This proposal in human population and quantitative genetics will provide powerful ways to investigate psychiatric disorders. Specifically to: (a) Develop models to analyze simultaneously in families a threshold character and a correlated quantitative measure (e.g., a diagnosis with a biochemical or psychosocial measure); (b) Implement multivariate analysis of quantitative traits in families taking into account variable family structure and method of ascertainment, and incorporate indices into path analytic models to measure components of the liability for a disorder; (c) Extend multifactorial segregation analysis to half-siblings in order to detect genetic effects and to children in order to relate adult and child psychopathology; (d) Incorporate follow-up data into genetic models to study diagnostic unreliability and stability in a family study; (e) Extend the use of survival analysis for family data; (f) Investigate assortative mating and dynamic models of familial resemblance; and (g) Apply these techniques to several family data sets. Long term objectives are to develop genetic and non-genetic transmission models which are realistic representations of the familial distributions of psychiatric illneses, develop techniques to test nosological hypotheses and resolve phenotypic heterogeneities, develop techniques to detect specific environmental and genetic factors, provide documented computer programs to the scientific community, and collaborate with others to study a broad spectrum of psychiatric and medical disorders. Methods include theoretical, computer implementation and simulation, and data analysis. First, theoretical issues in genetic epidemiology will be resolved, then path analytic and multivariate models will be extended and numerical techniques improved. Next, computer programs will be implemented and simulations used to assess operating characteristics. Finally, the methods will be applied to data. Genetic effects are important in many psychiatric disorders, but the ways in which they interact with the environment to produce an illness are unknown. This research will enable the definition of more etiologically homogeneous subgroups of affected individuals, the characterization of specific modes of transmission, improved risk prediction, and the discovery of relevant pre-morbid characteristics.
| Romeis, James C; Heath, Andrew C; Xian, Hong et al. (2005) Heritability of SF-36 among middle-age, middle-class, male-male twins. Med Care 43:1147-54 |
| Romeis, James C; Grant, Julia D; Knopik, Valerie S et al. (2004) The genetics of middle-age spread in middle-class males. Twin Res 7:596-602 |
| Xian, Hong; Scherrer, Jeffrey F; Madden, Pamela A F et al. (2003) The heritability of failed smoking cessation and nicotine withdrawal in twins who smoked and attempted to quit. Nicotine Tob Res 5:245-54 |
| Saccone, Nancy L; Neuman, Rosalind J; Saccone, Scott F et al. (2003) Genetic analysis of maximum cigarette-use phenotypes. BMC Genet 4 Suppl 1:S105 |
| Scherrer, Jeffrey F; Xian, Hong; Bucholz, Kathleen K et al. (2003) A twin study of depression symptoms, hypertension, and heart disease in middle-aged men. Psychosom Med 65:548-57 |
| Rice, John P; Neuman, Rosalind J; Saccone, Nancy L et al. (2003) Age and birth cohort effects on rates of alcohol dependence. Alcohol Clin Exp Res 27:93-9 |
| Eisen, Seth A; Chantarujikapong, Sunanta; Xian, Hong et al. (2002) Does marijuana use have residual adverse effects on self-reported health measures, socio-demographics and quality of life? A monozygotic co-twin control study in men. Addiction 97:1137-44 |
| Fu, Q; Heath, A C; Bucholz, K K et al. (2002) A twin study of genetic and environmental influences on suicidality in men. Psychol Med 32:11-24 |
| Rice, J P (2001) Diagnosis as a covariate in sib-pair linkage analysis. Am J Med Genet 105:55-6 |
| Rice, J P; Saccone, N L; Rasmussen, E (2001) Definition of the phenotype. Adv Genet 42:69-76 |
Showing the most recent 10 out of 67 publications
