Scholarlink

<p>This article examines the human body’s adaptive responses to obesity from biological, behavioral, and evolutionary perspectives. It explores how ancient survival mechanisms, such as fat storage during scarcity, have persisted but become maladaptive in modern contexts of food abundance and sedentary lifestyles. Using the Thrifty Gene Hypothesis and General Adaptation Syndrome (GAS), the study investigates how chronic stress and genetic predispositions contribute to obesity. Chronic stress, as described in GAS, is linked to obesity through mechanisms like prolonged cortisol elevation, which promotes fat storage, particularly in the abdominal region, and disrupts hunger and satiety regulation. The article also explores the possibility that contemporary chronic stress may cause the body to buffer stressful conditions through fat accumulation. While the Thrifty Gene Hypothesis suggests that genetic traits evolved to optimize energy storage during scarcity, contributing to obesity in modern environments, it remains controversial. Critics argue that it oversimplifies obesity’s causes, such as lifestyle and environmental factors. Although genetic variations influencing obesity susceptibility continue to evolve, the physiological mechanisms of fat storage and stress adaptation have remained largely unchanged since ancient times.</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

Human adaptation response to obesity

  • 期刊论文

  • 发表日期：

    2025年4月27日

查看全文
  • Alireza Jahanbani,
  • Davood Rezazadeh,
  • Elham Sajadi,
  • Mahdiyeh Haj Hosseini,
  • Deniz Ketabchi,
  • Narges EskandariRoozbahani

摘要

This article examines the human body’s adaptive responses to obesity from biological, behavioral, and evolutionary perspectives. It explores how ancient survival mechanisms, such as fat storage during scarcity, have persisted but become maladaptive in modern contexts of food abundance and sedentary lifestyles. Using the Thrifty Gene Hypothesis and General Adaptation Syndrome (GAS), the study investigates how chronic stress and genetic predispositions contribute to obesity. Chronic stress, as described in GAS, is linked to obesity through mechanisms like prolonged cortisol elevation, which promotes fat storage, particularly in the abdominal region, and disrupts hunger and satiety regulation. The article also explores the possibility that contemporary chronic stress may cause the body to buffer stressful conditions through fat accumulation. While the Thrifty Gene Hypothesis suggests that genetic traits evolved to optimize energy storage during scarcity, contributing to obesity in modern environments, it remains controversial. Critics argue that it oversimplifies obesity’s causes, such as lifestyle and environmental factors. Although genetic variations influencing obesity susceptibility continue to evolve, the physiological mechanisms of fat storage and stress adaptation have remained largely unchanged since ancient times.