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So the neurotransmitters are the 'chemicals' and if they deviate from 'normal' levels, concentrations etc., they are in 'imbalance'? And this then causes depression. That is a very unfortunate leap from a probabilistic correlation to a simple mechanistic causation hypothesis. Even "seperable"separable neural dysfunctions" are a very far cry from understanding just a subset of symptoms, let alone "depression".

So the neurotransmitters are the 'chemicals' and if they deviate from 'normal' levels, concentrations etc., they are in 'imbalance'? And this then causes depression. That is a very unfortunate leap from a probabilistic correlation to a simple mechanistic causation hypothesis. Even "seperable neural dysfunctions" are a very far cry from understanding just a subset of symptoms, let alone "depression".

So the neurotransmitters are the 'chemicals' and if they deviate from 'normal' levels, concentrations etc., they are in 'imbalance'? And this then causes depression. That is a very unfortunate leap from a probabilistic correlation to a simple mechanistic causation hypothesis. Even "separable neural dysfunctions" are a very far cry from understanding just a subset of symptoms, let alone "depression".

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This gave an overview of eight currently competing models, chemical imbalance quote singled out here. Taking some hints on how scientific theories originate, operate and outlast others might be useful. Well, if 'chemical imbalance' indeed is able to do so:

Yes. At best this theory is onan oversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised, but sells very well.

Yes. At best this theory is on oversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised.

This gave an overview of eight currently competing models, chemical imbalance quote singled out here. Taking some hints on how scientific theories originate, operate and outlast others might be useful. Well, if 'chemical imbalance' indeed is able to do so:

Yes. At best this theory is an oversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised, but sells very well.

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So why is this theory still so popular? Just because a chemical imbalance can be chemically balanced? With marketable drugsdrugs, of course?

The "Chemical Imbalance" Explanation for Depression: Origins, Lay Endorsement, and Clinical Implications:
Modern chemical imbalance hypotheses of depression originated in the mid-20th century, spurred by important discoveries such as the efficacy of chlorpromazine for psychosis; findings that monoamines exist within the central nervous system (CNS) and act as neurotransmitters; and an early understanding of monoamine synthesis, storage, release, and deactivation. Such discoveries also quickened the emergence of psychopharmacology as a discipline and helped lead to the eventual widespread practice of using prescription drugs to treat mental disorders also (e.g., Healy, 2001). […]
Also interfering with response-equals-causation logic are findings that in many clinical trials, antidepressants have exhibited either no or very modest advantages in comparison with placebos (Kirsch, Moore, Scoboria, & Nicholls, 2002; Kirsch, Scoboria, & Moore, 2002).
So Where Do We Stand Today?
In sum, the pathophysiology of depression remains poorly understood (Hindmarch, 2001; Hirschfeld, 2000), and a simplistic chemical imbalance explanation for depression likely lacks ade- quate validity (Hindmarch, 2002). Monoamine deficiencies continue to be mentioned by some researchers as a potential cause of depression (e.g., Bianchi et al., 2002), but others have declared simply that the monoamine hypothesis “is incorrect” (Owens, 2004, p. 6). Researchers have increasingly turned toward investigations of other potential biological causes of depression (e.g., Hindmarch, 2001; Leonard, 2000; McEwen, 1999). Related efforts to identify distinct brain changes before, during, and after depression treatment are also ongoing (e.g., Cook et al., 2005; Sheline, 2003).

However, there are currently no widely available anatomical, chemical, or other biological tests that reliably distinguish the brains of depressed persons from nondepressed persons (e.g., Antonuccio et al., 1999). Multiple etiological models (including biological, environmental, and interactional) of depression remain viable at present.
The Chemical Imbalance Explanation as Cultural Narrative Despite its flaws, the chemical imbalance explanation remains the potentially dominant cultural story of depression etiology in the United States (e.g., Smith, 1999). However, cultural narratives of mental illness do not necessarily reflect an objective reality or universal understanding. Different historical and cultural traditions frame depressive experiences within different contexts, thereby promoting and/or limiting particular symptoms and shaping different understandings and meanings of depression and its appro- priate treatment. Such narratives are probably best conceptualized as social constructions that must be understood within the cultural context that socializes, interprets, and responds to them (Marsella & Kaplan, 2002). […]
Currently, depression is not diagnosed via objective chemical tests, nor is treatment guided by any such tests. If depression did result primarily from a known chemical imbalance, such tests would likely be available and in widespread use, and depression would be easily and quickly resolved for most patients.

Yes. At best this theory is on oversimplificationoversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised.

So why is this theory still so popular? Just because a chemical imbalance can be chemically balanced? With marketable drugs, of course?

Yes. At best this theory is on oversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised.

So why is this theory still so popular? Just because a chemical imbalance can be chemically balanced? With marketable drugs, of course?

The "Chemical Imbalance" Explanation for Depression: Origins, Lay Endorsement, and Clinical Implications:
Modern chemical imbalance hypotheses of depression originated in the mid-20th century, spurred by important discoveries such as the efficacy of chlorpromazine for psychosis; findings that monoamines exist within the central nervous system (CNS) and act as neurotransmitters; and an early understanding of monoamine synthesis, storage, release, and deactivation. Such discoveries also quickened the emergence of psychopharmacology as a discipline and helped lead to the eventual widespread practice of using prescription drugs to treat mental disorders also (e.g., Healy, 2001). […]
Also interfering with response-equals-causation logic are findings that in many clinical trials, antidepressants have exhibited either no or very modest advantages in comparison with placebos (Kirsch, Moore, Scoboria, & Nicholls, 2002; Kirsch, Scoboria, & Moore, 2002).
So Where Do We Stand Today?
In sum, the pathophysiology of depression remains poorly understood (Hindmarch, 2001; Hirschfeld, 2000), and a simplistic chemical imbalance explanation for depression likely lacks ade- quate validity (Hindmarch, 2002). Monoamine deficiencies continue to be mentioned by some researchers as a potential cause of depression (e.g., Bianchi et al., 2002), but others have declared simply that the monoamine hypothesis “is incorrect” (Owens, 2004, p. 6). Researchers have increasingly turned toward investigations of other potential biological causes of depression (e.g., Hindmarch, 2001; Leonard, 2000; McEwen, 1999). Related efforts to identify distinct brain changes before, during, and after depression treatment are also ongoing (e.g., Cook et al., 2005; Sheline, 2003).

However, there are currently no widely available anatomical, chemical, or other biological tests that reliably distinguish the brains of depressed persons from nondepressed persons (e.g., Antonuccio et al., 1999). Multiple etiological models (including biological, environmental, and interactional) of depression remain viable at present.
The Chemical Imbalance Explanation as Cultural Narrative Despite its flaws, the chemical imbalance explanation remains the potentially dominant cultural story of depression etiology in the United States (e.g., Smith, 1999). However, cultural narratives of mental illness do not necessarily reflect an objective reality or universal understanding. Different historical and cultural traditions frame depressive experiences within different contexts, thereby promoting and/or limiting particular symptoms and shaping different understandings and meanings of depression and its appro- priate treatment. Such narratives are probably best conceptualized as social constructions that must be understood within the cultural context that socializes, interprets, and responds to them (Marsella & Kaplan, 2002). […]
Currently, depression is not diagnosed via objective chemical tests, nor is treatment guided by any such tests. If depression did result primarily from a known chemical imbalance, such tests would likely be available and in widespread use, and depression would be easily and quickly resolved for most patients.

Yes. At best this theory is on oversimplification. More accurate now, it seems the outlook is that a once promising hypothesis has failed to provide a convincing explanation for the causes nor the 'cures', has failed to accurately predict the outcomes of medications and other interventions, and plainly way too often does not work as advertised.

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