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

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

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

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

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

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Food Reward Friday

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This week's lucky "winner"... peanut M + M's!!!


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Does "Metabolically Healthy Obesity" Exist?

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

Does metabolically healthy obesity exist?

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Food Reward Friday

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


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Beans, Lentils, and the Paleo Diet

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

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

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

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

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

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

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Recent and Upcoming Appearances

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Smarter Science of Slim

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

Super Human Radio

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

The Reality Check podcast

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

Obesity Society conference

Next Thursday 11/9, I'll be speaking at the 2013 Obesity Society conference in Atlanta.  My talk is titled "The Glial Response to Obesity is Reversible", and it will be about my work on the reversibility of obesity-associated hypothalamic neuropathology in mice.  My talk will be part of the session "Neuronal Control of Satiety" between 3:00 and 4:30, specific time pending.  See you there!

Buckwheat Crepes Revisited

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

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

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

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New Post on Eat Move Sleep Blog

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

Sleep and Genetic Obesity Risk

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

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

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Speaking in Lisbon on October 5

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

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

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

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

Is Refined Carbohydrate Addictive?

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

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

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

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

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

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More Thoughts on Cold Training: Biology Chimes In

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

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

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

Biology of Temperature Regulation

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Reflections on the 2013 Ancestral Health Symposium

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

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

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

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

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

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

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

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

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

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

AHS Talk This Saturday

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For those who are attending the Ancestral Health Symposium this year, my talk will be at 9:00 AM on Saturday.  The title is "Insulin and Obesity: Reconciling Conflicting Evidence", and it will focus on the following two questions:
  1. Does elevated insulin cause obesity; does obesity cause elevated insulin; or both?
  2. Is there a unifying hypothesis that's able to explain all of the seemingly conflicting evidence cited by each side of the debate?
I'll approach the matter in true scientific fashion: stating hypotheses, making rational predictions based on those hypotheses, and seeing how well the evidence matches the predictions.  I'll explore the evidence in a way that has never been done before (to my knowledge), even on this blog.

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

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

Food Reward Friday

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

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

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Food Reward Friday

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


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Brown Fat: It's a Big Deal

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

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

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

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

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

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


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The Genetics of Obesity, Part III

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Genetics Loads the Gun, Environment Pulls the Trigger

Thanks to a WHS reader* for reminding me of the above quote by Dr. Francis Collins, director of the US National Institutes of Health**.  This is a concept that helps reconcile the following two seemingly contradictory observations:
  1. Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
  2. Diet and lifestyle have a large impact on obesity risk.  The prevalence of obesity has tripled in the last 30 years, and the prevalence of extreme obesity has increased by almost 10-fold.  This is presumably not enough time for genetic changes to account for it.
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