You aren’t what you eat, you become what you eat

Abstract

AbstractObesity (and the consequent obesity epidemic) is a complex, adaptive process, taking place over a time span of many years. Energy intake is recognized as a potentially important driver of obesity, especially in the context of an identifiable energy imbalance which, it is surmised, must lead to weight gain. Similarly, energy expenditure must play an important role. However, both show an enormous degree of individual variation. Therefore, measuring them is an exceedingly difficult task, especially in the context of large populations and long time periods. It has been argued that population-level observed weight gain can be traced back to very small daily energy imbalances while, at the same time, positing that a much larger maintenance energy gap is responsible for maintaining the energy requirements of the increased weight population. In this paper we examine the relation between BMI and energy intake as functions of age. The convexity of the BMI curves as a function of age and gender demonstrate the enhanced obesity risk apparent in young adults and women, and imply that no settling points exist at the population level. Consistent with other studies, overall weight increases are consistent with a very small daily energy imbalance, about 7 cal. Consumption as a function of age shows a small, steady, linear decrease of about 8 cal per year, and can be associated with a maximal energy excess/deficit of about 250cal for the youngest and oldest age groups. By examining weight differences between age groups as a function of age, we argue that this excess/deficit is an important motor for the observed weight differences, and argue that the apparent energy imbalance of 250 cal, due to excess consumption, leads to an effective imbalance of only 7 cal due to the existence of various physiological and behavioral mechanisms that enhance weight homeostasis and effectively reduce the energy excess from 250 cal to 7 cal. We discuss several possibilities for such mechanisms.