Rounded Agony
Hard to live, hard to die
- Aug 8, 2022
- 786
As I continue to wait in an apparently eternal limbo for a community psychiatry referral to clear, I've been bouncing about reading shit that will help me navigate the appointment when/if it ever happens. Well, after coming across an interesting tidbit in an article about long-term negative life consequences tending to mess with dopamine pathways (thus marginalizing the holy grail/first-line serotonin approach), I found the following on Wikipedia's antidepressant page of all places. Thankfully all the links are intact - always cite your sources, kids!
From the section on Pharmacology:
I plan to cite this information if I am ever told by someone that antidepressants, specifically SSRIs, would be good for me.
*Edited to remove a non-essential section and add underlines.*[/justify]
From the section on Pharmacology:
"A major 2022 systematic umbrella review by Joanna Moncrieff and colleagues showed that the serotonin theory of depression was not supported by the evidence from a wide variety of areas.[142] The authors concluded that there is no association between serotonin and depression and there is no support for depression being caused by low serotonin activity or concentrations.[142] Other literature had described the lack of support for the theory previously.[147][148][149] In many of the expert responses to the review, it was stated that the monoamine hypothesis had long already been abandoned by psychiatry.[150][151] This is in spite of about 90% of the general public in Western countries believing the theory to be true and many in the field of psychiatry continuing to promote the theory up to recent times.[151][149]
...
The serotonin and monoamine hypotheses of depression have been heavily promoted by the pharmaceutical industry (e.g., in advertisements) and by the psychiatric profession at large despite the lack of evidence in support of them.[147][148][141][153][149][154] In the case of the pharmaceutical industry, this can be attributed to obvious financial incentives, with the theory creating bias against non-pharmacological treatments for depression.[154][147][148][141]
An alternative theory for antidepressant action proposed by certain academics such as Irving Kirsch is that they work largely or entirely via placebo mechanisms.[155][156][157] This is supported by meta-analyses of antidepressant randomized controlled trials, which consistently show that placebo groups in trials improve about 80 to 90% as much as antidepressant groups on average[155][158] and that antidepressants are only marginally more effective for depression than placebos.[159][160][161][162][163] The difference between antidepressants and placebo corresponds to an effect size (SMD) of about 0.3, which in turn equates to about a 2- to 3-point additional improvement on the 0–52-point (HRSD) and 0–60-point (MADRS) depression rating scales used in trials.[159][160][161][162][163] This small advantage of antidepressants over placebo is often statistically significant and is the basis for their regulatory approval, but is sufficiently modest that its clinical significance is doubtful.[164][165][160][163] Moreover, the small advantage of antidepressants over placebo may simply be a methodological artifact caused by unblinding due to the psychoactive effects and side effects of antidepressants, in turn resulting in enhanced placebo effects and apparent antidepressant efficacy.[155][163][156] Placebos are not purely psychological phenomenon, but have been found to modify the activity of several brain regions and to increase levels of dopamine and endogenous opioids in the reward pathways.[166][167][168] It has been argued by Kirsch that although antidepressants may be used efficaciously for depression as active placebos, they are limited by significant pharmacological side effects and risks, and therefore non-pharmacological therapies, such as psychotherapy and lifestyle changes, which can have similar efficacy to antidepressants but do not have their adverse effects, ought to be preferred as treatments in people with depression.[169]
The placebo response, or the improvement in scores in the placebo group in clinical trials, is not only due to the placebo effect, but is also due to other phenomena such as spontaneous remission and regression to the mean.[155][170] Depression tends to have an episodic course, with people eventually recovering even with no medical intervention, and people tend to seek treatment, as well as enroll in clinical trials, when they are feeling their worst.[171][170] In meta-analyses of trials of depression therapies, Kirsch estimated based on improvement in untreated waiting-list controls that spontaneous remission and regression to the mean only account for about 25% of the improvement in depression scores with antidepressant therapy.[155][172][173][174][171] However, another academic, Michael P. Hengartner, has argued and presented evidence that spontaneous remission and regression to the mean might actually account for most of the improvement in depression scores with antidepressants, and that the substantial placebo effect observed in clinical trials might largely be a methodological artifact.[170] This suggests that antidepressants may be associated with much less genuine treatment benefit, whether due to the placebo effect or to the antidepressant itself, than has been traditionally assumed.[170]"
I plan to cite this information if I am ever told by someone that antidepressants, specifically SSRIs, would be good for me.
*Edited to remove a non-essential section and add underlines.*[/justify]
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some of the writing there was actually pretty funny, some quite heartbreaking...
