While some people may use aromatherapy as their form of health resources for dealing with stress, there are others who simply let their stress build.

But what they don’t realize is that they may be taking out their aggression in their sleep. According to a new study published in Head & Face Medicine, people who are stressed by problems in their daily lives or constantly having trouble at work may be more likely to grind their teeth at night.

The unconscious grinding of one’s teeth, which is otherwise known as Sleep Buxism, is extremely common with people who are trying to escape the problems of their daily lives. While this may be viewed as a de-stresser, it’s not healthy for a human’s teeth.

“Bruxing can lead to abrasive tooth wear, looseness and sensitivity of teeth, and growth and pain in the muscles responsible for chewing. Its causes are still relatively unknown, but stress has been implicated,” explained lead researcher Maria Giraki. For individuals who are prone to sleep bruxism, taking nutritional supplements such as calcium may boost the strength of teeth.

The purpose of sleep remains one of the greatest unsolved mysteries in science. Although we spend roughly one-third of life asleep, researchers still do not know why.

While sleep is often thought to have evolved to play an unknown but vital role inside the body, a new theory now suggests it actually developed as a method to better deal with the outside world.

Sleep is often seen as bad for survival. Sleeping animals might be vulnerable to predators and cannot eat, mate, scout for prey, care for relatives or perform other behaviors key to getting by. As such “it’s been thought that sleep must serve some as-yet unidentified physiological or neural function that can’t be accomplished when animals are awake,” said sleep researcher Jerome Siegel at the University of California at Los Angeles.

However, Siegel noted that a number of species could make do without sleep for long spans of time.

For instance, newborn dolphins and killer whales and their mothers show an almost total lack of what might be called sleep in other animals — that is, extended periods of immobility — for several weeks after birth, when these animals normally migrate. Similar findings are seen in birds during migrations, “where birds can fly for days on end without stopping,” he explained.

“So you have to start thinking — if sleep has a vital universal function, how are they able to survive without it?” Siegel said.

Carnivores get their Zzzz’s
In a survey of the sleep times of a broad range of animals, Siegel found that carnivores sleep more than omnivores, which in turn sleep more than herbivores. To him, this suggested the role of sleep was linked to an animal’s niche in its ecosystem.

One example Siegel cited was the big brown bat, which sleeps 20 hours a day, perhaps the record for mammals.

“One might suppose this animal sleeps so much because of some unknown function that sleep has for it,” Siegel said. “But it seems more easily explained by the fact that it preys on moths and mosquitoes that only come out at dusk and are active for only a few hours before the temperature falls and they can’t function. If it spent more time awake, it would spend more energy but not be as successful at hunting, and if it came out in the day it would be exposed to predatory birds that can see much better than it can.”

Siegel proposes the main function of sleep is to increase an animal’s efficiency and minimize its risk by controlling how a species behaves with regards to its surroundings.

“All species have times when they need to be active and ones where they don’t, and so you can see species optimizing their periods of inactivity in response to their environment,” Siegel said. “I’m saying that sleep helps animals adapt to the world around them.”

Other theories abound
There are many other theories as to what the function of sleep is. These include:

• A role in learning — either helping to form new connections between brain cells or pruning unnecessary ones.
• Reversing damage from oxidative stresses incurred while awake.
• Promoting longevity.

However, Siegel contends that sleep cannot be explained by the relative size of the brain, lifespan, body size, “and other such variables that have been intensively examined over the years with conflicting and confusing results.”

For instance, “if one knows the size or brain size of different animals you cannot predict or explain their sleep time or depth. The baboon has the same total sleep time and total REM sleep time as the guinea pig,” he said. “The long-living elephant has one of the shorted sleep times whereas the long-living bat has one of the longest sleep times.”

Siegel emphasized, “My theory doesn’t mean that significant things don’t happen in sleep — it just means there is no vital universal function for sleep. A whole spectrum of things are accomplished better in sleep than awake in some animals, such as digesting food, but it doesn’t mean the function of sleep is digestion.”

U.S. researchers said:

Many nights of too little sleep when the body’s rhythm says it is time to snooze have cumulative detrimental effects on how a person performs and could be a safety risk, the researchers wrote in the journal Science Translational Medicine.

“Insufficient sleep over multiple sleep-wake cycles causes performance to deteriorate much faster for every additional hour we spend awake, particularly during the biological night,” lead author Dr. Daniel Cohen of Brigham and Women’s Hospital in Boston said in a telephone interview.

On average, a person needs about eight hours a night to preserve performance, said Cohen, a neurologist. Acute sleep loss is being awake for more than 24 hours in a row and chronic sleep loss is getting only about four to seven hours of sleep per night, he said.

Cohen’s team tracked nine healthy volunteers — five men and four women — to see what effect a combination of acute sleep loss, chronic sleep loss and biological sleep rhythm might have on their ability to function.

The researchers found that while most participants caught up on acute sleep loss with a single night of 10 hours sleep, those with chronic sleep loss showed deteriorating performance for each hour spent awake.

The volunteers were kept in a hospital for 38 days and lived on various sleep cycles. They were tested every four hours to measure alertness and attentiveness.

Cohen said researchers know that three days is not enough to recover from chronic sleep loss, but they still do not know how many days or weeks may be needed.

Cohen said people may not realize that they have a chronic sleep debt because it slowly builds over weeks.

“We can falsely feel like we’ve recovered quickly from chronic sleep loss because recent sleep makes us feel relatively restored early the next day,” he said.

“People may be largely unaware that they are chronically sleep-deprived,” he said. “It’s when they then stay up and try to pull an all-nighter that they are much more vulnerable to sudden sleepiness, inattentiveness and … potentially accidents and errors.”

A urine test that can differentiate between dangerous and safe snoring is possible, say researchers at the University of Chicago.

They looked at 90 children referred to a clinic to be evaluated for breathing problems in sleep, and 30 controls.

A number of proteins were increased in the urine of the children diagnosed with dangerous snoring.

The research is published in the American Journal of Respiratory and Critical Care Medicine.

The team say their findings need to be repeated but may lead to a simple test.

Sleep tests

The children all had standard overnight tests and some were classified as having obstructive sleep apnoea (OSA).

OSA can lead to mental, behavioural, cardiovascular and metabolic problems in children. It is estimated that up to 3% of all children up to the age of nine may suffer from it.

The researchers collected the children’s first sample of urine on the morning after the sleep study.

They used a process with fluorescent dyes to separate and characterise the proteins in the urine and found three proteins at higher concentrations in the urine of children with OSA: urocortin 3, orosomucoid and uromodulin.

Another protein, kallikrein 1, was at lower levels in the urine.

The scientists say further research is needed to work out which proteins work best for a test and the right time to get the urine sample.

They think that it may be possible to develop a simple colour-based test like a pregnancy kit that can be done by doctors or parents.

Diagnostic screening

“It was rather unexpected that the urine would provide us with the ability to identify OSA” said Dr David Gozal, who led the research.

“If we can develop this further we might be able to screen children for OSA for a fraction of the cost of keeping them in a sleep clinic overnight, and it would overcome the huge waiting lists for such screening.”

Ian Balfour, a respiratory consultant at the Royal Brompton Hospital, which carries out many sleep studies on children, said: “OSA is a big problem in children with large tonsils or who are obese.

“Some overweight children with this problem have to use ventilators to sleep at night.

“This is an interesting finding – the implication is that the children’s renal and kidney function is being affected by their OSA.

“But the research is too far from being something practical doctors and patients would be able to use.”

Dr Paul Gringras, consultant in Paediatric Neurodisability and Sleep Medicine at the Evelina Children’s Hospital, agreed that OSA was an important condition because of its harmful impact on physical health as well as learning and behaviour.

“The specialist centres that can accurately identify true cases are few, and at full capacity” he said.

“It is appealing to look at certain proteins from a single urine sample that could make the diagnosis.

“This study is the first step towards this possibility, but more work is needed to check the test is reliable, when the best time of day is to perform the test, and, finally, to simplify the biochemical tests so that they are easier to carry out.”

A new study suggests that older men who suffer from restless leg syndrome (RLS) may also be at risk for erectile dysfunction.

A new study published in the journal Sleep suggests that erectile dysfunction was 16 percent more prevalent in men who suffered from restless leg syndrome symptoms between five and 14 times a month. Similarly, those who had RLS symptoms more than 15 times a year were 78 percent more likely to suffer from erectile dysfunction.

The study conducted a survey of 23,119 men with an average age of 69. It was found that 4 percent of men suffered from restless leg syndrome and 41 percent had erectile dysfunction.

The prevalence of erectile dysfunction increased with age. Researchers noted that both problems relate to the nervous system, posing as a link.

“The mechanisms underlying the association between RLS and erectile dysfunction could be caused by hypofunctioning of dopamine in the central nervous system, which is associated with both conditions,” said lead author Xiang Gao.

Nutritional supplements such as zinc and vitamin C may help improve erectile function.

Teenagers when

Of 15,500 12 to 18-year-olds studied, those who went to bed after midnight were 24% more likely to have depression than those who went before 2200.

And those who slept fewer than five hours a night had a 71% higher risk of depression than those who slept eight hours, the journal Sleep reports.

It is estimated 80,000 UK children and young people have depression.

The researchers from Columbia University Medical Center in New York looked at data from 15,500 teenagers collected in the 1990s.

One in 15 of those studied were found to have depression.

As well as the higher risk of depression, those who were set a bedtime by their parents of after midnight were 20% more likely to think about suicide than those whose bedtime was 2200 or earlier.

Those who had less than five hours sleep a night were thought to have a 48% higher risk of suicidal thoughts compared with those who had eight hours of sleep.

Teenagers who reported they “usually get enough sleep” were 65% less likely to be depressed.

Depression and suicidal thoughts were also more likely in girls, older teenagers and in those who had a lower self-perception of how much parents care about them.

Most of the parents of the adolescents in the study set a bedtime of 2200 or earlier.

A quarter set a bedtime of 2400 or later.

On average the teenagers were having seven hours and 53 minutes sleep a night – less than the nine hours recommended at that age.

Study leader Dr James Gangwisch said although it it was possible that youngsters with depression struggle to sleep, the fact that parental set bedtimes were linked with depression suggests that a lack of sleep is somehow underpinning the development of the condition.

He said a lack of sleep could affect emotional brain responses and lead to moodiness that hindered the ability to cope with daily stresses.

This moodiness could affect judgment, concentration and impulse control.

Regular exercise

“Adequate quality sleep could therefore be a preventative measure against depression and a treatment for depression,” he added.

Sarah Brennan, chief executive at the mental health charity YoungMinds, said: “Enough sleep, good food and regular exercise are all essential to stay emotionally healthy.

“Nearly 80,000 children and young people suffer with depression, yet we are still failing to provide our young people with the help and support to cope with it and prevent it.

“Providing parents with information about how to look after your body, for example by getting enough sleep, and how to get help if they are worried about their teenager, will ensure problems are tackled early and prevent serious mental health conditions such as depression.”

New discoveries into how the body clock works could provide clues to help combat jet lag, research suggests.

A University of Manchester team studied special cells which they say play an important role in regulating a person’s body clock.

The cells had been thought to be inactive during the day – but their research found the opposite is true.

It is hoped the findings may also pave the way to combating sleep disorders triggered by body clock malfunctions.

Professor Hugh Piggins, an expert in neuroscience at the university, said the research will allow a new approach to being able to tune our daily clock.

Two cells

The Manchester research turns on its head the idea that the brain keeps the body clock on track by firing more cells during daylight and very few during the night.

“The traditional model said the clock and the brain communicated to the rest of the brain via the number of electrical impulses that the brain cells were producing,” Prof Piggins told the BBC World Service’s Health Check programme.

“These impulses would travel around the brain, telling it what time of day it is.

“What we’ve found is in fact that there are at least two types of cells in this part of the brain.”

These brain cells behave unlike any other cell seen so far, and contain a key gene – per1 – which allows them to sustain unusually high levels of “excitability”.

The cells becoming so “excited” that they seem quiet or even dead; but then later they calm down, recover and become normally active again.

It is this activity which tells the human body when to be awake.

Sleep dysfunction

Prof Piggins added: “There’s a lot of interest in the pharmaceutical industry, obviously, to try to develop chemical treatments to reset your daily clock to help counteract things like jetlag.

“Or, perhaps more importantly, different kind of sleep disorders for which dysfunctions in this clock are often involved.”

This study marks the first time these “quiet” cells have been studied.

“This may mean that elsewhere in the brain there are cells like this that can also survive these very unusual conditions.”

While nutritional supplements such as ginko biloba may help with improving memory, a study from Northwestern University indicates that even though the participants were in a deep sleep, they were able to hear sounds that enhanced their memory when they awoke.

The study played 25 different sounds while the participants slept, including a cat meowing and a tea kettle whistle.

Previously, the participants were asked to drag matching objects across a computer screen as a way of spatial learning. It was found the participants were more accurate in the exercise their nap with the sounds.

Researchers believe that this study may be key in determining how sleep affects memory retention.

“We are beginning to see that deep sleep actually is a key time for memory processing,” said senior author Ken Paller.

Paller added that this study will open the door to many questions and that further research is needed to understand how memory process during the sleep stage.

The two individuals also performed a great service to science: As participants in sleep research conducted by the University of California, San Francisco, the subjects’ unusual sleep patterns led researchers to a specific gene for “short sleepers.”

The discovery of the gene, known as Dec2, was published in August in Science and became the first gene in humans known to control sleep quantity. The idea that a gene might determine sleep duration seemed improbable prior to this study, but the researchers also replicated the effect in mice and in fruit flies.

“Without that you could not convince anyone, not even myself,” says Ying-Hui Fu, Ph.D, one of the UCSF researchers.

It’s an important discovery, but not because it explains why so few Americans get the requisite eight hours of sleep; the fact that it was found in only two participants out of several hundred means that it’s likely the gene is rare.

Instead, the finding gives researchers an essential clue about what role other genes might play in sleep regulation. It’s becoming increasingly clear that the answer to improving sleep lies in identifying the vulnerabilities of our genetic makeup and understanding how our poor sleep habits can exacerbate them.

The Role of Genes

Though the discovery of the short-sleeper gene was the first of its kind, other researchers have connected sleep apnea to a gene variation and narcolepsy to a gene mutation. These disorders disrupt the normal sleep cycle in maddening and sometimes life-threatening ways.

Sleep apnea, which affects an estimated 12 million Americans, causes arrested or shallow breathing during the night. Carriers of this marker are twice as likely to suffer from the common disorder, which also predisposes sufferers to higher risk for stroke, cardiovascular disease and heart attacks.

Narcolepsy, a far less common disorder that affects only 135,000 Americans, is associated with a mutated gene that causes abnormal processing of neurotransmitters known to play a role in wakefulness. The brain of a narcolepsy sufferer fails to regulate the sleep-wake cycle normally, sending the person into sporadic fits of sleep, unwillingly, throughout the day.

Stanford professor and researcher Dr. Emmanuel Mignot, who is director of the university’s Center for Narcolepsy, discovered the gene mutation and variation for narcolepsy and sleep apnea in 1999 and 2001, respectively.

Mignot’s hunch — and it’s just opinion until science proves him right — is that the spectrum of sleep disorders that also includes insomnia, nightmares and sleepwalking can also be traced back to genetic causes. Recent research has shown that even restless legs syndrome, long a punch line in pop culture that in fact keeps 12 million Americans awake at night, is strongly associated with gene variations.

What intrigues Mignot is how people respond to such sleep disruptions, particularly those that lead to chronic sleep deprivation.

“Some people will be extremely impaired and some people won’t care at all,” he says, noting that scientists control for factors like participant demographics and sleep hygiene and get the same resulst. “It’s clear that some people have fundamentally different needs independent of the environment, and they’re likely genetic.”

The Black Box of Sleep

David F. Dinges, Ph.D., chief of the division of sleep and chronobiology at the University of Pennsylvania School of Medicine, knows this phenomenon well. Data gathered from his studies of several hundred participants has shown time and again that when sleep is chronically reduced, individuals have markedly different responses to handling that deprivation. Yet when they get the same amount of adequate sleep, behavior remains consistent.

Researchers have no scientific explanation for this — yet. Fu, Mignot and Dinges all strongly believe it has to do with gene variations, but for now the field remains — as Fu calls it — a black box.

In the meantime, the 40 million Americans who suffer from chronic sleep disorders will have to manage their conditions through medication, improved sleep hygiene and cognitive behavioral therapy.

The former is a common-sense approach to sleep that focuses on simple steps like maintaining a regular sleep schedule, eliminating distractions like noise and abstaining from caffeine and alcohol close to bedtime. The latter is a form of therapy that aims to help the sleepless cope with their condition by teaching them a variety of coping skills, including yoga and meditation.

Dinges hopes that research will lead to the discovery of key genes that determine and affect our sleep cycles, enabling medicine to provide personalized diagnoses and treatments for those who don’t sleep well.

“It’s not an issue of broken or bad genes,” says Dinges. “We want to use that information in a personalized way to help people understand what environmental things will put them a risk because of their genetic variations.”

Sleep deprivation makes it harder for the brain to memorize newly learned information, and scientists may have found a way around that problem.

Writing in Nature, University of Pennsylvania graduate student Christopher G. Vecsey, professor Ted Abel, PhD, and colleagues identify a chemical chain reaction linked to sleep deprivation — and a possible solution.

The researchers used electrical shocks to train lab mice not to move in certain cages, and then deprived some of the mice of sleep for five hours. Those sleep-deprived mice were worse at remembering not to move around in those cages than mice that had been allowed to sleep.

When deprived of sleep, the mice made more of an enzyme called phosphodiesterase 4 (PDE4). In turn, the surplus of PDE4 caused a shortfall of a compound called cAMP, which is involved in forming new memories in a brain area called the hippocampus.

The researchers ran the tests on more mice. And this time, they injected some of the mice with rolipram, an experimental drug that blocks PDE4. For comparison, other mice got placebo shots.

The mice got those shots right after being trained not to move in certain cages, but before sleep deprivation. Sleep-deprived mice that had gotten the rolipram shot aced the memory test; they remembered not to scurry around the cages where they were likely to get shocked.

The researchers aren’t recommending rolipram for sleep-deprived people.

But they say their study shows that “it may be possible” to make drugs that target PDE4, and that such drugs “may prove useful in the treatment of the cognitive effects of sleep deprivation.”