Maternal Alcohol Use Disorder Research Articles

Parental substance use disorder and risk of intellectual disability in offspring in Sweden: a national register study

Intellectual disability (ID) is a disorder with unknown aetiology in many cases. Maternal alcohol use is a known risk factor for ID, but less is known about the importance of maternal and paternal substance use disorder (SUD) and risk of ID in offspring. Data from multiple nationwide registers were used to create a cohort of children born from January 01, 1978 to December 31, 2002. All participants were born in Sweden, had available parental identification information and did not emigrate or die before age 12 (n=1,940,820). Logistic regression modelling was performed with exposure defined as having a parent who received any SUD diagnosis, including alcohol use disorder (AUD) and drug use disorder (DUD). The outcome was registration of diagnosis of any form of ID. First, we analysed the risk of ID if parental SUD was registered prior to childbirth with stepwise adjustment of multiple covariates. Second, the effect of timing of SUD diagnosis in relation to childbirth was analysed. Of 37,410 offspring with parental SUD registered prior to birth, 3.0% (n=1110) had any form of ID compared to 1.2% (n=23,168) of those 1,903,410 individuals without parental SUD prior birth. Parental SUD prior birth was associated with an increased risk of any form of ID (Odds Ratio [OR]: 2.3 [2.2-2.5]), with ORs similar for maternal (OR: 2.3 [2.1-2.5]) and paternal SUD (OR: 2.3 [2.1-2.5]). These ORs were reduced but remained statistically significant after adjusting for parental education, migration, psychiatric comorbidity, and co-parent SUD (OR parental SUD: 1.6 [1.5-1.8]; OR maternal SUD: 1.4 [1.2-1.5]; OR paternal SUD: 1.6 [1.5-1.7]). Parental SUD was associated with increased risk of ID in offspring irrespective of timing of diagnosis, but if mothers or fathers were diagnosed with AUD during pregnancy (OR maternal AUD: 5.0 [3.1-8.2]; OR paternal AUD: 2.8 [2.2-3.6]), the risk was significantly greater than if the AUD diagnosis was first registered after childbirth (OR maternal AUD: 1.9 [1.8-2.0]; OR paternal AUD: 1.6 [1.6-1.7]). Both paternal and maternal SUD were associated with an increased risk of ID in offspring, with greatest risk observed when AUD was diagnosed during pregnancy. Possible mechanisms may involve shared genetic and environmental factors, including toxic effects from alcohol intake. These findings have clinical implications in suggesting that parental SUD in either parent represents a possibly modifiable risk factor to consider when developing prevention, diagnostics and treatment programs for children with ID. Stockholm County Council, the Research Council of the Swedish Alcohol Retailing Monopoly, Fredrik and Ingrid Thurings stiftelse, Academy of Finland, the Swedish Research Council and the Swedish Research Council for Health, Working Life and Welfare, Nordforsk by the Nordic Council of Ministers and the Polish Medical Research Agency.

Elucidating the Links Between Mother and Father Alcohol Use Disorder and Adolescent Externalizing Psychopathology: A Test of Transmission Specificity Within Competing Factor Structures and Genetic and Environmental Liabilities.

Parental alcohol use disorder (AUD) is a substantiated risk factor for adolescent externalizing psychopathology; however, the level of specificity at which risk from parental AUD is transmitted to adolescent offspring should be interrogated further. The current study modeled competing factor structures of psychopathology in a sample of 502 adolescent twin pairs (Mage = 13.24years) and tested associations with mother and father AUD. The bifactor model exhibited the best fit to the data when contrasted with correlated factors and general factor models. Paternal AUD predicted the externalizing and internalizing correlated factors, the adolescent P-factor but not the residual externalizing and internalizing factors, and the general factor. No significant associations with maternal AUD were noted. Lastly, the latent factors of adolescent psychopathology were all moderately heritable (h2 = 0.44-0.59) and influenced by the nonshared environment. Shared genetic factors primarily explained externalizing and internalizing covariance. Findings suggest that efforts to mitigate risk in offspring of fathers exhibiting AUD require broader approaches that address the full range of adolescent symptomology.

Maternal Alcohol-Use Disorder and Child Outcomes

OBJECTIVES: Investigate the relationship between maternal alcohol-use disorder and multiple biological and social child outcomes, including birth outcomes, child protection, justice contact, and academic outcomes for both Indigenous and non-Indigenous children. METHODS: Women with a birth recorded on the Western Australian Midwives Notification System (1983–2007) and their offspring were in scope. The exposed cohort were mothers with an alcohol-related diagnosis (International Classification of Diseases, Ninth Revision and International Classification of Diseases, 10th Revision) recorded in an administrative data set and their offspring (non-Indigenous: n = 13 969; Indigenous: n = 9635). The exposed cohort was frequency matched with mothers with no record of an alcohol-related diagnosis and their offspring (comparison cohort; non-Indigenous: n = 40 302; Indigenous: n = 20 533). RESULTS: Over half of exposed non-Indigenous children (55%) and 84% of exposed Indigenous children experienced ≥1 negative outcome. The likelihood of any negative outcome was significantly higher for the exposed than the comparison cohort (non-Indigenous: odds ratio [OR] = 2.67 [95% confidence interval (CI) = 2.56–2.78]; Indigenous: OR = 2.67 [95% CI = 2.50–2.85]). The odds were greatest for children whose mothers received a diagnosis during pregnancy (non-Indigenous: OR = 4.65 [95% CI = 3.87–5.59]; Indigenous: OR = 5.18 [95% CI = 4.10–6.55]); however, numbers were small. CONCLUSIONS: The effects of maternal alcohol-use disorder are experienced by the majority of exposed children rather than a vulnerable subgroup of this population. These findings highlight the need for universal prevention strategies to reduce harmful alcohol use and targeted interventions to support at-risk women and children.

Are Parental Alcohol Use Disorder Histories Associated With Offspring Behavior Problems at Age 2?

Studies of clinical and high-risk samples have demonstrated associations between parental alcohol use disorders (AUDs) and offspring's internalizing and externalizing behavior problems during adolescence and early adulthood. It remains unclear, however, whether associations between parental AUD histories and offspring behavior problems are evident among very young offspring who were not directly exposed to a parent who experienced an active AUD episode during the child's lifetime. The present study sought to evaluate internalizing and externalizing behavior problems among young children as a function of paternal and maternal AUD histories and associated clinical features. The community sample consisted of 160 families with a 2-year-old child and parents who did not experience an AUD episode since the child was born. Parental AUD histories and associated clinical features were evaluated with semistructured interviews, and parental reports of child internalizing and externalizing behaviors were assessed with an age-appropriate behavior checklist. In contrast to previous findings from clinical and high-risk samples, when paternal and maternal AUD histories and associated clinical features were evaluated as predictors of child behavior problems, no statistically significant associations were detected (βs ranged from .01 to .18). Moderating effects of sex of the offspring were also not significant. Parental AUD histories do not appear to confer risk for offspring internalizing or externalizing behavior problems at age 2. The emergence of such behavior problems may be limited to specific developmental periods during childhood or reflect the impact of direct exposure to parents with alcohol-related problems.

Trauma exposure and post-traumatic stress disorder among youth in a high-risk family study: Associations with maternal and paternal alcohol use disorder

This study presents findings regarding the prevalence of trauma exposure and Posttraumatic Stress Disorder (PTSD) based on discrete types of trauma (physical, sexual, witnessed violence, and non-assaultive trauma) among 3404 youth in a family study of Alcohol Use Disorder (AUD). Data from the Collaborative Study on the Genetics of Alcoholism (COGA) were used to examine associations of parent AUD with offspring’s childhood trauma exposure, and with lifetime diagnosis of DSM-IV PTSD among White and Black participants aged 12-35.Of 3404 youth, 59.7% had parents affected by AUD and 78% experienced ≤1 traumatic event before age 18. AUD in one or both parents was associated with physical, sexual, and witnessed violence among Whites. Among African Americans, maternal AUD was associated with sexual assault. The lifetime PTSD rate among youth exposed to childhood trauma was 8.6%, and mother-only AUD was significantly associated with lifetime PTSD among participants in both groups. PTSD among youth in this study were somewhat higher (7.9% to 8.83%) than those found in general population studies of the same demographic (5% to 6.8%). Maternal AUD appears to be a salient risk factor for sexual assault before age 18 among Black and development of lifetime PTSD among White youth.

Maternal Alcohol-Use Disorder and Child Outcomes.

Investigate the relationship between maternal alcohol-use disorder and multiple biological and social child outcomes, including birth outcomes, child protection, justice contact, and academic outcomes for both Indigenous and non-Indigenous children. Women with a birth recorded on the Western Australian Midwives Notification System (1983-2007) and their offspring were in scope. The exposed cohort were mothers with an alcohol-related diagnosis (International Classification of Diseases, Ninth Revision and International Classification of Diseases, 10th Revision) recorded in an administrative data set and their offspring (non-Indigenous: n = 13 969; Indigenous: n = 9635). The exposed cohort was frequency matched with mothers with no record of an alcohol-related diagnosis and their offspring (comparison cohort; non-Indigenous: n = 40 302; Indigenous: n = 20 533). Over half of exposed non-Indigenous children (55%) and 84% of exposed Indigenous children experienced ≥1 negative outcome. The likelihood of any negative outcome was significantly higher for the exposed than the comparison cohort (non-Indigenous: odds ratio [OR] = 2.67 [95% confidence interval (CI) = 2.56-2.78]; Indigenous: OR = 2.67 [95% CI = 2.50-2.85]). The odds were greatest for children whose mothers received a diagnosis during pregnancy (non-Indigenous: OR = 4.65 [95% CI = 3.87-5.59]; Indigenous: OR = 5.18 [95% CI = 4.10-6.55]); however, numbers were small. The effects of maternal alcohol-use disorder are experienced by the majority of exposed children rather than a vulnerable subgroup of this population. These findings highlight the need for universal prevention strategies to reduce harmful alcohol use and targeted interventions to support at-risk women and children.

Predicting risk for Alcohol Use Disorder using longitudinal data with multimodal biomarkers and family history: a machine learning study.

Predictive models have succeeded in distinguishing between individuals with Alcohol use Disorder (AUD) and controls. However, predictive models identifying who is prone to develop AUD and the biomarkers indicating a predisposition to AUD are still unclear. Our sample (n = 656) included offspring and non-offspring of European American (EA) and African American (AA) ancestry from the Collaborative Study of the Genetics of Alcoholism (COGA) who were recruited as early as age 12 and were unaffected at first assessment and reassessed years later as AUD (DSM-5) (n = 328) or unaffected (n = 328). Machine learning analysis was performed for 220 EEG measures, 149 alcohol-related single nucleotide polymorphisms (SNPs) from a recent large Genome-wide Association Study (GWAS) of alcohol use/misuse and two family history (mother DSM-5 AUD and father DSM-5 AUD) features using supervised, Linear Support Vector Machine (SVM) classifier to test which features assessed before developing AUD predict those who go on to develop AUD. Age, gender, and ancestry stratified analyses were performed. Results indicate significant and higher accuracy rates for the AA compared with the EA prediction models and a higher model accuracy trend among females compared with males for both ancestries. Combined EEG and SNP features model outperformed models based on only EEG features or only SNP features for both EA and AA samples. This multidimensional superiority was confirmed in a follow-up analysis in the AA age groups (12-15, 16-19, 20-30) and EA age group (16-19). In both ancestry samples, the youngest age group achieved higher accuracy score than the two other older age groups. Maternal AUD increased the model's accuracy in both ancestries' samples. Several discriminative EEG measures and SNPs features were identified, including lower posterior gamma, higher slow wave connectivity (delta, theta, alpha), higher frontal gamma ratio, higher beta correlation in the parietal area, and 5 SNPs: rs4780836, rs2605140, rs11690265, rs692854, and rs13380649. Results highlight the significance of sampling uniformity followed by stratified (e.g., ancestry, gender, developmental period) analysis, and wider selection of features, to generate better prediction scores allowing a more accurate estimation of AUD development.

Family history of alcohol use disorder is associated with brain structural and functional changes in healthy first-degree relatives

BackgroundNeuroimaging studies of vulnerability to Alcohol Use Disorder (AUD) have identified structural and functional variations which might reflect inheritable features in alcohol-naïve relatives of AUD individuals (FH+) compared to controls having no such family history (FH-). However, prior research did not simultaneously account for childhood maltreatment, any clinically significant disorder and maternal AUD. Therefore, we mainly aimed to investigate the brain structure and reward-related neural activations (fMRI), using whole-brain analysis in FH+ young adults with no prevalent confounders. Methods46 FH+ and 45 FH- male and female participants had no severe childhood maltreatment exposure, neither any psychiatric disorder or AUD, nor a prenatal exposure to maternal AUD. We used a 3 T MRI coupled with a whole brain voxel-based method to compare between groups the grey matter volumes and activations in response to big versus small wins during a Monetary Incentive Delay task. The Childhood Trauma Questionnaire score was used as confounding variable in the analyses to account for the remaining variance between groups. ResultsCompared to FH- controls, FH+ participants had smaller grey matter volumes in the frontal and cingulate regions as well as in the bilateral nucleus accumbens and right insula. The FH+ participants’ fMRI datasets denoted a blunted activation in the middle cingulum with respect to FH- controls’ during the processing of reward magnitude, and a greater activation in the anterior cingulum in response to anticipation of a small win. ConclusionsFamily history of alcohol use disorder is linked to structural and functional variations including brain regions involved in reward processes.

Parental alcohol use disorder with and without other mental disorders and offspring alcohol use disorder.

To examine the association between parental alcohol use disorder (AUD) with and without other mental disorders and offspring AUD. Using data from Danish nationwide registers, we identified 15477 offspring with parental AUD and 154392 reference individuals from the general population. Parental AUD was defined as registration for AUD treatment. Parental mental disorders were identified in medical registers and comprised psychotic, mood, anxiety, personality, drug use, and other non-alcohol-related mental disorders. AUD in offspring was identified from medical, pharmacy, treatment and cause of death registers. Hazard ratios (HRs) of AUD were estimated using Cox regression models. AUD in one or both parents was associated with higher risks of AUD in offspring compared with reference individuals. Paternal AUD plus other mental disorder (HR=2.27, 95% confidence interval (CI): 2.10-2.46) and paternal AUD alone (HR=2.21, 95% CI: 2.07-2.36) were associated with higher offspring AUD risk. Similarly, maternal AUD plus other mental disorder (HR=3.02, 95% CI: 2.66-3.43) and maternal AUD alone (HR=2.57, 95% CI: 2.20-3.01) were associated with higher offspring AUD risk. Offspring with parental AUD are at increased risk of AUD irrespective of exposure to other parental mental disorders.

The role of parent and offspring sex on risk for externalizing psychopathology in offspring with parental alcohol use disorder: a national Swedish study.

The substantial literature showing that offspring of parents with alcohol use disorder (AUD) is at increased risk for externalizing psychopathology rarely examines the differential effects of parental and offspring sex. This literature also has other important limitations, such as modest sample sizes and use of unrepresentative samples. Using a large, nationwide Swedish sample, we aim to investigate the roles of parental and offspring sex in externalizing psychopathology among offspring with parental AUD. AUD diagnosis and externalizing measures were obtained from national registries. Associations between outcomes and parental AUD were examined using logistic regressions. Parental and offspring sex effects were examined with interaction terms. Risks for externalizing disorders were increased in sons and daughters with parental AUD, with significant differences between sons and daughters for criminal behavior; maternal AUD had a greater impact than paternal AUD (regardless of offspring sex), but having two parents with AUD increased risk for all outcomes substantially more than having one parent; and maternal AUD increased risk of drug abuse for daughters more than sons, while paternal AUD increased risk of AUD and criminal behavior for sons more than daughters. Offspring of parents with AUD areat increased risk for externalizing psychopathology. Maternal and paternal AUD differentially affected sons' vs. daughters' risks for AUD, drug abuse, and criminal behavior. The transmission of psychopathology within the externalizing spectrum appears to have sex-specific elements.

Maternal alcohol use disorders and depression in emerging adulthood: Examining the relevance of social ties, childhood adversity, and socioeconomic status

A number of recent studies have found that alcohol use disorders (AUDs) among parents are associated with higher levels of depression in their adult children. However, these studies have not considered whether several important social conditions in childhood help explain this association. Using a large sample of young adults from the National Longitudinal Surveys of Youth 1979 Children and Young Adults (NLSY79-CY), this study examines changes in the relationship between maternal AUDs and depression in emerging adulthood after controlling for three clusters of variables related to childhood social ties, adversity, and socioeconomic status. After models adjust for these factors, the association is reduced, but maternal AUDs remain a robust predictor of depression in emerging adulthood. These findings highlight the intergenerational consequences of AUDs and the need to develop interventions that supplement children's social support and economic circumstances.

The effects of maternal alcohol use disorders on childhood relationships and mental health.

Despite millions of children living in the turmoil of their parents' active alcoholism or the aftermath of past abuse, research to date has not (1) provided a comprehensive examination of the effects of maternal alcohol use disorders (AUDs) on children's social ties outside of their relationships with parents, or (2) considered whether the number and quality of childhood social ties alter the effects of maternal AUDs on children's mental health. Using data from the National Longitudinal Surveys of Youth 1979 Children and Young Adults, analysis examined the influence of maternal AUDs on the number and quality of children's ties with siblings, extended family and family friends, peers, and neighborhood members. The analysis also considered how children's social ties influenced the association between maternal AUDs and children's internalizing and externalizing problems. Children of alcoholic mothers had similarly sized networks but more distant relationships with siblings and friends, negative interactions with classmates, and isolating neighborhoods. Controlling for these aspects of children's social ties substantially reduced mental health disparities between children of alcoholic mothers and other children. Findings support the view that maternal alcohol use disorders have the potential to damage children's mental health while also setting into motion long-term relationship problems. Future research should examine the networks of children who experience parental AUDs to further clarify the social processes that link parental AUDs to children's mental health.

Pregnancy outcomes of mothers with an alcohol-related diagnosis: a population-based cohort study for the period 1983-2007.

To examine fetal outcomes of mothers with an alcohol-related diagnosis. Population-based cohort. Western Australia (WA). Births on the WA Midwives Notification System (1983-2007). Infants of mothers with an alcohol-related diagnosis [International Classification of Disease (ICD), 9th/10th revisions] recorded on WA health data sets (non-Aboriginal n = 13 807; Aboriginal n = 9766) were identified through the WA data linkage system. A comparison cohort of infants born to mothers without an alcohol diagnosis was frequency matched on maternal age, year of birth of the offspring, and Aboriginal status (non-Aboriginal n = 40 148; Aboriginal n = 20 643). Poisson regression-generated adjusted relative risk (aRR) and 95% confidence intervals (95% CIs) for small for gestational age (SGA), preterm birth, and low-Apgar score, calculated separately for non-Aboriginal and Aboriginal infants of mothers with an alcohol diagnosis recorded during pregnancy and any alcohol diagnosis. Population-attributable fractions were calculated. The aRR for non-Aboriginal infants when a maternal alcohol diagnosis was recorded during pregnancy ranged from 1.79 (95% CI 1.42-2.16) for SGA to 2.57 (95% CI 1.69-4.27) for preterm birth <32 weeks of gestation, and for Aboriginal infants ranged from 2.69 (95% CI 2.28-3.16) to 1.99 (95% CI 1.40-2.84), respectively. The highest population-attributable fractions were for any alcohol diagnosis and for Aboriginal infants. For Aboriginal births, approximately 9% (95% CI 4.74-12.97) and 10.1% (95% CI 5.50-14.49) of moderate and very preterm births, respectively, and 24.4% (95% CI 13.5-21.2%) of SGAs were attributable to having a mother with any alcohol-related diagnosis. Mothers with an alcohol diagnosis are at increased risk of poor pregnancy outcomes. The public health impact of maternal alcohol-use disorders on fetal outcomes is significant.

Parent and Child Psychopathology and Suicide Attempts among Children of Parents with Alcohol Use Disorder

Parents with psychopathology such as alcohol use disorder (AUD) that confers risk for suicide attempt (SA) may have children who are more likely to develop such psychopathology and to attempt suicide, suggesting that risk may be “transmitted” from parents to children. We examined this phenomenon during the transition from childhood to adolescence, when risk for SA increases dramatically. A cohort of 418 children were examined at average age 9.4 (range 7–14) years at enrollment (Time 1, childhood) and approximately 5 years later, prior to reaching age 18 (Time 2, adolescence). One or both biological parents, oversampled for AUD, were also interviewed. Structural equation models (SEM) examined father-child, mother-child, and either/both parent-child associations. The primary outcome was SA over follow-up among offspring, assessed at Time 2. As hypothesized, parental antisocial personality disorder predicted conduct disorder symptoms in offspring both during childhood and adolescence (parent-child model, father-child model) and maternal AUD predicted conduct disorder symptoms during childhood (mother-child model). However, we did not find evidence to support transmission of depression from parents to offspring either during childhood or adolescence, and parent psychopathology did not show statistically significant associations with SA during adolescence. In conclusion, we conducted a rare study of parent-to-child “transmission” of risk for SA that used a prospective research design, included diagnostic interviews with both parents and offspring, and examined the transition from childhood to adolescence, and the first such study in children of parents with AUD. Results provided mixed support for hypothesized parent-child associations.

Dental Hospital Admissions in the Children of Mothers with an Alcohol-Related Diagnosis: A Population-Based, Data-Linkage Study

To investigate the relationship between maternal alcohol-use disorder and dental hospital admissions in children up to 5 years of age. Mothers with an International Classification of Diseases, 9th revision/10th revision alcohol-related diagnosis, a proxy for alcohol-use disorder, were identified through the Western Australian data-linkage system. Exposed mothers were frequency-matched by maternal age, Aboriginal status, and child's birth year to randomly selected comparison mothers without an alcohol diagnosis. Linkage with the Midwives Notification System (1983-2002) identified all births of these mothers; "exposed" (non-Aboriginal, n = 11,171; Aboriginal, n = 8145) and comparison cohorts (non-Aboriginal, n = 32,508; Aboriginal, n = 16,719). Dental hospital admissions were identified through linkage with Hospital Morbidity Data (1983-2007) (3.2% exposed; 3.0% comparison) and cases of fetal alcohol syndrome (n = 84) through linkage with the Western Australian Register of Developmental Anomalies. ORs and 95% CIs for having a dental admission (International Classification of Diseases, 9th revision: 520-529; International Classification of Diseases, 10th revision: K0-K14.9) were generated by the use of generalized estimating equations, which we adjusted for potential confounding factors (aOR). Children of mothers with an alcohol-related diagnosis had increased adjusted odds of gingivitis and periodontal diseases (aOR 1.67; 95% CI 1.12-2.51) and "other" diseases of the lip and oral mucosa (aOR 1.56; 95% CI 1.21-2.01). Diseases of the salivary glands were increased only in Aboriginal children of mothers with an alcohol-related diagnosis (aOR 2.65; 95% CI 1.09-6.44). Children diagnosed with fetal alcohol syndrome had increased ORs of any dental admission (aOR 2.58; 95% CI 1.30-5.11). Maternal alcohol-use disorder was associated with dental admissions related to disorders of the soft tissues, but questions remain regarding perinatal influences on dental admissions and disease.

Maternal Alcohol Use and Sudden Infant Death Syndrome and Infant Mortality Excluding SIDS

Improvements in the rate of infant mortality (death in first year of life) have not occurred in recent years. This study investigates the association between maternal alcohol-use disorder and sudden infant death syndrome (SIDS) and infant mortality not classified as SIDS using linked, population-based health and mortality data. Exposed mothers were identified through the presence of an International Classification of Diseases 9/10 alcohol diagnosis, a proxy for alcohol-use disorder, recorded on health, mental health, and/or drug and alcohol datasets (1983-2005). Comparison mothers without an alcohol diagnosis were frequency matched to exposed mothers on maternal age within maternal race and year of birth of their children. All offspring with their birth recorded on the Midwives Notification System compose the exposed (n = 21 841) and comparison (n = 56 054) cohorts. Cases of SIDS (n = 303) and infant mortality excluding SIDS (n = 598) were identified through linkage with the Western Australian Mortality Register. Analyses were conducted by using Cox regression and results presented as adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). The highest risk of SIDS occurred when a maternal alcohol diagnosis was recorded during pregnancy (aHR 6.92, 95% CI 4.02-11.90) or within 1 year postpregnancy (aHR 8.61, 95% CI 5.04-14.69). An alcohol diagnosis recorded during pregnancy more than doubled the risk of infant deaths (excluding SIDS) (aHR 2.35, 95% CI 1.45-3.83). Maternal alcohol-use disorder is attributable for at least 16.41% (95% CI 9.73%-23.69%) of SIDS and 3.40% (95% CI 2.28%-4.67%) of infant deaths not classified as SIDS. Maternal alcohol-use disorder is a significant risk factor for SIDS and infant mortality excluding SIDS.

Alcohol Use Disorders in Schizophrenia

Comorbid alcohol use disorders (AUDs) in schizophrenia are associated with increased morbidity, more inpatient treatment, and violent offending. It is of clinical importance to identify those with schizophrenia who may go on to develop an alcohol use disorder; however, the risk factors are not well understood. The aim of this study was to identify risk factors for the development of an AUD in patients after they had been diagnosed with schizophrenia. We conducted a retrospective case-control study of 12,653 individuals diagnosed with ICD-defined schizophrenia in Sweden in 1973-2004, using data from national registers. We tested the associations between individual factors (marital status, immigrant status, and previous violent offending), sociodemographic factors (income and education), and parental risk factors (AUDs, psychosis, and violent offending) ICD-defined and AUD development using logistic regression modeling. Over a median follow-up of 17.3 years, 7.6% of patients had at least 1 hospital diagnosis of AUD. After adjustment for gender and age at diagnosis in a multivariate regression model, previous violent offending (OR = 2.1; 95% CI, 1.8-2.5), low education (OR = 1.3; 95% CI, 1.1-1.5), maternal AUD (OR = 1.9; 95% CI, 1.4-2.7), and paternal AUD (OR = 1.9; 95% CI, 1.5-2.3) remained independently associated with increased risk of patient AUD. AUDs are a common sequela of schizophrenia. Risk factors that could be identified at the time of first presentation include low educational attainment, previous violent offending, and parental history of AUDs and may inform clinical treatment and follow-up of those most at risk.

The Contribution of Parental Alcohol Use Disorders and Other Psychiatric Illness to the Risk of Alcohol Use Disorders in the Offspring

Few population-based studies have investigated associations between parental history of alcoholism and the risk of alcoholism in offspring. The aim was to investigate in a large cohort the risk of alcohol use disorders (AUD) in the offspring of parents with or without AUD and with or without hospitalization for other psychiatric disorder (OPD). Longitudinal birth cohort study included 7,177 men and women born in Copenhagen between October 1959 and December 1961. Cases of AUD were identified in 3 Danish health registers and cases of OPD in the Danish Psychiatric Central Register. Offspring registration with AUD was analyzed in relation to parental registration with AUD and OPD. Covariates were offspring gender and parental social status. Both maternal and paternal registration with AUD significantly predicted offspring risk of AUD (odds ratios 1.96; 95% CI 1.42 to 2.71 and 1.99; 95% CI 1.54 to 2.68, respectively). The association between maternal, but not paternal, OPD and offspring AUD was also significant (odds ratios 1.46; 95% CI 1.15 to 1.86 and 1.26; 95% CI 0.95 to 1.66, respectively). Other predictors were male gender and parental social status. A significant interaction was observed between paternal AUD and offspring gender on offspring AUD, and stratified analyses showed particularly strong associations of both paternal and maternal AUD with offspring AUD in female cohort members. Parental AUD was associated with an increased risk of offspring AUD independent of other significant predictors, such as gender, parental social status, and parental psychiatric hospitalization with other diagnoses. Furthermore, this association appeared to be stronger among female than male offspring. The results suggest that inherited factors related to alcoholism are at least as important in determining the risk of alcoholism among daughters as among sons.

Maternal alcohol use disorder and offspring ADHD: disentangling genetic and environmental effects using a children-of-twins design

Children of alcoholics are significantly more likely to experience high-risk environmental exposures, including prenatal substance exposure, and are more likely to exhibit externalizing problems [e.g. attention deficit hyperactivity disorder (ADHD)]. While there is evidence that genetic influences and prenatal nicotine and/or alcohol exposure play separate roles in determining risk of ADHD, little has been done on determining the joint roles that genetic risk associated with maternal alcohol use disorder (AUD) and prenatal risk factors play in determining risk of ADHD. Using a children-of-twins design, diagnostic telephone interview data from high-risk families (female monozygotic and dizygotic twins concordant or discordant for AUD as parents) and control families targeted from a large Australian twin cohort were analyzed using logistic regression models. Offspring of twins with a history of AUD, as well as offspring of non-AUD monozygotic twins whose co-twin had AUD, were significantly more likely to exhibit ADHD than offspring of controls. This pattern is consistent with a genetic explanation for the association between maternal AUD and increased offspring risk of ADHD. Adjustment for prenatal smoking, which remained significantly predictive, did not remove the significant genetic association between maternal AUD and offspring ADHD. While maternal smoking during pregnancy probably contributes to the association between maternal AUD and offspring ADHD risk, the evidence for a significant genetic correlation suggests: (i) pleiotropic genetic effects, with some genes that influence risk of AUD also influencing vulnerability to ADHD; or (ii) ADHD is a direct risk-factor for AUD.