Vitamins and Health Archives - Page 2 of 3 - Health Tips From The Professor

Do B Vitamins Reduce Heart Disease Risk?

February 23, 2016 by Dr. Steve Chaney

What Role Do B Vitamins Play in a Heart Healthy Lifestyle?

Author: Dr. Stephen Chaney

Two weeks ago I shared some studies that challenge the claim that vitamin E doesn’t reduce heart attack risk. To close out “Heart Health” month, I want to share some information that may change how you think about B vitamins and heart disease risk. Once again, you’ve seen the headlines: “B Vitamins Do Not Reduce the Risk of Heart Disease”. In fact, these headlines have been repeated so many times that virtually every expert thinks that it has to be true. Once again, I’m going to share some information with you that I learned from a seminar by Dr. Jeffrey Blumberg who disagrees with this commonly held belief.

Dr. Blumberg is a Professor in the Friedman School ofNutrition Science and Policy at Tufts. Dr. Blumberg has over 200 publications in peer-reviewed scientific journals. He is considered one of the world’s top experts on supplementation, and his specialty is conducting and analyzing clinical studies. He believes that the media has seriously misinterpreted the studies on B vitamins and heart disease risk. You might call this “The Rest of the Story” because you (and your doctor) definitely did not hear this part of the story in the news.

Do B Vitamins Reduce Heart Disease Risk?

The study in question is called the “Heart Outcomes Prevention Evaluation-2“. In that study a group of middle aged men and women received 2.5 mg of folate, 50 mg of vitamin B6 and 1 mg of vitamin B12 versus a placebo and were followed for an average of 5 years.

The headlines that you may have seen said “B vitamins do not reduce the risk of major cardiovascular events in patients with vascular disease”. But, the headlines did not tell the whole story.

In the first place, that was only true for heart attacks and cardiovascular death. Strokes were reduced by 25%. I don’t know about you, but I consider strokes to be fairly major.

However, even when we focus on heart attacks and cardiovascular deaths the headlines didn’t tell the whole story. You see, even the best intentioned studies sometimes contain fatal flaws that aren’t obvious until after the study has been completed.

The Flaws In The Study

There were two major flaws in this study.

Flaw #1 was that 70% of the study subjects were eating foods fortified with folate and had adequate levels of that nutrient in their bloodstream before the study started.

For those people who were already getting enough folate in their diet, B vitamin supplementation didn’t make much of a difference. However, for those people not getting adequate levels of folate in their diet, B vitamin supplementation decreased their risk of heart disease by ~15%.

Flaw #2 was that ~90% of the people in the study had a history of coronary artery disease and most of them were already on cholesterol lowering medications.

To understand why this is a problem you have to understand both the proposed mechanism by which B vitamin supplementation has been proposed to lower the risk of heart disease AND how the cholesterol lowering drugs work.

Deficiencies of folate, B6 and B12 are thought to increase the risk of heart disease because the B vitamin deficiency causes an increase in homocysteinelevels in the blood, and high homocysteine levels are thought to increase inflammation – which is a risk factor for heart disease. So supplementation with folate, B6 and B12 has been proposed to decrease heart disease risk by decreasing inflammation.

The problem is that the most commonly used cholesterol lowering medications also decrease inflammation.So you might not be surprised to learn that those people who had a history of coronary artery disease(and were taking cholesterol lowering medication that reduces inflammation) did not receive much additional benefit from B vitamin supplementation.

For those people in the study who were not taking cholesterol lowering medication, B vitamin supplementation also reduced their risk of heart attacks by ~15% – but there were too few people in that group for the results to be statistically significant.

So the headlines from this study really should have said “B vitamins do not reduce the risk of heart attacks or cardiovascular deaths in people who are already getting adequate folate from their diet or in people who are taking drugs that reduce the bad effects of B vitamin deficiency”. But that kind of headline just wouldn’t sell any newspapers.

What Does This Study Mean For You?

There are two very important take-home lessons from this study.

Lesson #1: Once again this study makes the point that supplementation makes the biggest difference when people have an increased need. The studies discussed in Vitamin E and Heart Disease two weeks ago illustrated increased need because of age, pre-existing disease, and genetic predisposition. This study illustrated increased need because of inadequate diet.

Lesson #2: This study also illustrates a problem that is becoming increasingly common in studies of supplementation. It is considered unethical to not provide participants in both groups with what is considered the standard of care for medical practice. In today’s world the standard of care includes multiple drugs with multiple side effects, and some of those drugs may have the same mechanism of action as the supplement.

I have discussed this problem in the context of omega-3 fatty acids and heart disease in a previous “Health Tips From the Professor,” Is Fish Oil Really Snake Oil? In many cases it is no longer possible to ask whether supplement X reduces the risk of a particular disease. It is now only possible to ask whether supplement X provides any additional benefit for patients who are taking multiple drugs, with multiple side effects. That’s not the question that many of my readers are interested in.

The Bottom Line

Headlines have proclaimed for years the “B Vitamins Do Not Reduce Heart Disease Risk”. Dr. Jeffrey Bloomberg of Tufts University has reviewed one of the major studies behind this claim and found the headlines to be misleading.

For example, the study showed that B vitamin supplementation reduced strokes by 25%, which is a pretty significant finding in itself.

When he analyzed the portion of the study looking at heart attacks, he found two major flaws:

#1: 70% of the people in the study were already getting adequate amounts of B vitamins from their diet and would not be expected to benefit from supplementation. For the 30% who weren’t getting adequate amounts of B vitamins from their diet, supplementation reduced their risk of heart attack by 15%.

#2: 90% of the people in the study were taking a drug that masks the beneficial effects of B vitamin supplementation. For the 10% who weren’t taking the drug, supplementation with B vitamins also reduced their risk of heart attack by 15%, but there were too few people in that group for the results to be statistically significant.

Obviously, there were only a handful of people in the study who weren’t getting enough B vitamins from their diet AND weren’t on medication, so we have no idea what the effect of B vitamin supplementation was in that group.

Once again this study makes the point that supplementation makes the biggest difference when people have an increased need. The studies discussed in “Health Tips From the Professor” two weeks ago illustrated increased need because of age, pre-existing disease, and genetic predisposition. This study illustrated increased need because of inadequate diet.

This study also illustrates a problem that is becoming increasingly common in studies of supplementation. It is considered unethical to not provide participants in both groups with what is considered the standard of care for medical practice. In today’s world the standard of care includes multiple drugs, some of which may have the same mechanism of action as the supplement.

In many cases it is no longer possible to ask whether supplement X reduces the risk of a particular disease. It is now only possible to ask whether supplement X provides any additional benefit for patients who are taking multiple drugs, with multiple side effects. That’s not the question that many of my readers are interested in.

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.

Vitamin E And Heart Disease

February 9, 2016 by Dr. Steve Chaney

Does Vitamin E Reduce Heart Attack Risk?

Author: Dr. Stephen Chaney

Since February is “Heart Health Month”, I thought I would share some information with you that might change how you think about vitamin E and heart disease risk. You’ve seen the headlines: “Vitamin E Does Not Reduce the Risk of Heart Disease”. In fact, these headlines have been repeated so many times that virtually every expert thinks that it has to be true. Let me share the opinion of one expert who disagrees. This week I’m going to share some information with you that I learned from a seminar by Dr. Jeffrey Blumberg from Tufts University.

But first let me tell you who Dr. Blumberg is. Dr. Blumberg is a Professor in the Friedman School of Nutrition Science and Policy at Tufts. Dr. Blumberg has over 200 publications in peer-reviewed scientific journals. He is considered one of the world’s top experts on supplementation.

Now back to what I learned at his seminar. Dr. Blumberg’s specialty is conducting and analyzing clinical studies, and his perspective on some very influential clinical studies is a bit different from what you may have heard from media reports. He believes that the media has seriously misinterpreted several recent studies. You might call this “The Rest of the Story” because you (and your doctor) definitely did not hear this part of the story in the news.

Does Vitamin E Reduce Heart Disease Risk In Women?

Let’s start with vitamin E and the risk of cardiovascular disease in women. The most influential study on this subject was the Women’s Health Study (Lee et al., JAMA, 294:56-65, 2005). This was a major study in which 39,876 women were given either 600 IU of vitamin E every other day or a placebo and followed for 10 years.

The headlines said “Vitamin E Supplements Do Not Reduce Risk Of Cardiovascular Death, Heart Attack And Stroke In Women”. That was true if you looked at the total population of women in the study.

But Dr. Blumberg pointed out that when you looked at women who were 65 or older in that study vitamin E supplementation caused a…

24% decrease in cardiovascular deaths,

26% decrease in major cardiovascular events,

21% decrease in venous thromboembolism (blood clots forming in the veins),

…and all of these decreases were statistically highly significant. That’s important because the risk of heart disease in pre-menopausal women is extremely low. It’s the over 65 group who have a high risk of heart disease.

Perhaps the headlines should have said: “Vitamin E reduces the risk of cardiovascular disease and cardiovascular deaths in those women at high risk of heart attacks”. But, of course, they didn’t. Perhaps that wasn’t considered newsworthy.

Other Studies On Vitamin E and Heart Disease Risk In Women

If this were the only study suggesting the vitamin E might benefit women at high risk of having a heart attack or stroke, it might be easy to dismiss it, but it’s not the only study showing this effect.

For example, a subsequent study called the “Women’s Antioxidant Cardiovascular Study” looked at the effect of 600 IU of vitamin E every other day on cardiovascular events in 8171 women health professionals (Cook et al, Archives of Internal Medicine, 167:1610-1618, 2007).

Once again the headlines said that vitamin E supplementation had no effect on cardiovascular events in women. But, when the authors looked at those women who already had cardiovascular disease at the beginning of the study (and were, therefore, at high risk of suffering a cardiovascular event during the study) vitamin E supplementation caused a 23% decreased risk of heart attack, stroke and cardiovascular death.

Another important study was the HOPE (Heart Outcomes Prevention Evaluation) study (Levy et al, Diabetes Care, 27: 2767, 2004). The overall study results were similar to several other recent trials – no significant effect of vitamin E supplementation on cardiovascular health in the population group as a whole.

However, by the time that study was performed it was clear that a particular genetic variation in the haptoglobin gene called the haptoglobin 2-2 genotype lead to a significant increase in oxidative damage to the vascular wall (the professor will collect your quizes at the end of this email).

When the data were reanalyzed by genotype, it became clear that people with the haptoglobin 2-2 genotype experienced a significant decrease in both heart attack and cardiovascular death with vitamin E supplementation. This finding has been confirmed by a subsequent double-blind, placebo-control study specifically designed to look at the cardioprotective effects of vitamin E in people with different haptoglobin genotypes (Milman et al, Arterioscler. Thromb. Vasc. Biol., 24: 136, 2008).

In short, the headlines from all three studies should have said: “Vitamin E reduces the risk of cardiovascular disease and cardiovascular deaths in those women at high risk of heart attacks” – and, it doesn’t appear to matter whether the increased risk is due to age, pre-existing disease, or genetic predisposition.

Does Vitamin E Reduce Heart Disease Risk In Men?

For men the most influential study was called the “Physician’s Health Study II” (H. D. Sesso et al, JAMA, 300: 2123-2133, 2008). In this study male physicians aged 40-84 were invited to participate in a double-blind clinical trial in which they were randomly assigned into groups who were given 400 IU of vitamin E every other day or placebo. They were followed for an average of 8 years during which data on both total mortality and cardiovascular mortality were obtained.

Once again, the headlines read “Vitamin E Does NotPrevent Cardiovascular Disease in Men”. But let me tell you what Dr. Blumberg said so that you understand “The Rest of the Story”. It starts by looking at the selection process for the Physician Health Studies.

Dr. Sesso and his colleagues sent out a letter asking 261,248 male physicians in the US if they would be willing to participate in the study. Only 112,528 responded and, of those responding, only 59,272 indicated that they were willing to participate. Of those who said that they were willing to participate only 32,223 met the selection criteria.

The exclusion criteria eliminated anyone who already had suffered a heart attack, stroke, angina or was on a blood thinner – in other words those people who were at greatest risk of suffering a heart attack or stroke during the study.

Finally, the study had an 18 week “run in” period to eliminate those people who were unwilling or unable to comply with the study protocol. This eliminated another 10,000 participants, leaving only 22,071 participants – less than 10% of the original.

This is where it gets really interesting. Dr. Sesso and his colleagues used publicly available databases to evaluate total and cardiovascular mortality in each group (H. D. Sesso et al, Controlled Clinical Trials, 23: 686-702, 2002). It turns out that at each stage of the selection process the incidence of both total and cardiovascular mortality during the 8-year period decreased.

In fact, the doctors who were actually included in the study were 67% less likely to die from all causes and 73% less likely to die from cardiovascular disease than the male physician population as a whole.

The bottom line is that the selection process eliminated almost all of the physicians at significant risk of having a heart attack or stroke during the study. The only ones who were actually enrolled in the study were those physicians who were at very low risk for having a fatal heart attack or stroke – or dying from any cause – during the study.

So the headlines describing this study should have read “Vitamin E Does Not Prevent Cardiovascular Disease in Men Who Are At Very Low Risk Of Heart Attack And Stroke”.The irony is that there was nothing wrong with the design of the study. It’s probably just a male ego thing. Guys who were unhealthy just didn’t want to participate in a study that might show how unhealthy they really were.

What Does This Mean For You?

These studies illustrate the true story of supplementation. For those of us who are at low risk of disease, supplementation is just a form of health insurance. But for those of us at high risk of disease, supplementation can make a huge difference in our health. That increased risk can be due to many things, as we have seen in the studies above. It can be due to poor diet, age, pre-existing disease, and/or genetic predisposition.

The problem is that most of us don’t really know whether we are at low risk or high risk until it’s too late. For millions of Americans the first sign of heart disease is sudden death.

The Bottom Line

The experts have been saying for years that vitamin E does not reduce the risk of heart disease. That claim is true, if you look at the general population, most of which is at low risk of developing heart disease – at least during the time frame of the clinical studies. However, when you look at people who are at high risk of developing heart disease, the answer is different.

For example, when you look at clinical studies with women, vitamin E significantly decreased the risk of heart attacks in women who…

Were over 65,

Had pre-existing heart disease at the beginning of the study,

Or, had a genetic predisposition to heart disease.

The headlines from these studies should have read “Vitamin E reduces the risk of cardiovascular disease in those women at high risk of heart attacks”, but they didn’t.

For men the story is a bit different. The Physician’s Health Study is considered the definitive study on the subject. However, most of the unhealthy male physicians either didn’t enroll in the study or dropped out before its completion. In fact, the doctors who were actually included in the study were 67% less likely to die from all causes and 73% less likely to die from cardiovascular disease than the male physician population as a whole. The headlines describing this study should have read “Vitamin E Does Not Prevent Cardiovascular Disease in Men Who Are At Very Low Risk Of Heart Attack And Stroke”.

These studies illustrate the true story of supplementation. For those of us who are at low risk of disease, supplementation is just a form of health insurance. But for those of us at high risk of disease, supplementation can make a huge difference in our health. That increased risk can be due to many things, as we have seen in the studies above. It can be due to poor diet, age, pre-existing disease, and/or genetic predisposition.

The problem is that most of us don’t really know whether we are at low risk or high risk until it’s too late. For millions of Americans the first sign of heart disease is sudden death.

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 Calcium Supplements Prevent Bone Fractures? – Part1

January 26, 2016 by Dr. Steve Chaney

Why The Recent Headlines May Be Misleading

Author: Dr. Stephen Chaney

Does calcium help prevent bone fractures? Osteoporosis is a debilitating and potentially deadly disease associated with aging. It affects 54 million Americans. It can cause debilitating back pain and bone fractures. 50% of women and 25% of men over 50 will break a bone due to osteoporosis. Hip fractures in the elderly due to osteoporosis are often a death sentence.

For that reason, the RDA for calcium has been set at 1,000 to 1,200 mg/day to reduce the risk of osteoporosis, and calcium supplements are often recommended to reach that target.However, recent headlines are proclaiming that calcium supplements do not actually prevent bone fractures and might increase your risk of a heart attack. Are the RDA recommendations wrong? Should you throw out your calcium supplements?

In this article I will review the article behind the study and help you put it into perspective. After all, you don’t really want to know whether calcium supplementation is beneficial for the average adult. You want to know whether it will be beneficial for you.

Let me start by putting the heart attack myth to rest. I have covered this in detail in a previous “Health Tips From The Professor” article, Calcium Supplements Increase Heart Attack Risk . If you don’t want to go to the trouble of reading my previous article, the short version is that:

Most of the studies suggesting an increased risk of heart attacks are flawed.

A very large study (74,000 women followed for 24 years) has shown fairly convincingly that calcium supplements do not increase heart attack risk. If anything, they decrease heart attack risk.

Unfortunately, like most other nutrition myths, this one is still being repeated – even after it has been refuted by subsequent studies.

Bone Metabolism and Osteoporosis

Before you can truly understand osteoporosis and how to prevent it, you need to know a bit about bone metabolism. We tend to think of our bones as solid and unchanging, much like the steel girders in an office building. Nothing could be further from the truth. Our bones are dynamic organs that are in a constant change throughout our lives.

Cells called osteoclasts and osteoblasts constantly break down old bone (a process called resorption) and replace it with new bone (a process called accretion). Without this constant renewal process our bones would quickly become old and brittle (I’ll discuss more about this next week when I talk about the side effects of drugs commonly used to increase bone density).

When we are young the bone building process exceeds bone resorption and our bones grow in size and in density. During most of our adult years, bone resorption and accretion are in balance so our bone density stays constant. However, as we age bone the bone building process (accretion) slows down and we start to lose bone density. Eventually our bones look like Swiss cheese and break very easily. This is called osteoporosis.

We should also think of our bones as calcium reservoirs. We need calcium in our bloodstream 24 hours a day for our muscles, brain, and nerves to function properly, but we only get calcium in our diet at discrete intervals. Consequently, when we eat our body tries to store as much calcium as possible in our bones. Between meals, we break down bone material so that we can release the calcium into our bloodstream that our muscle, brain & nerves need to function.

If we lead a “bone healthy” lifestyle, all of this works perfectly. We build strong bones during our growing years, maintain healthy bones during our adult years, and only lose bone density slowly as we age – maybe never experiencing osteoporosis. We always accumulate enough calcium in our bones during meals to provide for the rest of our body between meals.

What is a “bone healthy” lifestyle, you might ask. Because calcium is a major component of bone, the medical and nutrition communities have long focused on calcium as a “magic bullet” that can assure bone health. Once the importance of vitamin D was understood, it was added to the equation. For years we have been told that if we just get enough calcium and vitamin D in our diets, we would build strong bones when we were young, maintain bone density most of our adult years, and lose bone density as slowly as possible as we age.It is this paradigm that the current study challenges.

Do Calcium Supplements Prevent Bone Fractures?

$prevent bone fractures$ Let’s start by looking at the study behind the headlines (Tai et al, British Medical Journal, BMJ/2015; 351:h4183 doi: 10.1136/bmj.h4183). This was a meta-analysis that included 15 studies (1533 participants) looking at dietary sources of calcium and 51 studies (12,257 participants) looking at calcium supplementation in women.

The results of the meta-analysis were thought provoking, but do not exactly support the headlines you have been reading. For example:

The headlines say “Calcium Supplements Do Not Prevent Broken Bones”.

This study did not actually look at calcium supplementation and the risk of bone fractures. That was a previous study (Boland et al, BMJ 2015, 351:h4580) by the same authors.
This study showed that calcium supplementation increased bone density by 0.7-1.8%, which the authors concluded was sufficient to reduce fracture risk by about 5-10%. That’s a disappointingly small effect, but it is not zero – as the headlines suggested.

The headlines say “It’s better to get your calcium from food than from supplements”.

This study showed that it did not matter whether the calcium came from food or from supplements. The increase in bone density was identical.

Garbage-In, Garbage-Out

Meta-analyses such as this one can be very strong, but they can also suffer from the “garbage-in, garbage-out” phenomenon. In short, if most of the studies that went into the meta-analysis were poorly designed, the conclusions of the meta-analysis will be unreliable.

The problem is that many of the individual studies were conducted 10, 20, 30 or 40 years ago when our knowledge of bone metabolism was incomplete.

Thirty or 40 years ago it was “state of the art” to just use a calcium supplement. Then we learned that adequate vitamin D was essential for efficient calcium utilization.

Most of the studies included in this meta-analysis looked at calcium supplementation without vitamin D. Only 13 of the studies (25%) included vitamin D.

Ten or 20 years ago it was “state of the art” to just use a calcium supplement with vitamin D. Then we learned that the blood level of 25-hydroxyvitamin D (the active form of vitamin D in the bloodstream) did not necessarily reflect vitamin D intake from the diet. In today’s world a study in which the 25-hydroxy vitamin D level is not measured should be considered sub-standard.

Only 18 (35%) of the studies measured baseline 25-hydroxy vitamin D levels.

If dietary calcium intake at baseline is already adequate, it is illogical to expect additional calcium to significantly increase bone density.

The baseline calcium intake was <800 mg/day (clearly inadequate) in only 26 (51%) of the studies. Baseline calcium intake was either not determined in the other studies or was already in the adequate range prior to supplementation.

In the future, we will probably want to include exercise as a component in the study (more about that next week). None of the studies included exercise as a component

In short, by today’s standards many, if not most, of the studies included in the meta-analysis had an inadequate design.

If I had designed the meta-analysis, I would have been a lot more restrictive in the studies I included.

I would have started by including only studies in which the baseline intake of calcium was <800 mg/day. If you want to critically evaluate whether calcium supplementation has a beneficial effect, you need to start with people who have an inadequate dietary intake of calcium. If their diets are already calcium sufficient, supplementation is unlikely to have any benefit.

At the very least I would only include studies that used calcium supplements containing 400-800 IU of vitamin D as well. In fact, based on the latest data, I would make sure that the calcium supplement I used also contained adequate levels of magnesium, vitamin K, zinc, copper and manganese. All of those have been shown to be important for bone formation and we cannot assume they are present at sufficient levels in their diet (more about that next week).

I would only include studies that measured blood levels of 25-hydroxy vitamin D at baseline and following supplementation with vitamin D so that we knew that the 25-hydroxy vitamin D level was sufficient to support optimal calcium utilization.

Finally, I would only include studies that specifically measured the effect of exercise on calcium utilization or included exercise as an integral part of their study.

The number of studies included in the meta-analysis would be much less, but they would all be high quality studies.

Finally, the authors also noted that a number of studies in the supplement group showed significantly greater (2.5 – 5.0%) increase in bone density. They dismissed them as outliers. I would have preferred a closer look at those studies to see if there was anything about the population group or study design that might explain the greater bone density increase in those studies.

Apples and Oranges

Because the authors included a wide variety of clinical studies, they were able to state that “Increases in bone mineral density were similar in trials of calcium monotherapy [calcium by itself] versus co-administered calcium and vitamin D…and in trials where baseline dietary calcium intake was <800 [clearly insufficient] versus >800 [probably sufficient] mg/day.” This could be considered a strength of their meta-analysis, but they are only valid comparisons if other important features of the studies being compared were uniform – i.e. they were comparing apples to apples.

But what if they were comparing apples and oranges?

For example, we know that vitamin D is required for efficient calcium utilization. When the authors compared studies having a baseline calcium intake of <800 mg/day with studies having a baseline calcium intake of >800 mg/day, they did not even check to see whether use of vitamin D was evenly distributed between the two groups. If most of the studies with a baseline calcium intake of <800 mg/day did not include vitamin D with their calcium supplements, the authors would be comparing apples and oranges. The comparison would be invalid.

Similarly, we also know that if calcium intake at baseline is adequate, adding more calcium is unlikely to increase bone density significantly. When the authors compared studies with and without vitamin D, they did not even check to see whether baseline calcium intake was evenly distributed between the two groups. If the participants in most of the studies utilizing supplements providing both calcium and vitamin D were already consuming sufficient calcium at baseline, they would be comparing apples to oranges. Again, the comparison would be invalid.

The authors of the meta-analysis simply did not provide the detail needed to determine whether their comparisons were apples to apples or apples to oranges. Thus, what seemed to be a strength of their study is actually a major weakness.

The Bottom Line

A recent study has reported that the RDA recommendation of 1,000 – 1,200 mg/day of calcium for people over 50 provides only a minimal increase in bone density (0.7-1.8%) over the first year or two. This translates into a very small (5-10%) decrease in risk of bone fractures. It did not matter whether the calcium came from dietary sources or from supplementation. The authors concluded that adding extra calcium to the diet, whether from food or supplements, was not a very efficient way to increase bone density and prevent fractures.

This study suffers from some serious flaws. It is a meta-analysis of previous clinical trials looking at the effects of calcium on bone density. Meta-analyses can be very strong studies because they average the effects of many individual studies. However, meta-analyses can also suffer from the “garbage-in, garbage-out” phenomenon. Simply put, the quality of the meta-analysis is only as good as the studies that go into it. In this case the meta-analysis included many clinical studies that were done 10, 20, 30 and even 40 years ago. Based on what we now know about bone metabolism, the design of many of those early studies was clearly inadequate (details are given in the article).

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.

Heart Disease Risk and Multivitamins

December 1, 2015 by Dr. Steve Chaney

Author: Dr. Stephen Chaney

It’s so confusing. One week vitamins are going to reduce your heart disease risk and cancer risk. The next week they are worthless. They might even kill you. So when you saw the recent headlines suggesting that multivitamin-mineral supplement use might decrease heart disease risk in women, you probably weren’t sure what to think.

More to the point, you may be thinking “Why is it so hard to get this right? Why can’t scientists decide once and for all whether vitamins are beneficial or not?”

Perhaps, the best way to understand the significance of the present study is to look at the strengths and limitations of previous studies. Then we can start to gain perspective on why it is so difficult to come to a definitive conclusion about this very important question.

How Good Is The Evidence That Multivitamin Use Doesn’t Reduce Heart Disease Risk?

Medical authorities are fond of telling you, with a great deal of confidence, that studies have conclusively proven multivitamin use does not decrease heart disease risk. However, in fact, that conclusion is based on only a few studies, and those studies have their limitations.

For example, the Physician’s Health Study II (Sesso et al, JAMA, 308: 1751-1760, 2012) reported that use of a multivitamin-mineral supplement for 11 years did not decrease cardiovascular incidence or mortality. It was a double-blind, placebo controlled clinical study. That’s the best kind of study, so it would be tempting to consider the case closed.

However, this study looked at a very small segment of the population. The participants were all male, primarily non-Hispanic whites, well to do, highly educated and health conscious. It also turns out that the participants that were in the poorest health and had the poorest health habits tended to drop out of the study and were not included in the final data analysis.

That means that the vast majority of participants in the study were at low risk of heart disease and were eating relatively healthy diets. Those are the people who would be least likely to benefit from supplementation. In short, this study proved beyond a reasonable doubt that the people least likely to benefit from supplementation did, in fact, not benefit from supplementation.

The studies that medical authorities quote as proving their case for women have all looked at antioxidant supplements and cardiovascular disease. There are three double-blind, placebo controlled studies that have all come to the conclusion that antioxidant supplements do not decrease cardiovascular risk in women. Once again, it might be tempting to consider the case closed.

However, in two of those studies (Lee et al, JAMA, 294: 56-65, 2005; Cook et al, Archives of Internal Medicine, 167: 1610-1618, 2007) when they looked at the subset of women who were at high risk of cardiovascular disease (either because of age or pre-existing disease), antioxidant supplements significantly decreased the risk of cardiovascular events and cardiovascular deaths. In short, these studies showed that those people most likely to benefit from supplementation, did, in fact, benefit from supplementation.

Finally, medical authorities have chosen to completely ignore a recent study reporting that multivitamin use significantly decreased heart attack risk in women, especially if they had been using the multivitamins for 5 years or more (Rautiainen et al, American Journal of Clinical Nutrition, 92: 1251-1256, 2010). In short, previous studies have not conclusively proven much of anything except that it is really hard to get definitive answers to this kind of question.

Does Multivitamin Use Decrease Cardiovascular Disease Risk In Women?

The current study (Bailey et al, Journal of Nutrition, 145: 572-580, 2015) compared multivitamin use in 8678 adults(65% women) 40 years or older, from the USDA’s NHANES III database and compared it with cardiovascular death reports in the National Death Index 18 years later.

At the time of the NHANES III study, 45% of the adults surveyed had used some kind of supplement within the past 30 days. When the researchers broke the data down further:

21% were using multivitamin-mineral supplements (3 or more vitamins and 1 or more minerals)

14% were using multivitamin supplements (3 or more vitamins, no minerals).

Among multivitamin-mineral and multivitamin supplement users, only 46% had been using them for 3 years or more.

When they compared supplement usage with cardiovascular deaths 18 years later, the results were as follows:

When they asked if multivitamin-mineral or multivitamin use at the beginning of the study affected cardiovascular mortality 18 years later, the answer was a clear no.

When they looked at women, use of a multivitamin-mineral supplement for 3 years or more was associated with a 35% decreased risk of cardiovascular mortality.

However, they did not find any cardiovascular benefit from long term use of a multivitamin supplement alone for women. From this, they concluded that the beneficial effects of the multivitamin-mineral supplement came from one of the minerals, most likely magnesium or calcium.

There was a slight hint that multivitamin use might be beneficial for men, but the number of cardiovascular deaths in that group was too small for the results to be statistically significant.

What Does This Study Mean?

This study suggests that long term use of a multivitamin-mineral supplement may decrease the risk of cardiovascular disease deaths in women. Whether long term multivitamin use also reduces risk of cardiovascular disease in men is an open question. This study is consistent with another recent study looking at multivitamin use in women (Rautiainen et al, American Journal of Clinical Nutrition, 92: 1251-1256, 2010). However, these studies are just a piece of the puzzle. It will take time and more studies before we will really be able to definitively say whether or not multivitamin use can decrease the risk of heart disease, or any other disease.

How Can You Reduce Your Heart Disease Risk?

The surest way to reduce your risk of heart disease is to develop a heart healthy lifestyle.

Lose weight and/or maintain ideal body weight. Overweight and obesity dramatically increase all of the major risk factors for heart disease – LDL cholesterol, triglycerides, diabetes, hypertension and inflammation.

Exercise for more than 30 minutes – 3 times or more/week. Regular exercise reduces the risk of heart disease by 30-40%.

Follow a diet low in saturated fat and trans-fat (substitute monounsaturated fats like olive oil and omega-3 fats); low in sugars and artificial sweeteners; and high in fiber, whole grains, legumes, fruits, vegetables, and fish.

Work with your physician to control predisposing diseases such as diabetes and hypertension.

What about supplementation? What role does it play in a heart healthy lifestyle? At present it’s pretty clear that the scientific community cannot definitively prove whether supplementation reduces the risk of heart disease or not. All the available evidence suggests that supplementation is most likely to prove beneficial for those who are at highest risk for heart disease and/or are most likely to be deficient in key nutrients – either because of poor diet or genetic variations that increase nutrient requirements.

In the best of all possible worlds we would know who was at high risk for heart disease and who was deficient in key nutrients. We would know who would benefit from supplements and who would not, but we don’t live in the best of all possible worlds.

Most people don’t know they are at risk for heart disease until it is too late. For far too many people the first symptom of heart disease is sudden death.
Genetics can greatly increase the need for key nutrients, and most people are completely unaware of those genetic predispositions until it is too late. In the future, we may be able to design genetic tests to determine individual nutritional requirements with precision, but we are decades away from that Utopian age at present.

Finally, many people are either blissfully unaware how unhealthy their diet is, or they just don’t want to do anything about it.

For all of the reasons above, I recommend a balanced supplementation program as part of a heart healthy lifestyle. The supplements most likely to be beneficial are a multivitamin-mineral supplement, antioxidants, omega-3s, and B vitamins. I have covered the evidence for the role of each of these nutrients in preserving heart health in previous issues of “Health Tips From the Professor”. Of course, I do not recommend supplementation as an alternative to a heart healthy lifestyle. Taking a multivitamin along with your Big Mac is probably not going to do much for your heart health.

The Bottom Line

A recent study reported that women who used a multivitamin – mineral supplement for 3 years or more decreased their risk of dying from heart disease over the next 18 years by 35%. The men in the study may have received some benefit from multivitamin – mineral supplementation, but the numbers were not large enough to be statistically significant.

This study is fully consistent with the results of a previous study with women. However, when we look at all of the available studies it is not possible to definitively conclude whether supplementation decreases the risk of heart disease or not.

All of the available evidence suggests that supplementation is most likely to be beneficial for those people who are at highest risk of heart disease and/or are most likely to be deficient in key nutrients.

In the best of all possible worlds we would know who was at high risk for heart disease and who was deficient in key nutrients. We would know who would benefit from supplements and who would not, but we don’t live in the best of all possible worlds.

Most people don’t know they are at risk for heart disease until it is too late. For far too many people the first symptom of heart disease is sudden death.
Genetics can greatly increase the need for key nutrients, and most people are completely unaware of those genetic predispositions until it is too late. In the future, we may be able to design genetic tests to determine individual nutritional requirements with precision, but we are decades away from that Utopian age at present.

Finally many people are either blissfully unaware how unhealthy their diet is, or they just don’t want to do anything about it.

For the reasons above, I recommend a balanced supplementation program as part of a heart healthy lifestyle. The supplements most likely to be beneficial are a multivitamin-mineral supplement, antioxidants, omega-3s, and B vitamins.

Of course,I do not recommend supplementation as an alternative to a heart healthy lifestyle. Taking a multivitamin along with your Big Mac is probably not going to do much for your heart health.

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.

Vitamin D and Multiple Sclerosis | Preventive Care?

October 27, 2015 by Dr. Steve Chaney

Author: Dr. Stephen Chaney

A new study (Mokry et al, PLOS Medicine, DOI: 10.1371/journal.pmed.1001866, August 25, 2015) suggests that people who are genetically prone to low vitamin D levels are at increased risk of developing multiple sclerosis (MS). To understand the importance of this study and what it means for us, we need to first review what is already known about vitamin D and multiple sclerosis.

MS is an autoimmune disease in which the immune system attacks the myelin sheath that coats our nerves. Conceptually, that’s the equivalent of a fraying cord on a lamp. Eventually, the cord is going to start shorting out and the lamp won’t work very well. On a very basic level MS is similar. As our myelin sheath is damaged over time, our nervous system starts working less well.

The earliest evidence that vitamin D status might be associated with MS was the observation that the prevalence of MS was highest for people who lived in northern regions with little exposure to sunlight.

Numerous studies since then have shown that MS patients generally have lower 25-hydroxy vitamin D levels in their blood.

These studies clearly show an association between low vitamin D status and MS, but association does not prove causation. There are two limitations of association studies that significantly reduce their predictive value – reverse causation and confounding factors.Those are both somewhat highfalutin scientific terms, so let me put them in plain English – and in terms that are relevant to our discussion of vitamin D status and MS.

Reverse causation simple means that the MS might have caused low vitamin D status. For example, individuals with MS might spend less time outdoors because of their physical limitations. That would result in less sun exposure, which would decrease their blood levels of 25-hydroxy vitamin D.

A confounding factor would be something else that increased the risk for MS and happened to be associated with low vitamin D status. Suppose, for example, that exercise decreased the risk of MS. People who spend most of their time inside in front of a TV or computer screen would have low levels of exercise and low sun exposure. If it was the lack of exercise rather than the low vitamin D status that actually predisposed to MS, lack of exercise would be a confounding factor for any clinical study comparing vitamin D status with risk of developing MS.

What Can Genetics Tell Us About The Relationship Between Vitamin D and Multiple Sclerosis?

The authors of this study had previously identified mutations in 4 genes that decrease blood levels of 25-hydroxy vitamin D (the most commonly used measure of vitamin D status). In this study(Mokry et al, PLOS Medicine, DOI: 10.1371/journal.pmed.1001866, August 25, 2015)they analyzed the frequency of those genetic mutations in 14,498 MS cases compared with 24,091 healthy controls. Their study showed:

Genetic mutations that decrease 25-hydroxy vitamin D levels are associated with a significant increase in the risk of developing MS.

Based on the relationship of those mutations with 25-hydroxy vitamin D levels, they calculated that every 50% increase in 25-hydroxy vitamin D levels was associated with a 50% decreased risk of developing MS.

This was a very large, well designed study. It has some limitations of its own, but because it used a genetic approach it largely avoids the concern about reverse causation and confounding factors. In short, this study strongly supports the conclusion from previous studies that low vitamin D status significantly increases the risk of developing MS.

The authors concluded “The identification of vitamin D as a causal susceptibility factor for MS may have important public health implications, since vitamin D insufficiency is common, and vitamin D supplementation is both relatively safe and cost effective.”

Is Vitamin D Supplementation Effective In Preventing And Treating MS?

The authors of the study also concluded “These findings provide the rationale for further investigating the therapeutic benefits of vitamin D supplementation in preventing the onset and progression of MS.”

While more studies are still needed, the Nurses’ Health Study (Munger et al, Neurology, 62: 60-65, 2004) provides pretty convincing evidence that vitamin D supplementation can prevent the onset of MS. That study followed 187,563 nurses for at least 4 years, during which time 173 of them developed MS. The study showed that supplementation with 400 IU/day of vitamin D reduced the risk of developing MS by 40%.

The efficacy of vitamin D supplementation in preventing the progression of MS is much less well established. Several studies have shown that low vitamin D status is associated with higher levels MS relapse and more rapid progression of MS symptoms.However, studies of vitamin D supplementation conducted to date have been too small and too short in duration to be definitive.

What Is The Significance Of This Study?

On one hand MS is a very rare disease, affecting around 0.1% of the adult population. On the other hand, it is a debilitating disease. If something as simple as assuring adequate vitamin D status can reduce the risk of developing MS by 40-50%, it is an important public health measure, especially since 40% of the US population has insufficient blood levels of vitamin D (Looker et al, American Journal of Clinical Nutrition, 88: 1519-1527, 2008).

What Does This Study Mean For You?

What does this study mean for you and me? We already know that adequate vitamin D status is essential for building strong bones, and there is pretty good evidence that adequate vitamin D status is important for a strong immune system. Now we can add autoimmune diseases to the list. It is pretty clear that adequate vitamin D status is important for preventing MS. It may help prevent other autoimmune diseases as well.

One interesting wrinkle for MS is that it may be vitally important to assure adequate vitamin D in our younger years. Studies looking at people who grow up in northern latitudes and then move south and vice versa suggest that the risk of developing MS is much more strongly associated with sun exposure during the first 10-15 years of life than with sun exposure later in life.

It is, therefore, not just important that we assure adequate vitamin D status for ourselves. It may be even more important that we assure that our kids and grandkids have adequate vitamin D status.

The problem is that in today’s world we are told to slather industrial strength sunscreen on ourselves from head to foot before we leave the house and very few foods in nature provide significant amounts of vitamin D, so most of us rely primarily on vitamin D fortified dairy products and supplements to assure adequate intake of vitamin D. Click here for the latest RDA recommendations for vitamin D intake.

Some people do appear to need greater than RDA levels of vitamin D because they don’t metabolize vitamin D efficiently. They can have adequate intake of vitamin D, but their blood levels of 25-hydroxy vitamin D are low. I recommend that you ask your doctor to check your 25-hydroxy vitamin D levels at your next physical. If they are low, work out a vitamin D supplementation regimen with your doctor to bring your 25-hydroxy vitamin D levels into the optimal range.

The Bottom Line

A recent study showed that genetic mutations which decrease 25-hydroxy vitamin D levels are associated with a significantly increased risk of developing MS. Based on the relationship of those mutations with 25-hydroxy vitamin D levels, the investigators calculated that every 50% increase in 25-hydroxy vitamin D levels was associated with a 50% decreased risk of developing MS. This study strongly supports the conclusion from previous studies that low vitamin D status significantly increases the risk of developing MS.

An earlier Nurses’ Health Study has shown that supplementation with 400 IU/day of vitamin D decreases the risk of developing MS by 40%.

The authors of the most recent study concluded “The identification of vitamin D as a causal susceptibility factor for MS may have important public health implications, since vitamin D insufficiency is common, and vitamin D supplementation is both relatively safe and cost effective.” I agree.

While MS is a very rare disease, it can be devastating. This alone, is a good enough reason to be sure that you maintain adequate vitamin D status.

There is evidence that vitamin D status in our childhood years may be more important than our vitamin D status in later years for determining our risk of developing MS. It is, therefore, not just important that we assure adequate vitamin D status for ourselves. It may be even more important that we assure that our kids and grandkids have adequate vitamin D status.

While these and other studies demonstrate the health benefits of maintaining adequate vitamin D status, many Americans don’t do a good job of it. Government surveys show that 40% of Americans are deficient in vitamin D. That’s because we are continually being advised to slather on industrial strength sunscreen before we leave the house, and most naturally occurring foods are relatively poor sources of vitamin D.

While the evidence that vitamin D supplementation is effective for preventing MS is strong, evidence that vitamin D supplementation can slow the progression of MS is inconclusive at present. More and better studies are needed before we will have a definitive answer to this question.

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.

ADHD Diet VS Medication for ADHD

October 6, 2015 by Dr. Steve Chaney

Author: Dr. Stephen Chaney

I came across a headline in our local newspaper recently that said “Try Nutrition, Not Drugs, for ADHD”. The article made claims like “No good evidence exists to support the ADHD disease hypothesis” and “…on numerous occasions we have seen ADHD symptoms completely disappear without medication”.

As a scientist, I am always a little skeptical about bold claims that run counter to established scientific wisdom. However, the authors of this article implied that their claims were based on a 2012 article in Pediatrics, which is a highly respected journal in its field, so I decided to investigate the article (Millichap and Yee, Pediatrics, 129: 1-8, 2012).

The article was written by two pediatricians with extensive experience treating children with ADHD. The article turned out to be a pretty thorough review of the literature on nutritional approaches for controlling ADHD. It did not approach the rigor of a meta-analysis study. Rather, it is what I refer to as an “interpretive review”. By that I mean that the clinical studies were interpreted in part on the basis of their clinical experience in treating children with ADHD.

Interpretive reviews can be either good or bad, depending on the objectiveness of the reviewers. In this case, I was familiar with many of the clinical studies they reviewed and found their interpretations to be accurate, so I decided to share their conclusions with you.

Is an ADHD Diet Better Than Medication For ADHD?

They reviewed all of the major nutritional approaches that have been used over the years to control ADHD. Let me start by saying that they are not wild-eyed proponents of “a nuts and berries diet cures all”. In fact, they use medications as the primary intervention for most of their ADHD patients. They advocate an ADHD diet approach when:

Medicines fail or there are adverse reactions (side effects).

The parents or the patients prefer a more natural approach.

There are symptoms or signs of a mineral deficiency (more about that below).

There is a need to substitute an ADHD-free healthy diet for an ADHD-linked diet (Simply put, if the child’s diet is bad enough, there are multiple benefits from switching to a healthier diet – a possible reduction in ADHD symptoms is just one of them.)

I will summarize their key findings below:

Do Omega-3 Fatty Acids Reduce ADHD Symptoms?

The authors reported that a number of studies have shown that children with ADHD tend to have low levels of essential fatty acids, especially the omega-3 fatty acids. They cite several studies which showed significant improvement in reading skills and reductions in ADHD symptoms when children with ADHD were give omega-3 supplements, but also noted that other studies showed no effect.They postulated that some children may benefit more from omega-3 supplementation than others.

They routinely use doses of 300-600 mg of omega-3s with their ADHD patients. They find that this intervention reduces ADHD symptoms in many children, but does not completely eliminate the need for medications.

My Two Cents: I have previously reported on the improvement in reading skills(Omega-3’s Improve Reading Skills) and reduction in ADHD symptoms (Can Fish Oil Make Children Smarter?) when children were given omega-3 supplements. In both cases, it was the children with the lowest omega-3 levels who benefitted most. No surprise there. Whether it will help your child is anyone’s guess. However, it is a natural approach with no side effects. It is certainly worth trying.

Does the Elimination of Food Additives Reduce ADHD Symptoms?

The current interest in food additives and ADHD originated with the Feingold diet. The Feingold diet eliminated food additives, foods with salicylates (apples, grapes, luncheon meats, sausage, hot dogs and drinks containing artificial colors and flavors), and chemical preservatives (e.g. BHA and BHT). It was popularized in the 1970s when some proponents claimed that it reduced ADHD symptoms in 50% of the children treated. After clinical studies showed that only a small percentage of children actually benefitted from this diet, it rapidly fell out of favor.

However, Millichap and Yee pointed out that more recent studies have shown that the subset of children who responded to the Feingold diet were not a “statistical blip”. A recent review of the literature reported that when children with suspected sensitivities to food additives were challenged with artificial food colors, 65–89% of them displayed ADHD symptoms.

My Two Cents: I have previously reported on the effects of artificial food colors on ADHD (Do Artificial Colors Cause Hyperactivity?). The studies I reviewed in this article reported that up to 28% of children with ADHD were sensitive to the amount of artificial food colors in the typical western diet and that removing those food colors resulted in a significant improvement in ADHD symptoms. Plus, those studies were just looking at food colors – not the hundreds of other food additives in the average American child’s diet.

I consider food additives to be problematic for many reasons. Even if doesn’t reduce their ADHD symptoms, eliminating as many of those food additives as possible is probably a good idea. It doesn’t need to be complicated. Just replacing processed foods and sodas with fresh fruits and vegetables and with low fat milk and natural fruit juices diluted with water to reduce their sugar content might make a significant difference in your child’s ADHD symptoms.

Food Sensitivities

Even natural foods can be a problem for children with food sensitivities, and it appears that there may be a large percentage of hyperactive children with food sensitivities. Millichap and Yee reported that elimination diets (diets that eliminate all foods which could cause food sensitivity) improve behavior in 76-82% of hyperactive children.

Even though this approach can be very effective Millichap and Yee don’t normally recommend it for their patients because it is difficult and time-consuming. The elimination diet is very restrictive and needs to be followed for a few weeks. Then individual foods need to be added back one at a time until the offending food(s) are identified. (They reported that antigen testing is not a particularly effective way of identifying food sensitivities associated with hyperactivity)

My Two Cents: I have previously reported on the link between food sensitivities and hyperactivity (What Causes ADHD?). I agree with Millichap and Yee that elimination diets are difficult and view this as something to be tried after all other natural approaches have failed. However, if there is a particular food that causes hyperactivity in your child, identifying it and eliminating it from their diet could just be something that will benefit them for the rest of their life.

Sugar

This is a particularly interesting topic. Many parents are absolutely convinced that sugary foods cause hyperactivity in their children, but the experts are saying that clinical studies have disproven that hypothesis. They claim that sugar has absolutely no effect on hyperactivity.

Millichap and Yee have an interesting perspective on the subject. They agree that clinical studies show that a sugar load does not affect behavior or cognitive function in small children, but they point to numerous clinical studies showing that the reactive hypoglycemia that occurs an hour or two after a sugar load adversely affects cognitive function in children, and that some children are more adversely affected than others.

My Two Cents: Reducing intake of refined sugars in your child’s diet makes sense for many reasons, especially considering the role of sugar intake in obesity. If your child has a tendency towards reactive hypoglycemia, it may also reduce ADHD symptoms.

Does Eliminating Iron and Zinc Deficiencies Reduce ADHD Symptoms?

Millichap and Yee reporting some studies suggested that iron and zinc deficiencies may be associated with ADHD symptoms, and recommend supplementation with an iron or zinc supplement when there is a documented deficiency.

My Two Cents: A simpler and less expensive approach would be a children’s multivitamin to prevent the possibility of iron or zinc deficiency. Of course, I would recommend that you choose one without artificial colors, preservatives and sweeteners.

Does Eating A Healthy Diet Reduce ADHD Symptoms?

Millichap and Yee closed their review by discussing a recent study in Australia that reported a significant reduction in ADHD symptoms in children eating “Healthy” diets (fish, vegetables, tomato, fresh fruit, whole grains & low fat dairy products) compared to children eating “Western” diets (Fast foods, red meat, processed meats, processed snacks, high fat dairy products & soft drinks). This is the ADHD diet approach, along with omega-3 supplementation, that they recommend most frequently for their patients.

My Two Cents: I wholeheartedly agree. In fact, if you and your family were to follow a “Healthy” diet instead of a “Western” diet it would likely have numerous health benefits. Plus, you are automatically removing ADHD triggers like food additives and sugar from your child’s diet.

The Bottom Line

A recent review of natural approaches for controlling ADHD symptoms (Millichap and Yee, Pediatrics, 129: 1-8, 2012) is both good news and bad news. The good news is that there are multiple nutritional approaches that can significantly reduce ADHD symptoms. These include:

Use of omega-3 supplements. They recommended 300-600 mg/day.

Removal of food additives (particularly food colors) from the diet.

Identification of food sensitivities and removal of those foods from the diet.

Reducing the amount of simple sugars in the diet.

Elimination of iron and zinc deficiencies if they exist (Iron deficiency is relatively common in American children. Zinc deficiency is not.) Alternatively, I recommend a children’s multivitamin to prevent iron and zinc deficiencies in the first place.

Eating a healthy diet rather than a Western diet. This also has the benefit of reducing the amount of food additives and sugars in the diet.

The bad news is that each of these approaches seems to work only in a subset of children with ADHD.

If you are a parent who is interested in a natural alternative to ADHD stimulant medications this means you may need to be patient and try several natural approaches until you find the one(s) that work(s) best for your child. The benefit of making the effort is that all of these approaches will also improve the health of your child in other important ways, and none of them have any side effects.

Unfortunately, the physician with only about 10 minutes to spend with each patient (which is increasingly the medical model in this country), may not have time to explore natural options. Medications are much easier to prescribe. You may need to be the one who takes the responsibility of exploring natural alternatives for your child.

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

Is Vitamin E Deficiency Common in the US

September 22, 2015 by Dr. Steve Chaney

Does Vitamin E Matter?

Author: Dr. Stephen Chaney

A headline claiming “Over 90% of Twentysomethings Have Suboptimal Vitamin E Status” caught my eye the other day, so I decided to investigate further. If you have been following all of the information and misinformation about vitamin E in the online media, you are probably confused – and this headline just adds to the confusion. There are probably three basic questions you want answered:

Is the latest study valid? Are most Americans vitamin E deficient?

Does it matter? Vitamin E has been described as “a vitamin in search of a disease”. If there are no diseases associated with vitamin E deficiency, should we even be concerned if most Americans are vitamin E deficient?

Is there any value to vitamin E supplementation? You will see claims that vitamin E supplementation has been proven not to work. Are these claims valid?

Let me guide you through the maze. I will start by analyzing the study behind the current headlines.

Are Americans Vitamin E Deficient?

The best food sources of vitamin E are nuts, seeds and unrefined vegetable oils, followed by green leafy vegetables. Since these foods are not abundant in the American diet, it is no surprise that previous studies have shown that 83% of US children and 91% of US adults do not consume the recommended 12 mg/day of vitamin E. Consequently, the 2015 Dietary Guidelines Advisory Committee identified vitamin E as a “shortfall nutrient”.

This study (McBurney et al, PLoS One 10(8): e0135510 doi: 10.1371/journal.pone.0135510) took the next logical step by asking whether the inadequate intake of vitamin E lead to inadequate blood levels of the vitamin. The authors analyzed data from 7,922 participants who had their blood levels of alpha-tocopherol (the most abundant form of vitamin E) determined in the 2003-2006 National Health and Nutrition Examination Survey (NHANES).

They subdivided participants into those who used no supplements (4049) and those who used supplements (3873). (Note: The supplement users were not necessarily using vitamin E supplements, but many were using a multivitamin supplement containing vitamin E). The authors compared the study participant’s blood levels of vitamin E with the Institute of Medicine standard for vitamin E deficiency (12 umol/L) and with a standard they set for adequate vitamin E levels (30 umol/L). Here are the results of their analysis:

People who did not use supplements had lower blood levels of vitamin E (24.9 umol/L) than those who used supplements (33.7 umol/L). No surprise here.

Only 0.6% of Americans were clinically deficient in vitamin E (blood levels < 12 umol/L). The prevalence of vitamin E deficiency did not vary significantly with age, gender or ethnicity.

When they looked at the people not using supplements, the percentage with suboptimal vitamin E status (blood levels < 30 umol/L) varied significantly by age, but was not significantly affected by gender or ethnicity. In this analysis the percentage with suboptimal vitamin E status was:

7% for ages 20-30.
8% for ages 31-50
2 % for ages 51 and above

Were The Headlines Correct?

Technically speaking the headlines were correct. 92.7% of Americans aged 20-30 who used no supplements had suboptimal blood levels of vitamin E as defined in this study. When you combined both supplement users and non-users, the percentage with suboptimal blood levels of vitamin E was only slightly less (87.4%). However, there are a couple of important caveats:

There is no internationally recognized standard for adequate blood levels of vitamin E. The authors had a reasonable rationale for choosing 30 umol/L as their standard for adequate blood levels, but they also acknowledged that the Estimated Average Requirement of vitamin E from food (12 mg/day) would result in a blood level of 27.9 umol/L, so their standard may be a bit high.

The average blood level of vitamin E for non-supplement users was 24.9 umol/L. While that is less than adequate, it is only slightly low – especially if the lower standard of 27.9 umol/L is used.

I think it would be more accurate to say that a large percentage of Americans have blood levels of vitamin E that are slightly below what is considered adequate but are far above what could be considered clinically deficient. The question then becomes “Does it matter?”

Does Vitamin E Matter?

Let me start with a little perspective. In the United States diseases like scurvy, pellagra and beriberi are things of the past. We simply don’t see deficiency diseases anymore. What we do see are intakes of essential nutrients that are slightly below optimal. Vitamin E is no different.

If we focus on suboptimal nutrient intake by itself, the answer would probably be that it doesn’t matter. Suboptimal nutrition is seldom enough to cause poor health by itself.

However, we also need to take into account individual differences that affect the need for essential nutrients. Poor health is much more likely to arise when suboptimal intake of one or more essential nutrients is coupled with increased needs due to genetic predisposition, risk factors that predispose to disease, and/or pre-existing disease.

With this perspective in mind, we are ready to ask whether suboptimal intake of vitamin E or any other essential nutrient matters. The answer is pretty simple. It doesn’t matter for everyone, but it matters very much for those individuals with increased needs.

If we had a good way of assessing individual nutritional needs, it would be easy to say who needed supplements and who didn’t. The problem is that we currently have no good way of assessing individual needs for essential nutrients. We simply cannot predict who will and who won’t be affected by suboptimal nutrient intake. That is why millions of Americans take supplements on a daily basis.

Is There Any Value To Vitamin E Supplementation?

That brings us to the final question. Is vitamin E supplementation a waste of money? You’ve probably already heard that most studies have failed to show any benefit from vitamin E supplementation, but you may be asking “How can that be when we also know that most Americans are getting suboptimal levels of vitamin E in their diet?”

With the perspective I described above in mind, the answer is pretty simple. Those studies have been asking the wrong question. They have been asking whether vitamin E supplements benefit everyone. They haven’t asked whether vitamin E supplements benefit people with increased needs.

When you ask that question the answer is very different. Let me give you three examples – one representing each of the kinds of increased need I described above:

In the Women’s Health Study (JAMA, 294: 56-65, 2005) vitamin E supplementation had no effect on heart attack or stroke in the general population. But when they looked at women over 65 (those at highest risk for heart disease), vitamin E supplementation reduced heart attack and stroke by 25% and cardiovascular deaths by 49%

In the Women’s Antioxidant Cardiovascular Study (Archives Internal Medicine, 167: 1610-1618, 2007) vitamin E supplementation again had no effect on cardiovascular events overall. But when they looked at the women who had cardiovascular disease at the start of the study, vitamin E supplementation decreased cardiovascular events by 23%.

In the Heart Outcome Prevention Evaluation Study (Diabetes Care, 27: 2767, 2004; Atherosclerosis, Thrombosis & Vascular Biology, 24: 136, 2008) vitamin E supplementation had no effect overall on heart attacks or cardiovascular deaths. But when they looked at a population who had a haptoglobin genotype that significantly increases the risk of heart disease, vitamin E supplementation significantly decreased the risk of both heart attacks and cardiovascular deaths.

The Bottom Line

Recent headlines saying that over 90% of young Americans have suboptimal vitamin E status are technically correct, but a bit overstated. It probably would have been more accurate to say that most Americans have slightly suboptimal vitamin E status.

The important question then becomes “Do marginal nutritional deficiencies matter?” The answer is pretty simple. Marginal nutritional deficiencies do not matter for everyone. However, they matter very much for those people who have increased needs for that nutrient due to genetic predisposition, risk factors for disease or pre-existing disease.

If we had a good way of assessing individual nutritional needs, it would be easy to say who needed supplements and who didn’t. However, we don’t have a good way of assessing increased needs for most nutrients, which is why many Americans use supplements on a daily basis.

As for all of those studies saying that vitamin E supplementation has no benefit, they are a bit misleading because they are asking the wrong question. They are asking whether vitamin E supplementation benefits everyone. They are not asking whether vitamin E supplementation benefits people with increased needs. When you ask that question the answer is very different (see examples in the article above).

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

How To Prevent Memory Loss?

July 28, 2015 by Dr. Steve Chaney

A New Study Shows B Vitamins and Omega-3s May Prevent Memory Loss

Author: Dr. Stephen Chaney

Want to know how to prevent memory loss? Every once in a while a breakthrough study comes along that has the potential to change paradigms. A recent study (Jerneren et al, Am J Clin Nutr, 102: 215-221, 2015) looking at the potential of B vitamins and omega-3s to slow brain shrinkage in the elderly is just such a study. It has the potential to forever change the way we think about preserving brain health as we age.

One of the most terrifying aspects of aging is the thought that we might literally lose our minds. On one hand, it seems to be an almost inevitable part of the aging process. Every year millions of older Americans develop mild cognitive impairment, and as they age many of them progress on to dementia or Alzheimer disease. In fact, one recent study (Plassman et al, Ann Neurol, 70: 418-426, 2014) estimated that for individuals 72 and older in the United States every 6 years:

8 million will develop mild cognitive impairment.
4 million will develop dementia.
3 million will develop Alzheimer disease.

Unfortunately, there is no effective drug treatment for preventing this cognitive decline, and there don’t appear to be any promising new drugs on the horizon. So it is only natural to ask whether there are diet and lifestyle changes that might reduce the rate of cognitive decline as we age.

As I discussed in previous issues of “Health Tips From the Professor” there are clinical studies suggesting that B vitamins and omega-3 fatty acids can both slow the brain shrinkage and cognitive decline associated with aging. Unfortunately, there are also clinical studies that have come up empty. They have found no effect of B vitamins or omega-3 fatty acids on brain shrinkage or cognitive decline. Because of these conflicting clinical results, many experts are simply not ready to endorse natural approaches for preventing cognitive decline.

That’s what makes the current study (Jerneren et al, Am J Clin Nutr, 102: 215-221, 2015) paradigm-changing. If this study is correct, you need both B vitamins and omega-3 fatty acids together to prevent cognitive decline. Neither one will work without the other.

That would explain a lot! The previous studies have not been designed to test the effects of both B vitamins and omega-3 fatty acids simultaneously. Whether or not the diets of previous study participants were adequate with respect to B vitamins and omega-3s was a matter of pure chance. If the diets were adequate in both B vitamins and omega-3s, the study outcome might be positive. If the diets were only adequate in just one or the other, the outcome would almost assuredly be negative.

Why Might B Vitamins and Omega-3s Both Be Required for Brain Health?

It is easy to understand why B vitamins and omega-3s each might be important for preventing cognitive decline individually. Cognitive decline is closely associated with elevated levels of homocysteine, a toxic amino acid metabolite, and multiple clinical studies have shown that the combination of folic acid, vitamin B12 and vitamin B6 is effective at lowering homocysteine levels.

The omega-3 fatty acids are an integral part of the myelin sheath that coats our neurons. You can think of myelin as being like the plastic coating on an electrical wire that allows the electrical current to travel from one end of the wire to the other without shorting out. Myelin plays essentially the same role for our neurons.

But what is the possible connection between B vitamins and omega-3s with regard to brain health? The authors of this study had an interesting hypothesis. It turns out that when homocysteine levels are elevated due to B vitamin deficiency methionine levels and the levels of a number of downstream metabolites, including phosphatidylcholine, are reduced – and phosphatidylcholine is what delivers omega-3 fatty acids to the brain.

If their hypothesis is correct, adequate levels of B vitamins are required to deliver omega-3 fatty acids to the brain. That means that omega-3 fatty acids would only be effective at preventing brain shrinkage and/or cognitive decline in studies where the subjects were receiving adequate B vitamins as well.

Conversely, if we assume, as the authors suggested, that the real role of B vitamins is to assure the presence of enough phosphatidylcholine to deliver omega-3 fatty acids to the brain, B vitamins would be effective only in clinical studies where the subjects were also getting sufficient omega-3s from their diet.

B Vitamins and Omega-3s Together May Be How To Prevent Memory Loss

The study itself included 168 adults over the age of 70 (average age = 77) with mild cognitive impairment at the beginning of the study. Half of them were given a high dose B vitamin supplement (800 ug folic acid, 500 ug vitamin B12, and 20 mg vitamin B6), and the other half were given a placebo.

Brain MRI scans were performed at the beginning of the study and again 2 years later to measure brain volume. Blood levels of omega-3 fatty acids were assessed at the beginning of the study. When the data were analyzed at the end of the study, the subjects with blood omega-3 levels of >590 umole/L were classified as having high omega-3 status, and subjects with blood omega-3 levels <390 umole/L were classified as having low omega-3 status.

The results were pretty striking:

B vitamin treatment reduced brain shrinkage by up to 70% over a two year period in adults over the age of 70.

The B vitamin treatment was only effective when the subjects were deficient in B vitamins at the beginning of the study, as indicated by elevated homocysteine levels.

The B vitamin treatment was also only effective in subjects with high omega-3 status. The B vitamin treatment had no benefit in subjects with low omega-3 status.

What Is The Significance Of This Study?

In today’s scientific world, “gold standard” clinical studies are considered to be those in which a single variable is evaluated in a double-blind, placebo-controlled clinical trial. Unfortunately, this reductionist approach can sometimes lead to misleading and confusing results.

For example, I once attended a session in which a world renowned expert was giving his talk on colon cancer. He said, “I can show you, unequivocally, that colon cancer risk is significantly decreased by a lifestyle that includes a high-fiber diet, a low-fat diet, adequate calcium, adequate B-vitamins, exercise and weight control. But I can’t show you that any one of them, by themselves, is effective.”

The question that came to me as I heard him speak was: “What’s the message that a responsible scientist or responsible health professional should be giving to their patients or the people that they’re advising?” You’ve heard experts saying: “Don’t worry about the fat” “Don’t worry about calcium.” “Don’t worry about B-vitamins.” “Don’t worry about fiber.” “None of them can be shown to decrease the risk of colon cancer.” Is that the message that we should be giving people? Or should we really be saying what that doctor said many years ago – that a lifestyle that includes all of those things significantly decreases the risk of colon cancer?

Similarly, in a recent “Health Tips From the Professor” I shared a study, Alzheimers Hope, showing that a holistic program involving exercise, a healthy diet, socialization and memory training significantly reduced cognitive decline in the elderly. Once again, it has been very difficult to reproducibly show that any of those interventions individually prevent cognitive decline.

That is what makes the current study so exciting. It is a single study, and it is a relatively small study. It definitely needs to be repeated. However, it has the potential to be a paradigm-shifting study.

Previous studies looking at the effect of B vitamins and omega-3s on brain shrinkage and/or cognitive decline have been inconsistent. Many have shown a benefit, but some have not. But, until now, none of the studies have looked at B vitamins and omega-3s together. If this study is correct, all future studies should examine the effect of both B vitamins and omega-3s together. The paradigm will have been forever changed.

Does It Matter?

The important question is whether this is just an academic discussion or does it really matter? If most older adults were getting adequate amounts of omega-3s and B vitamins in their diet, this would merely be an academic discussion. Unfortunately, that is not the case.

Our oceans and rivers are becoming more and more polluted, and many people are avoiding fish because of concerns about heavy metal or PCB contamination. There is also an increasing emphasis on eating “sustainable” fish. That usually means the fish are farm raised, and farm raised fish are the most likely to be contaminated with PCBs, which is unfortunate. For example, I recently went to a nice restaurant that had a delicious sounding salmon dish on their menu. They could guarantee that the salmon was sustainably raised, but they couldn’t guarantee it was PCB-free. I chose not to eat the salmon.

It is no wonder that many adults aren’t getting enough omega-3s in their diet. In a recent “Health Tips From the Professor,” Do women get enough omeg-3 during pregnancy I reported a study showing that a shocking 75% of pregnant and lactating Canadian women were not getting enough omega-3s in their diet! Other studies suggest those of us in the United States don’t do much better.

We don’t do much better with respect to B vitamins either. For example:

The most frequent cause of B12 deficiency is the age related loss of the ability to absorb vitamin B12 in the upper intestine. This affects 10-30% of people over the age of 50.

Chronic use of acid-suppressing medications such as Prilosec, Nexium, Tagamet, Pepcid and Zantac also decreases B12 absorption and increases the risk of B12 deficiency. Millions of Americans use those drugs on a daily basis.

Overall, B12 deficiency has been estimated to affect about 40% of people over 60 years of age.

Deficiency of the enzyme methylenetetrahydrofolate reductase (MTHFR) substantially increases the requirement for folic acid. About 10% of the US population has this enzyme deficiency.

About 25% of Americans have low blood levels of B6

Clearly, this is not just an academic argument. Millions of older Americans are deficient in B vitamins or omega-3s or both.

The Bottom Line

A recently published study looked at the effect of high dose B vitamin supplementation on brain shrinkage over a two year periods in adults over 70 (average age 77) with mild cognitive impairment at the beginning of the study. This study differed from all previous studies in that it also measured omega-3 fatty acid levels in the blood at the beginning of the study to assess omega-3 status.

B vitamin treatment reduced brain shrinkage by up to 70% over the two year period compared to placebo.

The B vitamin treatment was only effective when the subjects were deficient in B vitamins at the beginning of the study, as indicated by elevated homocysteine levels.

The B vitamin treatment was also only effective in subjects with high omega-3 status at the beginning of the study. If they had low omega-3 status, the B vitamin supplementation was ineffective.

This study has the potential to forever shift the paradigm for preventing cognitive decline in the elderly. Past studies have looked at the effect of B vitamins and omega-3s at reducing cognitive decline separately, and these studies have been inconsistent. If this study is correct, consistent benefits will only be seen when both B vitamins and omega-3 fatty acids are present at adequate levels.

This is a concern because millions of older Americans are deficient in B vitamins or omega-3s or both.

How to prevent memory loss? Of course, B vitamins and omega-3s are just part of a holistic approach for preventing cognitive decline. Weight control, exercise, a healthy diet, adequate sleep, socialization, and memory training (mental exercise) are also important if we want to retail our full mental capacity into our 90s and beyond.

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 Supplements Cause Cancer?

May 20, 2015May 19, 2015 by Dr. Steve Chaney

The Kernel of Truth Behind the Scary Headlines

Author: Dr. Stephen Chaney

Once again the sky is falling! Some of the recent headlines have been downright scary. You’ve probably seen headlines saying things like “The American Association for Cancer Research reports that dietary supplements increase cancer risk” and “A recent study shows that taking extra vitamins and minerals may do more harm than good”. You’re probably asking yourself if you should throw away those vitamin and mineral supplements that you have been taking.

Let me start by correcting some of the more misleading statements in the recent headlines:

• This was not a position statement from the American Association for Cancer Research. It was a talk presented by a single scientist at the American Association for Cancer Research annual meeting.

• This was not a new study. The talk was based on a paper published in 2012 (Martinez et al., Journal of the National Cancer Institute, 104: 732-739, 2012).

• This was not even a study. It was a review of previously published studies.

• When you read the paper you find that the majority of studies found no effect of supplementation on cancer risk, a few suggested that supplementation might decrease cancer risk, and a very few suggested that supplementation might increase cancer risk. However, the scientist giving the talk at the American Association for Cancer Research meeting choose to emphasize the few studies suggesting increased risk.

Should We Worry About A Few Studies Suggesting Increased Cancer Risk?

The important question is whether we should be concerned about even a few studies suggesting that supplementation increases cancer risk. As a research scientist I am not particularly concerned. That’s because I realize that there is always some variability in the results of clinical trials.

• Sometimes that’s because an individual clinical study was poorly designed. Those are studies that are easy to eliminate from consideration.

• However, many times we do not know why an individual study is an “outlier”. We only know that it is different from all the other studies. Good scientists base their opinions on the weight of the evidence from all available clinical studies, not individual studies – particularly if the individual studies are outliers.

Unfortunately, that’s not the way it works in the “real world”. In the real world individual studies that support a particular viewpoint are often quoted over and over until they become “generally accepted as true” – even if multiple subsequent studies have come to the opposite conclusion. They become what I call “nutrition myths”.

In this issue of “Health Tips From the Professor” I will briefly debunk some of these nutrition myths about the cancer risk of supplementation by exposing the clinical studies that were poorly designed and/or have been contradicted by multiple subsequent studies.

However, there is often a “kernel of truth” buried in all the hype. This kernel of truth is the main focus of this issue because it should guide our decisions about supplementation – not the scary headlines.

Antioxidants & Cancer Risk – A Poorly Designed Study

One of the most widely quoted studies supporting the claim that antioxidant supplements increase the risk of cancer was a meta-analysis of 66 published clinical studies (American Journal of Clinical Nutrition, 297: 842-857, 2007). It came to the conclusion that consumption of extra vitamins A, E, and beta-carotene were associated with up to a 16% increased risk of cancer. However, that study included only those studies in which adverse outcomes were reported. 400 studies with no adverse outcomes were ignored.

More to the point, another group of scientists came back and re-analyzing the same data set a couple of years later (Nutrients, 2: 929-949, 2010). When they looked at same 66 studies included in the original meta-analysis, they reported that 60% of the studies showed no effect of supplementation; 36% of studies showed a benefit of supplementation; and only 4% showed an increased cancer risk.

You might ask yourself, “If only 4% of the studies showed any increase in cancer risk, how could the meta-analysis of all 66 studies report a 16% increase in cancer risk?” That’s because of a statistical quirk. In a meta-analysis the outcome of a single very large study can swamp the conclusions of multiple smaller studies. In this case, the increased cancer risk reported in the original meta-analysis was almost entirely due to a single study in which participants using vitamin E were also on hormone replacement therapy. That’s a concern because we now know that hormone replacement therapy significantly increases cancer risk.

In short, this was a flawed study, but it is cited over and over as “proof” that antioxidant supplementation may increase cancer risk.

Examples of Nutrition Myths Disproved by Subsequent Studies

Antioxidants & Cancer Risk

I have covered this topic in a previous “Health Tips From the Professor” so I’ll just give you a brief summary here. In short, the flawed paper suggesting that antioxidants has been followed by several major studies that have come to the opposite conclusions. For example:

• One study followed 24,000 adults in Germany for 11 years and found that those consuming antioxidant supplements at the beginning of the study had a 48% decrease in cancer mortality and a 42% decrease in overall mortality (European Journal of Nutrition, 51: 407-413, 2012).

• A US study followed 15,000 male physicians for 10 years and found that multivitamin supplementation decreased cancer incidence by 8% (JAMA, 308: 1871-1880, 2012).

• Another study with the same group of 15,000 physicians found that vitamin C and E supplements had no effect on cancer risk over an 8 year period. But, when the study was extended by an additional 3.8 years vitamin C supplementation decreased the risk of colon cancer by 46% (American Journal of Clinical Nutrition, 100: 915-923, 2014).

• Finally, a study of 7,728 women with invasive breast cancer showed that multivitamin use increased breast cancer survival by 30% (Breast Cancer Research & Treatment, 141: 495-505, 2013).

Folic Acid & Cancer Risk

I have also covered this topic in a previous “Health Tips From the Professor”, so, once again, I will be brief.

• The study (JAMA, 297: 2351-2359, 2007) that is widely quoted as suggesting that folic acid supplementation might increase the risk of developing colon cancer in people over 50 didn’t actually look at colon cancer. It looked at adenomas in the colon. That is an important distinction because adenomas are benign. They can develop into a cancerous lesion over time, but that is not inevitable.

• Two major studies since then (American Journal of Clinical Nutrition, 94: 1053-1062, 2011 and Gastroenterology, 141: 98-105, 2011) have reported that folic acid supplementation does not increase the risk of colon cancer.

• In fact, the second study showed that people with the highest intake of both folic acid from supplementation and folates from food significantly decreased their risk of developing colon cancer.

The Kernel of Truth Behind the Headlines

While the scary headlines about supplements causing cancer are clearly misleading, I would be doing my readers a disservice if I didn’t discuss the kernel of truth behind the headlines.

Let me start by saying that I am not a big fan of high dose, high purity individual supplements. In foods vitamins and minerals tend to occur in a natural balance. When we take individual nutrients in high doses, they often interfere with our body’s ability to absorb and utilize similar nutrients from the foods we eat. We create an imbalance.

That is the “kernel of truth” behind the headlines. High dose, high purity supplements have the potential to create nutritional imbalances. They have the potential to cause harm. Let me give you some examples in the context of cancer risk.

• Alpha-tocopherol is the most abundant form of vitamin E in foods. However, there are many other forms of vitamin E in foods and high dose, pure alpha-tocopherol suppresses their absorption. This is a potential concern because some of them – gamma-tocopherol and the tocotrienols, for example – are more effective than alpha-tocopherol at reducing the risk of certain cancers in animal studies. This selective anticancer effect has not yet been demonstrated in humans, but it does raise some concern about the use of high dose, high purity alpha-tocopherol supplements.

• Antioxidants are generally found in combination in foods, not as isolated nutrients. This is important because antioxidants work together. For example, vitamin E reduces free radicals to chemically unstable intermediates that have the potential to damage cells and cause cancer. A selenium-containing enzyme is required to convert these unstable intermediates into completely harmless compounds. This is thought to be the reason why a recent study found that high dose alpha-tocopherol increased prostate cancer risk in men with low selenium status, but not in men with high selenium status (Journal of the National Cancer Institute, doi: 10.1093/jnci/djt456, 2014).

• Beta-carotene is the most abundant carotenoid in foods, but there are many other naturally occurring carotenoids – some of which appear to have unique anticancer activity in animal studies. This has been suggested as the reason why several studies have shown that diets high in carotenoids decrease the risk of lung cancer in smokers, but high dose beta-carotene alone appears to increase the risk of lung cancer in smokers.

• B vitamins are best utilized in balance. That is especially true for folic acid, B12 and B6, which probably explains a recent study that suggested high dose B6 and folic acid supplements were associated with an increased risk of mortality, but a B complex supplement containing the same doses of both folic acid and B6 was not associated with increased mortality (Archives of Internal Medicine, 171: 1625-1633, 2011).

Do Supplements Cause Cancer?

Now that you understand the “kernel of truth” behind the headlines you can better understand why some experts recommend getting our vitamins and minerals from foods rather than supplements. While I understand the logic behind that recommendation, I consider it an imperfect solution to the problem for three reasons:

#1: Most of us don’t eat the way that we should. The USDA tells us that only 3-5% of Americans eat a healthy diet on a daily basis.

#2: Most of us don’t eat enough variety of foods. Even if we eat some healthy foods, we won’t get the balance of essential nutrients we need unless we eat a wide variety of healthy foods.

#3: Some of us have increased nutritional needs. Poor diet, genetic predisposition and poor health can all increase our needs for certain essential nutrients – and we may not know about those increased needs until it is too late.

Supplementation to fill nutritional gaps is still a good choice for many Americans, but I recommend avoiding the high dose, high purity individual supplements. For example:

• Choose a supplement that contains all the naturally occurring forms of vitamin E and selenium in addition to alpha-tocopherol.

• Choose a supplement that contains a variety of carotenoids, not just pure beta-carotene.

• Choose a supplement that contains the B vitamins in balance, not just high dose individual B vitamins like folic acid or vitamin B6.

I could go on, but I think you get the idea. If you take individual high purity, high dose supplements you might actually increase your cancer risk. For the most part, the increased cancer risk has not been proven, but it is theoretically possible. A better approach is to choose supplements that are designed to mimic the balance of vitamins and minerals found in the foods we eat.

The Bottom Line

• Ignore the scary headlines warning that supplement use may increase your risk of cancer. For the most part, those headlines are based on a few flawed studies that have been refuted by multiple subsequent studies which have come to the opposite conclusion.

• However, there is a kernel of truth behind the idea that certain supplements might have the potential to increase cancer risk. High dose, high purity individual supplements such as alpha-tocopherol, beta-carotene and folic can interfere with our body’s ability to absorb or utilize related nutrients that are important for cancer prevention. In short, high dose, high purity supplements can create nutrient imbalances that have the potential to increase cancer risk.

• That doesn’t mean that we need to avoid supplements entirely. It does mean that we need to make wise choices about the supplements we use. My recommendations are:

o Choose a supplement that contains all the naturally occurring forms of vitamin E and selenium in addition to alpha-tocopherol.

o Choose a supplement that contains a variety of carotenoids, not just pure beta-carotene.

o Choose a supplement that contains the B vitamins in balance, not just high dose individual B vitamins like folic acid or vitamin B6.

o I could go on, but you get the idea. You want to choose supplements that are designed to mimic the balance of nutrients we find in nature.

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.

Vitamin D Deficiency

January 13, 2015 by Dr. Steve Chaney

What Is The Real Vitamin D Story?

Author: Dr. Stephen Chaney

If you are like most people, you probably don’t know what to believe about vitamin D deficiency. Some experts tout vitamin D as a miracle nutrient that will help you lead a longer, healthier life. They leave you with the impression that everyone should be supplementing with vitamin D.

Other experts tell you that the supposed benefits of vitamin D are all hype. They tell you not to waste your money on vitamin D supplements.

When you pull back the curtain and look at the clinical studies behind the headlines, a pattern begins to emerge.

Most of the studies that support a role for vitamin D in preventing heart disease, preventing cancer and extending life have been population studies. They have compared populations with low vitamin D intake with populations with adequate vitamin D intake. While population studies are good for suggesting associations, they have their limitations:

Population studies are good at suggesting associations, but they do not prove cause and effect.

With population studies it is also very difficult to eliminate what scientists call “confounding variables”. Let me give you an example. Suppose someone had low 25-hydroxyvitamin D levels in their blood because they sat around all day watching TV and never got out in the sun. If they got sick you wouldn’t really know whether it was due to low 25-hydroxyvitamin D levels or due to inactivity. In this case, inactivity would be a confounding variable.

On the other hand, most of the studies that fail to find any benefit of vitamin D are double blind, placebo-controlled intervention studies in which one group was given supplemental vitamin D and the other group was given a placebo. While these studies are considered the most reliable clinical studies, they have their limitations as well.

In the case of vitamin D many of these studies were done with a cross section of the population in which most of the participants already had adequate blood levels of 25-hydroxyvitamin D at the start of the study. Those studies are incapable of telling us whether correcting a vitamin D deficiency would have been beneficial.

Even when the intervention studies focus on participants with low vitamin D status at the start of the trial they have another significant limitation. They are all short term studies. Typically, the best of these studies last no more than a couple of years. Longer term studies are far too expensive. In contrast, diseases such as heart disease and cancer take decades to develop. A one or two year intervention with vitamin D simply may not be sufficient to correct the damage caused by decades of vitamin D deficiency

This is the current dilemma that is creating all of the confusion in the vitamin D story. For the most part, population studies and intervention studies are coming to very different conclusions. And both kinds of studies have inherent limitations that are difficult to overcome.

Fortunately, a new kind of clinical study has been developed in recent years that overcomes the limitations of both population studies and intervention studies.

A New Kind of Clinical Study

The new approach is something called mendelian randomization. I apologize for the scientific jargon, but let me explain. In this case you are separating your population based on genetic variation rather than on the basis of biochemical or behavioral differences.

For example, in the clinical study I will describe in a minute the population was separated into groups based on genetic variations in the DHCR7 and CYP2R1 genes. The first gene is involved in the biosynthesis of cholesterol, which is a precursor of vitamin D, and the second gene converts vitamin D to 25-hydroxyvitamin D. Both genes affect blood levels of 25-hydroxyvitamin D.

This kind of study has several unique strengths:

Genetic variations are unaffected by confounding variables such as sun exposure, obesity, smoking, inactivity, and poor diet. If the study population is large enough, those confounding variables will be equally distributed among groups that are selected solely on the basis of genetic variations.

These studies are long term by definition. If someone has a genetic variant that lowers their 25-hydroxyvitamin D level, it will do so for their entire lifetime. They can increase their vitamin D status by sun exposure, for example, but their blood levels of 25 hydroxyvitamin D will always be less than someone with equal sun exposure who does not have that genetic variant.

Because these studies reflect lifelong exposure to 25-hydroxyvitamin D they are ideally suited for measuring the effect of vitamin D status on mortality and diseases that take decades to develop.

Do Vitamin D Genes Affect Mortality?

This study (S. Afzal et al, The British Medical Journal, 2014;p 349:g6330 doi: 10.1136/bmj.g6330) combined the data from three clinical studies conducted in Copenhagen between 1976 and 2013. The age of the participants ranged from 20 to 100 years and the follow-up was 6-19 years. 95,766 participants in these studies were genotyped for variants in the DHCR7 and CYP2R1 genes which were known to affect 25-hydroxyvitamin D levels. 35,334 of those participants also had blood 25-hydroxyvitamin D levels determined. By the end of the study 10,349 of the participants had died.

The individual genetic variants included in this study caused a relatively small (1.9 nmol/L) decrease in blood levels of 25-hydroxyvitamin D. However, because this was a very large study and the participants with those genetic variants were exposed to lower 25-hydroxyvitamin D levels for their entire lifespan, the decreased 25-vitamin D levels were associated with significant increases in all cause mortality and cancer mortality, but not with increased cardiovascular mortality.

When they extrapolated to a genetically caused 20 nmol/L decrease in 25-hydroxyvitamin D, the decrease in 25-hdroxyvitamin D was associated with a 30% increase in all cause mortality and a 30% increase in cancer mortality.

What Kind Of Studies Are Needed Next?

The authors noted that this is the first study of its kind, so it obviously needs to be confirmed by other large mendelian randomization studies that test the link between vitamin D status and mortality.

Ideally, it should also be verified by double blind, placebo controlled intervention studies, but that may not be possible. If one really wanted to verify this study, the intervention study should start with a population group with 25-hydroxyvitamin D levels at least 20 nmol/L below what is considered adequate and provide them with enough supplemental vitamin D to increase their 25-hydroxyvitamin D to the adequate range. That is difficult, but doable.

However, the intervention study would also need to be long enough (decades perhaps) to prevent cancer from developing. That kind of study will probably never be done.

The Bottom Line

The relationship between vitamin D status and mortality has been investigated with a new type of clinical study based on what is called mendelian randomization. Population groups were segregated based on genetic variations in two genes that affect blood 25-hydroxyvitamin D levels (a measure of vitamin D status).

This study concluded that a genetically determined decrease of 20 nmol/L in blood 25-hydroxyvitamin D was associated with a 30% increase in all cause mortality and a 30% increase in cancer mortality, but had no significant effect on cardiovascular mortality.

This kind of study is particularly strong because it measures the affect of lifelong exposure to 25-hydroxyvitamin D. This is important when assessing the effect of vitamin D status on mortality and diseases such as cancer that take decades to develop. In contrast, the double blind, placebo controlled intervention studies that are consider the “Gold Standard” for clinical studies may be too short term to adequately assess the effect of vitamin D status on cancer or all cause mortality.

This study supports the benefit of maintaining optimal vitamin D status, but it is the first clinical study of its kind and needs to be confirmed by other studies.

In the meantime, there is no harm to in maintaining your blood levels of 25-hydroxyvitamin D in the optimal range through diet, sun exposure and supplementation. This study suggests it just may help you live a longer, healthier life.

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