Sleep: Impacts on Older Adult Health
A good night’s rest is key to wellness.
Sleep complaints are common among older adults; more than one-half report experiencing some kind of sleep difficulty, such as falling asleep, staying asleep, or not feeling rested most or all of the time.1 Up to 70% report at least one symptom of insomnia, such as difficulty falling asleep, difficulty staying asleep, and waking early in the morning.2 Poor sleep, in turn, is associated significantly with various comorbidities among older adults, including cognitive decline, diabetes, falls, and mood disorders. Increasing research suggests that sleep may play a causal role in each of these areas and that sleep may also be an important target for treating and preventing many such chronic conditions.
How Sleep Changes With Age
Older adults also experience different kinds of sleep than their younger counterparts. For example, they typically experience less slow wave sleep, spend more time in lighter non–rapid eye movement (NREM) stages of sleep, and have shorter and fewer NREM-REM sleep cycles.3 Possibly because of these changes in nighttime sleep, 1 in 4 older adults also experiences sleepiness during the day sufficient to impair normal daily activities, and older adults unsurprisingly are more prone to napping during the day.4
Some research suggests, counterintuitively, that sleep is not significantly associated with cognitive function in older adults. A 2015 review found little evidence of an association between either short sleep or sleep fragmentation and cognitive measures in adults older than 60 years.6 The same review noted that in several cross-sectional studies, increased nighttime awakenings are correlated with improved cognitive performance among older adults.7,8 A separate review of experimental studies on sleep deprivation found that although sleep deprivation results in poorer cognitive performance in younger adults, the effect is less pronounced or nonexistent among older adults.5
By contrast, a 2016 meta-analysis and review found that there’s a significant association between sleep and cognition in older adults. Specifically, both short and long sleep duration were associated with poorer multiple-domain performance, executive function, verbal memory, and working memory performance.9 Furthermore, while much of the research on sleep and cognition in older adults relies on subjective reports of sleep, several large studies relying on objective measurements showed an association between poor sleep and cognitive function in aging populations.10-13
All research on sleep and cognition discussed so far has been cross-sectional, comparing sleep and cognition when both variables were measured at a single point in time in older age. But there’s another question to consider regarding sleep and cognition—namely, do sleep patterns earlier in life influence cognition in older age? An array of longitudinal studies suggests the answer is yes: Poor sleep in middle age predicts cognitive decline years into the future.
In one study of adults aged 45–69 years, participants’ sleep duration was assessed on two different occasions five years apart. On the latter occasion, their cognitive function was also measured via six different cognition tests. Those who reported an adverse change in sleep length between the first assessment and the second assessment (that is, a decrease from six, seven, or eight hours of sleep or an increase from seven or eight hours of sleep) had worse performance on most of the cognition tests.14 In another study of middle-aged adults, self-reported sleep length and quality predicted cognitive decline as measured in a telephone interview 22 years later.15 Thus, there’s reason to believe that sleep disturbances in middle-age promote cognitive impairments years later.6
Alzheimer’s Disease and Other Dementias
The accumulation of amyloid-β (Aβ) and its subsequent formation into amyloid plaques is a hallmark of AD. According to Bryce Mander, PhD, an assistant professor of psychiatry and human behavior in the School of Medicine at the University of California, Irvine, classic rodent models of AD have shown that amyloid pathology in interstitial fluid in the brain follows a circadian rhythm. “It rises when they’re awake, and it goes down when they’re asleep,” Mander says. “If you sleep-deprive the rodents, you increase the plaques in the brain. This was one of the first pieces of evidence that actively disrupting or reducing sleep was actually increasing amyloid plaque production.”
In humans, multiple cross-sectional studies have now linked poor sleep with greater Aβ burden.21,22 Although cross-sectional research cannot speak to causality, several experimental studies do suggest the link is causal. One study of middle-aged men found that after a night of normal sleep, Aβ burden in cerebrospinal fluid decreased by 6%. However, after a night of sleep deprivation, no such reduction occurred.23 Similarly, a second small study of healthy controls found that just one night of sleep deprivation produced a significant increase in Aβ burden relative to baseline measurements after a night of normal sleep.24
Although it’s clear that poor sleep increases risk of AD, the precise mechanisms are less clear. Two have been proposed, according to Mander. The first is that there’s a fundamental difference between how neurons fire in wakefulness vs sleep that increases amyloid production. “Neurons are much more metabolically active, use much more oxygen, and so build up more oxidative stress in wakefulness relative to non-REM sleep—and those are all mechanisms that are linked to Aβ production,” Mander says. The other proposed mechanism relates to the glymphatic system, which is the mechanism the brain uses to deal with waste. “Essentially, the glymphatic system power-washes the brain, flushing cerebrospinal fluid from the brain to wash away all the external toxins and proteins that may damage neurons,” Mander says. This process occurs preferentially during NREM sleep; thus, the theory is that if NREM sleep is disrupted, it disrupts the brain’s ability to flush toxins. Either way, however, what appears clear is that poor sleep likely plays a causal role in AD and that addressing sleep may in turn may be key to preventing or delaying AD.
Experimental research in the general population has shown that restricting and disrupting sleep both produce impairments in markers of cardiometabolic health. Specifically, acute short-term sleep restriction raises blood pressure,25,26 induces insulin resistance,27-30 impairs glucose tolerance,31 prompts inflammation,32,33 and leads to weight gain.34
Although research on lipids is not entirely inconsistent,35 some studies suggest that sleep affects lipid levels. One study involving both an experimental and observational component found that restricting sleep increased expression of genes in inflammatory pathways and decreased expression of genes relating to cholesterol transport. Short sleep was also associated with lower HDL, an important risk factor for cardiovascular disease. Such research suggests that sleep deprivation may influence cardiovascular health by modifying inflammatory and cholesterol pathways all the way down at the level of gene expression.36
These experimental studies were short term and were conducted in the general adult population, not among older adults. However, observational studies among older adults suggest long-term associations.
For instance, multiple studies have found that both short and long sleep duration are associated with poorer glycemic control and with elevated risk of prediabetes and incident type 2 diabetes mellitus.37-41 Similarly, multiple studies have found a significant association between insufficient sleep duration and obesity.42,43 However, the research on obesity has not always been consistent, and a 2016 review concluded that the relationship between sleep duration and obesity, if one exists, appears stronger in younger adults than in older adults.44 A factor that may explain some of the inconsistency is that many studies on sleep and obesity have relied on self-report. Older adults experience high rates of sleep disorders, which may cause a misperception of time spent sleeping and misreporting on self-reports. Indeed, at least one cross-sectional study found no relationship between sleep and obesity in older adults when relying on self-reports, but did find a significant association when using actigraphy to measure sleep objectively. Specifically, short sleep duration, long sleep duration, and sleep fragmentation were all associated with increased obesity risk.45
In the general adult population, sleep duration has been linked to cardiovascular disease46-49 and to hypertension, an important risk factor for cardiovascular disease.50-52 However, the link between hypertension and sleep duration appears to weaken with age. A number of studies have found that the association is either reduced or nonexistent in older adults—possibly because other risk factors for hypertension may obscure any association.51,53-56 With cardiovascular disease, by contrast, there’s some evidence that the association with sleep remains significant with age.57-59 A cohort study of 400,000 Taiwanese adults found that extreme sleep duration (both short and long) predicted substantially increased risk of death from coronary heart disease, and that the associations were stronger in older vs younger adults.60
As for mechanisms, the autonomic nervous system is one suspected player, according to Knutson. “What we think is happening is that impaired sleep or insufficient sleep is eliciting a stress response, and we know chronic stress elevation is associated with cardiometabolic risk.” The endocrine system is likely also involved, Knutson adds. Sleep deprivation and impairment could prompt changes in the regulation and production of, say, appetite hormones, leading in turn to increased food intake, obesity, and then cardiometabolic disorders. “The production of a lot of hormones seem to change in short-term experimental studies in response to sleep restriction and impairment,” Knutson says.
There remains debate about whether sleep problems themselves increase the risk of fall or whether fall risk is increased by the medications used to treat sleep difficulties. Most studies have not examined sleep issues independently from medication use. However, in one prospective study, self-reported short sleep duration of five hours or less per night at baseline was associated with increased odds of having two or more falls in the subsequent year, independent of benzodiazepine use.68
Mood and Suicide
The relationship between sleep and depression appears to be bidirectional. A 2017 meta-analysis found that self-reported sleep disturbances increased the risk of the development, worsening, and reoccurrence of depression. But the reverse also held true: Participants with depression were more likely to experience both onset and worsening of sleep disturbances.71
Poor sleep is likewise associated with an elevated risk of suicide. In a 10-year case-control observational study, older adults with self-reported poor sleep quality were 1.4 times more likely to die by suicide than were participants who slept well. This association remained even after adjusting for depressive symptoms.72
According to Katie L. Stone, PhD, senior scientist at the California Pacific Medical Center Research Institute and an adjunct professor in the department of epidemiology and biostatistics at the University of California, San Francisco, the mechanisms by which sleep may affect mood may involve both direct and indirect pathways. While biological factors could be involved, the fact that sleep influences other aspects of health could also play a role. “Anecdotally, if you sleep poorly and it impacts other aspects of your quality of life, of your health in general, that could negatively impact mood. It could be just one aspect of an overall general lack of well-being,” Stone says. The bidirectional nature of mood disorders and sleep problems is also important to bear in mind, she adds. “If you’re sleeping poorly and it impacts mood, then that also interferes with your ability to sleep. It becomes a cyclical pattern of one contributing to the other.”
Implications for Clinicians
The issue of treatment is still complex, unfortunately. “We do have very good, well-established, evidence-based treatments for disorders such as insomnia and sleep-disordered breathing,” Dzierzewski says. However, it’s not always clear what effect sleep treatments will have on other health conditions, such as cognitive impairment. Some experimental research has explored this question, but with disappointing results.73 “The vast majority of studies of sleep treatments have not shown the widespread improvements in cognition that we would like to have seen,” Dzierzewski says.
Similarly, the efficacy of sleep interventions for improving depression is not yet clear. “We don’t know the extent to which some of those changes that occur are reversible,” Stone says. In the general adult population, there is some early evidence that sleep interventions improve mood.74 But some research suggests that such interventions may not have as much impact among older adults. For example, in one study, a brief behavioral treatment for insomnia improved multiple insomnia symptoms (including sleep onset latency, wake after sleep onset, total sleep time, sleep efficiency, and sleep quality ratings) as measured by actigraphy. However, the treatment did not improve symptoms of depression over the reductions seen in controls.75
According to Dzierzewski, some of the lackluster results so far, at least with respect to cognition, may simply be due to the short duration of the studies. “If someone has been sleeping poorly for a decade, improvement of sleep over four to six weeks may not be enough time to show improvements in cognition,” he says. Both Dzierzewski and Stone agree that better studies are needed to show the potential influence of sleep interventions on comorbid conditions.
But regardless of whether sleep interventions improve cognition or influence depression, Dzierzewski believes sleep problems should be treated—preferably using cognitive behavioral therapy rather than medication. “We don’t have definitive answers about whether intervening on sleep could reduce the risk or thwart the progression of AD or other dementias,” Dzierzewski says. “However, you’re not going to harm someone by treating sleep problems, and improving their sleep would at a minimum improve quality of life.”
— Jamie Santa Cruz is a health and medical journalist based in Parker, Colorado.
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