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Night eating syndrome is negatively associated with sleep, severity of anxiety and depression. Our findings suggest that there is a complex relation between NES and depression, and it is recommended that depressed patients be evaluated for NES.

Schizophrenia has substantial variation in symptom severity, course of illness, and overall functioning. Earlier age of onset (AOO) is consistently associated with negative outcomes and yet the causes of this association are still unknown. We used a multiplex, extended pedigree design (total N = 771; 636 relatives from 43 multigenerational families with at least 2 relatives diagnosed with schizophrenia and 135 matched controls) to examine among the schizophrenia relatives (N = 103) the relationship between AOO and negative and positive symptom severity, cognition, and community functioning. Most importantly, we assessed whether there are shared genetic effects between AOO and negative symptoms, positive symptoms, cognition, and community functioning. As expected, earlier AOO was significantly correlated with increased severity of negative and positive symptoms and poorer cognition and community functioning among schizophrenia patients. Notably, the genetic correlation between AOO of schizophrenia and negative symptoms was significant (Rg = −1.00, p = .007). Although the genetic correlations between AOO and positive symptoms, cognition, and community functioning were estimated at maximum and in the predicted direction, they were not statistically significant. AOO of schizophrenia itself was modestly heritable, although not significant and negative symptoms, positive symptoms, and cognition were all strongly and significantly heritable. In sum, we replicated prior findings indicating that earlier AOO is associated with increased symptom severity and extended the literature by detecting shared genetic effects between AOO and negative symptoms, suggestive of pleiotropy.

Background Both bipolar disorder and major depressive disorder are characterized by difficulties in emotion regulation. Little is known about which specific emotion regulatory patterns may be transdiagnostic versus disorder specific, and how such patterns change as a function of current mood states. Methods This preliminary investigation examined specific patterns of self-reported trait emotion regulation difficulties and mindfulness-based regulations strategies across four groups: remitted adults with bipolar I disorder (BD-remitted; n = 32), currently manic adults with bipolar I disorder (BD-manic; n = 19), remitted adults with major depressive disorder (MDD-remitted; n = 32), and healthy controls (CTL; n = 30). Results All three clinical groups reported significantly greater difficulties with emotion regulation and decreased overall mindfulness-based strategies. Conclusions These results suggest that increased emotion regulation difficulties, decreased mindfulness, and increased emotion-driven impulsivity may be transdiagnostic across mood disorders and states, and that impulsivity may be particularly impaired during periods of mania.

BackgroundBipolar disorder is associated with heightened and persistent positive emotion (Gruber in Curr Dir Psychol Sci 20:217–221, 2011; Johnson in Clin Psychol Rev 25:241–262, 2005). Yet little is known about information processing biases that may influence these patterns of emotion responding.MethodsThe current study adopted eye-tracking methodology as a continuous measure of sustained overt attention to monitor gaze preferences during passive viewing of positive, negative, and neutral standardized photo stimuli among remitted bipolar adults and healthy controls. Percentage fixation durations were recorded for predetermined areas of interest across the entire image presentation, and exploratory analyses were conducted to examine early versus late temporal phases of image processing.ResultsResults suggest that the bipolar and healthy control groups did not differ in patterns of attention bias.ConclusionsFindings provide insight into apparently intact attention processing despite disrupted emotional responding in bipolar disorder.

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Risk for schizophrenia peaks during early adulthood, a critical period for brain development. Although several influential theoretical models have been proposed for the developmental relationship between brain pathology and clinical onset, to our knowledge, no study has directly evaluated the predictions of these models for schizophrenia developmental genetic effects on brain structure. To address this question, we introduce a framework to estimate the effects of schizophrenia genetic variation on brain structure phenotypes across the life span. Five-hundred and six participants, including 30 schizophrenia probands, 200 of their relatives (aged 12-85 years) from 32 families with at least two first-degree schizophrenia relatives, and 276 unrelated controls, underwent MRI to assess regional cortical thickness (CT) and cortical surface area (CSA). Genetic variance decomposition analyses were conducted to distinguish among schizophrenia neurogenetic effects that are most salient before schizophrenia peak age-of-risk (i.e., early neurodevelopmental effects), after peak age-of-risk (late neurodevelopmental effects), and during the later plateau of age-of-risk (neurodegenerative effects). Genetic correlations between schizophrenia and cortical traits suggested early neurodevelopmental effects for frontal and insula CSA, late neurodevelopmental effects for overall CSA and frontal, parietal, and occipital CSA, and possible neurodegenerative effects for temporal CT and parietal CSA. Importantly, these developmental neurogenetic effects were specific to schizophrenia and not found with nonpsychotic depression. Our findings

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