Hello To The World Health Organization (WHO)…


I get views regularly from organizations as diverse as the WHO (World Health Organization) and the MHRA, to the US government and the European Medicines Authority. It’s interesting that the WHO were viewing today, because it was back in 2002, that the WHO reported that Paroxetine (Seroxat/Paxil) topped the list of withdrawal symptoms for SSRI drugs.

http://news.bbc.co.uk/2/hi/health/1382551.stm

 

“Dr Healy told BBC News Online, of the 100m people world-wide who were on Seroxat, one in 1,000 could have a suicidal reaction.”

Withdrawal problems

A World Health Organization report which ranked antidepressants in order of withdrawal problems found Seroxat was the hardest to come off.

 

Ian Hudson of The MHRA (ex-GSK Employee)Bluffs And Blunders His Way Through A Grilling By Andy Vickery At A Paxil Induced Suicide Trial (2000)


I have to say I have been incensed watching a video of Dr Ian Hudson of the MHRA when he was defending (his employer at the time) GSK from allegations that Paxil/Seroxat caused a suicide in the US. Hudson did everything he could to defend Paxil/Seroxat  but in many ways he slipped up. This video was recorded in 2000. At this time I would have been on Seroxat for two years, I had no idea that this trial was even happening, there was no access to the web, or information back then- people like me were left suffering in the dark. Some people didn’t make it through, the side effects were too much, and they killed themselves. Akathsia is one of the most crippling and disturbing side effects of any psychiatric drug. On Seroxat I had weeks, often months of regular bouts of akathisa, I wouldn’t wish it on my worst enemy- it was hell, beyond hell actually, it was utterly devastating. I can understand completely how Akathisia would drive some people to kill themselves, I don’t know how I endured it, maybe my youth had something to do with it- often youth protects us from extreme events because we can endure more- and Seroxat was torture, absolute torture.

At the time that Dr Ian Hudson was defending his employers in a Seroxat suicide trial in the US, and denying that Seroxat was even associated with Akathisia, I was probably  climbing up the walls in my bedroom, rocking like a lunatic, crying and pulling on my scalp, feeling like every atom in my body was on fire, intensely suicidal, feeling like my skin was literally burning and crawling off my bones-  but all the while completely unaware that I was experiencing akathisa from Seroxat.

I didn’t even know what akathsia was.

However, I’m sure that Ian Hudson knew what Akathisa was though..

Ian hudson is now the CEO of the MHRA (the Medicines Regulator in the UK). At the time of his video deposition in this Paxil/Seroxat suicide trial- he was the ‘World-wide safety director’ of GSK (the manufacturer of Seroxat).

Imagine that ‘wordwide safety director’ of one of the most controversial drugs of the past 20 years …

I wonder what Ian Hudson’s view is now of Seroxat?

Does he still think that there is no relationship between Seroxat and Suicide?

Does he still think that there is no evidence of a cause and effect relationship of Akathsia with Seroxat?

If so, then why does GSK warn now of these effects in their PILs?

According to the GSK PIL (screen grab below)- Seroxat can cause Akathsia in around 1 in 1000 people.

Seroxat was prescribed to millions of people since it was first licensed 25 years ago- in 1991. So how many people went on to kill themselves because of Akathsia from Paxil/Seroxat? How many people lost their health? How many people killed themselves in the agonizing withdrawals? Can Hudson give us the new stats on that?

He is, after all, now the chief at the medicines regulator, and although he once defended Seroxat for GSK in court, maybe his new role as a patient protector- as opposed to a drug company lackey- he would be able to re-define his views for us and warn the public about the dangers of Seroxat?

Personally I wouldn’t even trust GSK’s PILs, if they say it’s one in 1000, it’s probably one in 100 or worse… they are proven liars and deceivers, nothing can be trusted from them given their track record. They are totally sociopathic when it comes to harming consumers of their drugs and denying that harm when it is revealed. But even if we take 1 in 1000 as an average estimate, that’s a lot of Akathsia from Seroxat.

But according to Ian- Seroxat doesn’t cause Akathsia, so which is it Ian does Seroxat cause Akathisia or not? The PIL says it does, but you said it didn’t…

Maybe Ian would like to-fulfill his role- and protect others from anymore Seroxat horror?

And maybe Ian would now like to do the right thing and apologize to all the people who killed themselves or felt suicidal, or lost their livelihoods, their relationships, and years of their lives, to Seroxat side effects?…

Or maybe he just doesn’t give a damn…

Either way, the whole thing stinks to high heaven in my opinion..

https://www.medicines.org.uk/emc/PIL.3185.latest.pdf

ian-hudsonseroxat-2

http://www.healyprozac.com/Trials/Tobin/Depositions/hudson-depo.txt

 

   Okay.  Dr. Hudson, does Paxil have an
 
        23  association with akathisia?
 
        24  A.    I've seen some case reports of
 
        25  akathisia.  I'm aware that there have been
 
 
 
                     SPHERION DEPOSITION SERVICES
                            (713) 650-3500

 
                   IAN R. B. HUDSON, M.R.C.P., M.D.
                                                     42
 
         1  some cases of akathisia, so it is something
 
         2  that we have received case reports about.
 
         3  Q.    Do you believe, as Worldwide Safety
 
         4  Director of SmithKline Beecham, that Paxil
 
         5  causes some patients to become akathisic?
 
         6  A.    I've seen no evidence to suggest a cause
 
         7  and affect relationship between Paroxetine and
 
         8  akathisia.  I've seen some case reports, but
 
         9  I've seen nothing that suggests a cause and
 
        10  affect relationship

Dr Ian Hudson (Ex GSK Employee and Current Head Of The MHRA- UK Medicines Regulator) Defends Paxil (Seroxat) In US Court Case… Exclusive- From Bob Fiddaman’s Blog…


 

http://fiddaman.blogspot.ie/2016/09/exclusive-dr-ian-hudson-in-defence-of.html

Monday, September 12, 2016

EXCLUSIVE: Dr Ian Hudson: In Defence of the Suicide Pill

A chance meeting, a discussion, a common interest.

That’s all it needs at times to stumble upon something you’ve been seeking for close to 10 years.

Video depositions have always fascinated me, they are better than the written depositions that we see within court documents. Most notably they show the subject answering questions, they show the subject in a much different light, they show the subject being evasive and choosing not to answer questions that may jeopardise the party he is appearing for. Moreover, they can be seen at later dates, when the subject has moved on to a different company or, in this instance, to head of the British drug regulator, the MHRA.

Ian Hudson is the former World Safety Officer for SmithKline Beecham, today they are more commonly known as GlaxoSmithKline or GSK.

On Friday, December 15, 2000, Ian Hudson, who at the time was still employed by GSK, gave a deposition in relation to a case that was to be tried in Wyoming a year or so after this deposition was taken, the result of which found that Paxil was, in fact, a proximate cause of the deaths in this case.

The case in question was brought against GSK by the relatives of a man, Donald Schell, who killed himself and three others after taking the drug Paxil,

Here is Ian Hudson’s video testimony. It’s a bit scratchy in places and the audio drops but it is the first time this has been seen in public.
.
Ian Hudson is the current Chief Executive of the MHRA, the British drug regulator who regulate the drugs you and I take.

You can draw your own conclusions as to whether or not you think Ian Hudson is forthright with his answers in this deposition.

A transcript of the video deposition can be found here.

Ian Hudson was being asked questions by US attorney, Andy Vickery.

(GSK are currently defending another Paxil related suicide in the US – The Stewart Dolin files can be seen here)


Paroxetine (Paxil/Seroxat) And Cognitive Impairment


http://qz.com/720419/when-meds-didnt-cure-my-depression-i-tried-retraining-my-brain-waves-instead/

“….But my experiences with psychotropic medication have shown similar problems. I started on paroxetine (the Paxil generic) in my 20s. It abruptly stopped working in my 30s—while I was taking it—and I slogged through five other medication trials before I found an effective replacement. Since then, paroxetine has been identified as having anti-cholinergic effects, which can include cognitive impairment and memory loss…”

Glad to see that the side effects of Cognitive Impairment from Paroxetine are beginning to be recognized in some media…

The ‘brain fog’ from Paroxetine never fully goes away..

http://i2.cdn.turner.com/cnn/2016/images/04/18/risacheretal_jamaneurology_final_inpress_041116.pdf

How Many People Have To Die Or Be Damaged For Life Before The Regulators Pull Seroxat (Paxil/Paroxetine) From The Market?


I had Akathisa multiple times on my 3 and a half agonizing years on Seroxat- how many people were driven to suicide or self harm etc from the horror of Seroxat/Paxil induced Akathsia?

In the following document, from 2006 (ten years ago now) Dr Peter Breggin drew attention to GSK’s suppression of the dangerous Akathisia side effect from Paxil:

See here

Ethical Human Psychology and Psychiatry, Volume 8, Number 2, Summer 2006

SPECIAL REPORT PART II

How GlaxoSmithKline Suppressed

Data on Paxil-Induced Akathisia:

Implications for Suicidality and

Peter R. Breggin, MD

This is the second in a series of Special Reports on previously suppressed data con-
cerning the selective serotonin reuptake inhibitor (SSRI) antidepressant Paxil (paroxetine) and its capacity to cause violence and suicide. The data were contained in a report that I wrote as a medical expert for a product liability suit against the manufacturer of Paxil, Lacuzong v. GlaxoSmithKline (GSK).1 After taking Paxil 10 mg for 3 days, Mr. Lacuzong drowned his two children and himself in a bathtub. The case was eventually ‘‘resolved’’ without the details of the settlement being made public.

The drug company denied all allegations.

My product liability report was based on numerous sources, most notably a 3-day trip

to the drug company offices to examine its internal files concerning how Paxil was re-
searched, developed, and marketed. Until these Special Reports, the information in these files had not been made public.

Since the publication of my first special report concerning how the manufacturer of

Paxil hid and manipulated data concerning Paxil-induced suicide (Breggin, 2006), the

FDA and the drug company, GlaxoSmithKline, have issued statements confirming that depressed adults of all ages taking the antidepressant have an increased rate of suicidality compared to depressed adults taking placebo (Kraus, 2006). These adults with major depressive disorder suffered a 6.4 times increase in the rate of suicidal ideation and behavior compared to the controls receiving the sugar pill (0.32% vs. 0.05%).

This meta-analysis of placebo-controlled clinical trials also focused on young adults who were prescribed Paxil for anxiety disorders as well as depression. In this broader diagnostic group, young adults (ages 18–24) who were given Paxil were also at increased risk for suicidality.

Summarizing these data, Paxil increased suicidality in depressed adults of all ages and also in young adults with depression, dysthymia, panic disorder, generalized anxiety disorder, and obsessive compulsive disorder.

The rates of Paxil-induced suicidality will be much higher in actual clinical practice where the drug exposure typically lasts much longer than 4–6 weeks, patient monitoring is much less thorough, multiple drugs often exacerbate adverse drug reactions, and many patients are already suicidal.

2006 Springer Publishing Company 91

92 Special Report Part II

By admitting that Paxil causes suicidality in adults, the FDA and GlaxoSmithKline confirmed observations I have been making in my publications and trial testimony for more than a decade (e.g., Breggin, 1997, 2001; Breggin & Breggin, 1994). The FDA and the drug company released their results within weeks after the publication of my initial special report in EHPP, which showed that the drug company had been suppressing the relevant data for many years (Breggin, 2006).

My first Special Report, ‘‘Court Filing Makes Public My Previously Suppressed Analysis of Paxil’s Effects,’’ described how recent court proceedings made my product liability report available to the public despite previously successful efforts by GSK to suppress it. My initial Special Report provided excerpts from my product liability analysis concerning how the drug company manipulated data concerning Paxil-induced suicidality. For example, GSK’s analysis of suicidality left out two attempted suicides and two completed suicides on Paxil, and exaggerated the number of suicidal acts on placebo. The company also reduced the apparent significance of suicide related events by providing separate analyses of overdose, suicide attempt, and suicidality. It is more useful and meaningful to combine all suicide-related activities into one category, suicidality.

For Special Report Part II, I have excerpted sections from my product liability report concerning how the drug company hid both the rates for Paxil-induced akathisia and the relationship between akathisia and suicidality. Akathisia is a drug-induced inner agitation or dysphoria that causes a person to feel compelled to move about. The painful feelings associated with akathisia have been compared to torture and often make people feel as if they are going ‘‘crazy.’’ People who suffer from akathisia often voice dramatic descriptions such as ‘‘electricity streaming through my veins,’’ ‘‘horrible jagged feelings inside my head’’ or ‘‘something pinching my nerves all over my body.’’ These vivid, desperate descriptions

can be mistaken for delusions or hallucinations (American Psychiatric Association, 1994,

2000; Breggin, 1997).

 

When the FDA initially approved Paxil in December 29, 1992, it had already been reported that SSRI antidepressants tend to induce extremely high rates of akathisia. For example, Lipinski, Mallaya, Zimmerman, and Pope (1992) described five cases and, based on a review of the literature, they estimated that Prozac (fluoxetine) causes akathisia in 9.7%–25% of patients. Since the 1970s, studies of neuroleptic-induced akathisia have demonstrated that akathisia causes severe emotional disturbances, including aggression, suicidality, and a worsening of psychosis (van Putten, 1975; van Putten & Marder, 1987; Breggin, 1983, 1997). In the early 1990s, clinical reports began to link Prozac-induced akathisia to severe, acute, and obsessive suicidality (e.g., Rothschild & Locke, 1991; Teicher, Glod, & Cole, 1990).

In 1994, the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM- IV, 1994, pp. 744–746) attempted to sum up the available clinical and research data concerning drug-induced akathisia. It stated, ‘‘Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts.’’ It also linked akathisia to ‘‘worsening of psychotic symptoms or behavioral dyscontrol.’’ The manual focused on neuroleptic-induced akathisia but made clear that the same problems are associated with SSRI antidepressant- induced akathisia: ‘‘Serotonin specific reuptake inhibitor antidepressant medications may produce akathisia that appears to be identical in phenomenology and treatment response to Neuroleptic-Induced Acute Akathisia.’’2

Because it was already known that SSRI-induced akathisia causes suicidality, violence, and overall mental deterioration, it was beholden on GSK to conduct a careful analysis

Special Report Part II 93 of Paxil-induced akathisia. It was also beholden on the company to look for a link between Paxil-induced akathisia and mental or behavioral abnormalities. Instead, GSK went to extreme lengths to hide the fact that Paxil causes akathisia and that the some Paxil akathisia cases were associated with suicidality.

SSRI antidepressants can cause suicidality and violence through means other than aka- thisia, including drug-induced agitation, depression, and mania. Patients who were previ- ously depressed can be pushed into states of agitated depression or manic-like reactions

(Breggin, 2003). The stimulating effects of SSRIs, from akathisia and agitation to mania, are responsible for causing some of the most severe mental and behavioral aberrations.

Some progress has been made by the Food and Drug Administration (FDA) in warning about the risks associated with SSRI stimulation or activation (reviewed in Breggin, 2005). The agency now requires antidepressant labels to carry several warnings related to over- stimulation and akathisia including the following: Clinical Worsening and Suicide Risk: Patients, their families and caregivers should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hy- pomania, mania, and other unusual changes in behavior, worsening of depression, and suicidal ideation, especially early during antidepressant treatment and when the dose is adjusted up or down. (FDA, 2005a, p. 2)

The FDA also requires antidepressant labels to carry a black box warning about the increased risk of suicidality in children who take these drugs (FDA, 2005a). Although specific warning about the increased risk of suicidality in adults who take these antidepressants is not required, the FDA has issued a Public Health Advisory about the potential danger in adults (FDA, 2005b). The data disclosed in this Special Report should lend scientific weight to the FDA’s concerns and encourage a specific label warning about the increased risk of suicidality in adults taking SSRI antidepressants such as Paxil.

The following excerpts from my product liability report dated July 21, 2001, focus on akathisia. In addition to examining how GSK manipulated or suppressed data concerning akathisia, these findings confirm a link between Paxil-induced akathisia and suicidality. The data also confirm that these severe reactions can occur beginning with the first dose of the drug and that they often occur within the first few days of the initial exposure.

My product liability report can be found in its entirety on my website, www. breggin.com. It covers numerous additional concerns about how GSK researched, developed, and marketed Paxil.

EXCERPTS FROM THE REPORT AND AFFIDAVIT OF PETER R. BREGGIN,

MD, IN THE CASE OF LACUZONG V. GLAXOSMITHKLINE

III. Eliminating Akathisia as Preferred Term and as an Investigator’s Term

(1) Definition of Akathisia. Akathisia is a neurological disorder caused by medica-
tions. Stedman’s Medical Dictionary, 27th edition (2000) defines akathisia as ‘‘A syndrome characterized by an inability to remain in a sitting posture, with motor restlessness and a feeling of muscular quivering.’’ The American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, IV (DSM-IV) (1994; 2000) describes akathisia in the context of neuroleptic drugs, but [as noted in the DSM-IV] the clinical manifestations are

94 Special Report Part II the same when akathisia is induced by SSRI antidepressants. The DSM-IV observes that akathisia includes the following symptoms: [S]ubjective complaints of restlessness and at least one of the following observed move-
ments: fidgety movements or swinging of the legs while seated, rocking from foot to foot or ‘‘walking on the spot’’ while standing, pacing to relieve the restlessness, or an inability to stand still for at least several minutes. (p. 744)

In general, if the subjective experience of agitation, anxiety, irritability or similar feelings are accompanied by voluntary motor movements, such as pacing or foot swinging, the syndrome is identified as akathisia.

(2) Akathisia, Violence, and Suicide. The DSM-IV states without qualification,

‘‘Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts’’

(p. 745).

There is a considerable body of literature to confirm the association between akathisia and violence and suicide. I have reviewed some of the literature in Breggin and Breggin

(1994) and Breggin (1997) [most recently in Breggin 2003] in regard to psychiatric drugs in general and specifically the SSRIs of which Paxil is a member. Teicher et al. (1993) reviewed SSRI-induced violence and suicide. More recently, Glenmullen (2000) devoted a significant portion of a book to reviewing the literature and discussing SSRI-induced violence and suicide.

(3) The Expurgation of Akathisia. It is extremely important for physicians to know that a drug can cause akathisia. Akathisia, as a term, signals the dangers of emotional anguish and the potential for inducing suicide and violence. It is not only fraudulent but also hazardous to patients to hide that a drug can cause akathisia. It is especially dangerous when the drug is being used to treat depression, because akathisia in depressed patients is especially likely to drive them to suicidal or violent acts.

Akathisia was systematically eliminated by SKB (now GSK) as a preferred term from the U.S. and non-U.S. studies. This meant that symptoms typical of akathisia would not be coded as akathisia, but as something else, such as agitation or central nervous system stimulation. (Preferred terms are the words used to describe specific adverse effects, such as akathisia, agitation, or mania. They are selected from a codebook provided by the FDA. If akathisia is not listed by the company as a preferred term in its plan or protocol for a study, then investigators will code or list akathisia as something else, such as agitation. Almost any term is less threatening than akathisia.)

Remarkably, akathisia does not even appear as an investigator’s term on any U.S. reports that I located. It appears only as an investigator’s term in about one dozen non- U.S. reports, whereas symptoms attributable to akathisia abound in the summaries of the U.S. reports of adverse drug reactions. From this it must be concluded that SKB not only removed akathisia from any lists of preferred terms, it also must have communicated to the principal investigators that the term should not be used in any of the adverse drug reports or clinical summaries. Clearly SKB preferred not to let the FDA or the medical profession know that Paxil causes akathisia. Indeed, they left it out of the section entitled ‘‘Adverse Experiences in Clinical Trials: Worldwide Data’’ (Section V—NDA. PAR Safety Summary 20-Nov- 1989, pp. 83–88; also see Table V.7, p. 114).

Similarly, akathisia was left out of the section entitled ‘‘Adverse Experience which occurred during active treatment—U.S. Phase II & III Studies,’’ ‘‘Nervous System’’ Special Report Part II 95 (Appendix V.8, in NDA 20031-Vol 422 November 1989, pp. 189/190–275/276). There is no listing at all for akathisia but many reports of related restlessness and nervousness. (4) Akathisia Slips Through in Non-U.S. Reports. Nonetheless, some akathisia reports slipped through in non-U.S. reports. In the section entitled ‘‘Adverse Experiences which occurred during active treatment-Non-US Phase II-III Studies,’’ V.1, pp. 129–199, we located 13 explicit reports of akathisia and motor akathisia (a synonym). In addition, there were many descriptions of akathisia listed under other preferred terms.

(5) The FDA Adds Akathisia to the Paxil Label. Eventually the FDA insisted that SKB add akathisia as a postmarketing finding without insisting on causation. The demand came in a letter in September 1993 from the FDA’s Paul Leber to SKB (SB 0000247). Had the FDA been informed during premarketing of the large number of cases of akathisia in association with Paxil, it would have been in a position to more firmly determine causation.

In response, a label version created by SKB and dated 2.05.94 does add akathisia and EPS as postmarketing findings.3 They should have been put in the label as a premarketing finding involving multiple cases (p. 000022). One of the two reports cited by the FDA was received from Ireland. However, the company already had many reports of akathisia in its possession from Europe, but must have failed to inform the FDA.

To repeat, the FDA required a mention of akathisia in the label based on merely two postmarketing reports, although SKB already had about one dozen explicitly identified akathisia reports in its possession from the non-U.S. premarketing studies and, as we shall document, dozens of other akathisia cases coded under different preferred terms, such as agitation and central nervous system stimulation, in the U.S. premarketing studies.

(6) How the FDA Codes Akathisia. The FDA has developed a coding system for adverse reaction terms. The dictionary is entitled ‘‘COSTART: Coding Symbols for The-
saurus of Adverse Reaction Terms.’’ I have the Fifth Edition (1995) in my library, but it has not changed in regard to akathisia. Like any other pharmaceutical company, SKB was supposed to base its collection and analysis of adverse reaction data on the COSTART system. This is discussed, for example, in an SKB Memorandum, ‘‘FDA Conversation

Record’’ (9.5.91), which memorializes a conversation with the FDA’s Thomas Laughren concerning, among other things, the use of COSTART terms (SB 0000158). In fact, the memo comments that Laughren (the ‘‘Division,’’ meaning the FDA’s Division of Neu- ropharmacological Drug Products) would make decisions about what terms to cut from the label.

From the beginning, COSTART has coded akathisia as akathisia. That is, the preferred term for akathisia is akathisia. This was true during the development of the first SSRI, Prozac.

Therefore, SKB deviated from the FDA’s coding system in order to classify cases of akathisia as something else, such as agitation. In reclassifying akathisia, as well as stopping the use of the term in general, SKB made it impossible for the FDA or anyone else to

accurately determine the total number of patients who suffered from akathisia as a result of taking Paxil. This was extremely fraudulent.

(7) Purposefulness of the Fraud Concerning Akathisia. The fraud had to be carried out with full knowledge, because it was well known that the original SSRI, Prozac, caused akathisia. The original Prozac label listed akathisia but estimated its occurrence as ‘‘infre- quent.’’ It quickly became apparent, however, that Prozac-induced akathisia was common 96 Special Report Part II and dangerous. In 1989, Joseph Lipinksi and his colleagues from McLean Hospital and

Harvard Medical School published five cases of Prozac-induced akathisia involving con- siderable emotional disturbance. Based on a literature review, the researchers estimated the rate of Prozac-induced akathisia at between 9.7% and 25%. In June 1990, the Public Citizen Health Research Group (related to Ralph Nader’s organization) in their Health

Letter similarly estimated the rate of Prozac-induced akathisia as 15%–25%. Furthermore, as reports by Teicher et al. (1990) and Rothschild and Locke (1991) illustrate, SSRI- induced akathisia as a potential cause of suicide and violence was a subject of discussion in the literature even before the approval of Paxil.

In the next section, we shall find a direct link between suicide and stimulation, in-
cluding akathisia, in SKB’s own NDA files.4

IV. Reanalysis of Preferred Terms in U.S. Trials

In addition to akathisia, Paxil commonly causes a variety of related symptoms of central nervous system stimulation (CNS), including CNS stimulation itself, anxiety, agitation, nervousness, irritability, and insomnia. These symptoms of stimulation are extremely im- portant because they, too, are associated with suicide and violence (Breggin & Breggin,

1994; Breggin 1997 [and more recently, Breggin 2003]). It is common knowledge in the medical profession that stimulation can induce depressed patients to make acts of suicide.Therefore, it is extremely important for physicians to know that an antidepressant drug causes stimulation, and it is fraudulent and dangerous to hide that information from them.

Unfortunately, SKB not only tried to hide the facts about Paxil-induced stimulation and akathisia, the company made false claims concerning Paxil in this regard. I have already documented that the FDA protested at times against these false claims. As another example, SKB developed a lengthy document entitled ‘‘Paxil (paroxetine hydrochloride):

Hospital Formulary Product Information’’ (SB 0000261, dated December 11, 1992). In it, SKB claimed that Paxil was effective in ‘‘depressed patients with associated symptoms of anxiety’’ (SB 0000271) and that the drug possessed an adverse reaction profile with ‘‘a low incidence of nervousness, agitation, and anxiety.’’ These statements are false. In fact, as the FDA stated (see previous) and as we shall continue to document, Paxil causes nervousness, agitation, irritability, anxiety, and related symptoms of stimulation in a large percentage of depressed patients, often in the first 3 days.

We shall also find that cases of akathisia were hidden in company-defined preferredterms (i.e., terms preferred by the drug company such as agitation, anxiety, stimulation, nervousness, and tremor).

The following is a reanalysis of several categories of CNS-related adverse effects that the company organized according to its selected preferred terms:

(1) Preferred Term Agitation. Agitation had 75 entries (pp. 191–193). A total of

49 of 75 agitation patients were in fact suffering from akathisia. Of these, 47 were described

by the term ‘‘restless’’ and 10 mentioned leg or foot (one case) movement. As the defi nition of akathisia indicated (see previous), these cases are most likely akathisia. Consistent with the Lacuzong case, 21 occurred in the first 1 to 3 days. Another 11 occurred in 4 to 5 days. Again consistent with the Lacuzong case, seven cases developed on low doses of 10 mg.

(2) Preferred Term Anxiety. Of the 86 reports in the category for ‘‘anxiety,’’ 24 were described as ‘‘tense’’ and 1 as ‘‘restlessness.’’ Although it is not as definitive as in the case Special Report Part II 97 of the preferred term ‘‘agitation,’’ many of these cases were probably akathisia. Of great importance, 26 occurred in the first 1 to 3 days. Another 9 occurred in 4 to 5 days; 8 occurred at the 10 mg dose.

(3) Preferred Term Nervousness. Under the category ‘‘nervousness’’ (pp. 235–238), 44 of 91 were probably related to akathisia. They were identified by the following terms: pacing, jumpy, jittery, and fidgety. Jittery was the most common. In all, 23 of 91 reports occurred in the first 1 to 3 days. Another 15 occurred in 4 to 5 days.

(4) Preferred Term Tremor. Under the ‘‘Preferred Term Tremor,’’ there were a very

large number of reports (pp. 268–273) that I have not fully evaluated. Many were related to akathisia.

V. Analysis of Akathisia in the Non-U.S. Phase II and III Clinical Trials

(1) Reports of Akathisia by Investigator Term. Unlike in the United States, a few

cases of akathisia were reported using the investigator’s term akathisia in the non-U.S.

Phase II–III studies (for Aropax, another brand name for paroxetine, November 1989,

Appendix V.1). They were coded under the preferred term CNS stimulation rather than

under akathisia:

Patient # Onset—days

1. 2218 072 (p. 137) NA

2. NA (p. 138) 1

3. 664 015 (pl 138) 1

4. NA (p. 138) 9

5. 664 012 (p. 139) 2

6. NA (p. 139) -6

7. 6 162 005 (p. 139) 4—Suicide attempt

8. NA (p. 139) 5

NA indicates Not Available.

(2) Akathisia Linked to Suicide Attempt. Of the eight patients diagnosed with aka-
thisia, only four were identified by patient number [and therefore could be traced back to their detailed clinical reports]. Of the four identified patients diagnosed with akathisia, one (25%) attempted suicide. Furthermore, the patient attempted suicide on the same day as the akathisia report (see NDA Suicide Report, Appendix 2, page 17).

It is very important to have the company identify the other four patients.

(3) Rapidity of Akathisia Onset. Of special importance to the Lacuzong case, aka-
thisia often begins within the first few days of treatment. Of the four identified patients, one did not have onset data. Of the seven patients with onset data, all were diagnosed in 9 or fewer days of treatment. Six were diagnosed within 1 week of treatment. Three were diagnosed within 1 to 2 days of treatment.

(4) Reports of ‘‘Motor Akathisia’’ by Investigator Term. Motor akathisia is identical to akathisia. The term simply emphasizes the external manifestation of the symptoms.

There were five cases:

Patient # Date of Onset

1. 7119 028 (p. 157) 16

2. 7119 058 (p. 157) 120

98 Special Report Part II

3. 7121 003 (p. 158 21

4. 7124 012 (p. 158) 6—Suicide (completed)

5. 7126 008 (p. 158) 28

(5) Motor-Akathisia Linked to Suicide. Of the five patients diagnosed with ‘‘motor

akathisia,’’ 1 (20%) committed suicide. Thus, of the 13 identified patients diagnosed with ‘‘akathisia’’ or ‘‘motor akathisia,’’ 2 (15%) attempted or completed suicide.

(6) Completed Suicides Linked to CNS Adverse Effects, Including Akathisia. We

have been able to trace five completed suicide cases to their original case summaries. Of the five patients who successfully committed suicide on Paxil, all were diagnosed with

CNS-related AERs (Adverse Event Reports) before suicide. Of those five cases, at least

two presuicide diagnoses (40%), agitation and motor akathisia, were related to stimulation

and/or akathisia. All of them had CNS adverse drug reactions.

The following are the five completed suicide cases followed by the investigator terms

for their adverse drug reactions.

1. 1.13.126 ‘‘severe insomnia’’

2. 2206.005 light-headedness, drowsiness, malaise

3. 2406.149 ‘‘restlessness (agitation)’’

4. 6.47. 003 vertigo

5. 7124–012 motor akathisia. ‘‘mild hyperkinesia’’

VI. Rapid Onset of Adverse Drug Reactions (ADRs) Documented From the

Spontaneous Reporting System

Postmarketing data from the Spontaneous Reporting System dated July 1993 confirms

that severe ADRs can develop in the first day or two of treatment, including reactions

that adversely affect behavior (NDA20031; SB 0000912). Here is a small sample excerpted

or extracted from the Adverse Experience Reports.

Day 1: Afraid, agitated, insomnia, tension. (p. 000152)

Day 1: EPS reaction. (p. 000156)

Day 1: Tremors, restlessness, tearful. (p. 000187)

Day 1 or 2: Disorientation, insomnia. (p. 000081)

Day 1: Severe akathisia. (p. 000340)

Day 1: Extremely restless, felt like screaming, dysphoric. (p. 000543)

Day 1: Hallucinations. (p. 000579)

Day 1: Hallucinations of insects and objects moving, dizzy. (p. 000507)

Day 1: Drugged, out of body, shaky. (p. 000487)

Day 1: Amnesia. (p. 000467)

Day 1: Distressed, hot flashes, sort of breath. (p. 000416)

Day 1: Distressed, hot flashes. (p. 000417)

Day 2: Dystonia. (p. 000138)

Day 2: Hallucination. (p. 000471)

Day 2: Bugs crawling, feeling high. (p. 000472)

Day 2: Drastic blood-sugar drop. (p. 000482)

Day 2: Numbness all over. (p. 000513)

Day 3: Severe muscle spasms. (p. 140)

Special Report Part II 99

Day 3: Dystonia, anxiety. (p. 172)

Day 3: Suicide attempt. (p. 000106)

Day 4: Insomnia, could not walk or talk on 10 mg. (p. 000372)

Day 5: Extreme agitation, jumped out window, disappeared 2 days. (p. 000554)

Day 5: Extremely jittery, very dizzy. (p. 115)

VII. The Role of ‘‘Central Nervous System Stimulation,’’ ‘‘Irritability,’’ and

‘‘Excitement’’ in Suicide and Violence

(1) Stimulation and Irritability in U.S. Trials. ‘‘Irritability’’ is used in psychiatry to

describe the emotional hyper-reactivity of individuals that can lead to inappropriate or

immoderate hostility and violence. It is closely related to excitability. (See, for example,

Stedman’s Medical Dictionary, 2000, or the PDR Medical Dictionary, 1995.)

Irritability is a much stronger term in psychiatry than in common use. In the Diagnostic

and Statistical Manual of Mental Disorders, IV (1994), a diagnosis of Substance-Induced

Mood Disorder can be made on the basis of any of ‘‘irritable mood’’ by itself (p. 374).

Appendix V.8, ‘‘Adverse Experiences Which Occurred During Active Treatment: U.S.

Phase II-III Trials’’ (SB 0000669, p. 198, stamped 199), lists CNS Stimulation as a preferred

term. In the category of CNS Stimulation, investigator terms were usually related to abnormal behavioral reactions, such as ‘‘irritable,’’ ‘‘irritability,’’ and ‘‘increased irritability.’’

There were 19 reports relating to irritability. There were 7 reports related to ‘‘excite-
ment’’ and ‘‘intense rushes of excitement.’’ Other reports were related to feeling ‘‘wired’’ and ‘‘wound up.’’

Of these approximately 41 patients with 50 reports of Central Nervous System stimu-
lation, many occurred early in treatment. Eight occurred within 1 to 2 days of the start

of treatment. Five adverse events occurred at the 10 mg dose, none of which were in the

1- to 2-day period.

(2) Anxiety and Suicide From Non-U.S. Phase II and III Studies. A hand count of ‘‘agitation’’ as the preferred term (NDA 420 November 1989, p. 128 ff) disclosed 43 reports, including one completed suicide (2406 149) on the 32nd day of Paxil ex-
posure. A hand count of ‘‘anxiety’’ as the preferred term disclosed 63 reports, with three attempted suicides on the same day, 3 days after the report and 19 days after the report.

Once again there is evidence that suicide is related to stimulation (akathisia, agitation, anxiety) from Paxil.

NOTES

1. Formerly known as SmithKline Beecham (SKB).

2. Bold in original. All quotes from p. 745. The same points are made in identical language in

the more recent edition (American Psychiatric Association, 2000, p. 801).

3. EPS (extrapyramidal symptoms) include a broad array of drug-induced neurological reactions, including akathisia.

4. The NDA (new drug application) contains all documents pertaining to the drug approval process, including all clinical trial data, evaluations of safety and efficacy, proposed advertising and marketing materials, the proposed label for the drug, and communications with the FDA.

100 Special Report Part II

REFERENCES

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders, fourth

edition (DSM-IV). Washington, DC: American Psychiatric Association.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders, fourth

edition, text revision (DSM-IV-TR). Washington, DC: American Psychiatric Association.

Breggin, P. (1983). Psychiatric drugs: Hazards to the brain. New York: Springer Publishing Company.

Breggin, P. (1997). Brain-disabling treatments in psychiatry: Drugs, electroshock and the FDA. New

York: Springer Publishing Company.

Breggin. (2001). The antidepressant fact book. Cambridge, MA: Perseus Books.

Breggin, P. (2003). Suicidality, violence, and mania caused by selective serotonin reuptake inhib-
itors: A review and analysis. Ethical Human Sciences and Services, 5, 225–246.

Breggin, P. (2005). Recent U.S., Canadian and British regulatory agency actions concerning anti-
depressant-induced harm to self and others: A review and analysis. Ethical Human Psychology

and Psychiatry, 7, 7–22.

Breggin, P. (2006). Court filing makes public my previously suppressed analysis of Paxil’s effects.

Ethical Human Psychology and Psychiatry, 8, 77–84.

Breggin, P., & Breggin, G. (1994). Talking back to Prozac. New York: St. Martin’s Press.

Food and Drug Administration. (2005a, January 26). Suicide labeling for antidepressants. Retrieved

May 25, 2006, from http://www.fda.gov

Food and Drug Administration. (2005b, June 30). FDA Public Health Advisory: Suicidality in adults

being treated with antidepressant medication. Retrieved May 25, 2006, from http://www.fda.org

Glenmullen, J. (2000). Prozac backlash. New York: Simon & Schuster.

Kraus, J. E. (2006, May). Dear healthcare professional: Important prescribing information [for Paxil].

Philadelphia: GlaxoSmithKline. Retrieved from http://www.fda.gov

Lipinksi, J., Jr., Mallaya, G., Zimmerman, P., & Pope, H., Jr. (1989, September). Fluoxetine-induced

akathisia: Clinical and theoretical implications. Journal of Clinical Psychiatry, 50, 339–352.

Rothschild, A., & Locke, C. (1991, December). Reexposure to fluoxetine after serious suicide at-
tempts by three patients: The role of akathisia. Journal of Clinical Psychiatry, 52, 491–493.

Teicher, M., Glod, C., & Cole, J. (1990). Emergence of intense suicidal preoccupation during

fluoxetine treatment. American Journal of Psychiatry, 147, 207–210.

van Putten, T. (1975). The many faces of akathisia. Comprehensive Psychiatry, 16, 43–47.

van Putten, T., & Marder, S. (1987). Behavioral toxicity of antipsychotic drugs. Journal of Clinical

Psychiatry, 48(Suppl.), 13–19.

Paxil/Seroxat/Aropax (Paroxetine) : “Question Of Drug’s Label Goes To Trial…”


http://www.chicagolawbulletin.com/paxil-2-16-16.aspx

Question on drug’s label goes to trial

paxil-2-16-16,ph02

James B. Zagel
Law Bulletin staff writer

A federal judge has again declined to throw out a lawsuit accusing the maker of the anti-depressant Paxil of liability in the suicide of a Chicago lawyer who took a generic version of the drug.

In a written opinion last week, U.S. District Judge James B. Zagel rejected the argument that the negligence claims brought under Illinois law by Stewart Dolin’s wife are pre-empted by federal law.

Wendy Dolin filed the suit in Cook County Circuit Court, and GlaxoSmithKline (GSK) removed it to federal court under diversity jurisdiction.

The suit maintains the labels on Paxil and its generic version are false and misleading because they failed to warn of an increased risk of suicide in adults over the age of 24.

In a motion for summary judgment, GSK argued such a warning is pre-empted by the Federal Food, Drug and Cosmetic Act.

Zagel didn’t see it that way.

A failure-to-warn claim is preempted by federal law, he wrote, citing Wyeth v. Levine, 555 U.S. 555 (2009), only if there is “clear evidence” the U.S. Food and Drug Administration would not have approved the warning the plaintiff alleges is required by state law.

GSK presented no such evidence, Zagel wrote.

In 2007, he wrote, the FDA invited GSK to discuss the option of keeping language on Paxil’s label warning of the possibility of an increased risk of suicide or suicidal thoughts in adults.

GSK didn’t take the FDA up on that invitation, Zagel wrote.

GSK, he wrote, did not ask for a formal meeting with the FDA and did not ask to include additional language on the label concerning Paxil’s possible effect on adults.

Under those circumstances, GSK failed to meet the “demanding burden” of showing it would have been futile to seek permission from the FDA to add an adult suicide warning on Paxil’s label, Zagel held.

Wendy Dolin is represented by attorneys who include R. Brent Wisner of Baum, Hedlund, Aristei & Goldman P.C. in Los Angeles.

The lead attorney for GSK is Alan S. Gilbert of Dentons U.S. LLP.

Neither attorney could be reached for comment.

In 2010, Stewart Dolin killed himself by leaping in front of a Chicago Transit Authority train at the Blue Line station at Washington and Dearborn streets in the Loop.

Dolin, 57, was a partner in Reed, Smith LLP.

He had started taking a generic version of Paxil, the brand-name version of paroxetine hydrochloride, six days before he committed suicide.

In addition to alleging the warning on the paroxentine label was inadequate, Wendy Dolin contends GSK concealed and manipulated data concerning the drug.

GSK wanted to obscure the fact that paroxetine carries a 6.7 times higher risk of suicide in adults who take the drug compared to those who take a placebo, Dolin contends.

In 2014, Zagel dismissed all claims against Mylan Inc., which made the paroxetine taken by Dolin.

But he held GSK must face claims under Illinois law of common-law negligence, negligent misrepresentation and product liability based on a negligence theory.

In the 2014 opinion, Zagel conceded GSK did not manufacture the paroxetine taken by Dolin.

But the federal Hatch-Waxman Act requires that a generic drug’s design and warning label must match those of the name-brand drug, Zagel wrote.

Therefore, he held, the brand-name maker must in some circumstances face claims based on the warnings on the generic version’s label.

In last week’s opinion, Zagel declined to reverse his 2014 ruling.

Noting that GSK and Wendy Dolin plan to call expert witnesses to the stand during the trial, Zagel also declined to hold that the Paxil’s label is adequate as a matter of law.

And Zagel rejected arguments that the doctor who prescribed Paxil for Stewart Dolin knew of the drug’s risk and, therefore, GSK could not be liable in Dolin’s suicide.

The doctor’s testimony suggests he didn’t know of the increased risk of suicide in adults over 24, Zagel wrote, and he relied on the 2010 Paxil label before prescribing the drug.

The suit is to go to trial on Sept. 19.

Zagel issued the opinion Thursday in Wendy B. Dolin v. SmithKline Beecham Corp., No. 12 C 6403.

Seroxat: GSK’s ‘Thalidomide Moment’?….


I have long been calling the Seroxat scandal ‘the mental health thalidomide’… I even sub-headed this blog with ‘Seroxat the mental health thalidomide’, when I set it up 9 years ago…

In the following article, by academic Redmond O’ Hanlon, Redmond discusses the implications of GSK’s notorious Seroxat Study 329..

Redmond calls this ‘Psychiatry’s Thalidomide Moment’

I think it was GSK’s thalidomide moment..

Psychiatry has had its thalidomide moment regularly since its inception..

The scale of harm which psychiatry has caused for over a century now is colossal..

Seroxat caused death and destruction on a much larger scale than Thalidomide, and GSK’s 3 Billion dollar Fine (see whistleblower Greg Thorpe’s complaint to the Dept of Justice here) lists endless pages of harm to consumers from several drugs over decades..

GSK have their thalidomide moment regularly too, at least once a year it seems.. Myodil, Seroxat, Avandia, Pandemrix, Wellbutrin…

..they really do live up to their nick-name of ‘Global Serial Killers’..

 

 


http://www.madinamerica.com/2015/11/study-329-psychiatrys-thalidomide-moment-part-2/

Study 329: Psychiatry’s Thalidomide Moment, Part 2

Nobody has retracted or apologized for a study that was an academic disgrace—but a marketing coup for GSK—which may well have caused untold numbers of deaths, suicide attempts and irreversible anguish to myriad families. Can we stand idly by when we’re told that it “accurately reflects the honestly-held views of the clinical investigator authors who do not agree that the article is false, fraudulent or misleading.”? What is the current market value of the honestly-held views of people who tell lies?

I’d like to reflect on a few major aspects of Study 329 and the recent BMJ restoration study (RS) which raise fundamental ethical issues, and which pose some theoretical problems or raise other important issues which haven’t yet been scrutinized. And, by counterpointing Paxil against Thalidomide, I shall suggest that a seismic cultural shift has made studies like Keller’s almost inevitable.

1. Ethics and Academic Integrity

Study 329 forces us to confront the ethical question once again, before it’s too late, and question the claim that the investigators were chosen only for their expertise, their interest in the subject and their capacity to recruit volunteers.  Might they not have been in the pay of GSK, or have been friends, ex-students or colleagues of people like Biederman, Keller, Krystal or Nemeroff? Or chosen for their commitment to drug solutions, regardless of awkward research findings, in line with the FDA which wrote at the time that there may be negative findings even in trials of drugs they know really work? Even at the initial stages, then, there was plenty of room for manoeuvre, allowing GSK and its (paid?) investigators to take advantage of a fuzzy diagnostic category, to cherry-pick the subjects most likely to produce favourable outcomes and to discount the gravity or relative severity of an adverse event if it suited their purposes.

The sociopathic lack of remorse and moral consciousness shown by GSK, Keller, et al., became most shockingly apparent early on, in GSK’s serial re-writing and occlusion of troubling data — designed to stop negative results leaking out to doctors, the public or their sales staff. In fact, a GSK internal memo showed that the company knew that their studies had failed to demonstrate efficacy since at least 1998; and in 2003 the MHRA revealed that GSK’s own studies showed that the drug actually trebles the risk of suicidal thoughts and behaviour in depressed children. Outside the Holocaust, I’ve never come across a more chilling, amoral or sociopathic memo than the one they sent out to senior management, clarifying their decision “to effectively manage the dissemination of these data in order to minimize any potential negative commercial impact…It would be commercially unacceptable to include a statement that efficacy had not been demonstrated, as this would undermine the profile of paroxetine.”  In the same cynical vein, an email from a PR executive working for GSK said: “Originally we had planned to do extensive media relations surrounding this study until we actually viewed the results. Essentially the study did not really show it was effective in treating adolescent depression, which is not something we want to publicize.”

An important ethical barometer is the prevalence of authors’ conflicts of interest (COIs), though it is really a wider, cultural, problem, for a large majority of medical and science journals in the world have no COI policy. While we weren’t told about the authors’ COIs here, we now know those of Keller, Ryan, and of GSK employee Mc. Cafferty, whose affiliation was hidden. We know, for example, that Shelley Jofre sent emails to Dr. Ryan in 2002 asking questions about the safety of Paxil, whereupon this “independent” researcher forwarded them to GSK, asking for advice on how to respond to her! We know also, thanks to Peter Doshi, the extent to which Karen Wagner was beholden to BP. I have since followed up her case: it beggars belief.  Hunting down the COI hare of the other “authors” could bring to light some very damning evidence indeed.

The prevalence of ghostwriting is another disturbing example of ethical indifference: David Healy, who has monitored this phenomenon rigorously for years, estimates that up to 50% of apparently serious academic psychiatric studies are ghostwritten. Could this be a devious way of getting around the ban on off-label promotion?

The rampant, unethical ubiquity of ghost writing has sullied the reputation of numerous academics and their institutions in the U.S. Hannah Arendt’s reflection is apposite here: “When all are guilty, no one is; confessions of collective guilt are the best possible safeguard against the discovery of culprits, and the very magnitude of the crime the best excuse for doing nothing.” Here, however, we have no confession of collective guilt; not surprising, since guilt implies a minimal moral conscience, which was so rare here and among Chemie-Grünenthal’s (C-G) top brass in the thalidomide tragedy, some of whom had seen active service in the camps, and most of whom had impeccable Nazi credentials. This brings to mind those studies some years ago showing that a large proportion of industry CEOs could be classified as sociopaths: another indicator of a huge cultural shift. Are we now simply facing the inevitable consequences of rampant neo-liberal economics?

We could of course argue that this entire affair could be reduced to just one issue: is there any justification for ghost-written academic studies, especially when they have serious safety implications? If it is deemed to be professionally acceptable, then the “authors” of Study 329 have committed no sin at all: it’s just par for the course. After all, PLoS Medicine, which has been leading the charge against ghostwriting, found that only 13 of the top 50 medical schools in the U.S. have a policy that prohibits it.

At a 2011 U. Toronto conference on ghostwriting, Trudo Lemmens, a law professor, said that biomedical ghostwriting is a public health issue needing serious attention, since erroneous use of pharmaceuticals is a leading cause of hospitalization. Many studies, like Keller’s, contribute to that by hiding adverse events, negative data, and over-emphasizing benefits, so academics fronting such studies are responsible for any ensuing prescriptions and harms. Yet there seems to be no backing in law for those wanting to hold academics legally and professionally accountable: ghostwriting is perfectly legal, widely practiced yet officially considered unethical, so universities are nicely protected when they routinely protect shady researchers, who bring them prestige and large research grants. McGill, though, showed commendable rigour and oversight in the Sherwin/Wyeth case.

Doshi and Healy have no doubt that Study 329 was ghostwritten, but I’m not yet absolutely sure about this, though the circumstantial evidence is overwhelming. Keller’s recent letter defending his study and criticizing the RS does indicate that the “authors” were centrally involved at all stages of the study. Could they be forced to take an oath on this, as was Sally Laden? I’m still very unclear about which authors knew what, if anything: the much- compromised JAMA tried, unsuccessfully, to find this out when first offered the article. Keller’s slippery filmed statements and his facial language made me very suspicious indeed, as he repeatedly dodged interviewers with statements like: “I don’t remember matters like this…I never read such tables.”

However, let’s now suppose it wasn’t ghost written, then Keller has painted himself into an inescapable corner, since the only excuse he could proffer for producing scholarly work that drew conclusions contradicting the raw data was that it was, in fact, ghost written. Either that or they produced scholarship that would not have been accepted from an undergraduate, but was accepted by the editor of a prestigious journal who brushed aside THE JOURNAL’S OWN REVIEWERS’ DEEP RESERVATIONS about the study.  Why?

2. Pseudo-science, Lies, Damn Lies, and Statistics

Another ethical casualty of Study 329 was peer review, a protocol designed to guarantee the integrity, independence and rigour of published scholarship: JAMA followed the protocol strictly, and rejected the study, but JAACAP did not. How did it get away with so few official criticisms or sanctions? The story behind the editor’s ultimate acceptance of it could prove very incriminating, and throw up even more serious questions about academe’s failure to uphold minimal standards by publishing a labyrinth of lies, half-truths and lies by omission. The intellectual dishonesty displayed here by members of a prestigious Ivy League university is a bloody blot on the escutcheon of American academic integrity. Standards like this in very high places should not be tolerated by any academic community worth its salt.

The RS also highlighted an area which is rarely discussed: statistical analysis. We have become hung up on whether the results of a trial had statistical or clinical significance, but this study reminds us of the value of patient narratives, “merely anecdotal” reports and descriptive statistics, as did the thalidomide tragedy. Here, the commitment to descriptive statistics was abandoned, probably because they might have allowed non-specialists to make judgments and informed decisions, whereas more sophisticated techniques offered a smokescreen to hide behind for years, thus allowing billions to accrue. How many of us are sufficiently qualified to evaluate what the statisticians tell us, and how they tell it?  Unsurprisingly, GSK told us that they employed the best ones here: this may well have been the only true statement they uttered. It was in their interest to hire the top people, pay them a fortune and make it clear that, without making fools of themselves professionally, they should choose designs, protocols and methods of analysis likely to give the required positive results.

Jureidini’s team forces us to radically critique another untouchable: RCTs, whose status, integrity and even utility must now be thrown into question. Following Breggin, Cohen, Doshi, Harrow, Healy, Kirsch, Moncrieff, Timimi, Whitaker et al., we RCT sceptics now have much more precise ammunition to fight with. In their wake, can we continue to have faith in any previous RCTs and meta-analyses when so many negative trial results are never published and when fundamentals like blinding and adherence to protocols are so flagrantly flouted? Is this just the tip of a very large, murky and treacherous iceberg? After all, Study 329 was published in a top journal, yet deviated from the original protocols, added several new outcome measures, sometimes after un-blinding, and drew conclusions directly at odds with their own findings. In particular, I am deeply suspicious about its level of sustained adherence to blinding protocols.

Over the years, we have had many scandalous instances of unethical manipulation which allowed BP an easy ride. Keller et al. gave us an egregious example of this when they disbanded reliance on Hamilton, but never registered the change, blithely declaring that since the profession had moved beyond Ham-D between 1993 and 1998, they needed to look at other more appropriate measures! As we say in Dublin: ”Pull the other one, it has bells on it!” I know of no evidence that he was right, and their unseemly scratching around for scales, criteria and about 20 new secondary outcomes that might show Paxil in a more favourable light was sad, desperate, even comical.

In short, we’ve had many reasons to be extremely sceptical of RCTs and critical of the uses to which they have been put: Study 329, for example, was merely a super-lucrative advertisement for a dangerous, addictive drug with doubtful benefits and numerous toxic side-effects. (In 2002 over two million paediatric Paxil prescriptions were written in the USA alone, just in time to beat the patent deadline.) Now whereas the law, the FDA and blind faith in RCTs bought an awful lot of time for GSK to make many billions unimpeded in subsequent years, a modest number of academic articles and individual “anecdotal” reports from doctors between 1958 and 1961 stopped thalidomide in its tracks by 1962. They didn’t hang about too long in those days: one critic was scandalized that C-G knew for six whole weeks of the dangers posed by thalidomide!

The RS, then, may well deal a mortal blow to our naïve faith in academic integrity, our bedazzlement by RCTs, and to our easy acceptance of them as gold-standard benchmarks of truth and rigour. It should, at the very least, put them in their place as one potential, yet fallible, tool in the arsenal of psychiatry, but one that should never be allowed to usurp the centrality of the empathic, dialogic relationship between a singular patient and healer, nor the full story of individual suffering, which is obfuscated by algorithms and statistical averages.

On the other hand, the RS might also, paradoxically, provoke a more positive, nuanced view of RCTs, suggesting that some modicum of scientific respectability could be maintained, but NOT IN THE PRESENT VENAL CULTURE: Jureidini et al. have shown us what they might yield if carried out rigorously by top independent researchers putting in Herculean work for no financial gain: had their study appeared in 2003 many wasted billions and many, many lives might have been saved. But how often are we going to get such a highly qualified, deeply committed, hard-working group together in the present climate, with its routine financial inducements? Should we not, perhaps, use the thalidomide case to reconsider the value of strong, repeated “anecdotal” pointers, thus emphasizing individual stories of psychotropic drug use and the withdrawal therefrom? David Healy, Luke Montagu and James Davies have given us a very strong lead in this domain.

Another problem hovering over, but not addressed, by both studies is that of causality: in psychiatric and neuroscientific discourse there’s a lot of slippery semantic skating going on – “linked to,” “associated with,” ”implicated in,” “correlated with,” and the like, but rarely “caused by.” This is not always helpful, but it does bespeak an understandable and judicious reluctance to assign one cause to any outcome.  The Study 329 authors cleverly exploited this difficulty when they tried to minimize serious adverse effects related to treatment by declaring that “causality cannot be determined conclusively.” A single cause for any illness can rarely be proven conclusively – even in cancer, as a number of commentators have pointed out. Thalidomide, however, does appear to have been the sole cause of all those awful deformities; but even in a case like PKU, which is habitually deemed to have a purely genetic aetiology, the gene will not express itself if rigorous environmental controls are put in place – in this case, diet.

Now while it seems clear that judges, biomedical academics and psychiatrists have grossly underestimated antidepressants’ (ADs) contribution to suicidal behaviour, it is also possible to overstate the case by insisting that a given SSRI caused violent, murderous or suicidal behaviour, thus negating the potential impact of other confounding variables. Yet some, but not many judges, taking the advice of people like Peter Breggin and David Healy, have declared that an AD like Prozac had indeed induced a murder.  But, pace both of these great fighters, I’d suggest that legal sanctions would be far easier to obtain if we focussed not on a conclusive single cause for a violent act, but on the very high risk factors associated with a given SSRI and on the full personal and contextual story.

3. The Matter of Suicide

In the opening of The Myth of Sisyphus, Camus argued that suicide is the only serious philosophical question, but for many, suicidal ideation (SI) is a dangerous by-product of SSRI consumption; a serious adverse effect. And further, SI means different things to different researchers.  For some, it is a particular preoccupation with suicide, ranging from regular random thoughts, to more sustained and frequent thoughts of suicide. For others, however, SI includes suicidal gestures or behaviours such as the planning or rehearsing of the act, incomplete attempts, or more serious attempts designed to fail. Even the MedDRA confuses the issue by coding suicidal ideation OR self-harm OR attempted suicide as suicide events. The RS rightly criticizes Keller for using the term “emotional lability” to fudge the severity and differences in suicidal behaviours, but have they not also engaged in some fudging by lumping suicidal thinking and events under one heading, “suicide-related adverse events”?

There is too much fuzzy thinking here: surely logic and scientific rigour oblige us to clarify our terms and avoid assigning the same weight to SI and clear suicide attempts, since most people who have suicidal ideation do not go on to end their lives, even though it must be considered a (low?) risk factor for suicide? To put this in context, it was estimated that in 2008-9 over 8.3 million adults aged 18+ in the U.S. reported suicidal thoughts in the previous year, but of these, only one adult in 140, 60,000 people, actually took their own lives. SI does not usually mean that someone wants to die, but that s/he does have a desperate need to express her/his hopelessness, impotence, overwhelming pain or collapse of meaning. It may often be a natural strategy employed in a hopeless situation: an imaginative rehearsal or symbolic expression of entrapment in the reptilian freeze response; of the impossibility of fight, flight or social engagement, to put it in terms of Polyvagal Theory.

I’m suggesting, then, that we must beware of falling into the trap of dramatizing or pathologizing something that may be absolutely normal, even healthy, in certain circumstances: for example, if one is homeless, disadvantaged or marginalized, living in unbearable social conditions, or trying to deal with overwhelming loss or failure the lack of SI would surely be a highly dissociative move.

Pain, danger and thoughts of suicide often attend the birth-pangs of any major life transition or change in status, as it did for Tolstoy and J.S. Mill. (See James Davies’ fascinating book, The Importance of Suffering.) Camus’s Meursault normalizes suicide  by reminding us that everyone at some time has wanted to kill the one s/he loves: for adolescents needing to separate and carve out their own identity such thoughts are routine, healthy, and not necessarily caused by SSRIs. And for them SI can be one way of managing the maelstrom of hormonal turmoil, passionate intensity, emotional lability and high-risk behaviour attending the scary transition from childhood to adulthood. It may simply well be a way of saying that s/he sees no meaning in life and cannot go on this way any more, especially at a time of collapse in traditional values.

We need to remember, too, that modern adolescence, bereft of mentors, is a particularly fraught, unstable time, in which risky behaviour is far more common than in childhood or adulthood; one in which accidents are the main cause of death, followed by suicide, regardless of any SSRI consumption. (See Sarah-Jayne Blakemore’s research on risk-taking behaviour in adolescents.) For example, in one recent case it became clear that a vicious racism had fueled multiple murders in a local school. In another, a recent school killer’s notebooks showed that he was in a state of absolute despair because doctors had told him he was condemned to live with “a broken brain” for life.

However, well-documented adolescent suicide attempts do have to be taken very seriously, even though they may well be just last-ditch screams for help or understanding: after all, David Healy and others point out that for every eleven suicide attempts there’s one actual suicide.

I believe, then, that it is important to de-emphasize and downgrade SI since the term is used too loosely and can a have a positive valency. Why not confine the term solely to thoughts, and prioritize clear suicidal behaviours? And, taking into account the wider cultural framework, would it not make more sense for judges and researchers to focus on the individual contexts and narratives subtending acts of serious self-harm, clear suicide attempts and very uncharacteristic acts of violence? Drug are usually part of a much bigger story, which we neglect at our peril.  Why not, then, let the law get on with assessing the strength of the circumstantial evidence and decide whether a given drug is a major contributor to a suicide beyond any reasonable doubt?

4. Neo-liberal Culture

Martin Keller recently made the point that since nobody has been able to pin anything on the authors, there’s obviously nothing to apologize for. The terrible thing is that he’s right: they have merely acted in a way that is condoned by academic journals, the FDA and the universities; sanctioned by the psychiatric establishment and the wider culture which makes it so easy for negative findings to run for cover, since there is no firm regulatory obligation to report all the results from clinical trials. In this case, Brown is in the dock, but numerous U.S. academic establishment have been regularly shamed, even though a few of them, like Harvard, have had the courage and integrity to come clean in similar cases, so why not Brown, whose officials conveniently lost some vital incriminating data? (Precisely the same thing happened with a vital incriminating registered letter at the C-G thalidomide trial.) Harvard did take some nebulous action against Biederman et al., but only when the scale of the deceit had become too blatant to hide. It is quite shameful that most U.S. universities routinely offer no comment when the media or people like Senator Grassley ask the tough questions about questionable research or COIs. Indeed, Grassley has said that they seem incapable of monitoring the COIs of faculty. Like the all-powerful gun lobby that even Obama can do little to tame, Marcia Angell’s 800-lb. gorilla has run amok, and thumbs its nose with impunity at the helpless Sorcerer’s Apprentice. And at all of us who protest so loudly and so often. But is this enough? Do the times not demand more concrete, radical action?

Is Study 329, then, not just one more shocking example of the mercantile values and the druggy doxa that permeate our entire culture? Obama’s choice when appointing the new FDA director is a stark incarnation of just how bad things are. So, before we all get too righteous and complacent we mustn’t forget that JAACAP, GSK, Keller et al. are simply following the ethos of our culture in which ethics and transparency have been all but abandoned, even at the top. Earlier this year, Scott, Rucklidge and Mulder studied the adherence, from 2009-13, by the editors of the five leading psychiatric journals to their own pious protocols of oversight and integrity, concluding that “most trials were either not prospectively registered, changed POMs or the timeframes at some point after registration or changed participant numbers.” When such oversight is so loose at the top, to whom do we turn for safe, rigorous research and unbiased guidelines? Quis custodiet ipsos custodes when they countenance criminal acts?

The Study 329 affair, then, underscores the fact that there is strong, but implicit, cultural permission given to BP and amoral academics for their chicanery since trial periods are so short, and post-marketing surveillance so weak and random. Our modern blind-eye culture has no problem with FDA laxity, blatant academic corruption and an increasingly perfunctory oversight by Congress and the law which permits direct-to-consumer marketing and off-label prescription, which in turn allows BP to profitably dispense with honesty, science or FDA approval.

Counterpointing the thalidomide with the Paxil affair, then, helps us to highlight a monumental shift in culture and values that lies very deep in the neo-liberal psyche, transcending Big Pharma, the universities et al. In the thalidomide case, the culture of the 60s enabled the remarkable integrity, rigour and persistence of the FDA’s Frances Kelsey who seems to have been fully backed by the FDA directorate, though one historian of the FDA wrote that she encountered some opposition there. And where she was supported by the wider culture, which subsequently lavished awards and encomia on her, our culture both encourages and rewards the likes of Keller et al. So in 40 years the 1962 amendment, designed to ensure the efficacy and safety of drugs, was emasculated, abused and disempowered by Big Pharma PR and cynical academics. Had thalidomide arrived in 1994 and been researched by such people, the laxity of the FDA, enabled by an ethics-free drug culture, would likely have ensured its continued presence on the market for years, producing millions of deformed babies facing early death or wrecked lives. Fortunately for mothers and new-borns back then academics had integrity: and the meteoric rise of BP power, allied to the prestige and often spurious truth-value of RCTs, was still some way off. Thus a small number of early academic studies, often in the BMJ, and many “merely anecdotal” reports, succeeded in ousting the drug before it got into its stride.

But, once again, what we’re really talking about here is a seismic cultural shift, over 40 years, which is underwritten by government and the law; one which finds no place for ethics, which favours permissive drug regulation, and a neo-liberal ethos in psychiatric practice, academia and the press.

Redmond O'Hanlon

Redmond O’Hanlon is an academic who has taught university courses in Ireland, the U.S. and Oxford, where he wrote his doctorate. He is at present tidying up the final draft of a book  which attempts to bring some insights from the worlds of psychology, philosophy and the arts into critical psychiatry, with special emphasis on the importance of narrative, and on the dangerous fantasy of psychiatric diagnoses. His particular interests are depression, ADHD, trauma, the so-called personality disorders – and the greatest scam of them all, “schizophrenia.”

GSK’s Patrick Vallance Casually Glosses Over The Deaths Of Kids From Seroxat (Paxil/Aropax)


Page_1

Patrick Vallance: “Alltrials is not pushing for that level of data availability and neither are we”

“If I’m a shareholder, which I am, I don’t want a company to be hiding something that might come to light”…

Yesterday I posted an interview with GSK’s CEO Andrew Witty. In that interview Witty was very clearly (and visibly) uncomfortable when questioned by BBC’s Newsnight’s Evan Davis about GSK’s bribery scandal in China and their corruption of doctors.

Andrew Witty’s awkward body language said it all.

See here for more


In an interview (see Audio above) with BBC 4’s ‘Life Scientific‘ radio series today with Jim Al-Khalili, GSK’s (head of R and D and admitted GSK share-holder) Patrick Vallance, is asked about Seroxat harming kids, and his response is really very unsettling. He casually glosses over the harm to (potentially) millions of kids from GSK’s dangerous Paroxetine (Paxil/Seroxat/Aropax) over the past 15 years in a very matter of fact way, as if he was discussing a certain flavor of tooth-paste or the symptoms of a very mild head ache.

Vallance says (when asked about Seroxat killing kids)  that:

“It’s inevitable that side effects things will occur from time to time”

“I’d rather know them than not know them”

(but isn’t this the whole point Pat- we weren’t warned of the side effects such as suicide, withdrawal and self harm so many millions of people didn’t know the side effects and were harmed by Seroxat- me included- purely on the basis that we didn’t know and were not told about them).

Wow, is that really your answer to the Seroxat scandal Pat? It’s inevitable that people get killed and maimed is it? It’s inevitable that GSK push drugs like Seroxat on under 18’s (when GSK knew from its own studies that Seroxat could harm them). That’s inevitable, all above board and expected is it? Is it all just inevitable really because that’s the nature of the drugs business? Or do scandals like Seroxat happen because of human greed, profit and sociopathic corporate behavior? I’d go with the latter…

It’s inevitable that it might rain tomorrow, it is not inevitable for a drug company to push its dangerous anti-depressant on young people when it knew it might make them kill themselves… How about making sure that your drugs are safe? Now there’s a novel idea Pat…

When asked about GSK’s endorsement of Alltrials GSK’s Pat Vallance admits that the Alltrials agenda is not about access to data at all ( data is the meat of the drugs industry, without access to it we just don’t know the dangers or efficacy of the drugs we take- see study329.org for more). Vallance also spins the well worn GSK yarn that they have been always publishing their trials on the clinical trials register but the truth (and what the GSK spin machine always omits) is that GSK were forced by two separate department of justice investigations into the company which have compelled them to publish trials- they did not do this willingly).

When asked by the interviewer, Jim Al-Khalili : “Is this about making clinical trial data available to all people”?

Pat Vallance responds that: “Alltrials is not pushing for that level of availability and neither are we”

Vallance’s answer is really very telling, and it reveals why GSK were so eager to jump on board the Alltrials/Ben Goldacre bandwagon. Access to data is what is needed here, not access to drug company’s published trials. Alltrials is a red herring, it gives GSK more control, and Ben Goldacre really has a lot to answer for in this regard. However since he seems to be enamored with Witty and Vallance, I won’t hold my breath for him to challenge them anytime soon. (I’ve written about these issues here, and Dr David Healy’s been banging the drum about Alltrials on his blog too- see here).

Furthermore, one of the only ways to get access to the data, is often only through litigation or department of justice investigations etc. People shouldn’t have to wait decades before they know the harms of a drug Mr Vallance. This is not acceptable nor inevitable. Seroxat has harmed immeasurably.  The long term damage hasn’t even begun to be assessed.

Just like Andrew Witty, your attitude towards those damaged by your drugs like seroxat seems to be… “well that’s just tough”..

And your company still makes a profit on Seroxat, it’s still being sold, which means that you and Witty are still profiting directly (and knowingly) from death, human damage, addiction and child suicide…

How nice for you both..

Ugh..

In The BMJ: Nurse Explains The Devastating Consequences Of Being Prescribed Seroxat (Paxil) At Age 20…


What’s the difference between an 18 year old and a 20 year old in terms of side effects of Seroxat? (Seroxat is banned for under-18’s but that didn’t stop GSK from pushing it, nor did it stop them from pushing it in adults).
I was 21 when I was prescribed Seroxat, and I was upped my dose to 40mg at one point..
This nurse was zombified on 5mg after a few weeks…
Try it for years.. how do you imagine that would turn out?
GSK have literally being poisoning people to death with Seroxat..
It’s a disgrace…

http://www.bmj.com/content/351/bmj.h4629/rr-1

Feature Research Conduct

No correction, no retraction, no apology, no comment: paroxetine trial reanalysis raises questions about institutional responsibility

BMJ 2015; 351 doi: http://dx.doi.org/10.1136/bmj.h4629 (Published 16 September 2015) Cite this as: BMJ 2015;351:h4629

Paroxetine trial reanalysis raises questions about institutional responsibility

I wanted to say thank you for publishing this article. I was once on Paxil myself, as a newly 20 year old, for panic disorder without agoraphobia. While taking just 1/4 of the normal starting dose (5mg was my dose), I displayed flat affect and a “zombie” like appearance. This was within several weeks, about two. I then became suicidal.

For something that is supposed to be an ANTI-depressant, I’m amazed at how PRO mental disorder it truly was.

I’m a very happy woman, and was always a happy teenager. This was not normal. The small, sane part of my brain told me I needed to tell someone I was feeling this way, but I didn’t want to – they would try to stop me if I did tell someone. I will never forget what that feeling was like, and I truly wonder if I am a PTSD patient now because of it.

In the end, I did try to hurt myself. I was very lucky to have my mother and a very close friend stop me and take me to the doctor. They pulled me off Paxil completely and switched me to another SSRI and a benzodiazepine to ease the withdrawal side effects from the Paxil. I’ve been on this SSRI ever since, and it has now been about 10 years.

Everytime I see an article like this, my heart breaks. I truly hope that this research saves other adolescents from experiencing what I went through. I wouldn’t wish it on my worst enemy.

Competing interests: No competing interests

From Bob Fiddaman: Seroxat Implicated In Fatal Sierre Bus Crash Tragedy


http://fiddaman.blogspot.ie/2015/10/did-seroxat-trigger-fatal-sierre-2012.html

Monday, October 05, 2015

Did Seroxat Trigger the Fatal Sierre 2012 Bus Crash?







Sierre, Switzerland, March 2012

There were 52 on board, 28 people perished, 22 of them were children. The other 24 pupils, all aged between 10 and 12, were injured, including three who were hospitalized with severe brain and chest injuries.

The exact cause of the crash has never been determined. The driver, Geert Michiels (34), also perished in the crash. An investigation showed that Michiels was not intoxicated.

A full investigation into the crash was carried out by Swiss Chief Prosecutor Olivier Elsig, the results of which were inconclusive. He ruled out the involvement of a third party, shortcomings in the road surface or the tunnel infrastructure. Excessive speed, alcohol or technical problems with the vehicle were also ruled out. He, at no point, could determine whether or not Geert Michiels carried out an act of homicide/suicide with the vehicle. In fact the final report leaves more questions than it does answers.

Michiels had driven the coach through a tunnel, he mounted the curb, made no attempt to apply the brakes, and crashed head-on into a short wall. Photographs of the scene were taken by one of the parents whose daughter was killed in the crash. Her photo’s, taken whilst visiting the tunnel sometime after the tragedy, show how Michiels mounted the pavement and made no attempt to steer the coach back into the road, opting instead to drive straight into a wall. (Photos here)

Just by looking at the photos of the scene one has to ask why Michiels did not steer the bus to the right upon mounting the curb. One also has to ask why he never took his foot off the accelerator and, more importantly, never applied the brakes. As humans we have a basic instinct of survival, it kicks in when our lives are put in danger. Imagine, if you will, a pool of water. You are swimming blissfully when an undercurrent starts to pull you down. Do you fight for survival or do you just relax and let the current pull you under?

Michiels mounted the curb (Fig 1) and continued to travel at a rate of 99/101km (about 62mph) – I refer to my pool analogy – what happened to Michiels survival instinct?

Fig 1
If fig 1 has you thinking why didn’t Michiels steer to the right then you’ll be surprised that the 3D image comes from the original investigation. It has fallen under heavy criticism from the parents of some of the victims.
This from Foundation Busramp Sierre, a group calling for independent research to be carried out into the crash.
“This is a 3D reconstruction that has been released by the Swiss authorities in connection with the study, on which the trajectory of the bus in the veiligheidsnis is displayed. However, this 3D reconstruction is incorrect. In this image, the distance between the bus and side wall must have been a half bus width (approximately 1m25). The actual distance between bus and side wall was not even 25 centimeters.”
 
The actual width of the pavement can be seen in Fig 2. As you can see it would have been quite easy for Michiels to steer to the right to avoid the oncoming wall (Fig 3)
Fig 2
Fig 3
 
 



The autopsy results of Geert Michiels (above), revealed that his left coronary artery was blocked at least 60 percent due to fat deposits. This disease (atherosclerosis) can lead to heart rhythm disturbances or even a heart attack. The autopsy also revealed traces of paroxetine in the system, paroxetine is the generic name of Seroxat, also known as Paxil.

According to information Michiels had been taking Seroxat for several years, he had been prescribed it as, at the time, he was going through a divorce. However, he was, at the time of the accident, in the process of tapering off. (more on this later). Furthermore, during the initial investigation, it was learned that Michiels took the drug for two years and that the standard dose was reduced by half in early 2012. The intention was to eventually phase out the use completely. If the standard dose was 20mg then a reduction of 10mg could possibly have been too drastic.

Unsatisfied with the findings of  Swiss Chief Prosecutor Olivier Elsig, the parents of some of the children, who died in the crash, employed the services of the Dutch-based forensic agency Independent Forensic Services (IFS).

IFS found that Michiels made two clear movements seconds before the crash, consciously and with the intention of running the bus into the wall of the tunnel.

“The driver at no time lost control of the steering wheel,” IFS researcher Selma Eikenboom told Dutch TV. “He made those movements consciously, with some force. Then he drove straight on for several seconds and into the wall. That’s not something you do if you’re feeling faint.” Asked if this demonstrated his suicidal intent, she said. “That’s a conclusion you may draw for yourself. This is technical evidence that speaks for itself.”

According to Dutch lawyer Job Knoester, acting for the parents, Michiels’ medication, Seroxat or paroxetine, has been implicated in cases of suicide and serious aggression aimed at others. “If you know that, then the matter has to be investigated,” he said. “It seems as if the Swiss didn’t want to look into the question at all.”

Armed with this new evidence the parents applied to the Swiss courts, in essence they wanted the investigation reopened. The federal tribunal dismissed the appeal.

Lawyer Job Knoester from The Hague, counsel for some parents, said after the dismissal of the appeal, “The parents want to know why their children died.” He added that the Swiss court never carried out their own reconstruction of the disaster and no research had been done on the side-effects of Seroxat.

Don Schell

In February, 1998, Don Schell (60), a non-violent family man and doting grandfather, took a .22 calibre pistol and a 357 magnum in the middle of the night and shot dead the three people in the world dearest to him – his wife Rita, his daughter Deb and baby Alyssa. Then he killed himself.

In 2001, a jury of five women and three men ruled that taking Paxil was the proximate cause of the deaths of Schell and his wife, daughter and granddaughter. The jury ruled that GlaxoSmithKline, the manufacturers of Paxil, were 80 percent responsible for the deaths. It held Schell 20 percent responsible. (Source)

David Carmichael

In 2004, while taking the antidepressant Paxil, Toronto fitness expert David Carmichael took his 11-year-old son Ian to a hotel room in London, Ont., and strangled him.

Charged with first-degree murder, Carmichael was found not criminally responsible because of a mental disorder and transferred to the Brockville Mental Health Centre. On Dec 4, 2009, he received an absolute discharge from the Ontario Review Board.

According to Health Canada: “A small number of patients taking drugs of this type may feel worse instead of better … They may experience unusual feelings of agitation, hostility or anxiety, or have impulsive or disturbing thoughts that could involve self-harm or harm to others.”

David’s website, which goes into detail of the tragedy can be viewed here. A 10 minute segment aired by CTV W-Five regarding David’s story can also be viewed here.

The two cases are striking. In the Schell case we have a jury pretty much speaking for the dead to protect the living. In the Carmichael case we have the evidence given by the actual person responsible for the homicide.

Geert Michiels holds all the answers to the fatal Sierre coach crash, yet, it appears, nobody is willing to investigate the link between Seroxat and homicide/suicide. Nobody is willing to allow Michiels to give his version of events from beyond the grave.

Swiss Chief Prosecutor Olivier Elsig’s final report told us nothing, in fact, the report just tells us what didn’t cause the crash. Investigations like this are all about eliminating so one can arrive at a conclusion – the report was inconclusive. At no point, has Elsig investigated the possible link between Seroxat and homicide/suicide, it begs the question, why?

Geert Michiels was employed by De Lijn Vlaams-Brabant, a company run by the Flemish government in Belgium to provide public transportation. The coach he was driving on that fateful evening was owned by TopTours in Belgium. I wrote the following email to them…

Dear REDACTED,

I am doing some research into tour bus driver protocols with regard to driving whilst under the influence of prescription medication.

Do TopTours have any protocol in place where driver’s are either…

a) required to let TopTours know that they are on medication

b) required to stay off work until they have finished their course of prescription medication.

I have more questions but this will do for now.

Thanks in advance for your reply.

Regards


TopTours failed to reply.

I find it quite remarkable that the investigation failed to look into the fact that Michiels was tapering from a drug known to cause severe withdrawal problems, problems that have been, for years, downplayed by the manufacturer, GlaxoSmithKline. In fact, it recently came to light that Glaxo had known about the withdrawal problems (in adults) for some years, but failed to carry out their own clinical studies into this problem, furthermore, they kept this information from the public (See Seroxat – Project 1059 Laden With Withdrawal Problems)

If reports are correct that Michiels dosage of Seroxat had been halved in efforts to wean him off then we have a potential time bomb. The reduction of Seroxat by half was poor advice. I, myself, struggled tapering off Seroxat – it took me around 19 months just to taper from 40mg per day to 22mg per day – I was using the liquid formulation of Seroxat and tapering by just 0.5 mg per week. In the end, I went cold turkey and suffered horrendous side effects, one of which was seeking confrontation – I actually went out into a country park in the early hours of the morning looking/hoping I would encounter trouble. It’s all detailed in my book, The evidence, however, is clear, the Seroxat scandal.

Furthermore, Michiels and his wife, Evy Laermans, were allegedly at loggerheads with his decision to drive coaches. Michiels worked part-time but had, unbeknownst to Laermans, asked the coach company if they could offer him a full-time position. Laermans knew nothing about this as her speech at a commemoration for the victims shows. She said that Geert was giving up and that he was killed during one of his last trips. (Source)

Could the disagreements between Michiels and his wife have led to him deliberately crashing the coach, could this irrational thinking have been brought on by the reduction of Seroxat?

Going cold turkey on Seroxat is not recommended, the side-effects are too severe. And here’s where the investigation failed.

This from Michiels wife…

He (Michiels) had taken no pill taken before the accident.

Michiels was in withdrawal, this fact is unquestionable.

The current patient information leaflet for Seroxat says..

Possible withdrawal effects when stopping treatment.

Side effects.

  • Feeling dizzy, unsteady or off-balance
  • Feeling anxious
  • Feeling restless or agitated
  • Tremor (shakiness)
  • Feeling confused or disorientated
  • Visual disturbances

The patient information leaflet is written by GlaxoSmithKline, there is no mention of Seroxat causing completion of suicidal or homicidal acts in adults. They do, however, say…

Some people have had thoughts of harming or killing themselves while taking Seroxat or soon after stopping treatment. Some people have experienced aggression while taking Seroxat.

“Soon after stopping treatment” is the key here.

If Michiels, as his wife suggested, had stopped taking his treatment then, even the manufacturer of Seroxat claim, “Some people have had thoughts of harming or killing themselves while taking Seroxat or soon after stopping treatment.”

Why was this overlooked by Swiss Chief Prosecutor Olivier Elsig?

And what of Michiels treating physician? Was he interviewed at any stage of the original investigation – he, assuming it was a he, could have thrown light on the exact dose of Seroxat Michiels was taking, he/she could have also explained why he/she decided to tell Michiels to reduce his dosage by half – what protocol was Michiels physician following here?

Here we have a bunch of parents wishing for answers – they are each left in limbo until they get these answers. Every stone must be turned, every nook and cranny should be delved into. You cannot just dismiss something on a whim then move on to other matters in an investigation. It’s half-assed to claim that this was just an “accident” when such stark evidence exists that there may be more to it than that.

It must also be noted that we have a grieving wife too. Evy Laermans lost her husband on that fateful night so she too should deserve some respect here. She, rightly so, is defending the name of her husband. It would be difficult for any of the parents to feel any sympathy or indeed empathy for Michiels. Whatever way you paint it, he was in charge of the motor vehicle when it crashed. There are other factors here too. The finger of blame, or partial blame, could be pointed at Michiels doctor for suggesting such a drastic taper – then of course we have the pharmaceutical company that market and manufacture Seroxat – GlaxoSmithKline. They are, it appears covered though. The small, insignificant warning on the patient information leaflet is almost like a disclaimer for such tragedy’s.

In the case of Don Schell (above) we saw the jury return a verdict. They attributed 80% of the blame to Seroxat manufacturers GlaxoSmithKline and 20% of the blame to Don Schell. The Swiss Chief Prosecutor Olivier Elsig has took the easy way out here, he has laid no blame on anyone, to do so would, no doubt, cause conflict, especially where GlaxoSmithKline are concerned. Elsig is sitting on the fence, he’s not wishing to rock the boat and this attitude is hindering the process of grief for the parents.

This case should be reopened. We may never be able to determine if Seroxat played a part in this tragedy but we should certainly put it on the table and, for the record, state that it may have induced a psychotic episode in Michiels. It needs to be an official statement here and not one of grieving parents, who will always be seen as people unwilling to accept that this was just an “accident”, nothing more, nothing less.

Operating any form of transport whilst under the influence of mind-altering drugs should also be looked into. The Federal Aviation Administration (FAA) don’t allow pilots on certain medications to operate aircraft, why, then, should coach companies be any different? In fact, back in 2010, the FAA cited Paxil as having a “severe withdrawal syndrome.”

With this knowledge, is it feasible to suggest that the coach company who hired the services of Michiels need to, at the very least, put something in place so no driver under the influence of psychiatric medication, is ever allowed to operate one of their vehicles again?

People should be talking about the possibilities in this case and not brushing them under the carpet. I doubt if the parents will ever find conclusive proof that Michiels deliberately crashed the coach into a brick wall, I doubt, if, indeed, Michiels did crash the coach deliberately, that the families will be able to determine whether or not Seroxat played a part in his decision making. It should, at the very least, be investigated and maybe listed as a possible causation.

I’m reminded of a scene from the movie Jaws. Matt Hooper (Richard Dreyfuss) is an expert in the field of sharks and shark attacks.

Hooper, examining the remains of the first victim, describes the post-mortem into his tape recorder.

Hooper: [to the m.e. and Brody] This was no boat accident!
Hooper: [to Brody] Did you notify the Coast Guard about this?
Brody: No. It was only local jurisdiction.
Hooper: [continues post-mortem] The left arm, head, shoulders, sternum and portions of the rib cage are intact…
Hooper: [lifts up the severed arm] This is what happens. It indicates the non-frenzied feeding of a large squalus – possibly Longimanus or Isurus glauca. Now… the enormous amount of tissue loss prevents any detailed analysis; however the attacking squalus must be considerably larger than any normal squalus found in these waters. Didn’t you get on a boat and check out these waters?
Brody: No.
Hooper: Well, this is not a boat accident! And it wasn’t any propeller; and it wasn’t any coral reef; and it wasn’t Jack the Ripper! It was a shark.

The parents of the children who perished in the Sierre coach crash have now formed a group. Foundation Busramp Sierre are calling for “Independent research into what really happened.”

In related news, Wendy B. Dolin, wife of the deceased, Stewart Dolin, charges that GSK negligently failed to warn her and her husband of what it knew to be a significant risk of suicide associated with Paxil (Seroxat).  – The full complaint can be read here.

Bob Fiddaman