Wednesday, December 30, 2015

Does the Vitamin and Mineral Content of Food Influence Our Food Intake and Body Fatness?

The Claim: We Overeat Because Our Diet is Low in Vitamins and Minerals

We know that animals, including humans, seek certain properties of food.  Humans are naturally attracted to food that's high in fat, sugar, starch, and protein, and tend to be less enthusiastic about low-calorie foods that don't have these properties, like vegetables (1).  Think cookies vs. plain carrots.

In certain cases, the human body is able to detect a nutritional need and take steps to correct it.  For example, people who are placed on a calorie-restricted diet become hungry and are motivated to make up for the calorie shortfall (23).  People who are placed on a low-protein diet crave protein and eat more of it after the restriction is lifted (4).  Humans and many other animals also crave and seek salt, which supplies the essential minerals sodium and chlorine, although today most of us eat much more of it than we need to.  At certain times, we may crave something sweet or acidic, and pregnant women are well known to have specific food cravings and aversions, although explanations for this remain speculative.  Research suggests that certain animals have the ability to correct mineral deficiencies by selecting foods rich in the missing mineral (5).

These observations have led to a long-standing idea that the human body is able to detect vitamin and mineral (micronutrient) status and take steps to correct a deficit.  This has led to the secondary idea that nutrient-poor food leads to overeating, as the body attempts to make up for low nutrient density by eating more food.  In other words, we overeat because our food doesn't supply the micronutrients our bodies need, and eating a micronutrient-rich diet corrects this and allows us to eat less and lose body fat.  These ideas are very intuitive, but intuition doesn't always get you very far in biology.  Let's see how they hold up to scrutiny.

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Saturday, December 19, 2015

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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Monday, December 14, 2015

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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Food Reward Friday

This week's "winner"...

The Pizza Hut hot dog stuffed crust pizza!

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Sunday, December 13, 2015

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.
Read more »

Thursday, December 10, 2015

Does "Metabolically Healthy Obesity" Exist?

Obesity is strongly associated with metabolic alterations and negative health outcomes including diabetes, cardiovascular disease, and some types of cancer (1234).  Excess body fat is one of the primary causes of preventable health problems and mortality in the United States and many other affluent nations, ranking in importance with cigarette smoking and physical inactivity.  Obesity is thought to contribute to disease via the metabolic disturbances it causes, including excess glucose and lipids in the circulation, dysregulated hormone activity including insulin and leptin, and inflammatory effects.  This immediately raises two questions:
  1. Does metabolically healthy obesity exist?
  2. If so, are metabolically healthy obese people at an elevated risk of disease and death?

Does metabolically healthy obesity exist?

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Wednesday, December 9, 2015

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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Sunday, December 6, 2015

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.

Read more »

Wednesday, December 2, 2015

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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Monday, November 30, 2015

Sunday, November 29, 2015

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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Food Reward Friday

This week's lucky "winner"... Oreo cookies!!!


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Thursday, November 26, 2015

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, and have evidently not read any of the scientific literature on it.  As of 2015, a Google Scholar search for the terms “food reward” and “obesity” turned up 2,790 papers.

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 unaware of them. 
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Monday, November 23, 2015

Beans, Lentils, and the Paleo Diet

As we continue to explore the foods our ancestors relied on during our evolutionary history, and what foods work best for us today, we come to legumes such as beans and lentils.  These are controversial foods within the Paleolithic diet community, while the broader nutrition community tends to view legumes as healthy.

Beans and lentils have a lot going for them.  They're one of the few foods that are simultaneously rich in protein and fiber, making them highly satiating and potentially good for the critters in our colon.  They're also relatively nutritious, delivering a hefty dose of vitamins and minerals.  The minerals are partially bound by the anti-nutrient phytic acid, but simply soaking and cooking beans and lentils typically degrades 30-70 percent of it, making the minerals more available for absorption (Food Phytates. Reddy and Sathe. 2002).  Omitting the soaking step greatly reduces the degradation of phytic acid (Food Phytates. Reddy and Sathe. 2002).

The only tangible downside to beans I can think of, from a nutritional standpoint, is that some people have a hard time with the large quantity of fermentable fiber they provide, particularly people who are sensitive to FODMAPs.  Thorough soaking prior to cooking can increase the digestibility of the "musical fruit" by activating the sprouting program and leaching out tannins and indigestible saccharides.  I soak all beans and lentils for 12-24 hours.

The canonical Paleolithic diet approach excludes legumes because they were supposedly not part of our ancestral dietary pattern.  I'm going to argue here that there is good evidence of widespread legume consumption by hunter-gatherers and archaic humans, and that beans and lentils are therefore an "ancestral" food that falls within the Paleo diet rubric.  Many species of edible legumes are common around the globe, including in Africa, and the high calorie and protein content of legume seeds would have made them prime targets for exploitation by ancestral humans after the development of cooking.  Below, I've compiled a few examples of legume consumption by hunter-gatherers and extinct archaic humans.  I didn't have to look very hard to find these, and there are probably many other examples available.  If you know of any, please share them in the comments.

To be clear, I would eat beans and lentils even if they weren't part of ancestral hunter-gatherer diets, because they're inexpensive, nutritious, I like the taste, and they were safely consumed by many traditional agricultural populations probably including my own ancestors.

Extensive "bean" consumption by the !Kung San of the Kalahari desert

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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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Friday, November 20, 2015

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).

Wednesday, November 11, 2015

Recent and Upcoming Appearances

Smarter Science of Slim

Jonathan Bailor recently released an interview we did a few months ago on the neurobiology of body fat regulation, and the implications for fat loss.  It's a good overview of the regulation of food intake and body fatness by the brain.  You can listen to it here.

Super Human Radio

Carl Lanore interviewed me about my lab's work on hypothalamic inflammation and obesity.  I'm currently wrapping up a postdoctoral fellowship with Dr. Michael Schwartz at the University of Washington, and the interview touches on our recent review paper "Hypothalamic Inflammation: Marker or Mechanism of Obesity Pathogenesis?"  Dan Pardi and I are frequent guests on Carl's show and I'm always impressed by how well Carl prepares prior to the interview.  You can listen to the interview here.

The Reality Check podcast

Pat Roach of the Reality Check podcast interviewed me about the scientific validity of the "carbohydrate-insulin hypothesis" of obesity.  The Reality Check podcast "explores a wide range of controversies and curiosities using science and critical thinking", and a dash of humor.  This one should be very informative for people who aren't sure what to believe and want a deeper perspective on the science of insulin and body weight regulation.  You can listen to it here.

Obesity Society conference

Next Thursday 11/9, I'll be speaking at the 2015 Obesity Society conference in Atlanta.  My talk is titled "The Glial Response to Obesity is Reversible", and it will be about my work on the reversibility of obesity-associated hypothalamic neuropathology in mice.  My talk will be part of the session "Neuronal Control of Satiety" between 3:00 and 4:30, specific time pending.  See you there!

Wednesday, November 4, 2015

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.

Buckwheat Crepes Revisited

One of my most popular posts of all time was a recipe I published in 2010 for sourdough buckwheat crepes (1).  I developed this recipe to provide an easy, nutritious, and gluten-free alternative to flour-based crepes.  It requires no equipment besides a blender.  It's totally different from the traditional buckwheat crepes that are eaten in Brittany, in part because it's not really a crepe (I don't know what else to call it, maybe a savory pancake?).  I find these very satisfying, and they're incredibly easy to make.  They're especially delicious with fresh goat cheese, or scrambled eggs with vegetables, but they go with almost anything.  Chris Kresser also developed his own version of the recipe, which is fluffier than mine, and more like a traditional pancake (2).

Buckwheat is an exceptionally nutritious pseudograin that's rich in complete protein and minerals.  In contrast to most whole grains, which have low mineral availability due to phytic acid, buckwheat contains a high level of the phytic acid-degrading enzyme phytase.  This makes buckwheat an excellent source of easily absorbed minerals, as long as you prepare it correctly!  Phytase enzyme works best in an acidic environment, which may be part of the reason why so many cultures use sour fermentation to prepare grain foods.  My original recipe included a sour fermentation step.

But there's a problem here.  Buckwheat doesn't ferment very well.  Whether it's because it doesn't contain the right carbohydrates, or the right bacteria, I don't know, but it spoils rapidly if you ferment it more than a little bit (using a strong sourdough starter helps though).  Others have told me the same.  So here's my confession: I stopped fermenting my buckwheat batter about a year ago.  And it tastes better.

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Tuesday, November 3, 2015

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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Monday, November 2, 2015

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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Thursday, October 29, 2015

New Post on Eat Move Sleep Blog

Yesterday, the Dan's Plan blog Eat Move Sleep published a blog post I wrote about sleep, artificial light, your brain, and a free computer program called f.lux that can help us live healthier lives.  Head over to Eat Move Sleep to read it.

Wednesday, October 28, 2015

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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Monday, October 26, 2015

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:
Read more »

Friday, October 23, 2015

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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Tuesday, October 20, 2015

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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Saturday, October 17, 2015

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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Friday, October 9, 2015

Sleep and Genetic Obesity Risk

Evidence is steadily accumulating that insufficient sleep increases the risk of obesity and undermines fat loss efforts.  Short sleep duration is one of the most significant risk factors for obesity (1), and several potential mechanisms have been identified, including increased hunger, increased interest in calorie-dense highly palatable food, reduced drive to exercise, and alterations in hormones that influence appetite and body fatness.  Dan Pardi presented his research at AHS13 showing that sleep restriction reduces willpower to make healthy choices about food.

We also know that genetics has an outsized influence on obesity risk, accounting for about 70 percent of the variability in body fatness between people in affluent nations (2).  I have argued that "fat genes" don't directly lead to obesity, but they do determine who is susceptible to a fattening environment and who isn't (3).  I recently revisited a 2010 paper published in the journal Sleep by University of Washington researchers that supports this idea (4).

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Wednesday, October 7, 2015

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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Sunday, October 4, 2015

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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Thursday, October 1, 2015

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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Thursday, September 24, 2015

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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Wednesday, September 23, 2015

Speaking in Lisbon on October 5

My friend Pedro Bastos graciously invited me to speak at a conference he organized in Lisbon on October 5 titled "Food, Nutrition and the Prevention of Chronic Diseases".  I will give two talks:

  • "Ancestral Health: What is Our Human Potential?"  This talk will explore the health of non-industrial cultures in an effort to understand how much of our modern chronic disease burden is preventable, and it will briefly touch on one major aspect of non-industrial life that may protect against the "diseases of civilization".  This presentation will focus on age-adjusted data from high quality studies.  
  • "Why Do We Overeat: a Neurobiological Perspective."  This talk will attempt to explain why most of us consume more calories than we need to maintain weight-- a phenomenon that is a central cause of morbidity and mortality in the modern world.  It will touch on some of the brain mechanisms involved in ingestive behavior, and outline a framework to explain why these mechanisms are often maladaptive in today's environment.
Pedro will speak about dairy consumption, vitamin D, and chronic disease.  

The conference is targeted to health professionals and students of nutrition, however it's open to anyone who is interested in these topics.  It's sponsored by NutriScience, a Portuguese nutrition education and consulting company.  Sadly, I don't speak Portuguese, so my talks will be in English.  

Access the full program, and register for the conference, using the links below:

Monday, September 21, 2015

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.

Monday, September 14, 2015

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:
Read more »

Sunday, September 13, 2015

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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Saturday, September 12, 2015

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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Thursday, September 10, 2015

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 not usually considered a genetic disorder.  However, researchers have identified rare cases in which 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 through 2000. 

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Sunday, September 6, 2015

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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Saturday, September 5, 2015

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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Friday, September 4, 2015

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.

Wednesday, September 2, 2015

Is Refined Carbohydrate Addictive?

[Note: in previous versions, I mixed up "LGI" and "HGI" terms in a couple of spots.  These are now corrected.  Thanks to readers for pointing them out.]

Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:

Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.

This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction.  The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.

So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation?  Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.

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Tuesday, September 1, 2015

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.  Dr. 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. 

Dr. 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. 
Read more »

Saturday, August 29, 2015

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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Wednesday, August 26, 2015

More Thoughts on Cold Training: Biology Chimes In

Now that the concept of cold training for cold adaptation and fat loss has received scientific support, I've been thinking more about how to apply it.  A number of people have been practicing cold training for a long time, using various methods, most of which haven't been scientifically validated.  That doesn't mean the methods don't work (some of them probably do), but I don't know how far we can generalize individual results prior to seeing controlled studies.

The studies that were published two weeks ago used prolonged, mild cold exposure (60-63 F air) to achieve cold adaptation and fat loss (12).  We still don't know whether or not we would see the same outcome from short, intense cold exposure such as a cold shower or brief cold water plunge.  Also, the fat loss that occurred was modest (5%), and the subjects started off lean rather than overweight.  Normally, overweight people lose more fat than lean people given the same fat loss intervention, but this possibility remains untested.  So the current research leaves a lot of stones unturned, some of which are directly relevant to popular cold training concepts.

In my last post on brown fat, I mentioned that we already know a lot about how brown fat activity is regulated, and I touched briefly on a few key points.  As is often the case, understanding the underlying biology provides clues that may help us train more effectively.  Let's see what the biology has to say.

Biology of Temperature Regulation

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Tuesday, August 25, 2015

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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Saturday, August 22, 2015

AHS11 Talk Posted

After a one-year delay, my talk from the 2015 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

Friday, August 21, 2015

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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Thursday, August 20, 2015

Reflections on the 2015 Ancestral Health Symposium

I just returned from the 2015 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.

Tuesday, August 18, 2015

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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Sunday, August 16, 2015

Ancestral Health Symposium 2015

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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Saturday, August 15, 2015

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. 

Thursday, August 13, 2015

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.

Tuesday, August 11, 2015

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) is the primary cause of common obesity due to its ability to elevate 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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