Figorilli Michela, Velluzzi Fernanda, Redolfi Stefania
Sleep Disorder Research Center, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Obesity Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Nutr Metab Cardiovasc Dis. 2025 Jun;35(6):104014. doi: 10.1016/j.numecd.2025.104014. Epub 2025 Mar 15.
Obesity and sleep disorders are highly prevalent conditions with profound implications for public health. Emerging evidence highlights a bidirectional relationship between these two conditions, with each exacerbating the other in a complex interplay of behavioral, physiological, and hormonal mechanisms. Sleep deprivation and poor sleep quality contribute to energy imbalance through dysregulation of appetite hormones (e.g., leptin and ghrelin), increased caloric intake, and reduced physical activity. Conversely, sleep disorders such as obstructive sleep apnea syndrome (OSAS), insomnia, and restless leg syndrome (RLS) are significantly more common in individuals with obesity.
This review explores the pathophysiological mechanisms underlying this relationship, including the roles of inflammation, autonomic dysregulation, and neuroendocrine pathways. Sleep loss exacerbates metabolic syndrome components, including insulin resistance and dyslipidemia, further perpetuating weight gain. Similarly, obesity-induced sleep disorders lead to pro-inflammatory states, vascular dysfunction, and sympathetic overactivation, compounding cardiometabolic risks. Specific conditions like OSA and RLS are examined as models of this interdependence, emphasizing their shared pathways and clinical implications.
The bidirectional link between obesity and sleep disorders underscores the importance of integrating sleep assessment and management into obesity treatment strategies. Addressing this relationship could mitigate the progression of cardiometabolic comorbidities and improve overall health outcomes. Moreover, the intertwined dynamics between obesity, sleep disorders, and mental health-mediated by inflammatory pathways, hormonal dysregulation, and neurobehavioral factors-highlight the critical need for integrated treatment approaches targeting physical, psychological, and sleep-related dimensions to enhance health and quality of life.
肥胖和睡眠障碍是高度普遍的状况,对公众健康有着深远影响。新出现的证据突显了这两种状况之间的双向关系,在行为、生理和激素机制的复杂相互作用中,二者相互加剧。睡眠剥夺和睡眠质量差通过食欲激素(如瘦素和胃饥饿素)失调、热量摄入增加以及身体活动减少导致能量失衡。相反,睡眠障碍如阻塞性睡眠呼吸暂停低通气综合征(OSAS)、失眠和不安腿综合征(RLS)在肥胖个体中明显更为常见。
本综述探讨了这种关系背后的病理生理机制,包括炎症、自主神经调节异常和神经内分泌途径的作用。睡眠不足会加剧代谢综合征的组成部分,包括胰岛素抵抗和血脂异常,进一步使体重增加持续存在。同样,肥胖引起的睡眠障碍会导致促炎状态、血管功能障碍和交感神经过度激活,增加心脏代谢风险。像OSA和RLS等特定状况作为这种相互依存关系的模型进行了研究,强调了它们共同的途径和临床意义。
肥胖与睡眠障碍之间的双向联系强调了将睡眠评估和管理纳入肥胖治疗策略的重要性。解决这种关系可以减轻心脏代谢合并症的进展并改善整体健康结果。此外,肥胖、睡眠障碍和心理健康之间由炎症途径、激素失调和神经行为因素介导的相互交织的动态关系,突显了迫切需要针对身体、心理和睡眠相关维度的综合治疗方法,以提高健康水平和生活质量。