PROZAC WITHDRAWAL: Woman Runs Away From Home: Kentucky

Paragraphs six and seven  read:  “Kelsey had been depressed and was taking several medications but decided to quit some of them cold turkey, particularly Prozac, Larry Kelsey said.”

“The sheriff said that Kelsey left with only $80 in cash, and although she has diabetes, she didn’t take any of her medication with her. He added that as of Thursday morning, no one had yet heard from her.”

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PROZAC: Personality Change: Later He Died: England

Paragraph 14 reads:  “In January 2008,
he saw Dr Francis Roberson, of the Ridgeway Medical
Practice in Plympton, Plymouth, complaining of anxiety and panic attacks.
He was prescribed anti-depressant
drugs.”

Later, Mathew saw Dr Stephen Robinson at the same
medical practice, and was prescribed the
anti-depressant fluoextine  [Prozac]  as the original
prescription was causing unpleasant side-effects and had done little to ease his
anxiety.”

Paragraphs 21 through 24 read:  “Mr Swan, of Tern
Gardens, Plympton, Plymouth, said he noticed a change

in Mathew’s behaviour from early in 2008.

He became
more distant, was fidgety and restless and would
fall asleep suddenly. Mr Swan said he also witnessed Mathew suffer a panic
attack in a bank queue.”

He said Mathew also became disillusioned
with his work that he had previously loved,
and had various run-ins with colleagues.”

This, said Mr Swan, was

totally out of character.

http://www.thisisplymouth.co.uk/news/Plymouth-man-died-inhaling-aerosol-gases/article-1320479-detail/article.html

Plymouth man died after inhaling aerosol gases

Tuesday, September 08, 2009, 11:45

5 readers have commented on
this story.
Click
here to read their views.

A TWENTY-TWO-year-old apprentice
electrician who died from inhaling a deodrant aerosol was suffering from
undiagnosed medical condition which meant he was more at risk from the gases in
the can, an inquest heard.

Mathew Burrows was found dead in bed by his
father in Churchdown, Glos, just weeks after he had moved from Plymouth to start
a new life with his dad.

After the tragedy, a pathologist found Mathew
was suffering from Hashimoto’s Thyroiditis, a condition which meant the butane
and propane in the spray were more likely to kill him, the Cheltenham inquest
was told.

Mathew, of Farrant Avenue, Churchdown, Glos, who had a history
of anxiety and panic attacks, was found dead by his father on Sept 14 last
year.

Recording a verdict of accidental death, Gloucestershire coroner
Alan Crickmore said there were a limited number of explanations as to how Mathew
came to inhale the gases.

He said he was sadly drawn to the conclusion
that Mathew inhaled deliberately although he was ‘absolutely satisfied’ this was
not intended to cause harm to himself.

The inquest heard that the day
before he was found dead Mathew had enjoyed a family day out at the Newent Onion
Fayre.

His father, Andrew Burrows, said he found his son’s body under a
duvet when he took him a cup of tea at around 9am.

Later, when a scene of
crime officer and a policeman moved Mathew, an aerosol can of deodorant was
found in the bed.

The inquest heard that Mathew had moved to Gloucester
area from Plymouth to be closer to his girlfriend, Charlotte
Morton.

Described by his mother, Tracy Brown, from Plymouth, as a ‘happy
lad, bright and popular,’ the inquest heard that Mathew had seen his doctor in
November 2007 after suffering palpitations.

Blood tests and an
electro-cardiograph were carried out and found to be normal.

In January
2008, he saw Dr Francis Roberson, of the Ridgeway Medical Practice in Plympton,
Plymouth, complaining of anxiety and panic attacks. He was prescribed
anti-depressant drugs.

Later, Mathew saw Dr Stephen Robinson at the same
medical practice, and was prescribed the anti-depressant fluoextine as the
original prescription was causing unpleasant side-effects and had done little to
ease his anxiety.

Over the next six months, Dr Robinson increased
Mathew’s dosage to 60mg and his condition was improving. Dr Robinson also
referred Mathew to a confidential counselling service for young people, called
The Zone.

After Mathew’s move to the Gloucester area, he was seen by Dr
Tim Macmorland of the Churchdown Surgery on September 4 and they discussed his
anxiety and panic attacks.

Dr Macmorland arranged for Mathew to see the
community psychiatric nurse with a view to future appointments with a
psychiatrist and a psychologist and for a full range of blood tests to be
carried out.

When asked by the coroner whether he had any concerns about
Mathew’s behaviour, Dr Macmorland said: ‘No, I did not. He was looking forward
to his new life in Gloucester. He looked relaxed and talked freely and
openly.’

In a statement read to the inquest, Mrs Brown said her son had
passed the first year of an electrical apprenticeship with distinction. When she
saw him over the August Bank Holiday weekend, he ‘seemed really
settled.’

Witness Michael Swan said he had known Mathew since he was 15
and became very close describing him as his family’s ‘surrogate son.’

Mr
Swan, of Tern Gardens, Plympton, Plymouth, said he noticed a change in Mathew’s
behaviour from early in 2008.

He became more distant, was fidgety and
restless and would fall asleep suddenly. Mr Swan said he also witnessed Mathew
suffer a panic attack in a bank queue.

He said Mathew also became
disillusioned with his work that he had previously loved, and had various
run-ins with colleagues.

This, said Mr Swan, was totally out of
character.

His father, Andrew, told the inquest he left Mathew watching
television at around 10.30pm on Saturday, September 13. They had enjoyed a
family trip to the onion fayre and later they had shared a bottle of wine over
dinner.

The next morning Mr Burrows found his son lying face down on his
bed under the duvet.

He was cold and when he tried to rouse him, there
was no movement or reaction. Mathew was later pronounced dead by
paramedics.

He was such a happy-go-lucky guy. He never demonstrated any
behaviour that would lead him to anything like that,” said Mr
Burrows.

Consultant forensic toxicologist Dr Simon Elliott told the
inquest that analysis of lung, brain and blood tissue revealed the presence of
butane and propane gases used as propellants in aerosol cans and cigarette
lighters.

Dr Elliott said investigation of blood and urine samples
revealed levels of alcohol above the legal drink-drive limit but way below any
fatal concentrations, and the presence of anti-depressant drug fluoextine that
fell within the range that could lead to fatal consequences in some
circumstances.

Dr John McCarthy, a consultant pathologist, said post
mortem examinations revealed that Mr Burrows had been suffering with Hashimoto’s
Thyroiditis, a condition that might simulate the symptoms of a depressive
illness.

Earlier, the inquest had heard from thyroid disease expert Dr
Edward Coombes who said such a condition could make a sufferer at risk of heart
failure.

Dr McCarthy said after studying the toxicology reports it was
more likely than not that the inhalation of butane and propane caused a sudden
cardiac arrest.

The coroner, giving his verdict, said the primary care
Mathew had received in Plymouth and Gloucester was of a high standard and there
had been no diagnostic reason for his thyroid problem to have been
spotted.

Mr Crickmore said the amount of relatively safe anti-depressants
at the lower end of the toxicity scale were not the direct cause of death nor
was the alcohol in his system.

He said that on the balance of
probabilities, it was likely that Mathew inhaled sufficient amounts of butane
and propane to get into his system and he accepted Dr Coombes point that his
heart, sensitised by the thyroiditis, put him at more risk.

Verdict:
Accidental.

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PROZAC: Woman Develops Hypomania: Later Diagnosed as Bipolar as They All Are!

NOTE FROM Ann Blake-Tracy (www.drugawareness.org): This little piece on antidepressant-induced bipolar disorder ends with the following questions: “What about you? If you went to the doctor for depression, were you prescribed an antidepressant alone? Were you asked if you’d ever had “high” moods? Did the antidepressant bring on mania or hypomania?”

When you consider that the rate of diagnosis for Bipolar Disorder increased by 4000% in a recent 10 year period that the numbers of those answering a resounding YES to those questions is VERY HIGH!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

I have publicly stated over and over again and will say it once again, “Antidepressants are the biggest CAUSE of Bipolar Disorder on the planet!”

1. Mania is a continuous series of mild seizures in the brain.

2. Seizures come from over stimulation of the brain.

3. ANTI – depressants, or the opposite of a depressant – a stimulant.

4. The over stimulation of the brain (especially from the shock of abrupt withdrawal from an antidepressant) leads to mania and the diagnosis of Bipolar Disorder.

Fourth sentence reads: “. It takes hindsight to see that what I thought was “normal” behavior in response to Prozac was in fact at least mild hypomania.”

http://bipolar.about.com/b/2009/08/31/bipolar-depression-and-antidepressants.htm

Bipolar Depression and Antidepressants

Monday August 31, 2009

My first psychiatric diagnosis was major depression, and my first psychiatric medication was Prozac. It was prescribed by my GP, not by a psychiatrist. I had a one-week follow-up visit, and then I was turned loose. It takes hindsight to see that what I thought was “normal” behavior in response to Prozac was in fact at least mild hypomania. Someone even called me “the poster child for Prozac.” This was in 1994, and I wasn’t diagnosed with bipolar disorder until 1999, after another antidepressant did a similar thing.

What about you? If you went to the doctor for depression, were you prescribed an antidepressant alone? Were you asked if you’d ever had “high” moods? Did the antidepressant bring on mania or hypomania?

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PAXIL TRIAL: Glaxo Executive’s Memo Suggested Burying Drug Studies (Update4)

An executive of GlaxoSmithKline Plc, the world’s second-biggest drugmaker, talked about burying negative studies linking its antidepressant drug Paxil to birth defects, according to a company memo introduced at a trial.
“If neg, results can bury,” Glaxo executive Bonnie Rossello wrote in a 1997 memo on what the company would do if forced to conduct animal studies on the drug. The memo was read during opening statements in the trial of a lawsuit brought by the family of a child born with heart defects.

The Philadelphia trial is the first of more than 600 cases alleging that London-based Glaxo knew Paxil caused birth defects and hid those risks to pump up profits.

NOTE BY Ann Blake-Tracy (www.drugawareness.org): In my small church congregation in Utah (maybe 100 families) there were two cases of SSRIs birth defects that I was aware of. In one case the mother was on Paxil and the other was a mother on Prozac. Both babies had to have heart surgery at birth or not long after. Because of that the number of 600 cases that have been filed is no surprise to me at all other than the number seems small in comparrison.

http://www.bloomberg.com/apps/news?pid=20670001&sid=ae8Ie3hNoafw

Glaxo Executive’s Memo Suggested Burying Drug Studies (Update4)
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By Jef Feeley and Margaret Cronin Fisk

Sept. 15 (Bloomberg) — An executive of GlaxoSmithKline Plc, the world’s second-biggest drugmaker, talked about burying negative studies linking its antidepressant drug Paxil to birth defects, according to a company memo introduced at a trial.

“If neg, results can bury,” Glaxo executive Bonnie Rossello wrote in a 1997 memo on what the company would do if forced to conduct animal studies on the drug. The memo was read during opening statements in the trial of a lawsuit brought by the family of a child born with heart defects.

The Philadelphia trial is the first of more than 600 cases alleging that London-based Glaxo knew Paxil caused birth defects and hid those risks to pump up profits. The drug, approved for U.S. use in 1992, generated about $942 million in sales last year, 2.1 percent of Glaxo’s total revenue.

The family of Lyam Kilker claims Glaxo withheld information from consumers and regulators about the risk of birth defects and failed to properly test Paxil. Kilker’s mother, Michelle David, blames Paxil for causing life-threatening heart defects in her 3-year-old son.

Glaxo officials urged scientists to withhold information about Paxil’s risks from a paper laying out the company’s “core safety philosophy” for the drug, said Sean Tracey, a lawyer for Kilker and David, in his opening statement in the trial.

“They said if there’s any doubt, take it out,” Tracey told jurors. “They do not want to scare anybody. It’s a very competitive marketplace. It’s a multibillion-dollar industry.”

‘Rare Thing’

Glaxo executives contend that the boy’s heart defect wasn’t caused by Paxil, Chilton Varner, one of the company’s lawyers, told jurors today in her opening statement. In court filings, Glaxo has said it appropriately tested and marketed the antidepressant drug.

“When Lyam Kilker was born in 2005, GSK had not received notice” of his specific type of heart defect in connection with Paxil use, Varner said. “The numbers will tell you the defect is a rare thing.”

The Paxil label at that time reported about animal studies, “including the rate of deaths,” she said.

Glaxo didn’t target pregnant women and its sales force didn’t use strong-arm tactics to push prescriptions, Varner said. “Whatever the marketing was, it played no role in Ms. David’s doctors’ decision to prescribe Paxil or Ms. David’s decision” to take the drug, she said.

Rat Studies

Glaxo officials purchased the compound sold as Paxil from a Danish company that had done animal studies showing young rats died after taking low doses of the drug, Tracey said in his opening statement.

One of the company’s scientists noted in internal documents in 1980 that information in the rat studies suggested Paxil “could be” a cause of birth defects, Tracey said. Still, the drugmaker refused for almost 20 years to do studies on why the young rats died, he added.

Tracey told jurors they would see documents in the trial that the company hadn’t turned over to regulators or congressional investigators. “You are going to see docs that have never seen light of day before,” he said.

For example, Tracey pointed to a 1998 internal review by Glaxo of all reports of side effects tied to Paxil and officials found “an alarmingly high number” of birth-defect reports. Even with those concerns, the report was never turned over to the U.S. Food and Drug Administration and “the alarming language” was deleted from it, the lawyer said.

In 2001, the company received a letter from a woman who used Paxil during her pregnancy and decided to abort her fetus after tests showed it had birth defects, Tracey said.

Internal Report

In analyzing the woman’s case, Glaxo officials concluded in an internal report that it was “almost certain” the fetus’s birth defects were caused by his mother’s Paxil use, the family’s lawyer added. Still, the company didn’t turn over its analysis to the FDA or beef up the drug’s warning label, Tracey said.

It wasn’t until after the FDA ordered Glaxo and other makers of antidepressants in 2003 to do more safety studies on their products that Glaxo officials publicly acknowledged that Paxil increased the risk of birth defects, Tracey said.

The lawyer for David, a college nursing student who was a former cheerleader for the National Basketball Association’s Philadelphia 76ers, told jurors that Glaxo hid Paxil’s problems to protect its profits.

Paxil is “the No. 1 asset to this day this company has ever owned,” the attorney said.

‘Quite Different’

Varner said she will present “quite different” evidence on animal tests tied to Paxil.

“The animal testing did not suggest Paxil caused birth defects,” Varner said. The FDA considered the tests when it approved the drug for use by U.S. consumers in 1992, she said.

When Glaxo officials considered offering Paxil for sale in Japan, internal records show executives worried in 1994 they might have to do more safety testing on the antidepressant, said Dr. David Healy, an Irish psychiatrist testifying as an expert for Kilker’s family in the case.

It may be the “type of study we wish to avoid,” Jenny Greenhorn, an official in Glaxo’s international regulatory affairs unit, said in a memo.

Glaxo also is fighting suits in the U.S., Canada and the U.K. over claims that Paxil, also known by the generic name paroxetine, causes homicidal and suicidal behavior. The company has settled some suicide claims, though terms of the settlements haven’t been released.

New York Settlement

In 2004, the drugmaker agreed to pay the state of New York $2.5 million to resolve claims that officials suppressed research showing Paxil may increase suicide risk in young people. The settlement also required Glaxo to publicly disclose the studies.

The company’s provision for legal and other non-tax disputes as of June 30 was 1.7 billion pounds ($2.8 billion), the company said in a July 22 regulatory filing that didn’t mention the Paxil litigation.

“We do not disclose our legal reserves for any specific litigation matter,” Glaxo spokesman Kevin Colgan said earlier this month.

Glaxo American depositary receipts, each representing two ordinary shares, fell 68 cents, or 1.7 percent, to $38.76 in New York Stock Exchange composite trading today. Glaxo fell 14 pence, or 1.2 percent, to 1,175.5 pence in London.

The case is Kilker v. SmithKline Beecham Corp. dba GlaxoSmithKline, 2007-001813, Court of Common Pleas, Philadelphia County, Pennsylvania.

To contact the reporters on this story: Jef Feeley in Philadelphia jfeeley@bloomberg.net; Margaret Cronin Fisk in Southfield, Michigan, at mcfisk@bloomberg.net.

Last Updated: September 15, 2009 17:03 EDT

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PROZAC: Woman Threatens State Patrolman: Missouri

HOW SAD!!! Reminds me of a talk I had with parents in Louisiana just last week who are completely overwhelmed dealing with a daughter with similar problems – ALL BECAUSE OF THE WIDESPREAD PRESCRIBING OF THESE DEADLY AND VERY ADDICTIVE PRESCRIPTION DRUGS!!!! They know she can get them from just about any doctor around.
Doctors have truly become our biggest drug pushers in this country! What on earth are we doing to our children?!!! How can so many families be left alone to deal with this – never knowing from one minute to the next if they are going to find their child unresponsive and dying due to yet another overdose of these drugs?
This country is in SO MUCH trouble and it has NOTHING to do with any outside threat to our nation – it is within.
Ann Blake-Tracy, Executive Director,
International Coalition for Drug Awareness
Author: Prozac (ETC): Panacea or Pandora? – Our
Serotonin Nightmare! & Audio: Help! I Can’t Get Off
My Antidepressant/Antipsychotic, ect. ()
Paragraphs three & four read:  “According to the criminal complaint, when Parsley made contact with West  ‘her speech was slurred and her eyes were bloodshot and glassy.’  He adds that he did not notice an odor of intoxicants on her.”SSRI Stories note:  “

 

“West reportedly admitted she had taken Xanax and Prozac at 6 a.m. After failing sobriety tests, West was placed under arrest.”

Hostility”  is listed as an Infrequent, but not Rare, reaction to Prozac in the Physicians Desk Reference.

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Lori White – Prozac for 2 1/2 years

Hi, my name is Lori White. I live in Sandy, Utah, and am a mother of 5 children, and grandmother of 7.

After being married for 12 years, I became a single mom for the next 9 years, during which time I had 4 teenagers at the same time. Depression runs in my family, and after a very difficult divorce, I found myself spending a lot of time in bed, especially when the children were in school. It was hard to cope with life, and I cried easily and found it difficult to stop crying.

Eventually I found a wonderful man and remarried, but every time there was a problem with one of the children, I would sink back into a depression. If I dropped the children off at school and one of them said, “Duh, Mom!” , I would shrink into myself, feel very incapable, and wonder what I had done to have my children hate me so much!

My doctor took pity on me, and put me on Prozac 8 years ago. When I was on the medication, I felt wonderful! I had NO problems!! And neither did anyone else! I was not affected by anyone else’s sad life or situations, and didn’t, couldn’t, cry.

After being on the medication for 6 years, I was introduced to a wonderful product, Classic, made by the Reliv company. After taking it for 6 months, I decided to go off the Prozac, which I did over a 3 week period. I found that I could cry again, could sympathize with others, and feel sad, but it didn’t last–I could stop crying, and I could feel happy again when I chose to.

I have been off Prozac now for 2 1/2 years, and just don’t have the cloud of gloom sitting on my shoulder that I had before going on it. When something sad or difficult happens in my life, it doesn’t bury me–I may cry, go to bed really feeling down, but when I wake up in the morning, I am fine–able to cope and put the problem in perspective.

Sincerely,
Lori

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Antidepressant Romance Fuels “Premedicated” Murder

Note From Ann Blake-Tracy: I must say that in the 20 years I have been specializing in adverse reactions to antidepressants and lecturing and writing about these drugs this is possibly the best article I have ever read on the overall problem with antidepressants!! EXCELLENT WORK!!!
The only thing I might have added is that the hypothesis behind the serotonin THEORY (everyone keeps forgetting it is a theory and not a fact) is backwards. According to research serotonin is elevated in depression, anxiety, violence, mania, psychosis, etc. NOT low. What is low is the ability to metabolize serotonin.
Now enjoy the article! As I said, it is excellent!!
Dr. Ann Blake-Tracy, Executive Director,
International Coalition for Drug Awareness

Website: www.drugawareness.org & www.ssristories.drugawareness.org
Author: Prozac: Panacea or Pandora? – Our Serotonin Nightmare
& CD or audio tape on safe withdrawal: “Help! I Can’t Get
Off My Antidepressant!”
Order Number:

August 17th, 2009

From The Desk of The People’s Chemist:

Are antidepressant’s a silent killer? Read more to learn how to avoid “Premedicated Murder.” Then visit my blog at http://www.thepeopleschemist.com/blog to leave your comments. I want to hear your voices on this! This is one of the most important articles I’ve ever written. Invest 6 minutes into your health by reading this.

Antidepressant Romance Fuels “Premedicated” Murder

By Shane “The People’s Chemist” Ellison

I wish medicine wasn’t so damn complicated. If it weren’t, people would see how Big Pharma cleverly plays prescription cupid to hook the masses into an antidepressant romance. Fueled by dreamy ads, sexy actors, and medical experts who get paid to give pharmaceutical fellatio, the romance has grown into a full-fledged orgy.

Antidepressants are among the best selling drugs, yet not one single diagnostic test supports their effectiveness. Romance makes for great business. But, are patients getting the love they deserve or are they facing another life threatening disaster akin to the Vioxx fiasco (killing an estimated 30,000 people who could have just used aspirin)? Perhaps the chemical facts behind antidepressants will give way to reality and help Americans sever ties to the deadly affair.

Life can be a bitch at times. Everyone knows it and Big Pharma profits from it. To answer our cries for happiness, they sell us a slew of molecules ripe with supposed happy atoms purported to elicit wanton pleasure. It’s a pipe dream. Like a parent who doesn’t like their daughter dating drug reps or psychiatrists, the FDA started using Black Box Warnings to inform us that, “Antidepressants, compared to placebo, increase the risk of suicidal thinking and behavior in children in short term studies.” Psychiatrists quickly refuted this.

Massaging our fears, Dr. McAllister-Williams of the Institute of Neuroscience at Newcastle University publicly insisted that “I believe they work and have an acceptable risk: benefit ratio for many patients.” Taking his cue, psychiatrists from around the world did what they do best: Ignore scientific ethics and get on their knees for Big Pharma.

In a vulgar display of medical ineptitude, prescribing habits surged. From 1996 to 2006, use of antidepressants increased 50% among children, 73% among adults and a ghastly 100% among the elderly – so much for Black Box Warnings. Why not rename them Profit Warnings? As prescribing habits have surged, so has antidepressant reality.

The so called disease of a “serotonin” chemical imbalance among depressed patients has never been proven. The Journal of Psychiatry and Neuroscience recently reminded doctors that, “Brain serotonin cannot be directly measured” and that even in the deceased, “Serotonin levels are unstable, within 24 hours of death.” Therefore, “direct evidence that serotonin is low in depressed persons is unavailable.”

Panicked, psychiatry hypothesized yet another cause of a chemical imbalance: Bad genes. Apparently, select people (basically anyone with a heartbeat) have a defective gene that makes them susceptible to depression – and drugs, drugs and more drugs can save them from the scourge of sadness. Bio-babble like “alleles” and “transporter genes” were thrown around like condoms at a high school pep rally. The jargon confused everyone. And in their dizzy stupor, most were convinced that it must mean one thing: antidepressants are the Holy Grail to attaining happiness. Psychiatry was once again renewed with the stench of pharmaceutical pheromones. But it didn’t last.

Thanks to scientific methodology, the industry was slapped with the facts. The New York Times delivered the blow and wrote, “One of the most celebrated findings in modern psychiatry – that a single gene helps determine one’s risk of depression in response to a divorce, a lost job or another serious reversal – has not held up to scientific scrutiny.”

You don’t need science to disprove the antiquated, reductionist propaganda surrounding the chemical imbalance theory. You only need the common sense of a child.

The human brain floats in thousands, billions or maybe even trillions of brain chemicals – all working in orchestra like unison to confer proper brain function. Even serotonin exists not as a single molecule, but instead as an ever changing chemical cascade of 5-htp, niacin, L-tryptophan, quinolinate, kynurenine and more. You’d have to be Paris Hilton or a psychiatrist to miss this logic and adhere to the simplistic serotonin imbalance theory.

With no such thing as a chemical imbalance or “depression inducing genes,” psychiatry did what any organization would do in the face of impending demise: Get the U.S Government to do their dirty work.

Today, an insidious collusion between Big Pharma and Big Government is doling out drugs paid for by our tax dollars to foster children, to our U.S. Troops, and to the elderly at breakneck speeds. With so many being drugged, a harsh reality is emerging: Antidepressant romance fuels “premedicated murder.”

While researching my upcoming book, Over-The-Counter Natural Cures (SourceBooks, October), I uncovered stories of horrific suicide and rage that occurred after being medicated with antidepressants. But none more disturbing than the Chris Wood story. Doped up on his prescribed cocktail of antidepressants – all three of them – he shot his 33 year old wife Francie and their three children – Chandler, 5, Gavin, 4, and Fiona, 2. Shockingly, in his drug damaged mind, they weren’t “dead enough” and gruesome decapitation followed. Afterwards, he picked up a shotgun and killed himself. This isn’t an isolated incident.

Among our US troop, suicide and rage is at an all time high – in direct correlation to mass prescribing. The same trend exists among teens as seen by the ever growing act of spraying classmates with bullets. Psychiatrists don’t seem to be alarmed with these trends, or at all interested in seeing the obvious correlations. In an attempt to “leave no American un-medicated,” they encourage subjective mental screening tests for the rest of us as a means of converting healthy people into psychiatric patients.

Psychiatry wants to position antidepressants as the cure for the premedicated violence. So to counter the growing evidence that their drugs are the cause, they insist that, “The only evidence that would be acceptable is the demonstration in a double blind trial that a difference in suicide rates was consistently seen. There is no evidence at all for a differential suicide attempt rate with antidepressants. Suicidal thoughts are an integral part of depression.” Here comes the backhand.

Writing for the Journal of American Physicians and Surgeons, Dr. Joel Kauffman elucidates that combined clinical trials on antidepressants show five times the risk of suicide among the treated compared to placebo.

The suicide/aggression trend is not inexplicable from a chemistry viewpoint. Using the latest cloning techniques and laboratory methods, it’s been shown that antidepressants elicit “neurotransmitter hijacking.” This may be partially responsible for the mental state that causes a person to gruesomely murder their loved ones, then put a shotgun to their chin and pull the trigger.

Once swallowed, antidepressants sail past the blood brain barrier and congregate on top of “neurotransmitter recyclers.” This can prevent the cellular “recycling factories” from activating previously used neurotransmitters like serotonin or any of its chemical cousins. With nowhere to go, the inactive brain compounds get “hijacked” by recycling facilities found in other regions of the brain. This would be similar to a square peg being shoved into a round hole. As shown by Baylor College of Medicine, the recycling facilities of key neurotransmitters, like dopamine (round), begin to retrieve serotonin (square) into dopamine vesicles. A dastardly consequence ensues.

Commenting on the hijacking, CNN publicized that, “Antidepressant drugs actually create a perilous brain imbalance.” And Psychiatric Times hypothesized that blocking transporters on cell bodies could drop neurotransmitter levels in the synapse. Is it true?

To measure if neurotransmitter hijacking leads to an empty synapse, you can simply look for clinical manifestations of poor neurotransmitter function (like Parkinson’s disease, which is due to poor output of dopamine) among antidepressant users. As far back as 1995, the American Journal of Medicine showed that 37% of all prescriptions for the treatment of Parkinson’s disease are due to Psychiatric drug use. Case closed. These antidepressant actions are the exact opposite of the claimed “neurotransmitter boosting” actions purported by most doctors!

Once neurotransmitter hijacking takes place, pharmacopossession (due to poor neurotransmitter function) may also set in. As patients come fully under the spell of antidepressants, the brain can become so scrambled that all normal reality and reason are overwritten by a new confusing and violent agenda. A new personality arises – one with homicidal and suicidal tendencies. And for an ever increasing number of antidepressant users, these tendencies are manifesting as premedicated murder – the deliberate killing as a result of being medicated in advance.

Unbalanced by drugs, the brain of an antidepressant user faces a slew of mind altering outcomes. What kind? What was Chris Wood thinking and feeling prior to committing premedicated murder of his family while pharmacopossessed? To answer these questions just go back to the beginning of this article and read the “profit warning” that comes with every Prozac prescription. It’s all there in black and white.

Even though the FDA “compels” drug companies to warn the public about antidepressant risks, their “death grip” on the medical industry has kept doctors and patients from knowing the real extent of the danger. Dr. Catherine DeAngelis, editor of the Journal of the American Medical Association said that “Pharma’s influence on medicine is so blatant now you’d have to be deaf, blind and dumb not to see it.” I guess psychiatrists are all three since they continue to ignore science and romance the masses with promises of happiness courtesy of antidepressants.

Before your doctor gives you an antidepressant, ask him to read you the Black Box Warning that comes with your prescription. This will ensure that the potential romance quickly gives way to reality and that you don’t succumb to premedicated murder.

About the Author

Shane Ellison’s entire career has been dedicated to the study of molecules – how they give life and how they take from it. He was a two-time recipient of the prestigious Howard Hughes Medical Institute Research Grant for his research in biochemistry and physiology. He is a best selling author, holds a master’s degree in organic chemistry, and has first-hand experience in drug design. Learn to get lean fast like is Mom (photos included) at http://www.ampmfatloss.com

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ANTIDEPRESSANTS: Murder-Suicide: 81 Year Old Man Kills Wife & Self: En…

Note From Ann Blake-Tracy: I do not know if I can tolerate reading another one of these stories!
This last week I went to the Iowa State Fair for the first time with my daughter and her family who were visiting. While riding the trolley through the fair the man sitting across from me asked an elderly couple as they got off how many years they had been together.
They answered that it was 53 years. And he wished them the best for their next 53 years together.
They smiled and said “Thank you.”
As we drove on I looked at the man across from me and said, “As long as neither of them take an antidepressant they should do okay.” And I went on to share with them how many of the absolutely horrifying reports we are getting of elderly couples, married for many years, killing one another.
I then returned home to open this report of yet another horrific tragedy for a couple who had been married a few years longer than the couple I had just met on the trolley  . . . there is just no excuse for this to continue! How sad! I is NORMAL for a man who has worked all of his life to become depressed if he has to sell his business. It is NOT a reason to medicate him!
What an absolutely horrific way to end a life of 60 years together. I hope their children know what really happened in the loss of their parents instead of one woman I met after one of my lectures who came forward crying. As she reached me she said, “I cannot thank you enough for helping me to finally have answers to why my father killed my mother and then himself 20 years ago while taking one of the older antidepressants!”
Dr. Ann Blake-Tracy, Executive Director,
International Coalition for Drug Awareness

Website: www.drugawareness.org & www.ssristories.drugawareness.org
Author: Prozac: Panacea or Pandora? – Our Serotonin Nightmare
& CD or audio tape on safe withdrawal: “Help! I Can’t Get
Off My Antidepressant!”
Order Number:

Paragraph seven reads:  “The court heard how Mr Mann became depressed after he sold his business in 2000 and from 2002 to 2005 was placed on anti-depressants, and again in 2008 after a reoccurrence of the mental illness.”

http://www.yorkshireeveningpost.co.uk/news/Depressed-pensioner-bludgeoned-wife-to.5548006.jp

Depressed pensioner bludgeoned wife to death before drowning himself

Published Date:
12 August 2009
By Charles Heslett

A pensioner bludgeoned his wife of almost 60 years to death before drowning himself in the bath.

Police discovered the body of retired sales rep Doreen Mann, 80, sprawled in the living room of the house she shared with husband Kenneth.

The retired factory owner, 81, was found dead upstairs face down in a bath full water wearing only his vest and underpants.

Officers took away a hammer, a craft knife and another knife from the scene at Foxroyd Lane, Thornhill Edge, Dewsbury, after the alarm was raised by a visiting mental health nurse on December 23 last year (2008].

An investigation was launched at the time by West Yorkshire Police’s Homicide & Murder Inquiry Team.

But Detective Sergeant Ian Lawrie told Wednesday’s inquest at Huddersfield Coroner’s Court that no-one else was being sought in connection with the death of the couple, who were both born in Leeds and had been married for 57 years.

The court heard how Mr Mann became depressed after he sold his business in 2000 and from 2002 to 2005 was placed on anti-depressants, and again in 2008 after a reoccurance of the mental illness.

On December 18, 2008, he and his wife were visited by psychiatrist Dr Vinood Shukla and a psychiatric nurse, the court heard.

A psychiatric nurse came to the red-bricked home called Kendoreen, where the couple had lived for 21 years, at 2.30pm on December 23.

After getting no answer from the front door apart from the couple’s barking collie dog, the nurse saw a bathroom light on and called police.

Detectives found the two knives and the hammer close to Mrs Mann’s body.

Her cause of death was later found to be a blow to her head and cut wounds to her neck and forearms.

Mr Mann’s corpse was found in an upstairs bathroom, face down in a full bath – his cause of death was given as self-drowning.

Barbara Moore told the inquest three weeks before her sister’s death Doreen had said she feared her husband might harm her.

West Yorkshire Coroner Roger Whittaker described the deaths as a “double tragedy”.

He recorded a verdict that Mrs Mann was unlawfully killed and that her husband drowned.

Mr Whittaker said he was satisfied that the balance of Mr Mann’s mind was disturbed at the time of his death and “that imbalance…was present at the time of the death of his wife“.

Mr Whittaker added that Mr Mann had given no indication on December 18 that he intended to harm his wife and that Mrs Mann had raised no similar concerns.

But the coroner said lessons “had been learned” by the mental health trust involved.

A South West Yorkshire Partnership NHS Foundation Trust spokeswoman said: “The Trust re-iterates its sincere sympathies to the family and others affected by these tragic deaths.

“The circumstances have been thoroughly investigated, and we are grateful to the family for their input into this.

“Sadly, we cannot change the tragic events that happened but we can learn from them and a number of changes have been made as a result.”

These included: Improved systems for referrals between services and exchange of information; Improved training for staff on assessing risk; Improved record keeping following home visits.

The spokeswoman added: “The investigation findings have been shared with the family and we are continuing to offer support as appropriate.”

The full article contains 574 words and appears in n/a newspaper.
Page 1 of 1

  • Last Updated: 12 August 2009 4:14 PM
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  • Location: Leeds

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Kauffman Study – (SSRI) Drugs: More Risks Than Benefits?

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009

SSRI Bombshell by Joel M. Kauffman, Ph.D. Tuesday, March 31st, 2009

Selective Serotonin Reuptake Inhibitor (SSRI) Drugs: More Risks Than Benefits?

Joel M. Kauffman, Ph.D.

ABSTRACT

Anecdotal reports have suggested that selective serotonin reuptake inhibitors (SSRIs) may cause suicidal or violent behavior in some patients. Because of the publicity surrounding certain events, and the numerous lawsuits that have been filed, a review of benefits and risks is needed.

At most 30% of patients receive a benefit from SSRIs beyond the large placebo effect in certain mental conditions, especially depression, according to a recent meta-analysis of published trials. An equally recent meta-analysis of all SSRI trials submitted to the FDA showed a small benefit for the severely depressed patients only. Many early unpublished trials did not show any benefit. Adverse effects are common, occurring in up to 75% of subjects.

Severe adverse effects may be underreported.

Meta- analyses of controlled trials did not include any actual suicides or murders, but only suicidality, some finding, in 1991 and 2007, no evidence even of suicidality.

Other meta-analyses using many of the same trials found that suicidality doubled to 1 in 500 on SSRIs compared with placebo or non-SSRI antidepressants, but did not include any actual suicides or murders. The trial designs were devised by SSRI makers to prevent reports of suicides, by eliminating subjects with the slightest trace of suicidal tendencies. Retrospective studies by others showed actual suicides on SSRIs with a relative risk (RR) of 2–3 compared with non-SSRI antidepressants, with an increased incidence of 123/100,000. Lower doses than the smallest available ones were found to maintain benefits in a majority of patients while reducing risks.

table_03_zoloftbusted1

[PLEASE NOTE THAT THE SSRISTORIES DATABASE REFERRED TO BY DR. KAUFFMAN IN THIS STUDY IS NO LONGER POSTED AT THE URL LISTED ABOVE BUT HAS BEEN MOVED TO THE URL www.ssristories.NET ]

No causal connection between SSRIs and suicide and/or violence has been proved; neither has it been ruled out. Physicians need to be vigilant, and aware of legal precedents that may subject them to enhanced liability when prescribing these drugs. The Genesis of SSRIs Fluoxetine (Prozac in the U.S., see Table 1), introduced in 1988 to combat depression, was the fourth selective serotonin reuptake inhibitor (SSRI) on the U.S. market, after being seriously considered by Eli Lilly as an antihypertensive drug. Unlike the earlier “tricyclics” (amitripyline, clomipramine, dothiepin, imipramine, etc.) and other drug classes, SSRIs acted on the brain to raise levels of the neurotransmitter serotonin without raising the levels of norepinephrine. This was thought to be a benefit in treatment of depression, and later anxiety, panic, social phobia, obsessive- compulsive disorder (OCD) , and many other conditions. The SSRIs listed in Table 1 are among the most frequently prescribed in the U.S., and compete with the five non- SSRIs shown, and others.

ssri-drug-table1

Benefits of SSRIs

A prominent recent meta-analysis of Bridge et al. included 27 trials of SSRIs for three defined mental conditions: major depressive disorder (MDD), OCD, and non-OCD anxiety disorders. Benefits, compared with placebo, were found to be highly statistically significant. For MDD, data from 13 trials showed benefit in 61% vs. 50% on placebo, a gain of 11% absolute (NNT=10), <0.001 for all ages of participants. For OCD, data from six trials showed benefit in 52% vs. 32% on placebo, a gain of 20% absolute (NNT=5), <0.001 for all ages. For non-OCD anxiety, data from 6 trials showed benefit in 69% vs. 39% on placebo, a gain of 30% absolute (NNT=3), <0.001 for all ages. These results represent the maximum expectation of benefit from SSRIs since 22 of the 27 trials were financially supported by SSRI makers, and thus subject to the routinely positive bias of industry-sponsored clinical trials. Jay S. Cohen, M.D., author of the 2001 book , wrote that half his patients did well on fluoxetine, but he noted a high incidence (50%) with side-effects. Cohen also cited a pre-approval study showing that the standard 20 mg per day starting dose helped 65% of patients, while 5 mg helped 54%, so Cohen became one of the pioneers in using lower doses before Lilly made them available. The 1996 entry for paroxetine, at least, confirmed that the 17 most common side-effects were dose-dependent.

In four observational cohort studies of four common SSRIs reported by physicians as part of the prescription-event monitoring program in the UK, with more than 10,000 patients in each drug group, only 36% of the physicians reported fluvoxamine as effective, compared with 60% for fluoxetine, sertraline, and paroxetine. These possible benefit rates, which include the placebo effect, parallel the percentage of patients remaining on the drug for 2 months.

See: Over Dose: the Case Against the Drug Companies

An old trial of placebo for anxious and depressed subjects reduced distress in 43%. Three meta-analyses of the antidepressant literature that appeared in the 1990s independently concluded that two-thirds of the effectiveness attributed to SSRIs is actually placebo effect. In a series of nine controlled studies on hospitalized patients with depression, 57% of those given placebo showed improvement in 2–6 weeks. A 1998 meta-analysis of 47 trials on antidepressant medication including SSRIs indicated that 75% of the response to them was duplicated by placebo. This meta-analysis was criticized on several grounds. Therefore, Irving Kirsch, Ph.D., of the University of Connecticut, with other authors, obtained data submitted to the FDA on every placebo-controlled clinical trial on the six most widely used SSRIs, and published a meta-analysis on 47 trials, finding a small, clinically insignificant effect.

This work was updated in 2008:

Analyses of datasets including unpublished as well as published clinical trials reveal smaller effects that fall well below recommended criteria for clinical effectiveness. Specifically, a meta-analysis of clinical trial data submitted to the U.S. Food and Drug Administration (FDA) revealed a mean drug–placebo difference in improvement scores of 1.80 points on the Hamilton Rating Scale of Depression (HRSD), whereas the National Institute for Clinical Excellence (NICE) used a drug–placebo difference of three points as a criterion for clinical significance when establishing guidelines for the treatment of depression in the United Kingdom. Kirsch et al. concluded that the updated findings from 35 carefully vetted trials suggest that, compared with placebo, the four new- generation antidepressants ( fluoxetine, venlfaxine, nefazodone, and paroxetine) do not produce clinically significant improvements in depression in patients who initially have moderate or even severe depression.

They show statistically significant but clinically minor effects only in the most severely depressed patients. Moreover, the significance of the effect probably is based on a decreased responsiveness to placebo, rather than increased responsiveness to medication. Given these results, the researchers conclude that there is little reason to prescribe new- generation antidepressant medications to any but the most severely depressed patients unless alternative treatments have been ineffective. In addition, they write that the decreased placebo response in extremely depressed patients, combined with a response to antidepressants comparable to that of less severely depressed patients, is a potentially important insight that should be investigated further.

Even these unimpressive findings exaggerated the benefits of antidepressants. In three fluoxetine trials and in the three sertraline trials for which data were reported, the protocol allowed replacement of patients who, in the investigators’ judgment, were not improving after 2 weeks. The trials also included a 1–2 week washout period, during which patients were given a placebo prior to randomization. Those whose scores improved 20% or more were excluded from the study. In 25 trials, the use of other psychoactive medication was reported. In most trials, a chloral hydrate sedative was permitted in doses ranging from 500 mg to 2,000 mg per day. Other psychoactive medication was usually prohibited but still reported as having been taken in several trials.

Perhaps such considerations led David Healy, M.D., an SSRI expert, to his conclusion that “…these drugs do not convincingly work….” His evidence came from early unpublished clinical trials whose results were revealed to him at FDA hearings. For fluoxetine, Healy noted four trials with a positive result and four without. For sertraline, only one of five early studies showed benefit. Because of the huge placebo effect, 32–75%, most physicians unfamiliar with the studies revealing this effect are likely, in my opinion, to say that one-third to two-thirds of their patients are improved on SSRIs. This would also explain Dr. Jay S. Cohen’s findings on lower doses of fluoxetine.

SSRIs reportedly interact with 40 other drugs to cause “serotonin syndrome.”

This presents as twitching, tremors, rigidity, fever, confusion, or agitation. Serotonin/norepinephrine reuptake inhibitors (SNRIs) also may cause serotonin syndrome by interactions. Most tricyclic depressants do not have these interactions, with the exception of amitriptyline.

In a controlled trial of paroxetine vs. clomipramine sponsored by GlaxoSmithKline, 75% of the subjects had an adverse effect on paroxetine, 21% had a severe adverse effect, and 13% committed a suicidal act (1 in 8). The 1996 entry for paroxetine lists 17 side-effects with an incidence of ≥ 5% for approved doses.

They are: asthenia, sweating, constipation, decreased appetite, diarrhea (up to 15%), dry mouth (up to 21%), nausea (up to 36%), anxiety, dizziness, nervousness, paresthesia, somnolence (up to 22%), tremor (up to 15%), blurred vision, abnormal ejaculation, impotence, and other male genital disorders. Fully 31 additional side effects with an incidence at least 1% greater than placebo were listed, including uncontrollable yawning.

Murder, suicide, and suicidality were NOT [emphasis added] included.

Nor were they on comparable lists for fluvoxamine, or sertraline. For fluvoxamine, suicide were separately listed as “infrequent.”

For fluoxetine, suicidal ideation was listed as a voluntary report not proved to be drug related. For sertraline, suicidal ideation and attempt were listed separately as “infrequent.”

The entry for venlafaxine was: “…the possibility of a suicide attempt is inherent in depression.” Not found in the was weight gain, which Cohen lists as a serious side effect.

Typical dropout rates in recent trials are claimed to be 5% (see below), but these must be short trials, or trials with a run-in period. In a meta-analysis of 62 earlier trials with a total of 6,000 subjects, the mean total dropout rate and the proportion of dropouts due to side effects appear comparable to results in general practice: total dropout rates of between 30% and 70% have been reported by 6 weeks, of which some 30%–40% are attributed to side effects and the rest to failure of treatment. Early findings of severe adverse effects by SSRI makers came to light only after the class was established. Of 53 healthy volunteer studies on fluoxetine, the results of only 12 were openly reported.

From 35 healthy volunteer studies on paroxetine, pre-launch, the results of only 14 appeared. From 35 pre-launch healthy volunteer studies on sertraline, only seven appeared. Among the unpublished trials, there was one in which all volunteers dropped out because of agitation (akathisia). In published work on sertraline, data excluded material on behavioral toxicity, including at least one suicide of a Adverse Effects of healthy volunteer, and in a different trial, 2 of 20 volunteers became intensely suicidal. This last is consistent with the dropout rate of 5% for agitation alone in actual trials. It is also consistent with Lilly’s animal studies, in which previously friendly cats treated with fluoxetine started growling and hissing—an unheeded warning.

Just a year after fluoxetine was introduced, Bill Forsyth of Maui, Hawaii, had taken it for only 12 days when he committed one of the first murder/suicides attributed to any SSRI.

In the same year Joseph Wesbecker killed eight others and himself in a Louisville, Ky., printing plant where he worked, after 4 weeks on fluoxetine. Yet as early as 1986, clinical trials showed a rate of 12.5 suicides per 1,000 subjects on fluoxetine vs. 3.8 on older non-SSRIs vs. 2.5 on placebo! An internal 1985 Lilly document found even worse results and said that benefits were less than risks. Such documents were released into the public domain by Lilly as part of the settlement in the Wesbecker case. Fifteen more “anecdotes” of murder/suicide, three with sertraline, were listed by DeGrandpre.

Lilly’s denials of a link to murder/suicide on national television and elsewhere cited a sponsored meta-analysis in in 1991, which exonerated fluoxetine as a cause of suicidal acts or thoughts without even mentioning actual murder or suicide. This study included only 3,067 patients of the 26,000 in the clinical trials it utilized. None of the trials had a declared endpoint of suicidality.

Some of the trials had been rejected by the FDA. No mention was made that Lilly had had benzodiazepines co-prescribed to minimizethe agitation that had been recognized with fluoxetine alone. The 5% dropout rate for anxiety and agitation (akathisia) would have taken out the most likely candidates for suicide. Nevertheless, the 1991 study had its intended effect. For example, in 2006 a 900-page tome entitled , which was aimed at attorneys, cited this study, and failed lawsuits concerning SSRIs. The 2007 meta-analysis by Bridge et al. may be influenced by indirect conflicts of interest that are hard to prove based on the financial disclosures.

Their paper pooled excess risk above placebo for “suicidal ideation/suicide attempt” from 27 trials. The excess risk was said to be 0.7% and statistically significant across all indications, but significant within each indication. Of the 27 trials, only five were sponsored by the drug maker, and one of these, the 2004 Treatment for Adolescents with Depression (TADS) study of fluoxetine, had the highest rate of suicidality—7% above placebo. Most of the same trials were used in a meta-analysis by the FDA, which found a statistically significant excess risk of 2% (4% vs. 2% on placebo, 1 in 50 more). Bridge et al. used a random-effects calculation, while the FDA used a fixed-effects calculation.

In commenting on the negative findings, Bridge et al. write: “No study [in our meta-analysis] was designed to examine suicidal ideation/suicide attempt as a study outcome, and in fact most trials were conducted in patients who had been carefully screened to exclude youths at risk.” No actual murders or suicides associated with SSRI use were reported. Did the designs of the studies preclude detection or reporting?

The Bridge meta-analysis was not just a vindication of SSRIs, as communicated to the by Gilbert Ross, M.D., Medical Director of the American Council on Science & Health. Ross went further, commenting that the FDA “Black Box warning” (see below) was counterproductive because it was discouraging the use of antidepressants! Ross speculated that the lethal rampage of the Virginia Tech shooter might have resulted from premature cessation of medications.

SSRIs in general have long lifetimes in the body. Fluoxetine and its active metabolite in particular have a half-life of 16 days, according to the 1996 . In a reexamination of trials in which suicides or attempts during the inadequate washout period were not blamed on the drug, it was shown that the relative risk (RR) of suicidal acts ranged from 3 for sertraline to 10 for fluoxetine.

A concurrent meta-analysis of 24 trials by Kaizar et al. utilized Bayesian statistics, a valid choice, in my opinion, because data do not have to follow a Gaussian or normal curve to yield valid results, and this method can be used to revise probabilities to determine whether a specific effect was due to a specific cause. They found an association between SSRI use and suicidality with odds ratios of 2.3 (95% confidence interval [CI] 1.3-3.8), when the diagnosis was MDD, not OCD, anxiety, nor ADHD. Non-SSRI antidepressants were said to have no association with suicide. This supports the FDA’s findings and requirement, as of October, 2004, for a Black Box warning for all SSRIs, to monitor children and adolescents for suicidality. Kaizar et al. were concerned that there were no completed suicides among 4,487 subjects in the trials; that the trial times were too short at median length of 8 weeks; and that in 10 of the 12 MDD studies, Again, there was no citation of actual suicides associated with SSRIs and no citation of Healy’s work.

Healy reviewed epidemiologic studies that have been cited to exonerate SSRIs. One was analyzed by Healy to show a threefold increase in suicidality compared with other antidepressants.While “treatment-related activation” has been considered primarily with regard to suicidality, it can lead to harm to others as well as to self. Healy summarized data on “hostile episodes” provided by GlaxoSmithKline from placebo-controlled trials with paroxetine in subjects of all ages: 9,219 on paroxetine and 6,455 on placebo. The rubric of “hostility” was used in the trial to code for aggression and violence, including homicide, homicidal acts, and homicidal ideation, as well as aggressive events and “conduct disorders.” No homicides were reported from these trials.

Overall, during both therapy and withdrawal, the RR was 2.1 for hostile events. In children with OCD the RR was 17. Separately, in healthy volunteer studies, hostile events occurred in 3 of 271 subjects on paroxetine vs. none of 138 on placebo. In trials of sertraline on depressed children submitted by Pfizer, 8 of 189 subjects discontinued for aggression, agitation, or hyperkinesis (a coding term for akathisia), compared with 0 of 184 on placebo. In clinical practice, the term akathisia has been restricted to demonstrable motor restlessness, but if that is the only effect, it would have been called dyskinesia according to Healy, who cites four studies linking akathisia to both suicide and homicide.

Actual suicides were combined with suicide attempts in a 2005 meta-analysis of 702 trials of SSRIs vs. either placebo or an active non-SSRI control. Studies were rejected if the citation was a review, a result of duplicate publication, too short, crossover, or had no reporting of actual or attempted suicide. The studies meeting the criteria included 88,000 patients. For attempted suicide, the RR was 2.3 for SSRIs vs. placebo (95% CI, 1.14-4.55). The number needed to treat to harm (sometimes called the “reverse NNT”) was 1 in 684. There was no difference in actual suicide. Of the 702 trials, 104 failed to report adverse events below a certain pre-set limit of 3%, 5%, or 10% of patients. Only 493 trials reported dropout rates, with a mean of 29%, and the mean follow-up time was only 11 weeks. Thus, there was clearly gross underreporting of adverse effects. PDR children and adolescents with an elevated baseline risk of suicide were excluded.

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009 9

More importantly, because actual suicides are involved, Healy cited a study by Donovan et al. that demonstrated a RR=3.4 ( <0.01) for SSRIs compared with all non-SSRI antidepressants involving 222 actual suicides, of which 41 were among patients who had an SSRI within a month of their suicide. Also the British Drug Safety Research Unit recorded more than 110 suicides in 50,000 patients taking an SSRI, an incidence of 219/100,000 compared with 96/100,000 for the non-SSRI mirtazepine (Remeron), an increase of 123/100,000, or 1 in 813 (Table 2). Thus the RR for actual suicide in patients taking SSRIs was 2.3 (or 2.8 for paroxetine). Even here, though, no murders were listed.

In another study cited by Healy, Jick et al. reported 143 actual suicides among 172,598 patients taking antidepressants. The relative risk of suicide in patients taking fluoxetine was 2.1, compared with those taking the tricyclic antidepressant dothiepin. The risk was not age-dependent. SSRI makers keep insisting that there will be more suicides if SSRIs are used as frequently as now. But the RR of 2–3 shown in studies is a number that the number of suicides that may have been prevented, so SSRI use is associated with more suicides, not fewer.

The International Coalition for Drug Awareness in cooperation with the Prozac Survivors Support Group has produced a website on which about 1,600 violent incidents associated with SSRI use are described ( www.ssristories.net ). The first column on the type of incident (murder, school shooting, etc.) is a hot link to a publicly available description of the incident, typically a local newspaper article. A selection of 10 entries (rows) is presented here as Table 3. About 360 suicides are tallied as well as about 400 murder incidents, many of which were multiple murders, each linked to 26 not net includesSSRIs Provide 1,600 Anecdotes of Violence SSRI use (Rosie Meysenburg, personal communication, 2008 .

As the number of “anecdotes” exceeds 1,600—hardly a small number—the association of SSRIs with murder/suicide, often combined, must be taken seriously. The SSRI website was searched to find combined murder/suicide incidents attributed to a specific SSRI. There were three for fluvoxamine, four for citalopram, 10 each for paroxetine and sertraline, and 31 for fluoxetine. Where the studies above substantiated suicide from SSRI use, the total on the SSRI website of 48 simultaneous murder/suicide incidents associated with SSRI use ties together SSRIs and murder. Since there were about two murders per suicide, we may infer that the murder rate on SSRIs could be about 250/100,000. Since no clinical trial involving multiple homicides is ever likely to be run, no firmer evidence is likely to be found. Healy noted that much of the evidence for suicide and murder came from the efforts of journalists and lawyers.
Note that the website carries a prominent warning that “withdrawal can often be more dangerous than continuing on a medication.” Nine violent events cited elsewhere—seven court cases of homicide (one attempted) and two assaults—were associated with specific SSRIs: three with paroxetine, three with sertraline, two with fluoxetine, and one with venlafaxine. Skeptics have cast doubt on whether the prescribed SSRIs were actually taken, especially since many medical records of juveniles were sealed. In the Columbine, Colo., shootings the toxicology report showed “therapeutic” levels of fluvoxamine in one of the shooters. The Red Lake, Minn., shooter had fluoxetine found, according to news items referenced on the website.

A 2004 editorial in by Simon Wessely, M.D., a spokes- man for Eli Lilly, and Robert Kerwin, Ph.D, cited only a single paper by Healy as a source of claims of suicidality that have found a receptive media audience. Tellingly, the only study described at length is by Jick et al. on the correlation of SSRI use and “attempted suicide,” in which the rates on dothiepin, amitriptyline, fluoxetine and paroxetine were not statistically different. Actual suicides in this study (seven on SSRIs) were not mentioned by Wessely and Kerwin, nor were the 143 suicides in Jick’s earlier paper. Jick et al. have been supported partially by GlaxoSmithKline and Pfizer. No study that reported actual suicides on SSRIs was described in detail, let alone refuted. Wessely and Kerwin wrote: “The problem is that depression is unequivocally and substantially associated with suicide and self-harm.” True, but this not the truth.

Table 2. Suicides Related to SSRIs or Mirtazapine

table_02_zoloftbusted1

The legal defense by Lilly, repeated by the media and others, is that any suicides are caused by the condition, depression, not by their drug—whether the violence is associated with short-term drug use, long-term drug use, increased doses, withdrawal, or rechallenge. There is no website, as far as I know, for violent acts committed by persons who never received SSRIs, or for total violent acts; hence the denominator for violent acts is not known. Also unknown is the fraction of potentially violent persons who are treated with SSRIs, or of persons treated with SSRIs who are potentially violent. The published studies on actual suicide, however, compare patients on SSRIs with similar patients on non- SSRI antidepressants or placebo. Children diagnosed with OCD, not depression, also became suicidal on SSRIs, as did healthy volunteers.

Actual two- to threefold increases in suicide rates have been demonstrated as well as they could be. How else could such effects be demonstrated? Who would submit, and what institutional review board or human subjects committee would approve a study explicitly designed to show whether assaultive, homicidal, or other violent behavior increases in subjects prescribed the study drug?

Denial by SSRI makers of culpability for these risks continues to this day. Whether physicians’ acting on the Black Box warnings of 2004 and 2007 for all SSRIs will diminish the incidence of murders and suicides is not yet known. Following the introduction of fluoxetine in 1988, only a year passed before an early user committed multiple murders and suicide; many other examples followed. More than 200 lawsuits have been begun by users of SSRIs and victims’ families charging wrongful death or failure to warn; these have had mixed outcomes. There is now legal precedent for SSRIs as a cause of murder, and the maker of the SSRI is potentially liable for damages, according to David Healy.

Eli Lilly responded with total denial to the lawsuits claiming a link between fluoxetine and violence. Several claims were settled out of court with secret details and no admission of guilt. The Australian David Hawkins was freed from a murder charge by a finding of temporary insanity caused by using sertraline. Tim Tobin of Wyoming won $6.4 million from SmithKline Beecham when a jury found that a murder/suicide committed by Donald Schell was attributable to use of paroxetine. There are four other homicide cases in which the SSRI was deemed to have contributed, resulting in a suspended sentence in one case and an insanity verdict in another.

One case of homicide, with a guilty verdict and a life sentence, followed a judicial ruling that akathisia was associated with SSRI use, but that a causal relationship with homicide could not be argued; thus the link of an SSRI with homicide was disallowed. This was in direct conflict with the findings of the four trials cited above. The SSRI website was searched to find murders related to a specific SSRI whose perpetrators were acquitted based on temporary SSRI-induced insanity. There were two cases with sertraline, four cases with paroxetine, and four cases with fluoxetine. So a precedent has been established for legal recognition that an SSRI can be a cause for murder, and that the drug maker can be found liable for damages. The notices of suicidality for the SSRIs found in the PDR or package inserts before 2004 did not really warn of actual suicide or murder.

200 SSRI-related Lawsuits

The Black Box warning of 2004 about possible suicide in children under 18 years of age did not cover adults or murder at any age, so potential liability for the SSRI makers still exists. In 2007 the warning was extended to persons under age 25 years. David Healy was quoted as saying that the warning was overdue, and that the risk was not likely to disappear above age 25. This was shown by the trials from GlaxoSmithKline on paroxetine cited above.

Antidepressants are extraordinarily difficult to assess for risks or benefits in trials. At most, 11%–30% of patients with depression or related conditions who take SSRIs actually benefited beyond the placebo effect on normal doses. Of the perceived benefit, 32%–67% can be attributed to the placebo effect. Adverse effects, mostly dose-dependent, will appear in up to 75% of patients on normal doses. Of these, studies suggest that suicidality will be observed in an additional 2%–13% (1 in 50 to 1 in 9) of patients on normal doses, beyond what is seen on placebo or many non-SSRI antidepressant drugs. This is sufficiently frequent that a typical prescribing physician should observe examples in routine practice.

The actual suicide rate could be about 123/100,000 (1 in 813) higher in patients on SSRIs than in those on tricyclics or placebo. Studies show that many more suicides are on normal doses of SSRIs beyond what is seen on placebo or many non-SSRI antidepressant drugs. Available data suggest that actual murders may be committed at about the rate of 250/100,000 (1 in 400) SSRI-treated patients beyond what is seen on placebo or many non-SSRI antidepressantdrugs, and that many more murders will be attempted on normal doses as well. While correlation does not prove causation, and results of court trials are not medical science, the data for suicide are solid, and the association of murder with suicide is very suggestive. Now that there is a stronger Black Box warning, physicians who ignore it may be liable for damages; the warning primarily protects the manufacturers of SSRIs. There is obviously great peril in drawing conclusions about causat i on from press report s or court decisions.

While manufacturers have a vested interest in exonerating their drugs, plaintiffs have an interest in blaming it, and defendants in exonerating themselves. We need careful, independent analysis of existing study data. In addition to randomized controlled trials, evidence from basic science ( neuropharmacology) and challenge/dechallenge/rechallenge investigations needs to be sought. Both the public and individual patients are imperiled by an incorrect answer to the pressing questions about these widely prescribed drugs. Future studies may show lower levels of murder and suicide with close supervision, and with better matching of this drug type to patient type.

Conclusionsattemptedsimultaneous
Joel M. Kauffman, Ph.D.

Acknowledgements:
Joel M. Kauffman, Ph.D., professor of chemistry emeritus at the
University of the Sciences, 600 S. 43rd St., Philadelphia, PA 19104-4495,
Contact: kauffman@bee.net.

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Frances E. H. Pane edited the manuscript. David Moncrief piqued my interest by providing a review copy of by Richard DeGrandpre.
The Cult of Pharmacology: How America Became the World’s Most Troubled Drug Culture

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009 11
Potential conflicts of interest: The author has neither a financial interest in any drug mentioned, nor in any alternate treatments for treating any mental illness.

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Kirsch I, Deacon BJ, Huedo-Medina TB, et al. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. 2008;5(2):e45. doi:10.1371/journal.pmed.0050045.

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New York Times:Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009

USA Trade Name Generic Name:
SSRIs
Celexa
Luvox
Paxil
Prozac
Zoloft
non-SSRIs
Effexor
Remeron
Serzone
Wellbutrin
(UK)
citalopram
fluvoxamine
paroxetine
fluoxetine
sertraline
venlafaxine
mirtazapine
nefazodone
bupropion
dothiepin USA Trade Name Generic Name
SSRIs
Celexa
Luvox
Paxil
Prozac
Zoloft
non-SSRIs
Effexor
Remeron
Serzone
Wellbutrin
(UK)
citalopram
fluvoxamine
paroxetine
fluoxetine
sertraline
venlafaxine
mirtazapine
nefazodone
bupropion
dothiepin

Physicians Desk Reference (PDR)
Joel M. Kauffman, Ph.D.
Table 1. Commonly Prescribed SSRIs and Other Antidepressants Selective Serotonin Reuptake Inhibitor (SSRI) Drugs:
More Risks Than Benefits?

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009 7 Physicians Desk Reference (PDR)
Joel M. Kauffman, Ph.D.
Table 1. Commonly Prescribed SSRIs and Other Antidepressants Selective Serotonin Reuptake Inhibitor (SSRI) Drugs:
More Risks Than Benefits?

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009 7

JAMAwhole12,69210,98313,74112,73450,15013,554

10 dead, 7 wounded: dosage increased one week before rampage
15 year old shoots two teachers, killing one: then kills himself
Columbine High School: 15 dead, 24 wounded
Four dead, twenty injured after Prozac withdrawal
Teen shoots at two students: kills his father
Jury finds Paxil was cause of murder-suicide
Man cleared of charges due to Paxil withdrawal defense
Not guilty by reason of Prozac induced insanity: mother kills daughter
Nine dead, 12 wounded in workplace shooting
11 year old hangs himself: lawsuit

Journal of American Physicians and Surgeons Volume 14 Number 1 Spring 2009

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DEPRESSION MED: Woman Stabs To Death A Man On A Stairwell: Australia

Paragraph three reads:  “Defence solicitor Bernie Balmer said Epshtein was on medication for anxiety, bipolar, depression, pain and one to lower her heart rate.”

http://www.theage.com.au/national/woman-in-court-over-stabbing-murder-20090803-e6l0.html

Woman in court over stabbing murder

Steve Butcher

August 3, 2009 – 12:04PM

A 21-year-old woman charged with the stabbing murder last week of a man in a St Kilda stairwell has appeared in court.

A lawyer for Natasha Epshtein told Melbourne Magistrates Court today his client had been treated by two doctors for five separate health conditions.

Defence solicitor Bernie Balmer said Epshtein was on medication for anxiety, bipolar, depression, pain and one to lower her heart rate.

Epshtein appeared before Deputy Chief Magistrate Dan Muling in a low-cut, black t-shirt with close-cropped hair and tattoos on her upper chest.

She is charged with murdering Peter James Len on July 30.

Mr Balmer said she would consent to a DNA sample being taken at a later date.

She was remanded to appear again on November 30.

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