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Chronic sleep deprivation and the impact “sleep debt” has on functioning and thinking cannot be reversed by one good night’s sleep, new research suggests.

While a night of good sleep can make you feel and operate better in the short run, the ill effects of long-term sleep loss linger much longer.

In fact, “chronic sleep loss from six hours of sleep per night for two weeks causes a similar level of impairment as staying awake for 24 hours,” said the study’s lead author, Dr. Daniel A. Cohen, a neurologist and sleep medicine specialist affiliated with Brigham and Women’s Hospital and Beth Israel Deaconess Medical Center, both in Boston.

Chronically sleep-deprived people are “vulnerable to sudden sleepiness, errors and accidents,” Cohen added, describing the vulnerability as something that won’t disappear after a full night of “catch-up” sleep.

Cohen and his colleagues report their findings in the Jan. 13 issue of Science Translational Medicine.

They note that 16 percent of Americans are believed to routinely sleep six hours a day or less.

Such chronic sleep deprivation is thought to be most prevalent in professions that involve shift work and overtime, such as trucking and transportation, the military, the health-care industry and emergency-response organizations. Many such workers try to cope with long stretches of insufficient sleep — and the safety hazards such sleep debt poses — by sleeping for longer periods whenever they can.

But does this type of catch-up strategy help restore alertness? To find out, the researchers tracked the behavior of nine healthy men and women, 21 to 34 years old. Participants were put on a three-week sleep-wake schedule that involved staying awake for 33 hours, followed by 10 hours of sleep.

This chronic sleep deprivation routine — which they said mimicked, for example, the typical on-call schedule of a resident physician — meant that the participants slept just 5.6 hours for every 24-hour period.

Data on a second group of participants, who slept a more normal eight hours in every 24-hour period, were used as a point of comparison.

The team found that in the immediate aftermath of a 10-hour sleep period, the sleep-deprived participants did perform within normal parameters on cognitive function and reaction-time testing.

However, as the study progressed, the now chronically sleep-deprived participants’ ability to recover full function after each 10-hour sleep began to fade. Their motor skills, as well as their ability to focus, pay attention and remain alert, all weakened over the ensuring 33-hour wake period.

Relatively normal reaction times for the sleep-deprived also dissipated significantly as day turned to night. The researchers attributed this to the interplay between chronic sleep deprivation and the body’s circadian rhythms.

The bottom line: People who build up a “chronic sleep debt” during the week in the hope that they can then “pay it back” with a full night or two of sleep on the weekend are in for a disappointment.

“A long night of sleep can largely hide the effects of chronic sleep loss,” Cohen said. But he said the sense of regaining full function is illusory.

“At this point,” Cohen noted, “we still do not know how many normal sleep-wake cycles it takes to catch up on chronic sleep loss.”

Gregg D. Jacobs, a sleep specialist with the Sleep Disorders Center at University of Massachusetts Memorial Medical Center in Boston, said that “sleep loss is not a one-size-fits-all phenomenon” and cautioned against generalizing too much from the findings.

“The sleep schedule they studied is similar to what residency physicians would experience,” he noted. “However, very few people other than resident physicians ever undergo a sleep schedule like this. Sleep loss in daily life is much more modest for most people.”

Jacobs also noted that the participants were relatively young and that older adults often need less sleep. And he added that sleep loss and an individual’s related performance can often depend on how motivated a person is to execute a task, which can be different depending on whether sleep loss and performance is job-related or not.

“The problem with lab studies on sleep loss,” he stressed, is that “they do not generalize well to daily life.”

SOURCES: Daniel A. Cohen, M.D., research fellow, division of sleep medicine, Brigham and Women’s Hospital, and staff neurologist, Beth Israel Deaconess Medical Center, Boston; Gregg D. Jacobs, Ph.D., sleep specialist, Sleep Disorders Center, University of Massachusetts Memorial Medical Center, Worcester, Mass.;

New research raises the possibility that people who have the highest levels of a chemical known as BPA in their urine are more likely to be diagnosed with heart disease.

But the findings don’t prove that bisphenol A (BPA) actually causes heart disease — one scientist even suggests other factors may be at play — and researchers can’t explain why statistics suggest that urinary levels of the chemical dropped by one-third over just two years during the last decade.

Still, the numbers raise more questions about BPA, which is found in a huge variety of plastic products. “The risks associated with exposure to BPA may be small, but they are relevant to very large numbers of people,” said study author Tamara S. Galloway, a researcher at the University of Exeter in England.

BPA, which is used to make hard, clear plastic and epoxy resin, is found in everyday items, from food and drink containers to electronic and medical equipment.

It has been linked to sexual dysfunction, heart disease, cancer, diabetes and even hyperactivity in girls. But the chemical industry questions the validity of studies and contends that BPA is safe.

“Studies of this type are very limited in what they tell us about potential impacts on human health. While they can provide helpful information on where to focus future research, by themselves they cannot and should not be used to demonstrate that a particular chemical can cause a particular effect. The public should be confident that BPA is one of the most studied chemicals. Regulatory bodies from around the world have recently completed scientific evaluations and found BPA safe in food-contact products, including canned foods and beverages,” stated Steven G. Hentges, of the American Chemistry Council’s Polycarbonate/BPA Global Group.

“The study itself does not establish a cause-and-effect relationship between BPA exposure and heart disease. In addition, the robustness of these limited findings is questionable, as fewer than 50 participants self-reported health conditions without medical confirmation,” Hentges added.

Galloway and colleagues sought to confirm the results of their previous research that showed a link between BPA exposure and heart disease. They compared data regarding BPA levels in urine from 2003-2004 (in 1,455 people) to 2005-2006 (in 1,493 people), and reported their findings in the Jan. 13 edition of the online journal PLoS ONE.

The researchers don’t know why the levels dropped by one-third over just two years, although they speculate that decreased use of BPA may explain it.

After adjusting their figures to reduce the chance that they’ll be thrown off by factors such as the age, gender and race of the subjects, the researchers found that high urinary levels of BPA boosted the risk of heart disease by 1.3 to 1.4 times compared to those with low levels.

That doesn’t necessarily mean BPA makes people have heart problems. Galloway acknowledged that heart disease could somehow affect the way that the body deals with BPA and might boost its levels.

“All we can say is that the two are associated, and that the association has now been shown in two independent study populations, making it unlikely to be a chance finding,” Galloway said.

Another possible factor is the diet of those who had high BPA levels, said Dr. Hugh S. Taylor, director of Yale University School of Medicine’s division of reproductive endocrinology and infertility.

“People who eat out of cans and plastic have higher BPA levels, however they also have a lot of other reasons to have heart disease. Bad diets are clearly a cause of heart disease as well,” he said. “This study is interesting and should make people concerned; it does not prove that BPA causes heart disease.”

To find out if one thing causes another, scientists often turn to the “gold standard” in medical research: a randomized, controlled double-blind study. In this case, people would be randomly assigned to either be exposed to BPA or not, then researchers would watch to see that happened.

However, in regards to potentially harmful BPA exposure, “this would be unacceptable to any ethics committee,” Galloway said. “Also, based on the current data, it would likely be very hard to find enough people for the control group who did not have detectable levels of BPA in their urine.”

In other words, almost everyone has BPA in their system, making it harder to figure out exactly what it does, if anything, to the body.

SOURCES: Tamara Galloway, Ph.D., professor, ecotoxicology, University of Exeter, U.K.; Hugh S. Taylor, M.D., director, division of reproductive endocrinology and infertility, Yale University School of Medicine, New Haven, Conn.; Steven G. Hentges, Polycarbonate/BPA Global Group, American Chemistry Council;

educed dosages of dopamine agonists, drugs routinely used to treat Parkinson’s disease, can cause symptoms similar to those experienced by addicts in withdrawal, such as anxiety, panic attacks, pain, dizziness and drug cravings, researchers say.

The symptoms of what the researchers have dubbed “dopamine agonist withdrawal syndrome” have been linked to a disruption in levels of dopamine in the brain, according to the study published in the Jan. 12 issue of the Archives of Neurology.

“Like cocaine and methamphetamines, dopamine agonists work by stimulating the reward pathways in the brain,” senior study author Dr. Melissa J. Nirenberg, said in a news release from Weill Cornell Medical Center.

“For this reason, it makes sense that they would engender similar withdrawal symptoms, particularly in those with high cumulative drug exposure,” explained Nirenberg, associate director of the Parkinson’s Disease and Movement Disorders Institute at New York-Presbyterian Hospital/Weill Cornell Medical Center and an assistant professor of neurology and neuroscience at Weill Cornell Medical College.

Dopamine agonists are used as an alternative to the drug L-DOPA, which can cause side effects in patients with Parkinson’s, such as involuntary movements. The dopamine agonist drugs — pramipexole (Mirapex) and ropinirole (Requip) — are also approved for treatment of restless legs syndrome.

In the study, researchers looked at the medical records of 93 people with Parkinson’s disease, 26 of whom lowered their doses of the dopamine agonist drugs. Five of these patients — 19 percent — experienced dopamine agonist withdrawal syndrome. Three of the five patients couldn’t adjust to the withdrawal symptoms and had to stay on the dopamine agonists, which can cause impulse control disorders, such as compulsive behaviors related to gambling, shopping, eating or sexual activity.

SOURCE: Weill Cornell Medical Center, news release