Using an adoption design to collect data on biological and adoptive parents of children adopted at birth, this study explored a possible mechanism through which heritable characteristics of adopted children evoke adoptive parent responses and lead to reciprocal influences between adoptive parent and adopted child behavior. Participants were 25 male and 20 female adoptees, 12-18 years of age, having either a biological parent with substance abuse /dependency or antisocial personality or a biological parent with no such history. The study found that psychiatric disorders of biological parents were significantly related to children's antisocial/hostile behaviors and that biological parents' psychiatric disorders were associated with adoptive parents' behaviors. This genotype-environment association was largely mediated by adoptees' antisocial / hostile behaviors. Results also suggest that the adoptee's antisocial/hostile behavior and adoptive mother's parenting practices affect each other.Genetic factors are frequently hypothesized to be involved in the way children select, modify, and create the environments that they experience (Scarr & McCartney, 1983). Although emerging evidence from a behavioral genetic perspective during the past decade suggests that heritable characteristics of children influence measures of family environment (e.g., Hur &

Environmental effects and genetic-environmental interaction account for significant variability in adoptee aggressivity, conduct disorder, and adult antisocial behavior and have important implications for the prevention and intervention of conduct disorder and associated conditions such as substance abuse and aggressivity.

This study confirms the model of two independent genetic factors involved in drug abuse/dependence and previous findings that disturbed adoptive parents are associated with adoptee drug abuse/dependency.

Given evidence of chronic inflammation in bipolar disorder (BD), we tested the efficacy of aspirin and minocycline as augmentation therapy for bipolar depression. Ninety-nine depressed outpatients with BD were enrolled in a 6 week, double-blind, placebo-controlled trial, and randomized to one of four groups: active minocycline (100 mg b.i.d.) + active aspirin (81 mg b.i.d.) (M + A); active minocycline + placebo aspirin (M + P); placebo-minocycline + active aspirin (A + P); and placebo-minocycline + placebo aspirin (P + P). A blinded interim analysis mid-way through the study led to the dropping of the M + P and A + P arms from further enrollment giving numbers per group who were included in the final analysis of: 30 (M + A), 18 (M + P), 19 (A + P), and 28 (P + P). When the study started, there were three primary outcome measures. Based on the results of the interim analysis, the primary outcome variable, response to treatment as defined by >50% decrease in Montgomery–Äsberg Depression Rating Scale (MADRS) score was maintained. The other two (i.e., the change in mean MADRS score from baseline to end of study and the remission rate, with remission being defined as a score of <11 on the MADRS) were reduced to exploratory outcome measures because the interim analysis indicated that the study was adequately powered to test differences in response rate but not the mean change in MADRS scores or remission rates. CRP and IL-6 were assayed to measure inflammation. Urinary thromboxane B2 (11-D-TXB2) concentrations, which were significantly increased at baseline in the combined BD sample (n = 90) vs. a healthy control group (n = 27), served as an indirect marker of cyclooxygenase (COX) activity. In a two-group analysis, the M + A group showed a greater response rate than the P + P group (p(one-tailed) = 0.034, OR = 2.93, NNT = 4.7). When all four arms were included in the analysis, there was a main effect of aspirin on treatment response that was driven by both the M + A and the A + P groups (p(two-tailed) = 0.019, OR = 3.67, NNT = 4.0). Additionally, there was a significant 3-way interaction between aspirin, minocycline, and IL-6, indicating that response to minocycline was significantly greater in participants in the M + P group with higher IL-6 concentrations. Further, participants in the M + P group who responded to treatment had significantly greater decreases in IL-6 levels between baseline and visit 7 vs. non-responders. Regarding the exploratory outcomes, there was a main effect for aspirin on the remission rate (χ12 = 4.14, p(2t) = 0.04, OR = 2.52, NNT = 8.0). There was no significant main effect of aspirin or minocycline on the mean change in MADRS score across visits. Aspirin and minocycline may be efficacious adjunctive treatments for bipolar depression. Given their potential import, additional studies to confirm and extend these findings are warranted.

Weight gain rate during inpatient treatment for AN was a significant predictor of short-term clinical outcome after discharge. It is unclear whether weight gain rate exerts a causal effect or is rather a marker for readiness to tolerate weight restoration and engage in the recovery process.