The Kitava study continues to get more and more interesting in later publications. Dr. Lindeberg and his colleagues continued exploring disease markers in the Kitavans, perhaps because their blood lipid findings were not consistent with what one would expect to find in a modern Western population with a low prevalence of CVD.
In their next study, the researchers examined Kitavans' insulin levels compared to Swedish controls. This paper is short but very sweet. Young Kitavan men and women have a fasting serum insulin level considerably lower than their Swedish counterparts (KM 3.9 IU/mL; SM 5.7; KW 3.5; SW 6.2). Kitavan insulin is relatively stable with age, whereas Swedish insulin increases. In the 60-74 year old group, Kitavans have approximately half the fasting serum insulin of Swedes. One thing to keep in mind is that these are average numbers. There is some overlap between the Kitavan and Swedish numbers, with a few Kitavans above the Swedish mean.
In figure 2, they address the possibility that exercise is the reason for Kitavans' low insulin levels. Kitavans have an activity level comparable to a moderately active Swedish person. They divided the Swedes into three categories: low, medium, and high amounts of physical activity at work. The people in the "low" category had the highest insulin, followed by the "high" group and then the "medium" group. The differences were small, however, and Kitavans had far lower serum insulin, on average, than any of the three Swedish groups. These data show that exercise can not explain Kitavans' low insulin levels.
The researchers also found that they could accurately predict average Swedish and Kitavan insulin levels using an equation that factored in age, BMI and waist circumference. This shows that there is a strong correlation between body composition and insulin levels, which applies across cultures.
Now it's time to take a step back and do some interpreting. First of all, this paper is consistent with the idea (but does not prove) that elevated insulin is a central element of overweight, vascular disease and possibly the other diseases of civilization. While we saw previously that mainstream blood lipid markers do not correlate well with CVD or stroke on Kitava, insulin has withstood the cross-cultural test.
In my opinion, the most important finding in this paper is that a high-carbohydrate diet does not necessarily lead to elevated fasting insulin. This is why I think the statement "carbohydrate drives insulin drives fat" is an oversimplification. With a properly-functioning pancreas and insulin-sensitive tissues (which many people in industrial societies do not have), a healthy person can eat a high-carbohydrate meal and keep blood glucose under control. Insulin definitely spikes, but it's temporary. The rest of the day, insulin is at basal levels. The Kitavans show that insulin spikes per se do not cause hyperinsulinemia.
So this leads to the Big Question: what causes hyperinsulinemia?? The best I can give you is informed speculation. Who has hyperinsulinemia? Industrial populations, especially the U.S. and native populations that have adopted Western foods. Who doesn't? Non-industrial populations that have not been affected by Western food habits, including the traditional Inuit, the Kuna, the traditional Masai and the Kitavans.
We can guess that total fat, saturated fat and carbohydrate do not cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also guess that there's not some specific food that protects these populations, since they eat completely different things. Exercise also can not completely account for these findings. What does that leave us with? Western food habits. In my opinion, the trail of metabolic destruction that has followed Westerners throughout the world is probably due in large part to industrial foods, including refined wheat flour, sugar and seed oils.
I'm not the first person to come up with this idea, far from it. The idea that specific types of carbohydrate foods, rather than carbohydrate in general, are responsible for the diseases of civilization, has been around for at least a century. It was an inescapable conclusion in the time of Weston Price, when anthropologists and field physicians could observe the transitions of native people to Western diets all over the world. This information has gradually faded from our collective consciousness as native cultures have become increasingly rare. The Kitava study is a helpful modern-day reminder.
Showing posts with label Cardiovascular disease. Show all posts
Showing posts with label Cardiovascular disease. Show all posts
Cardiovascular Risk Factors on Kitava, Part II: Blood Lipids
The findings in the previous post are all pretty much expected in a population that doesn't get heart disease. However, things started to get interesting when Lindeberg's group measured the Kitavans' serum lipids ("cholesterol"). Kitavan and Swedish total cholesterol is about the same in young men, around 174 mg/dL (4.5 mmol/L). It rises with age in older Swedish men but not Kitavans.
Doctors commonly refer to total cholesterol over 200 mg/dL (5.2 mmol/L) as "high", so Kitavan men are in the clear. On the other hand, Kitavan women should be dying of heart disease left and right with their high middle-age cholesterol of 247 mg/dL (6.4 mmol/L)! That's actually higher than the value for Swedish women of the same age, who are far more prone to heart disease than Kitavans.
The fun doesn't stop there. Total cholesterol isn't a good predictor of heart attack risk, but there are better measures. LDL on Kitava is lower in males than in Sweden, but for females it's about the same until old age. HDL is slightly lower than Swedes' at middle and old age, and triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) comparable to Swedes, who suffer from a high rate of cardiovascular mortality.
Kitavan smokers had a lower HDL than nonsmokers, yet still did not develop CVD. Smoking is considered one of the most powerful risk factors for cardiovascular disease in Western populations. I think it's worth noting, however, that Kitavans tend to be light smokers.
These data are difficult to reconcile with the hypothesis that certain patterns of blood lipids cause CVD. Kitavans, particularly the women, have a blood lipid profile that should have them clutching their chests, yet they remain healthy.
There is a theory of the relationship between blood lipids and CVD that can explain these data. Perhaps blood lipids, rather than causing CVD, simply reflect diet composition and other lifestyle factors. Both on Kitava and in the West, low HDL and elevated triglycerides imply a high carbohydrate intake. Low-carbohydrate diets consistently raise HDL and lower triglycerides. On Kitava, carbohydrate comes mostly from root crops. In the West, it comes mostly from processed grains (typically wheat) and sugar. So the blood lipid pattern that associates best with CVD and the metabolic syndrome in the West is simply a marker of industrial food intake.
Doctors commonly refer to total cholesterol over 200 mg/dL (5.2 mmol/L) as "high", so Kitavan men are in the clear. On the other hand, Kitavan women should be dying of heart disease left and right with their high middle-age cholesterol of 247 mg/dL (6.4 mmol/L)! That's actually higher than the value for Swedish women of the same age, who are far more prone to heart disease than Kitavans.
The fun doesn't stop there. Total cholesterol isn't a good predictor of heart attack risk, but there are better measures. LDL on Kitava is lower in males than in Sweden, but for females it's about the same until old age. HDL is slightly lower than Swedes' at middle and old age, and triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) comparable to Swedes, who suffer from a high rate of cardiovascular mortality.
Kitavan smokers had a lower HDL than nonsmokers, yet still did not develop CVD. Smoking is considered one of the most powerful risk factors for cardiovascular disease in Western populations. I think it's worth noting, however, that Kitavans tend to be light smokers.
These data are difficult to reconcile with the hypothesis that certain patterns of blood lipids cause CVD. Kitavans, particularly the women, have a blood lipid profile that should have them clutching their chests, yet they remain healthy.
There is a theory of the relationship between blood lipids and CVD that can explain these data. Perhaps blood lipids, rather than causing CVD, simply reflect diet composition and other lifestyle factors. Both on Kitava and in the West, low HDL and elevated triglycerides imply a high carbohydrate intake. Low-carbohydrate diets consistently raise HDL and lower triglycerides. On Kitava, carbohydrate comes mostly from root crops. In the West, it comes mostly from processed grains (typically wheat) and sugar. So the blood lipid pattern that associates best with CVD and the metabolic syndrome in the West is simply a marker of industrial food intake.
Cardiovascular Risk Factors on Kitava, Part I: Weight and Blood Pressure
The Kitavans are an isolated population free of cardiovascular disease and stroke, despite the fact that more than three quarters of them smoke cigarettes (although not very frequently). They eat a carbohydrate-heavy, whole-foods diet that is uninfluenced by modern food habits and consists mostly of starchy root crops, fruit, vegetables, coconut and fish. Their intake of grains and processed foods is negligible.
Naturally, when Dr. Lindeberg's group discovered that Kitavans don't suffer from heart disease or stroke, they investigated further. In the second paper of the series, they analyzed the Kitavans' "cardiovascular risk factors" that sometimes associate with heart disease in Western populations, such as overweight, hypertension, elevated total cholesterol and other blood lipid markers.
Kitavans are lean. Adult male body mass index (BMI) starts out at 22, and diminishes with age. For comparison, Swedes begin at a BMI of 25 and stay that way. Both populations lose muscle mass with age, so Kitavans are staying lean while Swedes are gaining fat. The average American has a BMI of about 28, which is considered overweight and 2 points away from being obese.
Kitavans also have a low blood pressure that rises modestly with age. This is actually a bit surprising to me, since other non-industrial groups like the Kuna do not experience a rise in blood pressure with age. Compared with Swedes, Kitavans' blood pressure is considerably lower at all ages.
In the next post, I'll discuss the Kitavans' blood lipid numbers ("cholesterol"), which challenge current thinking about heart disease risk factors.
Naturally, when Dr. Lindeberg's group discovered that Kitavans don't suffer from heart disease or stroke, they investigated further. In the second paper of the series, they analyzed the Kitavans' "cardiovascular risk factors" that sometimes associate with heart disease in Western populations, such as overweight, hypertension, elevated total cholesterol and other blood lipid markers.
Kitavans are lean. Adult male body mass index (BMI) starts out at 22, and diminishes with age. For comparison, Swedes begin at a BMI of 25 and stay that way. Both populations lose muscle mass with age, so Kitavans are staying lean while Swedes are gaining fat. The average American has a BMI of about 28, which is considered overweight and 2 points away from being obese.
Kitavans also have a low blood pressure that rises modestly with age. This is actually a bit surprising to me, since other non-industrial groups like the Kuna do not experience a rise in blood pressure with age. Compared with Swedes, Kitavans' blood pressure is considerably lower at all ages.
In the next post, I'll discuss the Kitavans' blood lipid numbers ("cholesterol"), which challenge current thinking about heart disease risk factors.
The Kitavans: Wisdom from the Pacific Islands
There are very few cultures left on this planet that have not been affected by modern food habits. There are even fewer that have been studied thoroughly. The island of Kitava in Papua New Guinea is host to one such culture, and its inhabitants have many profound things to teach us about diet and health.
The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate.
From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples.
Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ.
Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.
Now for a few relevant facts before we really start diving in:
Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from near-complete carnivory to plant-rich omnivory. But it does not include large amounts of industrial foods.
In the next few posts, I'll discuss more specific data about the health of the Kitavans.
The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate.
From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples.
Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ.
Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.
Now for a few relevant facts before we really start diving in:
- Kitavans are moderately active. They have an activity level comparable to a moderately active Swede, the population to which Dr. Lindeberg draws frequent comparisons.
- They have abundant food, and shortage is uncommon.
- Their good health is probably not related to genetics, since genetically similar groups in the same region are exquisitely sensitive to the ravages of industrial food. Furthermore, the only Kitavan who moved away from the island to live a modern life is also the only fat Kitavan.
- Their life expectancy at birth is estimated at 45 years (includes infant mortality), and life expectancy at age 50 is an additional 25 years. This is remarkable for a culture with limited access to modern medicine.
- Over 75% of Kitavans smoke cigarettes, although in small amounts. Even the most isolated societies have their modern vices.
For the whole of PNG, no case of IHD or atherothrombotic stroke has been reported in clinical investigations and autopsy studies among traditionally living Melanesians for more than seven decades, though an increasing number of myocardial infarctions [heart attacks] and angina pectoris in urbanized populations have been reported since the 1960s.Dementia was not found except in in two young Kitavans, who were born handicapped. The elderly remained sharp until death, including one man who reached 100 years of age. Kitavans are also unfamiliar with external cancers, with the exception of one possible case of breast cancer in an elderly woman.
Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from near-complete carnivory to plant-rich omnivory. But it does not include large amounts of industrial foods.
In the next few posts, I'll discuss more specific data about the health of the Kitavans.
Vitamin K2, menatetrenone (MK-4)
Weston Price established the importance of the MK-4 isoform of vitamin K2 (hereafter, K2) with a series of interesting experiments. He showed in chickens that blood levels of calcium and phosphorus depended both on vitamin A and K2, and that the two had synergistic effects on mineral absorption. He also showed that chickens preferred eating butter that was rich in K2 over butter low in K2, even when the investigators couldn't distinguish between them. Young turkeys fed K2-containing butter oil along with cod liver oil (A and D) also grew at a much faster rate than turkeys fed cod liver oil alone.
He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.
Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.
Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.
Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.
Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status.
The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.
I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.
Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.
Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.
Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).
He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.
Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.
Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.
Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.
Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status.
The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.
I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.
Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.
Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.
Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).
Masai and Atherosclerosis
I've been digging deeper into the health of the Masai lately. A commenter on Chris's blog pointed me to a 1972 paper showing that the Masai have atherosclerosis, or hardening of the arteries. This interested me so I got my hands on the full text, along with a few others from the same time period. What I found is nothing short of fascinating.
First, some background. Traditional Masai in Kenya and Tanzania are pastoralists, subsisting on fermented cow's milk, meat and blood, as well as traded food in modern times. They rarely eat fresh vegetables. Contrary to popular belief, they are a genetically diverse population, due to the custom of abducting women from neighboring tribes. Many of these tribes are agriculturalists. From Mann et al: "The genetic argument is worthless". This will be important to keep in mind as we interpret the data.
At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow's milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat. Here is the reference for all this. Milk fat is about 50% saturated. That means the Muran gets 33% of his calories from saturated fat. This population eats more saturated fat than any other I'm aware of.
How's their cholesterol? Remarkably low. Their total serum cholesterol is about half the average American's. I haven't found any studies that broke it down further than total cholesterol. Their blood pressure is also low, and hypertension is rare. Overweight is practically nonexistent. Their electrocardiogram readings show no signs of heart disease. They have exceptionally good endurance, but their grip strength is significantly weaker than Americans of African descent. Two groups undertook autopsies of male Masai to look for artery disease.
The first study, published in 1970, examined 10 males, 7 of which were over 40 years old. They found very little evidence of atherosclerosis, even in individuals over 60. The second study, which is often used as evidence against a high-fat diet, was much more thorough and far more interesting. Mann et al. autopsied 50 Masai men, aged 10 to 65. The single most represented age group was 50-59 years old, at 13 individuals. They found no evidence of myocardial infarction (heart attack) in any of the 50 hearts. What they did find, however, was coronary artery disease. Here's a figure showing the prevalence of "aortic fibrosis", a type of atherosclerotic lesion:
It looks almost binary, doesn't it? What could be causing the dramatic jump in atherosclerosis at age 40? Here's another figure, of total cholesterol (top) and "sudanophilia" (fatty streaks in the arteries, bottom). Note that the Muran period is superimposed (top).
There appears to be a pattern here. Either the Masai men are eating nothing but milk, meat and blood and they're nearly free from atherosclerosis, or they're eating however they please and they have as much atherosclerosis as the average American. There doesn't seem to be much in between.
Here's a quote from the paper that I found interesting:
This may suggest that you can eat a wide variety of foods and be healthy, except industrial grain products (particularly white flour), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.
First, some background. Traditional Masai in Kenya and Tanzania are pastoralists, subsisting on fermented cow's milk, meat and blood, as well as traded food in modern times. They rarely eat fresh vegetables. Contrary to popular belief, they are a genetically diverse population, due to the custom of abducting women from neighboring tribes. Many of these tribes are agriculturalists. From Mann et al: "The genetic argument is worthless". This will be important to keep in mind as we interpret the data.
At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow's milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat. Here is the reference for all this. Milk fat is about 50% saturated. That means the Muran gets 33% of his calories from saturated fat. This population eats more saturated fat than any other I'm aware of.
How's their cholesterol? Remarkably low. Their total serum cholesterol is about half the average American's. I haven't found any studies that broke it down further than total cholesterol. Their blood pressure is also low, and hypertension is rare. Overweight is practically nonexistent. Their electrocardiogram readings show no signs of heart disease. They have exceptionally good endurance, but their grip strength is significantly weaker than Americans of African descent. Two groups undertook autopsies of male Masai to look for artery disease.
The first study, published in 1970, examined 10 males, 7 of which were over 40 years old. They found very little evidence of atherosclerosis, even in individuals over 60. The second study, which is often used as evidence against a high-fat diet, was much more thorough and far more interesting. Mann et al. autopsied 50 Masai men, aged 10 to 65. The single most represented age group was 50-59 years old, at 13 individuals. They found no evidence of myocardial infarction (heart attack) in any of the 50 hearts. What they did find, however, was coronary artery disease. Here's a figure showing the prevalence of "aortic fibrosis", a type of atherosclerotic lesion:
It looks almost binary, doesn't it? What could be causing the dramatic jump in atherosclerosis at age 40? Here's another figure, of total cholesterol (top) and "sudanophilia" (fatty streaks in the arteries, bottom). Note that the Muran period is superimposed (top).
There appears to be a pattern here. Either the Masai men are eating nothing but milk, meat and blood and they're nearly free from atherosclerosis, or they're eating however they please and they have as much atherosclerosis as the average American. There doesn't seem to be much in between.
Here's a quote from the paper that I found interesting:
We believe... that the Muran escapes some noxious dietary agent for a time. Obviously, this is neither animal fat nor cholesterol. The old and the young Masai do have access to such processed staples as flour, sugar, confections and shortenings through the Indian dukas scattered about Masailand. These foods could carry the hypothetical agent."
This may suggest that you can eat a wide variety of foods and be healthy, except industrial grain products (particularly white flour), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.
The French Paradox
According to the World Health Organization, 82 out of every 100,000 French men between ages 35 and 74 died as a result of cardiovascular disease (CVD) in the year 2000. In that same year, 216 out of 100,000 men between the same ages in the U.S. succumbed to the same disease.
According to the Food and Agriculture Organization of the UN, during roughly the same time period, the average French person ate slightly more total fat and almost three times more animal fat than the average American. Animal fats came from dairy, lard, red meats, fish and poultry, and contributed to a much higher overall saturated fat intake in the French. This has been called the "French paradox", the paradox being that saturated fat is supposed to cause CVD.
Researchers have been scrambling to identify the factor that is protecting French hearts from the toxic onslaught of saturated fat. What could possibly be preventing the buttery sludge coursing through their arteries from killing them on the spot? One hypothesis is that wine is protective. Although the modern French don't actually drink much more alcohol than Americans on average, wine contains a number of molecules that are potentially protective.
One of these that has gotten a lot of attention is resveratrol, an activator of SIRT1, a deacetylase enzyme that is involved in stress resistance and lifespan regulation. But lo and behold, it turns out that there isn't enough of it in wine to be helpful. Now researchers are turning their attention to a class of molecules called procyanidins, but I suspect that this will turn up negative as well. The protective molecule is probably ethanol, but no one wants to hear that because it doesn't resolve the paradox.
As a person with a French background who has spent quite a bit of time in France, the notion of a French paradox is insulting. It implies that the French are eating an unhealthy diet, but are somehow miraculously protected by a compound they're ingesting by accident. Any French person will tell you there is no paradox. When you make a commitment to seek out the freshest, most delicious ingredients available and cook them yourself, your diet will be healthier than if you count the grams of this and that on your TV dinner.
There's more. Americans consume almost twice the amount of sugar as the average French person. I find this surprising, given the large amount of sugar I've seen on French tables, but I think it speaks to the huge amount of sugar we consume in the US. Much of it probably comes from the high-fructose corn syrup in soda. I'll save my rant about that for another time.
Another thing that stands out about French food habits is the absence of snacking. Mealtimes in France tend to be well-defined, and grazing is looked down upon. I think this is probably essential for maintaining adequate insulin sensitivity in the face of (delicious) refined carbohydrates like baguette.
And finally, the French enjoy their food more than the average nation. I wouldn't underestimate the value of this for health and overall well-being.
So what was the paradox again? I can't remember. Maybe a more parsimonious explanation of the data is that saturated fat isn't so bad after all, and enjoying wholesome food and limiting sugar is the true prescription for health.
Thanks to Gaetan Lee for the creative commons photo.
Cardiovascular Risk Factors on Kitava, Part III: Insulin
The Kitava study continues to get more and more interesting in later publications. Dr. Lindeberg and his colleagues continued exploring disease markers in the Kitavans, perhaps because their blood lipid findings were not consistent with what one would expect to find in a modern Western population with a low prevalence of CVD.
In their next study, the researchers examined Kitavans' insulin levels compared to Swedish controls. This paper is short but very sweet. Young Kitavan men and women have a fasting serum insulin level considerably lower than their Swedish counterparts (KM 3.9 IU/mL; SM 5.7; KW 3.5; SW 6.2). Kitavan insulin is relatively stable with age, whereas Swedish insulin increases. In the 60-74 year old group, Kitavans have approximately half the fasting serum insulin of Swedes. One thing to keep in mind is that these are average numbers. There is some overlap between the Kitavan and Swedish numbers, with a few Kitavans above the Swedish mean.
In figure 2, they address the possibility that exercise is the reason for Kitavans' low insulin levels. Kitavans have an activity level comparable to a moderately active Swedish person. They divided the Swedes into three categories: low, medium, and high amounts of physical activity at work. The people in the "low" category had the highest insulin, followed by the "high" group and then the "medium" group. The differences were small, however, and Kitavans had far lower serum insulin, on average, than any of the three Swedish groups. These data show that exercise can not explain Kitavans' low insulin levels.
The researchers also found that they could accurately predict average Swedish and Kitavan insulin levels using an equation that factored in age, BMI and waist circumference. This shows that there is a strong correlation between body composition and insulin levels, which applies across cultures.
Now it's time to take a step back and do some interpreting. First of all, this paper is consistent with the idea (but does not prove) that elevated insulin is a central element of overweight, vascular disease and possibly the other diseases of civilization. While we saw previously that mainstream blood lipid markers do not correlate well with CVD or stroke on Kitava, insulin has withstood the cross-cultural test.
In my opinion, the most important finding in this paper is that a high-carbohydrate diet does not necessarily lead to elevated fasting insulin. This is why I think the statement "carbohydrate drives insulin drives fat" is an oversimplification. With a properly-functioning pancreas and insulin-sensitive tissues (which many people in industrial societies do not have), a healthy person can eat a high-carbohydrate meal and keep blood glucose under control. Insulin definitely spikes, but it's temporary. The rest of the day, insulin is at basal levels. The Kitavans show that insulin spikes per se do not cause hyperinsulinemia.
So this leads to the Big Question: what causes hyperinsulinemia?? The best I can give you is informed speculation. Who has hyperinsulinemia? Industrial populations, especially the U.S. and native populations that have adopted Western foods. Who doesn't? Non-industrial populations that have not been affected by Western food habits, including the traditional Inuit, the Kuna, the traditional Masai and the Kitavans.
We can guess that total fat, saturated fat and carbohydrate do not cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also guess that there's not some specific food that protects these populations, since they eat completely different things. Exercise also can not completely account for these findings. What does that leave us with? Western food habits. In my opinion, the trail of metabolic destruction that has followed Westerners throughout the world is probably due in large part to industrial foods, including refined wheat flour, sugar and seed oils.
I'm not the first person to come up with this idea, far from it. The idea that specific types of carbohydrate foods, rather than carbohydrate in general, are responsible for the diseases of civilization, has been around for at least a century. It was an inescapable conclusion in the time of Weston Price, when anthropologists and field physicians could observe the transitions of native people to Western diets all over the world. This information has gradually faded from our collective consciousness as native cultures have become increasingly rare. The Kitava study is a helpful modern-day reminder.
In their next study, the researchers examined Kitavans' insulin levels compared to Swedish controls. This paper is short but very sweet. Young Kitavan men and women have a fasting serum insulin level considerably lower than their Swedish counterparts (KM 3.9 IU/mL; SM 5.7; KW 3.5; SW 6.2). Kitavan insulin is relatively stable with age, whereas Swedish insulin increases. In the 60-74 year old group, Kitavans have approximately half the fasting serum insulin of Swedes. One thing to keep in mind is that these are average numbers. There is some overlap between the Kitavan and Swedish numbers, with a few Kitavans above the Swedish mean.
In figure 2, they address the possibility that exercise is the reason for Kitavans' low insulin levels. Kitavans have an activity level comparable to a moderately active Swedish person. They divided the Swedes into three categories: low, medium, and high amounts of physical activity at work. The people in the "low" category had the highest insulin, followed by the "high" group and then the "medium" group. The differences were small, however, and Kitavans had far lower serum insulin, on average, than any of the three Swedish groups. These data show that exercise can not explain Kitavans' low insulin levels.
The researchers also found that they could accurately predict average Swedish and Kitavan insulin levels using an equation that factored in age, BMI and waist circumference. This shows that there is a strong correlation between body composition and insulin levels, which applies across cultures.
Now it's time to take a step back and do some interpreting. First of all, this paper is consistent with the idea (but does not prove) that elevated insulin is a central element of overweight, vascular disease and possibly the other diseases of civilization. While we saw previously that mainstream blood lipid markers do not correlate well with CVD or stroke on Kitava, insulin has withstood the cross-cultural test.
In my opinion, the most important finding in this paper is that a high-carbohydrate diet does not necessarily lead to elevated fasting insulin. This is why I think the statement "carbohydrate drives insulin drives fat" is an oversimplification. With a properly-functioning pancreas and insulin-sensitive tissues (which many people in industrial societies do not have), a healthy person can eat a high-carbohydrate meal and keep blood glucose under control. Insulin definitely spikes, but it's temporary. The rest of the day, insulin is at basal levels. The Kitavans show that insulin spikes per se do not cause hyperinsulinemia.
So this leads to the Big Question: what causes hyperinsulinemia?? The best I can give you is informed speculation. Who has hyperinsulinemia? Industrial populations, especially the U.S. and native populations that have adopted Western foods. Who doesn't? Non-industrial populations that have not been affected by Western food habits, including the traditional Inuit, the Kuna, the traditional Masai and the Kitavans.
We can guess that total fat, saturated fat and carbohydrate do not cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also guess that there's not some specific food that protects these populations, since they eat completely different things. Exercise also can not completely account for these findings. What does that leave us with? Western food habits. In my opinion, the trail of metabolic destruction that has followed Westerners throughout the world is probably due in large part to industrial foods, including refined wheat flour, sugar and seed oils.
I'm not the first person to come up with this idea, far from it. The idea that specific types of carbohydrate foods, rather than carbohydrate in general, are responsible for the diseases of civilization, has been around for at least a century. It was an inescapable conclusion in the time of Weston Price, when anthropologists and field physicians could observe the transitions of native people to Western diets all over the world. This information has gradually faded from our collective consciousness as native cultures have become increasingly rare. The Kitava study is a helpful modern-day reminder.
Cardiovascular Risk Factors on Kitava, Part II: Blood Lipids
The findings in the previous post are all pretty much expected in a population that doesn't get heart disease. However, things started to get interesting when Lindeberg's group measured the Kitavans' serum lipids ("cholesterol"). Kitavan and Swedish total cholesterol is about the same in young men, around 174 mg/dL (4.5 mmol/L). It rises with age in older Swedish men but not Kitavans.
Doctors commonly refer to total cholesterol over 200 mg/dL (5.2 mmol/L) as "high", so Kitavan men are in the clear. On the other hand, Kitavan women should be dying of heart disease left and right with their high middle-age cholesterol of 247 mg/dL (6.4 mmol/L)! That's actually higher than the value for Swedish women of the same age, who are far more prone to heart disease than Kitavans.
The fun doesn't stop there. Total cholesterol isn't a good predictor of heart attack risk, but there are better measures. LDL on Kitava is lower in males than in Sweden, but for females it's about the same until old age. HDL is slightly lower than Swedes' at middle and old age, and triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) comparable to Swedes, who suffer from a high rate of cardiovascular mortality.
Kitavan smokers had a lower HDL than nonsmokers, yet still did not develop CVD. Smoking is considered one of the most powerful risk factors for cardiovascular disease in Western populations. I think it's worth noting, however, that Kitavans tend to be light smokers.
These data are difficult to reconcile with the hypothesis that certain patterns of blood lipids cause CVD. Kitavans, particularly the women, have a blood lipid profile that should have them clutching their chests, yet they remain healthy.
There is a theory of the relationship between blood lipids and CVD that can explain these data. Perhaps blood lipids, rather than causing CVD, simply reflect diet composition and other lifestyle factors. Both on Kitava and in the West, low HDL and elevated triglycerides imply a high carbohydrate intake. Low-carbohydrate diets consistently raise HDL and lower triglycerides. On Kitava, carbohydrate comes mostly from root crops. In the West, it comes mostly from processed grains (typically wheat) and sugar. So the blood lipid pattern that associates best with CVD and the metabolic syndrome in the West is simply a marker of industrial food intake.
Doctors commonly refer to total cholesterol over 200 mg/dL (5.2 mmol/L) as "high", so Kitavan men are in the clear. On the other hand, Kitavan women should be dying of heart disease left and right with their high middle-age cholesterol of 247 mg/dL (6.4 mmol/L)! That's actually higher than the value for Swedish women of the same age, who are far more prone to heart disease than Kitavans.
The fun doesn't stop there. Total cholesterol isn't a good predictor of heart attack risk, but there are better measures. LDL on Kitava is lower in males than in Sweden, but for females it's about the same until old age. HDL is slightly lower than Swedes' at middle and old age, and triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) comparable to Swedes, who suffer from a high rate of cardiovascular mortality.
Kitavan smokers had a lower HDL than nonsmokers, yet still did not develop CVD. Smoking is considered one of the most powerful risk factors for cardiovascular disease in Western populations. I think it's worth noting, however, that Kitavans tend to be light smokers.
These data are difficult to reconcile with the hypothesis that certain patterns of blood lipids cause CVD. Kitavans, particularly the women, have a blood lipid profile that should have them clutching their chests, yet they remain healthy.
There is a theory of the relationship between blood lipids and CVD that can explain these data. Perhaps blood lipids, rather than causing CVD, simply reflect diet composition and other lifestyle factors. Both on Kitava and in the West, low HDL and elevated triglycerides imply a high carbohydrate intake. Low-carbohydrate diets consistently raise HDL and lower triglycerides. On Kitava, carbohydrate comes mostly from root crops. In the West, it comes mostly from processed grains (typically wheat) and sugar. So the blood lipid pattern that associates best with CVD and the metabolic syndrome in the West is simply a marker of industrial food intake.
Cardiovascular Risk Factors on Kitava, Part I: Weight and Blood Pressure
The Kitavans are an isolated population free of cardiovascular disease and stroke, despite the fact that more than three quarters of them smoke cigarettes (although not very frequently). They eat a carbohydrate-heavy, whole-foods diet that is uninfluenced by modern food habits and consists mostly of starchy root crops, fruit, vegetables, coconut and fish. Their intake of grains and processed foods is negligible.
Naturally, when Dr. Lindeberg's group discovered that Kitavans don't suffer from heart disease or stroke, they investigated further. In the second paper of the series, they analyzed the Kitavans' "cardiovascular risk factors" that sometimes associate with heart disease in Western populations, such as overweight, hypertension, elevated total cholesterol and other blood lipid markers.
Kitavans are lean. Adult male body mass index (BMI) starts out at 22, and diminishes with age. For comparison, Swedes begin at a BMI of 25 and stay that way. Both populations lose muscle mass with age, so Kitavans are staying lean while Swedes are gaining fat. The average American has a BMI of about 28, which is considered overweight and 2 points away from being obese.
Kitavans also have a low blood pressure that rises modestly with age. This is actually a bit surprising to me, since other non-industrial groups like the Kuna do not experience a rise in blood pressure with age. Compared with Swedes, Kitavans' blood pressure is considerably lower at all ages.
In the next post, I'll discuss the Kitavans' blood lipid numbers ("cholesterol"), which challenge current thinking about heart disease risk factors.
Naturally, when Dr. Lindeberg's group discovered that Kitavans don't suffer from heart disease or stroke, they investigated further. In the second paper of the series, they analyzed the Kitavans' "cardiovascular risk factors" that sometimes associate with heart disease in Western populations, such as overweight, hypertension, elevated total cholesterol and other blood lipid markers.
Kitavans are lean. Adult male body mass index (BMI) starts out at 22, and diminishes with age. For comparison, Swedes begin at a BMI of 25 and stay that way. Both populations lose muscle mass with age, so Kitavans are staying lean while Swedes are gaining fat. The average American has a BMI of about 28, which is considered overweight and 2 points away from being obese.
Kitavans also have a low blood pressure that rises modestly with age. This is actually a bit surprising to me, since other non-industrial groups like the Kuna do not experience a rise in blood pressure with age. Compared with Swedes, Kitavans' blood pressure is considerably lower at all ages.
In the next post, I'll discuss the Kitavans' blood lipid numbers ("cholesterol"), which challenge current thinking about heart disease risk factors.
The Kitavans: Wisdom from the Pacific Islands
There are very few cultures left on this planet that have not been affected by modern food habits. There are even fewer that have been studied thoroughly. The island of Kitava in Papua New Guinea is host to one such culture, and its inhabitants have many profound things to teach us about diet and health.
The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate.
From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples.
Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ.
Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.
Now for a few relevant facts before we really start diving in:
Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from near-complete carnivory to plant-rich omnivory. But it does not include large amounts of industrial foods.
In the next few posts, I'll discuss more specific data about the health of the Kitavans.
The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate.
From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples.
Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ.
Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.
Now for a few relevant facts before we really start diving in:
- Kitavans are moderately active. They have an activity level comparable to a moderately active Swede, the population to which Dr. Lindeberg draws frequent comparisons.
- They have abundant food, and shortage is uncommon.
- Their good health is probably not related to genetics, since genetically similar groups in the same region are exquisitely sensitive to the ravages of industrial food. Furthermore, the only Kitavan who moved away from the island to live a modern life is also the only fat Kitavan.
- Their life expectancy at birth is estimated at 45 years (includes infant mortality), and life expectancy at age 50 is an additional 25 years. This is remarkable for a culture with limited access to modern medicine.
- Over 75% of Kitavans smoke cigarettes, although in small amounts. Even the most isolated societies have their modern vices.
For the whole of PNG, no case of IHD or atherothrombotic stroke has been reported in clinical investigations and autopsy studies among traditionally living Melanesians for more than seven decades, though an increasing number of myocardial infarctions [heart attacks] and angina pectoris in urbanized populations have been reported since the 1960s.Dementia was not found except in in two young Kitavans, who were born handicapped. The elderly remained sharp until death, including one man who reached 100 years of age. Kitavans are also unfamiliar with external cancers, with the exception of one possible case of breast cancer in an elderly woman.
Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from near-complete carnivory to plant-rich omnivory. But it does not include large amounts of industrial foods.
In the next few posts, I'll discuss more specific data about the health of the Kitavans.
Vitamin K2, menatetrenone (MK-4)
Weston Price established the importance of the MK-4 isoform of vitamin K2 (hereafter, K2) with a series of interesting experiments. He showed in chickens that blood levels of calcium and phosphorus depended both on vitamin A and K2, and that the two had synergistic effects on mineral absorption. He also showed that chickens preferred eating butter that was rich in K2 over butter low in K2, even when the investigators couldn't distinguish between them. Young turkeys fed K2-containing butter oil along with cod liver oil (A and D) also grew at a much faster rate than turkeys fed cod liver oil alone.
He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.
Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.
Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.
Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.
Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status.
The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.
I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.
Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.
Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.
Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).
He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.
Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.
Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.
Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.
Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status.
The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.
I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.
Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.
Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.
Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).
Masai and Atherosclerosis
I've been digging deeper into the health of the Masai lately. A commenter on Chris's blog pointed me to a 1972 paper showing that the Masai have atherosclerosis, or hardening of the arteries. This interested me so I got my hands on the full text, along with a few others from the same time period. What I found is nothing short of fascinating.
First, some background. Traditional Masai in Kenya and Tanzania are pastoralists, subsisting on fermented cow's milk, meat and blood, as well as traded food in modern times. They rarely eat fresh vegetables. Contrary to popular belief, they are a genetically diverse population, due to the custom of abducting women from neighboring tribes. Many of these tribes are agriculturalists. From Mann et al: "The genetic argument is worthless". This will be important to keep in mind as we interpret the data.
At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow's milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat. Here is the reference for all this. Milk fat is about 50% saturated. That means the Muran gets 33% of his calories from saturated fat. This population eats more saturated fat than any other I'm aware of.
How's their cholesterol? Remarkably low. Their total serum cholesterol is about half the average American's. I haven't found any studies that broke it down further than total cholesterol. Their blood pressure is also low, and hypertension is rare. Overweight is practically nonexistent. Their electrocardiogram readings show no signs of heart disease. They have exceptionally good endurance, but their grip strength is significantly weaker than Americans of African descent. Two groups undertook autopsies of male Masai to look for artery disease.
The first study, published in 1970, examined 10 males, 7 of which were over 40 years old. They found very little evidence of atherosclerosis, even in individuals over 60. The second study, which is often used as evidence against a high-fat diet, was much more thorough and far more interesting. Mann et al. autopsied 50 Masai men, aged 10 to 65. The single most represented age group was 50-59 years old, at 13 individuals. They found no evidence of myocardial infarction (heart attack) in any of the 50 hearts. What they did find, however, was coronary artery disease. Here's a figure showing the prevalence of "aortic fibrosis", a type of atherosclerotic lesion:
It looks almost binary, doesn't it? What could be causing the dramatic jump in atherosclerosis at age 40? Here's another figure, of total cholesterol (top) and "sudanophilia" (fatty streaks in the arteries, bottom). Note that the Muran period is superimposed (top).
There appears to be a pattern here. Either the Masai men are eating nothing but milk, meat and blood and they're nearly free from atherosclerosis, or they're eating however they please and they have as much atherosclerosis as the average American. There doesn't seem to be much in between.
Here's a quote from the paper that I found interesting:
This may suggest that you can eat a wide variety of foods and be healthy, except industrial grain products (particularly white flour), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.
First, some background. Traditional Masai in Kenya and Tanzania are pastoralists, subsisting on fermented cow's milk, meat and blood, as well as traded food in modern times. They rarely eat fresh vegetables. Contrary to popular belief, they are a genetically diverse population, due to the custom of abducting women from neighboring tribes. Many of these tribes are agriculturalists. From Mann et al: "The genetic argument is worthless". This will be important to keep in mind as we interpret the data.
At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow's milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat. Here is the reference for all this. Milk fat is about 50% saturated. That means the Muran gets 33% of his calories from saturated fat. This population eats more saturated fat than any other I'm aware of.
How's their cholesterol? Remarkably low. Their total serum cholesterol is about half the average American's. I haven't found any studies that broke it down further than total cholesterol. Their blood pressure is also low, and hypertension is rare. Overweight is practically nonexistent. Their electrocardiogram readings show no signs of heart disease. They have exceptionally good endurance, but their grip strength is significantly weaker than Americans of African descent. Two groups undertook autopsies of male Masai to look for artery disease.
The first study, published in 1970, examined 10 males, 7 of which were over 40 years old. They found very little evidence of atherosclerosis, even in individuals over 60. The second study, which is often used as evidence against a high-fat diet, was much more thorough and far more interesting. Mann et al. autopsied 50 Masai men, aged 10 to 65. The single most represented age group was 50-59 years old, at 13 individuals. They found no evidence of myocardial infarction (heart attack) in any of the 50 hearts. What they did find, however, was coronary artery disease. Here's a figure showing the prevalence of "aortic fibrosis", a type of atherosclerotic lesion:
It looks almost binary, doesn't it? What could be causing the dramatic jump in atherosclerosis at age 40? Here's another figure, of total cholesterol (top) and "sudanophilia" (fatty streaks in the arteries, bottom). Note that the Muran period is superimposed (top).
There appears to be a pattern here. Either the Masai men are eating nothing but milk, meat and blood and they're nearly free from atherosclerosis, or they're eating however they please and they have as much atherosclerosis as the average American. There doesn't seem to be much in between.
Here's a quote from the paper that I found interesting:
We believe... that the Muran escapes some noxious dietary agent for a time. Obviously, this is neither animal fat nor cholesterol. The old and the young Masai do have access to such processed staples as flour, sugar, confections and shortenings through the Indian dukas scattered about Masailand. These foods could carry the hypothetical agent."
This may suggest that you can eat a wide variety of foods and be healthy, except industrial grain products (particularly white flour), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.
The French Paradox
According to the World Health Organization, 82 out of every 100,000 French men between ages 35 and 74 died as a result of cardiovascular disease (CVD) in the year 2000. In that same year, 216 out of 100,000 men between the same ages in the U.S. succumbed to the same disease.
According to the Food and Agriculture Organization of the UN, during roughly the same time period, the average French person ate slightly more total fat and almost three times more animal fat than the average American. Animal fats came from dairy, lard, red meats, fish and poultry, and contributed to a much higher overall saturated fat intake in the French. This has been called the "French paradox", the paradox being that saturated fat is supposed to cause CVD.
Researchers have been scrambling to identify the factor that is protecting French hearts from the toxic onslaught of saturated fat. What could possibly be preventing the buttery sludge coursing through their arteries from killing them on the spot? One hypothesis is that wine is protective. Although the modern French don't actually drink much more alcohol than Americans on average, wine contains a number of molecules that are potentially protective.
One of these that has gotten a lot of attention is resveratrol, an activator of SIRT1, a deacetylase enzyme that is involved in stress resistance and lifespan regulation. But lo and behold, it turns out that there isn't enough of it in wine to be helpful. Now researchers are turning their attention to a class of molecules called procyanidins, but I suspect that this will turn up negative as well. The protective molecule is probably ethanol, but no one wants to hear that because it doesn't resolve the paradox.
As a person with a French background who has spent quite a bit of time in France, the notion of a French paradox is insulting. It implies that the French are eating an unhealthy diet, but are somehow miraculously protected by a compound they're ingesting by accident. Any French person will tell you there is no paradox. When you make a commitment to seek out the freshest, most delicious ingredients available and cook them yourself, your diet will be healthier than if you count the grams of this and that on your TV dinner.
There's more. Americans consume almost twice the amount of sugar as the average French person. I find this surprising, given the large amount of sugar I've seen on French tables, but I think it speaks to the huge amount of sugar we consume in the US. Much of it probably comes from the high-fructose corn syrup in soda. I'll save my rant about that for another time.
Another thing that stands out about French food habits is the absence of snacking. Mealtimes in France tend to be well-defined, and grazing is looked down upon. I think this is probably essential for maintaining adequate insulin sensitivity in the face of (delicious) refined carbohydrates like baguette.
And finally, the French enjoy their food more than the average nation. I wouldn't underestimate the value of this for health and overall well-being.
So what was the paradox again? I can't remember. Maybe a more parsimonious explanation of the data is that saturated fat isn't so bad after all, and enjoying wholesome food and limiting sugar is the true prescription for health.
Thanks to Gaetan Lee for the creative commons photo.
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