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Using data from a prospective birth cohort, we aimed to test for an association between exposure to tobacco smoke in utero or during early development and the experience of hypomania assessed in young adulthood.
We used data on 2957 participants from a large birth cohort (Avon longitudinal study of parents and children [ALSPAC]). The primary outcome of interest was hypomania, and the secondary outcome was “hypomania plus previous psychotic experiences (PE)”. Maternally-reported smoking during pregnancy, paternal smoking and exposure to environmental tobacco smoke (ETS) in childhood were the exposures of interest. Multivariable logistic regression was used and estimates of association were adjusted for socio-economic, lifestyle and obstetric factors.
There was weak evidence of an association between exposure to maternal smoking in utero and lifetime hypomania. However, there was a strong association of maternal smoking during pregnancy within the sub-group of individuals with hypomania who had also experienced psychotic symptoms (OR = 3.45; 95% CI: 1.49–7.98; P = 0.004). There was no association between paternal smoking, or exposure to ETS during childhood, and hypomania outcomes.
Exposure to smoking in utero may be a risk factor for more severe forms of psychopathology on the mood-psychosis spectrum, rather than DSM-defined bipolar disorder.
This study investigated differences in cognitive performance between middle-aged adults with and without a lifetime history of mood disorder features, adjusting for a range of potential confounders.
Cross-sectional analysis of baseline data from the UK Biobank cohort. Adults aged 40–69 (n = 143,828) were assessed using measures of reasoning, reaction time and memory. Self-reported data on lifetime features of major depression and bipolar disorder were used to construct groups for comparison against controls. Regression models examined the association between mood disorder classification and cognitive performance, adjusting for sociodemographic, lifestyle and clinical confounders.
Inverse associations between lifetime history of bipolar or severe recurrent depression features and cognitive performance were attenuated or reversed after adjusting for confounders, including psychotropic medication use and current depressive symptoms. Participants with a lifetime history of single episode or moderate recurrent depression features outperformed controls to a small (but statistically significant) degree, independent of adjustment for confounders. There was a significant interaction between use of psychotropic medication and lifetime mood disorder features, with reduced cognitive performance observed in participants taking psychotropic medication.
In this general population sample of adults in middle age, lifetime features of recurrent depression or bipolar disorder were only associated with cognitive impairment within unadjusted analyses. These findings underscore the importance of adjusting for potential confounders when investigating mood disorder-related cognitive function.
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