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Background <p>Statin therapy has been associated with increased risk of type 2 diabetes (T2D). We investigated the relationship between Low-Density Lipoprotein Cholesterol (LDL-C) plasma concentrations and incident T2D and evaluated the modifying effect of statin therapy in a large population-based cohort.</p> Methods <p>Individuals free of T2D and cardiovascular disease at baseline were followed longitudinally for the development of new-onset T2D. Cox proportional hazards models were applied to evaluate the associations of LDL-C levels and statin therapy with T2D risk.</p> Results <p>From a population of 202,545 individuals, we selected 13,674 participants free of T2D and cardiovascular disease (of whom 52% were on statins), who were followed for a median of 71.6&#xa0;months (IQR 34.5–149.9), during which 1,819 (13%) developed incident T2D. Cox multiple regression analysis revealed a significant inverse association between LDL-C plasma levels and incident T2D (<i>p</i> &lt; 0.001). When stratifying LDL-C into quartiles [i.e. low (&lt; 84&#xa0;mg/dL), medium (≥ 84 to &lt; 107&#xa0;mg/dL), high (≥ 107 to &lt; 131&#xa0;mg/dL), and very high (≥ 131&#xa0;mg/dL)], we observed that patients with LDL-C &lt; 84&#xa0;mg/dL had the highest risk of developing T2D. The interaction between statin therapy and T2D incidence was significant only in the very high LDL-C group, where statin users had a greater risk than non-users (p = 0.018); in the other three LDL-C groups, statin therapy did not significantly modify the association between LDL-C and T2D risk.</p> Conclusions <p>Taken together, our findings demonstrate a strong inverse association between LDL-C and incident T2D in the general population. The increased risk of T2D at lower LDL-C levels appears to be independent of statin use, supporting the role of LDL-C as a potential biomarker of T2D susceptibility.</p> Graphical Abstract <p></p>

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A six-year longitudinal study identifies a statin-independent association between low LDL-cholesterol and risk of type 2 diabetes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月11日

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  • Maria Lembo,
  • Valentina Trimarco,
  • Daniela Pacella,
  • Raffaele Izzo,
  • Stanislovas S. Jankauskas,
  • Roberto Piccinocchi,
  • Paola Gallo,
  • Luca Bardi,
  • Gaetano Piccinocchi,
  • Carmine Morisco,
  • Stefano Cristiano,
  • Giovanni Esposito,
  • Giuseppe Giugliano,
  • Maria Virginia Manzi,
  • Gaetano Santulli,
  • Bruno Trimarco

摘要

Background

Statin therapy has been associated with increased risk of type 2 diabetes (T2D). We investigated the relationship between Low-Density Lipoprotein Cholesterol (LDL-C) plasma concentrations and incident T2D and evaluated the modifying effect of statin therapy in a large population-based cohort.

Methods

Individuals free of T2D and cardiovascular disease at baseline were followed longitudinally for the development of new-onset T2D. Cox proportional hazards models were applied to evaluate the associations of LDL-C levels and statin therapy with T2D risk.

Results

From a population of 202,545 individuals, we selected 13,674 participants free of T2D and cardiovascular disease (of whom 52% were on statins), who were followed for a median of 71.6 months (IQR 34.5–149.9), during which 1,819 (13%) developed incident T2D. Cox multiple regression analysis revealed a significant inverse association between LDL-C plasma levels and incident T2D (p < 0.001). When stratifying LDL-C into quartiles [i.e. low (< 84 mg/dL), medium (≥ 84 to < 107 mg/dL), high (≥ 107 to < 131 mg/dL), and very high (≥ 131 mg/dL)], we observed that patients with LDL-C < 84 mg/dL had the highest risk of developing T2D. The interaction between statin therapy and T2D incidence was significant only in the very high LDL-C group, where statin users had a greater risk than non-users (p = 0.018); in the other three LDL-C groups, statin therapy did not significantly modify the association between LDL-C and T2D risk.

Conclusions

Taken together, our findings demonstrate a strong inverse association between LDL-C and incident T2D in the general population. The increased risk of T2D at lower LDL-C levels appears to be independent of statin use, supporting the role of LDL-C as a potential biomarker of T2D susceptibility.

Graphical Abstract