Adverse Psychiatric Reactions Information Link (April) conference – book now

Book now for APRIL’s third conference in London November 6th 2008: Adverse psychiatric side effects of medicines: What’s your responsibility? Download pdf here Download word format here.

APRIL was founded by Millie Kieve who began researching ADR’s after the death of daughter Karen in 1995.

With additional session on coming off medicines ‘how to prepare and cope with withdrawal’.

Speakers and Panel include:
Professor Munir Pirmohamed
Professor of Pharmacogenetics, Liverpool University. Leader in ADR Research

Professor David Healy
Professor of Psychological Medicine University of Wales Author of The Antidepressant Era

Charles Medawar
Founder Social Audit, Specialist Medicines Policy & Drug Safety co-author Medicines out of Control

Dr Anita Holdcroft
Emeritus Professor of Anaesthesia, Imperial College London. Anaesthesia ADR analysis paper 07

Professor Heather Ashton
Emeritus Professor Clinical Psychopharmacology Newcastle University

Dr Joanna Moncrieff
Sen.Lecturer/Hon.Consultant Psychiatrist Author of The Myth of the Chemical Cure

Dr Simon Maxwell
Edinburgh Uni/ British Pharmacological Soc. Med Schools Council Safe Prescribing Working Group

Dr Andrew Herxheimer
Clin.Pharm. co-author Seroxat ADR Review International Journal of Risk and Safety in Medicine.

Nigel Meadows
H.M.Coroner Manchester City District

Bob Johnson
James Nayler Foundation psychiatrist author of Emotional Health

Dr John Halliday
Pharmacology & Therapeutics Sub Dean King’s College, London

Dr Ben Goldacre
Medical doctor writer broadcaster (The Guardain ‘Bad Science’ regular column)
Peter Walsh CEO Action Against Medical Accidents

Clare Milford-Haven
Clare’s son James died by suicide 10 days after having anaesthesia

Millie Kieve
Founder of the charity APRIL will speak about the patient experience, lack of awareness and how this is costing lives

I’d like to suggest Dr Alastair Benbow attends – and someone from the MHRA… maybe Ian Hudson? No doubt the pair of them could learn a thing or two – and if either of you gents can make it – then lunch is on me.



Brown University, Keller and Study 329 – cracks beginning to show at last?

I’ve written a lot before about Marty Keller and Study 329 and so has Aubrey Blumsohn at Scientific Misconduct – in fact Dr Blumsohn has written to Brown University about Keller and his ‘research’.

It’s about time someone from Brown and/or Keller himself had the balls to stand up and explain themselves.

Now at last we might be starting to see some cracks begining to show thanks to student journalists at Brown University. This from Healthcare Renewal:

Brown University Student Journalists Dare to Report on Paxil/ Seroxat, Study 329 and GSK

We have published a few posts about the controversy about the clinical research supporting the use of paroxetine (Paxil, Seroxat in the UK, made by GlaxoSmithKline) in depression (here, here, here, and here.) This controversy includes allegations that clinical research funded by GSK was manipulated, and that the company’s marketing for the drug was unsupported by clinical evidence. GSK settled a case alleging fraud in the marketing of Paxil by then NY Attorney General Eliot Spitzer in 2004. A recent article provided arguments and evidence that Study 329, a clinical trial of paroxetine for adolescents, was manipulated , allegedly at least with the acquiescence of Brown University Psychiatry Chair Dr Martin Keller. [Jureidini JN, McHenry LB, Mansfield PR. Clinical trials and drug promotion: selective reporting of study 329. Int J Risk Safety Med 2008; 20: 73-81. Link here.] A book entirely devoted to this controversy, Side Effects by Alison Bass, who started reporting on the case in 1999 for the Boston Globe, was just published.

I am a still proud alumnus of Brown University (undergraduate and medical). I was a full-time faculty member at the University from 1994-2004, and am still a clinical faculty member. Despite Dr Keller’s and the University’s central role in the case, at least as alleged by Ms Bass and by Jureidini et al, there has only been silence about the case here in Rhode Island.

That just changed. Intrepid reporters from the Brown Daily Herald published two stories on the GSK/ Paxil/ Keller controversy. Both included some important original reporting, as well as providing clear summaries of the issues at hand.

The first article dealt mainly with Keller’s alleged conflicts of interest. This article provided confirmation that Senator Charles Grassley (R-Iowa) and the US Senate Finance Committee is, in fact, investigating Dr Keller and Brown University in connection with the controversy. It also included other original reporting, including an acknowledgement from GlaxoSmithKline Director of US Media Relationships Sarah Alspach that the company had provided the committee with full information about the compensation it gave Dr Keller.

The second provided a quite clear explanation of the allegations about the manipulation of Study 329. This article also included results of an interview with Dr Jon Jureidini, the author of an article that dissected study 329, and suggested that it had been manipulated to enhance the apparent benefits of paroxetine, and diminish its apparent risks. The reporters noted that Jureidini was “confident that data in Study 329 were deliberately misrepresented.” They were also able to obtain an internal GSK document that acknowledged that study 329 did not prove the efficacy of the drug.

The BDH reporters, Chaz Firestone and Chaz Kelsh, in my opinion, did a fine job, clearly explaining the issues, and digging out some new facts on the case.

Nonetheless, the BDH reporters were not able to get Dr Keller to talk to them, despite several attempts. They were not able to get anyone in the University administration to discuss any substantive aspects of the case. The highest ranking University official who would talk to them was Provost David Kertzer. He asserted that the University “can’t discuss particular cases of possible claims of wrongdoing and what we do about them.”

In my opinion, and as I said to the reporters, one of the most distressing aspects of this case is the refusal of Dr Keller or anyone in the University to deal with the content of the case. Very serious allegations have been made. If they can be refuted, they should be. If not, stonewalling only increases the impression that the University administration has something to hide.

Furthermore, the case raises important issues about science and clinical medicine. Universities are supposed to be where people can conduct free enquiry. There seems to be no free enquiry at Brown into the issues raised by this case. University administrators should be encouraging free enquiry. Here, they seem to be doing their best to avoid, if not stifle it.

Today, the BDH published its own editorial on the case, suggesting that Dr Keller’s “actions directly affect the integrity of the University.” If so, the University community should, at the very least, be discussing these actions, how they affect this integrity, and what ought to be done about it. Unfortunately, I am not optimistic that there will be an open discussion of these issues, even after the brave publication of these articles. The University administration seems to have some reason they want to clamp a lid on this case, and I am afraid they will continue to do so. The medical school faculty, lacking tenure and remembering what happened to previous dissenters like Dr David Kern, are likely to be too scared to push that lid away. Woe unto Brown.

See also comments on the Alison Bass Blog, PharmaGossip, and Pharmalot.

MHRA report finds healthcare blogs as influential as old media

I’m playing catch-up here with some old(ish) news from earlier in September.

Bob Fiddaman (author of Seroxat Sufferers) recently had a meeting with the MHRA, which you can read about here – there’s a full transcript of the meeting.

Bob’s meeting coincided with the release by the MHRA of a report it had commissioned about itself, Seroxat and blogs… you can download the entire 248 page document here. It’s a 12.1mb file, as it includes the report and many letters from patients and members of Parliament who wrote to complain about Seroxat.

Now read on for an American viewpoint on all this – from Furious Seasons:

Earlier this year, the MHRA–Britain’s FDA–got a report from a British web consulting firm analyzing the influence and popularity of various online information sources for people interested in learning more about Seroxat (Paxil’s UK name) and the MHRA. It’s not clear why the MHRA commissioned the study, but apparently the agency realized it was being pounded by numerous British bloggers over its role in letting a problematic anti-depressant stay on the market with few warnings for consumers about withdrawal problems and other side effects, so the agency apparently wanted to learn how much impact all these newfangled blogs were having.

What the MHRA learned from this report (6.4 MB pdf) is that blogs and the people who write them are as influential as many traditional media websites and traditional corporate websites and are more influential than are many well-financed healthcare websites such as WebMD. The report only looked at how influential blogs were as regards the MHRA and Seroxat (as opposed to the FDA and Paxil) to give the whole thing a British slant.

Included among influential and popular blogs in no particular order were Pharmalot (US), Seroxat Sufferers, Seroxat Secrets (UK), the Carlat Psychiatry Blog (US), Furious Seasons (my All-American blog), Clinical Psychology and Psychiatry (US) and Health Care Renewal (US). For popularity and influence, we ranked right up there with wire services, the London (UK), Times and the Wall Street Journal and only slightly trailed the BBC and the New York Times. This is all quite astonishing when you think about it–underfinanced blogs having as much influence as the WSJ! Unthinkable! US blogs that barely mention the MHRA (and usually write about Paxil not Seroxat) being more influential than WebMD–the world has come undone for sure!

You can skim the report for yourself and draw your own conclusions. Obviously, there are going to be biases in how the report’s analyses were done and what search terms were used and so on (you’d get different results if the consultants had gone after the FDA and Paxil), but what the MHRA has learned reminds me of what political parties and the mainstream media learned about US political blogs in 2004 and that is that they cannot ignore them. The reading public has voted with its eyeballs and has decided that blogs matter, and matter in some cases much more than Big Pharma’s own websites and more than pharma-funded health care sites like WebMD. And that my friends smells like victory.

I simply cannot wait until the FDA figures this phenomenon out for itself. Advertisers too.

Posted in MHRA. 2 Comments »

Is Clinical Depression Caused by a Serotonin Imbalance?

This from Chemical (thanks to Truthman30):

“In a sense there are two entirely different discussions going on about the theory: In the media and the advertisements serotonin deficiency is presented as simple and straightforward, but in scientific circles it is treated as tenuous at best.  In scientific circles the debate seems to be not so much about the strength of the theory but about the appropriateness of using it with patients given the lack of clear data – one prominent academic psychiatrist states that the serotonin theory is a metaphor which he will not use with his own patients; another practicing psychiatrist states that that the evidence presented by Dr. Kramer “doesn’t mean much” in clinical practice but admits to telling patients they have a chemical imbalance all the same.

We continue to wonder if the scientific evidence justifies such behavior, let alone massive marketing campaigns which inform the general public that depression is the result of a serotonin imbalance. In the matter of informed consent, we question whether patients who are told they have a chemical imbalance really understand how little direct evidence there is for the theory.”

[Now read on:]

Is Clinical Depression Caused by a Serotonin Imbalance? A Response to Peter Kramer

Jonathan Leo, Ph.D.
Jeffrey Lacasse, Ph.D.


The claim that depression is caused by an imbalance of serotonin is often made in the mainstream media. In a recent paper in Society we report on our efforts to examine the supporting evidence used by journalists who make such claims. We corresponded with a pharmaceutical company, several psychiatrists, and the National Institute of Mental Health. For the most part we received few citations of scientific papers, and those that were cited did not provide evidence for a causal connection between serotonin and depression. In our experience, there are few scientists familiar with the data that will publicly defend the serotonin theory of depression.

We also believe that debate between researchers holding conflicting viewpoints is an essential part of scientific progress. We were therefore pleased to see that Peter Kramer, author of Listening to Prozac, recently posted a defense of the theory on his blog. Dr. Kramer had previously made public comments responding to critiques of the serotonin theory in 2006, stating, “While it’s true that one could say that these drug companies are using a very oversimplified metaphor – and a metaphor for something that may not even exist at all – it’s also wrong to suggest that it has no relationship to contemporary theories of mood regulation.

Since we agreed with this statement, we were intrigued by Dr. Kramer’s recent defense of the serotonin theory. In his blog posting, Dr. Kramer cites evidence to support the serotonin theory, much of it from a recent review article in the New England Journal of Medicine. All of the studies Kramer discusses are interesting research projects, but for us, the important question is: Do these studies provide enough scientific evidence to support the ubiquitous statements in the media about depression?  As just a few examples:  “Mental illness are simply chemical imbalances,” or “Depression is thought to be caused by a chemical imbalance in the brain.” Below, we analyze the evidence presented.


Alteration in 5-HT1B Receptor Function by p11 in Depression-Like States (2006) Science, 311: p77. In reference to this paper, Kramer states: “Other studies have found that serotonin receptors function less efficiently in depressed patients. A protein named p11 is implicated: depressed patients have less of it in the brain.”  The paper in question is a four page paper that examines the interaction of the serotonin 1B receptor with p11 in rodents. Out of the four pages, the authors devote one sentence to p11 in humans. In what can only be called a preliminary report, as very few details are supplied, the authors report that p11 mRNA is decreased in the anterior cingulate cortex in patients who suffered from depression (p.79). The study used fifteen patients and fifteen controls. Seven of the patients committed suicide. Patients who commit suicide are very likely not a fair representation of the average patient diagnosed with depression, but this problem aside, the authors do not mention whether the patients had a history of medication exposure – an obvious question.

An e-mail inquiry and subsequent reply from E. Fuller Torrey, the head of the Stanley Foundation, which supplied the brains for the study, confirmed that the majority of the patients had been prescribed medication – whether they filled these prescriptions and/or took the medications is unknown. Dr. Torrey did mention that one possibility is that the patients who committed suicide stopped taking their medication, implying that the lack of medication was a contributing factor to their suicide. Thus the lower level of p11 in the depressed patients could be due to long-term antidepressant use, to the withdrawal effect, or to a combination of both. Therefore, a major piece of evidence that Kramer uses to defend the serotonin theory is a comparison of 15 patients with a history of medication use, which was only one minor component of a larger study.  We do not think that our concern with prior medication use is excessive. In the words of Ross Baldessarini, professor of psychiatry,  “Almost any psychotropic drug that’s given for more than a few weeks leads to changes in brain function such that when you stop, the brain has to reset its thermostat.”

Major Depressive Disorder, New England Journal of Medicine (NEJM), 358:55. In this review article, the authors discuss numerous avenues of research into depression. While the authors discuss serotonin they do not supply any direct evidence for the idea that low serotonin is the cause of depression. For instance, they discuss tryptophan depletion studies. Tryptophan is a rate limiting enzyme involved in serotonin production in the brain. It was originally hypothesized that tryptophan depletion would lead to low serotonin, which in turn would lead to a lowering of mood. Yet, as the authors point out, in healthy subjects this has not been the case.

The authors also discuss an oft-cited study by Caspi et al. which investigated common polymorphisms of the promoter for the serotonin transporter gene.  Yet, the NEJM’s piece also includes the oft-made characterization about the study, which leaves out some important details. According to the NEJM, “Caspi et al. found that 5-HTTTLPR predicted depression only in association with defined life stresses” (p. 56).  However, this needs to be qualified by pointing out two important points: 1) Just the presence of the short form of the gene did not predict depression – after all following major life stressors only 35% of the short form carriers developed depression (If 65% of the carriers do not develop depression, it seems hard to characterize it as predictive). One needs to qualify the statement in the NEJM by saying that carriers of the short form were more likely than carriers of the long form to develop depression after major life stressors (It is the comparison that is important). Yet, besides pointing out that it is the difference between long and short form that is important, even more qualifications are warranted. 2) In addition, “defined life stressors” must be qualified; the carriers of the short form were at a disadvantage only if they were exposed to three or more major life stressors.  For those people who only suffered one or two life stressors, the findings were reversed and the patients with the short form actually were less likely to be depressed – in this case the short form was protective (See Figure 3, p. 389 of the Caspi study). A subsequent study by Shelley Taylor and her colleagues at UCLA found that people with two copies of the gene’s short form were actually less likely to have depression symptoms if they had positive childhood experiences.

Also of note with the Caspi study is that the marker in question is not a rare mutation found in only a small percentage of the population. Approximately 70% of the population carries this “susceptibility” gene. One possible conclusion is that they have not discovered something unique about the subset of people diagnosed with depression, but have discovered something about human nature in general. Of course there are mechanisms in the makeup of the human brain that respond to environmental stressors. But finding these mechanisms does not mean that we have found a marker for a disease. If 70% of us have a gene that plays a role in our response to stress should this be considered “normal” or “pathological?” Complicating interpretation of this data, while some studies have found similar results to Caspi, other groups have not (Gillespie, 2005).

Kramer also touches on the efficacy of the SSRIs when he says, “The NEJM notes that a third of depressed patients do not respond to antidepressants. In those who do respond, what the authors call ‘the monoamine-deficiency hypothesis extended’ remains the most powerful explanation of the drugs’ mechanism of action.” Leaving efficacy aside, it is important to point out that showing how a drug acts at the molecular level does not necessarily equate to understanding the etiology of a condition – in this case determining that a drug acts on the serotonin receptor or serotonin system does not prove that depression is caused by low serotonin. If we followed the logic that “mechanism equals disease” then we could assume that every drug with a behavioral effect on the nervous system does so because of a chemical imbalance – something which is certainly not true. In many cases a drug will relieve a symptom but not treat the root cause of the problem. Take a long distance runner with a pulled muscle. Pain medication will relieve the pain – a symptom – but we do not attribute the cause of the pulled muscle to a chemical imbalance. Many drugs – both legal and illegal – act on the monoamine system: SSRIs, amphetamines, methylphenidate [Ritalin], mushrooms, coffee, cocaine, etc.

The authors of the NEJM piece state: “A strong point of the monoamine theory is its predictive power. Almost every compound that has been synthesized or discovered for the purpose of inhibiting norepinephrine or serotonin reuptake has been proved to be a clinically effective antidepressant.” We would go one step further and point out that based on the predictive power of the monoamine theory, even though the legal and illegal drugs have similar pharmacological properties, the chemical imbalance theory will only be applied to the use of drugs sold by a pharmaceutical company. Take the performance enhancing effects of amphetamines. If they are sold by a pharmaceutical company to improve classroom performance in a child this is considered acceptable, but selling amphetamines to a baseball player seeking to increase his batting average, can get you five to ten – and the player can wind up unemployed. The justification for the difference between the two scenarios? One case involves treatment for a supposed chemical imbalance, and one case involves a cheater. The demarcation between the two scenarios is not based on the pharmacological profile of amphetamines but on marketing and societal mores.

Elevated Monoamine Oxidase A Levels in the Brain: An Explanation for the Monoamine Imbalance of Major Depression,” Archives of General Psychiatry, 63, 1209-1216. This is one of the more interesting papers on this topic. MAO-A is an enzyme that breaks down the neurotransmitters serotonin, norepinephrine, and dopamine. The authors’ hypothesis is that MAO-A levels are higher in the brain during untreated depression, which they believe could explain the monoamine theory of major depression. They used positron emission tomography (PET) scanning on 17 patients diagnosed with depression and 17 healthy patients, and measured their levels of MAO-DVs, an indicator of MAO-A. The group of depressed patients had higher mean (average) levels of MAO-A. Thus, one interpretation is that these higher levels of MAO-A enzymes cause major depression. After critically appraising this paper, we have several questions:

Does this paper establish that increased MAO-A is the cause of major depression? Or, alternatively, does it simply document an association? We wonder if higher mean MAO-A among a group of depressives might be a sign of depression, rather than the cause. Consider that many people get nervous before public speaking, and, frequently, their heart rate quickens and their blood pressure goes up. But most people would not say that high blood pressure is the biochemical explanation for public speaking anxiety. Similarly, how do we know that lower MAO-A in depressed individuals is not simply a sign of depression, rather than the cause? Certainly, further experiments are required before causal claims can be made regarding MAO-A in depression.

Have the results been replicated? The answer is no. This is a study of 17 depressives and 17 healthy patients in Canada. Time will tell if independent research teams are able to replicate this finding with other patients. Certainly, important findings should be replicated, repeatedly, by as many different research teams as possible. The history of science, and in particular psychiatric science, is full of exciting preliminary findings followed by failed replication attempts.

Are the results specific to depression? Keep in mind that MAO does not just break down serotonin, but also norepinephrine and dopamine. These three neurotransmitters are implicated in almost every DSM-IV-defined mental disorder. In future experiments, rather than healthy volunteers, it would be interesting to see patients diagnosed with major depression compared to patients diagnosed with other non-affective mental disorders (e.g., ADHD). Until such experiments are performed, we think many will question whether these findings are specific to depression.

Below, we have created a figure with content similar to figure 2, p.1212, in their article. (We cannot reproduce the original figure due to copyright). This figure is most similar to the results presented for the midbrain, hippocampus, and putamen. The pattern holds true less so for the results from the posterior cingulated cortex and thalamus.

What do we make of the fact that there is overlap between healthy and depressed patients? Several healthy patients have higher levels of MAO-A than depressed patients, and some depressed patients have lower levels of MAO-A than healthy patients. For instance, in the figure above, if we consider that the healthy patients have “normal” levels of MAO-A, then eight out of the seventeen depressed patients would fall in the normal range, or conversely 7 of the healthy patients would fall in the same range as the depressed patients. In other words, while there might be differences in group means, this does not mean that individual patients can be identified on the basis of their MAO-A levels. This is quite different than the diagnosis of diabetes, a medical condition to which clinical depression is often compared, in which lab tests are used to accurately diagnose patients.

Are the author’s conclusions congruent with the existing clinical trial data? Recent research has challenged the efficacy of SSRIs. For instance, a recent systematic review concluded, “Among adults with moderate to severe major depression in the clinical trials we reviewed, paroxetine was not superior to placebo in terms of overall treatment effectiveness and acceptability” (Barbui, Toshiaki, & Cirpiani, 2008, p. 296). We are confused as to how such findings line up with the proposal that serotonin imbalance causes depression. Michael Thase, an academic psychiatrist and pharmaceutical company-funded clinical trialist, has proposed that one or two out of ten patients prescribed an SSRI have a clinically significant response. Would proponents of the chemical imbalance theory interpret this to mean that 80-90% of patients prescribed SSRIs do not have a serotonin imbalance?

To top it all off, there are many debatable issues regarding statistical reporting, generalizability, and the other issues that face all such small neuroimaging studies.

Thus, while the Meyer study is an interesting piece of research, and is an important contribution to the field (and we certainly look forward to seeing future reports of MAO) we do question using it, as Kramer does, as primary evidence in support of the idea that depression is caused by low serotonin. In other words, the problem lies not with the ongoing laboratory research, but with prematurely drawing conclusions from these data.


We are pleased that Kramer has put in writing what he thinks is the best evidence for the serotonin theory, however, we are concerned that readers of his blog may mistakenly conclude that there is indeed powerful new evidence for the serotonin theory. As we have shown, an in-depth look at these studies finds the results to be tentative, at best. Hypotheses regarding serotonin and depression have been generated that need to be rigorously tested, as has been the case for forty years.

Overall, this discussion illustrates the difficulties of the scientific process and the perils of justificationary thinking. If a psychiatrist begins with the belief that serotonin deficiency causes depression and proceeds from there, there will always be studies to be cited. Unfortunately, much of this evidence collapses under critical scrutiny.

We would prefer a more rigorous scientific model. Important components would include replication, acceptance and integration of counter-evidence, active attempts to falsify the theory being tested, and a solid grasp of the methodological limitations involved with the research. Fortunately, we find that most scientists are quite aware of these limitations. In fact, when scientists discuss the biological basis of mood with other scientists, it is almost as if there are a set of ground rules that everyone agrees with, such as: (a) There are extremely subtle nuances to many of these studies; (b) it is important to refrain from drawing too many conclusions from the latest findings; (c) finding a biological difference between people diagnosed with depression and “normals” does not automatically warrant the jump to causation; and (d) environmental triggers play an extremely important role in why someone’s mood might be lowered. Yet, in the popular press all these qualifications disappear and instead the public is inundated with declarations that “mental disorders are caused by chemical imbalances.”

In a sense there are two entirely different discussions going on about the theory: In the media and the advertisements serotonin deficiency is presented as simple and straightforward, but in scientific circles it is treated as tenuous at best.  In scientific circles the debate seems to be not so much about the strength of the theory but about the appropriateness of using it with patients given the lack of clear data – one prominent academic psychiatrist states that the serotonin theory is a metaphor which he will not use with his own patients; another practicing psychiatrist states that that the evidence presented by Dr. Kramer “doesn’t mean much” in clinical practice but admits to telling patients they have a chemical imbalance all the same.

We continue to wonder if the scientific evidence justifies such behavior, let alone massive marketing campaigns which inform the general public that depression is the result of a serotonin imbalance. In the matter of informed consent, we question whether patients who are told they have a chemical imbalance really understand how little direct evidence there is for the theory.

We encourage reporters to dig deeper and to question whether the evidence in support of the theory justifies simplistic claims about the cause of depression, and to carefully consider the claims made by  psychiatrists and other experts about the serotonin theory. In his blog posting, Kramer argues that the miserably depressed Zoloft Ovoid creature is smarter than the critics have made him or her out to be. We agree with Kramer that the Ovoid is intelligent, however, given its ability to convince the media that there is substantial evidence in support of the serotonin theory, it appears that the Ovoid’s talents seem to lie in the marketing, and not the scientific, realm.

Pharma Giles – gone but not forgotten

I had this comment today – you simply must follow the link… thanks to ‘Blogger’:

For all of you missing the Pharmagiles blog I am reproducing the amusing Childrens Story of Medicine Book created by the legendary PharmaGiles.

Come on MHRA – admit Seroxat/Paxil really is addictive…

No one seems to want to admit Seroxat/Paxil is addictive… not Glaxo, not the FDA, not the World Health Organisation, not the MHRA… it seems the only people who are prepared to stand up and say Seroxat is addictive are those of us who actually took the drug.

I thought I was right to say I was addicted to Seroxat because I was totally dependent on the drug as I found I could not stop taking it without suffering terrible physical and mental withdrawal symptoms… a simple and straightforward enough premise. In fact The Oxford Pocket Dictionary of Current English (date: 2008) agrees with me, defining addiction as: the fact or condition of being addicted to a particular substance, thing, or activity.

In a recent meeting with Bob Fiddaman, Kent Woods of the MHRA disagreed as he repeated the big pharma mantra about the definition of ‘addiction’: “8. KW noted that the term “addiction” ought to be reserved for circumstances which typically entailed cravings leading to increase in dosage…”

Well Kent, I’ve got some news for you – I have no time for semantics designed to protect drug manufacturers (or the MHRA) while you sit there and ignore patients’ experiences.

I was addicted to Seroxat. It is an addictive drug.

Here are some more definitions of Addiction:

More drug marketing by the back door – Servier take a bow

A colleague sent me this news item about research that shows SSRIs DON’T actually work – and they also ruin your sleep (bear with me – this is a good one).

BARCELONA, Spain — September 1, 2008. A Scottish study — Long-Term Antidepressant Treatment Without Active Management Hardly Induces Remission: presented at ECNP By Judith Moser, MD — identified a group of patients in primary care who are on long-term and stable treatment with selective serotonin reuptake inhibitors (SSRIs). A substantial proportion of patients displayed prevailing residual depressive and anxiety symptoms as well as sleep problems in spite of their treatment.

Alan Wade, MD, CPS Clinical Research Centre, Glasgow, Scotland, presented the study at a poster session on September 1 here at the 21st European College of Neuropsychopharmacology (ECNP) Congress.

Patients who were prescribed standard doses of antidepressants by their general practitioners without active management due to repeat prescriptions were identified from prescribing records in the West of Scotland.

Patients were invited to complete a questionnaire; 316 out of 893 questionnaires were completed and returned (35%).

 Each patient completed a Hospital Anxiety and Depression Scale (HADS). Simple Laekert questionnaires enquired about specific sleep symptoms; furthermore, the response to individual questions was analysed.

If patients are to have a good quality of life, it is important that the antidepressant treatment leads to remission with a minimal number of residual symptoms. 

Nevertheless, as the HADS results showed, most of the patients still displayed significant residual symptoms, despite the long-term treatment. 

Seventeen percent of patients still showed severe depression and 29% severe anxiety. No significant association was reported between the duration of SSRI treatment and the mean anxiety and depression scores.

Anxiety and sleep symptoms were prominent in over half of the population and interfered with the patients’ daily lives as reported by them. Only a minority of patients were satisfied with their sleep, and 29% perceived their sleep problem as a significant stressor.

The majority of patients (61.19%) had not reported their sleep problems to the general practitioner. Of those who had, 50.59% received a hypnotic medication. Treatment of insomnia often turned out to be helpful but led to long-term use in half of the patients. “The patients adjusted their lifestyles to this chronic illness,” Dr. Wade concluded. “They are just not actively treated well enough to get really well, so there are several questions to be asked in the future.”

Funding for this study was provided by Servier.

If only there was a new anti depressant that didn’t ruin your sleep… oh hold on… what’s this I wrote about in May this year when Depression Alliance found themsleves helping in the marketing effort for Valdoxan:

Interestingly, French company Servier, makes Valdoxan (agomelatine) which is an antidepressant, but with added qualities. Says Servier
“the drug’s unique profile could make it an exciting and innovative
product, but it will face stiff competition from top-selling
antidepressants already established in the market… As well as treating
the main symptoms of depression, the drug also helps to
improve daytime alertness by normalising the timing and continuity of
sleep, a problem that Servier says is common in patients.

That’s handy. So Valdoxan could be just the thing patients need – as
the new survey from Depression Alliance has discovered that sleep
disturbance is a real problem. But hold on, The development of this survey and the report into its findings were undertaken in partnership with and funded by Servier Laboratories Limited.

That’s a bit of a coincidence isn’t it?

And here’s another coincidence – Servier Laboratories this week [02 March 2006] confirmed the UK agency support behind its new anti-depressant, Valdoxan. Athena Medical PR
secured the contract to steer the brand to market. The drug is the
French firm’s first foray into the UK mental health arena, with
Valdoxan poised to enter the controversial and crowded market ‘during

Valdoxan combines antidepressant efficacy with ‘favourable’ side effects – it has the additional benefit of sleep regulation in depressive patients, according to data unveiled last year.

Well that’s two pieces of ‘research’ (that Servier has funded) that will useful in its sales pitch for Valdoxan. I bet boxes and boxes of reprints of both pieces of ‘research’ have been mailed to GPs and handed over by Servier drug reps as they pass out the free samples of the new wonder antidepressant, Valdoxan.

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