The idea that depression and other mental health conditions are caused by an imbalance of chemicals in the brain is so deeply ingrained in our psyche that it seems almost sacrilegious to question it.

Direct-to-consumer-advertising (DCTA) campaigns, which have expanded the size of the antidepressant market (Donohue et al., 2004), revolve around the claim that SSRIs (the most popular class of antidepressants) alleviate depression by correcting a deficiency of serotonin in the brain.

For example, Pfizer’s television advertisement for Zoloft states that “depression is a serious medical condition that may be due to a chemical imbalance”, and that “Zoloft works to correct this imbalance.”

Other SSRI advertising campaigns make similar claims. The Effexor website even has a slick video explaining that “research suggests an important link between depression and an imbalance in some of the brain’s chemical messengers. Two neurotransmitters believed to be involved in depression are serotonin and norepinephrine.” The video goes on to explain that Effexor works by increasing serotonin levels in the synapse, which is “believed to relieve symptoms of depression over time.”

These days serotonin is widely promoted as the way to achieve just about every personality trait that is desirable, including self-confidence, creativity, emotional resilience, success, achievement, sociability and high energy. And the converse is also true. Low serotonin levels have been implicated in almost every undesirable mental state and behavioral pattern, such as depression, aggressiveness, suicide, stress, lack of self-confidence, failure, low impulse control, binge eating and other forms of substance abuse.

In fact, the idea that low levels of serotonin cause depression has become so widespread that it’s not uncommon to hear people speak of the need to “boost their serotonin levels” through exercise, herbal supplements or even sexual activity. The “chemical imbalance” theory is so well established that it is now part of the popular lexicon.

It is, after all, a neat theory. It takes a complex and heterogeneous condition (depression) and boils it down to a simple imbalance of two to three neurotransmitters (out of more than 100 that have been identified), which, as it happens, can be “corrected” by long-term drug treatment. This clear and easy-to-follow theory is the driving force behind the $12 billion worth of antidepressant drugs sold each year.

However, there is one (rather large) problem with this theory: there is absolutely no evidence to support it. Recent reviews of the research have demonstrated no link between depression, or any other mental disorder, and an imbalance of chemicals in the brain (Lacasse & Leo, 2005; (Valenstein, 1998).

The ineffectiveness of antidepressant drugs when compared to placebo cast even more doubt on the “chemical imbalance” theory. (See my recent articles Placebos as effective as antidepressants and A closer look at the evidence for more on this.)

Folks, at this point you might want to grab a cup of tea. It’s going to take a while to explain the history of this theory, why it is flawed, and how continues to persist in light of the complete lack of evidence to support it. I will try to be as concise as possible, but there’s a lot of material to cover and a lot of propaganda I need to disabuse you of.

Ready? Let’s start with a bit of history.

The history of the “chemical imbalance” theory

The first antidepressant, iproniazid, was discovered by accident in 1952 after it was observed that some tubercular patients became euphoric when treated with this drug. A bacteriologist named Albert Zeller found that iproniazid was effective in inhibiting the enzyme monoamine oxydase. As its name implies, monoamine oxydase plays an essential role in inactivating monoamines such as epinephrine and norepinephrine. Thus, iproniazid raised levels of epinephrine and norepinephrine which in turn led to stimulation of the sympathetic nervous system - an effect thought to be responsible for the antidepressant action of the drug.

At around the same time, an extract from the plant Rauwolfia serpentina was introduced into western psychiatry. This extract had been used medicinally in India for more than a thousand years and was thought to have a calming effect useful to quite babies, treat insomnia, high blood pressure, insanity and much more. In 1953 chemists at Ciba, a pharmaceutical company, isolated the active compound from this herb and called it reserpine.

In 1955 researchers at the National Institutes of Health reported that reserpine reduces the levels of serotonin in the brains of animals. It was later established that all three of the major biogenic amines in the brain, norepinephrine, serotonin, and dopamine, were all decreased by reserpine (again, in animals).

In animal studies conducted at around the same time, it was found that animals administered reserpine showed a short period of increased excitement and motor activity, followed by a prolonged period of inactivity. The animals often had a hunched posture and an immobility that was thought to resemble catatonia (Valenstein, 1998). Since reserpine lowered levels of serotonin, norepinephrine and dopamine, and caused the effects observed in animals, it was concluded that depression was a result of low levels of biogenic amines. Hence, the “chemical imbalance” theory is born.

However, it was later found that reserpine only rarely produces a true clinical depression. Despite high doses and many months of treatment with reserpine, only 6 percent of the patients developed symptoms even suggestive of depression. In addition, an examination of these 6 percent of patients revealed that all of them had a previous history of depression. (Mendels & Frazer, 1974) There were even reports from a few studies that reserpine could have an antidepressant effect (in spite of reducing levels of serotonin, norepinephrine and dopanmine).

As it turns out, that is only the tip of the iceberg when it comes to revealing the inadequacies of the “chemical imbalance” theory.

The fatal flaws of “chemical imbalance” theory

As Elliot Valenstein Ph.D., Professor Emeritus of psychology and neuroscience at Michigan University, points out in his seminal book Blaming the Brain, “Contrary to what is often claimed, no biochemical, anatomical or functional signs have been found that reliably distinguish the brains of mental patients.” (p. 125)

In his book, Valenstein clearly and systematically dismantles the chemical imbalance theory:

1. Reducing levels of norepinephrine, serotonin and dopamine does not actually produce depression in humans, even though it appeared to do so in animals.
2. The theory cannot explain why there are drugs that alleviate depression despite the fact that they have little or no effect on either serotonin or norepinephrine.
3. Drugs that raise serotonin and norepinephrine levels, such as amphetamine and cocaine, do not alleviate depression.
4. No one has explained why it takes a relatively long time before antidepressant drugs produce any elevation of mood. Antidepressants produce their maximum elevation of serotonin and norepinephrine in only a day or two, but it often takes several weeks before any improvement in mood occurs.
5. Although some depressed patients have low levels of serotonin and norepinephrine, the majority do not. Estimates vary, but a reasonable average from several studies indicates that only about 25 percent of depressed patients actually have low levels of these metabolites.
6. Some depressed patients actually have abnormally high levels of serotonin and norepinephrine, and some patients with no history of depression at all have low levels of these amines.
7. Although there have been claims that depression may be caused by excessive levels of monoamine oxydase (the enzyme that breaks down serotonin and norepinephrine), this is only true in some depressed patients and not in others.
8. Antidepressants produce a number of different effects other than increasing norepinephrine and serotonin activity that have not been accounted for when considering their activity on depression.

Another problem is that it is not now possible to measure serotonin and norepinephrine in the brains of patients. Estimates of brain neurotransmitters can only be inferred by measuring the biogenic amine breakdown products (metabolites) in the urine and cerebrospinal fluid. The assumption underlying this measurement is that the level of biogenic amine metabolites in the urine and cerebrospinal fluid reflects the amount of neurotransmitters in the brain. However, less than one-half of the serotonin and norepinephrine metabolites in the urine or cerebrospinal fluid come from the brain. The other half come from various organs in the body. Thus, there are serious problems with what is actually being measured.

Finally, there is not a single peer-reviewed article that can be accurately cited to support claims of serotonin deficiency in any mental disorder, while there are many articles that present counterevidence. Furthermore, the Diagnostic and Statistical Manual of Mental Disorders (DSM) does not list serotonin as the cause of any mental disorder. The American Psychiatric Press Textbook of Clinical Psychiatry addresses serotonin deficiency as an unconfirmed hypothesis, stating “Additional experience has not confirmed the monoamine depletion hypothesis” (Lacasse & Leo, 2005).

When all of this evidence is taken in full, it should be abundantly clear that depression is not caused by a chemical imbalance.

But, as Valenstein shrewdly observes, “there are few rewards waiting for the person who claims that “the emperor is really nude” or who claims that we really do not know what causes depression or why an antidepressant sometimes helps to relieve this condition.”

How have we been fooled?

There are several reasons the idea that mental disorders are caused by a chemical imbalance has become so widespread (and none of them have anything to do with the actual scientific evidence, as we have seen).

It is known that people suffering from mental disorders and especially their families prefer a diagnosis of “physical disease” because it does not convey the stigma and blame commonly associated with “psychological problems”. A “physical disease” may suggest a more optimistic prognosis, and mental patients are often more amenable to drug treatment when they are told they have a physical disease.

Patients are highly susceptible to Direct-to-Consumer-Advertising (DCTA). It has been reported that patients are now presenting to their doctors with a self-described “chemical imbalance” (Kramer, 2002). This is important because studies show that patients who are convinced they are suffering from a neurotransmitter defect are likely to request a prescription for antidepressants, and may be skeptical of physicians who suggest other interventions such as cognitive behavioral therapy (DeRubeis et al., 2005). It has also been shown that anxious and depressed patients “are probably more susceptible to the controlling influence of advertisements (Hollon MF, 2004).

The benefit of the chemical imbalance theory for insurance companies and the pharmaceutical industry is primarily economic. Medical insurers are primarily concerned with cost, and they want to discourage treatments (such as psychotherapy) that may involve many contact hours and considerable expense. Their control over payment schedules enables insurance companies to shift treatment toward drugs and away from psychotherapy.

The motivation of the pharmaceutical companies should be fairly obvious. As mentioned previously, the market for antidepressant drugs is now $12 billion. All publicly traded for-profit companies are required by law to increase the value of their investor’s stock. Perhaps it goes without saying, but it is a simple fact that pharmaceutical companies will do anything they legally (and sometimes illegally) can to maximize revenues.

Studies have shown that the advertisements placed by drug companies in professional journals or distributed directly to physicians are often exaggerated or misleading and do not accurately reflect scientific evidence (Lacasse & Leo, 2005). While physicians deny they are being influenced, it has been shown repeatedly that their prescription preferences are heavily affected by promotional material from drug companies (Moynihan, 2003). Research also suggests that doctors exposed to company reps are more likely to favor drugs over non-drug therapy, and more likely to prescribe expensive medications when equally effective but less costly ones are available (Lexchin, 1989). Some studies have even shown an association between the dose and response: in other words, the more contact between doctors and sales reps the more doctors latch on to the “commercial” messages as opposed to the “scientific” view of a product’s value (Wazana, 2000).

The motivation of psychiatrists to accept the chemical imbalance theory is somewhat more subtle. Starting around 1930, psychiatrists became increasingly aware of growing competition from nonmedical therapists such as psychologists, social workers and counselors. Because of this, psychiatrists have been attracted to physical treatments like drugs and electroshock therapy that differentiate them from nonmedical practitioners. Psychiatry may be the least respected medical specialty (U.S. General Accounting Office report). Many Americans rejected Fruedian talk therapy as quackery, and the whole field of psychiatry lacks the quality of research (randomized, placebo-controlled, double-blind experiments) that serves as the gold-standard in other branches of medicine.

Dr. Colin Ross, a psychiatrist, describes it this way:

Of course there are also many “benefits” to going along with the conventional “chemical imbalance” theory, such as free dinners, symphony tickets, and trips to the Caribbean; consultancy fees, honoraria and stock options from the pharmaceutical companies; and a much larger, growing private practice as the $20 billion spent by drug companies on advertising brings patients to the office. Psychiatrists are just human, like the rest of us, and not many of them can resist all of these benefits.

In sum, the idea that depression is caused by a chemical imbalance is a myth. Pharmaceutical ads for antidepressants assert that depression is a physical diseases because that serves as a natural and easy segue to promoting drug treatment. There may well be biological factors which predispose some individuals toward depression, but predisposition is not a cause. The theory that mental disorders are physical diseases ignores the relevance of psychosocial factors and implies by omission that such factors are of little importance.

Stay tuned for future articles on the psychosocial factors of depression, the loss of sadness as a normal response to life, and the branding of new psychological conditions as a means of increasing drug sales.

Recommended resources

• Blaming the Brain, by Elliot Valenstein Ph.D.
• Rethinking Psychiatric Drugs, by Grace Jackson M.D.
• America Fooled: The truth about antidepressants, antipsychotics and how we’ve been deceived, by Timothy Scott Ph.D.
• The Loss of Sadness, by Alan Horwitz and Jerome Wakefield
• The Myth of the Chemical Cure, by Joanna Moncrieff

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The tricky thing about doing scientific research, as I explained in last week’s article, is that conflicts of interest between doctors, researchers and pharmaceutical companies have become so prevalent that the results of even studies published in prominent, peer-reviewed journals cannot be taken at face value.

One must ask: was the study designed properly? Do the author’s conclusions match their own data? Have the authors reported all of the relevant results? Who funded the study, and what role did they have in choosing the subjects, overseeing the methodology and publishing the results?

When looking at a body of research, one must also consider whether there are unpublished studies on the topic and what the effect of those studies might be. This is particularly true in the case of antidepressants, where it has been estimated that approximately 23% of studies have not been published. Why? Because those studies had even less favorable results than those studies that have been published, and the drug companies who paid for them are under no legal obligation (currently - hopefully this might change in the future) to publish study results.

With that in mind, let’s consider Stephan’s comment and each of the points he brings up in turn:

I want to thank Stephan again for his comment and for raising these important issues.

Let’s start with the parts that I agree with. Certainly, depression has become so broad a term that some have argued that it is an essentially meaningless clinical designation. Unlike other conditions that have measurable physiological markers, people that are diagnosed as depressed do not usually have any features that categorically distinguish them from other people. The sorts of problems that are diagnosed as depression can very considerably depending upon which diagnostic criteria are used, the interpretation of those criteria, and cultural and professional attitudes.

In their book The Loss of Sadness, Horwitz and Wakefield point out that the diagnosis of depression has now come to include transient and completely appropriate responses to life such as sadness after the passing of a loved one, disappointment after the loss of a job or anxiety about financial troubles. They argue, very convincingly, that the DSM IV criteria for depression do not adequately distinguish between what they call “normal sadness” and depression, and the result has been the almost complete medicalization of our emotional response to life. I will be writing an article on this very soon, as I believe it’s a critical perspective to understand in our exploration of depression and antidepressants.

Secondly, I certainly cannot argue with the statement that “antidepressants work for some people”. However, the important questions to ask in relation to that statement are:

• Why do antidepressants work
• How do antidepressants work?
• Whom do they work for?

Why are these questions important? Because if it turns out that antidepressants do not have any specific drug effects (raising serotonin, for example), and work only because people expect or desire them to work (like placebos), or because of non-specific drug effects (such as sedation or stimulation), then the logic behind prescribing antidepressants at all becomes quite tenuous to say the least - especially when their side effects and risks are taken into consideration.

Now let’s consider each point in turn.

What Stephan says about the dangers of meta-analysis are true. However, the same danger applies to overestimating the efficacy of antidepressants. There may be some people who are “responders” who have a response to the drug that is significantly higher than placebo; however, there may also be “nonresponders” whose response to the drug was significantly lower than placebo. There is no indication that antidepressants work on a particular subset of people, and no one has identified who this subset is and why they are helped by antidepressants when others are not.

Kirsch’s analysis that antidepressants do not have a clinically meaningful advantage over placebo (”The Emperor’s New Drugs“) has been almost universally accepted within the scientific community. Kirsch’s and his colleagues invoked the Freedom of Information Act to obtain access to the FDA database of controlled trials used in the initial approval for the most popular antidepressants. According to researcher David O. Antonuccio in his article “Antidepressants: A Triumph of Marketing Over Science?“, it is difficult to imagine a database that would offer a more fair opportunity to evaluate the efficacy of antidepressants.

The fact that Kirsch found that antidepressants were no more effective than placebo is surprising, in a way, because these results come from studies that were underwritten and designed by the drug companies themselves under conditions most favorable to the active drug condition. In other words, the deck was stacked from the start in favor of the drugs, and they still didn’t come out ahead.

Since a drug must be shown to be superior to placebo in order to be approved, placebo effects are incredibly annoying to drug companies and they do everything they can to minimize the impact of placebo in their studies. The fact that the FDA allows them to use these techniques is, in my mind, blatant corruption. Consider the following methods used in the studies Kirsch analyzed (and most studies, for that matter):

1. Placebo washout period: During the first two weeks of the study, everyone is on a placebo. The subjects that respond best to placebo are eliminated from the study. This potentially removes both antidepressant nonresponders (i.e. those that were on an antidepressant before the study starts who get better when they are taken off of it) and placebo resopnders (i.e. those that are not on antidepressants before the study and who respond to placebo). Imagine the converse: an antidepressant washout procedure that eliminates all of the antidepressant responders before a study begins! Such a procedure would surely be considered bias.
2. Penetration of the blind: the double-blind in these studies (where neither the patients nor doctors are supposed to know who is taking the drug and who is taking the placebo) is likely to be unintentionally broken because of the pattern of side effects in the active and inactive drug conditions (Greenberg & Fisher, 1997). When efforts are made to ensure the integrity of the blind, drug effects are diminished. For example, a recent review of the Cochrane database of antidepressant studies using “active placebos” (making side effects more difficult to detect) found very small, non-significant differences between drug and placebo, suggesting that trials using inert placebos overestimate drug effects (Moncrieff, Wessely & Hardy, 2001)
3. Replacement of non-responders: at least six of the studies Kirsch reviewed (of 38) allowed replacement of nonresponders. This means that during the first two weeks of the study, those that were not responding to the drug were removed from the study!
4. Use of sedative medication: Most studies allowed the prescription of a sedative concurrent with the antidepressant. Since other studies have shown that sedatives are as effective in treating depression as antidepressants, how can we possibly know whether the antidepressant effect obtained (if there was one) in these studies was due to the antidepressant drug or the sedative? There are at least 6 points on the 52-point HAM-D scale that the doctors use to determine whether a patient is depressed or not that are related to sleep and favor medications with sedative properties. Since the mean difference between patients taking drugs and patients taking placebos in the studies Kirsch analyzed was only 2 points, it is entirely possible that this small difference is only due to the effects of the sedatives used in the studies and has nothing to do with a true antidepressant drug effect.
5. Reliance on clinician ratings: Given that patients tend to report smaller differences than clinicians (Moncrieff, 2001) one certainly wonders how the pattern of results would change using self-report measures like the Beck Depression Inventory.

Frankly, considering the bias against placebo described above, it is simply amazing that placebo still nearly matched the effects of the drug. Imagine what the results might look like if the trials had been performed without these “anti-placebo” measures!

Also, Kirsch et al. pointed out that the overall active drug effects may have been further inflated because mean results were not reported from several studies that found nonsignificant differences between placebo and active drugs.

The advantage to using the FDA database for analysis is considerable. It contains all of the data from initial trials, published or not, and therefore is not subject to the usual publication bias. (As I mentioned earlier in the article, drug companies simply don’t publish negative results. This is known as the “file drawer” phenomenon, since they probably just stuff those studies in some file drawer hoping they will never be found). Antidepressants are significantly more effective than inert placebos in about two-thirds of published trials. However, in the FDA database which includes unpublished trials, Kirsch found that medication outperformed placebo less than half of the time (in 20 of 46 trials).

Although Kirsch’s study is a meta-analyses, he is also looking directly at the results of individual trials. When less than half of individual trials show any advantage for the active drug over placebo, one must really wonder whether these drugs have any specific “antidepressant” effects.

Now on to the next point.

Actually, it’s not the case that antidepressants work in animal models. According to Joanna Moncrieff in her book The Myth of the Chemical Cure, it is rarely mentioned that all animal models of depression produce variable results according to where they are conducted. “In other words,” she says, “they are unreliable.” In addition to this, they fail to select specifically for antidepressants and responses are obtained with drugs that are not generally considered to be antidepressants (i.e. amphetamines, opiates, antihistamines, antipsychotics, atropine, pentobarbital, zinc and antibiotics).

Also, the SSRIs (the most popular class of antidepressant drugs) typically fail to have any response in the forced swim test, which is one of the most common antidepressant screening tests. In this test, rats are placed in a tank of water from which they cannot escape. The time until they give up trying to escape is measured, on the assumption that the state of giving up is akin to depression. It is thought that antidepressants should prolong the time to giving up. However, the SSRIs have no such effect.

Finally, other tests for depression also frequently show that non-antidepressant drugs (sedatives, stimulants, antihistamines, etc) yield “false positive” results.

I’m not so sure we shouldn’t banish them from planet Earth, to tell you the truth.

Longitudinal follow-up studies (which study the effects of antidepresants over the long term - not just the 6-8 week periods the clinical trials look at) show very poor outcomes for people treated for depression both in the hospital and in the community, and the overall prevalence of depression is rising despite increased use of antidepressants (Moncrieff & Kirsch, 2006). Two studies that assessed outcome in depressed patients treated with and without drugs found that people prescribed antidepressants had a slightly worse outcome than those not prescribed them, even after baseline severity had been taken into account (Brugha TS et al, 1992; Ronalds C et al., 1997). No comparable studies exist that show a better outcome in people prescribed antidepressants.

Outside short-term randomized clinical trials there is virtually no evidence that antidepressants have changed the outcome of depression. The evidence that does exist suggests that they may have possibly made it worse. Depression is more common today than before antidepressants were introduced and the outcome has not improved. Epidemiological trends show that the more antidepressants are prescribed, the more prevalent depression is. Sharply rising levels of antidepressant prescribing since the 1990s have been accompanied by increased prevalence of depressive episodes (Patten 2004) and by rising levels of sickness absence for depression (Moncrieff & Pomerleau 2000).

Finally, there is a growing body of research suggesting that antidepressants worsen the chronicity, if not severity, of depression in many patients. Even relatively short-term exposure to antidepressants has been shown to cause chemical and even anatomical changes in the body and brain that could predispose patients to further depressive episodes (Jackson, “Rethinking Psychiatric Drugs“)

Some might argue that antidepressants are important to stave off suicide in very depressed patients. However, there is no evidence that antidepressants reduce the risk of suicide or suicide attempts in comparison with a placebo in clinical trials (Kahn et al. 2000). In fact, rates have actually increased in some age groups and in some countries despite increased antidepressant prescribing (Moncrieff & Kirsch 2006), and when antidepressant trials have been re-analyzed to compensate for erroneous methodologies, the SSRIs have consistently revealed a risk of suicide (completed or attempted) of between two to four times higher than placebo (ackson, “Rethinking Psychiatric Drugs“)

And we haven’t even talked about side effects yet! Since this article is already very long, I’ll save that for another day. Suffice to say that these are not harmless drugs and the side effects can be severe and potentially fatal.

So I ask you, fair readers, when you add all of this up, should doctors continue to prescribe antidepressants? Let’s see what researchers who have been studying antidepressants and depression for decades have to say:

Moncrieff has actually suggested that the term “antidepressant” is a misnomer, because the drugs have not been demonstrated to have a consistent and specific effect against depression.

If antidepressant drugs were the only option for treating depression, one might still be able to make an argument for their use in spite of their lack of efficacy and risks. However, it has repeatedly been shown that aerobic exercise, light therapy, Cognitive Behavioral Therapy, St. John’s Wort, bibliotherapy (prayer) and perhaps acupuncture (more studies are needed) are just as effective for treating depression as antidepressants - with few, if any, adverse effects. In fact, in the case of exercise many of the side effects produced are beneficial (e.g. better overall health and wellness).

Considering that antidepressants are likely no more effective than placebos, have not improved (and perhaps worsened) long-term outcomes, may increase the risk of suicidal and violent behavior and have significant many other significant side effects and risks, including potentially permanent changes in the brain which predispose patients to further depression… and considering that there are well-established alternatives that are just as effective, if not more so, in treating depression with almost no adverse effects and significantly fewer costs, I see no compelling reason to continue prescribing antidepressants.

Obviously many other people are posing this question, particularly in the medical community. Kirsch’s research has been so widely accepted that the debate has not centered around his conclusions, but on the implications of those conclusions. Ironically, it has been suggested by more than one commentator that although we now know that antidepressants aren’t effective, we should continue to prescribe them - if only in an attempt to elicit a placebo effect.

Huh? Let me explain. One major reason people respond to placebo in antidepressant trials is that they expect the drug to work. They expect it to work because of all of the promotion they’ve seen, newspaper and magazine articles they’ve read, and personal testimonials they’ve heard. What would happen if it became known that antidepressants are, in fact, not effective and that they could actually make depression worse. Bye bye placebo effect.

So some researchers and doctors have actually suggested that we should go on promoting the delusion that antidepressants are effective so that people who are taking them will continue to believe that they are working, which of course significantly increases the chance that they will work.

If these drugs were not so potentially dangerous and harmful, and if there were not proven alternatives, I could almost go along with this deception - although it does raise some very interesting ethical questions. However, the drugs are potentially dangerous and harmful, and there are proven alternatives, so I cannot agree with this approach.

In closing, I just want to remind anyone who is currently taking an antidepressant and thinking about stopping that it is essential you do so under your doctor’s supervision. You will have to gradually taper off of your medication - do not stop abruptly!

As always, I welcome your comments and questions.

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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.

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

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Much of what I write may challenge your current beliefs and contradict what you’ve heard about depression and antidepressants. My hope is that today’s post about the influence of the pharmaceutical industry on doctors, researchers and patients will inspire you to re-examine what you’ve been told so far and approach everything you hear in the future with a “healthy skepticism”.

The truth is that all of our beliefs about depression have been tainted, quite intentionally, by the more than $20 billion spent each year by pharmaceutical companies to promote their drugs (an amount greater than the gross domestic product of all but 70 of the world’s richest nations). In 2000, the pharmaceutical industry had a combined lobbying and campaign contribution budget of $200 million - larger than any other industry (Wayne & Peterson, 2001). The industry has 625 registered lobbyists, more than there are members of congress (Wayne & Peterson, 2001). The industry also underwrites about 70% of clinical drug trials in the United States (DeAngelis et al., 2001).

Consumer Reports has detailed the marketing strategies used by drug companies, including:

• giving free samples and information to doctors
• advertising in medical journals
• using “ask your doctor” media advertisements aimed directly at the consumer (the U.S. and New Zealand are the only two countries that allow this)
• sponsoring promotional dinner meetings with substantial gifts or even cash provided for attendees
• paying consultants to speak at scientific meetings where it is possible to circumvent FDA guidelines that require disclosure of side effects
• funding only those research projects that have a high likelihood of producing favorable results for a particular drug company’s product
• terminating negative studies before they are ready for publication
• not publishing studies with negative results
• offering to pay journalists to cover their products
• helping to fund patient advocacy and other public interest groups so the consumer group appears to be publicly carrying the banner of a particular drug

How can we possibly rely on information that is so inexorably intertwined with corporate interests? Corporations have very little motivation to share information that could harm sales of their products, as they are required by law to maximize profits for their shareholders. On the contrary, they have much incentive to do everything in their power to suppress such information. Several studies have shown that researchers who produce data that is contrary to the interests of the pharmaceutical industry risk legal, professional, or even personal attack - directly or indirectly financed by the industry. (Bosley, 2002; Healy, 2002; Monbiot, 2002).

As researcher David Antonuccio points out in his excellent article Antidepressants: A Triumph of Marketing over Science?:

Clinical trials are the basis of approval of new drugs by the FDA, but their reliability is seriously in doubt because of three major flaws: conflicts of interest on the part of investigators; inappropriate involvement of research sponsors in their design and management; and publication bias in disseminating their results. (Quick, 2001)

The situation has become so dire that in September of 2001 the editors of 13 leading medical journals published a joint editorial in which they said:

Huh? Wouldn’t you expect researchers to have these rights already? In many cases, they don’t.

The editor of the prestigious New England Journal of Medicine argued in a separate editorial that the editors didn’t go far enough in their rebuke:

The conflicts of interest between researchers and drug companies is bad enough. But what’s even more distressing is that many doctors do not even read the research to learn about the drugs they are prescribing. Jerry Avorn, a Harvard Medical School professor and drug researcher is a leading authority on how physicians are educated about new drugs. He acknowledges that most physicians have only minimal knowledge about drug studies. Instead, Dr. Avorn has this to say about where most physicians get their knowledge about drugs:

There are now over 90,000 pharmaceutical reps walking the halls of medical offices around the U.S. Since there are less than 600,000 office-based doctors in the U.S. today, there is approximately one full-time drug rep for every six physicians. The drug reps bring free food for office staff, free samples for distribution to patients, free pens, free textbooks and other free gifts. They are also sometimes authorized to provide free vacations for physicians who would enjoy spending a weekend with other physicians in places like Hawaii or the Caribbean hearing the latest “research” on the effectiveness of a drug. In 2006, the pharmaceutical industry spent $2 billion on these types of events alone.

Does all of this advertising and promotion actually influence doctors? You bet it does. A government report found that in just one year the most heavily advertised drugs had prescription increases of 25% (U.S. General Accounting Office, 2002). There is even a formula that generally applies to drug advertising: each dollar spent on advertising increases sales by $4.

Even more discouraging than the influence of drug companies on doctors is the influence of patients who’ve been subjected to drug company advertising on doctors! A study published in the Journal of the American Board of Family Practitioners reported that 49% of patient requests for drugs or other requests prompted by “direct-to-consumer” advertising were not clinically appropriate. Yet 7 out of 10 times, physicians gave into the requests. (And that is by their own admission; there is likely a percentage of physicians who do not want to admit they write prescriptions or order tests on the basis of patient requests.)

The influence of advertising on doctors and patients is particularly relevant in the case of antidepressants. By a wide margin the largest amount spent on advertising by drug companies was on antidepressant promotion - a whopping $367 million dollars per week!(U.S. General Accounting Office, 2002) In fact, it appears that DTC advertising may be the single most effective way a drug company can increase the number of people who are diagnosed with depression and then will begin taking antidepressants (Donohue, 2004).

I could go on, but I think you get the point. As consumers and patients we simply cannot rely on profit-driven drug companies to give us accurate information about their products. And unfortunately, because of the massive conflicts of interest that exist between researchers, physicians and the pharmaceutical industry - we cannot necessarily rely on our doctors or even scientific studies to show us the way.

Luckily for us, there are still studies being done by independent researchers and those brave enough to risk the ire of the drug companies that we can turn to for honest, unbiased data. Unsurprisingly, these studies often have very different results than those sponsored by the industry. Thanks to the Freedom of Information Act, some researchers have even been able to access the studies done by the drug companies that they never published (obviously the ones that were least favorable to their drugs).

When these independent and unpublished studies are analyzed, a very different picture of depression and the efficacy of antidepressants begins to emerge.

Contrary to popular belief:

You might be shocked by some of these statements. Though I was already very skeptical about antidepressants before beginning this research, I myself have been blown away by the complete lack of evidence supporting the theory that depression is a biological disease and the very strong evidence that antidepressants are no more effective than placebo.

I’ll be writing in more detail about several of the points to come in the coming weeks, so please stay tuned!

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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.

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

• Natural Prevention of Heart Disease Guidelines
• The Truth About Cholesterol Brochure
• Resources for further learning
• Recommended tests for heart disease
• Recent New York Times article questioning efficacy of cholesterol-lowering drugs

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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…

You 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.

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:

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:

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

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:

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

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

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

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

• Handouts from my recent public talk on cholesterol
• Dr. Uffe Ravnskov’s “The Cholesterol Myths”
• The International Network of Cholesterol Skeptics

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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.

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

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