Fructose intake from sugar-sweetened beverages is associated with a greater risk of hyperandrogenism in women: UK Biobank cohort study.

Miguel E Rentería, Pomme I H G Simons, Martijn C G J Brouwers, Huadong Chen, Amée M Buziau

Journal: European journal of endocrinology 2024;190(1):104-112

PMID: 38291515

Abstract

OBJECTIVE

To assess the association between fructose consumption and serum sex hormone-binding globulin (SHBG), (free) testosterone, and risk of hyperandrogenism in a population-based cohort.

DESIGN

An observational and genetic association study in participants of the UK Biobank (n = 136 384 and n = 383 392, respectively).

METHODS

We assessed the relationship of (1) the intake of different sources of fructose (ie, total, fruit, fruit juice, and sugar-sweetened beverages [SSBs]) and (2) rs2304681 (a missense variant in the gene encoding ketohexokinase, used as an instrument of impaired fructose metabolism), with SHBG, total and free testosterone levels, and risk of hyperandrogenism (free androgen index >4.5).

RESULTS

The intake of total fructose and fructose from fruit was associated with higher serum SHBG and lower free testosterone in men and women and lower risk of hyperandrogenism in women. In contrast, fructose intake from SSB (≥10 g/day) was associated with lower SHBG in men and women and with higher free testosterone levels and risk of hyperandrogenism in women (odds ratio [OR]: 1.018; 95% confidence interval [CI]: 1.010; 1.026). Carriers of the rs2304681 A allele were characterized by higher circulating SHBG (both men and women), lower serum free testosterone (women), and a lower risk of biochemical hyperandrogenism (OR: 0.997, 95% CI: 0.955; 0.999; women) and acne vulgaris (OR: 0.975, 95% CI: 0.952; 0.999; men and women combined).

CONCLUSIONS

The consumption of ≥10 g/day fructose from SSB, corresponding to ≥200 mL serving, is associated with a 2% higher risk of hyperandrogenism in women. These observational data are supported by our genetic data.

© The Author(s) 2024. Published by Oxford University Press on behalf of European Society of Endocrinology.

Address: Department of Internal Medicine, Division of Endocrinology and Metabolic Diseases, Maastricht University Medical Center, Maastricht, The Netherlands.; Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands.; School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, The Netherlands.; Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Australia.; School of Biomedical Sciences, Faculty of Health, Queensland University of Technology (QUT), Brisbane, Australia.; Department of Internal Medicine, Division of Endocrinology and Metabolic Diseases, Maastricht University Medical Center, Maastricht, The Netherlands.; Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands.; School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, The Netherlands.; Department of Internal Medicine, Elkerliek Hospital, Helmond, The Netherlands.; Department of Internal Medicine, Division of Endocrinology and Metabolic Diseases, Maastricht University Medical Center, Maastricht, The Netherlands.; School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, The Netherlands.
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