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Biological psychiatry, or biopsychiatry is an approach to psychiatry that aims to understand mental disorder in terms of the biological function of the nervous system. It is interdisciplinary in its approach and draws on sciences such as neuroscience, psychopharmacology, biochemistry, genetics and physiology to form theories about the biological bases of behaviour and psychopathology. [1][2][3][4]

While there is some overlap between biological psychiatry and neurology, the latter generally focuses on disorders where gross or visible pathology of the nervous system is apparent, such as epilepsy, cerebral palsy, encephalitis, neuritis, Parkinson's disease and multiple sclerosis. There is some overlap with neuropsychiatry, which typically deals with behavioural disturbance in the context of apparent brain disorder.

Biological psychiatry and other approaches to mental illness are not mutually exclusive, but may simply attempt to deal with the phenomena at different levels of explanation. Because of the focus on the biological function of the nervous system, however, biological psychiatry has been particularly important in developing and prescribing drug-based treatments for mental disorder.

In practice, however, psychiatrists may advocate both medication and psychological therapies when treating mental illness. The therapy is more likely to be conducted by clinical psychologists, psychotherapists, occupational therapists or other mental health workers who are more specialised and trained in non-drug approaches.[5][6]

The history of the field extends back to the ancient Greek physician Hippocrates,[7] but the term biological psychiatry was first used in peer-reviewed scientific literature in 1953. The term is more commonly used in the US than in some other countries such as the UK. [8] The field, however, is not without its critics and the phrase "biological psychiatry" is sometimes used by those critics as a term of disparagement.

Scope and detailed definitionEdit

Biological Psychiatry is a branch of Psychiatry where the focus is chiefly on researching & understanding the biological basis of major mental disorders such as Unipolar & Bipolar Affective (Mood) Disorders, Schizophrenia & Organic Mental Disorders such as Alzheimers Disease. This knowledge has been gained using imaging techniques, psychopharmacology, neuroimmunochemistry & so on. Discovering the detailed interplay between neurotransmitters and the understanding of the neurotransmitter fingerprint of psychiatric drugs such as Clozapine has been a helpful result of the research. On a research level, it includes all possible biological bases of behavior - biochemical, genetic, physiological, neurological and anatomical. On a clinical level, it includes various therapies, such as drugs, diet, avoidance of environmental contaminants, exercise, and alleviation of the adverse effects of life stress[9], all of which can cause measurable biochemical changes.[10] The biological psychiatrist views all of these as possible etiologies of or remedies for mental health disorders.

However, the biological psychiatrist typically does not discount psychoanalytic approaches (talk therapies). Medical psychiatric training generally includes both psychodynamic and biological approaches.[5] Accordingly, psychiatrists are usually comfortable with a dual approach: "psychotherapeutic methods...are as indispensable as psychopharmacotherapy in a modern psychiatric clinic"[6],

Basis for biological psychiatryEdit

Sigmund Freud developed psychotherapy in the early 1900s, and through the 1950s this technique was prominent in treating mental health disorders.

However in the late 1950s, the first modern antipsychotic and antidepressant drugs were developed: Chlorpromazine (also known as Thorazine), the first widely-used antipsychotic, was synthesized in 1950, and iproniazid, one of the first antidepressants, was first synthesized in 1957. In 1959 imipramine, the first tricyclic antidepressant, was developed.

Based significantly on clinical observations of the above drug results, in 1965 the seminal paper "The catecholamine hypothesis of affective disorders" was published.[11] It articulated the "chemical imbalance" hypothesis of mental health disorders, especially depression. It formed much of the conceptual basis for the modern era in biological psychiatry.[12]

Although the "chemical imbalance" hypothesis has been significantly revised since 1965, many newer medications (such as fluoxetine and other SSRIs) were developed based on the underlying theories of the hypothesis. More recent research points to deeper underlying biological mechansisms as the possible basis for several mental health disorders.[13][14]

Modern brain imaging techniques allow noninvasive examination of neural function in patients with mental health disorders, however this is currently experimental. With some disorders it appears the proper imaging equipment can reliably detect certain neurobiological problems associated with a specific disorder.[15][16] If further studies corroborate these experimental results, future diagnosis of certain mental health disorders could be expedited using such methods.

Another source of data indicating a significant biological aspect of some mental health disorders is twin studies. Identical twins have the same nuclear DNA, so carefully constructed studies may indicate the relative importance of environmental and genetic factors on the development of a particular mental health disorder.

The results from this research and the associated hypotheses form the basis for biological psychiatry and the treatment approaches in a clinical setting.

Scope of clinical biological psychiatric treatment Edit

While psychiatrists often combine both psychodynamic ("talk therapy") and biological approaches, this discussion covers mainly the biological aspects.

Since various biological factors can affect mood and behavior, psychiatrists often evaluate these before initiating further treatment. Such factors include hormone levels (especially thyroid), diet (especially alcohol and caffeine), and amount/quality of regular sleep and exercise.

Biological treatment of mental health disorders is not limited to drugs. Non-drug treatments include diet and exercise modifications, and in some severe cases treatments such as transcranial magnetic stimulation or electroconvulsive therapy may be indicated.

Diagnostic processEdit

Correct diagnosis is important for mental health disorders, otherwise the condition could worsen, resulting in a negative impact on both the patient and the healthcare system.[17] Another problem with misdiagnosis is that a treatment for one condition might exacerbate other conditions.[18][19] In other cases apparent mental health disorders could be a side effect of a serious biological problem such as concussion,[20] brain tumor,[21][22] or hormonal abnormality,[21][23][24][25] which could require medical or surgical intervention.

Disorders and biologic treatmentEdit

HistoryEdit

Early 20th centuryEdit

Sigmund Freud was originally focused on the biological causes of mental illness. Freud's professor and mentor, Ernst Wilhelm von Brücke, strongly believed that thought and behavior were determined by purely biological factors. Freud initially accepted this and was convinced that certain drugs (particularly cocaine) functioned as antidepressants. He spent many years trying to "reduce" personality to neurology, a cause he later gave up on before developing his now well-known psychoanalytic theories.[26]

Nearly 100 years ago, Harvey Cushing, the father of neurosurgery, noted that pituitary gland problems often cause mental health disorders. He wondered whether the depression and anxiety he observed in patients with pituitary disorders were caused by hormonal abnormalities, the physical tumor itself, or both.[21]

Mid 20th centuryEdit

An important point in modern history of biological psychiatry was discovery of modern antipsychotic and antidepressant drugs. Chlorpromazine (also known as Thorazine), an antipsychotic, was first synthesized in 1950, and iproniazid, one of the first antidepressants, was first synthesized in 1957. In 1959 imipramine, the first tricyclic antidepressant, was developed. Research into the action of these drugs led to the first modern biological theory of mental health disorders called the catecholamine theory, later broadened to the monoamine theory, which included serotonin. These were popularly called the "chemical imbalance" theory of mental health disorders.

Late 20th centuryEdit

Starting with fluoxetine (marketed as Prozac) in 1988, a series of monoamine-based antidepressant medications belonging to the class of selective serotonin reuptake inhibitors were approved. These were no more effective than earlier antidepressants, but generally had fewer side effects.[27] Most operate on the same principle, which is modulation of monoamines (neurotransmitters) in the neuronal synapse. Some drugs modulate a single neurotransmitter (typically serotonin). Others affect multiple neurotransmitters, called dual action or multiple action drugs. They are no more effective clinically than single action versions. That most antidepressants invoke the same biochemical method of action may explain why they are each similarly effective in rough terms. Recent research indicates antidepressants often work but are somewhat less effective than earlier thought.[28]

Problems with catecholamine/monoamine hypothesesEdit

The monoamine hypothesis was compelling, especially based on apparently successful clinical results with early antidepressant drugs, but even at the time there were discrepant findings. Only a minority of patients given the serotonin-depleting drug reserpine became depressed; in fact reserpine even acted as an antidepressant in many cases. This was inconsistent with the initial monoamine theory which said depression was cased by neurotransmitter deficiency.

Another problem was the time lag between antidepressant biological action and therapeutic benefit. Studies showed the neurotransmitter changes occurred within hours, yet therapeutic benefit took weeks.

To explain these behaviors, more recent modifications of the monoamine theory describe a synaptic adaptation process which takes place over several weeks. Yet this alone does not appear to explain all of the therapeutic effects. [29]

Latest biological hypotheses of mental health disordersEdit

New research indicates different biological mechanisms may underlie some mental health disorders, only indirectly related to neurotransmitters and the monoamine "chemical imbalance theory."[14]

Recent research indicates a biological "final common pathway" may exist which both electroconvulsive therapy[30] and most current antidepressant drugs have in common. These investigations show recurrent depression may be a neurodegenerative disorder, disrupting the structure and function of brain cells, destroying nerve cell connections, even killing certain brain cells, and precipitating a decline in overall cognitive function.[14]

In this new biological psychiatry viewpoint, neuronal plasticity is a key element. Increasing evidence points to various mental health disorders as a neurophysiological problem which inhibits neuronal plasticity.[31][32][33]

This is called the neurogenic hypothesis of depression. It promises to explain pharmacological antidepressant action[13][34], including the time lag from taking the drug to therapeutic onset, why downregulation (not just upregulation) of neurotransmitters can help depression, why stress often precipitates mood disorders,[35] and why selective modulation of different neurotransmitters can help depression. It may also explain the neurobiological mechanism of other non-drug effects on mood, including exercise, diet and metabolism.[36] Lastly, by identifying the neurobiological "final common pathway" into which most antidepressants funnel, it may allow rational design of new medications which target only that pathway. This could yield drugs which have fewer side effects, are more effective and have quicker therapeutic onset.[14]

Criticism Edit

Main article: Biopsychiatry controversy

A vocal minority of patients, activists and mental health care professionals, including some psychiatrists, dispute biological psychiatry as a scientific concept or as having a proper empirical basis, for example arguing that there are no known biomarkers for recognised psychiatric conditions. This position has been represented in scholarly journals such as The Journal of Mind and Behavior [37], The American Journal of Orthopsychiatry [How to reference and link to summary or text], and Ethical Human Psychology and Psychiatry, which publishes material specifically countering "the idea that emotional distress is due to an underlying organic disease." [38] Alternative theories and models instead view mental disorder as non-biomedical and might explain it in terms of, for example, emotional reactions to negative life circumstances or to acute trauma.

The movement, bolstered by groups with similar criticisms of biological psychiatry (such as the Church of Scientology), is often labeled, sometimes derogatorily, as Anti-psychiatry. Others with an anti-psychiatry point of view do not dispute the notion that certain behavior phenotypes have an organic basis, but dispute the labeling of neurological differences as disordered and inferior (see, for example, the autism rights movement and the neurodiversity concept).

Fields such as social psychiatry, clinical psychology and sociology tend to offer non-biomedical accounts of mental distress and disorder and are sometimes critical of biopsychiatry.

ReferencesEdit

  1. On-Line Medical Dictionary. Dept. of Medical Oncology, University of Newcastle upon Tyne.
  2. Webster's Dictionary definition of biological psychiatry. Webster's Dictionary.
  3. Purpose of Society of Biological Psychiatry. Society of Biological Psychiatry.
  4. Infoplease dictionary definition of Biological Psychiatry. Infoplease dictionary.
  5. 5.0 5.1 Harvard/Cambridge psychiatric training syllabus. Dept. of Psychiatry Harvard Medical School.
  6. 6.0 6.1 Vetulani, J. (November 2001). Biological basis of psychiatry.. Psychiatry Pol. PMID 11877886.
  7. Payk, T.R.. Historical treatment of depression. The Delano Report.
  8. Bennett, A.E. (October 1953). Biological Psychiatry. American Journal of Psychiatry 4 (110): 244-52. PMID 13092281.
  9. McEwen, B.S. (September 2005). Stressed or stressed out: what is the difference?. Journal of Psychiatry and Neuroscience. PMID 16151535.
  10. Hendricks H., et al. (2005). Metabolism, mood and cognition in aging: the importance of lifestyle and dietary intervention. Neurobiology Aging. PMID 16290269.
  11. Schildkraut J J, et al. (November 1965). British psychiatry in the 20th century--observations from a psychiatric journal.. The American Journal of Psychiatry. PMID 5319766.
  12. Psychobiology Of Major Affective Disorders. Massachusetts General Mental Health Center.
  13. 13.0 13.1 Duman, R.S. (2004). Depression: a case of neuronal life and death?. Biological Psychiatry. PMID 15271581.
  14. 14.0 14.1 14.2 14.3 Depression: Beyond Serotonin. Psychology Today Magazine.
  15. Johnson, M.R. (2006). A Functional Magnetic Resonance Imaging Study of Working Memory Abnormalities in Schizophrenia.. Biological Psychiatry. PMID 16503328.
  16. Whalley H.C., et al. (2006). Functional Imaging as a Predictor of Schizophrenia.. Biological Psychiatry. PMID 16460690.
  17. Pini S., et al. (April-June 1999). Detection and management of mental distress and psychiatric disorders in primary care settings.. Epidemiologia e psichiatria sociale. PMID 10540512.
  18. Goldberg JF (May 2003). When do antidepressants worsen the course of bipolar disorder?. Journal of Psychiatric Practice. PMID 15985931.
  19. Practice Guideline for the Treatment of Patients with Bipolar Disorder. American Psychiatric Association. URL accessed on April 20, 2006.
  20. Ryan LM, et al. (November 2003). Post concussion syndrome. International Review of Psychiatry. PMID 15276952.
  21. 21.0 21.1 21.2 Weitzner, M. (1998). Neuropsychiatry and pituitary disease: an overview.. Psychotherapy and Psychosomatics. PMID 9667059.
  22. Sobrinho LG (1998). Emotional aspects of hyperprolactinemia.. Journal of Psychiatric Practice. PMID 15985931.
  23. Sonino N (1998). Psychosomatic aspects of Cushing's disease.. Psychotherapy and Psychosomatics. PMID 9667061.
  24. Larisch R, et al. (September 2004). Depression and anxiety in different thyroid function states.. Hormone and Metabolic Research. PMID 15486818.
  25. Fink G, et al. (November 1999). Androgen actions on central serotonin neurotransmission: relevance for mood, mental state and memory.. Behavioural Brain Research. PMID 10553690.
  26. Boeree, George C.. Sigmund Freud. Shippensburg University.
  27. Hotopf M., et al. (1996). Are SSRIs a cost-effective alternative to tricyclics?. British Journal of Psychiatry. PMID 8730935.
  28. Ban, T.A. (2001). Pharmacotherapy of depression: a historical analysis.. Journal of Neural Transmission. PMID 11478422.
  29. Korn, Martin L.. Serotonin and Norepinephrine Antidepressant Effects. Medscape.
  30. Ongür D., et al. (2004). A role for glia in the action of electroconvulsive therapy.. Harvard Review of Psychiatry. PMID 15590574.
  31. Duman C.H., et al. (2005). Neurobiology and treatment of anxiety: signal transduction and neural plasticity.. Handb Exp Pharmacol. PMID 16594263.
  32. Warner-Schmidt J.L., et al. (2006). Hippocampal neurogenesis: opposing effects of stress and antidepressant treatment.. Hippocampus. PMID 16425236.
  33. Perera, T.D. (2000). Neurogenesis and depression.. Journal of Psychiatric Practice. PMID 15990493.
  34. Kodama M., et al. (2004). Chronic olanzapine or fluoxetine administration increases cell proliferation in hippocampus and prefrontal cortex of adult rat.. Biological Psychiatry. PMID 15476686.
  35. Duman, R.S. (2004). Role of neurotrophic factors in the etiology and treatment of mood disorders.. Neuromolecular Medicine. PMID 15001809.
  36. Newton, S.S. (2005). Regulation of neurogenesis and angiogenesis in depression.. Curr Neurovasc Res. PMID 16181076.
  37. http://www.umaine.edu/JMB/archives/volume11/11_3-4_1990summerautumn.html
  38. Breggin, Peter R. Ethical Human Psychology and Psychiatry. Springer Publishing.

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