Why Are We Overweight? Part 2

Last installment, I discussed a recent article by Professor Katarina T. Borer that addresses the overweight epidemic currently sweeping the world. Specifically, I provided background information regarding how homeostatic mechanisms that operate to maintain normalcy within the body should correct this progressive increase in body fat retention via the influence of the hormones insulin and leptin, which circulate in the blood and enter the brain at levels proportional to body fat content. The take-home message was that these hormones will be present in greater quantities when an energy surplus is in effect and investigators have found that when either of these is administered directly into the brain of an animal, it will tend to eat less. This is precisely what would be predicted by a homeostatic model of control because it would help to restore normalcy (i.e., an ‘ideal’ body fat level) in the face of abnormal conditions (an energy surplus). Furthermore, these hormones should also affect how much energy we expend; for example, their presence should facilitate an elevation of both the resting metabolic rate and our level of spontaneous physical activity. The end result should be that a ‘set point’ will be established and body fat levels will remain relatively stable in the face of changing conditions. Obviously, this is not the way things have been going of late.

Before I detail Professor Borer’s findings, I want to address reader feedback concerning last month’s column and, specifically, a misunderstanding regarding the role of the hormones that I mention above. It is natural to reduce things to a good vs. bad mentality when dealing with diet and exercise and, indeed, this has been done with insulin and leptin such that they are now considered evil purveyors of the overweight epidemic that is currently taking place. This is why some readers couldn’t understand why I appear to paint them in a positive light. The bottom line is that when these hormones are circulating in excess quantity, it is a bad thing because it means you are already storing excess fat. However, if homeostatic regulation had been working properly, they would have also reversed the factors that got you into the predicament in the first place. It is also important to recognize that the ability of a hormone to exert its effect depends not only upon its presence, but also on the receptiveness of sites that must be amenable to its influence. In this regard, chronic elevation of these hormones tends to desensitize receptors and this condition also characterizes the overweight and associated diseased state.

In summary, it’s easy to see why insulin and leptin carry a negative stigma; however, it’s also important to realize that if homeostatic control was acting properly, their initial influence would have addressed the problem before things got so far out of hand. Furthermore, if a homeostatic system of the regulation of body fat was in effect, body fat levels would not deviate substantially from person to person outside a narrow range determined primarily by genetics. This means that much like body temperature, humans would all store a similar amount of fat. The fact that this is clearly not the case suggests that humans exhibit non-homeostatic control of the regulation of energy balance and this forms the basis of the aforementioned article.

Professor Borer begins by citing previous research confirming that feeding in humans and animals is strongly influenced by non-homeostatic factors such as the palatability of food, sensory diversity, food availability, portion size and social facilitation. Furthermore, humans and animals do not respond in a homeostatic manner with respect to the caloric density of foods such that when calorically-dense foods comprise a major portion of the diet, fat gain will inevitably occur. Human and animal weights also tend to level off at vastly different plateaus depending upon food presentation/availability and variable opportunities/necessities for physical activity. Finally, it is interesting to note that subjective feelings of hunger have been shown to be significantly suppressed during and after intense exercise; for example, long duration, high-intensity exercise sessions create a significant short-term negative energy balance. This is contrary to what would be expected. In conjunction with the fact that intravenous nutrient infusions and enforced inactivity also tend to result in deficient caloric metering, these findings provide for a growing body of evidence that confirms a relationship between energy balance, putative energy-regulating hormones, appetite and actual food intake that does not conform to a simple homeostatic model (e.g., the set-point theory).

The fact that weight gain doesn’t serve to blunt appetite and increase movement in humans suggests that non-homeostatic responses to an energy surplus are in effect. In this regard, it is interesting to note that circulating insulin and leptin do rise in response to an energy surplus/fat gain as would be predicted by the homeostatic model of control; however, they do not act to either lower energy intake or raise energy expenditure. Instead, an energy deficit actually increases spontaneous physical activity and an energy surplus tends to lower it. Professor Borer then proceeds to detail recent findings from her laboratory that help to explain why this might be the case.

This article was originally published in New Living Magazine, which can be accessed on-line at www.newliving.com.





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