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Changes in alcohol intake and serum urate changes: longitudinal analyses of annual medical examination database
  1. Sho Fukui1,2,3,
  2. Masato Okada2,
  3. Tomohiro Shinozaki4,
  4. Takahiro Asano2,
  5. Takehiro Nakai2,
  6. Hiromichi Tamaki2,
  7. Mitsumasa Kishimoto2,5,
  8. Hiroshi Hasegawa3,
  9. Takeaki Matsuda3,
  10. Javier Marrugo1,
  11. Sara K Tedeschi1,
  12. Hyon Choi6,7,
  13. Daniel H Solomon1
  1. 1 Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Immuno-Rheumatology Center, St. Luke's international Hospital, Tokyo, Japan
  3. 3 Department of Emergency and General Medicine, Kyorin University School of Medicine, Tokyo, Japan
  4. 4 Department of Information and Computer Technology, Faculty of Engineering, Tokyo University of Science, Tokyo, Japan
  5. 5 Department of Nephrology and Rheumatology, Kyorin University School of Medicine, Tokyo, Japan
  6. 6 Arthritis Research Canada, Richmond, Virginia, Canada
  7. 7 Division of Rheumatology, Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Dr Sho Fukui, Brigham and Women's Hospital, Boston, Massachusetts, USA; sfukui{at}; Professor Daniel H Solomon; dsolomon{at}


Introduction Despite the established cross-sectional association between alcohol intake and serum urate (SU), its longitudinal association remains unknown. This study aimed to determine whether changes in alcohol intake have a clinically relevant association with SU change.

Method We conducted retrospective analyses using systematically collected annual medical examination data from October 2012 to October 2022 in a Japanese preventive medicine centre. The exposure was changes in alcohol intake between two consecutive visits. The association of SU changes with alcohol intake changes was estimated by mixed-effect linear regression with adjustment for relevant covariates.

Results We analysed 63 486 participants (median age, 47.0 years; 55% women; 58.6% regular alcohol drinkers with a median of 1.4 drinks/day) with 370 572 visits. The median SU level was 5.3 mg/dL, and 506 (0.8%) participants had diagnoses of gout or hyperuricemia without medication use during the study period. Decreasing one daily alcohol intake had a clinically small association with SU changes (−0.019 (95% CI: −0.021 to –0.017) mg/dL). Beer had the largest association with SU (−0.036 (95% CI: −0.039 to –0.032) mg/dL for one beer decrease). Complete discontinuation of any alcohol from a mean of 0.8 drinks/day was associated with −0.056 mg/dL (95% CI: −0.068 to –0.043) decrease in SU; the association became larger in hyperuricemic participants (−0.110 mg/dL (95% CI: −0.154 to –0.066) for alcohol discontinuation from a mean of 1.0 drinks/day).

Conclusions This study revealed changes in alcohol intake had small associations with SU change at the general Japanese population level. Complete discontinuation of alcohol in hyperuricemic participants had only modest improvement in SU.

  • Gout
  • Epidemiology
  • Crystal arthropathies

Data availability statement

No data are available. Data is not available publicly because of the regulations in our institution. Data were analysed using STATA software (V.17.1, StataCorp). The codes used in this study are available upon reasonable request from the corresponding author (SF).

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Data availability statement

No data are available. Data is not available publicly because of the regulations in our institution. Data were analysed using STATA software (V.17.1, StataCorp). The codes used in this study are available upon reasonable request from the corresponding author (SF).

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  • Handling editor Josef S Smolen

  • Contributors SF, MO and DHS contributed to the original conception and design of this study, which TS, TA, TN, HT, MK, HH, TM, JM, SKT and HC reviewed and corrected. SF collected data with support from MO, TS, TA, TN, HT, MK, HH and TM. SF performed data analysis with support from TS, JM, SKT, HC and DHS. SF, JM, SKT and DHS initially interpreted the data, and other authors advised on the interpretation. SF drafted the original manuscript, which was critically reviewed and revised by all other authors. All authors have read and approved the final version of the manuscript. SF took responsibility for the integrity of the data and the accuracy of the data analysis. SF accepts full responsibility for the work and/or the conduct of the study, had access to the data, and controlled the decision to publish.

  • Funding This study was supported by NIH funding P30 AR072577 (PI: DHS).

  • Competing interests HT reports personal fees from Chugai Pharmaceutical, AbbVie, Ono Pharmaceutical, Kyowa-Kirin, Takeda Pharmaceutical, Astellas Pharma, Tanabe-Mitsubishi, GSK, Pfizer, Dai-ichi-Sankyo, Eisai, Illy-lily and Ayumi, outside the submitted work. MK reports consulting fees and honoraria from AbbVie, Amgen, Asahi-Kasei Pharma, Astellas, Ayumi Pharma, BMS, Celgene, Chugai, Daiichi-Sankyo, Eisai, Eli Lilly, Gilead, Janssen, Kyowa Kirin, Novartis, Ono Pharma, Pfizer, Tanabe-Mitsubishi, Teijin Pharma, and UCB Pharma, outside the submitted work. SKT reports consulting fees from Novartis.DS reports research grants from CorEvitas, Janssen, Moderna, and Novartis, and royalties from UpToDate. All other authors have no conflict of interest.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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