Hey Junior your being a prick. For everyone else the cholesterol studies are interesting and there are thousands more to read on this subject. I could also have posted studies supporting a low fat diet, but I could not find one study supporting a total Vegan diet (not really, I didn't look). When it's used as a religion Vegan is capitalized. http://tinyurl.com/2okasb The effects of a very-low-carbohydrate, high-saturated-fat weight-loss diet ... CONCLUSION: An LC does not impair FMD. We observed beneficial effects of both diets on most of the CVD risk factors measured. http://preview.tinyurl.com/2e9p85 Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet. Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS. http://preview.tinyurl.com/26orme Westernizing diets influence fat intake, red blood cell fatty acid composition, and health in remote Alaskan Native communities in the center for Alaska Native health study. CONCLUSIONS: Diets emphasizing traditional Alaskan Native foods were associated with a fatty acid profile promoting greater cardiovascular health than diets emphasizing Western foods. http://preview.tinyurl.com/2f8md3 Cholesterol levels did not increase in the Atkins group and systolic blood pressure decreased, although not significantly. Our patient will likely lose weight if she is able to continue with any of these diets. Although the evidence evaluating increased cardiovascular events in patients on the Atkins diet is not strong, the available evidence does not show that the Atkins diet increases this risk. http://preview.tinyurl.com/yvzfwu A randomized trial of a low-carbohydrate diet for obesity. The low-carbohydrate diet was associated with a greater improvement in some risk factors for coronary heart disease. I posted links to some Atkins type diets just to show everything isn't black and white when it comes to our body. I personally don't like the Atkins diet. These are a few of the literally hundreds of published studies showing the cholesterol question isn't answered yet. Once you start reading up on this some you will find evidence supporting both sides. I also think a big part of diet is finding out what works for the individual, we are not all wired the same.
Great links guys; I will post some really interesting studies when I get a chance. The bottom line: Big pharma has done an amazing sales pitch in convincing the world (while literally bribing doctors - it's true) that your cholesterol 'scores' should be low. Cholesterol lowering medications have been so incredibly profitable for pharma companies, it's hard to quantify the amount of money that has been made. There is scant evidence that eating the 'usual' suspects (eggs, butter, meat) raises cholesterol levels. There is scant evidence of any relationship between levels of LDL or HDL cholesterol and cardiovascular disease. Yet these allegations are now accepted as gospel among most people, and even many physicians (though not all). Here's a good start in unwinding these myths - make sure to read this article very carefully, because it is quite excellent in explaining how modern medicine has gotten the basics of 'cause and effect' wrong, yet again: http://www.nytimes.com/2008/01/27/opinion/27taubes.html?th&emc=th Whatâs Cholesterol Got to Do With It? By GARY TAUBES Published: January 27, 2008 THE idea that cholesterol plays a key role in heart disease is so tightly woven into modern medical thinking that it is no longer considered open to question. This is the message that emerged all too clearly from the recent news that the drug Vytorin had fared no better in clinical trials than the statin therapy it was meant to supplant. Vytorin is a combination of cholesterol-lowering drugs, one called Zetia and the other a statin called Zocor. Because the two drugs lower LDL cholesterol by different mechanisms, the makers of Vytorin (Merck and Schering-Plough) assumed that their double-barreled therapy would lower it more than either drug alone, which it did, and so do a better job of slowing the accumulation of fatty plaques in the arteries â which it did not. Heart disease specialists who were asked to comment on this turn of events insisted that the result implied nothing about their assumption that LDL cholesterol is dangerous, only about whether it is always medically effective to lower it. But this interpretation is based on a longstanding conceptual error embedded in the very language we use to discuss heart disease. It confuses the cholesterol carried in the bloodstream with the particles, known as lipoproteins, that shuttle that cholesterol around. There is little doubt that certain of these lipoproteins pose dangers, but whether cholesterol itself is a critical factor is a question that the Vytorin trial has most definitely raised. Itâs a question that needs to be acknowledged and addressed if weâre going to make any more headway in preventing heart disease. To understand the distinction between cholesterol and lipoproteins it helps to know something of the history of cholesterol research. 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 â high-density, low-density and very low-density. The National Institutes of Health financed a handful of studies to determine whether these âcholesterol fractionsâ 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, âtotal cholesterol per se is not a risk factor for coronary heart disease at all.â The cholesterol in low-density lipoproteins was deemed a âmarginal risk factorâ 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 âbadâ cholesterol and high-density lipoproteins carry âgoodâ cholesterol. And then the precise terminology was jettisoned in favor of the common shorthand. The lipoproteins LDL and HDL became âgood cholesterolâ and âbad cholesterol,â 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, weâve 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 âmarginal risk factorâ 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 weâve 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. Itâs 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. So it is reasonable, after the Vytorin trial, to question the role of LDL cholesterol in heart disease. Not whether statins help prevent heart disease, but whether they work exclusively, or at all, by this mechanism. There are numerous other ways in which statins might be effective. They reduce inflammation, which is now considered a risk factor for heart disease. They act to keep artery walls healthy. And statins act on lipoproteins as much as on the cholesterol inside them. They decrease the total number of low-density and very low-density lipoproteins in the blood, including the smallest and densest form of LDL, which is now widely believed to be particularly noxious. Because medical authorities have always approached the cholesterol hypothesis as a public health issue, rather than as a scientific one, weâre repeatedly reminded that it shouldnât be questioned. Heart attacks kill hundreds of thousands of Americans every year, statin therapy can save lives, and skepticism might be perceived as a reason to delay action. So letâs just trust our assumptions, get people to change their diets and put high-risk people on statins and other cholesterol-lowering drugs. Science, however, suggests a different approach: test the hypothesis rigorously and see if it survives. If the evidence continues to challenge the role of cholesterol, then rethink it, without preconceptions, and consider what these other pathways in cardiovascular disease are implying about cause and prevention. A different hypothesis may turn out to fit the facts better, and one day help prevent considerably more deaths.
Actually, they are 9 games under. 34-36-7 means that they won 34, lost 36 in regulation, and lost 7 in overtime. There are only 4 teams worse than the Islanders.
March 27, 2007 Special Report: Coronary Calcification Predicts Future Heart Attacks and Coronary Death. Cholesterol Not Found To Be A Significant Risk Factor By Bill Sardi A striking report just published in the New England Journal of Medicine indicates the accumulation of calcium in coronary arteries, and not cholesterol, more accurately predicts a future heart attack or other heart trouble, far more than cholesterol or other standard risk factors. This report gives evidence of a major misdirection by modern medicine - the creation of cholesterol phobia in the population at large. Prior studies show use of cholesterol-lowering drugs does not reduce mortality rates for coronary artery disease. This report follows a front-page report in Business Week Magazine declaring cholesterol-lowering drugs to be of marginal value. The study involved 6722 men and women, ~age 60, who were studied for a period of 3.8 years (median). None had coronary artery disease at the beginning of the study. Subjects who experienced an adverse coronary event (heart attack, angina, placement of a stent, coronary death) were more likely to be taking cholesterol-lowering drugs (~28%) than those who did not experience such an event (~16%). Furthermore, subjects who experienced a heart attack or angina had about the same total cholesterol (~199) as subjects who did not (~194). Cholesterol barely met statistical significance whereas calcium was a highly predictive factor. Traditionally-used risk factors, such as C-reactive protein (a marker of inflammation), triglycerides, HDL cholesterol and greater body mass, were not predictive for a future coronary artery event. Among subjects whose coronary artery calcium score was zero, their risk for any adverse coronary event was only about one-half of 1% (0.0044), or less than 1 in 200, whereas those with a coronary calcium score over 300, about 8.0% experienced an adverse event involving coronary arteries (0.0804), or about 8 in 100, an 18-fold difference (1800%!), over the 3.8 year period. This study shows the risk for a future heart attack is nil for those with a calcium arterial score of zero. This data helps to explain why hundreds of thousands of Americans experience a sudden-death heart attack with low-to-normal cholesterol. Most heart attacks emanate in the four coronary arteries that supply the heart with oxygenated blood. About 50% of arterial plaque is calcium and only 3% is cholesterol. Arterial calcium can be measured by use of a CT scan (called an Agatston score, for Dr. Arthur Agatston, South Beach Miami, Florida cardiologist). About 70% of white males, 52% of black males, 57% of Hispanic males and 59% of Chinese males, have coronary calcium scores greater than zero. The calcium arterial scores for women are about half that of males owing to the fact they donate calcium to their offspring during pregnancy and lactation and control calcium via estrogen throughout their fertile years. Calcium begins to accumulate in coronary arteries in males as soon as full growth is achieved, around age 18. Women begin to accumulate calcium in their arteries with the onset of menopause or early hysterectomy. It was recently reported that postmenopausal women who take calcium supplements increase their risk for a heart attack by about 45%. [British Medical Journal 2008 Feb 2; 336 (7638): 262-6] In the early 1990s British cardiologist Stephen Seely noted that countries which consume that highest amount of calcium (New Zealand, Ireland, North America, Scandinavian countries), mostly from dairy products, have the highest rates of cardiovascular disease. [International Journal Cardiology 1991 Nov; 33(2):191-8] Sixty-four percent (64%) of subjects who experienced any coronary event were current or former smokers compared to about 50% of those who did not experience a heart attack or other adverse event. [Coronary Calcium as a Predictor of Coronary Events in Four Racial or Ethnic Groups, New England Journal of Medicine 358: 1336-45, March 27, 2008]
Calcium consumption is high in the west, there are lots of cultures that get way less calcium and more magnesium and they don't have osteoperosis. The Cholesterol thing is just ridiculous, always was. All they knew was that artery walls were cracking and part of the repair was done with cholesterol so they jump to the conclusion somehow that less cholesterol is better...