Some people have reacted negatively to the idea of a reduced-reward diet because it strikes them as difficult or unsustainable. In this post, I'll discuss my thoughts on the practicality and sustainability of this way of eating. I've also thrown in a few philosophical points about reward and the modern world.
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How Does Gastric Bypass Surgery Cause Fat Loss?
Gastric bypass surgery is an operation that causes food to bypass part of the digestive tract. In the most common surgery, Roux-en-Y bypass, stomach size is reduced and a portion of the upper small intestine is bypassed. This means that food skips most of the stomach and the duodenum (upper small intestine), passing from the tiny stomach directly into the jejunum (a lower part of the upper small intestine)*. It looks something like this:
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Liposuction and Fat Regain
If body fat really is actively regulated by the body, rather than just being a passive result of voluntary food intake and exercise behaviors, then liposuction shouldn't be very effective at reducing total fat mass in the long run. People should return to their body fat "setpoint" rather than remaining at a lower fat mass.
Teri L. Hernandez and colleagues recently performed the first ever randomized liposuction study to answer this question (1). Participants were randomly selected to either receive liposuction, or not. They were all instructed not to make any lifestyle changes for the duration of the study, and body fatness was measured at 6 weeks, 6 months and one year by DXA.
At 6 weeks, the liposuction group was significantly leaner than the control group. At 6 months, the difference between the two groups had decreased. At one year, it had decreased further and the difference between the groups was no longer statistically significant. Furthermore, the liposuction group regained fat disproportionately in the abdominal area (belly), which is more dangerous than where it was before. The investigators stated:
Teri L. Hernandez and colleagues recently performed the first ever randomized liposuction study to answer this question (1). Participants were randomly selected to either receive liposuction, or not. They were all instructed not to make any lifestyle changes for the duration of the study, and body fatness was measured at 6 weeks, 6 months and one year by DXA.
At 6 weeks, the liposuction group was significantly leaner than the control group. At 6 months, the difference between the two groups had decreased. At one year, it had decreased further and the difference between the groups was no longer statistically significant. Furthermore, the liposuction group regained fat disproportionately in the abdominal area (belly), which is more dangerous than where it was before. The investigators stated:
We conclude that [body fat] is not only restored to baseline levels in nonobese women after small-volume liposuction, but is redistributed abdominally.This is consistent with animal studies showing that when you surgically remove fat, total fat mass "catches up" to animals that had no fat removed (2). Fat mass is too important to be left up to chance. That's why the body regulates it, and that's why any satisfying resolution of obesity must address that regulatory mechanism.
Food Reward: a Dominant Factor in Obesity, Part VIII
Further reading
I didn't come up with the idea that excessive food reward increases calorie intake and can lead to obesity, far from it. The idea has been floating around the scientific literature for decades. In 1976, after conducting an interesting diet study in humans, Dr. Michel Cabanac stated that the "palatability of the diet influences the set point of the ponderostat [system that regulates body fatness]" (1).
Currently there is a growing consensus that food reward/palatability is a major contributor to obesity. This is reflected by the proliferation of review articles appearing in high-profile journals. For the scientists in the audience who want more detail than I provide on my blog, here are some of the reviews I've read and enjoyed. These were written by some of the leading scientists in the study of food reward and hedonics:
Palatability of food and the ponderostat. Michel Cabanac, 1989.
Food reward, hyperphagia and obesity. Hans-Rudolf Berthoud et al., 2011.
Reward mechanisms in obesity: new insights and future directions. Paul J. Kenny, 2011.
Relation of obesity to consummatory and anticipatory food reward. Eric Stice, 2009.
Hedonic and incentive signals for body weight control. Emil Egecioglu et al., 2011.
Homeostatic and hedonic signals interact in the control of food intake. Michael Lutter and Eric J. Nestler, 2009.
Opioids as agents of reward-related feeding: a consideration of the evidence. Allen S. Levine and Charles J. Billington, 2004.
Central opioids and consumption of sweet tastants: when reward outweighs homeostasis. Pawel K. Olszewski and Allen S. Levine, 2007.
Oral and postoral determinants of food reward. Anthony Sclafani, 2004.
Reduced dopaminergic tone in hypothalamic neural circuits: expression of a "thrifty" genotype underlying the metabolic syndrome? Hanno Pijl, 2003.
If you can read all these papers and still not believe in the food reward hypothesis... you deserve some kind of award.
I didn't come up with the idea that excessive food reward increases calorie intake and can lead to obesity, far from it. The idea has been floating around the scientific literature for decades. In 1976, after conducting an interesting diet study in humans, Dr. Michel Cabanac stated that the "palatability of the diet influences the set point of the ponderostat [system that regulates body fatness]" (1).
Currently there is a growing consensus that food reward/palatability is a major contributor to obesity. This is reflected by the proliferation of review articles appearing in high-profile journals. For the scientists in the audience who want more detail than I provide on my blog, here are some of the reviews I've read and enjoyed. These were written by some of the leading scientists in the study of food reward and hedonics:
Palatability of food and the ponderostat. Michel Cabanac, 1989.
Food reward, hyperphagia and obesity. Hans-Rudolf Berthoud et al., 2011.
Reward mechanisms in obesity: new insights and future directions. Paul J. Kenny, 2011.
Relation of obesity to consummatory and anticipatory food reward. Eric Stice, 2009.
Hedonic and incentive signals for body weight control. Emil Egecioglu et al., 2011.
Homeostatic and hedonic signals interact in the control of food intake. Michael Lutter and Eric J. Nestler, 2009.
Opioids as agents of reward-related feeding: a consideration of the evidence. Allen S. Levine and Charles J. Billington, 2004.
Central opioids and consumption of sweet tastants: when reward outweighs homeostasis. Pawel K. Olszewski and Allen S. Levine, 2007.
Oral and postoral determinants of food reward. Anthony Sclafani, 2004.
Reduced dopaminergic tone in hypothalamic neural circuits: expression of a "thrifty" genotype underlying the metabolic syndrome? Hanno Pijl, 2003.
If you can read all these papers and still not believe in the food reward hypothesis... you deserve some kind of award.
Food Reward: a Dominant Factor in Obesity, Part VII
Now that I've explained the importance of food reward to obesity, and you're tired of reading about it, it's time to share my ideas on how to prevent and perhaps reverse fat gain. First, I want to point out that although food reward is important, it's not the only factor. Heritable factors (genetics and epigenetics), developmental factors (uterine environment, childhood diet), lifestyle factors (exercise, sleep, stress) and dietary factors besides reward also play a role. That's why I called this series "a dominant factor in obesity", rather than "the dominant factor in obesity".
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Food Reward: a Dominant Factor in Obesity, Part VI
Reward Centers can Modify the Body Fat Setpoint
Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain. It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1). Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2). I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3). The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
Earth's Best Organic 2nd Fruit Variety Pack, 4-Ounce Jars (Pack of 12)
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Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain. It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1). Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2). I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3). The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
Earth's Best Organic 2nd Fruit Variety Pack, 4-Ounce Jars (Pack of 12)
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Food Reward: a Dominant Factor in Obesity, Part V
Non-industrial diets from a food reward perspective
In 21st century affluent nations, we have unprecedented control over what food crosses our lips. We can buy nearly any fruit or vegetable in any season, and a massive processed food industry has sprung up to satisfy (or manufacture) our every craving. Most people can afford exotic spices and herbs from around the world-- consider that only a hundred years ago, black pepper was a luxury item. But our degree of control goes even deeper: over the last century, kitchen technology such as electric/gas stoves, refrigerators, microwaves and a variety of other now-indispensable devices have changed the way we prepare food at home (Megan J. Elias. Food in the United States, 1890-1945).
To help calibrate our thinking about the role of food reward (and food palatability) in human evolutionary history, I offer a few brief descriptions of contemporary hunter-gatherer and non-industrial agriculturalist diets. What did they eat, and how did they prepare it?
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In 21st century affluent nations, we have unprecedented control over what food crosses our lips. We can buy nearly any fruit or vegetable in any season, and a massive processed food industry has sprung up to satisfy (or manufacture) our every craving. Most people can afford exotic spices and herbs from around the world-- consider that only a hundred years ago, black pepper was a luxury item. But our degree of control goes even deeper: over the last century, kitchen technology such as electric/gas stoves, refrigerators, microwaves and a variety of other now-indispensable devices have changed the way we prepare food at home (Megan J. Elias. Food in the United States, 1890-1945).
To help calibrate our thinking about the role of food reward (and food palatability) in human evolutionary history, I offer a few brief descriptions of contemporary hunter-gatherer and non-industrial agriculturalist diets. What did they eat, and how did they prepare it?
Read more »
Healthy Skeptic Podcast
Chris Kresser has just posted our recent interview/discussion on his blog The Healthy Skeptic. You can listen to it on Chris's blog here. The discussion mostly centered around body fat and food reward. I also answered a few reader questions. Here are some highlights:
- How does the food reward system work? Why did it evolve?
- Why do certain flavors we don’t initially like become appealing over time?
- How does industrially processed food affect the food reward system?
- What’s the most effective diet used to make rats obese in a research setting? What does this tell us about human diet and weight regulation?
- Do we know why highly rewarding food increases the set point in some people but not in others?
- How does the food reward theory explain the effectiveness of popular fat loss diets?
- Does the food reward theory tell us anything about why traditional cultures are generally lean?
- What does cooking temperature have to do with health?
- Reader question: How does one lose fat?
- Reader question: What do I (Stephan) eat?
- Reader question: Why do many people gain fat with age, especially postmenopausal women?
Fast Food, Weight Gain and Insulin Resistance
CarbSane just posted an interesting new study that fits in nicely with what we're discussing here. It's part of the US Coronary Artery Risk Development in Young Adults (CARDIA) study, which is a long-term observational study that is publishing many interesting findings. The new study is titled "Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis" (1). The results speak for themselves, loud and clear (I've edited some numbers out of the quote for clarity):
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Food Reward: a Dominant Factor in Obesity, Part III
Low-Fat Diets
In 2000, the International Journal of Obesity published a nice review article of low-fat diet trials. It included data from 16 controlled trials lasting from 2-12 months and enrolling 1,910 participants (1). What sets this review apart is it only covered studies that did not include instructions to restrict calorie intake (ad libitum diets). On average, low-fat dieters reduced their fat intake from 37.7 to 27.5 percent of calories. Here's what they found:
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In 2000, the International Journal of Obesity published a nice review article of low-fat diet trials. It included data from 16 controlled trials lasting from 2-12 months and enrolling 1,910 participants (1). What sets this review apart is it only covered studies that did not include instructions to restrict calorie intake (ad libitum diets). On average, low-fat dieters reduced their fat intake from 37.7 to 27.5 percent of calories. Here's what they found:
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Clarifications About Carbohydrate and Insulin
My statements about carbohydrate and insulin in the previous post seem to have kicked up some dust! Some people are even suggesting I've gone low-fat! I'm going to take this opportunity to be more specific about my positions.
I do not think that post-meal insulin spikes contribute to obesity, and they may even oppose it. I'm not aware of anyone who researches metabolism for a living who thinks post-meal insulin spikes contribute to obesity, and after having looked into it, I understand why. It's not a controversial issue in my field as far as I can tell. Elevated fasting insulin is a separate issue-- that's a marker of insulin resistance. It's important not to confuse the two. Does insulin resistance contribute to obesity? I don't know, but it's hypothetically possible since insulin acts like leptin's kid brother in some ways. As far as I can tell, starch per se and post-meal insulin spikes do not lead to insulin resistance.
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I do not think that post-meal insulin spikes contribute to obesity, and they may even oppose it. I'm not aware of anyone who researches metabolism for a living who thinks post-meal insulin spikes contribute to obesity, and after having looked into it, I understand why. It's not a controversial issue in my field as far as I can tell. Elevated fasting insulin is a separate issue-- that's a marker of insulin resistance. It's important not to confuse the two. Does insulin resistance contribute to obesity? I don't know, but it's hypothetically possible since insulin acts like leptin's kid brother in some ways. As far as I can tell, starch per se and post-meal insulin spikes do not lead to insulin resistance.
Read more »
Healthy Skeptic Podcast and Reader Questions
Chris Kresser, Danny Roddy and I just finished recording the podcast that will be released on May 24th. It went really well, and we think you'll find it informative and maybe even practical!
Unfortunately, we only got around to answering three of the questions I had selected:
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Unfortunately, we only got around to answering three of the questions I had selected:
- How does one lose fat?
- What do I (Stephan) eat?
- Why do many people gain fat with age, especially postmenopausal women?
Read more »
Paleolithic Diet Clinical Trials, Part V
Dr. Staffan Lindeberg's group has published a new paleolithic diet paper in the journal Nutrition and Metabolism, titled "A Paleolithic Diet is More Satiating per Calorie than a Mediterranean-like Diet in Individuals with Ischemic Heart Disease" (1).
The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).
One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).
With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.
There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.
A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).
A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.
If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.
*Intakes were determined using 4-day weighed food records.
**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.
The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).
One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).
With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.
There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.
A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).
A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.
If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.
*Intakes were determined using 4-day weighed food records.
**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.
The Twinkie Diet for Fat Loss
The Experiment
I've received several e-mails from readers about a recent experiment by nutrition professor Mark Haub at Kansas State university (thanks to Josh and others). He ate a calorie-restricted diet in which 2/3 of his calories came from junk food: Twinkies, Hostess and Little Debbie cakes, Dorito corn chips and sweetened cereals (1). On this calorie-restricted junk food diet (800 calorie/day deficit), he lost 27 pounds in two months.
Therefore, junk food doesn't cause fat gain and the only thing that determines body fatness is how much you eat and exercise. Right?
Discussion
Let's start with a few things most people can agree on. If you don't eat any food at all, you will lose fat mass. If you voluntarily force-feed yourself with a large excess of food, you will gain fat mass, whether the excess comes from carbohydrate or fat (2). So calories obviously have something to do with fat mass.
But of course, the situation is much more subtle in real life. Since a pound of body fat contains roughly 3,500 calories, eating an excess of 80 calories per day (1 piece of toast) should lead to a weight gain of 8 lbs of fat per year. Conversely, if you're distracted and forget to eat your toast, you should lose 8 lbs of fat per year, which would eventually be dangerous for a lean person. That's why we all record every crumb of food we eat, determine its exact calorie content, and match that intake precisely with our energy expenditure to maintain a stable weight.
Oh wait, we don't do that? Then how do so many people maintain a stable weight over years and decades? And how do wild animals maintain a stable body fat percentage (except when preparing for hibernation) even in the face of food surpluses? How do lab rats and mice fed a whole food diet maintain a stable body fat percentage in the face of literally unlimited food, when they're in a small cage with practically nothing to do but eat?
The answer is that the body isn't stupid. Over hundreds of millions of years, we've evolved sophisticated systems that maintain "energy homeostasis". In other words, these systems act to regulate fat mass and keep it within the optimal range. The evolutionary pressures operating here are obvious: too little fat mass, and an organism will be susceptible to starvation; too much, and an organism will be less agile and less efficient at locomotion and reproduction. Energy homeostasis is such a basic part of survival that even the simplest organisms regulate it.
Not only is it clear that we have an energy homeostasis system, we even know a thing or two about how it works. Early studies showed that lesioning a part of the brain called the ventromedial hypothalamus causes massive obesity (3; this is also true in humans, when a disruption results from cancer). Investigators also discovered several genetic mutations in rats and mice that result in massive obesity*. Decades-long research eventually demonstrated that these models have something in common: they all interfere with an energy homeostasis circuit that passes information about fat mass to the hypothalamus via the hormone leptin.
The leptin system is a classic negative feedback loop: the more fat mass accumulates, the more leptin is produced. The more leptin is produced, the more the hypothalamus activates programs to reduce hunger and increase energy expenditure, which continues until fat mass is back in the optimal range. Conversely, low fat mass and low leptin lead to increased hunger and energy conservation by this same pathway**.
So if genetic mutants can become massively obese, I guess that argues against the idea that voluntary food intake and energy expenditure are the only determinants of fat mass. But a skeptic might point out that these are extreme cases, and such mutations are so rare in humans that the analogy is irrelevant.
Let's dig deeper. There are many studies in which rodents are made obese using industrial high-fat diets made from refined ingredients. The rats eat more calories (at least in the beginning), and gain fat rapidly. No big surprise there. But what may come as a surprise to the calorie counters is that rodents on these diets gain body fat even if their calorie intake is matched precisely to lean rodents eating a whole food diet (4, 5, 6). In fact, they sometimes gain almost as much fat as rodents who are allowed to eat all the industrial food they want. This has been demonstrated repeatedly.
How is this possible? The answer is that the calorie-matched rats reduce their energy expenditure to a greater degree than those that are allowed free access to food. The most logical explanation for this behavior is that the "set point" of the energy homeostasis system has changed. The industrial diet causes the rodents' bodies to "want" to accumulate more fat, therefore they will accomplish that by any means necessary, whether it means eating more, or if that's not possible, expending less energy. This shows that a poor diet can, in principle, dysregulate the system that controls energy homeostasis.
Well, then why did Dr. Haub's diet allow him to lose weight? The body can only maintain body composition in the face of a calorie deficit up to a certain point. After that, it has no choice but to lower fat mass. It will do so reluctantly, at the same time increasing hunger, and reducing lean mass***, muscular strength and energy dedicated to tissue repair and immune function. However, I hope everyone can agree that a sufficient calorie deficit can lead to fat loss regardless of what kind of food is eaten. Dr. Haub's 800 calorie deficit qualifies. I think only a very small percentage of people are capable of maintaining that kind of calorie deficit for more than a few months, because it is mentally and physically difficult to fight against what the hypothalamus has decided is in your best interest.
My hypothesis is that, in many people, industrial food and an unnatural lifestyle lead to gradual fat gain by dysregulating the energy homeostasis system. This "breaks" the system that's designed to automatically keep our fat mass in the optimal range by regulating energy intake, energy expenditure and the relative partitioning of energy resources between lean and fat tissue. This system is not under our conscious control, and it has nothing to do with willpower.
I suspect that if you put a group of children on this junk food diet for many years, and compared them to a group of children on a healthy diet, the junk food group would end up fatter as adults. This would be true if neither group paid any attention to calories, and perhaps even if calorie intake were identical in the two groups (as in the rodent example). The result of Dr. Haub's experiment does not contradict that hypothesis.
So do calories matter? Yes, but in a healthy person, all the math is done automatically by the hypothalamus and energy balance requires no conscious effort. In 2010, many people have already accumulated excess fat mass. How that may be sustainably lost is another question entirely, and a more challenging one in my opinion. As they say, an ounce of prevention is worth a pound of cure. There are many possible strategies, with varying degrees of efficacy that depend highly on individual differences, but I think overall the question is still open. I discussed some of my thoughts in a recent series on body fat regulation (7, 8, 9, 10, 11).
* ob/ob and db/db mice. Zucker and Koletsky rats. Equivalent mutations in humans also result in obesity.
** Via an increase in muscular efficiency and perhaps a decrease in basal metabolism. Thyroid hormone activity drops.
*** Loss of muscle, bone and connective tissue can be compensated for by strength training during calorie restriction. Presumed loss of other non-adipose tissues (liver, kidney, brain, etc.) is probably not affected by strength training.
I've received several e-mails from readers about a recent experiment by nutrition professor Mark Haub at Kansas State university (thanks to Josh and others). He ate a calorie-restricted diet in which 2/3 of his calories came from junk food: Twinkies, Hostess and Little Debbie cakes, Dorito corn chips and sweetened cereals (1). On this calorie-restricted junk food diet (800 calorie/day deficit), he lost 27 pounds in two months.
Therefore, junk food doesn't cause fat gain and the only thing that determines body fatness is how much you eat and exercise. Right?
Discussion
Let's start with a few things most people can agree on. If you don't eat any food at all, you will lose fat mass. If you voluntarily force-feed yourself with a large excess of food, you will gain fat mass, whether the excess comes from carbohydrate or fat (2). So calories obviously have something to do with fat mass.
But of course, the situation is much more subtle in real life. Since a pound of body fat contains roughly 3,500 calories, eating an excess of 80 calories per day (1 piece of toast) should lead to a weight gain of 8 lbs of fat per year. Conversely, if you're distracted and forget to eat your toast, you should lose 8 lbs of fat per year, which would eventually be dangerous for a lean person. That's why we all record every crumb of food we eat, determine its exact calorie content, and match that intake precisely with our energy expenditure to maintain a stable weight.
Oh wait, we don't do that? Then how do so many people maintain a stable weight over years and decades? And how do wild animals maintain a stable body fat percentage (except when preparing for hibernation) even in the face of food surpluses? How do lab rats and mice fed a whole food diet maintain a stable body fat percentage in the face of literally unlimited food, when they're in a small cage with practically nothing to do but eat?
The answer is that the body isn't stupid. Over hundreds of millions of years, we've evolved sophisticated systems that maintain "energy homeostasis". In other words, these systems act to regulate fat mass and keep it within the optimal range. The evolutionary pressures operating here are obvious: too little fat mass, and an organism will be susceptible to starvation; too much, and an organism will be less agile and less efficient at locomotion and reproduction. Energy homeostasis is such a basic part of survival that even the simplest organisms regulate it.
Not only is it clear that we have an energy homeostasis system, we even know a thing or two about how it works. Early studies showed that lesioning a part of the brain called the ventromedial hypothalamus causes massive obesity (3; this is also true in humans, when a disruption results from cancer). Investigators also discovered several genetic mutations in rats and mice that result in massive obesity*. Decades-long research eventually demonstrated that these models have something in common: they all interfere with an energy homeostasis circuit that passes information about fat mass to the hypothalamus via the hormone leptin.
The leptin system is a classic negative feedback loop: the more fat mass accumulates, the more leptin is produced. The more leptin is produced, the more the hypothalamus activates programs to reduce hunger and increase energy expenditure, which continues until fat mass is back in the optimal range. Conversely, low fat mass and low leptin lead to increased hunger and energy conservation by this same pathway**.
So if genetic mutants can become massively obese, I guess that argues against the idea that voluntary food intake and energy expenditure are the only determinants of fat mass. But a skeptic might point out that these are extreme cases, and such mutations are so rare in humans that the analogy is irrelevant.
Let's dig deeper. There are many studies in which rodents are made obese using industrial high-fat diets made from refined ingredients. The rats eat more calories (at least in the beginning), and gain fat rapidly. No big surprise there. But what may come as a surprise to the calorie counters is that rodents on these diets gain body fat even if their calorie intake is matched precisely to lean rodents eating a whole food diet (4, 5, 6). In fact, they sometimes gain almost as much fat as rodents who are allowed to eat all the industrial food they want. This has been demonstrated repeatedly.
How is this possible? The answer is that the calorie-matched rats reduce their energy expenditure to a greater degree than those that are allowed free access to food. The most logical explanation for this behavior is that the "set point" of the energy homeostasis system has changed. The industrial diet causes the rodents' bodies to "want" to accumulate more fat, therefore they will accomplish that by any means necessary, whether it means eating more, or if that's not possible, expending less energy. This shows that a poor diet can, in principle, dysregulate the system that controls energy homeostasis.
Well, then why did Dr. Haub's diet allow him to lose weight? The body can only maintain body composition in the face of a calorie deficit up to a certain point. After that, it has no choice but to lower fat mass. It will do so reluctantly, at the same time increasing hunger, and reducing lean mass***, muscular strength and energy dedicated to tissue repair and immune function. However, I hope everyone can agree that a sufficient calorie deficit can lead to fat loss regardless of what kind of food is eaten. Dr. Haub's 800 calorie deficit qualifies. I think only a very small percentage of people are capable of maintaining that kind of calorie deficit for more than a few months, because it is mentally and physically difficult to fight against what the hypothalamus has decided is in your best interest.
My hypothesis is that, in many people, industrial food and an unnatural lifestyle lead to gradual fat gain by dysregulating the energy homeostasis system. This "breaks" the system that's designed to automatically keep our fat mass in the optimal range by regulating energy intake, energy expenditure and the relative partitioning of energy resources between lean and fat tissue. This system is not under our conscious control, and it has nothing to do with willpower.
I suspect that if you put a group of children on this junk food diet for many years, and compared them to a group of children on a healthy diet, the junk food group would end up fatter as adults. This would be true if neither group paid any attention to calories, and perhaps even if calorie intake were identical in the two groups (as in the rodent example). The result of Dr. Haub's experiment does not contradict that hypothesis.
So do calories matter? Yes, but in a healthy person, all the math is done automatically by the hypothalamus and energy balance requires no conscious effort. In 2010, many people have already accumulated excess fat mass. How that may be sustainably lost is another question entirely, and a more challenging one in my opinion. As they say, an ounce of prevention is worth a pound of cure. There are many possible strategies, with varying degrees of efficacy that depend highly on individual differences, but I think overall the question is still open. I discussed some of my thoughts in a recent series on body fat regulation (7, 8, 9, 10, 11).
* ob/ob and db/db mice. Zucker and Koletsky rats. Equivalent mutations in humans also result in obesity.
** Via an increase in muscular efficiency and perhaps a decrease in basal metabolism. Thyroid hormone activity drops.
*** Loss of muscle, bone and connective tissue can be compensated for by strength training during calorie restriction. Presumed loss of other non-adipose tissues (liver, kidney, brain, etc.) is probably not affected by strength training.
Obesity and the Brain
Nature Genetics just published a paper that caught my interest (1). Investigators reviewed the studies that have attempted to determine associations between genetic variants and common obesity (as judged by body mass index or BMI). In other words, they looked for "genes" that are suspected to make people fat.
There are a number of gene variants that associate with an increased or decreased risk of obesity. These fall into two categories: rare single-gene mutations that cause dramatic obesity, and common variants that are estimated to have a very small impact on body fatness. The former category cannot account for common obesity because it is far too rare, and the latter probably cannot account for it either because it has too little impact*. Genetics can't explain the fact that there were half as many obese people in the US 40 years ago. Here's a wise quote from the obesity researcher Dr. David L. Katz, quoted from an interview about the study (2):
So, what do the genes do? Of those that have a known function, nearly all of them act in the brain, and most act in known body fat regulation circuits in the hypothalamus (a brain region). The brain is the master regulator of body fat mass. It's also the master regulator of nearly all large-scale homeostatic systems in the body, including the endocrine (hormone) system. Now you know why I study the neurobiology of obesity.
* The authors estimated that "together, the 32 confirmed BMI loci explained 1.45% of the inter-individual variation in BMI." In other words, even if you were unlucky enough to inherit the 'fat' version of all 32 genes, which is exceedingly unlikely, you would only have a slightly higher risk of obesity than the general population.
There are a number of gene variants that associate with an increased or decreased risk of obesity. These fall into two categories: rare single-gene mutations that cause dramatic obesity, and common variants that are estimated to have a very small impact on body fatness. The former category cannot account for common obesity because it is far too rare, and the latter probably cannot account for it either because it has too little impact*. Genetics can't explain the fact that there were half as many obese people in the US 40 years ago. Here's a wise quote from the obesity researcher Dr. David L. Katz, quoted from an interview about the study (2):
Let us by all means study our genes, and their associations with our various shapes and sizes... But let's not let it distract us from the fact that our genes have not changed to account for the modern advent of epidemic obesity -- our environments and lifestyles have.Exactly. So I don't usually pay much attention to "obesity genes", although I do think genetics contributes to how a body reacts to an unnatural diet/lifestyle. However, the first part of his statement is important too. Studying these types of associations can give us insights into the biological mechanisms of obesity when we ask the question "what do these genes do?" The processes these genes participate in should be the same processes that are most important in regulating fat mass.
So, what do the genes do? Of those that have a known function, nearly all of them act in the brain, and most act in known body fat regulation circuits in the hypothalamus (a brain region). The brain is the master regulator of body fat mass. It's also the master regulator of nearly all large-scale homeostatic systems in the body, including the endocrine (hormone) system. Now you know why I study the neurobiology of obesity.
* The authors estimated that "together, the 32 confirmed BMI loci explained 1.45% of the inter-individual variation in BMI." In other words, even if you were unlucky enough to inherit the 'fat' version of all 32 genes, which is exceedingly unlikely, you would only have a slightly higher risk of obesity than the general population.
Sleep Post Correction
An astute commenter pointed out that I misread the numbers in the paper on sleep and fat loss. I wrote that out of the total 3.0 kg lost, the high-sleep group lost 2.4 kg as fat, and the low-sleep group lost 1.4 kg of fat out of 2.9 kg total.
In fact, the high-sleep group lost 1.4 out of 2.9 kg as fat, and the low-sleep group lost 0.6 out of 3.0 kg as fat. So I got the numbers all mixed up. Sorry for the mistake. The main point of the post still stands though: sleep deprivation negatively influences body composition.
The correct numbers are even more interesting than the ones I made up. Even in the high-sleep group, nearly half the body weight lost by simple calorie restriction was lean mass. That doesn't make calorie restriction look very good!
In the sleep-deprived group, 80% of the weight lost by calorie restriction came out of lean mass. Ouch!
That illustrates one of the reasons why I'm skeptical of simple calorie restriction as a means of fat loss. When the body "wants" to be fat, it will sacrifice lean mass to preserve fat tissue. For example, the genetically obese Zucker rat cannot be starved thin. If you try to put it on a severe calorie-restricted diet, it will literally die fat because it will cannibalize its own lean mass (muscle, heart, brain, etc.) to spare the fat. That's an extreme example, but it illustrates the point.
The key is not only to balance energy intake with expenditure (which the brain does automatically when it's working correctly), but to allocate energy appropriately to lean and fat mass.
In fact, the high-sleep group lost 1.4 out of 2.9 kg as fat, and the low-sleep group lost 0.6 out of 3.0 kg as fat. So I got the numbers all mixed up. Sorry for the mistake. The main point of the post still stands though: sleep deprivation negatively influences body composition.
The correct numbers are even more interesting than the ones I made up. Even in the high-sleep group, nearly half the body weight lost by simple calorie restriction was lean mass. That doesn't make calorie restriction look very good!
In the sleep-deprived group, 80% of the weight lost by calorie restriction came out of lean mass. Ouch!
That illustrates one of the reasons why I'm skeptical of simple calorie restriction as a means of fat loss. When the body "wants" to be fat, it will sacrifice lean mass to preserve fat tissue. For example, the genetically obese Zucker rat cannot be starved thin. If you try to put it on a severe calorie-restricted diet, it will literally die fat because it will cannibalize its own lean mass (muscle, heart, brain, etc.) to spare the fat. That's an extreme example, but it illustrates the point.
The key is not only to balance energy intake with expenditure (which the brain does automatically when it's working correctly), but to allocate energy appropriately to lean and fat mass.
Have Seed Oils Caused a Multi-Generational Obesity Epidemic?
In 2006, Drs. Gerard Ailhaud and Philippe Guesnet hypothesized that industrial seed oils such as corn, soybean, safflower, sunflower and cottonseed oil are at least partially responsible for the current obesity epidemic (1). These oils were not a significant part of the human diet until very recently, yet they have been promoted due to their supposed ability to prevent cardiovascular disease. The Western world has been living a massive uncontrolled experiment ever since.
Linoleic acid is an omega-6 polyunsaturated fatty acid (PUFA) that makes up a large proportion of seed oils. It's a very bioactive molecule, in part because it's the precursor of two classes of signaling molecules (eicosanoids and endocannabinoids), some of which influence the development of fat tissue and regulate appetite.
Linoleic acid is an omega-6 polyunsaturated fatty acid (PUFA) that makes up a large proportion of seed oils. It's a very bioactive molecule, in part because it's the precursor of two classes of signaling molecules (eicosanoids and endocannabinoids), some of which influence the development of fat tissue and regulate appetite.
Dr. Ailhaud and his colleagues pointed out that not only are people eating far more linoleic acid than ever before; that very same linoleic acid is accumulating in our fat tissue and showing up in breast milk. Here are a few graphs to illustrate the point. The first graph is of PUFA consumption in the US over the last century, primarily reflecting seed oil intake (based on USDA food disappearance records):
Here's a graph of added fat intake based on USDA data. Added animal fats such as butter and lard have remained stable since 1970 (although total animal fat intake has declined), while seed oil consumption has gone from high to higher:
The following graph shows linoleic acid accumulation in human body fat over the last few decades in Western nations (mostly the US). I put this together based on two references (2, 3). I didn't find any data from the US past 1986. Linoleic acid, unlike most other fatty acids, accumulates disproportionately in body fat (4):
And finally, linoleic acid in the breast milk of US mothers, from Dr. Ailhaud's 2006 paper (the black dots):
In 2009, Dr. Ingeborg Hanbauer published a paper showing that when mice are fed a diet with a poor omega-6:3 balance (77:1), after three generations they develop adult obesity (5). Mice fed the same diet with a better omega-6:3 balance (9.5:1) did not develop obesity, and remained smaller overall. This shows that PUFA imbalance can cause multi-generational effects resulting in obesity and excessive tissue growth. Cmdr. Joseph Hibbeln, a collaborator of Dr. Bill Lands, was an author. The thing I don't like about this paper is they didn't quantify the obesity by measuring fat mass, so we have to take the authors' word that they had more fat.
This week, Dr. Florence Massiera and collaborators published a similar paper titled “A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations” (6). Drs. Ailhaud and Guesnet were both on this paper. They showed that a 35% fat diet with an omega-6:3 ratio of 28 caused obesity that progressively increased over four generations of mice. Although this study was more detailed than the study by Dr. Hanbauer and colleagues, it lacked a comparison group with a more favorable omega-6:3 balance to show that the obesity was specifically the result of omega-6:3 imbalance, rather than the fact that the diet was higher in fat overall or some other aspect of its composition.
If this is true in humans, it would be a straightforward explanation for the obesity epidemic that has plagued the Western world in recent decades. It would explain why the epidemic began in children around 1970, but didn’t show up in adults until about 1980. It would explain why the epidemic is less severe in Europe, and even less so in Asia. And of course, it correlates well with trends in seed oil consumption. This graph is based on US NHANES survey data:
We already know that a number of prenatal factors can have an effect on adult body fat levels in rodents, and observational studies have suggested that the same may apply to humans. If a mother’s body fat is full of linoleic acid, she will pass it on to the fetus as it grows, and after birth in breast milk, influencing its development.
As long-time followers of Whole Health Source know, I suspect industrial seed oils contribute to many of our modern ills. I can’t say for sure that seed oils are responsible for the current obesity epidemic, but the evidence certainly gives me pause. In any case, seed oils are an unnatural part of the human diet and it won’t hurt anyone to avoid them. The half-life of linoleic acid in fat tissue is about two years, so reducing it is a long-term prospect.
Paleolithic Diet Clinical Trials Part IV
Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells.
After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.
Patients were put on two different diets for 3 months each. The first was a "conventional diabetes diet". I read a previous draft of the paper in which I believe they stated it was based on American Diabetes Association guidelines, but I can't find that statement in the final draft. In any case, here are the guidelines from the methods section:
As has been reported in other studies, paleolithic dieters ate fewer total calories than the comparison group. This is part of the reason why I believe that something in the modern diet causes hyperphagia, or excessive eating. According to the paleolithic diet studies, this food or combination of foods is neolithic, and probably resides in grains, refined sugar and/or dairy. I have my money on wheat and sugar, with a probable long-term contribution from industrial vegetable oils as well.
Were the improvements on the paleolithic diet simply due to calorie restriction? Maybe, but keep in mind that neither group was told to restrict its caloric intake. The reduction in caloric intake occurred naturally, despite the participants presumably eating to fullness. I suspect that the paleolithic diet reset the dieters' body fat set-point, after which fat began pouring out of their fat tissue. They were supplementing their diets with body fat-- 13 pounds (6 kg) of it over 3 months.
The other notable difference between the two diets, besides food types, was carbohydrate intake. The diabetes diet group ate 56% more carbohydrate than the paleo diet group, with 42% of their calories coming from it. The paleolithic group ate 32% carbohydrate. Could this have been the reason for the better outcome of the paleolithic group? I'd be surprised if it wasn't a factor. Advising a diabetic to eat a high-carbohydrate diet is like asking someone who's allergic to bee stings to fetch you some honey from your bee hive. Diabetes is a disorder of glucose intolerance. Starch is a glucose polymer.
Although to be fair, participants on the diabetes diet did improve in a number of ways. There's something to be said for eating whole foods.
This trial was actually a bit of a disappointment for me. I was hoping for a slam dunk, similar to Lindeberg's previous study that "cured" all 14 patients of glucose intolerance in 3 months. In the current study, the paleolithic diet left 8 out of 13 patients diabetic after 3 months. What was the difference? For one thing, the patients in this study had well-established diabetes with an average duration of 9 years. As Jenny Ruhl explains in her book Blood Sugar 101, type II diabetes often progresses to beta cell loss, after which the pancreas can no longer secrete an adequate amount of insulin.
This may be the critical finding of Dr. Lindeberg's two studies: type II diabetes can be prevented when it's caught at an early stage, such as pre-diabetes, whereas prolonged diabetes may cause damage that cannot be completely reversed though diet. I think this is consistent with the experience of many diabetics who have seen an improvement but not a cure from changes in diet. Please add any relevant experiences to the comments.
Collectively, the evidence from clinical trials on the "paleolithic diet" indicate that it's a very effective treatment for modern metabolic dysfunction, including excess body fat, insulin resistance and glucose intolerance. Another way of saying this is that the modern industrial diet causes metabolic dysfunction.
Paleolithic Diet Clinical Trials
Paleolithic Diet Clinical Trials Part II
One Last Thought
Paleolithic Diet Clinical Trials Part III
After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.
Patients were put on two different diets for 3 months each. The first was a "conventional diabetes diet". I read a previous draft of the paper in which I believe they stated it was based on American Diabetes Association guidelines, but I can't find that statement in the final draft. In any case, here are the guidelines from the methods section:
The information on the Diabetes diet stated that it should aim at evenly distributed meals with increased intake of vegetables, root vegetables, dietary fiber, whole-grain bread and other whole-grain cereal products, fruits and berries, and decreased intake of total fat with more unsaturated fat. The majority of dietary energy should come from carbohydrates from foods naturally rich in carbohydrate and dietary fiber. The concepts of glycemic index and varied meals through meal planning by the Plate Model were explained [18]. Salt intake was recommended to be kept below 6 g per day.The investigators gave the paleolithic group the following advice:
The information on the Paleolithic diet stated that it should be based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts, while excluding dairy products, cereal grains, beans, refined fats, sugar, candy, soft drinks, beer and extra addition of salt. The following items were recommended in limited amounts for the Paleolithic diet: eggs (≤2 per day), nuts (preferentially walnuts), dried fruit, potatoes (≤1 medium-sized per day), rapeseed or olive oil (≤1 tablespoon per day), wine (≤1 glass per day). The intake of other foods was not restricted and no advice was given with regard to proportions of food categories (e.g. animal versus plant foods). The evolutionary rationale for a Paleolithic diet and potential benefits were explained.Neither diet was restricted in calories. After comparing the effects of the two diets for 3 months, the investigators concluded that the paleolithic diet:
- Reduced HbA1c more than the diabetes diet (a measure of average blood glucose)
- Reduced weight, BMI and waist circumference more than the diabetes diet
- Lowered blood pressure more than the diabetes diet
- Reduced triglycerides more than the diabetes diet
- Increased HDL more than the diabetes diet
As has been reported in other studies, paleolithic dieters ate fewer total calories than the comparison group. This is part of the reason why I believe that something in the modern diet causes hyperphagia, or excessive eating. According to the paleolithic diet studies, this food or combination of foods is neolithic, and probably resides in grains, refined sugar and/or dairy. I have my money on wheat and sugar, with a probable long-term contribution from industrial vegetable oils as well.
Were the improvements on the paleolithic diet simply due to calorie restriction? Maybe, but keep in mind that neither group was told to restrict its caloric intake. The reduction in caloric intake occurred naturally, despite the participants presumably eating to fullness. I suspect that the paleolithic diet reset the dieters' body fat set-point, after which fat began pouring out of their fat tissue. They were supplementing their diets with body fat-- 13 pounds (6 kg) of it over 3 months.
The other notable difference between the two diets, besides food types, was carbohydrate intake. The diabetes diet group ate 56% more carbohydrate than the paleo diet group, with 42% of their calories coming from it. The paleolithic group ate 32% carbohydrate. Could this have been the reason for the better outcome of the paleolithic group? I'd be surprised if it wasn't a factor. Advising a diabetic to eat a high-carbohydrate diet is like asking someone who's allergic to bee stings to fetch you some honey from your bee hive. Diabetes is a disorder of glucose intolerance. Starch is a glucose polymer.
Although to be fair, participants on the diabetes diet did improve in a number of ways. There's something to be said for eating whole foods.
This trial was actually a bit of a disappointment for me. I was hoping for a slam dunk, similar to Lindeberg's previous study that "cured" all 14 patients of glucose intolerance in 3 months. In the current study, the paleolithic diet left 8 out of 13 patients diabetic after 3 months. What was the difference? For one thing, the patients in this study had well-established diabetes with an average duration of 9 years. As Jenny Ruhl explains in her book Blood Sugar 101, type II diabetes often progresses to beta cell loss, after which the pancreas can no longer secrete an adequate amount of insulin.
This may be the critical finding of Dr. Lindeberg's two studies: type II diabetes can be prevented when it's caught at an early stage, such as pre-diabetes, whereas prolonged diabetes may cause damage that cannot be completely reversed though diet. I think this is consistent with the experience of many diabetics who have seen an improvement but not a cure from changes in diet. Please add any relevant experiences to the comments.
Collectively, the evidence from clinical trials on the "paleolithic diet" indicate that it's a very effective treatment for modern metabolic dysfunction, including excess body fat, insulin resistance and glucose intolerance. Another way of saying this is that the modern industrial diet causes metabolic dysfunction.
Paleolithic Diet Clinical Trials
Paleolithic Diet Clinical Trials Part II
One Last Thought
Paleolithic Diet Clinical Trials Part III
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