Which Supplements Are Good For Your Heart?

February 7, 2023 by Dr. Steve Chaney

How Should You Interpret This Study?

Author: Dr. Stephen Chaney

February 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?

This 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-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?

In 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.

Omega-3s:

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 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.

β-carotene:

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.

Can Diet Alter Your Genetic Destiny?

March 25, 2014 by Dr. Steve Chaney

Disease Is Not Inevitable

Author: Dr. Stephen Chaney

Many people seem to have the attitude that if obesity [or cancer, heart disease or diabetes] runs in their family, it is their destiny. They can’t really do anything about it, so why even try?

Most of us in the field of nutrition have felt for years that nothing could be further from the truth. But our belief was based on individual cases, not on solid science. That is no longer the case.

Recent scientific advances have given us solid proof that it is possible to alter our genetic destiny. A family predisposition to diabetes, for example, no longer dooms us to the same fate.

I’m not talking about something like the discredited Blood Type Diet. I’m talking about real science. Let me start by giving you an overview of the latest scientific advances.

Can Diet Alter Your Genetic Destiny?

The answer to this question is YES, and that answer lies in a relatively new scientific specialty called nutrigenomics – the interaction between nutrition and genetics. There are three ways in which nutrition and genetics interact:

1) Your genetic makeup can influence your nutrient requirements.

The best characterized example of this is methylene tetrahydrofolate reductase (MTHFR) deficiency. MTHFR deficiency increases the requirement for folic acid and is associated with neural tube defects and other neurological disorders, dementia, colon cancer & leukemia.

In spite of what some blogs and supplement manufacturers would have you believe, supplementation with around 400 IU of folic acid is usually sufficient to overcome the consequences of MTHFR deficiency. 5-methylene tetrahydrofolate (also sold as methyl folate or 5-methyl folate) offers no advantage in absorption, bioavailability or physiological activity (Clinical Pharmacokinetics, 49: 535-548, 2010; American Journal of Clinical Nutrition, 79: 473-478, 2004).

This is just one example. There are hundreds of other genetic variations that influence nutrient requirements – some known and some yet unknown.

2) A healthy diet can reduce your genetic predisposition for disease.

This perhaps the one that is easiest to understand. For conceptual purposes let us suppose that your genetic makeup were associated with high levels of inflammation. That would predispose you to heart disease, cancer and many other diseases. However, a diet rich in anti-inflammatory nutrients could reduce your risk of those diseases.

This is just a hypothetical example. I’ll give some specific examples in the paragraphs below.

3) Diet can actually alter your genes.

This is perhaps the most interesting scientific advance in recent years. We used to think that genes couldn’t be changed. What you inherited was what you got.

Now we know that both DNA and the proteins that coat the DNA can be modified, and those modifications alter how those genes are expressed. More importantly, we now know that those modifications can be inherited.

Perhaps the best characterized chemical modification of both DNA and proteins is something called methylation. Methylation influences gene expression and is, in turn, influenced by nutrients in the diet like folic acid, vitamin B12, vitamin B6, choline and the amino acid methionine.

Again this is just the “tip of the iceberg”. We are learning more about how diet can alter our genes every day.

Examples Of How Diet Can Alter Genetic Predisposition

Heart Disease

Perhaps the most impressive recent study is one that looked at the effect of diet on 20,000 people who had a genetic predisposition to heart disease (PLOS Medicine, October 2011, doi/10.1371/journal.pmed.1001106).

These people all had a genetic variant 9p21 that causes a 2 fold increased risk of heart attack. The study showed that a diet rich in fruits, vegetables and nuts reduced their risk of heart attack to that of the general population.

Another study, the Heart Outcomes Prevention Evaluation (HOPE) study (Diabetes Care, 27: 2767, 2004; Arteriosclerosis, Thrombosis and Vascular Biology, 24: 136, 2008), looked at genetic variations in the haptoglobin gene that influence cardiovascular risk. The haptoglobin 2-2 genotype increases oxidative damage to the arterial wall, which significantly increases the risk of cardiovascular disease.

When the authors of this study looked at the effect of vitamin E, they found that it significantly decreased heart attacks and cardiovascular deaths in people with the haptoglobin 2-2 genotype, but not in people with other haptoglobin geneotypes.

There was also a study called the ISOHEART study (American Journal of Clinical Nutrition, 82: 1260-1268, 2005; American Journal of Clinical Nutrition, 83: 592-600, 2006) that looked at a particular genetic variation in the estrogen receptor which increases inflammation and decreases levels of HDL. As you might expect, this genotype significantly increases cardiovascular risk.

Soy isoflavones significantly decreased inflammation and increased HDL levels in this population group. But they had no effect on inflammation or HDL levels in people with other genotypes affecting the estrogen reception.

To put this in perspective, these studies are fundamentally different from other studies you have heard about regarding nutritional interventions and heart disease risks. Those studies were looking at the effect of diet or supplementation in the general population.

These studies are looking at the effect of diet or supplementation in people who were genetically predisposed to heart disease. These studies show that genetic predisposition [to heart disease] does not have to be your destiny. You can change the outcome!

Cancer

A healthy diet (characterized by high intakes of vegetables, fruits, whole grain products and low intakes of refined grain products) compared with the standard American diet (characterized by high intakes of refined grain products, desserts, sweets and processed meats) results in a pattern of gene expression that is associated with lower risk of cancer. (Nutrition Journal, 2013 12:24).

A healthy lifestyle (low fat diet, stress management and exercise) in men with prostate cancer causes downregulation of genes associated with tumor growth (PNAS, 105: 8369-8374).

Sulforaphane, a nutrient found in broccoli, turns on genes that suppress cancer.

Diabetes

A study reported at the 2013 meeting of the European Association for the Study of Diabetes showed that regular exercise activated genes associated with a lower risk of type 2 diabetes

Cellular Stress Response

A diet rich in antioxidant fruits and vegetables activates the cellular stress response genes that protect us from DNA damage, inflammation and reactive oxygen species (BMC Medicine, 2010 8:54).

Resveratrol, a nutrient found in grape skins and red wine, activates genes associated with DNA repair and combating reactive oxygen species while it reduces the activity of genes associated with inflammation, increased blood pressure and cholesterol production.

To put these last three examples (cancer, diabetes and cellular stress response) in perspective, they show that diet and supplementation can alter gene expression – and that those alterations are likely to decrease disease risk.

Obesity

Finally, an animal study suggests that maternal obesity may increase the risk of obesity in the offspring by increasing their taste preference for foods with lots of sugar and fats (Endocrinology, 151: 475-464, 2010).

The Bottom Line:

The science of nutrigenomics tells us that diet and genetics interact in some important ways:

1) Your genetic makeup can influence your requirement for certain nutrients.

For example, methylene tetrahydrofolate reductase (MTHFR) deficiency increases your requirement for folic acid.

Contrary to what many blogs would have you believe, folic acid is just as effective as 5-methylene tetrahydrofolate (also sold as methyl folate or 5-methyl folate) at correcting MTHFR deficiency.

2) Healthy diet and lifestyle can overcome genetic predisposition to certain diseases. The best established example at present is for people genetically predisposed to heart disease, but preliminary evidence suggests that the risk of other diseases such as diabetes and cancer are altered by your diet.

3) Diet can actually alter gene expression – for better or worse depending on your diet. Those alterations not only affect your health, but they may affect your children’s health as well.

4) Nutrigenomics is a young science and many of the individual studies should be considered preliminary. However, the scientific backing is become stronger every day for what many experts in the field have believed for years.

“Your genes do not have to be your destiny. Healthy diet and lifestyle can overcome a genetic predisposition to many diseases.”

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 Selenium & Vitamin E Increase Prostate Cancer Risk?

March 11, 2014 by Dr. Steve Chaney

Should Men Avoid Those Supplements?

Author: Dr. Stephen Chaney

You’ve probably seen the headlines saying “Supplementation with selenium and vitamin E increases the risk of prostate cancer.” The authors of the study even said “Men aged greater than 55 should avoid supplements with either vitamin E or Se (selenium) at doses that exceed recommended dietary intakes.”

In a recent “Health Tips From The Professor” I debunked the headlines saying “Omega-3 fatty acids increase prostate cancer risk“.

What about vitamin E and selenium? Is it true that they increase prostate cancer risk? If you are a man over 55, should you be concerned? Should you stop using supplements containing vitamin E and selenium?

Do Selenium & Vitamin E Increase Prostate Cancer Risk?

Previous Studies On Selenium, Vitamin E And Prostate Cancer Risk

The study that generated the initial excitement in the field was the Nutrition Prevention of Cancer (NPC) Trial that ended in 1998 (Clark et al, British Journal of Urology, 81: 730-734, 1998; Duffield-Lillico et al, British Journal of Urology, 91: 608-612, 2003).

That study showed that supplementing men who had low blood levels of selenium with 200 ug/day of selenium decreased their prostate cancer risk by 65%.

It was followed by a second, much larger trial called the Selenium and Vitamin E Cancer Prevention Trial (SELECT) (Lipmann et al, JAMA, 301: 39-51, 2009). It looked at supplementation with 200 ug/day of selenium and/or 400 IU/day of synthetic alpha-tocopherol.

The SELECT study found no protective effect of either selenium or vitamin E on prostate cancer risk, but did suggest that vitamin E might actually cause a slight increase in prostate cancer risk.

The Study That Generated The Headlines

The authors of the study that generated the recent headlines (Kristal et al, Journal of the National Cancer Institute, doi: 10.1093/jnci/djt456, 2014) were attempting to find a simple explanation for the unexpected results of the SELECT study.

They hypothesized that the baseline selenium status at the beginning of the study might have influenced the outcome of supplementation. Kristal et al reanalyzed the data from the SELECT trial, comparing the effect of selenium and vitamin E supplementation in men with low selenium status and men with high selenium status.

However, at face value their data were confusing rather simplifying. They found:

Supplementation with selenium had no effect on prostate cancer risk in men with low selenium status, but increased prostate cancer risk by 91% in men with high selenium status.

Conversely, supplementation with 400 IU of vitamin E had no effect on prostate cancer risk in men with high selenium status, but increased prostate cancer risk by 63% in men with low selenium status.

Based on this hodge-podge of data, they concluded that “Men aged greater than 55 should avoid supplements with either vitamin E or Se (selenium) at doses that exceed recommended dietary intakes.” That was the statement that generated the headlines. Was that recommendation justified?

What Do Other Experts Say?

There was an editorial evaluation of the paper by some of the top expects in the field in the same journal (Frankel et al, Journal of the National Cancer Institute, doi: 10.1093/jnci/dju005, 2014) that provided thoughtful explanations of the confusing data in the paper by Kristal et al. They examined three questions:

1) Why did the SELECT study find no effect of selenium supplementation in men with low selenium status, while the earlier NPC trial found a 65% decrease in prostate cancer risk?

The authors of the editorial pointed out that the lowest baseline selenium status in the SELECT trial was much higher than the lowest baseline selenium status in the previous NPC trial. In fact the baseline selenium status in the SELECT trial was at a level in which no effect of selenium supplementation would have been expected based on the results from the NPC trial.

The authors speculated that the addition of selenized yeast to animal feed has improved selenium status in the US population to the point where selenium supplementation can no longer be expected to reduce prostate cancer risk.

2) Why did selenium supplementation increase prostate cancer risk in men with high selenium status, but not in men with low selenium status?

The authors pointed out that for selenium there is a very narrow range between sufficient intake and toxicity. The daily value (DV) for selenium is 90 ug/day and the recommended upper limit (UL) for selenium intake is 400 ug/day.

The average selenium intake for adult men in this country is 151 ug/day. That’s just the average. It’s not hard to imagine that adding 200ug/day of selenium to men at the highest selenium intake could move them into the toxic range.

3) Why did vitamin E supplementation increase prostate cancer risk in men with low selenium status, but not in men with high selenium status?

In part, the authors felt that the pure alpha-tocopherol used in the SELECT trial was not optimal. Pure alpha-tocopherol interferes with the absorption of the other naturally occurring forms of vitamin E, such as gamma-tocopherol – which is the form of vitamin E that decreases prostate cancer risk in animal studies.

The authors also noted that vitamin E and selenium work together to inactivate free radicals in cell membranes. Vitamin E reduces the free radicals to a chemically unstable intermediate that still has the potential to damage membranes. A selenium-containing enzyme is required to convert that unstable intermediate into a completely harmless compound.

So when vitamin E is present in much higher levels than selenium, as it was in the group with low baseline selenium status, unstable radicals can accumulate and membrane damage can occur. The authors felt that this was the most likely explanation of the increased prostate cancer risk when men with low selenium status were supplemented with high dose vitamin E.

The authors of the editorial had a much more nuanced interpretation of the data reported by Kristal et al. If you read their evaluation carefully you would likely conclude that you should avoid high dose selenium supplements. However, rather than simply avoiding vitamin E supplements, you should choose vitamin E supplements that contain all of the naturally occurring vitamin E forms and contain near DV amounts of selenium.

These recommendations would be a much better fit to the data, but don’t lend themselves to dramatic headlines – so the editorial has been largely ignored by the press.

The Bottom Line:

1) Ignore the scary headlines about selenium and vitamin E causing prostate cancer. You can continue to use your supplements as long as you choose ones that are well balanced.

2) Conversely, if you are at risk of prostate cancer, there is no good evidence that supplementation with either selenium or vitamin E will reduce your risk.

3) The results of this study are fully consistent with my longstanding recommendation to follow a holistic approach to supplementation and to avoid high dose single nutrient supplements.

4) There is no reason to supplement with 200 ug/day of selenium. If you are already getting good amounts of selenium from your diet, that dosage could be toxic and may actually increase your risk of cancer. Make sure that your supplements have no more than the DV (70 ug) of selenium.

5) Avoid high purity alpha-tocopherol supplements. Look for vitamin E supplements containing the full spectrum of tocopherols and tocotrienols in addition to alpha-tocopherol. In addition, make sure that your vitamin E supplement also contains selenium at near DV levels.

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.

Are Multivitamins A Waste Of Money?

December 24, 2013 by Dr. Steve Chaney

Don’t Throw Your Vitamins Away Yet

Author: Dr. Stephen Chaney

The Professor is annoyed. Two things really irritate me:

Charlatans who cherry pick studies to “prove” that their snake oil supplements will cure what ails you.
Doctors who proclaim that vitamins are a waste of money without understanding the science behind the studies they are quoting.

Are Multivitamins A Waste Of Money?

You’ve seen the headlines telling you that “the experts” have concluded that multivitamins are a waste of money. You might be wondering “What’s behind these headlines? Who are these experts, and what is their evidence?”

Let’s start at the beginning. The article (Gualler et al., Annals of Internal Medicine, 159: 850-851, 2013) that generated all of the headlines was an editorial, which means it is an opinion piece, not a scientific study. It represents the opinion of five very prominent doctors, but it is, at the end of the day, just their opinion. Many other well respected experts disagree with their opinion.

They based their editorial on three recently published studies:

The first study reported that vitamin and mineral supplements did not decrease the risk of heart disease and cancer in healthy individuals (Fortmann et al., Annals of Internal Medicine, 159, doi: 10.7326/003-4815-159-12-201312170-00729)

The second study reported that multivitamins did not affect cognitive function in healthy male physicians aged 65 and older (Gradstein et al, Annals of Internal Medicine, 159, 806-814, 2013)

The third study concluded that multivitamins did not reduce the risk of a second heart attack in patients who had previously had a heart attack and were receiving appropriate medical therapy.

These were all large, well designed studies, so it would be tempting to conclude that the headlines were right. Maybe vitamins are a waste of money.

But, what if the whole underlying premise of these studies was flawed? Let’s examine that possibility by examining the flawed premises behind these and other studies.

What’s Wrong With These Studies?

#1) These studies were too narrowly focused.

Multivitamins and individual vitamins and minerals are not magic bullets. They are not drugs. They are meant to fill nutritional gaps in our diet – not prevent or cure disease. We should be asking whether holistic approaches can prevent or cure disease – not whether individual nutrients can do so.

One of the examples that I love to use, because it really made an impression on me as a young scientist, occurred at an International Cancer Symposium I attended more than 30 years ago. I attended a session in which an internally renowned expert was giving his talk on colon cancer. He said, “I can show you, unequivocally, that colon cancer risk is significantly decreased by a lifestyle that includes a high-fiber diet, a low-fat diet, adequate calcium, adequate B-vitamins, exercise and weight control. But I can’t show you that any one of them, by themselves, is effective.”

The question that came to me as I heard him speak was: “What’s the message that a responsible scientist or responsible health professional should be giving to their patients or the people that they’re advising?” You’ve probably heard experts saying:

“Don’t worry about the fat content of your diet. It can’t be shown to increase the risk of colon cancer.”
“Don’t worry about calcium. It doesn’t decrease the risk of colon cancer”
“Don’t worry about B-vitamins. They don’t decrease the risk”
“Don’t worry about fiber. It can’t be shown to decrease the risk either”

But, is that the message that we should be giving people – that nothing matters? Shouldn’t we really be saying what that doctor said many years ago – that a lifestyle that includes all of those things significantly decreases the risk of colon cancer?

#2) These studies were destined to fail.

It’s almost impossible to prove that any single intervention prevents disease when you are starting with a healthy population (something we scientists refer to as a primary prevention study).

For example, in “Health Tips From the Professor” just a couple of weeks ago I shared with you that even when you combine all of the published studies with tens of thousands of patients, it is impossible to prove that stain drugs prevent heart attacks in healthy individuals.

If you can’t show that statins prevent heart disease in healthy people, why would you expect to be able to show that vitamins or minerals prevent heart attacks in healthy people?

I can’t resist pointing out that this perfectly illustrates the pro-drug, anti-supplement bias that is so prevalent among many of my medical colleagues. I haven’t seen a single editorial or headline suggesting that statin drugs might be a waste of money for healthy individuals.

#3) These studies simply asked the wrong questions.

For example, the third study described in the editorial was asking whether multivitamins reduced the risk of a second heart attack in patients who were receiving “appropriate medical therapy”. What does “appropriate medical therapy” mean, you might ask? It means that those patients were on 4 or 5 drugs, with all of their side effects.

In reality the study was not asking whether multivitamins reduced the risk of a second heart attack. The study asked whether multivitamins had any additional benefits for individuals who were taking 4 or 5 drugs to reduce their risk of a second heart attack. That’s a totally different question.

There are lots of examples of this paradigm. For example, 17 years ago the Cambridge Heart Antioxidant Study showed that vitamin E significant decreased heart attack risk in patients with severe cardiovascular disease (Stephens et al, The Lancet, 347: 781-786, 1996). Patients in that study were taking one or two medications. However, in today’s world that would be considered unethical. The standard medical treatment for high risk heart disease patients today is 4 or 5 drugs, and when patients are receiving that many medications it is no longer possible to demonstrate a benefit of vitamin E. The story is similar for omega-3 fatty acids.

That poses a dilemma. What recent studies show is that individual nutrients don’t reduce the risk of a second heart attack in someone who is receiving “standard of care” medical treatment.

But that’s not the question I am interested in. I’d like to know whether natural approaches might be just as effective as the drugs or whether natural approaches might allow one to use fewer drugs or lower doses. I’d like to avoid all of the side effects of those drugs if I could.

What about you? What questions would you like answered? Do these studies answer those questions?

What Was Overlooked In Those Studies

The studies did show conclusively that there were no harmful effects from supplementing except for high dose beta-carotene in smokers. Somehow that information never made it into the headlines.

The Bottom Line

Don’t pay much attention to the reports that supplements don’t work and are a waste of money. Those studies are fundamentally flawed.

Don’t pay much attention to the reports claiming that vitamins will hurt you. Except for beta-carotene in smokers the latest studies showed no evidence of harm.

On the other hand, don’t expect miracles from your vitamins. If you spend your time sitting in front of the TV set eating pizza & drinking sodas, popping a vitamin pill won’t prevent much of anything.

Finally, holistic approaches are often as effective as drug therapy – without the side effects. Your vitamins can be an important part of a holistic approach to better health that includes weight control, a good diet and exercise.

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.

Are Cholesterol Lowering Drugs Right For You?

January 11, 2023November 19, 2013 by Dr. Steve Chaney

Do Statins Really Work?

Author: Dr. Stephen Chaney

Statins – those ubiquitous drugs used to lower cholesterol levels – are big business!

Over 20 million Americans are currently being treated with statin drugs at a cost that runs into billions of dollars every year. And cardiologists have just recommended that another 20 million Americans consider using cholesterol lowering drugs. 44% of the men and 22% of the women in this country are now being told that they should be using statin drugs.

Some of my cardiologist friends are so convinced that statin drugs prevent death from heart attacks that they have said, only half-joking, that we should just add statins to the water supply.

Are Cholesterol-Lowering Drugs Right For You?

Is the faith of doctors in the power of statin drugs to prevent death from heart disease justified? To answer that question in full we need to look at people who have already survived a heart attack and people who have never had a heart attack separately.

If you’ve already had a heart attack the evidence is clear cut.

If you have had a heart attack, there is good evidence that statins will reduce your risk of dying from a second heart attack.

In the technical jargon of the scientific world that is referred to as secondary prevention.

But what about those millions of Americans who are being prescribed statin drugs who have never had a heart attack? This is something we scientists refer to as primary prevention.

What Do The Studies Actually Say About Statins And Primary Prevention?

Here the evidence is not clear at all. Two major reports have cast doubt on the assumption that statins actually do prevent heart attacks in people who have not already had a first heart attack.

In the first study, Dr. Kausik Ray and colleagues from Cambridge University in England performed a meta-analyis of 11 clinical studies involving over 65,000 participants (Ray et al, Arch. Int. Med., 170: 1024-1031, 2010). They focused on those participants in the studies who had not previously had a heart attack (primary prevention).

They found that the use of statins over an average of 3.7 years had no statistically significant effect on mortality. In short, statins had no effect on the risk of dying from heart disease or any other cause.

Dr. Sreenivasa Sechasai, one of the doctors involved in the study, said “We didn’t find a significant reduction in death despite having such a huge sample size. This is the totality of evidence in primary prevention. So if we can’t show a reduction with this data, it is unlikely to be there.”

The second study was a Cochrane Systemic Review of statins published January 19th, 2011. It stated that there was not enough scientific evidence to recommend the use of statins in people with no previous history of heart disease with some caveats (see below).

To help you understand the significance of that conclusion, let me give you a bit of background:

First you need to understand that the Cochrane Collaboration is an independent, non-profit organization that carefully reviews the scientific evidence behind medical treatments and proposed medical treatments.

Cochrane Reviews are considered the “Holy Grail” of evidence-based medicine (ie. medicine based on the best scientific evidence rather than what the pharmaceutical companies would have you believe).

So when a Cochrane Review concludes that there isn’t enough evidence to recommend use of statins in patients with no prior history of heart disease that is pretty big news in the medical world.

How Should These Studies Be Interpreted?

Please don’t misinterpret what I am saying. The Cochrane Review said that statin drugs are overprescribed, but it did not say that everyone who has not had a heart attack will not benefit from statins. It said that there are a number of risk factors that need to be considered in evaluating individual patients for statin use.

Simply put, that means that it is not as simple as saying that everyone with no previous history of heart disease should not be on statin drugs.

If you are currently taking statin drugs and you have no previous history of heart disease, you may want to discuss with your physician whether the Cochrane Review of statin drugs changes their opinion of whether se of those drugs is still warranted for you.

But the bottom line is that only your physician is trained to take into account all of the factors that increase your risk of heart disease and the best therapeutic approach for reducing your risk of heart attack.

There Is A Double Standard In The Medical Community

More importantly, these studies highlight the difficulty in showing that anything works when you start out with a healthy group of adults with no prior evidence of disease (primary prevention).

And, the way that doctors have responded to primary prevention studies shows that there is a double standard in how primary prevention trials are interpreted in the medical community. For example:

There is no good evidence that statins prevent fatal heart attacks in healthy people.

However, because statins do work in high risk patients, most doctors recommend their use by millions of Americans who have never had a heart attack.

There is also no good evidence that nutrients like vitamin E and omega-3 fatty acids prevent fatal heart attacks in healthy people.

However, there is evidence that both vitamin E and omega-3 fatty acids prevent heart attacks in high risk patients, yet most doctors will tell you they are a waste of money.

It is food for thought.

The Bottom Line

1) Statin drugs clearly save lives when used by people who have already had a heart attack.

2) On the other hand, there is no proof that statin drugs prevent heart attacks in people who have not previously had a heart attack

3) Statin drugs do have side effects. Increased risk of diabetes, liver damage, muscle damage and kidney failure are the best documented, although memory loss has also been reported.

4) I am not recommending that you stop using statin drugs without consulting your doctor. I am suggesting that you discuss the benefits and risks of statin drug use with your doctor.

5) Perhaps the most important poin tto come out of these studies is that it almost impossible to prove the benefit of any intervention in a primary prevention trial. If you can’t prove that statins work in healthy people, it is not surprising that it is difficult to prove that other interventions work.

6) Finally, the way that these studies have been interpreted shows that there is a clear double standard in how the medical community evaluates primary intervention trials.

Statin drugs don’t show any benefit in a primary prevention setting, yet most doctors still recommend them.

Vitamin E and omega-3 fatty acids don’t show any benefit in a primary prevention setting, and most doctors recommend against them.

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.