Increased risk of myocardial infarction in depressed patients with type 2 diabetes.

OBJECTIVE: To investigate major depressive disorder (MDD), which complicates the course of type 2 diabetes and is associated with an increased risk of cardiovascular disease and death. This risk may be due to a greater susceptibility for myocardial infarction (MI) in depressed patients with type 2 diabetes compared with nondepressed patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Veterans Administration electronic medical records were analyzed to identify a cohort free of cardiovascular disease in fiscal years 1999 and 2000, aged 25 to 80 years. ICD-9-CM codes were used to create a four-level risk group indicating 1) neither diabetes nor MDD (n = 214,749), 2) MDD alone (n = 77,568), 3) type 2 diabetes alone (n = 40,953), and 4) comorbid MDD and type 2 diabetes (n = 12,679). Age-adjusted Cox proportional hazards models were computed before and after adjusting for baseline sociodemographic and time-dependent covariates. RESULTS: After adjusting for covariates, patients with type 2 diabetes alone and patients with MDD alone were at ∼30% increased risk for MI, and patients with type 2 diabetes and MDD were at 82% increased risk for MI (hazard ratio 1.82 [95% CI 1.69-1.97]) compared with patients without either condition. CONCLUSIONS: Compared with patients with only diabetes or only MDD, individuals with type 2 diabetes and MDD are at increased risk for new-onset MI. Monitoring cardiovascular health in depressed patients with type 2 diabetes may reduce the risk of MI in this especially high-risk group.

Antidepressant drug compliance: reduced risk of MI and mortality in depressed patients.

BACKGROUND: The long-term risk of myocardial infarction (MI) associated with use of antidepressants is uncertain, especially for nontricyclic antidepressants. The present study uses a national Veterans Affairs cohort to test whether antidepressants increase or decrease risk of MI and all-cause mortality. METHODS: US Department of Veterans Affairs patient records were analyzed to identify a cohort free of cardiovascular disease in fiscal years 1999 and 2000, aged 25-80 years, who had an International Classification of Diseases, Ninth Revision, Clinical Modification code indicating an episode of depression (n=93,653). Incident MI and all-cause mortality were modeled in patients who received 12 weeks or more of antidepressant pharmacotherapy as compared with 0-11 weeks during follow-up. Age-adjusted Cox proportional hazard models were computed before and after adjusting for baseline sociodemographics and time-dependent covariates. RESULTS: Receipt of 12 or more weeks of continuous antidepressant therapy was associated with significantly reduced rates of incident MI across classes of antidepressants: selective serotonin reuptake inhibitor (SSRIs) (hazard ratio [HR] 0.48; 95% confidence interval [CI], 0.44-0.52), serotonin-norepinephrine reuptake inhibitors (SNRIs) (HR 0.35; 95% CI, 0.32-0.40), tricyclic antidepressants (TCAs) (HR 0.39; 95% CI, 0.34-0.44), and "Other" (HR 0.41; 95% CI, 0.37-0.45). Risk of all-cause mortality also was decreased with receipt of 12 weeks of pharmacotherapy with all classes of antidepressants (SSRI, SNRI, TCA, Other), with HRs ranging from 0.50 to 0.66. CONCLUSIONS: Across classes of antidepressants, 12 weeks of pharmacotherapy appears to be safe in terms of MI risk. Although the mechanism for this association remains uncertain, it is possible that compliance with pharmacotherapy for depression reflects compliance with cardiovascular medications. It also is possible that a direct drug effect or improved depressed mood may attenuate the risk of MI in depressed patients.

Commentary: the role of mentored internships for systems engineering in improving health care delivery.

The authors advise the adoption of mentored internships in systems engineering, conducted at academic hospitals, directed by physicians, epidemiologists, and health administrators and overseen by faculty at attendant schools of engineering. Such internships are anticipated to directly address the immediate objectives of administrators and clinicians. Additionally, this affords future generations of health care engineers the opportunity to learn the language and methodology of the medical sciences to provide a common ground for the analysis and understanding of medical systems. In turn, this should foster collaboration between the principal stakeholders in health care delivery--practitioners, administrators, engineers, and researchers--in the collective efforts to improve the quality of services provided.

Anxiety disorders increase risk for incident myocardial infarction in depressed and nondepressed Veterans Administration patients.

BACKGROUND: Depression is a risk factor for incident myocardial infarction (MI), but little is known about the independent or additive risk from anxiety disorders. METHODS: In a 7-year retrospective cohort design, we identified a cohort free of cardiovascular disease in fiscal years 1999 and 2000 that contained 96,612 patients between 25 and 80 years of age who had an International Classification of Diseases, Ninth Revision, Clinical Modification code indicating a diagnosis of depression in 2000 (baseline) and 259,387 patients without depression. Cox proportional hazards models stratified by depression were computed to test for a main effect of anxiety disorder unspecified, generalized anxiety disorder, panic disorder, social phobia, obsessive-compulsive disorder, and posttraumatic stress disorder (PTSD) on risk of incident MI. The models were adjusted for multiple MI risk factors and sociodemographics. RESULTS: Depressed as compared to nondepressed Veterans Administration patients were at increased risk for incident MI (HR 1.39; 95% CI 1.34-1.45). In nondepressed patients those with anxiety disorder unspecified (HR 1.34; 95% CI 1.21-1.47), panic disorder (HR 1.43; 95% CI 1.11-1.83), and PTSD (HR 1.25; 95% CI 1.16-1.36) were at increased risk for incident MI. The independent risk associated with anxiety disorders was reduced in patients comorbid for depression. CONCLUSIONS: In Veterans Administration patients free of heart disease in 1999 and 2000, those with depression, anxiety disorder unspecified, panic disorder, and PTSD were at increased risk of incident MI. Anxiety disorders are independent risk factors for MI. Depression partially accounts for the effect of anxiety disorders on risk of MI in patients with both conditions.

Predisposición genética común en la depresión mayor y el trastorno de estrés postraumático en hombres / Common genetic liability to major depression and posttraumatic stress disorder in men

Fundamento: La depresión mayor (DM) y el trastorno de estrés postraumático (TEPT) se caracterizan por su elevada comorbilidad. No se ha cuantificado el grado hasta el cual una predisposición genética común explica la etiología de su asociación y tiene importantes implicaciones para la investigación y la prevención. Métodos: Este artículo presenta un análisis de los datos de 6.744 miembros del Vietnam Era Twin Registry. La DM y el TEPT se evaluaron mediante el Diagnostic Interview Schedule-III-R en 1991–1992. Se efectuó un modelado bivariante de gemelos para determinar la etiología genética y ambiental de la asociación DM-TEPT. Resultados: El modelo con el mejor ajuste de la asociación DM-TEPT incluyó una correlación genética sustancial (r = 0,77; IC95%, 0,50-1,00) y una correlación modesta ambiental específica individual (r = 0,34; IC del 95%, 0,19–0,48). Una predisposición genética común explicó el 62,5% de la comorbilidad DM-TEPT. Las influencias genéticas comunes a la DM explicaron el 15% de la varianza total en el riesgo de TEPT y el 58% de la varianza genética en el TEPT. Las influencias ambientales específicas individuales comunes a la DM solo explicaron el 11% de la varianza ambiental individual específica en el TEPT. Limitaciones: Los participantes del presente estudio eran veteranos de la guerra de Vietnam y los hallazgos no pueden generalizarse a civiles, mujeres u otras cohortes. Conclusiones: La comorbilidad DM-TEPT se explica en gran parte por influencias genéticas comunes. La superposición genética sustancial entre ambos implica que los genes involucrados en la etiología de la DM son potentes candidatos para el TEPT y al contrario. Las influencias ambientales en ambos explican un menor grado su covariación y parecen ser en su mayor parte específicas de trastorno. Se requiere más investigación para identificar los factores ambientales que influyen en el desarrollo de la DM comparado con el TEPT en el contexto de una predisposición genética común (AU)

Background: Major depression (MD) and posttraumatic stress disorder (PTSD) are highly comorbid. The degree to which a common genetic liability explains the etiology of the MD-PTSD association has not been quantified and has important implications or research and prevention. Methods: This paper presents an analysis of data from 6744 members of the Vietnam Era Twin Registry. MD and PTSD were assessed using the Diagnostic Interview Schedule-III-R in 1991–92. Bivariate twin modeling was conducted to determine the genetic and environmental etiology of the MD-PTSD association. Results: The best-fitting model for the MD-PTSD association included a substantial genetic correlation (r = 77; 95% CI, .50–1.00) and a modest individual-specific environmental correlation (r = .34; 95% CI, .19–48). Common genetic liability explained 62.5% of MD-PTSD comorbidity. Genetic influences common to MD explained 15% of the total variance in risk for PTSD and 58% of the genetic variance in PTSD. Individual-specific environmental influences common to MD explained only 11% of the individualspecific environmental variance in PTSD. Limitations: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts. Conclusions: MD-PTSD comorbidity is largely explained by common genetic influences. Substantial genetic overlap between MD and PTSD implies that genes implicated in the etiology of MD are strong candidates for PTSD and vice versa. Environmental influences on MD and PTSD explain less of their covariation and appear to be largely disorder-specific. Research is needed to identify environmental factors that influence the development of MD versus PTSD in the context of common genetic liability (AU)

Depression increases risk of incident myocardial infarction among Veterans Administration patients with rheumatoid arthritis.

OBJECTIVE: This study evaluates whether depression is a risk factor for incident myocardial infarction (MI) in Department of Veterans Affairs (VA) patients with rheumatoid arthritis (RA) between 30 and 79 years of age. METHODS: We used a retrospective cohort study of 15,634 patients with RA. Diagnoses and sociodemographic data were obtained from VA administrative and pharmacy databases between fiscal years 1999 and 2006. Entry into the cohort required 2 years of patient time with no evidence of cardiovascular disease. Cox proportional hazard models with time-dependent covariates were computed to determine whether RA patients with depression as compared to RA patients without depression were at increased risk for MI during the maximum 6-year follow-up period. RESULTS: Unadjusted analyses indicated depressed RA patients were 1.4 times more likely than nondepressed RA patients to have an MI during follow-up. These results remained significant (HR=1.4; 95% CI: 1.1-1.8) in the adjusted Cox proportional hazards model which included the effects of sociodemographics and known physical risks (e.g., diabetes) for MI. CONCLUSIONS: Depressed RA patients, without a history of cardiovascular disease, are 40% more likely to have a heart attack as compared to those without depression. These data demonstrate a rapid (within 6 years) transition to MI following onset of depression in RA patients. Increased monitoring of depression and heart disease status in this patient population may be warranted which in turn may result in longer duration of life.

Genetic and environmental contributions to nicotine, alcohol and cannabis dependence in male twins.

AIMS: To compute the common and specific genetic and environmental contributions to nicotine dependence (ND) alcohol dependence (AD) and cannabis dependence (CD). DESIGN: Twin model. PARTICIPANTS: Data from 1874 monozygotic and 1498 dizygotic twin pair members of the Vietnam Era Twin Registry were obtained via telephone administration of a structured psychiatric interview in 1992. MEASUREMENTS: Data to derive life-time diagnoses of DSM-III-R ND, AD and CD were obtained via telephone administration of the Diagnostic Interview Schedule. FINDINGS: The best-fitting model allowed for additive genetic contributions and unique environmental influences that were common to all three phenotypes. Risks for ND and AD were also due to genetic and unique environmental influences specific to each drug. A specific shared environmental factor contributed to CD. CONCLUSIONS: These results suggest that the life-time co-occurrence of ND, AD and CD is due to common and specific genetic factors as well as unique environmental influences, and vulnerability for CD is also due to shared environmental factors that do not contribute to ND and AD. The majority of genetic variance is shared across drugs and the majority of unique environmental influences are drug-specific in these middle-aged men. Because differences between models allowing for specific genetic versus shared environment were small, we are most confident in concluding that there are specific familial contributions-either additive genetic or shared environment-to CD.

Measured environmental contributions to cannabis abuse/dependence in an offspring of twins design.

Genetic and environmental factors are known to contribute to cannabis abuse/dependence (CAD). We sought to determine the magnitude of the contribution from measured environmental variables to offspring cannabis dependence in a design that controls for familial vulnerability. Data come from a study of 725 twin members of the Vietnam Era Twin Registry, 720 of their biological offspring (age 18-32 years) and 427 mothers. Data were obtained on offspring perception of family and peer support and substance use behaviors and offspring CAD. After adjusting for familial risk, and environmental covariates, CAD was significantly more likely among male offspring (OR=2.73; 95% CI: 1.69-4.41). Offspring CAD was associated with reporting: siblings used illicit drugs (OR=3.40; 95% CI: 1.81-6.38), a few friends used drugs (OR=2.72; 95% CI: 1.04-7.09), a quarter or more friends used drugs (OR=8.30; 95% CI: 3.09-22.33) and one-half or more 12th grade peers used drugs (OR=3.17; 95% CI: 1.42-7.08). Perceived sibling, friend and school peer substance use are strongly associated with CAD in young adults even after accounting for latent familial risk and for multiple measured intra-family and extra-family environmental influences.

Posttraumatic stress disorder; combat exposure; and nicotine dependence, alcohol dependence, and major depression in male twins.

Combat exposure is associated with increased risk of psychiatric and substance use disorders in veterans. However, it is not known whether combat exposure independently increases risk for these disorders or whether this association is accounted for by genetic vulnerability common to posttraumatic stress disorder (PTSD). This article tests competing explanations for the association of combat exposure and PTSD with nicotine dependence (ND), alcohol dependence (AD), and major depression (MD). Data were obtained from 6099 members of the Vietnam Era Twin Registry, a national registry of male-male twin pairs who served in the military during the Vietnam era. Twin models were fit to estimate the genetic and environmental variance common and specific to Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition, lifetime diagnoses of PTSD, combat trauma, and 3 comorbid conditions: ND, AD, and MD. Variance specific to ND, AD, and MD was due to genetic factors (48%, 36%, and 12%, respectively) and unique environmental factors (36%, 42%, and 58%, respectively). After accounting for variance common to PTSD, no residual genetic and environmental variance overlapped between combat and ND, combat and AD, and combat and MD. Combat exposure is not independently associated with lifetime ND, AD, and MD. The association of combat exposure with these 3 disorders is due to genetic and unique environmental contributions in common with PTSD. These findings suggest comorbid PTSD may represent a genetically mediated vulnerability to psychopathology after trauma.

A Latent Class Analysis of DSM-III-R Pathological Gambling Criteria in Middle-Aged Men: Association with Psychiatric Disorders.

PURPOSE: : This study was designed to empirically derive latent classes based on PG criteria and to assess the association between nongambling psychiatric disorders and specific classes. METHODS: : A total of 8138 community-based middle-aged men were surveyed, and 2720 were assessed for Diagnostic Interview Schedule, Version 3, Revised (DIS-III-R) pathologic gambling (PG). Latent class analysis (LCA) was applied to Diagnostic and Statistical Manual Version 3, Revised (DSM-III-R) criteria to identify gambling classes. χ and logistic regression models evaluated the association between gambling classes and lifetime psychiatric disorders. RESULTS: : The final model included 4 classes: class 0 (ie, 5418 individuals who never gambled 25 or more times per year) and classes 1-3 (identified by the LCA and comprising 2720 respondents assessed for PG). For the 9 individual criteria of PG, endorsement percentages ranged from 2%-6%, 4%-58%, and 53%-100% for classes 1-3, respectively. Nongambling psychiatric disorders were differentially associated with the 4 gambling classes, and psychopathology was more common in groups more frequently acknowledging PG criteria. CONCLUSIONS: : Empirical support is provided for distinct classes of gambling behaviors demonstrating differential associations with individual PG criteria and nongambling psychiatric disorders. The data-driven categorization of gambling behaviors provides direction for research on defining, preventing, and treating syndromal and subsyndromal PG.

Common genetic liability to major depression and posttraumatic stress disorder in men.

BACKGROUND: Major depression (MD) and posttraumatic stress disorder (PTSD) are highly comorbid. The degree to which a common genetic liability explains the etiology of the MD-PTSD association has not been quantified and has important implications for research and prevention. METHODS: This paper presents an analysis of data from 6744 members of the Vietnam Era Twin Registry. MD and PTSD were assessed using the Diagnostic Interview Schedule-III-R in 1991-92. Bivariate twin modeling was conducted to determine the genetic and environmental etiology of the MD-PTSD association. RESULTS: The best-fitting model for the MD-PTSD association included a substantial genetic correlation (r=.77; 95% CI, .50-1.00) and a modest individual-specific environmental correlation (r=.34; 95% CI, .19-.48). Common genetic liability explained 62.5% of MD-PTSD comorbidity. Genetic influences common to MD explained 15% of the total variance in risk for PTSD and 58% of the genetic variance in PTSD. Individual-specific environmental influences common to MD explained only 11% of the individual-specific environmental variance in PTSD. LIMITATIONS: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts. CONCLUSIONS: MD-PTSD comorbidity is largely explained by common genetic influences. Substantial genetic overlap between MD and PTSD implies that genes implicated in the etiology of MD are strong candidates for PTSD and vice versa. Environmental influences on MD and PTSD explain less of their covariation and appear to be largely disorder-specific. Research is needed to identify environmental factors that influence the development of MD versus PTSD in the context of common genetic liability.

Training practitioners in evidence-based chronic disease prevention for global health.

Too often, public health decisions are based on short-term demands rather than long-term research and objectives. Policies and programmes are sometimes developed around anecdotal evidence. The Evidence-Based Public Health (EBPH) programme trains public health practitioners to use a comprehensive, scientific approach when developing and evaluating chronic disease programmes. Begun in 2002, the EBPH programme is an international collaboration. The course is organized in seven parts to teach skills in: 1) assessing a community's needs; 2) quantifying the issue; 3) developing a concise statement of the issue; 4) determining what is known about the issue by reviewing the scientific literature; 5) developing and prioritizing programme and policy options; 6) developing an action plan and implementing interventions; and 7) evaluating the programme or policy. The course takes an applied approach and emphasizes information that is readily available to busy practitioners, relying on experiential learning and includes lectures, practice exercises, and case studies. It focuses n using evidence-based tools and encourages participants to add to the evidence base in areas where intervention knowledge is sparse. Through this training programme, we educated practitioners from 38 countries in 4 continents. This article describes the evolution of the parent course and describes experiences implementing the course in the Russian Federation, Lithuania, and Chile. Lessons learned from replication of the course include the need to build a "critical mass" of public health officials trained in EBPH within each country and the importance of international, collaborative networks. Scientific and technologic advances provide unprecedented opportunities for public health professionals to enhance the practice of EBPH. To take full advantage of new technology and tools and to combat new health challenges, public health practitioners must continually improve their skills.

Differential etiology of posttraumatic stress disorder with conduct disorder and major depression in male veterans.

BACKGROUND: Epidemiologic studies reveal that posttraumatic stress disorder (PTSD) is highly comorbid with both conduct disorder and major depression in men. The genetic and environmental etiology of this comorbidity has not been examined. METHODS: Data were analyzed from 6744 middle-aged male-male monozygotic and dizygotic twins from the Vietnam Era Twin Registry. Conduct disorder, major depression, and PTSD were assessed via telephone interview using the Diagnostic Interview Schedule for the DSM-III-R in 1992. Structural equation modeling was used to estimate additive genetic, shared environmental, and individual-specific environmental effects common and specific to conduct disorder, major depression, and PTSD. RESULTS: The association between conduct disorder and PTSD was explained primarily by common shared environmental influences; these explained 10% (95% confidence interval: 6%-17%) of the variance in PTSD. The association between major depression and PTSD was largely explained by common genetic influences; these explained 19% (95% confidence interval: 11%-26%) of the variance in PTSD. CONCLUSIONS: Our findings suggest that different etiologic mechanisms explain the association of conduct disorder and major depression with PTSD in male veterans. If replicated in other populations, results suggest research aimed at identifying specific genetic and environmental factors that influence PTSD may benefit from starting with those that have been more consistently and strongly associated with major depression and conduct disorder.

Common genetic risk of major depression and nicotine dependence: the contribution of antisocial traits in a United States veteran male twin cohort.

Many studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

Nicotine dependence subtypes: association with smoking history, diagnostic criteria and psychiatric disorders in 5440 regular smokers from the Vietnam Era Twin Registry.

Studies suggest empirically derived subtypes of nicotine dependence exist in young adult populations with short smoking careers. It is not known if classes of dependence exist in middle aged smokers with longer smoking careers and whether these classes reflect quantitative or qualitative differences. It is not known if psychiatric disorders are associated with classes of nicotine dependence. Nicotine dependence symptoms were obtained from a 1992 administration of the Diagnostic Interview Schedule. Latent Class Analyses (LCA) was computed using data from 5440 members of the Vietnam Era Twin Registry. LCA was used to derive significantly different classes of nicotine dependence, which were assessed for their association with smoking history, nicotine dependence, and other psychiatric disorders. The LCA model which best fit the data was a 4 class solution characterized by severity. Age onset of regular smoking decreased with more severe classes. Cigarette consumption, failed cessation and psychiatric disorders were associated with more severe classes. Empirically derived subtypes of nicotine dependence are mostly characterized by increasing severity. Suggestions for refinement of nicotine dependence diagnostic criteria are discussed.

Evidence for specificity of transmission of alcohol and nicotine dependence in an offspring of twins design.

Alcohol dependence (AD) and nicotine dependence (ND) have been shown to co-occur. Results from twin studies implicate the role of genetics in the etiology of both ND and AD with substantial, yet incomplete, overlap. To test for specificity of transmission of AD and ND in an offspring of twins sample we analyzed data from a study of adolescent and adult offspring of twin fathers ascertained from the Vietnam Era Twin Registry. This sample consists of 1213 twin fathers, 862 biologic or rearing mothers, and 1270 offspring. Offspring were allocated to one of four risk groups for AD based on twin fathers' zygosity and father's and cotwins AD history. Offspring DSM-IV AD and ND were measured by structured diagnostic interview. Paternal AD and ND were significantly associated with offspring AD and ND, respectively. Bivariate probit regression results suggest specificity for transmission of AD and ND. This remained constant after controlling for offspring demographics and psychopathology and maternal AD and ND. Despite the substantial genetic overlap between the two disorders, there is evidence for genetic effects specific for AD and ND.

Exposure to paternal alcoholism does not predict development of alcohol-use disorders in offspring: evidence from an offspring-of-twins study.

OBJECTIVE: 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). METHOD: 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. RESULTS: 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. CONCLUSIONS: 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.

Adolescent alcohol use is a risk factor for adult alcohol and drug dependence: evidence from a twin design.

BACKGROUND: Early alcohol use is associated with abuse and dependence of licit and illicit substances later in life. The role of genetic and environmental factors in this association is not conclusive. METHOD: In 1992, data on substance use, abuse/dependence and psychiatric disorders were collected from 8169 male twin members of the Vietnam Era Twin Registry. The interview obtained age of onset of regular drinking (one drink/month for 6 or more months). Regression analyses of twin pairs discordant for early alcohol use tested whether the association between early drinking (before age 17) and adult substance use and abuse/dependence remained after controlling for genetic factors, family environment and covariates. Twin models tested for common genetic and/or environmental influences on early drinking and adult alcohol dependence and ever use and abuse/dependence on marijuana and other drugs. RESULTS: Co-twin analyses suggested the association between early regular alcohol use and adult alcohol dependence, marijuana and other drug use, and marijuana and other drug abuse/dependence could not be entirely explained by common genetic and shared family environmental factors. Genetic contributions to early regular drinking were significantly correlated with those on use of marijuana (rA=0.59), use of other drugs (rA=0.64), alcohol dependence (rA=0.54) and abuse/dependence of marijuana and other drugs (rA=0.63 and 0.66). Small but significant unique environmental correlations (rE range 0.11-0.22) indicated that familial factors could not entirely explain the association between early alcohol use and later substance use, abuse and dependence. CONCLUSIONS: Early regular drinking is associated with later alcohol dependence and use, abuse/dependence on drugs. The association is not entirely explained by genetic or shared family environmental factors. This suggests unique environmental factors contribute to transitions from early regular alcohol drinking to use, abuse and dependence on alcohol and other substances.

Heritability of SF-36 among middle-age, middle-class, male-male twins.

OBJECTIVE: We sought to examine the relative importance of genetic and environmental factors for the MOS SF-36; a widely used, valid, and reliable measure of health-related quality of life and to discuss incorporating genetic influences into health services research. DATA SOURCES: Data are from a nationally distributed, nonclinical cohort of 2928 middle age, middle-class, male-male twin members of the Vietnam Era Twin Registry. STUDY DESIGN: This was a secondary data analysis, classic twin heritability analysis. DATA COLLECTION: A telephone survey was used to collect information on alcohol-related problems and health services use, including the SF-36. PRINCIPAL FINDINGS: Variance component analyses indicated that additive genetic factors accounted for 17% to 33% of the variance for each of the 8 domains of the SF-36. Shared environment accounted for 0% to 12% of the variance for each domain, with the majority of variance for each domain accounted for by nonshared, or unique environment and error. Physical and mental health summary measures indicated that approximately one-third of the variance was accounted for by additive genetic factors and the remainder accounted for by nonshared environment and error. Clinical condition, history of alcohol dependence, had a small-but-significant influence for all domains. Including condition proved to be a better-fitting model. However, confidence intervals temper uniform statistical significance for genetic factors. CONCLUSIONS: This study assessed the heritability of the SF-36 in a nonclinical, community sample of middle age, middle-class all-male twins. The moderate genetic effects on SF-36 domain and summary measures are new findings and thus may affect interpretations of SF-36 as a measure of health-related quality of life. Ideally, trait-based measures should identify genetic sources of variation and thus help understand any bias of the true effects of SF-36. Still the majority of variance is accounted for by nonshared or unique environmental factors and error. By extension, increased understanding of the importance of genetic and environmental factors that influence either predictors or outcomes of interest will expand the level of scientific debate in health services research and improve predictability.