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codeunknown
Posts: 22615
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Joined: 7/14/2004
Member: #704
8/11/2008  1:18 AM
Posted by BlueSeats:
Posted by codeunknown:

Here's a hint, Blueseats, don't declare that paradigms are changing when the authors of the article themselves don't. Once again, its not my goal to embarass you or put you on the spot but I keep wondering why you're, rather uncharacteristically, making these wild proclamations.

Truth be told, when you do chose to embarrass someone you do it so thoroughly and meticulously that it's worth being the victim just for the show. I'm clearly baiting you, don't stop now! And thanks for the flattery about being a favorite poster. Right back at you.

That said, I do believe the paradigm is shifting, and the momentum will pick up as better tests are conducted.


To cut to the chase, you've unfortunately garbled this article as well - the authors are making a satiety argument and protein (found in far greater quantities in eggs as opposed to bagels) has, by far, been shown to be the major component implicated in satiety. Just in case you don't believe me, the article you posted is a follow-up to a 2005 article these authors presented -- the conclusion of that article is that "Compared to an isocaloric, equal weight bagel-based breakfast, the egg-breakfast induced greater satiety and significantly reduced short-term food intake."

Now, keep in mind and this is of utmost importance, the article above doesn't even attempt to control for total fat, saturated fat or total caloric intake in the whole diet - merely the breakfast component is controlled -- and this, of course, was done intentionally because disparities in weight gain can only occur through changes in input or output. They are NOT AT ALL exploring the relationship between cholesterol, heart disease or saturated fat as you might have hoped; they are simply making the case that there may be a synergistic relationship between conscious dieting + an egg breakfast and short-term satiety and, thus, weight loss. For the sake of completion, it should also have raised a red flag to you that E vs. B data is not presented in the abstract - if there is no discrepancy between those groups, perhaps the pyschological compomenent is dominant and that realization should have prompted, at least, a randomization across diet history. But, again, it seems that you're not so interested in objectively evaluating the data as in claiming some sort of strange victory.

I understand that. But the same is true for fats. It's one of the great failures of the low fat diet approach. Fat calories, which are much more satiating than glucose and other simple sugars, are generally replaced by carbohydrates (and far too often refine grains) which surge insulin levels and leave people hungry. Eventually insulin resistance can set in. Diet compliance becomes a major issue too because carbs are a lot more addictive than fats. Typically people are far more likely to splurge in things like breads, cookies, chips, chocolate, etc, than they are on, say, animal fat or olive oil.

I don't have an agenda here - I don't own Lipitor stock - although I should. In fact, the more heart disease there is, the more CABG surgeries I do, the more money I make. So Blue, as a buddy and easily one of my favorite posters on this site, I'm not asking you to "blindly" follow my wisdom but it might do you well to at least consider my >30 years of experience leading research in this field and dissecting the literature before telling me and the rest of us that we're missing some major paradigm shift that never occurred.

I understand that you have a very high IQ, are well schooled, know a sh-t load about many things, and can write about things I'll never understand with a vocabulary so broad I can barely read it. But that doesn't make you right. Nor can I say I know you to be wrong. What I am saying is there is compelling evidence that calls your position into question, and more and more people are carrying the drum.

There are just to many holes in your theory. Low fat diets have been the rage for what, 20-30 years now but obesity is up. Smoking is down and people consume less saturated fats, yet heart disease is just as high. Cultures with higher intake of saturated fats have lower rates of heart disease. So what gives?

Great. I'm not sure where that leaves us. I'm not sure what paradigm is shifting. I'm not sure where exactly your objection lies along the lipid hypothesis. I'm not sure why you value crude epidemiology over large, controlled clinical trials. I'm not sure why you think that I'm discounting other undiscovered risk factors when I'm merely making the case for serum LDL and saturated fat as important risk factors. And so I'm not really sure how to respond without provoking a sarcastic, baiting post. So the show, in which you consider yourself a victim, is officially over.


Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
AUTOADVERT
codeunknown
Posts: 22615
Alba Posts: 9
Joined: 7/14/2004
Member: #704
8/11/2008  1:24 AM
Posted by BlueSeats:



I understand that. It's a shotcoming of the test, Everyone already knew protien is more satiating than empty carbs. And they could have used egg whites to prove that.


[Edited by - blueseats on 08-11-2008 01:04 AM]

Its not necessarily a shortcoming of the study. Their goal isn't so much to distinguish between the ability of proteins and fats to produce satiety as much as be able to make a practical recommendation for weight loss. And eggs over bagels in the morning is what they found. Do I agree? Not until we've read the full text.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
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Joined: 11/6/2005
Member: #1024
8/11/2008  1:28 AM
Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.
codeunknown
Posts: 22615
Alba Posts: 9
Joined: 7/14/2004
Member: #704
8/11/2008  1:38 AM
Posted by BlueSeats:

Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.


I can't really say without seeing the published article. Among the first questions I'd ask is how the two groups were divided and whether any other lifestyle changes took place? Like did they pick up a pack of Marlboros? etc.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
Alba Posts: 41
Joined: 11/6/2005
Member: #1024
8/11/2008  1:47 AM
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:

Here's a hint, Blueseats, don't declare that paradigms are changing when the authors of the article themselves don't. Once again, its not my goal to embarass you or put you on the spot but I keep wondering why you're, rather uncharacteristically, making these wild proclamations.

Truth be told, when you do chose to embarrass someone you do it so thoroughly and meticulously that it's worth being the victim just for the show. I'm clearly baiting you, don't stop now! And thanks for the flattery about being a favorite poster. Right back at you.

That said, I do believe the paradigm is shifting, and the momentum will pick up as better tests are conducted.


To cut to the chase, you've unfortunately garbled this article as well - the authors are making a satiety argument and protein (found in far greater quantities in eggs as opposed to bagels) has, by far, been shown to be the major component implicated in satiety. Just in case you don't believe me, the article you posted is a follow-up to a 2005 article these authors presented -- the conclusion of that article is that "Compared to an isocaloric, equal weight bagel-based breakfast, the egg-breakfast induced greater satiety and significantly reduced short-term food intake."

Now, keep in mind and this is of utmost importance, the article above doesn't even attempt to control for total fat, saturated fat or total caloric intake in the whole diet - merely the breakfast component is controlled -- and this, of course, was done intentionally because disparities in weight gain can only occur through changes in input or output. They are NOT AT ALL exploring the relationship between cholesterol, heart disease or saturated fat as you might have hoped; they are simply making the case that there may be a synergistic relationship between conscious dieting + an egg breakfast and short-term satiety and, thus, weight loss. For the sake of completion, it should also have raised a red flag to you that E vs. B data is not presented in the abstract - if there is no discrepancy between those groups, perhaps the pyschological compomenent is dominant and that realization should have prompted, at least, a randomization across diet history. But, again, it seems that you're not so interested in objectively evaluating the data as in claiming some sort of strange victory.

I understand that. But the same is true for fats. It's one of the great failures of the low fat diet approach. Fat calories, which are much more satiating than glucose and other simple sugars, are generally replaced by carbohydrates (and far too often refine grains) which surge insulin levels and leave people hungry. Eventually insulin resistance can set in. Diet compliance becomes a major issue too because carbs are a lot more addictive than fats. Typically people are far more likely to splurge in things like breads, cookies, chips, chocolate, etc, than they are on, say, animal fat or olive oil.

I don't have an agenda here - I don't own Lipitor stock - although I should. In fact, the more heart disease there is, the more CABG surgeries I do, the more money I make. So Blue, as a buddy and easily one of my favorite posters on this site, I'm not asking you to "blindly" follow my wisdom but it might do you well to at least consider my >30 years of experience leading research in this field and dissecting the literature before telling me and the rest of us that we're missing some major paradigm shift that never occurred.

I understand that you have a very high IQ, are well schooled, know a sh-t load about many things, and can write about things I'll never understand with a vocabulary so broad I can barely read it. But that doesn't make you right. Nor can I say I know you to be wrong. What I am saying is there is compelling evidence that calls your position into question, and more and more people are carrying the drum.

There are just to many holes in your theory. Low fat diets have been the rage for what, 20-30 years now but obesity is up. Smoking is down and people consume less saturated fats, yet heart disease is just as high. Cultures with higher intake of saturated fats have lower rates of heart disease. So what gives?

Great. I'm not sure where that leaves us. I'm not sure what paradigm is shifting. I'm not sure where exactly your objection lies along the lipid hypothesis. I'm not sure why you value crude epidemiology over large, controlled clinical trials. I'm not sure why you think that I'm discounting other undiscovered risk factors when I'm merely making the case for serum LDL and saturated fat as important risk factors. And so I'm not really sure how to respond without provoking a sarcastic, baiting post. So the show, in which you consider yourself a victim, is officially over.



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.
BlueSeats
Posts: 27272
Alba Posts: 41
Joined: 11/6/2005
Member: #1024
8/11/2008  1:54 AM
Posted by codeunknown:
Posted by BlueSeats:

Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.


I can't really say without seeing the published article. Among the first questions I'd ask is how the two groups were divided and whether any other lifestyle changes took place? Like did they pick up a pack of Marlboros? etc.

Under what conditions would you tell them to go back to their original high saturated fat diet?
codeunknown
Posts: 22615
Alba Posts: 9
Joined: 7/14/2004
Member: #704
8/11/2008  2:00 AM
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:

Here's a hint, Blueseats, don't declare that paradigms are changing when the authors of the article themselves don't. Once again, its not my goal to embarass you or put you on the spot but I keep wondering why you're, rather uncharacteristically, making these wild proclamations.

Truth be told, when you do chose to embarrass someone you do it so thoroughly and meticulously that it's worth being the victim just for the show. I'm clearly baiting you, don't stop now! And thanks for the flattery about being a favorite poster. Right back at you.

That said, I do believe the paradigm is shifting, and the momentum will pick up as better tests are conducted.


To cut to the chase, you've unfortunately garbled this article as well - the authors are making a satiety argument and protein (found in far greater quantities in eggs as opposed to bagels) has, by far, been shown to be the major component implicated in satiety. Just in case you don't believe me, the article you posted is a follow-up to a 2005 article these authors presented -- the conclusion of that article is that "Compared to an isocaloric, equal weight bagel-based breakfast, the egg-breakfast induced greater satiety and significantly reduced short-term food intake."

Now, keep in mind and this is of utmost importance, the article above doesn't even attempt to control for total fat, saturated fat or total caloric intake in the whole diet - merely the breakfast component is controlled -- and this, of course, was done intentionally because disparities in weight gain can only occur through changes in input or output. They are NOT AT ALL exploring the relationship between cholesterol, heart disease or saturated fat as you might have hoped; they are simply making the case that there may be a synergistic relationship between conscious dieting + an egg breakfast and short-term satiety and, thus, weight loss. For the sake of completion, it should also have raised a red flag to you that E vs. B data is not presented in the abstract - if there is no discrepancy between those groups, perhaps the pyschological compomenent is dominant and that realization should have prompted, at least, a randomization across diet history. But, again, it seems that you're not so interested in objectively evaluating the data as in claiming some sort of strange victory.

I understand that. But the same is true for fats. It's one of the great failures of the low fat diet approach. Fat calories, which are much more satiating than glucose and other simple sugars, are generally replaced by carbohydrates (and far too often refine grains) which surge insulin levels and leave people hungry. Eventually insulin resistance can set in. Diet compliance becomes a major issue too because carbs are a lot more addictive than fats. Typically people are far more likely to splurge in things like breads, cookies, chips, chocolate, etc, than they are on, say, animal fat or olive oil.

I don't have an agenda here - I don't own Lipitor stock - although I should. In fact, the more heart disease there is, the more CABG surgeries I do, the more money I make. So Blue, as a buddy and easily one of my favorite posters on this site, I'm not asking you to "blindly" follow my wisdom but it might do you well to at least consider my >30 years of experience leading research in this field and dissecting the literature before telling me and the rest of us that we're missing some major paradigm shift that never occurred.

I understand that you have a very high IQ, are well schooled, know a sh-t load about many things, and can write about things I'll never understand with a vocabulary so broad I can barely read it. But that doesn't make you right. Nor can I say I know you to be wrong. What I am saying is there is compelling evidence that calls your position into question, and more and more people are carrying the drum.

There are just to many holes in your theory. Low fat diets have been the rage for what, 20-30 years now but obesity is up. Smoking is down and people consume less saturated fats, yet heart disease is just as high. Cultures with higher intake of saturated fats have lower rates of heart disease. So what gives?

Great. I'm not sure where that leaves us. I'm not sure what paradigm is shifting. I'm not sure where exactly your objection lies along the lipid hypothesis. I'm not sure why you value crude epidemiology over large, controlled clinical trials. I'm not sure why you think that I'm discounting other undiscovered risk factors when I'm merely making the case for serum LDL and saturated fat as important risk factors. And so I'm not really sure how to respond without provoking a sarcastic, baiting post. So the show, in which you consider yourself a victim, is officially over.



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.


For millenia, our ancestors lived on average 30 years less than us, taken by infections and the like before heart disease had the opportunity to manifest itself. Smouldering heart disease went undetected because we didn't have the benefits of EKGs and echocardiograms. Our ancestors also excercised. They didn't smoke. And the portions they ate were likely less as a gazelle only comes around once in a while. Even then they were eaten by wild game before 45, so their efforts were in vain. So, if getting eaten at 45 is doing well, I'm pleased to have surpassed those lofty expectations.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
codeunknown
Posts: 22615
Alba Posts: 9
Joined: 7/14/2004
Member: #704
8/11/2008  2:02 AM
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:

Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.


I can't really say without seeing the published article. Among the first questions I'd ask is how the two groups were divided and whether any other lifestyle changes took place? Like did they pick up a pack of Marlboros? etc.

Under what conditions would you tell them to go back to their original high saturated fat diet?

After controlled studies that apply to their population.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
Alba Posts: 41
Joined: 11/6/2005
Member: #1024
8/11/2008  2:21 AM
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:

Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.


I can't really say without seeing the published article. Among the first questions I'd ask is how the two groups were divided and whether any other lifestyle changes took place? Like did they pick up a pack of Marlboros? etc.

Under what conditions would you tell them to go back to their original high saturated fat diet?

After controlled studies that apply to their population.

That's a bit vague. What's being tested, what's being controlled and how are you defining their population?

Can you cite similar studies that have been applied to similarly healthy, high saturated fat ingesting populations and demonstrate the kind of useful information they generated, how it was applied, and the outcome of those applications?
codeunknown
Posts: 22615
Alba Posts: 9
Joined: 7/14/2004
Member: #704
8/11/2008  2:33 AM
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:

Code, I'm still interested in hearing how you reconcile this:

I showed in the other excerpts reports of African tribesmen who thrive on healthy saturated fats, but when they are introduced to Western industrialized diets their cholesterol and heart disease sky rocket. The sad thing is that in this society, rather than being told to return to their native, healthy, high saturated fat diet, they will be told to consume more Lean Cuisine and Nabisco crackers that proclaim themselves to be "part of a healthy low fat diet". This overdose of carbs and sugars will drive up their insulin levels, leading to insulin resistance and predispose them to diabetes and heart disease. IOW, they will told to more strictly adhere to the high carbohydrate and over processed oils that corrupted their health in the first place. They'll be left under-nourished, carb addicted, hungry and insulin resistant - thusly predisposed to diabetes and heart disease. Then they'll be put on statins. But never to go back to their wholesome high fat diet.


I can't really say without seeing the published article. Among the first questions I'd ask is how the two groups were divided and whether any other lifestyle changes took place? Like did they pick up a pack of Marlboros? etc.

Under what conditions would you tell them to go back to their original high saturated fat diet?

After controlled studies that apply to their population.

That's a bit vague. What's being tested, what's being controlled and how are you defining their population?

Can you cite similar studies that have been applied to similarly healthy, high saturated fat ingesting populations and demonstrate the kind of useful information they generated, how it was applied, and the outcome of those applications?

Do you ever sleep, man?

I'll try and answer your questions to the best of my ability if I get the chance within the week. Still, given the plethora of studies I've already posted and described, it shouldn't be hard to imagine the kind of study I'd be going for. Giving you particular inclusion criteria would require me to know a little more about their culture in order to anticipate potential pitfalls. LDL, HDL, CHD events etc. would be among the most obvious outcome variables.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
Alba Posts: 41
Joined: 11/6/2005
Member: #1024
8/11/2008  3:07 AM
Code, don't sweat the request, it wont move the discussion forward. But seriously, have you ever had a patient with high cholesterol and sought out a population specific study and prescribed accordingly? Your first post suggests otherwise - you follow guidelines you say all clinicians follow:
Posted by codeunknown:


The bottom line is that the commercial message that an elevation in LDL or "bad" cholesterol increases cardiovascular incidents and mortality is absolutely true. Conversely, reducing LDL with dietary decreases in saturated fat or statin therapy invariably prevents heart attacks and strokes in a population. To give you a feel for the numbers, prospective studies have long shown that statin therapy reduces non-fatal cardiac events by 35% and fatal cardiac events by 25%. The correlation between LDL levels and mortality has been so bulletfroof that there are guidelines that all clinicians follow:

LDL level
<100 Optimal
100-129 Near optimal
130-159
160-189 High
>190 Very high


So when was the last time you returned a chap to a high saturated fat diet rather than drugs?

----



Studies that Challenge the Lipid Hypothesis

While it is true that researchers have induced heart disease in some animals by giving them extremely large dosages of oxidized or rancid cholesterol—amounts ten times that found in the ordinary human diet—several population studies squarely contradict the cholesterol-heart disease connection. A survey of 1700 patients with hardening of the arteries, conducted by the famous heart surgeon Michael DeBakey, found no relationship between the level of cholesterol in the blood and the incidence of atherosclerosis.9 A survey of South Carolina adults found no correlation of blood cholesterol levels with "bad" dietary habits, such as use of red meat, animal fats, fried foods, butter, eggs, whole milk, bacon, sausage and cheese.10 A Medical Research Council survey showed that men eating butter ran half the risk of developing heart disease as those using margarine.11

Mother's milk provides a higher proportion of cholesterol than almost any other food. It also contains over 50% of its calories as fat, much of it saturated fat. Both cholesterol and saturated fat are essential for growth in babies and children, especially the development of the brain.12 Yet, the American Heart Association is now recommending a low-cholesterol, lowfat diet for children! Commercial formulas are low in saturated fats and soy formulas are devoid of cholesterol. A recent study linked lowfat diets with failure to thrive in children.13

Numerous surveys of traditional populations have yielded information that is an embarrassment to the Diet Dictocrats. For example, a study comparing Jews when they lived in Yemen, whose diets contained fats solely of animal origin, to Yemenite Jews living in Israel, whose diets contained margarine and vegetable oils, revealed little heart disease or diabetes in the former group but high levels of both diseases in the latter.14 (The study also noted that the Yemenite Jews consumed no sugar but those in Israel consumed sugar in amounts equaling 25-30% of total carbohydrate intake.) A comparison of populations in northern and southern India revealed a similar pattern. People in northern India consume 17 times more animal fat but have an incidence of coronary heart disease seven times lower than people in southern India.15 The Masai and kindred tribes of Africa subsist largely on milk, blood and beef. They are free from coronary heart disease and have excellent blood cholesterol levels.16 Eskimos eat liberally of animal fats from fish and marine animals. On their native diet they are free of disease and exceptionally hardy.17 An extensive study of diet and disease patterns in China found that the region in which the populace consumes large amounts of whole milk had half the rate of heart disease as several districts in which only small amounts of animal products are consumed.18 Several Mediterranean societies have low rates of heart disease even though fat—including highly saturated fat from lamb, sausage and goat cheese—comprises up to 70% of their caloric intake. The inhabitants of Crete, for example, are remarkable for their good health and longevity.19 A study of Puerto Ricans revealed that, although they consume large amounts of animal fat, they have a very low incidence of colon and breast cancer.20 A study of the long-lived inhabitants of Soviet Georgia revealed that those who eat the most fatty meat live the longest.21 In Okinawa, where the average life span for women is 84 years—longer than in Japan—the inhabitants eat generous amounts of pork and seafood and do all their cooking in lard.22 None of these studies is mentioned by those urging restriction of saturated fats.

The relative good health of the Japanese, who have the longest life span of any nation in the world, is generally attributed to a lowfat diet. Although the Japanese eat few dairy fats, the notion that their diet is low in fat is a myth; rather, it contains moderate amounts of animal fats from eggs, pork, chicken, beef, seafood and organ meats. With their fondness for shellfish and fish broth, eaten on a daily basis, the Japanese probably consume more cholesterol than most Americans. What they do not consume is a lot of vegetable oil, white flour or processed food (although they do eat white rice.) The life span of the Japanese has increased since World War II with an increase in animal fat and protein in the diet.23 Those who point to Japanese statistics to promote the lowfat diet fail to mention that the Swiss live almost as long on one of the fattiest diets in the world. Tied for third in the longevity stakes are Austria and Greece—both with high-fat diets.24

As a final example, let us consider the French. Anyone who has eaten his way across France has observed that the French diet is just loaded with saturated fats in the form of butter, eggs, cheese, cream, liver, meats and rich patés. Yet the French have a lower rate of coronary heart disease than many other western countries. In the United States, 315 of every 100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. In the Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkably low 80 per 100,000.25 This phenomenon has recently gained international attention as the French Paradox. (The French do suffer from many degenerative diseases, however. They eat large amounts of sugar and white flour and in recent years have succumbed to the timesaving temptations of processed foods.)

A chorus of establishment voices, including the American Cancer Society, the National Cancer Institute and the Senate Committee on Nutrition and Human Needs, claims that animal fat is linked not only with heart disease but also with cancers of various types. Yet when researchers from the University of Maryland analyzed the data they used to make such claims, they found that vegetable fat consumption was correlated with cancer and animal fat was not.26

# DeBakey, M, et al, JAMA, 1964, 189:655-59
# Lackland, D T, et al, J Nutr, Nov 1990, 120:11S:1433-1436
# Nutr Week, Mar 22, 1991, 21:12:2-3
# Alfin-Slater, R B, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, R S Goodhartand M E Shils, eds, Lea and Febiger, Philadelphia, 1980, 131
# Smith, M M, and F Lif****z, Pediatrics, Mar 1994, 93:3:438-443
# Cohen, A, Am Heart J, 1963, 65:291
# Malhotra, S, Indian Journal of Industrial Medicine, 1968, 14:219
# Kang-Jey Ho, et al, Archeological Pathology, 1971, 91:387; Mann, G V, et al, Am J Epidemiol, 1972, 95:26-37
# Price, Weston, DDS, Nutrition and Physical Degeneration, 1945, Price-Pottenger Nutrition Foundation, San Diego, CA, 59-72
# Chen, Junshi, Diet, Life-Style and Mortality in China: A Study of the Characteristics of 65 Chinese Counties, Cornell University Press, Ithica, NY
# Willett, W C, et al, Am J Clin Nutr, June 1995, 61(6S):1402S - 1406S; Perez-Llamas, F, et al, J Hum Nutr Diet, Dec 1996, 9:6:463-471; Alberti-Fidanza, A, et al, Eur J Clin Nutr, Feb 1994, 48:2:85-91
# Fernandez, N A, Cancer Res, 1975, 35:3272; Martines, I, et al, Cancer Res, 1975, 35:3265
# Pitskhelauri, G Z, The Long Living of Soviet Georgia, 1982, Human Sciences Press, New York, NY
# Franklyn, D, Health, September 1996, 57-63
# Koga, Y et al, "Recent Trends in Cardiovascular Disease and Risk Factors in the Seven Countries Study: Japan," Lessons for Science from the Seven Countries Study, H Toshima, et al, eds, Springer, New York, NY, 1994, 63-74
# Moore, Thomas J, Lifespan: What Really Affects Human Longevity, 1990, Simon and Schuster, New York, NY
# O'Neill, Molly, NY Times, Nov 17, 1991
# Enig, Mary G, Ph D, et al, Fed Proc, Jul 1978, 37:9:2215-2220

Sorry, the numbers didn't copy but they are the footnotes 9-26 in succession
BlueSeats
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8/11/2008  3:28 AM
I'm just curious, has anybody ever seen a documentary on primitive people who live off the land who are obese and with high incidences of heart disease?

Cause I know one thing for sure, you can take people from anywhere in the world and bring them here and feed them our diet and watch them get fat and line up for the standard diabetes and statin protocol. In fact, you don't even have to bring them here, just set them up with Pepsi, Nabisco, Nestle, General Foods, hydrogenated oils, pasteurized/homogenized growth hormone and antibiotic filled milk, etc, and it will happen for them right over there.

but lets not grasp the obvious, we could always quibble over whether they get more exercise (duh) or eat less calories (duh) and deceive ourselves that their diet of natural foods is really no better than ours. So instead we can waste time conducting studies to determine that a fat, protein and nutrient rich food, like a whole egg, in fact stays with you longer than a nutritionally deficient refined starch, that the body quickly converts to glucose (sugar).

Instead of emulating cultures that work, we harp on some single entity in our diet, like animal fat, which theoretically would happen to be close to what they're eating. But even that isn't because even our meat isn't allowed to follow a natural diet. We feed our animals corn, hormones and antibiotics when cows should be eating grass, and chickens should be eating grubs and worms.

But still we need more research to figure out how to keep eating crap and still stay healthy. We have these really smart doctors and researchers and they hang their hats on dumb studies and encourage us to eat dub products, like Coffee Mate instead of organic cream, or oils turned into plastic (Margarine) because in their world unadulterated fats, which man has lived on since he was an itch in Adam's pants, is no longer considered good for us. Much better that we should eat plasticized substitutes.

-----

An Example of Junk Science

By Mary Enig, PhD

While the establishment is finally recognizing the dangers of trans fatty acids, conventional dietary gurus continue to warn the public about the alleged dangers of saturated fats. In this article, we will look at a study published in 1997 in the American Journal of Cardiology (79:350-354) used to justify avoidance of red meat and butterfat, the two main sources of saturated fatty acids in the Western diet.

Arthur Agatston, author of the best-selling South Beach Diet refers to this research when he states: "The major problem I have with the Atkins Diet is the liberal intake of saturated fats. There is evidence now that immediately following a meal of saturated fats, there is dysfunction in the arteries, including those that supply the heart muscle with blood. As a result, the lining of the arteries (the endothelium) is predisposed to constriction and clotting. Imagine: Under the right (or rather, wrong) circumstances, eating a meal that’s high in saturated fat can trigger a heart attack! In addition, after a high-fat meal certain elements in the blood called remnant particles, persist for longer than is healthy. These particles contribute to the buildup of plaque in the vessel wall." Agatston recommends consuming polyunsaturated and monounsaturated vegetable oils, including tub spreads, rather than animal fats like butter.

In the study, carried out by Robert A. Vogel and his team at the University of Maryland School of Medicine, ten volunteers were tested for "endothelial function" by measuring the diameter
change in the brachial artery using ultrasound after a high-fat and a lowfat meal, each of 900 calories.(The endothelium is the lining of the arteries.) The high-fat meal contained 50 grams of fat and the lowfat meal contained--according to the authors--0 grams of fat. (Actually, no food is completely devoid of fat, even skim milk.)

"Flow-mediated vascularity" did decrease more in the high-fat group compared to the lowfat group. Interestingly, LDL-cholesterol declined slightly for both groups but in the lowfat
group, the so-called good HDL-cholesterol also declined, whereas it remained stable in the high-fat group. Blood pressure declined in the high-fat group, but rose in the lowfat group. Most significantly, blood glucose rose in the lowfat group, but declined slightly and then returned to baseline in the high-fat group.

For years we have been hearing that high-fat foods raise so-called bad LDL-cholesterol and blood pressure and therefore contribute to heart disease. But since that didn’t happen in this study, the authors have declared that an inherently subjective measurement of "endothelial function" is a better marker for heart disease.

But was it saturated fat that caused the decline in endothelial function? The high-fat meal consisted of an egg McMuffin, sausage McMuffin, two hash brown patties and a noncaffeinated beverage. The lowfat meal consisted of Frosted Flakes, skimmed milk and orange juice. According to the authors, the high fat meal contained 50 grams of fat, of which 14 were saturated fat. So only 28 percent of the fat in the high-fat meal was saturated. The rest was a combination of trans fats, monounsaturated and polyunsaturated fat, any one of which, or all together are the likely culprits in the decline in endothelial function. But Agatston (along with the study authors) blames the adverse effects on saturated fats!

The lowfat meal that won the endothelial-function contest is obviously a terrible meal--extremely high in sugar and devoid of nutrients. Yet it does have one thing going for it--it is unlikely that Frosted Flakes, skim milk or orange juice contain MSG, whereas the high-fat meal certainly contained MSG in the sausage and hash browns. If the bread contained soy, which it probably did, this would be another source of MSG. The presence of MSG in the high-fat meal provides a likely explanation for the decline in endothelial function.

The subjects in this study ate junk food and the research itself can only be described as junk. The study was designed so poorly that no conclusions can be drawn from it. In order to test the effects of saturated fat on endothelial function, the researchers should have provided two identical meals of simple whole foods, except for the addition of a mostly saturated fat such as suet or coconut oil to one of the meals. Then, to compare the effects of the various fats with saturated fat, the researchers should have repeated the experiment adding a mostly monounsaturated fat, such as olive oil, to one of the meals, a high-trans fat such as vegetable shortening and finally a polyunsaturated fat such as corn oil.

To correlate their findings--temporary decline in endothelial function--with long-term effects such as heart disease, the authors should have been able to cite numerous studies; but they cite only one, which postulates a chronic decline in endothelial function with atherosclerosis. They provide no evidence that the temporary decline in endothelial function observed in this study is associated with atherosclerosis in the long term or can "trigger a heart attack."

As it becomes more and more obvious that cholesterol levels have little predictive value for heart disease--and that saturated fats in fact have little or no effect on cholesterol levels anyway--researchers are searching for other ways to demonize saturated fats. The study carried out by Vogel and his team can only be characterized as "garbage in, garbage out," a "grasping-at-straws" attempt to stem the change in consumer eating habits towards real, whole foods.

[Edited by - blueseats on 08-11-2008 04:02 AM]
BlueSeats
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8/11/2008  10:18 AM
Posted by codeunknown:
Posted by BlueSeats:



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.


For millenia, our ancestors lived on average 30 years less than us, taken by infections and the like before heart disease had the opportunity to manifest itself. Smouldering heart disease went undetected because we didn't have the benefits of EKGs and echocardiograms. Our ancestors also excercised. They didn't smoke. And the portions they ate were likely less as a gazelle only comes around once in a while. Even then they were eaten by wild game before 45, so their efforts were in vain. So, if getting eaten at 45 is doing well, I'm pleased to have surpassed those lofty expectations.

You seem to be saying that by dying by 45 those people were spared from heart disease that might have manifested itself later on. But in our culture today doctors are finding fit to put kids on statins as early as age 8. For us, the manifestations of obesity, diabetes and heart disease are revealed well before age 45. Are there any hunter/gatherers today that is also true for?
EnySpree
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8/11/2008  11:52 AM
You guys are going "in" with this thread.

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codeunknown
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8/11/2008  5:33 PM
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.


For millenia, our ancestors lived on average 30 years less than us, taken by infections and the like before heart disease had the opportunity to manifest itself. Smouldering heart disease went undetected because we didn't have the benefits of EKGs and echocardiograms. Our ancestors also excercised. They didn't smoke. And the portions they ate were likely less as a gazelle only comes around once in a while. Even then they were eaten by wild game before 45, so their efforts were in vain. So, if getting eaten at 45 is doing well, I'm pleased to have surpassed those lofty expectations.

You seem to be saying that by dying by 45 those people were spared from heart disease that might have manifested itself later on. But in our culture today doctors are finding fit to put kids on statins as early as age 8. For us, the manifestations of obesity, diabetes and heart disease are revealed well before age 45. Are there any hunter/gatherers today that is also true for?

Are you serious? What 8 year old kids do you know that regularly get statins? I don't know of any 8 year old kids getting statins unless they have a serious genetic disorder (ex. familial hypercholesterolemia), in which case their natural history is a heart attack in their early 20s. Would you prefer they die eating your ill-conceived diet of lard and saturated fat?

For your edification, clinical manifestations of heart disease before the age of 45 are a quite unusual occurrence, giving rise to a search for an underlying disorder - primary hypertension, uncontrolled type 1 diabetes etc. So you're off the mark there too.

Keep your hunters and gatherers alive past 50 and the incidence of cardiovascular events skyrockets.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
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8/11/2008  6:10 PM
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.


For millenia, our ancestors lived on average 30 years less than us, taken by infections and the like before heart disease had the opportunity to manifest itself. Smouldering heart disease went undetected because we didn't have the benefits of EKGs and echocardiograms. Our ancestors also excercised. They didn't smoke. And the portions they ate were likely less as a gazelle only comes around once in a while. Even then they were eaten by wild game before 45, so their efforts were in vain. So, if getting eaten at 45 is doing well, I'm pleased to have surpassed those lofty expectations.

You seem to be saying that by dying by 45 those people were spared from heart disease that might have manifested itself later on. But in our culture today doctors are finding fit to put kids on statins as early as age 8. For us, the manifestations of obesity, diabetes and heart disease are revealed well before age 45. Are there any hunter/gatherers today that is also true for?

Are you serious? What 8 year old kids do you know that regularly get statins? I don't know of any 8 year old kids getting statins unless they have a serious genetic disorder (ex. familial hypercholesterolemia), in which case their natural history is a heart attack in their early 20s. Would you prefer they die eating your ill-conceived diet of lard and saturated fat?

Below is a policy on a clinical report appearing in the July issue of Pediatrics, the peer-reviewed, scientific journal of the American Academy of Pediatrics (AAP).

For Release: July 7, 2008, 12:01 am (ET)

The American Academy of Pediatrics has issued new cholesterol screening and treatment recommendations for children. The policy statement, “Lipid Screening and Cardiovascular Health in Childhood,” recommends cholesterol screening of children and adolescents with a family history of high cholesterol or heart disease. It also recommends screening patients whose family history is unknown or those who have other factors for heart disease including obesity, high blood pressure or diabetes. Screening should take place after age two, but no later than age 10. The best method for testing is a fasting lipid profile. If a child has values within the normal range, testing should be repeated in three to five years. For children who are more than eight years old and who have high LDL concentrations, cholesterol-reducing medications should be considered. Younger patients with elevated cholesterol readings should focus on weight reduction and increased activity while receiving nutritional counseling. The statement also recommends the use of reduced-fat dairy products, such as two percent milk, for children as young as one year of age for whom overweight or obesity is a concern.

Maybe you're right, maybe statins are a blessing, in light of the fact the low fat diet is failing our population so miserably and obesity, diabetes and heart disease are at epidemic levels.

For your edification, clinical manifestations of heart disease before the age of 45 are a quite unusual occurrence, giving rise to a search for an underlying disorder - primary hypertension, uncontrolled type 1 diabetes etc. So you're off the mark there too.

I know plenty of men on stains pre 45, or right around that mark. Clearly these underlying disorders are also rapidly escalating.

We're 30 years into the low fat approach and it's gotten us nowhere.
Keep your hunters and gatherers alive past 50 and the incidence of cardiovascular events skyrockets.

Studies?

Doesn't make sense. Which are the hunter-gatherers with epidemic proportions of obesity, hypertention and diabetes that equally predispose them to CVD?
BasketballJones
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8/11/2008  6:26 PM
https:// It's not so hard.
codeunknown
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8/11/2008  6:41 PM
Here's a small compilation of evidence I put together against dietary saturated fat and serum LDL cholesterol as mediators of heart disease. With caveats about stroke and distinctions between the variety of fats. For you, Blue, to attain a slightly better understanding of those "dumb" studies.

Feel free to survey the body of evidence or pick and choose select studies.

---

Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Circulation 2002; 106:3143.

Broedl, UC, Geiss, HC, Parhofer, KG. Comparison of current guidelines for primary prevention of coronary heart disease. J Gen Intern Med 2003; 18:190.

Wallis, EJ, Ramsay, LE, Ul Haq, I, et al. Coronary and cardiovascular risk estimation for primary prevention: Validation of a new Sheffield table in the 1995 Scottish health survey population. BMJ 2000; 320:671.

Pekkanen, J, Linn, S, Hetgg, G, et al. Ten-year mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease. N Engl J Med 1990; 322:1700.

Gould, AL, Rossouw, JE, Santanello, NC, et al. Cholesterol reduction yields clinical benefit: Impact of statin trials. Circulation 1998; 97:946.

Ballantyne, CM, Grundy, SM, Oberman, A, et al. Hyperlipidemia: diagnostic and therapeutic perspectives. J Clin Endocrinol Metab 2000; 85:2089.

D'Agostino RB, Sr, Grundy, S, Sullivan, LM, Wilson, P. Validation of the Framingham Coronary Heart Disease Prediction Scores: Results of a Multiple Ethnic Groups Investigation. JAMA 2001; 286:180.

Bastuji-Garin, S, Deverly, A, Moyse, D, Castaigne, A. The Framingham prediction rule is not valid in a European population of treated hypertensive patients. J Hypertens 2002; 20:1973.

Brindle, P, Emberson, J, Lampe, F, et al. Predictive accuracy of the Framingham coronary risk score in British men: prospective cohort study. BMJ 2003; 327:1267.

Liu, J, Hong, Y, D'Agostino RB, Sr, et al. Predictive value for the Chinese population of the Framingham CHD risk assessment tool compared with the Chinese Multi-Provincial Cohort Study. JAMA 2004; 291:2591.

Fedder, DO, Koro, CE, L'Italien, GJ. New National Cholesterol Education Program III guidelines for primary prevention lipid-lowering drug therapy: Projected impact on the size, sex, and age distribution of the treatment-eligible population. Circulation 2002; 105:152.

Kinosian, B, Glick, H, Garland, G. Cholesterol and coronary heart disease: Predicting risks by levels and ratios. Ann Intern Med 1994; 121:641.

Steyn, K, Sliwa, K, Hawken, S, et al. Risk factors associated with myocardial infarction in Africa: the INTERHEART Africa study. Circulation 2005; 112:3554.

Otvos, JD, Collins, D, Freedman, DS, et al. Low-density lipoprotein and high-density lipoprotein particle subclasses predict coronary events and are favorably changed by gemfibrozil therapy in the Veterans Affairs High-Density Lipoprotein Intervention Trial. Circulation 2006; 113:1556.

Cui, Y, Blumenthal, RS, Flaws, JA, et al. Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality. Arch Intern Med 2001; 161:1413.

Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344:1383.

Sacks, FM, Pfeffer, MA, Moye, LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med 1996; 335:1001.

Shepherd, J, Cobbe, SM, Ford, I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995; 333:1301.

Sever, PS, Dahlof, B, Poulter, NR, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003; 361:1149.

Downs, JR, Clearfield, M, Weis, S, et al for the AFCAPS/TexCAPS Research Group. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: Results of AFCAPS/TexCAPS. JAMA 1998; 279:1615.

Kumana, CR, Cheung, BM, Lauder, IJ. Gauging the impact of statins using number needed to treat. JAMA 1999; 282:1899.

Marchioli, R, Marfisi, RM, Carcini, F, Tognoni, G. Meta-analysis, clinical trials, and transferability of research results into practice: The case of cholesterol-lowering interventions in the secondary prevention of coronary heart disease. Arch Intern Med 1996; 156:1158.

Wilt, TJ, Bloomfield, HE, MacDonald, R, et al. Effectiveness of statin therapy in adults with coronary heart disease. Arch Intern Med 2004; 164:1427.

MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360:7.

Brown, BG, Zhao, XQ, Sacco, DE, Albers, JJ. Lipid lowering and plaque regression. New insights into prevention of plaque disruption and clinical events in coronary disease. Circulation 1993; 87:1781.
Pedersen, TR, Kjekshus, J, Berg, K, et al. Cholesterol lowering and the use of healthcare resources: Results of the Scandinavian Simvastatin Survival Study. Circulation 1996; 93:1796.

Kane, JP, Malloy, MJ, Ports, TA, et al. Regression of coronary atherosclerosis during treatment of familial hypercholesterolemia with combined drug regimens. JAMA 1990; 264:3007.

Grundy, SM, Balady, GJ, Criqui, MH, et al. When to start cholesterol-lowering therapy in patients with coronary heart disease. A statement for healthcare professionals from the American Heart Association Task Force on Risk Reduction. Circulation 1997; 95:1683.

Grundy, SM, Cleeman, JI, Merz, CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation 2004; 110:227.
Cannon, CP, Braunwald, E, McCabe, CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med 2004; 350:1495.

de Lemos, JA. Blazing, MA, Wiviott, SD, et al. Early Intensive vs a delayed conservative simvastatin strategy in patients with acute coronary syndromes. JAMA 2004; 292:1307.

Grover, SA, Coupal, L, Hu, XP. Identifying adults at increased risk of coronary disease. How well do the current cholesterol guidelines work? JAMA 1995; 274:801.

Ramsay, LE, Haq, IU, Yeo, WW, et al. Targeted lipid lowering drug therapy for primary prevention of coronary disease: An updated Sheffield table. Lancet 1996; 348:387.

Anderson, KM, Odell, PM, Wilson, PWF, et al. Cardiovascular disease risk profiles. Am Heart J 1991; 121:293.

Johannesson, M, Jonsson, B, Kjiekshus, J, et al for the Scandinavian Simvastatin Survival Study Group. Cost effectiveness of simvastatin treatment to lower cholesterol levels in patients with coronary heart disease. N Engl J Med 1997; 336:332.

Tsevat, J, Kuntz, KM, Orav, EJ, et al. Cost-effectiveness of pravastatin therapy for survivors of myocardial infarction with average cholesterol levels. Am Heart J 2001; 141:727.

Perreault, S, Hamilton, VH, Lavoie, F, et al. Treating hyperlipidemia for the primary prevention of coronary disease: Are higher doses of lovastatin cost-effective? Arch Intern Med 1998; 157:375.

Manninen, V, Tenkanen, L, Koskinen, P, et al. Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: Implications for treatment. Circulation 1992; 85:37.

Law, MR, Thompson, SG, Wald, NJ. Assessing possible hazards of reducing serum cholesterol. Br Med J 1994; 308:373.

Hebert, PR, Gaziano, JM, Chan, KS, Hennekens, CH. Cholesterol lowering with statin drugs, risk of stroke, and total mortality. An overview of randomized trials. JAMA 1997; 278:313.

Muldoon, MF, Manuck, SB, Mendelsohn, AB, et al. Cholesterol reduction and non-illness mortality: meta-analysis of randomised clinical trials. BMJ 2001; 322:11.

Golomb, BA, Kane, T, Dimsdale, JE. Severe irritability associated with statin cholesterol-lowering drugs. QJM 2004; 97:229.

Lloyd-Jones, DM, O'Donnell, CJ, D'Agostino, RB, et al. Applicability of cholesterol-lowering primary prevention trials to a general population: The Framingham Heart Study. Arch Intern Med 2001; 161:949.
Cashin-Hemphill, L, Mack, WJ, Pogoda, JM, et al. Beneficial effects of colestipol-niacin on coronary atherosclerosis. A 4-year follow-up. JAMA 1990; 264:3013.

Brown, G, Albers, JJ, Fisher, LD, et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med 1990; 323:1289.

Andrade, SE, Walerks, AM, Gottlieb, LK, et al. Discontinuation of antihyperlipidemic drugs — Do rates reported in clinical trials reflect rates in primary care settings? N Engl J Med 1995; 332:1125.

Pedersen, TR, Berg, K, Cook, TJ, et al. Safety and tolerability of cholesterol lowering with simvastatin during 5 years in the Scandinavian Simvastatin Survival Study. Arch Intern Med 1996; 156:2085.

Sacks, FM, Tonkin, AM, Craven, T, et al. Coronary heart disease in patients with low LDL-cholesterol: benefit of pravastatin in diabetics and enhanced role for HDL-cholesterol and triglycerides as risk factors. Circulation 2002; 105:1424.

Collins, R, Armitage, J, Parish, S, et al. MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 2003; 361:2005.

Colhoun, HM, Betteridge, DJ, Durrington, PN, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet 2004; 364:685.

Kearney, PM, Blackwell, L, Collins, R, et al. Efficacy of cholesterol-lowering therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis. Lancet 2008; 371:117.

Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106:3143.

Shepherd, J, Blauw, GJ, Murphy, MB, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet 2002; 360:1623.

Kaiser, FE. Cholesterol and the older adult. South Med J 1993; 86:2511.

Rosenson, RS. Beyond low-density lipoprotein cholesterol: A perspective on low high-density lipoprotein disorders and Lp(a) lipoprotein excess. Arch Intern Med 1996; 156:1278.

Harper, CR, Jacobson, TA. New perspectives on the management of low levels of high-density lipoprotein cholesterol. Arch Intern Med 1999; 159:1049.

Butowski, PF, Winder, AF. Usual care dietary practice, achievement and implications for medication in the management of hypercholesterolemia: Data from the UK Lipid Clinics Programme. Eur Heart J 1998; 19:1328.

Jenkins, DJ, Kendall, CW, Marchie, A, et al. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. JAMA 2003; 290:502.

Stefanick, ML, Mackey, S, Sheehan, M, et al. Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med 1998; 339:12.

Effects of pravastatin in patients with serum total cholesterol levels from 5.2 to 7.8mmol/liter (200 to 300 mg/dl) plus two additional atherosclerotic risk factors. The Pravastatin Multinational Study Group for Cardiac Risk Patients. Am J Cardiol 1993; 72:1031.

Byington, RP, Jukema, JW, Salonen, JT, et al. Reduction in cardiovascular events during pravastatin therapy: Pooled analysis of clinical events of the Pravastatin Atherosclerosis Intervention Program. Circulation 1995; 92:2419.

Denke, MA, Adams-Huet, B, Nguyen, AT. Individual cholesterol variation in response to a margarine- or butter-based diet: A study in families. JAMA 2000; 284:2740.

Henkin, Y, Shai, I, Zuk, R, et al. Dietary treatment of hypercholesterolemia: Do dietitians do it better? A randomized, controlled trial. Am J Med 2000; 109:549.

Hsia, J, Rodabough, R, Rosal, MC, et al. Compliance with National Cholesterol Education Program dietary and lifestyle guidelines among older women with self-reported hypercholesterolemia. The Women's Health Initiative. Am J Med 2002; 113:384.

Canner, PL, Berge, KG, Wenger, NK. Fifteen year mortality in coronary drug project patients: Long-term benefit with niacin. J Am Coll Cardiol 1986; 8:1245.

Keech, A, Simes, RJ, Barter, P, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005; 366:1849.

Rubins, HB, Robins, SJ, Collins, D, et al, for the Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. N Engl J Med 1999; 341:410.

Larsen, ML, Illingworth, DR. Drug treatment of dyslipoproteinemia. Med Clin North Am 1994; 78:225.

Levy, RI, Troendle, AJ, Fattu, JM. A quarter century of drug treatment of dyslipoproteinemia, with a focus on the new HMG-CoA reductase inhibitor fluvastatin. Circulation 1993; 87:III45.

Illingworth, DR, Stein, EA, Mitchel, YB, et al. Comparative effects of lovastatin and niacin in primary hypercholesterolemia. A prospective trial. Arch Intern Med 1994; 154:1586.

Sprecher, DL, Abrams, J, Allen, JW, et al. Low-dose combined therapy with fluvastatin and cholestyramine in hyperlipidemic patients. Ann Intern Med 1994; 120:537.

Jones, P, Kafonek, S, Laurora, I, et al for the CURVES Investigators. Comparative dose efficacy study of atorvastatin versus simvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol 1998; 81:582.

Bakker-Arkema, RG, Davidson, MH, Goldstein, RJ, et al. Efficacy and safety of a new HMG CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia. JAMA 1996; 276:128.

Davidson, M, McKenney, J, Stein, E, et al., for the Atorvastatin Study Group I. Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. Am J Cardiol 1997; 79:1475.

Jones, PH, Davidson, MH, Stein, EA, et al. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol 2003; 92:152.

Jula, A, Marniemi, J, Huupponen, R, et al. Effects of Diet and Simvastatin on Serum Lipids, Insulin, and Antioxidants in Hypercholesterolemic Men: A Randomized Controlled Trial. JAMA 2002; 287:598.

Fruchart, JC, Brewer, HB, Leitersdorf, E. Consensus for the use of fibrates in the treatment of dyslipoproteinemia and coronary heart disease. Am J Cardiol 1998; 81:912.

Staels, B, Dallongeville, J, Auwerx, J, et al. Mechanism of action of fibrates on lipid and lipoprotein metabolism. Circulation 1998; 98:2088.

Grundy, SM, Mok, HY, Zech, L, Berman, M. Influence of nicotinic acid on metabolism of cholesterol and triglycerides in man. J Lipid Res 1981; 22:24.

Probstfield, JL, Hunninghake, DB. Nicotinic acid as a lipoprotein-altering agent. Therapy directed by the primary physician. Arch Intern Med 1994; 154:1557.

Pearson, TA, Laurora, I, Chu, H, Kafonek, S. The lipid treatment assessment project (L-TAP): a multicenter survey to evaluate the percentages of dyslipidemic patients receiving lipid- lowering therapy and achieving low-density lipoprotein cholesterol goals. Arch Intern Med 2000; 160:459.

Glasziou, PP, Irwig, L, Heritier, S, et al. Monitoring cholesterol levels: measurement error or true change?. Ann Intern Med 2008; 148:656.

Posner, B, Cobb, JL, Belanger, A, et al. Dietary lipid predictors of coronary heart disease in men. Arch Intern Med 1991; 151:1181.

Hegsted, DM, Ausman, LM, Johnson, JA, Dallal, GE. Dietary fat and serum lipids: An evaluation of the experimental data. Am J Clin Nutr 1993; 57:875.

Meyer, KA, Kushi, LH, Jacobs, DR Jr, Folsom, AR. Dietary fat and incidence of type 2 diabetes in older Iowa women. Diabetes Care 2001; 24:1528.

Fuentes, F, Lopez-Miranda, J, Sanchez, E, et al. Mediterranean and low-fat diets improve endothelial function in hypercholesterolemic patients. Ann Intern Med 2001; 134:1115.

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Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
codeunknown
Posts: 22615
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8/11/2008  7:22 PM
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:
Posted by codeunknown:
Posted by BlueSeats:



My position is that when minimally adulterated foods are eaten in sensible amounts all these nettlesome issues become moot. We wouldn't be obese, we wouldn't need doctors telling us how to eat (after all homo sapiens did pretty well for hundreds of thousands of years without MDs telling them what to eat) and like so many primitive cultures, we wouldn't care about our cholesterol because we wouldn't be plagued by heart disease.

But because our food has become industrialized, refined, stripped of nutrients, molecularly altered, etc, we now need scientists to try to figure out how to maintain a healthy metabolism when that used to be a non issue.

Trying to villianize foods here that work very well elsewhere just makes no sense to me.

I'm gonna keep the topic going, feel free to jump in when so motivated. And I look forward to hearing your answers to some of the basic questions I've been posing.


For millenia, our ancestors lived on average 30 years less than us, taken by infections and the like before heart disease had the opportunity to manifest itself. Smouldering heart disease went undetected because we didn't have the benefits of EKGs and echocardiograms. Our ancestors also excercised. They didn't smoke. And the portions they ate were likely less as a gazelle only comes around once in a while. Even then they were eaten by wild game before 45, so their efforts were in vain. So, if getting eaten at 45 is doing well, I'm pleased to have surpassed those lofty expectations.

You seem to be saying that by dying by 45 those people were spared from heart disease that might have manifested itself later on. But in our culture today doctors are finding fit to put kids on statins as early as age 8. For us, the manifestations of obesity, diabetes and heart disease are revealed well before age 45. Are there any hunter/gatherers today that is also true for?

Are you serious? What 8 year old kids do you know that regularly get statins? I don't know of any 8 year old kids getting statins unless they have a serious genetic disorder (ex. familial hypercholesterolemia), in which case their natural history is a heart attack in their early 20s. Would you prefer they die eating your ill-conceived diet of lard and saturated fat?

Below is a policy on a clinical report appearing in the July issue of Pediatrics, the peer-reviewed, scientific journal of the American Academy of Pediatrics (AAP).

For Release: July 7, 2008, 12:01 am (ET)

The American Academy of Pediatrics has issued new cholesterol screening and treatment recommendations for children. The policy statement, “Lipid Screening and Cardiovascular Health in Childhood,” recommends cholesterol screening of children and adolescents with a family history of high cholesterol or heart disease. It also recommends screening patients whose family history is unknown or those who have other factors for heart disease including obesity, high blood pressure or diabetes. Screening should take place after age two, but no later than age 10. The best method for testing is a fasting lipid profile. If a child has values within the normal range, testing should be repeated in three to five years. For children who are more than eight years old and who have high LDL concentrations, cholesterol-reducing medications should be considered. Younger patients with elevated cholesterol readings should focus on weight reduction and increased activity while receiving nutritional counseling. The statement also recommends the use of reduced-fat dairy products, such as two percent milk, for children as young as one year of age for whom overweight or obesity is a concern.

Maybe you're right, maybe statins are a blessing, in light of the fact the low fat diet is failing our population so miserably and obesity, diabetes and heart disease are at epidemic levels.

For your edification, clinical manifestations of heart disease before the age of 45 are a quite unusual occurrence, giving rise to a search for an underlying disorder - primary hypertension, uncontrolled type 1 diabetes etc. So you're off the mark there too.

I know plenty of men on stains pre 45, or right around that mark. Clearly these underlying disorders are also rapidly escalating.

We're 30 years into the low fat approach and it's gotten us nowhere.
Keep your hunters and gatherers alive past 50 and the incidence of cardiovascular events skyrockets.

Studies?

Doesn't make sense. Which are the hunter-gatherers with epidemic proportions of obesity, hypertention and diabetes that equally predispose them to CVD?

Because you know plenty of men under 45 getting statins, does that mean they have had a clinical manifestation of coronary heart disease? Try again. They're treated preemptively as would your cavemen if they had lipid studies performed.

You AAP article reitterates what I said. You screen kids with a familial history of hypercholesterolemia. And you treat familial hypercholesterolemia, in its various forms, with statins because those folks get premature heart attacks. In other words, you're treating kids with genetic predispositions to dyslipidemia. Your average husky kid isn't getting statins.

Why do the hunters and gathers have to have an equal predisposition to CHD? That has no bearing on the fact that their incidence of heart disease would go up with longer lifespans. And it also has no bearing on the fact that their heart disease is underestimated because of the prevalence of premature death - being eaten etc.
Sh-t in the popcorn to go with sh-t on the court. Its a theme show like Medieval times.
BlueSeats
Posts: 27272
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8/11/2008  8:21 PM



Unfortunately I don't have access to those studies, but I'll be sure to give them all the attention that you gave to the citations I presented that challenge the Lipid Hypothesis. But which ones are better than the egg vs bagel, or McMuffin and soda vs Frosted Flakes and orange juice study?


Code, in all seriousness though, thanks for the dialog - you've been a good sport and it's been fun. But it makes no sense for me to go mano a mano with you. I'll just stick to presenting information I find interesting for other's consideration.

However, on the matter of access, if you could pull these studies for me and present them I'd love to take a peek. I'd be most appreciative. Google just won't do.

Contrary to conventional medical wisdom, the Framingham study did not find that a high-fat diet doomed people to a heart attack. A subgroup of Framingham participants was assessed for their intake of saturated fats, dietary cholesterol and overall calories. None had any effect on the development of heart disease.

The idea that a low-fat diet prevents heart disease lives on, despite a 2001 review of all relevant clinical trials. The combined results showed that reducing or modifying dietary fat intake had no effect on heart disease mortality or total mortality .

Hooper et al. British Medical Journal, 3/31/01
-----------------------


The Framingham Heart Study is often cited as proof of the lipid hypothesis. This study began in 1948 and involved some 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals-those who consumed little cholesterol and saturated fat and those who consumed large amounts. After 40 years, the director of this study had to admit:

"In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . .

We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."3

Castelli, William, Arch Int Med, Jul 1992, 152:7:1371-1372

The study did show that those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease; but weight gain and cholesterol levels had an inverse correlation with fat and cholesterol intake in the diet.4

Hubert H, et al, Circulation, 1983, 67:968; Smith, R and E R Pinckney, Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of the Literature, Vol 2, 1991, Vector Enterprises, Sherman Oaks, CA
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