Can Diet Alter Your Genetic Destiny?

Disease Is Not Inevitable

Author: Dr. Stephen Chaney

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

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

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

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

Can Diet Alter Your Genetic Destiny?

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

1)     Your genetic makeup can influence your nutrient requirements.

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

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

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

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

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

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

3)     Diet can actually alter your genes.

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

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

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

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

Examples Of How Diet Can Alter Genetic Predisposition

Mature Man - Heart Attack Heart Disease

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

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

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

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

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

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

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

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

Cancer

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

Diabetes

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

Cellular Stress Response

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

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

Obesity

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

The Bottom Line:

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

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

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

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

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

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

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

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

Do Selenium & Vitamin E Increase Prostate Cancer Risk?

Should Men Avoid Those Supplements?

 Author: Dr. Stephen Chaney

Vitamin EYou’ve probably seen the headlines saying “Supplementation with selenium and vitamin E increases the risk of prostate cancer.” The authors of the study even said “Men aged greater than 55 should avoid supplements with either vitamin E or Se (selenium) at doses that exceed recommended dietary intakes.”

In a recent “Health Tips From The Professor” I debunked the headlines saying “Omega-3 fatty acids increase prostate cancer risk“.

What about vitamin E and selenium? Is it true that they increase prostate cancer risk? If you are a man over 55, should you be concerned? Should you stop using supplements containing vitamin E and selenium?

Do Selenium & Vitamin E Increase Prostate Cancer Risk?

Previous Studies On Selenium, Vitamin E And Prostate Cancer Risk

The study that generated the initial excitement in the field was the Nutrition Prevention of Cancer (NPC) Trial that ended in 1998 (Clark et al, British Journal of Urology, 81: 730-734, 1998; Duffield-Lillico et al, British Journal of Urology, 91: 608-612, 2003).

That study showed that supplementing men who had low blood levels of selenium with 200 ug/day of selenium decreased their prostate cancer risk by 65%.

It was followed by a second, much larger trial called the Selenium and Vitamin E Cancer Prevention Trial (SELECT) (Lipmann et al, JAMA, 301: 39-51, 2009). It looked at supplementation with 200 ug/day of selenium and/or 400 IU/day of synthetic alpha-tocopherol.

The SELECT study found no protective effect of either selenium or vitamin E on prostate cancer risk, but did suggest that vitamin E might actually cause a slight increase in prostate cancer risk.

The Study That Generated The Headlines

The authors of the study that generated the recent headlines (Kristal et al, Journal of the National Cancer Institute, doi: 10.1093/jnci/djt456, 2014) were attempting to find a simple explanation for the unexpected results of the SELECT study.

They hypothesized that the baseline selenium status at the beginning of the study might have influenced the outcome of supplementation. Kristal et al reanalyzed the data from the SELECT trial, comparing the effect of selenium and vitamin E supplementation in men with low selenium status and men with high selenium status.

However, at face value their data were confusing rather simplifying. They found:

  • Supplementation with selenium had no effect on prostate cancer risk in men with low selenium status, but increased prostate cancer risk by 91% in men with high selenium status.
  • Conversely, supplementation with 400 IU of vitamin E had no effect on prostate cancer risk in men with high selenium status, but increased prostate cancer risk by 63% in men with low selenium status.

Based on this hodge-podge of data, they concluded that “Men aged greater than 55 should avoid supplements with either vitamin E or Se (selenium) at doses that exceed recommended dietary intakes.” That was the statement that generated the headlines. Was that recommendation justified?

What Do Other Experts Say?

There was an editorial evaluation of the paper by some of the top expects in the field in the same journal (Frankel et al, Journal of the National Cancer Institute, doi: 10.1093/jnci/dju005, 2014) that provided thoughtful explanations of the confusing data in the paper by Kristal et al. They examined three questions:

1)     Why did the SELECT study find no effect of selenium supplementation in men with low selenium status, while the earlier NPC trial found a 65% decrease in prostate cancer risk?

  • The authors of the editorial pointed out that the lowest baseline selenium status in the SELECT trial was much higher than the lowest baseline selenium status in the previous NPC trial. In fact the baseline selenium status in the SELECT trial was at a level in which no effect of selenium supplementation would have been expected based on the results from the NPC trial.

The authors speculated that the addition of selenized yeast to animal feed has improved selenium status in the US population to the point where selenium supplementation can no longer be expected to reduce prostate cancer risk.

2)     Why did selenium supplementation increase prostate cancer risk in men with high selenium status, but not in men with low selenium status?

  • The authors pointed out that for selenium there is a very narrow range between sufficient intake and toxicity. The daily value (DV) for selenium is 90 ug/day and the recommended upper limit (UL) for selenium intake is 400 ug/day.

The average selenium intake for adult men in this country is 151 ug/day. That’s just the average. It’s not hard to imagine that adding 200ug/day of selenium to men at the highest selenium intake could move them into the toxic range.

3)     Why did vitamin E supplementation increase prostate cancer risk in men with low selenium status, but not in men with high selenium status?

  • In part, the authors felt that the pure alpha-tocopherol used in the SELECT trial was not optimal. Pure alpha-tocopherol interferes with the absorption of the other naturally occurring forms of vitamin E, such as gamma-tocopherol – which is the form of vitamin E that decreases prostate cancer risk in animal studies.
  • The authors also noted that vitamin E and selenium work together to inactivate free radicals in cell membranes. Vitamin E reduces the free radicals to a chemically unstable intermediate that still has the potential to damage membranes. A selenium-containing enzyme is required to convert that unstable intermediate into a completely harmless compound.

So when vitamin E is present in much higher levels than selenium, as it was in the group with low baseline selenium status, unstable radicals can accumulate and membrane damage can occur. The authors felt that this was the most likely explanation of the increased prostate cancer risk when men with low selenium status were supplemented with high dose vitamin E.

The authors of the editorial had a much more nuanced interpretation of the data reported by Kristal et al. If you read their evaluation carefully you would likely conclude that you should avoid high dose selenium supplements. However, rather than simply avoiding vitamin E supplements, you should choose vitamin E supplements that contain all of the naturally occurring vitamin E forms and contain near DV amounts of selenium.

These recommendations would be a much better fit to the data, but don’t lend themselves to dramatic headlines – so the editorial has been largely ignored by the press.

The Bottom Line:

1)     Ignore the scary headlines about selenium and vitamin E causing prostate cancer. You can continue to use your supplements as long as you choose ones that are well balanced.

2)     Conversely, if you are at risk of prostate cancer, there is no good evidence that supplementation with either selenium or vitamin E will reduce your risk.

3)     The results of this study are fully consistent with my longstanding recommendation to follow a holistic approach to supplementation and to avoid high dose single nutrient supplements.

4)     There is no reason to supplement with 200 ug/day of selenium. If you are already getting good amounts of selenium from your diet, that dosage could be toxic and may actually increase your risk of cancer. Make sure that your supplements have no more than the DV (70 ug) of selenium.

5)     Avoid high purity alpha-tocopherol supplements. Look for vitamin E supplements containing the full spectrum of tocopherols and tocotrienols in addition to alpha-tocopherol. In addition, make sure that your vitamin E supplement also contains selenium at near DV levels.

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

Are Multivitamins A Waste Of Money?

Don’t Throw Your Vitamins Away Yet

Author: Dr. Stephen Chaney

ProfessorThe Professor is annoyed. Two things really irritate me:

  • Charlatans who cherry pick studies to “prove” that their snake oil supplements will cure what ails you.
  • Doctors who proclaim that vitamins are a waste of money without understanding the science behind the studies they are quoting.

Are Multivitamins A Waste Of Money?

You’ve seen the headlines telling you that “the experts” have concluded that multivitamins are a waste of money. You might be wondering “What’s behind these headlines? Who are these experts, and what is their evidence?”

Let’s start at the beginning. 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 is an opinion piece, not a scientific study. It represents the opinion of five very prominent doctors, but it is, at the end of the day, just their opinion. Many other well respected experts disagree with their opinion.

They based their editorial on three recently published studies:

  • The first study reported that vitamin and mineral supplements did not decrease the risk of heart disease and cancer in healthy individuals (Fortmann et al., Annals of Internal Medicine, 159, doi: 10.7326/003-4815-159-12-201312170-00729)
  • The second study reported that multivitamins did not affect cognitive function in healthy male physicians aged 65 and older (Gradstein et al, Annals of Internal Medicine, 159, 806-814, 2013)
  • The third study concluded that multivitamins did not reduce the risk of a second heart attack in patients who had previously had a heart attack and were receiving appropriate medical therapy.

These were all large, well designed studies, so it would be tempting to conclude that the headlines were right. Maybe vitamins are a waste of money.

But, what if the whole underlying premise of these studies was flawed? Let’s examine that possibility by examining the flawed premises behind these and other studies.

What’s Wrong With These Studies?

#1) These studies were too narrowly focused.

MultivitaminsMultivitamins and individual vitamins and minerals are not magic bullets. They are not drugs. They are meant to fill nutritional gaps in our diet – not prevent or cure disease. We should be asking whether holistic approaches can prevent or cure disease – not whether individual nutrients can do so.

One of the examples that I love to use, because it really made an impression on me as a young scientist, occurred at an International Cancer Symposium I attended more than 30 years ago. I attended a session in which an internally renowned expert was giving his talk on colon cancer. He said, “I can show you, unequivocally, that colon cancer risk is significantly decreased by a lifestyle that includes a high-fiber diet, a low-fat diet, adequate calcium, adequate B-vitamins, exercise and weight control. But I can’t show you that any one of them, by themselves, is effective.”

The question that came to me as I heard him speak was: “What’s the message that a responsible scientist or responsible health professional should be giving to their patients or the people that they’re advising?” You’ve probably heard experts saying:

  • “Don’t worry about the fat content of your diet. It can’t be shown to increase the risk of colon cancer.”
  • “Don’t worry about calcium. It doesn’t decrease the risk of colon cancer”
  • “Don’t worry about B-vitamins. They don’t decrease the risk”
  • “Don’t worry about fiber. It can’t be shown to decrease the risk either”

But, is that the message that we should be giving people – that nothing matters? Shouldn’t we really be saying what that doctor said many years ago – that a lifestyle that includes all of those things significantly decreases the risk of colon cancer?

#2) These studies were destined to fail.

It’s almost impossible to prove that any single intervention prevents disease when you are starting with a healthy population (something we scientists refer to as a primary prevention study).

For example, in “Health Tips From the Professor” just a couple of weeks ago I shared with you that even when you combine all of the published studies with tens of thousands of patients, it is impossible to prove that stain drugs prevent heart attacks in healthy individuals.

If you can’t show that statins prevent heart disease in healthy people, why would you expect to be able to show that vitamins or minerals prevent heart attacks in healthy people?

I can’t resist pointing out that this perfectly illustrates the pro-drug, anti-supplement bias that is so prevalent among many of my medical colleagues. I haven’t seen a single editorial or headline suggesting that statin drugs might be a waste of money for healthy individuals.

#3) These studies simply asked the wrong questions.

For example, the third study described in the editorial was asking whether multivitamins reduced the risk of a second heart attack in patients who were receiving “appropriate medical therapy”. What does “appropriate medical therapy” mean, you might ask? It means that those patients were on 4 or 5 drugs, with all of their side effects.

In reality the study was not asking whether multivitamins reduced the risk of a second heart attack. The study asked whether multivitamins had any additional benefits for individuals who were taking 4 or 5 drugs to reduce their risk of a second heart attack. That’s a totally different question.

There are lots of examples of this paradigm. For example, 17 years ago the Cambridge Heart Antioxidant Study showed that vitamin E significant decreased heart attack risk in patients with severe cardiovascular disease (Stephens et al, The Lancet, 347: 781-786, 1996). Patients in that study were taking one or two medications. However, in today’s world that would be considered unethical. The standard medical treatment for high risk heart disease patients today is 4 or 5 drugs, and when patients are receiving that many medications it is no longer possible to demonstrate a benefit of vitamin E. The story is similar for omega-3 fatty acids.

That poses a dilemma. What recent studies show is that individual nutrients don’t reduce the risk of a second heart attack in someone who is receiving “standard of care” medical treatment.

But that’s not the question I am interested in. I’d like to know whether natural approaches might be just as effective as the drugs or whether natural approaches might allow one to use fewer drugs or lower doses. I’d like to avoid all of the side effects of those drugs if I could.

What about you? What questions would you like answered? Do these studies answer those questions?

What Was Overlooked In Those Studies

The studies did show conclusively that there were no harmful effects from supplementing except for high dose beta-carotene in smokers. Somehow that information never made it into the headlines.

The Bottom Line

  • Don’t pay much attention to the reports that supplements don’t work and are a waste of money. Those studies are fundamentally flawed.
  • Don’t pay much attention to the reports claiming that vitamins will hurt you. Except for beta-carotene in smokers the latest studies showed no evidence of harm.
  • On the other hand, don’t expect miracles from your vitamins. If you spend your time sitting in front of the TV set eating pizza & drinking sodas, popping a vitamin pill won’t prevent much of anything.
  • Finally, holistic approaches are often as effective as drug therapy – without the side effects. Your vitamins can be an important part of a holistic approach to better health that includes weight control, a good diet and exercise.

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 Cholesterol Lowering Drugs Right For You?

Do Statins Really Work?

Author: Dr. Stephen Chaney

Do statins really work?Statins – those ubiquitous drugs used to lower cholesterol levels – are big business!

Over 20 million Americans are currently being treated with statin drugs at a cost that runs into billions of dollars every year. And cardiologists have just recommended that another 20 million Americans consider using cholesterol lowering drugs. 44% of the men and 22% of the women in this country are now being told that they should be using statin drugs.

Some of my cardiologist friends are so convinced that statin drugs prevent death from heart attacks that they have said, only half-joking, that we should just add statins to the water supply.

Are Cholesterol-Lowering Drugs Right For You?

Is the faith of doctors in the power of statin drugs to prevent death from heart disease justified? To answer that question in full we need to look at people who have already survived a heart attack and people who have never had a heart attack separately.

If you’ve already had a heart attack the evidence is clear cut.

  • If you have had a heart attack, there is good evidence that statins will reduce your risk of dying from a second heart attack.
  • In the technical jargon of the scientific world that is referred to as secondary prevention.

But what about those millions of Americans who are being prescribed statin drugs who have never had a heart attack? This is something we scientists refer to as primary prevention.

What Do The Studies Actually Say About Statins And Primary Prevention?

Here the evidence is not clear at all. Two major reports have cast doubt on the assumption that statins actually do prevent heart attacks in people who have not already had a first heart attack.

In the first study, Dr. Kausik Ray and colleagues from Cambridge University in England performed a meta-analyis of 11 clinical studies involving over 65,000 participants (Ray et al, Arch. Int. Med., 170: 1024-1031, 2010). They focused on those participants in the studies who had not previously had a heart attack (primary prevention).

  • They found that the use of statins over an average of 3.7 years had no statistically significant effect on mortality. In short, statins had no effect on the risk of dying from heart disease or any other cause.
  • Dr. Sreenivasa Sechasai, one of the doctors involved in the study, said “We didn’t find a significant reduction in death despite having such a huge sample size. This is the totality of evidence in primary prevention. So if we can’t show a reduction with this data, it is unlikely to be there.”

The second study was a Cochrane Systemic Review of statins published January 19th, 2011.  It stated that there was not enough scientific evidence to recommend the use of statins in people with no previous history of heart disease with some caveats (see below).

To help you understand the significance of that conclusion, let me give you a bit of background:

  • First you need to understand that the Cochrane Collaboration is an independent, non-profit organization that carefully reviews the scientific evidence behind medical treatments and proposed medical treatments.
  • Cochrane Reviews are considered the “Holy Grail” of evidence-based medicine (ie. medicine based on the best scientific evidence rather than what the pharmaceutical companies would have you believe).
  • So when a Cochrane Review concludes that there isn’t enough evidence to recommend use of statins in patients with no prior history of heart disease that is pretty big news in the medical world.

How Should These Studies Be Interpreted?

Please don’t misinterpret what I am saying. The Cochrane Review said that statin drugs are overprescribed, but it did not say that everyone who has not had a heart attack will not benefit from statins. It said that there are a number of risk factors that need to be considered in evaluating individual patients for statin use.

  • Simply put, that means that it is not as simple as saying that everyone with no previous history of heart disease should not be on statin drugs.
  • If you are currently taking statin drugs and you have no previous history of heart disease, you may want to discuss with your physician whether the Cochrane Review of statin drugs changes their opinion of whether se of those drugs is still warranted for you.
  • But the bottom line is that only your physician is trained to take into account all of the factors that increase your risk of heart disease and the best therapeutic approach for reducing your risk of heart attack.

There Is A Double Standard In The Medical Community

More importantly, these studies highlight the difficulty in showing that anything works when you start out with a healthy group of adults with no prior evidence of disease (primary prevention).

And, the way that doctors have responded to primary prevention studies shows that there is a double standard in how primary prevention trials are interpreted in the medical community. For example:

  • There is no good evidence that statins prevent fatal heart attacks in healthy people.
  • However, because statins do work in high risk patients, most doctors recommend their use by millions of Americans who have never had a heart attack.
  • There is also no good evidence that nutrients like vitamin E and omega-3 fatty acids prevent fatal heart attacks in healthy people.
  • However, there is evidence that both vitamin E and omega-3 fatty acids prevent heart attacks in high risk patients, yet most doctors will tell you they are a waste of money.

It is food for thought.

The Bottom Line

1)    Statin drugs clearly save lives when used by people who have already had a heart attack.

2)    On the other hand, there is no proof that statin drugs prevent heart attacks in people who have not previously had a heart attack

3)    Statin drugs do have side effects. Increased risk of diabetes, liver damage, muscle damage and kidney failure are the best documented, although memory loss has also been reported.

4)    I am not recommending that you stop using statin drugs without consulting your doctor. I am suggesting that you discuss the benefits and risks of statin drug use with your doctor.

5)    Perhaps the most important poin tto come out of these studies is that it almost impossible to prove the benefit of any intervention in a primary prevention trial. If you can’t prove that statins work in healthy people, it is not surprising that it is difficult to prove that other interventions work.

6)   Finally, the way that these studies have been interpreted shows that there is a clear double standard in how the medical community evaluates primary intervention trials.

  • Statin drugs don’t show any benefit in a primary prevention setting, yet most doctors still recommend them.
  • Vitamin E and omega-3 fatty acids don’t show any benefit in a primary prevention setting, and most doctors recommend against them.

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.

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