Christian Glatz

Bio: Christian Glatz is an academic researcher from German Aerospace Center. The author has contributed to research in topics: Sleep disorder & Polysomnography. The author has an hindex of 1, co-authored 1 publications receiving 60 citations.

Sleep and circadian rhythm disruption in psychiatric and neurodegenerative disease

Abstract: Sleep and circadian rhythm disruption are frequently observed in patients with psychiatric disorders and neurodegenerative disease. The abnormal sleep that is experienced by these patients is largely assumed to be the product of medication or some other influence that is not well defined. However, normal brain function and the generation of sleep are linked by common neurotransmitter systems and regulatory pathways. Disruption of sleep alters sleep-wake timing, destabilizes physiology and promotes a range of pathologies (from cognitive to metabolic defects) that are rarely considered to be associated with abnormal sleep. We propose that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms. The stabilization of sleep may be a means by which to reduce the symptoms of--and permit early intervention of--psychiatric and neurodegenerative disease.

Burden of Disease from Environmental Noise: Quantification of Healthy Life Years Lost in Europe

Abstract: The health impacts of environmental noise are a growing concern. At least one million healthy life years are lost every year from traffic-related noise in the western part of Europe. This publication summarises the evidence on the relationship between environmental noise and health effects, including cardiovascular disease, cognitive impairment, sleep disturbance, tinnitus, and annoyance. For each one, the environmental burden of disease methodology, based on exposure-response relationship, exposure distribution, background prevalence of disease and disability weights of the outcome, is applied to calculate the burden of disease in terms of disability-adjusted life-years. Data are still lacking for the rest of the WHO European Region. This publication provides policy-makers and their advisers with technical support in their quantitative risk assessment of environmental noise. International, national and local authorities can use the procedure for estimating burdens presented here to prioritize and plan environmental and public health policies.

Cardiovascular effects of environmental noise exposure

Abstract: The role of noise as an environmental pollutant and its impact on health are being increasingly recognized. Beyond its effects on the auditory system, noise causes annoyance and disturbs sleep, and it impairs cognitive performance. Furthermore, evidence from epidemiologic studies demonstrates that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, and stroke. Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. This review focuses on the cardiovascular consequences of environmental noise exposure and stresses the importance of noise mitigation strategies for public health.

Environmental stressors and cardio-metabolic disease: part II-mechanistic insights.

Abstract: Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.