The effect of insufficient sleep on the heart is a relatively new area of study. Research to date has linked inadequate sleep—which is defined in studies as sleeping six or fewer hours per night—to an increased risk of heart disease and stroke, as well as a lower life expectancy. Poor sleep has been associated with heightened blood pressure and other cardiovascular-disease risk factors, such as obesity.
According to the National Heart, Lung, and Blood Institute (NHLBI) at the NIH, adults of all ages need seven to eight hours of sleep every night. When you lose sleep or choose not to sleep the recommended number of hours, the NHLBI says, you accumulate sleep “debt,” which can affect your health. (See https://www.nhlbi.nih.gov/health/health-topics/topics/sdd/howmuch.)
Increasingly, Americans do not spend enough time each day sleeping.
“Typical daily sleep duration has been declining among adults in the United States for more than a generation,” write physicians in the 2006 article, “Association of Usual Sleep Duration With Hypertension: The Sleep Heart Health Study,” published in the journal, Sleep, “with median sleep duration falling from 8 hours per night in the 1950s to 7 hours per night in recent years, with more than one-third now sleeping fewer than 7 hours per night.”
Most of this reduction, say the authors, is voluntary, as people report watching TV, using the Internet, or working as reasons for not getting enough sleep. Since 2006, when their article was published, I would speculate that the average number of hours of sleep per night has declined. Distractions from sleep—texting, streaming—have only multiplied.
There are three types of studies that explore the links between sleep habits and the risk of developing cardiovascular disease and other disorders. The first is the sleep-deprivation study in which healthy research volunteers are deprived of sleep and examined for short-term physiological changes that could trigger disease. According to the Division of Sleep Medicine at Harvard Medical School, such studies have revealed many “potentially harmful effects” usually associated with “increased stress,” such as “increased blood pressure, impaired control of blood glucose, and increased inflammation.”
Cross-sectional epidemiological studies, in which large populations of subjects answer questionnaires about their sleep habits and any diseases they may have, have linked both reduced and increased (more than nine hours per night) sleep duration to hypertension, diabetes, and obesity. Cross-sectional studies have obvious drawbacks: They rely on self-reporting, which may not be accurate, and also present a chicken-and-egg dilemma: Respondents may have a disease that affects their sleep.
The most convincing type of evidence that long-term sleep habits are associated with the development of cardiovascular and other diseases, according to Harvard’s sleep medicine division, comes from longitudinal epidemiological studies. In such studies, the sleep habits and disease patterns of initially healthy individuals are tracked over time. Such studies suggest an association between long-term inadequate sleep and hypertension/heart disease, as well as diabetes and obesity. (Which begs the question whether a change in sleep patterns could reverse a disease process.)
I have not extensively researched the nexus between poor sleep and disease and lack the expertise to incisively evaluate the study reports that I have read. It seems to me that it’s difficult to account for confounding factors, such as diet and exercise. I can tell you that a 2011 European Heart Journal review of 15 medical studies involving almost 475,000 people found that “short sleepers” had a 48 percent increased risk of developing or dying from coronary heart disease in a seven to 25-year follow-up period, depending on the study. Their risk of developing or dying from a stroke during this same time was quantified as 15 percent greater than those who had adequate sleep.
I also can tell you that after broadly reviewing the available experimental data, a Harvard-based team of physicians and scientists determined that short-term sleep deprivation “altered” blood pressure, inflammation, autonomic tone, and hormones “in a direction that is recognized to contribute to the development of cardiovascular disease, most importantly, atherosclerosis.” (Janet M. Mulligan et al, “Cardiovascular, Inflammatory and Metabolic Consequences of Sleep Deprivation,” Progress in Cardiovascular Diseases 51(4): 294-302 (2009), available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403737/.)
But it’s also true that, to quote Dr. Phyllis C. Zee, a neurology professor and director of the Sleep Disorders Program at Northwestern University School of Medicine: “Lack of sleep doesn’t necessarily cause heart disease.”
Inadequate sleep, Zee says in a recent WebMD article, “really increases the risk factors for heart disease.” It does not cause it. To understand how or why this would be so, you have to understand the nature and characteristics of sleep.
Nature of Sleep
I daresay everyone knows that sleep is essential to good health and well-being. Sleep promotes optimal functioning of bodily processes and restores our alertness. It is a normal state of decreased responsiveness to external stimuli, a time of reduced activity.
Once thought to be an inactive state during which the brain literally shut down, sleep has been understood for more than 50 years to be a dynamic state during which repair, rejuvenation, and energy conservation occur. Complex humoral (bodily fluids), neurochemical, and neuronal (nerves) networks affect the “sleep-wake state.”
We humans are “programmed” by two interacting systems to sleep each night. They are 1) our internal biological clock, also known as our circadian pacemaker or rhythm; and 2) our sleep-wake homeostat. Each is referred to as a sleep “driver.”
Our clock, which is controlled by the suprachiasmatic nucleus in the hypothalamus (an important part of the brain), regulates the cycling of many of our functions every 24 hours, including when we sleep and wake. The sleep-wake homeostat regulates our need for sleep based on how long we’ve been awake. Together, these two mechanisms determine the timing of our transitions from wakefulness to sleep and sleep to wakefulness. Once asleep, our brains “turn on” characteristic patterns of electrical activity that vary as our sleep progresses through different periods.
Sleep is composed of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. NREM sleep is divided into three stages, called N1, N2, and N3; REM sleep is denoted as stage R. Each stage is recognizable by a characteristic electrical pattern on an electroencephalogram (EEG), which measures brain activity, and by the presence or absence of eye movements. I will not discuss particulars of these brain-wave patterns, except to say that in the progression from N1 to N3, the waves become slower and more synchronized, and the eyes remain still. Each stage also has a distinct physiologic regulation.
Healthy adults begin sleep with NREM sleep. According to the Harvard sleep medicine division, “The transition from wakefulness to N1 occurs seconds to minutes after the start of the slow eye movements seen when a person first begins to nod off.” N1 typically lasts just one to seven minutes. N2, which follows, generally lasts 10 to 25 minutes. N3, the third stage of NREM sleep, lasts 20 to 40 minutes and is known as “slow-wave” or “deep” sleep. During N3, it may be very difficult to awaken someone.
After the N3 stage, a series of body movements usually signals an “ascent” to lighter NREM sleep stages. A five- to 10-minute period of N2 typically precedes the initial REM sleep episode, which may last only one to five minutes. REM sleep episodes, during which most (but not all) dreaming occurs, become longer during the night.
NREM and REM sleep alternate in a cyclical fashion throughout a typical night.
Altogether, REM sleep comprises about 20 to 25 percent of total sleep in healthy adults. It is an active state during which the firing rate of most neurons throughout the brain increases, as compared with NREM sleep. Brain-activity patterns during REM sleep are more random and variable than the regular patterns seen in NREM sleep.
The first NREM-REM sleep cycle lasts between 70 and 100 minutes; the average length of later cycles is about 90 to 120 minutes. Scientists speculate that specific sequences of NREM-REM occur to optimize both physical and mental recuperation, as well as memory consolidation.
Research suggests, according to the Harvard sleep experts, that memory consolidation, a process by which a memory becomes stable, takes place only during sleep. Acquisition of information to be consolidated and recall of that information as memory occur only during wakefulness.
Physiological Changes During Sleep
During wakefulness, our body temperature, blood pressure, and levels of oxygen, carbon dioxide, and glucose in the blood remain constant, so as to enable optimal functioning. During sleep, these physiological demands are generally reduced.
It has long been known that when we sleep, our body temperature decreases by about 1 to 2 degrees F., and our blood pressure drops. One of the possible functions of sleep, say experts, is to give the heart a chance to rest from the constant demands it confronts during wakefulness. Both heart rate and blood pressure reduce during NREM sleep.
All bets are off, however, with REM sleep, when blood pressure and heart rate increase from NREM, and changes in blood flow cause erections in males and clitoris swelling in females. The reasons for these neural and physiological changes during REM sleep are not known, but may be related to nervous system activity during dreams. (Interestingly, during REM, we are temporarily paralyzed, so that we don’t act out our dreams.)
As we progress from wakefulness through the stages of non-REM sleep, our breathing rate decreases slightly and becomes regular, unlike in wakefulness, when our breathing is variable with our activities. During REM sleep, however, our respiratory pattern becomes more irregular again, and our breathing rate increases.
Among other physiological activities, our kidney function slows during sleep, and the production of urine is decreased. Sleep also induces an increase in the release of human growth hormone (HGH), which plays a critical role in human growth and development, muscle mass, and muscle strength. This increase suggests, according to experts, that cell repair and growth may be an important function of sleep.
Besides HGH, our sleeping bodies secrete other hormones that help to control appetite (our caloric demand reduces), energy metabolism—conserving it—and glucose processing. Obtaining too little sleep upsets the balance of these and other hormones. Poor sleep has been associated, for example, with increases in the secretion of insulin after a meal. Higher levels of insulin, the hormone that regulates glucose metabolism, are associated with obesity, which is a risk factor for diabetes and heart disease.
According to the Harvard Division of Sleep Medicine, numerous epidemiological studies have revealed that adults who regularly sleep less than five hours per night have a “greatly increased risk of having or developing diabetes.” Apparently, an increase in insulin resistance, when the body does not use insulin properly, is associated with insufficient sleep. (Some sleep studies focus exclusively on the links between poor sleep and obesity and diabetes.)
If you don’t get enough sleep, the nightly dip in blood pressure during NREM sleep, which constitutes most of your sleep, does not occur. Your heart is not de-stressing. It does not get the rest it needs.
A lack of sleep “puts your body under stress,” writes the NHLBI in its excellent lay publication, Your Guide to Healthy Sleep, “and may trigger the release of more adrenaline, cortisol, and other stress hormones during the day. These hormones keep your blood pressure from dipping during sleep, which increases your risk for heart disease.”
Short-term experimental sleep restriction for as little as one night has been reported to increase blood pressure in both healthy and hypertensive subjects.
According to the Sleep Heart Health Study authors (above), who conducted a community-based, prospective cohort study of the cardiovascular consequences of obstructive sleep apnea/hypopnea: “Usual sleep duration above or below the median of 7 to less than 8 hours per night is associated with an increased prevalence of hypertension, particularly at the extreme of less than 6 hours per night.”
(The Sleep Heart Health Study, funded in part by the NHLBI, involved nearly 6,000 subjects who had sleep disorders. The primary aim of the research was not to analyze sleep duration and hypertension, but to study the relationship between hypertension and sleep apnea.)
Lack of sleep is also thought to contribute to inflammation, and, if chronic, to cardiovascular risk.
Studies have found that people who habitually or repeatedly do not get enough sleep have higher than normal blood levels of C-reactive protein (CRP), which is a major marker of inflammation. CRP has been shown to be predictive of cardiovascular morbidity. Researchers have suggested that sleep loss may be one of the ways that inflammatory processes are activated or triggered.
Dr. Zee, the chief of neurology/sleep medicine at Northwestern medical school, neatly summarizes some key basics to keep in mind when considering how poor sleep may affect our health:
*Good-quality sleep decreases the work of your heart, as blood pressure and heart rate go down at night.
*People who are sleep-deprived show less variability in their heart rate, meaning that instead of fluctuating normally, the heart rate usually stays elevated. (This is during wakefulness.)
*Shortened sleep can increase C-reactive protein, which is released with stress and inflammation. High CRP is a risk factor for atherosclerosis and heart disease.
*Shortened sleep interferes with appetite regulation. You may end up eating more and gaining weight or eating foods that are less healthy for your heart.
*Lack of sleep can increase insulin resistance, which is a risk factor for the development of type 2 diabetes and heart disease.
To access the NHLBI’s booklet, “Your Guide to Healthy Sleep,” which was last updated in 2011, click on https://www.nhlbi.nih.gov/files/docs/public/sleep/healthy_sleep.pdf.
Next up: My last blog in National Heart Month.