Contents - Previous - Next

This is the old United Nations University website. Visit the new site at

Nutritional requirements

Nutrition and educational achievement: part I. malnutrition and behavioural test indicators

Ernesto Pollitt and Nita Lewis
Human Nutrition Center, School of Public Health, University of Texas, Houston, Texas


The purpose of this paper is to depict the role of nutrition as a determinant of formal educational achievement. First, an evaluation is made of the role of nutrition in shaping aptitudes and abilities of the pre-school child. A basic educational proposition is that school success will depend, in part, on the capabilities of the student at the beginning of his formal education (1). The paper also looks at the role of nutrition once the child is in school. Accordingly, from a longitudinal perspective, the substantive difference between these two periods lies in their focus on the developmental implications when the nutrition variable affects the child.

Somewhat arbitrarily, a distinction is made between possible behavioural effects of malnutrition, i.e., iron deficiency or protein-energy malnutrition (PEM), and the co-variations that may be established between nutritional and behavioural indicators in populations where malnutrition is not a major public health problem. Part I of this paper deals with the former and Part II will deal with the latter. This distinction exemplifies the differences in the concerns of developing countries and those of the industrialized countries.

Neither part presents an exhaustive review of the literature. Studies are often selectively cited to substantiate statements made; in other instances (especially when the focus is on areas where there is scarcity of information) studies are reviewed in some detail. Also, it should be pointed out that the issue of mechanisms whereby nutrition factors offset behaviour is not discussed.


In this section the focus is restricted to highly prevalent forms of malnutrition, mostly in developing countries, and for which evidence of an impact of malnutrition is established or suggested. Specifically, the association between behaviour and the nutritional anomalies of protein-calorie malnutrition, iron deficiency and anaemia, iodine deficiency, and avitaminosis A are discussed.

Protein-Energy Malnutrition (PEM)

"Most children with PEM are generally born into, and develop in, an unsanitary environment with few early opportunities for learning and psychosocial stimulation, and are constantly exposed to agents that will lead to infectious diseases" (2). Because of the total impact of the environment on development, individuals with a history of malnutrition are likely to have specific deficiencies in cognitive function or learning ability (for detailed literature reviews, see 3, 4). The isolation of specific PEM effects on cognition has been a troublesome methodological problem.

From the available published information, the following inferences are warranted.

  1. Severe PEM occurring throughout most of the first two years of life in children living in populations where malnutrition is endemic generally results in severe cognitive deficits (5 9). In the absence of an appropriate rehabilitation programme (10, 11) or change to a stimulating home environment (12), this deficit will restrict the chances that the child has of taking advantage of the formal educational system (13 - 19).
  2. Severe PEM secondary to a biological disorder (e.g., pyloric stenosis) during the first two years of life in children not exposed to poverty conditions may, but generally does not, leave cognitive deficits that interfere with school learning (20 - 23).
  3. Infants and young children of comparatively short stature (an indicator of nutritional history) within populations where malnutrition is endemic are likely to perform less well than children of average height from the same community on tests of intelligence or on tests of specific cognitive processes (24, 25). Accordingly, their school achievement will probably not be up to the level of their comparatively taller peers from the same populations (26).
  4. Infants and pre-school children with a history of moderate to severe malnutrition who are exposed to stimulating home environments (12), or to long-term nutrition and psychosocial stimulation programmes may be partly, if not totally, rehabilitated from their cognitive deficits (10, 11, 27). Although data supporting this issue are not yet available, the rehabilitation may be successful enough to expect them to compete satisfactorily with their peers in school.

Iron Deficiency and Anaemia

Data from two recent experimental studies indicate that in preschool children, particular process features of cognition, such as selective attention, vigilance, or rehearsal strategies for memory function, may be altered by iron deficiency with (28) and without anaemia (29). (For detailed review of literature, see 30.) The study of Pollitt, et al. (29) suggests that there may be some adverse functional consequences in cases of mild iron deficiency, which were previously identified as falling within the normal variability of iron status in children. Oski and Honig (28) and Pollitt, et al. (29) found that iron-repletion therapy was followed by a reversal of all previously detected cognitive deficits.

It may be inferred that the iron-deficient pre-school child will not have learning difficulties once he or she reaches the school setting if the sideropenia is reversed. On the other hand, these data suggest that school-age children may have learning difficulties if they are iron-deficient (see the section on iron deficiency in the school-age child in Part II of this paper).

One other developmental issue that requires further research is whether long-term, chronic iron deficiency during the first year of life can have long-lasting effects. The experimental work cited above does not address the issue of the timing of the deficiency. One study investigated possible long-term effects of iron deficiency (31). In a sample of 61 children, 32 developed iron-deficiency anaemia between six and 18 months of age (Hb. 6.1- 9.5 g/dl). Twenty-nine infants received neonatal iron dextran injections and were not anaemic (Hb. 11.5- 23.9 g/dl) during this age period. Neurological evaluation performed six or seven years later showed that the iron-deficient group had more "soft neurological signs" than found in the controls. Unfortunately, because these data were presented in an abstract, there is no way of critically assessing the soundness of the study design and findings.

Iodine Deficiency

Severe iodine deficiency results in hypothyroidism, a pathological state characterized by an impairment in synthesizing thyroid hormone. Unless the thyroid gland is nonfunctional or absent, the impairment is accompanied by goitre, or thyroid gland enlargement, which results from hyperstimulation of the thyroid gland. Severe endemic goitre- which is generally the result of a diet deficient in iodine (32)- has been clearly associated with endemic cretinism in different world regions (33, 34). A cretin is characterized by severe intellectual retardation, dysarthria, and possibly deafness. With few, if any, exceptions, cretins are not able to attend school because of their severe intellectual limitations. They represent the most dramatic example of the way a nutritional deficiency may stop a child from taking advantage of the formal educational system (34).

A continuum of neurological impairment resulting from iodine deficiency has also been postulated. One end-point of the continuum is cretinism, while the other extreme is a milder neurological impairment (35). Although little argument exists about the association between goitre and severe mental retardation and cretinism, there is considerable controversy about the validity of the the continuum hypothesis.

Evidence recently accumulated from studies on the effect of iodized oil on pregnant women in populations with a high prevalence of iodine deficiency provides some support for the continuum hypothesis (36, 37). These data also suggested that the adverse effects of iodine deficiency on the central nervous system begin in the early stages of foetal life.

In Ecuador, a study was conducted comparing the IQs of children in two communities (37). In one, iodized oil was injected into every member of the community; the other community served as a control. Children in the treatment community were selected for the study if they were at least 36 months old, and if treatment of their mothers had occurred either prior to conception or between the fourth and fifth months of foetal life. They were then matched by age and sex with children from the non-treated population. The difference in the Stanford Binet IQ for the children of the mothers treated during gestation and the controls was not statistically significant. On the other hand, the mean IQ for the offspring of the women treated prior to conception was much higher and statistically different from that of controls. Treatment, therefore, had a differential effect on intelligence dependent on its timing.

When it was initiated during the second trimester of pregnancy, it did not appear to prevent mild intellectual retardation in the offspring. Conversely, it had a demonstrably salutary effect when it was given before embryogenesis.

Although it is now possible to eradicate iodine deficiency and goitre in most populations (32) through appropriate prophylactic programmes, this specific nutritional deficiency still represents a major public health problem (38).

Vitamin A and Xerophthalmia

Vitamin-A deficiency causes abnormalities in tissue metabolism and resultant weight loss, nervous disorders, reduced resistance to infection, and eye lesions that progressively worsen until blindness occurs (see 39, p.5). These lesions, xerophthalmia and kerotomalacia, are most frequently found in young children and are often accompanied by protein-energy malnutrition. Lesions form on the eyes after the fluids that lubricate the conjunctiva dry up. This process is reversible by treatment with vitamin A. Left untreated, however, the condition worsens until the eyes are irreversibly blind.

From the data available, it appears that of the survivors of severe xerophthalmia, 25 per cent are totally blind, 50 to 60 per cent are partially blind, and 15 to 25 per cent have unimpaired sight. Data sources are such that the total annual number of cases of blindness resulting from xerophthalmia is impossibie to determine (39, p.9). A first estimate of 20,000 per year by McLaren (40) was raised to 100,000 per year in 1970; but this figure has yet to be confirmed (39).

The effects of the blindness resulting from xerophthalmia on a child are self-evident. Loss of vision is a severe handicap to the individual and to the family. To our knowledge, no studies have been done to determine how many children never attend school as a result of xerophthalmia, or how school performance is affected by varying degrees of visual handicap.


The data reviewed here have shown that nutrition factors should be considered as inputs in the educational attainment process of children. These inputs can be defined in connection with the timing of their effects. They may affect aptitudes and abilities of pre-school children, and determine in part the degree of success the child will have later within the school. They may also affect the student directly once he/she is embarked upon formal education.

In the pre-school period, nutritional deficiencies may become sufficient causes for the exclusion of the child from participating in the regular school system (e.g., cretinism and xerophthalmia secondary to endemic iodine and vitamin-A deficiency, respectively). PEM generally is not a sufficient cause of cognitive derangements, but it is often a substantive component of a sufficient cause. When PEM (and possibly iron-deficiency anaemia) is part of an economically impoverished environment, the probabilities are very high that the cognitive competence of a child will be adversely affected. In the absence of appropriate rehabilitation his or her future school performance will not be satisfactory, or at least not up to the level of peers.

Once the child is in school, iron deficiency can affect his or her cognitive function. Specifically, it can interfere with selective processes, such as attention, vigilance, or rehearsal strategies for memory operations. Yet it is not known whether these effects restrict learning ability. At best, a probability statement can be advanced indicating that in the presence of iron deficiency the likelihood of successful school achievement is decreased.


1. L. Alexander and J. Simmons, "The Determinants of School Achievement in Developing Countries: The Educational Production Function," International Bank for Reconstruction and Development, Staff Working Paper No. 201 (Washington, 1975).

2. UNESCO, "Nutrition in Educational Policy and Planning," Draft Report of a UNESCO Consultation, 11 - 14 Sept. 1979, Uppsala, Sweden (unpublished).

3. J. Cravioto and E.R. DeLicardie, "Nutrition, Mental Development, and Learning," in F. Falkner and J.M. Tanner, eds., Human Growth, vol. 3: Neurobiology and Nutrition (Plenum Press, New York, 1979).

4, E. Pollitt and C. Thomson, "Protein-Calorie Malnutrition and Behavior: A View from Psychology," in R, Wurtman and J. Wurtman, eds., Nutrition and the Brain, vol.. 2 ((Raven Press, New York, 1977).

5. L. Brockman and H. Ricciuti, "Severe Protein-Calorie Malnutrition and Cognitive Development in Infancy and Early Childhood," Developmental Psychology, 4: 312 (1971).

6. F. Monckeberg, "Effects of Early Marasmic Malnutrition on Subsequent Physical and Psychological Development," in N.S. Scrimshaw and J.E. Gordon, eds., Malnutrition, Learning, and Behavior (MIT Press, Cambridge, Massachusetts, 1969).

7. E. Pollitt and D. Granoff, "Mental and Motor Development of Peruvian Children Treated for Severe Malnutrition," Revista Interamer. Psichol., 1: 93 (1967).

8. U.S. Yatkin and D.S. McLaren, "The Behavioral Development of Infants Recovering from Severe Malnutrition," J. Mental Defic. Res.,14: 25 (1970),

9. J. Cravioto and B. Robles, "Evolution of Adaptive and Motor Behavior during Rehabilitation from Kwashiorkor," Am. J. Orthopsych., 35:499 ;1965).

10. S. Grantham-McGregor, M. Stewart, C. Powell, and W.N. Schofield, "Effect of Stimulation on Mental Development of Malnourished Child," Lancet, ii: 20011979).

11. J. Cravioto and R. Arrieta, "Stimulation and Mental Development of Mainourished Infants," Lancet, ii: 899 (1979).

12. M. Winick, K. Meyer-Katchadurian, and R.C. Harris, "Malnutrition and Environmental Enrichment by Early Adoption,"Science, 190:1173 (1975).

13. H.G. Birch, C. Pineiro, E. Alcalde, T. Toca, and J. Cravioto, "Relation of Kwashiorkor in Early Childhood and Intelligence at School Age," Pediat. Res., 5: 579 (1971).

14. J.K. Howard, "Calorie Intake and Intelligence: A Study Among Bantu School Children," Central Afr. J. Med., 12: 63 (1966).

15. V. Cabak and R. Najdanvic, "Effect of Undernutrition in Early Life on Physical and Mental Development," Arch. Dis. Childh., 40:523 (1965).

16. L.D. Edwards and L.J. Craddock, "Malnutrition and intellectual Development. A Study in School-Age Aboriginal Children at Walgett, N.S.W.," Med. J. Austral., 5 May 1973, p. 330.

17. M.B. Stoch and P,M. Smythe, "Fifteen Year Developmental Study on Effects of Severe Undernutrition during Infancy on Subsequent Physical Growth and Intellectual Functioning," Arch. Dis Childh., 51: 327 (1976).

18. S.A. Richardson, H.G. Birch, E. Grabie, and K. Yoder, "The Behavior of Children in School Who Were Severely Malnourished in the First Two Years of Life," J. Hlth. Soc. Behav., 13: 276 (1972).

19. S.A. Richardson, H.G. Birch, and M.E. Hertzig, "School Performance of Children Who Were Severely Malnuourished in Infancy," Amer. J. Mental Defic., 77: 623 (1973).

20. C.E. Ellis and D.E. Hill, "Growth, Intelligence and School Performance in Children with Cystic Fibrosis Who Have Had an Episode of Malnutrition during Infancy," J. Pediat., 87: 565 (1975).

21. P,S. Klein, G.B. Forbes, and P.R. Nader, "Effects of Starvation in Infancy (Pyloric Stenosis) on Subsequent Learning Abilities," J. Pediat., 87: 8 (1975).

22. J.D. Lloyd-Still, I. Hurwitz, P.H. Wolff, and H. Shwachman, "Intellectual Development after Severe Malnutrition in Infancy," Pediatrics, 54: 306 (1974).

23. H.B. Valman, "Intelligence after Malnutrition Caused by Neonatal Resection of the lleum," Lancet, 1: 425 (1974).

24. J. Cravioto, E. DeLicardie, and H. Birch, "Nutrition, Growth and Neurointegrative Development: An Experimental and Ecologic Study," Pediatrics (supplement), part II, 38 (1966).

25. R. Klein, H. Freeman, J. Kagan, C. Yarbrough, and J.P. Habicht, "Is Big Smart? The Relation of Growth to Cognition," J. Hlth Soc. Behav., 13: 219 (1972).

26. M. Irwin, P.L. Engle, C. Yarbrough, R.E. Klein, and J. Townsend, "The Relationship of Prior Ability and Family Characteristics to School Attendance and School Achievement in Rural Guatemala," Child Develop., 49 (1978).

27. H. McKay, L. Sinisterra, A. McKay, H. Gomez, and P. Lioreda, "Cognitive Growth in Colombian Malnourished Preschoolers," Science, 200: 270 (1978).

28. F. Oski and A. Honig, "The Effects of Therapy on the Developmental Scores of Iron-Deficient Infants," d. Pediat., 92: 21 (1978).

29. E. Pollitt, D. Greenfield, and R. Leibel, "Behavioral Effects of Iron Deficiency among Preschool Chlidren in Cambridge, Massachusetts," Fed. Proc., 37: 487 (1978).

30. R.L. Leibel, D.B. Greenfield, and E. Pollitt, "Iron Deficiency: Behavior and Brain Biochemistry," in M. Winick, ea., Nutrition in Pre- and Postnatal Development (Plenum Press, New York, 1979).

31. R.J. Cantwell, "The Long-Term Neurological Sequelae of Anemia in Infancy," Pediat. Res., 8: 342 (1974).

32. F.W. Clements, "Endemic Goitre," in G.H. Beaton and J.M. Bengoa, eds., Nutrition in Preventive Medicine (World Health Organization, Geneva,1976).

33. J.B. Stanbury, ea., Endemic Goiter (Pan American Health Organization,Washington, 1969).

34. J.B. Stanbury and R.L. Kroc, "Human Development and the Thyroid Gland: Relation to Endemic Cretinism," Adv. Exper. Med. Biol., vol. 30 (1972).

35. L.S. Greene, "Hyperendemic Goiter, Cretinism, and Social Organization in Highland Ecuador," in L.S. Greene, ea., Malnutrition, Behavior and Social Organization (Academic Press, New York, 1977).

36. R. Fierro-Benítez, I. Ramírez, E. Estrella, C. Jaramllio, C. Díaz, and J. Urresta, "Iodized Oil in the Prevention of Endemic Goiter and Associated Defects in the Andean Region of Ecuador: I. Program Design, Effects on Goiter Prevalence, Thyroid Function, and Iodine Excretion," in J.B. Stanbury, ea., Endemic Goiter (Pan American Health Organization, Washington, 1969).

37. R. Fierro-Benítez, l. Ramírez, E. Estrelia, and J.B. Stanbury, "The Role of Iodine in Intellectual Development in an Area of Endemic Goiter," in J.T. Dunn and G.A. Medeiros, eds., Endemic Goiter and Cretinism: Continuing Threats to World Health (Pan American Health Organization, Washington, 1974).

38. OPS (Organización Panamericana de la Salud), Politícas Nacionales de Alimentación y Nutrición, Publicación Científica No.328 (PAHO, Washington, 1976).

39. WHO (World Health Organization), Vitamin A Deficiency and Xerophthalmia, Report of a Joint WHO/USAID Meeting (Technical Report Series No. 590, WHO, Geneva, 1976).

40. D.S McLaren, Malnutrition and the Eye (Academic Press, New York, 1963).

Contents - Previous - Next