TOO EERY!!!!!! Re: Boy’s meds might give clinician pause today

Tuesday, 19 August 2008
This is ALL TOO
EERY!!!!! Just yesterday I was at Von Maur in Omaha with Mark and
Donna Taylor as we stopped while driving from Salt Lake City to Des Moines!
What sent chills down my spine, even though I was too tired to feel much
after driving for about 12 hours straight with only a couple hours break, was
what I learned when I dropped Mark and Donna off at Whole Foods to pick up a few
groceries while I played on the lawn with my puppy. And as I played with
him I looked up and saw Von Maur. I caught my breath and thought “But it
does not look like a mall from here, maybe it is just another Von Maur store,
not the one where all those people died last year.”
So when the next person stopped to play with my little dog I asked
them if that happened to be the mall where the shooting was last year.
When they said yes I thought I would fall over from the shock of it all!!
Because last December 4th when I last drove through Omaha I stopped across
the street (right where I was yesterday) from Von Maur at the Omaha Whole Foods
Market and asked if we could arrange for me to come and speak to warn
people in the Omaha area about the dangers of antidepressants. I then left
waiting for them to call me.
But it was the following day that Robbie walked into that mall shooting. It
resulted in NINE deaths due to his long-term use of antidepressants. Yesterday,
almost a year later I realized how closely tied all of this was as I
stood there just across the street with the first boy shot at Columbine High
School knowing I personally left warning just the day before the shooting.
The most sickening statement about this never ending nightmare comes
from the question Mark asked me as we stood there yesterday. He wanted to
know whether the Whole Foods had ever called back wanting to schedule
a lecture. I had to tell him they had not.
And now today this article comes out talking about Robbie’s long-term use
of antidepressants? I noticed they did not even explain the withdrawal he was in
at the time which causes the REM Sleep Behavior Disorder at an even higher rate
than being on one does.
The whole combination of these experiences  . . .  these things
never stop taking my breath away!!!
When we look at the info in this article we realize that I was years too
late anyway even though I made an attempt to stop this one just the
day before it happened. What is being done now to babies in the wombs of the
moms who take these drugs is CRIMINAL!!! And the same holds true for all those
in their youth who are given these drugs!! How very terrible! And if they
continue to attempt to push the Mother’s Act to get more pregnant and
nursing moms on these drugs . . . . WATCH OUT!
But in saying that, let me add that I do believe there is hope to turn
those effects around if you know enough about alternative treatments.
Ann Blake-Tracy
In a message dated 8/17/2008 9:36:49 P.M. Central America Standard T, writes:

One of the Journal Articles on SSRI Stories
states:  “Sentence 5 of the Abstract reads:  “Experimental
studies in rodents show that administration of SSRIs during a key
developmental window creates changes in brain circuitry and maladaptive
behaviors that persist into adulthood.”

Developmental effects of SSRIs: lessons learned
from animal studies

Xenia Boruea, b, John Chena, b and Barry G.

aUniversity of Virginia Medical Scientist
Training Program and University of Virginia Neuroscience Graduate Program,
Charlottesville, VA 22904, United States

bUniversity of Virginia, Department of
Biology, Charlottesville, VA 22904, United States

Received 1 June
2007;  accepted 19 June 2007.  Available online 7 July 2007.


Selective serotonin reuptake inhibitors (SSRIs) are
utilized in the treatment of depression in pregnant and lactating women. SSRIs
may be passed to the fetus through the placenta and the neonate through
breastfeeding, potentially exposing them to SSRIs during peri- and postnatal
development. However, the long-term effects of this SSRI exposure are still
largely unknown. The simplicity and genetic amenability of model organisms
provides a critical experimental advantage compared to studies with humans.
This review will assess the current research done in animals that sheds light
on the role of serotonin during development and the possible effects of SSRIs.
Experimental studies in rodents show that administration of SSRIs during a key
developmental window creates changes in brain circuitry and maladaptive
behaviors that persist into adulthood. Similar changes result from the
inhibition of the serotonin transporter or monoamine oxidase, implicating
these two regulators of serotonin signaling in developmental changes.
Understanding the role of serotonin in brain development is critical to
identifying the possible effects of SSRI exposure.

Serotonin; Neurotransmitter; CNS development
Corresponding author at:
University of Virginia, Department of Biology, Gilmer Hall
071, Box 400328, Charlottesville, VA 22904, United States. Tel.: +1 434 243
6794; fax: +1 434 243 5315.

At 08:06
AM 8/17/2008, jay baadsgaard wrote:

Sunday    August 17, 2008

Boy’s meds might give
clinician pause today



Robbie Hawkins was prescribed medications to combat anxiety
disorders, hyperactivity and depression for roughly half of his 19

In 1992, when Robbie was 4, a psychiatrist prescribed
Ritalin, a stimulant used to treat attention-deficit hyperactivity disorder,
and Mellaril, an antipsychotic.

When Robbie was hospitalized that
December, those medications were discontinued in favor of the
antidepressant Pamelor, which he took for at least 10

Although all three medications still are prescribed,
research has shown limitations or flaws in each that would give a clinician
today greater pause before prescribing them to a


Ritalin: A well-regarded trial
study published last year involving preschoolers showed that
while some children benefit from Ritalin, younger children may be
more sensitive to its side effects. Those can include decreased appetite,
sleep loss, irritability and emotionality, said Dr. Mary Margaret Gleason,
the lead author of psychiatric medication treatment guidelines for
preschoolers published in the Journal of the American Academy of Child &
Adolescent Psychiatry.

Mellaril: This antipsychotic is
typically prescribed for schizophrenia. Robbie took a low dose to help him
settle down and fall asleep. Tests have found that Mellaril causes
some patients serious heart problems, such as changing the rhythm and
electrical conduction of the heart, Gleason said. The U.S. Food and Drug
Administration recommends prescribing it only to schizophrenic
patients who have not responded to other antipsychotic drugs.

Pamelor: Newer antidepressants have fewer side effects and a wider
tolerance, said Dr. Graham Emslie, the chief of child and adolescent
psychiatry at Children’s Medical Center in Dallas. Research also has shown
that Pamelor isn’t as effective in young children, Gleason said, although it
can help some children with attention-deficit hyperactivity disorder or loss
of urinary control.

When Robbie was 15, he was treated with the
antidepressant Effexor XR. Two years later, he was prescribed the
antidepressant Zoloft after attempting suicide.

He refused both
medications after taking each for less than two months, according to
juvenile court records.

Nearly all antidepressants, including the
three prescribed to Robbie, now carry a required “black box”
warning on their labels. The FDA began ordering such warnings three
years ago, after clinical trials suggested that some drugs increased the
risk of suicidal thinking and behavior in children and teens, particularly
when first given or when the dosage changed.

No research has
been conducted to determine whether antidepressants taken
by children or teens have long-term effects, Gleason

Robbie wasn’t taking antidepressants last
December when he killed eight people, severely wounded others and
committed suicide at Von Maur, although an autopsy detected therapeutic
amounts of the prescription drug diazepam, a tranquilizer known by the trade
name Valium.

The drug had not been prescribed to him.

has approved only one antidepressant — Prozac — for use in children, but
psychiatrists can use their discretion to prescribe

Gleason called the decision to prescribe psychiatric
medication to children “a complicated balancing act” that pits the risk of
continuing illness against the risks associated with

“By the time (parents) seek mental health care, they’re
really in a lot of distress, the child’s in a lot of distress (and) the
impact of the illness is pervading the child’s life,” she said.
Contact the Omaha World-Herald newsroom

©2008 Omaha World-Herald®. All rights reserved. This material may not be
published, broadcast, rewritten, displayed or redistributed for any purpose
without permission from the Omaha

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My Effexor Withdrawal Story

“There were times where it seemed like I could barely sort out how to walk or breath.”

I have been through a good number of meds for depression and mood stabilizers. Never have I experienced any withdrawal effects until now. In December of 2003 the Effexor “lost its efficacy.” Turns out that 6 months drug trials do not show that this antidepressant frequently just stops working. I was taking 75 mg Effexor (immediate release) in the morning and after work. Once I was stabilized on Wellbutrin XR my psychiatrist put me on a taper of 75 mg, 50 mg, 25 mg for one or two weeks each. In February of 2004 I was on the 25 mg when my dad died. We stopped the taper figuring there was enough going on.

I did not realize it at the time but I was experiencing withdrawal during the taper. I thought it was just something in me acting up. (I am one of the over 50% of folks with bipolar who are also addicts – toss of a coin I guess – clean since March 24, 2003.) I was real irritable, poor coordination, light headed/weird feeling in the back of my scull, hallucinations from the corner of my eye, extreme confusion. There were times where it seemed like I could barely sort out how to walk or breath. Not to mention I became acutely aware of the sexual side effects I had unknowingly been experiencing from the Effexor.

So now it is May of 2004 and we decided to finish the taper. I was on 12.5 mg for a week and now I have been on 0 mg for 2 days. This is hell. I had withdrawal on the 12.5 mg but it was OK. I was real irritable with everyone, emotional, all the symptoms that I experienced before. Within 3 days things were OK and then by the 4 everything seemed back to normal. But the withdrawal from 0 mg is the worst. Added to the list of symptoms are intense flu like stomach sensations, and sobbing jags. Usually they are 5-10 second jags and happen for no reason. It happened 4 times while watching “Where the heart is.” This is not a movie that should make a person cry 4 times. Now that it is the second day with no Effexor the crying jags have gotten longer and more intense. Now there are tears whereas before there were none. I do feel like the crying is helping to mourn my father’s death some more.

I feel like the first day I put down dope. Part of the reason I stay clean is because I never want the feeling of having 1 day clean. I see people come in with a few days clean and the misery and pain is so clear. They help to remind me how much it sucks to get clean. That it is so much easier to stay clean than to get clean. I have not used but here I am feeling like I just walked into the rooms.

I don’t know if I am looking to get into a lawsuit but I do not understand why Effexor is still prescribed. I know that the reason it is still on the market is because it is still bought. Drug companies are in the business of making money so I do not really blame them. If the med stops selling the company will take it off the market. However doctors are in the business of making people well. It is the doctor I hold responsible more than the drug company. Is Effexor being prescribed out of ignorance or is there a unique benefit that outweighs the risks of withdrawal symptoms? I don’t know. I do know that I need to talk to my psychiatrist about it. I also know that I have heard a bunch of people saying they are Effexor and I have been telling! them to get off as soon as possible.

Thanks for letting me share.

Jon Faber

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Matt’s Story

“On July 18, 2003, I lost my son to suicide after 10 weeks of being on the antidepressant Lexapro.”

Matt was a healthy and happy child who grew up in a loving home, the youngest of six. He was athletic and outgoing, well liked by his peers and adults as well. Matt was a good student, with a strong sense of right and wrong, a kind heart, and a sound faith in God. He loved sports and music, and was always joking around with his family and friends. Oh, he could be stubborn when he thought he had a point, and he was known to procrastinate with the best of them. He was a joy to us always. Then, during his senior year in high school, things started to change.

He became withdrawn and was having trouble sleeping. He lost interest in his friends, school, his job, his college plans, and basketball (the thing he loved most). Matt turned 18 on April 25, 2003. A week later he began treatment for “clinical depression” (his first episode). There were several things that could have contributed to his depression, though most were normal “growing up” situations. One thing we do know is that Matt was suffering from post traumatic stress. At the age of 13, he was hit by a car on his bike. He suffered a frontal lobe head injury, but every indication was that he recovered well from that accident. Still, five years later, he began reliving the accident as though it had just happened. He was having nightmares and panic attacks, but Matt was NOT suicidal.

The counselor that he was seeing was shocked and visibly shaken by Matt’s death. He said that he never saw any indication that Matt would do such a thing. The medication was prescribed ( by a family practice doctor) to help correct a “chemical imbalance” which we were told is at the root of depression. He began taking Lexapro during the second week of May. We were told the side effects could be nausea, insomnia, headaches, dizziness. Did anyone say “and suicidal behavior”? NO!!!

I am devastated to think that something we were giving my son to help him could have literally taken him from us. At the very least, we should have been warned to be on the look out for certain signs. Signs I have since learned are danger signs, such as anxiety and akathisia. I had never heard that word before, but I now believe that Matt was experiencing it. I realize that I have gone on at length, and still there is so much more I could say. Our lives have been ripped apart, and I’ll always wonder “What If”” he hadn’t been taking that medicine? Would he still be here?

Nothing can bring my son back. I would just like to share our story with other parents who may be helped before it’s too late.

I would also like to hear what others have to say about Lexapro. My e-mail address is I welcome hearing from anyone who has an interest in this look forward to hearing from you. Thank you. Celeste

Celeste Steubing

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Doctor Tells Patient that Antidepressants Treat Pain

“I realize that these antidepressants messed up my brain chemistry.”


I have been diagnosed with Occipital Neuralgia (Nerve Pain in the Occipital Region of the head) by a number of different doctors. I have tried different medications to relieve the nerve pain, but none of them seemed to relieve the pain completely. One doctor suggested I try an antidepressant. I told him that I wasn’t depressed, just in pain. He told me th antidepressants help treat chronic pain. Thus, I decided to try this antidepressant called Paxil for my nerve pain.

I took it for six months, but wish I hadn’t! After six months, I felt like I couldn’t think straight (I was in a zombie like state), had memory loss, gained weight, experienced sexual dysfunction, etc. I came off Paxil cold turkey, but realized that was a mistake (I didn’t realize at the time that I was suppose to come off these type of medications very, very slowly). The doctor wanted me back on the medication, but didn’t provide an explanation. I told him why would I go back on a medication that has these side effects. I didn’t go back on the medication. I became severally depressed (even though I wasn’t depressed before taking the Paxil).

I almost lost my job because of my depressed mood. I honestly don’t know how I managed to keep it. After about 6 months of no medication I was given short doses (a weeks’ worth) of anti-inflammatory steroids for my nerve pain. That made my depression worse. I read later that steroids deplete serotonin. I started to develop nerve pain down the back of my legs. I think the Depression and nerve pain down the back of my legs was caused by my brain chemistry being altered by Paxil and then the introduction of another medication made the brain chemistry worse (I didn’t think about this at that time).

So by now I had Depression, Occipital Neuralgia and nerve pain down the back of my legs. Another doctor suggested that I try a different antidepressant. I told him of the unpleasant experience I had with Paxil. He recommended that I try Prozac. Told me it was different from Paxil. I tried it, but was very weary because of my experience with Paxil. The only reason I tried it was because I wanted rid of the Depression, Occipital Neuralgia and the nerve pain down the back of my legs.

After about four months on Prozac, I encountered similar side effects to the Paxil. The only difference instead of weight gain, I experienced weight loss. I came off this medication, but this time very, very slowly. I learned my lesson from my Paxil days. While on the Prozac it didn’t really help my depression or nerve pain down the back of my legs. I was still depressed, had the Occipital Neuralgia and the nerve pain down the back of my legs. I didn’t know what to do. I tried some exercise, but just didn’t feel right.

I know that Paxil and Prozac had something to do with the way I was feeling. The Depression and nerve pain down the back of my legs became to much, that I went on another antidepressant called Celexa. I told my doctor about the experiences I had on Paxil and Prozac. He told me this is a newer antidepressant and has fewer side effects than Paxil and Prozac. I took that for about 1 and 1/2 years. It took care of my Depression, but didn’t really take care of the nerve pain down the back of my legs. I eventually came off the because of the side effects. The side effects of Celexa were similar to Paxil, but not as harsh.

I am still stuck with Depression, Occipital Neuralgia and nerve pain down the back of my legs. I realize that these antidepressants messed up my brain chemistry. I have ordered PROZAC: PANACEA OR PANDORA? By Ann Blake Tracy, PhD. I hope this book can provide some answers and solutions. I am also considering taking the herb St John’s Wort, but will read the book first to see if I can get any answers/solutions to my problems.

Is there any action I can take against the makers of these drugs and the doctors that prescribed them to me? All of this has happened over a four year period. I have had the Occipital Neuralgia a lot longer than that.



This is Survivor Story number 21.
Total number of stories in current database is 48

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3/15/2002 • Rare Neurologic Syndrome Linked to Antidepressant

3/15/2002 • Rare Neurologic Syndrome Linked to Antidepressant

Jim Rosack

Psychiatric News March 15, 2002 Volume 37 Number 6, p. 31

Neurologists warn other clinicians that SSRIs could contribute to a potential increase in certain patients‚ risk of having a rare form of stroke.
Rare Neurologic Syndrome Linked to Antidepressant

Jim Rosack

Psychiatric News March 15, 2002 Volume 37 Number 6, p. 31

Neurologists warn other clinicians that SSRIs could contribute to a potential increase in certain patients‚ risk of having a rare form of stroke.

A new report from a group of neurologists warns that combinations of medications that modulate brain levels of serotonin, including SSRIs and other antidepressants, could lead to a relatively rare form of stroke due to marked vasoconstriction.

The report, which appeared in the January issue of Neurology, includes case studies of three patients who developed Call-Fleming syndrome, which is characterized by sudden-onset severe headache, focal neurological deficits, and seizures. Although rare, the syndrome is most commonly seen in women.

The first patient studied, a 46-year-old woman, developed a “worst ever” headache, nausea, and blurred vision, which were followed a few days later by escalating neurological symptoms. The woman‚s medications included sertraline and trazadone, and for two days prior to developing symptoms, she had taken an over-the-counter cold remedy that contained dextromethorphan. Diagnostic testing confirmed severe, diffuse, intracranial vasoconstriction, including a 70 percent constriction of the origin of the vertebral artery.

In addition, several areas of ischemic stroke were identified. Within a week of discontinuing both the sertraline and the cold remedy, the women was discharged in markedly improved condition.

The second case described a 45-year-old woman who developed a sudden, “explosive” headache, again with accompanying nausea. Four weeks earlier, she had been started on paroxetine 40 mg and clonazepam 0.25 mg for a recurrence of major depression. Shortly before the onset of the headache, she had taken a cold remedy with dextromethorphan and pseudoephedrine. Again, severe, bilateral vasoconstriction was demonstrated on cerebral angiography, and MRI demonstrated multiple areas of ischemic stroke. The patient‚s paroxetine was discontinued, and her symptoms subsided. Interestingly, four months later, this patient again had a worsening of her depression and was prescribed mirtazapine. Within two weeks she again developed headaches, which resolved when the mirtazapine was stopped.

The third patient was a 34-year-old male who developed an “explosive” headache with sensitivity to light, nausea, and extreme fatigue. His family history included migraine syndrome, and as a result, he was treated with sumatriptan, a common migraine medication known to be a serotonin receptor agonist that causes significant cerebral vasoconstriction. Following a second dose of that drug later the same day, the patient had a generalized seizure, and an MRI five days later showed multiple bilateral ischemic areas.

Although the patient denied any use of illicit drugs, recent cocaine use was suspected.

Aneesh Singhal, M.D., the primary author of the report, has seen about a dozen similar cases in his practice. Although he believes that Call-Fleming syndrome is rare, he told Psychiatric News that it includes a number of conditions that are often labeled in different ways, and thus the syndrome may be underrecognized.

“This is a preliminary observation; it needs confirmation,” he stressed. “It ‚s important to note that it is not the individual drugs, that by themselves might enhance the risk [of stroke from vasoconstriction], but rather the combination of drugs,” he told Psychiatric News.

“It is conceivable that someone who has a migraine syndrome, is trying to lose weight, and is depressed, which is not an uncommon situation, may take three or four agents, and thus have increased risk of vasoconstriction and end up with stroke.”

Singhal said that differential diagnosis needs to include the possibility of serotonin-induced vasoconstriction in any patient who has a sudden onset of severe headaches that are not explained by any of the accepted causes, most commonly a subarachnoid hemorrhage. “If the known causes are ruled out, you have to remember that there is one more cause, and that is vasoconstriction.”

Singhal said patients who are taking serotonin-modulating medications should be routinely asked about the presence of moderate to severe, persistent or recurrent headaches. He stressed that although headache is a common side effect of many of these medications, when the headache is recurrent or sustained and moderate or severe, medications should be at least temporarily suspended, and the cause of the headache investigated.

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2/28/2002 • Antidepressant drug trials turn away most of the depressed population

2/28/2002 • Antidepressant drug trials turn away most of the depressed population

Mark Zimmerman, associate professor of psychiatry and human behavior, director of outpatient psychiatry at Rhode Island Hospital

Brown University

While antidepressants are among the most frequently prescribed medications, most patients treated for major depression in a typical outpatient psychiatric practice would not qualify to take part in a clinical trial for a new antidepressant drug, according to a new Brown University study.

Antidepressant drug trials turn away most of the depressed population

Mark Zimmerman, associate professor of psychiatry and human behavior, director of outpatient psychiatry at Rhode Island Hospital

Brown University

While antidepressants are among the most frequently prescribed medications, most patients treated for major depression in a typical outpatient psychiatric practice would not qualify to take part in a clinical trial for a new antidepressant drug, according to a new Brown University study.

Trials to determine the effectiveness of antidepressants have historically evaluated only a small subset of depressed individuals with a very specific clinical profile. People diagnosed with other psychiatric problems and people with mild depression are among those excluded, says the study, which appears in the March 2002 American Journal of Psychiatry.

“When you take any medicine you assume it‚s been found to be effective for your condition,” said Mark Zimmerman, associate professor of psychiatry and human behavior, director of outpatient psychiatry at Rhode Island Hospital, and the study‚s lead researcher. “No one knows for sure whether antidepressants are effective for most of the patients we treat.”

As few as 15 percent of 346 depressed patients evaluated in the Rhode Island Hospital Department of Psychiatry outpatient clinic would have met the eligibility requirements of a standard drug trial, depending on the criteria.

To determine whether the clinic patients would qualify for the drug studies, the researchers reviewed inclusion and exclusion criteria used in 31 antidepressant trials published from 1994 to 1998 in five leading psychiatric journals. Many of the studies excluded patients who had psychotic features, a history of manic episodes, suicide risk, unstable medical illnesses, or a history of drug or alcohol abuse. Several also excluded subjects with eating disorders, obsessive-compulsive disorder or panic disorder.

Nearly all of the studies excluded patients who fell below a cutoff score on a measure of symptom severity, even though they were diagnosed with major depression. “We are not aware of any other medical condition in which individuals with the disorder are routinely excluded because they are not sick enough,” said Zimmerman.

“Drug companies are concerned that individuals with mild depression will respond just as well to a placebo as they will to antidepressant medication,” said Zimmerman. “However, this represents a sizable number of individuals who are prescribed these medicines, especially by primary care physicians.”

The researchers conducted diagnostic evaluations of patients at the Rhode Island Hospital Department of Psychiatry outpatient practice, a group ranging in age from 16 to 65. Excluding patients with any of the features commonly used in efficacy trials eliminated two-thirds of the patients. If patients with an anxiety disorder were also excluded, then more than 85 percent of the patients would not have qualified for a drug study of antidepressants ˆ yet more than 90 percent of the patients in the study for whom prescribing information was available were being treated with antidepressants at the time of the evaluation.

Some extrapolation of antidepressant studies by clinicians will always be necessary, Zimmerman said. It would be impossible to establish the effectiveness of antidepressant medications in every conceivable population of depressed patients. But the current practice of limiting studies to only “pure” moderate-to-severely ill depressives may skew the findings of drug trials, he added. If antidepressants are, in fact, not effective for some of these large subgroups of depressed individuals, their prescription incurs an unjustifiable exposure of risks and side effects, and alternative treatments need to be considered.

Opening antidepressant trials to patients with a wider range of symptoms would allow researchers to learn whether any specific subsets respond or do not respond to a drug. The question now is whether government mandates are necessary to make trials more inclusive, Zimmerman said. There is little motivation for drug companies ˆ whose primary aim is to show that their medication is safe and that it works for some patients ˆ to do this.

“Drug companies have been correct in assuming that if they show their medicine works for a highly select group of depressed patients, physicians will use it for all patients,” said Zimmerman.

This study was supported by grants from the National Institutes of Mental Health. Zimmerman worked with Jill I. Mattia, clinical assistant professor, and Michael A. Posternak, research fellow, in the Department of Psychiatry and Human Behavior at Brown University.

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Effexor gave me the urge to take my life.

“Anybody who says Effexor is not dangerous is lying”


I am 36 years old with 2 children. Last year was a traumatic year, splitting up with my children’s father, losing a baby, working 46 hours per week and starting another relationship with mentally cruel man. In September my doctor put me on Effexor 75mg for depression, which started me on a downward spiral with hideous side effects.

Anybody who says Effexor is not dangerous is lying. After 2 months on the drug, I stuck a hose to my exhaust pipe of my car, took 2 sleeping tablets so I would not wake up and get out, and went to sleep. EIGHT hours later I awoke, and drove home dejected and angry. All of this was on 300mg of Effexor. I plummeted even further, slashing my wrists over 100 times, and never once did I miss a dose.

I was sleeping approx 4 hours per night, put on 10 kilos with no real change in my diet and the brain zaps were very real. I decided to wean myself off the tablets against my doctors advise, and had the worst week of my life. Fast-forward to now 6 weeks later, and I truly believe Effexor gave me the urge to take my life. I feel fantastic, in control and nearly normal. I no longer plot my death or have the urge to cut. The only thing I can thank Effexor for is sorting out my true friends in this world. My suicide attempts were very serious ones, not telling anybody beforehand and by all accounts I should be dead. If it were not for unleaded petrol, I would be. The difference is, it would not be from suicide, it would have been from Effexor.



This is Survivor Story number 43.
Total number of stories in current database is 48

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Baum, Hedlund, Aristei, Guilford & Schiavo vs. Glaxo Smithkline Corporation

Baum, Hedlund, Aristei, Guilford & Schiavo vs. Glaxo Smithkline Corporation

Suit: Antidepressant is Addictive

A lawsuit contends the manufacturer of the popular anti-depressant Paxil concealed evidence that the drug can be addictive

Baum, Hedlund, Aristei, Guilford & Schiavo vs. Glaxo Smithkline Corporation


Suit: Antidepressant is Addictive

To learn more, go to

A lawsuit contends the manufacturer of the popular anti-depressant Paxil concealed evidence that the drug can be addictive.

The lawsuit was filed Friday on behalf of 35 people from around the country who say they suffered symptoms ranging from electric-like shocks to suicidal thoughts after discontinuing use of the drug.

The lawsuit, which seeks class-action status and unspecified damages, says GlaxoSmithkline PLC concealed the possibility of physical and psychological withdrawal symptoms from the drug. It alleges fraud, deceit, negligence, liability, and breach of warranty.

There was no immediate comment from the British-based company. Calls to its U.S. offices after business hours Friday were not returned.

Introduced on the U.S. market in 1992, Paxil is the country’s second-largest selling anti-depressant.

Paul Domb, 42, of Miami, said that after he stopped taking Paxil last year, he suffered from convulsions, night sweats, and suicidal thoughts for about six weeks.

He said he thought the problems had to do with recent heart surgery, but after researching his symptoms he concluded they were caused by his withdrawal from Paxil.

“I stopped taking this drug … and it destroyed me. It almost killed me,” he said.

In June, a Wyoming jury awarded $8 million in damages to the family of a man after determining that Paxil caused him to kill his wife, daughter and granddaughter before committing suicide.

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4/23/2001 – Matt Miller's Zoloft tragedy featured in UK article

When Depression Turns Deadly:
Can Antidepressants Transform Despair into Suicide?

Saturday, April 21, 2001

When Matt Miller’s family moved to a bigger house in a new neighbourhood in
Kansas City, Mo., the athletic 13-year-old with thick blond hair found that
he couldn’t penetrate the cliques at his new school. He was a nobody, an

“He was angry at us, he was angry at the school, his grades suffered. He
wasn’t himself,” said his father, Mark Miller.

The boy’s teachers recommended that he see a psychiatrist, who prescribed
Zoloft, an antidepressant in the same chemical family as Prozac.
The doctor said it would help Matt’s mood, make him feel better about
himself. The boy started taking the pills and seemed to be in good spirits
for a few days.

But then he began showing signs of intense nervousness and agitation. He
couldn’t sit still, his father remembers. He kept kicking people under the
table. His eyes were sunken and he couldn’t sleep, yet he had a restless

After six days on the drug, on July 28, 1997, Matt hanged himself in his
bedroom closet.

“Suicide always takes you by surprise, but no one could have imagined that
Matt would have done that,” Miller said in an interview. “There was no
previous attempt, no serious threat of it, no note, no premeditation.
“It was a very impulsive act I am convinced was brought about by the
stimulant nature of the drug.”

Miller has launched a lawsuit against Pfizer Inc., which makes Zoloft. He is
one of about 200 people who have sued — so far unsuccessfully — the makers
of Prozac and similar products. The plaintiffs contend that the drugs, known
as selective serotonin reuptake inhibitors, caused their loved ones to kill
themselves and, in some cases, hurt or kill others as well.
One of the few cases to go to trial so far was that of William Forsyth, a
63-year-old wealthy Hawaii businessman who stabbed to death his wife of 37
years and then killed himself in 1993. At the time, he had been taking
Prozac for 11 days for panic attacks.

In 1999, a jury in the civil lawsuit cleared Prozac of liability in the
deaths. Forsyth’s adult children began another suit last year accusing Eli
Lilly and Co., the maker of the drug, of covering up damaging details about
the antidepressant.

Chief among the scientific experts who have given people, including Miller
and Forsyth’s children, reason to believe that a link may exist between
antidepressants and suicide is Dr. David Healy, whom Miller has engaged as
an expert witness in his suit.

Healy is a well-known British psychiatrist who argues that Prozac and
similar drugs may trigger suicide in some patients, and that there should be
warning labels on the products.

To Miller, Healy is a hero, a crusading scientist with the guts and
credibility to challenge the powerful, multinational drug companies in an
era in which many researchers and institutions depend on them for funding.
But discussing the down side of Prozac does not appear to have been a good
career move. Healy’s blunt expression of his views may have cost him a job
at the Centre for Addiction and Mental Health, a teaching hospital
associated with the University of Toronto. The centre had been recruiting
him for months, but last year rescinded his written job offer after he gave
a speech warning that Prozac may trigger suicide in some patients.

Eli Lilly Canada Inc. is a major corporate donor to the centre, but
university and hospital officials say their decision had nothing to do with
wanting to please the drug company or to avoid damaging future fundraising
efforts. They say their reasons are confidential.
Healy says the only explanation he was offered was that his lecture
“solidified” the view that he was not a good fit.

For Eli Lilly’s part, it points out that a U.S. Food and Drug Administration
panel of experts voted six to three against requiring Prozac to carry a
suicide-risk warning label. In September of 1991, the FDA concluded that
there was no credible evidence of a causal link between the use of
antidepressant drugs, including Prozac, and suicides or violent behaviour.
And a paper published in March of 1991 by Jerrold Rosenbaum of Massachusetts
General Hospital found that patients on Prozac were not prone to suicide any
more than patients on other medication.

Eli Lilly said, in a written response to questions from The Globe and Mail:
“There is, to the contrary, published scientific evidence showing that
Prozac and medicines like it actually protect against such behaviour —
reducing aggressive and suicidal thoughts and behaviour.”

When Prozac was introduced in the late 1980s, it was billed as a wonder drug
that could combat depression with far fewer risks than previous medications,
including the danger of an overdose or problems when mixed with alcohol.
Prozac and drugs like it — Zoloft, Paxil and Luvox — were said to help
with emotional limitations such as low self-esteem and fear of rejection.
Prozac was a commercial as well as a medical miracle, sold to an estimated
40 million people worldwide since it hit the market.

The drug boosts levels of the neurotransmitter serotonin, which seems to
improve the mood of patients. But within a few years of Prozac’s launch came
hints that it brought out a dark side in a small fraction of users.
Martin Teicher, a researcher at Harvard University, published an article in
the American Journal of Psychiatry in 1990 that discussed six cases in which
patients became intensely preoccupied with suicide after taking the drug.
Other scientists also found a potential link between Prozac and suicide.

Healy says in one of his published papers that Eli Lilly scientists
collaborated with the FDA on designing an experiment that would measure how
serious the problem was, but they then decided against conducting it.
Instead, in 1991, Eli Lilly published an analysis of data taken from
existing trials. Its conclusion? There was no increase of suicidal thoughts
or suicide among depressed patients taking Prozac.

But Healy says in the paper that data from only about one-eighth of the
patients in the clinical trials were included. No mention was made that some
had been prescribed a sedative that may have alleviated an intense nervous
state that can lead to suicide, which is called akathisia, he says.
The analysis also did not point out that 5 per cent of patients dropped out
of the studies because they were anxious and agitated and may have been
suffering from akathisia, Healy says.

Another document, dated Nov. 13, 1990, shows that company scientists were
pressured by executives to soften physicians’ reports of suicidal thoughts
or suicide attempts, according to Harvard psychiatrist Joseph Glenmullen,
who obtained the document and is author of the book Prozac Backlash.
Additional evidence about the potential risks can be found in the patent for
a second-generation Prozac pill, which Eli Lilly has licensed. The patent
says the new and improved Prozac would decrease side effects including:
“nervousness, anxiety, and insomnia,” as well as “inner restlessness
(akathisia), suicidal thoughts and self-mutilation.”

But at the same time, Eli Lilly says these symptoms are not associated in
any significant way with taking the current version of Prozac.
The new Prozac — which incidentally was co-developed by Teicher, one of the
drug’s early critics — isn’t yet on the market, Last year, Healy published a
study in the journal Primary Care Psychiatry that said two of 20 healthy
volunteers taking an antidepressant in the same family as Prozac reported
feeling suicidal.

But by his calculations, probably 40,000 people have committed suicide while
on Prozac since its launch, above and beyond the number who would have taken
their own lives if their condition had been left untreated.

The German government now requires warning labels, and Britain is
considering them. Canada and the United States do not.
Healy says he is not opposed to Prozac and thinks that it can do a lot of
good. But he says it is unethical and irresponsible not to warn doctors
about the potential dangers, and believes Eli Lilly chose not to do so to
maximize profits.

He says family doctors seem to be increasingly prescribing Prozac and other
antidepressants to children and now to women complaining of severe
premenstrual symptoms, yet patients in North America do not have to be told
about the potential risks.

Eli Lilly and the other drug companies argue that depression, not
antidepressants, are to blame for suicides. Pfizer is trying to have Healy
barred from testifying in the Miller case, questioning his credibility as an
expert witness.

So what are Canadian consumers to think? Jacques Bradwejn, chairman of the
psychiatry department at the University of Ottawa, says he has reviewed the
literature and agrees with the FDA and Eli Lilly that there is no evidence
that Prozac and similar drugs cause more suicides than would have occurred
if patients had not been treated.

But a small number of patients — even as many as 1 per cent — may fall
into a nervous state that could trigger suicide, he said, adding that more
research is needed to better understand the problem.

While Prozac may be overprescribed for patients who are not truly ill,
Bradwejn worries that the message that the Prozac is dangerous will do more
harm than good for those who are moderately to severely depressed.
“If the message is too alarmist, it could have a very negative effect on


A study by Dr. David Healy found that two of 20 healthy volunteers taking a
selective serotonin reuptake inhibitor in the same family as Prozac reported
suicidal feelings. This is the story of one of those people, a 30-year-old
woman who didn’t know what drug she was taking, as recorded in the study.
“On the Friday she telephoned early in the morning, distressed and tearful
from the previous night. Her conversation was garbled. She described almost
going out and killing herself. . .

“The night previously she had felt complete blackness all around her. . . .
She felt hopeless and alone. It seemed that all she could do was to follow a
thought that had been planted in her brain by some alien force.
“She suddenly decided she should go and throw herself in front of a car,
that this was the only answer. It was as if there was nothing out there
apart from the car. . . . She didn’t think of her partner or child. She was
walking out the door when the phone went. This stopped the tunnel of
suicidal ideation.

“She later became distraught at what she had nearly done and guilty that she
had not thought of her family.”

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6/28/2000 – Antidepressant medication use and breast cancer risk

As most of you have already read in my book, Dr. Lorne Brandes linked
antidepressants to cancer in a 1992 study. Now we have additional evidence
that this is happening with one of the leading cancer killers in women –
breast cancer. This study indicates that long term use is the biggest culprit
in breast cancer with 2 years of use of the older tricyclic antidepressants ev
en doubling the rate of cancers and Paxil showing a substantial increase as
well. “Use of tricyclic medications for greater than 2 years, however, may be
associated with a twofold elevation, and use of paroxetine [Paxil] may be
associated with a substantial increase in breast cancer risk.”

We are always grateful to have any of you update us on important issues such
as this so that we can notify others. A special thank you goes out to our
Norwegian director, Svein Reseland, for updating us on this study and for the
assistance he has contributed over the years. It is a pleasure to work with

Ann Blake-Tracy, Executive Director,
International Coalition For Drug Awareness

Am J Epidemiol 2000 May 15;151(10):951-7 Related Articles, Books

Antidepressant medication use and breast cancer risk.

Cotterchio M, Kreiger N, Darlington G, Steingart A

Division of Preventive Oncology, Cancer Care Ontario, Toronto, Canada.

[Medline record in process]

Experimental and epidemiologic studies suggest that antidepressant medication
use may be associated with breast cancer risk. This hypothesis was
investigated using a population-based case-control study; cases diagnosed in
1995-1996 were identified using the Ontario Cancer Registry, and controls
were randomly sampled from an Ontario Ministry of Finance database. Data were
collected using a self-administered questionnaire, and multivariate logistic
regression was used to estimate odds ratios and 95% confidence intervals.
Adjusted odds ratio estimates ranged from 0.7 to 0.8 and were not
statistically significant for “ever” use of antidepressants, tricyclics, and
selective serotonin reuptake inhibitors. Compared with no antidepressant use,
use of tricyclic antidepressants for greater than 2 years’ duration was
associated with an elevated risk of breast cancer (odds ratio (OR) = 2.1, 95%
confidence interval (CI): 0.9, 5.0). Of the six most commonly reported
antidepressant medications, only paroxetine use was associated with an
increase in breast cancer risk (OR = 7.2, 95% CI: 0.9, 58.3). Results from
this study do not support the hypothesis that “ever” use of any
antidepressant medications is associated with breast cancer risk. Use of
tricyclic medications for greater than 2 years, however, may be associated
with a twofold elevation, and use of paroxetine may be associated with a
substantial increase in breast cancer risk.

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