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.
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  • Last Updated: 12 August 2009 4:14 PM
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  • 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_ (http://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%).
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/F1)
View larger version (30K):
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(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/F1)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/F1)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/F1)

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.

View this table:
_[in this window]_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/T1)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/T1)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/T1)
Table 1. Baseline Characteristics of the Subjects and Recruitment According
to Study Center.

View this table:
_[in this window]_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/T2)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/T2)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/T2)
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.
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/F2)
View larger version (21K):
_[in this window]_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/F2)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/F2)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/F2)
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).
View this table:
_[in this window]_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/T3)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/T3)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/T3)
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) ).
View this table:
_[in this window]_
(http://content.nejm.org/cgi/content/full/NEJMoa0804633v2/T4)
_[in a new window]_
(http://content.nejm.org/cgi/content-nw/full/NEJMoa0804633v2/T4)
(http://content.nejm.org/cgi/powerpoint/NEJMoa0804633v2/T4)
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.
References
1. Benjamin RS, Costello EJ, Warren M. Anxiety disorders in a pediatric
sample. J Anxiety Disord 1990;4:293-316. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1016/0887-6185(90)90027-\
7&link_type=DOI)
_[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1990EJ54500002&link_type=I\
SI
)
2. Birmaher B, Yelovich AK, Renaud J. Pharmacologic treatment for
children and adolescents with anxiety disorders. Pediatr Clin North Am
1998;45:1187-1204. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1016/S0031-3955(05)70069\
-9&link_type=DOI) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000076256400011&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=9884682&link_type=MED)
3. Achenbach TM, Howell CT, McConaughy SH, et al. Six-year predictors
of problems in a national sample of children and youth: I. Cross-informant
syndromes. J Am Acad Child Adolesc Psychiatry 1995;34:336-347. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1097/00004583-199503000-\
0002

0&link_type=DOI) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1995QK02500020&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=7896676&link_type=MED)
4. Ferdinand RF, Verhulst FC. Psychopathology from adolescence into
young adulthood: an 8-year follow-up study. Am J Psychiatry 1995;152:1586-1594.
_<NOBR Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=ajp&resid=152/11/1\
586
)
5. Pine DS, Cohen P, Gurley D, Brook J, Ma Y. The risk for
early-adulthood anxiety and depressive disorders in adolescents with anxiety
and
depressive disorders. Arch Gen Psychiatry 1998;55:56-64. _<NOBR Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=archpsyc&resid=55/\
1/56
)
6. Pine DS. Child-adult anxiety disorders. J Am Acad Child Adolesc
Psychiatry 1994;33:280-281. _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1994MT23000019&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=8150802&link_type=MED)
7. Gurley D, Cohen P, Pine DS, Brook J. Discriminating depression and
anxiety in youth: a role for diagnostic criteria. J Affect Disord
1996;39:191-200. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1016/0165-0327(96)00020-\
1&link_type=DOI) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1996VA95900004&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=8856423&link_type=MED)
8. Shaffer D, Fisher P, Dulcan MK, et al. The NIMH Diagnostic Interview
Schedule for Children Version 2.3 (DISC-2.3): description, acceptability,
prevalence rates, and performance in the MECA study. J Am Acad Child Adolesc
Psychiatry 1996;35:865-877. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1097/00004583-199607000-\
00012&link_type=DOI
) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1996UT65000012&link_type=I\
SI
)
_[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=8768346&link_type=MED)
9. Klein R. Anxiety disorders. In: Rutter M, Taylor E, Hersov L, eds.
Child and adolescent psychiatry: modern approaches. 3rd ed. London: Blackwell
Scientific, 1995:351-74.
10. Kendall PC, Treating anxiety disorders in children: results of a
randomized clinical trial. J Consult Clin Psychol 1994;62:100-111. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1037/0022-006X.62.1.100&
link_type=DOI) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1994MW67500015&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=8034812&link_type=MED)
11. Kendall PC, Flannery-Schroeder E, Panichelli-Mindel SM,
Southam-Gerow M, Henin A, Warman M. Therapy for youths with anxiety disorders:
a second
randomized clinical trial. J Consult Clin Psychol 1997;65:366-380. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1037/0022-006X.65.3.36
6&link_type=DOI) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1997XA22300002&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=9170760&link_type=MED)
12. Birmaher B, Axelson DA, Monk K, et al. Fluoxetine for the treatment
of childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry
2003;42:415-423. _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000181706500007&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=12649628&link_type=MED)
13. The Research Unit on Pediatric Psychopharmacology Anxiety Study
Group. Fluvoxamine for the treatment of anxiety disorders in children and
adolescents. N Engl J Med 2001;344:1279-1285. _<NOBR Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=nejm&resid=344/17/\
1279
)
14. James A, Soler A, Weatherall R. Cognitive behavioural therapy for
anxiety disorders in children and adolescents. Cochrane Database Syst Rev
2005;4:CD004690-CD004690. _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=16235374&link_type=MED)
15. Bridge JA, Iyengar S, Salary CB, et al. Clinical response and risk
for reported suicidal ideation and suicide attempts in pediatric
antidepressant treatment: a meta-analysis of randomized controlled trials. JAMA
2007;297:1683-1696. _<NOBR Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=jama&resid=297/15/\
1683
)
16. Diagnostic and statistical manual of mental disorders, 4th ed., text
rev.: DSM-IV-TR. Washington, DC: American Psychiatric Association, 2000.
17. Kendall PC, Hedtke KA. Cognitive-behavioral therapy for anxious
children: therapist manual. 3rd ed. Ardmore, PA: Workbook Publishing, 2006.
18. Idem. Coping Cat workbook. 2nd ed.. Ardmore, PA: Workbook
Publishing, 2006.
19. Kendall PC, Gosch E, Furr JM, Sood E. Flexibility within fidelity. J
Am Acad Child Adolesc Psychiatry 2008;47:987-993. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1097/CHI.0b013e31817eed2\
f&link_type=D

OI) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=18714195&link_type=MED)
20. Albano AM, Silverman WK. The anxiety disorders interview schedule
for DSM-IV, child version: clinician manual. New York: Oxford University Press,
1996.
21. Guy W, Bonato R, eds. CGI: Clinical Global Impressions. Chevy Chase,
MD: National Institute of Mental Health, 1970.
22. The Pediatric Anxiety Rating Scale (PARS): development and
psychometric properties. J Am Acad Child Adolesc Psychiatry 2002;41:1061-1069.
_[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1097/00004583-200209000-\
00006&link_type=DOI
) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000177597000006&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=12218427&link_type=MED)
23. Shaffer D, Gould MS, Brasic J, et al. A Children’s Global Assessment
Scale (CGAS). Arch Gen Psychiatry 1983;40:1228-1231. _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A1983RP17500010&link_type=I\
SI
)
_[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=6639293&link_type=MED)

24. Miller RG. Simultaneous statistical inference. New York:
McGraw-Hill, 1966.
25. Rynn MA, Siqueland L, Rickels K. Placebo-controlled trial of
sertraline in the treatment of children with generalized anxiety disorder. Am J
Psychiatry 2001;158:2008-2014. _<NOBR Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=ajp&resid=158/12/2\
008
)
26. Silverman WK, Pina AA, Viswesvaran C. Evidence-based psychosocial
treatments for phobic and anxiety disorders in children and adolescents. J Clin
Child Adolesc Psychol 2008;37:105-130. _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=18814641&link_type=MED)
27. Beidel DC, Turner SM, Sallee FR, Ammerman RT, Crosby LA, Pathak S.
SET-C versus fluoxetine in the treatment of childhood social phobia. J Am Acad
Child Adolesc Psychiatry 2007;46:1622-1632. _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000251141800011&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=18030084&link_type=MED)
28. Kendall PC, Hudson JL, Gosch E, Flannery-Schroeder E, Suveg C.
Cognitive-behavioral therapy for anxiety disordered youth: a randomized
clinical
trial evaluating child and family modalities. J Consult Clin Psychol
2008;76:282-297. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1037/0022-006X.76.2.282&\
link_type=DOI
) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000254539400010&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=18377124&link_type=MED)
29. Chambless DL, Hollon SD. Defining empirically supported therapies. J
Consult Clin Psychol 1998;66:7-18. _[CrossRef]_ (http://content
.nejm.org/cgi/external_ref?access_num=10.1037/0022-006X.66.1.7&link_type=DOI)
_[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000071929800002&link_type=I\
SI
)
_[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=9489259&link_type=MED)
30. Wagner KD, Berard R, Stein MB, et al. A multicenter, randomized,
double-blind, placebo-controlled trial of paroxetine in children and
adolescents
with social anxiety disorder. Arch Gen Psychiatry 2004;61:1153-1162. _<NOBR
Full Text]_
(http://content.nejm.org/cgi/ijlink?linkType=ABST&journalCode=archpsyc&resid=61/\
11/1153
)
31. March JS, Entusah AR, Rynn M, Albano AM, Tourian KA. A randomized
controlled trial of venlafaxine ER versus placebo in pediatric social anxiety
disorder. Biol Psychiatry 2007;62:1149-1154. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1016/j.biopsych.2007.02.\
025&link_type=DOI
)
_[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=000250905800012&link_type=I\
SI
) _[Medline]_
(http://content.nejm.org/cgi/external_ref?access_num=17553467&link_type=MED)
32. Kiesler DJ. Some myths of psychotherapy research and the search for
a paradigm. Psychol Bull 1966;65:110-136. _[CrossRef]_
(http://content.nejm.org/cgi/external_ref?access_num=10.1037/h0022911&link_type=\
DOI
) _[ISI]_
(http://content.nejm.org/cgi/external_ref?access_num=A19667673600005&link_type=I\
SI
)
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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6/26/2001 – Part 1 – Creating an Epidemic of Columbine Shooters!!!

This week I was interviewed on CNN about new “research” on treating anxiety
in children with the SSRI, Luvox.

[I will first send you research out of Australia about anxiety and serotonin
levels along with an e-mail that just came in from a mother whose son had his
life ruined by Luvox and then I will send the Washington Post article next on
the study.]

I must say that we have taken insanity to an all new height with this recent
study out on anxiety in children. The same drug Eric Harris was on in the
Columbine High School shooting, Luvox, is the drug that was used in this
study to treat anxiety in children. But look at what behavior was considered
to be abnormal enough to give this drug that has “psychosis” listed as a
“frequent” side effect!

“Extreme separation anxiety disorder, he said, would be displayed in a child
who avoided birthday parties and sleepovers. A medium-grade example would be
children who refused to sleep in their own rooms and wanted to get into bed
with their parents.”

Now I don’t know about the rest of you, but I had a child that often jumped
in bed with mom and did not like birthday parties very much. Given a choice
between waiting for children to grow out of that as opposed to drugging them
into psychosis, should not be a difficult choice at all!

We don’t get to enjoy these little children in our lives for very long.
Before we know it they are grown and gone. Why not enjoy the short time they
want to crawl into bed with mom and dad to be cuddled and reassured that
everything is okay? But to look at this as a serious mental disorder for
which they need to be drugged?!! This is greed beyond anything imaginable!

When we look at the science behind anxiety disorders the insanity grows by
leaps and bounds because medical research over the last several decades has
continued to show (as documented in Prozac: Panacea or Pandora?) that
anxiety, along with other mood disorders, is associated with ELEVATED levels
of serotonin, rather than decreased levels of serotonin. So in a patient
suffering from anxiety, WHY would we want to increase already elevated levels
of serotonin with an SSRI?

Dr. Murray Ellis at the Baker Medical Research Institute in Melbourne,
Australia found last year that 75% of those suffering from various anxiety
disorders had EIGHT times higher levels of serotonin even on days when they
did not demonstrate anxiety symptoms.

So, as I asked on CNN, I once again ask, “Why on earth would we want to do
anything to increase serotonin in those who already demonstrate symptoms of
ELEVATED serotonin?”

My heart aches for these children who were tortured and maimed as guinea
pigs, given this deadly drug for the sole purpose of increasing the profits
of those who still have their hands dripping with the blood of all the
Columbine victims.

Ann Blake-Tracy, Executive Director,
International Coalition For Drug Awareness
www.drugawareness.org
____________________________

http://theage.com.au/news/20000514/A59189-2000May13.html

Dramatic reversal in research on anxiety

By STEVE DOW
Sunday 14 May 2000

Startling and unexpected findings on panic disorder patients could
fundamentally change the way anxiety and anxiety-related depression are
treated.

The findings by Melbourne’s Baker Medical Research Institute, presented to a
recent scientific meeting and soon to be submitted to the medical journal The
Lancet, have unsettled scientists and turned upside down their ideas on brain
chemistry among the anxious.

But the evidence from the work by cardiologist Professor Murray Esler and
colleagues is so strong that it is being taken seriously.

The scientists tested the levels of the mood-regulating chemical serotonin in
20 patients who suffer panic attacks and found that, even on a good day, the
average levels of the chemical in the brains of at least 15 of the patients
were eight times higher than normal.

Until now, the theory has been that anxiety, panic and anxiety-related
depression are caused by a lack or underactivity of serotonin in the brain.
Based on this theory, the selective serotonin re-uptake inhibitor (SSRI)
wonder drugs that emerged in the ’90s – marketed as Prozac, Aropax and Zoloft
– are intended to increase serotonin around the brain neurons involved in
anxiety.

Professor Esler emphasised that the SSRIs were “great drugs” and should
remain worldwide bestsellers.

However, there were two important implications of the new research, he said.

First, the conventional view of how SSRIs operate has been challenged. It
would appear that the drugs are effective because, over time, they somehow
decrease, rather than increase, serotonin as originally thought.

Second, the new findings could spark drug companies to create drugs that stop
serotonin directly. Such a response might stop the common problem of
“serotonin agitation” experienced by many patients on SSRIs. These patients
experience increased anxiety in their first weeks of treatment on drugs such
as Prozac, Aropax and Zoloft; the drugs making the problem “worse before they
make it better”, Professor Esler said.

He said there was now compelling evidence that panic disorder and depression
were on a par with high blood pressure and smoking as risk factors for heart
disease. A study of several panic disorder patients had shown a spasm of
coronary arteries was common after an attack. One patient, a woman of 40,
suffered a clot and subsequent heart attack because of her panic disorder.

The Baker Institute wishes to recruit patients who suffer panic disorders and
depression for future studies. Contact the institute on 95224212.

NEWS 14: The Health Report
_____________________________________

Teenager on Luvox – aggressive, homicidal
3/26/01

This letter is for your feedback section on the net. In July of 1999 our son,
then 14 years old, was started on Luvox by a psychiatrist for treatment of
his compulsive behavior. We had actually taken him there for treatment of
depression, but the doctor said he was depressed because of his compulsive
disorder. As our son was 6 foot tall and 300+ pounds, the doctor eventually
had him on a dose up to 300 mg a day. Our son started to act very aloof and
irritable. When he was depressed he talked about killing himself, he would
sleep a lot, and he drew pictures of guns. But once on the Luvox, he became
aggressive towards us and would swing at us at the least provocation.

Just before Christmas he came up to me, his mother, and said, “Something is
wrong with me,” but he couldn’t explain it. I didn’t realize at all what he
meant. On Christmas he opened his gifts methodically with no expression on
his face. He had always loved this holiday and now he was acting like a
zombie.

In the winter of 2000, we got a call from his school that he had threatened
some people. The police were called. Apparently our son, who had never done
anything wrong in school or out, had been talking in the cafeteria about
killing the family of a girl he knew, then killing her. He went into graphic
detail and then looked at two boys who were sitting nearby listening and said
to them, “If you tell anyone, I’ll kill you”. The boys turned him in.

We found out through interviews the police had with other kids in the school
that our son had also plotted the same demise for another family of a girl he
knew. He had told this girl to her face. She and her family, however, knew
our son and knew this was not his normal behavior. They therefore did nothing
about it.

To make a long story short, he was arrested but not taken to jail
immediately because we begged to take him home and watch him 24 hours a day.
He had to be drug tested. He had to go to a partial program for troubled kids
for two weeks. He was given 10 days out of school suspension and the story,
of course, went all over the school. He lost his best friend because the
mother would not let him hang around with our son anymore. No one called to
support him or us. We were isolated from the community. We had to hire a
lawyer because the local police wanted to put him in jail. They had written
up a report that made our son look like he was insane. The report went to the
juvenile court and Children’s Services. We were visited by Children’s
Services and interviewed. Our son went through approximately three different
psychiatric evaluations; however, all of these were done after he was taken
off the Luvox. We had taken him off the drug after this all happened because
we were afraid it might have caused his behavior problem. I had read about
Columbine and knew the boy involved had been on Luvox too. The psychologists
who evaluated him found him to be fine except for depression; again, these
evaluations were after he was taken off the Luvox. Everyone who interviewed
him after he was off the Luvox could not believe he had threatened people
the way he did, he was not the same person.

We were lucky enough to have the case dismissed as it was our son’s first
offense as a juvenile and our state allows one mistake. They supposedly
closed the file, but the local police will have it open until our son is 18.
In the meantime, if he gets into any trouble, they will use it against him.

We pulled our son out of school and homeschooled him to keep him away from
the cruelty of the kids at school. We had to have him tutored and sent him to
summer school so that he could keep up with his class. He is now called a
“Sophomore” instead of a “Junior” because he was short 3/4ths of a credit,
even with all of our effort; although he will graduate with his class as a
Senior next year. The school told us he just won’t ever be a “Junior”. Our
son faces taunting to this day, not as bad as when he first went back to
school in the fall. A boy said “rape” next to him in class and a girl in the
class told her mother and the mother called the police about our son because
she had heard the story and thought he was the one talking about rape. The
guidance counselor told him this year that he has to watch everything that he
says. He cannot say certain words at school, like “gun”, “shoot”, “murder”,
etc because he could get in trouble.

This child will never be the same because of Luvox. His high school years are
a nightmare now and people in this small town will know him as being
“dangerous”. On the bright side, the families of the two girls that he
threatened refused to file any charges against our son because they knew this
was not his usual behavior and that something was “obviously wrong”.

The psychiatrist who gave our son the Luvox became very defensive immediately
after the episode and said that it was not the Luvox, it was our son. He said
that no cases had ever been won against SSRIs. He also told our son that what
he did was horrible, that nobody would ever forget it or forgive him and that
even if he went to another school, they would find out about it.

Can you imagine a psychiatrist saying this to a patient? Needless
to say, we left him after the legal aspect of the case was closed.

My son told me later that when he was on Luvox, he wasn’t afraid to do
anything. He said he had “no fear”.

We hope this will help make people aware of the dangers of Luvox and the
other SSRI drugs. I only wish there was some way to help the people like my
son who have lost so much to this drug.

Please do not print our name or our e-mail address.

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Is there a steroid effect with Prozac

“Wouldn’t it be wonderful if I regain my desire to write and paint when I finally get off Prozac?”

 

I was placed on Prozac a few years ago and tried to stop using it several times. Each time I did, I begin feeling dizzy at times and nauseous. Not long after I begin using Prozac, I started to ‘itch’. My ears itched especially, and the palms of my hand began to appear dry. Are there some ‘corticosteroids’ in Prozac?

[Note: You will find in Prozac: Panacea or Pandora? that there is a DOUBLING of Cortisol levels with only one 30mg dose of Prozac. This would give a VERY powerful corticosteroid effect.]

Now there’s a claim that antidepressants help women in menopause. What’s next?

Prozac is supposed to be now OKed for OCD. Well, it didn’t work for me. I did realize a particular habit it produced for me that was OCD. Every day at noon, I would drive to the same thrift shop stay for about 45 minutes then return to work. If I didn’t go I felt as though something was wrong. I really felt I had to go.

I must say, I believe MOST individuals have some form of OCD. Of course if a company can market a drug, initially meant for one disease, for another disease (problem) whatever euphemistic title applied, then the more $$$ for their corporation. I wonder if someday there will be a “Antidepressant,” rebellion because of the medicines/drugs/chemicals prescribed to persons.

Children are being doped up to keep them quiet so their parents can go to work and not worry about their ‘normal’ activities. I suppose certain mental problems are a continuing trend. “My kid is more of a problem than yours?” “I’m on more med that you?”

I realize I am ranting by writing, but I am so frustrated and disappointed. And, when one complains about such things, what’s one of the first, if NOT the first question one is asked, “How old is the person.” Then, too often, it’s the VICTIM on whom the FAULT is placed.

I know there was a time while taking alprazolam that showed bizarre conduct on my workplace in NJ. I told my supervisor I would apologizes to the person, but I was told NOT to because apparently my conduct was to be kept quiet. I was placed on leave of absence because of my condition. While that conduct occurred, I was under treatment and had been for some time. My conduct was definitely out of character, impulsive, and destructive to my reputation.

The snowball began when I commenced having panic attacks and was ultimately depressed I needed to see a doctor/psychiatrist/counselor. I saw all three. The first med. I was given was Xanax, then Imipramine, I have a list written somewhere, although the list may be got from my former physician, in NJ. Although, with the patient/physician confidentiality law, I suppose one has not access to the files.

I truly hope I can stop using Prozac. Presently I am not under a Dr care and auspices. When we left NJ nearly a year ago, I was given a Prozac prescription 3 month supply, I have been opening the capsules and dividing the contents by thirds. Every other day I would use a third. I suppose when the company I worked for 12 years downsized me in March 1999, I was also egotistically downsized.

That’s another thing, in the past I wrote poetry well, and in an instant. While using Prozac, I lost so much of my artistic desire that I actually became more depressed. Wouldn’t it be wonderful if I regain my desire to write and paint when I finally get off Prozac?

Sincerely

Lorraine B. Jacobs

 

7/2/2000

This is Survivor Story number 17.
Total number of stories in current database is 96

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The Aftermath of Antidepressants

The Aftermath Of Prozac, Zoloft, Luvox, Fen-Phen, & Many Other Serotonergic Drugs

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

Ann Blake-Tracy has specialized for 10 years in adverse reactions to serotonergic medications. She is the executive director of the International Coalition for Drug Awareness (www.drugawareness.org) and author of the book PROZAC:PANACEA OR PANDORA?

WARNING: IT SHOULD BE NOTED THAT A GRADUAL TAPERING OFF OF MEDICATIONS IS SAFEST WITHDRAWAL METHOD TO AVOID SERIOUS WITHDRAWAL EFFECTS

Often there is the terrible withdrawal associated with the SSRIs. Unless patients are warned to come very slowly off these drugs by shaving minuscule amounts off their pills each day, as opposed to cutting them in half or taking a pill every other day, they can go into terrible withdrawal which is generally delayed several months. This withdrawal includes bouts of overwhelming depression, terrible insomnia and fatigue, and can include life-threatening physical effects, psychosis, or violent outbursts.

Note: Keep in mind that these drugs are all serotonergic agents and clones or “copy cat” drugs of Prozac – the first SSRI antidepressant introduced to the market in America. Basically what applies to one, applies to the others. For instance we have more data out on Prozac because it has been around longer, but as the mode of action is the same for all of these meds the effects will be the same for the other drugs on this list as it is for Prozac. If we are discussing one drug, similar effects would be expected from any other company’s version of the drug. In fact it would be more honest to give them the titles of Prozac #1, Prozac #2,Prozac #3, etc. rather than the brand names they have been given, from the second clone, Zoloft, to the latest Prozac clone, Celexa.

My concern is that each new SSRI introduced seems to be a little stronger on serotonin reuptake and therefore potentially more dangerous. And the all too common practice of going from one SSRI to another blocks additional receptors and magnifies the harmful effects of these medications. It is crucial to learn that according to medical research the theory behind this group of drugs is invalid. Known as serotonin reuptake inhibitors. They are designed to block serotonin in the brain, thereby increasing brain levels of this neurotransmitter. Yet for three decades researchers have been intensely interested in serotonin because LSD and PCP produce their psychedelic effects by mimicking serotonin. Elevated serotonin is found in: psychosis or schizophrenia, mood disorders, organic brain disease, mental retardation, autism and Alzheimer’s. While low levels of the metabolism of serotonin (which also produces high serotonin), are found in those with: depression, anxiety, suicide, violence, arson, substance abuse, insomnia, violent nightmares, impulsive behavior, reckless driving, exhibitionism, hostility, argumentative behavior, etc. The drugs increase serotonin and decrease the metabolism of serotonin leading to any and all of the above results. This information is extremely crucial for patients and physicians to learn as soon as possible. We have a high rate of use of these drugs nationwide. Raising serotonin and lowering the metabolism of serotonin in such a large number of people can produce very serious, widespread and long term problems for all of society.

So why are we now in the 90’s being told that increased serotonin is good for us? Is it because it is good for the pocketbooks of the manufacturers? One manufacturer is running full page newspaper and magazine ads and half hour TV infomercials to bring in over $7 million daily, while on the other hand they are settling Prozac suicide cases for huge amounts of money in exchange for silence from victim’s families on the details of those settlements. The silence in the court cases insures that the drug will be allowed to finish out its patent time, thus bringing in the highest possible profits for the company. They know that with $7 million coming in daily, they can afford to settle a large number of lawsuits and still come out “smelling like a rose” financially.

Eli Lilly has been sued for Prozac related deaths in numerous state and federal courts with most of these cases being settled or dismissed – many were dismissed due to the unethical manipulation of the Wesbecker verdict
(see time line for details).

We have witnessed no decrease in suicide, but increases in murder/suicide, suicide, unwed pregnancies, domestic violence, manic-depression, MS, hypoglycemia, diabetes, bankruptcies, divorce, mothers (parents) killing children, road rage, school shootings, cancer, Chronic Fatigue Syndrome, and Fibromyalgia since these serotonergic drugs have become so popular and I relate it directly to the effects of these drugs.

The death toll has continued to climb drastically since I wrote PROZAC: PANACEA OR PANDORA? Some of the cases you may be familiar with are:

1. Mr. and Mrs. Phil Hartman (Zoloft), Prozac was found in the van of Mark Barton, the Atlanta day trader, who recently killed his family and others in a shooting spree before taking his own life;
2. Neal Furrow, in LA Jewish school shooting was reported to have been court ordered to be on Prozac along with several other medications;
3. The Salt Lake Family History Library shooting;
4. School shootings in Littleton, Colorado (Luvox), Atlanta, Georgia, Springfield, Oregon (Prozac), and Caldwell, Idaho;
5. Another boy in Pocatello, ID in 1998 who in seizure activity from Zoloft had a stand off at the school;
6. 15 year old Chris Shanahan (Paxil) in Rigby, ID who out of the blue killed a woman;
7. The shooting at the lottery in Connecticut last spring by Matthew Beck (Luvox) that left five dead in a murder/suicide;
8. The New York City Subway bombing by Edward Leary (Prozac);
9. Nick Mansies (Paxil) in New Jersey who was convicted of killing a little boy who was selling cookies door to door;
10. In Orange County, CA Dana Sue Gray (Paxil) who co-workers described as a very caring nurse killed several elderly people;
11. Officer Stephen Christian (Prozac) one of the finest officers on the Dallas Police force, who ran into a police substation shooting at fellow officers and was killed;
12. 13 year old Chris Fetters (Prozac) in Iowa who killed her favorite aunt;
13. David Rothman (Prozac) killed two co-workers and himself at the Dept. of Agriculture in Ingelwood, CA;
14. Williams Evans (Zoloft) shot one co-worker at the Ohio Bureau of Employment Services before shooting himself in Columbus, OH;
15. Winatchee, WA where 43 people were wrongfully imprisoned in a false accusation of sexual abuse “witch hunt” fury started by a child under the influence of Prozac and Paxil;
16. Christopher Vasquez (Zoloft) killed Michael Morrow in Central Park;
17. Megan Hogg (Prozac) duct taped the mouths and noses of her three little girls and took a handful of pills; Vera Espinoza (Prozac) in Randolph, VT shot her small son and daughter before shooting herself;
18. An elderly man (Prozac) in Layton, UT axed his wife and daughter to death;
19. Margaret Kastanis (Prozac) used a knife and hammer to kill her three children before stabbing herself to death;
20. An elderly man (Paxil) in Dallas, TX strangled his wife before shooting himself twice in the chest;
21. Larramie Huntzinger (Zoloft) blacked out and ran his car into three young girls killing two in Salt Lake City, UT;
22. Mary Hinkelman (Prozac), a nurse in Baroda, MI shot her two small daughters and her sister before shooting herself;
23. Lisa Fox (Prozac) shot her small son and her dog before shooting herself in Brighton, MI;
24. Debi Louselle (Zoloft) shot daughter and then herself in Salt Lake City, UT;
25. A father in Wyoming shot his wife, daughter and baby grand-daughter then himself after only days on Paxil;
26. A mother (Prozac) in Pleasant Grove, UT killed her 17 year old son with a sledge hammer while he slept before she attempted suicide by drinking Drano;
27. Larry Butz, a superintendent of schools in Ames, IA shot his wife, son and daughter before shooting himself – many cases pending in court are not mentioned.

This is only a handful of MANY, MANY more cases – there would not be room for anything else if I continued listing the cases.

A few additional famous victims: Princess Di (Prozac) and Dodi Fayed -via their driver Henri Paul (Prozac), Monica Lewinsky (Prozac, Zoloft, Effexor, Serzone and Phen-Fen), Chris Farley (Prozac), Pres. Clinton’s ex-partner Jim Mc Dougal (Prozac), Abby Hoffman (Prozac), Del Shannon (Prozac), Danielle Steele’s son (Prozac), INXS singer Michael Hutchence (Prozac), Sarah – Dutchess of York (Phen-Fen)

The latest figures show Prozac has about 44,000 adverse reports filed with the FDA. Out of those reports there are about 2,500 deaths with the large majority of them linked to suicide or violence.

The suicide statistics relating to women are shocking. According to the CDC there are about 30,000 suicides yearly in the United States. Out of those about 6,000 are women – a ratio of about 4.3 to 1, male to female. About twice as many women as men are treated for depression demonstrating that generally men are more than 8 times as lethal in their suicidal gestures as women. Women were known to use less lethal means until the SSRI antidepressants hit the market. But on Prozac and Paxil, women committed 40% of the suicides – many were strikingly violent and clearly leaving no
means for rescue. (Remember that because Prozac was the first of this group of drugs its track record gives us a vision of what is to come with other serotonergic antidepressants, especially when they are so powerful in the reuptake of serotonin.)

TIME LINE OF CRITICAL INFORMATION DISCOVERED SINCE THE BOOK:

*NOTE: Any documents beginning with PZ are Lilly documents on Prozac which have been ferreted out by attorneys and are now being used in lawsuits against the drug company. (Christian vs. Eli Lilly, by Vickery & Waldner, Houston, TX)

* Mid 1950’s: Dr. Felix Sulman began his research on those who suffer from high serotonin levels because of an inability to metabolize serotonin. He found that serotonin is a stress neuro-hormone leading even rabbits, the most docile of creatures, to be aggressive. He coined the term “serotonin irritation syndrome.” He found that those who were unable to break down serotonin would have the levels increase. They were in effect being poisoned by the serotonin produced by their own bodies, the irritation victims suffered from migraines, hot flashes, irritability, sleeplessness, pains around the heart, difficulty in breathing, a worsening of bronchial complaints, irrational tension and anxiety. . . horrifying nightmares. It also caused his volunteers to sleep badly – that is, always on the edge of consciousness so that they were not properly rested – and to wake after only a few hours of sleep.” (sleep apnea) He also found it caused pregnant women to abort.
* October, 1977: Slater, et.al., Inhibition of REM Sleep by Fluoxetine, a Specific Inhibitor of Serotonin Uptake, October 1977, at p. 385 – Prozac was found to affect sleep habits, specifically to suppress deep sleep, which the scientists call REM (rapid eye movement) sleep in cats. By the fourth day of drug treatment the cats receiving the larger doses, which had been friendly for years, began to growl and hiss. After cessation of the drug treatment, the cats returned to their usual friendly behavior in a week or two; those on the higher doses recovering more slowly. – – 1977: [PZ 1298 1999] “A total of six dogs from the high dose group were removed from treatment … due to severe occurrences of either aggressive behavior, ataxia, or anorexia.”]
* July 31, 1978: [PZ1061 1025-28, July 31, 1978] Human subjects began to be used by Lilly in controlled clinical trials. The first group of patients showed no improvement in their depression, but there were a “large number of reports of adverse reactions.” The first human to receive Prozac experienced “dystonia resembling an extrapyramidal reaction” – an uncontrollable, Parkinson-like shaking or trembling.
* July 23, 1979 [PZ 1297 969] The clinical studies in depression showed that “some patients have converted from severe depression to agitation within a few days; in one case the agitation was marked and the patient had to be taken off drug. In future studies the use of benzodiazepines to control the agitation will be permitted.”
* August 3, 1979: The clinical trials excluded patients who had serious suicidal risk. [E.g. control #001519, IND Protocol No. 14, August 3, 1979; PZ1135 695, July 2, 1986 memorandum of Dr. Wernicke].
* December 17, 1984: [PZ 65 449, report of Lilly to FDA] Lilly reported to the FDA that benzodiazepines and other sedatives were given with Prozac throughout the clinical trials. This was to help offset the stimulant effect of the drug. In a memorandum of Lilly scientist Charles Beasley [PZ 541 2007-08] issues of “agitation vs. sedation” and concomitant sedative medications like benzodiazepines (to control the agitation) are discussed. Concerns are that agitation in a suicidal patient can induce suicide.
* March 3, 1986 Lilly controlled the flow of information to the FDA and decided that suicide data on Prozac should not be evaluated, “in the safety-update for the FDA the number of suicides and suicide attempts will not be especially evaluated.” [PZ 879 1966, March 3, 1986 telex]
* September 12, 1986: German BGA very concerned with the risk of suicide and ultimately approved Prozac on the condition that physicians be warned of the risk of suicide and told to consider using sedatives and closely monitor patients. [PZ 878 1383, report of Lilly consultant Pohlmeier; PZ 2467 299, September 12, 1986] Lilly actually warned physicians in Germany and other countries that this measure “can be necessary” to minimize the risk of suicide, [PZ 1341 402, December 6, 1989 German warning; PZ 2469 490]
* February 7, 1990: In response to the Harvard study, Teicher, et al., Lilly’s top scientist, Leigh Thompson, told his fellow executives that “Lilly can go down the tubes if we lose Prozac”. [PZ 1941 827, February 7, 1990]. In the ensuing months Dr. Thompson spoke frequently with his principal FDA regulator about the issue, once at 6:15 in the morning. [PZ 391 1959, July 18, 1990]. Lilly later described the man as “our defender”. [PZ1941 2256, September 12, 1990]
* May 29, 1990, Lilly added “suicidal ideation” in the section dealing with post-marketing reports. [PZ883 562, July 26, 1990 memorandum]
* September 14, 1990: Contrary to the advice of his staff, Dr. Thompson told the Eli Lilly Board of Directors that suicide and hostile acts were probably, caused by the patients’ underlying disorders rather than Prozac. [PZ542 2101, September 14, 1990; PZ4002 889, Board Minutes]. The staff was concerned because they knew that this issue was never studied during the clinical trials.
* September 11, 1990: Note from Dr. Bruce Stadel, Chief of the Epidemiology Branch, attaching an analysis done by Dr. David Graham, Section Chief within the Epidemiology Branch, of Lilly’s July 17, 1990 submission to the FDA on the Prozac/suicidality/violence issue. The following factors were (a) brought to the attention of those in the higher echelons of the FDA, but (b) ignored, discounted or “trashed” by them: #1 Lilly’s analysis improperly excluded 76 out of 97 suicides; as Dr. Stadel expressed it, “[i]t is inappropriate in a safety analysis to exclude such a large proportion of case”; #2 Lilly admitted that its clinical trials “were not designed for the prospective evaluation of suicidality” and that “[i]n these trials, patients with current suicidal ideation were excluded”; #3 Lilly admitted that the HAMD-3 rating scale it used to assess suicidality in clinical trials was inadequate; and that Lilly’s statements about violence only demonstrated “how great under-reporting is” and that “[t]he actual data showed a higher percentage of treatment-emergent suicidality among fluoxetine (2.9% than tricyclic (0.8%) patients . . . [which percentage] was similar to that reported by Teicher.”
* July 1, 1992: A study lead by Dr. Lorne Brandes of the Manatoba Institute of Cell Biology in Winnipeg, Canada was published in CANCER RESEARCH linking the two most popular anti-depressants, Elavil and Prozac to cancer.
* 1994: A study headed by Howard Markell published in The Journal of Pediatrics showed LSD flashbacks and LSD reactions induced by Prozac.
* June 9, 1994: The New York Review of Books article by Dr. Sherwin Nuland slams Peter Kramer for pushing Prozac in his book Listening to Prozac. He pointed out that all docs are taught in med school this little poem about serotonin: “This man was addicted to moanin’, confusion, edema, and groanin’, intestinal rushes, great tricolored blushes, and died from too much serotonin.” He listed constriction of lungs and intestines, diarrhea, wheezing, flushing, mental confusion, tightening of bronchioles, and lessening conscious control over behavior from increases in serotonin. “Moreover, . . . it is still too early to arrive at a reliable estimate of possible dangers that may appear in the long term,” and 15% dropped out of the clinical trials on Prozac because of adverse reactions. He also discussed the similarity of serotonin to the psychedelics like LSD and PCP.
* November, 1994: Krystal JH, Webb E, Cooney N, et al., “Specificity of Ethanol-like Effects Elicited in Serotonergic and Noradrenergic Mechanisms,” ARCHIVES OF GENERAL PSYCHIATRY, Vol. 51, Issue 11, pgs 898-911, 1994 demonstrated that an increase in brain levels of either of two neurotransmitters, serotonin or noradrenalin, produces:
#1 a craving for alcohol,
#2 anger,
#3 anxiety.
They found this to be especially true for those who have a history of alcoholism. An increase serotonin in turn increases noradrenalin. Numerous reports have been made by reformed alcoholics who are being “driven” to alcohol again after being prescribed a serotonergic drug. And many other patients who had no previous history of alcoholism have continued to report an “overwhelming compulsion” to drink while using these drugs.

A few personal accounts:

#1 A young woman, a recovering alcoholic, reported that during the eight month period she had been using Prozac she found it necessary to attend AA meetings every day in order to fight off the strong compulsions to begin drinking again.
#2 In the Southeastern United States a middle aged psychologist, also a recovering alcoholic, after being prescribed Prozac, found herself needing to attend AA meetings morning, noon, and night to keep from destroying the sobriety she had achieved.
#3 A young father, who was Mormon and had never before in his life used alcohol, found himself drinking Ever Clear and exhibiting bizarre as well as violent behavior, after being prescribed Prozac and Ritalin.
#4 A young mother who had never used alcohol before began drinking large amounts within weeks of being prescribed Prozac and quickly found herself committed to a mental institution due to the psychotic behavior that resulted. Added to her Prozac prescription were anti-psychotic meds and electric shock treatments. She then began to experience seizures and was started on anti-seizure meds.
#5 A concerned neighbor reported her friend was drinking straight Vodka on a regular basis after being prescribed Zoloft. #6 A daughter reported her father, sober for 15 years, began drinking again on Prozac.

* December, 1994: Not guilty verdict on Wesbecker wrongful death suit against Lilly’s Prozac.
* Treatment emergent suicidality with Prozac has been demonstrated to be two to three times higher than any other anti-depressant. (Jick, et al., Antidepressants and Suicide)
* May, 1995: Judge John Potter who presided over the Wesbecker case filed documents to demand that Lilly be forced to disclose the secret deal they made with the plaintiffs to withhold very damaging evidence in exchange for settlement. In his pleading to the court Potter stated, “Lilly sought to buy not just the verdict, but the court’s judgment as well.” Potter accused Lilly of “giving the verdict the widest possible publicity” accompanied by the claim that Lilly had “proven in a court of law that Prozac was safe.” Furious with Lilly’s attempt to turn his courtroom into an advertising agency for Prozac, he claims his motion reflects “the court’s duty to protect the integrity of the judicial system.” He believes, as do prominent legal ethicists, that a full and open disclosure of the terms of the settlement is a necessary public safety issue.
* July, 1997: Mayo Clinic found that the increased serotonin, which produces blood clotting, was causing a gummy glossy substance to build up on heart valves. Dr. Heidi Connolly with the Divisions of Cardiovascular Diseases and Internal Medicine, who headed the study stated, “We do know that fenfluramine and phentermine [Fen-Phen] alter the way the brain chemical serotonin is metabolized, and serotonin that circulates in the blood can cause valve injury.” Fenfluramine produces a rapid release of serotonin, inhibits serotonin reuptake, and may also have receptor agonist activity. The study’s revelations should send a loud and very clear warning throughout the medical community concerning all serotonergic medications.
* August 25, 1997: Letter to Ann Blake-Tracy, “I caught the last part of your presentation on Radio Station KEX, Portland, while flipping through the dial last night. I was flabbergasted to hear you speak of the horrible potential side effects from Prozac, which I have been taking for approximately four years, particularly since I have been diagnosed recently with cardiomyalgia, severe artery disease, congestive heart failure and also Fibromyalgia. (I was a very “well” person prior to taking the Prozac and am now exhausted all the time, with horrible aching joints and considerable pain and a massive heart problem.) The adverse cardiovascular effects from Prozac, the one drug in this class of drugs out long enough to have somewhat of track record, are listed in the drug information sheet put out by the manufacturer. The “frequent” effects listed are hemorrhage and hypertension. The “infrequent” effects include very serious adverse effects: congestive heart failure, myocardial infarct, tachycardia, angina pectoris, arrhythmia, hypotension, migraine syncope and vascular headache.
* September, 1997: Redux and Phen-Fen were pulled from the market.
* October 20, 1997: Dr. Candace Pert, Research Professor at Georgetown University Medical Center, past head of the brain chemistry department at the National Institute of Health, and author of the new book, MOLECULES OF EMOTION, sounded an alarm in TIME, October 20. She stated, “I am alarmed at the monster that Johns Hopkins neuroscientist Solomon Snyder and I created when we discovered the simple binding assay for drug receptors 25 years ago. Prozac and other antidepressant serotonin-receptor-active compounds may also cause cardiovascular problems in some susceptible people after long-term use, which has become common practice despite the lack of safety studies.”
As we are being led to believe these drugs produce effects only in the brain, Dr. Pert accuses the medical profession of oversimplifying the action of these drugs and adds that “the public is being misinformed about the precision of these selective serotonin-uptake inhibitors.” It is critical that both physicians and patients be made aware of these adverse physical reactions. She points out that the medical profession not only oversimplifies the action of these drugs in the brain, but “ignores the body as if it exists merely to carry the head around!” And that, “these molecules of emotion regulate every aspect of our physiology.” The body plays a very significant role in how we feel and act the way we do. This fact can no longer be ignored. Serotonin and serotonin receptors exist throughout the body, as well as the brain, and every aspect of the body’s physiology is affected by these serotonergic medications. In fact approximately 90% of the body’s serotonin is produced in the intestinal tract. According to Dr. Michael Gershon of New York’s Columbia Presbyterian, this is the reason why Prozac produces so many gastrointestinal side effects.
* March, 1998: Two new studies published. One that shows Prozac so strongly inhibits one particular serotonin receptor that this produces both obesity and seizures and the other discusses the blockage of muscle and neuronal nicotinic acetylcholine receptors indicating interactions between the serotonergic and cholinergic systems in the central nervous system.
* April, 1998: Our next generation of guinea pigs – one month before a 15 year old on Prozac, Kip Kinkel, in Springfield OR killed his parents and two classmates the American Psychiatric Association and the American Academy of Pediatric Psychiatrists asked the FDA to consider the serotonergic antidepressants for use in children as young as two and drugs for anxiety, aggression and manic depression in babies only one month old! The use of Prozac among young children ages 6 – 12 has increased an alarming 400% from 1995 (51.000 new prescriptions) to 1996 (203,000 new prescriptions).
* June, 1999: CLINICAL PSYCHIATRY NEWS reported that Dr. Malcolm Bowers a psychiatrist at Yale has found that physicians are not paying enough attention to patient factors that could make initiation of SSRIs dangerous. He found that “SSRI-induced psychosis has accounted for 8% of all general hospital psychiatric admissions over a recent 14-month period.” And “What is surprising is that this particular group of side effects is really underplayed.” (The 8% figure represents over 150,000 SSRI induced psychotic breaks per year!!!!!!!)

WARNING: Children so often get coughs and colds, yet using a cough or cold medication with dextromethorphan could cause the serotonin syndrome, a very serious and potentially fatal adverse reaction and/or produce PCP reactions.

Serotonin syndrome remains an often misdiagnosed or unrecognized fatal reaction due to the medical profession being so uninformed about this drug-induced disorder.

Developing brains are far more vulnerable than adult brains and brain damage generally becomes more apparent after the brain is fully developed, rather than immediately. Increases in cortisol produce brain damage while medical research shows that one single 30mg dose of Prozac DOUBLES the level of cortisol. This drastic increase in cortisol causes a multitude of serious physical reactions including impairment of linear growth, as well as impairing the development and regeneration of the liver, kidneys, muscles, etc. In light of so many unspeakable tragedies, I have grown weary of all the silly philosophical discussions we have heard since Kramer’s LISTENING TO PROZAC came out. Patients are dying or having their health destroyed mentally as well as physically (when do we begin to discuss the very serious physical side effects associated with high levels of serotonin?). These patients and their families are frantically searching for answers while this research sits right under our noses and could easily be made available to them. The widespread use of Prozac and its clones is not a statement of either their safety or their effectiveness. It is a statement about the effectiveness of an infinite marketing budget and incredible advertising campaign! These drugs have very serious physical side effects, as well as dangerous psychiatric side effects.

To prevent further tragedy this medical research must be acknowledged and addressed in headline news without delay rather than remain buried in seldom read medical research documents as has been the case in the past with other mind- altering medications, once thought to be safe, which were subsequently prohibited by law, i.e. LSD, PCP, cocaine, etc.

PRAISE FOR PROZAC: PANACEA OR PANDORA?

“I started having bad reactions . . . Oct ’96 I found Prozac to be causing joint and muscle pain itself . . . 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 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 who are prepared to fight for the truth for the benefit of mankind.” Oct. 1998 note from a British nurse

“PROZAC: PANACEA OR PANDORA? is an incredible compilation of medical data that will lay the groundwork to educate other professionals and the general public about the new SSRI antidepressants – Prozac, Zoloft, Paxil, Luvox, Effexor and Serzone.” (Jeff Wise, psychologist, Salt Lake County Drug and Alcohol Abuse )

“In 15 years of reading books on drugs I have never read a book with more information or so well documented as PROZAC: PANACEA OR PANDORA?” (Dr. Kevin Millet, Bountiful, UT)

“As I lecture to physicians nationwide on the medical use of psychoactive drugs PROZAC: PANACEA OR PANDORA? always accompanies me in my brief case.” (Dr. Bruce Woolley, neuropsychopharmacologist, Brigham Young University)

“I found PROZAC: PANACEA OR PANDORA? fascinating reading and the most complete analysis of the various factors pertaining to the Prozac controversy.” (Attorney Donald Sokol, Susanville, CA)

“PROZAC: PANACEA OR PANDORA? literally saved my life, and if I’d known about it a year earlier, could have saved me untold grief and agony as well. It is the only collated, comprehensive source I know of for this information , . . .. this book described everything that had happened to me in great detail, gave scientific reasons why it happened, backed it all up with solid research, included testimonials from hundreds of others in the same situation, it immaculately details, explains, and refers one to the latest research on a whole hornet’s nest of ‘atypical’ side-and/or after-effects from the use of these antidepressants. It also contains information on how to reduce the severity of problems encountered while starting on or going off these meds.” (Nick Jameson, Prozac patient)

“Magnificent! This text is a monument to Ann Tracy’s tenacity and love for her fellow human beings.” (Dr. Paul Kennedy, N.J.)

“PROZAC: PANACEA OR PANDORA? has not left one question about these drugs unanswered! Ann Tracy has covered them all.” (Margaret McCaffery, N.Y. who lost her daughter, a neurosurgeon, in a Prozac suicide)

“The work Ann Blake-Tracy is doing is very important and she is truly a heroine.” (Dr. Candace Pert, Washington, DC, one of the two developers of the serotonin binding process which made possible the development of the serotonergic drugs. Dr. Pert has boldly stated, speaking of these serotonergic medications, “I am alarmed at the monsters I created!”)

WARNING: In sharing this information about adverse reactions to antidepressants I always recommend that you also give reference to my CD on safe withdrawal, Help! I Can’t Get Off My Antidepressant!, so that we do not have more people dropping off these drugs too quickly – a move which I have warned from the beginning can be even more dangerous than staying on the drugs!

The FDA also now warns that any abrupt change in dose of an antidepressant can produce suicide, hostility or psychosis. And these reactions can either come on very rapidly or even be delayed for months depending upon the adverse effects upon sleep patterns when the withdrawal is rapid! You can find the CD on safe and effective withdrawal helps here: http://store.drugawareness.org/

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