Does exposure to parental substance use disorders increase substance use disorder risk in offspring? A 5-year follow-up study.

BACKGROUND: This study examined the impact of exposure to parental substance use disorders (SUD) (alcohol or drug abuse or dependence) on the development of SUD in offspring. METHODS: The original sample was derived from pediatric and psychiatric ascertained females 6-17 years old with (N = 140) and without Attention Deficit Hyperactivity Disorder (ADHD; N = 122). At baseline, these groups had 143 and 131 biological siblings and 274 and 238 parents, respectively. All subjects and their family members were comprehensively and blindly assessed by structured psychiatric interviews for psychopathology and substance use. The female probands and their siblings were reassessed after a follow-up period of 5 years. RESULTS: At follow-up the mean age of offspring was 17.9 ± 4.20 years. Independently of ADHD, familial risk, and socioeconomic status, exposure to maternal drug use disorders, but not paternal drug use disorders, was significantly associated with the development of a drug use disorder in offspring (OR: 7.04; p = 0.03). There was a significant association between exposure to parental SUD during adolescence (relative to preschool or latency years) and SUD in offspring (OR: 3.61; p = 0.03). CONCLUSIONS: Exposure to maternal drug use disorders during adolescent years increased the risk for the development of a drug use disorder in a sample of females with and without ADHD and their siblings. Exposure to parental SUD during adolescence specifically increases the risk of SUD development in offspring.

Can pediatric bipolar-I disorder be diagnosed in the context of posttraumatic stress disorder? A familial risk analysis.

Despite ongoing concerns that traumatized children with severe symptoms of emotional dysregulation may be inappropriately receiving a diagnosis of pediatric bipolar-I (BP-I) disorder, this issue has not been adequately examined in the literature. Because both pediatric BP-I disorder and posttraumatic stress disorder (PTSD) are familial disorders, if children with both BP-I and PTSD were to be truly affected with BP-I disorder, their relatives would be at high risk for BP-I disorder. To this end, we compared patterns of familial aggregation of BP-I disorder in BP-I children with and without PTSD with age and sex matched controls. Participants were 236 youths with BP-I disorder and 136 controls of both sexes along with their siblings. Participants completed a large battery of measures designed to assess psychiatric disorders, psychosocial, educational, and cognitive parameters. Familial risk analysis revealed that relatives of BP-I probands with and without PTSD had similar elevated rates of BP-I disorder that significantly differed from those of relatives of controls. Pediatric BP-I disorder is similarly highly familial in probands with and without PTSD indicating that their co-occurrence is not due to diagnostic error.

Does sex moderate the clinical correlates of pediatric bipolar-I disorder? Results from a large controlled family-genetic study.

BACKGROUND: Since little is known as to whether sex differences affect the clinical presentation of pediatric BP-I disorder, it is an area of high clinical, scientific and public health relevance. METHODS: Subjects are 239 BP-I probands (65 female probands, 174 male probands) and their 726 first-degree relatives, and 136 non-bipolar, non-ADHD control probands (37 female probands, 99 male probands) and their 411 first-degree relatives matched for age and sex. We modeled the psychiatric and cognitive outcomes as a function of BP-I status, sex, and the BP-I status-gender interaction. RESULTS: BP-I disorder was equally familial in both sexes. With the exception of duration of mania (shorter in females) and number of depressive episodes (more in females), there were no other meaningful differences between the sexes in clinical correlates of BP-I disorder. With the exception of a significant sex effect for panic disorder and a trend for substance use disorders (p=0.05) with female probands being at a higher risk than male probands, patterns of comorbidity were similar between the sexes. Despite the similarities, boys with BP-I disorder received more intensive and costly academic services than girls with the same disorder. LIMITATIONS: Since we studied children referred to a family study of bipolar disorder, our findings may not generalize to clinic settings. CONCLUSIONS: We found more similarities than differences between the sexes in the personal and familial correlates of BP-I disorder. Clinicians should consider bipolar disorder in the differential diagnosis of both boys and girls afflicted with symptoms suggestive of this disorder.

Psychiatric comorbidity and functioning in a clinically referred population of adults with autism spectrum disorders: a comparative study.

To systematically examine the patterns of psychiatric comorbidity and functioning in clinically referred adults with autism spectrum disorders (ASD). Psychiatrically referred adults with and without ASD were compared on measures assessing for psychiatric comorbidity and psychosocial functioning. Sixty-three adults with ASD participated in the study (mean age: 29 ± 11 years). Adults with ASD in their lifetime suffered from a higher burden of psychiatric disorders (6 ± 3.4 vs. 3.5 ± 2.7; p < 0.001) including major depressive disorder and multiple anxiety disorders, and were functionally more impaired with a significant proportion having received both counseling and pharmacotherapy. Adults with ASD have high levels of psychiatric comorbidity and dysfunction comparable to a clinically referred population of adults without ASD.