The Case for the Food Reward Hypothesis of Obesity, Part II

In this post, I'll explore whether or not the scientific evidence is consistent with the predictions of the food reward hypothesis, as outlined in the last post.

Before diving in, I'd like to address the critique that the food reward concept is a tautology or relies on circular reasoning (or is not testable/falsifiable).  This critique has no logical basis.  The reward and palatability value of a food is not defined by its effect on energy intake or body fatness.  In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1).  In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2).  In rodents, it is measured by observing stereotyped facial responses to palatable and unpalatable foods, which are similar to those seen in human infants.  It is not a tautology or circular reasoning to say that the reinforcing value or pleasantness of food influences food intake and body fatness. These are quantifiable concepts and as I will explain, their relationship with food intake and body fatness can be, and already has been, tested in a controlled manner. 

1.   Increasing the reward/palatability value of the diet should cause fat gain in animals and humans

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The Case for the Food Reward Hypothesis of Obesity, Part I

Introduction

When you want to investigate something using the scientific method, first you create a model that you hope describes a natural phenomenon-- this is called a hypothesis.  Then you go about testing that model against reality, under controlled conditions, to see if it has any predictive power.  There is rarely a single experiment, or single study, that can demonstrate that a hypothesis is correct.  Most important hypotheses require many mutually buttressing lines of evidence from multiple research groups before they're widely accepted.  Although it's not necessary, understanding the mechanism by which an effect occurs, and having that mechanism be consistent with the hypothesis, adds substantially to the case.

With that in mind, this post will go into greater detail on the evidence supporting food reward and palatability as major factors in the regulation of food intake and body fatness.  There is a large amount of supportive evidence at this point, which is rapidly expanding due to the efforts of many brilliant researchers, however for the sake of clarity and brevity, so far I've only given a "tip of the iceberg" view of it.  But there are two types of people who want more detail: (1) the skeptics, and (2) scientifically inclined people who want mechanism.  This post is for them.  It will get technical at times, as there is no other way to convey the material effectively.

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Humans on a Cafeteria Diet

In the 1970s, as the modern obesity epidemic was just getting started, investigators were searching for new animal models of diet-induced obesity.  They tried all sorts of things, from sugar to various types of fats, but none of them caused obesity as rapidly and reproducibly as desired*.  1976, Anthony Sclafani tried something new, and disarmingly simple, which he called the "supermarket diet": he gave his rats access to a variety of palatable human foods, in addition to standard rodent chow.  They immediately ignored the chow, instead gorging on the palatable food and rapidly becoming obese (1).  Later renamed the "cafeteria diet", it remains the most rapid and effective way of producing dietary obesity and metabolic syndrome in rodents using solid food (2).

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Primal Docs

Chris Armstrong, creator of the website Celiac Handbook, has designed a new non-commercial website called Primal Docs to help people connect with ancestral health-oriented physicians.  It's currently fairly small, but as more physicians join, it will become more useful.  If you are a patient looking for such a physician in your area, or an ancestral health-oriented physician looking for more exposure, it's worth having a look at his site:

Primal Docs

Update 9/22: apparently there is already another website that serves a similar purpose and has many more physicians enrolled: Paleo Physicians Network.

Fat Tissue Insulin Sensitivity and Obesity

In this post, I'll discuss a few more facts pertaining to the idea that elevated insulin promotes the accumulation of fat mass.  

Insulin Action on Fat Cells Over the Course of Fat Gain

The idea that insulin acts on fat cells to promote obesity requires that insulin suppress fat release in people with more fat (or people who are gaining fat) to a greater extent than in lean people.  As I have written before, this is not the case, and in fact the reverse is true.  The fat tissue of obese people fails to normally suppress fatty acid release in response to an increase in insulin caused by a meal or an insulin injection, indicating that insulin's ability to suppress fat release is impaired in obesity (1, 2, 3).  The reason for that is simple: the fat tissue of obese people is insulin resistant.

There has been some question around the blogosphere about when insulin resistance in fat tissue occurs.  Is it only observed in obese people, or does it occur to a lesser extent in people who carry less excess fat mass and are perhaps on a trajectory of fat gain?  To answer this question, let's turn the clocks back to 1968, a year before Neil Armstrong first set foot on the moon. 

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Hyperinsulinemia: Cause or Effect of Obesity?

Is Elevated Insulin the Cause or Effect of Obesity?

The carbohydrate hypothesis, in its most popular current incarnation, states that elevated insulin acts on fat cells to cause fat storage, leading to obesity.  This is due to its ability to increase the activity of lipoprotein lipase and decrease the activity of hormone-sensitive lipase, thus creating a net flux of fat into fat cells.  I'm still not sure why this would be the case, considering that fat tissue becomes more insulin resistant as body fat accumulates, therefore insulin action on it is not necessarily increased.  Total fat release from fat tissue increases with total fat mass (1), demonstrating that insulin is not able to do its job of suppressing fat release as effectively in people who carry excess fat.  But let's put that problem aside for the moment and keep trucking.

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Catered Paleo Dinner with Yours Truly

Gil Butler, organizer of the Western Washington Paleo Enthusiasts group, has organized a catered "paleo" dinner on Sunday, October 9th.  He will be screening the first episode of "Primal Chef", Featuring Robb Wolf and others.  He invited me to give a short (20 minute) presentation, which I accepted.  There are still roughly 30 spots remaining [update 9/21-- the event is full].

The event will be in the Ballard neighborhood of Seattle and the price is $15.76 per person.  I will not be paid for this talk, it's just an opportunity to share ideas and meet people. 

Click here to register.

Book Review: The End of Overeating

The End of Overeating was written based on the personal journey of Dr. David A. Kessler (MD) to understand the obesity epidemic, and treat his own obesity in the process.  Kessler was the FDA commissioner under presidents George HW Bush and Bill Clinton.  He is known for his efforts to regulate cigarettes, and his involvement in modernizing Nutrition Facts labels on packaged food.  He was also the dean of Yale medical school for six years-- a very accomplished person. 

Kessler's book focuses on 1) the ability of food with a high palatability/reward value to cause overeating and obesity, 2) the systematic efforts of the food industry to maximize food palatability/reward to increase sales in a competitive market, and 3) what to do about it.  He has not only done a lot of reading on the subject, but has also participated directly in food reward research himself, so he has real credibility.  The End of Overeating is not the usual diet book baloney. 
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A Roadmap to Obesity

In this post, I'll explain my current understanding of the factors that promote obesity in humans.  

Heritability

To a large degree, obesity is a heritable condition.  Various studies indicate that roughly two-thirds of the differences in body fatness between individuals is explained by heredity*, although estimates vary greatly (1).  However, we also know that obesity is not genetically determined, because in the US, the obesity rate has more than doubled in the last 30 years, consistent with what has happened to many other cultures (2).  How do we reconcile these two facts?  By understanding that genetic variability determines the degree of susceptibility to obesity-promoting factors.  In other words, in a natural environment with a natural diet, nearly everyone would be relatively lean, but when obesity-promoting factors are introduced, genetic makeup determines how resistant each person will be to fat gain.  As with the diseases of civilization, obesity is caused by a mismatch between our genetic heritage and our current environment.  This idea received experimental support from an interesting recent study (3).

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Seed Oils and Body Fatness-- A Problematic Revisit

Anthony Colpo recently posted a discussion of one of my older posts on seed oils and body fat gain (1), which reminded me that I need to revisit the idea.  As my knowledge of obesity and metabolism has expanded, I feel the evidence behind the hypothesis that seed oils (corn, soybean, etc.) promote obesity due to their linoleic acid (omega-6 fat) content has largely collapsed.

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Food Palatability and Body Fatness: Clues from Alliesthesia

Part I: Is there a Ponderostat?

Some of the most important experiments for understanding the role of food palatability/reward in body fatness were performed by Dr. Michel Cabanac and collaborators in the 1970s (hat tip to Dr. Seth Roberts for the references).  In my recent food reward series (1), I referenced but did not discuss Dr. Cabanac's work because I felt it would have taken too long to describe.  However, I included two of his studies in my Ancestral Health Symposium talk, and I think they're worth discussing in more detail here.

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I Got Boinged, and Other News

The reaction to my post "The Carbohydrate Hypothesis of Obesity: a Critical Examination" has been overwhelmingly positive, particularly among the scientists I've heard from. 

On Saturday, the inimitable maker and writer Mark Frauenfelder posted a link to my post on the variety blog BoingBoing.  BoingBoing has been on my sidebar for three years, and it's the place I go when I need a break.  It's a fun assortment of science, news, technology and entertainment.  BoingBoing was originally a zine started by Frauenfelder and his wife in 1988, and it has been on the web since 1995.  Today, it has multiple contributing authors and it draws several hundred thousand hits per day.  I'm thrilled that Frauenfelder posted my article there.  Apparently he likes my blog.  Thanks!

I added a new section (IIB) to my original post.  It discusses what human genetics can teach us about the mechanisms of common obesity.  It is consistent with the rest of the evidence suggesting that body fatness is primarily regulated by the brain, not by fat tissue, and that leptin signaling plays a dominant role in this process. 

The Carbohydrate Hypothesis of Obesity: a Critical Examination

Introduction

I'd like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health.  Although it doesn't work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people.  For a subset of people, the results can be very impressive.  I consider that to be a fact at this point, but that's not what I'll be discussing here. 

What I want to discuss is a hypothesis.  It's the idea, championed by Gary Taubes, that carbohydrate (particularly refined carbohydrate) causes obesity by elevating insulin, thereby causing increased fat storage in fat cells.  To demonstrate that I'm representing this hypothesis accurately, here is a quote from his book Good Calories, Bad Calories:

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Ancestral Health Symposium Drama

My full Ancestral Health Symposium talk is not yet online, but reader bentlleyj74 found a link to a You Tube video of most of my exchange with Gary Taubes following the talk.  You can find it here.  I'm not sure who shot it, but if you'd like credit, please contact me. 

I think I did an adequate job responding to his questions, but as I'm not the best at thinking on my feet, I can do better.  So here are his questions and my more complete responses.  This was all during one question and answer session; it was essentially an extended interrogation.  I'm paraphrasing Gary's questions for the most part to make them more concise, although the sections in quotation marks are direct quotes:

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Ancestral Health Symposium

Last weekend I attended the Ancestral Health Symposium at the University of California, Los Angeles, organized by Aaron Blaisdell, Brent Pottenger and Seth Roberts with help from many others.  It was a really great experience and I'm grateful to have been invited.  I was finally able to meet many of the people who I respect and admire, but knew only through the internet.  I'm not going to make a list because it would be too long, but if you take a look at the symposium schedule, I think you'll understand where I'm coming from.  I was also able to connect with a number of Whole Health Source readers, which was great.  I recognized some of them from the comments section.  Now I know it wasn't just my mom with 57 Google accounts.

The symposium was the first of its kind, and represented many facets of the ancestral health community, including "Paleolithic" diet and exercise patterns, low-carbohydrate diets, Weston Price-style diets, traditional health-nutrition researchers as well as other camps.  For the most part they coexisted peacefully and perhaps even learned a thing or two from one another. 

I was very impressed by the appearance of the attendees.  Young men and women were fit with glowing skin, and older attendees were energetic and aging gracefully.  It would be hard to come up with a better advertisement for ancestrally-oriented diets and lifestyles.  I saw a lot of people taking the stairs rather than the elevator.  I like to say I'll take the elevator/escalator when I'm dead.  I think integrating exercise into everyday life is healthy and efficient.  Escalators and elevators of course make sense for people with physical disabilities or heavy suitcases.

The first talk was by Dr. Boyd Eaton, considered by many to be the grandfather of the paleolithic diet concept.  I was very impressed by his composure, humility and compassionate attitude.  Half his talk was dedicated to environmental and social problems.  Dr. Staffan Lindeberg gave a talk titled "Food and Western Disease", which covered his paleolithic diet clinical trials as well as other evidence supporting ancestral diets.  I like Dr. Lindeberg's humble and skeptical style of reasoning.  I had the great pleasure of having dinner with Dr. Lindeberg and his wife, Dr. Eaton, Pedro Bastos, Dr. Lynda Frassetto, Dr. Guy-Andre Pelouze and his son Alexandre.  Pedro gave a very nice talk on the complexities of traditional and modern dairy.  The following night, I was able to connect with other writers I enjoy, including Chris Masterjohn, Melissa McEwen, John Durant, and Denise Minger. 

Dr. Pelouze is a french cardiovascular surgeon who strongly supports the food reward/palatability concept of obesity.  We had a conversation the evening before the conference, during which he basically made the same points I was going to make in my talk.  He is particularly familiar with the research of Dr. Michel Cabanac, who is central to the food reward idea.  He eats an interesting diet: mostly raw, omnivorous, and extremely simple.  If I understood correctly, he mostly eats raw meat, fish, fruit and vegetables with little or no preparation.  He sometimes cooks food if he wants to, but most of it is raw.  He believes simple, raw food allows the body's satiety systems to work more effectively.  He has been eating this way for more than twenty years, and his son was raised this way and is now about my age (if I recall correctly, Alexandre has a masters and is studying for an MD, and ultimately wants to become an MD/PhD).  Both of them look very good, are full of energy and have a remarkably positive mental state.  Alexandre told me that he never felt deprived growing up around other children who ate pastries, candy et cetera.  They woke up early and ran six miles before the conference began at 8 am. 

I gave my talk on Friday.  Giving a talk is not like writing a blog post-- it has to be much more cohesive and visually compelling.  I put a lot of work into it and it went really well.  Besides the heat I got from from Gary Taubes in the question and answer session, the response was very positive.  The talk, including the questions, will be freely available on the internet soon, as well as other talks from the symposium.  Some of it will be familiar to people who have read my body fat setpoint and food reward series, but it's a concise summary of the ideas and parts of it are new, so it will definitely be worthwhile to watch it.  

We have entered a new era of media communication.  Every time someone sneezed, it was live tweeted.  There are some good aspects to it-- it democratizes information by making it more accessible.  On the other hand, it's sometimes low quality information that contains inaccurate accounts and quotes that are subsequently recirculated. 

It was a great conference and I hope it was the first of many.

Interview on Super Human Radio

Today, I did an audio interview with Carl Lanore of Super Human Radio.  Carl seems like a sharp guy who focuses on physical fitness, nutrition, health and aging.  We talked mostly about food reward and body fatness-- I think it went well.  Carl went from obese to fit, and his fat loss experience lines up well with the food reward concept.  As he was losing fat rapidly, he told friends that he had "divorced from flavor", eating plain chicken, sweet potatoes and oatmeal, yet he grew to enjoy simple food over time.

The interview is here.  It also includes an interview of Dr. Matthew Andry about Dr. Loren Cordain's position on dairy; my interview starts at about 57 minutes.  Just to warn you, the website and podcast are both full of ads.

Weight Gain and Weight Loss in a Traditional African Society

The Massas is an ethnic group in Northern Cameroon that subsists mostly on plain sorghum loaves and porridge, along with a small amount of milk, fish and vegetables (1, 2).  They have a peculiar tradition called Guru Walla that is only undertaken by men (2, 1):
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Simple Food: Thoughts on Practicality

Some people have reacted negatively to the idea of a reduced-reward diet because it strikes them as difficult or unsustainable.  In this post, I'll discuss my thoughts on the practicality and sustainability of this way of eating.  I've also thrown in a few philosophical points about reward and the modern world.
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How Does Gastric Bypass Surgery Cause Fat Loss?

Gastric bypass surgery is an operation that causes food to bypass part of the digestive tract.  In the most common surgery, Roux-en-Y bypass, stomach size is reduced and a portion of the upper small intestine is bypassed.  This means that food skips most of the stomach and the duodenum (upper small intestine), passing from the tiny stomach directly into the jejunum (a lower part of the upper small intestine)*.  It looks something like this:
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Liposuction and Fat Regain

If body fat really is actively regulated by the body, rather than just being a passive result of voluntary food intake and exercise behaviors, then liposuction shouldn't be very effective at reducing total fat mass in the long run.  People should return to their body fat "setpoint" rather than remaining at a lower fat mass. 

Teri L. Hernandez and colleagues recently performed the first ever randomized liposuction study to answer this question (1).  Participants were randomly selected to either receive liposuction, or not.  They were all instructed not to make any lifestyle changes for the duration of the study, and body fatness was measured at 6 weeks, 6 months and one year by DXA. 

At 6 weeks, the liposuction group was significantly leaner than the control group.  At 6 months, the difference between the two groups had decreased.  At one year, it had decreased further and the difference between the groups was no longer statistically significant.  Furthermore, the liposuction group regained fat disproportionately in the abdominal area (belly), which is more dangerous than where it was before. The investigators stated:

We conclude that [body fat] is not only restored to baseline levels in nonobese women after small-volume liposuction, but is redistributed abdominally.

This is consistent with animal studies showing that when you surgically remove fat, total fat mass "catches up" to animals that had no fat removed (2).  Fat mass is too important to be left up to chance.  That's why the body regulates it, and that's why any satisfying resolution of obesity must address that regulatory mechanism.

Food Reward: a Dominant Factor in Obesity, Part VIII

Further reading

I didn't come up with the idea that excessive food reward increases calorie intake and can lead to obesity, far from it.  The idea has been floating around the scientific literature for decades.  In 1976, after conducting an interesting diet study in humans, Dr. Michel Cabanac stated that the "palatability of the diet influences the set point of the ponderostat [system that regulates body fatness]" (1).  

Currently there is a growing consensus that food reward/palatability is a major contributor to obesity. This is reflected by the proliferation of review articles appearing in high-profile journals.  For the scientists in the audience who want more detail than I provide on my blog, here are some of the reviews I've read and enjoyed.  These were written by some of the leading scientists in the study of food reward and hedonics:

Palatability of food and the ponderostat.  Michel Cabanac, 1989.
Food reward, hyperphagia and obesity.  Hans-Rudolf Berthoud et al., 2011.
Reward mechanisms in obesity: new insights and future directions.  Paul J. Kenny, 2011.
Relation of obesity to consummatory and anticipatory food reward.  Eric Stice, 2009.
Hedonic and incentive signals for body weight control.  Emil Egecioglu et al., 2011.
Homeostatic and hedonic signals interact in the control of food intake.  Michael Lutter and Eric J. Nestler, 2009.
Opioids as agents of reward-related feeding: a consideration of the evidence.  Allen S. Levine and Charles J. Billington, 2004.
Central opioids and consumption of sweet tastants: when reward outweighs homeostasis.  Pawel K. Olszewski and Allen S. Levine, 2007.
Oral and postoral determinants of food reward.  Anthony Sclafani, 2004.
Reduced dopaminergic tone in hypothalamic neural circuits: expression of a "thrifty" genotype underlying the metabolic syndrome?  Hanno Pijl, 2003.

If you can read all these papers and still not believe in the food reward hypothesis... you deserve some kind of award.

Food Reward: a Dominant Factor in Obesity, Part VII

Now that I've explained the importance of food reward to obesity, and you're tired of reading about it, it's time to share my ideas on how to prevent and perhaps reverse fat gain.  First, I want to point out that although food reward is important, it's not the only factor.  Heritable factors (genetics and epigenetics), developmental factors (uterine environment, childhood diet), lifestyle factors (exercise, sleep, stress) and dietary factors besides reward also play a role.  That's why I called this series "a dominant factor in obesity", rather than "the dominant factor in obesity".
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Drug Cessation and Weight Gain

Commenter "mem", who has been practicing healthcare for 30+ years, made an interesting remark that I think is relevant to this discussion:

Recovering substance dependent people often put on lots of weight and it is not uncommon for them to become obese or morbidly obese.

This relates to the question that commenter "Gunther Gatherer" and I have been pondering in the comments: can stimulating reward pathways through non-food stimuli influence body fatness?  

It's clear that smoking cigarettes, taking cocaine and certain other pleasure drugs suppress appetite and can prevent weight gain.  These drugs all activate dopamine-dependent reward centers, which is why they're addictive.  Cocaine in particular directly inhibits dopamine clearance from the synapse (neuron-neuron junction), increasing its availability for signaling.
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Food Reward: a Dominant Factor in Obesity, Part VI

Reward Centers can Modify the Body Fat Setpoint

Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain.  It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1).  Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2).  I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3).  The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
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