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Exercise’s Impact on Cognition

/22 September 2021/ All MFN blog/

It’s not news that the brain changes with age. Significant changes in regions of the brain occur in healthy adults as they age, based on MRI studies.(1) The caudate, cerebellum, hippocampus, and association cortices shrunk substantially. This shrinkage in the hippocampus and the cerebellum accelerates with age. The hippocampus, the site for new memory formation, is involved with learning and emotion with a rich supply of estrogen and progesterone receptors. The cerebellum coordinates voluntary movements including all conscious muscular activity, balance, coordination, and speech.

Incidence of Dementia

The United States is experiencing both a declining birth rate and an increased average life span. This combination will increase the percentage of people over the age of 65 to 19.6%, resulting in a total of 71 million people by the year 2030.(2) The number of people over the age of 80 is also expected to increase to 19.5 million by 2030.(2) These changes will greatly increase the number of people with dementia since 6% to 10% of North American individuals aged 65 or older have dementia; this increases to 30% in those aged 85 or over.(3)

Dementia, or senility, is a difficult-to-define cluster of symptoms that include memory loss, loss of vocabulary, and loss of motor function in the absence of a change in the level of consciousness. Dementia can be measured qualitatively by verbal memory tests such as the Blessed Orientation-Memory-Concentration test, comprising six questions as listed in the following table:

The scores from each of the table’s six items are multiplied to produce a weighted score. Score 1 for each incorrect response; weighted error scores greater than 10 are consistent with dementia.(4)

Exercise Affects the Brain

The incidence of Alzheimer’s dementia can be used as a measurement of brain health.(5) As part of his study “Exercise Is Associated With Reduced Risk for Incident Dementia Among Persons 65 Years of Age and Older,” Eric B. Larson, MD, MPH, et al asked 1,740 mentally healthy men and women over the age of 65 how many days per week over the past year they had exercised for at least 15 minutes. The incidence of Alzheimer’s disease (AD) was significantly higher for individuals who exercised fewer than three times per week (19.7 per 1,000 person-years) compared with those who exercised more than three times per week (13 per 1,000 person-years). These results were not influenced by the E4 alleles on the apolipoprotein gene, which indicates a genetic predisposition for AD.

Laura Podewils et al studied the relationship between physical activity and dementia in 3,375 men and women over the course of 5.4 years.(6) Physical activity in these individuals over the age of 65 was assessed via the Minnesota Leisure Time Questionnaire. The subjects were questioned regarding the frequency and duration of their physical activity over the previous two weeks. Like Larson et al, this study found that increased exercise decreased the incidence of Alzheimer’s dementia.

The Mini-Mental State Exam can be used as a measure of cognitive ability or impairment. The 30-point questionnaire commonly used by health care providers screens for dementia, evaluates cognitive impairment, and follows cognitive change over time, making it an effective way to document an individual’s response to treatment.(7) Kristine Yaffe, MD, et al used the Mini-Mental State Exam to show that cognitive performance increases as the number of blocks walked per week increases.(8) The study involved 5,925 women over the age of 65 over a six- to eight-year period.

The most objective measure of cardiovascular fitness is the measurement of the maximum rate of oxygen consumption as measured during incremental exercise—milliliters of oxygen per kilogram of body mass per minute. A subjective measure of exercise amount or duration is not as accurate as the above direct measure, which is called maximum oxygen consumption or VO2 max. Deborah Barnes, PhD, et al conducted a six-year study of 349 individuals over the age of 55 measuring both VO2 max and subjective measures of fitness. Barnes found only the lower levels of VO2 max correlated with cognitive decline.(9) The four studies mentioned show a positive cognitive benefit from exercise. A meta-analysis performed by Colcombe and Kramer from 1966 to 2001 examined 18 studies of fitness training and cognitive function in nondemented older adults. They concluded that fitness training had a positive influence on cognition.(10)

Prospective controlled human studies provide more robust data than both animal and uncontrolled studies. Stanley J. Colcombe et al were the first to show in a prospective controlled setting that increases in cardiovascular fitness in humans results in increased functioning of the prefrontal and parietal cortices. These data suggest that increased cardiovascular fitness can affect improvements in the plasticity of the aging human brain and may serve to reduce both biological and cognitive senescence in humans.(11) In addition, women tended to exhibit the greater benefit.(12) In a literature review, Kramer et al complemented these data through the use of MRI, which is very accurate in the brain. Through this technique, Kramer and colleagues concluded that older adults who participated in the aerobic training group demonstrated a significant increase in gray matter volume in regions of the frontal and superior temporal lobe when compared with controls. The results suggest that even relatively short exercise interventions can begin to restore some of the losses in brain volume associated with normal aging.(12)

Animal studies offer some insight into how aerobic exercise benefits brain function. Aerobic exercise increases brain function in both young and old animals. Aerobic exercise increases the levels of brain-derived neurogenic factor (BDNF) and insulinlike growth factor 1 (IGF-1). BDNF has been shown to regulate neurotransmitters, including dopaminergic and cholinergic systems and may be playing an important role in the exercise-induced effects on the brain.(13) BDNF may be involved in the postexercise changes seen on a brain MRI. In addition, IGF-1 may be mediating the effects of exercise on BDNF, neurogenesis, and cognitive performance. Animal studies provide information on the effects of exercise that is difficult to obtain in human intervention studies. The sum of these animal studies overlaps with results from human studies and suggests that exercise is an effective enhancer of neurocognitive functioning in both young and old animals.(12)

AD, the most common form of dementia, shares many age-related pathophysiological features of type 2 diabetes, including insulin resistance, disrupted glucose metabolism in nonneural tissues, peripheral oxidative and inflammatory stress, amyloid aggregation, neural atrophy, and cognitive decline. Brain insulin resistance appears to be an early and common feature of AD, a phenomenon accompanied by IGF-1 resistance, promoting cognitive decline independent of classic AD pathology.(14) Such a large set of shared features suggests shared etiologies.

Recommendation

High-intensity interval training (HIIT) is a type of endurance training involving short periods of maximal effort followed by periods of maintenance or recovery effort. What can differ is the timing and type of endurance exercise. A typical cycling HIIT pattern may be four to six maximal 30-second cycling sprints separated by 4.5-minute recovery periods of comfortable cycling. When HIIT is compared with longer steady endurance training, the HIIT patterns show increased mitochondrial density in muscle cells and greater muscle performance improvements.(15,16)

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This article was featured in Today’s Geriatric Medicine.

Today’s Geriatric Medicine is a bimonthly trade publication offering news and insights for professionals in elder care.

Get a Free Subscription to Today’s Geriatric Medicine

 

This article was featured in the Jan/Feb 2016 issue of Today’s Geriatric Medicine (Vol. 9 No. 1 P. 26). Written by Robert Drapkin, MD

Robert Drapkin, MD, a medical oncologist and competitive bodybuilder in Clearwater, Florida, specializes in helping elderly adults achieve a healthful lifestyle to combat illnesses or disease and to extend lifespan.

 

References

1. Raz N, Lindenberger U, Rodrigue KM, et al. Regional brain changes in aging healthy adults: general trends, individual differences and modifiers. Cereb Cortex. 2005;15(11):1676-1689.

2. Chapman DP, Williams SM, Strine TW, Anda RF, Moore MJ. Dementia and its implications for public health. Prev Chronic Dis. 2006;3(2):A34.

3. Hendrie HC. Epidemiology of dementia and Alzheimer’s disease. Am J Geriatr Psychiatry. 1998;6(2 Suppl 1):S3-S18.

4. The Blessed Orientation-Memory-Concentration Test. University of Missouri Geriatric Examination Tool Kit website. http://geriatrictoolkit.missouri.edu/cog/bomc.pdf.

5. Larson EB, Wang L, Bowen JD, et al. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann Intern Med. 2006;144(2):73-81.

6. Podewils LJ, Guallar E, Kuller LH, et al. Physical activity, APOE genotype, and dementia risk: findings from the Cardiovascular Health Cognition Study. Am J Epidemiol. 2005;161(7):639-651.

7. Pangman VC, Sloan J, Guse L. An examination of psychometric properties of the mini-mental state examination and the standardized mini-mental state examination: implications for clinical practice. Appl Nurs Res. 2000;13(4):209-213.

8. Yaffe K, Barnes D, Nevitt M, Lui LY, Covinsky K. A prospective study of physical activity and cognitive decline in elderly women: women who walk. Arch Intern Med. 2001;161(14):1703-1708.

9. Barnes DE, Yaffe K, Satariano WA, Tager IB. A longitudinal study of cardiorespiratory fitness and cognitive function in healthy older adults. J Am Geriatr Soc. 2003;51(4):459-465.

10. Colcombe S, Kramer AF. Fitness effects on the cognitive function of older adults: a meta-analytic study. Psychol Sci. 2003;14(2):125-130.

11. Colcombe SJ, Kramer AF, Erickson KI, et al. Cardiovascular fitness, cortical plasticity, and aging. Proc Natl Acad Sci U S A. 2004;101(9):3316-3321.

12. Kramer AF, Erickson KI, Colcombe SJ. Exercise, cognition, and the aging brain. J Appl Physiol (1985). 2006;101(4):1237-1242.

13. Knüsel B, Winslow JW, Rosenthal A, et al. Promotion of central cholinergic and dopaminergic neuron differentiation by brain-derived neurotrophic factor but not neurotrophin 3. Proc Natl Acad Sci U S A. 1991;88(3):961-965.

14. Talbot K, Wang HY, Kazi H, et al. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. J Clin Invest. 2012;122(4):1316-1338.

15. Gibala M. Molecular responses to high-intensity interval exercise. Appl Physiol Nutr Metab. 2009;34(3):428-432.

16. Billat VL. Interval training for performance: a scientific and empirical practice. Special recommendations for middle- and long-distance running. Part I: anaerobic interval training. Sports Med. 2001;31(1):13-31.

Senior-and-Trainer

Dementia Doesn’t Invalidate Exercise Needs

/8 June 2021/ All MFN blog/

With careful capability assessment and appropriate program design, exercise regimens can improve walking, balance, and flexibility and reduce falls in patients with dementia.

“Ruth, sit down! Don’t get up on your own.”
Who is that? Why is she yelling at me? I need to get up. My legs are stiff and I want to go for a walk.

“Ruth, stop getting up. You’re going to fall.”
Stop yelling at me. Who are these people? I feel so anxious. All I want to do is go for a walk. Why can’t I just go for a walk? I have walked by myself my whole life.

In working with older adults, many of us have witnessed circumstances similar to this. Often staff wish to maintain the safety and security of individuals living with dementia by limiting their independent mobility and ambulation. But are we truly protecting these individuals who are at risk? What are the ramifications of our actions? Movement and mobility are important foundations to maintaining strength, balance, flexibility, and continence; reducing anxiety and depression; and maintaining social relationships.

To this point, the positive impact of exercise in older adults is well documented in the literature. Exercise programs have been found to result in more favorable physical, social, and emotional health status and fewer activities of daily living impairments in the elderly.(1) These optimistic results provide support for older adults’ exercise groups to improve quality of life and reduce the burden of care for at-risk populations, including those with dementia.

While many focus on the cognitive effects of dementia, the physical aspects are also pronounced. Frequently noted are gait changes including a decrease in step length, step height, and reduction in cadence. These are compounded by balance deficits associated with a reduction in coordination, proprioception, and vision. To further aggravate the situation, the physical effects also can result in expressive and receptive communication deficits. As a result, patients living with dementia can have difficulty communicating these issues, as well as pain.

Effects of Exercise on Individuals With Dementia

Randomized controlled trials of patients with dementia or mild cognitive impairment have indicated improved cognitive scores after six to 12 months of aerobic exercise when compared with a sedentary population.(2) Other benefits associated with aerobic activity include the reduction of osteoporosis and fracture risk,(3) as well as a reduction in mortality risk.(4) Aerobic activity has also been noted to have other beneficial effects on secondary diagnoses associated with dementia including depression,5 anxiety,6 and behavior management.(7)

While the exact causative reasons for these beneficial outcomes are not fully understood, many studies favor the view that the cerebrovascular benefits exercise has on other body systems can be applied to the neurodegenerative process of dementia. Furthermore, evidence exists that aerobic exercise reduces the progression of the neurodegenerative process through facilitation of neuroprotective factors and neuroplasticity.(8)

The positive effects of exercise have also been found in individuals living with dementia who are already experiencing negative physical outcomes. Toulotte et al studied the effects of physical training on frail patients with dementia with a history of falls.(9) The training group was noted to have improved walking, flexibility, and balance, and a reduction in falls. Furthermore, Huusko et al evaluated the impact with hip fracture patients who also had mild/moderate dementia. Those who received intensive rehab were found to have shorter lengths of hospital stay and greater ability to return to the community than those in the control group.(10)

Developing an Exercise Prescription

Regardless of the reasons behind the beneficial effects of exercise on individuals with dementia, it’s necessary to evaluate each patient individually before initiating an exercise program. This includes an interdisciplinary review of an individual’s age, prior exercise involvement, and comorbid medical conditions. Based on the findings, an appropriate exercise program can then be initiated using the American Heart Association’s recommendation of 150 minutes per week of moderately strenuous physical activity.(11) These minutes of exercise can be divided over any number of days per week and with any number of sessions per day. For patient tolerance purposes, these sessions are often kept to between 15 and 30 minutes.

What type of exercise is appropriate for a patient to perform? For individuals with dementia, similar to those without, it is important to focus on their interests. Understanding these interest levels requires investigation. For some patients, this investigation may be complicated by apathy, aggressive behaviors, pain, and communication difficulties.

Depending on the severity of the disease, a focused understanding of a patient’s short- and long-term memory recall is necessary. While older adults without dementia may have a strong recall of their short- and long-term interests, this may not be true of an individual with dementia. Therefore, for those with intact long-term memory, we need to obtain the relevant information. Maybe interests include running, ballroom dancing, bowling, bicycling, gardening, or swimming. If patients can’t physically perform these activities, should we just give up? Of course not. We need to improvise. For example, ballroom dancing may now require walkers, or bicycling may need to be on stationary recumbent bikes with scenery posted around the bicycle.

Case Study

Ms. T is a 53-year-old female who presented to the Hebrew Home at Riverdale skilled nursing facility with a diagnosis including vascular dementia. Prior to initiating a therapy-based warm water program, Ms. T required intermittent assistance walking with a rollator. Her cognition was limited to the point that she could not participate in interviews on the Minimum Data Set (MDS). Despite significant staff efforts to minimize any emotional or environmental disturbances, she experienced periods of agitation. She completed a standardized assessment of her mobility, utilizing the Timed Up and Go (TUG) assessment, completing it in 32 seconds.

At that time, a land- and water-based exercise program with a three-days-per-week frequency was initiated with a physical therapist and dance movement therapist. The hypothesis behind this program was that through the use of multiple therapeutic modalities, gains in strength, balance, cognition, emotional support, and socialization would be achieved. Strength, balance, and functional tasks including ambulation with buoyancy in multiple planes, rotational activities, plyometrics, and resistive activities were implemented. For cognition, behavioral management, and emotional support purposes, music, singing, mental imagery, and floatation were incorporated into individual sessions.

After two months of participating in this innovative program, Ms. T was walking independently without an assistive device. She had also demonstrated an improvement in TUG assessment, completing the test in 10 fewer seconds. Additionally, Ms. T was noted to have experienced an improvement in her cognition, as she was now able to participate in interviews for the MDS. Most meaningful was that Ms. T rediscovered her smile. Tenaya Cowsill, MS, R-DMT, LCAT-P, reported that “this program has been an incredibly meaningful source of joy, autonomy, and pride” for Ms. T.

The Power of Dance

Dance/movement therapy (DMT) is an evidence-based movement approach to psychosocial health and well-being. The American Dance Therapy Association defines DMT as “the psychotherapeutic use of movement to further the emotional, cognitive, physical, and social integration of the individual.”(12) Therapists are board-certified licensed mental health professionals who use movement as a tool to explore, support, and strengthen clients’ emotional needs and coping mechanisms.

DMT can result in both positive physical and emotional outcomes, including a “sense of community, decreasing the experience of emotional isolation, and enriched relational interaction.”(13) Because this modality comprises both verbal and nonverbal interventions, it is especially appropriate for older adults with memory loss who are affected by the expressive and receptive communication difficulties.

The American Dance Therapy Association describes the emotional benefits and processes in treatment for older adults. “Individuals’ capacities and incapacities are explored, and accompanying feelings are expressed. Mourning, frustration, joy, and laughter can be ritualized in group movement, allowing for emotional release and group bonding.”(14)

The physical benefits of exercise and movement have been detailed in previous sections of this article. DMT, which places a focus on mental and emotional health, provides additional benefits as its holistic process includes “physical activity or exercise [and also] … learning, attention, memory, emotion, rhythmic motor coordination, balance, gait, visuospatial ability, acoustic stimulation, imagination, improvisation, and social interaction.”(15)

Older adults, especially those living with memory loss, may struggle with coordinated movement due to changes in brain functioning. Dance therapy welcomes all levels of functioning, encouraging engagement from an individual’s baseline, wherever that may be.

The creative, fluid, psychodynamic process allows for relatedness and engagement with multiple levels of functioning. A primary practice of a dance/movement therapist is one of embodied mirroring defined as the “somatic attunement of the therapist in face-to-face engaged interaction,”(13) which physically communicates to individuals living with memory loss that they are seen and understood. In a time when communication is often impaired, embodied mirroring provides an important tool for validating a patient’s experience.(15) As clinician Kalila B. Homann, MA, LPC-S, BC-DMT, wrote, “Mirroring is practiced by the therapist in DMT as a way to enhance emotional resonance between a therapist and patient … when a therapist mirrors the client’s emotional movements, the therapist is communicating this understanding and acceptance nonverbally.”

On a neurological level this intervention activates the brain’s mirror neuron system. From the neuroscience lens, mirror neurons are thought to be the determining factor in our capacity for empathy and interrelatedness.(13,16) This neurophysiological process “coordinates auditory and visual perception of nonverbal communication by tracking movement and expression in others—replicating the patterns of activation in the brain of the observer.” A resident with memory loss thus experiences validation on a neurobiological level. In dementia, because of the changes in communication that often occur due to brain deterioration, the benefits of emotional attunement from a therapist cannot be overstated. This need for witnessing and validation is a basic human need that does not change with dementia.

Case Study

Ms. M was a 92-year-old woman living in a skilled nursing neighborhood at the Hebrew Home at Riverdale. She carried a diagnosis of mild memory impairment and was a vibrant and active member of the community. She expressed and demonstrated a love for music. She would ambulate throughout the home with her walker, attending a wide variety of programs and actively socializing.

After suffering a stroke, her life shifted. She became reliant on a wheelchair for mobility, and her speech, gait, balance, and cognition were all impaired. This medical event also triggered an exacerbation of major depression, something she had lived with throughout her life. Through working with the rehabilitation team, she demonstrated improvements in functioning; however, major depression remained an impediment to treatment. As her therapy was reaching completion, she was transitioned via a warm handoff to DMT twice weekly from her wheelchair.

During group sessions, she presented with bright affect and eye contact, which was supported and validated by the therapist facilitating the group. In the therapeutic group space, Ms. M was able to both verbally and nonverbally express her grief and frustration with her condition. She spoke about her depression and was able to verbally and physically process her feelings through creative expression within the therapeutic alliance. Ms. M was able to “engage physiological processes related to emotion and make them more available to the conscious mind,” as Homann’s writings suggest. Through increased awareness Ms. M was able to more fully process and express her depressive symptoms, enabling her to further her treatment.

As dance therapy progressed, Ms. M began to increase her interpersonal relatedness, making eye contact with peers, sharing memories and physical gestures of connection. Ali Schechter, LCAT, R-DMT, her dance/movement therapist, states: “[Ms. M’s] movement generates vitality which results in expression.” Through the therapeutic alliance, this expression was validated, supporting Ms. M’s improved mood state.

As her mood state improved through DMT, Ms. M expressed the desire to begin standing and walking again. In addition to mood state support, DMT focused on movement of the spine, core, and hips, aiding in body strengthening for standing. The interdisciplinary team referred her for further physical therapy, and she began standing and, at times, walking with her walker for short periods. She continues to be an active participant in DMT sessions.

Blending Therapy Modalities

Maintaining and improving fitness and well-being remains an important evidence-based practice in our society. This is further magnified for older adults, especially those living with dementia. While the benefits of fitness programs remain the same for this population, the prescription for achievement may require a blended approach. Therapies, inclusive of physical and dance/movement, share many common strengths and goals. Therefore, the ability of these modalities to partner provides opportunities for improved mental, physical, and emotional health. The goal in all treatment is the well-being of residents, and care teams should use interdisciplinary tools and modalities toward that goal.

Get a Free Subscription to Today’s Geriatric Medicine

This article was featured in Today’s Geriatric Medicine.

Today’s Geriatric Medicine is a bimonthly trade publication offering news and insights for professionals in elder care.

Get a Free Subscription to Today’s Geriatric Medicine

 

This article was featured in the March/April 2018 issue of Today’s Geriatric Medicine (Vol. 11 No. 2 P. 14). Written by David Siegelman and Mary Farkas.

 David Siegelman, PT, RAC-CT, is the vice president of rehabilitation at the Hebrew Home at Riverdale in Bronx, New York. In this role he oversees the operation of the short-term rehabilitation units, clinical documentation and reimbursement department, and rehabilitation department. Having entered the field as a physical therapist, he has demonstrated expertise in clinical and systems management in acute care hospitals and skilled nursing facilities over the past 20 years.

Mary Farkas, RDT, LCAT, CDP, is the director of therapeutic arts and enrichment programs at the Hebrew Home at Riverdale. She is a licensed creative arts therapist who specializes in the intersection of dementia, end-of-life care, and mental health.

 

References

  1. Hamar B, Coberley CR, Pope JE, Rula EY. Impact of a senior fitness program on measures of physical and emotional health and functioning. Popul Health Manag. 2013;16(6):364-372.
  2. Smith PJ, Blumenthal JA, Hoffman BM, et al. Aerobic exercise and neurocognitive performance: a meta-analytic review of randomized controlled trials. Psychosom Med. 2010;72(3):239-252.
  3. Rizzoli R, Bruyere O, Cannata-Andia JB, et al. Management of osteoporosis in the elderly. Curr Med Res Opin. 2009;25(10):2373-2387.
  4. Lee DC, Artero EG, Sui X, Blair SN. Mortality trends in the general population: the importance of cardiorespiratory fitness. J Psychopharmacol. 2010;24(4 Suppl):27-35.
  5. Conn VS. Depressive symptom outcomes of physical activity interventions: meta-analysis findings. Ann Behav Med. 2010;39(2):128-138.
  6. Dunn AL. Review: exercise programmes reduce anxiety symptoms in sedentary patients with chronic illnesses. Evid Based Ment Health. 2010;13(3):95.
  7. Teri L, Gibbons LE, McCurry SM, et al. Exercise plus behavioral management in patients with Alzheimer disease: a randomized controlled trial. JAMA. 2003;290(15):2015-2022.
  8. Ahlskog JE, Geda YE, Graff-Radford NR, Petersen RC. Physical exercise as a preventive or disease-modifying treatment of dementia and brain aging. Mayo Clin Proc. 2011;86(9):876-884.
  9. Toulotte C, Fabre C, Dangremont B, Lensel G, Thévenon A. Effects of physical training on the physical capacity of frail, demented patients with a history of falling: a randomised controlled trial. Age Aging. 2003;32(1):67-73.
  10. Huusko T, Karppi P, Avikainen V, Kautiainen H, Sulkava R. Randomised, clinically controlled trial of intensive geriatric rehabilitation in patients with hip fracture: subgroup analysis of patients with dementia. BMJ. 2000;321(7269):1107-1111.
  11. Nelson ME, Rejeski WT, Blair SN, et al. Physical activity and public health in older adults: recommendation from the American College of Sports Medicine and the American Heart Association. Circulation. 2007;116(9):1094-1105.
  12. What is dance/movement therapy? American Dance Therapy Association website. https://adta.org/. Retrieved January 7, 2018.
  13. Homann KB. Embodied concepts of neurobiology in dance/movement therapy practice. Am J Dance Ther. 2010;32(2):80-99.
  14. American Dance Therapy Association. Dance/movement therapy & the older adult. https://adta.org/wp-content/uploads/2015/12/DMT-with-the-Elderly.pdf. Accessed January 7, 2018.
  15. Kshytriya S, Barnstaple R, Rabinovich DB, DeSouza JFX. Dance and aging: a critical review of findings in neuroscience. Am J Dance Ther. 2015;37(2):81-112.
  16. Iacoboni M. Mirroring People: The New Science of How We Connect With Others. New York, NY: Farrar, Strauss and Giroux; 2008.
fitness-dumbells-exercise

Exercise and Dementia — Does Physical Activity Provide Cognitive Benefits?

/14 April 2021/ All MFN blog/

The World Health Organization recommends regular physical exercise—both aerobic and strength training—for older individuals as a means of reducing cognitive decline.1 However, studies on the effects of exercise on cognitive function in individuals with dementia have produced mixed results. While some research indicates a positive effect, other studies have failed to find clear benefits. Thus, the question remains: Is exercise actually effective at slowing down cognitive decline in individuals with dementia?

Evidence in Favor: Cognitive Benefits in Dementia

Repeated randomized controlled trials have found that various types of exercise programs produce cognitive benefits in dementia over a three- to four-month period. For example, one trial of 40 community-dwelling adults with mild to moderate dementia examined the impact of a four-month home-based exercise intervention consisting of strength and balance training exercises plus daily walking. Those in the exercise group showed improved scores on the Mini-Mental State Examination (MMSE) over baseline as compared with controls. (2) Similarly, a Belgian trial of 25 patients with moderate to severe dementia found that a program of daily physical exercises supported by music produced significant improvements in cognition on both the MMSE and the fluency subtest of the Amsterdam Dementia Screening Test 6 compared with controls. (3) Multiple other trials have produced similar results. (4-7)

A weakness of most randomized controlled trials showing a cognitive benefit of exercise in dementia is that the study populations have been small. One 2016 trial, however, tested a moderate- to high-intensity exercise intervention in a larger sample: 200 community-dwelling patients with mild Alzheimer’s disease (AD). Participants were randomized to either a supervised exercise group (one-hour sessions three times per week for four months) or to a control group. The study found no effect on cognition in the exercise group as a whole; however, in an exploratory analysis, the researchers found a possible beneficial impact on cognition among those who were most consistent in attending exercise sessions and who exercised at the greatest intensity, suggesting a dose-response relationship between exercise and cognition. (8)

Evidence Against: No Cognitive Benefits in Dementia

Although a range of studies suggest that exercise has a benefit for dementia treatment, other studies have found no such benefit. Such was the case, for example, with a 2017 Swedish trial of nearly 200 individuals with dementia in a nursing home setting. Participants were randomized either to a four-month high-intensity exercise intervention or to a seated attention control activity. The exercise intervention had no benefit for either global cognition or executive function over control, relative to baseline measures. This was true regardless of the sex of the participants, their forms of dementia, and their cognitive levels at baseline. (9)

In the case of the Swedish trial, the researchers hypothesized that the lack of benefit could be due to the fact that the exercise intervention focused on strength training rather than aerobic exercise. But a 2018 randomized control trial from British researchers produced no better results with aerobic exercise. In this large, carefully designed trial of almost 500 participants with mild to moderate dementia, participants were assigned to either an exercise group (which included both aerobic exercise and strength training) or to a usual-care group. Not only did exercise fail to produce cognitive benefits, but those in the exercise group actually demonstrated slightly worse cognition at the end of 12 months than did those in the usual care group. (10)

Mixed Results From Meta-Analyses and Systematic Reviews

The mixed results in individual randomized trials mirror the contradictory findings of several recent meta-analyses and systematic reviews.

Specifically, a 2015 systematic review of 17 randomized controlled trials found only very limited benefits of exercise in dementia—namely, researchers concluded that exercise programs may improve ability to do activities of daily living in dementia, but that exercise provides no benefits for cognition, neuropsychiatric symptoms, or depression. (11)

By contrast, however, two other recent meta-analyses reached the opposite conclusion and have affirmed the benefits of exercise—especially aerobic exercise—for cognition in dementia. The first of these meta-analyses, published in 2016, found that exercise has a positive benefit on cognition in both AD and other dementias and that both high-frequency and low-frequency exercise programs are beneficial. (12)

The second meta-analysis with a positive result, published in 2018, included 19 randomized controlled trials involving patients with AD as well as those at high risk of AD. This meta-analysis found that exercise interventions appear to slow cognitive decline in both groups—in those who have AD as well as in those at risk of the disease. (13)

Resolving the Inconsistencies

To make sense of the inconsistencies, a first point of note is that the research on exercise and its impact on cognition in dementia is still in its infancy. “There are a relatively small amount of studies that examine this relationship and there are still many unknowns due to limitations of the current literature,” says Gregory Panza, MS, an exercise physiologist at Connecticut’s Hartford Hospital and lead author of the 2018 meta-analysis referenced previously that found a positive benefit of aerobic exercise on cognition in dementia.

Not only are there a limited number of studies, but many of those that are available have been small and of relatively poor methodological quality. In fact, the authors of the 2015 systematic review that found no cognitive benefits of exercise in dementia explicitly noted that there was considerable unexplained heterogeneity in the analysis, and that the quality of the evidence was “very low.” (11)

With respect to meta-analyses in particular, Panza, a doctoral candidate in the department of kinesiology and the Human Performance Laboratory at the University of Connecticut, notes a major weakness of several analyses that have found a lack of impact of exercise on cognition: Namely, they have included mixed samples of people with multiple types of dementia (AD, vascular dementia, and other types of dementia) and analyzed them all together as one sample, rather than examining each group separately. “This is an issue because there are several physiological differences among the different types, and as a result, exercise may be affecting each type of dementia differently,” Panza says. Additionally, previous meta-analyses usually have failed to examine moderators such as age and gender. It’s important to examine moderators, he says, “because it gives you valuable information on which variables may be influencing the impact that the exercise is having on cognitive function.”

To address these limitations of previous research, Panza and his coauthors adhered to high-quality methodological reporting standards in their own 2018 meta-analysis, suggesting that their group’s finding of a positive cognitive benefit of exercise in dementia may carry more weight than the negative findings of some previous analyses. In their study, Panza and his colleagues also conducted within-group analyses (in which they compared cognitive changes both before and after the intervention for both the exercise and control groups), rather than merely conducting a between-group analysis as had previous meta-analyses. The within-group analysis allowed the group to take into account the cognitive decline that occurs naturally with untreated disease in the control group, and this analysis revealed the novel finding that exercise could improve cognition among controls. Overall, then, the Panza’s meta-analysis offers important support to the hypothesis that exercise can indeed slow cognitive decline in dementia.

Exercise in Midlife Protects Against Dementia

In addition to the evidence about the effect of exercise on cognition in individuals who already have dementia, there’s also a body of research on the effects of mid- to late-life exercise on future risk of cognitive impairment. (14) For instance, in a longitudinal study of women spanning 44 years, high levels of physical fitness were associated with a significantly reduced risk of dementia several decades later as compared with medium levels of physical fitness; in fact, high levels of physical fitness delayed onset of dementia by 9.5 years compared with medium fitness. (15)

Some research suggests that exercise may have especially significant benefits for individuals at highest genetic risk for dementia. A 2014 study, for instance, examined a group of 97 cognitively normal adults and compared how high vs low levels of physical activity correlated with each group’s hippocampal volume over the following 18 months. Researchers found that exercise had no apparent impact on hippocampal volume in those without genetic risk. But in those at genetic risk (that is, carriers of the APOE-E4 allele), low levels of physical activity were associated with a decline in hippocampal volume. This same group of less-active, higher-risk individuals was also more likely to show both cognitive and functional decline over the study period. (16)

According to Stephen Rao, PhD, Ralph and Luci Schey Endowed Chair at the Cleveland Clinic Lou Ruvo Center for Brain Health, a main mechanism by which exercise is thought to affect dementia risk is by affecting inflammation. “What exercise seems to be doing is reducing the amount of inflammation that ultimately is a very important factor in the progression of the disease. The disease is going on for 10 to 15 years prior to its diagnosis. So anything you can do to alter processes like inflammation can make a big dent in the rate of progression of the disease.”

To be clear, not all research shows a protective benefit of exercise against dementia: One 2018 systematic review and meta-analysis found that randomized controlled trials on exercise for dementia prevention are limited, but that the existing evidence does not show any significant effect of exercise in terms of reducing dementia risk. (17)

However, several other meta-analyses have come to the opposite conclusion. A 2011 meta-analysis of 15 prospective studies that included a total of more than 33,000 subjects without dementia concluded that all levels of physical exercise, from low to high, offer a significant and consistent protective effect (-35% or greater) against cognitive decline. (18) Similarly, a 2016 meta-analysis of 10 high-quality prospective observational cohort studies found that those who were more active had a 35% to 40% lower chance of developing AD than did those who were less active. (19)

Implications for Providers

According to Panza, there are still significant gaps in the research on exercise and dementia, and there’s a need for considerably more research using neuroimaging and molecular markers to examine the neuropsychological, electrophysiological, and pathophysiological effects that exercise has on dementia. Still, he recommends exercise—especially aerobic exercise—as a valuable treatment option for those who have dementia or are at risk. “Not only is there evidence that exercise can delay the onset of Alzheimer’s disease but the physical benefits of exercise may also help their patients keep their independence longer.”

Rao likewise acknowledges the unknowns, but he too affirms that exercise appears to be an important means of reducing dementia risk. “Exercise is key. It’s never too late. Providers should really encourage their patients to exercise, within reason, within their level of fitness.”

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This article was featured in Today’s Geriatric Medicine.

Today’s Geriatric Medicine is a bimonthly trade publication offering news and insights for professionals in elder care.

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This article was featured in the May/June 2019 issue of Today’s Geriatric Medicine (Vol. 12 No. 3 P. 6). Written by Jamie Santa Cruz, a health and medical writer in the greater Denver area. Reprinted with permission from Today’s Geriatric Medicine.


References

1. Physical activity and older adults. World Health Organization website. http://www.who.int/dietphysicalactivity/factsheet_olderadults/en. Accessed October 30, 2018.

2. Vreugdenhil A, Cannell J, Davies A, Razay G. A community-based exercise programme to improve functional ability in people with Alzheimer’s disease: a randomized controlled trial. Scand J Caring Sci. 2012;26(1):12-19.

3. Van de Winckel A, Feys H, De Weerdt W, Dom R. Cognitive and behavioural effects of music-based exercises in patients with dementia. Clin Rehabil. 2004;18(3):253-260.

4. Kemoun G, Thibaud M, Roumagne N, et al. Effects of a physical training programme on cognitive function and walking efficiency in elderly persons with dementia. Dement Geriatr Cogn Disord. 2010;29(2):109-114.

5. Arcoverde C, Deslandes A, Moraes H, et al. Treadmill training as an augmentation treatment for Alzheimer’s disease: a pilot randomized controlled study. Arq Neuropsiquiatr. 2014;72(3):190-196.

6. Öhman H, Savikko N, Strandberg TE, et al. Effects of exercise on cognition: The Finnish Alzheimer Disease Exercise Trial: a randomized, controlled trial. J Am Geriatr Soc. 2016;64(4):731-738.

7. Cancela JM, Ayán C, Varela S, Seijo M. Effects of a long-term aerobic exercise intervention on institutionalized patients with dementia. J Sci Med Sport. 2016;19(4):293-298.

8. Hoffmann K, Sobol NA, Frederiksen KS, et al. Moderate-to-high intensity physical exercise in patients with Alzheimer’s disease: a randomized controlled trial. J Alzheimers Dis. 2016;50(2):443-453.

9. Toots A, Littbrand H, Boström G, et al. Effects of exercise on cognitive function in older people with dementia: a randomized controlled trial. J Alzheimers Dis. 2017;60(1):323-332.

10. Lamb SE, Sheehan B, Atherton N, et al. Dementia And Physical Activity (DAPA) trial of moderate to high intensity exercise training for people with dementia: randomised controlled trial. BMJ. 2018;361:k1675.

11. Forbes D, Forbes SC, Blake CM, Thiessen EJ, Forbes S. Exercise programs for people with dementia. Cochrane Database Syst Rev. 2015;(4):CD006489.

12. Groot C, Hooghiemstra AM, Raijmakers PG, et al. The effect of physical activity on cognitive function in patients with dementia: a meta-analysis of randomized control trials. Ageing Res Rev. 2016;25:13-23.

13. Panza GA, Taylor BA, MacDonald HV, et al. Can exercise improve cognitive symptoms of Alzheimer’s disease? J Am Geriatr Soc. 2018;66(3):487-495.

14. Defina LF, Willis BL, Radford NB, et al. The association between midlife cardiorespiratory fitness levels and later-life dementia: a cohort study. Ann Intern Med. 2013;158(3):162-168.

15. Hörder H, Johansson L, Guo X, et al. Midlife cardiovascular fitness and dementia: a 44-year longitudinal population study in women. Neurology. 2018;90(15):e1298-e1305.

16. Smith JC, Nielson KA, Woodard JL, et al. Physical activity reduces hippocampal atrophy in elders at genetic risk for Alzheimer’s disease. Front Aging Neurosci. 2014;6:61.

17. de Souto Barreto P, Demougeot L, Vellas B, Rolland Y. Exercise training for preventing dementia, mild cognitive impairment, and clinically meaningful cognitive decline: a systematic review and meta-analysis. J Gerontol A Biol Sci Med Sci. 2018;73(11):1504-1511.

18. Sofi F, Valecchi D, Bacci D, et al. Physical activity and risk of cognitive decline: a meta-analysis of prospective studies. J Intern Med. 2011;269(1):107-117.

19. Santos-Lozano A, Pareja-Galeano H, Sanchis-Gomar F, et al. Physical activity and Alzheimer disease: a protective association. Mayo Clin Proc. 2016;91(8):999-1020.

Senior man in a gym talking to personal trainer

Sarcopenia & Diabetes: Untangling the Connections

/9 March 2021/ All MFN blog/

Muscle loss is a significant quality-of-life issue for patients with diabetes.

Diabetes is extremely common in the older adult population, affecting more than one-quarter of Americans aged 65 and older.(1) It’s increasingly recognized that individuals with type 2 diabetes—who comprise the vast majority of all diabetes cases—are vulnerable to sarcopenia—excessive age-related muscle loss. Although muscle loss can begin in persons with diabetes even at younger ages, it’s of particular concern among older adults.

“People with diabetes are living longer now, which is incredibly exciting,” says Rita Kalyani, MD, MHS, an associate professor of medicine in the division of endocrinology, diabetes, and metabolism at Johns Hopkins School of Medicine. But “it’s important to recognize [the potential for accelerated muscle loss] because it can significantly impact quality of life for people with diabetes and also mortality.”

What Is Sarcopenia?

Muscle loss is natural with advancing age. It is routine for individuals to lose 3% to 8% of their muscle mass per decade beginning at age 30, and the rate of decline is even higher after the about age 60.2 Muscle strength declines even more rapidly—at a rate of 3% to 4% per year in men and 2.5% to 3% per year in women by the age of 75.3

While some muscle loss is typical, sarcopenia refers to a condition of accelerated muscle loss. Earlier definitions of sarcopenia focused exclusively on loss of muscle mass as the key determinant of the condition, but more recent definitions have recognized that muscle strength and function are equally important for predicting adverse outcomes.(4-6) Thus, newer definitions for sarcopenia have included low walking speed and grip strength alongside low muscle mass.(5) Sarcopenia is associated with an increased risk of falls, functional decline, frailty, and mortality.(7)

How Strong Is the Connection Between Diabetes and Sarcopenia?

The link between diabetes and sarcopenia is well established. In a study of 810 Korean adults, 15.7% of participants with diabetes were found to have sarcopenia, compared with just 6.9% of participants without diabetes.(8) A later study led by the same author, also in Korea, produced similar findings: in a sample of 414 adults aged 65 or older, participants with type 2 diabetes had significantly lower muscle mass (defined as appendicular mass/height) than did those without diabetes.(9) A link between low muscle mass and diabetes has been found in several other populations as well.(5,10)

Multiple studies have also linked diabetes to reduced muscle strength. In a cross-sectional investigation of 1,391 adults aged 60 to 70 years from the Hertfordshire (UK) cohort study, men newly diagnosed with diabetes had significantly lower grip strength than did those without diabetes.11 The effect sizes were smaller in women, but the trend was the same for both genders. Similarly, among 1,840 participants aged 70 to 79 years in the Health, Aging, and Body Composition study, subjects with type 2 diabetes showed a greater loss of both muscle mass and a greater loss of leg strength and leg muscle quality (though not arm strength/quality) over three years, compared with those without diabetes.(12) These declines were attenuated after adjustment for demographics, body composition, physical activity, and other factors, but the association remained significant.

The association between sarcopenia and diabetes has led some researchers to argue that sarcopenia is probably one of the underlying mechanisms that explains the reduced functional ability and mobility that is often seen in older patients with type 2 diabetes.(13)

Mechanisms: How Diabetes Contributes to Sarcopenia

While diabetes accelerates the process of muscle loss, the mechanisms aren’t yet thoroughly understood. “There are probably multiple underlying pathways linking the observational findings that we see between type 2 diabetes and accelerated loss of muscle,” Kalyani says.

The presence of insulin resistance, which is the key feature of type 2 diabetes, appears to be a major pathway. “Insulin resistance is associated with decreased protein synthesis in the muscle,” Kalyani says. One of the key roles of insulin is to drive nutrients (ie, glucose) from the blood into skeletal muscle tissue and stimulate protein synthesis. In type 2 diabetes, however, insulin signaling is impaired; insulin is not able to effectively drive glucose into the muscle tissue, and the muscle cannot synthesize new protein rapidly enough to keep pace with natural muscle degradation.(13)

Insulin resistance is linked not only to decreased protein synthesis but also to mitochondrial dysfunction. Individuals with diabetes frequently have decreased mitochondrial function, which again appears to contribute to the impairment of muscle function (possibly in part because these mitochondrial alterations may increase insulin resistance).(5)

Diabetes can also promote sarcopenia via peripheral neuropathy. Approximately 30% to 50% of diabetes mellitus patients experience peripheral neuropathy, and the condition has been shown to be an independent risk factor for sarcopenia in individuals with diabetes.(14) “Nerves are needed to help the muscles contract properly,” says John Morley, MD, a professor of medicine in the division of geriatric medicine at the Saint Louis University School of Medicine. “My leg muscles are almost certainly contracting as I sit here. If I’ve got some degree of neuropathy, I won’t get the same amount of contraction.”

Still other factors also may play a role in causing muscle loss in the context of diabetes. People with diabetes frequently have higher than normal levels of inflammatory cytokines, including tumor necrosis factor and interleukin.(6) Such cytokines have been shown to have negative impacts on both muscle mass and strength in older adults.(15) In addition, “people with diabetes are also more likely to have hypothyroidism, and people with hypothyroidism get a myopathy of the legs as well,” Morley says. “So you should always be thinking, if you see a diabetic who’s lost a lot of muscle, ‘Could this be due to something else, like low thyroid’?”

Thus, a wide variety of factors likely contribute to the connection between diabetes and sarcopenia. Some data suggest that these varying mechanisms come into play even in individuals who are comparatively young or who are comparatively early in the disease process. Kalyani and her colleagues examined a group of 984 participants from the Baltimore Longitudinal Study of Aging and found that loss of muscle function as a result of hyperglycemia was seen in some patients who were only in their 40s. Interestingly, peripheral neuropathy appeared to be a contributing factor. Also of note in this investigation is the fact that hyperglycemia affected muscle strength and quality even for patients with blood glucose levels in the prediabetes range.(16)

A Bidirectional Association: How Muscle Loss Can Lead to Diabetes

Until recently, scholarly attention on the connection between diabetes and sarcopenia has focused on diabetes as a cause of sarcopenia. “Clinically the direction that we think about most is accelerated muscle loss being a complication of diabetes—that people who have diabetes develop accelerated muscle loss over time,” Kalyani says. “But it’s possible that the reverse direction is also true.”

Kalyani herself explored this hypothesis in a recent study of 1,855 US adults (baseline mean age of 58.9 years). She and her colleagues found that men—though not women—who had a higher percentage of total or leg lean body mass had a lower risk of developing diabetes over the seven-year average follow-up period, even after adjusting for race.(17) The findings are in line with a previous study of young and middle-aged Korean adults (median age of 39 years at baseline) showing that individuals in the lowest quartile of relative muscle mass had a two-fold higher risk of developing diabetes than did those in the highest quartile over an average of nearly three years of follow up.(18)

According to Kalyani, the findings make sense. “Skeletal muscle is the main site of glucose uptake in the body after we eat,” accounting for about 80% of glucose clearance in a healthy individual. “So if we don’t have enough skeletal muscle, then the glucose is not taken up by the body, and it stays in the blood. As a result, your glucose levels are higher, and over time that could lead to the development of diabetes,” Kalyani says.

A recent review on the bidirectional relationship between diabetes and sarcopenia supports Kalyani’s hypothesis, arguing that loss of skeletal muscle mass and function is both a cause and a consequence of diabetes. As for how muscle loss can cause diabetes, the review supports Kalyani’s assertion that muscle loss results in a diminished target for insulin, altering glucose regulation. But the review also notes another mechanism by which muscle loss can lead to diabetes—namely, it can contribute to a decreased metabolic rate and a decrease in physical activity, which can cause inter- and intramuscular adipose tissue accumulation, in turn leading to insulin resistance.(19)

One of the difficulties associated with type 2 diabetes is that the disease doesn’t necessarily produce obvious symptoms in the early stages, meaning that some patients may not be diagnosed until after they have already developed cardiovascular problems.

However, the recognition that loss of muscle strength predicts risk of diabetes has led to new possibilities for diagnosing type 2 diabetes in its earlier stages. A recent study led by researchers at Oakland University in Rochester, Michigan, used data from more than 5,000 participants in the National Health and Nutrition Examination Surveys to identify specific cut points of handgrip strength that take into account age, sex, and body weight and that indicate the presence of type 2 diabetes in adults that appear otherwise healthy.(20) According to the authors, these cut points can be a useful screening tool for identifying diabetes at earlier stages and getting patients into treatment sooner.

The Role of Blood-Glucose Management in Preventing Muscle Loss

The growing body of research on the connection between diabetes and sarcopenia has raised an important question: Does lowering blood glucose help preserve muscle mass?

According to Morley, there’s little research on that question, but diabetes medications that control blood glucose levels likely do have a role to play in treating (and preventing) muscle loss among older adults with diabetes. “If you’re using something like metformin or the gliptins, those improve insulin resistance. Improving insulin resistance will allow you to get more nutrients into your muscle tissue.”

The question of whether lowering blood glucose helps prevent sarcopenia is relevant because most clinical practice guidelines for older adults with diabetes recommend less aggressive glucose control as people get older. “The older adult population is heterogenous—there are some people who have long life expectancy, some have greater life expectancy, some are at greater risk for polypharmacy or hypoglycemia,” Kalyani says. “So in general glucose targets for older adults are not as strict as they are for younger adults.”

Unfortunately, Kalyani says, it’s possible that these relaxed targets may exacerbate muscle loss in vulnerable older adults. Key clinical trials on which clinical management guidelines for blood glucose have been based haven’t usually included older adults, so there’s no way to know at present. According to Kalyani, future research is needed to better understand the effects of glucose-lowering on muscle mass in older adults.

The Importance of Exercise

While diabetes medications may have a role to play in lowering blood glucose and in staving off muscle loss, Morley is adamant that no medication is as beneficial for treating sarcopenia as physical exercise. “The major treatment is resistance exercise,” Morley says. “You can argue that aerobic exercise is also useful, but if you’re going to do anything as a diabetic, you want to do resistance exercise to build your muscle bulk.” For older adults with sarcopenia, the key exercises he recommends are walking around the block four to five times, doing some weight lifting, and sitting in a chair and getting up ten times in a row as fast as possible.

Kalyani agrees on the importance of activity. “Physical exercise is always recommended,” in part to promote fat loss and maintain muscle mass, both of which can improve glucose levels. Those recommendations apply equally to both younger and older adults, she says. “As long as they can tolerate the exercise they are doing, we definitely recommend that, particularly muscle strengthening exercise and resistance activity.”

Recommendations for Clinicians

• Take seriously the fact that patients with type 2 diabetes are vulnerable to muscle loss. “Accelerated muscle loss is an underappreciated condition that occurs in people with type 2 diabetes. I don’t think it’s well recognized,” Kalyani says. One reason for the under-recognition, she says, is that most providers who treat diabetes aren’t geriatricians and thus aren’t as likely to be familiar with age-related muscle loss and how it can affect mobility. “It needs to be better recognized in clinical practice that this occurs at greater frequency in people with diabetes,” she says.

• Screen all individuals with diabetes for sarcopenia. Everyone aged 50 or older should also be screened, even if they don’t have diabetes, Morley says. “You can argue, ‘Well, I don’t really need to do that, I just need to get them out exercising, and they’ll do well,’ but people don’t do well if you don’t give them a diagnosis.”

As for a specific screening tool, Morley recommends SARC-F. This screen contains five questions that focus on a patients’ ability to lift and carry 10 pounds, their ease in walking across a room, their ease in rising from a chair, their ability to climb a flight of stairs, and the number of falls they have had in the last year. The questionnaire and scoring instructions are available at cgakit.com/sarc-f-questionnaire.

• Spend time making sure patients understand the importance of exercise. “Every clinician knows that diabetics should exercise and exercise is good for them,” Morley says. “Realistically, every diabetic should be in an exercise program. It should be covered by medical insurance, because that’s by far the best treatment for diabetes, period.” The problem, according to Morley, is that physicians often recommend exercise without driving home how thoroughly important it is. “[We need to] stress that this is more important than the drug.”

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This article was featured in the November/December 2020 issue of Today’s Geriatric Medicine.

Today’s Geriatric Medicine is a bimonthly trade publication offering news and insights for professionals in elder care.

Get a Free Subscription to Today’s Geriatric Medicine

 

This article was featured in the November/December 2020 issue of Today’s Geriatric Medicine (Vol. 13 No. 6 P. 14). Written by Jamie Santa Cruz, a health and medical writer in the greater Denver area. Reprinted with permission from Today’s Geriatric Medicine.

 

References

1. Centers for Disease Control and Prevention. National diabetes statistics report, 2020. https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Published 2020.

2. Volpi E, Nazemi R, Fujita S. Muscle tissue changes with aging. Curr Opin Clin Nutr Metab Care. 2004;7(4):405-410.

3. Wilkinson DJ, Piasecki M, Atherton PJ. The age-related loss of skeletal muscle mass and function: measurement and physiology of muscle fibre atrophy and muscle fibre loss in humans. Ageing Res Rev. 2018;47:123-132.

4. Sobestiansky S, Michaelsson K, Cederholm T. Sarcopenia prevalence and associations with mortality and hospitalisation by various sarcopenia definitions in 85–89 year old community-dwelling men: a report from the ULSAM study. BMC Geriatr. 2019;19(1):318.

5. Morley JE, Malmstrom TK, Rodriguez-Mañas L, Sinclair AJ. Frailty, sarcopenia and diabetes. J Am Med Dir Assoc. 2014;15(12):853-859.

6. Cruz-Jentoft AJ, Bahat G, Bauer J, et al. Sarcopenia: revised European consensus on definition and diagnosis [published correction appears in Age Ageing. 2019;48(4):601]. Age Ageing. 2019;48(1):16-31.

7. Cruz-Jentoft AJ, Sayer AA. Sarcopenia [published correction appears in Lancet. 2019;393(10191):2590]. Lancet. 2019;393(10191):2636-2646.

8. Kim TN, Park MS, Yang SJ, et al. Prevalence and determinant factors of sarcopenia in patients with type 2 diabetes: the Korean Sarcopenic Obesity Study (KSOS) [published correction appears in Diabetes Care. 2010;33(10):2294]. Diabetes Care. 2010;33(7):1497-1499.

9. Kim KS, Park KS, Kim MJ, Kim SK, Cho YW, Park SW. Type 2 diabetes is associated with low muscle mass in older adults. Geriatr Gerontol Int. 2014;14(Suppl 1):115-121.

10. Leenders M, Verdijk LB, van der Hoeven L, et al. Patients with type 2 diabetes show a greater decline in muscle mass, muscle strength, and functional capacity with aging. J Am Med Dir Assoc. 2013;14(8):585-592.

11. Sayer AA, Dennison EM, Syddall HE, Gilbody HJ, Phillips DI, Cooper C. Type 2 diabetes, muscle strength, and impaired physical function: the tip of the iceberg? Diabetes Care. 2005;28(10):2541-2542.

12. Park SW, Goodpaster BH, Strotmeyer ES, et al. Accelerated loss of skeletal muscle strength in older adults with type 2 diabetes: the health, aging, and body composition study. Diabetes Care. 2007;30(6):1507-1512.

13. Umegaki H. Sarcopenia and diabetes: hyperglycemia is a risk factor for age-associated muscle mass and functional reduction. J Diabetes Investig. 2015;6(6):623-624.

14. Yang Q, Zhang Y, Zeng Q, et al. Correlation between diabetic peripheral neuropathy and sarcopenia in patients with type 2 diabetes mellitus and diabetic foot disease: a cross-sectional study. Diabetes Metab Syndr Obes. 2020;13:377-386.

15. Jang HC. Sarcopenia, frailty, and diabetes in older adults. Diabetes Metab J. 2016;40(3):182-189.

16. Kalyani RR, Metter EJ, Egan J, Golden SH, Ferrucci L. Hyperglycemia predicts persistently lower muscle strength with aging. Diabetes Care. 2015;38(1):82-90.

17. Kalyani RR, Metter EJ, Xue QL, et al. The relationship of lean body mass with aging to the development of diabetes. J Endocr Soc. 2020;4(7):bvaa043.

18. Hong S, Chang Y, Jung HS, Yun KE, Shin H, Ryu S. Relative muscle mass and the risk of incident type 2 diabetes: a cohort study. PLoS One. 2017;12(11):e0188650.

19. Mesinovic J, Zengin A, De Courten B, Ebeling PR, Scott D. Sarcopenia and type 2 diabetes mellitus: a bidirectional relationship. Diabetes Metab Syndr Obes. 2019;12:1057-1072.

20. Brown EC, Buchan DS, Madi SA, Gordon BN, Drignei D. Grip strength cut points for diabetes risk among apparently healthy U.S. adults. Am J Prev Med. 2020;58(6):757-765.