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Increased discounting of delayed rewards may reflect a decision bias that contributes to excessive use of alcohol and, more generally, to an impulsive, disinhibitory predisposition that is characterized by a preference for immediate over long-term rewards. The current study examined the association between delay discounting of rewards and the co-variation among several types of disinhibitory problems that are often comorbid with alcohol dependence (AD). Lifetime problems with alcohol, marijuana, other drugs, childhood conduct disorder, and adult antisocial behavior were assessed in a sample of 426 young adults, 257 of whom had a lifetime diagnosis of AD. Higher delay discounting rates were associated with the covariation among all domains of disinhibitory problems and were not uniquely associated with any one domain. Higher delay discounting rates also were associated with lower intelligence, lower working memory capacity, and higher trait impulsivity. The results suggest that increased delay discounting of rewards may reflect aspects of a general vulnerability to externalizing, disinhibitory disorders. Keywords delay discounting; alcoholism; comorbidity; impulsivity; antisocial behavior Individuals with alcohol dependence (AD) tend to discount future rewards relative to immediate rewards at higher rates compared to those without AD (Bjork, Hommer, Grant, & Danube, 2004;Finn, 2002;Mitchell, Fields, D'Esposito, & Boettiger, 2005;Petry, 2001). This pattern of increased discounting of delayed rewards may reflect decision biases that contribute to excessive use of alcohol and, more generally, to an impulsive predisposition that is characterized by a preference for immediate over long-term rewards and reduced cognitive capacity (Finn, 2002;Mitchell, Fields, D'Esposito & Boettiger, 2005).However, because increased delayed discounting of rewards is thought to be a key component of impulsivity (Crean, de Wit, & Richards, 2000;Mitchell, 1999;Reynolds, 2006a) and because AD is highly comorbid with other disinhibitory disorders (Krueger et al., 2002), high rates of delay discounting also should be associated with other forms of disinhibitory psychopathology, such as childhood conduct disorder (CCD). In fact, considerable evidence suggests that this is the case. Abuse of and dependence on other substances, such as opiates, stimulants, and tobacco, also has been associated with increased delay discounting rates (Bornovalova, Correspondence concerning this article should be sent to Dr. Peter R. Finn, Department of Psychological and Brain Sciences, Indiana University, 1101 E. 10 th Street, Bloomington,, finnp@indiana.edu. Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this m...

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Importance Prenatal antidepressant exposure has been associated with adverse outcomes. Previous studies, however, may not have adequately accounted for confounding. Objective To evaluate alternative hypotheses for associations between first-trimester antidepressant exposure and birth and neurodevelopmental problems. Design, Setting, and Participants This retrospective cohort study included Swedish offspring born between 1996 and 2012 and followed through 2013 or censored by death or emigration. Analyses controlling for pregnancy, maternal, and paternal covariates, as well as sibling comparisons, timing of exposure comparisons, and paternal comparisons, were used to examine the associations. Exposures Maternal self-reported first-trimester antidepressant use and first-trimester antidepressant dispensations. Main Outcomes and Measures Preterm birth (< 37 gestational weeks), small for gestation age (birth weight < 2 SDs below the mean for gestational age), and first inpatient or outpatient clinical diagnosis of autism spectrum disorder and attention-deficit/hyperactivity disorder in offspring. Results Among 1,580,629 offspring (mean gestational age 279 days; 48.6% female; 1.4% [n = 22,544] with maternal first-trimester self-reported antidepressant use) born to 943,776 mothers (mean age at childbirth 30 years), 7.0% of exposed vs. 4.8% of unexposed offspring were preterm, 2.5% of exposed vs. 2.2% of unexposed were small for gestational age, 5.3% of exposed vs. 2.1% of unexposed were diagnosed with autism spectrum disorder by age 15, and 12.6% of exposed vs. 5.5% of unexposed were diagnosed by attention-deficit/hyperactivity disorder by age 15. At the population level, first-trimester exposure was associated with all outcomes, compared with unexposed offspring (preterm birth: OR = 1.5, 95% CI, [1.4, 1.6]; small for gestational age: OR = 1.2, 95% CI, [1.1, 1.3]; autism spectrum disorder: HR = 2.0, 95% CI, [1.8, 2.3]; attention-deficit/hyperactivity disorder: HR = 2.2, 95% CI, [2.0, 2.4]). However, in models that compared siblings while adjusting for pregnancy, maternal, and paternal traits, first-trimester antidepressant exposure was associated with preterm birth (OR = 1.3, 95% CI [1.2, 1.5]) but not with small for gestational age (OR = 1.0, 95% CI [0.8, 1.3]), autism spectrum disorder (HR = 0.8, 95% CI [0.6, 1.1]), or attention-deficit/hyperactivity disorder (HR = 1.0, 95% CI [0.8, 1.3]). Results from analyses assessing associations with maternal dispensations before pregnancy and paternal first-trimester dispensations were consistent with findings from the sibling comparisons. Conclusion and Relevance Among offspring born in Sweden, after accounting for confounding factors, first-trimester antidepressant exposure, compared to no exposure, was associated with a small increased risk of preterm birth but no increased risk of small for gestational age, autism spectrum disorder, or attention-deficit/hyperactivity disorder.

Background Preconception, prenatal, and postnatal maternal stress are associated with increased offspring psychopathology, but findings are inconsistent and need replication. We estimated associations between maternal bereavement stress and offspring autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, suicide attempt, and completed suicide. Methods Using Swedish registers, we conducted the largest population-based study to date examining associations between stress exposure in 738,144 offspring born 1992–2000 for childhood outcomes and 2,155,221 offspring born 1973–1997 for adult outcomes with follow-up through 2009. Maternal stress was defined as death of a first degree relative during 6 months before conception, across pregnancy, or the first two postnatal years. Cox proportional survival analyses were used to obtain hazard ratios (HR) in unadjusted and adjusted analyses. Results Marginal increased risk of bipolar disorder and schizophrenia following preconception bereavement stress was not significant. Third trimester prenatal stress increased risk of ASD (adjusted HR=1.58, 95% CI: 1.15–2.17) and ADHD (adjusted HR=1.31, 95% CI: 1.04–1.66). First postnatal year stress increased risk for offspring suicide attempt (adjusted HR=1.13, 95% CI: 1.02–1.25) and completed suicide (adjusted HR=1.51, 95% CI: 1.08–2.11). Bereavement stress during the second postnatal year increased risk of ASD (adjusted HR=1.30, 95% CI: 1.09–1.55). Conclusions Further research is needed on associations between preconception stress and psychopathological outcomes. Prenatal bereavement stress increases risk of offspring ASD and ADHD. Postnatal bereavement stress moderately increases risk of offspring suicide attempt, completed suicide, and ASD. Smaller previous studies may have overestimated associations between early stress and psychopathological outcomes.