New Study: Is a Calorie a Calorie?

A new study in JAMA led by Dr. Cara B. Ebbeling and colleagues purports to challenge the idea that all calories are equally fattening (1).  Let's have a look.  When thinking about the role of calorie intake in body fatness, there are basically three camps:

1.    Calories don’t matter at all, only diet composition matters.
2.    Calories are the only thing that matters, and diet composition is irrelevant.
3.    Calories matter, but diet composition may also play a role.

The first one is an odd position that is not very well populated.  The second one has a lot of adherents in the research world, and there’s enough evidence to make a good case for it.  It’s represented by the phrase ‘a calorie is a calorie’, i.e. all calories are equally fattening.  #1 and #2 are both extreme positions, and as such they get a lot of attention.  But the third group, although less vocal, may be closest to the truth. 
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Why Did Energy Expenditure Differ Between Diets in the Recent Study by Dr. Ludwig's Group?

As discussed in the previous post, a recent study by Dr. David Ludwig's group suggested that during weight maintenance following fat loss, eating a very low carbohydrate (VLC) diet led to a higher metabolic rate (energy expenditure) than eating a low-fat (LF) diet, with a low glycemic index (LGI) diet falling in between the two (1).  The VLC diet was 30 percent protein, while the other two were 20 percent.  It's important to note that these were three dietary patterns that differed in many ways, and contrary to claims that are being made in the popular media, the study was not designed to isolate the specific influence of protein, carbohydrate or fat on energy expenditure in this context. 

Not only did the VLC diet lead to a higher total energy expenditure than the LF and LGI diets, the most remarkable finding is that it led to a higher resting energy expenditure.  Basically, people on the VLC diet woke up in the morning burning more energy than people on the LGI diet, and people on the LGI diet woke up burning more than people on the LF diet.  The VLC dieters burned 326 more calories than the LF dieters, and 200 more than the LGI dieters.

It's always tempting to view each new study in isolation, without considering the numerous studies that came before it, but in this case it's essential to see this study through a skeptical lens that places it into the proper scientific context.  Previous studies have suggested that:

1. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are not trying to lose weight (2, 3).
2. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are being experimentally overfed, and if anything carbohydrate increases energy expenditure more than fat (4, 5).
3. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure during weight loss (6, 7, 8), and does not influence the rate of fat loss when calories are precisely controlled. 

This new study does not erase or invalidate any of these previous findings.  It fills a knowledge gap about the effect of diet composition on energy expenditure specifically in people who have lost weight and are trying to maintain the reduced weight.

With that, let's see what could have accounted for the differences observed in Dr. Ludwig's study.
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Interview with Aitor Calero of Directo al Paladar

Aitor Calero writes for the popular Spanish cooking and nutrition blog, Directo al Paladar ("straight to the palate").  We did a written interview a while back, and he agreed to let me post the English version on my blog.  The Spanish version is here and here.

Without further ado, here it is:

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What Causes Type 2 Diabetes, and How Can it be Prevented?

In the comments of the last post, we've been discussing the relationship between body fatness and diabetes risk.  I think this is really worth understanding, because type 2 diabetes is one of the few lifestyle disorders where 1) the basic causes are fairly well understood, and 2) we have effective diet/lifestyle prevention strategies that have been clearly supported by multiple controlled trials.

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New Review Paper by Yours Truly: High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

My colleagues Drs. Mario Kratz, Ton Baars, and I just published a paper in the European Journal of Nutrition titled "The Relationship Between High-Fat Dairy Consumption and Obesity, Cardiovascular, and Metabolic Disease".  Mario is a nutrition researcher at the Fred Hutchinson Cancer Research Center here in Seattle, and friend of mine.  He's doing some very interesting research on nutrition and health (with an interest in ancestral diets), and I'm confident that we'll be getting some major insights from his research group in the near future.  Mario specializes in tightly controlled human feeding trials.  Ton is an agricultural scientist at the University of Kassel in Germany, who specializes in the effect of animal husbandry practices (e.g., grass vs. grain feeding) on the nutritional composition of dairy.  None of us have any connection to the dairy industry or any other conflicts of interest.

The paper is organized into three sections:

1. A comprehensive review of the observational studies that have examined the relationship between high-fat dairy and/or dairy fat consumption and obesity, metabolic health, diabetes, and cardiovascular disease.
2. A discussion of the possible mechanisms that could underlie the observational findings.
3. Differences between pasture-fed and conventional dairy, and the potential health implications of these differences.

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How Should Science be Done?

Lately I keep running into the idea that the proper way to do science is to continually strive to disprove a hypothesis, rather than support it*.  According to these writers, this is what scientists are supposed to aspire to, but I've never actually heard a scientist say this.  The latest example was recently published in the Wall Street Journal (1).  This evokes an image of the Super Scientist, one who is so skeptical that he never believes his own ideas and is constantly trying to tear them down.  I'm no philosopher of science, but this idea never sat well with me, and it's contrary to how science is practiced. 
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Two Great Quotes About Obesity (technical)

By Dr. Hans-Rudolf Berthoud, from a recent paper, "The Neurobiology of Food Intake in an Obesogenic Environment" (1).  I came across it because it cites my review paper (2).  My perspective on obesity is similar to his.  From the abstract:

The modern lifestyle with its drastic changes in the way we eat and move puts pressure on the homoeostatic system responsible for the regulation of body weight, which has led to an increase in overweight and obesity. The power of food cues targeting susceptible emotions and cognitive brain functions, particularly of children and adolescents, is increasingly exploited by modern neuromarketing tools. Increased intake of energy-dense foods high in fat and sugar is not only adding more energy, but may also corrupt neural functions of brain systems involved in nutrient sensing as well as in hedonic, motivational and cognitive processing.

And a nice one from the conclusions:
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Lorcaserin: the Latest FDA-approved Obesity Drug

The FDA recently approved a new drug called lorcaserin (brand name Belviq) for the treatment of obesity.  Lorcaserin causes an average of 13 lbs (5.8 kg) of weight loss over a year, compared to 5 lbs (2.2 kg) for placebo (1), which is less than the other recently approved drug Qsymia (formerly Qnexa; topiramate/phentermine).

Learning about obesity drugs is always a good opportunity to gain insight into the mechanisms that underlie the development and reversal of obesity.  If you've been following this blog for a while, you already have a pretty good guess what organ this new drug acts on.  Make your guess and read on!

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Ancestral Health Symposium 2012

I recently returned from AHS12 and a little side trip to visit family.  The conference was hosted at Harvard University through the Harvard Food Law Society.  Many thanks to all the organizers who made it happen.  By and large, it went smoothly.

The science as expected ranged from outstanding to mediocre, but I was really encouraged by the presence and enthusiastic participation of a number of quality researchers and clinicians. The basic concept of ancestral health is something almost anyone can get behind: many of our modern health problems are due to a mismatch between the modern environment and what our bodies "expect".  The basic idea is really just common sense, but of course the devil is in the details when you start trying to figure out what exactly our bodies expect, and how best to give it to them.  I think our perspective as a community is moving in the right direction.

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AHS11 Talk Posted

After a one-year delay, my talk from the 2011 Ancestral Health Symposium is online with slides synched.  The talk is titled "Obesity: Old Solutions for a New Problem", and it's an overview of some of the research linking food reward to food intake and body fatness.  This is the talk that introduced a fundamentally new idea to the ancestral community: not only does the chemical composition of food matter, but also its sensory qualities-- in fact, the sensory qualities of food are among the primary determinants of food intake.  I didn't come up with the idea of course, I simply translated the research for a more general audience and put my own evolutionary spin on it.

The talk would be a bit different if I were to give it today, as my understanding of the subject has expanded, and my speaking skills have improved.  However, the central message remains as true today as it was a year ago.  You can find the talk here.

The slide synching was done by an extremely generous man named Ben Fury.  As you can see in the video, he did an excellent job.  Without Ben, this video would have remained in internet limbo forever.

Below, I've published a message from Ben explaining the interesting work that he does.  Please contact him if you think it's interesting.

A Message from Ben Fury

I was writing a book on health, fitness and diet in 2009 when my house burned down in the Station Fire, along with 165,000 acres of my beloved Angeles National Forest. Since then, I've had a series of people needing help come through my life, that have upgraded and morphed my talents...

Seniors with chronic pain, falls, brittle bones, and stiff shrunken muscles.
Diabetics with out of control blood sugars, going blind, and having limbs lopped off.
Neurologically challenged people with spastic limbs and foggy brains.
Fat, listless, unhappy people with no idea how they got that way, seeing no way out of the darkness.
Each of them needing help in different ways, but all with an underlying theme of what works to help heal our conditions:

•     Remove flour, sugar, beans, and heavily processed oils from our diet. Eat real food.
•     Get strong.
•     Get flexible.
•     Stop ceding health responsibility to outside forces, and take charge of our own wellness.
•     Only use truly evidence based medicine. Don't just pop the latest pill or get the latest surgery all the other people are doing. Be wary of the disease mongers in both the conventional and alternative camps.
•     Find our "happy thoughts." Use the simple restoratives of sleep, play, and reflection, to let go of pain, find inner peace, and let in joy and purposeful outer direction.

The methods to accomplish these goals are varied, and I have both non-profit and for-profit ventures to share them.
Their websites are currently in development.
The for-profit is BenFury.com
The non-profit is PainRelieversUSA.org , whose mission statement is:

To move beyond pain management...
and learn to live pain free.

Feel free to write to me  at: ben [at] benfury dot com

Does Calorie Restriction Extend Lifespan in Mammals?

Until about two years ago, the story went something like this: calorie restriction extends lifespan in yeast, worms, flies, and rodents.  Lifespan extension by calorie restriction appears to be biologically universal, therefore it's probably only a matter of time until it's demonstrated in humans as well.  More than 20 years ago, independent teams of researchers set out to demonstrate the phenomenon in macaque monkeys, a primate model closer to humans than any lifespan model previously tested.

Recent findings have caused me to seriously question this narrative.  One of the first challenges was the finding that genetically wild mice (as opposed to inbred laboratory strains) do not live longer when their calorie intake is restricted, despite showing hormonal changes associated with longevity in other strains, although the restricted animals do develop less cancer (1).  One of the biggest blows came in 2009, when researchers published the results of a study that analyzed the effect of calorie restriction on lifespan in 41 different strains of mice, both male and female (2).  They found that calorie restriction extends lifespan in a subset of strains, but actually shortens lifespan in an even larger subset.  Below is a graph of the effect of calorie restriction on lifespan in the 41 strains.  Positive numbers indicate that calorie restriction extended life, while negative numbers indicate that it shortened life:

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A Late Summer Harvest

It's been a good year for gardening in Seattle, at least in my garden.  Thanks to great new tools* and Steve Solomon's recipe for homemade fertilizer, my house has been swimming in home-grown vegetables all summer.  I'm fortunate that a friend lets me garden a 300 square foot plot behind her house.  Here's a photo of part of today's harvest; various kale/collards, zucchini, tomatoes and the last of the pole beans:

Perfect for the Eocene diet.  

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Calories and Carbohydrate: a Natural Experiment

In the lab, we work hard to design experiments that help us understand the natural world.  But sometimes, nature sets up experiments for us, and all we have to do is collect the data.  These are called "natural experiments", and they have led to profound insights in every field of science.  For example, Alzheimer's disease is usually not considered a genetic disorder.  However, researchers have identified rare cases where AD is inherited in a simple genetic manner.  By identifying the genes involved, and what they do, we were able to increase our understanding of the molecular mechanisms of the disease.

The natural experiment I'll be discussing today began in 1989 with the onset of a major economic crisis in Cuba. This coincided with the loss of the Soviet Union as a trading partner, resulting in a massive economic collapse over the next six years, which gradually recovered by 2000. 

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Nutrition Science Initiative (NuSI)

Some of you may have heard of an ambitious new nutrition research foundation called the Nutrition Science Initiative (NuSI).  In this post, I'll explain what it is, why it matters, and how I feel about it-- from the perspective of an obesity researcher. 

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More Thoughts on Macronutrient Trends

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

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Photos and More Gardening

I've needed new professional and blog photos for a long time.  My friend Adam Roe was in town recently, and he happens to be professional photographer, so he graciously offered to snap a few shots.  Despite less than ideal conditions, he did an outstanding job.  Here's a larger version of the photo on my profile (which Blogger shrinks down to a tiny thumbnail):

To see more of Adam's work, head over to his Facebook page, and don't forget to 'like' and share it if you enjoy it.  Adam is currently based in Berlin.

Gardening Update

Here's a photo of today's harvest (taken by me, not Adam; you can tell by the poor focus and primitive lighting):

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Candy at the Cash Register

Last week, the New England Journal of Medicine published an interesting editorial titled "Candy at the Cash Register-- a Risk Factor for Obesity and Chronic Disease."  This fits in well with our discussion of non-homeostatic eating, or eating in the absence of calorie need.

There are a few quotes in this article that I find really perceptive.

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Food Reward Fridays

Each Friday, I'm going to post a picture of a modern food so ridiculous it makes you want to laugh and cry at the same time.  I'm doing this for two reasons:

1. To raise awareness about the unhealthy, fattening foods that are taking over global food culture.  These are highly rewarding, highly palatable, energy-dense foods that drive people to eat in the absence of hunger, and continue eating beyond calorie needs.  In many cases, the foods have been specifically designed to maximize "craveability" and palatability.
2. Because it's funny.

Without further ado... the first lucky winner:

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Food Reward Friday

This week's lucky winner... the Hardee's MONSTER THICKBURGER!

Two 1/3 lb beef patties, four strips of bacon, three slices of American "cheese", mayo and bun.  This bad boy boasts 1,300 calories, 830 from fat, 188 from carbohydrate and 228 from protein.  Charred and fried processed meat, fake cheese, refined soybean oil mayo, and a white flour bun. You might as well just inject it directly into your carotid artery.  Add a large fries and a medium coke, and you're at 2,110 calories.  Who's hungry?  Actually I am.  

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An Encouraging Trend

I was in the Seattle/Tacoma airport today, and I noticed quite a few people taking the stairs even though they're flanked by escalators.  It's been my impression lately that more people are using stairs than even five years ago.  I used to be the only weirdo on the stairs, but today I shared them with about ten other people.  I know Seattle isn't necessarily representative of the nation as a whole, but I (optimistically) think of it as the vanguard in this respect.

One of the healthiest things a person can do is build exercise into daily life.  You don't have to be Usain Bolt or Lance Armstrong to reap the benefits of exercise.  In fact, evidence is accumulating that moderate exercise is healthier than extreme exercise.  Taking the stairs instead of the elevator/escalator, walking or jogging even a modest amount, or standing for part of the day, can have an immediate, measurable impact on metabolic health (1).

Maybe it's macho, but I'll feel defeated the day I need a giant energy-guzzling machine to take me up a 15 foot incline.  I have legs, and I intend to use them.  Escalators are good for people who are disabled or have very heavy bags, but the rest of us have an opportunity to use our bodies in a natural and healthy way.  Part of the problem is how buildings are designed.  Humans tend to take the path of least resistance, and if the first thing we come across is an elevator, and the stairs are grimy and tucked away down some side hallway, we'll tend to take the elevator.  Architects in some places are building in more prominent stairways to encourage gentle exercise throughout the day.

Food Reward Friday

This week's winner: the Taco Bell Doritos Locos Taco!

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Food Reward Friday

This week's winner: poutine!

While not as appetizing looking as the Monster Thickburger, poutine is probably more popular.  For those who aren't familiar, poutine is a large plate of French fries, topped with gravy and cheese curds.  It originated in Quebec, but has become popular throughout Canada and in the Northern US.

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Food Reward Friday

This week's winner... the Starbuck's Double Chocolaty Chip Frappuccino!

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

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

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

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

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Food Reward Friday

This week's "winner"... Kellogg's Krave cereal!

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

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

This week's "winner"...

The Pizza Hut hot dog stuffed crust pizza!

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The Potato Diet

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

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Extreme Flu Activity in the US

A friend of mine came down with a nasty flu recently.  I checked Google Flu Trends, and found that flu activity is currently at "intense" levels throughout the US.  This is the highest flu activity Google Flu Trends has recorded in the last six years (image from Google Flu Trends 1/3/12).

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Food Reward Friday

This week's "winner"... the Heart Attack Grill's Quadruple Bypass Burger!

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Overfeeding and Elevated Insulin

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

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Appearance on "Ask the Low-Carb Experts" Podcast Postponed

I was scheduled to appear on Jimmy Moore's show "Ask the Low-Carb Experts" this Thursday.  I don't consider myself a low-carb expert, but I do have expertise in obesity and metabolism, and Jimmy had invited me to discuss these topics on his show.

Due to a confluence of events, I've decided that this is not the best time to do the show.  I want to be clear that I don't intend this as a rebuke of Jimmy Moore or his show-- most of my reasons for postponing have nothing to do with Jimmy.  Thanks for your understanding.

Food Reward Friday

This week's "winner"... the Garbage Plate!!

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Dogs Eating Carbs

Five years ago, I had an interesting conversation with a veterinarian friend about dog food.  We were talking about diabetes in one of the dogs she was treating, and I remarked "that's what happens when you feed a carnivore carbohydrate".  She gave me a funny look.  At the time, I was seeing the world through the low-carb lens, and I remember thinking how bizarre it was that she didn't yield to my impeccable logic.  As they say, live and learn.

The journal Nature published a fascinating paper on the evolution of the domestic dog today (1).  Researchers compared the genome of wolves and domestic dogs to see what genetic changes accompanied domestication.

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Comment Published in Nature

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

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

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Food Reward Friday

This week's "winner"... the KFC Double Down sandwich!

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Announcing the Ideal Weight Program

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

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

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

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

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

What is the Ideal Weight Program?

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

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

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

Here's what you get when you sign up:

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

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

Ideal Weight Program



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

Comment Policy

Over the last year, I've noticed that the quality of the comments section here has deteriorated significantly, with a high proportion of poorly grounded and/or disrespectful comments, typically from anonymous or semi-anonymous people.  This is the nature of the Internet I suppose-- comments sections are rowdy places.  But ultimately I do have control over this, and I intend to exert it to maintain a higher level of information quality and decorum in my corner of the Internet.

For the foreseeable future, I'll be moderating comments.  Here are my criteria for deciding whether or not a comment will be published:

1. Value.  Comments should be well thought out, and points supported by research or at least solid logic.  Personal anecdotes are welcome as long as they aren't over-interpreted.  Thoughtful questions are also welcome, although I can't guarantee I'll answer them.  As always, anyone is free to disagree with me in a constructive manner, or simply offer a word of support.  
2. Respect.  Comments should be respectful to me and other commenters, and composed in a concise manner.  It isn't difficult to disagree in a respectful way.
3. On topic.  Comments should be at least somewhat relevant to the subject of the post.
4. Full name.  Attaching your full name to a comment means taking responsibility for what you write.  I'll continue to publish anonymous comments if they add value, but I'll be more likely to publish if you include your full name in your screen name, your profile, or at the bottom of your comment.
5. No ads.  I will not publish links to commercial sites that do not add value to the discussion, nor will I publish any other link I find objectionable.

Because I'll be moderating, I've decided to remove the captcha word authentication, which many people found difficult to use.  We'll see how that goes.  Since I have a lot on my plate, and Whole Health Source is a one-man show, I may not always moderate comments in a timely manner.  I apologize in advance for the inconvenience.  

Why Do We Eat? A Neurobiological Perspective. Part I

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

The Gatekeeper of Voluntary Behaviors

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Why Do We Eat? A Neurobiological Perspective. Part II

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

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

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

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

The Satiety System (Short-Term Energy Homeostasis)


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

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Why Do We Eat? A Neurobiological Perspective. Part III

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

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

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

The Energy Homeostasis System

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Why Do We Eat? A Neurobiological Perspective. Part IV

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

Age

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

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Why Do We Eat? A Neurobiological Perspective. Part V

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

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

The Hedonic System

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Why Do We Eat? A Neurobiological Perspective. Part VI

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

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

Behavioral Reinforcement

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Why Do We Eat? A Neurobiological Perspective. Part VII

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

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

Food 'Cost'

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Why Do We Eat? A Neurobiological Perspective. Part VIII

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

Why is Eating Behavior Regulated?

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

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Food Reward Friday

This week's lucky "winner"... an unnamed hot dog-laden Pizza Hut monstrosity with tempura shrimp and mayonnaise!

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Food Reward Friday

This week's "winner"... the Banana Split!

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Body Fatness and Cardiovascular Risk Factors

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

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Food Reward Friday

This week, Food Reward Friday is going to be a little bit different.  I've received a few e-mails from people who would like to see me write about some of the less obvious examples of food reward-- foods that are less extreme, but much more common, and that nevertheless promote overeating.  Let's face it, even though they're funny and they (sometimes) illustrate the principle, most people reading this blog don't eat banana splits very often, much less pizzas made out of hot dogs.

So this week's "winner" is something many of you have in your houses right now, and which was also the subject of an interesting recent study... potato chips!

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Salt Sugar Fat

I'd just like to put in a quick word for a book that will be released tomorrow, titled Salt Sugar Fat: How the Food Giants Hooked Us, by Pulitzer prize-winning author Michael Moss.  This is along the same lines as Dr. David Kessler's book The End of Overeating, which explains how the food industry uses food reward, palatability, and food cues to maximize sales-- and as an unintended side effect, maximize our waistlines.   Judging by Moss's recent article in New York Times Magazine, which I highly recommend reading, the book will be excellent.  I've pre-ordered it.

Your Brain on Potato Chips

Or, more accurately, a rat's brain on potato chips.  Last week, PLoS One published a very interesting paper by Dr. Tobias Hoch and colleagues on what happens in a rat's brain when it is exposed to a highly palatable/rewarding food (1).  Rats, like humans, overconsume highly palatable foods even when they're sated on less palatable foods (2), and feeding rats a variety of palatable human junk foods is one of the most effective ways to fatten them (3).  Since the brain directs all behaviors, food consumption is an expression of brain activity patterns.  So what is the brain activity pattern that leads to the overconsumption of a highly palatable and rewarding food?

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Does the Mediterranean Diet Reduce Cardiovascular Risk?

By now, most of you have probably heard about the recent study on the "Mediterranean diet" (1), a diet that was designed by diet-heart researchers and is based loosely on the traditional diet of Crete and certain other Mediterranean regions.  The popular press has been enthusiastically reporting this trial as long-awaited proof that the Mediterranean diet reduces the risk of cardiovascular events-- by a full 30 percent over a 4.8-year period.  I wish I could share their enthusiasm for the study.

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Food Reward Friday

This week's lucky "winner"... Yoplait Go-Gurt!

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Atherosclerosis in Ancient Mummies Revisited

Many of you are already aware of the recent study that examined atherosclerosis in 137 ancient mummies from four different cultures (1).  Investigators used computed tomography (CT; a form of X-ray) to examine artery calcification in mummies from ancient Egypt, Peru, Puebloans, and arctic Unangan hunter-gatherers.  Artery calcification is the accumulation of calcium in the vessel wall, and it is a marker of severe atherosclerosis.  Where there is calcification, the artery wall is thickened and extensively damaged.  Not surprisingly, this is a risk factor for heart attack.  Pockets of calcification are typical as people age.

I'm not going to re-hash the paper in detail because that has been done elsewhere.  However, I do want to make a few key points about the study and its interpretation.  First, all groups had atherosclerosis to a similar degree, and it increased with advancing age.  This suggests that atherosclerosis may be part of the human condition, and not a modern disease.  Although it's interesting to have this confirmed in ancient mummies, we already knew this from cardiac autopsy data in a variety of non-industrial cultures (2, 3, 4, 5).

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Food Reward Friday

This week's lucky "winner"... fried Coke!

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Food Reward Friday

This week's luck winner(s)... pastries!!

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Neuronal Control of Appetite, Metabolism and Weight

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

Rapid Pace of Scientific Progress

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Food Reward Friday

This week's "lucky" winner... milkshakes!

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Are Animal Crackers Paleo?

Every child loves animal crackers, those sweet and crunchy animal-shaped biscuits.  But are they compatible with a Paleo diet?  Some people might think they already know the answer, but consider this: our ancestors evolved on the African savanna, eating the plants and animals found there.  Inside each box of animal crackers is an assortment of tiny savanna creatures such as giraffes and elephants.

To get to the bottom of this, I interviewed Robert Pearson, CEO of Animal Cracker Products Inc., who explained to me how these crackers are made.

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Glucagon, Dietary Protein, and Low-Carbohydrate Diets

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

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

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Food Reward Friday

This week's lucky "winner"... energy bars!

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Book Review: Salt, Sugar, Fat

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

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Food Reward Friday

This week's lucky "winner"... ice cream!!

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Food Variety, Calorie Intake, and Weight Gain

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

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

This may seem counterintuitive, since variety in the diet is generally seen as a good thing.  In some ways, it is a good thing, however in this post we'll see that it can have a downside.
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Speaking at AHS13

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

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

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

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

The Neurobiology of the Obesity Epidemic

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

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

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Update

I haven't been putting much effort into blogging these past few weeks.  Frankly, a little break has been nice while I take care of other things in my life.  But I haven't been twiddling my thumbs.  Obesity research hasn't slowed down and there are many topics that I'd love to write about here if I had the time.  I'll be starting a new series soon on the genetics of obesity-- a fascinating subject.  I also plan to cover some of my recent publications on obesity and blood glucose control by the brain.  Last but not least, we will soon roll out a substantially upgraded version of the Ideal Weight Program.  Those who have already purchased the program will continue to have access to the new version.

Food Reward Friday

This week's "winner" will certainly be the most controversial yet... bacon!!

Bacon is a fatty cut of pork (typically side or back) that has been thinly sliced, cured, then cooked until crispy.  This results in a fatty, salty, savory flavor that almost everyone loves.  Bacon's extremely high calorie density, saltiness, and savory flavor give it a reward value that competes with chocolate and ice cream.  Sometimes it's even used to flavor chocolate and ice cream!

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Food Reward Friday

This week's lucky "winner"... cronuts!!

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Food Reward Friday

This week's lucky "winner"... low-carb gluten-free bacon chocolate mocha ice cream cake!!

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The Genetics of Obesity, Part I

Choosing the Right Parents: the Best Way to Stay Lean?

In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1).  They took advantage of one of the most useful tools in human genetics: identical twins.  This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb.   By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).

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Food Reward Friday

This week's lucky "winner"... beer!!

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The Genetics of Obesity, Part II

Rodents Lead the Way

The study of obesity genetics dates back more than half a century.  In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene.  They named this the "obese" (ob/ob) mouse.  Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.

At the time of discovery, no one knew where the mutations resided in the genome.  All they knew is that the mutations were in single genes, and they resulted in extreme obesity.  Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way.  Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned.  Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.

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Return to the Source Parkour Camp

For those who are interested in natural movement training, this summer my friend Rafe Kelley will be hosting an interesting three-day event near Bellingham, WA called "Return to the Source".  Rafe is skilled in a variety of movement disciplines and is the co-founder of the Seattle parkour gym Parkour Visions.  Parkour is a very fun sport that hones our natural ability to skillfully navigate physical obstacles, but it's usually done in an urban context.

The camp will take place from August 23-25.  Here's a description from the Parkour Visions site:

"This summer, return to the source of human movement with Parkour Visions as we explore the natural environment in and around Bellingham, WA. Rafe Kelley will introduce you to the benefits of training and playing in nature. You will learn how to adapt your technique and movement to moving effectively through woods, over rocks, and in trees during this unique, 3-day experience."

Watch this video if you want to see what you're in for.

Knowing Rafe, it will be fun and productive.  You can sign up through this page.

The Genetics of Obesity, Part III

Genetics Loads the Gun, Environment Pulls the Trigger

Thanks to a WHS reader* for reminding me of the above quote by Dr. Francis Collins, director of the US National Institutes of Health**.  This is a concept that helps reconcile the following two seemingly contradictory observations:

1. Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
2. Diet and lifestyle have a large impact on obesity risk.  The prevalence of obesity has tripled in the last 30 years, and the prevalence of extreme obesity has increased by almost 10-fold.  This is presumably not enough time for genetic changes to account for it.

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Zucchini: The Home Gardener's Worst Friend? With bonus garden-related rambling.

One of my main gardening goals has been to harvest more of something than I can eat, despite my limited gardening space here in the Emerald City.  I want the feeling of abundance that comes with having to preserve and give away food because I can't eat it all.

Enter zucchini.  My grandfather used to say that in New Jersey in summertime, you'd have to keep your car doors locked, otherwise the car would be full of zucchini the next time you got in!  In mid-May, I planted two starts from my local grocery store labeled "green zucchini", with no further information.  I put them in a bed that used to be a pile of composted horse manure, and that I had also cover cropped, mulched, fertilized, and loosened deeply with my broadfork.  They look pleased.

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Brown Fat: It's a Big Deal

Non-shivering thermogenesis is the process by which the body generates extra heat without shivering.  Shivering is a way for the body to use muscular contractions to generate heat, but non-shivering thermogenesis uses a completely different mechanism to accomplish the same goal: a specialized fat-burning tissue called brown fat.  Brown fat is brown rather than white because it's packed with mitochondria, the power plants of the cell.  Under cold conditions, these mitochondria are activated, using a specialized molecular mechanism called uncoupling* to generate heat.

The mechanism of brown fat activation has been worked out fairly well in rodents, which rely heavily on non-shivering thermogenesis due to their small body size.  Specialized areas of the hypothalamus in the brain sense body temperature (through sensors in the brain and body), body energy status (by measuring leptin and satiety signals), stress level, and probably other factors, and integrate this information to set brown fat activity.  The hypothalamus does this by acting through the sympathetic nervous system, which heavily innervates brown fat.  As an aside, this process works basically the same in humans, as far as we currently know.  Those who claim that rodent models are irrelevant to humans are completely full of hot air**, as the high degree of conservation of the hypothalamus over 75 million years of evolution demonstrates.

Two new studies concurrently published in the Journal of Clinical Investigation last week demonstrate what I've suspected for a long time: brown fat can be 'trained' by cold exposure to be more active, and its activation by cold can reduce body fatness.

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Food Reward Friday

This week's lucky winner... salted nuts!!

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Food Reward Friday

This week's lucky "winner"... cola!

Thirsty yet?  Visual cues such as these are used to drive food/beverage seeking and consumption behavior, which are used to drive profits.  How does this work?  Once you've consumed a rewarding beverage enough times, particularly as a malleable child, your brain comes to associate everything about that beverage with the primary reward you obtained from it (calories, sugar, and caffeine).  This is simply Pavlovian/classical conditioning*.  Everything associated with that beverage becomes a cue that triggers motivation to obtain it (craving), including the sight of it, the smell of it, the sound of a can popping, and even the physical and social environment it was consumed in-- just like Pavlov's dogs learned to drool at the sound of a bell that was repeatedly paired with food.

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AHS Talk This Saturday

For those who are attending the Ancestral Health Symposium this year, my talk will be at 9:00 AM on Saturday.  The title is "Insulin and Obesity: Reconciling Conflicting Evidence", and it will focus on the following two questions:

1. Does elevated insulin cause obesity; does obesity cause elevated insulin; or both?
2. Is there a unifying hypothesis that's able to explain all of the seemingly conflicting evidence cited by each side of the debate?

I'll approach the matter in true scientific fashion: stating hypotheses, making rational predictions based on those hypotheses, and seeing how well the evidence matches the predictions.  I'll explore the evidence in a way that has never been done before (to my knowledge), even on this blog.

Why am I giving this talk?  Two reasons.  First, it's an important question that has implications for the prevention and treatment of obesity, and it has received a lot of interest in the ancestral health community and to some extent among obesity researchers.  Second, I study the mechanisms of obesity professionally, I'm wrapping up a postdoc in a lab that has focused on the role of insulin in body fatness (lab of Dr. Michael W. Schwartz), and I've thought about this question a lot over the years-- so I'm in a good position to speak about it.

The talk will be accessible and informative to almost all knowledge levels, including researchers, physicians, and anyone who knows a little bit about insulin.  I'll cover most of the basics as we go.  I guarantee you'll learn something, whatever your knowledge level.

Reflections on the 2013 Ancestral Health Symposium

I just returned from the 2013 Ancestral Health Symposium in Atlanta.  Despite a few challenges with the audio/visual setup, I think it went well.

I arrived on Thursday evening, and so I missed a few talks that would have been interesting to attend, by Mel Konner, Nassim Taleb, Gad Saad, and Hamilton Stapell.  Dr. Konner is one of the progenitors of the modern Paleo movement.  Dr. Saad does interesting work on consummatory behavior, reward, and its possible evolutionary basis.  Dr. Stapell is a historian with an interest in the modern Paleo movement.  He got some heat for suggesting that the movement is unlikely to go truly mainstream, which I agree with.  I had the opportunity to spend quite a bit of time with him and found him to be an interesting person.

On Friday, Chris Kresser gave a nice talk about the potential hidden costs of eradicating our intestinal parasites and inadvertently altering our gut flora.  Unfortunately it was concurrent with Chris Masterjohn so I'll have to watch his talk on fat-soluble vitamins when it's posted.  I spent most of the rest of the day practicing my talk.

On Saturday morning, I gave my talk "Insulin and Obesity: Reconciling Conflicting Evidence".  I think it went well, and the feedback overall was very positive, both on the content and the delivery.  The conference is fairly low-carb-centric and I know some people disagree with my perspective on insulin, and that's OK.   The-question-and-answer session after the talk was also productive, with some comments/questions from Andreas Eenfeldt and others.  With the completion of this talk, I've addressed the topic to my satisfaction and I don't expect to spend much more time on it unless important new data emerge.  The talk will be freely available online at some point, and I expect it to become a valuable resource for people who want to learn more about the relationship between insulin and obesity.  It should be accessible to anyone with a little bit of background in the subject, but it will also be informative to most researchers.

After my talk, I attended several other good presentations.  Dan Pardi gave a nice talk on the importance of sleep and the circadian rhythm, how it works, how the modern world disrupts it, and how to fix it.  The relationship between sleep and health is a very hot area of research right now, it fits seamlessly with the evolutionary perspective, and Pardi showed off his high level of expertise in the subject.  He included the results of an interesting sleep study he conducted as part of his doctoral work at Stanford, showing that sleep restriction makes us more likely to choose foods we perceive as unhealthy.

Sleep and the circadian rhythm was a recurrent theme at AHS13.  A lot of interesting research is emerging on sleep, body weight, and health, and the ancestral community has been quick to embrace this research and integrate it into the ancestral health template.  I think it's a big piece of the puzzle.

Jeff Rothschild gave a nice summary of the research on time-restricted feeding, body weight and health in animal models and humans.  Research in this area is expanding and the results are pretty interesting, suggesting that when you restrict a rodent's feeding window to the time of day when it would naturally consume food (rather than giving constant access during both day and night), it becomes more resistant to obesity even when exposed to a fattening diet.  Rothschild tied this concept together with circadian regulation in a compelling way.  Since food is one of the stimuli that sets the circadian clock, Rothschild proposes to eat when the sun is up, and not when it's down, synchronizing eating behavior with the natural seasonal light rhythm.  I think it's a great idea, although it wouldn't be practical for me to implement it currently.  Maybe someday if I have a more flexible schedule.  Rothschild is about to publish a review paper on this topic as part of his master's degree training, so keep your eyes peeled.

Kevin Boyd gave a very compelling talk about malocclusion (underdeveloped jaws and crowded teeth) and breathing problems, particularly those occurring during sleep.  Malocclusion is a modern epidemic with major health implications, as Dr. Boyd showed by his analysis of ancient vs. modern skulls.  The differences in palate development between our recent ancestors (less than 200 years ago) and modern humans are consistent and striking, as Weston Price also noted a century ago.  Dr. Boyd believes that changing infant feeding practices (primarily the replacement of breast feeding with bottle feeding) is the main responsible factor, due to the different mechanical stimulation it provides, and he's proposing to test that hypothesis using the tools of modern research.  He's presented his research at prestigious organizations and in high-impact scientific journals, so I think this idea may really be gaining traction.  Very exciting.

I was honored when Dr. Boyd told me that my 9-part series on malocclusion is what got him interested in this problem (1, 2, 3, 4, 5, 6, 7, 8, 9).  His research has of course taken it further than I did, and as a dentist his understanding of malocclusion is deeper than mine.  He's a middle-aged man who is going back to school to do this research, and his enthusiasm is palpable.  Robert Corruccini, a quality anthropology researcher and notable proponent of the idea that malocclusion is a "disease of civilization" and not purely inherited, is one of his advisers.

There were a number of excellent talks, and others that didn't meet my standards for information quality.  Overall, an interesting conference with seemingly less drama than in previous years.