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Sarcopenia and Muscle Aging

Sarcopenia and Muscle Aging

Teaser: 

 


Click here to view the entire report from the 28th Annual Scientific Meeting of the Canadian Geriatrics Society

Sarcopenia and Muscle Aging

Speaker: Patrick Dehail, MD, PhD, Service de Médecine Physique et Réadaptation & EA 4136, CHU de Bordeaux, Université de Bordeaux 2; Bordeaux, France.

Dr. Patrick Dehail focused on the mechanisms and functional impact of and therapeutic approaches to sarcopenia and muscle aging.

Defining Sarcopenia
Sarcopenia is a progressive process of age-related muscle mass (MM) loss. Its prevalence is high, from 10-24% in 65-70-year-olds to over 30% in those over 80 years old.

Sarcopenia is characterized by a muscle mass index (MMI) (appendicular skeletal MM [kg]/height2 [m2]) at least two standard deviations lower than the MMI in a younger population.1 A threshold that takes into account muscle performance and describes MM loss that has a functional impact is of the greatest utility.

In older adults, MM loss is associated with increased fat mass. It is important to take these two processes into account because fat mass affects the consequences of sarcopenia.

Age-related Changes and Mechanisms Involved in Muscle Tissue
Sarcopenia is associated with muscle tissue changes such as a decrease in the number and atrophy of type II skeletal fibres, while type I fibres are more preserved (Figure 1). At the molecular level, aging is associated with a decreased expression of myosin heavy chain (MHC) IIa and IIx isoforms, while the level of expression of MHC I tends to remain constant. There is an increase in the total number of hybrid fibres coexpressing various MHC isoforms.
Mechanisms involved in muscle aging include motor unit changes, inactivity, and the dysregulation of muscle protein synthesis and apoptosis.

The aging process is associated with a 25-50% reduction of the a-motoneurons (a-MN). Small MN, which are more preserved than large a-MN, continue to innervate type I fibres. Over many years, the loss of large a-MN is compensated by a sprouting phenomenon: small MN will take over and innervate orphan type II muscle fibres, which will become type I fibres. Eventually, however, the new giant motor units constituted through the sprouting phenomenon are lost and, beyond a certain threshold, this loss will lead to a functional impact.

Inactivity is viewed as an etiologic factor of sarcopenia. However, it is not known whether inactivity is the consequence of neuromuscular changes (adaptation) or a factor contributing to these changes.

Dr. Dehail described the dysregulation of muscle protein synthesis as playing an important role in sarcopenia. Splanchnic sequestration diverts amino acids to the liver or the intestine. Secondly, insulin resistance, which is more prevalent in older adults, plays a role essentially by increasing proteolysis of muscular proteins. A decreased level of metabolic hormones (testosterone, GH-IGF1 axis, DHEA) also contributes to this dysregulation. Finally, the elevated level of proinflammatory cytokines (in particular, IL6 and TNF-a) seen in older adults stimulates proteolysis. Additionally, decreased MGF levels (a factor that stimulates the pool of satellite cells), and increased level of myostatin (a muscle growth inhibitor) and apoptosis also contribute to sarcopenia.

Aging is also associated with microcirculatory changes that affect muscle tissue.

Malnutrition, anorexia, and decreased vitamin D and vitamin D receptors (VDR) levels are common in older adults. Prevalence of vitamin D deficiency exceeds 90% in hospitalized older adults. Vitamin D affects protein synthesis and the functional capacity of muscle tissue. There is a correlation between the levels of 25-hydroxyvitamin D (25-OHD) and loss of muscular strength. Visser et al. showed that subjects with a 25-OHD level <25 nmol/l were more likely to lose their grip strength at 3 years. The decline of the circulating levels of 25-OHD was also associated with the decrease of walk speed and time to stand.2

Functional Impact of Muscle Aging
Muscle changes affect muscular performance and strength. Loss of muscular strength starts early but is relatively insignificant until 50-60 years of age. Isokinetic, concentric, and lower limb muscle strength are primarily affected. This loss is asymmetric relative to antagonist muscles.

The threshold of functional decline varies among individuals and also depends on the functional task. However, some authors suggest that there are clinical thresholds under which most persons will experience difficulties. For example, Janssen et al. showed that a MMI below 5.75 for women and 8.5 for men correlates with a higher risk of functional impairment.3 Ploutz-Snyder et al. calculated the ratio of knee extensors isometric strength/body weight, and estimated that a ratio below 3 Nm/kg was associated with a decline in functional ability, especially with locomotion (walk, stair climbing, sit-to-stand).4 Lauretani et al. suggest an even simpler method, where an isometric hand grip strength below 30 kg for men and 20 kg for women can allow to identify older persons with a decline in walk time or locomotor ability.5

From a functional point of view, loss of muscle power is more important, Dr. Dehail explained. It is required in many important basic activities such as sit-to-stand, stair climbing, or walking. Muscle power is extremely useful in loss of balance situations (falls) where a posture adjustment is necessary, and allows the older adult to remain functionally independent.

Aging is also associated with a reduced muscle quality (defined as the ratio of muscle strength/muscle mass). Voluntary movements are affected by the degradation of central drive conductivity and an increase in agonist-antagonist coactivations.The rheologic properties of skeletal muscle are also modified, with a prolongation of muscle contraction and half-relaxation times. Decreased tendon stiffness will lead to a poorer transmission of muscle strength to the motion segment.

Finally, Dr. Dehail ascribed particular importance to the ability to maintain a contraction level during sustained effort. Dr. Dehail and colleagues compared the “endurance coefficient” (EC) (ratio of the last three isokinetic muscle contractions strength/first muscle contraction strength) and the changes in loss of muscle strength in older and younger adults.6 Interestingly, the oldest and most fragile adults (mean age: 85) did not have a loss of strength, and their EC was close to 1. Older individuals (mean age: 75) showed an EC of 0.92, compared to 0.85 in young subjects (students). In fact, during a sustained effort, younger adults will first use type II fibres before switching to type I fibres. Older and hospitalized adults will use type I fibres from the beginning, giving them an endurance coefficient close to 1.

Therapeutic approaches
Resistance strength training

Dr. Dehail described resistance strength training as central to fighting sarcopenia and as the most efficient method available. All types of resistance strength training are suitable, but in practice it is important to adapt the exercises to the patient. Protocols vary, but it is suggested to do at least 3 training sessions per week, for 12 weeks, which is the time necessary for maximal strength gain.

During the first 3 weeks, results improve with no nervous or muscular adaptation. From weeks 3 to 6, strength gain is the highest, mostly due to an adaptation of the motor units (better recruitment, firing rate, and synchronization) and a decrease of muscular coactivations. From weeks 6 to12, muscular adaptations prevail (slight increase of MM and slight fibre hypertrophy). Beyond 12 weeks, no further gain is attained, but strength is maintained as long as the older adult continues training at the same schedule.

Dr. Dehail cited a study by Yarasheski et al. that showed that after 2 weeks of resistance strength training, muscle protein synthesis is similar in older (78-84 years old) and younger (23-32 years old) adults.7

In a systematic review, Latham et al. showed that older adults who follow a resistance strength training program gain significant muscle strength (20 to 200% increase of the 1 MR [maximal repetition], according to various studies).8
Resistance strength training improves muscle strength and power, and more modestly walking time, and sit-to-stand time, and lowers the risk of falls. However, the impact on ADLs or quality of life are unknown. Nutritional supplementation is also important and improves the results, especially in malnourished older subjects.

Drugs
According to Dr. Dehail, testosterone and growth hormone (GH) only improve muscular performance in hypogonadal individuals or individuals with a GH deficiency. DHEA shows no benefits in terms of muscular performance. Vitamin D lowers the risk of falls, but this benefit does not seem to be linked to improved muscle strength or power.

ACE inhibitors may be beneficial. An observational study showed favorable effects on muscle strength and mass. Controlled studies are needed for confirmation.

Other molecules are being studied, such as SARMs (selective androgen receptor modulators), myostatin antagonists, or some amino acids (leucine).

Conclusion
Sarcopenia is correlated with higher functional impairment of ADLs, and a higher risk of falls, physical frailty, and dependence. It is also associated with higher mortality, especially in sarcopenic hospitalized older adults, as they show a higher incidence of nocosomial infections.

Sarcopenia is associated with a clear increase of health care costs (about $900 extra per older patient/year in the US).

References

  1. Baumgartner RN, Koehler KM, Gallagher D, et al. Epidemiology of sarcopenia among the elderly in New Mexico. Am J Epidemiol 1998;147:755-63.
  2. Visser M, Deeg DJ, Lips P. Low vitamin D and high parathyroid hormone levels as determinants of loss of muscle strength and muscle mass (sarcopenia): the Longitudinal Aging Study Amsterdam. J Clin Endocrinol Metab 2003;88:5766-72.
  3. Janssen I, Baumgartner RN, Ross R, Rosenberg IH, Roubenoff R. Skeletal muscle cutpoints associated with elevated physical disability risk in older men and women. Am J Epidemiol 2004;159:413-21.
  4. Ploutz-Snyder LL, Manini T, Ploutz-Snyder RJ, et al. Functionally relevant thresholds of quadriceps femoris strength. J Gerontol A Biol Sci Med Sci 2002;57:B144-52.
  5. Lauretani F, Russo CR, Bandinelli S, et al. Age-associated changes in skeletal muscles and their effect on mobility: an operational diagnosis of sarcopenia. J Appl Physiol 2003;95:1851-60.
  6. Muller F, Dehail P, Bestaven E, et al. Maximal and sustained isokinetic lower-limb muscle strength in hospitalized older people. Muscle Nerve 2007;35:739-44.
  7. Yarasheski KE. Exercise, aging, and muscle protein metabolism. J Gerontol A Biol Sci Med Sci 2003;58:M918-22.
  8. Latham NK, Bennett DA, Stretton CM, et al. Systematic review of progressive resistance strength training in older adults. J Gerontol A Biol Sci Med Sci 2004;59:48-61.

Chronic Disease and Aging: A Global Challenge

Chronic Disease and Aging: A Global Challenge

Teaser: 

Click here to view the entire report from the 28th Annual Scientific Meeting of the Canadian Geriatrics Society

Chronic Disease and Aging: A Global Challenge

Speaker: Howard Bergman, MD, The Dr. Joseph Kaufmann Professor and Director, Division of Geriatric Medicine, McGill University, Montreal, QC; Co-Director: Solidage Research Group, Montreal, QC; Director, Quebec Research Network in Ageing/Fonds de Recherche en Santé du Québec, Montreal, QC; Chair, Advisory Board, Institute of Aging, Canadian Institutes of Health Research, Ottawa, ON.

Dr. Howard Bergman prefaced his discussion of the increasing burden of chronic disease and aging with a slide series featuring images of aging individuals from around the world. The photographs offered diverse examples of visible frailty and decline, as well as obvious health and resiliency into late age, highlighting the profound heterogeneity of aging adults.

Current Demographic and Epidemiologic Shifts

The world’s population is aging; the worldwide demographic and epidemiologic transitions associated with increasing life expectancy and a rapidly aging population is recognized as one of the challenges of our time. That the population of Western nations is aging is commonplace knowledge; however, this trend is not a limited but rather a worldwide shift.

There is an overall increase in life expectancy: over the last five decades, life expectancy at birth increased globally by almost 20 years, from 46.5 years in 1950-1955 to 66.0 years in 2000-2005. The global average annual growth rate of persons aged 80 years and over (3.8 %) is currently twice as high as the growth rate of the population aged 60 and over (1.9%). The 80-plus age group is expected to remain the fastest-growing segment of the population (Figure 1).

The demographic transition began earlier in the more developed countries, but poorer regions are currently experiencing similar changes within shorter time spans. When compared with demographic transitions in France, for example, Mexico is aging six times more rapidly. Dr. Bergman presented statistics showing that through 2050, 70% of the world’s older persons (80 and over) will be living in developing regions. In both developed and developing countries the complex effects of improved living conditions, education, medical care, and accessibility to health care are promoting longevity. Additionally in developing countries older adults are living longer due to improved sanitation, nutrition, and infection control.

This shift has led to an increase in the prevalence of chronic diseases and the potential number of older persons living with disability. These conditions pose important challenges to health care systems. Dr. Bergman cited a recent World Health Organization (WHO) report that ranked health care systems worldwide according to criteria that included the capacity of the care system to improve the health of the population, meet health care needs, assure quality of care, offer responsiveness and equity in the provision of that care, including toward vulnerable groups, and the cost efficiency of the system. France ranked first; indicators of Canada’s performance were ranked below expectation and were outmatched by countries thought to be on the margins of the developed standard, such as Colombia.

The Effort to Increase Active Life Expectancy
Increased longevity in both the developed and developing worlds often results in a longer period of life being spent with chronic disease.

The forces driving longevity are off-set by forces that serve as risk factors for the evolution of chronic disease such as poor dietary habits (the so-called worldwide “McDonaldization”), reduced physical activity, and increased tobacco use (particularly in developing countries as tobacco companies shift their focus away from the increasingly nonsmoking developed nations). Increased longevity also translates into prolonged exposure to chronic disease risk factors.

Health care systems around the world will increasingly struggle to manage a high proportion of older persons with disabilities and chronic disease, a segment of the population that is heterogeneous and has complex needs. This burden is also borne by older people themselves, along with their families, communities, and societies. Poorly managed chronic disease drives disability. If rates of disability can be mitigated, further improvements in life expectancy will result.

Signs of Improvement
Over the last several decades, researchers have witnessed an overall decrease in the rate of disability. Dr. Bergman cited data accrued from longitudinal studies of aging that show strong associations between lifestyle risks factors and the incidence of disability.

In the United States, it has been shown that improvements in individual health habits have led to increased survival and postponement of the age of onset of disability. Successfully implemented preventive strategies and screening protocols (e.g., prostate-specific antigen, bone density) have changed the onset of chronic disease. Additionally, improvements in health care systems, along with pharmaceutical and technological advances, have reduced disability related to the most disabling chronic diseases (hypertension, diabetes, hyperlipidemia). Improved surgical strategies for ailments affecting older adults (joint replacement, cataract surgery) have delayed or prevented disability. Finally, socioeconomic factors such as improved education, incomes, and working conditions have produced overall health improvements and reduced disability.

Emerging Challenges in the Developing World

The key question is whether the resources will be available to address the rapid changes in the developing world. Developing countries are experiencing sudden changes in a context of limited resources. Their health care systems are not optimally adapted to the complexity of managing and treating chronic disease, frailty, and dependence. Finally, socio-economic and demographic shifts are exerting a negative influence on health outcomes in the developing world: family members are not filling in supportive gaps as they once were, and transgenerational households are on the decline, as developing nations experience increased numbers of women in the paid workforce (rather than remaining informal caregivers), and children leaving their villages or going abroad in search of economic opportunity.

According to Dr. Bergman, a 1-2 year delay in the onset of disability/dependence can make a significant difference and directly reduces needs for long-term care and institutional resources. A shift toward an older population at risk for chronic disease and disability calls for health systems that on the one hand reduce the number of people who develop disability and lose independence, but on the other hand are able to provide for people who do develop disability and are dependent.

Not all strategies pursued in the developed world are transferable. Dr. Bergman observed that Canada relies on a strategy of screening and treatment of high-risk individuals, but this is ill-matched to the resources of developing countries. The WHO advocates health prevention and promotion in developing nations incorporating a community-based approach. If community health professionals were to implement strategies in the Asia/Pacific region that lowered blood pressure by 3 mmHg, this could lead to as many as 1 million fewer deaths from stroke by 2010, claimed one study Dr. Bergman cited. Another study by the WHO concerned a community-based intervention aimed at reducing salt intake in Tianjin, China, which had important effects of improving health knowledge, decreasing salt intake, and decreasing systolic blood pressure.

Dr. Bergman stated that research points toward a need for developed nations to better incorporate the community primary care approach to providing care for older persons with complex needs. This means accelerating the trend away from creating more “bricks and mortar” facilities (hospital and nursing home beds) toward strategies promoting living in the community. The latter have been associated with greater longevity. Governments need to invest in strategies supporting family/community involvement; integrate traditional healing resources, and train a workforce focused on mitigating the onset and effects of chronic disease.

Conclusion: International Collaboration and Knowledge Exchange to Support Effective Health Interventions
Effective interventions must go beyond instituting projects in one city or town, Dr. Bergman stated. Integrating improvements aimed at delaying onset of chronic disease must occur on a system-wide level. He encouraged listeners to consider how they could contribute to the effort and put the information he presented into their research perspectives. The effort to coordinate approaches and add to the evolving knowledge on frailty, studies on aging interventions, and information and policy exchange will help promote a coherent and responsive system of care that can meet this global challenge.

Telomeres, Telomerase and Aging

Telomeres, Telomerase and Aging

Teaser: 

 


Click here to view the entire report from the 28th Annual Scientific Meeting of the Canadian Geriatrics Society

Telomeres, Telomerase and Aging

Speaker: Chantal Autexier, Ph.D., Lady Davis Institute for Medical Research, Jewish General Hospital, and Bloomfield Center for Research in Aging; Departments of Anatomy and Cell Biology, and Medicine, McGill University, Montreal QC.

Dr. Chantal Autexier discussed the role of telomeres in the maintenance of genetic and cellular integrity, and how telomere disruption is involved in cellular senescence and the aging process.

Telomeres and Their Role in Cellular Integrity
Telomeres are noncoding repetitive DNA sequences (TTAGGG) that protect the ends of linear eukaryotic chromosomes. In humans, a shelterin complex of 6 main proteins binds telomeres.1 Both the structure and the length of telomeres are important for cellular integrity (Figure 1).

The telomeres are thought to prevent the cell’s damage response mechanisms from recognizing the ends of linear chromosomes as double-stranded DNA breaks, including those arising when chromosomes are damaged by stresses such as ionizing radiation. Interfering with telomere structure or length can lead to end-to-end fusions between chromosomes, chromosome instability and abnormalities, and cell division problems (cell senescence, cell death, or cells becoming cancerous).

In the body, most cells are unable to maintain telomere length from one division to the next, as the DNA replication machinery is unable to fully replicate the ends of chromosomes, leading to telomere shortening every time cells divide. Once a critical point—the Hayflick limit—is reached, most cells exit the cell cycle and undergo cell senescence. However, a small proportion of cells are able to re-enter the cell cycle, and this is usually associated with the lengthening of telomeres and the expression of telomerase, an enzyme directly involved in telomere formation and maintenance. Bodnar et al. have shown that forced expression of telomerase prevents telomere loss and growth arrest of normal human fibroblasts in culture and is sufficient for telomere lengthening and cell immortalization (extended lifespan).2

While most cells do not express telomerase, some cells do, such as stem cells, cells of the germ line, and 85% of cancer cells. Such cells are therefore able to maintain telomere length and structure through a large number of cell division cycles.

Telomere Shortening, Cell Senescence, and Tissue Aging
The process by which a cell exits the cell cycle is called replicative senescence. This can be triggered by various stresses, such as radiation damage and oxidative stress.3,4 In many cases, senescence is caused by, or associated with, loss of telomere integrity.

The cell cycle is controlled by multiple checkpoint mechanisms that sense DNA damage, activate repair mechanisms, and trigger cell death when damage cannot be repaired. Tumour suppressors are important cell cycle regulators that regulate cell senescence and death, ensuring that a cell with extensive damage dies or stops dividing. When these checkpoint proteins are absent or malfunctioning, damaged cells continue to grow. Although tumour suppressors protect an organism from the accumulation of damaged cells, they also contribute to tissue aging. As damaged and senescent cells are eliminated through cell death, cell pools responsible for tissue renewal and the maintenance of tissue function are depleted.

In humans and other organisms, tissues that undergo rapid self-renewal—lining of the gut, skin, hair follicles, and bone marrow—are the ones most affected by telomere shortening, cell senescence and cell death. Many age-related pathologies affect these tissues.

According to Dr. Autexier, many studies have shown a correlation between telomere shortening and replicative senescence, cell death and aging, and between telomere length maintenance, the presence of telomerase activity and cellular immortalization, longevity or cancer formation.

Telomere Disruption in Aging
Dr. Autexier explained that many characteristics of natural aging in humans are related to a decline in processes that require continuous cell renewal, or to defective safeguard mechanisms that prevent the occurrence and survival of cells with genomic abnormalities. These include declines in immune and bone marrow functions, skin thickness changes, reduced wound healing capacity, structural changes in epithelial tissues, loss of fertility, and increased incidence of cancer. Research now suggests that loss of telomere integrity is one of the key mechanisms that drive the aging and age-related pathologies.

Dr. Autexier described that premature human aging syndromes, such as Ataxia Telangiectasia, Werner Syndrome, and Dyskeratosis congenita (DKC), share phenotypic similarities with the normal aging process, such as cataracts, osteoporosis, hair graying, and neurodegeneration.5 These syndromes are associated with defects in genes implicated in the maintenance of genomic and telomeric integrity.

DKC phenotypes first present in tissues that undergo constant cell renewal, such as the gut, the epidermis, and the bone marrow.6,7 Patient populations with the autosomal dominant form of the disease demonstrate shorter telomeres, earlier disease onset and more severe symptoms with each successive generation. These results are consistent with a defective telomere maintenance process.

Various forms of DKC indeed arise from mutations in genes that are directly involved in maintaining telomere integrity. So far, DKC mutations have been identified in telomerase, in a component of the telomerase complex called hTR (human Telomerase RNA) and in the gene encoding Dyskerin, a protein that binds to hTR.8,9

The relationship between defective telomerase activity and the aging process was confirmed in the mTR knockout mouse model. Although these mice are viable, successive generations exhibit progressive shortening of telomeres and decreased fertility (the 6th generation being infertile).10 Interestingly, these mice also present reduced wound healing, hair loss and graying, reduced body weight, intestinal villi atrophy, bone marrow failure, and an increased incidence of cancer.11,12

Most phenotypes observed in this mouse model are similar to those seen in DKC patients and, to a certain extent, to age-related pathologies associated with normal human aging.13

Conclusion
Dr. Autexier closed by observing that there have been numerous studies in the last 4 years correlating telomere length and mortality, Alzheimer’s disease status, and longevity. Although these studies are generally correlative, it is interesting to see that more research is being done to look at telomere length as a marker for some diseases associated with aging.14,15,16

Telomere integrity is a key regulator of human aging and cancer formation, suggesting that proteins involved in telomere maintenance could represent molecular targets for therapeutic interventions in the fields of cancer and other age-related diseases.

References

  1. Blasco MA. Telomere length, stem cells and aging. Nat Chem Biol 2007;3:640-9.
  2. Bodnar AG, Ouellette M, Frolkis M, et al., Extension of life-span by introduction of telomerase into normal human cells. Science 1998;279:349-52.
  3. Campisi J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell 2005;120:513-22.
  4. Ithana K, Campisi J, Dimri GP. Mechanisms of cellular senescence in human and mouse cells. Biogerontol 2004;5:1-10.
  5. Hasty P, Campisi J, Hoeijmakers J, et al. Aging and genome maintenance: lessons from the mouse? Science 2003;299:1355-9.
  6. Kirwan M, Dokal I. Dyskeratosis congenita: a genetic disorder of many faces. Clin Genet 2008;73:103-12.
  7. Marciniak R, Guarente L. Human genetics. Testing telomerase. Nature 2001;413:370-3.
  8. Mitchell JR, Wood E, Collins K. A telomerase component is defective in the human disease dyskeratosis congenital. Nature 1999;402:551-5.
  9. Dokal I, Vulliamy T. Dyskeratosis congenita: its link to telomerase and aplastic anaemia. Blood Rev 2003;17:217-25.
  10. Blasco MA, Lee HW, Hande MP, et al. Telomere shortening and tumor formation by mouse cells lacking telomerase RNA. Cell 1997;91:25-34.
  11. Rudolph KL, Chang S, Lee HW, et al. Longevity, stress response, and cancer in aging telomerase-deficient mice. Cell 1999;96:701-12.
  12. Lee HW, Blasco MA, Gottlieb GJ, et al. Essential role of mouse telomerase in highly proliferative organs. Nature 1998;392:569-74.
  13. Marciniak RA, Johnson FB, Guarente L. Dyskeratosis congenita, telomeres and human ageing. Trends Genet 2000;16:193-5.
  14. Cawthon RM, Smith, KR, O’Brian E, et al. Association between telomere length in blood and mortality in people aged 60 years or older. Lancet 2003;361:393-5.
  15. Panossian LA, Porter VR, Valenzuela HF, et al. Telomere shortening in T cells correlates with Alzheimer’s disease status. Neurobiol Aging 2003;24:77-84.
  16. Nakamura K, Takubo K, Izumiyama-Shimomura N, et al. Telomeric DNA length in cerebral gray and white matter is associated with longevity in individuals aged 70 years or older. Experimental Gerontology 2007;42:944-50.

Sexuality in the Aging Couple, Part I: The Aging Woman

Sexuality in the Aging Couple, Part I: The Aging Woman

Teaser: 

Irwin W. Kuzmarov, MD, FRCSC, Assistant Professor, Department of Surgery (Urology), McGill University; Director of Professional and Hospital Services, Santa Cabrini Hospital, Montreal, QC; Past President, Canadian Society for the Study of the Aging Male.
Jerald Bain, BScPhm, MD, MSc, FRCPC, CertEndo, BA, Professor Emeritus, Department of Medicine, Department of Endocrinology and Metabolism, Mount Sinai Hospital; University of Toronto, Toronto, ON; Past President, Canadian Society for the Study of the Aging Male.

Sexuality and sexual activity do not end when a person reaches a certain age. Sexual desire and activity continue well into later life, and age is not a deterrent to a happy and healthy sex life. However, clinicians should be aware that the normal sexual response of men and women may change with aging. When sexual dysfunction occurs, studies show that men and women tend to view sexual dysfunction differently. Part I of this article addresses sexuality and sexual dysfunction in aging women; Part II (to appear in a forthcoming issue of Geriatrics & Aging) will address the male side of the picture. It is crucial that family doctors be aware of sexuality in the aging couple, and be able to evaluate and manage problems that may arise.
Key Words: aging, sexual activity, sexual dysfunction, women, testosterone therapy.

Age-Related Hearing Loss

Age-Related Hearing Loss

Teaser: 

Christopher Hilton, MD, Instructor, Department of Otolaryngology, University of Minnesota, Minneapolis, MN, USA.
Tina Huang, MD, Assistant Professor, Department of Otolaryngology, University of Minnesota, Minneapolis, MN, USA.

Age-related hearing loss (ARHL) is the most common neurosensory deficit associated with aging. It presents with a predictable pattern of sensorineural hearing loss, causing problems with communication that have been associated with depression and social isolation. Recent studies have improved our understanding of the etiology of ARHL on a molecular level. While treatment options exist with hearing aids and cochlear implants, prevention by identification and avoidance of key risk factors remains the best strategy for dealing with this disease.
Key words: presbycusis, age-related hearing loss, deafness, hearing aids, aging.

Personality Traits: Stability and Change with Age

Personality Traits: Stability and Change with Age

Teaser: 

Antonio Terracciano, PhD, Laboratory of Personality and Cognition, National Institute on Aging (NIA), National Institutes of Health (NIH), U.S. Department of Health and Human Services (DHHS), Baltimore, MD, USA.
Robert R. McCrae, PhD, Laboratory of Personality and Cognition, NIA, NIH, DHHS, Baltimore, MD, USA.
Paul T. Costa Jr., PhD, Laboratory of Personality and Cognition, NIA, NIH, DHHS, Baltimore, MD, USA.

Individual differences in personality traits are generally stable during adulthood; where there are changes, they are generally in the direction of greater maturity. The trends are similar for men and women and across cultures. With advancing age, people generally become more emotionally stable, agreeable, and conscientious, with better impulse control, but less active and less open to new actions and values than younger individuals. Those trajectories provide several insights into adult development, challenging some negative stereotypes about older adults and serving as a reminder that enduring individual differences are more important than age in understanding personality.
Key words: personality traits, aging, cross-cultural, depression, Alzheimer’s disease.

Nutritional Guidelines in Canada and the US: Differences between Younger and Older Adults

Nutritional Guidelines in Canada and the US: Differences between Younger and Older Adults

Teaser: 

Joan Pleuss, RD, MS, CDE, CD, Director, Bionutrion & Body Composition Units, Clinical & Translational Research Institute, Medical College of Wisconsin, Milwaukee, WI.

The requirement for some nutrients changes as adults age. The Dietary Reference Intakes, the 2007 Canada Food Guide, and the 2005 Dietary Guidelines for Americans (MyPyramid.gov) provide guidance for the consumer and the professional for nutritional needs throughout the life span. The Guidelines provide recommendations in user-friendly messages. MyPyramid.gov and the Food Guide allow the public to access information on the internet that is individualized for age, gender, and physical activity. The Dietary Reference Intakes provide the health professional with nutrition requirements for gender and specific age groupings through the entire lifespan. This article will address those nutrients whose requirements significantly change with adult aging.
Key words: Dietary Reference Intakes, Canada Food Guide, Dietary Guidelines of America, MyPyramid, aging, nutrition.

Aging in Africa

Aging in Africa

Teaser: 

Irene Turpie, MB, ChB, MSc, FRCP(C), FRCP (Glas), Professor Emeritus, McMaster University, Hamilton, Ontario.
Leigh Hunsinger, BA, Medical Student, McMaster University, Hamilton, Ontario.

Africa, with its many countries and ethnic groups, has a population of 800 million people and the highest rate of growth of the older adult population in the world. Urbanization and the HIV/AIDS epidemic are changing the traditional role of older adults. The epidemiological transition from acute infections to chronic diseases is occurring more slowly in Africa than in other continents but it is occurring. Many older persons are malnourished and live in poverty. Hypertension, stroke, osteoarthritis, chronic respiratory and mood disorders are expected to increase in incidence and are increasingly being identified in a continent without the resources or infrastructure as yet to mount preventive campaigns and to treat chronic health conditions. What is known about many older Africans is that they have the capacity to age well through daily exercise and healthy diets low in processed sugar and saturated fats. Aging Africans are generally regarded with respect and dignity. There is much that needs to be done to prevent deleterious aging outcomes for older adults in that continent and there is much we can learn about healthy aging and lifestyle prevention.
Key words: aging, Africa, epidemiological transition, developing nations, HIV/AIDS.

Unhealthy Alcohol Intake among Older Adults

Unhealthy Alcohol Intake among Older Adults

Teaser: 

Ann Schmidt Luggen, PhD, GNP, Professor Emeritus, Northern Kentucky University, Highland Heights, Kentucky, USA.

The number of older adults who drink to excess is not known, partly because primary health practitioners seldom screen for this problem. The signs of alcohol abuse are vague prior to late-stage liver failure and many of them are attributed to normal aging. Two types of alcohol dependence are commonly seen in older adults: type I is a late-onset alcohol dependence in which depression, chronic illness, or life changes such as retirement precipitate drinking, while type II is mainly genetic and reflects lifelong drinking that has not been previously identified by health professionals. Pharmacologic agents such as naltrexone and acamprosate have been shown in a number of clinical trials to be useful in care. A great many others are still in testing phases. Nonpharmacologic management is also effective, especially when teamed with drug therapy. Some of these are cognitive behavioural therapy, motivational enhancement therapy, and counselling that the primary care physician can do in the office, also known as the brief intervention approach. There is much that can be done if alcohol dependence is recognized.
Key words: alcohol, aging, older adults, dependence, liver disease.

The Impact of Anemia on Physical Function among Older Adults

The Impact of Anemia on Physical Function among Older Adults

Teaser: 

Cinzia Maraldi, MD, Department of Clinicial and Experimental Medicine, Division of Internal Medicine, Gerontology, and Geriatrics, University of Ferrara, Ferrrara, Italy; Department of Aging and Geriatric Research, College of Medicine, Institute on Aging, University of Florida, Gainesville, FL, USA.
Marco Pahor, MD, Department of Aging and Geriatric Research, College of Medicine, Institute on Aging, University of Florida; Geriatric Research, Education and Clinical Center (GRECC), Malcolm Randall Veteran’s Affairs Medical Center, Gainesville, FL, USA.

Maintaining independence is one of the major goals in geriatric care, and identification of modifiable conditions that may promote the onset and progression of disability is of paramount importance in the clinical approach to the older patient. Anemia is key among those factors that may affect physical function in older adults. It is a common condition that appears to predict the onset of functional decline and disability in older adults. Early diagnosis of anemia and identification of its underlying causes is important not only in order to prevent the condition from worsening but also to prevent its associated poor health outcomes.
Key words: anemia, aging, disability, hemoglobin, functional decline.