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Updated: Aug 23, 2025

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The Effect of Body Fat Distribution on Systemic Sclerosis.

Gonzalo Villanueva-Martin1, Marialbert Acosta-Herrera2, Martin Kerick1

  • 1Department of Cell Biology and Immunology, Institute of Parasitology and Biomedicine López-Neyra, CSIC, 18016 Granada, Spain.

Journal of Clinical Medicine
|October 27, 2022
PubMed
Summary
This summary is machine-generated.

This study found no causal link between obesity metrics like BMI and systemic sclerosis (SSc). However, a negative association was observed for waist-to-hip ratio adjusted for BMI, possibly due to gastrointestinal issues in SSc patients.

Keywords:
mendelian randomizationobesitysystemic sclerosis

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Area of Science:

  • Immunology
  • Genetics
  • Metabolic Disorders

Background:

  • Obesity is linked to chronic inflammation and immune-mediated diseases.
  • The specific role of obesity in systemic sclerosis (SSc) pathogenesis is not well understood.
  • Understanding obesity's impact on SSc is crucial for disease management and prevention.

Purpose of the Study:

  • To investigate the potential causal effects of body fat distribution on systemic sclerosis (SSc).
  • To analyze the relationship between body mass index (BMI), waist-to-hip ratio (WHR), and WHR adjusted for BMI (WHRadjBMI) and SSc risk.
  • To explore genetic correlations between obesity traits and SSc.

Main Methods:

  • Utilized a two-sample Mendelian randomization (2SMR) study design.
  • Employed genome-wide association study (GWAS) data for SSc, BMI, WHR, and WHRadjBMI.
  • Applied various Mendelian randomization (MR) methods including inverse-variance weight, MR-Egger, and multivariable models, alongside genetic correlation analyses (LDSC, pHESS).

Main Results:

  • No significant genetic correlation or causal relationship was found between BMI, WHR, and SSc.
  • A potential negative causal association was identified between WHRadjBMI and SSc.
  • This association may be influenced by gastrointestinal complications common in SSc patients.

Conclusions:

  • Obesity, as measured by common indices, does not appear to have a direct causal effect on the development of SSc.
  • Reverse causality, potentially driven by disease-related factors like gastrointestinal complications, may confound the observed associations.
  • Further research is needed to clarify the complex interplay between body composition, inflammation, and SSc.