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.

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Food Variety, Calorie Intake, and Weight Gain

Let's kick off this post with a quote from a 2001 review paper (1):

Increased variety in the food supply may contribute to the development and maintenance of obesity.  Thirty-nine studies examining dietary variety, energy intake, and body composition are reviewed. Animal and human studies show that food consumption increases when there is more variety in a meal or diet and that greater dietary variety is associated with increased body weight and fat.

This may seem counterintuitive, since variety in the diet is generally seen as a good thing.  In some ways, it is a good thing, however in this post we'll see that it can have a downside.
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Neuronal Control of Appetite, Metabolism and Weight

Last week, I attended a Keystone conference, "Neuronal Control of Appetite, Metabolism and Weight", in Banff.  Keystone conferences are small, focused meetings that tend to attract high quality science.  This particular conference centered around my own professional research interests, and it was incredibly informative.  This post is a summary of some of the most salient points.

Rapid Pace of Scientific Progress

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Why Do We Eat? A Neurobiological Perspective. Part VIII

In the (probably) last post of this series, I'll take the pieces that I've gradually outlined in previous posts, and put them together into a big-picture, common-sense framework for thinking about human eating behavior, and why we eat more today than ever before.

Why is Eating Behavior Regulated?

Let's start at the most fundamental level.  To be competitive in a natural environment, organisms must find rational ways of interacting with their surroundings to promote survival and reproduction.  One of the most important elements of survival is the acquisition of energy and chemical building blocks, either by photosynthesis, or (in the case of animals) eating other organisms.  This imperative drove the evolution of rational food seeking behaviors long before the emergence of humans, mammals, reptiles, amphibians, fish, worms, and even eukaryotes (organisms with nuclei).

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Why Do We Eat? A Neurobiological Perspective. Part VII

Welcome back to the series, after a bit of a hiatus!  In previous posts, we covered the fact that humans eat because we're motivated to eat, and many things can motivate us to eat.  These include factors related to energy need (homeostatic factors), such as hunger, and factors that have little to do with energy need or hunger (non-homeostatic factors).  These many factors are all processed in specialized brain 'modules' that ultimately converge on a central action selection system (part of the reward system); this is the part of you that decides whether or not to initiate eating behaviors.

This will be somewhat of a catch-all post in which I discuss cognitive, emotional, and habit influences on food intake.  Since these factors are not my specialty, I'll keep it brief, but I don't mean to suggest they aren't important.

Food 'Cost'

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Why Do We Eat? A Neurobiological Perspective. Part V

In previous posts, I explained that food intake is determined by a variety of factors that are detected by the brain, and integrated by circuits in the mesolimbic system to determine the overall motivation to eat.  These factors include 'homeostatic factors' that reflect a true energy need by the body, and 'non-homeostatic factors' that are independent of the body's energy needs (e.g. palatability, habit, and the social environment).

In this post, we'll explore the hedonic system, which governs pleasure.  This includes the pleasure associated with food, called palatability.  The palatability of food is one of the factors that determines food intake.

The Hedonic System

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Why Do We Eat? A Neurobiological Perspective. Part III

In the first post, I explained that all voluntary actions are driven by a central action selection system in the mesolimbic area (the reward system).  This is the part of you that makes the decision to act, or not to act.  This system determines your overall motivation to obtain food, based on a variety of internal and external factors, for example hunger, the effort required to obtain food, and the sensory qualities of food/drink.  These factors are recognized and processed by a number of specialized 'modules' in the brain, and forwarded to the reward system where the decision to eat, or not to eat, is made.  Researchers divide food intake into two categories: 1) eating from a true energy need by the body (homeostatic eating), e.g. hunger, and 2) eating for other reasons (non-homeostatic eating), e.g. eating for social reasons or because the food tastes really good.

In the second post of the series, we explored how the brain regulates food intake on a meal-to meal basis based on feedback from the digestive system, and how food properties can influence this process.  The integrated gut-brain system that accomplishes this can be called the satiety system.

In this post, we'll explore the energy homeostasis system, which regulates energy balance (energy in vs. energy out) and body fatness on a long term basis.

The Energy Homeostasis System

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Another China Tidbit

A final note about the Chinese study in the previous post: the overweight vegetable-eaters (read: wheat eaters) exercised more than their non-vegetable-eating, thin neighbors. So although their average calorie intake was a bit higher, their expenditure was as well. 

Although I speculated in the last post that affluent people might be eating more wheat and fresh vegetables, the data don't support that. Participants with the highest income level actually adhered to the wheat and vegetable-rich pattern the least, while low-income participants were most likely to eat this way.

Interestingly, education showed a (weaker) trend in the opposite direction. More educated participants were more likely to eat the wheat-vegetable pattern, while the opposite was true of less educated participants. Thus, it looks like wheat makes people more educated. Just kidding, that's exactly the logic we have to avoid when interpreting this type of study!

Wheat in China

Dr. Michael Eades linked to an interesting study yesterday on his Health and Nutrition blog. It's entitled "Vegetable-Rich Food Pattern is Related to Obesity in China."

It's one of these epidemiological studies where they try to divide subjects into different categories of eating patterns and see how health problems associate with each one. They identified four patterns: the 'macho' diet high in meat and alcohol; the 'traditional' diet high in rice and vegetables; the 'sweet tooth' pattern high in cake, dairy and various drinks; and the 'vegetable rich' diet high in wheat, vegetables, fruit and tofu. The only pattern that associated with obesity was the vegetable-rich diet. The 25% of people eating closest to the vegetable-rich pattern were more than twice as likely to be obese as the 25% adhering the least.

The authors of the paper try to blame the increased obesity on a higher intake of vegetable oil from stir-frying the vegetables, but that explanation is misleading. A cursory glance at table 3 reveals that the vegetable-eaters weren't eating any more fat than their thinner neighbors. Dr. Eades suggests that their higher carbohydrate intake (+10%) was partially responsible for the weight gain, but I wasn't satisfied with that explanation so I took a closer look.  Dr. Eades also pointed to their higher calorie intake (+120 kcal/day), which makes sense to me.

One of the most striking elements of the 'vegetable-rich' food pattern is its replacement of rice with wheat flour. The 25% of the study population that adhered the least to the vegetable-rich food pattern ate 7.3 times more rice than wheat, whereas the 25% sticking most closely to the vegetable-rich pattern ate 1.2 times more wheat than rice! In other words, wheat flour rather than rice was their single largest source of calories. This association was much stronger than the increase in vegetable consumption itself!

All of a sudden, the data make more sense. Wheat seems to associate with health problems in many contexts. Perhaps the reason we don't see the same type of association in American epidemiological studies is that everyone eats wheat. Only in a culture that has a true diversity of diet can you find a robust association like this. The replacement of rice with wheat may have caused the increase in calorie intake as well. Clinical trials of low-carbohydrate diets as well as 'paleolithic diets' have shown good metabolic outcomes from wheat avoidance, although one can't be sure what role wheat plays from those data.

I don't think the vegetables had anything to do with the weight gain, they were just incidentally associated with wheat consumption. But I do think these data are difficult to reconcile with the idea that vegetables protect against overweight.