“…10 Even if depression were to be associated with a specific biochemical disturbance, we have no current grounds to claim that antidepressant drugs act by reversing this abnormality. 12 Apart from placebo effects, antidepressants exert psychoactive effects that may reveal their identity to people taking part in placebo controlled trials, thus infringing the double blind design. Moreover, the psychoactive effects of antidepressants, such as the sedative effects of tricyclics and the possible emotional dampening effects of SSRIs, 13 may themselves impact on outcome measures.…”
Section: The Evidence On Antidepressant Effectsmentioning
confidence: 99%
“…The fact that psychoactive substances not normally considered to be antidepressants, including antipsychotics, stimulants, and benzodiazepines have similar effects to antidepressants in some trials, and that antidepressants themselves come from diverse chemical classes, supports the idea that it is the psychoactive and placebo effects of antidepressants, not their supposed effect on an underlying brain disorder, that accounts for the small differences observed between drugs and placebos in randomised controlled trials. 12 Despite this lack of evidence, we acknowledge that a substantial body of opinion continues to maintain that depression is a reversible, or partially reversible brain disease that can usefully be treated with drugs. The argument that this can best be understood as an 'ideology' deliberately maintained by those with a commercial interest in doing so is presented elsewhere, 14 although it is indicative of changes in this ideology that quetiapine is now being marketed in the US as a treatment for depression and bipolar disorder as well as its original indication, schizophrenia.…”
Section: The Evidence On Antidepressant Effectsmentioning
Despite NICE guidance that should have limited it, antidepressant prescribing continues to increase. Research evidence suggests that much if not all of the observed efficacy should be attributed to complex non-specific effects rather than 'restoration of disturbed brain chemistry'. According to this view the uncertain benefits of antidepressants are unlikely to outweigh the risks, suggesting the need to explore other approaches to treatment.
“…10 Even if depression were to be associated with a specific biochemical disturbance, we have no current grounds to claim that antidepressant drugs act by reversing this abnormality. 12 Apart from placebo effects, antidepressants exert psychoactive effects that may reveal their identity to people taking part in placebo controlled trials, thus infringing the double blind design. Moreover, the psychoactive effects of antidepressants, such as the sedative effects of tricyclics and the possible emotional dampening effects of SSRIs, 13 may themselves impact on outcome measures.…”
Section: The Evidence On Antidepressant Effectsmentioning
confidence: 99%
“…The fact that psychoactive substances not normally considered to be antidepressants, including antipsychotics, stimulants, and benzodiazepines have similar effects to antidepressants in some trials, and that antidepressants themselves come from diverse chemical classes, supports the idea that it is the psychoactive and placebo effects of antidepressants, not their supposed effect on an underlying brain disorder, that accounts for the small differences observed between drugs and placebos in randomised controlled trials. 12 Despite this lack of evidence, we acknowledge that a substantial body of opinion continues to maintain that depression is a reversible, or partially reversible brain disease that can usefully be treated with drugs. The argument that this can best be understood as an 'ideology' deliberately maintained by those with a commercial interest in doing so is presented elsewhere, 14 although it is indicative of changes in this ideology that quetiapine is now being marketed in the US as a treatment for depression and bipolar disorder as well as its original indication, schizophrenia.…”
Section: The Evidence On Antidepressant Effectsmentioning
Despite NICE guidance that should have limited it, antidepressant prescribing continues to increase. Research evidence suggests that much if not all of the observed efficacy should be attributed to complex non-specific effects rather than 'restoration of disturbed brain chemistry'. According to this view the uncertain benefits of antidepressants are unlikely to outweigh the risks, suggesting the need to explore other approaches to treatment.
“…Studies of serotonin receptors, for example, show increased levels in depression in some studies, decreased levels in other studies and no difference in some (Moncrieff & Cohen, 2006). There are claims that tryptophan depletion produces depression, but the research has involved people who had been previously treated with SSRIs, and studies with volunteers show no effects (Murphy, Smith, Cowen, Robbins & Sahakian, 2002).…”
Aims:This article explores an alternative understanding of how psychiatric drugs works that is referred to as the drug-centred model of drug action. Unlike the current diseasecentred model, which suggests that psychiatric drugs work by correcting an underlying brain abnormality, the drug-centred model emphasises how psychiatric drugs affect mental states and behaviour by modifying normal brain processes. The alterations produced may impact on the emotional and behavioural problems that constitute the symptoms of mental disorders.
Methods:Arguments are put forward that justify the consideration of the drug-centred model.The research necessary to support the prescription of drugs according to such a model is explored.
Results:Evidence from neurochemistry and comparative drug trials do not confirm the disease-centred model of drug action. Since psychiatric drugs are recognised to have mind and behaviour-altering properties, the drug-centred model constitutes a plausible alternative. The drug-centred model suggests research is needed to identify all the alterations produced by various sorts of drugs, both acute and long-term, and how these might interact with the symptoms and problems associated with different mental disorders. This requires detailed animal and volunteer studies and data from patients prescribed drug treatment long-term, along with placebo-controlled and comparative 3 trials that look at the overall impact of drug-induced alterations on well-being and functioning as well as symptoms. Research is also needed on alternative ways of fulfilling the function of drug treatment. The moral aspect of using drugs to modify behaviour rather than treat disease needs honest and transparent consideration.
Conclusions:It is hoped this discussion will encourage the psychiatric and pharmaceutical research community to provide more of the information that is required to use psychiatric drugs safely and effectively.
“…According to Moncrieff and Cohen [26], antidepressants have not been shown to cure depression and depression is not caused by an abnormal brain in need of cure. Rather, antidepressants serve to create an abnormal brain state, which causes a variety of manifestations including sedation, cognitive impairment, and stimulation.…”
Cognitive and pharmaceutical interventions and outcomes for depression are compared, with attention to their long-term effects on a range of negative schema. A subset of residual dysfunctional schema is identified and shown to influence patients during periods of mood or stress induction while under pharmaceutical treatment as well as following cessation of pharmaceutical interventions. The same dysfunctional schema, however, show a more effective and enduring pattern of positive modification in response to cognitive treatment. Medication is acknowledged to provide symptomatic relief from a subset of negative schema, without modifying a full complement of deeply rooted, tenacious negative beliefs. Patients medicated for depression, even in the absence of overt depressive symptoms, carry emotionally masked and dormant maladaptive schemas which may continue, through their carriers' thoughts and behaviors, to influence their own behavior and affect others in their environment who may or may not be medicated.
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