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You sleep at night and are active during the day that's how things work for humans, but theoretically if a human whose parents lived on earth were to be born in another planet resembling earth but the difference was that this planet has an 8.5 hour day, what kind of changes will this person undergo?if a human who grew up on earth suddenly had to move to this planet how would his body adapt? what would be the difference between a person who moves to this 8.5 hour day planet with the person that was born there? and would the person who was born on this planet be active for 4.25 hours and then sleep for the other 4.25?
Humans have evolved for 24 hour days and our bodies would not adapt well to this short of sleep/wake cycles (whether or not they were born there, unless they have been there for many generations and have been able to evolve for the new time). Our bodies would still want to spend about the same amount of time sleeping and being awake.
If we tried to adjust our sleep cycles to this planet with 8.5 hour days, we would experience many of the stresses that occur during jet lag (Google Scholar search), which can cause depression. Jet lag is identical to experiencing one day which is shorter or longer than the typical 24 hours.
The sunlight helps set our circadian rhythm, but 8.5 hours would be too fast. I thought I heard for an experiment that used mice that supports this, but I still haven't found the reference yet.
Nbogard referenced the article Plasticity of the Intrinsic Period of the Human Circadian Timing System, which showed that the circadian rhythm in humans can be altered by up to 0.65 hours by the use of lights. This is consistent with what I mentioned that the sunlight helps to set our circadian rhythm.
The best way to adapt would be to use artificial lighting to keep your days about 24 hour days (artificial light during waking hours, heavy curtains during sleeping hours), as mentioned in ThePopMachine's answer.
Actually, for your example it would be pretty easy to adapt. You just have a 25.5 hour day with 12.75 hours of day and 12.75 hours of night. Except you have a 4.25 hour period in the middle of the day where you stay inside and use lights (like in the evening for most people on Earth) and a 4.25 hour period at night where you make sure your eye mask is on.
Added convenience: there are three different choices of when to call day so it's good for shift work and there's no problem with traffic. Let's move there!
Your Body's Internal Clock and How It Affects Your Overall Health
We all feel the ebb and flow of daily life, the daily rhythms that shape our days. The most basic daily rhythm we live by is the sleep-wake cycle, which (for most) is related to the cycle of the sun. It makes us feel sleepy as the evening hours wear on, and wakeful as the day begins. Sleep-wake and other daily patterns are part of our circadian rhythms, (circum means "around" and dies, "day") which are governed by the body's internal or biological clock, housed deep within the brain.
But research has been finding that the body's clock is responsible for more than just sleep and wakefulness. Other systems, like hunger, mental alertness, and mood, stress, heart function, and immunity also operate on a daily rhythm.
The existence of the biological clock can be particularly apparent when it's off kilter: Jet lag and shift work can throw our normal patterns out of whack and take a toll on physical and mental health. Even shifting the clock an hour forward or backward when daylight savings time begins or ends can disrupt our biological clocks.
Disrupting our body's natural cycles can cause problems. Studies have found there are more frequent traffic accidents and workplace injuries when we spring forward and lose an hour of sleep. Heart patients are at greater risk for myocardial infarction in the week following the Daylight Savings time shift. But even more significant is that science continues to discover important connections between a disrupted clock and chronic health issues, from diabetes to heart disease to cognitive decline.
It turns out that the same genes and biological factors that govern our internal clock are also involved in how other body systems operate -- and break down. It can be hard to determine whether a disrupted clock leads to health problems, or whether it's the other way around.
We're beginning to understand more about how the clock interacts with and helps govern the function of other systems and affects our overall health. In fact, keeping your body's daily cycle on an even keel may be one of the best things you can do for your overall health.
YOUR BODY WANTS TO RUN LIKE A SWISS WATCH
The idea of a biological clock may sound like a quaint metaphor, but there is actually a very distinct brain region that is charged with keeping time: It is an area called the suprachiasmatic nucleus (or SCN), situated right above the point in the brain where the optic nerve fibers cross. This location enables the SCN to receive the cues it needs from light in the environment to help it keep time.
But genes also influence the body's clock and circadian rhythms. The system requires both types of input -- light and genes -- to keep it on track. To stay on the 24-hour cycle, the brain needs the input of sunlight through the eyes to reset itself each day. When humans are allowed to run off their body's clock apart from input from the sun, by being kept in continuous darkness, the body's daily cycle tends to lengthen to about 25 hours. And when people or animals lack the genes that help control the clock's cycle, their sleep-wake cycles can stray even further, or be absent completely. The need for both kinds of cues -- light and genes -- make the biological clock a classic example of how genes and the environment work in tandem to keep the system functioning well.
Our Behaviors and Body Functions Run on Cycle
Melatonin is one hormone responsible for our body's daily cycle. When night falls and there is less light input to the SCN, the production of melatonin, the hormone responsible for making us feel sleepy, goes up. When it's dark, more melatonin is secreted, which signals the brain to go into sleep mode. When the sun rises, melatonin secretion is inhibited, and the brain's awake circuits resume.
Other systems also follow a daily rhythm, many of which are controlled by hormones and other compounds that receive cues from the biological clock. For example, the hormones responsible for hunger and metabolism rise and fall over the course of the day. The chemicals involved in immune system function also vary. Compounds that encourage the inflammatory response rise at night, (which is why fevers tend to spike then), and those that inhibit it rise during the day.
This is likely because the body is better at fighting infection while it is at rest, and energy can be poured into the effort, rather than into other functions. And activity of the stress response system -- particularly in secretion of the stress hormone, cortisol -- is reduced during the nighttime hours, and heightened in the early morning.
Although there are certain areas of the body, like the heart, that are able to govern their own function to some degree, there is strong evidence that the body clock plays a major role in controlling many of these fluctuations (such as in blood sugar) over the 24-hour period.
ENVIRONMENTAL DISRUPTIONS TO THE BODY'S CLOCK
Some of the best knowledge we have about the roles the biological clock plays in our health come from instances in which the cycle gets out of sync. This can happen for different reasons, and we're just starting to understand them in greater detail. Sometimes we do things ourselves that disrupt our normal rhythms, like flying to a distant time zone. Sometimes it's other factors, (like genes or biology) that play a role.
Flying across the country on the red-eye is a prime example of how we can disrupt our own clocks, and a far more extreme example than the spring forward/fall back ritual in many parts of the U.S.
When jet lag sets in, we feel disoriented, foggy, and sleepy at the wrong times of day because, after changing time zones, our body clock tells us it's one time and the outside environment tells us it's another. In fact, jet lag can be considered one type of circadian rhythm disorder. It can be treated simply be allowing the body to adjust to the new time, although it may take several days for external cues (light) to help the internal clock catch up or fall back with its new cycle.
Shift work is another example of how we can get ourselves off-cycle, and this too can develop into a circadian rhythm disorder over the long term. People who work the night shift not only have a hard time with their sleep patterns (feeling sleepy at work or experiencing insomnia during the day), but other systems in their bodies can also feel the effects -- and they can be chronic. It's not been clear exactly why this connection exists, but weight gain or metabolic changes may be involved. These phenomena underline how particular behaviors or lifestyles can affect the body's clock, but there are other factors at play, like genetics and body chemistry.
BIOLOGICAL AND GENETIC DISRUPTIONS AND THEIR IMPLICATIONS FOR HEALTH
The interactions of the clock are complex, and their effects on different body systems are intricate, but we're starting to understand more about how the nuts and bolts of the clock work, and affect each system of the body, from our hearts to our moods.
Since the biological clock is, in fact, a biological entity, things can go wrong with it that may have less to do with lifestyle or the environment, and more to do with the mechanisms of the clock itself. For example, there's more to the clock-diabetes link than just turning our sleep cycle around, though sleep can make a difference.
The same genes that control the receptors for the sleep hormone melatonin are involved in insulin release, which could also play a role in diabetes risk. When melatonin receptor genes have mutations that damage the connection between the biological clock and insulin release people have a significantly higher risk of developing diabetes.
The Rhythms of the Heart
The heart is one organ that, although it can keep time by itself to some degree, relies on the brain's biological clock for cues. For years doctors and researchers have noticed that heart problems like fatal arrhythmias are more likely to occur at certain times of the day, both in the early morning and to a lesser degree, in the evening hours. Taking blood pressure medication in the evening seems to improve its effectiveness because it works with the body's circadian rhythms.
The reason for this has recently become clear: A genetic factor involved in the rhythm of the brain's clock also controls the electrical activity in the heart. Mice who are bred to lack this factor -- Kruppel-like factor 15 (KLF15) -- or have too much of it, have many more heart problems than normal mice. Understanding this clock-heart connection could help experts design drugs to reduce the risk of heart problems in people by stabilizing the levels of these compounds.
Immunity and Vaccinations
Most of us have experienced being more susceptible to getting sick when sleep-deprived. The reason for this appears to be that certain chemicals responsible for immune function, like cytokines, wax and wane throughout the day and sleep deprivation deprives us of their best effects. Animals who are given vaccines at specific times of the day, when certain proteins that sense bacterial invaders are highest, have a much stronger immune response, even weeks later. The same is very likely true for humans.
Body rhythms don't just enhance vaccines' ability to provide immunity they can affect the body's ability to battle infection on its own. When mice were exposed to a bacterial infection, the severity of their infection reflected the time of day they were infected.
It's not just in the lab that these effects are seen. Babies who are given vaccines in the afternoon -- and who sleep more right after -- have better immune responses to the innoculations. It's likely that the same effect is true in adults, since our immune systems fluctuate in similar ways.
Our internal clocks also have a hand in whether we feel up or down emotionally. People with mood disorders like depression, bipolar disorder, and seasonal affective disorder (SAD) have altered circadian rhythms. In fact, sleep disturbances, both sleeping too much and too little, are one of the key symptoms of depression and other mood disorders.
The relationship between body rhythms and mood is an intricate one, and likely has to do with how the brain chemical serotonin fluctuates in relation to the light-dark cycle and throughout the year as the days become longer and shorter. Mice bred to have problems with serotonin function also have seriously altered daily rhythms. People's serotonin levels increase during the part of the day when there is more light available.
The circadian rhythm-mental health connection has also been linked to disease states like Alzheimer's, Parkinson's, and Huntington's, and even autism spectrum disorder. Researchers are finding that disrupted daily rhythms can be good predictors for the development of mild cognitive impairment that comes with age, and even for dementia.
Experiments in fruit flies (which may seem a far cry from humans, but actually serve as excellent models in biological clock studies) show that degeneration in the brain occurs much more rapidly when there are problems in the functioning of a key clock gene, and the lifespans of the flies are significantly shortened. Knowing more about how the clock is related to cognitive function and decline could help experts predict -- and perhaps one day prevent -- it from occurring in humans as well.
Paying attention to the body's natural rhythms is probably more important to our health than we realize. It's not just sleep deprivation that affects our well-being, but it's also the alteration of our biological rhythms that can interfere with so many body functions, making us more prone to health problems like infection, mood problems, and even heart disease.
Why the biological clock becomes disrupted in certain people, or naturally with age, is not completely clear, but some have recently suggested that it could in part have to do with the aging of the eyes. Natural changes in the lens and even the development of cataracts let less light into the eye and, therefore, the brain and this can affect biological rhythms.
There are many other reasons our bodies' clocks can go out of sync, which probably involve a combination of genetic predisposition and lifestyle choices, such as alcohol consumption. Sometimes the clock can get unset -- as with the changes associated with daylight savings time, air travel, or shift work -- and there's only so much we can do until our body and its clock are in equilibrium again.
But keeping your schedule on track as much as possible is probably the best advice. You probably have a pretty good sense of your body's natural rhythms intuitively. Avoid disruptions to your eat-sleep cycles. Practice good sleep hygiene, and stick to a sleep schedule that works well for your body to keep the system in its natural rhythm. Turning in a little earlier, cutting back on caffeine late in the day, and saving that last bit of work for the morning rather than staying late up to finish it, can make a big difference in how your internal clock functions and in how you feel.
7 Answers 7
We actually have very little information on this question. I'm assuming from your "not interested in evolution" phrasing that you're interested in a 1 generation case, where a baby is born in low gravity and stays there. NASA is very interested in questions like this, because it helps them deal with the physiological effects of space on astronauts.
The answer is really complicated because the human body grows in response to stimuli. However, not all stimuli are gravity related. Some of our spinal growth after birth is due to gravity. However, bed-ridden children still grow to reasonably normal heights, so there are clearly many other factors wedged against each other to support spinal growth. (This would change if you opened the question to evolutionary effects, but in 1 generation, its a bit simpler).
The real issue for human growth in space is the few cases where we need gravity to develop. It is known that our hearts atrophy in space because they don't need to pump as much blood. It is not yet known if, in that atrophied state, it is strong enough to raise a healthy child. For all we know their immune system could be stunted because it didn't get enough oxygen! These unknowns are why we don't allow anyone but fully fit, grown adults into space. Our society believes it is not worth the risk.
If you want humans to be taller due to low gravity, I would look at what could cause a human to want to be taller. Look at gymnasts and contortionists. I guarantee nothing they do was ever "planned" for by genetics. They simply want to be more flexible, so they put their body into situations where it can grow into a more flexible shape. If there were strong advantages of being tall (such as reaching fruit of local fauna which grows tall and slender due to gravity), I think you would find remarkable effects, especially in the 1-3 year old region of a child's life. That would go doubly so with a few generations of social evolution, to build a family structure that raises children to want to be tall from a young age.
Sheesh, he's not interested in a multigenerational evolutionary hypothetical here.
Likely humans born in high gravity would develop stronger hearts, lungs, and musculature. Bones would likely be thicker as well, if not caused by developing in high G then from healing from constant breakage. (Falling would be very dangerous on a high G planet) Children would learn to walk slower and may be significantly shorter, no one would ride bicycles, and planes and off planet trips would be very expensive fuel wise.
Low G humans would likely lose the ability to survive in a normal G environment due to atrophy or, in children born on the planet, lack of development but it's doubtful that they would be rendered unable to survive in their own environment. Children would all ride unicycles but would be very jealous of the off-worlders who could fly pedalcopters. Depending on the lack of gravity low cost compressed air jetpacks may be available and people would not need to worry about falling from (again depending on the gravity) almost any height. Expect to see people safely disembarking from air transportation without needing it to land.
(this is my own theory related to a story line I'm working on, very unsure on it's validity, but it involves multiple generations during a prolonged space flight in a zero g environment. was actually going to post it to this forum eventually for input). I'm also working on the assumption that critical functions such as respiratory, circulatory, and digestion can continue to function in different gravities.
Assumptions. not only is it zero-g, but we are lacking sun exposure as well. Air pressure is earth like in the zero-g environment.
The human body will lengthen significantly if raised entirely in a zero g environment. Limbs will become longer, including the neck. Bone density will be significantly less and it's quite likely this being will weigh significantly less than a Human raised on Earth. Bone structure (although elongated) won't change in a single generation. however multiple generations in zero-g may start to see their bones loose rigidity, become flexible structures instead. Several generations later may result in a elongated semi-eel like being that can quickly bend around curves and corners of the ship/structure it resides in.
Hands could have an interesting change. Where a human on Earth needs to grip and pick-up things against the weight of gravity, and zero-g human would not. rather they would be spending most of their time on 'button' like interfaces. Gives me this image of elongated fingers exceedingly adept at a 'key press' up and down motion instead of a bulky hand designed to lift against the weight of gravity. Precision in a zero-g human would become more required than strength (precision often being sacrificed in favor of raw strength) and the hand will reflect that.
Muscle structure would also develop significantly differently. Where our strongest muscles (Glutes) tend to be focused on keeping us upright, a space child wouldn't have that same need to develop the ability to stand. Nor would walking muscles (Quads) have the pressure on them to grow to the strength a human on Earth's would. Pushing off would be the preferred locomotion of a zero-g human, perhaps giving them larger calf muscles in relation to their other muscles (yet still not as developed as one that needs to fight gravity on a constant basis.
Skin colour would also be significantly different as the pigments that protect us from the sun wouldn't be required. Don't ask why, but I have the image of eventually greying skin, especially over multiple generations.
We may develop a new 'sense' or a variation on one that we already have but don't much consider. Orienting yourself on Earth is a 2-d exercise for the most case. up and down are in relation to gravity and is easier to enforce. As divers and deep sea swimmers know, up and down isn't quite as simple to detect without this obvious gravitational pull. How exactly a zero-g human would learn to orient itself and perceive it's 3-d location could be considered a 'new sense' to some degree.
All of this is purely speculation as we really have no idea what a zero-g human would look like.
Scientist studies how modern life is messing with sleep
DULUTH, Minn.-Shadab Rahman's business is sleep, but it wasn't his dream job.
"I needed a summer research project," the Harvard Medical School instructor said. "The only available lab was in Toronto. . They studied sleep."
That was when Rahman, now 36, was an undergraduate with an interest in cardiovascular medicine. His summer in Toronto led to a second summer as a research associate at the same lab and then work at another Toronto lab with the same mentor as he achieved his doctorate degree.
Now an expert on the effect of light on sleep and circadian rhythm - the "body clock" that guides our daily patterns - Rahman will be in Duluth next month as one of the speakers during a Celebrate the Night Sky symposium.
Like organizers of that week of activities, Rahman is an advocate of darkness at night. Excess light at the wrong times of day, Rahman said recently during a phone interview from his office in Boston, "is a major problem."
During the interview, Rahman talked about light and darkness, sleep and not being able to sleep, our circadian rhythm and how it gets disrupted.
It turns out that blue light, not red or orange or green, is the light of choice for your intrinsically photosensitive retinal ganglion cells, also known as IPRGCs.
If you didn't know you had IPRGCs, don't feel bad. They weren't discovered until the early 2000s, Rahman said. They're lodged in the retina, and they have special photoreceptors called melanopsin. That's what triggers our body clock's response to light, Rahman said, and melanopsin's strongest response is to blue light.
Practical application: Rahman conducted a study in Toronto involving nurses who do shift work. The study involved using "blue blockers" to filter out blue light in an attempt to neutralize the disruption in their circadian rhythm. "Obviously every study has caveats, but we got some favorable results where the nurses were sleeping better after they used the intervention," he said.
The flip side is that blue light can enhance alertness, Rahman said. It's as effective as caffeine and preferable if you don't want to stay awake later - because the effect of blue light wears off much more quickly than the effect of caffeine.
There's no getting around the National Sleep Foundation recommendation for seven to eight hours of sleep, Rahman said. "Really, they recommend 7½, but that's for adults," he said. "For adolescents, it's much longer" - between nine and 10 hours.
But what about those highly successful people who say they get by on six, five or four hours of sleep at night?
It's artificial wakefulness, according to Rahman.
"The short-term effects (of being sleep-deprived) are typically increased sleepiness, drowsiness, cognitive detriments," he said. "And what's our solution to that? Drink coffee. . In the United States, we are the highest consumers of coffee. We chug down coffee all day. People are drinking coffee morning, afternoon, evening, just to stay awake. That just goes to show how sleep-deprived we are."
Does he practice what he preaches?
Yes, Rahman said. He tries to get 7½ hours of sleep at night. He drinks coffee, but only in the morning. "But having said that, I also have a 6-month-old and a 2½-year-old at home, so that's not ideal conditions for sleep."
We come with a body clock that runs on a 24-hour cycle - nearly, Rahman said.
Your personal body clock might run on a 23.5-hour cycle or a 24.5-hour cycle. The average body clock cycle is 24.2 hours.
Light allows your body clock to adjust to make up the difference, Rahman said. But it's a problem for some people who are blind - those whose retinas have been destroyed. If that's you, and you have a 24.2-hour body clock, you'll be off by 12 minutes on any given day. In 10 days, you'll be off by 120 minutes - two hours.
"So if you go to sleep at midnight tonight and your body clock can't adjust to the light-dark cycle . then in 10 days you're going to . feel sleepy at 2 a.m.," he said.
Incidentally, the 24-hour clock doesn't apply just to humans, or just to mammals, but to all living beings, Rahman said.
"There are clocks in tube worms that are miles under the ocean," he said. "They are never exposed to light, and yet they have a body clock."
Astronauts in the International Space Station have two challenges to their circadian rhythm, Rahman said. They do shift work. And because they're circling the Earth, they have a 90-minute light-dark cycle. "And the human body is such that the body clock cannot adapt to a 90-minute light-dark cycle."
With NASA funding, Rahman and other researchers tested new LED lights for the space station to see what effect they might have on circadian rhythm. That study was done on the ground, but a second phase is underway in which use of the lights is being studied in the space station itself.
Many of us not only get too much light at night, we don't get enough during the day, Rahman said.
"We need light during the day," he said. "And that's why I always say you can't get enough light during the day if you're indoors."
That's because our ancestors spent their days outside, getting up to a million lux of light from the sun. Even a very bright light intensity indoors is only about 2,000 lux, Rahman said. If your office is in a basement and you have no windows, you might be getting 200-300 lux.
Conversely, the brightest campfires our ancestors lit after the sun went down produced no more than 5 lux of light, Rahman said. That much has a negligible effect on the body clock, he said. "But now that artificial light has come in you're getting exposed to 100 lux, 200 lux indoors at night."
All of that artificial light isn't just a bad thing for people who want to see the stars at night, according to Rahman. It disrupts our body clocks, and that negatively affects our health.
"Whenever we study clock disruption, it is obvious that it's associated with various different health disorders ranging from depression to diabetes, from various food disorders to cancer," he said. "You name it, clock disruption is bad."
Do you have trouble sleeping on your first night in a new place? There's a reason for that.
"First-night effect" invariably shows up in sleep studies, Rahman said. Their worst night of sleep will be their first night in the lab.
Our brains evolved that way, Rahman said. A new environment throws off the brain because it's always monitoring its surroundings for signs of danger, even when you're in the sleep state. It's not a deep sleep, and the brain continues evaluating unfamiliar sounds.
"Hotels can spend millions trying to give you the soft pillow, the hard pillow, this bed, that bed," Rahman said. "But it's not your environment. It's difficult to adjust overnight."
Some travelers compensate by bringing their own pillow, he said. Someone used to an urban environment might benefit from a "white noise" app if spending a night in a quiet, rural place.
"Light has profound effects on our biology other than vision," Rahman said. "And it can have a stimulating effect, and we should use it wisely. Just because we have artificial light doesn't mean that we can just abuse it."
Awakening to Sleep
SLEPT BADLY AGAIN last night. Perhaps you did, too. I was in a strange city and in a strange bed filled with the overabundant warmth of a hotel room. At home, I often come awake for an hour or two in the early morning, 3:30, 4. A thread of thought -- the merest particle of wakefulness -- presents itself, and soon the bedside light is on and I'm reading again or lying in the dark, thinking. I often put off going to bed, as I did last night, for no good reason. Like a kid with an 8:30 bedtime in the eternal twilight of summer, I can't quite bear to quit consciousness. The itch of waking won't subside. This is an old and by now not particularly troublesome habit, though its effects are sometimes tedious and grow more pronounced the older I get. Like almost everyone, I borrow more from sleep than I can ever hope to repay, and I can feel the debt being exacted whenever my attention dissipates. There are days when I wonder what it feels like to be fully awake.
You may have wondered the same, too. Almost everyone I know complains about sleep, and the refrain is usually ''Not enough.'' It's a subjective estimate, but accurate as far as it goes. The problem of sleep curtailment in late-20th-century Western society ''is so big,'' one prominent sleep researcher told me, ''that people just can't digest it. If you were to take people off the street, the vast majority would be sleep-deprived.'' There is a sense among many students of the subject that sleep deprivation is reaching crisis proportions. It is a problem not only for serious insomniacs, who total perhaps 17 percent of America's adult population, but also for the populace at large. People don't merely believe they're sleeping less they are in fact sleeping less -- perhaps as much as one and a half hours less each night than humans did at the beginning of the century -- often because they choose to do so.
In the last decade, the number of sleep-disorder clinics in the United States has grown to perhaps 1,500, 325 of them voluntarily accredited by the American Sleep Disorders Association. Despite this growth, sleep medicine is just now beginning to be taught in medical school, and only within the past year has the American Medical Association recognized sleep medicine as a self-designated specialty. At the University of Chicago Medical Center, Eve Van Cauter, a research professor of medicine, is beginning a major sleep-debt study that will, in her words, '⟞lineate the consequences of sleep curtailment for not only mood, not only cognition, not only performance, but also metabolism, cardiovascular function and immune function.''
Like many sleep researchers, Van Cauter argues that besides simply sleeping less, humans are no longer subjected to seasonal changes in the lengths of day and night. The seasonal fluctuations in conception rates associated with long winter nights, plainly evident before World War I, have essentially disappeared. We live in an artificial environment with an altered light-dark cycle, including, obviously, less exposure to true darkness and, perhaps not so obviously, less exposure to bright natural light because so many people work indoors. Shift workers especially -- perhaps 20 percent of America's work force -- find themselves in perpetual conflict with the social and environmental cues around them as a result, they experience higher rates of gastrointestinal and cardiovascular disease, as well as depression and infertility.
''The behavioral curtailment of sleep, the deletion of rest,'' Van Cauter says, ''is something that is unbelievably common. It probably has enormous health implications.'' Yet no one has done the long-term epidemiological studies needed to discover the true dimensions of chronic, culture-wide sleep deprivation or its effects on human health.
Like every scientist I talked to, Van Cauter regards as utterly unfounded the recent American fascination with, and embrace of, melatonin as a sleeping potion and all-purpose medicament. (You can now buy melatonin pills even in airport gift shops, thus creating an enormous uncontrolled experiment with a substance that is being used in a test study in the Netherlands as a contraceptive agent.) But as Van Cauter says: ''If people didn't have a problem with sleep, melatonin wouldn't sell. Its popularity is a demonstration of the fact that huge amounts of people feel they don't sleep the way they would like to.'' And if people didn't have a problem with waking -- getting up in the morning and staying alert during the day -- we probably wouldn't have made such a cult of the coffee bean or rigged our bedrooms with alarm clocks meant to catapult us into consciousness.
More and more, it seems, the convergent Western cultures of work and entertainment aspire to make machines of us all, to create an electronic, robotized atemporality that conflicts with the biological constraints inherent in being human. (That it's possible to regard our biology as a 'ɼonstraint'' suggests how far we've already gone in this direction.) Visible fatigue is an acceptable pledge of earnestness and ambition, and there is a profound reluctance in the business world even to acknowledge the subject of sleep loss. Hearing people talk about their sleeping habits is a little like hearing them talk about their digestion. An unexpected note of pride creeps in, as if the person doing the talking were his own prize county-fair steer. Some people -- a tiny minority -- worry that they sleep too much to prosper in these frenetic times. The only individuals who seem content are the ones who cheerfully announce how little sleep they need, and they are often making it up. How we sleep is widely, if implicitly, taken to be an index of things that have little to do with sleep -- emotional balance, competitiveness, sensitivity, toughness.
The poet Sir Philip Sidney called sleep ''the poor man's wealth, the prisoner's release, the indifferent judge between the high and low.'' But it's easier, I've found, to say what sleep is -- to name it metaphorically -- than to state what it does or what the widespread effects of gradual, long-term sleep loss in our society might be. Asking what sleep is for sounds like the kind of guileless question philosophers ask, like asking what time is for. It grows curiouser and curiouser the more you think about it. In fact, it's hard to talk about sleep without talking about time.
To see what I mean, imagine a world with no artificial illumination, only the light of day and the dark of night, a planet where the intensity of light varies predictably in ways that are connected to, but not caused by, the passage of time. Imagine, too, that over billions of years organisms evolve that reflect in their bodily systems the relation between light and time in their environment. They develop sensors (eyes) to register the presence or absence of light. They develop internal clocks -- genes and cells and clusters of cells capable of generating a biological night and a biological day. They develop pathways along which these sensors and clocks can communicate. Even if light were to disappear for weeks or months at a stretch, the rhythms of biological day and night -- what scientists call circadian rhythms -- would still be produced at precise intervals within the bodies of these organisms. But biological time and external light aren't completely independent. Sunrise and nightfall recalibrate the internal clocks of these creatures, so that in winter their biological night is long and in summer it is short. Call this life on earth 40,000 years ago.
Now imagine one such organism with the temerity to light up the night. It fashions lamps of pitch, animal fat, petroleum, inert gases. It ignores what its cells still remember, that light -- even artificial light -- has the power to regulate biological clocks. It begins to pretend that every night is a midsummer's night only a few hours long. A society full of beings like this would be able to accomplish remarkable things with the extra time it had on its hands. It could build mighty cities. It could establish eminent bodies, like the Sleep Research Society and the American Sleep Disorders Association and the American Board of Sleep Medicine and the Society for Research on Biological Rhythms. It could foster scientists and doctors whose working lives were spent studying the interactions among light, time and sleep. It could even send sleepless writers to interview those scientists and doctors.
But what it would never, ever elect to do again is turn out the lights and roost when the chickens roost. The one thing this society seems to have wanted all along was to stay up way past its evolutionary bedtime. But the clock we are trying to fool is our own clock, our inherent circadian rhythms. Ultimately, a 'ɼlock'' is a weak metaphor for the power of those rhythms, which control, among other things, the timing of variations in body temperature, cardiovascular rates and the secretion of substances like melatonin in the pineal gland, prolactin and human growth hormone in the pituitary and cortisol in the adrenal gland. Taken as a whole, these variations define not only the internal state of our bodies but also the condition of consciousness itself. And yet as scientists come closer to understanding the mechanisms of circadian rhythms -- and as sleep deprivation emerges as a major public health issue -- they find themselves still confronting the enigma of sleep's purpose itself. It's a puzzle that goes right to the root of our nature.
I GOT A CALL at 6:20 A.M. a couple of months ago from William Dement, who has for many years been one of the pre-eminent sleep researchers in the United States. He woke me out of a sound slumber, which is one of the things he does for a living, although for most of his career he has done it in a laboratory at Stanford University. In 1951, when he was a medical student, Dement joined the sleep lab run by Nathaniel Kleitman, a professor of physiology at the University of Chicago Medical School and to many the father of modern sleep research. Just after Dement's arrival, a graduate student in Kleitman's lab named Eugene Aserinsky discovered, in his sleeping research subjects, rapid eye movement, or REM. It was an enormous discovery, after which, Dement has written, ''it was, thus, no longer possible to think of sleep as one state.'' (REM sleep in adult humans constitutes 20 to 25 percent of a good night's sleep. The rest of the sleep cycle is made up of four non-REM stages, the most important of which, some researchers believe, is slow-wave sleep, also about 20 to 25 percent of a night's sleep.)
In his opus ''Sleep and Wakefulness,'' first published in 1939, Kleitman defined sleep as 'ɺ periodic temporary cessation or interruption of the waking state, the latter being the prevalent mode of existence for the healthy adult.'' This has a strangely normative ring to it, a privileging, natural enough, of the waking condition. It supposes that sleep is largely a kind of absence, an abeyance of what makes humans human. Now, 45 years later, Dement was phoning from Jackson, Miss., where he had been meeting with the staff of Trent Lott, the Senate majority leader, trying to draw Congressional attention to sleep disorders and their treatment. The character of Dement's work has changed over the years from analyzing the shape of sleep in the laboratory to focusing public attention on sleep as a vital health issue. The trajectory of Dement's career suggests the sweeping changes that have occurred in the understanding of sleep. As the physiological mechanisms of sleep become better understood, doctors are better able to alleviate sleep disorders. Doctors can now bring about what Dement calls 'ɺ miracle of restoration'' to many patients, including those who suffer from obstructive sleep apnea, a chronic, pharyngeal blockage of normal breathing during sleep, which affects between 1 and 4 percent of adults.
As long as sleep was considered little more than an interruption of the waking state, it was treated as a convenient window through which to view the dreaming mind. Being interested in sleep was just a different way of being interested in consciousness. Much of the early sleep research in this century was based on the assumption, as one biologist put it, that ''humans had potentially evolved out of the constraints of the environment.'' But what if, as seems increasingly apparent, that turns out to be impossible? What if the environment is inescapable? What if sleep is a physiological product equivalent to consciousness and not just a state of suspension in which the mind is suddenly untrammeled? For one thing, most common-sense notions about the relation between sleep and waking fall apart.
After the discovery, in 1929, that electrical activity in the human brain could be traced over the surface of the skull, it became conventional to characterize the stages of sleep in terms of their brain-wave patterns, as recorded in an electroencephalogram, or EEG. The literature of sleep positively bristles with descriptions not of slumber itself but of the shapes a moving pen inscribes upon a moving piece of paper: sleep spindles, K-complex waves, alpha waves, theta waves, delta waves -- the impulses of a sleeping brain whose protective shell has been studded with electrical sensors in accordance with the International 10-20 Electrode Placement System. In other words, it became customary to regard sleep mainly as an artifact of the brain.
This made sense. The passage from consciousness -- a brain function, after all -- into unconsciousness is the kind of telltale sign that's hard to overlook. But in the early 1970's, it was discovered that in the rodent hypothalamus a small cluster of perhaps 10,000 cells, called the suprachiasmatic nucleus, or SCN, plays a major part in controlling the circadian rhythms of the body, the alternation between biological day and night. The SCN receives light input from retinal ganglion cells, and so it is able to adjust the body clock using the external rhythms of night and day. If you damage the SCN in rats, you change the distribution (but not the quantity) of their sleep. There are difficulties in making the inferential leap from the physiology of rodents, most of whom are nocturnal, to the physiology of humans, who are diurnal. But the hypothesis, based on increasingly strong evidence, is that in humans, too, the SCN is one of the major centers where circadian rhythms -- although not sleep itself -- are produced. And yet circadian rhythms, even though they appear to originate in the brain, don't affect the brain alone. Nor do the circadian clocks (there is evidence of at least two) simply switch on at night and off in the day, or vice versa.
The body's circadian rhythms are always functioning, but they produce different outputs at different times in a cycle that, left on its own, without light input or behavioral cues, lasts slightly longer than 24 hours. In fact, the very idea of circadian rhythms has the effect of uniting waking and sleeping into a single, carefully equilibrated system, so that it becomes impossible to ask what sleep is for without asking what waking is for. It also becomes impossible to imagine that humans have somehow escaped the evolutionary imperative of their environment. Circadian rhythms attune the human organism to the external environment, but they also coordinate the internal operations of the body. To argue that humans have somehow evolved away from the constraints of their environment ignores the fact that the human body is always to a certain extent producing its environment -- a bodily environment that is extraordinarily stable, as it is in all mammals.
IT IS 7:57 A.M. on the Dan Ryan Expressway. A Wednesday. ''I-94 East,'' the signs read, though the lane I'm in, like the neighboring lanes, is bearing due south. Other drivers seem discomfited, but they know exactly how long it's going to take to get where they're going, and I don't. Again and again, I-94 divides into local and express lanes, and that is what time seems to do as morning overcomes Chicago. Every minute splits into local and express, and not a single person in Cook County takes the local. Like flight controllers, the radio traffic-jocks call out coordinates, indecipherable to a visitor. Along the rail platforms, waiting Chicagoans look out across the tumid lanes of I-94.
The rain beats down. The wind blows. The towers of downtown Chicago stand entangled in a low ceiling the color of charcoal and pigeon. Darkness is piling up toward winter, the season of long nights, but the city is hardwired into a different kind of time: market time, phone time, Web time, grid time, tube time, train time, drive time, flight time, bank time, lab time, work time -- all of them synchronized, to one degree or another, with atomic time, a second of which, according to the National Institute of Standards and Technology, equals 'ɹ,192,631,770 periods of the radiation corresponding to the transition between the two hyperfine levels of the ground state of the cesium-133 atom.'' Time slips away at nine billion cesium ticks per second. It never sleeps. It asks of these commuters only that they never sleep, too. They are trying to oblige, looking out with bloodshot eyes at brake lights as numerous and motile and waterlogged as cranberries in a bog. On the Dan Ryan Expressway it is not yet a hyperfine day.
I had come to Chicago to visit the Sleep Research Laboratory at the University of Chicago. It is on South Drexel Avenue, near the hospital-fortress-complex of the University of Chicago Medical School, where small, jumpy bunches of interns and residents, wearing the white coats given to the professionally sleep-deprived, linger in the courtyard before the university bookstore, which also houses an espresso bar. South Drexel is a quiet, tree-lined avenue with the domestic flavor of a side street in the northern Bronx, and No. 5743 has a shabby, misleadingly obsolescent feel to it. In a second-floor office overlooking the street, I found Dr. Wallace Mendelson, a psychiatrist who is a co-director of the sleep lab and who is the president of the Sleep Research Society. For a decade, at SUNY Stony Brook and at the Cleveland Clinic, Mendelson studied the molecular workings of sleeping pills, and he is currently doing research on the brain receptors where sleeping pills conduct their business. He is looking, he told me, for more powerful and safer sleeping pills.
It had occurred to me, after reading a number of studies on human sleep, that humans, in addition to their other sleep problems, are notoriously inaccurate witnesses of their own repose. They have trouble judging how long and how well they have slept. How, after all, do you gauge a quantum of your own unconsciousness? Mendelson cited, for my consideration, a perplexing subgroup of insomniacs, a highly unusual example of the trouble humans have in estimating their sleep. ''These are people,'' he said, ''who come to the doctor bitterly complaining of insomnia. So you do a study on these persons. You turn out the lights, and five minutes later their eyes are closed, they're breathing slowly and quietly, they're not moving and their EEG is showing a sleep pattern. They stay that way for eight hours, yet you wake them up in the morning and they say: 'See? I told you I wouldn't sleep.' ''
Mendelson's colleague Allan Rechtschaffen, who is about to retire as head of the University of Chicago Sleep Research Lab, once performed an experiment that had a bearing on this problem of sleep cognition. He invited self-described good sleepers and self-described bad sleepers to spend the night in the laboratory. When a subject had been asleep for 10 minutes, judging by behavior and brain-wave patterns, Rechtschaffen went into the room, woke the subject and asked him what he had been doing. The good sleepers said, ''I was asleep.'' The bad sleepers said, ''I was awake, of course.''
''I repeated the experiment, to see if it was true,'' Mendelson said. 'ɺnd it was. My addition to the story was to use a sleeping pill -- Halcion originally, but I've subsequently done it with Ambien,'' which is a brand name for zolpidem, the most often prescribed sleeping pill in America. ''I gave poor sleepers a placebo one night and a sleeping pill the next. Keep in mind that I'm describing in black and white what was a statistical finding. But basically, when you gave the insomniacs a placebo and woke them and asked, 'Were you awake or asleep?' they said, as predicted, 'I was awake.' When you gave them a sleeping pill and woke them and asked them the same question, they said, 'I was asleep.' The theory we're beginning to operate under is that maybe what sleeping pills do to the EEG is less important than the fact that they change your perception of whether or not you're awake.''
Perhaps the task of the next generation of sleeping pills will be to produce the illusion that we have slept well and deeply when in fact we have not. This would make sense if the consequences of sleep loss were more benign. But the penalties for what might be called catastrophic sleep loss are well known. Allan Rechtschaffen has done a famous series of experiments in which rats were wakened to death. Rats deprived of total sleep died in two and a half weeks, after their thermoregulatory systems collapsed. Rats deprived of REM sleep died in five weeks. (No one knows how soon a rat would die if, like the insomniac subgroup Mendelson described, it merely believed it had been deprived of sleep.)
Rechtschaffen's office is on the third floor of 5743 South Drexel. He is an affable, intellectually generous man -- dressed in khakis and a polo shirt, he looks as though his impending retirement were less a withdrawal than an embarkation -- but there's something minatory about the approach to his lair. Many small, neatly lettered signs appear on doors and file-cabinet drawers and bookshelves and three-ring-binder hole-punches, signs intended to maintain order in the kingdom of sleep, to insure that the chattels of at least one office in this building remain where they belong. I asked Rechtschaffen the question that had begun to prey upon me: What is sleep for?
He recounted several prominent theories. Some of them sound ridiculously self-evident (sleep is for rest), but others address the evolutionary origin of sleep, its Darwinian purpose, and in doing so they try to factor in an almost unimaginable number of variables having to do with behavioral adaptation, ecological niches and problems of body size. But what it all boils down to is an irreducible puzzle. ''Take respiration,'' Recht schaffen said. ''It helps a lot of things. Respiration will help you to talk, to laugh, to whistle, to play the tuba, but that's not the main function. Sleep facilitates survival. That's the bottom line. What is it about sleep that's essential for survival? That's the key question.'' He paused, ruefully, and then said, ''I can't answer that question.
''We know an awful lot about the physiology of sleep,'' he added with a faintly valedictory air. ''Sleep has now been very well described. But the question of the function of sleep has not been solved. The overriding fact is that there's no one theory that's accepted by the majority of sleep researchers. Now, we have a lot of leads about what the function of sleep might be. But we haven't nailed it down. So that a third of our lives still remains for the most part a mystery.''
On the second floor of No. 5743, Wallace Mendelson had put it a slightly different way: ''Nobody has the faintest idea what the function of any specific stage of sleep is.''
UNDERLYING ALL the intricacies of the human circadian system and all the atemporal elements in modern life that affect our natural periodicity, there is, of course, the greater periodicity of the human organism, the passage from birth to death, to be reckoned with. Mary Carskadon's office is in the Bradley Sleep Lab of Brown University's Butler Campus, a peaceful, tree-shaded enclave off Blackstone Avenue in Providence, R.I. The hour is suppertime, and Carskadon, who looks exhausted, has spent the entire day in the classroom. Behind her desk, however, sits the personification of alertness, a handsome chinchilla-like rodent named Prince David, who is a member of the species Octodon degu, the commonest mammal in Chile. Degus have a number of qualities that make them interesting to sleep researchers and especially to Carskadon. They're diurnal, like humans, and they mature relatively slowly, which allows Carskadon to study their adolescent sleep patterns much as she studies the sleep patterns of middle-school and high-school students.
The research question that drives Carskadon is all too familiar to parents: Why has this bright, happy child who used to be raring to go at 6 A.M. turned into this morose adolescent you can't get out of bed? Behind Carskadon, Prince David, with the nicely tuned circadian precision that makes rodents so beloved of sleep researchers, climbs onto his wheel and begins his appointed rounds. Carskadon says: ''It became really evident as I looked at surveys gathered here at Brown that there's a clear delay in the timing of sleep across early adolescence. Weɽ thought that this was all due to psychosocial factors. For example, most parents hold out staying up later as a reward. Going to bed early is a punishment. I became intrigued by the possibility that there might actually be a biological process going on as well. It's a big shift. It's a very salient phenomenon.''
Carskadon's hypothesis is that the entry into adolescence and the dislocations of mood and conduct associated with it mark the maturing of the circadian system. ''We see that same pattern,'' she says, ''throughout the rest of adulthood -- what we call a midday trough.'' That is the period roughly between 1 and 4 P.M. when sleep looms, existence pales and, not coincidentally, there is a significant rise in the number of traffic and industrial accidents. (A parallel trough, familiar to anyone who has known the despair of early morning, occurs between 1 and 4 A.M., the time when humans are likeliest to mourn credit card debt and to die.) In their sleep patterns, as in almost everything else, adolescents are making the passage to adulthood, which is why they seem so odious to adults and to one another.
But that passage has, in fact, already begun in the darkness of the womb. Steven Reppert is a pediatrician who returned to basic research almost 20 years ago and now runs the Laboratory of Developmental Chronobiology at Harvard Medical School. His office is a glass-partitioned cubicle secreted along the short wall on the far side of his crowded lab in the Jackson Building at Massachusetts General Hospital. Reppert has a picture-window view of the apparatus of molecular biology and of his team of grad students and post-docs. He shares his office with a computer, a horizontal file of offprints and a framed cecropia moth. It was Reppert's love of moths -- and the question of how their metamorphoses are timed -- that led him into science. Reppert has precociously white hair, and when you ask him about the implications of any discovery, he is likely to answer by explaining how it will shape the discovery of future discoveries. In a scientist, this is a truly amiable trait.
''Many years ago,'' Reppert says, by which he means recently, ''we discovered that the biological clock in the SCN is actually working in the fetus.'' This begins, interestingly, even before the fetal brain can register the differences between light and dark. ''We did a number of experiments showing that the fetus was always in time with the mother. So we came up with this idea: Mom is functioning as the transducer for the fetal circadian system. She takes in light information to her circadian system, and then that is communicated to the fetal circadian system. There are two hormone transmitters. Mom's melatonin rhythm is a very precise marker of her circadian system. Melatonin is a small molecule, and it slips readily across biological barriers through the placenta. The second transmitter is dopamine, which occurs within the fetus itself, and its secretion is a way the fetal SCN incorporates other signals from the mother.''
The sleep patterns of an adolescent are not those of an infant -- and those of a 65-year-old are not those of a teen-ager. Like so much else in our lives, sleep is disrupted by the process of growing old. 'ɺs we age,'' Eve Van Cauter had explained to me, ''we lose the ability to produce deep sleep, and the intensity of the deep sleep is less. The initiation of deep sleep is associated with the release of human growth hormone and of prolactin. Particularly for older adults, in their seventh decade or so, there may be zero minutes of deep sleep and there may be zero micrograms of growth hormone being secreted.'' Not much is known about the role of prolactin, except in pregnant women. According to the Encyclopedia of Sleep and Dreaming, edited by Mary Carskadon, it is ''the most important hormone for production of casein, the essential protein in human breast milk.'' Human growth hormone controls the ratio of fat tissue to muscle mass, and it also affects bone metabolism, immunomodulation and other functions.
'ɺll of the cardiovascular and endocrine correlates of good sleep disappear in aging,'' Van Cauter added. The quality of sleep in humans begins to deteriorate as early as the late 30's, and when the quality of sleep goes, so goes its restorative effect on the endocrine and cardiovascular systems. And as sleep deteriorates, so, too, does one's emotional state. ''I think it's not an unreasonable hypothesis,'' Van Cauter said, ''that a lot of the effects of aging, including geriatric depression, could be ultimately traced to a sleep deficit.''
Like every scientist I talked to, Van Cauter is keenly aware of the tension between the timeless existence our culture is fabricating in this century and the deeply temporal, cyclical rhythm of life that marks our entire evolution as organisms. ''I see sleeping and waking as an oscillation,'' she said. ''Instead of being wide awake during the day and completely unconscious when we sleep, why don't we stay at an intermediate level and keep that throughout our life? Why do we oscillate? But everything oscillates in biology. It's apparently a more efficient way.'' The paradox is that as we sleep less and less, we come ever closer to that intermediate level -- half awake, half asleep and totally useless all the time. What we really need is a stronger oscillation.
'ɺLL WAKEFULNESS IS SLEEP deprivation,'' William Dement said to me in mid-September. This was a phrase I would hear in my head for weeks, and it came to mind again as I sat in an office belonging to Joseph Takahashi, a professor of neurobiology and physiology at Northwestern University and a member of the National Science Foundation Center for Biological Timing. Takahashi has carried the search for the physical source of circadian rhythms down to the genetic level, the elemental substratum of organic life. His experiments have shown that there is a genetic as well as an environmental limit to the circadian rhythms at work in mammalian physiology. The weather outside his office was unbelievably foul. The wind had risen and waves from Lake Michigan were crashing into the bulwark of the Northwestern campus, just north of Chicago, in a manner that was all too emblematic of the collision between the periodic rhythms of human physiology and the unyielding demands of a 24-hour society.
I was looking at the activity record of a mouse. If you spend much time with sleep scientists you quickly learn how to read such charts. ''Mice have a beautiful behavior,'' Takahashi said, holding up a clear-plastic mouse cage with a wheel inside it. ''They run on a wheel. There's a switch, and when they run a signal goes to the computer. Simple.'' If a mouse is exposed to regular 12-hour periods of light and darkness, its activity record usually looks like perfectly vertical alternating bands of white (rest) and black (running) across a 48-hour span. (The hours are plotted on the horizontal axis, the days on the vertical axis.) But if the mouse is left in darkness for many days, its internal clock is not reset by light, and it adheres to its natural cycle -- 'ɿree-running rhythm,'' as the sleep people say. The average free-running circadian period for the strain of mice in Takahashi's lab is 23.7 hours. Because each activity episode and each sleep episode begins slightly earlier than it did the day before, the vertical bars on the activity record of a normal mouse kept in constant darkness will drift to the left as the days pass. For humans, the free-running circadian period is about 25 hours, which means that in a similar experiment the vertical bars on a human sleep-activity record would drift to the right.
I bother to explain all this because in Takahashi's office I was looking at an activity record that was shocking. It seemed almost ordinary for the first 20 days, while the mouse that produced it was on a fixed light-dark schedule. But when the lights were turned off for good, the cycle lengthened to 28 hours, and then it exploded. Suddenly the activity record looked like noise, an incoherent flickering of abbreviated light and dark dashes scattered all over the page for all the subsequent days of the experiment. This mouse plainly lacked any circadian guidance in the absence of environmental cues. It had failed to generate its own temporal environment. You can produce a similar effect in a rat by altering its brain, removing the SCN. But this mouse, whose SCN was intact, had two copies of a mutant allele of the 'ɼlock'' gene. If it had only one copy, it would show a lengthened circadian period of 24.8 hours, 'ɼlearly out of the distribution of normal mice,'' Takahashi said, but still perfectly regular. When this extraordinary activity record was produced, Takahashi's lab had seen only the phenotype of this mutant gene -- in other words, the mouse itself. Now they have found the gene. It is extremely likely that in humans too there is a clock gene, probably on chromosome 4.
A few of Takahashi's unusual mice will make their way east to Steven Reppert's lab, where they will breed and sleep and run and, in the language of science, be sacrificed. There Reppert will repeat an experiment he has already performed on normal mice. He will take cells from the SCN of newborn mice likely to show this mutation and culture them on a slide that has been implanted with tiny electrodes. The electrodes will record the firing rates -- the chemical discharges -- of the individual SCN neurons that happen to lie directly on top of them. ''We've been able to take these cells,'' Reppert said, speaking of ordinary mouse cells, 'ɺnd monitor them the way you would monitor the whole animal, for 42 days. That pervasive circadian aspect of behavior -- the precise rhythms of wheel-running, for instance -- we can now track in the firing rhythm of a single cell. We think the circadian clock is cell-autonomous. In other words, everything that it takes to make the molecular, biochemical, cellular oscillation can be found in one cell.'' The question Reppert hopes to answer with Takahashi's mutant mice is this: Do cells from their SCN fire in a different pattern than SCN cells from ordinary mice?
There is other evidence about how circadian rhythm is produced at the cellular and genetic levels. A protein created by a gene called per (for period) in Drosophila melanogaster, the fruit fly, engenders what Takahashi calls 'ɺ beautiful oscillation in the RNA cycle.'' The proteins created by per and another clock-related gene in the fruit fly, called tim (for timeless), also pair up to form what Reppert calls two interdependent auto regulatory transcription feedback loops, which are directly affected by light acting upon tim. ''What that means,'' Reppert explained, ''is that the protein that is made in the cell by these genes seems to feed back on its own production. When it reaches a certain level, it shuts off. If you get the time kinetics appropriate, then this would be self-sustaining.'' This is one version -- there are several -- of what the circadian clock looks like at the most fundamental level. The relevant genes encode the creation of proteins, and those proteins interact with light, and with one another, to produce the timepiece in Drosophila and perhaps, analogously, in us.
''Why do we oscillate?'' Eve Van Cauter asks. These genes and their protein feedback loops are some of the reasons. They exemplify the discontinuous logic of sleep, a logic in which the answer to the question ''What is sleep for?'' is 'use we oscillate.''
I found myself staring, in Takahashi's office, at the white space on the activity record of a normal mouse, which I had been using for comparison. The white space represents light, and light, on a human activity record, means waking. The white space seemed to be posing a question of its own: What is waking for? Same answer: Because we oscillate. Stop oscillating and you're dead. It had become apparent to me that the circadian system -- of which sleep, like the full moon passing across the night sky, is only the most visible marker -- is an enormously subtle means of integrating environmental input with a complex suite of physiological outputs.
I had just become used to the idea that sleep is a physiological artifact of the circadian system when I realized that waking -- consciousness -- is not merely the transparent state of being it seems to be. It, too, is being generated by the body's circadian rhythms. It has a shape and a hormonal substratum all its own. This was not necessarily news, but it reminded me a little of the moment when you first realize that the eye is not a window, even into the soul, but an organ with its own opacity. It makes you wonder.
WILL THERE SOMEDAY BE HUMANS WHO are born with a purposely altered clock gene? Will we go that far to accommodate a sleepless society? Perhaps. But perhaps there is a simpler, already innate solution to the problem of sleep curtailment, one that depends on our oscillatory nature. Modern sleep -- severely delimited sleep -- is largely a cultural product. It is only, at most, a few centuries old, a result of our profound conviction that we can control the details of our biological destiny. But what did sleep in the era of our evolutionary emergence look like? What was sleep like before television, before electric lights, before the industrial revolution, before agriculture?
Something like an answer has been provided by Thomas Wehr, who is chief of the Clinical Psychobiology Branch of the National Institutes of Mental Health in Bethesda, Md. While Wehr was studying melatonin secretion, which is, as he says, 'ɺ chemical transducer of nighttime and season,'' he found himself wondering, Have humans preserved a mechanism for perceiving seasonal change, the way animals have? To answer this question, he devised an experiment in which volunteers subjected themselves in the laboratory to a sleep schedule based on the duration of a midwinter's night at the latitude of Washington -- about 14 hours. In other words, they spent 14 hours in darkness, from 6 P.M. to 8 A.M., every night for at least a month, just as the aboriginal occupants of Lafayette Park would have done every winter until they died of malaria.
''We decided,'' Wehr told me, ''to take a more general look at what human biology could be like in a longer night -- to reanimate a prehistoric mode. We measured all the usual things: temperature, hormones, melatonin secretion, the EEG patterns in sleep.''
What Wehr found was remarkable. The first night the volunteers slept 11 hours, and in the first weeks of the experiment they repaid 17 hours of accumulated sleep debt -- i.e., they slept 17 hours longer than they would have called normal for the same period. It took three weeks for a sleep pattern to stabilize, and when it did it lasted about eight and a quarter hours per night. But it was not consolidated sleep, and it was not just sleep. Over time, Wehr explained, 'ɺnother state emerged, not sleep, not active wakefulness, but quiet rest with an endocrinology all its own.''
Each night the volunteers lay in a state of quiet rest for two hours before passing abruptly into sleep. They slept in an evening bout that lasted four hours. Then they awoke out of REM sleep into another two hours of quiet rest, followed by another four-hour bout of sleep and another two hours of quiet rest before rising at 8 A.M. This pattern of divided sleep, separated by rest, is called a bimodal distribution of sleep, and it is typical of the sleep of many mammals living in the wild, which is to say that it is atypical of humans living in modern Western society. Yet in a forthcoming article, to be published in a volume called ''Progress in Brain Research,'' Wehr concludes that ''in long nights . . . human sleep resembles that of other mammals to a much greater extent than has been appreciated.'' Bimodal sleep, punctuated by quiet rest, was a pattern to which modern Americans reverted almost as soon as they were given the chance.
''In healthy people,'' Wehr remarked, ''this bimodal pattern of sleep would be called a sleep disorder, although the resemblance to animal sleep confirms its naturalness. And as people get older they revert to this pattern of divided sleep. Perhaps it gets harder to override it.''
I asked Wehr whether any of his subjects had gone crazy lying in the dark during those long nights.
None had. 'ɺnyone could do it,'' he said.
And having done it, Wehr's subjects remarked that never before had they felt awake. Wehr measured their daytime sleepiness using a variation of a conventional method called the Multiple Sleep Latency Test, which was devised by Mary Carskadon and William Dement. Essentially, the M.S.L.T. measures the speed at which you fall asleep while lying quietly in a dark room. Not only did Wehr's subjects '𧿮l more awake, they were more awake.''
What late-20th-century Americans seem to expect from sleep is simply sleep -- a single, uninterrupted dose of slumber delivered in a sleek package that doesn't get in the way of a busy schedule. And, Eve Van Cauter said, ''Perhaps for the human, who has been able to consolidate sleep and stay awake for long periods of time and achieve things that take a long period of time to achieve, that may be part of our success as a species.''
But what has been sacrificed as human sleep has become more and more condensed and less and less seasonal is an open question. Living year-round on midsummer time, with long days and short nights, ''has obtained,'' Wehr writes, 'ɿor so many generations that modern humans no longer realize that they are capable of experiencing a range of alternative modes that may once have occurred on a seasonal basis in prehistoric times but now lie dormant in their physiology.'' While humans worry about how much further we can compact our actual sleep time, we've already jettisoned six nightly hours of quiet winter rest. In a most meaningful sense, those are transitional hours. Once in the night and once in the early morning, Wehr's volunteers woke out of REM sleep, which is strongly associated with dreaming, into a period of quiet wakefulness quite distinct from daytime wakefulness. Perhaps as we've learned, over time, to sleep a less characteristically mammalian sleep, we've also learned to sleep a less human sleep.
''It is tempting to speculate,'' Wehr writes, ''that in prehistoric times this arrangement provided a channel of communication between dreams and waking life that has gradually been closed off as humans have compressed and consolidated their sleep. If so, then this alteration might provide a physiological explanation for the observation that modern humans seem to have lost touch with the wellspring of myths and fantasies.''
''IT IS FOR THE DOCTORS TO DECIDE WHETHER sleep is such a necessity that our very life depends on it,'' wrote Montaigne. But this is the kind of science you can do at home. Tonight, in New York, the sun will set at 4:50. It rises at 7:19 tomorrow morning. That's 14 hours and 29 minutes of darkness. All you have to do is turn out the lights, put out the cat and unplug the phone. Don't get restless.
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While sleep is crucial for day-to-day functioning, it’s also crucial for health. As psychologists were discovering the architecture of sleep, epidemiologists were beginning to assess its impact on our bodies. “In the 1960s, there were a number of large community-based studies that sought to figure out what the real causes of death were in the community,” says Michael Grandner, the director of sleep and health research at the University of Arizona. Large-scale epidemiological projects like the Framingham heart study (begun in 1948) and the Alameda County study (begun in 1965) helped to create the maxims that dominate public health to this day—smoking kills, diet and exercise factor into heart disease, alcohol is dangerous—but hidden in all that data was another finding: In meta-analyses of these large-scale studies, “you get this u-shape for mortality,” Grandner says. Both too much sleep (longer than eight hours) and too little sleep (shorter than six hours) put people at higher odds for early death. (According to Grandner, there’s a clearer consensus around the idea that too little sleep is bad for health the effects of too much sleep remain an open and debated question.)
In 2002, Grandner’s mentor, Daniel Kripke, a psychiatrist at the University of California, San Diego, published a report compiling data from more than 1 million men and women aged 30 to 102. “The best survival was found among those who slept seven hours per night,” the study found. Says Grandner: “This was, and still is, the largest study ever on this topic and arguably the most clear.”
To understand why scientists hypothesize that poor sleep causes poor health, we need to dive into the smallest components of the human body. It is here scientists have made the biggest leaps in connecting sleep with overall health. Over the last two decades, there has been a shift in the way scientists understand sleep, explains Allan Pack, who researches sleep and genomics at the University of Pennsylvania’s Perelman School of Medicine. “The idea was you go to sleep, the brain shuts down, something happens that’s helpful to” your brain, Pack says. Now, however, “one of the things we know is there’s not only a clock in your brain controlling the sleep-wake pattern, there are clocks in every tissue, essentially.”
Scientists have discovered “clock genes,” tiny bits of DNA that act like a biological metronome: By regularly flipping on and off, they help the body maintain its sense of time. And not only are these clocks in every tissue in every human, or in every tissue in every mammal, but they can be found in “virtually every organism on the surface of the planet,” says Michael Twery, the director of the National Institutes of Health’s National Center on Sleep Disorders Research. Cycles in activity and rest are fundamental in the architecture of life.
Messing with these cycles—essentially throwing the body’s metronome off beat—throws the whole body off beat. “When you have situations like the mistiming of sleep, or not enough sleep, you can conceivably alter clock [gene] function and then alter the expression of all these important genes that are regulating things like metabolism, or skeletal muscle function, pancreatic function,” says John Hogenesch, a chronobiologist at the University of Pennsylvania who studies clock genes in mammals. Like toxins in the food chain, the effects accumulate upward from there: Cells that have their clock genes disrupted don’t produce the right proteins, those proteins then don’t regulate tissues well, and organ systems show strain.
In the late 1990s, an invention called the microarray—a computer chip that allows researchers to study how many genes are turned on in a given cell—burst open this research. Now, scientists could watch, in near-real time, what was happening to cells in animals that had been denied sleep. They didn’t look healthy. “When you keep animals awake, you get this phenomenon called the unfolded protein response,” Pack explains. Proteins are the building blocks of the cell. If the proteins are poorly constructed, or, in science speak, unfolded—like a Lego block with a misshapen connector—they won’t work. “Then you either have got to destroy them or what happens is they aggregate into lumps,” Pack says. “And you get these protein aggregates, which are very toxic to the cell.”
How those disruptions in the cell come to affect entire organ systems isn’t entirely understood. But evidence from molecular biology, epidemiology, and psychology points to the idea that poor sleep is a risk factor for heart disease, diabetes, and obesity—which are all ailments that disproportionately affect black communities. In America, blacks are 33 percent more likely to die from heart disease than the population at large, 1.7 times more likely to have diabetes, and 1.5 times more likely to be obese. For every 100,000 blacks, it’s estimated that heart disease takes away 1,691.1 years of potential life in a given year. For whites, that figure is 900.9 years.
Overall, if we factor out deaths caused by aging, the mortality rate for black men—from all causes—in the United States is 1,104 per 100,000, according to the Centers for Disease Control and Prevention. For white men, the mortality rate is 878.5 deaths per 100,000. For white women, that figure is 630.8 per 100,000 for black women, it’s 752.5. Could sleep explain part of the difference between blacks and whites?
The best scientists are always skeptical, and the sleep researchers I spoke to were no exception. “It’s plausible to suggest racial differences in sleep, whatever the cause, might potentially be one, maybe a small piece,” Grandner says. “It’s probably not explaining the whole thing or a large fraction of it, but could be playing a role in some of these health disparities.”
One thing, however, is certain: Sleep disparities do exist. “I think we can say there’s a great deal of evidence that there are race differences,” Lauderdale says. And given the link between sleep and well-being, it seems clear that those differences are worth taking seriously as a matter of public health.
On the question of how to explain the black-white sleep gap itself, researchers have a number of related theories. (There is a consensus that innate biological differences between blacks and whites are not a factor.) The stress caused by discrimination is one strong possibility. In the San Diego sleep study, Tomfohr’s team knew, going in, that slow-wave sleep is very sensitive to stress—which is, in turn, our body’s signal to remain vigilant against perceived threats, including discrimination. “That was our thought: If people are feeling really discriminated against, then of course they are not going to want to get into a really deep stage of sleep,” she says.
After the participants’ stays in the San Diego lab, researchers had them take a survey, designed to assess the level of discrimination they felt on any given day. (Participants were asked to agree or disagree with statements, including “In my life, I have experienced prejudice because of my ethnicity” and “My ethnic group is often criticized in this country.”) Armed with this information, Tomfohr and her colleagues could then determine a correlation between discrimination and sleep. And it turned out that there was, in fact, a correlation: More discrimination meant less slow-wave sleep. “If you can take out that discrimination piece, the average African American and the average Caucasian look at lot more similar,” she says. “It’s not perfect, but in terms of sleep, a lot of the disparity goes away.”
Danielle L. Beatty Moody, a psychologist at the University of Maryland, Baltimore County, conducted a similar test while working as a post-doctoral scholar in the psychiatry department of the University of Pittsburgh in the late 2000s. People who are discriminated against, she believes, carry worry throughout the day. And that worry literally keeps them up at night. “It’s uncomfortable for them to sleep because they are thinking back over mistreatment, thinking back over maltreatment, thinking back over bias they experienced,” she says. “In thinking about those experiences, they are getting more aroused, more cognitive arousal, which does the opposite of what you need it to do to go to sleep.”
Lauren Hale, a professor of preventive medicine at Stony Brook University and the founding editor in chief of the journal Sleep Health, makes a similar but slightly different point: She argues that sleep is a reflection of a person’s agency. The more control you have over your life—the more freedom you have financially, the more freedom you have to live where you choose, the more control you have over what you eat and when you eat it, the more you have the luxury of possessing the time and equipment to exercise—the more likely you are able to create an environment that fosters good sleep. “[S]keptics cannot argue that people with poor sleep habits simply ‘choose’ to sleep poorly,” Hale and a co-author wrote in 2010. “Sleep should be viewed as a consequence of something other than choice.”
Neighborhoods also appear to matter when it comes to sleep health. “I have never seen a study that hasn’t shown a direct association between neighborhood quality and sleep quality,” Hale tells me. “Those two are linked.” And black families are more likely to live in poorer neighborhoods, even if they are middle-income. (“Even among white and black families with similar incomes, white families are much more likely to live in good neighborhoods—with high-quality schools, day-care options, parks, playgrounds and transportation options,” wrote David Leonhardt recently in The New York Times, summarizing the results of a Stanford study by Sean Reardon.)
Feelings of safety are key here. Hale theorizes that—as with discrimination—noisy, unsafe, disorderly neighborhoods increase stress and the need for vigilance. “If you know somebody in your neighborhood who has had a break-in, you might feel pretty uncomfortable shutting your eyes falling asleep while your two or three children are sleeping in the room next door and no one else is there to protect them,” she says. “And that type of insecurity, whether it’s financial or physical safety, is more common among people who don’t have control over their environment, because if you did have control over your environment, you’d say, ‘I’m getting out of here.’”
Hale has been involved in several studies that compare levels of disorder in a neighborhood—as measured by cleanliness, crime, presence of graffiti, and so on—with sleep and health. Overall, she finds, poor sleep can explain 20 percent of the difference between the good health found in rich neighborhoods and the bad health found in poor ones. “Based on these results, targeted interventions designed to promote sleep quality in disadvantaged neighborhoods (e.g., community-based sleep promotion and noise-level ordinances) could help to improve the physical health of residents in the short-term,” Hale writes in one of her co-authored papers in the journal Preventive Medicine. And while “community-based sleep promotion” may sound like an impossibly vague intervention, there are, in fact, programs underway that show how it might be done.
Some of the more practical research aimed at helping black Americans to sleep better is being conducted by Girardin Jean-Louis, a charismatic Haitian-born psychologist who runs a lab dedicated to sleep and health disparities at New York University’s Center for Healthful Behavior Change. When I first started reporting on this topic, Jean-Louis’s name was brought up in just about every conversation. “What I think is innovative about what Dr. Jean-Louis is doing is that he goes into the community and finds out from the stakeholders what we need to do and works with them,” says Kristen Knutson, a biomedical anthropologist at the University of Chicago who has been studying the link between sleep and health outcomes.
It’s 84 degrees and rising on a Saturday in August when I go to see Jean-Louis’s work in action. In the St. Albans community of Jamaica, Queens, Azizi Seixas—a member of Jean-Louis’s team—takes the stage outside Christ Church International. Congregants and community members sit under tents in the closed-off street adjacent to the church, which, despite its coral-pink bricks, is as nondescript and industrial as the self-storage facility next door.
Today is the church’s annual health fair. Six tents line the street. At one, passersby can get their blood pressure or blood-sugar levels taken (though I don’t see any who do). Another station is giving away free reflexology foot massages (much more popular).
Seixas is here to recruit participants for a yearlong study that Jean-Louis’s lab is conducting. St. Albans—a working- to middle-class community that is almost entirely black—isn’t the poorest neighborhood in the city, but it suffers from the same stressors as many other minority areas: people working multiple jobs at odd hours people struggling to pay for mortgages while taking care of their families. “People have two or three jobs—they don’t get enough sleep,” the nurse manning the blood-pressure station tells me. “You come in [from one job], you get five or six minutes sleep—or maybe two hours of sleep—then you have to go out to another job. They don’t realize. They just think, ‘Oh, I’m tired.’ They don’t realize they’re developing a problem that’s greater than being just tired.”
Thirty percent of adult residents in the greater Jamaica area are obese. The death rate from diabetes in Jamaica is higher than in both Queens and New York City as a whole. Jamaica also has one of the highest rates of heart-attack hospitalizations in the city. “When you don’t sleep well, guess what happens?” Seixas asks the crowd from the stage. “Over time, that builds up, and it builds up, and it builds up, and what we have found is that many of the times, the hypertension—the high blood pressure—the diabetes, all those health conditions are associated. They have something to do with sleep.”
Seixas directs those assembled to a station that NYU has set up for free sleep screenings. They’ll ask for history of snoring, insomnia, and daytime sleepiness. Their specific target is to identify people at risk for obstructive sleep apnea, a potentially deadly disorder where a person intermittently stops breathing during sleep. These cessations, called apneas, can occur hundreds of times in a night, and each generally lasts 10 to 30 seconds.
People with sleep apnea get truly awful sleep. Essentially, it’s a condition that maximizes all of the health problems related to short sleep duration. Like short sleepers, people with sleep apnea are at higher risk for high blood pressure, diabetes, and weight gain. “We take some of these people with hypertension, and we give them antihypertensive medications. Often times, what we find is there is a subset of people, primarily blacks, where they don’t respond to the hypertensive medication,” Seixas tells me. “What we found in our studies is that a lot of these people have undetected, untreated sleep disorders, particularly sleep apnea.”
As with sleep problems more generally, there is a racial disparity when it comes to sleep apnea. “Not only does it seem like they’re more likely to have the disorder, they’re less likely to make it to a doctor to have treatment prescribed, and even if they get treatment prescribed, they’re less adherent and don’t use it as much,” Knutson says. “So, all across, from step A to step Z of getting treated, there are disparities.” In the June Sleep report, 12.8 percent of blacks in the cohort had sleep apnea 7.4 percent of whites did. An overview paper in the 2015 Annual Review of Public Health cites 14 percent of blacks as having the condition—the figures for whites are around half that—and also states that sleep apnea is four to six times as prevalent in black children. (It’s hard to say how prevalent sleep apnea is—among blacks, whites, or in the overall population—because apneas are usually so short that people don’t remember waking up from them.)
Apnea is just one aspect of Jean-Louis’s work on sleep. One unit of his lab is looking into the noise levels of different New York neighborhoods and then determining their impacts on sleep and blood pressure. In another program, the lab is restricting one hour of sleep in a group of adults for 12 weeks to see how the change affects their bodies. They also have an NIH-funded program designing a website for sleep-health education. When I visit their offices a few days after the health fair, the team—a diverse collection of academics in their 20s and 30s—is debating whether a stock image of a black man sleeping next to a bowl of food is appropriate for the education website.
Until 2000, Jean-Louis was focused on lab-based work at the University of California, San Diego, researching under Daniel Kripke. But he found that the controlled, sterile environment wasn’t satisfying. “You have got to be in the community where you are actually touching people’s lives,” he says. “To me, this is more rewarding.”
While Jean-Louis was in San Diego, evidence was mounting that not only were blacks not getting good sleep but they were more at risk for sleep disorders. San Diego is only about 5 percent black—a figure not conducive to research on race—so Jean-Louis took a position at SUNY Downstate College of Medicine in Brooklyn, a place where he just had to step outside to be immersed in the black community. He and his childhood friend and frequent collaborator Ferdinand Zizi—a sleep-health researcher as well—would go to churches, barber shops, beauty salons, and community centers to recruit people for focus groups and find out what was holding their sleep health back.
What they found was a community unfamiliar with sleep health and hesitant to undergo lab tests. One of their studies tracked 421 black patients who were referred to get tested for sleep apnea. Just 38 percent showed up to get a diagnosis (even though all were called by the doctor to remind them of their appointments). Of those 38 percent, nearly all received a positive diagnosis. Many of those referred for sleep tests were obese, hypertensive, and had high cholesterol. Missing out on sleep treatments meant they were missing out on an opportunity to manage those conditions as well.
Jean-Louis joined NYU in 2013. In his current study—which is being funded by the NIH at a cost of $423,750—he and his colleagues are trying to figure out whether simple interventions could better diagnose and treat minorities for sleep apnea. (For the first year, the study was only for blacks now it has been opened up to all minorities.) Hence the team’s visit to places like Christ Church International. “Girardin’s studies are pioneering,” says Twery of the NIH, “in the sense he is doing community-based research to understand the cultural basis of the problem and how to improve the health of these communities.”
At the health fair, if community members are identified as being at risk for sleep apnea, they’re invited to join the study. Once in the study, they are first assigned a peer health educator. This person, who usually lives in the same community, guides the participants through the process of getting a diagnosis and then helps them adhere to treatments.
“People like stories. They like you to engage them,” Jean-Louis says. “So you might find the first five to ten minutes, you’re just talking about their lives.” He believes this is the key aspect of the intervention. The idea is to be sensitive to any wariness patients may have of medical institutions and not to blame them for lacking knowledge. In his papers, he calls this approach culturally tailored education. “When people feel you value them, you value their time, they’ll do it. But you just can’t show up with a clipboard and asking questions,” he explains.
The health educators—who have six weeks of training—remain in contact with the participants for a year, acting as health coaches and guiding them toward treatment goals. “Until people are able to understand what sleep apnea is about, they’re going to be resistant,” Lystra Harry, one of the educators, tells me. “Whatever decision they choose to make, we respect it.” Not everyone will get a diagnosis, but everyone will be educated in sleep health, which could help alleviate problems of short sleep as well.
Jean-Louis says he has preliminary data that shows this approach is working. People who receive culturally tailored sleep education are, he says, four times more likely to make an appointment for a follow-up exam. “And once they are in, they will actually stay in,” he says.
For privacy reasons, the NYU team wouldn’t put me in touch with any participants in the study. But the lead peer health educator introduced me to her sister, Kimberly Turner, a 55-year-old African American resident of Canarsie, Brooklyn, who had been diagnosed with sleep apnea. Before she was diagnosed, she told me, she felt like she was in the Twilight Zone. Time seemed to disappear. A coworker sitting next to her would suddenly vanish. She’d stop at a red light and then, an instant later, car horns would be blaring at her. She would wonder: “Did that really happen?” She hadn’t realized she was falling asleep during the day. “You start to question everything,” she says.
Turner was tired all the time. She woke up with terrible headaches. All the clues pointing toward apnea were there, but she didn’t realize something might be wrong with her breathing during sleep until her husband told her. “He just literally said that I stopped breathing, and I was like, ‘You’re kidding me, I don’t stop breathing.’ I had never really heard of it at that point.”
On the advice of her doctor, she was referred for an overnight polysomnography sleep study. It took some convincing (“You have to sleep in this unknown place the whole night, and I didn’t want to do it”), but she eventually agreed. Two minutes into Turner’s sleep study it had to be stopped. “I stopped breathing too many times,” she says.
After being diagnosed, Turner was prescribed a CPAP (continuous positive airway pressure) mask to wear at night. It’s cumbersome and “a mood killer,” she says, but it keeps her airways open. Since treatment, her life has turned around. She’s more alert. Her headaches are gone.
The theory guiding Jean-Louis’s work is that sleep disorders like Turner’s are a significant contributor to racial health gaps in this country—and if we could treat all those cases, there would be a meaningful reduction in health disparities. “Untreated sleep apnea leads to cardiovascular disease if not death,” Jean-Louis says. “There are many times we go, we give talks in churches, and we hear stories of people who died, and we always say to ourselves, ‘You know, I think that was untreated sleep apnea.’ We can’t have a 35-year-old African American male go to bed and not wake up the next day. That doesn’t make any sense.”
Sleep apnea is the most extreme manifestation of the sleeping problems that disproportionately affect black Americans. But focusing on community-based health education—as Jean-Louis is doing—may help not just with sleep apnea but with other sleeping problems, too. And if his interventions work, they could be scaled up.
Indeed, whether it’s through community health fairs or schools, sleep education probably needs to become more widespread. “What really brings me hope is that in a conversation with new parents or a conversation with middle-school students and their teachers, you can have a tremendous impact,” says Orfeu Buxton, a sleep-medicine researcher with appointments at Harvard and Penn State who occasionally gives talks at schools. The benefits of good sleep aren’t hard to market. “You talk about being happy, looking better, being healthier, all these different things, and I don’t know which one is going to hit for which person, but once you give the explanation of how big an impact sleep has on absolutely everything, younger people are turning the corner, I think.”
For kids, Buxton thinks that having schools start later would encourage healthy sleep habits at an early age. For adults, workplaces can also adjust: Buxton and colleagues at Harvard have found that in nursing homes where managers were more supportive of work-life balance, employees were more likely to get more sleep.
Both state governments and Washington could play a role by encouraging employers to adopt company wellness programs that reward good sleep. (Most critically, these programs should seek to reach shift workers who live in an almost constant state of jet lag.) In fact, at every level of government, there are policy decisions—whether on neighborhood noise levels or public safety or the placement of public housing—that provide good opportunities to consider, and perhaps improve, how people sleep.
One point of optimism is that this subject, though relatively new, is being well-supported by the NIH. The majority of the studies cited in this article received some funding from the NIH, which has identified decreasing health disparities as a research priority. Since 1993, according to Twery, there have been more than 10,000 NIH-funded sleep research projects published.
Ultimately, sleep may offer researchers a way to attack seemingly even more intractable health problems—including those that disproportionately affect black Americans. “Not only might sleep be a potential causal factor in health disparities making things worse, it might be a potential place to help the situation,” Grandner says. “If you take someone who is not getting enough sleep, and you increase their sleep, can that prevent some of these things”—obesity, diabetes, heart disease—“over time? That’s still an open question.”
Tomfohr also sees some cause for optimism. “I don’t think this is totally fatalistic,” she says. “My hope is that this is addressable from multiple levels—that we can identify people who are at risk for sleeping poorly, and then we can do good interventions to help them sleep better, so this isn’t a sentence towards getting cardiovascular disease, or getting sick, or getting diabetes. I have a hopeful feeling about this.”
Increased Oxygen Delivery
Once oxygen is deposited into the bloodstream by the lungs, the body must also increase your homeostasis heart rate during exercise to deliver oxygen to the cells to once again maintain homeostasis. The increase in heart rate boosts the speed at which your arteries and capillaries can deliver oxygen to needy cells.
It also increases how fast these blood vessels can deliver the broken-down components of recent foods you have consumed. Both products are necessary for energy creation to occur through aerobic respiration.
6. Wearable Health Devices Market Trends
To perform a complete market analysis of WHDs, it is necessary to understand the market segments of these type of devices and then follow market lines to analyse specific markets. This approach will allow us to understand market values and trends in surrounding areas, which can also be possible target areas in a near future.
Wearable devices market value is in constant grow and this year it is estimated to reach a value of approximately $12 billion. It is a market that is in constant growth, if we think that in 2010 the market was only $6.3 million, it is possible to understand that in these recent years it has increased substantially (around 200 hundred percent) . According to IDTechEx, in terms of global revenue, the following five year’s trend is to increase at a higher rate as it can be seen in Figure 6 .
Horizontal bar graphic showing the total revenue in billions ($) (left axis) from 2015 to 2017, and estimated until 2026. The blue line shows the revenue growth rate in billions ($) (right axis). Adapted from .
Wearable devices market can be categorized according to the classification shown in Figure 7 . According to this study made by ABI Research , from 2017 to 2019 the use of wearable devices in healthcare will constantly increase and can undergo the market value of wearables for sport/activity purposes. This fact is a good indicator for WHDs companies that have the aim to develop products for healthcare applications . The smart clothing market that is still nowadays very small but its trend is to increase, reaching around $8.1 million in 2019 and is estimated to reach around $26 million in 2022 .
Horizontal bar graphic showing the trend of global market value of wearable computing devices, in millions, between 2017 and 2019. Adapted from .
With the technology and internet of things (IoT) revolution, the healthcare wearable devices segment is increasing and with this the telehealth sector is also rapidly changing. In 2014 it was predicted that this year the revenues of telehealth devices and services reach $4.5 billion, which is almost the double of the 2017 value of $2.8 billion . The number of home healthcare monitoring devices connected to a data center also has a growing trend considering the past years ( Figure 8 A) according to a study made by Berg Insight . In this study it is possible to understand the evolution of this trend in the sector of home medical monitoring devices: diabetes care devices blood pressure monitors multi-parameter patient monitoring apnea and sleep monitors holter monitors and heart rate meters. Although most of these device cannot have wearable features, it is possible to conclude that this is a continuous growing market segment, creating a market opportunity for the growth of WHDs in home healthcare for following years.
(A) Connected home medical monitoring devices (in millions) 2011 to 2017  (B) The world market for telehealth from 2014 divided in the main areas (CHF-congestive heart failures COPD-chronic obstructive pulmonary disease) .
Healthcare ambulatory monitoring segment, according to a study made by IHS Inc. (London, UK)  can be divided in several areas according to the diseases or the type of monitoring, resulting in five main areas: ( Figure 8 B): congestive heart failures (CHF) chronic obstructive pulmonary disease (COPD) diabetes hypertension and mental Health. This study conclusion is that mobile telehealth solutions are going to become the standard in remote patient monitoring, leading to a larger market for the WHDs.
It is important to mention a fact regarding this market analysis: mobile health technology worldwide market in 2011 was about $1.2 billion and it is expected to reach an amazing $11.8 billion value this year, an important fact that supports the use of WHDs combined with mobile technology .
Manifestations and Prevalence
Parasomnias are unpleasant or undesirable behaviors or experiences that occur during entry into sleep, during sleep, or during arousals from sleep (AASM, 2005). They are categorized as primary parasomnias, which predominantly occur during the sleep state, and secondary parasomnias, which are complications associated with disorders of organ systems that occur during sleep. Primary parasomnias can further be classified depending on which sleep state they originate in, REM sleep, NREM, or others that can occur during either state (Table 3-4).
Selected Primary Sleep Parasomnias.
Parasomnias typically manifest themselves during transition periods from one state of sleep to another, during which time the brain activity is reorganizing (Mahowald and Schenck, 2005). Activities associated with parasomnias are characterized by being potentially violent or injurious, disruptive to other household members, resulting in excessive daytime sleepiness, or associated with medical, psychiatric, or neurological conditions (Mahowald and Ettinger, 1990).
Disorders of Arousal, NREM
Disorders of arousal are the most common type of parasomnia, occurring in as much as 4 percent of the adult population (Ohayon et al., 1999) and up to 17 percent of children (Klackenberg, 1982). Typically the arousals occur during the first 60 to 90 minutes of sleep and do not cause full awakenings, but rather partial arousal from deep NREM sleep. Disorders of arousal manifest in a variety of ways, from barely audible mumbling, disoriented sleepwalking, to frantic bouts of shrieking and flailing of limbs (Wills and Garcia, 2002).
Individuals who experience confusional arousals exhibit confused mental and behavioral activity following arousals from sleep. They are often disoriented in time and space, display slow speech, and blunted answers to questions (AASM, 2005). Episodes of resistive and even violent behavior can last several minutes to hours. Confusional arousals are more than three to four times more prevalent in children compared to individuals 15 years or older (around 3 percent) (Ohayon et al., 2000). They can be precipitated by forced arousals, particularly early in an individual’s sleep cycle.
Sleepwalking is characterized by a complex series of behaviors that culminate in walking around with an altered state of consciousness and impaired judgment (AASM, 2005). Individuals who are sleepwalking commonly perform routine and nonroutine behaviors at inappropriate times and have difficulty recalling episodic events. Like confusional arousals, the prevalence of sleepwalking is higher in children than adults (AASM, 2005). There appears to be a genetic predisposition for sleepwalking. Children who have both parents affected by sleepwalking are 38 percent more likely to also be affected (Klackenberg, 1982 Hublin et al., 1997).
Sleep terrors are characterized by arousal from SWS accompanied by a cry or piercing scream, in addition to autonomic nervous system and behavioral manifestations of intense fear (AASM, 2005). Individuals with sleep terrors are typically hard to arouse from sleep and, when they are awoken, are confused and disoriented. There does not appear to be a significant gender or age difference in prevalence or incidence of sleep terrors (AASM, 2005).
Disorders Associated with REM Sleep
Rapid Eye Movement Sleep Behavior Disorder
REM sleep behavior disorder is characterized by a complex set of behaviors that occur during REM sleep, including mild to harmful body movements associated with dreams and nightmares (AASM, 2005). Normally during REM sleep, muscles are temporarily paralyzed however, in REM sleep behavior disorder this paralysis is absent, thus allowing individuals to “play out” their dreams. The overall prevalence in the general population is estimated to be less than half a percent, slightly higher in older persons (AASM, 2005), and affecting men more frequently than women.
REM sleep behavior disorder is frequently associated with neurological disorders and it has been suggested that it could be an early sign of neurodegeneration (Olson et al., 2000). At least 15 percent of individuals with Parkinson’s disease (Comella et al., 1998 Gagnon et al., 2002) and 44 percent of individuals with multiple system atrophy (Plazzi et al., 1997 1998) also suffer from REM sleep behavior disorder. There are a number of effective pharmacological treatments, including a long-acting benzodiazepine (Schenck and Mahowald, 1990), clonazepam (Schenck et al., 1993), and dopamine agonists (Bamford, 1993 Fantini et al., 2003).
Nightmare disorder is characterized by recurrent disturbances of dreaming that are disturbing mental experiences that seem real and sometimes cause the individual to wake up. If awoken, individuals commonly have difficulty returning to sleep. Nightmares often occur during the second half of a normal period of sleep. Dream content involves a distressing theme, typically imminent physical danger. During nightmares, individuals experience increased heart and respiration rates (Fisher et al., 1970 Nielsen and Zadra, 2000).
Nightmares commonly affect children and adolescents and decrease in frequency and intensity as an individual grows older (AASM, 2005). Drugs and alcohol can trigger nightmares. Prevalence rates are also higher in individuals suffering from acute stress disorder and posttraumatic stress disorder.
Humans are naturally adapted to lowland environment where oxygen is abundant.  When people from the general lowlands go to altitudes above 2,500 metres (8,200 ft) they experience altitude sickness, which is a type of hypoxia, a clinical syndrome of severe lack of oxygen. Some people get the illness even at above 1,500 metres (5,000 ft).  Complications include fatigue, dizziness, breathlessness, headaches, insomnia, malaise, nausea, vomiting, body pain, loss of appetite, ear-ringing, blistering and purpling of the hands and feet, and dilated veins.   
The sickness is compounded by related symptoms such as cerebral oedema (swelling of brain) and pulmonary oedema (fluid accumulation in lungs).   For several days, they breathe excessively and burn extra energy even when the body is relaxed. The heart rate then gradually decreases. Hypoxia, in fact, is one of the principal causes of death among mountaineers.   In women, pregnancy can be severely affected, such as development of high blood pressure, called preeclampsia, which causes premature labour, low birth weight of babies, and often complicated with profuse bleeding, seizures, and death of the mother.  
An estimated 81.6 million people worldwide are estimated to live at an elevation higher than 2,500 metres (8,200 ft) above sea level, of which 21.7 million are in Ethiopia, 12.5 million in China, 11.7 million in Colombia, 7.8 million in Peru and 6.2 million in Bolivia.  Certain natives of Tibet, Ethiopia, and the Andes have been living at these high altitudes for generations and are protected from hypoxia as a consequence of genetic adaptation.   It is estimated that at 4,000 metres (13,000 ft), every lungful of air only has 60% of the oxygen molecules that people at sea level have.  Highlanders are thus constantly exposed to a low oxygen environment, yet they live without any debilitating problems.  One of the best documented effects of high altitude is a progressive reduction in birth weight. It has been known that women of long-resident high-altitude population are not affected. These women are known to give birth to heavier-weight infants than women of lowland inhabitants. This is particularly true among Tibetan babies, whose average birth weight is 294–650 (
470) g heavier than the surrounding Chinese population and their blood-oxygen level is considerably higher. 
The first scientific investigations of high-altitude adaptation was done by A. Roberto Frisancho of the University of Michigan in the late 1960s among the Quechua people of Peru.   Paul T. Baker, Penn State University, (in the Department of Anthropology) also conducted a considerable amount of research into human adaptation to high altitudes, and mentored students who continued this research.  One of these students, anthropologist Cynthia Beall of Case Western Reserve University, began to conduct research on high altitude adaptation among the Tibetans in the early 1980s, still doing so to this day. 
Scientists started to notice the extraordinary physical performance of Tibetans since the beginning of Himalayan climbing era in the early 20th century. The hypothesis of a possible evolutionary genetic adaptation makes sense.  The Tibetan plateau has an average elevation of 4,000 metres (13,000 ft) above sea level, and covering more than 2.5 million km 2 , it is the highest and largest plateau in the world. In 1990, it was estimated that 4,594,188 Tibetans live on the plateau, with 53% living at an altitude over 3,500 metres (11,500 ft). Fairly large numbers (about 600,000) live at an altitude exceeding 4,500 metres (14,800 ft) in the Chantong-Qingnan area.  Where the Tibetan highlanders live, the oxygen level is only about 60% of that at sea level. The Tibetans, who have been living in this region for 3,000 years, do not exhibit the elevated haemoglobin concentrations to cope with oxygen deficiency as observed in other populations who have moved temporarily or permanently at high altitudes. Instead, the Tibetans inhale more air with each breath and breathe more rapidly than either sea-level populations or Andeans. Tibetans have better oxygenation at birth, enlarged lung volumes throughout life, and a higher capacity for exercise. They show a sustained increase in cerebral blood flow, lower haemoglobin concentration, and less susceptibility to chronic mountain sickness than other populations, due to their longer history of high-altitude habitation.  
Individuals can develop short-term tolerance with careful physical preparation and systematic monitoring of movements, but the biological changes are quite temporary and reversible when they return to lowlands.  Moreover, unlike lowland people who only experience increased breathing for a few days after entering high altitudes, Tibetans retain this rapid breathing and elevated lung-capacity throughout their lifetime.  This enables them to inhale larger amounts of air per unit of time to compensate for low oxygen levels. In addition, they have high levels (mostly double) of nitric oxide in their blood, when compared to lowlanders, and this probably helps their blood vessels dilate for enhanced blood circulation.  Further, their haemoglobin level is not significantly different (average 15.6 g/dl in males and 14.2 g/dl in females),  from those of people living at low altitude. (Normally, mountaineers experience >2 g/dl increase in Hb level at Mt. Everest base camp in two weeks.  ) In this way they are able to evade both the effects of hypoxia and mountain sickness throughout life. Even when they climbed the highest summits like Mt. Everest, they showed regular oxygen uptake, greater ventilation, more brisk hypoxic ventilatory responses, larger lung volumes, greater diffusing capacities, constant body weight and a better quality of sleep, compared to people from the lowland. 
In contrast to the Tibetans, the Andean highlanders, who have been living at high altitudes for no more than 11,000 years, show different pattern of haemoglobin adaptation. Their haemoglobin concentration is higher compared to those of lowlander population, which also happens to lowlanders moving to high altitude. When they spend some weeks in the lowland their haemoglobin drops to average of other people. This shows only temporary and reversible acclimatisation. However, in contrast to lowland people, they do have increased oxygen level in their haemoglobin, that is, more oxygen per blood volume than other people. This confers an ability to carry more oxygen in each red blood cell, making a more effective transport of oxygen in their body, while their breathing is essentially at the same rate.  This enables them to overcome hypoxia and normally reproduce without risk of death for the mother or baby. The Andean highlanders are known from the 16th-century missionaries that their reproduction had always been normal, without any effect in the giving birth or the risk for early pregnancy loss, which are common to hypoxic stress.  They have developmentally acquired enlarged residual lung volume and its associated increase in alveolar area, which are supplemented with increased tissue thickness and moderate increase in red blood cells. Though the physical growth in body size is delayed, growth in lung volumes is accelerated.  An incomplete adaptation such as elevated haemoglobin levels still leaves them at risk for mountain sickness with old age.
Among the Quechua people of the Altiplano, there is a significant variation in NOS3 (the gene encoding endothelial nitric oxide synthase, eNOS), which is associated with higher levels of nitric oxide in high altitude.  Nuñoa children of Quechua ancestry exhibit higher blood-oxygen content (91.3) and lower heart rate (84.8) than their counterpart school children of different ethnicity, who have an average of 89.9 blood-oxygen and 88–91 heart rate.  High-altitude born and bred females of Quechua origins have comparatively enlarged lung volume for increased respiration. 
Blood profile comparisons show that among the Andeans, Aymaran highlanders are better adapted to highlands than the Quechuas.   Among the Bolivian Aymara people, the resting ventilation and hypoxic ventilatory response were quite low (roughly 1.5 times lower), in contrast to those of the Tibetans. The intrapopulation genetic variation was relatively less among the Aymara people.   Moreover, when compared to Tibetans, the blood haemoglobin level at high altitudes among Aymarans is notably higher, with an average of 19.2 g/dl for males and 17.8 g/dl for females.  Among the different native highlander populations, the underlying physiological responses to adaptation are quite different. For example, among four quantitative features, such as are resting ventilation, hypoxic ventilatory response, oxygen saturation, and haemoglobin concentration, the levels of variations are significantly different between the Tibetans and the Aymaras.  Methylation also influences oxygenation. 
The peoples of the Ethiopian highlands also live at extremely high altitudes, around 3,000 metres (9,800 ft) to 3,500 metres (11,500 ft). Highland Ethiopians exhibit elevated haemoglobin levels, like Andeans and lowlander peoples at high altitudes, but do not exhibit the Andeans’ increase in oxygen content of haemoglobin.  Among healthy individuals, the average haemoglobin concentrations are 15.9 and 15.0 g/dl for males and females respectively (which is lower than normal, almost similar to the Tibetans), and an average oxygen saturation of haemoglobin is 95.3% (which is higher than average, like the Andeans).  Additionally, Ethiopian highlanders do not exhibit any significant change in blood circulation of the brain, which has been observed among the Peruvian highlanders (and attributed to their frequent altitude-related illnesses).  Yet, similar to the Andeans and Tibetans, the Ethiopian highlanders are immune to the extreme dangers posed by high-altitude environment, and their pattern of adaptation is definitely unique from that of other highland peoples. 
The underlying molecular evolution of high-altitude adaptation has been explored and understood fairly recently.  Depending on the geographical and environmental pressures, high-altitude adaptation involves different genetic patterns, some of which have evolved quite recently. For example, Tibetan adaptations became prevalent in the past 3,000 years, a rapid example of recent human evolution. At the turn of the 21st century, it was reported that the genetic make-up of the respiratory components of the Tibetan and the Ethiopian populations are significantly different. 
Substantial evidence in Tibetan highlanders suggests that variation in haemoglobin and blood-oxygen levels are adaptive as Darwinian fitness. It has been documented that Tibetan women with a high likelihood of possessing one to two alleles for high blood-oxygen content (which is odd for normal women) had more surviving children the higher the oxygen capacity, the lower the infant mortality.  In 2010, for the first time, the genes responsible for the unique adaptive traits were identified following genome sequencing of 50 Tibetans and 40 Han Chinese from Beijing. Initially, the strongest signal of natural selection detected was a transcription factor involved in response to hypoxia, called endothelial Per-Arnt-Sim (PAS) domain protein 1 (EPAS1). It was found that one single-nucleotide polymorphism (SNP) at EPAS1 shows a 78% frequency difference between Tibetan and mainland Chinese samples, representing the fastest genetic change observed in any human gene to date. Hence, Tibetan adaptation to high altitude becomes the fastest process of phenotypically observable evolution in humans,  which is estimated to have occurred a few thousand years ago, when the Tibetans split up from the mainland Chinese population. The time of genetic divergence has been variously estimated as 2,750 (original estimate),  4,725,  8,000,  or 9,000  years ago. Mutations in EPAS1, at higher frequency in Tibetans than their Han neighbours, correlate with decreased haemoglobin concentrations among the Tibetans, which is the hallmark of their adaptation to hypoxia. Simultaneously, two genes, egl nine homolog 1 (EGLN1) (which inhibits haemoglobin production under high oxygen concentration) and peroxisome proliferator-activated receptor alpha (PPARA), were also identified to be positively selected in relation to decreased haemoglobin nature in the Tibetans. 
Similarly, the Sherpas, known for their Himalayan hardiness, exhibit similar patterns in the EPAS1 gene, which further fortifies that the gene is under selection for adaptation to the high-altitude life of Tibetans.  A study in 2014 indicates that the mutant EPAS1 gene could have been inherited from archaic hominins, the Denisovans.  EPAS1 and EGLN1 are definitely the major genes for unique adaptive traits when compared with those of the Chinese and Japanese.  Comparative genome analysis in 2014 revealed that the Tibetans inherited an equal mixture of genomes from the Nepalese-Sherpas and Hans, and they acquired the adaptive genes from the sherpa-lineage. Further, the population split was estimated to occur around 20,000 to 40,000 years ago, a range of which support archaeological, mitochondria DNA and Y chromosome evidence for an initial colonisation of the Tibetan plateau around 30,000 years ago. 
The genes (EPAS1, EGLN1, and PPARA) function in concert with another gene named hypoxia inducible factors (HIF), which in turn is a principal regulator of red blood cell production (erythropoiesis) in response to oxygen metabolism.    The genes are associated not only with decreased haemoglobin levels, but also in regulating energy metabolism. EPAS1 is significantly associated with increased lactate concentration (the product of anaerobic glycolysis), and PPARA is correlated with decrease in the activity of fatty acid oxidation.  EGLN1 codes for an enzyme, prolyl hydroxylase 2 (PHD2), involved in erythropoiesis. Among the Tibetans, mutation in EGLN1 (specifically at position 12, where cytosine is replaced with guanine and at 380, where G is replaced with C) results in mutant PHD2 (aspartic acid at position 4 becomes glutamine, and cysteine at 127 becomes serine) and this mutation inhibits erythropoiesis. The mutation is estimated to occur about 8,000 years ago.  Further, the Tibetans are enriched for genes in the disease class of human reproduction (such as genes from the DAZ, BPY2, CDY, and HLA-DQ and HLA-DR gene clusters) and biological process categories of response to DNA damage stimulus and DNA repair (such as RAD51, RAD52, and MRE11A), which are related to the adaptive traits of high infant birth weight and darker skin tone and are most likely due to recent local adaptation. 
The patterns of genetic adaptation among the Andeans are largely distinct from those of the Tibetan, with both populations showing evidence of positive natural selection in different genes or gene regions. However, EGLN1 appears to be the principal signature of evolution, as it shows evidence of positive selection in both Tibetans and Andeans. Even then, the pattern of variation for this gene differs between the two populations.  Among the Andeans, there are no significant associations between EPAS1 or EGLN1 SNP genotypes and haemoglobin concentration, which has been the characteristic of the Tibetans.  The whole genome sequences of 20 Andeans (half of them having chronic mountain sickness) revealed that two genes, SENP1 (an erythropoiesis regulator) and ANP32D (an oncogene) play vital roles in their weak adaptation to hypoxia. 
The adaptive mechanism of Ethiopian highlanders is quite different. This is probably because their migration to the highland was relatively early for example, the Amhara have inhabited altitudes above 2,500 metres (8,200 ft) for at least 5,000 years and altitudes around 2,000 metres (6,600 ft) to 2,400 metres (7,900 ft) for more than 70,000 years.  Genomic analysis of two ethnic groups, Amhara and Oromo, revealed that gene variations associated with haemoglobin difference among Tibetans or other variants at the same gene location do not influence the adaptation in Ethiopians.  Identification of specific genes further reveals that several candidate genes are involved in Ethiopians, including CBARA1, VAV3, ARNT2 and THRB. Two of these genes (THRB and ARNT2) are known to play a role in the HIF-1 pathway, a pathway implicated in previous work reported in Tibetan and Andean studies. This supports the concept that adaptation to high altitude arose independently among different highlanders as a result of convergent evolution. 
What to know about general adaptation syndrome
General adaptation syndrome is a three-stage response that the body has to stress. But what do the different stages involve and what examples are there of GAS in action?
Stress is sometimes thought of as a mental pressure, but it also has a physical effect on the body. Understanding the stages the body goes through when exposed to stress helps people become more aware of these physical signs of stress when they occur.
This article explores what general adaption syndrome (GAS) is, its different stages, and when it may occur. It also considers how people can better manage their response to stress.
Share on Pinterest GAS describes the way the body responds to stress.
Hans Selye, a Vienna-born scientist, working in the 20th century, was the first person to describe GAS.
Selye found that rats displayed a similar set of physical responses to several different stressors. The latter included cold temperatures, excessive physical exertions, and injection with toxins.
The scientist explained GAS as the body’s way of adapting to a perceived threat to better equip it to survive. A paper on Selye’s GAS theory was published in The Journal of Clinical Endocrinology in 1946.
The three stages of GAS are:
What happens within the body during each of these stages is explored below.
Alarm reaction stage
At the alarm reaction stage, a distress signal is sent to a part of the brain called the hypothalamus. The hypothalamus enables the release of hormones called glucocorticoids.
Glucocorticoids trigger the release of adrenaline and cortisol, which is a stress hormone. The adrenaline gives a person a boost of energy. Their heart rate increases and their blood pressure rises. Meanwhile, blood sugar levels also go up.
These physiological changes are governed by a part of a person’s autonomic nervous system (ANS) called the sympathetic branch.
The alarm reaction stage of the GAS prepares a person to respond to the stressor they are experiencing. This is often known as a “fight or flight” response.
During the resistance stage, the body tries to counteract the physiological changes that happened during the alarm reaction stage. The resistance stage is governed by a part of the ANS called the parasympathetic.
The parasympathetic branch of the ANS tries to return the body to normal by reducing the amount of cortisol produced. The heart rate and blood pressure begin to return to normal.
If the stressful situation comes to an end, during the resistance stage, the body will then return to normal.
However, if the stressor remains, the body will stay in a state of alert, and stress hormones continue to be produced.
This physical response can lead to a person struggling to concentrate and becoming irritable.
After an extended period of stress, the body goes into the final stage of GAS, known as the exhaustion stage. At this stage, the body has depleted its energy resources by continually trying but failing to recover from the initial alarm reaction stage.
Once it reaches the exhaustion stage, a person’s body is no longer equipped to fight stress. They may experience:
If a person does not find ways to manage stress levels at this stage, they are at risk of developing stress-related health conditions.