A few months ago, I published a post about the Pima Indians (Akimel O'odham) of Arizona. The Pima are one of the most heart-wrenching examples of the disease of civilization afflicting a society after a nutrition transition. Traditionally a healthy agricultural people, they now have some of the highest rates of obesity and diabetes in the world.
The trouble all started when their irrigation waters were diverted upstream in the late 19th century. Their traditional diet of corn, beans, squash, fish, game meats and gathered plant foods became impossible. They became dependent on government food programs, which provided them with white flour, sugar, lard and canned goods. Now they are the subjects of scientific research because of their staggering health problems.
I'm happy to report that after more than 30 years of activism, lawsuits and negotiation, the Pima and neighboring tribes have reached an agreement with the federal government that will restore a portion of their original water. Of the 2 million acre-feet of water the Pima were estimated to have used since before the 16th century, the settlement will restore 653,500. An acre-foot is approximately the personal water use of one household. The settlement also provides federal funds for reconstructing old irrigation canals.
Now we will see how the Pima will use it. Will they return to an agricultural lifestyle, perhaps with the advantages of modern technology? Or will they lease the water rights for money and continue to live off Western foods? Perhaps some of both. They are definitely aware that Western food is causing their health problems, and that they could regain their health by eating traditional foods. However, white flour "fry bread", sugar and canned meat have been around for so long they are also a cultural tradition at this point. Only time will tell which path they choose.
Water for the Pima
A few months ago, I published a post about the Pima Indians (Akimel O'odham) of Arizona. The Pima are one of the most heart-wrenching examples of the disease of civilization afflicting a society after a nutrition transition. Traditionally a healthy agricultural people, they now have some of the highest rates of obesity and diabetes in the world.
The trouble all started when their irrigation waters were diverted upstream in the late 19th century. Their traditional diet of corn, beans, squash, fish, game meats and gathered plant foods became impossible. They became dependent on government food programs, which provided them with white flour, sugar, lard and canned goods. Now they are the subjects of scientific research because of their staggering health problems.
I'm happy to report that after more than 30 years of activism, lawsuits and negotiation, the Pima and neighboring tribes have reached an agreement with the federal government that will restore a portion of their original water. Of the 2 million acre-feet of water the Pima were estimated to have used since before the 16th century, the settlement will restore 653,500. An acre-foot is approximately the personal water use of one household. The settlement also provides federal funds for reconstructing old irrigation canals.
Now we will see how the Pima will use it. Will they return to an agricultural lifestyle, perhaps with the advantages of modern technology? Or will they lease the water rights for money and continue to live off Western foods? Perhaps some of both. They are definitely aware that Western food is causing their health problems, and that they could regain their health by eating traditional foods. However, white flour "fry bread", sugar and canned meat have been around for so long they are also a cultural tradition at this point. Only time will tell which path they choose.
The trouble all started when their irrigation waters were diverted upstream in the late 19th century. Their traditional diet of corn, beans, squash, fish, game meats and gathered plant foods became impossible. They became dependent on government food programs, which provided them with white flour, sugar, lard and canned goods. Now they are the subjects of scientific research because of their staggering health problems.
I'm happy to report that after more than 30 years of activism, lawsuits and negotiation, the Pima and neighboring tribes have reached an agreement with the federal government that will restore a portion of their original water. Of the 2 million acre-feet of water the Pima were estimated to have used since before the 16th century, the settlement will restore 653,500. An acre-foot is approximately the personal water use of one household. The settlement also provides federal funds for reconstructing old irrigation canals.
Now we will see how the Pima will use it. Will they return to an agricultural lifestyle, perhaps with the advantages of modern technology? Or will they lease the water rights for money and continue to live off Western foods? Perhaps some of both. They are definitely aware that Western food is causing their health problems, and that they could regain their health by eating traditional foods. However, white flour "fry bread", sugar and canned meat have been around for so long they are also a cultural tradition at this point. Only time will tell which path they choose.
Conflict of Interest
The U.S. National Cholesterol Education Program (NCEP) is a government organization that educates physicians and the general public about the "dangers" of elevated cholesterol. They have a panel that creates official guidelines for the reduction of cardiovascular disease risk. They contain target cholesterol levels, and the usual recommendations to eat less saturated fat and cholesterol, and lose weight.
They recommend keeping LDL below 100 mg/dL, which would place tens of millions of Americans on statins.
I was reading Dr. John Briffa's blog today and he linked to a government web page disclosing NCEP panel members' conflicts of interest. It's fairly common in academic circles to require conflict of interest statements, so a skeptical audience can decide whether or not they think someone is biased. The 9-member NECP panel was happy to indulge us:
They recommend keeping LDL below 100 mg/dL, which would place tens of millions of Americans on statins.
I was reading Dr. John Briffa's blog today and he linked to a government web page disclosing NCEP panel members' conflicts of interest. It's fairly common in academic circles to require conflict of interest statements, so a skeptical audience can decide whether or not they think someone is biased. The 9-member NECP panel was happy to indulge us:
Every company in bold is a statin manufacturer. This is outrageous! These are the people setting official government blood cholesterol target values for the entire country! Eight out of nine of them should be dismissed immediately, and replaced by people who can do a better job of pretending to be impartial!Dr. Grundy has received honoraria from Merck, Pfizer, Sankyo, Bayer, Merck/Schering-Plough, Kos, Abbott, Bristol-Myers Squibb, and AstraZeneca; he has received research grants from Merck, Abbott, and Glaxo Smith Kline.
Dr. Cleeman has no financial relationships to disclose.
Dr. Bairey Merz has received lecture honoraria from Pfizer, Merck, and Kos; she has served as a consultant for Pfizer, Bayer, and EHC (Merck); she has received unrestricted institutional grants for Continuing Medical Education from Pfizer, Procter & Gamble, Novartis, Wyeth, AstraZeneca, and Bristol-Myers Squibb Medical Imaging; she has received a research grant from Merck; she has stock in Boston Scientific, IVAX, Eli Lilly, Medtronic, Johnson & Johnson, SCIPIE Insurance, ATS Medical, and Biosite.
Dr. Brewer has received honoraria from AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Esperion, and Novartis; he has served as a consultant for AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Sankyo, and Novartis.
Dr. Clark has received honoraria for educational presentations from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer; he has received grant/research support from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer.
Dr. Hunninghake has received honoraria for consulting and speakers bureau from AstraZeneca, Merck, Merck/Schering-Plough, and Pfizer, and for consulting from Kos; he has received research grants from AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, and Pfizer.
Dr. Pasternak has served as a speaker for Pfizer, Merck, Merck/Schering-Plough, Takeda, Kos, BMS-Sanofi, and Novartis; he has served as a consultant for Merck, Merck/Schering-Plough, Sanofi, Pfizer Health Solutions, Johnson & Johnson-Merck, and AstraZeneca.
Dr. Smith has received institutional research support from Merck; he has stock in Medtronic and Johnson & Johnson.
Dr. Stone has received honoraria for educational lectures from Abbott, AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, Pfizer, Reliant, and Sankyo; he has served as a consultant for Abbott, Merck, Merck/Schering-Plough, Pfizer, and Reliant.
Conflict of Interest
The U.S. National Cholesterol Education Program (NCEP) is a government organization that educates physicians and the general public about the "dangers" of elevated cholesterol. They have a panel that creates official guidelines for the reduction of cardiovascular disease risk. They contain target cholesterol levels, and the usual recommendations to eat less saturated fat and cholesterol, and lose weight.
They recommend keeping LDL below 100 mg/dL, which would place tens of millions of Americans on statins.
I was reading Dr. John Briffa's blog today and he linked to a government web page disclosing NCEP panel members' conflicts of interest. It's fairly common in academic circles to require conflict of interest statements, so a skeptical audience can decide whether or not they think someone is biased. The 9-member NECP panel was happy to indulge us:
They recommend keeping LDL below 100 mg/dL, which would place tens of millions of Americans on statins.
I was reading Dr. John Briffa's blog today and he linked to a government web page disclosing NCEP panel members' conflicts of interest. It's fairly common in academic circles to require conflict of interest statements, so a skeptical audience can decide whether or not they think someone is biased. The 9-member NECP panel was happy to indulge us:
Every company in bold is a statin manufacturer. This is outrageous! These are the people setting official government blood cholesterol target values for the entire country! Eight out of nine of them should be dismissed immediately, and replaced by people who can do a better job of pretending to be impartial!Dr. Grundy has received honoraria from Merck, Pfizer, Sankyo, Bayer, Merck/Schering-Plough, Kos, Abbott, Bristol-Myers Squibb, and AstraZeneca; he has received research grants from Merck, Abbott, and Glaxo Smith Kline.
Dr. Cleeman has no financial relationships to disclose.
Dr. Bairey Merz has received lecture honoraria from Pfizer, Merck, and Kos; she has served as a consultant for Pfizer, Bayer, and EHC (Merck); she has received unrestricted institutional grants for Continuing Medical Education from Pfizer, Procter & Gamble, Novartis, Wyeth, AstraZeneca, and Bristol-Myers Squibb Medical Imaging; she has received a research grant from Merck; she has stock in Boston Scientific, IVAX, Eli Lilly, Medtronic, Johnson & Johnson, SCIPIE Insurance, ATS Medical, and Biosite.
Dr. Brewer has received honoraria from AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Esperion, and Novartis; he has served as a consultant for AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Sankyo, and Novartis.
Dr. Clark has received honoraria for educational presentations from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer; he has received grant/research support from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer.
Dr. Hunninghake has received honoraria for consulting and speakers bureau from AstraZeneca, Merck, Merck/Schering-Plough, and Pfizer, and for consulting from Kos; he has received research grants from AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, and Pfizer.
Dr. Pasternak has served as a speaker for Pfizer, Merck, Merck/Schering-Plough, Takeda, Kos, BMS-Sanofi, and Novartis; he has served as a consultant for Merck, Merck/Schering-Plough, Sanofi, Pfizer Health Solutions, Johnson & Johnson-Merck, and AstraZeneca.
Dr. Smith has received institutional research support from Merck; he has stock in Medtronic and Johnson & Johnson.
Dr. Stone has received honoraria for educational lectures from Abbott, AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, Pfizer, Reliant, and Sankyo; he has served as a consultant for Abbott, Merck, Merck/Schering-Plough, Pfizer, and Reliant.
Eating Down the Food Chain
Europe once teemed with large mammals, including species of elephant, lion, tiger, bear, moose and bison. America was also home to a number of huge and unusual animals: mammoths, dire wolves, lions, giant sloths and others.
The same goes for Australia, where giant kangaroos, huge wombats and marsupial 'lions' once roamed.
What do these extinctions have in common? They all occurred around when humans arrived. The idea that humans caused them is hotly debated, because they also sometimes coincided with climactic and vegetation changes. However, I believe the fact that these extinctions occurred on several different continents about when humans arrived points to an anthropogenic explanation.
A recent archaeological study from the island of Tasmania off the coast of Australia supports the idea that humans were behind the Australian extinctions. Many large animals went extinct around the time when humans arrived in Australia, but that time also coincided with a change in climate. What the new study shows is that the same large animals survived for another 5,000 years in Tasmania... until humans arrived there from the mainland. Then they promptly went extinct. That time period didn't correspond to a major climate change, so it's hard to explain it away.
It's a harsh reality that our big brains and remarkable adaptability give us the power to be exceptionally destructive to the environment. We're good at finding the most productive niches available, and exploiting them until they implode. Jared Diamond wrote an excellent book on the subject called Collapse, which details how nearly every major civilization collapse throughout history was caused at least in part by environmental damage. It's been a hallmark of human history since the beginning.
I don't think it will take much to convince you that the trend has accelerated in modern times. Ocean life, our major source of nutrient-rich wild food, has already been severely depleted. The current extinction rate is estimated to be over 1,000 times the baseline, pre-modern level, and rising.
Humans have always been top-level predators. We kill and eat nutrient-dense prey that is often much larger than we are. But today, the extinction of such walking meat lockers has caused us to eat down the food chain. We're turning to jellyfish and sea cucumbers and... gasp... lobsters!
While it's true that we've probably always eaten things like shellfish and insects, I find it disturbing that we've depleted the oceans to the point where we can no longer sustainably eat formerly abundant carnivorous fish like tuna. We need to make a concerted effort to preserve these species because extinction is permanent.
I don't want to live in a future where the only thing on the menu is bacteria patties, the other other other other white meat.
Eating Down the Food Chain
Europe once teemed with large mammals, including species of elephant, lion, tiger, bear, moose and bison. America was also home to a number of huge and unusual animals: mammoths, dire wolves, lions, giant sloths and others.
The same goes for Australia, where giant kangaroos, huge wombats and marsupial 'lions' once roamed.
What do these extinctions have in common? They all occurred around when humans arrived. The idea that humans caused them is hotly debated, because they also sometimes coincided with climactic and vegetation changes. However, I believe the fact that these extinctions occurred on several different continents about when humans arrived points to an anthropogenic explanation.
A recent archaeological study from the island of Tasmania off the coast of Australia supports the idea that humans were behind the Australian extinctions. Many large animals went extinct around the time when humans arrived in Australia, but that time also coincided with a change in climate. What the new study shows is that the same large animals survived for another 5,000 years in Tasmania... until humans arrived there from the mainland. Then they promptly went extinct. That time period didn't correspond to a major climate change, so it's hard to explain it away.
It's a harsh reality that our big brains and remarkable adaptability give us the power to be exceptionally destructive to the environment. We're good at finding the most productive niches available, and exploiting them until they implode. Jared Diamond wrote an excellent book on the subject called Collapse, which details how nearly every major civilization collapse throughout history was caused at least in part by environmental damage. It's been a hallmark of human history since the beginning.
I don't think it will take much to convince you that the trend has accelerated in modern times. Ocean life, our major source of nutrient-rich wild food, has already been severely depleted. The current extinction rate is estimated to be over 1,000 times the baseline, pre-modern level, and rising.
Humans have always been top-level predators. We kill and eat nutrient-dense prey that is often much larger than we are. But today, the extinction of such walking meat lockers has caused us to eat down the food chain. We're turning to jellyfish and sea cucumbers and... gasp... lobsters!
While it's true that we've probably always eaten things like shellfish and insects, I find it disturbing that we've depleted the oceans to the point where we can no longer sustainably eat formerly abundant carnivorous fish like tuna. We need to make a concerted effort to preserve these species because extinction is permanent.
I don't want to live in a future where the only thing on the menu is bacteria patties, the other other other other white meat.
Saharan Hunter-Gatherers Unearthed
The media recently covered an archaeological discovery in Niger that caught my attention. In the middle of the Sahara desert, researchers found a hunter-gatherer burial site containing over 200 graves ranging from about 10,000 to 4,500 years old. During this period, the region was lush and productive.
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
Among the Tenerian graves was a heart-rending burial tableaux [SIC!!]: A young woman was lying on her side. Pollen under her body suggested that she was placed on a bed of flowers. Lying on their sides facing her were two young children, their fingers interlocked with hers, leaving a tangle of bones.Haha, I couldn't let the spelling error slide, it should be 'tableau'. Hey, I'm half French, give me a break.
Saharan Hunter-Gatherers Unearthed
The media recently covered an archaeological discovery in Niger that caught my attention. In the middle of the Sahara desert, researchers found a hunter-gatherer burial site containing over 200 graves ranging from about 10,000 to 4,500 years old. During this period, the region was lush and productive.
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
There were two groups: the Kiffian, who were powerful hunters and fishermen, and the Tenerian, who were smaller pastoralists (herders) and fishermen.
Individuals at the Kiffian sites averaged over 6 feet tall, with some reaching 6' 8". They were powerfully muscled, and found with the remains of elephants, giraffes, pythons, giant perch and other large game.
Not that you have to be Conan the Barbarian to kill an elephant. Forest pygmies traditionally hunt elephants, and there's a picutre in Nutrition and Physical Degeneration to prove it. They use stealth, agility and an intimate knowledge of their prey to make up for their small size and primitive weapons.
Both the Kiffians and the Tenerians had excellent dental development and health. Take a look at some of the pictures. Those are the teeth of a wild Homo sapiens. Straight, free of decay and with plenty of room for the wisdom teeth. They must have had good dentists.
Both cultures also showed a high level of intelligence and empathy. They were found with decorated pottery shards and their bodies were arranged in imaginative and empathetic ways. A man was buried sitting on a tortoise shell. A mother was buried with her two children. Here's the picture. I can't say it better than the LA Times:
Among the Tenerian graves was a heart-rending burial tableaux [SIC!!]: A young woman was lying on her side. Pollen under her body suggested that she was placed on a bed of flowers. Lying on their sides facing her were two young children, their fingers interlocked with hers, leaving a tangle of bones.Haha, I couldn't let the spelling error slide, it should be 'tableau'. Hey, I'm half French, give me a break.
Fit at 70
In my professional life, I study neurodegenerative disease, the mechanisms of aging, and what the two have in common. I was reading through a textbook on aging a few months ago, and I came across an interesting series of graphs.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
Fit at 70
In my professional life, I study neurodegenerative disease, the mechanisms of aging, and what the two have in common. I was reading through a textbook on aging a few months ago, and I came across an interesting series of graphs.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
The first graph showed the average cardiorespiratory endurance of Americans at different ages. It peaks around 30 and goes downhill from there. But the author of this chapter was very intelligent; he knew that averages sometimes conceal meaningful information. The second graph showed two lines: one representing a man who was sedentary, and the other representing a man who exercised regularly for his entire life. The data were from real individuals. The endurance of the first man basically tracked the national average as he aged. The endurance of the second man remained relatively stable from early adulthood until the age of 70, after which it declined noticeably.
We aren't taking care of ourselves for nothing, ladies and gentlemen. We're doing it because the stakes are high. Just look at Jack LaLanne, the fitness buff. He's been working out regularly and eating a whole foods diet since before I was born, and he's still pumping iron every day at 93.
Kitava: Wrapping it Up
There's a lot to be learned from the Kitava study. Kitavans eat a diet of root vegetables, coconut, fruit, vegetables and fish and have undetectable levels of cardiovascular disease (CVD), stroke and overweight. Despite light smoking. 69% of their calories come from carbohydrate, 21% from fat and 10% from protein. This is essentially a carbohydrate-heavy version of what our paleolithic ancestors ate. They also get lots of sunshine and have a moderately high activity level.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, and most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This raises the possibility that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and withholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? White flour and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from near-complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed seed oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, and most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This raises the possibility that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and withholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? White flour and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from near-complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed seed oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
Kitava: Wrapping it Up
There's a lot to be learned from the Kitava study. Kitavans eat a diet of root vegetables, coconut, fruit, vegetables and fish and have undetectable levels of cardiovascular disease (CVD), stroke and overweight. Despite light smoking. 69% of their calories come from carbohydrate, 21% from fat and 10% from protein. This is essentially a carbohydrate-heavy version of what our paleolithic ancestors ate. They also get lots of sunshine and have a moderately high activity level.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, and most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This raises the possibility that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and withholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? White flour and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from near-complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed seed oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
The first thing we can say is that a high intake of carbohydrate is not enough, by itself, to cause overweight or the diseases of civilization. It's also not enough to cause insulin resistance. I sent an e-mail to Dr. Lindeberg asking if his group had measured Kitavans' glucose tolerance. He told me they had not. However, I can only guess they had good glucose control since they suffered from none of the complications of unmanaged diabetes.
The Kitavan diet is low in fat, and most of the fat they eat is saturated because it comes from coconuts. Compared to Americans and Swedes, they have a high intake of saturated fat. So much for the theory that saturated fat causes CVD... They also have a relatively high intake of fish fat, at 4g per day. This gives them a high ratio of omega-3 to omega-6 fatty acids, with plenty of DHA and EPA.
Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This raises the possibility that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and withholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? White flour and sugar maybe?
Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness.
The Kitavan diet is one path to vibrant health. Like many other non-industrial groups, Kitavans eat whole, natural foods that are broadly consistent with what our hunter-gatherer ancestors would have eaten. It amazes me that as humans, we can live well on diets that range from near-complete carnivory to plant-rich omnivory. We are possibly the most adaptable species on the planet.
The ideal diet for humans includes a lot of possibilities. I believe the focus on macronutrients is misguided. There are examples of cultures that were/are healthy eating high-fat diets, high-carbohydrate diets and everything in between. What they do not eat is processed grains, particularly wheat, refined sugar, industrially processed seed oils and other modern foods. I believe these are unhealthy, and this is visible in the trail of destruction they have left around the globe. Its traces can be found in the Pacific islands, where close genetic relatives of the Kitavans have become morbidly obese and unhealthy on a processed-food diet.
Cardiovascular Risk Factors on Kitava, Part IV: Leptin
Leptin is a hormone that is a central player in the process of weight gain and chronic disease. Its existence had been predicted for decades, but it was not identified until 1994. Although less well known than insulin, its effects on nutrient disposal, metabolic rate and feeding behaviors place it on the same level of importance.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others. This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so it's possible that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at industrial food.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others. This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so it's possible that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at industrial food.
Cardiovascular Risk Factors on Kitava, Part IV: Leptin
Leptin is a hormone that is a central player in the process of weight gain and chronic disease. Its existence had been predicted for decades, but it was not identified until 1994. Although less well known than insulin, its effects on nutrient disposal, metabolic rate and feeding behaviors place it on the same level of importance.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others. This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so it's possible that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at industrial food.
Caloric intake and expenditure vary from day to day and week to week in humans, yet most people maintain a relatively stable weight without consciously adjusting food intake. For example, I become hungry after a long fast, whereas I won't be very hungry if I've stuffed myself for two meals in a row. This suggests a homeostatic mechanism, or feedback loop, which keeps weight in the body's preferred range. Leptin is the major feedback signal.
Here's how it works. Leptin is secreted by adipose (fat) tissue, and its blood levels are proportional to fat mass. The more fat, the more leptin. It acts in the brain to increase the metabolic rate, decrease eating behaviors, and inhibit the deposition of fat. Thus, if fat mass increases, hunger diminishes and the body tries to burn calories to regain its preferred equilibrium.
The next logical question is "how could anyone become obese if this feedback loop inhibits energy storage in response to fat gain?" The answer is a problem called leptin resistance. In people who are obese, the brain no longer responds to the leptin signal. In fact, the brain believes leptin levels are low, implying stored energy is low, so it thinks it's starving. This explains the low metabolic rate, increased tendency for fat storage and hyperphagia (increased eating) seen in many obese people. Leptin resistance has reset the body's preferred weight 'set-point' to a higher level.
Incidentally, some reaserchers have claimed that obese people gain fat because they don't fidget as much as others. This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so it's possible that obese people fidget less than thin people due to their leptin resistance. In other words, they fidget less because they're fat, rather than the other way around.
The problem of leptin resistance is well illustrated by a rat model called the Zucker fatty strain. The Zucker rat has a mutation in the leptin receptor gene, making its brain unresponsive to leptin signals. The rat's fat tissue pumps out leptin, but its brain is deaf to it. This is basically a model of severe leptin resistance, the same thing we see in obese humans. What happens to these rats? They become hyperphagic, hypometabolic, obese, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome.
This shows that leptin resistance is sufficient to cause many of the common metabolic problems that plague modern societies. In humans, it's a little known fact that leptin resistance precedes the development of obesity, insulin resistance, and impaired glucose tolerance! Furthermore, humans with leptin receptor mutations or impaired leptin production become hyperphagic and severely obese. This puts leptin at the top of my list of suspects.
So here we have the Kitavans, who are thin and healthy. How's their leptin? Incredibly low. Even in young individuals, Kitavan leptin levels average less than half of Swedish levels. Beyond age 60, Kitavans have 1/4 the leptin level of Swedish people. The difference is so great, the standard deviations don't even overlap.
This isn't surprising, since leptin levels track with fat mass and the Kitavans are very lean (average male BMI = 20, female BMI = 18). Now we are faced with a chicken and egg question. Are Kitavans thin because they're leptin-sensitive, or are they leptin-sensitive because they're thin?
There's no way to answer this question conclusively using the data I'm familiar with. However, in mice and humans, leptin resistance by itself can initiate a spectrum of metabolic problems very reminiscent of what we see so frequently in modern societies. This leads me to believe that there's something about the modern lifestyle that causes leptin resistance. As usual, my microscope is pointed directly at industrial food.
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 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 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.
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.
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.
Letter to the Editor
I wrote a letter to the New York Times about their recent article "The Overflowing American Dinnerplate", which I reviewed here. The letter didn't get accepted, so I will publish it here:
In the article "The Overflowing American Dinner Plate", Bill Marsh cites USDA data showing a 59% increase in fat consumption from 1970 to 2006, coinciding with the doubling of the obesity rate in America. However, according to Centers for Disease Control NHANES nutrition survey data, total fat intake in the US has remained relatively constant since 1971, and has actually decreased as a percentage of calories. The apparent discrepancy disappears when we understand that the USDA data Marsh cites are not comprehensive. They do not include the fat contained in milk and meat, which have been steadily decreasing since 1970.
The change Marsh reported refers primarily to the increasing use of industrially processed vegetable oils such as soybean oil. These have gradually replaced animal fats in our diet over the last 30 years. Since overall fat intake has changed little since the 1970s, it cannot be blamed for rising obesity.
Letter to the Editor
I wrote a letter to the New York Times about their recent article "The Overflowing American Dinnerplate", which I reviewed here. The letter didn't get accepted, so I will publish it here:
In the article "The Overflowing American Dinner Plate", Bill Marsh cites USDA data showing a 59% increase in fat consumption from 1970 to 2006, coinciding with the doubling of the obesity rate in America. However, according to Centers for Disease Control NHANES nutrition survey data, total fat intake in the US has remained relatively constant since 1971, and has actually decreased as a percentage of calories. The apparent discrepancy disappears when we understand that the USDA data Marsh cites are not comprehensive. They do not include the fat contained in milk and meat, which have been steadily decreasing since 1970.
The change Marsh reported refers primarily to the increasing use of industrially processed vegetable oils such as soybean oil. These have gradually replaced animal fats in our diet over the last 30 years. Since overall fat intake has changed little since the 1970s, it cannot be blamed for rising obesity.
Rats on Junk Food
If diet composition causes hyperphagia, we should be able to see it in animals. I just came across a great study from the lab of Dr. Neil Stickland that explored this in rats. They took two groups of pregnant rats and fed them two different diets ad libitum, meaning the rats could eat as much as they wanted. Here's what the diets looked like:
The rest of the paper is interesting as well. Pups born to mothers who ate junk food while pregnant and lactating had a greater tendency to eat junk than pups born to mothers who ate rat chow during the same period. This underscores the idea that poor nutrition can set a child up for a lifetime of problems.
The animals were fed two types of diet throughout the study. They were fed either RM3 rodent chow alone ad libitum (SDS Ltd, Betchworth, Surrey, UK) or with a junk food diet, also known as cafeteria diet, which consisted of eight different types of palatable foods, purchased from a British supermarket. The palatable food included biscuits, marshmallows, cheese, jam doughnuts, chocolate chip muffins, butter flapjacks, potato crisps and caramel/chocolate bars.It's important to note that the junk food-fed rats had access to rat chow as well. Now here's where it gets interesting. Rats with access to junk food in addition to rat chow ate 56% more calories than the chow-only group! Here's what they had to say about it:
These results clearly show that pregnant rats, given ad libitum access to junk food, exhibited hyperphagia characterised by a marked preference for foods rich in fat, sucrose and salt at the expense of protein-rich foods, when compared with rats that only had access to rodent chow. Although the body mass of dams was comparable among all groups at the start of the experiment, the increased energy intake in the junk food group throughout gestation was accompanied by an increase in body mass at G20 [gestational day 20] with the junk food-fed dams being 13 % heavier than those fed chow alone.Hmm, this is remarkably reminiscent of what's happening to a certain group of humans in North America right now: give them access to food made mostly of refined grains, sugar, and industrially processed vegetable oil. They will prefer it to healthier food, to the point of overeating. The junk food then drives hyperphagia by interfering with the body's feedback loops that normally keep feeding behaviors and body fat within the optimal range. These data support the hypothesis that metabolic damage is the cause of, not the result of, "super-sized" food portions and other similar cultural phenomena.
The rest of the paper is interesting as well. Pups born to mothers who ate junk food while pregnant and lactating had a greater tendency to eat junk than pups born to mothers who ate rat chow during the same period. This underscores the idea that poor nutrition can set a child up for a lifetime of problems.
Rats on Junk Food
If diet composition causes hyperphagia, we should be able to see it in animals. I just came across a great study from the lab of Dr. Neil Stickland that explored this in rats. They took two groups of pregnant rats and fed them two different diets ad libitum, meaning the rats could eat as much as they wanted. Here's what the diets looked like:
The rest of the paper is interesting as well. Pups born to mothers who ate junk food while pregnant and lactating had a greater tendency to eat junk than pups born to mothers who ate rat chow during the same period. This underscores the idea that poor nutrition can set a child up for a lifetime of problems.
The animals were fed two types of diet throughout the study. They were fed either RM3 rodent chow alone ad libitum (SDS Ltd, Betchworth, Surrey, UK) or with a junk food diet, also known as cafeteria diet, which consisted of eight different types of palatable foods, purchased from a British supermarket. The palatable food included biscuits, marshmallows, cheese, jam doughnuts, chocolate chip muffins, butter flapjacks, potato crisps and caramel/chocolate bars.It's important to note that the junk food-fed rats had access to rat chow as well. Now here's where it gets interesting. Rats with access to junk food in addition to rat chow ate 56% more calories than the chow-only group! Here's what they had to say about it:
These results clearly show that pregnant rats, given ad libitum access to junk food, exhibited hyperphagia characterised by a marked preference for foods rich in fat, sucrose and salt at the expense of protein-rich foods, when compared with rats that only had access to rodent chow. Although the body mass of dams was comparable among all groups at the start of the experiment, the increased energy intake in the junk food group throughout gestation was accompanied by an increase in body mass at G20 [gestational day 20] with the junk food-fed dams being 13 % heavier than those fed chow alone.Hmm, this is remarkably reminiscent of what's happening to a certain group of humans in North America right now: give them access to food made mostly of refined grains, sugar, and industrially processed vegetable oil. They will prefer it to healthier food, to the point of overeating. The junk food then drives hyperphagia by interfering with the body's feedback loops that normally keep feeding behaviors and body fat within the optimal range. These data support the hypothesis that metabolic damage is the cause of, not the result of, "super-sized" food portions and other similar cultural phenomena.
The rest of the paper is interesting as well. Pups born to mothers who ate junk food while pregnant and lactating had a greater tendency to eat junk than pups born to mothers who ate rat chow during the same period. This underscores the idea that poor nutrition can set a child up for a lifetime of problems.
Hyperphagia
One of the things I didn't mention in the last post is that Americans are eating more calories than ever before. According to Centers for Disease Control NHANES data, in 2000, men ate about 160 more calories per day, and women ate about 340 more than in 1971. That's a change of 7% and 22%, respectively. The extra calories come almost exclusively from refined grains, with the largest single contribution coming from white wheat flour (correction: the largest single contribution comes from corn sweeteners, followed by white wheat flour).
Some people will see those data and decide the increase in calories is the explanation for the expanding American waistline. I don't think that's incorrect, but I do think it misses the point. The relevant question is "why are we eating more calories now than we were in 1971?"
We weren't exactly starving in 1971. And average energy expenditure, if anything, has actually increased. So why are we eating more? I believe that our increased food intake, or hyperphagia, is the result of metabolic disturbances, rather than the cause of them.
Humans, like all animals, have a sophisticated system of hormones and brain regions whose function is to maintain a proper energy balance. Part of the system's job is to keep fat mass at an appropriate level. With a properly functioning system, feedback loops inhibit hunger once fat mass has reached a certain level, and also increase resting metabolic rate to burn excess calories. If the system is working properly, it's very difficult to gain weight. There have been a number of overfeeding studies in which subjects have consumed huge amounts of excess calories. Some people gain weight, many don't.
The fact that fat mass is hormonally regulated can be easily seen in other mammals. When was the last time you saw a fat squirrel in the springtime? When was the last time you saw a thin squirrel in the fall? These events are regulated by hormones. A squirrel in captivity will put on weight in the fall, even if its daily food intake is not changed.
A key hormone in this process is leptin. Leptin levels are proportional to fat mass, and serve to inhibit hunger and eating behaviors. Under normal conditions, the more fat tissue a person has, the more leptin they will produce, and the less they will eat until the fat mass has reached the body's preferred 'set-point'. The problem is that overweight Westerners are almost invariably leptin-resistant, meaning their body doesn't respond to the signal to stop eating!
Leptin resistance leads to hyperphagia, overweight and the metabolic syndrome (a common cluster of symptoms that implies profound metabolic disturbance). It typically precedes insulin resistance during the downward slide towards metabolic syndrome.
I suspect that wheat, sugar and perhaps other processed foods cause hyperphagia. It's the same thing you see when wheat is first introduced to a culture, even if it's replacing another refined carbohydrate. I believe hyperphagia is secondary to a disturbed metabolism. There's something about the combination of refined wheat, sugar, processed vegetable oils and other industrial foods that reached a critical mass in the mid-70s. The shift in diet composition disturbed our normal hormonal profile (even more than it was already disturbed), and sent us into a tailspin of excessive eating and unprecedented weight gain.
Some people will see those data and decide the increase in calories is the explanation for the expanding American waistline. I don't think that's incorrect, but I do think it misses the point. The relevant question is "why are we eating more calories now than we were in 1971?"
We weren't exactly starving in 1971. And average energy expenditure, if anything, has actually increased. So why are we eating more? I believe that our increased food intake, or hyperphagia, is the result of metabolic disturbances, rather than the cause of them.
Humans, like all animals, have a sophisticated system of hormones and brain regions whose function is to maintain a proper energy balance. Part of the system's job is to keep fat mass at an appropriate level. With a properly functioning system, feedback loops inhibit hunger once fat mass has reached a certain level, and also increase resting metabolic rate to burn excess calories. If the system is working properly, it's very difficult to gain weight. There have been a number of overfeeding studies in which subjects have consumed huge amounts of excess calories. Some people gain weight, many don't.
The fact that fat mass is hormonally regulated can be easily seen in other mammals. When was the last time you saw a fat squirrel in the springtime? When was the last time you saw a thin squirrel in the fall? These events are regulated by hormones. A squirrel in captivity will put on weight in the fall, even if its daily food intake is not changed.
A key hormone in this process is leptin. Leptin levels are proportional to fat mass, and serve to inhibit hunger and eating behaviors. Under normal conditions, the more fat tissue a person has, the more leptin they will produce, and the less they will eat until the fat mass has reached the body's preferred 'set-point'. The problem is that overweight Westerners are almost invariably leptin-resistant, meaning their body doesn't respond to the signal to stop eating!
Leptin resistance leads to hyperphagia, overweight and the metabolic syndrome (a common cluster of symptoms that implies profound metabolic disturbance). It typically precedes insulin resistance during the downward slide towards metabolic syndrome.
I suspect that wheat, sugar and perhaps other processed foods cause hyperphagia. It's the same thing you see when wheat is first introduced to a culture, even if it's replacing another refined carbohydrate. I believe hyperphagia is secondary to a disturbed metabolism. There's something about the combination of refined wheat, sugar, processed vegetable oils and other industrial foods that reached a critical mass in the mid-70s. The shift in diet composition disturbed our normal hormonal profile (even more than it was already disturbed), and sent us into a tailspin of excessive eating and unprecedented weight gain.
Subscribe to:
Posts (Atom)