Thermogenic foods such as pepper may enhance the thermic effects of food.
The thermic effect of food (TEF) is the postprandial rise in energy expenditure that is due to the processing of ingested food. It was first shown by Seguin and Lavoisier in 1793 when they measured an increase in oxygen utilisation following food ingestion. Generally protein foods produce greater thermogenesis postprandially compared to carbohydrates and fat because amino acid metabolism is more complex than the processing of non-nitrogenous energy. Postprandially, protein can increase thermogenesis by between 25 to 40 %, glucose by between 6 to 8 %, and fat by between 2 to 3 %. Therefore the thermic effect of food can vary considerably, depending on the macronutrient profile of the meal. Because the thermic effect of food is part of the total energy expenditure, the question as to whether it contributes to the obesity process is of importance to nutritional scientists. Therefore many studies have investigated the thermic effect of foods in obese and lean subjects in order to determine its contribution to weight gain.
The hypothesis that the thermic effect of food is blunted in the obese and overweight is controversial. While some studies show reduced postprandial thermogenesis in obese individuals, some show no difference between obese and control subjects. However, much of this difference may result from methodological differences between the studies. Obesity may therefore be associated with a reduced thermic effect of food, but only under certain circumstances. In a review of the topic published in 2012, the authors examined some of the factors that may be required to see a reduction in postprandial thermogenesis in the obese1. To do this they analysed 49 studies and collated the data to find common variables that may account for the presence of a blunted thermic effect of food. The results showed that studies using glucose infusions consistently found blunted postprandial thermogenesis in obese individuals. The authors concluded from this that the blunted thermic effect of food in obesity is related to the degree of insulin resistance.
The negative results found in some studies may therefore relate to a number of factors including study design. However, of particular relevance might be that the thermic effect of food does not relate directly to obesity, but some associated condition. The review cited above suggests that it is not the degree of obesity that is the determining factor but the degree of insulin resistance. Because insulin resistance can vary between the obese, the degree of attenuation of the thermic effect of food can also vary. This last point is important because similar problems were associated with determining changes to the resting metabolic rate in obesity. Initially it was assumed that resting metabolic rate might be lower in the obese, but it was consistently shown that obese individuals had higher resting metabolic rates. Subsequent research showed it was not the level of obesity that determined the resting metabolic rate, but he degree of lean muscle tissue. Because obese individuals tend to have more muscle, they also tend to have high resting metabolic rates.
That the sympathetic nervous response to eating is diminished in obese individuals explains the mechanism by which postprandial thermogenesis is blunted. This suggest that foods that stimulate the sympathetic nervous system may be of benefit in raising the thermic effect of food in the obese. However, if the blunted thermogenesis is caused by metabolic dysfunction, any attempt to artificially raise that response would not be addressing the root cause of the problems and therefore could not be considered sustainable. Methylxanthines, capsaicinoids and alkaloids from plants known to stimulate the central nervous system that could increase the thermic effect of food in obese individuals should only be considered short-term solutions. Redressing the cause of the problem, the metabolic dysfunction caused by insulin resistance would be the only effective long term solution. This would require dietary changes to reverse the insulin resistance with particular emphasis on the removal of sources of fructose from the diet.
