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Bill Sardi
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Posted May 5, 2013: by Bill Sardi
Even the chairman of the department of cardiovascular medicine at the Cleveland Clinic is disturbed by the Food & Drug Administration’s late Friday night approval of a combination drug intended to reduce circulating cholesterol levels. The FDA approved Liptruzet (Zetia + generic Lipitor, chemically known as Ezetimibe and Atorvastatin) that lowers cholesterol but has not been shown to reduce the risk of cardiovascular disease or death, a fact its maker does not dispute. This newly approved drug will sell for about $5.50 per pill or $2007/year. Lipitor is the historically best-selling statin cholesterol drug whose patent expired in 2011. Zetia works by reducing cholesterol absorption from foods while Lipitor interferes with the liver’s natural production of cholesterol.
This development is quite surprising given that the FDA said it is going to pay more attention to what are called “primary end points” in drug approvals, such as mortality, rather than just factors that correlate with but may not cause disease. Or in some circumstances there may be drugs that address relevant measures of disease, but over-inhibition of inflammation or blood sugar or blood pressure, for example, obviously can be problematic.
In recent years the FDA has come under criticism for approval of drugs based upon measurable correlations of disease, such as blood pressure, blood sugar or cholesterol, while not factoring in the ultimate end point — survival. In fact, all statin cholesterol-lowering drugs from their inception in the late 1970s with Mevacor, were approved on the basis of lowering blood cholesterol concentrations, not cardiac death.
Therefore some anti-inflammatory drugs and anti-diabetic drugs were approved by the FDA only to be removed from the market due to elevated mortality rates. The liver-toxic statin drugs remain on the market, despite their inability to demonstrate they avert mortal heart attacks. This may be surprising to patients with heart disease who have been sternly lectured they will incur a heart attack if they don’t take a statin drug. But John Abramson MD, author of OVERDOSED AMERICA, slammed the door on statin drugs when he analyzed the top ten statin drug trials and found these drugs did not reduce mortality among healthy adults for coronary artery disease.
A recent analysis found that cholesterol, statin drug use and aspirin did not reduce mortality for cardiovascular disease. Elevated blood sugar (diabetes), not cholesterol, was found to be the primary factor involved in cardiovascular death among middle-aged adults. A more recent study shows cholesterol accurately indicates risk for cardiac death slightly better than pure chance while elevated blood sugar is highly predictive of mortality from heart disease.
One wonders why and how statins were so rapidly and widely adopted when data did not back their safety or efficacy. But this writer as alerted readers to the fact that statin drugs reduce testosterone levels and may part of a covert population control agenda.
As a side topic, if cholesterol is not a valid marker of coronary artery disease, then what is?
There has been a growing body of evidence in recent years that uric acid is an independent predictor of mortality among high-risk patients with cardiovascular disease. One of the largest studies of its kind, known as NHANES I, conducted among thousands of patients, and found that individuals with the highest uric acid levels were at the greatest risk for cardiac death. This landmark study was published 13 years ago in the Journal of the American Medical Association and has not been heeded by modern medicine.
In a study conducted in Israel, the rate of cardiovascular disease was 11.6% for women with the highest uric acid levels compared to 5.0-6.5% among men with lower uric acid levels. For men, the highest rate of cardiovascular disease occurrence was 14.0% for the highest uric acid levels compared with 10.8% among men in the lowest uric acid group.
A striking study shows that among 78,707 healthy people, free of cardiovascular disease, increasing uric acid levels are significantly associated risk for cardiovascular disease events (heart attacks, strokes) double that of changes in high-density lipoprotein (HDL) “good” cholesterol. Elevated uric acid is considered causal, not just associated with, heart and blood vessel disease.
While statin drugs don’t significantly reduce cardiac death rates, they do slightly reduce risk for non-mortal heart attacks, which may in fact be due to their demonstrated ability to mildly reduce uric acid levels.
Convincing data shows that drugs (allopurinol) used to treat elevated uric acid levels significantly reduce risk for cardiovascular disease.
Despite this evidence, uric acid is still being debated as a marker for mortality in heart disease.
This health writer has pointed to arterial calcium deposits being the primary culprit in coronary artery disease, and upon further investigation, it is found that blood serum uric acid levels serve as a marker for coronary artery calcification. High uric acid levels correlate with arterial stiffness, which is usually induced by calcifications, not cholesterol.
More concerning, uric acid levels in the normal range as associated with increased risk for heart and blood vessel disease. This can be explained by the fact blood analysis presents what is called the reference range or commonly-found range for various measures in blood samples, it often does not represent disease range.
Researchers note that uric acid levels are routinely obtained but clinicians may not be alerted to their significance. acid.
In turn, uric acid may be a result of excessive iron stores in the body. In one study 20.7% of individuals with high uric acid had high iron storage (ferritin) levels versus 8.8% of individuals with low uric acid levels. The relationship between high uric acid levels and high iron stores is confirmed by other studies as well.
The enzyme xanthine oxidase is the precursor for uric acid. There are many natural xanthine oxidase inhibitors which can be used to control uric acid, virtually all of them being iron-binding molecules called polyphenols.
One study found molecules from the Asian raisin tree (myricetin), from red onions or red apple peel (quercetin), parsley (apigenin) inhibit xanthine oxidase at very low concentrations. Extracts from cranberries, purple grape juice and black tea similarly inhibit this enzyme. In another study of twelve natural molecules, an extract from blue skullcap (esculetin) or Chinese skullcap (baicalin) displayed the strongest ability to inhibit xanthine oxidase. Cherries are also known to lower uric acid levels, tart cherries in particular.
High doses of vitamin C, averaging 500 milligrams or more, also significantly reduce uric acid levels. IP6 rice bran extract, which serves as an iron-binder and is available as a dietary supplement, has also been found to reduce uric acid levels. © 2013 Bill Sardi, Knowledge of Health, Inc.
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