The important thing to remember in determining one's risk of heart attack and stroke is that in my opinion — and that of a growing number of experts — your cholesterol level no longer plays a role.

Cholesterol — to me and to others that have researched the subject — is now considered to be irrelevant to the process of atherosclerosis. Family history is perhaps the strongest determinant. If your father, mother, an aunt or uncle, died prematurely from a heart attack or stroke, you are definitely in the high risk category.

Other risk factors are a history of cigarette smoking, obesity, a sedentary life style — with minimal to no exercise — and the presence of diabetes.

Nearly a decade ago, many of those who study statin drugs concluded that the modest benefit of statins is derived not from cholesterol inhibition, but by suppression of inflammation.

Statin drugs were designed to inhibit the synthesis of cholesterol by suppression of the mevalonate pathway, which also is responsible for the synthesis of CoQ10, dolichols, selenoproteins and other biochemicals vital for cellular function.

The drug companies did not have much to say about this collateral damage when they first marketed statins. It was so much easier for the pharmaceutical reps to say “statins inhibit cholesterol” than to tell the entire truth when promoting statins to the medical community.

I learned this truth progressively through my independent statin research. Inhibition of CoQ10 and dolichols is responsible for most of the side effects associated with statin use.

Throughout the early phase of statin marketing, doctors felt the modest benefits were from cholesterol inhibition. You can imagine the surprise, over ten years ago, to learn that statins had another effect on an intracellular transcriptase known as nuclear factor kappa B (NF-kB) that mediated inflammation.

All this time when we thought the modest statin benefit was from cholesterol lowering it was apparently from the inhibition of inflammation. This in my mind was the truth behind the benefit of statins. The entire three decades of statin use before this discovery had been nothing but an anti-cholesterol con job.

But there is more, far more. Statin blockade of the mevalonate pathway by reductase inhibition (that's what all statins do — read it on the package insert) had proven to be dosage dependent and the higher the dose of statin needed to achieve desired cholesterol levels, the more profound the collateral damage and adverse reactions.

Because NF-kB was already present in the cells as an intra-cellular transcriptase, relatively tiny statin doses gave the desired anti-inflammatory effect with minimal, if any, effect on the mevalonate pathway and therefore stable levels of cholesterol, CoQ10, dolichols and selenoproteins.

A low dose statin would, I believe, in most subjects give the desired anti-inflammatory effect with no significant effect on the mevalonate pathway. If your present statin dose significantly lowers your cholesterol, in my opinion you are taking too much.

Low dose statins used in this manner give the benefit of statins without the side effects that have plagued statin users from the very beginning.

It is important to understand that our best estimate is that fewer than 10% of statin reactions are reported to the U.S. Food and Drug Administration (FDA) making the numbers you are about to see even more astonishing. Here is a presentation of FDA statin damage reports for the decade ending 2014.
http://www.spacedoc.com/articles/faers-statin-review

Of particular interest to me have been the reports of rhabdomyolysis hospitalizations especially when one applies the 12% mortality rate for statin associated deaths.

Over 1300 deaths from this cause have been reported just in this past decade making the total number of statin associated rhabdomyolysis deaths probably in excess of 2,000.

I can recall in 2004 the media furor surrounding Bayer’s decision to remove its problematic Baycol from the shelves due to 52 deaths from statin induced rhabdomyolysis while today I can't interest any media person to pick up the story.

Perhaps we have become so hardened to the statin adverse reactions stories that we as a society can now accept this number of deaths without a whisper of anguish.

Now some of you reading this will think that I am just an antagonist, contradicting pharmaceutical company and government opinions for the sake of it. That is not the case.

For example, the U.S. Government have just released their Dietary Guidelines for 2015 to 2020. These recommendations are updated every five years. Notably absent from the new recommendations are the limits on daily cholesterol consumption. In 2010 we were advised to keep dietary cholesterol below 300 mg per day. See the new guidelines here:

http://health.gov/dietaryguidelines/2015/guidelines/chapter-1/a-closer-look-inside-healthy-eating-patterns/

Here is what we are told now:

“A few foods, notably egg yolks and some shellfish, are higher in dietary cholesterol but not saturated fats. Eggs and shellfish can be consumed along with a variety of other choices within and across the subgroup recommendations of the protein foods group.”

So after close to forty years of the message to avoid eggs because they are high in cholesterol, we are now told that eggs are fine because they are low in saturated fat. Cholesterol in the diet is no longer a concern.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

January 2016