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Sleepless in L.A.

Everyone craves a good night’s sleep, but for far too many people it’s an elusive dream.

By Kathy Svitil
Photography by Ann Johansson


It is 8:45 p.m. on a Monday night in April as I pull my car into the parking lot near the UCLA sleep lab, which is housed in what used to be the emergency room of the old UCLA Medical Center. Only a few cars are in the lot - not surprising, given the hour - so I easily find a spot.

Like most adults, I don't always sleep well. I find myself staring at the ceiling at 3 a.m. more often than I'd like. But I wouldn't characterize my sleep difficulties as severe enough to warrant an overnight evaluation hooked up to an array of sensors. Nevertheless, I'm here to spend the night at the sleep lab for just that purpose.

Tens of millions of Americans routinely suffer from some kind of sleep difficulty - insomnia, night terrors, sleepwalking, narcolepsy, restless legs, sleep apnea and more. It's not just medical issues that are to blame. "Modern society has contributed to the problem of sleeplessness," UCLA pulmonologist and sleep specialist Michelle Zeidler, M.D., says. "The increase in work hours, commute time and time spent on various technologies after hours has curtailed the amount of time we spend sleeping."

Whatever the cause of this epidemic, sleeplessness accounts for $16 billion in annual healthcare expenses and $50 billion in lost productivity, according to the National Institutes of Health. Drowsy drivers, says the National Highway Traffic Safety Administration, cause at least 100,000 car crashes a year, with an estimated 71,000 injuries and 1,550 fatalities. Studies have shown that chronically reduced or disrupted sleep raises the risk of other health problems, such as obesity, diabetes and cardiovascular disease, on top of creating a whole society of really tired people.

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"Sleep has an enormous impact on society and health," notes sleep specialist and neurologist Alon Avidan, M.D., M.P.H., director of the UCLA Sleep Disorders Center, which is made up of the newly renovated Westwood sleep lab, the outpatient Sleep Disorders Clinic and research facilities. "A good night's sleep needs to be considered preventive medicine, just like a healthy diet and exercise."

At 9:30 p.m., my technologist, William, starts hooking me up to an intimidating tangle of multicolored wires. "I can connect these in my sleep, but I've never counted just how many there are," he quips about the electrodes that he's fastening to the back of my head, forehead, temples, chin, chest, abdomen and legs. These wires, which are plugged into a box strung around my neck, will track my brain waves, eye movements, heart rate and leg movements, among other variables, while I sleep. Elastic straps are secured over my chest and stomach, connected to still more leads, and a blood-oxygen reader is clamped to my left index finger.

Around 11:30 p.m., William comes back to outfit me with a final accessory - a clear tube in each nostril to sense oxygen levels in my exhaled air - and to connect all the wires to the lab's central monitoring station in an adjacent room. After shutting off the lights, he speaks via an intercom and runs me through exercises to calibrate the instruments ("look up and down," "look side to side," "breathe deeply") then leaves me to my dreams. I can't say I'm enjoying this much, but by midnight, despite the tubes, straps and wires, I begin to nod off.
For decades, researchers have debated the function of sleep. One of the most widely accepted theories holds that sleep is a crucial period of down time during which our bodies can recover from damage. Rapid-eye-movement, or REM, sleep - dreaming sleep - by contrast, has long been considered vital for memory formation and learning. "The question 'Why do we sleep?' usually is posed as some kind of a mystery," sleep researcher Jerome Siegel, Ph.D., says, "because we perceive sleep as something maladaptive, as a vulnerable state." It is a period when we are at risk of predation and unable to perform functions like eating or mating that are vital to our survival. "It's an anthropomorphic view, because humans like to stay awake, and suggests that to persist, sleep must have some function that balances out this huge 'penalty' of sleeping," he says.

"I bought into this, too," admits Dr. Siegel, head of the Center for Sleep Research at the Jane and Terry Semel Institute for Neuroscience and Human Behavior at UCLA. Now, however, based on observations of the sleep habits and lifestyles of a variety of animals, he has a different view. Sleep, he says, is adaptive because it restricts behavior, allowing humans and other animals to increase their metabolic efficiency and decrease energy usage while simultaneously reducing the risk of predation and injury.

In his studies of dolphins, for example, Dr. Siegel has found that, although they have large brains, these creatures don't seem to have long periods of unresponsiveness that would indicate they're sleeping as we humans might. Indeed, he notes, "brain-wave recordings show activity that is typical of deep sleep on only one side of the brain at a time, but never bilaterally" - as if a dolphin's typical state-of-rest is half-awake, half-asleep.

But this lack of sleep, in dolphins, at least, seems to have no adverse cognitive effects, Dr. Siegel says. "In one study, dolphins had to press a paddle every 30 seconds for five days, and they did just fine. There was no deterioration of performance, and no rebound after." The same imperviousness to sleep deprivation has also been noted in migratory birds, he says, and more recently in other animals.

Not all animals, of course, can so effectively skip sleep. Some are champion sleepers. Case in point: North America's big brown bat. An insect-eater, the bat is awake only for about four hours a day, just around dusk when insects are most plentiful. "If the bats were active earlier, the insects wouldn't be there, and if they are up earlier, they would be vulnerable to predation by large predatory birds," Dr. Siegel says. Because the sleeping brain runs at a lower metabolic setting, the bats save energy even as they minimize their risk. Big cats like lions behave similarly, he says: "They hunt, they eat, and then the best thing for them to do is go back to the den with their babies and sleep."

To Dr. Siegel, all of this evidence suggests that the amount of sleep a given species needs is determined by varying factors such as the time necessary to hunt, eat, mate and care for young, as well as predation dangers during periods of activity. "Sleeping," he says, "is the best thing you can do if you want to pass your genes along, after you take care of the necessities of life."

Of course, even though our sleep needs may be hard-wired into us, we humans don't always experience problem-free slumber. In fact, as we age, sleep difficulties become commonplace. One reason, says a team of UCLA researchers headed by Chancellor Gene D. Block, Ph.D., a professor of psychiatry and biobehavioral sciences, is a change in the brain's master circadian clock - a brain region known as the suprachiasmatic nucleus, or SCN - which controls the sleep-wake cycle. In 2011, Chancellor Block and neuroscientist Christopher Colwell, Ph.D., head of the UCLA Laboratory of Circadian and Sleep Medicine, reported a dramatic difference in the neural output of the SCN in middle-aged mice compared to young mice. In young mice, the scientists discovered high levels of activity during the day and much lower activity levels at night; in middle-aged animals, the day-night difference was far smaller.

This type of decline affects the clock's ability to influence the rest of the body, leading to a "transient feeling of disruption that feels like jet lag," says Dr. Colwell, who is now investigating the mechanism behind the change. One idea is that aging leads to a chronic inflammation of the central nervous system that, in turn, disrupts the neural activity of the clock. Such inflammation is also seen in neurodegenerative disorders like Parkinson's disease, in which - not coincidentally, Dr. Colwell says - the neural output of the SCN is also diminished. Alternatively, the decreased activity of the SCN may be due to an age-related malfunction in mitochondria, cells' energy-producing structures.

The researchers are certain, however, that the effect is not due to changes in the molecular clockwork found inside single cells; rather, it is due to a functional change in the ability of cells of the SCN to communicate with the rest of the body. And that means it may be possible to override the change and reduce or reverse age-related sleep problems. For example, it might help to time exercise to an optimal point in the body's activity cycle - "The late afternoon could be best for exercise, while the same exercise late at night might further disrupt the sleep cycle," Dr. Colwell says - or to regulate when and what one eats, or use light to recalibrate one's clock.

The light flips on at 5:50 a.m., startling me awake. William enters the room to tell me it's morning, more or less, and the testing is done. As he removes the nasal tube, peels off electrodes and unfastens the chest and abdominal straps, he tells me that my sleep was, for the most part, uneventful.

A few minutes later, I'm seeing my night mapped out as tracings on a monitor, with separate lines for eye movements, respiration rate, oxygen levels and other variables. There is one anomaly, at 12:56 a.m., a minor episode of sleep apnea, during which my breathing stopped for 13 seconds. To me, it sounds like 13 seconds too long, but compared to the actual patients in the sleep lab, who sometimes stop breathing for many tens of seconds or even minutes, over and over again throughout the night, it is literally nothing more than a blip on a computer screen.

Although an estimated 60-million Americans regularly experience insomnia - it is the most frequently cited reason that patients seek medical help for sleep difficulties - the complaint is uncommon among patients over-nighting at UCLA's eight-bed sleep lab. For a patient with insomnia, a sleep study won't reveal much more than can be obtained from a thorough clinical history. People who can't fall asleep, after all, are acutely aware of their predicament and don't need to be tethered to miles of wires to tell them what their problem is.

Sleep apnea - abnormal pauses in breathing during sleep, like my 13-second lapse - is, on the other hand, the most common reason patients seek a sleep evaluation. It also is one of the most severe sleep disorders, notes Dr. Avidan. In fact, Dr. Avidan says, the relationship between sleep and medical disorders is bidirectional; sleep quality is affected by the presence and severity of medical disorders as well as the medications used to treat them, and poor sleep quality can itself contribute to medical disorders.

According to the National Institute of Neurological Disorders and Stroke, some 18-million Americans suffer from sleep apnea. Most have what is known as obstructive sleep apnea, or OSA, which occurs when the muscles in the throat, soft palate and tongue periodically relax during sleep and droop, causing the airway to narrow or to be blocked, preventing the flow of oxygen to the lungs. After several seconds to a couple of minutes, the sleeper wakes up, snorting loudly or gasping for air, then falls asleep again, usually unaware that he or she ever awoke - though his or her bed partner, rousted from a peaceful slumber, will be keenly aware of the problem. The cycle is repeated, sometimes dozens of times an hour, hundreds of times a night.

Daytime fatigue (which, surprisingly, isn't a universal symptom) and irritable sleep partners aren't the only result. According to neurobiologist Ron Harper, Ph.D., sleep apnea - or "sleep-disordered breathing" - can cause damage to a number of vital brain areas, including those that regulate blood pressure, serve memory functions, assist in warding off depression and anxiety, and help in executive function. "The damage appears as loss and injury to brain cells, supporting tissue and nerve fibers, and impaired brain responses when asking the brain to respond to manipulations that normally raise blood pressure," says Dr. Harper, a distinguished professor of neurobiology at the David Geffen School of Medicine at UCLA.

Using high-resolution magnetic resonance imaging, Dr. Harper and colleagues found that several areas of the brains of patients with OSA are smaller in volume than the same brain areas of control subjects without the sleep disorder. In particular, brain structures called the mammillary bodies - so-called because they resemble small breasts - are nearly 20-percent smaller in patients with OSA. These structures, located on the underside of the brain, are critical for short-term memory formation.

"We were shocked to see how much mammillary-body volumes had declined in OSA patients," Dr. Harper says. "This was the first evidence that OSA was accompanied by damage to this memory region." His research also has identified similar brain-volume losses and different signs of injury in other regions, including the hippocampus, also involved in memory formation, and the anterior cingulate cortex, which, among other functions, plays a role in depression and anxiety.

What's going on? Dr. Harper proposes that these brain areas are shrinking because their constituent cells are literally being starved to death. And the reason why, he suspects, is low levels of thiamine and magnesium. A frequently noted characteristic of OSA patients is that they sweat profusely at night. That happens because the sympathetic nervous system, which maintains the body's homeostasis and regulates sweating, is too active, partially as a result of damage to brain areas that regulate sympathetic activity; this over-activity also causes blood vessels to constrict, raising blood pressure.

"These people lose a lot of water, which flushes out nutrients that are water-soluble, including magnesium and thiamine, or vitamin B1," Dr. Harper says. One function of thiamine in the body is to transport glucose into cells to "feed" them, a process that is aided by magnesium. When thiamine and magnesium levels are low, "the cells, excessively activated because of low oxygen during apnea, can't be adequately fed, and they die," he says.

Although there is still no proof that thiamine levels are low in folks with OSA, the vitamin deficiency would be especially problematic. When individuals with OSA stop breathing, their cells become oxygen-starved and, as a consequence, become very active, which increases their need for glucose; without thiamine and magnesium, glucose never reaches those hungry cells.

If brain structures are being damaged by the repeated episodes of low oxygen that are characteristic of sleep apnea, the key to preventing that damage is maintaining normal oxygen levels. For most OSA patients receiving treatment, that level is accomplished with a continuous positive airway pressure, or CPAP, device. A CPAP device consists of a mask that fits snugly over the nose, through which a tube delivers a steady stream of air that provides enough air pressure to keep the tissues of the mouth and throat from collapsing. Although effective, the machines can be cumbersome and obtrusive. "People experience discomfort with the interface and congestion," among other problems, says UCLA pulmonologist and sleep specialist Ravi Aysola, M.D. "But in my practice, people want their sleep disorder addressed, and if they are committed to treatment, they will adjust. Some of my patients become what I like to call 'CPAP evangelists,'" he says. "They tell everyone how it changes their life."

Other patients, Dr. Aysola acknowledges, never adjust to the machines. They may, however, get relief from behavioral or lifestyle changes - change their sleep position, cut out alcohol or drugs, lose weight - or through the use of a dental device that helps keep the airway open. "The best treatment that is never used isn't the best treatment," he says, "so if people can't get used to the CPAP device, we still encourage them to come back into the sleep clinic, because there are many other things they can do."

By 6:30 a.m., I'm dressed and ready to leave the sleep lab, my adventure over. After nearly 12 hours, I know a little more than I used to about my sleep patterns. I'm sometimes subject to brief episodes of apnea, and at times when I sleep on my back and during REM sleep my oxygen level dips a bit. All-in-all, nothing dramatic to worry about, although I'm sure I'll continue to struggle with the occasional sleepless 3 a.m.

As I hit the still-empty freeway and head east into the sunrise, well over an hour early for work, I'm already looking forward to my next night of (hopefully) peaceful slumber - perchance to dream.


Kathy Svitil is co-director of news and lead science writer for the California Institute of Technology.

To read more about clinical sleep medicine and the UCLA Sleep Disorders Center, click on the link to this article at:

 





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