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Effects of Nutritional Deficiency

The widespread notion that what we eat affects how we think has been difficult to prove. Even for the most flagrant example of poor nutrition, starvation in Third World countries, such a precept has not been indisputably demonstrated. [Pg.71]

What are the interactions between diet/nutrition and cognitive capacity Presumably, neuronal function is most vulnerable during brain cell division and myelin maturation, i.e., during gestation and infancy. Chronic, severe protein-calorie malnutrition at this stage is associated with mental retardation. Conclusions as to whether nutritional supplementation prevents this behavioural pathology are hampered by intervention effects not easily dissected, notably amelioration of other medical conditions and of the psychosocial milieu. Early childhood malnutrition has been extensively reviewed, and only the salient aspects will be considered in this paper. [Pg.71]

Cultural and genetic factors limit the applicability of these studies to health care in the United States. Though the effects of mild to moderate malnutrition are more subtle, they may also be more prevalent than previously assumed. These considerations apply to micronutrient status, such as for iron in children, and to a spectrum of adult deficiencies, primarily [Pg.71]

Mark J. Rosenthal and James S. Goodwin Department of Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131. [Pg.71]

Draper (ed.), Advances in Nutritional Research Plenum Press, New York 1985 [Pg.71]


RIO. Ruchman, I., The effect of nutritional deficiencies on the development of neutralising antibodies and associated changes in cerebral resistance against the virus of Western Equine Encephalomyelitis. J. Immunol. 53, 51-74 (1946). [Pg.235]

There may also he an effect of selenium deficiency on vitamin E nutrition. Selenium deficiency causes a specific pancreatic atrophy, which is unresponsive to vitamin E supplements. In turn, this leads to impaired secretion of lipase, and hence impaired absorption of dietary lipids in general that will affect the absorption of vitamin E (Thompson and Scott, 1970). [Pg.121]

Duerden JM and Bates CJ (1985) Effect of riboflavin deficiency on lipid metabolism of liver and brown adipose tissue of sucking rat pups. British Journal of Nutrition 53, 107-15. [Pg.422]

Mock DM, Johnson SB, and ffolman RT (f988a) Effects of biotin deficiency on serum fatty acid composition evidence for abnormalities in humans. Journal of Nutrition 118,342-8. [Pg.441]

Selenium is known to be an essential micronutrient for humans and animals therefore, inadequate as well as excessive selenium intake can cause adverse health effects. The Food and Nutrition Board of the National Research Council has established adequate intakes (AI) of 15-20 pg/day for infants based on the selenium content of milk of well nourished, but unsupplemented, mothers (NAS 2000). No data were available on which to base RDAs for children or adolescents and so the RDAs for children and adolescents are extrapolated from adult values. Studies of selenium deficient populations suggest that children are more susceptible to the effects of selenium deficiency and have the highest need for selenium of any individuals in the population (Chen et al. 1980 Yang et al. 1988). [Pg.188]

Copper deficiency is extremely rare, and there is no evidence that copper ever need be added to a normal diet. Even in chnical states associated with hypocupremia (sprue, celiac disease, and nephrotic syndrome), effects of copper deficiency usually are not demonstrable. Anemia due to copper deficiency has been described in individuals who have undergone intestinal bypass surgery, in those who are receiving parenteral nutrition, in malnourished infants, and in patients ingesting excessive amounts of zinc. While an inherited disorder affecting copper transport (Menkes disease) is associated with reduced activity of several copper-dependent enzymes, this disease is not associated with hematological abnormalities. [Pg.940]


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