Myths & Truths

Debunking popular myths and replacing them with scientifically-validated facts

Where’s the beef?

March 26, 2009 in Cancer, Food & Nutrition, Myths & Truths | 18 comments

roast beef You might have seen an article in your newspaper or online touting a recent study published in the Archives of Internal Medicine that “strongly” linked red meat consumption with cancer and an increased risk of death. Heck, how could you miss it? Google shows 547 new articles about the study, and it was mentioned in just about every major newspaper in the U.S.

(That’s not an accident, by the way. It’s an intentional attack by the tyrannical meat-hating scientific majority, the same folks who brought us the “cholesterol causes heart disease” and “saturated fat is bad for you” myths.)

Trouble is – as is so often the case – the study is deeply flawed. In fact, anyone with training in research methodology might find themselves wondering “where’s the beef?” after they read it. In the end it’s just another piece of worthless propaganda parading as medical research. It tells us a lot more about the biases and motives of the researchers, and the incompetence of the media reporting on it, than it does about the effect of red meat consumption on human health.

Here are my “top 10″ reasons to ignore this study and continue to eat your grass-fed, organic red meat:

It was an observational study. Observational studies can show an association between two variables (i.e red meat consumption and death), but they can never show causation (i.e. that eating red meat caused the deaths). A simple example of the difference between correlation and causation is that elevated white blood cell count is correlated with infections. But that doesn’t mean elevated white blood cell counts cause infections!
The relative risk reduction (RRR) was slightly over 1.0. Most researchers don’t pay attention to an RRR under 2.0, due to the notorious difficulties involved with this type of research.
Two articles were published in the American Journal of Clinical Nutrition at around the same time that directly contradicted these results. The first study pooled data from 13 studies and found that risk of colorectal cancer was not associated with saturated fat or red meat intake. The second study found that there was no difference in mortality between vegetarians and meat eaters.
The authors didn’t adequately control for other dietary factors known to increase morbidity and mortality. As another commentator pointed out in her analysis of this study, “Americans get their “cancer causing” red meat served to them on a great big white bun with a load of other carbohydrates (soda, chips, fries) and inflammation-causing n-6 vegetable oils (chips, fries, salad dressings) on the side.” It’s more likely (based on other studies, including the two mentioned above) that the increase in deaths was caused by the junk food surrounding the red meat and not by the meat itself.
The basis of measurement is a “detailed questionnaire”. Questionnaires about one’s diet are always error prone as remarkably few people remember accurately what they eat on any given day, let alone over a period of years. Furthermore, most people lie about what they actually eat, especially now that proper diet has been given a quasi-religious significance and eating poorly is equated with being morally inferior.
Check out this quote from the Archives of Internal Medicine study:

“Red meat intake was calculated using the frequency of consumption and portion size information of all types of beef and pork and included bacon, beef, cold cuts, ham, hamburger, hotdogs, liver, pork, sausage, steak, and meats in foods such as pizza, chili, lasagna, and stew”.

In other words, even those people who ate things like hot dogs and hamburgers (with buns made of refined white flour), and who ate pizza (on refined white flour crusts) were included in the ‘red meat’ group. Also, those who ate processed or cured meats, such as ham, bacon, sausage, hot dogs, or cold cuts (with possible nitrates) were included in the ‘red meat’ group. And those who ate prepared food (with unknown additives and preservatives) such as pizza, chili, lasagna, and stew were also included in the ‘red meat’ group. Therefore, this study does absolutely nothing to prove that red meat, and not these processed and highly refined foods, is the culprit.
The quality of the meat consumed in the study was not taken into account. Highly processed and adulterated “factory-farmed” meats like salami and hot dogs are lumped together with grass-fed, organic meat as if they’re the same thing. It’s likely that very little of the meat people ate in the study was from pasture-fed animals. Factory fed animals are fed corn (high in polyunsaturated, omega-6 fat), antibiotics, and hormones, all of which negatively impact human health.
We don’t know anything about the lifestyles of the different study groups. Were they under stress? Did they lose their jobs? Did they have other illnesses? Did they live in a toxic environment? All of these factors contribute significantly to disease and mortality.
We don’t know if the people in the study ate more sugar, processed food, artificial sweeteners, preservatives, additives or fast food – all of which are known to cause health problems.
We don’t know if the people who ate more red meat were better off financially than the people who ate less red meat, and thus had more exposure to the “medical industrial complex” – which, as you know from my previous article, kills more than 225,000 people per year and is the 3rd leading cause of death in this country.

I could go on, but I think you get the idea. Nothing to see here, folks. Move along.

Me? I’m gonna go have a big, juicy, grass-fed steak.

Further recommended reading

Meat and Mortality. A great critique of the study by Dr. Michael Eades, author of Protein Power.
More on Meat & Sustainability. A Challenge to Environmentalists.
The Red Scare. Another insightful analysis over at Mark’s Daily Apple.

The failure of U.S. healthcare

February 28, 2009 in Medical Industrial Complex, Myths & Truths | 2 comments

failure The U.S. spent 16 percent of its Gross Domestic Product (GDP) – a cool $2 trillion – on health care in 2005.¹ Considering this enormous expenditure, we should have the best medicine in the world. We should be reversing disease, preventing disease, and doing minimal harm. However, careful and objective review shows the opposite.

The U.S. ranks just 34th in the world in life expectancy and 29th for infant mortality. Of 13 countries in a recent comparison, the United States ranks an average of 12th (second from bottom) for 16 available health indicators.²

40 million people in this country do not have health insurance. The exorbitant cost of health care seems to be tolerated based on the assumption that better health results from more expensive care, despite studies that as many as 20% to 30% of patients receive contraindicated care.³

Even worse, a recent study by Dr. Barbara Starfield published in 2000 in the prestigious Journal of the American Medical Association demonstrated that iatrogenic incidents (events caused by medical intervention) are the 3rd leading cause of death in this country, causing more than 250,000 deaths per year. Only heart disease and cancer kill more people.

Dr. Starfield estimates that, each year, medical errors and adverse effects of the health care system are responsible for:

116 million extra physician visits
77 million extra prescriptions
17 million emergency department visits
8 million hospitalizations
3 million long-term admissions
199,000 additional deaths
$77 billion in extra costs

As grim as they are, these statistics are likely to be seriously underestimated as only about 5 to 20% of iatrogenic incidents are even recorded^{analyses which have taken these oversights into consideration estimate that medical care is in fact the leading cause of death in the U.S. each year.}

^{Starfield believes that a major contributor to the poor performance of the United States on health indicators is the high degree of income inequality in this country. Countless studies in the medical literature document the adverse effects of low socioeconomic position on health. New research suggests the adverse effects not only of low social position but, especially, low relative social position in industrialized countries.⁶}

Perhaps the words “health care” have given us the illusion that medicine is about health. In fact, western medicine is not a purveyor of healthcare but of disease-care. When the number one killer in a society is the health care system, that system has no excuse except to address its own urgent shortcomings. Unfortunately, until this happens partaking in allopathic medicine itself is one of the highest causes of death as well as one of the most expensive ways to die.

Park, A. America’s Health Check Up. 11/20/2008. Time Magazine Online. ↩
Starfield B. Primary Care: Balancing Health Needs, Services, and Technology. New York, NY: Oxford University Press; 1998. ↩
Schuster M, McGlynn E, Brook R. How good is the quality of health care in the United States? Milbank Q. 1998;76:517-563 ↩
Leape LL. Error in medicine. JAMA . 1994 Dec 21;272(23):1851-7. ↩
injuryboard.com. General Accounting Office study sheds light on nursing home abuse. July 17, 2003 . Available at: http://www.injuryboard.com/view.cfm/Article=3005. Accessed December 17, 2003 ↩
Wilkinson R. Unhealthy Societies: The Afflictions of Inequality. London, England: Routledge; 1996. ↩

How to increase your risk of heart disease

August 5, 2008 in Food & Nutrition, Heart Disease, Myths & Truths | 7 comments

vegetable oil Easy! 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.

Low-carb diet best for weight loss

July 16, 2008 in Food & Nutrition, Myths & Truths | 7 comments

steak and veggies A study was just published in the New England Journal of Medicine on July 17th comparing the effectiveness and safety of three different weight loss diets. 322 moderately obese subjects were assigned to one of three diets: low-fat, restricted-calorie; Mediterranean, restricted-calorie; or low-carbohydrate, non-restricted calorie.

The rate of adherence to the study diet was 95% at year one and 85% at year two. Among the 272 participants who completed the intervention, the mean weight losses were 3.3 kg for the low-fat group, 4.6 kg for the Mediterranean-diet group, and 5.5 kg for the low-carbohydrate group.

Perhaps more significantly, the relative reduction in the ratio of total cholesterol to HDL was 20% in the low carbohydrate group while only 12% in the low-fat group. Among the 35 subjects with diabetes, changes in fasting plasma glucose and insulin levels were more favorable among those assigned to the Mediterranean diet than among those assigned to the low-fat diet.

Unfortunately, the bias against saturated fat and animal products that is still so prevalent in the mainstream (in spite of the lack of evidence to support it) prevailed in this study. The research team advised those following the low-carb diet to “choose vegetarian sources of fat and protein” and moderate their consumption of saturated fats and meat.

This suggests that the low-fat dieters may have consumed a substantial portion of their calories as fat in the form of omega-6 polyunsaturated fatty acids. Excess intake of omega-6 fatty acids contributes to a host of problems including heart disease, diabetes, and cancer; but even more relevant to this study and its results is the fact that omega-6 fatty acids can cause increased water retention. And as everyone knows, increased water retention equals increased weight.

This certainly causes me to wonder how much more dramatic the results of this study might have been if the low-carb subjects were encouraged to significantly restrict their consumption of omega-6 fats (which cause water retention, and thus weight gain) and replace them with saturated fats (which do not cause water retention). What is remarkable is that in spite of the consumption of omega-6 fats, the low-carb group still lost more weight than both the low-fat and Mediterranean groups. That’s a strong endorsement for the benefits of a low-carb diet for weight loss.

The low-carb and Mediterranean (to a lesser degree) diet also had other benefits beyond promoting weight loss and improving cholesterol measures. The level of high-sensitivity C-reactive protein decreased significantly only in the Mediterranean and ow-carb group, with the low-carb group again showing the greatest decrease (29% vs. 21%). C-reactive protein is a measure of inflammation that has been positively correlated with heart disease in recent studies. Once again, one must wonder if the reduction would have been even greater in the low-carb group had the subjects been told to restrict their intake of omega-6 fats, which are known to promote inflammation.

Another interesting finding is that although caloric intake was only restricted in the low-fat and Mediterranean diet groups, the low-carb group also ended up eating fewer calories during the diet. Many people who follow a low-carb, high protein/high fat diet find that they spontaneously eat less because additional protein, and in particular fat, leads to greater levels of satiety (satisfaction).

One limitation of the study is that it relied on self-reported dietary intake (this is true of almost every dietary study except those performed in tightly controlled conditions, such as an inpatient facility). However, the study was somewhat unique in that it was conducted in a workplace at a research center with an on-site medical clinic. It also had several other strengths. The drop-out rate was exceptionally low for a study of this kind; all participants started simultaneously; the duration was relatively long (2 years); the study group was relatively large; and the monthly measurements of weight remitted a better understanding of the weight-loss trajectory than other studies.

The “chemical imbalance” myth

June 30, 2008 in Depression, Myths & Truths | 58 comments

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:

Reducing levels of norepinephrine, serotonin and dopamine does not actually produce depression in humans, even though it appeared to do so in animals.
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.
Drugs that raise serotonin and norepinephrine levels, such as amphetamine and cocaine, do not alleviate depression.
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.
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.
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.
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.
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

A closer look at antidepressants

June 26, 2008 in Depression, Myths & Truths | 15 comments

magnifying glass I’d like to thank everyone for their comments, both online and “offline” about my recent “Placebos as Effective as Antidepressants” article. Some very good questions were raised in a comment from Stephan, author of the highly recommended Whole Health Blog that I would like to address in today’s article.

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 fully agree with you about the “chemical imbalance” thing; it’s incredibly dense. They try to spin it like you were born with depression and there’s nothing you can do about it but take a drug. I have a friend who’s into mood disorder research and I’ve talked to him about that meta-analysis showing no significant effect of ADs.

First of all, he has no dog in the fight because his interest in mood disorders is purely academic. I can vouch for his lack of bias toward antidepressants. Here’s what he told me. Basically, what we call “depression” is actually a collection of related disorders. Antidepressants only work on a subset of them.

There are “responders” and “non-responders” in any group of people who receive antidepressants. For responders, antidepressants can be very effective. When you do a meta-analysis where you’re averaging everyone with “depression” together, the effect of an antidepressant will be small or nonexistent because of the heterogeneity. So this is a problem with saying that antidepressants aren’t effective based on that analysis.

I don’t have a problem believing that antidepressants work for some people. They certainly work in animal models of depression, where there is no placebo effect. I don’t think we should banish them from planet Earth. But I do think the fact that we use them so much points to a bigger problem that we should be addressing by other means.”

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