Honors Project--Smith College, Northampton, Mass., 2010. / Includes bibliographical references (p. 43-46)

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Thesis. 1976. M.S.--Massachusetts Institute of Technology. Dept. of Nutrition and Food Science. / Microfiche copy available in Archives and Science. / Vita. / Bibliography: leaves 69-78. / M.S.

It has been well documented that protein calorie malnutrition (PCM) gives rise to physiological and behavioral deficits. These deficits include changes in emotional, exploratory and social behaviors of the malnourished organism. In particular, previous research has demonstrated that Feci from infancy results in avoidance of and failure to initiate social interactions as well as decreased contact with the environment, which in turn, further disrupt emotional and social development. This study examined the effects of chronic protein malnutrition on the social behavior of adult rhesus macaques by experimentally testing the hypothesis that deficient monkeys, unlike normal well-fed ones, are more likely to avoid social encounters than to seek them out. In addition, the animals' social interactions were recorded and analyzed. Subjects consisted of eleven adult rhesus monkeys (Macaca mulatta). Five were fed a protein-deficient diet (3.0 % of total kilocalories) and six were fed adequate amounts of protein (14 % of total kilocalories) from birth. After habituation to the test apparatus, subjects were trained to perform an operant response which opened a sliding door. During training, the response allowed access to food. In the final testing, opening the door allowed access to a social partner. If the subject performed the response and released a social partner, the social behaviors of the pair was recorded for ten minutes. Each subject was given three opportunities, on three separate occasions, to release every other subject. Protein-deficient subjects habituated to the experimental apparatus and acquired a simple operant response at the same rate as the control subjects. The protein-deficient monkeys, however, failed to generalize this operant response as rapidly as the control monkeys. As predicted, protein-deficient monkeys performed an operant response allowing access to a social partner less frequently than did the control monkeys. For like-diet pairings both the control and deficient subjects released approximately 60% of their partners; however, controls were far more likely to release a dissimilar diet partner (84% probability) than were deficient subjects (39% probability). Diet condition of the releasor was a significant factor, whereas diet condition of the release was not. Variables which could confound these findings were examined. It was found that: 1. The difference between diet groups was not accounted for by proximity of home cages; 2. Sex of the animals was not a confounding factor; 3. Although body weight and diet condition were highly correlated, body weight alone did not exert an effect above and beyond that of diet condition; 4. Dominance status, although correlated with both diet condition and body weight, showed only a weak correlation with the likelihood of one subject releasing another when the effect of diet condition was partialed out. In summary, diet condition played the major determining role in the frequency of release rates. Social behavior data was collected throughout the final phase of the experiment. Both groups of animals exhibited minimal play and sexual behaviors. Protein-deficient monkeys were more submissive than their matched controls. Subjects deviated most dramatically from one another in two behavioral clusters: disturbed (defined as self-stimulatory, autistic-like behaviors) and exploratory behaviors. Deficient monkeys engaged in more disturbed behaviors, while control monkeys engaged in more exploratory behaviors. Results are discussed in terms of behavioral similarity to social isolate animals, and possible nutritional-environmental interaction leading to chronic or persistent deficits in social development.

Protein deficiency may increase susceptibility to gastrointestinal (GI) parasitic infections, possibly as a result of impaired systemic and/or intestinal effector responses induced by downregulation of Th2 cytokines and/or upregulation of Th1 cytokines. To test this hypothesis, female BALB/c mice (n = 18/diet) were fed a control (24%), marginal (7%), or deficient (3%) protein diet and given a challenge infection with the GI nematode, Heligmosomoides polygyrus. The 3% mice had higher worm burdens at 1, 2 and 4 weeks post-challenge infection (pci), lower increases in serum IgE, reduced intestinal eosinophilia, and depressed mucosal mast cell proliferation and activation at 1 to 2 weeks pci. To determine whether these suppressed effector responses in the 3% mice were associated with altered spleen and mesenteric lymph node (MLN) cytokine profiles, cells were restimulated in vitro with parasite antigen and cytokine concentrations were measured. Deficient MLN cells secreted significantly less IL-4 and more IFN-gamma at 1--2 weeks pci than did control MLN cells. Deficient spleen cells also secreted more IFN-gamma at 2 weeks pci compared with control spleen cells. From RT-PCR analyses, the 3% mice also had lower IL-4 mRNA expression in spleen and MLN at 1--2 weeks pci. Our study supports the hypothesis that protein deficiency exacerbates the survival of a GI nematode parasite by decreasing IL-4 (Th2) and increasing IFN-gamma (Th1) early in the infection, leading to reduced gut and systemic Th2 effector responses.

Two experiments were undertaken to evaluate the baby pig as a biomedical model with which to study Protein-Calorie malnutrition. In the first experiment, 32Yorkshire and Yorkshire X Landrace pigs weaned at 21 days were fed either an 18% or 4% protein ration. Blood samples were taken biweekly from the anterior vena cava and the serum samples analyzed for calcium, phosphorus, glucose, cholesterol, lactic dehydrogenase, glutamic oxaloacetic transaminase, amylase, a 1ka1ine phosphatase, total protein, albumin and blood urea nitrogen. Significant (p ≤.01) treatment effects were observed for total protein, albumin, amylase, alkaline phosphatase, lactic dehydrogenase, cholesterol, calcium and phosphorus. In the second experiment, 40 Yorkshire and Yorkshire X Landrace pigs weaned at 28 days were fed rations containing 18%, 10%, 8%, 6%, and 4% protein. Blood samples were again taken biweekly and serum samples were analyzed for the same parameters as in trial one. In addition, serum copper, iron, magnesium, and zinc were measured. The livers of any animals which died on the low protein diets, were fat extracted, and the level of fat compared to that obtained from livers of animals killed as suckling pigs at a slaughter plant. Total body water was determined on three animals on the 18% ration and three on the h% ration utilizing tritiated water as a tracer. Total protein, albumin, amylase, lactic dehydrogenase, calcium, phosphorus, copper, iron and magnesium correlated well with dietary protein intake. Significant treatment effects were observed for total body water and fat content of the liver. An attempt was made to find a biochemical parameter which might be used in diagnosing developing protein calorie malnutrition. The results of the study would indicate that serum phosphate and amylase are the most sensitive parameters to dietary protein intake. Not every lesion or biochemical serum change occurring in man was reproduced in the present study. Nevertheless, characteristic symptoms such as the development of fatty liver, growth retardation, abnormal hair texture, hypoalbuminemia, and apathy were reproduced in the protein deficient swine. The baby pig would therefore appear to be a good model for the study of protein-calorie malnutrition. / Land and Food Systems, Faculty of / Graduate

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