Research paperClinical features of bipolar spectrum with binge eating behaviour
Introduction
It has been suggested that identification of clinical sub-phenotypes might help further the understanding of the genetic architecture of bipolar disorder (MacQueen et al., 2005, Saunders et al., 2008, Schulze, 2010), and that bipolar disorder with a comorbid eating disorder (ED) might represent one such sub-phenotype (Liu et al., 2016; McElroy et al., 2015). For example, in a genome-wide association analysis (GWAS) comparing 184 bipolar patients with a best estimate diagnosis of bulimia nervosa (BN) or anorexia nervosa (AN) with bipolar patients without ED comorbidity and with healthy controls, the most significant genome finding was within SOX2-OT (p=8.9×10−8 for rs 4854912) with a secondary peak in the adjacent FXR1 gene (p=1.2×10−6 for rs 1805576) on chromosome 3q26.33 (Liu et al., 2016). The authors concluded that their findings replicated a prior association of SOX2-OT with EDs, that clinical sub-phenotypes have utility, and that different clinical presentations of bipolar disorder may reflect differential genetic contributions.
By contrast, in an analysis of data from the Bipolar Disorder Genome Study Consortium, part of the Genetic Association Information Network (GAIN), our group found that bipolar disorder plus broadly-defined BE (used as a proxy for a comorbid ED since formal ED diagnoses were not available) was associated with genetic variants in the apoprotein B gene (Winham et al., 2014). It is unknown, however, how many bipolar patients with BE have a formal ED diagnosis, and whether the presence of BE in the absence of an ED diagnosis is clinically relevant in bipolar disorder. Indeed, it is also unknown how best to define the bipolar-ED sub-phenotype or even if there is more than one such sub-phenotype. Specifically, should the bipolar-ED sub-phenotype be defined as bipolar disorder with a comorbid syndromal ED or could it be bipolar disorder co-occurring with some aspect of ED psychopathology, such as BE?
We thus wondered whether the presence of BE, regardless of the presence of a formal ED, might signify an important clinical sub-phenotype that could inform genetic studies of bipolar disorder. This is important because BE is more easily assessed than syndromal EDs per se, and genetic studies require extremely large sample sizes. Hence, bipolar disorder with comorbid BE could be a more efficiently assessed sub-phenotype than bipolar disorder with a co-occurring ED, thereby saving valuable time when assessing phenotypes of large samples of bipolar individuals for genetic studies.
To address this question, we evaluated the prevalence and correlates of different levels of BE among 1114 patients with bipolar 1 disorder, bipolar II disorder, or schizoaffective disorder, bipolar type participating in a genetic biobank. We refer to all of these patients as having bipolar spectrum disorder.
Section snippets
Study design
Participants for this study were derived from The Mayo Clinic Bipolar Biobank (Frye et al., 2015). Entry criteria for the Biobank were a diagnosis of bipolar I disorder, bipolar II disorder, or schizoaffective disorder, bipolar type; no current suicidal ideation or psychosis; and age 18 through 80 years (Frye et al., 2015). The protocol was approved by an institutional review board at each study site, and every participant provided written informed consent to be included in the Biobank.
As
Discussion
Using the EDDS, we found 30% of patients with bipolar spectrum disorder had any BE and 27% had BE plus an ED diagnosis. Thus, the majority of patients with BE had an ED diagnosis (90%). Our finding that 30% of bipolar spectrum patients had BE and that 27% had BED or BN is consistent with epidemiologic and clinical studies reporting elevated rates of BE, BED, and BN in individuals with bipolar disorder (or the reverse) (Hudson et al., 2007, Javaras et al., 2008, Kessler et al., 2013, McElroy et
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