The three principle components of daily energy expenditure (EE) are resting EE, diet-induced thermogenesis (DIT) and activity-related EE. DIT is the energy produced after a meal, contributing 10-15% to total EE. DIT is also known as the thermic effects of food. Observations in the 1980s from animal studies that thermogenesis contributes significantly to the regulation of body fat, have led to a hypothesis that a defect in DIT may cause obesity in humans. However the evidence from numerous human studies is conflicting, the reasons for which are unclear.
DIT arises from a combination of heat production from BAT and other UCP-rich tissues and from the energy required for the processing and storing nutrients. Thus only one component of DIT is heat energy. DIT is usually quantified by indirect calorimetry from gas exchange. Because indirect calorimetry does not measure heat, we questioned whether post-prandial heat dissipated is reliably quantified as DIT. We employed infrared thermography to independently assess thermogenesis by measuring skin temperatures overlying supraclavicular BAT depots. Thermogenic activity of BAT was stimulated by cold and by a meal which induced a parallel increase in energy production. These stimulatory effects on BAT thermogenesis were inhibited by glucocorticoids. However glucocorticoids enhanced postprandial energy production (‘DIT’) in the face of reduced BAT thermogenesis and stimulated lipid synthesis. The increase in energy production correlated significantly with the increase in lipogenesis. As energy cannot be destroyed (first law of thermodynamics), the energy which would have been dissipated as heat after a meal, is channelled into lipid synthesis (storage). These findings provide the strongest evidence that DIT may not necessary reflect true thermogenesis (heat production). When quantified by indirect calorimetry, DIT can be a friend or foe of energy balance depending on the thermogenic fraction. The assumption that gas exchange-derived DIT reflects energy loss from heat production is likely to explain the controversy on the role of DIT in obesity.