Childhood adversity and sleep are associated with symptom severity in perinatal women presenting for psychiatric care.

This study leverages psychiatric intake data from treatment-seeking perinatal women aiming to explore the understudied associations between childhood adversity, sleep quality, and severity of perinatal mental illness in this population. The sample is 578 perinatal women presenting for initial evaluation to a university-based perinatal psychiatry clinic. At intake, we collected demographics, adverse childhood experiences (ACEs), sleep quality, and diagnosis and symptom severity of depression, anxiety, and posttraumatic stress disorder (PTSD). Clinician-rated diagnoses showed that 65% of women met criteria for major depression, 23% for generalized anxiety disorder and 4% for PTSD; almost 30% of women had childhood adversity and 98.2% reported poor perinatal sleep quality. Regression analyses revealed differential associations between ACEs and sleep quality and perinatal mood symptoms; ACEs were significantly associated with pregnancy and postpartum PTSD, whereas sleep quality was associated with perinatal depression and generalized anxiety. Screening for ACEs and sleep quality during perinatal intake has high clinical utility, as these two factors significantly contribute to symptom severity across peripartum.

Antisocial alcoholism and serotonin-related polymorphisms: association tests.

Central serotonin dysfunction appears to be related to a subtype of alcoholism with antisocial impulsive features (type II; antisocial alcoholism). The serotonergic deficit may be associated with greater impulsivity, which in turn facilitates both alcohol dependence and antisocial behavior. The present study tested association of antisocial impulsive alcoholism with candidate genes related to serotonergic neurotransmission, using families. Eight markers were assayed using polymerase chain reaction: tryptophan hydroxylase (intron 7), the serotonin transporter SLC6A4 (VNTR 9/12), HTTLPR, the three serotonin receptor types HTR1B (G861C), HTR2A (T102C) and HTR2C (Cys23Ser), monoamine oxidase A (T1460C), and (CA)(n). Eligible probands had early age of onset of alcoholism, child conduct disorder, and two or more symptoms of adult Antisocial Personality Disorder. This sample included 35 probands, their parents, and some siblings (n = 116). Association tests were conducted using the Haplotype Relative Risk method for antisocial alcoholism diagnosis and the George-Elston regression method (the S.A.G.E. program ASSOC) for quantitative antisocial alcoholism severity. Haplotype Relative Risk analyses were not significant at the 0.05 level for any of the markers. Trends suggestive for future research occurred for tryptophan hydroxylase and HTR2A. Quantitative ASSOC analyses showed significant marker effects (P < 0.05) for both monoamine oxidase A markers, which were in linkage disequilibrium. Antisocial alcoholism symptom severity was higher with monoamine oxidase A C homozygotes or hemizygotes, indicating that low monoamine oxidase activity may be important. Future studies are needed to examine joint and interactive effects of serotonin-related markers.