Last October, I participated in a panel discussion organized by the Harvard Food Law Society in Boston. The panel included Drs. Walter Willett, David Ludwig, Robert Lustig, and myself, with Corby Kummer as moderator. Dr. Willett is the chair of the Harvard Department of Nutrition; Dr. Ludwig is a professor of nutrition and pediatrics at Harvard; Dr. Lustig is a professor of clinical pediatrics at UCSF; and Kummer is a food writer and senior editor for The Atlantic.
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Saturday, 5 May 2012
Saturday, 28 April 2012
Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part I
In the previous post, I explained that Otzi descended in large part from early adopters of agriculture in the Middle East or nearby. What I'll explain in further posts is that Otzi was not a genetic anomaly: he was part of a wave of agricultural migrants that washed over Europe thousands of years ago, spreading their genes throughout. Not only that, Otzi represents a halfway point in the evolutionary process that transformed Paleolithic humans into modern humans.
Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?
There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe. One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains. The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle. These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals. We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming.
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Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?
There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe. One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains. The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle. These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals. We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming.
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Tuesday, 24 April 2012
Lessons From Ötzi, the Tyrolean Ice Man. Part III
There are two reasons why I chose this time to write about Otzi. The first is that I've been looking for a good excuse to revisit human evolutionary history, particularly that of Europeans, and what it does and doesn't tell us about the "optimal" human diet. The second is that Otzi's full genome was sequenced and described in a recent issue of Nature Communications (1). A "genome" is the full complement of genes an organism carries. So what that means is that researchers have sequenced almost all of his genes.
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Monday, 23 April 2012
Hunger is your best friend: It makes natural foods taste delicious and promotes optimal nutrient partitioning
One of the biggest problems with modern diets rich in industrial foods is that they promote unnatural hunger patterns. For example, hunger can be caused by hypoglycemic dips, coupled with force-storage of fat in adipocytes, after meals rich in refined carbohydrates. This is a double-edged post-meal pattern that is induced by, among other things, abnormally elevated insulin levels. The resulting hunger is a rather unnatural type of hunger.
By the way, I often read here and there, mostly in blogs, that “insulin suppresses hunger”. I frankly don’t know where this idea comes from. What actually happens is that insulin is co-secreted with a number of other hormones. One of those, like insulin also secreted by the beta-cells in the pancreas, is amylin – a powerful appetite suppressor. Amylin deficiency leads to hunger even after a large carbohydrate-rich meal, when insulin levels are elevated.
Abnormally high insulin levels – like those after a “healthy” breakfast of carbohydrate-rich cereals, pancakes etc. – lead to abnormal blood glucose dips soon after the meal. What I am talking about here is a fall in glucose levels that is considerable, and that also happens very fast – illustrated by the ratio between the lengths of the vertical and horizontal black lines on the figure below, from a previous post ().
Those hypoglycemic dips induce hunger, because the hormonal changes necessary to apply a break to the fall in glucose levels (which left unchecked would lead to death) leave us with a hormonal mix that ends up stimulating hunger, in an unnatural way. At the bottom of those dips, insulin levels are much lower than before. I am not talking about diabetics here. I am talking about normoglycemic folks, like the ones whose glucose levels are show on the figure above.
On a diet primarily of natural foods, or foods that are not heavily modified from their natural state, hunger patterns tend to be better synchronized with nutrient deficiencies. This is one of the main advantages of a natural foods diet. By nutrients, I do not mean only micronutrients such as vitamins and minerals, but also macronutrients such as amino and fatty acids.
On a natural diet, nutrient deficiencies should happen regularly. Our bodies are designed for sporadic nutrient intake, remaining most of the time in the fasted state. Human beings are unique in that they have very large brains in proportion to their overall body size, brains that run primarily on glucose – the average person’s brain consumes about 5 g/h of glucose. This latter characteristic makes it very difficult to extrapolate diet-based results based on other species to humans.
As hunger becomes better synchronized with nutrient deficiencies, it should promote optimal nutrient partitioning. This means that, among other things: (a) you should periodically feel hungry for different types of food, depending on your nutrient needs at that point in time; (b) if you do weight training, and fell hungry, some muscle gain should follow; and (c) if you let hunger drive food consumption, on a diet of predominantly natural foods, body fat levels should remain relatively low.
In this sense, hunger becomes your friend – and the best spice!
By the way, I often read here and there, mostly in blogs, that “insulin suppresses hunger”. I frankly don’t know where this idea comes from. What actually happens is that insulin is co-secreted with a number of other hormones. One of those, like insulin also secreted by the beta-cells in the pancreas, is amylin – a powerful appetite suppressor. Amylin deficiency leads to hunger even after a large carbohydrate-rich meal, when insulin levels are elevated.
Abnormally high insulin levels – like those after a “healthy” breakfast of carbohydrate-rich cereals, pancakes etc. – lead to abnormal blood glucose dips soon after the meal. What I am talking about here is a fall in glucose levels that is considerable, and that also happens very fast – illustrated by the ratio between the lengths of the vertical and horizontal black lines on the figure below, from a previous post ().
Those hypoglycemic dips induce hunger, because the hormonal changes necessary to apply a break to the fall in glucose levels (which left unchecked would lead to death) leave us with a hormonal mix that ends up stimulating hunger, in an unnatural way. At the bottom of those dips, insulin levels are much lower than before. I am not talking about diabetics here. I am talking about normoglycemic folks, like the ones whose glucose levels are show on the figure above.
On a diet primarily of natural foods, or foods that are not heavily modified from their natural state, hunger patterns tend to be better synchronized with nutrient deficiencies. This is one of the main advantages of a natural foods diet. By nutrients, I do not mean only micronutrients such as vitamins and minerals, but also macronutrients such as amino and fatty acids.
On a natural diet, nutrient deficiencies should happen regularly. Our bodies are designed for sporadic nutrient intake, remaining most of the time in the fasted state. Human beings are unique in that they have very large brains in proportion to their overall body size, brains that run primarily on glucose – the average person’s brain consumes about 5 g/h of glucose. This latter characteristic makes it very difficult to extrapolate diet-based results based on other species to humans.
As hunger becomes better synchronized with nutrient deficiencies, it should promote optimal nutrient partitioning. This means that, among other things: (a) you should periodically feel hungry for different types of food, depending on your nutrient needs at that point in time; (b) if you do weight training, and fell hungry, some muscle gain should follow; and (c) if you let hunger drive food consumption, on a diet of predominantly natural foods, body fat levels should remain relatively low.
In this sense, hunger becomes your friend – and the best spice!
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Tuesday, 17 April 2012
Lessons From Ötzi, the Tyrolean Ice Man. Part II
Otzi's Diet
Otzi's digestive tract contains the remains of three meals. They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2). The meat came from three different animals-- chamois, red deer and ibex. The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.
Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3). He died in the spring with a belly full of einkorn wheat. Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year. However, he also clearly ate meat and used leather made from his prey. Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.
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Otzi's digestive tract contains the remains of three meals. They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2). The meat came from three different animals-- chamois, red deer and ibex. The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.
Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3). He died in the spring with a belly full of einkorn wheat. Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year. However, he also clearly ate meat and used leather made from his prey. Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.
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Monday, 16 April 2012
Exercise and Food Intake
The New York Times just published an article reviewing some of the recent research on exercise, food intake and food reward, titled "Does Exercise Make You Overeat?". I was planning to write about this at some point, but I don't know when I'd be able to get around to it, and the NYT article is a fair treatment of the subject, so I'll just point you to the article.
Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less. Alex Hutchinson discussed this point recently on his blog (1). Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat. Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat. There is a lot of individual variability here. The average obese person won't lose a substantial amount of fat through exercise alone. However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people. On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward.
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Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less. Alex Hutchinson discussed this point recently on his blog (1). Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat. Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat. There is a lot of individual variability here. The average obese person won't lose a substantial amount of fat through exercise alone. However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people. On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward.
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Hormonal reductionism is as myopic as biochemical reductionism
Biochemistry-based arguments can be very misleading. Yet, biochemistry can be extremely useful in the elucidation of diet and lifestyle effects that are suggested by well-designed studies of humans. If you start with a biochemistry-based argument though, and ignore actual studies of humans, you can easily convince someone that glycogen-depleting exercise (e.g., weight training) is unhealthy, because many health markers change for the worse after that type of exercise. But it is the damage caused by glycogen-depleting exercise that leads to health improvements, via short- and long-term compensatory adaptations ().
Biochemistry is very helpful in terms of providing “pieces for the puzzle”, but biochemical reductionism is a problem. Analogous to biochemical reductionism, and perhaps one example of it, is hormonal reductionism – trying to argue that all diet and lifestyle effects are mediated by a single hormone. A less extreme position, but still myopic, is to argue that all diet and lifestyle effects are mostly mediated by a single hormone.
One of my own “favorite” hormones is adiponectin, which I have been discussing for years in this blog (). Increased serum adiponectin has been found to be significantly associated with: decreased body fat (particularly decreased visceral fat), decreased risk of developing diabetes type 2, and decreased blood pressure. Adiponectin appears to also have anti-inflammatory and athero-protective properties.
As a side note, typically women have higher levels of serum adiponectin than men, particularly young women. Culturally we have a tendency to see young women as “delicate” and “vulnerable”. Guess what? Young women are the closest we get to “indestructible” in the human species. And there is an evolutionary reason for that, which is that fertile women have been in our evolutionary past, and still are, the bottleneck of any population. A population of 100 individuals, where 99 are men and 1 is a woman, will quickly disappear. If it is 99 women and 1 fertile man, the population will grow; but there will also be some problems due to inbreeding. Even if the guy is ugly the population will grow; without competition, he will look very cute.
Jung and colleagues measured various hormone levels in 78 obese people who had visited obesity clinics at five university hospitals (Ajou, Ulsan, Catholic, Hanyang and Yonsei) in Korea (). Those folks restricted their caloric intake to 500 calories less than their usual intake, and exercised, for 12 weeks. Below are the measured changes in tumor necrosis factor α (TNF-α, now called only TNF), interleukin-6 (IL-6), resistin, leptin, adiponectin, and interleukin-10 (IL-10).
We see from the table above that the hormonal changes were all significant (all at the P equal to or lower than 0.001 level except one, at the P lower than 0.05 level), and all indicative of health improvements. The serum concentrations of all hormones decreased, with two exceptions – adiponectin and interleukin-10, which increased. Interleukin-10 is an anti-inflammatory hormone produced by white blood cells. The most significant increase of the two was by far in adiponectin (P = .001, versus P = .041 for interleukin-10).
Now, should we try to find a way of producing synthetic adiponectin then? My guess is that doing that will not lead to very positive results in human trials; because, as you can see from the table, hormones vary in concert. At the moment, the only way to “supplement” adiponectin is to lose body fat, and that leads to concurrent changes in many other hormones (e.g., TNF decreases).
Trying to manipulate one single hormone, or build an entire health-improvement approach based on its effects, is myopic. But that is what often happens. Leptin is a relatively recent example.
One reason why biochemistry is so complex, with so many convoluted processes, is that evolution is a tinkerer that is “blind” to complexity. Traits appear at random in populations and spread if they increase reproductive success; even if they decrease survival success, by the way ().
Evolution is not an engineer, and is not even our “friend” (). To optimize our health, we need to “hack” evolution.
Biochemistry is very helpful in terms of providing “pieces for the puzzle”, but biochemical reductionism is a problem. Analogous to biochemical reductionism, and perhaps one example of it, is hormonal reductionism – trying to argue that all diet and lifestyle effects are mediated by a single hormone. A less extreme position, but still myopic, is to argue that all diet and lifestyle effects are mostly mediated by a single hormone.
One of my own “favorite” hormones is adiponectin, which I have been discussing for years in this blog (). Increased serum adiponectin has been found to be significantly associated with: decreased body fat (particularly decreased visceral fat), decreased risk of developing diabetes type 2, and decreased blood pressure. Adiponectin appears to also have anti-inflammatory and athero-protective properties.
As a side note, typically women have higher levels of serum adiponectin than men, particularly young women. Culturally we have a tendency to see young women as “delicate” and “vulnerable”. Guess what? Young women are the closest we get to “indestructible” in the human species. And there is an evolutionary reason for that, which is that fertile women have been in our evolutionary past, and still are, the bottleneck of any population. A population of 100 individuals, where 99 are men and 1 is a woman, will quickly disappear. If it is 99 women and 1 fertile man, the population will grow; but there will also be some problems due to inbreeding. Even if the guy is ugly the population will grow; without competition, he will look very cute.
Jung and colleagues measured various hormone levels in 78 obese people who had visited obesity clinics at five university hospitals (Ajou, Ulsan, Catholic, Hanyang and Yonsei) in Korea (). Those folks restricted their caloric intake to 500 calories less than their usual intake, and exercised, for 12 weeks. Below are the measured changes in tumor necrosis factor α (TNF-α, now called only TNF), interleukin-6 (IL-6), resistin, leptin, adiponectin, and interleukin-10 (IL-10).
We see from the table above that the hormonal changes were all significant (all at the P equal to or lower than 0.001 level except one, at the P lower than 0.05 level), and all indicative of health improvements. The serum concentrations of all hormones decreased, with two exceptions – adiponectin and interleukin-10, which increased. Interleukin-10 is an anti-inflammatory hormone produced by white blood cells. The most significant increase of the two was by far in adiponectin (P = .001, versus P = .041 for interleukin-10).
Now, should we try to find a way of producing synthetic adiponectin then? My guess is that doing that will not lead to very positive results in human trials; because, as you can see from the table, hormones vary in concert. At the moment, the only way to “supplement” adiponectin is to lose body fat, and that leads to concurrent changes in many other hormones (e.g., TNF decreases).
Trying to manipulate one single hormone, or build an entire health-improvement approach based on its effects, is myopic. But that is what often happens. Leptin is a relatively recent example.
One reason why biochemistry is so complex, with so many convoluted processes, is that evolution is a tinkerer that is “blind” to complexity. Traits appear at random in populations and spread if they increase reproductive success; even if they decrease survival success, by the way ().
Evolution is not an engineer, and is not even our “friend” (). To optimize our health, we need to “hack” evolution.
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