Heart Disease

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devolutionResearch by an Iowa State University scientist due to be published this month in the journal Proceedings of the National Academy of Sciences indicates that cholesterol-lowering drugs (statins) may lessen brain function.

The results of the study show that drugs that inhibit the liver from making cholesterol may also keep the brain from making cholesterol, which is vital to efficient brain function.

“If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters,”, said Yeon-Kyun Shin, the lead researcher. “Neurotransmitters affect the data-processing and memory functions. In other words – how smart you are and how well you remember things.”

Cholesterol is abundant in the tissue of the brain and nervous system. Myelin, which covers nerve axons to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, is over one fifth cholesterol by weight. Even though the brain only makes up 2% of the body’s weight, it contains 25% of its cholesterol.

We now know that the formation of synapses, or connections between neurons, is directly dependent on the availability of cholesterol.

The formation of these synapses are what give us the ability to remember and learn. The benefits of sleep for memory formation and learning are in part a result of increased cholesterol synthesis during sleep.

“If you try to lower the cholesterol by taking medicine that is attacking the machinery of cholesterol synthesis in the liver, that medicine goes to the brain too. And then it reduces the synthesis of cholesterol which is necessary in the brain,” said Shin.

This study is yet another strike against statin drugs, which have numerous side effects and are not effective in reducing mortality for the vast majority of the population. Please see my recent article, The Truth About Statin Drugs, for more on why statins are probably not a good idea for you and your loved ones.

inflammationA recent study published in the American Journal of Pathology adds to the already considerable body of evidence which suggests that inflammation is a primary cause of heart attacks and strokes.

In an article I wrote last year, Preventing Heart Disease Without Drugs, I reviewed the current scientific understanding of what causes heart disease. If you’ve been following this blog, you know that inflammation and oxidative damage – not saturated fat and cholesterol – are the primary causes of heart disease.

I wrote:

Inflammation is the body’s response to noxious substances. Those substances can be foreign, like bacteria, or found within our body, as in autoimmune diseases like rheumatoid arthritis. In the case of heart disease, inflammatory reactions within atherosclerotic plaques can induce clot formation.

When the lining of the artery is damaged, white blood cells flock to the site, resulting in inflammation. Inflammation not only further damages the artery walls, leaving them stiffer and more prone to plaque buildup, but it also makes any plaque that’s already there more fragile and more likely to burst.

Oxidative damage is a natural process of energy production and storage in the body. Oxidation produces free radicals, which are molecules missing an electron in their outer shell. Highly unstable and reactive, these molecules “attack” other molecules attempting to “steal” electrons from their outer shells in order to gain stability. Free radicals damage other cells and DNA, creating more free radicals in the process and a chain reaction of oxidative damage.

Normally oxidation is kept in check, but when oxidative stress is high or the body’s level of antioxidants is low, oxidative damage occurs. Oxidative damage is strongly correlated to heart disease. Studies have shown that oxidated LDL cholesterol is 8x greater stronger a risk factor for heart disease than normal LDL.

The data from this study provide further support for the “oxidative response to inflammation” hypothesis described above. The researchers found that inflammation leads to a reduction of mature collagen in atherosclerotic plaques, leading to thinner caps that are more likely to rupture. This is important because other studies have shown that it is not atherosclerosis alone, but the rupture of the atherosclerotic plaques, that causes heart attacks and strokes.

It follows, then, that if we want to prevent heart disease we need to do everything we can to minimize inflammation and oxidative damage.

Top four causes of oxidative damage & inflammation

  1. Stress
  2. Smoking
  3. Poor nutrition
  4. Physical inactivity

By focusing on reducing or completely eliminating, when possible, the factors in our life that contribute to oxidative stress and inflammation, we can drastically lower our risk for heart disease.

For more in-depth information about each of these factors and how to minimize your risk of heart disease without drugs, please refer to Preventing Heart Disease Without Drugs.

eggs

ATTN: Bay Area Healthy Skeptic readers!

I am once again offering my free public talk next week in Berkeley, CA which debunks the myth that cholesterol causes heart disease. We’ll also explore the true causes of heart disease as well as simple dietary and lifestyle changes you can make to protect yourself and your loved ones.

If you have family or friends that live in the area that might benefit from this information, please let them know about the talk.

Thursday, January 29th from 7:00 – 9:00 PM

Acupuncture & Integrated Medicine College, Berkeley (AIMC Berkeley)
2550 Shattuck Avenue (at Blake)

10-minute walk south on Shattuck from Downtown Berkeley BART

510.666.8248 ext. 106

www.aimc.edu

For over 50 years, the medical establishment has vigorously promoted the notion that high cholesterol is a primary risk factor for coronary heart disease, and that a diet high in saturated fat and cholesterol causes heart disease. These hypotheses are widely accepted as fact by physicians and the general public alike, despite the overwhelming body of evidence that suggests otherwise.

During this two-hour talk, we’ll review scientific studies demonstrating that:

  1. High cholesterol is not the primary of cause heart disease..
  2. Diets high in saturated fat and cholesterol don’t cause heart disease.
  3. Consumption of so-called “heart healthy” vegetable oils is linked to heart disease, cancer and many other conditions.
  4. Statin drugs don’t reduce the risk of death for most people, and have dangerous side effects and complications.

You’ll also learn the latest theories on what causes heart disease and a truly “heart healthy” approach to diet and lifestyle that is supported by both modern science and centuries of traditional wisdom.

The presentation draws on more than 150 peer-reviewed studies published in major journals and the work of an impressive list of physicians, scientists and researchers who question the connection between cholesterol and heart disease.

pregnant womanBack in July I posted an article called Statins For Pregnant Women and Kids? criticizing a research study that actually recommended statins for pregnant women.

Well, it appears that even mainstream scientists are beginning to acknowledge the very real risks that statins present for pregnant mothers and fetuses.

Current clinical guidelines already recommend that women who are pregnant should stop taking statins but the advice is based on the knowledge that cholesterol is essential for normal fetal development.

But new research from The University of Manchester has shown that even water-soluble or ‘hydrophilic’ statins, such as pravastatin, can affect placental development leading to worse pregnancy outcomes.

According to Dr. Melissa Westwood, a Senior Lecturer in Endocrinology based at the Maternal and Fetal Health Research Centre at St. Mary’s Hospital, Manchester:

“Our study examined the effects that both lipophilic and hydrophilic statins had on a key biological system that is crucial for maintaining the normal function of the placenta, which acts as the nutrient-waste exchange barrier between mother and fetus.”

Fat-soluble statins like cerivastatin were already known to adversely affect the placenta, resulting in reducing growth. But the researchers also found that pravastatin – the water-soluble statin thought to be potentially compatible for use in pregnancy – had the same detrimental effect.

“These results clearly show that the effect of statins on the placenta is not dependent on their lipophilicity as had previously been suggested,” said Dr Westwood, whose findings are published in the Journal of Cellular and Molecular Medicine.

“While hydrophilic statins have not been reported to increase the incidence of fetal malformations, our research suggests that they will have a detrimental effect on placental growth, which is likely to result in poor pregnancy outcome.

“Healthcare professionals should continue to advise women to avoid the use of any type of statin once they plan to start a family or when a pregnancy is suspected or confirmed.

pill bottle with warningI’d like to bring your attention to two recently published studies which highlight the dangers of antidepressant drugs and maintaining low cholesterol levels.

Low Serum Cholesterol May Be Associated With Suicide Attempt History

I’ve written before about the association of low cholesterol with aggressive and violent behavior as well as an increased risk of suicide. A recent study published in the Journal of Clinical Psychiatry adds weight to the already considerable body of evidence suggesting that low cholesterol is dangerous to your health.

In this study ‘low cholesterol’ was defined as less than 160mg/dL (4.16 mmol/L). This level has been noted several times in the medical literature as a level below which suicide is more likely. And you should note that this level is well within what is considered ‘healthy’ by a cholesterol-lowering, drug pushing health industry.

This is consistent with studies showing that low blood cholesterol levels are associated with suicide and that cholesterol levels in certain areas of the brain are lower in those who commit suicide by violent means than in those who commit suicide by non-violent means.

Cholesterol is a health-promoting substance. It is a critical component of cell membranes, the precursor to all steroid hormones, a precursor to vitamin D, and the limiting factor that brain cells need to make connections with one another called synapses, making it essential to learning and memory.

If you understand the vital role cholesterol plays in health – especially in the brain – it’s not difficult to figure out why low cholesterol could increase the risk of suicide and violent behavior.

This is yet another reason to avoid cholesterol-lowering statin drugs. If you haven’t read it already, you might want to check out my post called Cholesterol Doesn’t Cause Heart Disease.

(J Clin Psychiatry October 21, 2008: e1-e8; pii: ej07m03866)

Two Antidepressants Taken During Pregnancy Linked To Heart Anomalies In Babies

In another disturbing study, researchers from Israel, Italy and Germany found that pregnant women taking two popular antidepressants, paroxetine (Paxil) and fluoxetine (Prozac), were three and four times more likely to give birth to children with heart problems.

Researchers have advised women taking the drugs to continue unless they are advised to stop by their doctor or consultant.

I’ve written extensively here about the risks of antidepressant drugs, especially for pregnant women. In my recent post Statins For Pregnant Women and Kids? I presented evidence that statin drugs can cause birth defects and changes in the brain that predispose the child to emotional problems later in life. Here’s a brief excerpt:

Back in 2004, a report in the New England Journal of Medicine showed that the use of statins in the first trimester of pregnancy was associated with birth defects, especially severe central nervous system defects and limb deformities. In fact, 20 out of 52 women exposed to statins gave birth to offspring with such defects, which represents a birth defect rate of 38 percent, nearly 20 times the background rate of birth defects!

If you’re pregnant or considering getting pregnant, please – for the sake of your baby – speak to your psychiatrist or doctor about getting off antidepressant drugs before you conceive.

mouth full of pillsIf you read the papers or watch the news you’ve probably heard about the recently published JUPITER study, advertised with bold headlines such as “Cholesterol drug causes risk of heart attack to plummet” and “Cholesterol-fighting drug shows wider benefit”. If you’ve been following this blog (and perhaps even if you haven’t), you are by now aware that such claims cannot be taken at face value.

You might suspect, for example, that the study was sponsored by a drug company and authored by researchers with financial interests tied to those drug companies. You might wonder if these associations could possibly – just possibly – influence not only the results of the study, but how those results are reported. You might also find yourself questioning the objectivity of a study with the title “Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin” (JUPITER).

If you’re asking yourself these questions, you are definitely on the right track. The study was indeed sponsored by a drug company, AstraZeneca. And each author of this study received money in the form of grants, consulting fees and honoraria from pharmaceutical companies – in some cases up to twelve different companies, including AstraZeneca, the study sponsor. Take a look at this list detailing the financial interests of the study authors (now required by the New England Journal of Medicine and other prominent publications):

Dr. Ridker reports receiving grant support from AstraZeneca, Novartis, Merck, Abbott, Roche, and Sanofi-Aventis; consulting fees or lecture fees or both from AstraZeneca, Novartis, Merck, Merck–Schering-Plough, Sanofi-Aventis, Isis, Dade Behring, and Vascular Biogenics; and is listed as a coinventor on patents held by Brigham and Women’s Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease, including the use of high-sensitivity C-reactive protein in the evaluation of patients’ risk of cardiovascular disease. These patents have been licensed to Dade Behring and AstraZeneca. Dr. Fonseca reports receiving research grants, lecture fees, and consulting fees from AstraZeneca, Pfizer, Schering-Plough, Sanofi-Aventis, and Merck; and Dr. Genest, lecture fees from AstraZeneca, Schering-Plough, Merck–Schering-Plough, Pfizer, Novartis, and Sanofi-Aventis and consulting fees from AstraZeneca, Merck, Merck Frosst, Schering-Plough, Pfizer, Novartis, Resverlogix, and Sanofi-Aventis. Dr. Gotto reports receiving consulting fees from Dupont, Novartis, Aegerion, Arisaph, Kowa, Merck, Merck–Schering-Plough, Pfizer, Genentech, Martek, and Reliant; serving as an expert witness; and receiving publication royalties. Dr. Kastelein reports receiving grant support from AstraZeneca, Pfizer, Roche, Novartis, Merck, Merck–Schering-Plough, Isis, Genzyme, and Sanofi-Aventis; lecture fees from AstraZeneca, GlaxoSmithKline, Pfizer, Novartis, Merck–Schering-Plough, Roche, Isis, and Boehringer Ingelheim; and consulting fees from AstraZeneca, Abbott, Pfizer, Isis, Genzyme, Roche, Novartis, Merck, Merck–Schering-Plough, and Sanofi-Aventis. Dr. Koenig reports receiving grant support from AstraZeneca, Roche, Anthera, Dade Behring and GlaxoSmithKline; lecture fees from AstraZeneca, Pfizer, Novartis, GlaxoSmithKline, DiaDexus, Roche, and Boehringer Ingelheim; and consulting fees from GlaxoSmithKline, Medlogix, Anthera, and Roche. Dr. Libby reports receiving lecture fees from Pfizer and lecture or consulting fees from AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Merck, Pfizer, Sanofi-Aventis, VIA Pharmaceuticals, Interleukin Genetics, Kowa Research Institute, Novartis, and Merck–Schering-Plough. Dr. Lorenzatti reports receiving grant support, lecture fees, and consulting fees from AstraZeneca, Takeda, and Novartis; Dr. Nordestgaard, lecture fees from AstraZeneca, Sanofi-Aventis, Pfizer, Boehringer Ingelheim, and Merck and consulting fees from AstraZeneca and BG Medicine; Dr. Shepherd, lecture fees from AstraZeneca, Pfizer, and Merck and consulting fees from AstraZeneca, Merck, Roche, GlaxoSmithKline, Pfizer, Nicox, and Oxford Biosciences; and Dr. Glynn, grant support from AstraZeneca and Bristol-Myers Squibb. No other potential conflict of interest relevant to this article was reported.

Now, the fact that these researchers receive money from all of these drug companies doesn’t mean that they are dishonest or that their data are invalid. However, if you think these conflicts of interest do not influence the outcomes of clinical research, then I suggest you read an article I published a few months ago called When It Comes To Drug Claims, Skepticism Is Healthy.

Now that you’ve put on your “Healthy Skeptic” goggles, we can move on and more closely examine the study itself. There are several things you need to be aware of as we discuss it.

First, although the press articles claim that the study looked at statin use in healthy populations, the subjects were people who had normal cholesterol but high CRP levels. CRP, or C-Reactive Protein, is a measure of inflammation in the body. It is now widely accepted even in the mainstream medical community that inflammation is a major risk factor for heart disease. And because inflammation is a sign of an underlying disease process, these patients were not, in fact, “healthy” as claimed.

There is little doubt that statins reduce inflammation, which can help prevent atherosclerosis. It appears that the benefits of statins are mainly due to this characteristic, rather than to their cholesterol-lowering effects. So it’s no surprise that the statins reduced rates of heart disease and mortality in this population that had inflammation going into the study.

I should also mention, however, that the predictive value of CRP for heart disease is highly controversial. Though some studies show a correlation between high CRP levels and heart disease, many others do not. Many physicians feel that CRP is not a useful indicator in clinical practice.

The second thing you need to be aware of is the difference between relative and absolute risk reduction. Relative risk reduction (RRR) measures how much the risk is reduced in the experimental group compared to a control group. Absolute risk reduction (ARR) is just the absolute difference in outcome rates between the control and treatment groups.

To make this more clear, let’s consider an example. Say that 2000 people enter a study for a particular drug and 1000 of them are randomized to placebo. At the end of the study, one person in the drug group died versus two people in the placebo group. The relative risk reduction of the drug group would thus be 50% (0.002 – 0.001/0.002). That sounds really impressive! The headline for this study might read “New drug reduces chance of dying by 50%!”. While technically true, you can see how misleading this can be. Why? Because when most people read that headline, they will interpret it to mean that if they take that drug, their risk of dying will be reduced by 50%, which is not even close to being true.

The absolute risk reduction, on the other hand, is always a much more modest number. Using the same example above, the absolute risk reduction in the drug group would have been a paltry one-tenth of a percent, or 0.1% (0.002 – 0.001). That’s not a very catchy headline, is it? “New drug reduces risk of dying by one-tenth of a percent”. It just doesn’t grab you the same way. But this is actually a more realistic view of what happened in the study and what we could expect to happen in the real world.

In fact, one could just as accurately say that in this hypothetical study, a patient has a 1-in-1000 (0.1%) chance of their life being saved by the drug. Said another way, 1,000 patients would have to be treated with this drug in order to save a single life. This measurement is called the Needed Number to Treat, and is another means for interpreting the results of clinical trials.

With that in mind, let’s examine the data from the JUPITER study. The actual numbers were 198 deaths out of 8901 in the statin group and 247 deaths out of 8901 in the placebo group. The relative risk reduction for total mortality (deaths) in the drug group was 19.8% [(247/8901 - 198/8901) / (247/8901)]. That means that the risk of death for people taking Crestor was 19.8% smaller than those taking placebo.

But what happens when we look at the absolute risk reduction numbers? According to the data, 2.77% (0.02774) of people taking the placebo died after two years versus 2.24% (0.02224) of people taking Crestor. This amounts to a difference of 0.55%, or one-half of one percent.

Here’s a graphical illustration of the difference in mortality between the Crestor and placebo group:

jupiter graph

If you’re having trouble making much of a difference, I don’t blame you!

To make this even more clear, let’s use the Needed Number to Treat method of evaluating these results. According to the study data, 182 people would have to be treated with Crestor for two years in order to save a single life.

Now that may not sound like a large number to you, especially if yours was one of the lives saved. However, when evaluating the viability of any potential treatment three considerations (above and beyond the efficacy of the treatment) must be taken into account: cost, side effects, and alternatives.

Let’s look at cost first. The cost of one patient taking Crestor for one year is approximately $1,300. Therefore, to prevent 49 deaths 8,901 people would have to take Crestor for two years at a cost of $23 million dollars. That is an enormously expensive treatment by any measure.

Second, this particular study did not register significant side effects in the statin group. This is very fishy, though, since nearly every other study on statins to date has shown significant side effects and the approval of Crestor itself was delayed by the FDA due to concern about Crestor side effects.

While all statins are associated with rare instances of rhabdomyolysis, a breakdown of muscle cells, Crestor had shown in studies before its approval that the potentially deadly disease had surfaced in seven people. Crestor’s potential muscle- and liver-damaging side effects become more worrisome and difficult to justify in patients who are essentially healthy.

What’s more, the study only lasted two years. That’s not long enough to adequately establish safety for the drug, especially if people are going to use it “preventatively”, which means they could be taking it for several years and even decades. Statins have caused cancer in every single animal study to date. Since cancer can take up to 25 years to develop after initial exposure to the carcinogen, we simply cannot know at this point that statins won’t also significantly increase the risk of cancer in adults.

Finally, before jumping on the statin bandwagon and recommending that we spend billions of dollars treating healthy people with Crestor, we should consider if there isn’t a less costly and risky way of preventing deaths due to inflammation and heart disease.

Wouldn’t you know it, there sure is!

For the last decade medical research has increasingly demonstrated that heart disease is caused not by high cholesterol levels, but by inflammation and oxidative damage. A full explanation of these mechanisms is beyond the scope of this post, but for more details you can read two previous articles: Cholesterol Doesn’t Cause Heart Disease and How To Increase Your Risk of Heart Disease.

So, if we want to prevent and even treat heart disease, we need to address the causes of inflammation and oxidative damage. Again, there’s not room to go into great detail on this here but in general the primary causes of inflammation and oxidative damage are 1) a diet high in polyunsaturated oil (PUFA) and refined flour and sugar, 2) lack of physical activity, 3) stress and 4) smoking.

We can thus prevent heart disease by avoiding PUFA and refined/processed food, getting adequate exercise, reducing stress and not smoking. These simple dietary and lifestyle changes are likely to produce even better results than a statin, for a fraction of the cost and without any side effects. In fact, the only side effects of this approach are improved physiological and psychological health! For more specific recommendations, read my article Preventing Heart Disease Without Drugs.

Taking a statin to “prevent” inflammation and heart disease is rather like bailing water with a pail to prevent a boat from sinking instead of simply plugging the leak. Unfortunately, our entire health care system is oriented around “bailing water with a pail”, which is to say treating the symptoms of disease, instead of “plugging the leak”, or addressing the causes of disease before it develops. The reason this is the case is because there’s a lot more money to be made from drugs, surgery and other costly interventions than there is from encouraging people to eat well, exercise and reduce stress.

Even if we ignore all of the issues I’ve pointed out above, the best thing we can say about this study is that a small group of unusual patients – those with low LDL-cholesterol AND high C-reactive protein – may slightly decrease their risk for all-cause mortality by taking a drug that costs them almost $1,300 per year and slightly increases their risk for developing diabetes.

That’s the best spin possible given the data from this study. Compare that to the mainstream media headlines, and you’ll have a clear understanding of how financial conflicts of interest are seriously damaging the integrity and value of clinical research.

At least the media wasn’t completely fooled. They did manage to at least include the perspective of sane doctors who questioned the desirability of millions of relatively healthy people taking drugs for the rest of their lives. According to the Wall Street Journal:

Moreover, despite large relative benefits, the actual number of patients helped was small. Those on the drug suffered 142 major cardiovascular events compared with 251 on placebo, a difference of 109. Dr. Hlatky said that raises questions about the cost-effectiveness of CRP screening and the value of putting millions of low-risk patients on medication for the rest of their lives.

From the New York Times:

Some consumer advocates and doctors raised concerns about the expense of putting relatively healthy patients on statins, which would cost the health system billions of dollars.

From Fox News:

About 120 people would have to take Crestor for two years to prevent a single heart attack, stroke or death, said Stanford University cardiologist Dr. Mark Hlatky. He wrote an editorial accompanying the study published online by the New England Journal of Medicine.

“Everybody likes the idea of prevention. We need to slow down and ask how many people are we going to be treating with drugs for the rest of their lives to prevent heart disease, versus a lot of other things we’re not doing” to improve health, Hlatky said.

If you know of someone who is considering a statin after reading about the JUPITER study, please do them a favor and send them a link to this article first. They should hear both sides of the story before making such a significant decision.

vegetable oilEasy! Just follow Dr. Steinberg’s recent recommendations.

Dr. Daniel Steinberg, author of “The Cholesterol Wars”, has just issued new recommendations proposing that “proposing that aggressive intervention to lower cholesterol levels as early as childhood is the best approach available today to reducing the incidence of coronary heart disease.”

In a review article published in the August 5, 2008 issue of the American Heart Association journal Circulation, Steinberg and his colleagues stat that “with a large body of evidence proving that low cholesterol levels equate with low rates of heart disease, “…our long-term goal should be to alter our lifestyle accordingly, beginning in infancy or early childhood” and that “…instituting a low-saturated fat, low-cholesterol diet in infancy (7 months) is perfectly safe, without adverse effects…”

I don’t know whether to scream or cry when I read this stuff. Or both. Why? Because Dr. Steinberg’s dietary recommendations – if embraced by parents – are sure to increase the risk of heart disease and cause developmental problems in the children unfortunate enough to adopt them.

Let’s take a closer look at each part of the article on ScienceDaily.com describing the new recommendations and see if Steinberg’s claims make any sense.

According to Steinberg, progress has been made in the treatment of coronary heart disease in adults with cholesterol lowering drugs like statins. However, while studies show a 30% decrease in death and disability from heart disease in patients treated with statins, 70% of patients have cardiac events while on statin therapy.

Progress in treating heart disease? What progress? Heart disease is the #1 cause of death in the U.S. today. In the early part of the 20th Century, heart disease was relatively unknown. I would hardly call that progress.

As for statins, please refer to my previous article “The Truth About Statin Drugs” for a more accurate appraisal of the effectiveness (or lack thereof) of statins. In short, statins don’t reduce the risk of death in 95% of the population, including healthy men with no pre-existing heart disease, women of any age and the elderly. While statin drugs do reduce mortality for young and middle-aged males with pre-existing heart disease, the benefit is small and not without significant adverse effects, risks and costs.

For example, in the six largest studies done on statins and mortality to date, the absolute risk reduction ranged from -0.3% to 3.3%. In two of those studies, statins actually increased the risk of death. In an analysis of this data, the UK Medical Research Council determined that even if you were in the 5% of the population that statins benefit, you’d have to take a statin for 30 years at a cost of $42,000 just to add nine months (best case) to your life.

Even that scenario is entirely hypothetical, because statins cause cancer in lab animals. Although this hasn’t been shown in humans to date, the window between exposure to a carcinogen and development of cancer can be as long as 25 years for humans. Since no one has been on statins for that long, there is still reason to believe that they might have the same effect in humans that they do on animals.

Progress? I don’t think so.

In fact, they propose that lowering low-density lipoproteins (the so-called “bad cholesterol”) to less than 50 mg./dl. even in children and young adults is a safe and potentially life-saving standard, through lifestyle (diet and exercise) changes if possible. Drug treatment may also be necessary in those at very high risk.

“Bad cholesterol”? That’s so 1975. It is well accepted even within the mainstream scientific community today that normal LDL cholesterol (so-called “bad cholesterol”) is not a risk factor for heart disease. Instead, it is the oxidation of the polyunsaturated fatty acid in the membrane of the LDL particle (when the level of antioxidants in the diet is insufficient to protect them) that contributes to heart disease.

Therefore, the only LDL cholesterol that could be called “bad” is oxidized LDL.
And what promotes oxidation of the LDL particle? Eating polyunsaturated fat (found in vegetable oils, nuts and seeds and in almost all processed food). Of course, these are exactly the fats the American Heart Association has promoted as “heart-healthy” for decades.

In addition to promoting oxidation of LDL particles, polyunsaturated fats contribute directly to atherosclerosis and heart attacks. 75% of arterial plaque is made up of unsaturated fat, of which 50% is polyunsaturated (only 25% is saturated). The greater the concentration of polyunsaturated fat in the plaque, the more likely it is to rupture. Such ruptures, and the ensuing blood clots that form, are a primary cause of heart attacks.

Another well-established cause of heart disease is inflammation. Omega-6 polyunsaturated fats, which constitute a large percentage of caloric intake for most Americans, are known to promote inflammation. Indeed, excess linoleic acid (LA) in the diet from vegetable oil has been shown to contribute directly to heart disease.

So, the notion that saturated fat “clogs arteries” and causes heart attacks is totally false. It is actually polyunsaturated fat – the so-called “heart-healthy fat – which has those effects.

If people’s lives weren’t at stake the irony of such a situation might be almost funny. As it stands it’s one of the great public health tragedies of modern times.

And what about the notion that eating cholesterol raises cholesterol levels in the blood? It turns out to be false – and Steinberg even admits as much in his own book. There are two parts of the hypothesis that cholesterol causes heart disease. The first part, called the “diet-heart hypothesis”, is that eating cholesterol in the diet raises cholesterol levels in the blood. The second part, called the “lipid hypothesis”, holds that high cholesterol levels in the blood cause heart disease.

We’ve already addressed the “lipid hypothesis” above. As for the “diet-heart hypothesis”, Steinberg clearly states in his book that there is little evidence to support it. Tightly controlled egg-feeding studies have shown that eating cholesterol only raises cholesterol levels in about 30% of the population (”hyper-responders”).

However, these same studies showed that egg consumption led to an increase in “light, fluffy LDL” that was actually protective against heart disease. Why? Because these large, buoyant LDL particles are protected against oxidation.

Finally, what about saturated fat? Does it cause heart disease as Steinberg suggests? Once again, the evidence squarely contradicts Dr. Steinberg’s claim. In 22 of 26 published studies there was no significant relationship between saturated fat intake and either coronary or all-cause mortality. Among the studies that Dr. Steinberg failed to mention in his book or in his recent recommendation:

  • Rose, et al. (1965): Replacing animal fat with corn oil for two years lowered serum cholesterol by 23 mg/dL but quadrupled cardiac and total mortality.
  • Sydney Diet-Heart Study (1978): Replacing animal fat with vegetable fat for five years lowered cholesterol by five percent but increased total mortality by 50 percent.

What’s more, in the few studies where saturated fat restriction did reduce deaths from heart disease, deaths from cancer, brain hemorrhage, suicide & violent death went up! In his book The Great Cholesterol Con, Anthony Colpo concludes:

“If saturated fats caused even a portion of the damage for which they are frequently blamed, their negative effects should be readily and repeatedly demonstrable in controlled clinical trials. However, after excluding the results of the poorly designed and sloppily conducted northern European studies, it quickly becomes apparent that there does not exist a single tightly controlled trial which shows that saturated fat restriction can save even a single life.”

There are two more claims made by Dr. Steinberg that I need to address.

“lowering low-density lipoproteins to less than 50mg/dL even in children and young adults is a safe and potentially life-saving standard.”

As stated above, there is absolutely no evidence that lowering LDL protects against heart disease. More than 40 trials have been performed to see if cholesterol lowering can prevent heat attacks. When all the results were pooled together, just as many died in the treatment groups as the control groups.

But what is most disturbing to me about Steinberg’s statement is the idea that lowering LDL to such unnatural levels is a “safe and potentially life-saving standard”. Cholesterol is a vital substance in our bodies. 50% of all cell membranes are made up of cholesterol; it is a precursor to sex hormones which govern fertility, reproduction and sexual development; it is an antioxidant that helps prevent free radical damage; and it is needed particularly by infants and children to ensure proper development of the brain and nervous system.

In fact, evidence in adults shows that low cholesterol levels can be dangerous and even life-threatening:

  • Low cholesterol is associated with increased total mortality in elderly people.
  • Framingham (1987): “There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.” In other words, as cholesterol fell death rates went up.
  • Honolulu Heart Program (2001): “long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”
  • J-LIT (2002): The highest death rate was observed among those with lowest cholesterol (under 160mg/dl); the lowest death rate was observed with those whose cholesterol was between 200-259mg/dl.

Low cholesterol has also been associated with increased rates of cancer, depression, violent and aggressive behavior, and suicide.

With that in mind, how could anyone possibly claim that reducing cholesterol to extremely low levels in children is “safe”?

“Drug treatment may also be necessary in those [children] at very high risk.

I’m not even sure where to start with this one, except to recommend that people like Dr. Steinberg be prosecuted for making such unfounded, irresponsible and dangerous recommendations.

According to the American Academy of Pediatrics:

“Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.”

Which is to say there is no evidence suggesting that cholesterol levels in kids are a risk factor for adult heart disease.

Furthermore, as we have already discussed, cholesterol is absolutely essential for brain development. Lowering brain levels of cholesterol in children, whose brains are still developing at a rapid rate, could have dire consequences.

Surely Dr. Steinberg must be aware of this? There is nothing controversial about the role of cholesterol in brain development. You can find this information in any physiology or biochemistry textbook. So why – especially in light of the lack of evidence linking cholesterol to heart disease in kids – is he suggesting that we give statins to children?

I really have no idea. In all likelihood Dr. Steinberg means well and believes he’s acting in the interest of our children. But I cannot understand how a respected medical doctor and researcher could overlook such an elementary and important fact and ignore the weight of scientific evidence.

We’ve all heard the saying “when all you’ve got is a hammer, everything looks like a nail.” When someone like Dr. Steinberg has invested so much of their life and energy into the theory that cholesterol causes heart disease, I guess it’s hard to let it go.

One of my favorite researchers, Chris Masterjohn, has just launched a new blog called “The Daily Lipid” where he writes about fats, cholesterol and health. Chris is pursuing a Ph.D. in Molecular and Cell Biology and is one of the most knowledgeable contemporary writers on cardiovascular health that I’m aware of. With his permission, I am cross-posting the first two articles on his blog – which you should definitely consider adding to your blogroll!

pregnant woman

Statins for pregnant women?

Statin manufacturers, the sycophantic researchers they pay, and the shameless hucksters who sell them are always up to no good, but their recent attempts to market them to pregnant women are simply horrifying.

According to a recent news article published in Mail online, researchers from liverpool believe that taking statins during pregnancy might help women avoid caesarean sections by promoting more robust uterine contraction. They hope to begin human trials in three to five years.

Somehow, the author of this article failed to react with the shock and horror appropriate to the situation — which should be the same shock and horror with which we would react to the suggestion that pregnant women should take thalidomide to avoid morning sickness.

Back in 2004, a report in the New England Journal of Medicine showed that the use of statins in the first trimester of pregnancy was associated with birth defects, especially severe central nervous system defects and limb deformities. In fact, 20 out of 52 women exposed to statins gave birth to offspring with such defects, which represents a birth defect rate of 38 percent, nearly 20 times the background rate of birth defects!

Even before this report was published, researchers already knew that statins caused birth defects in animal experiments, and the FDA already required the drugs to carry a label warning pregnant women to stay away from them. The article linked to above stated the following:

“FDA took this action because it was recognized that fetal cholesterol synthesis was essential for development, and because animals given statins during pregnancy had offspring with a variety of birth defects,” [one of the study's authors] said.

Less than a year later, Merck and Johnson & Johnson jointly asked the FDA for permission to market an over-the-counter statin. One of the concerns about the proposal was the risk to pregnant women. USA Today reported:

The FDA classifies Mevacor and other statins as pregnancy category X, which means they are not supposed to be taken by pregnant women. Not only have category X drugs been linked to fetal abnormalities in animal or human studies, but the FDA also has declared that the benefits of taking them do not outweigh potential risks.

According to the same article, Merck made a disturbing admission:

“Of course, there will be women who take it off-label,” acknowledges Merck executive Edwin Hemwall, referring to the use of non-prescription Mevacor by women under 55.

And what could prompt women to use statins during pregnancy against recommendations? Certainly a news article declaring that statins might prevent the need for caesarean sections and their associated complications could prompt some women to do so.

So what ground-breaking research made these Liverpool researchers so confident that taking drugs associated with twenty times the normal rate of major birth defects during pregnancy might be a good idea that they put out a press release declaring this confidence to the public before any trials were even under way?

Well, according to the article:

Tests have already shown that raising levels of cholesterol interferes with womb tissue’s ability to contract.
Really. Raising levels of cholesterol. You might wonder how they accomplished that. Did they use cholesterol-raising drugs? I don’t know of any drugs that do that. Did they use egg yolks, or the dreaded dietary villain — gasp — saturated fats?

No, the story is quite different.

The apparent basis for this ridiculous statin cheerleading is a 2004 study published by researchers from the University of Liverpool in the American Journal of Physiology — Cell Physiology entitled “Increased cholesterol decreases uterine activity: functional effects of cholesterol alteration in pregnant rat myometrium.”

Rather than feeding anything to pregnant women or pregnant rats, the researchers took pregnant rats and killed them. So the first thing we can say is that statins might help you deliver a baby if your doctor kills you first.

Then they extracted the uterine tissue and either extracted cholesterol from it with a chemical solvent called methyl beta-cyclodextrin, or enriched it either with cholesterol mixed with this solvent or with LDL (which they didn’t measure for oxidation prior to use). Then they added drugs to induce contraction under either cholesterol-depleted or cholesterol-enriched conditions, and found that contraction was greater under cholesterol-depleted conditions.

So now we know that — wait, what is it we know?

Well, quite clearly, we don’t know anything that we can have any confidence has any physiological relevance at all. That is, except the fact that statins cause birth defects in animals, and they increase the rate of birth defects in humans by nearly twenty times, primarily by causing severe defects of the central nervous system and limb deformities.

To add to that, we also know that the vast majority of humans conceived with Smith-Lemli-Opitz Syndrome (SLOS), a genetic inability to synthesize enough cholesterol, die of spontaneous abortion in the first 16 weeks of gestation. Those who live long enough to be born suffer from mental retardation, autism, facial and skeletal malformations, visual dysfunctions and failure to thrive.

Statins for pregnant women? I don’t think so.

Article written by Chris Masterjohn

Statins for 8-year old children?

child with drug

The American Academy of Pediatrics recently announced new recommendations for giving cholesterol-lowering drugs to children as young as eight years old. They also recommend giving low-fat milk to infants as young as one year old.

The New York Times published several articles on this, first announcing the recommendation the day the academy made it, then describing the backlash of saner doctors and other members of the public against it, and finally editorializing that while they were first “appalled” at the recommendation, after reading the report they were more dismayed at the state of our children’s health.

Concerning this frightful state of children’s health, the Times reported the following:

“We are in an epidemic,” said Dr. Jatinder Bhatia, a member of the academy’s nutrition committee who is a professor and chief of neonatology at the Medical College of Georgia in Augusta. “The risk of giving statins at a lower age is less than the benefit you’re going to get out of it.”

Dr. Bhatia said that although there was not “a whole lot” of data on pediatric use of cholesterol-lowering drugs, recent research showed that the drugs were generally safe for children.

An epidemic of what? High cholesterol? Not according to the academy’s report, which states that cholesterol levels in children declined between 1966 and 1994 and stayed the same between 1994 and 2000.

No, we are in an epidemic of obesity. As the Times reported:

But proponents say there is growing evidence that the first signs of heart disease show up in childhood, and with 30 percent of the nation’s children overweight or obese, many doctors fear that a rash of early heart attacks and diabetes is on the horizon as these children grow up.

Is there any evidence that statins lead to weight loss? If there is, I am not aware of it.

The point is immaterial, because the academy doesn’t claim to have any evidence for its position in the first place. For example, its report states the following:

Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.
And further down:

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.

In other words, they don’t know what level of cholesterol is risky and at what age it starts posing a risk, but they will nevertheless assume that there is some level that does start to pose a risk at some age and they will thus have to make a guess just what that level and what that age is.

The report discusses evidence that the “metabolic syndrome” and the “recent epidemic of childhood obesity” are tied to the risk of diabetes and heart disease and evidence that even modest weight loss at a level of five to seven percent is sufficient to prevent diabetes. Yet somehow instead of making a recommendation about how to more effectively lose weight the authors derive from this data a much less logical but much more profitable conclusion that 8-year-olds should be put on statins.

As to the recommendation to feed infants low-fat milk, the Times reported the following:

The academy also now recommends giving children low-fat milk after 12 months if a doctor is concerned about future weight problems. Although children need fat for brain development, the group says that because children often consume so much fat, low-fat milk is now appropriate.

This is rather remarkable, because the academy attributed the drop in childhood cholesterol levels to the successes of the anti-fat, anti-cholesterol campaign that began in the 1950s. But now children no longer need milkfat because they are getting plenty of fat. Well which is it? Are they getting more fat now or less fat?

Of course milkfat is also a source of choline, along with liver and egg yolks, which is essential to brain development.

But even this misses the point. Cholesterol is essential to brain development!

One of the first articles I added to my section on the functions of cholesterol was an article entitled “Learning, Your Memory, and Cholesterol.” It discusses the evidence uncovered eight years ago that cholesterol is the limiting factor for the formation of synapses, which are the connections between neurons that allow learning and memory to take place.

Lowering brain levels of cholesterol can be detrimental at any age beacause of this, but the consequences for children — whose brains are still developing at a much more rapid rate — could be much more dire.

No doubt, most researchers and medical doctors mean well and are honestly trying to help our children. But surely someone in these drug companies must know that cholesterol is necessary for brain development, and that cholesterol-lowering drugs reduce mental performance in adults. Surely they must know that if we raise our next generation of children on statins during the critical periods of brain development, we may raise a whole generation with compromised intelligence.

And if that’s the case, are they trying to dumb us down? Sometimes it seems like that’s the case.

Article written by Chris Masterjohn

tropical paradiseIn the last two weeks alone three articles have appeared in the scientific press about new studies reporting on vitamin D’s many crucial roles in the body. Along with promoting strong bones, a healthy immune system and protection against some types of cancer, recent studies suggest vitamin D can treat heart failure, protect against heart attacks and reduce the risk of death from both cardiovascular and overall causes.

Back in April I wrote an article called “Throw Away Your Sunscreen” about the protective effects of exposure to sunlight against melanoma. Despite conventional wisdom that tells us to avoid sun exposure at all costs, it turns out that the vitamin D our bodies synthesize when exposed to UV light is a first line of defense against developing melanoma.

In an article published on June 9 in Archives of Internal Medicine, scientists reported that low levels of vitamin D are associated with a higher risk of myocardial infarction (heart attack) in men. The study showed that rates of cardiovascular disease-related deaths are increased at higher latitudes and during the winter months, and are lower at lower altitudes.

In an article published in the July issue of the Journal of Cardiovascular Pharmacology, on June 12, researchers found that vitamin D directly contributes to cardiovascular fitness. In fact, University of Michigan pharmacologist Robert U. Simpson, Ph.D. thinks it’s apt to call vitamin D “the heart tranquilizer”. Simpson and his team discovered that treatments with activated vitamin D prevented heart muscle cells from hypertrophy, a condition in which the heart becomes enlarged and overworked in people with heart failure.

Finally, in a study published on June 23 in the Archives of Internal Medicine, a team of Austrian scientists revealed that low blood levels of vitamin D appear to have an increased risk of death overall and from cardiovascular causes. Harald Donbig, M.D. and his colleagues studied 25-hydroxyvitamin D and 1,25 dihydroxyvitamin D levels in 3,258 consecutive patients (average age 62 years) who were scheduled for coronary angiography testing at a single medical center between 1997 and 2000.

During 7.7 years of follow-up, death rates from any cause and from cardiovascular causes were higher among individuals in the lower one-half of 25-hydroxyvitamin D levels and the lowest one-fourth of 1,25-dihydroxyvitamin D levels. These associations remained when researchers controlled for other factors such as coronary artery disease, physical activity and co-occurring diseases.

So what does all this mean to you? A recent consensus panel estimated that about 50 – 60 percent of older individuals in North America and the rest of the world do not have satisfactory vitamin D status, and the situation is similar for younger individuals. Blood levels of vitamin D lower than 20 to 30 nanograms per milliliter have been associated with falls, fractures, cancer, autoimmune dysfunction, cardiovascular disease and hypertension.

To put it blankly, that means half of all people around the world are deficient in vitamin D and therefore at increased risk for serious and potentially fatal conditions.

Low 25-hydroxyvitamin D levels are also correlated with markers of inflammation such as C-reactive protein, as well as signs of oxidative damage to cells, Donbig’s study revealed. In a previous article, I explained that inflammation and oxidative damage (not cholesterol) are the primary causes of the worldwide heart disease epidemic. Inflammation and oxidative damage are also contributing factors to diabetes, metabolic syndrome, cancer and many other diseases.

So how does vitamin D work its magic? It acts as a potent hormone in more than a dozen types of tissues and cells in the body, regulating expression of essential genes and rapidly activating already expressed enzymes and proteins. In the heart, vitamin D binds to specific vitamin D receptors and produces its “calming”, protective effects.

There are essentially three ways to obtain vitamin D: exposure to UV light, food and supplements. The most effective of all of these methods is exposure to sunlight. Full-body exposure of pale skin to summer sunshine for 30 minutes without clothing or sunscreen can result in the synthesis of between 10,000 and 20,000 IU of vitamin D. At most latitudes outside of the tropics, however, there are substantial portions of the year during which vitamin D cannot be obtained from sunlight; additionally, environmental factors including pollution and the presence of buildings can reduce the availability of UVB light.

In northern latitudes or during winter months when the sun isn’t shining, I recommend taking 1 tsp./day of high-vitamin cod liver oil (Green Pasture or Radiant Life are two brands I recommend) to ensure adequate vitamin D (and vitamin A) intake. You can also eat vitamin D-rich foods such as herring, duck eggs, bluefin tuna, trout, eel, mackerel, sardines, chicken eggs, beef liver and pork. If you follow this approach further supplementation should not be necessary.

Before closing, I must mention (briefly) the issue of vitamin D toxicity. Vitamin D is widely considered to be the most toxic of all vitamins, and dire warnings are often issued to avoid excess sun exposure and vitamin D in the diet on that basis. The discussion of vitamin D toxicity has failed to take into account the interaction between vitamins A, D and K. Several lines of evidence suggest that vitamin D toxicity actually results from a relative deficiency of vitamins A and K.
So, the solution is not to avoid sun exposure or sources of vitamin D in the diet. Rather, it ensure adequate vitamin D intake (through sunlight and food) and to increase the intake (through diet and/or supplements) of vitamins A & K. Stay tuned for a future post on the interaction between vitamins A, D & K and their relevance to human health.

THS recommendations:

  • Throw away your sunscreen. Use coconut and sesame oil if needed, and moderate your exposure to sun to avoid frequent sunburn.
  • Get an hour or two of exposure to sunlight each day if possible. Don’t cover your skin (or your child’s skin) completely when out in the sun.
  • In northern latitudes or during winter months when the sun isn’t shining, take 1 tsp./day of high-vitamin cod liver oil (Green Pasture or Radiant Life are two brands I recommend) to ensure adequate vitamin A & D intake.
  • Eat vitamin D-rich foods such as herring, duck eggs, bluefin tuna, trout, eel, mackerel, sardines, chicken eggs, beef liver and pork.
  • Make sure to eat enough vitamin K. Primary sources in the diet are natto, hard and soft cheeses, egg yolks, sauerkraut, butter and other fermented foods. Make sure to choose dairy products from grass-fed animals if possible.

Suggested Links

  • The Vitamin D Miracle: Is it For Real?
  • From Seafood to Sunshine: A New Understanding of Vitamin D Safety
  • Vitamin D Toxicity Redefined

veggie basket In today’s article we’ll discuss how to prevent heart disease without drugs. If you haven’t already read Part 1 of this series, which examined the problems with statin drugs, and Part 2, which debunks the myth that cholesterol causes heart disease, you might want to do that before reading this article.

Last week I mentioned the INTERHEART study, which looked at the relationship between heart disease and lifestyle in 52 countries around the world. What this study revealed is that approximately 90% of heart disease could be prevented by simple changes to diet and lifestyle.

Let’s just make this crystal clear: 9 out of 10 cases of heart disease are completely preventable without drugs. With sales of statin drugs reaching close to $30 billion this year with Lipitor alone bringing in close to $14 billion, this might come as some surprise. But the pharmaceutical companies are, quite literally, invested in people taking their cholesterol-lowering drugs in spite of the complete lack of evidence that lowering cholesterol prevents heart disease.

In order to understand the changes we need to make to prevent heart disease, we have to briefly examine what causes it. By now you know that the answer is not “cholesterol”. In fact, as I mentioned briefly in last week’s article, the two primary contributing mechanisms to heart disease are inflammation and oxidative damage.

Inflammation is the body’s response to noxious substances. Those substances can be foreign, like bacteria, or found within our body, as in autoimmune diseases like rheumatoid arthritis. In the case of heart disease, inflammatory reactions within atherosclerotic plaques can induce clot formation.

When the lining of the artery is damaged, white blood cells flock to the site, resulting in inflammation. Inflammation not only further damages the artery walls, leaving them stiffer and more prone to plaque buildup, but it also makes any plaque that’s already there more fragile and more likely to burst.

Oxidative damage is a natural process of energy production and storage in the body. Oxidation produces free radicals, which are molecules missing an electron in their outer shell. Highly unstable and reactive, these molecules “attack” other molecules attempting to “steal” electrons from their outer shells in order to gain stability. Free radicals damage other cells and DNA, creating more free radicals in the process and a chain reaction of oxidative damage.

Normally oxidation is kept in check, but when oxidative stress is high or the body’s level of antioxidants is low, oxidative damage occurs. Oxidative damage is strongly correlated to heart disease. Studies have shown that oxidated LDL cholesterol is 8x greater stronger a risk factor for heart disease than normal LDL.

Since there may be some confusion on this point, I want to make it clear: normal LDL cholesterol is not a risk factor for heart disease in most populations, but oxidated LDL cholesterol is. This points to oxidation as the primary risk factor, not cholesterol. Why? Because when an LDL particle oxidizes, it is the polyunsaturated fat that oxidizes first. The saturated fat and the cholesterol, hidden deep within the core of the lipoprotein, are the least likely to oxidize.

It follows, then, that if we want to prevent heart disease we need to do everything we can to minimize inflammation and oxidative damage.

Top four causes of oxidative damage & inflammation

  1. Stress
  2. Smoking
  3. Poor nutrition
  4. Physical inactivity

By focusing on reducing or completely eliminating, when possible, the factors in our life that contribute to oxidative stress and inflammation, we can drastically lower our risk for heart disease. Let’s take a brief look at each risk factor.

Stress

In the INTERHEART study, stress tripled the risk of heart disease. This was true across all countries and cultured that were studies. The primary mechanism by which stress causes heart disease is by dysregulating the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is directly intertwined with the autonomic nervous system, and it governs the “fight-or-flight” response we experience in reaction to a stressor.

Continued activation of this “fight-or-flight” response leads to hyper-arousal of the sympathetic nervous system, which in turn leads to chronically elevated levels of cortisol. And elevated levels of cortisol can cause both inflammation and oxidative damage.

Stress management, then, should be a vital part of any heart disease prevention program. In fact, some researchers today believe that stress may be the single most significant factor in the cause and prevention of heart disease. There are several proven methods of stress reduction, including mindfulness-based stress reduction (MBSR), acupuncture and biofeedback. It doesn’t matter which method you choose. It just matters that you do it, and do it regularly.

Smoking

I assume that you are already well aware of the dangers of smoking, so I won’t spend much time on this one. For the purposes of this discussion, I will point out that smoking as few as 1-4 cigarettes a day has been shown to increase the risk of heart disease by 40%. But smoking 40 cigarettes a day increases that risk by 900%.

So if you smoke and you’re concerned about heart disease – quit.

Nutrition

Over the past century we’ve seen a consistent decline in the consumption of traditional, nutrient-dense foods in favor of highly processed, nutrient-depleted products. The flawed hypothesis that cholesterol causes heart disease has wrongly identified health-promoting foods like meat, organ meats, eggs and dairy products as harmful, and replaced them with toxic, processed alternatives such as chips, white breads, pastries, crackers, cookies, frozen foods, candy and soda.

There are two ways that nutrition contributes to heart disease: too much of the wrong foods, and not enough of the right ones.

The average American gets 57% of his/her calories from highly refined cereal grains and polyunsaturated (PUFA) oils. The #3 source of calories, behind grains and PUFA, is sugar and high-fructose corn syrup. Refined grains, polyunsaturated oils and sugar are all major contributors to both inflammation and oxidative damage.

Not only do refined carbohydrates, vegetable oils and sugar contribute to inflammation and oxidative damage, they are also completely devoid of micronutrients that would protect us from these processes. Meats, fruits and vegetables are all high in antioxidants that prevent oxidative damage, and rich in other micronutrients that play important roles in preventing heart disease.

More than 85% of Americans are not getting the federally recommended five servings of fresh fruit and vegetables each day. The intake of dark leafy green or yellow/orange veggies for the average American is equivalent to 18g – one-half of one small carrot. Iceberg lettuce, tomatoes, french fries, orange juice and bananas constitute 30% of fruit and vegetable intake for most Americans.

Many people know that the “Standard American Diet” is extremely unhealthy. But what most do not know is that the so-called “heart-healthy” diet that has been vigorously promoted for decades actually contributes to heart disease! The “heart-healthy” diet is high in refined carbohydrates and polyunsaturated oils, which, as we have seen, cause inflammation and oxidative damage.

On the other hand, saturated fats (which have been demonized by the medical mainstream) such as butter, coconut oil, lard, tallow and ghee are protected against oxidation and possess many other important health benefits. These fats are the ones we need to be eating to protect ourselves from heart disease.

It is extremely important to buy organic meat, eggs and dairy products that come from animals that have been raised on fresh pasture rather than in commercial, factory feedlots. See this article and this one for more information on why this is so essential.

Finally, it must be pointed out that not all “organic” products are healthy. Most packaged food (including organic cereals, crackers, chips and so-called “nutrition bars”) are full of highly refined carbohydrates, sugar, and vegetable oils. And by now, I don’t need to tell you what that means!

So what would a truly heart healthy diet look like, then? Download my Guidelines for Natural Prevention of Heart Disease to find out.

Physical Inactivity

Physical inactivity is likely a major causative factor in the explosive rise of coronary heart disease in the 20th century. During the vast majority of evolutionary history, humans have had to exert themselves to obtain food and water. Even at the turn of the 20th century in the U.S., a majority of people had jobs that required physical activity (farmers, laborers, etc.) Now the majority of the workforce has sedentary occupations with little to no physical activity at all.

Currently more than 60% of American adults are not regularly active, and 25% of the adult population is completely sedentary. People that are physically inactive have between 1.5x and 2.4x the risk of developing heart disease.

On the other hand, regular exercise reduces both inflammation and oxidative damage. Even relatively low levels of activity are protective – as long as they are consistent. A public review at Harvard University showed that 30-minutes of moderate physical activity on most days of the week decreases deaths from heart disease by 20-30%.

The best strategy for people struggling to find time to exercise is to make it part of their daily life (i.e. riding a bike or walking to work, choosing the stairs over the escalator or elevator, etc.)

When combined, the four strategies listed above will significantly reduce your chances of getting heart disease – without taking a single pill of any kind.

If you already have heart disease, or you are at high risk for heart disease (overweight, high blood pressure, diabetic, etc.), then you may need additional support. See my

Recommended articles

 

In last week’s article about the ineffectiveness of statin drugs in reducing mortality in most populations I promised I would follow-up with an article on drug-free prevention of heart disease. I will do that this week, but it occurred to me that the first article in this series should have been one that dispels the myth that cholesterol causes heart disease. Understanding that is the key to the prevention strategies that will follow in the next article. So without further ado…

butterYou are all no doubt acquainted with the popular hypothesis on cholesterol and heart disease. It has two parts: first, that eating cholesterol in the diet raises cholesterol levels in the blood; and two, that high cholesterol levels in the blood cause heart disease.

You might be surprised to learn that neither of these statements is true. The first one is relatively easy to dispatch. In the Framingham Heart Study, which is the longest-running and perhaps most significant study on heart disease done to date, it was demonstrated that intake of cholesterol in the diet had absolutely no correlation with heart disease. If you look at the graph below, you’ll see that both men and women with above average intake of cholesterol had nearly identical rates of heart disease as men and women with below average intake of cholesterol.

framingham

In fact, the “diet-heart hypothesis”, which is the scientific name for the idea that eating cholesterol causes heart disease, has even been discounted by the researchers who were responsible for its genesis. Ancel Keys, who in many ways can be considered the “father” of the cholesterol-heart disease hypothesis, had this to say in 1997:

“There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”

This is a reference to early studies performed on chickens and rabbits where they force-fed these animals high-levels of cholesterol. Since rabbits and chickens are mostly vegetarian, their physiology is not adapted for processing such large amounts of dietary cholesterol, so it’s no surprise they developed atherosclerosis. The mistake was assuming that the results of this experiment could be extrapolated to humans, who are omnivores with significant differences in physiology.

The second tenet of the cholesterol-heart disease hypothesis, the notion that high cholesterol levels in the blood cause heart disease, is referred to as the “lipid hypothesis” in the scientific community. Though it still accepted as gospel truth by the general public and many medical professionals, most researchers now believe the primary causes of heart disease are inflammation and oxidative stress. Unfortunately, the rest of us haven’t gotten the memo, so to speak, that cholesterol isn’t the cause of heart disease.

It would take several articles to explain this in complete detail, but I’d like to give at least a brief summary here.

If cholesterol caused heart disease, it should be a risk factor in 1) all ages, 2) both sexes and 3) all populations around the world (barring any protective factor, of course). Also, if cholesterol caused heart disease we would expect that lowering cholesterol would reduce heart disease. But none of these assumptions turn out to be true.

The rate of heart disease in 65-year old men is ten times that of 45-year old men. Yet a recent study in the Journal of American Medical Association indicated that high LDL cholesterol is not a risk factor for from coronary heart disease (CHD) mortality or total mortality (death from any cause). It is extremely unlikely that a risk factor for a disease would stop being a risk factor at a time when that disease kills the greatest number of people. That is akin to suggesting that smoking causes lung cancer in young men, but somehow stops doing so in older men!

Another consistent thorn in the side of supporters of the “lipid hypothesis” is that women suffer 300% less heart disease than men, in spite of having higher average cholesterol levels. At the recent Conference on Low Blood Cholesterol, which reviewed 11 major studies including 125,000 women, it was determined that there was absolutely no relationship between total cholesterol levels and mortality from cardiovascular or any other causes.

Nor is cholesterol a risk factor in all populations around the world. In fact, some of the populations with the highest levels of blood cholesterol have among the lowest rates of heart disease, and vice versa. Dr. Malcom Kendrick, a well-known skeptic of the lipid-hypothesis, explains this very well in the video below:

Finally, more than 40 trials have been performed to determine whether lowering cholesterol levels can prevent heart disease. In some trials heart disease rates went down, in others they went up. But when the results of all of the trials were taken together, just as many people died in the treatment groups (who had their cholesterol levels lowered by drugs) as in the control groups (who had no treatment).

If you’re still skeptical after reading all of this, perhaps William Castelli, the director of the famed Framingham Heart Study mentioned above can convince you:

“Serum cholesterol is not a strong risk factor for CHD, in the sense that blood pressure is a strong risk factor for stroke or cigarette smoking is a risk factor for lung cancer.”

Or how about Frederick Stare, a long-time American Heart Association member and (former) proponent of the lipid hypothesis:

“The cholesterol factor is of minor importance as a risk factor in CVD. Of far more importance are smoking, hypertension, obesity, diabetes, insufficient physical activity, and stress.”

So there you have it. Contrary to popular belief, cholesterol is not a dangerous poison that causes heart disease. Rather, it is an essential nutrient present in the cell membranes of all tissues of all mammals, and has some very important functions in the body. In fact, in many studies low cholesterol has been associated with an increase in total mortality!

Again, the Framingham Study which followed 15,000 participants over three generations:

“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.”

In other words, as cholesterol fell death rates went up.

The Honolulu Heart Program study, with 8,000 participants, published in 2001:

“Long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”

And finally, the huge Japanese Lipid Intervention Trial with over 47,000 participants:

“The highest death rate observed was among those with lowest cholesterol (under 160mg/dl); lowest death rate observed was with those whose cholesterol was between 200-259mg/dl”

In other words, those with the lowest cholesterol had the highest death rate, and those with cholesterol levels that would today be called “dangerous” had the lowest death rate.

As you can see, not only does high cholesterol not cause heart disease, low cholesterol can actually be dangerous to your health. So toss out your vegetable oil and start eating butter and eggs again! But more on that next week…

Recommended links

pills and bills Statins have been almost universally hailed as “wonder drugs” by medical authorities around the world. The market for statins was $26 billion in 2005, and sales for Lipitor alone reached $14 billion in 2006. Merck and Bristol Myers-Squib are actively seeking “over-the-counter” (OTC) status for their statin drugs. Statins are prescribed to men and women, children and the elderly, people with heart disease and people without heart disease.

In fact, these drugs have a reputation for being so safe and effective that one UK physician, John Reckless (I’m not kidding – that’s actually his name!) has suggested that we put statins in the water supply.

That’s a bold suggestion, of course, and it begs the question: are statins really as safe and cost effective as mainstream medical authorities claim? The unequivocal answer is no.

Statins don’t increase survival in healthy people

Statins have never been shown to be effective in reducing the risk of death in people with no history of heart disease. No study of statins on this “primary prevention population” has ever shown reduced mortality in healthy men and women with only an elevated serum cholesterol level and no known coronary heart disease. (CMAJ. 2005 Nov 8;173(10):1207; author reply 1210.) In fact, an analysis of large, controlled trials prior to 2000 found that long-term use of statins for primary prevention of CHD produced a 1% greater risk of death over 10 years compared to placebo

Statins don’t increase survival in women

Despite the fact that around half of the millions of statin prescriptions written each year are handed to female patients, these drugs show no overall mortality benefit regardless of whether they are used for primary prevention (women with no history of heart disease) or secondary prevention (women with pre-existing heart disease). In women without coronary heart disease (CHD), statins fail to lower both CHD and overall mortality, while in women with CHD, statins do lower CHD mortality but increase the risk of death from other causes, leaving overall mortality unchanged. (JAMA study)

Statins don’t increase survival in the elderly

The only statin study dealing exclusively with seniors, the PROSPER trial, found that pravastatin did reduce the incidence of coronary mortality (death from heart disease). However, this decrease was almost entirely negated by a corresponding increase in cancer deaths. As a result, overall mortality between the pravastatin and placebo groups after 3.2 years was nearly identical.

This is a highly significant finding since the rate of heart disease in 65-year old men is ten times higher than it is in 45-year old men. The vast majority of people who die from heart disease are over 65, and there is no evidence that statins are effective in this population.

Do statins work for anyone?

Among people with CHD or considered to be at high risk for CHD, the effect of statins on the incidence of CHD mortality ranges from virtually none (in the ALLHAT trial) to forty-six percent (the LIPS trial). The reduction in total mortality from all causes ranges from none (the ALLHAT trial) to twenty-nine percent (the 4S trial).

However, the use of statins in this population is not without considerable risk. Statins frequently produce muscle weakness, lethargy, liver dysfunction and cognitive disturbances ranging from confusion to transient amnesia. They have produced severe rhabdomyolysis that can lead to life-threatening kidney failure.

Aspirin just as effective as statins (and 20x cheaper!)

Perhaps the final nail in the coffin for statins is that a recent study in the British Medical Journal showed that aspirin is just as effective as statins for treating heart disease in secondary prevention populations – and 20 times more cost effective! Aspirin is also far safer than statins are, with fewer adverse effects, risks and complications.

The bottom line

  1. Statin drugs do not reduce the risk of death in 95% of the population, including healthy men with no pre-existing heart disease, women of any age, and the elderly.
  2. Statin drugs do reduce mortality for young and middle-aged men with pre-existing heart disease, but the benefit is small and not without significant adverse effects, risks and costs.
  3. Aspirin works just as well as statins do for preventing heart disease, and is 20 times more cost effective.

So what if you are at risk for heart disease and you’d prefer not to take a statin? Other than aspirin, there are many clinically proven ways to prevent heart disease involving simple adjustments to diet and lifestyle. In fact, the recent INTERHEART study which looked at the incidence of heart disease in 52 countries revealed that over 90% of heart disease is preventable by diet and lifestyle modifications.

I’ll discuss these natural methods of preventing heart disease in my next post. Stay tuned!

Recommended links

  • Dangers of statin drugs: what you haven’t been told about cholesterol-lowering drugs
  • The effect of statins is not due to cholesterol lowering

egg The persistent myth that cholesterol causes heart disease has scared many of us away from eating eggs on a regular basis. But there is absolutely no research that links egg consumption to heart disease.

A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

You’ve probably been conditioned to believe that anything that raises LDL cholesterol (so-called “bad” cholesterol) should be avoided like the plague. But even the medical mainstream has come to recognize that all LDL cholesterol is not the same. It’s true that small, dense LDL particles have been linked to heart disease. This is primarily due to the fact that they are much more susceptible to oxidative damage than normal LDL cholesterol particles.

However, egg consumption increases the proportion of large, buoyant LDL particles that have been shown to be protective against heart disease. Egg consumption also shifts individuals from the LDL pattern B to pattern A. Pattern B indicates a preponderance of small, dense LDL particles (risk factors for heart disease), while pattern A indicates a preponderance of large, buoyant LDL particles (which protect us from heart disease). This is a good thing.

Eggs one of the most nutrient-dense foods available. One egg provides 13 essential nutrients, all in the yolk (contrary to popular belief, the yolk is far higher in nutrients than the white).

Eggs are an excellent source of B vitamins, which are needed for vital functions in the body, and also provide good quantities of vitamin A, essential for normal growth and development.

The vitamin E in eggs protects against heart disease and some cancers; eggs also contain vitamin D, which promotes mineral absorption and good bone health.

Eggs are rich in iodine, for making thyroid hormones, and phosphorus, essential for healthy bones and teeth.

Eggs are also good sources of antioxidants known to protect the eye. Therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts.

There’s absolutely no reason to limit your consumption of eggs to three to four per week, as recommended by “heart-healthy” nutritional guidelines. In fact, consuming two to three eggs per day would provide a better boost to your health and protection against disease than a multivitamin supplement. Eggs truly are one of nature’s superfoods.

It’s important, however, to make sure that you buy organic, pasture-raised eggs. Studies show that commercially-raised eggs are up to 19 times higher in pro-inflammatory omega-6 fatty acids. Unfortunately, almost all eggs sold in supermarkets – even the organic eggs sold at chains such as Whole Foods and Wild Oats – are not truly pasture-raised. To find these eggs, check your local farmer’s market or visit the Eat Wild website to locate a source in your area.

eggs
Attention Bay Area HEALTHY SKEPTIC readers!

I am offering a free public talk next week in Berkeley, CA which debunks the myth that cholesterol causes heart disease. We’ll also explore the true causes of heart disease as well as simple dietary and lifestyle changes you can make to protect yourself and your loved ones. See below for details. Hope to see you there!

Wednesday, May 21st from 7:00 – 9:00 PM
Acupuncture & Integrated Medicine College, Berkeley (AIMC Berkeley)
2550 Shattuck Avenue (at Blake)
10-minute walk south on Shattuck from Downtown Berkeley BART
510.666.8248 ext. 106

www.aimc.edu

For over 50 years, the medical establishment has vigorously promoted the notion that high cholesterol is a primary risk factor for coronary heart disease, and that a diet high in saturated fat and cholesterol causes heart disease. These hypotheses are widely accepted as fact by physicians and the general public alike, despite the overwhelming body of evidence that suggests otherwise.

During this two-hour talk, we’ll review scientific studies demonstrating that:

  1. High cholesterol doesn’t cause heart disease
  2. Low cholesterol worsens your physical and mental health and increases your chances of dying prematurely
  3. Diets high in saturated fat and cholesterol don’t cause heart disease, but they do promote health and longevity
  4. Consumption of so-called “heart healthy” vegetable oils is linked to heart disease, cancer and many other conditions

You’ll also learn the latest theories on what causes heart disease and a truly “heart healthy” approach to diet and lifestyle that is supported by both modern science and centuries of traditional wisdom.

The presentation draws on more than 150 peer-reviewed studies published in major journals and the work of an impressive list of physicians, scientists and researchers who question the connection between cholesterol and heart disease.

cheeseA study recently published by the European Prospective Investigation into Cancer and Nutrition (EPIC) has revealed that increased intake of vitamin K2 may reduce the risk of prostate cancer by 35 percent. The authors point out that the benefits of K2 were most pronounced for advanced prostate cancer, and, importantly, that vitamin K1 did not offer any prostate benefits.

The findings were based on data from more than 11,000 men taking part in the EPIC Heidelberg cohort. It adds to a small but fast-growing body of science supporting the potential health benefits of vitamin K2 for bone, cardiovascular, skin, brain, and now prostate health.

Unfortunately, many people are not aware of the health benefits of vitamin K2. The K vitamins have been underrated and misunderstood up until very recently in both the scientific community and the general public.

It has been commonly believed that the benefits of vitamin K are limited to its role in blood clotting. Another popular misconception is that vitamins K1 and K2 are simply different forms of the same vitamin – with the same physiological functions.

New evidence, however, has confirmed that vitamin K2’s role in the body extends far beyond blood clotting to include protecting us from heart disease, ensuring healthy skin, forming strong bones, promoting brain function, supporting growth and development and helping to prevent cancer – to name a few. In fact, vitamin K2 has so many functions not associated with vitamin K1 that many researchers insist that K1 and K2 are best seen as two different vitamins entirely.

A large epidemiological study from the Netherlands illustrates this point well. The researchers collected data on the vitamin K intakes of the subjects between 1990 and 1993 and measured the extent of heart disease in each subject, who had died from it and how this related to vitamin K2 intake and arterial calcification. They found that calcification of the arteries was the best predictor of heart disease. Those in the highest third of vitamin K2 intakes were 52 percent less likely to develop severe calcification of the arteries, 41 percent less likely to develop heart disease, and 57 percent less likely to die from it. (Geleijnse et al., 2004, pp. 3100-3105) However, intake of vitamin K1 had no effect on cardiovascular disease outcomes.

While K1 is preferentially used by the liver to activate blood clotting proteins, K2 is preferentially used by other tissues to deposit calcium in appropriate locations, such as in the bones and teeth, and prevent it from depositing in locations where it does not belong, such as the soft tissues.(Spronk et al., 2003, pp. 531-537) In an acknowledgment of the different roles played by vitamins K1 and K2, the United States Department of Agriculture (USDA) finally determined the vitamin K2 contents of foods in the U.S. diet for the first time in 2006. (Elder, Haytowitz, Howe, Peterson, & Booth, 2006, pp. 436-467)

Another common misconception is that human beings do not need vitamin K2 in their diet, since they have the capacity to convert vitamin K1 to vitamin K2. The amount of vitamin K1 in typical diets is ten times greater than that of vitamin K2, and researchers and physicians have largely dismissed the contribution of K2 to nutritional status as insignificant.

However, although animals can convert vitamin K1 to vitamin K2, a significant amount of evidence suggests that humans require preformed K2 in the diet to obtain and maintain optimal health. The strongest indication that humans require preformed vitamin K2 in the diet is that epidemiological and intervention studies both show its superiority over K1. Intake of K2 is inversely associated with heart disease in humans while intake of K1 is not (Geleijnse et al., 2004, pp. 3100-3105), and vitamin K2 is at least three times more effective than vitamin K1 at activating proteins related to skeletal metabolism. (Schurgers et al., 2007) And remember that in the study on vitamin K2’s role in treating prostate cancer, which I mentioned at the beginning of this article, vitamin K1 had no effect.

All of this evidence points to the possibility that vitamin K2 may be an essential nutrient in the human diet. So where does one find vitamin K2 in foods? The following is a list of the foods highest in vitamin K2, as measured by the USDA:

Foods high in vitamin K2

  • Natto
  • Hard cheese
  • Soft cheese
  • Egg yolk
  • Butter
  • Chicken liver
  • Salami
  • Chicken breast
  • Grond beef

Unfortunately, precise values for some foods that are likely to be high in K2 (such as organ meats) are not available at this time. The pancreas and salivary glands would be richest; reproductive organs, brains, cartilage and possibly kidneys would also be very rich; finally, bone would be richer than muscle meat. Fish eggs are also likely to be rich in K2.

It was once erroneously believed that intestinal bacteria are a major contributor to vitamin K status. However, the majority of evidence contradicts this view. Most of the vitamin K2 produced in the intestine are embedded within bacterial membranes and not available for absorption. Thus, intestinal production of K2 likely makes only a small contribution to vitamin K status. (Unden & Bongaerts, 1997, pp. 217-234)

On the other hand, fermented foods, however, such as sauerkraut, cheese and natto (a soy dish popular in Japan), contain substantial amounts of vitamin K2. Natto contains the highest concentration of K2 of any food measured; nearly all of it is present as MK-7, which research has shown to be a highly effective form. A recent study demonstrated that MK-7 increased the percentage of osteocalcin in humans three times more powerfully than did vitamin K1. (Schurgers & Vermeer, 2000, pp. 298-307)

It is important to note that commercial butter is not a significantly high source of vitamin K2. Dr. Weston A. Price, who was the first to elucidate the role of vitamin K2 in human health (though he called it “Activator X” at the time) analyzed over 20,000 samples of butter sent to him from various parts of the world. As mentioned previously in this paper, he found that the Activator X concentration varied 50-fold. Animals grazing on vitamin K-rich cereal grasses, especially wheat grass, and alfalfa in a lush green state of growth produced fat with the highest amounts of Activator X, but the soil in which the pasture was grown also influenced the quality of the butter. It was only the vitamin-rich butter grown in three feet or more of healthy top soil that had such dramatic curing properties when combined with cod liver oil in Dr. Price’s experiments and clinical practice.

Therefore, vitamin K2 levels will not be high in butter from grain-fed cows raised in confinement feedlots. Since the overwhelming majority of butter sold in the U.S. comes from such feedlots, butter is not a significant source of K2 in the diet for most people. This is yet another argument for obtaining raw butter from cows raised on green pasture.

New research which expands our understanding of the many important roles of vitamin K2 is being published at a rapid pace. Yet it is already clear that vitamin K2 is an important nutrient for human health – and one of the most poorly understood by medical authorities and the general public.

Recommended links

  • On the Trail of the Elusive X-Factor
  • The Vitamin You Need to Prevent Prostate Cancer
  • K2 Associated with Reduced Risk of Coronary Heart Disease

A recent article reported on the results of a trial of the cholesterol-lowering drug Zytorin, which is a combination of Zocor and Zeita – made by Merck and Schering-Plough.

Zocor and Zeita lower cholesterol by different mechanisms, so the idea was that combining them into a single drug (Vytorin) would dramatically lower cholesterol and, they assumed, reduce heart disease.

They got the first part right. Vytorin did indeed lead to dramatic reductions in cholesterol levels in those who took the drug. However, it also increased the risk of heart disease – exactly the opposite result they were hoping for.

The worst part about this is that Merck & Schering-Plough sat on this data for almost two years, while over five million people around the world continued to take a drug that was proven to nearly double the risk of heart disease. Congress has launched a full-scale investigation and the NY Times is publicly demanding a new law to prevent this from happening again.

Yesterday another article was published in the Times with an update on the investigation, including emails sent by the lead investigator on the Vytorin trial indicating that Merck & Schering-Plough were deliberately delaying publication of the results of this trial.

Yet another case of gross malfeasance by the pharmaceutical industry. Consumers beware.

Related articles

  • Accusations of Delays in Releasing Drug Results
  • Doubt Cast on Two Drugs Used to Lower Cholesterol
  • Editorial: Overpromoted Cholesterol Drugs

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