Causal relationships between schizophrenia and psoriasis: a two-sample Mendelian randomization study

Lusheng Miao1, Taosheng Miao2, Ying Zhang1

  • 1Department of Dermatology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

BMC Psychiatry
|March 21, 2025
PubMed
Abstract

Insights

This study used Mendelian randomization to find a causal link between schizophrenia and psoriasis vulgaris. Emotional states like tenseness and misery may mediate this link, possibly via oxidative stress in the HPA axis.

Area of Science:

  • Psychiatry and Dermatology
  • Genetic Epidemiology
  • Systems Biology

Background:

  • Inconsistent findings exist regarding the association between schizophrenia and psoriasis.
  • Previous studies have not definitively established a causal relationship.

Purpose of the Study:

  • To investigate the causal relationship between schizophrenia and psoriasis using Mendelian randomization (MR).
  • To identify potential mediators and underlying biological mechanisms linking these conditions.

Main Methods:

  • Employed Mendelian randomization (MR) with inverse variance weighting as the primary analysis.
  • Utilized a two-step MR approach to identify mediators.
  • Conducted pathway and functional enrichment analyses to explore mechanisms.

Main Results:

  • Confirmed a significant association between schizophrenia and psoriasis vulgaris (OR: 1.0010, p=0.008).
  • Genetic susceptibility to schizophrenia increased psoriasis vulgaris risk (OR: 1.18, p=0.016) but not psoriatic arthropathy.
  • Tenseness, tiredness, and misery were identified as potential mediators.
  • Oxidative stress-driven hypothalamic-pituitary-adrenal (HPA) axis pathways implicated.

Conclusions:

  • Established a significant causal link between schizophrenia and psoriasis vulgaris.
  • Identified psychological distress (tenseness, tiredness, misery) as potential mediators.
  • Suggests shared biological pathways involving oxidative stress and the HPA axis.

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