Denise Minger has just put up another great China Study post that's worth reading if you haven't already. Denise has been busy applying her statistics skills to the mountain of data the study collected. She noted in a previous post that wheat intake was strongly associated with coronary heart disease (CHD), the quintessential modern cardiovascular disease. I, and several other people, requested that she work her mathmagic to see if the association could be due to some other factor. For example, wheat is eaten mostly in the Northern regions of China, and CHD rates are generally higher at higher latitudes (vitamin D insufficiency?). This is true in Europe as well, and may be partly responsible for the purported benefits of the Mediterranean diet. You can mathematically determine if the association between wheat and CHD is simply due to the fact that wheat eaters live further North.
To make a long story short, nothing could explain the association except wheat itself, even latitude. Furthermore, she found a strong association between wheat intake and body mass index, typically a predictor of fat mass although we can't say that for sure. That finding echos a previous study in China where wheat eaters were more likely to be overweight than rice eaters (1, 2). Head over to Denise's post for the full story.
The China Study has major limitations built into its basic design, due to the fact that it was observational and pooled the blood samples of many individuals. Therefore, its findings can never prove anything, they can only suggest or be consistent with hypotheses. However, the study also has some unique advantages, such as a diversity of diets and regions, and the fact that people had presumably been eating a similar diet for a long time. I feel that Denise's efforts are really teasing out some useful information from the study that have been de-emphasized by other investigators.
There has been so little serious investigation into the health effects of wheat in the general population that I have to rely mostly on indirect evidence, such as the observation that the diseases of civilization tend to closely follow the introduction of white flour around the globe. Researchers studying celiac disease and other forms of gluten allergy, and the efforts of the paleolithic diet community in spreading that information (for example, Loren Cordain and Pedro Bastos), have been major contributors to understanding the health effects of wheat. Denise's analysis is one of the strongest pieces of evidence I've come by so far. One of these days, I'll post all of my references incriminating wheat. There are quite a few, although none of them is the smoking gun. I think there's enough indirect evidence that investigators should begin taking the idea seriously that wheat, particularly in the form of industrial flour products, may contribute to chronic disease in more than just a small subset of the population.
Showing posts with label overweight. Show all posts
Showing posts with label overweight. Show all posts
Thursday, September 2, 2010
Thursday, August 19, 2010
Tropical Plant Fats: Coconut Oil, Part II
Heart Disease: Animal Studies
Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.
The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:
Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.
In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.
What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.
Heart Disease: Human Studies
It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.
Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.
Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).
Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.
Coconut Oil and Body Fat
In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.
Coconut Oil and Cancer
Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.
The Bottom Line
There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.
* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.
Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.
The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:
- Sunflower oil plus added cholesterol
- Copra oil, a coconut oil pressed from dried coconuts, plus added cholesterol
- Freshly pressed virgin coconut oil, plus added cholesterol
Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.
In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.
What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.
Heart Disease: Human Studies
It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.
Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.
Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).
Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.
Coconut Oil and Body Fat
In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.
Coconut Oil and Cancer
Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.
The Bottom Line
There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.
* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.
Thursday, June 24, 2010
Interview with Jimmy Moore
About two months ago, I did an interview with Jimmy Moore of the Livin' la Vida Low Carb internet empire. I hardly remember what we talked about, but I think it went well. I enjoyed Jimmy's pleasant and open-minded attitude. Head over to Jimmy's website and listen to the interview here.
I do recall making at least one mistake. When discussing heart attacks,I said "atrial fibrillation" when I meant "ventricular fibrillation".
I do recall making at least one mistake. When discussing heart attacks,I said "atrial fibrillation" when I meant "ventricular fibrillation".
Wednesday, June 16, 2010
Low Micronutrient Intake may Contribute to Obesity
Lower Micronutrient Status in the Obese
Investigators have noted repeatedly that obese people have a lower blood concentration of a number of nutrients, including vitamin A, vitamin D, vitamin K, several B vitamins, zinc and iron (1). Although there is evidence that some of these may influence fat mass in animals, the evidence for a cause-and-effect relationship in humans is generally slim. There is quite a bit of indirect evidence that vitamin D status influences the risk of obesity (2), although a large, well-controlled study found that high-dose vitamin D3 supplementation does not cause fat loss in overweight and obese volunteers over the course of a year (3). It may still have a preventive effect, or require a longer timescale, but that remains to be determined.
Hot off the Presses
A new study in the journal Obesity, by Y. Li and colleagues, showed that compared to a placebo, a low-dose multivitamin caused obese volunteers to lose 7 lb (3.2 kg) of fat mass in 6 months, mostly from the abdominal region (4). The supplement also reduced LDL by 27%, increased HDL by a whopping 40% and increased resting energy expenditure. Here's what the supplement contained:
Vitamin A(containing natural mixed b-carotene) 5000 IU
Vitamin D 400 IU
Vitamin E 30 IU
Thiamin 1.5 mg
Riboflavin 1.7 mg
Vitamin B6 2 mg
Vitamin C 60 mg
Vitamin B12 6 mcg
Vitamin K1 25 mcg
Biotin 30 mcg
Folic acid 400 mcg
Nicotinamide 20 mg
Pantothenic acid 10 mg
Calcium 162 mg
Phosphorus 125 mg
Chlorine 36.3 mg
Magnesium 100 mg
Iron 18 mg
Copper 2 mg
Zinc 15 mg
Manganese 2.5 mg
Iodine 150 mcg
Chromium 25 mcg
Molybdenum 25 mcg
Selenium 25 mcg
Nickel 5 mcg
Stannum 10 mcg
Silicon 10 mcg
Vanadium 10 mcg
Although the result needs to be repeated, if we take it at face value, it has some important implications:
Does this mean we should all take multivitamins to stay or become thin? No. There is no multivitamin that can match the completeness and balance of a nutrient-dense, whole food, omnivorous diet. Beef liver, leafy greens and sunlight are nature's vitamin pills. Avoiding refined foods instantly doubles the micronutrient content of the typical diet. Properly preparing whole grains by soaking and fermentation is equivalent to taking a multi-mineral along with conventionally prepared grains, as absorption of key minerals is increased by 50-300% (10). Or you can eat root vegetables instead of grains, and enjoy their naturally high mineral availability. Or both.
Investigators have noted repeatedly that obese people have a lower blood concentration of a number of nutrients, including vitamin A, vitamin D, vitamin K, several B vitamins, zinc and iron (1). Although there is evidence that some of these may influence fat mass in animals, the evidence for a cause-and-effect relationship in humans is generally slim. There is quite a bit of indirect evidence that vitamin D status influences the risk of obesity (2), although a large, well-controlled study found that high-dose vitamin D3 supplementation does not cause fat loss in overweight and obese volunteers over the course of a year (3). It may still have a preventive effect, or require a longer timescale, but that remains to be determined.
Hot off the Presses
A new study in the journal Obesity, by Y. Li and colleagues, showed that compared to a placebo, a low-dose multivitamin caused obese volunteers to lose 7 lb (3.2 kg) of fat mass in 6 months, mostly from the abdominal region (4). The supplement also reduced LDL by 27%, increased HDL by a whopping 40% and increased resting energy expenditure. Here's what the supplement contained:
Vitamin A(containing natural mixed b-carotene) 5000 IU
Vitamin D 400 IU
Vitamin E 30 IU
Thiamin 1.5 mg
Riboflavin 1.7 mg
Vitamin B6 2 mg
Vitamin C 60 mg
Vitamin B12 6 mcg
Vitamin K1 25 mcg
Biotin 30 mcg
Folic acid 400 mcg
Nicotinamide 20 mg
Pantothenic acid 10 mg
Calcium 162 mg
Phosphorus 125 mg
Chlorine 36.3 mg
Magnesium 100 mg
Iron 18 mg
Copper 2 mg
Zinc 15 mg
Manganese 2.5 mg
Iodine 150 mcg
Chromium 25 mcg
Molybdenum 25 mcg
Selenium 25 mcg
Nickel 5 mcg
Stannum 10 mcg
Silicon 10 mcg
Vanadium 10 mcg
Although the result needs to be repeated, if we take it at face value, it has some important implications:
- The nutrient density of a diet may influence obesity risk, as I speculated in my recent audio interview and related posts (5, 6, 7, 8, 9).
- Many nutrients act together to create health, and multiple insufficiencies may contribute to disease. This may be why single nutrient supplementation trials usually don't find much.
- Another possibility is that obesity can result from a number of different nutrient insufficiencies, and the cause is different in different people. This study may have seen a large effect because it corrected many different insufficiencies.
- This result, once again, kills the simplistic notion that body fat is determined exclusively by voluntary food consumption and exercise behaviors (sometimes called the "calories in, calories out" idea, or "gluttony and sloth"). In this case, a multivitamin was able to increase resting energy expenditure and cause fat loss without any voluntary changes in food intake or exercise, suggesting metabolic effects and a possible downward shift of the body fat "setpoint" due to improved nutrient status.
Does this mean we should all take multivitamins to stay or become thin? No. There is no multivitamin that can match the completeness and balance of a nutrient-dense, whole food, omnivorous diet. Beef liver, leafy greens and sunlight are nature's vitamin pills. Avoiding refined foods instantly doubles the micronutrient content of the typical diet. Properly preparing whole grains by soaking and fermentation is equivalent to taking a multi-mineral along with conventionally prepared grains, as absorption of key minerals is increased by 50-300% (10). Or you can eat root vegetables instead of grains, and enjoy their naturally high mineral availability. Or both.
Tuesday, May 18, 2010
Intervew with Chris Kresser of The Healthy Skeptic
Last week, I did an audio interview with Chris Kresser of The Healthy Skeptic, on the topic of obesity. We put some preparation into it, and I think it's my best interview yet. Chris was a gracious host. We covered some interesting ground, including (list copied from Chris's post):
- The little known causes of the obesity epidemic
- Why the common weight loss advice to “eat less and exercise more” isn’t effective
- The long-term results of various weight loss diets (low-carb, low-fat, etc.)
- The body-fat setpoint and its relevance to weight regulation
- The importance of gut flora in weight regulation
- The role of industrial seed oils in the obesity epidemic
- Obesity as immunological and inflammatory disease
- Strategies for preventing weight gain and promoting weight loss
Friday, April 23, 2010
Have Seed Oils Caused a Multi-Generational Obesity Epidemic?
In 2006, Drs. Gerard Ailhaud and Philippe Guesnet hypothesized that industrial seed oils such as corn, soybean, safflower, sunflower and cottonseed oil are at least partially responsible for the current obesity epidemic (1). These oils were not a significant part of the human diet until very recently, yet they have been promoted due to their supposed ability to prevent cardiovascular disease. The Western world has been living a massive uncontrolled experiment ever since.
Linoleic acid is an omega-6 polyunsaturated fatty acid (PUFA) that makes up a large proportion of seed oils. It's a very bioactive molecule, in part because it's the precursor of two classes of signaling molecules (eicosanoids and endocannabinoids), some of which influence the development of fat tissue and regulate appetite.
Linoleic acid is an omega-6 polyunsaturated fatty acid (PUFA) that makes up a large proportion of seed oils. It's a very bioactive molecule, in part because it's the precursor of two classes of signaling molecules (eicosanoids and endocannabinoids), some of which influence the development of fat tissue and regulate appetite.
Dr. Ailhaud and his colleagues pointed out that not only are people eating far more linoleic acid than ever before; that very same linoleic acid is accumulating in our fat tissue and showing up in breast milk. Here are a few graphs to illustrate the point. The first graph is of PUFA consumption in the US over the last century, primarily reflecting seed oil intake (based on USDA food disappearance records):
Here's a graph of added fat intake based on USDA data. Added animal fats such as butter and lard have remained stable since 1970 (although total animal fat intake has declined), while seed oil consumption has gone from high to higher:
The following graph shows linoleic acid accumulation in human body fat over the last few decades in Western nations (mostly the US). I put this together based on two references (2, 3). I didn't find any data from the US past 1986. Linoleic acid, unlike most other fatty acids, accumulates disproportionately in body fat (4):
And finally, linoleic acid in the breast milk of US mothers, from Dr. Ailhaud's 2006 paper (the black dots):
In 2009, Dr. Ingeborg Hanbauer published a paper showing that when mice are fed a diet with a poor omega-6:3 balance (77:1), after three generations they develop adult obesity (5). Mice fed the same diet with a better omega-6:3 balance (9.5:1) did not develop obesity, and remained smaller overall. This shows that PUFA imbalance can cause multi-generational effects resulting in obesity and excessive tissue growth. Cmdr. Joseph Hibbeln, a collaborator of Dr. Bill Lands, was an author. The thing I don't like about this paper is they didn't quantify the obesity by measuring fat mass, so we have to take the authors' word that they had more fat.
This week, Dr. Florence Massiera and collaborators published a similar paper titled “A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations” (6). Drs. Ailhaud and Guesnet were both on this paper. They showed that a 35% fat diet with an omega-6:3 ratio of 28 caused obesity that progressively increased over four generations of mice. Although this study was more detailed than the study by Dr. Hanbauer and colleagues, it lacked a comparison group with a more favorable omega-6:3 balance to show that the obesity was specifically the result of omega-6:3 imbalance, rather than the fact that the diet was higher in fat overall or some other aspect of its composition.
If this is true in humans, it would be a straightforward explanation for the obesity epidemic that has plagued the Western world in recent decades. It would explain why the epidemic began in children around 1970, but didn’t show up in adults until about 1980. It would explain why the epidemic is less severe in Europe, and even less so in Asia. And of course, it correlates well with trends in seed oil consumption. This graph is based on US NHANES survey data:
We already know that a number of prenatal factors can have an effect on adult body fat levels in rodents, and observational studies have suggested that the same may apply to humans. If a mother’s body fat is full of linoleic acid, she will pass it on to the fetus as it grows, and after birth in breast milk, influencing its development.
As long-time followers of Whole Health Source know, I suspect industrial seed oils contribute to many of our modern ills. I can’t say for sure that seed oils are responsible for the current obesity epidemic, but the evidence certainly gives me pause. In any case, seed oils are an unnatural part of the human diet and it won’t hurt anyone to avoid them. The half-life of linoleic acid in fat tissue is about two years, so reducing it is a long-term prospect.
Sunday, April 18, 2010
Dinner with Taubes, Eades and Hujoel
Gary Taubes gave a lecture at UW last Thursday. Thanks to all the Whole Health Source readers who showed up. Gary's talk was titled "Why We Get Fat: Adiposity 101 and the Alternative Hypothesis of Obesity". He was hosted by Dr. Philippe Hujoel, the UW epidemiologist and dentist who authored the paper "Dietary Carbohydrates and Dental-Systemic Diseases" (1).
Gary's first target was the commonly held idea that obesity is simply caused by eating too much and exercising too little, and thus the cure is to eat less and exercise more. He used numerous examples from both humans and animals to show that fat mass is biologically regulated, rather than being the passive result of voluntary behaviors such as eating and exercise. He presented evidence of cultures remaining lean despite a huge and continuous surplus of food, as long as they stayed on their traditional diet. He also described how they subsequently became obese and diabetic on industrial foods (the Pima, for example).
He then moved into what he feels is the biological cause of obesity: excessive insulin keeping fat from exiting fat cells. It's true that insulin is a storage hormone, at the cellular level. However, fat mass regulation involves a dynamic interplay between many different interlacing systems that determine both overall energy intake and expenditure, as well as local availability of nutrients at the tissue level (i.e., how much fat gets into your fat tissue vs. your muscle tissue). I think the cause of obesity is likely to be more complex than insulin signaling.
He also offered the "carbohydrate hypothesis", which is the idea that carbohydrate, or at least refined carbohydrate, is behind the obesity epidemic and perhaps other metabolic problems. This is due to its ability to elevate insulin. I agree that refined carbohydrate, particularly white flour and sugar, is probably a central part of the problem. I'm also open to the possibility that some people in industrial nations are genuinely sensitive to carbohydrate regardless of what form it's in, although that remains to be rigorously tested. I don't think carbohydrate is sufficient to cause obesity per se, due to the many lean and healthy cultures that eat high carbohydrate diets*. Gary acknowledges this, and thinks there's probably another factor that's involved in allowing carbohydrate sensitivity to develop, for example excessive sugar.
I had the opportunity to speak with Gary at length on Thursday, as well as on Friday at dinner. Gary is a very nice guy-- a straightforward New York personality who's not averse to a friendly disagreement. In case any of you are wondering, he looks good. Good body composition, nice skin, hair and teeth (apologies to Gary for the analysis). Philippe and his wife took us out to a very nice restaurant, where we had a leisurely four-hour meal, and Dr. Mike Eades was in town so he joined us as well. Mike has a strong Southern accent and is also a pleasant guy. Philippe and his wife are generous and engaging people. It was a great evening. The restaurant was nice enough that I wasn't going to be picky about the food-- I ate everything that was put in front of me and enjoyed it.
* I'm talking about prevention rather than cure here. I acknowledge that many people have had great success losing fat using low-carbohydrate diets, including two gentlemen I met on Thursday.
Gary's first target was the commonly held idea that obesity is simply caused by eating too much and exercising too little, and thus the cure is to eat less and exercise more. He used numerous examples from both humans and animals to show that fat mass is biologically regulated, rather than being the passive result of voluntary behaviors such as eating and exercise. He presented evidence of cultures remaining lean despite a huge and continuous surplus of food, as long as they stayed on their traditional diet. He also described how they subsequently became obese and diabetic on industrial foods (the Pima, for example).
He then moved into what he feels is the biological cause of obesity: excessive insulin keeping fat from exiting fat cells. It's true that insulin is a storage hormone, at the cellular level. However, fat mass regulation involves a dynamic interplay between many different interlacing systems that determine both overall energy intake and expenditure, as well as local availability of nutrients at the tissue level (i.e., how much fat gets into your fat tissue vs. your muscle tissue). I think the cause of obesity is likely to be more complex than insulin signaling.
He also offered the "carbohydrate hypothesis", which is the idea that carbohydrate, or at least refined carbohydrate, is behind the obesity epidemic and perhaps other metabolic problems. This is due to its ability to elevate insulin. I agree that refined carbohydrate, particularly white flour and sugar, is probably a central part of the problem. I'm also open to the possibility that some people in industrial nations are genuinely sensitive to carbohydrate regardless of what form it's in, although that remains to be rigorously tested. I don't think carbohydrate is sufficient to cause obesity per se, due to the many lean and healthy cultures that eat high carbohydrate diets*. Gary acknowledges this, and thinks there's probably another factor that's involved in allowing carbohydrate sensitivity to develop, for example excessive sugar.
I had the opportunity to speak with Gary at length on Thursday, as well as on Friday at dinner. Gary is a very nice guy-- a straightforward New York personality who's not averse to a friendly disagreement. In case any of you are wondering, he looks good. Good body composition, nice skin, hair and teeth (apologies to Gary for the analysis). Philippe and his wife took us out to a very nice restaurant, where we had a leisurely four-hour meal, and Dr. Mike Eades was in town so he joined us as well. Mike has a strong Southern accent and is also a pleasant guy. Philippe and his wife are generous and engaging people. It was a great evening. The restaurant was nice enough that I wasn't going to be picky about the food-- I ate everything that was put in front of me and enjoyed it.
* I'm talking about prevention rather than cure here. I acknowledge that many people have had great success losing fat using low-carbohydrate diets, including two gentlemen I met on Thursday.
Tuesday, April 13, 2010
Interview with John Barban
I recently did a podcast interview with John Barban from the Adonis Lifestyle blog. We talked mostly about fat mass and the body fat "setpoint". As it turns out, what I said must have been at odds with John's philosophy, because he posted another podcast the next week that appears to be about why he disagrees with me!
Anyway, enjoy the interview.
I did another one recently with Jimmy Moore that's coming soon.
Anyway, enjoy the interview.
I did another one recently with Jimmy Moore that's coming soon.
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