The hypothalamus controls a number of different mechanisms that allow it to oxidise fuels to produce heat. One such mechanisms is the heat produced by consumption of a meal. This rise in body temperature following consumption of food is termed the thermic effect of food (TEF) and can represent a significant portion of the ingested energy (~5 to 10 %). By increasing the TEF the hypothalamus can increase the amount of wasted energy and this is one mechanism by which the body weight can be maintained despite fluctuations in energy intake. Generally larger more calorie dense meals produce a larger TEF which ensures that body fat accumulation does not become excessive. However, this mechanisms is dependent on the underlying biochemistry being fully functional. Evidence suggests that low quality foods are able to cause metabolic dysfunction which leads to insulin and leptin resistance, and that these conditions then cause the hypothalamus to lose its ability to correctly regulate the TEF, resulting in fat accumulation.
Evidence that the obese have a blunted TEF has been presented in the nutritional literature. The TEF is dependent on the release of catecholamine hormones such as adrenaline and noradrenaline and it has been shown that postprandially these hormones are in lower concentrations in the plasma of those with obesity. It is often assumed that the resting metabolic rate (RMR) of obese subjects is lower than that of non-obese subjects. However, this is not the case. For example, in one study researchers tested the RMR of obese women and non-obese subjects in a respiratory chamber and found that the obese women had significantly higher RMRs (2208 versus 1746 kcal per day in obese and non-obese women, respectively)1. However, when the authors measured the TEF following a liquid meal (17 % protein, 54 % carbohydrate and 29 % lipids) in the subject they found that the obese women had a significantly blunted TEF compared to the non-obese women.
In the obese women the TEF was 7.6 % of the energy content of the food whereas in the non-obese women it was 9.5 %. These results support a large body of other evidence that suggests that the TEF is blunted in obese people but that the RMR is not. When the obese women lost weight their thermogenic response to food was retested and it was found that it was still blunted (6.2 % of the energy content of the food). This supports the contention that the blunted thermogenic response to food is a result of an underlying metabolic dysfunction and is not due to the level of adiposity. The weight loss in the women was induced by a calorie restricted diet, and looking at the data it can be seen that while the subjects lost some body fat, a large amount of the lost weight was skeletal muscle. This loss of skeletal muscle will have significantly reduced the RMRs of the women. In combination with the blunted TEF, this would greatly increase the risk of regaining lost weight as body fat.
Dr Robert Barrington’s Nutritional Recommendation: The higher metabolic rate of the obese is thought to be due to the larger skeletal muscle masses they posses as a result of their larger body weights which requires a higher degree of structural support. Calorie restrictive weight loss results in a loss of this skeletal muscle mass and this in turn then lowers the RMR. Following forced calorie restriction people often therefore have both as blunted TEF and a reduced RMR. This is a perfect storm for weight regain in the form of fat, and is the reason that ‘dieting’ does not cause successful long term weight loss. Addition of caffeine to the diet can increase the TEF because it causes the release of catecholamines that are responsible for this effects. However, this will not correct the underlying cause of the blunted TEF, something that can only be achieved by consuming high quality foods.
RdB
