Forced calorie restriction and subsequent weight loss is associated with a reduction in body weight. However, this body weight includes substantial amounts of skeletal muscle. This is problematic because it ts the skeletal muscle mass that dictates the resting metabolic rate, and loss of muscle therefore downregulates energy utilisation. The down regulation of energy utilisation by the hypothalamus following energy restriction is a well known phenomenon that is evidenced in many studies that have investigated calorie restriction on the obese. For example, in a study published in the American Journal of Clinical Nutrition in 19841, researchers tested the thermogenic response of diabetic and non-diabetic obese subjects, before and after weight loss, in comparison to normal weight healthy control subjects. The obese subjects were classified as having normal glucose tolerance, impaired glucose tolerance or type 2 diabetes and were studied before and after losing between 10 and 35 kg of weight using an energy restricted diet for 6 months.
The results of the study showed that prior to weight loss, the glucose induced thermogenesis of the obese type 2 diabetics and those with normal glucose tolerance was significantly lower than pair matched subjects of the same age from the control group of healthy normal weight subjects. Those obese subjects with impaired glucose tolerance also had lower glucose induced thermogenesis compared to younger normal weight subjects, but not those of middle-aged. Following weight loss, the glucose induced thermogenesis of the obese subjects with normal glucose tolerance and impaired glucose tolerance fell even further, but those obese subjects with type 2 diabetes did not experience further drops. Therefore the weight loss experienced by the subjects significantly and deleteriously reduced the ability of the subjects to produce heat from a glucose load, suggesting that their thermogenic response to food had been compromised following weight loss. Indeed, this appears to be a common pattern when examining data from similar weight loss studies.
Weight loss is associated with a reduction in resting metabolic rate and a reduction in postprandial thermogenesis. The reason for this is because obesity is actually a metabolic disorder characterised by poor energy compartmentalisation and utilisation. Although the adipose tissue could be used as a ready source of energy, it is unavailable to the hypothalamus as an energy store due to metabolic aberrations. Obesity then is a disease of starvation. Taking a starving person and exposing them to the stress of calorie restriction will only cause counterregulatory mechanisms to be implemented by the hypothalamus in order to save energy. These mechanisms include a reduction in the available energy for physical activity, a reduction postprandial thermogenesis and a reduction in resting metabolic rate. Just as when a starving man is provided with food he rapidly gains weight, so a calorie restricted obese subject exposed to normal eating again will rapidly regain lost weight. This is the reason that forced calorie restriction is ineffective at causing weight loss.
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