15.1: Physical Aging in Late Adulthood
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Learning Objectives
By the end of this section, you will be able to:
- Understand reasons behind variation in life expectancy
- Explain the major theories about the physical aging process
- Describe the physical changes that occur in late adulthood
- Identify key changes in the brain during late adulthood
Myra has reached a significant milestone, her ninety-first birthday. She celebrated it with her children, who are in their late sixties, her middle-aged grandchildren, her great-grandchildren (who range from adolescents to emerging adults), and one great-great-grandchild (a particularly rambunctious toddler). Myra’s family is a snapshot of most of the stages of the human lifespan. As her loved ones revisit over family photos and videos, they smile and joke about the physical changes they see in each other today compared to the images from twenty or forty or sixty years ago.
This section on physical aging in late adulthood covers the ways the many different systems in our bodies physically change with time, including muscular, skeletal, sensory, nervous, respiratory, and cardiovascular systems. Research on life expectancy as well as theories about how and why people experience changes in later life help us to understand these processes.
Life Expectancy
Human beings know that life does not last forever (Figure 15.2). Having passed through infancy, childhood, adolescence, plus early, emerging and middle adulthood, everyone will experience late adulthood with declines in physical ability and health, eventually resulting in death. These changes may sound stark, but there are many reasons for optimism.
Research studying human longevity or life expectancy —the average age to which members of a species or subpopulation within a species will live—has revealed consistent positive trends over a long period of time. In fact, average human life expectancy has been steadily increasing worldwide for the past 100 years, from 34.1 years in 1913 to 71.0 years today (Dattani et al., 2023). This dramatic jump is likely due to decreases in infant mortality, improved living conditions, improvements in both quality of and access to health care, preventive measures such as vaccinations, and improved knowledge of health and nutrition. The gap in life expectancy between wealthier regions, which have more resources and more access to health care, and poorer areas of the world has also decreased over time, although there is still variability. Australia/Oceania has the highest life expectancy of 79.4 years, and Africa has the lowest of 61.7 years (Dattani et al., 2023). 1
In the United States, average life expectancy is around seventy-nine years, and women live six years longer than men on average. This tendency for women to live longer than men is also observed globally. A February 2020 report from the U.S. Census Bureau projected that life expectancy will likely continue to increase for the next forty years, surpassing eighty-five years by the year 2060 (Medina et al., 2020) (Figure 15.3). However, while projections are optimistic, future improvements in life expectancy are not guaranteed, and a variety of factors could influence them. For example, the COVID-19 pandemic was responsible for a global decline in life expectancy, ranging from 1 to 2.5 years (Arias et al., 2022; Dattani et al., 2023). Rising rates of obesity are also associated with lowered life expectancy in both developed and developing nations (Bansal & Jin, 2023). 2
Researchers also find variations in life expectancy within regions and populations in the same country. For example, in the United States, the highest-income individuals tend to live more than fourteen years longer than the lowest-income individuals (Chetty et al., 2016), and differences based on race and ethnicity are observed. Socioeconomic status accounts for most of the observed racial and ethnic differences in longevity (For the Health ABC Study, 2012). Group differences in financial stability, housing and neighborhood factors, education, community support and safety, health insurance, and access to healthy food and high-quality health care all likely contribute (Kaiser Family Foundation, 2023).
Some trends in the data are more difficult to interpret, however. In the United States, while Black residents have the lowest life expectancy at birth, this gap tends to narrow over the lifespan. After surviving to age eighty years, Black Americans tend to live longer than White Americans. This suggests that although Black Americans are disadvantaged in terms of life expectancy for much of the lifespan, those who reach advanced age may be more resilient than most. Hispanic Americans, in contrast, tend to have longer life expectancies across the entire life span (Arias & Xu, 2020). Understanding these group differences requires analyzing more factors than just socioeconomic status, such as lifestyle differences and genetic risk. National research on people of Asian and American Indian/Alaska Native heritage has only begun being collected in the last few years, with preliminary data showing the highest life expectancy for Asian Americans and the lowest for AI/AN (Arias et al., 2022).
Types and Theories of Aging
Researchers have identified different types of aging based on whether the process is typical or accelerated by disease or environmental influences. The most fundamental type of aging is primary aging , the natural process that has not been accelerated or worsened as a result of disease. Among its characteristics are subtle declines in processing speed and working memory and weakening of the skeletal and muscular systems (Birren & Cunningham, 1985; Othman et al., 2022).
Interventions in primary aging would slow the aging process, but little progress to achieve this has been made. Most interventions have instead focused on preventive measures to improve health, allowing individuals to remain in primary aging while delaying issues that would lead to secondary or tertiary aging (Barnes et al., 2021; Cartee et al., 2016; Cornelissen & Otsuka, 2017).
Next, secondary aging is accelerated and worsened by disease processes, lifestyle choices, or environmental factors (Birren & Cunningham, 1985; Othman et al., 2022). Rapid cognitive decline as a result of any form of dementia is an example of secondary aging, as are health problems resulting from a poor diet, a sedentary lifestyle, exposure to pollutants, and inadequate access to health care and other resources. This type of aging has been the largest focus of interventional efforts, including medical treatments to slow or reverse disease processes, lifestyle interventions to improve health, and social programs such as Medicaid/Medicare to open access to health-care resources.
Finally, tertiary aging describes the more rapid and general declines that may occur in the months and years prior to death (Birren & Cunningham, 1985; Othman et al., 2022). Examples include loss of mobility and terminal decline , the accelerated and nonnormative declines in cognitive ability that can occur one to five years before death (Hülür et al., 2016; Wilson et al., 2020).
Theories of aging are researched and refined based on studies in genetics, biochemistry, and human and animal studies. These theories are continually evolving, and do not paint a conclusive, universal picture. Many researchers recognize that causes of ages may vary and combine in the overall process of getting older and the development of age-related and other conditions. For example, the free radical theory, described below, may explain the development of certain conditions, but not others; it may be a definite cause of aging, but not a universal cause for all aging.
Hormonal Stress Theory
Some theories and research on aging focus on the diseases and health problems that become more common in later years. One such theory, the hormonal stress theory of aging (also called neuroendocrine theory) (Sapolsky, 1992), proposes that as people get older, stress hormones such as cortisol tend to stay elevated longer after a stressful response than they do at younger ages (Figure 15.4). These hormones have been positively correlated with hypertension, diabetes, cognitive decline, and cardiovascular disease (Novais et al., 2017; Thayer et al., 2021; Yiallouris et al., 2019). It’s therefore plausible that age-related increases in exposure to stress hormones could contribute to many of the health problems typically associated with age.
While stress hormones have short-term benefits, such as preparing the body for fight-or flight responses, research has shown that chronic exposure can have a direct negative effect on the health of many bodily systems. For example, cortisol alone has been linked to a variety of health issues, including depression, obesity, fatigue, cardiovascular health, and inflammation. These hormones may also lead to unhealthy behavioral responses, such as losing sleep or overeating during stressful times (O’Connor et al., 2021). Having a history of adverse childhood experiences is also associated with increased risk of negative health outcomes in adulthood, including cardiovascular disease, dementia, and depression (Dagnino et al., 2020; Godoy et al., 2021; Merrick et al., 2019; Tani et al., 2020).
Free Radical Theory
The free radical theory focuses on free radicals, unstable oxygen molecules that are a by-product of metabolizing the food we eat. Because they try to bond with other atoms or molecules to become stable, free radicals can cause small amounts of physical damage to tissues or cells as they attempt to stabilize (Ziada et al., 2020).
The free radical theory suggests that this damage accumulates as people age, eventually resulting in many of the health problems associated with aging. Some believe we may be able to minimize free radical damage by increasing the intake of antioxidants, substances naturally produced in the body and also common in many fruits and vegetables. Although some research supports the free radical theory, particularly with regard to specific conditions like cancer and heart disease, other studies have contradicted it; research on antioxidants so far is less conclusive (Aversa et al., 2016; Jomova et al., 2023; Ziada et al., 2020).
Cellular Clock Theory
The cellular clock theory suggests that cells can divide to reproduce themselves only a limited number of times. As they reach this number, the body is no longer able to replace old or damaged cells with new ones, theoretically resulting in many of the diseases and declines associated with aging. This idea was first developed by Leonard Hayflick, who discovered that cells could typically divide around forty to sixty times before cell division stops, a constraint sometimes referred to as “the Hayflick limit .” Hayflick suggested that some mechanism in the cell operated as a clock that eventually stopped future divisions (Hayflick, 1977). The idea has led many researchers to conclude that, unless lifespan extending interventions are developed, the maximum human lifespan is around 122 years (Blagosklonny, 2021).
What sort of mechanism would act as such a clock? Eventually, a potential answer has been found in telomeres. A telomere is the strand of DNA on the tip of each chromosome. Telomeres protect DNA, somewhat like the ends on shoelaces that keep them from unraveling. However, telomeres become shorter each time a cell divides, eventually becoming too short to serve their protective role, so the cell’s ability to divide ends (Shay & Wright, 2000).
One compelling bit of evidence supporting the cellular clock theory exists in a rare genetic condition called progeria , affecting around one in four million individuals (Figure 15.5). Progeria causes young children to develop many health problems and features typically associated with age, such as hair loss, joint problems, heart problems, fatigue, and shortness of breath. The skin and facial features also resemble those of older individuals, and the life expectancy of affected individuals is typically twelve to thirteen years (Hennekam, 2006). One of the characteristics of this condition is shorter-than-typical telomeres (Allsopp et al., 1992; Decker et al., 2009), providing strong evidence that telomeres play a role in the normal physical aging process.
Wear and Tear Theory
Another theory takes a more global and environmental look at physical aging. The wear and tear theory suggests that the use of our bodies results in unrepaired damage that accumulates over time, resulting in aging. However, the idea does not account for the body’s ability to repair and fix damage throughout life (Lipsky & King, 2015), and research does not provide strong support for this theory. In fact, more active humans (and other species) generally tend to be healthier and live longer, suggesting that the more we use our bodies, the longer they last (Mitteldorf, 2010; Sattaur et al., 2020).
Still, some research has suggested that although wear and tear may not explain the aging process overall, it could explain some age-related experiences. For example, athletes who engage in intense levels of activity might be at greater risk for joint problems later in life (Davies et al., 2019). Thus, it’s plausible that joint problems in later life could at least partly be predicted by extreme use and damage, consistent with the wear and tear theory.
Genetic Variability
Other research has focused on the idea that genes may play a role in physical and biological aging ([link]Figure 15_01_Age70[/link]). Part of this idea is based on knowledge about diseases that have a genetic component, such as breast cancer, coronary artery disease, and Huntingon’s disease. Inheriting a genetic tendency for one of these conditions can affect a person’s life expectancy and how well they maintain functioning with age. However, many research studies suggest that just the longevity of close relatives can be predictive of your own life expectancy. One such study demonstrated, in a very large sample of over 20,000 individuals, that having close relatives who survived to the top tenth percentile in longevity was strongly associated with living longer. This relationship did not exist for relatives who were not genetically related, such as spouses and in-laws, suggesting the relationship is largely genetic and not due to shared environments and lifestyles (van den Berg et al., 2019). Some evidence exists that variations in several specific genes, such as the APOE gene, are associated with longevity (MedlinePlus, 2022). Table 15.1 summarizes possible causes of biological aging.
| Possible Cause | Description | Overview |
|---|---|---|
| Hormonal stress | Levels of hormones such as cortisol stay elevated longer with increasing age, resulting in greater exposure as we get older. | This theory identifies factors that contribute to life-threatening conditions such as heart failure in later life. |
| Free radicals | Unstable molecules called free radicals cause damage that accumulates over the lifespan, resulting in many problems associated with aging. | Some research suggests that free radical damage could be a factor in some age-related declines. |
| Cellular clock | Cells are limited in their ability to divide due to shrinkage of protective telomeres over time. When they can no longer replace themselves, age-related declines result. | This theory has a great deal of support, including conditions such as progeria, in which short telomeres at birth result in a short life expectancy and the presence in childhood of many health problems typically seen in later life. |
| Wear and tear | The accumulation of unrepaired damage to the body over the lifespan results in the body eventually wearing out. | The body repairs most damage due to injury or use. The theory may, however, effectively predict late-age joint problems from extreme use and damage earlier in life. |
| Genetic variability | Certain alleles inherited from relatives may affect how long we live. | Some conditions associated with shorter life expectancy, like coronary artery disease, may be inherited. Also, there may be specific genes associated with longevity. |
Changes in the Body
So far, you’ve learned about theories attempting to understand and describe the physical aging process. The physiological changes during late adulthood affect various areas of the body. Changes in muscle and bone can affect mobility. Sensory abilities in vision and hearing may change. The appearance of skin and hair often show signs of aging, and internally, aging can affect organs like the heart and bladder, and also result in changes within the brain.
Link to Learning
Are you ageist? Take this quiz on ageism and learn more about the types of ageism and how they may impact you.
Musculoskeletal Changes and Mobility
The skeletal system is maintained by processes that create new bone tissue while removing old, maintaining bone density for most of the life span with the help of the sex hormones testosterone and estrogen . As levels of these hormones decline with age, however, so does our ability to maintain bone density (Chan & Duque, 2002; Dines & Garovic, 2024). This is especially problematic for women, who experience a large drop in estrogen following menopause (Bonnick, 2006). A condition characterized by extensive loss of bone mass and weakening of the bones, called osteoporosis , is therefore much more common in women than men. Among individuals over age sixty-five years, 27.1 percent of women have osteoporosis compared to 5.7 percent of men (Sarafrazi et al., 2021). Research suggests that the best ways to prevent osteoporosis are to eat a healthy diet with plenty of calcium, vitamin D, and protein; to exercise regularly (Figure 15.6), especially doing weight-bearing exercise; and to limit smoking and alcohol consumption (National Institute on Aging, 2022).
While osteoporosis is a loss of bone mass , sarcopenia is a loss of muscle mass that also occurs later in life. Generally, adults can expect to lose around 3 to 8 percent of muscle mass per decade after age thirty years. While this gradual decline is not very noticeable, it does accelerate after age sixty years (Volpi et al., 2004). Getting plenty of exercise including aerobic exercise and resistance training, consuming adequate amounts of protein, and maintaining adequate caloric intake have all been associated with decreasing age-related muscle loss. Research has shown that weight-training programs significantly increased strength and muscle power, even among individuals ages ninety years and older (Cadore et al., 2014). Other studies have demonstrated similar benefits for yoga, which has the added benefit of increasing flexibility (Green et al., 2019; Jeter et al., 2014). Research such as this suggests that while muscle loss is normative in later years, it is also reversible, and even the oldest individuals can gain strength and muscle with intentional efforts.
The loss of both muscle and bone mass can be a problematic combination. Weaker bones and muscles can hinder the ability to walk and increase the chance of falling. With less muscle protecting weaker bones, falls are more likely to result in fractures and other serious injuries (Colón et al., 2018). Additionally, weakened bones can actually break and cause a fall (Hamdy, 2017). An older adult may need to be inactive for many weeks while a broken bone heals, and inactivity can accelerate losses in both muscle and bone mass, making it more difficult to regain mobility after recovery. Weight-training and yoga interventions have been found to improve balance and reduce the risk of falling in addition to increasing muscle and bone mass and flexibility (Cadore et al., 2014; Green et al., 2019; Jeter et al., 2014).
Sensory Changes
Decline in visual acuity, the extent to which we can see clearly at a distance, typically begins in middle adulthood when the lens in the eye stiffens (Sjöstrand et al., 2011). As a result, many individuals who never had vision problems eventually need corrective eyewear. It is also typical to struggle to see things at close range as we age. This condition, called presbyopia , requires many middle-aged and older adults to use reading glasses.
Another eye condition that becomes common with age is the development of cataract s, cloudy areas on the typically clear lens of the eye caused by a buildup of protein. Cataracts result in blurry, less clear vision and impaired color vision, but they can be successfully treated with outpatient surgery (Figure 15.7). The condition age-related macular degeneration is characterized by blurring and potential loss of vision in the center of the field of vision as a result of damage to the macula , the central part of the retina. Peripheral vision is typically maintained. Much less common than cataracts, macular degeneration is more difficult to treat and is the leading cause of severe vision loss later in life. While there is no cure, some forms can be medically treated with injections (American Optometric Association, n.d.; Ashraf & Souka,2017; Hernández-Zimbrón et al., 2018).
Another condition common in later life, glaucoma , is typically associated with increased pressure inside the eye and resulting damage to the optic nerve, which can bring about permanent vision loss if not treated (Casson et al., 2012). This vision loss takes the form of “tunnel vision,” in which central vision is unaffected but peripheral vision is damaged (Figure 15.8). While some forms are genetic, most cases of glaucoma are difficult to predict and have been associated with environmental factors such as smoking. Generally, the risk increases considerably after age sixty years, although people with a family history of glaucoma or other risk factors can experience the disorder at much earlier ages, even in childhood (Doucette et al., 2015). Treatment typically consists of medicated eye drops and, if needed, surgery (Weinreb et al., 2014).
Another vision-related condition common in advanced age is dry eye syndrome , which occurs when eyes don’t produce enough tears. This is a primary aging change but can also be affected by hormonal changes, medications, and high blood pressure. Dry eye syndrome affects 20 percent of people over the age of eighty years (Sharma & Hindman, 2014). While it does not typically result in structural damage, it is still problematic because it has been associated with occasional blurry vision, pain, and sleep disturbances (Guo & Akpek, 2020).
Hearing also undergoes normative declines associated with age, called presbycusis . Presbycusis is not an overall decrease in the volume at which we hear sound in the environment. Instead, the ability to hear high-pitched tones is affected first (Huang & Tang, 2010). Many factors, including genetics, may play a role in its severity, but one of the most common predictors of hearing loss in older age is repeated or extreme exposure to loud noise throughout life (Huang & Tang, 2010). This type of hearing loss can also occur at younger ages when there is a lot of exposure to loud noise. A sample of seventeen-year-olds provided self-reported data about hearing issues, had objective hearing tests, and reported their music-listening behaviors with earbuds. Those who listened for longer durations and at louder volumes had more self-reported hearing problems and scored lower on hearing tests, even at their young age (Widén et al., 2017).
More recent data indicate that approximately one billion people between the ages of twelve and thirty-four years are at risk of hearing loss caused by listening to music at unsafe levels, either through devices like earbuds or at loud venues like concerts or clubs, and that this hearing loss is not only permanent but also accelerates late-life hearing loss (Dillard et al., 2022). Similar patterns are noted for people who spend a lot of time playing video games (Dillard et al., 2024). This research demonstrates not only that hearing loss can start much earlier in life but also that damage accumulates over time.
Life Hacks: Assessing and Protecting Your Hearing
As you read about the damage that listening to loud music can do to your hearing, did you find yourself thinking about your own listening habits as well as other noise exposure in your own life? If you have serious concerns about your hearing, you should be tested by a professional. Still, there are ways to get a general indication about whether you have experienced any age-related hearing loss, even at a young age.
You can find online hearing tests that play high-pitched tones of different frequencies that represent what can typically be heard by those under twenty-four, under thirty, under forty, and under fifty years of age. If you find yourself unable to hear the pitches typically heard among your age group, it could be an indication that you have experienced more age-related hearing loss than is typical for your age. If you continue on this trajectory, you may experience more hearing loss and at a younger age than most.
While this type of hearing loss is permanent, you can do things to minimize future loss, such as listening to music at lower volumes, wearing earplugs when attending loud concerts or clubs, and generally reducing your exposure to loud noise.
You can also use technology to measure your exposure to loud noises. If you have an Apple Watch, you can download the Noise App, which measures the sound levels in your environment and notifies you if it’s getting dangerously loud. The National Institute for Occupational Safety and Health Sound Level Meter App is similar, and available for iPhones. Apps for Android poducts are also available. If you have an iPhone or Apple Watch and want to participate in research that helps further understanding of noise exposure and hearing, the University of Michigan Apple Hearing Study is an interesting option where you can also learn more about your own exposure to sound and how it may be affecting your health.
Gender is also correlated with hearing loss in later life. On average, men have more hearing loss than women, a result believed to be partially related to hormonal differences and possibly even differences in the functioning of the cochlea , a snail-shaped fluid-filled chamber in the inner ear that transforms sound vibrations into electrical impulses sent to the brain for interpretation (Nolan, 2020). But this tendency varies across cultures, suggesting that it is also influenced by lifestyle and work-related differences in exposure to loud noise; men are more likely to work in noisy settings such as construction and more likely to engage in behaviors such as smoking that are associated with increased hearing loss (Cornelius et al., 2022; Jung et al., 2024; von Gablenz et al., 2020). Older adults who have avoided loud noise throughout their lives may experience only subtle declines.
Other age-related changes in the ear are not hearing related. A condition called vertigo causes dizziness or the sensation of moving when still. Vertigo is experienced in 30 percent of those sixty years of age and older (Fernández et al., 2015). It can have multiple causes, the most common being a buildup of calcium crystals in the ear canal. Treatments depend on the cause and severity and include medications and the Epley maneuver, a series of head movements intended to relocate the calcium deposits (Dommaraju & Perera, 2016).
Many issues unrelated to age, such as allergies, COVID-19, colds, and the flu, can result in short-term losses of smell and taste. Still, some age-related declines in these senses do occur, and while they’re not dangerous, they can lead to problems like reduced enjoyment of food. Older adults who take less pleasure in food may eat less and can develop unintended weight loss and malnutrition (National Institute on Aging, 2020).
Research findings about changes in the sense of touch have been inconsistent, but sensitivity to pain, temperature, and vibration does tend to decline with age (Wickremaratchi & Llewelyn, 2006). However, older adults are much more likely to report chronic or long-lasting pain as a serious problem that limits their functioning, quality of life, and social involvement. These reports are likely due to the increased prevalence of conditions, especially muscular and skeletal issues such as arthritis and sciatica, that contribute to joint, neck, and back discomfort (Domenichiello & Ramsden, 2019).
Skin and Hair Changes
Other physical changes include the aging of the skin, which becomes thinner and drier and loses elasticity and fat, making wrinkles more common. Injuries such as bruises and cuts can appear more pronounced and take longer to heal as we get older. Age spots and even skin cancer can also become more common.
Some changes are inevitable. Yet there is a great deal of diversity in the extent to which people experience age-related changes in the skin, some of which is strongly linked to environmental exposure throughout the lifespan. Skin dryness can be prevented by staying hydrated, applying moisturizers, and avoiding very dry climates, but the most influential factor in keeping your skin looking healthy and avoiding problems such as wrinkles, skin cancer, and age spots is to limit sun exposure throughout your life (Figure 15.9). This means consistently using sunscreen, wearing ultraviolet-protective clothing, and avoiding suntanning and sunburns (National Institute on Aging, 2017).
As you may guess, the two most prominent age-related changes to hair are thinning and graying. Graying is due to a loss of melanin production in the hair follicle. Both genetic factors and racial differences play a part. For example, the onset of graying typically ranges from the midthirties for White individuals to the mid-forties for Black individuals. Some environmental factors, such as sun exposure, contribute as well (Maymone et al., 2021). Hair loss is also thought to be strongly genetic. While both men and women can experience thinning hair with age, it is more common and severe among men, with 60 percent of men over age thirty years reporting hair loss . Men whose fathers and maternal grandfathers experienced hair loss are at the greatest risk. Regardless of family history, the risk of hair loss increases with age. (Chumlea et al., 2004).
Heart, Lung, and Bladder Changes
Less visually obvious are physical changes to the cardiovascular system, including stiffening and hardening of the arteries, which results in increasing rates of hypertension (high blood pressure). Plaque buildup inside the artery walls, often the product of a high-cholesterol diet, also increases with age and can limit blood flow. Problems such as these can damage and weaken the heart, potentially leading to heart failure (National Institute on Aging, 2018). In the United States, heart disease is the most common cause of death for people over age forty-five years, and the percentage of deaths from heart disease increases with age (Xu et al., 2021).
Men and women sometimes have different symptoms of heart disease; for example, women having a heart attack are more likely than men to have symptoms such as nausea and jaw pain without any chest pain (Lichtman et al., 2018), meaning that they often wait longer to get treatment and are likely to experience more heart damage as a result. Monitoring blood pressure and cholesterol, eating a healthy diet, and engaging in cardiovascular exercise are all important factors in maintaining a healthy cardiovascular system.
The efficiency of the respiratory system tends to peak around our midtwenties and then slowly declines (Sharma & Goodwin, 2006). Not noticeable for much of adulthood, these declines become more consequential in later life. For example, bone loss can make the ribs less elastic and less capable of expanding and contracting as we breathe. Combined with other changes in the lungs, this loss decreases lung capacity as we age (American Lung Association, 2023). Coughs also become weaker, limiting the ability to clear unwanted particles from the lungs (Lowery et al., 2013). The lungs are also more susceptible to infections such as the flu, COVID-19, and pneumonia, which can develop into more serious conditions in older adults due to the declining functioning of the immune system (American Lung Association, 2023).
Another physical change relates to the bladder and bladder control. Urinary incontinence can occur at any age but becomes increasingly common in later life. It is a product of urinary muscles not working appropriately due to a variety of reasons, such as weakening muscles, overactive bladder muscles, damage associated with chronic health problems, and the shifting of organs around the bladder. Incontinence can be more common among men, who may also experience inflammation or enlargement of the prostate. Medical treatment and behavioral options such as pelvic muscle/Kegel exercises are available, depending on the cause of the incontinence (National Institute on Aging, 2022).
Sleep Changes
The amount of sleep recommended and the average amount of sleep attained both decrease across the lifespan. Older adults should get about 7 to 8 hours of sleep per night (Chaput et al., 2018). Since circadian rhythms shift forward as we age, most people find themselves going to bed earlier and waking up earlier than when they were younger (Newsom & DeBanto, 2023). Chronic pain, dementia, and other health problems can bring sleeping challenges for older adults. Around half of older adults report frequent sleep problems, such as difficulty falling asleep and increased sleep disturbances after falling asleep. These problems have been positively correlated with mortality, increased risk of falls and other accidents, and declines in cognitive functioning (Crowly, 2011; Sivertsen et al., 2021).
Changes in the Brain
The brain undergoes several normative changes as we age. After the age of forty years, its volume decreases by 5 percent every ten years, a decline that may speed up after age seventy years and that seems more pronounced in men than women. While this decreasing volume likely has many contributing factors, it may be due to shrinking neurons, fewer synapses, and decreases in the volume of blood in the brain than to actual cell death (Peters, 2006; Sele et al., 2021).
The brain’s cortex , responsible for cognitive processes such as memory, problem-solving, and decision-making, is also growing thinner. Recent research suggests the process begins around the age of four years (Fjell et al., 2015), so thinning later in life continues a trend that has lasted most of the lifespan. This thinning trend may sound like a negative change, but much of it is associated with lifelong synaptic pruning, in which the brain gets rid of synapses and neurons that are no longer needed, thereby increasing its efficiency in processing information. Still, some research suggests that an accelerated thinning of the cortex can be associated with decreased cognitive ability (Fjell et al., 2015; Shaw et al., 2016).
Another factor contributing to decreasing brain volume is the loss of white matter . White matter is the inner portion of the brain, which consists of millions of axons, each covered with a fatty myelin sheath, giving a white appearance. While white matter was historically thought to be unimportant in brain function, it is now believed to allow different regions of the brain to communicate and may also play a role in learning (Fields, 2008). While the myelin on neurons continues to develop until the midtwenties, it then becomes relatively stable before starting to deteriorate after the age of forty years (Peters, 2006).
The loss of myelin may have more implications than reducing brain volume. The primary purpose of myelin on nerve cells is to insulate the axon, resulting in increases in speed and efficiency of the neuron. Research has found that the slowing of the brain in later life, seen in lower processing speed, for instance, can be accounted for by age-related declines in white matter (Kerchner et al., 2012).
Another change in the brain occurs in the hippocampi, the regions of the brain within each of the two temporal lobes that assist in the formation and retention of new memories. Structural changes occur that are associated with age-related memory declines (Yassa et al., 2011).
The brain also has mechanisms to preserve and assist its functioning despite these age-related changes. Neuroplasticity, or the brain’s ability to change in response to challenges or new experiences, typically decreases with age (Calabrese et al., 2013; Sorrells et al., 2018), and for a long time, it was thought that individuals developed only new synaptic connections, not new neurons, after birth. However, some research suggests the brain in later life is able to create new neurons, including in areas important for memory, like the hippocampus (Moreno-Jiménez et al., 2019). Some research examining neuroplasticity in older mice revealed that physical activity and exposure to an enriched environment resulted in the creation of new hippocampal neurons (Kempermann et al., 2002; Liu & Nusslock, 2018). Although these findings are specific to nonhuman animal research, they are consistent with research suggesting that older adults who live an active lifestyle with cognitive stimulation experience less cognitive decline and, in some cases, restoration of function following neurological impairment (Han et al., 2022; Stillman et al., 2020).
Other research has revealed increased functioning of the frontal lobe s in some older adults. The frontal lobes are responsible for many of our higher-level cognitive processes, such as decision-making and planning. Older adults who have increased activity in the frontal cortex tend to perform better on cognitive tasks. This increase in frontal lobe activity could thus be an example of neuroplasticity compensating for other declines in brain function (Goh & Park, 2009).
References
Allsopp, R. C., Vaziri, H., Patterson, C., Goldstein, S., Younglai, E. V., Futcher, A. B., Greider, C. W., & Harley, C. B. (1992). Telomere length predicts replicative capacity of human fibroblasts. Proceedings of the National Academy of Sciences of the United States of America , 89 (21), 10114–10118. doi.org/10.1073/pnas.89.21.10114
American Lung Association. (2023). Your aging lungs . https://www.lung.org/blog/your-aging-lungs
American Optometric Association. (n.d.). Senior vision: Over 60 years of age. https://www.aoa.org/healthy-eyes/eye...r-vision?sso=y
Arias, E., Tejada-Vera, B., Kochanek, K. D., & Ahmad, F. B. (2022). Provisional life expectancy estimates for 2021. Vital Statistics Rapid Release; no 23. National Center for Health Statistics. https://dx.doi.org/ 10.15620/cdc:118999
Arias, E., & Xu, J. (2020). United States life tables, 2018. National Vital Statistics Reports: From the Centers for Disease Control and Prevention, National Center for Health Statistics, National Vital Statistics System , 69 (12), 1–45. https://pubmed.ncbi.nlm.nih.gov/33270553/
Ashraf, M., & Souka, A. (2017). Aflibercept in age-related macular degeneration: Evaluating its role as a primary therapeutic option. Eye , 31 (11), 1523–1536. https://doi.org/10.1038/eye.2017.81
Aversa, R., Petrescu, R. V. V., Apicella, A., & Petrescu, F. I. (2016). One can slow down the aging through antioxidants. American Journal of Engineering and Applied Sciences, 9 (4), 1112–1126. https://doi.org/10.3844/ajeassp.2016.1112.1126
Bansal, S., & Jin, Y. (2023). Heterogeneous effects of obesity on life expectancy: A global perspective. Annual Review of Resource Economics, 15 , 433–554. doi.org/10.1146/annurev-reso...-022823-033521
Barnes, J. N., Pearson, A. G., Corkery, A. T., Eisenmann, N. A., & Miller, K. B. (2021). Exercise, arterial stiffness, and cerebral vascular function: Potential impact on brain health. Journal of the International Neuropsychological Society, 27 (8), 761–775. https://doi.org/10.1017/S1355617721000394
Birren, J. E., & Cunningham, W. R. (1985). Research on the psychology of aging: Principles, concepts and theory. In J. E. Birren & K. W. Schaie (Eds.), Handbook of the Psychology of Aging (2nd ed.). Van Nostrand Reinhold Company.
Blagosklonny, M. V. (2021). No limit to maximal lifespan in humans: How to beat a 122-year-old record. Oncoscience , 8 , 110–119. https://doi.org/10.18632/oncoscience.547
Bonnick, S. L. (2006). Osteoporosis in men and women. Clinical Cornerstone , 8 (1), 28–39. https://doi.org/10.1016/s1098-3597(06)80063-3
Cadore, E. L., Casas-Herrero, A., Zambom-Ferraresi, F., Idoate, F., Millor, N., Gómez, M., Rodríguez-Mañas, L., & Izquierdo, M. (2014). Multicomponent exercises including muscle power training enhance muscle mass, power output, and functional outcomes in institutionalized frail nonagenarians. AGE 36 , 773–785. https://doi.org/10.1007/s11357-013-9586-z
Calabrese, F., Guidotti, G., Racagni, G., & Riva, M. A. (2013). Reduced neuroplasticity in aged rats: A role for the neurotrophin brain-derived neurotrophic factor. Neurobiology of Aging , 34 (12), 2768–2776. https://doi.org/10.1016/j.neurobiolaging.2013.06.014
Cartee, G. D., Hepple, R. T., Bamman, M. M., & Zierath, J. R. (2016). Exercise promotes healthy aging of skeletal muscle. Cell Metabolism, 23 (6), 1034–1047. http://dx.doi.org/10.1016/j.cmet.2016.05.007
Casson, R. J., Chidlow, G., Wood, J. P. M., Crowston, J. G., & Goldberg, I. (2012). Definition of glaucoma: Clinical and experimental concepts. Clinical and Experimental Ophthalmology , 40 (4), 341–349. doi.org/10.1111/j.1442-9071.2012.02773.x
Chan, G., & Duque, G. (2002). Age-related bone loss: Old bone, new facts. Gerontology , 48 (2), 62–71. doi.org/10.1159/000048929
Chaput, J. P., Dutil, C., & Sampasa-Kanyinga, H. (2018). Sleeping hours: What is the ideal number and how does age impact this? Nature and Science of Sleep , 10 , 421–430. https://doi.org/10.2147/nss.s163071
Chetty, R., Stepner, M., Abraham, S., Lin, S., Scuderi, B., Turner, N., Bergeron, A., & Cutler, D. M. (2016). The Association between Income and Life Expectancy in the United States, 2001-2014. JAMA , 315 (16), 1750–1766. doi.org/10.1001/jama.2016.4226
Chumlea, W. C., Rhodes, T., Girman, C. J., Johnson-Levonas, A., Lilly, F. R. W., Wu, R., & Guo, S. S. (2004). Family history and risk of hair loss. Dermatology , 209 (1), 33–39. doi.org/10.1159/000078584
Colón, C. J. P., Molina-Vicenty, I. L., Frontera-Rodríguez, M., García-Ferré, A., Rivera, B. P., Cintrón-Vélez, G., & Frontera-Rodríguez, S. (2018). Muscle and bone mass loss in the elderly population: Advances in diagnosis and treatment. Journal of Biomedicine , 3 , 40–49. https://doi.org/10.7150/jbm.23390
Cornelissen, G., & Otsuka, K. (2017). Chronobiology of aging: A mini-review. Gerontology, 63 (2), 118–128. doi.org/10.1159/000450945
Cornelius, M. E., Loretan, C. G., Wang, T. W., Jamal, A., & Homa, D. M. (2022). Tobacco product use among adults – United States, 2020. Morbidity and Mortality Weekly Report, 71 (11), 397–405. https://doi.org/10.15585/mmwr.mm7111a1
Crowley, K. (2011). Sleep and sleep disorders in older adults. Neuropsychology Review , 21 , 41–53. https://doi.org/10.1007/s11065-010-9154-6
Dagnino, P., Ugarte, M. J., Morales, F., González, S., Saralegui, D., & Ehrenthal, J. C. (2020). Risk factors for adult depression: Adverse childhood experiences and personality functioning. Frontiers in Psychology, 11 , 594698. https://doi.org/10.3389/fpsyg.2020.594698
Dattani, S, Rodés-Guirao, L, Ritchie, H., Ortiz-Ospina, E., & Roser, M. (2023). Life expectancy. OurWorldInData.org. https://ourworldindata.org/life-expectancy
Davies, M. A. M., Kerr, Z. Y., DeFreese, J. D., Arden, N. K., Marshall, S. W., Guskiewicz, K. M., Padua, D. A., & Pietrosimone, B. (2019). Prevalence of and risk factors for total hip and knee replacement in retired National Football League athletes. American Journal of Sports Medicine , 47 (12), 2863–2870. doi.org/10.1177/0363546519870804
Decker, M. L., Chavez, E., Vulto, I., & Lansdorp, P. M. (2009). Telomere length in Hutchinson-Gilford Progeria Syndrome. Mechanisms of Ageing and Development , 130 (6), 377–383. https://doi.org/10.1016/j.mad.2009.03.001
Dillard, L. K., Arunda, M. O., Lopez-Perez, L., Martinez, R. X., Jiménez, L., & Chadha, S. (2022). Prevalence and global estimates of unsafe listening practices in adolescents and young adults: A systematic review and meta-analysis. BMJ Global Health, 7 , e010501. doi.org/10.1136/bmjgh-2022-010501
Dillard, L. K., Mulas, P., Der, C., Fu, X., & Chadha, S. (2024). Risk of sound-induced hearing loss from exposure to video gaming or esports: A systematic scoping review: BMJ Public Health, 2 (1), e000253. doi.org/10.1136/bmjph-2023-000253
Dines, V. A., & Garovic, V. D. (2024). Menopause and chronic kidney disease. Nature Reviews Nephrology , 20 , 4–5. https://doi.org/10.1038/s41581-023-00717-w
Domenichiello, A. F., & Ramsden, C. E. (2019). The silent epidemic of chronic pain in older adults. Progress in Neuro-psychopharmacology & Biological Psychiatry , 93 , 284–290. https://doi.org/10.1016/j.pnpbp.2019.04.006
Dommaraju, S., & Perera, E. (2016). An approach to vertigo in general practice. PubMed , 45 (4), 190–194. https://pubmed.ncbi.nlm.nih.gov/27052132
Doucette, L. P., Rasnitsyn, A., Seifi, M., & Walter, M. A. (2015). The interactions of genes, age, and environment in glaucoma pathogenesis. Survey of Ophthalmology , 60 (4), 310–326. https://doi.org/10.1016/j.survophthal.2015.01.004
Fernández, L., Breinbauer, H. A., & Delano, P. H. (2015). Vertigo and dizziness in the elderly. Frontiers in Neurology , 6 . https://doi.org/10.3389/fneur.2015.00144
Fields, R. D. (2008). White matter in learning, cognition and psychiatric disorders. Trends in Neurosciences , 31 (7), 361–370. https://doi.org/10.1016/j.tins.2008.04.001
Fjell, A. M., Grydeland, H., Krogsrud, S. K., Amlien, I., Rohani, D. A., Ferschmann, L., Storsve, A. B., Tamnes, C. K., Sala-Llonch, R., Due-Tønnessen, P., Bjørnerud, A., Sølsnes, A. E., Håberg, A. K., Skranes, J., Bartsch, H., Chen, C.-H., Thompson, W. K., Panizzon, M. S., Kremen, W. S., . . . Walhovd, K. B. (2015). Development and aging of cortical thickness correspond to genetic organization patterns. Proceedings of the National Academy of Sciences of the United States of America , 112 (50), 15462–15467. doi.org/10.1073/pnas.1508831112
For the Health ABC Study. (2012). Racial differences in mortality in older adults: Factors beyond socioeconomic status. Annals of Behavioral Medicine , 43 (1), 29–38. doi.org/10.1007/s12160-011-9335-4
Godoy, L. C., Frankfurter, C., Cooper, M., Lay, C., Maunder, R., & Farkouh, M. E. (2021). Association of adverse childhood experiences with cardiovascular disease later in life: A review. JAMA Cardiology, 6 (2), 228–235. doi.org/10.1001/jamacardio.2020.6050
Goh, J. O., & Park, D. C. (2009). Neuroplasticity and cognitive aging: The scaffolding theory of aging and cognition. Restorative Neurology and Neuroscience , 27 (5), 391–403. doi.org/10.3233/rnn-2009-0493
Green, E., Huynh, A., Broussard, L., Zunker, B., Matthews, J., Hilton, C. L., & Aranha, K. (2019). Systematic review of yoga and balance: Effect on adults with neuromuscular impairment. The American Journal of Occupational Therapy, 73 (1), 7301205150p1-7301205150p11. doi.org/10.5014/ajot.2019.028944
Guo, L., & Akpek, E. K. (2020). The negative effects of dry eye disease on quality of life and visual function. Turkish Journal of Medical Sciences , 50 (10), 1611–1615. https://doi.org/10.3906/sag-2002-143
Hamdy, R. C. (2017). Fractures and repeated falls. Journal of Clinical Densitometry, 20 (3), 425–431. https://doi.org/10.1016/j.jocd.2017.06.009
Han, Y., Yuan, M., Guo, Y.-S., Shen, X.-Y., Gao, Z.-K., & Bi, X. (2022). The role of enriched environment in neural development and repair. Frontiers in Cellular Neuroscience, 16 , 890666. https://doi.org/10.3389/fncel.2022.890666
Hayflick, L., & Finch, C. E. (1977). The cellular basis for biological aging. Handbook of the Biology of Aging , 159–186.
Hennekam, R. C. M. (2006). Hutchinson–Gilford progeria syndrome: Review of the phenotype. American Journal of Medical Genetics Part A , 140A (23), 2603–2624. doi.org/10.1002/ajmg.a.31346
Hernández-Zimbrón, L. F., Zamora-Alvarado, R., Ochoa-De la Paz, L., Vélez-Montoya, R., Zenteno, E., Gulías-Cañizo, R., Quiróz-Mercado, H., & González-Salinas, R. (2018). Age-related macular degeneration: New paradigms for treatment and management of AMD. Oxidative Medicine and Cellular Longevity , 2018 , 1–14. doi.org/10.1155/2018/8374647
Hill, L., & Artiga, S. (2023, May 23). What is driving widening racial disparities in life expectancy? KFF. https://www.kff.org/racial-equity-an...fe-expectancy/
Huang, Q., & Tang, J. (2010). Age-related hearing loss or presbycusis. European Archives of Oto-rhino-laryngology , 267 (8), 1179–1191. https://doi.org/10.1007/s00405-010-1270-7
Hülür, G., Ram, N., & Gerstorf, D. (2016). Terminal decline of function. In V. L. Bengtson & R. A. Settersten Jr. (Eds.), Handbook of theories of aging (3rd ed.). www.researchgate.net/profile...f-function.pdf
Jeter, P. E., Nkodo, A.-F., Moonaz, S. H., & Dagnelie, G. (2014). A systematic review of yoga for balance in a healthy population. Journal of Alternative and Complementary Medicine, 20 (4), 221–232. doi.org/10.1089/acm.2013.0378
Jomova, K., Raptova, R., Alomar, S. Y., Alwasel, S. H., Nepovimova, E., Kuca, K., & Valko, M. (2023). Reactive oxygen species, toxicity, oxidative stress, and antioxidants: Chronic diseases and aging. Archives of Toxicology, 97 , 2499–2574. https://doi.org/10.1007/s00204-023-03562-9
Jung, S.-H., Lee, Y. C., Shivakumar, M., Kim, J., Yun, J.-S., Park, W.-Y., Won, H.-H., Penn Medicine Biobank, & Kim, D. (2024). Association between genetic risk and adherence to healthy lifestyle for developing age-related hearing loss. BMC Medicine, 22 , 141. https://doi.org/10.1186/s12916-024-03364-5
Kaiser Family Foundation. (2023). What is driving widening racial disparities in life expectancy? https://www.kff.org/racial-equity-an...fe-expectancy/
Kempermann, G., Gast, D., & Gage, F. H. (2002). Neuroplasticity in old age: Sustained fivefold induction of hippocampal neurogenesis by long-term environmental enrichment. Annals of Neurology , 52 (2), 135–143. doi.org/10.1002/ana.10262
Kerchner, G. A., Racine, C. A., Hale, S., Wilheim, R., Laluz, V., Miller, B. L., & Kramer, J. H. (2012). Cognitive processing speed in older adults: Relationship with white matter integrity. PLOS ONE , 7 (11), e50425. https://doi.org/10.1371/journal.pone.0050425
Lichtman, J. H., Leifheit, E. C., Safdar, B., Bao, H., Krumholz, H. M., Lorenze, N. P., Daneshvar, M., Spertus, J. A., & D’Onofrio, G. (2018). Sex differences in the presentation and perception of symptoms among young patients with myocardial infarction: Evidence from the VIRGO study (Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients). Circulation, 137 (8), 781–790. doi.org/10.1161/CIRCULATIONAHA.117.031650
Lipsky, M. S., & King, M. (2015). Biological theories of aging. Disease-a-month , 61 (11), 460–466. https://doi.org/10.1016/j.disamonth.2015.09.005
Liu, P. Z., & Nusslock, R. (2018). Exercise-mediated neurogenesis in the hippocampus via BDNF. Frontiers in Neuroscience, 12 , 52. https://doi.org/10.3389/fnins.2018.00052
Lowery, E. M., Brubaker, A. L., Kuhlmann, E., & Kovacs, E. J. (2013). The aging lung. Clinical Interventions in Aging, 8, 1489–1496. https://doi.org/10.2147/cia.s51152
Maymone, M. B. C., Laughter, M., Pollock, S., Khan, I., Marques, T., Abdat, R., Goldberg, L. J., & Vashi, N. A. (2021). Hair aging in different races and ethnicities. The Journal of Clinical and Aesthetic Dermatology , 14 (1), 38–44. https://europepmc.org/article/MED/33584967
Medina, L., Sabo, S., & Vespa, J. (2020). Living longer: Historical and projected life expectancy in the United States, 1960 to 2060. U.S. Department of Commerce, U.S. Census Bureau. https://www.census.gov/content/dam/C...o/p25-1145.pdf
MedlinePlus (2022). Is longevity determined by genetics? National Library of Medicine. https://medlineplus.gov/genetics/und...its/longevity/
Merrick, M. T., Ford, D. C., Ports, K. A., Guinn, A. S., Chen, J., Klevens, J., Metzler, M., Jones, C. M., Simon, T. R., Daniel, V. M., Ottley, P., & Mercy, J. A. (2019). Vital signs: Estimated proportion of adult health problems attributable to adverse childhood experiences and implications for prevention—25 states, 2015–2017. Morbidity and Mortality Weekly Report, 68 (44), 999–1005. https://doi.org/10.15585/mmwr.mm6844e1
Mitteldorf, J. (2010). Aging is not a process of wear and tear. Rejuvenation Research , 13 (2–3), 322–326. doi.org/10.1089/rej.2009.0967
Moreno-Jiménez, E. P., Flor-García, M., Terreros-Roncal, J., Rábano, A., Cafini, F., Pallas-Bazarra, N., Ávila, J., & Llorens-Martín, M. (2019). Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease. Nature Medicine, 25 , 554–560. https://doi.org/10.1038/s41591-019-0375-9
National Institute on Aging. (2017). Skin care and aging. www.nia.nih.gov/health/skin-care-and-aging
National Institute on Aging. (2018). Heart health and aging. www.nia.nih.gov/health/heart-health-and-aging
National Institute on Aging. (2020). How smell and taste change as you age. www.nia.nih.gov/health/smell-and-taste
National Institute on Aging. (2022). Urinary incontinence in older adults. www.nia.nih.gov/health/urina...e-older-adults
Newsom, R., & DeBanto, J. (2023, September 19). Aging and sleep . Sleep Foundation. https://www.sleepfoundation.org/aging-and-sleep
Nolan, L. S. (2020). Age-related hearing loss: Why we need to think about sex as a biological variable. Journal of Neuroscience Research, 98 (9), 1705–1720. doi.org/10.1002/jnr.24647
Novais, A., Monteiro, S., Roque, S., Correia-Neves, M., & Sousa, N. (2017). How age, sex and genotype shape the stress response. Neurobiology of Stress , 6 , 4456. https://doi.org/10.1016/j.ynstr.2016.11.004
O’Connor, D. B., Thayer, J. F., & Vedhara, K. (2021). Stress and health: A review of psychobiological processes. Annual Review of Psychology , 72 , 663–688. doi.org/10.1146/annurev-psych-062520-122331
Othman, Z., Abdul Halim, A. S., Azman, K. F., Ahmad, A. H., Zakaria, R., Sirajudeen, K. N. S., Wijaya, A., & Ahmi, A. (2022). Profiling the research landscape on cognitive aging: A bibliometric analysis and network visualization. Frontiers in Aging Neuroscience, 14 , 876159. https://doi.org/10.3389/fnagi.2022.876159
Peters, R. (2006). Ageing and the brain. Postgraduate Medical Journal , 82 (964), 84–88. doi.org/10.1136/pgmj.2005.036665
Sapolsky, R. M. (1992). Stress, the aging brain, and the mechanisms of neuron death . MIT Press.
Sarafrazi, N., Wambogo, E. A., & Shepherd, J. A. (2021). Osteoporosis or low bone mass in older adults: United States, 2017 – 2018 . U.S. Department of Health and Human Services, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention. https://doi.org/10.15620/cdc:103477
Sattaur, Z., Lashley, L. K., & Golden, C. J. (2020). Wear and tear theory of aging. Essays in developmental psychology . Available at: https://nsuworks.nova.edu/cps_facbooks/732
Sele, S., Liem, F., Mérillat, S., & Jäncke, L. (2021). Age-related decline in the brain: A longitudinal study on inter-individual variability of cortical thickness, area, volume, and cognition. NeuroImage , 240 , 118370. https://doi.org/10.1016/j.neuroimage.2021.118370
Sharma, A., & Hindman, H. B. (2014). Aging: A predisposition to dry eyes. Journal of Ophthalmology , 2014 , 1–8. doi.org/10.1155/2014/781683
Sharma, G., & Goodwin, J. (2006). Effect of aging on respiratory system physiology and immunology. Clinical Interventions in Aging , 1 (3), 253–260. www.ncbi.nlm.nih.gov/pmc/articles/PMC2695176/
Shaw, M. E., Abhayaratna, W. P., Sachdev, P. S., Anstey, K. J., & Cherbuin, N. (2016). Cortical thinning at midlife: The PATH through life study. Brain Topography , 29 , 875–884. https://doi.org/10.1007/s10548-016-0509-z
Shay, J. W., & Wright, W. E. (2000). Hayflick, his limit, and cellular ageing. Nature Reviews Molecular Cell Biology , 1 , 72–76. https://doi.org/10.1038/35036093
Sivertsen, B., Pallesen, S., Friborg, O., Nilsen, K. B., Bakke, Ø. K., Goll, J. B., & Hopstock, L. A. (2021). Sleep patterns and insomnia in a large population-based study of middle-aged and older adults: The Tromsø study 2015–2016. Journal of Sleep Research, 30 (1), e13095. doi.org/10.1111/jsr.13095
Sjöstrand, J., Laatikainen, L., Hirvelä, H., Popovic, Z., & Jonsson, R. (2011). The decline in visual acuity in elderly people with healthy eyes or eyes with early age-related maculopathy in two Scandinavian population samples. Acta Ophthalmologica , 89 (2), 116–123. doi.org/10.1111/j.1755-3768.2009.01653.x
Sorrells, S. F., Paredes, M. F., Cebrian-Silla, A., Sandoval, K., Qi, D., Kelley, K. W., James, D., Mayer, S., Chang, J., Auguste, K. I., Chang, E. F., Gutierrez, A. J., Kriegstein, A. R., Mathern, G. W., Oldham, M. C., Huang, E. J., Garcia-Verdugo, J. M., Yang, Z., & Alvarez-Buylla, A. (2018). Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature, 555 , 377–381. https://doi.org/10.1038/nature25975
Stillman, C. M., Esteban-Cornejo, I., Brown, B., Bender, C. M., & Erickson, K. I. (2020). Effects of exercise on brain and cognition across age groups and health states. Trends in Neurosciences , 43 (7), 533–543. https://doi.org/10.1016/j.tins.2020.04.010
Tani, Y., Fujiwara, T., & Kondo, K. (2020). Association between adverse childhood experiences and dementia in older Japanese adults. JAMA Network Open, 3 (2), e1920740. doi.org/10.1001/jamanetworkopen.2019.20740
Thayer, J. F., Mather, M., & Koenig, J. (2021). Stress and aging: A neurovisceral integration perspective. Psychophysiology, 58 (7), e13804. doi.org/10.1111/psyp.13804
van den Berg, N., Rodríguez-Girondo, M., van Dijk, I. K., Mourits, R. J., Mandemakers, K., Janssens, A. A. P. O., Beekman, M., Smith, K. R., & Slagboom, P. E. (2019). Longevity defined as top 10% survivors and beyond is transmitted as a quantitative genetic trait. Nature Communications , 10 , 35. https://doi.org/10.1038/s41467-018-07925-0
Volpi, E., Nazemi, R., & Fujita, S. (2004). Muscle tissue changes with aging. Current Opinion in Clinical Nutrition and Metabolic Care, 7 (4), 405–410. doi.org/10.1097/01.mco.0000134362.76653.b2
von Gablenz, P., Hoffmann, E., & Holube, I. (2020). Gender-specific hearing loss in German adults aged 18 to 84 years compared to US American and current European studies. PLOS ONE , 15 (4), e0231632. https://doi.org/10.1371/journal.pone.0231632
Weinreb, R. N., Aung, T., & Medeiros, F. A. (2014). The pathophysiology and treatment of glaucoma. JAMA , 311 (18), 1901. doi.org/10.1001/jama.2014.3192
Wickremaratchi, M. M., & Llewelyn, J. G. (2006). Effects of ageing on touch. Postgraduate Medical Journal , 82 (967), 301–304. doi.org/10.1136/pgmj.2005.039651
Widén, S., Båsjö, S., Möller, C., & Kähäri, K. (2017). Headphone listening habits and hearing thresholds in Swedish adolescents. Noise Health , 19 (88), 125–132. doi.org/10.4103/nah.nah_65_16
Wilson, R. S., Yu, L., Leurgans, S. E., Bennett, D. A., & Boyle, P. A. (2020). Proportion of cognitive loss attributable to terminal decline. Neurology, 94 (1), e42–e50. doi.org/10.1212/WNL.0000000000008671
Xu, J. Q., Murphy, S. L., Kochanek, K. D., and Arias, E. (2021). Deaths: Final data for 2019. National Vital Statistics Reports, 70 (8). National Center for Health Statistics. https://dx.doi.org/10.15620/cdc:106058
Yassa, M. A., Mattfeld, A. T., Stark, S. M., & Stark, C. E. (2011). Age-related memory deficits linked to circuit-specific disruptions in the hippocampus. Proceedings of the National Academy of Sciences of the United States of America , 108 (21), 8873–8878. doi.org/10.1073/pnas.1101567108
Yiallouris, A., Tsioutis, C., Agapidaki, E., Zafeiri, M., Agouridis, A. P., Ntourakis, D., & Johnson, E. O. (2019). Adrenal aging and its implications on stress responsiveness in humans. Frontiers in Endocrinology, 10 . https://doi.org/10.3389/fendo.2019.00054
Ziada, A. S., Smith, M.-S. R., & Côté, H. (2020). Updating the free radical theory of aging. Frontiers in Cell and Developmental Biology , 8 . https://doi.org/10.3389/fcell.2020.575645