As we age, our sleep changes and, for many, this can lead to problems.

The fact that sleep problems are common among older adults is now well established. Indeed, 67% of the 1,506 adults aged between 55 and 84 interviewed for the 2003 National Sleep Foundation Survey reported experiencing one or more symptoms of a sleep problem at least a few nights a week. For example, about one fourth reported waking up too early and being unable to get back to sleep (23%). Also, 34% of the 55 to 64 year olds and 25% of the 65 to 84 year olds reported that their sleep quality had gotten somewhat or much worse than it was 10 years ago. In all, 13% of those interviewed had already been diagnosed with a sleep disorder (insomnia, sleep apnea, or restless legs syndrome [RLS]), and 9% were treated for it.1

Many factors may interfere with optimal sleep and wakefulness in older adults. Acute or chronic illness, the side effects caused by medication, mental health conditions, primary sleep disorders, and abrupt, uncontrollable changes in both social and personal life may all contribute to the development of sleep difficulties in the elderly.

The prevalence of primary sleep disorders (RLS, periodic leg movements during sleep, sleep apnea, and some parasomnias) starts to increase significantly in the middle years of life (40 to 60 years old). In 1994, Lavigne and Montplaisir2 demonstrated that the prevalence of RLS-related symptoms increases linearly with age, and they are reported by 18% to 23% of Canadians aged 60 and over. Others3 have found that 20% of women and 28% of men in a community-dwelling population had at least five apneic events per hour of sleep, which was significantly correlated with daytime sleepiness. REM behavioral disorder (RBD) is a parasomnia in which patients manifest undesirable and often violent behaviors during REM sleep. These behavioral manifestations result from the disappearance of the paralysis that generally accompanies REM sleep, and are related to the patient’s dreamscape. RBD occurs primarily after age 50, especially in men with a ratio of seven men for each woman with the disorder.4 The prevalence of RBD in the general population is estimated to be approximately 0.5%.5

The interrelationships between health and sleep are of great importance for the elderly. In fact, the prevalence and the incidence of insomnia after age 65 in the general population are dramatically lower in the healthiest individuals compared to those with coexisting medical and psychiatric diseases.6,7 Cardiovascular diseases, pulmonary diseases, chronic pain conditions, and dementia are all associated with morning fatigue and/or daytime sleepiness while also being a cause of poor nocturnal sleep quality.8 Psychiatric disorders also have acute symptoms that might contribute to sleep difficulties. For example, the association between major depression and insomnia is now well established.9 Finally, elderly individuals frequently take medication. Advanced age and frailty may increase their susceptibility to the adverse effects of medication.10,11

Sleep and Aging
Sleep changes occur from the cradle to the grave. Important modifications of the sleep-wake cycle also occur in “optimal aging” (in individuals free of any medical or psychiatric condition and who do not present specific sleep disorders). Compared to young subjects, elderly individuals show:

  • Earlier bedtimes and wake-up times12
  • More sleep during the day (naps)13
  • Less sleep during the night13,14
  • More awakenings during their sleep episode, especially in the second half of the night13,14
  • Lighter sleep; more stages 1 and 2 and less slow-wave sleep (SWS)14

The effects of aging on the sleep-wake cycle are gradual. Many sleep characteristics may change acutely and as early as in the 30s, while others will change only gradually and later on during a person’s life span. Subjective sleep complaints begin to increase significantly in the middle years of life. Almost all sleep parameters will show significant changes associated with the effects of aging between the ages of 20 and 60.

The results of our studies, focusing on this population, indicate that increasing age is associated with earlier bedtimes and wake times,15 less time asleep, more frequent awakenings of longer duration during sleep, less SWS, and higher percentages of the lighter stages of sleep.16 Furthermore, the quantitative evaluation of sleep EEG changes shows a consistent decrease in slow wave activity (SWA) during non-REM.17,18

It is important to note that members of the middle-aged population may be particularly at risk of suffering from the sleep disturbances that they are experiencing. Indeed, their multiple social, professional, and family responsibilities not only limit the strategies they may adopt to alleviate their sleep and alertness problems (fewer opportunities to nap and change sleep-wake schedules), but also aggravate the consequences of such problems (lower productivity level, higher risk for accidents, and irritability).

Why does sleep change with aging?
The mechanisms underlying these age-related sleep modifications are still unknown. According to actual models, it is the interaction between homeostatic and circadian processes that regulates the sleep-wake cycle. The homeostatic process represents the accumulation of sleep pressure with increasing time awake and its dissipation during a sleep episode. Thus, the longer an individual has been awake, the deeper his or her sleep (more SWS and SWA) will be, and vice versa. The circadian process is controlled by our biological clock, promoting wakefulness at certain times and sleep at others across the 24-hour day. People easily experience the influence of their biological clock when they start to perform night-work. Indeed, when their biological clock is not yet adjusted, they are working when it promotes sleep and sleeping when it promotes wakefulness. This situation generates important sleep and vigilance complaints. Precise interaction between the homeostatic and circadian processes is necessary in order to ensure optimal quality of both sleep and vigilance. Therefore, age-related sleep changes may be linked to modifications of the homeostatic and circadian processes individually, or of their interaction.

A number of hypotheses have been proposed to explain the sleep-wake modifications that occur with aging. These hypotheses include, among others:

  • A phase advance in the biological clock or a decrease in the strength of its signal;
  • An increase in the vulnerability of sleep when the biological clock promotes wakefulness;
  • Alterations to the homeostatic process controlling sleep intensity;
  • Higher rigidity of the biological clock to adapt after jet lag or shift work;
  • A reduction in the capacity of the biological clock to respond to its synchronizers (light).

Of course, these hypotheses are not mutually exclusive and more than one of these processes may be responsible for the age-related deterioration of the sleep-wake cycle. Studies are now testing many of these hypotheses. For example, the phase advance hypothesis has been able to predict age-related changes in the timing of bedtimes and wake times. According to this hypothesis, the phase advance of the biological clock would produce an earlier timing of the episode of high sleep propensity in the evening (this makes older people go to sleep earlier) and an earlier circadian wake signal in the morning (this makes older people wake up earlier). Although many studies have demonstrated a phase advance of the biological clock signal with aging, the underlying mechanisms have yet to be clarified.

Other authors have suggested that the sleep of older subjects may be particularly vulnerable at times when the biological clock is promoting wakefulness. The increasing number of complaints among elderly people concerning shift work and jet lag subjectively confirms this idea. Moreover, some objective studies in the laboratory also confirm that elderly and middle-aged subjects have more problems maintaining sleep when the biological clock sends a strong wake signal, as it does during daytime.19,20

The results of sleep deprivation studies in older subjects have indicated that, despite an increase in SWS during the recuperative sleep episode, the rebound of SWS may be less intense than in young subjects.21,22 These results suggest that older individuals’ sleep shows a reduced ability to respond to extended wakefulness. This may represent an alteration of homeostatic sleep regulation.

In conclusion, the mechanisms that spur the major age-related decrease in sleep consolidation, the marked diminution of SWS, and the lower tolerance of their sleep to a timing at which the biological clock promotes wakefulness are still unknown. More research is needed to confirm or rule out propositions. Finally, future animal and human research must focus on the underlying mechanisms in order to define new targets for prevention and intervention.

Are All Age-related changes bad?
For many healthy older individuals, age-related sleep modifications may go unnoticed and may not induce sleep or vigilance complaints. This suggests that aging may be associated with a reduction in the need for sleep. Stated differently, less sleep would be necessary to ensure optimal vigilance during the day as the person increases in age; however, the age-related alterations in the sleep-wake cycle may have negative effects on daily functioning. To test this hypothesis, studies must focus on the consequences of age-related modifications on all physical and psychological functions in which sleep plays a significant role (vigilance, cognition, brain plasticity, mood regulation, hormonal regulation, and immune system). A better understanding of the effects of age-related changes in sleep parameters is important not only for a more solid comprehension of the interrelation itself, but also in terms of treatment planning, implementation, and evaluation. A multidisciplinary collaboration between experts in the fields of sleep, psychology, neuropsychology, psychiatry, endocrinology, and neurology is necessary to achieve this goal.

Contributing factors
Many variables have been proposed as potentially significant contributors to the increase in vulnerability of the aging sleep-wake system to disturbances. These include stimulant consumption, menopause, and stress.

Caffeine is the most widely used central nervous system stimulant in North America and older individuals consume it on a regular basis. Caffeine is known to mimic some of the effects of aging on sleep. It decreases deep sleep and increases wakefulness across the night. It also lengthens sleep latency. Thus, it is quite possible that caffeine may lead to a more important disruption of sleep in older subjects compared to the young. Caffeine should then be consumed with moderation.

Very few studies have evaluated the effects of the menopausal state on objective sleep parameters in the laboratory, and the ones that have done so show inconsistent results. One study reported that about half of menopausal women complain about their sleep.23 These women are twice as inclined as premenopausal women to use sleeping pills, as they sleep less and suffer more often from insomnia symptoms; however, not every woman will experience the detrimental effects of menopause on sleep.24 Evidently, more studies are needed to define and understand the factors associated with sleep quality in menopause. The importance of vasomotor symptoms, such as night sweats and hot flashes, remains undetermined, but these symptoms also seem to play a role in menopausal women’s subjective complaints. The effects of hormonal therapy on polysomnographic sleep parameters will also require further clarification.

Finally, some researchers have proposed that aging can significantly increase the vulnerability of the sleep-wake cycle to the effects of stress. They have shown, for example, that a similar stress experience may have a more negative impact on the sleep of older subjects than that of the young.25

What Else needs to be done?
Fundamental and clinical research on sleep in aging has grown rapidly over the past decades, with important progress in the development of descriptive studies that characterize age-related sleep modifications over the life span; however, research on sleep in aging still faces important challenges. First, a better understanding of the mechanisms underlying age-related sleep modifications is necessary and requires a greater investment in research time and energy. This line of inquiry should involve fundamental human and animal research. Second, it is important to identify factors that may increase the vulnerability of the aging sleep-wake system to disturbances. These factors might include gender, menopause, stress, stimulant consumption, and psychiatric disorders. In addition, the consequences of age-related modifications to the sleep-wake cycle demand more thorough evaluation. These should include not only vigilance but also all functions to which evidence suggests that sleep makes a significant contribution. Finally, the development of preventive and therapeutic strategies to help the aging population cope with their sleep-wake cycle difficulties ought to be a research priority.

Caroline Drapeau, MPs, is a doctoral candidate; Isabelle Hamel-Hébert, BSc, is a master’s candidate; and Julie Carrier, PhD, is associate professor, all at the Department of Psychology, Université de Montreal, Montreal, Quebec, Canada.

References
1. National Sleep Foundation. 2003 Sleep in America Poll. Available at: http://www.sleepfoundation.org. Accessed July 28, 2005.
2. Lavigne G, Montplaisir J. Restless legs syndrome and sleep bruxism: prevalence and association among Canadians. Sleep. 1994;17:739-743.
3. Ancoli-Israel S, Kripke D, Klauber MR, Mason WJ, Fell R, Kaplan O. Sleep-disordered breathing in community-dwelling elderly. Sleep. 1991;14:486-495.
4. Schenck CH, Mahowald MW. REM sleep behavior disorder: clinical, developmental, and neuroscience perspectives 16 years after its formal identification in sleep. Sleep. 2002;25:120-138.
5. Ohayon MM, Caulet M, Priest RG. Violent behavior during sleep. J Clin Psychiatry. 1997;58:369-376.
6.Foley DJ, Monjan A, Simonsick EM, Wallace RB, Blazer DG. Incidence and remission of insomnia among elderly adults: an epidemiologic study of 6,800 persons over three years. Sleep. 1999;22(suppl 2):S366-S372.
7. Vitiello MV, Moe KE, Prinz PN. Sleep complaints cosegregate with illness in older adults: clinical research informed by and informing epidemiological studies of sleep. J Psychosom Res. 2002;53:555-559.
8. Carrier J, Bliwise DL. Sleep and circadian rhythms in normal aging. In: Dans Billiard M, ed. Sleep: Physiology, Investigations and Medicine. New York: Kluwer Academic Plenum Publishers; 2003:297-332.
9. Fava M. Daytime sleepiness and insomnia as correlates of depression. J Clin Psychiatry. 2004;65:27-32.
10. Swift CG. The clinical pharmacology of aging. Br J Clin Pharmacol. 2003;56:249-253.
11. Ancoli-Israel S, Cooke JR. Prevalence and comorbidity of insomnia and effect on functioning in elderly populations. J Am Geriatr Soc. 2005;53:S264-S271.
12. Weitzman ED, Moline ML, Czeisler CA, Zimmerman JC. Chronobiology of aging: temperature, sleep-wake rhythms and entrainment. Neurobiol Aging. 1982;3:299-309.
13. Feinberg I. Changes in sleep cycle patterns with age. J Psychiatr Res. 1974;10:283-306.
14. Redline S, Kirchner HL, Quan SF, Gottlieb DJ, Kapur V, Newman A. The effects of age, sex, ethnicity, and sleep-disordered breathing on sleep architecture, Arch Intern Med. 2004;164:406-418.
15. Carrier J, Paquet J, Morettini J, Touchette E. Phase advance of sleep and temperature circadian rhythms in the middle years of life in humans. Neuroscientific Letters. 2002;320:1-4
16. Carrier J, Monk TH, Buysse DJ, Kupfer DJ. Sleep and morningness-eveningness in the “middle” years of life (20-59y). J Sleep Res. 1997;6:230-237.
17. Carrier J, Land S, Buysse DJ, Kupfer DJ, Monk TH. The effects of age and gender on sleep EEG power spectral density in the middle years of life (ages 20-60 years old). Psychophysiology. 2001;38:232-242.
18. Dijk DJ, Beersma DG, Van Den Hoofdakker RJ. All night spectral analysis of EEG sleep in young adult and middle-aged male subjects. Neurobiol Aging. 1989;10:677-682.
19. Dijk DJ, Duffy JF, Riel E, Shanahan TL, Czeisler CA. Ageing and the circadian and homeostatic regulation of human sleep during forced desynchrony of rest, melatonin and temperature rhythms. J Physiol. 1999;516 (Pt 2):611-627.
20. Gaudreau H, Morettini J, Lavoie HB, Carrier J. Effects of a 25-h sleep deprivation on daytime sleep in the middle-aged. Neurobiol Aging. 2001;22:461-468.
21. Bonnet MH, Rosa RR. Sleep and performance in young adults and older normals and insomniacs during acute sleep loss and recovery. Biol Psychol. 1987;25:153-172.
22. Carskadon MA, Dement WC. Sleep loss in elderly volunteers. Sleep. 1985;8:207-221.
23. Ledesert B, Ringa V, Breart G. Menopause and perceived health status among the women of the French GAZEL cohort. Maturitas. 1994;20:113-120.
24. National Sleep Foundation. (1998). Women and Sleep Poll. Available at: http://www.sleepfoundation.org. Accessed July 28, 2005.
25. Vgontzas AN, Bixler EO, Wittman AM, et al. Middle-aged men show higher sensitivity of sleep to the arousing effects of corticotrophin-releasing hormone than young men: clinical implications. J Clin Endocrinol Metab. 2001;86:1489-1495.