Can You Be Fit and Fat?

YES: In fact, it's a worthy goal.
Steven Blair, PED, professor of exercise science, epidemiology and biostatistics at the University of South Carolina

It's better than being thin and unfit.
Overweight people who exercise just 150 minutes a week have half the risk of mortality of normal-weight people who don't exercise at all, according to research I conducted. That's not true once you move from overweight (meaning a body mass index, or BMI, of 25 to 29.9) to obese (a BMI of 30 or more). But being fit and a little fat seems to be fine.

Weight alone doesn't raise disease risk-lack of fitness does.
In one study, half of overweight adults and one-third of obese people who were active had normal blood pressure, cholesterol, triglycerides, and blood sugar, putting them at normal risk for heart disease and diabetes, which are both supposedly caused by weight.

Getting fit is more realistic than getting slim.
For most people, diets don't work in the long term. We ought to be thinking about different strategies. It's far easier for a fat person to get fit than thin.

You can't be obese and fit.
Unless you're in that tiny fraction of the population-like pro athletes or the very muscular-whose muscle mass explains their high BMI. For most people with a BMI of 30 or more, their fitness is reduced by their weight, and their risk of conditions like diabetes and heart disease goes up.

Exercise doesn't erase all the risks of being heavy.
Yes, physical activity is important, but so is watching what you eat. Most studies show that both diet and exercise are important for diabetes prevention, for instance. And a study in the journal Obesity suggests that people with the highest BMIs have unhealthy eating habits.

Playing down the problem of excess weight is dangerous.
If you're heavy, you can cut your mortality risk by eating well and exercising-but research suggests that even active obese people are at 91% greater risk of dying than active people of normal weight.

A Sign of the Times

Every now and then, I venture out to go shopping at mainstream chain clothing stores.  Although I find it onerous, there are certain things I can't get at thrift stores.  For example, I can never find nice jeans.

The last time I set foot in these stores was about two years ago.  It was tough to find pants my size at that time-- many stores simply didn't sell pants with a 30 inch waist.  This year, it was even harder, since some of the stores that formerly carried 30W pants no longer did.  I managed to find my usual 30W 30L size in two stores, but I had a bizarre experience in both cases.   I put them on, and they were falling off my waist.  Since my waist size hasn't changed in two years, and my old 30W 30L pants of the same brand still fit the same as they did when I bought them two years ago, I have to conclude that both stores have changed their definition of "30 inches".  My new size is 28W 30L, which is tough to find these days.
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60 Minutes Report on the Flavorist Industry

A reader sent me a link to a recent CBS documentary titled "Tweaking Tastes and Creating Cravings", reported by Morley Safer.

Safer describes the "flavorist" industry, entirely dedicated to crafting irresistible odors for the purpose of selling processed and restaurant food.  They focused on the company Givaudin.  Dr. David Kessler, author of The End of Overeating, makes an appearance near the end.

Here are a few notable quotes:

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New Review Papers on Food Reward

As research on the role of reward/palatability in obesity continues to accelerate, interesting new papers are appearing weekly.  Here is a roundup of review papers I've encountered in the last three months.  These range from somewhat technical to very technical, but I think they should be mostly accessible to people with a background in the biological sciences. 

Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction
Written by Dr. Nora D. Volkow and colleagues.  This paper describes the similarities between the mechanisms of obesity and addiction, with a focus on human brain imaging studies.  Most researchers don't think obesity is an addiction per se, but the mechanisms (e.g., brain areas important for reward) do seem to overlap considerably.  This paper is well composed and got a lot of media attention.  Dr. Volkow is the director of the National Institute on Drug Abuse, a branch of the National Institutes of Health.  The NIH is the main source of biomedical research funding in the US, and also conducts its own research.

Here's a quote from the paper:

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Another Simple Food Weight Loss Experience

Whole Health Source reader Sarah Pugh recently went on a six-week simple food (low reward) diet to test its effectiveness as a weight loss strategy, and she was kind enough to describe her experience for me, and provide a link to her blog where she discussed it in more detail (1). 

Consistent with the scientific literature and a number of previous reader anecdotes (2), Sarah experienced a reduction in appetite on the simple food diet, losing 15 pounds in 6 weeks without hunger.  In contrast to her prior experiences with typical calorie restriction, her energy level and mood remained high over this period.  Here's a quote from her blog:

Well, it looks like the theory that in the absence of nice palatable food, the body will turn quite readily to fat stores and start munching them up, is holding up. At the moment, the majority of the energy I use is coming from my insides, and my body is using it without such quibbles as the increased hunger, low energy, crappy thermo-regulation or bitchiness normally associated with severe calorie restriction.

I can't promise that everyone will experience results like this, but this is basically what the food reward hypothesis suggests should be possible, and it seems to work this way for many people.  That's one of the reasons why this idea interests me so much.

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A Brief Response to Taubes's Food Reward Critique, and a Little Something Extra

It appears Gary Taubes has completed his series critiquing the food reward hypothesis of obesity (1).  I have to hand it to him, it takes some cojones to critique an entire field of research, particularly when you have no scientific background in it.

The food reward hypothesis of obesity states that the reward and palatability value of food influence body fatness, and excess reward/palatability can promote body fat accumulation.  If we want to test the hypothesis, the most direct way is to find experiments in which 1) the nutritional qualities of the experimental diet groups are kept the same or at least very similar, 2) some aspect of diet reward/palatability differs, and 3) changes in body fat/weight are measured (for example, 2, 3, 4, 5, 6, 7, 8, 9).  In these experiments the hypothesis has both arms and one leg tied behind its back, because the most potent reward factors (energy density, sugar, fat) have nutritional value and therefore experiments that modify these cannot be tightly controlled for nutritional differences.  Yet even with this severe disadvantage, the hypothesis is consistently supported by the scientific evidence.  Taubes repeatedly stated in his series that controlled studies like these have not been conducted, apparently basing this belief on a 22-year-old review paper by Dr. Israel Ramirez and colleagues that does not contain the word 'reward' (10).

Another way to test the hypothesis is to see if people with higher food reward sensitivity (due to genetics or other factors) tend to gain more fat over time (for example, 11, 12, 13, 14, 15, 16).  In addition, studies that have examined the effect of palatability/reward on food intake in a controlled manner are relevant (17, 18, 19, 20, 21, 22), as are studies that have identified some of the mechanisms by which these effects occur (reviewed in 23).  Even if not all of the studies are perfect, at some point, one has to acknowledge that there are a lot of mutually buttressing lines of evidence here.  It is notable that virtually none of these studies appeared in Taubes's posts, and he appeared largely unaware of them. 
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Two Recent Papers by Matt Metzgar

This is just a quick post to highlight two recent papers by the economist and fellow health writer Matt Metzgar.

The first paper is titled "The Feasibility of a Paleolithic Diet for Low-income Consumers", and is co-authored by Dr. Todd C. Rideout, Maelan Fontes-Villalba, and Dr. Remko S. Kuipers (1).  They found that a Paleolithic-type diet that meets all micronutrient requirements except calcium (which probably has an unnecessarily high RDA) costs slightly more money than a non-Paleolithic diet that fulfills the same requirements, but both are possible on a tight budget. 

The second paper is titled "Externalities From Grain Consumption: a Survey", with Matt Metzgar as the sole author (2).  He reviews certain positive and negative externalities due to the effects of grain consumption on health.  The take-home message is that refined grains are unhealthy and therefore costly to society, whole grains are better, but grains in general have certain healthcare-related economic costs that are difficult to deny, such as celiac disease.

There are a lot of ideas floating around on the blogosphere, some good and others questionable.  Composing a manuscript and submitting it to a reputable scientific journal is a good way to demonstrate that your idea holds water, and it's also a good way to communicate it to the scientific community.  The peer review process isn't perfect but it does encourage scientific rigor.  I think Metzgar is a good example of someone who has successfully put his ideas through this process.  Pedro Bastos, who also spoke at the Ancestral Health Symposium, is another example (3).

Does High Circulating Insulin Drive Body Fat Accumulation? Answers from Genetically Modified Mice

The house mouse Mus musculus is an incredible research tool in the biomedical sciences, due to its ease of care and its ability to be genetically manipulated.  Although mice aren't humans, they resemble us closely in many ways, including how insulin signaling works.  Genetic manipulation of mice allows researchers to identify biological mechanisms and cause-effect relationships in a very precise manner.  One way of doing this is to create "knockout" mice that lack a specific gene, in an attempt to determine that gene's importance in a particular process.  Another way is to create transgenic mice that express a gene of interest, often modified in some way.  A third method is to use an extraordinary (but now common) tool called "Cre-lox" recombination (1), which allows us to delete or add a single gene in a specific tissue or cell type. 

Studying the relationship between obesity and insulin resistance is challenging, because the two typically travel together, confounding efforts to determine which is the cause and which is the effect of the other (or neither).  Some have proposed the hypothesis that high levels of circulating insulin promote body fat accumulation*.  To truly address this question, we need to consider targeted experiments that increase circulating insulin over long periods of time without altering a number of other factors throughout the body.  This is where mice come in.  Scientists are able to perform precise genetic interventions in mice that increase circulating insulin over a long period of time.  These mice should gain fat mass if the hypothesis is correct. 

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The Brain Controls Insulin Action

Insulin regulates blood glucose primarily by two mechanisms:

1. Suppressing glucose production by the liver
2. Enhancing glucose uptake by other tissues, particularly muscle and liver

Since the cells contained in liver, muscle and other tissues respond directly to insulin stimulation, most people don't think about the role of the brain in this process.  An interesting paper just published in Diabetes reminds us of the central role of the brain in glucose metabolism as well as body fat regulation (1).  Investigators showed that by inhibiting insulin signaling in the brains of mice, they could diminish insulin's ability to suppress liver glucose production by 20%, and its ability to promote glucose uptake by muscle tissue by 59%.  In other words, the majority of insulin's ability to cause muscle to take up glucose is mediated by its effect on the brain. 

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Harvard Food Law Society "Forum on Food Policy" TEDx Conference

Last Friday, it was my pleasure to attended and present at the Harvard Food Law Society's TEDx conference, Forum on Food Policy.  I had never been to Cambridge or Boston before, and I was struck by how European they feel compared to Seattle.  The conference was a great success, thanks to the dedicated efforts of the Food Law Society's presidents Nate Rosenberg, Krista DeBoer, and many other volunteers. 

Dr. Robert Lustig gave a keynote address on Thursday evening, which I unfortunately wasn't able to attend due to my flight schedule.  From what I heard, he focused on practical solutions for reducing national sugar consumption, such as instituting a sugar tax.  Dr. Lustig was a major presence at the conference, and perhaps partially due to his efforts, sugar was a central focus throughout the day.  Nearly everyone agrees that added sugar is harmful to the nation's health at current intakes, so the question kept coming up "how long is it going to take us to do something about it?"  As Dr. David Ludwig said, "...the obesity epidemic can be viewed as a disease of technology with a simple, but politically difficult solution".

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Losing Fat With Simple Food-- Two Reader Anecdotes

Each week, I'm receiving more e-mails and comments from people who are successfully losing fat by eating simple (low reward) food, similar to what I described here.  In some cases, people are breaking through fat loss plateaus that they had reached on conventional low-carbohydrate, low-fat or paleo diets.  This concept can be applied to any type of diet, and I believe it is an important characteristic of ancestral food patterns.

At the Ancestral Health Symposium, I met two Whole Health Source readers, Aravind Balasubramanian and Kamal Patel, who were interested in trying a simple diet to lose fat and improve their health.  In addition, they wanted to break free of certain other high-reward activities in their lives that they felt were not constructive.  They recently embarked on an 8-week low-reward diet and lifestyle to test the effectiveness of the concepts.  Both of them had previously achieved a stable (in Aravind's case, reduced) weight on a paleo-ish diet prior to this experiment, but they still carried more fat than they wanted to.  They offered to write about their experience for WHS, and I thought other readers might find it informative.  Their story is below, followed by a few of my comments.

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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

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.

Dietary Guidelines for Americans, My Way

I just saw this on BoingBoing.  Simple but true. 

This image was created by Adam Fields. 

The people who design government dietary guidelines are gagged by the fact that politics and business are so tightly intertwined in this country.  Their advice will never directly target the primary source of obesity and metabolic dysfunction-- industrially processed food-- because that would hurt corporate profits in one of the country's biggest economic sectors.  You can only squeeze so much profit out of a carrot, so food engineers design "value-added" ultrapalatable/rewarding foods with a larger profit margin.

We don't even have the political will to regulate food advertisements directed at defenseless children, which are systematically training them from an early age to prefer foods that are fattening and unhealthy.  This is supposedly out of a "free market" spirit, but that justification is hollow because processed food manufacturers benefit from tax loopholes and major government subsidies, including programs supporting grain production and the employment of disadvantaged citizens (see Fast Food Nation).

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".
Read more »

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.
Read more »

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.
Read more »

Food Reward: a Dominant Factor in Obesity, Part V

Non-industrial diets from a food reward perspective

In 21st century affluent nations, we have unprecedented control over what food crosses our lips.  We can buy nearly any fruit or vegetable in any season, and a massive processed food industry has sprung up to satisfy (or manufacture) our every craving.  Most people can afford exotic spices and herbs from around the world-- consider that only a hundred years ago, black pepper was a luxury item.  But our degree of control goes even deeper: over the last century, kitchen technology such as electric/gas stoves, refrigerators, microwaves and a variety of other now-indispensable devices have changed the way we prepare food at home (Megan J. Elias.  Food in the United States, 1890-1945). 

To help calibrate our thinking about the role of food reward (and food palatability) in human evolutionary history, I offer a few brief descriptions of contemporary hunter-gatherer and non-industrial agriculturalist diets.  What did they eat, and how did they prepare it? 
Read more »

Food Reward: a Dominant Factor in Obesity, Part IV

What is Food Reward?

After reading comments on my recent posts, I realized I need to do a better job of defining the term "food reward".  I'm going to take a moment to do that here.  Reward is a psychology term with a specific definition: "a process that reinforces behavior" (1).  Rewarding food is not the same thing as food that tastes good, although they often occur together. 

Read more »

Healthy Skeptic Podcast

Chris Kresser has just posted our recent interview/discussion on his blog The Healthy Skeptic.  You can listen to it on Chris's blog here.  The discussion mostly centered around body fat and food reward.  I also answered a few reader questions.  Here are some highlights:

• How does the food reward system work? Why did it evolve?
• Why do certain flavors we don’t initially like become appealing over time?
• How does industrially processed food affect the food reward system?
• What’s the most effective diet used to make rats obese in a research setting? What does this tell us about human diet and weight regulation?
• Do we know why highly rewarding food increases the set point in some people but not in others?
• How does the food reward theory explain the effectiveness of popular fat loss diets?
• Does the food reward theory tell us anything about why traditional cultures are generally lean?
• What does cooking temperature have to do with health?
• Reader question: How does one lose fat?
• Reader question: What do I (Stephan) eat?
• Reader question: Why do many people gain fat with age, especially postmenopausal women?

The podcast is a sneak preview of some of the things I'll be discussing in the near future.  Enjoy!

Fast Food, Weight Gain and Insulin Resistance

CarbSane just posted an interesting new study that fits in nicely with what we're discussing here.  It's part of the US Coronary Artery Risk Development in Young Adults (CARDIA) study, which is a long-term observational study that is publishing many interesting findings.  The new study is titled "Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis" (1).  The results speak for themselves, loud and clear (I've edited some numbers out of the quote for clarity):
Read more »

Food Reward: a Dominant Factor in Obesity, Part III

Low-Fat Diets

In 2000, the International Journal of Obesity published a nice review article of low-fat diet trials.  It included data from 16 controlled trials lasting from 2-12 months and enrolling 1,910 participants (1).  What sets this review apart is it only covered studies that did not include instructions to restrict calorie intake (ad libitum diets).  On average, low-fat dieters reduced their fat intake from 37.7 to 27.5 percent of calories.  Here's what they found:
Read more »

Clarifications About Carbohydrate and Insulin

My statements about carbohydrate and insulin in the previous post seem to have kicked up some dust!  Some people are even suggesting I've gone low-fat!  I'm going to take this opportunity to be more specific about my positions.

I do not think that post-meal insulin spikes contribute to obesity, and they may even oppose it. Elevated fasting insulin is a separate issue-- that's a marker of insulin resistance.  It's important not to confuse the two.  Does insulin resistance contribute to obesity?  I don't know, but it's hypothetically possible since insulin acts like leptin's kid brother in some ways.  As far as I can tell, starch per se and post-meal insulin spikes do not lead to insulin resistance.
Read more »

Healthy Skeptic Podcast and Reader Questions

Chris Kresser, Danny Roddy and I just finished recording the podcast that will be released on May 24th.  It went really well, and we think you'll find it informative and maybe even practical!

Unfortunately, we only got around to answering three of the questions I had selected:

1. How does one lose fat?
2. What do I (Stephan) eat?
3. Why do many people gain fat with age, especially postmenopausal women?

I feel guilty about that, so I'm going to answer three more right now.

Read more »

Administrative Note

My blog is being mercilessly ripped off by cheesy feed aggregators that are using my material for commercial gain, often without attribution.  I was able to ignore them when there were only one or two, and when they appeared far down the list on Google searches.  But at this point, there are 20+ rip-off sites that ride my coattails under questionable circumstances, and are getting decent Google rankings, so I've had enough.  I'm changing my feed settings so that I only partially syndicate my posts, and I'm adding a short plagiarism warning to each post.

What that means is that if you're using an RSS reader, you'll have to click through to my blog to read my material in full.  I apologize for the inconvenience, but I don't see any other solution.

Read more »

Ask Me a Question

On May 13th, I'll be recording a podcast with Chris Kresser of The Healthy Skeptic. Chris interviewed me about a year ago, and I thought it went well. Chris is a good host and asks interesting questions.

This time around, we're going to do things a bit differently. I'll start with a little overview of my current thoughts on obesity, then we'll answer reader questions. The show is going to be mostly about obesity and related matters, but I may answer a couple of questions that aren't related to obesity if they're especially interesting. There are two ways to leave questions: either in the comments section of this post, or the comments section of Chris's post. The show will air on May 24th.
Read more »

Food Reward: a Dominant Factor in Obesity, Part II

How to Make a Rat Obese

Rodents are an important model organism for the study of human obesity. To study obesity in rodents, you have to make them fat first. There are many ways to do this, from genetic mutations, to brain lesions, to various diets. However, the most rapid and effective way to make a normal (non-mutant, non-lesioned) rodent obese is the "cafeteria diet." The cafeteria diet first appeared in the medical literature in 1976 (1), and was quickly adopted by other investigators. Here's a description from a recent paper (2):

In this model, animals are allowed free access to standard chow and water while concurrently offered highly palatable, energy dense, unhealthy human foods ad libitum.

In other words, they're given an unlimited amount of human junk food in addition to their whole food-based "standard chow." In this particular paper, the junk foods included Froot Loops, Cocoa Puffs, peanut butter cookies, Reese's Pieces, Hostess Blueberry MiniMuffins, Cheez-its, nacho cheese Doritos, hot dogs, cheese, wedding cake, pork rinds, pepperoni slices and other industrial delicacies. Rats exposed to this food almost completely ignored their healthier, more nutritious and less palatable chow, instead gorging on junk food and rapidly attaining an obese state.

Investigators have known for decades that the cafeteria diet is a highly effective way of producing obesity in rodents, but what was interesting about this particular study from my perspective is that it compared the cafeteria diet to three other commonly used rodent diets: 1) standard, unpurified chow; 2) a purified/refined high-fat diet; 3) a purified/refined low-fat diet designed as a comparator for the high-fat diet. All three of these diets were given as homogeneous pellets, and the textures range from hard and fibrous (chow) to soft and oily like cookie dough (high-fat). The low-fat diet contains a lot of sugar, the high-fat diet contains a modest amount of sugar, and the chow diet contains virtually none. The particular high-fat diet in this paper (Research Diets D12451, 45% fat, which is high for a rat) is commonly used to produce obesity in rats, although it's not always very effective. The 60% fat version is more effective.

Consistent with previous findings, rats on every diet consumed the same number of calories over time... except the cafeteria diet-fed rats, which ate 30% more than any of the other groups. Rats on every diet gained fat compared to the unpurified chow group, but the cafeteria diet group gained much more than any of the others. There was no difference in fat gain between the purified high-fat and low-fat diets.

So in this paper, they compared two refined diets with vastly different carb:fat ratios and different sugar contents, and yet neither equaled the cafeteria diet in its ability to increase food intake and cause fat gain. The fat, starch and sugar content of the cafeteria diet was not able to fully explain its effect on fat gain. However, each diets' ability to cause fat gain correlated with its respective food reward qualities. Refined diets high in fat or sugar caused fat gain in rats relative to unpurified chow, but were surpassed by a diet containing a combination of fat, sugar, starch, salt, free glutamate (umami), interesting textures and pleasant and invariant aromas.

Although the cafeteria diet is the most effective at causing obesity in rodents, it's not commonly used because it's a lot more work than feeding pellets, and it introduces a lot of variability into experiments because each rat eats a different combination of foods.

How to Make an Obese Human Lean

In 1965, the Annals of the New York Academy of Sciences published a very unusual paper (3). Here is the stated goal of the investigators:

The study of food intake in man is fraught with difficulties which result from the enormously complex nature of human eating behavior. In man, in contrast to lower animals, the eating process involves an intricate mixture of physiologic, psychologic, cultural and esthetic considerations. People eat not only to assuage hunger, but because of the enjoyment of the meal ceremony, the pleasures of the palate and often to gratify unconscious needs that are hard to identify. Because of inherent difficulties in studying human food intake in the usual setting, we have attempted to develop a system that would minimize the variables involved and thereby improve the chances of obtaining more reliable and reproducible data.

Here's a photo of their "system":
It's a machine that dispenses bland liquid food through a straw, at the push of a button. They don't give any information on the composition of the liquid diet, beyond remarking that "carbohydrate supplied 50 per cent of the calories, protein 20 per cent and fat 30 per cent. the formula contained vitamins and minerals in amount adequate for daily maintenance."

Volunteers were given access to the machine and allowed to consume as much of the liquid diet as they wanted, but no other food. Since they were in a hospital setting, the investigators could be confident that the volunteers ate nothing else.

The first thing they report is what happened when they fed two lean people using the machine, for 16 or 9 days. Both of them maintained their typical calorie intake (~3,075 and ~4,430 kcal per day) and maintained a very stable weight during this period.

Next, the investigators did the same experiment using two "grossly obese" volunteers. Again, they were asked to "obtain food from the machine whenever hungry." Over the course of the first 18 days, the first (male) volunteer consumed a meager 275 calories per day. The second (female) volunteer consumed a ridiculously low 144 calories per day over the course of 12 days, losing 23 pounds. Without showing data, the investigators remarked that an additional three obese volunteers "showed a similar inhibition of calorie intake when fed by machine."

The first volunteer continued eating bland food from the machine for a total of 70 days, losing approximately 70 pounds. After that, he was sent home with the formula and instructed to drink 400 calories of it per day, which he did for an additional 185 days, after which his total weight loss was 200 lbs. The investigators remarked that "during all this time weight was steadily lost and the patient never complained of hunger or gastrointestinal discomfort." This is truly a starvation-level calorie intake, and to eat it continually for 255 days without hunger suggests that something rather interesting was happening in this man's body.

This machine-feeding regimen was nearly as close as one can get to a diet with no rewarding properties whatsoever. Although it contained carbohydrate and fat, it did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized. As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a "broken" metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. This also implies that obesity may not be a disorder, but rather a normal response to the prevailing dietary environment in affluent nations.

A second study by Dr. Michel Cabanac in 1976 confirmed that reducing food reward (by feeding bland food) lowers the fat mass setpoint in humans, using a clever method that I won't discuss for the sake of brevity (4). I learned about both of these studies through the writing of Dr. Seth Roberts, author of The Shangri-La Diet. I'd also like to thank Dr. Stephen Benoit, a researcher in the food reward field, for talking through these ideas with me to make sure I wasn't misinterpreting them.

I'd like to briefly remark that there's an anatomical basis for the idea of two-way communication between brain regions that determine reward and those that control body fatness. It's well known that the latter influence the former (think about your drive to obtain food after you've just eaten a big meal vs. after you've skipped a meal), but there are also connections from the former to the latter via a brain region called the lateral hypothalamus. The point is that it's anatomically plausible that food reward determines in part the amount of body fat a person carries.

Some people may be inclined to think "well, if food tastes bad, you eat less of it; so what!" Although that may be true to some extent, I don't think it can explain the fact that bland diets affect the calorie intake of lean and obese people differently. To me, that implies that highly rewarding food increases the body fat setpoint in susceptible people, and that food with few rewarding properties allows them to return to a lean state.

In the next few posts, I'll describe how food reward explains the effectiveness of many popular fat loss diets, I'll describe how this hypothesis fits in with the diets and health of non-industrial cultures, and I'll outline new dietary strategies for preventing and treating obesity and certain forms of metabolic dysfunction.

Food Reward: a Dominant Factor in Obesity, Part I

A Curious Finding

It all started with one little sentence buried in a paper about obese rats. I was reading about how rats become obese when they're given chocolate Ensure, the "meal replacement drink", when I came across this:

...neither [obesity-prone] nor [obesity-resistant] rats will overeat on either vanilla- or strawberry-flavored Ensure.

The only meaningful difference between chocolate, vanilla and strawberry Ensure is the flavor, yet rats eating the chocolate variety overate, rapidly gained fat and became metabolically ill, while rats eating the other flavors didn't (1). Furthermore, the study suggested that the food's flavor determined, in part, what amount of fatness the rats' bodies "defended."

As I explained in previous posts, the human (and rodent) brain regulates the amount of fat the body carries, in a manner similar to how the brain regulates blood pressure, body temperature, blood oxygenation and blood pH (2). That fact, in addition to several other lines of evidence, suggests that obesity probably results from a change in this regulatory system. I refer to the amount of body fat that the brain defends as the "body fat setpoint", however it's clear that the setpoint is dependent on diet and lifestyle factors. The implication of this paper that I could not escape is that a food's flavor influences body fatness and probably the body fat setpoint.

An Introduction to Food Reward

The brain contains a sophisticated system that assigns a value judgment to everything we experience, integrating a vast amount of information into a one-dimensional rating system that labels things from awesome to terrible. This is the system that decides whether we should seek out a particular experience, or avoid it. For example, if you burn yourself each time you touch the burner on your stove, your brain will label that action as bad and it will discourage you from touching it again. On the other hand, if you feel good every time you're cold and put on a sweater, your brain will encourage that behavior. In the psychology literature, this phenomenon is called "reward," and it's critical to survival.

The brain assigns reward to, and seeks out, experiences that it perceives as positive, and discourages behaviors that it views as threatening. Drugs of abuse plug directly into reward pathways, bypassing the external routes that would typically trigger reward. Although this system has been studied most in the context of drug addiction, it evolved to deal with natural environmental stimuli, not drugs.

As food is one of the most important elements of survival, the brain's reward system is highly attuned to food's rewarding properties. The brain uses input from smell, taste, touch, social cues, and numerous signals from the digestive tract* to assign a reward value to foods. Experiments in rats and humans have outlined some of the qualities of food that are inherently rewarding:

• Fat
• Starch
• Sugar
• Salt
• Meatiness (glutamate)
• The absence of bitterness
  
• Certain textures (e.g., soft or liquid calories, crunchy foods)
• Certain aromas (e.g., esters found in many fruits)
• Calorie density ("heavy" food)
  

We are generally born liking the qualities listed above, and aromas and flavors that are associated with these qualities become rewarding over time. For example, beer tastes terrible the first time you drink it because it's bitter, but after you drink it a few times and your brain catches wind that there are calories and a drug in there, it often begins tasting good. The same applies to many vegetables. Children are generally not fond of vegetables, but if you serve them spinach smothered in butter enough times, they'll learn to like it by the time they're adults.

The human brain evolved to deal with a certain range of rewarding experiences. It didn't evolve to constructively manage strong drugs of abuse such as heroin and crack cocaine, which overstimulate reward pathways, leading to the pathological drug seeking behaviors that characterize addiction. These drugs are "superstimuli" that exceed our reward system's normal operating parameters. Over the next few posts, I'll try to convince you that in a similar manner, industrially processed food, which has been professionally crafted to maximize its rewarding properties, is a superstimulus that exceeds the brain's normal operating parameters, leading to an increase in body fatness and other negative consequences.


* Nerves measure stomach distension. A number of of gut-derived paracrine and endocrine signals, including CCK, PYY, ghrelin, GLP-1 and many others potentially participate in food reward sensing, some by acting directly on the brain via the circulation, and others by signaling indirectly via the vagus nerve. More on this later.

Upcoming Talks

I'll be giving at least two talks at conferences this year:

Ancestral Health Symposium; "The Human Ecological Niche and Modern Health"; August 5-6 in Los Angeles. This is going to be a great conference. Many of my favorite health/nutrition writers will be presenting. Organizer Brent Pottenger and I collaborated on designing the symposium's name so I hope you like it.

My talk will be titled "Obesity; Old Solutions to a New Problem." I'll be presenting some of my emerging thoughts on obesity. I expect to ruffle some feathers!

Tickets are going fast so reserve one today! I doubt there will be any left two weeks from now.


TEDx Harvard Law; "Food Policy and Public Health"; Oct 21 at Harvard. My talk is tentatively titled "The American Diet: a Historical Perspective." This topic interests me because it helps us frame the discussion on why chronic disease is so prevalent today, and what are the appropriate public health measures to combat it. This should also be a great conference.

Obesity and the Fluid-in, Fluid-out Therapy for Edema

I recently attended a lecture by Dr. Arya M. Sharma here at the University of Washington. Dr. Sharma is a Canadian clinician who specializes in the treatment of obesity. He gave the UW Science in Medicine lecture, which is a prestigious invited lecture.

He spent a little bit of time pointing out the fallacy behind conventional obesity treatment. He used the analogy of edema, which is an abnormal accumulation of fluid in the body.

Since we know that the amount of fluid contained in the body depends on the amount of fluid entering the body and the amount of fluid leaving the body, the treatment for edema is obvious: drink less, pee more.

Of course, this makes no sense. It doesn't address the underlying cause of edema and it will not help the patient. Yet we apply that exact same logic to fat loss. Since the amount of energy contained in the body (in the form of fat) depends on the amount entering and the amount leaving, the solution is easy: eat less, move more. Well, yes, if you can stick to that program it will cause fat loss. But that's equivalent to telling someone with edema to drink less water. It will cause a loss of fluid, but it won't correct the underlying problem that caused excessive fluid retention in the first place.

For example, if you have edema because your heart isn't pumping effectively (cardiac insufficiency), the heart is the problem that must be addressed. Any other treatment is purely symptomatic and is not a cure.

The same applies to obesity. If you don't correct the alteration in the system that causes an obese person to 'defend' his elevated fat mass against changes*, anything you do is symptomatic treatment and is unlikely to be very effective in the long term. My goal is to develop a method that goes beyond symptomatic treatment and allows the body to naturally return to a lower fat mass. I've been doing a lot of reading and I have a simple new idea that I feel confident in. It also neatly explains the results of a variety of weight loss diets. I've dropped a few hints here and there, but I'll be formally unveiling it in the next couple of months. Stay tuned.


* The body fat homeostasis system. The core element appears to be a negative feedback loop between body fat (via leptin, and insulin to a lesser degree) and the brain (primarily the hypothalamus, but other regions are involved). There are many other elements in the system, but that one seems to set the 'gain' on all the others and guides long-term fat mass homeostasis. The brain is the gatekeeper of both energy intake and energy expenditure, and unconscious processes strongly suggest appropriate levels for both factors according to the brain's perceived homeostatic needs. Those suggestions can be overridden consciously, but it requires a perpetual high degree of discipline, whereas someone who has been lean all her life doesn't require discipline to remain lean because her brain is suggesting behaviors that naturally defend leanness. I know what I'm saying here may seem controversial to some people reading this, because it's contrary to what they've read on the internet or in the popular press, but it's not particularly controversial in my field. In fact, you'll find most of this stuff in general neuroscience textbooks dating back more than 10 years (e.g., Eric Kandel and colleagues, Principles of Neuroscience).

US Omega-6 and Omega-3 Fat Consumption over the Last Century

Omega-6 and omega-3 polyunsaturated fats (PUFA) are essential nutrients that play many important roles in the body. They are highly bioactive, and so any deviation from ancestral intake norms should probably be viewed with suspicion. I've expressed my opinion many times on this blog that omega-6 consumption is currently too high due to our high intake of refined seed oils (corn, soybean, sunflower, etc.) in industrial nations. Although it's clear that the quantity of omega-6 and omega-3 polyunsaturated fat have changed over the last century, no one had ever published a paper that attempted to systematically quantify it until last month (1).

Drs. Chris Ramsden and Joseph Hibbeln worked on this paper (the first author was Dr. Tanya Blasbalg and the senior author was Dr. Robert Rawlings)-- they were the first and second authors of a different review article I reviewed recently (2). Their new paper is a great reference that I'm sure I'll cite many times. I'm going to briefly review it and highlight a few key points.

1. The intake of omega-6 linoleic acid has increased quite a bit since 1909. It would have been roughly 2.3% of calories in 1909, while in 1999 it was 7.2%. That represents an increase of 213%. Linoleic acid is the form of omega-6 that predominates in seed oils.

2. The intake of omega-3 alpha-linolenic acid has also increased, for reasons that I'll explain below. It changed from 0.35% of calories to 0.72%, an increase of 109%.

3. The intake of long-chain omega-6 and omega-3 fats have decreased. These are the highly bioactive fats for which linoleic acid and alpha-linolenic acid are precursors. Arachidonic acid, DHA, DPA and EPA intakes have declined. This mostly has to do with changing husbandry practices and the replacement of animal fats with seed oils in the diet.

4. The ratio of omega-6 to omega-3 fats has increased. There is still quite a bit of debate over whether the ratios matter, or simply the absolute amount of each. I maintain that there is enough evidence from highly controlled animal studies and the basic biochemistry of PUFAs to tentatively conclude that the ratio is important. At a minimum, we know that excess linoleic acid inhibits omega-3 metabolism (3, 4, 5, 6). The omega-6:3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009, a 78% increase.

5. The biggest factor in both linoleic acid and alpha-linolenic acid intake changes was the astonishing rise in soybean oil consumption. Soybean oil consumption increased from virtually nothing to 7.4% of total calories, eclipsing all sources of calories besides sugar, dairy and grains! That's because processed food is stuffed with it. It's essentially a byproduct of defatted soybean meal-- the second most important animal feed after corn. Check out this graph from the paper:

I think this paper is an important piece of the puzzle as we try to figure out what happened to nutrition and health in the US over the last century.

Fat-ten-u

I recently bought the book Food in the United States, 1820s-1890. I came across an ad for an interesting product that was sold in the late 1800s called Fat-ten-u. Check your calendars, it's not April fools day anymore; this is for real. Fat-ten-u was a dietary supplement guaranteed to "make the thin plump and rosy with honest fleshiness of form." I found several more ads for it online, and they feature drawings of despondent, lean women and drawings of happy overweight women accompanied by enthusiastic testimonials such as this:

"FAT-TEN-U FOODS increased my weight 39 pounds, gave me new womanly vigor and developed me finely. My two sisters also use FAT-TEN-U and because of our newly found vigor we have taken up Grecian dancing and have roles in all local productions."

I'm dying to know what was in this stuff, but I can't find the ingredients anywhere.

I find this rather extraordinary, for two reasons:

• Social norms have clearly changed since the late 1800s. Today, leanness is typically considered more attractive than plumpness.
• Women had to make an effort to become overweight in the late 1800s. In 2011, roughly two-thirds of US women are considered overweight or obese, despite the fact that most of them would rather be lean.

A rhetorical question: did everyone count calories in the 1800s, or did their diet and lifestyle naturally promote leanness? The existence of Fat-ten-u is consistent with the idea that our bodies naturally "defended" a lean body composition more effectively in the late 1800s, when our diets were less industrialized. This is supported by the only reliable data on obesity prevalence in the 1890s I'm aware of: body height and weight measurements from over 35,000 Union civil war veterans aged 40-69 years old (1). In that group of Caucasian men, obesity was about 10% of what it is today in the same age group. Whether or not you believe that this sample was representative of the population at large, I can't imagine any demographic in the modern US with an obesity prevalence of 3 percent (certainly not 60 year old war veterans).

Here are two more ads for Fat-ten-u and "Corpula foods" for your viewing pleasure:

Great New Product

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Bozolol is an amazing nutritional supplement extracted from the bozolol berry, harvested wild in the heart of the Amazon rainforest. To the native Ilotaca tribe, the bozolol berry is sacred because it alters the molecules in your brain to make you smarter AND sexier.

Here's how it works: bozolol actually increases the uptake of fat-soluble vitamins from your food, while reducing inflammation in the arteries and helping you shed fat faster than a pork roast! Guaranteed! Learn more about it here. 

April fools!

Dr. Kevin Patterson on Western Diets and Health

A few readers have pointed me to an interesting NPR interview with the Canadian physician Kevin Patterson (link). He describes his medical work in Afghanistan and the Canadian arctic treating cultures with various degrees of industrialization. He discusses the "epidemiological transition", the idea that cultures experience predictable changes in their health as they go from hunter-gatherer, to agricultural, to industrial. I think he has an uncommonly good perspective on the effects of industrialization on human health, which tends to be true of people who have witnessed the effects of the industrial diet and lifestyle on diverse cultures.

A central concept behind my thinking is that it's possible to benefit simultaneously from both:

• The sanitation, medical technology, safety technology, law enforcement and lower warfare-related mortality that have increased our life expectancy dramatically relative to our distant ancestors.


• The very low incidence of obesity, diabetes, coronary heart disease and other non-infectious chronic diseases afforded by a diet and lifestyle roughly consistent with our non-industrial heritage.

But it requires discipline, because going with the flow means becoming unhealthy.

Randy Tobler Show: Welcome

This morning, I had a conversation with Dr. Randy Tobler on his radio show "Vital Signs", on 97.1 FM News Talk in St Louis. Dr. Tobler is an obstetrician-gynecologist with an interest in nutrition, fitness and reproductive endocrinology from a holistic perspective. He asked me to appear on his show after he discovered my blog and found that we have some things in common, including an interest in evolutionary/ancestral health. We talked about the history of the American diet, the health of non-industrial cultures, what fats are healthiest, and the difference between pastured and conventional meat/dairy-- we took a few questions from listeners-- it was fun.

The show is available as a podcast here (3/26 show), although as far as I can tell, you need iTunes to listen to it. My section of the show starts around 8:20.

To everyone who arrived here after hearing me on the air this morning: welcome! Here are a few posts to give you a feel for what I do here at Whole Health Source:

The Coronary Heart Disease Epidemic
US Weight, Lifestyle and Diet Trends, 1970-2007
Butter vs. Margarine Showdown
Preventing and Reversing Tooth Decay
The Kitavans: Wisdom from the Pacific Islands
Potatoes and Human Health, Part I, Part II and Part III
Traditional Preparation Methods Improve Grains' Nutritional Value
Real Food XI: Sourdough Buckwheat Crepes
Glucose Tolerance in Non-industrial Cultures
Tropical Plant Fats: Palm Oil
It's Time to Let Go of the Glycemic Index

Safflower Oil Study

A few people have sent me a new study claiming to demonstrate that half a tablespoon of safflower oil a day improves insulin sensitivity, increases HDL and decreases inflammation in diabetics (1). Let me explain why this study does not show what it claims.

It all comes down to a little thing called a control group, which is the basis for comparison that you use to determine if your intervention had an effect. This study didn't have one for the safflower group. What it had was two intervention groups, one given 6.4g conjugated linoleic acid (CLA; 50% c9t11 and 50% t10c12-CLA) per day, and one given 8g safflower oil. I have to guess that this study was originally designed to test the effects of the CLA, with the safflower oil group as the control group, and that the interpretation of the data changed after the results came in. Otherwise, I don't understand why they would conduct a study like this without a control group.

Anyway, they found that the safflower oil group did better than the CLA group over 16 weeks, showing a higher insulin sensitivity, higher HDL, lower HbA1c (a marker of average blood glucose levels) and lower CRP (a marker of inflammation). But they also found that the safflower group improved slightly compared to baseline, therefore they decided to attribute the difference to a beneficial effect of safflower oil. The problem is that without a control (placebo) group for comparison, there's no way to know if the improvement would have occurred regardless of treatment, due to the season changing, more regular check-ups at the doctor's office due to participating in a study, or countless other unforeseen factors. A control group is essential for the accurate interpretation of results, which is why drug studies always have placebo groups.

What we can say is that the safflower oil group fared better than the CLA group, because there was a difference between the two. However, what I think really happened is that the CLA supplement was harmful and the small dose of safflower oil had no effect. Why? Because the t10c12 isomer of CLA, which was half their pill, has already been shown by previous well-controlled studies to reduce insulin sensitivity, decrease HDL and increase inflammatory markers at a similar dose and for a similar duration (2, 3). The safflower oil group only looked good by comparison. We can add this study to the "research bloopers" file.

It's worth noting that naturally occurring CLA mixtures, similar to those found in pastured dairy and ruminant fat, have not been shown to cause metabolic problems such as those caused by isolated t10c12 CLA.