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.

Food Reward Friday

This week's "winner"...

The Pizza Hut hot dog stuffed crust pizza!

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.

Food Reward Friday

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

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.

Food Reward Friday

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

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.

Food Reward Friday

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

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 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.  

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:

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.

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):

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:

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. 

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. 

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.  

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:

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

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.

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!

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:

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. 

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.

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.

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:

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.

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. 

What Puts Fat Into Fat Cells, and What Takes it Out?

Body fatness at its most basic level is determined by the rate of fat going into vs. out of fat cells. This in/out cycle occurs regardless of conditions outside the cell, but the balance between in and out is influenced by a variety of external factors.  One of the arguments that has been made in the popular media about obesity goes something like this:  


A number of factors can promote the release of fat from fat cells, including:

Epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), glucagon, thyroid-stimulating hormone, melanocyte-stimulating hormone, vasopressin, and growth hormone

 But only two promote fat storage:

Insulin, and acylation-stimulating protein (ASP)*

Therefore if we want to understand body fat accumulation, we should focus on the latter category, because that's what puts fat inside fat cells.  Simple, right?

Can you spot the logical error in this argument?

A Pressure Cooker for the 21st Century

Pressure cookers are an extremely useful kitchen tool.  They greatly speed cooking and reduce energy usage by up to 70 percent.  This is because as pressure increases, so does the boiling point of water, which is the factor that limits cooking speed in water-containing foods (most foods).  If it weren't for my pressure cooker, I'd rarely eat beets or globe artichokes.  Instead of baking, boiling or steaming these for 60-90 minutes, I can have them soft as butter in 30.  But let's face it: most people are intimidated by pressure cookers.  They fear the sounds, the hot steam, and the perceived risk of explosion.  I escaped this because I grew up around them.

New Study Demonstrates that Sugar has to be Palatable to be Fattening in Mice

Dr. Anthony Sclafani's research group just published a study definitively demonstrating that high palatability, or pleasantness of taste, is required for sugar to be fattening in mice (1).  Dr. John Glendinning was lead author. Dr. Sclafani's group has done a lot of excellent research over the years.  Among other things, he's the person who invented the most fattening rodent diet in the world-- the 'cafeteria diet'-- composed of human junk food. 

Mice and rats love sweet food and drinks, just like humans.  If you give them a choice between plain water and sugar water, they'll overconsume the sugar water and become obese.  I have argued, based on a large body of evidence, that the reward value and palatability* of these solutions are important to this process (2, 3, 4).  This is really just common sense honestly, because by definition if the solution weren't rewarding the mice wouldn't go out of their way to drink it instead of water, the same way people wouldn't go out of their way to get soda if it weren't rewarding.  But it's always best to confirm common sense with research.

Sugar Intake and Body Fatness in Non-industrial Cultures

Around the world, non-industrial cultures following an ancestral diet and lifestyle tend to be lean. When they transition a modern diet and lifestyle, they typically put on body fat and develop the classic "diseases of civilization" such as diabetes and cardiovascular disease.  If we can understand the reasons why this health transition occurs, we will understand why these problems afflict us today.  Research has already identified a number of important factors, but today I'm going to discuss one in particular that has received a lot of attention lately: sugar.

There's an idea currently circulating that sugar is the main reason why healthy traditional cultures end up obese and sick.  It’s easy to find non-industrial cultures that are lean and don’t eat much sugar, and it’s easy to find industrial cultures that are obese and eat a lot of it.  But many factors are changing simultaneously there.  We could use the same examples to demonstrate that blue jeans and hair gel cause obesity.  If sugar is truly the important factor, then cultures with a high sugar intake, but an otherwise ancestral diet and lifestyle, should also be overweight and sick.  Let’s see if that's true. 

Calories Still Matter

The Centers for Disease Control's NHANES surveys documented a massive increase in obesity in the United States between the 1960-62 and 2007-2008 survey periods (1).  In 1960, 13 percent of US adults were obese, while in 2008 that number had risen to 34 percent.  The prevalence of extreme obesity increased from 0.9 to 6.0 percent over the same time period!

Something has changed, but what?  Well, the most parsimonious explanation is that we're simply eating more.  Here is a graph I created of our calorie intake (green) overlaid on a graph of obesity prevalence (blue) between 1970 and 2008:

How Bad is Fructose? David Despain Interviews Dr. John Sievenpiper

In my article "Is Sugar Fattening?", I discussed a recent review paper on fructose, by Dr. John Sievenpiper and colleagues (1).  It was the most recent of several review papers to conclude that fructose is probably not inherently fattening in humans, but that it can be fattening if it's consumed to excess, due to the added calories.  Dr. Sievenpiper and colleagues have also written other papers addressing the metabolic effects of fructose, which appear to be fairly minor unless it's consumed to excess (2, 3, 4, 5).  The senior author on these studies is Dr. David Jenkins at McMaster University.  David Despain, a science and health writer who publishes a nice blog called Evolving Health, recently interviewed Dr. Sievenpiper about his work.

It's an interesting interview and very timely, due to the recent attention paid to fructose in the popular media. This has mostly been driven by a couple of high-profile individuals-- an issue they discuss in the interview.  The interview, recent papers, and sessions at scientific conferences are part of an effort by researchers to push back against some of the less well founded claims that have received widespread attention lately.

Lower Blood Pressure Naturally

Recently, Chris Kresser published a series on dietary salt (sodium chloride) and health (1).  One of the issues he covered is the effect of salt on blood pressure.  Most studies have shown a relatively weak relationship between salt intake and blood pressure.  My position overall is that we're currently eating a lot more salt than at almost any point in our evolutionary history as a species, so I tend to favor a moderately low salt intake.  However, there may be more important factors than salt when it comes to blood pressure, at least in the short term. 

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part III

In previous posts, I reviewed some of the evidence suggesting that human evolution has accelerated rapidly since the development of agriculture (and to some degree, before it).  Europeans (and other lineages with a long history of agriculture)  carry known genetic adaptations to the Neolithic diet, and there are probably many adaptations that have not yet been identified.  In my final post in this series, I'll argue that although we've adapted, the adaptation is probably not complete, and we're left in a sort of genetic limbo between the Paleolithic and Neolithic state. 

Recent Genetic Adaptations are Often Crude

It may at first seem strange, but many genes responsible for common genetic disorders show evidence of positive selection.  In other words, the genes that cause these disorders were favored by evolution at some point because they presumably provided a survival advantage.  For example, the sickle cell anemia gene protects against malaria, but if you inherit two copies of it, you end up with a serious and life-threatening disorder (1).  The cystic fibrosis gene may have been selected to protect against one or more infectious diseases, but again if you get two copies of it, quality of life and lifespan are greatly curtailed (2, 3).  Familial Mediterranean fever is a very common disorder in Mediterranean populations, involving painful inflammatory attacks of the digestive tract, and sometimes a deadly condition called amyloidosis.  It shows evidence of positive selection and probably protected against intestinal disease due to the heightened inflammatory state it confers to the digestive tract (4, 5).  Celiac disease, a severe autoimmune reaction to gluten found in some grains, may be a by-product of selection for protection against bacterial infection (6).  Phenylketonuria also shows evidence of positive selection (7), and the list goes on.  It's clear that a lot of our recent evolution was in response to new disease pressures, likely from increased population density, sendentism, and contact with domestic animals.

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part II

In previous posts, I described how Otzi was (at least in large part) a genetic descendant of Middle Eastern agriculturalists, rather than being purely descended from local hunter-gatherers who adopted agriculture in situ.  I also reviewed evidence showing that modern Europeans are a genetic mixture of local European hunter-gatherers, incoming agricultural populations from the Middle East, neanderthals, and perhaps other groups.  In this post, I'll describe the evidence for rapid human evolution since the end of the Paleolithic period, and research indicating that some of these changes are adaptations to the Neolithic (agricultural/horticultural/pastoral) diet.

Humans have Evolved Significantly Since the End of the Paleolithic

Evolution by natural selection leaves a distinct signature in the genome, and geneticists can detect this signature tens of thousands of years after the fact by comparing many genomes to one another.  A landmark paper published in 2007 by Dr. John Hawks and colleagues showed that humans have been undergoing "extraordinarily rapid recent genetic evolution" over the last 40,000 years (1).  Furthermore:

Media Appearances

Last October, I participated in a panel discussion organized by the Harvard Food Law Society in Boston.  The panel included Drs. Walter Willett, David Ludwig, Robert Lustig, and myself, with Corby Kummer as moderator.  Dr. Willett is the chair of the Harvard Department of Nutrition; Dr. Ludwig is a professor of nutrition and pediatrics at Harvard; Dr. Lustig is a professor of clinical pediatrics at UCSF; and Kummer is a food writer and senior editor for The Atlantic. 

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part I

In the previous post, I explained that Otzi descended in large part from early adopters of agriculture in the Middle East or nearby.  What I'll explain in further posts is that Otzi was not a genetic anomaly: he was part of a wave of agricultural migrants that washed over Europe thousands of years ago, spreading their genes throughout.  Not only that, Otzi represents a halfway point in the evolutionary process that transformed Paleolithic humans into modern humans.

Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?

There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe.  One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains.  The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle.  These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals.  We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming. 

Lessons From Ötzi, the Tyrolean Ice Man. Part III

There are two reasons why I chose this time to write about Otzi.  The first is that I've been looking for a good excuse to revisit human evolutionary history, particularly that of Europeans, and what it does and doesn't tell us about the "optimal" human diet.  The second is that Otzi's full genome was sequenced and described in a recent issue of Nature Communications (1).  A "genome" is the full complement of genes an organism carries.  So what that means is that researchers have sequenced almost all of his genes. 

Lessons From Ötzi, the Tyrolean Ice Man. Part II

Otzi's Diet

Otzi's digestive tract contains the remains of three meals.  They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2).  The meat came from three different animals-- chamois, red deer and ibex.  The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.

Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3).  He died in the spring with a belly full of einkorn wheat.  Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year.  However, he also clearly ate meat and used leather made from his prey.  Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.

Exercise and Food Intake

The New York Times just published an article reviewing some of the recent research on exercise, food intake and food reward, titled "Does Exercise Make You Overeat?".  I was planning to write about this at some point, but I don't know when I'd be able to get around to it, and the NYT article is a fair treatment of the subject, so I'll just point you to the article.

Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less.  Alex Hutchinson discussed this point recently on his blog (1).  Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat.  Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat.  There is a lot of individual variability here.  The average obese person won't lose a substantial amount of fat through exercise alone.  However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people.  On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward. 

Next Primal Chef Event Sunday 5/20

Gil Butler has been working on a television show called Primal Chef, where he invites local chefs to make creative dishes from a list of Paleo ingredients, in a designated amount of time.  The format is reminiscent of Iron Chef.  The food is judged afterward by figures in the Paleo community.  Robb Wolf was a judge on the first episode.

Gil has invited me to be a judge on the next show, along with Sara Fragoso and Dr. Tim Gerstmar.  The next day, Sunday April 20th, Gil is organizing a catered Primal Chef event in Seattle, with Paleo dinner, speakers, entertainment, prizes, and a screening of part of Paleo Chef episode 1.  You can read the details and sign up here.  I won't be speaking because I don't have time to put together another talk right now, but I will be attending the event. 

Lessons From Ötzi, the Tyrolean Ice Man. Part I

This is Otzi, or at least a reconstruction of what he might have looked like.  5,300 years ago, he laid down on a glacier near the border between modern-day Italy and Austria, under unpleasant circumstances.  He was quickly frozen into the glacier.  In 1991, his slumber was rudely interrupted by two German tourists, which eventually landed him in the South Tyrol Museum of Archaeology in Italy. 

Otzi is Europe's oldest natural human mummy, and as such, he's an important window into the history of the human species in Europe.  His genome has been sequenced, and it offers us clues about the genetic history of modern Europeans.

Otzi's Story

Global Meat Production, 1961-2009

Total global meat production per person has steadily increased from 0.13 lbs per day in 1961 to 0.29 lbs per day in 2009*, a 120 percent increase over the last half century (currently in the US, average meat consumption is about half a pound per day).  Since meat consumption in the US and Europe has only increased modestly over time, this change mostly reflects greatly increased meat consumption over the last half century in developing countries** in Asia, Africa and South America.  In 1961, it's likely that most of the 0.13 pounds per day of meat was consumed in affluent countries such as the US, with not much consumed elsewhere (with some exceptions).  Historically, meat has always been expensive relative to other food sources in agricultural societies, so it's eaten by those who can afford it.

Eocene Diet Follow-up

Now that WHS readers around the globe have adopted the Eocene Diet and are losing weight at an alarming rate, it's time to explain the post a little more.  First, credit where credit is due: Melissa McEwen made a similar argument in her 2011 AHS talk, where she rolled out the "Cambrian Explosion Diet", which beats the Eocene Diet by about 470 million years.  It was probably in the back of my head somewhere when I came up with the idea.

April Fools day is good for a laugh, but humor often has a grain of truth in it.  In this case, the post was a jumping off point for discussing human evolution and what it has to say about the "optimal" human diet, if such a thing exists.  Here's a preview: evolution is a continuous process that has shaped our ancestors' genomes for every generation since the beginning of life.  It didn't end with the Paleolithic, in fact it accelerated, and most of us today carry meaningful adaptations to the Neolithic diet and lifestyle. 

The Eocene Diet

Warning -- Satire -- April Fool's Post

65 million years ago, a massive asteroid slammed into the Yucatan peninsula, creating a giant dust cloud that contributed to the extinction of terrestrial dinosaurs.  In the resulting re-adjustment of global ecosystems, a new plant tissue evolved, which paved the way for the eventual appearance of humans: fruit.  Fruit represents a finely crafted symbiosis between plants and animals, in which the plant provides a nourishing morsel, and the animal disperses the plant's seeds inside a packet of rich fertilizer.

Fruit was such a powerful selective pressure that mammals quickly evolved to exploit it more effectively, developing adaptations for life in the forest canopy.  One result of this was the rapid emergence of primates, carrying physical, digestive and metabolic adaptations for the acquisition and consumption of fruit and leaves.  Primates also continued eating insects, a vestige of our early mammalian heritage. 

Onward

In upcoming posts, I plan to pursue two main themes.  The first is a more comprehensive exploration of what determines eating behavior in humans, the neurobiology behind it, and the real world implications of this research.  The reward and palatability value of food are major factors, but there are others, and I've spent enough time focusing on them for the time being.  Also, the discussions revolving around food reward seem to be devolving into something that resembles team sports, and I've had my fill.

The second topic I'm going to touch on is human evolutionary history, including amazing recent insights from the field of human genetics.  These findings have implications for the nutrition and health of modern humans. 

I look forward to exploring these topics, and others, with all of you in the coming months.

Recent Media Appearances

Men's Health interviewed and quoted me in an article titled "Reprogram Your Metabolism", written by Lou Schuler.  Part of the article was related to the food reward concept.  I'm glad to see the idea gradually reaching the mainstream. 

Boing Boing recently covered an article by Dr. Hisham Ziauddeen and colleagues in Nature Reviews Neuroscience that questioned the idea that common obesity represents food addiction-- an idea that I often encounter in my reading.  Maggie Koerth-Baker asked me if I wanted to respond.  I sent her a response explaining that I agree with the authors' conclusions and I also doubt obesity is food addiction per se, as I have explained in the past, although a subset of obese people can be addicted to food.  I explained that the conclusions of the paper are consistent with the idea that food reward influences fat mass.  You can find my explanation here.

Food Reward: Approaching a Scientific Consensus

Review papers provide a bird's-eye view of a field from the perspective of experts.  Recent review papers show that many obesity researchers are converging on a model for the development of obesity that includes excessive food reward*, in addition to other factors such as physical inactivity, behavioral traits, and alterations in the function of the hypothalamus (a key brain region for the regulation of body fatness).  Take for example the four new review papers I posted recently by obesity and reward researchers:

Speaking at AHS12

I'll be giving a 40 minute presentation at the Ancestral Health Symposium this summer titled "Digestive Health, Inflammation and the Metabolic Syndrome".  Here's the abstract:

The “metabolic syndrome” is a cluster of health problems including abdominal obesity, insulin resistance, low-grade inflammation, high blood pressure and blood lipid abnormalities that currently affects one third of American adults.  It is the quintessential modern metabolic disorder and a major risk factor for diabetes, heart disease and certain cancers.  This talk will explore emerging links between diet, gut flora, digestive health and the development of the metabolic syndrome.  The audience will learn about factors that may help maintain digestive and metabolic health for themselves and the next generation.

Excessive fat mass is an important contributor to the metabolic syndrome, but at the same level of body fatness, some people are metabolically normal while others are extremely impaired.  Even among obese people, most of whom have the metabolic syndrome, about 20 percent are metabolically normal, with normal fasting insulin and insulin sensitivity, normal blood pressure, normal circulating inflammatory markers, and normal blood lipids.

What determines this?  Emerging research suggests that one factor is digestive health, including the bacterial ecosystem inside each person's digestive tract, and the integrity of the gut barrier.  I'll review some of this research in my talk, and leave the audience with actionable information for maintaining gastrointestinal and metabolic health.  Most of this information will not have been covered on this blog.

The Ancestral Health Symposium will be from August 9-12 at Harvard Law School in Boston, presented in conjunction with the Harvard Food Law society.  Tickets are currently available-- get them before they sell out!  Last year, they went fast.

See you there!

Qsymia (formerly Qnexa), the Latest Obesity Drug

There are very few obesity drugs currently approved for use in the US-- not because effective drugs don't exist, but because the FDA has judged that the side effects of existing drugs are unacceptable. 

Although ultimately I believe the most satisfying resolution to the obesity epidemic will not come from drugs, drugs offer us a window into the biological processes that underlie obesity and fat loss.  Along those lines, here's a quote from a review paper on obesity drugs that I think is particularly enlightening (1):

Boing!

I just had a featured article published on Boing Boing, "Seduced by Food: Obesity and the Human Brain".  Boing Boing is the most popular blog on the Internet, with over 5 million unique visitors per month, and it's also one of my favorite haunts, so it was really exciting for me to be invited to submit an article.  For comparison, Whole Health Source had about 72,000 unique visitors last month (200,000+ hits).

The article is a concise review of the food reward concept, and how it relates to the current obesity epidemic.  Concise compared to all the writing I've done on this blog, anyway.  I put a lot of work into making the article cohesive and understandable for a somewhat general audience, and I think it's much more effective at explaining the concept than the scattered blog posts I've published here.  I hope it will clear up some of the confusion about food reward.  I don't know what's up with the image they decided to use at the top. 

Many thanks to Mark Frauenfelder, Maggie Koerth-Baker, and Rob Beschizza for the opportunity to publish on Boing Boing, as well as their comments on the draft versions!

For those who have arrived at Whole Health Source for the first time via Boing Boing, welcome!   Have a look around.  The "labels" menu on the sidebar is a good place to start-- you can browse by topic.

Tweet

I've decided, on the sage advice of a WHS reader, to join the world of Twitter.  I'll be using it to announce new posts, as well as communicating papers that I find interesting, but either don't have time to blog about or think are too technical for a general audience.  My tag is "whsource".  Head on over to Twitter if you want to follow my tweets.

Palatability, Satiety and Calorie Intake

WHS reader Paul Hagerty recently sent me a very interesting paper titled "A Satiety Index of Common Foods", by Dr. SHA Holt and colleagues (1).  This paper quantified how full we feel after eating specific foods.  I've been aware of it for a while, but hadn't read it until recently.  They fed volunteers a variety of commonly eaten foods, each in a 240 calorie portion, and measured how full each food made them feel, and how much they ate at a subsequent meal.  Using the results, they calculated a "satiety index", which represents the fullness per calorie of each food, normalized to white bread (white bread arbitrarily set to SI = 100).  So for example, popcorn has a satiety index of 154, meaning it's more filling than white bread per calorie. 

One of the most interesting aspects of the paper is that the investigators measured a variety of food properties (energy density, fat, starch, sugar, fiber, water content, palatability), and then determined which of them explained the SI values most completely.

Soda-Free Sunday

Last Thursday, I received a message from a gentleman named Dorsol Plants about a public health campaign here in King County called Soda Free Sunday.  They're asking people to visit www.sodafreesundays.com and make a pledge to go soda-free for one day per week. 

Drinking sugar-sweetened beverages (SSBs), including soda, is one of the worst things you can do for your health.  SSB consumption is probably one of the major contributors to the modern epidemics of obesity and metabolic dysfunction.

I imagine that most WHS readers don't drink SSBs very often if at all, but I'm sure some do.  Whether you want to try drinking fewer SSBs, or just re-affirm an ongoing commitment to avoid them, I encourage you to visit www.sodafreesundays.com and make the pledge.  You can do so even if you're not a resident of King county.

Is Sugar Fattening?

Buckle your seat belts, ladies and gentlemen-- we're going on a long ride through the scientific literature on sugar and body fatness.  Some of the evidence will be surprising and challenging for many of you, as it was for me, but ultimately it paints a coherent and actionable picture.

By 2606, the US Diet will be 100 Percent Sugar

The US diet has changed dramatically in the last 200 years.  Many of these changes stem from a single factor: the industrialization and commercialization of the American food system.  We've outsourced most of our food preparation, placing it into the hands of professionals whose interests aren't always well aligned with ours.

It's hard to appreciate just how much things have changed, because none of us were alive 200 years ago.  To help illustrate some of these changes, I've been collecting statistics on US diet trends.  Since sugar is the most refined food we eat in quantity, and it's a good marker of processed food consumption, naturally I wanted to get my hands on sugar intake statistics-- but solid numbers going back to the early 19th century are hard to come by!  Of all the diet-related books I've read, I've never seen a graph of year-by-year sugar intake going back more than 100 years.

A gentleman by the name of Jeremy Landen and I eventually tracked down some outstanding statistics from old US Department of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005, which have appeared in two of my talks but I have never seen graphed anywhere else*.  These numbers represent added sweeteners such as cane sugar, high-fructose corn syrup and maple syrup, but not naturally occurring sugars in fruit and vegetables.  Behold:

Cigarette Smoking-- Another Factor in the Obesity Epidemic

Obesity rates in the US have more than doubled in the last 30 years, and rates of childhood obesity and extreme adult obesity have tripled.  One third of US adults are considered obese, and another third overweight.  This is the "obesity epidemic".

The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved.  However, there's another probable contributor that's often overlooked: declining smoking rates.  

Here's a graph I prepared of cigarette consumption over the last century in the US (1):

My TEDx Talk, "The American Diet: a Historical Perspective"

On October 21st, I spoke at the Harvard Food Law Society's TEDx conference, Forum on Food Policy.  The conference kicked off with three talks on nutrition, by Drs. Walter Willett, David Ludwig and myself.  My talk is only 17 minutes long as per TED format, but it's packed with research on both quantitative and qualitative changes in the US diet over the last two centuries.  It contains surprises for almost anyone, and I can guarantee you've never learned this much about the history of the US diet in 17 minutes.  The talk was titled "The American Diet: a Historical Perspective"; you can access it by following that link.

An Interview with Dr. C. Vicky Beer, Paleo-friendly MD

As I was preparing my recent article on the Paleo diet (1), I interviewed a local Paleo-friendly MD named C. Vicky Beer.  I was only able to include a snippet of the interview in the article, but I thought WHS readers would be interested to read the rest of the interview with Dr. Beer:

Paleo Diet Article in Sound Consumer

I recently wrote an article for my local natural foods grocery store, PCC, about the "Paleolithic" diet.  You can read it online here.  I explain the basic rationale for Paleo diets, some of the scientific support behind it, and how it can be helpful for people with certain health problems.  I focused in particular on the research of Dr. Staffan Lindeberg at the University of Lund, who has studied non-industrial populations using modern medical techniques and also conducted clinical diet trials using the Paleo diet.

Insulin and Obesity: Another Nail in the Coffin

There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness.  Some versions invoke insulin's effects on fat tissue, others its effects in the brain.  This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn't seem to have much if any impact on body weight in controlled trials). 

I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s.  However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness.  If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well. 

What Causes Insulin Resistance? Part VII

In previous posts, I outlined the factors I'm aware of that can contribute to insulin resistance.  In this post, first I'll list the factors, then I'll provide my opinion of effective strategies for preventing and potentially reversing insulin resistance.

The factors

These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance.  I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another. 

Three Announcements

Chris Highcock of the blog Conditioning Research just published a book called Hillfit, which is a conditioning book targeted at hikers/backpackers.  He uses his knowledge and experience in hiking and conditioning to argue that strength training is an important part of conditioning for hiking.  I'm also a hiker/backpacker myself here in the rugged and beautiful Pacific Northwest, and I also find that strength training helps with climbing big hills, and walking farther and more easily with a lower risk of injury.

Richard Nikoley of the blog Free the Animal has also published a book called Free the Animal: Beyond the Blog, where he shares his strategies for losing fat and improving health and fitness.  I haven't had a chance to read it yet, but Richard has a reasonable perspective on diet/health and a sharp wit. 

Also, my friend Pedro Bastos has asked me to announce a one-day seminar at the University of Lisbon (Portugal) by Dr. Frits Muskiet titled "Vitamins and Minerals: A Scientific, Modern, Evolutionary and Global View".  It will be on Sunday, Feb 5-- you can find more details about the seminar here.  Dr. Muskiet is a researcher at the Groningen University Medical Center in the Netherlands.  He studies the impact of nutrients, particularly fatty acids, on health, from an evolutionary perspective.  Wish I could attend. 

What Causes Insulin Resistance? Part VI

In this post, I'll explore a few miscellaneous factors that can contribute to insulin resistance: smoking, glucocorticoids/stress, cooking temperature, age, genetics and low birth weight.

Smoking

Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:

1. Increased inflammation
2. Increased circulating free fatty acids (4)

Paradoxically, since smoking also protects against fat gain, in the very long term it may not produce as much insulin resistance as one would otherwise expect.  Diabetes risk is greatly elevated in the three years following smoking cessation (5), and this is likely due to the fat gain that occurs.  This is not a good excuse to keep smoking, because smoking tobacco is one of the most unhealthy things you can possibly do.  But it is a good reason to tighten up your diet and lifestyle after quitting.

What Causes Insulin Resistance? Part V

Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance.  In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.

Carbohydrate and Fat

There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity.  What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people.  This will get at what causes insulin resistance in someone who does not already have it.

New Obesity Review Paper by Yours Truly

The Journal of Clinical Endocrinology and Metabolism just published a clinical review paper written by myself and my mentor Dr. Mike Schwartz, titled "Regulation of Food Intake, Energy Balance, and Body Fat Mass: Implications for the Pathogenesis and Treatment of Obesity" (1).  JCEM is one of the most cited peer-reviewed journals in the fields of endocrinology, obesity and diabetes, and I'm very pleased that it spans the gap between scientists and physicians.  Our paper takes a fresh and up-to-date look at the mechanisms by which food intake and body fat mass are regulated by the body, and how these mechanisms are altered in obesity.  We explain the obesity epidemic in terms of the mismatch between our genes and our current environment, a theme that is frequently invoked in ancestral health circles.

What Causes Insulin Resistance? Part IV

So far, we've explored three interlinked causes of insulin resistance: cellular energy excess, inflammation, and insulin resistance in the brain.  In this post, I'll explore the effects on micronutrient status on insulin sensitivity.

Micronutrient Status

There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post.  My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.

What Causes Insulin Resistance? Part III

As discussed in previous posts, cellular energy excess and inflammation are two important and interlinked causes of insulin resistance.  Continuing our exploration of insulin resistance, let's turn our attention to the brain.

The brain influences every tissue in the body, in many instances managing tissue processes to react to changing environmental or internal conditions.  It is intimately involved in insulin signaling in various tissues, for example by:

• regulating insulin secretion by the pancreas (1)
• regulating glucose absorption by tissues in response to insulin (2)
• regulating the suppression of glucose production by the liver in response to insulin (3)
• regulating the trafficking of fatty acids in and out of fat cells in response to insulin (4, 5)

Because of its important role in insulin signaling, the brain is a candidate mechanism of insulin resistance.

What Causes Insulin Resistance? Part II

In the last post, I described how cellular energy excess causes insulin resistance, and how this is triggered by whole-body energy imbalance.  In this post, I'll describe another major cause of insulin resistance: inflammation. 

Inflammation

In 1876, a German physician named W Ebstein reported that high doses of sodium salicylate could totally eliminate the signs and symptoms of diabetes in certain patients (Berliner Klinische Wochenschrift. 13:337. 1876). Following up on this work in 1901, the British physician RT Williamson reported that treating diabetic patients with sodium salicylate caused a striking decrease in the amount of glucose contained in the patients' urine, also indicating an apparent improvement in diabetes (2).  This effect was essentially forgotten until 1957, when it was rediscovered.

What Causes Insulin Resistance? Part I

Insulin is an ancient hormone that influences many processes in the body.  Its main role is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body's two main fuels), keeping them within a fairly narrow range*.  It does this by encouraging the transport of nutrients into cells from the circulation, and discouraging the export of nutrients out of storage sites, in response to an increase in circulating nutrients (glucose or fatty acids). It therefore operates a negative feedback loop that constrains circulating nutrient concentrations.  It also has many other functions that are tissue-specific.

Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids).  It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders. 

Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range?  The answer to that question is the crux of this post. 

New York Times Magazine Article on Obesity

For those of you who haven't seen it, Tara Parker-Pope write a nice article on obesity in the latest issue of NY Times Magazine (1).  She discusses  research showing  that the body "resists" fat loss attempts, making it difficult to lose fat and maintain fat loss once obesity is established.

High-Fat Diets, Obesity and Brain Damage

Many of you have probably heard the news this week:

High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods

Your brain cells are exploding with every bite of butter!  Just kidding.  The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1).  We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop.  I'm fourth author on the paper, so let me explain what we found and why it's important.  

The Questions

Among the many questions that interest obesity researchers, two stand out:

1. What causes obesity?
2. Once obesity is established, why is it so difficult to treat?

Our study expands on the efforts of many other labs to answer the first question, and takes a stab at the second one as well.  Dr. Licio Velloso and collaborators were the first to show in 2005 that inflammation in a part of the brain called the hypothalamus contributes to the development of obesity in rodents (2), and this has been independently confirmed several times since then.  The hypothalamus is an important brain region for the regulation of body fatness, and inflammation keeps it from doing its job correctly.

The Findings

Junk Free January

Last year, Matt Lentzner organized a project called Gluten Free January, in which 546 people from around the world gave up gluten for one month.  The results were striking: a surprisingly large proportion of participants lost weight, experienced improved energy, better digestion and other benefits (1, 2).  This January, Lentzner organized a similar project called Junk Free January.  Participants can choose between four different diet styles:

1. Gluten free
2. Seed oil free (soybean, sunflower, corn oil, etc.)
3. Sugar free
4. Gluten, seed oil and sugar free

Wheat, seed oils and added sugar are three factors that, in my opinion, are probably linked to the modern "diseases of affluence" such as obesity, diabetes and coronary heart disease.  This is particularly true if the wheat is eaten in the form of white flour products, and the seed oils are industrially refined and used in high-heat cooking applications.

If you've been waiting for an excuse to improve your diet, why not join Junk Free January?