In my article "Is Sugar Fattening?", I discussed a recent review paper on fructose, by Dr. John Sievenpiper and colleagues (1). It was the most recent of several review papers to conclude that fructose is probably not inherently fattening in humans, but that it can be fattening if it's consumed to excess, due to the added calories. Dr. Sievenpiper and colleagues have also written other papers addressing the metabolic effects of fructose, which appear to be fairly minor unless it's consumed to excess (2, 3, 4, 5). The senior author on these studies is Dr. David Jenkins at McMaster University. David Despain, a science and health writer who publishes a nice blog called Evolving Health, recently interviewed Dr. Sievenpiper about his work.
It's an interesting interview and very timely, due to the recent attention paid to fructose in the popular media. This has mostly been driven by a couple of high-profile individuals-- an issue they discuss in the interview. The interview, recent papers, and sessions at scientific conferences are part of an effort by researchers to push back against some of the less well founded claims that have received widespread attention lately.
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Lower Blood Pressure Naturally
Recently, Chris Kresser published a series on dietary salt (sodium chloride) and health (1). One of the issues he covered is the effect of salt on blood pressure. Most studies have shown a relatively weak relationship between salt intake and blood pressure. My position overall is that we're currently eating a lot more salt than at almost any point in our evolutionary history as a species, so I tend to favor a moderately low salt intake. However, there may be more important factors than salt when it comes to blood pressure, at least in the short term.
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Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part III
In previous posts, I reviewed some of the evidence suggesting that human evolution has accelerated rapidly since the development of agriculture (and to some degree, before it). Europeans (and other lineages with a long history of agriculture) carry known genetic adaptations to the Neolithic diet, and there are probably many adaptations that have not yet been identified. In my final post in this series, I'll argue that although we've adapted, the adaptation is probably not complete, and we're left in a sort of genetic limbo between the Paleolithic and Neolithic state.
Recent Genetic Adaptations are Often Crude
It may at first seem strange, but many genes responsible for common genetic disorders show evidence of positive selection. In other words, the genes that cause these disorders were favored by evolution at some point because they presumably provided a survival advantage. For example, the sickle cell anemia gene protects against malaria, but if you inherit two copies of it, you end up with a serious and life-threatening disorder (1). The cystic fibrosis gene may have been selected to protect against one or more infectious diseases, but again if you get two copies of it, quality of life and lifespan are greatly curtailed (2, 3). Familial Mediterranean fever is a very common disorder in Mediterranean populations, involving painful inflammatory attacks of the digestive tract, and sometimes a deadly condition called amyloidosis. It shows evidence of positive selection and probably protected against intestinal disease due to the heightened inflammatory state it confers to the digestive tract (4, 5). Celiac disease, a severe autoimmune reaction to gluten found in some grains, may be a by-product of selection for protection against bacterial infection (6). Phenylketonuria also shows evidence of positive selection (7), and the list goes on. It's clear that a lot of our recent evolution was in response to new disease pressures, likely from increased population density, sendentism, and contact with domestic animals.
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Recent Genetic Adaptations are Often Crude
It may at first seem strange, but many genes responsible for common genetic disorders show evidence of positive selection. In other words, the genes that cause these disorders were favored by evolution at some point because they presumably provided a survival advantage. For example, the sickle cell anemia gene protects against malaria, but if you inherit two copies of it, you end up with a serious and life-threatening disorder (1). The cystic fibrosis gene may have been selected to protect against one or more infectious diseases, but again if you get two copies of it, quality of life and lifespan are greatly curtailed (2, 3). Familial Mediterranean fever is a very common disorder in Mediterranean populations, involving painful inflammatory attacks of the digestive tract, and sometimes a deadly condition called amyloidosis. It shows evidence of positive selection and probably protected against intestinal disease due to the heightened inflammatory state it confers to the digestive tract (4, 5). Celiac disease, a severe autoimmune reaction to gluten found in some grains, may be a by-product of selection for protection against bacterial infection (6). Phenylketonuria also shows evidence of positive selection (7), and the list goes on. It's clear that a lot of our recent evolution was in response to new disease pressures, likely from increased population density, sendentism, and contact with domestic animals.
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Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part II
In previous posts, I described how Otzi was (at least in large part) a genetic descendant of Middle Eastern agriculturalists, rather than being purely descended from local hunter-gatherers who adopted agriculture in situ. I also reviewed evidence showing that modern Europeans are a genetic mixture of local European hunter-gatherers, incoming agricultural populations from the Middle East, neanderthals, and perhaps other groups. In this post, I'll describe the evidence for rapid human evolution since the end of the Paleolithic period, and research indicating that some of these changes are adaptations to the Neolithic (agricultural/horticultural/pastoral) diet.
Humans have Evolved Significantly Since the End of the Paleolithic
Evolution by natural selection leaves a distinct signature in the genome, and geneticists can detect this signature tens of thousands of years after the fact by comparing many genomes to one another. A landmark paper published in 2007 by Dr. John Hawks and colleagues showed that humans have been undergoing "extraordinarily rapid recent genetic evolution" over the last 40,000 years (1). Furthermore:
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Humans have Evolved Significantly Since the End of the Paleolithic
Evolution by natural selection leaves a distinct signature in the genome, and geneticists can detect this signature tens of thousands of years after the fact by comparing many genomes to one another. A landmark paper published in 2007 by Dr. John Hawks and colleagues showed that humans have been undergoing "extraordinarily rapid recent genetic evolution" over the last 40,000 years (1). Furthermore:
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Media Appearances
Last October, I participated in a panel discussion organized by the Harvard Food Law Society in Boston. The panel included Drs. Walter Willett, David Ludwig, Robert Lustig, and myself, with Corby Kummer as moderator. Dr. Willett is the chair of the Harvard Department of Nutrition; Dr. Ludwig is a professor of nutrition and pediatrics at Harvard; Dr. Lustig is a professor of clinical pediatrics at UCSF; and Kummer is a food writer and senior editor for The Atlantic.
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Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part I
In the previous post, I explained that Otzi descended in large part from early adopters of agriculture in the Middle East or nearby. What I'll explain in further posts is that Otzi was not a genetic anomaly: he was part of a wave of agricultural migrants that washed over Europe thousands of years ago, spreading their genes throughout. Not only that, Otzi represents a halfway point in the evolutionary process that transformed Paleolithic humans into modern humans.
Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?
There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe. One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains. The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle. These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals. We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming.
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Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?
There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe. One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains. The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle. These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals. We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming.
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Lessons From Ötzi, the Tyrolean Ice Man. Part III
There are two reasons why I chose this time to write about Otzi. The first is that I've been looking for a good excuse to revisit human evolutionary history, particularly that of Europeans, and what it does and doesn't tell us about the "optimal" human diet. The second is that Otzi's full genome was sequenced and described in a recent issue of Nature Communications (1). A "genome" is the full complement of genes an organism carries. So what that means is that researchers have sequenced almost all of his genes.
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Lessons From Ötzi, the Tyrolean Ice Man. Part II
Otzi's Diet
Otzi's digestive tract contains the remains of three meals. They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2). The meat came from three different animals-- chamois, red deer and ibex. The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.
Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3). He died in the spring with a belly full of einkorn wheat. Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year. However, he also clearly ate meat and used leather made from his prey. Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.
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Otzi's digestive tract contains the remains of three meals. They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2). The meat came from three different animals-- chamois, red deer and ibex. The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.
Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3). He died in the spring with a belly full of einkorn wheat. Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year. However, he also clearly ate meat and used leather made from his prey. Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.
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Exercise and Food Intake
The New York Times just published an article reviewing some of the recent research on exercise, food intake and food reward, titled "Does Exercise Make You Overeat?". I was planning to write about this at some point, but I don't know when I'd be able to get around to it, and the NYT article is a fair treatment of the subject, so I'll just point you to the article.
Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less. Alex Hutchinson discussed this point recently on his blog (1). Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat. Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat. There is a lot of individual variability here. The average obese person won't lose a substantial amount of fat through exercise alone. However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people. On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward.
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Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less. Alex Hutchinson discussed this point recently on his blog (1). Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat. Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat. There is a lot of individual variability here. The average obese person won't lose a substantial amount of fat through exercise alone. However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people. On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward.
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Next Primal Chef Event Sunday 5/20
Gil Butler has been working on a television show called Primal Chef, where he invites local chefs to make creative dishes from a list of Paleo ingredients, in a designated amount of time. The format is reminiscent of Iron Chef. The food is judged afterward by figures in the Paleo community. Robb Wolf was a judge on the first episode.
Gil has invited me to be a judge on the next show, along with Sara Fragoso and Dr. Tim Gerstmar. The next day, Sunday April 20th, Gil is organizing a catered Primal Chef event in Seattle, with Paleo dinner, speakers, entertainment, prizes, and a screening of part of Paleo Chef episode 1. You can read the details and sign up here. I won't be speaking because I don't have time to put together another talk right now, but I will be attending the event.
Gil has invited me to be a judge on the next show, along with Sara Fragoso and Dr. Tim Gerstmar. The next day, Sunday April 20th, Gil is organizing a catered Primal Chef event in Seattle, with Paleo dinner, speakers, entertainment, prizes, and a screening of part of Paleo Chef episode 1. You can read the details and sign up here. I won't be speaking because I don't have time to put together another talk right now, but I will be attending the event.
Lessons From Ötzi, the Tyrolean Ice Man. Part I
Otzi is Europe's oldest natural human mummy, and as such, he's an important window into the history of the human species in Europe. His genome has been sequenced, and it offers us clues about the genetic history of modern Europeans.
Otzi's Story
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Global Meat Production, 1961-2009
Total global meat production per person has steadily increased from 0.13 lbs per day in 1961 to 0.29 lbs per day in 2009*, a 120 percent increase over the last half century (currently in the US, average meat consumption is about half a pound per day). Since meat consumption in the US and Europe has only increased modestly over time, this change mostly reflects greatly increased meat consumption over the last half century in developing countries** in Asia, Africa and South America. In 1961, it's likely that most of the 0.13 pounds per day of meat was consumed in affluent countries such as the US, with not much consumed elsewhere (with some exceptions). Historically, meat has always been expensive relative to other food sources in agricultural societies, so it's eaten by those who can afford it.
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Eocene Diet Follow-up
Now that WHS readers around the globe have adopted the Eocene Diet and are losing weight at an alarming rate, it's time to explain the post a little more. First, credit where credit is due: Melissa McEwen made a similar argument in her 2011 AHS talk, where she rolled out the "Cambrian Explosion Diet", which beats the Eocene Diet by about 470 million years. It was probably in the back of my head somewhere when I came up with the idea.
April Fools day is good for a laugh, but humor often has a grain of truth in it. In this case, the post was a jumping off point for discussing human evolution and what it has to say about the "optimal" human diet, if such a thing exists. Here's a preview: evolution is a continuous process that has shaped our ancestors' genomes for every generation since the beginning of life. It didn't end with the Paleolithic, in fact it accelerated, and most of us today carry meaningful adaptations to the Neolithic diet and lifestyle.
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April Fools day is good for a laugh, but humor often has a grain of truth in it. In this case, the post was a jumping off point for discussing human evolution and what it has to say about the "optimal" human diet, if such a thing exists. Here's a preview: evolution is a continuous process that has shaped our ancestors' genomes for every generation since the beginning of life. It didn't end with the Paleolithic, in fact it accelerated, and most of us today carry meaningful adaptations to the Neolithic diet and lifestyle.
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The Eocene Diet
65 million years ago, a massive asteroid slammed into the Yucatan peninsula, creating a giant dust cloud that contributed to the extinction of terrestrial dinosaurs. In the resulting re-adjustment of global ecosystems, a new plant tissue evolved, which paved the way for the eventual appearance of humans: fruit. Fruit represents a finely crafted symbiosis between plants and animals, in which the plant provides a nourishing morsel, and the animal disperses the plant's seeds inside a packet of rich fertilizer.
Fruit was such a powerful selective pressure that mammals quickly evolved to exploit it more effectively, developing adaptations for life in the forest canopy. One result of this was the rapid emergence of primates, carrying physical, digestive and metabolic adaptations for the acquisition and consumption of fruit and leaves. Primates also continued eating insects, a vestige of our early mammalian heritage.
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Fruit was such a powerful selective pressure that mammals quickly evolved to exploit it more effectively, developing adaptations for life in the forest canopy. One result of this was the rapid emergence of primates, carrying physical, digestive and metabolic adaptations for the acquisition and consumption of fruit and leaves. Primates also continued eating insects, a vestige of our early mammalian heritage.
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Onward
In upcoming posts, I plan to pursue two main themes. The first is a more comprehensive exploration of what determines eating behavior in humans, the neurobiology behind it, and the real world implications of this research. The reward and palatability value of food are major factors, but there are others, and I've spent enough time focusing on them for the time being. Also, the discussions revolving around food reward seem to be devolving into something that resembles team sports, and I've had my fill.
The second topic I'm going to touch on is human evolutionary history, including amazing recent insights from the field of human genetics. These findings have implications for the nutrition and health of modern humans.
I look forward to exploring these topics, and others, with all of you in the coming months.
The second topic I'm going to touch on is human evolutionary history, including amazing recent insights from the field of human genetics. These findings have implications for the nutrition and health of modern humans.
I look forward to exploring these topics, and others, with all of you in the coming months.
Recent Media Appearances
Men's Health interviewed and quoted me in an article titled "Reprogram Your Metabolism", written by Lou Schuler. Part of the article was related to the food reward concept. I'm glad to see the idea gradually reaching the mainstream.
Boing Boing recently covered an article by Dr. Hisham Ziauddeen and colleagues in Nature Reviews Neuroscience that questioned the idea that common obesity represents food addiction-- an idea that I often encounter in my reading. Maggie Koerth-Baker asked me if I wanted to respond. I sent her a response explaining that I agree with the authors' conclusions and I also doubt obesity is food addiction per se, as I have explained in the past, although a subset of obese people can be addicted to food. I explained that the conclusions of the paper are consistent with the idea that food reward influences fat mass. You can find my explanation here.
Boing Boing recently covered an article by Dr. Hisham Ziauddeen and colleagues in Nature Reviews Neuroscience that questioned the idea that common obesity represents food addiction-- an idea that I often encounter in my reading. Maggie Koerth-Baker asked me if I wanted to respond. I sent her a response explaining that I agree with the authors' conclusions and I also doubt obesity is food addiction per se, as I have explained in the past, although a subset of obese people can be addicted to food. I explained that the conclusions of the paper are consistent with the idea that food reward influences fat mass. You can find my explanation here.
Food Reward: Approaching a Scientific Consensus
Review papers provide a bird's-eye view of a field from the perspective of experts. Recent review papers show that many obesity researchers are converging on a model for the development of obesity that includes excessive food reward*, in addition to other factors such as physical inactivity, behavioral traits, and alterations in the function of the hypothalamus (a key brain region for the regulation of body fatness). Take for example the four new review papers I posted recently by obesity and reward researchers:
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Speaking at AHS12
I'll be giving a 40 minute presentation at the Ancestral Health Symposium this summer titled "Digestive Health, Inflammation and the Metabolic Syndrome". Here's the abstract:
What determines this? Emerging research suggests that one factor is digestive health, including the bacterial ecosystem inside each person's digestive tract, and the integrity of the gut barrier. I'll review some of this research in my talk, and leave the audience with actionable information for maintaining gastrointestinal and metabolic health. Most of this information will not have been covered on this blog.
The Ancestral Health Symposium will be from August 9-12 at Harvard Law School in Boston, presented in conjunction with the Harvard Food Law society. Tickets are currently available-- get them before they sell out! Last year, they went fast.
See you there!
Excessive fat mass is an important contributor to the metabolic syndrome, but at the same level of body fatness, some people are metabolically normal while others are extremely impaired. Even among obese people, most of whom have the metabolic syndrome, about 20 percent are metabolically normal, with normal fasting insulin and insulin sensitivity, normal blood pressure, normal circulating inflammatory markers, and normal blood lipids.The “metabolic syndrome” is a cluster of health problems including abdominal obesity, insulin resistance, low-grade inflammation, high blood pressure and blood lipid abnormalities that currently affects one third of American adults. It is the quintessential modern metabolic disorder and a major risk factor for diabetes, heart disease and certain cancers. This talk will explore emerging links between diet, gut flora, digestive health and the development of the metabolic syndrome. The audience will learn about factors that may help maintain digestive and metabolic health for themselves and the next generation.
What determines this? Emerging research suggests that one factor is digestive health, including the bacterial ecosystem inside each person's digestive tract, and the integrity of the gut barrier. I'll review some of this research in my talk, and leave the audience with actionable information for maintaining gastrointestinal and metabolic health. Most of this information will not have been covered on this blog.
The Ancestral Health Symposium will be from August 9-12 at Harvard Law School in Boston, presented in conjunction with the Harvard Food Law society. Tickets are currently available-- get them before they sell out! Last year, they went fast.
See you there!
Qnexa, the Latest Obesity Drug
There are very few obesity drugs currently approved for use in the US-- not because effective drugs don't exist, but because the FDA has judged that the side effects of existing drugs are unacceptable.
Although ultimately I believe the most satisfying resolution to the obesity epidemic will not come from drugs, drugs offer us a window into the biological processes that underlie obesity and fat loss. Along those lines, here's a quote from a review paper on obesity drugs that I think is particularly enlightening (1):
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Although ultimately I believe the most satisfying resolution to the obesity epidemic will not come from drugs, drugs offer us a window into the biological processes that underlie obesity and fat loss. Along those lines, here's a quote from a review paper on obesity drugs that I think is particularly enlightening (1):
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Boing!
I just had a featured article published on Boing Boing, "Seduced by Food: Obesity and the Human Brain". Boing Boing is the most popular blog on the Internet, with over 5 million unique visitors per month, and it's also one of my favorite haunts, so it was really exciting for me to be invited to submit an article. For comparison, Whole Health Source had about 72,000 unique visitors last month (200,000+ hits).
The article is a concise review of the food reward concept, and how it relates to the current obesity epidemic. Concise compared to all the writing I've done on this blog, anyway. I put a lot of work into making the article cohesive and understandable for a somewhat general audience, and I think it's much more effective at explaining the concept than the scattered blog posts I've published here. I hope it will clear up some of the confusion about food reward. I don't know what's up with the image they decided to use at the top.
Many thanks to Mark Frauenfelder, Maggie Koerth-Baker, and Rob Beschizza for the opportunity to publish on Boing Boing, as well as their comments on the draft versions!
For those who have arrived at Whole Health Source for the first time via Boing Boing, welcome! Have a look around. The "labels" menu on the sidebar is a good place to start-- you can browse by topic.
The article is a concise review of the food reward concept, and how it relates to the current obesity epidemic. Concise compared to all the writing I've done on this blog, anyway. I put a lot of work into making the article cohesive and understandable for a somewhat general audience, and I think it's much more effective at explaining the concept than the scattered blog posts I've published here. I hope it will clear up some of the confusion about food reward. I don't know what's up with the image they decided to use at the top.
Many thanks to Mark Frauenfelder, Maggie Koerth-Baker, and Rob Beschizza for the opportunity to publish on Boing Boing, as well as their comments on the draft versions!
For those who have arrived at Whole Health Source for the first time via Boing Boing, welcome! Have a look around. The "labels" menu on the sidebar is a good place to start-- you can browse by topic.
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Palatability, Satiety and Calorie Intake
WHS reader Paul Hagerty recently sent me a very interesting paper titled "A Satiety Index of Common Foods", by Dr. SHA Holt and colleagues (1). This paper quantified how full we feel after eating specific foods. I've been aware of it for a while, but hadn't read it until recently. They fed volunteers a variety of commonly eaten foods, each in a 240 calorie portion, and measured how full each food made them feel, and how much they ate at a subsequent meal. Using the results, they calculated a "satiety index", which represents the fullness per calorie of each food, normalized to white bread (white bread arbitrarily set to SI = 100). So for example, popcorn has a satiety index of 154, meaning it's more filling than white bread per calorie.
One of the most interesting aspects of the paper is that the investigators measured a variety of food properties (energy density, fat, starch, sugar, fiber, water content, palatability), and then determined which of them explained the SI values most completely.
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One of the most interesting aspects of the paper is that the investigators measured a variety of food properties (energy density, fat, starch, sugar, fiber, water content, palatability), and then determined which of them explained the SI values most completely.
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Soda-Free Sunday
Last Thursday, I received a message from a gentleman named Dorsol Plants about a public health campaign here in King County called Soda Free Sunday. They're asking people to visit www.sodafreesundays.com and make a pledge to go soda-free for one day per week.
Drinking sugar-sweetened beverages (SSBs), including soda, is one of the worst things you can do for your health. SSB consumption is probably one of the major contributors to the modern epidemics of obesity and metabolic dysfunction.
I imagine that most WHS readers don't drink SSBs very often if at all, but I'm sure some do. Whether you want to try drinking fewer SSBs, or just re-affirm an ongoing commitment to avoid them, I encourage you to visit www.sodafreesundays.com and make the pledge. You can do so even if you're not a resident of King county.
Drinking sugar-sweetened beverages (SSBs), including soda, is one of the worst things you can do for your health. SSB consumption is probably one of the major contributors to the modern epidemics of obesity and metabolic dysfunction.
I imagine that most WHS readers don't drink SSBs very often if at all, but I'm sure some do. Whether you want to try drinking fewer SSBs, or just re-affirm an ongoing commitment to avoid them, I encourage you to visit www.sodafreesundays.com and make the pledge. You can do so even if you're not a resident of King county.
Is Sugar Fattening?
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By 2606, the US Diet will be 100 Percent Sugar
The US diet has changed dramatically in the last 200 years. Many of these changes stem from a single factor: the industrialization and commercialization of the American food system. We've outsourced most of our food preparation, placing it into the hands of professionals whose interests aren't always well aligned with ours.
It's hard to appreciate just how much things have changed, because none of us were alive 200 years ago. To help illustrate some of these changes, I've been collecting statistics on US diet trends. Since sugar is the most refined food we eat in quantity, and it's a good marker of processed food consumption, naturally I wanted to get my hands on sugar intake statistics-- but solid numbers going back to the early 19th century are hard to come by! Of all the diet-related books I've read, I've never seen a graph of year-by-year sugar intake going back more than 100 years.
A gentleman by the name of Jeremy Landen and I eventually tracked down some outstanding statistics from old US Department of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005, which have appeared in two of my talks but I have never seen graphed anywhere else*. These numbers represent added sweeteners such as cane sugar, high-fructose corn syrup and maple syrup, but not naturally occurring sugars in fruit and vegetables. Behold:
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Cigarette Smoking-- Another Factor in the Obesity Epidemic
Obesity rates in the US have more than doubled in the last 30 years, and rates of childhood obesity and extreme adult obesity have tripled. One third of US adults are considered obese, and another third overweight. This is the "obesity epidemic".
The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved. However, there's another probable contributor that's often overlooked: declining smoking rates.
Here's a graph of cigarette consumption over the last century in the US (1):
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The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved. However, there's another probable contributor that's often overlooked: declining smoking rates.
Here's a graph of cigarette consumption over the last century in the US (1):
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My TEDx Talk, "The American Diet: a Historical Perspective"
On October 21st, I spoke at the Harvard Food Law Society's TEDx conference, Forum on Food Policy. The conference kicked off with three talks on nutrition, by Drs. Walter Willett, David Ludwig and myself. My talk is only 17 minutes long as per TED format, but it's packed with research on both quantitative and qualitative changes in the US diet over the last two centuries. It contains surprises for almost anyone, and I can guarantee you've never learned this much about the history of the US diet in 17 minutes. The talk was titled "The American Diet: a Historical Perspective"; you can access it by following that link.
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An Interview with Dr. C. Vicky Beer, Paleo-friendly MD
As I was preparing my recent article on the Paleo diet (1), I interviewed a local Paleo-friendly MD named C. Vicky Beer. I was only able to include a snippet of the interview in the article, but I thought WHS readers would be interested to read the rest of the interview with Dr. Beer:
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Paleo Diet Article in Sound Consumer
I recently wrote an article for my local natural foods grocery store, PCC, about the "Paleolithic" diet. You can read it online here. I explain the basic rationale for Paleo diets, some of the scientific support behind it, and how it can be helpful for people with certain health problems. I focused in particular on the research of Dr. Staffan Lindeberg at the University of Lund, who has studied non-industrial populations using modern medical techniques and also conducted clinical diet trials using the Paleo diet.
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Insulin and Obesity: Another Nail in the Coffin
There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness. Some versions invoke insulin's effects on fat tissue, others its effects in the brain. This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn't seem to have much if any impact on body weight in controlled trials).
I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s. However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness. If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well.
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I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s. However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness. If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well.
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What Causes Insulin Resistance? Part VII
In previous posts, I outlined the factors I'm aware of that can contribute to insulin resistance. In this post, first I'll list the factors, then I'll provide my opinion of effective strategies for preventing and potentially reversing insulin resistance.
The factors
These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance. I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another.
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The factors
These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance. I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another.
Read more »
Three Announcements
Chris Highcock of the blog Conditioning Research just published a book called Hillfit, which is a conditioning book targeted at hikers/backpackers. He uses his knowledge and experience in hiking and conditioning to argue that strength training is an important part of conditioning for hiking. I'm also a hiker/backpacker myself here in the rugged and beautiful Pacific Northwest, and I also find that strength training helps with climbing big hills, and walking farther and more easily with a lower risk of injury.
Richard Nikoley of the blog Free the Animal has also published a book called Free the Animal: Beyond the Blog, where he shares his strategies for losing fat and improving health and fitness. I haven't had a chance to read it yet, but Richard has a reasonable perspective on diet/health and a sharp wit.
Also, my friend Pedro Bastos has asked me to announce a one-day seminar at the University of Lisbon (Portugal) by Dr. Frits Muskiet titled "Vitamins and Minerals: A Scientific, Modern, Evolutionary and Global View". It will be on Sunday, Feb 5-- you can find more details about the seminar here. Dr. Muskiet is a researcher at the Groningen University Medical Center in the Netherlands. He studies the impact of nutrients, particularly fatty acids, on health, from an evolutionary perspective. Wish I could attend.
Richard Nikoley of the blog Free the Animal has also published a book called Free the Animal: Beyond the Blog, where he shares his strategies for losing fat and improving health and fitness. I haven't had a chance to read it yet, but Richard has a reasonable perspective on diet/health and a sharp wit.
Also, my friend Pedro Bastos has asked me to announce a one-day seminar at the University of Lisbon (Portugal) by Dr. Frits Muskiet titled "Vitamins and Minerals: A Scientific, Modern, Evolutionary and Global View". It will be on Sunday, Feb 5-- you can find more details about the seminar here. Dr. Muskiet is a researcher at the Groningen University Medical Center in the Netherlands. He studies the impact of nutrients, particularly fatty acids, on health, from an evolutionary perspective. Wish I could attend.
What Causes Insulin Resistance? Part VI
In this post, I'll explore a few miscellaneous factors that can contribute to insulin resistance: smoking, glucocorticoids/stress, cooking temperature, age, genetics and low birth weight.
Smoking
Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:
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Smoking
Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:
- Increased inflammation
- Increased circulating free fatty acids (4)
Read more »
What Causes Insulin Resistance? Part V
Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance. In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.
Carbohydrate and Fat
There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity. What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people. This will get at what causes insulin resistance in someone who does not already have it.
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Carbohydrate and Fat
There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity. What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people. This will get at what causes insulin resistance in someone who does not already have it.
Read more »
New Obesity Review Paper by Yours Truly
The Journal of Clinical Endocrinology and Metabolism just published a clinical review paper written by myself and my mentor Dr. Mike Schwartz, titled "Regulation of Food Intake, Energy Balance, and Body Fat Mass: Implications for the Pathogenesis and Treatment of Obesity" (1). JCEM is one of the most cited peer-reviewed journals in the fields of endocrinology, obesity and diabetes, and I'm very pleased that it spans the gap between scientists and physicians. Our paper takes a fresh and up-to-date look at the mechanisms by which food intake and body fat mass are regulated by the body, and how these mechanisms are altered in obesity. We explain the obesity epidemic in terms of the mismatch between our genes and our current environment, a theme that is frequently invoked in ancestral health circles.
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What Causes Insulin Resistance? Part IV
So far, we've explored three interlinked causes of insulin resistance: cellular energy excess, inflammation, and insulin resistance in the brain. In this post, I'll explore the effects on micronutrient status on insulin sensitivity.
Micronutrient Status
There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post. My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.
Read more »
Micronutrient Status
There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post. My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.
Read more »
What Causes Insulin Resistance? Part III
As discussed in previous posts, cellular energy excess and inflammation are two important and interlinked causes of insulin resistance. Continuing our exploration of insulin resistance, let's turn our attention to the brain.
The brain influences every tissue in the body, in many instances managing tissue processes to react to changing environmental or internal conditions. It is intimately involved in insulin signaling in various tissues, for example by:
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The brain influences every tissue in the body, in many instances managing tissue processes to react to changing environmental or internal conditions. It is intimately involved in insulin signaling in various tissues, for example by:
- regulating insulin secretion by the pancreas (1)
- regulating glucose absorption by tissues in response to insulin (2)
- regulating the suppression of glucose production by the liver in response to insulin (3)
- regulating the trafficking of fatty acids in and out of fat cells in response to insulin (4, 5)
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What Causes Insulin Resistance? Part II
In the last post, I described how cellular energy excess causes insulin resistance, and how this is triggered by whole-body energy imbalance. In this post, I'll describe another major cause of insulin resistance: inflammation.
Inflammation
In 1876, a German physician named W Ebstein reported that high doses of sodium salicylate could totally eliminate the signs and symptoms of diabetes in certain patients (Berliner Klinische Wochenschrift. 13:337. 1876). Following up on this work in 1901, the British physician RT Williamson reported that treating diabetic patients with sodium salicylate caused a striking decrease in the amount of glucose contained in the patients' urine, also indicating an apparent improvement in diabetes (2). This effect was essentially forgotten until 1957, when it was rediscovered.
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Inflammation
In 1876, a German physician named W Ebstein reported that high doses of sodium salicylate could totally eliminate the signs and symptoms of diabetes in certain patients (Berliner Klinische Wochenschrift. 13:337. 1876). Following up on this work in 1901, the British physician RT Williamson reported that treating diabetic patients with sodium salicylate caused a striking decrease in the amount of glucose contained in the patients' urine, also indicating an apparent improvement in diabetes (2). This effect was essentially forgotten until 1957, when it was rediscovered.
Read more »
What Causes Insulin Resistance? Part I
Insulin is an ancient hormone that influences many processes in the body. Its main role is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body's two main fuels), keeping them within a fairly narrow range*. It does this by encouraging the transport of nutrients into cells from the circulation, and discouraging the export of nutrients out of storage sites, in response to an increase in circulating nutrients (glucose or fatty acids). It therefore operates a negative feedback loop that constrains circulating nutrient concentrations. It also has many other functions that are tissue-specific.
Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids). It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders.
Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range? The answer to that question is the crux of this post.
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Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids). It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders.
Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range? The answer to that question is the crux of this post.
Read more »
New York Times Magazine Article on Obesity
For those of you who haven't seen it, Tara Parker-Pope write a nice article on obesity in the latest issue of NY Times Magazine (1). She discusses research showing that the body "resists" fat loss attempts, making it difficult to lose fat and maintain fat loss once obesity is established.
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High-Fat Diets, Obesity and Brain Damage
Many of you have probably heard the news this week:
High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods
Your brain cells are exploding with every bite of butter! Just kidding. The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1). We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop. I'm fourth author on the paper, so let me explain what we found and why it's important.
The Questions
Among the many questions that interest obesity researchers, two stand out:
The Findings
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High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods
Your brain cells are exploding with every bite of butter! Just kidding. The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1). We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop. I'm fourth author on the paper, so let me explain what we found and why it's important.
The Questions
Among the many questions that interest obesity researchers, two stand out:
- What causes obesity?
- Once obesity is established, why is it so difficult to treat?
The Findings
Read more »
Junk Free January
Last year, Matt Lentzner organized a project called Gluten Free January, in which 546 people from around the world gave up gluten for one month. The results were striking: a surprisingly large proportion of participants lost weight, experienced improved energy, better digestion and other benefits (1, 2). This January, Lentzner organized a similar project called Junk Free January. Participants can choose between four different diet styles:
If you've been waiting for an excuse to improve your diet, why not join Junk Free January?
- Gluten free
- Seed oil free (soybean, sunflower, corn oil, etc.)
- Sugar free
- Gluten, seed oil and sugar free
If you've been waiting for an excuse to improve your diet, why not join Junk Free January?
