Does Carnitine Increase Heart Disease Risk?

April 8, 2014 by Dr. Steve Chaney

Carnitine: Dr. Jekyl or Mr. Hyde?

Author: Dr. Stephen Chaney

It’s both interesting and confusing when one Journal article appears talking about the dangers of a particular supplement and just a couple of weeks later another article appears talking about the benefits of that same supplement – especially when the conclusions of both articles are misrepresented in the media.

But that’s exactly what has just occurred with the supplement L-carnitine. Media reports of the first article trumpeted the headline “Cleveland Clinic study links L-carnitine to increased risk of heart disease”. Media reports of the second article featured the headline “Mayo Clinic review links L-carnitine to multiple health heart benefits”. As you might suspect, neither headline was completely accurate. So let me help you sort out the confusion about L-carnitine and heart health

What is Carnitine?

But first let me give you a little bit of background about L-carnitine. L-Carnitine is an essential part of the transport system that allows fatty acids to enter the mitochondria where they can be oxidized and generate energy. So it is an essential nutrient for any cell that has mitochondria and utilizes fatty acids as an energy source.

L-carnitine is particularly important for muscle cells, and the hardest working muscle cells in our body are those that pump blood through our hearts. So when we think of L-carnitine we should think of heart health first.

But that doesn’t mean that L-carnitine is an essential nutrient. In fact, our bodies generally make all of the L-carnitine that we need. There are some metabolic diseases that can prevent us from making L-carnitine or utilizing L-carnitine efficiently. People with those diseases benefit from L-carnitine supplementation, but those diseases are exceedingly rare.

There is some evidence that supplemental L-carnitine may be of benefit in individuals suffering from congestive heart failure and other diseases characterized by weakened heart muscles. Other than that there is little evidence that supplemental L-carnitine is beneficial for healthy individuals.

Does Carnitine Increase Heart Disease Risk?

Let’s look at the first study (Koeth et al, Nature Medicine, doi:10.1038/nm.3145, April 7, 2013) – the one that purportedly linked L-carnitine to increase risk of heart disease. The authors were trying to gain a better understanding of the well-established link between red meat consumption and cardiovascular disease risk. The classical explanation of this link has been the saturated fat and cholesterol content of the red meat.

However, several recent studies have questioned whether saturated fat and cholesterol actually increase the risk of cardiovascular disease (see last week’s article “Are Saturated Fats Good For You?”)

Since red meat is also high in L-carnitine, the authors hypothesized that it might be the L-carnitine or a metabolite of the L-carnitine that was associated with increased risk of heart disease in people consuming red meat.

The authors honed in on a metabolite of L-carnitine called trimethylamine-N-oxide or TMAO that is produced by bacteria in the intestine and had been previously shown to accelerate atherosclerosis in mice. They developed what they called an L-carnitine challenge. Basically, they gave their subjects an 8 ounce sirloin steak, which contains about 180 mg of L-carnitine, and measured levels of L-carnitine and TMAO in the blood one hour later and the urine 24 hours later. [I’m guessing they didn’t have much trouble finding volunteers for that study.]

When the subjects were omnivores (meaning meat eaters) they found a significant increase in both L-carnitine and TMAO in their blood and urine following the L-carnitine challenge. When they put the same subjects on broad-spectrum antibiotics for a week to wipe out their intestinal bacteria and repeated the L-carnitine challenge, they found an increase in L-carnitine but no increase in TMAO. This simply confirmed that the intestinal bacteria were required for the conversion of L-carnitine to TMAO.

Finally, because previous studies have shown that omnivores and vegetarians have very different populations of intestinal bacteria, they repeated their L-carnitine challenge in a group of vegans and found that consumption of the same 8 ounce sirloin steak by the vegans did not result in any significant increase in TMAO in either their blood or urine.

Armed with this information, the authors measured L-carnitine and TMAO concentrations in the fasting blood of 2595 patients undergoing cardiac evaluation in the Cleveland Clinic. They used an established protocol to assess the three-year risk for major adverse cardiac events in the patients they examined. They observed a significant association between L-carnitine levels and cardiovascular event risks, but only in subjects who also had high blood levels of TMAO.

Now it’s time to compare what the headlines said to what the study actually showed. The headlines said “L-carnitine linked to increased risk of heart disease”. What the study actually showed was that there were two things that were required to increase the risk of heart disease – L-carnitine and a population of intestinal bacteria that converted the L-carnitine to TMAO.

The major source of L-carnitine in the American diet is red meat, and habitual red meat consumption is required to support a population of intestinal bacteria that is capable of converting L-carnitine to TMAO. So the headlines should have read “red meat consumption linked to increased risk of heart disease”. But, of course, that’s old news. It doesn’t sell subscriptions.

Does Carnitine Decrease Heart Disease Risk?

The second study (DiNicolantonio et al, Mayo Clinic Proceedings, dx.doi.org/10.1016/j.mayocp.2013.02.007) was a meta-analysis. It reviewed 13 clinical studies involving 3629 people who had already had heart attacks and were given L-carnitine or a placebo after the heart attack.

In evaluating the results of this study it is useful to remember that a heart attack generally kills some of the heart muscle and weakens some of the surviving heart muscle. When the data from all of the studies was combined the authors reported a 27% reduction in all cause mortality, a 65% reduction in arrhythmias, and a 40% reduction in angina. However, there was no reduction in a second heart attack or the development of heart failure.

So perhaps the headlines describing this study were a little closer to being on target, but they failed to mention that these effects were only seen in people who had already suffered a heart attack and had weakened heart muscles. They also failed to mention that there was no decreased risk of a second heart attack or congestive heart failure.

The Bottom Line:

1) The first study should be considered preliminary. It needs to be confirmed by other studies. If it is true, it is not ground breaking. It merely gives us a fuller understanding of why red meat consumption may be linked to increased risk of heart disease and gives you yet another reason to minimize red meat consumption.

The study does raise the possibility that use of L-carnitine supplements may increase your risk of heart disease if you eat red meat on a regular basis, and that this same risk may not be associated with L-carnitine supplementation if you are a vegan. But the study did not directly test that hypothesis, and much more research is required before I would give it any weight.

2) The second study suggests that if you have already had a heart attack, you may want to consult with your physician about whether L-carnitine supplementation might be of benefit. Once again, this study is not ground breaking. We already knew that L-carnitine supplementation was helpful for people with weakened heart muscle. This study merely confirmed that.

Contrary to what the headlines suggested, this study provides no guidance about whether L-carnitine supplementation has any heart health benefits in people without pre-existing heart disease – and the bulk of existing literature suggests that it does not.

3) Finally, I realize that the major use of L-carnitine in the US market is in sports supplements purported to increase strength and endurance. The literature on that is decidedly mixed, but that’s another subject for another time.

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 Saturated Fats Good For You?

April 1, 2014 by Dr. Steve Chaney

Is Everything We Thought We Knew About Fats Wrong?

Author: Dr. Stephen Chaney

Bring out the fatted calf! Headlines are proclaiming that saturated fats don’t increase your risk of heart disease – and that they may actually be good for you.

The study (Annals of Internal Medicine, 160: 398-406, 2014) that attracted all the attention in the press was what we scientists call a meta-analysis. Basically, that is a study that combines the data from many clinical trials to improve the statistical power of the effect being studied.

And it was a very large study. It included 81 clinical trials that looked at the effects of various types of fat on heart disease risk.

Are Saturated Fats Good For You?

The answer to this question is a simple No. The headlines suggesting that saturated fats might be good for you were clearly misleading. The study concluded that saturated fats might not increase the risk of heart disease, but it never said that saturated fats were good for you.

In short, the study concluded that:

Saturated fats, monounsaturated fats and long-chain omega-6 polyunsaturated fats did not affect heart disease risk.

Long chain omega-3 polyunsaturated fats decreased heart disease risk [Note: The original version of the paper said that the decrease was non-significant, which is what the headlines have reported. However, after several experts pointed out an error in their analysis of the omega-3 data, the authors corrected their analysis, and the corrected data show that the decrease in risk is significant.]

Trans fats increased heart disease risk

If those conclusions are correct, they would represent a major paradigm shift. We have been told for years that we should limit saturated fats and replace them with unsaturated fats. Has that advice been wrong?

Is Everything We Thought We Knew About Fats Wrong?

Before we bring out the fatted calf and start heaping butter on our12 ounce steaks, perhaps we should look at some of the limitations of this study.

We Eat Foods, Not Fats

When the authors broke the data down into the effects of individual saturated and unsaturated fatty acids on heart disease risk some interesting insights emerge.

For example, with respect to saturated fats:

Both palmitic acid and stearic acid – which are abundant in palm oil and animal fats – increased the risk of heart disease.

On the other hand, margic acid – which is more abundant in dairy products – decreased the risk of heart disease.

So while the net effect of saturated fats on heart disease risk may be zero, these data suggest:

It is still a good idea to avoid fatty meats, especially red meats, if you want to reduce your risk of heart disease. When you focus on foods, rather than fats this fundamental advice has not changed in over 40 years! In next week’s “Health Tips From the Professor” I will share some of the latest research on the dangers of red meat.

With fatty dairy foods the situation is a little more uncertain. I’m not ready to tell you to break out the butter and whipped cream just yet, but recent research does suggest that dairy foods have some beneficial effects that may outweigh their saturated fat content.

With respect to omega-3 fatty acids:

alpha-linolenic acid – which is found in vegetable oils and nuts and is the most abundant omega-3 fatty acids in our diets – had no effect on heart disease risk.

On the other hand, EPA and DHA – which are found primarily in oily fish and omega-3 supplements – decreased heart disease risk by 20-25%.

Once again, while the net effect of omega-3 fatty acids on heart disease risk was very small, that’s primarily because most Americans consume mostly alpha-linolenic acid and very little EPA and DHA. This study shows that fish oil significantly reduces heart disease risk, which is fully consistent with the heart healthy advice of the American Heart Association and National Institutes of Health over the past decade or more.

What We Replace the Fats With Is Important

A major weakness of the current study is that it did not ask what the individual clinical trials were replacing the fatty acids with. Many of them were simply replacing the saturated fats with carbohydrates. To understand why that is important, you have to go back to the research of Dr. Ancel Keys.

The whole concept of saturated fats increasing the risk of heart disease is based on the groundbreaking research of Dr. Ancel Keys in the 50’s and 60’s. But, it is important to understand what his research showed and didn’t show.

His research showed that when you replaced saturated fats with monounsaturated fats and/or polyunsaturated fats the risk of heart disease was significantly reduced. He was the very first advocate of what we now call the Mediterranean diet. (He lived to 101 and his wife lived to 97, so he must have been on to something.)

Unfortunately, his diet advice got corrupted. The mantra became low fat diets, where the saturated fat was replaced with carbohydrates – mostly simple sugars and refined flours. Since diets containing a lot of simple sugars and refined flours also increase the risk of heart disease you completely offset the benefits of getting rid of the saturated fats.

Just in case you think that is outdated dietary advice, Dr. Key’s recommendations were confirmed by a major meta-analysis published in 2009 (American Journal of Clinical Nutrition, 89: 1425-1432, 2009). That study showed once again that replacing saturated fats with carbohydrates had no effect on heart disease risk, while replacing them with polyunsaturated fats significantly reduced risk.

The Bottom Line:

You can put the fatted calf back out to pasture. The headlines telling you that saturated fats don’t increase the risk of heart disease were overstated and misleading. This study does not represent a paradigm shift. In fact, when you analyze the study in depth it simply reaffirms much of the current dietary advice about fats.

1) When you simply replace saturated fats with carbohydrates, as did many of the studies in the meta-analysis that generated all of the headlines, there is little or no effect on heart disease risk. However, other studies have shown that when you replace the saturated fats with monounsaturated and polyunsaturated fats you significantly reduce heart disease risk.

In short, if you are interested in reducing your risk of heart disease, low fat diets may be of relatively little value while Mediterranean diets may be beneficial. No paradigm shift there. That sounds pretty familiar.

2) Fatty meats, especially red meats, appear to increase the risk of heart disease. No surprises there.

3) Alpha-linolenic acid, the short chain omega-3 fatty acid found in nuts, seeds and vegetable oils, does not decrease heart disease risk. However, EPA and DHA, the long chain omega-3 fatty acids found in fatty fish and fish oil supplements significantly decrease heart disease risk. That’s probably because the efficiency of conversion of alpha-linolenic acid to EPA & DHA in our bodies is only around 10%. No surprises there.

4) The study did suggest that dairy foods may decrease heart disease risk. While there are a few other studies supporting that idea, I’m not ready to break out the butter and whipped cream yet. More research is needed.

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

Can Diet Alter Your Genetic Destiny?

March 25, 2014 by Dr. Steve Chaney

Disease Is Not Inevitable

Author: Dr. Stephen Chaney

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

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

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

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

Can Diet Alter Your Genetic Destiny?

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

1) Your genetic makeup can influence your nutrient requirements.

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

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

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

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

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

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

3) Diet can actually alter your genes.

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

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

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

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

Examples Of How Diet Can Alter Genetic Predisposition

Heart Disease

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

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

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

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

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

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

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

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

Cancer

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

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

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

Diabetes

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

Cellular Stress Response

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

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

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

Obesity

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

The Bottom Line:

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

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

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

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

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

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

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

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

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

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 Dietary Polyphenols Associated With Longevity?

October 22, 2013 by Dr. Steve Chaney

Are Polyphenols The Fountain of Youth?

Author: Dr. Stephen Chaney

You’ve probably heard that resveratrol and other polyphenols in red wine can help mice live longer. But what about us? Are dietary polyphenols associated with longevity in humans?

Until recently nobody knew the answer to that question. However, a recent study (Zamora-Ros et al, J. Nutr. 143: 1445-1450, 2013) suggests that polyphenols may just help us live a bit longer.

Of course, the news headlines make it sound like a sure thing, and many of the manufacturers of polyphenol-containing supplements are already citing the study as “proof” that their products will make you live forever.

Polyphenols Are Everywhere:

So, let me give you some background information before I start diving into the study.

The term polyphenols includes some names you may recognize, such as flavonoids, isoflavones, anthrocyanidins and resveratrol, and many more that might look like the kind of names you might expect to find on a processed food label.

Polyphenols don’t just come from red wine. There are several hundred polyphenols in edible foods. Many fruits, vegetables (including beans like soybeans) and whole grains – the kinds of foods that every expert recommends for a healthy diet – are also great sources of polyphenols.

Most polyphenols are excellent antioxidants. Studies suggest that they may also exert antiinflammatory effects and may reduce the risk of heart disease, neurodegenerative disease and cancer. So it is not unreasonable to assume that they might enhance longevity.

An In-Depth Analysis Of The Study:

The study enrolled 807 men and women over the age of 65 (average age = 74, range = 67-81) from the Chianti region of Italy and followed them for 12 years. At the beginning of the study polyphenol intake of the participants was analyzed from a dietary recall form (polyphenol intake based on what they remembered eating) and from a 24 hour urine specimen (actual polyphenol intake).

During the 12 year follow-up, 34% of the participants died. Based on the dietary recall, there was no association between dietary polyphenol intake and mortality. However, based on urinary polyphenol content there was a 30% decrease in mortality for those with the highest dietary polyphenol intake (>650 mg/day) compared to those with the lowest polyphenol intake (<500 mg/day).

Strengths of the Study:

This is the very first study to actually investigate the relationship between dietary polyphenols and longevity in a meaningful way. The study was well designed and well executed.

The measurement of urinary polyphenol content is a strength of this study. Dietary recalls are often inaccurate. In fact, this study suggests that dietary recalls should probably not be used to estimate dietary polyphenol intake in future studies.

Weaknesses of the Study:

This was a first study of its kind, and like any other first study it needs to be confirmed by additional studies.

The study only measured associations, not cause and effect. Of course, it would be almost impossible to conduct a double blind, placebo controlled study of this duration – especially if one is using urinary excretion as a measure of polyphenol intake.

The study did not report the dietary sources of the polyphenols, although this information was presumably available from the dietary recalls. Because the study was conducted in the Chianti region of Italy it is probably pretty safe to assume that red wine contributed to the polyphenol intake. However, people in that region of Italy also tend to consume diets rich in fruits and vegetables. Hopefully, future studies will help determine whether some polyphenols are more important for longevity than others.

The Bottom Line:

1) Eat lots of fresh fruits and vegetables. They’ll make you healthier, and you just may live longer.

2) If you like red wine, drink it in moderation. Just don’t assume that it can substitute for a healthy diet. This study measured total polyphenols, not just red wine polyphenols.

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 There Really Such A Thing A Positive Stress?

October 17, 2013October 17, 2013 by Dr. Steve Chaney

Stress Can Be Your Friend

Author: Dr. Pierre DuBois

Do you consider yourself an optimist or a pessimist? When the going gets tough, the optimists among you can take heart—new research that has found that viewing stress positively can be of benefit to both the mind and body.

When the brain perceives stress (either physical or psychological), it reacts by releasing cortisol, adrenaline and norepinephrine to prepare the body for a “fight or flight” response. Fortunately for us, this response is not triggered in most people today as frequently as it once was or for the same kinds of reasons.

After all, relatively few of us are in life-threatening situations on a regular basis. Today’s “modern” stresses are more likely to be caused by wrestling with the IRS, trying to escape a traffic jam or competing with a coworker for a promotion.

It is interesting to note that stress, in itself, is not necessarily a negative thing. It is how we perceive it that makes it either good or bad for us. This is a hopeful discovery, as most people have only limited control over how much stress they experience. The everyday stresses of modern life are difficult to escape. But if we can train our minds to view them as a challenge rather than a threat, it could actually help to bring about better health.

Scientists from a handful of universities, including Yale University and Columbia University, examined the effects of stress on 300 investment bankers who had just emerged from a round of layoffs (I know it’s difficult to feel bad for the stress of investment bankers, but stay with me here). In the study, published in the Journal of Personality and Social Psychology, scientists divided the participants into two groups, and tried to alter the perception of half of them to view stress as debilitating and the other half to view it as an enhancement.

The first half of the participants were shown videos of people succumbing to stress. The other half were shown videos of people meeting challenges, such as sports figures accomplishing a difficult goal. The results showed that those who had a more optimistic view of stress had fewer health problems, including headaches and muscle pain, and performed better at work than the pessimistic group. In addition, levels of cortisol (the stress hormone) were lower in those who viewed stress as potentially enhancing.

There is actually a term for positive stress, called eustress, which was coined by endocrinologist Hans Selye in the 1970s. It has been proven that stress in moderation improves cognitive performance and improves memory.

Good stress involves the kind of challenges where we feel that we are in control and are accomplishing something. It boosts the immune system and can improve heart function. So eliminating all stress from our lives is probably not a good idea.

The stress to watch out for is the chronic, long-term emotional stress, which causes stress hormones to remain at persistently high levels, leading to many chronic ailments such as heart disease, high blood pressure and depression.

However, viewing certain stressors as challenges rather than threats can be a positive thing and can help ensure that you have a healthy, satisfying and exciting life.

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 Skipping Breakfast Increase Heart Disease Risk?

October 17, 2013September 10, 2013 by Dr. Steve Chaney

Should You Eat Breakfast Every Day?

Author: Dr. Stephen Chaney

Does skipping breakfast actually increase your risk of heart attacks? You’ve probably heard the saying “Eat breakfast like a king, lunch like a prince, and dinner like a pauper”.

You’ve probably also heard that skipping breakfast is associated with increased risk of things like:

obesity
high blood pressure
and diabetes

If you believe those associations are true, the latest study showing an association between skipping breakfast and heart disease risk just makes sense. After all, obesity, high blood pressure and diabetes all increase the risk of heart disease.

But, how good is the evidence skipping breakfast actually increases the risk of any of those things?

The evidence for the link between skipping breakfast and heart disease risk:

Let’s start with the current study linking breakfast skipping with heart disease (Cahill et al, Circulation, 128: 337-343, 2013) because its study design is similar to the studies linking breakfast skipping to obesity, high blood pressure and diabetes. This study surveyed the eating habits of 27,000 men (45+ years old) enrolled in the Health Professionals Follow-Up Study in 1992 and followed those men for 16 years.

The results were pretty dramatic. After correcting for other factors that might influence heart disease risk, the men who skipped breakfast were 27% more likely to develop heart disease over the next 16 years than the men who ate breakfast on a daily basis.

As impressive as the association between breakfast and heart disease was, there was an even more impressive association that never made it into the headlines.

There was no association between skipping breakfast and eating late in the evening. However, those men who ate late in the evening were 53% more like to develop heart disease than men who did not.

The pros and cons of the study:

The pros:

1) The strength of this study is that it is large (27,000 participants), long (16 years) and well designed. The results were statistically very significant.

The cons:

1) This study only shows associations. It does not prove cause and effect. Having said that, it would be really, really hard to design a placebo controlled study for breakfast versus no breakfast. So cause and effect is almost impossible to prove for this type of comparison.

2) The study did not ask what kind of breakfast the participants were eating. We don’t know whether the breakfasts were a Danish and coffee, an Egg McMuffin and hash browns or a high protein smoothie with perhaps some fruit or oatmeal– and, believe me, there is a difference among those three breakfasts!

The Bottom Line:

1) Eating breakfast is probably a good thing. Yes, the evidence that skipping breakfast increases heart disease risk is circumstantial, but it is also substantial. This is a large, well designed study.

2) Not all breakfasts are equal. You probably already knew that! I recommend a breakfast with fruit, nuts, whole grains in moderation and lean protein sources.

3) While this particular study only included men, previous studies suggest that the potential health risks of skipping breakfast are equally strong for women.

4) Finally, while skipping breakfast grabbed all the headlines, the data suggest that eating late at night is an even stronger predictor of heart disease risk.

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

Can Soft Drinks Cause Heart Disease?

October 17, 2013September 2, 2013 by Steve Chaney

Put Down That Soda

Author: Dr. Stephen Chaney

Can Soft Drinks Cause Heart Disease? For today’s “Health Tip” I’m going to paraphrase a quote from your some of your favorite action flicks: “Put down that soda and back away and nobody gets hurt.”

You see, the news about soft drinks keeps getting worse and worse! You’ve probably already heard that soft drink consumption leads to weight gain, pre-diabetes and possibly even diabetes because calories in liquid form do not affect appetite to the same extent as calories in solid form.

Soft Drink Consumption increases the risk of heart attack and stroke in women:

As if that weren’t bad enough, three recent studies suggest that soft drinks consumption is also associated with increased risk of heart attacks and stroke.

The first study looked at sweetened beverage consumption and risk of coronary heart disease in women (Fung et al, Am. J. Clin. Nutr., 89: 1037-1042, 2009).

This study followed 88,520 women enrolled in the Nurses Health Study for 24 years. Consumption of sugar-sweetened beverages (either sodas or non-carbonated sugar-sweetened beverages such as Hawaiian Punch, lemonade and other non-carbonated fruit drinks) was assessed from food-frequency questionnaires administered 7 times during the 24 years. And the total incidence of coronary events (both fatal and non-fatal) was recorded.

The results were striking. When they compared women who consumed as little as one sugar-sweetened beverage per day with women who consumed those beverages less than once per month, the increased risk of coronary heart disease was 23%. And when they compared women who consumed more than two sugar-sweetened beverage per day with women who consumed those beverages less than once per month, the increased risk of coronary heart disease was a whopping 35%.

Sodas are just as harmful for men:

And, in case you guys thought you were off the hook, a study has just been published showing similar results in men (de Koning et al, Circulation, March 12, 2012, Epub ahead of print). This study was a 22 year follow up of 42,883 men enrolled in the Men’s Health Professional study. The study design and results were very similar to the ones obtained previously in the Nurses Health Study except that this study did not distinguish between subjects consuming one sugar sweetened beverage a day and those consuming more than one each day.

When they compared men who consumed one or more sugar sweetened beverage a day to men who never consumed sugar-sweetened beverages, the increased risk of coronary heart disease was 20%.

Diet sodas are just as bad as regular sodas:

Finally, you may be saying that this information doesn’t apply to you because you only consume diet sodas or artificially sweetened non-carbonated beverages.

Unfortunately, you may not be off the hook either!

Another study published in January 2012 reported that diet soft drink consumption is also associated with increased risk of coronary heart disease – including strokes (Gardener et al, J. Gen. Intern. Med., DOI: 10.1007/sl11606-011-1968-2). This study followed 2564 men and women enrolled in the Northern Manhattan Study for 10 years.

The people in this study who consumed more than one diet soda or artificially sweetened beverage/day were 43% more likely to have a vascular event (heart attack or stroke) then the people consuming less than one diet beverage/month. This study is in line with previous studies showing that diet soda consumption is associated with increased risk of pre-diabetes and type 2 diabetes.

And, as I have pointed out in my previous “Health Tips”, there is no convincing evidence that diet sodas actually help prevent weight gain. Sure there are several published studies showing that when dietitians supervise the diets of the study participants, you can achieve weight loss by substituting diet beverages for sugar containing beverages.

However, two major studies have shown that when you look at free-living populations, consumption of diet beverages is associated with just as much weight gain as consumption of sugar containing beverages (Dhingra et al, Circulation,116: 480-488, 2007; Fowler et al,

Obesity, 16:1894-1900, 2008). Apparently, without a dietitian looking over our shoulder, we manage to make up for those lost calories somewhere else!

The Bottom Line:

So what’s the bottom line for you?

You should be aware that these studies just look at associations – not cause and effect – and they can be skewed by the characteristics of the study populations. For example, there were some striking inconsistencies between the 3 studies I cited that are likely due to differences in the population groups that they sampled. However, despite some differences from one study to the next, the weight of accumulating evidence seems to suggest that sodas – both sugar containing and diet – are really not good for us.

So it’s back to my original advice: “Just put down that soda and nobody gets hurt.” Water is sounding better and better!

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.