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Articles by K. S Kendler
Total Records ( 5 ) for K. S Kendler
  K. S Kendler and J. Myers

OBJECTIVE: Church attendance is one of the most consistent predictors of alcohol and nicotine consumption. The authors sought to clarify changes in the role of genetic and environmental factors in influencing church attendance and the interrelationship between church attendance and alcohol and nicotine use from early adolescence into adulthood. METHOD: The authors used data from two interview waves 6 years apart of 1,796 male twins from a population-based register, in which respondents were asked about current and past church attendance and psychoactive drug use. Structural twin models were fitted and tested using the Mx software program. RESULTS: As twins developed from childhood through adulthood, the influence of shared environmental factors on church attendance declined dramatically while genetic factors increased. In early and late adolescence, the negative correlations between church attendance and alcohol and nicotine consumption resulted largely from shared environmental factors. In adulthood, the inverse relationship between church attendance and substance use became stronger and arose largely from genetic factors. CONCLUSIONS: As individuals mature, they increasingly shape their own social environment in large part as a result of their genetically influenced temperament. When individuals are younger and living at home, frequent church attendance reflects a range of familial and social-environmental influences that reduce levels of substance use. In adulthood, by contrast, high levels of church attendance largely index genetically influenced temperamental factors that are protective against substance use. Using genetically informative designs such as twin studies, it is possible to show that the causes of the relationship between social risk factors and substance use can change dramatically over development.

  A. R Sanders , D. F Levinson , J Duan , J. M Dennis , R Li , K. S Kendler , J. P Rice , J Shi , B. J Mowry , F Amin , J. M Silverman , N. G Buccola , W. F Byerley , D. W Black , R Freedman , C. R Cloninger and P. V. Gejman

The Molecular Genetics of Schizophrenia (MGS2) project recruited an adult control sample of non-Hispanic European-ancestry (N=3,364) and African American (N=1,301) subjects.


Subjects gave consent to deposit phenotypic data and blood samples into a repository for general research use, with full anonymization of the sample. The authors compared the control sample with population census data for demographic data and with previous population surveys for anthropometrics and prevalences of psychiatric disorders as estimated by an Internet-administered questionnaire.


The full MGS2 control sample includes 4,665 subjects (European-ancestry: N=3,364; African American: N=1,301), of whom 3,626 were included in the MGS2 genome-wide association study (GWAS). The sample is generally demographically representative of the U.S. population, except for being older and more female, educated, and affluent, although all strata are represented. Self-reported ancestry was consistent with genotypic and census data. Lifetime prevalences for depressive, anxiety, and substance use diagnoses were higher than in previous population-based surveys, probably due to use of an abbreviated self-report instrument. However, patterns such as sex ratios, comorbidity, and demographic associations were consistent with previous reports. DNA quality for the Internet collected/evaluated control sample was comparable to that of the face-to-face case sample.


The Internet-based methods facilitated the rapid collection of large and anonymized non-Hispanic European-ancestry and African American control samples that have been validated as being generally representative for many aspects of demography, ancestry, and morbidity. Utilization of clinical screening data shared with the scientific community may permit investigators to select appropriate controls for some studies.

  K. S Kendler , C. O Gardner , A Fiske and M. Gatz

Context  Major depresssion (MD) and coronary artery disease (CAD) frequently co-occur. The mechanisms of comorbidity are uncertain.

Objective  To clarify sources of MD-CAD comorbidity.

Design  Major depression was assessed at the time of the personal interview, and CAD from hospital discharge records and death certificates.

Setting  Swedish population-based twin registry.

Participants  The study included 30 374 twins with a mean age of 57 years.

Main Outcome Measure  Modified DSM-IV diagnosis of MD or diagnosis of CAD.

Results  Lifetime association between MD and CAD was modest (odds ratio, ~1.3). In time-dependent Cox analyses, onset of CAD produced concurrent and ongoing hazard ratios for MD of 2.83 and 1.75. These risks increased if the diagnosis of CAD was restricted to myocardial infarction. Onset of MD increased the concurrent and ongoing hazard ratios for CAD to 2.53 and 1.17. The ongoing CAD risk was strongly associated with depressive severity and recurrence. Twin models showed that the modest comorbidity between MD and CAD in women arose primarily from shared genetic effects, although the genetic correlation was small (+0.16). In men, the source of comorbidity was moderated by age, being environmental in older members and largely genetic in younger members of the sample.

Conclusions  Although the MD-CAD relationship across the lifespan is modest, time-dependent models reveal stronger associations. The sustained effect of CAD onset on MD risk is much stronger than vice versa. The effect of MD on CAD is largely acute, and the longer-term effects are apparently mediated via depressive recurrence. When examined separately, in men, environmental effects, which are often acute, play a large role in MD-CAD comorbidity, whereas in women, chronic effects, which are in part genetic, are more important. In men, genetic sources of MD-CAD comorbidity are more important in younger members of the sample.

  K. S Kendler and C. O. Gardner

Context  Most environmental risk factors for psychiatric disorders cannot be studied experimentally, making causal attributions difficult. Can we address this question by using together 2 major methods for causal inference: natural experiments and specialized statistical methods?

Objective  To determine the causal relationship between dependent stressful life events (dSLEs) and prior depressive episodes (PDEs) and major depression (MD).

Design  Assessment of risk factors and episodes of MD at interview. Statistical analyses used the co-twin control and propensity score–matching methods.

Setting  General community.

Participants  Four thousand nine hundred ten male and female twins from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders.

Main Outcome Measure  Episodes of MD.

Results  We found that dSLEs were strongly associated with risk for MD in female (odds ratio [OR], 5.85) and male (4.55) twins in the entire sample and, at considerably lower levels, in female (2.29) and male (2.19) monozygotic twins discordant for dSLE exposure. A case-control sample matched on propensity score showed a moderate association in female (OR, 1.79) and male (1.53) twins. A PDE strongly predicted risk for MD in female (OR, 3.68) and male (5.20) twins in the entire sample. In monozygotic pairs discordant for exposure, the association was weaker in male (OR, 1.41) and absent in female (1.00) twins. A case-control sample matched on propensity score showed a moderate association between PDE and depressive episodes in male (OR, 1.58) and female twins (1.66).

Conclusions  Although dSLEs have a modest causal effect on the risk for MD, a large proportion of the observed association is noncausal. The same pattern is seen for PDEs, although the causal impact is somewhat more tenuous. For environmental exposures in psychiatry that cannot be studied experimentally, co-twin control and propensity scoring methods—which have complementary strengths and weaknesses—can provide similar results, suggesting their joint use can help with the critical question of causal inference.

  K. S Kendler and M. B. First

Two major approaches can be used for the up-coming revisions of DSM–V and ICD–10: an ‘iterative model’ in which incremental changes are made or a ‘paradigm shift model’ in which the existing approach is jettisoned in favour of a new nosological model. We explore each of these two approaches and conclude that although they both have strengths and limitations, our field is not currently ready for a paradigm shift.

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