Part of the reason the heart suffers so dramatically under the weight of sleep deprivation concerns blood pressure. Have a quick look at your right forearm and pick out some veins. If you wrap your left hand around that forearm, just below the elbow, and grip it, like a tourniquet, you will see those vessels start to balloon. A little alarming, isn’t it? The ease with which just a little sleep loss can pump up pressure in the veins of your entire body, stretching and distressing the vessel walls, is equally alarming. High blood pressure is so common nowadays that we forget the deathly toll it inflicts. This year alone, hypertension will steal more than 7 million people’s lives by way of cardiac failure, ischemic heart disease, stroke, or kidney failure. Deficient sleep is responsible for many of these lost fathers, mothers, grandparents, and beloved friends.
As with other consequences of sleep loss we’ve encountered, you don’t need a full night of total sleep deprivation to inflict a measurable impact on your cardiovascular system. One night of modest sleep reduction—even just one or two hours—will promptly speed the contracting rate of a person’s heart, hour upon hour, and significantly increase the systolic blood pressure within their vasculature.fn1 You will find no solace in the fact that these experiments were conducted in young, fit individuals, all of whom started out with an otherwise healthy cardiovascular system just hours before. Such physical fitness proves no match for a short night of sleep; it affords no resistance.
Beyond accelerating your heart rate and increasing your blood pressure, a lack of sleep further erodes the fabric of those strained blood vessels, especially those that feed the heart itself, called the coronary arteries. These corridors of life need to be clean and open wide to supply your heart with blood at all times. Narrow or block those passageways, and your heart can suffer a comprehensive and often fatal attack caused by blood oxygen starvation, colloquially known as a “massive coronary.”
One cause of a coronary artery blockage is atherosclerosis, or the furring up of those heart corridors with hardened plaques that contain calcium deposits. Researchers at the University of Chicago studied almost five hundred healthy midlife adults, none of whom had any existing heart disease or signs of atherosclerosis. They tracked the health of the coronary arteries of these participants for a number of years, all the while assessing their sleep. If you were one of the individuals who were obtaining just five to six hours each night or less, you were 200 to 300 percent more likely to suffer calcification of your coronary arteries over the next five years, relative to those individuals sleeping seven to eight hours. The deficient sleep of those individuals was associated with a closing off of the critical passageways that should otherwise be wide open and feeding the heart with blood, starving it and significantly increasing the risk of a coronary heart attack.
Although the mechanisms by which sleep deprivation degrades cardiovascular health are numerous, they all appear to cluster around a common culprit, called the sympathetic nervous system. Abandon any thoughts of love or serene compassion based on the misguiding name. The sympathetic nervous system is resolutely activating, inciting, even agitating. If needed, it will mobilize the evolutionarily ancient fight-or-flight stress response within the body, comprehensively and in a matter of seconds. Like an accomplished general in command of a vast military, the sympathetic nervous system can muster activity in a vast assortment of the body’s physiological divisions—from respiration, immune function, and stress chemicals to blood pressure and heart rate.
An acute stress response from the sympathetic nervous system, which is normally only deployed for short periods of time lasting minutes to hours, can be highly adaptive under conditions of credible threat, such as the potential of real physical attack. Survival is the goal, and these responses promote immediate action to accomplish just that. But leave that system stuck in the “on” position for long durations of time, and sympathetic activation becomes deeply maladaptive. In fact, it is a killer.
With few exceptions over the past half century, every experiment that has investigated the impact of deficient sleep on the human body has observed an overactive sympathetic nervous system. For as long as the state of insufficient sleep lasts, and for some time thereafter, the body remains stuck in some degree of a fight-or-flight state. It can last for years in those with an untreated sleep disorder, excessive work hours that limit sleep or its quality, or the simple neglect of sleep by an individual. Like a car engine that is revved to a shrieking extreme for sustained periods of time, your sympathetic nervous system is floored into perpetual overdrive by a lack of sleep. The consequential strain that is placed on your body by the persistent force of sympathetic activation will leak out in all manner of health issues, just like the failed pistons, gaskets, seals, and gnashing gears of an abused car engine.
Through this central pathway of an overactive sympathetic nervous system, sleep deprivation triggers a domino effect that will spread like a wave of health damage throughout your body. It starts with removing a default resting brake that normally prevents your heart from accelerating in its rate of contraction. Once this brake is released, you will experience sustained speeds of cardiac beating.
As your sleep-deprived heart beats faster, the volumetric rate of blood pumped through your vasculature increases, and with that comes the hypertensive state of your blood pressure. Occurring at the same time is a chronic increase in a stress hormone called cortisol, which is triggered by the overactive sympathetic nervous system. One undesirable consequence of the sustained deluge of cortisol is the constriction of those blood vessels, triggering an even greater increase in blood pressure.
Making matters worse, growth hormone—a great healer of the body—which normally surges at night, is shut off by the state of sleep deprivation. Without growth hormone to replenish the lining of your blood vessels, called the endothelium, they will be slowly shorn and stripped of their integrity. Adding insult to real injury, the hypertensive strain that sleep deprivation places on your vasculature means that you can no longer repair those fracturing vessels effectively. The damaged and weakened state of vascular plumbing throughout your body now becomes systemically more prone to atherosclerosis (arteries furring up). Vessels will rupture. It is a powder keg of factors, with heart attack and stroke being the most common casualties in the explosive aftermath.
Compare this cascade of harm to the healing benefits that a full night of sleep normally lavishes on the cardiovascular system. During deep NREM sleep specifically, the brain communicates a calming signal to the fight-or-flight sympathetic branch of the body’s nervous system, and does so for long durations of the night. As a result, deep sleep prevents an escalation of this physiological stress that is synonymous with increased blood pressure, heart attack, heart failure, and stroke. This includes a calming effect on the contracting speed of your heart. Think of your deep NREM sleep as a natural form of nighttime blood-pressure management—one that averts hypertension and stroke.
When communicating science to the general public in lectures or writing, I’m always wary of bombarding an audience with never-ending mortality and morbidity statistics, lest they themselves lose the will to live in front of me. It is hard not to do so with such compelling masses of studies in the field of sleep deprivation. Often, however, a single astonishing result is all that people need to apprehend the point. For cardiovascular health, I believe that finding comes from a “global experiment” in which 1.5 billion people are forced to reduce their sleep by one hour or less for a single night each year. It is very likely that you have been part of this experiment, otherwise known as daylight savings time.
In the Northern Hemisphere, the switch to daylight savings time in March results in most people losing an hour of sleep opportunity. Should you tabulate millions of daily hospital records, as researchers have done, you discover that this seemingly trivial sleep reduction comes with a frightening spike in heart attacks the following day. Impressively, it works both ways. In the autumn within the Northern Hemisphere, when the
clocks move back and we gain an hour of sleep opportunity time, rates of heart attacks plummet the day after. A similar rise-and-fall relationship can be seen with the number of traffic accidents, proving that the brain, by way of attention lapses and microsleeps, is just as sensitive as the heart to very small perturbations of sleep. Most people think nothing of losing an hour of sleep for a single night, believing it to be trivial and inconsequential. It is anything but.
SLEEP LOSS AND METABOLISM: DIABETES AND WEIGHT GAIN
The less you sleep, the more you are likely to eat. In addition, your body becomes unable to manage those calories effectively, especially the concentrations of sugar in your blood. In these two ways, sleeping less than seven or eight hours a night will increase your probability of gaining weight, being overweight, or being obese, and significantly increases your likelihood of developing type 2 diabetes.
The global health cost of diabetes is $375 billion a year. That of obesity is more than $2 trillion. Yet for the under-slept individual, the cost to health, quality of life, and a hastened arrival of death are more meaningful. Precisely how a lack of sleep sets you on a path toward diabetes and leads to obesity is now well understood and incontrovertible.
DIABETES
Sugar is a dangerous thing. In your diet, yes, but here I’m referring to that which is currently circulating in your bloodstream. Excessively high levels of blood sugar, or glucose, over weeks or years inflicts a surprising harm to the tissues and organs of your body, worsens your health, and shortens your life span. Eye disease that can end in blindness, nerve disease that commonly results in amputations, and kidney failure necessitating dialysis or transplant are all consequences of prolonged high blood sugar, as are hypertension and heart disease. But it is the condition of type 2 diabetes that is most commonly and immediately related to unregulated blood sugar.
In a healthy individual, the hormone insulin will trigger the cells of your body to swiftly absorb glucose from the bloodstream should it increase, as happens after eating a meal. Instructed by insulin, the cells of your body will open special channels on their surface that operate like wonderfully efficient roadside drains at the height of a downpour. They have no problem dealing with the deluge of glucose coursing down the transit arteries, averting what could otherwise be a dangerous flood of sugar in the bloodstream.
If the cells of your body stop responding to insulin, however, they cannot efficiently absorb glucose from the blood. Similar to roadside drains that become blocked or erroneously closed shut, the rising swell of blood sugar cannot be brought back down to safe levels. At this point, the body has transitioned into a hyperglycemic state. Should this condition persist, and the cells of your body remain intolerant to dealing with the high levels of glucose, you will transition into a pre-diabetic state and, ultimately, develop full-blown type 2 diabetes.
Early-warning signs of a link between sleep loss and abnormal blood sugar emerged in a series of large epidemiological studies spanning several continents. Independent of one another, the research groups found far higher rates of type 2 diabetes among individuals that reported sleeping less than six hours a night routinely. The association remained significant even when adjusting for other contributing factors, such as body weight, alcohol, smoking, age, gender, race, and caffeine use. Powerful as these studies are, though, they do not inform the direction of causality. Does the state of diabetes impair your sleep, or does short sleep impair your body’s ability to regulate blood sugar, thereby causing diabetes?
To answer this question, scientists had to conduct carefully controlled experiments with healthy adults who had no existing signs of diabetes or issues with blood sugar. In the first of these studies, participants were limited to sleeping four hours a night for just six nights. By the end of that week, these (formerly healthy) participants were 40 percent less effective at absorbing a standard dose of glucose, compared to when they were fully rested.
To give you a sense of what that means, if the researchers showed those blood sugar readings to an unwitting family doctor, the GP would immediately classify that individual as being pre-diabetic. They would start a rapid intervention program to prevent the development of irreversible type 2 diabetes. Numerous scientific laboratories around the world have replicated this alarming effect of short sleep, some with even less aggressive reductions in sleep amount.
How does a lack of sleep hijack the body’s effective control of blood sugar? Was it a blockade of insulin release, removing the essential instruction for cells to absorb glucose? Or had the cells themselves become unresponsive to an otherwise normal and present message of insulin?
As we have discovered, both are true, though the most compelling evidence indicates the latter. By taking small tissue samples, or biopsies, from participants at the end of the above experiments, we can examine how the cells of the body are operating. After participants had been restricted to four to five hours of sleep for a week, the cells of these tired individuals had become far less receptive to insulin. In this sleep-deprived state, the cells were stubbornly resisting the message from insulin and refusing to open up their surface channels. The cells were repelling rather than absorbing the dangerously high levels of glucose. The roadside drains were effectively closed shut, leading to a rising tide of blood sugar and a pre-diabetic state of hyperglycemia.
While many in the general public understand that diabetes is serious, they may not appreciate the true burden. Beyond the average treatment cost of more than $85,000 per patient (which contributes to higher medical insurance premiums), diabetes lops ten years off an individual’s life expectancy. Chronic sleep deprivation is now recognized as one of the major contributors to the escalation of type 2 diabetes throughout first-world countries. It’s a preventable contribution.
WEIGHT GAIN AND OBESITY
When your sleep becomes short, you will gain weight. Multiple forces conspire to expand your waistline. The first concerns two hormones controlling appetite: leptin and ghrelin.fn2 Leptin signals a sense of feeling full. When circulating levels of leptin are high, your appetite is blunted and you don’t feel like eating. Ghrelin, in contrast, triggers a strong sensation of hunger. When ghrelin levels increase, so, too, does your desire to eat. An imbalance of either one of these hormones can trigger increased eating and thus body weight. Perturb both in the wrong direction, and weight gain is more than probable.
Over the past thirty years, my colleague Dr. Eve Van Cauter at the University of Chicago has tirelessly conducted research on the link between sleep and appetite that is as brilliant as it is impactful. Rather than depriving individuals of a full night of sleep, Van Cauter has taken a more relevant approach. She recognized that more than a third of individuals in industrialized societies sleep less than five to six hours a night during the week. So in a first series of studies of healthy young adults of perfectly normal weight, she began to investigate whether one week of this societally typical short sleep was enough to disrupt levels of either leptin or ghrelin or both.
If you are a participant in one of Van Cauter’s studies, it feels rather more like a one-week stay at a hotel. You will get your own room, bed, clean sheets, a television, Internet access, etc.—everything except free tea and coffee, since no caffeine is allowed. In one arm of the experiment, you will be given an eight-and-a-half-hour sleep opportunity each night for five nights, recorded with electrodes placed on your head. In the other arm of the study, you are only allowed four to five hours of sleep for five nights, also measured with electrode recordings. In both study arms, you will receive exactly the same amount and type of food, and your degree of physical activity is also held constant. Each day, your sense of hunger and food intake are monitored, as are your circulating levels of leptin and ghrelin.
Using precisely this experimental design in a group of healthy, lean participants, Van Cauter discovered that individuals were far more ravenous when sleeping four to five hours a night. This despite being given the same amount of food and being similarly acti
ve, which kept the hunger levels of these same individuals under calm control when they were getting eight or more hours of sleep. The strong rise of hunger pangs and increased reported appetite occurred rapidly, by just the second day of short sleeping.
At fault were the two characters, leptin and ghrelin. Inadequate sleep decreased concentrations of the satiety-signaling hormone leptin and increased levels of the hunger-instigating hormone ghrelin. It was a classic case of physiological double jeopardy: participants were being punished twice for the same offense of short sleeping: once by having the “I’m full” signal removed from their system, and once by gaining the “I’m still hungry” feeling being amplified. As a result, participants just didn’t feel satisfied by food when they were short sleeping.
From a metabolic perspective, the sleep-restricted participants had lost their hunger control. By limiting these individuals to what some in our society would think of as a “sufficient” amount of sleep (five hours a night), Van Cauter had caused a profound imbalance in the scales of hormonal food desire. By muting the chemical message that says “stop eating” (leptin), yet increasing the hormonal voice that shouts “please, keep eating” (ghrelin), your appetite remains unsatisfied when your sleep is anything less than plentiful, even after a kingly meal. As Van Cauter has elegantly described to me, a sleep-deprived body will cry famine in the midst of plenty.
Why We Sleep Page 19