Why Are We Overweight? Part 3

Homeostasis is a blanket term that refers to the capacity for living organisms to maintain internal constancy despite disruptions in their external environment. Homeostatic mechanisms are critical for the survival of living beings because were it not for the body’s remarkable ability to adapt, its function would be severely compromised by any number of stressors that are encountered on a regular basis. However, there is a glaring example of a circumstance where human homeostatic control has not been functioning properly and as a result, a serious global health epidemic has emerged. That epidemic is overweight/obesity and in the last two installments, I laid the groundwork for a review of a recent article by Professor Katarina T. Borer that explains why this might be the case.

If you consider the health risks associated with excess body fat storage, it is intuitive to suggest that homeostatic mechanisms should keep surplus amounts from accumulating. Indeed, research performed by E.F. Adolph in 1947 supports this very notion. Specifically, Adolf showed that body weight in rats tends to stabilize and is defended at a given plateau at the end of their growth phase and refinement of his findings has led to a contemporary view of the homeostatic regulation of body fat that is known as the set-point theory. Within this schema, the central nervous system exerts its influence through circulating hormones that make you want to eat less and be more active when an energy surplus is present. Specifically, insulin and leptin will signal deviations from a normative body fat level to the hypothalamic centers of the brain that adjust our appetite, our metabolism and how active we choose to be. Consequently, a ‘set point’ will exist and the end result will be that much like body temperature, body fat levels will not deviate considerably over time. What is more, this tight homeostatic regulation should also ensure that all living humans will accumulate a relatively similar amount of fat (once again, think body temperature, which is virtually identical from person to person). Interestingly, this seems to be the case in the animal kingdom (e.g., you’d be hard-pressed to find an overweight tiger or a skinny elephant), but not for man. Consequently, it seems reasonable to suggest that there is a significant influence from non-homeostatic processes on how much energy we ingest and expend.

Professor Borer’s investigative objective was to examine the role of leptin and insulin in the control of human meal-to-meal eating and appetite. To do so, her research team recruited nine postmenopausal women to serve as subjects and for these individuals, energy balance was manipulated during their daily regimen by varying the energy content of their meals, imposing an additional energy cost due to exercise and infusing nutrients intravenously. Specifically, subjects were exposed to four treatment conditions – ingestion of a small amount of energy in the morning (i.e., eating a 100-calorie meal at 6 a.m.), expenditure of a large amount of energy in the morning (i.e., performing moderate-intensity exercise that cost 550 calories between 10 a.m. and noon) and two matching conditions where similar circumstances were encountered; however, intravenous nutrient infusions were given to replace the calories missing in the small meal and expended during the exercise session, respectively. While manipulating these factors, the researchers measured the hormones that should provide homeostatic control (i.e., the two mentioned above and also the gut peptide ghrelin, which acts in an opposing manner by stimulating hunger when a negative energy balance is in effect). They also measured changes in appetite, which were assessed with a visual analog scale. The four treatment conditions were compared to a control condition where the same subjects ate a large morning meal that contained 500 calories of energy. The researchers also measured how much their subjects ate during a subsequent midday meal at which point they were allowed to ingest as much as they desired.

The results from this study provide evidence that appetite is sensitive to the size and energy content of meals, but not to short-term fluctuations in energy balance that are imposed by exercise or intravenous nutrient infusions. In fact, exercise actually suppressed hunger and increased the perception of fullness! Furthermore, appetite also did not adjust appropriately to short-term fluctuations in energy balance during the subsequent meal; i.e., more food was not voluntarily consumed when energy deficits were present. Indeed, appetite and meal-to-meal eating appeared to be controlled by stomach capacity as opposed to the preceding energy deficit. However, despite appetite’s inability to respond appropriately under these circumstances, the putative appetite-controlling hormones did operate as predicted when these fluctuations were encountered; for example, plasma ghrelin increased and leptin decreased as a result of the small meal and the exercise session and both hormones also responded in an appropriate manner when the energy imbalance was corrected via nutrient infusion. The researchers concluded that human appetite and meal-to-meal eating are unresponsive to short-term variations in energy availability caused by inadequate meal size, energy expenditure during exercise or intravenous increases in nutrient energy even though the hormones that should regulate this behavior appear to respond in the appropriate manner. 

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





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