Apolipoprotein E genotype and memory in the sixth decade of life.

BACKGROUND: Virtually all adult studies of APOE genotypes and cognition have included individuals over 60. In older adults, epsilon 4 carriers may manifest greater cognitive asymmetries than non-epsilon 4 carriers even in the absence of overall mean differences. General cognitive ability may also be affected by aging and APOE genotype, but most studies have inadequately addressed this potential confound. The goals of this study were to examine, in middle age, the relationship of APOE genotype with episodic memory and verbal-visuospatial episodic memory asymmetries, after accounting for prior general cognitive ability. METHOD: We compared epsilon 4+ and epsilon 4- individuals in 626 male twins in their 50s. We examined verbal and visuospatial episodic memory and verbal-visual asymmetry scores after adjusting for cognitive ability at age 20. Analyses corrected for correlations between twin pair members. RESULTS: Compared with epsilon 4- individuals, epsilon 4 carriers performed significantly more poorly on verbal, but not visuospatial memory, manifested significantly greater cognitive asymmetry, and also had significantly more concerns about memory. At age 20, epsilon 4 carriers had higher general cognitive ability than epsilon 4- individuals, and current memory differences were enhanced after adjusting for age 20 cognitive ability. CONCLUSIONS: Small, but significant, APOE-epsilon 4-related memory deficits appear in the sixth decade of life in individuals who show no signs of preclinical dementia. The results partially support studies of older adults that suggest that increased cognitive asymmetries reflect risk for dementia and are associated with the APOE-epsilon 4 genotype. The results also highlight the potential problems of not having accurate data on prior cognitive ability.

Cardiac magnetic resonance imaging abnormalities in systemic lupus erythematosus: a preliminary report.

The purpose of this prospective, pilot study was to determine whether differences in myocardial T2 relaxivity can be identified among active systemic lupus erythematosus (SLE) patients with clinically suspected SLE myocarditis, other active SLE patients, inactive SLE patients and age and gender matched controls. Eleven consecutive female patients (six with active SLE and five with inactive SLE), and five age, gender and race matched healthy controls underwent imaging with echocardiography and cardiac magnetic resonance imaging (MRI). Echocardiographic measurements included left ventricular end diastolic (LVEDV) and end systolic volumes (LVESV), and mass (LVM) (all indexed to body mass); ejection fraction and cardiac output. The cardiac MRI measurement was the T2 relaxation time (an index of soft tissue signal, with higher levels suggestive of increased tissue water content). Patients with active SLE had significantly higher LVEDV and LVM than inactive SLE patients and healthy controls, and significantly larger LVESV than healthy controls. Myocardial T2 relaxation times were significantly higher in patients with active SLE compared to those with inactive SLE and to healthy controls, and remained higher even after excluding the two active SLE patients who had clinical myocarditis. The four active SLE patients who underwent repeat cardiac imaging studies after clinical improvement showed normalization of these myocardial abnormalities. The conclusion was that active SLE patients demonstrate abnormalities in myocardial structure manifested by high myocardial T2 relaxation times that normalized after clinical improvement in disease activity. These findings suggest that T2 relaxation values are a sensitive indicator of myocardial disease in patients with SLE and that myocardial T2 relaxation abnormality frequently occur in patients with active SLE, even in the absence of myocardial involvement by clinical criteria.

Clinical and laboratory assessment of distal peripheral nerves in Gulf War veterans and spouses.

BACKGROUND: The prevalence of symptoms suggesting distal symmetric polyneuropathy (DSP) was reported to be higher among deployed veterans (DV) to the Persian Gulf in 1990-1991 than to control non-deployed veterans (NDV). The authors therefore compared the prevalence of DSP by direct examination of DV and their spouses to control NDV and spouses. METHODS: The authors performed standardized neurologic examinations on 1,061 DV and 1,128 NDV selected from a cohort of veterans who previously participated in a national mail and telephone survey. Presence of DSP was evaluated by history, physical examination, and standardized electrophysiologic assessment of motor and sensory nerves. Similar examinations were performed without electrophysiologic tests in 484 DV spouses and 533 NDV spouses. Statistical analyses were performed with appropriate adjustments for the stratified sampling scheme. RESULTS: No differences between adjusted population prevalence of DSP in DV and NDV were found by electrophysiology (3.7% vs 6.3%, p = 0.07), by neurologic examination (3.1% vs 2.6%, p = 0.60), or by the methods combined (6.3% vs 7.3%, p = 0.47). Excluding veterans with non-military service related diseases that may cause DSP did not alter outcomes. DV potentially exposed to neurotoxins from the Khamisiyah ammunition depot explosion did not significantly differ in DSP prevalence compared to non-exposed DV. The prevalence of DSP in DV spouses did not differ from NDV spouses (2.7% vs 3.2%, p = 0.64). CONCLUSIONS: Neither veterans deployed during the Gulf War era nor their spouses had a higher prevalence of DSP compared to NDV and spouses.

A twin study of genetic and environmental influences on suicidality in men.

BACKGROUND: Previous studies that have examined genetic influences on suicidal behaviour were confounded by genetic vulnerability for psychiatric risk factors. The present study examines genetic influences on suicidality (i.e. suicidal ideation and/or suicide attempt) after controlling for the inheritance of psychiatric disorders. METHODS: Sociodemographics, combat exposure, lifetime DSM-III-R major depression, bipolar disorder, childhood conduct disorder, adult antisocial personality disorder, panic disorder, post-traumatic stress disorder, drug dependence, alcohol dependence and lifetime suicidal ideation and attempt were assessed in 3372 twin pairs from the Vietnam Era Twin Registry who were assessed in 1987 and 1992. Genetic risk factors for suicidality were examined in a multinomial logistic regression model. Additive genetic, shared environmental and non-shared environmental effects on suicidality were estimated using structural equation modelling, controlling for other risk factors. RESULTS: The prevalence of suicidal ideation and suicide attempt were 16.1% and 2.4% respectively. In a multinomial regression model, co-twin's suicidality, being white, unemployment, being other than married, medium combat exposure and psychiatric disorders were significant predictors for suicidal ideation. Co-twin's suicidality, unemployment, marital disruption, low education attainment and psychiatric disorders (except childhood conduct disorder) were significant predictors for suicide attempt. Model-fitting suggested that suicidal ideation was influenced by additive genetic (36%) and non-shared environmental (64%) effects, while suicide attempt was affected by additive genetic (17%), shared environmental (19%) and non-shared environmental (64%) effects. CONCLUSIONS: There may be a genetic susceptibility specific to both suicidal ideation and suicide attempt in men, which is not explained by the inheritance of common psychiatric disorders.

A twin study of generalized anxiety disorder symptoms, panic disorder symptoms and post-traumatic stress disorder in men.

Generalized anxiety disorder (GAD), panic disorder (PD) and post-traumatic stress disorder (PTSD) often co-occur. We investigated whether and to what degree genetic and environmental contributions overlap among symptoms of GAD, symptoms of PD and PTSD. Subjects were 3327 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of GAD symptoms, PD symptoms and PTSD. The liability for GAD symptoms was due to a 37.9% additive genetic contribution common to PD symptoms and PTSD. Liability for PD symptoms was due to a 20.7% additive genetic contribution common to GAD symptoms and PTSD, and a 20.1% additive genetic influence specific to PD symptoms. Additive genetic influences common to symptoms of GAD and PD accounted for 21.3% of the genetic variance in PTSD. Additive genetic influences specific to PTSD accounted for 13.6% of the genetic variance in PTSD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that these disorders each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

The genetics of pathological gambling.

Problem and pathological gambling (PG) occurs in about 5% of Americans. Gambling is associated with substantial psychosocial and psychiatric health problems, and the increasing ease of access to gambling may increase its future prevalence. Therefore, it is important to gain greater insight into the causes of PG. Family studies of PG are consistent with a substantial familial impact on vulnerability to PG. However, family studies cannot distinguish genetic from family environmental influences. By contrast, the study of twin pairs permits the genetic and environmental influences on PG to be estimated. The study of gambling behavior among 3,359 twin pair members of the Vietnam Era Twin Registry suggests that: (1) inherited factors explain a substantial proportion of the variance in the report of symptoms of gambling; (2) there is a single continuum of genetic vulnerability that underlies gambling problems of varying severities; and, (3) the co-occurrence of PG with conduct disorder, antisocial personality disorder, and alcohol abuse/dependence is partially explained by genes that influence both PG and these other psychiatric disorders. Neurophysiological correlates of gambling problems and genetically based differences in neurotransmitter systems may provide biological mechanisms that explain the genetic basis for a predisposition to PG.

Heritability of self-reported health.

OBJECTIVE: To explore the contribution of genes and environmental factors to variation in a common measure (i.e., a five-point--excellent, very good, good, fair, and poor--Likert scale) of self-reported health. DATA SOURCES: Data were analyzed from 4,638 male-male twin pair members of the Vietnam Era Twin (VET) Registry who responded to a 1987 health survey. STUDY DESIGN: Varying models for the relationship between genetic and environmental influences on self-reported health were tested in an attempt to explain the relative contributions of additive genetic, shared and nonshared environmental effects, and health conditions reported since 1975 to perceived health status. DATA COLLECTION: A mail and telephone survey of health was administered in 1987 to VET Registry twins. PRINCIPAL FINDINGS: Variance component estimates under the best-fitting model included a 39.6 percent genetic contribution to self-reported health. In a model which included the effect of health condition, genes accounted for 32.5 percent and health condition accounted for 15.0 percent of the variance in self-reported health. The magnitude of the genetic contribution to perceived health status was not significantly different in a model with or without health condition. CONCLUSIONS: These data suggest over one-third of the variability of self-reported health can be attributed to genes. Since perceived health status is a major predictor of morbidity, mortality, and health services utilization, future analyses should consider the role of heritable influences on traditional health services variables.

Genetic and environmental influences on posttraumatic stress disorder, alcohol and drug dependence in twin pairs.

We investigated whether and to what degree genetic and environmental contributions overlap among posttraumatic stress disorder (PTSD), alcohol dependence (AD) and drug dependence (DD). Subjects were 3304 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS-3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of DSM-III-R PTSD, AD and DD. The liability for PTSD was partially due to a 15.3% genetic contribution common to AD and DD and 20.0% genetic contribution specific to PTSD. Risk for AD was partially due to a 55.7% genetic contribution common to PTSD and DD. Genetic influences common to PTSD and AD accounted for 25.2% of the total risk for DD. Specific family environmental influence accounted for 33.9% of the total variance in risk for DD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that PTSD, AD and DD each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Improving residents' compliance with standards of ambulatory care: results from the VA Cooperative Study on Computerized Reminders.

CONTEXT: Computerized systems to remind physicians to provide appropriate care have not been widely evaluated in large numbers of patients in multiple clinical settings. OBJECTIVE: To examine whether a computerized reminder system operating in multiple Veterans Affairs (VA) ambulatory care clinics improves resident physician compliance with standards of ambulatory care. DESIGN, SETTING, AND PARTICIPANTS: A total of 275 resident physicians at 12 VA medical centers were randomly assigned in firms or half-day clinic blocks to either a reminder group (n = 132) or a control group (n = 143). During a 17-month study period (January 31, 1995-June 30, 1996), the residents cared for 12,989 unique patients for whom at least 1 of the studied standards of care (SOC) was applicable. MAIN OUTCOME MEASURES: Compliance with 13 SOC, tracked using hospital databases and encounter forms completed by residents, compared between residents in the reminder group vs those in the control group. RESULTS: Measuring compliance as the proportion of patients in compliance with all applicable SOC by their last visit during the study period, the reminder group had statistically significantly higher rates of compliance than the control group for all standards combined (58.8% vs 53.5%; odds ratio [OR], 1.24; 95% confidence interval [CI], 1.08-1.42; P =.002) and for 5 of the 13 standards examined individually. Measuring compliance as the proportion of all visits for which care was indicated in which residents provided proper care, the reminder group also had statistically significantly higher rates of compliance than the control group for all standards combined (17.9% vs 12.2%; OR, 1.57; 95% CI, 1.45-1.71; P<.001) and for 9 of the 13 standards examined individually. The benefit of reminders, however, declined throughout the course of the study, even though the reminders remained active. CONCLUSIONS: Our data indicate that reminder systems installed at multiple sites can improve residents' compliance to multiple SOC. The benefits of such systems, however, appear to deteriorate over time. Future research needs to explore methods to better sustain the benefits of reminders. JAMA. 2000;284:1411-1416.

Evidence for genetic influences common and specific to symptoms of generalized anxiety and panic.

BACKGROUND: Generalized anxiety disorder (GAD) and panic disorder (PD) often co-occur and have been shown to be heritable. Researchers have debated the validity of the distinction between GAD and PD. To test for distinction between disorders, we estimated the genetic and environmental contributions which were specific and common to GAD and PD in a cohort of male-male twin pairs. METHODS: Data were obtained from a telephone interview performed in 1992 utilizing the Diagnostic Interview Schedule Version 3-Revised. Interviews were administered to 6724 male-male monozygotic and dizygotic twin pair members of the Vietnam Era Twin Registry. We defined lifetime GAD by the report of six or more DSM-III-R symptoms and lifetime PD by the report of four or more DSM-III-R symptoms. RESULTS: The lifetime co-occurrence of GAD and PD was best explained by a model which did not include family environmental influences. The variance in risk for GAD was due to a 37.9% influence from additive genetic factors with the remainder due to unique environmental influences. The variance in risk for PD was due to a 22.6% additive genetic contribution which was common with GAD and a 21.2% non-additive genetic contribution specific to PD with the remainder of variance in risk for PD due to unique environmental influences. LIMITATIONS: Results may be limited to middle aged males. Model fitting with full diagnostic criteria was not possible due to low prevalences. CONCLUSIONS: Our data suggest a distinction in liability for GAD versus PD. The common genetic influence to GAD and PD may partially account for the risk of the co-occurrence of these disorders in a lifetime.

Self-Reported zygosity and the equal-environments assumption for psychiatric disorders in the Vietnam Era Twin Registry.

The equal-environments assumption (EEA) in twin studies of psychiatric disorders assumes that the family environment which contributes to risk for a disorder is equally correlated between monozygotic (MZ) and dizygotic (DZ) twin pairs. In a study of psychiatric disorders in female twins, Kendler and colleagues (1993) have demonstrated the utility of a test of the EEA which includes a specified family environmental factor defined by using measures of perceived zygosity. We tested the EEA assumption among 3155 male-male twin pair members of the Vietnam Era Twin Registry for the following DSM-III-R lifetime disorders: alcohol dependence, marijuana dependence, any illicit drug dependence, nicotine dependence, major depression, and posttraumatic stress disorder. The majority of MZ (81.6%; n = 1593) and DZ (90.2%; n = 1086) twin pairs agreed with the investigator's assigned zygosity. The best-fitting model for each of these disorders did not allow for a specified family environmental influence. These results support the usefulness of perceived zygosity in tests of the EEA. In male twin pairs, perceived zygosity has little impact on twin similarity for common psychiatric disorders.

The impact of sociodemographics, comorbidity and symptom recency on health-related quality of life in alcoholics.

OBJECTIVE: To obtain estimates of the relationship between alcoholism and health-related quality of life (HRQL) in twin pairs discordant for alcohol dependence. METHOD: In 1995, 1,258 male-male twin pair members of the Vietnam Era Twin Registry (total Registry N = 7.375 pairs) were administered a modified Medical Outcomes Study 36 Item Short Form (SF-36) and the Diagnostic Interview Schedule (DIS) to obtain measures of HRQL and a DSM-III-R criteria lifetime diagnosis of alcohol dependence. Mean within pair differences on eight separate SF-36 subscales were calculated for 436 remitted (no alcohol symptoms in the past 5 years) alcohol-dependent discordant twin pairs and for 194 recent (at least one alcohol symptom in the past 5 years) alcohol-dependent discordant pairs before and after adjustment for covariates. Covariates included lifetime physical illness, lifetime psychiatric disorders, lifetime drug dependence, lifetime nicotine dependence, current marital status, current income and severity. RESULTS: In the unadjusted analysis remitted alcoholic twins compared to their nonalcoholic co-twins reported significantly lower mean scores for six of eight SF-36 subscales. Recent alcoholic twins, compared to their nonalcoholic co-twins, reported significantly lower mean scores for all of the SF-36 subscales. However, after simultaneous adjustment for all covariates, no SF-36 subscale mean, except "vitality" among recent alcoholic twins, was significantly different between alcoholic twins and their nonalcoholic co-twins. CONCLUSIONS: Differences in HRQL between alcoholic and nonalcoholic co-twins is due to covariation from physical and psychiatric problems, drug and nicotine dependence, marital status, income and severity.

Interrelationship of genetic and environmental influences on conduct disorder and alcohol and marijuana dependence symptoms.

Data from the Vietnam Era Twin (VET) Registry were analyzed to explore the degree to which the same genetic and environmental factors contribute to childhood conduct disorder symptoms and to alcohol and marijuana dependence symptoms. Data on conduct disorder and alcohol and marijuana dependence were obtained from administration of the Diagnostic Interview Schedule to 1,856 monozygotic and 1,479 dizygotic male-male twin pair members of the VET Registry. Multivariate genetic models were compared to determine the genetic and environmental influences common and or specific to all three phenotypes. A full model that allowed for common genetic and environmental influences to all three phenotypes gave a good fit to the data, but the best fitting reduced model did not allow for a genetic influence on conduct disorder symptoms. Under the best fitting reduced model, genes explained 44.7% of the variance in risk for alcohol dependence symptoms. The genetic liability for symptoms of marijuana dependence was due to a 36.3% specific contribution and a 7.6% contribution from genes common with alcohol dependence symptoms. Family environmental contributions common to all three phenotypes explained 46.7%, 11.9%, and 21.3% of variance in risk for symptoms of conduct disorder, alcohol dependence, and marijuana dependence, respectively. Common family environmental factors contribute to risk of conduct disorder symptoms and alcohol and marijuana dependence symptoms. Common genetic influences contribute to risk of symptoms of alcohol dependence and marijuana dependence. While our findings suggest genes do not contribute to co-morbid conduct disorder symptoms, comparisons with other twin studies suggest that the role of genes in risk for conduct disorder remains uncertain.

Common genetic vulnerability for nicotine and alcohol dependence in men.

BACKGROUND: Nicotine and alcohol dependence often occur together. We examined data from male twin pairs to determine whether there are genetic or environmental influences common to nicotine and alcohol dependence, and, if so, to estimate the magnitude and correlation of these influences. METHODS: Subjects were 3356 male-male twin-pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised. Genetic model fitting was performed to estimate the magnitude and correlation of genetic and environmental contributions to lifetime nicotine and alcohol dependence. RESULTS: The heritability of nicotine dependence was 60.3% (95% confidence interval [CI], 55.4%-65.2%); that of alcohol dependence, 55.1% (95% CI, 49.7%-60.5%). The best-fitting model for the co-occurrence of lifetime nicotine and alcohol dependence included a substantial genetic correlation between both disorders (r = 0.68; 95% CI, 0.61-0.74) and a modest unique environmental correlation (r = 0.23; 95% CI, 0.14-0.32). CONCLUSIONS: These data suggest a common genetic vulnerability to nicotine and alcohol dependence in men. This common genetic influence may partially explain the clinical and epidemiological observations that alcoholics are often dependent smokers.

The heritability of alcoholism symptoms: "indicators of genetic and environmental influence in alcohol-dependent individuals" revisited.

There is consistent evidence from twin and adoption studies implicating genetic factors in the etiology of alcoholism, yet few studies have examined the role of genetic influences on individual symptoms of alcoholism. In a previous study of 113 male twins, Johnson et al. (1996a) identified 7 alcoholism symptoms that were more "genetic" and 14 that were more "environmental" (that is, non-genetic) in their etiology by examining symptom concordances among monozygotic and dizygotic twin pairs. The present study represents an attempt to replicate the results of this previous study and extend them by estimating the contribution of genetic factors to the variation in liability for different alcoholism symptoms. Subjects were 3356 male twin pairs from the Vietnam Era Twin Registry. Lifetime histories of alcoholism symptoms were assessed by a structured psychiatric telephone interview. The results of the previous study were not replicated. The correlations between symptom classifications as genetic and non-genetic in the present and previous study were nonsignificant and ranged from -0.27 to 0.11. However, within the present study the correlation between symptom classifications as genetic and non-genetic was statistically significant across random split-half subsamples (r = 0.59); nine alcoholism symptoms were consistently classified as genetic and six symptoms as non-genetic in their etiology. Model-fitting analyses applied to different alcoholism symptoms yielded heritability estimates ranging from 0.03 to 0.53 with broad and overlapping confidence intervals around these estimates, ranging from 0.00 to 0.65. The results of this study highlight the difficulty of identifying more or less heritable phenotypes in twin research, and suggest that it may not be possible to identify specific alcoholism symptoms that are more genetic in their etiology than others. Nevertheless, there appears to be potentially important variation in the relative magnitude of genetic influences for individual alcoholism symptoms, and exploring these differences may lead to further insights into the nosology and etiology of alcohol-related problems.

Sociodemographic and health status characteristics with prostate cancer screening in a national cohort of middle-aged male veterans.

OBJECTIVES: To characterize variables associated with obtaining prostate cancer screening in a nonclinical, nationally distributed, middle-aged male population. METHODS: Telephone interviews were administered to 2652 individual members of the Vietnam Era Twin Registry in 1992 and 1995. Dependent variables were self-report measures of having had a digital rectal examination (DRE) and/or a prostate-specific antigen (PSA) test in the past 5 years. Independent variables were current measures of age, household income, education, race, insurance, source of care, and lifetime measures of physical condition, psychiatric illness, and alcohol and nicotine dependence. RESULTS: Thirty-five percent of the sample reported having had a PSA and DRE within the past 5 years. Prevalence of obtaining either a PSA or DRE varied with age, income, education, and race. Subjects with a regular source of care, a regular physician, and health insurance reported higher rates of having had a DRE or PSA and DRE. Persons with a physical or psychiatric illness reported more screening. A multiple regression model revealed that having a regular source of care, having a regular physician, physical illness, psychiatric illness, minority status, higher income, and age predicted having had some form of screening. CONCLUSIONS: A substantial portion of middle-aged men have had both a PSA and DRE performed at least once in the preceding 5 years. It may be possible to further improve prostate cancer screening participation by directing educational programs at men who are not in contact with the healthcare system. If the PSA and DRE screening guidelines that are finally adopted discourage screening among low-risk men younger than age 50, educational programs that emphasize age screening criteria may be warranted.

Co-occurrence of abuse of different drugs in men: the role of drug-specific and shared vulnerabilities.

BACKGROUND: Previous research has demonstrated genetic and environmental influences on abuse of individual substances, but there is less known about how these factors may influence the co-occurrence of abuse of different illicit drugs. METHODS: We studied 3372 male twin pairs from the Vietnam Era Twin Registry. They were interviewed using the Diagnostic Interview Schedule, Version III, Revised to investigate the extent to which the abuse of different categories of drugs occurs together within an individual, as well as the possibility that genetic and environmental factors are responsible for observed co-occurrence. Co-occurrence was quantified using odds ratios and conditional probabilities. Multivariate biometrical modeling analyses were used to assess genetic and environmental influences on co-occurrence. RESULTS: Abusing any category of drug was associated with a marked increase in the probability of abusing every other category of drugs. We found evidence for a shared or common vulnerability factor that underlies the abuse of marijuana, sedatives, stimulants, heroin or opiates, and psychedelics. This shared vulnerability is influenced by genetic, family environmental, and nonfamily environmental factors, but not every drug is influenced to the same extent by the shared vulnerability factor. Marijuana, more than other drugs, was influenced by family environmental factors. Each category of drug, except psychedelics, had genetic influences unique to itself (ie, not shared with other drug categories). Heroin had larger genetic influences unique to itself than did any other drug. CONCLUSION: There are genetically and environmentally determined characteristics that comprise a shared or common vulnerability to abuse a range of illicit drugs.

Contribution of emotionally traumatic events and inheritance to the report of current physical health problems in 4042 Vietnam era veteran twin pairs.

OBJECTIVE: To determine the contributions of psychological trauma (exposure to combat during the Vietnam War), genetic factors, childhood experiences shared by twin siblings, and unmeasured experiences not shared by twin siblings to the reporting of current physical health problems a mean of 19 years after military service. METHODS: In 1987, a national sample of 2224 monozygotic and 1818 dizygotic male veteran members of the Vietnam Era Twin Registry participated in a survey of health. Genetic modeling was performed on cross-sectional physical health and combat exposure data derived from Registry twins. RESULTS: Combat experiences explained a small proportion (0.7-8.4%) of the variance in the report of hypertension, respiratory conditions, persistent skin conditions, gastrointestinal disorders, joint disorders, and hearing problems. Childhood experiences shared by siblings are not clearly related to any health problem studied. By contrast, genetic factors explain 31 to 54% and noncombat experiences not shared by siblings explain 45 to 66% of the variance in current physical health status. CONCLUSIONS: Greater than 90% of the variance in reported current physical health problems in Vietnam era veterans is attributable to inherited factors and unmeasured environmental experiences not shared by twin siblings. The traumatic experience of combat makes only a small contribution to the report of current physical health problems. These results do not preclude the possibility that combat influenced the prevalence of illness shortly after military service or that combat may influence the development of illness in the future.

Long-term reliability and validity of alcoholism diagnoses and symptoms in a large national telephone interview survey.

The long-term reliability and validity of telephone lay interview assessments of alcoholism were examined in the context of a large national community-based survey of over 8,000 male Vietnam era veterans. A subsample of 146 men was interviewed twice by telephone using the same structured interview an average of 15 months apart to evaluate the long-term reliability of alcoholism symptoms and diagnoses. In addition, a search of Department of Veterans Affairs patient treatment files of inpatient hospitalizations between 1970 and 1993 yielded a subsample of 89 interviewed men with a past discharge diagnosis of alcohol dependence. The test-retest reliability of alcohol abuse and alcohol dependence diagnoses was good, with kappa coefficients of 0.74 and 0.61, respectively. The reliability of individual alcoholism symptoms was fair to good, with kappas of 0.46 to 0.67. Ninety-six percent of individuals identified by Department of Veterans Affairs patient treatment files as having an alcohol dependence diagnosis were correctly diagnosed by the telephone interview. The results of the present study provide additional evidence for the long-term reliability and validity of lifetime alcoholism diagnoses, and suggest that the reliability and validity of telephone interview assessments of alcoholism are as good as that of an in-person interview. Telephone administration of structured psychiatric interviews appears to be an attractive alternative to in-person interviewing for gathering information about alcoholism and alcohol-related problems.

A registry-based twin study of depression in men.

BACKGROUND: The only large, registry-based twin study of depression using diagnostic criteria assessed by structured interview included only women. We present results from a comparable study of men. METHODS: Data were collected using a standardized telephone interview of men from the Vietnam Era Twin Registry. Both twins from 3372 pairs participated. Proband-wise concordance rates and biometric modeling were used to analyze the data. RESULTS: The diagnosis of major depression (MD), as defined by DSM-III-R, and the subtype of severe/psychotic MD were significantly affected by genetic (h2=0.36 and 0.39, respectively) and nonshared environmental (e2=0.64 and 0.61, respectively) factors but not by family environmental factors. Dysthymia and mild and moderate MD were affected by family environmental (c2=0.27, 0.08, and 0.14, respectively) and nonshared environmental (e2=0.73, 0.92, and 0.86, respectively) factors but not by genetic factors. Early-onset (before age 30 years) and late-onset (after age 30 years) MD were significantly affected by genetic (h2=0.47 and 0.10, respectively) and nonshared environmental (e2=0.53 and 0.90, respectively) factors. Early-onset MD was significantly more heritable than late-onset MD. CONCLUSIONS: The magnitude of genetic and environmental effects on depression in men is similar to that previously reported in women. Also similar to previous findings, more severe and earlier-onset depression may be more strongly affected by genetic factors, but differences in the reliability of reports of depression associated with severity may inflate estimates of the effect of the unique environment and deflate heritability estimates for less severe depression.