Parental Alcohol Use Disorder Research Articles

Disaggregating within- and between-person associations to test the aversive transmission of alcohol use in late adolescence through adulthood.

The theory of aversive transmission posits that children of parents who have an alcohol use disorder (AUD) may abstain or limit their own alcohol use because they believe themselves to be at risk of developing problems with alcohol. The present study examined relationships among parental AUD, perceived parental AUD, perceived risk for AUD, addiction avoidance reasons for limiting alcohol use, and alcohol use using a random intercept cross-lagged panel model. Participants (N = 805; 48% female; 28% Latinx) were from a longitudinal study investigating intergenerational transmission of AUD. Parental AUD, perceived parental AUD, perceived risk for AUD, addiction avoidance reasons for limiting alcohol use, and alcohol use (quantity, frequency, and frequency of heavy drinking) were measured every 5 years from late adolescence (Mage = 20) to adulthood (Mage = 32). Random intercept cross-lagged panel models tested whether there were stable between-person relations or time-varying within-person relations among these variables. At the between-person level, perceived parental AUD predicted greater addiction avoidance reasons for limiting alcohol use and greater perceived risk. Those with greater addiction avoidance reasons for limiting alcohol use were less likely to use any alcohol and drank less frequently. Parental AUD was associated with higher levels of alcohol use as well as perceived risk. No consistent cross-lagged paths were found at the within-person level. Study findings were at the between-person level rather than the within-person level. Future work on aversive transmission is needed to better understand this subgroup of children of parents with AUD. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Polygenic risk score for problematic alcohol use predicts heavy drinking and alcohol use disorder symptoms in young adulthood after accounting for adolescent alcohol use and parental alcohol use disorder

BackgroundGenome-wide association studies (GWAS) have identified hundreds of loci associated with alcohol-related traits. GWAS permit the calculation of polygenic risk scores (PRS), which aggregate genetic risk for a trait across the genome. To evaluate the usefulness of a PRS for problematic alcohol use (PAU)—which subsumes alcohol use disorder (AUD) and alcohol-related problems—we tested whether this PRS predicted heavy drinking and alcohol problems after accounting for family history of AUD and prior drinking history, robust and established predictors of PAU. MethodsParticipants (N=665) were European-ancestry members of the Michigan Longitudinal Study, a prospective family study with high rates (65%) of parental AUD. Participants reported their frequency of alcohol use, maximum drinks consumed in a 24-hour period, and alcohol use problems at four assessments in adolescence and young adulthood (11–29 years old). We used polygenic prediction via Bayesian regression and continuous shrinkage priors to create a PAU PRS using summary statistics from a meta-GWAS of PAU. ResultsAfter adjusting for demographic covariates, parental AUD, and drinking and alcohol use problems in early and mid/late adolescence, the PAU PRS was significantly associated with alcohol-related problems in young adulthood (β=.08, p=.047; R2=0.6%). The PAU PRS also had a significant indirect effect on alcohol use problems in young adulthood through earlier drinking and alcohol use problems (β=.02, p=.03). ConclusionsThe PAU PRS predicted alcohol problems in young adulthood after accounting for parental history of AUD and alcohol use in adolescence, providing evidence that genetic data uniquely inform the etiology of alcohol problems.

Mortality in adult children of parents with alcohol use disorder: a nationwide register study

Research suggests that adult children of parents with harmful alcohol use are at increased risk for premature death. This national cohort study investigated mortality in adult children of parents with alcohol use disorder (AUD), adjusting for sociodemographic variables. The study used 1973 to 2018 data from Swedish national registers to compare mortality risk in children who had ≥ 1 parent with AUD (ICD-10 code F10 and its ICD-8 and ICD-9 equivalents) (n = 122,947) and those who did not (n = 2,298,532). A Cox regression model adjusted for year of birth, sex, parental education, and childhood loss of a parent was used. Before the age of 18 years, about 5% of children born in Sweden lived with ≥ 1 parent who had a clinical diagnosis of AUD. Overall mortality was higher in adult children of parents with AUD: hazard ratio (HR) 1.76, 95% confidence interval (CI) 1.71–1.82. Mortality remained elevated after adjustments for sociodemographic factors (HR 1.45, 95% CI 1.40–1.50). Children of parents with AUD had increased mortality from all investigated causes. The highest excess risk was for death from drug-related causes (excluding accidental poisonings) (HR 3.08, 95% CI 2.74–3.46). For most causes, mortality was higher if the mother had AUD than if the father had AUD. Patterns of mortality were similar in both sexes. This study provides evidence that parental AUD raises the risk of offspring mortality from preventable causes such as drug use, suicide (HR 2.16, 95% CI 1.98–2.36), accident (HR 2.00, 95% CI 1.87–2.13), and assault (HR 1.76, 95% CI 1.38–2.24).

Origins of spousal cross-concordance for psychiatric disorders: a test of the social stress theory for alcohol use disorder.

The authors sought to clarify the impact of spousal psychiatric disorders of differing severity [major depression or anxiety disorders (DAD) v. bipolar disorder or nonaffective psychosis (BPN)] on proband risk for alcohol use disorder (AUD) during marriage. In a Swedish cohort (N = 744 628), associations between spousal DAD and BPN and proband AUD were estimated with Cox proportional hazards; associations between parental AUD, proband premarital AUD, and spousal lifetime DAD and BPN were estimated with logistic regression; and whether spousal DAD or BPN causally increased risk for AUD was evaluated with frailty models. Spousal premarital DAD, spousal marital-onset DAD, and spousal BPN (premarital or marital-onset) were associated with proband AUD during marriage [hazard ratios (HR) range 1.44-3.72]. Those with a parental or premarital history of AUD (v. without) were more likely to marry a spouse with DAD or BPN (odds ratios 1.22-2.77). Moving from an unaffected first spouse to a DAD-affected second spouse increased AUD risk in males (HR 2.90). Moving from an unaffected first spouse to a BPN-affected second spouse increased AUD risk (HRmales 3.96; HRfemales 5.64). Moving to an unaffected second spouse from a DAD-affected first spouse decreased AUD risk, with stronger evidence in females compared to males (HRmales 0.59; HRfemales 0.28). Associations between spousal DAD or BPN and proband AUD reflect both selection and causal effects. Marriage to a BPN-affected spouse has a particularly strong effect on AUD risk, with more modest effects for spousal DAD.

Heterogeneity in effects of parent-child separation on young-adult substance use disorder.

A large body of literature suggests that parent-child separation predicts child maladjustment. However, further advancement in methodology is needed to account for heterogeneity in types of separation. Additionally, given a lack of research examining different types of separation as predictors of offspring substance use, further research into this topic is warranted. The present study tested the relation between parent-child separation and young-adult substance use disorder (SUD), capturing heterogeneity in these effects based on group differences and measurement of separation. In a sample of 427 young adults from a larger longitudinal study oversampled for parental alcohol use disorder (AUD), effects of number and type of separations on SUD diagnosis were tested. Further, we explored whether these associations were moderated by gender, ethnicity, or parental AUD. Two underlying types of separation were found: parental health-related separation (i.e., parental death, hospitalization) and nonhealth-related separation (i.e., divorce, arrest). A higher sum of separations and greater nonhealth-related separation predicted higher odds of SUD. Greater health-related separation predicted lower odds of SUD. However, these effects were qualified by interactions with ethnicity and parental AUD. Although the vast majority of studies measure cumulative parent-child separation with sum scores, the present study demonstrates that measuring underlying "types" of cumulative separation also reveals important effects. Moreover, childhood separation is a significant risk factor for SUD. Future research on separation should implement methods to capture separation types and further account for potential effects of selection into separation types. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Risk of somatic disease and mortality in individuals of parents with alcohol use disorder: a register-based cohort study.

To estimate the risks of 12 types of somatic disease-alcohol-related, blood, cancer, circulatory, digestive, endocrine and metabolic, genitourinary, infectious, musculoskeletal, nervous, respiratory and skin-in individuals with parental alcohol use disorder (AUD) versus a reference population, and to estimate the risks of all-cause mortality and of death from an alcohol-related cause. Matched cohort study followed-up through nation-wide health registries. Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). Denmark. A total of 14 008 individuals born 1962-2003 of parents with AUD and 139 087 reference offspring randomly selected from the Danish Civil Registration System were followed from their 15th birthday and onward during 1970-2018. Follow-up time ranged between 2 423 955 and 3 208 366 person-years for somatic diseases and was 3 214 411 person-years for all-cause and alcohol-related mortality. Information on somatic disease was obtained from the Danish National Patient Registry. Causes of death were obtained from the Danish Cause of Death Registry. Individuals of parents with AUD had a higher risk of alcohol-related diseases (HR = 2.70, 95% CI = 2.24-3.24) compared with the reference individuals. Higher HRs among individuals with parental AUD compared with reference individuals were also observed in all other somatic diseases except for cancer. All-cause mortality (HR = 1.80, 95% CI = 1.63-2.00) and alcohol-related mortality (HR = 3.28, 95% CI = 2.11-5.08) were higher among individuals of parents with AUD compared with the reference individuals. No significant differences were found in relation to the gender of either parents or offspring. In Denmark, parental alcohol use disorder appears to predict alcohol-related and non-alcohol-related somatic morbidity and mortality in offspring.

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.

Understanding the Progression from Early Alcohol Use Experimentation to Alcohol Use Disorder: Testing Vulnerability by Experience Interactions Using a Two-Part Latent Growth Curve Model.

Most adolescents experiment with alcohol, but a smaller percentage advance to heavy alcohol use (AU) and AU disorder (AUD). Understanding for whom and how early risk leads to AUD is of interest to prevention, treatment, and etiology of AUD. Informed by developmental and behavioral neuroscience theory, the current study tested whether temperament (effortful control, surgency, and negative affect), peer AU (multi-reporter), and AU with parents' permission interacted to distinguish youth who experiment with alcohol from those who escalate to AUD. Community adolescents (N = 765, 53% female) were assessed annually for seven years (Mage = 11.8, range: 10-13 at Year 1; Mage = 18.7; range = 17-20 at year 7). Temperament by early experience interactions were expected to predict amount of AU. Amount of AU was expected to mediate the relationship between the interactions and AUD symptoms (assessed at Years 3 and 7, Mage = 13.8 and 18.7) above and beyond a range of confounds (e.g., problem behavior and parental AU and AUD). Supporting hypotheses, effortful control and surgency interacted with AU with parents' permission and peer AU, respectively, to predict higher amount of AU (R2 = 0.47) and AUD symptoms (R2 = 0.03). Results support developmental and behavioral neuroscience theory. High surgency and low effortful control in conjunction with peer AU and AU with parents' permission were associated with large effects on AU and moderate mediated effects through AU to AUD. AU with parents' permission was risky at low and high effortful control and protective when peers used alcohol.

A latent class analysis of alcohol and posttraumatic stress symptoms among offspring of parents with and without alcohol use disorder

The co-occurrence of posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) is widely known, yet few studies have examined whether and how AUD symptoms co-occur with PTSD symptom clusters of hypervigilance, avoidance/numbing, and re-experiencing. The purpose of this study was to examine potential overlap between AUD and posttraumatic stress symptomatology, and to characterize the resultant latent classes in terms of demographics, drinking behaviors, parental AUD, and specific traumas experienced (physical violence, sexual violence, and non-assaultive trauma). We hypothesized that classes would be differentiated by type and severity of AUD and PTS symptoms. Drawing from a sample of white and Black participants from the Collaborative Study on the Genetics of Alcoholism (COGA), we examined young adults between the ages of 18–35 who had experienced trauma (N = 2478). A series of LCA models based on the type of trauma experienced, posttraumatic stress symptoms and problematic alcohol use were then fitted to the data. A four-class solution provided the best fit, consisting of a low symptom class (N = 1134), moderate alcohol/low PTS severity (N = 623), mild alcohol/high PTS severity (N = 544), and high symptom severity (N = 177). Higher prevalence of sexual assault was associated with membership in high PTS severity classes, and parent AUD was associated with membership in each class, particularly when the mother or both parents had the disorder. Using person-centered methods such as LCA is a commonsense approach to understanding the heterogeneity of symptoms, trauma types, and individual-level characteristics associated with trauma-exposed individuals and comorbid AUD-PTSD, and our study is one of relatively few to empirically ascertain the co-occurrence of alcohol and PTS symptoms in a high-risk family sample.

Nature of the Causal Relationship Between Academic Achievement and the Risk for Alcohol Use Disorder

We evaluated the claim that interventions to improve academic achievement can reduce the risk for alcohol use disorder (AUD). Using nationwide data for individuals born in Sweden from 1972 to 1981 (n = 930,182), we conducted instrumental variable and co-relative analyses of the association between academic achievement and AUD with a mean 21.4-year follow-up. Our instrument, used in the instrumental variable analyses, was month of birth. Co-relative analyses were conducted in cousins, full siblings, and monozygotic twins discordant for AUD, with observed results fitted to a genetic model. The academic achievement-AUD association was modeled in Cox regression. AUD was assessed using national medical, criminal, or pharmacy registries. Later month of birth was significantly associated with poorer academic achievement. Lower standardized academic achievement had a strong relationship with the risk for subsequent AUD registration: hazard ratio (HR) [per SD] = 2.14 [2.11, 2.17]. Instrumental variable analysis produced a substantial but moderately attenuated association: HR = 1.52 [1.28, 1.80]. Controlling for modest associations between month of birth and parental education and AUD risk reduced the association to HR = 1.43 [1.20, 1.69]. Our genetic co-relative model fitted the observed data relatively well and estimated the academic achievement-AUD association in monozygotic twins discordant for academic achievement to equal an HR of 1.44 [1.35, 1.52]. Results were broadly similar when analyzed separately in males and females. Two distinct methods with different assumptions produced results suggesting that the association observed between academic achievement at age 16 and the risk for AUD into middle adulthood is partly causal, thereby providing support for interventions to improve academic achievement as a means to prevent later AUD risk.

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.

Parental Family History of Alcohol Use Disorder and Neural Correlates of Response Inhibition in Children From the Adolescent Brain Cognitive Development (ABCD) Study.

Youth whose parents have alcohol use disorder (AUD) are at higher risk for earlier initiation and greater magnitude of alcohol use, and have a higher likelihood of developing an AUD than their peers without parental history of AUD. This increased risk may be partly attributable to altered development of inhibitory control and related neural circuitry. This study examined neural activation during a motor response inhibition Stop Signal Task (SST) in substance-naïve youth aged 9 to 10years with and without parental family history of AUD. Baseline cross-sectional survey and functional magnetic resonance imaging (fMRI) data were drawn from 6,898 youth in the US-based Adolescent Brain Cognitive Development Study. Generalized additive mixed models were conducted to examine the association between maternal, paternal, and parental (both mother and father) family history of AUD with neural activation during successful and failed response inhibition. Family history interactions with sex and stratification by ethnicity were explored. Of 6,898 participants, 951 (14%) were family history positive for anyparental AUD. Paternal history of AUD was associated with greater activation for successful inhibition in the right medial orbital frontal gyrus, compared to youth with no family history. Maternal history of AUD was associated with greater activation for failed response inhibition among females in the cerebellum, compared to females with no such history. Parental history (both mother and father) of AUD was associated with greater activation during successful inhibition in the left paracentral gyri and left superior parietal lobule. Maternal history and parental history of AUD findings were accounted for by a family history of substance use disorder in general. All effect sizes were relatively small. Substance-naïve children with a parental family history of AUD exhibit greater neural activation in some regions of the fronto-basal ganglia and cerebellar networks when they successfully or unsuccessfully inhibit a response as compared to children with no such family history. This unique neural response pattern could reflect a compensatory response and may represent an inherent neurobiological vulnerability to risk-related behaviors in these youth which will be examined in future longitudinal analyses of this cohort.

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.

Effects of Observable Parent Alcohol Consequences and Parent Alcohol Disorder on Adolescent Alcohol Expectancies.

Parental drinking and parent alcohol use disorder (AUD) are known predictors of adolescent positive alcohol expectancies, but their link to negative expectancies is unclear. Research suggests that parent drinking may indirectly predict adolescent expectancies through exposure to parental drinking events. However, exposure to parent negative alcohol consequences may be more relevant to adolescents' expectancies. The present study tested the mediating effect of parent observable negative alcohol consequences in the association between parent AUD and adolescent expectancies. This study used parent and adolescent data from the Adult and Family Development Project. A total of 581 adolescents reported on their alcohol expectancies across 2 waves of data, and their parents reported on potentially observable alcohol-related negative consequences during the first wave. Past-year and lifetime parent AUD were assessed with diagnostic interviews across 6 waves of data. Mothers' observable consequences mediated the effect of her past-year AUD on adolescent negative expectancies in adolescence, but this effect did not hold at a 1.5-year follow-up. Mothers' lifetime AUD was the only prospective predictor of later adolescent negative expectancies. No father drinking variables predicted expectancies, and all models were invariant across child biological sex. Finally, older adolescent age prospectively predicted higher positive expectancies, whereas the adolescents' own drinking predicted lower negative expectancies. These findings, in line with other recent studies, suggest that exposure to mothers' negative experiences with alcohol may counterintuitively normalize negative alcohol effects. This may paradoxically increase risk for adolescents rather than buffering the effects of a family history of parental AUD.

Family structure and alcohol use disorder: a register-based cohort study among offspring with and without parental alcohol use disorder.

To assess whether parental alcohol use disorder (AUD) is associated with higher risks of living in a non-intact family and assess whether non-intact family structure is associated with higher risks of AUD in the offspring. Prospective cohort study. Danish nation-wide registries. A total of 9948 parental AUD offspring and 98 136 reference offspring from the Danish population. Family structure assessed at birth and at each birthday until age 15 as intact or non-intact (with mother only, father only or neither parent); years lived in an intact family defined as total number of years lived with both parents from birth until the 15th birthday; AUD defined as registration in medical, treatment and cause of death registries. Data were analyzed by Cox regression. At birth, 30.9% [95% confidence interval (CI) = 29.1-32.6] of parental AUD offspring and 10.7% (95% CI = 10.3-11.0) of reference offspring lived in a non-intact family. At age 15, the numbers were 84.6% (95% CI = 83.9-85.3) and 38.4% (95% CI = 38.1-38.7). Parental AUD was associated with a higher risk of offspring AUD [hazard ratio (HR) = 1.88, 95% CI = 1.74-2.02]. Offspring were at lower risk of AUD if they lived 15 years in an intact family compared with offspring who never lived in an intact family (HR = 0.67, 95% CI = 0.52-0.87 for those with parental AUD, and HR = 0.53, 95% CI = 0.48-0.59 for those whose parents did not have AUD). Findings were inconclusive as to whether or not an association was present between family structure and AUD among offspring with parental AUD and reference offspring. The prevalence of non-intact family structure appears to be higher in offspring of parents with alcohol use disorder (AUD) than among offspring from the general population. Parental AUD appears to be associated with increased risk of offspring AUD, and non-intact family structure appears to be associated with increased risk of offspring AUD regardless of parental AUD.

Intelligence in young adulthood and alcohol use disorders in a prospective cohort study of Danish men: the role of psychiatric disorders and parental psychiatric history

ObjectivesThe aims were to estimate the association between intelligence measured in young adulthood and risk of alcohol use disorders (AUD) in men and to investigate the potential modification of this...

The Degree of Multidimensional Severity of Alcohol Use Disorder among Treatment-Seeking Patients: Is There an Additive Effect of Parental Alcohol Use Disorder?

Background: The additive effect of parental alcohol use disorders (AUD) is conventionally defined as an increasing risk of the offspring developing AUD relative to family history negative, < family history positive with 1 parent (FHP1), < FHP2. The few studies on the additive effect of parental AUD have focused on the risk of development of offspring AUD and not on the degree of multidimensional AUD addiction severity. Aims: The aims of the present study were to examine the frequency of treatment-seeking outpatients exposed to FHP1 and FHP2 and whether addiction severity was impacted by the additive effect of parental AUD among AUD female and male offspring. Methods: This cross-sectional study was based on 3,361 consecutive treatment-seeking outpatients from 2006 to 2016, assessed by means of the ­European Addiction Severity Index (EUROP-ASI). The ­EUROP-ASI assessed multidimensional addiction severity, comprising alcohol and other drug use, somatic and psychiatric health status, family and other social status, economy and employment-related problems and criminal status composite scores at treatment entry. Results: Among females, 40.38% had FHP1 and 15.68% FHP2, whereas males had 40.90% FHP1 and 13.24% FHP2. No conventional additive effect was found on the composite scores among both genders. However, another type of synergistic additive effect, only manifesting with exposure to FHP2, was found for employment-related problems and psychiatric status composite scores among male offspring. Conclusions: Exposure to parental AUD is strikingly high among treatment-seeking outpatients. Nonetheless, the additive effect has a modest impact on multidimensional addiction severity and is mostly related to psycho-social impairment among treatment-seeking male offspring.

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.

Parental alcohol use disorder and offspring marital outcomes.

We tested whether parental alcohol use disorder (AUD) predicted adult offspring's likelihood of marriage and marriage to an AUD-affected spouse; whether effects differed as a function of the sex or number of affected parents; and whether they were robust to confounders. Sex-stratified Cox and logistic regression models. Sweden. A total of 1 171 070 individuals (51.40% male) born 1965-75. Obtained from legal, medical and pharmacy registries. Predictor was parent AUD. Outcomes were marriage and spouse AUD. Adjustments included offspring birth year and AUD; and parental education, marriage, divorce, criminal behavior and drug abuse. Male and female offspring of AUD-affected parents were more likely to marry at younger ages (<25), illustrative unadjusted hazard ratio (HR)age 20 =1.22 (1.17, 1.28) and 1.34 (1.20, 1.39) and were less likely to marry at older ages (>25), HRage 30 =0.79 (0.78, 0.81) and 0.82 (0.81, 0.84). Parental AUD was associated with higher odds of having an affected spouse for males and females, odds ratio (OR)=1.47 (1.38, 1.57) and 1.63 (1.56, 1.70). Effects were more pronounced for those with two versus one AUD-affected parent and adjustments attenuated effects negligibly. Daughters of affected mothers (versus fathers) were more likely to have AUD-affected husbands, OR=1.68 (1.54, 1.84) versus 1.56 (1.48, 1.64), while there was no difference in sons. In Sweden, parental alcohol use disorder (AUD) is associated with a higher probability of marriage at younger ages, a lower probability of marriage at older ages and a higher likelihood of marriage to an affected spouse compared with no parental AUD. Most of these effects become stronger when the number of AUD-affected parents increases from one to two, and most effects hold after controlling for parents' socio-economic status, marital history, other externalizing disorders and offspring's own AUD status. Daughters of affected mothers are more likely to have an affected spouse.

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.