Background <p>Recent studies suggest a link between residual cholesterol (RC) and hypertension, but the mechanisms remain unclear. Exploring modifiable factors like RC may contribute to chronic disease management.</p> Methods <p>A total of 1,788 individuals aged 45 years or older were selected from the China Health and Retirement Longitudinal Study (CHARLS), which was conducted from 2011 to 2020. Participants with a baseline BMI ≥ 24&#xa0;kg/m² or diagnosis of hypertension in 2013 or earlier were excluded. Here, baseline RC levels were treated as the exposure factor, BMI from the 2013 follow-up as the mediator, and incident hypertension from the 2015–2020 follow-up as the outcome variable. This study examined the effect of RC and BMI on hypertension by focusing on the role of BMI in the underlying mechanisms. Additionally, cross-sectional data from the 2011 CHARLS were included to validate the stability of the mediating relationships.</p> Results <p>After a two-year follow-up (2013), 186 participants (10.4%) developed overweight or obesity (BMI ≥ 24&#xa0;kg/m²). Within a median follow-up of five years (2015–2020), 24% (430 individuals) experienced the onset of hypertension. RC levels rising by 1 mmol/L were tied to a 4% increase in the risk of overweight/obesity (OR = 1.04, 95% CI: 1.01–1.08). Similarly, an increase of 1 mmol/L in RC was linked to a 30% increased risk of developing hypertension (HR = 1.3, 95% CI: 1.1–1.55). BMI-2013 was significantly associated with incident hypertension (OR = 1.07, 95% CI: 1.03–1.11). These findings remained stable after adjusting for covariates. BMI-2013 was identified as a key mediator in the connection between RC and hypertension, with an indirect effect of β = 0.008 (95% CI: 0.003–0.01, <i>p</i> = 0.02) and a total effect of β = 0.064 (95% CI: 0.017–0.110, <i>p</i> &lt; 0.001), accounting for 11.8% of the total effect (<i>P</i> = 0.02). Sensitivity analysis of the cross-sectional data suggested that the results were stable.</p> Conclusion <p>RC may contribute to hypertension development, with BMI potentially acting as a mediator. These findings highlight the importance of metabolic risk control in reducing the burden of chronic diseases.</p>

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Exploring the relationship between residual cholesterol, body mass index, and hypertension risk: a national cohort study

  • Tian-Qi Teng,
  • Jing Liu,
  • Meng-Meng Wang,
  • Ya-Qin Chen,
  • Jia-Chao Xu,
  • Zi-Han Dong,
  • Qing-Ying Jiao,
  • Ning Zhang,
  • Hai-Chu Yu

摘要

Background

Recent studies suggest a link between residual cholesterol (RC) and hypertension, but the mechanisms remain unclear. Exploring modifiable factors like RC may contribute to chronic disease management.

Methods

A total of 1,788 individuals aged 45 years or older were selected from the China Health and Retirement Longitudinal Study (CHARLS), which was conducted from 2011 to 2020. Participants with a baseline BMI ≥ 24 kg/m² or diagnosis of hypertension in 2013 or earlier were excluded. Here, baseline RC levels were treated as the exposure factor, BMI from the 2013 follow-up as the mediator, and incident hypertension from the 2015–2020 follow-up as the outcome variable. This study examined the effect of RC and BMI on hypertension by focusing on the role of BMI in the underlying mechanisms. Additionally, cross-sectional data from the 2011 CHARLS were included to validate the stability of the mediating relationships.

Results

After a two-year follow-up (2013), 186 participants (10.4%) developed overweight or obesity (BMI ≥ 24 kg/m²). Within a median follow-up of five years (2015–2020), 24% (430 individuals) experienced the onset of hypertension. RC levels rising by 1 mmol/L were tied to a 4% increase in the risk of overweight/obesity (OR = 1.04, 95% CI: 1.01–1.08). Similarly, an increase of 1 mmol/L in RC was linked to a 30% increased risk of developing hypertension (HR = 1.3, 95% CI: 1.1–1.55). BMI-2013 was significantly associated with incident hypertension (OR = 1.07, 95% CI: 1.03–1.11). These findings remained stable after adjusting for covariates. BMI-2013 was identified as a key mediator in the connection between RC and hypertension, with an indirect effect of β = 0.008 (95% CI: 0.003–0.01, p = 0.02) and a total effect of β = 0.064 (95% CI: 0.017–0.110, p < 0.001), accounting for 11.8% of the total effect (P = 0.02). Sensitivity analysis of the cross-sectional data suggested that the results were stable.

Conclusion

RC may contribute to hypertension development, with BMI potentially acting as a mediator. These findings highlight the importance of metabolic risk control in reducing the burden of chronic diseases.