Mark Sisson has been a central figure in the evolutionary health community since he began his weblog Mark's Daily Apple in 2006. He and his staff have been posting daily on his blog ever since. He has also written several other books, edited the Optimum Health newsletter, competed as a high-level endurance athlete, and served on the International Triathlon Union as the anti-doping chairman, all of which you can read about on his biography page. Mark is a practice-what-you-preach kind of guy, and if physical appearance means anything, he's on to something.
In 2009, Mark published his long-awaited book The Primal Blueprint. He self-published the book, which has advantages and disadvantages. The big advantage is that you aren't subject to the sometimes onerous demands of publishers, who attempt to maximize sales at Barnes and Noble. The front cover sports a simple picture of Mark, rather than a sunbaked swimsuit model, and the back cover offers no ridiculous claims of instant beauty and fat loss.
The drawback of self-publishing is it's more difficult to break into a wider market. That's why Mark has asked me to publish my review of his book today. He's trying to push it up in the Amazon.com rankings so that it gets a broader exposure. If you've been thinking about buying Mark's book, now is a good time to do it. If you order it from Amazon.com on March 17th, Mark is offering to sweeten the deal with some freebies on his site Mark's Daily Apple. Full disclosure: I'm not getting anything out of this, I'm simply mentioning it because I was reviewing Mark's book anyway and I thought some readers might enjoy it.
The Primal Blueprint is not a weight loss or diet book, it's a lifestyle program with an evolutionary slant. Mark uses the example of historical and contemporary hunter-gatherers as a model, and attempts to apply those lessons to life in the 21st century. He does it in a way that's empowering accessible to nearly everyone. To illustrate his points, he uses the example of an archetypal hunter-gatherer called Grok, and his 21st century mirror image, the Korg family.
The diet section will be familiar to anyone who has read about "paleolithic"-type diets. He advocates eating meats including organs, seafood, eggs, nuts, abundant vegetables, and fruit. He also suggests avoiding grains, legumes, dairy (although he's not very militant about this one), processed food in general, and reducing carbohydrate to less than 150 grams per day. I like his diet suggestions because they focus on real food. Mark is not a drill sergeant. He tries to create a plan that will be sustainable in the long run, by staying positive and allowing for cheats.
We part ways on the issue of carbohydrate. He suggests that eating more than 150 grams of carbohydrate per day leads to fat gain and disease, whereas I feel that position is untenable in light of what we know of non-industrial cultures (including some relatively high-carbohydrate hunter-gatherers). Although carbohydrate restriction (or at least wheat and sugar restriction) does have its place in treating obesity and metabolic dysfunction in modern populations, ultimately I don't think it's necessary for the prevention of those same problems, and it can even be counterproductive in some cases. Mark does acknowledge that refined carbohydrates are the main culprits.
The book's diet section also recommends nutritional supplements, including a multivitamin/mineral, antioxidant supplement, probiotics, protein powder and fish oil. I'm not a big proponent of supplementation. I'm also a bit of a hypocrite because I do take small doses of fish oil (when I haven't had seafood recently), and vitamin D in wintertime. But I can't get behind protein powders and antioxidant supplements.
Mark's suggestions for exercise, sun exposure, sleep and stress management make good sense to me. In a nutshell: do all three, but keep the exercise varied and don't overdo it. As a former high-level endurance athlete, he has a lot of credibility here. He puts everything in a format that's practical, accessible and empowering.
I think The Primal Blueprint is a useful book for a person who wants to maintain or improve her health. Although we disagree on the issue of carbohydrate, the diet and lifestyle advice is solid and will definitely be a vast improvement over what the average person is doing. The Primal Blueprint is not an academic book, nor does it attempt to be. It doesn't contain many references (although it does contain some), and it won't satisfy someone looking for an in-depth discussion of the scientific literature. However, it's perfect for someone who's getting started and needs guidance, or who simply wants a more comprehensive source than reading blog snippets. It would make a great gift for that family member or friend who's been asking how you stay in such good shape.
Showing posts with label low-carb. Show all posts
Showing posts with label low-carb. Show all posts
Wednesday, March 17, 2010
Sunday, January 31, 2010
The Body Fat Setpoint, Part IV: Changing the Setpoint
Prevention is Easier than Cure
Experiments in animals have confirmed what common sense suggests: it's easier to prevent health problems than to reverse them. Still, many health conditions can be improved, and in some cases reversed, through lifestyle interventions. It's important to have realistic expectations and to be kind to oneself. Cultivating a drill sergeant mentality will not improve quality of life, and isn't likely to be sustainable.
Fat Loss: a New Approach
If there's one thing that's consistent in the medical literature, it's that telling people to eat fewer calories does not help them lose weight in the long term. Gary Taubes has written about this at length in his book Good Calories, Bad Calories, and in his upcoming book on body fat. Many people who use this strategy see transient fat loss, followed by fat regain and a feeling of defeat. There's a simple reason for it: the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.
Therefore, what we need for sustainable fat loss is not starvation; we need a treatment that lowers the fat mass setpoint. There are several criteria that this treatment will have to meet to qualify:
Strategies: Diet Pattern
The most obvious treatment that fits all of my criteria is low-carbohydrate dieting. Overweight people eating low-carbohydrate diets generally lose fat and spontaneously reduce their calorie intake. In fact, in several diet studies, investigators compared an all-you-can-eat low-carbohydrate diet with a calorie-restricted low-fat diet. The low-carbohydrate dieters generally reduced their calorie intake and body fat to a similar or greater degree than the low-fat dieters, despite the fact that they ate all the calories they wanted (1). This suggest that their fat mass setpoint had changed. At this point, I think moderate carbohydrate restriction may be preferable to strict carbohydrate restriction for some people, due to the increasing number of reports I've read of people doing poorly in the long run on extremely low-carbohydrate diets (2).
Another strategy that appears effective is the "paleolithic" diet. In Dr. Staffan Lindeberg's 2007 diet study, overweight volunteers with heart disease lost fat and reduced their calorie intake to a remarkable degree while eating a diet consistent with our hunter-gatherer heritage (3). This result is consistent with another diet trial of the paleolithic diet in diabetics (4). In post hoc analysis, Dr. Lindeberg's group showed that the reduction in weight was apparently independent of changes in carbohydrate intake*. This suggests that the paleolithic diet has health benefits that are independent of carbohydrate intake.
Strategies: Gastrointestinal Health
Since the gastrointestinal (GI) tract is so intimately involved in body fat metabolism and overall health (see the former post), the next strategy is to improve GI health. There are a number of ways to do this, but they all center around four things:
Oligofructose is similar to inulin, a fiber that occurs naturally in a wide variety of plants. Good sources are jerusalem artichokes, jicama, artichokes, onions, leeks, burdock and chicory root. Certain non-industrial cultures had a high intake of inulin. There are some caveats to inulin, however: inulin and oligofructose can cause gas, and can also exacerbate gastroesophageal reflux disorder (9). So don't eat a big plate of jerusalem artichokes before that important date.
The colon is packed with symbiotic bacteria, and is the site of most intestinal fermentation. The small intestine contains fewer bacteria, but gut barrier function there is critical as well. The small intestine is where the GI doctor will take a biopsy to look for celiac disease. Celiac disease is a degeneration of the small intestinal lining due to an autoimmune reaction caused by gluten (in wheat, barley and rye). This brings us to one of the most important elements of maintaining gut barrier health: avoiding food sensitivities. Gluten and casein (in dairy protein) are the two most common offenders. Gluten sensitivity is widespread and typically undiagnosed (10).
Eating raw fermented foods such as sauerkraut, kimchi, yogurt and half-sour pickles also helps maintain the integrity of the upper GI tract. I doubt these have any effect on the colon, given the huge number of bacteria already present. Other important factors in gut barrier health are keeping the ratio of omega-6 to omega-3 fats in balance, eating nutrient-dense food, and avoiding the questionable chemical additives in processed food. If triglycerides are important for leptin sensitivity, then avoiding sugar and ensuring a regular source of omega-3 should aid weight loss as well.
Strategies: Micronutrients
As I discussed in the last post, micronutrient deficiency probably plays a role in obesity, both in ways that we understand and ways that we (or I) don't. Eating a diet that has a high nutrient density and ensuring a good vitamin D status will help any sustainable fat loss strategy. The easiest way to do this is to eliminate industrially processed foods such as white flour, sugar and seed oils. These constitute more than 50% of calories for the average Westerner.
After that, you can further increase your diet's nutrient density by learning to properly prepare grains and legumes to maximize their nutritional value and digestibility (11, 12; or by avoiding grains and legumes altogether if you wish), selecting organic and/or pasture-raised foods if possible, and eating seafood including seaweed. One of the problems with extremely low-carbohydrate diets is that they may be low in water-soluble micronutrients, although this isn't necessarily the case.
Strategies: Miscellaneous
In general, exercise isn't necessarily helpful for fat loss. However, there is one type of exercise that clearly is: high-intensity intermittent training (HIIT). It's basically a fancy name for sprints. They can be done on a track, on a stationary bicycle, using weight training circuits, or any other way that allows sufficient intensity. The key is to achieve maximal exertion for several brief periods, separated by rest. This type of exercise is not about burning calories through exertion: it's about increasing hormone sensitivity using an intense, brief stressor (hormesis). Even a ridiculously short period of time spent training HIIT each week can result in significant fat loss, despite no change in diet or calorie intake (13).
Anecdotally, many people have had success using intermittent fasting (IF) for fat loss. There's some evidence in the scientific literature that IF and related approaches may be helpful (14). There are different approaches to IF, but a common and effective method is to do two complete 24-hour fasts per week. It's important to note that IF isn't about restricting calories, it's about resetting the fat mass setpoint. After a fast, allow yourself to eat quality food until you're no longer hungry.
Insufficient sleep has been strongly and repeatedly linked to obesity. Whether it's a cause or consequence of obesity I can't say for sure, but in any case it's important for health to sleep until you feel rested. If your sleep quality is poor due to psychological stress, meditating before bedtime may help. I find that meditation has a remarkable effect on my sleep quality. Due to the poor development of oral and nasal structures in industrial nations, many people do not breathe effectively and may suffer from conditions such as sleep apnea that reduce sleep quality. Overweight also contributes to these problems.
I'm sure there are other useful strategies, but that's all I have for now. If you have something to add, please put it in the comments.
* Since reducing carbohydrate intake wasn't part of the intervention, this result is observational.
Experiments in animals have confirmed what common sense suggests: it's easier to prevent health problems than to reverse them. Still, many health conditions can be improved, and in some cases reversed, through lifestyle interventions. It's important to have realistic expectations and to be kind to oneself. Cultivating a drill sergeant mentality will not improve quality of life, and isn't likely to be sustainable.
Fat Loss: a New Approach
If there's one thing that's consistent in the medical literature, it's that telling people to eat fewer calories does not help them lose weight in the long term. Gary Taubes has written about this at length in his book Good Calories, Bad Calories, and in his upcoming book on body fat. Many people who use this strategy see transient fat loss, followed by fat regain and a feeling of defeat. There's a simple reason for it: the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.
Therefore, what we need for sustainable fat loss is not starvation; we need a treatment that lowers the fat mass setpoint. There are several criteria that this treatment will have to meet to qualify:
- It must cause fat loss
- It must not involve deliberate calorie restriction
- It must maintain fat loss over a long period of time
- It must not be harmful to overall health
Strategies: Diet Pattern
The most obvious treatment that fits all of my criteria is low-carbohydrate dieting. Overweight people eating low-carbohydrate diets generally lose fat and spontaneously reduce their calorie intake. In fact, in several diet studies, investigators compared an all-you-can-eat low-carbohydrate diet with a calorie-restricted low-fat diet. The low-carbohydrate dieters generally reduced their calorie intake and body fat to a similar or greater degree than the low-fat dieters, despite the fact that they ate all the calories they wanted (1). This suggest that their fat mass setpoint had changed. At this point, I think moderate carbohydrate restriction may be preferable to strict carbohydrate restriction for some people, due to the increasing number of reports I've read of people doing poorly in the long run on extremely low-carbohydrate diets (2).
Another strategy that appears effective is the "paleolithic" diet. In Dr. Staffan Lindeberg's 2007 diet study, overweight volunteers with heart disease lost fat and reduced their calorie intake to a remarkable degree while eating a diet consistent with our hunter-gatherer heritage (3). This result is consistent with another diet trial of the paleolithic diet in diabetics (4). In post hoc analysis, Dr. Lindeberg's group showed that the reduction in weight was apparently independent of changes in carbohydrate intake*. This suggests that the paleolithic diet has health benefits that are independent of carbohydrate intake.
Strategies: Gastrointestinal Health
Since the gastrointestinal (GI) tract is so intimately involved in body fat metabolism and overall health (see the former post), the next strategy is to improve GI health. There are a number of ways to do this, but they all center around four things:
- Don't eat food that encourages the growth of harmful bacteria
- Eat food that encourages the growth of good bacteria
- Don't eat food that impairs gut barrier function
- Eat food that promotes gut barrier health
Oligofructose is similar to inulin, a fiber that occurs naturally in a wide variety of plants. Good sources are jerusalem artichokes, jicama, artichokes, onions, leeks, burdock and chicory root. Certain non-industrial cultures had a high intake of inulin. There are some caveats to inulin, however: inulin and oligofructose can cause gas, and can also exacerbate gastroesophageal reflux disorder (9). So don't eat a big plate of jerusalem artichokes before that important date.
The colon is packed with symbiotic bacteria, and is the site of most intestinal fermentation. The small intestine contains fewer bacteria, but gut barrier function there is critical as well. The small intestine is where the GI doctor will take a biopsy to look for celiac disease. Celiac disease is a degeneration of the small intestinal lining due to an autoimmune reaction caused by gluten (in wheat, barley and rye). This brings us to one of the most important elements of maintaining gut barrier health: avoiding food sensitivities. Gluten and casein (in dairy protein) are the two most common offenders. Gluten sensitivity is widespread and typically undiagnosed (10).
Eating raw fermented foods such as sauerkraut, kimchi, yogurt and half-sour pickles also helps maintain the integrity of the upper GI tract. I doubt these have any effect on the colon, given the huge number of bacteria already present. Other important factors in gut barrier health are keeping the ratio of omega-6 to omega-3 fats in balance, eating nutrient-dense food, and avoiding the questionable chemical additives in processed food. If triglycerides are important for leptin sensitivity, then avoiding sugar and ensuring a regular source of omega-3 should aid weight loss as well.
Strategies: Micronutrients
As I discussed in the last post, micronutrient deficiency probably plays a role in obesity, both in ways that we understand and ways that we (or I) don't. Eating a diet that has a high nutrient density and ensuring a good vitamin D status will help any sustainable fat loss strategy. The easiest way to do this is to eliminate industrially processed foods such as white flour, sugar and seed oils. These constitute more than 50% of calories for the average Westerner.
After that, you can further increase your diet's nutrient density by learning to properly prepare grains and legumes to maximize their nutritional value and digestibility (11, 12; or by avoiding grains and legumes altogether if you wish), selecting organic and/or pasture-raised foods if possible, and eating seafood including seaweed. One of the problems with extremely low-carbohydrate diets is that they may be low in water-soluble micronutrients, although this isn't necessarily the case.
Strategies: Miscellaneous
In general, exercise isn't necessarily helpful for fat loss. However, there is one type of exercise that clearly is: high-intensity intermittent training (HIIT). It's basically a fancy name for sprints. They can be done on a track, on a stationary bicycle, using weight training circuits, or any other way that allows sufficient intensity. The key is to achieve maximal exertion for several brief periods, separated by rest. This type of exercise is not about burning calories through exertion: it's about increasing hormone sensitivity using an intense, brief stressor (hormesis). Even a ridiculously short period of time spent training HIIT each week can result in significant fat loss, despite no change in diet or calorie intake (13).
Anecdotally, many people have had success using intermittent fasting (IF) for fat loss. There's some evidence in the scientific literature that IF and related approaches may be helpful (14). There are different approaches to IF, but a common and effective method is to do two complete 24-hour fasts per week. It's important to note that IF isn't about restricting calories, it's about resetting the fat mass setpoint. After a fast, allow yourself to eat quality food until you're no longer hungry.
Insufficient sleep has been strongly and repeatedly linked to obesity. Whether it's a cause or consequence of obesity I can't say for sure, but in any case it's important for health to sleep until you feel rested. If your sleep quality is poor due to psychological stress, meditating before bedtime may help. I find that meditation has a remarkable effect on my sleep quality. Due to the poor development of oral and nasal structures in industrial nations, many people do not breathe effectively and may suffer from conditions such as sleep apnea that reduce sleep quality. Overweight also contributes to these problems.
I'm sure there are other useful strategies, but that's all I have for now. If you have something to add, please put it in the comments.
* Since reducing carbohydrate intake wasn't part of the intervention, this result is observational.
Friday, December 4, 2009
Dr. Rosedale Replies
A few months ago, I posted link to an article by Dr. Ron Rosedale and made a few comments about it. Dr. Rosedale has sent a reply to my comments, which I have agreed to publish as a new post because they may be of interest to readers. In the following exchange, my numbered comments are in quotes and Dr. Rosedale's replies follow them.
Dr. Rosedale's Comments
Furthermore, insulin's major purpose goes way beyond sugar. At the very least, it is a nutrient storage hormone being relevant not only in glucose storage, but also in fat and protein (amino acid) storage. It also plays a significant role in micronutrient storage and conversions. However, overwhelmingly more important, is insulin's role as a nutrient sensor greatly influencing genetic expression and modifying the rate of aging by up or down regulating maintenance and repair.
Stephan himself could answer this one. It's not the percent of calories from carbohydrates that is relevant; it is the absolute amount of non-fiber carbohydrates that is relevant as the glycemic load.
A few further comments on the Kitavans, though I really am not an expert on their diet:
I find that indigenous diets are only partially helpful as there are so many variables that can go unaccounted for. I prefer the more elementary sciences to form opinions. However, it sounds like there really isn't that much non-fiber carbohydrate in the diet and there is considerable fiber, fish and coconut oil, and moderate to low protein, all of which are quite fine for health. If it is known, the total gram quantities of macronutrients would be good to know. Another important point; what is their lifespan? It sounds like it might be long, but it would be nice to know a more accurate figure. It is not weight loss that we should be after, it is health as indicated by a long and youthful lifespan. Another point; though they (the Kitavans) may be doing well if one defines well as better than most human counterparts, it isn't really saying much. The majority of society eats so badly that it really is not difficult to eat a diet that is better. What I am after is not just better, but best. Perhaps one could take the Kitavan diet and improve upon it by reducing the non-fiber carbohydrate content and perhaps adding more beneficial fats and oils. It is quite possible, in fact probable, that there have been no human societies that have eaten an ideal diet. We can only use what modern science is telling us to come up with this.
My Reply to Dr. Rosedale
Thank you for your comments.
1. I agree with you that control of blood sugar is not insulin's only purpose, and that there are other mechanisms of blood glucose control. There were several papers published recently showing that type 1 diabetic rats (lacking insulin) can be restored to a normal blood glucose level and near-normal glucose tolerance by infusing leptin into the lateral or the third cerebral ventricles (1, 2). This was totally independent of insulin, because the rats weren't producing any. And yes, insulin signaling influences lifespan in a number of animal models.
However, insulin is still the primary controller of blood sugar under normal circumstances, as shown in type 1 diabetes where the primary defect is in insulin production. Furthermore, excessively elevated glucose is damaging per se, due to protein glycation, competition with vitamin C, etc. Therefore, the glucose-controlling function of insulin is important.
I do not agree that glucose from starch and fruit played an insignificant role in human evolution. A number of modern hunter-gatherers eat a significant amount of starch, and our ancestors probably did as well, as soon as they could cook. The timeline of cooking is debated, but we've probably been doing it for at least half a million years, or as long as Homo sapiens has existed. Fruit sugar is roughly 50% glucose, as is honey.
2. As someone who spent two years in the field of aging research, I don't see a scientific consensus on the idea that reproduction and aging are in balance with one another. The two correlate with one another in some, but not all models. I was at a seminar just the other day by Dr. Linda Partridge, from the Max Planck institute, and she was talking about her lifespan experiments in fruit flies. She was able to independently modify lifespan and fecundity using amino acid restriction, leading her to the conclusion that there is no link between the two in her model. She published these data recently in the journal Nature (reference).
Regarding the energy required for cellular maintenance, a little math is instructive here. I eat maybe 3,200 calories a day, which is normal for an active male of my weight. My basal metabolic rate is roughly 1,700 kcal per day. So 1,500 of my calories have already gone to moving my skeletal muscles. Of the basal metabolic rate, the vast majority comes from maintaining body temperature. Thermogenesis is why cold-blooded animals only need to eat a fraction of the calories mammals do. Then there's cardiac function, and smooth muscle activity, which eat up more calories. Then there are the energy-intensive cellular processes of maintaining ionic gradients across cell membranes (which is why the brain eats up 20% of our calories) and protein synthesis.
After you subtract out all those functions, only a small fraction of total caloric intake is left for other cellular processes. So the caloric needs for processes that combat cellular aging (DNA repair, etc.) are quite low, compared to overall energy requirements. This is consistent with the fact that naked mole rats, which live ten times longer than Rattus norvegicus, have a similar basal metabolic rate to one another. Keeping cells from being damaged is not a particularly energy-intensive process, and so we have to look elsewhere for the reason why it hasn't been prioritized by evolution.
3. The Kitavan diet is high in digestible starch. The foods they eat have been characterized for starch content, glycemic index, and fiber content. Their diet overall has a high glycemic load, is 69% carbohydrate by calories, and is similar in calories to the American diet. They have a low BMI, a low fasting insulin and low fasting glucose. I agree that there are many factors at play here, and the example of the Kitavans doesn't necessarily give carbohydrate a free pass in all situations. But it does show that a high carbohydrate intake, at least under certain circumstances, is compatible with low fasting insulin, high insulin sensitivity, leanness, and apparent good health.
I also agree that the Kitavans are not really a good model of longevity. Although they live a long time relative to other non-industrial cultures, and have individuals exceeding 95 years old, they don't have a longer average lifespan than people in affluent nations. One can guess that it's due to a lack of modern medical care to treat infectious diseases, and I think that's likely to play a role, but ultimately it's speculation. It's an open question whether you could improve their lifespan by reducing the non-fiber carbohydrate content of their diet, but I'm skeptical.
In the end, it's also an open question whether or not you can extend life by restricting carbohydrate. For the typical overweight American who responds well to carbohydrate restriction, it's reasonable to speculate that it might. For an insulin-sensitive, lean American, it's not clear that it would have much benefit, outside of reducing potentially harmful foods such as gluten and sugar. Although insulin signaling is probably tied up with lifespan in humans, as in many other species, no one has shown that post-meal insulin spikes caused by carbohydrate, as opposed to chronically elevated insulin and insulin resistance, is harmful. The story is not as simple as "more serum insulin = shorter lifespan".
Is there any evidence that carbohydrate restriction extends lifespan in a non-carnivorous mammal such as a rodent or monkey? I'm open to the possibility, but I haven't seen any studies. I'll look forward to them.
Dr. Rosedale's Comments
1. Dr. Rosedale says that insulin's ability to regulate blood sugar is a minor role, and that other hormones do the same thing. Tell that to a type 1 diabetic. Excessive blood glucose is Not Good, and that's what you get if there isn't enough insulin around.What I have said was that insulin does not control glucose levels in the blood, and that insulin's biological purpose (not ability) plays only a minor role in BS control... and that is a correct statement. Insulin reduces blood glucose by storing it for a rainy day as glycogen and fat, but not for the purpose of regulating blood sugar levels. The control of BS is in an upward direction, not a downward direction. The problem in our evolutionary history was to have enough BS for emergency anaerobic respiration and for those tissues that require it such as red blood cells. Lowering blood sugar was never a priority in our history. For one, it didn't rise much very often. There wasn't much glucose around. Uncooked rice and potatoes, etc., are mostly indigestible. The sugar that was around, such as in fruit, required considerable effort to obtain therefore lowered the sugar prior to obtaining it. Also, the sugar that is in fruit is largely fructose which doesn't convert that much into glucose but rather into fat in the liver. Even if it did raise blood sugar levels, even if it did cause diabetes in evolutionary time, nature would consider that irrelevant as it wouldn't have killed people prior to the reproductive years, only post-reproductively when nature doesn't give a damn.
Furthermore, insulin's major purpose goes way beyond sugar. At the very least, it is a nutrient storage hormone being relevant not only in glucose storage, but also in fat and protein (amino acid) storage. It also plays a significant role in micronutrient storage and conversions. However, overwhelmingly more important, is insulin's role as a nutrient sensor greatly influencing genetic expression and modifying the rate of aging by up or down regulating maintenance and repair.
2. I'm not convinced by the theory that organisms balance reproduction and repair, emphasizing one at the expense of the other. The amount of energy it takes to fuel cellular repair processes is negligible compared to the amount it takes to maintain body temperature, fuel the brain and contract skeletal muscles. Why not just have the organism eat an extra half-teaspoon of mashed potatoes to fuel the heat-shock proteins and make a little extra catalase? I think the true reasons behind lifespan extension upon caloric restriction will turn out to be more complex than a balance between reproduction and repair.Stephan does not have to be convinced. Almost everybody who studies the biology of aging is convinced that there is a dichotomy between reproduction and maintenance and repair and that biologically a cell can spend the majority of available resources towards one or the other, but not both. This can actually be shown genetically as the up or down regulation of the expression of genes regulating heat shock proteins, intracellular antioxidant systems, DNA repair enzymes, "garbage collection", etc versus the up or down regulation of genes which regulate reproductive behavior. It should also be noted that excessive reproductive behavior is, in individual cells of multicellular organisms, a strong predisposition to cancer. Furthermore, Stephan’s statement that it takes negligible energy for maintenance and repair is very wrong. In fact one could make the argument that almost all of the energy spent by both individual cells and by the cell societies of multi-celled organisms when not reproducing is towards maintenance and repair.
3. I disagree with the idea that carbohydrate itself is behind elevated fasting insulin and leptin. Just look at the Kitavans. They get 69% of their calories from high-glycemic-load carbohydrates, with not much fat (21%) or protein (10%) to slow digestion. Yet, they have low fasting insulin and remarkably low fasting leptin. I believe the fasting levels of these hormones are more responsive to macronutrient quality than quantity. In other words, what matters most is not how much carbohydrate is in the diet, but where the carbohydrate comes from. The modern Western combination of carelessly processed wheat, sugar and linoleic acid-rich vegetable oil seems to be particularly harmful.It is not where the carbohydrates come from, but where the carbohydrates go. In other words, what carbohydrates are digested into, i.e what the cells are being fed. Feeding them glucose, fructose, galactose and amino acids as energy (as opposed to using the amino acids whole as structural components) is bad.
Stephan himself could answer this one. It's not the percent of calories from carbohydrates that is relevant; it is the absolute amount of non-fiber carbohydrates that is relevant as the glycemic load.
A few further comments on the Kitavans, though I really am not an expert on their diet:
I find that indigenous diets are only partially helpful as there are so many variables that can go unaccounted for. I prefer the more elementary sciences to form opinions. However, it sounds like there really isn't that much non-fiber carbohydrate in the diet and there is considerable fiber, fish and coconut oil, and moderate to low protein, all of which are quite fine for health. If it is known, the total gram quantities of macronutrients would be good to know. Another important point; what is their lifespan? It sounds like it might be long, but it would be nice to know a more accurate figure. It is not weight loss that we should be after, it is health as indicated by a long and youthful lifespan. Another point; though they (the Kitavans) may be doing well if one defines well as better than most human counterparts, it isn't really saying much. The majority of society eats so badly that it really is not difficult to eat a diet that is better. What I am after is not just better, but best. Perhaps one could take the Kitavan diet and improve upon it by reducing the non-fiber carbohydrate content and perhaps adding more beneficial fats and oils. It is quite possible, in fact probable, that there have been no human societies that have eaten an ideal diet. We can only use what modern science is telling us to come up with this.
My Reply to Dr. Rosedale
Thank you for your comments.
1. I agree with you that control of blood sugar is not insulin's only purpose, and that there are other mechanisms of blood glucose control. There were several papers published recently showing that type 1 diabetic rats (lacking insulin) can be restored to a normal blood glucose level and near-normal glucose tolerance by infusing leptin into the lateral or the third cerebral ventricles (1, 2). This was totally independent of insulin, because the rats weren't producing any. And yes, insulin signaling influences lifespan in a number of animal models.
However, insulin is still the primary controller of blood sugar under normal circumstances, as shown in type 1 diabetes where the primary defect is in insulin production. Furthermore, excessively elevated glucose is damaging per se, due to protein glycation, competition with vitamin C, etc. Therefore, the glucose-controlling function of insulin is important.
I do not agree that glucose from starch and fruit played an insignificant role in human evolution. A number of modern hunter-gatherers eat a significant amount of starch, and our ancestors probably did as well, as soon as they could cook. The timeline of cooking is debated, but we've probably been doing it for at least half a million years, or as long as Homo sapiens has existed. Fruit sugar is roughly 50% glucose, as is honey.
2. As someone who spent two years in the field of aging research, I don't see a scientific consensus on the idea that reproduction and aging are in balance with one another. The two correlate with one another in some, but not all models. I was at a seminar just the other day by Dr. Linda Partridge, from the Max Planck institute, and she was talking about her lifespan experiments in fruit flies. She was able to independently modify lifespan and fecundity using amino acid restriction, leading her to the conclusion that there is no link between the two in her model. She published these data recently in the journal Nature (reference).
Regarding the energy required for cellular maintenance, a little math is instructive here. I eat maybe 3,200 calories a day, which is normal for an active male of my weight. My basal metabolic rate is roughly 1,700 kcal per day. So 1,500 of my calories have already gone to moving my skeletal muscles. Of the basal metabolic rate, the vast majority comes from maintaining body temperature. Thermogenesis is why cold-blooded animals only need to eat a fraction of the calories mammals do. Then there's cardiac function, and smooth muscle activity, which eat up more calories. Then there are the energy-intensive cellular processes of maintaining ionic gradients across cell membranes (which is why the brain eats up 20% of our calories) and protein synthesis.
After you subtract out all those functions, only a small fraction of total caloric intake is left for other cellular processes. So the caloric needs for processes that combat cellular aging (DNA repair, etc.) are quite low, compared to overall energy requirements. This is consistent with the fact that naked mole rats, which live ten times longer than Rattus norvegicus, have a similar basal metabolic rate to one another. Keeping cells from being damaged is not a particularly energy-intensive process, and so we have to look elsewhere for the reason why it hasn't been prioritized by evolution.
3. The Kitavan diet is high in digestible starch. The foods they eat have been characterized for starch content, glycemic index, and fiber content. Their diet overall has a high glycemic load, is 69% carbohydrate by calories, and is similar in calories to the American diet. They have a low BMI, a low fasting insulin and low fasting glucose. I agree that there are many factors at play here, and the example of the Kitavans doesn't necessarily give carbohydrate a free pass in all situations. But it does show that a high carbohydrate intake, at least under certain circumstances, is compatible with low fasting insulin, high insulin sensitivity, leanness, and apparent good health.
I also agree that the Kitavans are not really a good model of longevity. Although they live a long time relative to other non-industrial cultures, and have individuals exceeding 95 years old, they don't have a longer average lifespan than people in affluent nations. One can guess that it's due to a lack of modern medical care to treat infectious diseases, and I think that's likely to play a role, but ultimately it's speculation. It's an open question whether you could improve their lifespan by reducing the non-fiber carbohydrate content of their diet, but I'm skeptical.
In the end, it's also an open question whether or not you can extend life by restricting carbohydrate. For the typical overweight American who responds well to carbohydrate restriction, it's reasonable to speculate that it might. For an insulin-sensitive, lean American, it's not clear that it would have much benefit, outside of reducing potentially harmful foods such as gluten and sugar. Although insulin signaling is probably tied up with lifespan in humans, as in many other species, no one has shown that post-meal insulin spikes caused by carbohydrate, as opposed to chronically elevated insulin and insulin resistance, is harmful. The story is not as simple as "more serum insulin = shorter lifespan".
Is there any evidence that carbohydrate restriction extends lifespan in a non-carnivorous mammal such as a rodent or monkey? I'm open to the possibility, but I haven't seen any studies. I'll look forward to them.
Thursday, September 24, 2009
Another Fatty Liver Reversal, Part II
A month ago, I wrote about a reader "Steve" who reversed his fatty liver using a change in diet. Non-alcoholic fatty liver disease (NAFLD) is a truly disturbing modern epidemic, rare a few decades ago and now affecting roughly a quarter of the adult population of modern industrialized nations. Researchers cause NAFLD readily in rodents by feeding them industrial vegetable oils or large amounts of sugar.
Steve recently e-mailed me to update me on his condition. He also passed along his liver test results, which I've graphed below. ALT is a liver enzyme that enters the bloodstream following liver damage such as hepatitis or NAFLD. It's below 50 units/L in a healthy person*. AST is another liver enzyme that's below 35 units/L in a healthy person*.
Steve began his new diet in November of 2008 and saw a remarkable and sustained improvement in his ALT and AST levels:
Here's how Steve described his diet change to me:
* The cutoff depends on who you ask, but these numbers are commonly used.
How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
Fatty Liver Reversal
Another Fatty Liver Reversal
Steve recently e-mailed me to update me on his condition. He also passed along his liver test results, which I've graphed below. ALT is a liver enzyme that enters the bloodstream following liver damage such as hepatitis or NAFLD. It's below 50 units/L in a healthy person*. AST is another liver enzyme that's below 35 units/L in a healthy person*.
Steve began his new diet in November of 2008 and saw a remarkable and sustained improvement in his ALT and AST levels:
Here's how Steve described his diet change to me:I totally eliminated sugar, heavy starches, and grains. Started eating more whole, real foods, including things like grass-fed beef and pastured pork and eggs, began supplementing with good fats and omega-3 (pastured butter, coconut oil, cod liver oil). Ate more fruits and vegetables instead of refined carbs. Also completely gave up on the idea that I had to eat only "lean" meats. After my last results, the GI doc said that I wouldn't need the biopsy at all, that things were great, and that if I kept it up I "would live forever."He did experience some side effects from this diet though:
My triglycerides also went from pre-diet measures of 201 and 147 to post diet 86, 81, and 71.The liver is the body's "metabolic grand central station". It's essential for nutrient homeostasis, insulin sensitivity, detoxification, and hormone conversion, among other things. What's bad for the liver is bad for the rest of the body as well. Don't poison your liver with sugar and industrial vegetable oils.
The added bonus, of course, was that my weight went from 205 pounds to 162 pounds and my body fat percentage from 24% to 12% in the matter of five months--all without the typically excessive cardio I used to try unsuccessfully for weight loss.
* The cutoff depends on who you ask, but these numbers are commonly used.
How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
Fatty Liver Reversal
Another Fatty Liver Reversal
Wednesday, September 16, 2009
Diabetics on a Low-carbohydrate Diet
Diabetes is a disorder of glucose intolerance. What happens when a diabetic eats a low-carbohydrate diet? Here's a graph of blood glucose over a 24 hour period, in type II diabetics on their usual diet (blue and grey triangles), and after 5 weeks on a 55% carbohydrate (yellow circles) or 20% carbohydrate (blue circles) diet:
The study in question describes these volunteers as having "mild, untreated diabetes." If 270 mg/dL of blood glucose is mild diabetes, I'd hate to see severe diabetes! In any case, the low-carbohydrate, high-fat diet brought blood glucose down to an acceptable level without requiring medication.
It's interesting to note in the graph above that fasting blood glucose (18-24 hours) also fell dramatically. This probably reflects improved insulin sensitivity in the liver. The liver pumps glucose into the bloodstream when it's necessary, and insulin suppresses this. When the liver is insulin resistant, it doesn't respond to the normal signal that there's already sufficient glucose, so it releases more and increases fasting blood glucose. When other tissues are insulin resistant, they don't take up the extra glucose, also contributing to the problem.
Glycated hemoglobin (HbA1c), a measure of average blood glucose concentration over the preceding few weeks, also reflected a profound improvement in blood glucose levels in the low-carbohydrate group:
At 5 weeks, the low-carbohydrate group was still improving and headed toward normal HbA1c, while the high-carbohydrate group remained at a dangerously high level. Total cholesterol, LDL and HDL remained unchanged in both groups, while triglycerides fell dramatically in the low-carbohydrate group.
When glucose is poison, it's better to eat fat.
Graph #1 was reproduced from Volek et al. (2005), which re-plotted data from Gannon et al. (2004). Graph #2 was drawn directly from Gannon et al.
The study in question describes these volunteers as having "mild, untreated diabetes." If 270 mg/dL of blood glucose is mild diabetes, I'd hate to see severe diabetes! In any case, the low-carbohydrate, high-fat diet brought blood glucose down to an acceptable level without requiring medication. It's interesting to note in the graph above that fasting blood glucose (18-24 hours) also fell dramatically. This probably reflects improved insulin sensitivity in the liver. The liver pumps glucose into the bloodstream when it's necessary, and insulin suppresses this. When the liver is insulin resistant, it doesn't respond to the normal signal that there's already sufficient glucose, so it releases more and increases fasting blood glucose. When other tissues are insulin resistant, they don't take up the extra glucose, also contributing to the problem.
Glycated hemoglobin (HbA1c), a measure of average blood glucose concentration over the preceding few weeks, also reflected a profound improvement in blood glucose levels in the low-carbohydrate group:
At 5 weeks, the low-carbohydrate group was still improving and headed toward normal HbA1c, while the high-carbohydrate group remained at a dangerously high level. Total cholesterol, LDL and HDL remained unchanged in both groups, while triglycerides fell dramatically in the low-carbohydrate group.When glucose is poison, it's better to eat fat.
Graph #1 was reproduced from Volek et al. (2005), which re-plotted data from Gannon et al. (2004). Graph #2 was drawn directly from Gannon et al.
Sunday, June 28, 2009
Another Fatty Liver Reversal
Just to show it wasn't a fluke, reader "Steve" replicates the experiment:
The liver is a remarkable organ. Besides being your "metabolic grand central station", it's the only organ in the human body that can regenerate almost completely. It can be 75% obliterated, and it will grow back over time. Fatty liver and NASH are largely reversible.
I had a similar problem as what Sam described, and it just happened to coincide with my discovery of and commitment to a new eating plan (based on low/good carb, high in good fat and omega 3, and good protein--basically a mix of paleo, primal, low carb, whatever they call it). I consider myself lucky to have had great fortune in my timing of finding out about my fatty liver.And a later comment:
My ALT and AST [markers of liver damage] had been at 124 and 43 respectively, and then still at 80 and 30 in a follow up a few months later. I weighed in at about 205 (I'm 6'1.5" on a slimmish frame), which was my heaviest. I had been on a basic American (bad) diet. The whole thing shocked me, especially after a CT with contrast showed the fatty deposits on my liver (and prior to that, when the muddy ultrasound revealed a fatty liver and a possible pancreatic mass, later ruled out by the CT). Like Sam, though I was surely overweight, I was not fat or heavy. (Most people have noticed I look leaner, but are shocked when I disclose how much weight I have lost since they say "I cannot believe you had that much to lose.")
At about the same time I found out about my liver issue, I had been getting into reading about diet and health (something I had done once when I read the Zone stuff from Sears many years ago). I practically dove through Taubes, Eades, Cordain, and a bunch of blogs (including yours), and I made a commitment to fix my problem.
I started a pretty severe regimen at first, which included only protein and good fats with a minimal amount of non-starchy fruits and vegetables. Almost immediately, I started losing weight and body fat (as measured by an electrical impedance scale). I have always supplemented with fish oil, but I added krill oil and I also started eating grass-fed beef and pastured eggs and pastured pork as much as possible. I have added some coconut oil and pastured butter to my diet as well. I have dropped almost 40 pounds, I am down to about 10-11% body fat (from 24%), and my ALT/AST on my last test was 24/14 [normal]. I am getting another test soon, and I expect similar results.
I can add to the story that I first found out about the fatty liver on a routine new patient blood screening when I moved to a new town. I can also add that it took a bit of initiative on my part to get to the right diagnosis. The first doctor suspected hepatitis, but when blood work ruled that out, he ordered the imagining tests. Once I was referred to a GI specialist, it was a quick diagnosis. Still, I had to undertake myself to figure out the best diet. The GI recommended eliminating white bread, rice, pasta, starches, etc. but also recommended lowering fat intake. Having done some of my reading on diet and health, I knew to follow the former advice and to modify the latter to be "get plenty of fat, but make sure its the right kind."Steve took the initiative and fixed his damaged liver. He modified his GI doctor's advice based on what he had read about nutrition, with excellent results. I suspect his doctor will be all ears next time Steve comes into his office.
The liver is a remarkable organ. Besides being your "metabolic grand central station", it's the only organ in the human body that can regenerate almost completely. It can be 75% obliterated, and it will grow back over time. Fatty liver and NASH are largely reversible.
Friday, June 26, 2009
When Friedewald Attacks
I don't get very excited about nitpicking blood lipids. That's not to say they're not useful. There's definitely an association between blood lipids and certain health outcomes such as cardiovascular disease. The thing that tires me is when people uncritically interpret those associations as evidence that lipids are actually causing the problem.
Low-density lipoprotein, or LDL, is the cholesterol fraction that typically gets the most attention. High LDL associates with heart attack risk in Americans and some other groups. Statins reduce LDL and reduce heart attack risk in a subset of the population, and this has been used to support the idea that elevated LDL causes heart attacks. This is despite the fact that lowering LDL via diet doesn't seem to reduce heart attack risk (typically by reducing total fat and/or saturated fat). Statins may in fact work because they're anti-inflammatory, rather than because they reduce LDL. But both explanations are speculative at this point.
The fact remains that if you want to know if Mr. Jones is going to have a heart attack in the next five years, measuring his LDL will give you more information than not measuring his LDL. This association doesn't seem to apply to all cultures or to Americans eating atypical diets. Then you can get into the fractions that associate more tightly with heart attack risk, such as low HDL, high triglycerides, small dense LDL, etc. Triglycerides vary with HDL (that is, when trigs go up, HDL generally goes down) and the ratio also happens to be a predictor of insulin sensitivity. Total cholesterol is virtually useless for predicting heart attack risk in the general population. This is something I'll discuss in more detail at another time.
When you walk into the doctor's office and ask him to measure your cholesterol, the numbers you get back will generally be total cholesterol, LDL, HDL and triglycerides. All of those except LDL are measured directly. LDL is calculated using the Friedewald equation, which is (in mg/dL):
I had a lipid panel done a while back, just for kicks. My LDL, calculated by the Friedewald equation, was 131 mg/dL. Over 130 is considered high. Pass the statins! But wait, my triglycerides were 48 mg/dL, which is quite low. I found a paper through Dr. Eades' post that contains an equation for accurately calculating LDL in people whose triglycerides are below 100 mg/dL*. Here it is (mg/dL):
*This equation was designed for individuals with a total cholesterol over 250 mg/dL.
Low-density lipoprotein, or LDL, is the cholesterol fraction that typically gets the most attention. High LDL associates with heart attack risk in Americans and some other groups. Statins reduce LDL and reduce heart attack risk in a subset of the population, and this has been used to support the idea that elevated LDL causes heart attacks. This is despite the fact that lowering LDL via diet doesn't seem to reduce heart attack risk (typically by reducing total fat and/or saturated fat). Statins may in fact work because they're anti-inflammatory, rather than because they reduce LDL. But both explanations are speculative at this point.
The fact remains that if you want to know if Mr. Jones is going to have a heart attack in the next five years, measuring his LDL will give you more information than not measuring his LDL. This association doesn't seem to apply to all cultures or to Americans eating atypical diets. Then you can get into the fractions that associate more tightly with heart attack risk, such as low HDL, high triglycerides, small dense LDL, etc. Triglycerides vary with HDL (that is, when trigs go up, HDL generally goes down) and the ratio also happens to be a predictor of insulin sensitivity. Total cholesterol is virtually useless for predicting heart attack risk in the general population. This is something I'll discuss in more detail at another time.
When you walk into the doctor's office and ask him to measure your cholesterol, the numbers you get back will generally be total cholesterol, LDL, HDL and triglycerides. All of those except LDL are measured directly. LDL is calculated using the Friedewald equation, which is (in mg/dL):
LDL = TC - HDL - (TG/5)Low-carb advocates have known for quite some time that this equation fails to accurately predict LDL concentration outside certain triglyceride ranges. Dr. Michael Eades put up a post about this recently, and Richard Nikoley has written about it before as well. The reason low-carb advocates know this is that reducing carbohydrate generally reduces triglycerides, often below 100 mg/dL. This is the range at which the Friedewald equation becomes unreliable, resulting in artificially inflated LDL numbers that make you have a heart attack just by reading them.
I had a lipid panel done a while back, just for kicks. My LDL, calculated by the Friedewald equation, was 131 mg/dL. Over 130 is considered high. Pass the statins! But wait, my triglycerides were 48 mg/dL, which is quite low. I found a paper through Dr. Eades' post that contains an equation for accurately calculating LDL in people whose triglycerides are below 100 mg/dL*. Here it is (mg/dL):
LDL = TC/1.19 + TG/1.9 - HDL/1.1 - 38I ran my numbers through this equation. My new, accurate calculated LDL? 98 mg/dL. Even the U.S. National Cholesterol Education Panel wouldn't put me on statins with an LDL like that. I managed to shave 33 mg/dL off my LDL in 2 minutes. Isn't math fun?
*This equation was designed for individuals with a total cholesterol over 250 mg/dL.
Sunday, March 15, 2009
Paleopathology at the Origins of Agriculture
In April of 1982, archaeologists from around the globe converged on Plattsburgh, New York for a research symposium. Their goal:
There are some major limitations to studying human health by looking at bones. The most obvious is that any soft tissue pathology will have been erased by time. Nevertheless, you can learn a lot from a skeleton. Here are the main health indicators discussed in the book:
There's so much information in this book, the best I can do is quote pieces of the editor's summary and add a few remarks of my own. One of the most interesting things I learned from the book is that the diet of many hunter-gatherer groups changed at the end of the upper Paleolithic, foreshadowing the shift to agriculture. From pages 566-568:
One of the interesting things I learned from the book is that Mesolithic populations, groups that were halfway between farming and hunting-gathering, were generally as healthy as hunter-gatherers:
One pathology that seems to have decreased with the adoption of agriculture is arthritis. The authors speculate that it may have more to do with strenuous activity than other aspects of the lifestyle such as diet. Another interpretation is that the hunter-gatherers appeared to have a higher arthritis rate because of their longer lifespans:
And the final word:
...[to use] data from human skeletal analysis and paleopathology [the study of ancient diseases] to measure the impact on human health of the Neolithic Revolution and antecedent changes in prehistoric hunter-gatherer food economies. The symposium developed out of our perception that many widely debated theories about the origins of agriculture had testable but untested implications concerning human health and nutrition and our belief that recent advances in techniques of skeletal analysis, and the recent explosive increase in data available in this field, permitted valid tests of many of these propositions.In other words, they got together to see what happened to human health as populations adopted agriculture. They were kind enough to publish the data presented at the symposium in the book Paleopathology at the Origins of Agriculture, edited by the erudite Drs. Mark Nathan Cohen and George J. Armelagos. It appears to be out of print, but luckily I have access to an excellent university library.
There are some major limitations to studying human health by looking at bones. The most obvious is that any soft tissue pathology will have been erased by time. Nevertheless, you can learn a lot from a skeleton. Here are the main health indicators discussed in the book:
- Mortality. Archaeologists are able to judge a person's approximate age at death, and if the number of skeletons is large enough, they can paint a rough picture of the life expectancy and infant mortality of a population.
- General growth. Total height, bone thickness, dental crowding, and pelvic and skull shape are all indicators of relative nutrition and health. This is particularly true in a genetically stable population. Pelvic depth is sensitive to nutrition and determines the size of the birth canal in women.
- Episodic stress. Bones and teeth carry markers of temporary "stress", most often due to starvation or malnutrition. Enamel hypoplasia, horizontal bands of thinned enamel on the teeth, is probably the most reliable marker. Harris lines, bands of increased density in long bones that may be caused by temporary growth arrest, are another type.
- Porotic hyperostosis and cribra orbitalia. These are both skull deformities that are caused by iron deficiency anemia, and are rather creepy to look at. They're typically caused by malnutrition, but can also result from parasites.
- Periosteal reactions. These are bone lesions resulting from infections.
- Physical trauma, such as fractures.
- Degenerative bone conditions, such as arthritis.
- Isotopes and trace elements. These can sometimes yield information about the nutritional status, diet composition and diet quality of populations.
- Dental pathology. My favorite! This category includes cavities, periodontal disease, missing teeth, abscesses, tooth wear, and excessive dental plaque.
In Upper Paleolithic times nutritional health was excellent. The evidence consists of extremely tall stature from plentiful calories and protein (and some microevolutionary selection?); maximum skull base height from plentiful protein, vitamin D, and sunlight in early childhood; and very good teeth and large pelvic depth from adequate protein and vitamins in later childhood and adolescence...The level of skeletal (including cranial and pelvic) development Paleolithic groups exhibited has remained unmatched throughout the history of agriculture. There may be exceptions but the trend is clear. Cranial capacity was 11% higher in the upper Paleolithic. You can see the pelvic data in this table taken from Paleopathology at the Origins of Agriculture.
Adult longevity, at 35 years for males and 30 years for females, implies fair to good general health...
There is no clear evidence for any endemic disease.
There's so much information in this book, the best I can do is quote pieces of the editor's summary and add a few remarks of my own. One of the most interesting things I learned from the book is that the diet of many hunter-gatherer groups changed at the end of the upper Paleolithic, foreshadowing the shift to agriculture. From pages 566-568:
During the upper Paleolithic stage, subsistence seems focused on relatively easily available foods of high nutritional value, such as large herd animals and migratory fish. Some plant foods seem to have been eaten, but they appear not to have been quantitatively important in the diet. Storage of foods appears early in many sequences, even during the Paleolithic, apparently to save seasonal surpluses for consumption during seasons of low productivity.Why am I getting the feeling that these archaeologists have a better grasp of human nutrition than the average medical doctor or nutritionist? They have the Price-esque understanding that comes from comparing the diets and multi-generational health of diverse human populations.
As hunting and gathering economies evolve during the Mesolithic [period of transition between hunting/gathering and agriculture], subsistence is expanded by exploitation of increasing numbers of species and by increasingly heavy exploitation of the more abundant and productive plant species. The inclusion of significant amounts of plant food in prehistoric diets seems to correlate with increased use of food processing tools, apparently to improve their taste and digestibility. As [Dr. Mark Nathan] Cohen suggests, there is an increasing focus through time on a few starchy plants of high productivity and storability. This process of subsistence intensification occurs even in regions where native agriculture never developed. In California, for example, as hunting-gathering populations grew, subsistence changed from an early pattern of reliance on game and varied plant resources to to one with increasing emphasis on collection of a few species of starchy seeds and nuts.
...As [Dr. Cohen] predicts, evolutionary change in prehistoric subsistence has moved in the direction of higher carrying capacity foods, not toward foods of higher-quality nutrition or greater reliability. Early nonagricultural diets appear to have been high in minerals, protein, vitamins, and trace nutrients, but relatively low in starch. In the development toward agriculture there is a growing emphasis on starchy, highly caloric food of high productivity and storability, changes that are not favorable to nutritional quality but that would have acted to increase carrying capacity, as Cohen's theory suggests.
One of the interesting things I learned from the book is that Mesolithic populations, groups that were halfway between farming and hunting-gathering, were generally as healthy as hunter-gatherers:
...it seems clear that seasonal and periodic physiological stress regularly affected most prehistoric hunting-gathering populations, as evidenced by the presence of enamel hypoplasias and Harris lines. What also seems clear is that severe and chronic stress, with high frequency of hypoplasias, infectious disease lesions, pathologies related to iron-deficiency anemia, and high mortality rates, is not characteristic of these early populations. There is no evidence of frequent, severe malnutrition, so the diet must have been adequate in calories and other nutrients most of the time. During the Mesolithic, the proportion of starch in the diet rose, to judge from the increased occurrence of certain dental diseases [with exceptions to be noted later], but not enough to create an impoverished diet... There is a possible slight tendency for Paleolithic people to be healthier and taller than Mesolithic people, but there is no apparent trend toward increasing physiological stress during the mesolithic.Cultures that adopted intensive agriculture typically showed a marked decline in health indicators. This is particularly true of dental health, which usually became quite poor.
Stress, however, does not seem to have become common and widespread until after the development of high degrees of sedentism, population density, and reliance on intensive agriculture. At this stage in all regions the incidence of physiological stress increases greatly, and average mortality rates increase appreciably. Most of these agricultural populations have high frequencies of porotic hyperostosis and cribra orbitalia, and there is a substantial increase in the number and severity of enamel hypoplasias and pathologies associated with infectious disease. Stature in many populations appears to have been considerably lower than would be expected if genetically-determined maxima had been reached, which suggests that the growth arrests documented by pathologies were causing stunting... Incidence of carbohydrate-related tooth disease increases, apparently because subsistence by this time is characterized by a heavy emphasis on a few starchy food crops.Infectious disease increased upon agricultural intensification:
Most [studies] conclude that infection was a more common and more serious problem for farmers than for their hunting and gathering forebears; and most suggest that this resulted from some combination of increasing sedentism, larger population aggregates, and the well-established synergism between infection and malnutrition.There are some apparent exceptions to the trend of declining health with the adoption of intensive agriculture. In my observation, they fall into two general categories. In the first, health improves upon the transition to agriculture because the hunter-gatherer population was unhealthy to begin with. This is due to living in a marginal environment or eating a diet with a high proportion of wild plant seeds. In the second category, the culture adopted rice. Rice is associated with less of a decline in health, and in some cases an increase in overall health, than other grains such as wheat and corn. In chapter 21 of the book Ancient Health: Bioarchaeological Interpretations of the Human Past, Drs. Michelle T Douglas and Michael Pietrusewsky state that "rice appears to be less cariogenic [cavity-promoting] than other grains such as maize [corn]."
One pathology that seems to have decreased with the adoption of agriculture is arthritis. The authors speculate that it may have more to do with strenuous activity than other aspects of the lifestyle such as diet. Another interpretation is that the hunter-gatherers appeared to have a higher arthritis rate because of their longer lifespans:
The arthritis data are also complicated by the fact that the hunter-gatherers discussed commonly displayed higher average ages at death than did the farming populations from the same region. The hunter-gatherers would therefore be expected to display more arthritis as a function of age even if their workloads were comparable [to farmers].In any case, it appears arthritis is normal for human beings and not a modern degenerative disease.
And the final word:
Taken as a whole, these indicators fairly clearly suggest an overall decline in the quality-- and probably in the length-- of human life associated with the adoption of agriculture.
Saturday, December 13, 2008
The Myth of the High-Protein Diet
The phrase "low-carbohydrate diet" is a no-no in some circles, because it implies that a diet is high in fat. Often, the euphemism "high-protein diet" is used to avoid the mental image of a stick of butter wrapped in bacon. It's purely a semantic game, because there is no such thing as a diet in which the majority of calories come from protein. The ability of the human body to metabolize protein ends at about 1/3 of calories (1, 2), and the long-term optimum may be lower still. Low-carbohydrate diets (yes, the ones that are highly effective for weight loss and general health) are high-fat diets.
Healthy cultures around the world tend to consume roughly 10 to 20% of calories from protein:
Masai - 19%
Healthy cultures around the world tend to consume roughly 10 to 20% of calories from protein:
Masai - 19%
Kitava - 10%
Tokelau - 12%
Tokelau - 12%
Inuit - 20%, according to Stefansson
Kuna - 12%
Sweden - 12%
United States - 15%
Human milk - 6%
The balance comes from fat and carbohydrate. Ask a traditional Inuit. If there's no fat on your meat, you may as well starve. Literally. "Rabbit starvation" was a term coined by American explorers who quickly realized that living on lean game is somewhere between unhealthy and fatal.
In the early 1900s, anthropologist and explorer Vilhjalmur Stefansson lived for several years among completely isolated Canadian Inuit (Eskimo) who had never seen a white person before. They were literally a stone-age culture, completely uninfluenced by the modern world. They are representative of how some of our paleolithic ancestors would have lived. Here's Stefansson, quoted from My Life With the Eskimo (1913):
The balance comes from fat and carbohydrate. Ask a traditional Inuit. If there's no fat on your meat, you may as well starve. Literally. "Rabbit starvation" was a term coined by American explorers who quickly realized that living on lean game is somewhere between unhealthy and fatal.
In the early 1900s, anthropologist and explorer Vilhjalmur Stefansson lived for several years among completely isolated Canadian Inuit (Eskimo) who had never seen a white person before. They were literally a stone-age culture, completely uninfluenced by the modern world. They are representative of how some of our paleolithic ancestors would have lived. Here's Stefansson, quoted from My Life With the Eskimo (1913):
In certain places and in certain years, rabbits are an important article of diet, but even when there is an abundance of this animal, the Indians consider themselves starving if they get nothing else, - and fairly enough, as my own party can testify, for any one who is compelled in winter to live for a period of several weeks on lean meat will actually starve, in this sense: that there are lacking from his diet certain necessary elements, notably fat, and it makes no difference how much he eats, he will be hungry at the end of each meal, and eventually he will lose strength or become actually ill. The Eskimo who have provided themselves in summer with bags of seal oil can carry them into a rabbit country and can live on rabbits satisfactorily for months.
Dr. Loren Cordain, in his excellent paper "Plant-Animal Subsistence Ratios and Macronutrient Energy Estimations in Worldwide Hunter-Gatherer Diets", argues based on calculated estimates that historical hunter-gatherers generally consumed between 19 and 35% of calories from protein:
It's clear from the anthropological literature that hunter-gatherers did not go after representative animals. They went after the fattest animals they could find. They knew exactly which animals were fattest in which seasons, which individuals were likely to be fattest within a herd, and which bodyparts were fattest on an individual animal. For example, Stefansson describes how the Inuit relied on (extremely fat) seal in the spring, wolf in the summer, and caribou and bear in the fall and early winter. If necessary, they would discard lean meat in favor of tongue, marrow, internal organs, back fat and other fat-rich bodyparts. This was in order to obtain a minimum of 65% of calories from fat.
Hunter-gatherers would sometimes even provision themselves with enough fat in advance to last a lean season or two. This was true for dozens of tribes along the Northwest coast of North America that relied chiefly on animal foods. Here's another excerpt from My Life With the Eskimo:
Further, although the human body can theoretically tolerate up to 35% protein by calories, even that amount is probably not optimal in the long term. I think that's suggested by the fact that diverse cultures tend to find a source of fat and/or carbohydrate that keeps their protein intake roughly between 10 and 20%. I think it's fine to eat plenty of protein, and there's no need to deliberately restrict it, because your tastes will tell you if you're eating too much. However, "high-protein diet" as a euphemism for low-carbohydrate diet is a misnomer. Low-carbohydrate diets are, and have always been, high-fat diets.
This high reliance on animal-based foods coupled with the relatively low carbohydrate content of wild plant foods produces universally characteristic macronutrient composition ratios in which protein is elevated (19- 35% of energy) at the expense of carbohydrates (22- 40% of energy).Later, he states that the most plausible range of fat intakes is 28- 58%. I agree with his assertion that hunter-gatherer diets tended to be relatively high in protein compared with contemporary diets, but I think his protein numbers are a bit high. Why? Because he calculates macronutrient composition based on the whole-carcass fat content of "representative" animals such as deer.
It's clear from the anthropological literature that hunter-gatherers did not go after representative animals. They went after the fattest animals they could find. They knew exactly which animals were fattest in which seasons, which individuals were likely to be fattest within a herd, and which bodyparts were fattest on an individual animal. For example, Stefansson describes how the Inuit relied on (extremely fat) seal in the spring, wolf in the summer, and caribou and bear in the fall and early winter. If necessary, they would discard lean meat in favor of tongue, marrow, internal organs, back fat and other fat-rich bodyparts. This was in order to obtain a minimum of 65% of calories from fat.
Hunter-gatherers would sometimes even provision themselves with enough fat in advance to last a lean season or two. This was true for dozens of tribes along the Northwest coast of North America that relied chiefly on animal foods. Here's another excerpt from My Life With the Eskimo:
...[spring] is the season which the Eskimo give up to the accumulation of blubber for the coming year. Fresh oil is not nearly so palatable or digestible as oil that has been allowed to ferment in a sealskin bag through the summer, and besides that it is difficult often to get seals in the fall... Each family will in the spring be able to lay away from three to seven bags of oil. Such a bag consists of the whole skin of the common seal... This makes a bag which will hold about three hundred pounds of blubber, so that a single family's store of oil for the fall will run from nine hundred to two thousand pounds.That's a lot of oil! Some of it would have been used to light oil lamps, but much of it would have been eaten. I think Cordain's estimate of the protein intake of hunter-gatherers is a bit high due to his underestimating fat intake. His paper shows that if you break historical hunter-gatherer cultures into 10 groups based on their reliance on animal foods, the most numerous group (46 out of 229) obtained 85- 100% of their food from animal sources. In other words, approximately 20% of historical hunter-gatherers were carnivorous or nearly so. If the human protein ceiling is 35% of calories, that means roughly one fifth of hunter-gatherers ate 65% or more of their calories as fat. It also means carnivory and high-fat diets are not just anomalies, they are part of the human ecological niche. Zero out of 229 groups obtained less than 16% of calories from animal foods. Vegetarianism is not part of our niche.
Further, although the human body can theoretically tolerate up to 35% protein by calories, even that amount is probably not optimal in the long term. I think that's suggested by the fact that diverse cultures tend to find a source of fat and/or carbohydrate that keeps their protein intake roughly between 10 and 20%. I think it's fine to eat plenty of protein, and there's no need to deliberately restrict it, because your tastes will tell you if you're eating too much. However, "high-protein diet" as a euphemism for low-carbohydrate diet is a misnomer. Low-carbohydrate diets are, and have always been, high-fat diets.
Saturday, July 26, 2008
The Inuit: Lessons from the Arctic
The Inuit (also called Eskimo) are a group of hunter-gatherer cultures who inhabit the arctic regions of Alaska, Canada and Greenland. They are a true testament to the toughness, adaptability and ingenuity of the human species. Their unique lifestyle has a lot of information to offer us about the boundaries of the human ecological niche. Weston Price was fascinated by their excellent teeth, good nature and overall robust health. Here's an excerpt from Nutrition and Physical Degeneration:"In his primitive state he has provided an example of physical excellence and dental perfection such as has seldom been excelled by any race in the past or present...we are also deeply concerned to know the formula of his nutrition in order that we may learn from it the secrets that will not only aid in the unfortunate modern or so-called civilized races, but will also, if possible, provide means for assisting in their preservation."
The Inuit are cold-hardy hunters whose traditional diet consists of a variety of sea mammals, fish, land mammals and birds. They invented some very sophisticated tools, including the kayak, whose basic design has remained essentially unchanged to this day. Most groups ate virtually no plant food. Their calories came primarily from fat, up to 75%, with almost no calories coming from carbohydrate. Children were breast-fed for about three years, and had solid food in their diet almost from birth. As with most hunter-gatherer groups, they were free from chronic disease while living a traditional lifestyle, even in old age. Here's a quote from Observations on the Western Eskimo and the Country they Inhabit; from Notes taken During two Years [1852-54] at Point Barrow, by Dr. John Simpson:
These people [the Inuit] are robust, muscular and active, inclining rather to spareness [leanness] than corpulence [overweight], presenting a markedly healthy appearance. The expression of the countenance is one of habitual good humor. The physical constitution of both sexes is strong. Extreme longevity is probably not unknown among them; but as they take no heed to number the years as they pass they can form no guess of their own ages.One of the common counterpoints I hear to the idea that high-fat hunter-gatherer diets are healthy, is that exercise protects them from the ravages of fat. The Inuit can help us get to the bottom of this debate. Here's a quote from Cancer, Disease of Civilization (1960, Vilhjalmur Stefansson):
"They are large eaters, some of them, especially the women, eating all the time..." ...during the winter the Barrow women stirred around very little, did little heavy work, and yet "inclined more to be sparse than corpulent" [quotes are the anthropologist Dr. John Murdoch, reproduced by Stefansson].Another argument I sometimes hear is that the Inuit are genetically adapted to their high-fat diet, and the same food would kill a European. This appears not to be the case. The anthropologist and arctic explorer Vilhjalmur Stefansson spent several years living with the Inuit in the early 20th century. He and his fellow Europeans and Americans thrived on the Inuit diet. American doctors were so incredulous that they defied him and a fellow explorer to live on a diet of fatty meat only for one year, under the supervision of the American Medical Association. To the doctors' dismay, they remained healthy, showing no signs of scurvy or any other deficiency (JAMA 1929;93:20–2).
Yet another amazing thing about the Inuit was their social structure. Here's Dr. John Murdoch again (quoted from Cancer, Disease of Civilization):
The women appear to stand on a footing of perfect equality with the men, both in the family and the community. The wife is the constant and trusted companion of the man in everything except the hunt, and her opinion is sought in every bargain or other important undertaking... The affection of parents for their children is extreme, and the children seem to be thoroughly worthy of it. They show hardly a trace of fretfulness or petulance so common among civilized children, and though indulged to an extreme extent are remarkably obedient. Corporal punishment appears to be absolutely unknown, and children are rarely chided or punished in any way.Unfortunately, those days are long gone. Since adopting a modern processed-food diet, the health and social structure of the Inuit has deteriorated dramatically. This had already happened to most groups by Weston Price's time, and is virtually complete today. Here's Price:
In the various groups in the lower Kuskokwim seventy-two individuals who were living exclusively on native foods had in their 2,138 teeth only two teeth or 0.09 per cent that had ever been attacked by tooth decay. In this district eighty-one individuals were studied who had been living in part or in considerable part on modern foods, and of their 2, 254 teeth 394 or 13 per cent had been attacked by dental caries. This represents an increase in dental caries of 144 fold.... When these adult Eskimos exchange their foods for our modern foods..., they often have very extensive tooth decay and suffer severely.... Their plight often becomes tragic since there are no dentists in these districts.Modern Inuit also suffer from very high rates of diabetes and overweight. This has been linked to changes in diet, particularly the use of white flour, sugar and processed oils.
Overall, the unique lifestyle and diet of the Inuit have a lot to teach us. First, that humans are capable of being healthy as carnivores. Second, that we are able to thrive on a high-fat diet. Third, that we are capable of living well in extremely harsh and diverse environments. Fourth, that the shift from natural foods to processed foods, rather than changes in macronutrient composition, is the true cause of the diseases of civilization.
Thursday, July 17, 2008
New Low-carb Study
I know you’ve all heard the news about the new low-carb study in the New England Journal of Medicine by now, but I have to chime in. I‘m going to try to offer you a different perspective of the study that you may not have found elsewhere. First of all, this is a Rolls Royce of a study. It was large, well-controlled, and two years long. It was partly funded by the Atkins foundation, but it's a peer-reviewed study in a good journal and if anything the study design is slanted against the low-carbohydrate diet.
The study compared the weights and various health parameters of 322 overweight subjects put on one of three diets: a “low-fat diet”, a Mediterranean diet and a “low-carbohydrate diet”. The first two were calorie-restricted while the low-carb diet was not. First of all, the “low-fat” diet was not particularly low in fat. It was 30% fat by calories, only a few percent short of the US average. What they call low-fat in the study is actually a calorie-restricted version of the American Heart Association diet recommendation, which suggests:
“…30% of calories from fat, 10% calories from saturated fat, and an intake of 300 mg of cholesterol per day. The Participants were counseled to consume low-fat grains, vegetables, fruits, and legumes and to limit their consumption of additional fats, sweets and high-fat snacks.”
So henceforth, I’ll refer to it as the AHA diet rather than the low-fat diet.
The “low-carb” diet wasn’t particularly low in carbohydrate either. The low-carb group was only getting 10% fewer calories from carbohydrate than the low-fat or Mediterranean diet groups. Despite these problems, the low-carbohydrate diet was the most effective overall. It caused a weight loss of 5.5 kg (12 lb), compared to 4.6 kg (10 lb) and 3.3 kg (7.4 lb) for the Mediterranean and AHA diets, respectively.
One of the most amazing aspects of the study is that the low-carb diet was the only one that wasn’t calorie-restricted, yet it caused the most weight loss. People in the low-carb group naturally reduced their calorie intake over the course of the study, ending up with an intake similar to the AHA group.
The low-carb diet also came out on top in most of the markers of health they examined. It caused the largest drop in HbA1c, a measure of average blood glucose level. It caused the largest drop in C-reactive protein, a measure of inflammation (the Mediterranean diet also did well). And finally, it caused the biggest improvement in the triglyceride:HDL ratio. This ratio is the best blood lipid predictor of heart disease risk I’m aware of in modern Western populations. The lower, the better. They didn't calculate it in the study so I had to do it myself. Here's a graph of the change in trig:HDL ratio for each group over the course of the study:
Other interesting findings: despite the calorie restriction, diabetic participants on the AHA group actually saw a significant increase in fasting blood glucose.
I've speculated before that wheat and sugar may cause hyperphagia, or excessive eating. We can see from these results that reducing carbohydrate (and probably wheat) reduces overall caloric intake quite significantly. This squares with the findings of the recent Chinese study that showed an increase in calorie intake and weight, correlating with the replacement of rice with wheat as the primary carbohydrate. It also squares with diet trends in the US, where wheat consumption has risen alongside calorie intake and weight.
I'd love to know what the results would have looked like if they had gone on a true low-carbohydrate diet, or even simply eliminated grains and sugar.
The study compared the weights and various health parameters of 322 overweight subjects put on one of three diets: a “low-fat diet”, a Mediterranean diet and a “low-carbohydrate diet”. The first two were calorie-restricted while the low-carb diet was not. First of all, the “low-fat” diet was not particularly low in fat. It was 30% fat by calories, only a few percent short of the US average. What they call low-fat in the study is actually a calorie-restricted version of the American Heart Association diet recommendation, which suggests:
“…30% of calories from fat, 10% calories from saturated fat, and an intake of 300 mg of cholesterol per day. The Participants were counseled to consume low-fat grains, vegetables, fruits, and legumes and to limit their consumption of additional fats, sweets and high-fat snacks.”
So henceforth, I’ll refer to it as the AHA diet rather than the low-fat diet.
The “low-carb” diet wasn’t particularly low in carbohydrate either. The low-carb group was only getting 10% fewer calories from carbohydrate than the low-fat or Mediterranean diet groups. Despite these problems, the low-carbohydrate diet was the most effective overall. It caused a weight loss of 5.5 kg (12 lb), compared to 4.6 kg (10 lb) and 3.3 kg (7.4 lb) for the Mediterranean and AHA diets, respectively.
One of the most amazing aspects of the study is that the low-carb diet was the only one that wasn’t calorie-restricted, yet it caused the most weight loss. People in the low-carb group naturally reduced their calorie intake over the course of the study, ending up with an intake similar to the AHA group.
The low-carb diet also came out on top in most of the markers of health they examined. It caused the largest drop in HbA1c, a measure of average blood glucose level. It caused the largest drop in C-reactive protein, a measure of inflammation (the Mediterranean diet also did well). And finally, it caused the biggest improvement in the triglyceride:HDL ratio. This ratio is the best blood lipid predictor of heart disease risk I’m aware of in modern Western populations. The lower, the better. They didn't calculate it in the study so I had to do it myself. Here's a graph of the change in trig:HDL ratio for each group over the course of the study:
Other interesting findings: despite the calorie restriction, diabetic participants on the AHA group actually saw a significant increase in fasting blood glucose.
I've speculated before that wheat and sugar may cause hyperphagia, or excessive eating. We can see from these results that reducing carbohydrate (and probably wheat) reduces overall caloric intake quite significantly. This squares with the findings of the recent Chinese study that showed an increase in calorie intake and weight, correlating with the replacement of rice with wheat as the primary carbohydrate. It also squares with diet trends in the US, where wheat consumption has risen alongside calorie intake and weight.
I'd love to know what the results would have looked like if they had gone on a true low-carbohydrate diet, or even simply eliminated grains and sugar.
Saturday, July 5, 2008
Mortality and Lifespan of the Inuit
One of the classic counter-arguments that's used to discredit accounts of healthy hunter-gatherers is the fallacy that they were short-lived, and thus did not have time to develop diseases of old age like cancer. While the life expectancy of hunter-gatherers was not as high as ours today, most groups had a significant number of elderly individuals, who sometimes lived to 80 years and beyond. Mortality came mostly from accidents, warfare and infectious disease rather than chronic disease.
I found a a mortality table from the records of a Russian mission in Alaska (compiled by Veniaminov, taken from Cancer, Disease of Civilization), which recorded the ages of death of a traditionally-living Inuit population during the years 1822 to 1836. Here's a plot of the raw data:
Here's the data re-plotted in another way. I changed the "bin size" of the bars to 10 year spans each (rather than the bins above, which vary from 3 to 20 years). This allows us to get a better picture of the number of deaths over time. I took some liberties with the data to do this, breaking up a large bin equally into two smaller bins. I also left out the infant mortality data, which are interesting but not relevant to this post:
.png)
Excluding infant mortality, about 25% of their population lived past 60. Based on these data, the approximate life expectancy (excluding infant mortality) of this Inuit population was 43.5 years. It's possible that life expectancy would have been higher before contact with the Russians, since they introduced a number of nasty diseases to which the Inuit were not resistant. Keep in mind that the Westerners who were developing cancer alongside them probably had a similar life expectancy at the time. Here's the data plotted in yet another way, showing the number of individuals surviving at each age, out of the total deaths recorded:
It's remarkably linear. Here's the percent chance of death at each age:
In the next post, I'll briefly summarize cancer data from several traditionally-living cultures other than the Inuit.
I found a a mortality table from the records of a Russian mission in Alaska (compiled by Veniaminov, taken from Cancer, Disease of Civilization), which recorded the ages of death of a traditionally-living Inuit population during the years 1822 to 1836. Here's a plot of the raw data:
Here's the data re-plotted in another way. I changed the "bin size" of the bars to 10 year spans each (rather than the bins above, which vary from 3 to 20 years). This allows us to get a better picture of the number of deaths over time. I took some liberties with the data to do this, breaking up a large bin equally into two smaller bins. I also left out the infant mortality data, which are interesting but not relevant to this post: .png)
Excluding infant mortality, about 25% of their population lived past 60. Based on these data, the approximate life expectancy (excluding infant mortality) of this Inuit population was 43.5 years. It's possible that life expectancy would have been higher before contact with the Russians, since they introduced a number of nasty diseases to which the Inuit were not resistant. Keep in mind that the Westerners who were developing cancer alongside them probably had a similar life expectancy at the time. Here's the data plotted in yet another way, showing the number of individuals surviving at each age, out of the total deaths recorded:
It's remarkably linear. Here's the percent chance of death at each age:
In the next post, I'll briefly summarize cancer data from several traditionally-living cultures other than the Inuit.
Friday, July 4, 2008
Cancer Among the Inuit
I remember coming across a table in the book Eat, Drink and Be Healthy (by Dr. Walter Willett-- you can skip it) a few years back. Included were data taken from Dr. Ancel Keys' "Seven Countries Study". It showed the cancer rates for three industrialized nations: the US, Greece and Japan. Although specific cancers differed, the overall rate was remarkably similar for all three: about 90 cancers per 100,000 people per year. Life expectancy was also similar, with Greece leading the pack by 4 years (the data are from the 60s).
The conclusion I drew at the time was that lifestyle did not affect the likelihood of developing cancer. It was easy to see from the same table that heart disease was largely preventable, since the US had a rate of 189 per 100,000 per year, compared to Japan's 34. Especially since I also knew that Japanese-Americans who eat an American diet get heart disease just like European-Americans.
I fell prey to the same logic that is so pervasive today: the idea that you will eventually die of cancer if no other disease gets you first. It's easy to believe, since the epidemiology seems to tell us that lifestyle doesn't affect overall cancer rates very much. There's only one little glitch... those epidemiological studies compare the sick to the sicker.
Here's the critical fact that modern medicine seems to have forgotten: hunter-gatherers and numerous non-industrial populations throughout the world have vanishingly small cancer rates. This fact was widely accepted in the 19th century and the early 20th, but has somehow managed to fade into obscurity. I know it sounds unbelievable, but allow me to explain.
I recently read Cancer, Disease of Civilization by Vilhjalmur Stefansson (thanks Peter). It really opened my eyes. Stefansson was an anthropologist and arctic explorer who participated in the search for cancer among the Canadian and Alaskan Inuit. Traditionally, most Inuit groups were strictly carnivorous, eating a diet of raw and cooked meat and fish almost exclusively. Their calories came primarily from fat, roughly 80%. They alternated between seasons of low and high physical activity, and typically enjoyed an abundant food supply.
Field physicians in the arctic noted that the Inuit were a remarkably healthy people. While they suffered from a tragic susceptibility to European communicable diseases, they did not develop the chronic diseases we now view as part of being human: tooth decay, overweight, heart attacks, appendicitis, constipation, diabetes and cancer. When word reached American and European physicians that the Inuit did not develop cancer, a number of them decided to mount an active search for it. This search began in the 1850s and tapered off in the 1920s, as traditionally-living Inuit became difficult to find.
One of these physicians was captain George B. Leavitt. He actively searched for cancer among the traditionally-living Inuit from 1885 to 1907. Along with his staff, he performed 50,000 examinations a year for the first 15 years, and 25,000 a year thereafter. He did not find a single case of cancer. At the same time, he was regularly diagnosing cancers among the crews of whaling ships and other Westernized populations. It's important to note two relevant facts about Inuit culture: first, their habit of going shirtless indoors. This would make visual inspection for external cancers very easy. Second, the Inuit generally had great faith in Western doctors and would consult them even for minor problems. Therefore, doctors in the arctic had ample opportunity to inspect them for cancer.
A study was published in 1934 by F.S. Fellows in the U.S Treasury's Public Health Reports entitled "Mortality in the Native Races of the Territory of Alaska, With Special Reference to Tuberculosis". It contained a table of cancer mortality deaths for several Alaskan regions, all of them Westernized to some degree. However, some were more Westernized than others. In descending order of Westernization, the percent of deaths from cancer were as follows:
.png)
Keep in mind that all four of the Inuit populations in this table were somewhat Westernized. It's clear that cancer incidence tracks well with Westernization. By "Westernization", what I mean mostly is the adoption of European food habits, including wheat flour, sugar, canned goods and vegetable oil. Later, most groups also adopted Western-style houses, which incidentally were not at all suited to their harsh climate.
In the next post, I'll address the classic counter-argument that hunter-gatherers were free of cancer because they didn't live long enough to develop it.
The conclusion I drew at the time was that lifestyle did not affect the likelihood of developing cancer. It was easy to see from the same table that heart disease was largely preventable, since the US had a rate of 189 per 100,000 per year, compared to Japan's 34. Especially since I also knew that Japanese-Americans who eat an American diet get heart disease just like European-Americans.
I fell prey to the same logic that is so pervasive today: the idea that you will eventually die of cancer if no other disease gets you first. It's easy to believe, since the epidemiology seems to tell us that lifestyle doesn't affect overall cancer rates very much. There's only one little glitch... those epidemiological studies compare the sick to the sicker.
Here's the critical fact that modern medicine seems to have forgotten: hunter-gatherers and numerous non-industrial populations throughout the world have vanishingly small cancer rates. This fact was widely accepted in the 19th century and the early 20th, but has somehow managed to fade into obscurity. I know it sounds unbelievable, but allow me to explain.
I recently read Cancer, Disease of Civilization by Vilhjalmur Stefansson (thanks Peter). It really opened my eyes. Stefansson was an anthropologist and arctic explorer who participated in the search for cancer among the Canadian and Alaskan Inuit. Traditionally, most Inuit groups were strictly carnivorous, eating a diet of raw and cooked meat and fish almost exclusively. Their calories came primarily from fat, roughly 80%. They alternated between seasons of low and high physical activity, and typically enjoyed an abundant food supply.
Field physicians in the arctic noted that the Inuit were a remarkably healthy people. While they suffered from a tragic susceptibility to European communicable diseases, they did not develop the chronic diseases we now view as part of being human: tooth decay, overweight, heart attacks, appendicitis, constipation, diabetes and cancer. When word reached American and European physicians that the Inuit did not develop cancer, a number of them decided to mount an active search for it. This search began in the 1850s and tapered off in the 1920s, as traditionally-living Inuit became difficult to find.
One of these physicians was captain George B. Leavitt. He actively searched for cancer among the traditionally-living Inuit from 1885 to 1907. Along with his staff, he performed 50,000 examinations a year for the first 15 years, and 25,000 a year thereafter. He did not find a single case of cancer. At the same time, he was regularly diagnosing cancers among the crews of whaling ships and other Westernized populations. It's important to note two relevant facts about Inuit culture: first, their habit of going shirtless indoors. This would make visual inspection for external cancers very easy. Second, the Inuit generally had great faith in Western doctors and would consult them even for minor problems. Therefore, doctors in the arctic had ample opportunity to inspect them for cancer.
A study was published in 1934 by F.S. Fellows in the U.S Treasury's Public Health Reports entitled "Mortality in the Native Races of the Territory of Alaska, With Special Reference to Tuberculosis". It contained a table of cancer mortality deaths for several Alaskan regions, all of them Westernized to some degree. However, some were more Westernized than others. In descending order of Westernization, the percent of deaths from cancer were as follows:
.png)
Keep in mind that all four of the Inuit populations in this table were somewhat Westernized. It's clear that cancer incidence tracks well with Westernization. By "Westernization", what I mean mostly is the adoption of European food habits, including wheat flour, sugar, canned goods and vegetable oil. Later, most groups also adopted Western-style houses, which incidentally were not at all suited to their harsh climate.
In the next post, I'll address the classic counter-argument that hunter-gatherers were free of cancer because they didn't live long enough to develop it.
Subscribe to:
Posts (Atom)
