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.
Read more »
Showing posts with label overweight. Show all posts
Showing posts with label overweight. Show all posts
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.
Read more »
Read more »
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
Read more »
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 »
A Sign of the Times
Every now and then, I venture out to go shopping at mainstream chain clothing stores. Although I find it onerous, there are certain things I can't get at thrift stores. For example, I can never find nice jeans.
The last time I set foot in these stores was about two years ago. It was tough to find pants my size at that time-- many stores simply didn't sell pants with a 30 inch waist. This year, it was even harder, since some of the stores that formerly carried 30W pants no longer did. I managed to find my usual 30W 30L size in two stores, but I had a bizarre experience in both cases. I put them on, and they were falling off my waist. Since my waist size hasn't changed in two years, and my old 30W 30L pants of the same brand still fit the same as they did when I bought them two years ago, I have to conclude that both stores have changed their definition of "30 inches". My new size is 28W 30L, which is tough to find these days.
Read more »
The last time I set foot in these stores was about two years ago. It was tough to find pants my size at that time-- many stores simply didn't sell pants with a 30 inch waist. This year, it was even harder, since some of the stores that formerly carried 30W pants no longer did. I managed to find my usual 30W 30L size in two stores, but I had a bizarre experience in both cases. I put them on, and they were falling off my waist. Since my waist size hasn't changed in two years, and my old 30W 30L pants of the same brand still fit the same as they did when I bought them two years ago, I have to conclude that both stores have changed their definition of "30 inches". My new size is 28W 30L, which is tough to find these days.
Read more »
60 Minutes Report on the Flavorist Industry
A reader sent me a link to a recent CBS documentary titled "Tweaking Tastes and Creating Cravings", reported by Morley Safer.
Safer describes the "flavorist" industry, entirely dedicated to crafting irresistible odors for the purpose of selling processed and restaurant food. They focused on the company Givaudin. Dr. David Kessler, author of The End of Overeating, makes an appearance near the end.
Here are a few notable quotes:
Read more »
Safer describes the "flavorist" industry, entirely dedicated to crafting irresistible odors for the purpose of selling processed and restaurant food. They focused on the company Givaudin. Dr. David Kessler, author of The End of Overeating, makes an appearance near the end.
Here are a few notable quotes:
Read more »
New Review Papers on Food Reward
As research on the role of reward/palatability in obesity continues to accelerate, interesting new papers are appearing weekly. Here is a roundup of review papers I've encountered in the last three months. These range from somewhat technical to very technical, but I think they should be mostly accessible to people with a background in the biological sciences.
Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction
Written by Dr. Nora D. Volkow and colleagues. This paper describes the similarities between the mechanisms of obesity and addiction, with a focus on human brain imaging studies. Most researchers don't think obesity is an addiction per se, but the mechanisms (e.g., brain areas important for reward) do seem to overlap considerably. This paper is well composed and got a lot of media attention. Dr. Volkow is the director of the National Institute on Drug Abuse, a branch of the National Institutes of Health. The NIH is the main source of biomedical research funding in the US, and also conducts its own research.
Here's a quote from the paper:
Read more »
Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction
Written by Dr. Nora D. Volkow and colleagues. This paper describes the similarities between the mechanisms of obesity and addiction, with a focus on human brain imaging studies. Most researchers don't think obesity is an addiction per se, but the mechanisms (e.g., brain areas important for reward) do seem to overlap considerably. This paper is well composed and got a lot of media attention. Dr. Volkow is the director of the National Institute on Drug Abuse, a branch of the National Institutes of Health. The NIH is the main source of biomedical research funding in the US, and also conducts its own research.
Here's a quote from the paper:
Read more »
Another Simple Food Weight Loss Experience
Whole Health Source reader Sarah Pugh recently went on a six-week simple food (low reward) diet to test its effectiveness as a weight loss strategy, and she was kind enough to describe her experience for me, and provide a link to her blog where she discussed it in more detail (1).
Consistent with the scientific literature and a number of previous reader anecdotes (2), Sarah experienced a reduction in appetite on the simple food diet, losing 15 pounds in 6 weeks without hunger. In contrast to her prior experiences with typical calorie restriction, her energy level and mood remained high over this period. Here's a quote from her blog:
Read more »
Consistent with the scientific literature and a number of previous reader anecdotes (2), Sarah experienced a reduction in appetite on the simple food diet, losing 15 pounds in 6 weeks without hunger. In contrast to her prior experiences with typical calorie restriction, her energy level and mood remained high over this period. Here's a quote from her blog:
Well, it looks like the theory that in the absence of nice palatable food, the body will turn quite readily to fat stores and start munching them up, is holding up. At the moment, the majority of the energy I use is coming from my insides, and my body is using it without such quibbles as the increased hunger, low energy, crappy thermo-regulation or bitchiness normally associated with severe calorie restriction.I can't promise that everyone will experience results like this, but this is basically what the food reward hypothesis suggests should be possible, and it seems to work this way for many people. That's one of the reasons why this idea interests me so much.
Read more »
A Brief Response to Taubes's Food Reward Critique, and a Little Something Extra
It appears Gary Taubes has completed his series critiquing the food reward hypothesis of obesity (1). I have to hand it to him, it takes some cojones to critique an entire field of research, particularly when you have no scientific background in it.
The food reward hypothesis of obesity states that the reward and palatability value of food influence body fatness, and excess reward/palatability can promote body fat accumulation. If we want to test the hypothesis, the most direct way is to find experiments in which 1) the nutritional qualities of the experimental diet groups are kept the same or at least very similar, 2) some aspect of diet reward/palatability differs, and 3) changes in body fat/weight are measured (for example, 2, 3, 4, 5, 6, 7, 8, 9). Taubes repeatedly stated in his series that controlled studies like these have not been conducted, apparently basing this belief on a 22-year-old review paper by Dr. Israel Ramirez and colleagues that does not contain the word 'reward' (10). Another way to test the hypothesis is to see if people with higher food reward sensitivity (due to genetics or other factors) tend to gain more fat over time (for example, 11, 12, 13, 14, 15, 16). In addition, studies that have examined the effect of palatability/reward on food intake in a controlled manner are relevant (17, 18, 19, 20, 21, 22), as are studies that have identified some of the mechanisms by which these effects occur (reviewed in 23). Even if not all of the studies are perfect, at some point, one has to acknowledge that there are a lot of mutually buttressing lines of evidence here. It is notable that very few of these studies appeared in Taubes's posts.
Read more »
The food reward hypothesis of obesity states that the reward and palatability value of food influence body fatness, and excess reward/palatability can promote body fat accumulation. If we want to test the hypothesis, the most direct way is to find experiments in which 1) the nutritional qualities of the experimental diet groups are kept the same or at least very similar, 2) some aspect of diet reward/palatability differs, and 3) changes in body fat/weight are measured (for example, 2, 3, 4, 5, 6, 7, 8, 9). Taubes repeatedly stated in his series that controlled studies like these have not been conducted, apparently basing this belief on a 22-year-old review paper by Dr. Israel Ramirez and colleagues that does not contain the word 'reward' (10). Another way to test the hypothesis is to see if people with higher food reward sensitivity (due to genetics or other factors) tend to gain more fat over time (for example, 11, 12, 13, 14, 15, 16). In addition, studies that have examined the effect of palatability/reward on food intake in a controlled manner are relevant (17, 18, 19, 20, 21, 22), as are studies that have identified some of the mechanisms by which these effects occur (reviewed in 23). Even if not all of the studies are perfect, at some point, one has to acknowledge that there are a lot of mutually buttressing lines of evidence here. It is notable that very few of these studies appeared in Taubes's posts.
Read more »
Does High Circulating Insulin Drive Body Fat Accumulation? Answers from Genetically Modified Mice
The house mouse Mus musculus is an incredible research tool in the biomedical sciences, due to its ease of care and its ability to be genetically manipulated. Although mice aren't humans, they resemble us closely in many ways, including how insulin signaling works. Genetic manipulation of mice allows researchers to identify biological mechanisms and cause-effect relationships in a very precise manner. One way of doing this is to create "knockout" mice that lack a specific gene, in an attempt to determine that gene's importance in a particular process. Another way is to create transgenic mice that express a gene of interest, often modified in some way. A third method is to use an extraordinary (but now common) tool called "Cre-lox" recombination (1), which allows us to delete or add a single gene in a specific tissue or cell type.
Studying the relationship between obesity and insulin resistance is challenging, because the two typically travel together, confounding efforts to determine which is the cause and which is the effect of the other (or neither). Some have proposed the hypothesis that high levels of circulating insulin promote body fat accumulation*. To truly address this question, we need to consider targeted experiments that increase circulating insulin over long periods of time without altering a number of other factors throughout the body. This is where mice come in. Scientists are able to perform precise genetic interventions in mice that increase circulating insulin over a long period of time. These mice should gain fat mass if the hypothesis is correct.
Read more »
Studying the relationship between obesity and insulin resistance is challenging, because the two typically travel together, confounding efforts to determine which is the cause and which is the effect of the other (or neither). Some have proposed the hypothesis that high levels of circulating insulin promote body fat accumulation*. To truly address this question, we need to consider targeted experiments that increase circulating insulin over long periods of time without altering a number of other factors throughout the body. This is where mice come in. Scientists are able to perform precise genetic interventions in mice that increase circulating insulin over a long period of time. These mice should gain fat mass if the hypothesis is correct.
Read more »
Losing Fat With Simple Food-- Two Reader Anecdotes
Each week, I'm receiving more e-mails and comments from people who are successfully losing fat by eating simple (low reward) food, similar to what I described here. In some cases, people are breaking through fat loss plateaus that they had reached on conventional low-carbohydrate, low-fat or paleo diets. This concept can be applied to any type of diet, and I believe it is an important characteristic of ancestral food patterns.
At the Ancestral Health Symposium, I met two Whole Health Source readers, Aravind Balasubramanian and Kamal Patel, who were interested in trying a simple diet to lose fat and improve their health. In addition, they wanted to break free of certain other high-reward activities in their lives that they felt were not constructive. They recently embarked on an 8-week low-reward diet and lifestyle to test the effectiveness of the concepts. Both of them had previously achieved a stable (in Aravind's case, reduced) weight on a paleo-ish diet prior to this experiment, but they still carried more fat than they wanted to. They offered to write about their experience for WHS, and I thought other readers might find it informative. Their story is below, followed by a few of my comments.
Read more »
At the Ancestral Health Symposium, I met two Whole Health Source readers, Aravind Balasubramanian and Kamal Patel, who were interested in trying a simple diet to lose fat and improve their health. In addition, they wanted to break free of certain other high-reward activities in their lives that they felt were not constructive. They recently embarked on an 8-week low-reward diet and lifestyle to test the effectiveness of the concepts. Both of them had previously achieved a stable (in Aravind's case, reduced) weight on a paleo-ish diet prior to this experiment, but they still carried more fat than they wanted to. They offered to write about their experience for WHS, and I thought other readers might find it informative. Their story is below, followed by a few of my comments.
Read more »
The Case for the Food Reward Hypothesis of Obesity, Part II
In this post, I'll explore whether or not the scientific evidence is consistent with the predictions of the food reward hypothesis, as outlined in the last post.
Before diving in, I'd like to address the critique that the food reward concept is a tautology or relies on circular reasoning (or is not testable/falsifiable). This critique has no logical basis. The reward and palatability value of a food is not defined by its effect on energy intake or body fatness. In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1). In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2). In rodents, it is measured by observing stereotyped facial responses to palatable and unpalatable foods, which are similar to those seen in human infants. It is not a tautology or circular reasoning to say that the reinforcing value or pleasantness of food influences food intake and body fatness. These are quantifiable concepts and as I will explain, their relationship with food intake and body fatness can be, and already has been, tested in a controlled manner.
1. Increasing the reward/palatability value of the diet should cause fat gain in animals and humans
Read more »
Before diving in, I'd like to address the critique that the food reward concept is a tautology or relies on circular reasoning (or is not testable/falsifiable). This critique has no logical basis. The reward and palatability value of a food is not defined by its effect on energy intake or body fatness. In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1). In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2). In rodents, it is measured by observing stereotyped facial responses to palatable and unpalatable foods, which are similar to those seen in human infants. It is not a tautology or circular reasoning to say that the reinforcing value or pleasantness of food influences food intake and body fatness. These are quantifiable concepts and as I will explain, their relationship with food intake and body fatness can be, and already has been, tested in a controlled manner.
1. Increasing the reward/palatability value of the diet should cause fat gain in animals and humans
Read more »
The Case for the Food Reward Hypothesis of Obesity, Part I
Introduction
When you want to investigate something using the scientific method, first you create a model that you hope describes a natural phenomenon-- this is called a hypothesis. Then you go about testing that model against reality, under controlled conditions, to see if it has any predictive power. There is rarely a single experiment, or single study, that can demonstrate that a hypothesis is correct. Most important hypotheses require many mutually buttressing lines of evidence from multiple research groups before they're widely accepted. Although it's not necessary, understanding the mechanism by which an effect occurs, and having that mechanism be consistent with the hypothesis, adds substantially to the case.
With that in mind, this post will go into greater detail on the evidence supporting food reward and palatability as major factors in the regulation of food intake and body fatness. There is a large amount of supportive evidence at this point, which is rapidly expanding due to the efforts of many brilliant researchers, however for the sake of clarity and brevity, so far I've only given a "tip of the iceberg" view of it. But there are two types of people who want more detail: (1) the skeptics, and (2) scientifically inclined people who want mechanism. This post is for them. It will get technical at times, as there is no other way to convey the material effectively.
Read more »
When you want to investigate something using the scientific method, first you create a model that you hope describes a natural phenomenon-- this is called a hypothesis. Then you go about testing that model against reality, under controlled conditions, to see if it has any predictive power. There is rarely a single experiment, or single study, that can demonstrate that a hypothesis is correct. Most important hypotheses require many mutually buttressing lines of evidence from multiple research groups before they're widely accepted. Although it's not necessary, understanding the mechanism by which an effect occurs, and having that mechanism be consistent with the hypothesis, adds substantially to the case.
With that in mind, this post will go into greater detail on the evidence supporting food reward and palatability as major factors in the regulation of food intake and body fatness. There is a large amount of supportive evidence at this point, which is rapidly expanding due to the efforts of many brilliant researchers, however for the sake of clarity and brevity, so far I've only given a "tip of the iceberg" view of it. But there are two types of people who want more detail: (1) the skeptics, and (2) scientifically inclined people who want mechanism. This post is for them. It will get technical at times, as there is no other way to convey the material effectively.
Read more »
Humans on a Cafeteria Diet
Read more »
Hyperinsulinemia: Cause or Effect of Obesity?
Is Elevated Insulin the Cause or Effect of Obesity?
The carbohydrate hypothesis, in its most popular current incarnation, states that elevated insulin acts on fat cells to cause fat storage, leading to obesity. This is due to its ability to increase the activity of lipoprotein lipase and decrease the activity of hormone-sensitive lipase, thus creating a net flux of fat into fat cells. I'm still not sure why this would be the case, considering that fat tissue becomes more insulin resistant as body fat accumulates, therefore insulin action on it is not necessarily increased. Total fat release from fat tissue increases with total fat mass (1), demonstrating that insulin is not able to do its job of suppressing fat release as effectively in people who carry excess fat. But let's put that problem aside for the moment and keep trucking.
Read more »
The carbohydrate hypothesis, in its most popular current incarnation, states that elevated insulin acts on fat cells to cause fat storage, leading to obesity. This is due to its ability to increase the activity of lipoprotein lipase and decrease the activity of hormone-sensitive lipase, thus creating a net flux of fat into fat cells. I'm still not sure why this would be the case, considering that fat tissue becomes more insulin resistant as body fat accumulates, therefore insulin action on it is not necessarily increased. Total fat release from fat tissue increases with total fat mass (1), demonstrating that insulin is not able to do its job of suppressing fat release as effectively in people who carry excess fat. But let's put that problem aside for the moment and keep trucking.
Read more »
Book Review: The End of Overeating
The End of Overdating was written based on the personal journey of Dr. David A. Kessler (MD) to understand the obesity epidemic, and treat his own obesity in the process. Kessler was the FDA commissioner under presidents George HW Bush and Bill Clinton. He is known for his efforts to regulate cigarettes, and his involvement in modernizing Nutrition Facts labels on packaged food. He was also the dean of Yale medical school for six years-- a very accomplished person.
Kessler's book focuses on 1) the ability of food with a high palatability/reward value to cause overeating and obesity, 2) the systematic efforts of the food industry to maximize food palatability/reward to increase sales in a competitive market, and 3) what to do about it. He has not only done a lot of reading on the subject, but has also participated directly in food reward research himself, so he has real credibility. The End of Overeating is not the usual diet book baloney.
Read more »
Kessler's book focuses on 1) the ability of food with a high palatability/reward value to cause overeating and obesity, 2) the systematic efforts of the food industry to maximize food palatability/reward to increase sales in a competitive market, and 3) what to do about it. He has not only done a lot of reading on the subject, but has also participated directly in food reward research himself, so he has real credibility. The End of Overeating is not the usual diet book baloney.
Read more »
A Roadmap to Obesity
In this post, I'll explain my current understanding of the factors that promote obesity in humans.
Heritability
To a large degree, obesity is a heritable condition. Various studies indicate that roughly two-thirds of the differences in body fatness between individuals is explained by heredity*, although estimates vary greatly (1). However, we also know that obesity is not genetically determined, because in the US, the obesity rate has more than doubled in the last 30 years, consistent with what has happened to many other cultures (2). How do we reconcile these two facts? By understanding that genetic variability determines the degree of susceptibility to obesity-promoting factors. In other words, in a natural environment with a natural diet, nearly everyone would be relatively lean, but when obesity-promoting factors are introduced, genetic makeup determines how resistant each person will be to fat gain. As with the diseases of civilization, obesity is caused by a mismatch between our genetic heritage and our current environment. This idea received experimental support from an interesting recent study (3).
Read more »
Heritability
To a large degree, obesity is a heritable condition. Various studies indicate that roughly two-thirds of the differences in body fatness between individuals is explained by heredity*, although estimates vary greatly (1). However, we also know that obesity is not genetically determined, because in the US, the obesity rate has more than doubled in the last 30 years, consistent with what has happened to many other cultures (2). How do we reconcile these two facts? By understanding that genetic variability determines the degree of susceptibility to obesity-promoting factors. In other words, in a natural environment with a natural diet, nearly everyone would be relatively lean, but when obesity-promoting factors are introduced, genetic makeup determines how resistant each person will be to fat gain. As with the diseases of civilization, obesity is caused by a mismatch between our genetic heritage and our current environment. This idea received experimental support from an interesting recent study (3).
Read more »
Seed Oils and Body Fatness-- A Problematic Revisit
Anthony Colpo recently posted a discussion of one of my older posts on seed oils and body fat gain (1), which reminded me that I need to revisit the idea. As my knowledge of obesity and metabolism has expanded, I feel the evidence behind the hypothesis that seed oils (corn, soybean, etc.) promote obesity due to their linoleic acid (omega-6 fat) content has largely collapsed.
Read more »
Read more »
Food Palatability and Body Fatness: Clues from Alliesthesia
Part I: Is there a Ponderostat?
Some of the most important experiments for understanding the role of food palatability/reward in body fatness were performed by Dr. Michel Cabanac and collaborators in the 1970s (hat tip to Dr. Seth Roberts for the references). In my recent food reward series (1), I referenced but did not discuss Dr. Cabanac's work because I felt it would have taken too long to describe. However, I included two of his studies in my Ancestral Health Symposium talk, and I think they're worth discussing in more detail here.
Read more »
Some of the most important experiments for understanding the role of food palatability/reward in body fatness were performed by Dr. Michel Cabanac and collaborators in the 1970s (hat tip to Dr. Seth Roberts for the references). In my recent food reward series (1), I referenced but did not discuss Dr. Cabanac's work because I felt it would have taken too long to describe. However, I included two of his studies in my Ancestral Health Symposium talk, and I think they're worth discussing in more detail here.
Read more »
I Got Boinged, and Other News
The reaction to my post "The Carbohydrate Hypothesis of Obesity: a Critical Examination" has been overwhelmingly positive, particularly among the scientists I've heard from.
On Saturday, the inimitable maker and writer Mark Frauenfelder posted a link to my post on the variety blog BoingBoing. BoingBoing has been on my sidebar for three years, and it's the place I go when I need a break. It's a fun assortment of science, news, technology and entertainment. BoingBoing was originally a zine started by Frauenfelder and his wife in 1988, and it has been on the web since 1995. Today, it has multiple contributing authors and it draws several hundred thousand hits per day. I'm thrilled that Frauenfelder posted my article there. Apparently he likes my blog. Thanks!
I added a new section (IIB) to my original post. It discusses what human genetics can teach us about the mechanisms of common obesity. It is consistent with the rest of the evidence suggesting that body fatness is primarily regulated by the brain, not by fat tissue, and that leptin signaling plays a dominant role in this process.
On Saturday, the inimitable maker and writer Mark Frauenfelder posted a link to my post on the variety blog BoingBoing. BoingBoing has been on my sidebar for three years, and it's the place I go when I need a break. It's a fun assortment of science, news, technology and entertainment. BoingBoing was originally a zine started by Frauenfelder and his wife in 1988, and it has been on the web since 1995. Today, it has multiple contributing authors and it draws several hundred thousand hits per day. I'm thrilled that Frauenfelder posted my article there. Apparently he likes my blog. Thanks!
I added a new section (IIB) to my original post. It discusses what human genetics can teach us about the mechanisms of common obesity. It is consistent with the rest of the evidence suggesting that body fatness is primarily regulated by the brain, not by fat tissue, and that leptin signaling plays a dominant role in this process.
The Carbohydrate Hypothesis of Obesity: a Critical Examination
Introduction
I'd like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health. Although it doesn't work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people. For a subset of people, the results can be very impressive. I consider that to be a fact at this point, but that's not what I'll be discussing here.
What I want to discuss is a hypothesis. It's the idea, championed by Gary Taubes, that carbohydrate (particularly refined carbohydrate) causes obesity by elevating insulin, thereby causing increased fat storage in fat cells. To demonstrate that I'm representing this hypothesis accurately, here is a quote from his book Good Calories, Bad Calories:
Read more »
I'd like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health. Although it doesn't work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people. For a subset of people, the results can be very impressive. I consider that to be a fact at this point, but that's not what I'll be discussing here.
What I want to discuss is a hypothesis. It's the idea, championed by Gary Taubes, that carbohydrate (particularly refined carbohydrate) causes obesity by elevating insulin, thereby causing increased fat storage in fat cells. To demonstrate that I'm representing this hypothesis accurately, here is a quote from his book Good Calories, Bad Calories:
Read more »
Subscribe to:
Posts (Atom)