Is Vitamin D Overhyped?

April 23, 2014 by Dr. Steve Chaney

Are Clouds Gathering For the Sunshine Vitamin?

Author: Dr. Stephen Chaney

We’ve known for years that vitamin D plays an essential role in calcium metabolism and is important for bone health. In fact, the use of vitamin D to prevent and cure rickets is one of the greatest success stories in the field of nutrition.

However, in recent years a number of studies have suggested that adequate vitamin D status was also important in reducing the risk of cancer, heart disease, diabetes, infectious diseases and autoimmune diseases – as well as overall mortality. Suddenly it seemed as if vitamin D could leap over tall buildings in a single bound (I realize that I’m probably dating myself with that analogy).

So when I saw the headlines about a new study (Theodoratou et al, BMJ, 2014;348:g2035 doi: 10.1136/bmj.g2035) that concluded all of those benefits of vitamin D were unconfirmed, I was not surprised. After all there have been many examples of periods in which individual vitamins were reported to have miraculous benefits – only to have most of those benefits debunked by subsequent studies. I fully expected that would be the theme of this issue of “Health Tips From the Professor”.

But when I read the article I found that the study had multiple flaws (more about that latter). I also discovered that the same issue of the British Medical Journal had another, much better designed, study that came to the exact opposite conclusion (Chowdhury et al, BMJ 2014;348:g1903 doi: 10.1136/bmj.g1903).

Funny how only the first study made it into the headlines. It’s only the negative news that sells.

Is Vitamin D Overhyped?

The first study was a very large meta-analysis that included 107 systematic reviews, 74 meta-analyses of observation studies (studies that compare population groups) and 87 meta-analyses of randomized, placebo controlled trials. In case you were wondering, the total number of patients enrolled in these studies must have numbered in the hundreds of thousands.

The authors of the study reported that:

There was no relationship between vitamin D intake and cancer, heart disease, autoimmune disease, infectious diseases, diabetes and other diseases. In other words, they concluded that most of the recent excitement about vitamin D was just hype.

There was also no evidence that vitamin D increased bone density or reduced the risk of fractures and falls in older people – in contrast to many previous studies.

Based on this evidence the authors said “universal conclusions about vitamin Ds benefits cannot be drawn [from current data]” and that vitamin D “might not be as essential as previously thought in maintaining bone mineral density”.

Both of those statements are pretty revolutionary, but a study this large has to be true – right? The answer is a definite maybe. The problem is that many of the studies included in this meta-analysis were poorly designed by today’s standards. Remember the old saying “garbage in, garbage out”.

The Study Is Flawed

My specific criticisms of the study are:

1) The conclusions about vitamin D and bone density were seriously flawed. The authors acknowledged that previous studies have shown that calcium and vitamin D together increased bone density, but they considered calcium to be a confounding variable and only included clinical trials using vitamin D supplementation alone. That shows a complete misunderstanding of the biochemical role of vitamin D.

The purpose of vitamin D is to maintain constant levels of blood calcium, not to build strong bones.

When blood levels of calcium are high, vitamin D lowers it by depositing the calcium in bones.
When blood levels of calcium are low, vitamin D raises it by leaching calcium from bone.

That’s why vitamin D and calcium work together. It is utter nonsense to expect vitamin D to increase bone density or prevent fractures unless you make sure that calcium intake is at least adequate.

2) Most studies of vitamin D supplementation did not stratify the data based on low versus high levels of 25-hydroxy vitamin D at the beginning of the study. That’s important because you would only expect vitamin D supplementation to be of benefit in people with low levels of 25-hydroxy vitamin D to begin with. If their 25-hydroxy vitamin D levels are already optimal, vitamin D supplementation is unlikely to be of additional benefit.

3) Finally, the authors did not separate the studies based on whether vitamin D2 or vitamin D3 was used. That’s important because some recent studies have suggested that D3 is more beneficial than D2.

Is Vitamin D Beneficial After All?

The second study came to the exact opposite conclusions. It was also a very large study. It included 73 observational studies (849,412 participants) and 22 randomized, placebo controlled studies (30,716) participants. Here is what the authors of this study concluded.

High blood levels of 25-hydroxy vitamin D decreased the risk of heart disease by 35%, cancer by 14% and overall mortality by 35%.

Supplementation with vitamin D3 reduced overall mortality by 11%, while supplementation with vitamin D2 increased overall mortality by an insignificant 4%.

65% of the US population can be classified as vitamin D insufficient (blood levels of 25-hydroxy vitamin D of below 30 ng/ml) and 4% as severely deficient in vitamin D (blood levels below 10 ng/ml)

Vitamin D deficiency contributes to 13% of the deaths in the United States. For comparison the corresponding numbers for other major risk factors are: smoking – 20%, physical inactivity – 11% and alcohol – 9%.

About the only point on which the two studies agreed was that there is a need for more, better designed studies to clarify the benefits of vitamin D.

The Bottom Line:

1) Two studies were published in the April 2014 issue of the British Medical Journal. The first concluded that all of the supposed benefits of vitamin D – including increasing bone density – were not supported by the available data. The second study concluded that adequate intake of vitamin D significantly reduced deaths due to heart disease and cancer and also significantly reduced overall mortality. Somehow, only the first study made it into the headlines. Why does that not surprise me?

2) The suggestion in the first study that vitamin D may not be essential for strong bones is based on a complete misunderstanding of the role of vitamin D in the body. There are ample clinical studies showing that vitamin D and calcium together are essential for strong bones. Nobody who understands biochemistry would expect vitamin D to increase bone density in the absence of calcium, but the authors only considered studies that excluded calcium in drawing their conclusion that vitamin D did not increase bone density.

3) The only point of agreement between the two studies is that more and better studies are needed to sort out the benefits of vitamin D and what levels of vitamin D are optimal. I wholeheartedly agree.

4) My advice is to ignore the headlines telling you that vitamin D is dead. On the other hand, don’t get caught up in the hype and buy megadoses of vitamin D supplements. While the evidence is rock solid that vitamin D and calcium together are essential for strong bones, the jury is still out on some of the other health benefits of vitamin D.

5) If you are supplementing with vitamin D you should know that the RDAs for vitamin D are 600 IU for ages 1-70 and 800 IU over 70. The safe upper limit has been set at 4,000 IU. You should only go above that on a doctor’s advice.

6) However, people metabolize vitamin D with different efficiencies, so I strongly recommend that you get your blood levels of 25-hydroxy vitamin D tested and let your doctor help you determine how much vitamin D you should be getting.

7) Finally, a number of recent studies suggest that vitamin D3 may be more effective than vitamin D2, so I only recommend supplements that contain D3.

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 High Protein Diets Cause Cancer?

April 15, 2014 by Dr. Steve Chaney

How Much Protein Should We Eat?

Author: Dr. Stephen Chaney

The recent headlines suggesting that high protein diets may cause cancer, diabetes and premature death in middle aged Americans are downright scary. You are probably asking yourself:

“Is this new information?”

“Does this apply to me?”

“Should I radically change what I eat?”

In this issue of “Health Tips From the Professor” I will address each of these questions.

Do High Protein Diets Cause Cancer?

The study in question (Levine et al., Cell Metabolism, 19: 407-417, 2014) suggested that high protein diets were associated with increased risk of cancer, diabetes and premature death in Americans in the 50-65 age range. I will touch on all three of these observations, but it is the increased risk of cancer that generated the most headlines – and the most concern (The consequences of diabetes take years to manifest, and death seem to be a more distant concern for most people. Cancer is immediate and personal).

The study looked at 6,381 adults aged 50 and older (average age 65) from the NHANES III data base. (NHANES is a comprehensive database collected by the Centers for Disease Control and Prevention that consists of surveys and physical examinations and is designed to be representative of the health and nutritional status of the US population.)

The data collected consisted of a single diet questionnaire conducted when the subjects were enrolled in the study. Based on the diet questionnaire the authors of the study divided the group into those with low protein intake (<10% of calories), those with moderate protein intake (10-19% of calories) and those with high protein intake (>20% of calories). Overall death and mortality from various diseases over the next 18 years was obtained by linking the NHANES data with the National Death Index.

Based on preliminary data suggesting that the age of the population might influence the results (I won’t go into details here) the authors of the study decided to subdivide the dataset into people aged 50-65 and people over 65. When they did that, they came to the following conclusions:

1) In the 50-65 age group diets high in animal protein were associated with a:

45% increase in overall mortality

4-fold increase in cancer death risk

4-fold increase in diabetes death risk.

Diets with moderate protein intake were associated with intermediate increases in risk. Surprisingly, there was no increase in cardiovascular disease risk.

2) When they looked at people in the 50-65 age group consuming diets high in vegetable protein:

the increased overall mortality and increased in cancer mortality disappeared

the increased diabetes mortality was still seen.

3) In the 65+ age group high protein diets were associated with a:

28% decrease in overall mortality

60% decrease in cancer mortality.

The increased risk of diabetes related deaths was still observed. The authors did not distinguish between animal and vegetable protein in the over 65 age group.

All of that may seem to be a bit too complicated. At the risk of gross oversimplification I would summarize their message as follows:

Diets high in animal protein may be bad for you if you are in the 50-65 age range, but might actually be good for you if you are over 65.

Diets high in vegetable protein appear to be good for anyone over age 50 (The study didn’t look at younger age groups).

Is This New Information?

Let’s start by assuming that the conclusions of the authors are correct (more about that below).

When you boil their message down to its simplest components, the information isn’t particularly novel.

The idea that vegetable proteins may be better for you than animal proteins has been around for decades. There are a number of studies suggesting that diets high in animal protein increase the risk of cancer, heart disease, diabetes and overall death – although it is still not clear whether it is the animal protein itself or some other characteristic of populations consuming mostly animal protein that is the culprit.

Evidence has been accumulating over the past decade or so that protein needs increase as we age, so it is not surprising that this study found high protein diets to be beneficial for those of us over age 65.

What Do Other Experts Say?

Since this study has been released it has been roundly criticized by other experts in the field. Let me sum up their four main criticisms and add one of my own.

1) The protein intake data were based on a single dietary survey taken at the beginning of an 18 year study. The authors stated that a single dietary survey has been shown to be a pretty accurate indicator of what an individual is eating at the time of the survey. However, it is problematic to assume that everyone’s diet remained the same over an 18 year period.

2) The choice of less than 10% of calories from protein is also problematic. According to the Institute of Medicine standards anything below 10% is defined as inadequate protein intake, which can have long term health consequences of its own.

More importantly, only 7% of the population being studied (437 individuals) fell into this group. This is the baseline group (or put another way, the denominator for all of the comparisons). The conclusions of this study were based on comparing the other two groups to this baseline, and there were too few individuals in this group to be confident that the baseline is accurate.

This does not necessarily invalidate the study, but it does decrease confidence in the size of the reported effect – so forget the reported numbers like 45% increase in mortality and 4-fold increase in cancer deaths. They probably aren’t accurate.

3) The number of people in this study who died from diabetes was exceedingly small (68 total) and most of them already had diabetes when the study began. The experts concluded that the numbers were simply too low to draw any conclusions about protein intake and diabetes related deaths, and I agree with them.

4) While the study controlled for fat intake and carbohydrate intake, it did not control for weight. That is a huge omission. Overweight is associated with increased risk of cancer, diabetes and death, and vegetarians tend to weigh less than non-vegetarians.

5) I would add that there are many other differences between vegetarians and non- vegetarians that could account for most of the differences reported between diets high in animal and vegetable protein. For example:

The kinds of fat in the two types of diet are different, and that can be significant (see “Are Saturated Fats Good For You?”)

Some animal proteins may be more harmful than others (see “Does Carnitine Increase Heart Disease risk?”)

Vegetarians tend to be more health conscious and thus they tend to exercise more, consume more fiber, consume more fruits and vegetables, consume less fried food, and consume less processed and convenience foods – all of which are associated with decreased risk of cancer, diabetes and death.

The Bottom Line:

This is not a particularly strong study. Nor is it particularly novel. In fact, when you strip away the scary headlines and focus on what the data really show, the conclusions aren’t that different from what nutrition experts have been saying for years.

1) This study suggests that if you are in the 50-65 age range, diets high in animal protein may not be good for you (this study focused on increased risk of cancer death and overall mortality. Other studies have suggested that diets high in animal protein may increase the risk of cardiovascular death).

This is not a new idea. These data are consistent with a number of other studies. However, none of these studies adequately assess whether the increased risk is from the animal protein alone or from other characteristics of populations that consume a lot of animal protein.

2) This study also suggests that diets high in vegetable protein do not increase either cancer risk or all cause mortality. That’s also not new information. We’ve known for years that people who consume primarily vegetable protein appear to be healthier. Once again, it is not clear whether it is the vegetable protein itself that is beneficial or whether the benefit is due to other characteristics of populations who consume a lot of vegetable protein.

3) Does that mean that you need to become a vegetarian? It probably reflects my personal bias, but I am reminded of a Woody Allen Quote: “Vegetarians don’t live longer. It just seems that way”. I am also encouraged by studies suggesting that most of the health benefits of vegetarianism can be achieved by diets that consist of around 50% vegetable protein.

I would never discourage anyone from becoming a vegetarian, but if you aren’t ready for that, I would highly recommend that you aim for at least 50% vegetable protein in your diet.

4) Finally, this study suggests that a high protein diet is beneficial for people over 65. This is also not a completely novel idea. It is consistent with a lot of recent research.

My advice to those of you who, like me, are over 65 is to pay attention to high protein foods and make sure that they are an important part of your diet. I’m not suggesting that you go for the double bacon cheeseburger just because you are over 65. I would still aim for a significant percentage of vegetable protein as a part of a healthy diet at any age.

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.

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.