Familial Variation in Episode Frequency in Bipolar Affective Disorder

Fisfalen, Maria-Elena; Schulze, Thomas G.; DePaulo, J. Raymond; DeGroot, Leslie J.; Badner, Judith A.; McMahon, Francis J.

doi:10.1176/appi.ajp.162.7.1266

Cited by 64 publications

(40 citation statements)

References 33 publications

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“…In addition, relatives with ADHD were at increased risk of BPD; this is consistent with other studies suggesting that comorbid BPD and ADHD is a familial phenotype (Faraone et al, 2003). In addition to age of onset, other phenotypic features of BPD that have been reported to aggegate in families include polarity of illness onset (mania vs. depression) (Kassem et al, 2006), mood episode frequency (Fisfalen et al, 2005), psychosis (Potash et al, 2003, Saunders et al, 2007 and lithium-responsiveness (Grof et al, 2002), suicidality (Saunders et al, 2007), rapid-cycling (Saunders et al, 2007), and comorbid alcohol use disorders and panic disorder (Saunders et al, 2007).The familial nature of BPD does not in itself establish that genes contribute since both genes and environmental factors could cause familial aggregation. Two methods which do allow genetic effects to be teased apart from environmental ones are adoption studies and twin studies.…”

supporting

confidence: 88%

Genetics of bipolar disorder

Smoller

Gardner-Schuster²

2007

Curr Psychiatry Rep

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Bipolar disorder is a mood disorder characterized by impairing episodes of mania and depression. Twin studies have established that bipolar disorder is among the most heritable of medical disorders and efforts to identify specific susceptibility genes have intensified over the past two decades. The search for genes influencing bipolar disorder has been complicated by a paucity of animal models, limited understanding of pathogenesis, and the genetic and phenotypic complexity of the syndrome. Linkage studies have implicated several chromosomal regions as harboring relevant genes, but results have been inconsistent. It is now widely accepted that the genetic liability to bipolar disorder reflects the action of many genes of individually small effect, a scenario for which linkage studies are poorly suited. Thus, association studies, which are more powerful for the detection of modest effect loci, have become the focus of gene-finding research. A large number of candidate genes, including biological candidates derived from hypotheses about the pathogenesis of the disorder and positional candidates derived from linkage and cytogenetic studies, have been evaluated. Several of these genes have been associated with the disorder in independent studies (including BDNF, DAOA, DISC1, GRIK4, SLC6A4, and TPH2), but none has been established. The clinical heterogeneity of bipolar disorder and its phenotypic and genetic overlap with other disorders (especially schizophrenia, schizoaffective disorder, and major depressive disorder) has raised questions about the optimal phenotype definition for genetic studies. Nevertheless, genomewide association analysis, which has successfully identified susceptibility genes for a variety of complex disorders, has begun to implicate specific genes for bipolar disorder (DGKH, CACNA1C, ANK3). The polygenicity of the disorder means that very large samples will be needed to detect the modest effect loci that likely contribute to bipolar disorder. Detailed genetic dissection of the disorder may provide novel targets (both pharmacologic and psychosocial) for intervention.Bipolar disorder (BPD) is a common and serious mental disorder characterized by severe mood symptoms, including episodes of mania or hypomania and depression, occurring with a typically cyclical course. Lifetime risk for BPD has typically been reported to be approximately 1%, though recent estimates are as high as 4%. (Kessler et al., 2005). The personal and societal costs of BPD are enormous: even among adequately-treated individuals, relapse is common and the disorder can be profoundly disabling, resulting in serious economic burden (Kessler et al., 2006) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production pr...

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supporting

confidence: 88%

Genetics of bipolar disorder

Smoller

Gardner-Schuster²

2007

Curr Psychiatry Rep

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“…Although these retrospective estimates may reflect recall bias to some extent, they are still within the range of estimates reported in prospective studies and family studies. 37,38 Since the mean age at onset of BPD occurs at one of the most critical periods of educational, occupational, and social development, its consequences often lead to lifelong disability. Not only does the disorder begin at an early age but affected individuals spend an average of a decade of their lives in episodes of illness.…”

Section: Commentmentioning

confidence: 99%

Lifetime and 12-Month Prevalence of Bipolar Spectrum Disorder in the National Comorbidity Survey Replication

Merikangas¹,

Akiskal²,

Angst³

et al. 2007

Arch Gen Psychiatry

2,116

1,336

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Context: There is growing recognition that bipolar disorder (BPD) has a spectrum of expression that is substantially more common than the 1% BP-I prevalence traditionally found in population surveys.Objective: To estimate the prevalence, correlates, and treatment patterns of bipolar spectrum disorder in the US population.Design: Direct interviews.Setting: Households in the continental United States.Participants: A nationally representative sample of 9282 English-speaking adults (aged Ն18 years).Main Outcome Measures: Version 3.0 of the World Health Organization's Composite International Diagnostic Interview, a fully structured lay-administered diagnostic interview, was used to assess DSM-IV lifetime and 12-month Axis I disorders. Subthreshold BPD was defined as recurrent hypomania without a major depressive episode or with fewer symptoms than required for threshold hypomania. Indicators of clinical severity included age at onset, chronicity, symptom severity, role impairment, comorbidity, and treatment.Results: Lifetime (and 12-month) prevalence estimates are 1.0% (0.6%) for BP-I, 1.1% (0.8%) for BP-II, and 2.4% (1.4%) for subthreshold BPD. Most respondents with threshold and subthreshold BPD had lifetime comorbidity with other Axis I disorders, particularly anxiety disorders. Clinical severity and role impairment are greater for threshold than for subthreshold BPD and for BP-II than for BP-I episodes of major depression, but subthreshold cases still have moderate to severe clinical severity and role impairment. Although most people with BPD receive lifetime professional treatment for emotional problems, use of antimanic medication is uncommon, especially in general medical settings.Conclusions: This study presents the first prevalence estimates of the BPD spectrum in a probability sample of the United States. Subthreshold BPD is common, clinically significant, and underdetected in treatment settings. Inappropriate treatment of BPD is a serious problem in the US population. Explicit criteria are needed to define subthreshold BPD for future clinical and research purposes. Psychiatry. 2007;64:543-552 Arch Gen

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“…The much higher estimates of persistence of BPD are consistent with prospective studies in clinical samples and with family studies. 85,86 …”

Section: Persistencementioning

confidence: 99%