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Background <p>The long-term respiratory health effects of artificial sweetener consumption remain unclear. This study aimed to investigate the associations of artificial sweetener intake with the risk of chronic obstructive pulmonary disease (COPD) and lung function, and to explore the potential mediating role of circulating metabolites.</p> Methods <p>Habitual intake of artificial sweeteners (teaspoon/day) was assessed via multiple 24-h dietary recalls. The multivariate Cox proportional hazards regression was used to analyze the association between AS and risk of COPD, and linear regression was used to analyze associations with forced vital capacity (FVC) and forced expiratory volume in 1&#xa0;s (FEV<sub>1</sub>). A mediation analysis was conducted to assess the contribution of plasma metabolic biomarkers.</p> Results <p>A total of 164,656 participants were included. Over a median follow-up of 14.88&#xa0;years, 4132 incident COPD cases were identified. Compared with non-consumption, higher consumption of artificial sweeteners was associated with a 27% increased risk of COPD (HR = 1.27, 95% CI: 1.14, 1.40) and decreased lung function, including FVC (β: –39.48&#xa0;mL, 95% CI: -56.53, -22.43, <i>p</i> &lt; 0.001) and FEV<sub>1</sub> (β: –37.08&#xa0;mL, 95% CI:-50.91, -23.25, <i>p</i> &lt; 0.001). A significant positive dose–response relationship was observed between artificial sweetener intake and COPD risk, and a negative dose–response relationship between artificial sweetener intake and lung function parameters. Mediation analysis identified several key mediators, including lipids within intermediate-density and low-density lipoprotein particles, apolipoprotein B, and polyunsaturated fatty acids. Among these, phospholipids in large LDL showed the highest mediating effect (PM: 8.72%; 95% CI: 4.53%, 19.63%), followed by cholesteryl esters in IDL (PM: 8.68%; 95% CI: 4.78%, 20.58%). Beyond lipoprotein sub-fractions, apolipoprotein B served as a significant mediator (PM: 6.70%; 95% CI: 3.67%, 16.35%). Furthermore, key fatty acids were identified as significant mediators.</p> Conclusion <p>Higher intake of artificial sweeteners is associated with an elevated risk of COPD and impaired lung function. These associations are partially mediated through pathways related to lipoprotein metabolism and fatty acid profiles.</p> Graphical abstract <p></p>

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Artificial sweetener intake and risk of chronic obstructive pulmonary disease: a mediation analysis based on plasma metabolic biomarkers

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • Miaomiao Fan,
  • Yan Chen,
  • Xiaolin Yin,
  • Shasha Zhao,
  • Jian Feng,
  • Zhaoping Li,
  • Qihui Zhang,
  • Chen Jiang,
  • Hao Bai,
  • Liyong Chen

摘要

Background

The long-term respiratory health effects of artificial sweetener consumption remain unclear. This study aimed to investigate the associations of artificial sweetener intake with the risk of chronic obstructive pulmonary disease (COPD) and lung function, and to explore the potential mediating role of circulating metabolites.

Methods

Habitual intake of artificial sweeteners (teaspoon/day) was assessed via multiple 24-h dietary recalls. The multivariate Cox proportional hazards regression was used to analyze the association between AS and risk of COPD, and linear regression was used to analyze associations with forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). A mediation analysis was conducted to assess the contribution of plasma metabolic biomarkers.

Results

A total of 164,656 participants were included. Over a median follow-up of 14.88 years, 4132 incident COPD cases were identified. Compared with non-consumption, higher consumption of artificial sweeteners was associated with a 27% increased risk of COPD (HR = 1.27, 95% CI: 1.14, 1.40) and decreased lung function, including FVC (β: –39.48 mL, 95% CI: -56.53, -22.43, p < 0.001) and FEV1 (β: –37.08 mL, 95% CI:-50.91, -23.25, p < 0.001). A significant positive dose–response relationship was observed between artificial sweetener intake and COPD risk, and a negative dose–response relationship between artificial sweetener intake and lung function parameters. Mediation analysis identified several key mediators, including lipids within intermediate-density and low-density lipoprotein particles, apolipoprotein B, and polyunsaturated fatty acids. Among these, phospholipids in large LDL showed the highest mediating effect (PM: 8.72%; 95% CI: 4.53%, 19.63%), followed by cholesteryl esters in IDL (PM: 8.68%; 95% CI: 4.78%, 20.58%). Beyond lipoprotein sub-fractions, apolipoprotein B served as a significant mediator (PM: 6.70%; 95% CI: 3.67%, 16.35%). Furthermore, key fatty acids were identified as significant mediators.

Conclusion

Higher intake of artificial sweeteners is associated with an elevated risk of COPD and impaired lung function. These associations are partially mediated through pathways related to lipoprotein metabolism and fatty acid profiles.

Graphical abstract