The Chemical imbalance ‘theory’… come on Glaxo – PROVE it now

When I started taking Seroxat in 1997, I wanted to know how this great new drug worked – the PIL (the leaflet that came with the tablets told me)“it boosts the levels of serotonin in your brain and that’s what makes you stop feeling depressed” I was told. It’s a simple chemical imbalance said the PIL.

By 2003, GSK said in it “Seroxat is one of a group of medicines called selective serotonin reuptake inhibitors (SSRIs) and works by bringing the levels of serotonin back to normal.”

All lies.

The chemical imbalance ‘theory’ HAS NEVER BEEN PROVED. NEVER.

Finally by mid 2006 GSK was starting to get closer to admitting the truth in its PIL “It is not fully understood how Seroxat and other SSRIs work…” At least that’s what they tell us in the UK and USA… however today in Australia, Aropax (the Aussie name for Seroxat/Paxil) still works as it “corrects the chemical imbalance and so helps relieve the symptoms of depression.”

Now read on:

“The Media and the Chemical Imbalance Theory of Depression” by Jonathan Leo & Jeffrey R. Lacasse is a follow up to their seminal article in PLoS Medicine (2005), in which they debunked the “chemical imbalance” theory of depression.

The “chemical imbalance” theory in psychiatry rests on the observation that mood could be artificially manipulated with drugs-those which raised monoamine levels improved mood, while those which lowered amine levels led to depression, but it remained to be seen if naturally occurring fluctuations in neurotransmitter levels were responsible for, or caused, the ebb and flow of mood levels. As the authors point out, in spite of the enormous amount of money and time that has been spent in the quest to confirm the chemical imbalance theory, direct proof has never materialized. Moreover, during the past several decades, a significant amount of evidence has accumulated which calls the theory’s validity into question.

Of particular note, in the two years since publication of their PLoS article, not a single scientific article challenged their conclusion. Indeed, the chairman of FDA Psychopharmacology Advisory Committee acknowledged that the “chemical imbalance” theory was but a “useful metaphor”–as opposed to a valid hypothesis.

Another credible, evidence-based assessment of the “chemical imbalance” theory is to be found on the website of The Mental Health Service at McGill University: “The term ‘chemical imbalance’ is thrown around a lot these days. True conditions caused by chemical imbalances are relatively rare. All thoughts, feelings and motions in the brain are mediated by the release of chemicals in brain pathways. Every person’s brain is unique, leading each of us to have different traits and abilities. Just because your brain works in a particular way does not mean that you have a chemical imbalance. A certain amount of sadness, anxiety or other emotional upset is normal, and though we may be able to block these feelings by chemicals, this would tend to dehumanize us. Even when we use medication to help an individual with overwhelming emotions, most of the time this is not to repair a ‘chemical imbalance’ but simply to help contain symptoms.” (Link here)

However, invalid thought it may be, as Drs. Leo and Lacasse point out the “chemical imbalance” theory has had extraordinary commercial value for both the pharmaceutical industry and psychiatry: “With the advent of the chemical imbalance theory, the companies were no longer just providing soothing tonics, they were now providing medications to treat diseases, as exemplified by an early SSRI advertisement stating: “When serotonin is in short supply, you may suffer from depression.” The wording here is all-important. The advertisement takes a correlation between serotonin shortage and psychological stress-and even this is highly questionable and unverifiable in any individual case-and makes a leap of faith to the conclusion that depression is caused by a serotonin imbalance, not that psychological stress impacts the serotonin system. And the marketing did not stop with depression; eventually we were told that whatever our problems might be, whether anxiety, excessive shyness, depression, or the inability to pay attention, the underlying cause was a faulty transmitter level which could be rectified with a pill. A 2005 survey from the Harvard School of Public Health reported that nearly half of all Americans will at some point develop a mental illness, presumably from a chemical imbalance, with 29% developing an anxiety disorder and 20% a mood disorder.”

The “chemical imbalance” theory has provided promoters of psychoactive “feel good” prescription drugs with the means for distancing their products from illicit street drugs whose chemical action is almost indistinguishable. Whereas drugs used to “take the edge off” stress are typically considered street drugs and are consumed by “users” or “addicts,” substances used to rectify a “chemical imbalance” can be called medications–and these are legitimately consumed by patients.

A fly in the ointment occurred when Ricky Williams, the star running back for the Miami Dolphins who had been “diagnosed” with Social Anxiety Disorder, and for several years was paid by GlaxoSmithKline to promote Paxil for anxiety disorder, was described in 2002, by People magazine, as suffering from a “depression-like chemical imbalance that affects roughly three million Americans.” Williams tested positive for marijuana on several occasions. But while his marijuana use was frowned upon, his use of Paxil was considered acceptable. One was a medication supposed to treat a chemical imbalance, while the other was a drug signaling a lack of willpower.

However, Williams’ contract with Glaxo came to a sudden halt in 2004, when he stated that marijuana was ten times better than Paxil. What got him into hot water, Drs. Leo and Lacasse, note, was not so much praising the competition, but rather putting his sponsor’s “medication” in the same category as an illicit drug. Williams threatened the assumption underlying the conventional unsupportable divide between legal and illegal drug use. His juxtaposition threatened the most powerful industries–including professional sports, the pharmaceutical industry, psychiatry, and the mass media.

Another fly in the ointment raising questions about the validity of the dividing line between prescribed and illicit psychoactive substances, is a recent controlled clinical trial conducted by researchers at Johns Hopkins. The researchers ostensibly tested the “Mystical” effects of psilocybin, the active ingredient in mushrooms which is an illegal drug that causes hallucinations. However, two months after the trial they found that “79% of those prescribed psilocybin reported moderately or greatly increased levels of life satisfaction compared with those given a placebo. A majority said their mood, attitudes and behaviors had changed for the better.” [Link] No SSRI clinical trial had that high a rate of long-lasting improvements in mood, attitude and behavior.

The authors sent inquiries to reporters who mentioned the “chemical imbalance” theory as if it had been proven, asking for citations of such proof. The responses–or lack of responses–and the biased, pro-industry reporting about mental health treatments, are no less troubling than the biased reporting in the New York Times about the events leading up to the Iraq War.

“In hindsight, as the Times editors now acknowledge (5/326/04), Judith Miller’s war coverage was overly one-sided. Her fundamental flaw could be described as a lack of professional skepticism toward the Bush administration, as she willingly parroted what those pushing for war were saying, while giving little credence to the stance of the other side. Writing in the New York Review of Books, Michael Massing commented that the Times and Miller’s reporting were examples of media “submissiveness.”

This depiction could just as well apply to the media’s reporting of mental health issues. As just one example, in some cases, the media still go to the people responsible for the original problems. For instance, several of the researchers involved with the studies of SSRIs in children are still cited in the press even though the following information has come out about their published studies: they downplayed the suicide risk; they exaggerated the benefits; and the papers published under their names were actually written by ghostwriters paid by the pharmaceutical industry.

The Times editors have acknowledged both the problems with Miller’s reporting and their own lack of editorial oversight of her. It remains to be seen if members of the media will ever look inward and reflect on their role in the promotion of the chemical imbalance theory. (For those familiar with the New York Times’ coverage of mental health issues over the past 10 years, it is refreshing that after a series of health reporters who essentially abdicated their role as investigative journalists, there is a newer group of Times reporters with more skeptical inclination…

Thanks to the AHRP blog for this.

Both articles by Jonathan Leo and Jeffrey Lacasse are freely accessible. The first is here and the latest paper can be found here.

I’ve written on this issue before – to catch up please have a look here and here.

And remember this – the chemical imbalance ‘theory’ HAS NEVER BEEN PROVED. NEVER.

All it is, is a marketing idea – a sales tool.

Depression and sadness – at last some commonsense

This from today’s Times

Sadness: a natural antidote

Depression is at record levels, but is the condition being misdiagnosed? A book argues that many people are just sad and it’s natural

Victor Hugo once described melancholy as “the pleasure of being sad”. Few now have the chance to experience that pleasure.

Sadness, according to a group of influential American psychiatrists, has taken on a clinical alter ego – depression – and is steadily being medicated into oblivion. In Britain, 31 million prescriptions for antidepressants were issued last year, a record high. Our Prozac nation is now also steeped in Seroxat; we increasingly turn to serotonin boosters to soothe our sorrows.

And yet, as a powerful book points out, sorrow is not a disease but a natural emotion, as vital to our wellbeing as happiness. The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder argues that the ability to feel sad has survived hundreds of thousands of years of human evolution and must be of benefit.

“While depressive disorder certainly exists and can be a devastating condition warranting medical attention, the apparent epidemic (in depression) reflects the way the psychiatric profession has understood and reclassified normal human sadness as largely an abnormal experience,” write Allan Horwitz, professor of sociology at Rutgers University, and Jerome Wakefield, professor of social work at New York University.

Their book demonstrates how medicine has lost sight of the context in which people can become sad; the definition of depression requires only the appearance of symptoms such as insomnia, change in appetite and fatigue. As a result, people who are downcast for valid reasons, such as the end of a relationship or the loss of a job, can be mistakenly deemed depressive. Despite their natural reaction to a misfortune, they are crowded under the same diagnostic umbrella as the poor souls who feel sad for no reason; it is only the latter whose brains are functioning abnormally and require treatment.

Horwitz and Wakefield are respected academics in the field of mental health; their book has already prompted widespread soul-searching about how depression is defined. “[The authors] make a persuasive argument that has major public health implications,” comments Michael First, professor of clinical psychiatry at Columbia University Medical Centre and editor of the Diagnostic and Statistical Manual of Mental Disorders (fourth edition).

The DSM-IV, as this manual is known, is the checklist used by psychiatrists worldwide to diagnose all the mental disorders recognised by the American Psychiatric Association. The new edition, DSM-V, is set to be published in 2011; there is a growing call for major depressive disorder (which encompasses most depressive disorders) to be reframed in the terms that Horwitz and Wakefield suggest. But perhaps the most surprising string to the book’s bow is the author of its foreword: Robert Spitzer, professor of psychiatry at the New York State Psychiatric Institute. Spitzer is described by The New Yorker as “one of the most influential psychiatrists of the 20th century”. He was the driving force behind the third edition of the DSM; before its publication in the late Sixties, it was common for psychiatrists to differ wildly in their diagnoses of a condition in the same patient.

Spitzer’s work resulted in a reliable, comprehensive dictionary of definitions that all professionals could use; under his stewardship, the diagnostic manual became a universal compass helping medics to navigate the complex territory of mental disease with confidence.

He calls The Loss of Sadness a “brilliant tour de force” and a “water-shed” in the development of the field. More tellingly, Spitzer admits that “Dr Wakefield has critiqued my efforts in ways that I have largely become convinced are valid . . . (the DSM’s) diagnostic criteria specified the symptoms that must be present to justify a given diagnosis, but ignored any reference to the context in which they developed. In so doing, they allowed normal responses to stressors to be characterised as symptoms of disorder.”

The book, Spitzer reveals, “has caused me to rethink my own position . . .” It is probably the closest you will ever come to hearing a doctor of Spitzer’s stature admit that he was wrong. The book’s central thesis is that sadness seems always to have existed. All cultures experience sorrow; human infants are born with a tearjerking ability to express it. Even the type of grief we experience at various events is remarkably consistent: those who miss a life goal, such as a wanted promotion, feel pessimistic and tired, while the bereaved tend to cry and report physical pain. That chimpanzees, with whom human beings share a common ancestry, can appear mournful when life turns against them, indicates that sorrow has long been woven into the emotional fabric of human evolution.

These facts suggest that virtually everyone has an innate biological capacity to feel sad; so it is sensible to assume, as the authors do, that a good evolutionary reason lies behind the preservation of sadness as a psychological trait.

Dr Dylan Evans, an evolutionary psychologist and author of Emotion: The Science of Sentiment, says it is clear that the ability to feel sad has been honed over millions of years. “It must be an innate capacity that has come to us through evolution, because it is a basic, universal emotion,” he says. “People don’t have to learn to be sad; blind people who have never seen faces produce the same facial expressions. Just like other basic emotions, such as happiness, fear and disgust, sadness has all the hallmarks of an adaptation.”

Evans accepts, though, that the benefit that sorrow brings is not clear. “Disgust helps you to avoid rotting food, and fear makes you avoid wild animals and the dark. The function of sadness is more difficult to work out.”

“One possibility is that it makes you stop and reflect on what you’ve done, and it’s a way of stopping mistakes in the future. The problem with this is that sad people often don’t think logically or creatively, and don’t learn from their mistakes. Another theory is that it initiates support from other people.”

Only when intense sadness has no clear cause, or lingers longer than usual, should it be considered dysfunctional, and be treated medically. The Loss of Sadness points out that this distinction is not made in the way that major depressive disorder (MDD) is defined. In particular, it takes no account of personal circumstances (except for bereavement).

For a diagnosis of MDD in a person, he or she should have displayed at least five of the following nine symptoms over a two-week period (the five must include at least one of the first two symptoms): depressed mood; a lack of interest in activities; change in appetite or weight; insomnia; or hypersomnia (excessive sleep); a physical slowdown; loss of energy; feelings of worthlessness or guilt; inability to concentrate and make decisions; recurrent thoughts of death or suicide. In the case of bereavement, the symptoms must endure for at least two months.

A similar range of symptoms can happen naturally to a healthy person after a stressful event, such as an adulterous betrayal, failing a college test, learning that a child has cancer, or a public dressing-down. And without that context being specified, the authors write: “Contemporary psychiatry has inadvertently characterised intense normal suffering as disease”. In most cases of normal sadness, the suffering gradually subsides. But by then it is often too late – he or she is already wielding a prescription for Paxil or Prozac.

Evans agrees with the idea that normal sadness is overmedicalised; he sees this as a chance to discover the true function of sadness. “By giving Prozac out on a massive scale, we are, in effect, creating a huge social experiment in which sadness disappears.” Knowing what happens in its absence should give us a clue as to why we are born to feel sad.

Randall Nesse, a psychiatrist at the University of Michigan, once speculated that economic booms and busts were becoming more extreme because so many stressed-out investors and traders were on Prozac, which blunted their sense of caution. When the gambling is heavier, Nesse argued, the bubbles are more voluminous and the busts more spectacular.

“Anecdotally, people on antidepressants say that they feel untouchable,” Evans says. “They don’t seem to have that emotional immediacy that most of us have.” For severe depression, that is a good thing but in healthy individuals the antidepressants may be desensitising people to vital emotional cues from others. The idea that depression is often an unjustified medicalisation of a normal human emotion is gaining currency in this country, too. Earlier this month, Mark Rapley, professor of clinical psychology at the University of East London, organised a conference entitled “Demedicalising Misery”, featuring speakers who believe that much normal behaviour is wrongly classified as disease, and/or the benefits of antidepressants are oversold. The conference was a sell-out.

Rapley regards the current epidemic in depression as a social and cultural one, not a bona fide clinical one. “How is it that we have become so bamboozled that we fail to recognise certain human experiences, such as grief or sadness, for what they are?” Rapley asks.

And if depression is just normal sorrow, he rails, it’s reasonable that antidepressants are not correcting some fundamental, underlying brain deficiency: “If I have a severe headache and take aspirin to make me feel better, I don’t think of myself as having an aspirin deficiency. If I drink a couple of glasses of wine before I go to a party and then become the life and soul, I don’t regard myself as having an alcohol deficiency. If we don’t believe it for aspirin and Shiraz, why do we accept it for SSRIs (selective serotonin reuptake inhibitors, such as Prozac)?”

Rapley does not use the word “depression”; he says that he believes in being “unbearably sad, so sad that you can’t leave the house and you don’t think life is worth living. I call that what it is: unbearable sadness. I see nothing wrong with using substances to make yourself feel better. What I object to is the intellectual trickery, and how the drugs industry has made us believe that when we feel sad we have something fundamentally wrong with us that needs correcting.”

What does Seroxat do and just how is it supposed to work?

I’m sorry – run that by me again will you Glaxo…?

When I started taking Seroxat in 1997, I wanted to know how this great new drug worked – it boosts the levels of serotonin in your brain and that’s what makes you stop feeling depressed I was told. It’s a simple chemical imbalance – and the leaflet that came with the tablets told me “Remember you can’t become addicted to Seroxat.”

In 2002 the Patient Information Leaflet (PIL) still told us “these tablets are not addictive”, and that withdrawal problems “are not common and not a sign of addiction”.

“Remember you can’t become addicted to Seroxat.” had been dropped completely from the Patient Information Leaflet (PIL) by 2003 when GSK said in it “Seroxat is one of a group of medicines called selective serotonin reuptake inhibitors (SSRIs) and works by bringing the levels of serotonin back to normal.”

However by mid 2006 GSK admitted in the PIL “It is not fully understood how Seroxat and other SSRIs work…”

In 2007 the MHRA told us “A variety of factors can contribute to an individual’s predisposition to depression. Although it is believed that depression may be caused by a biochemical imbalance and it is recognised that serotonin plays a role in the development of depression it is considered that there is more than one final common pathway in the aetiology of depression, and we are not aware of an internationally agreed ’proper chemical balance of serotonin in the brain’ that would prevent or reduce the likelihood of experiencing depression.

As the precise role that serotonin plays in depression is still subject to ongoing research we really are not best placed to provide you with a response on this particular issue.”

I’m recapping on all this because in Australia it seems that Glaxo changed its mind yet again…. in Australia, “Aropax (the Aussie name for Seroxat/Paxil) corrects the chemical imbalance and so helps relieve the symptoms of depression. “

Go to Seroxat Sufferers to read some forthright views on this news item…

Go here to find out the shocking new prescribing information (in the UK at least).

Eternal sunshine

20 years of Prozac eh?

Writing today in the Guardian, Anna Moore, presents us with 20 things we should know about

It’s sold as happiness in a blister pack – a cure-all that has changed the way we think about wellbeing. As Prozac reaches its 20th birthday, Anna Moore presents 20 things you need to know about the most widely used antidepressant in the world

1: Depression has deepened
In 1971, when LY110141 – the compound that became Prozac – was developed, depression was rarely discussed and antidepressants largely restricted to the psychiatric unit. People went to their GPs with ‘anxiety’ and ‘nerves’. Tranquillisers such as Valium were a likely response.

Eli Lilly, the company behind Prozac, originally saw an entirely different future for its new drug. It was first tested as a treatment for high blood pressure, which worked in some animals but not in humans. Plan B was as an anti-obesity agent, but this didn’t hold up either. When tested on psychotic patients and those hospitalised with depression, LY110141 – by now named Fluoxetine – had no obvious benefit, with a number of patients getting worse. Finally, Eli Lilly tested it on mild depressives. Five recruits tried it; all five cheered up. By 1999, it was providing Eli Lilly with more than 25 per cent of its $10bn revenue.

Fluoxetine was handed to Interbrand, the world’s leading branding company (Sony, Microsoft, Nikon, Nintendo) for an identity. The name Prozac was picked for its zap: it sounded positive, professional, quick, proey, zaccy. It was marketed in an easy-to-prescribe ‘one pill, one dose for all’ formula and came when the medical profession and media were awash with horror stories about Valium addiction.

Prozac hit a society that was in the mood for it. National campaigns (supported by Eli Lilly) alerted GPs and the public to the dangers of depression. Eli Lilly funded 8m brochures (Depression: What you need to know) and 200,000 posters. Previous antidepressants were highly toxic, lethal if overdosed on and had other nasty side-effects. Prozac was pushed as entirely safe, to be doled out by anyone. It was the wonder drug, the easy answer, an instant up, neurological eldorado. When launch day dawned, patients were already asking for it by name.

Twenty years on, Prozac remains the most widely used antidepressant in history, prescribed to 54m people worldwide, and many feel they owe their lives to it. It is prescribed for depression, obsessive compulsive disorder, panic disorder, eating disorders and premenstrual dysphoric disorder (formerly known as PMT). In the UK, between 1991 and 2001, antidepressant prescriptions rose from 9m to 24m a year.

Strangely, depression has reached epidemic levels. Money and success is no defence: writers, royalty, rock stars, supermodels, actors, middle managers have all had it. Studies suggest that in America, depression more than doubled between 1991 and 2001. In the UK, an estimated one in six people will experience it – and it costs more than £9bn annually in treatment, benefits and lost revenue. Meanwhile, according to the World Health Organisation, depression is set to become second only to heart disease as the world’s leading disability by 2020.

20: Goodbye Prozac, hello Cymbalta
All good things come to an end, though, and in 2001, Prozac lost its patent. Eli Lilly lost $35m of its market value in one day – and 90 per cent of its Prozac prescriptions in a single year. Eli Lilly has now come back with Cymbalta, which it hopes will be the next Prozac. This was approved by America’s Food & Drug Administration despite another very shaky start. Traci Johnson, a healthy 19-year-old college student, hung herself in the Eli Lilly laboratory while testing the drug at high doses, in return for $150 a day. Cymbalta is a painkiller and antidepressant combined because, according to its logo, ‘Depression Hurts’. Read all about it, carry out a self-assessment checklist and watch some inspiring real-life stories on www.cymbalta.com

You can read all of Anna Moore’s article here.

Dr June Raine at the MHRA was warned about Seroxat 7 years ago

My good friend Bob Fiddaman, over at Seroxat sufferers writes:

Dr June Raine is the Director of the Post-Licensing Division at the Medicines and Healthcare Products Regulatory Agency (MHRA) and her responsibilities include all the issues that relate to medicines once they are authorised for use on the market.

Now, you have to ask yourself two fundamental questions here. Firstly, Dr June Raine is still the Director of the Post-Licensing Division at the MHRA – Why?

And secondly… Why have no criminal charges been brought against her?

Bob’s post Dr June Raine, MHRA knew 7 years ago tells the story of David Healy’s letter to her on the 7 June 2000. He wrote the day after the Court case in “Cheyenne, Wyoming… found GlaxoSmithKline guilty on several accounts including the count that Paroxetine can cause suicidality, that it specifically did so and contributed to the wrongful death of Don and Rita Schell as well as Deborah and Alyssa Tobin and that the company had been responsible for a failure to test and a failure to warn”.

David Healy wrote his letter in order to try and save lives.

As an expert witness in the Schell/Tobin case, Professor Healy had been granted access to Glaxo’s archives and had made shocking discoveries:

“What I found was that approximately 25% of the volunteers in the studies that I reviewed which were all of the healthy volunteer studies done prior to the filing of this drug for registration in the US and in the UK – 34 studies approximately in all. These yielded a 25% agitation, nervousness/akathisia rate. Some of the multiple does studies in healthy volunteers lasting 2-3 weeks yielded an up to 85% withdrawal rate in the volunteers.

All of their healthy volunteer studies were supposed to have been made available to me but not all were. Of the ones that were missing there was trace correspondence left in once indicating that the investigator had never witnessed such a level of problems in a study with healthy volunteers. Another study was a single dose study which in a dose dependent fashion yielded a 75% rate of severe adverse events most of which involved the central nervous system. There were other disturbing indications from one of the other missing studies.

Volunteers who had participated in the programme went on to suicidal acts. The relationship between their intake of paroxetine and later suicidal acts is a matter about which neither you nor SmithKline Beecham should be sanguine.

These studies were for the most part done on company employees. None of the studies bar the missing ones were done by investigators with a background in psychiatry. The investigators were general physicians with a primary interest in gastrointestinal problems who could not have been expected to detect mental problems of this sort that have concerned me and I would have thought should concern you”.

Professor Healy carried on:

“My testimony in this case also bore witness to sealed studies and other unreported data. It commented on the Montgomery Baldwin Study which yielded a projected rate of 45 suicide attempts in a group of recurrent brief depressive disordered patients on paroxetine per annum versus 12 on placebo. The figures were not statistically significant in great part one has to suggest because the company had terminated the study early. This termination and subsequent non-publication I would imagine the jury will have found and others will find significant.

Dr Hudson, currently of the MCA, was a witness for SmithKline in this case. He may well be able to give you further details on some of the issues involved. His testimony involved repeated reference to the fact that SmithKline Beecham cannot decide whether their drug had caused problems such as the wrongful death of Don and Rita Schell or Deborah and Alyssa Tobin or the wrongful deaths of many other people whose deaths have been reported to SmithKline even when these reports have been accompanied by the opinions of their treating physicians that the drug had indeed contributed to the problem. Dr Hudson’s testimony was that until controlled trials or other similar studies had proven in general that paroxetine could cause such problems that the company could not make decisions on any specific case”.

In conclusion he wrote:

“I think what will also be clear is that SmithKline Beecham recognised the presence of withdrawal syndromes in their volunteers from the early to mid 1980s. That withdrawal syndromes occurred at a much higher rate than occur on benzodiazepines. Nevertheless they applied for and have received from you and other regulators a licence to claim that their drug is effective in the prophylaxis of depression and these claims have been based on designs which almost certainly are designs better suited to show the presence of a withdrawal syndrome than designs suited to demonstrate prophylaxis in depressive disorders. A great number of people have in recent years been told that when they begin to feel ill on discontinuing treatment that this is the recrudescence of their mood disorder rather than a discontinuation syndrome from their drug. I would imagine that a great many such people and others on their behalf will feel extraordinarily let down and angry when faced with the evidence that I’ve been faced with”.

I think we all have to ask why June Raine and the MHRA did nothing in 2000 and still today they do nothing.

The best Kept Secret – SSRIs Do Not Work

The medicalization of distress has led to a dramatic rise in the use of antidepressants, however it is questionable whether patients are being told that in controlled clinical trials the drugs barely outperformed a placebo, says Jonathan Leo, Associate Professor of Neuroanatomy, Lincoln Memorial University, DeBusk College of Osteopathic Medicine.

Dr Leo also states that patients are not told that in many cases the symptoms of depression will improve within six months even without medication, or that many people have significant physiological problems when they try and get off the drugs. In the interest of informed consent, he notes, patients should be given all the facts before taking an antidepressant.

In 2004, a study of previously hidden unpublished data as well as published studies on five SSRIs, was conducted by Tim Kendall, deputy director of the Royal College of Psychiatrists’ Research Unit in London, to help analyze research to draw up the clinical guidelines for British regulators, and published in the Lancet.

Following his evaluation, Mr Kendall stated: “This data confirms what we found in adults with mild to moderate depression: SSRIs are no better than placebo, and there is no point in using something that increases the risk of suicide.”

In 2005, the British Medical Journal published another study that concluded that SSRIs are no more effective than a placebo and do not reduce depression.

SSRIs have been on the market less than 20 years so their long-term effects are still unknown. Barry Tuner, a professor of law and medical ethics in the UK, says mental illness has skyrocketed in the US because drug companies have marketed it and the US is facing a “societal catastrophe” if this is not reined in.

“In twenty years,” he warns, “a huge percentage of the population will be damaged by these medications and the recipients will have real mental disorders caused by the drugs.”

You can Evelyn Pringle’s latest article in full here.

A history of SSRIs

Over the years I have collected a few interesting documents and I think it’s just plain selfish to keep them to myself so I’m starting to share them with you.

The one for download here – A History of SSRIs is exactly what it says it is… a history of SSRIs.

You can read about the first SSRI – Zelmid – which was patented in 1972 and made it to market in 1982 before any of the others. I suppose not many of you remember Zelmid though as it was discovered in rare cases to cause a serious neurological disorder called Guillain-Barré Syndrome. This potentially fatal disorder led to the immediate removal of the drug from the market.

But Astra had already begun the development of a derivative of Zelmid, called alaproclate, when Zelmid ran into trouble. Alaproclate was being investigated for both depression and Alzheimer’s disease. But it caused liver problems in one strain of laboratory mice and this was enough to lead Astra to drop it. Shortly after this, Astra introduced an innovative antipsychotic, remoxipride, which looked like it would have significantly fewer side effects than older agents. Several months after its launch, however, remoxipride was reported to cause aplastic anemia in a small number of people and it too was withdrawn.

Notice a pattern here?

And did you know this about Prozac? As Eli Lilly were trying to launch Prozac in Germany they came up against a slight problem with the view of the German regulators on fluoxetine (Prozac) as of May 1984: “Considering the benefit and the risk, we think this preparation totally unsuitable for the treatment of depression”.

A History of SSRIs is an enlightening document – with a large section on Seroxat!

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