references anyone, re: correl'n (or not) betw cholesterol+heart dis.?
- Thread starter patandchickens
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patandchickens
Crazy Cat Lady
I *do* appreciate it, Wifezilla, I just can't see how to get from those articles to the info I am looking for. The first lacks references, and the second is on a pretty different topic (biochemistry, rather than epidemiology)Wifezilla said:
Thanks though,
Pat
abifae
Abinormal Butterfly
One would think. I'm equally frustrated by autism studies. No one has a definition yet. Let alone anything to test.patandchickens said:
I think the politics of funding are the bottom line in lack of good research. But I'm paranoid.
kcsunshine
Almost Self-Reliant
Too many people don't ask the right questions because their Dr. is a "God" figure and they follow blindly every he/she says to do without asking "why".
freemotion
Food Guru
Who funds studies?patandchickens said:
Who benefits from the perceived need to lower, lower, lower blood cholesterol?
Who funds the ones who fund the studies?
Who teaches the doctors that cholesterol needs to be lowered?
Any scientist who tried to scream about the dangers of trans fats a few decades ago could no longer get funding or sometimes even a job. Even now that the truth is out, most processed foods contain trans fats, even those labeled "0 Trans Fats!"
Cholesterol numbers and vascular disease....no different. Please post your findings here.....I hope you find some studies that are useful. Did you look at any of the citations from articles on www.westonaprice.org? I haven't had time.....
I remember hearing about a study of the information in the Framingham Study, some scientists took a second look and found that it did NOT prove the lipid hypothesis, but rather, those who ate a diet higher in cholesterol had fewer heart attacks and were more active and weighed less.
Wifezilla
Low-Carb Queen - RIP: 1963-2021
"In the 1950s, two hypotheses competed for attention among heart disease researchers. It had been known for decades that cholesterol was a component of atherosclerotic plaques, and people who have a genetic disorder that causes extremely high cholesterol levels typically have clogged arteries and heart attacks. As new technology enabled them to look more closely at lipoproteins, however, researchers began to suspect that these carrier molecules might play a greater role in cardiovascular disease than the cholesterol inside them. The cholesterol hypothesis dominated, however, because analyzing lipoproteins was still expensive and difficult, while cholesterol tests were easily ordered up by any doctor.
In the late 1960s, biochemists created a simple technique for measuring, more specifically, the cholesterol inside the different kinds of lipoproteins high-density, low-density and very low-density. The National Institutes of Health financed a handful of studies to determine whether these cholesterol fractions could predict the risk of cardiovascular disease. In 1977, the researchers reported their results: total cholesterol turned out to be surprisingly useless as a predictor. Researchers involved with the Framingham Heart Study found that in men and women 50 and older, total cholesterol per se is not a risk factor for coronary heart disease at all.
The cholesterol in low-density lipoproteins was deemed a marginal risk factor for heart disease. Cholesterol in high-density lipoproteins was easily the best determinant of risk, but with the correlation reversed: the higher the amount, the lower the risk of heart disease.
These findings led directly to the notion that low-density lipoproteins carry bad cholesterol and high-density lipoproteins carry good cholesterol. And then the precise terminology was jettisoned in favor of the common shorthand. The lipoproteins LDL and HDL became good cholesterol and bad cholesterol, and the lipoprotein transport vehicle was now conflated with its cholesterol cargo. Lost in translation was the evidence that the causal agent in heart disease might be abnormalities in the lipoproteins themselves.
The truth is, weve always had reason to question the idea that cholesterol is an agent of disease. Indeed, what the Framingham researchers meant in 1977 when they described LDL cholesterol as a marginal risk factor is that a large proportion of people who suffer heart attacks have relatively low LDL cholesterol.
So how did we come to believe strongly that LDL cholesterol is so bad for us? It was partly due to the observation that eating saturated fat raises LDL cholesterol, and weve assumed that saturated fat is bad for us. This logic is circular, though: saturated fat is bad because it raises LDL cholesterol, and LDL cholesterol is bad because it is the thing that saturated fat raises. In clinical trials, researchers have been unable to generate compelling evidence that saturated fat in the diet causes heart disease.
The other important piece of evidence for the cholesterol hypothesis is that statin drugs like Zocor and Lipitor lower LDL cholesterol and also prevent heart attacks. The higher the potency of statins, the greater the cholesterol lowering and the fewer the heart attacks. This is perceived as implying cause and effect: statins reduce LDL cholesterol and prevent heart disease, so reducing LDL cholesterol prevents heart disease. This belief is held with such conviction that the Food and Drug Administration now approves drugs to prevent heart disease, as it did with Zetia, solely on the evidence that they lower LDL cholesterol.
But the logic is specious because most drugs have multiple actions. Its like insisting that aspirin prevents heart disease by getting rid of headaches.
One obvious way to test the LDL cholesterol hypothesis is to find therapies that lower it by different means and see if they, too, prevent heart attacks. This is essentially what the Vytorin trial did and why its results argue against the hypothesis.
Other such tests have likewise failed to confirm it. A recent trial of torcetrapib, a drug that both raises HDL and lowers LDL cholesterol, was halted midstream because the drug seemed to cause heart attacks and strokes rather than prevent them. Estrogen replacement therapy also lowers LDL cholesterol, but it too has failed to prevent heart disease in clinical trials. The same goes for eating less saturated fat."
http://www.nytimes.com/2008/01/27/opinion/27taubes.html
In the late 1960s, biochemists created a simple technique for measuring, more specifically, the cholesterol inside the different kinds of lipoproteins high-density, low-density and very low-density. The National Institutes of Health financed a handful of studies to determine whether these cholesterol fractions could predict the risk of cardiovascular disease. In 1977, the researchers reported their results: total cholesterol turned out to be surprisingly useless as a predictor. Researchers involved with the Framingham Heart Study found that in men and women 50 and older, total cholesterol per se is not a risk factor for coronary heart disease at all.
The cholesterol in low-density lipoproteins was deemed a marginal risk factor for heart disease. Cholesterol in high-density lipoproteins was easily the best determinant of risk, but with the correlation reversed: the higher the amount, the lower the risk of heart disease.
These findings led directly to the notion that low-density lipoproteins carry bad cholesterol and high-density lipoproteins carry good cholesterol. And then the precise terminology was jettisoned in favor of the common shorthand. The lipoproteins LDL and HDL became good cholesterol and bad cholesterol, and the lipoprotein transport vehicle was now conflated with its cholesterol cargo. Lost in translation was the evidence that the causal agent in heart disease might be abnormalities in the lipoproteins themselves.
The truth is, weve always had reason to question the idea that cholesterol is an agent of disease. Indeed, what the Framingham researchers meant in 1977 when they described LDL cholesterol as a marginal risk factor is that a large proportion of people who suffer heart attacks have relatively low LDL cholesterol.
So how did we come to believe strongly that LDL cholesterol is so bad for us? It was partly due to the observation that eating saturated fat raises LDL cholesterol, and weve assumed that saturated fat is bad for us. This logic is circular, though: saturated fat is bad because it raises LDL cholesterol, and LDL cholesterol is bad because it is the thing that saturated fat raises. In clinical trials, researchers have been unable to generate compelling evidence that saturated fat in the diet causes heart disease.
The other important piece of evidence for the cholesterol hypothesis is that statin drugs like Zocor and Lipitor lower LDL cholesterol and also prevent heart attacks. The higher the potency of statins, the greater the cholesterol lowering and the fewer the heart attacks. This is perceived as implying cause and effect: statins reduce LDL cholesterol and prevent heart disease, so reducing LDL cholesterol prevents heart disease. This belief is held with such conviction that the Food and Drug Administration now approves drugs to prevent heart disease, as it did with Zetia, solely on the evidence that they lower LDL cholesterol.
But the logic is specious because most drugs have multiple actions. Its like insisting that aspirin prevents heart disease by getting rid of headaches.
One obvious way to test the LDL cholesterol hypothesis is to find therapies that lower it by different means and see if they, too, prevent heart attacks. This is essentially what the Vytorin trial did and why its results argue against the hypothesis.
Other such tests have likewise failed to confirm it. A recent trial of torcetrapib, a drug that both raises HDL and lowers LDL cholesterol, was halted midstream because the drug seemed to cause heart attacks and strokes rather than prevent them. Estrogen replacement therapy also lowers LDL cholesterol, but it too has failed to prevent heart disease in clinical trials. The same goes for eating less saturated fat."
http://www.nytimes.com/2008/01/27/opinion/27taubes.html
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- #18
patandchickens
Crazy Cat Lady
Now that is DEFINITELY helpful, Wifezilla, thank you!!! 
(Btw, did y'all read the link I posted earlier, it's interesting)
Search on this topic somewhat interrupted by frantic googling on consequences of grain overload in sheep who somehow butted open the latched chicken-bldg door and spent the afternoon with their snouts in the grain bag, eep,
Pat
(Btw, did y'all read the link I posted earlier, it's interesting)
Search on this topic somewhat interrupted by frantic googling on consequences of grain overload in sheep who somehow butted open the latched chicken-bldg door and spent the afternoon with their snouts in the grain bag, eep,
Pat
freemotion
Food Guru
Double eep!
- Thread starter
- #20
patandchickens
Crazy Cat Lady
Yeah, no kidding eeep. And nobody is replying to my post on BYH about it, aargh (of course people are *allowed* to have lives and not spend every moment in front of the computer, but, still).
AFAIK it was only the two 'teenagers', who've been on high-grain diets all their lives and are still getting free choice grain at night, so ti could have been worse... and aside from seeming too quiet at times (but ok at the moment) and *possibly* very slightly inflated, nothing awful has happened yet, but...
Argh.
Too much carbohydrates = bad
Pat
AFAIK it was only the two 'teenagers', who've been on high-grain diets all their lives and are still getting free choice grain at night, so ti could have been worse... and aside from seeming too quiet at times (but ok at the moment) and *possibly* very slightly inflated, nothing awful has happened yet, but...
Argh.
Too much carbohydrates = bad
Pat
