Agitated and depressed with a traumatic brain injury.

ObjectiveThis study aimed to examine among veterans whether 1) alcohol consumption patterns are associated with probability of psychiatric symptoms, and 2) alcohol use disorder (AUD) history explains psychiatric symptoms among nondrinkers.MethodData were collected from 3,003 veterans (20.5% women). Gender-stratified logistic models examined the association between alcohol consumption pattern and odds of symptoms of posttraumatic stress disorder (PTSD), depression, and suicidality. Two types of models were tested: four-group models comparing moderate drinkers to nondrinkers, light, and heavy drinkers; and five-group models separating nondrinkers by AUD history.ResultsIn four-group models for both genders, compared to moderate drinkers, hazardous drinkers were more likely to have psychiatric symptoms. Among men, nondrinkers were more likely to have symptoms of depression and suicidality but not PTSD. Among women, nondrinkers and light drinkers were more likely to have PTSD symptoms. In the five-group model for men, odds of symptoms were higher for nondrinkers with AUD history and hazardous drinkers. Compared to nondrinkers without AUD history and light drinkers, male nondrinkers with AUD history had higher odds of psychiatric symptoms. In the five-group model for women, odds of symptoms were higher for hazardous drinkers. Female nondrinkers with AUD history had higher odds of a positive depression screen. Odds of a positive PTSD screen were higher for female nondrinkers (with and without AUD history) and light drinkers.ConclusionsFor male veterans, there was a protective effect of moderate drinking (compared to abstinence) that disappeared when nondrinkers without AUD history were separated. However, results for women showed a protective effect of moderate drinking with regard to PTSD that persisted even when AUD history was taken into account.

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.

Two rapidly acting antidepressive treatment forms, namely, electroconvulsive therapy (ECT) and ketamine, possibly share a common mechanism of action primarily involving alterations of neurotransmission (glutamate and γ-aminobutyric acid levels). Because patients receiving ketamine and with a coexistent family history of an alcohol use disorder (AUD) seem to benefit from consistent and longer lasting antidepressive effects, we hypothesized better treatment response in ECT patients with an own history or a family history of an AUD. One hundred forty-one psychiatric inpatients with a major depressive episode, who were treated with ECT, were enrolled into this retrospective study. Age, sex, family or personal history of alcohol or benzodiazepine use disorder, ECT response data, and ECT treatment-related data were collected and analyzed with ordinal logistic regression and Fisher exact tests. Twenty-one percent of all patients had their own history of an AUD, 11% had their own history of a benzodiazepine use disorder, and 11% reported on a positive family history of alcohol or benzodiazepine use disorder. The logistic regression analyses revealed that only patient's own history of an AUD predicts a better ECT response (P = 0.031; odds ratio, 2.1; Fisher exact test, P = 0.006). Within the limitations of a retrospective study, a history of an AUD seems to be a positive predictor for an ECT response in patients experiencing a major depressive episode, which has not been found in 2 earlier studies. Findings are in line with neurobiological hypotheses of excitatory/inhibitory neurotransmitter changes with ketamine and ECT.

The present investigation examined the role of gender, family history of alcohol and drug use disorders, temperament, childhood behavior problems, and adult psychopathology, on adult alcohol use disorder (AUD) severity. Structural equation modeling was used to examine multiple etiological pathways to adult alcohol use disorder (AUD) severity. Participants included 335 treatment-seeking males and females with current or lifetime DSM-III-R alcohol dependence (96%) or abuse (4%) enrolled in one of five treatment outcome studies. Extensive assessment at treatment entry used a mixture of retrospective and current self-report. Results identified two significant paths associated with a latent factor of adult alcohol use disorder severity at entry to treatment. In Path 1, male gender and family history of drug use disorder predicted greater childhood behavior problems, which predicted antisocial personality disorder (ASPD), borderline personality disorder (BPD), and anxiety disorders (ADs), with anxiety disorders leading directly to alcohol use disorder severity. In Path 2, family history of alcohol use disorder predicted difficult temperament in childhood, which predicted borderline personality disorder, major depressive disorder (MDD) and anxiety disorders; both major depressive disorder and anxiety disorders in turn predicted alcohol use disorder severity at treatment entry. The present findings build on the literature on heterogeneity in developmental risk processes leading to the expression of adult alcohol use disorder symptomology among patients presenting for alcohol use disorder treatment.

Individuals with a family history (FH+) of alcohol use disorder (AUD) have a higher risk for developing an AUD than those with no family history (FH-) of AUD. In addition, FH+ individuals tend to perform worse on neuropsychological measures and show heightened impulsivity, which may be due to underlying differences in brain structure such as cortical thickness. The primary aim of this study was to investigate differences in cortical thickness in FH+ compared to FH- adolescents. Secondary aims were to (i) investigate differences in executive functioning and impulsivity, and (ii) examine associations between brain structure and behavior. Brain scans of 95 FH- and 93 FH+ subjects aged 13 to 18 were obtained using magnetic resonance imaging. FH+ subjects were required to have at least 1 biological parent with a history of an AUD. FH+ and FH- individuals had limited or no past alcohol use, thereby minimizing potential effects of alcohol. Subjects were evaluated on impulsivity and executive functioning tasks. Thicknesses of cortical lobes and subregions were analyzed using FreeSurfer. Regions showing group differences were examined for group-by-age interactions and correlations with neuropsychological and personality measures. FH+ adolescents had thinner cortices in frontal and parietal lobes, notably in the medial orbitofrontal, lateral orbitofrontal, and superior parietal cortices. The difference in cortical thickness between family history groups was strongest among the youngest subjects. FH+ subjects were also more impulsive and had poorer performance on a spatial memory task. These findings demonstrate frontal and parietal structural differences in FH+ adolescents that might underlie cognitive and behavioral characteristics associated with AUD risk.

To compare head and neck free flap outcomes and complications among patients with a history of alcohol use disorder. This is a multicenter retrospective study from January 1, 2010 to July 31, 2025 using data from 73 healthcare organizations in the United States. Adult patients 18 years or older with head and neck cancer undergoing non-bony or bony free flap reconstruction were divided based on presence or absence of a history of alcohol use disorder before surgery. Primary outcomes examined up to 30 days after surgery included flap failure, need for vascular repair, and flap revision. Patients with a history of alcohol use disorder within 6 months of surgery who underwent bony reconstruction had an increased risk of needing flap revision surgery and pneumonia (RR: 1.293[1.018, 1.642]; 1.947[1.337, 2.836]). A history of alcohol use disorder within 1 year prior to non-bony free flap surgery had a higher risk of flap revision. (RR: 1.218[1.008, 1.472]). Sepsis and pneumonia were noted to have increased risks in relation to alcohol use disorders (RR: 1.522[1.055, 2.196]; 2.011[1.568, 2.581]). The risk of flap failure was not associated with a history of alcohol use disorders (RR: 1.159[0.878, 1.531]). Alcohol use disorder within 6 months prior to surgery is associated with an increased risk of flap revision surgery for bony reconstruction cases. For both non-bony and bony free flaps, the risks of sepsis and pneumonia also increase significantly with alcohol use disorder. Level 3.

Hypertension and obesity are serious health problems that have been associated with an increased risk of cardiovascular disease (CVD). We recently showed a relationship between hypertension, obesity and cardiovagal control in a sample of Native and MexicanAmericans at high risk of alcohol use disorders (AUD). While studies have shown that Native and MexicanAmericans exhibit high rates of AUD, the consequences of AUD on CVD risk factors and their relationship with cardiovascular autonomic control is not well understood in these ethnic groups. This study investigated whether an association could be demonstrated between cardiovascular autonomic control and several CVD risk factors in Native and Mexican American men and women (n=228) who are literate in English and are residing legally in San Diego County. Participants with lifetime history of AUD showed higher rates of systolic and diastolic hypertension and obesity than participants without lifetime AUD. Lifetime AUD was significantly associated with reduced HR response to deep breathing (HRDB) measure of cardiovagal control, higher current drinking quantity, and obesity. Reduced HRDB was also associated with increased systolic pre-hypertension or hypertension (pre-/hypertension) and with higher diastolic blood pressure in a linear regression model that included several diagnostic and demographic variables. HRDB and time- and frequency-domain measures of cardiovagal control were significantly reduced in participants with diastolic pre-/hypertension. These data suggest that lower cardiovagal control may play a role in the prevalence of systolic and diastolic pre-/hypertension in a community sample with a history of alcohol and substance use disorders.

Objective To evaluate the risks of major wound healing complications in patients with a history of alcohol use disorder. Study Design Multicenter, retrospective cohort study from January 1, 2010 to July 31, 2025. Setting Sixty‐eight healthcare institutions in the United States. Methods Patients included were aged 18 years or older who had a history of mandible open reduction and internal fixation (ORIF). The patients were stratified into groups based on a history of alcohol use disorder. A total of 13,742 patients were included in the study. After propensity score matching, both groups with and without alcohol use disorder had 6871 patients. All major outcomes and complications including osteomyelitis, pseudoarthrosis, wound disruption, and nonunion/malunion were evaluated at 1, 3, and 6 months after surgery. Results Patients with a history of alcohol use disorder within 6 months before surgery had higher risks of wound disruption (RR: 1.45 [1.15‐1.84]), nonunion/malunion (RR: 1.31 [1.06‐1.63]), and infection (RR: 1.26 [1.09‐1.45]). By 3 and 6 months, they also showed increased risk of all three of these complications. Osteomyelitis after surgery was associated with a history of alcohol use disorder (RR: 1.26 [1.01‐1.57]). No patients had a significantly high rate of pseudoarthrosis after surgery. Conclusion Patients with a history of alcohol use disorder have a higher risk of complications involved with wound and bone healing following mandible ORIF. Level of Evidence Level 3.

Some sources report increases in alcohol use have been observed since the start of the COVID-19 pandemic, particularly among women. Cross-sectional studies suggest that specific COVID-19-related stressful experiences (e.g., social disconnection) may be driving such increases in the general population. Few studies have explored these topics among individuals with a history of Alcohol Use Disorders (AUD), an especially vulnerable population. Drawing on recent data collected by the Collaborative Study on the Genetics of Alcoholism (COGA; COVID-19 study N = 1651, 62% women, age range: 30–91) in conjunction with AUD history data collected on the sample since 1990, we investigated associations of COVID-19 related stressors and coping activities with changes in drunkenness frequency since the start of the pandemic. Analyses were conducted for those without a history of AUD (N: 645) and three groups of participants with a history of AUD prior to the start of the pandemic: (1) those experiencing AUD symptoms (N: 606), (2) those in remission who were drinking (N: 231), and (3) those in remission who were abstinent (had not consumed alcohol for 5+ years; N: 169). Gender-stratified models were also examined. Exploratory analyses examined the moderating effects of ‘problematic alcohol use’ polygenic risk scores (PRS) and neural connectivity (i.e., posterior interhemispheric alpha EEG coherence) on associations between COVID-19 stressors and coping activities with changes in the frequency of drunkenness. Increases in drunkenness frequency since the start of the pandemic were higher among those with a lifetime AUD diagnosis experiencing symptoms prior to the start of the pandemic (14% reported increased drunkenness) when compared to those without a history of AUD (5% reported increased drunkenness). Among individuals in remission from AUD prior to the start of the pandemic, rates of increased drunkenness were 10% for those who were drinking pre-pandemic and 4% for those who had previously been abstinent. Across all groups, women reported nominally greater increases in drunkenness frequency when compared with men, although only women experiencing pre-pandemic AUD symptoms reported significantly greater rates of increased drunkenness since the start of the pandemic compared to men in this group (17% of women vs. 5% of men). Among those without a prior history of AUD, associations between COVID-19 risk and protective factors with increases in drunkenness frequency were not observed. Among all groups with a history of AUD (including those with AUD symptoms and those remitted from AUD), perceived stress was associated with increases in drunkenness. Among the remitted-abstinent group, essential worker status was associated with increases in drunkenness. Gender differences in these associations were observed: among women in the remitted-abstinent group, essential worker status, perceived stress, media consumption, and decreased social interactions were associated with increases in drunkenness. Among men in the remitted-drinking group, perceived stress was associated with increases in drunkenness, and increased relationship quality was associated with decreases in drunkenness. Exploratory analyses indicated that associations between family illness or death with increases in drunkenness and increased relationship quality with decreases in drunkenness were more pronounced among the remitted-drinking participants with higher PRS. Associations between family illness or death, media consumption, and economic hardships with increases in drunkenness and healthy coping with decreases in drunkenness were more pronounced among the remitted-abstinent group with lower interhemispheric alpha EEG connectivity. Our results demonstrated that only individuals with pre-pandemic AUD symptoms reported greater increases in drunkenness frequency since the start of the COVID-19 pandemic compared to those without a lifetime history of AUD. This increase was more pronounced among women than men in this group. However, COVID-19-related stressors and coping activities were associated with changes in the frequency of drunkenness among all groups of participants with a prior history of AUD, including those experiencing AUD symptoms, as well as abstinent and non-abstinent participants in remission. Perceived stress, essential worker status, media consumption, social connections (especially for women), and relationship quality (especially for men) are specific areas of focus for designing intervention and prevention strategies aimed at reducing pandemic-related alcohol misuse among this particularly vulnerable group. Interestingly, these associations were not observed for individuals without a prior history of AUD, supporting prior literature that demonstrates that widespread stressors (e.g., pandemics, terrorist attacks) disproportionately impact the mental health and alcohol use of those with a prior history of problems.

Gambling disorder affects 0.5-2.4% of the population and shows strong associations with lifetime alcohol use disorder. Very little is known regarding whether lifetime alcohol use disorder can impact the clinical presentation or outcome trajectory of gambling disorder. Data were pooled from previous clinical trials conducted on people with gambling disorder, none of whom had current alcohol use disorder. Demographic and clinical variables were compared between those who did versus did not have lifetime alcohol use disorder. Of the 621 participants in the clinical trials, 103 (16.6%) had a lifetime history of alcohol use disorder. History of alcohol use disorder was significantly associated with male gender (relative risk [RR] = 1.42), greater body weight (Cohen's D = 0.27), family history of alcohol use disorder in first-degree relative(s) (RR = 1.46), occurrence of previous hospitalization due to psychiatric illness (RR = 2.68), and higher gambling-related legal problems (RR = 1.50). History of alcohol use disorder was not significantly associated with other variables that were examined, such as severity of gambling disorder or extent of functional disability. Lifetime alcohol use disorder was not significantly associated with the extent of clinical improvement in gambling disorder symptoms during the subsequent clinical trials. These data highlight that lifetime alcohol use disorder is an important clinical variable to be considered when assessing gambling disorder because it is associated with several untoward features (especially gambling-related legal problems and prior psychiatric hospitalization). The study design enabled these associations to be disambiguated from current or recent alcohol use disorder.

To identify risk factors for suicide attempts (SA) in individuals commencing treatment for a manic or mixed episode. A total of 3390 manic or mixed cases with bipolar disorder (BD) type I recruited from 14 European countries were included in a prospective, 2-year observational study. Poisson regression models were used to identify individual and treatment factors associated with new SA events. Two multivariate models were built, stratified for the presence or absence of prior SA. A total of 302 SA were recorded prospectively; the peak incidence was 0-12 weeks after commencing treatment. In cases with a prior history of SA, risk of SA repetition was associated with younger age of first manic episode (P = 0.03), rapid cycling (P < 0.001), history of alcohol and/or substance use disorder (P < 0.001), number of psychotropic drugs prescribed (P < 0.001) and initiation of an anticonvulsant at study entry (P < 0.001). In cases with no previous SA, the first SA event was associated with rapid cycling (P = 0.02), lifetime history of alcohol use disorder (P = 0.02) and initiation of an anticonvulsant at study entry (P = 0.002). The introduction of anticonvulsants for a recent-onset manic or mixed episode may be associated with an increased risk of SA. Further BD studies must determine whether this link is causal.

A family history (FH) of alcohol use disorder (AUD) is associated with increased personal risk for alcohol misuse and AUD. FH is also related to increased impulsivity as evidenced by performance on delay discounting tasks, representing a potential mechanistic link between FH and alcohol misuse. Delay discounting tasks assess individual differences in preferences for smaller, immediate versus larger, delayed rewards, the former being linked to substance misuse. Decision-making on such tasks is underpinned by multiple neural systems, including those supporting reward valuation, cognitive control, and future-oriented thinking. We hypothesized that FH would be associated with differences in one or more neural systems related to delay discounting, with these differences being related to increases in alcohol misuse in young adulthood. We tested 163 first-year college students (ages 18–19) with varying levels of familial risk for AUD on an fMRI delay discounting task. Alcohol misuse was self-reported at baseline and in three yearly follow-up surveys using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol misuse was modeled using a latent growth model, and we examined mediation between FH and alcohol misuse trajectory (AUDIT intercept and slope) through functional activation of brain regions implicated in reward valuation (nucleus accumbens), cognitive control (middle frontal gyrus), and future-oriented thinking (hippocampus). FH was associated with greater activation of the nucleus accumbens, which in turn predicted a steeper AUDIT slope. No other mediators were significant. Our results demonstrate that nucleus accumbens function may be a key mechanism by which FH increases risk for alcohol misuse and AUD.

Introduction: Liver is the most common site for intra-abdominal abscess. Pyogenic liver abscess is more common in men compared to women. Risk factors include diabetes mellitus and chronic hepatobiliary disease. Alcohol abuse is known to cause bone marrow suppression and compromised immune system. Limited data are available regarding clinical outcomes in patients with history of alcohol use disorder who are admitted with pyogenic liver abscess. Methods: Using National Inpatient Sample databases from 2016 to 2019. We identified patients presenting with pyogenic liver abscess, the population were then divided based on the presence and absence of alcohol use disorder using appropriate ICD-10-CM/PCS codes. STATA 16.0 software was used for the analysis. Pearson’s Chi-Square test was used to analyze categorical variable, whereas the student t-test was used to analyze continuous variables. Univariate and multivariate logistic regression was used to adjust for potential confounders. Primary outcome was in hospital mortality due to Pyogenic liver abscess in patients with alcohol use disorder. Results: Amongst total of 19,830 patients admitted with pyogenic liver abscess, 1,090 patients had history of alcohol use disorder and 18,740 patients did not. Both groups consisted predominantly of white male patients. Mean LOS was higher in alcohol use disorder group (8±6.08 days) than in non-alcohol use disorder group (7.35±6.34 days ) (P=< 0.001 ). Mean total hospitalization charges were higher in AUD group ($ 20,968) than in the non-AUD group ($ 18,994) (P= < 0.001) Conclusion: Patient with Pyogenic liver abscess with alcohol use disorder history had higher resource utilization, but less odds of mortality. (Table) Table 1. - In-patient outcome comparison of patients with history of alcohol use disorder presenting with pyogenic liver abscess PLA WITH AUD, N(%) PLA WITHOUT AUD, N(%) P value Total 1090(8.92) 18740(91.07) Primary Outcome OR 95 CI P value Mortality 0.511 0.067 - 3.86 < 0.001 Secondary Outcomes Mean Mean P value LOS(days) 8+/-6.08 7.35+/-6.34 < 0.001 Charges(US$) 20968 18994 < 0.001 Demographics Mean Age 57.65+/- 11.45 61.47+/-15.65 Female(%) 205(18.81) 7404(41)

To explore the genetic influence of a family history of alcohol use disorders and the dopamine transporter SLC6A3 (DAT1) and dopamine beta-hydroxylase (DBH) gene polymorphisms on the risk of severe complications (withdrawal seizures (AWS) and delirium tremens (DT)) during alcohol withdrawal in alcohol-dependent men. We investigated the effects of 3 previously reported candidate genetic variations: 40-bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the SLC6A3(DAT1) gene, and -1021 C/T (rs1611115) of DBH gene in 266 alcohol-dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD-10 during current alcohol withdrawal. Clinically important information and a family history of alcohol use disorders (FH) were obtained by semi-structured interview. Patients in SC group more often have positive FH (54.6% vs. 33%, p=0.001) and their age at first alcohol use (FAU) was lower (16±3.53y.o vs. 17±1.66 y.o, p=0.001). Logistic regression revealed that FH predicts severe complications in total (р=0.001) and DT (р=0.003), FAU independently predicts severe complications in total (р=0.008), AWS (р=0.04), DT (р=0.032), AWS+DT (р=0.048) and every year of delay alcohol use decreases the risk by 18-30%. The gene polymorphisms interact with FAU to decrease the FAU influence on the risk of AWS (T variant of DAT (rs27072), р=0.04), (AWS+DT) and DT (T variant of DBH (rs1611115), р=0.023 and р=0.06). The T variant of DAT (rs27072) is associated with FAU (p=0.007) and increases the risk of (AWS+DT) (р=0.036), but decreases the risk of AWS (р=0.038) and of DT (р=0.021) too, but only in interaction with positive FH. The 9 repeat variant (9R) of DAT VNTR is associated with AWS (p=0.009), but the risk of AWS (р=0.004) and of SC in total (р=0.001) are elevated only in 9R carriers with positive FH. The 9R independently increases the risk of DT (р=0.048) and the effect become more robust in 9R carriers with high density of FH (р=0.014). The gene x gene interaction decreases the risk of DT (р=0.055). According to an analysis of total cohort of patients, the T variant of DBH (rs1611115) is associated with any kind of manifestation of delirium in alcohol-dependent men (p=0.039). This study demonstrate the genetic influence of a family history of alcohol use disorders and DAT and DBH gene polymorphisms on the risk of withdrawal seizures and delirium tremens. The interaction of genetic variations with positive family history provides the most robust effect, the interaction of genetic variations with the age at first alcohol use may «protect» their carriers from negative influence of this «behavioral» risk factor. Replication in large cohorts of patients is necessary to verify these findings for subsequent use in prevention programs.

Differences in regional brain volumes as a function of family history (FH) of alcohol use disorder (AUD) have been reported, and it has been suggested that these differences might index genetic risk for AUD. However, results have been inconsistent. The aims of the current study were (i) to provide an updated descriptive review of the existing literature and (ii) to examine the association of FH with indices of subcortical volumes and cortical thickness in a sample of youth recruited based on FH status. To address aim 1, a literature search located 15 published studies comprising 1,735 participants. Studies were characterized according to population, analytic methods, regions of interest, and primary findings. To address the second aim, we examined volumetric and cortical thickness in a sample of 69 youth (mean age=19.71years, SD=0.79) recruited based on FH status and matched on drinking variables. Associations of sex and alcohol use with volumetric outcomes were also examined. Our descriptive review revealed an inconsistent pattern of results with respect to the presence, direction, and regional specificity of volumetric differences across FH groups. The most consistent finding, significantly smaller amygdala volumes in FH+ participants, was not replicated in all studies. In the current sample of youth, measures of subcortical volumes and cortical thickness did not significantly differ as a function of FH, sex, or their interaction. Evidence for FH group differences in regional brain volumes is inconsistent, and the current study failed to detect any group differences. Further research is needed to confirm the reproducibility of FH group differences and implications for AUD risk.