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 (2, 3). 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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Does "Metabolically Healthy Obesity" Exist?
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cancer,
Cardiovascular disease,
diabetes,
disease,
metabolic syndrome,
overweight
Obesity is strongly associated with metabolic alterations and negative health outcomes including diabetes, cardiovascular disease, and some types of cancer (1, 2, 3, 4). 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:
Does metabolically healthy obesity exist?
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- Does metabolically healthy obesity exist?
- If so, are metabolically healthy obese people at an elevated risk of disease and death?
Does metabolically healthy obesity exist?
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Beans, Lentils, and the Paleo Diet
As we continue to explore the foods our ancestors relied on during our evolutionary history, and what foods work best for us today, we come to legumes such as beans and lentils. These are controversial foods within the Paleolithic diet community, while the broader nutrition community tends to view legumes as healthy.
Beans and lentils have a lot going for them. They're one of the few foods that are simultaneously rich in protein and fiber, making them highly satiating and potentially good for the critters in our colon. They're also relatively nutritious, delivering a hefty dose of vitamins and minerals. The minerals are partially bound by the anti-nutrient phytic acid, but simply soaking and cooking beans and lentils typically degrades 30-70 percent of it, making the minerals more available for absorption (Food Phytates. Reddy and Sathe. 2002). Omitting the soaking step greatly reduces the degradation of phytic acid (Food Phytates. Reddy and Sathe. 2002).
The only tangible downside to beans I can think of, from a nutritional standpoint, is that some people have a hard time with the large quantity of fermentable fiber they provide, particularly people who are sensitive to FODMAPs. Thorough soaking prior to cooking can increase the digestibility of the "musical fruit" by activating the sprouting program and leaching out tannins and indigestible saccharides. I soak all beans and lentils for 12-24 hours.
The canonical Paleolithic diet approach excludes legumes because they were supposedly not part of our ancestral dietary pattern. I'm going to argue here that there is good evidence of widespread legume consumption by hunter-gatherers and archaic humans, and that beans and lentils are therefore an "ancestral" food that falls within the Paleo diet rubric. Many species of edible legumes are common around the globe, including in Africa, and the high calorie and protein content of legume seeds would have made them prime targets for exploitation by ancestral humans after the development of cooking. Below, I've compiled a few examples of legume consumption by hunter-gatherers and extinct archaic humans. I didn't have to look very hard to find these, and there are probably many other examples available. If you know of any, please share them in the comments.
To be clear, I would eat beans and lentils even if they weren't part of ancestral hunter-gatherer diets, because they're inexpensive, nutritious, I like the taste, and they were safely consumed by many traditional agricultural populations probably including my own ancestors.
Extensive "bean" consumption by the !Kung San of the Kalahari desert
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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
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!
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!
Related Posts:
Buckwheat Crepes Revisited
One of my most popular posts of all time was a recipe I published in 2010 for sourdough buckwheat crepes (1). I developed this recipe to provide an easy, nutritious, and gluten-free alternative to flour-based crepes. It requires no equipment besides a blender. It's totally different from the traditional buckwheat crepes that are eaten in Brittany, in part because it's not really a crepe (I don't know what else to call it, maybe a savory pancake?). I find these very satisfying, and they're incredibly easy to make. They're especially delicious with fresh goat cheese, or scrambled eggs with vegetables, but they go with almost anything. Chris Kresser also developed his own version of the recipe, which is fluffier than mine, and more like a traditional pancake (2).
Buckwheat is an exceptionally nutritious pseudograin that's rich in complete protein and minerals. In contrast to most whole grains, which have low mineral availability due to phytic acid, buckwheat contains a high level of the phytic acid-degrading enzyme phytase. This makes buckwheat an excellent source of easily absorbed minerals, as long as you prepare it correctly! Phytase enzyme works best in an acidic environment, which may be part of the reason why so many cultures use sour fermentation to prepare grain foods. My original recipe included a sour fermentation step.
But there's a problem here. Buckwheat doesn't ferment very well. Whether it's because it doesn't contain the right carbohydrates, or the right bacteria, I don't know, but it spoils rapidly if you ferment it more than a little bit (using a strong sourdough starter helps though). Others have told me the same. So here's my confession: I stopped fermenting my buckwheat batter about a year ago. And it tastes better.
Read more »
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.
Read more »
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New Post on Eat Move Sleep Blog
Yesterday, the Dan's Plan blog Eat Move Sleep published a blog post I wrote about sleep, artificial light, your brain, and a free computer program called f.lux that can help us live healthier lives. Head over to Eat Move Sleep to read it.
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Sleep and Genetic Obesity Risk
Evidence is steadily accumulating that insufficient sleep increases the risk of obesity and undermines fat loss efforts. Short sleep duration is one of the most significant risk factors for obesity (1), and several potential mechanisms have been identified, including increased hunger, increased interest in calorie-dense highly palatable food, reduced drive to exercise, and alterations in hormones that influence appetite and body fatness. Dan Pardi presented his research at AHS13 showing that sleep restriction reduces willpower to make healthy choices about food.
We also know that genetics has an outsized influence on obesity risk, accounting for about 70 percent of the variability in body fatness between people in affluent nations (2). I have argued that "fat genes" don't directly lead to obesity, but they do determine who is susceptible to a fattening environment and who isn't (3). I recently revisited a 2010 paper published in the journal Sleep by University of Washington researchers that supports this idea (4).
Read more »
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
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:
Related Posts:
Is Refined Carbohydrate Addictive?
[Note: in previous versions, I mixed up "LGI" and "HGI" terms in a couple of spots. These are now corrected. Thanks to readers for pointing them out.]
Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:
Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.
This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction. The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.
So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation? Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.
Read more »
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.
Read more »
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More Thoughts on Cold Training: Biology Chimes In
Now that the concept of cold training for cold adaptation and fat loss has received scientific support, I've been thinking more about how to apply it. A number of people have been practicing cold training for a long time, using various methods, most of which haven't been scientifically validated. That doesn't mean the methods don't work (some of them probably do), but I don't know how far we can generalize individual results prior to seeing controlled studies.
The studies that were published two weeks ago used prolonged, mild cold exposure (60-63 F air) to achieve cold adaptation and fat loss (1, 2). 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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The studies that were published two weeks ago used prolonged, mild cold exposure (60-63 F air) to achieve cold adaptation and fat loss (1, 2). 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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AHS Talk This Saturday
For those who are attending the Ancestral Health Symposium this year, my talk will be at 9:00 AM on Saturday. The title is "Insulin and Obesity: Reconciling Conflicting Evidence", and it will focus on the following two questions:
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.
- Does elevated insulin cause obesity; does obesity cause elevated insulin; or both?
- Is there a unifying hypothesis that's able to explain all of the seemingly conflicting evidence cited by each side of the debate?
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.
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Food Reward Friday
This week's lucky "winner"... cola!
Thirsty yet? Visual cues such as these are used to drive food/beverage seeking and consumption behavior, which are used to drive profits. How does this work? Once you've consumed a rewarding beverage enough times, particularly as a malleable child, your brain comes to associate everything about that beverage with the primary reward you obtained from it (calories, sugar, and caffeine). This is simply Pavlovian/classical conditioning*. Everything associated with that beverage becomes a cue that triggers motivation to obtain it (craving), including the sight of it, the smell of it, the sound of a can popping, and even the physical and social environment it was consumed in-- just like Pavlov's dogs learned to drool at the sound of a bell that was repeatedly paired with food.
Read more »
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.
Read more »
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The Genetics of Obesity, Part III
Genetics Loads the Gun, Environment Pulls the Trigger
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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:
- Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
- 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.
Related Posts:
The Genetics of Obesity, Part II
Rodents Lead the Way
The study of obesity genetics dates back more than half a century. In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene. They named this the "obese" (ob/ob) mouse. Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.
At the time of discovery, no one knew where the mutations resided in the genome. All they knew is that the mutations were in single genes, and they resulted in extreme obesity. Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way. Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned. Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.
Read more »
The study of obesity genetics dates back more than half a century. In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene. They named this the "obese" (ob/ob) mouse. Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.
At the time of discovery, no one knew where the mutations resided in the genome. All they knew is that the mutations were in single genes, and they resulted in extreme obesity. Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way. Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned. Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.
Read more »
Related Posts:
The Genetics of Obesity, Part I
Choosing the Right Parents: the Best Way to Stay Lean?
In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1). They took advantage of one of the most useful tools in human genetics: identical twins. This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb. By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).
Read more »
In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1). They took advantage of one of the most useful tools in human genetics: identical twins. This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb. By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).
Read more »
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Food Reward Friday
This week's lucky "winner"... low-carb gluten-free bacon chocolate mocha ice cream cake!!
Read more »
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Food Reward Friday
This week's "winner" will certainly be the most controversial yet... bacon!!
Bacon is a fatty cut of pork (typically side or back) that has been thinly sliced, cured, then cooked until crispy. This results in a fatty, salty, savory flavor that almost everyone loves. Bacon's extremely high calorie density, saltiness, and savory flavor give it a reward value that competes with chocolate and ice cream. Sometimes it's even used to flavor chocolate and ice cream!
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Bacon is a fatty cut of pork (typically side or back) that has been thinly sliced, cured, then cooked until crispy. This results in a fatty, salty, savory flavor that almost everyone loves. Bacon's extremely high calorie density, saltiness, and savory flavor give it a reward value that competes with chocolate and ice cream. Sometimes it's even used to flavor chocolate and ice cream!
Read more »
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Update
I haven't been putting much effort into blogging these past few weeks. Frankly, a little break has been nice while I take care of other things in my life. But I haven't been twiddling my thumbs. Obesity research hasn't slowed down and there are many topics that I'd love to write about here if I had the time. I'll be starting a new series soon on the genetics of obesity-- a fascinating subject. I also plan to cover some of my recent publications on obesity and blood glucose control by the brain. Last but not least, we will soon roll out a substantially upgraded version of the Ideal Weight Program. Those who have already purchased the program will continue to have access to the new version.
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The Neurobiology of the Obesity Epidemic
I recently read an interesting review paper by Dr. Edmund T. Rolls titled "Taste, olfactory and food texture reward processing in the brain and the control of appetite" that I'll discuss in this post (1). Dr. Rolls is a prolific neuroscience researcher at Oxford who focuses on "the brain mechanisms of perception, memory, emotion and feeding, and thus of perceptual, memory, emotional and appetite disorders." His website is here.
The first half of the paper is technical and discusses some of Dr. Rolls' findings on how specific brain areas process sensory and reward information, and how individual neurons can integrate multiple sensory signals during this process. I recommend reading it if you have the background and interest, but I'm not going to cover it here. The second half of the paper is an attempt to explain the obesity epidemic based on what he knows about the brain and other aspects of human biology.
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The first half of the paper is technical and discusses some of Dr. Rolls' findings on how specific brain areas process sensory and reward information, and how individual neurons can integrate multiple sensory signals during this process. I recommend reading it if you have the background and interest, but I'm not going to cover it here. The second half of the paper is an attempt to explain the obesity epidemic based on what he knows about the brain and other aspects of human biology.
Read more »
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Speaking at AHS13
The 2013 Ancestral Health Symposium will be held in Atlanta, GA, August 14-17. Last year was a great conference, and I look forward to more informative talks and networking. Tickets go fast, so reserve yours now if you plan to attend!
This year, I'll be speaking on insulin and obesity. My talk will be titled "Insulin and Obesity: Reconciling Conflicting Evidence". In this talk, I'll present the evidence for and against the idea that elevated insulin contributes to the development of obesity. One hypothesis states that elevated insulin contributes to obesity, while the other states that elevated insulin is caused by obesity and does not contribute to it. Both sides of the debate present evidence that appears compelling, and it often seems like each side is talking past the other rather than trying to incorporate all of the evidence into a larger, more powerful model.
There's a lot evidence that can be brought to bear on this question, but much of it hasn't reached the public yet. I'll explore a broad swath of evidence from clinical case studies, observational studies, controlled trials, animal research, physiology, and cell biology to test the two competing hypotheses and outline a model that can explain all of the seemingly conflicting data. Much of this information hasn't appeared on this blog. My goal is to put together a talk that will be informative to a researcher but also accessible to an informed layperson.
On a separate note, my AHS12 talk "Digestive Health, Inflammation and the Metabolic Syndrome" has not been posted online because the video recording of my talk has mysteriously disappeared. I think many WHS readers would be interested in the talk, since it covers research on the important and interdependent influence of gut health, inflammation, and psychological stress on the metabolic syndrome (the quintessential modern metabolic disorder). I'm going to try to find time to make a narrated slideshow so I can post it on YouTube.
This year, I'll be speaking on insulin and obesity. My talk will be titled "Insulin and Obesity: Reconciling Conflicting Evidence". In this talk, I'll present the evidence for and against the idea that elevated insulin contributes to the development of obesity. One hypothesis states that elevated insulin contributes to obesity, while the other states that elevated insulin is caused by obesity and does not contribute to it. Both sides of the debate present evidence that appears compelling, and it often seems like each side is talking past the other rather than trying to incorporate all of the evidence into a larger, more powerful model.
There's a lot evidence that can be brought to bear on this question, but much of it hasn't reached the public yet. I'll explore a broad swath of evidence from clinical case studies, observational studies, controlled trials, animal research, physiology, and cell biology to test the two competing hypotheses and outline a model that can explain all of the seemingly conflicting data. Much of this information hasn't appeared on this blog. My goal is to put together a talk that will be informative to a researcher but also accessible to an informed layperson.
On a separate note, my AHS12 talk "Digestive Health, Inflammation and the Metabolic Syndrome" has not been posted online because the video recording of my talk has mysteriously disappeared. I think many WHS readers would be interested in the talk, since it covers research on the important and interdependent influence of gut health, inflammation, and psychological stress on the metabolic syndrome (the quintessential modern metabolic disorder). I'm going to try to find time to make a narrated slideshow so I can post it on YouTube.
Related Posts:
Food Variety, Calorie Intake, and Weight Gain
Let's kick off this post with a quote from a 2001 review paper (1):
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Increased variety in the food supply may contribute to the development and maintenance of obesity. Thirty-nine studies examining dietary variety, energy intake, and body composition are reviewed. Animal and human studies show that food consumption increases when there is more variety in a meal or diet and that greater dietary variety is associated with increased body weight and fat.This may seem counterintuitive, since variety in the diet is generally seen as a good thing. In some ways, it is a good thing, however in this post we'll see that it can have a downside.
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Book Review: Salt, Sugar, Fat
Michael Moss is a Pulitzer prize-winning journalist who has made a career writing about the US food system. In his latest book, Salt, Sugar, Fat: How the Food Giants Hooked Us, he attempts to explain how the processed food industry has been so successful at increasing its control over US "stomach share". Although the book doesn't focus on the obesity epidemic, the relevance is obvious. Salt, Sugar, Fat is required reading for anyone who wants to understand why obesity is becoming more common in the US and throughout the world.
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Glucagon, Dietary Protein, and Low-Carbohydrate Diets
Glucagon is a hormone that plays an important role in blood glucose control. Like insulin, it's secreted by the pancreas, though it's secreted by a different cell population than insulin (alpha vs. beta cells). In some ways, glucagon opposes insulin. However, the role of glucagon in metabolism is frequently misunderstood in diet-health circles.
The liver normally stores glucose in the form of glycogen and releases it into the bloodstream as needed. It can also manufacture glucose from glycerol, lactate, and certain amino acids. Glucagon's main job is to keep blood glucose from dipping too low by making sure the liver releases enough glucose. There are a few situations where this is particularly important:
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The liver normally stores glucose in the form of glycogen and releases it into the bloodstream as needed. It can also manufacture glucose from glycerol, lactate, and certain amino acids. Glucagon's main job is to keep blood glucose from dipping too low by making sure the liver releases enough glucose. There are a few situations where this is particularly important:
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Are Animal Crackers Paleo?
Warning -- Satire -- April Fool's Post
Every child loves animal crackers, those sweet and crunchy animal-shaped biscuits. But are they compatible with a Paleo diet? Some people might think they already know the answer, but consider this: our ancestors evolved on the African savanna, eating the plants and animals found there. Inside each box of animal crackers is an assortment of tiny savanna creatures such as giraffes and elephants.
To get to the bottom of this, I interviewed Robert Pearson, CEO of Animal Cracker Products Inc., who explained to me how these crackers are made.
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Every child loves animal crackers, those sweet and crunchy animal-shaped biscuits. But are they compatible with a Paleo diet? Some people might think they already know the answer, but consider this: our ancestors evolved on the African savanna, eating the plants and animals found there. Inside each box of animal crackers is an assortment of tiny savanna creatures such as giraffes and elephants.
To get to the bottom of this, I interviewed Robert Pearson, CEO of Animal Cracker Products Inc., who explained to me how these crackers are made.
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Neuronal Control of Appetite, Metabolism and Weight
Last week, I attended a Keystone conference, "Neuronal Control of Appetite, Metabolism and Weight", in Banff. Keystone conferences are small, focused meetings that tend to attract high quality science. This particular conference centered around my own professional research interests, and it was incredibly informative. This post is a summary of some of the most salient points.
Rapid Pace of Scientific Progress
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Rapid Pace of Scientific Progress
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Atherosclerosis in Ancient Mummies Revisited
Many of you are already aware of the recent study that examined atherosclerosis in 137 ancient mummies from four different cultures (1). Investigators used computed tomography (CT; a form of X-ray) to examine artery calcification in mummies from ancient Egypt, Peru, Puebloans, and arctic Unangan hunter-gatherers. Artery calcification is the accumulation of calcium in the vessel wall, and it is a marker of severe atherosclerosis. Where there is calcification, the artery wall is thickened and extensively damaged. Not surprisingly, this is a risk factor for heart attack. Pockets of calcification are typical as people age.
I'm not going to re-hash the paper in detail because that has been done elsewhere. However, I do want to make a few key points about the study and its interpretation. First, all groups had atherosclerosis to a similar degree, and it increased with advancing age. This suggests that atherosclerosis may be part of the human condition, and not a modern disease. Although it's interesting to have this confirmed in ancient mummies, we already knew this from cardiac autopsy data in a variety of non-industrial cultures (2, 3, 4, 5).
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Does the Mediterranean Diet Reduce Cardiovascular Risk?
By now, most of you have probably heard about the recent study on the "Mediterranean diet" (1), a diet that was designed by diet-heart researchers and is based loosely on the traditional diet of Crete and certain other Mediterranean regions. The popular press has been enthusiastically reporting this trial as long-awaited proof that the Mediterranean diet reduces the risk of cardiovascular events-- by a full 30 percent over a 4.8-year period. I wish I could share their enthusiasm for the study.
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Your Brain on Potato Chips
Or, more accurately, a rat's brain on potato chips. Last week, PLoS One published a very interesting paper by Dr. Tobias Hoch and colleagues on what happens in a rat's brain when it is exposed to a highly palatable/rewarding food (1). Rats, like humans, overconsume highly palatable foods even when they're sated on less palatable foods (2), and feeding rats a variety of palatable human junk foods is one of the most effective ways to fatten them (3). Since the brain directs all behaviors, food consumption is an expression of brain activity patterns. So what is the brain activity pattern that leads to the overconsumption of a highly palatable and rewarding food?
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Salt Sugar Fat
I'd just like to put in a quick word for a book that will be released tomorrow, titled Salt Sugar Fat: How the Food Giants Hooked Us, by Pulitzer prize-winning author Michael Moss. This is along the same lines as Dr. David Kessler's book The End of Overeating, which explains how the food industry uses food reward, palatability, and food cues to maximize sales-- and as an unintended side effect, maximize our waistlines. Judging by Moss's recent article in New York Times Magazine, which I highly recommend reading, the book will be excellent. I've pre-ordered it.
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Food Reward Friday
This week, Food Reward Friday is going to be a little bit different. I've received a few e-mails from people who would like to see me write about some of the less obvious examples of food reward-- foods that are less extreme, but much more common, and that nevertheless promote overeating. Let's face it, even though they're funny and they (sometimes) illustrate the principle, most people reading this blog don't eat banana splits very often, much less pizzas made out of hot dogs.
So this week's "winner" is something many of you have in your houses right now, and which was also the subject of an interesting recent study... potato chips!
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So this week's "winner" is something many of you have in your houses right now, and which was also the subject of an interesting recent study... potato chips!
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Body Fatness and Cardiovascular Risk Factors
I recently revisited a really cool paper published in the Lancet in 2009 on body fatness, biomarkers, health, and mortality (1). It's a meta-analysis that compiled body mass index (BMI) data from nearly 900,000 individual people, and related it to circulating lipids and various health outcomes. This is one of the most authoritative papers on the subject.
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