In the last post we explored how trans fats are an underlying cause of inflammation that sets the stage for heart disease, a fact that is fairly well documented.  To be clear, rancid or oxidized oils that contain trans fats are themselves not the direct source of endogenous oxidized cholesterol (despite the similar name) and as previously discussed are a middle man in the heart disease process.  Their role is important to understand in the historical context of substituting healthy saturated fats with highly processed vegetable oils.  To understand the mechanism of heart disease, we will explore two fundamental causes – neither being a deficiency of statin drugs.

The first of these causes is calcification, or hardening of the arteries.  In short, calcification is the process whereby calcium is pathologically deposited into smooth tissue.  There are many causes of abnormal calcification including an excess of dietary or supplemental vitamin D2 (as opposed to the much lauded vitamin D3) as well as a lack of magnesium relative to calcium.  The ultimate result however is an abnormal shunting of calcium out of solution.  This includes the formation of kidney stones and the calcification of connective tissue known as osteoarthritis.

Once arterial vessels have succumbed to calcification and are exhibiting chronic inflammation (diagnosed on a lab test as high CRP) the missing piece is the process behind which these small dense LDL particles become oxidized.  The answer to that question is glycation, the second and arguably most fundamental underlying cause.

Glycation is the chemical process whereby a sugar bonds to a protein or fat molecule.  The LDL fraction of cholesterol (which is a protein that delivers fats) is particularly vulnerable to glycation by sugar in your bloodstream, the end result being an oxidized and therefore damaged molecule.  Once these molecules deliver their content and become smaller and more dense, they return to the liver for recycling but the attached sugars of glycation interferes with the process.  What results is a gummy substance that instead gets broken down by macrophages in the artery wall.  Over time, these glycated lipoproteins amass in calcified and inflamed tissue in the disease process known as atherosclerosis.  

From this vantage point we see that high blood sugar, which results from consuming an excess of sugars, fructose, and grains, is the instigating factor.  Trans fats potentiate the problem by contributing towards insulin resistance which further elevates blood sugar.

There is always more to the story, such as evidence of infectious agents irritating the coronary artery walls (smoking does this as well) and emotional and stress factors underlying heart disease, but the source of inflammation and the formation of oxidized cholesterol is the linch pin of the equation, without which heart disease would never have reached epidemic proportions.  Statins get their glory by removing some of the total cholesterol from the picture (both good and bad) and by virtue of that, yes, you will decrease the formation of arterial plaque.  What this shotgun approach fails to do however is address the mechanism behind cholesterol becoming oxidized.  Having less cholesterol available to become oxidized might be a sound argument for taking statins but considering the body’s need for cholesterol, blindly reducing total cholesterol out of context of the patient’s overall health is poor, non-specific medicine.

Although the research supports certain cohorts benefiting from taking statins (older men with a history of heart disease) the use of statins as a preventative strategy makes no sense.  What I find even more disturbing is the widespread prescribing of statins with little concern for side effects and without revaluation of the need for the drug once cholesterol levels have decreased.  I have correlated patients suffering from low libido and depression with cholesterol that has gone too low due to long-term statin use.  The need to lower cholesterol is debatable, especially considering the reasons given above, but even if there is a legitimate need to do so, there are many natural means that work within the body’s design and without the side effects attributed to statins.

In light of statins inability to address the underlying mechanism of heart disease, and the depletion of CoQ10 and healthy cholesterol for which they are notorious, one would be well advised to deeply consider the research and rationale behind the use of statins should the drug be prescribed to you.  If you are willing to make lifestyle, and particularly dietary changes, and utilize natural therapies to normalize heart disease markers, you can sidestep the need for a statin drug and earn a longer, healthier, and more empowered life.  It would be well deserved for being your own advocate and going against the status quo.

For more information on the research statistics on statins, please read this excellent literature review and analysis from Chris Kresser.


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