Bipolar disorder causes: Difference between revisions

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{{Bipolar disorder}}
{{Bipolar disorder}}
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==Overview==
==Overview==
According to the U.S. government's [[National Institute of Mental Health]] (NIMH), "There is no single cause for bipolar disorder—rather, many factors act together to produce the illness." "Because bipolar disorder tends to run in families, researchers have been searching for specific [[gene]]s passed down through generations that may increase a person's chance of developing the illness." "In addition, findings from gene research suggest that bipolar disorder, like other mental illnesses, does not occur because of a single gene.".<ref>{{cite web |url=http://www.nimh.nih.gov/publicat/bipolar.cfm#bp5 |title=What Causes Bipolar Disorder? |accessdate= |format= |work= |author=NIMH}}</ref> Psychological factors also play a strong role in the psychopathology of the disease, and the development of mania may depend on the occurrence of strssful life events, and the individuals ability to handle stress.
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==


It is well established that bipolar disorder is a genetically influenced condition which can respond very well to medication (Johnson & Leahy, 2004; Miklowitz & Goldstein, 1997; Frank, 2005).
===[[Psychosocial]] factors===
(See [[treatment of bipolar disorder]] for a more detailed discussion of treatment.)


Psychological factors also play a strong role in both the [[psychopathology]] of the disorder and the [[psychotherapeutic]] factors aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing [[prodromal]] symptoms before full-blown recurrence, and, practising the factors that lead to maintenance of [[remission (medicine)|remission]] (Lam et al, 1999; Johnson & Leahy, 2004; Basco & Rush, 2005; Miklowitz & Goldstein, 1997; Frank, 2005). Modern [[evidence based medicine|evidence based]] psychotherapies designed specifically for bipolar disorder when used in combination with standard medication treatment increase the time the individual stays well significantly longer than medications alone (Frank, 2005). These psychotherapies are [[interpersonal and social rhythm therapy]] for bipolar disorder, family focused therapy for bipolar disorder, psychoeducation, [[cognitive therapy]] for bipolar disorder, and [[prodrome]] detection. All except psychoeducation and prodrome detection are available as books.
*[[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>
Abnormalities in brain function have been related to feelings of [[anxiety]] and lower stress resilience. When faced with a very stressful, negative major life event, such as a failure in an important area, an individual may have his first major depression. Conversely, when an individual accomplishes a major achievement he may experience his first [[hypomanic]] or [[manic]] episode. Individuals with bipolar disorder tend to experience episode triggers involving either [[interpersonal]] or achievement-related life events. An example of interpersonal-life events include [[falling in love]] or, conversely, the death of a close friend. Achievement-related life events include acceptance into an elite graduate school or by contrast, being fired from work (Miklowitz & Goldstein, 1997). [[Childbirth]] can also trigger a postpartum psychosis for bipolar women, which can lead in the worse cases to infanticide.


The "kindling" theory<ref name=kindling>[http://www.bpinfo.net/kindling_theory.htm Link and reference involving kindling theory]</ref> asserts that people who are genetically predisposed toward bipolar disorder can experience a series of stressful events, each of which lowers the threshold at which mood changes occur. Eventually, a mood episode can start (and becomes recurrent) by itself. Not all individuals experience subsequent mood episodes in the absence of positive or negative life events, however.  
*[[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>


Individuals with late-[[adolescent]]/early [[adult]] onset of the disorder will very likely have experienced [[childhood]] anxiety and depression. Some argue that childhood-onset bipolar disorder should be treated early.
<br />
===[[Heritability]] or [[inheritance]]===


A [[family history (medicine)|family history]] of [[bipolar spectrum]] disorders can impart a genetic predisposition towards developing a bipolar spectrum disorder.<ref name=Genetic_Likelihood>[http://www.psycheducation.org/depression/risk.htm Genetics and Risk] PsychEducation.org</ref> Since bipolar disorders are [[polygenic]] (involving many genes), there are apt to be many unipolar and bipolar disordered individuals in the same family pedigree. This is very often the case (Barondes, 1998). [[Anxiety disorders]], clinical depression, [[eating disorders]], [[premenstrual dysphoric disorder]], [[postpartum depression]], postpartum psychosis and/or [[schizophrenia]] may be part of the patient's family history and reflects a term called "genetic loading."
*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>]
*[[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 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>
*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>
*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>


Bipolar disorder is not either environmental or physiological, it is multifactorial; that is, many genes and [[environmental factors]] conspire to create the disorder (Johnson & Leahy, 2004). Since bipolar disorder is so [[heterogeneous]], it is likely that people experience different pathways towards the illness (Miklowitz & Goldstein, 1997). Recent research done in Japan indicates a hypothesis of dysfunctional mitochondria in the brain (Stork & Renshaw, 2005)''
===[[Inflammation]]===


*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 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===


===Heritability or inheritance===  
*A number of [[neurotransmitters]] have been linked to this [[disorder]].
The disorder runs in families.<ref>
*[[Catecholamine]] [[hypothesis]], state that increase in [[epinephrine]] and [[norepinephrine]] causes [[mania]] and a decrease in [[epinephrine]] and [[norepinephrine]] causes [[depression]].
{{Citation
*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>
  | last = McGuffin
*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>
  | first = P
*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>.
  | 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> More than two-thirds of people with bipolar disorder have at least one close relative with the disorder or with unipolar major depression.


Studies seeking to identify the genetic basis of bipolar disorder indicate that susceptibility stems from multiple genes. Scientists are continuing their search for these genes, using advanced genetic analytic methods and large samples of families affected by the illness. The researchers are hopeful that identification of susceptibility genes for bipolar disorder, and the brain proteins they code for, will make it possible to develop better treatments and preventive interventions targeted at the underlying illness process.
===Neurophysiologic factors===


*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 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>
<br />
==References==
==References==


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

Biochemical factors

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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