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<p>Historical famine exposure has left enduring biological imprints that continue to shape health outcomes in modern environments characterized by nutritional abundance. This study examines the epigenetic legacies of famine, focusing on mechanistic pathways that predispose populations to obesity and metabolic disease. Drawing on epidemiological evidence from major twentieth-century famines, we integrate geographic mapping with intracellular cascade modeling to highlight how nutritional deprivation during critical developmental windows alters gene expression, endocrine regulation, and metabolic programming. These epigenetic modifications, including changes in DNA methylation and histone acetylation, persist across generations, influencing appetite regulation, insulin sensitivity, and adipose tissue metabolism. Our findings underscore the paradox whereby populations historically exposed to famine exhibit heightened vulnerability to obesity and type 2 diabetes when later confronted with caloric abundance. By visualizing famine events globally and linking them to long-term health risks, this work situates obesity not only as a lifestyle condition but also as a legacy of historical nutritional trauma. The study contributes to the developmental origins of health and disease framework, emphasizing the need for public health strategies that account for intergenerational epigenetic risk in addressing modern metabolic epidemics.</p>

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Epigenetic legacies of famine: mechanistic pathways to obesity in modern environments

  • 期刊论文

  • 发表日期：

    2026年8月5日

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  • Abbas S. Neamah,
  • Rasha H. Al-Rikabi,
  • Fadhel M. Lafta

摘要

Historical famine exposure has left enduring biological imprints that continue to shape health outcomes in modern environments characterized by nutritional abundance. This study examines the epigenetic legacies of famine, focusing on mechanistic pathways that predispose populations to obesity and metabolic disease. Drawing on epidemiological evidence from major twentieth-century famines, we integrate geographic mapping with intracellular cascade modeling to highlight how nutritional deprivation during critical developmental windows alters gene expression, endocrine regulation, and metabolic programming. These epigenetic modifications, including changes in DNA methylation and histone acetylation, persist across generations, influencing appetite regulation, insulin sensitivity, and adipose tissue metabolism. Our findings underscore the paradox whereby populations historically exposed to famine exhibit heightened vulnerability to obesity and type 2 diabetes when later confronted with caloric abundance. By visualizing famine events globally and linking them to long-term health risks, this work situates obesity not only as a lifestyle condition but also as a legacy of historical nutritional trauma. The study contributes to the developmental origins of health and disease framework, emphasizing the need for public health strategies that account for intergenerational epigenetic risk in addressing modern metabolic epidemics.