Which Supplements Are Good For Your Heart?

How Should You Interpret This Study? 

Author: Dr. Stephen Chaney 

strong heartFebruary is Heart Health month. So, it is fitting that we ask, “What is the status of heart health in this country?” The American Heart Association just published an update of heart health statistics through 2019 (CW Tsao et al, Circulation, 145: e153-e639, 2022). And the statistics aren’t encouraging. [Note: The American Heart Association only reported statistics through 2019 because the COVID-19 pandemic significantly skewed the statistics in 2020 and 2021].

The Good News is that between 2009 and 2019:

  • All heart disease deaths have decreased by 25%.
  • Heart attack deaths have decreased by 6.6%.
  • Stroke deaths have decreased by 6%.

The Bad News is that:

  • Heart disease is still the leading cause of death in this country.
  • Someone dies from a heart attack every 40 seconds.
  • Someone dies from a stroke every 3 minutes.

Diet, exercise, and weight control play a major role in reducing the risk of heart disease. Best of all, they have no side effects. They represent a risk-free approach that each of us can control.

But is there something else? Could supplements play a role? Are supplements hype or hope for a healthy heart?

All the Dr. Strangeloves in the nutrition space have their favorite heart health supplements. They claim their supplements will single-handedly abolish heart disease (and help you leap tall buildings in a single bound).

On the other hand, many doctors will tell you these supplements are a waste of money. They don’t work. They just drain your wallet.

It’s so confusing. Who should you believe? Fortunately, a recent study (P An et al, Journal of the American College of Cardiology, 80: 2269-2285, 2022) has separated the hype from the hope and tells us which “heart-healthy” supplements work, and which don’t.

How Was This Study Done?

Clinical StudyThis was a major clinical study carried out by researchers from the China Agricultural University and Brown University in the US. It was a meta-analysis, which means it combined the data from many published clinical trials.

The investigators searched three major databases of clinical trials to identify:

  • 884 randomized, placebo-controlled clinical studies…
  • Of 27 types of micronutrients…
  • With a total of 883,627 patients…
  • Looking at the effectiveness of micronutrient supplementation lasting an average of 3 years on either…
    • Cardiovascular risk factors like blood pressure, total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides…or…
    • Cardiovascular outcomes such as coronary heart disease (CHD), heart attacks, strokes, and deaths due to cardiovascular disease (CVD) and all causes.

[Note: Coronary heart disease (CHD) refers to build up of plaque in the coronary arteries (the arteries leading to the heart). It is often referred to as heart disease and can lead to heart attacks (myocardial infarction). Cardiovascular disease (CVD) is a more inclusive term that includes coronary heart disease, stroke, congenital heart defects, and peripheral artery disease.]

The investigators also included an analysis of the quality of the data in each of the clinical studies and rated the evidence of each of their findings as high quality, moderate quality, or low quality.

Which Supplements Are Good For Your Heart?

The top 3 heart-healthy supplements in this study were:

Omega-3s And Heart DiseaseOmega-3 Fatty Acids:

  • Increased HDL cholesterol and decreased triglycerides, both favorable risk factors for heart health.
  • Deceased risk of heart attacks by 15%, all CHD events by 14%, and CVD deaths by 7% (see definitions of CHD and CVD above).
  • The median dose of omega-3 fatty acids in these studies was 1.8 g/day.
  • The evidence was moderate quality for all these findings.

Folic Acid:

  • Decreased LDL cholesterol (moderate quality evidence) and decreased blood pressure and total cholesterol (low quality evidence).
  • Decreased stroke risk by 16% (moderate quality evidence).

Coenzyme Q10:

  • Decreased triglycerides (high quality evidence) and reduced blood pressure (low quality evidence).
  • Decreased the risk of all-cause mortality by 32% (moderate quality evidence).
  • These studies were performed with patients diagnosed with heart failure. Coenzyme Q10 is often recommended for these patients, so the studies were likely performed to test the efficacy of this treatment.

There were three micronutrients (vitamin C, vitamin E, and vitamin D) that did not appear to affect heart disease outcomes.

Finally, as reported in previous studies, β-carotene increased the risk of stroke, CVD mortality, and all-cause mortality.

In terms of the question I asked at the beginning of this article, this study concluded that:

  • Omega-3, folic acid, and coenzyme Q10 supplements represent hope for a healthy heart.
  • Vitamin C, vitamin E, and vitamin D supplements represent hype for a healthy heart.
  • β-carotene supplements represent danger for a healthy heart.

But these conclusions just scratch the surface. To put them into perspective we need to dig a bit deeper.

How Should You Interpret This Study?

Question MarkIn evaluating the significance of these findings there are two things to keep in mind.

#1: This study is a meta-analysis and meta-analyses have both strengths and weaknesses.

The strength of meta-analyses is that by combining multiple clinical studies they can end up with a database containing 100s of thousands of subjects. This allows them to do two things:

  • It allows the meta-analysis to detect statistically significant effects that might be too small to detect in an individual study.
  • It allows the meta-analysis to detect the average effect of all the clinical studies it includes.

The weakness of meta-analyses is that the design of individual studies included in the analysis varies greatly. The individual studies vary in things like dose, duration, type of subjects included in the study, and much more.

This is why this study rated most of their conclusions as backed by moderate- or low-quality evidence. [Note: The fact that the authors evaluated the quality of evidence is a strength of this study. Most meta-analyses just report their conclusions without telling you how strong the evidence behind those conclusions is.]

#2: Most clinical studies of supplements (including those included in this meta-analysis) have two significant weaknesses.

  • Most studies do not measure the nutritional status of their subjects prior to adding the supplement. If their nutritional status for a particular nutrient was already optimal, there is no reason to expect more of that nutrient to provide any benefit.
  • Most studies measure the effect of a supplement on a cross-section of the population without asking who would be most likely to benefit.

You would almost never design a clinical study that way if you were evaluating the effectiveness of a potential drug. So, why would you design clinical studies of supplements that way?

With these considerations in mind, let me provide some perspective on the conclusions of this study.

Coenzyme Q10:

This meta-analysis found that coenzyme Q10 significantly reduced all-cause mortality in patients with heart failure. This is consistent with multiple clinical studies and a recent Cochrane Collaboration review.

Does coenzyme Q10 have any heart health benefits for people without congestive heart failure? There is no direct evidence that it does, but let me offer an analogy with statin drugs.

Statin drugs are very effective at reducing heart attacks in high-risk patients. But they have no detectable effect on heart attacks in low-risk patients. However, this has not stopped the medical profession from recommending statins for millions of low-risk patients. The rationale is that if they are so clearly beneficial in high-risk patients, they are “probably” beneficial in low-risk patients.

I would argue a similar rationale should apply to supplements like coenzyme Q10.


This study found that omega-3 reduced both heart attacks and the risk of dying from heart disease. Most previous meta-analyses of omega-3s and heart disease have come to the same conclusion. However, some meta-analyses have failed to find any heart health benefits of omega-3s. Unfortunately, this has allowed both proponents and opponents of omega-3 use for heart health to quote studies supporting their viewpoint.

However, there is one meta-analysis that stands out from all the others. A group of 17 scientists from across the globe collaborated in developing a “best practices” experimental design protocol for assessing the effect of omega-3 supplementation on heart health. They conducted their clinical studies independently, and when their data (from 42,000 subjects) were pooled, the results showed that omega-3 supplementation decreased:

  • Premature death from all causes by 16%.
  • Premature death from heart disease by 19%.
  • Premature death from cancer by 15%.
  • Premature death from causes other than heart disease and cancer by 18%.

This study eliminates the limitations of previous meta-analyses. That makes it much stronger than the other meta-analyses. And these results are consistent with the current meta-analysis.

Omega-3s have long been recognized as essential nutrients. It is past time to set Daily Value (DV) recommendations for omega-3s. Based on the recommendations of other experts in the field, I think the DV should be set at 500-1,000 mg/day. I take more than that, but this would represent a good minimum recommendation for heart health.

folic acidFolic acid:

As with omega-3s, this meta-analysis reported a positive effect of folic acid on heart health. But many other studies have come up empty. Why is that?

It may be because, between food fortification and multivitamin use, many Americans already have sufficient blood levels of folic acid. For example, one study reported that 70% of the subjects in their study had optimal levels of folates in their blood. And that study also reported:

  • Subjects with adequate levels of folates in their blood received no additional benefit from folic acid supplementation.
  • However, for subjects with inadequate blood folate levels, folic acid supplementation decreased their risk of heart disease by ~15%.

We see this pattern over and over in supplement studies. Supplement opponents interpret these studies as showing that supplements are worthless. But a better interpretation is that supplements benefit those who need them.

The problem is that we don’t know our blood levels of essential nutrients. We don’t know which nutrients we need, and which we don’t. That’s why I like to think of supplements as “insurance” against the effects of an imperfect diet.

Vitamins E and D:

The situation with vitamins E and D is similar. This meta-analysis found no heart health benefit of either vitamin E or D. That is because the clinical studies included in the meta-analysis asked whether vitamin E or vitamin D improved heart health for everyone in the study.

Previous studies focusing on patients with low blood levels of these nutrients and/or at high risk of heart disease have shown some benefits of both vitamins at reducing heart disease risk.

So, for folic acid, vitamin E, and vitamin D (and possibly vitamin C) the take-home message should be:

  • Ignore all the Dr. Strangeloves telling you that these vitamins are “magic bullets” that will dramatically reduce your risk of heart disease.
  • Ignore the naysayers who tell you they are worthless.
  • Use supplementation wisely to make sure you have the recommended intake of these and other essential nutrients.


This meta-analysis reported that β-carotene increased the risk of heart disease. This is not a new finding. Multiple previous studies have come to the same conclusion.

And we know why this is. There are many naturally occurring carotenoids, and they each have unique heart health benefits. A high dose β-carotene supplement interferes with the absorption of the other carotenoids. You are creating a deficiency of other heart-healthy carotenoids.

If you are not getting lots of colorful fruits and vegetables from your diet, my recommendation is to choose a supplement with all the naturally occurring carotenoids in balance – not a pure β-carotene supplement.

The Bottom Line 

The Dr. Strangeloves in the nutrition space all have their favorite heart health supplements. They claim their supplements will single-handedly abolish heart disease (and help you leap tall buildings in a single bound).

On the other hand, many doctors will tell you these supplements are a waste of money. They don’t work. They just drain your wallet.

It’s so confusing. Who should you believe? Fortunately, a recent study has separated the hype from the hope and tells us which “heart-healthy” supplements work, and which don’t.

This study was a meta-analysis of 884 clinical studies with 883,627 participants. It reported:

  • Omega-3 supplementation deceased risk of heart attacks by 15% and all cardiovascular deaths by 7%.
  • Folic acid supplementation decreased stroke risk by 16%.
  • Coenzyme Q10 supplementation decreased the risk of all-cause mortality in patients with heart failure by 32%.
  • Vitamin C, vitamin E, vitamin D did not appear to affect heart disease outcomes.
  • β-carotene increased the risk of stroke, CVD mortality, and all-cause mortality.

For more details on this study and what it means for you, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

Do Statins Decrease Or Increase The Risk Of Parkinson’s Disease?

The Fine Print Behind The Misleading Headline

 Author: Dr. Stephen Chaney

 Human NeuronsI hadn’t paid much attention to the headlines saying “Statin Use May Decrease Parkinson’s Risk” until the other day when I happened to glance a couple of lines below the headline and spotted a statement saying “Study Shows That Discontinuation of Statin Therapy Increases Risk of Parkinson’s”.

 I immediately said to myself “That’s bizarre. There is a total disconnect between the headlines and the study.” If you really wanted to determine whether statin use reduced the risk of Parkinson’s, you would compare the incidence of Parkinson’s disease in a group of statin users and a matched group who did not use statins.

It turns out those studies have been done, and they were inconclusive – some studies showed a slight increase in Parkinson’s in statin users, some showed a slight decrease, and most showed no correlation between statin use and Parkinson’s.

In that context, this study could equally well have been interpreted as suggesting that statin use increased the risk of Parkinson’s, but somehow none of the headlines mentioned that possibility.

Are Both Possibilities Plausible?

 Let’s look at each possibility in detail. The reasoning is complex, but let me try to walk you through it.

 Could Statins Decrease The Risk Of Parkinson’s

 Parkinson’s is caused by the progressive degeneration of the brain neurons that produce a chemical messenger called dopamine that controls muscle movement. However, the causes of nerve degeneration in Parkinson’s patients are largely unknown.

Genetics may play a small role. Environmental toxins may play a role. But most experts feel that Parkinson’s patients produce an excess of free radicals, and it is the oxidative damage caused by those free radicals that results in the loss of the ability of neurons to produce dopamine.

But even that is not the whole answer. The brain is normally able to use coenzyme Q10, which is very abundant in brain, and other antioxidants to destroy free radicals before they damage brain neurons. Somehow in Parkinson’s patients free radical production and antioxidant production have gotten out of balance.

Advocates of the theory that statins may decrease the risk of Parkinson’s, point out that statins decrease oxidative damage. So if a person was predisposed to developing Parkinson’s and oxidative damage is a major cause of Parkinson’s, it is theoretically possible that statins could slow the progression to Parkinson’s while they were taking the drug. Of course, once they stopped taking the drug the oxidative damage to dopamine-producing neurons would resume and Parkinson’s would eventually develop.

In this model- Let’s call it Model A:

1)     Oxidative damage of dopamine-producing neurons was caused by some unspecified external agent.

2)     Statins protected the neurons from oxidative damage while they were being used.

3)     Once the statin drugs were discontinued oxidative damage resumed and the risk of developing Parkinson’s increased.

This is the model favored by the authors and repeated in all of the headlines you saw.

Could Statins Increase The Risk Of Parkinson’s?

Statins also interfere with the synthesis of cholesterol and coenzyme Q10, and these are both absolutely essential for brain function. Let’s start with cholesterol:

  •  20% of the body’s membrane cholesterol is found in the myelin sheath that coats the brain’s neurons (You can think of the myelin sheath as analogous to the plastic coating that insulates an electrical wire).
  • Cholesterol can’t cross the blood-brain barrier, which means that the brain cannot utilize cholesterol from the bloodstream . It has to make its own cholesterol.

As for coenzyme Q10:

  • It is not only a powerful antioxidant. It is also absolutely essential for cellular energy production.
  • The brain has tremendous energy requirements. The brain accounts for 20% of the energy utilization of our body. Neurons burn 2 times more energy than other cells in our body.

For both of these reasons, many experts have cautioned that statin drugs have the potential to cause neurodegenerative diseases such as Parkinson’s.  In this model – Lets call it model B:

1)     The statin drugs themselves are damaging the dopamine-producing neurons by inhibiting cholesterol and coenzyme Q10 synthesis in the brain.

2)     The antioxidant effects of the statin drugs were masking the damage caused by the statins while the drugs were being used.

3)     Once the statin drugs were discontinued the underlying damage was unmasked and the patients quickly developed Parkinson’s.

What Did The Study Actually Show?

The study (Lee et al, Neurology, 81: 410-416, 2013) looked at 43,810 statin users on the island of Taiwan. The Taiwanese Health System keeps extensive records of prescription use and health conditions of everyone on the island. It also requires that statin use be discontinued as soon as the patient reach their target of < 100 mg/dL LDL cholesterol, so they had the perfect population base to study what happens when you discontinue statin therapy.

The results were:

  • The patients who discontinued statin therapy were 42% less likely to develop Parkinson’s that those who continued on statin therapy. That result is consistent with both models A & B.
  • The increased risk of developing Parkinson’s when the drug was discontinued was only seen for the statin drugs like simvastatin and atorvastatin that are able to cross the blood brain barrier. That result is actually a bit more consistent with model B (Remember that the brain has to be able to make its own cholesterol and statins block cholesterol production).
  • When the study compared people using statin drugs to those not using statin drugs there was no significant difference in the prevalence of Parkinson’s – even for those statin drugs that cross the blood brain barrier. That means that merely being on a statin drug did not influence the risk of developing Parkinson’s. It was only when patients were on statin drugs for a period of time and were subsequently taken off statins that the risk of developing Parkinson’s was affected – and the effect was to increase risk! In the context of the first two findings, that result is also a bit more consistent with model B.

The Bottom Line:

If I were writing one of those medical blogs, I would have probably have gone with the party line and told you that statins decrease your risk of developing Parkinson’s. And if I were one of those health bloggers who never let the facts get in the way of a good story, I’d probably be scaring you with headlines saying that statins increase your risk of Parkinson’s.

But, I’m a scientist. I actually read the article, and I tell it to you like it is. Here’s your bottom line.

1)     Ignore the headlines. The study they are talking about can’t distinguish between statins increasing or decreasing the risk of Parkinson’s. Don’t let anyone tell you that reducing the risk of Parkinson’s is a side benefit of statin therapy. That simply has not been proven.

2)     The study does clearly show that discontinuing the statin drugs simvastatin and atorvastatin is associated with increased risk of developing Parkinson’s. That’s a big red flag for me, because 53% of patients discontinue statin therapy because of side effects, cost or other reasons.

3)     However, statin drugs do save lives, especially for people who have already had a heart attack, so talk with your doctor about the benefits and risks of statin drugs, and which statin drugs are best for you.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Health Tips From The Professor