Chemical imbalance

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Chemical imbalance is one theory about the cause of mental illness. Other causes that are debated include psychological and social causes.

The basic concept is that neurotransmitter imbalances within the brain are the main causes of psychiatric conditions and that these conditions can be improved with medication which corrects these imbalance. The phrase originated from the scientific study of brain chemistry. In the 1950s the monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants were accidentally discovered to be effective in the treatment of depression^[1]. These findings and other supporting evidence led Joseph Schildkraut to publish his paper called "The Catecholamine Hypothesis of Affective Disorders" in 1965.^[2] Schildkraut associated low levels of neurotransmitters with depression.

Research into other mental illnesses such as schizophrenia also found that too little activity of certain neurotransmitters was correlated to these disorders. In the scientific community this hypothesis has been referred to as the Monoamine Hypothesis. This hypothesis has been a major focus of research in the fields Pathophysiology and Pharmacotherapy for over 25 years ^[3] and led to the development of new classes of drugs such as SSRIs (selective-serotonin reuptake inhibitors)^[4]. This conceptual framework has been challenged within the scientific community, though no other demonstrably superior hypothesis has emerged. While the hypothesis has been shown to be simplistic and lacking, there is sufficient evidence to consider it as a useful heuristic in the aiding of our understanding of brain chemistry and explaining pharmacotherapy.^[3][5] Wayne Goodman, Chair of the U.S. Food and Drug Administration It may be noted, for example, that, while the most commonly prescribed medications for depression increase the availability of only one to three neurotransmitters, science has so far identified over 100 existing neurotransmitters in the human body. Manipulation of serotonin, norepinephrine and dopamine availability may fall far short of truly treating the larger picture of depression as a systemic disease. Psychopharmacological Advisory Committee, has described the serotonergic theory of depression as a "useful metaphor" for understanding depression, though not one that he uses with his own psychiatric patients.^[6] Recently, psychiatrist Peter Kramer stated that the serotonin theory of depression had been declared dead prematurely.^[7] Kramer argues that recent scientific research actually shows a definitive role for serotonin deficiency in depression. An analysis of the studies Kramer cites argues that such statements are premature.^[8]

Monoamine hypothesis

Monoamine Hypothesis is a biological theory stating that depression is caused by the underactivity in the brain of monoamines, such as dopamine, serotonin, and norepinephrine.

In the 1950s the monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants were accidentally discovered to be effective in the treatment of depression.^[1] These findings and other supporting evidence led Joseph Schildkraut to publish his paper called "The Catecholamine Hypothesis of Affective Disorders" in 1965.^[2] Schildkraut associated low levels of neurotransmitters with depression. Research into other mental impairments such as schizophrenia also found that too little activity of certain neurotransmitters were connected to these disorders.

The hypothesis has been a major focus of research in the fields pathophysiology and pharmacotherapy for over 25 years.^[3] and led to the development of new classes of drugs such as SSRIs (selective serotonin reuptake inhibitors).^[4]

Dopamine hypothesis

In studying the causes of schizophrenia, particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which triggers the release of dopamine may exacerbate the psychotic symptoms in schizophrenia.^[9] An influential theory, known as the Dopamine hypothesis of schizophrenia, proposed that a malfunction involving dopamine pathways was the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.^[10]

Criticisms

According to critics, the chemical imbalance hypothesis has been overpromoted and continues to be advanced as factual by pharmaceutical companies. They believe the general population and many journalists have accepted this hypothesis into their understanding of mental illness uncritically.^[11] They have pointed to the lack of an established chemical balance (without which, they claim, the notion of an "imbalance" is meaningless). Certain pharmaceutical companies such as Pfizer continue to promote drugs like Zoloft with advertisements asserting that mental illness may be due to chemical imbalances in the brain, and that their drugs work to "correct" this imbalance. ^[12] Most academics believe that the advertisements are oversimplified and don't fully explain what is happening. ^[13]

Chemical imbalances theories do not presume individual laboratory tests be obtained from a patient at the time of prescription, such as one would expect in the analogy to physical medicine. For example, someone suffering from schizophrenia is not given haloperidol on the basis of a laboratory test which shows that his or her dopamine level is too high.

Chemical imbalances theories distinguish, between 'side' and 'main' drug effects in recording the response to the drug. 'Side' effects are considered to be simple, direct, predictible, allowable effects which are merely 'physical' but do include often flattened affect and memory, emotive and cognitive effects. These drug effects may then be cited capriciously as further evidence to confirm the diagnosis as correct, confusing cause and effect.^{[citation needed]}

When 'improvement' is measured in industry research studies, attention is given only to the 'main' effect - typically a complex, indirect, interpersonal, perceptual, cultural change, thereby confusing cause with coincidence. There does not exist in chemical imbalance theories, effectiveness measures using standard social networks and associated tests before and after drugs administration.^{[citation needed]}

Chemical imbalance theories predominate in 'streamline' public sector medicine for lower social class and homeless persons, where drugs constitute the only form of treatment. There is much wishful thinking in attribution of drug effect, particularly in cases like schizophrenia, where there no longer exists a patient [non-drug user] control group available.^{[citation needed]}

See also

• BDNF

References