Is Meat Unhealthy? Part V
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In this post, I'll examine the possible relationship between meat intake and type 2 diabetes. Type 2 diabetes is the most common form of diabetes, and it is strongly linked to lifestyle factors.
Non-industrial cultures
Non-industrial cultures have an extremely low prevalence of diabetes, whether they are near-vegan or near-carnivorous. This is supported by blood glucose measurements in a variety of cultures, from the sweet potato farmers of the New Guinea highlands to the arctic Inuit hunters. Here is what Otto Schaefer, director of the Northern Medical Research Unit at Charles Camsell hospital in Edmonton, Canada, had to say about the Inuit in the excellent book Western Diseases (Trowell and Burkitt, 1981):
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Non-industrial cultures
Non-industrial cultures have an extremely low prevalence of diabetes, whether they are near-vegan or near-carnivorous. This is supported by blood glucose measurements in a variety of cultures, from the sweet potato farmers of the New Guinea highlands to the arctic Inuit hunters. Here is what Otto Schaefer, director of the Northern Medical Research Unit at Charles Camsell hospital in Edmonton, Canada, had to say about the Inuit in the excellent book Western Diseases (Trowell and Burkitt, 1981):
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Is Meat Unhealthy? Part IV
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In this post, I'll address the question: does eating meat contribute to weight gain?
Non-industrial cultures
I'll get right to the point: humans living in a non-industrialized setting tend to be lean, regardless of how much meat they eat. This applies equally to hunter-gatherers, herders, and farmers.
One of the leanest populations I've encountered in my reading is the 1960s Papua New Guinea highland farmers of Tukisenta. They ate a nearly vegan diet composed almost exclusively of sweet potatoes, occasionally punctuated by feasts including large amounts of pork. On average, they ate very little animal food. Visiting researchers noted that the residents of Tukisenta were "muscular and mostly very lean", and did not gain fat with age (1, Western Diseases, Trowell and Burkitt, 1981).
Another remarkably lean hunter-gatherer population is the !Kung San foragers of the Kalahari desert. The !Kung San are so lean that many of them would be considered underweight on the standard body mass index scale (BMI less than 18.5). Average BMI doesn't exceed 20 in any age category (The !Kung San, Richard Lee, 1979). Is this simply because they're starving? It is true that they don't always get as much food as they'd like, but on most days, they have the ability to gather more food than they need. The fact that they are able to reproduce normally suggests that they aren't starving. Richard Lee's detailed work with the !Kung San indicates that approximately 40 percent of their calories came from animal foods during his study period in the 1960s. This was mostly meat, with occasional eggs when available.
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Non-industrial cultures
I'll get right to the point: humans living in a non-industrialized setting tend to be lean, regardless of how much meat they eat. This applies equally to hunter-gatherers, herders, and farmers.
One of the leanest populations I've encountered in my reading is the 1960s Papua New Guinea highland farmers of Tukisenta. They ate a nearly vegan diet composed almost exclusively of sweet potatoes, occasionally punctuated by feasts including large amounts of pork. On average, they ate very little animal food. Visiting researchers noted that the residents of Tukisenta were "muscular and mostly very lean", and did not gain fat with age (1, Western Diseases, Trowell and Burkitt, 1981).
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| !Kung man gathering mongongo fruit/nuts. From The !Kung San, by Richard B. Lee. |
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Recent Interviews
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For those who don't follow my Twitter account (@whsource), here are links to my two most recent interviews.
Smash the Fat with Sam Feltham. We discuss the eternally controversial question, "is a calorie a calorie"? Like many other advocates of the low-carbohydrate diet, Feltham believes that the metabolic effects of food (particularly on insulin), rather than calorie intake per se, are the primary determinants of body fatness. I explain the perspective that my field of research has provided on this question. We also discussed why some lean people become diabetic. Feltham was a gracious host.
Nourish, Balance, Thrive with Christopher Kelly. Kelly is also an advocate of the low-carbohydrate diet for fat loss. This interview covered a lot of ground, including the insulin-obesity hypothesis, regulation of body fatness by the leptin-brain axis, how food reward works to increase calorie intake, and the impact of the food environment on food intake. I explain why I think proponents of the insulin-obesity hypothesis have mistaken association for causation, and what I believe the true relationship is between insulin biology and obesity. Kelly was also a gracious host. He provides a transcript if you'd rather read the interview in text form.
Smash the Fat with Sam Feltham. We discuss the eternally controversial question, "is a calorie a calorie"? Like many other advocates of the low-carbohydrate diet, Feltham believes that the metabolic effects of food (particularly on insulin), rather than calorie intake per se, are the primary determinants of body fatness. I explain the perspective that my field of research has provided on this question. We also discussed why some lean people become diabetic. Feltham was a gracious host.
Nourish, Balance, Thrive with Christopher Kelly. Kelly is also an advocate of the low-carbohydrate diet for fat loss. This interview covered a lot of ground, including the insulin-obesity hypothesis, regulation of body fatness by the leptin-brain axis, how food reward works to increase calorie intake, and the impact of the food environment on food intake. I explain why I think proponents of the insulin-obesity hypothesis have mistaken association for causation, and what I believe the true relationship is between insulin biology and obesity. Kelly was also a gracious host. He provides a transcript if you'd rather read the interview in text form.
Is Meat Unhealthy? Part II
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Over time, animals adapt to the foods they regularly consume. This is how archaeologists can, for example, determine that Triceratops was an herbivore and Tyrannosaurus was a carnivore just by looking at the structure of the skeleton. Adaptations to diet extend beyond skeletal structure, into digestion, metabolism, the brain, musculature, and other aspects of physical function. What is our evolutionary history with meat?
Human Evolutionary History with Meat: 200 to 2.6 Million Years Ago
Mammals evolved from ancestral "mammal-like reptiles" (therapsids, then cynodonts) approximately 220 million years ago (Richard Klein. The Human Career. 2009). Roughly 100 million years ago, placental mammals emerged. The earliest placental mammals are thought to have been nocturnal shrew-like beasts that subsisted primarily on insects, similar to modern shrews and moles. Mammalian teeth continued to show features specialized for insect consumption until the rise of the primates.
65 million years ago, coinciding with the evolution of the first fruiting plants, our ancestors took to the trees and became primates. For most of the time between then and now, our ancestors likely ate the prototypical primate diet of fruit, seeds, leaves/stems, and insects (1). Some primates also hunt smaller animals and thus eat the flesh of mammals, birds, reptiles, amphibians, and fish in addition to insects. However, the contribution of non-insect meat to the diet is usually small.
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Human Evolutionary History with Meat: 200 to 2.6 Million Years Ago
Mammals evolved from ancestral "mammal-like reptiles" (therapsids, then cynodonts) approximately 220 million years ago (Richard Klein. The Human Career. 2009). Roughly 100 million years ago, placental mammals emerged. The earliest placental mammals are thought to have been nocturnal shrew-like beasts that subsisted primarily on insects, similar to modern shrews and moles. Mammalian teeth continued to show features specialized for insect consumption until the rise of the primates.
65 million years ago, coinciding with the evolution of the first fruiting plants, our ancestors took to the trees and became primates. For most of the time between then and now, our ancestors likely ate the prototypical primate diet of fruit, seeds, leaves/stems, and insects (1). Some primates also hunt smaller animals and thus eat the flesh of mammals, birds, reptiles, amphibians, and fish in addition to insects. However, the contribution of non-insect meat to the diet is usually small.
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Is Meat Unhealthy? Part I
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Introduction
At Dr. McDougall's Advanced Study Weekend, I had the opportunity to hear a number of researchers and advocates make the case for a "plant-based diet", which is a diet containing little or no animal foods. Many of them voiced the opinion that animal foods contribute substantially to the primary killers in the US, such as heart disease and cancer. Some of the evidence they presented was provocative and compelling, so it stimulated me to take a deeper look and come to my own conclusions.
No matter what the health implications of meat eating turn out to be, I respect vegetarians and vegans. Most of them are conscientious, responsible people who make daily personal sacrifices to try to make the world a better place for all of us.
My Experience with Vegetarian and Vegan Diets
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At Dr. McDougall's Advanced Study Weekend, I had the opportunity to hear a number of researchers and advocates make the case for a "plant-based diet", which is a diet containing little or no animal foods. Many of them voiced the opinion that animal foods contribute substantially to the primary killers in the US, such as heart disease and cancer. Some of the evidence they presented was provocative and compelling, so it stimulated me to take a deeper look and come to my own conclusions.
No matter what the health implications of meat eating turn out to be, I respect vegetarians and vegans. Most of them are conscientious, responsible people who make daily personal sacrifices to try to make the world a better place for all of us.
My Experience with Vegetarian and Vegan Diets
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Obesity → Diabetes
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A new study adds to the evidence that the prevalence of type 2 diabetes is rapidly increasing in the US, and our national weight problem is largely to blame.
The Centers for Disease Control (CDC) currently estimates that a jaw-dropping 33 percent of US men, and 39 percent of US women, will develop diabetes at some point in their lives (1). Roughly one out of three people in this country will develop diabetes, and those who don't manage it effectively will suffer debilitating health consequences. Has the risk of developing diabetes always been so high, and if not, why is it increasing?
In the same issue of the Annals of Internal Medicine as the low-carb vs. low-fat study, appears another study that aims to partially address this question (2).
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The Centers for Disease Control (CDC) currently estimates that a jaw-dropping 33 percent of US men, and 39 percent of US women, will develop diabetes at some point in their lives (1). Roughly one out of three people in this country will develop diabetes, and those who don't manage it effectively will suffer debilitating health consequences. Has the risk of developing diabetes always been so high, and if not, why is it increasing?
In the same issue of the Annals of Internal Medicine as the low-carb vs. low-fat study, appears another study that aims to partially address this question (2).
Read more »
Metabolic Effects of a Traditional Asian High-carbohydrate Diet
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A recent study supports the notion that an 'ancestral diet' focused around high-starch agricultural foods can cultivate leanness and metabolic health.
John McDougall gave Christopher Gardner a hard time at the McDougall Advanced Study Weekend. Dr. Gardner conducts high-profile randomized controlled trials (RCTs) at Stanford to compare the effectiveness of a variety of diets for weight loss, cardiovascular and metabolic health. The "A to Z Study", in which Atkins, Zone, Ornish, and LEARN diets were pitted against one another for one year, is one of his best-known trials (1).
Dr. McDougall asked a simple question: why haven't these trials evaluated the diet that has sustained the large majority of the world's population for the last several thousand years? This is an agriculturalist or horticulturalist diet based around starchy foods such as grains, tubers, legumes, and plantains, and containing little fat or animal foods. Researchers have studied a number of cultures eating this way, and have usually found them to be lean, with good cardiovascular and metabolic health. Why not devote resources to studying this time-tested ancestral diet? I think it's a fair question.
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John McDougall gave Christopher Gardner a hard time at the McDougall Advanced Study Weekend. Dr. Gardner conducts high-profile randomized controlled trials (RCTs) at Stanford to compare the effectiveness of a variety of diets for weight loss, cardiovascular and metabolic health. The "A to Z Study", in which Atkins, Zone, Ornish, and LEARN diets were pitted against one another for one year, is one of his best-known trials (1).
Dr. McDougall asked a simple question: why haven't these trials evaluated the diet that has sustained the large majority of the world's population for the last several thousand years? This is an agriculturalist or horticulturalist diet based around starchy foods such as grains, tubers, legumes, and plantains, and containing little fat or animal foods. Researchers have studied a number of cultures eating this way, and have usually found them to be lean, with good cardiovascular and metabolic health. Why not devote resources to studying this time-tested ancestral diet? I think it's a fair question.
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Help Advance Diabetes Research
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A University of Virginia researcher named Hannah Menefee contacted me recently to ask for our help. She and her colleagues are conducting a study on how people with type 2 diabetes use Facebook to manage their health, and how that technology can be leveraged to support effective health communication.
If you have type 2 diabetes, and you'd like to participate in the study, please join their Diabetes Management Study Facebook group. There, you'll receive more information about the study, you'll receive a short survey, and you may be invited into one of the study phases.
If you have type 2 diabetes, and you'd like to participate in the study, please join their Diabetes Management Study Facebook group. There, you'll receive more information about the study, you'll receive a short survey, and you may be invited into one of the study phases.
My AHS14 Talk on Leptin Resistance is Posted
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The Ancestral Health Society just posted a video of my recent talk "What Causes Leptin Resistance?" Follow the link below to access it. Enjoy!
What Causes Leptin Resistance?
What Causes Leptin Resistance?
Thoughts on the McDougall Advanced Study Weekend
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For those of you who aren't familiar with him, Dr. John McDougall is a doctor and diet/health advocate who recommends a very low fat, high starch, whole food vegan diet to control weight and avoid chronic disease. He's been at it for a long time, and he's a major figure in the "plant-based diet" community (i.e., a diet including little or no animal foods).
Dr. McDougall invited me to participate in his 3-day Advanced Study Weekend retreat in Santa Rosa, CA. My job was to give my talk on insulin and obesity, and participate in a panel discussion/debate with Dr. McDougall in which we sorted through issues related to low-carb, Paleo, and the health implications of eating animal foods. I was glad to receive the invitation, because I don't see myself as a diet partisan, and I believe that my evidence-based information is applicable to a variety of diet styles. I saw the Weekend as an opportunity to extend my thoughts to a new community, challenge myself, and maybe even learn a thing or two. It was particularly interesting to compare and contrast the Advanced Study Weekend with the Ancestral Health Symposium, which is more Paleo- and low-carb-friendly.
General Observations
The attendees were a lot older than AHS attendees. I estimate that most of them were in their 60s, although there were some young people in attendance.
I don't place too much emphasis on peoples' personal appearance at conferences like this. You don't know what a person's background, genetics, or personal struggles may be, you don't know how closely they adhere to the program, and you don't know to what degree a group of people might be self-selected for particular traits*. But I will note that Dr. McDougall, his family, and many of the other starch-based/plant-based diet advocates tended to be extremely lean with low fat and muscle mass. They also tended to have a healthy and energetic appearance and demeanor. As I would expect, decades of exceptionally high starch intake hasn't made them obese or obviously ill.
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Dr. McDougall invited me to participate in his 3-day Advanced Study Weekend retreat in Santa Rosa, CA. My job was to give my talk on insulin and obesity, and participate in a panel discussion/debate with Dr. McDougall in which we sorted through issues related to low-carb, Paleo, and the health implications of eating animal foods. I was glad to receive the invitation, because I don't see myself as a diet partisan, and I believe that my evidence-based information is applicable to a variety of diet styles. I saw the Weekend as an opportunity to extend my thoughts to a new community, challenge myself, and maybe even learn a thing or two. It was particularly interesting to compare and contrast the Advanced Study Weekend with the Ancestral Health Symposium, which is more Paleo- and low-carb-friendly.
General Observations
The attendees were a lot older than AHS attendees. I estimate that most of them were in their 60s, although there were some young people in attendance.
I don't place too much emphasis on peoples' personal appearance at conferences like this. You don't know what a person's background, genetics, or personal struggles may be, you don't know how closely they adhere to the program, and you don't know to what degree a group of people might be self-selected for particular traits*. But I will note that Dr. McDougall, his family, and many of the other starch-based/plant-based diet advocates tended to be extremely lean with low fat and muscle mass. They also tended to have a healthy and energetic appearance and demeanor. As I would expect, decades of exceptionally high starch intake hasn't made them obese or obviously ill.
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What about the Other Weight Loss Diet Study??
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The same day the low-fat vs low-carb study by Bazzano and colleagues was published, the Journal of the American Medical Association published a meta-analysis that compared the effectiveness of "named diet programs". Many people have interpreted this study as demonstrating that low-carbohydrate and low-fat diets are both effective for weight loss, and that we simply need to pick a diet and stick with it, but that's not really what the study showed. Let's take a closer look.
Johnston and colleagues sifted through PubMed for studies that evaluated "named diet programs", such as Ornish, Atkins, LEARN, Weight Watchers, etc (1). In addition, the methods state that they included any study as low-carbohydrate that recommended less than 40% of calories from carbohydrate, was funded by the Atkins foundation, or was "Atkins-like". These criteria weren't extended to the low-fat diet: only studies of name-brand low-fat diets like the Ornish diet were included, while the meta-analysis excluded low-fat diet studies whose guidelines were based on recommendations from government and academic sources, even though the latter group represents the majority of the evidence we have for low-fat diets. The inclusion criteria were therefore extremely asymmetrical in how they represented low-carb and low-fat diets. This fact explains the unusual findings of the paper.
The abstract immediately activated my skeptic alarm, because it states that at the one-year mark, low-carbohydrate diets and low-fat diets both led to a sustained weight loss of about 16 pounds (7.3 kg). Based on my understanding of the weight loss literature, that number seems far too high for the low-fat diet, and also too high for the low-carbohydrate diet.
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Johnston and colleagues sifted through PubMed for studies that evaluated "named diet programs", such as Ornish, Atkins, LEARN, Weight Watchers, etc (1). In addition, the methods state that they included any study as low-carbohydrate that recommended less than 40% of calories from carbohydrate, was funded by the Atkins foundation, or was "Atkins-like". These criteria weren't extended to the low-fat diet: only studies of name-brand low-fat diets like the Ornish diet were included, while the meta-analysis excluded low-fat diet studies whose guidelines were based on recommendations from government and academic sources, even though the latter group represents the majority of the evidence we have for low-fat diets. The inclusion criteria were therefore extremely asymmetrical in how they represented low-carb and low-fat diets. This fact explains the unusual findings of the paper.
The abstract immediately activated my skeptic alarm, because it states that at the one-year mark, low-carbohydrate diets and low-fat diets both led to a sustained weight loss of about 16 pounds (7.3 kg). Based on my understanding of the weight loss literature, that number seems far too high for the low-fat diet, and also too high for the low-carbohydrate diet.
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Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence
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A new high-profile study compared the weight loss and cardiovascular effects of a low-carbohydrate diet vs. a low-fat diet. Although many studies have done this before, this one is novel enough to add to our current understanding of diet and health. Unlike most other studies of this nature, diet adherence was fairly good, and carbohydrate restriction produced greater weight loss and cardiovascular risk factor improvements than fat restriction at the one-year mark. Yet like previous studies, neither diet produced very impressive results.
The Study
Lydia A. Bazzano and colleagues at Tulane University randomly assigned 148 obese men and women without cardiovascular disease into two groups (1):
Results
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The Study
Lydia A. Bazzano and colleagues at Tulane University randomly assigned 148 obese men and women without cardiovascular disease into two groups (1):
- Received instructions to eat less than 40 grams of carbohydrate per day, plus one low-carbohydrate meal replacement per day. No specific advice to alter calorie intake. Met regularly with dietitians to explain the dietary changes and maintain motivation.
- Received instructions to eat less than 30 percent of calories from fat, less than 7 percent of calories as saturated fat, and 55 percent of calories from carbohydrate, plus one low-fat meal replacement per day. No specific advice to alter calorie intake. This is based on NCEP guidelines, which are actually designed for cardiovascular risk reduction and not weight loss. Met regularly with dietitians to explain the dietary changes and maintain motivation.
Results
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Science of Nutrition Podcast
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I recently did an interview with Seth Yoder, who has a master's degree in nutrition science and writes the blog The Science of Nutrition. Seth caught my attention recently with his withering review of The Big Fat Surprise, the latest book to claim that ideological/incompetent scientists and public policy makers got the science of nutrition backward and we should all be eating low-carb, high-fat, high-meat diets. I was impressed by how deeply Seth dug into the reference list, and how well he picked up on subtle but troubling misrepresentations of the evidence.
Last week, Seth and I got together at a local brewpub to do an interview. We were joined by Carrie Dennett, an MPH/RDN who has a nutrition blog and writes for the Seattle Times. I'd probably do a lot more interviews if I could ride my bike to them and have my interviewer buy me a drink.
Speaking of drinks, by the end of the interview I had a little buzz-- you might hear it in my voice if you listen closely. As usual, I had plenty to say about body fat regulation, food reward, and other topics, with plenty of side trips to discuss particularly fascinating studies. Also, the word of the day was 'compelling'.
Enjoy the interview!
Last week, Seth and I got together at a local brewpub to do an interview. We were joined by Carrie Dennett, an MPH/RDN who has a nutrition blog and writes for the Seattle Times. I'd probably do a lot more interviews if I could ride my bike to them and have my interviewer buy me a drink.
Speaking of drinks, by the end of the interview I had a little buzz-- you might hear it in my voice if you listen closely. As usual, I had plenty to say about body fat regulation, food reward, and other topics, with plenty of side trips to discuss particularly fascinating studies. Also, the word of the day was 'compelling'.
Enjoy the interview!
Can Hypothalamic Inflammation and Leptin Resistance be Reversed?
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A new study by yours truly begins to address the key question: can hypothalamic inflammation and leptin resistance be reversed?
Leptin is the primary hormonal regulator of body fatness in the human body (1). Secreted by fat tissue, it acts in many places in the body, but its most important effects on body weight occur via the brain, and particularly a brain region called the hypothalamus. The hypothalamus is responsible for keeping certain physiological variables within the optimal range, including blood pressure, body temperature, and body fatness.
In obesity, the brain loses its sensitivity to leptin, and this causes the body to begin 'defending' a higher level of body fatness, analogous to how a person with a fever 'defends' a higher body temperature (1). Once a person has become obese, it's difficult to return to true leanness because this system vigorously opposes major fat loss. Leptin resistance makes fat loss more difficult.
In rodent models, leptin resistance is caused at least in part by inflammatory signaling in the hypothalamus. We can observe this in multiple ways, but one common way is to look at the appearance of specific cells in the brain that change number, size, and shape when inflammation is present (2). These cells are called microglia and astrocytes. In addition to the work in rodents, we've published preliminary evidence that these same inflammatory changes occur in the hypothalamus of obese humans (2).
A key question is whether or not these inflammatory changes can be reversed. Is a person with leptin resistance doomed to have it forever, undermining fat loss efforts for the rest of his or her life? Or can it be corrected, possibly allowing easier and more sustainable fat loss? We just published a study in Endocrinology that begins to answer this question, using a mouse model of dietary obesity (3). I'm co-first author of this study along with my colleague Kathryn Berkseth, MD. My former mentor Mike Schwartz, MD is senior author.
The Study
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Leptin is the primary hormonal regulator of body fatness in the human body (1). Secreted by fat tissue, it acts in many places in the body, but its most important effects on body weight occur via the brain, and particularly a brain region called the hypothalamus. The hypothalamus is responsible for keeping certain physiological variables within the optimal range, including blood pressure, body temperature, and body fatness.
In obesity, the brain loses its sensitivity to leptin, and this causes the body to begin 'defending' a higher level of body fatness, analogous to how a person with a fever 'defends' a higher body temperature (1). Once a person has become obese, it's difficult to return to true leanness because this system vigorously opposes major fat loss. Leptin resistance makes fat loss more difficult.
In rodent models, leptin resistance is caused at least in part by inflammatory signaling in the hypothalamus. We can observe this in multiple ways, but one common way is to look at the appearance of specific cells in the brain that change number, size, and shape when inflammation is present (2). These cells are called microglia and astrocytes. In addition to the work in rodents, we've published preliminary evidence that these same inflammatory changes occur in the hypothalamus of obese humans (2).
A key question is whether or not these inflammatory changes can be reversed. Is a person with leptin resistance doomed to have it forever, undermining fat loss efforts for the rest of his or her life? Or can it be corrected, possibly allowing easier and more sustainable fat loss? We just published a study in Endocrinology that begins to answer this question, using a mouse model of dietary obesity (3). I'm co-first author of this study along with my colleague Kathryn Berkseth, MD. My former mentor Mike Schwartz, MD is senior author.
The Study
Read more »
Help Fund High-Quality Research on Diet and Health
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University of California, San Francisco researcher Dr. Ashley Mason has asked me to spread the word about a diet-health study she's preparing to conduct in collaboration with Dr. Lynda Frassetto. Dr. Frassetto is a widely recognized expert on mineral metabolism and bone health, and also one of the few researchers who has managed to wrangle funding to study the health impacts of a Paleolithic-style diet. Her findings have been quite provocative.
Together with their collaborators, Drs. Mason and Frassetto are preparing another diet-health trial to study the impact of two different diets on polycystic ovary syndrome, or PCOS. PCOS is a common hormonal disorder among reproductive-age women, and its signs and symptoms include ovarian cysts, excess hair growth, menstrual irregularity or absence, infertility, and obesity. Its causes are unknown, but insulin resistance is a core characteristic of it and is thought to play an important role. PCOS is thought to be influenced by diet and lifestyle.
A research team including Drs. Frassetto and Mason, as well as Drs. Umesh Masharani, Heather Huddleston, and Michael Cohn will test a Paleolithic-style diet and an American Diabetes Asssociation diet to see if either or both improves insulin resistance and menstrual cycle regularity for women with PCOS. Each diet will likely have beneficial effects, however it remains unknown which will be more effective at treating PCOS.
Currently, it's exceedingly difficult for researchers to land funding from the National Institutes of Health (NIH) to do nutrition-related research in the context of disease treatment or management, particularly if it involves a Paleo diet. Recognizing the important potential of fleshing out the relationship between diet and health, researchers are looking for other ways to fund their work. This study will give them the early data they need to start large, truly definitive studies of the links between diet and insulin resistance, and you can help make it happen.
Please check out their crowdfunding website to learn more about the study, the researchers, and make tax-deductible donations to support their work. And, if you're attending the Ancestral Health Symposium, one of the "backer" rewards is having lunch with the researchers.
Click here to see their crowdfunding site!
This post was prepared in part using content provided by Dr. Mason.
Together with their collaborators, Drs. Mason and Frassetto are preparing another diet-health trial to study the impact of two different diets on polycystic ovary syndrome, or PCOS. PCOS is a common hormonal disorder among reproductive-age women, and its signs and symptoms include ovarian cysts, excess hair growth, menstrual irregularity or absence, infertility, and obesity. Its causes are unknown, but insulin resistance is a core characteristic of it and is thought to play an important role. PCOS is thought to be influenced by diet and lifestyle.
A research team including Drs. Frassetto and Mason, as well as Drs. Umesh Masharani, Heather Huddleston, and Michael Cohn will test a Paleolithic-style diet and an American Diabetes Asssociation diet to see if either or both improves insulin resistance and menstrual cycle regularity for women with PCOS. Each diet will likely have beneficial effects, however it remains unknown which will be more effective at treating PCOS.
Currently, it's exceedingly difficult for researchers to land funding from the National Institutes of Health (NIH) to do nutrition-related research in the context of disease treatment or management, particularly if it involves a Paleo diet. Recognizing the important potential of fleshing out the relationship between diet and health, researchers are looking for other ways to fund their work. This study will give them the early data they need to start large, truly definitive studies of the links between diet and insulin resistance, and you can help make it happen.
Please check out their crowdfunding website to learn more about the study, the researchers, and make tax-deductible donations to support their work. And, if you're attending the Ancestral Health Symposium, one of the "backer" rewards is having lunch with the researchers.
Click here to see their crowdfunding site!
This post was prepared in part using content provided by Dr. Mason.
Fat and Carbohydrate: Clarifications and Details
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The last two posts on fat and carbohydrate were written to answer a few important, but relatively narrow, questions that I feel are particularly pertinent at the moment:
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- Was the US obesity epidemic caused by an increase in calorie intake?
- Could it have been caused by an increase in carbohydrate intake, independent of the increase in calorie intake?
- Does an unrestricted high-carbohydrate diet lead to a higher calorie intake and body fatness than an unrestricted high-fat diet, or vice versa?
- Could the US government's advice to eat a low-fat diet have caused the obesity epidemic by causing a dietary shift toward carbohydrate?
However, those posts left a few loose ends that I'd like to tie up in this post. Here, I'll lay out my opinions on the relationship between macronutrient intake and obesity in more detail. I'll give my opinions on the following questions:
- What dietary macronutrient composition is the least likely to cause obesity over a lifetime?
- What dietary macronutrient composition is best for a person who is already overweight or obese?
- Is fat inherently fattening and/or unhealthy?
From the beginning
Has Obesity Research Failed?
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I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates. According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.
Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*. What gives? Maybe if we just scrapped the whole endeavor we'd be better off.
Let's take a closer look at this argument and see how it holds up.
Why Do Research?
There are two fundamental reasons why we do research:
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Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*. What gives? Maybe if we just scrapped the whole endeavor we'd be better off.
Let's take a closer look at this argument and see how it holds up.
Why Do Research?
There are two fundamental reasons why we do research:
- To gather accurate information about the natural world. This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
- Practical applications. We want to solve problems and improve our lives.
If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.
Has Obesity Research Gathered Accurate Information?
A New Understanding of an Old "Obesity Gene"
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As with many of the genes in our genome, different people carry different versions of FTO. People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).
Despite being the most consistent hit in these genetic studies, FTO has remained a mystery. As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status. Yet its function is difficult to reconcile with a role in weight regulation:
- It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
- It's not primarily expressed in the brain or in body fat, but in all tissues.
- Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.
An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes. Typically, they tell us that obesity risk is associated with variability in a particular region of the genome. If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit. However, that's not always the case...
Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?
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Two human studies, published in 1995 and 2000, tested the effect of carbohydrate vs. fat overfeeding on body fat gain in humans. What did they find, and why is it important?
We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness. These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most). Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake? If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?
The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.
Horton et al.
Read more »
We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness. These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most). Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake? If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?
The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.
Horton et al.
Read more »
Garden Update: A Banner Year
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Things are warming up here in Seattle and the flowers are blooming. I just planted my first crops of the year-- potatoes and strawberries.
2013 was a banner year for my 500-square-foot urban vegetable garden, including my first experience growing and processing a grain. I never got around to posting about it last year-- so here it is.
Interbay mulch technique
In the fall of 2012, I tried a new technique for improving the soil called "Interbay mulching". This is a variation on sheet mulching, which involves placing uncomposted organic matter directly onto the garden soil in fall and letting it compost until the next growing season. To Interbay mulch, you simply cover your sheet mulch with burlap. This keeps everything moist, protects earthworms from bird predation so they can munch freely, and suppresses weeds. I used leaves (carbon) and spent coffee grounds from a local coffee shop (nitrogen) for my organic matter.
When I pulled back the burlap last spring, I was initially disappointed. The coffee grounds had disappeared completely, but there was still a lot of leaf matter left on the soil, indicating that it had only partially composted. However, I later decided that it had worked well, because the soil structure underneath was improved and it seemed to be enriched with significant organic matter as well as a large population of fat earthworms. The mulch suppressed weeds remarkably well, and the beds remained mostly clean for the rest of the season.
Those observations, combined with huge yields from the mulched beds, convinced me that it was worthwhile.
New tools
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2013 was a banner year for my 500-square-foot urban vegetable garden, including my first experience growing and processing a grain. I never got around to posting about it last year-- so here it is.
Interbay mulch technique
.JPG) |
| The bed on the right has been mulched with leaves, spent coffee grounds, and burlap sacks ($1/sack at the local hardware store). The beds on the left were planted with a rye-clover-vetch-pea cover crop. Paths are mulched with wood chips. |
When I pulled back the burlap last spring, I was initially disappointed. The coffee grounds had disappeared completely, but there was still a lot of leaf matter left on the soil, indicating that it had only partially composted. However, I later decided that it had worked well, because the soil structure underneath was improved and it seemed to be enriched with significant organic matter as well as a large population of fat earthworms. The mulch suppressed weeds remarkably well, and the beds remained mostly clean for the rest of the season.
Those observations, combined with huge yields from the mulched beds, convinced me that it was worthwhile.
New tools
Read more »
More Graphs of Calorie Intake vs. BMI
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In the last post, a reader commented that the correlation would be more convincing if I graphed calories vs. average BMI rather than the prevalence of obesity. It was a valid point, so I went searching for average BMI values from NHANES surveys. I dug up a CDC document that contains data from surveys between 1960 and 2002 (1). Because these data only cover five survey periods, we only get five data points to analyze, as opposed to the eight used in the last post. The document contains BMI values for men and women separately, so I averaged the two to approximate average BMI in the general adult population. It's also worth noting that I use the approximate midpoint of the survey period as the year.
First, a graph of average BMI over time. It went up:
Now, let's see how well average BMI correlates with calorie intake:
The correlation between calorie intake and obesity prevalence was remarkable, but this correlation is simply incredible. An R-squared value of 0.98 indicates that daily calorie intake and average BMI are almost perfectly correlated.
We can further deduce that each 100-calorie increase in daily food intake is associated with an 0.62-point increase in average BMI among US adults.
Calorie Intake and the US Obesity Epidemic
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Between 1960 and 2008, the prevalence of obesity in US adults increased from 13 to 34 percent, and the prevalence of extreme obesity increased from 0.9 to 6 percent (NHANES surveys). This major shift in population fatness is called the "obesity epidemic".
What caused the obesity epidemic? As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it. There are two main sources of data for US calorie intake. The first is NHANES surveys conducted by the Centers for Disease Control. They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased. The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors. However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.
Read more »
What caused the obesity epidemic? As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it. There are two main sources of data for US calorie intake. The first is NHANES surveys conducted by the Centers for Disease Control. They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased. The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors. However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.
Read more »
Uncovering the True Health Costs of Excess Weight
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Is excess weight hazardous to health, or can it actually be protective? This question has provoked intense debate in the academic community, in some cases even leading researchers to angrily denounce the work of others (1). There is good evidence to suggest that excess body fat increases the risk of specific diseases, including many of our major killers: diabetes, heart attack, stroke, heart failure, cancer, and kidney failure (2). Yet strangely, the studies relating excess weight to the total risk of dying-- an overall measure of health that's hard to argue with-- are inconsistent. Why?
Read more »
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New Position with Nestlé
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Warning -- Satire -- April Fool's Post
I'm happy to announce that I've accepted a Product Research and Development position with Nestlé Foods. Nestlé is known for its skillful application of 'neuromarketing'-- using neuroscience to enhance product development and sales-- and the company recruited me for my background in neuroscience and food reward.
As Whole Health Source readers know well, food reward has a major impact on food selection and consumption, and therefore it has huge potential as a product development strategy. Although product development by the food industry has always relied to some extent on a basic understanding of food reward, corporations still lag far behind the cutting edge of food reward research, and they are therefore missing out on a major opportunity to drive repeat purchase and consumption behavior and increase total sale volume. I plan to leverage science-corporate synergy to develop food product solutions that people LOVE*.
Even more exciting, Nestlé has asked me to lead a strategic partnership initiative with Coca-Cola to utilize neuromarketing to tailor beverage product development specifically for children, who have a somewhat different set of reward criteria than adults. We're excited to develop product solutions that kids LOVE* even more than current offerings, by scientifically designing new combinations of flavors, sweeteners, and totally safe habit-forming drugs such as caffeine.
Both companies have been very responsive to my nutritional concerns about processed foods, and so we're working together to make healthier products. Here are some of the changes we're discussing:
April Fools!!!!!!
* Learned Obedience Via Eating
I'm happy to announce that I've accepted a Product Research and Development position with Nestlé Foods. Nestlé is known for its skillful application of 'neuromarketing'-- using neuroscience to enhance product development and sales-- and the company recruited me for my background in neuroscience and food reward.
As Whole Health Source readers know well, food reward has a major impact on food selection and consumption, and therefore it has huge potential as a product development strategy. Although product development by the food industry has always relied to some extent on a basic understanding of food reward, corporations still lag far behind the cutting edge of food reward research, and they are therefore missing out on a major opportunity to drive repeat purchase and consumption behavior and increase total sale volume. I plan to leverage science-corporate synergy to develop food product solutions that people LOVE*.
Even more exciting, Nestlé has asked me to lead a strategic partnership initiative with Coca-Cola to utilize neuromarketing to tailor beverage product development specifically for children, who have a somewhat different set of reward criteria than adults. We're excited to develop product solutions that kids LOVE* even more than current offerings, by scientifically designing new combinations of flavors, sweeteners, and totally safe habit-forming drugs such as caffeine.
Both companies have been very responsive to my nutritional concerns about processed foods, and so we're working together to make healthier products. Here are some of the changes we're discussing:
- Adding vitamin C and cod liver oil to chocolate.
- Replacing a portion (1.7%) of the sugar in beverages with stevia across the board.
- Stealthily decreasing the portion size of beverages. To do this, we'll increase the thickness of the plastic bottles so the exterior of the bottle is the same size, but the actual beverage content is reduced by 0.2 oz.
- Getting these healthy snacks and beverages back into schools where kids can enjoy them!
April Fools!!!!!!
* Learned Obedience Via Eating
Corrections to the New Review Paper on Dietary Fat and Cardiovascular Risk
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The meta-analysis by Chowdhury et al. raised quite a furor from certain segments of researchers and the popular media. I find this reaction interesting. I usually write about obesity, which is a topic of great interest to people, but my post about the review paper received more than twice my usual traffic. People whose findings or opinions are questioned by the paper are aggressively denouncing it in the media, even calling for retraction (1). This resembles what happens every time a high-profile review paper is published that doesn't support the conventional stance on fatty acids and health (e.g., Siri-Tarino et al. [2], which despite much gnashing of teeth is still standing*). I'm not sure why this issue in particular arouses such excitement, but I find it amusing and disturbing at the same time. This kind of reaction would be totally out of place in most other fields of science, where aggressive public media outbursts by researchers are usually frowned upon.
As it turns out, the critics have a point this time. Significant errors were uncovered in the original version of the meta-analysis, which have been corrected in the current version (3). These include the following two errors, one of which alters the conclusion somewhat:
Read more »
As it turns out, the critics have a point this time. Significant errors were uncovered in the original version of the meta-analysis, which have been corrected in the current version (3). These include the following two errors, one of which alters the conclusion somewhat:
- The outcome of one observational study on omega-3 fatty acids was reported as slightly negative, when it was actually strongly positive. This changes the conclusion of the meta-analysis, making it somewhat more favorable to omega-3 consumption for cardiovascular protection.
- The authors left out two studies on omega-6 fatty acids. These didn't change the overall conclusions on omega-6.
Read more »
Book Review: Your Personal Paleo Code
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Chris Kresser has been a major figure in the ancestral health community for some time now. It's funny to recall that I was actually one of his first readers, back in the early days of his blog when it was called The Healthy Skeptic and the audience was small. Chris's readership rapidly eclipsed mine, and now he's in high demand for his ability to convey ideas clearly and offer practical solutions to important health concerns.
He recently published a book titled Your Personal Paleo Code, which also happens to be a New York Times bestseller. The primary goal of the book is to help you develop a diet and lifestyle that support health and well-being by starting from a generally healthy template and personalizing it to your needs. Let's have a look.
Introduction
Kresser opens with the poignant story of his own health problems, which began with an infectious illness in Indonesia and several courses of antibiotic therapy. After years of struggling with the resulting symptoms, trying a variety of diets, and finally accepting his condition, he was unexpectedly able to recover his health by adopting a personalized Paleo-like diet that included bone broth and fermented foods.
Why Paleo?
Read more »
He recently published a book titled Your Personal Paleo Code, which also happens to be a New York Times bestseller. The primary goal of the book is to help you develop a diet and lifestyle that support health and well-being by starting from a generally healthy template and personalizing it to your needs. Let's have a look.
Introduction
Kresser opens with the poignant story of his own health problems, which began with an infectious illness in Indonesia and several courses of antibiotic therapy. After years of struggling with the resulting symptoms, trying a variety of diets, and finally accepting his condition, he was unexpectedly able to recover his health by adopting a personalized Paleo-like diet that included bone broth and fermented foods.
Why Paleo?
Read more »
The Ultimate Detox: Your Kidneys
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The specter of unseen, unspecified toxins eroding our health is worth many millions of dollars in the United States and abroad. Companies offer "detox" supplements, beverages, and creams that supposedly rid us of supposed toxins, despite a complete lack of evidence that these products do anything at all*. This comes from an industry that excels at creating boogeymen and offering costly solutions for them.
If your wallet needs to lose weight, then these products are highly effective, otherwise it's probably best to save your money. Here's why.
The body is equipped with an extremely advanced system for excreting toxins. The kidneys are part of this system, and their design is genius. The basic functional unit of the kidney is the nephron, and the average kidney contains about a million of them. Nephrons have two major parts: a renal corpuscle and a renal tubule.
The renal corpuscle is the interface between the blood and the fluid that will eventually become urine. Blood is filtered by a fine "sieve" of cells that prevents everything larger than a small protein from passing into the renal tubule. Red blood cells, platelets, and most proteins stay on the blood side, while small proteins such as albumin, minerals, urea, glucose, water, and almost anything that would be considered a toxin** are allowed through into the renal tubule.
The renal tubule is a long tube that re-absorbs everything in this filtered blood that the body wants to keep. Water, minerals, albumin, glucose, amino acids, and other useful molecules are re-absorbed. Everything else ends up as urine and is excreted.
Can you see the genius of this design? Urine is blood, minus all the good stuff. Everything that isn't specifically recognized by the body as useful is excreted by default, no matter what it is. The body doesn't have to recognize each of the thousands of foreign compounds that make their way into our circulation each day. These substances are all out the door, by default.
Are you impressed by your kidneys yet? If not, consider this. Your kidneys filter your entire blood volume roughly 70 times per day. The reason you don't have to pee a liter a minute is that urine volume is reduced by 99 percent due to water reabsorption in the renal tubules.
This is why most drugs have to be taken on a regular basis, often several times per day. In concert with the detoxification enzymes of the liver, which tend to make drugs easier for the kidneys to excrete, the kidneys rapidly reduce the circulating concentration of drugs simply by excreting everything they don't recognize as useful.
Can a detox product improve upon 500 million years of kidney evolution***? I have my doubts.
* Exception: chelation therapy offered by a licensed medical practitioner for actual, diagnosed heavy metal poisoning. Second exception: strategies that use the word "detox" loosely to refer to removing unhealthy foods from the diet.
** Toxins tend to be very small-- either small organic molecules or minerals such as arsenic. Larger toxins such as proteins are uncommon in the circulation because proteins are generally not absorbed by the digestive tract. Toxic proteins have to be injected or otherwise directly introduced into the circulation, e.g. by a snake bite or a bacterial infection. But if you're bitten by a rattlesnake, I hope your first line of treatment won't be a detox kit from your local supplement store.
*** Kidneys are present in hagfish and lampreys, the most "primitive" living vertebrates.
If your wallet needs to lose weight, then these products are highly effective, otherwise it's probably best to save your money. Here's why.
The body is equipped with an extremely advanced system for excreting toxins. The kidneys are part of this system, and their design is genius. The basic functional unit of the kidney is the nephron, and the average kidney contains about a million of them. Nephrons have two major parts: a renal corpuscle and a renal tubule.
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| A nephron. In this image, the Bowman's capsule and glomerulus make up the renal corpuscle, and the proximal/distal tubules and the loop of Henle (#1-3) make up the renal tubule. Note the network of blood vessels (capillaries) that allow the transfer of water and other goodies from the tubule back into the blood. Image source. |
The renal tubule is a long tube that re-absorbs everything in this filtered blood that the body wants to keep. Water, minerals, albumin, glucose, amino acids, and other useful molecules are re-absorbed. Everything else ends up as urine and is excreted.
Can you see the genius of this design? Urine is blood, minus all the good stuff. Everything that isn't specifically recognized by the body as useful is excreted by default, no matter what it is. The body doesn't have to recognize each of the thousands of foreign compounds that make their way into our circulation each day. These substances are all out the door, by default.
Are you impressed by your kidneys yet? If not, consider this. Your kidneys filter your entire blood volume roughly 70 times per day. The reason you don't have to pee a liter a minute is that urine volume is reduced by 99 percent due to water reabsorption in the renal tubules.
This is why most drugs have to be taken on a regular basis, often several times per day. In concert with the detoxification enzymes of the liver, which tend to make drugs easier for the kidneys to excrete, the kidneys rapidly reduce the circulating concentration of drugs simply by excreting everything they don't recognize as useful.
Can a detox product improve upon 500 million years of kidney evolution***? I have my doubts.
* Exception: chelation therapy offered by a licensed medical practitioner for actual, diagnosed heavy metal poisoning. Second exception: strategies that use the word "detox" loosely to refer to removing unhealthy foods from the diet.
** Toxins tend to be very small-- either small organic molecules or minerals such as arsenic. Larger toxins such as proteins are uncommon in the circulation because proteins are generally not absorbed by the digestive tract. Toxic proteins have to be injected or otherwise directly introduced into the circulation, e.g. by a snake bite or a bacterial infection. But if you're bitten by a rattlesnake, I hope your first line of treatment won't be a detox kit from your local supplement store.
*** Kidneys are present in hagfish and lampreys, the most "primitive" living vertebrates.
Food Reward Friday
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This week's lucky "winner"... Kirkland Signature Cashew Clusters!!
WHS reader Brad Dieter mentioned these on Facebook the other day:
Nutrition tip of the day. Do not buy Cashew Clusters from Costco. You will eat an entire bag in one fell swoop. Sweet, salty, crunchy, and calorie dense, the perfect storm in Stephan Guyenet's model of overeating. I have n=1 data as proof.
n=1 quickly turned into n=6 as other people chimed in, including myself. I can attest to the fact that Cashew Clusters are like crack. Here's more evidence from their Amazon reviews:
"Addiction with less guilt!" These things are SO freaking good!!!... I'm eating some right now and I am having trouble keeping my hand out of the bag long enough to write this review!
"Delicious". I gave this as a gift to my girl friend... She loved it ! Heard there wasn't much sugar either. Seems the nuts were crispy and the clusters were very addicting, in a nice way. It lasted only for 6 days. [SG- each bag contains 4,800 calories]
"Buy these and you will be hooked for life!" One word "NUMMY!"... Very addicting.
Cashew Clusters are only about 11 percent sugar by calories, with the other 89 percent of calories coming from whole nuts and seeds. They're probably a healthy snack if you can eat them in moderation. Can you?
Snacktime in My Kitchen
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Here is a photo of all visible food in my kitchen:
Along the back wall, we have glass containers of raw nuts, unsalted roasted nuts, grains, and legumes. It's easy and attractive to organize your dry foods using inexpensive 2 quart Ball jars. They also have the advantage of being moth-proof. On the left, we have fresh fruit and a few onions. On the far left in the background is our hand-cranked conical burr grinder, for occasional coffee (Skerton).
If I walk into my kitchen between meals, the only food available to eat without doing any cooking or reheating is unsalted nuts and fresh fruit. There is no other snack food in the kitchen. No chips, cookies, bars, popcorn, snack mix, candy, or anything else that's tempting and easy to grab and devour.
When it's mealtime, we eat good home-cooked food. When it isn't mealtime, we don't have anything available that we would eat without feeling genuinely hungry. If we do feel genuinely hungry, fresh fruit and unsalted nuts make a satisfying snack.
This is the way of my people.
What's the point? Eliminating tempting food cues from our surroundings and creating small barriers to food consumption decreases the quantity of food we eat while increasing the quality. Engineering a food environment that discourages eating for reasons other than hunger helps match food intake to the body's true energy needs, favoring leanness and health.
This is the way of my people.
What's the point? Eliminating tempting food cues from our surroundings and creating small barriers to food consumption decreases the quantity of food we eat while increasing the quality. Engineering a food environment that discourages eating for reasons other than hunger helps match food intake to the body's true energy needs, favoring leanness and health.
Mindless Eating
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You think you're in control of your eating behavior-- but you aren't
In 2005, Brian Wansink's research group published a remarkable study that demonstrates the powerful unconscious influence of the food environment on our consumption (1).
Volunteers were invited to a test kitchen to eat bowls of tomato soup for lunch. Each person was given a bowl containing 18 ounces of soup-- but there was a catch. Half the volunteers were given custom-made soup bowls that partially refilled as they ate, such that the soup level dropped more slowly.
5 Easy and Effective Ways to Eat Less
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Why do we overeat? Why is it hard to lose fat once we've gained it? Is there a way to comfortably and sustainably eat less and lose fat?
I recently did an interview with Armi Legge of Evidence Magazine that gives an overview of my thinking on these topics-- based on a large and compelling body of research that rarely reaches popular media sources in useful form.
At the end of the interview, Armi asks me to list my top five tips for reducing calorie intake. Enjoy!
Mysteries of Energy Balance and Weight Loss
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How to Lose Weight Effortlessly
You've probably seen this claim many times: a pound of fat contains 3,500 kilocalories (kcal). A slice of toast is 80 kcal. All you have to do is forego one slice of toast per day-- just a few percent of your total calorie intake-- and you will lose 8.3 lbs of fat per year. Fat loss is so easy!
This reasoning is extremely common both in the popular media and among researchers. Here's an example from the book Mindless Eating, by researcher Brian Wansink:
...the difference between 1,900 and 2,000 calories is one we cannot detect, nor can we detect the difference between 2,000 and 2,100 calories. But over the course of a year, this mindless margin would either cause us to lose ten pounds or to gain ten pounds. It takes 3,500 extra calories to equal one pound. It doesn't matter if we eat these extra 3,500 calories in one week or gradually over the entire year. They'll add up to one pound.
This is the danger of creeping calories. Just 10 extra calories a day-- one stick of Doublemint gum or three small Jelly Belly jelly beans-- will make you a pound more portly one year from today. Only three Jelly Bellys a day.
According to this reasoning, if I reduced my calorie intake by 80 kcal per day, I'd become skeletal in two years and vanish in a puff of smoke within 10 years*. All from a meager 3 percent reduction in calorie intake!
What's wrong here?
NutriScience Seminar in Lisbon with Lindeberg, Fontes, and Bastos
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My friend Pedro Bastos has asked me to spread the word about a seminar he's organizing in Lisbon titled "Evidence and Evolution-based Nutrition". It will include Staffan Lindeberg, Maelan Fontes, and Pedro Bastos-- three quality researchers in the area of evolutionary health-- I'm sure it will be interesting. Here's the flier:
Public Talk at the University of Virginia on Friday, January 17
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The talk will be titled "Why Do We Overeat? A Neurobiological Perspective". Here's the teaser:
Obesity is a leading cause of morbidity and mortality in industrialized nations, yet this is a relatively recent phenomenon. In the United States, increasing obesity prevalence has paralleled a gradual increase of daily energy intake. Why do most Americans eat more than we used to, and more than we need to maintain a lean state, despite negative consequences? This presentation will touch on the neurobiology of action selection, the neurobiology of energy homeostasis, and why our central nervous system hardware may not be up to the task of constructively navigating the modern food environment.The talk will be attended by medical students, but I also hope to have some doctors and researchers show up, as well as people from the broader Charlottesville community. It will be a thought-provoking talk regardless of your background, and it will touch on some of my own work.
The talk will be held in the main medical school auditorium, MEB 3110, on Friday, January 17 at noon. You can find driving directions and parking information by following this link. You'll probably have to park in a parking garage, either the Lee Street or Central Grounds garage (directions in the link).
For a map of the UVA health system, follow this link. The Medical Education Building is number 44 on the map, and the talk will be in room MEB 3110 on the 3rd floor of the building.
See you there!
Free e-Book and Ideal Weight Program 2.0 Announcement
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I'm happy to announce that we're releasing a free e-book titled Why do We Gain Fat, and How do We Lose it? An Introduction to the Science of Body Fat, by Dan Pardi and myself. This is a slimmed-down version of the longer, fully referenced e-book we offer as part of the Ideal Weight Program. In it, we provide a succinct overview of the science of body fat gain and loss, and the evidence base for our program. It also contains a schematic that ties together the various concepts in visual form. You can download it from the Dan’s Plan site by following this link to our program overview page.
Ideal Weight Program 2.0 Upgrades
Over the last year, Dan and I have been working hard to improve the Ideal Weight Program, both in response to user feedback and our own ideas for development. Here are some of the new features we offer in 2014:
- Four-week meal plans and shopping lists for the FLASH diet and the Simple Food Diet, as requested by Ideal Weight Program users. This is in addition to the recipes and cooking guides we already provide.
- The Protein Unit system. Research suggests there's an optimal amount of protein for appetite control and fat loss, depending on your height, weight, gender, and physical activity level. Our fat loss diets are high in protein, but how do you know you're getting the right amount? We've created a calculator that does it for you automatically, and explains how to apply your personalized Protein Unit value easily and intuitively using real food.
- Diet plates. These are visual guides to following our diets, based loosely on the intuitive USDA MyPlate design.
- Cheat sheets. Put these on your fridge to remind yourself of your diet and lifestyle guidelines, and daily protein unit goal.
- Updated guidance. We've refined a few things in the diet guidance documents.
At a time of year when many people want to shed excess holiday pounds and start down a leaner, healthier path, we offer the Ideal Weight Program 2.0. The program comes with a 30-day no-questions-asked refund policy so you can try it without risk. We think you'll love this program, but if it doesn't work for you, we're happy to refund your purchase price.
Financial disclosure: I receive a portion of the revenue from the sale of the Ideal Weight Program. I do not receive revenue from the sale of other products associated with Dan's Plan or the Ideal Weight Program (such as the Fitbit, cooking tools, and other programs).