Summary: A new study reports different subtypes of bipolar disorder tend to cluster within families, suggesting that even though there are genetic similarities that indicate overlap between subtypes, each has a different origin.
A new study published in Biological Psychiatry looks at the potential genetic distinctions between bipolar I and bipolar II disorders
The most common subtypes of bipolar disorder, bipolar I and bipolar II, stem-at least in part-from different biological causes, according to a new study published in Biological Psychiatry. Despite genetic overlap between the two subtypes, each subtype tended to cluster within families, suggesting a distinction between bipolar disorders I and II.
The study, by Dr. Jie Song of the Department of Clinical Neuroscience, Karolinska Institutet, Sweden, and colleagues helps settle controversy over the relationship between bipolar I and bipolar II disorders. Although genetic similarities indicate overlap between the subtypes, the new findings emphasize different origins. According to Song, this is contrary to a common notion among many clinicians that bipolar II disorder is merely a milder form.
“We have tended to view the two forms of bipolar disorder as variants of the same clinical condition. However, this new study highlights important differences in the heritable risk for these two disorders,” said Dr. John Krystal, Editor of Biological Psychiatry.
The study is the first nationwide family study to explore the difference between the two main subtypes of bipolar disorder. Dr. Song and colleagues analyzed the occurrence of the bipolar disorder subtypes in families from the Swedish national registers. Although a strong genetic correlation between bipolar I and bipolar II disorder suggests that they are not completely different, the family occurrence for each subtype was stronger than co-occurrence between the subtypes, indicating that bipolar I and bipolar II disorders tend to “run” in families separately, rather than occurring together.
“Within the context of our emerging appreciation of polygenic risk, where gene variations are implicated in several disorders, the new findings point to only partial overlap in the risk mechanisms for these two forms of bipolar disorder,” said Dr. Krystal.
The study also provided some additional clues that bipolar I and II disorders have distinct origins. Only bipolar disorder II showed gender differences-the proportion of females to males was higher in bipolar disorder II but not bipolar disorder I. And bipolar I clustered together in families with schizophrenia, which was not apparent for bipolar disorder II.
“Hopefully, our findings increase awareness of the need for refined distinctions between subtypes of mood disorder,” said Dr. Song. The distinction between the subtypes also has implications for treatment strategies for patients. Dr. Song added that future research is warranted to characterize new biomarkers to improve treatment and prognosis.
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Original Research: Abstract for “Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study” by Jie Song, Ralf Kuja-Halkola, Arvid Sjölander, Sarah E. Bergen, Henrik Larsson, Mikael Landén, and Paul Lichtenstein in Biological Psychiatry. Published online November 20 2017 doi:10.1016/j.biopsych.2017.11.014
Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study
Uncertainty remains whether bipolar I disorder (BDI) and bipolar II disorder (BDII) differ etiologically. We used a population-based family sample to examine the etiological boundaries between BDI and BDII by assessing their familial aggregation/coaggregation and by assessing the coaggregation between them and schizophrenia, depression, attention-deficit/hyperactivity disorder, eating disorders, autism spectrum disorder, substance use disorders, anxiety disorders, and personality disorders.
By linking Swedish national registers, we established a population-based cohort (N = 15,685,511) and identified relatives with different biological relationships. Odds ratios (ORs) were used to measure the relative risk of BDI and BDII in relatives of individuals diagnosed with BDI (n = 4309) and BDII (n = 4178). The heritability for BDI and BDII and the genetic correlation across psychiatric disorders were estimated by variance decomposition analysis.
Compared with the general population, the OR of BDI was 17.0 (95% confidence interval [CI] 13.1–22.0) in first-degree relatives of BDI patients, higher than that of BDII patients (OR 9.8, 95% CI 7.7–12.5). The ORs of BDII were 13.6 (95% CI 10.2–18.2) in first-degree relatives of BDII patients and 9.8 (95% CI 7.7–12.4) in relatives of BDI patients. The heritabilities for BDI and BDII were estimated at 57% (95% CI 32%–79%) and 46% (95% CI 21%–67%), respectively, with a genetic correlation estimated as 0.78 (95% CI 0.36–1.00). The familial coaggregation of other psychiatric disorders, in particular schizophrenia, showed different patterns for BDI and BDII.
Our results suggest a distinction between BDI and BDII in etiology, partly due to genetic differences.
“Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study” by Jie Song, Ralf Kuja-Halkola, Arvid Sjölander, Sarah E. Bergen, Henrik Larsson, Mikael Landén, and Paul Lichtenstein in Biological Psychiatry. Published online November 20 2017 doi:10.1016/j.biopsych.2017.11.014