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.
Minggu, 31 Agustus 2008
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.
Jumat, 29 Agustus 2008
My Conflict of Interest Disclosure
This blog does not bring me any revenue, direct or indirect. I publish it as a free service to my friends and family, and anyone else who's interested.
I don't allow advertising at this time, nor am I connected to any of the products or books I've mentioned in any way.
My meager salary is paid indirectly by the National Institutes of Health, which supports my research on neurodegenerative disease. This blog is a personal project of mine and the NIH has no influence over it, or knowledge of it.
My biases are all my own.
I don't allow advertising at this time, nor am I connected to any of the products or books I've mentioned in any way.
My meager salary is paid indirectly by the National Institutes of Health, which supports my research on neurodegenerative disease. This blog is a personal project of mine and the NIH has no influence over it, or knowledge of it.
My biases are all my own.
My Conflict of Interest Disclosure
This blog does not bring me any revenue, direct or indirect. I publish it as a free service to my friends and family, and anyone else who's interested.
I don't allow advertising at this time, nor am I connected to any of the products or books I've mentioned in any way.
My meager salary is paid indirectly by the National Institutes of Health, which supports my research on neurodegenerative disease. This blog is a personal project of mine and the NIH has no influence over it, or knowledge of it.
My biases are all my own.
I don't allow advertising at this time, nor am I connected to any of the products or books I've mentioned in any way.
My meager salary is paid indirectly by the National Institutes of Health, which supports my research on neurodegenerative disease. This blog is a personal project of mine and the NIH has no influence over it, or knowledge of it.
My biases are all my own.
Kamis, 28 Agustus 2008
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.
Walking Off 35 Pounds
In the 'before photo' here Debra Flinn weighs 216 pounds at her height of 5'5". She decided to take extreme measures to lose weight and planned on walking to a city that was 874 miles away.
It took her 66 days to do it (at an average daily walking mileage of 13 miles). When she got there she was 35 pounds lighter.
See her story and her 'after photo' here.
Rabu, 27 Agustus 2008
Ooops been gone a while
Right then, seeing as I have been tardy, let me bring you all up to speed. I had my unfill which was wonderful... too wonderful. I have been able to eat everything and it's dog.
So I booked to have a top up and had it done last Sunday. I had 0.5mls put back in (for free) and to be honest there is not a lot of difference. I have not been eating quite so much, but apart from that I am able to eat pretty much all things except for sliced bread/rolls.
I am finding that pitta is a really good thing for me to eat. I have had 3 pitta bread over the course of the day with hummus. Tonight's tea is roast gammon with cauliflower cheese and for afters we are having apple and blackberry crumble and custard.
I am not hungry right now, and all I have consumed all day has been pitta bread and hummus, orange juice and coffee.
If you asked me have I had a lot to eat today I would say "yes" and in the back of my min think "too much" but actually this is BECAUSE of the band causing the sensation of satisfaction. I only FEEL like I have eaten too much, when in fact I haven't.
I hope to see a difference with my eating with this fill. Not so tight that I cannot eat more than a bite, but enough so that I can keep healthy and just lose maybe even 1/2 pound per week.
I am conscious that I am not really at my 1 year out yet (Band Mk2 that is - counting November 9th as band day.), and I have lost about a 1/3rd of the weight I want to ideally lose. I hope to have knocked half the weight on its head by my Band (mk2) Anniversary.
What damage did I do to my weight whilst at open free for all... 4 lb gain. This was analysed as 1 pound of water, 1 pound of muscle and 2 pounds of fat. Not bad when you consider I ate like a hog for 2 weeks solid. Mind you, eating like a hog for someone with a band, whatever their restriction is like, is significantly reduced from the Hardcore Hog that I was pre banding!!
So, I am not going to update my weight bar and add on the 4pound gain, as I will feel horrible and it will put me in a bad place, and I will adjust it when I have lost 4 and a half pounds instead and then I will be happy.
I have exactly 6mls in my band.
I suffered with a lot of pain in my port over the last few days where I have had to resort to codeine (Thanks Dad! He gave me all 200 packets of 90 tablets given to him from the hospital after his cancer operation - bargain!). Codeine was the only thing that touched my pain before when my band broke. However, it was NOT that kind of pain, but really from the injection site. There has been no swelling, redness or anything else and I still definitely have restriction, so I am not worried, although paranoia did start to set in during the long sleepless night after the fill! Today is fine though and I have been decorating, sawing, painting and all kinds of stuff without a problem.
As for the normal lark... we have our new lodger Josh. He arrived this afternoon at 3:30 with all his stuff. He is really excited about staying and starting his apprenticeship etc. Seems like a nice lad. He has a brother aged 9 too so just like home really!
Right, over and out for today.
So I booked to have a top up and had it done last Sunday. I had 0.5mls put back in (for free) and to be honest there is not a lot of difference. I have not been eating quite so much, but apart from that I am able to eat pretty much all things except for sliced bread/rolls.
I am finding that pitta is a really good thing for me to eat. I have had 3 pitta bread over the course of the day with hummus. Tonight's tea is roast gammon with cauliflower cheese and for afters we are having apple and blackberry crumble and custard.
I am not hungry right now, and all I have consumed all day has been pitta bread and hummus, orange juice and coffee.
If you asked me have I had a lot to eat today I would say "yes" and in the back of my min think "too much" but actually this is BECAUSE of the band causing the sensation of satisfaction. I only FEEL like I have eaten too much, when in fact I haven't.
I hope to see a difference with my eating with this fill. Not so tight that I cannot eat more than a bite, but enough so that I can keep healthy and just lose maybe even 1/2 pound per week.
I am conscious that I am not really at my 1 year out yet (Band Mk2 that is - counting November 9th as band day.), and I have lost about a 1/3rd of the weight I want to ideally lose. I hope to have knocked half the weight on its head by my Band (mk2) Anniversary.
What damage did I do to my weight whilst at open free for all... 4 lb gain. This was analysed as 1 pound of water, 1 pound of muscle and 2 pounds of fat. Not bad when you consider I ate like a hog for 2 weeks solid. Mind you, eating like a hog for someone with a band, whatever their restriction is like, is significantly reduced from the Hardcore Hog that I was pre banding!!
So, I am not going to update my weight bar and add on the 4pound gain, as I will feel horrible and it will put me in a bad place, and I will adjust it when I have lost 4 and a half pounds instead and then I will be happy.
I have exactly 6mls in my band.
I suffered with a lot of pain in my port over the last few days where I have had to resort to codeine (Thanks Dad! He gave me all 200 packets of 90 tablets given to him from the hospital after his cancer operation - bargain!). Codeine was the only thing that touched my pain before when my band broke. However, it was NOT that kind of pain, but really from the injection site. There has been no swelling, redness or anything else and I still definitely have restriction, so I am not worried, although paranoia did start to set in during the long sleepless night after the fill! Today is fine though and I have been decorating, sawing, painting and all kinds of stuff without a problem.
As for the normal lark... we have our new lodger Josh. He arrived this afternoon at 3:30 with all his stuff. He is really excited about staying and starting his apprenticeship etc. Seems like a nice lad. He has a brother aged 9 too so just like home really!
Right, over and out for today.
Selasa, 26 Agustus 2008
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.
Senin, 25 Agustus 2008
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.
Jumat, 22 Agustus 2008
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.
Kamis, 21 Agustus 2008
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 smoking like chimneys. 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, but 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 suggests 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 witholding 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? Grains 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 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 vegetable 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.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
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, but 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 suggests 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 witholding 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? Grains 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 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 vegetable 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.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
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 smoking like chimneys. 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, but 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 suggests 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 witholding 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? Grains 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 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 vegetable 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.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
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, but 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 suggests 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 witholding 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? Grains 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 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 vegetable 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.
One last caveat. I do still believe in the efficacy of low-carbohydrate diets for weight loss and health. The Western diet and lifestyle can damage the metabolism severely, particularly glucose metabolism. It seems to be somewhat reversible, but it depends on the extent of the damage and the individual. People with a history of overweight or poor glucose control should be careful with carbohydrate. It's possible that some people will not be able to handle normal amounts of carbohydrate in any form. Be aware of what your body is telling you.
The Diabetes Miracle Diet
Michael lost 56 pounds recently over about five months. He says eating less of the same foods does not work.Instead he went on The 30-Day Diabetes Miracle
This is a vegetarian diet focused on lots of beans, oatmeal and vegetables. He also walked between 20 and 30 miles per week. His weight loss averaged between 2.5 and 3.5 pounds a week.
Rabu, 20 Agustus 2008
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 (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue 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 wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
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 (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue 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 wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
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 (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue 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 wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
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 (a variation on the "obesity is caused by sloth" theory). This is based on the observation that thin people fidget more than overweight people. Leptin also influences activity levels, so I would argue 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 wheat. Its lectins are capable of binding to and desensitizing the leptin and insulin receptors in vitro, as I wrote about before. Staffan Lindeberg proposed that grain lectins could be responsible for leptin resistance here. This is one of many possible mechanisms by which wheat could wreak metabolic damage, particularly in its industrially processed form.
Senin, 18 Agustus 2008
Todays roundup
I have loads of things on eBay at the moment. A car, some shoes, a face cream, art books, my dress that I wore to the wedding and other stuff.
Hopefully I might get some cash back!
So that's what I have spent most of the day doing... photographing stuff and entering reams of crap on eBay. Its so long winded. Something that has really annoyed me today is the fact that if you revise and item, once you have listed it on eBay that is, it changes the title for you. good huh? I think that's rubbish seeing as I chose my title and took ages on it.
Grrr
Bunk mate phoned today. Was wicked to catch up and her life has been just the same crazy whirlwind as mine... but not quite eh bunk mate? She thinks I am totally crazy and I guess she is right. HA HA.
Trish the Canadian lodger moved out today. Boo Hoo... but there we go.
Now, Bunk mate pointed out that people might be getting a tad lost in the comings and going of the lodgers and the cars...
Ok, here's a round up of the lodgers to date:
November 2007 - February 2008 Carina our German Girl
February 2008 - April 2008 Our two Spanish sweeties... Maria and Xandra
April - present Sue out lovely English Rose
April 2008 - June 2008 - Lotse the Hungarian truck driver
June 2008 - July 2008 - Lotse + Csilla his wife & Lilli their daughter!
June 2008 for 2 weeks Katie the Scottish news reader
June 2008 - August 18th Trish the Canadian Medieval history PHD student
So at the moment we have just Sue and her dog Dylan. In a week, Josh arrives. He is a young lad of 16 just about to start his apprenticeship and will be staying with us for at least 13 weeks... but more likely a year +.
Last night we went to Lotse and Csilla's for dinner with Sue. It was really great. They have moved into a 3 bedroom place and they invited us over for dinner. They are so grateful to us for helping them get started. Lilli, their daughter, is coeliac. They didnt know that they could get a lot of her food on prescription. She is so painfully thin its harrowing. They nearly wept at the thought of Lilli being able to eat bread, pizza, rolls and pasta. In Hungary their life was a bit awful I think. Anyway, to them its like they have arrived in Paradise. Weird considering I would give anything to go and live in Hungary!! HA HA.
So it was really nice to go there and see them settling into English life. What a massive decision huh? Their son Greg joins them in September also to make a new start. Really exciting for them.
So, lodger wise that's it really... waiting for next Tuesday to settle Josh in, but that should be no problem really.
Cars...
well, I wrote my red Rover off last December, remember? I bought the horrid Mondeo to tide me over. Then I bought my MG but just didn't get along with it. Now I have bought a Rover 25 which is much more 'ME' and sold the MG. DH had a company car until beginning of June. Then he bought a Rover 400 saloon. It was a big of a nadger, and he swapped it on the site called http://www.swapz.co.uk/ which is cool for a Citroen saxo. But he still needed a better small car. So we just got him an 02 plate Ford Fiesta with is totally great for him and he is thrilled. So we are now selling the saxo.
Its all go around here boyz and girlz!
I have only 2 more weeks of the holidays left and then I am right back in the thick of it again. I am going to put my prices up because its just ridiculous not to. The few new people I have got over the holidays have not blinked a bit at the £14 per lesson price tag. I am, after all, extremely cheap anyway! The going rate is £16 - and that's travelling to the teachers house... so I am a bit of a bargain. I cant be too cheap or I will look like rubbish. Hard huh?
Ok, roundup of today's food...
had the prawns thing this morning
had an apple
had a couple of cereal bars
dinner was cauliflower, creamed leeks and duchess potatoes. I didn't bother with meat as it makes me sick.
Then I had half a bottle red and another cereal bar.
That's all folks!
Hopefully I might get some cash back!
So that's what I have spent most of the day doing... photographing stuff and entering reams of crap on eBay. Its so long winded. Something that has really annoyed me today is the fact that if you revise and item, once you have listed it on eBay that is, it changes the title for you. good huh? I think that's rubbish seeing as I chose my title and took ages on it.
Grrr
Bunk mate phoned today. Was wicked to catch up and her life has been just the same crazy whirlwind as mine... but not quite eh bunk mate? She thinks I am totally crazy and I guess she is right. HA HA.
Trish the Canadian lodger moved out today. Boo Hoo... but there we go.
Now, Bunk mate pointed out that people might be getting a tad lost in the comings and going of the lodgers and the cars...
Ok, here's a round up of the lodgers to date:
November 2007 - February 2008 Carina our German Girl
February 2008 - April 2008 Our two Spanish sweeties... Maria and Xandra
April - present Sue out lovely English Rose
April 2008 - June 2008 - Lotse the Hungarian truck driver
June 2008 - July 2008 - Lotse + Csilla his wife & Lilli their daughter!
June 2008 for 2 weeks Katie the Scottish news reader
June 2008 - August 18th Trish the Canadian Medieval history PHD student
So at the moment we have just Sue and her dog Dylan. In a week, Josh arrives. He is a young lad of 16 just about to start his apprenticeship and will be staying with us for at least 13 weeks... but more likely a year +.
Last night we went to Lotse and Csilla's for dinner with Sue. It was really great. They have moved into a 3 bedroom place and they invited us over for dinner. They are so grateful to us for helping them get started. Lilli, their daughter, is coeliac. They didnt know that they could get a lot of her food on prescription. She is so painfully thin its harrowing. They nearly wept at the thought of Lilli being able to eat bread, pizza, rolls and pasta. In Hungary their life was a bit awful I think. Anyway, to them its like they have arrived in Paradise. Weird considering I would give anything to go and live in Hungary!! HA HA.
So it was really nice to go there and see them settling into English life. What a massive decision huh? Their son Greg joins them in September also to make a new start. Really exciting for them.
So, lodger wise that's it really... waiting for next Tuesday to settle Josh in, but that should be no problem really.
Cars...
well, I wrote my red Rover off last December, remember? I bought the horrid Mondeo to tide me over. Then I bought my MG but just didn't get along with it. Now I have bought a Rover 25 which is much more 'ME' and sold the MG. DH had a company car until beginning of June. Then he bought a Rover 400 saloon. It was a big of a nadger, and he swapped it on the site called http://www.swapz.co.uk/ which is cool for a Citroen saxo. But he still needed a better small car. So we just got him an 02 plate Ford Fiesta with is totally great for him and he is thrilled. So we are now selling the saxo.
Its all go around here boyz and girlz!
I have only 2 more weeks of the holidays left and then I am right back in the thick of it again. I am going to put my prices up because its just ridiculous not to. The few new people I have got over the holidays have not blinked a bit at the £14 per lesson price tag. I am, after all, extremely cheap anyway! The going rate is £16 - and that's travelling to the teachers house... so I am a bit of a bargain. I cant be too cheap or I will look like rubbish. Hard huh?
Ok, roundup of today's food...
had the prawns thing this morning
had an apple
had a couple of cereal bars
dinner was cauliflower, creamed leeks and duchess potatoes. I didn't bother with meat as it makes me sick.
Then I had half a bottle red and another cereal bar.
That's all folks!
From Size XXL to Medium
Carl, age 29, decided to get fit again. He's lost 50 pounds and gone from a size XXL to a size medium. His preferred way back to optimum health was to join a gym and start up kick-boxing. See his story and picture here.
The unrelated photo above is by livegym-showtime.
Shopping is getting to be a full time job for an accountant
1 Tesco Plain Flour 1.5kg
2 Pataks Madras Curry Paste Medium Hot Jar 283g
14 Golden Delicious Apples Class 1 Loose
4 Pot Noodle Chicken & M/Room 94g
1 Red Bull Energy Drink 250ml
2 Tesco Nas Orange Squash 750ml
1 Robinsons Hi-Juice Orange 1 Ltr
4 Tesco Thick All Butter Shortbread Fingers 250g
1 Frozen Cooked & Peeled King Prawns 250g
1 T.Salt & Vinegarcrunchy Sticks 150g
1 Tesco Prawn Crackers 60g
1 Walkers Wotsits Cheese 12pk
3 Tesco Spinach Ricotta Tortellini 250g
1 Ready To Eat Peach Punnet
1 Tesco 12 Mini Savoury Eggs 240g
2 Boklunder Schulte Bratwurst 540g
1 Dove Deodorant Fresh Antiperspirant Deodrant 150ml
1 Raid Fly And Wasp Killer 300ml
1 Tesco Value Cooked Ham 125g
1 Tesco Value Table Salt 1kg
1 Tesco Non Biological Powder 30 Wash/2.4kg
2 Tesco Value Chicken Breast Fillets 1kg
2 Go Tan Nasi Goreng Mealkit 380g
1 Lamb Whole Leg 1.4kg - 2.4kg
1 Go Cat Duck Rabbit & Chicken 950g
2 Tesco Chocolate Chip Chewy & Crisp Cereal Bar 6 Pack
2 Tesco Value Dishwasher Tabs 30's
1 Clean & Fresh Washing Up Liquid 1 Ltr
1 Tesco Floral Liquid Rim Plus 3 Refills
24 Tesco Uht Value Skimmed Milk 1 Litre
5 Felix Fish Variety Pack 6 X 400g
TOTAL
£104.74
Same EXACT shop... using equivalent brands in LIDL.... £77.88
That is a saving of nearly £27.00!!!!!!!! Thats a new pair of shoes!
I have decided that I have to be more frugal with my spending, and am choosing where to buy things rather than just going to Tesco like I always have done.
A year or two ago I never thought about the price of things. The weekly shop come to such & such and that was that. I didn't buy value all the time, nor did I look and compare prices. I just saw what I wanted and put it in the trolley. I am finding with rising costs that this is simply idiotic these days. I was in tesco teaching DS how to work out which olive oil to buy and it struck me that I was actually working out the price per litre and then seeing which one was better value on a basic necessity like olive oil. This was really concerning.
When I was looking at it all, there were several thoughts going through my mind. Firstly was DS needs to be able to do this. He needs to be able to convert £1.25 per litre/kilo into mls/grams. He needs to work out how much per litre a 500ml bottle of oil costing £3.65 is etc.
Secondly, how cunning supermarkets are. For example there are 10 bottles of oil on the shelf. Some are 500mls, some 1 ltr, some 750. They all are labelled by price, but because of the sizing of the bottles, you still cant work out which is cheaper. They have 'tried' to make it easier by underneath putting the price per litre... but it is NOT uniform! Sometimes they put price per half litre or in mls, so for someone who cannot do basic maths, this is a minefield.
It struck me that they need to uniformly put the price per litre, or per ml or whatever and stick to it. But of course they are not going to.
DS and were looking at all these bottles of oil, and we were sat down on the floor in the aisle doing these sums. People were staring at us like we were mad. I said to DS "Which one looks the most expensive" and "Which one looks the cheapest?" He chose the Bertolli light olive oil as the most expensive because the label looks lovely. He chose the plain glass tesco bottle of oil as the cheapest because of the label too and also by the price tag. He was right about the most expensive. But wrong about the cheapest. Right next to the bottle of Tesco olive oil was another bottle which looked exactly the same size. It was dearer by about 25p though. However, when you looked VERY closely this bottle was 1litre of oil, and the glass one next to it was 750mls. The 1litre bottle was PLASTIC. It was exactly the same shape and size as the 750ml one, but was infact the cheapest. Now, just rushing through with screaming kids, Mrs Joe Bloggs would pick up the 750ml no doubt, because 25p is still 25p and would not notice that actually the other WAS cheaper.
I think this is like deception. It amounts to it. They cover the prices with jargon, put different prices, different sizes etc and it baffles one. Cunning. Obviously its their job to be, but I think it terrible. Going to such lengths as that to gain a few pence.
It doesn't stop there... you by loose apples because you see that the packaged ones are dearer. Then you keep doing that and what do you find, the packed apples are now cheaper!! so you go back to packed, then a few weeks later the loose are in again. They swap it to maximise their success and your loss.
Who goes shopping for a pint of milk and comes out with that pint costing £50. Its a time old saying, but I know I do! They swap the shelves, move products practically weekly to get you traipsing through the store in the hope that you will spot a bargain! How much more of this kind of thing that we don't notice? I always used to wonder why you could smell bread as you walked in the shop, but the bakery section was at the far back of the store... Hmmm.
Anyway, I am getting my veg from a local farm shop. I asked the lady there to make me up a box of veg and salad. That way I can go in, get the goods and leave and it cuts down on impulse buying. I find that I never have enough veg to last the week, so I go shopping purely for vegetables 2 or 3 times a week and end up come out with all kinds of other crap.
I am doing my main shopping in Lidl once per week.
I am buying my washing detergent ONLY from ALDI because their Liquid wash is £2 per bottle and it does 30 washes!!! That's Unreal! It washes really well too.
This way I figure I am going to save myself about £50 - £65 a week on my shopping bills.
Needs must when the devil drives.
band land... I am going to have a top up, I think I wrote that already, on Sunday. I have had a good day today... some prawns in a ginger and garlic sauce that I saved and froze from the other week and an apple. Not gonna get very fat on that huh.
Yesterday was a bit of a bad day... not because of over eating, but being sick. I cant remember what I had for breakfast... I think a muesli bar... then I went to the city to buy some stuff for our box day anniversary celebration which is on the 30th (will explain all later). I was really hungry and bought some spinach falafel from waitrose. I ate one and should have stopped. I didn't and ate another only to have to be sick later. Then we went to Lotse and Csilla's for dinner. They made fried chicken and mash and tiramisu. I had some chicken, but had to throw it back up. I managed the potato and also the two helpings of tiramisu. Yum!
Today I have also added a cereal bar to my daily food intake. I have no idea what we are doing for dinner, but I want something nice!
2 Pataks Madras Curry Paste Medium Hot Jar 283g
14 Golden Delicious Apples Class 1 Loose
4 Pot Noodle Chicken & M/Room 94g
1 Red Bull Energy Drink 250ml
2 Tesco Nas Orange Squash 750ml
1 Robinsons Hi-Juice Orange 1 Ltr
4 Tesco Thick All Butter Shortbread Fingers 250g
1 Frozen Cooked & Peeled King Prawns 250g
1 T.Salt & Vinegarcrunchy Sticks 150g
1 Tesco Prawn Crackers 60g
1 Walkers Wotsits Cheese 12pk
3 Tesco Spinach Ricotta Tortellini 250g
1 Ready To Eat Peach Punnet
1 Tesco 12 Mini Savoury Eggs 240g
2 Boklunder Schulte Bratwurst 540g
1 Dove Deodorant Fresh Antiperspirant Deodrant 150ml
1 Raid Fly And Wasp Killer 300ml
1 Tesco Value Cooked Ham 125g
1 Tesco Value Table Salt 1kg
1 Tesco Non Biological Powder 30 Wash/2.4kg
2 Tesco Value Chicken Breast Fillets 1kg
2 Go Tan Nasi Goreng Mealkit 380g
1 Lamb Whole Leg 1.4kg - 2.4kg
1 Go Cat Duck Rabbit & Chicken 950g
2 Tesco Chocolate Chip Chewy & Crisp Cereal Bar 6 Pack
2 Tesco Value Dishwasher Tabs 30's
1 Clean & Fresh Washing Up Liquid 1 Ltr
1 Tesco Floral Liquid Rim Plus 3 Refills
24 Tesco Uht Value Skimmed Milk 1 Litre
5 Felix Fish Variety Pack 6 X 400g
TOTAL
£104.74
Same EXACT shop... using equivalent brands in LIDL.... £77.88
That is a saving of nearly £27.00!!!!!!!! Thats a new pair of shoes!
I have decided that I have to be more frugal with my spending, and am choosing where to buy things rather than just going to Tesco like I always have done.
A year or two ago I never thought about the price of things. The weekly shop come to such & such and that was that. I didn't buy value all the time, nor did I look and compare prices. I just saw what I wanted and put it in the trolley. I am finding with rising costs that this is simply idiotic these days. I was in tesco teaching DS how to work out which olive oil to buy and it struck me that I was actually working out the price per litre and then seeing which one was better value on a basic necessity like olive oil. This was really concerning.
When I was looking at it all, there were several thoughts going through my mind. Firstly was DS needs to be able to do this. He needs to be able to convert £1.25 per litre/kilo into mls/grams. He needs to work out how much per litre a 500ml bottle of oil costing £3.65 is etc.
Secondly, how cunning supermarkets are. For example there are 10 bottles of oil on the shelf. Some are 500mls, some 1 ltr, some 750. They all are labelled by price, but because of the sizing of the bottles, you still cant work out which is cheaper. They have 'tried' to make it easier by underneath putting the price per litre... but it is NOT uniform! Sometimes they put price per half litre or in mls, so for someone who cannot do basic maths, this is a minefield.
It struck me that they need to uniformly put the price per litre, or per ml or whatever and stick to it. But of course they are not going to.
DS and were looking at all these bottles of oil, and we were sat down on the floor in the aisle doing these sums. People were staring at us like we were mad. I said to DS "Which one looks the most expensive" and "Which one looks the cheapest?" He chose the Bertolli light olive oil as the most expensive because the label looks lovely. He chose the plain glass tesco bottle of oil as the cheapest because of the label too and also by the price tag. He was right about the most expensive. But wrong about the cheapest. Right next to the bottle of Tesco olive oil was another bottle which looked exactly the same size. It was dearer by about 25p though. However, when you looked VERY closely this bottle was 1litre of oil, and the glass one next to it was 750mls. The 1litre bottle was PLASTIC. It was exactly the same shape and size as the 750ml one, but was infact the cheapest. Now, just rushing through with screaming kids, Mrs Joe Bloggs would pick up the 750ml no doubt, because 25p is still 25p and would not notice that actually the other WAS cheaper.
I think this is like deception. It amounts to it. They cover the prices with jargon, put different prices, different sizes etc and it baffles one. Cunning. Obviously its their job to be, but I think it terrible. Going to such lengths as that to gain a few pence.
It doesn't stop there... you by loose apples because you see that the packaged ones are dearer. Then you keep doing that and what do you find, the packed apples are now cheaper!! so you go back to packed, then a few weeks later the loose are in again. They swap it to maximise their success and your loss.
Who goes shopping for a pint of milk and comes out with that pint costing £50. Its a time old saying, but I know I do! They swap the shelves, move products practically weekly to get you traipsing through the store in the hope that you will spot a bargain! How much more of this kind of thing that we don't notice? I always used to wonder why you could smell bread as you walked in the shop, but the bakery section was at the far back of the store... Hmmm.
Anyway, I am getting my veg from a local farm shop. I asked the lady there to make me up a box of veg and salad. That way I can go in, get the goods and leave and it cuts down on impulse buying. I find that I never have enough veg to last the week, so I go shopping purely for vegetables 2 or 3 times a week and end up come out with all kinds of other crap.
I am doing my main shopping in Lidl once per week.
I am buying my washing detergent ONLY from ALDI because their Liquid wash is £2 per bottle and it does 30 washes!!! That's Unreal! It washes really well too.
This way I figure I am going to save myself about £50 - £65 a week on my shopping bills.
Needs must when the devil drives.
band land... I am going to have a top up, I think I wrote that already, on Sunday. I have had a good day today... some prawns in a ginger and garlic sauce that I saved and froze from the other week and an apple. Not gonna get very fat on that huh.
Yesterday was a bit of a bad day... not because of over eating, but being sick. I cant remember what I had for breakfast... I think a muesli bar... then I went to the city to buy some stuff for our box day anniversary celebration which is on the 30th (will explain all later). I was really hungry and bought some spinach falafel from waitrose. I ate one and should have stopped. I didn't and ate another only to have to be sick later. Then we went to Lotse and Csilla's for dinner. They made fried chicken and mash and tiramisu. I had some chicken, but had to throw it back up. I managed the potato and also the two helpings of tiramisu. Yum!
Today I have also added a cereal bar to my daily food intake. I have no idea what we are doing for dinner, but I want something nice!
Minggu, 17 Agustus 2008
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. What drives fat accumulation is chronically high insulin (hyperinsulinemia), which the Kitavans do not have. 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 safely rule out that total fat, saturated fat and carbohydrate cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also safely rule out that there's some specific food that protects these populations, since they eat completely different things. Exercise is also not a compelling explanation, based on the data above and others. 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 wheat and refined sugar.
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. What drives fat accumulation is chronically high insulin (hyperinsulinemia), which the Kitavans do not have. 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 safely rule out that total fat, saturated fat and carbohydrate cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also safely rule out that there's some specific food that protects these populations, since they eat completely different things. Exercise is also not a compelling explanation, based on the data above and others. 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 wheat and refined sugar.
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. What drives fat accumulation is chronically high insulin (hyperinsulinemia), which the Kitavans do not have. 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 safely rule out that total fat, saturated fat and carbohydrate cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also safely rule out that there's some specific food that protects these populations, since they eat completely different things. Exercise is also not a compelling explanation, based on the data above and others. 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 wheat and refined sugar.
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. What drives fat accumulation is chronically high insulin (hyperinsulinemia), which the Kitavans do not have. 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 safely rule out that total fat, saturated fat and carbohydrate cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also safely rule out that there's some specific food that protects these populations, since they eat completely different things. Exercise is also not a compelling explanation, based on the data above and others. 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 wheat and refined sugar.
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.
Jumat, 15 Agustus 2008
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. Some of the best predictors in Western populations are low HDL and high triglycerides (these are also markers of the metabolic syndrome). It's well established that HDL goes down on a high-carbohydrate diet, and triglycerides go up. That's exactly what we see in Kitavans. Their HDL is slightly lower than Swedes' at middle and old age, and their triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) equal to or worse than 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 won't discuss LDL much because it's a weak predictor, but in case you're interested, it's lower in Kitavan males than Swedish males. It's about the same in Kitavan and Swedish females until old age, when Swedish LDL goes up.
These data seriously challenge the theory 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.
I have a theory of the relationship between blood lipids and CVD that can explain these data. I believe that 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 grain and sugar 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. Some of the best predictors in Western populations are low HDL and high triglycerides (these are also markers of the metabolic syndrome). It's well established that HDL goes down on a high-carbohydrate diet, and triglycerides go up. That's exactly what we see in Kitavans. Their HDL is slightly lower than Swedes' at middle and old age, and their triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) equal to or worse than 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 won't discuss LDL much because it's a weak predictor, but in case you're interested, it's lower in Kitavan males than Swedish males. It's about the same in Kitavan and Swedish females until old age, when Swedish LDL goes up.
These data seriously challenge the theory 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.
I have a theory of the relationship between blood lipids and CVD that can explain these data. I believe that 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 grain and sugar 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. Some of the best predictors in Western populations are low HDL and high triglycerides (these are also markers of the metabolic syndrome). It's well established that HDL goes down on a high-carbohydrate diet, and triglycerides go up. That's exactly what we see in Kitavans. Their HDL is slightly lower than Swedes' at middle and old age, and their triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) equal to or worse than 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 won't discuss LDL much because it's a weak predictor, but in case you're interested, it's lower in Kitavan males than Swedish males. It's about the same in Kitavan and Swedish females until old age, when Swedish LDL goes up.
These data seriously challenge the theory 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.
I have a theory of the relationship between blood lipids and CVD that can explain these data. I believe that 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 grain and sugar 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. Some of the best predictors in Western populations are low HDL and high triglycerides (these are also markers of the metabolic syndrome). It's well established that HDL goes down on a high-carbohydrate diet, and triglycerides go up. That's exactly what we see in Kitavans. Their HDL is slightly lower than Swedes' at middle and old age, and their triglycerides are higher on average. Judging by these numbers, Kitavans should have cardiovascular disease (CVD) equal to or worse than 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 won't discuss LDL much because it's a weak predictor, but in case you're interested, it's lower in Kitavan males than Swedish males. It's about the same in Kitavan and Swedish females until old age, when Swedish LDL goes up.
These data seriously challenge the theory 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.
I have a theory of the relationship between blood lipids and CVD that can explain these data. I believe that 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 grain and sugar intake.
Kamis, 14 Agustus 2008
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. 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. 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.
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