The Neurobiology of the Obesity Epidemic

I recently read an interesting review paper by Dr. Edmund T. Rolls titled "Taste, olfactory and food texture reward processing in the brain and the control of appetite" that I'll discuss in this post (1).  Dr. Rolls is a prolific neuroscience researcher at Oxford who focuses on "the brain mechanisms of perception, memory, emotion and feeding, and thus of perceptual, memory, emotional and appetite disorders."  His website is here.

The first half of the paper is technical and discusses some of Dr. Rolls' findings on how specific brain areas process sensory and reward information, and how individual neurons can integrate multiple sensory signals during this process.  I recommend reading it if you have the background and interest, but I'm not going to cover it here.  The second half of the paper is an attempt to explain the obesity epidemic based on what he knows about the brain and other aspects of human biology.


Dr. Rolls kicks it off with a brief discussion of genetics, just enough to conclude that it can't be responsible for the current obesity epidemic.  I've edited the references out to streamline the text.

These are of some importance, with some of the variance in weight and [resting metabolic rate] in a population of human subjects attributable to inheritance. However, the ‘obesity epidemic’ that has occurred since 1990 cannot be attributed to genetic changes, for which the time scale is far too short, but instead to factors such as the increased palatability, variety and availability of food which are some of the crucial drivers of food intake and the amount of food that is eaten in our changed modern environment and that are described later.

I'll note here that the idea of a gene-environment mismatch is the foundation of the ancestral health concept.  Although it has become fashionable in some academic circles to criticize the ancestral health/Paleo community for "idealizing the past", being unscientific, etc., in reality this fundamental concept is widely accepted and cited in the biomedical literature (as shown above and below).  Few researchers would disagree that a gene-environment mismatch is at the root of the modern obesity epidemic, and therefore that it is valuable to understand where our species came from in our effort to combat obesity. Although some of the critiques of the ancestral health community are legitimate, they often reek of academic snobbery and ingroup identity reinforcement.  The fundamental concept is sound and already widely accepted, so why not cooperate and try to refine it instead of ostentatiously rejecting the community attempting to advance it?

Dr. Rolls then moves on to discuss what has changed about our environment that has increased food intake.  You might find this familiar:

The fundamental concept this leads to about some of the major causes of obesity is that, over the last 30 years, sensory stimulation produced by the taste, smell, texture and appearance of food, as well as its availability, have increased dramatically, yet the satiety signals produced by stomach distension, satiety hormones, etc. have remained essentially unchanged, so that the effect on the brain's control system for appetite is to lead to a net average increase in the reward value and palatability of food which over rides the satiety signals, and contributes to the tendency to be overstimulated by food and to overeat.

Again referencing the mismatch between our evolutionary context and modern environment, Dr. Rolls discusses the ability of food palatability to increase food intake beyond the body's normal 'stop signal' that would ordinarily constrain food intake when an appropriate number of calories have been eaten:

A factor in obesity (as described in section ‘Brain processing of the sensory properties and pleasantness of food’) is food palatability, which with modern methods of food production can now be greater than would have been the case during the evolution of our feeding control systems. These brain systems evolved so that internal signals from for example gastric distension and glucose utilisation could act to decrease the pleasantness of the sensory sensations produced by feeding sufficiently by the end of a meal to stop further eating. However, the greater palatability of modern food may mean that this balance is altered, so that there is a tendency for the greater palatability of food to be insufficiently decreased by a standard amount of food eaten, so that extra food is eaten in a meal.

He also covers sensory-specific satiety, another factor in food intake.  This phenomenon is the reason why we eat more total food when food variety is high, as explained here.

Sensory-specific satiety is the decrease in the appetite for a particular food as it is eaten in a meal, without a decrease in the appetite for different foods, as shown earlier. It is an important factor influencing how much of each food is eaten in a meal, and its evolutionary significance may be to encourage eating of a range of different foods, and thus obtaining a range of nutrients. As a result of sensory-specific satiety, if a wide variety of foods is available, overeating in a meal can occur. Given that it is now possible to make available a very wide range of food flavours, textures and appearances, and that such foods are readily available, this variety effect may be a factor in promoting excess food intake.

And a word about calorie density:

Although gastric emptying rate is slower for high-energy density foods, this does not fully compensate for the energy density of the food. The implication is that eating energy dense foods (e.g. high-fat foods) may not allow gastric distension to contribute sufficiently to satiety. Because of this, the energy density of foods may be an important factor that influences how much energy is consumed in a meal.

It's worth noting that although fat is a factor in calorie density, it's not the only factor.  High-fat foods can be moderate in calorie density (e.g. avocado), and high-carbohydrate foods can be high in calorie density (e.g. crackers).  That being said, all else being equal, higher-fat foods do tend to have a higher calorie density.

The reasoning Dr. Rolls presents in his paper is why I frequently say that the obesity epidemic is due in large part to increased availability of calorie-dense, highly palatable and rewarding foods.  This statement neatly summarizes some of the main factors that influence food intake: food accessibility, calorie density, food variety, palatability, and reward.

I hope this all sounds familiar to regular WHS readers.  The idea is that the brain integrates a variety of factors, both internal and external, into its (mostly unconscious) decision-making process of whether or not to eat.  Some factors increase the probability of eating, while others decrease it.  Changes in these factors (e.g. changes in the food environment due to technological progress) can alter the probability of eating, alter total food intake, and ultimately alter body fatness.  Here's an image summarizing this process, from the last post in my series "Why Do We Eat? A Neurobiological Perspective" (2):