A graduate of Harvard Medical School and the founder and director of The Center for Mind-Body Medicine in Washington, DC, Dr. Gordon has been helping people to recover from depression without drugs for almost 40 years. If what you’ve been learning on The Healthy Skeptic about depression and antidepressants rings true, you’ll love Dr. Gordon’s work.

The web-based series, called “A Natural Approach for Treating Depression,” will include video lessons focused on four of Dr. Gordon’s main themes to treating depression and is based on Dr. Gordon’s treatment program, which he developed and has been teaching around the world for almost 40 years.

Dr. Gordon’s program asserts that prescription antidepressants are often ineffective and create significant side effects. He teaches natural self-care techniques, such as relaxation exercises, physical exercise, proper nutrition and others, that have been proven to successfully treat depression and its symptoms. The program allows the patient to take an active, effective role in their own healing. The series and its related downloadable resources for participants are free.

If you or anyone you know is suffering from depression and could use some extra guidance, I would highly recommend this program. Dr. Gordon writes with clarity, compassion and decades of firsthand experience in treating patients with depression. Although I haven’t yet heard him speak or teach, I can say with confidence from reading his book that his online program will be an invaluable resource to those struggling with depression.

For more information and to sign up, follow this link.

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• Placebo as Effective as Antidepresants
• When it Comes to Drug Claims, Skepticism is Healthy
• A Closer Look at Antidepressants
• The “Chemical Imbalance” Myth
• Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Drugs
• The Dark Side of Antidepressants
• The Heart of Depression
• The Stress-Depression Link
• Treating Depression Without Drugs - Part I
• Treating Depression Without Drugs - Part II
• Treating Depression Without Drugs - Part III

selected offsite articles

• Efficacy of Antidepressants in Adults
• The Emperor’s New Drugs: An Analysis of Antidepressant Medication Data Submitted to the U.S. Food and Drug Administration
• Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration
• Antidepressants: A Triumph of Marketing Over Science?
• Antidepressants and Placebos: Secrets, Revelations, and Unanswered Questions
• Do Antidepressants Cure or Create Abnormal Brain States?
• The Antidepressant Debate
• Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature

Books: serotonin hypothesis & antidepressants

• America Fooled: The Truth About Antidepressants, Antipsychotics And How We’ve Been Deceived, by Timothy Scott Ph.D
• Rethinking Psychiatric Drugs: A Guide for Informed Consent, by Grace Jackson M.D.
• The Myth of the Chemical Cure: A Critique of Psychiatric Drug Treatmentby Joanna Moncrieff, M.D.
• Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Drugs, by Peter Breggin M.D.
• Brain Disabling Treatments in Psychiatry: Drugs, Electroshock, and the Psychopharmaceutical Complex, by Peter Breggin M.D.
• Blaming the Brain: The Truth About Drugs and Mental Health, by Elliot Valenstein Ph.D

Books: holistic treatment of depression

• Unstuck: Your Guide to the Seven-Stage Journey Out of Depression, by James S. Gordon M.D.
• The Depression Book: Depression as an Opportunity for Spiritual Growth, by Cheri Huber
• The Mindful Way through Depression: Freeing Yourself from Chronic Unhappiness, by Mark Williams, Zindel Segal, John Teasdale, Jon Kabat-Zinn
• Spiritual Emergency (New Consciousness Reader), by Stanislav Grof M.D.
• Turning Suffering Inside Out, by Darlene Cohen
• When Things Fall Apart, by Pema Chodron

tapes & cds

• Mindfulness-Based Stress Reduction
• “Mini-Moves” (great for daytime relaxation & improving sleep)
• Unconditional Self-Acceptance

nutrition

• Principles of Healthy Diets

handouts

• Natural Treatment & Prevention of Depression

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The World Health Organization states that depression is the leading cause of disability, affecting more than 120 million people worldwide. Antidepressants are now the most popular class of drugs in the U.S., and their use has been growing rapidly over the past two decades. From 1990 to 2000, prescriptions for SSRIs (the leading class of antidepressant drugs) rose by a staggering 1300%. In the last year alone, 30 million patients in the U.S. spent over $12 billion on antidepressants.

However, despite their aggressive promotion and widespread use, recent evidence suggests that antidepressants are not as effective as we have been led to believe. Other studies have raised concerns about the long-term safety of antidepressant drugs, including a potential increase in suicidal behavior in both children and adults.

In this two-hour presentation, you’ll learn about several non-drug treatments that are clinically proven to be at least as effective as antidepressants for relieving depression in all but the most severe cases. We will also review various theories on the nature and causes of depression, drawing upon both modern science and traditional wisdom.

Date: Wednesday, September 24th

Time: 7:00 - 9:00 PM

Location:
Acupuncture & Integrative Medicine College (AIMC)

2550 Shattuck Ave (at Blake)
Berkeley, CA 94704
MAP

AIMC is an easy, 10-minute walk south on Shattuck from downtown Berkeley BART.

Cost: Free

Click here to download a PDF flyer for the event.

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People taking prescription antidepressants appear to drive worse than people who aren’t taking such drugs, and depressed people on antidepressants have even more trouble concentrating and reacting behind the wheel.

These were the conclusions of a study recently released at the Annual Convention of the American Psychological Association.

The group taking antidepressants who reported a high number of symptoms of depression performed significantly worse than the control group on several of the driving performance tasks.

Participants in the study had to make a series of common driving decisions, such as reacting to brake lights, stop signs or traffic signals while being distracted by speed limit signs, pylons, animals, other cars, helicopters or bicyclists. The simulation tested steering, concentration and scanning.

This is, of course, further evidence that antidepressants create rather than cure abnormal brain states.

And one more reason, of many, not to take them.

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In the last few articles in my series on antidepressants and depression, I have presented evidence demonstrating that - despite popular belief - depression is not caused by a deficiency of serotonin in the brain.

However, this of course does not suggest that depression is completely divorced from biochemical processes in the body. The brain is a “living orchestra” of complex, interconnected systems that are in continuous relationship with one another. Everything from the food that we eat to the chemicals we’re exposed to in our environment to the hormones we produce effects the functioning of the brain.

This will likely come as no surprise to you. It’s simply common sense. But as you may have noticed, in the world of scientific research common sense must first be proven according to the established standards of scientific proof before it is accepted.

Such has been the case with the link between stress and depression. I’ll wager that if I asked ten people on the street whether chronic stress caused depression, probably all ten of them would say “yes”. However, scientific proof of the causal link between chronic stress and depression has only begun to emerge over the past few years. It has been known for much longer that depressed people have elevated levels of cortisol (an indicator of chronic stress), but it was not known whether those elevated levels were the result or cause of depression.

In 2006 Ardyfio & Kim published a study indicating that chronic hypercortisolemia (elevated cortisol levels in the blood) causes anxiety-related behavior in mice. These results suggest that elevated cortisol levels may contribute to the symptom profile of depression rather than simply being a consequence of it.

Ardyfio & Kim’s study also confirmed the results of other studies which suggest that while acute stress is adaptive (helps us adjust to our changing circumstances), chronic stress has detrimental effects on the brain and behavior. Indeed, chronic stress has been linked to a wide variety of modern diseases, including (but not limited to) heart disease, cancer, diabetes, autoimmune disease, irritable bowel syndrome and fibromyalgia.

In a more recent study published in 2007, work stress was demonstrated to precipitate diagnosable depression and anxiety-related disorders in previously healthy, young individuals. The authors point out that stressful work conditions predict poor mental health, and that currently as many as 40% of people are exposed to work stress. (That’s funny, I would have thought the number to be closer to 100%).

The relationship between psychological job demands and the risk of depression and anxiety was graded; in study members exposed to high psychological job demands the risk was two times higher than in those with low demands. The combination of multiple work stressors conferred an even higher risk, especially in men.

Once again, this probably does not come as a surprise to you. It makes sense that high stress at work may cause depression and anxiety. But, believe it or not, this is relatively recent news to the mainstream scientific establishment.

Finally, in a study published today, researchers have shown how cortisol (one of the stress hormones) regulates brain neurotransmission in both the short and long term and enables neuronal connections to adapt.

In the short term, cortisol increases the mobility of receptors found on the surface of neurons, thus allowing synaptic connections to adapt more effectively to the demands of brain activity. The stress hormone might be considered as an “alarm” that mobilizes the receptors for action. This behavior is adaptive, as it helps the organism (us) prepare and mobilize for action when faced with stress (a threat).

However, in the case of prolonged stress (which is the type of stress most prevalent in modern life) cortisol actually reduces synaptic plasticity. Lack of receptor mobility contributes to a lack of adaptation, which of course, is bad news for us.

The relevance to all of these studies to our recent discussion about depression and its treatment is this: stress is likely a significant contributing factor to depression for most people, and stress-management should play an important role in the treatment of depression.

Stress-management strategies are drug-free, non-invasive, cost-effective and have a wide range of beneficial “side effects” such as happiness, relaxation, improved sleep, more energy, improved libido, increased productivity, and protection from the legion of diseases that have been linked to stress.

In short, there is absolutely no reason not to include stress management in your treatment regimen for depression, or in your daily life even if you are currently healthy and free of disease.

There are many ways to reduce stress, including meditation, prayer, gentle movement (yoga, tai chi, Feldenkrais), exercise, deep relaxation techniques, spending time in nature, listening to music. What’s most important is that you find something that works for you and stick with it.

Mindfullness-Based Stress Reduction (MBSR), created by Dr. Jon Kabat-Zinn, is a very successful approach that has been clinically proven in well-designed studies to reduce pain and stress and improve health. I recommend his book Full Catastrophe Living, as well as the CD recordings of the techniques.

I also recommend a system of gentle movement and breathing exercises called “mini-moves”. Although they are marketed as a treatment for insomnia, the creator (Michael Krugman) of the system believes (quite correctly) that the best way to cure insomnia is to manage daytime stress successfully. You can download the “Secrets of Sounder Sleep” audio here. They are very simple and can be performed in as little as 5-15 minutes at a time.

I’ve used both of these systems myself with great success.

Next week will be the final article in the depression series (for now): drug-free alternatives to treating depression. Until then…

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Today’s article is the sixth in an ongoing series on antidepressants and depression. It’s long, so you might want to print it out or go grab a cup of tea. If you are visiting the blog for the first time, or you haven’t had a chance to read the previous articles, you might find it helpful to do so before diving into this one.

The treatment of depression with drugs is based on the enormous collective delusion that psychiatric drugs act by correcting a chemical imbalance in the brain. As a result, a large percentage of the population has been convinced to take drugs in order to deal with the problems of daily life. Everything from break-ups to job difficulties to worries about the future have been transformed into “chemical problems”.

The myth that depression is caused by a chemical imbalance has permeated public consciousness, changing the way we view our lives and ourselves. We have become, in the words of sociologist Nicholas Rose, a society of “neurochemical selves”, recoding our moods and ills in terms of the supposed functioning of our brain chemicals and acting on ourselves in light of this belief.

This is reflected in the growing market for non-prescription products claiming to “enhance serotonin levels” in health food shops and on the Internet, and the cascade of claims that everything from chocolate to exercise makes you feel good because it “balances brain chemicals”. It also largely explains the 1300% growth between 1990 and 2000 in prescriptions of selective serotonin reuptake inhibitors (SSRIs), the most popular class of antidepressant drugs.

Yet, as I have explained in a previous article, there is no evidence to support the notion that depression is associated with an abnormality or imbalance of serotonin (or any other brain chemical), or that antidepressants work by reversing such a problem. Moreover, recent meta-analyses (Kirsh et al. 2008; Kirsh et al. 2004) suggest that antidepressants have only a small advantage over placebo, and that this advantage is most likely clinically meaningless. It has never been demonstrated that antidepressants act in a specific, disease-centered manner, nor have antidepressants ben shown to be superior to other drugs with psychoactive properties (Moncrieff & Cohen, 2006).

In spite of the complete lack of evidence supporting their use, one still often hears the familiar refrain “yes, but drugs are necessary in some cases!” This statement may in fact be true, but not because drugs have been demonstrated to be effective for certain types of depression or with certain patients. Instead, drugs may be necessary in a society where traditional social support structures which play a therapeutic role have completely broken down.

Studies have shown that most individuals with a healthy social support network are able to easily handle major stressors in life. When that network is underdeveloped or non-existent, it is far more likely that depression will occur (Wade & Kendler, 2000).

It has been observed, for example, that schizophrenia and other mental disorders occur less frequently and have a much more favorable prognosis in so-called “Third World” countries than in the West (Sartorious et al 1986). The influence of culture has been mentioned as an important determinant of differences in both the course and outcome of mental illness.

In developing countries strong connections between family members, kin groups and the local community are more likely to be intact. In addition, cultural, religious and spiritual beliefs in these societies provide a context in which symptoms of depression and other mental illness can be understood outside of the label of medical disease or pathology. Possession and rites of passage are two examples of such contexts.

In the West, however, these traditional support structures have been replaced by new cultural norms that do not offer support or therapeutic value to people experiencing mental distress. Among the socio-cultural factors identified by researchers as having a negative influence in Western societies are: extreme nuclearization of the family and therefore lack of support for mentally ill members of the kin group; covert rejection and social isolation of the mentally ill in spite of public assertions to the contrary; immediate sick role typing and general expectation of a chronic mental illness if a person shows an acute psychotic reaction; and the assumption that a person is insane if beliefs or behavior appear somewhat strange or “irrational”.

Therefore, in the West depression is far more likely to occur because of the breakdown of strong family and community support structures, the stigmatization of mental illness, the belief (perpetuated by drug companies) that all mental illness is “chronic”, and the lack of any cultural, religious or spiritual support for people who do not share the consensus view of reality. Statistics measuring the prevalence of depression around the world bear this out. According to the World Health Organization, if current trends continue, by the year 2020 depression will be the leading cause of disability in the West.

In contrast, in developing countries that have not yet fully adopted Western culture transient (i.e. temporary) psychotic reactions and brief depressive episodes are more common than chronic mental illness. When an individual begins to experience distress, the surrounding family and community respond with sympathy, support and traditional therapeutic resources. Surrounded by a rich support structure, the individual is able to return relatively quickly to healthy mental functioning - without drugs.

The cultural differences in the incidence of and response to mental illness suggests something that may be entirely obvious to you but has been largely forgotten in contemporary discussions about depression: that it cannot be properly defined or understood without considering the social context in which it occurs.

In other words, depression is both an individual and a social disease.

Unsurprisingly, epidemiological evidence has tied depression to poor housing, poverty, unemployment and precarious or stressful working conditions. Imagine, for example, a single parent working two low-paying jobs trying to support her child with no family or close friends nearby to help and little time to spend with them even if they were present. Or consider a child that spends most of his days in a school that doesn’t value his style of learning, eats a steady diet of sugar and processed food and lives with an alcoholic parent who is verbally and perhaps physically abusive. It makes perfect sense that both of these individuals could frequently feel sad, hopeless and even desperate. But are these individuals “depressed”?

Even if we agree that the intense feelings they are experiencing could be labeled as “depression”, perhaps a more relevant question might be this: is depression always a pathology? Or is it possible that much of what we call depression is simply a natural and entirely human response to certain circumstances in life?

This is exactly what Allan Horwitz and Jerome Wakefield argue in their book “The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder“. The authors point out that the current epidemic of depression has been made possible by a change in the psychiatric definition of depression that allows the classification of normal sadness as a disease, even when it is not.

Horwitz and Wakefield define normal sadness as having three components: it is context-specific; it is of roughly proportionate intensity to the provoking loss/stimulus; and it tends to end roughly when the loss or situation ends, or else it gradually ceases as coping mechanisms adjust individuals to new circumstances.

The hypothetical examples I gave above of the single parent and the child living in an abusive home environment undoubtedly meet Horwitz & Wakefield’s criteria for “normal sadness”. The feelings occur in a specific context and are roughly proportionate to the circumstances. And though we can’t know this for sure since our example is hypothetical, one might assume that if the conditions of their lives were more favorable they may not feel so sad, hopeless and desperate. Nevertheless, in the West today both of these individuals would almost certainly be labeled as depressed and treated with psychoactive drugs.

While I appreciate the importance of Horwitz and Wakefield’s distinction between normal sadness and depression, I believe it is incomplete. In their framework, there must be some stimulus such as the death of a loved one, the loss of a job or the end of a relationship in order for someone to “escape” the depression label. Yet such events are not the only causes of discontent.

Regardless of economic status people in the West live in increasing isolation and alienation from each other, their communities and the natural world. Phone and email have replaced face-to-face interaction. The impersonality of big-box chain stores and strip mall outlets have replaced the intimacy and familiarity of the local corner store. The pace of life has become so fast that most people feel they are struggling just to get by. And even though we are far richer as a nation now, studies show that people today are not as happy as they were in the 1950s.

Sociologist Alain Ehrenberg has recently suggested that depression is a direct result of the new conceptions of individuality that have emerged in modern societies (Ehrenberg 2000). In societies that celebrate individual responsibility and personal initiative, the reciprocal of that norm of active self-fulfillment is depression - now largely defined as a pathology involving a lack of energy or an inability to perform the tasks required for work or relations with others. The continual incitements to action, to choice, to self-realisation and self-improvement act as a norm in relation to which individuals govern themselves, and against which differences are judged as pathologies.

Another way to speak of this change is as an increase in psychological stress. It is difficult to accurately compare stress levels today to those of the past, but sociologists like Juliet B. Schorr at Harvard University have observed that Americans (and likely people in all Western societies) are working longer hours, often with less pay, and have far less time for leisure. Since recent studies have identified a causal link between work stress and depression, one can safely make the assumption that the increase in work hours together with the decrease in leisure time could very well be contributing to the epidemic of depression.

Consider a middle-class individual living in an “exurban” housing tract 100 miles from their workplace. Each day they commute for two hours in each direction, fighting traffic all the way. Their job lacks any relevance or meaning to them and is simply done to make money and survive, without any joy or satisfaction. They have little control or agency at work and spend there day performing trivial tasks that do not challenge or engage them. They do not know their neighbors, they are disconnected from nature, and perhaps they have recently gone through a painful divorce.

If this person is experiencing apathy, sadness and a lack of enthusiasm for life, does that mean they are depressed? And even if we do label their condition as “depression”, can we truly understand or treat them successfully without addressing the circumstances (or root causes) of this person’s so-called depression?

There is little doubt that the people who seek treatment for depression are suffering. But should psychological and emotional suffering always be viewed as “something to get rid of”? Despite claims made by the companies who market antidepressant drugs, suffering cannot be pulled out of the brain like a splinter from the foot. Great religious and spiritual traditions from around the world view suffering as an avenue to greater understanding of oneself, life and God. Suffering can be viewed as a signal drawing our attention to issues in our life that need to be addressed.

If we simply use chemicals to diminish these signals and numb ourselves from their effects, we lose the opportunity to grow, evolve and heal. According to world-renowned psychiatrist David Healy, when strong feelings are suppressed by rejecting them or with drugs, people become “binded” to their own psychological or spiritual state. Psychiatric drugs blunt and confuse essential emotional signals and make it very difficult for people to know what they are really feeling. And because the pharmacological effects of drugs impair mental functioning, they can reinforce the patient’s sense of helplessness and dependence upon chemicals - even when those chemicals are preventing them from full recovery.

People who are depressed have lost touch with their hopes and dreams. Yet they wouldn’t be depressed if they did not still have a vision for a better life. If drugs are used to obliterate the feelings of discontent or suffering, the connection to that vision for a better life may be lost.

One might legitimately wonder, then, whether it is wise to attempt to treat such complex human and social problems with chemicals. Such a treatment strategy can only be useful if the goal is to perpetuate the status quo, to continue with “business as usual” at all costs, rather than addressing the psychosocial problems that are at the root of the discontent.

The message that drugs can cure our problems has profound consequences. Individual human beings with their unique life histories and personal characteristics have been reduced to biochemical entities and in this way the reality of human experience and suffering is denied (Moncrief 2008). People have come to view themselves as “victims of their own biology”, rather than as autonomous individuals with the power to make positive changes in their lives.

At another level such an exclusive focus on drug treatment allows governments and institutions to ignore the social and political reasons why so many people feel discontented with their lives. This is not surprising, of course. Both governments and corporations stand to benefit from maintaining the status quo and are often threatened by social change.

The “disease-centered” model of depression is presented as objective, unassailable fact, but it is instead an ideology (Moncrieff 2008). All forms of ideology convey a partial view of human experience and activities that is motivated by a particular interest; in this case, the interest of multinational pharmaceutical companies. The best selling drugs today are those that are taken indefinitely. This has fueled the drug companies’ efforts to label depression as a chronic, lifelong disease in spite of epidemiological studies which indicate that, even when untreated, depressive episodes tend to last no longer than nine months.

In her article called “Disease Mongering in Drug Promotion“, Barbara Mintzes describes the effort of pharmaceutical companies to “widen the boundaries of treatable illness in order to expand markets for those who sell and deliver treatments”. This phenomenon is known as “disease mongering”, and involves several tactics including the introduction of new, questionable diagnoses; the promotion of drugs as the first line of defense for problems not previously considered medical; the expansion of current definitions of mental illness; and the inflation of disease prevalence rates.

In a blatant example of the last strategy, pharmaceutical companies have estimated in their promotional literature that up to one-third of people worldwide have a mental illness. This ridiculous (and in my opinion, transparent) claim is not supported anywhere in the scientific literature. Peer-reviewed studies put the figure at significantly less than 5%.

It should be obvious that drug companies would be the first to benefit from such grossly overstated estimates of the prevalence of depression. In fact, executives in the pharmaceutical industry have even admitted as much. Thirty years ago Henry Madsen, the CEO of Merck, made some very candid comments as he approached his retirement. Suggesting he’d rather Merck to be more like chewing gum maker Wrigley’s, Gadsen said that it had “long been his dream to make drugs for healthy people.”

Sadly, Madsen’s dream has been realized with the advent of not only antidepressants, but also statins, antacids and other drugs sold to essentially healthy people. These medications are now the top-selling drugs around the world. (Madsen’s sense of morality may have been skewed, but he certainly was a visionary businessman.)

The field of psychiatry has largely collaborated with the pharmaceutical industry in defining intense and painful emotions as “disorders”. Diagnoses like “panic disorder” and “clinical depression” give a medical aura to powerful emotions and make them seem dangerous, pathological, unnatural or out of control. In an astute observation of this state of affairs, psychiatrist Steven Sharfstein remarked in the March, 2006 issue of Psychiatric News that the biopsychosocial model of depression has been replaced by the “bio-bio-bio” model.

It has now become common practice for psychiatrists to prescribe drugs on their very first visit with a patient, and to tell that patient that they will likely need to take drugs for the rest of their lives. Such a prognosis is offered in spite of the fact that no attempt has been made whatsoever to try proven, non-drug treatment alternatives such as psychotherapy and exercise!

The increasing rates of depression and poor long-term treatment outcomes clearly indicate that the current drug-centered strategy is not effective. For real progress to be made the psychological, social, economic and political roots of depression must be addressed. This will require a coordinated effort on the part of patients, physicians, communities and politicians. It will not be easy, because we are fighting deeply entrenched beliefs about the “biochemical” nature of depression as well as a $500 billion dollar pharmaceutical industry that is not likely to willingly give up the $20 billion in sales represented by antidepressants.

There is no doubt that the systemic changes I am describing are far more difficult to implement than administering a drug. Nevertheless, we must begin if we hope to heal ourselves, our culture and our world.

In the final article of the series, I will present proven non-drug alternatives for treating depression. Stay tuned!

Recommended books

• Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Medications, by Peter Breggin

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Although these drugs are generally considered to be safe by the media and amongst medical professionals and patients, a close look at the evidence suggests otherwise. Antidepressants have serious and potentially fatal adverse effects, cause potentially permanent brain damage, increase the risk of suicide and violent behavior in both children and adults, and increase the frequency and chronicity of depression. Chronic use of antidepressants also promotes dependency on drugs rather than empowering people to make positive life changes, and places a tremendous burden on healthcare systems in the U.S. and abroad - but I will discuss those issues in next week’s article.

Physiological side effects

The adverse effects of antidepressants include movement disorders, agitation, sexual dysfunction, improper bone development, improper brain development, gastrointestinal bleeding, and a variety of other lesser known problems. These are not rare events, but the most significant harm comes only after months or years of use, which leads to the false impression that antidepressants seem quite safe.

More than half of those beginning an antidepressant have one of the more common side effects (Brambilla et al. 2005).

While some side effects may not carry serious health risks, others do. Gastrointestinal bleeding can become a life-threatening condition, and improper bone development in children is a serious problem that can lead to increased skeletal problems and frequent bone fractures as they age. It has been shown that serotonin exposure in young mice impairs their brain’s cerebral development (Esaki et al. 2005), and many researchers believe that the use of SSRI medications in pregnant mothers and young children may predispose children to emotional disorders later in life (Ansorge et al. 2004).

Another problem with the side effects caused by antidepressants that is often not discussed is the likelihood that additional medications will be prescribed to control them. It is well-known that Prozac produces anxiety and agitation, so physicians often prescribe a sedative (typically a benzodiazapene) along with it. Since recent studies have shown that antidepressants cause gastrointestinal bleeding, doctors are starting to prescribe acid-inhibiting drugs such as Nexium to prevent this side effect. These drugs also inevitably cause side effects, which may lead to the prescription of even more drugs. (This is not uncommon, as I pointed out in last week’s article.)

Psychological side effects

Perhaps the best known psychological side effect of SSRIs is “amotivational syndrome”, a condition with symptoms that are clinically similar to those that develop when the frontal lobes of the brain are damaged. The syndrome is characterized by apathy, disinhibited behavior, demotivation and a personality change similar to the effects of lobotomy (Marangell et al. 2001, p.1059). All psychoactive drugs, including antidepressants, are known to blunt our emotional responses to some extent.

Clinical studies of SSRIs report that agitation is a common side effect. When Yale University’s Department of Psychiatry analyzed the admissions to their hospital’s psychiatric unit, they found that 8.1% of the patients were “found to have been admitted owing to antidepressant mania or psychosis” (Preda et al. 2001). Agitation is such a common side effect with SSRIs that the drug companies have consistently sought to hide it during clinical trials by prescribing a tranquilizer or sedative along with the antidepressant. Studies by Eli Lilly employees found that between 21% and 28% of patients taking Prozac experienced insomnia, agitation, anxiety, nervousness and restlessness, with the highest rates among people taking the highest doses (Beasley et al. 2001).

From their inception, antidepressants have been recognized as having a worrisome capacity to incite changes between episodes of depression (characterized by dysphoria, insomnia, low energy, poor concentration, reduced appetite and diminished libido) and episodes of mania (characterized by euphoria, increased activity, rapid speech, racing thoughts, diminished need for sleep, hypersexuality and diminished impulse control).

Several reports suggest that SSRIs are associated with movement disorders such as akathisia, Parkinson’s disease, dystonia (acute rigidity), dyskinesia (abnormal involuntary choreic movements) and tardive dyskiniesia (Gerber & Lynd 1998).

These movement disorders are serious enough on their own. However, what is even more alarming is the potential for akathisia to induce aggression and suicide. Akathisia, a condition of inner restlessness or severe agitation, is the most commonly occurring movement disorder associated with psychoactive drug use. Akathisia-related violence receives specific attention in the Diagnostic and Statistical Manual of Mental Disorders (DSM). Akathisia has been shown to increase violent behavior and suicide, and antidepressants are known to cause akathisia.

Suicide

After years of foot-dragging and thousands of excess suicides, the FDA finally admitted that “two to three children out of every hundred” could be expected to develop suicidal thoughts or actions as a result of antidepressant therapy (Harris 2004). The risk of suicide events for children receiving SSRIs has been three times higher than placebo. (Healy 2005). Amazingly, no bans or restrictions have been placed on their use in children in the U.S.

While the increased risk of suicide in children has become better known, most people are unaware that a similar risk exists for adults. When adult antidepressant trials were re-analyzed to compensate for erroneous methodologies, SSRIs have consistently revealed a risk of suicide (completed or attempted) that is two to four times higher than placebo (Healy 2005).

Turning short-term suffering into long-term misery

A growing body of research supports the hypothesis that antidepressants worsen the chronicity, if not severity, of depressive features in many subjects. Antidepressant therapy is often associated with the poorest outcomes. In a large, retrospective study in the Netherlands of more than 12,000 patients, antidepressant exposure was associated with the worst long term results. 72-79% of the patients who relapsed received antidepressants during their initial episode of depression. In contrast, only one of the patients who did not relapse received no antidepressants during or following the initial episode. (Weel-Baumgarten 2000)

Longitudinal (long-term) follow-up stuides show very poor outcomes for people treated for depression in both hospital and outpatient settings, and the overall prevalence of depression is rising despite increased use of antidepressants (Moncrieff & Kirsch 2006).

Epidemiological observations have long held that most episodes of depression end after three to six months. However, almost half of all Americans treated with antidepressants have remained on medication for more than a year (Antonuccio et al. 2004).

Long-term effects of antidepressants

Antidepressants have been shown to produce long-term, and in some cases, irreversible chemical and structural changes to the body and brain.

The administration of Prozac and Paxil raises cortisol levels in human subjects (Jackson 2005, p.90). Given the fact that elevated cortisol levels are associated with depression, weight gain, immune dysfunction, and memory problems, the possibility that antidepressants may contribute to prolonged elevations in cortisol is alarming to say the least.

In a study designed to investigate the anatomic effects of serotonergenic compounds, researchers at Thomas Jefferson University found that high-dose, short-term exposure to SSRIs in rats was sufficient to produce swelling and kinking in the serotonin nerve fibers (Kalia 2000). Research performed by a different team of investigators demonstrated a reduction in dendritic length and dendritic spine density, and in contrast to the previous study, these changes did not reverse even after a prolonged recovery period. The results were interpreted to suggest that chronic exposure to SSRIs may arrest the normal development of neurons.

I want to emphasize that what I’ve covered here is only the beginning of the story when it comes to the adverse effects of antidepressants. There are volumes of published research and many books which present this information with much more detail. I recommend Peter Breggin’s landmark “Brain Disabling Treatments in Psychiatry” and Grace Jackson’s “Rethinking Psychiatric Drugs” as resources if you are interested in pursuing this further.

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

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

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

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

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

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

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

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

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

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

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

The history of the “chemical imbalance” theory

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

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

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

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

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

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

The fatal flaws of “chemical imbalance” theory

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

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

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

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

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

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

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

How have we been fooled?

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

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

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

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

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

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

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

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

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

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

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

Recommended resources

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

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

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

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

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

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

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

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

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

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

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

Now let’s consider each point in turn.

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

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

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

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

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

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

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

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

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

Now on to the next point.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

As always, I welcome your comments and questions.

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

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

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

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

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

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

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

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

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

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

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

There are now over 90,000 pharmaceutical reps walking the halls of medical offices around the U.S. Since there are less than 600,000 office-based doctors in the U.S. today, there is approximately one full-time drug rep for every six physicians. The drug reps bring free