Scholarlink

Purpose <p>Bariatric surgery has proven effective in enhancing metabolic health and achieving sustainable weight loss for individuals with obesity. However, some patients experience adverse psychological outcomes and reduced quality-of-life post-surgery, potentially linked to&#xa0;changes in the gut–brain axis. This review aims to synthesize current evidence on the interplay between bariatric surgery-induced gut–brain axis modifications and patients’ psychological status.</p> Methods <p>A systematic literature search was conducted across PubMed, Web of Science, and Embase, prioritizing clinical studies, mechanistic investigations, and meta-analyses. Inclusion criteria encompassed English-language articles examining psychological parameters, gut-derived hormones, and gut microbiota in adults after Roux-en-Y gastric bypass or sleeve gastrectomy.</p> Results <p>Bariatric surgery fundamentally reprograms gut–brain communication through anatomical, endocrine, and neural plasticity mechanisms, a process associated with dual-edged metabolic benefits and neuropsychiatric risks. Mechanistic analyses suggest that postoperative dysregulation of GLP-1/PYY secretion, altered vagal afferent signaling, and sustained microbiota dysbiosis (reduced Bifidobacterium, elevated Proteobacteria) may represent potential correlates of these outcomes.</p> Conclusions <p>Studies have demonstrated significant associations between mood, quality of life, psychological status, and gut-derived hormones or microbiota.&#xa0;A comprehensive understanding of how bariatric surgery impacts gut–brain signaling pathways is critical for optimizing long-term therapeutic outcomes and enhancing patient quality of life.</p> Level of evidence <p>This manuscript is a Narrative Review. According to the grading criteria of the Oxford Centre for Evidence-Based Medicine (OCEBM), this manuscript is categorized as Level III–IV evidence.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Post-bariatric surgery quality-of-life decline: analysis of the gut–brain axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年9月2日

查看全文
  • Yuxuan Jiao,
  • Shaohui Zhu,
  • Huichao Xue,
  • Yihao Wang,
  • Yanfang Wang,
  • Dong Hou

摘要

Purpose

Bariatric surgery has proven effective in enhancing metabolic health and achieving sustainable weight loss for individuals with obesity. However, some patients experience adverse psychological outcomes and reduced quality-of-life post-surgery, potentially linked to changes in the gut–brain axis. This review aims to synthesize current evidence on the interplay between bariatric surgery-induced gut–brain axis modifications and patients’ psychological status.

Methods

A systematic literature search was conducted across PubMed, Web of Science, and Embase, prioritizing clinical studies, mechanistic investigations, and meta-analyses. Inclusion criteria encompassed English-language articles examining psychological parameters, gut-derived hormones, and gut microbiota in adults after Roux-en-Y gastric bypass or sleeve gastrectomy.

Results

Bariatric surgery fundamentally reprograms gut–brain communication through anatomical, endocrine, and neural plasticity mechanisms, a process associated with dual-edged metabolic benefits and neuropsychiatric risks. Mechanistic analyses suggest that postoperative dysregulation of GLP-1/PYY secretion, altered vagal afferent signaling, and sustained microbiota dysbiosis (reduced Bifidobacterium, elevated Proteobacteria) may represent potential correlates of these outcomes.

Conclusions

Studies have demonstrated significant associations between mood, quality of life, psychological status, and gut-derived hormones or microbiota. A comprehensive understanding of how bariatric surgery impacts gut–brain signaling pathways is critical for optimizing long-term therapeutic outcomes and enhancing patient quality of life.

Level of evidence

This manuscript is a Narrative Review. According to the grading criteria of the Oxford Centre for Evidence-Based Medicine (OCEBM), this manuscript is categorized as Level III–IV evidence.