By Dr. Mercola
Could it be possible that nearly everything your doctor and the media is telling you about high cholesterol and how it relates to heart disease and strokes is wrong?
The media and health experts have been giving out massive misinformation about cholesterol. In a thought-provoking two-part series, Dr. Ernest N. Curtis, a doctor of internal medicine and cardiology, puts to rest several decades-old studies that supposedly "proved" the cholesterol-heart disease link.
Debunking the Cholesterol "Science" and Unveiling the Truth
If high cholesterol and high-fat diets are really NOT the cause of heart disease, then how did this massive misinformation campaign start? It actually started more than 100 years ago when the Lipid Hypothesis or the Cholesterol Theory was developed by a German pathologist named Rudolph Virchow. After studying arterial plaques from corpses, he theorized that cholesterol in your blood led to the development of plaques in your arteries.
Meanwhile, in 1913 in St. Petersburg, Russia, Nikolaj Nikolajewitsch Anitschkow fed rabbits cholesterol and determined that it led to atherosclerotic changes (apparently no one questioned the fact that rabbits are herbivores and do not naturally consume cholesterol!). This started the notion that eating cholesterol leads to plaque deposits in your arteries, and at that time it was believed that all cholesterol in your blood was due to dietary sources.
This, of course, is not true, as it's now known that your liver makes about 75 percent of your body's cholesterol. That's right! Even if you didn't eat any cholesterol, you would still have cholesterol in your body, which is a good thing considering it's needed by every one of your cells to produce cell membranes.
Your diet is actually an afterthought when it comes to what your cholesterol levels will be, but this simple truth is largely ignored or unrealized even by many physicians.
In the early 1900s, the Cholesterol Theory was already taking root, but it received even more completely flawed support in the 1950s and subsequent years thereafter. The string of research that effectively solidified the cholesterol myth we know all too well today.
The Seven Countries' Study Incorrectly Links Dietary Fat to Heart Disease
Several decades ago, Dr. Ancel Keys published a seminal paper that serves as the basis for nearly all of the initial scientific support for the Cholesterol Theory. The study is known as the Seven Countries Study, that linked the consumption of dietary fat to coronary heart disease. What you may not know is that when Keys published his analysis that claimed to prove the link between dietary fats and coronary heart disease (CHD), he selectively analyzed information from only seven countries to prove his correlation, rather than comparing all the data available at the time -- from 22 countries.
As you might suspect, the studies he excluded were those that did not fit with his hypothesis, namely those that showed a low percentage fat in their diet and a high incidence of death from CHD as well as those with a high-fat diet and low incidence of CHD. If all 22 countries had been analyzed, there would have been no correlation found whatsoever; it should have been called the 22 Countries Study!
The nutrition community of that time completely accepted the hypothesis, and encouraged the public to cut out butter, red meat, animal fats, eggs, dairy and other "artery clogging" fats from their diets -- a radical change at that time that is still very much in force today.
Most of the experts I know believe that Dr. Keys' research was pivotal for perpetuating the low-fat approach to health. This is a major part of the solid science you will need to know if anyone seeks to disagree with you when you share this information; this study is really the foundation that triggered the massive emphasis on low-fat diets and the flawed belief that cholesterol is so pernicious.
More Flawed "Proof": The Framingham Study
The next major support for the cholesterol theory came from a study you have likely heard of called the Framingham Heart Study, which 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 who filled out detailed questionnaires about their lifestyle habits and diets. The study is credited with identifying heart disease risk factors, such as smoking, high blood pressure, lack of exercise and, yes, high cholesterol.
The cholesterol link was weak, as researchers noted those who weighed more and had abnormally high blood cholesterol levels were slightly more at risk for future heart disease, but widely publicized. What you don't hear about is the fact that the more cholesterol and saturated fat people ate, the lower their cholesterol levels.
In a 1992 editorial published in the Archives of Internal Medicine, Dr. William Castelli, a former director of the Framingham Heart study, stated:
"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. The opposite of what… Keys et al would predict…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."
The "MrFit" Study: Hypothesis Proven by Omission
The U.S. Multiple Risk Factor Intervention Trial (MRFIT), sponsored by the National Heart, Lung and Blood Institute, is another study that is highly misleading. It compared mortality rates and eating habits of over 12,000 men, and the finding that was widely publicized was that people who ate a low-saturated fat and low-cholesterol diet had a marginal reduction in coronary heart disease.
What did they leave out?
Their mortality from all causes was higher! As Mary Enig and Sally Fallon stated in The Truth About Saturated Fat:
"The few studies that indicate a correlation between fat reduction and a decrease in coronary heart disease mortality also document a concurrent increase in deaths from cancer, brain hemorrhage, suicide and violent death. After 10 years of lowering fat intake and not smoking, they found no significant difference in death from heart disease or total death compared to the control group of smokers, poor diet etc."
Statistical Lies: The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT)
Around the same time as the MRFIT study was the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost $150 million and is often cited to justify a low-fat diet, even though dietary factors were not tested in the study at all. Instead, the study tested the effects of cholestyramine, a cholesterol-lowering drug.
" Their statistical analysis of the results implied a 24% reduction in the rate of coronary heart disease in the group taking the drug compared with the placebo group; however, non-heart disease deaths in the drug group increased -- deaths from cancer, stroke, violence and suicide. Even the conclusion that lowering cholesterol reduces heart disease is suspect.
Independent researchers who tabulated the results of this study found no significant statistical difference in coronary heart disease death rates between the two groups. However, both the popular press and medical journals touted the LRC-CPPT as the long-sought proof that animal fats are the cause of heart disease …"
"After 10 years the number dying from coronary heart disease (CHD) plus those suffering a non-fatal myocardial infarction (NFMI) were totaled for both groups. The total incidence in the cholestyramine group was 7.0% and the control group 8.6%.
This small difference of 1.6% was reported as a 19% reduction in death and heart attack by using relative risk reduction (the difference of 1.6% is roughly 19% of 8.6) in place of the less misleading absolute risk reduction (1.6%). Furthermore, this tiny difference was given the designation of "statistically significant" by changing the criteria originally given for determination of significance after the data was in."
It is often the case that leaders who want to use the cholesterol agenda use statistics to "prove" their point.
Cholesterol Drug Benefits Perpetuated by Statistical Myths
The LRC-CPPT study was only able to show a meaningful benefit because it focused on relative risk reduction rather than absolute risk reduction. What's the difference? You can find a very simple explanation of relative risk vs. absolute risk at the Annie Appleseed Project web site, but let me sum it up here.
- Relative risk reduction is calculated by dividing the absolute risk reduction by the control event rate
- Absolute risk reduction is the decrease in risk of a treatment in relation to a control treatment
In plain English, here's what that means: let's say you have a study of 200 women, half of whom take a drug and half take a placebo, to examine the effect on breast cancer risk. After five years, two women in the drug group develop breast cancer, compared to four who took the placebo. This data could lead to either of the following headlines, and both would be correct:
"New Miracle Drug Cuts Breast Cancer Risk by 50%!"
"New Drug Results in 2% Drop in Breast Cancer Risk!"
How can this be?
The Annie Appleseed Project explains:
"The headlines represent two different ways to express the same data. The first headline expresses the relative risk reduction — the two women who took the drug (subjects) and developed breast cancer equal half the number (50%) of the four women who took the placebo (controls) and developed breast cancer.
The second headline expresses the absolute risk reduction — 2% of the subjects (2 out of 100) who took the drug developed breast cancer and 4% of the controls (4 out of 100) who took the placebo developed breast cancer — an absolute difference of 2% (4% minus 2%)."
You can now see why clinical trials, especially those funded by drug companies, will cite relative risk reductions rather than absolute risk reductions, and as a patient you need to be aware that statistics can be easily manipulated.
As STATS at George Mason University explains:
"An important feature of relative risk is that it tells you nothing about the actual risk."
How Statins Really Work Explains Why They Don't Really Work
A new look at statin cholesterol-lowering drugs from the Massachusetts Institute of Technology claims that no study has ever proven that statins improve all-cause mortality -- in other words, they don't prolong your life any longer than if you'd not taken them at all. And rather than improving your life, they actually contribute to a deterioration in the quality of your life, destroying muscles and endangering liver, kidney and heart function.
According to Stephanie Seneff, author of this stunning revelation:
"Statin drugs inhibit the action of an enzyme, HMG coenzyme A reductase, that catalyses an early step in the 25-step process that produces cholesterol. This step is also an early step in the synthesis of a number of other powerful biological substances that are involved in cellular regulation processes and antioxidant effects.
One of these is coenzyme Q10, present in the greatest concentration in the heart, which plays an important role in mitochondrial energy production and acts as a potent antioxidant …
Statins also interfere with cell-signaling mechanisms mediated by so-called G-proteins, which orchestrate complex metabolic responses to stressed conditions. Another crucial substance whose synthesis is blocked is dolichol, which plays a crucial role in the endoplasmic reticulum. We can't begin to imagine what diverse effects all of this disruption, due to interference with HMG coenzyme A reductase, might have on the cell's ability to function …
There can be no doubt that statins will make your remaining days on earth a lot less pleasant than they would otherwise be … "
It's widely known that statins lower your CoQ10 levels by blocking the pathway involved in cholesterol production -- the same pathway by which Q10 is produced. Statins also reduce the blood cholesterol that transports CoQ10 and other fat-soluble antioxidants.
The loss of CoQ10 leads to loss of cell energy and increased free radicals which, in turn, can further damage your mitochondrial DNA, effectively setting into motion an evil circle of increasing free radicals and mitochondrial damage.
There are no official warnings in the U.S. regarding CoQ10 depletion from taking statin drugs, and many physicians fail to inform you about this problem as well. Labeling in Canada, however, clearly warns of CoQ10 depletion and even notes that this nutrient deficiency "could lead to impaired cardiac function in patients with borderline congestive heart failure."
As your body gets more and more depleted of CoQ10, you may suffer from fatigue, muscle weakness and soreness, and eventually heart failure, so it is imperative if you take statin drugs that you take CoQ10 or, if you are over the age of 40, the reduced version called ubiquinol.
Statins May Even Cause Diabetes!
Statins carry other side effects as well, including diabetes. A meta-analysis, published in JAMA in June, concluded that those taking higher doses of statins were at increased risk of diabetes compared to those taking moderate doses. What this means is that the higher your dose, the higher your risk of developing diabetes.
The "number needed to harm" for intensive-dose statin therapy was 498 for new-onset diabetes—that's the number of people who need to take the drug in order for one person to develop diabetes. In even simpler terms, one out of every 498 people who are on a high-dose statin regimen will develop diabetes. (The lower the "number needed to harm," the greater the risk factor is.)
(As a side note, the "number needed to treat" per year for intensive-dose statins was 155 for cardiovascular events. This means that 155 people have to take the drug in order to prevent one person from having a cardiovascular event.)
Aside from what I've already covered above, statin drugs are associated with a rather extensive list of harmful side effects, including:
Weakness Polyneuropathy (nerve damage in the hands and feet) Acidosis Dysfunction of the pancreas Muscle aches and pains Anemia Sexual dysfunction Cataracts Rhabdomyolysis, a serious degenerative muscle tissue condition Potential increase in liver enzymes so patients must be monitored for normal liver function Suppressed immune function Increased cancer risk
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So How Can You Optimize Your Cholesterol Levels?
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The most effective way to optimize your cholesterol profile and prevent heart disease is via diet and exercise. It's actually quite simple too. Remember that 75 percent of your cholesterol is produced by your liver, which is influenced by your insulin levels.
Therefore, if you optimize your insulin level, you will automatically optimize your cholesterol and reduce your risk of both diabetes and heart disease. There is NO magic pill to cure heart disease, as the underlying cause is insulin resistance caused by eating too many sugars, grains and especially fructose.
So, my primary recommendations for safely regulating your cholesterol and reducing your risk of heart disease include:
- Reduce, with the plan of eliminating grains and fructose from your diet. This is one of the best ways to optimize your insulin levels, which will have a positive effect on not just your cholesterol, but also reduces your risk of diabetes and heart disease, and most other chronic diseases. Use my Nutrition Plan to help you determine the ideal diet for you, and consume a good portion of your food raw.
- Get plenty of high quality, animal-based omega 3 fats, such as krill oil, and reduce your consumption of damaged omega-6 fats (trans fats, vegetable oils) to balance out your omega-3 to omega-6 ratio.
- Include heart-healthy foods in your diet, such as olive oil, coconut and coconut oil, organic raw dairy products and eggs, avocados, raw nuts and seeds, and organic grass-fed meats.
- Optimize your vitamin D levels by getting proper sun exposure or using a safe tanning bed.
- Exercise daily. Make sure you incorporate peak fitness exercises, which also optimizes your human growth hormone (HGH) production.
- Avoid smoking or drinking alcohol excessively.
- Be sure to get plenty of good, restorative sleep.