Rethinking Statins

By Stephen T. Sinatra, M.D., F.A.C.C., F.A.C.N., C.N.S., C.B.T.

In June of 2011, the Food and Drug Administration (FDA) issued a warning about the increased risk of muscle pain and weakness (myopathy) from high-dose Zocor (simvastatin), a popular cholesterol-lowering statin drug. Specifically, the agency cited the 80-milligram dose of the medication in its warning and cautioned against prescribing such a high amount to new patients in particular.

I applaud the FDA action, but feel the warning falls far short of what the public needs to know. The fact is that statins and severe cholesterol-reduction can contribute to memory problems, cognition difficulties, cataracts, liver problems, polyneuropathy, impotence, and immune decline. And since many statin side effects are underreported or dismissed by doctors, the problems with these drugs are really more serious and widespread than officials let on and medication labels admit.

The basic trouble with statins is that they inhibit the body’s production of CoQ10. That’s the equivalent of throwing a biochemical monkey wrench into your body’s machinery, because CoQ10 is essential for the generation of cellular energy. Without sufficient CoQ10, energy production will lag and cell function will suffer. The key to counteracting statin-related problems, as I have said for years, is to take a minimum of 200 mg of CoQ10 daily in divided doses, as well as to supplement with other important nutrients like magnesium, carnitine, and ribose—all of which protect and fortify the energy-producing structures inside cells known as mitochondria. Unfortunately, there are approximately 60 million people on statins in the U.S. and very few of them will ever be told by their doctors to take CoQ10, let alone any other supplements to prevent side effects.

Questioning the Cholesterol Connection

Years ago, like practically every other cardiologist, I was a staunch believer in cholesterol lowering. Cholesterol was the bad boy of heart disease and statin drugs were the blessed solution. But throughout my clinical practice I observed that my cardiac patients developed heart problems whether their cholesterol was high or normal, which made me realize that cholesterol wasn’t the sole perpetrator. It was just one of many accomplices in the disease process. Then, with the emergence of research in the late 1990s pointing to inflammation as the real cause of heart disease, I totally dumped the cholesterol theory.

Simply put, cholesterol is not the problem. Cholesterol is absolutely critical to the body in so many ways, including as an essential raw material for cell membranes and sex hormones. Instead, the real problem is the current cardiology obsession to slash cholesterol to ever lower and lower levels. And the fact that many doctors are trying to achieve this radical cholesterol reduction by using ever stronger statin drugs and prescribing statins for prevention to people without heart disease is compounding the problem.

Last July, the European Cardiology Society gave official sanction to treating “dyslipedemia” (the phony term for “high” cholesterol as defined by Big Pharmafunded researchers) with statins at the “highest dose possible or highest tolerable dose.” The announced goal: to reach the target LDL cholesterol level of below 70 mg/dL for very high-risk patients and below 100 for high-risk patients. If those targets aren’t possible, then doctors should aim for a 50-percent reduction in LDL, according to the Euro docs. But such cholesterol-cutting goals fly in the face of increasing questions about the efficacy of statins and the decades-long cholesterol-lowering paradigm. For instance:

  • A review of major statin trials involving more than 32,000 patients revealed a significant increase (12 percent) in the risk of diabetes at high doses compared to lower doses.
  • Studies have linked the potential for dementia with a decline in cholesterol. A University of Kentucky study showed that aged dogs who underwent routine statin treatment exhibited cognitive deficits compared to non-treated older dogs.
  • A 2010 review by British researchers of 11 major studies, involving more than 65,000 patients, failed to find evidence for the benefit of statin therapy for high-risk primary prevention. Beatrice Golomb, M.D., a statin expert from the University of California/San Diego, commented that the study supports what we should already know, “that for patients without established heart disease, statins are more risky than helpful.”
  •  In a statistical analysis published in 2010 of databases from 368 general practices in England and Wales, involving more than 225,000 statin users, researchers found significant associations with myopathy, cataracts, acute renal failure, and moderate or serious liver dysfunction.

Reevaluating Results

Some particularly persuasive papers have also been written by cardiologist Michel de Lorgeril, M.D., from the French National Center of Scientific Research in Grenoble. He challenged the results of the highly publicized JUPITER study. The particular statin being studied in this trial was Crestor (rosuvastatin) and the results hailed Crestor’s ability to decrease the risk of developing cardiovascular disease.

De Lorgeril’s report pointed out that nine of the authors in the study had financial relationships with AstraZeneca, the manufacturer of Crestor and sponsor of the study, and that such conflicts of interest are a common denominator in statin-related studies. His critique also noted that most published cholesterol-lowering drug trials since 2005 have been negative or ambiguous. He argued that the recent studies “strongly suggest” that the results of previous, highly positive statin trials between 1994 and 2004 “should be carefully re-examined by experts independent from the pharmaceutical industry.” “The next question,” he wrote, “would be whether it is not time for a full reappraisal of the theory according to which cholesterol-lowering results in a significant protection against cardiovascular morbidity and mortality.” I couldn’t agree more.

My Statin/Cholesterol Bottom Line

In 2003, I wrote a letter to the Southern Medical Journal and strongly questioned the practice of cholesterol-lowering to treat cardiovascular disease. To me, the emerging research was clearly showing the importance of inflammation over cholesterol, and that where statins could excel was when used in high-risk patients with known heart disease. Specifically, the best candidates for a statin are males with low HDL (below 30 mg/dL) and established coronary artery disease (CAD). The benefits these men derive from statin drugs are not from any cholesterol-lowering effect but from the ability of statins to thin the blood and defuse inflammation. Women with high cholesterol in the absence of CAD have no business taking statins. There is no substantial evidence that the drugs do anything for them.

A growing number of cardiology skeptics, myself included, would love to see a thorough re-evaluation of the whole cholesterol theory. But statins represent a $17 billion annual cash cow for Big Pharma, so I don’t expect that to happen anytime soon.


  • Preiss D, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy. JAMA. 2011;305(24):2556–2564.
  • Tong J, et al. A scissors mechanism for stimulation of SNARE-mediated lipid mixing by cholesterol. Proc Natl Avad Sci USA. 2009;106(13):5141–5146.
  • Stewart R, et al. Twenty-six–year change in total cholesterol levels and incident dementia: the Honolulu-Asia Aging Study. Arch Neurol. 2007:64(1):103–107.
  • Martin SB, et al. Coenzyme Q10 and cognition in atorvastatin treated dogs. Neurosci Lett. 2011:501(2):92–95.
  • Ray KK, et al. Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65,229 participants. Arch Intern Med. 2010;170(12):1024–1031.
  • Hippisley-Cox J, Coupland C. Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database. BMJ. 2010;340:c2197.
  • de Lorgeril M, et al. Cholesterol lowering, cardiovascular diseases, and the rosuvas-tatin-JUPITER controversy. Arch Intern Med. 2010;170(12):1032–1036.
  • de Lorgeril M, et al. Recent cholesterol-lowering drug trials: new data, new questions. J Lipid Nutr. 2010;19(1):65–79.
  •  Sinatra S. Is cholesterol lowering with statins the gold standard for treating patients with cardiovascular disease? South Med J. 2003:96(3):220–222.

This article originally appeared in the November 2011 issue of Dr. Sinatra’s monthly written newsletter, Heart, Health & Nutrition. HMDI has reprinted this article with permission from Healthy Directions, LLC (© 2011 Healthy Directions, LLC).

Leave a Reply


  1. marfi nerys

    on January 26, 2014 at 11:31 pm

    that I do not take Rosuvastatina, COQ10
    have recomended if take this for high colesterol,

  2. marfi nerys

    on January 26, 2014 at 11:42 pm

    that I do not take Rosuvastatina, have COQ 10, you recommended if I take this
    only for high colesterol. have high pressure.

  3. GJB

    on June 15, 2014 at 11:12 pm

    My new lab results are TC 360- HDL 71.8 – LDL 275,6 Trig 63. I am a female & 63 years old. My doc wants me on Crestor, but I don’t want to take because of the info re same. Take Bystolic for elevated BP. Any suggestions?

  4. kitty

    on December 23, 2014 at 11:44 pm

    “Women with high cholesterol in the absence of CAD have no business taking statins. ” — THANK YOU! Very happy to read about reservations with using statins for primary prevention. Just had a call from my primary care – almost in the same boat as GJB except for LDL at 191, HDL 59; Tirg 63. 55 years old; no hypertension (without drugs;), no diabetes, never-smoker. He suggested to spend 3 months trying lifestyle changes, but beyond tweaking the diet a little, exercising more and maybe losing 5-7 pounds or so (I weight 132 now at 5’2″ so it’s not like I have a lot of room there without it showing on my skin) which I was planning to lose anyway to fit in size 5 dresses, there isn’t much I can do. I told I’ll try lifestyle but not drugs.

  5. Steve

    on February 25, 2020 at 1:24 pm

    I’m a 67 year old white male. I was told 4 1/2 years ago that I had a high bg, in fact that I was diabetic. I went on a keto diet lost 70 lbs and now weigh 145 lbs and have an Ha1c of 5.0, triglycerides of 69, hdl of 56. However at my LDL has risen from 110 when diagnosed with diabetes to 220 – it seemed to go up in a straight line as the weight came off. My cardiologist is hounding me to take a statin because as he says it will save my life. I’m active fit and healthy otherwise. My doctor will speak of nothing else and says I’m in denial about my CVD. I am not in denial, I’m confused and worried. I couldn’t have lost the weight and achieved a 5.0 a1c without having strong self control.
    I would appreciate any suggestions about the statins. I hear Keto professional experts say all the time to find another doctor, but I have found this impossible as practically all of them think alike with respect to the risk calculator and statins.


  6. HeartMD Editor

    on March 11, 2020 at 5:23 pm

    Hi Steve, Dr. Sinatra says, “your Triglyceride-to-HDL ratio is just over 1, which is excellent. That level is correlated with low risk of CVD (cardiovascular disease). By a high BG, I assume you mean blood glucose. I do recommend statin medication in men over 70 with documented heart disease. You are only 67. So if there is no evidence you have any CVD, I would probably hold off prescribing a statin if you were my patient.”

  7. Steve

    on March 17, 2020 at 9:51 am

    Thank you for answering my post. Since then I’ve had a CAC test where I scored 625 Agatston – so I have relented and started taking a low dose statin Rosuvastatin 5mg. Had another blood test and my other markers are even better than before (tri 52 hdl 60 ldl c 168 chol 235). I understand that I’m a good candidate for statin therapy, however, my concern is one of tracking the ldl’s that are being removed from my blood. If the ldl is the nice fluffy non oxidized type I really don’t care how much of that I have, so the problem for me is that i don’t know if those small oxidized ldl’s are being removed to a significant degree as the standard blood test doesn’t tell me that. I need to know how to track the targeted oxidized ldl’s to know if the statin is working to an affective degree. How does one do that?

    Thanks so much for responding

  8. HeartMD Editor

    on March 24, 2020 at 11:09 pm

    Steve, you would need to consult with your personal MD to see what labs in your area test for particle size. Your MD can also work with you and your insurance company to determine the frequency for follow-up testing for reimbursement. Maybe these articles I wrote may help:
    Regardless of the LDL, remember that low-dose statins have antioxidant and “blood-thinning” (anti-coagulation) effects as well, which shall support your overall circulation.
    Best wishes,
    Dr. Sinatra

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