Whole Foods!! Keifer is not very hard to make either. I've seen the culturing stuff for sale on the internet recently somewhere, you boil milk, put the culturing stuff in it and let it set overnight. Any milk probably works but the goat milk is better in some regards.. the stuff is addicting almost.. I guess once you have the cultured stuff you keep some for culturing the next batch.. my guess is that goats are range fed more than cows since goats are so useful for cleaning up weeds.....
For sure, but if you can do prevention via changing your diet it costs nothing basically. You substitute good foods for bad ones and your food budget is not affected much. I'm in California, I've met several people that cured their own cancers, one after the doctors gave up on her. I had a friend that would go to the doctor, get the diagnosis, find out what was prescribed for what he had, look up how the medicine was derived, get the herb it was derived from, put it in capsules and the doctors would get pissed at him for it!! His medicine was working great but they didn't like that!! I cured bursitis with Hyaluronic Acid, went to the doctor, told him about it when he asked how my shoulder was doing, his reply was "if you cured yourself with a supplement then you weren't diagnosed properly".. my reply to that was a big upraised middle digit salute to doctors. I can't stand those bastards. Everything in their thinking is geared to you handing over all your wealth.. "it's genetic", "herbs are dangerous", "you don't know enough"... ad nauseum...
Great stuff! Great link! Thanks! And keep it coming guys! "The predictive power of a high cholesterol is overrated. In the 30 year follow-up of the Framingham cohort for instance, high cholesterol was not predictive after the age of forty-seven.2 It is not a strong predictor for women, Canadian men and patients with established CHD either. In Russia, low cholesterol is a predictor of CHD2 and individuals with familial hypercholesterolemia may live just as long and have a risk of CHD just as low as that of normal people.3 No doubt the statins lower coronary mortality, but the size of the effect is unimpressive. In the CARE trial for instance, the odds of escaping death from a heart attack in five years for a patient with CHD was 94.3%, which improved to 95.4% with statin treatment. For healthy people with high cholesterol the effect is even smaller; in the WOSCOPS trial, the figures were 98.4% and 98.8%, respectively. These figures do not take into account possible side effects which usually appear more often. In animal experiments the statins have proven carcinogenic. In the CARE trial statin treatment was followed by more breast cancer. In the EXCEL trial, total mortality after just one year was much higher in those receiving statins. Unfortunately the trial was stopped before further observations could be made.2 We need more experience before introducing mass-prevention with potentially carcinogenic drugs."
http://www.nytimes.com/2008/01/27/opinion/27taubes.html Amazing op/ed by someone with credibility on the matter. WHAT'S 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. Gary Taubes is the author of âGood Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control and Disease.â
I know some people that have been prescribed aspirin while others have been told to take fish oil capsules. I wonder why some doctors pick one over the other.
Total Cholesterol and all it's pernicious subfractions are largely a function of lifestyle. What's you are putting in your mouth. Saturated fat will trash your health. Trans fat is "10X" worse. Dean Ornish and his "Lifestyle" program is a good read.
Look at this killthesunshine. Look how saturated fat was consumed in larger amounts in the past, but less heart disease. Now people eat much less saturated fat, but more heart disease? So yes, you are right, it is about what people are eating, but saturated fat is not the problem from the evidence. Trans fat, overprocessed food is something to look at in my opinion. http://trusted.md/blog/vreni_gurd/2007/04/06/saturated_fat_the_misunderstood_nutrient
This is not about eating excessive amount of anything. For example. Carrots are good for you, and healthy right? They have vitamin A, that is good for you. But vitamin A es fat soluble too. If you have too much vitamin A, it is stored in the liver, toxic and unhealthy. So does that mean vitamin A is bad? No. So eating all meat diet in excess could have harmful effect on lipids, but does that mean saturated fat is bad? No.
Do you agree that what we eat plays a predominate role in our health and the health of our lipids? i think you do otherwise you wouldn't bother to post this topic. so how much saturated fat do we need to consume? we know how how much Vit A for optimum health, how much saturated and trans fat??