Study: Lack of sleep may cause brain to “eat” itself
ST. LOUIS — Make sure you get enough shut-eye. According to a new study lack of sleep may cause your brain to “eat” itself.
Scientists say burning the midnight oil can cause your brain to break down more of its cells and connectors. Researchers say this could explain why a chronic lack of sleep puts people at risk of Alzheimer’s disease, dementia and other neurological disorders.
This is an excerpt from the “Sleep Duration” study:
Sleep patterns of quantity and quality are affected by a variety of cultural, social, psychological, behavioral, pathophysiological, and environmental influences and have shown secular trends alongside changes in the modern society requiring longer hours of work, more shift-work and 24-7 availability of commodities, curtailing the duration of sleep to fewer hours per day across westernized populations. This has led to increased reporting of fatigue, tiredness, and excessive daytime sleepiness. Lack of sleep also exerts deleterious effects on a variety of systems with detectable changes in metabolic, endocrine, and immune pathways.
Over the last few decades there has been growing evidence to suggest that too little sleep and too much sleep are associated with adverse health outcomes, including total mortality, cardiovascular disease, type 2 diabetes, hypertension and respiratory disorders, obesity in both children and adults, and poor self-rated health.
The relationship between duration of sleep and mortality has been often described as a U-shaped association, although other studies have not found such a uniform effect or have found no association. It is believed that different mechanisms may underlie such associations at either end of the distribution of sleep duration. Given the variety of studies, the large differences in the types and sizes of populations examined, the duration of follow-up, and the size of the effects, it is difficult to draw immediate conclusions on the consistency of the associations at either end of the distribution of sleep duration and at its effect size. The latter is important in public health to ascertain the likely impact at population level, if amenable to modification.
The aims of this study were to (a) systematically review published prospective population-based studies, (b) carry out a meta-analysis to assess whether the global evidence supports the presence of a relationship between either short or long duration of sleep and all-cause mortality, and (c) obtain a quantitative estimate of the risk to assess the consistency and potential public health relevance. A meta-analysis allows the combination of the results of different studies, increasing the overall statistical power and the precision of estimates while controlling for bias and limiting random error.