Volume 12, Issue 61
Using these conventional heart treatments could cause a heart attack

Wow! A blockbuster review article just came out last month about one of my least favorite — and Big Pharma's most loved drugs. I'm talking about statin drugs. These drugs came out about 20 years ago and I don't even want to guess how much money the drug companies have made. I'm thinking it comes real close to our national debt! The drug companies initially pushed statins as a preventive for atherosclerosis and heart disease. And now, they push them as the best thing ever for just about anything that ails you. But the authors of a new paper published in a peer reviewed medical journal are possibly blowing the lid off these dangerous drugs. According to their report, the indiscriminate use of these drugs might actually be responsible for more cardiovascular deaths than they supposedly prevent.

The bombshell comes in the very first line in the paper. "In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels." Well, we already know that statin drugs are mitochondrial suppressants. The FDA has made that clear. But did you know that they also suppress the function of vitamin K2? Vitamin K2 is the cofactor for matrix Gla-protein activation, which is the enzyme that protects the arteries from calcification. Because of the vitamin K2 suppression, the authors predict that statin use is increasing the calcification of the arteries of those taking the drugs. But that's not all.

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Statins also inhibit the biosynthesis of selenium-containing enzymes. One of the most critical selenium enzymes is glutathione peroxidase. Glutathione peroxidase is an essential enzyme for the control of free radical damage. When glutathione peroxidase is inhibited, free radical damage, aging, and degenerative disease is accelerated. But that is not all selenium does. One of the signs of an interruption in selenium-activated protein synthesis is congestive heart failure. Is the increased use of statin drugs one of the reasons that we are seeing an increasing number of cases of heart failure these days? The authors of the new study wonder.

Based on these and other observations, the authors of this paper conclude with this amazing statement about statin drugs which are supposed to be protecting the hearts and blood vessels of those taking them, "Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated." This is an astonishing quote to appear in a peer reviewed scientific journal about a drug that is routinely pushed on almost every American.

Right now statin drug use has been associated with diabetes, dementia, fatigue, weakness, muscle wasting, and mitochondrial toxicity. Now we can possibly add congestive heart failure and calcified atherosclerosis to the list. I have written many times before about how the studies very clearly show that statin drugs offer no benefit at all in people with elevated cholesterol readings, but who do not already have heart disease. Even in those who do, the benefit is questionable, especially when we see all the serious side effects. Now we have to wonder if they are actually making things worse.

If you are taking a statin drug just because your cholesterol levels are high and you have no history of heart disease, reconsider taking it. There are much better ways to avoid a heart attack, including nattokinase, fish oil, and CoQ10.

And when you hear all the great marketing campaigns that Big Pharma and Big Medicine put on, don't forget to be very skeptical. You just might live longer and better with that attitude.

Yours for better health,

Okuyama H1, Langsjoen PH, Hamazaki T, et al. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.

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