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.

How Stretching Can Hurt Your Muscles

March 20, 2014 by Dr. Steve Chaney

Preventing & Healing Repetitive Strain Injuries – Part 3

Author: Julie Donnelly, LMT

These past two weeks we took a look at how muscles move the body, and why muscles cause pain. Then we looked at why strengthening isn’t always the best thing to do, in fact how it could even cause more pain. And finally today we’ll discuss why stretching can actually cause muscles to tear. I call this the Stretching Misconception.

Stretching Shouldn’t Hurt!

Have you ever felt so tight when you tried to move a joint that you decided to stretch? The odds are that you answered “yes” to that question. However, many people complain that they feel worse after stretching than they did before stretching.

Before getting into the specifics of the stretching misconception there are two words that need to be clarified. Many people confuse the word “spasm” with “cramp”. A cramp (also called a “Charlie horse”) normally involves all of the fibers of a muscle, and is when a muscle suddenly contracts totally. A spasm is like tying a knot in the center of the muscle and while it may only involve a few fibers; there can be multiple spasms throughout the muscle.

Each spasm feels like a bump when you slide your fingers deeply down the length of the muscle. These spasms normally form over an extended period of time, often from repetitive strain on the muscle fibers. Spasms are at the heart of the stretching misconception, so it is important that you think of a spasm as a knot in the muscle fibers in order to understand why it can hurt to stretch.

As I mentioned in Part I of this series, a muscle begins on a stationary bone, crosses over a joint, and then inserts into a moveable bone. When the muscle pulls on the moveable bone, the joint moves, however, if the muscle has a “knot” in it you can actually cause micro-tears to the fibers as you stretch.

How Stretching Can Hurt Your Muscles

Think of this analogy: visualize a strong tree with a rope tied to it. The rope is the perfect length to attach to a flexible tree without bending the second tree. You can imagine if you pulled on the rope the flexible tree would bend over, and if you let go of the rope, the flexible tree would stand up straight again. This is a simple explanation of how a muscle pulls on a bone and causes the joint to move.

However, if you tied a knot in the rope, the tree would bend. If you tied a second knot, the tree would bend even further. If you then tried to stretch the rope so the flexible tree was standing straight, you would cause the knot to get tighter and the remaining rope would have to overstretch on both sides of the knot in order for the flexible tree to stand up straight.

This is exactly what is happening when you have a spasm, or multiple spasms, in your muscle. As you stretch you are causing the knot within the muscle to get tighter, and you are also causing the fibers on either side of the spasm to overstretch. This overstretching may cause the fibers to actually tear either along the length of the muscle, or where the fibers attach to the bone at either end of the muscle. This can be avoided by simply massaging the muscle to release the spasm before you stretch.

It’s now easy to understand why the repetitive movements that you do on a regular basis will cause the muscle to ultimately shorten into knots that we call spasms or trigger points. As I mentioned, when you try to stretch a spasm you can be causing yourself potential problems, and may even tear the muscle fibers.

Fortunately there is a solution. First you need to release the spasms that are causing the muscle to tie up into a knot, and then you can safely stretch. TriggerPointYoga was designed and developed to first eliminate the spasms in the muscle you will be stretching, and then continues to give four separate session of traditional yoga poses – two for the upper body and two for the lower body. You will gain flexibility and range-of-motion without injuring your muscle fibers.

Julie Donnelly is an internationally respected muscular therapist specializing in the treatment of chronic pain and sports injuries. She has co-authored several self-treatment books, including The 15 Minute Back Pain Solution, Treat Yourself to Pain-Free Living and Carpal Tunnel Syndrome-What You Don’t Know CAN Hurt You. Julie is also the co-developer of TriggerPoint Yoga. She teaches Julstro self-treatment workshops nationwide and is a frequent presenter at Conventions and Seminars. Julie may be contacted through her websites: http://www.julstro.com and http://www.TriggerPointYoga.com.

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.

How Strengthening Can Hurt Your Muscles

March 13, 2014 by Dr. Steve Chaney

Preventing & Healing Repetitive Strain Injuries – Part 2

Author: Julie Donnelly, LMT

In part I of this series we explored “how” muscles cause joint pain and prevent us from moving easily and without pain. In Part II we’ll take a look at the “why.”

When a person can’t freely move a joint they are frequently told they need to strengthen the muscle that moves the joint, but this is often a serious misconception. Let’s look at this further so it will become clear.

Most people have heard the term Repetitive Strain Injury (RSI), but they don’t have a clear concept of how that affects them on a daily basis.

Repetitive Strain Injuries (RSIs)

Repetitive strain injuries happen when a muscle does the same movement over and over, causing the muscle to develop an excess of Hydrogen ions (H+), which is a part of lactic acid. Lactic acid was once thought to be the “bad guy” that created spasms/knots in your muscles. Then research showed that lactic acid has two components, one is called lactate and it is an important piece of energy production, and the other is H+, which is the acid byproduct of energy production and is the cause of the spasms.

Your body has the ability to flush out H+, but if you are exercising, or repetitively doing the same movement, you are creating more H+ than your body can eliminate. The scales tip and the excess lactic acid will cause the muscle fibers to contract into a spasm. The spasm is usually formed slowly so you don’t notice it until it is so evolved that the fibers are twisted into a knot and are putting a strain on the insertion point at the joint.

Strengthening vs Lengthening

When you can’t bend a joint, such as your elbow, you are often told to strengthen the muscle that pulls on the joint, in this case, the biceps. However, you actually need to lengthen your triceps.

In fact, I tell my clients to first look at the area where they are feeling pain, and then find out which muscle inserts at that point. If you can’t bend a joint, I tell people to look at what muscles should be stretching to enable the joint to move. The likelihood is great that the tight muscle is the cause your problem.

You’ll be amazed at how quickly you will regain full range-of-motion when you release the “straps that are holding you bound” by lengthening the contracted muscles.

Another piece of the strengthening misconception occurs when a person feels they are losing power in their muscle. Many times the person isn’t feeling any pain in their body, just a general feeling of loss of strength. You know you are exercising, but still you aren’t as strong as you were, so you feel you need to increase your strengthening exercises.

How Strengthening Can Hurt Your Muscles

To demonstrate this topic we’ll use the biceps of the upper arm as our example. I do a lot of my work with endurance athletes, athletes who are power lifters or simply individuals who exercise to the extreme. I’ve seen how they are in severe pain, sometimes to the point where they can’t do even the simplest movements without having not only pain but also losing power.

Often they lose power because the pain is too sharp when they go to lift the weight, or do pull ups. Other times they just feel like they are having weakness in the muscle, which makes them more determined to exercise that muscle even more. What has happened is the muscle is now too short to have any pulling power.

Look at the graphic to the left. Many endurance athletes look just like this drawing, and some people think this is the picture of strength. However what is happening is the biceps muscles have been shortened to the point where he can’t completely straighten his arm, so he has actually lost power.

But you don’t need to be an endurance athlete to have this experience. If any muscle in your body is shortened by spasms, whether they are from doing a repetitive movement or from exercise, you will also lose strength in those muscle fibers.

Consider this: if you couldn’t move your body, but you wanted to pull a heavy object toward you, you would stretch your arm out all the way and then pull on the object. If you stepped closer to the object so your arm is now bent, you can see that you wouldn’t have as much strength to move the heavy object. In the same way, when a muscle is already shortened by either a spasm or a static contraction, it won’t have the full pulling power it needs to function properly. You need to lengthen the fibers to their optimal length so they can pull with full strength.

You stretch, but often people will complain that the muscles aren’t stretching, or they hurt worse after the stretch than they did before stretching. This brings us to the “stretching misconception,” which will be explained in Part III of this trilogy.

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.

How Muscles Cause Joint Pain

March 6, 2014 by Dr. Steve Chaney

Preventing & Healing Repetitive Strain Injuries – Part 1

Author: Julie Donnelly, LMT

Using the words “pain” and “free” in the same sentence causes people who love to exercise laugh since it seems to be a contradiction of terms, but it is not only possible, it’s easy to achieve. It is understood that exercising, or even just daily living, causes muscles to ache and will also put stress on joints.

When the pain begins you are told to use “RICE” (Rest, Ice, Compression, Elevation) – but you don’t have the time, or you simply don’t want to rest! So, you keep going and just as you’ve been told, it gets worse, even to the point where you may need to stop your world!

You’ve also come to realize that resting (when you do decide to rest) only lasts for a short time, and then the pain returns. The good news is you can be a pain-free; you just need to know how to find the source of your pain and then how to effectively treat it.

How Muscles Cause Joint Pain

RICE certainly works immediately after having a traumatic injury, but repetitive stress on your muscles requires treatment of the knots that are putting tension onto the tendons and joints. Getting back to basic anatomy will help to unravel the misconceptions that plague both athletes and non-athletes alike. Once you understand the logic of why you are feeling pain, you will know exactly what needs to be done to immediately release a muscle-related pain anywhere in your body.

This is NOT going to be a complicated lesson in Anatomy & Physiology, but I’ve found that a little knowledge of the body goes a long way. I’m going to put the proper names for the muscles and tendons into a parenthesis so if you want to actually see the muscles that are causing you pain you’ll be able to look them up.

I always tell the clients I work with “the most challenging part is finding where the source of the pain is located, and then treating it is easy”. This article will help you to find the source of your problem. Let’s begin at the beginning…

The Basics – How a Joint Moves

Movement is a simple process:

1. A muscle originates on a bone.

2. It then merges into a tendon.

3. The tendon crosses over the joint to insert into a movable bone.

4. When the muscle contracts it pulls on the tendon. The tendon then pulls on the moveable bone and your joint moves.

Example: The Muscles of Your Upper Leg

All joints have two (or more) muscles that determine the degree and angle that the joint will move. While one muscle is contracting, the other muscle must relax and stretch. A good example of this principle are the muscles of your upper leg. (quadriceps and hamstrings).

The quadriceps originate on the front of your hip (pelvis), merge into a thick tendon (patella tendon) and cross over the knee cap to insert onto the front of your shinbone (tibia). When they contract normally you fully extend your leg so it becomes straight. Meanwhile, your hamstrings originate on the lower edge at the back of your pelvis; go down the back of your thigh, with the tendons crossing over the back of your knee and inserting onto the back side/top of the lower leg bone.

Consider this analogy, if you attached your pants to the front of your shinbone, and then pulled up at the waist, you would feel the pressure at your knee and you also wouldn’t be able to bend your knee. Likewise, since your quadriceps originate up at the front of your pelvis and insert into your shinbone, when your quadriceps are tight they can’t stretch and you can’t bend your knee.

For example, to demonstrate an analogy of what tight hamstrings would do, consider what would happen if you bent your leg and then attached your pants to the bottom of your posterior pelvis (the bone you sit on, at the top of your thigh) and the back of your knee, you wouldn’t be able to open your leg up straight. But, clearly, you don’t have a knee problem, you have tightness in the upper thigh (hamstring) preventing your knee from moving.

When this has happened you begin to feel stiffness and a lack of your full strength. Some therapists will tell you that you need to strengthen your thigh (quadriceps) muscles. You may also think you need to stretch your hamstrings, but stretching a spasm is counter-productive and can actually make the spasm become more complicated while over-stretching the rest of the muscle fiber.

In Part II we’ll look at the first misconception – strengthening the muscle will heal the pain.

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.

Will Non-GMO Foods Be Less Nutritious?

March 4, 2014 by Dr. Steve Chaney

The Unintended Consequences of the Proposed Non-GMO Labeling Laws

Author: Dr. Stephen Chaney

Post Foods recently announced that their Grape Nuts cereal will be completely non-GMO. General Foods followed suit by announcing that their Original Cheerios will also be non-GMO. That’s good news, right?

Maybe, but it turns out that the new non-GMO Grape Nuts will no longer contain vitamins A, D, B12 or riboflavin, and the amount of riboflavin in a serving of Cheerios decreased from 25% of the daily recommended value (DV) to 2% of the DV.

The cereal manufacturers claim that their new cereals are more wholesome, but one nutrition expert said “The new products are arguably less healthy given their lower vitamin content.”

I’ve never been one to claim that throwing a few vitamins into a serving of cereal turns it into a nutrition powerhouse, but the decreased vitamin content of the new non-GMO cereals does raise a few questions.

Why were the vitamins removed?

Did it have anything to do with the cereals being non-GMO?

Does this mean that the non-GMO processed foods of the future will be less nutritious than the foods they replace?

The cereal manufacturers were mum when asked these questions, so we will need to rely on some scientific sleuthing and a bit of intuition to get the answers.

The Flaw in The Proposed Non-GMO Labeling Laws

I first discussed this topic a few months ago in a “Health Tips From The Professor” article titled “When is GMO Non-GMO?” I received a lot of irate comments from people who take every word on the non-GMO websites and videos as the gospel truth. (The professor has never been one to shy away from controversy when he sees claims that aren’t based on good science.)

However, I think my article was misunderstood by some of my readers, so let me review my conclusions briefly:

There are definitely environmental concerns around the widespread use of GM crops – especially those that allow heavy pesticide and herbicide usage.

There are potential health concerns related to the consumption of unprocessed GM foods and proteins derived from GM foods – although those heath concerns have been blown way out of proportion in the media.

If the proposed Non-GMO labeling laws stopped there, they would be scientifically justified. But they go one step further by requiring that processed foods labeled as non-GMO cannot contain any ingredient obtained from a GM source. There is no scientific justification for this.

Nutrients (sugars, oils & vitamins) derived from GM sources are chemically and biologically indistinguishable from those same nutrients derived from non-GMO sources.

The intentions of the proposed non-GMO labeling laws are good, but whenever you go beyond what good science supports there are often unintended consequences – such as the vitamin-depleted non-GMO cereals that the food manufacturers have just announced.

Will Non-GMO Foods Be Less Nutritious?

To understand the answer to that question, let’s look at what probably happened to the vitamins in the non-GMO cereals.

In today’s world many vitamins are purified from genetically modified microorganisms – bacteria & yeast that have been modified to overproduce certain vitamins. In evaluating the significance of that statement, here are a few facts to consider:

1) We have gotten vitamins from these sources for many years.

B vitamins have been obtained from yeast for at least a hundred years.

A significant portion of the vitamins we absorb on a daily basis are made by bacteria in our gut.

2) The only difference today is that these microorganisms have been genetically modified to overproduce the vitamins.

3) These are naturally sourced vitamins.

The microorganisms are the same ones that have provided these vitamins for generations.

The enzymes used by the microorganisms to make the vitamins are the same.

4) There is no downside to the use of GM organisms as a source of natural vitamins.

There is no environmental risk from the use of these GM microorganisms. They don’t contain any dangerous genes that could wreak havoc if they escaped from the food processing plants.

Because the purified vitamins are indistinguishable from those obtained from non-GMO sources, there are also no health risks.

5) The advantage of using these GM organisms is clear. It substantially lowers the cost of vitamins and allows them to be used in the mass market – for example, in popular breakfast cereals.

6) Most food manufacturers can’t simply use non-GMO sourced vitamins and raise their prices.

A recent poll showed that 53% of Americans prefer non-GMO foods, but only 11% are willing to pay more for those foods

What Does the Future Hold?

Even though they are scientifically flawed, the proposed non-GMO labeling laws will probably become the law in several states in the near future. (Good science has never played much of a role in political decisions.)

Currently, there simply aren’t enough non-GMO vitamins available to supply the mass market – even if price were no concern. So, in the short term, many non-GMO processed foods are likely to be less nutritious than the foods they will replace – as we just saw with Grape Nuts and Cheerios.

However, most people feel that American ingenuity and the law of supply and demand will eventually result in a bigger supply of reasonable priced non-GMO vitamins. When that happens non-GMO processed foods will be just as nutritious as the older GM versions.

However, at this point nobody knows how long that will take.

The Bottom Line:

1) There is a scientific basis for environmental and potential health concerns regarding genetically modified whole foods and the protein extracted from these foods.

2) However, proposed non-GMO labeling laws would require that a processed food be labeled as genetically modified if it contains any nutrient purified from a genetically modified organism.

3) There is no scientific justification for this requirement. Purified vitamins from GM and non-GM microorganisms are chemically and biologically indistinguishable. Furthermore, the GM microorganisms used to produce the vitamins pose no environmental or health risks.

4) Non-GMO vitamins (vitamins prepared from non-GMO microorganisms) are currently in short supply and are very expensive compared to vitamins prepared from GM microorganisms.

5) Consequently, the unintended consequence of these proposed non-GMO labeling laws will likely be that many of the new non-GMO processed foods will contain fewer vitamins and, therefore, will be less nutritious than the foods they replace – at least in the short term. The new non-GMO Grape Nuts and Cheerios may be just the tip of the iceberg.

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 Toxic Chemicals Lowering Our IQ?

February 25, 2014 by Dr. Steve Chaney

Is Chemical Brain Drain A Pandemic?

Author: Dr. Stephen Chaney

In a past issue of “Health Tips From the Professor” I examined the evidence suggesting that toxic chemicals in the home could cause childhood asthma. That is alarming because asthma can predispose individuals to other diseases and affects quality of life.

But, what if that were only the tip of the iceberg? For example, a recent headline stated: “More Toxic Chemicals [In Our Environment] Are Damaging Children’s Brains”. If that headline is true, it’s downright scary.

The authors of this study suggested that toxic chemicals which are abundant in our environment can cause decreases in IQ and aggressive or hyperactive behavior in children – and that those changes may be permanent.

The Study Behind The Headlines

The paper that generated the headlines (Grandjean & Landrigan, The Lancet Neurology, 13: 330-338, 2014) was a review of the literature, not an actual clinical study.

Based on published clinical studies, the authors identified 12 chemicals commonly found in the environment as developmental neurotoxins (toxins that interfere with normal brain development) based. [If you would like to find out what those “Dirty Dozen” chemicals are and where they are found, click here.]

This finding compares with 6 developmental neurotoxins that they were able to identify in a similar study in 2006.

The authors were not claiming that the number or amount of toxic chemicals changed between 2006 and 2014. They were saying that science has advanced to the point where we can classify six more chemicals that have been in our environment for years as developmental neurotoxins.

Even more worrisome, the authors postulate that many more environmental neurotoxins remain undiscovered.

Are Toxic Chemicals Lowering Our IQ?

To answer that question, you need to look at some of the studies they cited in their review. For example:

Elevated blood lead levels in children are associated with as much as a 7 point decrease in IQ (Lamphear et al, Environmental Health Perspectives, 113: 894-899, 2005).

Elevated fluoride levels in drinking water are also associated with as much as a 7 point decrease in IQ (Choi et al, Environmental Health Perspectives, 120: 1362-1368, 2012).

The effects of many of the toxic chemicals on IQ were difficult to quantify, but the authors estimated that exposure of US children to just 3 of the chemicals (lead, methymercury and organophosphate pesticides) was sufficient to lower their average IQ by 1.6 points.

What Are The Potential Consequences?

The authors spoke of the environmental neurotoxins they identified as representing a “silent pandemic of a chemical brain drain” that could cost the US economy billions of dollars.

One of the blog posts I read on this topic summarized the consequences in a very graphic manner. It said:

If one child’s IQ is reduced by 5 points, it doesn’t appear to make a big difference. For example, that child might be:

A little slower to learn
A little shorter of attention
A little less successful at tests and at work

That might result in $90,000 in lost lifetime earnings

However, if the average IQ of every child in the US were decreased by 5 points, the effect becomes significant:

Only half as many members of the next generation would be “intellectually gifted”.
Twice as many of the next generation would be “intellectually impaired”
Lost productivity could be in the billions

Of course, statements like that are a bit over the top. Drs. Grandjean and Landrigan did not claim that the net effect of the chemicals they identified was a 5 point drop in IQ. Nor did they claim that all US children were affected equally.

Still, it’s enough to make you think.

Are Toxic Chemicals Causing Behavior Problems?

The authors cited numerous studies linking the chemical neurotoxins they identified to aggression and hyperactivity. But perhaps the most compelling reason to suspect that environmental chemicals may be affecting brain development is the spiraling incidence of developmental disorders such as autism and ADHD. For example:

Autism has increased by 78% since 2007 and now affects 1 of 88 eight year old children.

ADHD has increased by 43% since 2003 and now affects 11% of children age 4-17.

Some of this increase could be due to better diagnosis of these conditions, but nobody believes that all of it is due to improved diagnosis. The authors claim that much of this increase is likely due to environmental exposure to the kinds of developmental neurotoxins they identified.

Is The Science Solid?

This is a difficult area of research. You can’t do the gold standard double-blind, placebo-controlled clinical trial. Nobody in their right mind would give one group of children toxic chemicals and the other group a placebo.

The studies cited in this paper were mostly population studies. Basically this means that they compared children with exposure to certain toxic chemicals to a control group that was as similar as possible to the first group except that their exposure to the toxic chemicals was less.

The limitation of this kind of study is obvious. We are usually comparing children from different locations or of different backgrounds. We almost never know if we have controlled for all possible variables so that the groups are truly identical.

As a consequence it becomes important to ask how many studies come to the same conclusion. For some of the toxic chemicals, such as lead, methymercury and organophosphate pesticides, the weight of evidence is very strong. For some of the newer additions to their list of developmental neurotoxins, it is pretty clear that the chemicals have neurotoxic properties, but the significance of those effects on the developing human brain are hard to quantify at this point.

The Bottom Line:

1) A recent review claims that there is a good scientific basis for classifying at least 12 environmental chemicals as developmental neurotoxins that are likely to reduce IQ and contribute to behavioral problems in US children. [If you would like to find out what those “Dirty Dozen” chemicals are and where they are found, click here.]

2) The science behind the claims in this review is solid, but not iron-clad.

3) However, there are times when we need to simply ask ourselves: “What if it were true?” The consequences of lowered IQ and developmental behavioral problems are so significant that it may not make sense to wait until we have unassailable scientific evidence before we act.

4) We all need to be guardians of our personal environment. But, it is not easy. The “Dirty Dozen” chemicals identified in this study come from many sources:

Some are industrial pollutants. For those, we need lobby for better environmental regulation.

Some are persistent groundwater contaminants. For those we need to drink purified water whenever possible.

Some are insecticides and herbicides used in agriculture. For those we need to buy organic, locally grown produce when feasible.

Some are found in common household products and furnishings. For those we need to become educated label readers and use non-toxic products in our home whenever possible.

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.