Should Statins Be Used Preventatively? - Dr. Carolyn Dean MD ND

Should Statins Be Used Preventatively?

January 20, 2021

When I went to medical school in the mid 70s, my class was coached that we should prescribe medications for as short a time as possible to treat a patient with specific condition but stop the drugs when a patient has recovered. That was 50 years ago. In the past decade or two, drugs are being prescribed “for life.” The concerns I’ve always had about drug side effects escalated dramatically. Taking a drug for two weeks compared to two to three decades is not something that has ever been scientifically studied – and will only be a retrospective exercise and too late to stop because of negative effects.

I’ve written about statins, their overuse and side effects in over a dozen blogs and in my Magnesium Miracle book. This particular blog today is inspired by a Medscape report “Who Benefits From Taking a Statin, and When?” The subtitle says it all “On Fundamentally Restructuring Our Thinking Regarding Primary Prevention of Cardiovascular Disease.” This 2020 research article is in the prestigious journal Circulation.

The authors’ premise is how to offer preventive therapeutics to young adult patients. It actually sounds like an attempt to justify what most doctors want to do – give everyone statin drugs “just in case” they might help prevent heart disease.

The fact that atherosclerosis does not affect everyone is said by the authors to “remain elusive” however in the same breath they say “the most important determinants have been known for nearly 60 years…the associations of serum cholesterol concentrations and systolic blood pressure with the incidence of coronary heart disease.” And they assert that “Currently, we have a clear understanding how cumulative exposure to atherogenic lipid fractions drives the process of atherosclerosis across the lifespan through a complex interplay of genetic and lifestyle determinants.”

So, cholesterol exposure over time causes coronary artery disease – “through a complex interplay of genetic and lifestyle determinants.” And that’s the extent of their comments on genetic and lifestyle factors in heart disease.

Since the Human Genome Project only found 23,000 human genes and researchers had to admit that epigenetics controlled genes, there is a lot we can explore about genes. We now know that genes are turned on and off by nutrients – especially magnesium and the B vitamins. As for lifestyle – we know that nutrition and nutrients are also responsible for coronary artery disease. But none of that is explored in this article.

Here’s how I describe heart disease and magnesium in my eBook, Sixty-Five Conditions Associated With Magnesium Deficiency.

The heart, specifically the left ventricle, has the highest amount of magnesium in the whole body. Magnesium deficiency is common in people with heart disease; taking magnesium can reduce that risk. For example, I think magnesium deficiency and calcium excess from calcium supplements should be the first area of investigation to solve the problem of higher incidence of heart attack in women.

Research indicates that calcium enters the cells by way of calcium channels that are jealously guarded by magnesium. Magnesium, at a concentration 10,000 times greater than that of calcium in the cells, allows only a certain amount of calcium to enter to create the necessary electrical transmission or muscle firing, and then immediately helps to eject the calcium once the work is done.

Why? If calcium accumulates in the cell, it causes hyperexcitability and eventually calcification that disrupts cell function. Too much calcium entering cells can cause symptoms of heart disease (such as angina, high blood pressure, and arrhythmia), asthma, or headaches. But if there is enough magnesium, it acts as the body’s natural calcium channel blocker.

In the Medscape article, I was concerned that statin side effects were not discussed. Instead they are described as being “generally well-tolerated and safe drugs to lower low-density lipoprotein cholesterol levels and consequently lower ASCVD risk.” Statins are “the most studied drug classes” and have become the reason that “statins are recommended for primary prevention in patients with extremely high low-density lipoprotein levels, patients with diabetes mellitus, and patients with the greatest short-term (ie, 10-year) predicted risk of ASCVD, because these groups are deemed to derive the greatest short-term benefit from treatment.”

Then the authors make their pitch for life-long statin intervention and say “About 20 years ago, ASCVD prevention became a more holistic endeavor when treatment recommendations were based on risk factors placed into the context of an individual’s age, sex, and interactions with other risk factors. This was done using coronary risk prediction models, with the most well-known based on data from the Framingham Heart Study.”

I’m particularly offended that they use the word holistic – which is universally associated with alternative medicine – to describe their approach to use life-long statins. They talk about transitioning from short term to long-term “expected” benefit. They don’t know that these benefits will occur but they “expect” they will occur. They cite studies that statins lower LDL.

The fact that’s it’s all about “expectations” is born out in the study they use to promote life-long statins. I’ll capitalize the offending words. It’s a “a thought-provoking MODELING study on the EXPECTED benefits of long-term statin use in YOUNGER individuals. The results are based on data from 3148 participants, age 30 to 59 years, without ASCVD, and not qualifying for statin treatment under current guidelines. Two different CONCEPTUAL biological ASSUMPTIONS were tested. ANTICIPATED benefits, expressed as absolute and relative ASCVD risk reduction over a 30-year horizon, were calculated across several MODEL PARAMETERS. THE STUDY THEREBY NOT ONLY PROVIDES TOOLS TO UNDERSTAND “IF” TAKING A STATIN SHOULD BE CONSIDERED, BUT ALSO “WHEN” STATIN INITIATION SHOULD BE CONSIDERED.

After slinging around words like MODELING, CONCEPTUAL, ANTICIPATED, and EXPECTED it’s obvious that this is not a research study but a computer simulation. And the researchers make an erroneous simulated conclusion that “high-intensity statin use could prevent 51% to 71% of premature ASCVD events among patients age 30 to 39 years when treated for 30 years, which amounts to almost 1.4 million events in the United States.”

Seriously? I’m not a statistician but just plain commonsense tells me that this study is full of flaws and will lead many doctors astray. I know the problem with many allopathic doctors is their lack of exposure to alternatives. They don’t read the cholesterol critics and they have no awareness of the nutritional and nutrient therapies that lower cholesterol. Instead, they are acutely aware of the failures in their practice where patients with heart disease do not respond to statins so they HOPE that giving these drugs to younger and younger people might “prevent” problems.

The authors even say that “The effectiveness of statins has mostly been studied in middle-aged and older individuals during relatively short treatment periods. It remains unknown to what extent results from these trials can be extrapolated to younger individuals. So far, there is no clear reason to believe that statins are not effective in this setting.”

I say, “hope” and “extrapolating” are not useful clinical strategies. A better strategy is to begin by reading the cholesterol critics and see what they have to say. My favorite is Dr. Malcolm Kendrick who has written extensively on statins and maintains that statins do not extend life expectancy. Dr. Kendrick doesn’t necessarily talk about alternatives. For that insight you can read what I have to say in The Magnesium Miracle. Here is an excerpt:

What is not normal is the high amounts of oxidized cholesterol (cholesterol abnormally bound with oxygen) that we eat in processed foods, fast foods, and fried foods. In addition, chlorine, fluoride in water, pesticides, and other environmental pollutants can oxidize cholesterol in the body. It is this oxidized cholesterol that researchers are concerned about when it comes to heart disease.[1] What is most interesting about oxidized cholesterol is that means cholesterol is an antioxidant. Cholesterol is sweeping up toxins in the body and trying to eliminate them and in the process becomes oxidized. So, cholesterol is not the problem – toxicity from chlorine, fluoride, pesticides, and other environmental pollutants is the real problem.

Regular use of antioxidants such as magnesium, vitamin E, vitamin A, and vitamin C can lower oxidized cholesterol levels because they deal with the toxins that overload the body and spill into the cholesterol pool. Magnesium is likely the most powerful antioxidant in the body and there is compelling evidence that magnesium therapy reduces cholesterol levels,[2] [3] [4] even when there is a genetic risk factor present for hypercholesterolemia.[5]

Unfortunately, there are no visible physical symptoms of high cholesterol beyond the associated signs of a bad diet, sedentary lifestyle, smoking, alcohol intake, and stress. You have to find it on a blood test. A poor diet with a high intake of saturated and polyunsaturated fats, hydrogenated oils, fried foods, meat, sugar, coffee, and alcohol will elevate cholesterol levels, especially when a person lacks fiber from whole grains and vegetables. Add a sedentary lifestyle with weight gain, and cholesterol increases.

The very diet that promotes elevated cholesterol also causes magnesium deficiency.

Most doctors do not have knowledge, time, or inclination to educate patients about correct eating habits that could reduce their cholesterol; instead they rely on medication to treat the problem. To be fair, many patients don’t have the inclination to comply even if their doctor recommends a change in diet, exercise, or weight loss. Adding magnesium supplementation to lifestyle changes, however, gives patients more dramatic improvement and the incentive to embrace change.

Magnesium is a Natural Statin

Magnesium acts by the same mechanisms as statin drugs to lower cholesterol. Every metabolic activity in the body depends on enzymes. Making cholesterol, for example, requires a specific enzyme called HMG-CoA reductase. Magnesium slows down this enzymatic reaction when it is present in sufficient quantities. It’s the same enzyme that statin drugs target and inhibit. However, magnesium is the natural way that the body has evolved to control cholesterol when it reaches a certain level, whereas statin drugs are used to destroy the whole process.

This means that if sufficient magnesium is present in the body, cholesterol will be limited to its necessary functions—the production of hormones and the maintenance of cell membranes—and will not be produced in excess. Magnesium is also responsible for several other lipid-altering functions that are not even shared by statin drugs. Magnesium is necessary for the activity of an enzyme that lowers LDL, the “bad” cholesterol; it also lowers triglycerides and raises the “good” cholesterol, HDL. Another magnesium-dependent enzyme converts omega-3 and omega- 6 essential fatty acids into prostaglandins, which are required for heart and overall health.



 Goldberg B, Heart Disease, Future Medicine Publishing, Tiburon, CA, 1998.

[2] Altura BT et al., “Magnesium dietary intake modulates blood lipid levels and artherogenesis.” Proc Natl Acad Sci, vol. 87, no. 5, pp. 1840–1844, 1990.

[3] Singh RB et al., “Does dietary magnesium modulate blood lipids?” Biol Trace Elem Res, vol. 30, pp. 50–64, 1991.

[4] Corica F et al., “Effects of oral magnesium supplementation on plasma lipid concentrations in patients with non-insulin-dependent diabetes mellitus.” Magnesium Res, vol. 7, pp. 43–46, 1994.

[5] Durlach J, “Commentary on recent epidemiological and clinical advances.” Magnesium Research, vol. 9, no. 2, pp. 139–141, 1996.

Want more health info like this?

Subscribe to receive FREE health tips from Dr. Carolyn Dean. We won't spam you or sell your information.