Background <p>Dietary fiber is inversely associated with metabolic syndrome (MetS); however, the mechanistic pathways and the consistency of this association across key demographic strata remain quantitatively unclear, which hinders the development of precise public health guidance.</p> Methods <p>This cross-sectional study included 7703 U.S. adults from the National Health and Nutrition Examination Survey (NHANES, 2010–2020). We employed survey-weighted logistic regression to assess the association between dietary fiber density (g/1000&#xa0;kcal) and MetS (defined by NCEP-ATP III criteria). Mediation analysis was conducted to decompose the total association into pathways operating through systemic inflammation (log-transformed high-sensitivity C-reactive protein [hs-CRP]) and insulin resistance (HOMA-IR). We further evaluated effect modification by body mass index (BMI) categories.</p> Results <p>Each 1&#xa0;g/1000&#xa0;kcal increase in dietary fiber density was associated with a 4% reduction in the odds of MetS (<i>OR</i> = 0.96, 95% <i>CI</i>: 0.94–0.99). This inverse association was partially mediated by lower hs-CRP levels (proportion mediated: 7.4%, <i>P</i> = 0.023), with sensitivity analyses confirming robustness to additional lifestyle adjustments. The association was consistent across all BMI categories (interaction <i>P</i> &gt; 0.62), suggesting homogeneous associations for normal-weight, overweight, and obese individuals.</p> Conclusions <p>In a nationally representative sample of U.S. adults, higher dietary fiber density is associated with a lower risk of metabolic syndrome. This association is partly explained by lower levels of systemic inflammation rather than by improvements in insulin resistance, and it is uniformly present across body weight statuses. These findings support the potential universal relevance of increasing fiber intake for MetS prevention and highlight anti-inflammatory pathways as a key area for mechanistic focus.</p>

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Dietary fiber and metabolic syndrome in NHANES: mediation through inflammation and modifications by population characteristics

  • Qingqing Zhang,
  • Di Wu,
  • Fengyun Guo,
  • Shengnan Yang,
  • Lijing Bao,
  • Ruiying Zhang,
  • Ping Wang

摘要

Background

Dietary fiber is inversely associated with metabolic syndrome (MetS); however, the mechanistic pathways and the consistency of this association across key demographic strata remain quantitatively unclear, which hinders the development of precise public health guidance.

Methods

This cross-sectional study included 7703 U.S. adults from the National Health and Nutrition Examination Survey (NHANES, 2010–2020). We employed survey-weighted logistic regression to assess the association between dietary fiber density (g/1000 kcal) and MetS (defined by NCEP-ATP III criteria). Mediation analysis was conducted to decompose the total association into pathways operating through systemic inflammation (log-transformed high-sensitivity C-reactive protein [hs-CRP]) and insulin resistance (HOMA-IR). We further evaluated effect modification by body mass index (BMI) categories.

Results

Each 1 g/1000 kcal increase in dietary fiber density was associated with a 4% reduction in the odds of MetS (OR = 0.96, 95% CI: 0.94–0.99). This inverse association was partially mediated by lower hs-CRP levels (proportion mediated: 7.4%, P = 0.023), with sensitivity analyses confirming robustness to additional lifestyle adjustments. The association was consistent across all BMI categories (interaction P > 0.62), suggesting homogeneous associations for normal-weight, overweight, and obese individuals.

Conclusions

In a nationally representative sample of U.S. adults, higher dietary fiber density is associated with a lower risk of metabolic syndrome. This association is partly explained by lower levels of systemic inflammation rather than by improvements in insulin resistance, and it is uniformly present across body weight statuses. These findings support the potential universal relevance of increasing fiber intake for MetS prevention and highlight anti-inflammatory pathways as a key area for mechanistic focus.