VTE

August 5, 2014 by Dr. Steve Chaney

Benefits of Omega-3

Author: Dr. Stephen Chaney

When a blood clot ends up in your lungs, it can be deadly. But that blood clot didn’t start out in your lungs. It initially formed in your veins where it is referred to as a thrombus. Then it broke off and migrated to your lungs – a process called venous thromboembolism or VTE. Venous thromboembolism is the third most common form of cardiovascular disease, killing around 100,000 Americans each year.

What if something as simple as adding more omega-3 fatty acids to your diet could dramatically decrease your risk of VTE? That’s exactly what a recent study (Hansen-Krone et al, J. Nutr., 144: 861-867, 2014) has suggested. It claims that one of the benefits of omega-3 in your diet may be to help prevent venous thromboembolism.

What Is Venous Thromboembolism or VTE?

As described above, venous thromboembolism starts when a blood clot (also called a thrombis) forms in a vein. About 2/3 of the time, the blood clot forms in the deep veins in the leg (called deep vein thrombosis or DVT) and stays there before eventually dissolving. The symptoms of deep vein thrombosis or DVT are generally leg pain and swelling.

About 1/3 of the time, the clot breaks loose and travels to the lung where it blocks blood flow to a portion of the lung (a process called pulmonary embolism). The symptoms of pulmonary embolism are severe shortness of breath, chest pain when breathing or coughing, and death! While the first two symptoms are pretty frightening, it’s the last symptom (death) that we’d really like to avoid.

Why Might Omega-3s Prevent Venous Thromboembolism or VTE?

One of the benefits of Omega-3s is they have been shown to reduce inflammation and platelet aggregation, two of the most important risk factors for venous thromboembolism. So it is logical to think that omega-3s might help reduce the risk. However, good scientists don’t rely on logic alone. They test their hypotheses by doing clinical studies.

Unfortunately, the results of previous clinical studies have been mixed. One study showed a protective effect of omega-3s, but two other studies found no correlation between omega-3 fatty acid intake and VTE. However, these studies had some significant limitations:

They were all performed with populations in the United States where fish consumption is relatively low and many of the fish have low omega-3 content. As a consequence omega-3 fatty acid intake was low and there wasn’t much of a range in intake.

Some of the studies did not ask about the use of omega-3 supplements. In a country where 37% of the population takes fish oil supplements, that is a huge omission.

They did not measure omega-3 fatty acid levels in the blood to verify that their dietary surveys were accurate.

Do Omega-3s Prevent Venous Blood Clots or DVT?

The current study (Hansen-Krone et al, J. Nutr., 144: 861-867, 2014) followed 23,631 people aged 25-97 from Tromso, Norway for 16 years.

The participants filled out a comprehensive dietary survey at the time of enrollment where they indicated the number of times per week they ate fish and how often they used fish oil supplements.

The scientists in charge of the study verified the estimated omega-3 intake from the dietary analysis in a subgroup of the population by measuring omega-3 fatty acid levels in their blood.

Finally, they utilized Norway’s excellent health records to determine how many of the people in their trial experienced a venous thromboembolism – either fatal or non-fatal.

The results were pretty impressive:

Blood level measurements of omega-3 fatty acids verified the omega-3 intake estimates from the dietary survey. There was a direct correlation between estimated intake and blood levels of the omega-3 fatty acids.

Those participants who ate fish most often (≥3 times/week) were 22% less likely to experience a VTE than those who ate fish least often (1-2 times/week). That difference was borderline significant.

Those participants who ate fish most often and took fish oil supplements were 48% less likely to experience a venous thromboembolism than those who ate fish least often and took no fish oil supplements. That difference was highly significant.

Strengths & Weaknesses of the Study

Since not all of the previous clinical studies have reached the same conclusion, it is important to look at the strengths and weaknesses of the study compared to the previous studies.

Strengths of the Study:

Tromso is located on the northeast coast of Norway, so fish consumption is high and most of the local fish are excellent sources of omega-3 fatty acids. Consequently, omega-3 intake was relatively high, which significantly increases the chance of seeing an effect if one exists. Fish consumption in the US is generally lower and not all of the fish consumed are good sources of omega-3s.

The study also took into account the use of omega-3 supplements. Some of the US studies did not.

The estimates of omega-3 intake from the dietary survey were verified by blood analysis of omega-3 fatty acids.

Weaknesses of the Study:

The amount of omega-3 fatty acids in the supplements was not recorded, so it is unclear what level of omega-3 fatty acid intake was required to see a significant decrease in VTE risk. This will make it difficult for future investigators to repeat the study.

They did not measure other nutrients that might affect the venous thromboembolism risk.

The Bottom Line

1) VTE is a serious condition with a high rate of mortality.

2) A recent study suggests that a combination of high fish consumption and fish oil supplement use may significantly decrease the risk of venous thromboembolism.

3) It is interesting to note that even three servings/week of omega-3 rich fish was not enough to cause a significant decrease in venous thromboembolism risk. It required additional omega-3s from fish oil supplements before the decreased risk was significant.

4) Not all previous studies have come to the same conclusion. So while the most recent study had several improvements in design compared to previous studies, the case can’t be considered closed. More studies are clearly needed.

5) This study suggests that omega-3 fatty acids may help prevent VTE from occurring. You should not consider them to be a treatment for the condition. If you are experiencing symptoms of venous thromboembolism (leg pain and swelling for deep vein thrombosis (DVT) or shortness of breath and pain when breathing for pulmonary embolism), don’t reach for your fish oil capsules. Call your doctor right away.

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.

Risk Factors of Prostate Cancer

July 29, 2014 by Dr. Steve Chaney

Vitamin D Deficiency?

Author: Dr. Stephen Chaney

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.”

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 MultiVitamins a Waste of Money?

July 22, 2014 by Dr. Steve Chaney

The Multivitamin Controversy You Never Heard About

Author: Dr. Stephen Chaney

Are multivitamins a waste of money? You probably saw the recent headlines telling you that “the experts” have concluded that multivitamins are a waste of money. The article (Gualler et al., Annals of Internal Medicine, 159: 850-851, 2013) that generated all of the headlines was an editorial, which means it was an opinion piece, not a scientific study. It represented the opinion of five very prominent doctors, but it was, at the end of the day, just their opinion.

At the time I pointed out fallacies of their arguments in a “Health Tips From the Professor” article (MultiVitamins-Waste Money?). But, what do I know? I have only published 114 papers in peer reviewed journals and two book chapters on nutrition.

It turns out that I’m not the only expert who feels this way. Five very prominent experts recently published rebuttals concluding that the authors of the original editorial ignored “decades of nutrition research and diet monitoring of the U.S. population to reach this misleading conclusion” (Frei et al, Annals of Internal Medicine, 160: 807-809, 2014).

Who Are These Experts?

Before I share what these experts said, I should probably share their qualifications:

Balz Frei, PhD

Distinguished Professor of Biochemistry & Biophysics & Director of the Linus Pauling Institute, Oregon State University
203 publications

Bruce N. Ames, PhD

Director of the Nutrition & Metabolism Center, Children’s Hospital Oakland Research Institute
540 publications

Jeffrey B. Blumberg, PhD

Professor, Freidman School of Nutrition Science and Policy and Director of the Antioxidants Research Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University
>300 publications

Walter C. Willet, MD, DrPH

Chair of the Department of Nutrition, Harvard School of Public Health
1,422 publications

Thomas R. Friberg, MD, MS

Professor of Ophthamology and Director of the Medical & Surgical Retinal Division of the University of Pittsburg School of Medicine
Principle investigator for the AREDS and AREDS II clinical studies.
134 publications

As you can see, these are not just your run of the mill scientists. They are the top experts in the field.

Are You Wasting Your Money On Multivitamins?

Are multivitamins a waste of money? What did these experts say?

They started by pointing out that few people in the United States follow the USDA dietary guidelines, and “consequently, most people in the United States even in cities like Raleigh, Durham, and Chapel Hill are not well nourished”. Specifically:

93% of U.S. adults don’t get enough vitamins D & E from their diet.
71% of U.S. adults don’t get enough vitamin K from their diet.
61% of U.S. adults don’t get enough magnesium from their diet.
50% of U.S. adults don’t get enough calcium and vitamin A from their diet.

They also pointed out that adequate intake of micronutrients is essential for normal body function and to support good health. Specifically:

Vitamins A, D, iron and zinc are required for normal immune function
Folic acid is required for neurological development. For example, “A multivitamin supplying folic acid dramatically decreases the risk of neural tube defects and is recommended for women of childbearing age.”
The AREDS and AREDS II studies have established the value of supplementation in preventing vision loss due to age-related macular degeneration.

They pointed out that largest (15,000 male physicians) and longest (13 years) randomized, placebo controlled trial of a multivitamin (the Physician’s Health Study II) showed a:

8% reduction in cancer incidence and a 12% reduction in cancer deaths
9% reduction in cataract formation

Finally, they pointed out that the claims that supplement use might actually increase mortality were overemphasized. Specifically:

The claims that high dose vitamin E increase mortality have been refuted by subsequent studies. I have discussed that in detail in my eBook, “The Myths of the Naysayers” (available for free to all subscribers of “Health Tips From the Professor”).
Only 1.1% of the U.S. population consumes more than the recommended upper limit for vitamin A (10,000 IU/day).
The only warning that actually holds up is that smokers should avoid high dose beta-carotene.
More importantly, all of those concerns involved high dose individual supplements. There is no evidence for any risk from taking a daily multivitamin.

In summary, the experts concluded: “Taking a daily multivitamin and mineral supplement not only helps fill known nutritional gaps in the diet of most persons in the United States (thereby ensuring normal body function and supporting good health), but may have the added benefit of helping to reduce the risk for chronic disease.”

The Bottom Line

1) Are multivitamins are a waste of money? No. That was simply the opinion of one group of experts. Other experts have come to the exact opposite conclusion.

2) Of course, it was only the negative opinion that made the headlines. Somehow the opinion that multivitamins are valuable for most Americans never got the attention of the press.

3) According to the experts mentioned in this article, multivitamins play an important role in filling well documented nutrition gaps in the U.S. population, assuring normal body function and helping preserve good health. There is evidence that they may have a modest role in reducing the risk for chronic diseases, and there is no evidence that multivitamin supplements increase the risk of mortality.

4) Of course, you shouldn’t expect miracles from your multivitamin. It’s not going to help you leap tall buildings in a single bound. Your multivitamin should just be one small part of your holistic health program of diet, exercise, weight control and supplementation.

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

Do Calcium Supplements Increase Heart Attack Risk?

July 15, 2014 by Dr. Steve Chaney

Calcium Confusion

Author: Dr. Stephen Chaney

Should you avoid calcium supplements? Do calcium supplements increase heart disease risk? If you’ve been reading some of the recent headlines in magazines, newspapers and current health articles, that’s exactly what you might think.

And, after years of telling us that calcium supplements may be important for bone health, even some doctors are now recommending that their patients avoid calcium supplements. So what’s the truth? What should you believe?

Can Gut Bacteria Make You Fat?

July 14, 2014July 8, 2014 by Dr. Steve Chaney

Gut Bacteria, Diet and Obesity

Author: Dr. Stephen Chaney

Can gut bacteria make you fat? It has been known for some time that the types of bacteria found in the intestines of obese people are different than those found in the intestines of lean individuals. But no one really knew the significance, if any, of that observation. Did obesity favor certain types of intestinal bacteria, or did certain types of intestinal bacteria favor obesity?

Obese individuals are often insulin resistant, and insulin resistance can cause higher sugar levels in the blood, urine and intestine. So it was easy to assume that obesity simply favored the growth of different types of bacteria in the intestine. However, recent studies have suggested that certain types of bacteria in our intestines may actually cause obesity.

Can Gut Bacteria Make You Fat?

For example, one study (Vijay-Kumar et al, Science, 328: 228-231, 2010) compared a strain of mice that are genetically predisposed to obesity with wild type (genetically lean) mice. They first looked at the intestinal bacteria. It turned out that the obese mice and lean mice had the same differences in intestinal bacteria that obese and lean humans have. And just like obese humans the obese mice ate more, displayed insulin resistance, and had elevated levels of triglycerides, cholesterol and blood sugar (They were pre-diabetic).

The investigators then decided to test the hypothesis that the particular bacterial strains found in the intestines of genetically obese mice might be causing their insulin resistance and obesity.

In the first experiment they killed off the intestinal bacteria in the genetically obese mice by putting high dose antibiotics in their food. Depleting the intestinal bacteria created some health problems for the mice, but it completely prevented the insulin resistance, overeating and obesity normally observed with this strain of mice.

In the second experiment they sterilized the intestines of the genetically lean mice and then colonized their intestines with intestinal bacteria from the genetically obese mice. When they did this, the genetically lean mice developed many of the characteristics of the genetically obese mice including insulin resistance, overeating, obesity and hyperglycemia.

In short, when their guts became colonized with bacteria from obese mice, the genetically lean mice became overweight and developed diabetes. Based on these experiments and other studies the scientists hypothesized that the wrong kinds of intestinal bacteria can make a significant contribution to insulin resistance, which in turn can lead to overeating and obesity. In short, they concluded that bad gut bacteria may make you fat.

The Battle of The Bacteria

In a second study (Walker et al, Science, 341: 1079-1089, 2013) the intestines of germ free mice were colonized with gut bacteria from lean and obese humans. The results were essentially the same as in the first study. That is, the mice who received gut bacteria from lean humans stayed lean and those who received gut bacteria from obese humans became obese.

But then the investigators asked two really interesting questions:

1) If you mixed the two types of bacteria, which one would win “the battle of the bacteria”?

For this experiment they took mice that had received gut bacteria from lean humans and mice that had received gut bacteria from obese humans and put them in the same cage. It turns out that since mice eat each other’s poop, they pick up each other’s intestinal bacteria. (No, I am not suggesting that you…)

The results of this experiment were (envelop please): The “lean” bacteria won out. They became the predominant bacteria in the intestines of all of the mice in the cage. Furthermore, none of the mice became obese – even the ones that had originally been inoculated with gut bacteria from obese humans.

2) Are the types of bacteria in the intestine influenced by diet?

In the previous experiment the mice were eating standard mouse chow – which is pretty healthy if you are a mouse. So the investigators decided to ask what would happen if they ate foods that were similar to really good and really bad human diets. They devised two types of diets for the mice – one that was high in fresh fruits & vegetable and low in fat (the good diet) and one that was high in fat and low in fresh fruits and vegetables (the bad diet).

On the good diet, the results were the same as in the previous experiment. On the bad diet the “lean” bacteria never grew in the intestines of the mice inoculated with bacteria from obese humans and those mice went on to become obese.

This study confirmed that the wrong kind of gut bacteria can cause obesity, but it also showed that diet can influence the type of bacteria that can grow in the intestine – something I talked about in an earlier issue of “Health Tips From the Professor” Our Gut Bacteria Are What We Eat.

The Bottom Line

1) Does this mean that you should rush out and buy some probiotics (good bacteria) as part of your weight loss strategy? The simple answer is no. That would be premature. These studies were performed in mice. Although similar results have been reported in humans (for example, Jumpertz et al, Am. J. Clin. Nutr., 94: 58-65, 2011), those studies are very preliminary at present. In addition, genetics and diet obviously played a role in the results. In short, we are a long way from knowing to what extent intestinal bacteria might contribute to obesity in humans.

2) However, there are many very good reasons to make sure that you supply friendly bacteria to your intestinal track on a regular basis. For example, we know that bad bacteria in your intestine can compromise your immune system, convert foods that you eat to cancer causing chemicals, and cause chronic inflammation – which contributes to a number of major diseases. Can gut bacteria make you fat? We can’t yet say whether good bugs will help keep you slim, but we do know that they can help keep you healthy.

3) Finally, while we can’t yet say whether probiotic supplements can help you lose weight, it is becoming increasing clear that healthy diets (low fat, high fiber diets with lots of fresh fruits and vegetables) support the type of intestinal bacteria that can make you slim. This is yet one more reason why a healthy diet is so important if you want to stay slim and healthy.

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 Grilled Meat Increase Prostate Cancer Risk?

July 5, 2014July 1, 2014 by Dr. Steve Chaney

Author: Dr. Stephen Chaney

Want Cancer With That Burger?

Its summer and you have most likely already visited a backyard bbq. One question that you probably won’t hear from your host or hostess is “Would you like some cancer with that burger?” But, perhaps that is exactly the question that they should be asking.

You probably already knew that red meat consumption may increase your risk of cancer. But, did you know that grilling that red meat may increase your risk of cancer even more?

You probably didn’t really want to know that when fat from the meat hits the hot coals, carcinogens form that are deposited on the meat.

You probably also didn’t want to know that when you cook meat to high temperatures the amino acids in the meat combine to form cancer causing substances.

And you really didn’t want to know that a recent study showed that people who consume well-done red meat were 60% more likely to develop advanced pancreatic cancer.

Does Grilled Meat Increase Prostate Cancer Risk?

This study compared 531 people ages 40-79 who had recently been diagnosed with advanced prostate cancer with 527 matched controls. Both groups were asked about their dietary intake of meats, usual meat cooking methods and doneness of the meat.

The results were quite striking:

Increased consumption of hamburgers was associated with a 79% increased risk of advanced prostate cancer.

Increased consumption of processed meat was associated with a 57% increased risk of advanced prostate cancer.

Grilled red meat was associated with a 63% increased risk of advanced prostate cancer.

Well done red meat was associated with a 52% increased risk of advanced prostate cancer.

However, those percentages are a little bit difficult to compare, because “increased consumption” was defined relative to what the usual consumption or cooking practice was. So put another way, weekly consumption of…

3 or more servings of red meat or…

1.5 or more servings of processed meat or…

1 or more servings of grilled or well done red meat…

…were associated with a 50% increased risk of advanced prostate cancer.

In contrast, consumption of white meat was not associated with increased cancer risk, no matter what the cooking method was used.

Is It Possible To Enjoy Your Cookouts Without Increasing Cancer Risk?

Our local newspaper recently carried some tips by Dr. Denise Snyder from the Duke University School of Nursing in Durham, NC on how you could reduce the risk of giving your guests cancer the next time you are the chef at your backyard bbq.

Here are her suggestions:

Grill fruits and vegetables instead of meat. That was her idea, not mine. My editorial comment would be that grilling white meat (fish or chicken) is also OK.

Use the lowest temperature that will cook your food thoroughly and keep the grill rack as high as possible.

Use a meat thermometer so that you can make sure that as soon as the meat is thoroughly cooked you remove it from the grill. We usually overcook the meat to make sure that it is done.

Shorten your grill time by microwaving the meat first, using thinner leaner cuts of meat or cutting up the meat and making kabobs.

Trim as much fat from the meat as possible before you cook it.

Line your grill rack with aluminum foil poked with holes. This allows the fat to drip down but minimizes the exposure of the meat to the carcinogens formed when the fat hits the coals.

Marinate your meats before grilling. That has been shown to reduce the formation of cancer causing chemicals.

And, of course, avoid processed meats like hot dogs and sausage completely because they have been shown to increase the risk of cancer and diabetes (British Journal of Cancer, 106: 603-607, 2012; American Journal of Clinical Nutrition, doi: 10.3945/ajcn.111.018978, 2011) no matter how they are cooked.

So here’s to a healthier backyard bbq. Bon appétit!

The Bottom Line

1) You already knew that red meat and processed meats may increase your risk of cancer, but how you cook your red meat also matters. Grilling your meat and/or cooking it until it is well done appear to significantly increase your risk of developing advanced prostate cancer.

2) In contrast, consumption of white meat was not associated with increased cancer risk, no matter what the cooking method was used.

3) I’ve included several tips on how you can reduce the cancer risk associated with grilling red meats in the article above so you can enjoy both your cookouts and your health.

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

Do Diet Sodas Make You Fat?

June 24, 2014 by Dr. Steve Chaney

Should You Kick the Diet Soda Habit?

Author: Dr. Stephen Chaney

We are consuming ever increasing amounts of diet sodas to combat the obesity epidemic. In 1960 14% of the U.S. population was obese and 3.3% of us consumed diet sodas. By 2010 41% of the U.S. population was obese and 20% of us were consuming diet sodas. It’s pretty clear that diet sodas aren’t helping us solve the obesity epidemic, but are they actually part of the problem?

You’ve probably seen the headlines questioning whether diet sodas actually help you lose weight. In fact many of the headlines imply the diet sodas will cause you to gain weight. Two of the more sensational headlines I came across said “Think diet sodas help you lose weight? Not so, Purdue study finds”, and “Can diet sodas actually cause more weight gain than regular sodas?”

Let me start with the first headline. The Purdue publication referred to in the headline (Swithers, Trends in Endocrin. & Metab., 24: 431-441) wasn’t really a study, it was an opinion piece. That simply means that it was a review where the references were selected on the basis of the author’s opinion. That’s OK if you clearly label it as an opinion piece, which Dr. Swithers did.

Now for the second headline: There is no good evidence that diet sodas will cause you to gain more weight than regular sodas. However, a number of published studies suggest that consumption of diet sodas is associated with weight gain – sometimes just as much weight gain as consumption of the sugar sweetened sodas they replace.

Do Diet Sodas Make You Fat?

The evidence that Dr. Swithers (Trends in Endocrin. & Metab., 24: 431-441) cited was pretty impressive.

For example, the San Antonio Heart Study recorded consumption of diet sodas and regular sugar sweetened sodas in 3,862 adults (average age 44) and measured the increase in BMI (a measure of obesity) over the next 7-8 years. That study found:

Individuals consuming >21 diet sodas/week were almost 2-fold more likely to become overweight or obese than individuals consuming no sodas.

There was a clear dose response effect, with a 41% increased risk of becoming overweight or obese for each can or bottle of diet soda consumed/day.

The increase in weight associated with diet soda consumption was just as great for those who were at normal weight at the beginning of the study as it was for those who were obese at the beginning of the study.

In this study the increase in weight associated with soda consumption was greater for diet sodas than it was for regular sodas.

Another major study (Circulation, 116: 480-488, 2007) recorded diet and regular soda consumption in 6039 participants in the Framingham Heart Study (average age 53) and measured the increase in obesity (along with other parameters associated with metabolic syndrome or pre-diabetes) over the next 4 years. This study found:

Individuals consuming one or more sodas/day had a 48% increased risk of becoming obese compared to people with infrequent soda consumption.

In this study the weight increase associated with soda consumption was virtually the same for diet sodas and regular sodas.

Are These Studies True?

These, and similar studies have been criticized because they are looking at associations, which do not prove cause-and-effect. For example, it’s not always clear whether the people in those studies gained weight because they were consuming diet sodas or consumed diet sodas because they were overweight.

That argument is less persuasive for the San Antonio Heart Study, because the weight gain associated with diet soda consumption was also seen with people who were at normal weight at the beginning of the study. Still there is a need for good double blind, placebo controlled intervention studies.

There have been very few intervention studies in which one group of subjects were told to drink only diet sodas and the other group only regular sodas. Unfortunately, in those studies the total caloric intake of the diet soda group was also restricted. So while the diet soda group did lose weight, it’s not clear whether that weight loss was due to the diet sodas or the overall caloric restriction of the diet.

You may have also seen the recent headlines from a study showing that people consuming diet sodas gained no more weight than people consuming water (Obesity, 22: 1415-1421, 2014). But once again, both groups were given detailed instructions on how to restrict total calories. Almost any diet will work if you have a dietitian looking over your shoulder and telling you how to restrict calories.

So what is the average consumer to think? On the one hand, dietitians and health professionals are telling you to drink diet sodas if you want to lose weight. On the other hand, you keep seeing these headlines saying the diet sodas may not help you lose weight or may even cause you to gain weight.

Of all the recent blogs and online articles on the topic, the only one I actually recommend reading is from WebMD (http://www.webmd.com/diet/features/diet-sodas-and-weight-gain-not-so-fast).

WebMD often adheres to the AMA line, but I found this to be a very balanced analysis of the science behind the question of whether diet sodas help or hinder weight loss.

How Could Diet Sodas Possibly Cause Weight Gain?

The million dollar question is: How could diet sodas possibly cause weight gain? After all, they contain no calories. I think the most useful perspective from the Web MD article is that it’s probably not the diet sodas themselves that cause weight gain. It’s what we eat with the diet sodas that cause the weight gain. Here are a couple of quotes I found particularly enlightening.

Dr. Barry Popkin, a colleague from the University of North Carolina, calls it the “Big Mac and Diet Coke” mentality. He says: “Especially in America, we have a lot of people who eat high-fat, high-sugar diets, but also drink diet sodas.”

Why is that? Dr. David Katz from Yale University has research suggesting that artificial sweeteners may condition people to want to eat more sweet foods. He says: “Our taste buds don’t really differentiate between sweet in sugar and sweet from, say, aspartame. The evidence that this sweet taste is addictive is pretty clear. What I have seen in my patients is that those who drink diet soda are more vulnerable to processed foods with added sugars.”

There is some independent evidence to back up that hypothesis. For example, one recent study showed that rats given artificially sweetened yoghurt with their rat chow ate more rat chow and gained more weight than rats fed sugar-sweetened yoghurt with their rat chow (Behavioral Neuroscience, 122: 161-173, 2008). Another study in humans showed that consumption of artificial sweeteners activates a portion of the brain associated with cravings for sweets (Physiology & Behavior, 107: 560-567, 2012).

However, this viewpoint is controversial. Some experts think that the association between diet sodas and weight gain is psychological rather than physiological. Simply put, when people consume diet drinks they feel that they can splurge elsewhere.

The Bottom Line

Once again there is no magic bullet. There is no good evidence that diet sodas will help you lose weight unless you carefully control the calories in everything else you eat. And, diet sodas may just cause you to gain weight because they make you crave the very foods that are worst for your waistline.

In addition, there may be other good reasons not to consume diet sodas. For example, recent studies have shown that consumption of diet sodas may be linked to increased risk of metabolic syndrome or pre-diabetes (Circulation, 116: 480-488, 2007) and heart disease (see Does Sugar Cause Heart Disease? and Can Soft Drinks Cause Heart Disease?

My recommendations are to drink water, herbal teas, unsweetened tea & coffee or unsweetened mineral water or seltzer – perhaps with a splash of fruit juice.

Finally, there is no substitute for a healthy, calorie controlled diet; exercise; and lifestyle change if you want to lose weight and keep it off.

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 Sugar Cause Heart Disease?

June 17, 2014 by Dr. Steve Chaney

Is Sugar No Longer Your Best Friend?

Author: Dr. Stephen Chaney

Sugar has gotten a lot of bad press in recent years. You’ve probably already heard that high sugar intake is associated with inflammation, obesity and diabetes. As if that weren’t bad enough, the latest headlines proclaim that added sugar may also increase our risk of fatal heart disease. Are those headlines true? And if they are true, what should you do about it?

Sugar Basics – The Truth About Sugar

There are three facts about sugar that almost every expert agrees with:

The sugars that occur naturally in foods like fruits and vegetables are generally not a problem unless you are a diabetic. It is the added sugars in our diet that we should be concerned with.

The amount of added sugars in the American diet has increased dramatically since the founding of this country. Based on data from the US Department of Commerce and the USDA, the amount of added sugar in the American diet has gone from 6.3 pounds/year in 1822 to over 100 pounds/year in 2000. Put another way, we have gone from consuming the amount of sugar in a 12 oz soda every 5 days in 1822 to every 7 hours in 2000.

The lion’s share of that added sugar is coming from sodas and similar sugary beverages. The amounts are: sodas and other sugar-sweetened beverages (37.1%), grain-based desserts (13.7%), fruit drinks (8.9%), dairy desserts (6.1%) and candy (5.8%).

Beyond that there is little agreement among experts. When I was a young man the sugar “villains” were glucose and sucrose. Then it was sugar alcohols. Today it is high-fructose corn syrup and maltodextrin. Tomorrow it will be something else.

In reality there are no sugar heroes and no sugar villains. The harmful effects of added sugars are based almost entirely on:

The amount of added sugars in the diet…and…

The type of foods those added sugars are found in.

For more information, watch my video “The Truth About Sugar”.

Does Sugar Cause Heart Disease?

The study behind the headlines (Yang et al, JAMA Internal Medicine, 174: 516-524, 2014) followed 11,733 participants in the 3^rd National Health And Nutrition Examination Survey (NHANES III) for an average of 14.6 years. (NHANES studies are designed to represent a cross section of the adult US population). Sugar intake was based on the average of two dietary surveys for most of the participants, and cardiovascular deaths were determined from the NHANES III Linked Mortality Files.

The average intake of added sugar in the American population was around 16% of total calories (compared to around 1% of total calories in 1822). For comparison purposes, the authors divided the population into three groups based on added sugar consumption:

Those consuming less than 10% of calories from added sugar (28.6% of the population).

Those consuming between 10% and 25% of calories from added sugars (46.4% of the population).

Those consuming more than 25% of calories from added sugars (25.0% of the population).

When the groups with the 10-25% and >25% of calories from added sugars were compared to the <10% group with respect to cardiovascular deaths, the results were pretty striking.

The group consuming 10-25% of calories from added sugars had a 30% increased risk of dying from heart disease

And the group consuming >25% of calories from added sugars had a 275% increased risk of dying from heart disease!

This association between added sugar consumption and risk of cardiovascular death was independent of age, sex, race/ethnicity, educational attainment, physical activity, HEI score (a measure of overall diet quality and BMI (a measure of obesity).

The Strengths And Weaknesses of This Study

Strengths:

This was a particularly large, well designed study.

This study is consistent with a number of early studies suggesting that added sugar intake increases the risk of cardiovascular death. See, for example “Can Soft Drinks Cause Heart Disease?”

Weaknesses:

The main weakness of this study is that it measures associations only. It does not prove cause and effect.

Should You Switch To Diet Sodas?

You may be thinking that you should switch to diet sodas – and perhaps artificially sweetened snacks and desserts as well. It only makes sense that if sugar is the problem, artificial sweeteners must be the answer. Wrong! The latest research suggests that diet sodas may be just as bad as the sugar-sweetened sodas.

I have already shared one study with you that linked consumption of diet sodas with increased risk of heart disease (see “Can Soft Drinks Cause Heart Disease?”). The link between diet sodas and heart disease has now been supported by another major clinical study reported by Dr. Ankur Vyas from University of Iowa, March 30, 2014 at the American College of Cardiology’s 63^rd Annual Scientific Session.

This study followed 60,000 women with an average age of 62.8 years who were enrolled in the Woman’s Health Initiative Observational Study for 9 years. They reported that compared to women who never or rarely drank diet sodas, those who consumed two or more diet sodas/day were:

30% more likely to suffer heart attacks and strokes…and…

50% more likely to die from cardiovascular disease.

What Can You Drink?

By now you are probably asking yourself: “If regular sodas, diet sodas, other sugary and diet beverages, and even most fruit juices are out, what else can I drink? Is there anything left?”

It’s not quite as daunting as it seems at first. It may take some time to re-educate your taste buds, but your health is worth it. Here are some healthy alternatives:

My #1 recommendation is always water. If you crave some flavor, add lemon, mint, or your favorite fruits. Herbal teas are another flavorful, healthy choice.

If you crave caffeine, go for green tea, regular tea or coffee – without sweeteners, of course.

If you crave the carbonation, start with unsweetened mineral water or seltzer and add you favorite flavorings.

The Bottom Line:

1) The evidence is getting stronger every day that too much added sugar in our diet is linked to increased risk of death from cardiovascular disease. If you are consuming >25% of calories from added sugars the increased risk is almost 3-fold!

2) The evidence from this study suggests that it would be prudent to keep added sugars below 10% of calories. For most Americans this represents around 200 calories/day from added sugars. That compares with the World Health Organization’s recommendation that added sugars be <10% of calories, the Institute of Medicine’s recommendation that added sugars be <25% of calories, and the American Heart Association’s recommendation that added sugars be <100 calories for women and <150 calories for men.

3) There are no sugar heroes and villains. The amount of added sugar in the diet is much more important than the kind of sugar. The food that the sugar is found in is also very important, with sodas and similar sugar-sweetened beverages being the worst offenders (See my video “The Truth About Sugar” for more information).

4) Artificial sweeteners are not the solution. A recent study with postmenopausal women suggests that consumption of as few as two diet sodas a day increases the risk of heart attacks and strokes by 30% and cardiovascular death by 50%.

5) Don’t despair. You won’t have to go thirsty. There are lots of healthy alternatives available (see above).

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

Are The Benefits Of Resveratrol A Myth?

June 10, 2014 by Dr. Steve Chaney

Is Resveratrol Dead?

Author: Dr. Stephen Chaney

It 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.

Can Chocolate Help You Lose Weight?

June 3, 2014 by Dr. Steve Chaney

A Candy a Day Keeps The Weight Away?

Author: Dr. Stephen Chaney

Sometimes you come across news that just seems too good to be true. The recent headlines saying that you can lose weight just by eating chocolate are a perfect example. Your first reaction when you heard that was probably “Sure, when pigs fly!”

But, it’s such an enticing idea – one might even say a deliciously enticing idea. And, in today’s world enticing ideas like this quickly gain a life of their own. Two popular books have been written on the subject. Chocolate diet plans are springing up right and left. A quick scan of the internet even revealed a web site saying that by investing a mere $1,250 in a training course you could become a “Certified Chocolate Weight Loss Coach” earning $50,000/year.

If you like chocolate as much as most people you are probably wondering could it just possibly be true?

Can Eating Chocolate Help You Lose Weight?

The idea that chocolate could help you lose weight does have some support. There are actually three published clinical studies suggesting that chocolate consumption is associated with lower weight (European Journal of Clinical Nutrition, 62: 247-253, 2008; Nutrition Research, 31: 122-130, 2011; Archives of Internal Medicine, 172: 519-521, 2012).

While that sounds pretty impressive, they were all cross-sectional studies. That means they looked at a cross section of the population and compared chocolate intake with BMI (a measure of obesity). Cross sectional studies have a couple of very important limitations:

1) Cross sectional studies merely measure associations. They don’t prove cause and effect. Was it the chocolate that caused the lower weight, or was it something else that those populations were doing? We don’t really know.

2) Cross sectional studies don’t tell us why an association occurs. In many ways this is the old chicken and egg conundrum. Which comes first? In this case the question is whether the people in the studies became obese because they ate less chocolate – or did they eat less chocolate because they were obese and were trying to control their calories? Again, we have no way of knowing.

If Pigs Could Only Fly

Chocolate is relatively rich in fat and high in calories. It’s not your typical diet food. On the surface it seems fairly implausible that eating chocolate could actually help you lose weight.

Scientists love to poke holes in implausible hypotheses, so it is no surprise that a recent study (PLOS ONE, 8(8) e70271) has poked some huge holes in the “chocolate causes weight loss” hypothesis.

This study analyzed data from over 12,000 participants in the Atherosclerosis Risk in Community (ARIC) Study. This was also a cross sectional study, but it was a prospective cross sectional study (That’s just a fancy scientific term which means that the study followed a cross section of the population over time, rather than just asking what that population group looked like at a single time point).

The authors of the study assessed frequency of chocolate intake and weight for each individual in the study at two separate time points 6 years apart. The results were very interesting:

When they looked at a cross section of the population at either time point, their results were the same as the previous three studies – namely those who consumed the most chocolate weighed less. So the data are pretty consistent. Overweight people consume less chocolate. But, that still doesn’t tell us why they consume less chocolate.

However, when they followed the individuals in the study over 6 years, those who consumed the most chocolate gained the most weight. The chocolate eaters were skinnier than the non-chocolate eaters at the beginning of the study, but they gained more weight as the study progressed. And, the more chocolate they consumed the more weight they gained over the next 6 years. [No surprise here. Calories still count.]

When they specifically looked at the population who had developed an obesity related illness between the first and second time point, they found that by the end of the study those participants had:

– Decreased chocolate intake by 37%

– Decreased fat intake by 4.5%

– Increased fruit intake by 20%

– Increased vegetable intake by 17%

In short, this study is more consistent with the “obesity causes reduced chocolate intake” model than the “reduced chocolate intake causes obesity” model. Simply put, if you are trying to lose weight, sweets like chocolate are probably among the first things to go.

Of course, even prospective cross sectional studies have their limitations. Double blind, placebo controlled studies are clearly needed to resolve this question. The only published study of this type has reported a slight weight gain associated 25 g/day of dark chocolate, but the study was too small and too short in duration to draw firm conclusions.

In summary, more studies are needed, but the current evidence does not support the “miracle diet food” claims for chocolate.

The Bottom Line:

1) Pigs still haven’t learned how to fly. As enticing as it may sound, the weight of current evidence does not support the claims that chocolate is a miracle diet food or that eating chocolate every day is a sensible strategy for losing weight.

2) On the other hand, dark chocolate is probably one of the healthier dessert foods. There is no reason not to enjoy an occasional bite of chocolate as part of a healthy, calorie-controlled 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.