Bipolar disorder causes: Difference between revisions

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==Overview==
==Overview==
A number of factors can be involved in bipolar disorder including genetic, biochemical, psychodynamic, and environmental factors. paternal age increase the risk of bipolar disorder in one’s offspring that could be due to increased genetic mutations during spermatogenesis. Stressful life events may be associated with onset of bipolar disorder and a more severe course of illness.The disorder runs in families. More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar major depression. Bipolar disorder is associated with immune system dysregulation.
A number of factors can be involved in bipolar disorder including [[genetic]], [[biochemical]], [[Psychodynamics|psychodynamic]], and [[Environmental factor|environmental]] factors. paternal age increase the risk of bipolar disorder in one’s offspring that could be due to increased [[genetic]] [[mutations]] during [[spermatogenesis]]. Stressful life events may be associated with onset of bipolar disorder and a more severe course of illness.The disorder runs in families. More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar [[Major depressive disorder|major depressio]]<nowiki/>n. Bipolar disorder is associated with [[immune system]] dysregulation.


==Causes==
==Causes==


===Psychosocial factors===
===[[Psychosocial]] factors===


*paternal age increase the risk of bipolar disorder in one’s offspring that could be due to increased genetic mutations during spermatogenesis.  As an example, a national registry study found that the risk of bipolar disorder in offspring of fathers 45 years and older was six times greater.<ref name="pmid24499422">{{cite journal| author=Chudal R, Gissler M, Sucksdorff D, Lehti V, Suominen A, Hinkka-Yli-Salomäki S | display-authors=etal| title=Parental age and the risk of bipolar disorders. | journal=Bipolar Disord | year= 2014 | volume= 16 | issue= 6 | pages= 624-32 | pmid=24499422 | doi=10.1111/bdi.12182 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24499422  }}</ref>
*[[Paternal age effect|Paternal age]] increase the risk of bipolar disorder in [[offspring]] due to increased [[genetic mutations]] during [[spermatogenesis]].  As an example, a national registry study found that the risk of bipolar disorder in offspring of fathers 45 years and older was six times greater.<ref name="pmid24499422">{{cite journal| author=Chudal R, Gissler M, Sucksdorff D, Lehti V, Suominen A, Hinkka-Yli-Salomäki S | display-authors=etal| title=Parental age and the risk of bipolar disorders. | journal=Bipolar Disord | year= 2014 | volume= 16 | issue= 6 | pages= 624-32 | pmid=24499422 | doi=10.1111/bdi.12182 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24499422  }}</ref>


*Stressful life events may be associated with onset of bipolar disorder and a more severe course of illness. It is more common among individuals who reported a history of childhood physical abuse.<ref name="pmid22806701">{{cite journal| author=Sugaya L, Hasin DS, Olfson M, Lin KH, Grant BF, Blanco C| title=Child physical abuse and adult mental health: a national study. | journal=J Trauma Stress | year= 2012 | volume= 25 | issue= 4 | pages= 384-92 | pmid=22806701 | doi=10.1002/jts.21719 | pmc=3805363 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22806701  }}</ref><ref name="pmid25597794">{{cite journal| author=Janiri D, Sani G, Danese E, Simonetti A, Ambrosi E, Angeletti G | display-authors=etal| title=Childhood traumatic experiences of patients with bipolar disorder type I and type II. | journal=J Affect Disord | year= 2015 | volume= 175 | issue=  | pages= 92-7 | pmid=25597794 | doi=10.1016/j.jad.2014.12.055 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25597794  }}</ref>
*[[Stress]]  and  a history of childhood [[physical abuse]] associated with onset of bipolar disorder and a more severe course of [[illness]].<ref name="pmid22806701">{{cite journal| author=Sugaya L, Hasin DS, Olfson M, Lin KH, Grant BF, Blanco C| title=Child physical abuse and adult mental health: a national study. | journal=J Trauma Stress | year= 2012 | volume= 25 | issue= 4 | pages= 384-92 | pmid=22806701 | doi=10.1002/jts.21719 | pmc=3805363 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22806701  }}</ref><ref name="pmid25597794">{{cite journal| author=Janiri D, Sani G, Danese E, Simonetti A, Ambrosi E, Angeletti G | display-authors=etal| title=Childhood traumatic experiences of patients with bipolar disorder type I and type II. | journal=J Affect Disord | year= 2015 | volume= 175 | issue=  | pages= 92-7 | pmid=25597794 | doi=10.1016/j.jad.2014.12.055 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25597794  }}</ref>


<br />
<br />
===Heritability or inheritance===
===[[Heritability]] or [[inheritance]]===


*The disorder runs in families.<ref>
*More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar [[Major depressive disorder|major depression.<ref> {{Citation  | last = McGuffin  | first = P  | last2 = Rijsdijk  | first2 = F  | last3 = Andrew  | first3 = M  | last4 = Sham  | first4 = P  | last5 = Katz  | first5 = R  | last6 = Cardno  | first6 = A  | title = The Heritability of Bipolar Affective Disorder and the Genetic Relationship to Unipolar Depression  | journal = Archives of General Psychiatry  | volume = 60  | issue = 5  | pages = 497-502  | year = 2003  | url = http://archpsyc.ama-assn.org/cgi/content/abstract/60/5/497 }} </ref>]][./Bipolar_disorder_causes#cite_note-4 <span class="mw-reflink-text"><nowiki>[4]</nowiki></span>]
{{Citation
*[[Genes]] that are involved in bipolar disorder have been studied, but no single [[gene]] has been identified.<ref name="pmid23663951">{{cite journal| author=Craddock N, Sklar P| title=Genetics of bipolar disorder. | journal=Lancet | year= 2013 | volume= 381 | issue= 9878 | pages= 1654-62 | pmid=23663951 | doi=10.1016/S0140-6736(13)60855-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23663951  }}</ref> it may involve many [[genes]] with small effects.<ref name="pmid16603476">{{cite journal| author=Finn CT, Smoller JW| title=Genetic counseling in psychiatry. | journal=Harv Rev Psychiatry | year= 2006 | volume= 14 | issue= 2 | pages= 109-21 | pmid=16603476 | doi=10.1080/10673220600655723 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16603476  }}</ref>
   | last = McGuffin
*Studies found several [[genetic]] variants are associated with bipolar disorder. One possible [[locus]] is [[CACNA1C]], which codes for a [[calcium channel]] that is involved in channel gating.<ref name="pmid236639512">Craddock N, Sklar P (2013) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23663951 Genetics of bipolar disorder.] ''Lancet'' 381 (9878):1654-62. [http://dx.doi.org/10.1016/S0140-6736(13)60855-7 DOI:10.1016/S0140-6736(13)60855-7] PMID: [https://pubmed.gov/23663951 23663951]</ref><ref name="pmid18711365">{{cite journal| author=Ferreira MA, O'Donovan MC, Meng YA, Jones IR, Ruderfer DM, Jones L | display-authors=etal| title=Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. | journal=Nat Genet | year= 2008 | volume= 40 | issue= 9 | pages= 1056-8 | pmid=18711365 | doi=10.1038/ng.209 | pmc=2703780 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18711365  }}</ref> other [[genes]] are ''[[ANK3]],'' and ''[[CLOCK]]'' [[genes]] especially bipolar type I disorder.<ref name="pmid18317468">{{cite journal| author=Sklar P, Smoller JW, Fan J, Ferreira MA, Perlis RH, Chambert K | display-authors=etal| title=Whole-genome association study of bipolar disorder. | journal=Mol Psychiatry | year= 2008 | volume= 13 | issue= 6 | pages= 558-69 | pmid=18317468 | doi=10.1038/sj.mp.4002151 | pmc=3777816 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18317468  }}</ref><ref name="pmid17379666">{{cite journal| author=Roybal K, Theobold D, Graham A, DiNieri JA, Russo SJ, Krishnan V | display-authors=etal| title=Mania-like behavior induced by disruption of CLOCK. | journal=Proc Natl Acad Sci U S A | year= 2007 | volume= 104 | issue= 15 | pages= 6406-11 | pmid=17379666 | doi=10.1073/pnas.0609625104 | pmc=1851061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17379666  }}</ref>
   | first = P
*A [[meta-analysis]] suggests that other [[biologic]] pathways are [[cardiac]] [[Adrenergic|β-adrenergic]] [[Cell signaling|signaling]], [[cardiac hypertrophy]] signaling, [[Corticotropin-releasing hormone|corticotropin releasing hormone]] [[Cell signaling|signaling]], [[endothelin 1]] [[Cell signaling|signaling]], [[glutamate]] [[Cell signaling|signaling]], and [[phospholipase C]] [[Cell signaling|signaling]].<ref name="pmid24718920">{{cite journal| author=Nurnberger JI, Koller DL, Jung J, Edenberg HJ, Foroud T, Guella I | display-authors=etal| title=Identification of pathways for bipolar disorder: a meta-analysis. | journal=JAMA Psychiatry | year= 2014 | volume= 71 | issue= 6 | pages= 657-64 | pmid=24718920 | doi=10.1001/jamapsychiatry.2014.176 | pmc=4523227 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24718920  }}</ref>
   | last2 = Rijsdijk
*In addition, a meta-analysis studies identified three [[Single nucleotide polymorphism|single-nucleotide polymorphisms]] on [[Chromosome|chromosomes]] 3 and 10. One of them is located on a brain expressed [[gene]] that encodes [[Calcium channels|calcium channel subunits]]; [[calcium signaling]] regulates [[neuronal]] [[growth]] and [[development]].<ref name="pmid23453886">{{cite journal| author=Serretti A, Fabbri C| title=Shared genetics among major psychiatric disorders. | journal=Lancet | year= 2013 | volume= 381 | issue= 9875 | pages= 1339-1341 | pmid=23453886 | doi=10.1016/S0140-6736(13)60223-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23453886  }}</ref><ref name="pmid23453885">{{cite journal| author=Cross-Disorder Group of the Psychiatric Genomics Consortium| title=Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. | journal=Lancet | year= 2013 | volume= 381 | issue= 9875 | pages= 1371-1379 | pmid=23453885 | doi=10.1016/S0140-6736(12)62129-1 | pmc=3714010 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23453885  }}</ref>
   | first2 = F
   | last3 = Andrew
   | first3 = M
   | last4 = Sham
   | first4 = P
   | last5 = Katz
   | first5 = R
   | last6 = Cardno
   | first6 = A
   | title = The Heritability of Bipolar Affective Disorder and the Genetic Relationship to Unipolar Depression
   | journal = Archives of General Psychiatry
   | volume = 60
   | issue = 5
   | pages = 497-502
   | year = 2003
   | url = http://archpsyc.ama-assn.org/cgi/content/abstract/60/5/497
}}
</ref> More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar major depression.
*Genes that are involved in bipolar disorder have been studied, but no single gene has been identified.<ref name="pmid23663951">{{cite journal| author=Craddock N, Sklar P| title=Genetics of bipolar disorder. | journal=Lancet | year= 2013 | volume= 381 | issue= 9878 | pages= 1654-62 | pmid=23663951 | doi=10.1016/S0140-6736(13)60855-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23663951  }}</ref> it may involve many genes with small effects.<ref name="pmid16603476">{{cite journal| author=Finn CT, Smoller JW| title=Genetic counseling in psychiatry. | journal=Harv Rev Psychiatry | year= 2006 | volume= 14 | issue= 2 | pages= 109-21 | pmid=16603476 | doi=10.1080/10673220600655723 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16603476  }}</ref>
*Studies have found that several genetic variants are associated with bipolar disorder. One possible locus is CACNA1C, which codes for a calcium channel that is involved in channel gating.<ref name="pmid236639512">Craddock N, Sklar P (2013) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23663951 Genetics of bipolar disorder.] ''Lancet'' 381 (9878):1654-62. [http://dx.doi.org/10.1016/S0140-6736(13)60855-7 DOI:10.1016/S0140-6736(13)60855-7] PMID: [https://pubmed.gov/23663951 23663951]</ref><ref name="pmid18711365">{{cite journal| author=Ferreira MA, O'Donovan MC, Meng YA, Jones IR, Ruderfer DM, Jones L | display-authors=etal| title=Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. | journal=Nat Genet | year= 2008 | volume= 40 | issue= 9 | pages= 1056-8 | pmid=18711365 | doi=10.1038/ng.209 | pmc=2703780 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18711365  }}</ref> other genes that have been found to be involved as well ''ANK3,'' and ''CLOCK'' genes especially bipolar type I (BPI) disorder.<ref name="pmid18317468">{{cite journal| author=Sklar P, Smoller JW, Fan J, Ferreira MA, Perlis RH, Chambert K | display-authors=etal| title=Whole-genome association study of bipolar disorder. | journal=Mol Psychiatry | year= 2008 | volume= 13 | issue= 6 | pages= 558-69 | pmid=18317468 | doi=10.1038/sj.mp.4002151 | pmc=3777816 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18317468  }}</ref><ref name="pmid17379666">{{cite journal| author=Roybal K, Theobold D, Graham A, DiNieri JA, Russo SJ, Krishnan V | display-authors=etal| title=Mania-like behavior induced by disruption of CLOCK. | journal=Proc Natl Acad Sci U S A | year= 2007 | volume= 104 | issue= 15 | pages= 6406-11 | pmid=17379666 | doi=10.1073/pnas.0609625104 | pmc=1851061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17379666  }}</ref>
*A meta-analysis of genetic studies of bipolar disorder suggests that other biologic pathways are cardiac β-adrenergic signaling, cardiac hypertrophy signaling, corticotropin releasing hormone signaling, endothelin 1 signaling, glutamate signaling, and phospholipase C signaling.<ref name="pmid24718920">{{cite journal| author=Nurnberger JI, Koller DL, Jung J, Edenberg HJ, Foroud T, Guella I | display-authors=etal| title=Identification of pathways for bipolar disorder: a meta-analysis. | journal=JAMA Psychiatry | year= 2014 | volume= 71 | issue= 6 | pages= 657-64 | pmid=24718920 | doi=10.1001/jamapsychiatry.2014.176 | pmc=4523227 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24718920  }}</ref>
*In addition, a meta-analysis of genome-wide association studies identified three single-nucleotide polymorphisms on chromosomes 3 and 10. One of the polymorphisms was located on a brain expressed gene that encodes calcium channel subunits; calcium signaling regulates neuronal growth and development.<ref name="pmid23453886">{{cite journal| author=Serretti A, Fabbri C| title=Shared genetics among major psychiatric disorders. | journal=Lancet | year= 2013 | volume= 381 | issue= 9875 | pages= 1339-1341 | pmid=23453886 | doi=10.1016/S0140-6736(13)60223-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23453886  }}</ref><ref name="pmid23453885">{{cite journal| author=Cross-Disorder Group of the Psychiatric Genomics Consortium| title=Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. | journal=Lancet | year= 2013 | volume= 381 | issue= 9875 | pages= 1371-1379 | pmid=23453885 | doi=10.1016/S0140-6736(12)62129-1 | pmc=3714010 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23453885  }}</ref>


===Inflammation===
===[[Inflammation]]===


*Bipolar disorder is associated with immune system dysregulation. Separate meta-analyses have each found that cytokines (eg, interleukin-4 and tumor necrosis factor-alpha) and cytokine receptors are elevated in patients with bipolar disorder<ref name="pmid23419545">{{cite journal| author=Modabbernia A, Taslimi S, Brietzke E, Ashrafi M| title=Cytokine alterations in bipolar disorder: a meta-analysis of 30 studies. | journal=Biol Psychiatry | year= 2013 | volume= 74 | issue= 1 | pages= 15-25 | pmid=23419545 | doi=10.1016/j.biopsych.2013.01.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23419545  }}</ref>
*Bipolar disorder is associated with [[immune system]] dysregulation. [[Cytokines]] (eg, [[Interleukin 4|interleukin-4]] and [[tumor necrosis factor-alpha]]) and [[Cytokine receptor|cytokine receptors]] are elevated in patients with bipolar disorder<ref name="pmid23419545">{{cite journal| author=Modabbernia A, Taslimi S, Brietzke E, Ashrafi M| title=Cytokine alterations in bipolar disorder: a meta-analysis of 30 studies. | journal=Biol Psychiatry | year= 2013 | volume= 74 | issue= 1 | pages= 15-25 | pmid=23419545 | doi=10.1016/j.biopsych.2013.01.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23419545  }}</ref>
*A meta-analysis of 11 studies found that levels of C reactive protein were higher in patients than controls, and the difference was small to moderate.<ref name="pmid25742201">{{cite journal| author=Dargél AA, Godin O, Kapczinski F, Kupfer DJ, Leboyer M| title=C-reactive protein alterations in bipolar disorder: a meta-analysis. | journal=J Clin Psychiatry | year= 2015 | volume= 76 | issue= 2 | pages= 142-50 | pmid=25742201 | doi=10.4088/JCP.14r09007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25742201  }}</ref>
*A meta-analysis found that levels of [[C-reactive protein|C reactive protein]] were higher in patients than controls, and the difference was small to moderate.<ref name="pmid25742201">{{cite journal| author=Dargél AA, Godin O, Kapczinski F, Kupfer DJ, Leboyer M| title=C-reactive protein alterations in bipolar disorder: a meta-analysis. | journal=J Clin Psychiatry | year= 2015 | volume= 76 | issue= 2 | pages= 142-50 | pmid=25742201 | doi=10.4088/JCP.14r09007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25742201  }}</ref>


=== Biochemical factors ===
===[[Biochemical]] factors===


* A number of neurotransmitters have been linked to this disorder.
*A number of [[neurotransmitters]] have been linked to this [[disorder]].
* Catecholamine hypothesis, state that increase in epinephrine and norepinephrine causes mania and a decrease in epinephrine and norepinephrine causes depression.
*[[Catecholamine]] [[hypothesis]], state that increase in [[epinephrine]] and [[norepinephrine]] causes [[mania]] and a decrease in [[epinephrine]] and [[norepinephrine]] causes [[depression]].
* Drugs that increase levels of monoamines, including serotonin, norepinephrine, or dopamine, can all potentially trigger mania for instance drug of abuse like cocaine.<ref name="pmid291795762">{{cite journal| author=Starzer MSK, Nordentoft M, Hjorthøj C| title=Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis. | journal=Am J Psychiatry | year= 2018 | volume= 175 | issue= 4 | pages= 343-350 | pmid=29179576 | doi=10.1176/appi.ajp.2017.17020223 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29179576  }}</ref>
*Drugs that increase levels of [[Monoamine|monoamines]], including [[serotonin]], [[norepinephrine]], or [[dopamine]], can all potentially trigger [[mania]] for instance [[Abuse|drug of abuse]] like [[cocaine]].<ref name="pmid291795762">{{cite journal| author=Starzer MSK, Nordentoft M, Hjorthøj C| title=Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis. | journal=Am J Psychiatry | year= 2018 | volume= 175 | issue= 4 | pages= 343-350 | pmid=29179576 | doi=10.1176/appi.ajp.2017.17020223 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29179576  }}</ref>
* Patients with substance use-induced psychosis may develop schizophrenia or bipolar disorder within five years.<ref name="pmid29179576">{{cite journal| author=Starzer MSK, Nordentoft M, Hjorthøj C| title=Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis. | journal=Am J Psychiatry | year= 2018 | volume= 175 | issue= 4 | pages= 343-350 | pmid=29179576 | doi=10.1176/appi.ajp.2017.17020223 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29179576  }}</ref>
*Patients with substance use-induced psychosis may develop schizophrenia or bipolar disorder within five years.<ref name="pmid29179576">{{cite journal| author=Starzer MSK, Nordentoft M, Hjorthøj C| title=Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis. | journal=Am J Psychiatry | year= 2018 | volume= 175 | issue= 4 | pages= 343-350 | pmid=29179576 | doi=10.1176/appi.ajp.2017.17020223 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29179576  }}</ref>
* A postmortem study of the frontal lobes of individuals with these disorders revealed that the glutamate levels were increased<ref name="pmid175742162">{{cite journal| author=Hashimoto K, Sawa A, Iyo M| title=Increased levels of glutamate in brains from patients with mood disorders. | journal=Biol Psychiatry | year= 2007 | volume= 62 | issue= 11 | pages= 1310-6 | pmid=17574216 | doi=10.1016/j.biopsych.2007.03.017 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17574216  }}</ref>.        
*A [[Postmortem|postmortem study]] of the [[frontal lobes]] of individuals with these disorders revealed that the [[glutamate]] levels were increased<ref name="pmid175742162">{{cite journal| author=Hashimoto K, Sawa A, Iyo M| title=Increased levels of glutamate in brains from patients with mood disorders. | journal=Biol Psychiatry | year= 2007 | volume= 62 | issue= 11 | pages= 1310-6 | pmid=17574216 | doi=10.1016/j.biopsych.2007.03.017 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17574216  }}</ref>.


=== Neurophysiologic factors ===
===Neurophysiologic factors===


* A meta-analysis by Houenou et al found decreased activation of gray matter in a cortical-cognitive brain network, which has been associated with the emotion regulation in patients with bipolar disorder.  <ref name="pmid21470688">{{cite journal| author=Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M | display-authors=etal| title=Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses. | journal=J Affect Disord | year= 2011 | volume= 132 | issue= 3 | pages= 344-55 | pmid=21470688 | doi=10.1016/j.jad.2011.03.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21470688  }}</ref>  
*A meta-analysis shows that decreased activation of [[Grey matter|gray matter]] in a cortical-cognitive brain network, which has been associated with the emotion regulation in patients with bipolar disorder.  <ref name="pmid21470688">{{cite journal| author=Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M | display-authors=etal| title=Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses. | journal=J Affect Disord | year= 2011 | volume= 132 | issue= 3 | pages= 344-55 | pmid=21470688 | doi=10.1016/j.jad.2011.03.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21470688  }}</ref>
*   There is functional and anatomic alterations in brain networks. for instance, there is activation in ventral limbic brain regions that mediate the experience of emotions. <ref name="pmid214706882">{{cite journal| author=Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M | display-authors=etal| title=Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses. | journal=J Affect Disord | year= 2011 | volume= 132 | issue= 3 | pages= 344-55 | pmid=21470688 | doi=10.1016/j.jad.2011.03.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21470688  }}</ref>    
*There is functional and [[anatomic]] alterations in [[brain]] networks. for instance, there is activation in [[ventral]] [[Limbic system|limbic]] [[brain]] regions that mediate the experience of [[emotions]]. <ref name="pmid214706882">{{cite journal| author=Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M | display-authors=etal| title=Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses. | journal=J Affect Disord | year= 2011 | volume= 132 | issue= 3 | pages= 344-55 | pmid=21470688 | doi=10.1016/j.jad.2011.03.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21470688  }}</ref>


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Latest revision as of 09:43, 16 August 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nuha Al-Howthi, MD[2]

Overview

A number of factors can be involved in bipolar disorder including genetic, biochemical, psychodynamic, and environmental factors. paternal age increase the risk of bipolar disorder in one’s offspring that could be due to increased genetic mutations during spermatogenesis. Stressful life events may be associated with onset of bipolar disorder and a more severe course of illness.The disorder runs in families. More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar major depression. Bipolar disorder is associated with immune system dysregulation.

Causes

Psychosocial factors


Heritability or inheritance

Inflammation

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Neurophysiologic factors

  • A meta-analysis shows that decreased activation of gray matter in a cortical-cognitive brain network, which has been associated with the emotion regulation in patients with bipolar disorder. [19]
  • There is functional and anatomic alterations in brain networks. for instance, there is activation in ventral limbic brain regions that mediate the experience of emotions. [20]


References

  1. ↑ Chudal R, Gissler M, Sucksdorff D, Lehti V, Suominen A, Hinkka-Yli-Salomäki S; et al. (2014). "Parental age and the risk of bipolar disorders". Bipolar Disord. 16 (6): 624–32. doi:10.1111/bdi.12182. PMID 24499422.
  2. ↑ Sugaya L, Hasin DS, Olfson M, Lin KH, Grant BF, Blanco C (2012). "Child physical abuse and adult mental health: a national study". J Trauma Stress. 25 (4): 384–92. doi:10.1002/jts.21719. PMC 3805363. PMID 22806701.
  3. ↑ Janiri D, Sani G, Danese E, Simonetti A, Ambrosi E, Angeletti G; et al. (2015). "Childhood traumatic experiences of patients with bipolar disorder type I and type II". J Affect Disord. 175: 92–7. doi:10.1016/j.jad.2014.12.055. PMID 25597794.
  4. ↑ McGuffin, P; Rijsdijk, F; Andrew, M; Sham, P; Katz, R; Cardno, A (2003), "The Heritability of Bipolar Affective Disorder and the Genetic Relationship to Unipolar Depression", Archives of General Psychiatry, 60 (5): 497–502
  5. ↑ Craddock N, Sklar P (2013). "Genetics of bipolar disorder". Lancet. 381 (9878): 1654–62. doi:10.1016/S0140-6736(13)60855-7. PMID 23663951.
  6. ↑ Finn CT, Smoller JW (2006). "Genetic counseling in psychiatry". Harv Rev Psychiatry. 14 (2): 109–21. doi:10.1080/10673220600655723. PMID 16603476.
  7. ↑ Craddock N, Sklar P (2013) Genetics of bipolar disorder. Lancet 381 (9878):1654-62. DOI:10.1016/S0140-6736(13)60855-7 PMID: 23663951
  8. ↑ Ferreira MA, O'Donovan MC, Meng YA, Jones IR, Ruderfer DM, Jones L; et al. (2008). "Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder". Nat Genet. 40 (9): 1056–8. doi:10.1038/ng.209. PMC 2703780. PMID 18711365.
  9. ↑ Sklar P, Smoller JW, Fan J, Ferreira MA, Perlis RH, Chambert K; et al. (2008). "Whole-genome association study of bipolar disorder". Mol Psychiatry. 13 (6): 558–69. doi:10.1038/sj.mp.4002151. PMC 3777816. PMID 18317468.
  10. ↑ Roybal K, Theobold D, Graham A, DiNieri JA, Russo SJ, Krishnan V; et al. (2007). "Mania-like behavior induced by disruption of CLOCK". Proc Natl Acad Sci U S A. 104 (15): 6406–11. doi:10.1073/pnas.0609625104. PMC 1851061. PMID 17379666.
  11. ↑ Nurnberger JI, Koller DL, Jung J, Edenberg HJ, Foroud T, Guella I; et al. (2014). "Identification of pathways for bipolar disorder: a meta-analysis". JAMA Psychiatry. 71 (6): 657–64. doi:10.1001/jamapsychiatry.2014.176. PMC 4523227. PMID 24718920.
  12. ↑ Serretti A, Fabbri C (2013). "Shared genetics among major psychiatric disorders". Lancet. 381 (9875): 1339–1341. doi:10.1016/S0140-6736(13)60223-8. PMID 23453886.
  13. ↑ Cross-Disorder Group of the Psychiatric Genomics Consortium (2013). "Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis". Lancet. 381 (9875): 1371–1379. doi:10.1016/S0140-6736(12)62129-1. PMC 3714010. PMID 23453885.
  14. ↑ Modabbernia A, Taslimi S, Brietzke E, Ashrafi M (2013). "Cytokine alterations in bipolar disorder: a meta-analysis of 30 studies". Biol Psychiatry. 74 (1): 15–25. doi:10.1016/j.biopsych.2013.01.007. PMID 23419545.
  15. ↑ Dargél AA, Godin O, Kapczinski F, Kupfer DJ, Leboyer M (2015). "C-reactive protein alterations in bipolar disorder: a meta-analysis". J Clin Psychiatry. 76 (2): 142–50. doi:10.4088/JCP.14r09007. PMID 25742201.
  16. ↑ Starzer MSK, Nordentoft M, Hjorthøj C (2018). "Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis". Am J Psychiatry. 175 (4): 343–350. doi:10.1176/appi.ajp.2017.17020223. PMID 29179576.
  17. ↑ Starzer MSK, Nordentoft M, Hjorthøj C (2018). "Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis". Am J Psychiatry. 175 (4): 343–350. doi:10.1176/appi.ajp.2017.17020223. PMID 29179576.
  18. ↑ Hashimoto K, Sawa A, Iyo M (2007). "Increased levels of glutamate in brains from patients with mood disorders". Biol Psychiatry. 62 (11): 1310–6. doi:10.1016/j.biopsych.2007.03.017. PMID 17574216.
  19. ↑ Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M; et al. (2011). "Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses". J Affect Disord. 132 (3): 344–55. doi:10.1016/j.jad.2011.03.016. PMID 21470688.
  20. ↑ Houenou J, Frommberger J, Carde S, Glasbrenner M, Diener C, Leboyer M; et al. (2011). "Neuroimaging-based markers of bipolar disorder: evidence from two meta-analyses". J Affect Disord. 132 (3): 344–55. doi:10.1016/j.jad.2011.03.016. PMID 21470688.

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