As seen is this Medical Paper
Article summary:
From the Essay
Antidepressants are assumed to work on the specific neurobiology of depressive disorders according to a “disease-centred” model of drug action. However, little evidence supports this idea.
An alternative, “drug-centred,” model suggests that psychotropic drugs create abnormal states that may coincidentally relieve symptoms. Drug-induced effects of antidepressants vary widely according to their chemical class—from sedation and cognitive impairment to mild stimulation and occasionally frank agitation. Results of clinical trials may be explained by drug-induced effects and placebo amplification.
No evidence shows that antidepressants or any other drugs produce long-term elevation of mood or other effects that are particularly useful in treating depression.
We propose in this Essay that an alternative “drug-centred” model can better explain observed drug effects in psychiatric conditions. This drug-centred model suggests that instead of relieving a hypothetical biochemical abnormality, drugs themselves cause abnormal states, which may coincidentally relieve psychiatric symptoms.All of which is interesting, but looks at a way to keep using the drugs without knowing what is really going on. The advantadge is that it drops the pretense that they know what is going on. So I suppose this is a weird half step forward, without addressing the actual situation.
Alcohol's disinhibiting effects may relieve symptoms of social phobia, but that does not imply that alcohol corrects a chemical imbalance underlying social phobia. Sedation may lessen high arousal, present in many acute psychiatric situations. Drugs that induce indifference, such as neuroleptics or opiates, may help reduce the distress of acute psychotic symptoms. Low-dose stimulants may help improve attention and concentration in the short term.
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Antidepressants are believed to exert their therapeutic effects by acting on brain monoamines, which are believed to be important determinants of mood. However, in a circular chain of logic, the monoamine theory of depression was itself formulated primarily in response to observations that early antidepressants increased brain monoamine levels
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The idea that antidepressant drugs target a specific biological state that produces depression strongly justifies the disease model of depression and its medical treatment. Therefore, abandoning the disease-centred model of antidepressant action squarely challenges the notion of depression as a biologically based medical disease.
The argument presented here supports claims that the medical concept of depression obscures the diversity of problems and experiences that come to be so labelled, and that social explanations and interventions have been undervalued.
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