Alcohol Use Disorder In Offspring Research Articles

Parental risk constellations and future alcohol use disorder (AUD) in offspring: A combined HUNT survey and health registries study.

We examined the risk of developing a future alcohol use disorder (AUD) among offspring of families with different constellations of parental risk factors. We analyzed a sample of 8,774 offspring (50.2% male) from 6,696 two-parent families who participated in the Nord-Trøndelag Health Study in Norway when offspring were 13-19 years old in 1995-1997 or 2006-2008. Based on population registry information and parental Nord-Trøndelag Health Study self-reports, families were classified via Latent Profile Analysis into fiver risk constellations reflecting parents' education, drinking quantities and frequencies, and mental health. Information about AUD-related diagnoses, treatments, and prescriptions for all offspring in the period between 2008 and 2016 was obtained from 3 national health registries and pooled to reflect any AUD. The likelihood of AUD in offspring was examined with a set of nested logistic regression models. Registry records yielded 186 AUD cases (2.1%). Compared with the lowest-risk constellation, offspring from two constellations were more likely to present with AUD in unadjusted analyses. After adjusting for all covariates, including offspring's alcohol consumption and witnessing parental intoxication during adolescence, AUD risk remained elevated and statistically significant (adjusted odds ratio = 2.34, 95% confidence interval = 1.14, 4.85) for offspring from the constellation characterized by at least weekly binge drinking, low education, and poor mental health in both parents. Weekly binge drinking by both parents was associated with future AUD risk among community offspring in Norway when clustered with additional parental risks such as poor mental health and low educational attainment. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

The Search for Contributors to Low Rates of Recognition of Paternal Alcohol Use Disorders in Offspring From the San Diego Prospective Study.

The most efficient approach for establishing family histories (FHs) asks informants about disorders in their relatives (a Family History Method [FHM]). However, FHMs underestimate family diagnoses. We evaluated if accuracies of young adult offspring report of their father's alcohol use disorders (AUDs) related to the age, sex, education, and/or substance-related patterns/problems of either the young adult informants or their AUD fathers. Data from the San Diego Prospective Study (SDPS), a multigenerational 35-year investigation, compared father/offspring pairs where the proband father's alcohol problems were correctly (Group 1) or incorrectly (Group 2) noted by offspring. In the key analysis, Group 1 versus 2 results were entered into bootstrapped backward logistic regression analyses predicting Group 1 membership. Five proband and one offspring characteristic were associated with correct identification of their father's alcohol problems. None of these related to age, education, or sex. Characteristics associated with correct FHM diagnoses included the father's FH of AUDs, self-report of drinking despite social/interpersonal or physical/psychological alcohol-related problems, spending much time related to alcohol, and his having a religious preference. The single offspring item predicting correct identification of the father's problems was the number of DSM alcohol problems of the offspring. In the SDPS, FHM sensitivity was most closely related to the father's drinking characteristics, not the offspring characteristics. While unique aspects of SDPS families potentially limit generalizability of results, the data demonstrate how the FHM can offer important initial steps in the search for genetically related AUD risks in a subset of families.

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.

The number of biological parents with alcohol use disorder histories and risk to offspring through age 30

ObjectiveWe investigated associations between the number of parents with histories of alcohol use disorder (AUD) and several offspring (proband) variables through age 30: occurrence of AUD and, separately, alcohol dependence; onset age of the initial AUD episode; time to recovery from the first AUD episode; number of distinct AUD episodes; and cumulative duration of AUD across episodes. MethodsOffspring data were collected during four assessment waves of a longitudinal epidemiological study of psychiatric disorders with a regionally representative sample. The reference sample included 730 offspring with diagnostic data from at least one parent. Offspring were assessed with semi-structured diagnostic interviews between mid-adolescence and young adulthood and parents were assessed when offspring were approximately 24 years of age. ResultsAs the number of parents with AUD increased, offspring risk for AUD and alcohol dependence also increased. Latent growth model results indicated that offspring AUD risk trajectories increase in severity as a function of the number of parents with AUD. This pattern of results was not observed for other AUD course-related features in offspring (i.e., number of distinct episodes; months required for recovery from initial episode; cumulative duration across episodes). ConclusionsThe number of parents with a history of AUD is associated with overall offspring risk for AUD and alcohol dependence and elevated AUD risk trajectories through age 30. The number of parents with AUD may be a more relevant risk factor for onset-related characteristics of AUD in offspring than for its longitudinal course.

Predictors of Increases in Alcohol Problems and Alcohol Use Disorders in Offspring in the San Diego Prospective Study.

The 35-year-long San Diego Prospective Study documented 2-fold increases in alcohol problems and alcohol use disorders (AUDs) in young-adult drinking offspring compared to rates in their fathers, the original probands. The current analyses use the same interviews and questionnaires at about the same age in members of the 2 generations to explore multiple potential contributors to the generational differences in adverse alcohol outcomes. Using data from recent offspring interviews, multiple cross-generation differences in characteristics potentially related to alcohol problems were evaluated in 3 steps: first through direct comparisons across probands and offspring at about age 30; second by backward linear regression analyses of predictors of alcohol problems within each generation; and finally third through R-based bootstrapped linear regressions of differences in alcohol problems in randomly matched probands and offspring. The analyses across the analytical approaches revealed 3 consistent predictors of higher alcohol problems in the second generation. These included the following: (i) a more robust relationship to alcohol problems for offspring with a low level of response to alcohol; (ii) higher offspring values for alcohol expectancies; and (iii) higher offspring impulsivity. The availability of data across generations offered a unique perspective for studying characteristics that may have contributed to a general finding in the literature of substantial increases in alcohol problems and AUDs in recent generations. If replicated, these results could suggest approaches to be used by parents, healthcare workers, insurance companies, and industry in their efforts to mitigate the increasing rates of alcohol problems in younger generations.

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 relation of parent alcohol disorder to young adult drinking outcomes mediated by parenting: Effects of developmentally limited versus persistent parent alcohol disorder

BackgroundParent alcohol use disorder (AUD) is a well-established risk factor for the development of offspring AUD and is associated with poor parenting. However, few studies have examined heterogeneity in trajectories of parental AUD and its influence on adolescent offspring drinking, and no studies to date have considered the differential risk to offspring conferred by parental AUDs that are limited to early adulthood. Specifically, AUDs limited to the period of emerging adulthood may confer less risk to a child's environment as recovery following emerging adulthood coincides with the typical ages of entry into the parenting role. The present study tested whether parental AUDs developmentally limited to emerging adulthood (DLAUD) transmit less risk for alcohol problems and alcohol consumption in offspring compared to offspring of parents with AUDs spanning across multiple developmental periods (persistent AUD), as mediated by positive parenting strategies. MethodPathways were examined using longitudinal mediation models (N = 361) comparing offspring with parental DLAUD, persistent AUD, and no AUD. ResultsParents with DLAUD do not transmit the same risk for alcohol problems to offspring as parents with persistent AUD (B = 0.173, SE = 0.067, p < .05); more offspring alcohol problems were associated with persistent AUD than with DLAUD. Positive parenting mediated the transmission of risk from parental AUD to offspring alcohol problems (B = 0.040, SE = 0.019, p < .05) and consumption (B = 0.019, SE = 0.011, p < .05) only when comparing persistent AUD vs. no parental AUD. ConclusionFindings suggest that the developmental period in which parents' recovery occurs is a useful way to categorize “recovered” AUDs versus current AUDs.

Does exposure to parental substance use disorders increase offspring risk for a substance use disorder? A longitudinal follow-up study into young adulthood

ObjectiveThe main aim of this study was to examine the risk of exposure to parental substance use disorders (SUD; alcohol or drug abuse or dependence) on the risk for SUD in offspring with and without attention deficit hyperactivity disorder (ADHD) followed into young adult years. MethodsSubjects were derived from two longitudinal case-control studies of probands of both sexes, 6–17 years, with and without DSM-III-R ADHD and their parents. Probands were followed for ten years into young adulthood. Probands with a parental history of non-nicotine SUD were included in this analysis. Exposure to SUD was determined by active non-nicotine parental SUD while the parent was living with their child after birth. Cox proportional hazard models were used to calculate the risk of non-nicotine SUD in offspring. Results171 of the 404 probands reassessed at ten-year follow up had a family history of parental SUD. 102 probands were exposed to active parental SUD. The average age of our sample was 22.2 ± 3.5 years old. Exposure to maternal but not paternal SUD increased offspring risk for an alcohol use disorder in young adulthood independently of ADHD status (OR: 2.7; 95% CI: 1.1, 6.9; p = 0.04). ConclusionExposure to maternal SUD increases the risk for an alcohol use disorder in offspring ten years later in young adult years irrespective of ADHD status.

The clinical features of alcohol use disorders in biological and step‐fathers that predict risk for alcohol use disorders in offspring

Given that Alcohol Use Disorder (AUD) is clinically heterogeneous, can we, in a large epidemiological sample using public registries, identify clinical features of AUD cases in biological and step-fathers that index, respectively, genetic and familial-environmental risk for AUD in their offspring? From all father-offspring pairs where the father had AUD and the offspring was born 1960-1990, we identified not-lived-with (NLW) biological fathers (n = 38,376) and step-father pairs (n = 9,711). The relationship between clinical and historical features of the father's AUD and risk for AUD in offspring was assessed by linear hazard regression. Age at first registration for AUD and recurrence of AUD registration were significantly stronger predictors of risk for AUD in the offspring of NLW fathers than in step-fathers. By contrast, number of AUD registrations in NLW fathers and step-fathers were equally predictive of risk for AUD in offspring. However, while the number of step-father AUD registrations that occurred when he was living them with significantly predicted risk for AUD in his step-children, the number of registrations that occurred when not residing with his step-children was unassociated with their AUD risk. In an epidemiological sample, we could meaningfully differentiate between features of AUD in fathers that indexed genetic risk which was transmitted to biological offspring (early age at onset and recurrence) versus indexed environmental risk (registrations while rearing) which increased risk in step-children.

An extended Swedish national adoption study of alcohol use disorder.

Alcohol use disorder (AUD) runs strongly in families. It is unclear to what extent the cross-generational transmission of AUD results from genetic vs environmental factors. To determine to what extent genetic and environmental factors contribute to the risk for AUD. Follow-up in 8 public data registers of adoptees, their biological and adoptive relatives, and offspring and parents from stepfamilies and not-lived-with families in Sweden. In this cohort study, subtypes of AUD were assessed by latent class analysis. A total of 18,115 adoptees (born 1950-1993) and 171,989 and 107,696 offspring of not-lived-with parents and stepparents, respectively (born 1960-1993). Alcohol use disorder recorded in medical, legal, or pharmacy registry records. Alcohol use disorder in adoptees was significantly predicted by AUD in biological parents (odds ratio, 1.46; 95% CI, 1.29-1.66) and siblings (odds ratio, 1.94; 95% CI, 1.55-2.44) as well as adoptive parents (odds ratio, 1.40; 95% CI, 1.09-1.80). Genetic and environmental risk indices created from biological and adoptive relatives acted additively on adoptee AUD liability. Results from biological and adoptive relatives were replicated and extended from examinations of, respectively, not-lived-with parents and stepparents. Multivariate models in these families showed that AUD in offspring was significantly predicted by AUD, drug abuse, psychiatric illness, and crime in not-lived-with parents and by AUD, drug abuse, crime, and premature death in stepparents. Latent class analyses of adoptees and offspring of not-lived-with parents with AUDs revealed 3 AUD classes characterized by (1) female preponderance and high rates of psychiatric illness, (2) mild nonrecurrent symptoms, and (3) early-onset recurrence, drug abuse, and crime. These classes had distinct genetic signatures in the patterns of risk for various disorders in their not-lived-with parents and striking differences in the rates of recorded mood disorders. Parent-offspring transmission of AUD results from both genetic and environmental factors. Genetic risk for AUD reflects both a specific liability to AUD and to other externalizing disorders. Environmental risk reflects features of both parental psychopathology and other aspects of the rearing environment. Alcohol use disorder is a heterogeneous syndrome and meaningful subtypes emerged from latent class analysis, which were validated by patterns of disorders in biological parents and specific psychiatric comorbidities. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent-offspring resemblance.

Impact of the Number of Parents With Alcohol Use Disorder on Alcohol Use Disorder in Offspring

Although parental alcohol use disorder (AUD) increases risk for alcohol problems in offspring, no studies have evaluated the odds of AUD in offspring based on the number of biological parents with AUD (0, 1, or 2) in a population-based national sample. The purpose of this study was to investigate the relationship between the number of AUD parents and prevalence of AUD in offspring. This study utilized data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions, which assessed AUD using the Alcohol Use Disorder and Associated Disabilities Interview Schedule-DSM-IV Version (main outcome variable). We analyzed the sample (n = 40,374) to investigate the effect of the number of AUD parents on lifetime AUD in offspring. In a subgroup analysis, gender differences were examined. 22% of adults in the United States had at least 1 biological parent with AUD. Compared with offspring of non-AUD parents, offspring of 1 AUD parent had a 2.5-fold increase (AOR = 2.51; 95% CI, 2.38-2.66) and offspring of 2 AUD parents had a 4.4-fold increase (AOR = 4.44; 95% CI, 3.93-5.02) in the odds of lifetime AUD. Each additional AUD parent increased the odds of AUD in offspring in an additive pattern. Female offspring were more vulnerable to the impact of parental AUD than male offspring (OR = 1.17 in offspring of 1 AUD parent; OR = 1.48 in offspring of 2 AUD parents). Offspring of AUD parents had heightened odds of lifetime AUD, with an additive parental effect. Awareness of this risk can be useful for clinicians to educate individuals with AUD parents about prevention and intervention.

Exposure to Paternal Alcoholism Does Not Predict Development of Alcohol-Use Disorders in Offspring: Evidence From an Offspring-of-Twins Study

Using an offspring-of-twins design, we tested the hypothesis that exposure to paternal alcoholism during the child's first 12 years will increase offspring risk for subsequent alcohol-use disorders (AUD). Structured psychiatric interviews assessed history of psychiatric and substance-use disorders in Vietnam Era Twin Registry fathers (n = 512), their offspring (n = 877), and mothers of the offspring (n = 507). Exposure was defined as the fathers' endorsement of any Diagnostic and Statistical Manual of Mental Disorders (DSM), Fourth Edition, AUD symptom, according to the Lifetime Drinking History assessment (administered in 1999), at any time between off- spring ages 0-12 years; all fathers had satisfied DSM, Third Edition, Revised (DSM-III-R), criteria for alcohol dependence in a 1992 diagnostic interview. Cox proportional hazards models were fit to predict time to first symptom of abuse/dependence in offspring. Off- spring exposed to paternal alcoholism were significantly more likely to develop an AUD when compared with offspring of nonalcoholic fathers (hazard ratio [HR] = 1.51; 95% confidence interval [CI]: 1.10-2.07). Although offspring unexposed to paternal alcoholism did not significantly differ from control offspring (HR = 1.50, 95% CI: 0.93-2.41), the magnitude of association was similar to that in the exposed offspring. There were no significant differences in AUD between offspring of alcoholics who were exposed and those who were not exposed to paternal alcoholism, as long as fathers had satisfied DSM-III-R criteria for alcohol dependence at some point in their lives. There does not appear to be a relationship between exposure to paternal alcoholism during childhood and development of an AUD in offspring. Genetic and high-risk environmental factors that are correlated with lifetime paternal alcoholism may be stronger predictors of offspring AUD than fathers' problem drinking. Future research should be encouraged, using more comprehensive analyses, to examine the role of family genetic influences and other family environmental influences on offspring alcohol outcomes.

Relation of attachment style to family history of alcoholism and alcohol use disorders in early adulthood

The present study examined the association between paternal alcoholism and attachment style in early adulthood and sought to determine whether attachment style might, at least partially, mediate intergenerational risk for alcoholism. The current report focuses on the cross-sectional relation between family history (FH) of alcoholism, attachment styles, and alcohol use disorders (AUD) when cohort members were, on average, 29 years old ( N=369; 46% male; 51% FH+). Results indicated that FH+ participants were more likely to have insecure attachment, characterized by fearful-avoidant and dismissed-avoidant styles. Additionally, fearful-avoidant and dismissed-avoidant attachment styles were related to the presence of an AUD even after controlling for sex and FH ( P<0.05). There was little evidence, however, that attachment style mediated the relation between paternal alcoholism and AUD in offspring; the FH-AUD association was only negligibly reduced when the effect of attachment style was controlled. Our findings suggest that insecure attachment style is a risk factor for AUD, independent of familial risk for alcoholism.

Alcohol use disorder among adolescents: impact of paternal alcoholism on drinking behavior, drinking motivation, and consequences.

This study examined the impact of an Alcohol Use Disorder (AUD) in biological fathers on drinking history, context, motivation, and consequences in male and female adolescents dichotomized according to the presence or absence of an AUD. Main effects for paternal history of an AUD were not found on any variable. Significant interactions were observed between father-son diagnostic status with respect to age of first alcohol use (p < 0.001) and peer relationships (p < 0.001). No significant interactions were observed between father-daughter diagnostic status. As expected, adolescents with AUD differed from adolescents without AUD on numerous variables pertaining to drinking behavior, history, and consequences. These findings indicate that there is no strong or pervasive effect of paternal AUD on adolescent offspring's AUD characteristics.