Can Fish Oil Make Children Smarter?

May 20, 2014 by Dr. Steve Chaney

When Do Omega-3 Supplements Make Sense?

Author: Dr. Stephen Chaney

We know that the omega-3 fatty acids found in fish oil are critically important for brain development. But will they really help our kids learn better? Some studies suggest that they do, while other studies have come up empty. Why is this? More importantly, what does it mean for your children? Will fish oil supplements help or not?

I’ve selected today’s study (Portillo-Reyes et al, Research in Developmental Disabilities, 35: 861-870, 2014) because it sheds some light on those important questions.

Can Fish Oil Make Children Smarter?

This study looked at the effect of supplementation for 3 months with 360 mg of EPA + DHA on cognitive function of malnourished Mexican children, ages 8-12 years old. The children came from poor neighborhoods where foods rich in omega-3 fatty acids were seldom available. Low intake of omega-3 fatty acids was confirmed by a food frequency survey.

Cognition was assessed based on a battery of 16 standardized cognition tests at the beginning of the study and again 3 months later.

The results were fairly clear cut. The children receiving the fish oil supplements showed significant gains in mental processing speed, visual-motor coordination, perceptual integration, attention span and executive function compared to children receiving a placebo. In case you were wondering, the first three most strongly affect a child’s ability to learn and last two affect their tendency to display ADHD symptoms.

What Is the Significance of This Study?

There are a lot of things not to like about the study:

It was a small study (59 children total)
Blood levels of omega-3 fatty acids were not determined.
It was a short term study (12 months would have been better).
Measuring the ability to learn is difficult. Experts in the field differ about which cognitive tests are best. I’m not taking a position on the adequacy of the tests they were using because that is not my area of expertise.
Because it was done in a poor region of Mexico, one could argue that its applicability to children in this country is uncertain.

So why even mention this study? That’s because it illustrates an important principle – one that is often ignored in the design and interpretation of clinical studies.

Simply put, the principle is that not everyone will benefit equally from supplementation. It is the malnourished and the sick who will benefit most. When you focus your clinical studies on those groups you are most likely to observe a benefit of supplementation. When you focus your study on well nourished, healthy individuals it will be much more difficult to observe any benefit. And if you perform a meta-analysis of all studies, without evaluating the studies on the basis of need – nutrition status and health status – benefits will also be much more difficult to demonstrate.

This study is just one example of that principle. In an earlier “Health Tips From the Professor” (Can DHA Help Johnny Read?) I reported on a study looking at the effect of DHA supplementation on reading ability of English schoolchildren. In that study, it was the children who were most deficient in DHA and started with the lowest reading skills who benefitted most from DHA supplementation.

What does all of this mean to you?

If you are a parent, you may be asking if a study done with Mexican children eating poor diets has any relevance for your kids. In today’s world of pop tarts and pizza it just might. Most children don’t order sardines on their pizza. As a consequence, many American children don’t get enough omega-3 fatty acids in their diet.

Should your children be getting more omega-3s in their diet? A recent study concluded that most American children only get 20-40 mg/day of DHA from their diet. So if your child’s food preferences don’t include salmon, sardines and the like – and if your child is experiencing learning issues or problems with ADHD, you might consider adding fish oil supplements to their diet. There’s no need to megadose. The international standard is around 200 mg/day of DHA for children 7 or older.

If you are one of those people who is confused by conflicting headlines about the benefits of supplementation, you may want to look at the studies behind those headlines and ask if supplementation would have been likely to provide any benefit in the subjects studied.

The Bottom Line:

1) A recent study reported that supplementation with fish oil significantly improved learning skills in children consuming a diet that was deficient in omega-3 fatty acids.

2) If your children are not consuming foods rich in omega-3 fatty acids such as coldwater fish, you might wish to make sure that they are getting adequate levels of omega-3 fatty acids in their diet. Most experts recommend around 200 mg/day for children over 7.

3) This study also illustrates the principle that supplementation is most likely to be of demonstrable benefit to those who have the worst diets and the greatest need. That doesn’t mean that supplementation won’t benefit everyone, but it does mean that it may be difficult to prove the value of supplementation in healthy people consuming a good diet.

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

Do Omega-3s Lower Blood Pressure?

May 6, 2014May 6, 2014 by Dr. Steve Chaney

The Good News About Fish Oil

Author: Dr. Stephen Chaney

High blood pressure or hypertension is a major problem in this country. Over 60% of Americans have high blood pressure. Only 47% of those with hypertension are adequately controlled. 20% of them don’t even know that they have high blood pressure.

In this case, ignorance is definitely not bliss. That’s because high blood pressure significantly increases the risk of stroke, heart attacks and congestive heart failure.

The causes of high blood pressure are many. Genetics, obesity, lack of exercise, sodium, alcohol, saturated fats and too few fresh fruits and vegetables all play a role. Age also plays a role. As we age, our blood vessels become less flexible and our blood pressure rises by about 0.6 mm Hg per year.

Medications can help, but many of them have significant side effects and often aren’t fully effective in controlling blood pressure. That’s why natural approaches are so important.

Because there are so many causes of hypertension, natural approaches for lowering your blood pressure are not simple. Natural approaches start with weight loss, restricting sodium intake, increasing physical activity, moderating alcohol intake and something called the DASH diet. In short, there is not just one simple change that you can make that will totally eliminate hypertension. It requires a complete lifestyle change.

That’s why the latest study on the effect of omega-3s on blood pressure is so exciting. If the headlines are true, adding omega-3s to your diet may be one of the most effective things you can do to lower your blood pressure naturally. So let’s examine the study to see if the headlines are accurate.

How Was The Study Designed?

This study (Miller et al, American Journal of Hypertension, doi:10.1093/ajh/hpu024) was a very large, well designed study. It is a meta-analysis of 70 randomized, placebo controlled clinical studies. Key characteristics of these studies were:

The mean study duration was 69 days. That means these beneficial effects occur relatively quickly.

The mean EPA + DHA dose was 3.8 g/day (range = 0.2 – 15 g/day). A wide range of doses was included.

The EPA & DHA came from all sources (seafood, EPA+DHA fortified foods, fish oil, algal oil, and purified ethyl esters. The source did not affect the outcome.

Olive oil was the most commonly used placebo, with omega-6 vegetable oils being used as placebos in a few studies. The choice of placebo did not affect the outcome.

None of the people in these studies were taking blood pressure lowering medications. That means these studies were specifically designed to see whether omega-3s lowered blood pressure, not whether they had any additional benefit for people already taking medications. This is important because if you only focus on groups who are already taking multiple medications, you tend to obscure the beneficial effects of omega-3s (see my recent Health Tip “Is Fish Oil Really Snake Oil?”)

Do Omega-3s lower Blood Pressure?

The authors of the study reported that:

Compared to placebo, EPA+DHA reduced systolic blood pressure (that’s the upper reading) by 1.52 mm Hg and diastolic blood pressure (that’s the lower reading) by 0.99 mm Hg.

When they looked at those participants who already had high blood pressure, the numbers were even more impressive – a 4.51 mm Hg decrease in systolic blood pressure and a 3.05 mm Hg decrease in diastolic blood pressure. That’s important because for each 2 mm Hg reduction in blood pressure there is a 6% decrease in stroke mortality, a 4% decrease in heart disease mortality, and a 3% decrease in total mortality.

More to the point, the authors of the study concluded that “A decrease of 4.51 mm Hg in systolic blood pressure among those with high blood pressure could help an individual avoid having to take medication to control blood pressure levels”.

When they looked at the study participants who had normal blood pressure the numbers were still significant – a 1.25 mm Hg decrease in systolic blood pressure and a 0.62 decrease in diastolic blood pressure. The authors pointed out that this could prevent, or at least delay, the age-related progression towards hypertension.

The effect of omega-3s on systolic blood pressure (4.51 mm Hg decrease) was comparable to the most successful lifestyle interventions – 3-10 mm Hg decrease for 10 pound weight loss, 4-9 mm Hg decrease for increased physical activity, 2-8 mm Hg decrease for sodium restriction, and 2-4 mm Hg for decreased alcohol consumption.

A dose of at least 1 gm/day of EPA+DHA was required for a significant decrease in systolic blood pressure, and a dose of over 2 gm/day was required for a significant decrease in both systolic and diastolic blood pressure

While this is a single study, it is consistent with a number of previous studies in this area. Based on the existing body of literature I would recommend omega-3s as part of a holistic approach for keeping your blood pressure under control.

The Bottom Line:

1) A recent meta-analysis of 70 published clinical studies (AJH, doi: 10.1093/ajh/hpu024) has shown fairly convincingly that omega-3 fatty acids are effective at lowering blood pressure. Moreover, this study is consistent with a number of previous studies. The evidence appears to be strong enough for omega-3s to be considered as part of a holistic approach to keeping your blood pressure under control.

2) If you already have high blood pressure, you should know that omega-3s caused blood pressure to decrease by 4.51 mm Hg in people like you. The authors of the study concluded that this decrease in blood pressure is large enough that some people may be able to avoid blood pressure medicines entirely. For others addition of omega-3s to their diet will likely allow their physicians to reduce the dose of medications required to keep their blood pressure under control – thus minimizing the side effects of the medications.

3) If you already have slightly elevated blood pressure that has not yet progressed to clinical hypertension, you should know that omega-3s also give a modest decrease in blood pressure in people like you. The authors of the study concluded that this decrease was enough to prevent or delay the age-related onset of hypertension.

4) The effect of omega-3s on reducing blood pressure is equivalent to the most successful lifestyle changes (weight loss, increased physical activity, sodium restriction and alcohol moderation). That doesn’t mean that you should pop fish oil pills and forget the other lifestyle changes. The idea is to combine as many of those lifestyle changes as possible so that you may never have to worry about high blood pressure again.

5) You need at least 1 gm/day of EPA+DHA to reduce systolic blood pressure and more than 2 gm/day to reduce both systolic and diastolic blood pressure.

6) Contrary to the hype you may have been reading elsewhere, the source of EPA+DHA didn’t matter. The only caveat is that many people really struggle with trying to get 1-2 gm/day of EPA+DHA from fish. It’s a bit too much of a good thing.

7) Don’t think of hypertension as a “Do it yourself” project. Hypertension is a silent killer. It’s one of those diseases where the first symptom is often sudden death – or, even worse, a life that is no longer worth living. Work with your physician. Let them help you find the right balance between lifestyle changes (including omega-3s) and medications to keep your blood pressure under control.

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 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.

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.

Are Dietary Supplements Safe?

March 18, 2014 by Dr. Steve Chaney

It’s a Jungle Out There

Author: Dr. Stephen Chaney

It’s a jungle out there. You probably already know that there are some bad players in the food supplement industry. There are companies that make products that don’t work, products that haven’t been tested for safety and efficacy, products are contaminated, and even products that are dangerous. There are some companies that even make products that contain dangerous drugs – drugs that can kill you.

Are Dietary Supplements Safe?

A recent report (Harel et al, JAMA Internal Medicine, doi: 10.1001/jamaintermed.2013.379) states that between January of 2004 and December of 2012 there were 465 drugs that were subject to a class I recall by the FDA. A class I recall is for cases in which there is a reasonable probability that use of or exposure to a product will cause serious adverse health consequences or death.

Now here’s the scary part: 98% of those recalls were for dietary supplements. The worst offenders were sexual enhancement products (40%), bodybuilding products (31%) and weight loss products (27%). And these weren’t all foreign-made products. 74% were manufactured in the United States.

[Note: If you are good at math, you will have noticed that leaves 0% for recalls of all other dietary supplements].

It’s A Jungle Out There

A perfect example of this scandalous behavior in certain segments of the food supplement industry is the DMAA saga. You may recall that I mentioned this in a recent “Health Tips From the Professor” titled “Are Fat Burning Supplements Safe?” Let me give you a very brief overview of that report, followed by the latest developments.

DMAA is short for dimethylamylamine. It is a stimulant that is chemically very similar to the ephedrine class of chemicals. The less reputable supplement manufacturers often add stimulants to their weight loss and bodybuilding products.

Stimulants do raise metabolic rate so they help with weight loss. They have no effect on athletic performance, but the athletes often feel like they have more energy – so they are popular in bodybuilding products. The problem is that many stimulants are dangerous. They can increase heart rate, cause arrhythmia, and they can kill people.

Because supplements with ephedra, another close realative of ephedrine, killed a bunch of people, the FDA forced supplement manufacturers to remove it from their products a number of years ago. You might have thought that the manufacturers would decide that adding stimulants to their products wasn’t a good idea. But no, they just substituted DMAA for ephedra. And guess what? The inevitable happened again. Two US soldiers died following DMAA usage in 2012.

The DMAA Scandal

The story really gets scandalous from here. The military ordered the removal of all DMAA containing products from U.S. Army and Air Force exchanges, but the FDA did not act. So what happened? Just about what you’d expect. Companies like GNC pulled their DMAA containing products from military bases, but continued to sell them from all their other stores.

Several months later the FDA finally acted. It sent a warning letter to all US manufacturers of DMAA containing products asking them to stop using DMAA as an ingredient in their supplements. All of the companies agreed to stop using it except one – USPLabs.

USPLabs claimed that DMAA could be found in geranium, which is an approved herbal ingredient, so they continued to use it. And GNC continued to sell their DMAA containing products in all its nonmilitary stores.

Finally, on April 11, 2013 the FDA issued a strongly worded warning about DMAA. The FDA warning said that by then there had been 86 reports of illnesses and deaths associated with supplements containing DMAA, and the preponderance of scientific evidence showed that DMAA was not a natural constituent of geranium.

The FDA said that they would take all possible means to get DMAA containing products off the market. A cynic might point out that the FDA did not act until the night before a high profile exposé on DMAA was scheduled to appear on NBC.

Finally, USPLabs threw in the towel and said that they would reformulate their DMAA containing products. A cynic might suspect that they will just substitute yet another stimulant for DMAA.

And, what about GNC? They said “It [DMAA] will be positioned out of stores, probably over the next five or six months as we sell existing inventory”. You don’t need a cynic to interpret that statement.

It wasn’t until the FDA raided their warehouses and removed all remaining DMAA-containing products that the DMAA story was over.

So what’s the bottom line for you? It is a jungle out there. Don’t fall for the hype and fancy claims. Do your homework, and stick with a company you can trust.

The Bottom Line:

1) When you hear headlines about dietary supplements killing people, you should realize that the bad players are found in only 3 types of dietary supplements – sexual enhancement products, bodybuilding products and weight loss products.

2) Just for perspective you should contrast any concerns about the safety of dietary supplements with:

The more than 35,000 deaths/year from properly prescribed medications…and…

The 8,000 deaths/year in US hospitals due to medication errors (Journal of General Internal Medicine, 25: 774-779, 2010)

3) When choosing supplements in that class use your common sense. Avoid those supplements promising magical gains in sexual prowess, increased muscle mass or weight loss.

4) Stick with a supplement company you can trust – one that is committed to only making supplements of proven benefit, and never making supplements that could cause any harm.

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

Do Selenium & Vitamin E Increase Prostate Cancer Risk?

March 11, 2014 by Dr. Steve Chaney

Should Men Avoid Those Supplements?

Author: Dr. Stephen Chaney

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

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

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

Do Selenium & Vitamin E Increase Prostate Cancer Risk?

Previous Studies On Selenium, Vitamin E And Prostate Cancer Risk

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

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

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

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

The Study That Generated The Headlines

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

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

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

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

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

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

What Do Other Experts Say?

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

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

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

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

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

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

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

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

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

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

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

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

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

The Bottom Line:

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

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

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

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

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

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

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.

Does Leucine Trigger Muscle Growth?

January 28, 2014 by Dr. Steve Chaney

What Does The Perfect Post-Workout Protein Shake Look Like?

Author: Dr. Stephen Chaney

If you work out on a regular basis and read any of the “muscle magazines”, you’ve seen the ads. “Explode Your Muscles.” “Double Your Gains.” They all claim to have the perfect post-workout protein shake, backed by science. They all sound so tempting, but you know that some of them have to be scams.

I told you about some of the sports supplements to avoid in a previous “Health Tips From the Professor”. In this issue, I’m going to ask “What does the perfect post-workout protein shake look like?”

For years athletes have been using protein beverages containing branched chain amino acids after their workouts to maximize muscle gain and recovery. There was some science behind that practice, but the major questions were unanswered. Nobody really knew:

How much protein is optimal?

What kind of protein is optimal?

What amount of branched chain amino acids is optimal?

Are some branched chain amino acids more important than others?

Does the optimal amount of branched chain amino acids depend on the amount of protein?

As a consequence, after workout protein supplements were all over the map in terms of protein source, protein amount, branched amino acid amount and type of branched chain amino acids. Fortunately, recent research has clarified many of these questions.

How Much And What Kind Of Protein Do You Need?

Recent research has shown that the optimal protein intake for maximizing muscle gain post workout is 15-20 gm for young adults (Katsanos et al, Am J Clin Nutr 82: 1065-1073, 2005; Moore et al, Am J Clin Nutr, 89: 161-168, 2009) and 20-25 gm for older adults (Symons et al, Am J Clin Nutr 86: 451-456, 2007).

More protein isn’t necessarily better. The effect of protein intake on post workout muscle gain maxes out at around 25 gm for young adults and 30 gm for older adults (Symons et al, J Am Diet Assoc 109: 1582-1586, 2009).

Whey protein is the best choice for enhancing muscle gain immediately after a workout. Other protein sources (soy, casein, chicken) are better choices for sustaining muscle gain over the next few hours.

Does Leucine Trigger Muscle Growth?

It turns out that leucine is the only branched chain amino acid that actually stimulates muscle protein synthesis (Am J Physiol Endocrinol Metab 291: E381-E387, 2006). And protein is what gives muscles their strength and their bulk.

Recent research has shown that 2-3 gm of leucine (2 gm for young adults; 3 gm for older adults) is sufficient to maximize post workout muscle gain if protein levels are adequate (Am J Physiol Endocrinol Metab 291: E381-E387, 2006).

Unanswered Questions About Optimizing Muscle Gain Post-Workout

Do the other branched chain amino acids play a supporting role, or is leucine alone sufficient to drive post-workout muscle gain?

Can leucine still help maximize post-workout muscle gain if protein intake is inadequate? If so, how much leucine is needed?

Does Leucine Enhancement Improve Low Protein Shakes?

A recent study (Churchward-Venne et al, Am J Clin Nutr, 99: 276-286, 2014) seems to answer those two questions. The authors compared the effect of 5 protein-amino acid combinations on muscle protein synthesis in 40 young men (~21 years old) following unilateral knee-extensor resistance exercise. The protein shakes contained:

25 gm of whey protein, which naturally contains 3 gm of leucine (high protein)

6.25 gm of whey protein, which naturally contains 0.76 gm of leucine (low protein)

6.25 gm of whey protein with 3 gm of leucine (low protein, low leucine)

6.25 gm of whey protein with 5 gm of leucine (low protein, high leucine)

6.25 gm of whey protein with 5 gm of leucine + added isoleucine and valine (the other branched chain amino acids). (low protein, branched chain amino acids).

The results were clear cut:

The high protein shake (25 gm of protein) was far superior to the low protein shake (6.25 gm of protein) at enhancing post workout protein synthesis. This is consistent with numerous other published clinical reports.

Adding 3 gm of leucine to the low protein shake had no effect on post-workout protein synthesis, but 5 gm of added leucine made the low protein shake just as effective as the high protein shake at supporting post-workout protein synthesis.

In short, leucine can improve the effectiveness of a low protein shake, but you need more leucine than if you chose the high protein shake to begin with.

Adding extra branched chain amino acids actually suppressed the effectiveness of leucine at enhancing post-workout protein synthesis. These data suggest:

Leucine probably is the major amino acid responsible for the muscle gain reported in many of the previous studies with branched chain amino acids.

If the other branched chain amino acids play a supporting role in the muscle gain, the quantities that occur naturally in the protein are probably enough. Adding more may actually reduce the effectiveness of leucine at stimulating muscle gain.

While this is a single study, it is consist with numerous other recent clinical studies. It simply helps clarify whether leucine can increase the effectiveness of a low protein supplement. It also clarifies the role of branched chain amino acids.

Also, while this study focused on protein synthesis, numerous other studies have shown that optimizing post-workout protein and leucine intake results in greater muscle gain (for example, Westcott et al., Fitness Management, May 2008)

The Bottom Line

Research on post-workout nutrition to optimize muscle gain from the workouts has come a long way in recent years. It is now actually possible to make rational choices about the best protein supplements and foods to support your workouts.

If you are a young adult (17-30), you should aim for 15-20 gm of protein and about 2 gm of leucine after your workout.

If you are an older adult (50+), you should aim for 20-25 gm of protein and 3 gm of leucine after your workout.

If you are in between you are on your own. Studies haven’t yet been done in your age group, but it’s reasonable to assume that you should aim for somewhere between the extremes.

If you are getting the recommended amounts of whey protein, the leucine level will also be optimal. If you are using other protein sources you may want to choose ones with added leucine.

The research cited above shows that you can make a low protein supplement effective by adding lots of leucine, but that’s going to require artificial flavors and sweeteners to cover up the taste of that much leucine. I would recommend choosing one that provided adequate protein to begin with.

While the research in this area is still somewhat fluid, I would avoid protein supplements with added branched chain amino acids other than leucine. If the paper I cited above is correct you probably get all of the other branched chain amino acids you need from your protein and adding more may actually interfere with the effect of leucine on muscle gain.

I’d pretty much forget all the other “magic ingredients” in post-workout supplements. If you’re a novice there is some evidence that arginine and HMB may be of benefit, but if you have been working out for more than 6 months, the evidence is mixed at best. As for the rest, the clinical studies are all over the map. There’s no convincing evidence that they work.

Whey protein is the best choice for enhancing muscle gain immediately after your workout. Soy and casein are better choices for sustaining muscle gain over the next few hours. If you’re looking at meat protein, chicken is a particularly good choice. Four ounces of chicken will provide the protein and leucine you need to sustain muscle gain for several hours.

Even if you are not working out, recent research on dietary protein and leucine has important implications for your health. In a recent “Health Tips From the Professor” I shared research showing that optimizing protein and leucine intake helps to increase muscle retention and maximize fat loss when you are losing weight.

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.

Could Omega-3s Improve Reading Skills?

January 21, 2014 by Dr. Steve Chaney

Can DHA Help Johnny Read?

Author: Dr. Stephen Chaney

If you are like most parents, you want to do everything you can to assure that your kids have the skills they need to succeed in school, and reading probably tops the list of necessary skills. If your child is reading below their age level, could something as simple as better nutrition improve their reading ability?

Recent studies have shown that the omega-3 fatty acids, especially DHA, play a very important role in normal brain function – especially memory, focus, concentration, and attention span.

I have shared with you previous studies which have shown that optimal DHA intake in pregnant women plays an important role in the early mental development of their children. On the other end of the age spectrum, studies have shown that optimal omega-3 fatty acid intake in older adults can delay cognitive decline.

I have also shared with you studies showing that omega-3 fatty acid supplementation in children with ADD and ADHD significantly reduce their symptoms. What about children without hyperactivity? Could omega-3 fatty acids affect their ability to learn?

Many Children Are Deficient in Omega-3 Fatty Acids

The Food and Nutrition Board has not yet set US standards for DHA intake, but the international standard is 200 mg for children 7 years old and older. Unfortunately, cod liver oil is a thing of the past, and foods rich in DHA are not particularly popular with children. Consequently, most children in this country are only getting around 20-40 mg of DHA per day.

And that shows up in their blood levels of omega-3 fatty acids. A recent study in England looked at blood levels of omega-3 fatty acids in 493 seven to nine year olds with below average reading performance who were enrolled in Oxfordshire primary schools (P. Montgomery et al, PLoS ONE, doi: 10.1371/journal.pone.0066697).

All of them had low blood levels of omega-3 fatty acids (both DHA and EPA), and the blood levels of omega-3 fatty acids were directly related to their reading ability. In non-scientific language that simply means that those with the poorest reading abilities had the lowest blood levels of omega-3 fatty acids.

This study is particularly significant because another study by the same group showing that DHA supplementation improved reading skills in underperforming children.

Could Omega-3s Improve Reading Skills?

This study (Richardson et al., PLoS ONE 7: e43909.doi:10.1371/journal.pone.0043909) looked at 362 normal 7-9 year old children enrolled in mainstream primary schools in Oxfordshire, England.

These children were all reading at significantly below the average for their grade levels. The study excluded children with specific medical difficulties that might affect their ability to read, children who were already taking medications expected to affect behavior or learning, children for whom English was not their first language, and children who were already eating fish more than twice a week or taking omega-3 supplements.

The children were given either supplements containing 600 mg of DHA per day or a placebo containing corn and soybean oil. At the end of 16 weeks the children were rescored on a standardized reading test.

The results were quite interesting. When the scientists looked at children reading in the lower third of their class, the affect of DHA on their ability to read was non-significant. However, when they looked at the children who were performing in the bottom 20% of their class with respect to reading, DHA supplementation resulted in a 20% improvement in their reading score. And when they looked at children in the bottom 10% of their class with respect to reading, DHA supplementation resulted in a 50% increase in reading scores. These changes were highly significant.

To put this in perspective, the children performing in the bottom 20% of their class improved their reading efficiency by around 0.8 months with respect to their normal reading age, and the children in the bottom 10% of their class improved their reading efficiency by around 1.9 months with respect to their normal reading age.

Strengths and Weaknesses of The Studies

On The Minus Side:

First and foremost we must remember that nutrition is only one of many factors that can affect reading performance in children. You shouldn’t think of DHA as a magic bullet that will cure your child’s reading problems by itself.

This is a single pair of studies that need to be replicated.

This study does not establish the optimal dose of DHA needed to improve reading in underperforming children. Until dose response studies have been done we don’t know whether 600 mg is needed or whether simply making sure that the children reach the recommended 200 mg per day of DHA would be sufficient.

On The Plus Side:

Both of these were very well controlled studies, and they complemented each other perfectly. One study showed that students with the poorest reading ability had the lowest blood levels of DHA. The other study showed that children with the poorest reading ability experienced the greatest improvement with DHA supplementation.

These studies were not done with third world children. They were studies with normal, healthy children in a prosperous European country.

These studies are fully consistent with previous studies looking at the effects of DHA on cognition in children.

The Bottom Line

What does this study mean for parents whose children may be struggling with their reading in school?

The lead author concluded: “We have shown that in the mainstream, general population, something as simple as DHA can benefit reading abilities in underperforming children.”

It’s perhaps not that ironclad yet. But if your kid or grandkid is reading below their grade level, DHA supplementation is both safe and inexpensive. It’s worth giving it a try.

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 Two Biggest Misconceptions About Supplementation

December 31, 2013 by Dr. Steve Chaney

Secrets You Need To Know

Author: Dr. Stephen Chaney

In last week’s “Health Tips From The Professor” I told you the truth behind the headlines that vitamins are a waste of money. This week I’m going to be talking about the two biggest misconceptions that people have about supplementation. These are two secrets you need to know.

The Two Biggest Misconceptions About Supplementation

I won’t keep you in suspense. The answer is pretty simple. The two biggest misconceptions about supplementation that I hear over and over are:

1) Supplementation can cure disease

2) It doesn’t matter what you eat (or what supplements you take)

Of course, those statements don’t tell you much by themselves, so let’s delve into the subject more deeply.

Misconception #1: Supplementation can cure disease.

I don’t know how many times I’ve been asked “I have “disease X”. What supplements should I take? – as if supplements were drugs that can be taken to cure a disease.

We shouldn’t think of supplements as drugs that cure diseases. We should think of them as providing the nutrients that are the building blocks of health – or perhaps the ammunition that the body uses to fight diseases. Diseases, after all, are an abnormal state of being, and our bodies have an amazing capacity to fight those diseases.

When we have infections or cancer our body activates its immune system to fight it. When we have inflammation our body tries to put out the fire. When we have damage to our DNA – our genetic information – our body tries to repair it. The list is almost endless. Our bodies are wondrously designed!

Our immune systems require nutrients like protein, B vitamins, antioxidants, zinc and iron. The omega-3 fatty acids, anti-oxidants and polyphenols like resveratrol are anti-inflammatory. Nutrients like antioxidants and polyphenols support DNA repair.

So proper diet and supplementation are not “magic bullets” that cure diseases. They are simply the building blocks that allow the body to do what it does best.

And because no two of us are alike the nutrients that we need the most to allow our bodies to do their job efficiently may be different for each one of us.

So while there is no magic food or supplement that will cure a specific disease, a healthy diet and a holistic approach to supplementation can often work wonders.

Misconception #2: It doesn’t matter what you eat.

This is the flip side of the coin. I often come across people who have been told by the “experts” that the cause of their disease was not related to diet so they shouldn’t worry about what they eat. They are also usually told that supplementation will not do any good.

Let’s take the most extreme example – genetically caused diseases or serious degenerative diseases like multiple sclerosis or Parkinson’s for which the causes are still not fully understood.

It is generally true that these diseases were not caused by poor diet (MS may be the exception because there is some evidence that it can be caused by inadequate vitamin D during childhood). And I know many people who take the “expert’s” advice to heart and eat whatever they like and consider supplementation a waste of money.

Is that a sound approach? Let’s consider.

Any nutritionist will tell you that an inadequate diet can lead to malaise, low energy, inflammation, weakened immune system and impaired wound healing – just to name a few maladies. Even if you don’t end up with the symptoms of a nutritional deficiency, a poor diet can rob you of energy and vitality.

If you layer the consequences of a poor diet on top of the underlying disease, your chances of being able to cope with the disease and function optimally are greatly diminished.

I have come across many people with very serious diseases who are able to function at a very high level through proper diet and a holistic approach to supplementation.

Diet and supplementation did not cure their disease as they quickly discover if they stop supplementing and go back to the way they used to eat, but in many cases you would consider them to be perfectly healthy as long as they keep doing what they have been doing.

The Bottom Line

1) There is no perfect food or supplement that is capable of curing disease, but if you give your body the nutrients that it needs it often has the ability to heal itself.

2) Proper diet and supplementation can make a difference even if the disease was not caused by poor nutrition.

3) Each of us have unique nutritional needs so a holistic approach to diet and supplementation is best.

I didn’t specifically talk about weight control and exercise, but you should know from my previous “Health Tips From The Professor” that I consider them to be an essential part of any holistic health program.

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.