Chapter 10. Biological Rhythms and Sleep
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Michelle Roberts Health editor, BBC News online Sharing a bed with a newborn increases the risk of sudden infant death syndrome fivefold, research claims. The risk applies even if parents avoid tobacco, alcohol and drugs - other factors firmly linked to cot deaths. The BMJ Open research compared nearly 1,500 cot deaths with a control group of more than 4,500 parents. Current guidance in the UK is that parents should decide where their baby sleeps, but says the safest option is in a crib or cot in the same room. No consensus Many other countries, such as the US and the Netherlands, go further and say parents should not share a bed with their baby for the first three months of his or her life. Prof Bob Carpenter, from the London School of Hygiene & Tropical Medicine, carried out the analysis and says the UK should now follow suit and "take a more definitive stance against bed-sharing for babies under three months". The government said it had asked the public health watchdog NICE to urgently examine its guidance on co-sleeping in light of this new study. BBC © 2013
Link ID: 18179 - Posted: 05.21.2013
20:00 13 May 2013 by Douglas Heaven Genes in cells throughout the body switch on and off throughout the day in a coordinated way. Or at least they should. In people with clinical depression, genes in their brain tissues appear to be significantly out of sync – a finding that could lead to new treatments for the condition. We know from previous studies that genes in cells elsewhere, such as the skin, follow a 24-hour cycle of activity. But identifying patterns of genetic activity in a living brain isn't easy to do. "We always assumed we would have a clock [in our brain]," says Huda Akil at the University of Michigan in Ann Arbor. "But it had never been shown before." Akil and her colleagues examined the brains of 55 people with a known time of death, looking at around 12,000 genes in tissues from six brain regions. By matching the time of death with molecular signs of genetic activity – whether each gene was actively expressing itself or not – the team identified hundreds of genes that follow a daily cycle. Sudden death Akil says it was important to look at the brains of individuals who had died suddenly – through a heart attack or car accident, for example. Slower deaths can cause dramatic changes in the brain that would have obscured what they were looking for, but sudden death freezes the genetic activity. "We can capture an instant," she says. © Copyright Reed Business Information Ltd.
By Samyukta Mullangi A recent article in NYTimes  declared that the rising rate of suicides among our baby boomer generation now made suicides, by raw numbers alone, a bigger killer than motor vehicle accidents! Researchers quoted within the article pointed to complex reasons like the economic downturn over the past decade, the widespread availability of opioid drugs like oxycodone, and changes in marriage, social isolation and family roles. Then I scrolled down, as I always do, to peruse some of the readers’ comments, and that’s when I paused. I suppose in hindsight that I had expected readers to exclaim at the shocking statistics (suicide rates now stand at 27.3 per 100,000 for middle aged men, 8.1 per 100,000 for women), or lament over personal stories of relatives or friends who took their own lives. While I certainly saw a few such comments, I was amazed to discover the number of readers who were sympathetic to the idea of suicide. “Molly” wrote “Why is suicide usually looked upon as a desperate and forbidden act? Can’t we accept that in addition to poverty, loneliness, alienation, ill health, life in world [sic] that is sometimes personally pointless means that death is a relief? I believe the right to die, in a time and place (and wishfully peacefully without violence) is a basic human right.” This post was ‘recommended’ by 351 other readers at the time of this essay being written. © 2013 Scientific American
By VATSAL G. THAKKAR IN the spring of 2010, a new patient came to see me to find out if he had attention-deficit hyperactivity disorder. He had all the classic symptoms: procrastination, forgetfulness, a propensity to lose things and, of course, the inability to pay attention consistently. But one thing was unusual. His symptoms had started only two years earlier, when he was 31. Though I treat a lot of adults for attention-deficit hyperactivity disorder, the presentation of this case was a violation of an important diagnostic criterion: symptoms must date back to childhood. It turned out he first started having these problems the month he began his most recent job, one that required him to rise at 5 a.m., despite the fact that he was a night owl. The patient didn’t have A.D.H.D., I realized, but a chronic sleep deficit. I suggested some techniques to help him fall asleep at night, like relaxing for 90 minutes before getting in bed at 10 p.m. If necessary, he could take a small amount of melatonin. When he returned to see me two weeks later, his symptoms were almost gone. I suggested he call if they recurred. I never heard from him again. Many theories are thrown around to explain the rise in the diagnosis and treatment of A.D.H.D. in children and adults. According to the Centers for Disease Control and Prevention, 11 percent of school-age children have now received a diagnosis of the condition. I don’t doubt that many people do, in fact, have A.D.H.D.; I regularly diagnose and treat it in adults. But what if a substantial proportion of cases are really sleep disorders in disguise? © 2013 The New York Times Company
By Russell Foster "Making teens start school in the morning is ‘cruel,’ brain doctor claims." So declared a British newspaper headline in 2007 after a talk I gave at an academic conference. One disbelieving reader responded: "This man sounds brain-dead." That was a typical reaction to work I was reporting at the time on teenage sleep patterns and their effect on performance at school. Six years on, there is growing acceptance that the structure of the academic day needs to take account of adolescent sleep patterns. The latest school to adopt a later start time is the UCL Academy in London; others are considering following suit. So what are the facts about teenage slumber, and how should society adjust to these needs? The biology of human sleep timing, like that of other mammals, changes as we age. This has been shown in many studies. As puberty begins, bedtimes and waking times get later. This trend continues until 19.5 years in women and 21 in men. Then it reverses. At 55 we wake at about the time we woke prior to puberty. On average this is two hours earlier than adolescents. This means that for a teenager, a 7 a.m. alarm call is the equivalent of a 5 a.m. start for people in their 50s. Precisely why this is so is unclear, but the shifts correlate with hormonal changes at puberty and the decline in those hormones as we age. However, biology is only part of the problem. Additional factors include a more relaxed attitude to bedtimes by parents, a general disregard for the importance of sleep, and access to TVs, DVDs, PCs, gaming devices, cellphones, and so on, all of which promote alertness and eat into time available for sleep. © 2013 The Slate Group, LLC.
By David Levine Sleep deprivation is a quick and efficient way to treat depression. It works 60 to 70 percent of the time—far better than existing drugs—but the mood boost usually lasts only until the patient falls asleep. As an ongoing treatment, sleep deprivation is impractical, but researchers have been studying the phenomenon in an effort to uncover the cellular mechanisms behind depression and remission. Now a team at Tufts University has pinpointed glia as the key players. The researchers previously found that astrocytes, a star-shaped type of glial cell, regulate the brain chemicals involved in sleepiness. During our waking hours, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention impairments. The neurotransmitter causes this pressure by binding to adenosine receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger. In the new study, published online January 15 in the journal Translational Psychiatry, the scientists investigated whether this process is responsible for the antidepressant effects of sleep deprivation. Mice with depressivelike symptoms were administered three doses of a compound that triggers adenosine receptors, thus mimicking sleep deprivation. Although the mice continued to sleep normally, after 12 hours they showed a rapid improvement in mood and behavior, which lasted for 48 hours. © 2013 Scientific American
Published by scicurious under Behavioral Neuro It's late. I've got a lot on my plate. A lot to do. And most of us do. So here I am, burning the midnight oil along with many of my neighbors. I usually count myself lucky to get 7 hours a night, and I AM lucky. For many parents or other caregivers, for example, 7 hours is unheard-of luxury. Is it just me? Probably not. Most of us don't get enough sleep, and those who don't sleep? Snack. But why? And what does this mean for issues like obesity? We know that there has been an increase in obesity in this country. And many people are asking why. There are probably lots of reasons involved: too much sugar, too little exercise, genetics, too much fat. But what about sleep? It turns out that getting less sleep is a risk factor for obesity, but...how are sleep and weight gain related? It turns out that sleep, or lack thereof, can have a lot of influence on how much we need to eat and how much we feel like eating. For example, sleep deprivation changes hunger hormone levels, which can change food intake, and some scientists hypothesize that decreased sleep can change energy expenditure as well. But in order to understand just how lack of sleep influences weight gain, well you need to sleep deprive some people. The authors took 8 men and 8 women who reported getting an average of 8 hours of sleep per night into an inpatient facility. They were taken off caffeine one week before the study and were told to stick to 9 hours of sleep opportunity (stay in bed 9 hours) per night for the first week. They also were put on a diet that was calibrated exactly to maintain their current weight. Copyright © 2013
By Stephani Sutherland Scientists have long known that once we nod off, certain memories grow stronger. One recent theory suggests that forgetting, too, is an essential function of sleep [see “Sleep's Secret Repairs,” by Jason Castro; Scientific American Mind, May/June 2012]. Researchers now suspect that post-traumatic stress disorder (PTSD) may emerge from flaws in sleep's forgetting process. Two studies presented at the 2012 meeting of the Society for Neuroscience in New Orleans indicate that sleep might offer a window of opportunity for weakening memories and providing relief from lingering reminders of trauma. Neuroscientists believe that during sleep, a memory-elimination routine cleans out obsolete information by physically weakening synapses, the junctions between communicating neurons. Gina Poe, a neuroscientist at the University of Michigan, found in mice that for synapses to lose strength, levels of the neurotransmitter noradrenaline must drop. Noradrenaline levels typically fall during REM sleep in rodents and humans, but in people with PTSD the amount stays high throughout sleep. Normalizing noradrenaline with pharmaceuticals, Poe says, “could absolutely be a key target to actually cure PTSD through normal sleep.” In a separate experiment, researcher Asya Rolls of Stanford University hijacked memory remodeling in sleeping mice to make a traumatic association less scary. Rolls and her colleagues conditioned mice to fear the scent of jasmine flowers by pairing the smell with a foot shock. When the mice slept, they released a puff of jasmine. Under normal circumstances, the smell would reactivate and bolster the memory, a process that requires newly made structural proteins. The researchers gave some mice a drug that prevented the manufacture of these building blocks in a key fear-memory area. When these mice woke up, they no longer responded to the odor with fearful behavior, indicating that the memory had been successfully disrupted. The findings might someday translate to a new kind of sleep-based therapy in people whose traumatic experiences are tied to specific sounds and smells—such as the noise of a bomb going off—that can be presented to their sleeping brain. © 2013 Scientific American
Barry Gordon, professor of neurology and cognitive science at the Johns Hopkins University School of Medicine, replies: We are aware of a tiny fraction of the thinking that goes on in our minds, and we can control only a tiny part of our conscious thoughts. The vast majority of our thinking efforts goes on subconsciously. Only one or two of these thoughts are likely to breach into consciousness at a time. Slips of the tongue and accidental actions offer glimpses of our unfiltered subconscious mental life. The intrusive thoughts you may experience throughout the day or before bed illustrate the disconcerting fact that many of the functions of the mind are outside of conscious control. Whether we maintain true control over any mental functions is the central debate about free will. Perhaps this lack of autonomy is to be expected as the foundations for almost all the mind's labors were laid long before our ancestors evolved consciousness. Even deliberate decisions are not completely under our power. Our awareness only sets the start and the end of a goal but leaves the implementation to unconscious mental processes. Thus, a batter can decide to swing at a ball that comes into the strike zone and can delineate the boundaries of that zone. But when the ball comes sailing through, unconscious mental functions take over. The actions required to send him to first base are too complex and unfold too quickly for our comparatively slow conscious control to handle. © 2013 Scientific American
By Rachel Ehrenberg A computer can decode the stuff of dreams. By comparing brain activity during sleep with activity patterns collected while study participants looked at certain objects, a computer learned to identify some contents of people’s unconscious reveries. “It’s striking work,” says cognitive psychologist Frank Tong of Vanderbilt University in Nashville, who was not involved in the research. “It’s a demonstration that brain activity during dreaming is very similar to activity during wakefulness.” The work, reported April 4 in Science by Japanese researchers led by Yukiyasu Kamitani of Advanced Telecommunications Research Institute International, adds to somewhat scant knowledge of how the brain constructs dreams, says Tong. The research could lead to a better understanding of what the brain does during different states of consciousness, such as those experienced by some coma patients. Dreams are a bit of a black box and difficult to study. Experiments with mice have revealed aspects of sleep and dreaming, such as how the experiences contribute to forming memories. But a mouse can’t tell you what it dreamed about. And the sleep stage that’s richest in dreams — REM sleep — typically kicks in about 90 minutes after a person conks out, making it time consuming to gather data on dreams. The noisy fMRI brain scanning machine doesn’t help. To skirt these experimental issues, the researchers recorded brain activity in three adult male volunteers during the early stages of sleep. After the subjects had dozed off, they were repeatedly awakened and asked for detailed reports on what they had seen while sleeping. In an example, one participant stated: “Well, there were persons, about three persons, inside some sort of hall. There was a male, a female and maybe like a child. Ah, it was like a boy, a girl and a mother. I don't think that there was any color.” © Society for Science & the Public 2000 - 2013
by Gisela Telis Insomniacs desperate for some zzzs may one day have a safer way to get them. Scientists have developed a new sleep medication that has induced sleep in rodents and monkeys without apparently impairing cognition, a potentially dangerous side effect of common sleep aids. The discovery, which originated in work explaining narcolepsy, could lead to a new class of drugs that help people who don't respond to other treatments. Between 10% and 15% of Americans chronically struggle with getting to or staying asleep. Many of them turn to sleeping pills for relief, and most are prescribed drugs, such as zolpidem (Ambien) and eszopiclone (Lunesta), that slow down the brain by binding to receptors for GABA, a neurotransmitter that's involved in mood, cognition, and muscle tone. But because the drugs target GABA indiscriminately, they can also impair cognition, causing amnesia, confusion, and other problems with learning and memory, along with a number of strange sleepwalking behaviors, including wandering, eating, and driving while asleep. This has led many researchers to seek out alternative mechanisms for inducing sleep. Neuroscientist Jason Uslaner of Merck Research Laboratories in West Point, Pennsylvania, and colleagues decided to tap into the brain's orexin system. Orexin (also known as hypocretin) is a protein that controls wakefulness and is missing in people with narcolepsy. Past studies successfully induced sleep by inhibiting orexin, but had not looked into its effects on cognition. The researchers developed a new orexin-inhibiting compound called DORA-22 and confirmed that it could induce sleep in rats and rhesus monkeys as effectively as the GABA-modulating drugs. © 2010 American Association for the Advancement of Science.
Link ID: 17994 - Posted: 04.05.2013
By ANAHAD O'CONNOR Doctors have plenty of good reasons to persuade people with sleep apnea to get it treated. The widespread disorder causes disruptions in breathing at night, which can ruin sleep and raise the likelihood of problems like obesity and fatigue. The standard treatment for the condition, a mask worn at night that delivers continuous positive airway pressure, or CPAP, significantly improves apnea, even though many people don’t like to wear it. But the mask may do more than restore normal breathing at night. Some research suggests it reduces inflammation, benefiting overall health. Many studies have looked at the link between sleep apnea and high levels of inflammatory markers. To get a clearer picture of the connection, a team of researchers recently carried out a meta-analysis that pooled data from two dozen trials involving over 1,000 patients. It was published last month. The data suggested that treating apnea with CPAP significantly reduces levels of two proteins associated with inflammation: tumor necrosis factor and C-reactive protein, or CRP. Sleep apnea is a risk factor for several severe chronic conditions like Type 2 diabetes and heart disease. It’s not clear whether apnea helps drive the development of these disorders or vice versa. But reducing inflammation may be one way in which treatment with CPAP reverses some of the long-term consequences of the sleep disorder. THE BOTTOM LINE: Treating sleep apnea with positive airway pressure helps to lower systemic inflammation, which might prevent some of the other problems associated with the disorder. Copyright 2013 The New York Times Company
By Markham Heid As if physical fatigue and a foggy brain weren't bad enough, restless nights may also harm your heart. A new multi-year study published in the European Heart Journal finds evidence of a substantial link between insomnia and the risk of heart failure. For more than 11 years, a study team from several Scandinavian universities tracked the sleeping habits and heart failure rates of more than 50,000 men and women. The researchers focused on the three major hallmarks of insomnia: trouble falling asleep, trouble staying asleep, and waking up still feeling fatigued. Unfortunately, the results of their analysis are enough to keep a person up at night: Among participants who experienced just one of those symptoms "occasionally" or "often," rates of heart failure increased 5% and 14%, respectively, compared to those who didn't struggle with sleep. But for those who experienced all three symptoms frequently, heart failure rates more than tripled, says study co-author Lars Laugsand, PhD, of the Norwegian University of Science and Technology. "Insomnia is a disorder marked by hyperarousal," Laugsand says. So instead of the restful state you should experience while sleeping, insomnia increases activity in your sympathetic nervous system, which in turn releases a flood of stress hormones into your bloodstream. This hormonal surge appears to boost blood pressure, which explains why periods of insomnia can make you feel like your heart is pounding or your body is overheating. © 2013 NBCNews.com
Link ID: 17971 - Posted: 04.01.2013
By Melissa Healy, Listening in on the electrical currents of teenagers’ brains during sleep, scientists have begun to hear the sound of growing maturity. It happens most intensively between the ages of 12 and 161 / 2: After years of frenzied fluctuation, the brain’s electrical output during the deepest phase of sleep — the delta, or slow-wave phase, when a child’s brain is undergoing its most restorative rest — becomes practically steady. That reduced fluctuation in electroencephalogram signals appears to coincide with what neuroscientists have described as major architectural changes in the brain that pave the way for cognitive maturity. While babies, toddlers and young children are taking in and making sense of the world, their brain cells are wiring themselves together willy-nilly, creating super-dense networks of interwoven neurons. But as we reach and progress through adolescence, neuroscientists have observed, a period of intensive “synaptic pruning” occurs in which those networks are thinned and the strongest and most evolutionarily useful remain. In a study published last week, scientists from the University of California at Davis say they believe the slowed fluctuations observed during the delta phase of teens’ sleep may be evidence of that pruning process at work. And since major mental illnesses such as schizophrenia appear to take root during adolescence, the authors of the study say the changing architecture of sleep may offer clues as to how and when mental illness sets in. © 1996-2013 The Washington Post
By Gary Stix A little shuteye refreshes. Right, but what does that really mean? Not talking here about leaping out of bed ready for a five-mile run upon awakening, but rather about what’s happening at the level of individual brain cells deep inside your head. A new study by R. Douglas Fields, a pioneer in researching out-of-the-mainstream brain areas and neural activity, holds one promising suggestion. Fields’s team at the National Institutes of Child Health and Development in Bethesda, Maryland, built on an earlier observation that during sleep (or even when just chilling out), neural signals travel the “wrong way” in cells of a critical region of the hippocampus, the brain structure involved with forming some types of new memories. The new study by Fields demonstrates, in a lab dish, that this reverse trafficking functions as a form of “editing,” a physical paring back of inessential parts of a brain cell to ensure that you don’t forget what you learned the previous day. Specifically, electrical signals in the CA1 area of the hippocampus reverse direction like the opposite flow of cars during the evening rush hour. The spiking electrical pulses move up instead of down the long extensions of nerve cells known as axons. The train of spikes pass through the cell body where the nucleus resides before reaching the ends of thousands of tiny branching tendrils called dendrites. © 2013 Scientific American
Link ID: 17938 - Posted: 03.23.2013
Nursing home residents who take a class of sleep medications that includes Lunesta and Ambien may be at higher risk for hip fractures compared with those who do not take these nonbenzodiazepine hypnotic drugs, according to a Harvard Medical School study. The study involved more than 15,000 nursing home residents who were on average 81 years old and were documented by Medicare to have had a hip fracture between July 2007 and December 2008. Nearly 11 percent of the residents with hip fractures took these drugs. Residents who took the prescription sleep medications were 66 percent more likely to sustain a hip fracture than those who did not. The risk was greater among new users of the medications and those suffering mild to moderate mental and physical decline. Those who took the medication for less than two months were more than twice as likely to fracture their hip, the study found. Nonbenzodiazepenes have been known to alter memory, attention, and balance, which may be why there is a greater risk of physical injury when taking the medication, the researchers wrote. Based on the findings, nursing home staff should try to treat sleep problems using nondrug strategies first, such as increased daytime activity and discouraging daytime napping, according to the researchers. © 2012 NY Times Co
by Jennifer Viegas Roosters are genetically programmed to crow with the dawn, finds a new study that could also help to explain why dogs bark and cats meow. Previously it was unknown if crowing roosters were simply reacting to their environment. “‘Cock-a-doodle-doo’ symbolizes the break of dawn in many countries,” Takashi Yoshimura of Nagoya University, who worked on the study, was quoted as saying in a press release. “But it wasn’t clear whether crowing is under the control of a biological clock or is simply a response to external stimuli.” That’s because things like a car’s headlights can set a rooster off too, as anyone who has lived near these birds knows. To solve the mystery, Yoshimura and colleagues kept roosters under round-the-clock dim lighting. This didn’t deter the roosters. No matter what, they kept crowing each morning just before dawn. The researchers say this is proof that the vocalizing is entrained to a circadian rhythm. In short, the roosters are genetically programmed to crow at a certain time. At some point, the rising sun set the roosters’ internal clock, so now they crow every 24 hours. Most animals, and plants too, have such an internalized timing mechanism. That’s why we tend to eat, sleep, exercise and more at around the same times. By consciously being aware of the schedule, our body has a chance to adapt to it, so well-functioning circadian rhythms are often tied to good health. © 2013 Discovery Communications, LLC.
Keyword: Biological Rhythms
Link ID: 17919 - Posted: 03.19.2013
By TARA PARKER-POPE The best path to a healthy weight may be a good night’s sleep. For years researchers have known that adults who sleep less than five or six hours a night are at higher risk of being overweight. Among children, sleeping less than 10 hours a night is associated with weight gain. Now a fascinating new study suggests that the link may be even more insidious than previously thought. Losing just a few hours of sleep a few nights in a row can lead to almost immediate weight gain. Sleep researchers from the University of Colorado recruited 16 healthy men and women for a two-week experiment tracking sleep, metabolism and eating habits. Nothing was left to chance: the subjects stayed in a special room that allowed researchers to track their metabolism by measuring the amount of oxygen they used and carbon dioxide they produced. Every bite of food was recorded, and strict sleep schedules were imposed. The goal was to determine how inadequate sleep over just one week — similar to what might occur when students cram for exams or when office workers stay up late to meet a looming deadline — affects a person’s weight, behavior and physiology. During the first week of the study, half the people were allowed to sleep nine hours a night while the other half stayed up until about midnight and then could sleep up to five hours. Everyone was given unlimited access to food. In the second week, the nine-hour sleepers were then restricted to five hours of sleep a night, while the sleep-deprived participants were allowed an extra four hours. Copyright 2013 The New York Times Company
When the mind is at rest, the electrical signals by which brain cells communicate appear to travel in reverse, wiping out unimportant information in the process, but sensitizing the cells for future sensory learning, according to a study of rats conducted by researchers at the National Institutes of Health. The finding has implications not only for studies seeking to help people learn more efficiently, but also for attempts to understand and treat post-traumatic stress disorder — in which the mind has difficulty moving beyond a disturbing experience. During waking hours, electrical signals travel from dendrites — antenna-like projections at one end of the cell — through the cell body. From the cell body, they then travel the length of the axon, a single long projection at the other end of the cell. This electrical signal stimulates the release of chemicals at the end of the axon, which bind to dendrites on adjacent cells, stimulating these recipient cells to fire electrical signals, and so on. When groups of cells repeatedly fire in this way, the electrical signals increase in intensity. Dr. Bukalo and her team examined electrical signals that traveled in reverse?from the cell’s axon, to the cell body, and out its many dendrites. The reverse firing, depicted in this diagram, happens during sleep and at rest, appearing to reset the cell and priming it to learn new information. It was previously known that, during sleep, these impulses were reversed, arising from waves of electrical activity originating deep within the brain. In the current study, the researchers found that these reverse signals weakened circuits formed during waking hours, apparently so that unimportant information could be erased from the brain. But the reverse signals also appeared to prime the brain to relearn at least some of the forgotten information. If the animals encountered the same information upon awakening, the circuits re-formed much more rapidly than when they originally encountered the information.
US researchers have found a link between working night shifts and the risk of ovarian cancer. A study of more than 3,000 women suggested that working overnight increased the risk of early-stage cancer by 49% compared with doing normal office hours. One possible explanation was disruption of the sleep hormone melatonin, the researchers said. But experts warned more work was needed and there might be other explanations. It does however follow an earlier association made between shift work and breast cancer. The International Agency for Cancer Research has previously identified working shift patterns that disrupt the body's natural "clock" as a probable cause of cancer. In the latest investigation, researchers looked at 1,101 women with advanced ovarian cancer, 389 with borderline or early disease and 1,832 women without the condition. Overall, a quarter with advanced cancer said they had worked night shifts, compared with a third of those with borderline disease and one in five of the control group. Analysis of the data showed a 24% increased risk of advanced cancer and 49% increased risk of early-stage disease for night workers compared with those who worked during the day. But the results were only significant for women over the age of 50, the researchers reported in Occupational and Environmental Medicine. And the risk did not seem to increase for those who had worked night shifts for the longest. BBC © 2013