VITAMIN A DEFICIENCY AND MORTALITY
Item
- Title
- VITAMIN A DEFICIENCY AND MORTALITY
- extracted text
-
RF_NUT_1_SUDHA
July 19, 1990
THE NEW ENGLAND.JOURNAL OF MEDICINE
160
A RANDOMIZED, CONTROLLED TRIAL OF VITAMIN A IN CHILDREN WITH SEVERE
MEASLES
Gregory D. Hussey, M.B., M.Sc.(Lond.), and Max Klein, M.B., F.C.P.fS.A.)
Abstract Background. Measles kills about 2 million
children annually, and there is no specific therapy for the
disease. It has been suggested that vitamin A may be of
benefit in the treatment of measles.
Methods. We conducted a randomized, double-blind
trial involving 189 children who were hospitalized at a re
gional center in South Africa because of measles compli
cated by pneumonia, diarrhea, or croup. The children (me
dian age, 10 months) were assigned to receive either
vitamin A (total dose, 400,000 IU of retinyl palmitate, given
orally; n = 92) or placebo (n = 97), beginning within five
days of the onset of the rash. At base line, the characteris
tics of the two groups were similar.
Results. Although clinically apparent vitamin A defi
ciency is rare in this population, the children’s serum reti
nol levels were markedly depressed (mean [xSEM],
0.405±0.021 m™oI per liter [11.6±0.6 nd per deciliter]),
and 92 percent of them had hyporetinemia (serum retinol
level <0.7 Mmol per liter [20 ng per deciliter]). Serum con-
centrations of retinol-binding protein (mean, 30.1 ±2.0 mg
per liter) and albumin (mean, 33.4±0.5 g per liter) were
also low. As compared with the placebo group, the chil
dren who received vitamin A recovered more rapidly
from pneumonia (mean, 6.3 vs. 12.4 days, respective
ly; P<0.001) and diarrhea (mean, 5.6 vs. 8.5 days;
P<0.00l), had less croup (13 vs. 27 cases; P = 0.03),
and spent fewer days in the hospital (mean, 10.6 vs. 14.8
days; P = 0.01). Of the 12 children who died, 10 were
among those given placebo (P = 0.05). For the group
treated with vitamin A, the risk of death or a major compli
cation during the hospital stay was half that of the control
group (relative risk, 0.51; 95 percent confidence interval,
0.35 to 0.74).
■
Conclusions. Treatment with vitamin A reduces mor
bidity and mortality in measles, and all children with severe
measles should be given vitamin A supplements, whether
or not they are thought to have a nutritional deficiency.
(N Engl J Med 1990; 323:160-4.)
EASLES remains a devastating disease, Tor
which specific therapy is lacking. Hopes for its
control and eventual eradication rest on immuniza
tion, but measles kills about 2 million children each
year1 and cripples an untold number through blind
ness2 and lung disease.3'4 The idea that vitamin A mayhave a protective effect in measles was first suggested
more than 50 years ago3 but was ignored until Barclay
et al.,1’ in a randomized clinical trial, found twice as
many deaths in the control group (12 of 92) as among
children given high doses of vitamin A (6 of 88).’'
Although the overall results did not reach statistical
significance, vitamin A was significantly protective in
the group under two years of age.6
That vitamin A should be of benefit in measles is
biologically plausible.7 Measles depresses serum levels
of vitamin A,8 " and hyporetinemia (a serum retinol
level below 0.7 Mmol per liter [20 Mg per deciliter]) is
associated with increased mortality from the disease,
particularly in children under two years of age."
In almost every known infectious disease, vitamin A
deficiency is known to result in greater frequency,
severity, or mortality.12 Increased susceptibility to in
fection was one of the first features of nutritional
vitamin A deficiency to be recognized,13 and even mild
deficiency appears to be associated with an increased
risk of pneumonia, diarrhea, and death in child
hood."’17 According to Scrimshaw ct al., “no nutri
tional deficiency in the animal kingdom is more
consistently synergistic with infection than that of
vitamin A.”12 They list nearly 50 studies (including 8
in humans) of diseases of bacterial, viral, or pro
tozoan origin in which vitamin A deficiency resulted
in increased frequency, severity, or mortality.12 In
fact, vitamin A is sometimes referred to as the “antiinfective” vitamin.18
We embarked on this study because measles is a
pressing problem in our part of the world19 and be
cause the results of Barclay et al.6 and the circum
stantial evidence appeared promising. Subsequently,
acting on the same evidence, the World Health Or
ganization recommended routine vitamin A supple
mentation for all children with measles in regions
where vitamin A deficiency was a recognized problem
and suggested that elsewhere “in countries where the
fatality rate of measles is 1% or higher it would be
sensible to provide vitamin A supplements to all chil
dren diagnosed with measles.”20 One difficulty with
this advice is that in the communities in which measles
poses the greatest problem, the mortality rate is often
unknown. Another is that the recommendation is
based on the less than conclusive evidence from the
only two studies to have addressed the question of
vitamin A therapy in measles.5,6 These are some of the
reasons why vitamin A supplementation is still not
given routinely to children who are seriously ill with
measles in South Africa, and presumably elsewhere.
M
From the Department of Baediatrks and Child Health. University of Cape
Town. Cape Town. South Africa. Address reprint requests to Dr. Klein at the Red
Cross War Memorial Children’s Hospital. Rondebosch 7700. South Africa.
Methods
Children with acute measles who required hospital admission for
the treatment of associated complications were entered in a ran
domized. double-blind, placebo-controlled trial to assess the effect
of oral vitamin A on morbidity and mortality. The study was limit
ed by a priori considerations to a fixed termination date, with a
maximal enrollment of 200 cases. It was conducted from March to
July 1987 al (he City Hospital for Infectious Diseases, a regional
center serving a population of about 2 million in Cape Town and
THE NEW ENGLAND JOURNAL OE MEDICINE
surrounding areas. The Medical Faculty’s ethics and research com
mittee approved the study protocol.
Patient Selection aod Randomization
All children under 13
quantify the chromatographic results (Spcctra-Phy^o. San Jose.
Calif.). Retinol-binding protein was measured by rz:..d immunodiffusion with a commercial kit (L(’-Partigen, Behnr«C"rrke, Mar
burg, Federal Republic of Germany). Chest radiograrS and other
investigations were performed when indicated.
Assessment of Outcomes
Patients in the trial
400.000 IL! (120 mg) ol
appropriate, but no additional vitamin supplements. One of the
Outcomes were assessed solely on the basis of (.•.aval criteria.
The outcome variables used were death and the seventh ol illness,
as indicated by the duration of the hospital stay, t.’.c duration of
pneumonia or diarrhea; the incidence of “.postmekLo" croup or
herpes stomatitis; and the need for a transfer to the Red Cross War
Memorial Children's Hospital for intensive care. Pneumonia was
defined as the presence of tachypnea (frequency of respiration >40
per minute) with retractions, crackles, or wheezes Diarrhea was
defined as the passage of four or more liquid stools a day. Measles
croup was defined as croup presenting on or within a day of admis
sion. Croup that developed subsequently was categorized as post
measles.
Statistical Analysis
Initial Investigations
The children's weight and height were recorded, and a venous-
for Health Statistics. 21 Hemoglobin levels, white-cell counts (by
Coulter model S5, Coulter Electronics, Hialeah, Fla.), and diflerential counts were estimated, and scrum was stored at — 70°C. Scrum
levels of total protein and albumin were measured by automated
analysis (Astra-8, Beckman Instruments, Brea, Calif.). Serum con-
The data were analyzed by computer with the Ept-1 nib program
(version 3, USD, Stone Mountain, Ga.). Categorical data2’ (e.g.,
the number of patients per group) were evaluated by die chi-square
test, with Yates' correction for continuity applied routinely,2’1 or by
Fisher’s exact test when the expected number in a cell was five or
less.24 Confidence intervals for the relative risks were calculated
according to the method of Greenland and Robins.2’ Continuous
data23 (e.g., vitamin level) were compared by the nonparamctric
Kruskal-Wallis test.23,2* All P values reported are tuo-tailcd, with
values of less than 0.05 considered statistically significant.
formancc liquid chromatography (Dupont Instruments, Wilming-
Results
A programmable integrator
Exclusion of Patients
Table 1. Base-Line Clinical findings in 189 Children with
Measles, According to Treatment Group.
*
Characteristic
Age (mo)
<6
6— 12
13-23
&24
Malc/fcmale
Mixed race/black
Weight for aget
<5th percentile
Height for agc+
<5th percentile
Weight for heightt
<5lh percentile
Rash (days)t
Diarrhea
No pneumonia
Pneumonia
No diarrhea
Pneumonia and diarrhea
Herpes stomatitis
Measles croup§
No. or
7
117
37
28
189
95
178
178
70
152
30
146
24
122
13
Placebo
(N = 97)
Vitamin A
(N « 92)
15.06 (8. 10, 15)
7
64
18
12
56/41
29/68
81.5 (74. 84, 92)
51
96.0 (93, 97. 100)
25
89.0 (82. 88. 95)
15.89 (8. 10. 17)
4
53
19
16
53/39
24/68
85.7 (77. 85, 96)
44
97.1 (93. 96. 101)
27
90.3 (84. 91. 97)
29
1.91 (1. 2, 2)
75
13
74
17
62
1
4
77
17
77
12
60
9
•Values in italics are means, followed in parentheses by 25th percentiles, medians, and 75th
percentiles All other v;dues are numbers of patients.
r Expressed as a percentage of the 50th percentile of the standards of the National Center fur
Health Statistics.
iP<0.05 for the comparison between groups.
5No patients with me asles croup required airway interventions
Of 224 patients under 13 years of age who were
admitted to the hospital with measles during the
study, 35 were excluded from the trial. In 12 of these
cases the rash was present for five or more days, in
2 vitamin A had previously been given, in 18 consent
could not be obtained because the child was unaccom
panied by a parent on admission, and in 3 the parents
refused consent. Hence, 189 patients were entered in
the trial. There were no exclusions for xerophthalmia
or withdrawals after entry.
Base-Line Characteristics
The placebo and treatment groups were generally
comparable (Tables 1 and 2), except that the patients
in the vitamin A group were admitted about 12 hours
earlier in terms of the duration of the rash and had
lower serum levels of total protein and albumin than
those in the placebo group. Two thirds of the children
were 12 months old or younger (median. 10 months;
range, 2 months to 5 years), and most were boys (58
percent). Blacks predominated (72 priccnt), and, the
remainder were of mixed race. The live white patients
admitted with measles were excluded: consent was re
fused in the cases of two, and three wcr<
*
more than 13
years old. The hospital is open to all. Immunization
and socioeconomic factors are thought tf) account for
differences in racial makeup between (l»«- study popu
lation and the general population H y
ars
*
of age or
■1__ i_
THE NEW ENGLAND JOURNAL OF MEDICINE
Table 2. Base-Line Blood and Serum Values, According
to Treatment Group.
July 19, 1990
under in Cape Town (57 percent
mixed race, 25 percent black, 18
percent white).27 Heights were not
Characteristic*
Patients
Placebo
Vitamin a
measured for 11 patients. Height
for age was below the fifth percen
mean (25lh. 50th. and 75th percentile)
tile in 52 children (29 percent) — a
Hemoglobin (g/dl)
177
10.73(10. 10.6. 11.5)
10.78(10, 10.5. 11.7)
prevalence similar to that in the lo
Hematocrit (%)
177
32.4 (30.32.5.35)
32.8 (30,32. 35)
cal reference population.211 Weight
Leukocytes (X 10“’/litcr)
177
8.63 (6.3. 7.7. 10.2)
8.99(6.2.8.15, 10.25)
for age (below the fifth percentile in
Lymphocytes (xl0"’/liter)
177
3.39 (2. 3.1, 4.2)
3.42(1.8. 2.9. 4.3)
50 percent), and weight for height
Total protein (g/litcr )1
155
58.54 (55. 57. 62)
53.94 (51. 54. 58)
(below the fifth percentile in 39
Albumin (g/litcr)t
34.5 (32,34. 37)
32.4 (29.33. 35)
percent) were considered to reflect
RBP (mg/liter)
156
29.6 (14. 18. 30)
30.48 (14. 17. 37)
Vitamin A (retinol) (/zg/dl)
156
12.19(7.7. 10.7, 14.4)
10.95 (6.7, 9 5. 12.6)
short-term weight losses from
131
12.84 (11.4, 15.1, 46.5)
Age <2 yr
II.1 (6.7.9.5.12 4)
measles211,3" rather than preexisting
25
Age >2 yrt
8.38 (7.1, 8.1, 10.5)
10.29(6.4. 10.5. 13.6)
acute prolein-energy malnutrition,
Hyporctinemia
143
68§
75§
since that occurs in 1 percent or less
Vitamin E (mg/liter)
156
7 94 (5.5. 7.8. 9.4)
6.84 (4.7. 6.8. 8 8)
of the local reference population.28
A combination of pneumonia and
diarrhea was the usual indication
retinol-binding protein. To convert grains of hemoglobin per deciliter to millimoles per liter, multiply by 0.6206; to convert
for hospital admission (64 percent).
micrograms of vitamin A per deciliter to micromoles per liter, multiply by 0.03491; and to convert milligrams of vitamin E
Diarrhea (16 percent), pneumo
tP<0.05 for the comparison between groups
nia (13 percent), or measles croup
(7 percent) appearing as isolated
symptoms precipitated the other
^Indicates the number of cases of hyporctinemia (scrum retinol concentration <0.7 jxmol per liter |20 pg per deciliter])
admissions.
No blood samples were obtained from 15 patients,
in the placebo group as in the vitamin A group
and only partial results were available for another 19
(P<0.001), and 66 percent of the children with chron
(Table 2). Serum levels were low for total protein
ic pneumonia (>10 days) were in the placebo group
(mean [±SE], 56.2±0.7 g per liter), albumin (mean,
(P = 0.008). Similarly, diarrhea continued for a third
33.4±0.46 g per liter), retinol-binding protein (mean,
longer in the placebo group (PC0.001), and 72 percent
30.1
±2.02 mg per liter), and vitamin A as retinol of the children with chronic diarrhea were in that
(mean, 0.405±0.021 /zmol per liter [11.6±0.6 /xg
group (P = 0.023). Postmeasles croup was more com
per deciliter]). Low levels of total protein principal
mon in the placebo group (P = 0.033), as was herpes
ly reflect depressed serum albumin concentrations
stomatitis (P = 0.08). Finally, the hospital stay of
(r2 = 72.6 percent, PC0.001). Serum retinol levels
the survivors was shorter by a third in the vitamin
were below the lower limit of the normal range (0.7
A-treated group (P = 0.004).
/zmol per liter [20 jig per deciliter]) in 92 percent of
Overall, 77 children had adverse outcomes (Table
the children (143 of 156), and 46 percent (72) had
3), of whom 52 were in the placebo group (P = 0.004).
levels below 0.35 /zmol per liter (10 pg per deciliter),
As compared with the children in the placebo group,
placing them at risk for xerophthalmia,31 although no
the children treated with vitamin A were at lower rela
tive risk for death (relative risk, 0.21; 95 percent confi
cases of this were observed. Vitamin E levels were in
the normal range.
dence interval, 0.05 to 0.94), prolonged pneumonia
2=10 days (relative risk, 0.44; 95 percent confidence
Outcome
interval, 0.24 to 0.80), prolonged diarrhea &10 days
(relative risk, 0.40; 95 percent confidence interval,
The children who received vitamin A had markedly
0.19 to 0.86), postmeasles croup (relative risk, 0.51; 95
diminished mortality and morbidity (Table 3), with
no clinically apparent adverse effects. Of the 12 chil
percent confidence interval, 0.28 to 0.92), airway in
dren who died (6.3 percent), 10 were in the placebo
tervention (relative risk, 0.35; 95 percent confidence
interval, 0.10 to 1.26), herpes stomatitis (relative risk,
group (P = 0.046). The children who died were 5 to
0.23; 95 percent confidence interval, 0.05 to 1.06), and
29 months of age, and seven were boys. Death oc
the need for intensive care (relative risk, 0.38; 95 per
curred 3 to 32 days after admission (median, 10.5).
Pneumonia3,32 caused 10 deaths, and the two remain
cent confidence interval, 0.13 to 1.16). The overall risk
for an adverse outcome in children treated with vita
ing children died after 15 and 32 days, respectively, of
min A was half that in the control group (relative risk,
fulminant sepsis following chronic diarrhea and mea
0.51; 95 percent confidence interval, 0.35 to 0.74). Of
sles-induced kwashiorkor. Croup was present as an
the 77 children who had adverse outcomes, only 2
incidental finding in 5 of the 10 children who died of
pneumonia.
were 3=2 years of age (P = 0.002), and the risk in a
Cases of pneumonia lasted almost twice as long
child ®2 years old was substantially lower than in
Vol. 323
No. 3
THE NEW ENGLAND JOURNAL OI- MEDICINE
Table 3. Mortality and Morbidity in 189 Children with Measles, According
to Treatment Group.*
163
treatment may reasonably be as
cribed to correction of the tissue
deficit
of vitamin A. We do not
Relative Risk
Placebo
(N - 92)
(95% CD
*
P Vai ue
(N « 97)
know, however, whether the deficit
Characteristic
was rectified by increases in the
0.21 (0.05-0.94)
2
0.046
10
Death
scrum retinol concentration or by
Age at death (mo)
0
<6
some other mechanism, since sc
rum retinol levels were not meas
i
13-23
ured after therapy.
1
0
>24
Hyporetinemia appears almost
Pneumonia (days)
6.53 (3. 5. 8.5)
<0.001
12.37 (5. 8. 17)
Duration
invariable in children with severe
0.44 (0.24-0.80)
>10
12
0.008
29
measles,811 as in this study, and
Diarrhea (days)
the reduction in the scrum retinol
5.61 (3. 5. 7)
<0.001
Duration
8.45 (5. 7. 10)
0.40 (0.19-0.86)
>10
0.023
21
level is associated with increasing
27
13
0.51 (0.28-0.92)
Postmcaslcs croup
0.033
ly severe disease." Since many of
0.35
(0.10-1.26)
9
3
0.16
With airway intervention
these data come from populations
2
0.23 (0.05-1.06)
0.08
9
Herpes stomatitis
in which nutritional vitamin A defi
0.38 (0.13-1.16)
0.13
Intensive care
ciency is a known problem,8’10 it has
0.51 (0.35-0.74)
<0.001
Adverse outcome?
52
25
been inferred that hyporetinemia
0.004
Hospital stay (days)§
15.24 (8. II. 19)
10.52 (7, 9. 13)
in measles represents the exhaus
tion of hepatic stores.6,7,20 There is
percentiles, medians, and 75th percentiles. All other values arc numbers of patients.
a possible alternative mechanism,
however. Hyporetinemia may oc
^Defined as death, pneumonia >10 days in duration, diarrhea >10 days in duration, postmexsles croup, or transfer for
cur in the presence of adequate he
SRefers to children who survived
patic stores of vitamin A when the
stores arc not mobilized fast enough
to meet demand.36 This has been found in fever, pneu
younger children (relative risk, 0.15; 95 percent confi
monia, rheumatoid arthritis, hepatitis, acute tonsil
dence interval, 0.02 to 0.91). No child with a serum
litis, and rheumatic fever36; in protein-energy mal
retinol concentration &0.7 /zmol per liter (20 /J-g per
nutrition38; and now also in measles.8 Inadequate
deciliter) died, but the smallness of this group (n =
mobilization of hepatic stores may therefore underlie
14) leaves the significance of the finding in doubt.
the hyporetinemia in children with severe measles
Discussion
from Kinshasa, Zaire," and Cape Town, where nutri
tional vitamin A deficiency is uncommon. A study
The results of our randomized, controlled trial indi
25 years ago showed vitamin A deficiency to be rare
cate a remarkable protective effect of vitamin A in
in Cape Town, even in children with severe protein
severe measles, notwithstanding the provision of good
energy malnutrition,38 and it still appears to be rare.
general medical care and the presence of complicated
A search of the computer data-base listing of inpa
advanced disease. Vitamin A reduced the death rate
tients at our children’s hospital, which predominantly
by more than half and the duration of pneumonia,
serves the local underprivileged community, found
diarrhea, and hospitalization by about one third. Vi
only three instances of clinical vitamin A deficiency
tamin A also appeared to reduce the incidence of her
among 161,381 children admitted over a 13-year peri
pes stomatitis and the need for intensive care. The
od, with no cases since 1985.
consistency of benefit with respect to all measures of
In view of the evidence that hyporetinemia may
outcome is noteworthy, since mortality is not a sensi
occur in the presence of adequate hepatic stores of
tive criterion. Because of their reliance on mortality
vitamin A38 and in populations not known to be defi
rates, previous studies of measles5,6 lacked the statis
cient in vitamin A," it would seem prudent to proceed
tical power to establish the benefit of vitamin A
therapy.
on the assumption that previous nutritional adequacy
may not ensure against the development of hyporctinThe favorable response to vitamin A therapy may
emia in severe measles. For all children seriously ill
be understood in terms of the very high incidence (92
with measles, vitamin A replacement should thus be
percent) of hyporetinemia in our patients (Table 2).
provided at the dose given by Barclay et al.6 (400,000
Hyporetinemia implies a state of vitamin A deficiency
at the tissue level, since there are virtually no periph
IU), which proved effective and safe in our study. A
eral-tissue stores of vitamin A except in the retina.33’36
lower dose (100,000 to 200,000 IU) is recommended
by the World Health Organization,20 but its efficacy in
Serum retinol levels below 0.7 ginol per liter (20 /xg
per deciliter) appear to be inadequate for the body’s
measles has yet to be established.
biologic needs.33 Oral vitamin A is absorbed well even
It may be asked whether it is cost effective to advo
in patients with diarrhea,37 so the observed effects of
cate treatment with vitamin A for all children with
THE NEW ENGLAND JOURNAL OF MEDICINE
severe measles. Clearly, children under two years of
age are at highest risk of an adverse outcome and
derive the most benefit from vitamin A. When re
sources are scarce, such children should be given pri
ority. In our study, however, half the children over
two years of age were at risk of xerophthalmia because
of serum retinol levels below 0.35 jumol per liter
(10 jig per deciliter),31 and hence they should have
vitamin A prophylaxis. Thus, when resources permit,
all children with severe measles should be given sup
plemental vitamin A.
We are indebted lo many colleagues for constructive criticism; to
Mr. R. Sayed, statistician to the Department of Community Health
preliminary analyses; to Glaxo (South Africa), for the donation of
our computer; to the nursing staff of the City Hospital for Infectious
Diseases for invaluable assistance and to the hospital’s medical su
perintendent, Dr. P.J.W. Roux, for providing facilities; to Mr. A.F.
Rodriques for searching the data base of patients of the Red Cross
War Memorial Children’s Hospital; to the medical superintendent,
Dr. R.O. Simpson, for giving access to the data base; to the McCauI
Bell Bequest of the Institute of Child Health, University of
Cape Town, for a grant to Professor H. de V. Hcesc that provided
funding for the assays of vitamins and retinol-binding protein; and
to Ms. Frances Pocock for performing these assays in the Institute
laboratory.
References
Grant JP. The state of the world's children. 1988. Oxford: Oxford Universi
ty Press. 1988:3.
Foster A. Sommer A. Childhood blindness from comcal ulceration in Afri
ca: causes, prevention, and treatment. Bull World Health Organ 1986;
64:619-23.
Warner JO, Marshall WC. Crippling lung disease after measles and adeno
virus infection. Br J Dis Chest 1976; 70:89-94.
Kaschula RO. Druker J, Kipps A. Late morphologic consequences of mea
sles: a lethal and debilitating lung disease among the poor. Rev Infect Dis
1983; 5:395-404.
Ellison JB. Intensive vitamin therapy in measles. BMJ 1932; 2:708-11.
Barclay AJG, Foster A. Sommer A. Vitamin A supplements and mortality
related to measles: a randomised clinical trial. BMJ 1987; 294:294-6.
Vitamin A for measles. Lancet 1987; 1:1067-8.
Reddy V, Bhaskaram P. Raghuramulu N. ct al. Relationship between mea
sles. malnutrition, and blindness: a prospective study in Indian children. Am
J Clin Nutr 1986; 44:924-30.
Inua M. Duggan MB. West CE, et al. Postmeasles corneal ulceration in
children in northern Nigeria: the role of vitamin A. malnutrition and mea
sles. Ann Trap Pacdiatr 1983; 3:181-91.
Varavithya W. Stoecker B. Chaiyaratana W. Kittikool J. Vitamin A status
of Thai children with measles. Trap Gcogr Med 1986; 38:359-61.
Markowitz LE. Nzilambi N, Driskell WJ. et al. Vitamin A levels and
mortality among hospitalized measles patients. Kinshasa. Zaire. J Trop
Pediatr 1989; 35:109-12
July 19, 1990
12. Scrimshaw NS, Taylor CE, Gordon JE. Interactions of nutrition and infec
tion. WHO monograph series no. 57. Geneva: World Health Organization,
1968.
13. Lassen HCA. Vitamin A deficiency and resistance against a specific infec
tion: preliminary report. J Hyg (Lond) 1930; 30:300-10.
14. Milton RC. Reddy V, Naidu AN. Mild vitamin A deficiency and childhood
morbidity — an Indian experience. Am J Clin Nutr 1987; 46:827-9.
15. Sommer A, Katz J, Tarwotjo I. Increased risk of respiratory disease and
diarrhea in children with preexisting mild vitamin A deficiency. Am J Clin
Nutr 1984;40:1090-5.
16. Sommer A. Tarwotjo I, Hussaini G. Susanto D. Increased mortality in
children with mild vitamin A deficiency. Lancet 1983; 2:585-8.
17. Sommer A, Tarwotjo I, Djunacdi E, etal. Impact of vitamin A supplementa
tion on childhood mortality: a randomised controlled community trial. Lan
cet 1986; 1:1169-73.
18. Green HN, Mcllanby E. Vitamin A as an anti-infective agent. BMJ 1928;
2:691-6.
19. Reynolds LG, Hussey G, Kettles AN. Continuing scourge of measles. S Afr
Med J 1987; 71:611.
20. Expanded programme on immunization- programme for the prevention of
blindness nutrition. Joint WHO/UNICEF statement: vitamin A for measles.
Wkly Epidemiol Rec 1987; 62:133-4.
21. Hamill PV. Drizd TA. Johnson CL. Reed RB. Roche AF, Moore WM
Physical growth- National Center for Health Statistics percentiles. Am J Clin
Nutr 1979; 32:607-29.
22. Catignani GL, Bicri JG. Simultaneous determination of retinol and alpha
tocopherol in serum or plasma by liquid chromatography. Clin Chem 1983;
29:708-12.
23. Rosner B. Fundamentals of biostatistics. 2nd ed. Boston: Duxbury Press,
1986.
24. Siegel S. Nonparametric statistics for the behavioral sciences. New York:
McGraw-Hill, 1956.
25. Greenland S, Robins JM. Estimation of a common effect parameter from
sparse follow-up data. Biometrics 1985; 41:55-68.
26. Behrman RE. Vaughan VC III. Nelson WE. Nelson textbook of pediatrics.
13th ed. Philadelphia: W.B. Saunders, 1987.
27. Central Statistical Services, Pretoria. Population Census 1985. Report no.
02-85-02. Pretoria, South Africa: Government Printer, 1986.
28. Hugo-Hamman CT, Kibel MA, Michie CA, Yach D. Nutrition status of
pre-school children in a Cape Town township. S Afr Med J 1987; 72:353-
29. Axton JH. Measles and the state of nutrition. S Afr Med J 1979; 55:12530. Morley D. Paediatric priorities in the developing world. London: Butter
worths, 1973:207-30.
31. Vitamin A deficiency and xerophthalmia: Report of a joint WHO/USAID
meeting. WHO Tech Rep Ser 1976; 590:1-88.
32. Kipps A, Kaschula RO. Virus pneumonia following mcasles:.a virological
and histological study of autopsy material. S Afr Med J 1976; 50:10838.
33. Olson JA. Vitamin A, retinoids, and carotenoids. In: Shils ME, Young VR,
eds. Modem nutrition in health and disease. 7th ed. Philadelphia: Lea &
Febiger, 1988:292-312.
34. Pitt GA. The assessment of vitamin A status. Proc Nutr Soc 1981; 40:173-8.
35. Olson JA. Metabolism of vitamin A. Biochem Soc Trans 1986; 14:928-30.
36. Barker BM. Vitamin A. In: Barker BM, Bender DA, eds. Vitamins in
medicine. Vol. 2. 4th ed. London: Heinemann, 1983:211-90.
37. Molla A, Islam A. Molla AM. Jahan F. Change in scrum vitamin A concen
tration after an oral dose in children with diarrhea. J Pediatr 1983; 103:1000-
38. KonnoT, Hansen JD, Truswell AS, Woodd-Walker R, Becker D. VitaminA deficiency and protein-calorie malnutrition in Cape Town. S Afr Med J
1968; 42:950-5.
IWT (
Research from the South
Vitamin A supplements and mortality related to measles:
a randomised clinical trial
ANDREW J G BARCLAY,
ALLEN FOSTER,
Abstract
One hundred and eighty children admitted with measles were
randomly allocated to receive routine treatment alone or with
additional large doses of vitamin A (200 000IU orally immediately
and again the next day). Baseline characteristics of the two
groups were virtually identical for age, severity of measles, and
vitamin A and general nutritional states. In 91% of the children
serum vitamin A concentrations were less than 0-56 umol/1. Of
the 88 subjects given vitamin A supplements, six (7%) died; of the
92 controls, 12 (13%) died (p=0-13). This difference in mortality
was most obvious for children aged under 2 years (one death out
of 46 children receiving supplements versus seven deaths out of
42 controls; p<0-05) and for cases complicated by croup or
laryngotracheobronchitis. Mortality was several times higher in
marasmic than in better nourished children, regardless of study
allocation (p<0-01).
ALFRED SOMMER
nourished children to less than those observed in non-infected
malnourished children.’-’ Measles probably increases utilisation of
vitamin A, and children with marginal liver stores of the vitamin
may thus develop acute vitamin A deficiency, resulting in eye
damage and possibly increased mortality from respiratory and
diarrhoeal causes. Indeed, measles is an important risk factor in the I
development of severe vitamin A deficiency and xerophthalmia in
Asia.” 14 It is also a particularly virulent disease among African
children, accounting for most cases of childhood blindness and for
considerable mortality.10 " 1517 Recent data suggest that vitamin
A deficiency may be prevalent in areas of Africa, including
Tanzania.16
This hospital based study sought to determine the effect of high
dose vitamin A supplements taken during early infection with
measles on subsequent mortality in African children.
Patients and methods
Introduction
Recent reports from Indonesia have shown that children with
clinically mild vitamin A deficiency have a fourfold increase in
mortality from all causes- and a threefold increase in the incidence
of respiratory and diarrhoeal diseases.-’ Vitamin A supplements
reduced preschool age childhood mortality by over 30%.' After
reviewing some 50 reports of the effect of vitamin A deficiency on
bacterial, viral, protozoal, and helminthic infections in man and
animals Scrimshaw et al concluded that “no nutritional deficiency is
more consistently synergistic with infectious disease than that of
vitamin A.”' At the time that they wrote this they were unable to
find data concerning the interaction between vitamin A and
measles.
Vitamin A is essential for the maintenance of normal epithelial
tissues throughout the body. In the absence of vitamin A mucosal
epithelium undergoes squamous metaplasia, with a concomitant
decrease in cell turnover.Measles is a viral disease that infects
and damages epithelial tissues throughout the body."’ " The
disease can also decrease serum concentrations of vitamin A in well
Mvumi Hospital, Dodoma, Tanzania
ANDREW J G BARCLAY, mb, dtch, chief of paediatrics
ALLEN FOSTER, MD, frcs, chief of ophthalmology
International Center for Epidemiologic and Preventive Ophthalmology, Dana
Center, Wilmer Eye Institute and School of Public Health, Johns Hopkins
Medical Institutions, Baltimore, United States
ALFRED SOMMER, MD, director
Correspondence and requests for reprints to: Dr A Sommer, Wilmer 120, Johns
Hopkins Hospital, Baltimore, MD 21205, United States.
Mvumi Hospital is a rural general hospital in central Tanzania relatedle
the church. Paediatric patients are drawn almost entirely from the local
population, which comprises subsistence farmers living in a fairly arid
environment. The staple diet is millet eaten with a green vegetable relish. 1
There is only one harvest a year, in April to May, and that is dependents
good rains. The rains in 1982 were very bad. leaving conditions of near
famine for many, but the rains and harvest in 1983 were good. Malnutrition i
is a great problem in children. About a quarter of all children admitted an
severely malnourished, and only 30% have a weight for age above 80% of th:
standard.-’" Anaemia is also common. The general paediatric background is
more fully described elsewhere i A J G Barclay., unpublished).
We attempted to include in this study every child with measles presenting i
to the hospital from September 1982 to November 1983, a period that |j
included an entire measles season. Measles was diagnosed on clinical I
grounds that included a history of prodromal disease and the presence of J •
typical rash. On admission all children were given a full clinical examination [
by the paediatrician. Shortly after admission they were seen by a member oi >
the eye department. They were all weighed and measured by the nurses and i
had their haemoglobin concentration measured and a blood slide examined'
by staff in the hospital laboratory.
A venous blood sample was taken on admission for estimation of vitamin
A state. Half of the subjects were then randomly allocated to receive vitamin'
A (200000 IU in oil orally immediately and again the next day); the othtf •
children were given standard treatment. Randomisation was accomplished I
by sequential assignment of single digits from a random numbers table, odd j
digits dictating one group and even the other. Which children received i
vitamin A was known to the paediatrician but not recorded in the gener-y |
notes: study allocation was therefore not known by any other staff dealing ■
with care of the children. Other main therapeutic sources of vitamin A-~l°f
example, multivitamins —are not routinely given and therefore were
received by any children in the trial. The two groups were treated identical ;
in the ward, fed the same diet, and given antibiotics or further investigate I
as indicated by their clinical condition.
Deaths caused by measles were taken to be deaths occurring within one
month of onset of the rash. Most patients were still in the ward when thtf p
died; three returned of their own accord and were readmitted with dysentetf I
or diarrhoea and died quickly and two ran away moribund and died at horn
*I
295
R.selinc blood samples were allowed to clot and were then spun down.
, serum "’3S separated and stored in a deep freeze within four hours of
V- c the sample. The serum was later shipped to Baltimore, where
• .e'nmidon"°f vitamin A (as retinol) was measured by high performance
ehromatography. 2’ Because of losses in transport biochemical
Jjtern'inat*ons are available for only 38 recipients of vitamin A and
<7 control5 ■
1 A the study was designed to assess the beneficial impact of vitamin A
'• 0|cments, and there was no biological, clinical, or epidemiological reason
su'!s\ispect any deleterious effects from added vitamin A, results were
Io. .^j with a single tail normal deviate (z) and Fisher’s exact test.
TABLE in—Complications and associated mortality
No (%) of children with
complications
No ■ % of children who died
Complication
vitamin A
Controls
vi tamin A
Pneumonia
Otitis media
Croup or
laryngotracheobronchitis
Dysentery
Haemorrhagic rash
Oral candidiasis
38(43)
19(22)
47(51)
20(22)
3 S,
i S:
7(15)
3(15'
8 (9)
2 (2)
28(32)
9(10)
13(14)
6 (7)
34(37)
5 (5)
i(50;
1 (4)
1(11)
4(3!)
3(50)
4(12)
1(20)
Controls
Jesuits
• Two hundred and twelve patients with measles were admitted during the
Thirty two were excluded from the trial, all but six before randomisa. D because of corneal ulcers (seven patients, who were automatically given
vitamin A and are reported on separately2-’); death within 24 hours of
^mission (five); running away within 24 hours (one); receiving vitamin A
before admission (nine); and admission while rhe study coordinator was
absent (10)- Of the ISO children in the trial, 11 did not have their height
recorded and 15 did not have their haemoglobin concentration measured.
The distribution of baseline characteristics of recipient and control
children was similar, including age (mean recipient 29-5 v mean control 30'7
months), weight for age (72% c 75% of standard), weight for height (83% v
J6% of standard), haemoglobin concentration (85 v 89 g/1), interval between
onset of rash and admission (3
*5
o 3*4 days), and scrum vitamin A
conceUEtion (0 30 v 0-32 umol/1). Only 9% of patients had serum vitamin
A coa^bations greater than 0-53 umoL 1.
S8 children given vitamin A, six (7%) died (table I). Of the 92
controls, 12 (13%) died. Despite the large clinical difference small numbers
■ imiit its significance (p=0-13). The difference was most obvious for children
aged under 2 years (p<0-05).
TABLE 1—Mortality of children admitted with measles
Aje
'months)
vitamin A
Controls
<9
9-11
17.73
24-35
36-47
48-59
560
14
12
20
]]
]]
9
10
23
16
13
12
15
Total
88
vitamin A
1 15'
2 t 77'
1 .9>
1(13)
2(22)
2(20)
3(13)
2(13)
1 iS)
2(13)
6 17)
12(13)
1
Twem. five children (14%) were marasmic, and 104 (58%) were
underweight as assessed by weight for age (table II). The mortality of
tMrasmic children was several times higher than that of better nourished
children. regardless of whether they had received vitamin A or not (p<001,
tailed resit In every nutritional category mortality was lower for vitamin
•'recipients.
Complications, usually already present at the time of admission, were
dually common in the two groups, but mortality from such complications
higher in the control group (table III). Pneumonia was the commonest
complication, affecting 85 children. Croup complicated measles in 13 of the
n—ITcigArfor age and mortality
1
No of.children in study
No (%) who died
vitamin A
Controls
vitamin A
Controls
Total
■u
47
17
27
Sl
8
1 (4)
I (21
4(24)
3(H)
6(11)
3(38)
4 (8)
7 (7)
7(28)
Total
92
6 (7)
12(13)
88
---------P°"”aSe or median National Center for Health Statistics standard.19
18(10)
60.^o
control group, of whom four (31%) died; in contrast, of eight children with
croup given vitamin A, none died. Very few children had dysentery; of those
who did, half died.
Discussion
Children randomised to receive vitamin A did not differ from the
control group in baseline age, nutritional state, duration of illness,
prevalence of complications, or haemoglobin or serum vitamin A
concentrations. Mortality was twice as high in the control group as
in the treated group, almost all of the difference being accounted for
by children aged under 2 years (p<0-05).
Although the numbers were small, there was a remarkable
consistency in the beneficial impact of vitamin A supplements on
complicating illness and nutritional strata. This was especially
obvious among children with croup or laryngotracheobronchitis.
No child who received vitamin A died of laryngotracheobronchitis,
whereas four in the control group died. Laryngotracheobronchitis is
a particularly difficult condition to treat with limited resources.
Because repair of epithelial surfaces in children with early vitamin A
deficiency may be poor, with a tendency to develop into squamous
metaplasia of the respiratory tract,” they may suffer increased
susceptibility to laryngotracheobronchitis or its consequences.
Malnutrition is common in and around Mvumi, and the nutri
tional state of this study group is not atypical of general paediatric
admissions. Children with low weight for age and weight for
height, not shown) had the highest mortality in both study groups.
Recent community studies have shown a varying relation between
premorbid general nutritional state and death from measles, but
most dealt with milder disease/’-’* Schrimshaw et al noted a
decrease in mortality from measles in children fed a vegetable
extract rich in protein that may have contained considerable
amounts of vitamin A.27 In our study vitamin A recipients suffered
lower mortality in every nutritional stratum.
The vitamin A concentrations among the children in our study
were all very low, much lower than that reported by workers in
Nigeria.12 This is explained partly by the different analytical
methods, populations, and diet. Tielsch and Sommer found that
children with vitamin A concentrations of less than 0'53 ttmol.l, a
category that would include over 90% of our study group, were at
very high risk of developing corneal ulcers.11
Vitamin A deficiency may be a large factor in determining the
outcome of measles in Africa, just as it seems to affect morbidity and
mortality in Asia.11 When a child with marginal vitamin A stores
gets measles available vitamin A is quickly depleted, presumablyreducing the ability to resist secondary infections or their conse
quences, or both.2’12 This would exacerbate the already reduced
immunocompetence thought to be associated with measles infec
tion.”
Further trials in different parts of Africa are urgently needed to
define the role of vitamin A deficiency in measles morbidity and
mortality and the importance of vitamin A supplements in their
control.
We thank Ms Agatha Rider for analysing the serum vitamin A concentra
tions. This study was partly supported by cooperative agreement No 0267
296
BRITISH MEDICAL JOURNAL
VOLUME 294
31 JANUARY
between the office of nutrition, United States Agency for International
Development, and the International Center for Epidemiologic and Preven
tive Ophthalmology.
■tphthalmii;
childhood corneal ulceration. Bull WHO fin pr
over A. Sommer A. Cornell ulceration, measles and childhood blindncs
Ophthalmol (in press).
. EurrA/r.UedJ 1977:54:3M-
nutrition and mortality in Bangladesh. Bull WHO 1981;59:901-8.
**
aby P, Hukh J, Lisse IM, Smits AJ. Measles mortality, state of nutrition and family siruciur
community study from Guinea-Bissau. 7 Infect Du 1983:147:693-701
26 Aaby P, Bukh J, Lisse IM, a al. Determinants of measles mortality in a rural area of Guit
Bissau: crowding, age, and malnutrition..? TropPcdiatr 1984;30:164-8
27 Scrimshaw NS, Salmon JB, Bruch HA. Gordon JE. Measles, diarrhoea and nutritional deficit
in the germ free
30 Kochanowski BA, Ross AC. Stimulation of humoral immunity by vitamin A during suckling^
post weaning in the rat. 7 SuirCtn press).
I975;iii 522.
MATERIA NON MEDICA
On the beach
The lights of Ardcniinny across the waters of Loch Long go out one by one as
the bleak November evening moves imperceptibly into night. Now and
again a gap in the blackness above allows moonlight to sparkle on the lapping
waves, a welcome relief from the soaking northerly squalls that chill and
dishearten. On the foreshore a dozen oyster catchers are busily feeding as the
tide ebbs. No sign of the rafts of ciders or the shags or even the gulls so
conspicuous by day. A Scottish sea loch has its charms even on a winter’s
night.
But this is no birdwatchers’ outing. This is Coulport beach, right next to
the naval base that will act as home to Britain’s Trident submarines. We are
fiu^iembers of the local peace group who have chosen to spend a Friday
here. Our vigil is peaceful bur not silent. We sing hymns, we chatter,
and the laughter pervades even those dreaded small hours which the doctor
on call knows and hates so keenly. We watch the comings and goings of the
base and the swarms of Ministry of Defence police—and they in turn watch
us, bin in a much more sophisticated way. Though we speak to two
policemen, we are unable to speak to the majority of the workers as they are
bussed in and out, and our protest is made simply by our presence.
Dawn slowly creeps over the pines, and the birds return. The day shift
replaces the night shift and it is time to extinguish the driftwood fire.
Have we changed anything? Nuclear weapons are an emotive issue. For
those of us who see them as the greatest danger to public health of our time it
is vital to protest, and I remember Edmund Burke’s words: “Nobody made a
greater mistake than he who did nothing because he could only do a little.”
At the very' least, for a short while we were at peace with our consciences.—
KENNETH F mclean, Denny, Stirlingshire.
Music buffs
Orpington has culture. Never mind that it has little history'. In fact Queen
Elizabeth I stayed at the manor once, and there is the Buff Orpington
chicken, but until rhe railway was electrified it was only a small place,
mentioned in the Domesday Book but overshadowed by the neighbour
which it now dwarfs, St Mary Cray. Today it is a pleasant middle class
dormitory suburb, perhaps slightly less refined than Petrs Wood, with a fast
train to London taking a mere 20 minutes, but only three miles from the real
country—at least until the green belt is raped by the mushrooming plans for
houses and out of town leisure precincts with which the developers hope to
fill the green fields between us and rhe M25.
Opposite our house is St Olave’s School, relocated from the shadow of
Southwark Cathedral. The hall, with its brick columns, gallery, and,
clerestoried root, has excellent accoustics and lor some lime now it has been
the setting fora yearly recital programme featuring world famous musicians.
You buy a ticket for the whole scries, and it is always sold out. There is
always a wonderful flower arrangement on the stage (our next door
neighbour docs them). To get the seat of your choice you must appear
early—up to an hour early—and recently we were seated in the gallery for the
first time to hear the Takacs String Quartet play Haydn and Bartok and then,
with Michael Collins, Brahms’s Clarinet Quintet in B Minor, with a little
Mozart for an encore. It was a superb performance, but you come to expect
this at St Olave’s. We are lucky. Not many people can boast fine concerts less
than a minute from their house.
It is interesting to observe a large audience from above. You can spot the
people you know, run a detailed survey of the incidence of pattern baldness,
watch the smaller children growing weary, and, above all, sense the
absorption and enjoyment of a crowd in a way which is impossible when you
arc within it. The audience was spellbound by the Brahms and the Haydn.
Not a cough barked, not a programme rustled. But Bartok’s String Quarid
A’o 4 is not easy listening, and during that the throng seethed, wriggled, and
fidgeted. There was manifest discomfort.
Oh yes, Orpington has culture. But perhaps it is not quite ready for
Bartok.—Andrew bamji, Orpington.
Some hosts ask their guests to take off their shoes when entering a carpeted hot#Does this increase the spread of tinea pedis. What discreet prophylactic measu#
are recommended?
>
Whereas this is clearly the subject for a fascinating study, there is lit^
information on the risks of transferring desquamated but infected skin scafc
to others via a carpet. Clearly many of the skin scales are exfoliated onjj
socks and into footwear and provided that socks are worn these showprovide some sort of a barrier. One study from Belgium suggested tb'
carpets were a potential source of desquamated hair from cats with ring
!
*®
infection.1 The actual proof, however, that shed hairs could cause infec^
in members of the household is difficult to establish. Presumably, the
prophylaxis is that if guests are asked to take their shoes off they should'
*
persuaded to leave their socks on.—R J hay, consultant dermatoloS1*
London.
jj
I De Vroey C. Epidemiology of ringworm (DermalophyrosisX Seminars in Dermatology ISSS'?-1^
The New England
Journal of Medicine
©Copyright. 1990, by the Massachusetts Medical Society
Volume 323
OCTOBER 4, 1990
Number 14
REDUCED MORTALITY AMONG CHILDREN IN SOUTHERN INDIA RECEIVING A SMALL
WEEKLY DOSE OF VITAMIN A
Laxmi Rahmathullah, M.B., B.S., D.T.P.H., Barbara A. Underwood, Ph.D.,
Ravilla D. Thulasiraj, M.B.A., Roy C. Milton, Ph.D., Kala Ramaswamy, M.Sc.,
Raheem Rahmathullah, and Ganeesh Babu, B.Com.
Abstract Background. Clinical vitamin A deficiency af
fects millions of children worldwide, and subclinical defi
ciency is even more common. Supplemental vitamin A has
been reported to reduce mortality among these children,
but the results have been questioned.
Methods. We conducted a randomized, controlled,
masked clinical trial for one year in southern India involv
ing 15,419 preschool-age children who received either 8.7
Mmol (8333 III) of vitamin A and 46 Mmol (20 mg) of vita
min E (the treated group) or vitamin E alone (the control
group). Vitamin supplements were delivered weekly by
community health volunteers who also recorded mortality
and morbidity. Weekly contact was made with at least 88
percent of the children in both study groups. The base-line
characteristics of the children were similar and document
ed a high prevalence of vitamin A deficiency and undernu■ trition.
Results. One hundred twenty-five deaths occurred, of
which 117 were not accidental. The risk of death in the
group treated with vitamin A was less than half that in the
control group (relative risk, 0.46; 95 percent confidence
interval, 0.30 to 0.71). The risk was most reduced among
children under 3 years of age (6 to 11 months — relative
risk, 0.28; 95 percent confidence interval, 0.09 to 0.85; 12
to 35 months — relative risk, 0.46; 95 perebnt confidence
interval, 0.26 to 0.81) and among those who were chron
ically undernourished, as manifested by stunting (relative
risk, 0.11; 95 percent confidence interval, 0.03 to 0.36).
The symptom-specific risk of mortality was significantly
associated with diarrhea, convulsions, and other infectionrelated symptoms.
Conclusions. The regular provision of a supplement of
vitamin A to children, at a level potentially obtainable from
foods, in an area where vitamin A deficiency and under
nutrition are documented public health problems contribut
ed substantially to children's survival; mortality was re
duced on average by 54 percent. (N Engl J Med 1990;
323:929-35.)
WENTY to 40 million children worldwide are
estimated fo have at least mild vitamin A defi
ciency, and nearly half are said to reside in India.'
Controlled field trials in an area of endemic vitamin
A deficiency in Indonesia revealed a reduction of
34 percent in mortality among infants and young
children given high-dose vitamin A supplements,2
and a reduction of up to an estimated 75 percent3
after periodic mass treatment with large-dose (209
Mmol [200,000 IU]) vitamin A. Reductions in mor
tality of 11 to 45 percent were reported after the nor
mal marketing of vitamin A-fortified monosodium
glutamate.4 The results of these studies and an earlier
observational trial in Indonesia5 have been questioned
because of aspects of the study designs6 and because
the mortality data provided no cause-specific infor-
mation and were obtained retrospectively, assuming
compliance.4
Clarifying the role of vitamin A deficiency in child
health and survival and defining successful, sustain
able control measures have broad public health, pub
lic policy, and programmatic importance. For this rea
son, we conducted a randomized, placebo-controlled,
masked clinical trial among 15,419 preschool-age chil
dren using a small, weekly dose of vitamin A (8.7
Mmol [8333 IU]) given directly to the children by
community health volunteers. We monitored morbid
ity and mortality weekly for one year. The dose of
vitamin A was meant to simulate the amount that
could be obtained from food, if food consumption was
near the level recommended by international groups
(approximately 1 to 1.4 Mmol [300 to 400 Mg] of vita
min A daily7,8).
T
From the Aravind Children's Hospital and Aravind Eye Hospital, Madurai.
India (L.R.. R.D.T., K.R., R.R. G.B.); the Office of International Programs
(B.A.U.) and the Biometry and Epidemiology Program (R.C.M.), National Eye
Institute. Bethesda. Md. Address reprint requests to Dr. Underwood at the Na
tional Eye Institute. Bldg. 31. Rm. 6A-17, 9000 Rockville Pike. Bethesda. MD
20892.
Supported by a grant from the Ford Foundation, New Delhi, India.
Methods
The study was carried out in three drought-prone, economically
and environmentally deprived panchajat unions (local-government
areas) in the Trichy district of Tamil Nadu in southern India. The
people of the area had been underserved by child-care programs,
including the national program of administering a large-dose (209
930
THE NEW ENGLAND JOURNAL OF MEDICINE
Mmol) supplement of vitamin A every six months. A survey of all
children under 60 months of age in the study area revealed that only
1 percent had participated in this program.
The study was reviewed and approved by the human-subjects
internal review boards of the Indian Council of Medical Research
and the Aravind Eye Hospital. Informed consent was obtained from
the leaders of the panchayal unions and then from the individual
families at the time of the base-line survey.
Survey Personnel and Procedures
All the communities within the areas selected for study were
mapped by locally recruited enumerators. A house-by-house demo
graphic and socioeconomic survey was carried out by specially
trained local workers
*
who also obtained from each mother a fiveyear history of mortality among her preschool-age children. House
holds with children under 60 months of age were identified and
assigned a census number.
Two medical-examination teams were formed, consisting of a
medical officer, nurses, and child-care and social workers. The
child-care and social workers were trained to undertake ocular ex
aminations, anthropometric measurements, and a morbidity histo
ry. The ocular examination was checked by the medical officer who
conducted the medical examination and verified the morbidity his
tory. The ocular examination was repeated by the same trained
fieldworkers after six months of intervention, and all the indexes
measured at base line were reassessed by the medical teams at the
end of the study.
A finger-prick blood sample and a dietary history detailing the
frequency of intake of locally available foods containing vitamin A9
were obtained from a randomly selected 2 percent of the children by
specially trained community workers.
At the base-line medical examination, all the children with symp
toms of xerophthalmia, including night blindness, were treated with
a large-dose combination of vitamin A (209 Mmol) and vitamin E
(46 Mmol), and they’ continued to be followed as part of the study.
The data were analyzed both including and excluding them. Chil
dren with symptoms of xerophthalmia at the six-month and final
ocular examinations were treated in a similar manner. All the chil
dren were given the large-dose supplement during their final medi
cal examination at the end of the study.
The children’s height (or length for those under 24 months) was
measured to the nearest centimeter with a calibrated board. Weight
was determined to the nearest 0.1 kg with a hanging Salter scale.
The ocular examination was performed with the classification
criteria of the World Health Organization.10 A history of night
blindness was obtained by interviewing the mother about the inci
dence in her children of malai ken, a term used in Tamil Nadu to
describe the commonly recognized symptom of “evening eyes,” the
inability to see well in dim light. The same term was subsequently
used by the community health volunteers to monitor the occurrence
of night blindness on a weekly basis.
Fieldworkers were aware that they were involved in a study to
determine the effect on morbidity of giving vitamins, but they were
not told that the study was specifically one of vitamin A or that
mortality was an outcome variable.
Randomization
Because of the varied population density in the panchayal unions,
we used a cluster-sampling design. From the 15,419 children identi-'
fied and examined at base line, 206 clusters were formed on the
basis of the minimal and maximal workloads that could be expected
from the community health volunteers. The majority of clusters
consisted of 50 to 100 children 6 to 60 months of age. The clus
ters were arranged according to population size; after a ran
dom start, they were assigned alternately to the treated or control
groups. The adequacy of randomization in achieving matching
according to base-line data was checked for the following char
acteristics: age and sex distribution, onc-month history' of di
arrhea and respiratory disease, anthropometric indexes of nu
tritional status, xerophthalmia status, five-year retrospective history
of mortality of children under five, household economic and
Oct. 4, 1990
hygienic status, and serum retinol levels. Matching was satisfactory
at base line for all the variables examined.
Implementation and Management
Community health volunteers were trained to dispense the sup
plement, collect morbidity data, and record mortality according to a
standard procedure. The volunteers visited each home assigned to
them every week for 52 weeks. During the visits they recorded ill
nesses according to symptoms and duration and checked for any
deaths. They dispensed the appropriate liquid supplement directly
into the mouth of the study child from a calibrated, color-coded
amber bottle. Community health volunteers knew that they were
responsible for dispensing from one color-coded bottle, but they
were unaware of what it contained other than vitamins.
Trained supervisors were each assigned to oversee seven or eight
community health volunteers. The supervisors were responsible for
weekly meetings with the volunteers to verify the completeness of
the morbidity-data forms for the previous week and to review their
proper use. The supervisors also collected the dispensers each week
and distributed refilled bottles. In addition, they checked the accu
racy of the data gathered from a random 5 percent of the house
holds weekly.
A block officer met every week with the supervisors to review the
forms and procedures, discuss problems, and provide refilled bottles'
for delivery to the community health volunteers. The supervisors
were informed weekly of the performance — in terms of rates of
contact and accuracy in data recording — of the community health
volunteers for whom they were responsible. Evidence of problems
was sought and the difficulties were remedied within a two-week
period. Unannounced spot checks on households were conducted by
block officers and headquarters staff.
Data were verified and then recorded on diskettes with use .of
portable computers in the field offices. The diskettes were sent week
ly to the headquarters office, where they were again checked for
completeness and accuracy. The procedures for personnel and data
management allowed close surveillance and a two-week feedback to
the field staff regarding their performance, thus giving them time to
correct any possible errors.
Supplements
Liquid supplements (kindly provided by Hoffmann-LaRoche,
Basel, Switzerland) were provided in color-coded aluminum cans
containing approximately 1 liter each. The appearance and taste of
the solutions were identical. The solution containing vitamin A was
prepared to contain, approximately the following: 8.7 Mm°l (8333
IU or 2500 Mg) of vitamin
palmitate and 46 Mmol (20 mg) of
vitamin E per milliliter dissolved in peanut oil. The placebo solution
contained approximately 46 Mmol (20 mg) of vitamin E per millili
ter dissolved in peanut oil.
The stability of the solutions was checked by HoffmannLaRoche initially and after I, 3, 6, and 12 months of storage, at
room temperature, 35°C, and 45°C, in both the dispenser bottles
and the aluminum flasks. In the flasks there was no loss of vitamin
A and about a 10 percent loss of vitamin E, and in the bottles there
was a loss of less than 5 percent of vitamin A after one year or less at
room jemperature and at 35°C. Stability was also checked by ran
domly withdrawing dispensers from the study areas halfway
through and at the end of the study. The field-laboratory analyses,
done approximately 18 to 24 months after the supply had been
received in India and used under the conditions of storage prevail
ing in the field, revealed a vitamin A loss of approximately 25
percent.
Data Monitoring
Six months after the weekly distribution began, a data-monitoring committee reviewed the data, summarized according to dose
color code only. No one associated with the study was aware of the
color code, which was held by Hoffmann-LaRoche until the study
ended. Although differences were evident in the mortality trends of
the study groups after six months, they could not be associated
Vol. 323
No. 14
931
THE NEW ENGLAND JOURNAL OE MEDICINE
unambiguously with the incidence, severity, or duration of morbid
ity. The committee concluded that the study should continue.
Table 1. Doses Missed and Minimal Amount of Vita
min A Received during 52 Weeks of Intervention.
Statistical Analysis
Randomization according to cluster rather than according to
child introduced a moderate increase (about 30 percent) in the
variance of the estimators of the relative risk of death in the treated
group as compared with the control group. Relative risks, signifi
cance, and confidence intervals were therefore calculated according
to the duster design." The risk of death among the controls was
used as the reference value for relative risk'of death: a relative risk"
*bf 0.5 means that the risk in the treated group was half that among
the controls, or conversely, that the risk among the controls was
twice that in the treated group. All ages were adjusted to reflect age
at the start of the intervention, which began on the same dale for all
the children.
—Nutritional status was assessed_wi(h_use_of the CASP anthropometric software package (version 3.0J provided by the U-S-.Centers ■
’ for Discasc~CohlroI. Values more than 2 SD below .th?.reference.
value were considered abnormal?
No OF
Doses Missed
Children
(N « 15.419)
Minimai Amount
Received’
0
41.8
38.7
6.9
3.2
2.0
453 (433.000)
410(390.000)
366 (349,000)
322 (307.000)
279 (266,000)
227 (216,000)
183 (174,000)
fimol (!Ul
6-10
11-15
16-20
21-26
27-31
>31
0.7
5.0
Results
Mortality data and associated morbidity are report
ed here. An analysis of morbidity in the 15,419 chil
dren is currently under way.
Contact with the Children
During each of the 52 weeks of the study, at least 88
percen t of the children were contactedfTKere was~ri'd
difference in rates of contact_between the treated and
contrdl"groups'.-The” reasons for lack of contact (of
which some children’had’more fliarTmieJTnp^dcd
moving from the study area (10 percent), temporary
absence (13 percent), refusal to participate (28 per
cent), sickness (29 percent), and other reasons (30
percent). Table 1 summarizes the study contact and
compliance in terms of the number of weeks the dose
was missed. Nearly 42 percent of the children received
all the doses. For those in the treated group, this was
equivalent to more than 453 jzmol (433,000 IU) of
vitamin A, or approximately the amount available in
the commonly used large-dose supplement (209 p.mol
every six months). More than 90 percent of the chil
dren received at least 322 /nmol (307,000 IU), which is
equivalent to more than 70 percent of what they
would have received in a large-dose supplement.
Base-Line Characteristics
Sex, age, xerophthalmia status, serum retinol level,
and nutritional status at base line are shown in Table
2.
There were no substantial differences in these in
dexes between the control and treated groups. Al
though the study was meant to include only children
from 6 to 60 months of age, birth records were un
available, and our recall records include a small num
ber of younger (1.8 percent) and older (5.4 percent)
children.
The base-line prevalence of xerophthalmia was 11
percent. The risk of xerophthalmia did not differ ac’ cording to sex, except for a slight predominance
among boys after three years of age. Thirty-seven per
cent of the serum retinol values from the randomly
sampled subgroup (n = 280) were =50.70 prnol per
liter, and 21 percent were SO.35 p.mol per liter. The
prevalence of vitamin A deficiency in each of the clini
cal and biochemical categories thus exceeded the
World Health Organization’s criteria for a public
health problem.10 Seven cases of active corneal in
volvement (category X2, X3A, or X3B) were seen
Table 2. Base-Line Characteristics of the Study
Population.
Characteristic
Percentage of
Children
Sex
Male
Female
Age (mo)
*
<5
12-23
24-35
*36-47
48-60
61-71
Xerophthalmia status!
XN
X1B
X2. X3A, X3B
XS
Serum retinol Gimol/liter)
<0.35
0.351-0.70
0.701-1.05
>1.05
Nutritional status!
Stunted
Wasted
Stunted and wasted
Normal
Unknown
•Age at the start of intervention.
+XN indicates night blindness. XIB Bildt’s spot. X2 comeal xerosis.
X3A comeal ulceration or keratomalacia of less than one third of the
comeal surface. X3B corneal ulceration or keratomalacia of one third or
tAs determined with the CASP anthropometric software package. Stunt
ed indicates height for age < the mean minus 2 SD and weight for height >
the mean minus 2 SD; wasted indicates height for age > the mean minus
2 SD and weight for height < the mean minus 2 SD; stunted and wasted
indicates height for age < the mean minus 2 SD and weight for height < the
mean minus 2 SD; and normal indicates height for age > the mean minus
932
THE NEW ENGLAND JOURNAL OF MEDICINE
(four in the control group and three in the treated
group). Night blindness accounted for about one third
and Bitot’s spots for about two thirds of the milder
cases of xerophthalmia.
Seventy-two percent of the children were classified
by anthropometry as undernourished (defined as
more than 2 SD below the reference mean). Approximately one third of the children were stunted, 18 percenf stuntecT'and wasted, and 23 percent wasted (Ta
ble 2). ^Stunting thus affected a somewhat larger^
proportion of the children than wasting, indicating
that prolonged malnutrition was more common than.
acute undernutrition among the study children.
The five-year history of mortality among children
under five years of age taken at base line was not
significantly different between families of control and
families of treated children (data not shown).
Mortality Outcome
There were! 25 deaths in the.study population duc
king the 52 weeks of surveillance^for an overall mortal
ity rate of 8.1 per 1000. Eight of these deaths, however, involved accidents unrelated to symptoms that
could have been associated with the intake ofyritamin
A: animal bite (two deaths), drowning (three), poison
ing (one), and falling (twb)VFiye of the accidental
deaths were in the treated group and three in the con
trol group.
Figure 1 shows the cumulative deaths according to
study group. Regardless of treatment, girls were at
somewhat higher risk of death than boys, BuTnot sig
nificantly so (relative risk, 1.5 in the control group and
1.2 in the freafed’gFoup). Vifamin A significantly, re
duced the risk of death for both sexes, the effect being
somewhat larger for girls (relative risk, 0.41 for girls
[P<0.01] and 0.52 for boys [PC0.05]).
Figure 1. Cumulative Deaths Monitored Weekly, According to
Study Group.
The solid line represents the group treated with vitamin A, and the
line broken by squares the control group. Children who died in
accidents (five in the treated group and three in the control group)
are included.
Oct. 4, 1990
Table 3 shows the mortality according to age and
study group for the 117 nonaccidental deaths..The risk
of death in the group receiving vitamin A was 46 per
cent of that in the control group. The relative risk was.
reduced most for infants (relative risk, 0.28; 95 percent
confidence interval, 0.09 to 0.85) and those 12 to 35_
months of age (relative risk, 0.46T95- percent confidence ihterval,'0.26 to 0.81); it was less than L0 in all
age groups..Excluding the children who had received
the high-dose supplement at any time or who received
it only at base line did not substantially change the
age-specific relative risks shown in Table 3. In addition, these relative risks were not significantly changed
by excluding those who did not receive the study sup
plements for more than seven consecutive weeks
(n = 1863) or those who did not receive the supple
ments for more than four weeks on four occasions
(n = 11). These exclusions were designed to minimize
any possible confounding due to a differential partici
pation effect or missing the supplements for a pro
longed period.
Among the nonaccidental deaths, 18 occurred
among children with xerophthalmia at base line. All
18 occurred in children overT2~mphths of age (12
children in the control group^agKSfjin the treated
group). The death ratg^amoWSSffiTdren with xe
rophthalmia was 10.6 pcf 1000, ascompared.with 7.2
per 1000 amopg tffe children without xerophthalmia.
Table>K'shows the symptom- and disease-specific
relative risk of death in the treated and control groups.
According to the “verbal autopsy,” there were too few
deaths specifically assocjateWfcth the symptoms of
respiratory discase-arftrmalnmrition to provide a reli
able relative'Yisk. Excluding these two categories of
symptoms, the relative risk was consistently lower for
the treated group — and signifi<?5ntly so, except for
deaths associated with measles. More than 40 percent
of thejieaths were associated with diarrhea, 16 percertfwith measles, and the remainder with symptoms
suggesting other infections>..
Table 5 shows the mortality according to treatment
group and base-line nutritional status.. Data on nutri.-.
~ tional status were massing for 469 children (3 percent),
among whom 7 died (6 in the control group and 1 in
the treated group). Among the children not treated
with vitamin.A (the control group), the death rate of
those who were both stunted and wasted was 1.5 tp
2 times higher than the death rate of those who were
either stunted or wasted, and it was 2.7 times higher
than the rate of normal children. Thus, the risk of
death was increased by acute undernutrition superim
posed on chronic malnutrition. But the effect of treat
ment with vifamin A was pronounced (relative risk,
0.11; P = 0.0f; 95 percent confidence interval, 0.03 to
0.36) among stunted children, whereas it was not sig
nificant among wasted, stunted and wasted, or normal
children.
A hierarchical log-linear model was used to assess
the multivariate relation among death, treatment, age,
Vo!. 323
No. 14
THE NEW ENGLAND JOURNAL OF MEDICINE
sex, and nutritional status. The significant association
between treatment and death persisted when adjusted
simultaneously for age, sex, and nutritional status.
Table 4. Symptom- and Disease-Specific Mortality,
According to Treatment Group.
Symptoms or
Discussion
The results of this community-based, masked con
trolled field trial clearly indicate that in an area where
clinical vitamin A deficiency and chronic undernutri
tion are common, ensuring a constant consumption of
vitamin A at least equivalent to the.recommended di
etary allowance enhanced children’s survival. In
Indonesia, somewhat similar effects among preschool
age children (a 45 percent reduction in mortality)
were reported with vitamin A-fortified monosodium
glutamate when it was a consistent part of the food
' supply.4
For the one-year follow-up period the overall mor
tality rate among children 6 to 60 months of age was
8.1
per 1000 in our study, comparable to the 7.8 per
1000 for the 12- to 71-month age group reported by the
Aceh, Indonesia, study.2 It was higher, however, than
Table 3. Mortality, According to Age and Study Group.
Study Grout
0-11 Mo
Control
Treated
12-35 Mo
Control
Treated
2^36 Mo
Control
Treated
Total
Control
Treated
Age-adjusted total
Children
No. OF
Deaths
Cumulative,
Mortality Rate
Relative Risk*
678
689
14
4
0.021
0.006
'. 0.28 (0.09. 0.85)+
3185
3179
52
24
0.016
0.008
0.46 (0.26. 0.81)$
3792
3896
14
9
0.004
0.002
0.63 (0.26, 1.50)
7655
7764
80
37
0.010
0.005
0.46 (0.29. 0.71)$
0.46 (0.30. 0.7J)$
•Relative risk for the treated group, as compared with the control group Values in parentheses are 95 percent confidence limits.
+P - 0.05.
$P = 0.01.
the 5 per 1000 reported from an area near Hyderabad,
India, where a placebo-controlled, blinded trial with a
high-dose supplement has also been performed.12
These rates are considerably below the 20 per 1000
reported as the national average for India.12 We moni
tored infant mortality in the study area for a one-year
period in 1988 and 1989 and obtained a rate of 64 per
1000, a figure somewhat lower than the 83 per 1000
reported for Tamil Nadu in 198213 and the 98 per 1000
for India generally.14 The mortality rate among in
fants less than 6 months old was 42 per 1000 live
births, and among those 6 to 11 months old it was 22
per 1000. We were unable to find any reliable informa
tion on mortality rates among one-to-five-year-olds in
Tamil Nadu. The lower mortality figures we report
undoubtedly reflect in part the well-recognized effect
of the frequent contact of households with trained
fieldworkers.12,15 Nonetheless, because the contact was
comparable in our two study groups, the efficacy of
933
Control Treated
Group
Group
Measles
Diarrhea
Respiratory
Malnutrition
Convulsions
Other
Total deaths
12
33
7
16
12
19
80
3
6
37
Relative Risk*
0.58 (0.17, 1.92)
0.48 (0.24, 0.96)+
—
—
0.25 (0.07. 0.85)+
0.31 (0.12. O.78)t
tr - o.o5
vitamin A supplementation at the level of the recom
mended dietary allowance in reducing mortality by 54
percent remains evident; mortality rates were 10.5 per
1000 in the control group as compared with 4.8 per
1000 in the treated group.
We found an insignificant sex-related difference in
the risk of death without regard to treatment. Treat
ment with vitamin A reduced the risk of mortality in
both sexes, but the reduction was somewhat greater
among girls. This finding contrasts with that reported
from Indonesia, in which a significant treatment effect
of large-dose supplementation was found only in boys,
among whom the prevalence of xerophthalmia was
also higher.2 In our study, the prevalence of xeroph
thalmia at base line was not significantly different be
tween the sexes until after three years of age, whereas
the effect on mortality of treatment with vitamin A
was pronounced among the younger groups.
The efficacy of our low-dose supplementation was
considerably higher than the 34 percent reduction in
mortality reported after high-dose supplementation in
Indonesia as determined by intention-to-treat analyTable 5. Mortality, According to Nutritional Status.*
Nutritional Status
Cumulative
and Study Group
Children Deaths Mortality Rate
Unknown
Control
Treated
Stunted
Control
Treated
Wasted
Control
Treated
Stunted and wasted
Control
Treated
Normal
Control
Treated
Relative Risk*
201
268
6
l
0.030
0.004
0.13 (0.01, 1.14)
2385
2418
27
3
0.011
0.001
0.11 (0.03. 0.36)$
1806
1798
14
10
0.008
0.006
0.72 (0.30. 1.72)
1373
1340
22
14
0.016
0.010
0.65 (0.30, 1.41)
1890
1940
1]
9
0.006
0.005
0.80 (0.32. 2.00)
•The categories of nutritional status are defined in Table 2.
tRelative risk for the treated group, as compared with the control group. Values in parentheses are 95 percent confidence limits.
tP - 0.01.
934
THE NEW ENGLAND JOURNAL OF MEDICINE
sis,2 but lower than the estimated 75 percent reduction
reported with an analysis based on actual receipt of
the capsules? The estimate based on receipt of
the capsules was derived from a total of only 18
deaths over a four-month follow-up period. As the
authors noted, its validity awaits verification by
a study that ensures consistent, periodic verification
of compliance in taking the large-dose supplement,
which has not been a feature of most large-scale pro
grams to date.16
Vitamin A was most efficacious in children under
three years of age, most prominently in infants. This
finding contrasts with reports from Indonesia. In the
Aceh study the effect of treatment was most marked
among those 60 to 71 months old,2 and in the study
involving vitamin A-fortified monosodium glutamate,
mortality was reduced by 11 percent among infants
and 45 percent among preschoolers. 4 In the mono
sodium glutamate study the infants probably received
a considerable portion of their food as breast milk,
^nd the effect of the program would therefore be
Expected to be less. The reasons for the discrepancy
between our results and those of the Aceh study
are less clear but may be related to the relative level
of underlying malnutrition in the two study pop
ulations. Our base-line prevalence of xerophthalmia
was 11 percent, as compared with about 1 to 2 percent
in Indonesia, and only 25 percent of the Indian
children had normal anthropometric features, where
as at least 40 to 69 percent of the Indonesian chil
dren were classified within 10 percent of the me
dian standards of the U.S. National Center for Health
Statistics.
In accordance with many reports from developing
countries where vitamin A deficiency is endemic, diar
rhea was associated with the highest number of
deaths, followed by measles and symptoms associated
with other infections — convulsions, jaundice, and en
cephalitis, for example. The protective effect of vita
min A was significant for all these conditions except
measles. This finding contrasts with hospital-based
Kase-control reports from Africa, in which the protec
tive effect of very large doses of vitamin A was excep
tionally high in'measles.1’-18 Previous studies suggest
that measles is a less severe disease in India than in
Africa, and that factors other than vitamin A — the
severity of concurrent malnutrition, for example —
may be a more critical determinant of measles-associ
ated morbidity and mortality.1’-20 It may also be that a
large dose of vitamin A is required to prevent a fatal
outcome in severe measles complicated by vitamin A
deficiency.
. Prolonged undernutrition,_as evidenced by stunt
ing, characterized nearly_one third of the children jn
our study at basejine, and a continuous supply of
vitamin A reduced the risk of dying to one-ninth that
of the controls. The protective effect of vitamin .A was”
unremarkable in children with wasting, an indicator
of acute malnutrition, and in those with normal an
thropometric features. Stunting reflects — in addition
Oct. 4, 1990
to an inadequate food supply— many characteristics
'’dfsocial deprivation that are frequently found in poor
'Households—Qur data_suggest that these persistent’
' ecological and physiologic insults undermine the abili- ‘
ty of a child who is deficient in vitamin A to ward off a
fatal outcome when confronted by an infection. The
programmatic implication of this is that maximal re
ductions in mortality can be expected from vitamin A
prophylaxis targeted to children who are chronically
undernourished and to those with superimposed acute
malnutrition. .
Children with xerophthalmia are reported to be at
4 to 12 times the risk of death of neighboring chil
dren with normal eyes, and the risk increases with
the increasing severity of symptoms? The mortality
rate among children with xerophthalmia in our study
was about 50 percent higher than among children
without the condition (7.2 vs. 10.6 per 1000). When
we adjusted for those who received a large dose of
vitamin A because of xerophthalmia, the treatment
effect of the continued small dose persisted — that is,
half as many died among those who continued to
receive the weekly supplement as among those who
did not.
Sommer et al? noted that daily consumption of the
recommended dietary allowance was the ideal ap
proach to vitamin A prophylaxis, but considered it to
be impractical from a programmatic point of view and
chose distribution of the large-dose capsule every six
months instead. Sommer et al. subsequently com
mented that the single most important limitation to
achieving the maximal effect with large-dose capsules
was inadequate contact and verification of compli
ance3; the large-dose approach requires careful moni
toring of distribution channels to avoid possible over
dosing. In contrast, our approach involving frequent
low doses showed that when the supplement is pro
vided at a safe dosage level in an easily dispensed
form, community workers can be effective in attaining
high rates of contact and verification if there is also
an appropriate managerial and supervisory system.
Importantly, the efficacy of supplementation at the
level of the recommended dietary allowance suggests
that a similar effect could be achieved by an equiva
lent supply of vitamin A from foodstuffs, an approach
that would potentially address other nutritional defi
ciencies as well.
References
United Nations Administrative Committee on Coordination-Subcommittee
on Nutrition. First report on the world nutrition situation. Geneva: United
Nations. 1987:36.
2.
Sommer A. Tarwotjo I. Djunacdi E. et al. Impact of vitamin A supplementa
tion on childhood mortality: a randomised controlled community trial. Lan
cet 1986; 1:1169-73.
3.
Tarwotjo 1. Sommer A, West KP Jr, Djunaedi E, Mele L. Hawkins B.
Influence of participation on mortality in a randomized trial of vitamin A
prophylaxis. Am J Clin Nutr 1987; 45:1466-71.
4.
Muhilal, Permeisih D, Idjradinata YR, Muherdiyantiningsih, Karyadi D.
Vitamin A-fortificd monosodium glutamate and health, growth, and sur
vival of children: a controlled field trial. Am J Clin Nutr 1988; 48:1271-
I.
5.
Sommer A. Tarwotjo I, Hussaini G, Susanto D. Increased mortality in
children with mild vitamin A deficiency. Lancet 1983; 2:585-8.
Vol. 323
6.
7.
8.
9.
10.
II.
No. 14
THE NEW ENGLAND JOURNAL OF MEDICINE
Subcommittee on Vitamin A Deficiency Prevention and Control. Food and
Nutrition Board. National Research Council. Vitamin A supplementation:
methodologies for field trials. Washington. D.C.: National Academy Press,
1987.
Requirements of vitamin A. iron, folate and vitamin B,,: report of a Joint
FAO/WHO Expert Consultation. No. 23 of FAO food and nutrition series.
Rome: Food and Agricultural Organization of the United Nations. 1988.
Subcommittee on the Tenth Edition of the RDAs, Food and Nutrition Board.
Commission on Life Sciences, National Research Council. Recommended
dietary allowances. IOth cd. Washington. D.C.: National Academy Press,
1989.
Underwood BA. Chavez M, Hankin J, ct al. Guidelines for the development
of a simplified dietary assessment to identify groups at risk for inadequate
intake of vitamin A. In: Report of International Vitamin A Consultative
Group (1VACG)&. Washington, DC.: International Life Sciences Insti
tute-Nutrition Foundation. 1989.
Control of vitamin A deficiency and xerophthalmia: report of a joint
WHO/UNICEF/USAID/Hclcn Keller Intcmational/IVACG meeting WHO
Tech Rep Ser 1982,672:1-64.
Cochran WG. Sampling techniques. 2nd ed. New York: John Wiley,
1963:65.
935
12. Gopalan C. Vitamin A and child mortality. Nulr Found India Bull 1990;
13. UNICEF. 1988 Asian and Pacific atlas of children in national development.
Thailand- Viscom Center Ltd.. 1987.
14. The state of the world's children 1990. New Delhi, India: Oxford University
Press for UNICEF. 1990:76.
15. Gopalan C. Vitamin A deficiency and child mortality. Nutr Found India
Bull 1986;7:1-2.
16. Underwood BA. Vitamin A prophylaxis programs in developing countries:
past experiences and future prospects. Nutr Rev 1990; 48:265-74.
17. Barclay AJG. Foster A. Sommer A Vitamin A supplements and mortal
ity related to measles: a randomised clinical trial. BMJ 1987; 294.29418. Husscy GD, Klein M. A randomized, controlled trial of vitamin A in chil
dren with severe measles. N Engl J Med 1990; 323.160-4.
19. Reddy V. Bhaskaram P. Raghuramulu N. et al. Relationship between mea
sles. malnutrition, and blindness: a prospective study in Indian children. Am
J Clin Nutr 1986; 44:924-30.
20. Markowitz LE. Nzilambi N, Driskell WJ. ct al. Vitamin A levels and
mortality among hospitalized measles patients. Kinshasa. Zaire. J Trop
Pediatr 1989; 35:109-12.
LOCATION ON CHROMOSOME 15 OF THE GENE DEFECT CAUSING MARFAN SYNDROME
Katariina 'Kainui.ainen, Cand.Med., Leena Pulkkinen, M.Sci., Aslak Savolainen, M.D.,
Ilkka Kaitila, M.D., Ph.D., and Leena Peltonen, M.D., Ph.D.
Abstract Background. Marfan syndrome, “the found
ing member" of the heritable disorders of connective tis
sue, is a common autosomal dominant disorder with high
ly variable clinical manifestations in the skeletal, ocular,
and cardiovascular systems. The fundamental defect
leading to this disease has escaped definition despite dec
ades of research efforts by several groups of investi
gators.
Methods and Results. Using linkage analyses with
polymorphic markers of the human genome, we mapped
the genetic defect to chromosome 15 in five families with
Marfan syndrome. With three polymorphic markers we ob
tained definitive proof of linkage in these families (lod
score = 3.92, B = 0.0+0.11). The most probable location
of the gene for the disease is currently D15S45 (lod
score = 3.32, B = 0.0+0.12).
Conclusions. The chromosomal localization of the
mutation in Marfan syndrome is a first step toward the
isolation and characterization of the defective gene and
serves as a diagnostic test in families in which cosegrega
tion of these markers with the disease has been con
firmed. (N Engl J Med 1990; 323:935-9.)
ARFAN syndrome is one of the most common
inherited connective-tissue disorders, with an
estimated prevalence of 40 to 60 cases per million pop
ulation.1 It is inherited in an autosomal dominant
fashion, although it is sporadic in 15 percent of cases.1
The most prominent clinical manifestations of the dis
order occur in the skeletal, ocular, and cardiovascular
systems.1 Diagnosis has been problematic because of
the extreme variability of clinical expression. The cur
rent diagnostic criteria were established at the Sev
enth International Congress on Human Genetics in
1986 and defined at the First International Sympo
sium on Marfan Syndrome in 1988.2,3 These criteria
include “more specific manifestations,” which are ec-
topia lentis, aortic-root dilatation, aortic dissection,
and dural ectasia;, and “other manifestations” in the
musculoskeletal, cardiovascular, ocular, integumen
tary, pulmonary, and central nervous systems. The
penetrance of the disease is considered complete, but
variable expression of its clinical manifestations is the
rule even within a single family.4
Despite intensive research carried out in various
laboratories, nothing is known about the genetic de
fect leading to Marfan syndrome. Several abnormali
ties of connective-tissue proteins have been observed
in patients,5-11 but their role as the primary defect in
the disease is unclear. In fact, linkage analyses have
allowed many of the genes coding for these proteins to
be excluded as the defective gene in the syndrome.
The excluded genes include genes coding for Type I,
Type II, and Type III collagens and fibronectin, as
well as genes coding for one polypeptide chain of Type
V and Type VI collagens.12-15
Over the past four years we have been collecting
information on Finnish families with Marfan syn
drome. We studied eight three-generation families,
each with a minimum of three living members who
were affected. In these families, linkage analysis of
M
From the Laboratory of Molecular Genetics, National Public Health Institute.
Helsinki (K.K., L. Peltonen); the Department of Clinical Genetics. Kuopio Uni
versity Central Hospital, Kuopio, Finland (L. Pulkkinen); the First Department
of Medicine. Helsinki University Central Hospital. Helsinki (A.S.); and the De
partment of Medical Genetics. University of Helsinki, Helsinki (I.K.). Ad
dress reprint requests to Dr. Peltonen at the Laboratory of Molecular Genetics,
National Public Health Institute. Mannerhcimintic 166, SF-00300 Helsinki.
Finland.
Supported by grants from the Academy of Finland, the Paulo Foundation, the
Meilahti Foundation, the Research Foundation of Farmos, and the Orion Medical
Company.
I
N<J T
1342
Howarth PH, Durham SR, Lee TH, Kay AB, Church MK, Holgate ST.
Influence of albuterol, cromolyn sodium and ipratropium bromide on
the airway and circulating mediator responses to allergic bronchial
21.
9.
Cockcroft DW, Murdock KY. Comparative effects of inhaled
salbutamol, sodium cromoglycate and beclomethasone dipropionate on
and increased bronchial responsiveness to histamine. J Allergy Clin
Immunol 1987; 79:734-40.
Barnes PJ. A new approach to the treatment of asthma. N Engl J Med
1989;321:1517-27.
Brittain RT. Approaches to a long-acting, selective Pj-adrenoceptor
II.
stimulant. Lung 1990; 168 (suppl): 111-14.
12.
Johnson M. The pharmacology of salmeterol. Lung 1990; 168 (suppl):
115-19.
13.
Butchers PR, Cousins SA, Vardey CJ. Salmeterol: a potent and
long-acting inhibitor of the release of inflammatory and spasmogenic
mediators from human lung. BrJ Pharmacol 1987; 92 (suppl): 745P.
14.
Boyd G, Anderson K, Carter R. A placebo controlled comparison of the
10.
15.
hours. Thorax 1989; 56: 14IP.
Ullman A, Svedmyr N. Salmeterol, a new long acting inhaled beta 2
patients. Thorax 1988; 43: 674-78.
16. Chai H, Farr RS, Forehlich LA, et aL Standardization of bronchial
inhalation challenge. J Allergy CUn Immunol 1975; 56:323-27.
Oxford: Blackwell Scientific Publications, 1987.
19.
20.
DEC 1,1990
THE LANCET
8.
Mediator release after endobronchial challenge in patients with
respiratory allergy. J Allergy CUn Immunol 1990; 50: 906-13.
Ahrens RC, Harris JB, Milaven G, Annis L, Ries R. Use of bronchial
provocation with histamine to compare the pharmacodynamics of
inhaled albuterol with metaproterenol in patients wth asthma. J Allergy
Clin Immunol 1987; 79:876-82.
Nials AT, Butchers PR, Colman RA, Johnson M, Vardey CJ. Salmeterol
and formoterol: are they both long-acting betaj-adrenoceptor agonists?
BrJ Pharmacol 1990; 90 (suppl) 120P.
MacOnchie JG, Foster JK, Fowler P, Thomas M. An initial comparison
of salmeterol and salbutamol against histamine-induced
bronchoconstriction in healthy subjects. BrJ Clin Pharmacol 1988; 25:
115P.
22.
Dahl R, Pederson B. Influence of ncdocromil sodium on the dual
asthmatic reaction after allergen challenge; a double-blind, placebocontrolled study. Eur J Respir Dis 1986; 69 (suppl 147): 263-65.
23.
Hood SK, Twentyman OP, Holgate ST. Altering baseline airway calibre
does not affect responsiveness in asthmatic subjects. Thorax 1989; 44:
350P.
24.
DcMonchy JGR, Kauffinan HF, Venge P, et al. Bronchoalveolar
eosinophilia during allergen-induced late reactions. Am Rev Respir Dis
1985;131:373-76.
25.
Metzger WJ, Richerson HB, Warden K, Monick M, Hunrunghake GW.
Bronchoalveolar lavage of allergic asthmatic patients following allergen
provocation. Chest 1986; 89:477-83.
26.
Persson CGA. Role of plasma exudation in asthmatic airways. Lancet
1986; i: 1126-29.
27.
Baker AJ, Fuller RW. Anti-inflammatory effect of salmeterol on human
alveolar macrophages. Am Rev Respir Dis 1990; 141: A394.
28.
Fuller RW, O’Maliy G, Baker AJ, MacDermot J. Human alveolar
macrophage activation: inhibition by Forskolin but not
Pj-adrenoccptor stimulation or phosphodiesterase inhibition. Palm
Pharmacol 1988; 1:101-06.
29.
Twentyman OP, Finnerty JP, Holgate ST. The inhibitory effect of
nebulised albuterol on the early and late asthmatic reactions and
increase in airways responsiveness provoked by inhaled allergen in
asthma. Am Rev Respir Dis (in press).
30.
Twentyman OP, Finnerty JP, Holgate ST. Salbutamol inhibits the
allergen-induced late asthmatic reaction and increase in responsiveness.
Clin Exp Allergy 1990; 20 (suppl 1): 94.
Palmqvist
31.
M, Bolder B, Lowhager O, Melander B, Svedmyr N,
Wahlandcr L. Late asthmatic reaction prevented by inhaled albuterol
and formoterol. J Allergy Clin Immunol 1989; 83: 244.
Effect of massive dose vitamin A on morbidity and
mortality in Indian children
K. VlJAYARAGHAVAN
G. RADHAIAH
K. V. Rameshwar Sarma
The effect of vitamin A supplementation on
preschool child morbidity and mortality was
assessed in a prospective double-blind placebocontrolled study around Hyderabad, India. Every
six months 200 000IU vitamin A was given to 7691
children (treatment group) whereas 8084 children
received a placebo (control group). Morbidity and
mortality data were collected every three months.
Risk of respiratory infection was higher in children
with mild xerophthalmia than in children with
normal eyes. Vitamin A supplementation had no
effect on morbidity status. Mortality rates were
similar in the two groups; it was highest in children
who did not receive either vitamin A or placebo.
The findings suggest that vitamin A supplemen
tation alone may not reduce child mortality.
Lancet 1990; 336:1342-45.
B. SURYA PRAKASAM
Vinodini Reddy
children survive? Thus, the morbidity and mortality due to
vitamin A deficiency is very high, even ifonly that associated
directly with severe xerophthalmia is considered.
Studies from Indonesia suggest that even mild vitamin
A deficiency is associated with increased morbidity/
mortality in children.1'* Furthermore, vitamin A
supplementation was shown to reduce the mortality rate by
about 30%.’ These observations have generated much
interest world wide about the role of vitamin A in child
survival. Analysis of available data in India indicated that
respiratory disease developed twice as often in children with
mild xerophthalmia as in children with normal eyes?
However, this study was retrospective and the sample size
was not adequate to assess mortality.
We have done a prospective study in a rural community to
assess the effect of vitamin A supplementation on morbidity
and mortality in preschool children.
Introduction
Children and methods
Vitamin A deficiency is widespread in India and in several
other developing countries. About 5-10% of children have
conjunctival xerosis and Bitot spots. Severe deficiency of
vitamin A with comeal involvement is more serious. There
are about 500 000 new cases ofxerophthalmia, halfof which
lead to blindness, each year in India, Bangladesh, the
Philippines, and Indonesia combined.1 Only 30% of these
The study was done between January, 1987, and January, 1989,
in five primary health centres, which served 84 villages (total
population of about 165 000) in one of the backward districts of
ADDRESSES: National Institute of Nutrition, Hyderabad500007, India (K. Vijayaraghavan. MSc. G. Radhaiah. MSc. B. Surya
Prakasam. MSc. K. V. R. Sarma, MO, V. Reddy. MO). Correspondence to
Dr K. Vijayaraghavan.
VOL 336
THE LANCET
TABLE I—DISTRIBUTION OF CHILDREN BY AGE AND SEX
Age (yr)
<1
1-2
>2 <3
>3 <4
>4 <5
Treatment
Control
Total
868,855
867/871
889/882
890’884
369/316
913/922
■ 880/901
934/902
972/910
374/376
1781/1777
1747/1772
1823/1784
1862/1794
743/692
Total
3883/3808
4073'4011
7956/7819
1343
TABLE III—CHILD MORTALITY ACCORDING TO DOSES OF
VITAMIN A OR PLACEBO
Group (1-5 yr)
No of doses
Vitamin A
Placebo
0
397 (17-6)
2274 (9-7)
4405 (2-3)
638 (17-2)
1857(10 8)
4511 (2-2)
2
Values are of no of cases (no of deaths/1000).
Values ate for M/F.
The overall incidence rates according to ocular status were
calculated by addition of incidences for the five intervals and are
presented per 100 child intervals. Morbidity rates for diarrhoea and
respiratory infections were calculated by: (Cases of given morbidity
during all the observation periods - total number of child
intervals) x 100. Relative risk of morbidity in children with
xerophthalmia was calculated by: incidence ofmorbidity in children
with xerophthalmia - incidence of morbidity in children without
xerophthalmia. Confidence intervals for relative risk were also
calculated. We calculated morbidity rates separately, taking into
consideration the vitamin A status during the interim between the
initial clinical examination and the examination six months later.
There were thus four groups: mild xerophthalmia both at baseline
and six-months later; mild xerophthalmia at baseline, normal six
months later; normal at baseline, mild xerophthalmia six months
later; and normal both at baseline and six months later. The
morbidity and mortality rates were calculated for each of these
groups.
We also analysed data, allowing for the anthropometric status of
the children. They were divided into 2 groups with 80%
weight-for-height as the cut-off level. The effect of vitamin A
supplementation was assessed by calculation of morbidity and
mortality rates according to the number of doses of vitamin A or
placebo received by the children—ie, rates were calculated for no
dose, one dose, and two dose groups.
Andhra Pradesh in India. The villages were allocated randomly into
two groups—treatment and control.
All preschool children (1-5 years old) in the treatment areas
received vitamin A (200000 IU) according to the national
programme of blindness prevention; children in control areas
received a placebo, which consisted of arachis oil—the same oil base
used in the vitamin A concentrate. There had been no distribution
of vitamin A in this area before the study was started. We intended
to give at least two doses of vitamin A or placebo to all children. At
the time of administration, some children were not available at their
homes because they had gone out of the village or had gone to field
with their parents. Hence, some children received two doses, and
some received only one dose. Those children who could not be
contacted on both occasions received no dose. The trial was double
blind: the investigators and medical officers did not know which
were the treatment and which were the control areas. They were not
aware whether the dose they were distributing was vitamin A or
placebo. Decoding was done only after data had been collected.
Households with preschool children were identified. Mothers
were contacted by trained field workers at their homes once every
three months after vitamin A or placebo had been given, and
information about morbidity, with particular reference to
diarrhoea, respiratory infection, and measles, was obtained for the
previous one month in the local language. Diarrhoea was defined as
the passing ofthree or more loose motions a day. Respiratory disease
was defined as the presence of clinically significant cough with or
without expectoration. The same investigators collected mortality
data during the three-monthly home visits by questioning parents
about each child. The villages were revisited in the same order.
A clinical examination for signs ofvitamin A deficiency was done
by trained medical officers at the time of the baseline survey and
therafter every six months until completion of the study. The first
dose was distributed soon after the first clinical examination.
Children were examined in adequate light with a loupe. Standard
diagnostic criteria for xerophthalmia were used. Mothers were
questioned about nightblindness with appropriate terms in the local
language. Children with comeal involvement were given immediate
treatment and dropped from the study; those with mild
xerophthalmia were managed in the same way as nonxerophthalmic (normal) children. Anthropometric measurements,
such as weight and weight-for-height, were done every six months
on each alternate child. Weight was measured with a beam balance
and weight-for-height was measured by a leanness board.7
In about 5% of households, supervisory staff randomly checked
morbidity and mortality data and receipt of vitamin A or placebo
about 2-3 weeks after the investigators. Children who had night
blindness (XN), conjunctival xerosis (XIA), or Bitot spots (X1B)
were classified as mild xerophthalmia and those without eye signs as
normal. All the data were analysed by computer. Incidence of
diarrhoea and of respiratory diseases was calculated separately for
each three-month interval.
Results
15 775 children between the ages of 1 and 5 years were
studied (7691 treatment, 8084 control) (table I). The two
groups were similar at baseline with respect to income
status, distribution of weight for age, and crude birth and
death rates. The distribution of children according to age
and sex was similar in the two groups. About 6% of the
children had night blindness and Bitot spots at baseline;
after vitamin A administration, the prevalence was 1 -3% in
the treatment areas and 2-9% in the control areas. About
58% of the treatment group had received two doses of
vitamin A and 34% had received at least one dose—ie, about
92% of the children had received one or more doses of
vitamin A. In the control area 57% of children had received
two doses and 32% had received one dose of placebo.
Risk of respiratory infection was significantly higher in
children who had mild xerophthalmia, either at the initial
clinical examination or six months later. However, the
incidence was higher in the group whose eyes were normal at
baseline but in whom xerophthalmia developed during the
six months period (table II). There was no relation between
risk of diarrhoea and ocular status. When weight-for-height
was considered, there was no difference in morbidity of
TABLE II-INCIDENCE OF INFECTIONS ACCORDING TO VITAMIN A STATUS
Clinical vitamin A status
Baseline
After 6 months
Mild xerophthalmia
Mild xerophthalmia
Normal
Normal
Mild xerophthalmia
Normal
Mild xerophthalmia
Normal
*p<0 05;tp<001.
Diarrhoea
Respiratory infection
Incidence (%)
Relative risk
Incidence (%)
Relative risk
8-6
8-2
9-5
7-3
119
113
1-31
1-0
166
17-5
22-5
12-9
*1-29
*
1-35
1-741
1-0
1344
THE LANCET
TABLE IV—ODDS-RATIOS OF DEATH WITH INDEPENDENT
VARIABLE
No of doses
Independent variable
Vitamin A
Sex
Schedule tribe
Agriculture labourer
Other labourer
Father illiterate
Age (mo)
2
1-10
1-22
146
2-61
1 10
0-95t
1
0
120
080
*
341
198
097
096
0-931
092
1-76
*
405
083
226
271
093t
•p<0-01; tp<0 05; tp<0 001 foe association with mortality.
children with or without xerophthalmia. There was no
beneficial effect of vitamin A supplementation on morbidity
status compared with placeoo.
Mortality was higher in children with xerophthalmia than
in those with normal eyes (number of cases, 403 vs 5318;
death rate/1000,4-96 vs 2-26) but relative risk (2-27) was not
statistically significant. After the intervention programme
was started there were no differences in mortality rates
between treatment and control groups (table III). Mortality
was higher in children who had not received any dose of
either vitamin A or placebo. There was a significant
reduction in mortality in the group which had received two
doses of vitamin A or placebo compared with those who had
received one dose or no dose. Results of logistic regression
analysis, including variables such as age, sex, father’s
educational status, caste, and number of doses, indicated
that there was a higher mortality in younger children and in
those who belonged to scheduled tribes (table IV).
Discussion
The role of vitamin A in maintaining the integrity of the
epithelium in the respiratory and gastrointestinal tracts is
well recognised. In laboratory animals, vitamin A deficiency
leads to alterations in the mucosal lining of these sites, so
they are more vulnerable to bacterial invasion.8 Similar
changes can account for a higher incidence of infections in
human vitamin A deficiency which leads to higher
mortality. However, the available evidence is not
unequivocal. In the Indonesian study3 xerophthalmia was
associated with increased risk of both diarrhoea and
respiratory infection, whereas in our study the incidence of
respiratory infection, but not of diarrhoea, was higher in
vitamin A deficient children. In both studies, morbidity data
were collected ■every three months and recall of events of
such a long interval may not be very accurate. However,
even in an earlier study carried out on Hyderabad slum
children, in which morbidity data were collected weekly,
mild xerophthalmia was associated with increased risk of
respiratory infection, but not diarrhoea? The influence of
other environmental factors on diarrhoea may perhaps be
greater than that of vitamin A deficiency.
The relation between vitamin A deficiency and mortality
is even more complex because of other confounding factors,
and is difficult to interpret. Several workers have shown that
the risk of death is very high in children with severe comeal
xerophthalmia.’ However, most of these children also have
severe protein energy malnutrition and infections, which
can independently contribute to the high mortality. It is
therefore difficult to say how much of this mortality is due to
vitamin A deficiency itself.
The prevalence of severe vitamin A deficiency with
comeal involvement is low, whereas mild deficiency, as
DEC 1, 1990
evidenced by night blindness, conjunctival xerosis, and
Bitot spots, is much more common. In our study, we found
no significant association between mild xerophthalmia and
mortality in children. There was no difference in the
mortality rates of children who received vitamin A or
placebo. Our results differ from those reported by Sommer
et al,5 who showed that mortality in Indonesia was reduced
by as much as 34% after vitamin A supplementation.
However, the design of the Indonesian study was criticised
because it was not double-blind, sufficient care was not
taken to eliminate contact effect between investigators and
community, and ascertainment of deaths was not by active
surveillance.10
We attempted to take care of these criticisms to a large
extent. However, one of the limitations of our study was the
low child mortality that we recorded in the study areas
compared with the reported national average. Although, it
can be argued that this might have invalidated the results,
the mortality rates observed in our study are not very
different from those of the Indonesian study.
It is noteworthy that mortality in the non-recipient
children (no dose group) was higher in the experimental and
placebo groups than in those who had received the
supplement. Likewise, in Indonesia, Tarwotjo et al13
reported a substantially higher mortality among non
recipients than among controls of the same age and sex.
These observations may be due to differences in the health
care received by the two groups; frequent contacts by the
project staff, both in treatment and in control villages, may
have motivated the community to seek health care and use
the services better. Although, the field investigators were
instructed to avoid active intervention, seriously ill children
were referred to the nearest health centre for treatment. As
Gopalan13 pointed out, it would not have been possible to
have accomplished their jobs successfully if the investigators
had not earned the cooperation of the families by giving
some advice on health care.
Sommer et al3 had suggested that reduction in child
mortality may be due to reduction in morbidity, such as
diarrhoea and respiratory infections. Administration of
vitamin A had no impact on morbidity in our study, despite
an association of mild xerophthalmia with increased
incidence of respiratory infection; this could be due to the
influence of other environmental factors.' Alternatively, the
high inddence of respiratory infection in mild
xerophthalmia was an association only and was not causally
related. The relation between vitamin A defidency and
mortality can vary in different regions depending on
morbidity pattern, sodocconomic characteristics, diet, and
health care practices. Thus, vitamin A supplementation
alone cannot be expected to improve child survival in all
ecological and cultural settings; this does not deny the
importance of vitamin A supplementation to improve
nutrition status. Prevention of blindness is a good enough
reason to strengthen the continuing vitamin A programme
combined with other health care services, it can have a better
impact on child health.
We thank Dr G. V. S. Nagabhushana Rao, Medical and Health Services,
Government of Andhra Pradesh, for cooperation and help in conducting the
study. The valuable suggestions and guidance received from Dr K.
Ramachandran, All India Institute of Medical Sciences, New Delhi, about
dam analysis is gratefully acknowledged.
I.
2.
REFERENCES
Sommer A, Hussaini G, Tarwotjo I, Susanto D. Incidence, prevalence
and scale of blinding malnutrition. Laiuet 1981; i: 1407-08.
Menon K, Vijayaraghavan K. Sequelae of severe xerophthalmia: a follow
-
VOL 336
3.
4.
5.
6.
7.
1345
THE LANCET
village health guides. Ind Pediatr 1985; 22:669-75.
up study. Am J Clin Nutr 1980; 33: 218-20.
Wilhem DL. Regeneration of the tracheal epithelium in the vitamin A
Sommer A, Katz J, Tarwotjo I. Increased risk of respiratory disease and 8.
deficient rat. J Pathol Bacterio! 1954; 67:361-65.
diarrhoea in children with pre-existing mild vitamin A deficiency. AmJ
Clin Nutr 1984; 40: 1090-95.
9.
Sommer A. Nutritional blindness and keratomalacia. New York: Oxford
Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in
University Press, 1982.
children with mild vitamin A deficiency. Lancet 1983; ii: 585-88.
10.
Mamdani M, Ross DA. Vitamin A supplementation and child survival:
Sommer A, Tarwotjo I, Djunaedi E, ct al. Impact of vitamin A
Magic bullet or false hope? London: EPC Publication, 1988;
supplementation on childhood mortality: a randomised controlled
no 19:36.
community trial. Lancet 1986; i: 1169-73.
11.
Tarwotjo I, Sommer A, West Jr KP, et al. Influence of paucipation on
Milton RC, Reddy V, Naidu AN. Mild vitamin A deficiency and
mortality in a randomised trial of vitamin A prophylaxis. Am J Clin
childhood morbidity: an Indian experience. Am J Clin Nutr 1987; 46:
Nutr 1987; 45: 1466-71.
827-29.
12.
Gopalan C. Vitamin A deficiency and child mortality. NFI Bull 1986; 7;
6-7.
Vijayaraghavan K, Rao DH, Rao TV. Assessment of nutritional status by
Infective dermatitis of Jamaican children: a marker
for HTLV-I infection
Lois LaGrenade Barrie Hanchard Valerie Fletcher
Beverley Cranston
in Jamaican children infective dermatitis is a
chronic eczema associated with refractory
nonvirulent Staphylococcus aureus or betahaemolytic streptococcus infection of the skin and
nasal vestibule. 14 children between the ages of 2
and 17 years with typical infective dermatitis,
attending the dermatology clinic at the University
Hospital of the West Indies in Jamaica, were tested
for antibody to human T-lymphotropic virus type 1
(HTLV-1). All were seropositive, whereas 11
children of similar age with atopic eczema were all
negative. In 2 of 2 cases of infective dermatitis, the
biological mother was HTLV-1 seropositive. None
of the 14 patients showed signs of adult T-cell
leukaemia/lymphoma, though experience with
previous cases of infective dermatitis indicates the
possibility of such progression.
William Blattner
groins; (8) generalised fine papular rash; (c) chronic nasal discharge
in the absence of other causes of rhinitis; (d) positive cultures for 3
aureus or beta-haemolytic streptococci from nasal discharge and/or
skin lesions. No patient had aJifctory of blood transfusion. 11
patients with atopic eczema from this same clinic served as controls:
their dermatitis was mainly flexural, they did not have chronic nasal
discharge, and 3 aureus and beta-haemolytic streptococci were
recovered from the skin only in the presence of secondary infection.
In each patient the full blood count was done including total
lymphocyte count and percentage eosinophils, and smears were
examined for the presence of atypical polylobated lymphocytes.
Serum was tested for HTLV-I antibodies by enzyme linked
immunosorbent assay (Dupont) with confirmation by recombinant
p21e enhanced western blot (Biotech/Dupont), core and envelope
antibodies being required for a positive result. Swabs from nasal
discharges and skin were cultured by routine methods for bacterial
pathogens. Skin biopsy was performed in 4 patients who were
refractory to treatment and lymph node biopsy in 2 patients who
had persistent generalised lymphadenopathy.
Lancet 1990; 336:1345-47.
Results
Introduction
In 1966 Sweet1 described a unique dermatitis in Jamaican
children which he called infective dermatitis.1 The following
year Walshe2 documented the clinical features and
bacteriology of this disease in 25 Jamaican children, noting
an association with Staphylococcus aureus and betahaemolytic streptococcus infection and a poor response to
treatment.
Typically the condition begins acutely without preceding
infantile eczema. The dermatitis can be controlled with
long-term antibiotics but relapses prompdy when these are
discontinued. The resistance to treatment, the frequent
exacerbations, and the infections with bacteria that are
usually non-virulent raised the possibility that infective
dermatitis is a disorder of immunosuppression. We have
looked for an association with human T-lymphotropic virus
type 1 (HTLV-I) infection.
5 boys and 9 girls had infective dermatitis (current ages 3-16
years, mean 8, median 8 5); 3 boys and 8 girls had atopic
dermatitis (current ages 2-12 years, mean 7, median 7). All
the children had low socioeconomic backgrounds.
All 14 infective dermatitis patients were positive for
HTLV-I antibodies (confirmed by western blot), as were
both the biological mothers whom we tested; by contrast,
none of the 11 children with atopic dermatitis was antibody
positive. The table shows the results of nasal swabs and skin
swabs from the infective dermatitis patients. In 2 of the 11
children with atopic dermatitis 3 aureus and betahaemolytic streptococci were grown from obviously
infected lesions.
Of the children with infective dermatitis 11 had normal
white blood cell and differential counts and 3 had a raised
neutrophil count compatible with bacterial infection. 12 had
a normal haemoglobin level and 2 were mildly anaemic (with
Patients and methods
Among 147 consecutive patients between the ages of2 and 17 years,
referred to the dermatology outpatients clinic at the University
Hospital of the West Indies between March, 1989, and March,
1990,14 met the clinical definition of infective dermatitis—namely,
(a) severe exudative eczema with crusting, involving the scalp,
eyelid margins, perinasal skin, retroauricular areas, axillae, and
ADDRESSES: Departments of Medicine and Pathology.
University of the West Indies. Mona, Jamaica (L LaGrenade.
MRCP. B. Hanchard. FRCPC. V. Fletcher, MB, B. Cranston, BSc);
National Institutes of Health, Bethesda. Maryland. USA (W.
Blattner, MO). Correspondence to Dr W. Blattner. National Cancer
Institute. Executive Plaza North (room 434). Bethesda. MD 20892.
USA
rv<jT '’-S’
The Lancet • Saturday 24 May 1986
BrtlPACT OF VITAMIN A SUPPLEMENTATION
®>.
ON CHILDHOOD MORTALITY
U 5 Randomised Controlled Community Trial
Alfred Sommer
g?; EdiDjunaedi
® -A. A. Loeden
Ignatius Tarwotjo
Keith P. West, Jr
Robert Tilden
Lisa Mele
and the Aceh Study Group
X - Internationa! Center for Epidemiologic and Preventive
-^Ophthalmology, Dana Center of the Wilmer Institute and School of
■ Public Health, Johns Hopkins University, Baltimore, Maryland;
Directorate of Nutrition and National Center for Health
^Research and Development, Ministry of Health, Government of
if; -Indonesia; and Helen Keller International, New York, USA
• Summary
450 villages in northern Sumatra were
;
randomly assigned to either participate in a
i vitamin A supplementation scheme (n = 229) or serve for 1
I par as a control (n = 221). 25 939 preschool children were
i aamined at baseline and again 11 to 13 months later.
s Capsules containing 200 000 IU vitamin A were distributed
g to preschool children aged over 1 year by local volunteers 1 to
13 months after baseline enumeration and again 6 months
Slater. Among children aged 12-71 months at baseline,
a nottaiity in control villages (75/10 231, 7-3 per 1000) was
149% greater than in those where supplements were given
| (53/10 919,4-9 per 1000)(p<0-05). The impact ofvitamin A
j supplementation seemed to be greater in boys than in girls.
| These results support earlier observations linking mild
I vitamin A deficiency to increased mortality and suggest that
?< supplements given to vitamin A deficient populations may
ij decrease mortality by as much as 34%.
I
Introduction
! A LONGITUDINALobservational study in rural central Java
I indicated that children with ocular signs of mild vitamin A
1 deficiency were more likely than neighbourhood controls to
! die, that mortality was directly related to severity ofvitamin A
i deficiency, and that poor survival was probably attributable,
■it least partly, to high, rates of respiratory disease and
diarrhoea.' ’ We report’here the results of a randomised,
controlled, community trial of vitamin A prophylaxis in
northern Sumatra.
Subjects and Methods
The study was carried out in Aceh Province, which is at the
conhern tip of Sumatra and where xerophthalmia is prevalent.’*’5
depopulation is ethnically distinct from that of Java, where the
'trlier observational study had been conducted.I )
For political and administrative reasons a cluster sampling
i shenie was employed. The sampling frame consisted of 2048
I ’dhges in Aceh Utara and Pidie, two contiguous rural kabupatens
I ■■districts) chosen because they had no current or planned
| ‘-relopment projects or vitamin Asupplementation schemes. From
'random start, 450 villages were systematically selected for the
I Sudy; these were then randomised for capsule distribution after the
feline examination (programme villages, n = 229) or after the
■ollow-up examination (control villages, n = 221). 18 villages from
l^ong those still in rhe sampling frame were substituted for
[ Saccnt villages found to have started vitamin A supplementation
^‘Ore the baseline survey.
All members of the two study teams, each consisting of an
ophthalmologist (team leader), a nurse, an anthropometrist, a
dietary interviewer, five enumerators, and a driver, all fluent in the
local dialect received a month’s classroom, hospital, and field
training. The enumerators, responsible for collecting demographic
data, were unaware that mortality was a research question. Stan
dardisation exercises were done before and regularly throughout the
study. First, each village was visited to identify households
containing children aged 0-5 years and to mark their dwellings.
Within 2 days the village was visited by the full team. Enumerators
visited every house containing preschool children, collected
socioeconomic, demographic, and medical data, and rounded up
children at a central point for their clinical examination. Dates of
birth were ascertained by reference to local events charted on the
Muslim calendar and.then translated to their roman equivalent by
the use of a specially prepared conversion table. Eyes were
examined with a focused light and 2X loupes and diagnoses were
made according to standard diagnostic criteria.5,6 Parents were
carefully questioned about the presence of nightblindness. 5’' They
were also asked about a history ofdiarrhoea (4 or more loose, watery
stools per day), of fever or cough lasting at least 24 h in the previous
7 days, and of “ever having” measles.
Recumbent length (if less than 24 months old) or standing height
(if 24 months or older) to the nearest 0-1 cm, and weight (using a
calibrated Salter scale) to the nearest 0-1 kg, were measured on a
10% subsample of all study children.
All children with active xerophthalmia at baseline examination
received at least one large dose ofvitamin A and were referred to the
local health unit. They were excluded from the analyses of
subsequent morbidity and mortality. All children received vitamin
A at the follow-up examination 9-13 months later.
Teams first visited villages between September, 1982, and
August, 1983, and follow-up visits were made by the same team in
the same sequence 9-13 months later. The variation in follow-up
time resulted from attempts to minimise rhe potential confounding
influence of the xMuslim fasting month and post-fasting holidays.
Standard capsules (supplied by UNICEF) were given to every
child aged 1-5 years in programme villages, by a local volunteer
trained to do so. The capsule nipple was snipped off and the
contents (200 000 IU vitamin A and 40 IU vitamin E) were
expressed into the child’s mouth. This volunteer kept a list of
children treated and issued the household with a distribution card.
The first dose was given 1-3 months after the baseline examination
and the second 6-8 months later. A distribution monitor visited
each village 2-4 weeks after the scheduled distribution and
interviewed 10% of eligible households. If coverage was less than
80% the local distributor was encouraged to reach children
previously missed.
All data were collected on precoded forms, entered onto diskettes,
and shipped to the data management facility at the International
Center for Epidemiologic and Preventive Ophthalmology, Johns
Hopkins University, where the information was processed with the
SIR data management package run on an IBM 4341 computer.
Statistical analyses were made with SIR, SAS, and GLIM software.
Statistical tests for significance and development of confidence
intervals were adjusted for clustering associated with randomisation
by village rather than by individual, and for the small number of
events expected and observed in any one village by applying poisson
regression with extra-poisson variation to account for natural
variability in mortality among villages.8,9 Two-tailed tests were
used.
The study was designed to examine overall differences between
non-infant preschool-age children in programme versus control
villages, on the assumption that mortality would be reduced by at
"deast 20% and allowing for an alpha error of0* 05 and a beta error of
8491 © The Lancet Ltd, 1986
THELANCET.MAYjj,
L.1985
1168
Sugar and Obesity
At a conference on the link between sugar and obesity, organised in
London on May 7 by the Sugar Bureau, ProfJohn Durnin (Institute
of Physiology, University of Glasgow) reviewed research on the
subject, found much of it inconclusive, and came to the view that
sugar intake did not play an important part in the development of
obesity. He stated: “It is unfortunate that absolute proofone way or
another is unattainable because it leaves the field open to the
nutritional missionary who is prepared to ignore the considerable
weight of scientific evidence pointing clearly to no link between
sugar and obesity”.
A one-day meeting on Advances in Physiological Measu *
■
Applied to Audiology is to take place at the Postgraduate
District Hospital, York, on Thursday, May 29: Graham Frost, De0
Audiological Physics, Royal National Throat, Nose and Ear Hosn
Inn Road, London WC1X 8DA.
■P''al-Cr^
A 2-day meeting entitled NHS Health Economics Group will kl
*
•'
the James Grade Centre, Birmingham, on May 29-30: John Todd fr '*■
Medical Officer, Sheffield Health Authority, Westbrook Hou»e Sh, ’
Road, Sheffield S118EU
’
°'*
A one-day meeting on Gastrointestinal Medicine is to take place Tv
Royal College of Physicians, London, on Friday, May 30: Barbara Ca
*^
Institute ofBiology, 20 Queensberry Place, London SW7 2DZ (01-581Si)1*’
University of Edinburgh
Prof R. E. Kendell,professor of psychiatry, has been elected dean
of the faculty of medicine with effect from Oct 1.
Diary of the Week
MAY 18to 24
A one-day course on Managing a Clinical Team will be held at the British
Postgraduate Medical Federation, London WC1, on Tuesday, May 20: Mrs E.
Macklin, Education Department, British Postgraduate Medical Federation,
33 Millman Street, London WC1N 3EJ (01-831 6222).
A one-day meeting entitled The Assurance of Quality in Medical
Imaging is to be held at the Middlesex Hospital Medical School, London Wl,
on Wednesday, May 21: Mrs S. Gaffey, Assistant Secretary’, British Institute
of Radiology, 36 Portland Place, London WIN 3DG (01-580 4085).
A one-day workshop on Child Care Law for Medical Practitioners will
take place at the Charing Cross and Westminster Medical School, London W6,
on Wednesday, May 21: Sue Hilton, British Association for Adoption and
Fostering, 11 Southwark Street, London SEI IRQ.
Monday, 19th
ROYAL COLLEGE OF RADIOLOGISTS, 2 Caricon House Terrace, London SWiy
4.30
pm Prof M. A, Ferguson-Smith: The .Molecular Pathology ofSex Deierninn'
INSTITUTE OF DERMATOLOGY, St John’s Hospital for Diseases of the Skin, ut
Street, Leciester Square, London WC2H 7BJ
4.45 pm Dr C. H. Cameron: Virus Diseases of the Skin.
INSTITUTE OF NEUROLOGY, National Hospital, Queen Square, London Wiv
3BG
5 30 pm Dr Arnold Starr (California): Auditory Memory Deficits in Man and their
Evaluation with Event Related Potential.
ST GEORGE’S HOSPITAL MEDICAL SCHOOL, 3rd Floor, Lanesborough \Tjc,
Cranmer Terrace, London SW17 ORE
12.30
pm Film—Laser Surgery For Cervical Intraepithelial Neoplasia.
Tuesday, 20th
INSTITUTE OF DERMATOLOGY
A one-day meeting on Multiple Sclerosis Research will take place at the
Town Hall, Stourbridge, on Thursday, May 22: Michele Jones, Extel
Consultancy 4 Bouveric Street, London EC4Y SAB (01-353 5272).
ICRF CANCER EPIDEMIOLOGY AND CLINICAL TRIALS UNIT, Ida Greta
A one-day conference on Dementia—Action on Training is to be held at
the Royal College of Physicians, 9 Queen Street, Edinburgh, on Thursday,
May 22: Jan Killeen, Co-ordinator, Scottish Action on Dementia, 33 Castle
Street, Edinburgh EH2 3DN (031-225 5000).
Wednesday, 21st
INSTITUTE OF ORTHOPAEDICS, Middlesex Hospital, Mortimer Street, LonJoa
Wl
A one-day conference on Care in the Community—Voluntary and
Statutory Services is to be held at the County Hall, Norwich, on Thursday,
May 22: Conference Department, Royal Society of Health, RSH House, 38a
St George’s Drive, London SW1V 4BH (01-630 0121).
A one-day meeting entitled Topics in Cardiac Transplantation will take
place at the Royal Society ofMedicine, London W1, on Thursday, May 22: Dr
B. T. Marsh, Library and Scientific Research Section, Royal Society of
Medicine, 1 Wimpole Street, London Wl (01-408 2119).
5 pm ProfM. A. Epstein; EB Vims Vaccines—Current Progress and Future Strategies
7 pm Mr E. O’G. Kirwin: Assessment of the Problem Back.
ROYAL FREE HOSPITAL, Pond Street, London NW3 2QG
5 pm Dr Robert Henderson (New Haven): Microelectrode Studies of Isolated
Hepatocytes.
NORTHWICK PARK HOSPITAL AND CLINICAL RESEARCH CENTRE.
Watford Road, Harrow, Middlesex HA! 3UJ
I pm Mrs T. Rutter: Development ofa District Drugs Guide and Possible Relevance w
General Practice.
CHACE POSTGRADUATE MEDICAL CENTRE, Chase Farm Hospital, Tic
Ridgeway, Enfield, Middlesex
DURHAM POSTGRADUATE MEDICAL CENTRE, Dryburn Hospital, Durham
A one-day meeting on Aspects of Forensic Science is to take place at the
Pharmaceutical Society of Great Britain, London SEI, on Friday, May 23:
Analytical Division, Royal Society of Chemistry, Burlington House, London
W1V0BN (01-437 8656).
Thursday, 22nd
MANCHESTER MEDICAL SOCIETY, John Rylands University Library, Oxford
Road, Manchester M13 9PP
5.30
pm Prof M. Clarke: Epidemiology in a New Medical SchooL
A one-day workshop entitled An Encounter with Educational Ideas will
be held at St Bartholomew’s Hospital Medical College, London ECI, on
Friday, May 23: Maureen Gyle, Association for the Study of Medical
Education, 2 Roseangle, Dundee, Scotland DD1 4LR (0382 26801).
Friday, 23rd
CARDIOTHORACIC INSTITUTE, Fulham Road, London SW3 6HP
8 am Dr Peter Cole: Bacterial Subterfuge
A one-day meeting entitled Facing the Void-Death, Loss and
Redundancy is to rake place at the British Postgraduate Medical Federation,
London WC1, on Wednesday, May 28: Mrs E. Macklin, Education
Department, British Postgraduate Medical Federation, 33 Millman Street,
London WC1N 3EJ (01-831 6222).
Rationale for and Results from a Randomised Double-blind Trial of TeW
chlorodecaoxygen Anion Complex in Wound Healing.—We apologise to Dr JHinz and his colleagues for errors in their April 12 paper (p 825). Fig i andfig
were transposed. In table II the number of missing controls should have beJ>
134. The formula in the first line on p828should have read y=a^t c.Ta 4
III should have been:
______________ ______
| TCDO
*
Control
Wound diagnosis
P -
A one-day workshop on Research into Restoration ofHealth—Models,
Method, Markers and Measurements will be held at the Charing Cross
and Westminster Medical School, London W6, on Wednesday, May 28: Pam
Edwards, Cardiac Department, Charing Cross Hospital, Fulham Palace Road,
Hammersmith, London W6 8RF (01-748 2040 Ext 2191).
A 2-day symposium entitled Pharmaceutical Industry Interfaces is to be
held at the Royal College of Physicians, London NW1, on May 28-29: Mrs J.
Wase-Bailey, Association ofMedical Advisers in the Pharmaceutical Industry,
20 Queensberry Place, London SW7 2DZ (01-589 9076).
Correction
Venous ulcers
Postoperative problem wounds
Arterial ulcers
Other wounds
.-0-1414 ; -0-41471
-0-1414
-0-3757f
-0-2422
-0-1414
-0-1414 |1 -0-2422
«0-W!
«o-ooi
«0-001
«o-wl
•q unaifected by diagnosis (sec text).
fAlso significantly better (p <0-01) than values for TCDO (arterial ulcers) and tP’
TCDO (other wounds).
THE LANCET, MAY
0-2 (1-tailed). Stratified subgroup analyses arc, strictly speaking,
inappropriate, and, because of the small numbers, not verv reliable.
Although Indonesian government regulations proscribe
administration of vitamin A prophylactically to infants, a
considerable proportion of them received capsules nonetheless, so
the impact on infant mortality was also examined.
All study procedures were approved by a steering committee
consisting of representatives of the Indonesian Center for Nutrition
Research, the Directorate of Community Health Services, the
provincial health authorities, Johns Hopkins University, and Helen
Keller International.
Results
29 236 preschool-aged children were enumerated at
baseline. Follow-up information was available on 89 ■ 0% of
the programme children and 88 • 4% of the controls. The age
and sex distribution of children lacking follow-up was
identical in the two groups.
Baseline Characteristics
Of the 25 939 children with baseline and follow-up
information, details of the initial ocular examination are
available for 91-9% of programme children and 90-5% of
controls. Active xerophthalmia was more prevalent in
controls than in the programme group (2 • 25 versus T 88%),
but the difference was not significant and was accounted for
almost entirely by the males (table I). Xerophthalmia was
more prevalent among males than females, especially among
controls. Xerophthalmia prevalence was negligible during
the first 2 years of life (less than 0 • 5%).
TABLE 1—BASELINE PREVALENCE OF ACTIVE XEROPHTHALMIA
No of patients with:
Bitot’s spots'
(MB)
Active
*xerophthalmia
(XN, XIB. X3)
136 (/•//%)
150 (/-CT)
143 (/•/£%)
164 (/-CT)
231 (/-CT)
256 (2-25%)
69 (/•/-/%)
88(1 -.58%)
72(1-19%)
\02 (!•&%}
120 (1-99%}
150 (2-CT)
*.66(/-/2
v)
61 (/•//%)
69 (/•/;%)
59 (1-07%) |
108 (/ -CT)
103 (/d?X.)
Night
blindness’
Programme (n = 12 281)
Control (n ■ 11 378)
Mules
Programme (n = 6043)
Control (n = 5533)
Females
Programme (n = 5881)
Control (n = 5494)
• Prevalence rates for XN and XIB are not mutually exclusive. For “active
xerophthalmia" an individual was counted only once. There were only 6
patients with corneal ulceration (X3), 3 in each group. Conjunctival and
corneal xerosis were excluded as being potentially less reliable.'’
-f-Incluces 357 programme and 301 control children whose sex was unknown.
TABLE ll-AGE ANDSEX DISTRIBVTION ON NONXEROI’UTHALMIC
CHILDREN
-
Programme
Control
*
Total
12 991 (100%)
112 209 (100%)
Male
Female
Total
Baseline age (months)
<12
12-23
24-35
36-47
48-59
60-71
Total
6365(50%)
6243 (50%)
12 608(100%)
5975 (.50%)
5888 (50%)
11 863 (100%)
2074 (16-0%)
1979 (15- 2%)
2086(16-1%)
2274(17-5%)
1887 (14-5%)
2686 (20- 7%)
\2 986 (100-0%)
1979(16-2%)
1941 (15-9%)
2072(17-0%)
2016(16-5%)
1724 (14-2%)
2465 (20-2%)
12 197 (100-0%)
'Includes infants, as well as children on whom age and/or sex arc unavailable.
-f-Sex not known for some children.
||||
The age and sex distributions of the non-xeronh l ’
children in the two groups were similar (table
disproportionate number of children purported to b ■
6th year of life probably includes children really in
and 7th years, as has been noted previously.5 Progra
S
control children were also similar for most other b
demographic and socioeconomic variables in ^dr
occupation of the head of the household, maternal cdu ""-Ma
source of drinking water, distance to the nearest elen/^3
school, and distance to the nearest health centre. ' ^d 'r,
The two groups were also similar in most health var' kRS
such as recent history of fever or cough or of ever havi k
measles; relative risks of these variables for the two
■
differed by less than 5% (table III) except for diarrfo^1 recent history being 23% commoner among control tL’
programme children (p=<0-05), with the greatest excess 1
girls. Recent diarrhoea was commonest during the 2nd
'
of life, when the frequency was 9 • 8% in programme villa^ '
and 10 • 7% in control villages. Thereafter it steadily declined "i
The most objective baseline health variable was nutritional ’
status. Anthropometric indices were similar for the tw
groups, both total and sex-specific (table IV).10 ■
In 99% of children in the two study groups, the interval
between baseline and follow-up examination was at least 11
months, and for 59%, at least 12 months. This interval did
not vary among age-sex-specific categories by more than
±2%.
Vitamin A Distribution Level
Of our three methods of monitoring for capsule
administration only interrogation of the child’s guardian(s)
proved feasible. Report forms provided by the local
distributors were largely illegible, and most cards issued to
households were faded, torn, or lost.
Over 93% of preschool children (12-71 months at baseline)
living in programme villages received at least one large dose
of vitamin A between baseline and follow-up examinations;
CABLE 111—BASELINE MORBIDITY VARIABLES
Cough’
Measlcsf
Diarrhoea'
Relative risk
compared
Control
Programme
Total
no
positive
no
positive
for control
12 781
12 781
11 753
12 781
31-2
45-7
IT. I
7-1
11 555
II 555
10 059
11 555
32-7
46-7
21'7
8-7
1-05
1-02
0-97
1-23
* Present in past seven days. Dal. missing on 210progranimechildrenand65l
controls.
j-Anv lime in past. Smaller denominator because ofchange in question shonlr
after survey began.
,
TABLE IV—BASE LINE ANTHROI’OAtE' FRY
|
—
Height for age (% of median) *
<85+
85-89
90-94
>95
Weight for height (% of median)
*
<80
80-89
^90
Programme
(n=1382)
Control
(n= 1271)__
8’9%
8-2%
23-9%
43-0%
24-9%
37-8%
*725%
3-0%
38-3%
58-6%
y /VO
*6%
35
60-7%___ _
■Median NCHS standards.” Represents 10% subsample of children.
fLess than 1 • 5% of children m either group were below 80% of median.
1171
TABLE Vl-AGE AND SEX-SPECIFIC MORTALITY DURING FOLLOW-UP
Programme villages
Baseline
age
(months)
Both sexes
12-23
24-35
36-47
48-59
60-71
Total
*
preschool
Control villages
Proportion
dying
Rate
per
1000
Proportion
dying
Rate
per
1000
RR
19/1979
14/2086
11/2274
' 5/1887
4/2686
*69
A• j
4*8
2*6
1 1,5
22/1941
25/2072
8/2016
7/1724
13/2465
11'3
*112
4*0
4-1
5*3
1.1,
1*81
0*83
1*58
3-53
53/10 917
4*9
75/10 230
7*4
48/2074
*1
23
55/1979
*8
27
*03,
(1
Infants (<12)
*Total
(0-71)
■ Malesf
0-11
Total
(0-71)
; ;$■;> received two doses (table V). In every age-group coverage
i if boys and girls differed by less than 1%.
|SIn theory, only two-thirds of the infants were eligible for
it capsule and less than one-quarter for two. Surprisingly,
g®o received at least one capsule and almost 62% both. This
[discrepancy may reflect disregard of normal government
guidelines or of small differences in age.
SOnly 1% of control subjects received any capsule,
presumably obtained at the health centres by children
presenting with xerophthalmia.
Impact on Xerophthalmia and Mortality
L The prevalence of active xerophthalmia in programme
tillages declined from 1 • 9% at baseline to 0- 3% at follow-up
and that in the control villages declined from 2 • 3% to 1 • 2%.
These changes meant that the risk of xerophthalmia in
control villages relative to that in programme villages rose
from 1-2 at baseline to 4-0 at follow-up (p<0'05). Sexipecific prevalence rates followed a similar pattern.
During rhe follow-up period 75 preschool study children
com control villages and 53 from programme villages died,
living mortality rates of 7-4 and 4-9 per 1000, respectively
(p<0-O5, two-tailed) (table VI). The relative risk of dying in
control versus programme villages was therefore 1-51 (95%
confidence limits 1-03, 2-28)", equivalent to a reduction in
mortality in programme villages of 34%. Infants in control
tillages had a mortality rate 21% greater than those in
programme villages.
To compare age/sex/study group-specific mortality,
children were classed as preschool children and infants (table
;1). Both infant and preschool control boys died 70% more
^quently than did those in the programme villages. The
■dative risk of death for boys in control versus programme
Ullages was 1-69(95% confidence limits 1 ■ 14,2 - 51). Excess
Mortality was less pronounced among control girls, in whom
’was limited to preschool children.
To examine further the effect of large doses ofvitamin A on
Mortality, cumulative sex-specific mortality rates for prekhool children were calculated every month after baseline
^amination (see accompanying figure). Boys and girls show
"oilar patterns: mortality in control villages was initially the
6me as (females) or lower (males) than that in programme
’Mages; with time, mortality in control villages gradually
Fcmaksf
0-11
Total
(0-71)
101/12 991
7*8
130/12 209
2*8)4:
*73,
(0
1*97)4:
*01,
(1
1*36
1*85)4:
*6
10
18/1014
28/5348
*817
5*2
29/970'
44/4998
*929
8-8
1-68
1*69
46/6362
7*2
73/5968
*2
12
1*69
* 14,2-51)4:
(1
28/994
23/5245
*228
4*
25/942
27/4933
“A - 1
*904
1-25
51/6239
8*2
52/5875
...
*71,
(0
1*09
1*71)4:
•Includes children with age unknown
•f* Excludes children for whom age and/or sex are unknown.
4=95<5’b confidence limits.
exceeded mortality in programme villages, a trend which was
more pronounced in boys; by the end ofthe follow-up period,
2-4 months after the second dose of vitamin A, cumulative
mortality had reached a plateau in programme villages, but it
continued to climb in control villages. The pattern among
infant boys mimicked that of preschool boys. Cumulative
mortality among infant girls in control villages was virtually
indistinguishable from that in programme villages.
examination for preschool children (aged 12-71 months at
baseline examination).
First dose given during months 1-3; second a mean of 6 months later.
Males—denominator for first 12 months in programme villages, 5351 (no
further deaths); in control villages, 5005 initially, 3046 during the last month.
Females—denominator for first 12 months in programme villages, 5249 (no
further deaths); in control villages, 4946 initially and 2978 during the last
month.
THE LANCET, MAY 24,'j^-j
Discussion
Mortality rates have been reported to be higher inmalnourished children in hospital with xerophthalmia than
in those with normal eyes."112 However, another study has
shown that in children admitted to hospital for
xerophthalmia, severe malnutrition was the most important
factor associated with mortality? Interpretation of these
studies is hindered by the biases inherent in family
motivation and hospital admission criteria, and the impact
intensive therapy has on mortality.
In a longitudinal study of 4000 preschool-aged Javanese
children we found that children with mild xerophthalmia
(night blindness, Bitot’s spots, or the two conditions
together—a ranking shown to be closely correlated with
serum vitamin A levels’’') died at four times the rate for their
non-xerophthalmic peers; the excess mortality was related to
the severity of the xerophthalmia; and this “dose-related”
risk was independent of the child’s general nutritional
status.1,2 The shape ofthe dose-response curve suggested that
subclinical vitamin A deficiency (ie, in the absence of
detectable xerophthalmia) was also associated with increased
mortality. Follow-up of surviving children revealed that
respiratory and diarrhoeal diseases were 2*-4
times more
likely to have developed in those who had been
xerophthalmic than in their non-xerophthalmic peers?
Again, vitamin A status seemed to be more important than
anthropometric status in predicting morbidity.
The present study was thus undertaken, partly to
determine whether supplements of vitamin A given to
preschool children (12-71 months ofage) would reduce their
mortality by at least 15%. Ideally all “treatment” children
would have received at least the recommended daily
allowance. But this would have required a special,
impracticable delivery system. Instead we opted for the
regular Indonesian government scheme of twice-a-year
administration of UNICEF-supplied capsules by trained
local volunteers, although we realised that it did not cover
infants. The Government of Indonesia would not condone
the use of placebos but field-workers collecting demographic
data were unaware that mortality was a research issue.
Strict randomisation of the 450 study villages seemed to
have worked reasonably well. The populations were similar
in most baseline characteristics investigated except for
xerophthalmia and history of recent diarrhoea, which were
slightly more prevalent among the controls. The differences
between programme and control populations in mortality
were out of proportion to their baseline differences; the
baseline difference in diarrhoeal history was greatest for
females, whereas excess mortality was greatest for males; and
the most objective, quantifiable baseline indices of health
status, weight-for-height and height-for-age, were virtually
identical in the two groups on both an age and sex specific
basis.
There was no evidence during the course of the study of
differences in economic or medical initiatives in the study
area, though clearly the vitamin A status throughout the
province was improving as shown by a substantial reduction
in prevalence of xerophthalmia between the 1978 nationwide
survey and the baseline examination in the present study.
The reduction in prevalence of xerophthalmia in control
villages during our study may have been part of the general
spontaneous improvement, which is the reason for having
controls?’6 The mortality rates in this study were also lower
than previously recorded for Java,1’ where rates seem to be
falling, and more closely resemble those of neighb0•' ■ ?'
“medium” infant mortality rate countries (eg, Phi|jD • 3 $
Malaysia, Thailand), where the median mortality"?--®
preschool-aged children is 3 per 1000.14
.. 10 -
Results were strongly positive, even jn 'l ". Sa
“intent-to-treat" analysis. Xerophthalmia prevalences * . '
preschool children living in programme villages declin j?.'J
85%, a result similar to those obtained in other car a ?■
conducted pilot trials,’’1’17 and it confirms thel, a|
distribution rate of capsules reported. Preschool co
children died 1 • 5 times more frequently than did program ° -‘1
children (95% confidence limits 1 -03, 2-28), equivalent
1
34% reduction in non-infant mortality among residents'01 1
programme villages. To control for baseline differences
1
prevalence of xerophthalmia and history of recent diarrh "" •
between programme and control villages, the proportion^- 1
children with xerophthalmia or recent history ofdiarrhoeas J
baseline was included as a covariate (predictor variable) in ,hc
analysis. Mortality results (relative risks and their confidence
limits) were nearly identical when either xerophthalmia alone
or when both xerophthalmia and diarrhoea were included in
the analysis.
.
Although the study was not designed to investigate
subgroups, and the numbers concerned preclude definite
conclusions, they provide additional evidence consistent with
the beneficial impact of vitamin A supplementationmortality among controls was greater at almost every age
including the first year of life; the difference in cumulative
mortality increased with time, even though male and female
controls had initial mortality rates that were the same as or
lower than those in programme villages; the impact was
greatest among boys, in whom vitamin A deficiency is
generally far more prevalent;’’l7'20 and among boys, the timerelated mortality pattern corresponded with the expected
temporal impact of capsule distribution. This interna!
consistency and agreement with previous studies is more
important than the size of the p value or width of the
confidence limits, which are direct consequences of the
enormous sample size required.
,
These results are especially encouraging for the following
reasons: capsule distribution was less than universal and
probably missed those who needed it most;21 single largedose supplementation maintains raised serum vitamin A
levels for only 1-3 months;22 distribution did not start until
1-3 months after enumeration; xerophthalmic controls took
vitamin A at health centres; and those in whom the grearest
impact might have been expected (children xerophthalmicat
baseline) were treated and dropped from the analysis.
1
1
I
|
'
i
:
|
4
I"
j
1
'
|
I
]
1
i
,
1
i
»
|
]
How vitamin A reduces mortality remains uncertain, j
Vitamin A deficiency is, associated with changes in surface •
epithelium and these may disrupt normal barrier function,
support bacterial growth (as seen on the conjunctiva2’ and
presumably the bladder21), and obstruct smaller branches of I
the tracheobronchial tree. Abnormalities in systemic immune
competence associated with vitamin A deficiency may also be
as important in contributing to mortality; in animals at leas', |
vitamin A deficiency interferes with humoral and especially |
cell-mediated immunity.2”2' Limited data suggest similar
effects in man.2” High doses of vitamin A given to otherwise |
normal animals have been reported to produce a non-spec“'6’
adjuvant-like increase in resistance to infection." 2 e
response to the high doses given in our study was unlikely to |
be due to non-specific changes. The children came from3 i
vitamin A deficient population’’’ and the impact "
J
1173
> ined. The rise in blood retinyl ester levels after one large
Kof vitamin A given to deficient patients do not last for
J’5" than 8-12 weeks;22,10 and holo-retinol-binding-protein
rise,.bin not above normal levels.10'11
presence of the study teams was unlikely to have
riflojnced the results ofour study because the only difference
,P ,et.n programme and control villages in their interaction
— h study personnel consisted of at most two contacts in 12
fcnths
the loca' v‘tamin A distributor in treatment
-phis distributor was neither trained nor instructed to
"S-Lriake any other intervention.
.^iiarnin A status probably modulates the incidence and
Verity
disease caused by a variety of pathogenic
■Linisms. The impact that vitamin A supplementation will
Son mortality will therefore depend upon a constellation
iffactors, including the prevalence and severity of vitamin A
agjdency; the frequency of exposure to pathogenic
-nanisms, size of the inoculum, and their virulence; and the
.^sence and degree of other adverse influences with which
{je young child must contend (eg, malnutrition, parasitic
tod). The results of the study reported here and those done in
hra1’1 confirm the importance that vitamin A deficiency in
thildhood has on mortality in Indonesia and show the impact
[hat supplementation can have on child survival.
nTbis study was carried out under cooperative agreement DSAN-CA-0267
rjh the Office of Nutrition, United States Agency for international
Development, with additional financial assistance from Hoffinan-La Roche,
y T Vicks, Ford Foundation, UNICEF, and the Asian Foundation for rhe
-Prevention of Blindness.
ICThe Aceh Study Group includes the following professional stall', apart front
pose listed as authors: Dr Akbar I’andji, Dr Koesdiono. Dr Daniel Kraushar,
red Dr Hugh R. Taylor; Barbara Hawkins, Imam Satibi. and William
Bumenbaum. Dr Scott Zcger developed the statistical methodology.
■ Correspondence should be addressed to A. S., Dana Center for Preventive
Ophthalmology, Wilmer Institute 120, 600 North Wolfe Street, Baltimore,
'Mityland 21205, USA.
PRE-OPERATIVE IDENTIFICATION OF
PATIENTS AT HIGH RISK OF DEEP VENOUS
THROMBOSIS AFTER ELECTIVE MAJOR
ABDOMINAL SURGERY
Henry M. Sue-Ling
David Johnston
Michael J. McMahon
Peter R. Philips1
J. Andrew Davies
University Departments of Medicine and Surgery,
General Infirmary, Leeds, and Health Care Research Unit,
University of Newcastle upon Tyne
Eighteen items of clinical and laboratory
information were measured on the day
before operation in 85 patients who underwent elective major
abdominal surgery. Postoperatively, deep venous thrombosis
(DVT) was detected by l2’I-ftbrinogen scan in 23 patients.
Stepwise logistic discriminant analysis was used to identify
factors which predicted DVT. Seven such factors were
identified, which were then used to construct a predictive
index. In descending order of predictive power, they were:
age, euglobulin lysis time (ELT), previous abdominal
surgery, varicose veins, antithrombin III concentration,
cigarette smoking, and platelet count. Pre-operatively, the
predictive index correctly identified 91% of the patients in
whom DVT developed, and wrongly allocated to the highrisk group 19% of those in whom it did not. A shortened
version of the predictive index based only on age and ELT
(1= - 11 - 5+0• 133 age+ 0-006 ELT) was 91% sensitive and
63% specific in the prediction ofDVT. Ina prospective study
of 43 patients, this shortened predictive index correctly
identified pre-operatively 93% of patients in whom DVT
developed, and wrongly allocated to the high-risk group only
17% of those in whom it did not.
Summary
Introduction
DEEP venous
thrombosis
(DVT) develops
in
approximately 30% of general surgical patients after elective
major abdominal surgery.12 Prophylactic measures, such as
the administration of low-dose heparin or dextran,
significantly reduce the frequency of postoperative deep
venous thrombosis and pulmonary embolism.i-’ However,
A. SOMMER AND OTHERS: REFERENCES—continued
Reference! continued at foot of next column
A/UT I ■ G
COMMUNITY HEALTH CELL
No: 367, 'Srinivasa Niiaya'
Jakkasandra, I Main, 1 Block,
Koramangala,
BANGALORE - 5G0 034.
REDUCED MORTALITY AMONG CHILDREN IN SOUTHERN INDIA RECEIVING A SMALL
WEEKLY DOSE OF VITAMIN A
Laxmi Rahmathullah, M.B., B.S., D.T.P.H., Barbara A. Underwood, Ph.D.,
Ravilla D. Thulasiraj, M.B.A., Roy C. Milton, Ph.D., Kala Ramaswamy, M.Sc.,
Raheem Rahmathullah, and Ganeesh Babu, B.Com.
Abstract Background. Clinical vitamin A deficiency af
fects millions of children worldwide, and subdinical defi
ciency is even more common. Supplemental vitamin A has
been reported to reduce mortality among these children,
but the results have been questioned.
Methods. We conducted a randomized, controlled,
masked clinical trial for one year in southern India involv
ing 15,419 preschool-age children who received either 8.7
/xmol (8333 IU) of vitamin A and 46 p.mol (20 mg) of vita
min E (the treated group) or vitamin E alone (the control
group). Vitamin supplements were delivered weekly by
community health volunteers who also recorded mortality
and morbidity. Weekly contact was made with at least 88
percent of the children in both study groups. The base-line
characteristics of the children were similar and document
ed a high prevalence of vitamin A deficiency and undernu
trition.
Results. One hundred twenty-five deaths occurred, of
which 117 were not accidental. The risk of death in the
group treated with vitamin A was less than half that in the
control group (relative risk, 0.46; 95 percent confidence
interval, 0.30 to 0.71). The risk was most reduced among
children under 3 years of age (6 to 11 months — relative
risk, 0.28; 95 percent confidence interval, 0.09 to 0.85; 12
to 35 months — relative risk, 0.46; 95 percent confidence
interval, 0.26 to 0.81) and among those who were chron
ically undernourished, as manifested by stunting (relative
risk, 0.11; 95 percent confidence interval, 0.03 to 0.36).
The symptom-specific risk of mortality was significantly
associated with diarrhea, convulsions, and other infectionrelated symptoms.
Conclusions. The regular provision of a supplement of
vitamin A to children, at a level potentially obtainable from
foods, in an area where vitamin A deficiency and under
nutrition are documented public health problems contribut
ed substantially to children's survival; mortality was re
duced on average by 54 percent. (N Engl J Med 1990;
323:929-35.)
WENTY to 40 million children worldwide are
estimated to have at least mild vitamin A defi
ciency, and nearly half are said to reside in/India.1
Controlled field trials in an area of endemic/vitamin
A deficiency in Indonesia revealed a reduction of
34 percent in mortality among infants arid young
children given high-dose vitamin A supplements,2
and a reduction of up to an estimated 75 percent3
after periodic mass treatment with large-dose (209
/xmol [200,000 IU]) vitamin A. Reductions in mor
tality of 11 to 45 percent were reported after the nor
mal marketing of vitamin A-fortified monosodium
glutamate.4 The results of these studies and an earlier
observational trial in Indonesia5 have been questioned
because of aspects of the study designs6 and because
the mortality data provided no cause-specific infor-
mation and were obtained retrospectively, assuming
compliance.4
Clarifying the role of vitamin A deficiency in child
health and survival and defining successful, sustain
able control measures have broad public health, pub
lic policy, and programmatic importance. For this rea
son, we conducted a randomized, placebo-controlled,
masked clinical trial among 15,419 preschool-age chil
dren using a small, weekly dose of vitamin A (8.7
/xmol [8333 IU]) given directly to the children by
community health volunteers. We monitored morbid
ity and mortality weekly for one year. The dose of
vitamin A was meant to simulate the amount that
could be obtained from food, if food consumption was
near the level recommended by international groups
(approximately 1 to 1.4 /xmol [300 to 400 p.g] of vita
min A daily7,8).
T
From the Aravind Children's Hospital and Aravind Eye Hospital, Madurai,
India (L.R.. R.D.T., K.R., R.R, G.B.); the Office of International Programs
(B.A.U.) and the Biometry and Epidemiology Program (R.C.M.), National Eye
Institute, Bethesda. Md. Address reprint requests to Dr. Underwood at the Na
tional Eye Institute, Bldg. 31, Rm. 6A-I7, 9000 Rockville Pike. Belhesda. MD
20892.
Supported by a grant from the Ford Foundation, New Delhi, India.
Methods
The study was carried out in three drought-prone, economically
and environmentally deprived panchayat unions (local-government
areas) in the Trichy district of Tamil Nadu in southern India. The
people of the area had been underserved by child-care programs,
including the national program of administering a large-dose (209
Reprinted from the New England Journal of Medicine
323:929-935 (October 4), 1990
930
THE NEW ENGLAND JOURNAL OF MEDICINE
/xmol) supplement of vitamin A every six months. A survey of all
children under 60 months of age in the study area revealed that only
1 percent had participated in this program.
The study was reviewed and approved by the human-subjects
internal review boards of the Indian Council of Medical Research
and the Aravind Eye Hospital. Informed consent was obtained from
the leaders of the panchayat unions and then from the individual
families at the time of the base-line survey.
Survey Personnel and Procedures
All the communities within the areas selected for study were
mapped by locally recruited enumerators. A house-by-house demo
graphic and socioeconomic survey was carried out by specially
trained local workers, who also obtained from each mother a fiveyear history of mortality among her preschool-age children. House
holds with children under 60 months of age were identified and
assigned a census number.
Two medical-examination teams were formed, consisting of a
medical officer, nurses, and child-care and social workers. The
child-care and social workers were trained to undertake ocular ex
aminations, anthropometric measurements, and a morbidity histo
ry. The ocular examination was checked by the medical officer who
conducted the medical examination and verified the morbidity his
tory. The ocular examination was repeated by the same trained
fieldworkers after six months of intervention, and all the indexes
measured at base line were reassessed by the medical teams at the
A finger-prick blood sample and a dietary history detailing the
frequency of intake of locally available foods containing vitamin A9
were obtained from a randomly selected 2 percent of the children by
specially trained community workers.
At the base-line medical examination, all the children with symp
toms of xerophthalmia, including night blindness, were treated with
a large-dose combination of vitamin A (209 ^imol) and vitamin E
(46 Atmol), and they continued to be followed as part of the study.
The data were analyzed both including and excluding them. Chil
dren with symptoms of xerophthalmia at the six-month and final
ocular examinations were treated in a similar manner. All the chil
dren were given the large-dose supplement during their final medi
cal examination at the end of the study.
The children’s height (or length for those under 24 months) was
measured to the nearest centimeter with a calibrated board. Weight
was determined to the nearest 0.1 kg with a hanging Salter scale.
The ocular examination was performed with the classification
criteria of the World Health Organization.10 A history of night
blindness was obtained by interviewing the mother about the inci
dence in her children of malai ken, a term used in Tamil Nadu to
describe the commonly recognized symptom of “evening eyes,” the
inability to see well in dim light. The same term was subsequently
used by the community health volunteers to monitor the occurrence
of night blindness on a weekly basis.
Fieldworkers were aware that they were involved in a study to
determine the effect on morbidity of giving vitamins, but they were
not told that the study was specifically one of vitamin A or that
mortality was an outcome variable.
Randomization
Because of the varied population density in the panchayat unions,
we used a cluster-sampling design. From the 15,419 children identi
fied and examined at base line, 206 clusters were formed on the
basis of the minimal and maximal workloads that could be expected
from the community health volunteers. The majority of clusters
consisted of 50 to 100 children 6 to 60 months of age. The clus
ters were arranged according to population size; after a ran
dom start, they were assigned alternately to the treated or control
groups. The adequacy of randomization in achieving matching
according to base-line data was checked for the following char
acteristics: age and sex distribution, one-month history of di
arrhea and respiratory disease, anthropometric indexes of nu
tritional status, xerophthalmia status, five-year retrospective history
of mortality of children under five, household economic and
Oct. 4, 1990
hygienic status, and serum retinol levels. Matching was satisfactory
at base line for all the variables examined.
Implementation and Management
Community health volunteers were trained to dispense the sup
plement, collect morbidity data, and record mortality according to a
standard procedure. The volunteers visited each home assigned to
them every week for 52 weeks. During the visits they recorded ill
nesses according to symptoms and duration and checked for any
deaths. They dispensed the appropriate liquid supplement directly
into the mouth of the study child from a calibrated, color-coded
amber bottle. Community health volunteers knew that they were
responsible for dispensing from one color-coded bottle, but they
were unaware of what it contained other than vitamins.
Trained supervisors were each assigned to oversee seven or eight
community health volunteers. The supervisors were responsible for
weekly meetings with the volunteers to verify the completeness of
the morbidity-data forms for the previous week and to review their
proper use. The supervisors also collected the dispensers each week
and distributed refilled bottles. In addition, they checked the accu
racy of the data gathered from a random 5 percent of the house
holds weekly.
A block officer met every week with the supervisors to review the
forms and procedures, discuss problems, and provide refilled bottles
for delivery to the community health volunteers. The supervisors
were informed weekly of the performance — in terms of rates of
contact and accuracy in data recording — of the community health
volunteers for whom they were responsible. Evidence of problems
was sought and the difficulties were remedied within a two-week
period. Unannounced spot checks on households were conducted by
block officers and headquarters staff.
Data were verified and then recorded on diskettes with use of
portable computers in the field offices. The diskettes were sent week
ly to the headquarters office, where they were again checked for
completeness and accuracy. The procedures for personnel and data
management allowed close surveillance and a two-week feedback to
the field staff regarding their performance, thus giving them time to
correct any possible errors.
Supplements
Liquid supplements (kindly provided by Hoffmann-LaRoche,
Basel, Switzerland) were provided in color-coded aluminum cans
containing approximately 1 liter each. The appearance and taste of
the solutions were identical. The solution containing vitamin A was
prepared to contain approximately the following: 8.7 gmol (8333
IU or 2500 jig) of vitamin A palmitate and 46 /zmol (20 mg) of
vitamin E per milliliter dissolved in peanut oil. The placebo solution
contained approximately 46 /xmol (20 mg) of vitamin E per millili
ter dissolved in peanut oil.
The stability of the solutions was checked by HoffmannLaRoche initially and after 1, 3, 6, and 12 months of storage, at
room temperature, 35°C, and 45°G, in both the dispenser bottles
and the aluminum flasks. In the flasks there was no loss of vitamin
A and about a 10 percent loss of vitamin E, and in the bottles there
was a loss of less than 5 percent of vitamin A after one year or less at
room temperature and at 35°C. Stability was also checked by ran
domly withdrawing dispensers from the study areas halfway
through and at the end of the study. The field-laboratory analyses,
done approximately 18 to 24 months after the supply had been
received in India and used under the conditions of storage prevail
ing in the field, revealed a vitamin A loss of approximately 25
percent.
Data Monitoring
Six months after the weekly distribution began, a data-monitoring committee reviewed the data, summarized according to dose
color code only. No one associated with the study was aware of the
color code, which was held by Hoffmann-LaRoche until the study
ended. Although differences were evident in the mortality trends of
the study groups after six months, they could not be associated
Vol. 323
No. 14
SUPPLEMENTAL VITAMIN A AND CHILD MORTALITY — RAHMATHULLAH ET AL.
unambiguously with the incidence, severity, or duration of morbid
ity. The committee concluded that the study should continue.
Table 1. Doses Missed and Minimal Amount of Vita
min A Received during 52 Weeks of Intervention.
Statistical Analysis
Randomization according to cluster rather than according to
child introduced a moderate increase (about 30 percent) in the
variance of the estimators of the relative risk of death in the treated
group as compared with the control group. Relative risks, signifi
cance, and confidence intervals were therefore calculated according
to the cluster design." The risk of death among the controls was
used as the reference value for relative risk of death: a relative risk
of 0.5 means that the risk in the treated group was half that among
the controls, or conversely, that the risk among the controls was
twice that in the treated group. All ages were adjusted to reflect age
at the start of the intervention, which began on the same date for all
the children.
Nutritional status was assessed with use of the CASP anthropo
metric software package (version 3.0) provided by the U.S. Centers
for Disease Control. Values more than 2 SD below the reference
value were considered abnormal.
931
No. OF
Doses Missed
Percent of
Children
(N = 15,419)
Minimal Amount
Received*
nmol (IU)
0
41.8
38.7
6-10
11-15
16-20
21-26
27-31
>31
3.2
2.0
0.7
5.0
453 (433,000)
410(390,000)
366 (349,000)
322 (307,000)
279 (266,000)
227 (216.000)
183 (174,000)
tion: 453/xmol - (maximal number of doses missed x 8.7/rmol) = min
imal amount received.
Results
Mortality data and associated morbidity are report
ed here. An analysis of morbidity in the 15,419 chil
dren is currently under way.
Contact with the Children
During each of the 52 weeks of the study, at least 88
percent of the children were contacted. There was no
difference in rates of contact between the treated and
control groups. The reasons for lack of contact (of
which some children had more than one) included
moving from the study area (10 percent), temporary
absence (13 percent), refusal to participate (28 per
cent), sickness (29 percent), and other reasons (30
percent). Table 1 summarizes the study contact and
compliance in terms of the number of weeks the dose
was missed. Nearly 42 percent of the children received
all the doses. For those in the treated group, this was
equivalent to more than 453 p.mol (433,000 IU) of
vitamin A, or approximately the amount available in
the commonly used large-dose supplement (209 p.mol
every six months). More than 90 percent of the chil
dren received at least 322 ju.mol (307,000 IU), which is
equivalent to more than 70 percent of what they
would have received in a large-dose supplement.
Base-Line Characteristics
Sex, age, xerophthalmia status, serum retinol level,
and nutritional status at base line are shown in Table
2.
There were no substantial differences in these in
dexes between the control and treated groups. Al
though the study was meant to include only children
from 6 to 60 months of age, birth records were un
available, and our recall records include a small num
ber of younger (1.8 percent) and older (5.4 percent)
children.
The base-line prevalence of xerophthalmia was 11
percent. The risk of xerophthalmia did not differ ac
cording to sex, except for a slight predominance
among boys after three years of age. Thirty-seven per
cent of the serum retinol values from the randomly
sampled subgroup (n = 280) were =50.70 /xmol per
liter, and 21 percent were ^0.35 /xmol per liter. The
prevalence of vitamin A deficiency in each of the clini
cal and biochemical categories thus exceeded the
World Health Organization’s criteria for a public
health problem.10 Seven cases of active corneal in
volvement (category X2, X3A, or X3B) were seen
Table 2. Base-Line Characteristics of the Study
Population.
Characteristic
Sex
Male
Female
Age (mo)
*
«S5
12-23
24-35
36-47
48-60
61-71
Xerophthalmia status!
XN
X1B
X2, X3A, X3B
XS
Serum retinol (/zmol/Iiter)
=50.35
0.351-0.70
0.701-1.05
>1.05
Nutritional status!
Stunted
Wasted
Stunted and wasted
Normal
Unknown
Percentage of
Children
52
48
1.8
7 1
20.0
21.2
22.1
22.4
5.4
77
7.2
0.05
0.07
21.4
16.1
16.4
46.1
31
23
18
25
3
•Age at the start of intervention.
tXN indicates night blindness, X1B Bildt's spot, X2 comeal xerosis,
X3A corneal ulceration or keratomalacia of less than one third of the
comeal surface, X3B corneal ulceration or keratomalacia of one third or
tAs determined with the CASP anthropometric software package. Stunt
ed indicates height for age < the mean minus 2 SD and weight for height >
the mean minus 2 SD; wasted indicates height for age > the mean minus
2 SD and weight for height < the mean minus 2 SD; stunted and wasted
indicates height forage < the mean minus 2 SD and weight for height < the
mean minus 2 SD; and normal indicates height for age the mean minus
2 SD and weight for height the mean minus 2 SD.
932
THE NEW ENGLAND JOURNAL OF MEDICINE
Oct. 4, 1990
Table 3 shows the mortality according to age and
study group for the 117 nonaccidental deaths. The risk
of death in the group receiving vitamin A was 46 per
cent of that in the control group. The relative risk was
reduced most for infants (relative risk, 0.28; 95 percent
confidence interval, 0.09 to 0.85) and those 12 to 35
months of age (relative risk, 0.46; 95 percent confi
dence interval, 0.26 to 0.81); it was less than 1.0 in all
age groups. Excluding the children who had received
the high-dose supplement at any time or who received
it only at base line did not substantially change the
age-specific relative risks shown in Table 3. In addi
tion, these relative risks were not significantly changed
by excluding those who did not receive the study sup
plements for more than seven consecutive weeks
(n = 1863) or those who did not receive the supple
ments for more than four weeks on four occasions
(n = 11). These exclusions were designed to minimize
Mortality Outcome
any possible confounding due to a differential partici
There were 125 deaths in the study population dur
pation effect or missing the supplements for a pro
ing the 52 weeks of surveillance, for an overall mortal
longed period.
ity rate of 8.1 per 1000. Eight of these deaths, how
Among the nonaccidental deaths, 18 occurred
ever, involved accidents unrelated to symptoms that
among children with xerophthalmia at base line. All
could have been associated with the intake of vitamin
18 occurred in children over 12 months of age (12
A: animal bite (two deaths), drowning (three), poison
children in the control group and 6 in the treated
ing (one), and falling (two). Five of the accidental
group). The death rate among children with xe
deaths were in the treated group and three in the con
rophthalmia was 10.6 per 1000, as compared with 7.2
trol group.
per 1000 among the children without xerophthalmia.
Figure 1 shows the cumulative deaths according to
Table 4 shows the symptom- and disease-specific
study group. Regardless of treatment, girls were at
relative risk of death in the treated and control groups.
somewhat higher risk of death than boys, but not sig
According to the “verbal autopsy,” there were too few
nificantly so (relative risk, 1.5 in the control group and
deaths specifically associated with the symptoms of
1.2
in the treated group). Vitamin A significantly re respiratory disease and malnutrition to provide a reli
duced the risk of death for both sexes, the effect being
able relative risk. Excluding these two categories of
somewhat larger for girls (relative risk, 0.41 for girls
symptoms, the relative risk was consistently lower for
[P<0.01] and 0.52 for boys [PC0.05]).
the treated group — and significantly so, except for
deaths associated with measles. More than 40 percent
of the deaths were associated with diarrhea, 16 per
cent with measles, and the remainder with symptoms
suggesting other infections.
Table 5 shows the mortality according to treatment
group and base-line nutritional status. Data on nutri
tional status were missing for 469 children (3 percent),
among whom 7 died (6 in the control group and 1 in
the treated group). Among the children not treated
with vitamin A (the control group), the death rate of
those who were both stunted and wasted was 1.5 to
2 times higher than the death rate of those who were
either stunted or wasted, and it was 2.7 times higher
than the rate of normal children. Thus, the risk of
death was increased by acute undernutrition superim
posed on chronic malnutrition. But the effect of treat
ment with vitamin A was pronounced (relative risk,
0.11; P = 0.01; 95 percent confidence interval, 0.03 to
Figure 1. Cumulative Deaths Monitored Weekly, According to
0.36) among stunted children, whereas it was not sig
Study Group.
nificant among wasted, stunted and wasted, or normal
The solid line represents the group treated with vitamin A, and the
children.
line broken by squares the control group. Children who died in
A hierarchical log-linear model was used to assess
accidents (five in the treated group and three in the control group)
are included.
the multivariate relation among death, treatment, age,
(four in the control group and three in the treated
group). Night blindness accounted for about one third
and Bitot’s spots for about two thirds of the milder
cases of xerophthalmia.
Seventy-two percent of the children were classified
by anthropometry as undernourished (defined as
more than 2 SD below the reference mean). Approxi
mately one third of the children were stunted, 18 per
cent stunted and wasted, and 23 percent wasted (Ta
ble 2). Stunting thus affected a somewhat larger
proportion of the children than wasting, indicating
that prolonged malnutrition was more common than
acute undernutrition among the study children.
The five-year history of mortality among children
under five years of age taken at base line was not
significantly different between families of control and
families of treated children (data not shown).
Vol. 323
SUPPLEMENTAL VITAMIN A AND CHILD MORTALITY — RAHMATHULLAH ET AL.
No. 14
sex, and nutritional status. The significant association
between treatment and death persisted when adjusted
simultaneously for age, sex, and nutritional status.
Table 4. Symptom- and Disease-Specific Mortality,
According to Treatment Group.
Control
Symptoms or
Discussion
Table 3. Mortality, According to Age and Study Group.
0-11 Mo
Control
Treated
12-35 Mo
Control
Treated
>36 Mo
Control
Treated
Total
Control
Treated
Age-adjusted total
No. OF
Children
Deaths
Cumulative
Mortality Rate
678
689
14
4
0.021
0.006
0.28 (0.09, 0.85)t
3185
3179
52
24
0.016
0.008
0 46 (0.26, 0.81)
*
3792
3896
14
9
0.004
0.002
0.63 (0.26, 1.50)
7655
7764
80
37
0.010
0.005
0.46 (0.29, 0.71)
*
Relative Risk*
0.46 (0.30, 0.71)
*
‘Relative risk for the treated group, as compared with the control group. Values in parenthctP = 0.05.
Relative Risk*
Group
no. of children
The results of this community-based, masked con
trolled field trial clearly indicate that in an area where
clinical vitamin A deficiency and chronic undernutri
tion are common, ensuring a constant consumption of
vitamin A at least equivalent to the recommended di
etary allowance enhanced children’s survival. In
Indonesia, somewhat similar effects among preschool
age children (a 45 percent reduction in mortality)
were reported with vitamin A-fortified monosodium
glutamate when it was a consistent part of the food
supply.4
For the one-year follow-up period the overall mor
tality rate among children 6 to 60 months of age was
8.1 per 1000 in our study, comparable to the 7.8 per
1000 for the 12- to 71-month age group reported by the
Aceh, Indonesia, study.2 It was higher, however, than
Study Group
933
*P = 0.01.
the 5 per 1000 reported from an area near Hyderabad,
India, where a placebo-controlled, blinded trial with a
high-dose supplement has also been performed.12
These rates are considerably below the 20 per 1000
reported as the national average for India.12 We moni
tored infant mortality in the study area for a one-year
period in 1988 and 1989 and obtained a rate of 64 per
1000, a figure somewhat lower than the 83 per 1000
reported for Tamil Nadu in 198213and the 98 per 1000
for India generally.14 The mortality rate among in
fants less than 6 months old was 42 per 1000 live
births, and among those 6 to 11 months old it was 22
per 1000. We were unable to find any reliable informa
tion on mortality rates among one-to-five-year-olds in
Tamil Nadu. The lower mortality figures we report
undoubtedly reflect in part the well-recognized effect
of the frequent contact of households with trained
fieldworkers.12’15 Nonetheless, because the contact was
comparable in our two study groups, the efficacy of
Measles
Diarrhea
Respiratory
Malnutrition
Convulsions
Other
Total deaths
12
33
3
16
12
19
80
3
6
37
0.58(0.17, 1.92)
0.48 (0.24, 0.96)t
—
—
0.25 (0.07, 0.85)t
0.31 (0.12, 0.78)t
•Relative risk for the treated group, as compared with the control group.
Values in parentheses are 95 percent confidence limits.
tP = 0.05.
vitamin A supplementation at the level of the recom
mended dietary allowance in reducing mortality by 54
percent remains evident; mortality rates were 10.5 per
1000 in the control group as compared with 4.8 per
1000 in the treated group.
We found an insignificant sex-related difference in
the risk of death without regard to treatment. Treat
ment with vitamin A reduced the risk of mortality in
both sexes, but the reduction was somewhat greater
among girls. This finding contrasts with that reported
from Indonesia, in which a significant treatment effect
of large-dose supplementation was found only in boys,
among whom the prevalence of xerophthalmia was
also higher.2 In our study, the prevalence of xeroph
thalmia at base line was not significantly different be
tween the sexes until after three years of age, whereas
the effect on mortality of treatment with vitamin A
was pronounced among the younger groups.
The efficacy of our low-dose supplementation was
considerably higher than the 34 percent reduction in
mortality reported after high-dose supplementation in
Indonesia as determined by intention-to-treat analy
Table 5. Mortality, According to Nutritional Status.
*
Nutritional Status
and Study Group
Unknown
Control
Treated
Stunted
Control
Treated
Wasted
Control
Treated
Stunted and wasted
Control
Treated
Normal
Control
Treated
Children
Cumulative
Mortality Rate
201
268
0.030
0.004
0.13(0.01,1.14)
2385
2418
Relative Risk!
0.011
0.001
0.11 (0.03,0.36)
*
1806
1798
14
10
0.008
0.006
0.72(0.30,1.72)
1373
1340
22
14
0.016
0.010
0.65 (0.30, 1.41)
0.006
0.005
0.80 (0.32, 2.00)
1890
1940
♦The categories of nutritional status are defined in Table 2.
tRclativc risk for die treated group, as compared with the control group. Values in parenthe
ses arc 95 percent confidence limits.
tP - 0.01.
934
Oct. 4, 1990
THE NEW ENGLAND JOURNAL OF MEDICINE
sis,2 but lower than the estimated 75 percent reduction
reported with an analysis based on actual receipt of
the capsules.3 The estimate based on receipt of
the capsules was derived from a total of only 18
deaths over a four-month follow-up period. As the
authors noted, its validity awaits verification by
a study that ensures consistent, periodic verification
of compliance in taking the large-dose supplement,
which has not been a feature of most large-scale pro
grams to date.16
Vitamin A was most efficacious in children under
three years of age, most prominently in infants. This
finding contrasts with reports from Indonesia. In the
Aceh study the effect of treatment was most marked
among those 60 to 71 months old,2 and in the study
involving vitamin A—fortified monosodium glutamate,
mortality was reduced by 11 percent among infants
and 45 percent among preschoolers.4 In the mono
sodium glutamate study the infants probably received
a considerable portion of their food as breast milk,
and the effect of the program would therefore be
expected to be less. The reasons for the discrepancy
between our results and those of the Aceh study
are less clear but may be related to the relative level
of underlying malnutrition in the two study pop
ulations. Our base-line prevalence of xerophthalmia
was 11 percent, as compared with about 1 to 2 percent
in Indonesia, and only 25 percent of the Indian
children had normal anthropometric features, where
as at least 40 to 69 percent of the Indonesian chil
dren were classified within 10 percent of the me
dian standards of the U.S. National Center for Health
Statistics.
In accordance with many reports from developing
countries where vitamin A deficiency is endemic, diar
rhea was associated with the highest number of
deaths, followed by measles and symptoms associated
with other infections — convulsions, jaundice, and en
cephalitis, for example. The protective effect of vita
min A was significant for all these conditions except
measles. This finding contrasts with hospital-based
case-control reports from Africa, in which the protec
tive effect of very large doses of vitamin A was excep
tionally high in measles.17,18 Previous studies suggest
that measles is a less severe disease in India than in
Africa, and that factors other than vitamin A — the
severity of concurrent malnutrition, for example —
may be a more critical determinant of measles-associ
ated morbidity and mortality.19,20 It may also be that a
large dose of vitamin A is required to prevent a fatal
outcome in severe measles complicated by vitamin A
deficiency.
Prolonged undernutrition, as evidenced by stunt
ing, characterized nearly one third of the children in
our study at base line, and a continuous supply of
vitamin A reduced the risk of dying to one-ninth that
of the controls. The protective effect of vitamin A was
unremarkable in children with wasting, an indicator
of acute malnutrition, and in those with normal an
thropometric features. Stunting reflects — in addition
to an inadequate food supply — many characteristics
of social deprivation that are frequently found in poor
households. Our data suggest that these persistent
ecological and physiologic insults undermine the abili
ty of a child who is deficient in vitamin A to ward off a
fatal outcome when confronted by an infection. The
programmatic implication of this is that maximal re
ductions in mortality can be expected from vitamin A
prophylaxis targeted to children who are chronically
undernourished and to those with superimposed acute
malnutrition.
Children with xerophthalmia are reported to be at
4 to 12 times the risk of death of neighboring chil
dren with normal eyes, and the risk increases with
the increasing severity of symptoms.5 The mortality
rate among children with xerophthalmia in our study
was about 50 percent higher than among children
without the condition (7.2 vs. 10.6 per 1000). When
we adjusted for those who received a large dose of
vitamin A because of xerophthalmia, the treatment
effect of the continued small dose persisted — that is,
half as many died among those who continued to
receive the weekly supplement as among those who
did not.
Sommer et al.2 noted that daily consumption of the
recommended dietary allowance was the ideal ap
proach to vitamin A prophylaxis, but considered it to
be impractical from a programmatic point of view and
chose distribution of the large-dose capsule every six
months instead. Sommer et al. subsequently com
mented that the single most important limitation to
achieving the maximal effect with large-dose capsules
was inadequate contact and verification of compli
ance3; the large-dose approach requires careful moni
toring of distribution channels to avoid possible over
dosing. In contrast, our approach involving frequent
low doses showed that when the supplement is pro
vided at a safe dosage level in an easily dispensed
form, community workers can be effective in attaining
high rates of contact and verification if there is also
an appropriate managerial and supervisory system.
Importantly, the efficacy of supplementation at the
level of the recommended dietary allowance suggests
that a similar effect could be achieved by an equiva
lent supply of vitamin A from foodstuffs, an approach
that would potentially address other nutritional defi
ciencies as well.
References
1.
United Nations Administrative Committee on Coordination-Subcommittee
on Nutrition. First report on the world nutrition situation. Geneva: United
Nations, 1987:36.
2.
Sommer A, Tarwotjo I, Djunaedi E, et al. Impact of vitamin A supplementa
tion on childhood mortality: a randomised controlled community trial. Lan
cet 1986; 1:1169-73.
3.
Tarwotjo I, Sommer A, West KP Jr, Djunaedi E, Mele L, Hawkins B.
Influence of participation on mortality in a randomized trial of vitamin A
prophylaxis. Am J Clin Nutr 1987; 45:1466-71.
4.
Muhilal, Permeisih D, Idjradinata YR, Muherdiyantiningsih, Karyadi D.
Vitamin A-fortified monosodium glutamate and health, growth, and sur
vival of children: a controlled field trial. Am J Clin Nutr 1988; 48:1271-
5.
Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in
children with mild vitamin A deficiency. Lancet 1983; 2:585-8.
Vol. 323
MARFAN SYNDROME GENE AND CHROMOSOME 15 — KA1NULAINEN ET AL.
Subcommittee on Vitamin A Deficiency Prevention and Control, Food and
Nutrition Board, National Research Council. Vitamin A supplementation:
methodologies for field trials. Washington, D.C.: National Academy Press,
1987.
Requirements of vitamin A, iron, folate and vitamin B)2: report of a Joint
FAO/WHO Expert Consultation. No. 23 of FAO food and nutrition series.
Rome: Food and Agricultural Organization of the United Nations, 1988.
Subcommittee on the Tenth Edition of the RDAs. Food and Nutrition Board,
Commission on Life Sciences, National Research Council. Recommended
dietary allowances. 10th cd. Washington, D.C.: National Academy Press,
1989.
Underwood BA, Chavez M, Hankin J, et al. Guidelines for the development
of a simplified dietary assessment to identify groups at risk for inadequate
intake of vitamin A. In: Report of International Vitamin A Consultative
Group (IVACG)®. Washington, D.C.: International Life Sciences Insti
tute-Nutrition Foundation, 1989.
Control of vitamin A deficiency and xerophthalmia: report of a joint
WHO/UNICEF/USAID/Helcn Keller Intcmational/IVACG meeting. WHO
Tech Rep Ser 1982; 672:1-64.
Cochran WG. Sampling techniques. 2nd ed. New York: John Wiley,
1963:65.
12.
935
Gopalan C. Vitamin A and child mortality. Nutr Found India Bull 1990;
UNICEF. 1988 Asian and Pacific atlas of children in national development.
Thailand: Viscom Center Ltd., 1987.
The state of the world’s children 1990. New Delhi, India: Oxford University
Press for UNICEF, 1990:76.
15.
Gopalan C. Vitamin A deficiency and child mortality. Nutr Found India
Bull 1986; 7:1-2.
16.
Underwood BA. Vitamin A prophylaxis programs in developing countries:
past experiences and future prospects. Nutr Rev 1990; 48:265-74.
17 Barclay AJG, Foster A, Sommer A. Vitamin A supplements and mortal
ity related to measles: a randomised clinical trial. BMJ 1987; 294:29413.
14.
Hussey GD, Klein M. A randomized, controlled trial of vitamin A in chil
dren with severe measles. N Engl J Med 1990; 323:160-4.
Reddy V, Bhaskaram P, Raghuramulu N, et al. Relationship between mea
sles, malnutrition, and blindness: a prospective study in Indian children. Am
J Clin Nutr 1986; 44:924-30.
20.
Markowitz LE, Nzilambi N, Driskell WJ, et al. Vitamin A levels and
mortality among hospitalized measles patients, Kinshasa, Zaire. J Trop
Pcdiatr 1989; 35:109-12.
18.
19.
©Copyright, 1990, by the Massachusetts Medical Society
Printed in the U.S.A.
THE NEW ENGLAND JOURNAL OF MEDICINE is published
weekly in the English language by the Massachusetts Medical
Society (Waltham, MA, USA). Material printed in the Journal is
covered by copyright. No part of this reprint may be reproduced or
transmitted in any form without written permission. All rights re
served. Direct permission requests to the Permissions Depart
ment at the USA subscription office. Editorial office: 10 Shattuck
Street, Boston, MA 02115, USA. SUBSCRIPTIONS: Subscrip
tion offices: 1440 Main Street, Waltham, MA 02154-1649, USA;
P.O. Box 1123, Commerce Court Postal Station, Toronto, Ontario
M5L 1K1, Canada; and Saxon Way, Melbourn, Royston, Herts
SG8 6NJ, UK. Subscription prices: USA: $79 per year (interns,
residents $47 per year; students $41 per year). Outside USA:
Canadian dollars drawn on a Canadian bank: C$122 per year
(interns, residents C$88 per year; students C$73 per year).
Pounds sterling drawn on a UK bank: £75 per year (interns, resi
dents, and students £51 per year). US dollar payments accepted
at current rate of exchange pro rata to the pound. Payments and
correspondence for all subscriptions delivered to Japan should
be sent directly to Nankodo Co., Ltd., 42-6, Hongo 3-chome,
Bunkyo-ku, Tokyo 113, Japan. Rates are subject to change with
out notice. Sample copies available on request.
Consumer Collective for
Organic Foods________
839, 23rd Main, 10th Cross, II Phase.J.P.Nagar,
Bangalore, 560 078
Telephone :6635963
coco NEWS:August 15,1995
Life. Death, I'ood and Medicine
Agriculture and indigenous systems of
health care in our country are more than
2000 years old. The advent of western
science & technology in various spheres
of human activity have mystified the
common sense approach and discredited
indigenous wisdom world over.
An interesting reading and thought
provoking question raised by Ken Taylor
founder member of the Minnesota Food
Association.........
"My comparison of the conventional
systems of agriculture and medicine
goes something like this: Both systems
are based on the assumption (perhaps
subconsciously) that death is the
enemy and can be defeated. Through
human cleverness (technology) we will
be able to identify the problem and fix
it, and because we think we can, we
should. The language of the two
systems is different. In medicine, it's
called a cure”. In U.S. agriculture, it's
called "feeding the world". This
assumption
represents
the
fundamental flaw in both systems,
because it violates a basic law of
nature - death is part of life. Denial of
this reality only delays action and
increases consequences.
In medicine, this belief that death is
the enemy to be defeated at all costs
tends to put physicians' focus on the
disease entity, not the human being
who is the patient. In this scenario, the
patient becomes the medium or the
pathway to the problem to be solved."
In agriculture, the enemy is death
from
starvation, and
exploding
population growth is the "disease" to
be cured. Food production becomes
the treatment to defeat that disease.
As this treatment is relentlessly
pursued, the planet, or patient, is put
at risk because the diagnosis of
population growth requires all the
wondrous production enhancing tools
that our industries and universities
can make available. Whatever gets in
the way of production is zapped with
some poison or tools.
The sustainable agriculture movement
and the alternative health care
movement have a lot in common and
much to learn from each other....
Wouldn't it be wonderful for |an|
unlikely coalition to form, of urban
and rural exiles of the agriculture and
medical priesthoods? It is lime for a
community -oriented coalition of
people who have identified their
common ground as concern for their
food and their health, with a
commitment to reclaim responsibility
for the complete cycle of their lives
and for the life of the earth. Will this
require a miracle?
It is encouraging that queries on organic
fanning, its nuances and availability of
organically produced food are trickling in
everyday at the coco office.
Welcome new members to the coalition
of producers and consumers.
A two kg batch of wood charcoal
powder passing through mesh 60 packed
upto a height of 8-10 cm can
decontaminate about 14 insecticide
residues in the range of 20 mg present in
400 litres of water.
!
Excerptedfrom
Insecticide pollution in potable water
resources in rural areas
The consumption of pesticides used to
increase the agricultural production, to
minimise the food loss during storage is
increasing in India for the last two
decades. BHC and DDT constitute about
50% of the total consumption ol
pesticides in India. Certain pesticides are
persistent and result in the contamination
of water resources due to spray drift,
direct application run off resulting from
rainfall and irrigation. A comprehensive
review illustrated how the surviving
insecticide residues have polluted soil,
water, food and air, thereby causing the
death of several species of birds aquatic
species and other organism.
A survey has been conducted to
investigate
the
magnitude
of
contamination of water resources with
pesticide residues in rural areas of
Mysore District. The studies revealed
that all the water samples invariably
contained BHC and some of the samples
showed DDT and methyl parathion
residues.
A decontamination technique has been
described to remove pesticide residues
from water. To protect public health a
pesticide
residue
decontamination
technique in potable water is described.
(G.
SURYANARAYANA
RAJU,
K.
VISWESWARIAllJ. M. M. GALINDO
AMANULLA KHAN and S. K. MAJUMDI'IR
Infestation Control and Pesticides
Discipline, Central Food Technological
Research Institute.
Mysore - 570013, India)
TURMERIC Cnrenina domestiea
Turmeric is a perennial plant with a short
stem and tufted leaves. It originated in
India and Southeast -Asia where it grows
in deciduous monsoon forest, and has
now reached worldwide distribution. It
thrives up to 2000 metres in places with
a rainfall of 1000 -2000 in. It grows well
on loams and alluvial soils. It can be
grown as a mixed cultivation with
vegetables.
It has insecticidal and
rcpcllant
properties.
act as a preventive against several dietary
carcinogens.
liirgctJLusccti
Army worms
Caterpillars
Cowpea beetle
Grain borer
Lesser grain borer
Mites
Rice flour beetle
Rice weevil
Turmeric boiled in milk along with a dash
of black pepper powder may be taken
two or three times a day for sore throat,
cough, cold.
Pharyngitis and other acute respiratory
infections.
A hot poultice made of turmeric powder
applied three to four times a day alleviate
the pain of abscesses.
For fissures on sole of the feet, mix some
castor oil with turmeric powder and
apply.
Methods of Use
There is relatively little information from
practical experience on the use of
insecticidal plants and most of it refers to
storage protection:
* PERIES in Sri Lanka describes the
following method
-Turmeric root is shredded and cow
urine added. The mixture is diluted with
water in proportions between 1 : 2 and 1
: 6 and used against insects and in
particular against caterpillars. The exact
quantities are not given.
-Threads can be dipped in grated
turmeric and stretched over the fields
which have then a repellent effect.
* In trials a turmeric preparation caused
a 90 - 100 % death rate of the army
worm (Spodoptera litura) in 2 days.
Dried rhizomes were grated and
extracted with acetone and the solution
was diluted with 5 parts of water.
Naturc_ciuie:
Turmeric has anti -cancer activity.
Research at the N1N Hyderabad
confirmed the anti mutagenic effects of
turmeric in humans, reporting that it may
Nutritious
extinction
crops
threatened
with
Finger millet (Elcusinc eornciinii)
Ragi is know by different names such as
ragica, mandua, madira. nagli, regain and
kepai in different parts of India. Ragi is
grown in Karnataka, Tamil Nadu,
Andhra, Orissa, Maharasthra, Bihar,
Uttar Pradesh and Gujarat.
Many varieties of Ragi existed in these
different parts of the country where they
were traditionally grown. Some of the
varieties that have been favorites with
farmers for example from one district in
Deccan region described in the
Gazetteer.
Ilullupore Ragi
Gidda bill Ragi
Karigidda Ragi
Jenu goodu Ragi
Madayana Ragi
Hasaru Kambi
Dodda Ragi
Jade shanka Ragi
Rudrajede
AhU/lgu Ragi
Karimurukalu
Balepatta
Biliragi
Green open
Green compact
Violet compact
Green open
Violet open
Green open
Green open
Green compact
Violet compact
(Iruun open
Green open
Green open
Green open
These strains had their very unique
characteristic.
For
instance,
Madayanagiri which is along duration
variety with open earheads were best
suited to the area. The varietal names
given by the farmers speak for the
characteristics of these varieties. Ragi as
a crop is one of the hardiest, suited to the
dry land tracts, and can withstand severe
drought conditions, reviving again with
remarkable vigour.
The crop
is
remarkably free from pest and diseases.
The Ragi grain can be stored for long
periods, even upto 50 years without
damage.
Varieties in Ragi differ in colour of the
grains and in lheir sizes. A deep brown
colour is the predominant colour of most
varieties, but shades of this colour
ranging from orange red at one end and
very deep brown, almost black at the
other, are met with. Differences in
quality of the grain are also recognised.
These are probably due to variations in
the composition of the grain. Apart from
all the above meritorious characteristics,
Ragi is a highly nutritious millet.
Nutrients per 100 gms of Ragi
Protein
Phosphorous
7.3 gms
283 mg
Energy
Iron
Calcium
Carotene
328 Kcal
42 mg
Ragi has been an important part of the
every day food intake. Ragi is powdered
and is used in dinbrent ways. In the
vernacular, they are known as 'mudde1.
Toli',kanji', and 'seri' for children. Ragi
preparations are enriched nutritionally
with locally available greens and pulses
to make a complete food. The flattened
roti resembles maize tortilla. Mudde from
the flour is prepared by steaming the
dough and making it into balls. The flour
is also suspended in cold water
containing a little butler milk and is left
overnight for mild fermentation. The
slurry is then cooked to prepare
porridge.
Malting of Ragi has been a traditional
process in certain parts of India. It is
mostly used for feeding young children.
Among the tropical cereals, linger millets
possess very high malting characteristics.
In order to malt, the millet is cleaned and
steeped in water for at least 16 hours.
Then it is allowed to germinate for two
days. This is de vegetated and the green
malt is scpnrnlcd by grinding. The sieved
portion is dried and malt
Hour is
obtained. This is added to the malted
flour of mung (Phascolus aureus) and has
an excellent nutritive value as food for
children and invalids.
Popping the finger millet is another
way of cooking the grain. Since the
grain cannot be debranned, popping is
an excellent way of retaining (he fibre
content and preparing ready-to-eat
foods. The grain can be processed in a
temperature of 250 C, with low
moisture content. This flour is
consumed along with jaggery and milk
anlits traditionally called 'hurihitil.'
Interested in travelling, languages,
cooking and enjoying good food.
Profiles of Coco Members
From (his newsletter, we intend biinging
out brief profiles of COCO members.
This time, we feature Anjela Sudharshan
and Bhavani Krishnakumar.
Address:
10, I Cross, I Main,
Dollar Layout,
J.P Nagar, IV Phase,
Bangalore 560 078
Tel: 6652712
AnjaJAjujelalSiulharslian.
Recipes
Spent the first 10 years since 1977 as a
junior/middlc level executive handling
consumer electronic goods for aspects of
inventory control, purchase, retailing,
general
merchandising
and
office
administration. For the last six years
involved in the rural development work
through NGO's on various aspects of
development like gender, sustainable
agriculture, environment and awareness
building.
Interested in working for conservation of
environment , rural poor, cooking and
travelling.
Bhiiviini Krishnakumar
Bhavani Krishnakumar is a bharata
natyam dancer, having undergone
training in this art for more than 30
years. She has performed on stage
several times, with the notable ones being
in National Centre for Performing Ails
and Godrej Theatre in Bombay, Krishna
Ghana Sabha and Vani Mahal in Madras.
1 ler last performance was in December
1993 at National Centre for Performing
Ails at Bombay.
Love for physical fitness has led her to
aerobics. She is now an instructor for
aerobics in a local gym.
You are encouraged to contribute new
and interesting recipes that you come
across.
Here's one by Laxnri
’
Soya uprna
Ingtitdieiil:;.
One cup soya (soaked overnight);
Chillies (Green and red), two each;
Scraped Coconut: two to three tbs;
Jeera: 1/2 tsp;
Mustard seeds: 1/2 tsp;
Turmeric powder: 1/4 tsp;
Aesofctida: a pinch;
Salt to taste;
Coriander and curry leaves;
Oil: two tbs;
Method:
Pressure cook the soaked soya and grind
it to paste along with aesofctida, chillies
and salt. I leal the oil in a saucepan and
when hot, add mustard, jeera and
turmeric. When the mustard sputters, add
the ground soya with coconut, coriander
and curry leaves. Cook it on medium
flame for three to four minutes. Serves
four.
Design and Layout: Krishnakumar
A/UT 1- 2>
11.
12.
13
14.
15.
16
17
18
19
Indian I Icalth Sector. EPW. vol. 28. no. 24. pp. 1207-10.1993.
Banerji, D., India’s National Tuberculosis Programme, Indian Journal of
Tuberculosis. 40:61-82.1992.
Dubos R , Man. Medicine and Environment, London, Penguin Books. 1968.
Banerji. D..Thc Knowledge of1 iuman Nutrition and the Peoples ofthe World, World
Review ofNutrition and Dietetics. Basel. Karger, pp. 1-23, 1988.
Sukhatme P. V.. The Incidence ofProtein Deficiency in Relation to Different Diets in
India. British Journal ofNutrition. 24(4): 1477-1480,1972.
NIHFW, National Revie w ofImmunization Programme in India, New Delhi,
NIHFW, 1989
ICMR. Nutrient Requirements and Recommended Dietary Allowances for Indians - A
Report of the Expert Group ofthe Indian Council of Medical Research. ICMR. New
Delhi. 1992.
Gopalan. C.. Stunting. Significance and Implications for Public I icalth Policy, Paper
presented at the NestleNutrition Workshop on Linear Growth Retardation in Less
Dev eloped Countries. Bangkok. March 1986, Published in Gopalan C.. Nutrition.
I Icalth and National Development. NFI. New Delhi, 1986.
Sat\ anaxayana. K.. Rao, B.S.N. and Srikantia. S.G., Nutrition and Work Output. Ind
J \utr Dietet . 16: 170-174. 1979
Zurbrigg S . Rakku’s Story - Structures of III I Icalth and the Sources ofChange.
Centre for Social Action. Bangalore. 1984.
s
I
Ld
B 2a, Ue^b a_
ISSUES FOR DEBATE
Health and Nutrition:
People, Policies and
Politics
Ritu Priya
82
An intensive debate occurred on issues relating to poverty, nutrition
and health in the seventies and early eighties declining soon
thereafter (Dandekar,1 Sukhatme,2 Gopalan,’). Prof. Sukhatme and
the Edmundsons presented one side of the debate in a more devel
oped and sophisticated form in their book, Diet, Disease and
*
Development
Today, when ‘poverty’ is being sought to be erased from national
planning and health policy, this book is an important document for
public debate regarding evolving public health and development
perspectives suited to the specific context of India and other
developing countries. The authors’ articulation of their perspective
allows it to be interpreted as anti-poor and to be used by anti-poor
social forces. It is important to reopen the debate and deal with
recent as well as earlier issues.
The Context of Contemporary Public Health Perspectives
The latest document largely setting the current trend in health
planning is the World Bank’s World Development Report: Investing
in Health.
*
It looks at health planning entirely from the point of view
63
of finance and the role of financial structures in changing or
ascertaining certain kinds of human behaviour. Presenting a plan for
a techno-centric, modem, expert-based, marketized health service
system with extreme commodification of health, it appears as the
most practical in the given socio-political and economic context
because it is entirely in tune with the centralized organisational
structures, the current economic structural changes and the elite,
urban oriented development model. The book authored by Sukhatme
and the two Edmundsons tends, in large part, to provide ‘scientific’
support to this approach and is. therefore, important to read and
analyse. But that is not all one should read into it. Contradictions
within its perspective offer ideas for other creative possibil ities as
well.
At the other end of the ideological spectrum from the World Bank,
we have the perspective articulated by the Bhore Committee (GO1,
1946)6and followed up by others attempting to adapt it in the light of
practical experience and changing conditions. One major drawback
of the Bhore Committee was that it assumed sufficiency of resources
and permitted itself the luxury of looking at every aspect of health
— services without emphasizing the need to prioritize (Qadeer and
Priya 1992).’ The suggestions for a complete public sector medical
care system such as Britain’s National Health Service too would
require unrealistic economic resource inputs from the state. This
book, on the other hand, gives primary consideration to the problem
of resources in the implementation of public health programmes and
insists on low resource input options. In fact, it may be faulted for its
over-balancing on the other side; cutting on absolute basics on the
plea of resource constraints. Later work (ICSSR-ICMR 1982.’ Antia
1993’) argues for a public health policy based on encouragement to
people’s action, use of indigenous systems of knowledge, panchayati
raj as an instrument of wielding people’s control over development
efforts and services and an efficient, well-funded public sector.
While success stories of this approach are available largely through
NGO efforts in small pockets, this perspective seems to be somehow
unable to come to grips with the existing socio-political situation. It
does not indicate the process by which societal conditions, very
adverse to implementation of the model presented, are to be turned in
a more conducive direction.
Between these two extreme models lie others which propose a mix of
the two. For instance, there is the suggestion of identifying a package
of services through an epidemiological approach including the
concept ofcommunity felt need, people’s health related perception
and behaviour, the decentralisation of services and due attention to
the high degree of disparities in th
*e socio-economic structure of
developing societies (Banerji 1993).10 This perspective acknowledges
the primacy of the political process in development planning. It
recognizes that implementation of a holistic approach is dependent
on processes which manage to break the socio-political constraints
on it. Meanwhile, it sees the developing of appropriate principles and
methods of health planning and then making them widely understood
dhd accepted as the primary tasks before public health scholars. The
planning ofthe National Tuberculosis Programme (NTP) is offered
as an example of appropriate planning." That the NTP has not
succeeded in practice shows how isolated appropriate efforts cannot
work unless the overall health service system is conducive to it.
This book presents another ‘in-between’ perspective. Its limitation is
that it attempts to address the issues of‘culture’ without addressing
the issues of social structure. Combining the-two would be a potent
mixture for change towards a more healthy society. Focussing
exclusively on any one is a travesty of the human reality. An
exclusive reliance on the former is likely to support the status quo in
an extremely unhealthy society.
The Book
This book brings together the ideas developed by Professor
Sukhatme over thirty-seven years (twenty-seven as Director of
Statistics, FAO, Rome and then, since 1981, as President.
Maharashtra Association for the Advancement of Science. Pune) as
also by his disciples Wade C. Edmundson (also a statistician) and
Stella A. Edmundson (a nutritionist). Their understanding of several
public health problems is put together to present a perspective on
how both health and development can be effectively promoted in
developing countries. In the process it makes one reflect upon the
economics of health and the relationship between science, policy,
politics and social trends.
The authors’ general perspective emphasizes health as a dynamic
process, a resultant of the interplay between mind and body, and of
65
the internal milieu with the external environment. In their view, an
understanding of the ecology of health must inform all health
planning with due consideration of the interaction between different
components of the external environment - the physical, the biologi
cal, the economic and the cultural - which sets the boundaries within
which the internal environment adjusts to maintain stability and
normal function. Therefore, health and economic development must
be examined together in all their complexity.
The principles underlying their policy guidelines emphasise the
importance of human resource development (basically education and
health) as the primary focus of developmental activity by govern
ments of developing countries. Economic growth alone is not enough
to improve health. “Human resource development is the key causal
priority motivating economic growth” (p. 8).
Secondly, improving health in the developing world is a matter of
setting priorities, particularly given the low health budgets. The
authors advocate the use of the cost-benefit approach for determining
intervention priorities.
66
Thirdly “give what the people want” (p. 29) is offered as the starting
point for any health improvement programme: easy-to-do cures for
their ailments; health workers treating them with courtesy, patience
and regard; giving people advice but allowing them the right not to
carry it out.
Analysing the health situation in developing countries, with the
specific cases of India and Indonesia, the authors spell out the well
accepted scenario that malnutrition and infectious diseases are the
major sources of ill-health in developing countries, that children
under five are the most affected age group, and, that there is more illhealth in rural rather than in urban areas.
The authors accept that dietary inadequacies and infectious disease
are strongly synergistic, one compounding the problems created by
the other, but see disease as a more important component ofhealth
than diet. Three scientific arguments are presented in support of this
contention. The direct scientific basis for this statement comes from a
statistical analysis of the factors leading to increase in life expect
ancy in Japan from 1949 to 1963. This contention is further
supported by their old statistical argument (part ofthe well-known
public debate between Professors Sukhatme and V.M. Dandekar in
the early 1980s) that people adapt to low energy intakes with little
functional loss and therefore the quality of food intake is not a major
problem. Here the authors also invoke the synergism between disease
and nutritional status to hypothesise that the low manifestation of
quantitative food deficiency is due to the disease load and its
siphoning off of the adequate dietary intake. This line of argument is
pushed further by a discussion of protein vitamin-A and iron
deficiency, and goiter; that the primary responsibility for the existing
forms of malnutrition lies in the quality of diets. Thus, as a correc
tive, what is needed are either changes in eating habits, or specific
nutrient additives.
The book also contains a detailed discussion on the microbiological
and pharmacological aspects of the major infectious diseases diarrhoea and dysentery, pneumonia, malaria, helminthic ’infec
tions’. There is, however, little consideration of their ecological
correlates.
Following this analysis, the authors make some concrete recommendations for health policy and programmes:
I.
2.
3.
4.
Direct action against disease needs to be given priority over
action against malnutrition.
Common diseases should be tackled largely through self-care by
lay persons with basic medical services handled by primary
health workers. Education of villagers in relevant modem
scientific knowledge, use of indigenous medical practitioners and
folk knowledge is recommended.
The importance of curative care is underlined even as a part of
public health programmes aiming at prevention. This is what
people want most. In the authors’ view, after it is provided,
people will start seeing the purpose of preventive measures.
Public health measures such as provision of safe water and
latrines, environmental sanitation, etc. though desirable, “are
costly and difficult, specially in the villages. Simple behavioural
change in the individual without extensive-government
intervention " (p. 150) is emphasized as the feasible method of
prevention of disease. At the.safne time, the authors see the
government programme for immunisation of children against the
67
six vaccine preventable diseases as an important intervention.
Involvingpeoplejn the Universal Immunisation Programme and
using knowledge of local customs and beliefs to make it
acceptable is stated to be crucial for its successful implementa
tion.
5.
The authors categorically reject supplementary feeding
programmes as an answer to the problem of malnutrition in
children. Quality ofdiets should be improved through educating
people in using locally available foods, fortification in marketed
products and specific supplements to be given by the medical
system. These measures plus the control of diseases which
compound the effect ofdietary deficiencies, are the preferred
means of improving nutritional status.
6.
Besides behavioural changes being brought about through health
education by primary health care workers, a more appropriate
primary school syllabus is recommended as the starting point
for improving rural people’s culture and lifestyle to decrease
morbidity and increase economic productivity.
gg In addition to the three “Rs” the appropriate curriculum is meant to
— equip the child with an understanding of his/her surroundings via
focusing on relevant health, agricultural and social issues using a mix
of traditional and modem knowledge sources and technologies.
The Perspective: Its Significance and Limitations
The principles set out in this book for public health theory, policy
making and practice are important contributions to the current debate
in public health. However, it does appear that the authors miss out
some elements crucial to the wholesome application of those very
principles when they analyse the health situation and when they diaw
out guidelines for public health policy. These are discussed below,
since ignoring them would undermine the power of fhe conceptual
principles offered by the authors.
Principle 1
One of the primary principles enunciated in the book is being holistic
and ecological with sensitivity to complexity and diversity. The
authors themselves go well beyond the cliched use of phrases like
‘inter-sectoral coordination’, ‘inter-disciplinarity ’ and ‘environment
friendliness.’ In their words: “There is a tendency for economic and.
technologic theory to be too simplistic... The real world where human
beings interact with their environment is a complex place with room
only fora holistic social and technological approach (p. vii).”
The authors remind us of the power of the individual human being,
an element often missing in the epidemiologically generated, large
numbers-based public health approaches. The introduction of this
conceptual element can well make public health more effective in
understanding human reality and in dealing with it.
Similarly, they highlight the situational specificity of health and
disease in different human populations. They emphasize the role of
the physical, biological, economic, and cultural environment in
causing health and disease. This understanding is widely shared
today. On the other hand, the conceptual significance of adaptation
by human groups to their ecological setting is still to be fully
appreciated, thougn it has been discussed by other scholars (Dubos
1968,'2 Banerji I988n).
This perspective also provides a counter to the ‘universal’, ‘neutral’
view of medicine and public health. The belief that ‘West is best’ is
questioned by this ecological view of health.
The authors’ work demonstrates how problems ofdifferent locations
may not only need different solutions, but that they also need to be
defined differently. As some earlier studies in the early seventies had
highlighted, protein deficiency in India needed to be interpreted
differently from how it had to be seen in children in the African
context, given the differences in dietary patterns (Sukhatme, 1972).14
The malnutrition in African children primarily demonstrated protein
deficiency, because of the reliance on carbohydrate-rich cassava
based weaning diets with almost no proteins. In India, the cereal and
pulses-based diets carry the correct proportion of carbohydrates and
proteins, and thus, malnutrition is a reflection of the inadequacy of
quantity.
Fallacy 1
In dealing with such inter-country, inter-regional differences, the
authors neglect internal disparities (other than gender) within the
population of a geographical region. They constantly refer to poverty,
but largely only to show how it is not a barrier to better health,
except in very extreme situations. They suggest that lack of
69
education is the prime reason for the poor being unable to raise their
standard of living. The specificity of the economic and social
environment of the poor and thereby the difference in the meaning of
physical and cultural adaptation as compared to the better off in the
some society is totally ignored.
and development is seen primarily in terms of increase in economic
productivity. HRD for human well-being finds no mention at all. The
perspective on adaptation to low intakes and their dismissal of
‘hunger’ as an issue (only starving to death or loss'of economic work
output being of real consequence) is consistent with this approach to
Principle 2
Another important principle presented in the book is the necessity of
giving importance and respect to the perceptions of rural peoples of
the developing countries. Their need for curative care as the primary
service of any health system, their desire to be treated with respect
and dignity, the recognition that they are not just helpless beings in
the hands of power-wielders but have their own means of dealing
with problems are important insights for the planning and implemen
tation of a public health service.
HRD.
Fallacy 2
Yet, when it comes to the underfed and chronically malnourished, the
authors say that only "a very small proportion of these are actually
'starving to death’. They are suffering from ‘psychic hunger’ and
70 malnutrition, but not from physiologic ‘starvation’ ” (p. 74). This
means that most of those who feel that they are not being able to fill
their stomachs adequately and want more food must not be ‘given
what they want’ because they are not "physiologically starving” nor
are they economically more productive when they eat more!
Principle 3
The authors take great care to emphasize human resource develop
ment (HRD). They argue against the macro-economistic model of
development which suggests that economic growth and industrial
development automatically bring social development. They also
speak of a spiritually higher form of human beings who "can mould
their minds as well as their bodies” in a healthy manner, whose
“egoism is tempered with the knowledge that self interest is often
well served by group interest", "need, not greed" forming the basis
of community action, etc.
Fallacy 3However, the rationale they offer for HRD is an entirely economic
one: that HRD will stimulate economic development. This is a
constant refrain throughout the book. The link between better health
The societal goal is thus to be an increase in national economic
productivity, even HRD being geared towards that goal. The hungry
must leam to adapt better to their hunger and primarily develop
culturally and spiritually not economically! Not once is there a
mention of how the better off of the world are to develop culturally
and spiritually; how their lifestyles must change to improve their own
health and that of the poor. This expectation of dichotomised social
values in the present world (with an upsurge of egalitarian demo
cratic aspirations at all levels of society) is a majorflaw in the
practicalfeasibility ofthe process the authors suggest for better
health and development. There has to be a consistency between
socially articulated values and the values one wants to see
inculcated in individuals.
Principle 4
Shaping of values, attitudes and behaviour is an important aspect of
social policy. In this regard, the authors progress beyond mere
‘health education’ to the overall educational system. Formal
educational channels are proposed as the basis for changing people’s
knowledge levels and behaviour so as to promote self-care and
community action and inculcate an ecological perspective.
Fallacy 4
One may grant that education which helps people deal more
effectively with their environment is an important intervention for the
deprived groups to improve their material conditions and health. But
it is not enough. For it to happen at all requires that the educators and
the better-off sections allow the deprived groups the space to gain
self-confidence and support them in the expression of their full
potential. What process the authors envisage to build such a social
environment is not clear. The entire tenor of the argument detracts
from any humanistic trend ifnot provide the basis for its opposite,
i.e., anti-poor tendencies.
Fallacy 5
Similarly, the advocacy of prioritizing of interventions by the cost
benefit approach also demonstrates the contradictions in the authors’
application of the stated principles. This method evaluates individual
interventions for their economic cost and for the benefits they
provide in terms of the cure of specific health problems. This limits
one to specific interventions without examining their interlinkages.
It does not take social costs or benefits into account.
The access of all citizens to all basic needs warrants little prioritizing
but that is what the authors do. How can one prioritize between
‘satisfying people's hunger' and ‘cure ofillness' specially if one is
to "give people what they want"? We must, of course, exam ine
various optional ways of meeting each of these basic needs and find
out the optimal one within tire given economic, social, cultural and
organisational constraints. There we can use the cost-benefit analysis
as one ofthe many tools which will help identify the optimal method
ofintervention.
In fact, their very methodology in field studies and data analyses is
72 indicative oftheir perspective towards development. Take, for
instance, the indices used by them. The use of mortality and life
expectancy rather than incidence and prevalence of disease or the
gaining of physical stature as the measures of health status is one
example. The use of economic activity alone for measuring work
output as against economic activity plus domestic and social
activities is another. We will discuss these at greater length in the
next section. Here it is sufficient to appreciate that consideration of
the quality of life is missing from the indices which form the bases of
the authors’ scientific arguments.
Fallacy 6
The interventions highlighted as solutions to each of the health
problems discussed in the book do not deal with any problem in a
manner that links it to other health problems or to its basic social and
environmental causes. Another aspect which finds no place in the
author’s perspective is the role of developmental interventions in
shaping of societal concepts and values around health.
Consider the Universal Immunisation Programme. Compared to
immunisation as the prime measure for decreasing morbidity and
mortality from the six vaccine preventable diseases, other general
measures would minimise a whole range of diseases - these six as
well several.more common ones which are responsible for a greater
quantum of childhood morbidity and mortality. For instance, safe
water supply and excreta disposal would not only deal with
poliomyelitis but also control the larger problems of diarrhoea and
dysentery, typhoid etc. Similarly, improving the nutritional status of
children will minimise the complications and mortality secondary to
measles as well as to the more common diarrhoea, dysentery,
pneumonia, tuberculosis and other respiratory diseases. The general
measures would improve other aspects of human lives as well and
increase well-being in general. In addition, they would provide
concrete shape to an ecological perspective. Immunisation promotes
the view that freedom from disease can be bought or acquired
through an injection while the general measures convey messages of
a hygienic lifestyle, environmental sanitation, etc-, as important for
health.
The authors put the latter at low priority because they see them as
costly and difficult to implement. However, if locally appropriate
technologies are used, if the community is convinced of their
usefulness and actively involved, such measures may not be too
difficult to implement. Professor Sukhatme’s own project in eight
villages near Pune seems to testify to this (p. 254-55). As for the
cost, it too will not be high as these appropriate technologies are
generally cheaper and more so if all thebenefits of these measures are
counted. Nor is mass immunisation as cheap and easy to implement
as is often made out to be. Maintenance of an effective cold chain,
administration of vaccines in the right manner and adequate coverage
are difficult things to ensure under our conditions. The National
Evaluation of the UIP (N1HFW, 1989)15 clearly shows the failure in
implementation even within the ‘intensive programme’ districts
which got special resources and devoted extra attention to UIP.
The technocentric, commodified nature of interventions selected as
priorities by the authors will convey messages contrary to what is
expected from the ‘appropriate curriculum’ for primary education. It
is likely that the concrete expression of health interventions will have
greater impact than any formal education. In addition, when the
overall developmental process is moving towards a more
homogenising, consumerist culture, the creative use of local genius
and knowledge is likely to be weakened further by the proposed
interventions.
Science and Policy
The relationship between science, policy and socio-political
perspective seems to explain the nature of discrepancies between the
conceptual principles stated by the authors and their work. The
methodology and analysis used in their scientific studies produce
results which support certain kinds of policy objectives and go
counter to other perspectives. Let me take up specific examples to
examine these links.
Protein Deficiency: Then and Now
Prof. Sukhatme had earlier made significant interventions in health
policy debates. In the early seventies, international agencies were
harping on protein deficiency and its serious implications for
developing countries in terms of physical and mental retardation of
large proportions of their populations. Influenced by the newly
marketed technologies for producing high protein foods, they
Zl advocated special forti fication of foods, promotion of high protein
foods, etc. At that time, Prof. Sukhatme highlighted data from India
which showed that the common diets of cereals and pulses provided
adequate proteins if eaten in quantities sufficient to fulfil calorie
requirements. The deficiency was primarily of calories due to under
feeding. He demonstrated statistically how this led to utilisation of
proteins for conversion into calories rather than body building and
therefore a secondary deficiency of protein (Sukhatme, 1972).13
Alongwith the work of scientists such as Gopalan and his colleagues
at the National Institute of Nutrition, this helped to effectively stem
the ‘protein gap’ hysteria.
In this book, the authors take a slightly different position on protein
deficiency, arguing that, “All things being equal, qualitative protein
deficiency is more likely to occur than quantitative energy defi
ciency. However, quantitative energy deficiency may cause
qualitative protein deficiency” (p. 37). While this statement presents
the physiological picture, it does not take the cultural and social
reality into account. In fact, read together with their contention that
“In the future more emphasis needs to be placed on the quality of the
diet and less on the quantity of food intake” (p. 75), it leads to a
complete reversal of Prof. Sukhatme’s earlier contribution to the
understanding of nutritional problems and to nutrition policy of the
seventies! From earlier demonstrating how quantitative energy
deficiency does in reality lead to protein deficiency in a majority of
the malnourished (Sukhatme 1972),15 they now state that this may
happen (as in the quote above). Can this change in position be
accounted for, at least in part, by the change in policy issues they
choose to address at the two points of time? Earlier the question was
whether to give primacy to protein deficiency or to calorie defi
ciency. Today the question being posed is of giving primacy to
disease control or to increasing nutritional intakes of the undernour
ished.
Variability and Energy Requirements
Sukhatme’s second major contribution has been in highlighting the
variability in calorie requirements between individuals with similar
weights engaging in similar amounts of physical work as also within
the same individual from day to day. His data analysis shows that
while intakes of large numbers average out in similar ways, an
individual’s energy balance may not be negative even if intakes are
below the mean or the Recommended Dietary Allowance (RDA) for
calories (Sukhatme, 1981)? This was a significant point to be made
at a time when RDAs had come to be used by medical persons,
nutritionists and dietitians as sacred numbers in assessing and
deciding each individual’s diet. This is patently a misinterpretation
and misuse of statistical averages whose purpose is to facilitate
comparison across groups of a large number of individuals.
Sukhatme’s argument would have served the cause of nutrition
science and its praxis greatly had this point been taken up ad
equately. However, it seems to have got lost as the use of RDAs
largely continues as before.
Sukhatme then went on to propose that instead of the mean, two
standard deviations below the mean of intakes in the group be taken
as the cut-off point while labelling diets as adequate or inadequate in
terms of proteins or calories. This needs to be examined further.
If the physiological nutrient requirements of individuals with a
certain body weight, age and activity level in a population follow a
normal Gaussian curve, the natural RDA of 50% of the individuals
in a population will fall below the mean (‘m’), of 16.5% below mean
minus standard deviation (‘m-s’) and of 0.25% below *m-2s ’. Thus,
individuals even below m-2s may be getting their full physiological
requirement because persons ofany population may actually need
only those few calories. However, dietary intakes are dependent not
just on physiological need but also on the cultural pattern and
psychological state of the individual, on the one hand, and the access
to food items both in terms ofthe types of foodstuffs and their
quantity, on the other. Individual physiological nutrient requirements
are difficult to establish as a result of these three, what statistically
are conventionally called, ‘confounding variables’ and because of
natural variability. Epidemiological measures such as RDAs are
available but only for purposes of assessing and planning for large
populations. Modem nutrition science should take the logic of
Sukhatme’s argument seriously. The ICMR Expert Group on RDAs
did dwell on the question of variability while resetting RDAs (ICMR
1992).1’ However, the scientific argument needs to be taken further.
Nutrition science needs to incorporate within its body ofknowledge
yg the nature of variations in nutrient needs and in dietary patterns
meant to meet those needs.
The understanding of variability offers possibilities of advancing the
horizons of science by relating it to the complexity of diversity in
physiological, ecological and social contexts. However, Sukhatme’s
own recommendation ofusing *m-2s ’ for setting dietary requirements
only lowers the RDA to another arbitrary numerical point; it does
not make the conceptual shift his own perspective demands.
The reason given for this shift of cut-off point from ‘m’ to ‘m-2s’
was that use of the former puts too many people in the.undernourished category even when many ofthem are not adversely
affected by their low intake. For some, this may be their natural
requirement (as expected of persons at the margins of any random
distribution curve) while others adapt to the low intakes js an ‘autoregulatory process’ and without any functional loss. Attempting to
raise their calorie intakes would be a waste of public effort and
resources. The basis ofhis policy proposal was cutting down the
waste ofresources.
Those disagreeing with his proposition of‘adaptation to low intakes
as a healthy process’ based their argument on two issues. One was
that low intakes lowered economic work output thus also perpetuat
ing poverty (Dandekar 1982, Gopalan 1983). Secondly, that
individuals who have ‘adapted’ to a poverty situation are the end
result of a process which involves deterioration of physiological
functions and high levels of morbidity in early life. Many succumbed
to this morbidity and are martyred on the way to ‘adaptation’, while
others who survive become physically stunted. Acceptance of
stunting as ‘healthy adaptation’ is only legitimation of a process
involving high costs to the community and the individual (Gopalan
1986).16
For the past couple of decades, Sukhatme and the Edmundsons have
been studying the two relationships challenging the normal adapta
tion hypothesis -the relationship between calorie intake and work
output and the relationship between nutrition and morbidity-mortality
levels.
In terms of work output they find that economic work output is not
significantly different between those with different calorie intakes.
The work by the Edmundsons among the villagers of Indonesia and
India has shown that people adapt to low energy intakes by (i) a
slowing ofgrowth and resultant reduction in body mass leading to
less food energy utilisation for a given amount ofphysical work,
(ii) greater metabolic efficiency in energy use, more by decrease in
basal metabolic rate but also by some decrease in energy usedfor
work, and, (Hi) decrease in time and energy spent on leisure
activity (resting, social and religious activity). Thus persons with
low energy intakes can perform more economically productive work
per unit of food energy consumed.
This may well be considered good adaptation from the economic
policy makers point of view. However, econom ic work output is
hardly a direct measure of physiological work capacity, because it is
modified significantly by other economic and social factors such as
possibilities within the occupation to increase output, the incentives
and motivations for harder work inputs, etc. A study by the National
Institute of Nutrition eliminated these factors and showed that those
with higher weights and heights at age five, and in adulthood at the
time of measuring work output, had significantly greater work output
as compared to their counterparts with lower weights and heights, if
habitual physical work done by them was the same. Habituation to
greater physical work improved performance giving an illusion of
healthy adaptation. However, a physiological parameter of adapta
tion for physical work, the increase in heart rate with increasing
work, showed the latter group to be poorly adapted, i.e., the same
intensive work put greater stress on the body of the village boys with
lower weights and heights than with higher body measurements
(Satyanarayana et al, 1979).” The lower work output of those with
lesser physical growth and the evidence of greater stress on them
indicates a lower level of physiological adaptation in the malnour
ished.
These findings differ significantly from those of Sukhatme and the
Edmundsons. Satyanarayana et al have extricated the natural
processes from their social overlay by taking the latter into account
methodologically. Sukhatme and the Edmundsons examine the
phenomenon from the point of view of a socially set goal, that of
maximum physical activity for economic output by human beings
who avail of the least possible resources. We must clearly distin— guish between the description of phenomena from these two points of
view when using such information for policy formation, specially
since there may not be universal agreement on the definition of social
goals.
Disease vs. Diet
The second argument against the acceptance of healthy ‘adaptation’
to chronic undemutrition is sought to be countered by the authors of
this book by making the point that infectious diseases are more
important in determining health status than malnutrition. They
attempt to do this through a statistical correlation of data on diets and
on five major diseases causing death with life expectancy at birth
(LEO). The data pertains to Japan from 1949 to 1963. They find that
diet and disease indices together explain 99.6% of the change in
LEO. Using some “complex statistical analyses” they find that on
separating out the effects of the two, “the fall in disease mortality (of
the five major causes) accounted for fully 60% or more of the
increase in life expectancy, whereas the improvement in nutritional
sufficiency accounted for only 40% or less of the improvement in
health (measured as LEO)” (p. 16). They conclude that “disease was
more important than diet”!
As a scientific conclusion, this statement is on very shaky ground. It
is well known that in situations of chronic undemutrition. deaths
directly due to malnutrition are few. It is rather that the severity of
diseases and mortality due to them is high in the malnourished. Thus
malnutrition increases the mortality due to disease. The statistical
correlation of diet and disease does not take this synergism into
account. Also, taking total mortality rates for the five most common
causes of death as the index of disease status is bound to show higher
statistical correlation with LEO than if actual morbidity rates are
used. With these biases inherent in the statistical analysis, if
nutritional sufficiency was still found to account for 40% of the
improvement in health, can that be said to be a crucial difference
compared to 60% by fall in disease mortality? Can this be legiti
mately further extended to guide policy?
The exact weightage of diet and nutrition in determining health status
is neither scientifically established yet, nor is it likely to be the same
in any two situations - so intertwined and complex is the relationship.
That is why, giving a ‘scientific’ basis for priority to disease control
over malnutrition control, facilitates the evasion of difficult policy
decisions addressing a broader canvas, including agricultural policy —
and the social distribution of resources. This is yet another instance
of policy issues impinging on the making of science as knowledge.
The understanding of the phenomenon of healthy human adaptation
to the environment is meaningful only when its limits are also stated.
While the various elements forming the environment, the physical,
economic, cultural and biological, interact with each other, the
extreme form of one can overwhelm the impact of others and produce
an environment beyond the limits of normal adaptability.
Due to the specificity of environmental settings of different human
groups, the degree of impact of each factor varies. If we divide
societies very ciudely into three broad economic groups, concepts
like ‘wasteful feeding' and ‘psychic hunger’ apply primarily to the
well-off of the 'developed countries and to the elite of the develop
ing ’ countries in whom disease related to over-nutrition is much
more common than in the rest of the population. The picture ofwelladjusted diets but nutritional deficiencies due to the stress of
infectious disease loads presented in this book, could well apply to
the middle class of ‘developing’ countries. In their case it could be
In Conclusion
Thus, in spite of all its contradictions, the importance of the book lies
in the principles it carries into public health planning and the issues a
critical reading of it reveal.
pertinent to debate whether additional dietary intakes to provide a
safety margin is the solution or priority be given to the control of
infectious diseases. Probably a combination of the two will better
reflect the ‘cultural adaptation’ in practice.
For the poor, the external environmental conditions are largely
beyond the limits within which adaptation can occur without
detractingfrom expression ofhuman potential. Their process of
adaptation for survival is at high human cost. Other than the high
childhood morbidity and mortality and the lowered physiological
work capacity discussed earlier, the decrease in non-economic work
including resting and social activityfound by Edmundson's own
studies means a decline in human well-being. The decrease in
leisure and social time would also be a major barrier to the indi
vidual and community action recommended by the authors as the
starting point
Education for better living is also likely to achievedittle benefits
because, as other scholars have estimated and Sukhatme’s early work
on protein deficiency shows, the poor traditionally have “the best
80 diets within their economic resources”. In addition, it has been amply
demonstrated that women of poor households are not able to attend '
adequately to child care and on maintaining hygiene because of being
over-worked and lack of many physical resources (e.g. Zurbrigg,
1984). Therefore, unless the structural constraints to healthy
adaptation of the poor are simultaneously highlighted and addressed,
the health and development for the poor is unlikely to be achieved.
While the health service system may have little direct role in
overcoming the structural constraints, it is for holistic public health
to point out these linkages. Denying or obscuring them will only be
counter-productive to the purpose of science as a ‘truthful description
of reality’ or for the policy aims of health and development for all.
Only when public health focusses on such issues, are the overall
planners and policy makers likely to take a holistic view of develop
ment and health. The decision to address or not address these issues
is a political one - the third comer ofthe triangle, 'science' and
‘policy 'forming the other two. It is a decision each one of us
concerned with health issues will have to take.
The contradictions in the application of their stated conceptual
principles do not detract from the significance of the ideas them
selves. In fact, the book allows one to examine how the enunciated
principles, which are humanistically incontrovertible and very
worthy ofemphasis in the present health and development scenario,
can get moulded into inhuman, anti-poor arguments. The authors’
conclusions from their empirical studies make us realize the
importance of public health analysis distinguishing between a
scientific understanding of natural processes and a scientific study of
the relationship between the natural processes and social factors
(e.g., on the issue of diet and work output). Both are of value, more
so if their boundaries are respected and their linkages recognised.
The fallacies in the book highlight the need for consideration of
prescriptions for problems of poverty and health in terms of societal
processes of change, not restricting them to a programmatic
orientation alone. They also highlight the need for a universally
accepted clear definition of terms often used today, such as ‘holistic’
public health.
References
DandekarV.M.. MeasuremcntofUndemutrition.FifthGopalanOranon.Nutrition
Societydflndia,NIN,Hyderabad, 1982.
Sukhatme. P V.Measiiringrhe Incidence oHJndemutrition.fW. 15(23): 1034-36.
1981.
3.
Gopalan, C„ Small'is Healthy? For the Poor, Not for the Rich!, AF7 Bulletin October.
NFl.New Delhi, 1983.
4.
Edmundson W.C.. Sukhatme P. V. and Edmundson S.A., Diet. Disease oral
Development, Macmillan India Ltd., New Delhi. 1992.
5.
World Bank. World Development Report - Investing in Health, OUP. Washington,
1993.
6.
GOI, Report ofthe Health Survey and Development Committee, vol. 4. Delhi.
ManagerofPublications 1946.
7.
Qadeer I and Priya R.. Planning for Health in Independent India. Paper presented at a
Seminar on ’ Understandingindependent India’, March 6-8,1992. School of.Social
Sciences. JNU.NewDelhi. 1992.
8.
ICSSR-ICMR. Health for All: An Alternative Strategy - Report ofa Study Group set
upjointly by ICSSR and 1CMR, Indian Institute of Education. Pune. 1981.
9.
Antia, N.H., World Bank and India’s Health. EPW, December25. vol. 28. pp. 2383’ 2887, 1993.
10.
Banctji, D.,.Simplistic Approach to Health Policy Analysis - World Bank Team on
I.
2.
rwr
WEDNESDAY,
JUNE 4,1997
‘Fish is idealfoodfor thought9
Kochi, June 3: Fish is the
best food for human brain,
nerves and eyes, according to
nutritional experts.
A group of500 nutrition exp
erts and scientists met at Barecelona and recommended
regular intake of fish by preg
nant and nursing mothers
and young children as fish con
tains great of docosahexaen
oic acid (DBA)—a long chain
of omega-3 poly saturate—
which accounts for 25 per cent
of the fat content of the brain,
reports the latest newsletter
of the Marine Products Export
Development Authority here.
It was also pointed out at the
meet that breast milk also con
tains small amounts of the
acid which is needed by a foe
tus.
If the mother's diet does not
include enough fish, then she
may not be able to supply the
DHA that the foetus needs,
say scientists.
In animals a shortage of
DHA makes them less intellig
ent, less capable of learning
and generally more disturbed
in behaviour while in humans
a low DHA supply could result
in poorer eye sight and slower
development in babies and
perhaps hyperactivity and
dyslexia in childhood the sci
entists' who participated in
the meet pointed out.
The meet also pointed out
that among human adults, a
poor DHA supply was likely to
cause depression, aggressive
behaviour, perhaps even schi
zophrenia.
It was recommended that
fish should be taken at least
twice a week by all and two to
three times a week by pregn
ant and nursing mothers.
It was also suggested that
for children it was important
to encourage fish eating from
an early age.
The meet had urged the ind
ustry to develop more fish pro
ducts aimed specifically at the
young children, the newslet
ter adds. PTI
VOLUNTARY HEALTH ASSOCIATION OF INDIA
C-14, COMMUNITY CENTRE, S.D.A.,
NEW DELHI 110 016
PHONES : 652007, 652008
GRAM: "VOLHEALTH" New Delhi-110016
B-41
VITAMIN A DEFICIENCY
Kamala S. Jayarao*
Vitamin A deficiency in pre-school children is
yet one more nutritional disorder of public
health importance in many developing coun
tries. It contributes'to a significant propor
tion of preventable blindness, a self-explana
tory tragic situation. Some ophthalmologists
in India believe that the problem of blindness
due to cataract is seen in a greater proportion
and hence demands greater attention than
vitamin A deficiency.
However, in my
opinion, such problems should not be viewed
with a statistician’s mind. Cataract is a
disorder of adulthood whereas hypovita
minosis A has its peak between 1 and 10
years of age. Thus young children become
blind before they can see anything of the
world and become a soci-economic burden.
It is hence that vitamin A deficiency should
be looked upon as a public health problem.
Vitama A deficiency, like other nutritional
disorders of childhood, is seen mainly in the
poorer classes and is mostly due to inadequate
intake of foods rich in vitamin A. As in the
case of PCM (Protein Calorie Malnutrition),
the foundations for vitamin A deficiency may
be said to be laid down during foetal life it
self. The intake of vitamin A by pregnant
mothers of the poorer classes is very low and
their serum vitamin A levels are also low1,2.
They may therefore be expected to transfer
smaller amounts of the vitamin to the foetus.
The breast milk of such mothers also has low
concentrations of vitamin A. The levels being
not more than 200/Pg per 24 hours3. The
*
National Institute of Nutrition, Hyderabad—500-007.
infant thus is not only born with low stores
of vitamin A but receives low quantities of
it during the immediate post-natal life. In
spite of this, however, ocular signs of vitamin
A deficiency are rarely seen in the first 6
months of life. One may hence believe that
this amount of vitamin A is probably ad
equate during infancy. I say this because as
yet there are no techniques by which vitamin
A requirements can be reliably assessed.
Beyond 6 months of age the vitamin A intake
drastically falls because
(1)
(2)
the breast milk output diminishes
the infant does not receive any extra
milk (either animal or formula made)
(3)
the weaning foods being largely based
on cereals contain virtually no retinol
and only small amounts of B-carotene,
As you are all aware retinol is found in high
concentrations only in animal foods. Plant
foods contain only carotenes, of which Bcarotene is nutritionally the most important.
The absorption of B-carotene is not as gocd as
that of retinol and its biological availablity
is also poor. Hence 11 Pg B-carotene is equi
valent to only 0.251 Pg retinol. Diet surveys
have showed that pre-school children in
South India receive only 300-500 I.U. vitamin
A daily, mostly as B-carotene, through their
diets4, ’.
In pre-school children the inci
dence of ocular signs of vitamin A deficiency
is quite high. In children of school-going age,
(
the incidence is higher but the lesions are
mainly Bitot’s spots and conjunctival xerosis.
Below 5 years, comeal xerosis and kerato
malacia are more frequent and hence the
condition is of more serious concern in this
age period. The reason for this age pattern
is not known; this may include factors like
the serveri ty of the deficiency, requirements
for growth, influence of infections and pre
sence of PCM etc. The incidence of vitamin
A deficiency in children with kwashiorkor
and marasmus is higher than in children with
milder degrees of PCM.
Ocular manifestations of vitamin A
deficiency
The first functional evidence of vitamin A
deficiency is night blindness. Being subjective,
it is difficult to establish its presence in
children, but in most cases the mother do
notice that rhe children do not see well at
dusk The conjunctival lesions include xerosis
and Bitot's spot. In adults and adolescents,
Bitot’s spots do not always respond to vita
min A therapy and hence their association
with vitamin A deficiency has been questio
ned But in pre-school children they do
disappear with therapy and are generally in
dicative of vitamin A deficiency. The con
junctival lesions do not interfere with vision
but may be considered as red signals, indi
cating the presence of vitamin A deficiency
of sufficiently high degree.
Blindness due to vitamin A deficiency is due
to cornal involvement corneal xerosis (the
drv, hazy cornea) leading to keratomalacia
(necrosis of cornea), the irreversible stage.
2
)
2.
Comeal xerosis can progress rapidly
to keratomalacia and must be treated imme
diately. Since it is necessary to raise the
serum vitamin A levels rapidly, it is not ad
visable to start the treatment with oral pre
parations. Recent studies show that the rise
in serum vitamin A levels is delayed when
oily preparations are injected6.
Hence it is
advocated that children with comeal xerosis
and children with kwashiorkot and vitamin A
deficiency be given an intramuscular injection
of water-miscible preparation of vitamin A,
immediately on diagnosis and again, 48-72
hours later. This may be followed up with
oral therapy; oral therapy should be with
oily preparations. Repeated parenteral ad
ministration is not recommended for fear of
inducing acute hypervitammosis A.
Prevention
1. The ideal way. to control and prevent
vitamin A deficiency would be to provide the
children with foods rich in preformed vitamin
A like eggs, liver, milk and milk products,
butter, ghee, etc. However, this being the
ideal method, it may not be expected to take
shape in the near future.
2. In the present economic circumsta
nces, the next method would be to ensure
adequate intakes of B-carotene (1200-1600//tg
daily for children, 3000/ Pg for adults and
4500/Ag for pregnant and lactating, women).
This entails intake of good amounts of, green
leaves (beetroot leaves, cairot leaves, arwi-
ka-sag, methi, hara dhaniya, sarson, lajagira,
palak, muli-ka-sag etc.) and fruits (jack fiult,
mango, orange, papita, tomatoes, etc.) This
need vigorous nutrition education to the
1.
Conjunctival xerosis and Bitot’s spots community. In certain communities, this
may be treated with oral preparations of may call for change in feed habits and
Therapy
vitamin A- Therapy for at least 4 weeks will
ensure fair storage of the vitamin in the
body.
correction of wrong notions like believing
that fruits cases cough and coles or gieens
cause diarrhoea, etc.
In view of the serious nature of the defi
despite vigorous vitamin A therapy.
ciency, it is necessary that some public health
importantly it must also be remembered that
measures be taken for prevention rather than
rely on the above two idealistic approaches.
McLaren7 suggested that since the human
liver has a large capacity to store vitamin A,
this programme is mainly intended to pre
vent the development of serious eye lesions
which could lead to permanenr blindness;
massive prophplactic doses of vitamin A
may be given to control vitamin A deficiency,
Following on this suggestion, the National
Institute of Nutrition at Hyderabad had
carried out field trials and .concluded that
oral administration of 200,000 I. U. of
vitamin A (as palmitate) every six months
during the first 5 years of life, will consi
derably reduce the incidence of ocular signs
Of vitkmin A deficiency8.
It was found
during this study that 75-90% of the children
are protected from developing any sign of
vitamin A deficiency and also, no new case of
keratomalacia occurred during this period.
Following the recommendation of Institute7.
States in India had accepted in principle to
implement this programme. These States are
Andhra Pradesh, Bihar, Karnataka,
Kerala,
Orissa, Tamil Nadu and West Bengal (these
cover the southern and eastern regions where
vitamin A deficiency is rampant). The early
stages of the trials at Karnataka were follo
wed up by this Institute and the results con
firmed the earlier observations.9.
The programme has now been taken up in
Indonesia and Philippines, also. I may, how
ever, mention here that not’ everyone is
willing to accept the efficacy of this pro
gramme. Dr. Pereira from Vellore (Tamil
Nadu) has some reservations ragarding this
programme10' 11. However, a group from
West Bengal12 have conducted a similar study
and observed total elimination of night blind
ness and no new cases of Bitot’s spot. In
those who already had the latter, the lesion
disappeared in only some children.. It must
be remembered here that in older children
and adults, Bitot’s spot may not disappear
More
this regime may not totally eliminate vitamin
A deficiency.
The aqueous preparation of massive-dose
vitamin A is made available by the Family
Planning Units of the Union Ministry of
Health and of the States where the pro
gramme is running. It is also supplied by
the Anglo-French Drug Company (Pardon
me I I have no vested interest; I am only
giving you information).
Those of you who are concerned with vita
min A deficiency may also be interestd to
know that there is an organisation called the
Xerophthalmia Club (supported by the Royal
Commonwealth Society for the Blind, U.K.).
They bring out bulletins which give infornaticn on various programmes the world
over, aimed at prevention of vitamin A defi
ciency blindness.
The Voluntary Health
Association of India has brought out some
pamphlets on this subject, in English as well
as regional languages, which will be helpful
to the paramedical workers. Those interes
ted may wiite to the following addresses :
Xerophthalmia Club
Nuffield.Lab. of Ophthalmology
Oxford, U.K.
Voluntary Health Association of India
C-14, Community Centre
Safdarjung Development Area
New Delhi - 110016
The World Health Chronicle (30:117,
1976) has an article which touches on
some of the points discussed here.
(
4
References
)
8.
Swaminathan, M,C., Susheela, T.
P. and Thimmayamma B. V. S.
(1970), Amer. J. Clin. Nutr.
23 : 119.
9.
Annual Report (Jan. 1872-Dec.
1972). National Institute, Hydera
bad, 1973, p. 102.
1.
Shankar, K. (1962), Ind. J. Med.
Res. 50 : 113.
2.
Venkatachalam, P. S. Belavady, B.
and Gopalan, C. (1962), J. Pediat.
61: 262.
3.
Pereira, S. M. and Begum, A.
Belavady, B. and Gopalan, C. 10.
(1069), Amer. J. Clin. Nutr.
(1959), Ind. J. Med. Res. 47 : 234.
22 : 858.
Sunderaraj, R., Begum, A., JesuPereira, S. M. and Begum, A.
dian, C. and Pereira, S. M., (1969), 11.
(1971), Arch. Childh. 46 : 525.
Ind. J. Med. Res. 57 : 375.
4.
5.
Sinha, D.P. and Bang, F.B. (1976),
Rao, N. P., Singh, D. and Swami- 12.
Amer. J. Clin. Nutr. 29 : 110nathan, M.C. (1969) Ind. J. Med.
Res. 57 : 2132.
6.
Srikantia, S. G. (1976), World
Review of Nutrition and Diete Ackno wled gement
tics, Vol. 20 (Kargar, S. Basle),
We are grateful for permission to
pp. 185-230.
reproduce this article from Medico
McLaren, D. S. (1964), Nutr. Rev. Friend Circle Bulletin No. 8, August
1976.
22 : 289.
7.
Printed at Jsb Printing Press, A-30/1, Naralna Industrial Area, Phase-I,
New Delhi- 110028
V~IT " ■[
should
dly
drumstick leaves is the main causative factor. The cdtmaon man does hot
have to strive to buy the expensive yellow fruits, instead he can use
leafy vegetables.
Our government has made a provision for the prevention of nutritional
blindness in the form of a program "Vitamin A prophylaxis program".
You need to know, about this service, because Vitamin A should be available
in every Primary Health Centre, and it is there for the benefit of your
children.
Oo.think about what action
3 Hydro retinol (Vitamin A%) is found in fresh water fish and occurs
mixed ’with retionl.
ketinoic acid (Vitamin A acid) in which the alcohol has been oxidised
shares some of the actions, of retinol. It is important in promoting
growth' and controlling differentiation and naintainence of epithalial
tissue in Vitamin A deficient animals, but is ineffective in restoring
visual, auditory or reproductive function in certain species where ’retinol
is active.
- 2 -
Physiology
Vitamin A is a nutrient which is necessary for good health.
L._It has an essential.Jtole in-Xhe-function-of -the. retinal (inner) layer
2.
3.
3.
of the eye.
In growth and differentiation of epithelial tissue.
Growth of bone and embryonic development.
Stabilising effect on various membranes.
5. Progression of premalignant characterestics is slowed or reversed in
experimental animals.
-In Vitamin Jk deficient .animals nuclear RUA synthesis is diminished.
Adaption to dark is a function of both rods and cones. Primary adaptation
is by the cones and completed in few minutes .2rfery adaptation is a function
of rods and not completed for 30, minutes.
When human beings are fed diets
deficient in Vitamin A, their ability for dark adaptation is reduced.
Rod
vision is affected more than cone vision.
Vitamin A plays an important role in the induction and control of epithelial
differentiation in mucus secreting or keratinizing tissues.
In the absence
of retinol, mucus cells disappear and atrophy of epithelium occurs, and is
replaced by stratified keratinizing epithelium.
The suppression of normal
secretion leads to irritation and infection.
Vitamin A deficiency and protein malnutrition are the two most serious
nutritional deficiency diseases in the world today. Vitamin A deficiency
can be fatal in young children with marasmus or kwashiorkor.
Mild Vitamin A deficiency manifests in skin lesions like hyperkeratosis and
infections, but the most recognisable is night blindness even though its
onset occurs when Vitamin A depletion is severe.
Vitamin A is fat soluble.
Absorption is reduced when diets are low in protein.
After absorption-most Vitamin A stored in liver. Symptom of Vitamin A
/occurs
deficiencyTwhen concentration falls below 10-20 ug/dl.
When there is protein deficiency plasma levels of Vitamin A falls,
replenishment with calories and protein is then required. During infections
Vitamin A level falls, partially because of increased urinary excretion.
Pregnancy increases demand of Vitamin A. Concentration of Vitamin A in fatal
blood is less than maternal blood. Colostrum and milk offers the new born
an,adequate supply of Vitamin A.
1 USP Unit of Vitamin A = 0.3 ug retinol
0.6 ug of B carotene
3...
- 3 -
Manifestation of Vitamin A deficiency
Eye
Xerophthalmia (dryness of eye)
Bitots spots
Keratomalacia (destruction of the eye)
Respiratory tract
Increased respiratory infection
Skin
Dry skin, papular eruptions on extremities.
Genito Urinary
Urinary calculi (from Epithelial debris forming foci)
Impaired spermatogenesis
Abortion
Malformed offspring
GI Tract
Diarrhoea, due to alteration in intestinal epithalium and
metaplasia of pancreatic duct epithalia.
Sweat glands : Atrophy
Bone : Faulty modeling of bone
Miscellaneous : Taste, smell and hearing decreased.
Recommended daily intake of Vitamin A
Infants : 300 units
Children (1-10 years) - 250-400 units
11 years and above : 575-750 units
Women during pregnancy and lactation - 1200 units
Vitamin A content in 100 gms.
Mango
Papaya
Banana
1120 I.U.
640 I.U.
200 I.U.
Guava
Jackfruit
160 I.U.
160 I.U.
Cabbage
Leaves of drumstick
1800 I.U.
12,000 I.U.
Spinach
Carrots
13,000 I.U.
20,000 I.U.
Sweet Potatoes
6000 I.U.
Butter
3500 I.U.
Egg
Cod Liver Oil
1500 I.U.
200,000 I.U.
Milk
Breast - 1898 I.U./litre ; Cow's - 1025 I.U./litre
Meat
100 I.U.
6000 to 60,000 I.U.
Liver
Vitamin A deficiency and Nutritional Blindness
Vitamin A deficiency is the single most frequent cause of blindness among
pre-school children in developing countries.
Young children are at the greatest risk because Vitamin A requirements
are proportionately greater than other groups and because they suffer
most from infections.
)
s
Blinding corneal destruction is most frqquent between the ages of 6 months
to 8 years. (WHO Ho.29/1985. "in point of fact
)
*
As long as the infant is on mother's milk there is little danger of
xerophthalmia.
But diluted substitute milk, or weaning foods which lacks
Vitamin A can bring on the disease.
■' :
A sick child loses appetite and in addition' the illness may interfere
with the body's ability to absorb and use Vitamin A in the food, and
then the Vitamin A stored in the liver is grained.
The foundation for Vitamin A deficiency may
life itself.
be laid down during foetal
If the intake of Vitamin A by p pregnant woman is low,
then transfer of Vitamin A to the foetus is low.
mothers will also be low-
Breast milk of such
Plant foods contain B carotene, but its absorption is not as good as
retinol, which is found in high concentration in animal foods.
Surveys in South India conducted by Dr. Swaminat.han have shown that pre
school children receive only 9 units of Vitamin A daily, and so incidence
of ocular signs are high. In the school going age, the incidence is
higher, but mainly include Bitot’s spots and conjunctional xerosis.
Below 5 years, corneal xerosis and keratomalacia are more frequent.
Tie first symptom of xerophthalmis is often night blindness.
A mother
finds her child no longer moves about easily in the house.
Xerophthalmia means dry eye.
Another early sign is the appearance of white foamy spots on the white
part of the eye, called Bitot's spots.
The dryness then gives way to softening of the corneal tissue with
resultant ulceration, destruction of the eye and blindness.
- 5 Treatment of xerophthalmia VJHO 1982
Vitamin A
Immediately
Day 2
Day 14
200,000 I.U. by month
Under 12 months :
"
the dosage
Diarrhoea and Vitamin A :
Nutritional blindness occurs in areas who~>. diarrhoea
is common among children, and this is not q chance happening.
Children who lack Vitamin A in their diet ire at risk not only of
blindness, but also of getting diarrhoea arrf other infections.
Repeated
attacks of diarrhoea may bring about the finhl eye damage which
destroys sight.
The combined effects of poverty and ignorance'add to the problem.
During an episode of diarrhoea, food intake is limited, and absorption
decreased. Diarrhoea occurs
more often ,and more seriously in
malnourished children who have poor stores of Vitamin A in the liver.
A study in Bangladesh showed that at least half'the children who had
e
serious xerophthalmia had suffered from diarrhoea the previous month.
In an Indonesian study, the children with xerophthalmia were 5 times
as likely to have had diarrhoea in the last week as children without
signs of Vitamin A deficiency.
i
However prospective study undertaken by MIN Hyder- bad, showed that
malnutrition does not increase the frequency of di iirhoea or duration,
but affects the severity of the .episode itself.
(Indian Journal of Paediatrics Vol.52, Sept.-Oct. ’35, 418, 463-67)
70% of water miscible Vitamin A is absorbed in a chili’ with diarrhoea.
A dose of Vitamin A is advisable before ORS is started').
6...
- 6 Measles and Vitamin A
The incidence of corneal lesions in measles is 3%.
Serum levels of Vitamin A show a drop during the measles episode,
returning to premeasles level within 8 weeks after the acute episode
without Vitamin A supplementation.
■
Superficial punctate keratopathy was idestified in 15% of children.
None of these children showed mild signs oc xerophthalmia. Measles per
se may cause corneal damage, followed by si condary bacterial infection.
Vitamin A deficiency could weaken the strve ural integrity of the cornea
itself. (UNICEF Vitamin A consultancy Susri T. Eastman April 1986)
A large dose of Vitamin A may not help during the acute attack, but is
likely to reduce the risk of post measles corneal involvement, in children
with low Vitamin A stores.
Protein Calorie Malnutrition (PCM) and Vitamin A
The incidence of Vitamin A deficiency in children with kwashiorkor and
of PCM.
narasmus is higher than in children with milder -
Corneal lesions have been rarely seen in children suffering from rinor
grades of PCM.
In Severe protein deficiency, Vitamin A in the diet does not reach the
liver and Vitamin A in the liver is not available for use.
Thus.a
functional deficiency of Vitamin A may occur in kwashiorkor, independent
of its dietary intake.
Arroyave suggests that if the rate of growth were accelerated by the
supplementation with proteins alone, the clinical manifestations of
Vitamin A deficiency may suddenly become more ser pis.
(Am J. Clin. Nuti 22:1119, 1969)
- 7 -
Vitamin A status can be improved by jiving a food source of Vitamin
A or 3 Carotene without changing exin; ing habitual diets of children
belonging to poor income groups.
—
Acute Respiratory Infection
Even mild degrees of Vitamin A shortag:.can lamage the body's
protective epithelial surfaces which In: intestinal, respiratory,-.
urinary tracts and the eyes.
Alfred Soqraer et al described in a stud/ 'of Indonesian children, that
those with mild xerophthalmia developed respiratory disease at twice
the rate of children with normal eyes. T$e risk of respiratory disease
was more closely associated with Vitamin A status than with general
nutritional status.
.
8..
SO?a
1.
EPIDEMIOLOGICAL
STUDIES
Prevalence of ocular signs of Vitamin A deficiency in preschool children
(3 rural and 3 urban areas of India).
(ICMR Technical Report Series No.26 studies on preschool children).
Age Years
% prevalence
Sample Size
Conj.
• xerosis
Bitot
spots
Corneal
lesions
1 - 2
2-3
4687
4257
1.6
’3.9
1.1
2,5
0.1
0.15
3-4
4-5
4029
5379
5.6
5.9
3.5
4.5
0.1
0.1
Pooled data of ten states over time act mlly suggests that the prevalence
of Bitot spots in rural India has increased almost 3 fold between 1974
and 1982.
(S.G. Srikantia, The Problem of Vitamin A deficiency in Indian Children,
UNICEF, 1985).
Prevalence rate shows seasonal variations, being higher in summer, hence
the timing of the administration of massive’, doses, of Vitamin A, is
important.
2.
The report for the Royal Commonwealth Society for the Blind, stated in
1978 that there would be 220000 children in 1-5 year age group, with
corneal lesions at any point of time.
It has been suggested that prevalence rated >f 0.5% Bitot's spots or
0.01% active corneal lesions may be used ns cut off levels and by either
criteria, Vitamin A deficiency is of Public H i-nlth Importance.
3.
School Children : Studies were done in Baroda, involving 2000 school
children 9-12% of children were found to be Vitamin A deficient.
4.
Measles : A study in Andhra Pradesh looked into the relationship between
measles and blindness. 3% of a large sample of children with measles
had corneal manifestations.
(Tenth IVACG meeting, Hyderabad, 1985 - Bhaskaran 15Vinodini Reddy
and Roy Milton).
5< Diarrhoeal Disease : More than 27000 children in 450 villages in North
Sumatra were studies by Alfred Sommers et al.
Results showed that children with mild xerophthalmia are at 2-3 times
greater risk of infection and 4-12 times greater risk of dying compared
to children with normal Vitamin A status.
9...
- 9 -
UNICEF reports a range of 30-42000 children blinded each year in India from
Vitamin A deficiency.
Pattern of Vitamin A intake
From a study of NNMB, intake of Vitamin A is widely different between
individual families, states, and within a state from one year to another.
Table :Vitamin A intake :: ug/consumption > mit in ten states : Rural (NNMB)
19/5
1978
Year
1981
1984
Kerala
107
97
350
236
Tamil Nadu
Karnataka
135
185
158
213
211
209
190
276
Andhra Pradesh
232
35
296
220
Maharashtra
296
: 14
MA
27.1
Gujarat
300
• 2--0
264
304
Madhya Pradesh
344
192
NA
533
191
387
337
495
207
NA
1078
NA
NA
NA
472
350
State
West Bengal
Uttar Pradesh
;
Orissa
.
MA : Not Available
Vitamin A Intake : ug/consumption unit in Ten Urb an Areas 1975.-73 (NNMB)
Mean
Range
Slums Dwellers
Industrial workers
248
352
119 - 434
116 - 482
Low Income Groups
332
232 - 382
Food Sources
Green leafy vegetables and milk.
10..
- 10 -
NATIONAL
PROGRAMME :
The Govt, of India in 1970 launched a national Vitamin A prophylaxis
Programme for the prevention of blindness in children in the endemic states.
The cost works out to 50 paise per child per year.
India was one of the first countries to involve itself in systematic applied
research in Vitamin A deficiency investigating the effectiveness and
ility • of using a megadose Vitamin A distribution.
Vitamin A deficiency blindness prevention is within the Govt.'s 20 point
programme.
Till a few years ago the existing maternal and child Health and Family
Welfare organisations were responsible for running the programme. Since
the Integrity Child Development Services (ICDS) was introduced in 1976,
this agency too is concerned.
In rural areas the programme is implemented through the PMC and its
subcentres, under the supervision of the Medical Officer of the Primary
Health Care (PHC).
The paramedical staff are responsible for identifying the target children
and ensuring that the dose is delivered, supplies of Vitamin A come from
the Directorate of Health Services, New Delhi.
In the ICDS programme, the Aganwadi worker is responsible for identifying
target children and ensuring that the massive dose is distributed.
The Village Health Guide assists the ANM in the program.
An evaluation of the programme done in 1973 involved 13 states.
In only 21 of 59 rural areas studied was the programme effective.
(40% coverage).
' 11...
- 11
Community awareness of the programme was poor.
Functionaries themselves were not aware of all aspects of the programme.
Vitamin A supplies were irregular arid insufficient.
Health education was poor.
(Vijayraghavan K and Prahlad Rao N, Nut. Rap. International 25,431, 1982). .
Target Coverage : There was a fall from 76’ in 81/82 to 65Z in 82/83.
The number.of doses do not indicate whether the same children have received
both doses.
Applied Nutrition Programme :
This programme helps rural communities grow more food and consume them.
Objectives are :
(a)
to impart nutrition education
(b)
to improve the nutrition intake and dietary habits of nursing arid
expectant mothers and children through promoting local production of
protective foods.
(c)
(d)
to set up community kitchens and school gardens.
to set up poultry, fishing units and centres for animal husba-dry.
It would have been possible to encourage people to grow foods containing
Vitamin A, but the lack of land, water and education, contributed to poor
impact of this programme.
.
12..
- 12 Massive Dose Prophylaxis :
•
It has been suggested that 200,000 I.U. given once every 6 months effectively
protects; both against Bitot spots and corneal lasi'Bs.in rural areas and
urban slums.
The massive dose approach when properly implemented leads to a substantial
reduction in the prevalence of Bitot’s spots.
Studies in NIM Hyderabad have shown that the prevalence of corneal lesions
showed a reduction of almost 80% in areas where the massive dose was
effectively delivered.
However on the basis of falling serum Vitamin A levels well before 6 months
after dosing, it has been suggested that it is desirable to administer the
dose once every 4 months instead of 6 months.
Breast feeding to.protect sight
The unborn child gets Vitamin A from its mother through the placenta. If
the mother has an inadequate diet, the new born has an insufficient store
of Vitamin A.
Young children need a small but regular supply of Vitamin A in-the diet.
The highest concentrations occur in colostrum (secretion of breast in the
first few days after, delivery). If the child is not given colostrum a
valuable source of Vitamin A is lost.
The amount of Vitamin A in the breast milk gradually decreases but is higher
than in cow's milk. ■
Breast feeding protects against xerophthalmia.
When the mother's diet is Vitamin A deficient mothers can be given a mega
dose 200,000 I.U. by month after delivery so the breast milk will contain
enough Vitamin A for at least 3-4 months.
Too much Vitamin A can do harm, doses more than 10,000 I.U. should not be
given to a pregnant woman.
Children who are not breast fed have 6-8 times greater chance of developing
xerophthalmia, than those receiving breast milk.
(Treating the whole child :
Diarrhoea Dialogue, Issue 21, June '85)
13...
- 13 Pharmaceutical Preparations of Vitamin A :
The megadose products of Vitamin A are as follows
(1)
Aquasol A caps. (USV)
Water soluble, Vitamin A 50,000 I.U./Cap.
30 costs 11.02
Also Injection 50,000 I.U./ml.
3 Amps. 4.86
(2)
Arovit (Roche)
Vit. A 50,000 I.U. Tab.
4. Cone. Vitamin A solution (Seamless)
each gram contains 50,000 I.U.
3 costs 1.96
5. Vitamin A injectiOn (3PL). Each ml.
Also injection Vitamin A 100,000 I.U., 300,000 I.U./ml.
contains 10
3 X 1 ml costs 4.00
Arovit drops Vitamin A 150,000 I.U. per ml. 7.5 ml.
costs 5.05 Rs.
(3)
Carbfral (Duphar)
Vitamin A 50,000 I.U. Tab.
30 costs 6.72 3s.
Also injection Vitamin A 50,000 I.U./ml.
/.Injection
Oily preparations of/Vitamin A are of no use, as they are released very
slowly.
The rational programme for prevention of Vitamin A deficiency utilises the
Vitamin A. syrups manufactured in India. The main source is from Indian
Drugs and Pharmaceuticals producing bottles containing 100 ml. concentration
Vitamin A solution. Each ml. contains 100,000 I.U. Vitamin A. A spoon
of 2 ml. size is included with the bottle.
The State Trading Corporation monitors supply and demand.
estimated by the Dept, of Family Welfare.
Demand is
Vitamin A is mainly produced by Roche, who also supply Indian Drugs and
Pharmaceuticals. They have also assisted Xerala State Drugs.
However several Pharmaceuticals prepare multiple vitamin preparations,
containing Vitamin A.
<
The production figures of Vitamin A for the period 84-87 are
85
198460.58 1WJ
Target : 105 MMu
86
198561.03 MMu
Target : 120 I@iu
87
198669.34
The import of Vitamin A
1983-84
1984-85
20.346 MMu
12.685 "
The production of Vitamin A falls for short of targets '.
14...
-14-
Food Fortificaticn by Vitrain A :
Milk is fortified with Vitamin A to contain a final level of 3,500 I.U.
per litre. All of this is consumed in the cities, and does not even reach
the slum population who need it most. However the recent information is
that fortification of milk is being discontinued.
Hiltone : A preparation made of 50% milk and 50% groundnut protein is being
fortified with Vitamin A, in 5 large cities. It is used in Govt, sponsored
feeding programmes, but would be restricted to the peripheries of the cities
where niltone is produced.
Vanaspati is fortified with Vitamin A to contain 25 I.U. per gm. Storage
and cooking losses may be 50 to 70%.
Besides intake of Vanaspati by
preschool children is very low.
Modern bread is fortified with Vitamin A.
Common salt fortified with Vitamin A has low stability.
iodine and iron is being considered.
Fortification with
Countries in Central America are using
sugar fortified with Vitamin A to prevent blindness.
Hyper Vitaminosis A
Overzealous Vitamin A therapy, eg. increased intake during acne, pregnancy,
lactation, can cause the following :- Irritability
- Headache
- Vomiting
- Decreased appetite
- Dry skin
- Skin Peeling
- Reddening of skin
- Enlarged liver, spleen
- Increased intracranial, pressure
- Tender hard swelling on extremities, occiput
Once the Vitamin is withdrawn, most signs and symptoms disappear within
a week.
Pregnant women should not take excess Vitamin A as congenital abnorraalities
can occur.
eg. Multivitaplex forte (Pfizer) is a multiple Vitamin therapy, one cap
a day is advised.
This cap. contains 10,000 I.U. of Vitamin A and taken
daily could lead to overdosage.
15...
- 16 -
Issues that arise :
1)
While we wish to prevent nutritional blindness by improved nutrition,
teaching people to grow and use green leafy vegetables, and fruits
(yellow), the scarcity of land, water, the exploitation of the tribals,
deforestation, increasing prices of basic commodities, use of fruits
in preparing costly and junk soft drinks, increased exports all make
us wonder where to begin
2)
In a health awareness programme, recognising early signs of the.disease
is essential. Are PHC and ICDS workers being taught the earliest signs
of Vitamin A deficiency - like stumbling in the dark due to night
blindness, identifying Bitot's spots ? Do these workers use every
opportunity in teaching people about nutrition, or do they mechanically
dole out Vitamin A ?
3)
-In- the strategy for Vitamin A distribution :
- age groups in months need to be specified instead of saying 1-6 years.
- -fixed times for Vitamin A distribution needs to bo done after ■
identifying the target beneficiaries.
- those who do not come to the clinic need to be given Vitamin A at the
home.
- the same child should get Vitamin A twice in the year.
- ICDS programme workers should not confire to 2-5 years age group.
- lactating mothers and pregnant women need to be included as beneficiarii
- sick children with measles, diarrhoea, PCM need to be beneficiaries.
- the special 2 ml. spoon has to be used, not the ordinary tea spoon.'
- registers to be maintained so that supply, utilisation and related
problems can be identified.
4)
Vitamin A production, as seen from the figures is far below the targets.
There is increasing import of Vitamin A. Vitamin A is not mentioned
in Category I list of essential drugs for national Health Programs.
We need a policy for increased production of essential. medicines like
Vitamin A, and curbing hazardous and irrational drugs.
Prepared by Dr. Susy Aya Pam, MD
People's Education for Health Action
:b: 22.4.88
- 17 QUESTIOHHAIHE - Vitamin A prophylaxis programme
1.
Do you have a programme for distribution of Vitamin A in your area ?
2.
Where is the Vitamin A obtained from ?
3.
Who distributes Vitamin A solution ?
4.
Who are the beneficiaries in this programme ?
5.
Where is the Vitamin A given, home/health centre ? and how often ?
6.
Is a special 2 ml. spoon used for this purpose, or is a tea spoon
used ?
7.
What are the problems in this program, is Vitamin A supply erratic,
lack of awareness among people, irregular visit by health worker etc.?
8.
Is a register maintained for this programme, can you give us a specimen
copy ?
9.
Are simple messages of consuming leafy vegetables and yellow cruits
to obtain Vitamin A, propagated ?
10.
What are your suggestions for improving this programme ?
11.Do you have children with keratomalacia (WPW) in your area ?
We would like you to participate in the Vitamin A prophylaxis programme.
In this context, can you fill in the above questionnaire and mail it
to us ?
:b:
VOLUNTARY HEALTH ASSOCIATION OF INDIA
40, Institutional Area
South of I I T
Near Qutab Hotel
New Delhi 110016
665018
Ph.Nos :663071
668072
3TCP.Y
0?
VITAMIN
A
”ith 3^-42,300 children blinded each year"in India'frob Vitamin A
deficiency,- it ia essential far us to know the. st -ry of Vitamin A.
This is a brief backgrounder on Vitamin A. Several issues arise.from
this story and we would appreciate your feedback. .Y.pu.-.may begin to .yonder
why nutritional blindness should bo an.entity at ail, when it ip easily
preventable.
Ignorance Of'the nutritive value of many edible-green leaves, like.
drumstick leaves is the main causative factor. The common man does not
have to strive to buy the expensive yellow fruits, instead- he can use
leafy vegetables.
Our Government has made a provision for the prevention of nutritional
blindness in the. form of a program "Vitamin A prophylaxis program".
You need to know about this service, because -Vitamin’A should ' be available
in every Primary-Health Centre,- and-it is there for.ths ‘benefit of .your ...
children.
.
.
HISTORY :
Might blindness was’apparently first described-in Egypt around 1500 PC
and topical treatment with roasted or fried liver was wisely fee amended I
Hippocrates later suggested eating beef liver’as a dure-'for t'-o Aioordor.
Experimental observations led to the discovery of Vitamin n-Aerap.it aalmia
(dryness and thickening of the- conjunction) -;cs recognised in 'lorld I
as a result a decrease in the content of butter fat in the diet.
Steenbock (1919) observed that Vitamin A content of vegetables varies
with the'degree of pigmentation, and led to'the discovery of.the chemical
nature of the vitamin.
CHEMISTRY :
.. .
Euler, and associate, and ’loose (1929) demonstrated that the plant pigment
carotene (Provitamin A) is a potent source of Vitamin A.
3 Carotene is the active carotenoid found in plants. Retinol (Vitamin
Aj.) a primary alcohol is present in .esterified from in the tissues of
animals and salt water fishes, in the liver.
3 Hydro retinol (Vitamin Ax) is found in fresh water fish and occurs
mixed with retionl.
Retinoic acid (Vitamin A acid) in which the alcohol has been oxidised
shares some of the actions, of retinol. It is important in promoting
growth and controlling differentiation and maintainence of epithalial
tissue in Vitamin A 'deficient animals, but is ineffective in restoring
visual, auditory or reproductive function in certain species where retinol
is active.
- 2 -
Physiology
Vitamin A is a nutrient which is necessary for good health.
1.
It has an. essential role in the function ofthe retinal (inner) layer-
of the eye.
2.
In growth and differentiation of epithelial tissue.
3,
Growth of bone and embryonic development.
3. Stabilising effect on various membranes.
5.
Progression of premalignant characteristics. is- slowed or reversed in
experimental animals.
In Vitamin. A deficient animals. jmjcIoar RNA synthesis is diminished.
Adaption to dark is a function of both rods and cones. Primary adaptation
is by the cones and completed in few minutes Artey adaptation is a function
of rods and not completed for 30, minutes.
When human beings are fed diets
deficient in Vitamin A, their ability for dark adaptation, is reduced.
Pod
vision is affected more than cone vision.
Vitanri p A plays an important role in the induction and control of epithelial
differentiation in mucus secreting or keratinizing tissues.
In the absence
of ratinol, mucus cells disappear and atrophy of epithelium occurs, and is
replaced by stratified keratinizing epithelium.
The suppression of normal
secretion leads to irritation and infection.
Vitamin A deficiency and protein malnutrition are the two most serious
nutritional deficiency diseases in the world today. Vitamin A deficiency
can be fatal in young children with marasmus or kwashiorkor.
Mild Vitamin A deficiency manifests in skin lesions like hyperkeratosis and
infections, but the most recognisable is night blindness even though its
onset occurs when Vitamin A depletion is severe.
Vitamin A is fat soluble.
Absorption is reduced when diets are low in protein.
After absorption.most Vitamin A stored in liver. Symptom of Vitamin A
/occurs
deficiency/when’toncentration falls below 10-20 ug/dl.
When there is protein deficiency plasma levels of Vitamin A falls,
replenishment with calories and protein is then required. During infections
Vitamin A level falls, partially because of increased urinary excretion.
Pregnancy increases demand of Vitamin A. Concentration of Vitamin A in fatal
blood is less than maternal blood. Colostrum and milk offers the new born
an adequate supply of Vitamin A.
1 USP Unit of Vitamin A « 0.3 ug retinol
0.6 ug of B carotene
3...
- 3 -
Manifestation of Vitamin A deficiency
Eye
Xerophthalmia (dryness of eye)
Bitots spots
Keratomalacia (destruction of the eye)
Respiratory tract
Increased respiratory infection
Skin
Dry skin, papular eruptions on extremities.
Genito Urinary
Urinary calculi (from Epithelial debris forming foci)
Impaired spermatogenesis
Abortion
Malformed offspring
GI Tract
Diarrhoea, due to alteration in intestinal epithalium and
metaplasia of pancreatic duct epithalia.
Sweat glands : Atrophy
Bone : Faulty modeling of bone
Miscellaneous : Taste, smell and hearing decreased.
Recommended daily intake of Vitamin A
Infants : 300 units '
Children (1-10 years) - 250-400 units
11 years and above : 575-750 units
Women during pregnancy and lactation - 1200 units
Vitamin A content in 100 gms.
Mango
Papaya
Banana
1120 I.U.
640 I.U.
200 I.U.
Guava
Jackfruit
160 I.U.
160 I.U.
Cabbage
Leaves of drumstick
1800 I.U.
12,000 I.U.
Spinach
Carrots
13,000 I.U.
20,000 I.U.
Sweet Potatoes
6000 I.U.
Butter
3500 I.U.
Egg
Cod Liver Oil
1500 I.U.
200,000 I.U.
Milk
Breast - 1898 I.U./litre ; Cow's - 1025 I.U./litre
Meat
Liver
6000 to 60,000 I.U.
100 I.U.
- 4 Vitamin A Deficiency and Nutritional Blindness
Vitamin A deficiency is the single most frequent cause of blindness among
pre-school children in developing countries.
Young children are at the greatest risk because Vitamin A requirements
are proportionately greater than other groups and because they suffer
most from infections.
Blinding corneal destruction is most frequent between the ages of 6 months
to 6 years. (WHO No.29/1985. ''in point of fact
)
*
As long as the infant is on mother's milk there is little danger of
xerophthalmia.
But diluted substitute mil’:, or weaning foods which lacks
Vitamin A can bring on the disease.
A sick child loses appetite and in addition the illness may interfere
with the body's ability to absorb and use Vitamin A in the food, and
then the Vitamin A stored in .the liver is drained.
The foundation for Vitamin A deficiency may
life itself.
be laid down during foetal
If the intake of Vitamin A by a pregnant woman is low,
then transfer of Vitamin A to the foetus is low.
mothers will also be low*
Breast milk of such
Plant foods contain B carotene, but its absorption is not as good as
retinol, which is found in high concentration in animal foods.
Surveys in South India conducted by Dr. Swaminathan have shown that pre
school children receive only 9 units of Vitamin A daily, and so incidence
of ocular signs are high. In the school going age, the incidence is
higher, but mainly include Bitot's spots and conjunctional xerosis.
Below 5 years, corneal xerosis and keratomalacia are more frequent.
The first symptom of xerophthalmia is often night blindness.
A mother
finds her child no longer moves about easily in the house.
Xerophthalmia means dry eye.
Another early sign is the appearance of white foamy spots on the white
part of the eye, called Bitot's spots.
The dryness then gives way to softening of the corneal tissue with
resultant ulceration, destruction of the eye and blindness.
- 5 Treatment of xerophthalmia 'FIO 1982
Vitamin A
Immediately
Day 2
Day 14
200,000 I.U. by month
Under 12 months : | the dosage
Diarrhoea and Vitamin A :
Nutritional blindness occurs in areas whe.
*e
diarrhoea
is common among children, and this is not □ chance happening.
Children who lack Vitamin A in their diet are at risk not only of
Repeated
blindness, but also of getting diarrhoea ard other infections.
attacks of diarrhoea may bring about the final eye damage which
destroys sight.
The combined effects of poverty and ignorance add to the problem.
During an episode of diarrhoea, food intake is limited, and absorption
decreased. Diarrhoea occurs
more often .and more seriously in
malnourished children who have poor stores of Vitamin A in.the liver.
A study in Bangladesh showed that at least halfthe children who had
serious xerophthalmia had suffered from diarrh- ea the previous month.
In an Indonesian study, the children with xerop’ thalmia were 5 times
as likely to have had diarrhoea in the last week as children without
signs of Vitamin A deficiency.
However prospective study undertaken by WIN Hyderabad, showed that
malnutrition does not increase the frequency of diarrhoea or duration,
but affects the severity of the episode itself.
(Indian Journal of Paediatrics Vol.52, Sept.-Oct. ’85, 418, 463-67)
70S of water miscible Vitamin A is absorbed in a chi?j’. with diarrhoea.
A dose of Vitamin A is advisable before ORS is started-
.
6..
- 6 Measles and Vitamin A
The incidence of corneal lesions in measles is 3%.
Serum levels of Vitamin A show a drop during the measles episode,
returning to premeasles level within 8 weeks after the acute episode
without Vitamin A supplementation.
Superficial punctate keratopathy was idert Lfied in 15% of children.
None of these children showed mild signs a" xerophthalmia. Measles per
se may cause corneal damage, followed by secondary bacterial infection.
Vitamin A deficiency could weaken the strut; ural integrity of the cornea
itself. (UNICEF Vitamin A consultancy Susa i T. Eastman April 1986)
A large dose of Vitamin A may not help during the acute attack, but is
likely to reduce the risk of post measles corneal involvement, in children
with low Vitamin A stores.
Protein Calorie Malnutrition (PCM) and Vitam-n A
The incidence of Vitamin A deficiency in children with kwashiorkor and
of PCM.
oar^smus is higher than in children with milder *
Cornenl lesions have been rarely seen in children suffering from minor
grades of PCM.
In Severe protein deficiency, Vitamin A in the dj.et does not reach the
liver and Vitamin A in the liver is not available for use.
Thus a
functional deficiency of Vitamin A may occur in kwashiorkor, independent
of its dietary intake.
Arroyave suggests that if the rate of growth were accelerated by the
supplementation with proteins alone, the clinical manifestations of
Vitamin A deficiency may suddenly become more serious.
(Am J. Clin. Nuti 22:1119, 1969)
Vitamin A status can be improved by .iving a food source of Vitamin
A or B Carotene without changing exi r, ing habitual diets of children
belonging to poor income groups.
Acute Respiratory Infection
Even mild degrees of Vitamin A shortage can damage the body's
protective epithelial surfaces which line intestinal, respiratory,
urinary tracts and the eyes.
Alfred Sommer et al described in a study "of Indonesian children, that
those with mild xerophthalmia developed respiratory disease at twice
the rate of children with normal eyes. 'Tie risk of respiratory disease
was more closely associated with Vitamin A status than with general
nutritional status;
.
8..
SOME
1.
EPIDEMIOLOGICAL
STUDIES
Prevalence of ocular signs of Vitamin A deficiency in preschool children
(3 rural and 3 urban areas of India).
(ICMR Technical Report Series No.26 studies on preschool children).
Age Years
% prevalence
Sample Size
Con j.
cerosis
Bitot
spots
Corneal
lesions
1-2
2-3
4687
4257
1.6
3.9
1.1
2,5
0.1
0.15
3-4
4-5
4029
5379
5.6
5.9
3.5'
4.5
0.1
0.1
Pooled data of ten states over time actually suggests that the prevalence
of Bitot spots in rural India has increased almost 3 fold between 1974
and 1982.
(S.G. Srikantia, The Problem of Vitamin 1 deficiency in Indian Children,
UNICEF, 1985).
Prevalence rate shows seasonal variations, being higher in summer, hence
the timing of the administration of massi’e doses, of Vitamin A, is
important.
2.
The report for the Royal Commonwealth Society for the Blind, stated in
1978 that there would be 220000 children in 1-5 year age group, with
corneal lesions at any point of time.
It has been suggested that prevalence rated of 0.5% Bitot’s spots or
0.01% active corneal lesions may be used as cut off levels and by either
criteria, Vitamin A deficiency is of Public Health Importance.
3.
School Children : Studies were done in Baroda, involving 2000 school
children 9-12% of children were found to be Vitamin A deficient.
'4. Measles : A study in Andhra Pradesh looked into the relationship between
measles and blindness. 3% of a large sample of children with measles
had corneal manifestations.
(Tenth IVACG meeting, Hyderabad, 1985 - Bhaskaran
and Roy Milton).
Vinodini Reddy
Diarrhoeal Disease : More than 27000 children in 450 villages in North
Sumatra were studies by Alfred Sommers et al.
Results showed that children with mild xerophthalmia are at 2-3 times
greater risk of infection and 4-12 times greater risk of dying compared
to children with normal Vitamin A status.
9...
- 9 UNICEF reports a range of 30-42000 children blinded each year in India from
Vitamin A deficiency.
Pattern of Vitamin A intake
From a study of NNMB, intake of Vitamin A. is widely different between
individual families, states, and within a.state from one year to another.
Table :Vitamin A intake :: ug/consumption upit in ten states :: Rural (NNMB)
1975
1978
Year
1981
1934
Kerala
107
97
350
236
Tamil Nadu
’58
211
Karnataka
135
185
190
276
Andhra Pradesh
232
35
296
220
Maharashtra
296
3 )4
NA
271
State
209
Gujarat
300
2> 0
264
304
Madhya Pradesh
344
192
NA
’.Jest Bengal
Uttar Pradesh
533
191
387 ’
337
495
207
NA
1078
NA
Orissa
NA
NA
472
350
NA : Not Available
Vitamin A Intake : ug/consumption unit in Ten Urban Areas 1975-78 (NNMB)
Mean
Range
Slums Dwellers
Industrial workers
248
352
119 - 434
116 - 482
Low Income Groups
332
232 - 382
Food Sources :- Green leafy vegetables and milk.
10...
- 10 -
NATIONAL PROGRAMME :
The Govt, of India in 1970 launched a National Vitamin A prophylaxis
Programme for the prevention of blindness in children in the endemic states.
The cost works out to 50 paise per child per year.
India was one of the first countries to involve itself in systematic applied
research in Vitamin A deficiency investigating the effectiveness and
f.rsi’ality _■ of using a megadose Vitamin A distribution.
Vitamin A deficiency blindness prevention is within the Govt.'s 20 point
programme.
Till a few years ago the existing maternal and child Health and Family
Welfare organisations were responsible for running the programme. Since
the Integrity Child Development Services (ICDS) was introduced in 1976,
this agency too is concerned.
In rural areas the programme is implemented through the PHC and its
subcentres, under the supervision of the Medical Officer of the Primary
Health Care (PHC).
The paramedical staff are responsible for identifying the target children
and ensuring that the dose is delivered, supplies of Vitamin A come from
the Directorate of Health Services, Nev/ Delhi.
In the ICDS programme, the Aganwadi worker is responsible for identifying
target children and ensuring that the massive dose ie distributed.
The Village Health Guide assists the ANN in the program.
An evaluation of the programme done in 1978 involved 13 states.
In only 21 of 59 rural areas studied was the programme effective.
(40% coverage).
11...
- 11 -
Community awareness1 of the programme was pc r.
Functionaries themselves were not aware of all aspects of the programme.
Vitamin A-. supplies were irregular and insufficient.
Health education was poor.
(Vijayraghavan K and Prahlad Rao N, Nut. Sep. International 25,431, 1982).
Target Coverage : There was a fall from 76
*
in 81/82 to 65Z in 82/83.
The number of doses do not indicate whether the same children have received
both doses.
Applied Nutrition Programme :
This programme helps rural communities grow more food and consume them.
Objectives are :
(a)
to impart nutrition education
(b)
to improve the nutrition intake and dietary habits of nursing and
expectant mothers and children through promoting local production _Qf
protective foods.
(c)
(d)
to set up community kitchens and school gardens.
to set up poultry, fishing units and centres for animal husbandry.
It would have been possible to encourage people to grow foods containing
Vitamin A, but the lack of land, water and education, contributed to poor
impact of this programme.
- 12 Massive Dose Prophylaxis :
It has been suggested that 200,000 I.U. given once every 6 months effectively
protects, both against Bitot spots and corneal le.-oi;bs,in rural areas and
urban slums.
The massive dose approach when properly implemented leads to a substantial
reduction in the prevalence of Bitot's spots.
<
»
Studies in NIN Hyderabad have shown that the prevalence of corneal lesions
showed a reduction of almost 80^ in areas where the maSsive dose was
effectively delivered.
However on the basis of falling serum Vitamin A levels’well before 6 months
after dosing, it has been suggested that it is desirable to administer the
dose once every 4 months instead of 6 months.
'
Bre^t feeding to protect sight
The unborn child gets Vitamin A from its mother through the placenta. If
the mother has an inadequate diet, the new born has an'insufficient store
of Vitamin A.
Young children need a small but regular supply of Vitamin A in the diet.
The highest concentrations occur in colostrum (secretion of breast in the
first few days after delivery). If the child is not given colostrum a
valuable source of Vitamin A is lost.
The amount of Vitamin A in the breast milk gradually decreases but is higher
than in cow's milk.
‘
Breast feeding protects against xerophthalmia.
When the mother's diet is Vitamin A deficient mothers can be given a mega
dose 200,000 I.U. by month after delivery so the breast milk will contain
enough Vitamin A for at least 3-4 months.
Too much Vitamin A can do harm, doses more than 10,000 I.U. should not be
given to a pregnant woman.
Children who are not breast fed have 6-8 times greater chance of developing
xerophthalmia, than those receiving breast milk.
(Treating the whole child :
Diarrhoea Dialogue, Issue 21, June ’85)
13...
- 13 -
iccutical Prennrations of Vitamin A :
The megadose products of Vitamin A are as follows
(1) Aquasol A caps. (USV) •
Hater soluble, Vitamin A 50,000 I.U./Cap.
30 costs 11.02
Also Injection 50,000 I.U./ml.
3 Amps. 4.86
(2) Arovit (Roche)
Vit.
50,000 I.U. Tab.
4.
Cone. Vitamin A solution (Seamless)
each gram contains 50,000 I.U.
3 costs 1.96
5.
Vitamin A Injection (BPL). Each ml.
Also injection Vitamin A 100,000 I.U., 300,000 I.U./ml.
contains 10,
3 X 1 ml costs 4.00
Arovit drops Vitamin A 150,000 I.U. per ml. 7.5 ml.
costs 5.05 Rs.
(3) Carofral (Duphar)
Vitamin A 50,000 I.U. Tab.
'30 costs 6.72 As.
Alon injection Vitamin A 50,000 I.U./ml.
/.Injection
Oily preparations of/.Vitamin A are of no use, as they are released very
slowly.
The rational programme for prevention of Vitamin A deficiency utilises the
Vitamin A syrups manufactured in India. The main source is from Indian
Drugs and Pharmaceuticals producing bottles containing 100 ml. concentration
Vitamin A solution. Each ml. contains 100,000 I.U. Vitamin A. A spoon
of 2 ml. size is included with the bottle.
The State Trading Corporation monitors supply and demand.
estimated by the Dept, of Family Welfare.
Demand is
Vitamin A is mainly produced by Roche, who also supply Indian Drugs and
Pharmaceuticals. They have also assisted Kerala State Drugs.
However several Pharmaceuticals prepare multiple vitamin preparations,
containing Vitamin A.
The production figures of Vitamin A for the period 84-87 are
1984-85
Target : 105 MMu
60.58 MMU
1985-86
51.03 MMu
Target : 120 MMu
1936-87
69.34 MMu
The import of Vitamin A
1983-84
1984-85
20.345 MMu
12.585 "
Tie production of Vitamin A falls for short of targets ’.
14...
- 14 -
Food Fortification by Vit~iin A :
Milk is fortified with Vitamin A to contain a final level of 3,500 I.U.
per litre. All of this is consumed in the cities, and does not even reach
the slum population who need it most. However the recent information is
that fortification of milk is being discontinued.
Miltone : A preparation made of 50% milk and 50% groundnut protein is being
fortified with Vitamin A, in 5 large cities. It is used in Govt, sponsored
feeding programmes, but would be restricted to the peripheries of the cities
where niltone is produced.
Vanaspati is fortified with Vitamin A to contain 25 I.U. per gm. Storage
and cooking losses may be 50 to 70%.
Besides intake of Vanaspati by
preschool children is very low.
Modern bread is fortified with Vitamin A.
Common salt fortified with Vitamin A has low stability.
iodine and iron is being considered.
Fortification with
Countries in Central America are using
sugar fortified with Vitamin A to prevent blindness.
Hyper Vitnminosis A
Overzealous Vitamin A therapy, eg. increased intake during acne, pregnancy,
lactation, can cause the following
- Irritability
- Headache
- Vomiting
- Decreased appetite
- Dry skin
- Skin Peeling
- Reddening of skin
- Enlarged liver, spleen
- Increased intra cranial. pressure
- Tender hard swelling on extremities, occiput
Once the Vitamin is withdrawn, most signs and symptoms disappear within
a week.
Pregnant women should not take excess Vitamin A as congenital abnormalities
can occur.
eg. Multivitaplex forte (Pfizer) is a multiple Vitamin therapy, one cap
a day is advised.
This cap. contains 10,000 I.U. of Vitamin A and taken
daily could lead to overdosage.
15...
- 15 -
Study by V~IAI of Jhelu Village :
Dr. Arora and Miss D. David conducted a study to assess the magnitude of
Vitamin A deficiency in Jhelu Village of Rajasthan.
Jhelu is 20 kia. away from the PNC in Mathania, and the nearest subcentre
is at Gagadi, 5 km. away.
There is no ICDS Project in the area.
Of a study of 150 children, 2/3 were below 6 years and 1/3 were in the
school going 'ige, above 6 years Distribution of 150 children showing signs
of Vitamin A deficiency.
Affected
No.
Normal a
Under 2 years
32
87.5
12.5
2-5 years
68
55.8
44.2
6-14 years
50
58
42
Age
Sex distribution of 55 Vitamin A deficient children
m
£
Belov/ 2 years
2-6 years
2
16
2
14
6-14 years
14
7
32
23
/made
Plans are being/for action and follow up,
16...
- 16 -
Issues that arise :
1)
While we wish to prevent nutritional blindness by improved nutrition,
teaching people to grow and use green leafy vegetables, and fruits
(yellow), the scarcity of land, water, the exploitation of the tribals,
deforestation, increasing prices of basic commodities, use of fruits
in preparing costly and junk soft drinks, increased exports all make
us wonder where to begin
2)
In a health awareness programme, recognising early signs of the disease
is essential. Are PHC and ICDS workers being taught the earliest signs
of Vitamin A deficiency - like stumbling in the dark due to night
blindness, identifying Bitot’s spots ? Do these workers use every
opportunity in teaching people about nutrition, or do they mechanically
dole out Vitamin A?
.
3)
In the strategy for Vitamin A distribution :.
~
- age groups in months need to be specified instead of saying l-$ years.
- fixed tines for Vitamin A distribution needs to be done after
identifying the target beneficiaries.
- those who do not come to the clinic need to be given Vitamin A at the
home.
- the same child should get Vitamin \ twice in the year.
- ICDS programme workers should not confine to 2-5 years age group.
- lactating mothers and pregnant women need to be included as beneficiaries
- sick children with measles, diarrhoea, PC!
*!
need to be beneficiaries.
- the special 2 ml, spoon has to be used, not the ordinary tea spoon.
- registers to be maintained so that supply, utilisation and related
problems can be identified.
4)
Vitamin A production, as seen from the figures is far below the ,targets.
There is increasing import of Vitamin A. Vitamin A is not mentioned
in Category I list of essential drugs for National Health Programs.
We need a policy for increased production of esaenti?! medicines like
Vitamin A, and curbing hazardous and irrational drugs.
Prepared by Dr. Susy Aya Ram, MD
People’s Education for Health Action
:b: 22.4.88
- 17 -
QUESTIONNAIRE - Vitamin A prophylaxis progranme
1.
Do you have a programme for distribution of Vitamin A in your area ?
2.
’/here is the Vitamin A obtained from ?
3.
Who distributes Vitamin A solution ?
4.
Who are the beneficiaries in this programme ?
5. Where is the Vitamin A given, horae/health centre ? and how often ?
6. Is a special 2 ml. spoon used for this purpose, or is a tea spoon
used ?
7.
What are the problems in this program, is Vitamin A supply erratic,
lack of awareness among people, irregular visit by health worker etc.?
8.
Is a register maintained for this programme, can you give us a specimen
copy ?
9.
Are simple messages of consuming leafy vegetables and yellow fruits
to obtain Vitamin A, propagated ?
10.’‘/hat are your suggestions for improving this programme ?
11.Do you have children with keratomalacia
in your area ?
We would like you to participate in the Vitamin A prophylaxis programme.
In this context, can you fill in the above questionnaire and mail it
to us ?
VOLUNTARY HEALTH ASSOCIATION OF INDIA
40, Institutional Area
South of I I T
Near Qutab Hotel
New Delhi 110016
665018
Ph.Mos :663071
668072
International Council
of Scientific Unions
Committee on the Teaching of Science
NUTRITION,
AND
THE QUALITY OF LIFE
Professor C. den Hartog and Dr C.E. West
for the International Union of Nutritional Science
NUTRITION AND THE QUALITY OF LIFE
In order to understand the relationship between “nutrition” and the
“quality of life”, it is desirable that the two terms be defined as well as
possible. Many definitions have been given for “nutrition”. We would
like to use that proposed by the Dutch Nutrition Council which states:
“Nutrition is the process of choosing and utilising food, its assimilation
by the human body and the resulting effect on health”. It is much more
difficult to define “quality of life”. One of the reasons for this is that
the expectations from life differ enormously between individuals. What
a Kalahari bushman or a Fulani herdsman expects of life is completely
different to that expected by the upper middle class, let alone the very
rich in the USA, China or the Netherlands. Nevertheless, there are a
few elementary needs which are the same for everyone: safety, a sense
of security, a sense of belonging, housing and freedom from worry
about having food each day. One is reminded of the prayer: “Give us
this day our daily bread”; the first requirement of life.
Good nutrition is therefore a sine qua non condition for the quality of
life. The condition of the mind and body is to a large extent determined
by nutrition. Incidental consequences of incorrect nutrition, such as
food poisoning, occasionally eating too little or too much, or the
occasional eating of food of poor quality, do not affect the quality of
life. It is the diet over a long period which is one of the determinants of
the quality of life.
The quality of life begins at birth
The way in which a child enters the world has a considerable influence
on his future life. For example there is a great deal of difference
perceptible between the birth of many children in the Third World and
those in affluent countries.
It has become apparent in the last few years that inadequate maternal
nutrition often produces, generation upon generation, children with
incomplete brain development and the chance of a lower IQ for the rest
of their lives compared with children with adequate maternal nutrition.
In the Western World, the two most important factors during pregnancy
which can impair a child’s development are excessive smoking and the
excessive use of alcohol by the mother. One could argue that heavy
smoking has nothing to do with nutrition. However, this is not so.
Smoking indirectly and adversely influences the supply of oxygen and
nutrients via the placenta to the unborn child. Compared with children
bom to women who do not smoke, when the mother smokes the risk of
having a premature baby doubles and the average birthweight is 150 to
400g lower, while the cranial circumference is smaller. Carbon
monoxide and nicotine are both toxic to the placenta and the children
of mothers who have smoked during pregnancy have lower iron
reserves in the bone marrow. The placenta is also smaller than usual.
This last trait is also found when excessive alcohol is used by a pregnant
mother and is coupled with intellectual retardation and some physical
abnormalities in the newborn baby. It is clear that these children will
not grow up to become “normal” adults and will remain on the negative
side of the quality norm, only being able to hold their own with the
support of others.
Influence of nutrition during childhood
The influence of nutrition during childhood can be positive as well as
negative and can therefore improve or diminish the quality of life. In
any case, as far as nutrition is concerned, what happens during child
hood helps to determine subsequent physical and mental health. Here
too, the problems differ from culture to culture and are likewise
dependent upon the availability of food. In many cultures, the concept
that food has a spiritual value is conveyed to children from a very early
age and these values remain throughout life. The spiritual value of food
is externally manifested in the form of sacrifices to gods, fasts, taboos
and magical happenings. In monotheistic religions, prayer is usually an
essential element for communication with God and is often associated
with food. Muslims, for example, use eating as a means of worshipping
God through prayer, fasting and other religious customs. Thus the
relationship between food and the worship of God takes an important
place in the quality of life.
Food is expensive in developing countries; the money required to
provide food for a family often represents a very high proportion of the
total income of the family. Thus the amount of food available is often
not sufficient for survival, optimum growth, and physical development.
High child mortality and retarded growth of young children are, we
feel, signs of a reduced quality of life.
Slightly retarded growth and remaining smaller do not in themselves
necessarily diminish the quality of life. They are only signs that less
than optimal development has taken place. However, when there is
high child mortality, one can presume that not only do the strong
survive but also that many have sustained permanent damage from the
serious malnutrition and infections suffered.
The role of breastmilk in providing a well-balanced diet and protection
against infection, especially in less developed countries, cannot be
overemphasized. It is particularly unfortunate that many mothers in
these countries do not continue breastfeeding for a sufficient period
of tune. Breastmilk can usually provide all the food required by an
infant up to age of 6 months. The reasons for giving up breastfeeding
early are many and varied but one factor responsible has been the
marketing strategy of companies selling breastmilk substitutes. In
affluent societies, the use of breastmilk substitutes has less influence on
the subsequent development of children than is the case in the Third
World. Welfare can be temporarily damaged by infections or over
feeding but permanent adverse effects have not been confirmed with
the exception of possible allergies to proteins of cow’s milk.
The period in which a child is an infant and toddler (up to 3 years) is
one in which the child is particularly vulnerable: the chance of a good
quality of life in the future can be jeopardized during this time. Proof
for this is provided by children who survive severe malnutrition due to
deficiencies of vitamin A, vitamin D, or iodine.
Severe vitamin A deficiency leads not only to night blindness which is
reversible but also to xerophthalmia (“dry eyes”) and keratomalacia.
The deficiency of vitamin A produces a lesion in the cornea of the eye
ultimately resulting in its perforation and therefore irreversible loss of
vision. Between 50,000 and 100,000 people mostly children under the
age of 3 years become blind in this way each year throughout the
world.
Vitamin D deficiency is a frequently occurring phenomenon which can
be prevented not only by ingestion of pre-formed vitamin D but also by
exposure to sunlight which converts a precursor in the skin to the
vitamin. Deficiency of vitamin D produces rickets with permanent
harmful effects to the skeleton. In Western countries with good child
care facilities, rickets has been reduced to a minimum. However,
rickets does occur in a number of countries where one would not expect
it because of the abundance of sunshine. This is the case among very
young children of some black African tribes who are kept in dark tents
for a long time and among women of Bedouin tribes who spend most
of their lives in dark tents. The Bedouin women often also suffer from
osteomalacia which produces a great deal of pain in the pelvis. This is
often in addition to rickets which gives rise to a deformed pelvis making
the process of child birth difficult.
Goitre is one of the most widely occurring dietary diseases and results
from iodine deficiency caused by the flushing away of iodine from the
earth’s surface. This can lead to retardation in children ranging from
real cretinism to growth retardation, decreased metabolism and
decreased physical and mental capacity.
It should be said that intervention programmes aimed at reducing the
incidence and severity of malnutrition due to dificiencies of vitamin A,
vitamin D and iodine and also to protein and energy deficiency have
been very effective. The developed world has a responsibility to
continue helping developing countries overcome these serious problems
of malnutrition.
Impaired quality of life in adults related to nutrition
This often occurs in adults as the result of undernutrition or over-eating
(a form of malnutrition) during youth. Nevertheless, adulthood has its
own syndromes which detract from optimal health and working
capacity. In developing countries, the main problem for adults is lack of
energy rather than lack of protein. Lack of energy in adults causes
bodily exertion to be reduced to a minimum in order to keep a balance
between energy intake and energy expenditure. Under such conditions,
it is impossible for physical activity to reach a desirable level thus giving
an apparent air of laziness.
In affluent countries, the problems are more complicated and often
result from over-eating or failing to eat a well-balanced diet. Many
diseases with a nutritional basis occur including cardiac and vascular
diseases, gall bladder disease, cirrhosis of the liver, and carcinoma of
the colon. Not only does an individual suffer from such a disease but
the society suffers because of reduced working capacity and increased
absentee rates in the workforce and because of premature death.
Correction of the nutritional problems in affluent countries presents a
task of similar magnitude to correction of the nutritional problems in
developing countries. Detrimental nutritional factors can exist for years
before disease symptoms become apparent. As much research is yet to
be carried out to determine the role of food constituents in nutritional
diseases such as those mentioned above, it is not possible to implement
completely effective prevention programmes. Prevention is made more
difficult not only because the disease exists before symptoms become
apparent but also because the willingness of individuals to change their
eating habits is only minimal.
Finally in this section on adults, mention should be made of dental
caries and also of the use of alcohol. It could be asked “How much does
dental caries influence the quality of life?”. Is it normal that a high
percentage of adults should be left with none of their own teeth? Just
because it occurs frequently, this situation should not be regarded as
the norm. Dental caries is a disease which must be fought right from
the beginning in youth but, because such technically perfect dentures
are available, it is barely considered a defect. In the same way, the
excessive use of alcohol by many young adults in so-called advanced
countries is becoming to be regarded as the norm. However, many
such people are ruining their health through cirrhosis of the liver which
often leads to premature death.
6
The Aged
The aim of nutrition, in so far as this influences the quality of life, is
to reach old age in good health without disablement from nutritionassociated diseases or aberrations such as cardiac or vascular diseases,
advanced osteoporosis, high blood pressure or apoplexy. As people
get older, it is difficult to change their eating habits. Thus it is desirable
to establish good eating habits at an early age and to modify the diet to
maintain a good, balanced, age-related diet with increasing age.
Positive influences
V
An overview of diets and nutrition mainly having a negative influence
on the quality of life has been presented above. It is just as useful to
consider how a diet can exert a positive influence and contribute to
optimal physical and mental health. This is a diet which throughout life
is adapted to the specific requirements at each different age period.
It is not possible to describe such a diet in the limited space available.
However, it should include all nutrients in sufficient qualities and the
right proportions to enable the body to meet all reasonable demands
made of it both internally and externally with as little stress as possible
to its natural defence and adaption mechanisms. The diet can be made
up from an amazing array of foods depending on the availability and
acceptability of the foods within the culture concerned. Such aspects as
hygiene and the absence of toxins should be taken into account.
Good diet should begin at an early age. In fact, as mentioned earlier,
it should begin before the baby is born with good nutrition for the
mother. In developing countries, the mother is usually faced with
nutritional deficiencies while in developed countries, it is more
important for mothers to abstain from smoking and not to consume
excessive amounts of alcohol. Breastfeeding of babies should be
encouraged throughout the world as it provides the child with the best
chance of being healthy.
e
evised Note of May 3, 2001
W'Atf'7 ~
'
thing into account feedback received; please see alsocomments ofMFC members in the Annual Meet
Organising Committee at the end ofthis note)
An Outline for the MFC 2002 Annual Meet on Food and Nutritional Security
n Food Security
ood security appears to be about getting rid of hunger and ensuring “two square meals” per day for
.’erybody. What kind of food? Who produces the food? How much control do people, especially the
jorest of the poor, have over the production, distribution and consumption of the kinds of food?
losely related is the question of whether the kind of food available and being consumed ensures long-term
Fritional security — the latter term understood as being able to access sufficient number of calories for
1 persons in one's family for sustained periods of time, access that would hopefully lead to better health
id quality of life. How many calories are really necessary for various occupation groups and what has been
e progress in this regard since the last decade? Can poor people purchase the required calories at the wage
veis actually on offer on farms and fields? In Gujarat for instance the minimum wage for farm labour is
cound Rs 80/- per day but nobody really gets it all the time.
utritional Issues
f medical scientific interest is: Why are specific nutritional anemia being caused? What is the etiology and
lidemiology of the same? On the other hand why are some kinds of deficiency (Vit A for example) appeal'
be diminishing? What are the other medical and health consequences’of these deficienceis? And what are
e new problems coming to fore with life style changes and changes in the kinds of food available? (See
'so note bn nutritional security at the end by S.Sridhar)
ole of State Policies, Markets, Technology and Ecology
dsewhere, increasing nutritional insecurity seems to be related to increasing deforestation; loss of control
ver common natural resources such as forest, water and land; the decrease in the availability and variety
•'vegetables (for instance greens), cereals (decrease in millets), food grains and edible oils; major shifts in
tricuiture from cash to commercial crops and the consequent'ecological imbalance and scarcity of food
id animal fodder.
' practice we need to examine, the feasibility of distributing free food to people who are unemployed or
ndlcss and poor and subject to droughts, cyclones and other natural calamities. In fact many of these
itural events, including earthquakes, need not end up as livelihood and nutritional calamities. What can
e do to prevent such catastrophic consequences?
'hat are the new roles of the state, the market and civil society in ensuring food and nutritional security
ith a “reforming"’ Government of India? This is of concern especially as the one of the major nutritional
ilicy interventions, the PDS, is being diluted. What and how effective have been the other policy
terventions - the ICDS and the mid-day meal schemes and Take Home Ration schemes. What will be the
u
feet ol the slow winding up of the Food Corporation of India? there is talk also of toning down the role
'the Agricultural Prices Commission, the one which fixes procurement prices.
f extreme concern are suicides among farmers and the apparent increase in immiserisation of all kinds of
asons, poor and not so poor. Some of these seem to be related to rapid shifts in government policies of
cnort-import, the increasingly adverse terms of trade for the indigenous producer, the dumping or
herwise of food and other industrial items of (what used to be) local production and consumption.
ow many of these are indeed related to the green revolution technology of farming and how many to other
ctors out of control of the farmer, for instance spiraling debt and lack of farm insurance? A closely related
sue is the kinds of rural and urban indebtedness and its long-term effect on nutrition, health and food
Tailability at the house hold level. Are Grameen bank type solutions (banking for the poor), increasingly
ivocated by Indian NGOs, the answer?
O
f special interest are gender differentials and any new insights coming out of recent studies including the
test round of census.
rith the inroads of WTO, or rather the easy succumbing to WTO logic by our policy makers (for instance,
e hasty removal of QRs on a host of items), we need to worry about what are the practical crop rotation
ternatives for farmers in the tussle between the market, growing more cash crops, soil nutrient depletion
£ id self-dependence. Can India afford to buy food in the international markets using money earned li'om
Spoils. Is it moral to export food (as we have recently done with rice, wheat and sugar) when our own poor
c starving? Why have prices of agricultural commodities fallen post-WTO while food prices have not
• lien?
a
£ i. similar look at the inroads made by shrimp farming in states like Tamil Nadu is in order, as the
aditional reliance on growing cereals for sustenance seems to have been sacrificed, and therefore more
rectly assured food security. A related issue is the investment of high technology fishing/trawling in the
W Tastal areas (blue revolution?) over the past 20 years and the actual effects on food and nutritional status of
e fishermen, especially the poorer among them.
ct another area of related interest is an examination of the 30-year old romance with soya beans, especially
7 farmers in M.P.. Now what has been the real life consequences of this dedication to soya beans
specially as pulse production seems to have come down (not the only reason for pulse production decline
iwever). What also has been the nutritional consequences of emphasis on wheat and rice as “prestige”
-reals as compared to say ragi, jowar, maize and other millets and the consequent decline in production of
“ c latter? What is happening to our combined resource base of ground water, soil and pest ecology, thanks
the Green Revolution and now the market? People have shifted to cash crops. Is there any alternative
g|W)Ssiblc?
O
Iso of interest is to ask why in spite of the many warnings about impoverishment, both rich and poor
;ople still subscribe, at least in Gujarat, to the Operation Flood led dairy farming? Some other data, from
ajasthan and West Bengal, however seem to indicate dairying actually results in per capita decline of the
zailability of milk in villages and therefore likely to have adverse nutritional consequences.
... . 'e nvcu to think oi diitereni nutritional ano tooo security policies across ciasses ana cultures ana as wei.
: across geo-climatic zones.
W
?.od Security and Ill Health Promoting Work
ow do we resolve the apparently obvious health-related tension between campaigns against tobacco and
in masala on the one hand and the unemployment of so many tobacco growing farmers and labourers,
?edi workers, tendu leaf collectors — many of them being really poor — if all of them were to shift from
bacco? (Beedi making is one of the largest sectors of employment after agriculture and construction).
Security and Ideology of Self-Reliance
H
"
jgl
41
—
“
4}
national self-reliance as an ideology, which was a major theme of our independence movement and our
jdy politic till the seventies, out of fashion? Or rather, we need to ask why has something so
immonsensical become out of fashion. Are we hurtling towards a market-led economy in the name of
rst and, now second generation, reforms without perfecting our act as a welfare state? (It is to be
membered most of the highly industrialised states of Europe have sound welfare mechanisms in place so
at people do not go hungry'.) What kind of food security are we providing with increase in hire and fire
jlicies (as per the recent budget of 2001, firms up to 1000 workers need not take permission to get rid of
orkers), of mindless disinvestment of PSUs.? We are told by economists that it is good for all of us in the
ng-term. How true is this assertion?
related issue of interest is, why has China, once touted as an example of a society with high equity, given
collective farming and communes and gone for market-led mechanisms? Closer home, what has been the
dance sheet at the end of the day of land reforms in West Bengal (Operation Barga)?
rhat indeed are the nutritional consequences of the market-led economy, of the Mcdonalds, Pepsis and
okes, Cargill salt and Monsanto seeds? Do we leave it to the wisdom of the system, some new invisible
md to take care of all the damage? What are the implications of patents, biotechnology, genetically
odified foods and organisms, and the onrush of MNCs in “value-added” food industry? Is free trade fair
ade?
as nutritional quality and food security really increased on the whole even as the percentage of people
How poverty line seems to have decreased? Is there any special role for health activists in all this? Is the
:ily solution to go back to an ecoconscious, welfare society - if so how do we do it?
iote on Nutritional Security
ince the major concern of the meet is to be food security, a number of issues in nutrition can be identified
at should contribute to a better understanding of food security and a rational approach for achieving the
ime. It may be enough to limit discussion on nutrition to background papers, especially if these are
ireful ly conceived. Hie issues that I can think of as meriting attention are:
1. Major nutritional deficiencies in India: nutritional anemia, protein-energy malnutrition (child and
adult), selected micronutrient deficiencies (vitamin A, iodine, etc): trends, current status,
contribution to morbidity / mortality! quality of life.
An examination of the regional I sociocultural differences in nutritional status (both under- and over
nutrition).
An examination of the changes over the last few decades in the understanding of the pathogenesis of
specific nutritional derangements, and implications of these on for policies related to agriculture and
food security.
4.
The nutritional impact of PDS, ICDS, MDM, TINT and other such programs - expected and actual.
The possible and actual effevis of then dilution.
5.
Potential and actual nutritional implications of recent policy changes related to food production,
procurement, distribution, etc.. Evidence for changes in nutritional status in vulnerable populations
of countries opting for major macroeconomic policy changes.
6.
Evidence for regional and gender differences in health indicators attributable to differences in
traditional dietary practices. Urbanisation and improvement/decrease in food security. Potential and
actual effects of a host of macro and micro factors on nutritional and health indicators: recent rapid
changes in lifestyles, particularly diets, availability of processed foods, worsening fuel crisis,
availability of cooking time, availability of time for cooking and differential calorie requirements at
different stages in life starting from weaning; Evidence for factors that influence such changes.
7.
Evidence for diminishing biodiversity in food sources. Potential or actual impact of this specifically
on local I regional health indicators, and generally on other biodiversity including human diversity, if
any.
8.
Genetically modified foods and their potential impact on nutrition and health.
9.
Any relevant studies available on traditional concepts of evaluating food value vis-a -vis variations
in food / nutritional needs of different individuals / families / communities, and prescriptions and
proscriptions that follow: their correlates in modem nutrition, and relevance of loss of such
traditional practices for nutrition / health status. Intrafamily food distribution over the years across
various classes and castes; Research needs in nutrition in its relation to food / agriculture policies.
eena Shairughna’s Comments
’ve gone through your background paper and
aiizc that you have laid out a very broad framework,
id a whole range of issues have been raised which
ay be classified into the following:
Access to food.
Wages and Food
Nutritional problems in relation to a large no. of
iriahles
Famine and Food security
Other Calamities
Role of the state eg. Nutritional Programmes,
DS., 1CDS., Procurement prices ,
Agriculture related, such as cash cropping, WTO.
xport Markets
WHO campaigns against tobacco and and it's effect
i food security and livelihoods.
Land reforms, collective farming. Indebtedness,
id its impact on food security
). Right to food.
I. GM foods, Biodiversity and implications for food
:curity.
c Problems of procurement, storage, and
Fsuibution.
3 Others
suppose each of these areas are important,and need
scussion and lend themselves to activism, however I
onder about our strengths, and how do we handle the
ne way out is to identify papers or paper writers,
id then structure the theme around the topics
ivered. We could try to avoid issues which are of
letorical value and /or common knowledge, such as
;ology, environment., and our great past kind of
ipers., unless there is some compelling evidence.
ven Sridhar's note starts off with
>ecificities,but ends up covering all the above
sues. Please do comment and let me know whether Pm
Isreading the problem.
Padmini Swaminathan’s Comments
i have the following suggestions to offer:
1] Let us use the MAM to discuss the theme of Food Security & Nutrition
•n
4|
in me veils. k eiis may ucuiae io uisvucss it jointly or separately
Jr both. At the Meet we could also zero in on a few key issues and take
'esponsibility for presentations, getting papers, etc.
21 the Note on Nutrition issues that have been circulated sketches a wide
ranvas. At the MAM we need to attempt some form of synthesization so that
.he issues are not only put in perspective but also in a manageable form.
An this T have the following extremely tentative format to suggest:
41, al Conceptual and Methodological Issues:
lloic I have m rmnd the debate generated by the two main methods that
tave been used to assess the extent of undernutrition in different pails
* ofthe world, namely, the FAO approach and the WHO approach. The FAO
approaches the problem through food availability statistics; the WHO
* proceeds to study the problem through observed conditions of human body
and basic functionings-lhe so-called anlluopometric approaches.
The consequences and limitations of relying on these approaches have to be
W analytically and empirically delineated with their differential
implications for policy.
b] Issues related to Data on Nutrition, both qualitative and
quantitative:
Few' would disagree with the notion that habitual intake below the
^plorie expenditure required is inadequate. The problems arise when this
— general definition is to be operationalized.
▼ It would be interesting to learn from scholars like Veena Shatrughna how
•.lie Indian State , has, through Bodies like the NNIMB, defined and
4| joerationalized the undemutrition/malnutrition question. 1’he questions of
data can themselves be split up into the following:
4^
i] The What question—what constitutes under/malnutrition
ii]The Who question—Identification of the population or segments ofthe
population who are undernourished.Is there a disproportionate emphasis
jii small children and women as victims of undemutrition to the exclusion
if adolescents and men?
iii]The 'When question-When in life is the risk of undernutrition
Highest? Do w;e have longitudinal observations ofthe same individuals
to answer the question, to what extent anthropometric failure early
in life is the explanation for short stature in adulthood and other
.complications.
"ivj Tlie Where question- location of undernutrition geographically and
4|
amone segments w’ithin a geographic population.
’•. ] The Why question-explanation for undernutrition [ food availability'
failures only or more substantively, income or entitlement failures]
lu Consequences of Undcniutiilion; Do we have concrete case studies
linking nutrition to particular debilitating diseases. Additionally
how docs one go about looking for and generating such data
♦
IV Policy Implications of Approaches adopted
Lam stessingthe aspect of Approach adopted since the policy
implications can be diametrically different depending on what approach we
idopt. Therefore we need to be aware ofthe possibility that the
mdamental
reasons for undemutrition are different in different parts of the world
aid also across countries. For example, literature shows that in
Sub-Saharan Africa the chief human problem is not low supply of food and
orimary undernutrition but rather grossly inadequate health care for large
sections of the population. In South Asia on the other hand, where the
anthropometric status ofthe population is far worse than in Africa, and
►chore mortality is considerably lower', primary undcniuirition is a chief
suspect for the overall deprivation. Action plans that fail to recognise
meh differences over space and time arc doomed to fail
I sc? the last section ofthe draft Outline, that oh Nutritional Security,
ong with the formulation of issues by Padmini, as forming the format for
e Annual meet. I say this for three reasons:W i) that this section of the draft provides an overview of all the issues,
4P' other sections only detail those issues.
Z) that many of the conceptual and methodological issues which were
rbjects of debate in the '60s and '70s (eg those raised by Sukhatme and
opalan), and settled in favour of the more holistic and pro-poor
41 jrspective, are again being restated in reverse arguments, almost ignoring
e earlier debates. They are currently providing the 'technical'
stification for ’medicalisation' ofthe nutrition problem and for narrow,
" chnocentric policy approaches.
3) mfc has the onus of debating and taking positions on the 'technical'
sues of'nutrition science' and its inherent concepts and methodologies.
admini's note points to these very' clearly.
4^
Therefore I would suggest that the Note on Nutritional Security in the
-aft be at the beginning of the Outline paper rather than at the end. Also
nt it incorporate points TT (on conceptual and methodological issues) and
/ ( on policy implications) of Padmini's note.
11/19/0112-.0S
1 ’zT@0r0tM
■ A@0
030" 0
' 0^pBp0p0pa>0aa@' 00
a@0a> @p> @PP a0 @0 £=> 0 P' a.0 &> 0 IP a
• ' ^p0p0p0p0p-^'^@'0p0pbBz?pp00p0P’0pa@' &@'0p0pbBi
N/U7-J.
MORE DEATHS DUE TO VTTMIN A IN ASSAM
Subject: MORE DEATHS DUE TO VTTMIN A IN ASSAM
Date: Sun, 18 Nov 2001 04:28:13 +0000
From: "umesh kapil" <kapilumesh@hotmail.com>
To: secy.wcd@sb.nic.in
CC: kapilumesh@hotmail.com
Respected Sir
I am enclosing
Assam.
furthur update on deaths due to vitamin A administration in
Dr. Umesh Kapil
Additional Professor
Department of Human Nutrition
AIIMS, New Delhi, 110029
kapilumeshfihotmail.com
3 more Vitamin A deaths in Assam
TIMES OF INDIA 18.11.2001
P P SINGH
TIMES NEWS NETWORK
GUWAHATI: At least three more children have died in Assam after taking
Vitamin A dose in a Unicef-sponsored programme, taking the toll to seven
though unofficial reports put the figure at eight, said state Health
Minister Dr. Bhumidar Barman.
Barman, while talking to this correspondent said that there have been three
more deaths in Kokrajhar district in Balagaon Relief Gamp under Gosaigaon
sub-division, but he felt these were too late for any reaction to the
Vitamin doses.
However, according to sources, the two infants — Duler Hasda aged five and
Bali Hasda aged three — both daughters of Saran Hasda had died on 15th of
November. The vitamin doses were administered on 12th and 13th of this
month, it is learn that the district administration exhumed the bodies and
has sent them to Kokrajhar hospital for post-mortem.
Another child, Vijay Topo, aged three, son of Etua Topo also died on
Saturday morning in the same relief camp according to sources in Kokrajhar.
His body has also been sent for post mortem.
When contacted the DC Kokrajhar, Dr. Ashish K Bhutani, while confirming the
news informed that he has seized all the used and unused bottles of Vitamin
A. He said the much talked_af. five_ml.cups.were not seized with these
indicating normal two ml spoons were used for. administering the vitamin.
This may_mean that the deaths were not due to over doze as has been
suggested by the state health minister.
Dr. Barman said though originally he had also opined that the deaths might
be due to overdose it seems the contents of the bottles could also be
responsible thus bringing the manufacturers of the Vitamin A also into the
picture.
He said that orders for the suspension of two doctors and one pharmacist who
were in charge of three booths where deaths took place earlier in the three
districts of Cachar, Sonitpur and Nalbari have been issued.
However, cachar DC P K Das said that no medical officer there has so far
been suspended.
ill'1
Dr. Barman said with the latest deaths being reported action against more
medical staff would be taken. According to the Health Minister two nurses
and one Anganwadi worker have also been suspended in the three districts of
\
aaxa§aB»M&axa°aaxa°Qa
(
MORE DEATHS DUE TO VITMIN A IN ASSAM
Cachar, Sonitpur and Nalbari
Vitamin A deaths: Screening was not done
SHANKHADEEP CHOUDHURY
TIMES NEWS NETWORK
GUWABATI: were enough precautions taken by the state government-Unicef
combine in Assam during the now-tainted Pulse Vitamin A programme?
Not really, it seems, if the minutest of risks are taken into consideration.
£
The basic public health question that has been raised in the aftermath of
the tragedy is whether a screening should have been done before Vitamin A
drops were administered to children to eliminate all risks, whatsoever.
Already, seven children have died after consuming Vitamin A drops in various
parts of Assam under a joint Unicef-Assam government programme. Red faced
authorities, while suspecting that it happened because of ah overdose, have
ordered a enquiry besides suspending six health officials till now.
Nutritionists and child specialists here feel that a screening should have
been made mandatory, even though some of them agree that this might be
physically impossible in a public health programme for the masses.
The logic, as city-based nutritionist Nahid Pasha says, is very simple.
"Vitamin is given in the form of retinol. If the child has a liver disorder
and the retinol binding capacity is reduced^ then it can cause toxicity and
he is not fit to receive Vitamin A. Therefore, a screening by me“dicos~±s
needed to ensure that a child is not suffering from a liver disorder or
diarrhoea", she feels.
Agrees another prominent Guwahati paedetrician, Dr Rajkumar Kayal:
"Sometimes, children are intolerant to a megadose of Vitamin A either per se
or because of some underlying ailments, and hence, theoretically speaking, a
screening would eliminate all such risks of ailments."
" However, he added: "Of course, I understand that this might be practically
impossible. Hence, the next best thing to do would be to adhere, to strict
guidelines on dosage, and at the same time, to preferably impart this
Vitamin A only to really vulnerable sections -children with malnutrition, or
with clinical Vitamin"A deficiency, or’with measles, or with chronic
diarrhoea."
However, Unicef authorities - while agreeing that no screening was conducted
- have a different opinion. Pat Engle, unicef's chief of child development
and nutrition, when contacted over telephone in New Delhi, pointed out:
"Globally, children are generally not screened, except for age, for a public
health campaign, including Vitamin A. Children are screened for age, but
there are no other criteria mentioned in the Government of India policy for
vitamin A. Preventative supplementation of Vitamin A, in fact, has been on
in India for~’the las t twenty.years,. "
Get ynnr frff download of MSN Explorer at http://explorer.msn.com/intl.asp
(W- I .
PREPARE AND SERVE SAFE MEALS
As a homemaker, you have the important
job of preparing and serving safe whole
some meals for your family. There are
many things you can do to make food safe.
When you prepare' and serve food it is
important to-• select good quality food
• keep yourself clean
• keep dishes and equipment clean
• keep the cooking and eating area clean.
Food can become unsafe to eat if it is-• served by a person carrying disease
germs
• served in soiled dishes
• eaten with dirty utensils and hands.
Keep everything clean. Cleanliness helps
to keep away disease germs. Clean food
is likely to be safe food.
MAKE MEALS SAFE
Some foods are eaten raw, others are
cooked. Either way, they should be clean.
You can prepare foods to make them safe
for you and your family.
Some foods spoil quicker than others.
Foods made of milk, eggs, meat, poultry,
fish or shellfish may contain harmful
bacteria that grow rapidly. These bacteria
can cause food to spoil. Spoiled foods will
make you sick.
When preparing these foods:
• store them for a very short time
• prepare in clean containers
• cook thoroughly
• serve immediately
• don't save leftovers.
3
Some Illnesses Are Caused by Food
TO PREVENT SPREAD BY
FOOD
ILLNESS
FOODS USUALLY
INVOLVED
WAYS
Bacillary
dysentery
Moist or prepared foods;
milk, other dairy products
or water contaminated with
excreta.
Strict personal cleanliness in food
preparation; keeping moist foods cool
during storage periods; cooking foods
before serving; getting rid of flies.
Persons with dysentery should not
handle food. Dispose of human wastes
safely.
Brucellosis Raw contaminated milk,
(Undulant
dairy products, or meat.
fever, Malta
fever,
Bang's
disease)
Get rid of brucellosis from livestock
by vaccinating young animals and
slaughtering infected older animals.
Boil milk used to drink or to make
other dairy products.
Diphtheria
Make the milk safe by boiling. Search
for the per son carrying the illness and
isolate him from other people.
Milk contaminated by
humans with the illness.
Scarlet feve- Foods contaminated by a
or septic
discharge from the mouth
sore throa' or nose of a person who
has disease germs in his
body, whether he is sick,
about to get sick, or
immune.
Boil milk used for drinking or to make
other dairy products. Keep persons
with the disease from handling food.
Separate them from other people.
Milk from cows with udder
infections caused by these
organisms.
Botulism
Home canned foods, or some Cook canned meat and vegetables
times commercially pre
thoroughly before serving. Boil 15
pared foods.
minutes and stir to make sureyouheat
all parts.
Amoebic
dysentery
Water contaminated with
sewage. Moist food con
taminated with human
excreta.
Protect your water supply. Use safe
drinking water. If you are not sure
water is safe, boil it for 10 minutes.
Be clean in preparing food. Dispose of
human excreta properly.
Trichinosis
Raw or undercooked pork
and pork products.
Cook these foods thoroughly. Cook
garbage fed to swine. Get rid of rats
in hog lots.
Salmonel
losis
Cracked or dirty eggs con
taminated with poultry
excreta, meat meal, bone
meal, or fish meal. Poultry
meat contaminated by un
sanitary handling.
Use only clean eggs with sound shells.
Soiled eggs should be washed. Handle
poultry meat and eggs under clean
conditions. Store them ina cold place.
Cook thoroughly and refrigerate if not
eaten at once. After handling raw eggs
or poultry, wash your hands thoroughly.
USE SAFE WATER
You need safe water to prepare foods and beverages. Water is likely to
be safe when it comes from acity water supply or a sanitary well. Your
local health officials can tell you how to make a sanitary well.
If you are not sure water is safe, boil it at least 10 minutes in a clean
container. Store in a clean covered container.
Use this boiled water for:
• drinking
• preparing dried, condensed
or evaporated milk
* making cold beverages
Foods Eaten Cooked
Cooking food will destroy most harmful
bacteria. Most foods should be washed
before cooking. Wash them before cutting
into small pieces.
Wash meat, fish, and poultry with a clean
damp cloth to remove dirt or chipped
bones. Do not let them soak in water.
They will come out soft and may lose
some of their natural juices.
Green leafy vegetables may need to be
washed several times to remove dirt,
insects, and worms. Lift leafy vegetables
from the water. The dirt and sand settles
to the bottom of the container.
* making ice
• washing fruits and vegetables
* washing dishes.
If there is mold, bruised or spoiled spots,
or insect damage, cut away these spots
before eating the food.
Foods Grown in Night Soil
Some foods such as fruits and vegetables
may come in contact with human excreta
or night soil. These foods need special
care.
Untreated night soil may carry disease
germs. There is no known way to treat
night soil at home so that it is safe. Never
use it to fertilize your garden.
Foods Eaten Raw
All fresh fruits and vegetables that are to
be eaten raw should be washed thoroughly
in safe water.
Washing fruits and vegetables helps re
move any sand, dirt, or pesticides that
might be on them.
5
Protect yourself and your family from
germs in human waste:
If there is a danger any night soil has
gotten into your garden, cook your vege
tables. Do not eat them raw.
Any fruit that falls on ground that has been
fertilized with night soil should be cooked,
particularly if it cannot be peeled.
Sometimes water from irrigation ditches
contains night soil. This water is not safe.
If you hav6 to use this water for watering
your garden and fruit trees, cook vege
tables and fruits to make them safe.
Foods Sprayed with Pesticides
In many countries, gardens and fruit trees
are sprayed with pesticides to get rid of
insects. Washing fruits and vegetables will
help remove these sprays.
Ask your health department sanitarian or
other health officials to tell you howto get
rid of these sprays on food.
Leftover Foods
All leftover foods should be stored in a
clean covered container.
If the food has been cooked, cool it
quickly. Place the container in cold water.
Do not cover tightly until it is cool. Put a
clean cloth over the container until the
food is cooled.
After food is cooled, cover the container
tightly. Place the container in a cool
place. If possible, store it in anicelessor
mechanical refrigerator or a cave.
Foods made with milk, eggs, meat, fish,
or poultry spoil rapidly. In hot climates
without refrigeration, never save them for
another meal.
All cooked leftover foods should be re
heated to make them safe to eat. Heat well
for 15 minutes.
USE SAFE MILK
Milk is one of our best foods. Fresh milk
can have harmful bacteria in it. To make
fresh milk safe, bring it to a boil.
Rinse with water that has been boiled
for 10 minutes. Be sure to wash the
cloth strainer.
Milk that you buy from a modern dairy
usually will be safe. If it is not you can
make it safe at home.
2. Pour milk through the strainer into the
container for heating. It is best not to
heat more than 2 quarts at a time.
Make milk safe by boiling soon after milk
ing if possible.
3.
Place the container over the fire and
bring the milk to a boil. Stir with a
ladle or a wooden spoon.
4.
As soon as the milk boils, remove the
container from the fire.
5.
Place the container in a basin of cold
water. Change the water often to cool
the milk quickly.
How to Make Milk Safe at Home
1. Be sure all your utensils are clean.
Wash utensils and containers first in
cold water to remove any milk or fat,
then wash them in hot soapy water.
6
f)
Boy in Pakistan is boiling milk to make it safe.
6.
7.
Put the cooled milk into clean bottles
or pottery jars that have been washed
in safe water, and cover.
How to Use Dried Milk
Keep milk in a cool place. Iceless or
mechanical refrigerators or caves are
ideal places for storing milk.
Sprinkle dry milk on top of safe, luke
warm water. Mix well. Mix a fresh supply
of milk for each meal.
Fluid milk is prepared by mixing one part
of dried milk with four equal parts of safe
water.
7
Keep Meat, Fish and Poultry
Covered
These foods should be kept covered--
• in the market
* on the way to your home
* in your home.
They should be wrapped loosely to allow
air to circulate. Flies and other insects
like to feed on these foods.
In the market, cheese cloth or other loosely
woven cloth could be used. In some coun
tries, food is protected from flies by
screened containers.
On the way from the market to your home,
these foods should be wrapped. If the seller
does not wrap them, take wrappings with
you. You may use paper, large clean leaves
or clean cloths.
At home, keep foods covered. If they are
wrapped with paper, leaves or a clean
cloth, loosen the wrapping. Air needs to
circulate around these foods. Store in a
cool place until used.
Food sold in the market is protected by a screen.--Ghana.
Homemakers ehoose fresh vegetables in a market in Egypt.
$
Cereals and Breads
Select cereals free from weevils, dirt, and
stones. When you pick the grain up in
your hand, it should feel heavy. If it feels
light, insects may have eaten some of the
grain. Insects eat the best part of grains.
bread helps to avoid dirt, flies, and other
insects.
Fresh Fruits and Vegetables
When selecting fresh fruits and vege
tables, avoid wilted, shriveled or decayed
ones.
Bread should be free from mold.
Keep bread covered at the market, on the
way home, and in your home. Covering
10
Green leafy vegetables should have afresh
and attractive color, no yellow streaks or
spots, or damage by insects or worms.
Milk and Cheese
in a damp place. Look for insect and
rodent damage.
Fresh milk should be free of insects and
dirt. It should have a fresh, not a sour
smell. Be sure it is in a clean covered
container. Sour milk is sold in many
markets.
Some kinds of cheese are made with a
mold in them. This type of cheese is safe.
Mold that forms on the outside of cheese is
not safe to eat.
Dry milk that has a strong flavor and is
lumpy may be old or may have been stored
Do not buy cheese that has been damaged
by insects or rodents.
STORE FOOD !N A CLEAN PLACE
Whether you buy food or grow it, youmust
have a place to store it properly until you
are ready to use it. Good storage saves
time, money, and food. Select suitable con
tainers and plan to keep foods cool, dry and
free from dirt, insects, and rodents.
Food that is not carefully stored attracts
insects and rodents. They may carry
disease germs.
Dry foods such as grains, salt and sugar
may be stored in pottery or glass jars,
tin cans or bottles. These containers with
tight covers may be kept on open shelves
in a cupboard.
* keep your home and surroundings
clean
• keep garbage in a covered container
Perishable foods like--
* feed garbage to animals or burn or
bury it
* fresh meat, fish and poultry
• some fresh fruits and vegetables
* milk, butter, margarine, cream and
leftovers
should be kept in a cool place.
When possible, store these foods in covered
containers in an iceless or mechanical
refrigerator, food safe, cave, or window
box.
In cool climates, some fruits and vege
tables may be stored from 4 to 6 weeks
tin cellars or in outdoor pits dug in the
ground.
Remember-• keep foods cool
• keep foods covered .
To control these pests you should--
• keep all food in covered containers
• burn or bury trash
• use a sanitary latrine
• ask government officials abouttheuse
of pesticides.
You may need to use pesticides to get rid
of household pests. Ask your sanitarian of
the health department or other officials to
help you. They can tell you how to control
them.
Keep poisons for killing insects and rodents
away from children, food, dishes, and
cooking utensils. Mark containers which
hold poisons clearly, and store in a safe
place. Poisons can make you and your
family sick.
KEEP YOURSELF CLEAN
Develop good personal habits. Wash your
hair every 10 days or 2 weeks. Do not
let hair fall into food--wear a scarf, net or
cap. Never comb or fix your hair where
food is being prepared.
Wear clean clothing. Wash your clothing
often. Use clean aprons to protect your
dress. Change clothing when it becomes
dirty.
Don't cough, sneeze, or spit near food or
dishes. You could spread disease germs.
Never lick your fingers or thumbs. Wash
your hands.
Don't scratch your head or touch your face
when preparing food.
When tasting foods for
separate fork or spoon.
flavor, use a
If you have a cut or scratch, wash it with
soap and water, cover with a clean cloth.
Keep sores covered so that flies and dirt
cannot get on them.
If possible, you should see a doctor if you
have sores or ulcers.
Wash Your Hands Often
Remember, harmful germs are all about
you. They are on your body, hair, face,
and clothes. If you do not keep clean and
healthy, you can spread germs.
Disease germs of amoebic dysentery, food
poisoning and typhoid fever can be spread
by unwashed hands. Get into the habit of
washing your hands often with soap and
clean safe water.
Several ways you can spread disease germs
when preparing and serving food are by
having:
Wash your hands before you:
• infected sores on your hands
• unwashed hands
• a contagious disease.
Scratches and Cuts
The sore on your hand may have disease
germs. Those germs can get into the food
you are preparing.
Later you eat this food. In awhile youmay
get a stomach ache. The germs traveled
from your hand to your food and then to
your stomach. If your family eats the same
food, they will be sick too.
12
• handle food, dishes or other eating
utensils
• set the table
• eat
* feed the children.
Wash hands after you:
•
•
•
•
*
*
•
go to the latrine
use a handkerchief
handle animals
clean animal pens
work in gardens
cough or sneeze
wipe your eyes, even when you use a
cloth
handle a baby or sick person.
Keep your fingernails cut short. Dirt and
disease germs gather under long nails.
Care of a Person with a
Contagious Disease
Such diseases as diptheria and scarlet
fever are contagious. This means they can
be spread from one person to another.
See a doctor if possible.
A person with a contagious disease should
not prepare food. Have some other member
of the family do it.
KEEP EQUIPMENT AND DISHES CLEAN
Equipment and dishes used for preparing
and serving meals must be:
• kept clean
* stored in a clean, safe place-
Remember, if equipment and dishes are
cleaned immediately after they are used,
it will take less time and the job will be
easier for you.
Care of Dishes, Pots and Pans
ft
Dishes, glasses, silverware, pots, pans
and other cooking utensils used for pre
paring food should be washed after each
use.
Washing and rinsing dishes carefully helps
to prevent the spread of disease germs
to you and your family.
To wash dishes, use water as hot as your
hands can stand. Use soap in the wash
water. Pour hot water that has been
boiled for 10 minutes over the dishes to
rinse them. This rinse water should not
contain soap and should be clear and clean.
Let the dishes dry in the air. Air drying
is the safest and easiest way if the dishes
are protected from dust, flies, insects, and
animals.
13
If you use towels to dry dishes, be sure
the towels are clean.
Care of Large Equipment
Burned-on food, smoke, rust and other
stains need special cleaning with a scour
ing material. Wood ashes, sand and
pebbles, salt, and other local materials
can be used. Commercial scouring powders
are good, if available.
The stove and oven should be thoroughly
cleaned at least once aweek. Food that has
spilled should be wiped off after each meal.
Store clean dishes in a clean, ventilated
place, free from insects and rodents.
Other equipment, such as the iceless or
mechanical refrigerator, stools, chairs,
and cupboards, need to be cleaned often
to keep them clean and safe. Scrub with
soapy water and rinse with Clear water. If
you have a sink, it should be cleaned
thoroughly at least once a day.
Care of Babies’ and Sick
Person’s Dishes
Babies' dishes and dishes for the sick
need special care. Wash these dishes
separately with hot soapy water and rinse
with clear water.
Then place each person's dishes in a
separate container. Cover the dishes with
clean water. Boil for 10 minutes. Drain.
Air dry. Store separately from the dishes
the rest of the family uses.
Store Dishes, Pots and Pans
in a Clean Place
All eating and cooking utensils should be
stored in a clean, dry place. Dishes and
glasses should be stored in an enclosed
cupboard, if possible. Store eating utensils
in a drawer, if possible.
Large pieces of cooking equipment, such as
pots and pans, can be turned upside down
on open shelves, a table or counter to
help keep out dirt, insects and rodents.
KEEP THE COOKING AND EATING AREA CLEAN
Painting or whitewashing the walls helps
keep the place clean. It will be amore at
tractive and pleasant place to work.
Have good air circulation to remove odors,
grease and smoke. A stove with a chimney
will help to keep out smoke.
Take pride in keeping the place where you
cook and eat clean and orderly. Keeping
these areas clean will help to keep away
household pests and avoid sickness. Keep
all animals, dogs, cats, pigs, and chickens
out of this area. They can spread disease
germs.
14
Some people screen windows to keep out
mosquitoes and other insects. They use
metal screening, mosquito netting, or
other available material.
Scrub the table and chairs often.
A clean kitchen is a more pleasant place
to work. When your kitchen is clean, you
will be proud of it and the food you pre
pare in it.
Keep the Working Surface Clean
Dispose of Garbage
and Waste Water
After each meal is served, clean the work
surface or table with soap and water. If
water is scarce or expensive, cover the
work surface with clean paper or large
clean leaves.
Put all good scraps in a covered garbage
container. Do not let them fall on the floor.
They attract household pests and pets.
Be sure the leaves have not been sprayed
with insecticide. After you are through
preparing the meal, burn the paper or
leaves. Then the work surface will not
need to be cleaned each time.
Waste foods can be fed to animals, used
for fertilizer, burned or buried. When
garbage is used to feed pigs, boil it for
30 minutes. This keeps pigs healthy and
prevents spread of trichinosis from food
scraps. Be careful that there are no bones,
glass, or metal in garbage fed to pigs.
Wash the garbage container with soap and
water each time it is emptied.
Keep the Floor Clean
Sweep the floor after meals to pick up food
scraps that have fallen to the floor.
Sweep after food is prepared and served,
not while food is being prepared or served.
Dust rises in the air and will fall on the
food and on work tables. Dampen the broom
when sweeping to avoid scattering dust.
If the floor is made of washable material
such as wood or cement, or is covered with
linoleum, wash it with soap and water to
keep it clean.
Don't throw garbage in the yard. It at
tracts insects and animals.
You Coin use waste water on your garden.
Some homes have a sink with septic tank
and a cess pool for disposing of waste
water.
If you do not have a sink, dig a hole in the
yard and fill it with rocks. Empty the waste
water into this hole. The water will seep
through the rocks into the earth.
Use a separate container for trash. When
the container is full, burn or bury the
trash.
MAKE EATING A PLEASANT TIME
Almost everyone enjoys eating. To help
make eating time pleasant, serve food in
clean containers, in a clean, cheerfulplace.
If flies or other insects are a problem,
the serving dishes should be kept covered.
Remove the cover just long enough to serve
each member of the family.
In many countries, all members of a
family sit down together to eat. Each
person should have his own dishes and
utensils to eat with at a table.
Use serving forks, spoons, spatulas or
ladles to serve food to each member of
the family. Do not touch the prepared food
with your hands.
15
Sometimes there are not enough dishes and
utensils so all members of a family can
eat at one time. No one should eat out
of the same container or use utensils
that another person has used until they
have been washed. Washing helps to destroy
disease germs.
When setting the table-• keep your hands off the tines of forks,
the blades of knives, the bowls of
spoons
• do not touch the rims of glassware or
cups
• keep fingers off the inside of bowls and
plates.
If cloth or paper napkins are used, each
person should have his own. Paper napkins
should be burned after use. Cloth napkins
should be washed in very hot soapy water.
Rinse in clean water and, when possible,
hang in the sun to dry.
EQUIPMENT IS IMPORTANT
Good equipment helps you to:
• prepare and serve safe meals
• keep your home clean.
A piece of equipment needed in one country
may not be practical in another. The kind
and amount of equipment needed will de
pend on the jobs you do in your own kitchen.
When you have good equipment to store,
prepare and serve food, you are helping
to avoid the spread of harmful bacteria.
Storing foods in covered containers off
the floor or ground helps to protect them
from dirt, insects and rodents.
An iceless or mechanical refrigerator
helps to keep perishable foods such as
meat, fish, poultry, milk and eggs for a
longer time.
16
Containers for garbage and trash help to
keep your home clean.
Find out what equipment is available in the
markets. Buying commercial equipment
may cost less than making it.
If you do plan to make equipment, you
should find out if the materials you need
are available. You should figure the costs
to make the equipment before you start the
project. Your husband can help you make
the heavy pieces of equipment.
Do not have more equipment than you can
use.
EQUIPMENT FOR PREPARING FOOD
Your work area can be a table or a counter over a cup
board. Although food is sometimes prepared on aboard
on the floor or ground, a table or a counter is better
because dirt and dust cannot get into the food so
easily.
Use a hardwood board to cut or chop foods on.
Cover with a clean cloth to use for rolling out pastry.
A paddle, a long, flat board 4 or 5 inches wide and
tapered at one end, can be used for stirring large
containers of food and for removing foods from the
oven.
Vegetable brushes can be made of coconut shells and
other local materials.
You will need several containers of wood, pottery,
metal, or enamel to prepare and mix foods, and
several to wash and peel fruits and vegetables into.
Gourds or calabashes may be used.
A rotary beater or wire whip is used to beat eggs
and mix powdered milk with water. A wire whip can
be made at home.
Funnels made of metal, wood, or plastic are used
to pour liquids into containers with small openings.
A sieve can be made by punching holes in a large
tin can. It can be made of metal or screening.
17
A bottle opener is a hook used to remove caps from
bottles. A can opener is made of metal with a sharp
cutting edge. There are many different types.
You may need several types and sizes of knives.
Keep the blades sharp. Store out of the reach of
children.
Ladles made of metal, wood, or gourds are used to
take foods such as rice, flour, sugar and beans out of
cans and to serve juicy foods.
Measuring cups made of aluminum, tin, glass or
gourds can be used to measure ingredients for cooking.
Measuring spoons, usually made of metal, wood, or
plastic, are to measure salt, pepper, spices, sugar
and flavoring.
A mortar is a heavy vessel to put grain in. A pestle
is used to crush grain in the vessel. It is impor
tant to keep them clean. Wash them after each use and
set in the sun to dry.
A grater can be made from one long side of a can by
punching holes of different sizes on the can. Bind the
edges with small strips of wood. Use it to grate
cheese, vegetables and spices. It may also be used to
grate soap for dish washing or laundry. Keep it clean.
Store it where children cannot reach it.
A hand-operated grinder can be used to grind foods
at home. They are available in many countries.
Grinding stone. Used in many countries for grinding
grains, peppers and other spices.
18
<s-
EQUIPMENT FOR COOKING
Many different types of stoves are made in countries
around the world. When the stove is inside your house,
try to have one with a chimney. This will keep the
smoke out and help to keep your home clean.
An oven can be made of oil drums, kerosene cans,
mud, clay or bricks. Many times the oven is separate
from the stove. If the oven is placed inside your house,
be sure it has a chimney.
A double boiler may be made from two cans, one
smaller than the other. It should have a cover. The
bottom can is filled with water and the smaller can
containing food is placed inside the can with water.
Cook sauces or other foods which need to be cooked
very-slowly in a double boiler.
Pots for cooking can be made of aluminum, cast iron
or clay. The number and size you need depends on the
amount and kinds of food you prepare. They should
have lids and handles. A lip makes pouring easier.
They should not be too heavy to lift when full.
Pans for baking may be made of tin, aluminum or
stainless steel. They are used for baking breads,
casseroles, meats, cakes, pies, and cookies.
Pot holders are used to handle hot pots, pans, spoons
and other hot utensils. You can make them by sewing
several thicknesses of cloth and binding the edges.
They should be about 6 inches square.
19
EQUIPMENT FOR SERVING
Food is placed on the table in large serving dishes.
From these, the food is taken to put on each, person s
own dish.
Cups or glasses are used to drink from. Each person
should have his own.
Knives, forks, spoons or chopsticks made of stain
less steel, aluminum, tin, silver or wood are used to
eat with. Each person served should have his own.
Tablecloths or place mats are made of closely woven
washable material. You can make them at home. They
are placed between the dishes and table to keep the
table clean.
Napkins may be made of cloth or paper. They are
placed on your lap to protect your clothing while you
are eating, you can also wipe your hands or face on
them.
A table can be made at home. It should be made of
material that is easy to clean.
Stools or chairs can be made at home. Place them
around the table to sit on when eating.
EQUIPMENT AND SUPPLIES FOR CLEANING UP
Dish pans are used for washing and rinsing dishes,
glassware, silverware, and cooking utensils.
A brush, dishmop, or cloth is used for washing
dishes, pots and pans, etc. They may be made of local
materials.
Tongs made of metal or wood can also be used to
lift dishes out of hot rinse water.
Dish baskets made of wire mesh or woven fibers
are used to dip dishes into boiling hot rinse water.
A
w
Put dishes on a shallow drain pan made of metal or
plastic when they are lifted from boiling hot rinse
water.
Dish towels can be used to dry dishes, pots and pans.
They can be made at home. But it is more sanitary
to air dry dishes.
A dish drying rack can be made of wood, bamboo,
metal or plastic.
Wash pans are used to wash hands often when pre
paring foods. Towels for drying hands are made of
closely woven cloth or paper.
Use a towel drying rack or line to air towels well and
raise them from the ground. This keeps them out of the
reach of children.
-■J
A broom may be bought or made of tough grass or
palm leaves tied firmly to a wooden or bamboo pole.
A dust pan may be made of an oblong tin can and a long
stick. Use it to collect dust and any waste food or
trash that has fallen on the floor.
You need cleaning cloths for washing work areas.
Keep a separate one to clean the stove.
A scrub pail can be used to hold water and soap for
washing the floor or large equipment. An oil can with
the top cut off maybe used.
21
A soap dish is used to save bar soap. It needs to be
dried from time to time.
Trash can. May be made of metal, wood, or card
board. It needs a tight fitting cover. Used to collect
paper, tin cans, and other trash.
A garbage can may be made from a large tin can, such
as a kerosene can. It should have a tight fitting cover
and be waterproof. Handles on each side and the cover
make it easier to use. It is used to collect food wastes
such as peelings, scraps, and bones.
r
STORAGE EQUIPMENT
Cupboards can be hung on the wall or stood on the
floor. They are made of wood, packing cases, bamboo,
or other local materials. Storing food, dishes and eat
ing utensils in a cupboard saves space. It also pro
tects them from dust and animals. A cupboard placed
above the washing up area will save time and effort
in carrying clean utensils.
Containers of metal, pottery, glass, or coconut shells
are used to store dry foods such as sugar, salt, flour,
or spices. They should have tight fitting covers to
keep out insects, rodents and dirt. Containers for
storing safe water may be made of pottery, metal or
wood.
Knife holder will store knives safely out of reach of
children. A drawer is better because it keeps knives
clean as well as safe.
Storage shelves are used to store small covered
containers holding food. Shelves should be attached to
a strong wall.
Hooks made of bamboo, wood pegs, a nail or wire are
used to hang equipment on. They are useful in a small
space because they keep the kitchen tidy.
22
F
"MaSfa Cnn " for VA adminktArtion k GniMTMasu: Cut) ” Im VA admiiiiilarliou L Chjiltv
Subject: "Magic Cup " for VA administartion is Guilty
Date: Sat, 24 Nov 2001 07:33:40 +0000
From: "umesh kapil" <kapilumesh@hotmail.coin>
To: nfi@bol.net,in
Dera Sir
I hope you find this information useful
kapil
USE OF NEV? CONTRAPTION IN THE YA DISTRIBUTION
No one owns up, all blame cups and spoons
In Assam, paramedics contradict each other on how they gave Vitamin A to
village kids
SAMUDRA GUPTA KASHYAF
•
The commonly held theory is that the children fell ill from an overdose of
Vitamin A, apparently because medical staff were using cups for the first
time, instead of the usual spoons, to dole it out.
His boss Dr Ashok Kumar Choudhury, sub-divisional medical officer and in
charge of the Bihdiya phc, echoed Basumatary, adding ruefully that despite
this ''care taken by us for fear of overdose'', seven children were
diagnosed with complaints of vomiting and loose motions. One of those who
attended the training session and administered the dose was Sanika Begum, a
fourth grade female attendant (FA, in official parlance). Sanika, who's been
with the health department for over 20 years, said
"she'd been shown neither medicine nor cup the hour-long session, held three
days before the actual programme. She and the 25 others were just told, in
theory, how to go about the dosage."
Get your FREE download of MSN Explorer at http;//explorer.msn.com/intl.asp
l-'vvd: Vit A related deaths in Assam...dia from the BMJ: (http://bmj.com)
Subject: Fwd: Vit A related deaths in Assam , India from the BMJ: (http://bmi.com)
Date: Fri. 23 Nov 2001 11:11:02 +0000
From: "umesh kapil" <kapilumesh@hotmail.com >
To: secy.wcd@sb.nic. in
Dr.R.V. V. Ayyar
Secretary
Government of India
Department of Women and Child Development
Ministry of Human Rsource Development
Shastri Bhawan
New Delhi
Respected Sir,
Here is an update for you on deaths in assam related with Vitamin a
administration from "The British Medical Journnal " one of the most
reputed medical journal in the world
with regards
Dr Umesh Kapil
Additional Professor Public Health Nutrition
Department of Human Nutrition
All India Institute of Medical Sciences,
New Delhi 110 029,
INDIA
Phone O: +91-11-6593383, R: 6195105,6185105
Fax: +91-11-6862663
email.kapilumesh@hotmail.com
>From: "umeshkapil" <kapilumesh@hotmail .com>
>To: < kapi1umesh@hotmai1.com>
>Subject: Vit A related deaths in Assam , India from the BMJ:
> (http: //bmi . com)
>Date: Thu, 22 Nov 2001 22:52:03 -0800
umeshkapil (kapilumesh@hotmail.com) has sent this article to you from BMJ:
>
>Deaths trigger fresh controversy over vitamin A programme in India
>http://www.bmj . com: 80/ccri/content/full/323/7323/1206?eaf
Get your FREE download of MSN Explorer at http://explorer.msn.com/intl.asp
UN vitaiBifl A eamf-aign in Maunfer fire iLaneet,VeL 3S8, No.929S, 24 Novembe
Subject'. UN vitamin A campaign in India under Tire :Lancet, Vol. 358, No.9295,24 Novembe
Dale: Tue, 27 Nov 2001 04:41:44 +0000
From: "umesh kapil" <kapikune-f5h@Jiotniail.com>
To: 8yyar@hub.nic. in
CC: kapikimesh@hotmail.com
Subject:
UN vitamin A campaign in India under fire
Lancet, Vol. 3SS, No.9295, 2d November, 2001.
Author: Marcie_Francis@americanchemistry.com
Dates
11/26/01 7:00 Aid
UN vitamin A campaign in India under
fire
Indian public-health experts have criticised a UNICEF campaign to
treatchildren with vitamin A deficiency after 15 infanta died in Assam
allegedly after an overdose ofvitamin A administered during a state-wide
campaign on Nov 11. According to the Assam state government 700 children of
3-2 million who were given the vitamin
A dose, are ill. The federal and
state governments and UNICEF are investigating the deaths.
"The figures
being reported are all overestimates. He will first share our findings with
the government", said Pat Engle, a UNICEF official. Umesh Kapil (Human
Nutrition Unit, All India Institute of Medical Sciences, New
Delhi)questioned the need for the campaign. "Surveys conducted by Indian
Council of Medical Research
in 1999 in Dibrugarh and Nagaon districts of
Assam revealed that only 0'3$ of children were
suffering from Bitot's
spots, a marker of vitamin A deficiency", he said. The "campaign approach
is wholly uncalled for . . . Mild forms of vitamin Adeficiency are seen in
highly deprived pockets and this does not justify a programme of
universaldistribution of
vitamin A supplements", said C Gopalan, Director
General, Nutrition Foundationof India, who pioneered vitamin A prophylaxis
in India in the 1970s.However Kapil noted that since 1970 government trained
health workers used spoons with a 2ml marking for administering vitamin A
doses. "In Assam, a 5 ml cup was provided,instead of a
spoon. Health
workers were possibly not properly trained . . . and overdose of vitamin A
occurred", said Kapil.
Assam's health minister, Bhumidhar Barman, has warned UNICEF that legal
actionwill be taken if tests show the syrup was contaminated. It has also
been suggested that the syrup may have been
out of date. However UNICEF
has said that the syrup has an expiry date of March, 2003, and
passed independent quality control checks in India.
^hDinesh C Sharma
Get your FREE download of MSN Explorer at http://explorer.msn.com/intl.asp
1 of 1
11/27/01 2:46 PM
Experts wonder whether all children need Vitamin A
Subject: Experts wonder whether all children need Vitamin A
Date: Mon, 19 Nov 2001 14:03:13 +0000
From: "umesh kapil" <kapilumesh@hotmail.com>
To: secy.wcd@sb.nic.in
Guwahati, Monday, November 19, 2001
Experts wonder whether all children need Vitamin A
NEW DELHI, Nov 18 - Even as authorities try to find out what went wrong
causing the death of some children after Vitamin A administration in Assam,
questions are being raised whether all children need to be administered
vitamin A doses, reports PTI. Experts agree that overdose of vitamin A
cannot be fatal although it can cause some problems like diarrhoea and
vomitting. UNICEF, the agency involved in the State programme, said it had
sent a team to Assam which would re-examine the quality of Vitamin A used.
"We have sent an expert to the State to know the factual position regarding
this incident. The postmortem report is also awaited and by Monday all
reports are likely to be available", A R Nanda, Secretary Family~Welfare,
told PTI. It was not_ a Centre-sponsored programme but a State government
programme in collaboration with UNICEF. The administration was done in
"campaign mode" in which effort is'made to administer a particular drug of
vaccine to all the children of a specific age group, he said, clarifying
that the Centre was not against the campaign mode with regard to Vitamin A
administration, Nanda said, "we favoured combining of this programme with
immunisation programme".
Guidelines on administering Vitamin A as micronutrient which have been
circulated to the States say that it can be given along with measles vaccine
and should be repeated after six months. The guidelines also prescribes the
age of children and the appropriate dose. Dr Umesh Kapil from AIIMS
Gastroenterology and Human Nutrition Department, who was among gxperts who
framed guidelines last September on Vitamin A administration, came out
heavily against the international agency involved saying Government of India
guidelines should be followed in national programmes. "These agencies are
going to the States, which can make modifications in Government of India
guidelines according to their needs, and convincing them.for switching over'
to campaign mode", Kapil said. In India, campaign mode was not needed' forVitamin A administration which should be given as part of routine health
care programmes, he said.
j
|
Kapil said campaign mode was needed only in areas which had large number of
cases of illness associated with Vitamin A deficiency. But there is no such
epidemic in the country. Comparing Vitamin A administration with polio
programme, being followed in campaign mode, Kapil said polio was a
communicable disease and if 90 per cent children are immunised against it.
it would lead to development of herd immunity. Vitamin A-related problems
JjEwUt-were non-communicable and all children did not require vitamin A
j
supplementation, he said. For example, Kapil said, a child having half a
.—
rCLX kilogram of milk every day did not need additional Vitamin A. Even an ICMR
/ i'b
study in the country's 18 districts, including two from Assam - DibrugarK”
1
- r
Snd Nagaon - did not find Vitamin A deficiency as a public health_problem,
'
Kapil said. But UNICEF insisted that all children in India needed Vitamin A
supplementation. Covering all the children by combining vitamin A doses with ■
immunisation programme was difficult.
'
>
According to the data available, only 17 per cent children in India have
received any Vitamin A dosage during past six months, it said. The agency,
however, admitted that Indian government had requested it not to combine
Vitamin administration with campaign. On the quality of Vitamin A used,
UNICEF's chief of Child Development and Nutrition in India, Pat Engle said
the agency uses locally produced Vitamin A doses which were tested
beforehand. "Our'team is right now in field and samples would be tested
again. We do not need risk contamination" Engle said, adding there was a
"fierce response" to the incident. There was always a small risk with
vitamin A administration but it was shortlived, she said, adding one per
.1 of 2
11/20/01 937
Experts wonder whether aD children need Vitamin A
cent children globally show symptoms like vomitting and diarrhoea, while
about 3.2 millipn_children were scheduled to be administered vitamin A in
the campaign, only 720 were hospitalised which comes to even less than point
25 per cent, she said, so far death/has not been reported by an overdose of
vitamin A, Engle said. Kapil also agreed saying reactions can occur in
children who already have some health problems and are severely
malnourished.
However, Kapil cautioned that there might be some "commercial interests" in
pursuing Vitamin A programme in campaign mode as there was only one company
in the world which was producing Vitamin A. The best method was to supply
Vitamin A through other sources like green leafy vegetables, Kapil said.
But, UNICEF said studies in India indicated that only 50 per cent of Vitamin
A need was met through fruits and vegetables. While in developed countries,
vitamin A needs are met through foods which are fortified with this vitamin,
in countries like India there was hardly any food fortification. Besides,
the poor would not be able to afford such food items, Engle said. Speaking
against fortification of food products with Vitamin A, Kapil said what was
true for developed world might riot be suitable to India. The country had to
set priorities as to whether it would provide Vitamin A which costs about Rs
four, cost of administration included, or other essential drugs like that
for'Malaria, which causes many deaths in the country, he said. Meanwhile,
Government now plans to reiterated earlier guidelines on Vitamin A
administration and would advise States to be cautious in the administration
of the vitamin.
Get your free download of MSN Explorer at http://explorer.msn.com/intl.asp
2of2
11/20/01 9:37
I HEALTH
Blaming the dispenser
The Assam Human Rights Commission indicts the State government
for the vitamin A-related deaths of 23 children in November.
R. RAMACHANDRAN
HE
Assam
Human
Rights
Commission (AHRC) has held the
Government of Assam responsible for the
vitamin A related (deaths of 23 children
T
after a “high dose vitamin A supplementa
tion” campaign in th-. v ,'.u in November
last. In its inquiry r
■■ submitted to t’z
StateChiei Secret.'r,'n.
n
// iisai.l
Wcurred owing m lap.':: c
■ m <•■'
“agencies or instnuremt.in.'.
pubii.
functionaries” of the govern mem, whether
the children died “due to vitamin ' poisoning or toxicity or allergy or coincident
with the administration of vitamin A
The mass administration campaign in
the “pulse mode” approach, conducted to
combat vitamin A deficiency (VAD) with
the assistance and support of the United
Nations Children’s Fund (UNICEF), tar
geted 3.17 million children in the one to
five age group. The high dose supplemen
tation involved administering 2 ml (0.2
million International Units, or 60 mg) on
a single day on November 11 and covered
2.8 million children. This resulted in 23
deaths and several hundred children suf
fered adverse toxicity effects {Frontline,
December 21, 2001). Unlike two earlier
rounds in Assam, which were linked to
According to AHRC Chairman justice
R.K. Manisana Singh, the Commission
undertook a suo mom inquiry into the
episode which, in its view, amounted to a
primafacie case of human rights violation.
However, .ir.v its jurisdiction was gov
erned by the Human Rights Act of 1993,
v.:::
; ef human rights violat:»-> i • .. p
■ .-.v’.... ai’d not a private
in :
'e?l.
r.-vri'...'
.my pending lit
ci':: or t,-'::-.
in any court of
i: .- .’.rnong
•irwitdfr.g -•...tries, the
C' -amission d:>i i'e
■ t‘~: authority to
the
ci NGO: like
UNICEF.
Twenty-two children died within a
week ol administration. One child died on
November 19. According to the report, 15
of these were in the one to three age group.
Significantly, two cases were outside the
target group - seven-month-old infant and
a five-and-a-half year old child. Under the
Central government recommended vita
min A intervention programme, the target
age group is nine months to three years.
The AHRC considered two questions.
One was whether the deaths were coinci
dent with the vitamin A administration,
andnotdueto vitamin A - a view expressed
by some experts, given the high under five
mortality rate (U5MR) in Assam. The sec
ond question was whether there was any
polio campaigns, the one conducted violation ofhuman rights by any public ser
orf November 11 was a stand-alone vita vant, and if so what steps should be taken
min A campaign as per the recommenda by the government.
tions of the National Consultation of
In order to substantiate the theory of
December 2000 that vitamin A supple coincidence, in his submission to the
mentation should not be linked to pulse Commission the Director of Health
polio campaigns.
Services ofAssam had providedastatement
Significantly, the report has refrained detailing the cases of 31 children who died
from blaming UNICEF. One of the sus in the first post-week of the campaign. Of
pected causes for the deaths was the uni these eight had not received vitamin A.
lateral switch by UNICEF to the use of a
However, having considered the caus
5 ml dispenser. The Government ofIndia’s es of death from a medico-legal perspec
stated norm is a 2 ml dose. The dispensing tive, the Commission has rejected this
health workers were reportedly not warned premise on the grounds that die signs and
of this or trained adequately. The Report, symptoms preceding the deaths of several
however, takes cognisance of the feet that children were attributable to vitamin A tox
a change in methods ofdispensing in some icity or allergy, and distinct from other
areas might have resulted in the adminis causes of common poisoning.
tration ofa higher dose and that some chil
Further, a forensic examination of the
dren may have suffered side effects due to viscera (stomach, kidney and liver) of two
the plastic cup measuring out a mega dose. cases (of two years and three years respec
FRONTLINE. FEBRUARY 15. 2002
tively) was positive for vitamin A poison
ing. The Commission has requested the
authority concerned to preserve the viscera
for future investigations. It also said that
the opinions of experts were too theoreti
cal and could not be accepted in the con
text of the case. Based on these
considerations, the report has argued that
there exists a strong prima facie case that
some of the children died owing to vitamin
A administration.
The Commission’s conclusion with
regard to the second question brings a bet
ter perspective to its conclusion with regard
to the first. It has pointed out that the pam
phlet (in Assamese) distributed to the
health workers as part of the training did
not contain any warning to the workers and
the parents or guardians of the children
about the possible side effects of high dose
vitamin A administration. Also, the train
ing did not give any consideration to the
health status of the child and the pamphlet
did not caution workers against giving vit
amin A to sick or ailing children. Nor did
it indicate whether vitamin A should be
administered to a child suffering from
chronic vitamin A toxicity, as even 2 ml
may be a mega dose in such a case. Vitamin
A may have precipitated the death of chil
dren already suffering from gastroenteritis,
viral fever and other childhood diseases, the
report has said.
It has pointed out that, significantly,
the leaflet also did not warn the workers
against exceeding the 2 ml limit while mea
suring out with a 5 ml cup. The supervi
sion provided, in the form of one doctor
for 10 booths, was also not sufficient to
ensure
safe
administration.
The
Commission has also drawn attention to
the report of the government analyst, the
State Drug Testing Laboratory, Assam, in
respect of the quality of vitamin A drawn
from Batch No. VSD 22, which indicated
“possible loss of potency on storage”.
Acknowledging the importance of the
vitaminAsupplementation programme, it
has made a set of recommendations for
future campaigns, which includes exami
nation of the quality of vitamin A, exclu
sion ofsick and ailing children, supervision
with one doctor per booth, warning against
exceeding the dosage of 2 ml and that the
dispenser should not have a capacity in
excess of 2 ml.
The Chief Secretary and the Commi
ssioner and Secretary of Health and Family
Welfare Department will have to respond
to the AHRC report, as well as state the
actions taken, within two months. ■
83
B SCIENCE AND TECHNOLOGY
Policy and perspective
A critique of the Science and Technology Policy-2001.
R. RAMACHANDRAN
OR die last three months, the draft of
a new science and technology (S&T)
policy document has been under discus
sion among the science administrators of
the country. Called the Science and
Technology Policy-2001 (STP—2001),
this draft of October 29, 2001, was pre
pared by a drafting committee set up by the
Ministry ofScienceandTechnology under
the chairmanship of Goverdhan Mehta,
Director of the Indian Institute ofScience
(IISc), Bangalore, and the then president
of the Indian National Science Academy
(INSA). The Mehta Committee has also
come out with a document oudining the
Action Plan and Implementation Strategy
framework along with the STP-2001.
However, the pertinent question is:
what necessitated the enunciation ofa new
policy? In terms ofpast policy enunciations
in S&T, what we have today is the expres
sion of a political commitment to science
in the form of the Scientific Policy
Resolution (SPR) of 1958 and the
Technology Policy Statement of 1983
(TPS-1983). The development ofS&T in
the country has been guided all these years
by these basic documents. In 1992-93,
Minister
for
S&T
Rangarajan
Kumaramangalam proposed a Technology
Policy. The Technology Policy Statement
of 1993 (TPS-1993) was “aimed at giving
a renewed sense of purpose to indigenous
technology for its accelerated development
and use in the context of the Industrial
Policy Statement of 1991 and keeping in
view the need to adhere to international
quality systems as well as preserve the envi
ronment.’’ Following the processes of eco
nomic reforms and industrial liberalisation
that were initiated during the same period,
it was a political initiative on the part ofthe
Minister, rather than an initiative from the
scientific community. The draft TPS1993, as a revision to TPS-1983, was cir
culated ■ among scientific institutions,
Central and State level scientific depart
ments, scienrocrats and technocrats and
the public for discussion. The draft was dis
cussed at various levels but the policy, for
reasons best known to the government, the
change of party in power certainly being
F
one, never saw the light of day.
Later,
the Scientific Advisory
Committee to the Cabinet (SACC), under
the chairmanship ofthe Principal Scientific
Adviser (PSA) to the government, A.P.J.
Abdul Kalam, resurrected the TPS-1993
document to give it a new shape in the light
of the ongoing process ofglobalisation and
the emerging ground realities that indige
nous technology development will have to
face in the wake of trade regimes under the
World Trade Organisation (WTO) sys
tem. The draft document prepared by the
SACC was submitted to Human Resource
Development Minister Murli Manohar
Joshi after it was discussed and approved
by the advisory committee comprising
eminent scientists and the empowered
committee comprising essentially secre
taries to the government that function
under the PSA.
The Minister called a discussion meet
ing to consider the SACC draft at the end
of which he, in his wisdom, decided to set
up yet another drafting committee under
the IISc director. (Informed observers say
that this provided evidence of the chasm
that had developed between the Minister
and Abdul Kalam, as a fallout ofwhich the
scientist is believed to have quit office.)
According to reliable sources, the
Mehta Committee includes scientists
whose views are close to the Bharatiya
Janata Party’s perspective on S&T devel
opment. In fact, one component ofthe new
draft, pertaining to integration of science
teaching with the “extensive knowledge
acquired over long civilisational experi
ence", is susceptible to the interpretation
that it legitimises subjects such as Vedic
Mathematics and Astrology. Although the
SACC draft was not made public, people
in the know said that the Mehta
Committee’s draft was somewhat different
from the SACC draft.
The draft has been pur up at the web
sites of various scientific departments and
the scientific academies in a bid to solicit
comments from the scientific community.
The comments are to be considered by the
new SACC headed by R. Chidambaram,
the new PSA. The original idea was to
evolve a final policy document to be
announced at the December 2001 session
of rhe Indian Science Congress in
Lucknow. Politically speaking, this was to
parallel the announcement of TPS-1983
by Prime Minister Indira Gandhi.
However, it appears that the process could
not be completed in time.
Besides the imperatives warranted by
the process ofglobalisation and the impact
of the WTO regime, the apparent aim of
the SACC was to integrate both the S&T
policy statements in a single document
instead ofthe earlier separate documents of
1958 and 1983. In fact, in the otherwise
excellendy phrased SPR, the importance
given to technology development was only
secondary. It said: “...technolog}’ can only
grow out of the study of science and its
applications." While the truth ofthe state
ment cannot be denied, the focus of
wording of the SPR was to foster and
ture science in the country. The sharp dis
tinction between science and technology is
no longer possible with the advances currendy in evidence, especially in the emerg
ing field of biotechnology where the rime
and space difference between discovery and
application has become extremely short.
Conversely, high technology is increasing
ly being used in the laboratory to do mod
em basic research. From such a perspective,
a single document may seem reasonable.
However, the way the SPR was word
ed did not imply that technolog}' develop
ment itself was not on the same footing as
science. In feet, following the clearing of
the SPR, the identification of the steps
involved in the implementation ofthe SPR
and the task ofworking out a plan ofaction
was taken up by the government, resulting
in three national level conferences (in 1958,
1963 and 1970) that brought togethei^^
entists, educationists and industrial:^
Moreover, a round-table conference of
young scientists was called by the Prime
Minister in 1967 to ger their perspectives
on critical issues.
The setting up of the National
Committee on Science and Technology
(NCSD in 1971, at the initiative of C.
Subramaniam, was an important step
towards systematic planning in the S&T
sector. In 1973, the NCST brought out a
policy document tided “An Approach to
Science and Technology Plan". It was a
classic document that addressed all the rel
evant i-sues concerning die demand and
supply components of S&T development
- forward, backward and horizontal or
■e:.t-sector.il linkages, fiscal issues and
t.n.littg patterns, industrial participation
.
investment in research and develop-
ns^
NuT-1Page 1 of 1
Community Health Cell
From:
To:
Subject:
"umesh kapii" <kapilurnesh@notmaii.com >
<kuber_routela@hotmail.com>
Saturday, April 26, 2003 2’51 Piv1
IDA-lndia.txt
Fwd: iron deficiency anemia-india
Dear colleague,
i am sending y ou a recent publication as an attachment entitled "Prevention and control of iron
deficiency anemia amongst young children". 1 hope you will find it informative and useful.
With personal regards
UmeAh. KawSL
(Dr Umesh Kapil)
Additional Professor Public Health Nutrition
Department of Human Nutrition
All India Institute of Medical Sciences,
New Delhi 110 029. INDIA tei No. (R) 91-11-26195105, (Off) 26593383
For All details of Past, Present and Future of IDD in India-Please Visit Web Site iddindia.20m.com
From' "umesh kapii"
To: kapilumesh@hotmail.com
Subject: Iron deficiency anemia-india
Date: Fri, 25 Apr 2003 07:10:43 +0000
Hot new gizmos. Check 'em out. Right now!
Dear colleague,
I am sending you a recent publication as an attachment entitled "Prevention and control of iron
deficiency anemia amongst young children". I hope you will find it informative and useful.
With personal regards
UmeAh(Dr Umesh Kapil)
Additional Professor Public Health Nutrition
Department of Human Nutrition
Ail India Institute of Medical Sciences,
New Delhi 110 029, INDIA (el No, (R) 91-11-26195105, (Off) 26593383
For All details of Past, Present and Future of IDD in India-Please Visit Web Site iddindia.20m.com
responsibilities of Anaganwadi Worker and Auxiliary Nurse Midwife, which
can be utilized for distribution of the IFA.. Various contact points like
measles immunization (9 months), DPT booster (16 months) and take home
distribution of IFA. Other village level developmental
functionaires/voluntary persons available in the community may also be
utilized for IFA supplementation, monitoring the compliance and side
effects and for counseling the mother about the benefits of IFA. An
umesh Kapil,
Professor,
Department of Human Nutrition,
All India Institute of Medical Sciences,
New Delhi, 110 029,
1. National family Health Survey—India (NFHS—II) 1998—99, International
Institute of Population Sciences. Measures International, Demographic
Health Survey, 2000.
2. Seshadri S, Hirode K, Naik P, Shah A, Gupta N. An effective
intervention to reduce the prevalence of anemia in children.
Indian J
Med Res, 1984, 80: 164-173.'
3. Indian Council of Medical Research. Studies on preschool children.
ICMR Tech Rep Ser No 26. National Institute or Nurition. Hyderabad,
1977.
4. Raman L, Pawashe AB, Vasanthi G, Parvati CH, Vasumathi N, Rawal A.
Plasma ferritin in the assessment of iron status on Indian infants.
Indian Pediatr 1990; 27: 705-713.
5. Gomber S, Kumar S, Rusia U, Gupta P, Agarwal KN, Sharma S. Prevalence
and etiology of nutritional anemias in early childhood in an urban slum.
Indian J Med Res 1998; 107: 269-273.
6. singla rn, Agarwal KN, Singh rm, Reddy hCG, Tripathi AM, Agarwal dk.
Deficiency anemia in pre-school children - Estimation of prevalence
based on response to hematinic supplementation. J Trop Pediatr 1982; 26:
deficiency anemia. In: Nutrition in Children, Developing Country
Concerns. Eds. Sachdev HPS and Choudhury P, NewDelhi, 1st edition 1994,
pp 492-524.
8.
Preventing iron defieincy in women and children technical consensus
on Key Issues. 7-9 October 1998, UNICEF, UNU, WHO, MT, Technical Group
International Nutrition Foundation, USA 1998.
9.
Zlotkin S. Current issues for the prevention and treatment of iron
deficiency anemia. Indian Pediatr 2002; 39: 125-128.
10.
Scrimashaw N. 1990. Functional Significance of Iron Deficiency. In:
Functional Significance of Iron Deficiency. Third Tuinual Nutrition
Workshop. Eds. Enwonwu, C, Meharry Medical College, Nashville, TN, USA,
1990, pp 1-14.
11.
Drapppr
Child development and Iron Dcfi-cicncy: Early Action is
Critical for Healthy Mental, Physical and Social Development. Oxford
Brief, I The Inter-national Nutritional Anemia Consultative Group.
Washington, D.C., USA, 1997.
AN INDIAN VIEW
PERSPECTIVE
POINT FROM
A
COMMUNITY
HEALTH
1. At the dawn of the new millennium, with all its new wealth, knowledge and technology base, it is critical
we take an honest and hard look at the hunger and food security situation of the poorest among us. They
continue to suffer and be marginalised even while government commitments are made in global UN
conferences that reaffirm their fundamental human rights and their access to adequate food.
We here offer an evidence-based synthetic situation analysis of India... which holds one fifth of the world's
population.
2. A 1996-97 survey (NIN, 1999) revealed the disturbing magnitude of the problem in comparison with
earlier surveys in tire country. Smaller studies and news reports reinforce the findins. 48% of
households had chronic energy deficiencies; in two decades, the proportion of well-nourished children
under 6 years increased only from 5.9% to 8.9%; stunting was at 57%; a decreasing trend in intake of
protein, energy, iron and calcium was also documented as was a lower consumption of cereals, millets and
pulses in all states plus inadequate consumption of milk, milk products, sugar, and green leafy vegetables:
the IMR in 10 states has stagnated or even worsened during the past 5 years; the proportion of low birth
weight babies continues to be a high 30%.
However the most significant finding was that nutrition and food security was being severely compromised
by the economic development policies being applied:
The proportion of landless households increased from 30-41% in ten years and there was a fragmentation
of the landholding size contributing to increased food insecurity; (prices of agricultural commodities were
crashing causing distress among poor farmers;) during the same 10 years, the average per capita income per
month increased by the equivalent of only approximately 50 pence at constant prices. Other sources report
that an increase in suicides, indebtedness, unemployment and migration is being seen; lack of money is
causing delayed marriages, mass marriages, pawning of household assets and overall impoverishment.
3.
In the state of Karnataka, where we live, hunger and hidden hunger remains widely prevalent, adversely
affecting children’s physical and intellectual development with the consequent negative impacts on
households/families. affected communities and the nation.
4.
This situation is symptomatic of deep societal disparities and compels us and tire international
community to address the root causes of poverty and hunger, namely social, economic and political
injustice.
Broader people-centred policies, access to markets, the lifting of agricultural subsidies in the North and
greater social security in the South, the removal of barriers to developing countries international trade, a
halt to the negative effects of globalization and trade liberalization are all needed to reverse the negative
social effects we are seeing, including adverse nutritional effects.
Public distribution systems which make essential food grains available to people are being forced to rise
prices and reduce coverage rather than helping to increase equity and act as genuine safety nets.
5.
Development strategies wich changed agricultural practices in India are
depleting the soil of micronutrients; this is passed on to foods. In the meantime pharmaceutical houses
aggressively market vitamins and minerals and influence government agencies to introduce them into
mass-based health programmes for women and children. Genetically modified crops and foods are being
quietly introduced as well.
6.
The role of the state is being eroded. Between 1990 and 2000, in Karnataka, expenditure on nutrition
interventions declined 4.3% a year (in real terms) adversely affecting nutrition support services. World
Bank Ioans are being taken for health and nutrition while structural adjustment and global trade agreements
increase economic vulnerability and food insecurity of a large majority.
7.
In this context, the Indian Peoples Health Charter adopted by a widely representative counttywide group
in a National Health Assembly in Calcutta in December 2000, expressed strong concerns and made
concrete demands regarding agriculture, trade, pricing and public health . The global Peoples Charter for
Health adopted by the Peoples Health Assembly in Dhaka in December 2000 also raised these concerns
(www.phamovement.org) and a worldwide movement is now being organised to systematically follow-up
on these issues.
8.
Given this reality -at the end of 2001 and five years after the WFS- we have more unanswered
questions than answers. Where exactly are we in relation to its 1996 Plan of Action? and Where do we see
economic and social rights taking central stage in the struggle against hunger and malnutrition? What is
being done to address the root causes of malnutrition and the ineffectiveness of nutrition programmes we
currently see being implemented? Can collective peoples rights (as much as individual human rights), as
well as the social accountability of the big players be more clearly put on the agenda? These seem to be
urgent agenda issues for a more assertive and better inter-connected civil society.
Drs.Thelma and Ravi Narayan. Community Health Cell. Bangalore, India, sochara@vsnl.com
NUT- I •
THE LANCET
Saturday 13 July 1991
y0] 338
No 8759
[original articles]
Efficacy of vitamin A in reducing preschool child
mortality in Nepal
Keith P. West, Jr R. P. Pokhrel Joanne Katz
Steven C. LeClerq Subarna K. Khatry
SharadaR. Shrestha Elizabeth K. Pradhan
James M. Tielsch M. R. Pandey Alfred Sommer
Community trials of the efficacy of vitamin A
"supplementation in reducing preschool childhood
mortality have produced conflicting results. To
resolve the question, a randomised, double-masked,
placebo-controlled community trial of 28 630
children aged 6-72 months was carried out in rural
Nepal, an area representative of the Gangetic flood
plain of South Asia. Randomisation was carried out
by
administrative
ward;
the
vitamin-Asupplemented children received 60 000 retinol
equivalents every 4 months and placebo-treated
children received identical capsules containing 300
retinol equivalents. After 12 months, the relative risk
of death in the vitamin-A-supplemented compared
with the control group was 0-70 (95% confidence
interval 0-56-0-88), equivalent to a 30% reduction in
mortality. The trial, which had been planned to last 2
years, was discontinued. The reduction in mortality
was present in both sexes (relative risk for boys 0-77;
for girls 0-65), at all ages (range of relative risks
0'83-0-50), and throughout the year (0-76-0-67).
The reduction in mortality risk was not affected by
acute nutritional status, as measured by arm
circumference. Thus, periodic vitamin A delivery in
<he community can greatly reduce child mortality in
developing countries.
'
Lancet 1991; 338: 67-71.
;
V itamin A deficiency is associated with an increased risk
n‘ childhood morbidity1-3 and mortality4 in developing
countries. Community trials of vitamin A supplementation
ln Indonesia5* and India7 reported annual reductions in
Preschool child mortality of 34% to 54%. However, another
Introduction
'
■
field trial in India failed to confirm a reduction in child
mortality with vitamin A;8 thus, concern was raised about
the potential impact of improved vitamin A nutrition on
child survival across different cultures.’-11
Asa follow-up to the original large-dose vitamin A trial in
Indonesia,3 a community trial in rural Nepal was
undertaken to assess the efficacy of vitamin A
supplementation every 4 months in reducing preschool
child mortality. Such supplementation is recommended by
the World Health Organisation for prevention of
xerophthalmia13 and may represent an achievable delivery
schedule for child survival.
Study population and methods
A randomised, double-masked, placebo-controlled vitamin A
supplementation trial was carried out from September, 1989, to
December, 1990, in the rural, plains (Terai) district of Sariahi. This
area was selected because it has endemic vitamin A deficiency,13 no
previous vitamin A supplementation programme, and ecological,
cultural, and demographic similarities to the Gangetic floodplain
communities of South Asia, with which it is continuous; the factor
enhances the general applicability of the findings.
29 local development units, each containing 9 administrative
wards, were selected for the trial. In 1988 the area had a population
of 144000 with about 28.000 children (19-0%) under 5 years of age
(Census Report of the District Public Health Office, Sariahi, Nepal,
ADDRESS: Dana Center for Preventive Ophthalmology, Wilmer
Eye Institute. The Johns Hopkins Schools of Medicine and
Public Health. Baltimore. Maryland. USA (K. P. West. Jr, DrPH, J.
Katz. MS, S. C. LeClerq. BS, E. K. Pradhan, BA J. M. Tielsch, PhD, Prof A
Sommer, Mb); National Society for the Prevention of Blindness
and World Health Organisation Prevention of Blindness
Programme, Kathmandu. Nepal (R. P. Pokhrel, PROS, S. K. Khatry. —•
FRCS, S. R. Shrestha. MPH); and the Ministry of Health of His
Majesty's Government. Kathmandu, Nepal (M. R. Pandey, FRCS).
Correspondence to Dr K. P. West Jr, Dana Center for Preventive
Ophthalmology, Wilmer Eye Institute 120, 600 North Wolfe Street
Baltimore. Maryland 21205. USA
THE LANCET
68
TABLE I—BASELINE CHARACTERISTICS OF STUDY CHILDREN
Nof%;
Sex
Male
Female
Age (mo)
6-11
12-23
24-35
36—47
48-60
Measles during previous 4 mo
*
Morbidity > 1 day during previous
week}
Diarrhoea
Dysentery
High fever
Persistent cough
Arm circumference (cm)
<11-5
11-5-12-4
12-5-13-4
*5
>13
Total:
Xerophthalmia^
Control
(n = 12 264)
Vitamin A
(n = 12 541)
6265 (511)
5999 (48-9)
6479 (517)
6062 (483)
1290 (10'S)
2806 (22'9)
2696 (22'0)
2624 (21-4)
2848 (232)
759 (62)
1356 (108)
2827 (22 5)
2827 (22 5)
2595 (20 7)
2936 (234)
639 (51)
1214 (11:0)
506 (46)
1882 (170)
1609 (14 5)
1244 (110)
508 (45)
1936 (17-1)
1720 (15-2)
420(38)
1032 (9-4)
2859 (261)
6652 (607)
10 963
66 (35)
380 (34)
1109 (99)
2836 (25 3)
6890 (61 4)
11215
52 (2-6)
•Data missing for 69 controls and 42 vitamin A children.
(about 90% of children).
tNot measured on 2627 (7 7%) children at baseline.
§Nightblindness. Bitot's spots, corneal xerosis, keratomalacia; assessed in a random
15% sample of 40 wards (n = 4274 children: 1871 control, 2024 vitamin A, 379 not
1989). Signed statements of consent were obtained from all 29
chairmen on behalf of their communities. Participation of wards,
households, and children in the jrialwas voluntary at all times. __
The ward served as the unit of trHmient “allocation. Local
development units were ordered by geographic:areas_and wardsby__
population size within each local development unit After a random
start, eac&of the 261 wards was systematically allocated to one of
four coded batches of supplements. Two codes contained a
standard 60 000 pg retinol equivalent (200 000IU) dose of vitamin
A and two served as control, containing 300 retinol equivalents
(1000 IU) of vitamin A (retinyl palmitate in arachis oil; Roche,
Basel, Switzerland). All supplements contained 40 IU vitamin E as
an antioxidant The supplements were given as single-dose gelatin
capsules of identical taste and appearance. Every 4 months two
capsules of each code, sampled from the study area, were analysed
for vitamin A potency by a local laboratory unaware of their code.
The mean retinol contents were 53 300 (SD 3513) and 246 (27)
retinol equivalents, which is equivalent to 89% and 82% potency
for the vitamin A (n = 19) and control (n=20) capsules,
respectively.
All households in a ward were visited by trained field staffevery 4
months for a year. At baseline, children of 60 months and younger
were enrolled; at follow-up visits only infants bom during the study
were later enrolled. Birth dates of children were determined by
means oflocal events and Nepali astrological calendars. At each visit
infants aged 6-11 months received half the contents of a capsule
(6 drops of oil)j equivalent to either 30 000 or 150 retinol
equivalents, respectively, and children of 12 months and older
received the whole contents of the capsule. After repeated
household visits when children were absent, capsules were left in the
home and the parents were asked to administer them. Families and
childen who moved within a ward were followed at each visit; those
who moved out of a ward (less than 2% per round) were declared
withdrawn at the next household visit. At each visit, a child’s
capsule receipt and vital status were recorded, left mid-upper arm
circumference was measured with an insertion tape,14 and 7-day
morbidity and4-month measles histories were taken. Children of 12
months and older with an arm circumference below 11-5 cm were
referred to local health posts. At the time of enrolment household
VOL 338: JULY 13,1991
TABLE II—HOUSEHOLD CHARACTERISTICS AT TIME OF ENTRY
_________ Noffl
Control
Vitamin A
Mother’s age (yr)
<20
20-29
>30
Total
Mother’s education (any)
History of 1 child death
Occupation of head of household
Labourer
Other
Total
Household owns radio
Preschool child/infant death in
previous year
860 (8-6)
5586 (55 9)
3540 (354)
9986
912 (91)
4177 (41'9)
873 (8 7)
5662 (561)
3551 (35-2)
10086
1018(101)
4200 (420)
5218 (580)
2250 (250)
1536 (170)
9004
1832 (203)
5288 (581)
2174 (239)
1636 (180)
9098
1942 (213)
355 (3'9)
374 (41)
and demographic indicators were assessed, including maternal
histories of previous child mortality by the Brass method.15
At baseline an ocular survey was carried out in a 15% random
sample of wards (n = 40). Children were examined for
xerophthalmia at a central site by an ophthalmologist (S. K. K.) or a
senior ophthalmic assistant. Chance-corrected inter-observer
agreement,16 based on 1001 independent replicates, was excellent
(x = 0-93). A history of night blindness (“ratandho/ratauni”) was
elicited from parents for children of 12 months and older. All
xerophthalmic and severely ill children were treated with vitamin A
and referred to local health posts for follow-up, as indicated. These
children are included in the analysis. Full details of this substudy
will be published elsewhere.
Child deaths were identified by means of the regular 4-monthly
census and by an independent-vital events surveillance-every-2
months in every ward. A “verbal autopsy” interview was carried
out, usually within 2 months of death, for all children who died.
Data were reviewed and probable causes of death were assigned
independently by two physicians. Differences in assignment were
discussed and a consensus cause of death assigned.
Capsule codes were broken and the four groups merged into
control and vitamin A treatment groups. Baseline differences were
tested by chi-square.17 All analyses were carried out on an
intention-to-treat basis. Computed mortality rates were based on
child-years of observation. Relative risks were derived with all
variance and 95% confidence interval estimates17 adjusted to
account for the design effect18—ie, the ward rather than individual.
serving as the unit of treatment allocation. Mortality rates and
TABLE III—INTERVAL-SPECIFIC AND ANNUAL MORTALITY OF
CHILDREN 6-72 MONTHS OF AGE
Time interval (x to x +4)
0-4 mo
4-8 mo
8-12 mo ' 0-12 mo
28 630
1807
2018
No entered at x
24 805
14 143
834
1045
Control
12 264
14 487
12 541
973
973
Vitamin A
Withdrawals
533
207
152
Control
174
569
214
Vitamin A
154
201
Child deaths
210
76
72
Control
62
152
53
48
Vitamin A
51
*
Child-years
12795
4505
4241
Control
4049
13 175
4633
Vitamin A
4147
4395
Mortality (per
1000 child-years)
164
16-9
170
Control
15-3
11-5
11 '4
Vitamin A
11-6
0-70
0-67
Relative risk
068
0-76
(95% CI)
(0-50—1 15) (0 45-100) (0-45-0-99) (0-56-0-88)
•Children who were withdrawn or who died during an interval were i
months of observation.
— 7
TABLE IV—ANNUAL MORTALITY OF CHILDREN AGED 6-72
MONTHS BY AGE AND SEX
Vitamin A
Control
—
ST
Male
Childyears Deaths
69
THE LANCET
VOL 338: JULY 13,1991
MR
Childyears Death
MR
6531
89
13 6
6821
72
10-6
Female
6263
121
19-3
6354
80
12-6
Age (mo)
Ml
1315
47
35-8
1393
39
280
12-23
2725
75
275
2790
53
190
24-35
2592
31
120
2724
27
9-9
36-47
2633
28
10-6
2657
18
6-8
48-59
2573
25
9-7
2649
13
4-9
60-72
956
4
4-2
964
2
21
Relative
risk
(95% Cl)
TABLE V—ANNUAL MORTALITY OF CHILDREN AGED 6-72
MONTHS BY NUTRITIONAL STATUS AND AGE
Control
circum
ference
(cm)
Childyears Deaths
Vitamin A
MR
Childyears Death
0-77
(0-55-109)
065
(0-48-089)
Children
aged 6-11
mo
<11-5
132
14
106-3
126
12
0-78
(0 49-1-25)
069
(0-47-1-01)
083
(0 47-1-50)
064
(0-33-1-24)
0-51
(0-24-107)
0-50
(008-3-29)
11-5-12-4
261
12
45-9
267
6
12-5-13-4
392
8
20-4
432
10
>13-5
346
6
17-3
387
6
179
5
MR = mortality rate (per 1000 child-years).
relative risks were calculated across strata ofage, sex, and nutritional
status. A Poisson regression model19 was fitted to estimate the effect
of vitamin A on mortality with simultaneous adjustment for each of
these factors.
The study protocol was approved by the Nepal Health Research
Council in Kathmandu, Nepal, and by the Joint Committee on
Clinical Investigation at the Johns Hopkins University School of
Medicine in Baltimore, USA.
MR
Relative
risk
(95% Cl)
94-9
0-89
(0-37-2-12)
225 _Q49_
(0-17-1-41)
23-1
113
(0-40-3-16)
15-5
0-89
0-25-3-11)
0-73
27-9
(0-20-2-62)
Unknown
184
7
38-0
Children
17-72 mo
<11-5
208
61
293-3
191
33
172-6
11-5-12-4
721
15
20-8
759
24
31-6
12-5-13-4
2132
30
12-9
2371
16
6-7
*5
>13
6986
35
50
7150
29
4-1
Unknown 1232
22
17-9
1310
11
8-4
0-59
(0-39-0-90)
1-52
(0-7’£3$8)
0-52
(0-27-1-00)
0-82
(0-48-1-41)
0-47
(0-21-1-03)
MR “mortality rate (per 1000 child-years).
The initial 24 805 children plus 3825 infants who entered
the 6-11 month age range at the first or second 4-monthly
visits (1879 controls, 1946 vitamin A) provided a total of
Results
28 630 children who contributed 25 970 child-years of
observation for this analysis (table III). There were 362
24 805 children aged 6-60 months entered the trial at
deaths during the 12 month period. The annual mortality
baseline (12 264 in the control group and 12 541 in the
vitamin A group), which represented more than 96% of all | rate was 16-4 per 1000 child-years in the control group and
I
11-5 per 1000 child-years in the vitamin A group, which
children of eligible age in the study area. The two groups of
children were very similar in their distributions of 1 givesaprotectiverelativeriskof0-70(95% CI 0-5<W)-88) for
a 30% reduction in child mortality. This CI and all others
demographic and clinical characteristics (table I). The
reflect a 23% increase in the estimated variance due to the
pooled prevalence of xerophthalmia in the random
design effect. The difference in risk increased from the first
subsample of wards was 3 0%.
to the second interval of dosing and then remained stable '
Treatment groups were also practically identical on more
than 25 characteristics assessed in all participating
during the third interval, which indicates a sustained effect.
households, including risk factors commonly associated
The effect of vitamin A was evident across sex and age
with preschool child mortality (table II). In both treatment
strata (table IV). There was a slightly greater reduction in
groups, at least one of the liveborn children of 42% of
mortality in girls than in boys. The excess female/male
mothers had died, and 4% of households reported at least
mortality ratio was somewhat smaller in the vitamin A than
one preschool child death during the previous year. During
in the control group (relative risk 1-19 vs 1-42). The.
the year before the trial in both treatment groups, the
protective effect of vitamin A was consistent at each age and,
estimated infant mortality rate was 82 per 1000 livebirths
except for children aged 24-35 months, became stronger
and the 1-4-year-old mortality rate was 12-13 per 1000
with age (table IV).
children per year. Thus, the two groups showed no
The effect of acute nutritional status on the impact of
differences in many risk factors for mortality and by
vitamin A during a subsequent 4-month interval was
reported past mortality at the outset and were taken to
examined separately in infants and older children (table V).
represent the same population.
‘
Although
arm circumference was measured at least once in
Capsule coverage remained high and equal in each group
97% of the children, only 89% were measured at each visit,
'hroughout the trial—about 88% of children in each group
thus reducing by 11 % the number of child-intervals for this
received the capsule contents from the staff at each visit.
analysis. In 8 of 10 age-status-specific strata, including the
Capsules were left in the home for about 10% of children at
most malnourished and the best nourished children,
each visit, of whom about 65% were estimated (by history
vitamin-A-supplemented children had lower mortality
On ^low-up of a subsample) to have received the capsule
(p<0 05 by Wilcoxon signed rank test). No trend in the”
contents from the parents. Thus, about 93% of all eligible
Y’ddren in each group received a supplement at each visit.
t least 74% of all enrolled children in each group were
own to receive their full quota of supplements; only 2%
1 ed to receive any supplement.———————
effect was observed with severity of wasting.
Multivariate analysis did not change the effect estimate.
The relative risk of death in the vitamin A group, after
simultaneous adjustment for the effects of sex, age, and
THE LANCET
70
nutritional status by Poisson regression, was 0-72 (95% CI
0-55-0-95).
Based on 358 completed verbal autopsy reports, vitamin
A seemed to reduce mortality ascribed to diarrhoea or
dysentery (relative risk 0-61), wasting malnutrition (0-65),
uncertain (infectious) causes (0-52), and measles (0-24).
These “probable causes” accounted for 28%, 20%, 19%,
and 4% of all deaths, respectively, in the combined groups.
There was no apparent effect on mortality due to acute lower
respiratory infection (1-29) or other miscellaneous causes
(101), which accounted for 18% and 11%, respectively, of
all deaths.
Discussion
Since the initial report from Indonesia on the
effectiveness of periodic,
large-dose vitamin A
supplementation in reducing child mortality,5 there have
been several attempts to clarify the effect of vitamin A on
child survival in different populations. Most trials have
reported a profound effect, but one trial did not show a
significant reduction in child mortality,8 for reasons which
remain unclear.
'
*
11
More frequent supplementation of children with vitamin
A may have a greater effect on child survival than less
frequent dosing—supply of about half of a preschool child’s
daily requirement by way of fortification reduced mortality
by 46% in Indonesia,6 and weekly vitamin A doses of 2500
retinol equivalents reduced mortality by 54% in south
India.7
The reduction in mortality was slightly greater in girls
than in boys, which accords with the south Indian study.7 As
in Indonesia,5 the effect of vitamin A in Nepal was stronger
with age, reaching a 50% reduction in mortality in the fifth
and sixth years of life. By contrast, the south Indian trial
found the greatest effect among infants 6-11 months of age.7
This variability may reflect differences in the age specificity
and severity of vitamin A deficiency and other determinants
.of child mortality in different populations. Given the wide
confidence intervals for all age-specific findings in all
studies, it may also be chance variation.
A very small arm circumference (less than 11-5 cm) at the
start of each interval was associated with a very high risk of
mortality (table v), despite referral of such children to local
health posts. However, acute nutritiona! status did not seem
to modify the protective effect of vitamin A. A consistent
effect of vitamin A across categories of wasting was also
observed in south India, although its effect was stronger in
stunted children.7
It is likely that vitamin A modifies the incidence,
duration, or severity of life-threatening infectious illness, as
seen with severe measles.20-21 The verbal autopsy suggested
that vitamin A had no effect on mortality attributed to acute
. lower respiratory infection. This finding is surprising,
because there is evidence that"vitamin A deficiency is linked
to increased risk of respiratory infection.22 However,the
40% reduction in deaths attributed to diarrhoea and
dysentery is consistent with evidence that closely links mild
xerophthalmia to risk of protracted diarrhoea.21"25 The
substantial reduction in mortality from measles (76%) is
consistent with vitamin A measles intervention trials20-21
from Africa and the weekly supplementation trial from
India.
This trial provides a firm estimate of the efficacy of
large-dose vitamin A prophylaxis in an endemically
vitamin-A-defident population. The large sample size, the
similarity of the treatment groups, the high coverage while
VOL 338: JULY 13,199|
minimising visits to avoid a “contact” effect,7 the checking
of capsule potency, and the high level of ascertainment help
to support the validity of the findings. A 30% reduction in
preschool child mortality predicts that, in Nepal alone
where 2% or more of preschool children are
xerophthalmic,26 more than 15 000 deaths could be^averted
each year by adequate nourishment of children with vitamin .
A. In south Asia 0
7-1 • 1 million child deaths could probably
*
be prevented annually by adequate vitamin A nourishment i
in the preschool years (J. Humphrey and colleagues,
unpublished).
Although periodic, large-dose delivery may lead to a more
modest reduction in child mortality than more frequent,
smaller doses, this approach is a feasible strategy for most
developing countries seeking to reduce child mortality with
vitamin A by means of immediately available and affordable
delivery systems.27
Periodic dosing should not preclude, or compete with,
efforts to improve the local food supply and dietary vitamin 4
A intake by vulnerable groups (eg, by means of gardens,
dietary counselling, and fortification). However, there may
be a compelling reason, in terms of child survival, to control i
vitamin A deficiency quickly through periodic
supplementation while longer-term solutions are pursued, j
This study was carried out under cooperative agreement no DAN I
0045-A-5094 between the Office of Nutrition, US Agency for International
Development (USAID), Washington, DC, and the Dana Center for '■
Preventive Ophthalmology (DCPO). It was a joint undertaking benven
DCPO and the National Society for the Prevention of Blindness,
Kathmandu, Nepal. The study was funded by USAID, with financial and
technical assistance from Task Force Sight and Life (Roche, Basel), the
United Nations Children’s Fund (UNICEF), Nepal, and NIH grant no
RRO4O6O.
The Sariahi Study Group (in addition to the authors) included Dr B. D.
Chataut, Dr R. Adhikari, Dr D. Calder, Dr J. Gmunder, Lai-Chu See, J.
Humphrey, J. Canner, L. Clement, N. N. Achariya, D. N. Mandal, T. RSakya, B. B. Shrestha. U. Khadka. R. K. Shrestha, M. D. Thapa, and S. R.
Ranjit. We thank Prof James Tonascia for helpful statistical advice and
oversight ofthe data safety and monitoring committee; the committee’s other
members, Dr F. Davidson, Dr M. R. Pandcy, Dr I. Tarwotjo, and Mr D._
Piet; and Y. Vaidya and K. B. Shrestha at the Central Food Research
Laboratory in Kathmandu for the analyses of vitamin A supplements.
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
■
W
Sommer A, Katz J, Tarwotjo I. Increased risk of respiratory disease and
diarrhoea in children with preexisting mild vitamin A deficiency. Am]
Clin Nutr 1984; 40:1090-95.
Milton RC, Reddy V, Naidu AN. Mild vitamin A deficiency and
childhood morbidity—an Indian experience. AmJ Clin Nutr 1987;4&
827-29.
Bloem MW, Wedel M, Egger RJ, ct al. Mild vitamin A deficiency and
risk of respiratory track diseases and diarrhea in preschool and school
children in Northeastern Thailand. AmJ Epidemiol 1990; 131:332-39Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in
children with mild vitamin A deficiency. Lancet 1983; ii: 585-88.
Sommer A, Tarwotjo I, Djunaedi E, ct al. Impact of vitamin A
supplementation on childhood mortality: a randomised controlled
community trial. Lancet 1986; i: 1169-73.
Muhilal, Permcisih D, Idjradinata YR, ct al. Vitamin A-fortified
monosodium glutamate and health, growth, and survival of children: a
controlled field trial. Am J Clin Nutr 1988; 48:1271-76.
Rahmathullah L, Underwood BA, Thulasiraj RD, ct al. Reduced ,
mortality among children in Southern India receiving a small wceHl
dose of vitamin A. N EnglJ Med 1990; 323:929-35.
Vijayaraghavan K, Radhalah G, Prakasam BS, et al. Effect of massM
dose vitamin A on morbidity and mortality in Indian children. Land1
1990; 336:1342-45.
Thumham DI. Vitamin A and childhood mortality. Lancet 1991; 337°
232.
Reddy V, Vijayaraghavan K. Vitamin A and childhood mortality. Lancd
1991; 337:232.
/
Sommer A, West KP Jr. Vitamin A and childhood mortality. La,tCil
1991; 337:925.
/
N UT-|.
Journal of Glaucoma
3:12-16. Raven Press. New York
C 1994 Raven Press. Ltd.
Automated Perimetry: A Study of the Glaucoma Hemifield
Test for the Detection, of Early Glaucomatous Visual
Field Loss
*'iRemo Susanna, Jr., m.d., tMarcelo Teixeira Nicolela, m.d.,
tDanilo Sone Soriano, m.d., and +Celso Antonio De Carvalho, m.d.
*Department of Ophthalmology. Albert Einstein Israelite Hospital, and ^Ophthalmology Department, Faculty of
Medicine, University of Sdo Paulo IFMUSP), Sdo Paulo, Brazil
Summary: In order to verify the ability of the Glaucoma Hemifield Test in
detecting early glaucomatous alterations, as well as its sensitivity, specificity,
and reproducibility, 78 glaucoma patients, glaucoma suspects, and normals
were selected. In those eyes who presented alterations of the optic disc sug
gestive of glaucomatous damage, but with no typical lesions in the visual field,
the test was positive in 18.4% of the cases. The sensitivity, specificity, and
reproducibility of the test were 100, 100. and 83.3%, respectively. Key Words:
Automated perimetry—Optic disc—Glaucoma Hemifield Test.
One of the major objectives of perimetry in glau
coma is to detect any possible evidence of lesion at
the earliest possible stage in order to prevent its
progression by using the appropriate therapeutic
treatment. In this sense, the automated perimetry
has been helpful, allowing the detection of visual
field defects at an earlier stage than manual perim
etry (1-5).
Numerous strategies have been developed in
computerized perimetry with the objective of in
crease its sensitivity in the detection of early glau
comatous alterations (6-9). In 1985, Duggan et al.
(10) proposed a test in which the visual sensitivity
thresholds were compared across the horizontal
field meridian. Preliminary studies (10) have shown
that the specificity and sensitivity of the detection
of early glaucomatous lesion by this method
reached 94% and 92%, respectively, based on Gold-
mann perimetry. Such a fact is based on the obser
vation. originally described by Hart and Becker (II)
and confirmed by Mikelberg and Drance (12) and by
Drance et al. (13) that the loss in the visual field in
glaucoma occurs asymmetrically along the horizon
tal meridian.
Later, in 1989 (14), a similar test is incorporated
to the Humphrey Field Analyzer (STATPAC 2)
with the name Glaucoma Hemifield Test (GHT),
which provides an analysis based on difference of
probability scores across the horizontal field merid
ian and also detects alterations if the two corre
sponding clusters have a total depression of sensi
tivity (Fig. 1).
The present study was done in order to verify
how early the GHT detects glaucomatous alter
ations and also its specificity, sensitivity, and re
producibility.
Received Julv 13. 1992. Revised August 11. 1992. Accepted
July 7. 1993.
Address correspondence and reprint requests to Dr. R.
Susanna Jr. at Av. Sao Gualter 99. Alto de Pinheiros. Sao PauloSP. CEP 05455. Brazil.
A total of 160 patients who have done at least
three perimeiric.examinations with_tbe Humphrey's
C30-2 automated perimetry program were studied.
.
12
PATIENTS AND METHODS
13
A UTO.MA TED PERIMETR Y
sual field defect. 1C: Those with CD of 3=0.7 asso
ciated with an IOP of >22 mm Hg.
Group 2. Consisting of those eyes with a typical
visual field defect, characterized by a nasal step
and/or a paracentral or arcuated scotomas, consist
ing in two or more adjacent points shown in the
probability graph (p < 0.05) of pattern deviation.
and reproducible in at least two perimetries.
Group 3. Consisting of those eyes in which there
isn’t the clinical impression of glaucomatous dam
age of the optic nerve head, which was defined by a
C/D of <0.4 and contralateral asymmetry of <0.1
and no typical visual field defect.
The last two visual field examinations of each
patient were considered for the study of reproduc
ibility of the GHT. Only the last visual field of each
patient was considered for the studies of sensitivity
and specificity, and also to study how early the
GHT is able to detect glaucomatous alterations.
FIG. 1. A scheme of the Glaucoma Hemifield Test, with the
five superior clusters of points which are compared with their
mirror image clusters in the inferior meridian. (From ref. 14.
with permission.)
In each case, maximum—intraocular- pressure .
(IOP) presented during the follow-up period was
noted) The vertical cup to disc ratio (C/D) was analyzed from stereoscopic photographs of the optic
disc by two experimental observers who didn’t
know other data from the patients.
The eyes were classified into three groups, the
first being further subdivided into three. Eyes that
could not be classified in these three groups were
excluded. Only patients who had the same size of
optic disc were considered. When two eyes of the
same patient matched the criteria to be included in
this study, we selected only one eye randomly.
Also, patients with retinal or optic nerve disease
besides glaucoma were excluded. No patients were
under pilocarpine or other miotic medication. Only
visual field tests performed with pupil diameter of
>3 mm were considered.
The following groups were defined:
Group 1. Consisting of those eyes in which there
is a clinical impression of glaucomatous damage of
the optic nerve.head without, however, exhibiting
typical glaucoma periiaetric-dfifectsUas defined in
group 2). 1A: Those which presented C/D of >0.5,
showing an asymmetry with the contralateral eye of
>0.2 and IOP of >22 mm Hg. IB: Primary open
angle glaucoma patients with one eye with CD of
>0.5 independently of the IOP levels in which the
contralateral eye showed typical glaucomatous vi
RESULTS
Seventy-eight patients matched the criteria estab
lished above. They were 39 males and 39 females.
The interval between the last two visual field exam
inations of each patient ranged from three to 26
months (average of 10.4 ±5.9 months).
Group 1 consisted of 38 eyes from 38 patients.
nine eyes belong to subgroup 1A. 20 eyes to IB, and
nine eyes to 1C. Thirty-seven patients had visual
acuity of 3=20/30. and only one patient had visual
acuity of 20/40. From a total of 38 eyes, the GHT
was positive in seven eyes (18.4%; confidence lim
its from 12.4 to 24.4%"). Table 1 shows the data
from group 1.
Group 2 consisted of 23 eyes belonging to 23 pa
tients. The visual acuity of these patients ranged
from 20/20 to 20/100, and 17 patients had visual acu
ity of >20/30 (73.9%). The GHT was positive in all
eyes from this group.
Group 3 included 17 eyes from 17 patients with
out clinical evidences of optic nerve damage and no
typical visual field defect. The GHT was negative in
all eyes of this group. The visual acuity of all pa
tients was equal to or better than 20/25. Table 2
shows the data from groups 2 and 3.
Table 3 shows the distribution of visual acuity in
the three groups. There wasn't a statistical differ
ence between the visual acuity of patients from
" For a coefficient of 95%.
J Glaucoma, Vol. 3, No. I. 1994
14
R. SUSANNA, JR. ET AL.
TABLE 1. Data from group 1
Subgroup A
Subgroup B
Subgroup C
Total
GHT
/
Sex
No.
patients
M
F
9
20
9
38
5
14
5
24
4
14
Age
(mean ± PD)
50.7 ±10.1
56.3 ± 13.6
52.8 ± 16.3
54.2 ± 13.8
N '
1 1
% pos.
11.1
4 1
2
7 :
20.0
22:2
18.4
CL (%)
1.2-21
11.5-28.5
8.4-36
12.4-24.4
M. male: F, female; PD, pattern deviation; N, number of positives GHT; % pos.,
percentage of positive GHT; CL. confidence limits, for a coefficient of 95%.
groups 1 and 3, but the visual acuity of both was
statistically different from patients of group 2 (p <
0.0001, x2 test).
There was a high statistical difference between
the groups 1 and 3 in respect to the positivity of the
GHT (p = 0.0055, Student’s t test).
The results of the GHT obtained in the two visual
field tests were the same in 65 eyes of the 78 eyes
studied (83.3%). From the 33 eyes in which the first
GHT was positive, 25 remained positive in the sec
ond test (75.8%). From the 45 eyes in which the first
GHT was negative, 40 eyes remained negative in
the second test (88.9%).
The average interval of time between the two
GHT of each patient in the group in which they
were reproducibles and in the group in which they
were not were 10.71 ± 6.02 and 8.69 ± 5.40 months,
respectively. This difference was not statistically
significant (p = 0.13, Student’s t test).
DISCUSSION
Perimetric study is essential for the early diagno
sis of glaucomatous lesion as well as in the evalua
tion of its progression. However, some authors sug
gest that the visual field damage appears only when
a significant number of nerve fibers was lost (1518). In this sense, the automated perimetry offers a
great help, because it can detect the damage at an
earlier stage than the manual perimetry (1-5). Fur
thermore, several analytic strategies have been de
veloped with this objective (6-10).
One of these methods, the GHT, is based on the
observation that the damage on the visual field oc
curs asymmetrically along the horizontal meridian
(11-13). In this test, clusters of points located su
periorly are compared with their mirror image be
low the horizontal meridian. The comparisons are
based on the pattern deviation probability map. A
visual field is considered “outside normal limits”
when the difference between any mirror image is
larger than is found in 1% of the normal population,
or when the total depression in any two correspond
ing clusters is greater than is found in 0.5% of the
normal population. A visual field is considered
“borderline” when the difference or the total de
pression of any mirror image clusters is greater than
is found in 3% of the normal population. The result
“generalized reduction of sensitivity" is when the
sensitivity of the most normal region of the field is
lesser than is found in 0.5% of the normal popula
tion. Another possible result is “abnormal high sen
sitivity,” which is when the sensitivity of the field is
higher than is found in 0.5% of the population. In
this study, the results “outside normal limits” and
“generalized reduction of sensitivity” were consid
ered a positive test.
To study how early this test would detect incipi
ent perimetric alterations in glaucoma, we selected
eyes in which there was a clinical impression of
glaucomatous damage of the optic disc without any
typical alterations in the visual field.
TABLE 3. Visual acuity from patients
Group 1
TABLE 2. Data from groups 2 and 3
Group 2
Group 3
Sex
GHT
No.
patients
M
F
Age
(mean ± PD)
N
% pos.
23
17
8
7
15
10
66.1 ± 12.2
50.5 * 12.6
23
0
100.0
0
M, male: F. female; PD. pattern deviation; N. number of positives
GHT: % pos.. percentage of positive GHT.
J Glaucoma. Vol. 3, No. /. 1994
20/20
20/25
20/30
20/40
20/60
20/100
Group 2
Group 3
No.
(%)
No.
(%)
No.
(%)
29
5
3
1
. (76.3)
(13.16)
(7.9)
(2.6)
—
8
7
2
4
1
1
(34.8)
(30.4)
(8.7)
(17.4)
(4.3)
(4.3)
15
2
(88.2)
(11.8)
—
No., number of eyes; %, percentage of eyes.
—.
__
_ _
—
AUTOMATED PERIMETRY
In the general population, few eyes with a CD
>0.5 and a contralateral asymmetry bigger than 0.2
are encountered. Weisman et al. (19) verified that a
vertical asymmetry >0.2 occurs in only 4% of the
population. When associated with a CD >0.5, it
occurs in 31% of glaucomatous eyes and in only
0.7% of eyes without this condition. Shin et al. (20)
showed that 32% of patients with a high IOP and a
CD >0.5 developed perimetric alterations. Wilensky (21), studying a group with an IOP of >25 mm
Hg, observed the appearance of visual field loss in
27.3% of cases in a 6-year follow-up.
It is also known that the percentage of perimetric
alterations encountered in eyes whose contralateral
eye already has glaucomatous lesion is significantly
greater than in other patients (22), principally when
associated with a CD bigger than 0.5 (23).
Another group of patients suspected of present
ing alterations in the optic disc due to glaucoma are
those which show a cup disc >0.7. Cup discs of
such magnitude occur in only 1-2% of the popula
tion (24,25) and, when associated with high IOP,
have an even greater possibility of being patho
logical. There is the possibility that these eyes
have a large congenital scleral rim or even a con
genital asymmetry, which may cause a false impres
sion of a pathological cup disc (26). However, the
association with high IOP suggests glaucomatous
damage.
Thus, it is likely that certain number of eyes
which we selected for Group 1 present anatomic
lesions of the optic nerve disc due to glaucoma,
without presenting characteristics perimetric alter
ations detectable by the GHT.
In this group, the GHT was positive in 18.4% of
the cases. When we study the three subgroups iso
lated, we notice that in the subgroup A the GHT
was positive in 11.1% of the eyes, in the subgroup B
in 20.0%, and in the subgroup C in 22.2%.
Among the seven positive GHT in group 1, four
showed the result “outside normal limits” and
three showed “generalized reduction of sensitiv
ity.” Although there was a small number of pa
tients. it seems that both criteria have the same sen
sitivity to detect the first alteration in patients from
group 1. It’s important to emphasize that these pa
tients haven't been treated with Pilocarpine or other
miotic drugs, which could reduce the global sensi
tivity of the visual field, and all patients with posi
tive GHT had visual acuity 3=20/25.
In order to test the sensitivity of the method, we
apply it in patients already known to present glau-
15
comalous perimetric alterations. The GHT was pos
itive in all 23 eyes studied (sensitivity of 100%).
Katz et al. (27) reported the GHT’s sensitivity of
92%, slightly lower than our result. Also Duggan et
al. (10) and Sommer et al. (28) reported a sensitivity
of 94 and 97%, respectively, using a test similar to
the GHT, called the differential threshold test.
To verify specificity, eyes with vertical cup disc
of <0.4 without asymmetry, that is to say eyes with
no clinical evidences of lesion, were chosen. In this
group the GHT proved negative in all eyes (speci
ficity of 100%). Katz et al. (27) reported for the
GHT a similar result. Comparing the results of this
group with those of the first one, a high statistical
difference was found, showing that the glaucoma
suspect population (group 1) differs from the normal
population (group 3).
The reproducibility of a test is also of consider
able importance in establishing its reliability. In the
present study, the general reproducibility was
83.3%. When we divide the eyes in two groups.
those where the first GHT were positive showed a
reproducibility of 75.8%. Those where the first
GHT were negative showed a reproducibility of
88.9%. It would be possible that the time between
the tests might influence its reproducibility. This
was not the case in our study, as the average inter
val between the tests in the group where it was
reproducible compared with the group where.it was
not reproducible was not statistically different.
This study showed that 18.4% of the patients who
present clinical impression of damage of optic disc
without typical visual field defect showed a positive
GHT. As we were interested only in studying the
GHT. we disregarded the value of MD (mean devi
ation), SF (short-term fluctuation), and other crite
ria to detect visual field defects. It is possible that if
we considered them, the number of eyes with visual?
field defects would increase. In contrast, all eyes
without this clinical impression of damage of the
optic disc showed a negative GHT. Therefore, the
GHT seems to be an important tool in the detection
of visual field damage in glaucoma suspects. How
ever. 81.6% of the eyes that had clinical evidences
of lesion of the optic disc showed a normal GHT.
Although it’s possible that some of these eyes might
have only an apparent glaucomatous damage of the
optic disc, this is unlikely to occur in all of these
eyes. These data are in agreement with the findings
reported by Quigley et al. (29) that a substantial loss
of nervous fiber is necessary before the first visual
field defect can be detected.
J Glaucoma. Vol. 3. No. I. /W
- Media
RF_NUT_1_SUDHA.pdf
Position: 2236 (3 views)