Does Resveratrol Improve Blood Sugar Control?

May 27, 2014 by Dr. Steve Chaney

Is The Promise of Resveratrol True?

Author: Dr. Stephen Chaney

It was just a few years ago that resveratrol was the latest “miracle nutrient”. It was featured on Dr. Oz and on 60 Minutes. It was hot! Today you see dueling headlines. The headlines one week proclaim the benefits of resveratrol. Next week’s headlines say that it’s all hype. What’s a person to believe?

Let me take you behind the headlines to look at the actual studies and answer some important questions.

1) What do we actually know about the benefits of resveratrol?

2) Is the evidence for beneficial effects of resveratrol where it should be considering the number of clinical studies that have been published?

3) What additional studies need to be done before we can be sure that resveratrol is beneficial?

4) Should you wait until we are absolutely certain resveratrol is beneficial, before you start using it? This is perhaps the most important question of all.

To answer those questions, let’s examine the study behind one of the latest headlines, namely: “Resveratrol Improves Blood Sugar Control in Diabetics”. One of the promises of resveratrol has been that it might help diabetics and pre-diabetics who struggle with blood sugar control. However, this promise was based on animal studies. The study that generated the headlines in question was a meta-analysis of recently published human clinical trials in this area (Liu et al, Am. J. Clin. Nut., 2014, doi: 10.3945/ajcn.113.082024).

Does Resveratrol Improve Blood Sugar Control?

The meta-analysis included 11 published placebo controlled double blind clinical studies looking at the effects of resveratrol supplementation on fasting blood sugar levels, insulin levels, hemoglobin A1c (a measure of blood sugar control) and insulin resistance (a measure closely associated with type 2 diabetes).

A strength of this meta-analysis is the fact that it included 11 clinical studies. However, a weakness of this analysis is that these studies utilized a wide variety of resveratrol doses (10 mg/day to 1 gram/day), a wide variety of end points and both diabetic and non-diabetic patients. That means that there were only a few studies with common population groups, resveratrol doses, and end points.

The conclusions of the study (and the headlines you may have seen) were that:

• Resveratrol appeared to improve blood sugar control (based on improvements in fasting blood sugar levels, insulin levels, hemoglobin A1c and insulin resistance) in diabetics.

• No consistent effect of resveratrol on blood sugar control was seen in non-diabetics.

How Good Are These Studies?

While these studies are very promising, they are bot definitive. There were only 3 published clinical studies in diabetics. While all 3 of the studies showed a positive effect of resveratrol supplementation:

• The doses used were different in each study (ranging from 10 mg/day to 1 gram/day)

• Each study measured different end points (one measured blood glucose, insulin levels, hemoglobin A1c and insulin resistance, one measured blood glucose and hemoglobin A1c and the third measured insulin resistance).

As a research scientist I would like to see more studies done at comparable doses and measuring the same end points – we scientists always want more studies.

Similarly, there was not enough consistency in the studies with non-diabetics to draw a firm conclusion. (3 were with obese patients, 3 were with patients with cardiovascular disease, 1 was with patients with metabolic syndrome and 1 was with perfectly healthy subjects.)

If you really wanted to see if something like resveratrol helps non-diabetics with blood sugar control, you would want to start with people who are already experiencing some difficulties with blood sugar control (pre-diabetics or patients with metabolic syndrome) and follow them for a couple of years to see if resveratrol reduces the number of them who become diabetic.

Are The Headlines Just Hype?

Does that mean that the blood sugar benefits of resveratrol are just hype? The answer is no. There is a difference between “very promising, but not yet definitive” and “hype”. We shouldn’t be surprised that human studies on the health benefits of resveratrol are not yet definitive. Science moves slowly. It often takes decades of scientific research before promising concepts are widely accepted by the scientific community.

When a research area is as young as this one, we sometimes need to go beyond the clinical studies and look at the totality of evidence. In this case:

• In mice resveratrol exerts its beneficial effects by turning on a specific anti-aging gene called SIRT1 (Cell Metabolism, 15: 675-690, 2012). In humans, resveratrol appears to activate the same genetic pathways as in mice (Journal of Clinical Endocrinology & Metabolism, 96: 1409-1414, 2011).

• In obese mice resveratrol improves markers of blood sugar control (Nature, 444: 337-342, 2006). Published clinical studies in diabetic humans also show improvements in blood sugar control (Journal of Clinical Nutrition, 2014, doi: 10.3945/ajcn.113.082024).

So while more and better clinical studies are needed to be absolutely certain that resveratrol helps improve blood sugar control, the evidence supporting that effect is substantial.

What Should You Do?

The ONLY important question for each of you is probably: “Should I wait a decade or two until we are absolutely sure about the health benefits of resveratrol before I take a resveratrol supplement?” That question is ultimately yours to answer. It’s all about benefits and risk.

Benefits – In animal studies resveratrol clearly improves blood sugar control. The human clinical studies published to date are consistent with the animal studies.

Risk – Current data suggest that resveratrol appears to be safe, even at high doses. For example, one recent study indicated that up to 5 gm/day is safe (Cancer Epidemiology BioMarkers & Prevention, volume 16:1246-1262, 2007), but I wouldn’t personally recommend exceeding 100-200 mg/day.

The Bottom Line:

1) Don’t get too excited about the headlines suggesting that resveratrol might help improve blood sugar control in diabetics. The few human clinical studies that have been published to date are consistent with previous animal studies. That is very promising, but more studies are needed before we can be absolutely confident that resveratrol supplementation is beneficial for diabetics.

2) Similarly, don’t be discouraged by the headlines suggesting that resveratrol does not help with blood sugar control in non-diabetics. Those results are preliminary as well.

3) That doesn’t mean that the headlines are just hype. It takes decades to accumulate definitive proof that any kind of food or nutrient offers proven benefits, and the bulk of human clinical research on reveratrol has occurred in the last couple of years. We are exactly where we should expect to be at this point in time.

4) With something as promising as resveratrol, the real question becomes whether you can afford to wait a decade or two until you know whether the potential benefits have been definitely proven. That question is up to you. On the plus side, current data suggest that resveratrol is highly promising for blood sugar control. In addition, resveratrol appears to be safe, even at high doses, but I wouldn’t personally recommend exceeding 100-200 mg/day.

5) We already know that weight control, exercise and a healthy diet improve blood sugar control. You should think of resveratrol as something you may wish to add to a healthy lifestyle, not as a substitute for a healthy lifestyle.

6) If you are diabetic and decide to try a resveratrol supplement, be sure to work with your physician so they can modify your dose of insulin or blood sugar medication as necessary.

7) Finally, you may be asking whether resveratrol supplements are even necessary. Can’t you just get all the resveratrol you need from a glass or two of red wine? Stay tuned. I’ll have the answer to that question in a couple of weeks.

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 Fish Oil Make Children Smarter?

May 20, 2014 by Dr. Steve Chaney

When Do Omega-3 Supplements Make Sense?

Author: Dr. Stephen Chaney

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

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

Can Fish Oil Make Children Smarter?

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

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

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

What Is the Significance of This Study?

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

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

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

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

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

What does all of this mean to you?

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

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

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

The Bottom Line:

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

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

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

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

Our Gut Bacteria Are What We Eat

May 13, 2014 by Dr. Steve Chaney

We Grow What We Eat

Author: Dr. Stephen Chaney

The 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.

Do Omega-3s Lower Blood Pressure?

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

The Good News About Fish Oil

Author: Dr. Stephen Chaney

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

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

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

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

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

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

How Was The Study Designed?

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

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

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

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

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

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

Do Omega-3s lower Blood Pressure?

The authors of the study reported that:

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

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

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

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

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

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

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

The Bottom Line:

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

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

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

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

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

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

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

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

Do Artificial Colors Cause Hyperactivity?

April 29, 2014 by Dr. Steve Chaney

Color Them Hyperactive

Author: Dr. Stephen Chaney

Each year between 3 and 10% of school aged children are diagnosed with attention deficit/hyperactivity disorder (ADHD), also known as hyperactivity.

Most of these children are currently being treated with drugs. And these drugs have side effects – ranging from relatively minor (loss of appetite, weight loss, insomnia and mood swings) to major (suicidal thoughts, psychotic behavior and drug abuse).

So it is only natural for parents to ask whether there is a more natural approach that they could follow and, more specifically, whether diet could make a difference.

The Feingold Diet And Hyperactivity

To answer that question let’s start by looking at just one aspects of children’s diets – the increasing prevalence of artificial food colors and preservatives in the diet. The average child today is consuming over 10 pounds of food additives every year!

The idea that food additives – specifically artificial colors and preservatives – might be responsible for hyperactivity was first raised by Dr. Ben Feingold over 30 years ago. He devised the Feingold Diet – a diet that was free of artificial food colors, preservatives
and other artificial food additives.

Some small scale clinical studies suggested that the diet might be successful and millions of parents used the diet for their hyperactive children with great success.

But the medical authorities pooh-poohed the Feingold Diet. They pointed out that when parents are putting their child on a special diet they are also giving that child more attention – and it might be the parent’s increased attention that decreased the child’s hyperactive behavior.

They also pointed out when you eliminate food additives from the diet you are decreasing the “junk” food and increasing fresh fruits and vegetables – in short the child’s diet is much healthier.

So eventually the Feingold Diet lost popularity – but the idea that artificial food colors & preservatives might trigger hyperactivity has refused to go away.

Do Artificial Colors Cause Hyperactivity?

In fact, a couple of recent studies have substantially strengthened the link between artificial ingredients and hyperactivity.

The first study was a meta-analysis of 15 previous studies looking at the effect of artificial food colors and preservatives on hyperactivity (Journal of Developmental & Behavioral Pediatrics, 25: 423-434, 2004).

This meta-analysis concluded that artificial food colors & preservatives caused an increase in hyperactivity in 28% of the children tested.

Almost all of the children in those previous studies were selected for the study because they had been diagnosed as hyperactive (ADHD). However, a more recent study looked at 297 children from Southampton England who had not been diagnosed as hyperactive (Lancet, 370: 1560-1567, 2007).

After an 8 week elimination phase in which artificial food colors and preservatives were removed from their diets, they were given a one week challenge consisting of fruit juice containing one of two different mixtures of four artificial food colors and the preservative sodium benzoate or a placebo.

The amount of artificial food colors and sodium benzoate in the fruit juice drinks was designed to match the average amount found in the English diet (which isn’t all that different from the American diet).

Once again, the results were clear. The amount of artificial food colors and preservatives found in the typical child’s diet is enough to trigger hyperactivity in many children.

The Bottom Line

So what does that mean to you if you have a hyperactive child? Could the simple act of eliminating artificial colors, flavors & preservatives from your child’s diet eliminate hyperactivity and give you back that calm, sweet child that you love?

The available data suggest that removing artificial food additives from your child’s diet can make a difference in their behavior, but I tend to side with experts who suggest that a holistic approach is best.
Eliminating food additives from your child’s diet is important, but also make sure the diet is a healthy one, that your child is getting all of the nutrients that they need and that they are getting all of the attention and support that they need.

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?

April 23, 2014 by Dr. Steve Chaney

Are Clouds Gathering For the Sunshine Vitamin?

Author: Dr. Stephen Chaney

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

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

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

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

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

Is Vitamin D Overhyped?

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

The authors of the study reported that:

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

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

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

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

The Study Is Flawed

My specific criticisms of the study are:

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

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

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

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

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

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

Is Vitamin D Beneficial After All?

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

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

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

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

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

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

The Bottom Line:

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

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

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

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

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

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

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

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

Do High Protein Diets Cause Cancer?

April 15, 2014 by Dr. Steve Chaney

How Much Protein Should We Eat?

Author: Dr. Stephen Chaney

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

“Is this new information?”

“Does this apply to me?”

“Should I radically change what I eat?”

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

Do High Protein Diets Cause Cancer?

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

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

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

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

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

45% increase in overall mortality

4-fold increase in cancer death risk

4-fold increase in diabetes death risk.

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

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

the increased overall mortality and increased in cancer mortality disappeared

the increased diabetes mortality was still seen.

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

28% decrease in overall mortality

60% decrease in cancer mortality.

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

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

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

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

Is This New Information?

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

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

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

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

What Do Other Experts Say?

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

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

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

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

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

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

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

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

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

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

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

The Bottom Line:

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

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

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

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

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

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

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

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

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

Does Carnitine Increase Heart Disease Risk?

April 8, 2014 by Dr. Steve Chaney

Carnitine: Dr. Jekyl or Mr. Hyde?

Author: Dr. Stephen Chaney

It’s both interesting and confusing when one Journal article appears talking about the dangers of a particular supplement and just a couple of weeks later another article appears talking about the benefits of that same supplement – especially when the conclusions of both articles are misrepresented in the media.

But that’s exactly what has just occurred with the supplement L-carnitine. Media reports of the first article trumpeted the headline “Cleveland Clinic study links L-carnitine to increased risk of heart disease”. Media reports of the second article featured the headline “Mayo Clinic review links L-carnitine to multiple health heart benefits”. As you might suspect, neither headline was completely accurate. So let me help you sort out the confusion about L-carnitine and heart health

What is Carnitine?

But first let me give you a little bit of background about L-carnitine. L-Carnitine is an essential part of the transport system that allows fatty acids to enter the mitochondria where they can be oxidized and generate energy. So it is an essential nutrient for any cell that has mitochondria and utilizes fatty acids as an energy source.

L-carnitine is particularly important for muscle cells, and the hardest working muscle cells in our body are those that pump blood through our hearts. So when we think of L-carnitine we should think of heart health first.

But that doesn’t mean that L-carnitine is an essential nutrient. In fact, our bodies generally make all of the L-carnitine that we need. There are some metabolic diseases that can prevent us from making L-carnitine or utilizing L-carnitine efficiently. People with those diseases benefit from L-carnitine supplementation, but those diseases are exceedingly rare.

There is some evidence that supplemental L-carnitine may be of benefit in individuals suffering from congestive heart failure and other diseases characterized by weakened heart muscles. Other than that there is little evidence that supplemental L-carnitine is beneficial for healthy individuals.

Does Carnitine Increase Heart Disease Risk?

Let’s look at the first study (Koeth et al, Nature Medicine, doi:10.1038/nm.3145, April 7, 2013) – the one that purportedly linked L-carnitine to increase risk of heart disease. The authors were trying to gain a better understanding of the well-established link between red meat consumption and cardiovascular disease risk. The classical explanation of this link has been the saturated fat and cholesterol content of the red meat.

However, several recent studies have questioned whether saturated fat and cholesterol actually increase the risk of cardiovascular disease (see last week’s article “Are Saturated Fats Good For You?”)

Since red meat is also high in L-carnitine, the authors hypothesized that it might be the L-carnitine or a metabolite of the L-carnitine that was associated with increased risk of heart disease in people consuming red meat.

The authors honed in on a metabolite of L-carnitine called trimethylamine-N-oxide or TMAO that is produced by bacteria in the intestine and had been previously shown to accelerate atherosclerosis in mice. They developed what they called an L-carnitine challenge. Basically, they gave their subjects an 8 ounce sirloin steak, which contains about 180 mg of L-carnitine, and measured levels of L-carnitine and TMAO in the blood one hour later and the urine 24 hours later. [I’m guessing they didn’t have much trouble finding volunteers for that study.]

When the subjects were omnivores (meaning meat eaters) they found a significant increase in both L-carnitine and TMAO in their blood and urine following the L-carnitine challenge. When they put the same subjects on broad-spectrum antibiotics for a week to wipe out their intestinal bacteria and repeated the L-carnitine challenge, they found an increase in L-carnitine but no increase in TMAO. This simply confirmed that the intestinal bacteria were required for the conversion of L-carnitine to TMAO.

Finally, because previous studies have shown that omnivores and vegetarians have very different populations of intestinal bacteria, they repeated their L-carnitine challenge in a group of vegans and found that consumption of the same 8 ounce sirloin steak by the vegans did not result in any significant increase in TMAO in either their blood or urine.

Armed with this information, the authors measured L-carnitine and TMAO concentrations in the fasting blood of 2595 patients undergoing cardiac evaluation in the Cleveland Clinic. They used an established protocol to assess the three-year risk for major adverse cardiac events in the patients they examined. They observed a significant association between L-carnitine levels and cardiovascular event risks, but only in subjects who also had high blood levels of TMAO.

Now it’s time to compare what the headlines said to what the study actually showed. The headlines said “L-carnitine linked to increased risk of heart disease”. What the study actually showed was that there were two things that were required to increase the risk of heart disease – L-carnitine and a population of intestinal bacteria that converted the L-carnitine to TMAO.

The major source of L-carnitine in the American diet is red meat, and habitual red meat consumption is required to support a population of intestinal bacteria that is capable of converting L-carnitine to TMAO. So the headlines should have read “red meat consumption linked to increased risk of heart disease”. But, of course, that’s old news. It doesn’t sell subscriptions.

Does Carnitine Decrease Heart Disease Risk?

The second study (DiNicolantonio et al, Mayo Clinic Proceedings, dx.doi.org/10.1016/j.mayocp.2013.02.007) was a meta-analysis. It reviewed 13 clinical studies involving 3629 people who had already had heart attacks and were given L-carnitine or a placebo after the heart attack.

In evaluating the results of this study it is useful to remember that a heart attack generally kills some of the heart muscle and weakens some of the surviving heart muscle. When the data from all of the studies was combined the authors reported a 27% reduction in all cause mortality, a 65% reduction in arrhythmias, and a 40% reduction in angina. However, there was no reduction in a second heart attack or the development of heart failure.

So perhaps the headlines describing this study were a little closer to being on target, but they failed to mention that these effects were only seen in people who had already suffered a heart attack and had weakened heart muscles. They also failed to mention that there was no decreased risk of a second heart attack or congestive heart failure.

The Bottom Line:

1) The first study should be considered preliminary. It needs to be confirmed by other studies. If it is true, it is not ground breaking. It merely gives us a fuller understanding of why red meat consumption may be linked to increased risk of heart disease and gives you yet another reason to minimize red meat consumption.

The study does raise the possibility that use of L-carnitine supplements may increase your risk of heart disease if you eat red meat on a regular basis, and that this same risk may not be associated with L-carnitine supplementation if you are a vegan. But the study did not directly test that hypothesis, and much more research is required before I would give it any weight.

2) The second study suggests that if you have already had a heart attack, you may want to consult with your physician about whether L-carnitine supplementation might be of benefit. Once again, this study is not ground breaking. We already knew that L-carnitine supplementation was helpful for people with weakened heart muscle. This study merely confirmed that.

Contrary to what the headlines suggested, this study provides no guidance about whether L-carnitine supplementation has any heart health benefits in people without pre-existing heart disease – and the bulk of existing literature suggests that it does not.

3) Finally, I realize that the major use of L-carnitine in the US market is in sports supplements purported to increase strength and endurance. The literature on that is decidedly mixed, but that’s another subject for another time.

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

Are Saturated Fats Good For You?

April 1, 2014 by Dr. Steve Chaney

Is Everything We Thought We Knew About Fats Wrong?

Author: Dr. Stephen Chaney

Bring out the fatted calf! Headlines are proclaiming that saturated fats don’t increase your risk of heart disease – and that they may actually be good for you.

The study (Annals of Internal Medicine, 160: 398-406, 2014) that attracted all the attention in the press was what we scientists call a meta-analysis. Basically, that is a study that combines the data from many clinical trials to improve the statistical power of the effect being studied.

And it was a very large study. It included 81 clinical trials that looked at the effects of various types of fat on heart disease risk.

Are Saturated Fats Good For You?

The answer to this question is a simple No. The headlines suggesting that saturated fats might be good for you were clearly misleading. The study concluded that saturated fats might not increase the risk of heart disease, but it never said that saturated fats were good for you.

In short, the study concluded that:

Saturated fats, monounsaturated fats and long-chain omega-6 polyunsaturated fats did not affect heart disease risk.

Long chain omega-3 polyunsaturated fats decreased heart disease risk [Note: The original version of the paper said that the decrease was non-significant, which is what the headlines have reported. However, after several experts pointed out an error in their analysis of the omega-3 data, the authors corrected their analysis, and the corrected data show that the decrease in risk is significant.]

Trans fats increased heart disease risk

If those conclusions are correct, they would represent a major paradigm shift. We have been told for years that we should limit saturated fats and replace them with unsaturated fats. Has that advice been wrong?

Is Everything We Thought We Knew About Fats Wrong?

Before we bring out the fatted calf and start heaping butter on our12 ounce steaks, perhaps we should look at some of the limitations of this study.

We Eat Foods, Not Fats

When the authors broke the data down into the effects of individual saturated and unsaturated fatty acids on heart disease risk some interesting insights emerge.

For example, with respect to saturated fats:

Both palmitic acid and stearic acid – which are abundant in palm oil and animal fats – increased the risk of heart disease.

On the other hand, margic acid – which is more abundant in dairy products – decreased the risk of heart disease.

So while the net effect of saturated fats on heart disease risk may be zero, these data suggest:

It is still a good idea to avoid fatty meats, especially red meats, if you want to reduce your risk of heart disease. When you focus on foods, rather than fats this fundamental advice has not changed in over 40 years! In next week’s “Health Tips From the Professor” I will share some of the latest research on the dangers of red meat.

With fatty dairy foods the situation is a little more uncertain. I’m not ready to tell you to break out the butter and whipped cream just yet, but recent research does suggest that dairy foods have some beneficial effects that may outweigh their saturated fat content.

With respect to omega-3 fatty acids:

alpha-linolenic acid – which is found in vegetable oils and nuts and is the most abundant omega-3 fatty acids in our diets – had no effect on heart disease risk.

On the other hand, EPA and DHA – which are found primarily in oily fish and omega-3 supplements – decreased heart disease risk by 20-25%.

Once again, while the net effect of omega-3 fatty acids on heart disease risk was very small, that’s primarily because most Americans consume mostly alpha-linolenic acid and very little EPA and DHA. This study shows that fish oil significantly reduces heart disease risk, which is fully consistent with the heart healthy advice of the American Heart Association and National Institutes of Health over the past decade or more.

What We Replace the Fats With Is Important

A major weakness of the current study is that it did not ask what the individual clinical trials were replacing the fatty acids with. Many of them were simply replacing the saturated fats with carbohydrates. To understand why that is important, you have to go back to the research of Dr. Ancel Keys.

The whole concept of saturated fats increasing the risk of heart disease is based on the groundbreaking research of Dr. Ancel Keys in the 50’s and 60’s. But, it is important to understand what his research showed and didn’t show.

His research showed that when you replaced saturated fats with monounsaturated fats and/or polyunsaturated fats the risk of heart disease was significantly reduced. He was the very first advocate of what we now call the Mediterranean diet. (He lived to 101 and his wife lived to 97, so he must have been on to something.)

Unfortunately, his diet advice got corrupted. The mantra became low fat diets, where the saturated fat was replaced with carbohydrates – mostly simple sugars and refined flours. Since diets containing a lot of simple sugars and refined flours also increase the risk of heart disease you completely offset the benefits of getting rid of the saturated fats.

Just in case you think that is outdated dietary advice, Dr. Key’s recommendations were confirmed by a major meta-analysis published in 2009 (American Journal of Clinical Nutrition, 89: 1425-1432, 2009). That study showed once again that replacing saturated fats with carbohydrates had no effect on heart disease risk, while replacing them with polyunsaturated fats significantly reduced risk.

The Bottom Line:

You can put the fatted calf back out to pasture. The headlines telling you that saturated fats don’t increase the risk of heart disease were overstated and misleading. This study does not represent a paradigm shift. In fact, when you analyze the study in depth it simply reaffirms much of the current dietary advice about fats.

1) When you simply replace saturated fats with carbohydrates, as did many of the studies in the meta-analysis that generated all of the headlines, there is little or no effect on heart disease risk. However, other studies have shown that when you replace the saturated fats with monounsaturated and polyunsaturated fats you significantly reduce heart disease risk.

In short, if you are interested in reducing your risk of heart disease, low fat diets may be of relatively little value while Mediterranean diets may be beneficial. No paradigm shift there. That sounds pretty familiar.

2) Fatty meats, especially red meats, appear to increase the risk of heart disease. No surprises there.

3) Alpha-linolenic acid, the short chain omega-3 fatty acid found in nuts, seeds and vegetable oils, does not decrease heart disease risk. However, EPA and DHA, the long chain omega-3 fatty acids found in fatty fish and fish oil supplements significantly decrease heart disease risk. That’s probably because the efficiency of conversion of alpha-linolenic acid to EPA & DHA in our bodies is only around 10%. No surprises there.

4) The study did suggest that dairy foods may decrease heart disease risk. While there are a few other studies supporting that idea, I’m not ready to break out the butter and whipped cream yet. More research is needed.

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

Can Diet Alter Your Genetic Destiny?

March 25, 2014 by Dr. Steve Chaney

Disease Is Not Inevitable

Author: Dr. Stephen Chaney

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

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

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

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

Can Diet Alter Your Genetic Destiny?

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

1) Your genetic makeup can influence your nutrient requirements.

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

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

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

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

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

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

3) Diet can actually alter your genes.

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

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

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

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

Examples Of How Diet Can Alter Genetic Predisposition

Heart Disease

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

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

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

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

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

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

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

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

Cancer

A healthy diet (characterized by high intakes of vegetables, fruits, whole grain products and low intakes of refined grain products) compared with the standard American diet (characterized by high intakes of refined grain products, desserts, sweets and processed meats) results in a pattern of gene expression that is associated with lower risk of cancer. (Nutrition Journal, 2013 12:24).

A healthy lifestyle (low fat diet, stress management and exercise) in men with prostate cancer causes downregulation of genes associated with tumor growth (PNAS, 105: 8369-8374).

Sulforaphane, a nutrient found in broccoli, turns on genes that suppress cancer.

Diabetes

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

Cellular Stress Response

A diet rich in antioxidant fruits and vegetables activates the cellular stress response genes that protect us from DNA damage, inflammation and reactive oxygen species (BMC Medicine, 2010 8:54).

Resveratrol, a nutrient found in grape skins and red wine, activates genes associated with DNA repair and combating reactive oxygen species while it reduces the activity of genes associated with inflammation, increased blood pressure and cholesterol production.

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

Obesity

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

The Bottom Line:

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

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

For example, methylene tetrahydrofolate reductase (MTHFR) deficiency increases your requirement for folic acid.

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

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

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

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

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

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