December 26, 2008
More Sleep Reduces Coronary Artery Calcification

Some people want to know which vitamin pills to take to slow aging. But I see far bigger benefits from focusing on the basics first. Here's an example of a basic good health practice with big benefits. Get enough sleep to reduce calcification of your arteries.

One extra hour of sleep per night appears to decrease the risk of coronary artery calcification, an early step down the path to cardiovascular disease, a research team based at the University of Chicago Medical Center reports in the Dec. 24/31 issue of JAMA. The benefit of one hour of additional sleep was comparable to the gains from lowering systolic blood pressure by 17 mm Hg.

About 12 percent of those in the study, healthy volunteers in their 40s, first developed coronary artery calcification over five years of follow-up. Calcified arteries, however, were found in 27 percent of those who slept less than five hours a night. That dropped to 11 percent for those who slept five to seven hours and fell to six percent for those who slept more than seven hours a night.

The benefits of sleep appeared to be greater for women. They did not vary according to race.

"The consistency and the magnitude of the difference came as a surprise," said study director Diane Lauderdale, PhD, associate professor of health studies at the University of Chicago Medical Center.

Sleep might benefit by lowering blood pressure or maybe stressed-out people just have less time for sleep.

The authors suggest three possible ways that shorter sleep could connect to calcification. First, there may be some factor not yet identified that can both reduce sleep duration and increase calcification. Second, although blood pressure measured during examinations did not seem to explain the association, blood pressure generally declines during sleep, so the 24-hour average blood pressure of those who sleep less may be higher, and that could lead to calcification. Finally, stress or a stress hormone like cortisol, which has been tied to decreased sleep and increased calcification, may play a role. Cortisol data were not available for all study participants.

You can't miss out on sleep without it costing you in a variety of ways. Reduced sleep for a single night increases harmful inflammatory response in the body.

Philadelphia, PA, September 2, 2008 – Loss of sleep, even for a few short hours during the night, can prompt one's immune system to turn against healthy tissue and organs. A new article in the September 15th issue of Biological Psychiatry, by the UCLA Cousins Center research team, reports that losing sleep for even part of one night can trigger the key cellular pathway that produces tissue-damaging inflammation. The findings suggest a good night's sleep can ease the risk of both heart disease and autoimmune disorders such as rheumatoid arthritis.

UCLA Cousins Center researchers reported similar results in 2006 as well.

Sleeps helps you learn complicated tasks too.

Share |      Randall Parker, 2008 December 26 03:31 PM  Aging Cardiovascular Studies

bbm said at December 26, 2008 6:03 PM:

Again, you can not leap from association to cause and effect.

For example, is it not plausible that being ¨type A¨ could cause both tendency to reduced sleep hours and increase risk for CAD?

These types of association studies are crap.

Randall Parker said at December 26, 2008 9:52 PM:


First off, I included an excerpt about different mechanisms, not all of which ran from lack of sleep toward calcification.

However, I also linked back to previous post on a report which showed increased inflammation from making people lose part of a night's sleep. Also, in that previous post's comments I reported on what the effects are from modafinil. All this is consistent with the arrow of causation starting from the lack of sleep. This study doesn't exist in isolation.

James Bowery said at December 30, 2008 5:50 AM:

'One night' sleep deprivation stimulates hippocampal neurogenesis
Grassi Zucconi G, Cipriani S, Balgkouranidou I, Scattoni R.
Department of Cellular and Environmental Biology,
University of Perugia, Perugia, Italy.
Brain Res Bull. 2006 Apr 28;69(4):375-81.


Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12h during their physiological period of rest, and were injected with bromodeoxyuridine 4h and 2h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.

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