Posted Aug 16, 2017 at 11:34 AMUpdated Aug 17, 2017 at 9:51 AM
He was charged with operating under the influence after a crash in Brockton – but it wasn’t related to alcohol consumption, police said.
BROCKTON – A Middleboro man was charged with operating under the influence after a crash in Brockton – but it wasn’t because of alcohol consumption, police said.
Jacob R. McMahon, 25, of Middleboro, was charged with negligent operation of a motor vehicle, disobeying motor vehicle rules and regulations, and operating under the influence of drugs, after he crashed into a parked car in Brockton on Sunday night, according to Brockton police.
At first, McMahon tried to drive away, but heavy damage to his Volkswagen Jetta stopped him from doing so, following the collision at 282 Green St. at 11:22 p.m., Brockton police said.
“He attempted to flee the scene,” said Brockton police Lt. William Hallisey, referring to a police report from the incident. “The Jetta was too badly damaged for him to flee.”
“Police did not detect an odor of alcohol, but he was unsteady on his feet,” Hallisey said. “His eyelids appeared heavy. It looked like he was about to go to sleep. He had trouble keeping his eyes open and maintaining balance. … He said he took one (Paxil pill).”
McMahon hurt his head during the crash, police said.
“He said he struck his head on the windshield,” Hallisey said.
McMahon was not arrested and was instead issued a summons, and he was transported to Good Samaritan Medical Center for treatment and testing.
Hallisey said that McMahon was expected to be tested for drug use as part of the ongoing investigation.
When the results of clinical trials aren’t made public, the consequences can be dangerous — and potentially deadly.
Consider the case of the anti-depressant Paxil, produced by the drug company SmithKline Beecham (now part of GlaxoSmithKline). GSK got approval from the FDA in 1999 for treatment of depression in adults, but not in teenagers. That meant that while doctors could prescribe the drug to adolescents — a so-called “off label” prescription — GSK could not promote the drug to doctors for that purpose.
But the company did just that, according to criminal and civil complaints filed by the Justice Department and a suit by then-New York Attorney General Eliot Spitzer. What’s more, the Justice Department claimed, GSK selectively and misleadingly released information about three studies it had conducted of the drug: It hired a consulting company to write a journal article that played up evidence from one study that the drug worked better as a treatment for pediatric depression than a placebo, played down (better) evidence from the same study that it hadn’t, and soft-pedaled the side effects.
These side effects included suicidal thoughts and actions.
It buried two other studies, the Justice Department noted, in which Paxil had failed to show efficacy in treating depression.
In the end, GSK paid the US government $3 billion in fines for illegal and misleading promotion Paxil and other drugs, and, in 2004, the FDA required manufacturers to put a “black box” warning label on Paxil and other antidepressants about the potential risks of increased suicidal thoughts and actions when used in children and teenagers.
In 2015, researchers published a second look at the data and clinical study reports underlying the study GSK had relied on for promoting Paxil’s use in adolescents. They affirmed the drug “was ineffective and unsafe in this study.” This was part of a much bigger problem afflicting drug research, they said: “There is a lack of access to data from most clinical randomised controlled trials, making it difficult to detect biased reporting.”
You might think a crisis of that scope, involving teenage suicide and billions of dollars, would rouse the scientific establishment to make sure that the results of all clinical trials be made public. But it didn’t happen. Despite public campaigns, and even legal requirements, many clinical trials still report results publicly late or not at all. What, if anything, will prod researchers — and universities and drug companies — to act?
The issue at stake here isn’t the FDA’s approval process. The FDA makes drugmakers go through an intensive application process before it deems new drugs or medical devices safe and effective. When drug companies seek FDA approval for a drug or device, they aren’t allowed to cherry-pick which results they report. The agency requires that companies submit plans outlining all trials they’ll submit for approval, and scrutinizes the trial results (even conducting its own statistical review). But the FDA does not ensure that all of those trial results also enter the public view.
That means doctors and researchers trying to get a full picture of a drug’s effects are out of luck.
During the Paxil legal battles, there was not yet a law in the United States requiring that clinical trials publicly share their results. What is remarkable is that today there is such a law — yet researchers and companies often ignore it.
Some researchers do share their trial results through journal publications. However, one synthesis of studies on the topic found that from one quarter to one half of clinical trials are never published — or are published only years after trials end. In that same report, from 2012, new research found that roughly half of all trials funded by the National Institutes of Health remained unpublished 30 months after the end of a trial (though 68 percent were ultimately published at some point). The reasons for delays and non-publication vary, from researchers’ lack of interest in reporting negative results — the infamous “file drawer problem” — to constraints on the time of researchers.
Progress on transparency legislation
The research transparency movement has been gaining steam, but still can’t declare victory. A 1997 federal requirement mandated that researchers register some trials in a public database (those pertaining to serious or life-threatening diseases). Then in 2005, an association of medical journals started requiring that any study published in one of their publications be registered in an online database before the time of first patient enrollment. That didn’t guarantee results would be made public, but it at least provided an incentive to researchers to make some information about the trial available.
A few years later, an even bigger shift occurred. Congress passed the FDA Amendments Act of 2007, which required that “applicable clinical trials” register and publicly report results within one year of trial completion. (The requirement excluded some trials, such as Phase 1 trials of drug safety as opposed to efficacy.) The site ClinicalTrials.gov, run by the National Library of Medicine, had started posting general information about trials in 2000 — so sick people could sign up, for example — but now became the place where those results were posted. And the law included a penalty: Those who failed to report on time could face fines of up to $10,000 per day.
Yet nearly a decade later, it’s clear that many researchers and institutions basically ignore the law. They report trials late or not at all, but the FDA has yet to levy a fine. An investigation by the health journalism organization STAT, published in December 2015, looked at about 9,000 trials across 98 institutions, from 2008 to 2015. Of trials that were required by the FDA to report their results, 74 percent of industry trials were either not reported or reported late. The figure, maybe surprisingly, was even worse for academic institutions: 90 percent late or unreported.
By STAT’s calculation, if the FDA had enforced the law using the $10,000-per-day day fine, it could have collected over $25 billion since 2008, funding the agency several times over.
And the thrust of STAT’s conclusions has beenechoed by other investigations. (After the Paxil episode, GSK, for its part, has been posting trial results to the company website; it also fares better than many other companies and institutions in several recent transparency scorecards.)
A medical culture too comfortable with non-publication and non-reporting
Why hasn’t the FDA enforced the 2007 law on publicizing results, and why hasn’t it levied financial penalties?
One reason, according to several of those that I spoke with, including Deborah Zarin, director of ClinicalTrials.gov, is that the 2007 law contained ambiguity about some of the requirements, including which trials were subject to the law.
Jennifer Miller, founder of Bioethics International, agrees that some researchers have been, at least till very recently, uncertain about whether the 2007 law applied to their trial. The language used in the law to describe applicable studies included the phrase “controlled clinical trials,” and there was some uncertainty about which trials would count as “controlled.” “How can you impose fines on an ambiguous law?” Miller said.
Researchers I spoke to emphasized, however, that clinical trial results are not just a legal issue: It’s an ethical matter, too. Regardless of the law, shouldn’t reporting results be part of the culture of doing clinical trials?
If so, there’s a problem with the current culture. Researchers are rewarded primarily for publishing as much as possible in the highest-ranked journals that they can, says Joseph Ross, an associate professor of medicine at Yale and an associate editor at JAMA Internal Medicine. “There’s no clear incentive for investigators to have a member of their staff do everything required by ClinicalTrials.gov. It gets deprioritized because it is a substantial amount of work, and investigators don’t put it at the top of their list.”
Competition may play a role. Someone who is running a trial might think: “My competitor has similar molecules in the pipeline, why should I tell them why it failed so that they don’t pump money into it?” says Tomasz Sablinski, co-founder of the drug development firm Transparency Life Sciences, who was previously with the pharmaceutical company Novartis.
How to change the norms, so that there’s an internal commitment to reporting results from researchers and institutions? Steven Goodman, an associate dean and professor of medicine at Stanford, notes that it will be important for institutions to provide education to researchers on how to report results, and pay for staff support.
AllTrials, a nonprofit organization founded by medical doctor and public intellectual Ben Goldacre, took on the mission of pushing for clinical trial transparency. AllTrials, which started in the UK and also has a campaign in the US, thinks the laws don’t go far enough: None of the regulations governing clinical trial reporting require sharing results retroactively (that is, before the laws are passed), which leaves many results for already-approved drugs unreported.
Goldacre also collaborated with a web developer and scientist, Anna Powell-Smith, to create the automatically updated Trials Tracker. The tracker scans ClinicalTrials.gov and PubMed to identify how many clinical trials have been reported by companies and institutions with 30 clinical trials or more. After working on transparency for many years, Goldacre believes “naming and shaming” is the main thing that will really grab the attention of those who haven’t reported their trials.
Momentum seems to be gathering, although the Trump administration’s commitment to the cause remains uncertain. In September 2016, Health and Human Services, which oversees the FDA, issued a “final rule” clarifying and expanding the requirements of the 2007 law: It specifies what was meant by “controlled clinical trials,” among other things. (“All interventional studies with prespecified outcome measures.”) The rule also expands the scope of the requirement to include results from certain trials of new drugs and devices which haven’t yet been approved by the FDA.
The National Institutes of Health (NIH) also announced a policy in September 2016 requiring that all its grant recipients publicly report their clinical trial results. The NIH policy and HHS final rule took effect on January 18. Will the organizations ramp up pressure to comply with the law, and will researchers take this obligation seriously? It’s too soon to say.
The obligation to research participants
One reason to care about whether clinical trial results are shared is that hundreds of thousands of patients have put themselves on the line as research subjects. We owe it to them not to let the information their participation enabled get stuck in a file drawer.
“If we made a pact with a person to enter into this experiment, then we have an ethical and scientific obligation to have the results out there, no matter what happened,” said Stanford’s Goodman.
Everyone who conducts a clinical trial should report their results, whatever the outcome. It’s the law, and it’s past time that it was followed. When researchers fail to do so, we should point that out early and often — for the sake of public health.
Stephanie Wykstra is a freelance writer and consultant with a focus on research transparency. She has recently worked with nonprofits including AllTrials USA and Robert Wood Johnson Foundation. Twitter: @Swykstr.
So BBC panorama are airing a Panorama investigation tonight into anti-depressant induced violence, and of course, even before the documentary has aired, we have all the pro-SSRI mouthpieces (most notably from the Royal college of Psychiatry UK) coming out en masse to condemn it before it has even been broadcast.
This is no surprise considering the Royal college of psychiatry and most of its members (not just UK psychiatrists but global psychiatrists) have long been in the pocket of the pharmaceutical industry. Of course, most of the mainstream media outlets, fail to mention that very significant fact.
However, despite the melodrama, it was interesting to note the position of Mind (the UK’s biggest and most respected mental health charity) who said:
….”Stephen Buckley, head of information at Mind, said: “Millions of people take SSRIs and other antidepressants and many find them useful in managing their mental health problems. “Side effects from medication can be serious but it’s important to recognise that severe side effects such as those explored in this programme are incredibly rare. “Anyone prescribed medication for a mental health problem should be fully informed about the drug and its side effects so they can make an informed choice about whether it’s the right treatment for them.”…
Stephen Buckley, from Mind, is wise to err on the side of caution, and that is part of what his job entails, however isn’t it interesting that he does not disagree with the findings of the documentary? He says that “severe side effects such as those explored in this programme are incredibly rare“. I agree with him, somewhat, antidepressant induced violent acts are relatively rare, however, anti-depressant induced violent thoughts are perhaps more common than most people realize.
Many people have antidepressant induced violent thoughts and impulses, it’s just Russian Roulette that decides who will act on them, and who won’t..
Seroxat (GSK’s notorious SSRI) causes aggression, akathisia (a feeling of unbearable anxiety), and violent thoughts/dreams/impulses; the whole class of SSRI drugs can cause these reactions. Many tens of thousands of people have been saying this about them for decades. I have experienced these side effects myself, from Seroxat.
There is no disputing this.
Of course, the (owned by the Pharmaceutical industry) Royal College of Psychiatry, and the other organizations with vested interests, will dismiss my experiences, and those of others who were harmed by SSRI’s, as merely anecdotal, but in the same breath they will quote (anecdotally) that that ‘these medicines save lives’. They will then quote the vague and mysterious ‘evidence based medicine’ to back up their stance, but what they won’t tell you is that the ‘evidence base’ is entirely unreliable, and in most cases -utterly corrupted, and in the worse cases- outright lies. They won’t tell you that the pharmaceutical industry is among the most corrupt industries on the planet (see Whisleblower Greg Thorpe’s GSK felony complaint here), and that death from psychiatric drugs in particular is a staggeringly high outcome for many.
A PRESCRIPTION For Murder? is a BBC documentary focusing on the potential effects of prescription antidepressants.
But what is it about? And when can you watch it? Here’s what we know…
What is A Prescription For Murder?
This new Panorama documentary looks into whether prescription antidepressants can turn you into a killer.
Over 40 million prescriptions for SSRI antidepressants were handed out by doctors last year in the UK.
Panorama reveals the devastating side effects on a tiny minority that can lead to psychosis, violence, possibly even murder.
With exclusive access to psychiatric reports, court footage and drug company data, reporter Shelley Jofre investigates the mass killings at the 2012 midnight premiere of a Batman movie in Aurora, Colorado. Twenty-four-year-old PhD student James Holmes, who had no record of violence or gun ownership, murdered 12 and injured 70.
Did the SSRI antidepressant he had been prescribed play a part in the killings?
Panorama has uncovered other cases of murder and extreme violence which could be linked to psychosis developed after the taking of SSRIs – including a father who strangled his 11-year-old son.
Panorama asks if enough is known about this rare side effect, and if doctors are unwittingly prescribing what could be a prescription for murder.
When is A Prescription for Murder? on?
You can catch the show at 9pm on Wednesday July 26, 2017.
If you miss it, you can catch it again on the BBC iPlayer.
Who is Shelley Jofre?
Shelley is a journalist who was born in Irvine, Ayrshire.
She began her career back in 1995 and is now one of the top investigators for Panorama.
Shelley is married and has a daughter.
Who is James Homes and what was the Aurora massacre?
James Eagan Holmes was born December 13, 1987 and is an American convicted mass murder.
He was responsible for the Aurora cinema shooting that killed 12 people and injured 70 others at a Century movie theatre in Aurora, Colorado, on July 20, 2012.
He walked into a midnight screening of Batman movie The Dark Knight Rises and threw two gas canisters into the audience.
Many in the audience thought it was a publicity stunt until he began spraying the crown with the shotgun, then the assault rifle and finally the pistol.
A witness said he went outside and and shot people as they ran.
Cops apprehended Holmes in his car behind the cinema within minutes of the shooting. He told them that he was “The Joker”.
On August 7 2015 Holmes was sentenced to life in prison without parole, avoiding the death penalty because the jury could not come to a unanimous decision.
James Holmes, a young man with no record of violence, murdered 12 people watching Batman in a Colorado cinema in 2012.
Did an SSRI antidepressant, prescribed by a doctor, play a part in the killings?
He slumps wild-eyed across the desk from detectives, with a mess of badly dyed red hair, his clothes hanging off him.
James Holmes looks every inch the monster who coldly executed 12 innocent people and injured dozens more at a midnight screening of the Batman film, The Dark Knight Rises.
Holmes had carried out the killings with an arsenal of weaponry he had accumulated in the preceding weeks. He had planned the shootings down to the tiniest detail, even booby-trapping his own apartment with home-made bombs to divert police resources while he launched the attack.
Watching a recording of his interview at the police station, conducted just hours after he carried out one of the worst mass shootings in recent US history, who could feel anything but loathing for this callous 24-year-old graduate student? When asked how to spell his surname, Holmes cockily replies, “Like Sherlock”.
When left alone with paper bags on his hands to secure forensic evidence, he’s caught on camera using them to talk to one another, like sock puppets.
The only hint he may have some inkling of what he’s just done is when he asks a detective, “There wasn’t any children hurt?” In fact, six-year-old Veronica Moser-Sullivan was the youngest of Holmes’s victims that night in July 2012 – killed as she watched the movie premiere with her mother at the packed cinema in Aurora, Colorado.
Americans have become wearily accustomed to mass shootings. Usually, in the days and weeks that follow, some kind of warped explanation emerges – be it terrorism, revenge or a predisposition to violence. It’s highly unusual for the perpetrator to be taken alive. Usually they are killed or kill themselves at the scene.
Holmes survived, and as the evidence stacked up it looked like another tragic collision of mental breakdown with America’s lax gun laws.
Holmes’s Glock 22 Pistol photographed on the bonnet of his car
Why else would a clever, shy guy with no history of violence, from a loving home, carry out such a heinous attack? Holmes had no enemies, no terrorist ideology to drive him on.
But the student had been seeing a psychiatrist at the University of Colorado Denver and this was no barrier to him buying a handgun, tear gas, full body armour and a semi-automatic rifle.
.223 M&P Assault Rifle photographed outside the cinema
Before he faced a court of law, Holmes was evaluated by a number of psychiatrists. No two doctors reached exactly the same conclusion. There were diagnoses of schizophrenia, schizoid personality disorder, schizotypal disorder – or no diagnosable disorder at all. Some thought Holmes couldn’t legally be held responsible for his crime, on grounds of insanity. Others disagreed, arguing he still knew right from wrong when he carried out the shootings.
When these questions came before a jury two years ago, the verdict was unanimous. Holmes was found guilty on all counts of murder and multiple counts of attempted murder.
Judge Carlos Samour Jr said:
He was led from the dock to jeers of “loser”, as his bewildered parents Bob and Arlene looked on, to begin one of the longest prison terms in US history – 12 life sentences plus 3,318 years in prison. He only narrowly escaped the death penalty.
Holmes is being held in solitary confinement at a maximum security prison in an undisclosed state, because the nature of his crimes make him a target for other prisoners. That’s how he will spend the rest of his days.
Like any other casual observer skimming over the court reporting online, I thought justice had been done, and that this was where Holmes’s story ended. Then I spoke to psycho-pharmacologist and long-time campaigner on the potential dangerous side effects of antidepressants, Prof David Healy.
Healy had been hired as an expert witness in the James Holmes case and had visited him in jail before the trial. The public defender appointed to represent Holmes wanted Healy to evaluate whether the antidepressant sertraline (also known as Lustral in the UK and Zoloft in the US), which Holmes had been prescribed, could have played a role in the mass murder.
Prof David Healy
I have worked with David Healy in the past on a number of investigative films for the BBC’s current affairs programme, Panorama.
These films revealed cases where people with no previous history of suicidal thoughts or violence went on to seriously harm themselves or others after being thrown into a state of mental turmoil by the newer generation of SSRI antidepressants, such as paroxetine and fluoxetine.
Before meeting Holmes, Healy doubted the pills had played a part. But by the end of his prison visit he had reached a controversial conclusion.
He was never called to give evidence at the trial of James Holmes, but he told me in August 2016 that he would have told the court:
SSRIs are thought to work by boosting serotonin levels to the brain.
Stephen Buckley, from mental health charity Mind, says:
He adds that no-one should stop taking medication suddenly, without advice from a health professional.
“If anyone is concerned that they may be experiencing harmful side effects they should speak to their doctor or pharmacist about alternatives.”
Prof Wendy Burn, president of the Royal College of Psychiatrists, says: “In all treatments – from cancer to heart disease – medicines which do good can also do harm. This applies in psychiatry. Current evidence from large-scale studies continues to show that for antidepressants the benefits outweigh the risks.”
David Healy maintains that while antidepressants can be a lifesaver for some, for others they can cause more harm than the original problems they were prescribed to treat.
But what makes a young man plan over months a mass shooting, then carry it out with cold precision? Could antidepressants possibly do that?
‘He was too good’
Arlene and Bob Holmes sat through every day of their son’s trial but rejected all approaches to talk in public about their son out of respect for the victims and their families.
However, a book that Arlene wrote, When the Focus Shifts: The Prayer Book of Arlene Holmes 2013-2014, gives an insight into her thoughts in the run-up to the trial in April 2015.
Arlene and Bob Holmes arrive at the court building
In one section, she describes the effects of taking the lowest dose of an SSRI antidepressant in March 2014:
She continues: “I sit through church service and sift through the Bible, uninspired. I’m fuzzy. Weird dreams. Crying used to be a release. Now I cannot cry, or laugh. I hate this feeling.”
Arlene Holmes, a nurse, wrote that she stopped taking the pills before the trial, telling her doctor she wanted to be able to feel things and to cry if she wanted to.
If she had a bad experience with an SSRI antidepressant, what would she make of David Healy’s view of her son’s case?
I contacted the couple’s lawyer explaining my own background in investigating antidepressants and suggesting that Arlene and Bob Holmes might hold information that could, ultimately, help prevent future tragedies.
A few weeks later an email from Arlene dropped into my inbox. Short and to the point, it requested more information and asked me not to share her contact details with anyone.
“Some people bear my family ill will,” she wrote.
When we finally spoke on the phone, it became clear Arlene and Bob had never seriously considered the effect antidepressants might have had on their son’s behaviour. In fact, they hadn’t even known of David Healy’s involvement as a pre-trial expert witness.
Persuaded that exploring their son’s case in depth may ultimately help others, they reluctantly agreed to a filmed interview. It wouldn’t help their son – they know he will spend the rest of his life in prison.
Approaching their low-rise detached home in a neat suburb of San Diego, what struck me was the sheer ordinariness – a man out washing his car, another mowing his lawn, kids playing baseball in the park. Inside, the Holmes’ house is modest, understated – just like Arlene and Bob.
“We are an introverted family,” says Arlene. “We are not showy but we like having people around. We care about the larger picture in society and we are Christians, we go to church.”
The couple have struggled to understand how their boy could cause so much hurt and pain to others.
“Not in your wildest dreams would you think your son would shoot strangers,” says Arlene. “For someone who loved kids and dogs and always did his homework and his chores. You can’t believe it is possible for anyone to cause that much harm, let alone the man you raised.”
She says they never saw any signs of violence, and that her son had not shown any interest in drink or drugs.
“In retrospect, I think he was too good. Maybe I should have worried about the fact he was so good, but as a mother you can worry about just about anything.”
Bob Holmes, a retired statistician, is a man of few words.
“He was never interested in guns or really even a violent kid, that’s why it was surprising. It came out of nowhere. He seemed happy enough, just pretty much a normal everyday kid growing up, so…” Bob’s voice trails off as though he can’t bear to finish the thought.
They say there had been ups and downs along the way but little to mark them out from any other family.
They moved home when James was 13 and he found the transition hard. He was quiet but he had friends and took part in sports. He cruised through his academic work at school and, later, as an undergraduate.
Bob and Arlene speak about taking James to a counsellor:
The first real hump in the road was when Holmes applied to six top universities to study for a doctorate in neuroscience. Academically bright, his shyness in interviews appeared to work against him. He was rejected by all of them.
“He came home and he just kind of didn’t do much of anything for a while, and he just kind of hung out,” says Bob.
Arlene says her son was sleeping a lot and not going out much.
“So I got mad and I said, ‘You are done with college, you need to do something.’”
Holmes took his mother’s advice and found a job working night shifts in a pill factory while he applied to more universities.
In 2011, he accepted an offer to study neuroscience at University of Colorado Denver and started in the autumn. Not his first choice, says his mother, but it all seemed to be working out fine.
“He still was happy to be at Colorado, talked to us about eventually settling and he eventually borrowed money to buy a town house on the outskirts of Denver,” she says.
Very few of Holmes’s former friends are willing to talk, but one – a young man who knew him well as an undergraduate – spoke to me on condition of anonymity. The Holmes he knew and liked was just as Bob and Arlene described – shy, polite, frugal and smart.
They used to play video games together – strategy games, not the violent kind, he says. There was the occasional beer, but no drugs, parties or girls.
“We were pretty nerdy,” he says.
Discovering someone he was close to could commit mass murder had been “a profound experience”. When he heard what his friend had done, he knew something must have happened to him.
“I still don’t know how to make sense of it,” he says.
Someone who spent time with Holmes in the crucial months before the shootings was Hillary Allen, a fellow graduate student on the neuroscience programme at CU Denver.
Sometimes the friendship was hard work.
“He was kind of quiet and kept to himself. He did have a kind of a quirky sense of humour,” says Allen.
“We were part of a group of scientists so I think everyone’s a bit odd. Maybe he was a little bit more odd than the rest of us, maybe more socially awkward.”
Socially awkward. It’s a phrase that comes up time and again to describe Holmes. It’s what led him to make contact with the university counselling department in the spring of 2012, just months before the shootings.
Cracks had started to appear in Holmes’s apparently effortless success. Over the Christmas break he was diagnosed with glandular fever. Tired and ill for the first couple of months of 2012, he kept going to classes, but his work was going downhill.
The shy and anxious Holmes found giving presentations in front of his classmates particularly hard.
His first proper relationship with fellow graduate student Gargi Datta had also come to an end. Datta didn’t want to speak to me, but according to Arlene Holmes the break-up hit her son hard.
“It was a cordial break-up. That’s the word he used, ‘cordial’. They both parted as friends.”
It was Datta who suggested Holmes seek help at the campus student wellness centre. On 21 March 2012, James Holmes had his first appointment there with psychiatrist Dr Lynne Fenton.
Sifting through the mountain of court testimony and evidence, this date sticks out.
Does it – as the prosecution would argue – mark the point at which Holmes first acknowledges he’s struggling mentally in the perfect storm of his relationship breakdown, academic problems and long-standing social anxiety? A storm that explains why he decided he had nothing to lose and everything to gain from killing as many people as he could?
Or was that date significant – as David Healy would say – because it was the day Lynne Fenton prescribed to James Holmes the antidepressant, sertraline?
First page of Holmes’s notebook
In his first meeting with Lynne Fenton, Holmes was hard to engage but described his anxiety around people. And during that 45-minute session worrying details emerged that he’d never talked about with his family.
Holmes said he was having thoughts of killing people three or four times a day.
Although it sounds alarming, Fenton didn’t regard him as dangerous at that point. The thoughts were abstract, there was no plan or, it seemed, any real intent. She prescribed the antidepressant sertraline to ease his anxiety and obsessive thoughts.
Holmes in custody
In later prison interviews with court-appointed forensic psychiatrist Dr William Reid, Holmes said he’d had intrusive thoughts like this since his teens. Not of actually killing people, rather of wishing them dead to escape from awkward social situations.
According to Reid, these kinds of intrusive thoughts are not uncommon.
“He wasn’t talking about a vengeful hatred,” he says. “He was talking about an aversion to mankind. Being around much of mankind was uncomfortable to him and it wasn’t very rewarding to him so he wanted to avoid it.”
With hindsight, it provides a clear motive, according to Colorado District Attorney, George Brauchler, who successfully prosecuted the case. He says Holmes had a long-standing hatred of mankind – that’s why he killed so many people.
As he puts it, Holmes was “evil”.
District Attorney, George Brauchler
Brauchler says Holmes kept his evil desires at bay until it became clear he wasn’t going to get what he wanted to be happy.
It’s a persuasive argument, and one some experts, and ultimately the jurors, had no trouble in accepting. But the timeline of what happened between Holmes’s first prescription of sertraline and the shootings wasn’t explored at trial.
When you scrutinise that timeline, it raises serious questions about the role of the widely prescribed antidepressant.
Page from Holme’s notebook
Just before he carried out the shootings, Holmes posted to Fenton a notebook he had written in. At times rambling, it gives some contemporaneous insight into his troubled mind. Both William Reid and David Healy agree it’s a valuable piece of evidence.
Holmes wrote about the initial effects of going on sertraline.
The first evidence that his thoughts of killing were turning real came in an online conversation with Gargi Datta on 25 March, four days after starting on sertraline.
At Holmes’s trial, Datta testified that at first she thought he was joking.
But as she challenged him, the details of his delusional theory spilled out.
This theory about increasing his so-called “human capital” by actually killing people was quite different to the abstract thoughts he’d had up until then about wishing people dead to get out of uncomfortable social situations.
Psychiatrists I’ve spoken to agree it was delusional, a sign of psychosis.
Datta was asked in court if he’d ever said anything delusional before this chat. She confirmed he hadn’t.
Forensic psychiatrist Dr Philip Resnick, from Ohio, was engaged as a prosecution expert. He was not called to give evidence at trial.
Dr Philip Resnick
In his first interview on the subject, he told me the “human capital” conversation with Datta was a key moment.
“I don’t think we have evidence of a plan to do it [kill] with an intention to do it before the human capital theory,” he says.
Holmes went back to see psychiatrist Lynne Fenton two days after telling Datta about human capital but he didn’t mention it to her. He did tell Fenton the medication hadn’t helped his obsessive thoughts. She doubled the dose of sertraline from 50mg to 100mg.
David Healy believes this made Holmes’s mental state worse:
He adds: “But when they are causing a problem, increasing the dose is a recipe for disaster.”
Nearly a fortnight after the dose increase on 9 April, the previously shy and awkward Holmes made a move on his classmate, Hillary Allen. His texts to her became uncharacteristically bold. One hot day he messaged her about the clothes she was wearing in class.
“Oh Hillary, Why yuh gotta distract me with those short shorts…?”
“I remember receiving that and just like kind of blushing and being like, I don’t remember what I said, but kind of trying to laugh it off and just trying not to create an awkward situation,” she says.
For David Healy, this was further evidence of the effect sertraline was having on Holmes.
At his fourth appointment with Lynne Fenton on 17 April, Holmes told her his homicidal thoughts had increased, though he still didn’t tell her about his human capital delusion. Fenton’s notes of that meeting documented a decline in his mental state.
“Psychotic level thinking… Guarded, paranoid, hostile thoughts he won’t elaborate on,” she wrote.
Whatever effect the sertraline was having, it certainly wasn’t helping. Healy firmly believes the psychotic-level thinking Fenton noted was a consequence of the medication.
At this appointment, Fenton upped the dose to 150mg. At Holmes’s trial she told the court this was the dose she had always been aiming for.
“It isn’t on her radar that this drug could be causing the kinds of problems that he’s having,” Healy says.
Fenton declined to be interviewed, but a statement from the University of Colorado Denver says patient-doctor confidentiality laws forbid her from talking about Holmes’s care without his consent, which he has not given.
By May, Holmes’s “mission”, as he later described it, got real. He began spending large amounts of money accumulating
weapons. In the notebook he wrote:
By this time, Holmes’s coursework had badly deteriorated. He gave a disastrous final presentation and then failed his exams. He was offered the chance to re-sit but on 11 June dropped out of university. Just before that, he had one last meeting with psychiatrist Lynne Fenton and her colleague.
Holmes’s final presentation
They were so concerned by his state of mind at this appointment they offered to keep treating him free of charge, but Holmes refused. Fenton had the power to detain Holmes under a mental health hold, but she told his trial she felt there were insufficient grounds.
She did contact the campus security team to ask for criminal-record and weapon-permit checks. Holmes was given the all clear. He never told Fenton about the weapons he’d bought or the plans he was making.
Fenton also called Holmes’s mother.
“She said, ‘Do you know that he is not going to continue in school?’” Arlene tells me. “I thought that was the purpose of her phone call, and I said, ‘Did he ask you to call me?’ And she said, ‘No he didn’t want me to call you and he didn’t want you to worry.’
If you haven’t listened to James Moore’s podcast series you really should.
James has notched up 29 Podcasts so far, and I think they are brilliant.
Stevie was prescribed Seroxat in 1996. Like many others, she was told by her doctor (from the propaganda of GSK at the time) that she had a chemical imbalance and that Seroxat would fix this. This was all nonsense of course, and merely just a marketing ploy to get more people on these drugs. More drugs and more patients on them- means more money for Glaxo’s coffers…
GSK are felons, proven criminals and fraudsters, do you think they tell the truth about their drugs?
Of course they don’t.
Do you think they care about people who suffer side effects?
Lyam David-Kilker was born on 24 October 2005, the second son of Michelle David and Miles Kilker of Bensalem, Pennsylvania. At birth he seemed like a normal, happy, healthy infant, but all that soon changed. His breathing was labored, and he became lethargic and lost his appetite. His parents took him to the doctors, who delivered devastating news. Lyam was born with multiple cardiac defects: a hole in his atrial septum, a hole in his ventricular septum, along with transposition of the great arteries—the same condition which afflicted Christiane and Amery’s son Daniel. Lyam required two open-heart surgeries and spent the first six months of his life in the hospital.
Shortly before conceiving, Michelle David had been prescribed Paxil for mild anxiety and occasional panic attacks, and she continued to take the drug throughout her pregnancy. After Miles Kilker heard a commercial message on television for the law firm linking Paxil to congenital heart defects, Michelle called the number and was referred to Sean Tracey, a personal injury lawyer from Houston.
During the trial, the plaintiff’s lawyers cited a couple of 2001 emails to GlaxoSmithKline from a woman (not Michelle David) who had taken Paxil while pregnant. The woman’s name was redacted from all court documents. The first email from her, dated 31 May, read:
“My name is [redacted]. I was diagnosed with panic disorder about four-and-a-half years ago. Since that time I’ve been taking Paxil, which is truly a miracle drug. I’ve been panic-free with this drug and have been able to go on with a normal life.
“I was married in October of 2000.My husband and I found out we were pregnant at Christmas time. I was so excited. I love children. The only problem is that I carried the baby to six months gestation and then had to have a termination.
“The doctors diagnosed my son with Truncus arteriosis. They said he would not lead a normal childhood and would most likely not make it through the open heart surgery that he would need as soon as he was delivered (if he was able to make it to that time). To say the least, I was absolutely distraught with this news.I thought this was something that I did, was because I stayed on the Paxil for selfish reasons.
“I wanted to know if you could direct me to any information you might have of any woman that has taken Paxil and still had healthy babies. My husband and I are ready to try again to get pregnant in the next month or two. I am so nervous. I don’t want to stop taking my miracle pill. But, then again, if there is a chance that this might hurt or affect the baby I want to know upfront. And I will somehow stop taking it for the time being.
“Please contact me as soon as possible. I love everything this drug has done for me. I am so thankful that your company had this available for me.I just want to continue to have a normal life and have the child that I always wanted. Please contact me as soon as possible.
“Please don’t forget about me,Thank you.”
“Thank you for your inquiry. We are attaching a copy of our current product information for Paxil. Please review the section on use during pregnancy. Further questions about your treatment should be directed to the physician, pharmacist or healthcare provider who has the most complete information about your medical condition. Because patient care is individualized, we encourage patients to direct questions about their medical condition and treatment to their physician. We believe that because your physician knows your medical history, he or she is best suited to answer your questions.
“Our drug information department is available to answer any questions your physician or pharmacist may have about our products. Your healthcare professional can call our drug information department at 1-888…”.
Congenital malformations associated with this drug
At that time, the prescribing information for Paxil made no mention of the number of reports of congenital malformations associated with this drug, and it was company policy not to tell doctors, patients, or pharmacists, either.
On 1 June, the mystery woman wrote again:
“This response is in regards to an e-mail that I had sent you previously. I was asking to see if you have any or are in the process of any clinical trials for women who are currently on Paxil and pregnant. I wanted to find out information to see how many women were on Paxil during pregnancy and if they were able to successfully have healthy babies.
“I am in no way insinuating your product did this to my child. I love the product, and I don’t think I could have gotten through my panic attacks without the wonderful help of this miracle drug. I just want to start to try and get pregnant again soon. I do not want to put my unborn child through anything that would hurt him/her.
“Please, if you do not have this information, where is this information held? Does anyone do studies like this?Please, any information you may give me would be great.Thanks again for your help.”
GSK responded to the mystery woman’s query by certified mail, asking her to sign a form authorizing the release of her medical records to GSK. The letter never reached her—it was returned as “undeliverable” by the US Postal Service. GSK apparently made no further efforts to communicate with her, although they did send a Medwatch report to the FDA, stating that “mother’s concurrent medications and medical conditions were not specified.” An internal GSK document, dated 13 June 2001, stated the link between Paxil and the cardiac defects suffered by the mystery woman’s unborn fetus was “almost certain.”
Lawyers for GSK argued that somebody must have checked the “almost certain” box by mistake. The jury didn’t buy it, and on 29 October 2009 awarded $2.5 million to Lyam Kilker.
Lyam survived, but hardly unscathed. For the rest of his life he will suffer from high blood pressure and diminished energy, and he will need repeat surgeries to replace the grafts covering the holes in his heart.
On 2 July 2012, the United States Department of Justice announced that GlaxoSmithKline had agreed to pay $3 billion to settle claims of illegal marketing of its products, including Paxil—the largest such payout in history. The same day the settlement was announced, the value of GSK shares rose 1.3%.
David Healy is a Professor of Psychiatry at Bangor University and the author of Pharmageddon, and he also testified as an exert witness at the Kilker trial. In a telephone interview he blasted SmithKline Beecham for not following up on early indications that paroxetine could cause birth defects. “They didn’t do what they ought to have done, do the kind of studies that they ought to have done.” He likened their attitude to that of tobacco company executives confronted with evidence of the harm their product could cause: “Let’s not look too closely at this.”
The mystery woman was later identified as Joanne Thomas, and she subsequently filed a wrongful death suit against GSK. On 27 November 2013, the Common Pleas Court of Philadelphia ruled against her on the grounds that the developing fetus (whom she called Ryan) had not reached the age of viability when the pregnancy was terminated. The certificate of fetal death listed Ryan’s gestational age as 21 ¬Ω weeks, whereas 3 days before the pregnancy was terminated, a cardiologist estimated Ryan’s age at 22 weeks. According to Pennsylvania law, a fetus is not considered “viable” until the age of 23 weeks.
Next: Part 4: “Patient safety is our highest concern”
Friday 26 May 2017 14.00 BST Last modified on Saturday 27 May 2017 00.10 BST
My daughter Renske met her boyfriend Samarie on the train. She was heading from the Netherlands to Switzerland; he was an asylum seeker from Benin. They got chatting and exchanged phone numbers. That was how it started. They had a good relationship. He was attentive and they were very respectful towards each other. They spent holidays with me and my wife Lieuwkje.
Just before midnight on 13 April 2011, I saw on the news that a girl had been killed in Baflo, where Renske lived. About an hour later, they showed a picture of the scene, and I recognised her flat. I called the police and said, “I think my daughter is the victim of the incident in Baflo.” At 5am, two officers came to the house and we learned what had happened.
Samarie had picked up a fire extinguisher in the hall and beaten Renske to death. When an officer tried to arrest him, he grabbed his pistol and shot him dead. Samarie was then shot by police five times and taken to hospital. I couldn’t believe it; in the two years that we’d known Samarie, I had never seen him lose his temper. It was so far removed from the man we knew that we couldn’t make sense of it. It was immediately clear to my wife and I that he needed help, and we wanted to try to be there for him; to understand what had happened.
Initially, I thought it was connected to Samarie’s asylum claim. The day before the killing, his final appeal had been rejected and he was told he was being deported. Five weeks later I went to his flat and found a strip of pills. I knew Samarie was taking antidepressants, but I didn’t know what sort. The label said paroxetine, which is a selective serotonin reuptake inhibitor (SSRI), and as a psychologist I knew there are risks associated with it. From talking to Samarie’s psychiatrist, I discovered that he was reducing his dose. I read that in a small number of cases there have been severe side-effects to SSRIs, including outbursts of extreme violence, usually when the dose is being changed.
After a month or two, we contacted his lawyer, but we couldn’t see Samarie because he was still in the prison hospital. We wrote him a letter and he replied saying how sorry he was. In September we visited him for the first time. We wanted to see for ourselves that he was genuinely remorseful. Samarie came into the room in tears, and he and my wife Lieuwkje hugged each other. I shook his hand. We didn’t talk a lot. He was still limping from his injuries.
From then on, we visited once a month. At first, we talked about what had happened with Renske. He said he’d been in a state of anxiety all day and had tried to get help. They had an argument and she tried to stop him walking out; that was when he hit her. When I asked if he had an explanation, he said: “No, you know how much I love her.” The visits allowed us to bear the grief together; it was our way of coping.
The idea of writing a book together came to me in 2014 after Samarie’s trial. He was sentenced to 28 years in prison for double murder. I thought, the circumstances of my daughter’s death are so extraordinary that I need to find a way to put it in words. Renske was a caring, modest young woman. She and Samarie had dreamed of living together one day. As well as losing her, we had lost them as a couple.
Samarie’s sentence was reduced on appeal to five and a half years. Instead of premeditated murder, he was found to have diminished responsibility for the killing of Renske and partial responsibility for the death of the police officer; the appeal court ruled that he had been in a psychotic state. He has now completed his sentence, and been transferred to psychiatric care.
We continue to visit and support Samarie. It’s not about whether we forgive him. What happened can never be erased, for him or for us. I can understand people thinking it’s unbelievable that we can even look each other in the eye, but this is our way of dealing with it. I’ve never thought it was the wrong decision.
Courts are not a place you can make jokes. I started off with a confident pitch:
If you owe a bank a million pounds, you have a problem but if you owe the bank a billion …
I didn’t get much further. It felt like several GSK lawyers popped up, addressing the judge with words to the effect that he’s talking about banking your honor, this is not his area of expertise. The judge accepted their objections and I didn’t get to complete the analogy.
Nobody knew what I was talking about anyway – pounds? What are pounds?
Judge Hart also ruled out the following image. So the jury never got to see it.
A lot of my testimony centered on working through each of the ways to hide the data listed here. The exhibit couldn’t be shown but this is what was covered – in some ways too well. There were documents showing correspondence between GSK and FDA on many of these points leaving the jury wondering whether GSK or FDA were more to blame.
Many of the things that were done were shocking. GSK and other companies dumped withdrawal related suicidal acts into the placebo arm of trials, inflating the risks of placebo and breaching FDA regulations in the process. A good deal of this was so blatant that the jury must have been left wondering whether FDA reviewers were asleep or out to lunch.
Suicidal events were coded under the heading of emotional lability. When a journalist and lawyers independently spotted this coding trick and it became a public issue, emails circulated within FDA asking what emotional lability actually was, and where it had come from. But Andy Bayman for GSK could show the jury the documents sent into FDA which showed suicidal events clearly coded as emotional lability. This naturally cast doubt on whether FDA could have been as ignorant of what was going on as FDA head honchos later claimed to be.
Another egregious trick was the use of patient exposure years. This gives rise to the Space Shuttle fallacy. If you calculate lives lost per miles traveled the Space Shuttle may be the safest means of transport in the universe. But it takes a brave person to go on one.
This is because in terms of exit from and entry to earth’s atmosphere the shuttle is highly risky – just like antidepressants where its the starting and stopping that are the problem. GSK and other companies continued some people who were happy as clams on their paroxetine for lengthy periods of time and mixed these with the patients having difficulties to dilute the problem. All of sudden, per year on treatment, the antidepressants looked safe. This is a legitimate approach for some problems but not for this one.
Another trick was putting suicidal events in a neurological category that also included dizziness and headache. These happen so commonly they drown out the signal from suicidal events.
Every time a maneuver like this was exposed, GSK looked bad. They looked like they owed the jury and the public money – a million dollars. The problem is though, they hold all the data. No one could give the jury the data from these GSK trials and say “here you are – its not rocket science – you work out what this data shows”.
While this is the case GSK effectively owe us Billions and its us who have the problem. They own us. And don’t seem to be under any onus to stop owning us.
But GSK interrupted my efforts to lighten the jury’s day by making this remark. A Court is not a place for this kind of thing.
Saturday 6 May 2017 08.30 BST Last modified on Saturday 6 May 2017 20.51 BST
Sarah never planned to take antidepressants for 14 years. Three years after she began taking them, when she was 21, she went to her GP and asked to stop: 20mg of Seroxat a day had helped her live with anxiety and panic attacks, but she began to feel uncomfortable about being on medication all the time. Her doctor advised her to taper down her medication carefully.
At once, “I was a mess,” she says. “I thought I was losing my mind. My appetite completely went. I lost the best part of two stone. I was anxious constantly. My mouth was dry. It was difficult to sit and be calm.” She became withdrawn, refusing to see friends, and remembers asking her mother to get her a couple of boxes of paracetamol, thinking, “I’m going to have to take all these tablets, because I can’t live like this.”
Sarah’s doctor encouraged her to go back up to 20mg. “Within a week, I was much better. I feel anger when I look back. That wasn’t me relapsing, that was withdrawal. But I was so unwell, I didn’t stop to think, ‘I’ve never had this before.’ I truly thought it was me. Now the only reason I am on the drug is because I am dependent upon it. And that is not good enough.”
Prescriptions of SSRIs (selective serotonin reuptake inhibitors), the most common type of antidepressant, have doubled in the past decade. There are now more than 70m prescriptions dispensed in the UK in a year, the “greatest rise” of any drug in the last year, according to NHS research. But while the side-effects of starting and then withdrawing from these drugs are reasonably well known (the patient information leaflet accompanying the SSRI Seroxat is six pages long), there is very little research into the long-term effects of using antidepressants.
Last year, an all-party parliamentary group began hearing evidence as to whether there is a link between a measurable rise in mental health disability claims – 103% between 1995 and 2014 – and that in antidepressant prescriptions. (Claims for other conditions fell by 35% in the same period.) “We need to have a serious rethink about current levels of prescribing, because it may well be that the drugs are in fact contributing to the disability burden,” Dr Joanna Moncrieff, a consultant psychiatrist and senior lecturer at University College London, told the committee.
Reports both anecdotal and clinical have included side-effects such as constant pain, an altered sense of smell, taste or hearing, visual problems, burning hands and feet; food or drug intolerances and akathisia (the medical term for a deep inner restlessness). When a patient begins tapering down their dosage, these effects are generally ascribed to the drug leaving their system; if it is long after withdrawal is supposed to be over, however, patients are often disbelieved (according to the drug companies, withdrawal should take just two weeks for most people, though they acknowledge that for some it can be months).
Professor David Healy, director of the department of psychological medicine at Cardiff University and author of 22 books on psychopharmacology, believes that antidepressants are overprescribed. “If you go into your average doctor – if you’ve been off the drug for half a year or more – and you complain [of a range of symptoms] and say, ‘I think it’s caused by this pill I was on’, he or she would say, ‘It’s been out of your body for months. You’re neurotic, you’re depressed. All we need to do is put you on another pill.’”
GPs, Healy says, are “relying on your word, and if it’s a choice between believing what you say and relying on what drug companies say to them, they [tend to] believe the drug companies”. Healy, who has been a consultant for, and expert witness against, most of the major pharmaceutical companies, has long argued that long-term side-effects are routinely ignored or misunderstood.
But many experts believe these drugs do more good than harm. “Most of the people I see who have moderate to severe depression benefit from them,” says Daniel Smith, a professor of psychiatry and researcher into bipolar disorder at the University of Glasgow. For some, medication can be no less than “transformative. It can get them through a really critical period of their life.”
However, when it comes to long-term impact, especially after a person stops taking SSRIs, Smith says it can be hard to work out which symptoms relate to the drug use and which to the underlying conditions. “There’s obviously an issue of cause and effect. How can we be certain the SSRI caused it? Depression affects libido and sexual interest. How much [of the reported effects] is depression and/or anxiety symptoms coming back?”
SSRIs have been around for more than 40 years, but grew in popularity in the late 1980s and 90s after pharmaceutical company Eli Lilly launched fluoxetine, otherwise known as Prozac. Time magazine put the drug on its cover twice, asking, “Is Freud finished?” and describing SSRIs as “mental health’s greatest success story”. In 2001, a landmark report on a clinical trial into paroxetine (sold as Seroxat in North America and Paxil in the UK), called Study 329, concluded that it demonstrated “remarkable efficacy and safety”. Study 329 led directly to a massive increase in prescriptions: by 2003, worldwide sales of Seroxat (manufactured by GlaxoSmithKline) were worth £2.7bn.
But concerns were raised about the study –the US food and drug administration (FDA) officer who reviewed the data disagreed with the findings, calling it a failed trial – and in 2015 the British Medical Journal published a re-evaluation. Seven authors went through as many of the thousands of individual case reports as they could, and found not only that “the efficacy of paroxetine… was not statistically or clinically different from placebo”, but that “there were clinically significant increases in harms, including suicidal ideation and behaviour”. The original study reported 265 adverse reactions; the BMJ found 481. The re-evaluation also found that psychiatric responses were grouped together with “dizziness” and “headaches”, rather than given their own category. In 2003, the UK banned the use of Seroxat by anyone under 18; and in 2004 the FDA required a “black box warning” on all antidepressants, its strictest level of patient warning.
“Patient safety is our number one priority,” a GlaxoSmithKline (GSK) spokesperson tells me. “We believe we acted responsibly in researching paroxetine, monitoring its safety once it was approved and updating its labelling as new information became available.”
Many SSRI users report blunted emotions, even long after they have ceased taking pills, and an impact on sexual function. “They should be called anti-sex drugs rather than antidepressant drugs,” says Jon Jureidini, a child psychiatrist of 30 years’ standing, a professor of psychiatry and paediatrics at the University of Adelaide and co-author of the BMJ study, “It’s more reliably predictable that they’re going to get rid of sexual function than it is that they’re going to get rid of depression.” Again, some people find this persists long after they cease taking the drug. One person I spoke to, Kevin, had taken Prozac for six months when he was 18; now 38, he hasn’t had an erection since.
Last September, Healy and colleagues published a further examination of the data gathered for Study 329. This data followed the trial participants for six months after they started taking paroxetine (the “continuation phase”) and while they were tapered off it. GSK, which in 2004 published a clinical study report, had argued that “the long-term safety profile of paroxetine in adolescents appears similar to that reported following short-term dosing”. Healy and co, however, concluded that the “continuation phase did not offer support for longer-term efficacy”. More alarmingly, they found that the taper phase, when patients were being taken off the drugs, was the riskiest of all, showing a “higher proportion of severe adverse events per week of exposure”. This, they said, opens up the risk of a “prescribing cascade”, whereby drug side-effects are thought to be symptoms, so are treated with further drugs, causing further side-effects and further prescriptions – thus increasing the risk of long-term prescription drug-dependency.
In October, the British Medical Association published its response to a two-year fact-finding exercise into long-term use of psychoactive drugs. It noted that while benzodiazepines, z-drugs, opioid and antidepressants are “a key therapeutic tool”, that their use can “often lead to a patient becoming dependent or suffering withdrawal symptoms… the evidence and insight presented to us by many charity and support groups… shows us that the ‘lived experience’ of patients using these medications is too often associated with devastating health and social harms”; it was therefore, the report concluded, a “significant public health issue”.
The BMA made three key recommendations: first, and most urgently, that the UK government establish a 24-hour helpline for prescribed drug dependence; second, that it establish well-resourced specialist support units; and third, that there should be clear guidance on prescription, tapering and withdrawal management (they found the current approach to antidepressants, in particular, to be inconsistent: too many patients were suffering “significant harm”). There are also increasingly urgent calls for studies into long-term effects that are not funded by drug companies, because, Moncrieff says: “We don’t have very much data. This research is really important, but hasn’t been done. It’s a massive blind spot. It’s extraordinary – or maybe, given the pressures and interests at work, not extraordinary at all – that it hasn’t been filled.”
In March this year, members of the BMA, along with MPs and researchers from Roehampton University, went to parliament to lobby Public Health England, armed with research estimating that there are 770,000 long-term users of antidepressants in England alone, at a cost of £44m to the NHS per year (a figure that does not account for the cost of GP appointments, or the impact of side-effects, withdrawal effects and disability payments).
“I think you have to adopt a very conservative approach,” says psychiatrist Jon Jureidini. “These are brain-altering drugs, and our overall experience with brain-altering drugs of all kinds is that they tend to have a detrimental effect on some proportion of people who take them long term. All we know about the benefits is from short-term symptom-reduction studies. The careful prescriber needs to say, ‘Well, in balancing the likely benefits and harms, I need to be very cautious about how much benefit I’m expecting, and I need to be very generous about the possibility that the harms might be more than they appear to be.’”
Quite a few long-term users, such as those I spoke to below (and who wished to be anonymous), would agree.
‘Tapering off is the hardest thing I’ve ever done’:Sarah, 32; has taken Seroxat for 14 years
I was prescribed Seroxat when I was 18, the year I started university. I grew up with a disabled sister, so things at home were very stressful, and I had a history of anxiety and panic attacks. I had counselling, but the problems persisted, so I went back to the GP. I don’t remember everything that was said, but there was no conversation about side-effects.
Within the first two weeks of starting Seroxat, I remember I was sitting in the front room watching TV when out of nowhere I had this intense feeling of heat, like an electric shock. It started in my hands, went all the way up my arms and through to my head.
The GP said it was probably just my body getting used to the drug. And after a few weeks the weird sensations did ease off. I had a fabulous time at university. I still had panic attacks, and there were certain situations I would avoid – as I still do – so it wasn’t a wonder drug, but there were no major problems.
But in 2006 I tried to come off it. There were a couple of Panorama documentaries about the side-effects and I was starting to become concerned. The GP said, “That’s fine, but do it gradually, over three weeks.”
I immediately became incredibly unwell. I thought I was losing my mind. I was going to work, but it was difficult to get through the day. My mouth was so dry, I was constantly drinking water. I had bizarre thoughts – not hallucinations – that were frightening or distressing. I had a strong sense of detachment from reality.
Eventually, the doctor said, “Look, you coming off is obviously not working: we need to get you back to 20mg.” Within a week I was much better.
A few years later, when I realised my mental health was getting worse, even though I was on the medication, I started to do some research, reading case studies about withdrawal. I find it so offensive when a GP says, “This is who you are.” I didn’t have these symptoms 10 years ago. I didn’t have this sense of detachment. I saw various psychiatrists. They just kept saying, “The drug is safe, you need to be on it.” A couple of others told me the reason I was having these problems was because I wasn’t taking enough. Another said, “If you were diabetic, you’d take insulin and you wouldn’t have an issue. Why are you so bothered about taking this drug?”
I’ve been on it since I was 18, so I don’t know who I am without it, as an adult. Who knows? I might have all kinds of problems, but I need to know I’ve tried. Tapering off is the hardest thing I’ve ever done. It’s taken me three years just to get from 20mg to 5mg. I’m no longer with my partner – we were together for six years. I believe Seroxat has played a part: it affected my moods, it made my anxiety worse and, by necessity, I’ve had to be selfish, really. I don’t want to say all my problems are to do with Seroxat, because they’re not. But I do believe that it has caused me harm.
‘I don’t have much of an interest in interacting romantically or physically with the opposite sex’: Jake, 24; took SSRIs for eight years
I had been dealing with symptoms of OCD and anxiety for a lot of my childhood. It’s in my family, affecting two siblings and one parent. I was prescribed Zoloft when I was 12; I took a variety of SSRIs, Zoloft to Prozac to Lexapro, and then two others, for eight years.
Did they help? You know, I can’t really tell you, because I got through school. I got high marks, I had a lot of friends. So, in that sense, they must have helped. That’s the thing: for people with major depression, it’s easy to say, this has a measurable effect. But I kept taking them just because that’s what I’ve always done.
I went to university right out of school. I did very poorly. I had a bit of a breakdown, isolating myself, not sleeping. I was still on medication. I came home and enrolled at a community college. That was my worst period – I was very depressed. And I started to think, “I’ve been on these medications a long time. I’m not doing well – why not get off them?” I don’t recommend this at all to anyone, but I stopped going to a psychiatrist and took myself off.
For months I had trouble sleeping. I was jittery. I had brain zaps. My anxiety was pretty ramped up. I would feel numbness in my extremities – generally my arms. My psychiatrist told me these were just normal withdrawal symptoms, and they’d be gone in four to six weeks: “Anything you feel beyond that is your anxiety and depression returning.” Basically, if you still feel anything beyond this window that the medical community has established, it’s all in your head.
Eventually I went back to school full-time, and I remember doing OK, feeling somewhat better.
I’ve now been drug-free for four years. What’s lasted are the sexual side-effects. They were definitely worse in withdrawal than they had been on the drug, even though I didn’t really realise or understand it at the time, primarily because I started to take SSRIs at 12. While my brother took the same medicine over the same period and had a normal sexual life, I had a lack of sexual interest. I had erections, and I have regularly masturbated my entire life. But I don’t have much of an interest in interacting romantically or physically with the opposite sex.
I didn’t even start thinking about sex until a couple of years ago. It’s almost like I woke up one day and thought, “OK!” I started getting these windows – days or weeks – when normal sexual feelings would appear. But they’re new to me and I don’t know what to do about them. And because I don’t know what to do, I get anxious, and the anxiety kills any feeling – and then I’m anxious because I’ve lost all my feeling.
Online, I’ve come across a big asexual community. Some also took antidepressants; I think there are a lot of people like me out there. I’d like to think that if I keep going to counselling and sleeping and eating properly, I can rectify these things.
In the end, it’s about pros and cons. If you’re lying in bed and can’t get up, is it better to function? If it was up to me, I’d say that, barring extreme circumstances, nobody under 18 should be prescribed these things. Your brain develops around them. Drug companies should be thinking of the long-term effect on people who can’t even consent.
‘If I missed a dose, I’d get shocks down the side of my body’:Chris, 43; has been taking Seroxat for 26 years
I was originally prescribed Seroxat for mild anxiety about my GCSEs. It was 1991, about the time GlaxoSmithKline released Seroxat. I was one of the first people to be given it.
I was prescribed 20mg, the basic dose, to start with. It helped me: I got through school, I went to uni, I went to work. But I had side-effects from the off: profuse sweating, low libido. I’m quite a placid person, but I became aggressive. I never suffered, in the beginning, with the suicidal thoughts that people talk about now, but what I did notice was that if I missed a dose – especially after eight years of taking it – I’d get shocks down the side of my body. I’d be nauseous, my limbs would become weak. I’d be in a constant state of confusion and was very impatient. I couldn’t communicate well with people. I said this to the doctor, and he said, “We’ll up the dose to 40mg.” That was 1998.
The 10 years after that weren’t too bad. I managed to work, as a sales rep, for 18-20 years. But by 2012, by which time I was up to 60mg, I had tried on numerous occasions to withdraw. I tried to go back to 20mg, but my words became slurry, so the doctor put me back up to 60mg.
By the time I was 38, even that wasn’t enough. I tried to take my life. The doctor wouldn’t prescribe a higher dose. I couldn’t do my job, I couldn’t concentrate, I couldn’t drive. A psychiatrist once said to me that coming off Seroxat is harder than quitting heroin. That really hit home.
I have now been unable to work for four years. I’m still seeing a psychiatrist. I’ve also been diagnosed with fibromyalgia: constant tiredness, aches in the neck, and in the lower back and lower limbs. I’m 43 and still live with my mum and dad.
I also have no libido. Since the age of 30, I have had no feelings in that regard whatsoever. I have had relationships, but they’ve all failed. I haven’t been in a relationship for 10 years, which is a long time to go without sex, but I just don’t get the urge.
I don’t really have emotions, to tell you the truth. The drug takes your emotions away. I’m sort of existing, not living.
And when the drugs do work…
‘I wanted to be able to feel good when good things were happening, bad when bad things were happening’
I suppose I was a depression snob. A purist. Why should I take antidepressants? Yes, there was something rubbish about crying all the time, not functioning, being unable to answer simple questions because of the fug in my head. But, hey, at least I was true to myself.
My depression went back to my late teens. I didn’t like to think of myself as depressive, because depressives were losers. And I didn’t think I fitted the bill: I was pretty funny and able, and I could get girlfriends. I guess most depressives don’t think they fit the bill.
It might have been genetic. My dad had paralysing depression, and so did his father. As a young boy, I’d spent three years off school with encephalitis – an inflammation of the brain that is often fatal. Survivors are often left with depression.
I remember as a teenager being on holiday in Greece with friends. The weather was gorgeous, and I thought, “Why can’t it piss down, because then at least I’d have a reason to feel this way?”
That is what I always craved – objectivity. To be able to feel good when good things were happening, to feel bad when bad things were happening. I hated the fact that my feelings rarely correlated to what was going on in my outer world.
In my 20s, I got by. I held down a good job, fell in love, had kids, made friends, had a pretty good life. But things came to a head when my best friend killed herself. I’d find myself weaving in between traffic wondering what the impact would be like. I took a period off work and gratefully accepted my Prozac prescription.
Things had changed since I first rejected them. Prozac looked cool (lovely green-and-white pills) and rock bands wrote great songs about it (even if REM’s Shiny Happy People was supposed to be dystopic). After telling people I was off work with depression, I ended up feeling like a priest at confessional. It turned out that virtually everybody I knew was a depressive and pilling their way out of it; now it was “our secret”.
Initially, Prozac made me feel sick. And then magically, after a couple of weeks, I felt lighter, as if something had been lifted. I could hear questions properly, answer logically, enjoy a sunny day.
My partner said I was transformed. Occasionally, I would try to come off the pills and felt rubbish again – not more rubbish than I had before, but the same. So I returned, and after a while, I thought, “What’s the point of even thinking about coming off the pills if they make life work for me?”
There are times now when I wonder if I weep and fret and withdraw too much, and whether I’m becoming immune to the Prozac. But on balance I think not, because life is still so much better than it was.
If Prozac was no longer working for me, would I stop taking it? Probably. Would I stop taking antidepressants full stop? I doubt it. I’d simply look for another super pill.