One of the most common pieces of advice in the health-nutrition world is that we should focus our carbohydrate intake on slowly-digesting carbohydrates, because they make us feel more full than rapidly-digesting carbohydrates. Rapidly-digesting carbohydrates, such as potatoes, stand accused of causing us to overeat, resulting in obesity, diabetes, and many other chronic ailments. Is this true?
Showing posts sorted by relevance for query glycemic. Sort by date Show all posts
Showing posts sorted by relevance for query glycemic. Sort by date Show all posts
Wednesday, April 22, 2015
Saturday, August 28, 2010
Saturated Fat, Glycemic Index and Insulin Sensitivity: More Evidence
Insulin is a hormone that drives glucose and other nutrients from the bloodstream into cells, among other things. A loss of sensitivity to the insulin signal, called insulin resistance, is a core feature of modern metabolic dysfunction and can lead to type II diabetes and other health problems. Insulin resistance affects a large percentage of people in affluent nations, in fact the majority of people in some places. What causes insulin resistance? Researchers have been trying to figure this out for decades.*
Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).
The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another common concept in the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fatness (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.
All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).
A large new study just published in the American Journal of Clinical nutrition has taken the evidence to a new level (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:
In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.
Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations may be limited by reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!
* Excess body fat is almost certainly a major cause. When fat mass increases beyond a certain point, particularly abdominal fat, the fat tissue typically becomes inflamed. Inflamed fat tissue secretes factors which reduce whole-body insulin sensitivity (12, 13). The big question is: what caused the fat gain?
Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).
The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another common concept in the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fatness (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.
All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).
A large new study just published in the American Journal of Clinical nutrition has taken the evidence to a new level (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:
- High saturated fat, high glycemic index
- High monounsaturated fat, high glycemic index
- High monounsaturated fat, low glycemic index
- Low fat, high glycemic index
- Low fat, low glycemic index
In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.
Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations may be limited by reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!
* Excess body fat is almost certainly a major cause. When fat mass increases beyond a certain point, particularly abdominal fat, the fat tissue typically becomes inflamed. Inflamed fat tissue secretes factors which reduce whole-body insulin sensitivity (12, 13). The big question is: what caused the fat gain?
Monday, September 2, 2013
Is Refined Carbohydrate Addictive?
[Note: in previous versions, I mixed up "LGI" and "HGI" terms in a couple of spots. These are now corrected. Thanks to readers for pointing them out.]
Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:
Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.
This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction. The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.
So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation? Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.
Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:
Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.
This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction. The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.
So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation? Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.
Saturday, January 30, 2016
Testing the Insulin Model: A Response to Dr. Ludwig
Dr. David Ludwig, MD, recently published a response to my critique of the carbohydrate-insulin-obesity hypothesis. This is good because he defends the idea in more detail than I've encountered in other written works. In fact, his piece is the most scientifically persuasive defense of the idea I can recall.
Before we dig in, I want to emphasize that this is science, not tribal warfare. The goal is to arrive at the best answer, rather than to win an argument. I'm proceeding in good faith, based on my belief that Ludwig and I are both serious people who care about science and human health, and I hope my audience will do the same. That said, let's get to it.
Before we dig in, I want to emphasize that this is science, not tribal warfare. The goal is to arrive at the best answer, rather than to win an argument. I'm proceeding in good faith, based on my belief that Ludwig and I are both serious people who care about science and human health, and I hope my audience will do the same. That said, let's get to it.
Thursday, March 19, 2009
The Glycemic Index: A Critical Evaluation
The glycemic index (GI) is a measure of how much an individual food elevates blood sugar when it's eaten. To measure it, investigators feed a person a food that contains a fixed amount of carbohydrate, and measure their blood glucose response over time. Then they determine the area under the glucose curve and compare it to a standard food such as white bread or pure glucose.
Each food must contain the same total amount of carbohydrate, so you might have to eat a big plate of carrots to compare with a slice of bread. You end up with a number that reflects the food's ability to elevate glucose when eaten in isolation. It depends in large part on how quickly the carbohydrate is digested/absorbed, with higher numbers usually resulting from faster absorption.
The GI is a standby of modern nutritional advice. It's easy to believe in because processed foods tend to have a higher glycemic index than minimally processed foods, high blood sugar is bad, and chronically high insulin is bad. Yet many people have criticized the concept. Why?
Blood sugar responses to a carbohydrate-containing foods vary greatly from person to person. For example, I can eat a medium potato and a big slice of white bread (roughly 60 g carbohydrate) with nothing else and only see a modest spike in my blood sugar. I barely break 100 mg/dL and I'm back at fasting glucose levels within an hour and a half. You can see a graph of this experiment here. That's what happens when you have a well-functioning pancreas and insulin-sensitive tissues. Your body shunts glucose into the tissues almost as rapidly as it enters the bloodstream. Someone with impaired glucose tolerance might have gone up to 170 mg/dL for two and a half hours on the same meal.
The other factor is that foods aren't eaten in isolation. Fat, protein, acidity and other factors slow carbohydrate absorption in the context of a normal meal, to the point where the GI of the individual foods become much less pronounced.
Researchers have conducted a number of controlled trials comparing low-GI diets to high-GI diets. I've done an informal literature review to see what the overall findings are. I'm only interested in long-term studies-- 10 weeks or longer-- and I've excluded studies using subjects with metabolic disorders such as diabetes.
The question I'm asking with this review is, what are the health effects of a low-glycemic index diet on a healthy normal-weight or overweight person? I found a total of seven studies on PubMed in which investigators varied GI while keeping total carbohydrate about the same, for 10 weeks or longer. I'll present them out of chronological order because they flow better that way.
One issue with this literature that I want to highlight before we proceed is that most of these studies weren't properly controlled to isolate the effects of GI independent of other factors. Low GI foods are often whole foods with more fiber, more nutrients, and a higher satiety value per calorie than high GI foods.
Study #1. Investigators put overweight women on a 12-week diet of either high-GI or low-GI foods with an equal amount of total carbohydrate. Both were unrestricted in calories. Body composition and total food intake were the same on both diets. Despite the diet advice aimed at changing GI, the investigators found that both groups' glucose and insulin curves were the same!
Study #2. Investigators divided 129 overweight young adults into four different diet groups for 12 weeks. Diet #1: high GI, high carbohydrate (60%). Diet #2: low GI, high carbohydrate. Diet #3: high GI, high-protein (28%). Diet #4: low GI, high protein. The high-protein diets were also a bit higher in fat. Although the differences were small and mostly not statistically significant, participants on diet #3 improved the most overall in my opinion. They lost the most weight, and had the greatest decrease in fasting insulin and calculated insulin resistance. Diet #2 came out modestly ahead of diet #1 on fat loss and fasting insulin.
Study #3. At 18 months, this is by far the longest trial. Investigators assigned 203 healthy Brazilian women to either a low-GI or high-GI energy-restricted diet. The difference in GI between the two diets was substantial; the high-GI diet was supposed to be double the low-GI diet. This was accomplished by a number of differences between diets, including different types of rice and higher bean consumption in the low-GI group. Weight loss was a meager 1/3 pound greater in the low-GI group, a difference that was not statistically significant at 18 months. Changes in estimated insulin sensitivity were not statistically significant.
Study #4. The FUNGENUT study. In this 12-week intervention, investigators divided 47 subjects with the metabolic syndrome into two diet groups. One was a high-glycemic, high-wheat group; the other was a low-glycemic, high-rye group. After 12 weeks, there was an improvement in the insulinogenic index (a marker of early insulin secretion in response to carbohydrate) in the rye group but not the wheat group. Glucose tolerance was essentially the same in both groups.
What makes this study unique is they went on to look at changes in gene expression in subcutaneous fat tissue before and after the diets. They found a decrease in the expression of stress and inflammation-related genes in the rye group, and an increase in stress and inflammation genes in the wheat group. They interpreted this as being the result of the different GIs of the two diets.
Further research will have to determine whether the result they observed is due to the glycemic differences of the two diets or something else.
Study #5. Investigators divided 18 subjects with elevated cardiovascular disease risk markers into two diets differing in their GI, for 12 weeks. The low-glycemic group lost 4 kg (statistically significant), while the high-glycemic group lost 1.5 kg (not statistically significant). In addition, the low-GI group ended up with lower 24-hour blood glucose measurements. This study was a bit strange because of the fact that the high-GI group started off 14 kg heavier than the low-GI group, and the way the data are reported is difficult to understand. Perhaps these limitations, along with the study's incongruence with other controlled trails, are what inspired the authors to describe it as a pilot study.
Study #6. 45 overweight females were divided between high-GI and low-GI diets for 10 weeks. The low-GI group lost a small amount more fat than the high-GI group, but the difference wasn't significant. The low-GI group also had a 10% drop in LDL cholesterol.
Study #7. This was the second-longest trial, at 4 months. 34 subjects with impaired glucose tolerance were divided into three diet groups. Diet #1: high-carbohydrate (60%), high-GI. Diet #2: high-carbohydrate, low-GI. Diet #3: "low-carbohydrate" (49%), "high-fat" (monounsaturated from olive and canola oil). The diet #1 group lost the most weight, followed by diet #2, while diet #3 gained weight. The differences were small but statistically significant. The insulin and triglyceride response to a test meal improved in diet group #1 but not #2. The insulin response also improved in group #3. The high-GI group came out looking pretty good.
[Update 10/2011-- please see this post for a recent example of a 6 month controlled trial including 720 participants that tested the effect of glycemic index modification on body fatness and health markers-- it is consistent with the conclusion below]
Overall, these studies do not support the idea that lowering the glycemic index of carbohydrate foods is useful for weight loss, insulin or glucose control, or anything else besides complicating your life. I'll keep my finger on the pulse of this research as it expands, but for the time being I don't see the glycemic index per se as a significant way to combat fat gain or metabolic disease.
Each food must contain the same total amount of carbohydrate, so you might have to eat a big plate of carrots to compare with a slice of bread. You end up with a number that reflects the food's ability to elevate glucose when eaten in isolation. It depends in large part on how quickly the carbohydrate is digested/absorbed, with higher numbers usually resulting from faster absorption.
The GI is a standby of modern nutritional advice. It's easy to believe in because processed foods tend to have a higher glycemic index than minimally processed foods, high blood sugar is bad, and chronically high insulin is bad. Yet many people have criticized the concept. Why?
Blood sugar responses to a carbohydrate-containing foods vary greatly from person to person. For example, I can eat a medium potato and a big slice of white bread (roughly 60 g carbohydrate) with nothing else and only see a modest spike in my blood sugar. I barely break 100 mg/dL and I'm back at fasting glucose levels within an hour and a half. You can see a graph of this experiment here. That's what happens when you have a well-functioning pancreas and insulin-sensitive tissues. Your body shunts glucose into the tissues almost as rapidly as it enters the bloodstream. Someone with impaired glucose tolerance might have gone up to 170 mg/dL for two and a half hours on the same meal.
The other factor is that foods aren't eaten in isolation. Fat, protein, acidity and other factors slow carbohydrate absorption in the context of a normal meal, to the point where the GI of the individual foods become much less pronounced.
Researchers have conducted a number of controlled trials comparing low-GI diets to high-GI diets. I've done an informal literature review to see what the overall findings are. I'm only interested in long-term studies-- 10 weeks or longer-- and I've excluded studies using subjects with metabolic disorders such as diabetes.
The question I'm asking with this review is, what are the health effects of a low-glycemic index diet on a healthy normal-weight or overweight person? I found a total of seven studies on PubMed in which investigators varied GI while keeping total carbohydrate about the same, for 10 weeks or longer. I'll present them out of chronological order because they flow better that way.
One issue with this literature that I want to highlight before we proceed is that most of these studies weren't properly controlled to isolate the effects of GI independent of other factors. Low GI foods are often whole foods with more fiber, more nutrients, and a higher satiety value per calorie than high GI foods.
Study #1. Investigators put overweight women on a 12-week diet of either high-GI or low-GI foods with an equal amount of total carbohydrate. Both were unrestricted in calories. Body composition and total food intake were the same on both diets. Despite the diet advice aimed at changing GI, the investigators found that both groups' glucose and insulin curves were the same!
Study #2. Investigators divided 129 overweight young adults into four different diet groups for 12 weeks. Diet #1: high GI, high carbohydrate (60%). Diet #2: low GI, high carbohydrate. Diet #3: high GI, high-protein (28%). Diet #4: low GI, high protein. The high-protein diets were also a bit higher in fat. Although the differences were small and mostly not statistically significant, participants on diet #3 improved the most overall in my opinion. They lost the most weight, and had the greatest decrease in fasting insulin and calculated insulin resistance. Diet #2 came out modestly ahead of diet #1 on fat loss and fasting insulin.Study #3. At 18 months, this is by far the longest trial. Investigators assigned 203 healthy Brazilian women to either a low-GI or high-GI energy-restricted diet. The difference in GI between the two diets was substantial; the high-GI diet was supposed to be double the low-GI diet. This was accomplished by a number of differences between diets, including different types of rice and higher bean consumption in the low-GI group. Weight loss was a meager 1/3 pound greater in the low-GI group, a difference that was not statistically significant at 18 months. Changes in estimated insulin sensitivity were not statistically significant.
Study #4. The FUNGENUT study. In this 12-week intervention, investigators divided 47 subjects with the metabolic syndrome into two diet groups. One was a high-glycemic, high-wheat group; the other was a low-glycemic, high-rye group. After 12 weeks, there was an improvement in the insulinogenic index (a marker of early insulin secretion in response to carbohydrate) in the rye group but not the wheat group. Glucose tolerance was essentially the same in both groups.
What makes this study unique is they went on to look at changes in gene expression in subcutaneous fat tissue before and after the diets. They found a decrease in the expression of stress and inflammation-related genes in the rye group, and an increase in stress and inflammation genes in the wheat group. They interpreted this as being the result of the different GIs of the two diets.
Further research will have to determine whether the result they observed is due to the glycemic differences of the two diets or something else.
Study #5. Investigators divided 18 subjects with elevated cardiovascular disease risk markers into two diets differing in their GI, for 12 weeks. The low-glycemic group lost 4 kg (statistically significant), while the high-glycemic group lost 1.5 kg (not statistically significant). In addition, the low-GI group ended up with lower 24-hour blood glucose measurements. This study was a bit strange because of the fact that the high-GI group started off 14 kg heavier than the low-GI group, and the way the data are reported is difficult to understand. Perhaps these limitations, along with the study's incongruence with other controlled trails, are what inspired the authors to describe it as a pilot study.
Study #6. 45 overweight females were divided between high-GI and low-GI diets for 10 weeks. The low-GI group lost a small amount more fat than the high-GI group, but the difference wasn't significant. The low-GI group also had a 10% drop in LDL cholesterol.
Study #7. This was the second-longest trial, at 4 months. 34 subjects with impaired glucose tolerance were divided into three diet groups. Diet #1: high-carbohydrate (60%), high-GI. Diet #2: high-carbohydrate, low-GI. Diet #3: "low-carbohydrate" (49%), "high-fat" (monounsaturated from olive and canola oil). The diet #1 group lost the most weight, followed by diet #2, while diet #3 gained weight. The differences were small but statistically significant. The insulin and triglyceride response to a test meal improved in diet group #1 but not #2. The insulin response also improved in group #3. The high-GI group came out looking pretty good.
[Update 10/2011-- please see this post for a recent example of a 6 month controlled trial including 720 participants that tested the effect of glycemic index modification on body fatness and health markers-- it is consistent with the conclusion below]
Overall, these studies do not support the idea that lowering the glycemic index of carbohydrate foods is useful for weight loss, insulin or glucose control, or anything else besides complicating your life. I'll keep my finger on the pulse of this research as it expands, but for the time being I don't see the glycemic index per se as a significant way to combat fat gain or metabolic disease.
Sunday, October 23, 2011
Harvard Food Law Society "Forum on Food Policy" TEDx Conference
Last Friday, it was my pleasure to attended and present at the Harvard Food Law Society's TEDx conference, Forum on Food Policy. I had never been to Cambridge or Boston before, and I was struck by how European they feel compared to Seattle. The conference was a great success, thanks to the dedicated efforts of the Food Law Society's presidents Nate Rosenberg, Krista DeBoer, and many other volunteers.
Dr. Robert Lustig gave a keynote address on Thursday evening, which I unfortunately wasn't able to attend due to my flight schedule. From what I heard, he focused on practical solutions for reducing national sugar consumption, such as instituting a sugar tax. Dr. Lustig was a major presence at the conference, and perhaps partially due to his efforts, sugar was a central focus throughout the day. Nearly everyone agrees that added sugar is harmful to the nation's health at current intakes, so the question kept coming up "how long is it going to take us to do something about it?" As Dr. David Ludwig said, "...the obesity epidemic can be viewed as a disease of technology with a simple, but politically difficult solution".
Dr. Robert Lustig gave a keynote address on Thursday evening, which I unfortunately wasn't able to attend due to my flight schedule. From what I heard, he focused on practical solutions for reducing national sugar consumption, such as instituting a sugar tax. Dr. Lustig was a major presence at the conference, and perhaps partially due to his efforts, sugar was a central focus throughout the day. Nearly everyone agrees that added sugar is harmful to the nation's health at current intakes, so the question kept coming up "how long is it going to take us to do something about it?" As Dr. David Ludwig said, "...the obesity epidemic can be viewed as a disease of technology with a simple, but politically difficult solution".
Thursday, June 28, 2012
New Study: Is a Calorie a Calorie?
A new study in JAMA led by Dr. Cara B. Ebbeling and colleagues purports to challenge the idea that all calories are equally fattening (1). Let's have a look. When thinking about the role of calorie intake in body fatness, there are basically three camps:
1. Calories don’t matter at all, only diet composition matters.
2. Calories are the only thing that matters, and diet composition is irrelevant.
3. Calories matter, but diet composition may also play a role.
The first one is an odd position that is not very well populated. The second one has a lot of adherents in the research world, and there’s enough evidence to make a good case for it. It’s represented by the phrase ‘a calorie is a calorie’, i.e. all calories are equally fattening. #1 and #2 are both extreme positions, and as such they get a lot of attention. But the third group, although less vocal, may be closest to the truth.
1. Calories don’t matter at all, only diet composition matters.
2. Calories are the only thing that matters, and diet composition is irrelevant.
3. Calories matter, but diet composition may also play a role.
The first one is an odd position that is not very well populated. The second one has a lot of adherents in the research world, and there’s enough evidence to make a good case for it. It’s represented by the phrase ‘a calorie is a calorie’, i.e. all calories are equally fattening. #1 and #2 are both extreme positions, and as such they get a lot of attention. But the third group, although less vocal, may be closest to the truth.
Friday, September 16, 2016
Do Blood Glucose Levels Affect Hunger and Satiety?
You've heard the story before: when you eat carbohydrate-rich foods that digest quickly, it sends your blood sugar and insulin levels soaring, then your blood sugar level comes crashing back down and you feel hungry and cranky. You reach for more carbohydrate, perpetuating the cycle of crashes, overeating, and fat gain.
It sounds pretty reasonable-- in fact, so reasonable that it's commonly stated as fact in popular media and in casual conversation. This idea is so deeply ingrained in the popular psyche that people often say "I have low blood sugar" instead of "I'm hungry" or "I'm tired". But this hypothesis has a big problem: despite extensive research, it hasn't been clearly supported. I've written about this issue before (1).
A new study offers a straightforward test of the hypothesis, and once again finds it lacking.
The study
It sounds pretty reasonable-- in fact, so reasonable that it's commonly stated as fact in popular media and in casual conversation. This idea is so deeply ingrained in the popular psyche that people often say "I have low blood sugar" instead of "I'm hungry" or "I'm tired". But this hypothesis has a big problem: despite extensive research, it hasn't been clearly supported. I've written about this issue before (1).
A new study offers a straightforward test of the hypothesis, and once again finds it lacking.
The study
Saturday, January 9, 2016
Always Hungry? It's Probably Not Your Insulin.
David Ludwig, MD, recently published a new book titled Always Hungry? Conquer cravings, retrain your fat cells, and lose weight permanently. The book is getting widespread media coverage. Ludwig is a professor of pediatrics at the Harvard Medical School and a professor of nutrition at the Harvard School of Public Health. He's a pediatric endocrinologist, but his primary focus is research, particularly the impact of nutrition on hunger, calorie expenditure, and body weight. Although I sometimes disagree with how he interprets evidence, he has made significant and useful contributions to the scientific literature in these areas, and I also support his efforts to find policy solutions to curb the intake of sweetened beverages and other junk foods. In the grand scheme of things, he's an ally in the fight to improve the American diet.
Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2). He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance. And the primary culprit is insulin. You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.
According to this view, overeating is irrelevant. We gain fat because our insulin levels are too high, leading our fat tissue to take up too much fat, and other tissues to take up too much glucose, causing our blood energy levels to drop and resulting in fat gain, hunger, and fatigue. The ultimate cause of the problem is the rapidly-digesting carbohydrate and sugar we eat. This idea is encapsulated by Ludwig's quote, "Overeating doesn't make you fat. The process of getting fat makes you overeat" (3).
Here are eleven facts that may make you question this line of reasoning:
Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2). He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance. And the primary culprit is insulin. You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.
According to this view, overeating is irrelevant. We gain fat because our insulin levels are too high, leading our fat tissue to take up too much fat, and other tissues to take up too much glucose, causing our blood energy levels to drop and resulting in fat gain, hunger, and fatigue. The ultimate cause of the problem is the rapidly-digesting carbohydrate and sugar we eat. This idea is encapsulated by Ludwig's quote, "Overeating doesn't make you fat. The process of getting fat makes you overeat" (3).
Here are eleven facts that may make you question this line of reasoning:
Monday, March 23, 2009
More Thoughts on the Glycemic Index
In the last post, I reviewed the controlled trials on the effect of the glycemic index (GI) of carbohydrate foods on health. I concluded that there is not much evidence that a low GI diet is better for health than a high GI diet.
It is true that for the "average" individual the GI of carbohydrate foods can affect the glucose and insulin response somewhat, even in the context of an actual meal. If you compare two meals of very different GI, the low GI meal will cause less insulin secretion and cause less total blood glucose in the plasma over the course of the day (although the differences in blood glucose may not be large in all individuals).
But is that biologically significant? In other words, do those differences matter when it comes to health? I would argue probably not, and here's why: there's a difference between post-meal glucose and insulin surges within the normal range, and those that occur in pathological conditions such as diabetes and insulin resistance. Chronically elevated insulin is a marker of metabolic dysfunction, while post-meal insulin surges are not (although glucose surges in excess of 140 mg/dL indicate glucose intolerance). Despite what you may hear from some sectors of the low-carbohydrate community, insulin surges do not necessarily lead to insulin resistance. Just ask a Kitavan. They get 69% of their 2,200 calories per day from high-glycemic starchy tubers and fruit (380 g carbohydrate), with not much fat to slow down digestion. Yet they have low fasting insulin, very little body fat and an undetectable incidence of diabetes, heart attack and stroke. That's despite a significant elderly population on the island.
Furthermore, in the 4-month GI intervention trial I mentioned last time, they measured something called glycated hemoglobin (HbA1c). HbA1c is a measure of the amount of blood glucose that has "stuck to" hemoglobin molecules in red blood cells. It's used to determine a person's average blood glucose concentration over the course of the past few weeks. The higher your HbA1c, the poorer your blood glucose control, the higher your likelihood of having diabetes, and the higher your cardiovascular risk. The low GI group had a statistically significant drop in their HbA1c value compared to the high GI group. But the difference was only 0.06%, a change that is biologically meaningless.
OK, let's take a step back. The goal of thinking about all this is to understand what's healthy, right? Let's take a look at how carbohydrate foods are consumed by cultures that rarely suffer from obesity or metabolic disease. Cultures that rely heavily on carbohydrate generally fall into three categories: they eat cooked starchy tubers, they grind and cook their grains, or they rely on grains that become very soft when cooked. In the first category, we have Africans, South Americans, Polynesians and Melanesians (including the Kitavans). In the second, we have various Africans, Europeans (including the villagers of the Loetschental valley), Middle Easterners and South Americans. In the third category, we have Asians, Europeans (the oat-eating residents of the outer Hebrides) and South Americans (quinoa-eating Peruvians).
The pattern here is one of maximizing GI, not minimizing it. That's not because high GI foods are inherently superior, but because traditional processing techniques that maximize the digestibility of carbohydrate foods also tend to increase their GI. I believe healthy cultures around the world didn't care about the glycemic index of foods, they cared about digestibility and nutritional value.
The reason we grind grains is simple. Ground grains are digested more easily and completely (hence the higher GI). Furthermore, ground grains are more effective than intact grains at breaking down their own phytic acid when soaked, particularly if they're allowed to ferment. This further increases their nutritional value.
The human digestive system is delicate. Cows can eat whole grass seeds and digest them using their giant four-compartment stomach that acts as a fermentation tank. Humans that eat intact grains end up donating them to the waste treatment plant. We just don't have the hardware to efficiently extract the nutrients from cooked whole rye berries, unless you're willing to chew each bite 47 times. Oats, quinoa, rice, beans and certain other starchy seeds are exceptions because they're softened sufficiently by cooking.
Grain consumption and grinding implements appear simultaneously in the archaeological record. Grinding has always been used to increase the digestibility of tough grains, even before the invention of agriculture when hunter-gatherers were gathering wild grains in the fertile crescent. Some archaeologists consider grinding implements one of the diagnostic features of a grain-based culture. Carbohydrate-based cultures have always prioritized digestibility and nutritional value over GI.
Finally, I'd like to emphasize that some people don't have a good relationship with carbohydrate. Diabetics and others with glucose intolerance should be very cautious with carbohydrate foods. The best way to know how you deal with carbohydrate is to get a blood glucose meter and use it after meals. For $70 or less, you can get a cheap meter and 50 test strips that will give you a very good idea of your glucose response to typical meals (as opposed to a glucose bomb at the doctor's office). Jenny Ruhl has a tutorial that explains the process. It's also useful to pay attention to how you feel and look with different amounts of carbohydrate in your diet.
It is true that for the "average" individual the GI of carbohydrate foods can affect the glucose and insulin response somewhat, even in the context of an actual meal. If you compare two meals of very different GI, the low GI meal will cause less insulin secretion and cause less total blood glucose in the plasma over the course of the day (although the differences in blood glucose may not be large in all individuals).
But is that biologically significant? In other words, do those differences matter when it comes to health? I would argue probably not, and here's why: there's a difference between post-meal glucose and insulin surges within the normal range, and those that occur in pathological conditions such as diabetes and insulin resistance. Chronically elevated insulin is a marker of metabolic dysfunction, while post-meal insulin surges are not (although glucose surges in excess of 140 mg/dL indicate glucose intolerance). Despite what you may hear from some sectors of the low-carbohydrate community, insulin surges do not necessarily lead to insulin resistance. Just ask a Kitavan. They get 69% of their 2,200 calories per day from high-glycemic starchy tubers and fruit (380 g carbohydrate), with not much fat to slow down digestion. Yet they have low fasting insulin, very little body fat and an undetectable incidence of diabetes, heart attack and stroke. That's despite a significant elderly population on the island.
Furthermore, in the 4-month GI intervention trial I mentioned last time, they measured something called glycated hemoglobin (HbA1c). HbA1c is a measure of the amount of blood glucose that has "stuck to" hemoglobin molecules in red blood cells. It's used to determine a person's average blood glucose concentration over the course of the past few weeks. The higher your HbA1c, the poorer your blood glucose control, the higher your likelihood of having diabetes, and the higher your cardiovascular risk. The low GI group had a statistically significant drop in their HbA1c value compared to the high GI group. But the difference was only 0.06%, a change that is biologically meaningless.
OK, let's take a step back. The goal of thinking about all this is to understand what's healthy, right? Let's take a look at how carbohydrate foods are consumed by cultures that rarely suffer from obesity or metabolic disease. Cultures that rely heavily on carbohydrate generally fall into three categories: they eat cooked starchy tubers, they grind and cook their grains, or they rely on grains that become very soft when cooked. In the first category, we have Africans, South Americans, Polynesians and Melanesians (including the Kitavans). In the second, we have various Africans, Europeans (including the villagers of the Loetschental valley), Middle Easterners and South Americans. In the third category, we have Asians, Europeans (the oat-eating residents of the outer Hebrides) and South Americans (quinoa-eating Peruvians).
The pattern here is one of maximizing GI, not minimizing it. That's not because high GI foods are inherently superior, but because traditional processing techniques that maximize the digestibility of carbohydrate foods also tend to increase their GI. I believe healthy cultures around the world didn't care about the glycemic index of foods, they cared about digestibility and nutritional value.
The reason we grind grains is simple. Ground grains are digested more easily and completely (hence the higher GI). Furthermore, ground grains are more effective than intact grains at breaking down their own phytic acid when soaked, particularly if they're allowed to ferment. This further increases their nutritional value.
The human digestive system is delicate. Cows can eat whole grass seeds and digest them using their giant four-compartment stomach that acts as a fermentation tank. Humans that eat intact grains end up donating them to the waste treatment plant. We just don't have the hardware to efficiently extract the nutrients from cooked whole rye berries, unless you're willing to chew each bite 47 times. Oats, quinoa, rice, beans and certain other starchy seeds are exceptions because they're softened sufficiently by cooking.
Grain consumption and grinding implements appear simultaneously in the archaeological record. Grinding has always been used to increase the digestibility of tough grains, even before the invention of agriculture when hunter-gatherers were gathering wild grains in the fertile crescent. Some archaeologists consider grinding implements one of the diagnostic features of a grain-based culture. Carbohydrate-based cultures have always prioritized digestibility and nutritional value over GI.
Finally, I'd like to emphasize that some people don't have a good relationship with carbohydrate. Diabetics and others with glucose intolerance should be very cautious with carbohydrate foods. The best way to know how you deal with carbohydrate is to get a blood glucose meter and use it after meals. For $70 or less, you can get a cheap meter and 50 test strips that will give you a very good idea of your glucose response to typical meals (as opposed to a glucose bomb at the doctor's office). Jenny Ruhl has a tutorial that explains the process. It's also useful to pay attention to how you feel and look with different amounts of carbohydrate in your diet.
Sunday, December 19, 2010
Potato Diet Interpretation
If you read my post on December 16th, you know that Chris Voigt saw remarkable fat loss and improvements in health markers as a result of two months of eating almost nothing but potatoes. This has left many people scratching their heads, because potatoes are not generally viewed as a healthy food. This is partially due to the fact that potatoes are very rich in carbohydrate, which also happens to be a quickly digested type, resulting in a high glycemic index. The glycemic index refers to the degree to which a particular food increases blood glucose when it's eaten, and I've questioned the relevance of this concept to health outcomes in the past (1, 2, 3). I think Mr. Voigt's results once again argue against the importance of the glycemic index as a diet-health concept.
It's often pointed out that potatoes are low in vitamins and minerals compared to vegetables on a per-calorie basis, but I think it's a misleading comparison because potatoes are much more calorie-dense than most vegetables. Potatoes compare favorably to other starchy staples such as bread, rice and taro.
Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).
On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But of course, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.
Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?
I believe Mr. Voigt's diet lowered his fat mass 'setpoint'. In other words, for whatever reason, the diet made his body 'want' to be leaner that it already was. His body began releasing stored fat that it considered excess, and therefore he had to eat less food to complete his energy needs. You see this same phenomenon very clearly in rodent feeding studies. Changes in diet composition/quality can cause dramatic shifts in the fat mass setpoint (5, 6). Mr. Voigt's appetite would eventually have returned to normal once he had stabilized at a lower body fat mass, just as rodents do.
Rodent studies have made it clear that diet composition has a massive effect on the level of fat mass that the body will 'defend' against changes in calorie intake (5, 6). Human studies have shown similar effects from changes in diet composition/quality. For example, in controlled diet trials, low-carbohydrate dieters spontaneously reduce their calorie intake quite significantly and lose body fat, without being asked to restrict calories (7). In Dr. Staffan Lindeberg's Paleolithic diet trials, participants lost a remarkable amount of fat, yet a recent publication from his group shows that the satiety (fullness) level of the Paleolithic group was not different from a non-Paleolithic comparison group despite a considerably lower calorie intake over 12 weeks (8, 9). I'll discuss this important new paper soon. Together, this suggests that diet composition/quality can have a dominant impact on the fat mass setpoint.
One possibility is that cutting the wheat, sugar, most vegetable oil and other processed food out of Mr. Voigt's diet was responsible for the fat loss. Many people find, for example, that they lose fat simply by eliminating wheat from their diet.
Another possibility that I've been exploring recently is that changes in palatability (pleasantness of flavor) influence the fat mass setpoint. There is evidence in rodents that it does, although it's not entirely consistent. For example, rats will become massively obese if you provide them with chocolate flavored Ensure (a meal replacement drink), but not with vanilla or strawberry Ensure (10). They will defend their elevated fat mass against calorie restriction (i.e. they show a physiological starvation response when you try to bring them down to a lower weight by feeding them less chocolate Ensure) while they're eating chocolate Ensure, but as soon as you put them back on unpurified rodent pellets, they will lose fat and defend the lower fat mass. Giving them food in liquid or paste form often causes obesity, while the same food in solid pellet form will not. Eating nothing but potatoes is obviously a diet with a low overall palatability.
So I think that both a change in diet composition/quality and a decrease in palatability probably contributed to a decrease in Mr. Voigt's fat mass setpoint, which allowed him to lose fat mass without triggering a starvation response (hunger, fatigue).
The rest of his improvements in health markers were partially due to the fat loss, including his decreased fasting glucose, decreased triglycerides, and presumably increased insulin sensitivity. They may also have been partially due to a lack of industrial food and increased intake of certain micronutrients such as magnesium.
One of the most striking changes was in his calculated LDL cholesterol ("bad" cholesterol), which decreased by 41%, putting him in a range that's more typical of healthy non-industrial cultures including hunter-gatherers. Yet hunter-gatherers didn't eat nothing but potatoes, often didn't eat much starch, and in some cases had a high intake of fat and saturated fat, so what gives? It's possible that a reduced saturated fat intake had an impact on his LDL, given the relatively short timescale of the diet. But I think there's something mysterious about this setpoint mechanism that has a much broader impact on metabolism than is generally appreciated. For example, calorie restriction in humans has a massive impact on LDL, much larger than the impact of saturated fat (11). And in any case, the latter appears to be a short-term phenomenon (12). It's just beginning to be appreciated that energy balance control systems in the brain influence cholesterol metabolism.
Mr. Voigt's digestion appeared to be just fine on his potato diet, even though he generally ate the skins. This makes me even more skeptical of the idea that potato glycoalkaloids in common potato varieties are a health concern, especially if you were to eliminate most of the glycoalkaloids by peeling.
I asked Mr. Voigt about what foods he was craving during the diet to get an idea of whether he was experiencing any major deficiencies. The fact that Mr. Voigt did not mention craving meat or other high-protein foods reinforces the fact that potatoes are a reasonable source of complete protein. The only thing he craved was crunchy/juicy food, which I'm not sure how to interpret.
He also stopped snoring during the diet, and began again immediately upon resuming his normal diet, perhaps indicating that his potato diet reduced airway inflammation. This could be due to avoiding food allergies and irritants (wheat anyone?) and also fat loss.
Overall, a very informative experiment! Enjoy your potatoes.
*Until the last 5.5 weeks, when he deliberately stuffed himself beyond his appetite because his rapid weight loss worried him. Yet, even with deliberate overfeeding up to his estimated calorie requirement of 2,200 calories per day, he continued to lose weight. He probably was not quite reaching his calorie goal, or his requirement is higher than he thought.
It's often pointed out that potatoes are low in vitamins and minerals compared to vegetables on a per-calorie basis, but I think it's a misleading comparison because potatoes are much more calorie-dense than most vegetables. Potatoes compare favorably to other starchy staples such as bread, rice and taro.
Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).
On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But of course, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.
Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?
I believe Mr. Voigt's diet lowered his fat mass 'setpoint'. In other words, for whatever reason, the diet made his body 'want' to be leaner that it already was. His body began releasing stored fat that it considered excess, and therefore he had to eat less food to complete his energy needs. You see this same phenomenon very clearly in rodent feeding studies. Changes in diet composition/quality can cause dramatic shifts in the fat mass setpoint (5, 6). Mr. Voigt's appetite would eventually have returned to normal once he had stabilized at a lower body fat mass, just as rodents do.
Rodent studies have made it clear that diet composition has a massive effect on the level of fat mass that the body will 'defend' against changes in calorie intake (5, 6). Human studies have shown similar effects from changes in diet composition/quality. For example, in controlled diet trials, low-carbohydrate dieters spontaneously reduce their calorie intake quite significantly and lose body fat, without being asked to restrict calories (7). In Dr. Staffan Lindeberg's Paleolithic diet trials, participants lost a remarkable amount of fat, yet a recent publication from his group shows that the satiety (fullness) level of the Paleolithic group was not different from a non-Paleolithic comparison group despite a considerably lower calorie intake over 12 weeks (8, 9). I'll discuss this important new paper soon. Together, this suggests that diet composition/quality can have a dominant impact on the fat mass setpoint.
One possibility is that cutting the wheat, sugar, most vegetable oil and other processed food out of Mr. Voigt's diet was responsible for the fat loss. Many people find, for example, that they lose fat simply by eliminating wheat from their diet.
Another possibility that I've been exploring recently is that changes in palatability (pleasantness of flavor) influence the fat mass setpoint. There is evidence in rodents that it does, although it's not entirely consistent. For example, rats will become massively obese if you provide them with chocolate flavored Ensure (a meal replacement drink), but not with vanilla or strawberry Ensure (10). They will defend their elevated fat mass against calorie restriction (i.e. they show a physiological starvation response when you try to bring them down to a lower weight by feeding them less chocolate Ensure) while they're eating chocolate Ensure, but as soon as you put them back on unpurified rodent pellets, they will lose fat and defend the lower fat mass. Giving them food in liquid or paste form often causes obesity, while the same food in solid pellet form will not. Eating nothing but potatoes is obviously a diet with a low overall palatability.
So I think that both a change in diet composition/quality and a decrease in palatability probably contributed to a decrease in Mr. Voigt's fat mass setpoint, which allowed him to lose fat mass without triggering a starvation response (hunger, fatigue).
The rest of his improvements in health markers were partially due to the fat loss, including his decreased fasting glucose, decreased triglycerides, and presumably increased insulin sensitivity. They may also have been partially due to a lack of industrial food and increased intake of certain micronutrients such as magnesium.
One of the most striking changes was in his calculated LDL cholesterol ("bad" cholesterol), which decreased by 41%, putting him in a range that's more typical of healthy non-industrial cultures including hunter-gatherers. Yet hunter-gatherers didn't eat nothing but potatoes, often didn't eat much starch, and in some cases had a high intake of fat and saturated fat, so what gives? It's possible that a reduced saturated fat intake had an impact on his LDL, given the relatively short timescale of the diet. But I think there's something mysterious about this setpoint mechanism that has a much broader impact on metabolism than is generally appreciated. For example, calorie restriction in humans has a massive impact on LDL, much larger than the impact of saturated fat (11). And in any case, the latter appears to be a short-term phenomenon (12). It's just beginning to be appreciated that energy balance control systems in the brain influence cholesterol metabolism.
Mr. Voigt's digestion appeared to be just fine on his potato diet, even though he generally ate the skins. This makes me even more skeptical of the idea that potato glycoalkaloids in common potato varieties are a health concern, especially if you were to eliminate most of the glycoalkaloids by peeling.
I asked Mr. Voigt about what foods he was craving during the diet to get an idea of whether he was experiencing any major deficiencies. The fact that Mr. Voigt did not mention craving meat or other high-protein foods reinforces the fact that potatoes are a reasonable source of complete protein. The only thing he craved was crunchy/juicy food, which I'm not sure how to interpret.
He also stopped snoring during the diet, and began again immediately upon resuming his normal diet, perhaps indicating that his potato diet reduced airway inflammation. This could be due to avoiding food allergies and irritants (wheat anyone?) and also fat loss.
Overall, a very informative experiment! Enjoy your potatoes.
*Until the last 5.5 weeks, when he deliberately stuffed himself beyond his appetite because his rapid weight loss worried him. Yet, even with deliberate overfeeding up to his estimated calorie requirement of 2,200 calories per day, he continued to lose weight. He probably was not quite reaching his calorie goal, or his requirement is higher than he thought.
Monday, September 29, 2008
Acne: Disease of Civilization
I often focus on the bigger facets of the disease of civilization. Things like cardiovascular disease and cancer, which are major killers and the subject of intensive research. But the disease of civilization is a spectrum of disorders that affects the body in countless ways, large and small.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.
In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.
The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.
They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.
Saturday, February 5, 2011
Assorted Thoughts About the 2010 Dietary Guidelines
In the past week, I've been rooting through the USDA's 2010 Dietary Guidelines (1). Here are a few of my thoughts.
Positive
One of the things I've been enjoying recently is watching health authorities shift away from a nutrient-oriented philosophy in favor of a more food-oriented philosophy. For example, I recently read a nice editorial by Drs. Dariush Mozaffarian and David S. Ludwig (not associated with the USDA) that encapsulates this (2). Here's a quote:
Although the 2010 guidelines are too focused on nutrients for my taste, they do spend some time talking about food groups and eating patterns, for example, recommending an increase in the consumption of vegetables, fruit, whole grains and seafood. They also recommend Mediterranean and plant-focused eating patterns. Although I don't think their recommendations quite hit the mark, they do reflect a shift in thinking.
Another thing I enjoyed about the Guidelines is the table on page 12 of chapter 2, which shows just how messed up the average American diet is. The number one source of calories in all age groups is "grain-based desserts". The next five in adults are yeast breads, chicken dishes, soda/sports drinks, alcohol and pizza. To see typical American food habits presented like this just blows me away. They call this the "obesogenic environment"; the idea that we're surrounded by tasty but unhealthy food and situations that favor the consumption of it. I agree.
The Guidelines also contain a surprisingly accurate one-sentence review of the glycemic index literature:
The first problem is the creation of the category "solid fats and added sugars", abbreviated SoFAS. With the creation of this term, they lump pastured butter together with Crisco and Red Hots. If they've been hiding the evidence that pastured butter, virgin coconut oil or red palm oil contribute to heart disease, I'd like to see it so I can stop eating them!
Another problem is their list of recommendations to curb the obesity epidemic. They say:
Jokes aside, I do think energy balance is a huge issue, perhaps even the central issue in chronic disease risk in affluent nations. The basic problem is that Americans are eating more calories than is optimal, and they have a very hard time stopping. It's not because they have less willpower than their stoic ancestors, it's because their bodies have decided that overweight/obesity is the new lean, and they defend that higher level of fat mass against changes. Simply telling an overweight person to eat fewer calories, without changing the dietary context, is not very effective in the long term, due to compensatory mechanisms including hunger and increased metabolic efficiency (fewer calories burned for the same muscular exertion).
What does the USDA recommend to lose fat or maintain leanness?
At one point, they talk about changes in the US diet that have corresponded with the obesity epidemic:
Conclusion
Although the 2010 USDA Dietary Guidelines show some promising trends, and contain some good information, I hope you can find a better source than the USDA for your nutrition advice.
Positive
One of the things I've been enjoying recently is watching health authorities shift away from a nutrient-oriented philosophy in favor of a more food-oriented philosophy. For example, I recently read a nice editorial by Drs. Dariush Mozaffarian and David S. Ludwig (not associated with the USDA) that encapsulates this (2). Here's a quote:
Nutritional science has advanced rapidly, and the evidence now demonstrates the major limitations of nutrient-based metrics for prevention of chronic disease. The proportion of total energy from fat appears largely unrelated to risk of cardiovascular disease, cancer, diabetes, or obesity. Saturated fat—targeted by nearly all nutrition-related professional organizations and governmental agencies—has little relation to heart disease within most prevailing dietary patterns. Typical recommendations to consume at least half of total energy as carbohydrate, a nutrient for which humans have no absolute requirement, conflate foods with widely divergent physiologic effects (eg, brown rice, white bread, apples). Foods are grouped based on protein content (chicken, fish, beans, nuts) despite demonstrably different health effects. With few exceptions (eg, omega-3 fats, trans fat, salt), individual compounds in isolation have small effects on chronic diseases. Thus, little of the information found on food labels’ “nutrition facts” panels provides useful guidance for selecting healthier foods to prevent chronic disease.Tell it! Although he doesn't use the word nutritionism, that's basically what he's arguing against. Dr. Mozaffarian seems to represent the less reductionist school of nutrition, which is a more informed version of what nutrition pioneers such as Sir Edward Mellanby, Dr. May Mellanby, Dr. Weston Price and Sir Robert McCarrison advocated.
In contrast with discrete nutrients, specific foods and dietary patterns substantially affect chronic disease risk, as shown by controlled trials of risk factors and prospective cohorts of disease end points
Although this approach may seem radical, it actually represents a return to more traditional, time-tested ways of eating. Healthier food-based dietary patterns have existed for generations among some populations.
Although the 2010 guidelines are too focused on nutrients for my taste, they do spend some time talking about food groups and eating patterns, for example, recommending an increase in the consumption of vegetables, fruit, whole grains and seafood. They also recommend Mediterranean and plant-focused eating patterns. Although I don't think their recommendations quite hit the mark, they do reflect a shift in thinking.
Another thing I enjoyed about the Guidelines is the table on page 12 of chapter 2, which shows just how messed up the average American diet is. The number one source of calories in all age groups is "grain-based desserts". The next five in adults are yeast breads, chicken dishes, soda/sports drinks, alcohol and pizza. To see typical American food habits presented like this just blows me away. They call this the "obesogenic environment"; the idea that we're surrounded by tasty but unhealthy food and situations that favor the consumption of it. I agree.
The Guidelines also contain a surprisingly accurate one-sentence review of the glycemic index literature:
Strong evidence shows that glycemic index and/or glycemic load are not associated with body weight; thus, it is not necessary to consider these measures when selecting carbohydrate foods and beverages for weight management.Negative
The first problem is the creation of the category "solid fats and added sugars", abbreviated SoFAS. With the creation of this term, they lump pastured butter together with Crisco and Red Hots. If they've been hiding the evidence that pastured butter, virgin coconut oil or red palm oil contribute to heart disease, I'd like to see it so I can stop eating them!
Another problem is their list of recommendations to curb the obesity epidemic. They say:
The current high rates of overweight and obesity among virtually all subgroups of the population in the United States demonstrate that many Americans are in calorie imbalance—that is, they consume more calories than they expend. To curb the obesity epidemic and improve their health, Americans need to make significant efforts to decrease the total number of calories they consume from foods and beverages and increase calorie expenditure through physical activity.Looks like we have Sherlock Holmes on the case. Now that we have this information, all we have to do is tell overweight people to eat less and they'll be lean again! What's that, they already know and it's not working?? Someone should tell the USDA.
Jokes aside, I do think energy balance is a huge issue, perhaps even the central issue in chronic disease risk in affluent nations. The basic problem is that Americans are eating more calories than is optimal, and they have a very hard time stopping. It's not because they have less willpower than their stoic ancestors, it's because their bodies have decided that overweight/obesity is the new lean, and they defend that higher level of fat mass against changes. Simply telling an overweight person to eat fewer calories, without changing the dietary context, is not very effective in the long term, due to compensatory mechanisms including hunger and increased metabolic efficiency (fewer calories burned for the same muscular exertion).
What does the USDA recommend to lose fat or maintain leanness?
- Count calories. Doesn't work for most people, although I acknowledge that it is physically possible to lose fat (and lean mass) by restricting calories.
- Reduce sweetened beverages. Thumbs up.
- Serve smaller portions. As far as I know, this rests exclusively on very short-term studies that showed that food consumed at a single meal or three is reduced if portion size is smaller. I guess it can't hurt to try it, but I'm not convinced it will have any effect on long-term body fatness. I think restaurant portion sizes have probably increased because people eat more, rather than the other way around, although both could be true.
- Eat foods that are less calorie dense. I think vegetables are healthy, but is it because they're less calorie-dense? Why is dietary fat intake generally not associated with obesity if it's the most calorie-dense substance? Why do many people lose body fat eating energy-dense low-carbohydrate diets? Not convinced, but I'm feeling open minded about this one.
- Exercise more and watch less TV. Exercise is good. But don't let it make you hungry, because then you'll eat more!
At one point, they talk about changes in the US diet that have corresponded with the obesity epidemic:
Average daily calories available per person in the marketplace increased approximately 600 calories, with the greatest increases in the availability of added fats and oils, grains, milk and milk products, and caloric sweeteners.Let me edit that so it's more complete:
Average daily calories available per person in the marketplace increased approximately 600 calories per day, 250 calories of which were actually consumed (USDA and NHANES). Added fats increased, due to a large increase in seed oil intake, but total fat intake remained approximately the same because of a roughly equal decrease in fatty meat and whole milk consumption (USDA and NHANES). Grain intake, predominantly wheat, increased, as did the consumption of refined sweeteners, predominantly high-fructose corn syrup (USDA).It reads a bit differently once you have a little more information, doesn't it? Animal fat intake declined considerably, and was replaced by seed oils, in parallel with the obesity and diabetes epidemics. Maybe it contributed, maybe it didn't, but why not just be forthright about it? People appreciate honesty.
Conclusion
Although the 2010 USDA Dietary Guidelines show some promising trends, and contain some good information, I hope you can find a better source than the USDA for your nutrition advice.
Monday, March 1, 2010
Book Review: S.P.E.E.D.
This book was sent to me by Matt Schoeneberger, who co-authored it with Jeff Thiboutot. Both have master's degrees in exercise science and health promotion. S.P.E.E.D. stands for Sleep, Psychology, Exercise, Environment and Diet. The authors have attempted to create a concise, comprehensive weight loss strategy based on what they feel is the most compelling scientific evidence available. It's subtitled "The Only Weight Loss Book Worth Reading". Despite the subtitle that's impossible to live up to, it was an interesting and well-researched book. It was a very fast read at 205 large-print pages including 32 pages of appendices and index.
I really appreciate the abundant in-text references the authors provided. I have a hard time taking a health and nutrition book seriously that doesn't provide any basis to evaluate its statements. There are already way too many people flapping their lips out there, without providing any outside support for their statements, for me to tolerate that sort of thing. Even well-referenced books can be a pain if the references aren't in the text itself. Schoeneberger and Thiboutot provided appropriate, accessible references for nearly every major statement in the book.
Chapter one, "What is a Healthy Weight", discusses the evidence for an association between body weight and health. They note that both underweight and obesity are associated with poor health outcomes, whereas moderate overweight isn't. While I agree, I continue to maintain that being fairly lean and appropriately muscled (which doesn't necessarily mean muscular) is probably optimal. The reason that people with a body mass index (BMI) considered to be "ideal" aren't healthier on average than people who are moderately overweight may have to do with the fact that many people with an "ideal" BMI are skinny-fat, i.e. have low muscle mass and too much abdominal fat.
Chapter 2, "Sleep", discusses the importance of sleep in weight regulation and overall health. They reference some good studies and I think they make a compelling case that it's important. Chapter 3, "Psychology", details psychological strategies to motivate and plan for effective weight loss.
Chapter 4, "Exercise", provides an exercise plan for weight loss. The main message: do it! I think they give a fair overview of the different categories of exercise and their relative merits, including high-intensity intermittent training (HIIT). However, the exercise regimen they suggest is intense and will probably lead to overtraining in many people. They recommend resistance training major, multi-joint exercises, 1-3 sets to muscular failure 2-4 days a week. I've been at the higher end of that recommendation and it made my joints hurt, plus I was weaker than when I strength trained less frequently. I think the lower end of their recommendation, 1 set of each exercise to failure twice a week, is more than sufficient to meet the goal of maximizing improvements in body composition in most people. My current routine is one brief strength training session and one sprint session per week (in addition to my leisurely cycle commute), which works well for me on a cost-benefit level. However, I was stronger when I was strength training twice a week and never going to muscular failure (a la Pavel Tsatsouline).
Chapter 5, "Environment", is an interesting discussion of different factors that promote excessive calorie intake, such as the setting of the meal, the company or lack thereof, and food presentation. While they support their statements very well with evidence from scientific studies, I do have a lingering doubt about these types of studies: as far as I know, they're all based on short-term interventions. Science would be a lot easier if short-term always translated to long term, but unfortunately that's not the case. For example, studies lasting one or two weeks show that low glycemic index foods cause a reduction in calorie intake and greater feelings of fullness. However, this effect disappears in the long term, and numerous controlled trials show that low glycemic index diets have no effect on food intake, body weight or insulin sensitivity in the long term. I reviewed those studies here.
The body has homeostatic mechanisms (homeostatic = maintains the status quo) that regulate long-term energy balance. Whether short-term changes in calorie intake based on environmental cues would translate into sustained changes that would have a significant impact on body fat, I don't know. For example, if you eat a meal with your extended family at a restaurant that serves massive portions, you might eat twice as much as you would by yourself in your own home. But the question is, will your body factor that huge meal into your subsequent calorie intake and energy expenditure over the following days? The answer is clearly yes, but the degree of compensation is unclear. Since I'm not aware of any trials indicating that changing meal context can actually lead to long-term weight loss, I can't put much faith in this strategy (if you know otherwise, please link to the study in the comments).
Chapter 6, "Diet", is a very brief discussion of what to eat for weight loss. They basically recommend a low-calorie, low-carb diet focused on whole, natural foods. I think low-carbohydrate diets can be useful for some overweight people trying to lose weight, if for no other reason than the fact that they make it easier to control appetite. In addition, a subset of people respond very well to carbohydrate restriction in terms of body composition, health and well-being. The authors emphasize nutrient density, but don't really explain how to achieve it. It would have been nice to see a discussion of a few topics such as organ meats, leafy greens, dairy quality (pastured vs. conventional) and vitamin D. These may not help you lose weight, but they will help keep you healthy, particularly on a calorie-restricted diet. The authors also recommend a few energy bars, powders and supplements that I don't support. They state that they have no financial connection to the manufacturers of the products they recommend.
I'm wary of their recommendation to deliberately restrict calorie intake. Although it will clearly cause fat loss if you restrict calories enough, it's been shown to be ineffective for sustainable, long-term fat loss over and over again. The only exception is the rare person with an iron will who is able to withstand misery indefinitely. I'm going to keep an open mind on this question though. There may be a place for deliberate calorie restriction in the right context. But at this point I'm going to require some pretty solid evidence that it's effective, sustainable, and doesn't have unacceptable side effects.
The book contains a nice bonus, an appendix titled "What is Quality Evidence"? It's a brief discussion of common logical pitfalls when evaluating evidence, and I think many people could benefit from reading it.
Overall, S.P.E.E.D. was a worthwhile read, definitely superior to 95% of fat loss books. With some caveats mentioned above, I think it could be a useful resource for someone interested in fat loss.
I really appreciate the abundant in-text references the authors provided. I have a hard time taking a health and nutrition book seriously that doesn't provide any basis to evaluate its statements. There are already way too many people flapping their lips out there, without providing any outside support for their statements, for me to tolerate that sort of thing. Even well-referenced books can be a pain if the references aren't in the text itself. Schoeneberger and Thiboutot provided appropriate, accessible references for nearly every major statement in the book.
Chapter one, "What is a Healthy Weight", discusses the evidence for an association between body weight and health. They note that both underweight and obesity are associated with poor health outcomes, whereas moderate overweight isn't. While I agree, I continue to maintain that being fairly lean and appropriately muscled (which doesn't necessarily mean muscular) is probably optimal. The reason that people with a body mass index (BMI) considered to be "ideal" aren't healthier on average than people who are moderately overweight may have to do with the fact that many people with an "ideal" BMI are skinny-fat, i.e. have low muscle mass and too much abdominal fat.
Chapter 2, "Sleep", discusses the importance of sleep in weight regulation and overall health. They reference some good studies and I think they make a compelling case that it's important. Chapter 3, "Psychology", details psychological strategies to motivate and plan for effective weight loss.
Chapter 4, "Exercise", provides an exercise plan for weight loss. The main message: do it! I think they give a fair overview of the different categories of exercise and their relative merits, including high-intensity intermittent training (HIIT). However, the exercise regimen they suggest is intense and will probably lead to overtraining in many people. They recommend resistance training major, multi-joint exercises, 1-3 sets to muscular failure 2-4 days a week. I've been at the higher end of that recommendation and it made my joints hurt, plus I was weaker than when I strength trained less frequently. I think the lower end of their recommendation, 1 set of each exercise to failure twice a week, is more than sufficient to meet the goal of maximizing improvements in body composition in most people. My current routine is one brief strength training session and one sprint session per week (in addition to my leisurely cycle commute), which works well for me on a cost-benefit level. However, I was stronger when I was strength training twice a week and never going to muscular failure (a la Pavel Tsatsouline).
Chapter 5, "Environment", is an interesting discussion of different factors that promote excessive calorie intake, such as the setting of the meal, the company or lack thereof, and food presentation. While they support their statements very well with evidence from scientific studies, I do have a lingering doubt about these types of studies: as far as I know, they're all based on short-term interventions. Science would be a lot easier if short-term always translated to long term, but unfortunately that's not the case. For example, studies lasting one or two weeks show that low glycemic index foods cause a reduction in calorie intake and greater feelings of fullness. However, this effect disappears in the long term, and numerous controlled trials show that low glycemic index diets have no effect on food intake, body weight or insulin sensitivity in the long term. I reviewed those studies here.
The body has homeostatic mechanisms (homeostatic = maintains the status quo) that regulate long-term energy balance. Whether short-term changes in calorie intake based on environmental cues would translate into sustained changes that would have a significant impact on body fat, I don't know. For example, if you eat a meal with your extended family at a restaurant that serves massive portions, you might eat twice as much as you would by yourself in your own home. But the question is, will your body factor that huge meal into your subsequent calorie intake and energy expenditure over the following days? The answer is clearly yes, but the degree of compensation is unclear. Since I'm not aware of any trials indicating that changing meal context can actually lead to long-term weight loss, I can't put much faith in this strategy (if you know otherwise, please link to the study in the comments).
Chapter 6, "Diet", is a very brief discussion of what to eat for weight loss. They basically recommend a low-calorie, low-carb diet focused on whole, natural foods. I think low-carbohydrate diets can be useful for some overweight people trying to lose weight, if for no other reason than the fact that they make it easier to control appetite. In addition, a subset of people respond very well to carbohydrate restriction in terms of body composition, health and well-being. The authors emphasize nutrient density, but don't really explain how to achieve it. It would have been nice to see a discussion of a few topics such as organ meats, leafy greens, dairy quality (pastured vs. conventional) and vitamin D. These may not help you lose weight, but they will help keep you healthy, particularly on a calorie-restricted diet. The authors also recommend a few energy bars, powders and supplements that I don't support. They state that they have no financial connection to the manufacturers of the products they recommend.
I'm wary of their recommendation to deliberately restrict calorie intake. Although it will clearly cause fat loss if you restrict calories enough, it's been shown to be ineffective for sustainable, long-term fat loss over and over again. The only exception is the rare person with an iron will who is able to withstand misery indefinitely. I'm going to keep an open mind on this question though. There may be a place for deliberate calorie restriction in the right context. But at this point I'm going to require some pretty solid evidence that it's effective, sustainable, and doesn't have unacceptable side effects.
The book contains a nice bonus, an appendix titled "What is Quality Evidence"? It's a brief discussion of common logical pitfalls when evaluating evidence, and I think many people could benefit from reading it.
Overall, S.P.E.E.D. was a worthwhile read, definitely superior to 95% of fat loss books. With some caveats mentioned above, I think it could be a useful resource for someone interested in fat loss.
Tuesday, July 7, 2015
What Properties Make a Food "Addictive"?
Although the concept of food addiction remains controversial, there's no doubt that specific foods can provoke addiction-like behaviors in susceptible people. Yet not all foods have this effect, suggesting that it's related to specific food properties. A new study aims to identify the properties that make a food "addictive".
Introduction
Introduction
Friday, January 27, 2012
Insulin and Obesity: Another Nail in the Coffin
There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness. Some versions invoke insulin's effects on fat tissue, others its effects in the brain. This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn't seem to have much if any impact on body weight in controlled trials).
I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s. However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness. If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well.
I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s. However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness. If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well.
Sunday, January 15, 2012
What Causes Insulin Resistance? Part V
Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance. In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.
Carbohydrate and Fat
There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity. What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people. This will get at what causes insulin resistance in someone who does not already have it.
Carbohydrate and Fat
There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity. What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people. This will get at what causes insulin resistance in someone who does not already have it.
Monday, April 22, 2013
Book Review: Salt, Sugar, Fat
Michael Moss is a Pulitzer prize-winning journalist who has made a career writing about the US food system. In his latest book, Salt, Sugar, Fat: How the Food Giants Hooked Us, he attempts to explain how the processed food industry has been so successful at increasing its control over US "stomach share". Although the book doesn't focus on the obesity epidemic, the relevance is obvious. Salt, Sugar, Fat is required reading for anyone who wants to understand why obesity is becoming more common in the US and throughout the world.
Saturday, October 2, 2010
Potatoes and Human Health, Part III
Potato-eating Cultures: the Quechua
The potato is thought to have originated in what is now Peru, on the shores of lake Titicaca. Native Peruvians such as the Quechua have been highly dependent on the potato for thousands of years. A 1964 study of the Quechua inhabitants of Nuñoa showed that they obtained 74% of their calories from potatoes (fresh and chuños), 10% from grains, 10% from Chenopodia (quinoa and cañihua), and 4% from animal foods. Total energy intake was 3,170 calories per day (1).
In 2001, a medical study of rural Quechua men reported an average body fat percentage of 16.4% (2). The mean age of the volunteers was 38. Body fat did increase slowly with age in this population, and by age 65 it was predicted to be about 20% on average. That's below the threshold of overweight, so I conclude that most men in this population are fairly lean, although there were a few overweight individuals.
In 2004, a study in rural Quechua women reported a body fat percentage of 31.2% in volunteers with a mean age of 35 (3). Body fat percentage was higher in a group of Quechua immigrants to the Peruvian capital of Lima. Among rural women, average fasting insulin was 6.8 uIU/mL, and fasting glucose was 68.4 mg/dL, which together suggest good insulin sensitivity and glucose control (4). Insulin and glucose were considerably lower in the rural group than the urban group. Blood pressure was low in both groups. Overall, this suggests that overweight is common among Quechua women.
Rural Quechua are characteristically short, with the average adult man standing no more than 5' 2" (2). One might be tempted to speculate that this reflects stunting due to a deficient diet. However, given the fact that nearly all non-industrial populations, including contemporary hunter-gatherers, are short by modern standards, I'm not convinced the Quechua are abnormal. A more likely explanation is that industrial foods cause excessive tissue growth in modern populations, perhaps by promoting overeating and excessive insulin and IGF-1 production, which are growth factors. I first encountered this hypothesis in Dr. Staffan Lindeberg's book Food and Western Disease.
I don't consider the Quechua diet to be optimal, but it does seem to support a reasonable level of metabolic health. Rural Quechua men subsisting on potatoes are relatively lean, while women are often overweight, though less overweight than urban Quechua who eat fewer potatoes. Unfortunately, I don't have more detailed data on other aspects of their health, such as gastrointestinal health.
Potato-eating Cultures: the Aymara
The Aymara are another potato-dependent people of the Andes, who span Peru, Bolivia and Chile. The first paper I'll discuss is titled "Low Prevalence of Type II Diabetes Despite a High Body Mass Index in the Aymara Natives From Chile", by Dr. Jose Luis Santos and colleagues (5). In the paper, they show that the prevalence of diabetes in this population was 1.5%, and the prevalence of pre-diabetes was 3.6%. The prevalence of both remained low even in the elderly. Here's a comparison of those numbers with figures from the modern United States (6):
That's quite a difference! The prevalence of diabetes in this population is low, but not as low as in some cultures such as the Kitavans (7, 8).
Now to discuss the "high body mass index" referenced in the title of the paper. The body mass index (BMI) is the relation between height and weight, and often, but not always, reflects fatness. The average BMI of this population was 24.9, which is very close to the cutoff between normal and overweight (25).
Investigators were surprised to find such a low prevalence of diabetes in this population, despite their apparent high prevalence of overweight. Yet if you've seen pictures of rural native South Americans, you may have noticed they're often built short and thick, with wide hips and big barrel chests. Could this be confounding the relationship between BMI and body fatness? To answer that question, I found another paper that estimated Aymara body fat using skinfold measurements (9). That study reported that both men and women remained relatively lean throughout life (ages 4-65), with only two of 23 subjects classified as overweight on the basis of body fat percentage, and none classified as obese.
Back to the first paper. In this Aymara group, blood pressure was on the high side. Serum cholesterol was also a bit high for a traditionally-living population, but still lower than most modern groups (~188 mg/dL). I find it very interesting that the cholesterol level in this population that eats virtually no fat was the same as on Tokelau, where nearly half of calories come from highly saturated coconut fat (10, 11). Fasting insulin is also on the high side in the Aymara, which is also interesting given their good glucose tolerance and low prevalence of diabetes. This could be related to differences in the measurement assay rather than a true difference in fasting insulin, since these assays were often not standardized between studies.
Together, this shows that a lifetime of high-carbohydrate, high-glycemic food does not necessarily lead to overweight or metabolic problems in the context of a traditional diet and lifestyle.
Potato-eating Cultures: the Irish
Potatoes were introduced to Ireland in the 17th century. They were well suited to the cool, temperate climate, and more productive than any other crop. By the early 18th century, potatoes were the main source of calories, particularly for the poor who ate practically nothing else. In 1839, the average Irish laborer obtained 87% of his calories from potatoes (12). In 1845, the potato blight Phytophthora infestans struck, decimating potato plantations nationwide and creating the Great Famine.
There isn't much reliable information on the health status of the Irish prior to the famine, besides reports of vitamin A deficiency symptoms (13) due to the fact that neither of the primary articles of diet, potatoes and buttermilk, provide significant vitamin A. However, the Irish at the time had a very high fertility rate, and anecdotal reports described them as healthy and attractive (14):
Starting nearly a century ago, a few researchers decided to feed volunteers potato-only diets to achieve various research objectives. The first such experiment was carried out by a Dr. M. Hindhede and published in 1913 (described in 15). Hindhede's goal was to explore the lower limit of the human protein requirement and the biological quality of potato protein. He fed three healthy adult men almost nothing but potatoes and margarine for 309 days (margarine was not made from hydrogenated seed oils at the time), all while making them do progressively more demanding physical labor. They apparently remained in good physical condition. Here's a description of one of his volunteers, a Mr. Madsen, from another book (described in 16; thanks to Matt Metzgar):
Just yesterday, Chris Voigt of the Washington State Potato Commission embarked on his own n=1 potato feeding experiment as a way to promote Washington state potatoes. He'll be eating nothing but potatoes and a little fat for two months, and getting a full physical at the end. Check out his website for more information and updates (18). Mr. Voigt has graciously agreed to a written interview with Whole Health Source at the end of his experiment. He pointed out to me that the Russet Burbank potato, the most popular variety in the United States, is over 135 years old. Stay tuned for more interesting facts from Mr. Voigt in early December.
Observational Studies
With the recent interest in the health effects of the glycemic index, a few studies have examined the association between potatoes and health in various populations. The results are all over the place, with some showing positive associations with health, and others showing negative associations (19, 20, 21). As a whole, I find these studies difficult to interpret and not very helpful.
Anecdotes
Some people feel good when they eat potatoes. Others find that potatoes and other members of the nightshade family give them digestive problems, exacerbate their arthritis, or cause fat gain. I haven't encountered any scientific research to substantiate claims that nightshades aggravate arthritis or other inflammatory conditions. However, that doesn't necessarily mean there aren't individuals who are sensitive. If potatoes don't agree with you, by all means avoid them.
The Bottom Line
You made it to the end! Give yourself a pat on the back. You deserve it.
In my opinion, the scientific literature as a whole, including animal and human studies, suggests rather consistently that potatoes can be a healthy part of a varied diet for most people, and they probably do not generally promote digestive problems, fat gain, or metabolic dysfunction. Nevertheless, I wouldn't recommend eating nothing but potatoes for any length of time. If you do choose to eat potatoes, follow these simple guidelines:
The potato is thought to have originated in what is now Peru, on the shores of lake Titicaca. Native Peruvians such as the Quechua have been highly dependent on the potato for thousands of years. A 1964 study of the Quechua inhabitants of Nuñoa showed that they obtained 74% of their calories from potatoes (fresh and chuños), 10% from grains, 10% from Chenopodia (quinoa and cañihua), and 4% from animal foods. Total energy intake was 3,170 calories per day (1).
In 2001, a medical study of rural Quechua men reported an average body fat percentage of 16.4% (2). The mean age of the volunteers was 38. Body fat did increase slowly with age in this population, and by age 65 it was predicted to be about 20% on average. That's below the threshold of overweight, so I conclude that most men in this population are fairly lean, although there were a few overweight individuals.
In 2004, a study in rural Quechua women reported a body fat percentage of 31.2% in volunteers with a mean age of 35 (3). Body fat percentage was higher in a group of Quechua immigrants to the Peruvian capital of Lima. Among rural women, average fasting insulin was 6.8 uIU/mL, and fasting glucose was 68.4 mg/dL, which together suggest good insulin sensitivity and glucose control (4). Insulin and glucose were considerably lower in the rural group than the urban group. Blood pressure was low in both groups. Overall, this suggests that overweight is common among Quechua women.
Rural Quechua are characteristically short, with the average adult man standing no more than 5' 2" (2). One might be tempted to speculate that this reflects stunting due to a deficient diet. However, given the fact that nearly all non-industrial populations, including contemporary hunter-gatherers, are short by modern standards, I'm not convinced the Quechua are abnormal. A more likely explanation is that industrial foods cause excessive tissue growth in modern populations, perhaps by promoting overeating and excessive insulin and IGF-1 production, which are growth factors. I first encountered this hypothesis in Dr. Staffan Lindeberg's book Food and Western Disease.
I don't consider the Quechua diet to be optimal, but it does seem to support a reasonable level of metabolic health. Rural Quechua men subsisting on potatoes are relatively lean, while women are often overweight, though less overweight than urban Quechua who eat fewer potatoes. Unfortunately, I don't have more detailed data on other aspects of their health, such as gastrointestinal health.
Potato-eating Cultures: the Aymara
The Aymara are another potato-dependent people of the Andes, who span Peru, Bolivia and Chile. The first paper I'll discuss is titled "Low Prevalence of Type II Diabetes Despite a High Body Mass Index in the Aymara Natives From Chile", by Dr. Jose Luis Santos and colleagues (5). In the paper, they show that the prevalence of diabetes in this population was 1.5%, and the prevalence of pre-diabetes was 3.6%. The prevalence of both remained low even in the elderly. Here's a comparison of those numbers with figures from the modern United States (6):
That's quite a difference! The prevalence of diabetes in this population is low, but not as low as in some cultures such as the Kitavans (7, 8).Now to discuss the "high body mass index" referenced in the title of the paper. The body mass index (BMI) is the relation between height and weight, and often, but not always, reflects fatness. The average BMI of this population was 24.9, which is very close to the cutoff between normal and overweight (25).
Investigators were surprised to find such a low prevalence of diabetes in this population, despite their apparent high prevalence of overweight. Yet if you've seen pictures of rural native South Americans, you may have noticed they're often built short and thick, with wide hips and big barrel chests. Could this be confounding the relationship between BMI and body fatness? To answer that question, I found another paper that estimated Aymara body fat using skinfold measurements (9). That study reported that both men and women remained relatively lean throughout life (ages 4-65), with only two of 23 subjects classified as overweight on the basis of body fat percentage, and none classified as obese.
Back to the first paper. In this Aymara group, blood pressure was on the high side. Serum cholesterol was also a bit high for a traditionally-living population, but still lower than most modern groups (~188 mg/dL). I find it very interesting that the cholesterol level in this population that eats virtually no fat was the same as on Tokelau, where nearly half of calories come from highly saturated coconut fat (10, 11). Fasting insulin is also on the high side in the Aymara, which is also interesting given their good glucose tolerance and low prevalence of diabetes. This could be related to differences in the measurement assay rather than a true difference in fasting insulin, since these assays were often not standardized between studies.
Together, this shows that a lifetime of high-carbohydrate, high-glycemic food does not necessarily lead to overweight or metabolic problems in the context of a traditional diet and lifestyle.
Potato-eating Cultures: the Irish
Potatoes were introduced to Ireland in the 17th century. They were well suited to the cool, temperate climate, and more productive than any other crop. By the early 18th century, potatoes were the main source of calories, particularly for the poor who ate practically nothing else. In 1839, the average Irish laborer obtained 87% of his calories from potatoes (12). In 1845, the potato blight Phytophthora infestans struck, decimating potato plantations nationwide and creating the Great Famine.
There isn't much reliable information on the health status of the Irish prior to the famine, besides reports of vitamin A deficiency symptoms (13) due to the fact that neither of the primary articles of diet, potatoes and buttermilk, provide significant vitamin A. However, the Irish at the time had a very high fertility rate, and anecdotal reports described them as healthy and attractive (14):
As far as fecundity is concerned, the high nutritional value of the potato diet might have played a significant role, but little supportive evidence has been presented so far... What is known is that the Irish in general and Irish women in particular were widely described as healthy and good-looking. Adam Smith's famous remark that potatoes were "peculiarly suitable to the health of the human constitution" can be complemented with numerous observations from other contemporary observers to the same effect.Controlled Feeding Studies
Starting nearly a century ago, a few researchers decided to feed volunteers potato-only diets to achieve various research objectives. The first such experiment was carried out by a Dr. M. Hindhede and published in 1913 (described in 15). Hindhede's goal was to explore the lower limit of the human protein requirement and the biological quality of potato protein. He fed three healthy adult men almost nothing but potatoes and margarine for 309 days (margarine was not made from hydrogenated seed oils at the time), all while making them do progressively more demanding physical labor. They apparently remained in good physical condition. Here's a description of one of his volunteers, a Mr. Madsen, from another book (described in 16; thanks to Matt Metzgar):
In order to test whether it was possible to perform heavy work on a strict potato diet, Mr. Madsen took a place as a farm laborer... His physical condition was excellent. In his book, Dr. Hindhede shows a photograph of Mr. Madsen taken on December 21st, 1912, after he had lived for almost a year entirely on potatoes. This photograph shows a strong, solid, athletic-looking figure, all of whose muscles are well-developed, and without excess fat. ...Hindhede had him examined by five physicians, including a diagnostician, a specialist in gastric and intestinal diseases, an X-ray specialist, and a blood specialist. They all pronounced him to be in a state of perfect health.Dr. Hindhede discovered that potato protein is high quality, providing all essential amino acids and high digestibility. Potato protein alone is sufficient to sustain an athletic man (although that doesn't make it optimal). A subsequent potato feeding study published in 1927 confirmed this finding (17). Two volunteers, a man and a woman, ate almost nothing but potatoes with a bit of lard and butter for 5.5 months. The man was an athlete but the woman was sedentary. Body weight and nitrogen balance (reflecting protein gain/loss from the body) remained constant throughout the experiment, indicating that their muscles were not atrophying at any appreciable rate, and they were probably not putting on fat. The investigators remarked:
The digestion was excellent throughout the experiment and both subjects felt very well. They did not tire of the uniform potato diet and there was no craving for change.In one of his Paleo Diet newsletters titled "Consumption of Nightshade Plants (Part 1)", Dr. Loren Cordain referenced two feeding studies showing that potatoes increase the serum level of the inflammatory cytokine interleukin-6 (22, 23). However, one study was not designed to determine the specific role of potato in the change (two dietary factors were altered simultaneously), and the other used potato chips as the source of potato. So I don't find these studies particularly relevant to the question at hand.
Just yesterday, Chris Voigt of the Washington State Potato Commission embarked on his own n=1 potato feeding experiment as a way to promote Washington state potatoes. He'll be eating nothing but potatoes and a little fat for two months, and getting a full physical at the end. Check out his website for more information and updates (18). Mr. Voigt has graciously agreed to a written interview with Whole Health Source at the end of his experiment. He pointed out to me that the Russet Burbank potato, the most popular variety in the United States, is over 135 years old. Stay tuned for more interesting facts from Mr. Voigt in early December.
Observational Studies
With the recent interest in the health effects of the glycemic index, a few studies have examined the association between potatoes and health in various populations. The results are all over the place, with some showing positive associations with health, and others showing negative associations (19, 20, 21). As a whole, I find these studies difficult to interpret and not very helpful.
Anecdotes
Some people feel good when they eat potatoes. Others find that potatoes and other members of the nightshade family give them digestive problems, exacerbate their arthritis, or cause fat gain. I haven't encountered any scientific research to substantiate claims that nightshades aggravate arthritis or other inflammatory conditions. However, that doesn't necessarily mean there aren't individuals who are sensitive. If potatoes don't agree with you, by all means avoid them.
The Bottom Line
You made it to the end! Give yourself a pat on the back. You deserve it.
In my opinion, the scientific literature as a whole, including animal and human studies, suggests rather consistently that potatoes can be a healthy part of a varied diet for most people, and they probably do not generally promote digestive problems, fat gain, or metabolic dysfunction. Nevertheless, I wouldn't recommend eating nothing but potatoes for any length of time. If you do choose to eat potatoes, follow these simple guidelines:
- Don't eat potatoes that are green, sprouting, blemished, or damaged
- Store them in a cool, dark place. They don't need to be refrigerated but it will extend their life
- Peel them before eating if you rely on them as a staple food
Saturday, March 26, 2011
Randy Tobler Show: Welcome
This morning, I had a conversation with Dr. Randy Tobler on his radio show "Vital Signs", on 97.1 FM News Talk in St Louis. Dr. Tobler is an obstetrician-gynecologist with an interest in nutrition, fitness and reproductive endocrinology from a holistic perspective. He asked me to appear on his show after he discovered my blog and found that we have some things in common, including an interest in evolutionary/ancestral health. We talked about the history of the American diet, the health of non-industrial cultures, what fats are healthiest, and the difference between pastured and conventional meat/dairy-- we took a few questions from listeners-- it was fun.
The show is available as a podcast here (3/26 show), although as far as I can tell, you need iTunes to listen to it. My section of the show starts around 8:20.
To everyone who arrived here after hearing me on the air this morning: welcome! Here are a few posts to give you a feel for what I do here at Whole Health Source:
The Coronary Heart Disease Epidemic
US Weight, Lifestyle and Diet Trends, 1970-2007
Butter vs. Margarine Showdown
Preventing and Reversing Tooth Decay
The Kitavans: Wisdom from the Pacific Islands
Potatoes and Human Health, Part I, Part II and Part III
Traditional Preparation Methods Improve Grains' Nutritional Value
Real Food XI: Sourdough Buckwheat Crepes
Glucose Tolerance in Non-industrial Cultures
Tropical Plant Fats: Palm Oil
It's Time to Let Go of the Glycemic Index
The show is available as a podcast here (3/26 show), although as far as I can tell, you need iTunes to listen to it. My section of the show starts around 8:20.
To everyone who arrived here after hearing me on the air this morning: welcome! Here are a few posts to give you a feel for what I do here at Whole Health Source:
The Coronary Heart Disease Epidemic
US Weight, Lifestyle and Diet Trends, 1970-2007
Butter vs. Margarine Showdown
Preventing and Reversing Tooth Decay
The Kitavans: Wisdom from the Pacific Islands
Potatoes and Human Health, Part I, Part II and Part III
Traditional Preparation Methods Improve Grains' Nutritional Value
Real Food XI: Sourdough Buckwheat Crepes
Glucose Tolerance in Non-industrial Cultures
Tropical Plant Fats: Palm Oil
It's Time to Let Go of the Glycemic Index
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