Biological psychiatry
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'''Biological psychiatry''', or '''biopsychiatry''' is an approach to [[psychiatry]] that aims to understand [[mental disorder]] in terms of the [[biology|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]].<ref name="Cancerweb">
{{cite web
| url = http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=biological+psychiatry
| title = On-Line Medical Dictionary
| publisher = Dept. of Medical Oncology, University of Newcastle upon Tyne
}}</ref><ref name="Webster">
{{cite web
| url = http://www.websters-online-dictionary.org/Bi/Biological_Psychiatry.html
| title = Webster's Dictionary definition of biological psychiatry
| publisher = Webster's Dictionary
}}</ref><ref name="Sobp">
{{cite web
| url = http://www.sobp.org/purpose.asp
| title = Purpose of Society of Biological Psychiatry
| publisher = Society of Biological Psychiatry
}}</ref><ref name="Infoplease">
{{cite web
| url = http://www.infoplease.com/ipd/A0342210.html
| title = Infoplease dictionary definition of Biological Psychiatry
| publisher = Infoplease dictionary
}}</ref>
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 psychologist]]s, [[psychotherapist]]s, [[occupational therapist]]s or other mental health workers who are more specialised and trained in non-drug approaches.<ref name="Harvard">
{{cite web
| url = http://medapps.med.harvard.edu/psych/education-residency.htm
| title = Harvard/Cambridge psychiatric training syllabus
| publisher = Dept. of Psychiatry Harvard Medical School
}}</ref><ref name="Vetulani">
{{cite journal
| author = Vetulani, J.
| year = 2001
| month = November
| title = Biological basis of psychiatry
| journal = Psychiatry Pol
| pmid = 11877886
}}</ref>
The history of the field extends back to the ancient Greek physician [[Hippocrates]],<ref name ="Delano">
{{cite web
| url = http://www.delano.com/ReferenceArticles/Depression-Historical.html
| title = Historical treatment of depression
| author = Payk, T.R.
| publisher = The Delano Report
}}</ref> 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.<ref name="Bennett">
{{cite journal
| author = Bennett, A.E.
| year = 1953
| month = October
| title = Biological Psychiatry
| journal = American Journal of Psychiatry
| volume = 4
| issue = 110
| pages = 244–52
| pmid = 13092281
}}</ref> 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 definition==
{{see also|Biological psychology}}
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 and Bipolar Affective (Mood) Disorders, Schizophrenia and Organic Mental Disorders such as Alzheimers Disease. This knowledge has been gained using imaging techniques, psychopharmacology, neuroimmunochemistry and 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,<ref name="McEwen">
{{cite journal
| author = McEwen, B.S.
| year = 2005
| month = September
| title = Stressed or stressed out: what is the difference?
| journal = Journal of Psychiatry and Neuroscience
| pmid = 16151535
}}</ref> all of which can cause measurable biochemical changes.<ref name="Hendricks">
{{cite journal
| author = Hendricks H., ''et al.''
| year = 2005
| title = Metabolism, mood and cognition in aging: the importance of lifestyle and dietary intervention
| journal = Neurobiology Aging
| pmid = 16290269
| doi = 10.1016/j.neurobiolaging.2005.10.005
| volume = 26
| pages = 1
}}</ref> The biological psychiatrist views all of these as possible [[etiology|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.<ref name="Harvard">
{{cite web
| url = http://medapps.med.harvard.edu/psych/education-residency.htm
| title = Harvard/Cambridge psychiatric training syllabus
| publisher = Dept. of Psychiatry Harvard Medical School
}}</ref> Accordingly, psychiatrists are usually comfortable with a dual approach: ''"psychotherapeutic methods...are as indispensable as psychopharmacotherapy in a modern psychiatric clinic"'',<ref name="Vetulani">
{{cite journal
| author = Vetulani, J.
| year = 2001
| month = November
| title = Biological basis of psychiatry
| journal = Psychiatry Pol
| pmid = 11877886
}}</ref>
==Basis for biological psychiatry==
[[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.<ref name ="Schildkraut">
{{cite journal
| author = Schildkraut J J, ''et al.''
| year = 1965
| month = November
| title = British psychiatry in the 20th century--observations from a psychiatric journal
| journal = The American Journal of Psychiatry
| pmid = 5319766
}}</ref> 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.<ref name="MGMHC">
{{cite web
| url = http://www.massmentalhealthcenter.org/research/programs-programpages-majoraffective.htm
| title = Psychobiology Of Major Affective Disorders
| publisher = Massachusetts General Mental Health Center
}}</ref>
Although the "chemical imbalance" hypothesis has been significantly revised since 1965, many newer medications (such as [[fluoxetine]] and other [[SSRI]]s) 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.<ref name="DumanRS">
{{cite journal
| author = Duman, R.S.
| year = 2004
| title = Depression: a case of neuronal life and death?
| journal = Biological Psychiatry
| pmid = 15271581
| doi = 10.1016/j.biopsych.2004.02.033
| volume = 56
| pages = 140
}}</ref><ref name ="PsyToday">
{{cite web
| url = http://www.psychologytoday.com/articles/pto-19990301-000031.html
| title = Depression: Beyond Serotonin
| publisher = Psychology Today Magazine
}}</ref>
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.<ref name="Johnson">
{{cite journal
| author = Johnson, M.R.
| year = 2006
| title = A Functional Magnetic Resonance Imaging Study of Working Memory Abnormalities in Schizophrenia
| journal = Biological Psychiatry
| pmid = 16503328
| doi = 10.1016/j.biopsych.2005.11.012
| volume = 60
| pages = 11
}}</ref><ref name="Whalley">
{{cite journal
| author = Whalley H.C., ''et al.''
| year = 2006
| title = Functional Imaging as a Predictor of Schizophrenia
| journal = Biological Psychiatry
| pmid = 16460690
| doi = 10.1016/j.biopsych.2005.11.013
| volume = 60
| pages = 454
}}</ref> 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 ==
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 process==
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.<ref name="PiniS">
{{cite journal
| author = Pini S., ''et al.''
| year = 1999
| month = April-June
| title = Detection and management of mental distress and psychiatric disorders in primary care settings
| journal = Epidemiologia e psichiatria sociale
| pmid = 10540512
}}</ref> Another problem with misdiagnosis is that a treatment for one condition might exacerbate other conditions.<ref name="GoldbergJF">
{{cite journal
| author = Goldberg JF
| year = 2003
| month = May
| title = When do antidepressants worsen the course of bipolar disorder?
| journal = Journal of Psychiatric Practice
| pmid = 15985931
| doi = 10.1097/00131746-200305000-00002
| volume = 9
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}}</ref><ref name="AMAGuideline">
{{cite web
| url = http://www.psych.org/psych_pract/treatg/pg/bipolar_revisebook_index.cfm
| title = Practice Guideline for the Treatment of Patients with Bipolar Disorder
| publisher = American Psychiatric Association
| accessmonthday = April 20
| accessyear = 2006
}}</ref> In other cases apparent mental health disorders could be a side effect of a serious biological problem such as concussion,<ref name="RyanLM">
{{cite journal
| author = Ryan LM, ''et al.''
| year = 2003
| month = November
| title = Post concussion syndrome
| journal = International Review of Psychiatry
| pmid = 15276952
| doi = 10.1080/09540260310001606692
| volume = 15
| pages = 310
}}</ref> brain tumor,<ref name="Weitzner">
{{cite journal
| author = Weitzner, M.
| year = 1998
| title = Neuropsychiatry and pituitary disease: an overview
| journal = Psychotherapy and Psychosomatics
| pmid = 9667059
| doi = 10.1159/000012272
| volume = 67
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}}</ref><ref name="SobrinhoLG">
{{cite journal
| author = Sobrinho LG
| year = 1998
| title = Emotional aspects of hyperprolactinemia
| journal = Journal of Psychiatric Practice
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}}</ref> or hormonal abnormality,<ref name="Weitzner" /><ref name="SoninoN">
{{cite journal
| author = Sonino N
| year = 1998
| title = Psychosomatic aspects of Cushing's disease
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}}</ref><ref name="LarischR">
{{cite journal
| author = Larisch R, ''et al.''
| year = 2004
| month = September
| title = Depression and anxiety in different thyroid function states
| journal = Hormone and Metabolic Research
| pmid = 15486818
| doi = 10.1055/s-2004-825925
| volume = 36
| pages = 650
}}</ref><ref name="FinkG">
{{cite journal
| author = Fink G, ''et al.''
| year = 1999
| month = November
| title = Androgen actions on central serotonin neurotransmission: relevance for mood, mental state and memory
| journal = Behavioural Brain Research
| pmid = 10553690
| doi = 10.1016/S0166-4328(99)00082-0
| volume = 105
| pages = 53
}}</ref> which could require medical or surgical intervention.
==Disorders and biologic treatment==
*[[Seasonal affective disorder]]: [[light therapy|Light box]], [[SSRI]]s
*[[Depression (mood)|Clinical depression]]: SSRIs[(Prozac)], SNRIs [[Effexor]], atypical antidepressants: ([[Wellbutrin]], [[Remeron]]), [[electroconvulsive therapy]], [[transcranial magnetic stimulation]]
*[[Bipolar disorder]]: [[Lithium Carbonate]], [[valproic acid]], [[Lamictal]], [[Carbamazepine]]
*[[Schizophrenia]]: Includes [[haloperidol]], [[clozapine]], [[olanzapine]], [[risperidone]], [[Quetiapine]], [[Ziprasidone]] and other [[Antipsychotic]]s
*[[Generalized anxiety disorder]]: SSRIs, [[benzodiazepine]]s, [[buspirone]]
*[[Obsessive-compulsive disorder]]: [[Clomipramine]], SSRIs [[citalopram]]
==History==
====Early 20th century====
[[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 [[psychoanalysis|psychoanalytic]] theories.<ref name="Boeree">
{{cite web
| url = http://www.ship.edu/~cgboeree/freud.html
| title = Sigmund Freud
| author = Boeree, George C.
| publisher = Shippensburg University
}}</ref>
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.<ref name="Weitzner" />
====Mid 20th century====
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 century====
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.<ref name="Hotopf">
{{cite journal
| author = Hotopf M., ''et al.''
| year = 1996
| title = Are SSRIs a cost-effective alternative to tricyclics?
| journal = [[British Journal of Psychiatry]]
| pmid = 8730935
}}</ref> 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.<ref name="Ban">
{{cite journal
| author = Ban, T.A.
| year = 2001
| title = Pharmacotherapy of depression: a historical analysis
| journal = Journal of Neural Transmission
| pmid = 11478422
| doi = 10.1007/s007020170047
| volume = 108
| pages = 707
}}</ref>
====Problems with catecholamine/monoamine hypotheses====
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 caused 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.<ref name="Korn">
{{cite web
| url = http://www.medscape.com/viewarticle/436395
| title = Serotonin and Norepinephrine Antidepressant Effects
| author = Korn, Martin L.
| publisher = Medscape
}}</ref>
==Latest biological hypotheses of mental health disorders==
New research indicates different biological mechanisms may underlie some mental health disorders, only indirectly related to neurotransmitters and the monoamine "chemical imbalance theory."<ref name ="PsyToday" />
Recent research indicates a biological "final common pathway" may exist which both [[electroconvulsive therapy]]<ref name="Ongur">
{{cite journal
| author = Ongür D., ''et al.''
| year = 2004
| title = A role for glia in the action of electroconvulsive therapy
| journal = Harvard Review of Psychiatry
| pmid = 15590574
}}</ref> 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.<ref name="PsyToday" />
In this new biological psychiatry viewpoint, [[Plasticity (brain)|neuronal plasticity]] is a key element. Increasing evidence points to various mental health disorders as a neurophysiological problem which inhibits neuronal plasticity.<ref name="DumanCH">
{{cite journal
| author = Duman C.H., ''et al.''
| year = 2005
| title = Neurobiology and treatment of anxiety: signal transduction and neural plasticity
| journal = Handb Exp Pharmacol
| pmid = 16594263
| doi = 10.1007/3-540-28082-0_11
| volume = 169
| pages = 305
}}</ref><ref name="Warner-Schmidt">
{{cite journal
| author = Warner-Schmidt J.L., ''et al.''
| year = 2006
| title = Hippocampal neurogenesis: opposing effects of stress and antidepressant treatment
| journal = Hippocampus
| pmid = 16425236
| doi = 10.1002/hipo.20156
| volume = 16
| pages = 239
}}</ref><ref name="Perera">
{{cite journal
| author = Perera, T.D.
| year = 2000
| title = Neurogenesis and depression
| journal = Journal of Psychiatric Practice
| pmid = 15990493
| doi = 10.1097/00131746-200011000-00003
| volume = 6
| pages = 322–333
}}</ref>
This is called the neurogenic hypothesis of depression. It promises to explain pharmacological antidepressant action,<ref name="DumanRS">
{{cite journal
| author = Duman, R.S.
| year = 2004
| title = Depression: a case of neuronal life and death?
| journal = Biological Psychiatry
| pmid = 15271581
| doi = 10.1016/j.biopsych.2004.02.033
| volume = 56
| pages = 140
}}</ref><ref name="Kodama">
{{cite journal
| author = Kodama M., ''et al.''
| year = 2004
| title = Chronic olanzapine or fluoxetine administration increases cell proliferation in hippocampus and prefrontal cortex of adult rat
| journal = Biological Psychiatry
| pmid = 15476686
| doi = 10.1016/j.biopsych.2004.07.008
| volume = 56
| pages = 570
}}</ref> 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,<ref name="DumanRS2">
{{cite journal
| author = Duman, R.S.
| year = 2004
| title = Role of neurotrophic factors in the etiology and treatment of mood disorders
| journal = Neuromolecular Medicine
| pmid = 15001809
| doi = 10.1385/NMM:5:1:011
| volume = 5
| pages = 011
}}</ref> 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.<ref name="Newton">
{{cite journal
| author = Newton, S.S.
| year = 2005
| title = Regulation of neurogenesis and angiogenesis in depression
| journal = Curr Neurovasc Res
| pmid = 16181076
}}</ref> 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.<ref name="PsyToday" />
== Criticism ==
{{main|Biopsychiatry controversy}}
A vocal minority of patients, [[activists]], and psychiatrists dispute biological psychiatry as a scientific concept or as having a proper empirical basis, for example arguing that there are no known [[Biomarker (medicine)|biomarkers]] for recognised psychiatric conditions. This position has been represented in niche [[academic journals]] such as ''The Journal of Mind and Behavior''<ref>[http://www.umaine.edu/JMB/archives/volume11/11_3-4_1990summerautumn.html Journal of Mind and Behavior<!-- Bot generated title -->]</ref> and ''Ethical Human Psychology and Psychiatry'', which publishes material specifically countering "the idea that emotional distress is due to an underlying organic disease."<ref name="EHPP">
{{cite web
| url = http://www.springerpub.com/journal.aspx?jid=1559-4343
| title = ''Ethical Human Psychology and Psychiatry''
| author = Breggin, Peter R
| publisher = Springer Publishing}}</ref> 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. <ref> {{cite book
| last = Arieti
| first = Silvano
| title = Interpretation of Schizophrenia
| publisher = Aronson
| date = 1994}}</ref>
Fields such as [[social psychiatry]], [[clinical psychology]], and [[sociology]] may offer non-biomedical accounts of mental distress and disorder for certain aliments and are sometimes critical of biopsychiatry. Social critics believe biopsychiatry fails to satisfy the [[scientific method]] because they believe there is no [[Falsifiability|testable]] biological evidence of mental disorders. Thus, these critics view biological psychiatry as a [[pseudoscience]] attempting to portray psychiatry as a biological science.
[[R.D. Laing]] argued that attributing mental disorders to biophysical factors was often flawed due to the diagnostic procedure. The "complaint" is often made by a family member, not the patient, the "history" provided by someone other than patient, and the "examination" consists of observing strange, incomprehensible behavior. Ancillary tests (EEG, PET) are often done after diagnosis, when treatment has begun, which makes the tests [[Blind experiment| non-blind ]] and incurs possible [[Confirmation bias| confirmation bias]].
==References==
<references/>
==See also==
* [[Biological psychology]]
* [[Psychiatry]]
==External links==
*[http://www.biopsychology.com/news/ Biological Psychology Links]
* [http://www.nytimes.com/2006/04/20/health/20psych.html?ex=1146196800&en=f315a6be44ef7a9b&ei=5070&emc=eta1 NYTimes.com] - 'Study Finds a Link of Drug Makers to Psychiatrists', Benedict Carey, ''[[New York Times]]'' ([[April 20]], [[2006]])
* [http://www.psychologytoday.com/articles/pto-19990301-000031.html PsychologyToday.com] - 'Depression: Beyond Serotonin: Much more than a chemical imbalance, depression is a disorder of mind, brain, and body', Hara Estroff Marano, ''[[Psychology Today]]'' (March, 1999)
{{Psychiatry}}
[[it:Psichiatria biologica]]
[[ru:Биологическая психиатрия]]
[[fi:Biologinen psykiatria]]
[[sv:Biologisk psykiatri]]
[[pt:Psiquiatria biológica]]
[[Category:Psychiatry]]