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Tips on taking a power nap

Posted Sep 16 2008 7:12am

For many of us, taking an afternoon nap is a great way to refresh when we’re feeling sleepy. The September 2008 issue of Harvard Men’s Health Watch discusses napping, its risks, its benefits, and tips to make it work for you.

People who are sleep deprived feel groggy during the day and may fall asleep when they least want to, perhaps at their desks or, worse, behind the steering wheel. Poor sleep at night may be caused by simply not devoting enough time to sleep or by medical problems that disrupt sleep, such as restless legs syndrome and obstructive sleep apnea. And in some cases, daytime sleepiness can result directly from medical problems such as depression or an underactive thyroid.

Voluntary napping, on the other hand, is not a sign of sleep deprivation, illness, or aging. In fact, a “power nap” can be helpful as well as enjoyable. Many studies of shift workers and other volunteers have reported that a nap as brief as 20 minutes can improve alertness, psychomotor performance, and mood.

Naps, however, aren’t trouble-free. One problem is sleep inertia, or grogginess and disorientation that may accompany awakening from deep sleep. The second problem is nighttime wakefulness.

To get the benefit of a quick snooze without being caught napping, Harvard Men’s Health Watch suggests the following tips:

• Plan to take your nap at a good time in your daily sleep-wake cycle; for many people, sometime between noon and 4 p.m. is best.
• Don’t sleep too long; a 20- to 40-minute nap may refresh your day without keeping you up at night.
• Give yourself 10 to 15 minutes to wake up fully before you resume a demanding task (Newswise).

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Could eating broccoli, or Broccosprouts, or other cruciferous vegetables (even wasabi) regularly help patients with chronic lung disease like COPD? It just might.

According to recent research from Johns Hopkins Medical School, a decrease in lung concentrations of NRF2-dependent antioxidants, key components of the lung’s defense system against inflammatory injury, is linked to the severity of chronic obstructive pulmonary disease (COPD) in smokers. Broccoli is known to contain a compound that prevents the degradation of NFR2.

The findings were published in the second issue for September 2008 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

COPD, or emphysema, is the fourth-leading cause of death in the U.S. and affects more than 16 million Americans.

In this study, researchers examined tissue samples from the lungs of smokers with and without COPD to determine if there were differences in measured levels of NRF2 expression and the level of its biochemical regulators, including KEAP1, which inhibits NRF2, and DJ-1, which stabilizes it. Dr. Biswal had previously shown that disruption in NRF2 expression in mice exposed to cigarette smoke caused early onset of severe emphysema.

When compared to non-COPD lungs, the lungs of patients with COPD showed markedly decreased levels of NRF2-dependent antioxidants, increased oxidative stress markers, a significant decrease in NRF2 protein with no change in NRF2 mRNA levels (indicating that it was expressed, but subsequently degraded), and similar KEAP1 levels, but a marked decrease in the level of DJ-1.

“NRF2-dependent antioxidants and DJ-1 expression was negatively associated with severity of COPD,” wrote principle investigator, Shyam Biswal, Ph.D., an associate professor in the Bloomberg School’s Department of Environmental Health Sciences and Division of Pulmonary and Critical Care at the Johns Hopkins School of Medicine. “Therapy directed toward enhancing NRF2-regulated antioxidants may be a novel strategy for attenuating the effects of oxidative stress in the pathogenesis of COPD.”

While clinical trials to date of antioxidants have been disappointing in improving the clinical course of patients with COPD, this study points to a possibility of benefit from restoring NRF2 levels in damaged lungs by reducing the action of KEAP1, which is an inhibitor of NRF2. “[I]ncreasing NRF2 may also restore important detoxifying enzymes to counteract other effects of tobacco smoke,” wrote Peter Barnes, D.M., of the National Heart and Lung Institute in London, in the accompanying editorial. “This has been achieved in vitro and in vivo by isothiocyanate compounds, such as sulforaphane, which occurs naturally in broccoli and [wasabi].”

Sulforaphane has been shown to be able to restore antioxidant gene expression in human epithelial tissue in which DJ-1 has been reduced. Isothiocyanate compounds such as that found in broccoli inhibit KEAP1, and thus prevent it from degrading NRF2, according to Dr. Barnes. There are many cruciferous vegetables that contain isothiocyanates, and perhaps cruciferous veggies should be considered a type of “functional food”.

“Future studies should target NRF2 as a novel strategy to increase antioxidant protection in the lungs and test its ability to decrease exacerbations and improve lung function in patients with COPD,” concluded Dr. Biswal.

John Heffner, MD, past president of the ATS, commented that “mounting evidence over several decades underscores the importance of oxidant-mediated damage for the development of COPD in addition to other lung diseases. This study adds greater precision to our understanding of the specific antioxidants that may protect the lung against emphysema to allow clinical trials based on valid pathophysiologic principles” (Newswise).

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