Please stop the psychiatric torture of Rebecca Merhav now !
by Justice lover
A letter by Benjamin Merhav to the Minister for Mental Health, Victoria, Austrlia :
Ms Lisa Neville,
the Minister for Mental Health,
Melbourne.
Dear Minister,
this is a call for your urgent intervention in the case of Rebecca Merhav, my daughter, whose life is at risk, her well being compromised, and her human rights trampled on by the treating psychiatrist of Junction Clinic.
Although her superior did phone me on 18th February and let me know that it is his intention to withdraw the Seroquel from Rebecca's compulsory drug intake, she is still forced to consume 400mg Seroquel tablet every day in that institution where she is detained.
Obviously, this proves the cynical and arbitrary character of her "treatment" by her treating psychitrist, who as always shows complete disregard for Rebecca's and my (on her behalf) reasoned and well researched objections to the that compulsory "treatment",disregard for Rebecca's well being, and for her right to life.
To my complaint during a phone conversation today the treating psychitrist's superior insists that the Seroquel is causing "improvement" for Rebecca, therefore she must continue to consume the daily 400mg of the poison. All that he was prepared to do for Rebecca was to check personally that claim of "improvement", and Rebecca would have to wait until next week at least to know his opinion.
There are many good reasons to let Rebecca taper off the "Antipsychotic" drugs, cancel the CTO and allow her return to normal life. Here are some of them :
1. Rebecca has been forced for over 30 years now to consume all kinds of psychiatric poisons (wrongly forced on her as "medications" for an "illness" she never had !). In other words, she has been used as a laboratory animal to test on her those poisons. As Rebecca's father I know and testify that there was nothing wrong with her when she was first ordered to be detained for "observation" at the request of her angry mother ( for refusing to do the home chores).
2. The so called "psychotic episodes" that she has had since then were the direct result of the "Antipsychotic" drugs she was forced to take, and/or the sudden withdrawal from them whenever she absconded from her psychiatric detention. As I mentioned in my previous letter this was confirmed to me by a British veteran psychiatrist, whose email was immediately forwarded by me to the treating psychiatrist, but she continues to ignore it.
3. Those 30 years of compulsory psychiatric "treatment" amount to continuous 30 years of physical and mental torture of an innocent person, and for no good reason even from a psychiatric point of view, as she never was a danger to anybody, including herself. Her best years of life were ruined as a result, and she would never be able to have children, even if the CTO and her psychiatric torture were to stop tomorrow. Why continue to further punish her for the rest of her life which is in danger of being cut short as a result of the psychiatric poisons already forced into her ?
4. Recent independent research proves that the so called "Atypical Antipsychotic" drugs - of which the Seroquel and the Risperdal are a part - are not more helpful than the old "Antipsychotic" drugs.They are not helpful, yet they carry more deadly dangers for the consumer, including sudden death. Therfore, even if all the psychiatric labels attached to Rebecca were correct, and she would have been "mentally ill" accordingly, why force on her poisons which carry the risks of death, brain damage, and a long list of other dangerous diseases if she is no danger to anybody ?
5. There are proven alternative healing methods which Rebecca can choose from, if she would need any, following a complete tapering of the Seroquel and Risperdal, why not give a chance to try the alternatives ? Surely, if all fails and she would be back to psychiatric "treatment" it would never be too late to force on her again the "Antipsychotic" poisons !
6. Despite 30 years of psychiatric torture and humiliation Rebecca has proven to be of strong character and of unheard of resilience ! Does she not deserve to be respected now, at the age of 45, and be listened to so as to allow her to return to normal life after all those incredible sufferings inflicted on her so far ? She wants to resume normal life, but the psychiatric poisons turn her into a disabled person, not to mention the horrible stigma attached to all former psychiatric patients !
Please stop the psychiatric torture of my daughter now !
Sincerely, Benjamin Merhav
Wednesday, February 27, 2008
Monday, February 25, 2008
MORE ON THE BIG PHARMA RACKET OF ANTIDEPRESSANTS
by Justice Lover
Following is a scientific report of research done to test Big Pharma-psychiatry claims to the "beneficial" effects of SSRI Antidepressants for people who suffer from depression.
The conclusion of the report's authors is that the "benefits" to consumers are no more than those of a placebo !
Add that to the horrendous dangers and deadly risks associated with consumption of and/or sudden withdrawal from those Antidepressants and you must reach the conclusion that here is a very deadly racket imposed on the unsuspecting public by Big Pharma and by the shrinks under the false cover of "medical treatment" !
Here is the report :
http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045
Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration by
Irving Kirsch1*, Brett J. Deacon2, Tania B. Huedo-Medina3, Alan Scoboria4, Thomas J. Moore5, Blair T. Johnson3
1 Department of Psychology, University of Hull, Hull, United Kingdom, 2 University of Wyoming, Laramie, Wyoming, United States of America, 3 Center for Health, Intervention, and Prevention, University of Connecticut, Storrs, Connecticut, United States of America, 4 Department of Psychology, University of Windsor, Windsor, Ontario, Canada, 5 Institute for Safe Medication Practices, Huntingdon Valley, Pennsylvania, United States of America
Background
Meta-analyses of antidepressant medications have reported only modest benefits over placebo treatment, and when unpublished trial data are included, the benefit falls below accepted criteria for clinical significance. Yet, the efficacy of the antidepressants may also depend on the severity of initial depression scores. The purpose of this analysis is to establish the relation of baseline severity and antidepressant efficacy using a relevant dataset of published and unpublished clinical trials.
Methods and Findings
We obtained data on all clinical trials submitted to the US Food and Drug Administration (FDA) for the licensing of the four new-generation antidepressants for which full datasets were available. We then used meta-analytic techniques to assess linear and quadratic effects of initial severity on improvement scores for drug and placebo groups and on drug–placebo difference scores. Drug–placebo differences increased as a function of initial severity, rising from virtually no difference at moderate levels of initial depression to a relatively small difference for patients with very severe depression, reaching conventional criteria for clinical significance only for patients at the upper end of the very severely depressed category. Meta-regression analyses indicated that the relation of baseline severity and improvement was curvilinear in drug groups and showed a strong, negative linear component in placebo groups.
Conclusions
Drug–placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.
Funding: The authors received no specific funding for this study..
Competing Interests: IK has received consulting fees from Squibb and Pfizer. BJD, TBH, AS, TJM, and BTJ have no competing interests.
Academic Editor: Phillipa Hay, University of Western Sydney, Australia
Citation: Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, et al. (2008) Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration. PLoS Med 5(2): e45 doi:10.1371/journal.pmed.0050045
Received: January 23, 2007; Accepted: January 4, 2008; Published: February 26, 2008
Copyright: © 2008 Kirsch et al.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abbreviations: d, standardized mean difference; FDA, US Food and Drug Administration; HRSD, Hamilton Rating Scale of Depression; LOCF, last observation carried forward; NICE, National Institute for Clinical Excellence; SDc, standard deviation of the change score
* To whom correspondence should be addressed. E-mail: i.kirsch@hull.ac.uk
Editors' Summary
Background.
Everyone feels miserable occasionally. But for some people—those with depression—these sad feelings last for months or years and interfere with daily life. Depression is a serious medical illness caused by imbalances in the brain chemicals that regulate mood. It affects one in six people at some time during their life, making them feel hopeless, worthless, unmotivated, even suicidal. Doctors measure the severity of depression using the “Hamilton Rating Scale of Depression” (HRSD), a 17–21 item questionnaire. The answers to each question are given a score and a total score for the questionnaire of more than 18 indicates severe depression. Mild depression is often treated with psychotherapy or talk therapy (for example, cognitive–behavioral therapy helps people to change negative ways of thinking and behaving). For more severe depression, current treatment is usually a combination of psychotherapy and an antidepressant drug, which is hypothesized to normalize the brain chemicals that affect mood. Antidepressants include “tricyclics,” “monoamine oxidases,” and “selective serotonin reuptake inhibitors” (SSRIs). SSRIs are the newest antidepressants and include fluoxetine, venlafaxine, nefazodone, and paroxetine.
Why Was This Study Done?
Although the US Food and Drug Administration (FDA), the UK National Institute for Health and Clinical Excellence (NICE), and other licensing authorities have approved SSRIs for the treatment of depression, some doubts remain about their clinical efficacy. Before an antidepressant is approved for use in patients, it must undergo clinical trials that compare its ability to improve the HRSD scores of patients with that of a placebo, a dummy tablet that contains no drug. Each individual trial provides some information about the new drug's effectiveness but additional information can be gained by combining the results of all the trials in a “meta-analysis,” a statistical method for combining the results of many studies.
A previously published meta-analysis of the published and unpublished trials on SSRIs submitted to the FDA during licensing has indicated that these drugs have only a marginal clinical benefit. On average, the SSRIs improved the HRSD score of patients by 1.8 points more than the placebo, whereas NICE has defined a significant clinical benefit for antidepressants as a drug–placebo difference in the improvement of the HRSD score of 3 points. However, average improvement scores may obscure beneficial effects between different groups of patient, so in the meta-analysis in this paper, the researchers investigated whether the baseline severity of depression affects antidepressant efficacy.
What Did the Researchers Do and Find?
The researchers obtained data on all the clinical trials submitted to the FDA for the licensing of fluoxetine, venlafaxine, nefazodone, and paroxetine. They then used meta-analytic techniques to investigate whether the initial severity of depression affected the HRSD improvement scores for the drug and placebo groups in these trials. They confirmed first that the overall effect of these new generation of antidepressants was below the recommended criteria for clinical significance. Then they showed that there was virtually no difference in the improvement scores for drug and placebo in patients with moderate depression and only a small and clinically insignificant difference among patients with very severe depression. The difference in improvement between the antidepressant and placebo reached clinical significance, however, in patients with initial HRSD scores of more than 28—that is, in the most severely depressed patients. Additional analyses indicated that the apparent clinical effectiveness of the antidepressants among these most severely depressed patients reflected a decreased responsiveness to placebo rather than an increased responsiveness to antidepressants.
What Do These Findings Mean?
These findings suggest that, compared with placebo, the new-generation antidepressants do not produce clinically significant improvements in depression in patients who initially have moderate or even very severe depression, but show significant effects only in the most severely depressed patients. The findings also show that the effect for these patients seems to be due to decreased responsiveness to placebo, rather than increased responsiveness to medication. Given these results, the researchers conclude that there is little reason to prescribe new-generation antidepressant medications to any but the most severely depressed patients unless alternative treatments have been ineffective. In addition, the finding that extremely depressed patients are less responsive to placebo than less severely depressed patients but have similar responses to antidepressants is a potentially important insight into how patients with depression respond to antidepressants and placebos that should be investigated further.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050045.
The MedlinePlus encyclopedia contains a page on depression (in English and Spanish)
Detailed information for patients and caregivers is available on all aspects of depression (including symptoms and treatment) from the US National Institute of Medical Health and from the UK National Health Service Direct Health Encyclopedia
MedlinePlus provides a list of links to further information on depression
Clinical Guidance for professionals, patients, caregivers and the public is provided by the UK National Institute for Health and Clinical Excellence
Introduction
Meta-analyses of antidepressant efficacy based on data from published trials reveal benefits that are statistically significant, but of marginal clinical significance [1]. Analyses of datasets including unpublished as well as published clinical trials reveal smaller effects that fall well below recommended criteria for clinical effectiveness. Specifically, a meta-analysis of clinical trial data submitted to the US Food and Drug Administration (FDA) revealed a mean drug–placebo difference in improvement scores of 1.80 points on the Hamilton Rating Scale of Depression (HRSD) [2], whereas the National Institute for Clinical Excellence (NICE) used a drug–placebo difference of three points as a criterion for clinical significance when establishing guidelines for the treatment of depression in the United Kingdom [1].
Mean improvement scores can obscure differences in improvement within subsets of patients. Specifically, antidepressants may be effective for severely depressed patients, but not for moderately depressed patients [1,3,4]. The purpose of the present analysis is to test that hypothesis (see Text S1 for the QUOROM checklist).
Conventional meta-analyses are often limited to published data. In the case of antidepressant medication, this limitation has been found to result in considerable reporting bias characterized by multiple publication, selective publication, and selective reporting in studies sponsored by pharmaceutical companies [5]. To avoid publication bias, we evaluated a dataset that includes the complete data from all trials of the medications, whether or not they were published.
Specifically, we analyzed the data submitted to the FDA for the licensing of four new-generation antidepressants for which full data, published and unpublished, were available. As part of the licensing process, the FDA requires drug companies to report “all controlled studies related to each proposed indication” ([6] emphasis in original). Thus, there should be no reporting bias in the dataset we analyze.
Methods
Study Retrieval
Following the Freedom of Information Act (FOIA) [7], we requested from the FDA all publicly releasable information about the clinical trials for efficacy conducted for marketing approval of fluoxetine, venlafaxine, nefazodone, paroxetine, sertraline, and citalopram, the six most widely prescribed antidepressants approved between 1987 and 1999 [2], which represent all but one of the selective serotonin reuptake inhibitors (SSRIs) approved during the study period. In reply, the agency provided photocopies of the medical and statistical reviews of the sponsors' New Drug Applications. The FDA requires that information on all industry-sponsored trials be submitted as part of the approval process; hence the files sent to us by the FDA should contain information on all trials conducted prior to the approval of each medication. This strategy omits trials conducted after approval was granted.
Although sponsors are required to submit information on all trials, the FDA public disclosure did not include mean changes for nine trials that were deemed adequate and well controlled but that failed to achieve a statistically significant benefit for drug over placebo. Data for four of these trials were available from a pharmaceutical company Web site in January 2007 and were obtained from the GlaxoSmithKline clinical trial register (http://ctr.gsk.co.uk/Summary/paroxetine/studylist.asp).
We also identified published versions of the FDA trials via a PubMed literature search (from January 1985 through May 2007) using the keywords depression; depressive; depressed; and placebo; specific names of antidepressant medications; and names of investigators from the FDA trials. Potentially relevant studies were also identified through references of retrieved and review articles and from a partially overlapping list of published versions of trials submitted to the Swedish drug regulatory authority [5]. Using a standardized protocol, all retrieved abstracts and publications were compared to the FDA trials. The match between each published study and its corresponding FDA trial was independently established with 100% agreement by two investigators (BJD and a research assistant).
Selection
Forty-seven clinical trials were identified in the data obtained from the FDA. The trial flow is illustrated in Figure 1. Inclusion of a drug type for which unsuccessful trials were excluded biases overall results in favor of that drug type, in a way that is akin to publication bias. The purpose in using the FDA dataset is precisely to avoid this type of bias by including all trials of each medication assessed. Therefore, we present analyses only for those medications for which mean change scores on all trials were available.
Figure 1. QUOROM Flow Chart
Validity Assessment
The FDA requires that rigorous standards be followed for the conduct of all efficacy trials for marketing approval [8] and also sets specific agency standards for clinical trials of antidepressant drugs [9]. In addition, the FDA independently reviews the clinical trial methods, statistical procedures, and results. The FDA dataset includes analyses of data from all patients who attended at least one evaluation visit, even if they subsequently dropped out of the trial prematurely. Results are reported from all well-controlled efficacy trials of the use of these medications for the treatment of depression. FDA medical and statistical reviewers had access to the raw data and evaluated the trials independently. The findings of the primary medical and statistical reviewers were verified by at least one other reviewer, and the analysis was also assessed by an independent advisory panel. Following FDA standards, all trials were randomized, double-blind, placebo-controlled trials. None used cross-over designs. Patients had been diagnosed as suffering from unipolar major depressive disorder using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria.
Given the above review process, we deemed it appropriate to include all studies deemed adequate and well controlled by FDA reviewers, especially as these are the data upon which the decision to approve these medications was based. Other validity criteria might yield different conclusions. In this review, some of the characteristics that may relate to the quality of trials were coded and assessed as possible moderator variables (e.g., interval of trial). The studies have similar methodological characteristics and were well controlled; therefore the methodological characteristics did not affect the final results.
Study Characteristics
In order to generalize the findings of the clinical trial to a larger patient population, FDA reviewers sought a completion rate of 70% or better for these typically 6-wk trials. Only four of the trials reported reaching this objective, and completion rates were not reported for two trials. Attrition rates were comparable between drug and placebo groups. Of those trials for which these rates were reported, 60% of the placebo patients and 63% of the study drug patients completed a 4-, 5-, 6-, or 8-wk trial. Thirty-three trials were of 6-wk duration, six trials were 4 wk, two were 5 wk, and six were 8 wk. Patients were evaluated on a weekly basis. For this meta-analysis, the data were taken from the last visit prior to trial termination.
Thirty-nine trials focused on outpatients: three included both inpatients and outpatients, three were conducted among the elderly (including one of the trials with both inpatients and outpatients), and two were among patients hospitalized for severe depression. No trial was reported for the treatment of children or adolescents.
Replacement of patients who investigators determined were not improving after 2 wk was allowed in three fluoxetine trials and in the three sertraline trials for which data were reported. The trials also included a 1- to 2-wk washout period during which patients were given placebo, prior to random assignment. Those whose scores improved 20% or more were excluded from the study prior to random assignment. The use of other psychoactive medication was reported in 25 trials. In most trials, a chloral hydrate sedative was permitted in doses ranging from 500 mg to 2,000 mg per day. Other psychoactive medication was usually prohibited but still reported as having been taken in several trials.
Meta-Analytic Data Synthesis
We conducted two types of data analysis, one in which each group's change was represented as a standardized mean difference (d), which divides change by the standard deviation of the change score (SDc) [10], and another using each study's drug and placebo groups' arithmetic mean (weighted for the inverse of the variance) as the meta-analytic “effect size” [11].
The first analysis permitted a determination of the absolute magnitude of change in both the placebo and treatment groups. Results permitted a determination of overall trends, analyses of baseline scores in relation to change, and for both types of models, tests of model specification, which assess the extent to which only sampling error remains unexplained. The results in raw metric are presented comparing both groups, but because of the variation of the SDcs, the standardized mean difference was used in moderator analyses in order to attain better-fitting models [12]. These results are compared to the criterion for clinical significance used by NICE, which is a three-point difference in Hamilton Rating Scale of Depression (HRSD) scores or a standardized mean difference (d) of 0.50 [1].
As known SDcs were related to mean baseline HRSD scores, these scores were used to impute missing SDc values, taking into account both the baseline and its quadratic form and any potential interaction of these terms with group (but in fact, there was no evidence that SDcs depended on treatment group). One trial reported SDcs for its drug and placebo groups that were less than 25% the size of the other trials; because preliminary analyses also revealed that this trial was an outlier, these two standard deviations were treated as missing and imputed. In total, SDcs were known for 28 groups, could be calculated from other inferential statistics in nine comparisons (18 groups), and were imputed in 12 comparisons (24 groups) (47.38%) [13,14].
Overall analyses evaluated both random- and fixed-effects models to assess effect size magnitude; because the same trends appeared for both, for simplicity we present only the fixed-effects results. We also assumed fixed-effects assumptions in order to analyze moderators for both groups. Both Q [15] and I2 [16] indices were used to assess inconsistencies from the models, not only to infer the presence or absence of homogeneity, but also (in the case of I2) to assess the degree of inconsistencies among trials [17]. We assumed fixed-effects models in analyzing moderators using meta-regression procedures [11]. Analyses examining linear and quadratic functions for baseline levels of severity used zero-centered forms of this variable [18].
A last, mixed-effects analysis for the amount of change used a random-effects constant along with fixed-effects moderator dimensions; these models provide more conservative assessments of moderation [19].
Because the same scale was used as the primary dependent variable in all of these trials, we were also able to represent results in their original metric [11]. This form of analysis makes results more easily interpretable in terms of clinical significance because mean change scores are analyzed directly, rather than being converted into effect sizes. The analytic weights are derived from the sample size and the SDc [11]. Finally, to show directly the amount of improvement for each study's drug group against its placebo group, we calculated the difference between the change for the drug group minus the change for the placebo group, leaving the difference in raw units and deriving its analytic weight from its standard error [11,12,20]. Analyses used these weights to examine these controlled outcomes both overall and to determine the extent to which drug-related change is a function of initial severity.
Results
Trial Flow
Mean improvement scores were not available in five of the 47 trials (Figure 1). Specifically, four sertraline trials involving 486 participants and one citalopram trial involving 274 participants were reported as having failed to achieve a statistically significant drug effect, without reporting mean HRSD scores. We were unable to find data from these trials on pharmaceutical company Web sites or through our search of the published literature. These omissions represent 38% of patients in sertraline trials and 23% of patients in citalopram trials. Analyses with and without inclusion of these trials found no differences in the patterns of results; similarly, the revealed patterns do not interact with drug type.
The purpose of using the data obtained from the FDA was to avoid publication bias, by including unpublished as well as published trials. Inclusion of only those sertraline and citalopram trials for which means were reported to the FDA would constitute a form of reporting bias similar to publication bias and would lead to overestimation of drug–placebo differences for these drug types. Therefore, we present analyses only on data for medications for which complete clinical trials' change was reported. The dataset comprised 35 clinical trials (five of fluoxetine, six of venlafaxine, eight of nefazodone, and 16 of paroxetine) involving 5,133 patients, 3,292 of whom had been randomized to medication and 1,841 of whom had been randomized to placebo.
Mean Change
Baseline HRSD scores, improvement, and sample sizes in drug and placebo groups for each clinical trial are reported in Table 1. As in the FDA files, studies are identified by protocol numbers. The data from these trials can be obtained from the FDA using FOIA requests and citing the medication name and protocol number. The table also includes references to published reports of the data abstracted from the FDA files, when they could be found (using the search methods described above). Studies in which data only from selected sites of a multisite study were published are not cited in the table.
We have also excluded published reports in which dropouts have been removed from the data. For each of the trials, the pharmaceutical companies had submitted to the FDA data in which attrition was handled by carrying forward the last observation carried forward (LOCF) on the patient, which was the basis in all cases of the FDA review. These data and their corresponding citations appear in the table. Even in the LOCF data, there sometimes are some minor discrepancies between the published version and the version submitted to the FDA. In some cases, for example, the N is slightly larger in the published studies than in the data reported to the FDA. Further complicating this problem is the fact that occasionally, the company has published a trial more than once, with slight discrepancies in the data between publications. Data in the table are those reported to the FDA.
Table 1.
Baseline HRSD Scores, Sample Sizes, and Raw and Standardized Improvement with Confidence Intervals, as Reported to the FDA for Drug and Placebo Groups
Confirming earlier analyses [2], but with a substantially larger number of clinical trials, weighted mean improvement was 9.60 points on the HRSD in the drug groups and 7.80 in the placebo groups, yielding a mean drug–placebo difference of 1.80 on HRSD improvement scores. Although the difference between these means easily attained statistical significance (Table 2, Model 3a), it does not meet the three-point drug–placebo criterion for clinical significance used by NICE. Represented as the standardized mean difference, d, mean change for drug groups was 1.24 and that for placebo 0.92, both of extremely large magnitude according to conventional standards. Thus, the difference between improvement in the drug groups and improvement in the placebo groups was 0.32, which falls below the 0.50 standardized mean difference criterion that NICE suggested. The amounts of change for drug and placebo groups varied widely around their respective means, Q(34)s = 51.80 and 74.59, p-values < i2s =" 34.18" style="font-weight: bold; font-style: italic;">Table 2.
Models of Improvement in Depression Scores Based on Group Assignment (Drug versus Placebo) and Initial Depression Severity (as Gauged by HRSD)
Drug and Initial Severity Trends in Change
Moderator analyses examined whether drug type, duration of treatment, and baseline severity (HRSD) scores related to improvement. Although drug type and duration of treatment were unrelated to improvement, the drug versus placebo difference remained significant, and amount of improvement was a function of baseline severity (Table 2, Model 1a). Specifically, the amount of improvement depended markedly on the quadratic function of baseline severity, but the linear function of baseline severity interacted with assignment to drug versus placebo (Model 1b). Specifically, as Figure 2 shows, improvement from baseline operated as a -shaped curvilinear function in relation to baseline severity, with those at the lowest and highest levels experiencing smaller gains, whereas those in-between experienced larger gains; the slope for placebo declined as severity increased, whereas the slope for drug was slightly positive. The difference between drug and placebo exceeded NICE's 0.50 standardized mean difference criterion at comparisons exceeding 28 in baseline severity. Further analyses indicated that drug type did not moderate this affect. Although venlafaxine and paroxetine had significantly (p < ds =" 0.42" d =" 0.22)" d =" 0.50." d =" 0.50." p =" 0.003)," p =" 0.0586," style="font-weight: bold; font-style: italic;">Discussion
Using complete datasets (including unpublished data) and a substantially larger dataset of this type than has been previously reported, we find that the overall effect of new-generation antidepressant medications is below recommended criteria for clinical significance. We also find that efficacy reaches clinical significance only in trials involving the most extremely depressed patients, and that this pattern is due to a decrease in the response to placebo rather than an increase in the response to medication.
Similar to prior reports [3,4], this analysis of U.S. FDA data for four new-generation antidepressants suggests an association between initial severity and the benefit of antidepressant medication. Unlike prior studies, we restricted our analysis to complete datasets that included all trials conducted, whether published or not. Thus, simple publication bias cannot underlie the results. We compared drug–placebo differences in improvement to criteria for clinical efficacy, and we used meta-regression procedures [11] to identify the relation of severity to improvement. Although we were able to replicate previously reported decreases in the placebo response as a function of increasing baseline severity, we found no linear relation between severity and response to medication.
NICE used a three-point difference in HRSD change scores, or a standardized mean difference of 0.50, as criteria of clinical significance [1]. By that criterion, the differences between drug and placebo were not clinically significant in clinical trials involving either moderately or very severely depressed patients, but did reach the criterion for trials involving patients whose mean initial depression scores were at the upper end of the very severe depression category (mean HRSD baseline 28; Figures 2–4). Given these data, there seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit.
A prior meta-analysis of published data only reported a very small significant difference between the antidepressant effect of fluoxetine and venlafaxine, but did not assess the effect of baseline severity as a moderator [23]. Our analyses failed to reveal any effect of drug type on efficacy or on the relation between severity and efficacy. It is possible that differences associated with drug type might be found with the inclusion of clinical trials conducted after the approval process, but analyses of head-to-head comparisons suggest that they are not likely to be large enough to be of clinical importance [23].
The response to placebo in these trials was exceptionally large, duplicating more than 80% of the improvement observed in the drug groups. In contrast, the effect of placebo on pain is estimated to be about 50% of the response to pain medication [24–26]. A substantial response to placebo was seen in moderately depressed groups and in groups with very severe levels of depression. It decreased somewhat, but was still substantial, in groups with the most-severe levels of depression.
Although baseline severity related to degree of improvement in the drug groups, the pattern was not linear. Instead, patients who by APA criteria were moderately depressed and those at the very high end of the severely depressed category (i.e., those with initial HRSD scores greater than 28) showed less improvement than those at the lower end of the severely depressed category. The curvilinear relation depended on only one trial of moderately depressed patients. When that outlier trial is excluded, there is no relation between baseline severity and antidepressant response. However, all of the other trials were with groups with mean initial HRSD scores in the very severe range (i.e., 23).
What is missing from the FDA data, however, are clinical trials with patients with initial depression scores in the severe range (19–22), and there was only one study with patients in the moderately depressed range. Had groups with a wider array of baseline depression scores been assessed, the curvilinear pattern might have been more obvious; in which case, clinically significant benefits for severely depressed patients might have been obtained. To perform this task in an unbiased way, it would be necessary for data for all approved medications to be available, even those gathered after the medication is approved. Having all the information available would also obviate the need to impute missing standard deviations, a limitation of the current investigation. Public availability of complete data on approved mediations might be made a condition of approval to solve these problems.
Finally, although differences in improvement increased at higher levels of initial depression, there was a negative relation between severity and the placebo response, whereas there was no difference between those with relatively low and relatively high initial depression in their response to drug. Thus, the increased benefit for extremely depressed patients seems attributable to a decrease in responsiveness to placebo, rather than an increase in responsiveness to medication.
Supporting Information
Text S1. QUOROM Checklist
(33 KB DOC)
Acknowledgments
Author contributions. IK abstracted baseline data from the FDA dataset, conceived the analyses, analyzed the data, and wrote the initial draft. BJD established correspondence between trials reported in the FDA dataset and those reported in the GlaxoSmithKline clinical trial register, abstracted the data from those trials, checked baseline data for trials in the FDA dataset, identified published versions of the FDA trials, and abstracted the data from those trials. TJM obtained the data from the FDA, and TJM and AS abstracted improvement data from that dataset. TBH and BTJ joined the project during the review process, analyzed the data, and assisted with subsequent drafts of the manuscript.
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(Emphasis by Justice Lover)
by Justice Lover
Following is a scientific report of research done to test Big Pharma-psychiatry claims to the "beneficial" effects of SSRI Antidepressants for people who suffer from depression.
The conclusion of the report's authors is that the "benefits" to consumers are no more than those of a placebo !
Add that to the horrendous dangers and deadly risks associated with consumption of and/or sudden withdrawal from those Antidepressants and you must reach the conclusion that here is a very deadly racket imposed on the unsuspecting public by Big Pharma and by the shrinks under the false cover of "medical treatment" !
Here is the report :
http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045
Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration by
Irving Kirsch1*, Brett J. Deacon2, Tania B. Huedo-Medina3, Alan Scoboria4, Thomas J. Moore5, Blair T. Johnson3
1 Department of Psychology, University of Hull, Hull, United Kingdom, 2 University of Wyoming, Laramie, Wyoming, United States of America, 3 Center for Health, Intervention, and Prevention, University of Connecticut, Storrs, Connecticut, United States of America, 4 Department of Psychology, University of Windsor, Windsor, Ontario, Canada, 5 Institute for Safe Medication Practices, Huntingdon Valley, Pennsylvania, United States of America
Background
Meta-analyses of antidepressant medications have reported only modest benefits over placebo treatment, and when unpublished trial data are included, the benefit falls below accepted criteria for clinical significance. Yet, the efficacy of the antidepressants may also depend on the severity of initial depression scores. The purpose of this analysis is to establish the relation of baseline severity and antidepressant efficacy using a relevant dataset of published and unpublished clinical trials.
Methods and Findings
We obtained data on all clinical trials submitted to the US Food and Drug Administration (FDA) for the licensing of the four new-generation antidepressants for which full datasets were available. We then used meta-analytic techniques to assess linear and quadratic effects of initial severity on improvement scores for drug and placebo groups and on drug–placebo difference scores. Drug–placebo differences increased as a function of initial severity, rising from virtually no difference at moderate levels of initial depression to a relatively small difference for patients with very severe depression, reaching conventional criteria for clinical significance only for patients at the upper end of the very severely depressed category. Meta-regression analyses indicated that the relation of baseline severity and improvement was curvilinear in drug groups and showed a strong, negative linear component in placebo groups.
Conclusions
Drug–placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.
Funding: The authors received no specific funding for this study..
Competing Interests: IK has received consulting fees from Squibb and Pfizer. BJD, TBH, AS, TJM, and BTJ have no competing interests.
Academic Editor: Phillipa Hay, University of Western Sydney, Australia
Citation: Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, et al. (2008) Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration. PLoS Med 5(2): e45 doi:10.1371/journal.pmed.0050045
Received: January 23, 2007; Accepted: January 4, 2008; Published: February 26, 2008
Copyright: © 2008 Kirsch et al.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abbreviations: d, standardized mean difference; FDA, US Food and Drug Administration; HRSD, Hamilton Rating Scale of Depression; LOCF, last observation carried forward; NICE, National Institute for Clinical Excellence; SDc, standard deviation of the change score
* To whom correspondence should be addressed. E-mail: i.kirsch@hull.ac.uk
Editors' Summary
Background.
Everyone feels miserable occasionally. But for some people—those with depression—these sad feelings last for months or years and interfere with daily life. Depression is a serious medical illness caused by imbalances in the brain chemicals that regulate mood. It affects one in six people at some time during their life, making them feel hopeless, worthless, unmotivated, even suicidal. Doctors measure the severity of depression using the “Hamilton Rating Scale of Depression” (HRSD), a 17–21 item questionnaire. The answers to each question are given a score and a total score for the questionnaire of more than 18 indicates severe depression. Mild depression is often treated with psychotherapy or talk therapy (for example, cognitive–behavioral therapy helps people to change negative ways of thinking and behaving). For more severe depression, current treatment is usually a combination of psychotherapy and an antidepressant drug, which is hypothesized to normalize the brain chemicals that affect mood. Antidepressants include “tricyclics,” “monoamine oxidases,” and “selective serotonin reuptake inhibitors” (SSRIs). SSRIs are the newest antidepressants and include fluoxetine, venlafaxine, nefazodone, and paroxetine.
Why Was This Study Done?
Although the US Food and Drug Administration (FDA), the UK National Institute for Health and Clinical Excellence (NICE), and other licensing authorities have approved SSRIs for the treatment of depression, some doubts remain about their clinical efficacy. Before an antidepressant is approved for use in patients, it must undergo clinical trials that compare its ability to improve the HRSD scores of patients with that of a placebo, a dummy tablet that contains no drug. Each individual trial provides some information about the new drug's effectiveness but additional information can be gained by combining the results of all the trials in a “meta-analysis,” a statistical method for combining the results of many studies.
A previously published meta-analysis of the published and unpublished trials on SSRIs submitted to the FDA during licensing has indicated that these drugs have only a marginal clinical benefit. On average, the SSRIs improved the HRSD score of patients by 1.8 points more than the placebo, whereas NICE has defined a significant clinical benefit for antidepressants as a drug–placebo difference in the improvement of the HRSD score of 3 points. However, average improvement scores may obscure beneficial effects between different groups of patient, so in the meta-analysis in this paper, the researchers investigated whether the baseline severity of depression affects antidepressant efficacy.
What Did the Researchers Do and Find?
The researchers obtained data on all the clinical trials submitted to the FDA for the licensing of fluoxetine, venlafaxine, nefazodone, and paroxetine. They then used meta-analytic techniques to investigate whether the initial severity of depression affected the HRSD improvement scores for the drug and placebo groups in these trials. They confirmed first that the overall effect of these new generation of antidepressants was below the recommended criteria for clinical significance. Then they showed that there was virtually no difference in the improvement scores for drug and placebo in patients with moderate depression and only a small and clinically insignificant difference among patients with very severe depression. The difference in improvement between the antidepressant and placebo reached clinical significance, however, in patients with initial HRSD scores of more than 28—that is, in the most severely depressed patients. Additional analyses indicated that the apparent clinical effectiveness of the antidepressants among these most severely depressed patients reflected a decreased responsiveness to placebo rather than an increased responsiveness to antidepressants.
What Do These Findings Mean?
These findings suggest that, compared with placebo, the new-generation antidepressants do not produce clinically significant improvements in depression in patients who initially have moderate or even very severe depression, but show significant effects only in the most severely depressed patients. The findings also show that the effect for these patients seems to be due to decreased responsiveness to placebo, rather than increased responsiveness to medication. Given these results, the researchers conclude that there is little reason to prescribe new-generation antidepressant medications to any but the most severely depressed patients unless alternative treatments have been ineffective. In addition, the finding that extremely depressed patients are less responsive to placebo than less severely depressed patients but have similar responses to antidepressants is a potentially important insight into how patients with depression respond to antidepressants and placebos that should be investigated further.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050045.
The MedlinePlus encyclopedia contains a page on depression (in English and Spanish)
Detailed information for patients and caregivers is available on all aspects of depression (including symptoms and treatment) from the US National Institute of Medical Health and from the UK National Health Service Direct Health Encyclopedia
MedlinePlus provides a list of links to further information on depression
Clinical Guidance for professionals, patients, caregivers and the public is provided by the UK National Institute for Health and Clinical Excellence
Introduction
Meta-analyses of antidepressant efficacy based on data from published trials reveal benefits that are statistically significant, but of marginal clinical significance [1]. Analyses of datasets including unpublished as well as published clinical trials reveal smaller effects that fall well below recommended criteria for clinical effectiveness. Specifically, a meta-analysis of clinical trial data submitted to the US Food and Drug Administration (FDA) revealed a mean drug–placebo difference in improvement scores of 1.80 points on the Hamilton Rating Scale of Depression (HRSD) [2], whereas the National Institute for Clinical Excellence (NICE) used a drug–placebo difference of three points as a criterion for clinical significance when establishing guidelines for the treatment of depression in the United Kingdom [1].
Mean improvement scores can obscure differences in improvement within subsets of patients. Specifically, antidepressants may be effective for severely depressed patients, but not for moderately depressed patients [1,3,4]. The purpose of the present analysis is to test that hypothesis (see Text S1 for the QUOROM checklist).
Conventional meta-analyses are often limited to published data. In the case of antidepressant medication, this limitation has been found to result in considerable reporting bias characterized by multiple publication, selective publication, and selective reporting in studies sponsored by pharmaceutical companies [5]. To avoid publication bias, we evaluated a dataset that includes the complete data from all trials of the medications, whether or not they were published.
Specifically, we analyzed the data submitted to the FDA for the licensing of four new-generation antidepressants for which full data, published and unpublished, were available. As part of the licensing process, the FDA requires drug companies to report “all controlled studies related to each proposed indication” ([6] emphasis in original). Thus, there should be no reporting bias in the dataset we analyze.
Methods
Study Retrieval
Following the Freedom of Information Act (FOIA) [7], we requested from the FDA all publicly releasable information about the clinical trials for efficacy conducted for marketing approval of fluoxetine, venlafaxine, nefazodone, paroxetine, sertraline, and citalopram, the six most widely prescribed antidepressants approved between 1987 and 1999 [2], which represent all but one of the selective serotonin reuptake inhibitors (SSRIs) approved during the study period. In reply, the agency provided photocopies of the medical and statistical reviews of the sponsors' New Drug Applications. The FDA requires that information on all industry-sponsored trials be submitted as part of the approval process; hence the files sent to us by the FDA should contain information on all trials conducted prior to the approval of each medication. This strategy omits trials conducted after approval was granted.
Although sponsors are required to submit information on all trials, the FDA public disclosure did not include mean changes for nine trials that were deemed adequate and well controlled but that failed to achieve a statistically significant benefit for drug over placebo. Data for four of these trials were available from a pharmaceutical company Web site in January 2007 and were obtained from the GlaxoSmithKline clinical trial register (http://ctr.gsk.co.uk/Summary/paroxetine/studylist.asp).
We also identified published versions of the FDA trials via a PubMed literature search (from January 1985 through May 2007) using the keywords depression; depressive; depressed; and placebo; specific names of antidepressant medications; and names of investigators from the FDA trials. Potentially relevant studies were also identified through references of retrieved and review articles and from a partially overlapping list of published versions of trials submitted to the Swedish drug regulatory authority [5]. Using a standardized protocol, all retrieved abstracts and publications were compared to the FDA trials. The match between each published study and its corresponding FDA trial was independently established with 100% agreement by two investigators (BJD and a research assistant).
Selection
Forty-seven clinical trials were identified in the data obtained from the FDA. The trial flow is illustrated in Figure 1. Inclusion of a drug type for which unsuccessful trials were excluded biases overall results in favor of that drug type, in a way that is akin to publication bias. The purpose in using the FDA dataset is precisely to avoid this type of bias by including all trials of each medication assessed. Therefore, we present analyses only for those medications for which mean change scores on all trials were available.
Figure 1. QUOROM Flow Chart
Validity Assessment
The FDA requires that rigorous standards be followed for the conduct of all efficacy trials for marketing approval [8] and also sets specific agency standards for clinical trials of antidepressant drugs [9]. In addition, the FDA independently reviews the clinical trial methods, statistical procedures, and results. The FDA dataset includes analyses of data from all patients who attended at least one evaluation visit, even if they subsequently dropped out of the trial prematurely. Results are reported from all well-controlled efficacy trials of the use of these medications for the treatment of depression. FDA medical and statistical reviewers had access to the raw data and evaluated the trials independently. The findings of the primary medical and statistical reviewers were verified by at least one other reviewer, and the analysis was also assessed by an independent advisory panel. Following FDA standards, all trials were randomized, double-blind, placebo-controlled trials. None used cross-over designs. Patients had been diagnosed as suffering from unipolar major depressive disorder using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria.
Given the above review process, we deemed it appropriate to include all studies deemed adequate and well controlled by FDA reviewers, especially as these are the data upon which the decision to approve these medications was based. Other validity criteria might yield different conclusions. In this review, some of the characteristics that may relate to the quality of trials were coded and assessed as possible moderator variables (e.g., interval of trial). The studies have similar methodological characteristics and were well controlled; therefore the methodological characteristics did not affect the final results.
Study Characteristics
In order to generalize the findings of the clinical trial to a larger patient population, FDA reviewers sought a completion rate of 70% or better for these typically 6-wk trials. Only four of the trials reported reaching this objective, and completion rates were not reported for two trials. Attrition rates were comparable between drug and placebo groups. Of those trials for which these rates were reported, 60% of the placebo patients and 63% of the study drug patients completed a 4-, 5-, 6-, or 8-wk trial. Thirty-three trials were of 6-wk duration, six trials were 4 wk, two were 5 wk, and six were 8 wk. Patients were evaluated on a weekly basis. For this meta-analysis, the data were taken from the last visit prior to trial termination.
Thirty-nine trials focused on outpatients: three included both inpatients and outpatients, three were conducted among the elderly (including one of the trials with both inpatients and outpatients), and two were among patients hospitalized for severe depression. No trial was reported for the treatment of children or adolescents.
Replacement of patients who investigators determined were not improving after 2 wk was allowed in three fluoxetine trials and in the three sertraline trials for which data were reported. The trials also included a 1- to 2-wk washout period during which patients were given placebo, prior to random assignment. Those whose scores improved 20% or more were excluded from the study prior to random assignment. The use of other psychoactive medication was reported in 25 trials. In most trials, a chloral hydrate sedative was permitted in doses ranging from 500 mg to 2,000 mg per day. Other psychoactive medication was usually prohibited but still reported as having been taken in several trials.
Meta-Analytic Data Synthesis
We conducted two types of data analysis, one in which each group's change was represented as a standardized mean difference (d), which divides change by the standard deviation of the change score (SDc) [10], and another using each study's drug and placebo groups' arithmetic mean (weighted for the inverse of the variance) as the meta-analytic “effect size” [11].
The first analysis permitted a determination of the absolute magnitude of change in both the placebo and treatment groups. Results permitted a determination of overall trends, analyses of baseline scores in relation to change, and for both types of models, tests of model specification, which assess the extent to which only sampling error remains unexplained. The results in raw metric are presented comparing both groups, but because of the variation of the SDcs, the standardized mean difference was used in moderator analyses in order to attain better-fitting models [12]. These results are compared to the criterion for clinical significance used by NICE, which is a three-point difference in Hamilton Rating Scale of Depression (HRSD) scores or a standardized mean difference (d) of 0.50 [1].
As known SDcs were related to mean baseline HRSD scores, these scores were used to impute missing SDc values, taking into account both the baseline and its quadratic form and any potential interaction of these terms with group (but in fact, there was no evidence that SDcs depended on treatment group). One trial reported SDcs for its drug and placebo groups that were less than 25% the size of the other trials; because preliminary analyses also revealed that this trial was an outlier, these two standard deviations were treated as missing and imputed. In total, SDcs were known for 28 groups, could be calculated from other inferential statistics in nine comparisons (18 groups), and were imputed in 12 comparisons (24 groups) (47.38%) [13,14].
Overall analyses evaluated both random- and fixed-effects models to assess effect size magnitude; because the same trends appeared for both, for simplicity we present only the fixed-effects results. We also assumed fixed-effects assumptions in order to analyze moderators for both groups. Both Q [15] and I2 [16] indices were used to assess inconsistencies from the models, not only to infer the presence or absence of homogeneity, but also (in the case of I2) to assess the degree of inconsistencies among trials [17]. We assumed fixed-effects models in analyzing moderators using meta-regression procedures [11]. Analyses examining linear and quadratic functions for baseline levels of severity used zero-centered forms of this variable [18].
A last, mixed-effects analysis for the amount of change used a random-effects constant along with fixed-effects moderator dimensions; these models provide more conservative assessments of moderation [19].
Because the same scale was used as the primary dependent variable in all of these trials, we were also able to represent results in their original metric [11]. This form of analysis makes results more easily interpretable in terms of clinical significance because mean change scores are analyzed directly, rather than being converted into effect sizes. The analytic weights are derived from the sample size and the SDc [11]. Finally, to show directly the amount of improvement for each study's drug group against its placebo group, we calculated the difference between the change for the drug group minus the change for the placebo group, leaving the difference in raw units and deriving its analytic weight from its standard error [11,12,20]. Analyses used these weights to examine these controlled outcomes both overall and to determine the extent to which drug-related change is a function of initial severity.
Results
Trial Flow
Mean improvement scores were not available in five of the 47 trials (Figure 1). Specifically, four sertraline trials involving 486 participants and one citalopram trial involving 274 participants were reported as having failed to achieve a statistically significant drug effect, without reporting mean HRSD scores. We were unable to find data from these trials on pharmaceutical company Web sites or through our search of the published literature. These omissions represent 38% of patients in sertraline trials and 23% of patients in citalopram trials. Analyses with and without inclusion of these trials found no differences in the patterns of results; similarly, the revealed patterns do not interact with drug type.
The purpose of using the data obtained from the FDA was to avoid publication bias, by including unpublished as well as published trials. Inclusion of only those sertraline and citalopram trials for which means were reported to the FDA would constitute a form of reporting bias similar to publication bias and would lead to overestimation of drug–placebo differences for these drug types. Therefore, we present analyses only on data for medications for which complete clinical trials' change was reported. The dataset comprised 35 clinical trials (five of fluoxetine, six of venlafaxine, eight of nefazodone, and 16 of paroxetine) involving 5,133 patients, 3,292 of whom had been randomized to medication and 1,841 of whom had been randomized to placebo.
Mean Change
Baseline HRSD scores, improvement, and sample sizes in drug and placebo groups for each clinical trial are reported in Table 1. As in the FDA files, studies are identified by protocol numbers. The data from these trials can be obtained from the FDA using FOIA requests and citing the medication name and protocol number. The table also includes references to published reports of the data abstracted from the FDA files, when they could be found (using the search methods described above). Studies in which data only from selected sites of a multisite study were published are not cited in the table.
We have also excluded published reports in which dropouts have been removed from the data. For each of the trials, the pharmaceutical companies had submitted to the FDA data in which attrition was handled by carrying forward the last observation carried forward (LOCF) on the patient, which was the basis in all cases of the FDA review. These data and their corresponding citations appear in the table. Even in the LOCF data, there sometimes are some minor discrepancies between the published version and the version submitted to the FDA. In some cases, for example, the N is slightly larger in the published studies than in the data reported to the FDA. Further complicating this problem is the fact that occasionally, the company has published a trial more than once, with slight discrepancies in the data between publications. Data in the table are those reported to the FDA.
Table 1.
Baseline HRSD Scores, Sample Sizes, and Raw and Standardized Improvement with Confidence Intervals, as Reported to the FDA for Drug and Placebo Groups
Confirming earlier analyses [2], but with a substantially larger number of clinical trials, weighted mean improvement was 9.60 points on the HRSD in the drug groups and 7.80 in the placebo groups, yielding a mean drug–placebo difference of 1.80 on HRSD improvement scores. Although the difference between these means easily attained statistical significance (Table 2, Model 3a), it does not meet the three-point drug–placebo criterion for clinical significance used by NICE. Represented as the standardized mean difference, d, mean change for drug groups was 1.24 and that for placebo 0.92, both of extremely large magnitude according to conventional standards. Thus, the difference between improvement in the drug groups and improvement in the placebo groups was 0.32, which falls below the 0.50 standardized mean difference criterion that NICE suggested. The amounts of change for drug and placebo groups varied widely around their respective means, Q(34)s = 51.80 and 74.59, p-values < i2s =" 34.18" style="font-weight: bold; font-style: italic;">Table 2.
Models of Improvement in Depression Scores Based on Group Assignment (Drug versus Placebo) and Initial Depression Severity (as Gauged by HRSD)
Drug and Initial Severity Trends in Change
Moderator analyses examined whether drug type, duration of treatment, and baseline severity (HRSD) scores related to improvement. Although drug type and duration of treatment were unrelated to improvement, the drug versus placebo difference remained significant, and amount of improvement was a function of baseline severity (Table 2, Model 1a). Specifically, the amount of improvement depended markedly on the quadratic function of baseline severity, but the linear function of baseline severity interacted with assignment to drug versus placebo (Model 1b). Specifically, as Figure 2 shows, improvement from baseline operated as a -shaped curvilinear function in relation to baseline severity, with those at the lowest and highest levels experiencing smaller gains, whereas those in-between experienced larger gains; the slope for placebo declined as severity increased, whereas the slope for drug was slightly positive. The difference between drug and placebo exceeded NICE's 0.50 standardized mean difference criterion at comparisons exceeding 28 in baseline severity. Further analyses indicated that drug type did not moderate this affect. Although venlafaxine and paroxetine had significantly (p < ds =" 0.42" d =" 0.22)" d =" 0.50." d =" 0.50." p =" 0.003)," p =" 0.0586," style="font-weight: bold; font-style: italic;">Discussion
Using complete datasets (including unpublished data) and a substantially larger dataset of this type than has been previously reported, we find that the overall effect of new-generation antidepressant medications is below recommended criteria for clinical significance. We also find that efficacy reaches clinical significance only in trials involving the most extremely depressed patients, and that this pattern is due to a decrease in the response to placebo rather than an increase in the response to medication.
Similar to prior reports [3,4], this analysis of U.S. FDA data for four new-generation antidepressants suggests an association between initial severity and the benefit of antidepressant medication. Unlike prior studies, we restricted our analysis to complete datasets that included all trials conducted, whether published or not. Thus, simple publication bias cannot underlie the results. We compared drug–placebo differences in improvement to criteria for clinical efficacy, and we used meta-regression procedures [11] to identify the relation of severity to improvement. Although we were able to replicate previously reported decreases in the placebo response as a function of increasing baseline severity, we found no linear relation between severity and response to medication.
NICE used a three-point difference in HRSD change scores, or a standardized mean difference of 0.50, as criteria of clinical significance [1]. By that criterion, the differences between drug and placebo were not clinically significant in clinical trials involving either moderately or very severely depressed patients, but did reach the criterion for trials involving patients whose mean initial depression scores were at the upper end of the very severe depression category (mean HRSD baseline 28; Figures 2–4). Given these data, there seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit.
A prior meta-analysis of published data only reported a very small significant difference between the antidepressant effect of fluoxetine and venlafaxine, but did not assess the effect of baseline severity as a moderator [23]. Our analyses failed to reveal any effect of drug type on efficacy or on the relation between severity and efficacy. It is possible that differences associated with drug type might be found with the inclusion of clinical trials conducted after the approval process, but analyses of head-to-head comparisons suggest that they are not likely to be large enough to be of clinical importance [23].
The response to placebo in these trials was exceptionally large, duplicating more than 80% of the improvement observed in the drug groups. In contrast, the effect of placebo on pain is estimated to be about 50% of the response to pain medication [24–26]. A substantial response to placebo was seen in moderately depressed groups and in groups with very severe levels of depression. It decreased somewhat, but was still substantial, in groups with the most-severe levels of depression.
Although baseline severity related to degree of improvement in the drug groups, the pattern was not linear. Instead, patients who by APA criteria were moderately depressed and those at the very high end of the severely depressed category (i.e., those with initial HRSD scores greater than 28) showed less improvement than those at the lower end of the severely depressed category. The curvilinear relation depended on only one trial of moderately depressed patients. When that outlier trial is excluded, there is no relation between baseline severity and antidepressant response. However, all of the other trials were with groups with mean initial HRSD scores in the very severe range (i.e., 23).
What is missing from the FDA data, however, are clinical trials with patients with initial depression scores in the severe range (19–22), and there was only one study with patients in the moderately depressed range. Had groups with a wider array of baseline depression scores been assessed, the curvilinear pattern might have been more obvious; in which case, clinically significant benefits for severely depressed patients might have been obtained. To perform this task in an unbiased way, it would be necessary for data for all approved medications to be available, even those gathered after the medication is approved. Having all the information available would also obviate the need to impute missing standard deviations, a limitation of the current investigation. Public availability of complete data on approved mediations might be made a condition of approval to solve these problems.
Finally, although differences in improvement increased at higher levels of initial depression, there was a negative relation between severity and the placebo response, whereas there was no difference between those with relatively low and relatively high initial depression in their response to drug. Thus, the increased benefit for extremely depressed patients seems attributable to a decrease in responsiveness to placebo, rather than an increase in responsiveness to medication.
Supporting Information
Text S1. QUOROM Checklist
(33 KB DOC)
Acknowledgments
Author contributions. IK abstracted baseline data from the FDA dataset, conceived the analyses, analyzed the data, and wrote the initial draft. BJD established correspondence between trials reported in the FDA dataset and those reported in the GlaxoSmithKline clinical trial register, abstracted the data from those trials, checked baseline data for trials in the FDA dataset, identified published versions of the FDA trials, and abstracted the data from those trials. TJM obtained the data from the FDA, and TJM and AS abstracted improvement data from that dataset. TBH and BTJ joined the project during the review process, analyzed the data, and assisted with subsequent drafts of the manuscript.
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(Emphasis by Justice Lover)
Sunday, February 24, 2008
MORE ON THE BIG PHARMA-PSYCHIATRY "ANTIPSYCHOTIC" RACKET
by Justice Lover
Psychiatrists are Medical Doctors. They have gained their academic MD because they have proved themselves as knowledgeable in all branches of science which make up the medical profession. They cannot be excused for being misled by Big Pharma's marketing propaganda.
If laymen have been aware of Big Pharma's rackets, then certainly the "experts" must have been aware too !
The willingness of shrinks to betray their patients in return for Big Pharma bribes is certainly no excuse, rather additional proof of the complicity of psychiatry in the crimes against humanity by Big Pharma !
The following AHRP report provides further proof for the criminal court which would try and convict both psychiatry and its practitioners along with the Big Pharma chiefs over their horrendous crimes against humanity !
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org and http://ahrp.blogspot.com
FYI
Two reports deal with antipsychotic drugs. The Philadelphia Inquirer (below)
examines the real life, severe adverse effects of antipsychotic drugs in
children.
A full page promotional report in today's New York Times Business section,
for the second time in six months helps boost Eli Lilly shares by
publicizing Lilly's latest, promotional hype for its claimed "breakthrough"
antipsychotic-in-development (LY2140023). The drug targets glutamate
receptors which Lilly's President of Research predicts "this area will heat
up here; this will be an area where there will be a lot of investment."
http://www.nytimes.com/2008/02
Whereas the old neuroleptics (a.k.a. antipsychotics) targeted dopamine
receptors, the second generation neuroleptics were hailed as the "wonder
drugs" of the 1990s. They were approved for use in adults with
schizophrenia and later for adults with bipolar disorder.
These drugs were marketed by selling a myth-the "dopamine" myth. And that
myth paid off in billions of dollars in sales-but failed to improve quality
of life for patients. Indeed, overwhelming evidence of these drugs'
debilitating, life-threatening adverse effects emerged, it became apparent
these toxic drugs undermine the health of those who take them.
In addition to acute weight gain, these drugs trigger hyperglycemia, insulin
resistant diabetes, strokes, and deaths. FDA's MedWatch database reveals
that pain killers (opiates and analgesics) and antipsychotics have been
linked to the greatest number of reported drug-induced deaths. The media,
however, has downplayed those statistics. See:
http://www.furiousseasons.com
erdal_clozaril_and_paxil
http://ahrp.blogspot.com/2007
Indeed, the toxic effects and lethal risks of the second generation
neuroleptics (a.k.a. antipsychotics) have been deliberately concealed from
consumers and (to a large extent) from physicians prescribing them. FDA
officials accommodated manufacturers by failing to examine the adverse event
data in the agency's files--at least, that's what FDA officials claimed.
Thanks to FDA's complicity in concealing these drugs' severe health hazards,
and the media's uncritical dissemination of industry-generated enthusiasm
for their latest drug, antipsychotic drugs, whose efficacy is now
acknowledged to be marginal, have become industry's blockbuster sellers.
Of note, leading schizophrenia researchers (Dr. Bita Moghaddam) who are
pursuing the glutamate hypothesis now readily admit that the current drugs
don't work-and have dangerous adverse effects: "Basically, we're still using
the same one-size-fits-all, anti-psychotic drugs that we've been using since
the late 1950s. These medications, called neuroleptics, block the actions of
dopamine, one of the neurotransmitters that relay messages between neurons
in the brain. Typically, neuroleptic drugs reduce paranoia and
hallucinations but offer little or no relief from other symptoms of
schizophrenia such as jumbled thoughts and social withdrawal.
Moreover,neuroleptics often cause severe side effects, including uncontrollable
tremors, huge weight gains and dangerous increases in patients' blood
lipids."
http://mac10.umc.pitt.edu/u
846&-Find
Despite their proven ineffectiveness and life-shortening severe adverse
effects, these drugs became blockbuster sellers, thanks in large measure to
aggressive marketing-including an industry-controlled scheme that led mental
health providers to prescribe these drugs as first line treatments. See,
TMAP medication guidelines: http://www.ahrp.org/infomail
TMAP guidelines resulted in taxpayers being saddled with underwriting most
of the cost--70% to 80%--for antipsychotics through Medicaid.
So far, eighteen State Attorneys General are suing antipsychotic drug
manufacturers for marketing fraud. Eli Lilly has reached astronomical
Zyprexa-diabetes settlements--$1.2 billion+-- with 31,000 plaintiffs on
condition that the evidence remain secret. Another 1,200 cases are open.
What is the nature of the evidence about Zyprexa that the company is willing
to pay billions to conceal?
Even as leading psychopharmacologists, such as Dr. Carol Tamminga, now
acknowledge: "In fact, the treatment for schizophrenia is at best partial
and inadequate," these drugs became the standard of care on the basis of
marketing hype.
Worst of all, antipsychotic use has exploded among America's young people
who are not even remotely psychotic-as documented by Vanderbilt University.
Even as psychiatrists cannot even agree whether the diagnosis bipolar
disorder exists in children, or whether using such toxic drugs is an
appropriate response, antipsychotics are widely and irresponsibly prescribed
for children as chemical restraints to "manage" bad behavior.
The data shows that children, even more than adults, suffer severe adverse effects.
For example, Risperdal induces gynecomastia (development of abnormally large
mammary glands in males resulting in breasts). Young boys have had to
undergo mastectomies as a result of taking the drug. And children have
developed insulin resistant diabetes.
The widespread use of these toxic drugs in children will be viewed by future
generations as a medical catastrophe. The drugs' long-term adverse effects
are not even studied for fear such studies would undercut sales.
We are skeptical that the "glutamate hypothesis" underpinning the latest
antipsychotics-in-development is likely to become the "breakthrough"
treatment--just as the previous antipsychotic drugs targeting dopamine
receptors, and the current drugs targeting dopamine and serotonin, proved
unsuccessful. The fact is, a major problem with all drugs whose action
affects functions in the central nervous system (CNS). CNS drugs, including
antidepressants, antipsychotics, anxiolytics, anti-convulsants, and
painkillers, cannot be programmed to target only one specific emotion (e.g.,
depression, psychosis).
Neither can these drugs' action within a neuroreceptor system-such as the dopamine or serotonin or glutamate receptor system--be limited to the brain. The drugs are extremely toxic and their action interferes with normal metabolic, cardiovascular and hormonal
function. This chronic interference with normal function in the body's major
systems triggers life-threatening chronic diseases.
Though the current antipsychotics are now maligned even by leading
psychiatrists they are still being widely prescribed, causing irreparable
harm. How does such prescribing square with the Hippocratic Oath, "First,
do no harm" ? In this era of commercially-driven drug marketing and
physician prescribing practices, even lethal drugs become blockbuster
sellers...
See also:
http://ahrp.blogspot.com/2007
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
The following link is to the relevant article in the The Philadelphia Inquirer :
http://www.philly.com/philly
s.html
Death, Destruction, Lies, Deceit, Bribes, Corruption by Big Pharma, the senior partners of psychiatry
by Justice LoverThe following article is by Brian Milke
Father of Sarina Angel
COPES Foundation
Together with Camille Milke, Sarina's mother, and Amy Philo, a Zoloft survivor,they are leading the struggle against Big Pharma and demanding the immediate legal ban on "Antidepressants" which killed Sarina.
Death, Destruction, Lies, Deceit, Bribes, Corruption
by Brian Milke
|
All the makings of a good movie or a great novel? Where do you think writers get their inspiration? I say one week as a fly on the wall inside Big Pharma would give them enough material for a lifetime!
Big Pharma execs and attorneys themselves would make the best authors and screen writers. Not only do they have the knowledge of all of these vile events (and many more) but think of the imagination and forward thinking they must also posses.
From a business standpoint, it is almost admirable and awe-inspiring; the way Big Pharma controls the industry and the world to protect their cash cows. I said almost - if it wasn't for the fact that these loathsome and wicked acts are all too real. People become very creative when it comes to money; and money, of course, is what fuels this hideous beast known as Big Pharma. It stretches out like a multi-tentacled monster controlling, altering or completely blocking every harpoon hurled its direction. Money causes and in-turn enables the beast to infiltrate everywhere, everyone and everything.
Imagine fighting an opponent that knows your next move even before you do. That has anticipated every path that you may use to harm it and has closed those paths down. That has intertwined itself and infiltrated every mean with which you may hope to get any form of a victory.
Yes the beast has thought of that. Whether you are looking for the ultimate goal of destruction, some sort of recourse or just some honest answers from it, the road blocks are already in place.
The beast’s tentacles reach from the White House to your house and everywhere in-between. To the news media, to your government officials, to the school systems, to your doctors, to your pharmacists and to your medicine cabinet. Plus many of its tentacles have off spring that bi-furcate to perform double duty.
The tentacle that encases the FDA, for example comes in the front door promising miracle drugs and a better way of life while, at the same time, coming in the back with inaccurate test results, threats and bribes. The FDA is being used! They are a front for drug dealers with more cash to go around than any third world cartel ever had. If anyone questions Big Pharma, the FDA has placed itself to protect them and even take the fall if need be. Like some over zealous secret service agent taking one for the president they stand between anyone who would dare threaten their leader. Big Pharma just produces it. All the FDA has to do is approve it for use and be the front man. Forget the fact that approval was based on incorrect reporting of the facts; that many members of the FDA have ties that should be considered a conflict of interest or that Big Pharma is paying for all this! Big Pharma runs the FDA. It's no secret. All it takes is money.
The tentacles have a grip on modern medicine too. Not just psychiatry either. We're talking about general practitioners, nurse practitioners and counselors who have all been empowered with mind altering psychotics. There are also the drug distributors, drug reps, salespeople, and pharmacists too. Big Pharma has everything from free lunches and promotional material to cash for prescribing their products more. They hide the truth with false reports, fixed studies, mislabeling of adverse reactions and non-reporting of negative test results. They also use their influence with the FDA and clever advertising to create the perceived need for every person to take their drugs. Most anyone who goes to the doctor today will walk out with "FREE SAMPLES" of the SSRI Antidepressant of the doctors choosing (in other words the one that has courted and wooed the doctor the most in any manner necessary).
How convenient for them to market a drug labeled "Anti-Depressants" that actually cause depression! They also cause a large number of other horrific side effects such as suicide, homicide, diabetes, heart disease, mania and akethisia! The purported cure is making us sick! Selective Serotonin Reuptake Inhibitor (SSRI) Anti-Depressants by definition and by Big Pharma's own admittance raise levels of the "feel good" hormone Serotonin in the brain. Excess serotonin has been proven to cause mental disorders not prevent them! Through all the tests and trials and experiments on people, SSRI's have yet to be proven effective in treating depression. Effectiveness is not a concern of Big Pharma, however. They have positioned their drugs to sell and sell big whether they work or not. In fact the list of off-label prescriptions is growing so rapidly, Big Pharma is assured that this Beast they have created will be nearly impossible to defeat. As many as 75% of the prescriptions written for SSRI's were for treatments not approved by the FDA. SSRI's are being prescribed for such things as pain, insomnia, anxiety, shyness, menstrual discomfort, dementia, restless leg syndrome, eating disorders and many others (most if not all of which are just made up) with little or no proof of effectiveness. In addition, a sub-market is being created for hundreds of other drugs that are used to counter the side effects of the original drug!
It's also extremely convenient for Big Pharma that these drugs are so very difficult to stop taking! Once on them, the worst thing you can do is stop abruptly. Too many times we hear in the news how the person who shot those people, drowned their child, murdered their parents or set themselves on fire recently stopped taking their medication. Big Pharma’s answer is don't stop! What type of sick and twisted company will take someone’s tragedy and spin it to promote the very thing that caused the problem?
Even our children are under direct attack by the tentacles of Big Pharma. When they go to school they are subjected to hundreds of other people who are on these medications. Any student or staff member on SSRI's has the potential to be a ticking bomb. What's more, when the ticking stops you don't know if they will implode or explode. Now our children are even being screened in the schools for potential disorders which, of course, are automatically treated with SSRI Anti-Depressants and other medications. 90% of our kids who have gone through the screening process walk out with a prescription! "Teen Screen" is supported, financially and otherwise, by Big Pharma in an effort to create more paying customers. Their goal is to screen all school age children; millions of which will end up on psychiatric drugs!
Big Pharma is also trying to create patients in the womb! Another would be victim is the pregnant mother and her unborn child. The latest of the beast’s efforts to control the world is "The Mothers Act" Bill which would have Government mandated testing of as many pregnant women and new mothers as possible for depression and then treat them with antidepressants! This is despite the myriad of studies showing a link between antidepressants and violence, abortion and birth defects. Being pregnant or a new mom is stressful enough without being on a medication that has been proven to make people "crazy"! There are worse things than depression! On December 8, 2005, the FDA issued a public health advisory to report that women who take Paxil in early pregnancy are at an approximately 2-fold increased risk of having an infant born with a cardiac defect compared to the general population. Another study finds that infants exposed to SSRI's in late pregnancy showed a 6-times greater risk of developing the lung disorder known as persistent pulmonary hypertension of the newborn (PPHN), a condition that, despite treatment, results in the death of approximately 10 to 20 percent of affected infants.
Alert the public you say? Why not just tell them the truth about what Big Pharma is doing? They surely will not allow this to continue once they know, right? The beast has thought of that too. As always, we've been beaten to the punch. There's another tentacle that has already alerted the public! And they're telling us more nearly every day about the dangers of SSRI Anti-Depressants. They tell us this horrific news and reveal unconsciousable side effects but they do it with smiley faces and cartoon characters to create a rosy public perception. They use direct to consumer advertising to boost this perception to a point where the drugs are revered. So many organizations, such as ours, "The COPES Foundation", "The International Coalition for Drug Awareness" and many others are continually making attempts to educate the public of the horrors of Big Pharma and the caustic chemicals they promote but they ALREADY KNOW! They know because their best bud, Big Pharma, told them so! They don't see the mealy beast for what it is. They feel the tentacle around them but think it's comforting! They think it protects them! They don't know they are victims! Victims of Deceit, of Corruption, of Death and of Criminals with Forward thinking.
Big Pharma has high ranking politicians, high powered lawyers, decision making officials in psychiatry, coveted news media and others in positions of power in place to defend it when needed. These tentacles seem to act separately and independently until called upon and then seamlessly become a part of the beast putting in or taking out legislation as need be; thwarting any attempts of litigation with counter suits, invasions of privacy and threats; inventing new illnesses and spewing the lies and propaganda of the drug companies to the unsuspecting public.
Don't they care that people are killing themselves and others because of these medications? I think they do. Not for the normal, humanitarian reasons however. We see it as the loss of a loved one. The loss of our daughter, someone’s mother, someone’s sister. They see it is a loss of revenue! They care because each person who dies is one less potential customer. One less person to feed the thriving beast.
What is to be done? Do we keep throwing stones just to see them be swatted away? Do we continue to tell people the information they don't want to hear? Do we alienate our friends and family by imposing this pile of information on them? Do we talk to legislators and the news media (those that may have not gotten wrapped in tentacles yet)? YES to all of the above. What options do we have? We won't sit idle. Others may but we won't. Remember what I said? People become very creative when it comes to money. The key to this is people. People have the power. Unfortunately, people are not as strong as we would like them to be. We've learned they can be a down right disapointment. But maybe things will be different. We will be here to support each other. We will not fade away! We will work together against the beast. I have to believe we will make a difference. I KNOW we WILL make a difference. For Sarina, for our family, for your families and for the world. I was going to say I've learned not to expect too much from people but that would be inaccurate. Now, more than ever, I expect so very much from all of us. Give me and the world a reason to hope. A reason to believe. WE WILL NOT BACK DOWN!
Brian Milke
Father of Sarina Angel
COPES Foundation
Big Pharma execs and attorneys themselves would make the best authors and screen writers. Not only do they have the knowledge of all of these vile events (and many more) but think of the imagination and forward thinking they must also posses.
From a business standpoint, it is almost admirable and awe-inspiring; the way Big Pharma controls the industry and the world to protect their cash cows. I said almost - if it wasn't for the fact that these loathsome and wicked acts are all too real. People become very creative when it comes to money; and money, of course, is what fuels this hideous beast known as Big Pharma. It stretches out like a multi-tentacled monster controlling, altering or completely blocking every harpoon hurled its direction. Money causes and in-turn enables the beast to infiltrate everywhere, everyone and everything.
Imagine fighting an opponent that knows your next move even before you do. That has anticipated every path that you may use to harm it and has closed those paths down. That has intertwined itself and infiltrated every mean with which you may hope to get any form of a victory.
Yes the beast has thought of that. Whether you are looking for the ultimate goal of destruction, some sort of recourse or just some honest answers from it, the road blocks are already in place.
The beast’s tentacles reach from the White House to your house and everywhere in-between. To the news media, to your government officials, to the school systems, to your doctors, to your pharmacists and to your medicine cabinet. Plus many of its tentacles have off spring that bi-furcate to perform double duty.
The tentacle that encases the FDA, for example comes in the front door promising miracle drugs and a better way of life while, at the same time, coming in the back with inaccurate test results, threats and bribes. The FDA is being used! They are a front for drug dealers with more cash to go around than any third world cartel ever had. If anyone questions Big Pharma, the FDA has placed itself to protect them and even take the fall if need be. Like some over zealous secret service agent taking one for the president they stand between anyone who would dare threaten their leader. Big Pharma just produces it. All the FDA has to do is approve it for use and be the front man. Forget the fact that approval was based on incorrect reporting of the facts; that many members of the FDA have ties that should be considered a conflict of interest or that Big Pharma is paying for all this! Big Pharma runs the FDA. It's no secret. All it takes is money.
The tentacles have a grip on modern medicine too. Not just psychiatry either. We're talking about general practitioners, nurse practitioners and counselors who have all been empowered with mind altering psychotics. There are also the drug distributors, drug reps, salespeople, and pharmacists too. Big Pharma has everything from free lunches and promotional material to cash for prescribing their products more. They hide the truth with false reports, fixed studies, mislabeling of adverse reactions and non-reporting of negative test results. They also use their influence with the FDA and clever advertising to create the perceived need for every person to take their drugs. Most anyone who goes to the doctor today will walk out with "FREE SAMPLES" of the SSRI Antidepressant of the doctors choosing (in other words the one that has courted and wooed the doctor the most in any manner necessary).
How convenient for them to market a drug labeled "Anti-Depressants" that actually cause depression! They also cause a large number of other horrific side effects such as suicide, homicide, diabetes, heart disease, mania and akethisia! The purported cure is making us sick! Selective Serotonin Reuptake Inhibitor (SSRI) Anti-Depressants by definition and by Big Pharma's own admittance raise levels of the "feel good" hormone Serotonin in the brain. Excess serotonin has been proven to cause mental disorders not prevent them! Through all the tests and trials and experiments on people, SSRI's have yet to be proven effective in treating depression. Effectiveness is not a concern of Big Pharma, however. They have positioned their drugs to sell and sell big whether they work or not. In fact the list of off-label prescriptions is growing so rapidly, Big Pharma is assured that this Beast they have created will be nearly impossible to defeat. As many as 75% of the prescriptions written for SSRI's were for treatments not approved by the FDA. SSRI's are being prescribed for such things as pain, insomnia, anxiety, shyness, menstrual discomfort, dementia, restless leg syndrome, eating disorders and many others (most if not all of which are just made up) with little or no proof of effectiveness. In addition, a sub-market is being created for hundreds of other drugs that are used to counter the side effects of the original drug!
It's also extremely convenient for Big Pharma that these drugs are so very difficult to stop taking! Once on them, the worst thing you can do is stop abruptly. Too many times we hear in the news how the person who shot those people, drowned their child, murdered their parents or set themselves on fire recently stopped taking their medication. Big Pharma’s answer is don't stop! What type of sick and twisted company will take someone’s tragedy and spin it to promote the very thing that caused the problem?
Even our children are under direct attack by the tentacles of Big Pharma. When they go to school they are subjected to hundreds of other people who are on these medications. Any student or staff member on SSRI's has the potential to be a ticking bomb. What's more, when the ticking stops you don't know if they will implode or explode. Now our children are even being screened in the schools for potential disorders which, of course, are automatically treated with SSRI Anti-Depressants and other medications. 90% of our kids who have gone through the screening process walk out with a prescription! "Teen Screen" is supported, financially and otherwise, by Big Pharma in an effort to create more paying customers. Their goal is to screen all school age children; millions of which will end up on psychiatric drugs!
Big Pharma is also trying to create patients in the womb! Another would be victim is the pregnant mother and her unborn child. The latest of the beast’s efforts to control the world is "The Mothers Act" Bill which would have Government mandated testing of as many pregnant women and new mothers as possible for depression and then treat them with antidepressants! This is despite the myriad of studies showing a link between antidepressants and violence, abortion and birth defects. Being pregnant or a new mom is stressful enough without being on a medication that has been proven to make people "crazy"! There are worse things than depression! On December 8, 2005, the FDA issued a public health advisory to report that women who take Paxil in early pregnancy are at an approximately 2-fold increased risk of having an infant born with a cardiac defect compared to the general population. Another study finds that infants exposed to SSRI's in late pregnancy showed a 6-times greater risk of developing the lung disorder known as persistent pulmonary hypertension of the newborn (PPHN), a condition that, despite treatment, results in the death of approximately 10 to 20 percent of affected infants.
Alert the public you say? Why not just tell them the truth about what Big Pharma is doing? They surely will not allow this to continue once they know, right? The beast has thought of that too. As always, we've been beaten to the punch. There's another tentacle that has already alerted the public! And they're telling us more nearly every day about the dangers of SSRI Anti-Depressants. They tell us this horrific news and reveal unconsciousable side effects but they do it with smiley faces and cartoon characters to create a rosy public perception. They use direct to consumer advertising to boost this perception to a point where the drugs are revered. So many organizations, such as ours, "The COPES Foundation", "The International Coalition for Drug Awareness" and many others are continually making attempts to educate the public of the horrors of Big Pharma and the caustic chemicals they promote but they ALREADY KNOW! They know because their best bud, Big Pharma, told them so! They don't see the mealy beast for what it is. They feel the tentacle around them but think it's comforting! They think it protects them! They don't know they are victims! Victims of Deceit, of Corruption, of Death and of Criminals with Forward thinking.
Big Pharma has high ranking politicians, high powered lawyers, decision making officials in psychiatry, coveted news media and others in positions of power in place to defend it when needed. These tentacles seem to act separately and independently until called upon and then seamlessly become a part of the beast putting in or taking out legislation as need be; thwarting any attempts of litigation with counter suits, invasions of privacy and threats; inventing new illnesses and spewing the lies and propaganda of the drug companies to the unsuspecting public.
Don't they care that people are killing themselves and others because of these medications? I think they do. Not for the normal, humanitarian reasons however. We see it as the loss of a loved one. The loss of our daughter, someone’s mother, someone’s sister. They see it is a loss of revenue! They care because each person who dies is one less potential customer. One less person to feed the thriving beast.
What is to be done? Do we keep throwing stones just to see them be swatted away? Do we continue to tell people the information they don't want to hear? Do we alienate our friends and family by imposing this pile of information on them? Do we talk to legislators and the news media (those that may have not gotten wrapped in tentacles yet)? YES to all of the above. What options do we have? We won't sit idle. Others may but we won't. Remember what I said? People become very creative when it comes to money. The key to this is people. People have the power. Unfortunately, people are not as strong as we would like them to be. We've learned they can be a down right disapointment. But maybe things will be different. We will be here to support each other. We will not fade away! We will work together against the beast. I have to believe we will make a difference. I KNOW we WILL make a difference. For Sarina, for our family, for your families and for the world. I was going to say I've learned not to expect too much from people but that would be inaccurate. Now, more than ever, I expect so very much from all of us. Give me and the world a reason to hope. A reason to believe. WE WILL NOT BACK DOWN!
Brian Milke
Father of Sarina Angel
COPES Foundation
Camille Milke, Eternal "Mommy" of Sarina Angel
Yesterday, Today, Tomorrow and Forever........
My Beautiful Baby Girl, 1/26/86 - 10/28/07, 21 years 9 months 3 days
Latitude: 35°12'44.77"N Longitude:106°42'29.32"W
COPES Foundation (Coalition Of Parents Enduring Suicide)
Founder and President, Main - 505-269-2286, Fax - 505-213-0999
SarinasVoice@aol.com
www.COPESFoundation.com
www.ILoveYouSarina21.last-memories.com
NM Director of the International Coalition for Drug Awareness
www.DrugAwareness.org
Yesterday, Today, Tomorrow and Forever........
My Beautiful Baby Girl, 1/26/86 - 10/28/07, 21 years 9 months 3 days
Latitude: 35°12'44.77"N Longitude:106°42'29.32"W
COPES Foundation (Coalition Of Parents Enduring Suicide)
Founder and President, Main - 505-269-2286, Fax - 505-213-0999
SarinasVoice@aol.com
www.COPESFoundation.com
www.ILoveYouSarina21.last
NM Director of the International Coalition for Drug Awareness
www.DrugAwareness.org
Saturday, February 23, 2008
RECENT CIVIL ACTIONS FOR DAMAGES AGAINST BIG PHARMA BY STATE ATTORNEYS GENERAL IN THE USA REGARDING THE "ANTIPSYCHOTIC" DRUGS RACKET
by Justice Lover
The following report was emailed to me today by AHRP :
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org/ and http://ahrp.blogspot.com/
FYI
Cong. Bart Stupak and Cong. John Dingell, the chairman of the House Energy and Commerce Committee, threatened to hold Health and Human Services Secretary Michael Leavitt in contempt for refusing to turn over FDA briefing documents subpoenaed by the committee in its probe over an antibiotic and a blood thinner linked to four deaths.
Sec. Leavitt oversees the FDA and other health care agencies. The documents in question were used to prepare FDA Commissioner, Andrew von Eschenbach,MD, for his appearance before House lawmakers last year. The commissioner testified that FDA did not use the flawed safety study to approve Ketek. But Cong. Stupak called that statement untrue and subpoenaed von Eschenbach's notes to determine if he lied under oath.The agency has said there was no intention to deceive the public.
Cong. Stupak called on Dr. von Eschenbach to step down because he hasdemonstrated "a total lack of leadership."
Underscoring FDA officials' disregard for the agency's mission--which is to protect the public health, and ensure that scientifically validated information is disseminated about prescription drugs--the agency has just issued proposed guidelines that would overturn the prohibition against drug manufacturers disseminating information to encourage doctors to prescribe their drug for "off-label" unapproved uses.
In essence, top FDA officials are serving as industry's handmaiden by attempting to legitimize illegal marketing activities.
Representative Henry Waxman, said the proposed rule "caters to the industry's desire to market their products without adequate testing or review." The Food, Drugs, and Cosmetics Act prohibits companies from promoting off-label uses of approved drugs.FDA would protect these manufacturers from deceptive marketing by accepting industry-sponsored and industry controlled articles containing false and misleading information. Such commercially sponsored articles have been shown to inflate the claimed benefits---while concealing the lethal risks.
The proposed FDA rule would legitimize the very activities that have led State Attorneys General and the Justice Department to sue Big Pharmacompanies.For example, 18 states are suing manufacturers of the so-called 'atypical' antipsychotic drugs--the most toxic harm-producing psychotropics--for off-label marketing:
9 states are suing Eli Lilly regarding Zyprexa: Alaska, Louisiana,Mississippi, Montana, New Mexico, Pennsylvania, South Carolina, Utah andWest Virginia. 6 states are suing Janssen regarding Risperdal: Arkansas, Louisiana,Montana, South Carolina, Texas and Pennsylvania. 3 states are suing AstraZeneca regarding Seroquel: Pennsylvania, SouthCarolina, and now, Montana . See the complaint posted at http://www.helenair.com/extras/complaint.pdf
AHRP applauds Cong. Stupak for calling a spade a spade.We would further recommend calling for the removal of the top echelon of FDA's Center for Drug Evaluation and Research (CDER).These officials have systematically relegated scientific evidence to file drawers and lent the seal of approval to lethal drugs that caused tens of thousands of Americans to die. That is a colossal disservice of an agency mandated to protect the public health.
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
(Emphasis by Justice Lover)
Wednesday, February 20, 2008
USA Supreme Court Favors Big Pharma
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org/ and http://ahrp.blogspot.com/
FYI
American Consumers no longer have any recourse from being harmed by defective drugs, vaccines or medical devices that carry the FDA seal of approval..The US Supreme Court has just rendered a decision giving the biotech drug and device industry immunity from liability for marketing defective products that kill.
Unless and until Congress acts to protect the American citizen (or direct democracy would replace the present plutocracy - Justice Lover ), let consumer beware.Do not for a split second trust prescription drug or medical device manufacturers--and by no means trust the FDA.
The FDA seal of approval is a license to market even poorly tested,defective drugs, vaccines and medical devices that kill.
Our only recourse is to vote for those who will stand up to Big Pharma (and still better : replace plutocracy with direct democracy !
- Justice Lover ) and legislate laws to protect our health--rather than industry's profits.
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
Following is the link to the relevant USATODAY report :
http://www.usatoday.com/money/industries/health/2008-02-20-medical-device-suits_N.htm
(Emphasis by Justice lover)
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org/ and http://ahrp.blogspot.com/
FYI
American Consumers no longer have any recourse from being harmed by defective drugs, vaccines or medical devices that carry the FDA seal of approval..The US Supreme Court has just rendered a decision giving the biotech drug and device industry immunity from liability for marketing defective products that kill.
Unless and until Congress acts to protect the American citizen (or direct democracy would replace the present plutocracy - Justice Lover ), let consumer beware.Do not for a split second trust prescription drug or medical device manufacturers--and by no means trust the FDA.
The FDA seal of approval is a license to market even poorly tested,defective drugs, vaccines and medical devices that kill.
Our only recourse is to vote for those who will stand up to Big Pharma (and still better : replace plutocracy with direct democracy !
- Justice Lover ) and legislate laws to protect our health--rather than industry's profits.
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
Following is the link to the relevant USATODAY report :
http://www.usatoday.com/money/industries/health/2008-02-20-medical-device-suits_N.htm
(Emphasis by Justice lover)
Tuesday, February 19, 2008
MORE ON THE BIG PHARMA-PSYCHIATRY "ANTIDEPRESSANTS" RACKET AND ITS VICTIMS AROUND THE WORLD
by Justice Lover
Most of the crimes against humanity perpetrated by Big Pharma and by its bribed shrinks are concentrated in the production and use of two groups of deadly pharmaceutical drugs : the SSRI "Antidepressants" and the "Antipsychotic" neuroleptics. Many thousands of innocent people have lost their live as a result of consumption (forced by the shrinks in most cases) of those poisons.
Yet those poisons ,prescribed by the shrinks , brought Big Pharma a huge increase in colossal profits, and with it a huge increase in the rate of bribes for the shrinks. In a word, it is a racket, a very deadly racket ,that must be stopped immediately, if thousands of lives are to be saved !
Following are 2 reports. One was emailed to me by AHRP, the other was downloaded from
http://www.ssristories.com/ . Both concern the "Antidepressants" racket.
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org/ and http://ahrp.blogspot.com/
FYI
“Two articles in today's New York Times, "Reports of Gunman's Use of Antidepressant Renew Debate Over Side Effects," and "Midlife Suicide RisesNearly 20%, Puzzle Researchers," represent a watershed for the Times.
Implicit in these reports are two evidence-based acknowledgments.Antidepressants, which had been touted as an effective treatment in reducing suicides, have been proven to increase the risk of suicide. What's more these drugs have been implicated in deadly violence.
The Times acknowledges the undeniable, but long denied, link between use of SSRI Antidepressants drugs and unprovoked explosive violence:"Over the years, the antidepressant Prozac and its cousins, including Paxiland Zoloft, have been linked to suicide and violence in hundreds ofpatients."Indeed, a website maintained by two mothers on a truth mission, Sara Bostockand Rosie Meysenburg, www.ssristories.com, lists 2,000 news reports linking SSRIs to violence.
These drugs' label warnings were only added after critics of pharmaceutical industry's concealment of drug hazards brought to public light the nature and severity of these drugs' adverse side-effects. Indeed, both the FDA and the MHRA in the UK failed for over a decade to examine the safety data in their own file drawers.
The Prozac label--which is identical for all SSRIs--warns about a cluster of drug-induced withdrawal symptoms that are associated with violent outbursts:"Discontinuation of Treatment with Prozac -During marketing of Prozac and other SSRIs and SNRIs...there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following:dysphoric mood, irritability, agitation, dizziness, sensory disturbances(e.g., paresthesias such as electric shock sensations), anxiety, confusion,headache,lethargy, emotional lability, [i.e. suicidal behavior] insomnia, and hypomania.
While these events are generally self-limiting, there have been reports of serious discontinuation symptoms. Patients should be monitored for these symptoms when discontinuing treatment with Prozac."The concealment of these drugs' lethal effects for over a decade led unsuspecting physicians to prescribe them widely. The consequences of such uninformed prescribing can be counted in preventable human casualties.
SSRI Antidepressants have been linked to a string of US school shooters--including Steven Kazmieczak, who shot and killed five students at Northern Illinois University.Ms. Bostock, an observer and suicide survivor, told the Times: "my main wish is that medical professionals, regulatory authorities and other scientists will examine closely the entire medical and treatment history of the perpetrators of these violent incidents in which innocent people are victims."
By contrast, the Times reports that "psychiatrists say the debate on such side effects, particularly suicide in the last four years, has driven patients from drugs that could help save their lives." That claim is without scientific foundation: help save lives how-by increasing the risk of suicide?
The claim is a faith-based position that defies the documented evidence.Another Times report focuses on the finding of a new five-year analysis of the nation's death rates, recently released by the federal Centers for Disease Control and Prevention. This study found that the suicide rate among 45-to-54-year-olds increased nearly 20% from 1999 to 2004--and for women 45to 54, the rate leapt to 31%.During these same years, sales and prescription data for SSRI Antidepressants skyrocketed--as documented by IMS Health, see:http://www.imshealth.com/ims/portal/front/articleC/0,2777,6599_18731_77056778,00.htmlandhttp://ahrp.blogspot.com/2007/05/eternal-sunshine-20-things-you-need-to.html
The alarming INCREASE in suicides among middle aged persons during a period of INCREASED use of SSRI Antidepressants refutes propaganda masquerading as scientific reports-including FDA's limited focus on children and young adults.
The authors of several reports attempt to control the commercial damage in the wake of valid safety information. These authors claimed that the recently added Black Box warnings about the increased suicide risk were the CAUSE for increased suicides.Two such reports were published in Feb. 2005:Julio Licinio, MD, and Ma-Ling Wong, M.D., of UCLA. Nature Reviews Drug Discovery. posted online at<www.nature.com/cgi-taf/DynaPage.taf?file=/nrd/journal/v4/n2/abs/nrd1634-fs.html
Robert Gibbons, Ph.D., of University of Illinois, Chicago, and J. John Mann,M.D., a professor of psychiatry at Columbia and chief of psychiatric research at New York State Psychiatric Institute. Arch Gen Psychiatry,posted at: http://archpsyc.ama-assn.org/cgi/content/abstract/62/2/165These authors claimed that most persons who did commit suicide did so because of untreated mental illness. Their judgment may have been clouded by conflicts of interest.The Times reports that Andrew C. Leon, a professor of biostatistics in psychiatry at Cornell, suggested that a drop in the use of hormone replacement therapy after 2002 might be implicated in the "puzzling 28.8 percent rise in the suicide rate among women ages 50 to 54." He is quoted speculating: "It may be that without the therapy, more women fell into depression."
Psychiatrists in the service of industry who refuse to acknowledge the evidence and alter psychiatry's practices accordingly, exhibit their utter disregard for science. In so doing they demonstrate an affinity to the Flat Earth Society and other adherents to junk science.”
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
The two relevant articles in The New York Times are here : http://www.nytimes.com/2008/02/19/us/19depress.html
http://www.nytimes.com/2008/02/19/us/19suicide.html?sq=suicide&st=nyt&scp=2&pagewanted=print
===========================
http://www.ssristories.com/
SSRI Stories
Antidepressant Nightmares
“This website is a collection of 2100+ news stories with the full media article available, mainly criminal in nature, that have appeared in the media (newspapers, TV, scientific journals) or that were part of FDA testimony in either 1991, 2004 or 2006, in which antidepressants are mentioned.
Antidepressants have been recognized as potential inducers of mania and psychosis since their introduction in the 1950s. Klein and Fink1 described psychosis as an adverse effect of the older tricyclic antidepressant imipramine. Since the introduction of Prozac in December, 1987, there has been a massive increase in the number of people taking antidepressants. Preda and Bowers2 reported that over 200,000 people a year enter a hospital with antidepressant-associated mania and/or psychosis. The subsequent harm from this prescribing can be seen in these 2100+ stories.
These stories have been collected over a period of years by two directors of the International Coalition for Drug Awareness (ICFDA). Their focus has been on Selective Serotonin Reuptake Inhibitors (SSRIs), of which Prozac was the first. Other SSRIs are Zoloft, Paxil (Seroxat), Celexa, Sarafem (Prozac in a pink pill), Lexapro, and Luvox. Other newer antidepressants included in this list are Remeron, Anafranil and the SNRIs Effexor, Serzone and Cymbalta as well as the dopamine reuptake inhibitor antidepressant Wellbutrin (also marketed as Zyban).
A public health problem of epidemic proportions
The Physicians' Desk Reference lists the following adverse reactions (side effects) to antidepressants among a host of other physical and neuropsychiatric effects: manic reaction (mania, e.g. kleptomania, pyromania, dipsomania), emotional lability (or instability), abnormal thinking, alcohol abuse, hallucinations, hostility, lack of emotion, paranoid reaction, amnesia, confusion, agitation, delirum, delusions, hysteria, psychosis, sleep disorders, abnormal dreams, and discontinuation (withdrawal) syndrome.
Adverse reactions are especially likely when starting or discontinuing the drug, increasing or lowering the dose or when switching from one SSRI to another SSRI. Adverse reactions are often diagnosed as bipolar disorder when the symptoms could be entirely iatrogenic (treatment induced).
Withdrawal, especially abrupt withdrawal, from any of these medications can also cause severe neuropsychiatric and physical symptoms. It is important to withdraw extremely slowly from these drugs, usually over a period of a year or more, under the supervision of a qualified and experienced specialist.
In addition to the adverse reactions listed in the Physicians' Desk Reference, the FDA published a Public Health Advisory on March 22, 2004 which states (in part): "Anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia (severe restlessness), hypomania, and mania have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric." (Click Links button at bottom of this page for a direct link to this FDA Warning.)
Most of the stories on this site describe events which occurred after the year 2000. The increase in online news material and the efficiency of search engines has greatly increased the ability to track stories. Even these 2100+ documented stories only represent the tip of an iceberg since most stories do not make it into the media. There are 45 cases of bizarre behavior, 28 school shootings/incidents, 49 road rage tragedies, 10 air rage incidents, 32 postpartum depression cases, over 500 murders (homicides), over 180 murder-suicides and other acts of violence including workplace violence on this site.
There is a grave concern among advocates that adverse reactions are greatly underestimated by the public, the medical profession and the regulatory authorities. Each of these stories in our list can be interpreted as an adverse reaction and in most cases we have highlighted the portion of the article that refers to evidence of bizarre behavioral change consistent with drug reaction. In some stories causation is acknowledged and the juxtaposition of these stories with those where it goes unrecognized as well as the repetition of themes and circumstances is chilling. If indeed medications played a significant role in all these tragedies, then this is a public health problem of epidemic proportions on a global scale. “
(Emphasis by Justice Lover)
by Justice Lover
Most of the crimes against humanity perpetrated by Big Pharma and by its bribed shrinks are concentrated in the production and use of two groups of deadly pharmaceutical drugs : the SSRI "Antidepressants" and the "Antipsychotic" neuroleptics. Many thousands of innocent people have lost their live as a result of consumption (forced by the shrinks in most cases) of those poisons.
Yet those poisons ,prescribed by the shrinks , brought Big Pharma a huge increase in colossal profits, and with it a huge increase in the rate of bribes for the shrinks. In a word, it is a racket, a very deadly racket ,that must be stopped immediately, if thousands of lives are to be saved !
Following are 2 reports. One was emailed to me by AHRP, the other was downloaded from
http://www.ssristories.com/ . Both concern the "Antidepressants" racket.
ALLIANCE FOR HUMAN RESEARCH PROTECTION
Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org/ and http://ahrp.blogspot.com/
FYI
“Two articles in today's New York Times, "Reports of Gunman's Use of Antidepressant Renew Debate Over Side Effects," and "Midlife Suicide RisesNearly 20%, Puzzle Researchers," represent a watershed for the Times.
Implicit in these reports are two evidence-based acknowledgments.Antidepressants, which had been touted as an effective treatment in reducing suicides, have been proven to increase the risk of suicide. What's more these drugs have been implicated in deadly violence.
The Times acknowledges the undeniable, but long denied, link between use of SSRI Antidepressants drugs and unprovoked explosive violence:"Over the years, the antidepressant Prozac and its cousins, including Paxiland Zoloft, have been linked to suicide and violence in hundreds ofpatients."Indeed, a website maintained by two mothers on a truth mission, Sara Bostockand Rosie Meysenburg, www.ssristories.com, lists 2,000 news reports linking SSRIs to violence.
These drugs' label warnings were only added after critics of pharmaceutical industry's concealment of drug hazards brought to public light the nature and severity of these drugs' adverse side-effects. Indeed, both the FDA and the MHRA in the UK failed for over a decade to examine the safety data in their own file drawers.
The Prozac label--which is identical for all SSRIs--warns about a cluster of drug-induced withdrawal symptoms that are associated with violent outbursts:"Discontinuation of Treatment with Prozac -During marketing of Prozac and other SSRIs and SNRIs...there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following:dysphoric mood, irritability, agitation, dizziness, sensory disturbances(e.g., paresthesias such as electric shock sensations), anxiety, confusion,headache,lethargy, emotional lability, [i.e. suicidal behavior] insomnia, and hypomania.
While these events are generally self-limiting, there have been reports of serious discontinuation symptoms. Patients should be monitored for these symptoms when discontinuing treatment with Prozac."The concealment of these drugs' lethal effects for over a decade led unsuspecting physicians to prescribe them widely. The consequences of such uninformed prescribing can be counted in preventable human casualties.
SSRI Antidepressants have been linked to a string of US school shooters--including Steven Kazmieczak, who shot and killed five students at Northern Illinois University.Ms. Bostock, an observer and suicide survivor, told the Times: "my main wish is that medical professionals, regulatory authorities and other scientists will examine closely the entire medical and treatment history of the perpetrators of these violent incidents in which innocent people are victims."
By contrast, the Times reports that "psychiatrists say the debate on such side effects, particularly suicide in the last four years, has driven patients from drugs that could help save their lives." That claim is without scientific foundation: help save lives how-by increasing the risk of suicide?
The claim is a faith-based position that defies the documented evidence.Another Times report focuses on the finding of a new five-year analysis of the nation's death rates, recently released by the federal Centers for Disease Control and Prevention. This study found that the suicide rate among 45-to-54-year-olds increased nearly 20% from 1999 to 2004--and for women 45to 54, the rate leapt to 31%.During these same years, sales and prescription data for SSRI Antidepressants skyrocketed--as documented by IMS Health, see:http://www.imshealth.com/ims/portal/front/articleC/0,2777,6599_18731_77056778,00.htmlandhttp://ahrp.blogspot.com/2007/05/eternal-sunshine-20-things-you-need-to.html
The alarming INCREASE in suicides among middle aged persons during a period of INCREASED use of SSRI Antidepressants refutes propaganda masquerading as scientific reports-including FDA's limited focus on children and young adults.
The authors of several reports attempt to control the commercial damage in the wake of valid safety information. These authors claimed that the recently added Black Box warnings about the increased suicide risk were the CAUSE for increased suicides.Two such reports were published in Feb. 2005:Julio Licinio, MD, and Ma-Ling Wong, M.D., of UCLA. Nature Reviews Drug Discovery. posted online at<www.nature.com/cgi-taf/DynaPage.taf?file=/nrd/journal/v4/n2/abs/nrd1634-fs.html
Robert Gibbons, Ph.D., of University of Illinois, Chicago, and J. John Mann,M.D., a professor of psychiatry at Columbia and chief of psychiatric research at New York State Psychiatric Institute. Arch Gen Psychiatry,posted at: http://archpsyc.ama-assn.org/cgi/content/abstract/62/2/165These authors claimed that most persons who did commit suicide did so because of untreated mental illness. Their judgment may have been clouded by conflicts of interest.The Times reports that Andrew C. Leon, a professor of biostatistics in psychiatry at Cornell, suggested that a drop in the use of hormone replacement therapy after 2002 might be implicated in the "puzzling 28.8 percent rise in the suicide rate among women ages 50 to 54." He is quoted speculating: "It may be that without the therapy, more women fell into depression."
Psychiatrists in the service of industry who refuse to acknowledge the evidence and alter psychiatry's practices accordingly, exhibit their utter disregard for science. In so doing they demonstrate an affinity to the Flat Earth Society and other adherents to junk science.”
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
The two relevant articles in The New York Times are here : http://www.nytimes.com/2008/02/19/us/19depress.html
http://www.nytimes.com/2008/02/19/us/19suicide.html?sq=suicide&st=nyt&scp=2&pagewanted=print
===========================
http://www.ssristories.com/
SSRI Stories
Antidepressant Nightmares
“This website is a collection of 2100+ news stories with the full media article available, mainly criminal in nature, that have appeared in the media (newspapers, TV, scientific journals) or that were part of FDA testimony in either 1991, 2004 or 2006, in which antidepressants are mentioned.
Antidepressants have been recognized as potential inducers of mania and psychosis since their introduction in the 1950s. Klein and Fink1 described psychosis as an adverse effect of the older tricyclic antidepressant imipramine. Since the introduction of Prozac in December, 1987, there has been a massive increase in the number of people taking antidepressants. Preda and Bowers2 reported that over 200,000 people a year enter a hospital with antidepressant-associated mania and/or psychosis. The subsequent harm from this prescribing can be seen in these 2100+ stories.
These stories have been collected over a period of years by two directors of the International Coalition for Drug Awareness (ICFDA). Their focus has been on Selective Serotonin Reuptake Inhibitors (SSRIs), of which Prozac was the first. Other SSRIs are Zoloft, Paxil (Seroxat), Celexa, Sarafem (Prozac in a pink pill), Lexapro, and Luvox. Other newer antidepressants included in this list are Remeron, Anafranil and the SNRIs Effexor, Serzone and Cymbalta as well as the dopamine reuptake inhibitor antidepressant Wellbutrin (also marketed as Zyban).
A public health problem of epidemic proportions
The Physicians' Desk Reference lists the following adverse reactions (side effects) to antidepressants among a host of other physical and neuropsychiatric effects: manic reaction (mania, e.g. kleptomania, pyromania, dipsomania), emotional lability (or instability), abnormal thinking, alcohol abuse, hallucinations, hostility, lack of emotion, paranoid reaction, amnesia, confusion, agitation, delirum, delusions, hysteria, psychosis, sleep disorders, abnormal dreams, and discontinuation (withdrawal) syndrome.
Adverse reactions are especially likely when starting or discontinuing the drug, increasing or lowering the dose or when switching from one SSRI to another SSRI. Adverse reactions are often diagnosed as bipolar disorder when the symptoms could be entirely iatrogenic (treatment induced).
Withdrawal, especially abrupt withdrawal, from any of these medications can also cause severe neuropsychiatric and physical symptoms. It is important to withdraw extremely slowly from these drugs, usually over a period of a year or more, under the supervision of a qualified and experienced specialist.
In addition to the adverse reactions listed in the Physicians' Desk Reference, the FDA published a Public Health Advisory on March 22, 2004 which states (in part): "Anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia (severe restlessness), hypomania, and mania have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric." (Click Links button at bottom of this page for a direct link to this FDA Warning.)
Most of the stories on this site describe events which occurred after the year 2000. The increase in online news material and the efficiency of search engines has greatly increased the ability to track stories. Even these 2100+ documented stories only represent the tip of an iceberg since most stories do not make it into the media. There are 45 cases of bizarre behavior, 28 school shootings/incidents, 49 road rage tragedies, 10 air rage incidents, 32 postpartum depression cases, over 500 murders (homicides), over 180 murder-suicides and other acts of violence including workplace violence on this site.
There is a grave concern among advocates that adverse reactions are greatly underestimated by the public, the medical profession and the regulatory authorities. Each of these stories in our list can be interpreted as an adverse reaction and in most cases we have highlighted the portion of the article that refers to evidence of bizarre behavioral change consistent with drug reaction. In some stories causation is acknowledged and the juxtaposition of these stories with those where it goes unrecognized as well as the repetition of themes and circumstances is chilling. If indeed medications played a significant role in all these tragedies, then this is a public health problem of epidemic proportions on a global scale. “
(Emphasis by Justice Lover)
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