Lawsuits for Serious SSRI Birth Defects are Frequent

wide eyed baby pic

Lawsuits for Serious SSRI Birth Defects are Frequent

There are currently so many SSRI birth defect lawsuits that have been filed by families whose infants have been born with these defects that the cases are being consolidated in a massive legal action in the federal court system.

Among the health problems that women claim were caused in their infants because of the use of SSRIs during pregnancy are:

* A life-threatening lung condition known as – Persistent Pulmonary Hypertension of the Newborn
*Club Foot
*Cleft Palate
*Cleft Lip
*Ventricular septal malformation
*Omphalocele
*Tetralogy of Fallot
*Limb deformities
*Genital defects
*Heart defects
*Abnormal intestinal defects
*Hydrocephalus
*Atrial septal defect
*Ventral septal defect

Now, the findings of a new study published in the British Medical Journal show that patients taking SSRIs may be at higher risk of developing an abnormal heart beat than patients who take other medications.

[What they are talking about here is the long QT interval that I have been discussing for years and included much information on this in the 2000 edition of Prozac: Panacea or Pandora? – Our Serotonin Nightmare.]

Among the birth defects identified in these SSRI lawsuits are nearly every one of the complaints the mothers had listed:

*Persistent Pulmonary Hypertension of the Newborn
*Heart defects
*Ventricular septal malformation
*Atrial septal defect
*Tetralogy of Fallot
*Cleft lip
*Cleft palate
*Club foot
*Omphalocele
*Limb deformities
*Genital defects
*Abnormal intestinal defects
*Hydrocephalus

In the new research linking SSRIs to increased risk of stroke, the findings of the research, which were published in the journal Neurology, the scientists found that the increased risk of stroke occurs most often during the first few weeks of treatment.

I will follow this up with new research just out that will demonstrate serious problems for the mother after pregnancy due to her use of antidepressants.

– See more at: http://www.resource4thepeople.com/defectivedrugs/SSRI-Birth-Defects.html#sthash.0BfFrwpA.dpuf

Ann Blake Tracy, Executive Director,
International Coalition for Drug Awareness
www.drugawareness.org & http://ssristories.drugawareness.org
Author: “Prozac: Panacea or Pandora? – Our Serotonin Nightmare – The Complete Truth of the Full Impact of Antidepressants Upon Us & Our World” & Withdrawal CD “Help! I Can’t Get Off My Antidepressant!

 

 

 

– See more at: http://www.resource4thepeople.com/defectivedrugs/SSRI-Birth-Defects.html#sthash.0BfFrwpA.dpuf

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Medical News Today: Antidepressants Produce Long-Term Depression

We read in the article below the following statements about long-term use of antidepressants producing long-term depression & withdrawal. Now all these researchers had to do to learn this sooner was read the research in my book when the first edition came out almost 20 years ago. Once again I repeat that the hypothesis behind antidepressants is INCORRECT/BACKWARDS!! And if the hypothesis is backwards the drugs are going to CAUSE what we are being told that they cure!
“. . . there are reasons to believe that antidepressant treatment itself may contribute to a chronic depressive syndrome. . .
In other words, prolonged exposure to antidepressants can induce neuroplastic changes that result in the genesis of antidepressant-induced dysphoric symptoms. The investigators propose the term ‘tardive dysphoria’ to describe such a phenomenon and describe diagnostic criteria for it. Tapering or discontinuing the antidepressant might reverse the dysphoric state. Antidepressant discontinuation may not provide immediate relief. In fact, it is likely that transient symptoms of withdrawal will occur in the initial 2-4 weeks following antidepressant discontinuation or tapering. However, after a prolonged period of antidepressant abstinence, one may see a gradual return to the patient’s baseline.”
Ann Blake-Tracy, Executive Director
International Coalition for Drug Awareness
www.drugawareness.org & www.ssristories.drugawareness.orgAuthor: Prozac: Panacea or Pandora? – Our Serotonin
Nightmare – The Complete Truth of the Full Impact of
Antidepressants Upon Us & Our World & Help! I
Can’t Get Off My Antidepressant!
 
http://www.medicalnewstoday.com/articles/218435.php
A New Troublesome Long-Term Effect Of Antidepressant Drugs; Tardive Dysphoria.
Editor’s Choice
Main Category: Depression
Also Included In: Psychology / Psychiatry
Article Date: 08 Mar 2011 – 0:00 PST

Treatment-resistantdepression (TRD) may be related to inadequate dosing of antidepressants or antidepressant tolerance. Alternatively, there are reasons to believe that antidepressant treatment itself may contribute to a chronic depressive syndrome. This study reports a case of antidepressant discontinuation in a TRD patient, a 67-year-old white man with onset of major depressive illness at the age of 45. He was homozygous for the short form of the serotonin transporter. He was treated off and on until the age of 59 and had been on an antidepressant continuously until the age of 67. Over the previous 2 years he had been depressed without any relief by medication or 2 electroconvulsive treatments. His medications at the time of evaluation included paroxetine 10 mg daily, venlafaxine 75 mg daily and clonazepam 3 mg daily. His 17-item Hamilton depression score was 22. Over the subsequent 6 months, he was started on bupropion and then tapered off all antidepressants, including the bupropion. His Hamilton depression score dropped to 18. The patient was not satisfied with his progress and sought another opinion to restart antidepressants. One year later, on duloxetine 60 mg daily, he continued to complain of unremitting depression.

A possible prodepressant effect of antidepressants has been previously proposed. Fava was the first to suggest that an antidepressant-related neurobiochemical mechanism of increasing vulnerability to depression might play a role in worsening the long-term outcome of the illness. Understanding of potential mechanisms of this phenomenon can be gleaned from observations regarding the short form of the serotonin transporter (5HTTR). Patients with the short form of the 5HTTR and prolonged antidepressant exposure, may be particularly vulnerable to antidepressant-related worsening. In other words, prolonged exposure to antidepressants can induce neuroplastic changes that result in the genesis of antidepressant-induced dysphoric symptoms. The investigators propose the term ‘tardive dysphoria’ to describe such a phenomenon and describe diagnostic criteria for it. Tapering or discontinuing the antidepressant might reverse the dysphoric state. Antidepressant discontinuation may not provide immediate relief. In fact, it is likely that transient symptoms of withdrawal will occur in the initial 2-4 weeks following antidepressant discontinuation or tapering. However, after a prolonged period of antidepressant abstinence, one may see a gradual return to the patient’s baseline.

Source: Journal of Psychotherapy and Psychosomatics, AlphaGalileo Foundation.

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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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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
  • Source: n/a
  • Location: Leeds

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NEJM: On Zoloft Homicidal Ideation Frequent In Those 17 & Under

Since I believe that people should always get credit for the hard work and contribution they make in life I want to give our thanks to Rosie Meysenburg for getting this out to us today and for her comments on it. Rosie has done so much, along with her husband Gene, in posting our years and years worth of work gathering these SSRI & SNRI cases together for the _www.ssristories.drugawareness.org_
(http://www.ssristories.drugawareness.org) site.

“This Adverse Event Report, from a study appearing in the New England Journal of Medicine, shows that of 133 children 17 & under on Zoloft there were 2 who reported “Homicidal Ideation”. There were no reports of “Homicidal Ideation” in the placebo group.

[According to the Physicians Desk Reference, a Frequent adverse reaction is one that occurs in 100 people or less.  Homicidal Ideation occurred in 1 in 66 children on Zoloft aged 17  and under.]

“According to the Physicians Desk Reference, a Frequent adverse reaction is one that occurs in 100 people or less. Homicidal Ideation occurred in 1 in 66 children on Zoloft aged 17 and under.

“This Adverse Event Report was the appendix for this study in the New England Journal of Medicine.”

adverse event report1.pdf

This Adverse Event Report was the appendix for this study in the New England Journal of Medicine:

http://content.nejm.org/cgi/content/full/NEJMoa0804633

And with this new information from the New England Journal of Medicine I want to include information out of Australia which is that Pfizer, the maker of Zoloft, along with the Therapeutic Goods Administration (TGA similar to our FDA), recommends that any SSRI antidepressant should not be prescribed to Australians under the age of 24. Funny, but I missed that warning from Pfizer for Americans under 24, didn’t you?

Next I will send that article that just came out over the weekend because it ties in so closely with this new information on Zoloft. And because there is so much to read in this article alone I am going to cut my comments at this point and let the article speak for itself.

Ann Blake-Tracy, Executive Director,
International Coalition for Drug Awareness
_www.drugawareness.org_ (https://www.drugawareness.org/) &
_www.ssristories.org_ (http://www.ssristories.org/)
Author of Prozac: Panacea or Pandora? – Our
Serotonin Nightmare & the audio, Help! I Can’t
Get Off My Antidepressant!!! ()

_atracyphd1@…_ (mailto:atracyphd1@…)

_http://content.nejm.org/cgi/content/full/NEJMoa0804633_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633)

Published at www.nejm.org October 30, 2008 (10.1056/NEJMoa0804633)
Cognitive Behavioral Therapy, Sertraline, or a Combination in Childhood
Anxiety

John T. Walkup, M.D., Anne Marie Albano, Ph.D., John Piacentini, Ph.D.,
Boris Birmaher, M.D., Scott N. Compton, Ph.D., Joel T. Sherrill, Ph.D., Golda
S. Ginsburg, Ph.D., Moira A. Rynn, M.D., James McCracken, M.D., Bruce Waslick,
M.D., Satish Iyengar, Ph.D., John S. March, M.D., M.P.H., and Philip C. Kendall, Ph.D.

ABSTRACT
Background Anxiety disorders are common psychiatric conditions affecting children and adolescents. Although cognitive behavioral therapy and selective serotonin-reuptake inhibitors have shown efficacy in treating these disorders, little is known about their relative or combined efficacy.

Methods In this randomized, controlled trial, we assigned 488 children between the ages of 7 and 17 years who had a primary diagnosis of separation anxiety disorder, generalized anxiety disorder, or social phobia to receive 14 sessions of cognitive behavioral therapy, sertraline (at a dose of up to 200 mg per day), a combination of sertraline and cognitive behavioral therapy, or a placebo drug for 12 weeks in a 2:2:2:1 ratio. We administered categorical and dimensional ratings of anxiety severity and impairment at baseline and at
weeks 4, 8, and 12.

Results The percentages of children who were rated as very much or much improved on the Clinician Global Impression “Improvement scale were 80.7% for combination therapy (P<0.001), 59.7% for cognitive behavioral therapy (P<0.001), and 54.9% for sertraline (P<0.001); all therapies were superior to placebo
(23.7%). Combination therapy was superior to both monotherapies (P<0.001).

Results on the Pediatric Anxiety Rating Scale documented a similar magnitude and pattern of response; combination therapy had a greater response than cognitive behavioral therapy, which was equivalent to sertraline, and all therapies were superior to placebo. Adverse events, including suicidal and homicidal
ideation, were no more frequent in the sertraline group than in the placebo group. No child attempted suicide. There was less insomnia, fatigue, sedation, and restlessness associated with cognitive behavioral therapy than with sertraline.

Conclusions
Both cognitive behavioral therapy and sertraline reduced the severity of anxiety in children with anxiety disorders; a combination of the two therapies had a superior response rate.

(ClinicalTrials.gov number,
NCT00052078 _[ClinicalTrials.gov]_
(http://content.nejm.org/cgi/external_ref?access_num=NCT00052078&link_type=CLINT\
RIALGOV
) .)

____________________________________
Anxiety disorders are common in children and cause substantial impairment in
school, in family relationships, and in social functioning._1_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R1) ,_2_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R2) Such disorders
also predict adult anxiety disorders and major depression._3_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R3) ,_4_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R4) ,_5_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R5) ,_6_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R6) Despite a high
prevalence (10 to 20%_3_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R3)
,_7_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R7) ,_8_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R8) ) and substantial
morbidity, anxiety disorders in childhood remain underrecognized and
undertreated._1_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R1)
,_9_

(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R9)

An improvement in outcomes for children with anxiety disorders would have important public health
implications.In clinical trials, separation and generalized anxiety disorders and social
phobia are often grouped together because of the high degree of overlap in
symptoms and the distinction from other anxiety disorders (e.g., obsessive compulsive disorder). Efficacious treatments for these disorders include cognitive behavioral therapy_10_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R10) ,_11_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R11) and
the use of selective serotonin-reuptake inhibitors (SSRIs)._12_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R12) ,_13_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R13)

However, randomized, controlled trials comparing cognitive behavioral therapy, the use of an SSRI, or the combination of both therapies with a control are lacking. The evaluation of combination therapy is particularly important because approximately 40 to 50% of children with these disorders do not have a response to short-term treatment with either monotherapy.
_14_(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R14) ,_15_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R15)

Our study, called the Child “Adolescent Anxiety Multimodal Study, was designed to address the current gaps in the treatment literature by evaluating the relative efficacy of cognitive behavioral therapy, sertraline, a combination of the two therapies, and a placebo drug. This article reports the results of short-term treatment.

Methods

Study Design and Implementation

This study was designed as a two-phase, multicenter, randomized, controlled trial for children and adolescents between the ages of 7 and 17 years who had separation or generalized anxiety disorder or social phobia. Phase 1 was a 12-week trial of short-term treatment comparing cognitive behavioral therapy, sertraline, and their combination with a placebo drug. Phase 2 is a 6-month open extension for patients who had a response in phase 1.

The authors designed the study, wrote the manuscript, and vouch for the data gathering and analysis. Pfizer provided sertraline and matching placebo free of charge but was not involved in the design or implementation of the study, the analysis or interpretation of data, the preparation or review of the manuscript, or the decision to publish the results of the study.

Study Subjects

Children between the ages of 7 and 17 years with a primary diagnosis of separation or generalized anxiety disorder or social phobia (according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision
[DSM-IV-TR]_16_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R16) ),
substantial impairment, and an IQ of 80 or more were eligible to participate. Children with coexisting psychiatric diagnoses of lesser severity than the three target disorders were also allowed to participate;
such diagnoses included attention deficit–hyperactivity disorder (ADHD) whilereceiving stable doses of stimulant and obsessive compulsive, post-traumatic stress, oppositional defiant, and conduct disorders. Children were excluded if they had an unstable medical condition, were refusing to attend school
because of anxiety, or had not had a response to two adequate trials of SSRIs or an adequate trial of cognitive behavioral therapy.

Girls who were pregnant or were sexually active and were not using an effective method of birth control
were also excluded. Children who were receiving psychoactive medications other than stable doses of stimulants and who had psychiatric diagnoses that made participation in the study clinically inappropriate (i.e., current majordepressive or substance-use disorder; type ADHD; or a lifetime history of bipolar, psychotic, or pervasive developmental disorders) or who presented an acute risk to themselves or others were also excluded.

Recruitment occurred from December 2002 through May 2007 at Duke University Medical Center, New York State Psychiatric Institute Columbia University Medical Center New York University, Johns Hopkins Medical Institutions, Temple University University of Pennsylvania, University of California, Los Angeles,and
Western Psychiatric Institute and Clinic University of Pittsburgh Medical Center. The protocol was approved and monitored by institutional review boards at each center and by the data and safety monitoring board of the National Institute of Mental Health. Subjects and at least one parent provided written informed consent.

Interventions

Cognitive behavioral therapy involved fourteen 60-minute sessions, which included review and ratings of the severity of subjects’ anxiety, response to treatment, and adverse events. Therapy was based on the Coping Cat program,_17_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R17) ,_18_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R18) which was adapted for the
subjects’ age and the duration of the study._19_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R19)

Each subject who was assigned to receive cognitive behavioral therapy received training in anxiety-management skills, followed by behavioral exposure to anxiety-provoking situations. Parents
attended weekly check-ins and two parent-only sessions. Experienced psychotherapists, certified in the Coping Cat protocol, received regular site-level and cross-site supervision.

Pharmacotherapy involved eight sessions of 30 to 60 minutes each that included review and ratings of the severity of subjects’ anxiety, their response to treatment, and adverse events. Sertraline (Zoloft) and matching placebo were administered on a fixed flexible schedule beginning with 25 mg per day and adjusted up to 200 mg per day by week 8. Through week 8, subjects who were considered to be mildly ill or worse and who had minimal side effects were eligible for dose increases.

Psychiatrists and nurse clinicians with experience in medicating children with anxiety disorders were certified in the study pharmacotherapy protocol and received regular site-level and cross-site supervision.
Pill counts and medication diaries were used to facilitate and document adherence. Combination therapy consisted of the administration of sertraline and cognitive behavioral therapy. Whenever possible, therapy and medication sessions occurred on the same day for the convenience of subjects.

Objectives
Study objectives were, first, to compare the relative efficacy of the three active treatments with placebo; second, to compare combination therapy with either sertraline or cognitive behavioral therapy alone; and third, to assess the safety and tolerability of sertraline, as compared with placebo. We hypothesized that all three active treatments would be superior to placebo and that combination therapy would be superior to either sertraline or cognitive behavioral therapy alone.

Outcome Assessments
We obtained demographic information, information on symptoms of anxiety, and data on coexisting disorders and psychosocial functioning using reports from both the subjects and their parents and from interviews of subjects and parents at the time of screening, at baseline, and at weeks 4, 8, and 12.

The interviews were administered by independent evaluators who were unaware of study-group assignments.
We used the Anxiety Disorders Interview Schedule for DSM-IV-TR, Child Version,_20_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R20) to establish diagnostic eligibility. The categorical primary outcome was the treatment response at week 12, which was defined as a score of 1 (very much improved) or 2 (much improved) on the Clinical Global Impression Improvement scale,_21_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R21) which ranges from 1 to 7, with lower scores indicating more improvement, as compared with baseline. A score of 1 or 2 reflects a substantial, clinically meaningful improvement in anxiety severity and normal functioning. The dimensional primary
outcome was anxiety severity as measured on the Pediatric Anxiety Rating Scale, computed by the summation of six items assessing anxiety severity, frequency, distress, avoidance, and interference during the previous week._22_(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R22)

Total scores on this scale range from 0 to 30, with scores above 13 indicating clinically meaningful anxiety. The Children’s Global Assessment Scale_23_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R23) was used to rate
overall impairment.

Scores on this scale range from 1 to 100; scores of 60 or lower are considered to indicate a need for treatment, and a score of 50 corresponds to moderate impairment that affects most life situations and is readily observable. Agreement among the raters was high for anxiety severity (r=0.85) and diagnostic
status (intraclass correlation coefficient= 0.82 to 0.88) on the basis of a videotaped review of 10% of assessments by independent evaluators that were performed at baseline and at week 12.

Adverse Events
Adverse events were defined as any unfavorable change in the subjects’ pretreatment condition, regardless of its relationship to a particular therapy. Serious adverse events were life-threatening events, hospitalization, or events leading to major incapacity. Harm-related adverse events were defined as thoughts of harm to self or others or related behaviors. All subjects were interviewed at the start of each visit by the study coordinator with the use of a standardized script. Identified adverse events and harm-related events were then evaluated and rated by each subject’s study clinician.

This report presents data on all serious adverse events, all harm-related adverse events, andmoderate and severe (i.e., functionally impairing) adverse events that occurred in 3% or more of subjects in any study group. The data and safety monitoring board of the National Institute of Mental Health performed a quarterly review
of reported adverse events. Given the greater number of study visits (and hence more reporting
opportunities) and the unblinded administration of sertraline in the combination-therapy group, the test of the adverse-event profile of sertraline focused on statistical comparisons between sertraline and placebo and sertraline and cognitive behavioral therapy.

Randomization and Masking
The randomization sequence in a 2:2:2:1 ratio was determined by a computer-generated algorithm and maintained by the central pharmacy, with stratification according to age, sex, and study center. Subjects were assigned to study groups after being deemed eligible and undergoing verbal reconsent with a study investigator. Subjects in the sertraline and placebo groups did not know whether they were receiving active therapy, nor did their clinicians. However, subjects who received combination therapy knew they were receiving active sertraline. The study protocol called for independent evaluators who completed assessments to be unaware of all treatment assignments.

Statistical Analysis
On the basis of previous studies,_10_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R10) ,_11_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R11) ,_12_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R12)
,_13_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R13) ,_14_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R14) ,_15_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R15)
we hypothesized that 80% of children in the combination-therapy group, 60% in either the sertraline group
or the cognitive-behavioral-therapy group, and 30% in the placebo group would be considered to have had a response to treatment at week 12. We determined that we needed to enroll 136 subjects in each active-treatment group and 70 subjects in the placebo group for the study to have a power of 80% to detect a minimum difference of 17% between any two study groups in the rate of response, assuming an alpha of 0.05 and a two-tailed test with no adjustment for multiple comparisons.

Analyses were performed with the use of SAS software, version 9.1.3 (SAS Institute). For categorical outcomes (including data regarding adverse events), treatments were compared with the use of Pearson’s chi-square test, Fisher’s exact test, or logistic regression, as appropriate. Logistic-regression models included the study center as a covariate. For dimensional outcomes, linear mixed-effects models (implemented with the use of PROC MIXED) were used to determine predicted mean values at each assessment point (weeks 4, 8, and 12)
and to test the study hypotheses with respect to between-group differences at week 12.

In each linear mixed-effects model, time and study group were included as fixed effects, with linear and quadratic time and time-by-treatment group interaction terms. Each model also began with a limited number of covariates (e.g., age, sex, and race), followed by backward stepping to identify thebest-fitting and most parsimonious model. In all models, random effects included intercept and linear slope terms, and an unstructured covariance was used to account for within-subject correlation over time. All comparisons were planned and tests were two-sided. A P value of less than 0.05 was considered to indicate statistical significance. The sequential Dunnett test was used to control the overall (familywise) error rate._24_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R24)

We analyzed data from all subjects according to study group. Sensitivity analyses were performed with the last observation carried forward (LOCF) and multiple imputation assuming missingness at random. Results were similar for the two missing-data methods. We report the results of the LOCF analysis because the
response rates were lower and hence provide a more conservative estimate of outcomes.

Results
Subjects
A total of 3066 potentially eligible subjects were screened by telephone
(_Figure 1_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#F1) ). Of these subjects, 761 signed consent forms and completed the inclusion and exclusion evaluation, 524 were deemed to be eligible and completed the baseline assessment, and 488 underwent randomization. Eleven subjects (2.3%) stopped
treatment but were included in the assessment (treatment withdrawals); 46 subjects (9.4%) stopped both treatment and assessment (study withdrawals).

On the basis of logistic-regression analyses, pairwise comparisons indicated that subjects in the cognitive-behavioral-therapy group were significantly less likely to withdraw from treatment than were those in the sertraline group (odds ratio, 0.33; 95% confidence interval [CI], 0.13 to 0.87; P=0.03) or the placebo
group (odds ratio, 0.24; 95% CI; 0.09 to 0.67; P=0.006). Of the 488 subjects who underwent randomization, 459 (94.1%) completed at least one postbaseline assessment, 396 (81.1%) completed all four assessments, and 440 (90.2%) completed the assessment at week 12. Subjects were recruited primarily through advertisements (52.2%) or clinical referrals (44.1%).
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Figure 1. Enrollment and Outcomes.

Subjects who are shown as having withdrawn from treatment discontinued their assigned therapy but continued to undergo study assessment. Subjects who are shown as having withdrawn from the study discontinued both therapy and assessment. CBT denotes cognitive behavioral therapy.

Of 14 possible sessions of cognitive behavioral therapy, the mean (±SD) number of sessions completed was 12.7±2.8 in the combination-therapy group and 13.2±2.0 in the cognitive-behavioral-therapy group. The mean dose of sertraline at the final visit was 133.7±59.8 mg per day (range, 25 to 200) in the combination-therapy group, 146.0±60.8 mg per day (range, 25 to 200) in the sertraline group, and 175.8±43.7 mg per day (range, 50 to 200) in the placebo group.

Demographic and Clinical Characteristics
There were no significant differences among study groups with respect to baseline demographic and clinical characteristics (_Table 1_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#T1) ). The mean age of participants was 10.7±2.8 years, with 74.2% under the age of 13 years.

There were nearly equal numbers of male and female subjects. Most subjects were white (78.9%), with
other racial and ethnic groups represented. Subjects came from predominantly middle-class and upper-middle-class families (74.6%) and lived with both biologic parents (70.3%). Most subjects had received the diagnosis of two or more primary anxiety disorders (78.7%) and one or more secondary disorders
(55.3%). At baseline, subjects had moderate-to-severe anxiety and impairment (_Table
2_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#T2) ).

Given the geographic diversity among study centers, there were significant differences among sites on several baseline demographic variables (e.g., race and socioeconomic status). Overall, these variables were equally distributed among study groups within each center; however, three centers had one instance each of
unequal distribution for sex, race, or socioeconomic status.

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Table 1. Baseline Characteristics of the Subjects and Recruitment According
to Study Center.

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Table 2. Key Outcomes at 12 Weeks.

Clinical Response
In the intention-to-treat analysis, the percentages of children who were rated as 1 (very much improved) or 2 (much improved) on the Clinical Global Impression–Improvement scale at 12 weeks were 80.7% (95% CI, 73.3 to 86.4) in the combination-therapy group, 59.7% (95% CI, 51.4 to 67.5) in the cognitive-behavioral-therapy group, 54.9% (95% CI, 46.4 to 63.1) in the sertraline group, and
23.7% (95% CI, 15.5 to 34.5) in the placebo group (_Table 2_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#T2) ).

With the study center as a covariate, planned pairwise comparisons from a logistic-regression model showed
that each active treatment was superior to placebo as follows: combination therapy versus placebo, P<0.001 (odds ratio, 13.6; 95% CI, 6.9 to 26.8); cognitive behavioral therapy versus placebo, P<0.001 (odds ratio, 4.8; 95% CI, 2.6 to 9.0); and sertraline versus placebo, P<0.001 (odds ratio, 3.9; 95% CI, 2.1 to 7.4). Similar pairwise comparisons revealed that combination therapy was superior to either sertraline alone (odds ratio, 3.4; 95% CI, 2.0 to 5.9; P<0.001) or cognitive behavioral therapy alone (odds ratio, 2.8; 95% CI, 1.6 to 4.8; P=0.001). However, there was no significant difference between sertraline and cognitive behavioral therapy (P=0.41).

There was no main effect for center (P=0.69); however, a comparison among centers according to study group revealed a significant difference in response to combination therapy but no differences with respect to the response to sertraline alone (P=0.15) or cognitive behavioral therapy alone (P=0.25).

Further evaluation of response rates revealed that the average response rate for combination therapy at one center was significantly lower than at the other centers (P=0.002). A sensitivity analysis of site response rates showed that when data from the one site were removed, the average response rate of the other sites was consistent with that of the full sample.

The mixed-effects model for the Pediatric Anxiety Rating Scale revealed a significant quadratic effect for time (P<0.001) and a significant quadratic time-by-treatment interaction for cognitive behavioral therapy versus placebo (P=0.01) but not for either combination therapy or sertraline versus placebo. In other words, as compared with placebo, cognitive behavioral therapy had a linear mean trajectory (_Figure 2_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#F2) ). Planned pairwise comparisons of the expected mean scores on the Pediatric Anxiety Rating Scale at week 12 revealed a similar ordering of
outcomes, with all active treatments superior to placebo, according to the following comparisons: combination therapy versus placebo, t=–5.94 (P<0.001); cognitive behavioral therapy versus placebo, t=–2.11 (P=0.04); and sertraline versus placebo, t=–3.15 (P=0.002). In addition, combination therapy was
superior to both sertraline alone (t=–3.26, P=0.001) and cognitive behavioral therapy alone (t=–4.73, P<0.001). No significant difference was found between sertraline and cognitive behavioral therapy (t=1.32, P=0.19). The same magnitude and pattern of outcome was found for the Clinical Global Impressio Severity
scale and the Children’s Global Assessment Scale.
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Figure 2. Scores on the Pediatric Anxiety Rating Scale during the 12-Week
Study.

Scores on the Pediatric Anxiety Rating Scale range from 0 to 30, with scores higher than 13 consistent with moderate levels of anxiety and a diagnosis of an anxiety disorder. The expected mean score is the mean of the sampling distribution of the mean.

Estimates of the effect size (Hedges’ g) and the number needed to treatbetween the active-treatment groups and the placebo group were calculated. Effect sizes are based on the expected mean scores on the Pediatric Anxiety
Rating Scale, derived from the mixed-effects model. The number needed to treat is based on the dichotomized, end-of-treatment scores on the Clinical Global Impression–Improvement scale with the use of LOCF. The effect size was 0.86 (95% CI, 0.56 to 1.15) for combination therapy, 0.45 (95% CI, 0.17 to 0.74) for
sertraline, and 0.31 (95% CI, 0.02 to 0.59) for cognitive behavioral treatment.

The number needed to treat was 1.7 (95% CI, 1.7 to 1.9) for combination therapy, 3.2 (95% CI, 3.2 to 3.5) for sertraline, and 2.8 (95% CI, 2.7 to 3.0) for cognitive behavioral therapy. Treatment and Study Withdrawals
Most treatment and study withdrawals were attributed to reasons other than adverse events (43 of 57, 75.4%) (_Table 3_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#T3) ).

Of the 14 withdrawals that were attributed to an adverse event, 11 (78.6%) were in the groups receiving either sertraline alone or placebo and consisted of 3 physical events (headache, stomach pains, and tremor) and 8 psychiatric adverse events (worsening of symptoms, 3 subjects; agitation or disinhibition, 3; hyperactivity, 1; and nonsuicidal self-harm and homicidal ideation, 1).
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Table 3. Subjects Who Withdrew from Treatment or the Study.

Serious Adverse Events
Three subjects had serious adverse events during the study period. One child in the sertraline group had a worsening of behavior that was attributed to the parents’ increased limit setting on avoidance behavior; the event was considered to be possibly related to sertraline. A child in the combination-therapy
group had a worsening of preexisting oppositional defiant behavior that resulted in psychiatric hospitalization; this event was considered to be unrelated to a study treatment. The third subject was hospitalized for a tonsillectomy, which was also considered to be unrelated to a study treatment
(_Table
4_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#T4) ).
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Table 4. Moderate-to-Severe Adverse Events at 12 Weeks.

Adverse Events
Subjects in the combination-therapy group had a greater number of study visits and therefore significantly more opportunities for elicitation of adverse events than did those in the other study groups, with a mean of 12.8±4.0 opportunities (range, 1 to 22) in the combination-therapy group, as compared with 9.9±3.6 (range, 1 to 14) in the sertraline group, 10.6±2.0 (range, 1 to 14) in the cognitive-behavioral-therapy group, and 9.7±4.2 (range, 1 to 14) in the placebo group (P<0.001 for all comparisons). Rates of adverse events,
including suicidal and homicidal ideation, were not significantly greater in the sertraline group than in the placebo group. No child in the study attempted suicide. Among children in the cognitive-behavioral-therapy group, there were fewer reports of insomnia, fatigue, sedation, and restlessness or fidgeting than in the sertraline group (P<0.05 for all comparisons). For a list of mild adverse events that were not associated with functional impairment, as well as moderate and severe events, see the _Supplementary Appendix_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633/DC1) ,

available with the full text of this article at www.nejm.org.

Discussion
Our study examined therapies that many clinicians consider to be the most promising treatments for childhood anxiety disorders. Our findings indicate that as compared with placebo, the three active therapies combination therapy with both cognitive behavioral therapy and sertraline, cognitive behavioral therapy alone, and sertraline alone — are effective short-term treatments for children with separation and generalized anxiety disorders and social phobia, with combination treatment having superior response rates. No physical,psychiatric, or harm-related adverse events were reported more frequently in the sertraline group than in the placebo group, a finding similar to that for SSRIs, as identified in previous studies of anxious children._12_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R12) ,_13_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R13) ,_25_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R25)

Few withdrawals from either treatment or the study were attributed to adverse events. Suicidal ideation and homicidal ideation were uncommon. No child attempted suicide during the study period. Since they were recruited at multiple centers and locations, the study subjects were racially and ethnically diverse. However, despite intense outreach, the sample did not include the most socioeconomically disadvantaged children.
Subjects were predominantly younger children and included those with ADHD and other anxiety disorders, factors that allow for generalization of the results to these populations.

Conversely, the exclusion of children and teens with major depression and pervasive developmental disorders may have limited the generalizability of the results to these populations.The observed advantage of combination therapy over either cognitive behavioral therapy or sertraline alone during short-term treatment (an improvement of 21 to 25%) suggests that among these effective therapies, combination therapy
provides the best chance for a positive outcome. The superiority of combination therapy might be due to additive or synergistic effects of the two therapies. However, additional contact time in the combination-therapy group, which was unblinded, and expectancy effects on the part of both subjects and
clinicians cannot be ruled out as alternative explanations.

Nonetheless, the magnitude of the treatment effect in the combination-therapy group (with two
subjects as the number needed to treat to prevent one additional event) suggests that children with anxiety disorders who receive quality combination therapy can consistently expect a substantial reduction in the severity of anxiety. An increased number of visits in the combination-therapy group resulted in increased opportunities for elicitation of adverse events. Consequently, the potential for expectancies among subjects, parents, and clinicians regarding the side effects of medications in the context of more visits may have increased the rate of some adverse events in the combination-therapy group and may limit conclusions that can be drawn regarding the rates of adverse events in combination therapy.

The positive benefit of cognitive behavioral therapy, as compared with placebo, adds new information to the existing literature._26_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R26)
The number needed to treat for cognitive behavioral therapy in this study (three subjects) is the same as that
identified in a meta-analysis of studies comparing subjects who were assigned to cognitive behavioral therapy with those assigned to a waiting list for therapy or to sessions without active therapy._14_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R14)

Our study’s test of cognitive behavioral therapy included children with moderate-to-severe anxiety and addresses criticism of previous trials that included children with only mild-to-moderate
anxiety._14_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R14)
Before our study, cognitive behavioral therapy for childhood anxiety was considered to be
“probably efficacious.”_26_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R26)

This evaluation of cognitive behavioral therapy and other recent studies_27_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R27)
,_28_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R28) suggests that
such therapy for childhood anxiety is a well-established, evidenced-based treatment._29_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R29)

Given that the risk of some adverse events was lower in the behavioral-therapy group than in the sertraline group, some parents and their children may consider choosing cognitive behavioral therapy as their initial treatment.

The results of our study confirm the short-term efficacy of sertraline for children with generalized anxiety disorder_25_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R25) and show that
sertraline is effective for children with separation anxiety disorder and social phobia. The number needed
to treat for sertraline in our study (three subjects) was the same as that previously identified in a meta-analysis_15_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R15) of six
randomized, placebo-controlled trials of SSRIs for childhood anxiety disorders._12_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R12) ,_13_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R13) ,_25_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R25)
,_30_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R30) ,_31_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R31)

These studies and others_27_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R27)
suggest that SSRIs, as a class, are the medication of choice for these conditions. The titration schedule that we used, which emphasized upward dose adjustment in the absence of response and adverse events, suggests that the average end-point dose of sertraline in this study is the highest dose consistent with good outcome and tolerability. No adverse events were observed more frequently in the sertraline group than in the placebo group. In contrast to the apparent risk of suicidal ideation and behavior in studies of depression in children and
adolescents,_15_ (http://content.nejm.org/cgi/content/full/NEJMoa0804633#R15) our study did not demonstrate any increased risk for suicidal behavior in the sertraline group. Given the benefit of sertraline alone or in combination with cognitive behavioral therapy and the limited risk of adverse events associated with the drug in our study, the well-monitored use of sertraline and other SSRIs in the treatment of childhood anxiety disorders is indicated.

Cognitive behavioral therapy and sertraline either in combination or as monotherapies appear to be effective treatments for these commonly occurring childhood anxiety disorders. Results confirm those of previous studies of SSRIs and cognitive behavioral therapy and, most important, show that combination
therapy offers children the best chance for a positive outcome. Our findings indicate that all three of the treatment options may be recommended, taking into consideration the family’s treatment preferences, treatment availability, cost, and time burden. To inform more prescriptive selection of patients for
treatment, further analysis of predictors and moderators of treatment response may identify who is most likely to respond to which_32_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#R32) of these
effective alternatives.
Supported by grants (U01 MH064089, to Dr. Walkup; U01 MH64092, to Dr.
Albano; U01 MH64003, to Dr. Birmaher; U01 MH63747, to Dr. Kendall; U01 MH64107,
to Dr. March; U01 MH64088, to Dr. Piacentini; and U01 MH064003, to Dr. Compton)
from the National Institute of Mental Health (NIMH).

Sertraline and matching placebo were supplied free of charge by Pfizer. Dr. Walkup reports receiving consulting fees from Eli Lilly and Jazz Pharmaceuticals and fees for legal consultation to defense counsel and
submission of written reports in litigation involving GlaxoSmithKline, receiving lecture fees from CMP Media, Medical Education Reviews, McMahon Group, and DiMedix, and receiving support in the form of free medication and matching placebo from Eli Lilly and free medication from Abbott for clinical trials funded by the NIMH; Dr. Albano, receiving royalties from Oxford University Press for the Anxiety Disorders Interview Schedule for DSM-IV, Child and Parent Versions, but not for interviews used in this study, and royalties from the Guilford Press; Dr. Piacentini, receiving royalties from Oxford University Press for treatmentmanuals on childhood obsessive compulsive disorder and tic disorders and from the Guilford Press and APA Books for other books on child mental health and receiving lecture fees from Janssen-Cilag; Dr. Birmaher, receiving consulting fees from Jazz Pharmaceuticals, Solvay Pharmaceuticals, and Abcomm, lecture fees from Solvay, and royalties from Random House for a book on children with bipolar disorder; Dr. Rynn, receiving grant support from Neuropharm, BoehringerIngelheim Pharmaceuticals, and Wyeth Pharmaceuticals, consulting fees from Wyeth, and royalties from APPI for a book chapter on pediatric anxiety disorders; Dr. McCracken, receiving consulting fees from Sanofi-Aventis and Wyeth, lecture fees from Shire and UCB, and grant support from Aspect, Johnson & Johnson, Bristol-Myers Squibb, and Eli Lilly; Dr. Waslick, receiving grant support from Baystate Health, Somerset Pharmaceuticals, and GlaxoSmithKline; Dr. Iyengar, receiving consulting fees from Westinghouse for statistical consultation; Dr. March, receiving study medications from Eli Lilly for an NIMH-funded clinical trial and receiving royalties from Pearson for being the author of the Multidimensional Anxiety Scale for Children, receiving consulting fees from Eli Lilly, Pfizer, Wyeth, and GlaxoSmithKline, having an equity interest in MedAvante, and serving on an advisory board for AstraZeneca and Johnson & Johnson; and Dr. Kendall, receiving royalties from Workbook Publishing for anxiety-treatment materials.

No other potential conflict of interest relevant to this article was reported.

The views expressed in this article are those of the authors and do not necessarily represent the official views of the NIMH, the National Institutes of Health, or the Department of Health and Human Services.
We thank the children and their families who made this study possible; and J. Chisar, J. Fried, R. Klein, E. Menvielle, S. Olin, J. Severe, D. Almirall, and members of NIMH’s data and safety monitoring board.
* The study investigators are listed in the Appendix.
(http://content.nejm.org/cgi/content/full/NEJMoa0804633#RFN1)

Source Information
From the Johns Hopkins Medical Institutions, Baltimore (J.T.W., G.S.G.); New York State Psychiatric Institute–Columbia University Medical Center, New York (A.M.A., M.A.R.); the University of California at Los Angeles, Los Angeles (J.P., J.M.); Western Psychiatric Institute and Clinic University of Pittsburgh Medical Center, Pittsburgh (B.B., S.I.); Duke University Medical Center, Durham, NC (S.N.C., J.S.M.); the Division of Services and Intervention Research, National Institute of Mental Health, Bethesda, MD (J.T.S.); Baystate
Medical Center, Springfield, MA (B.W.); and Temple University, Philadelphia
(P.C.K.).

This article (10.1056/NEJMoa0804633) was published at www.nejm.org on
October 30, 2008. It will appear in the December 25 issue of the Journal.
Address reprint requests to Dr. Walkup at the Division of Child and
Adolescent Psychiatry, Department of Psychiatry and Behavioral Sciences, Johns
Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287.
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Appendix
The following investigators participated in this study: Steering Committee:
J. Walkup (chair), A. Albano (cochair); Statistics–Experimental Design: S.
Compton, S. Iyengar, J. March; Cognitive Behavioral Therapy: P. Kendall, G.
Ginsburg; Pharmacotherapy: M. Rynn, J. McCracken; Assessment: J. Piacentini,
A. Albano; Study Coordinators: C. Keeton, H. Koo, S. Aschenbrand, L. Bardsley,
R. Beidas, J. Catena, K. Dever, K. Drake, R. Dublin, E. Fontaine, J. Furr, A.
Gonzalez, K. Hedtke, L. Hunt, M. Keller, J. Kingery, A. Krain, K. Miller, J.
Podell, P. Rentas, M. Rozenmann, C. Suveg, C. Weiner, M. Wilson, T. Zoulas;
Data Center: M. Fletcher, K. Sullivan; Cognitive Behavior Therapists: E.
Gosch, C. Alfano, A. Angelosante, S. Aschenbrand, A. Barmish, L. Bergman, S.
Best, J. Comer, S. Compton, W. Copeland, M. Cwik, M. Desari, K. Drake, E.
Fontaine, J. Furr, P. Gammon, C. Gaze, R. Grover, H. Harmon, A. Hughes, K.
Hutchinson, J. Jones, C. Keeton, H. Kepley, J. Kingery, A. Krain, A. Langley,
J. Lee, J. Levitt, J. Manetti-Cusa, E. Martin, C. Mauro, K. McKnight, T. Peris, K.
Poling, L. Preuss, A. Puliafico, J. Robin, T. Roblek, J. Samson, M.
Schlossberg, M. Sweeney, C. Suveg, O. Velting, T. Verduin; Pharmacotherapists:
M. Rynn, J. McCracken, A. Adegbola, P. Ambrosini, D. Axelson, S. Barnett, A. Baskina,
B. Birmaher, C. Cagande, A. Chrisman, B. Chung, H. Courvoisie, B. Dave, A.
Desai, K. Dever, M. Gazzola, E. Harris, G. Hirsh, V. Howells, L. Hsu, I.
Hypolite, F. Kampmeier, S. Khalid-Khan, B. Kim, D. Kondo, L. Kotler, M.
Krushelnycky, J. Larson, J. Lee, P. Lee, C. Lopez, L. Maayan, J. McCracken, R.
Means,L. Miller, A. Parr, C. Pataki, C. Peterson, P. Pilania, R. Pizarro, H. Ravi,
S. Reinblatt, M. Riddle, M. Rodowski, D. Sakolsky, A. Scharko, R. Suddath, C.
Suarez, J. Walkup, B. Waslick; Independent Evaluators: A. Albano, G.
Ginsburg, B. Asche, A. Barmish, M. Beaudry, S. Chang, M. Choudhury, B. Chu, S.
Crawley, J. Curry, G. Danner, N. Deily, R. Dingfelder, D. Fitzgerald, P.
Gammon, S. Hofflich, E. Kastelic, J. Keener, T. Lipani, K. Lukin, M. Masarik, T.
Peris, T. Piacentini, S. Pimentel, A. Puliafico, T. Roblek, M. Schlossberg, E.
Sood, S. Tiwari, J. Trachtenberg, P. van de Velde; Pharmacy: K. Truelove, H.
Kim; Research Assistants: S. Allard, S. Avny, D. Beckmann, C. Brice, B.
Buzzella, E. Capelli, A. Chiu, M. Coles, J. Freeman, M. Gringle, S. Hefton, D.
Hood, M. Jacoby, J. King, A. Kolos, B. Lourea-Wadell, L. Lu, J. Lusky, R. Maid, C.
Merolli, Y. Ojo, A. Pearlman, J. Regan, S. Rock, M. Rooney, N. Simone, S.
Tiwari, S. Yeager.

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Cushing’s Syndrome on Prozac–A Nurse’s Story

” (I) thought it was saving my life, while all the time it was insidiously and slowly killing me.”

 

I started having bad reactions in Oct. ’96. I found Prozac to be causing joint and muscle pain itself. I also became concerned that I was developing signs of Cushing’s Syndrome. I was very pro-Prozac until last October and wouldn’t have listened to anything said against it until I got problems (thought it was saving my life, while all the time it was insidiously and slowly killing me!) When I first heard about your book (Prozac: Panacea or Pandora?) on the Internet I was interested but quite skeptical. However, since reading it and having suffered so many problems with Prozac, I have come to the conclusion that the book is brilliant, and a life-line as far as I am concerned. I tried to fault the research and reasoning, but could not and still can’t. I would like to extend my thanks to you for your heroic stance on this enormously important issue. I have tremendous respect and admiration for your hard work, determination and courage in pursuing this subject so vigorously, against so much powerful opposition for the benefit of people like me. Your integrity puts many, if not most doctors and psychiatrists to shame. It is reassuring to find that there are a few people in the world who are prepared to fight for the truth for the benefit of mankind.

A.S., A British Nurse

 

9/1/1997

Years 2000 and Prior

This is Survivor Story number 37.
Total number of stories in current database is 96

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