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Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.
To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.
Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.
Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.
AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
There is evidence that patients with schizophrenia spectrum disorders present higher mortality in comparison with the general population. The aim of this study was to analyse the causes of mortality and sociodemographic factors associated with mortality, standardised mortality ratios (SMRs), life expectancy and potential years of life lost (YLL) in patients with schizophrenia spectrum disorders in Spain.
The study included a cohort of patients from the Malaga Schizophrenia Case Register (1418 patients; 907 males; average age 42.31 years) who were followed up for a minimum of 10 years (median = 13.43). The factors associated with mortality were analysed with a survival analysis using Cox's proportional hazards regression model.
The main causes of mortality in the cohort were circulatory disease (21.45%), cancer (17.09%) and suicide (13.09%). The SMR of the cohort was more than threefold that of the population of Malaga (3.19). The life expectancy at birth was 67.11 years old, which is more than 13 years shorter than that of the population of Malaga. The YLL was 20.74. The variables associated with a higher risk of mortality were age [adjusted hazard ratio (AHR) = 1.069, p < 0.001], male gender (AHR = 1.751, p < 0.001) and type of area of residence (p = 0.028; deprived urban zone v. non-deprived urban area, AHR = 1.460, p = 0.028). In addition, receiving welfare benefit status in comparison with employed status (AHR = 1.940, p = 0.008) was associated with increased mortality.
There is excess mortality in patients with schizophrenia spectrum disorders and also an association with age, gender, socioeconomic inequalities and receiving welfare benefits. Efforts directed towards improved living conditions could have a positive effect on reducing mortality.
Despite the robust body of work on cognitive aspects of bipolar disorder (BD), a clear profile of associated impairments in impulsivity, decision-making and risk-taking from studies that use behavioural measures has yet to be established. A systematic review, across four electronic databases (PsycINFO, MEDLINE/PubMed, ScienceDirect and Scopus), of literature published between January 1999 and December 2018 was carried out in accordance with the PRISMA statement. The protocol was registered on PROSPERO (CRD42018114684). A fixed-effect and random-effects meta-analysis using the Hedges' g (ES) estimate was performed. The analysis revealed significant impairment in BD individuals with medium effect sizes in various aspects of impulsivity – response inhibition (ES = 0.49; p < 0.0001), delay of gratification (ES = 0.54; p < 0.0001) and inattention (ES = 0.49; p < 0.0001) – and in decision-making (ES = 0.61, p = 0.0002), but no significant impairment in risk-taking behaviour (ES = 0.41; p = 0.0598). Furthermore, we found significant heterogeneity between studies for decision-making and risk-taking behaviour but not for impulsivity. Impaired risk-taking behaviour was significant in a subgroup of BD-I and euthymic individuals (ES = 0.92; p < 0.0001) with no significant heterogeneity. A stratification analysis revealed comparable results in euthymic and non-euthymic individuals for impulsivity. Our findings suggest that behaviour impulsivity is elevated in all phases of BD, representing a core and clinically relevant feature that persists beyond mood symptoms. More studies about decision-making and risk-taking are necessary to establish if they are impaired in BD and to analyze the role of mood state.
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