Aims <p>This study investigated the associations of polygenic risk score (PRS) and coffee consumption, as well as their interaction, with prediabetes and type 2 Diabetes Mellitus (T2DM) among participants in the southern Netherlands.</p> Methods <p>7668 participants were classified as normal glucose metabolism (NGM), prediabetes, or T2DM based on World Health Organization 2006 criteria. PRS (423 T2DM-related single nucleotide polymorphisms) and coffee consumption (via food frequency questionnaire) were categorized into tertiles (low, medium, and high) based on the population distribution. Multinomial logistic regression and dose–response analyses were performed to evaluate the cross-sectional associations between PRS and coffee consumption with prediabetes and T2DM.</p> Results <p>Fully adjusted analyses indicated that medium and high coffee consumption were associated with lower odds of prediabetes (odds ratios [ORs]: 0.80; 95% CI: 0.69, 0.92 and 0.83; 95% CI: 0.72, 0.96) and T2DM (ORs: 0.80; 95% CI: 0.70, 0.91 and 0.80; 95% CI: 0.70, 0.91). U-shaped associations were observed for both prediabetes and T2DM, with the overlapping range of 2.9–6.9 cups/day statistically associated with lower odds (OR &lt; 1) for both conditions. Additionally, participants in the PRS group had higher odds of prediabetes (OR: 1.58; 95% CI: 1.35, 1.86) and T2DM (OR: 3.16; 95% CI: 2.80, 3.56) compared to the low PRS group. No significant interaction was found between PRS and coffee consumption (<i>P</i> = 0.21).</p> Conclusions <p>No significant interaction was observed between coffee consumption and PRS for prediabetes and T2DM. Coffee consumption was associated with the prevalence of both conditions in a pattern that may be U-shaped. However, these associations appear to be population-specific and require validation in diverse populations to clarify gene-lifestyle interactions.</p>

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Interaction between coffee consumption and polygenic risk score in relation to diabetes: insights from the Maastricht study

  • Yufeng Rao,
  • Evan Yi-Wen Yu,
  • Tzu-Yao Lin,
  • Yiming Chen,
  • Yingfen Qin,
  • Annemarie Koster,
  • Simone J. P. M. Eussen,
  • Hans Bosma,
  • Tos T. J. M. Berendschot,
  • Carla J. H. van der Kallen,
  • Marleen M. J. van Greevenbroek,
  • Bastiaan E. de Galan,
  • Maurice P. Zeegers,
  • Anke Wesselius

摘要

Aims

This study investigated the associations of polygenic risk score (PRS) and coffee consumption, as well as their interaction, with prediabetes and type 2 Diabetes Mellitus (T2DM) among participants in the southern Netherlands.

Methods

7668 participants were classified as normal glucose metabolism (NGM), prediabetes, or T2DM based on World Health Organization 2006 criteria. PRS (423 T2DM-related single nucleotide polymorphisms) and coffee consumption (via food frequency questionnaire) were categorized into tertiles (low, medium, and high) based on the population distribution. Multinomial logistic regression and dose–response analyses were performed to evaluate the cross-sectional associations between PRS and coffee consumption with prediabetes and T2DM.

Results

Fully adjusted analyses indicated that medium and high coffee consumption were associated with lower odds of prediabetes (odds ratios [ORs]: 0.80; 95% CI: 0.69, 0.92 and 0.83; 95% CI: 0.72, 0.96) and T2DM (ORs: 0.80; 95% CI: 0.70, 0.91 and 0.80; 95% CI: 0.70, 0.91). U-shaped associations were observed for both prediabetes and T2DM, with the overlapping range of 2.9–6.9 cups/day statistically associated with lower odds (OR < 1) for both conditions. Additionally, participants in the PRS group had higher odds of prediabetes (OR: 1.58; 95% CI: 1.35, 1.86) and T2DM (OR: 3.16; 95% CI: 2.80, 3.56) compared to the low PRS group. No significant interaction was found between PRS and coffee consumption (P = 0.21).

Conclusions

No significant interaction was observed between coffee consumption and PRS for prediabetes and T2DM. Coffee consumption was associated with the prevalence of both conditions in a pattern that may be U-shaped. However, these associations appear to be population-specific and require validation in diverse populations to clarify gene-lifestyle interactions.