Background and aims: Adverse childhood experiences (ACEs) have been associated with various adverse health outcomes, potentially including digestive diseases. We conducted a population-based cross-sectional study aimed at examining the mediating effect of depression in the longitudinal relationship between ACEs and digestive diseases.
Methods: For this study, we recruited 5145 participants aged ≥ 45 years from the 2014 and 2015 waves of the China Health and Retirement Longitudinal Study (CHARLS). Multivariable mediation analysis with bootstrap resampling was used to assess the mediating role of depression in the association between ACEs and digestive diseases.
Results: In the 5145 middle-aged and older Chinese adults (mean age, 63.9 years), cumulative childhood adversity was found to be a significant predictor of the risk of digestive diseases (B = 0.023 per ACE, standard error (SE) = 0.005, P < 0.001). Depressive symptoms (prevalence, 28.1%) mediated 33.3% of this association (indirect effect = 0.0078, 95% confidence interval (CI): 0.0056–0.0101, P < 0.001), while the direct effect of ACE persisted (B = 0.0156, 95% CI: 0.0057–0.0259, P = 0.004).
Conclusions: ACEs are associated with a higher susceptibility to digestive diseases directly and through depression-mediated pathways. The findings of this study indicate that interventions targeting depression may attenuate the pathogenesis of digestive diseases in those with ACE, particularly in high-risk subgroups with ≥ 4 ACEs and concurrent depression (10-item Center for Epidemiologic Studies Depression Scale score ≥ 10).
Background and aims: Adverse childhood experiences (ACEs) have been associated with various adverse health outcomes, potentially including digestive diseases. We conducted a population-based cross-sectional study aimed at examining the mediating effect of depression in the longitudinal relationship between ACEs and digestive diseases.
Methods: For this study, we recruited 5145 participants aged ≥ 45 years from the 2014 and 2015 waves of the China Health and Retirement Longitudinal Study (CHARLS). Multivariable mediation analysis with bootstrap resampling was used to assess the mediating role of depression in the association between ACEs and digestive diseases.
Results: In the 5145 middle-aged and older Chinese adults (mean age, 63.9 years), cumulative childhood adversity was found to be a significant predictor of the risk of digestive diseases (B = 0.023 per ACE, standard error (SE) = 0.005, P < 0.001). Depressive symptoms (prevalence, 28.1%) mediated 33.3% of this association (indirect effect = 0.0078, 95% confidence interval (CI): 0.0056–0.0101, P < 0.001), while the direct effect of ACE persisted (B = 0.0156, 95% CI: 0.0057–0.0259, P = 0.004).
Conclusions: ACEs are associated with a higher susceptibility to digestive diseases directly and through depression-mediated pathways. The findings of this study indicate that interventions targeting depression may attenuate the pathogenesis of digestive diseases in those with ACE, particularly in high-risk subgroups with ≥ 4 ACEs and concurrent depression (10-item Center for Epidemiologic Studies Depression Scale score ≥ 10).
Background and aims: Tracheostomy is commonly performed in patients with a range of diseases. However, the relationship between tracheostomy and dysphagia remains controversial. Therefore, we conducted this retrospective study to determine whether tracheostomy affects swallowing function and to explore the characteristics of tracheostomy-associated dysphagia.
Methods: We enrolled 56 patients with tracheostomy who successfully underwent decannulation and analyzed the results of flexible endoscopic evaluation of swallowing (FEES) before and after decannulation.
Results: After decannulation, significant improvements were observed in swelling of the arytenoid cartilage (P < 0.001), secretion accumulation (P < 0.001), laryngeal sensation (P < 0.001), and clearance ability (P < 0.001). Swallowing function also improved significantly after decannulation, as evidenced by reductions in pyriform sinus residue (P < 0.001), vallecula residue (P < 0.001), and Penetration–Aspiration Scale scores (P < 0.001).
Conclusions: In patients with neurogenic dysphagia undergoing tracheostomy, the presence of a tracheostomy tube may impair laryngeal sensory function and clearance, leading to increased accumulation of secretions and swelling of the arytenoid cartilage. Furthermore, tracheostomy may aggravate dysphagia, resulting in increased pharyngeal residue and a higher risk of aspiration.
Background and aims: Tracheostomy is commonly performed in patients with a range of diseases. However, the relationship between tracheostomy and dysphagia remains controversial. Therefore, we conducted this retrospective study to determine whether tracheostomy affects swallowing function and to explore the characteristics of tracheostomy-associated dysphagia.
Methods: We enrolled 56 patients with tracheostomy who successfully underwent decannulation and analyzed the results of flexible endoscopic evaluation of swallowing (FEES) before and after decannulation.
Results: After decannulation, significant improvements were observed in swelling of the arytenoid cartilage (P < 0.001), secretion accumulation (P < 0.001), laryngeal sensation (P < 0.001), and clearance ability (P < 0.001). Swallowing function also improved significantly after decannulation, as evidenced by reductions in pyriform sinus residue (P < 0.001), vallecula residue (P < 0.001), and Penetration–Aspiration Scale scores (P < 0.001).
Conclusions: In patients with neurogenic dysphagia undergoing tracheostomy, the presence of a tracheostomy tube may impair laryngeal sensory function and clearance, leading to increased accumulation of secretions and swelling of the arytenoid cartilage. Furthermore, tracheostomy may aggravate dysphagia, resulting in increased pharyngeal residue and a higher risk of aspiration.
Ischemic stroke and Alzheimer's disease (AD) are leading causes of neurological disability and cognitive decline, respectively. Although traditionally studied as distinct disorders, growing evidence suggests that both conditions can be understood within a brain-heart disease framework characterized by disrupted oxygen and energy homeostasis. Acute cerebral ischemia can provoke secondary cardiac dysfunction, whereas chronic cardiovascular insufficiency may impair cerebral perfusion, disrupt neurovascular homeostasis, and accelerate cognitive decline. These reciprocal interactions support the concept of a bidirectional brain-heart axis that links neural and cardiac vulnerability. Within this cross-organ stress network, hypoxia-responsive signaling, metabolic reprogramming, mitochondrial dysfunction, neurovascular injury, and systemic inflammation contribute to adaptive and maladaptive responses across multiple organ systems. In this Review, we examine how brain-heart interactions shape responses to acute and chronic neurological injury, with particular emphasis on ischemic stroke and AD as representative models of acute and chronic oxygen-energy stress. We discuss mechanisms of metabolic adaptation, neurovascular remodeling, inflammatory activation, and hypoxia-inducible factor (HIF) signaling across the brain-heart axis, while highlighting evidence from experimental studies, single-cell analyses, and human clinical investigations. By integrating these findings, we propose a systems-level framework that may help explain how acute neurological injury, chronic neurodegeneration, and cardiometabolic stress converge over time and guide the development of more integrated therapeutic strategies.
Ischemic stroke and Alzheimer's disease (AD) are leading causes of neurological disability and cognitive decline, respectively. Although traditionally studied as distinct disorders, growing evidence suggests that both conditions can be understood within a brain-heart disease framework characterized by disrupted oxygen and energy homeostasis. Acute cerebral ischemia can provoke secondary cardiac dysfunction, whereas chronic cardiovascular insufficiency may impair cerebral perfusion, disrupt neurovascular homeostasis, and accelerate cognitive decline. These reciprocal interactions support the concept of a bidirectional brain-heart axis that links neural and cardiac vulnerability. Within this cross-organ stress network, hypoxia-responsive signaling, metabolic reprogramming, mitochondrial dysfunction, neurovascular injury, and systemic inflammation contribute to adaptive and maladaptive responses across multiple organ systems. In this Review, we examine how brain-heart interactions shape responses to acute and chronic neurological injury, with particular emphasis on ischemic stroke and AD as representative models of acute and chronic oxygen-energy stress. We discuss mechanisms of metabolic adaptation, neurovascular remodeling, inflammatory activation, and hypoxia-inducible factor (HIF) signaling across the brain-heart axis, while highlighting evidence from experimental studies, single-cell analyses, and human clinical investigations. By integrating these findings, we propose a systems-level framework that may help explain how acute neurological injury, chronic neurodegeneration, and cardiometabolic stress converge over time and guide the development of more integrated therapeutic strategies.
