Life Extension Magazine®

Nurse talking to patient on statin and Coq10

Consumer Confusion about Cholesterol and Statin Drugs

Statin drugs deplete the body’s CoQ10 and vitamin K. Restoring these nutrients can reduce symptoms of heart failure and alleviate statin drugs’ side effects.

Scientifically reviewed by: Dr. April Parks, MD, MS, in August 2023. Written by: Chancellor Faloon.


Statin drugs remain controversial because they are often overprescribed and present side effects such as fatigue and muscle pain.

Few physicians advise their patients that statins deplete CoQ10 from the body.

Restoring healthy levels of CoQ10 through supplementation has been shown to alleviate side effects as well as reduce the symptoms of heart failure.

If you or someone you know is on a statin, this article can help the patient and their physician make more educated decisions.

Statins and Heart Disease


Heart disease encompasses a range of cardiac disorders that include:

  • Chronic heart failure
  • Coronary artery disease
  • Valvular disease (such as aortic stenosis)
  • Sudden heart attack

Maintaining healthy levels of cholesterol is one way to help lower these risks.

There are people who question the evidence for the causal role of LDL cholesterol in atherosclerotic disease.

There is also disagreement about exactly which patient populations benefit most from cholesterol-lowering-type drugs called statins.

Concerns raised about statin drugs include:

  • In people without known heart disease, there does not appear to be a mortality benefit with statin drugs, and the harms can outweigh the benefits,1,2
  • Clinical trials of statins are largely industry-sponsored, and the original data in those studies are mostly unavailable to researchers,2,3 and
  • Lifestyle factors including tobacco usage, unhealthy diet, and sedentary lifestyle are thought to account for as much as 80% of cardiovascular risk.2,4

The sum of published research shows that:

  • Simple ways exist to diminish the most common statin-drug side effect,
  • In high-risk individuals, statins do reduce heart disease deaths and mortality from other causes, and
  • Comprehensive evaluation and control of cholesterol and other risk factors achieve the greatest reduction in heart disease risk.

Aging often results in an increase in cholesterol. This age-related increase in cholesterol is primarily composed of small, dense LDL particles, especially those oxidized, which promote the formation of harmful plaque in the arteries.

As the decades add up, the damage inflicted by these cholesterol particles injures blood vessels, eventually obstructing blood flow to the heart muscle, brain, and other organs.

If an aging individual with poor and worsening cholesterol does not want to make radical lifestyle and dietary changes, then proper statin drug therapy (usually at a much lower dose than commonly prescribed) should be considered.

Reducing Statin Side Effects


Cholesterol is carried through the blood by transporters called lipoproteins, of which LDL (low-density lipoprotein) is one.

Statins lead to robust reductions in LDL (“bad”) cholesterol and decreases in C-reactive protein, a marker of inflammation, including C-reactive protein and interleukin-6.7

Statins have clearly defined benefits for high-risk individuals, but their use in prevention in low-risk individuals is not supported by that science.

Researchers and clinicians have pointed out that in individuals at low risk of cardiovascular events, side effects of statins outweigh benefits.1,8

Life Extension® was among the first to note that statin drugs were being overprescribed, often at unnecessarily high doses.

Statins deplete the body’s levels of coenzyme Q10, which causes many outward side effects, like muscle pain (myalgias) along with potential multi-organ damage.

Evidence also shows that statins interfere with the synthesis of vitamin K2.9,10

The encouraging news is muscle pain caused by statins can be significantly reduced with the addition of coenzyme Q10.11-14

The statin-induced decrease in coenzyme Q10 and vitamin K2 can be corrected by taking supplemental CoQ10 and vitamin K2.

What you need to know

Cholesterol and Statins

  • Statins have clearly defined benefits for individuals at high risk for cardio-vascular events.
  • Statins lead to significant reduction in LDL (“bad”) cholesterol.
  • The body’s levels of coenzyme Q10 are depleted by statins.
  • Low CoQ10 blood levels have been associated with higher mortality in heart failure patients.
  • Statins interfere with the synthesis of vitamin K2, which helps promote arterial health.

CoQ10 Provides Support


A meta-analysis published in 2018 combined the results of 12 randomized, controlled trials that included a total of 575 patients.

This study concluded that coenzyme Q10 (CoQ10) supplementation ameliorated the muscle pain, cramps, weakness, and tiredness associated with statin drugs. It also showed that statins reduce CoQ10 levels by 16%-54%.14

In high-risk individuals (which includes a significant portion of the aging population), statin drugs help protect against cardiovascular disease, 15 including coronary artery occlusion and cerebral vascular insufficiency. In some observational studies, statin use showed potential in slowing aortic stenosis progression.16 Statins also reduce CoQ10 levels.11

New Data Support CoQ10’s Protective Effects

A clinical trial published in 2019 (after the 2018 meta-analysis showing the CoQ10 protective effect in statin users), demonstrated another approach to protect against statin-induced myalgia:11

Cut the statin drug dose in half.


Add a CoQ10 supplement.

In this study, 60 patients were selected who were all statin intolerant and had elevations in blood biomarkers (creatine kinase and liver transaminases) which have been correlated with statin-induced muscle pain.

After patients were taken off statins for a month, they were then put back on a half-dose statin for a month. At that point they were randomized to receive either 100 mg of CoQ10 (ubiquinone) or a placebo. The difference was dramatic:

In the group that received the CoQ10, 46.6% reported a reduction in pain scores.

In the group that received the placebo, only 6.6% reported a reduction in pain scores.

Blood markers of organ damage sometimes seen in statin drug patients decreased significantly in the CoQ10 group, while there was no significant change in biomarkers of muscle, liver, or kidney damage in the placebo group.

At the end of the study, participants in the CoQ10 group also had lower LDL and total cholesterol compared to the placebo group (not receiving CoQ10), and they accomplished this with just half the statin dose they were previously taking!

Low CoQ10 blood levels have been associated with higher mortality in heart failure patients.17

Continuing research shows that CoQ10 supplementation can effectively boost levels of this heart-essential nutrient, improving outcomes for heart failure patients.

In a recent study, researchers selected 142 patients who developed heart failure while on statins.12

Of these patients, 94% had diastolic heart failure (inability of their left ventricle to relax normally and properly fill) and 6% had systolic heart failure (lack of their left ventricle contracting normally and pumping blood out into circulation).

The patients were taken off statins and put on an average dose of 300 mg/day of CoQ10. The study primarily used the ubiquinol form of CoQ10, which is more readily absorbed into the bloodstream than ubiquinone.

By the end of follow-up (mean 2.8 years) the number of patients who had no limitations of physical activity increased from 8% to an astounding 79%.

For the patients with diastolic heart failure who received CoQ10, at final follow-up:

  • Approximately 34% had complete normalization of diastolic function,
  • 60% had sustained improvement in diastolic function, and
  • 25% showed improvement but not normalization of diastolic function.

For the patients who had systolic heart failure, ejection fraction increased by a mean of 12%.

Ejection fraction is the percentage of blood pumped out of the heart’s left ventricle with each beat. Measuring this percentage is essential to the proper evaluation and management of those with systolic heart failure.18

Why Early Statin Trials Were Short Term

Some critics of statins contend the research does not consistently show they reduce cardiovascular or all-cause mortality.

However, real-world obstacles stand in the way of long-term, placebo-controlled human trials designed to test the effects of statins or other interventions on mortality, which is the proof we need to establish a life-extending benefit.

A study evaluating human mortality would require many decades to produce meaningful results. Humans live longer than lab animals, which makes us more difficult to study, and makes such research prohibitively costly.

Other factors add to the complexity. People often change their diet, exercise, and lifestyle habits. Compliance with any nutritional or pharmaceutical intervention tends to be inconsistent. Additional confounding factors that are difficult to control are stress levels, environment, and individual genetics.

For these reasons, long-term, randomized, placebo-controlled trials of potentially life-extending interventions—such as statins—present an enormous challenge to the scientific community.

Newer Trials Show Reduced Mortality

But statin critics may be overlooking newer studies that are showing meaningful mortality benefits.

One large-scale meta-analysis published in 2016 showed that statins were significantly more effective for patients in reducing the odds of dying from coronary heart disease and from any cause, compared to control groups.21

Specifically, statin users had 31% lower odds of dying from coronary heart disease and 16% lower odds of dying from any cause, compared to controls.

20-Year Study Yields Robust Mortality Benefit


A study published in 2017 was one of the first to truly examine the impact of statin use over the long term.

This study analyzed evidence after the termination of a randomized, placebo-controlled statin trial. One arm of this study evaluated the effects of statins in men with LDL of 190 mg/dL or higher and without preexisting vascular disease.

This analysis divided a total of 5,529 men into two groups, those with LDL levels under 190 mg/dL and those with LDL levels at 190 mg/dL or higher.

The randomized, controlled phase of this trial was about five years and used a statin drug called pravastatin.

What makes this study significant is that the observational follow-up on patients was an additional 15 years, meaning the whole study population was followed for 20 years.22

Merck Received Patent for Combined Statin-CoQ10 Drug, but Never Brought it to Market


Merck and Co., Inc. is one of the world’s largest pharmaceutical companies. It was the first to introduce a statin drug, called lovastatin (Mevacor®), in the 1980s and then another statin called simvastatin (Zocor®) in the 1990s.

In 1989, the company filed for a patent on a drug that combined CoQ10 with a statin to reduce statin side effects. In 1990, they were awarded that patent, which was scheduled to expire in 2009.19

Merck never proceeded with clinical trials needed for FDA approval.

They may have decided that it was not worth spending hundreds of millions of dollars to conduct clinical trials and then develop a drug with CoQ10. Statin drugs are cheap to produce compared to coenzyme Q10, which is relatively expensive.

Merck’s patent, however, kept other drug companies from pursuing a combination statin-CoQ10. Still, a survey published in 2015 reported that 71% of cardiologists recommend CoQ10 to some of their patients.20

At the end of the 20-year follow-up, an analysis was done comparing the placebo group to men with LDL ≥ 190 mg/dL and originally assigned to the pravastatin group in the initial trial. Here are the findings over this 20-year period:

  • The risk of coronary heart disease mortality was reduced by 28% in pravastatin drug users,
  • Cardiovascular death was reduced by 25% and all-cause mortality by 18% respectively, in people remaining on pravastatin over this 20-year period.

In the participants whose LDL was lower than 190 mg/dL, pravastatin reduced the risk of coronary heart disease and major adverse cardiovascular events. The participants with LDL ≥190 mg/dL had greater reductions in cardiovascular and all-cause mortality from pravastatin treatment compared to placebo.

Increased Risk When LDL Particles Are Small and Dense

A high number of small, dense LDL particles has been associated with elevated heart disease risk.30

The reason is that circulating, small, dense LDL particles easily penetrate and damage the blood vessel wall. In addition, they are more prone to atherogenic modification, including oxidation.31

Oxidized LDL damages the delicate endo-thelial cells lining the blood vessel wall.32 Once the integrity of the endothelial barrier is compromised, additional oxidized LDL accumulates behind the arterial wall.

A critical step in the development of atherosclerosis is the adhesion of monocytes (a type of white blood cell) to the endothelial cells that line the artery walls.33,34

These monocytes enter the blood vessel lining and develop into macrophages whose job is to engulf oxidized LDL cholesterol. Accumulation of oxidized LDL particles in the macrophage leads to the formation of foam cells.33,34

The accumulation of foam cells, along with the proliferation of smooth muscle cells and excess connective tissue, are key drivers of atherosclerosis.33,34

Foam cells play a central role in the inflammation that drives the atherosclerosis process.35

The average LDL cholesterol level dropped by 23.3% from its baseline value in the treatment group of those with LDL ≥190 mg/dL.

This 23.3% reduction is still a considerable distance from what is generally accepted as a healthy LDL range, which is below 100 mg/dL for primary prevention of cardiovascular disease in people with low risk.23

For people with high risk, such as individuals who have already suffered a cardiovascular event, some experts recommended that they achieve LDL levels below 70 mg/dL.24

If LDL cholesterol had been brought down even further in the patients in the 20-year study using pravastatin, the risk of cardiovascular events and all-cause mortality would likely have fallen with it.

It is important to note that these relatively recent studies were published after many decades of criticism were lodged against statin drugs.

No one questions the side effects statins can inflict. Much has to do with excess dosing and prescribing statins to patients who did not need them, and not advising patients to supplement with CoQ10 and vitamin K2.

Statins Improve Health Outcomes in US Veterans

A new study published in July 2020 in the Journal of the American Medical Association (JAMA) found that statin use was associated with substantial risk reduction in all-cause mortality.39

The study recruited 326,981 veterans with a mean age of 81 years and followed them for a mean of 6.8 years from a clinical visit.

Compared to non-statin drug users, statin use was associated with a 25% reduction in all-cause mortality, 20% reduction in cardiovascular mortality, and an 8% reduction in a composite of atherosclerotic cardiovascular events.

Multiple Risk Factors for Cardiovascular Disease

There are some patients with high LDL cholesterol who do not have cardiovascular disease, while some with lower cholesterol do have it. These paradoxical findings have led some to downplay the risks posed by elevated LDL cholesterol. However, this does not mean that cholesterol plays no role in cardiovascular disease.

People sometimes forget that there are multiple risk factors contributing to the threat of every illness, and cardiovascular disease is no exception.

Scientific data accumulated over decades demonstrate that excess LDL cholesterol is one of the primary culprits.6

Impact of Apolipoprotein B

Apolipoprotein B is found on all non-HDL-cholesterol-carrying lipoprotein particles, such as LDL and VLDL.25

High apolipoprotein B is a recognized marker for damage to arterial walls and risk of atherosclerosis. This is important because the basic laboratory tests for lipids, including LDL, HDL, and total cholesterol and triglycerides, often don’t give the full picture of cardiovascular disease risk.

Research on certain populations shows a correlation between maintaining lifetime low levels of apolipoprotein B and a roughly 90% decreased risk of coronary artery disease.26

Elevated apolipoprotein B is a more reliable marker for cardiovascular disease than LDL,HDL, and total cholesterol.6,27-29

Despite intensive educational efforts, apolipo-protein B blood tests are not routinely incorporated into primary care medicine. The tragic result is a failure to prevent heart attacks, strokes, and other occlusive arterial diseases.

For Life Extension® readers, this problem was resolved when apolipoprotein B was added to the comprehensive Male and Female Panel blood tests they undergo each year.


Published data define the importance of maintaining optimal LDL and HDL cholesterol levels to lower heart disease risk.

Statins can help keep cholesterol levels in optimal ranges in those for whom diet and lifestyle measures aren’t enough.

To achieve the most significant heart disease risk reduction, one must monitor and address every risk factor related to heart diseases. That includes testing for apolipoprotein B and other atherogenic risk factors.

Controlling the vascular damage created by elevated LDL cholesterol levels is challenging. Altering one’s diet to reduce excess saturated fat intake might enable a lower statin drug dose to achieve optimal cholesterol levels.4,36-38

Anyone using a statin must ensure their coenzyme Q10 levels are not compromised.

This can be achieved by taking 100-200 mg a day of CoQ10, preferably the ubiquinol form. CoQ10 should be taken with the heaviest meal of the day that contains some fat, to facilitate its absorption.

Those with heart failure usually need to take around 400 mg of ubiquinol a day to achieve optimal CoQ10 blood levels.

Recent data also point to the value of vitamin K2 use with statin drugs. For those interested in supplementing with vitamin K who are taking Coumadin® or Jantoven® (warfarin), please discuss with your doctor first. The box on the next page describes what some warfarin users are doing to supplement with low-dose vitamin K2 under physician supervision.

These steps can lessen the side effects of statins and help to lower the risk of cardiovascular disease.

Vitamin K Antagonists, Food Sources of Vitamin K, and INR Variability

Warfarin is a drug that inhibits unwanted coagulation by interfering with vitamin K activity in the liver.

A frequently encountered problem with patients prescribed warfarin, a vitamin K antagonist, is the variability of INR.

INR (international normalization ratio) is a measurement of warfarin’s effect upon the tendency of the blood to clot through the extrinsic clotting pathway. This can be due to variation of dietary intake of rich food sources of vitamin K (e.g. green leafy vegetables).

Too much vitamin K can diminish the anti-coagulant effects of warfarin and produce unstable INR measurements.

In patients receiving warfarin with a goal INR of 2-3, the addition of low-dose oral vitamin K supplementation may help increase INR stability.

Some published research suggests that low-dose (around 45 mcg) vitamin K may help improve the stability of INR measurements—however, such a strategy should only be contemplated after full discussion with a patient’s physician and frequent blood testing (to include INR) to assess for the intended effect (i.e. INR stability).

Warfarin users seeking more details about this should log on to:

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.


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