I believe that I have a professional and moral obligation to question the prescription and widespread use of old-generation (SSRI class) anti-depressant medications such as Prozac, Zoloft, Paxil, Celexa and Luvox. I cannot condemn it: I am not qualified to make that judgement. Condemnation must be left to the credible experts, and their interpretation of the evidence. However, I share my concerns: that the manufacture, marketing, excessive prescription, and sale of these drugs has probably been dangerous and negligent.
This position is well-supported by references to credible and recent scientific opinion and evidence. Credible criticism first came to public attention when David Healy, a professor of psychiatry who lost his job for speaking out about the undeniable risk that SSRIs cause a small percentage of patients to kill themselves, which had not yet been addressed in the scientific literature.3 In January 2008, New England Journal of Medicine reported that drug manufacturers failed to publish every FDA-registered study4 that didn’t make SSRI anti-depressants look good.5 Then PLos Medicine followed up in February with the largest review of SSRI studies to date — including6 all the previously unpublished FDA studies, as discussed by Arstechnica.com. The effectiveness of anti-depressants has always been debatable, but this new analysis of all the evidence resulted in a particularly underwhelming picture of the efficacy of these drugs, which appear to be no more effective than sugar pills for most depression7 — though they may be modestly effective for severe depression.89 This is not a new expert opinion, but simply the most recent credible evidence to support an existing opinion. See the footnotes for full details, and please bear in mind the weight of this evidence as you read on.
I have a personal history with so-called “clinical” depression and bipolar disorder. In 1991, a psychiatrist not only diagnosed me with manic-depression (probably a misdiagnosis), but told me that I would be dead by suicide “within a year” — yikes! — if I did not accept pharmaceutical treatment in the form of SSRI antidepressants. Prozac was three years old then, and had been the most prescribed drug in history as of 1990. I walked out of that psychiatrist’s office, and later cured my own depression and mood swings through personal development.“Take this mood-altering drug or you’re dead within a year,” was probably not the voice of compassionate wisdom.
Fortunately, I recognized that “take this mood-altering drug or you’re dead within a year” was probably not the voice of compassionate wisdom. But, in fact, it was more dangerous than I knew.
Ely Lily is the manufacturer of Prozac. “The company’s internal documents, some dating to the mid-1980s, as well as government applications and patents, indicate that the pharmaceutical giant has known for years that its best-selling drug [Prozac] could cause suicidal reactions in a small but significant number of patients.”10
Taking Prozac could have induced my suicide rather than preventing it! The same is true for all the millions of people out there ingesting SSRI antidepressants. Scientific controversy about this allegation continues vigorously to this day, as any quick internet search can demonstrate (Google "SSRI suicide"). As long the truth remains elusive, there is a strong “better safe than sorry” case to be made against their use.
I have long condemned anti-depressants on the basis of general cynicism. I always knew or suspected that they have numerous alarming side effects, that they are marketed aggressively by some of the most profitable and unaccountable corporations in the world, and that their usage does not have a sound scientific rationale. These have been reason enough to suspect that they are more myth than medicine.
Yet, for all my cynicism, I foolishly had some faith that these drugs could not be all bad. I assumed that their side effects were more or less as reported in drug references, that the manufacturers’ power to obscure the facts is mitigated by government agencies, and that the physiological rationale for the drugs is at least intelligible.
As a health care professional, I have had the opportunity to learn otherwise. I have observed dozens of my own clients struggle with depression both with and without SSRI antidepressants, had numerous conversations with other complementary and conventional health care professionals on the subject, and read many articles and books.
Contrary to what I once assumed, the side-effects of anti-depressants are actually numerous, severe, potentially life-threatening, and not widely known or even understood. They cause a low but measurable rate of psychotic mania, for instance — equal to millions of people who have been reduced to quivering wrecks, their behaviour drastically altered, careers, marriages and lives lost. Withdrawal symptoms from SSRIs are even more problematic.
The power of the SSRI manufacturers is quite unchecked by government institutions like the American FDA. Indeed, there are documented cases of these companies successfully:
This is no surprise given the amount of money and conflicts of interest involved. For instance, President George Bush Sr. was on the board of directors of Eli Lilly & Co. (Prozac), and the head of the FDA during the Prozac approval now works for the pharmaceutical industry as a consultant!
Finally, the scientific rationale for anti-depressants is not, it turns out, very good at all. It is as clumsy as the rationale for electroshock therapy and lobotomy was historically. The popularity of anti-depressants is a continuation of the historical tendency to use “brain-disabling treatments” in psychiatry.11
It is important to understand that SSRIs quite literally just “mess with your head,” specifically interfering with the function of a common messenger molecule (serotonin), one of thousands of others, whose purpose and broad significance to brain function in general is only vaguely understood, and whose particular significance to depression is completely unknown. Consider this 2010 article in New Scientist, emphasizing how recent research has only emphasized our ignorance:
If you thought depression was caused by low serotonin levels, think again. It looks as if the brain chemistry of a depressed person is much more complex, with mounting evidence suggesting that too much serotonin in some brain regions is to blame.
The most sophisticated method known for even measuring serotonin levels in the brain — never mind understanding the significance of these measurements — is to grind up a piece of brain, spin it in a centrifuge, and measure the sum total of serotonin relative to other substances. And how about our ability to measure the amount of serotonin in any given synapse at any time? Exactly zero. Yet the marketing of these drugs would have us believe that they are extremely specific in their effects. It is simply not so.
Despite the commercials — treating depression pharmacologically is not treating something as simple as a low level of a single neurotransmitter. Measuring serotonin levels, even if practical, would likely be of no clinical value. Depression is a result of poor emotional regulation among various brain regions. Drugs are a blunt tool by which we can nudge brain function in a direction which, for some people, can change this regulation and reduce depression. It’s not really about the levels.
Given these limitations, the idea that we can diagnose a “chemical imbalance” in the brain is pure nonsese — even if we could measure it, we don’t know what normal brain chemistry is. Bear in mind also that no psychiatrist actually attempts to measure your brain chemistry before prescribing SSRIs. They don’t do it, of course, because they have not the slightest idea how to diagnose allegedly dysfunctional neurochemistry. They infer the idea of dysfunctional neurochemistry from your subjective symptoms (i.e. depression). That idea has achieved an outrageously disproprotionate credibility, seeming like certain knowledge to the layperson, when it fact the reality is that the nature of sertonin and related neurotransmitters remain almost completely mysterious to medical science.
The concept of a “chemical imbalance” in the human brain is one of the most fantastic oversimplifications in science, and one of the worst legacies of the modern pharmaceutical industry. A bowl of soup could have a chemical imbalance …
We do not prescribe medicines to “treat” brain chemistry, we prescribe medications that mess with it — to rock the boat, stir the soup — not because we know what to do to brain chemistry, but because it is something that we can do to brain chemistry. The precision is in the mechanism of effect, and not the consequences.
Indeed, the scientific rationale for these drugs is so bankrupt that to even call them “antidepressants” has more to do with marketing than science, and various studies have shown that they simply do not work as advertised.12 Antidepressants are, in fact, closely related to amphetamines like ecstasy and cocaine. Cocaine essentially does exactly the same kinds of things to the brain, only it messes with serotonin plus a few other molecules. You can think of anti-depressants as “simplified cocaine.” And also “legal cocaine.” It’s an incredibly blunt medical instrument that does not do anything except generally interfere with normal brain function.
It is not necessarily a bad thing to carefully “tinker” with your brain. Humans have a long history of finding ways to mess with our own heads. There are times in life when almost any change in mental state feels like an upgrade. But we need to be more realistic and acknowledge that this is what we’re really doing with SSRIs.
If the allegations against them are correct — and they seem to be — the presence and typical usage of these drugs in our society is just as unconsciounable as any snake oil ever was, only worse because of the massive scale. Too often we think of our civilization as scientifically sophisticated in all fields. Yet neurophysiology is still primitive in many ways, lacking in testable theories with the power to explain many mental phenomena — yet touted (marketed) as advanced. Consequently, medical malpractice is still common. It’s my responsibility as a health care professional to raise these concerns, even though there are more credible voices to be heard.
Indeed, please do not take my word for it. Although under-reported in the past, lately all of this information is readily available from other and more credible sources. If you are considering antidepressant medication, please do your homework first. If you are already taking antidepressant medication and want to quit safely, it is not sufficient to simply ask your physician. You must educate yourself.
There’s no denying that massage is pleasant — for most people — but its medical benefits are much less clear and proven than you might think. Myths about massage abound. Massage does not flush lactic acid out of cells, or meaningfully increase circulation, or reduce inflammation. It might reduce cortisol levels, but even that popular notion is far from proven, and it’s more likely that it’s wrong.13 Even in the unlikely event that massage actually does reduce cortisol levels, the phsyiology of stress is much too complex to assume cortisol reduction is in itself a meaningful, good thing. Cortisol levels after a massage do not give a meaningful picture of the organism, and there is no direct relationship between a temporary cortisol reduction and any health benefit. What matters is cortisol levels over time, but even that isn’t exactly straightforward: stress and cortisol have a complex and chaotic relationship regulated by many variables out of our control.
While many benefits of massage are still disconcertingly uncertain and hotly debated (by some), there are two truly proven ones. Dr. Christopher Moyer, a psychologist and massage researcher, explains that the only truly confirmed benefits of massage are its effects on mood (“affect”),14 specifically:
And more massage is probably even better. Dr. Moyer:
We made an interesting discovery concerning the effect of the treatment on state anxiety. When a series of massage therapy sessions was administered, the first session in the series provided significant reductions in anxiety, but the last session in the same series provided reductions that were almost twice as large. This pattern was consistent across every study we were able to examine, which strongly suggests that experience with massage therapy is an important predictor of its success, at least where anxiety is concerned. To put it another way, it is possible that the greatest benefits come about only when a person has learned how to receive massage therapy.
So this should be a no-brainer: getting a massage is a better idea than taking meds in almost every possible way. It’s probably not cheaper. But it’s definitely better.
I am a science writer, former massage therapist, and I was the assistant editor at ScienceBasedMedicine.org for several years. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook or Twitter.
The evidence of the benefit of cognitive behavioural therapy for depression may be declining: “modern CBT clinical trials seemingly provided less relief from depressive symptoms as compared with the seminal trials.” (Or it may not be: the importance of the “decline effect” has probably been exaggerated.)BACK TO TEXT
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BACKGROUND: Evidence-based medicine is valuable to the extent that the evidence base is complete and unbiased. Selective publication of clinical trials--and the outcomes within those trials--can lead to unrealistic estimates of drug effectiveness and alter the apparent risk-benefit ratio.
METHODS: We obtained reviews from the Food and Drug Administration (FDA) for studies of 12 antidepressant agents involving 12,564 patients. We conducted a systematic literature search to identify matching publications. For trials that were reported in the literature, we compared the published outcomes with the FDA outcomes. We also compared the effect size derived from the published reports with the effect size derived from the entire FDA data set.
RESULTS: Among 74 FDA-registered studies, 31%, accounting for 3449 study participants, were not published. Whether and how the studies were published were associated with the study outcome. A total of 37 studies viewed by the FDA as having positive results were published; 1 study viewed as positive was not published. Studies viewed by the FDA as having negative or questionable results were, with 3 exceptions, either not published (22 studies) or published in a way that, in our opinion, conveyed a positive outcome (11 studies). According to the published literature, it appeared that 94% of the trials conducted were positive. By contrast, the FDA analysis showed that 51% were positive. Separate meta-analyses of the FDA and journal data sets showed that the increase in effect size ranged from 11 to 69% for individual drugs and was 32% overall.
CONCLUSIONS: We cannot determine whether the bias observed resulted from a failure to submit manuscripts on the part of authors and sponsors, from decisions by journal editors and reviewers not to publish, or both. Selective reporting of clinical trial results may have adverse consequences for researchers, study participants, health care professionals, and patients.
From the abstract: “Drug-placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.”
Commenting on this paper, Ars Technica notes (see Just how good are current antidepressants?) that, “These trials include not just those that were published in peer-reviewed journals, but also unpublished trials that were registered with the FDA.” This is extremely important. Although it should be obvious, it helps that New England Journal of Medicine pointed it out recently: “Evidence-based medicine is valuable to the extent that the evidence base is complete and unbiased.” Yet they reported (see Turner) that the FDA has published studies of anti-depressants when they had positive outcomes, while studies with apparently negative results were “either not published (22 studies) or published in a way that, in our opinion, conveyed a positive outcome (11 studies)”!BACK TO TEXT
This was a careful review of the evidence about how well antidepressant medications work. The results were refreshingly different from the usual “more research needed” (although doubtless more research is still needed). What they learned: the worse the depression is, the better antidepressant medications seem work. They really do not work at all for minor depression, but “for patients with very severe depression, the benefit of medications over placebo is substantial.”
The authors were not surprised by the basic pattern, but they were surprised by how strong it was:
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What makes our findings both surprising and compelling is the high level of depression symptom severity that appears to be required for clinically meaningful drug/placebo differences to emerge, particularly given the evidence that the majority of patients receiving antidepressant medication in clinical practice present with scores below these levels.
Dr. Christopher Moyer explains that the only confirmed benefits of massage are its effects on mood (“affect”), specifically depression and anxiety. “Together, these effects on anxiety and depression are the most well-established effects in the MT research literature. They are especially important for us to understand not only for their own sake, but also because anxiety and depression exacerbate many other specific health problem.” He proposes that “the time is right to name a new subfield for massage therapy research and practice: affective massage therapy.”BACK TO TEXT