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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Speaking at AHS13

The 2013 Ancestral Health Symposium will be held in Atlanta, GA, August 14-17.  Last year was a great conference, and I look forward to more informative talks and networking.  Tickets go fast, so reserve yours now if you plan to attend!

This year, I'll be speaking on insulin and obesity.  My talk will be titled "Insulin and Obesity: Reconciling Conflicting Evidence".  In this talk, I'll present the evidence for and against the idea that elevated insulin contributes to the development of obesity.  One hypothesis states that elevated insulin contributes to obesity, while the other states that elevated insulin is caused by obesity and does not contribute to it.  Both sides of the debate present evidence that appears compelling, and it often seems like each side is talking past the other rather than trying to incorporate all of the evidence into a larger, more powerful model.

There's a lot evidence that can be brought to bear on this question, but much of it hasn't reached the public yet.  I'll explore a broad swath of evidence from clinical case studies, observational studies, controlled trials, animal research, physiology, and cell biology to test the two competing hypotheses and outline a model that can explain all of the seemingly conflicting data.  Much of this information hasn't appeared on this blog.  My goal is to put together a talk that will be informative to a researcher but also accessible to an informed layperson.

On a separate note, my AHS12 talk "Digestive Health, Inflammation and the Metabolic Syndrome" has not been posted online because the video recording of my talk has mysteriously disappeared.  I think many WHS readers would be interested in the talk, since it covers research on the important and interdependent influence of gut health, inflammation, and psychological stress on the metabolic syndrome (the quintessential modern metabolic disorder).  I'm going to try to find time to make a narrated slideshow so I can post it on YouTube.

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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Book Review: Salt, Sugar, Fat

Michael Moss is a Pulitzer prize-winning journalist who has made a career writing about the US food system.  In his latest book, Salt, Sugar, Fat: How the Food Giants Hooked Us, he attempts to explain how the processed food industry has been so successful at increasing its control over US "stomach share".  Although the book doesn't focus on the obesity epidemic, the relevance is obvious.  Salt, Sugar, Fat is required reading for anyone who wants to understand why obesity is becoming more common in the US and throughout the world.

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Glucagon, Dietary Protein, and Low-Carbohydrate Diets

Glucagon is a hormone that plays an important role in blood glucose control.  Like insulin, it's secreted by the pancreas, though it's secreted by a different cell population than insulin (alpha vs. beta cells).  In some ways, glucagon opposes insulin.  However, the role of glucagon in metabolism is frequently misunderstood in diet-health circles.

The liver normally stores glucose in the form of glycogen and releases it into the bloodstream as needed.  It can also manufacture glucose from glycerol, lactate, and certain amino acids.  Glucagon's main job is to keep blood glucose from dipping too low by making sure the liver releases enough glucose.  There are a few situations where this is particularly important:

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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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Body Fatness and Cardiovascular Risk Factors

I recently revisited a really cool paper published in the Lancet in 2009 on body fatness, biomarkers, health, and mortality (1). It's a meta-analysis that compiled body mass index (BMI) data from nearly 900,000 individual people, and related it to circulating lipids and various health outcomes.  This is one of the most authoritative papers on the subject.

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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 VI

In previous posts in this series, I explained that the brain (primarily the mesolimbic system) integrates various factors to decide whether or not to drive food seeking and consumption behaviors.  These include homeostatic factors such as hunger, and non-homeostatic factors such as palatability and the social environment.

In this post, I'll examine the reward system more closely.  This is the system that governs the motivation for food, and behavioral reinforcement (a form of learning).  It does this by receiving information from other parts of the brain that it uses to determine if it's appropriate to drive (motivate) food seeking behavior.  I covered its role in motivation in the first post of the series, so in this post I'll address reinforcement.

Behavioral Reinforcement

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Why Do We Eat? A Neurobiological Perspective. Part IV

In this post, I'll follow up on the last post with a discussion two more important factors that can affect energy homeostasis and therefore our food intake and propensity to gain fat: age and menopause.

Age

Although it often isn't the case in non-industrial cultures, in affluent nations most people gain fat with age.  This fat gain continues until old age, when many people once again lose fat.  This is probably related to a number of factors, three of which I'll discuss.  The first is that we tend to become less physically active with age.  The second, related factor is that we lose lean mass with age, and so energy expenditure declines.

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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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Why Do We Eat? A Neurobiological Perspective. Part II

In the last post, I explained that eating behavior is determined by a variety of factors, including hunger and a number of others that I'll gradually explore as we make our way through the series.  These factors are recognized by specialized brain 'modules' and forwarded to a central action selection system in the mesolimbic area (the reward system), which determines if they are collectively sufficient cause for action.  If so, they're forwarded to brain systems that directly drive the physical movements involved in seeking and consuming food (motor systems).

The term 'homeostasis' is important in biology.  Homeostasis is a process that attempts to keep a particular factor within a certain stable range.  The thermostat in your house is an example of a homeostatic system.  It reacts to upward or downward changes in a manner that keeps temperature in a comfortable range.  The human body also contains a thermostat that keeps internal temperature close to 98.6 F.  Many things are homeostatically regulated by the body, and one of them is energy status (how much energy the body has available for use).  Homeostasis of large-scale processes in the body is typically regulated by the brain.

We can divide the factors that determine feeding behavior into two categories, homeostatic and non-homeostatic.  Homeostatic eating is when food intake is driven by a true energy need, as perceived by the brain.  For the most part, this is eating in response to hunger.  Non-homeostatic eating is when food intake is driven by factors other than energy need, such as palatability, habitual meal time, and food cues (e.g. you just walked by a vending machine full of Flamin' Hot Cheetos).

We can divide energy homeostasis into two sub-categories: 1) the system that regulates short-term, meal-to-meal calorie intake, and 2) the system that regulates fat mass, the long-term energy reserve of the human body.  In this post, I'll give an overview of the process that regulates energy homeostasis on a short-term, meal-to-meal basis.

The Satiety System (Short-Term Energy Homeostasis)


The stomach of an adult human has a capacity of 2-4 liters.  In practice, people rarely eat that volume of food.  In fact, most of us feel completely stuffed long before we've reached full stomach capacity.  Why?

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Why Do We Eat? A Neurobiological Perspective. Part I

As with all voluntary movements, eating food is an expression of activity in the brain.  The brain integrates various inputs from around the body, and outside the body, and decides whether or not to execute the goal-directed behaviors of food seeking and consumption.  Research has uncovered a lot about how this process works, and in this series I'll give a simplified overview of what scientists have learned about how, and why, the brain decides to eat.

The Gatekeeper of Voluntary Behaviors

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Announcing the Ideal Weight Program

I often receive requests from people asking for my overall perspective on fat loss and health.  I share my opinions here, but they're scattered throughout hundreds of posts, there's a lot I haven't had a chance to write about, and I rarely give practical recommendations.  However, I knew I'd eventually put everything together into a cohesive fat loss program-- it was only a matter of finding the right opportunity.

That opportunity presented itself in 2011 when I met Dan Pardi, a researcher whose work focuses on sleep and food intake, and the CEO of a company called Dan's Plan.  I was immediately impressed by Dan because he stood out as someone with a high level of expertise in sleep and physical activity, as well as someone who has successfully lost a substantial amount of fat and kept it off for several years.

Dan and his team had developed a set of unique and engaging tools for tracking weight, sleep, and physical activity to help people maintain daily mindfulness over the simple fundamentals of health.  These tools are 100 percent free and incredibly easy to use, particularly if you sync them with an electronic scale and step counter.  When synced with these devices, the Dan's Plan website automatically uploads and displays your weight, sleep, and physical activity score, as well as integrating them all into a single user-friendly Health Zone Score that lets you know your overall performance at a glance.  Even if you have no interest in fat loss, I highly recommend using the free tracking tools on the Dan's Plan site-- I do.

In early 2012, Dan approached me about creating a fat loss program for Dan's Plan that incorporates their unique tracking tools.  This struck me as an excellent opportunity to create a diet and lifestyle program that combines sound science with exciting new technology.  Dan and I both brought science to the table, and Dan also brought the perspective gained from working with others to help them lose fat, as well as his own successful fat loss experience.  Dan and I have been working hard on this project, and we're finally ready to launch.

I'm happy to announce the Ideal Weight Program, an effective new system for fat loss and maintenance.

What is the Ideal Weight Program?

The Ideal Weight Program is a unique system for fat loss and maintenance that draws from the latest science on diet, physical activity, sleep, and behavior modification, and pairs it with engaging tools that help you define your goals and meet them.  It keeps you consistently focused on the everyday factors that really matter for fat loss, and gives you the skills you need to make sustainable diet and lifestyle changes.  Based on your own goals and priorities, you can choose one of two diet strategies for the initial fat loss phase:

• The Fat Loss and Sustainable Health (FLASH) diet, an intensive high-protein diet for rapid fat loss.
• The Simple Food Diet, a more flexible diet based on whole, natural foods specifically selected for fat loss.  One important goal of this diet is to teach healthy cooking skills, using recipes and tips provided.

These diets are designed to naturally promote a lower calorie intake and fat loss, without requiring calorie counting.  The Ideal Weight Program also includes important physical activity and sleep components, and explains why these are so critical for fat loss and health.  Dan and I discussed some of the principles underlying the Ideal Weight Program on Chris Kresser's podcast recently.

Here's what you get when you sign up:

• Detailed documents that walk you through the program
• Weight, sleep, and physical activity tracking tools tailored for fat loss
• Simple recipes and cooking tips that work with almost anything in your fridge
• Videos that explain the key concepts behind fat loss and maintenance
• An e-book explaining the scientific rationale behind the program

Signing up for the Ideal Weight Program gives you lifetime access to everything.  We've discounted the initial price, because we want to hear your feedback so that we can continue to improve the program over time.  If you follow the link below, first you'll be prompted to sign up for a basic Dan's Plan account, and once you have your account set up, you'll be able to purchase the Ideal Weight Program:

Ideal Weight Program



Financial disclosure: I will receive a portion of the revenue from the sale of the Ideal Weight Program.  I do not receive revenue from the sale of other products associated with Dan's Plan or the Ideal Weight Program (such as the Fitbit, cooking tools, and other programs).

Comment Published in Nature

I recently read an opinion piece by Gary Taubes in the scientific journal Nature, titled "Treat Obesity as Physiology, not Physics", in which he promoted NuSI and repeated the statement that obesity research is a "house of cards" because it focuses on calories in/out, at the expense of studying the "hormonal regulatory disorders" underlying obesity (1).  I wrote a letter to the editor in response to Taubes's commentary, which has been published in Nature (2).

I'm used to seeing these kinds of claims in the popular press at this point, but to see it published in a scientific journal is galling (even if it's in the opinion section).  This is the equivalent of a person who has never held an ax telling a group of lumberjacks they need to focus on cutting trees.  It's part of a disturbing trend of popular writers in the low-carb and Paleo world attacking researchers, and even entire fields of research, they have little understanding of.  Of course this only applies to a minority of the community, but this argumentation style smells of desperation and reflects poorly on the community as a whole.

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Overfeeding and Elevated Insulin

It's commonly accepted in the obesity research community that fat gain causes insulin resistance and an increase in circulating insulin, and that this is a major reason why obese people usually have insulin resistance and high circulating insulin. Part of the rationale is that substantial fat loss by almost any means improves insulin sensitivity and causes circulating insulin to decline, and substantial fat gain from deliberate overfeeding causes insulin sensitivity to decline and circulating insulin to increase.  I recently cited three references to support this contention on another blog, and was challenged, so I decided to revisit these references to make sure I had understood them correctly (1, 2, 3).  Since I took the time to do this, I figured I may as well write it up for my readers, since these studies are quite informative.

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The Potato Diet

In 2010, I wrote a series of blog posts on the health properties of potatoes (1, 2, 3).  The evidence showed that potatoes are non-toxic, filling per calorie, remarkably nutritious, and can be eaten as almost the sole source of nutrition for extended periods of time (though I'm not recommending this).  Traditional South American cultures such as the Quechua and Aymara have eaten potatoes as the major source of calories for generations without any apparent ill effects (3).  This is particularly interesting since potatoes are one of the highest glycemic and most insulin-stimulating foods known.

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Is it Time to Re-write the Textbooks on Insulin and Obesity? Part II

A new paper published on December 6th in the journal Science once again tackles the question of whether elevated insulin drives the development of obesity (1).  Mice were generated that lack Jun kinases 1 and 2 specifically in immune cells, impairing their ability to produce inflammation while having very few off-target effects.  These mice do not become insulin resistant when placed on a fattening diet, and their insulin levels do not increase one iota.  Are they protected from obesity?  People who read the last post should know the answer already.
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Is it Time to Re-write the Textbooks on Insulin and Obesity?

A recent study in Cell Metabolism by Dr. Arya Mehran and colleagues found a result that, according to a press release, "could overturn widely accepted notions about healthy eating habits" (1), and has set the Internet abuzz.

In this study, researchers generated mice that lack one copy of the pancreatic insulin gene, and compared them to mice carrying both copies (2).  Then, they exposed both groups to a fattening diet, and found that mice lacking one copy of the insulin gene secreted less insulin than the comparison group (i.e., they did not develop the same degree of hyperinsulinemia).  These mice were also completely resistant to fat gain, while the comparison group became obese.  The authors came to some rather grandiose conclusions based on these results, suggesting that the "accepted model" that hyperinsulinemia is the result of obesity is "incompatible with our results that put the insulin hypersecretion genetically upstream of obesity".  Ergo, diet causes hyperinsulinemia, which causes fat gain.  It's a familiar argument to those who frequent Internet diet-health circles, except in this case the hyperinsulinemia is caused by a high-fat diet.

The problem is that the "accepted model" they want to replace overnight didn't come out of thin air-- it emerged from a large body of research, which was almost completely ignored by the authors.  When carefully considered, this evidence suggests an alternative explanation for the results of Dr. Mehran and colleagues.

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More Thoughts on Macronutrient Trends

I had a brief positive exchange with Gary Taubes about the NuSI post.  He reminded me that there's an artifact (measurement error) in the USDA data on fat consumption in the year 2000 when they changed assessment methods.  Here are the USDA data on macronutrient consumption since 1970, corrected for loss (28.8%) but not corrected for the artifact:

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