Aims: 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. Data synthesis: 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. Conclusions: 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.

Obesity and sleep disorders: A bidirectional relationship

Figorilli M.
Primo
;
Velluzzi F.
Secondo
;
Redolfi S.
Ultimo
2025-01-01

Abstract

Aims: 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. Data synthesis: 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. Conclusions: 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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/450745
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