Sleep Disorders and Inflammatory Disease Activity
Sleep dysfunction is a highly prevalent condition that has long been implicated in accelerating disease states characterized by having an inflammatory component such as systemic lupus erythematosus, HIV, and multiple sclerosis. Inflammatory bowel disease (IBD) is a chronic, debilitating disease that is characterized by waxing and waning symptoms, which are a direct result of increased circulating inflammatory cytokines. Recent studies have demonstrated sleep dysfunction and the disruption of the circadian rhythm to result in an upregulation of inflammatory cytokines. Not only does this pose a potential trigger for disease flares but also an increased risk of malignancy in this subset of patients. This begs to question whether or not there is a therapeutic role of sleep cycle and circadian rhythm optimization in the prevention of IBD flares. Further research is needed to clarify the role of sleep dysfunction and alterations of the circadian rhythm in modifying disease activity and also in reducing the risk of malignancy in patients suffering from IBD.
Crohn's disease (CD) and ulcerative colitis (UC) are two distinct phenotypic patterns of inflammatory bowel disease (IBD) affecting ~1.5 million Americans, with >30,000 new cases diagnosed annually. They are both characterized by periods of asymptomatic remission interrupted by episodes of symptomatic disease flares or exacerbations. Although the specific etiology of IBD is not yet known, disease flares are thought to be multifactorial. Physiological and environmentalstressors cause an increase of circulating inflammatory cytokines resulting in a disease flare. In animal models, sleep deprivation has been shown to increase inflammatory cytokines tumor necrosis factor-α, interleukin(IL)-1β, IL-6, and CRP, clinical markers of IBD that maintain chronic inflammation and may incite acute exacerbations of IBD. Interestingly, some triggers differ in how they affect the two disease phenotypes. For example, smoking has been proven to induce flares in CD, but it decreases the likelihood of UC flares. Recently, sleep dysfunction and disruption in the circadian rhythm have been implicated as potential triggers for disease flares, predominantly in patients suffering from CD. Altered sleep also modifies the immune system), which may further affect the disease course in IBD. This can in turn affect sleep pattern, creating a vicious cycle, and may perpetuateinflammation. In addition, sleep dysfunction has recently been shown to accelerate tumor growth through recruitment of tumor-associated macrophages and Toll-like receptor 4(TLR4) signaling. This article will discuss the current hypothesis of how sleep dysfunction may affect disease activity in IBD and the potential for disease modification by improving sleep patterns.
Abstract and Introduction
Abstract
Sleep dysfunction is a highly prevalent condition that has long been implicated in accelerating disease states characterized by having an inflammatory component such as systemic lupus erythematosus, HIV, and multiple sclerosis. Inflammatory bowel disease (IBD) is a chronic, debilitating disease that is characterized by waxing and waning symptoms, which are a direct result of increased circulating inflammatory cytokines. Recent studies have demonstrated sleep dysfunction and the disruption of the circadian rhythm to result in an upregulation of inflammatory cytokines. Not only does this pose a potential trigger for disease flares but also an increased risk of malignancy in this subset of patients. This begs to question whether or not there is a therapeutic role of sleep cycle and circadian rhythm optimization in the prevention of IBD flares. Further research is needed to clarify the role of sleep dysfunction and alterations of the circadian rhythm in modifying disease activity and also in reducing the risk of malignancy in patients suffering from IBD.
Introduction
Crohn's disease (CD) and ulcerative colitis (UC) are two distinct phenotypic patterns of inflammatory bowel disease (IBD) affecting ~1.5 million Americans, with >30,000 new cases diagnosed annually. They are both characterized by periods of asymptomatic remission interrupted by episodes of symptomatic disease flares or exacerbations. Although the specific etiology of IBD is not yet known, disease flares are thought to be multifactorial. Physiological and environmentalstressors cause an increase of circulating inflammatory cytokines resulting in a disease flare. In animal models, sleep deprivation has been shown to increase inflammatory cytokines tumor necrosis factor-α, interleukin(IL)-1β, IL-6, and CRP, clinical markers of IBD that maintain chronic inflammation and may incite acute exacerbations of IBD. Interestingly, some triggers differ in how they affect the two disease phenotypes. For example, smoking has been proven to induce flares in CD, but it decreases the likelihood of UC flares. Recently, sleep dysfunction and disruption in the circadian rhythm have been implicated as potential triggers for disease flares, predominantly in patients suffering from CD. Altered sleep also modifies the immune system), which may further affect the disease course in IBD. This can in turn affect sleep pattern, creating a vicious cycle, and may perpetuateinflammation. In addition, sleep dysfunction has recently been shown to accelerate tumor growth through recruitment of tumor-associated macrophages and Toll-like receptor 4(TLR4) signaling. This article will discuss the current hypothesis of how sleep dysfunction may affect disease activity in IBD and the potential for disease modification by improving sleep patterns.
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