An Emerging GSK Scandal -(Tafenoquine) : Psychosis, Bipolar and Chronic Depression: Personal Account of an Australian Tafenoquine Veteran

Posted on June 27, 2016 by International Mefloquine Veterans’ Alliance
This is the personal account of an Australian soldier who deployed to Timor Leste with the 1st Battalion, Royal Australian Regiment (1 RAR) in 2000-2001. During this tour 1 RAR soldiers were used to trial the experimental quinoline anti-malarial drug tafenoquine, manufactured by GlaxoSmithKline, in one of a series of tafenoquine studies undertaken by the Army Malaria Institute. The Department of Defence claims that “there is no evidence that tafenoquine causes serious neuropsychiatric effects, either acute or chronic”, only by ignoring the fully documented medical histories of this veteran and many others like him.
Among the 492 tafenoquine trial subjects, not one single severe neuropsychiatric adverse event was attributed to their use of this drug in the published trial report. Yet there are scores who were subsequently diagnosed with serious, chronic psychiatric disorders including depression, anxiety, PTSD, bipolar and other personality disorders. Many were medically discharged from the Army and remain chronically ill, while the Department of Defence refuses to accept any responsibility or to undertake follow-up studies.
This account is typical among the survivors of the trial.
“I was put in the locked psychiatric ward at Townsville under close surveillance and remember being isolated with some other very mentally sick people. What I went through there in hospital can’t really be explained to someone who hasn’t crossed the line to insanity.” 

I was 19 years old when I was deployed on Operation Tanager to East Timor. To be a soldier was all I ever wanted to be and I joined  because I wanted to make a difference and help people. I was a soldier of 2 platoon Alpha Company 1 RAR, and I was prescribed Tafenoquine as part of the anti malaria drug trial in 2000.

A lot of things happened over there on tour that had a great impact on my life. It’s been 15 years since I returned home from that deployment and the following is a summary of what has happened after my battalion returned from war-like service on Anzac Day 2001.

Like most of us, I had some trouble adjusting to society when we came back to Australia. The first thing out of the ordinary for me was that I just felt like being alone. That wasn’t normal behavior for me and I turned down invitations from friends to just stay inside on my own for days. I felt a bit shut off and I became more withdrawn and in particular from strangers and civilians. I found when my mind was occupied with work though, I seemed to be doing alright and I didn’t really think it was a problem at the time.
Later that year in 2001 was where things started to go very wrong for me. My mind started to deteriorate over a period of 2 months which lead me for the first time down the path of mania. Initially I was in good health and felt great. I had a happy and positive outlook and a huge thirst for life. I felt really strong, confident, and powerful. I started noticing I seemed to have a lot more energy than ever before, and my thoughts began to slowly race.
Things that seemed difficult before were now quite simple to me. My mind was very sharp and fast and was getting faster each day. So much so that it began working overtime. In a space of 2 weeks I rarely slept, I remember walking the line between dreaming and being awake and thinking that I was fine, when in reality I had lost 20kg from over-exercising, looked exhausted and was talking so fast and rapidly shifting from one subject to the next that no one could understand me. I was becoming irritable, quick to anger and quicker to another emotion in an instant. Any fear or inhibitions holding me back were gone, and I would wake to a new day excited like it was an epic adventure. I started to believe I had a heightened sense of state as ordinary things or circumstances started to communicate with me on a second level to what I would normally understand. I found intricate meaning in anything that I was immersed in which would be entirely delusional to anyone but myself. I was completely irrational and psychotic, and it wasn’t until I didn’t show up for parade one morning that I completely lost it. I have trouble remembering, but I’m told that I was found in my room which was in a state of chaos, and I remember my boss bringing me some food and taking me to hospital.
I was put in the locked psychiatric ward at Townsville under close surveillance and remember being isolated with some other very mentally sick people. What I went through there in hospital can’t really be explained to someone who hasn’t crossed the line to insanity. To give you an indication of my thought process though, I believed I was at the centre of some extraordinary story where I’d been taken to a facility not of this Earth, and that the people I met were reincarnated versions of others I once knew.
To say the least, for me to come back to reality was a long, slow and difficult process. I had no idea what was happening to me, and was under very heavy drug sedation. I eventually came to grips with the fact that I was told I had a major psychotic episode and needed time in hospital to recover which played out to three months.
I was put on leave and sent home to be treated as my family tried to piece together what was happening. My memory of this time is hazy as I was heavily sedated and physically unable to get out of bed at times from the medication. After 4 or 5 visits to a Psychiatrist I was diagnosed with Bipolar Disorder. I didn’t know what that was and to this day I think doctors have a hard time understanding it themselves but the diagnosis lead me to understand that my future in the services was over. I lived and breathed the Army so this was very hard to take. The day I was told that I would be medically discharged was probably the most I’ve ever felt ashamed and lost.
A couple of amazing Vietnam Vets tried to help me when I was first discharged. I was still in a daze from the medication the doctors were trying to treat me with and frankly in a bit of shock from what I had been through. An advocate put together a case for me on my behalf. I kept quite a comprehensive written journal of my accounts in Timor but any evidence I had was not enough to support my claim for Bipolar Disorder.Timor was new and I needed to show evidence that I had been through a  stressor significant enough with the diagnosis of Bipolar Disorder being within 6 months of that stressor to warrant a claim.

When presenting my case coincidentally on Remembrance Day the Vets on the board asked whether I had been in any contacts or fired my weapon throughout the tour. When I answered no, I knew my claim would be denied and it was.
Since my discharge I’ve tried to live my life as best as I could, but I soon discovered new problems. I had my first taste of major anxiety and depression in early 2004. I slowly started withdrawing into myself and lost more and more of my personality over a few weeks to a point where my mind felt numb, and everything I did seemed like I was just going through the motions of basic communication. I felt on edge and my cognitive skills were almost freezing up as I couldn’t function or make a decision. This was new and I tried to escape from it by drinking heavily one night. I remember waking up the next morning frozen with what I now know is anxiety. I knew I needed to call for help but couldn’t work out what to say or how to do it and felt just about paralyzed in my mind. I had to once again recover and quit my job and move home for my family to take care of me.
What followed was a long drawn out depression. It would hold on to me and little I can do to this day can help it. When depression comes it comes, and I just have to hope for the best, but when it does come, suicidal thoughts come with it leading to suicidal ideation. In the trough of depression it’s close to the only thought that you have. You’re mind convinces you it’s the only choice that’s left to solve what’s happening. For me, it’s not a feeling of sadness, it’s a feeling of nothing at all. It’s just about the opposite of mania, you’re mind runs slowly, and simple tasks seem overwhelming. You just want to be alone, you don’t want to do anything, and you just want to die. I’ve had more depressive episodes than I can say, and have been close to being hospitalised for it on a number of occasions. They can last for months on end and the anti-depressant medication treatment I’ve had for it doesn’t seem to have any effect.
I was 23 by this stage after going through these two major episodes and started to have little hope for my future. I took a very basic job at a factory where I worked along side older people that had trouble mentally but were able to put in a days manual labour. It was hard for me because despite my psychological problems I was reasonably bright and young.
I had a lot of nightmares, and continue to have one vivid reoccurring one where I’m in a contact scenario back in Timor with my section. Each dream is in a new location but it’s always the same, I can’t seem to find my weapon while my mates and I comes under fire. I wake up in terror and a cold sweat. I find occasionally in social situations I get a similar cold sweat and I panic. I avoid anything army, in particular Anzac Day or anything that reminds me about my service which I find hard as some of my closest friends still serve and I have a respect for it. I’ve found in the past when I bring things up, or relive what I went through on deployment it often leads to me becoming unwell. 

The fear of that first psychotic episode is what keeps me in check. I’ve had several further manic episodes and they seem to come when I’m under stress. The most recent one I had was quite severe and I was starting to lose my grip on reality again with delusions and seeing signs in ordinary things. I’d take wild risks in decisions and not consider the consequences. Some of the thoughts I’ve had in these times I won’t mention but could have lead to some dangerous scenarios. I would show signs of violence, bursts of anger, just breaking down emotionally, and generally not be in control of myself. You try to use your brain to figure out how to solve the situation, but the problem is your brain is the part that’s broken. Each time I have an episode, my mind seems to be in a worse state than before. I get headaches, my short term memory deteriorates, and my focus or concentration to stay on a simple task at times seems more confused. People will talk to me and quite often I’m far away. Im still a bit unsure of the cause of what has happened to me. All I know is this – I went to Timor fit and healthy, and didn’t return that way and have never been the same since.

Despite what has happened to me, somewhere deep down is that 19 year old soldier that doesn’t give in. I fight to hold on to who I am, and not let things get to me. Some days I lose though, weather the storm and lock myself away from the world for a day or two, but I carry on.
I’ve managed to persevere and live a pretty good life of sorts really. There were long periods where I was healthy and it was here I managed to do really well. With the money I made in Timor, and from the factory I had a deposit to buy a house. I left the factory, studied, travelled, opened a business, got married and started a family. Throughout all this I’ve cycled through mental health problems and states of mania, depression and anxiety. Sometimes I have outbursts of these problems where they’re short lived or blend together.
In 2009 my girlfriend who is now my wife experienced what happens to me when I have a major depressive episode. She didn’t know what to do at first as I became more distant and withdrawn and slowly couldn’t communicate what was happening to me. It got pretty severe quite quickly and I ended up at hospital once again. This time I managed to get some help. I met with some new doctors who were a bit more in touch with young veterans. Since then I’ve been treated by a psychiatrist for Bipolar Disorder. After all this time with him I’ve rarely spoken about my deployment but talking with him has helped me stay on track with my condition. For a long time I was taking Epilem to control my moods, and sleeping medication when necessary to reduce the risk when I go high in mania but I’ve been drug free now for over 18 months and reasonably healthy. I know what the future holds for me though, and what has happened to me is permanent. I think what hurts me the most is putting my family through the process.
I owe my life to my family and friends. Without them or an understanding support network, I wouldn’t be here. Strangely, I’ve also found having looked after a dog has helped. It gets me out of the house and my dog’s outlook on life is pretty inspiring. Physical fitness or activities have also really helped when I’ve been depressed. Forcing myself to go out and be with friends. A job that keeps my mind occupied and gives me a purpose. The belief that no matter how deep or dark a depression is, that it will one day eventually pass. A good night sleep and not too much stress to set things off. I’ve found that having a sense of humor has helped me through the years. A Vietnam Vet once said to me that when you’re a digger, if you’re platoon went through a bad situation you would have a laugh along the way, and that’s how you get over things, deal and survive. I think also that none of us fought in Timor on our own.
Going on tour to help the East Timorese was one of the defining moments of my life. I haven’t been in contact with anyone I served with for nearly 15 years now and being isolated hasn’t really helped me. For a long time I literally thought I was a minority, mentally weak and just unfortunate for what happened to me. A friend recently sent me a link to the online group for us Timor vets and it’s answered a lot of questions. I hope to answer more and personally with what I went through hope to find peace in knowing that I wasn’t at fault for what I’ve suffered. I also hope to live the rest of my life as mentally healthy as I can, and that one day I can pay back my friends, family and the great people who have helped me.

‘Serial FCA Whistleblower’ Joe Piacentile Loses Claim Against WhistleBlower Greg Thorpe

Greg Thorpe regularly posts comments on articles on this blog, and his views are always honest. I applaud Greg for having the courage to be the first whistle-blower to speak out against GSK’s misdeeds back in the early 2000’s (see here), and I applaud him further for having the tenacity not to quit, particularly in the subsequent fight against opportunistic individuals, and the vultures that have encircled him, ever since he decided to put his life on the line 13 years ago. I know what it’s like to put your life on the line, to fight tooth and nail, and to self sacrifice everything for the greater good, and I also know what it takes to persevere even when the vultures, sociopaths, and psychos, are sniping at your heels.

It takes guts.

Greg is not afraid to speak the truth about GSK’s sham 3 Billion dollar fine (see here). He is not afraid to tell us that this fine was not justice at all but merely a quid pro quo sham- a gift to GSK. He’s not afraid to tell us what really happened behind the gloss of the media spin.

GSK’s 3 Billlion dollar fine was a white-wash. It will not deter them, or any other pharmaceutical company, from continuing to harm patients in the pursuit of profits. It was not a success for patient rights (as some have advertised it), it was a success for GSK, the industry (and the lawyers who feed off FCA claims). It was akin to a slap on the wrist for GSK and business as usual.

(see comments here).

Greg is not afraid to speak out against the whole damn stinking debacle.

The FCA (false claims act) has turned into a farce, and a highly lucrative industry (made up mainly of opportunists- lawyers and former ‘whistle-blowers’), and one individual who seems to have amassed a fortune from this new industry is Dr Joe Piacentile.

Dr Joe has apparently made up to 17 million by filing multiple FCA complaints against multiple pharmaceutical companies over several years.

Surely this kind of thing needs to be stopped in its tracks? How is it even ethical, or legal, to do this?

Is it not blatant opportunism and profiteering? Surely this kind of behavior debases the entire idea of law and of justice itself?

Dr Joe is part of an organization called Whistle Blowers Against Fraud. This organization is effectively a profit making enterprise. I see nothing on the WAF website about the dead and damaged patients from all the dodgy drugs they have allegedly exposed.

All I see (on these whistle-blower fishing websites) are advertisements about the billions of dollars of fines they have apparently recouped from the pharmaceutical industry.

I just see more greed..

And a lot of self promotion..


Dr Joe even admits on his own website (the Piacentile Family foundation) that he learned the in’s and out’s of how these fraudulent activities occur by being originally involved himself in defrauding America’s medicaid system.

In the mid-1980s, Dr. Joe was a partner in a national durable medical equipment company. In charge of a sales force of 160 employees, Dr. Joe grew sales from $1 million to $20 million in a mere three years. However, this early success did not end well. Dr. Joe and his partners each pled guilty to one count of fraud for reportedly “falsifying Medicare forms.” This brush with the justice system opened Dr. Joe’s eyes to the real damages caused by fraud and gave him a front row seat in observing the inner workings of the justice system’s prosecution of such crimes.

I understand that there probably has to be some financial incentive to blow the whistle on these huge companies and their wrong-doings, but surely making an entire career out of it has to be unethical?

Dr Piancentile has been controversial for many years now, precisely because of the reasons I have just outlined.

As recently as 2014 Dr Joe made headline news on NBC America because of a 100,000 dollar donation to President Obama. Dr Joe, it seems, was also seeking a pardon for his history of medicaid fraud.

I guess the medicaid fraud wasn’t good advertising for his Whistleblowers Against Fraud (WAF) venture?

“…A White House-backed advocacy group has fired one of its fundraisers and returned a $100,000 check she collected from a New Jersey doctor who is seeking a presidential pardon for Medicare fraud, officials of the group told NBC News.

Organizing for Action, or OFA, a political nonprofit set up last year to promote the president’s policies, confirmed that it dismissed consultant Samantha Maltzman this week after receiving inquiries from NBC News about a contribution she had brought in from Dr. Joseph Piacentile, who was convicted in 1991 for Medicare fraud and tax evasion.”…

Piacentile did not attend the dinner, removed from the guest list after OFA vetters flagged his felony conviction, according to the OFA official who spoke on condition of anonymity. His pardon application shows that he was sentenced in 1994 for Medicare fraud and tax evasion, serving six months in a halfway house and agreeing to a $900,000 consent judgment. He has since founded a whistleblowers group dedicated to exposing health care and other frauds…”

A recent judgment against Greg Thorpe, by Joe Piacentile, was denied.

In short, Dr Joe was attempting to seek over 800,000 dollars off Greg Thorpe despite already receiving multiple millions in payments from  the other so called ‘whistle-blowers’ involved in the original GSK FCA complaint.

Greg stood his ground.

Here is the judgement, in Greg’s favor…

2016.06.21 ORDER RE Granting Thorpe SJ

Psychiatrist Mickey Nardo’s Latest Post On GSK Study 329…

Posted on Wednesday 22 June 2016

David Healy, Jon Jureidini, Bernard Carroll, and Ben Goldacre

Some day there’ll be a best seller, a popular science book that will tell a story currently still in the making – and near the beginning the book will have a chapter about the interchange between David Healy and Charlie Nemeroff in Toronto in 2000 when Healy lost a new job because he talked about the potentially fatal side effects of SSRI [and Nemeroff, then boss of bosses] undermined his job change in retaliation. And there will be a piece about how Jon Jureidini, a pediatric psychiatrist, publicly protested a published study in 2003 that fraudulently claimed that a SSRI was safe and effective in adolescent depression. And that best-selling-author-to-be will add the efforts of Bernard Carroll and Bob Rubin in 2003 and later 2006 in exposing that same Charlie Nemeroff and others for promoting treatments they had a personal financial interest in without acknowledging those interests. Then there’s Ben Goldacre who will be cited for calling attention to the essential role of data transparency in bringing the truth to light with the AllTrials initiative, or getting at a major mechanism of deceit with his COMPare project. There will be so many more who will figure into this unfolding story. But right now, in spite of a lot of prequels, that book can’t be written because the story’s not over yet. Sure enough, there’s been progress but the main story line continues, lacking an in·place general solution…

Recently, the pioneers have been mighty busy. In September, David Healy, Jon Juriedini, and their colleagues republished the 2001 study that had become a paradigm for a jury-rigged Clinical Trial report, reanalyzing it from the original dataset using the author’s own Protocol and found that despite the earlier claims, the drug was neither effective nor safe in adolescents [Restoring Study 329: efficacy and harms of paroxetine and imipramine in treatment of major depression in adolescence]. Then in March, Jon Juriedini and some other colleagues were back with another SSRIs·in·adolescents·study, this time with access to internal documents showing again how a negative Clinical Trial had been published as positive [The citalopram CIT-MD-18 pediatric depression trial: Deconstruction of medical ghostwriting, data mischaracterisation and academic malfeasance]. This study had been used as a basis for FDA Approval, and used the same technique of altering the a priori protocol – something Ben Goldacre‘s COMPare project calls “outcome switching.”

We now know that this problem of misreported Clinical Trials will never be solved so long as the raw data remains hidden. Without access to that information, we’ll never put a stop to these dark days of pseudoscience in the medical literature. But that’s not enough, because it’s the analysis of that data where the misbehavior has been centered. Today, one of those pioneers has a blog post that suggests a viable next step, a concrete general solution to the problem:
Health Care Renewal
by Bernard Carroll
June 22, 2015

There is a disconnection between the FDA’s drug approval process and the reports we see in medical journals. Pharmaceutical corporations exploit this gap through adulterated, self-serving analyses, and the FDA sits on its hands. I suggest we need a new mechanism to fix the problem – by independent analyses of clinical trials data.

When they analyze and publish their clinical trials in medical journals, pharmaceutical corporations have free rein to shape the analyses. The FDA conducts independent analyses of the data submitted by the corporations, and it may deny or delay approval. But the FDA does not challenge the reports that flood our medical journals, both before and after FDA approval. It is no secret that these publications are routinely biased for marketing effect, but the FDA averts its gaze. That failure of the FDA – a posture known as enforcement discretion – has been well documented. The question is why? At the same time, exposing the biases has been difficult for outsiders because the data are considered proprietary secrets.
This is just a teaser. The whole post is on-line. In the next section, Carrol outlines the problem using Juriedini’s latest paper as a case example then proposes a solution:
A Specific Proposal
Our primary defense against such perversions of scientific reporting is fidelity to the registered IND protocol and plan of statistical analysis. The solution is not hard to see: We need independent analyses of clinical trials because we cannot trust the corporate analyses. In effect, we need something like the Underwriters Laboratory to verify the statistical analyses of clinical trials. Nobody takes the manufacturing corporation’s word for it concerning the safety and performance of X-ray machines or cardiac defibrillators. Why treat the statistical analysis of drug trials any differently? It’s highly technical work. Who should assume that responsibility? Why not the FDA? After all, they alone see all the data. My specific proposal is for Congress to mandate that the FDA analyze all clinical trials data strictly according to the registered protocols and analysis plans. That requirement should apply to new drugs or to approved drugs being tested for new indications. It should apply also to publications reporting new trials of approved drugs. Corporations and investigators should be prohibited from publishing their own in-house statistical analyses unless verified by FDA oversight.
There follows a section on why the time to act is at hand and the potential counterarguments:
It is time for Congress to grasp this nettle. The time for enforcement discretion is past, and we need Congress either to direct the FDA to act or to create a new mechanism of oversight. To do nothing would be unthinkable.

There are other suggested solutions beginning to appear and I’ll cover some of them in subsequent blog posts. But this one comes first because it’s the one that makes the most sense to me. In all of the work that went into our Paxil Study 329 paper where my part was the efficacy analysis, I became convinced that insisting that the analyses follow the a priori Protocol and Statistical Analysis Plan to the letter is the only way to insure that the analysis is worthwhile. After we finished our paper, I went back and looked and every questionable trial I’d looked at had suspicious variables. My problem was that finding those Protocols was spotty. My hat’s off to Goldacre’s team for being able to run them down. The other ubiquitous problem was from inappropriate statistical testing. So Carroll’s proposal seems right as rain. The FDA has the capabilities to do the analyses, and already does them in many cases.

I picked the four investigators up top, not because they work together, or even necessarily agree. I picked them because each has been a central part of my own growing understanding of a way out of this mess. My way of saying “thanks!”

Update: Dr. Carroll’s proposal was cross posted on Naked Capitalism with some interesting comments.

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


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. It covers numerous additional concerns about how GSK researched, developed, and marketed Paxil.



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.


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


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

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

being treated with antidepressant medication. Retrieved May 25, 2006, from

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

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.

Doctor Ben Goldacre Knows Best…


Note to Ben Goldacre (from me):

“….Missing data poisons the well for everybody. If proper trials are never done, if trials with negative results are withheld, then we simply cannot know the true effects of the treatments we use. Evidence in medicine is not an abstract academic preoccupation. When we are fed bad data, we make the wrong decisions, inflicting unnecessary pain and suffering, and death, on people just like us….”

Ben Goldacre 2012

“…As one of the authors of the RIAT restoration of Paxil Study 329 who was around for the whole process, I don’t actually know the answer to Leonie’s question about why it was so hard to get our paper published.

I don’t know if a Conflict of Interest had anything to do with that, but in a way, that’s the whole point – when there’s a significant Conflict of Interest, you can’t ever really know.

It’s a variable that can’t be evaluated.

So her question stands whether it can be answered or not. Should the original Study 329 report be retracted?

That’s not in our hands.

My choice would be that it should never have been published in the first place..”

(Comment by Mickey Nardo one of the authors of the BMJ published- RIAT Study on GSK’s Study 329 for Paroxetine in Adolescents on “Club 329”– David Healy’s Blog- ).

There is a fascinating debate happening over on Dr David Healy’s blog about a lecture which  Dr Ben Goldacre gave in Dublin’s Royal College of Surgeons last week. It all started when (patient activist, and blogger) Leonie Fennell (an attendee of the lecture)- published her opinion of Ben’s talk in a post on Dr Healy’s blog (titled ‘Club 329‘). The post seems to be sparking some very interesting reactions, not least from Ben Goldacre himself (who  incidentally has already accused Dr. Healy of misrepresenting his views because the post is published on Healy’s web-page).

Personally I don’t think that Leonie misrepresented Ben at all, and ironically, Ben claims that the audio of the lecture itself confirms this misrepresentation, when in fact- it does the opposite: it upholds, and confirms Leonie’s views.

You can listen to the audio here:

Ben released it on Twitter, and I thought it might be helpful (for clarity) to cut it to the exact parts which are under debate.

The following is Leonie’s full blog post, on Dr Healy’s blog.

I will follow underneath it with some commentary.

Club 329: Part 1

June, 7, 2016 | 24 Comments

The doctors prescribing the drugs don’t know they don’t do what they’re meant to. Nor do their patients. The manufacturers know full well, but they’re not telling. Drugs are tested by their manufacturers, in poorly designed trials, on hopelessly small numbers of weird, unrepresentative patients, and analysed using techniques that exaggerate the benefits.

Reboxetine is a drug I have prescribed. Other drugs had done nothing for my patient, so we wanted to try something new. I’d read the trial data before I wrote the prescription, and found only well-designed, fair tests, with overwhelmingly positive results. Reboxetine was better than a placebo, and as good as any other antidepressant in head-to-head comparisons. It’s approved for use by the Medicines and Healthcare products Regulatory Agency (the MHRA), which governs all drugs in the UK. Millions of doses are prescribed every year, around the world. Reboxetine was clearly a safe and effective treatment. The patient and I discussed the evidence briefly, and agreed it was the right treatment to try next. I signed a prescription.

But we had both been misled. In October 2010, a group of researchers was finally able to bring together all the data that had ever been collected on reboxetine, both from trials that were published and from those that had never appeared in academic papers. When all this trial data was put together, it produced a shocking picture. Seven trials had been conducted comparing reboxetine against a placebo. Only one, conducted in 254 patients, had a neat, positive result, and that one was published in an academic journal, for doctors and researchers to read. But six more trials were conducted, in almost 10 times as many patients. All of them showed that reboxetine was no better than a dummy sugar pill. None of these trials was published. I had no idea they existed.

It got worse. The trials comparing reboxetine against other drugs showed exactly the same picture: three small studies, 507 patients in total, showed that reboxetine was just as good as any other drug. They were all published. But 1,657 patients’ worth of data was left unpublished, and this unpublished data showed that patients on reboxetine did worse than those on other drugs. If all this wasn’t bad enough, there was also the side-effects data. The drug looked fine in the trials that appeared in the academic literature; but when we saw the unpublished studies, it turned out that patients were more likely to have side-effects, more likely to drop out of taking the drug and more likely to withdraw from the trial because of side-effects, if they were taking reboxetine rather than one of its competitors.

I did everything a doctor is supposed to do. I read all the papers, I critically appraised them, I understood them, I discussed them with the patient and we made a decision together, based on the evidence. In the published data, reboxetine was a safe and effective drug. In reality, it was no better than a sugar pill and, worse, it does more harm than good. As a doctor, I did something that, on the balance of all the evidence, harmed my patient, simply because unflattering data was left unpublished.

Nobody broke any law in that situation, reboxetine is still on the market and the system that allowed all this to happen is still in play, for all drugs, in all countries in the world. Negative data goes missing, for all treatments, in all areas of science. The regulators and professional bodies we would reasonably expect to stamp out such practices have failed us. These problems have been protected from public scrutiny because they’re too complex to capture in a soundbite. This is why they’ve gone unfixed by politicians, at least to some extent; but it’s also why it takes detail to explain. The people you should have been able to trust to fix these problems have failed you, and because you have to understand a problem properly in order to fix it, there are some things you need to know.

Drugs are tested by the people who manufacture them, in poorly designed trials, on hopelessly small numbers of weird, unrepresentative patients, and analysed using techniques that are flawed by design, in such a way that they exaggerate the benefits of treatments. Unsurprisingly, these trials tend to produce results that favour the manufacturer. When trials throw up results that companies don’t like, they are perfectly entitled to hide them from doctors and patients, so we only ever see a distorted picture of any drug’s true effects. Regulators see most of the trial data, but only from early on in a drug’s life, and even then they don’t give this data to doctors or patients, or even to other parts of government. This distorted evidence is then communicated and applied in a distorted fashion.

In their 40 years of practice after leaving medical school, doctors hear about what works ad hoc, from sales reps, colleagues and journals. But those colleagues can be in the pay of drug companies – often undisclosed – and the journals are, too. And so are the patient groups. And finally, academic papers, which everyone thinks of as objective, are often covertly planned and written by people who work directly for the companies, without disclosure. Sometimes whole academic journals are owned outright by one drug company. Aside from all this, for several of the most important and enduring problems in medicine, we have no idea what the best treatment is, because it’s not in anyone’s financial interest to conduct any trials at all.

Now, on to the details.

In 2010, researchers from Harvard and Toronto found all the trials looking at five major classes of drug – antidepressants, ulcer drugs and so on – then measured two key features: were they positive, and were they funded by industry? They found more than 500 trials in total: 85% of the industry-funded studies were positive, but only 50% of the government-funded trials were. In 2007, researchers looked at every published trial that set out to explore the benefits of a statin. These cholesterol-lowering drugs reduce your risk of having a heart attack and are prescribed in very large quantities. This study found 192 trials in total, either comparing one statin against another, or comparing a statin against a different kind of treatment. They found that industry-funded trials were 20 times more likely to give results favouring the test drug.

These are frightening results, but they come from individual studies. So let’s consider systematic reviews into this area. In 2003, two were published. They took all the studies ever published that looked at whether industry funding is associated with pro-industry results, and both found that industry-funded trials were, overall, about four times more likely to report positive results. A further review in 2007 looked at the new studies in the intervening four years: it found 20 more pieces of work, and all but two showed that industry-sponsored trials were more likely to report flattering results.

It turns out that this pattern persists even when you move away from published academic papers and look instead at trial reports from academic conferences. James Fries and Eswar Krishnan, at the Stanford University School of Medicine in California, studied all the research abstracts presented at the 2001 American College of Rheumatology meetings which reported any kind of trial and acknowledged industry sponsorship, in order to find out what proportion had results that favoured the sponsor’s drug.

In general, the results section of an academic paper is extensive: the raw numbers are given for each outcome, and for each possible causal factor, but not just as raw figures. The “ranges” are given, subgroups are explored, statistical tests conducted, and each detail is described in table form, and in shorter narrative form in the text. This lengthy process is usually spread over several pages. In Fries and Krishnan (2004), this level of detail was unnecessary. The results section is a single, simple and – I like to imagine – fairly passive-aggressive sentence:

“The results from every randomised controlled trial (45 out of 45) favoured the drug of the sponsor.”

How does this happen? How do industry-sponsored trials almost always manage to get a positive result? Sometimes trials are flawed by design. You can compare your new drug with something you know to be rubbish – an existing drug at an inadequate dose, perhaps, or a placebo sugar pill that does almost nothing. You can choose your patients very carefully, so they are more likely to get better on your treatment. You can peek at the results halfway through, and stop your trial early if they look good. But after all these methodological quirks comes one very simple insult to the integrity of the data. Sometimes, drug companies conduct lots of trials, and when they see that the results are unflattering, they simply fail to publish them.

Because researchers are free to bury any result they please, patients are exposed to harm on a staggering scale throughout the whole of medicine. Doctors can have no idea about the true effects of the treatments they give. Does this drug really work best, or have I simply been deprived of half the data? No one can tell. Is this expensive drug worth the money, or has the data simply been massaged? No one can tell. Will this drug kill patients? Is there any evidence that it’s dangerous? No one can tell. This is a bizarre situation to arise in medicine, a discipline in which everything is supposed to be based on evidence.

And this data is withheld from everyone in medicine, from top to bottom. Nice, for example, is the National Institute for Health and Clinical Excellence, created by the British government to conduct careful, unbiased summaries of all the evidence on new treatments. It is unable either to identify or to access data on a drug’s effectiveness that’s been withheld by researchers or companies: Nice has no more legal right to that data than you or I do, even though it is making decisions about effectiveness, and cost-effectiveness, on behalf of the NHS, for millions of people.

In any sensible world, when researchers are conducting trials on a new tablet for a drug company, for example, we’d expect universal contracts, making it clear that all researchers are obliged to publish their results, and that industry sponsors – which have a huge interest in positive results – must have no control over the data. But, despite everything we know about industry-funded research being systematically biased, this does not happen. In fact, the opposite is true: it is entirely normal for researchers and academics conducting industry-funded trials to sign contracts subjecting them to gagging clauses that forbid them to publish, discuss or analyse data from their trials without the permission of the funder.

This is such a secretive and shameful situation that even trying to document it in public can be a fraught business. In 2006, a paper was published in the Journal of the American Medical Association (Jama), one of the biggest medical journals in the world, describing how common it was for researchers doing industry-funded trials to have these kinds of constraints placed on their right to publish the results. The study was conducted by the Nordic Cochrane Centre and it looked at all the trials given approval to go ahead in Copenhagen and Frederiksberg. (If you’re wondering why these two cities were chosen, it was simply a matter of practicality: the researchers applied elsewhere without success, and were specifically refused access to data in the UK.) These trials were overwhelmingly sponsored by the pharmaceutical industry (98%) and the rules governing the management of the results tell a story that walks the now familiar line between frightening and absurd.

For 16 of the 44 trials, the sponsoring company got to see the data as it accumulated, and in a further 16 it had the right to stop the trial at any time, for any reason. This means that a company can see if a trial is going against it, and can interfere as it progresses, distorting the results. Even if the study was allowed to finish, the data could still be suppressed: there were constraints on publication rights in 40 of the 44 trials, and in half of them the contracts specifically stated that the sponsor either owned the data outright (what about the patients, you might say?), or needed to approve the final publication, or both. None of these restrictions was mentioned in any of the published papers.

When the paper describing this situation was published in Jama, Lif, the Danish pharmaceutical industry association, responded by announcing, in the Journal of the Danish Medical Association, that it was “both shaken and enraged about the criticism, that could not be recognised”. It demanded an investigation of the scientists, though it failed to say by whom or of what. Lif then wrote to the Danish Committee on Scientific Dishonesty, accusing the Cochrane researchers of scientific misconduct. We can’t see the letter, but the researchers say the allegations were extremely serious – they were accused of deliberately distorting the data – but vague, and without documents or evidence to back them up.

Nonetheless, the investigation went on for a year. Peter Gøtzsche, director of the Cochrane Centre, told the British Medical Journal that only Lif’s third letter, 10 months into this process, made specific allegations that could be investigated by the committee. Two months after that, the charges were dismissed. The Cochrane researchers had done nothing wrong. But before they were cleared, Lif copied the letters alleging scientific dishonesty to the hospital where four of them worked, and to the management organisation running that hospital, and sent similar letters to the Danish medical association, the ministry of health, the ministry of science and so on. Gøtzsche and his colleagues felt “intimidated and harassed” by Lif’s behaviour. Lif continued to insist that the researchers were guilty of misconduct even after the investigation was completed.

Paroxetine is a commonly used antidepressant, from the class of drugs known as selective serotonin reuptake inhibitors or SSRIs. It’s also a good example of how companies have exploited our long-standing permissiveness about missing trials, and found loopholes in our inadequate regulations on trial disclosure.

To understand why, we first need to go through a quirk of the licensing process. Drugs do not simply come on to the market for use in all medical conditions: for any specific use of any drug, in any specific disease, you need a separate marketing authorisation. So a drug might be licensed to treat ovarian cancer, for example, but not breast cancer. That doesn’t mean the drug doesn’t work in breast cancer. There might well be some evidence that it’s great for treating that disease, too, but maybe the company hasn’t gone to the trouble and expense of getting a formal marketing authorisation for that specific use. Doctors can still go ahead and prescribe it for breast cancer, if they want, because the drug is available for prescription, it probably works, and there are boxes of it sitting in pharmacies waiting to go out. In this situation, the doctor will be prescribing the drug legally, but “off-label”.

Now, it turns out that the use of a drug in children is treated as a separate marketing authorisation from its use in adults. This makes sense in many cases, because children can respond to drugs in very different ways and so research needs to be done in children separately. But getting a licence for a specific use is an arduous business, requiring lots of paperwork and some specific studies. Often, this will be so expensive that companies will not bother to get a licence specifically to market a drug for use in children, because that market is usually much smaller.

So it is not unusual for a drug to be licensed for use in adults but then prescribed for children. Regulators have recognised that this is a problem, so recently they have started to offer incentives for companies to conduct more research and formally seek these licences.

When GlaxoSmithKline applied for a marketing authorisation in children for paroxetine, an extraordinary situation came to light, triggering the longest investigation in the history of UK drugs regulation. Between 1994 and 2002, GSK conducted nine trials of paroxetine in children. The first two failed to show any benefit, but the company made no attempt to inform anyone of this by changing the “drug label” that is sent to all doctors and patients. In fact, after these trials were completed, an internal company management document stated: “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 year after this secret internal memo, 32,000 prescriptions were issued to children for paroxetine in the UK alone: so, while the company knew the drug didn’t work in children, it was in no hurry to tell doctors that, despite knowing that large numbers of children were taking it. More trials were conducted over the coming years – nine in total – and none showed that the drug was effective at treating depression in children.

It gets much worse than that. These children weren’t simply receiving a drug that the company knew to be ineffective for them; they were also being exposed to side-effects. This should be self-evident, since any effective treatment will have some side-effects, and doctors factor this in, alongside the benefits (which in this case were nonexistent). But nobody knew how bad these side-effects were, because the company didn’t tell doctors, or patients, or even the regulator about the worrying safety data from its trials. This was because of a loophole: you have to tell the regulator only about side-effects reported in studies looking at the specific uses for which the drug has a marketing authorisation. Because the use of paroxetine in children was “off-label”, GSK had no legal obligation to tell anyone about what it had found.

People had worried for a long time that paroxetine might increase the risk of suicide, though that is quite a difficult side-effect to detect in an antidepressant. In February 2003, GSK spontaneously sent the MHRA a package of information on the risk of suicide on paroxetine, containing some analyses done in 2002 from adverse-event data in trials the company had held, going back a decade. This analysis showed that there was no increased risk of suicide. But it was misleading: although it was unclear at the time, data from trials in children had been mixed in with data from trials in adults, which had vastly greater numbers of participants. As a result, any sign of increased suicide risk among children on paroxetine had been completely diluted away.

Later in 2003, GSK had a meeting with the MHRA to discuss another issue involving paroxetine. At the end of this meeting, the GSK representatives gave out a briefing document, explaining that the company was planning to apply later that year for a specific marketing authorisation to use paroxetine in children. They mentioned, while handing out the document, that the MHRA might wish to bear in mind a safety concern the company had noted: an increased risk of suicide among children with depression who received paroxetine, compared with those on dummy placebo pills.

This was vitally important side-effect data, being presented, after an astonishing delay, casually, through an entirely inappropriate and unofficial channel. Although the data was given to completely the wrong team, the MHRA staff present at this meeting had the wit to spot that this was an important new problem. A flurry of activity followed: analyses were done, and within one month a letter was sent to all doctors advising them not to prescribe paroxetine to patients under the age of 18.

How is it possible that our systems for getting data from companies are so poor, they can simply withhold vitally important information showing that a drug is not only ineffective, but actively dangerous? Because the regulations contain ridiculous loopholes, and it’s dismal to see how GSK cheerfully exploited them: when the investigation was published in 2008, it concluded that what the company had done – withholding important data about safety and effectiveness that doctors and patients clearly needed to see – was plainly unethical, and put children around the world at risk; but our laws are so weak that GSK could not be charged with any crime.

After this episode, the MHRA and EU changed some of their regulations, though not adequately. They created an obligation for companies to hand over safety data for uses of a drug outside its marketing authorisation; but ridiculously, for example, trials conducted outside the EU were still exempt. Some of the trials GSK conducted were published in part, but that is obviously not enough: we already know that if we see only a biased sample of the data, we are misled. But we also need all the data for the more simple reason that we need lots of data: safety signals are often weak, subtle and difficult to detect. In the case of paroxetine, the dangers became apparent only when the adverse events from all of the trials were pooled and analysed together.

That leads us to the second obvious flaw in the current system: the results of these trials are given in secret to the regulator, which then sits and quietly makes a decision. This is the opposite of science, which is reliable only because everyone shows their working, explains how they know that something is effective or safe, shares their methods and results, and allows others to decide if they agree with the way in which the data was processed and analysed. Yet for the safety and efficacy of drugs, we allow it to happen behind closed doors, because drug companies have decided that they want to share their trial results discretely with the regulators. So the most important job in evidence-based medicine is carried out alone and in secret. And regulators are not infallible, as we shall see.

Rosiglitazone was first marketed in 1999. In that first year, Dr John Buse from the University of North Carolina discussed an increased risk of heart problems at a pair of academic meetings. The drug’s manufacturer, GSK, made direct contact in an attempt to silence him, then moved on to his head of department. Buse felt pressured to sign various legal documents. To cut a long story short, after wading through documents for several months, in 2007 the US Senate committee on finance released a report describing the treatment of Buse as “intimidation”.

But we are more concerned with the safety and efficacy data. In 2003 the Uppsala drug monitoring group of the World Health Organisation contacted GSK about an unusually large number of spontaneous reports associating rosiglitazone with heart problems. GSK conducted two internal meta-analyses of its own data on this, in 2005 and 2006. These showed that the risk was real, but although both GSK and the FDA had these results, neither made any public statement about them, and they were not published until 2008.

During this delay, vast numbers of patients were exposed to the drug, but doctors and patients learned about this serious problem only in 2007, when cardiologist Professor Steve Nissen and colleagues published a landmark meta-analysis. This showed a 43% increase in the risk of heart problems in patients on rosiglitazone. Since people with diabetes are already at increased risk of heart problems, and the whole point of treating diabetes is to reduce this risk, that finding was big potatoes. Nissen’s findings were confirmed in later work, and in 2010 the drug was either taken off the market or restricted, all around the world.

Now, my argument is not that this drug should have been banned sooner because, as perverse as it sounds, doctors do often need inferior drugs for use as a last resort. For example, a patient may develop idiosyncratic side-effects on the most effective pills and be unable to take them any longer. Once this has happened, it may be worth trying a less effective drug if it is at least better than nothing.

The concern is that these discussions happened with the data locked behind closed doors, visible only to regulators. In fact, Nissen’s analysis could only be done at all because of a very unusual court judgment. In 2004, when GSK was caught out withholding data showing evidence of serious side-effects from paroxetine in children, their bad behaviour resulted in a US court case over allegations of fraud, the settlement of which, alongside a significant payout, required GSK to commit to posting clinical trial results on a public website.

Nissen used the rosiglitazone data, when it became available, and found worrying signs of harm, which they then published to doctors – something the regulators had never done, despite having the information years earlier. If this information had all been freely available from the start, regulators might have felt a little more anxious about their decisions but, crucially, doctors and patients could have disagreed with them and made informed choices. This is why we need wider access to all trial reports, for all medicines.

Missing data poisons the well for everybody. If proper trials are never done, if trials with negative results are withheld, then we simply cannot know the true effects of the treatments we use. Evidence in medicine is not an abstract academic preoccupation. When we are fed bad data, we make the wrong decisions, inflicting unnecessary pain and suffering, and death, on people just like us.


To the BBC, GSK, and The MHRA (medicines regulators in the UK) who were all viewing this afternoon. I wonder what interest you have in the story of one person who had a terrible time on GSK’s vile Seroxat drug? Surely you’d all have better things to do than bother with the random ramblings on my little blog? What is it you’re curious about? GSK whistle-blower Greg Thorpe’s recent comments on my blog, perhaps? Or the Yemen whistle blower who contacted me about GSK’s alleged corruption in Yemen? Or maybe it’s about Seroxat causing suicide in teens? (or is that old news now?), or maybe it’s just generally about Seroxat (Paxil) causing death and destruction to the lives of thousands of people?

I suppose, it could be any number of things. There is almost a decade of blog posts, and over 1000 of them in fact, so I’m sure there’s plenty of reading to be done.

Whatever it is, you can always e-mail me (not you GSK though) and find out more : 

There’s loads of information that I haven’t made public.

I’m sure there’s a ton of BBC documentaries to be made on the reams of subject matter I have explored over the years…

I’m taking a little break for a while, kinda worn out…

But my e-mail is always open…

What is Prescripticide?

What is prescripticide?

pill antidepressant SSRI medication

A newly created concept is gathering momentum on social media.

‘Prescripticide’ has been officially embraced by the internet, with the creation of a new Wikipedia page that defines it as a death caused by an adverse reaction to a prescription drug.

The word was coined in December 2015 by David Carmichael, who killed his son over a decade ago while experiencing an SSRI-induced psychosis.

Carmichael was charged with first-degree murder in the US, but after multiple psychiatric assessments the court found him not criminally responsible for his son’s death.

In an article published by web-based medical research group Rxisk, which advocates for improved drug education, Carmichael describes his experience after increasing his antidepressant dosage.

“Over a three-week period, I changed completely from being a loving, caring and nurturing father of two beautiful children to taking the life of my beloved son Ian, in a calm, organised state of delirium-psychosis,” says Carmichael.

Alongside other stories of alleged antidepressant-related homicides, Carmichael’s account is leading healthcare practitioners and mental health advocates to question whether SSRIs and other prescription drugs carry side effects that are more dangerous than previously thought.

The Wikipedia page also cites Danish medical researcher Dr Peter Gotzsche, co-founder of the Cochrane Collaboration, who has stated that prescription drugs are the third leading cause of death after heart disease and cancer.

Dr Gotzsche has written extensively against the widespread use of antidepressants and ‘Big Pharma’.


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