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1. The role of individual nutrient deficiencies in linear growth faltering

1.1. Energy

In most situations, interpretation of associations between energy (food) intake and linear growth is confounded by the fact that when food intake is low, the intake of many other nutrients will also be inadequate. However, two experimental approaches have shed some light on the question of whether energy deficiency affects linear growth. These include manipulating the energy content of infant formulas while keeping the content of other nutrients at adequate and/or constant levels, and the provision of supplemental energy alone to stunted children.

Fomon et al. (1977) examined the impact on infant growth of manipulating the energy content of infant formulas. Infants were fed either a modified skim milk formula or Similac between 112 and 167 days of age. The low-fat, low carbohydrate skim milk formula contained 36 kcal/dl, and although the volume consumed was greater than that of Similac, average energy intake was low and ranged from 519 to 575 kcal/day (Table 1). In contrast, Similac contained the recommended energy content of 67 kcal/dl and supported energy intakes between 609 and 718 kcal/day. The infants consumed substantially more protein from the low energy formula (which contained 3.56 g/dl protein vs 1.72 g/dl), and more of most minerals and vitamins. In these previously well-nourished infants, low energy intake had a negative impact only on ponderal gain, and did not affect linear growth.

Similar results were obtained when infants were fed a formula providing 54 kcal/dl vs 100 kcal/dl (Fomon et al., 1975). The two formulas contained similar concentrations of protein and micronutrients, and intake of these was substantially higher from the low energy formula because of the greater volume consumed. Between 8 and 41 days of age, weight gain was 29.8 ±4.9 g/day vs 41.0 ±10.4 g/day with the low vs high energy formulas respectively (P < 0.01), while length gain was unaffected (1.23 ±0.17 vs 1.26 ±0.17 mm/day).

In an interesting case study of an obese infant who required intravenous and enteral nutritional support, energy intake was reduced from approximately 70 to 50-55 kcal/day at 12 months of age. The intake of other nutrients was adequate. Her weight and fat (but not lean) tissue mass were markedly reduced while her length gain was unaffected (Peipert et al., 1992).

Table 1. Effect of energy intake on the weight and length of infants during 112-167 days of age

Energy intake (kcal/d)

Length gain (mm/d)

Weight gain (g/d)

Skim milk

575 1

0.72 ±0.09 4

13.4 ±4.5

565 2

0.68 ±0.17

11.4 ±6.5

519 3

0.69 ±0.15

11.3 ±3.5


718 1

0.66 ±0.19

18.1 ±4.3

681 2

0.76 ±0.19

19.3 ±5.3

609 3

0.72 ±0.14

16.1 ±4.2

1 Male infants (n = 15),
2 male infants (n = 14) and
3 female infants (n = 14) born one to two years later than the first group.
4 Mean ±SD. From Fomon et al. (1977).

There are conflicting results concerning whether supplementation with energy alone improves linear growth of stunted children. No effect on linear growth was found by Malcolm et al. (1970) and Lampl, Johnston & Malcolm (1978) in New Guinea, where taro or sweet potato supplied most of the nutrients and children were very stunted, but not wasted. Children, age 5.5 to 15.5 years, were provided with supplements of either more of their usual diet by increasing the number of meals from 3 to 5 per day, 30 g margarine/day., or 75 g skim milk/day for 13 weeks. Compared to the unsupplemented control group (Table 2), height increment was increased 40% by extra food, and 111% by skim milk; based on skinfold thickness, height was gained at the expense of fat stores. The margarine supplement did not increase linear growth. Weight gain was more rapid when either the skim milk or the margarine supplements were provided. In a second study, over a 32-week supplementation period 10 g/day of skim milk increased height increment by 85%, while 20 g/day increased it by 97%. Thus, additional energy did not increase the rate of linear gain in these stunted (but not wasted) children although it did increase weight gain and fatness.

In contrast, Gopalan et al. (1973) reported that undernourished Indian children, age 1 to 5 years, increased both their height and weight gain when their diet was supplemented daily with a high energy (310 kcal/day), low protein (3 g/day) cake for 14 months (Table 3). The cake was prepared from wheat flour, sugar and oil, and no micronutrients were added. The supplement was also effective in preventing the loss of height and weight gain which occurred in unsupplemented children affected with measles. These children were certainly malnourished because some of them developed kwashiorkor or marasmus during the study, but actual height and weight data were not provided. Thus, it is unclear whether they were stunted and/or wasted.

Table 2. Height and weight gain of stunted New Guinea schoolchildren supplemented with milk or energy alone



Height gain (cm)

Weight gain (kg)

Usual diet


1.10 ±0.12

0.50 ±0.13

Skim milk, 75 g/d + usual diet


2.32 ±0.11 1

1.21 ±0.10 2

Margarine, 30g/d + usual diet


0.96 ±0.11

1.05 ±0.18 3

5 meals vs usual 3 meals


1.54 ±0.13 4

0.47 ±0.14

1 Significantly greater than other 3 groups, P < 0.001;
2 significantly greater than usual or 5-meal groups, P < 0.001;
3 significantly greater than usual or 5-meal groups, P < 0.05;
4 significantly greater than usual or margarine groups, P < 0.05 From Malcolm (1970).

Table 3. Effect of energy supplements for 14 months on height and weight gain of undernourished Indian preschool-children

Age (years)

Height gain (cm)

Weight gain (kg)

Supplemented 1


Supplemented 1



9.3 (25) 2

6.5 (9)




9.5 (50)

7.8 (26)




9.1 (65)

7.4 (33)




8.4 (71)

7.3 (15)



1 Supplementation significantly increased height and weight gain at all ages;
2 number of children. From Gopalan et al. (1973)

Inexplicably, neither a high-energy (300 kcal/day), low protein snack with or without a vitamin-mineral supplement containing iron and zinc, improved rates of height or weight growth in 1-5 year old stunted and wasted Thai children (Gershoff et al., 1988).

1.2. Protein

Many investigators have observed an improvement in the linear growth of stunted children after supplementation with protein-rich foods such as milk, either alone or with other foods or nutrients, while others have not (Beaton & Ghassemi, 1982). However, there is little information on the specific role of protein in linear growth, because low protein intakes are usually accompanied not only by low energy intakes but by inadequate amounts of important micronutrients that are contained in dietary protein sources. These include iron, zinc, copper, calcium and vitamin A.

In the INCAP longitudinal intervention study in Guatemala there was no additional benefit for child growth of providing supplements that contained good quality protein (as atole, a mixture of dry skim milk and cereal) compared to supplemental energy alone (provided in a non-protein beverage called fresco). Energy intake was the important predictor of linear height (and weight) increments (Martorell & Klein, 1980). However, it is not certain that the beneficial effects of the atole were due to its energy content alone, because the dried skim milk and cereal in this supplement probably provided higher amounts of some micronutrients compared to fresco (Allen, in press a).

An important point is that in the INCAP intervention study severe growth stunting occurred even when protein and essential amino acid intakes were probably adequate. While atole supplements did improve linear growth, the infants and children receiving this supplement remained severely growth-stunted even though the energy intake of some of them exceeded the FAD/WHO requirement values, and protein intakes were two to three times higher than requirements in the majority of children. The INCAP investigators have stated that "although effects on length were clear, they were less than might have been expected given the level of supplement provided" (Martorell & Habicht, 1986). This suggests that other nutrients than protein or energy were inadequate in the atole. In the Nutrition CRSP, linear growth faltering was common in Egyptian, Kenyan and Mexican preschool-children even though their protein and essential amino acid intakes were adequate (Beaton, Calloway & Murphy, 1992).

The studies described above suggest that linear growth faltering, or subsequent failure to recover, can occur when intakes of energy and/or protein are adequate. This raises the question of the extent to which micronutrient deficiencies impair linear growth of human populations.

1.3. Zinc

1.3.1. Identification of zinc deficiency in the Middle East The effects of zinc deficiency on human growth were first described in Iran and Egypt (Prasad et al., 1963; Prasad, Halstead & Nadimi, 1972; Ronaghy et al., 1974; Halstead et al., 1972). In these locations zinc deficiency was associated with high phytate, high fiber, low protein diets, and with hookworm and schistosomiasis (Halstead et al., 1972), situations which may also have created other micronutrient deficiencies. The earliest zinc intervention trials were not successful in improving the linear growth of school-age boys (Carter et al., 1969; Mahloudji et al., 1975). Similarly, Ronaghy et al., (1969) found no growth benefit of providing 28 mg zinc/day plus iron, or 40 mg zinc/day plus iron and food, to short prepubertal Iranian boys, although it did improve the rate of maturation of their genitalia.

Because the supplemental zinc may have been poorly absorbed when consumed with the high fiber, high phytate Middle Eastern diets, or the studies were not of sufficient duration, Ronaghy et al. (1974) increased the amount of supplemental zinc to 40 mg/day for 13 year old moderately growth-retarded Iranian boys. Supplementation produced significant increases in height (at 182 days and 536 days), weight (at 536 days) and bone age (almost doubled at 536 days). This supplement also included 10 g/day of egg white protein, corn oil, minerals and vitamins, which failed to improve linear growth in the absence of zinc.

1.3.2. Zinc and growth of children in industrialized countries During the 1970s and 1980s there were several studies of the impact of zinc supplementation on short children in the United States and Canada (Table 4). Hambidge's group in Denver, Colorado, reported that short middle-income children had low hair zinc concentrations, impaired taste acuity and poor appetite (Hambidge et al., 1971). Later (Hambidge et al., 1976) they found that the height of 37% of children age 3-5 years, enrolled in a school program for low-income children, was at or below the 10th centile. Of these, 74% were Mexican-Americans. Hair and plasma zinc were lower than in children from a middle-income group, suggesting that inadequate zinc nutriture was common in the low-income families. In 1983 a zinc supplementation trial was performed on children 2-6 years old, with height-for-age below the 10th centile of NCHS reference values, and meeting two out of three of the following criteria: low dietary zinc, low plasma zinc, and low hair zinc. They were given a placebo or 5 mg zinc per day for a year. The zinc produced a 10% increase in height velocity which was significant within 6 months in the boys and the group as a whole, an increase in hair zinc, but no change in plasma zinc. The supplement increased food (energy) intake from 1280 to 1880 kcal/day in boys (Krebs, Hambidge & Walravens, 1984), but had no significant effect on either the food intake or linear growth of the girls.

Gibson et al. (1989) also showed a beneficial effect of zinc supplements on Caucasian Canadian boys with low height centiles. A supplement of 10 mg zinc/day was provided to 5-7 year olds, for 12 months. Only boys with a low initial hair zinc concentration responded to the supplement with faster linear growth. Energy intake and weight gain were unaffected.

Table 4. Zinc supplements and growth in industrialized countries


Age, status

mg Zn/d






Walravens, Krebs & Hambidge (1983)

2-6 y, short



+ 1, M 2

NS 3


Gibson et al. (1989)

5-7 y, short



+, M 4




Walravens, Hambidge & Koepfer (1989)

8-27 m, low wt




+, M


Walravens et al. (1992)

4-9 m, breast-fed



+, M

+, M

M = males.
1 Significant effect of treatment;
2 treatment effect is significant only in males;
3 not significant;
4 only males studied.

In Colorado, approximately 5 mg supplemental zinc per day for 6 months improved the weight-for-age of infants and preschool-children (age 8-27 months, mean 15 months) with the failure-to-thrive syndrome (weight below the 10th centile) (Walravens, Hambidge & Koepfer, 1989). Linear growth was not improved by the supplements. Possible explanations, apart from a lack of zinc deficiency, include selection on the basis of low weight-for-age rather than low length, and the relatively short duration of the study.

This research has been extended to answer the question of whether the smaller size of breast-fed infants in industrialized countries might be in part due to the decline in breast milk zinc concentrations that occurs during the first 6 months of lactation. Walravens et al. (1992) supplemented 4-9 month-old infants who were primarily breast-fed and born to low-income, immigrant families in France. When 5 mg zinc/day was provided, both weight and length gain increased significantly during the 3-month period. Length-for-age Z scores of supplemented infants were above NCHS reference values throughout the 3 months, while those of the placebo group fell slightly below reference values after 3 months. While some substitution of breast milk for weaning foods with lower zinc content cannot be definitively ruled out, these data are intriguing and need to be replicated in other settings. The nutritional implications of these results are not clear, because breast milk zinc content does not seem to be affected by poor maternal zinc status, nor increased by maternal zinc supplementation (Karra et al., 1989).

One intriguing aspect of the U.S., Canadian and French studies is that there was no obvious reason for the children to be zinc deficient. The U.S. children consumed quite generous amounts of animal products and a limited amount of ethnic foods, with an average pre-supplement zinc intake of 5.2 mg/day compared to 6.5 mg/day by children in middle-income families. It is possible that the onset of zinc deficiency occurred much earlier, perhaps in infancy, or that the zinc requirements of these stunted individuals were unusually high.

1.3.3. Zinc and growth of children in developing countries Data on zinc interventions to improve growth in developing countries are summarized in Table 5. In China, 1-6-year-old children with poor growth benefited from 1-2 mg zinc/day supplemented for 6 months, by significantly increasing weight and length gain (Chen et al., 1985).

A zinc intervention trial has been completed recently on children living in the Ecuadorian Andes (Dirren et al., in press). A national survey in Ecuador had found the prevalence of linear growth retardation in the rural Andes to be 67%. In addition 69% of children between 6 and 11 months were anemic, vitamin A status was marginal, riboflavin status poor and serum zinc was < 65 mg/dl in 35% of rural children. All children between 12 and 30 months of age in a community were enrolled and given 10 mg zinc/day or a placebo for 15 months. Anemic children were treated with iron. There was a significant increase in height starting at 3-6 months and becoming stronger with time. Over the 15-month period boys grew 1 cm more in the supplemented vs placebo group (P < 0.001) but girls only grew 0.6 cm more (P < 0.07). The supplement significantly increased the weight Z score of girls but not boys.

Table 5. Zinc supplements and growth in developing countries 1


Age 2, status

Supplement mg Zn/d

Duration of supplement (months)

Height gain

Weight gain



Xue-Cun et al. (1985)

12-72, short






Dirren et al. (in press)

12-48, all





The Gambia

Bates et al. (1993)

7-27, all







Golden & Golden (1981)

6-17, PEM






Castillo-Duran et al. (1987)

8, marasmic






Schlesinger et al. (1992)

8, marasmic



+, M


1 See Table 4 for abbreviations;
2 months.

Children as young as 7 months were included in a zinc supplementation trial in The Gambia (Bates et al., 1993). All children were enrolled from three villages in a region of endemic growth faltering, and provided with 70 mg zinc twice-weekly for 15 months. There was no impact of the supplement on length or weight gain, or on an extensive battery of biochemical, hormonal and immunological measures.

1.3.4. Zinc and growth of severely malnourished children Several studies have demonstrated a beneficial effect of supplementing severely malnourished children with zinc (Table 5). These include the provision of zinc supplements (0.16-1.0 mg/kg/day) to Jamaican children who had been fed soy or cow's milk formulas during recovery from protein-energy malnutrition (Golden & Golden, 1981). The supplements increased lean body mass and total body water at the expense of adipose tissue synthesis, and therefore improved the efficiency of utilization of dietary energy for weight gain.

Marasmic infants in Chile responded to zinc supplementation (2 mg/kg/day in addition to a vitamin-mineral supplement containing iron, copper and vitamin A) for 90 days, by increasing their weight-for-length but not their length-for-age or energy intake (Castillo-Duran et al., 1987). Schlesinger et al. (1992) observed that a zinc-fortified formula improved the linear growth of Chilean infants (average age 7 months) recovering from marasmus, compared to a non-fortified formula containing amounts of zinc (and other nutrients) used in standard infant formulas. Although weight-for-age and height-for-age Z scores were not different over the 105-day rehabilitation period, on the basis of length/age Z scores, growth was significantly faster by 30 days, compared to 60 days in the control group. This earlier growth spurt occurred only in the male infants. Immune response was also better in the zinc-supplemented group, although there was no effect on the number or duration of infectious episodes, suggesting that the beneficial effect on growth was not explained by lower morbidity.

Zinc supplements may have a greater impact on the linear growth of infants and children suffering from diarrhea. In this condition there are massive increases in fecal zinc (Naveh, Lightman & Zinder, 1982) as well as anorexia which reduces zinc intake; together the low intake and increased excretion cause balance to be strongly negative during the episode and lower for some time afterwards (Castillo-Duran, Vial & Uauy, 1988). Copper balance is similarly affected (Castillo-Duran & Uauy, 1988). Severe diarrhea can induce clinical zinc deficiency, indicated by an acrodermatitis-like rash and low serum alkaline phosphatase levels, which requires 200-300 mg zinc per day to reverse (Rothbaum, Maur & Farrell, 1982).

In Bangladesh, Behrens, Tomkins & Roy (1990) examined the effect of zinc supplementation on the growth of children age 3-24 months with acute diarrhea (less than 3 days). Children were supplemented with 15 mg/kg daily (approx. 90 mg/day) for 2 weeks, then followed at home. Zinc improved linear growth by 25%, mostly between 4 and 9 weeks after the diarrhea. Ponderal gains were not reported. Clearly, additional research is needed on the benefits of zinc supplementation for children recovering from malnutrition or diarrhea.

1.3.5. Summary of zinc and linear growth Zinc supplements improved the linear growth of short but generally well-nourished children in the United States and Canada. In these children selected for shortness, zinc did not affect weight gain. In contrast, supplements provided to failure-to-thrive (low weight-for-age) infants in the United States improved only weight. There is no known reason why these children in industrialized countries should be zinc deficient; because the children were selected on the basis of poor growth and evidence of zinc deficiency, they may represent a segment of the population with relatively high zinc requirements. In spite of the generally positive impact of zinc supplements on the growth of small children in wealthier countries, further work is needed to determine whether zinc nutritional status is an important determinant of linear growth retardation in developing countries.

1.4. Iron

Reports of the benefits of iron supplementation for the linear growth of anemic children have shown mixed results (Table 6). In 1966, Judisch, Naiman & Oski evaluated the records of 156 anemic infants and children under 3 years of age in a United States clinic. As a group they tended to be underweight, and one third of them had a low weight at birth. Their weight gain improved when they were supplemented with iron (6 mg/kg/day until 2 months after hemoglobin returned to normal). Linear growth data were not reported. In a British study, anemic infants (17-19 months) were provided with 24 mg iron/day plus vitamin C for 8 weeks. They had a 125% faster weight gain velocity than unsupplemented controls, which was greatest in those infants with the greatest hematological response to iron (Aukett et al., 1988). Again, length change was not measured.

Table 6. Iron supplements and growth'


Age 1, status

Duration of supplement (weeks)

Height gain

Weight gain


Carter et al. (1969)

11-18 y, short





Judisch, Naiman & Oski (1966)

<3 y, anemic





Aukett et al. (1986)

1.5 y, anemic





Chwang, Soemantri & Pollitt (1988)

8-13 y, anemic





Latham et al. (1990)

8 y, all




1 See Table 4 for abbreviations.

In Indonesia, where the staples are rice, cassava, maize and potatoes, anemic children age 8.2-13.5 years were treated for 12 weeks with 2 mg/kg/day iron (approx. 50 mg/day) (Chwang, Soemantri & Pollitt, 1988). Iron treatment significantly increased weight, height and arm circumference in the anemic group but not in non-anemic controls. Height increased from 132.1 cm to 132.7 cm over the 12 weeks in the supplemented anemic children, compared to 135.3 cm to 135.6 cm in the anemic placebo group. Weight changed from 26.5 kg to 27.6 kg in the anemics treated with iron, while untreated anemics gained very little (from 25.7 to 26.0 kg).

More recently, Latham et al. (1990) reported improvements in growth following 15 weeks of iron supplementation in young Kenyan school children. The supplements significantly increased weight gain (which was 2.1 kg/15 weeks compared to 1.2 kg in controls, P < 0.002), but had no effect on linear gain. Appetite was also improved after supplementation.

These mixed results might be explained in part by the difficulty of detecting significant growth differences in the relatively short periods during which iron supplements were given. Also because linear growth only improved in the anemic Indonesian children, whereas both anemic and non-anemic schoolchildren were studied in Kenya, it is quite possible that linear growth only responds to iron treatment if the child was initially anemic.

1.5. Copper

The main risk factors for copper deficiency in children are low birth weight, low copper intake (e.g. due to high intakes of cow's milk), and malabsorption and diarrhea. Children recovering from severe malnutrition have low copper stores and benefit from copper supplementation especially if fed high-energy, low-copper diets (Castillo-Duran et al., 1983). Castillo-Duran & Uauy (1989) found a beneficial effect on weight gain and weight-for-length of supplementation with 80 mg/kg/day copper for one month, in 11 children recovering from malnutrition. Only those with low serum copper and ceruloplasmin initially were found to benefit. Energy intake was also higher after supplementation. Length increase was greater but not significantly so, perhaps because of the short period of study and small number of subjects. Cordano, Baertl & Graham (1964) found an improvement in bone-maturation delay in four severely malnourished infants after copper therapy. Linear growth response was not reported.

1.6. Iodine

Iodine deficiency is endemic in some regions of the world, and when it is severe it can certainly cause substantial linear growth retardation (Greene, 1980). Marginal deficiency, the occurrence of which has probably been under estimated, is also associated with short height (see chapter by Neumann & Harrison in this issue). It is possible that iodine deficiency during fetal life has a persistent impact on later growth. In a region of Ecuador with severe iodine deficiency, interventions with iodinated oil failed to change children's growth (Ramirez et al., 1972). On the other hand, if women are given iodinated oil prior to conception, the birthweight of their infants is increased (Thilly et al., 1979). Because iodine status is adequate in many of the populations in which growth faltering occurs, it is probably not a major explanatory factor for the global prevalence of stunting. It is also a special case in that its level of intake is relatively independent of the adequacy of the food supply.

1.7. Vitamin A

Associations between linear growth stunting and night-blindness and/or conjunctival evidence of xerophthalmia, have been found in some studies (Mere et al., 1991; Brink et al., 1979; Santos et al., 1983; Muhilal et al., 1988) but not others (Tielsch et al., 1986; West et al., 1992). A more recent analysis of existing data from Indonesian preschool-children examined the relationship between spontaneous onset or recovery from clinical xerophthalmia (defined as a history of night-blindness as reported by the mother-those with corneal xerophthalmia were treated and excluded) and weight and height change during 3-month intervals (Tarwotjo et al., 1992). Children who had xerophthalmia at the beginning of a 3-month period, but who were normal at its end, gained weight at the same rate as non-xerophthalmic controls, but showed no improvement in linear growth rate. In contrast, those who changed from normal to xerophthalmic, or who were xerophthalmic throughout a 3-month period, grew significantly more slowly in both weight and height even controlling for diarrhea and respiratory infections at the start of each interval. The results imply that growth is slower in children with persistent xerophthalmia or with vitamin A status so marginal that it precipitated clinical symptoms. In those children who recovered spontaneously, the rate of weight gain increased; they regained more than half the weight they had lost during a period with xerophthalmia. However, their linear growth did not improve.

Because such associations may be caused by other nutrient deficiencies in children who are vitamin A deficient, it is necessary to evaluate the impact of vitamin A supplementation trials on growth. The results of such studies are inconsistent (Table 7). A randomized trial of vitamin A supplementation (60,000 mg retinol equivalents, every 6 months for a year), in an area of Indonesia with endemic vitamin A deficiency, stimulated weight gain of males by 110 g in those aged 2-3 years (not significant), by 190 g in 4 year-olds, and by 263 g in those aged 5 years (West et al., 1988). The higher gain of the 4 and 5 year-olds was statistically significant, but there was no effect at 1 year of age. The supplements had no effect on linear growth or on weight gain of girls. Multiple regression analysis controlling for morbidity did not change these results. In a different Indonesian population where many children had subclinical vitamin A deficiency, fortification of commercial monosodium glutamate with vitamin A improved linear but not ponderal growth (Muhilal et al., 1988). The effect was significant in 1-2 year-olds, perhaps reflecting the greater growth potential of the younger children.

One possible explanation for the different results between the two Indonesian projects is that linear growth benefits more from a sustained food fortification program than from a few large doses of the vitamin. However, this interpretation is complicated by a recent report from India, in which 15,419 children aged 6-60 months received weekly doses of 2,500 mg retinol for one year (Rahmathulla et al., 1991). The vitamin A supplement did not improve either linear or ponderal growth. The supplements also failed to alter the incidence, severity or duration of diarrhea or respiratory infections (although mortality fell by 54%). Because these Indian children were probably more malnourished than those in Indonesia, and the vitamin A was given weekly, a lack of growth response in this study is surprising.

Table 7. Vitamin A supplements and growth 1







West et al. (1969)

1-5 y

High dose every 6 mo


+, M 45 y 2


Muhilal et al. (1988)

1-5 y


+, MF 3 1,2,4 y



Rahmathulla et al. (1991)

0.5-5 y

Low dose every week



1 See Table 4 for abbreviations;
2 age at which treatment effect is significant;
3 treatment effect significant in males and females;
4 monosodium glutamate with vitamin A.

In summary, the reported impact of vitamin A intervention on growth is highly variable among studies. During spontaneous recovery from xerophthalmia, weight gain recovery may be more likely than height gain. Length gain was only improved in one study in which there was a sustained improvement in the vitamin supply through food fortification. Finally, in no study have supplements or food fortification benefited the growth of children under one year of age, when growth failure is most serious.

1.8. Summary and conclusions concerning single nutrient deficiencies and linear growth stunting

Interventions with single nutrients, in the case of all of the nutrients reviewed above, have produced conflicting results concerning their ability to reverse growth stunting. For example, zinc supplements have stimulated linear growth in some studies, ponderal growth in others, or have shown no effect. Certainly no single nutrient supplement had a major, consistent effect on linear growth. There are several possible explanations for the lack of consistency among studies. One is that short or underweight children were sometimes selected deliberately by the investigators, while in others all children in a group were studied. Other selection criteria that varied among studies were recent diarrhea or PEM, and the exclusion of severely anemic cases. The age of the children differed across studies and so did the amount and type of supplement used. Nevertheless, the amount of supplement provided in these interventions should have produced an impact on linear growth if that specific nutrient had been growth-limiting. It is therefore plausible that multiple, rather than single, growth-limiting nutrient deficiencies exist in the same children. In the next section this possibility is explored using data from the Nutrition CRSP and other studies.

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