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. 

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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

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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.
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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. 

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The Eocene Diet

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. 

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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:
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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 problemsincluding abdominal obesity, insulin resistance, low-grade inflammation, highblood pressure and blood lipid abnormalities that currently affects one thirdof American adults.  It is thequintessential modern metabolic disorder and a major risk factor for diabetes,heart disease and certain cancers.  Thistalk will explore emerging links between diet, gut flora, digestive health andthe development of the metabolic syndrome. The audience will learn about factors that may help maintain digestiveand 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!

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):
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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.

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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.

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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:

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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 of cigarette consumption over the last century in the US (1):
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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.

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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:

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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.
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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. 

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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. 
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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.

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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.

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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.

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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.

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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.

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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.

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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. 

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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.
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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

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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?