Depression

You are currently browsing the archive for the Depression category.

big pharma cartoonA new report due to be published in the May issue of the American Journal of Psychiatry shows that antidepressants aren’t all they’re cracked up to be.

But, faithful readers, you already knew that. Right?

The report is part of the National Institute of Mental Health-funded Sequenced Treatment Alternatives to Relieve Depression (STAR*D) project – the largest study of the treatment of depression conducted in the United States. It showed that findings from clinical studies used to gain FDA approval of antidepressants are not applicable to most patients with depression.

Researchers at the University of Pittsburgh Graduate School of Public Health compared symptoms and outcomes in depressed patients who met phase III study inclusion criteria to those who did not. Phase III studies for antidepressants determine the effectiveness of the drug in comparison to a placebo.

The inclusion criteria for these studies aren’t standardized or subject to any federal guidelines. Typically this means that patients with milder forms of depression, chronic depression, or other psychiatric or medical conditions in addition to short-term depression are excluded from studies.

In other words, the majority of “real world” patients with depression who end up taking antidepressants are excluded from clinical studies. It should be obvious why this is a problem. In a normal, clinical setting many patients with depression do also have other illnesses, such as diabetes, chronic fatigue syndrome or irritable bowel syndrome (IBS). It’s not unusual for them to have anxiety and insomnia, as well. In fact, it wouldn’t be presumptuous to expect that a depressed person might be suffering from a number of conditions that are either contributing to or caused by their illness.

Yet the only people that “qualify” for the clinical trials which determine whether antidepressants get approved by the FDA are those with short-term depression, no history of depression, no other psychiatric conditions such as anxiety, and no physical illnesses like heart disease or diabetes. This is the only subgroup of the general population for which we have any data on the efficacy of antidepressants.

By the same token, this means is that we have almost no clinical data on how antidepressants work for the “real world” patients who are most likely to be taking them. Indeed, after assessing 2,855 patients treated with citalopram (Celexa), the study authors found that fewer than one in four, or 22.2%, of the patients met the usual criteria for inclusion in phase III clinical trials.

According to study lead author, Stephen Wisniewski, Ph.D., professor of epidemiology and co-director of the Epidemiology Data Center, University of Pittsburgh Graduate School of Public Health, “This raises major concerns about whether results from traditional phase III studies can be generalized to most people with depression, who also often suffer from anxiety, substance abuse and other medical and psychiatric problems.”

When Wisniewski and his colleagues looked at the efficacy of antidepressants in those who did not meet phase III inclusion criteria - meaning the majority of people who take the drugs in real life - they found that their outcomes were much worse than those who did qualify for the trials. The depression remission rate in the patients who met the criteria was 34.4 percent, compared to only 24.7 percent in the ineligible group.

So, here’s the bottom line: antidepressants are nowhere near as effective as research suggests.

And that is really bad news for the drug companies, because research already suggests that antidepressants aren’t very effective at all. In fact, as I explained in a previous article, antidepressants are no more effective than placebo for most people. If antidepressants are no more effective than placebo in the patients that do meet phase III criteria, and we know that antidepressants are less effective for patients who don’t meet phase III criteria (the vast majority of “real world” depression patients), then couldn’t we assume that antidepressants are less effective than placebo for most patients?

Yes, we could.

For more information on this topic, check out this index of my articles (as well as selected off-site resources) on depression and antidepressants.

tibetan bowlEach week, it seems, more and more evidence pours in demonstrating the effectiveness of non-drug treatments for depression.

In a study, published December 1, 2008 in the Journal of Consulting and Clinical Psychology, MBCT proved as effective as maintenance anti-depressants in preventing a relapse and more effective in enhancing peoples’ quality of life. The study also showed MBCT to be as cost-effective as prescription drugs in helping people with a history of depression stay well in the longer-term.

Over the 15 months after the trial, 47% of the group following the MBCT course experienced a relapse compared with 60% of those continuing their normal treatment, including anti-depressant drugs. In addition, the group on the MBCT programme reported a higher quality of life, in terms of their overall enjoyment of daily living and physical well-being.

MBCT was developed by a team of psychologists from Toronto (Zindel Segal), Oxford (Mark Williams) and Cambridge (John Teasdale) in 2002 to help people who suffer repeated bouts of depression. It focuses on targeting negative thinking and aims to help people who are very vulnerable to recurring depression stop depressed moods from spiralling out of control into a full episode of depression.

Click here to read the full article.

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

Low Serum Cholesterol May Be Associated With Suicide Attempt History

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

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

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

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

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

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

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

Two Antidepressants Taken During Pregnancy Linked To Heart Anomalies In Babies

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

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

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

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

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

unstuck bookDr. James Gordon, a renowned psychiatrist and integrative medicine pioneer, is teaching a four-part online series beginning November 18th on treating depression naturally. Dr. Gordon is the author of Unstuck, which is in my opinion the most complete resource on the holistic treatment of depression available.

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.

person sleepingIn Part I and Part II of this series, we examined drug-free alternatives to treating depression including exercise, psychotherapy, light therapy, St. John’s Wort and acupuncture. We have learned that all of these treatments are at least as effective as antidepressants in the short term, and some (exercise and psychotherapy) are more effective in the long-term. All of these treatments have far fewer side effects, risks and complications than antidepressants. In fact, the only “side effects” of exercise and psychotherapy are positive ones: improved physiological and mental health!

Today we will look at other lifestyle-based approaches to treating depression without drugs. As I mentioned in the previous article, because 70% of research is funded by drug companies, many of these non-drug approaches have not been studied as extensively as antidepressant medication.

Nevertheless, there is enough data from clinical and epidemiological studies to support the following strategies - especially since they are superior to antidepressants from a “cost/risk - benefit” analysis. In other words, though some of the approaches I will propose in this article have not been exhaustively proven according to the standards of Western science, there are several lines of evidence supporting their effectiveness and without exception they have beneficial side effects and improve the quality of patient’s lives.

What’s more, all of these approaches can be combined together along with the treatments mentioned in the two previous articles to obtain the maximum effect. Based on the available evidence which we have extensively reviewed, these non-drug treatments should without a doubt be the first line of defense (as well as the second, third, fourth, etc.) in treating depression.

Nutrition

At some point in the future, I hope to dedicate an entire post (or perhaps more) to the subject of nutrition and depression. I personally believe that inadequate nutrition is a significant contributing factor to the continuously rising rates of depression in this country. Consequently, I also believe that proper nutrition can be one of the most effective treatments for depression.

For now, I will go over what I feel are the most important aspects of nutritional causes and treatment of depression, and hopefully address the subject in more detail later.

SUGAR

Diabetes is correlated with higher rates of depression. In 2005, researchers discovered a positive connection between higher levels of insulin resistance and severity of depressive symptoms in patients with impaired glucose tolerance, before the occurrence of diabetes. Based on these findings, it was suggested that insulin resistance could be the result of an increased release of counter-regulatory hormones linked to depression; however, this has not been confirmed.

Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia. Sugar can also cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes. Based on the study results above, this is one mechanism by which sugar could contribute to depression.

There is no doubt that increased sugar intake leads to hormonal changes that can lead to emotional instability. Therefore, people who are depressed (and all people, in fact) should significantly decrease their sugar consumption.

OMEGA-6 / OMEGA-3 RATIO

Anthropological evidence suggests that the intake of omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFA) during the Paleolithic era was roughly equal, whereas the present n-6 to n-3 PUFA in western countries has ben estimated to be between 10 and 25 to 1. The n-6 to n-3 PUFA imbalance has been due mainly to the increase in vegetable and seed oil use and the rise in consumption of processed foods (which contain these oils).

Two major studies have provided direct evidence for the role of the n-6 to n-3 PUFA ratio in depression. The studies found that depression is associated with significantly decreased total n-3 PUFA and increased n-6 to n-3 PUFA ratio (Maes et al. 1996; Maes et al. 1999) . A supporting study carried out in 1998 also found a significant depletion in total n-3 PUFA, and in particular DHA, in the erythrocyte membranes of depressed patients.

Epidemiological data show the trend in decreasing dietary n-3 PUFA consumption and the increasing evidence of depression, both over time and between nations (Hibbeln et al. 1995). Further investigation suggests that the significance lies in the increase in n-6 to n-3 ratio, rather than simply low n-3 intake alone, as these two fatty acids compete in binding to enzyme systems that produce chain elongation and further desaturation. A diet high in n-6 fatty acids prevents the incorporation of n-3 PUFA into cell membranes and phospholipids (Spector et al. 1985).

All polyunsaturated fatty acids - including n-3 PUFA - have been shown to make lipoproteins more vulnerable to oxidative damage (Reaven et al. 1991), and oxidative damage is a significant risk factor for heart disease, cancer and many other conditions. As mentioned above, n-6 consumption actually prevents the incorporation of n-3 into our cells. Therefore, rather than increasing our consumption of n-3 PUFA to treat depression, as is often suggested, it makes more sense to dramatically decrease our consumption of n-6 PUFA. This will help our bodies to incorporate the small, but adequate amount of n-3 PUFA we get in a whole-foods based diet. Avoiding n-6 PUFA (primarily found in vegetable and seed oils, and in animals fed vegetables high in n-6 like pigs and chickens) will not only alleviate depression, but also benefit our health in many other ways.

VITAMIN D

In a 1998 controlled experiment, Australian researchers found that vitamin D (400 and 800 IU), significantly enhanced positive affect when given to healthy individuals. Forty-four subjects were given 400 IU cholecalciferol, 800 IU cholecalciferol, or placebo for 5 days during late winter in a random double-blind study. Results on a self-report measure showed that vitamin D3 enhanced positive affect a full standard deviation and there was some evidence of a reduction in negative affect. The authors concluded: “vitamin D3 deficiency provides a compelling and parsimonious explanation for seasonal variations in mood” (Landsdowne & Provost, 1998).

In another study in 1999, the vitamin D scientist, Bruce Hollis, teamed up with Michael Gloth and Wasif Alam to find that 100,000 IU of vitamin D given as a one time oral dose improved depression scales better than light therapy in a small group of patients with seasonal affective disorder. All subjects in the vitamin D group improved in all measures and, more importantly, improvement in 25(OH)D levels levels was significantly associated with the degree of improvement (Gloth et al. 1999).

According to the Vitamin D Council:

To further strengthen the case that vitamin D deficiency causes some cases of depression, evidence should exist that the incidence of depression has increased over the last century. During that time, humans have reduced their sunlight exposure via urbanization (tall buildings and pollution reduce UVB ), industrialization (working inside reduces UVB exposure), cars (glass totally blocks UVB), clothes (even light clothing blocks UVB), sunblock and misguided medical advice to never let sunlight strike you unprotected skin.All these factors contribute to reduce circulating 25(OH)D levels.

Klerman and Weissman’s claim that major depression has increased dramatically over the last 80 years is one of the most famous (and controversial) findings in modern psychiatry. Something called recall bias (a type of selective remembering) may explain some of the reported increase, but does it explain it all?

If you suffer from depression, get your 25(OH)D level checked and, if it is lower than 35 ng/mL (87 nM/L), you are vitamin D deficient and should begin treatment. If you are not depressed, get your 25(OH)D level checked anyway. If it is lower than 35 ng/mL (87 nM/L), you are vitamin D deficient and should begin treatment.

Recommended intake is up to 5,000 IU per day of vitamin D through exposure to sunshine and/or supplementation. See this article on vitamin D to learn to calculate how much vitamin D is produced given a certain amount of exposure to sunlight, and to learn more about vitamin D supplementation. It is important to remember that D works synergistically with A & K2, so if you increase your intake of D you must also increase your intake of A & K2 to avoid D toxicity.

Finally, I’d like to share with you a comment I received from a reader about how he/she has cured depression with nutritional intervention. Note that I endorse just about every suggested step, with the exception of the significant increase in n-3 intake. Based on the evidence above, I suspect that his/her improvement was a result of the decrease in n-6 PUFA more than it was the increase in n-3 PUFA.

I suffered from depression, for many years–it was so bad that often I thought that the only answer for my life would be to end it. Thoughts of suicide danced through my mind frequently.

Early March 2008 I changed my diet completely:

–eliminated all processed foods

–eliminated all white foods; most important, eliminated sugar, which is the “white devil”

–eliminated all foods containing soy and corn; so I don’t eat the meat of animals that have been fed grains

–two years prior to March 2008 I stopped drinking sodas/soft drinks

–only meats that have been traditionally raised; meat from ruminants that have been grass fed; chickens that have been pastured (I get them with the head and feet); meat from pigs that have not been raised in confinement (I know the people who “produce” the pork that I eat–they feed their pigs food that is in season and local, and they allow their pigs to be pigs, and never slaughter them before their time)

–eliminated all the bad fats

–added good fats: coconut oil, palm kernel oil, [raw] butter from grass fed cows, lard (from the pigs described above), beef bone marrow fat (from grass fed and pastured cows), olive oil

–eat a tin of sardines (with the skin and bones) weekly

–eat wild Alaskan salmon weekly

–cut out grains; although, occassionally, I have a jones for those carbs, so I’ll eat some brown rice; sometimes I’ll have a bowl of steel-cut oats, which I have soaked overnight, and when I eat it, I add lots of butter and raw cream to it

–stopped eating out; I cook all of the meals that I eat

–only eat raw milk cheeses

–eggs from hens that have been pastured

–drink this mixture daily: raw milk, raw cream, 4-6 raw egg yolks, some unsulphured organic blackstrap molasses

–daily supplements of: cod liver oil, evening primrose oil, wheat germ oil, kelp powder, dessicated liver

–vegetables and fruit

–drink only when thirsty

–stopped wearing sunblock/sunscreen lotions; get out in the sun daily for 20-plus minutes

–exercise daily; I ride my bike everywhere (I live in San Francisco) or I walk

Following the reader’s advice will not only relieve depression, it will dramatically improve all aspects of your physical, emotional and mental health.

Adequate sleep and rest

Recent studies have definitively linked insomnia with depression and increased suicidal behavior. A research abstract that was presented on June 12 at SLEEP 2008, the annual meeting of the Associated Professional Sleep Societies, found a link between poor sleep and suicidal behavior among children and adolescents with depressive episodes. 83.8% of the depressed patients in the study had sleep disturbances, and there was a significant association between suicidal behavior and the presence of sleep complaints.

Another recent study confirmed the persistent nature of insomnia and the increased risk of subsequent depression among individuals with insomnia. According to the study, 17% - 50% of subjects with insomnia lasting just two weeks or longer developed a major depressive episode reported in a later interview.

Other research has indicated that insomnia can cause depressed mood and adversely affect endocrine function (Banks 2007).

Most Americans are chronically sleep deprived. The foundation’s 2001 national “Sleep in America” poll reported that almost seven out of 10 Americans experienced frequent sleep problems, and that most were undiagnosed. The same poll in 2003 found that 67 percent of older adults had frequent sleep problems and only one in eight had been diagnosed.

This alone could explain the epidemic increase in depression over the last several decades. But when sleep deprivation is added to other factors such as increased intake of n-6 PUFA, increased stress, the use of antidepressant drugs, the breakdown of family, community and other social support structures, it isn’t difficult at all to understand why so many of us are depressed.

The American Academy of Sleep Medicine (AASM) offers the following tips on how to get a good night’s sleep:

  • Follow a consistent bedtime routine.
  • Establish a relaxing setting at bedtime.
  • Get a full night’s sleep every night.
  • Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
  • Keep computers and TVs out of the bedroom.
  • Do not go to bed hungry, but don’t eat a big meal before bedtime either.
  • Avoid any rigorous exercise within six hours of your bedtime.
  • Make your bedroom quiet, dark and a little bit cool.
  • Get up at the same time every morning.

Stress Management

An increasing amount of evidence (along with common sense) indicates that chronic stress directly contributes to depression. Please see my recent article for more information about this.

I am not aware of any well-designed clinical trials examining the effects of stress reduction on depression. However, logic dictates that since stress is a cause of and contributing factor to depression, managing stress is an important aspect of treating depression.

One study published in 1995 showed that meditation can improve mood. Another small study demonstrated that mindfulness-based cognitive therapy (MBCT) significantly improved depression and reduced relapse. A series of studies and case studies have shown that biofeedback can also be effective for depression and mood disorders.

The reality is that there are many ways to manage and reduce stress, from yoga to meditation to mindfulness-based stress reduction to progressive relaxation techniques. The important thing is not which method you choose, but that you commit to something and do it on a regular basis.

Prayer & Spiritual Practice

You’re not going to see much scientific research into the role of prayer and spiritual practice in treating depression. Nevertheless, for as long as people have been “depressed” they have used their relationship with God, nature, a “higher power” or whatever guiding principles they embrace to get through difficult times.

People who are depressed often feel isolated, alienated or alone. A strong faith in God or in the interconnectedness of all life can re-establish a sense of belonging and support. Prayer and spirituality can also re-frame the depression one is experiencing in a larger and less “personal” context.

In my previous article called The Heart of Depression, we examined how cultural, religious and spiritual beliefs in these traditional 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.

The words and labels we use to “frame” our experience have tremendous power. In the U.S. today, depression is viewed as a sickness that must be cured, as a pathology, as a “biological disease”. 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”?

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.

Spirituality and prayer can help people who are suffering to understand their experience in a more empowering and self-validating context than what is offered by mainstream medicine. When one views their suffering as an opportunity for growth and evolution, rather than as a disease requiring treatment with drugs, it is far more likely that lasting, positive change will occur.

In the next and final article (for a while, at least) in my series on depression and antidepressants, I will summarize everything we’ve covered so far and offer my recommendations for treating depression holistically.

car crash

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.

lightboxIn the first article in this three-part series on treating depression without drugs, we established that several non-drug treatments are at least as effective in treating depression than antidepressants - with few, if any of their side effects. Specifically, we learned that both psychotherapy and exercise compare favorably with antidepressants for treating even serious depression in the short-term, and are both more effective than antidepressants in the long-term.

Today we will examine three other drug-free treatments for depression: light therapy, St. John’s Wort and acupuncture. In the final article, we will look at lifestyle-based treatments such as nutrition, adequate sleep and rest, stress management, pleasure and bibliotherapy (prayer or spiritual practice).

Light Therapy

Researchers at the National Institute for Mental Health are credited for the idea that perhaps more people are apt to become depressed during dark, dreary winter days than on bright, crisp spring days because they are not getting enough light. Since then, people around the world have begun to use “light therapy” to overcome Seasonal Affective Disorder. However, light therapy is also being used to successfully treat major depression at any time of the year.

Beginning the day sitting in front of a fluorescent light box that typically emits about 10,000 lux units of light has helped many people who might otherwise struggle with depression throughout the day. Bright light has been shown by numerous studies to act as a specific antidepressant in depressed patients. In a recent meta-analysis of published studies on light therapy and depression which appeared in the April 2005 issue of the American Journal of Psychiatry, the authors found that bright light treatment for nonseasonal depression is efficacious, with effect sizes equivalent to those in most antidepressant studies.

Once again, as was the case with both exercise and psychotherapy, the combining light therapy with antidepressants was no more effective than light therapy alone.

In contrast to exercise and psychotherapy, bright light therapy does occasionally have some side effects, including headache, eye strain, nausea and agitation. But these are very mild when compared against the side effect profile of antidepressants.

It is very important to note that some psychotropic medication (and psychotropic herbs such as St. John’s Wort) may increase sensitivity to light, so light therapy should probably not be combined with St. John’s Wort or antidepressants.

Some critics of light therapy have pointed out that it could be a placebo and there is no way to prove otherwise. It is not possible to keep someone from knowing whether they are being exposed to very bright light or the placebo (dim light). Therefore the “blind” is broken and patients will know whether they are receiving the active or “inert” treatment. Could it be that the positive effects of bright light are simply due to the assumption or expectation of the patients that they will improve, rather than a result of the bright light itself?

Sure it is. But perhaps a more important question is, “does it matter?” If we use Antonuccio’s criteria for evaluating a potential treatment (i.e. 1) first do no harm, 2) cost-benefit analysis) then it becomes clear that light therapy compares very favorably with antidepressants even if it is “merely a placebo”. As you will know if you’ve been following my blog, antidepressants could also be referred to as placebos because they have been shown to be no more effective than placebo in treating depression. The criteria for whether a drug gets approved or not by the FDA is that it must outperform placebo; otherwise, it is simply considered a placebo itself.

Although light therapy may have some side effects, they pale in comparison to those of antidepressants and, unlike antidepressants, light therapy poses no significant risks or long-term complications. A typical light therapy device costs between $200-$300, so over the long-term it is much more cost-effective than medication. Finally, light therapy is just as effective as pharmacotherapy for treating depression.

When all of this is taken together, light therapy is superior to antidepressants - even if it is a placebo.

St. John’s Wort

St. John’s Wort (Hypericum) is an herb that can be used to make tea, or the “active ingredients” with the herb that can be extracted and put into capsules. In Europe SJW is widely prescribed as an antidepressant, but in the U.S., it is available over-the-counter.

St. John’s Wort has repeatedly been shown to work as well as or better than antidepressants in double-blind, placebo-controlled studies. For example, compared to Paxil, depression scores fell more (56.6% vs. 44.8%) and side effects were less (Szegedi et al. 2005). Similar results were found for Prozac (Schulz 2002). A comparison with both Zoloft and Celexa found St. John’s Wort again performed as well as the antidepressant drug without as many side effects (Gastpar 2005; Gastpar 2006).

While St. John’s Wort is clearly as effective as antidepressants, the number of adverse effects is ten times less - being essentially equivalent to taking a placebo. The most common adverse events (1 per 300,000 treated cases) concern reactions of the skin exposed to light (due to potential increased photosensitivity caused by SJW and other psychotropic substances).

Please do note that St. John’s Wort is contraindicated for concurrent use with certain medications, including antidepressant drugs, coumarin-type anticoagulants, the immunosuppressants cyclosporine and tacrolimus, protease and reverse transcriptase inhibitors used in anti-HIV treatment and with certain antineoplastic (cancer) agents.

However, these potential interactions can be easily avoided with proper supervision from a health-care professional who is experienced with the use of St. John’s Wort.

Once again, to be accurate we must point out the possibility that St. John’s Wort is merely a placebo. If it is roughly as effective as antidepressants, and antidepressants are themselves placebo, then it follows that St. John’s Wort may also be a placebo. However, the same analyses that we used for light therapy applies here. The question is, how does St. John’s Wort compare against the primary treatment for depression - antidepressants? As we have seen, SJW is just as effective as antidepressants with only a fraction of the side effects, so there is absolutely no reason not to choose it over a synthetic antidepressant.

Before we move on to acupuncture, nutrition, rest and other lifestyle-based treatments for depression, I want to briefly discuss the criteria we’ve used so far for evaluating the effectiveness of a treatment. As I’m sure you’ve noticed, I am primarily basing the determination of the effectiveness (or lack thereof) of a treatment on well-designed, placebo-controlled, double-blind scientific studies.

I obviously have great respect for this method of inquiry and it has led (and continues to lead) to many important advances in medicine. However, it must be pointed out that this standard of proof has limitations. For example, 2/3 of medical research is funded by pharmaceutical companies. This means that the lines of investigations most often pursued in scientific research are those that are likely to lead to new therapies that can be monetized by the drug companies. There is little incentive for a drug company to dedicate research dollars to a study on how nutrition affects depression, unless there’s a product they can imagine marketing based on the study results. The result is that there are relatively few studies evaluating the effect of nutritional intake on depression.

Another limitation of double-blind, placebo-controlled research is that it is difficult (if not impossible) to maintain that standard with treatment modalities that depend on the unique interaction that happens between a practitioner and a patient. Western science is often skeptical, of course, that this interaction that occurs influences the treatment in any way. They do not understand how the interaction could influence the treatment, and what Western science does not understand, is often dismissed as “new-age fluff”.

What is remarkable about this is not just the arrogance of such a position, but also the ignorance it demonstrates. Over the last two decades, research into the placebo effect and growing understanding of how the nervous, endocrine and immune systems are inter-related have proven beyond a shadow of a doubt - according to the most rigorous Western scientific standards - that the interaction between a doctor or clinician and their patient absolutely influences the outcome of the treatment. In fact, many studies have shown that this interaction may be more important than the treatment itself; or, perhaps more accurately, the interaction is the treatment.

With this in mind, it becomes clear that the efficacy of acupuncture as a treatment for depression - or anything else - can never be accurately measured in a double-blind, placebo-controlled study. As much as Western science hates to admit this, we are not machines that respond in entirely an predictable manner given the same circumstances. There is no way to “standardize” the interaction that happens between an acupuncturist (or any healing professional) and a patient, because each person and, therefore, each relationship is unique.

Acupuncture

Considering all of the caveats above, can acupuncture help with depression? According to the Cochrane Database Systematic Review (the gold standard for medical research reviews today), “there is no evidence that medication was better than acupuncture in reducing the severity of depression.” In many of the studies they reviewed, acupuncture and electro-acupuncture either cured or remarkably improved depression scores, performing just as well as synthetic antidepressants.

However, it must also be noted that the studies were few in number, often poorly designed and did not have enough subjects to draw definitive conclusions. The authors of the review concluded that there was “insufficient evidence to determine the efficacy of acupuncture compared to medication”.

And of course, we always have the issue of placebo. It is possible that the benefit the patients are receiving comes from the interaction with the practitioner and their expectation that they will improve - rather than as a result of the needles themselves.

Once again, though, if we evaluate acupuncture based on a “cost-benefit” analysis, it compares very well against antidepressants. It has been shown to be at least as effective as medication in many studies as noted above, and the side effects are minimal when compared with antidepressants. Acupuncture has also been shown to be effective in treating other conditions that may occur alongside of depression, such as pain and stress.

Stay tuned for the third-part of this series which will consider lifestyle-based treatments such as nutrition, adequate sleep and rest, stress management, pleasure and prayer.

bicyclistThe most widely prescribed drugs in the U.S. are not for pain management, cholesterol lowering, heartburn or hypertension.

They’re for depression.

Last year doctors wrote $232.7 million prescriptions for antidepressants. That’s an increase of 25 million prescriptions since 2003 and translates into an estimated 30 million patients in the United States who spent $12 billion on antidepressants in 2007.

With numbers like these, a person might make these assumptions:

  • Antidepressants are effective treatments for depression
  • There are few, if any, effective alternatives to antidepressants

As reasonable as these assumptions would be based on the popularity of antidepressants, they are both wrong.

In my preceding articles in this ongoing series on depression and antidepressants, I’ve presented clear evidence that antidepressants are not effective for treating depression.

In this article and the following two, I will present evidence that several non-drug treatments for depression are at least as effective as antidepressants, with few (if any) of their side effects, risks and costs.

As you may recall from the previous articles in this series, recent meta-analyses have shown that antidepressants have no clinically meaningful advantage over placebos. What I have not yet pointed out is that the effectiveness of antidepressant drugs has probably been overstated due to methodological factors in the studies.

In the studies performed on antidepressant drugs, the people taking the drugs also received supportive weekly visits with doctors or researchers along with the medication. The resulting “therapeutic alliance” may have enhanced the efficacy of these drugs and given an inaccurate picture of their effectiveness in a managed care environment where antidepressants are often delivered in conjunction with infrequent visits to a physician or mental health professional.

We know from placebo research that the contact which occurs between the patient and practitioner can be a powerful treatment in itself. Therefore, the supportive visits that patients received during the drug trials could have easily amplified the effect of the drug and made it seem far more effective than it would be in a “normal” clinical situation where visits to a physician or psychiatrist are not regular or frequent.

With this in mind, it is very likely that antidepressants are less effective than placebos in normal clinical practice. Indeed, researcher Joanne Moncrieff has repeatedly pointed out that the term “antidepressant” is a misnomer. The drugs collectively referred to as “antidepressants” do not specifically treat depression (any more than placebo), and therefore should not be called “antidepressants” at all.

What are the alternatives, then, to treating depression? Imagine having a choice between five treatments. Treatment A produces a therapeutic response but also a large number of adverse effects including diarrhea, nausea, anorexia, sweating, forgetfulness, bleeding, seizures, anxiety, mania, sleep disruption and sexual dysfunction. Treatments B, C, D & E produce therapeutic responses similar to Treatment A, but with far fewer adverse effects and costs. Treatments B & C, in fact, have no adverse effects at all and have been shown to be significantly more effective than Treatment A in the long-term.

This is not, of course, simply a hypothetical question. Treatment A corresponds to the selective serotonin reuptake inhibitors (SSRIs) that have become so overwhelmingly popular. Treatment B is psychotherapy, which is as effective as antidepressants in the short term (even for serious depression), and is more effective in the long term. Treatment C is exercise, which has been reported to have lasting therapeutic benefits in the treatment of major depression with no “side effects” except for improved physiological and mental health. Treatment D is light therapy, which has been recently assessed in several clinical studies and is just as effective as antidepressant medication. Treatment E is St. John’s Wort, an herb that has been extensively studied and shown to be similar in efficacy to antidepressants with 10 times fewer adverse effects.

As depression researcher David Antonuccio points out, “whether one subscribes to the Hippocratic dictum ‘first do no harm’ or takes a cost-benefit approach to treatment, it is impossible to ignore the fact that antidepressants are not medically benign treatments. Antidepressants have serious side effects (listed above) as well as medical risks (including increased risk of dying) when combined with other medications - as is often the case in clinical settings. Antidepressants have been shown to cause potentially permanent changes to the brain that can predispose a patient to depression in the future, and the withdrawal symptoms of SSRIs are substantial for many, if not most, patients.

A frequent argument made by supporters of antidepressants is that patients with serious depression need antidepressants to stave off suicide. However, there is no evidence whatsoever that antidepressants reduce the risk of suicide or suicide attempts in comparison with placebo in clinical trials. On the contrary, in a recent analysis of the data that compensated for erroneous methodologies, Dr. Grace Jackson found that antidepressants increased the risk of suicide by two to four times in adults, and by three times in children (Jackson 2005, p.122)

It has also been demonstrated that recent sharp increases in antidepressant use have been accompanied by increased prevalence and duration of depressive episodes and rising levels of sickness absence (Patten 2004). Naturalistic studies have also shown that depressive episodes are more frequent and last longer among antidepressant users than among nonusers, and that sickness absence is more prolonged (Moncrieff 2006). Finally, long-term follow-up studies show very poor outcomes for people treated for depression with drugs, and the overall prevalence of depression is rising despite increased use of antidepressants (Fombonne 1994).

Please allow me to summarize the research and simplify the preceding paragraphs:

Antidepressants don’t work. If anything, they make things worse.

Now that we have firmly established the ineffectiveness and dangers of antidepressants, let’s look more closely at the alternatives. We will evaluate each treatment based on Antonuccio’s criteria above:

  • Does the treatment do any harm?
  • How do the “costs” compare with the “benefits”?

and we will also compare their efficacy with that of antidepressants.

Psychotherapy

Several studies show that psychotherapy (particularly cognitive therapy, behavioral activation, and interpersonal therapy) compares favorably with medication in the short-term, even when the depression is severe, and appears superior to medications over the long term (Antonuccio 2002). When medical cost offset, relapse and side effects are considered in a cost-benefit analysis, psychotherapy can be very cost-effective - particularly in a psychoeducational (e.g. therapist-assisted bibliotherapy) or group format (Antonuccio et al. 1997). Finally, studies show that most patients prefer psychotherapeutic intervention to drugs when given the choice. (Unfortunately, they are rarely given the choice; today, fewer than 10% of psychiatrists offer psychotherapy to their patients.)

It is important to note that several studies have shown that combined treatment (psychotherapy + medication, exercise + medication) produces inferior results when compared to the non-drug modality alone (Hollon et al. 1992). The failure of this combined approach is not surprising when one considers the counter-productive effects of invasive chemical interventions (e.g. suppression of REM sleep, elevation of cortisol, induction of mania).

Unfortunately, the mental health profession remains largely ignorant to this “tragedy of its own making”:

“Some investigators have argued that the relatively high relapse rate after drug treatment indicates that depression should be treated like a chronic medical disease requiring ongoing, long-term medical treatment indefinitely. This logic appears tautological: Drug treatment results in a higher relapse rate than cognitive-behavioral therapy; therefore, the patients should be maintained on drugs to prevent relapse.” (Antonuccio 1995)

Exercise

Several studies have shown that aerobic exercise is at least as effective as antidepressants in treating depression. For example, one recent study published in the American Journal of Preventative Medicine in 2005 indicated that the “public health dose” (5x/week frequency burning 17.5 kcal/kg/week) of exercise led to remission rates of 42%. For the sake of comparison, the Collaborative Depression Study, conducted by the National Institute for Mental Health, indicated remission rates of 36% for cognitive behavioral therapy and 42% for antidepressant medication.

A frequent criticism of exercise as a treatment for depression is the supposed lack of compliance in patients. The argument is that people who are depressed are too depressed to exercise. While this may be true in some cases, adherence rates in exercise studies were comparable to many medication trials, where rates vary from 60%-80%. Thus, evidence does not support the notion that exercise is not a feasible treatment for depressed patients.

Another benefit of exercise as a treatment for depression is that the only “side effects” are improved physiological and mental health. In contrast to antidepressants, exercise has no adverse effects whatsoever. Instead, it has a moderate reducing effect on anxiety, can improve physical self-perceptions and in some cases global self-esteem, and can enhance mood states and - in older adults - improve cognitive function.

In a study published in Psychosomatic Medicine in 2000, another important advantage of exercise over antidepressants was revealed. Participants in the exercise group were less likely to relapse than participants in the two groups receiving medication. Other studies have confirmed this effect, demonstrating that aerobic exercise is especially helpful in the prevention of relapse and recurrence of depression.

Once again, as was the case with psychotherapy, there was no benefit when combining antidepressant drugs with exercise. In fact, the opposite was the case, at least with respect to relapse for patients who initially responded well to treatment. According to the authors of the study:

“This was an unexpected finding because it was assumed that combining exercise with medication would have, if anything, an additive effect.

The authors go on to speculate on why antidepressant drugs would decrease the exercise’s beneficial effects on depression:

“One of the positive psychological benefits of systematic exercise is the development of a sense of personal mastery and positive self-regard, which we believe is likely to play some role in the depression-reducing effects of exercise. It is conceivable that the concurrent use of medication may undermine this benefit by prioritizing an alternative, less self-confirming attribution for one’s improved condition. Instead of incorporating the belief “I was dedicated and worked hard with the exercise program; it wasn’t easy, but I beat this depression,” patients might incorporate the belief that “I took an antidepressant and got better”.

It is also possible that the metabolic and physiological effects of antidepressants described above (suppression of REM sleep, elevated cortisol levels, etc.) could counteract the positive benefits of exercise to a certain degree.

In part II of this article I will discuss light therapy, St. John’s Wort and acupuncture as treatments for depression. In Part III I will examine other lifestyle modifications that can both prevent and treat depression, such as proper nutrition, stress management, getting adequate sleep, the experience of pleasure and prayer or spiritual practice.

stressed woman

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…

man on bench

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!

Please remember to always seek the guidance of a qualified psychiatrist when attempting to withdraw from psychoactive drugs. It is very dangerous to stop taking the drugs abruptly or to begin the withdrawal process without supervision. Psychiatrist Peter Breggin is considered to be one of the foremost experts in psychiatric drug withdrawal, and he has written a book (linked to below) for helping patients wean off of drugs. If you are considering stopping your medication, I recommend you read this book and discuss it with your doctor.

Recommended books

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

depressed personThis week’s article in my continuing series on depression and antidepressants will examine the physiological, psychological and social consequences of antidepressant use.

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.

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

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

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

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

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

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

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

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

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

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

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

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

The history of the “chemical imbalance” theory

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

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

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

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

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

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

The fatal flaws of “chemical imbalance” theory

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

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

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

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

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

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

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

How have we been fooled?

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

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

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

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

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

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

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

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

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

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

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

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

Recommended resources

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

magnifying glassI’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