Is Erythritol Bad For Your Heart?

March 28, 2023 by Dr. Steve Chaney

Who Should Be Concerned About Erythritol Intake?

Author: Dr. Stephen Chaney

Everyone is searching for the perfect sweetener. And if you were in the marketing department of Big Food Inc, the perfect sweetener would be defined as:

Natural, meaning that it is found in fruits, vegetables, or other plant foods.

Low in calories. Of course, a perfect sweetener would have zero calories because it is not metabolized in our bodies.

Low glycemic, meaning that it would have a minimal effect on blood sugar levels. Once again, a perfect sweetener would have zero effect on blood sugar levels.

Safe, meaning that it has no adverse effects on our health.

Sugar alcohols appear to meet all these criteria, so they have become the sweetener of choice for lots of highly processed foods. This is especially true for the sugar alcohol, erythritol, since it is currently the least expensive of the sugar alcohols.

So, a recent study (M Witowski et al, Nature Medicine, 2023) suggesting that erythritol might increase the risk of heart disease was quite surprising.

This is the first study to suggest a link between erythritol and heart disease, and it was a flawed study (I will discuss the flaws below).

Reputable scientists don’t put much credence in a weak first study like this one. We generally consider the conclusions of a first study like this one to be an unproven hypothesis at this point.

But we are cautious. There will be many follow-up, better designed studies, to test this hypothesis. Once these studies have been published, the scientific community will look at all the evidence and either issue a warning or conclude that there is no reason for concern.

But that doesn’t stop the Dr. Strangeloves of the world from warning you of the “dangers” of erythritol and telling you to avoid it at all costs.

For that reason, I felt it was appropriate to address this issue. I will:

Describe the study and its flaws.

Put the study into the broader perspective of what we know about sweeteners.

Identify the two population groups who should be most concerned about erythritol.

How Was The Study Done And What Did It Show?

This study can be divided into three parts.

#1: An Association Between Erythritol Blood Levels And Heart Disease.

There were three separate experiments included in this section of the study. In each experiment patients were recruited after visiting cardiac clinics for diagnostic procedures. The average age of these patients was 67 and 45% of them already had experienced a non-fatal heart attack prior to the study. In other words, these were all older patients with pre-existing heart disease who were at high risk of heart attack or stroke in the near future.

The first study was a metabolomic study. In simple terms this means that high-tech equipment and computing were used to measure hundreds of metabolites in the blood of the patients and, in this case, correlate each of them with the occurrence of heart attacks and strokes over the next three years.

This study identified 16 sugar alcohols and related metabolites in the blood of these patients that were associated with an increased risk of heart attack and stroke. (I will discuss the significance of this observation in more detail later.)

Because erythritol was among the top 6 compounds in terms of association with increased heart attack and stroke risk, and erythritol is the most commonly used sugar alcohol in processed foods, the next two studies focused on the association between blood levels of erythritol and heart attack/stroke risk. Their results were predictable.

High blood levels of erythritol were associated with an increased risk of heart attack and stroke over the next three years.

Flaws In This Portion Of The Study:

As the authors of the study pointed out, these studies were done with older patients with pre-existing heart disease who were at high risk of heart attack or stroke. They acknowledged that it is not known whether these associations exist with younger, healthier patients.

As the authors also pointed out, these are associations. They do not prove cause and effect. In particular, the studies did not measure the diet, exercise habits, and other lifestyle factors of these patients that may have contributed to their increased risk of heart attack and stroke.

When you look closely at the data, it is clear that the association is only seen at the highest blood levels of erythritol. Specifically, the blood levels of erythritol in these patients were divided into quartiles. The risk of heart attack and stroke in the first three quartiles (low to moderate blood levels of erythritol) were identical to the control. However, the fourth quartile (highest blood levels of erythritol) was associated with a dramatically increased risk of heart attack and stroke. That raises three important questions:

- “How much erythritol were patients in the fourth quartile consuming?”

- - The authors did not look at dietary intake of erythritol but did note a previous study estimated that Americans consume up to 30 grams of erythritol a day.

- 30 grams of erythritol a day is a huge amount of erythritol. Where does that erythritol come from?

- - Much of it comes from erythritol-containing highly processed foods like zero calorie sugar substitutes (either erythritol alone or erythritol mixed with artificial sweeteners to improve the taste); reduced- and low calorie carbonated and non-carbonated beverages; hard candy and cough drops, cookies, cakes, pastries, and bars; puddings and pie fillings; soft candies; syrups and toppings; ready to eat cereals; fruit novelty snacks; and frozen desserts.

- - But it is also found in foods you might not suspect, such as plant-based “milk” substitutes; chocolate and flavored milks; barbecue and tomato sauce, fruit-based smoothies, the syrup used in canned fruits, yoghurt; low calorie salad dressings; and salty snacks.

- - In other words, the only way anyone can consume 30 grams of erythritol in a day is to consume large quantities of erythritol-containing highly processed foods (I will discuss the significance of this observation later).

- “What else was different about patients in the fourth quartile?”

- - When you look carefully at the data, the patients in the fourth quartile were significantly older, with a higher incidence of diabetes, pre-existing coronary artery disease, previous non-fatal heart attacks, congestive heart failure, and greater triglycerides – all of which significantly increase their risk of heart attack and stroke.

#2: Mechanistic Studies:

Next the authors did in vitro and animal studies looking at the effect of high levels of erythritol on blood clotting.

These studies showed that high levels of erythritol promoted blood clotting both in vitro and in mice. The authors concluded that these studies provided a plausible mechanism for a link between high erythritol blood levels and increased risk of heart attack and stroke.

Flaws In This Portion Of The Study:

Other critics have pointed out that the assays used were not accurate models of blood clotting in humans. This particular critique is beyond my expertise, so I won’t comment further. However:

- As someone who was involved in cancer drug development for over 30 years, I know that in vitro and animal models are poor indicators of how things work in humans.

- And as a biochemist, I have two concerns:

- - The authors provided no mechanistic rationale for why erythritol would enhance blood clotting.

- - The authors made no effort to show that the effect of erythritol was unique. Would high levels of other sugar alcohols or other naturally occurring sugars have the same effect on blood clotting in their assays? We don’t know.

#3: Blood Levels Of Erythritol After Oral Intake.

Finally, the authors gave subjects 30 grams of erythritol and measured blood levels over the next several days.

This experiment showed that very high blood levels of erythritol were attained and maintained for at least two days before gradually decreasing to baseline. The authors concluded this experiment showed that it was feasible to attain and maintain high blood levels of erythritol for several days following a single ingestion of 30 grams of erythritol.

Flaws In This Portion Of The Study:

I have already pointed out that 30 grams per day is a huge amount of erythritol. However, erythritol in the diet will come from a variety of foods, some of which will contain components (fiber etc.) that slow the absorption of erythritol.

In contrast, the subjects in this experiment were given 300 ml of liquid containing 30 grams of erythritol and told to drink it in two minutes!

In other words, these subjects were consuming 30 grams of erythritol in 2 minutes rather than 24 hours, and they were consuming it in the most easily absorbable form. For a study like this, that makes the effective dose orders of magnitude greater than the amount of erythritol that anyone consumes from their diet over a 24-hour period. The study design was completely unrealistic.

Is Erythritol Bad For Your Heart?

As described above, this is the first study to suggest an association between erythritol and heart disease, and it was a highly flawed study.

It is also important to know that erythritol is not an artificial sweetener. It is found naturally in foods like grapes, peaches, pears, watermelons, and mushrooms. It is also found in some fermented foods like cheese, soy sauce, beer, sake, and wine.

It is also a byproduct of normal human metabolism, so we always have some of it circulating in our bloodstream. Our body knows how to handle low to moderate intakes of erythritol.

However, to help you really understand what this study means, I need to put it into the context of other studies. I will do this in story form (You will find more details about these studies in my book “Slaying The Food Myths”).

First, let’s look at highly processed food consumption:

Multiple recent studies have shown that high consumption of highly processed food is associated with increased risk of obesity, diabetes, heart disease, and premature death. We don’t know what it is about highly processed food consumption that is responsible for the increased risk, but it is unlikely to be just one thing.

As I pointed out above, the only way to achieve the high blood levels of erythritol associated with increased heart disease risk is to consume large quantities of erythritol-containing highly processed foods.

Next, let’s follow the history of sweeteners in highly processed foods.

When I was a young man, sucrose (table sugar) was added to most highly processed foods. Sucrose is found naturally in many fruits and vegetables. Small to moderate intake of sucrose in unprocessed and minimally processed foods posed no problem. However, large intakes of sugar in highly processed foods were found to increase the risk of obesity, diabetes, heart disease, and premature death.

At that point, sucrose became a “sugar villain”, and Big Food, Inc substituted fructose and high fructose corn syrup (a mixture of fructose and glucose) for sugar in their highly processed foods. As with sucrose, fructose is found naturally in many foods, and small to moderate intakes of fructose and high fructose corn syrup posed no health risks. However, large intakes of fructose and high fructose corn syrup in highly processed foods were found to increase the risk of obesity, diabetes, heart disease, and premature death.

Fructose and high fructose corn syrup then became the sugar villains. And because high fructose corn syrup is chemically and biologically indistinguishable from natural sugars like honey, date sugar, coconut sugar, it is likely that high intakes of these sugars in highly processed foods would cause the same problem.
So Big Food, Inc started relying on artificial sweeteners in their highly processed foods. But guess what? Recent studies have suggested that artificial sweeteners in highly processed foods are associated with obesity, diabetes, and heart disease.

That has caused Big Food, Inc to rely more on sugar alcohols in their highly processed foods, particularly erythritol because it is the least expensive of the sugar alcohols. Now the current study comes along and suggests that high intake of erythritol in highly processed foods may increase the risk of heart disease.

If this hypothesis is confirmed by better designed studies, it is not clear what Big Food, Inc will do next. The metabolomic study described above showed that high blood levels of several other sugar alcohols are associated with an increased risk of heart disease.

Hopefully, you are starting to see a pattern here. It’s time to ask the question, “Is it the sweetener, or is it the food?”

Clearly, it doesn’t matter what sweetener we are talking about. Large intake of any natural sweetener in the context of a diet rich in highly processed foods appears to have an adverse effect on our health. And we don’t know whether these adverse health effects are caused by the sweetener or some other component of the highly processed foods.

If you want to improve your health, the best solution is to decrease your intake of highly processed foods. That will automatically reduce your intake of sweeteners and other unhealthy components of highly processed foods and increase your intake of healthy components from the whole foods you will be eating instead.

Who Should Be Concerned About Erythritol Intake?

The authors of this study identified two groups who should be most concerned about erythritol consumption – diabetics and adherents of the keto diet.

Diabetics are at high risk because they are told to consume non-caloric sweeteners instead of sugars, and they are not told to avoid highly processed foods. Consequently, they consume much higher amounts of non-caloric sweeteners than the average American.

I must admit that I didn’t foresee keto adherents as a high-risk group. However, it appears that keto enthusiasts love their sweets as much as the rest of us, and the sweetener of choice for keto-friendly sweets is erythritol. The authors said that a single serving of keto ice cream contains 30 grams of erythritol. I can hardly imagine how much erythritol they must be getting in their diet.

And, once again, the best advice for both groups is to simply decrease the amount of highly processed food in their diet.

The Bottom Line

Erythritol is not an artificial sweetener. It is found naturally in foods like grapes, peaches, pears, watermelons, and mushrooms. It is also found in some fermented foods like cheese, soy sauce, beer, sake, and wine.

It is also a byproduct of normal human metabolism, so we always have some of it circulating in our bloodstream. Our body knows how to handle erythritol.

That is why it was a surprise when a recent study claimed that high intake of erythritol is associated with an increased risk of heart attack and stroke. The Dr. Strangeloves of the world are already starting to tell you that erythritol is deadly and you should avoid it at all costs. But reputable scientists are saying, “Not so fast”.

This is the first study to suggest an association between erythritol and heart disease, and it was a highly flawed study.

In fact, the study showed that low to moderate intakes of erythritol had no effect on heart disease risk. It was only the highest intake of erythritol that was associated with increased risk of heart disease. And given the distribution of erythritol in the American diet, the only way someone could take in that much erythritol is to consume large amounts of erythritol-sweetened highly processed foods.

A brief review of the literature on sweeteners reveals that this is a common pattern for every natural sweetener tested. Low to moderate intake of these sweeteners has no adverse health effects. However, high intake of every sweetener tested in the context of a highly processed food diet is associated with an increased risk of obesity, diabetes, heart disease, and premature death.

That raises the question, “Is it the sweetener, or is it the food?”

Clearly, it doesn’t matter what sweetener we are talking about. Large intake of any natural sweetener in the context of a diet rich in highly processed foods is likely to have an adverse effect on our health. And we don’t know whether these adverse health effects are caused by the sweetener or some other component of a highly processed food diet.

For more details on the study and information about which foods are likely to contain erythritol and the population groups who should be most concerned about erythritol consumption, 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

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.

Does Magnesium Protect Your Heart?

October 25, 2022 by Dr. Steve Chaney

Do You Need A Magnesium Supplement?

Author: Dr. Stephen Chaney

Getting an adequate amount magnesium from our diet should not be a problem. Magnesium is found in a wide variety of foods with the best sources being legumes (beans), nuts, seeds, whole grains, green leafy vegetables, and dairy foods.

The problem is:

None of these foods contain enough magnesium by themselves to provide the RDA (420 mg/day for men and 320 mg/day for women) for magnesium. We need to consume a variety of these foods every day – something most Americans aren’t doing.

These foods are decent sources of magnesium only in their unprocessed form. And most Americans consume more highly processed foods than whole, unprocessed foods.

Two to three servings of dairy provide a decent amount of magnesium, but many Americans are cutting back on dairy. And plant-based dairy substitutes often provide much less magnesium than the dairy food they replace.

Finally, green leafy vegetables (iceberg lettuce doesn’t count) don’t make it into the American menu as often as they should.

As a result, recent studies find that at least 50% of Americans are not getting enough magnesium in their diet. In fact, the average magnesium intake in this country is 268 mg/day for men and 234 mg/day for women. And the figures are not very different in other developed countries.

Does it matter? Recent studies have shown that an adequate intake of dietary magnesium is associated with lower risks of cardiovascular diseases (CVD) and all-cause mortality. This may be because of the of role of magnesium in supporting heart muscle contraction, normal heart rhythm, and blood pressure regulation. Adequate magnesium intake is also associated with lower risk of type 2 diabetes.

But what if you have already had a heart attack? Is it too late for magnesium to make a difference? A recent study (I Evers et al, Frontiers in Cardiovascular Medicine, August 12, 2022) was designed to answer this question.

The authors examined the effect of magnesium intake on cardiovascular disease (CVD) mortality, all-cause mortality, and coronary heart disease (CHD) mortality in patients who had experienced a recent heart attack.

[Note: CHD is defined as heart disease due to clogged coronary arteries, such as a heart attack. CVD includes CHD plus diseases caused by other clogged blood vessels, such as strokes and peripheral artery disease].

How Was The Study Done?

The authors used data from a previous study that had enrolled 4,365 Dutch patients aged 60-80 (average age = 69) who had experienced a heart attack within approximately 4 years prior to enrollment and followed them for an average of 12.4 years. All patients were receiving standard post-heart attack drug therapy.

The characteristics of the patients enrolled in the study were as follows:

Male 79%, female 21%
Average magnesium intake = 302 mg/day
Percent magnesium deficient: 72% of men and 67% of women
Percent taking magnesium supplements = 5.4%
Percent on drugs to lower blood pressure = 90%
Percent on statins = 86%
Percent on diuretics = 24%

Upon entry into the study the patients were asked to fill out a 203-item food frequency questionnaire reflecting their dietary intake over the past month. Trained dietitians reviewed the questionnaires and phoned the participants to clarify any unclear or missing items. The questionnaires were linked to the 2006 Dutch Food Composition Database to calculate magnesium intake and other aspects of their diets.

The patients were divided into 3 groups based on their energy adjusted magnesium intakes and those in the highest third (>322 mg/day) were compared to those in the lowest third (<238 mg/day) with respect to cardiovascular disease (CVD), all-cause mortality, and coronary heart disease (CHD) mortality.

The comparisons were statically adjusted for fiber intake (most magnesium-rich foods are also high fiber foods), diuretic use (diuretics reduce magnesium levels in the blood), age, sex, smoking, alcohol use, physical activity, obesity, education level, caloric intake, calcium, vitamin D, sodium from foods, potassium, heme iron, vitamin C, beta-carotenoids, polyunsaturated fatty acids, saturated fatty acids, overall diet quality based on the Dutch Dietary Guidelines, systolic blood pressure, kidney function, and diabetes. In other words, the data were adjusted for every conceivable variable that could have influenced the outcome.

Does Magnesium Protect Your Heart?

When those with the highest magnesium intake (>322 mg/day) were compared to those with the lowest intake (<283 mg/day):

Cardiovascular disease (CVD) mortality was reduced by 28%.

All-cause mortality was reduced by 22%.

Coronary heart disease (CHD) mortality was reduced by 16%, but that reduction was not statistically significant.

They then looked at the effect of some variables that might affect CVD risk on the results.

Diabetes, kidney function, iron intake, smoking, alcohol use, blood pressure, most dietary components and overall diet quality had no effect on the results.

The results were also not affected when patients using a magnesium supplement were excluded from the analysis. This suggests the effect of magnesium from diet and supplementation is similar.

However, diuretic use had a significant effect on the results.

- For patients using diuretics, high magnesium intake versus low magnesium intake reduced CVD mortality by 45%.

How Much Magnesium Do You Need?

You may have noticed that the difference between the highest magnesium intake group and the lowest intake group was, on average, only 39 mg/day. So, the authors also used a statistical approach that utilized data from each individual patient to produce a graph of magnesium intake versus risk of CVD, total, and CHD mortality. For all 3 end points the graphs showed an inverse, linear relationship between magnesium and mortality.

From this, the authors were able to calculate the effect of each 100mg/day increase in magnesium intake on mortality risk. Each 100mg/day of added magnesium reduced the risk of:

CVD mortality by 38%.

All-cause mortality by 30%.

CHD mortality by 33%, and these results were borderline significant.

The inverse relationship between magnesium intake was observed at intakes ranging from around 200 mg/day to around 450 mg/day, which represented the range of dietary magnesium intake in this Dutch population group.

This study did not define an upper limit to the beneficial effect of magnesium intake because the graphs had not plateaued at 450 mg/day, suggesting that higher magnesium intakes might give even better results.

The authors concluded, “We observed a strong, linear inverse association of dietary magnesium with CVD and all-cause mortality after a heart attack, which was most pronounced in patients who used diuretics. Our findings emphasize the importance of an adequate magnesium intake in CVD patients, on top of cardiovascular drug treatment.”

I might add that this is the first study to look at the effect of magnesium on long-term survival after a heart attack.

Do You Need A Magnesium Supplement?

As I said earlier, the best dietary sources of magnesium are beans, nuts, seeds, whole grains, green leafy vegetables, and dairy foods. And:

None of these foods contain enough magnesium by themselves to provide the RDA (420 mg/day for men and 320 mg/day for women) for magnesium.

These foods are decent sources of magnesium only in their unprocessed form.

When unprocessed, each of these foods provides 20 to 60 mg of magnesium per serving. If we use an average value of 40 mg/serving, you would need in the range of 8-10 servings/day of these foods in their unprocessed form to meet the RDA for magnesium.

You could get a more accurate estimate of the magnesium content of your diet using the “Magnesium Content of Selected Foods” table from the NIH Factsheet on Magnesium.

Now you are ready to ask yourself two questions:

Does my current diet provide the RDA for magnesium?

2. If not, am I willing to make the dietary changes needed to increase my magnesium levels to RDA levels?

If your answer to both questions is no, you should probably consider a magnesium supplement. A supplement providing around 200 mg of magnesium should bring all but the worst diets up to the recommended magnesium intake.

The current study did not define an upper limit for the beneficial effect of magnesium on survival after a heart attack but suggested that intakes above 450 mg/day might be optimal.

I do not recommend megadoses of magnesium, but intakes from diet and supplementation that slightly exceed the RDA appear to be safe. In their Magnesium Factsheet, the NIH states, “Too much magnesium…does not pose a health risk in healthy individuals because the kidneys eliminate excess amounts in the urine.”

The only concern is that magnesium from supplements is absorbed much more rapidly than magnesium from foods, and this can cause gas, bloating, and diarrhea in some individuals. For this reason, I recommend a sustained release magnesium supplement, so the magnesium is absorbed more slowly.

Finally, we should not consider magnesium as a magic bullet. The current study statistically eliminated every known variable that might affect survival after a heart attack, so it could estimate the beneficial effects of magnesium alone.

However, survival after a heart attack will likely be much greater if diet, exercise, and body mass are also optimized.

The Bottom Line

Recent studies have shown that an adequate intake of dietary magnesium is associated with lower risks of cardiovascular diseases (CVD) and all-cause mortality.

But what if you have already had a heart attack? Is it too late for magnesium to make a difference? A recent study of heart attack patients in Holland was designed to answer this question.

When heart attack patients with the highest magnesium intake (>322 mg/day) were compared to those with the lowest intake (<283 mg/day):

Cardiovascular disease (CVD) mortality was reduced by 28%.

All-cause mortality was reduced by 22%.

Coronary heart disease (CHD) mortality was reduced by 16%, but that reduction was not statistically significant.

The authors went on to look at the inverse linear relationship between magnesium intake and mortality risk. They found that each 100mg/day of added magnesium reduced the risk of:

CVD mortality by 38%.

All-cause mortality by 30%.

CHD mortality by 33%, and these results were borderline significant.

The authors concluded, “We observed a strong, linear inverse association of dietary magnesium with CVD and all-cause mortality after a heart attack…Our findings emphasize the importance of an adequate magnesium intake in CVD patients…”

I might add that this is the first study to look at the effect of magnesium on long-term survival of patients who have suffered a heart attack.

For more details on this study and my discussion of whether you might benefit from a magnesium supplement, 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.

The Omega-3 Pendulum

April 12, 2022 by Dr. Steve Chaney

Who Benefits Most From Omega-3s?

Author: Dr. Stephen Chaney

If you were around in the 60’s, you might remember the song “England Swings Like a Pendulum Do”. It was a cute song, but it had nothing to do with pendulums. This week I am talking about something that really does resemble a pendulum – the question of whether omega-3s reduce heart disease risk.

There is perhaps nothing more confusing to the average person than the “truth” about omega-3s and heart disease risk. The headlines and expert opinion on the topic swing wildly between “omega-3s reduce heart disease risk” to “omega-3s have no effect on heart disease risk” and back again. To me these swings resemble the swings of a pendulum – hence the title of this article.

Part of the reason for the wild swings is that journalists and most “experts” tend to rely on the latest study and ignore previous studies. Another contributing factor is that most journalists and experts read only the main conclusions in the article abstract. They don’t read and analyze the whole study.

So, in today’s “Health Tips From the Professor” I plan to:

Analyze 3 major studies that have influenced our understanding of the relationship between omega-3 intake and heart disease risk. I will tell you what the experts missed about these studies and why they missed it.

Summarize what you should know about omega-3 intake and your risk of heart disease.

Why Is The Role Of Omega-3s In Preventing Heart Disease So Confusing?

In answering that question, let me start with what I call “Secrets Only Scientists Know”.

#1: Each study is designed to disprove previous studies. That is a strength of the scientific method. But it guarantees there will be studies on both sides of every issue.

Responsible scientists look at all high-quality studies and base their opinions on the weight of evidence. Journalists and less-responsible “experts” tend to “cherry pick” the studies that match their opinions.

#2: Every study has its flaws. Even high-quality studies have unintended flaws. And I have some expertise in identifying unintended flaws.

I published over 100 papers that went through the peer review process. And I was involved in the peer review of manuscripts submitted by other scientists. In the discussion below I will use my experience in reviewing scientific studies to identify unintended flaws in 3 major studies on omega-3s and heart disease risk.

Next, let me share the questions I ask when reviewing studies on omega-3s and heart disease. I am just sharing the questions here. Later I will share examples of how these questions allowed me to identify unintended flaws in the studies I review below.

#1: How did they define heart disease? The headlines you read usually refer to the effect of omega-3s on “heart disease”. However, heart disease is a generic term. In layman’s terms, it encompasses angina, heart attacks, stroke due to blood clots, stroke due brain bleeds, congestive heart failure, impaired circulation, and much more.

Omega-3s have vastly different effects on different forms of heart disease, so it is important to know which form(s) of heart disease the study examined. And if the study included all forms of heart disease, it is important to know whether they also looked at the forms of heart disease where omega-3s have been shown to have the largest impact.

#2: What was the risk level of the patients in the study? If the patients in the study are at imminent risk of a heart attack or major cardiovascular event, it is much easier to show an effect than if they are at low risk.

For example, it is easy to show that statins reduce the risk of a second heart attack in someone who has just suffered a heart attack. These are high-risk patients. However, if you look at patients with high cholesterol but no other risk factors for heart disease, it is almost impossible to show a benefit of statins. These are low-risk patients.

If it is difficult to show that statins benefit low-risk patients, why should we expect to be able to show that omega-3s benefit low-risk patients?

[Note: I am not saying that statins do not benefit low-risk patients. I am just saying it is very difficult to prove they do in clinical studies.]

#3: How much omega-3s are the patients getting in their diet? The public reads the headlines. When the headlines say that omega-3s are good for their hearts, they tend to take omega-3 supplements. When the headlines say omega-3s are worthless, they cut back on omega-3 supplements. So, there is also a pendulum effect for omega-3 intake.

Omega-3s are fats. So, omega-3s accumulate in our cell membranes. The technical term for the amount of omega-3s in our cellular membranes is something called “Omega-3 Index”. Previous studies have shown that:

- An omega-3 index of 4% or less is associated with high risk of heart disease, and…

- An omega-3 index of 8% or more is associated with a low risk of heart disease.

When the omega-3 index approaches 8%, adding more omega-3 is unlikely to provide much additional benefit. Yet many studies either don’t measure or ignore the omega-3 index of patients they are enrolling in the study.

#4: How many and what drugs were the patients taking? Many heart disease patients are taking drugs that lower blood pressure, lower triglycerides, reduce inflammation, and reduce the risk of blood clot formation. These drugs do the same things that omega-3s do. This decreases the likelihood that you can see any benefit from increasing omega-3s intake.

The Omega-3 Pendulum

With all this in mind let’s examine three major double-blind, placebo-controlled studies that looked at the effect of omega-3s on heart disease risk and came to different conclusions. Here is a summary of the studies.

GISSI Study	ASCEND Study	VITAL Study
11,000 participants	15,480 participants	25,871 participants
Followed for 3.5 years	Followed for 7.4 years	Followed for 5.3 years
Europe	USA	USA
Published in 1999	Published in 2018	Published in 2019
Dose = 1 gm/day	Dose = 1 gm/day	Dose = 1 gm/day
20% ↓ in heart disease deaths	No effect on fatal or non-fatal heart attack or stroke	Significant ↓ in some forms of heart disease
45% ↓ in fatal heart attack or stroke – as effective as statins		Significant ↓ in heart disease risk for some patients

At first glance the study designs look similar, so why did these studies give such different results. This is where the unintended flaws come into play. Let’s look at each study in more detail.

The GISSI Study:

The patients enrolled in this study all had suffered a heart attack in the previous 3 months. They were at very high risk of suffering a second heart attack within the next couple of years.

Omega-3 intake was not measured in this study. But it was uncommon for Europeans to supplement with omega-3s in the 90’s. And European studies on omega-3 intake during that period generally found that omega-3 intake was low.

Patients enrolled in this study were generally taking only 2 heart disease drugs, a beta-blocker and a blood pressure drug.

The ASCEND Study:

The patients enrolled in this study had diabetes without any evidence of heart disease. Only 17% of the patients enrolled in the study were at high risk of heart disease. 83% were at low risk. Remember, it is difficult to show a benefit of any intervention in low-risk patients.

The average omega-3 index of patients enrolled in this study was 7.1%. That means omega-3 levels were near optimal at the beginning of the study. Adding additional omega-3s was unlikely to show much benefit.

Most of the patients in this study were on 3-5 heart drugs and 1-2 diabetes drugs which duplicated the effects of omega-3s.

That means this study was asking a very different question. It was asking whether omega-3s provided any additional benefit for patients who were already taking multiple drugs that duplicated the effects of omega-3s.

However, you would have never known that from the headlines. The headlines simply said this study showed omega-3s were ineffective at preventing heart disease.

Simply put, this study was doomed to fail. However, despite its many flaws the authors reported that omega-3s did reduce one form of heart disease, namely vascular deaths (primarily due to heart attack and stroke). Somehow this observation never made it into the headlines.

The VITAL Study:

This study enrolled a cross-section of the American population aged 55 or older (average age = 67). As you might suspect for a cross-section of the American population, most of the participants in this study were at low risk for heart disease. This limited the ability of the study to show a benefit of omega-3 supplementation in the whole population.

However, there were subsets of the group who were at high risk of heart disease (more about that below).

This study excluded omega-3 supplement users The average omega-3 index of patients enrolled in this study was 2.7% at the beginning of the study and increased substantially during the study. This enhanced the ability of the study to show a benefit of omega-3 supplementation.

Participants in this study were only using statins and blood pressure medications. People using more medications were excluded from the study. This also enhanced the ability of the study to show a benefit of omega-3 supplementation.

The authors reported that “Supplementation with omega-3 fatty acids did not result in a lower incidence of major cardiovascular events…” This is what lazy journalists and many experts reported about the study.

However, the authors designed the study so they could also:

Look at the effect of omega-3s on heart disease risk in high-risk groups. They found that major cardiovascular events were reduced by:

- 26% in African Americans.

- 26% in patients with diabetes.

- 17% in patients with a family history of heart disease.

- 19% in patients with two or more risk factors of heart disease.

Look at the effect of omega-3s on heart disease risk in people with low omega-3 intake. They found that omega-3 supplementation reduced major cardiovascular events by:

- 19% in patients with low fish intake.

Look at the effect of omega-3s on the risk of different forms of heart disease. They found that omega-3 supplementation reduced:

- Heart attacks by 28% in the general population and by 70% for African Americans.

- Deaths from heart attacks by 50%.

- Deaths from coronary heart disease (primarily heart attacks and ischemic strokes (strokes caused by blood clots)) by 24%.

In summary, if you take every study at face value it seems like the pendulum is constantly swinging from “omega-3s reduce heart disease risk” to “omega-3s are worthless” and back again. There appears to be no explanation for the difference in results from one study to the next.

However, if you remember that even good studies have unintended flaws and ask the four questions I proposed above, it all makes sense.

How is heart disease defined? Studies looking at heart attack and/or ischemic stroke are much more likely to show a benefit of omega-3s than studies that include all forms of heart disease.

Are the patients at low-risk or high-risk for heart disease? Studies in high-risk populations are much more likely to show a benefit than studies in low-risk populations.

What is the omega-3 intake of participants in the study? Studies in populations with low omega-3 intake are more likely to show a benefit of omega-3 supplementation than studies in populations with high omega-3 intake.

How many heart drugs are the patients taking? Studies in people taking no more than one or two heart drugs are more likely to show a benefit of omega-3 supplementation than studies in people taking 3-5 heart drugs.

When you view omega-3 clinical studies through the lens of these 4 questions, the noise disappears. It is easy to see why these studies came to different conclusions.

Who Benefits Most From Omega-3s?

The answers to this question are clear:

People at high risk of heart disease are most likely to benefit from omega-3 supplementation.

People with low omega-3 intake are most likely to benefit from omega-3 supplementation.

Omega-3 supplementation appears to have the biggest effect on heart attack and ischemic stroke (stroke due to blood clots). Its effect on other forms of heart disease is less clear.

Omega-3 supplementation appears to be most effective at preventing heart disease if you are taking no more than 1 or 2 heart drugs. It may provide little additional benefit if you are taking multiple heart drugs. However, you might want to have a conversation with your doctor about whether omega-3 supplementation might allow you to reduce or eliminate some of those drugs.

What about the general population? Is omega-3 supplementation useful for patients who are at low to moderate risk of heart disease?

If we compare omega-3 studies with statin studies, the answer would be yes. Remember that statins cannot be shown to reduce heart attacks in low-risk populations. However, because they are clearly effective in high-risk patients, the medical community assumes they should be beneficial in low-risk populations. The same argument could be made for omega-3s.

We also need to recognize that our ability to recognize those who are at high risk of heart disease is imperfect. For too many Americans, the first indication that they have heart disease is sudden death!

When I was still teaching, I invited a cardiologist to speak to my class of first year medical students. He told the students, only partly in jest, that he felt statins were so beneficial they “should be added to the drinking water”.

I feel the same way about omega-3s:

Most Americans do not get enough omega-3s in our diet.

Our omega-3 index is usually much closer to 4% (high risk of heart disease) than 8% (low risk of heart disease).

Many of us may not realize that we are at high risk of heart disease until it is too late.

And omega-3s have other health benefits.

For all these reasons, omega-3 supplementation only makes sense.

The Bottom Line

If you take every study at face value, there appears to be no explanation for the difference in results from one study to the next. However, if you recognize that even good studies have unintended flaws and ask four simple questions to expose these flaws, it all makes sense.

For the four questions you should ask when reviewing any omega-3 study and my recommendations for who benefits the most from omega-3 supplementation, 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.

Is Dairy Bad For Your Heart?

December 7, 2021 by Dr. Steve Chaney

Is Dairy Right For You?

Author: Dr. Stephen Chaney

We have been told for years that dairy foods are good for us. They are part of the USDA five food groups. In fact, they are part of the dietary recommendations of every government and most health organizations across the world.

And dairy foods are nutritious. They are excellent sources of calcium, potassium, protein, and vitamins A and B12. And if they are fortified, they are also an excellent source of vitamin D. Many health experts consider them essential for healthy bones. So, you might be saying, “Case closed. We should all be eating more dairy foods”.

But, not so fast. Many dairy foods are high in saturated fats. In fact, 65% of the fat in dairy foods is saturated. We have known for years that when saturated fats replace polyunsaturated fats in the diet, LDL cholesterol levels increase. And, as I reported in a previous issue of “Health Tips From the Professor” there is excellent evidence that replacing polyunsaturated fats with saturated fats substantially increases the risk of dying from heart attack, stroke, and other forms of heart disease.

The widely accepted message from these studies is that saturated fats raise LDL cholesterol levels and increases our risk of dying from heart disease. If we accept this message, it poses a dilemma. Dairy foods are nutritious. But they are high in saturated fat. What should we do?

The answer from the American Heart Association and most other health organizations is simple. We should eat low-fat dairy foods.

But this is where it gets really confusing. Dairy foods are composed of much more than saturated fats. And you have probably seen the claims that full fat dairy foods don’t increase the risk of heart disease.

So, what is the truth about full-fat dairy foods and heart health? In this issue of “Health Tips From The Professor” I review three recent studies and the recommendations of the Heart Foundation because they shed light on this question.

Is Dairy Bad For Your Heart?

Before I answer this question, I should point out that there are two ways of looking at it.

As I said above, the studies proving that saturated fats increase the risk of heart disease, substituted saturated fats for polyunsaturated fats and controlled every other aspect of the diet. That has led the American Heart Association and other organizations to recommend that we eat low-fat dairy foods.

However, when most people hear that recommendation, they simply substitute low-fat dairy for full-fat dairy foods without changing any other aspect of their diet or lifestyle. The first two studies were designed to see if that approach was effective for reducing heart disease risk.

The first study (KA Schmidt et al, American Journal of Clinical Nutrition, 114: 882-892, 2021) was a randomized controlled trial that compared the effect of low-fat dairy foods and full-fat dairy foods on heart health parameters.

The participants in this study were:

Average age = 62
56% male
75% white
Average weight = 214 pounds
All of them were prediabetic

All participants were told to stick with their usual diets (probably typical American diets) except for the amount and type of dairy foods added to their diet. During the first four weeks they restricted dairy consumption to 3 servings of nonfat dairy/week so they would all be starting with the same amount of dairy consumption. Then they were divided into 3 groups for the 12-week study:

Group 1 continued with 3 servings of nonfat dairy/week.
Group 2 added 3 servings of low-fat dairy/day to their usual diet.
Group 3 added 3 servings of high-fat dairy/day to their usual diet.

At the beginning of the study and again at the end of the 12-week study LDL cholesterol, HDL cholesterol, triglycerides, free fatty acids, and blood pressure were measured. The results were:

There was no difference in LDL cholesterol, HDL cholesterol, triglycerides, free fatty acids, or blood pressure in the three groups at the end of 12 weeks.

There was no also significant change in LDL cholesterol, HDL cholesterol, triglycerides, free fatty acids, or blood pressure during the study in any of the three groups.

The authors concluded, “A diet rich in full-fat dairy had no effect on fasting lipid profile or blood pressure compared with diets limited in dairy or rich in low-fat dairy. Therefore, dairy fat, when consumed as part of complex whole foods does not adversely affect these classic cardiovascular disease risk factors.”

[Note: The last sentence is key. Remember the “proof” that saturated fats increase LDL levels and increase the risk of heart disease come from studies in which saturated fats were substituted for polyunsaturated fats and every other aspect of the diet was carefully controlled.

In this study, and others like it, the effects of saturated fats are studied in a complex food (dairy) in the presence of an even more complex diet containing many foods that influence the risk of heart disease.]

The second study (J Guo et al, European Journal of Epidemiology 32: 269-287, 2017) was a meta-analysis of 29 studies with 938,465 participants looking at the association of full-fat dairy consumption with the risk of dying from heart disease.

Seven of the 29 studies were conducted in the United States. Of the remaining studies 3 were from Japan and Taiwan, 2 were from Australia, and 17 were from Europe.

The results of the study were:

There was no association between full-fat dairy, low-fat dairy, and total dairy consumption and risk of dying from heart disease.

When the results were broken down into individual dairy foods.

There was no association between milk consumption and risk of dying from heart disease.

Consumption of one serving/day of fermented dairy foods was associated with a 2% decreased risk of dying from heart disease.

The authors concluded, “The current meta-analysis of 29 prospective cohort studies suggested no association of total, high and low-fat dairy and milk with risk of cardiovascular disease. In addition, a possible role of fermented dairy was found in cardiovascular disease prevention, but the result was driven by a single study.” [I would add that this effect, if confirmed by subsequent studies, is extremely small (2%).]

The first two studies do not say that full-fat dairy foods are heart healthy for everyone, as some headlines would have you believe. Instead, these studies show fairly convincingly that simply switching from full-fat to low-fat dairy foods, without changing any other aspect of your diet and lifestyle, is not as effective at decreasing your risk of heart disease as some experts would have you believe.

The third publication (WC Willett and DS Ludwig, New England Journal of Medicine 382: 644-654, 2020) was a review of the effect of dairy foods on our health. One of the authors, Walter C Willett, is one of the top experts in the field. The review covered many topics, but I will focus on the section dealing with the effect of dairy foods on heart health.

This review took a more nuanced look at full-fat dairy foods and examined the effect of substituting full-fat dairy for other protein foods.

The review concludes, “The association of milk with the risk of cardiovascular disease depends on the comparison foods. In most cohort studies [such as the studies described above], no specific comparison was made; by default, the comparison was everything else in the diet – typically large amounts of refined grains, potato products, sugar, and meat.”

The review went on to say that previous studies have shown:

“Both full-fat and low-fat dairy foods…were associated with a lower risk [of cardiovascular disease and stroke] than…the same number of servings of red meat but with a higher risk than seen with the same number of servings of fish or nuts.”

“Dairy fat…was associated with a higher risk of cardiovascular disease than was polyunsaturated or vegetable fat.”

“For persons living in low-income countries where diets are very high in starch, moderate intake of dairy foods may reduce cardiovascular disease by providing nutritional value and reducing glycemic load [the amount of easily digestible carbohydrate in the diet].”

Is Dairy Right For You?

Now I am ready to answer the question posed at the beginning of this article, “Is dairy bad for your heart?” The answer is, “It depends”.

As described above, the effect of dairy on heart health depends on our overall diet. It also depends on our lifestyle, our weight, and our health.

In addition, clinical studies report averages, and none of us are average. We all have unique diets, lifestyles, health status, and genetic makeup.

So, what does this mean for you? Perhaps it is best summed up by the recommendations of Australia’s Heart Foundation which take health status, lifestyle, and genetic differences into account:

A heart healthy diet can include dairy, but it is not essential [with careful planning and/or supplementation you can get your calcium and protein elsewhere].

Milk, yogurt, and cheese are considered neutral for heart health, meaning they neither increase nor decrease the risk of heart disease for the average person. However, the recommendations vary depending on health status, genetics, and lifestyle:

- Low-fat milk, yogurt, and cheese are recommended for people with heart disease or high cholesterol because the fat in dairy foods can raise cholesterol more for these people. [Note: If cholesterol is elevated, it usually means that individual has a hard time regulating blood cholesterol levels because of obesity, genetics, or pre-existing disease. For these individuals, diets high in saturated fat are more likely to increase LDL cholesterol and risk of heart disease.]

- Full-fat milk, yogurt, and cheese can be part of a heart healthy diet for healthy people provided most of the fat in the diet comes from fish, nuts, seeds, and healthy oils. [Note: Overall diet is important.]

Choosing unflavored milk, yogurt, and cheese helps limit the amount of sugar in your diet.

Ice cream, cream, and dairy desserts should be eaten only sometimes and in small amounts because they have more sugar and fat, and less protein, vitamins, and minerals than other dairy foods.

Butter raises LDL cholesterol levels, especially in people who already have elevated cholesterol.

- There is no evidence that butter can be part of a heart healthy diet, so you should consider healthier options such as olive oil, avocado, nut butters, and spreads made with healthier oils, such as olive oil.

The Bottom Line

However, dairy foods have been controversial in recent years. Some experts claim that only low-fat dairy products can be heart healthy. Others claim that full-fat dairy foods are just as healthy as low-fat dairy foods.

I shared three recent publications and dietary recommendations from The Heart Foundation that shed light on these controversies.

The first study found that full-fat dairy foods did not increase LDL cholesterol, triglycerides, and other heart disease risk factors.

The second study was a meta-analysis of 29 clinical studies with almost one million people. It found that full-fat dairy foods did not increase the risk of dying from heart disease.

“Case closed”, you might say. However, these studies do not say that full-fat dairy foods are heart healthy for everyone, as some headlines would have you believe. Instead, these studies show fairly convincingly that simply switching from full-fat to low-fat dairy foods, without changing any other aspect of your diet and lifestyle, is not as effective at decreasing your risk of heart disease as some experts would have you believe.

Moreover, these studies do not account for the effect of overall diet, lifestyle, health status, and genetics on the risk of heart disease.

That is why I included the third study in my review. It took the overall diet into account and concluded the effect of full-fat dairy foods on heart disease risk depends on the overall diet.

For some diets full-fat dairy increases heart disease risk.

For other diets full-fat dairy has no effect on heart disease risk.

And for some diets full-fat dairy may even decrease heart disease risk.

Finally, I included recommendations of the Australian Heart Foundation because they included the effect of health status, lifestyle, and genetics in their recommendations.

For more details on the findings of the third study and the recommendations of the Heart Foundation, 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.

A Diet To Die For

September 14, 2021 by Dr. Steve Chaney

Which Diet Is Best?

Author: Dr. Stephen Chaney

Many clinical studies focus on the benefits or risks associated with individual components of our diet. For example, we have been told:

Saturated and trans fats are bad for us and monounsaturated and omega-3 fats are good for us.

Sugar and refined carbohydrates are bad for us, but complex carbohydrates are good for us.

However, we don’t eat saturated fats or sugars in isolation. They are part of a diet with many other foods. Do other foods in our diet affect the risks we associate with saturated fat or sugar? We don’t know.

Simply put, we don’t eat foods, we eat diets. We don’t eat saturated fats, we eat diets. It would be more helpful for the average person if research focused on which diets are good and bad for us instead of which foods are good and bad for us.

One recent study (JM Shikany et al, Journal of the American Heart Association, 10:e019158, 2021) did just that. It evaluated the effect of 6 different dietary patterns on the risk of sudden cardiac death (dropping dead from a stroke or heart attack).

It turns out that one of the diets significantly increases your risk of sudden cardiac death. I call that one, “A diet to die for”.

Another diet significantly decreases your risk of sudden cardiac death. I call that one, “A diet to live for”.

The other diets had no significant effect on the risk of sudden cardiac death.

You are probably wondering, “What were the diets?”; “Which diet is best?”; and “Which diet is worst?” I cover that below, but first we should look at how the study was designed.

How Was The Study Designed?

The study involved 21,069 participants in the REGARDS (Reasons for Geographical and Racial Differences in Stroke) clinical trial who were followed for an average of 10 years. This clinical trial enrolled:

30% of its participants from what is called the “the stroke belt” (North Carolina, South Carolina, Georgia, Tennessee, Alabama, Mississippi, Arkansas, and Louisiana).

20% of its participants from what is called “the stroke buckle” (the coastal plain of North Carolina, South Carolina, and Georgia).

50% of its participants from elsewhere in the continental United States.

At the beginning of the study, participants were given a medical exam and filled out an extensive questionnaire on diet.

Based on the diet analysis, the participants were ranked for adherence to six dietary patterns.

#1: The Convenience Pattern. This dietary pattern relied heavily on pre-packaged or restaurant meals, pasta dishes, pizza, Mexican food, and Chinese food.

#2: The Plant-Based Pattern. This dietary pattern relied heavily on vegetables, fruits, fruit juice, cereal, beans, fish, poultry, and yogurt.

#3: The Sweets Pattern. This dietary pattern relied heavily on added sugars, desserts, chocolate, candy, and sweetened breakfast foods.

#4: The Southern Pattern. This dietary pattern relied heavily on added fats, fried food, eggs and egg dishes, organ meats, processed meats, and sugar-sweetened beverages.

#5: The Alcohol and Salad Pattern. This dietary pattern relied heavily on beer, wine, liquor, green leafy vegetables, tomatoes, and salad dressing.

#6: The Mediterranean Pattern. Adherence to the Mediterranean dietary pattern was based on the well-established Mediterranean Diet Score.

Points are added for beneficial foods (vegetables, fruits, legumes, whole grain cereals, nuts, and fish).

Points are subtracted for detrimental foods (meat and dairy).

Points are added for a high ratio of monounsaturated fats to saturated fats (think diets rich in olive oil).

One point is added for moderate alcohol consumption, Zero or excess alcohol consumption is assigned 0 points.

The study looked at the correlation of these dietary patterns with the incidence of sudden cardiac death during the 10-year study.

A Diet To Die For

The results were striking.

The Southern Diet increased the 10-year risk of sudden cardiac death 2.2-fold. Basically, it doubled the risk.

- In people with no previous history of heart disease at the beginning of the 10-year study, the Southern Diet increased the risk of sudden cardiac death by 2.3-fold.

- In people with a previous history of heart disease at the beginning of the 10-year study, the Southern Diet increased the risk of sudden cardiac death by 2-fold.

The Mediterranean Diet decreased the 10-year risk of sudden cardiac death 41%.

- In people with no previous history of heart disease at the beginning of the 10-year study, the Mediterranean Diet decreased the risk of sudden cardiac death by 51%. Basically, it cut the risk in half.

- In people with a previous history of heart disease at the beginning of the 10-year study, the Mediterranean Diet decreased the risk of sudden cardiac death by 23%, but that decrease was not statistically significant.

None of the other diets had a significant effect on the 10-year risk of sudden cardiac death.

In the words of the authors, “We identified a trend towards an inverse association of the Mediterranean diet score and a positive association of adherence to the Southern dietary pattern with risk of sudden cardiac death.” [That is a fancy way of saying the Mediterranean diet decreased the risk of sudden cardiac death, and the Southern dietary pattern increased the risk of sudden cardiac death.]

Which Diet Is Best?

The Mediterranean Diet Is Best: In this analysis of the effects of 6 different dietary patterns on the risk of sudden cardiac death, it is obvious that the Mediterranean diet is best. It cut the risk of sudden cardiac death in half.

This should come as no surprise:

I have reported on a previous study showing that the Mediterranean diet decreases the risk of heart disease by 47%.

In the Woman’s Health Study the Mediterranean diet decreased the risk of sudden cardiac death by 36%.

In the Nurses’ Health Study there was an inverse association between the Mediterranean Diet Score and sudden cardiac death.

The Southern Dietary Pattern Was Worst. It doubled the risk of sudden cardiac death. As someone who grew up in the South, this comes as no surprise to me. Let me count the ways:

It starts with a breakfast of fried eggs, grits with “red-eye gravy” (a mixture of ham drippings and coffee), ham or sausage, and biscuits made with lots of lard and sugar.

When I was growing up, a snack might be an RC cola and moon pies (look that one up).

Dinner might be fried chicken and hushpuppies or fried fish and hushpuppies.

Instead of picnics we have pig pickins (which is pretty much what it sounds like).

And we boil our vegetables with fatback (pig fat) and sugar.

I could go on, but you get the picture. Don’t get me wrong, I have fond memories of the foods I ate while growing up in the South. I just don’t eat them much anymore.

Why Didn’t The Plant-Based Dietary Pattern Score Better? One of the surprises from this study was that the Plant-Based Dietary Pattern didn’t score better. After all, numerous studies have shown that mostly plant-based diets reduce the risk of heart disease. Why did it strike out in this study?

My feeling is that the study did not adequately describe a true Plant-Based Dietary Pattern. As I described above, participants following the Plant-Based Dietary Pattern were identified as having above average consumption of vegetables, fruits, fruit juice, cereal, beans, fish, poultry, and yogurt compared to others in this study. I have two concerns with this classification.

As described, this is a semi-vegetarian diet, while the best results for reducing heart disease risk are seen with strict vegetarian and lacto-ovo-vegetarian diets.

However, my biggest concern is that we don’t know what other foods they were consuming. Were they also consuming convenience foods? Were they consuming sweets? We don’t know.

That is very different from the two dietary patterns that stood out in this study.

50% of the participants in this study came the Southeastern region of the United States. So, when the study identified participants as following a Southern Dietary Pattern based on a few southern foods, it is likely that those participants ate many other southern foods as well.

If 50% of the participants in the study had come from the Loma Linda area of California where vegetarianism is much more common, the study might have done a better job of identifying participants consuming a plant-based diet.

While participants consuming the Mediterranean diet were more scattered geographically, the Mediterranean Diet Score used to identify people consuming a Mediterranean diet is much more detailed and has been validated in numerous previous studies.

In short, the Southern and Mediterranean Dietary Patterns may have stood out in this study because they provided a more precise distinction between those consuming a Southern or Mediterranean diet and those following other dietary patterns. If the Plant-Based Dietary Pattern had been more precisely described, it might have shown a statistically significant benefit as well.

The Bottom Line

Many clinical studies focus on the benefits or risks associated with individual components of our diet.

However, we don’t eat foods, we eat diets. It would be more helpful for the average person if research focused on which diets are good and bad for us instead of which foods are good and bad for us.

One recent study did just that. It evaluated the effect of 6 different dietary patterns on the risk of sudden cardiac death (dropping dead from a stroke or heart attack).

It turns out that the Southern diet doubles your risk of sudden cardiac death. I call that one, “A diet to die for”.

In contrast, the Mediterranean diet cuts your risk of sudden cardiac death in half. I call that one, “A diet to live for”.

The other diets had no significant effect on the risk of sudden cardiac death.

For more details on the study, why the Southern diet is so bad for us, and why the Mediterranean diet is so good for us, 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.

Omega 3 Supplementation And Heart Disease Risk

April 15, 2020April 14, 2020 by Dr. Steve Chaney

How Can You Reduce Your Risk Of Heart Disease?

I understand your confusion. One month the headlines say that omega 3 supplementation reduces the risk of heart disease. The next month headlines claim that omega 3 supplements are worthless. What is the truth about omega 3 supplementation and heart disease risk?

Let me start by sharing the two of the most recent studies on the topic. They are both very large, well designed studies. However, the reason I selected these two studies is that they approached the relationship between omega 3 supplementation and heart disease risk in very different ways but came to the same conclusion.

The first study (Y Hu et al, Journal of the American Heart Association, Volume 8, Issue 19, 1 October 2019) was a meta-analysis of 13 randomized controlled clinical studies looking at the relationship between omega 3 supplementation and heart disease risk.

The second study (Z-H Li et al, British Medical Journal, BMJ2020;368:m456) looked at the association between habitual omega 3 supplementation and heart disease risk.

Each of these studies had strengths and weaknesses, but they complemented each other. The weaknesses of one study were the strengths of the other study.

How Were The Studies Done?

Study #1: The 13 studies included in the meta-analysis had a total of 127,477 participants (mean age 64, 60% male, mostly overweight) who were given either an omega-3 supplement or a placebo.

40% of the participants had diabetes.

72% of the participants were on cholesterol lowering drugs and a variety of other medications.

Participants were followed for between 3 and 7.4 years (average follow-up period was 5 years).

The dose of omega 3s ranged between 376 and 4,000 mg/day.

The major strengths of this study were:

All 13 studies included in the meta-analysis were randomized, placebo controlled clinical trials.

The meta-analysis had a very large number of participants (nearly 130,000), so it was possible to accurately measure even small effects of omega 3 supplementation on heart disease risk.

The major weaknesses of this study were:

Most of the participants were already on multiple drugs that provided many of the same benefits as omega 3s, so it was impossible to assess the full effect of omega 3 supplementation on heart disease risk.

The duration of the clinical trials included in this meta-analysis was short compared to the decades required for heart disease to develop.

Most of the participants already had heart disease or were at high risk of developing heart disease. The people in these studies were not representative of the general population.

Study #2: The data for this study were obtained from the UK Biobank study which enrolled 427,678 participants (mean age 56, 45% male) from 22 medical centers across England, Scotland, and Wales. None of the participants had been diagnosed with heart disease or cancer at the time of enrollment.

At enrollment the participants filled out a detailed online questionnaire concerning their lifestyle, diet, diseases, medications, and supplement use. Among the questions was whether they habitually used fish oil supplements (Yes or No).

The participants were enrolled between 2006 and 2010 and followed for an average of 9 years.

31% of the participants were already taking omega 3 supplements on a regular basis at the time they enrolled in the study. This was the omega 3 supplementation group. The remaining 69% was the control group.

Only 10% of the participants were taking statin drugs or aspirin, probably because none of them had been diagnosed with heart disease.

Around 10% of the participants had high blood pressure and were taking blood pressure medications.

Most of the participants were slightly overweight but only 4% had diabetes.

The main strengths of this study were:

Very few of the participants were on medications. That means that medications did not interfere with the effect of omega 3 supplementation.

The participants were already using omega 3 supplements at the time of enrollment and were followed for an additional 9 years. That means that the duration of omega 3 supplement use was much longer than in the first study.

The participants were healthy and free of heart disease at the beginning of the study. That means that the results of this study focused more on prevention than on treatment. It also means the results are more applicable to the general population.

The main weakness of this study was:

It was an association study, which cannot prove cause and effect. In contrast, the first study was based on randomized, placebo controlled clinical trials, which can prove cause and effect.

In short, the weaknesses of the first study were strengths of the second study and vice-versa.

Omega 3 Supplementation And Heart Disease Risk

Study #1: The results from the meta-analysis of randomized, placebo-controlled clinical trials were that omega 3 supplementation:

Reduced heart attacks by 12%.

Reduced overall heart disease risk by 7%.

Reduced deaths from heart disease by 8%.

Because of the large number of participants included in the meta-analysis, all these reductions were highly significant.

The risk reduction was linearly related to the dose of omega-3s, but the study did not allow estimation of an optimal omega-3 dose.

The authors concluded: “Marine [fish oil] omega-3 supplementation lowers risk for heart attack, overall heart disease risk, and heart disease death…Risk reductions appear to be linearly related to marine omega-3 dose.”

Study #2: This study showed that regular use of omega-3 supplements:

Reduced deaths from all causes by 13%.

Reduced deaths from heart attacks by 20%.

Reduced deaths from all types of heart disease by 16%.

Because of the large number of participants, all these reductions were highly significant.

This study did not collect data on omega-3 dose, so the study did not allow estimation of an optimal omega-3 dose.

The authors concluded: “Habitual use of fish oil seems to be associated with a lower risk of all cause mortality and heart disease mortality…,supporting their use for the prevention of mortality from all causes and heart disease. Future studies are needed to examine the extent to which the dose of fish oil supplements influences the ability to achieve a clinically meaningful effect.”

While these studies did not provide information on the optimal omega 3 dose, a previous study concluded that an omega-3 intake of 835 mg/day or higher is needed to achieve clinically meaningful reductions in heart disease risk.

How Can You Reduce Your Risk Of Heart Disease?

These two studies support the value of omega 3 supplementation for reducing heart disease risk. However, while risk reductions were highly significant, the magnitude of risk reduction was relatively small. That means we should think of omega-3 supplementation as part of a holistic approach to reducing our health disease risk. It is just one piece of the puzzle.

With that in mind, here is what the American Heart Association recommends for reducing your risk of heart disease:

If you smoke, stop.

Choose good nutrition.

- Choose a diet that emphasizes vegetables, fruits, whole grains, low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts.

- Choose a diet that limits sweets, sugar-sweetened beverages, and red meats.

Reduce high blood cholesterol and triglycerides.

- Reduce your intake of saturated fat, trans fat and cholesterol and get moving.

- If diet and physical activity don’t get those numbers under control, then medication may be the next step.

Lower High Blood Pressure.

Be physically active every day.

- Aim for at least 150 minutes per week of moderate-intensity physical activity per week.

Aim for a healthy weight.

Manage diabetes.

Reduce stress.

Limit alcohol.

Add in omega-3 supplementation to these recommendations and you have a winning combination.

The Bottom Line

Two major studies have recently been published on the relationship between omega 3 supplementation and heart disease. I felt it was important to evaluate these studies together because:

They are both very large, well designed studies.

They approached the relationship between omega 3 supplementation and heart disease risk in very different ways but came to the same conclusion.

They complemented each other. The weaknesses of one study were the strengths of the other study.

These studies showed that omega 3 supplementation:

Reduced heart attacks by 12-20%.

Reduced overall heart disease risk by 7%.

Reduced deaths from heart disease by 8-16%.

Reduced deaths from all causes by 13%

While these studies did not provide information on the optimal omega 3 dose, a previous study concluded that an omega-3 intake of 835 mg/day or higher is needed to achieve clinically meaningful reductions in heart disease risk.

For more details and the American Heart Association recommendations on what else you can do to reduce your risk of heart disease, 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.

Is Fish Oil Really Snake Oil?

February 11, 2014 by Dr. Steve Chaney

Does Fish Oil Reduce Heart Disease Risk?

Author: Dr. Stephen Chaney

One of my readers recently sent me a video titled “Is Fish Oil Just Snake Oil?” and asked me to comment on it. The doctor who made the video claimed that the most recent studies had definitively shown that omega-3 fatty acids, whether from fish or fish oil, do not decrease the risk of heart attack, stroke or cardiovascular death. He went on to say that the case was closed. There was no point in even doing any more studies.

My reader, like many of you, was confused. Wasn’t it just a few years ago we were being told that clinical studies have shown that omega-3 fatty acids significantly reduce the risk of heart disease? Hadn’t major health organizations recommended omega-3 fatty acids as part of a heart health diet? What has changed?

The answer to the first two questions is a resounding YES, and “What has changed?” is THE story. Let me explain.

Fish Oil And Heart Disease Risk In Healthy People

If we look at intervention studies in healthy people (what we scientists refer to as primary prevention studies) the results have been pretty uniform over the years. In a primary prevention setting, fish oil cannot be shown to significantly reduce the risk of heart disease (Rizos et al, JAMA, 308: 1024-1033, 2012).

That’s not unexpected because it is almost impossible to show that any intervention significantly reduces the risk of heart disease in healthy populations. For example, as I pointed out in recent Health Tips From the Professor (“Do Statins Really Work?” and “Can An Apple A Day Keep Statins Away?”) you can’t even show that statins significantly reduce heart attack risk in healthy populations.

If you can’t prove that statins reduce the risk of heart attacks in a healthy population, it should come as no surprise that you can’t prove that fish oil reduce heart attacks in a healthy population. To answer that question we need to look at whether fish oil reduces the risk of heart attacks in high risk populations.

Fish Oil And Heart Disease Risk In Sick People – The Early Studies

Most of the early studies looking at the effect of fish oil in patients at high risk of cardiovascular disease (what we scientists refer to as secondary prevention studies) reported very positive results.

For example, the DART1 study (Burr et al, Lancet, 2: 757-761, 1989) and the US Physician’s Health Study (Albert et al, JAMA, 279: 23-28, 1998) reported a 29% decrease in total mortality and a 52% decrease in sudden deaths related to heart disease in patients consuming diets rich in omega-3 containing fish.

Even more striking was the GISSI-Prevenzione study (Marchioli et al, Lancet, 354: 447-455, 1999; Marchioli et al, Eur. Heart J, 21: 949-952, 2000; Marchioli et al, Circulation, 105: 1897-1903, 2002). This was a very robust and well designed study. It looked at the effect of a fish oil supplement providing 1 g/day of omega-3 fatty acids on the risk of a second heart attack in 11,323 patients who had survived a non-fatal heart attack within the last 3 months – a very high risk group.

The results were clear cut. Over the next 3.5 years supplementation with fish oil reduced overall death by 15% and sudden death due to heart disease by 30% compared to a placebo. And, if you looked at the first 4 months, when the risk of a second heart attack is highest, the fish oil supplement reduced the risk of overall death by 41% and sudden death by 53%.

The authors estimated that treating 1,000 heart attack patients with 1 g/day of fish oil would save 5.7 lives per year. That is almost identical to the 5.2 lives saved per 1,000 patients per year by the statin drug pravastatin in the LIPID trial (NEJM, 339: 1349-1357, 1998).

No wonder the American Heart Association said that patients “could consider fish oil supplementation for heart disease risk prevention.”

Fish Oil And Heart Disease Risk In Sick People – The Latest Studies

However, the most recent studies have been uniformly negative. For example, the ORIGIN trial (Bosch et al, NEJM, 367: 309-318, 2012) treated 12,536 patients who were considered at high risk of heart disease because of diabetes or pre-diabetes with either 1 g/day of fish oil or a placebo. This was also a robust, well designed study, and it found no effect of the fish oil supplement on either heart attacks or deaths due to heart disease.

Similarly, a recent meta-analysis looking at the combined effects of 14 randomized, double-blind, placebo-controlled trials in patients at high risk of heart disease found no significant effect of fish oil supplements on overall deaths, sudden death due to heart disease, heart attacks, congestive heart failure or stroke (Kwak et al, Arch. Int. Med., 172: 686-694, 2012).

No wonder you are confused by all of the conflicting studies. You must be wondering: “Is the American Heart Association wrong?” “Are fish oil supplements useless for reducing heart disease risk?”

What Has Changed Between The Early Studies & The Latest Studies?

When a trained scientist sees the outcome of well designed clinical studies change over time, he or she asks: “What has changed in the studies?” It turns out that a lot has changed.

1) In the first place the criteria for people considered at risk for heart attack and stoke have changed dramatically. Not only has the definition of high cholesterol” been dramatically lowered, but cardiologists now treat people for heart disease if they have inflammation, elevated triglycerides, elevated blood pressure, diabetes, pre-diabetes or minor arrythmia.

For example, the GISSI-Prevenzione study recruited patients who had a heart attack within the past three months, while the ORIGIN study just looked at people who had diabetes or impaired blood sugar control. While both groups could be considered high risk, the patients in the earlier studies were at much higher risk for an imminent heart attack or stroke – thus making it much easier to detect a beneficial effect of omega-3 supplementation.

2) Secondly, the standard of care for people considered at risk for heart disease has also changed dramatically. In the earlier studies patients were generally treated with one or two drugs – generally a beta-blockers and/or drug to lower blood pressure. In the more recent studies the patients generally receive at least 3 to 5 different medications – medications to lower cholesterol, lower blood pressure, lower triglycerides, reduce inflammation, reduce arrhythmia, reduce blood clotting, and medications to reduce the side effects of those medications.

Since those medications perform many of the beneficial effects of omega-3 fatty acids, it is perhaps no surprise that it is now very difficult to show any additional benefit of omega-3 fatty acids in patients on multiple medications.

The bottom line is that we are no longer asking the same question. The earlier studies were asking whether fish oil supplements reduce the risk of heart attacks or cardiovascular death in patients at high risk of heart disease. The more recent studies are asking whether fish oil supplements provide any additional benefits in a high risk population that is already on 3-5 medications to reduce their risk of heart disease.

However, the people who are writing the headlines you are reading (and the videos you are watching) are not making that distinction. They are pretending that nothing has changed in the way the studies are designed. They are telling you that the latest studies contradict the earlier studies when, in fact, they are measuring two different things.

Is Fish Oil Really Snake Oil?

Was the doctor who made the video “Is Fish Oil Just Snake Oil?” correct in saying that omega-3 fatty acids are ineffective at reducing the risk of heart disease? The answer is yes and no.

If you take the medical viewpoint that the proper way to treat anyone at the slightest risk of heart disease is with 3-5 medications – with all of their side effects, the answer seems to be pretty clear cut that adding fish oil to your regimen provides little additional benefit.

However, that is not the question that interests me. I’d like to know whether I can reduce my risk of heart attack and cardiovascular death by taking omega-3 fatty acids in place of those drugs – as the original studies have shown.

I’m sure many of my readers feel the same way.

The Bottom Line

Studies performed prior to 2000 have generally shown that fish oil supplements reduce the risk of a second heart attack in patients who have previously had a heart attack. One study even suggested that they were as effective as statin drugs at reducing heart attack risk in this population.

Recent studies have called into question the beneficial effects of fish oil supplements at reducing the risk of heart disease. However, these studies were performed with lower risk patients and the patients were on 3-5 medications to reduce their risk of heart attack or stroke.

The recent studies are no longer evaluating whether fish oil supplements can reduce the risk of heart disease. They are asking whether they have any additional beneficial effects for people taking multiple medications. That’s a totally different question.

So ignore the headlines saying that fish oil is snake oil. If you are content taking multiple medications to reduce your risk of heart disease, it is probably correct to say that omega-3 fatty acids provide little additional benefit.

However, if you are interested in a more holistic, drug-free approach to reducing your risk of heart disease, I still recommend omega-3 fatty acids as part of a heart healthy diet, as does the American Heart Association.

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.