Marianna Gasperi1, John N Krieger2, Matthew S Panizzon3, Jack Goldberg4, Dedra Buchwald5, Niloofar Afari6. 1. University of California, San Diego, CA; VA Center of Excellence for Stress and Mental Health, San Diego, CA. 2. University of Washington, Seattle, WA. 3. Center for Behavior Genetics of Aging, University of California, San Diego, CA. 4. University of Washington, Seattle, WA; Vietnam Era Twin Registry, Seattle, WA. 5. Elson S Floyd College of Medicine, Washington State University, Spokane, WA. 6. University of California, San Diego, CA; VA Center of Excellence for Stress and Mental Health, San Diego, CA. Electronic address: nafari@ucsd.edu.
Abstract
OBJECTIVE: To evaluate the genetic and environmental relationship among prostatitis and other urological conditions, including benign prostatic hyperplasia (BPH) and prostate cancer (CaP), a classical twin design and biometric modeling was used. While prostatitis-characterized by pain and voiding symptoms, no clear etiology, and functional and quality of life impairments-co-occurs with other urinary conditions, the degree of shared overlapping etiologic processes among them remains unclear. We examined the contribution of genetic and environmental factors to these conditions and the etiology of their associations at the level of genetic and environmental influences. METHODS: 4380 monozygotic and dizygotic male twin pairs from the Vietnam Era Twin Registry reported lifetime physician-diagnosed prostatitis (combined acute and chronic), bladder problems, enlarged prostate/BPH, and CaP. Multivariate biometrical modeling estimated the magnitude of genetic and environmental influences for each condition, as well as their genetic and environmental covariance. The common pathway model tested the assumption that covariation among these urinary conditions is determined by a single latent factor. RESULTS: Overall prevalence of prostatitis was 2.7%. Heritability estimates ranged from 19% for bladder problems to 42% for CaP. Significant shared environmental influences were present for CaP (12%), enlarged prostate/BPH (10%) but were smaller than genetic influences. A reduced one factor common pathway model provided the best fit, suggesting that covariation among the conditions is determined by a shared latent factor. CONCLUSION: We identified a common, genetically-influenced factor that accounts for much of the comorbidity among these 4 disease conditions. Nonshared environmental factors also make a significant contribution. Published by Elsevier Inc.
OBJECTIVE: To evaluate the genetic and environmental relationship among prostatitis and other urological conditions, including benign prostatic hyperplasia (BPH) and prostate cancer (CaP), a classical twin design and biometric modeling was used. While prostatitis-characterized by pain and voiding symptoms, no clear etiology, and functional and quality of life impairments-co-occurs with other urinary conditions, the degree of shared overlapping etiologic processes among them remains unclear. We examined the contribution of genetic and environmental factors to these conditions and the etiology of their associations at the level of genetic and environmental influences. METHODS: 4380 monozygotic and dizygotic male twin pairs from the Vietnam Era Twin Registry reported lifetime physician-diagnosed prostatitis (combined acute and chronic), bladder problems, enlarged prostate/BPH, and CaP. Multivariate biometrical modeling estimated the magnitude of genetic and environmental influences for each condition, as well as their genetic and environmental covariance. The common pathway model tested the assumption that covariation among these urinary conditions is determined by a single latent factor. RESULTS: Overall prevalence of prostatitis was 2.7%. Heritability estimates ranged from 19% for bladder problems to 42% for CaP. Significant shared environmental influences were present for CaP (12%), enlarged prostate/BPH (10%) but were smaller than genetic influences. A reduced one factor common pathway model provided the best fit, suggesting that covariation among the conditions is determined by a shared latent factor. CONCLUSION: We identified a common, genetically-influenced factor that accounts for much of the comorbidity among these 4 disease conditions. Nonshared environmental factors also make a significant contribution. Published by Elsevier Inc.
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