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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.

Cholesterol

healthy skeptic articles

Offsite Articles

  • What’s Wrong With ‘Politically Correct’ Nutrition?, Weston A. Price Foundation
  • The Soft Science of Dietary Fat, by Gary Taubes
  • The Skinny on Fats, by Sally Fallon & Mary Enig, Ph.D
  • The Oiling of America, by Mary Enig, Ph.D
  • High Cholesterol & Heart Disease: Myth or Truth?, by Chris Masterjohn

Websites

  • The Weston A. Price Foundation (excellent information about nutrition)
  • The International Network of Cholesterol Skeptics (group of physicians and researchers worldwide who challenge the “cholesterol-heart disease hypothesis
  • Cholesterol and Health (excellent, research-based website focused on debunking popular myths about cholesterol and heart disease)
  • Nourishing Our Children (must see for parents)
  • Wise Food Ways (see section on “where the wise foods are” for local food resources)
  • Eat Wild (for locating grass-fed meat and dairy products)
  • Real Milk (for health benefits of raw dairy products)

Books

  • The Cholesterol Myths, by Uffe Ravnskov M.D., Ph.D (written by a physician with a Ph.D in statistics; Dr. Ravnskov has been an independent researcher debunking the myths of cholesterol and saturated fat since the 70s)
  • The Great Cholesterol Con, by Anthony Colpo (*over 1400 references, but easy to read as well; highly recommended)
  • The Great Cholesterol Con, by Malcom Kendrick M.D. (lucid and humorous; a great introduction)
  • The Fluoride Deception, by Christopher Bryson (a lucid and well-researched analysis of the dangers of fluoride)
  • Nourishing Traditions, by Sally Fallon (the “bible” of traditional, whole-foods nutrition; information & recipes)
  • Wild Fermentation: The Flavor, Nutrition & Craft of Live-Culture Foods, by Sandor Katz (the best book on fermentation and live-culture foods I know of)
  • Full Moon Feast, by Jessica Prentice (an excellent introduction to the native nutrition lifestyle & a fantastic cookbook)

Handouts from cholesterol talk

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.

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.

corn kernelsThis week I’d like to bring your attention to three articles I came across on the web which illustrate the utter madness of mainstream medicine and nutrition.

The first article, “Beware of New Media Brainwashing About High Fructose Corn Syrup“, appeared on Mercola.com, a health advocacy site run by Dr. Joseph Mercola which I recommend. I agree with Dr. Mercola on most things, and even when we don’t agree the differences are relatively minor.

In his article Mercola warns consumers that The Corn Refiners Association is spending $20 to $30 million dollars on an advertising campaign to “rehabilitate” the reputation of high fructose corn syrup (HFCS), claiming that the product is “no worse for you than sugar.”

HFCS is now the #1 source of calories for children in the U.S., a staggering fact when research has clearly linked HFCS to obesity, diabetes, metabolic syndrome, high triglycerides, liver disease and more. On top of that, HFCS is almost always made with genetically modified corn.

Head on over to Mercola.com to read the rest of the article and learn why you and your children should be avoiding HFCS as much as possible. HFCS is found primarily in processed foods (in everything from hamburger buns to soda), so if you follow my general recommendation of eating a whole-foods diet you should have no trouble avoiding it.

The second article, “8-Year-Olds on Statins? A New Plan Quickly Bites Back“, was published in the New York Times on July 8. It describes new guidelines issued by the American Academy of Pediatrics recommending that statin drugs be prescribed to kids as young as 8 years old!

While some doctors applauded the idea (which is incomprehensible to me), others were “incredulous”. Why are they incredulous? Because there is absolutely no evidence suggesting that treating children with statins will prevent heart attacks or reduce mortality from heart disease. Furthermore, there are no data on the possible side effects from taking statins for 40 or 50 years. Since statins have caused cancer in several animal studies, there is no reason to assume that this is not a risk in humans - especially with such long-term use of the drugs.

If you’re not familiar with the dangers of statin drugs, I suggest you read my recent article “The Truth About Statin Drugs“. Not only are statins nowhere near as effective as claimed, they have serious adverse effects and risks - including death.

What’s more, statins have been neither studied nor approved for use with children. In other words, the American Pediatric Association wants to perform an uncontrolled experiment with statin drugs and our children. This is completely unacceptable in light of what we already know about these drugs.

This is yet another obvious example of how the massive conflicts of interest in the medical field, which I described in a previous article, cloud the judgment of otherwise well-meaning physicians and health organizations.

Head over to the New York Times to read the rest of the article.

The third article, “Popular Fish, Tilapia, Contains Potentially Dangerous Fatty Acid Combination” which appeared on ScienceDaily.com, revealed that farm-raised tilapia has very low levels of beneficial omega-3 fatty acids and, even worse, very high levels of omega-6 fatty acids.

This is particularly troublesome because tilapia has become one of the most highly consumed fish in the U.S. (mostly due to its low price), and that trend is expected to continue through 2010.

Researchers have found that tilapia has higher levels of omega-6 fatty acids than doughnuts. That’s scary.

The health risks of excessive amounts of omega-6 fatty acids in the diet are well established. In short, they are significant contributors to both inflammation and oxidative damage in the body. Inflammation and oxidative damage are major risk factors for heart disease, diabetes, cancer and many other diseases.

Wild-caught oily fish, on the other hand, contain a favorable ratio of omega-3 to omega-6 fatty acids and may actually protect against inflammation and oxidative damage?

So what’s the problem with tilapia, you ask? The problem is that they are raised on a “fish farm” where they are fed inexpensive corn-based feeds which contain short chain omega-6 fatty acids that the fish convert and store in their tissues. While this practice has kept the price of tilapia low, it has also transformed it into a toxic food.

Repeat after me: fish don’t eat corn. Fish don’t eat corn. Fish don’t eat corn.

(Cows don’t normally eat chicken parts, gummi bears and garbage, either; but they do in commercial feedlots where most of the meat in the U.S. is produced. I’ll save that for another day, though.)

What all of these articles share in common is 1) further evidence of the rampant conflicts of interest in our medical care system, 2) the complete lack of an objective, independent regulatory body that can protect consumers from the malfeasance of Big Pharma and Big Agrobusiness, 3) the general departure from common sense and traditional wisdom when it comes to health care and nutrition.

It’s absolute madness.

serotonin illustration“A theory that is wrong is considered preferable to admitting our ignorance.” - Elliot Vallenstein, Ph.D.

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:

“I also saw how badly biological psychiatrists want to be regarded as doctors and accepted by the rest of the medical profession. In their desire to be accepted as real clinical scientists, these psychiatrists were building far too dogmatic an edifice… pushing their certainty far beyond what the data could support.”

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

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

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