cancer

Risk Factors of Prostate Cancer

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Vitamin D Deficiency?

Author: Dr. Stephen Chaney

Vitamin D

Is vitamin D deficiency one of the risk factors of prostate cancer? What if something as simple as maintaining optimal vitamin D status could decrease your risk of prostate cancer? There is a lot of indirect evidence suggesting that vitamin D deficiency might affect your risk of developing prostate cancer. For example:

  • Prostate cancer incidence and vitamin D deficiency parallel each other. Both are highest in northern latitudes, in African American men, and in older men.
  • Prostate cancer mortality rates are highest for patients diagnosed in the winter and at Northern latitudes.

However, clinical studies looking at the correlation between 25-hydroxy vitamin D (the biologically active form of vitamin D in the blood) and prostate cancer incidence have been inconsistent. Because of this there has been considerable controversy in the scientific community as to whether or not there was any correlation between vitamin D deficiency and prostate cancer.

Vitamin D Deficiency and Cancer

That’s what makes the recent headlines suggesting that vitamin D is associated with decreased risk of aggressive prostate cancer so interesting. Does this study show low vitamin D to be one of the risk factors of prostate cancer? Have the conflicting data on vitamin D deficiency and prostate cancer finally been resolved or is this just another case of dueling headlines? Let’s start by looking at the study itself.

This study (Murphy et al, Clinical Cancer Research, 20: 2289-2299, 2014) enrolled 667 men, aged 40-79 (average age = 62), from five urology clinics in Chicago over a four year period. These were all men who were undergoing their first prostate biopsy because of elevated serum PSA levels or an abnormal DRE (that’s doctor talk for digital rectal exam – the least favorite part of every guy’s physical exam). The clinics also drew blood and measured each patient’s 25-hydroxy vitamin D level at the time of the prostate biopsy.

This study had a number of important strengths:

  • It was conducted at a northern latitude. Because of that 41.2% of the men in this study were vitamin D deficient (<20 ng/ml) and 15.7% were severely vitamin D deficient (<12 ng/ml). That’s important because you need a significant percentage of patients with vitamin D deficiency to have any chance of seeing an effect of vitamin D status on prostate cancer risk.
  • The study had equal numbers of African American and European American men. That’s important because African American men have significantly lower 25-hydroxy vitamin D status and significantly higher risk of prostate cancer than European American men.
  • All of the men enrolled in the study had elevated PSA levels or abnormal DREs. That’s important because it meant that all of the men enrolled in the study were at high risk of having prostate cancer. That made the correlation between vitamin D status and prostate cancer easier to detect.
  • This was the first study to correlate 25-hydroxyvitamin D levels with prostate biopsies at the time of biopsy. That’s important because it allowed the investigators to distinguish between aggressive tumors (which require immediate treatment and have a higher probability of mortality) and slow growing tumors (which may simply need to be monitored).

The results were pretty dramatic:

  • In African American men vitamin D deficiency (<20 ng/ml) was associated with an increased risk of prostate cancer diagnosis at time of biopsy.
  • In both European American and African American men severe vitamin D deficiency (<12 ng/ml) was associated with increased risk of aggressive prostate cancer diagnosis at time of biopsy.

The authors concluded: “Our work supports the hypothesis that 25-hydroxy vitamin D is a potential biomarker that plays a clinically significant role in prostate cancer, and it may be a useful modifiable risk factor in the disease”.

That’s “science speak” for “adequate vitamin D status may help prevent prostate cancer” or “low vitamin D may indeed be one of the risk factors of prostate cancer.”

VitaminD-smashes-cancer

Why Have Some Studies Failed To Find A Correlation Between Vitamin D Deficiency and Prostate Cancer?

The authors of the current study had an interesting hypothesis for why some previous studies have not seen an association between vitamin D status and prostate cancer risk. When you compare all of the previous studies, the strongest correlations between vitamin D deficiency and prostate cancer were the studies conducted at northern latitudes, in African American men, or focusing on aggressive prostate cancer as an end point.

That offers a few clues as to why other studies may have failed to find a link between vitamin D status and prostate cancer risk. For example:

  • The clue that the correlation between vitamin D deficiency and prostate cancer risk was strongest at northern latitudes and with African American men suggests that you need to have a significant percentage of subjects with deficient or very deficient levels of 25-hydroxy vitamin D before you can see a correlation. Other studies may have failed to show a correlation simply because most of the men in the study had normal vitamin D status.
  • The clue that the correlation is strongest for aggressive prostate cancer is more subtle. The authors hypothesized that prostate cancer develops over a lifetime. If that is the case, measuring vitamin D deficiency at the time of diagnosis may not represent the lifetime vitamin D status. The vitamin D status could have decreased because the men were older or had become overweight, or the vitamin D status could have changed simply because they moved from one geographical location to another.

In contrast, the progression from benign to aggressive prostate cancer is generally short term, so it would be affected by the most recent vitamin D status. If that is the case, then the vitamin D status measured at the time of diagnosis may more accurately reflect the vitamin D deficiency that affected the aggressiveness of the cancer.

 

The Bottom Line

1)     The latest study suggests that vitamin D deficiency (<20 ng/ml serum 25-hydroxy vitamin D) may significantly increase the risk of prostate cancer. The correlation between low vitamin D status and prostate cancer risk is strongest for African American men.

2)     The study also suggests that severe vitamin D deficiency (<12 ng/ml serum 25-hydroxyvitamin D) may significantly increase the risk of aggressive prostate cancer in both African American and European American men.

3)     This is a very well done study, and it is consistent with many, but not all, of the previous studies. Clearly more research needs to be done. Future research should be focused on high risk subjects and subjects with low vitamin D status so that the correlation between vitamin D status and prostate cancer risk can be adequately tested.

4)     This is another example of why I recommend that you have your serum 25-hydroxy vitamin D level measured on a regular basis and that you aim to keep it in the normal range (20-80 ng/ml). Some experts believe that 30-80 ng/ml is optimal.

5)     If you are African American, overweight, live in northern latitudes or it is winter, you may need supplemental vitamin D3. 1,000 – 4,000 IU/day of vitamin D3 is generally considered to be safe. If higher amounts are needed to normalize your 25-hydroxy vitamin D levels I recommend that you consult your physician for the appropriate dose.

 

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

Are The Benefits Of Resveratrol A Myth?

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Is Resveratrol Dead?

Author: Dr. Stephen Chaney

Red WineIt seems like just a few years ago that the headlines were proclaiming that resveratrol, a polyphenol found in red wines, grapes and chocolate, was the latest “super nutrient”. It was going to make you younger, smarter and healthier. You probably knew that all of the claims being made at the time could not be true.

But the latest headlines are claiming that resveratrol health benefits are all a myth. Has the resveratrol bubble burst? Was it all just hype?

Before you decide that resveratrol supplements are just a waste of money, let me take you behind the scenes and evaluate the latest study objectively. Let’s talk about what it showed, and didn’t show. But, before we look at the study, let’s review the history of resveratrol.

How Did The Resveratrol Story Get Started?

The resveratrol story started in the 1990’s when Dr. Serge Renaud at Bordeaux University coined the term “French Paradox” to describe the fact that cardiovascular disease incidence was relatively low in the French population despite the fact that they consumed diets high in saturated fat and cholesterol.

People immediately started asking what could possibly explain this discrepancy between the US and French populations? In other words, what could be protecting the French population from their high fat diet? One obviously difference between the French and Americans is that the French consume a lot more red wine – or at least they did before the “French Paradox” publicity turned red wine into a health food. Based on that difference, Dr. Renaud proposed that the French Paradox was due to the high red wine consumption in France.

But, red wine is an alcoholic beverage and overconsumption of alcoholic beverages is a major health problem for many people. And, while alcohol does have some cardiovascular benefits, alcohol consumption was pretty constant across countries.

So the next logical question was what other ingredients in red wine might explain their supposed health benefits. Polyphenols appear to have numerous health benefits, and resveratrol is the major polyphenol in red wine. So resveratrol became the “poster child” for the health benefits of red wine.

Even so, for years resveratrol was a “niche” supplement. It had a loyal following, but it wasn’t a big player in the nutritional supplement market. All that changed in 2009. Dr. David Sinclair at Harvard University had been studying genes that slow the aging process. He had screened thousands of naturally occurring small molecules in hopes of finding some that could turn on those anti-aging genes.

He announced that resveratrol and a few related polyphenols were the most potent activators of those anti-aging genes, and he went on to publish studies showing that resveratrol could help obese mice live longer and lean mice be healthier. All of a sudden resveratrol became a superstar.

But, does resveratrol also work in humans? There are many clinical studies that suggest it does. That’s why I was surprised by the recent headlines proclaiming that the supposed health benefits of resveratrol were myths. So once again, let’s look at the study behind the headlines.

Are The Benefits Of Resveratrol a Myth?

The study behind the headlines (Semba et al, JAMA Internal Medicine, doi: 10.1001/jamainternalmed.2014.1582) followed 783 men and women aged 65 years or older from the Chianti region of Italy for 9 years. None of the participants were taking resveratrol supplements. The investigators estimated resveratrol intake by measuring the concentrations of resveratrol metabolites in the urine.

The investigators measured all cause mortality and the prevalence of heart disease and cancer over the 9 year period and found no correlation between those outcomes and urinary resveratrol metabolites. From those data the authors concluded that “Resveratrol levels achieved with a Western diet did not have a substantial influence on health status or mortality risk of the population in this study.”

The Strengths And Weaknesses of The Study

There are really two important questions – what are the strengths and weaknesses of the study and what does the study actually show?

What are the strengths and weaknesses of the study?

  • A major strength of the study was the measurement of urinary resveratrol metabolites rather than relying on the less accurate dietary recall – although it should be noted that the assays used are relatively new and could benefit from further validation.
  • The main weakness is that it was a relatively small study in a relatively homogeneous population. Most of the resveratrol consumed by this population came from red wine and even the group with the lowest resveratrol intake was drinking 2-3 glasses of red wine per week (You don’t find many teetotalers in the wine growing regions of Italy).

What does the study actually show?

  • The level of resveratrol metabolites in this population directly correlated with alcohol consumption. And, the authors of the study concluded that since the study was done in the Chianti region of Italy, most of the resveratrol came from red wine. So the study actually suggests that red wine consumption has no effect on heart disease, cancer or longevity – in direct contradiction to Renaud’s French Hypothesis.
  • The conclusion that the amount of resveratrol one can obtain from diet alone is unlikely to provide health benefits needs to be replicated in a much larger population group with a wider range of resveratrol intakes from a wider variety of foods before it can be considered definitive.
  • Even if the amount of resveratrol in food does offer no significant health benefits, that information provides little or no guidance when we consider resveratrol supplements, which generally provide much higher levels of resveratrol.

The Bottom Line:

1)    Don’t pay too much attention to the headlines saying that the health benefits of resveratrol are a myth. The study behind the headlines was a small study in a relatively homogeneous population. If anything, it debunked the hypothesis that red wine consumption is responsible for the French Paradox.

2)    The study did suggest that the amount of resveratrol one can obtain from diet alone is unlikely to provide significant health benefits. While that may be true, it is irrelevant when considering resveratrol supplements because they provide much higher amounts of resveratrol.

3)    The clinical studies on resveratrol supplements are very encouraging, but not yet definitive (see, for example, my “Health Tips From the Professor” article on resveratrol and blood sugar control. That’s to be expected at this stage. It generally takes decades of studies before the scientific community reaches consensus on anything. In the meantime you will continue to see alternating headlines proclaiming the miracles and the myths of resveratrol.

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.

Our Gut Bacteria Are What We Eat

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We Grow What We Eat

Author: Dr. Stephen Chaney

BacteriaThe subtitle of this week’s “Health Tips From the Professor” is “We Grow What We Eat”.

No, this is not about each of us starting a backyard garden and literally growing what we eat – although that would probably be a good idea for most of us. I’m actually talking about the bacteria that we “grow” in our intestine.

Most of you probably already know about the concept of “good” and “bad” intestinal bacteria.

Evidence suggests that the “bad” bacteria and yeast in our intestine can cause all sorts of adverse health effects:

  • There is mounting evidence that they can compromise our immune system.
  • There is also evidence that they can create a “leaky gut” (you can think of this as knocking holes in our intestinal wall that allow partially digested foods to enter the circulation where they can trigger inflammation and auto-immune responses).
  • There is some evidence that they can affect brain function and our moods.
  • They appear to convert the foods that we eat into cancer causing chemicals which can be absorbed into the bloodstream.
  • Studies in mice even suggest that they can make us fat.

The list goes on and on…

The “good bacteria” are thought to crowd out the “bad” bacteria and prevent many of the health problems they cause.

In case you’re thinking that it seems a bit far-fetched to think that our intestinal bacteria could affect our health, let me remind you that we have about 100 trillion bacteria in our intestine compared to about 10 trillion cells in our body. They outnumber us 10 to 1.

For years we have thought of “bad” bacteria and yeast as originating from undercooked, spoiled or poorly washed foods that we eat and the “good” bacteria as originating from foods like yogurt and probiotic supplements.

But most of us have not thought that the kinds of foods we choose to eat on a daily basis can affect the kinds of bacteria we “grow” in our intestine – until now. You’ve heard for years that “We are what we eat”. Well it now appears that we also “grow what we eat”. I’m referring to a recent study by G. D. Wu et al (Science, 334: 105-108, 2011).

Our Gut Bacteria Are What We Eat

I’m going to get a bit technical here (Don’t worry. There won’t be a quiz). Scientists refer to the population of bacteria in our intestines as our “microbiome”. Previous studies have shown that people from all over the world tend to have one of two distinct microbiomes (populations of bacteria) in their intestines – Bacteroides or Prevotella. [Again, don’t let the specialized scientific terminology scare you. These are just the names scientists have given to these two distinctive populations of intestinal bacteria].

What this study showed was that people who habitually consumed high-fat/low-fiber diets (diets containing predominantly animal protein and saturated fats) tended to have the Bacteroides bacteria in their intestine, while people who habitually consumed low-fat/high-fiber diets (diets that are primarily plant based and are high in carbohydrate and low in meat and dairy) tended to have the Prevotella bacteria in their intestine. And surprisingly this appears to be independent of sex, weight and nationality.

Is This Important?

The research defining these two distinct microbiomes (populations of intestinal bacteria) and showing that they are influenced by what we eat is very new. At this point in time we know relatively little about the health benefits and risks associated with the Bacteroides and Prevotella microbiomes.

For example:

  • Most of the studies on the health effects of “bad intestinal bacteria” were based on the identification of one or two “bad bacteria” in the gut – not on the hundreds of bacterial species found in the Bacteroides microbiome. So we can’t say for sure that the Bacteriodes microbiome found in people with diets high in animal protein and saturated fats will cause the same health problems as the “bad bacteria”. Nor do we know for sure how important a role the Bacteriodes microbiome plays in the health consequences of consuming that kind of diet.
  • Similarly, many of studies on the health benefits of “good intestinal bacteria” have been based on probiotic supplements containing one or two bacterial species – not the hundreds of bacterial species found in the Prevotella microbiome. So we can’t really say if probiotics or even the Prevotella microbiome will convey the same health benefits seen in populations who consume vegetarian diets.

However, now that do we know that we “grow what we eat” there are numerous studies ongoing to define the benefits and risks associated with each type of bacterial population.

For example, I shared a study with you recently which shows that the intestinal bacteria in people who eat a lot of animal protein convert carnitine (which is also found in meat) to a compound called TMAO, which may increase the risk of heart attacks, and that the conversion of carnitine to TMAO does not occur in people who consume a vegetarian diet ( see “Does Carnitine Increase Heart Disease Risk”)

Stay tuned! I’ll keep you updated as more information becomes available.

The Bottom Line:

Most of the studies I report on are ones that you can act on right away. This one is different. This study introduces a whole new concept – one that raises as many questions as it answers. This makes us ask those “what if” questions.

1)     Previous studies have shown that most people have one of two different kinds of microbiomes (populations of bacteria) in their intestines. This study showed that diets high in animal protein and fat favored one kind of intestinal microbiome, while diets low in fat and high in fiber from fruits & vegetables favored another type of intestinal microbiome.

2)     With a few exceptions we don’t know yet how important a role these intestinal microbiomes play in determining the health consequences of different diets. However, because our intestinal bacteria outnumber the cells in our body by 10:1, it is tempting to ask “What if?”

3)     We also don’t yet know the extent to which probiotics (either from foods or supplements) can overcome the effects of a bad diet on our intestinal microbiome, but it is tempting to ask “What if?”

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 D Overhyped?

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Are Clouds Gathering For the Sunshine Vitamin?

Author: Dr. Stephen Chaney

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

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

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

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

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

Is Vitamin D Overhyped?

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

The authors of the study reported that:

  • There was no relationship between vitamin D intake and cancer, heart disease, autoimmune disease, infectious diseases, diabetes and other diseases. In other words, they concluded that most of the recent excitement about vitamin D was just hype.
  • There was also no evidence that vitamin D increased bone density or reduced the risk of fractures and falls in older people – in contrast to many previous studies.

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

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

The Study Is Flawed

My specific criticisms of the study are:

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

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

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

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

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

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

Is Vitamin D Beneficial After All?

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

  • High blood levels of 25-hydroxy vitamin D decreased the risk of heart disease by 35%, cancer by 14% and overall mortality by 35%.
  • Supplementation with vitamin D3 reduced overall mortality by 11%, while supplementation with vitamin D2 increased overall mortality by an insignificant 4%.
  • 65% of the US population can be classified as vitamin D insufficient (blood levels of 25-hydroxy vitamin D of below 30 ng/ml) and 4% as severely deficient in vitamin D (blood levels below 10 ng/ml)
  • Vitamin D deficiency contributes to 13% of the deaths in the United States. For comparison the corresponding numbers for other major risk factors are: smoking – 20%, physical inactivity – 11% and alcohol – 9%.
  • About the only point on which the two studies agreed was that there is a need for more, better designed studies to clarify the benefits of vitamin D.

The Bottom Line:

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

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

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

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

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

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

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

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

Do High Protein Diets Cause Cancer?

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How Much Protein Should We Eat?

Author: Dr. Stephen Chaney

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

  • “Is this new information?”
  • “Does this apply to me?”
  • “Should I radically change what I eat?”

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

Do High Protein Diets Cause Cancer?

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

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

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

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

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

  • 45% increase in overall mortality
  • 4-fold increase in cancer death risk
  • 4-fold increase in diabetes death risk.

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

Protein Shakes2)     When they looked at people in the 50-65 age group consuming diets high in vegetable protein:

  • the increased overall mortality and increased in cancer mortality disappeared
  • the increased diabetes mortality was still seen.

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

  • 28% decrease in overall mortality
  • 60% decrease in cancer mortality.

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

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

  • Diets high in animal protein may be bad for you if you are in the 50-65 age range, but might actually be good for you if you are over 65.
  • Diets high in vegetable protein appear to be good for anyone over age 50 (The study didn’t look at younger age groups).

Is This New Information?

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

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

  • The idea that vegetable proteins may be better for you than animal proteins has been around for decades. There are a number of studies suggesting that diets high in animal protein increase the risk of cancer, heart disease, diabetes and overall death – although it is still not clear whether it is the animal protein itself or some other characteristic of populations consuming mostly animal protein that is the culprit.
  • Evidence has been accumulating over the past decade or so that protein needs increase as we age, so it is not surprising that this study found high protein diets to be beneficial for those of us over age 65.

What Do Other Experts Say?

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

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

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

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

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

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

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

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

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

The Bottom Line:

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

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

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

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

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

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

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

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

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

Can Diet Alter Your Genetic Destiny?

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Disease Is Not Inevitable

Author: Dr. Stephen Chaney

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

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

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

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

Can Diet Alter Your Genetic Destiny?

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

1)     Your genetic makeup can influence your nutrient requirements.

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

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

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

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

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

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

3)     Diet can actually alter your genes.

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

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

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

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

Examples Of How Diet Can Alter Genetic Predisposition

Mature Man - Heart Attack Heart Disease

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

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

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

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

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

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

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

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

Cancer

  • A healthy diet (characterized by high intakes of vegetables, fruits, whole grain products and low intakes of refined grain products) compared with the standard American diet (characterized by high intakes of refined grain products, desserts, sweets and processed meats) results in a pattern of gene expression that is associated with lower risk of cancer.  (Nutrition Journal, 2013 12:24).
  • A healthy lifestyle (low fat diet, stress management and exercise) in men with prostate cancer causes downregulation of genes associated with tumor growth (PNAS, 105: 8369-8374).
  • Sulforaphane, a nutrient found in broccoli, turns on genes that suppress cancer.

Diabetes

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

Cellular Stress Response

  • A diet rich in antioxidant fruits and vegetables activates the cellular stress response genes that protect us from DNA damage, inflammation and reactive oxygen species (BMC Medicine, 2010 8:54).
  • Resveratrol, a nutrient found in grape skins and red wine, activates genes associated with DNA repair and combating reactive oxygen species while it reduces the activity of genes associated with inflammation, increased blood pressure and cholesterol production.

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

Obesity

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

The Bottom Line:

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

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

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

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

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

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

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

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

Does Cell Phone Use Lead to Brain Cancer?

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Author: Dr. Pierre DuBois

Does Cell Phone Use Lead To CancerThere are currently close to 6 billion cell phone subscriptions worldwide, and increased usage of cell phones has understandably led to a greater level of interest in how safe they are.

The main concern for our health is that mobile phones emit and receive electromagnetic radiation as a result of their need to communicate with relay towers, and some of this radiation is absorbed by the head when the phone is held up to the ear.

Whether or not the radiation (both the amount and the frequency) that a typical mobile phone user is likely to receive is potentially damaging to their health has been the subject of debate for some time.

Does Cell Phone Use Lead to Brain Cancer?

Anecdotal evidence that high mobile phone use can potentially lead to brain cancer is not hard to find. Newspapers and other media sources are only too ready to run such stories.

However, given that there are so many people using mobile communication so regularly, the chances are that someone is going to have a brain tumor at some point, whether or not there is any link with the amount of time they spend on their phone.

The obvious question is whether or not there is good reason to be concerned over how and how much you use your phone.

The Evidence Against Cell Phone Usage Leading To Brain Cancer

The most recent assessment of the scientific evidence of mobile phone safety was carried out by the European Commission Scientific Committee on Emerging And Newly Identified Health Risks (SCENIHR). They concluded that mobile phone usage was unlikely to increase the risk of developing brain tumors.

The most recent results from a long-term study by researchers from the Institute of Cancer Epidemiology at the Danish Cancer Society in Denmark also failed to find any link between mobile phone usage and the development of brain tumors or any other cancers of the nervous system.

This study was particularly significant in that it used most of the Danish population to determine if there was any difference in the incidence of brain cancer between mobile phone users and non-mobile phone users. Unsurprisingly, this work has been quoted frequently, especially by cell phone companies, as evidence that their products have now been given a completely clean bill of health.

The Evidence For Cell Phone Usage Leading To Brain Cancer

In contrast to the previous results, the conclusion of a 2010 paper published in the International Journal of Epidemiology on the subject suggested that while no overall link was found between two kinds of brain tumor and mobile phone usage, the data did point to a possible increase in the development of glioma-type tumors in the most intensive users

The authors also pointed out that since the new generations of smart phones are being used for even greater periods of time, especially by younger people, further and ongoing studies in this area are definitely merited.

In 2011, the World Health Organization (WHO) classified mobile phone radiation as “potentially carcinogenic to humans.” Following from this, many countries have adopted a precautionary approach and suggested moderation in cell phone usage. Using a hands-free kit to avoid holding a phone next to your head has also been advised.

While the available evidence suggests that low and normal usage of a mobile phone does not increase your risk of developing a brain tumor, it is probably wise to reduce your exposure to electromagnetic radiation as much as you can, and certainly to avoid spending long periods of the day with a phone next to your ear.

The Bottom Line:

  • The link between cell phone use and brain cancer is inconclusive at present. Most studies find no overall link, but suggest that certain types of brain cancers could be associated with cell phone use.
  • Experts recommend not holding cell phones next to your head for long periods of time.

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

Are Dietary Polyphenols Associated With Longevity?

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Are Polyphenols The Fountain of Youth?

Author: Dr. Stephen Chaney

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

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

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

Polyphenols Are Everywhere:

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

  • The term polyphenols includes some names you may recognize, such as flavonoids, isoflavones, anthrocyanidins and resveratrol, and many more that might look like the kind of names you might expect to find on a processed food label.
  • Polyphenols don’t just come from red wine. There are several hundred polyphenols in edible foods. Many fruits, vegetables (including beans like soybeans) and whole grains – the kinds of foods that every expert recommends for a healthy diet – are also great sources of polyphenols.
  • Most polyphenols are excellent antioxidants. Studies suggest that they may also exert antiinflammatory effects and may reduce the risk of heart disease, neurodegenerative disease and cancer. So it is not unreasonable to assume that they might enhance longevity.

An In-Depth Analysis Of The Study:

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

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

Strengths of the Study:

  • This is the very first study to actually investigate the relationship between dietary polyphenols and longevity in a meaningful way. The study was well designed and well executed.
  • The measurement of urinary polyphenol content is a strength of this study. Dietary recalls are often inaccurate. In fact, this study suggests that dietary recalls should probably not be used to estimate dietary polyphenol intake in future studies.

Weaknesses of the Study:

  • This was a first study of its kind, and like any other first study it needs to be confirmed by additional studies.
  • The study only measured associations, not cause and effect. Of course, it would be almost impossible to conduct a double blind, placebo controlled study of this duration – especially if one is using urinary excretion as a measure of polyphenol intake.
  • The study did not report the dietary sources of the polyphenols, although this information was presumably available from the dietary recalls. Because the study was conducted in the Chianti region of Italy it is probably pretty safe to assume that red wine contributed to the polyphenol intake. However, people in that region of Italy also tend to consume diets rich in fruits and vegetables. Hopefully, future studies will help determine whether some polyphenols are more important for longevity than others.

The Bottom Line:

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

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

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

Soy And Breast Cancer Recurrence

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The Truth About Soy And Breast Cancer

 Author: Dr. Stephen Chaney

SoybeanYou’ve probably heard the warnings: “Soy may increase the risk of breast cancer!” “Women with breast cancer shouldn’t use soy!”

The first warning was never true. Numerous clinical studies have shown that consumption of soy protein is associated with a lower risk of developing breast cancer.

Furthermore, the science behind the second warning has never been very strong. The concerns that soy might stimulate the growth of breast cancer cells was based primarily on cell culture experiments and one experiment in mice – even though a second experiment in mice came to the exact opposite conclusion.

Was The Hypothesis That Soy Could Increase The Risk Of Breast Cancer Recurrence Plausible?

The possibility that soy isoflavones could stimulate the growth of estrogen- responsive breast cancer was biochemically plausible because soy isoflavones bind to the estrogen receptor and have a very weak stimulatory effect (much weaker than estrogen itself).

Even that evidence was not definitive because soy isoflavones also turn on several tumor suppressor pathways in breast cells and help strengthen the immune system – so they could just as easily inhibit the growth of breast cancer cells.

However, because the concerns were plausible and had not been definitively disproved, most experts, including me, recommended for several years that women with estrogen- responsive breast cancer might want to avoid soy protein.

Has The Hypothesis Been Rigorously Tested?

In fact, the definitive clinical studies have been performed, and it turns out for women who are breast cancer survivors, consumption of soy foods does not increase either the risk of breast cancer recurrence or of dying from breast cancer.

The first of these studies was reported in the December 2009 issue of the Journal of the American Medical Association by researchers at Vanderbilt University and Shanghai Institute of Preventive Medicine (Shu et al, JAMA, 302: 2437-2443, 2009).

It was a large, well designed, study that enrolled 5042 Chinese women aged 20 to 75 years old who had been diagnosed with breast cancer and followed them for an average period of 3.9 years.

The women were divided into four groups based on the soy content of their diet (ranging from 5 grams/day to 15 grams/day). The results were clear cut. Breast cancer survivors with the highest soy intake had 25% less chance of breast cancer recurrence and 25% less chance of dying from breast cancer than the women with the lowest soy intake.

The effect was equally strong for women with estrogen receptor-positive and estrogen receptor negative cancers, for early stage and late stage breast cancer and for pre- and post-menopausal women. In short this was a very robust study.

The study also showed that soy protein intake did not interfere with tamoxifen, a drug that blocks the binding of estrogen to its receptor on cancer cells. Tamoxifen is used for both for treating estrogen-responsive breast cancer and preventing its recurrence. In this study, the reduction in the risk of breast cancer recurrence & death was just as great whether the breast cancer survivors were taking tamoxifen or not.

In fact, tamoxifen was protective only for women with low soy intake. It conferred no extra protection for the women at the highest level of soy intake because the soy isoflavones were also blocking the binding of estrogen to its receptor.

Other Clinical Studies

If that were the only published clinical study to test the soy-breast cancer hypothesis, I and other experts would be very cautious about making definitive statements. However, at least four more clinical studies have been published since then, both in Chinese and American populations. The studies have either shown no significant effect of soy on breast cancer recurrence or a protective effect. None of them have shown any detrimental effects of soy consumption by breast cancer survivors.

A meta-analysis of all 5 studies was published earlier this year (Chi et al, Asian Pac J Cancer Prev., 14: 2407-2412, 2013). This study combined the data from 11,206 breast cancer survivors in the US and China. Those with the highest soy consumption had a 23% decrease in recurrence and a 15% decrease in mortality from breast cancer.

The Bottom Line:

What does this mean for you if you are a breast cancer survivor?

1)     There are many reasons to include soy protein foods as part of a healthy diet. Soy foods are one of the highest quality vegetable protein sources and provide a great alternative to many of the high fat, high cholesterol animal proteins in the American diet.

2)     I personally feel that these studies are clear cut enough that breast cancer survivors no longer need to fear soy protein as part of a healthy diet.

3)     The responsible websites agree with this assessment. For example, WebMD and the American Institute for Cancer Research (AICR) both say that breast cancer survivors need no longer worry about eating moderate amounts of soy foods.

4)     The irresponsible websites (I won’t name names, but you know who they are) are still warning breast cancer survivors to avoid soy completely. As a scientist I really have problem with people who are unwilling to change their opinions in the face of overwhelming scientific evidence to the contrary.

5)     Of course, some of those bloggers have now shifted their arguments to say that it is unfermented or genetically modified soy that causes breast cancer. Those statements are equally bogus – but that’s another story for another time.

6)     Finally, I want to emphasize that the published studies merely show that soy does not increase the risk of breast cancer and is safe to use for breast cancer survivors. None of those studies suggest that soy is an effective treatment for breast cancer. The protective effects of soy are modest at best. If you have breast cancer, consult with your physician about the best treatment options for you.

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.

Health Tips From The Professor