Sleep Disorders and Inflammatory Disease Activity
Sleep Disorders and Inflammatory Disease Activity
Some of the most recent research on the effects of sleep dysfunction has focused on the effects of sleep fragmentation on the cellular signaling pathways and their role in the development of malignancy. Recent studies have correlated sleep fragmentation and the upregulation of proinflammatory and oncogenes, with particular focus on Tlr4. Hakim et al. sought to evaluate the effect of sleep fragmentation on tumor growth progression through Tlr4 signaling. Mice wereexposed to sleep fragmentation 1 week before engraftment of syngeneic tumor cells, with tumor analysis 4 weeks later. In addition, host contributions were compared through the use of mice deficient in Tlr4 or its effector molecules, namely TRIF or MYD88. Mice subjected to sleep fragmentation were noted to have alterations in the level of tumor-associated macrophages and also exhibited more aggressive tumor development, as evidenced by proximity to the tumor capsule. Interestingly, these aggressive features of tumor growth were abolished in a subset of TLR-4-deficient mice. These findings highlight the potential for sleep dysfunction to alter immune system signaling pathways, leading to an increased risk of malignancy. This is of particular importance in patients with IBD, as this population may already be at an increased risk for the development of malignancy). Accelerating and delaying the environmental light cycle results in the suprachiasmatic nuclei output shifting more rapidly than rhythm locomotor rhythms and the rhythms in peripheral tissues. Circadian disruptions occur in shift workers and appear to contribute to hypertension), diabetes), breast cancer, lung cancer, and elevated prostate-specific antigen. Shift work often entails changes in diet, exercise, and tobacco use, which can confound circadian rhythm and sleep disturbance studies.
Sleep Dysfunction and the Risk for Malignancy
Some of the most recent research on the effects of sleep dysfunction has focused on the effects of sleep fragmentation on the cellular signaling pathways and their role in the development of malignancy. Recent studies have correlated sleep fragmentation and the upregulation of proinflammatory and oncogenes, with particular focus on Tlr4. Hakim et al. sought to evaluate the effect of sleep fragmentation on tumor growth progression through Tlr4 signaling. Mice wereexposed to sleep fragmentation 1 week before engraftment of syngeneic tumor cells, with tumor analysis 4 weeks later. In addition, host contributions were compared through the use of mice deficient in Tlr4 or its effector molecules, namely TRIF or MYD88. Mice subjected to sleep fragmentation were noted to have alterations in the level of tumor-associated macrophages and also exhibited more aggressive tumor development, as evidenced by proximity to the tumor capsule. Interestingly, these aggressive features of tumor growth were abolished in a subset of TLR-4-deficient mice. These findings highlight the potential for sleep dysfunction to alter immune system signaling pathways, leading to an increased risk of malignancy. This is of particular importance in patients with IBD, as this population may already be at an increased risk for the development of malignancy). Accelerating and delaying the environmental light cycle results in the suprachiasmatic nuclei output shifting more rapidly than rhythm locomotor rhythms and the rhythms in peripheral tissues. Circadian disruptions occur in shift workers and appear to contribute to hypertension), diabetes), breast cancer, lung cancer, and elevated prostate-specific antigen. Shift work often entails changes in diet, exercise, and tobacco use, which can confound circadian rhythm and sleep disturbance studies.