Pilot Performance, Jet Lag and Sleep Deprivation

Night-time departures, early morning arrivals, and adjusting to several time zones in a matter of days can rattle circadian rhythms, compromise attention and challenge vigilance. And yet, these are the very conditions many pilots face as they contend with a technically challenging job in which potentially hundreds of lives are at stake.

In an article to be published in a forthcoming issue of Current Directions in Psychological Science, a journal of the Association for Psychological Science, John A Caldwell, a psychologist and senior scientist at Fatigue Science, a Honolulu business focusing on fatigue assessment, examines the problem of sleep deprived pilots by teasing out the complex interplay of inadequate sleep and circadian rhythms. He explains how airline industry solutions miss the point and then suggests other options.

Caldwell points out that "fatigue-related performance problems in aviation have been consistently underestimated and underappreciated, despite the fact that decades of research on pilots and other operational personnel has clearly established that fatigue from insufficient sleep significantly degrades basic cognitive performance, psychological mood, and fundamental piloting skills."

Evidence abounds. In 2004, a corporate airlines flight crashed as it approached Kirksville Regional Airport; in 2008, Honolulu based pilots of Go! Airlines overshot their destination by more than thirty miles because they fell asleep during a trip that was only fifty minutes long. A Northwest Airlines Flight overflew its destination by 150 miles because pilots had dozed off at the controls. In 2009, fifty people were killed when a Continental Connection flight en route from Newark to Buffalo crashed into a house. Pilots failed to respond properly to a stall warning and the flight went out of control.

After examining what went wrong, the NTSB concluded that, "the pilots' performance was likely impaired because of fatigue." Since 1990 the US National Transportation Safety Board has placed pilot fatigue on the Most Wanted List of safety related priorities.

Why? Because as fatigue increases, "accuracy and timing degrade, lower standards of performance are accepted, the ability to integrate information from individual flight instruments into a meaningful and overall pattern declines, and attention narrows. "

In one study, F-117 pilots were deprived of one night of sleep and then were tested on precision instruments. Not only did pilot errors on those instruments double after one night of sleep loss, pilots reported feeling depressed and confused.

Clearly fatigue is fundamentally the result of insufficient sleep, but for pilots the important issue is the consequences of that sleep loss when they are sitting at the control panel. The author suggests that "fatigue related risks increase substantially when (a) the waking period is longer than 16 hours, (b) the preduty sleep period is shorter than 6 hours, or (c) the work period occurs during the pilot's usual sleep hours."

"Regulators, and often the pilots themselves, have tried to address the fatigue problem by focusing on duty hours rather than focusing on the physiological factors that are truly responsible," Caldwell says. "The combination of insufficient sleep and circadian factors is at the heart of the fatigue problem in any operational context."

The two most important variables for alertness are recent sleep and the body's natural circadian rhythm, or "body clock." What that means is that when a pilot reports for duty, he or she should have had from seven to nine hours of good sleep within a reasonable period of time before work and that as often as possible, the work schedule is in some harmony with the pilot's natural daily rhythm.

The amount of time that a pilot is actually working is much less important. But that is the area airlines and regulators have focused on to address the problem. "Hours-of- service" regulations have been instituted to mitigate fatigue, but "that seems to be a function of convenience rather than science." Caldwell writes that in traditional regulatory approaches "one hour of daytime flight in one's home time zone after plenty of sleep is considered to generate the same amount of fatigue as an hour of nighttime flight" that was preceded by a transcontinental transition and sleep outside of a normal sleep cycle. Fortunately, new Federal Aviation Administration regulations better account for the true physiological nature of fatigue, but additional fatigue-management strategies are needed.

Caldwell acknowledges that the very nature of airline travel predisposes pilots to disrupted sleep schedules, but he points out several approaches that can both predict a truly impaired pilot and mitigate the consequences of a lack of sleep. There are some fatigue prediction models that can help determine the impact of work/rest schedules on aviator performance. Crew members should be educated on sleep hygiene so they can snag some restorative rest before duty or during layovers. Onboard cockpit napping should be authorized so that pilots will be able to compensate for a lack of sleep. And new wearable sleep-tracking technologies should be utilized to actually measure the pre-duty and layover sleep of flight crews so that they can better manage and optimize their own sleep.

"As a society, we must come to grips with the fact that the average adult needs 7-9 hours of sleep every single day," he says. "And there is no amount of willpower, professionalism, training, or money that will prevent the performance losses associated with the failure to routinely acquire sufficient sleep."

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Disrupted Internal Clock Means Higher Risk of Diabetes and Obesity

A study by researchers at Brigham and Women's Hospital (BWH) reinforces the finding that too little sleep or sleep patterns that are inconsistent with our body's "internal biological clock" may lead to increased risk of diabetes and obesity. This finding has been seen in short-term lab studies and when observing human subjects via epidemiological studies. However, unlike epidemiological studies, this new study provides support by examining humans in a controlled lab environment over a prolonged period, and altering the timing of sleep, mimicking shift work or recurrent jet lag.

The study will be electronically published on April 11, 2012 inScience Translational Medicine.

Researchers hosted 21 healthy participants in a completely controlled environment for nearly six weeks. The researchers controlled how many hours of sleep participants got, as well as when they slept, and other factors such as activities and diet. Participants started with getting optimal sleep (approximately 10 hours per night). This was followed by three weeks of 5.6 hours of sleep per 24-hour period and with sleep occurring at all times of day and night, thereby simulating the schedule of rotating shift workers. Thus, during this period, there were many days when participants were trying to sleep at unusual times within their internal circadian cycle-the body's "internal biological clock" that regulates sleep-wake and many other processes within our bodies. The study closed with the participants having nine nights of recovery sleep at the usual time.

The researchers saw that prolonged sleep restriction with simultaneous circadian disruption decreased the participants' resting metabolic rate. Moreover, during this period, glucose concentrations in the blood increased after meals, because of poor insulin secretion by the pancreas.

According to the researchers, a decreased resting metabolic rate could translate into a yearly weight gain of over 10 pounds if diet and activity are unchanged. Increased glucose concentration and poor insulin secretion could lead to an increased risk for diabetes.

"We think these results support the findings from studies showing that, in people with a pre-diabetic condition, shift workers who stay awake at night are much more likely to progress to full-on diabetes than day workers," said Orfeu M. Buxton, PhD, BWH neuroscientist and lead study author. "Since night workers often have a hard time sleeping during the day, they can face both circadian disruption working at night and insufficient sleep during the day. The evidence is clear that getting enough sleep is important for health, and that sleep should be at night for best effect."

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Scientists Change the Body's Biological Clock

The discovery of a major gear in the biological clock that tells the body when to sleep and metabolize food may lead to new drugs to treat sleep problems and metabolic disorders, including diabetes.

Scientists at the Salk Institute for Biological Studies, led by Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, showed that two cellular switches found on the nucleus of mouse cells, known as REV-ERBα and REV-ERBβ, are essential for maintaining normal sleeping and eating cycles and for metabolism of nutrients from food.

The findings, reported March 29 inNature, describe a powerful link between circadian rhythms and metabolism and suggest a new avenue for treating disorders of both systems, including jet lag, sleep disorders, obesity and diabetes.

"This fundamentally changes our knowledge about the workings of the circadian clock and how it orchestrates our sleep-wake cycles, when we eat and even the times our bodies metabolize nutrients," says Evans. "Nuclear receptors can be targeted with drugs, which suggests we might be able to target REV-ERBα and β to treat disorders of sleep and metabolism."

Nurses, emergency personnel and others who work shifts that alter the normal 24-hour cycle of waking and sleeping are at much higher risk for a number of diseases, including metabolic disorders such as diabetes. To address this, scientists are trying to understand precisely how the biological clock works and uncover possible targets for drugs that could adjust the circadian rhythm in people with sleep disorders and circadian-associated metabolic disorders.

In mammals, the circadian timing system is orchestrated by a central clock in the brain and subsidiary clocks in most other organs. The master clock in the brain is set by light and determines the overall diurnal or nocturnal preference of an animal, including sleep-wake cycles and feeding behavior.

Scientists knew that two genes, BMAL1 and CLOCK, worked together at the core of the clock's molecular machinery to activate the network of circadian genes. In this way, BMAL1 acts like the accelerator on a car, activating genes to rev up our physiology each morning so that we are alert, hungry and physically active.

Prior to this work REV-ERBα and β were thought to play only a minor role in these cycles, possibly working together to slow CLOCK-BMAL1 activity to make minor adjustments to keep the clock running on time.

However, genetic studies of two genes with similar functions can be very difficult and thus the real importance of REV-ERBα and β remained mysterious.

The Salk scientists got around this hurdle by developing mice in which both genes could be turned off in the liver at any point by giving them an estrogen derivative called tamoxifen. Now mice could develop normally to adulthood, at which point the scientists could turn off REV-ERBα and REV-ERBβ in their livers -- -- an organ crucial to maintaining the correct balance of sugar and fat in blood -- -- to see what effects it had on circadian rhythms and metabolism.

"When we turned off both receptors, the animal's biological clocks went haywire," says Han Cho, first author on the paper and a postdoctoral researcher in Evan's laboratory. "The mice started running on their exercise wheels when they should have been resting. This suggested REV-ERBα and REV-ERBβ aren't an auxiliary system that makes minor adjustments, but an integral part of the clock's core mechanism. Without them, the clock can't function properly."

Digging more deeply into the clockworks, the Salk scientists mapped out the genes that the REV-ERBs control to keep the body operating on the right schedule, finding that they overlap with hundreds of the same genes controlled by CLOCK and BMAL1. This and other findings suggested that the REV-ERBs, act as a break on the genes BMAL1 activates.

"We thought that the core of the clock was an accelerator, and that all REV-ERBα and REV-ERBβ did was to pull the foot off that pedal," says Evans. "What we've shown is that these receptors act directly as a break to slow clock activity. Now we've got a accelerator and a break, each equally important in creating the daily rhythm of the clock."

The scientists also found that the REV-ERBs control the activity of hundreds of genes involved metabolism, including those responsible for controlling levels of fats and bile. The mice in which REV-ERBα and REV-ERBβ were turned off had high levels of fat and sugar in their blood -- -- common problems in people with metabolic disorders.

"This explains how our cellular metabolism is tied to daylight cycles determined by the movements of the sun and the earth," says Satchidananda Panda, an associate professor in Salk's Regulatory Biology Laboratory and co-author on the paper. "Now we want to find ways of leveraging this mechanism to fix a person's metabolic rhythms when they are disrupted by travel, shift work or sleep disorders."

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Disruption of Biological Clocks Can Lead to Neurodegeneration, Early Death, Study Suggests

New research at Oregon State University provides evidence for the first time that disruption of circadian rhythms -- the biological "clocks" found in many animals -- can clearly cause accelerated neurodegeneration, loss of motor function and premature death.

The study was published inNeurobiology of Disease and done by researchers at OSU and Oregon Health and Science University. Prior to this, it wasn't clear which came first -- whether the disruption of biological clock mechanisms was the cause or the result of neurodegeneration.

"In these experiments, we showed through both environmental and genetic approaches that disrupting the biological clock accelerated these health problems," said Kuntol Rakshit, an OSU graduate fellow.

"There's a great deal of interest right now in studies on circadian rhythms, as we learn more about the range of problems that can result when they are disrupted," Rakshit said. "Ultimately we hope that this research will be taken from the laboratory to the bedside."

These studies were done with fruit flies, but the OSU scientists said previous research has indicated there are close parallels between them and humans. Some of the genes regulating circadian rhythms in flies are so important that they have been preserved through millions of years of separate evolution and still do the same thing in humans.

The biological clock, in humans and many other animals, is a complex genetic mechanism tuned to the 24-hour day and regular cycles of light, dark and sleep. It influences a wide range of biological processes, from fertility to hormone production, feeding patterns, DNA repair, sleep, stress reactions, even the effectiveness of medications. In humans, researchers have found strong correlations between disrupted clock mechanisms, aging, and neurologic diseases such as Alzheimer's and Huntington's disease.

The fruit flies used in this research carried two mutations, one that disrupts circadian rhythms and another that causes flies to develop brain pathologies during aging. These double mutants had a 32-50 percent shorter lifespan, lost much of their motor function, and developed significant "vacuoles" or holes in their brains far sooner than flies with a functional clock.

The decline and loss of clock function may be just the beginning of a damaging, circular process, said Jadwiga Giebultowicz, an OSU professor of zoology, member of the OSU Center for Healthy Aging Research and project leader.

"When the biological clock begins to fail, rhythms that regulate cell function and health get disrupted, and we now know that this predisposes the brain to neurodegeneration," Giebultowicz said. "But that neurodegeneration, in turn, may cause more damage to the clock function.

"A healthy biological clock helps protect against this damage," she said. "When the clock fails, the damage processes speed up."

Aging is closely associated with this process, Giebultowicz said, but it's not clear exactly how. Molecular clock oscillations decline during aging. Finding ways to restore them might form a possible therapy for biological clock damage and help to prevent disease, and work in that area will be part of future research.

Read more: http://www.sciencedaily.com/releases/2012/01/120110140225