The role of dietary fat in the regulation of energy intake was assessed by manipulating a conventional diet and measuring spontaneous food consumption. Twenty-four women each consumed a sequence of three 2-wk dietary treatments in which 15–20%, 30–35%, or 45–50% of the energy was derived from fat. These diets consisted of foods that were similar in appearance and palatability but differed in the amount of high-fat ingredients used. Relative to their energy consumption on the medium-fat diet, the subjects spontaneously consumed an 11.3% deficit on the low-fat diet and a 15.4% surfeit on the high-fat diet (p less than 0.0001), resulting in significant changes in body weight (p less than 0.001). A small amount of caloric compensation did occur (p less than 0.02), which was greatest in the leanest subjects (p less than 0.03). These results suggest that habitual, unrestricted consumption of low-fat diets may be an effective approach to weight control.

The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the ‘obesity epidemic’ – the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models – the general intake model and the dual intervention point model – that address this issue and might offer better ways to understand how body fatness is controlled.

OBJECTIVE: The objective of this study was to quantify the weight gain of freshmen during their first 12 weeks at Cornell University. In addition, students completed questionnaires that revealed particular behaviors and activities that were associated with weight gain. DESIGN: Serial, correlational study. SUBJECTS: A total of 68 freshmen from Cornell University. MEASUREMENT: A total of 60 students were weighed during the first week of the semester, then again 12 weeks later. They were also given a questionnaire to complete concerning their behavior during the previous 12 weeks. RESULTS: After adjusting for clothing weights, the mean weight gain of the freshmen was 1.9±2.4?kg, a value significantly different from 0. Two regression models generated from the questionnaire were fitted to the weight gain. The first linear regression model (Model 1) accounted for 58% of the variance and indicated that eating in the ‘all-you-can-eat’ dining halls accounted for 20% of the variance in weight gain. Snacking and eating high-fat ‘junk food’ accounted for anther 20%. When initial weight was used as a covariate (Model 2), the consumption of junk foods, meal frequency and number of snacks accounted for 47% of the variance. CONCLUSION: The study clearly demonstrated that significant weight gain during first semester college is a real phenomenon and can be attributed to tangible environmental stimuli. The weight gain is considerably greater than that observed in the population and may be useful as a model to test various techniques that may reduce or reverse the ‘epidemic’ of obesity observed in the general population.

Our conceptions of how malnutrition endured early in life affects brain development have evolved considerably since the mid-1960s. At that time, it was feared that malnutrition endured during certain sensitive periods in early development would produce irreversible brain damage possibly resulting in mental retardation and an impairment in brain function. We now know that most of the alterations in the growth of various brain structures eventually recover (to some extent), although permanent alterations in the hippocampus and cerebellum remain. However, recent neuropharmacological research has revealed long-lasting, if not permanent, changes in brain neural receptor function resulting from an early episode of malnutrition. These more recent findings indicate that the kinds of behaviors and cognitive functions impaired by malnutrition may be more related to emotional responses to stressful events than to cognitive deficits per se, the age range of vulnerability to these long-term effects of malnutrition may be much greater than we had suspected and the minimal amount of malnutrition (hunger) necessary to produce these long-term alterations is unknown.

The behavioral effects of early malnutrition and early environmental isolation were observed in male rats. Dietary and environmental manipulations occurred during the first 7 weeks of life, after which followed a 10-week recovery period. On the basis of several different responses, it was found that the behavioral effects of early malnutrition were exaggerated by the environmental isolation. In most cases, the behavioral effects of early malnutrition were completely eliminated by supplying "additional stimulation" early in life. Two theoretical mechanisms are proposed to explain these findings.