Posted by linkadge on July 19, 2006, at 19:33:57
In reply to Re: couldn't have said it better myself, posted by SLS on July 19, 2006, at 5:57:36
>They already have been.
I just don't understand how you can't envision all of the clincical trials that show nothing at all that never see the light of day.The argument too (surely you are not ignorant of) the fact that the use of active placebos often produce a significant narrowing of the gap between antidepressant and placebo sucess rates.
It has been well documented that patients' beleifs can often predict response to antidepressants.
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256CFC00521C5A
When taken in the context of active vs. placebo, it is not unreasonable to suggest that patients know when they are getting an active drug. When the patient comes to believe that they are recieving the active drug thats when these beliefs can play a significant role in the outcome of the trial. This is why active placebo's are so fiercely opposed by drug companies.
The following exerpts were taken from:
http://bjp.rcpsych.org/cgi/content/full/180/3/193
In addition, Greenberg et al found that the effects of older antidepressants compared with placebo were less than the effects of newer ones in a meta-analysis of three-arm trials comparing a new antidepressant and an old one with placebo (Greenberg et al, 1992). They suggested that this was due to reduced expectations of the performance of the older antidepressants.
Moncrieff et al (1998) found lower effect sizes in trials using active placebos
Quitkin et al also criticised the findings from active placebo-controlled trials on the basis that drug improvement rates were lower than expected.
The Hamilton Rating Scale for Depression (Hamilton, 1960) has been criticised because it contains a large number of items relating to sleep and anxiety, which is likely to favour any active drug with sedative properties. (Ie the highly sedating antihistamine derivitive TCAs)
Selective reporting of outcomes is a potential problem.
Failure to perform ‘intention to treat’ analysis has been shown to inflate apparent treatment effects in antidepressant trials (Bollini et al, 1999).
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Publication bias is also a concern (Antonuccio et al, 1999; Moncrieff, 2001) and a recent meta-analysis SHOWED THAT SPONSORSHIP WAS THE STRONGEST PREDICTOR OF OUTCOME IN COMPARITIVE TRIALS WITH SELECTIVE SEROTONIN REUPTAKE INHIBITORS (Freemantle et al, 2000).
*****************************It is agreed that there is great heterogeneity among such trials of antidepressants, with a substantial proportion finding no difference between drug and placebo.
Morris & Beck (1974) found that around a third of trials of tricyclic antidepressants were negative.
Rogers & Clay (1975) FOUND THAT 64% OF TRIALS OF IMIPRAMINE WERE NEGATIVE, and McNair (1974)
The Medical Research Council trial found no difference between imipramine and placebo on the main categorical outcome and negligible differences in individual symptoms (Medical Research Council, 1965).
Although it was reported that imipramine was superior to placebo at 3 weeks, there was no difference at the end of the 5-week treatment period or at the end of followup. In addition, the main report on efficacy excluded the 159 Black patients who were said to have shown a poorer response to imipramine (Raskin et al, 1970). (IE Rife with bias)
Recent studies are almost all conducted with out-patients and most are sponsored by the pharmaceutical industry. It is possible that there is a greater potential for placebo effects and therefore for amplified placebo effects in people with milder disorders. However, so few studies test the integrity of the double-masking that it is difficult to know to what extent this is the case (Even et al, 2000).
Many substances not conventionally classified as antidepressants have been found to be superior to placebo or to have equivalent efficacy to antidepressants in trials of treatment of depression. The list includes various neuroleptics (Robertson & Trimble, 1982), barbiturates (Blashki et al, 1971), benzodiazepines (Imlah, 1985), buspirone (Robinson et al, 1990), some stimulants (Rickels et al, 1970) and more recently Hypericum extract (Philipp et al, 1999). These observations might imply that depression is susceptible to a variety of non-disease-specific pharmacological actions such as sedation or psychostimulation, as well as the effects of suggestion.
I honestly don't see how you can conclude in such a cut and dry manner that antidepressants are unequivically effective.Linkadge
poster:linkadge
thread:662854
URL: http://www.dr-bob.org/babble/20060717/msgs/668382.html