Ann Rheum Dis 74:369-374 doi:10.1136/annrheumdis-2013-204067
  • Clinical and epidemiological research
  • Extended report

Familial aggregation of gout and relative genetic and environmental contributions: a nationwide population study in Taiwan

Open Access
  1. Michael Doherty1
  1. 1Department of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK
  2. 2Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, Taoyuan, Taiwan
  3. 3Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK
  4. 4Department of Public Health, College of Medicine, Chang Gung University, Taoyuan, Taiwan
  5. 5Biostatistics Core Laboratory, Molecular Medicine Research Centre, Chang Gung University, Taoyuan, Taiwan
  1. Correspondence to Dr Chang-Fu Kuo, Academic Rheumatology, Clinical Sciences Building, City Hospital, Nottingham NG51PB, UK; zandis{at}; mbxck2{at}
  • Received 3 June 2013
  • Revised 22 August 2013
  • Accepted 3 November 2013
  • Published Online First 21 November 2013


Objective To examine familial aggregation of gout and to estimate the heritability and environmental contributions to gout susceptibility in the general population.

Methods Using data from the National Health Insurance (NHI) Research Database in Taiwan, we conducted a nationwide cross-sectional study of data collected from 22 643 748 beneficiaries of the NHI in 2004; among them 1 045 059 individuals had physician-diagnosed gout. We estimated relative risks (RR) of gout in individuals with affected first-degree and second-degree relatives and relative contributions of genes (heritability), common environment shared by family members and non-shared environment to gout susceptibility.

Results RRs for gout were significantly higher in individuals with affected first-degree relatives (men, 1.91 (95% CI 1.90 to 1.93); women, 1.97 (95% CI 1.94 to 1.99)) and also in those with affected second-degree relatives (men, 1.27 (95% CI 1.23 to 1.31); women, 1.40 (95% CI 1.35 to 1.46)). RRs (95% CIs) for individuals with an affected twin, sibling, offspring, parent, grandchild, nephew/niece, uncle/aunt and grandparent were 8.02 (6.95 to 9.26), 2.59 (2.54 to 2.63), 1.96 (1.95 to 1.97), 1.93 (1.91 to 1.94), 1.48 (1.43 to 1.53), 1.40 (1.32 to 1.47), 1.31 (1.24 to 1.39), and 1.26 (1.21 to 1.30), respectively. The relative contributions of heritability, common and non-shared environmental factors to phenotypic variance of gout were 35.1, 28.1 and 36.8% in men and 17.0, 18.5 and 64.5% in women, respectively.

Conclusions This population-based study confirms that gout aggregates within families. The risk of gout is higher in people with a family history. Genetic and environmental factors contribute to gout aetiology, and the relative contributions are sexually dimorphic.

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