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Abstract

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

The aging of the world's population is a major contributor to the growing prevalence of the cardiometabolic syndrome (CMS) because older persons are more affected by the constellation of cardiovascular risk factors that constitute the syndrome. The prevalence of CMS has been related to the increasing prevalence of obesity, which is growing progressively even among older age groups. Indeed, obesity and aging are 2 overlapping mounting public health problems. It is currently accepted that CMS predicts cardiovascular mortality and/or the development of type 2 diabetes mellitus, and this is also true in studies including older persons. CMS is further complicated by modifications in body composition and fat redistribution during aging; older adults are at higher risk for developing central obesity and sarcopenia or sarcopenic obesity, a condition characterized by an important reduction in lean body mass associated with obesity, linked to an increased production of inflammatory adipokines that may alter insulin sensitivity and muscle mass and strength. A better understanding of the pathophysiologic mechanisms of sarcopenic obesity may help to elucidate the complex relationship between CMS and mortality/morbidity in older adults.

The world's population is aging, and since central obesity and other components of the cardiometabolic syndrome (CMS) (ie, hypertension [HTN] and dyslipidemia) are frequent in older populations, this may contribute to the growing prevalence of CMS.1–7 Older adults are at higher risk for developing sarcopenia, loss of muscle mass and strength, and central obesity secondary to the modifications in body composition and fat redistribution during aging.8 A state of chronic inflammation has been proposed to be the origin of sarcopenia,9 which may be triggered, at least in part, by proinflammatory agents produced in abdominal fat. This review covers data on the prevalence of CMS in older populations as well as on the power of CMS in the prediction of cardiovascular events and in the development of type 2 diabetes mellitus (DM) in this population and gives an overview of how sarcopenic obesity may relate to CMS.

Prevalence of CMS in Older Populations

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

The cluster of abdominal obesity, hyperglycemia and/or hyperinsulinemia, dyslipidemia, and elevated blood pressure that composes CMS has become a worldwide health disorder, which has led to increased risk of cardiovascular disease (CVD) and development of type 2 DM in different populations.1 The increased prevalence of CMS is particularly steep among the elderly.2–5 In addition, the consequences of CMS seem to be amplified in older persons, possibly because of physiologic changes associated with aging and/or the concurrence of chronic conditions more frequently observed during this period of life.6

Data from the Third National Health and Nutrition Examination Survey (NHANES III) and NHANES 1999–2000 have confirmed the high prevalence of CMS in the US population, according to the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP III) definition. The age-adjusted prevalence has also significantly increased from 24.1% in NHANES III (1988–1994) to 27.0% in NHANES 1999–2000, predicting a further rise in the incidence of DM and CVD in future years.7 A consistent observation among different populations is that the prevalence of CMS increases with age. In the United States, among adults aged 60 years or older, CMS prevalence is as high as 42%, compared with 7% in 20- to 29-year-old individuals.2 In a Swedish cohort of 70-year-old persons, 22.6%had CMS according to NCEP ATP III criteria. One-third of the total sample had at least 1 of the 5 criteria for CMS, with HTN being the most prevalent risk factor (68.3% in men and 50.2% in women), while abdominal obesity was the second most common risk factor (27.2% of men and 42.7% of women).4 A similar pattern was also found in nonwestern countries, such as Iran, where the prevalence was <10% in the 20- to 29-year-old age group, and rose to 38% in men and to 67% in women in the 60- to 69-year-old age group.3

The prevalence of CMS has been related to the escalating prevalence of obesity, which is growing progressively even among older age groups. Indeed, obesity and aging of the populations are 2 overlapping public health problems. Currently, >130 million Americans are either overweight (body mass index [BMI] >25) or obese (BMI >30)10; by 2050, the percentage of US citizens older than 65 years will reach 20% (vs 12% in 2004).11 In nursing homes in some states across the United States, there is a trend of elevated BMI among new admissions. In 2002, in nearly one-third of the nursing homes studied, >25% of their admissions had a BMI >30, and most of these patients required assistance from 2 individuals to get up and move around.12 Hence, the potential health benefits from reducing overweight and obesity are of major public health importance; doing so may lessen the burden of disease and disability linked to the aging population with CMS and excess body weight. Some controversy exists about the potential harms of obesity in the elderly, however, because the relative mortality risk by BMI is different according to age category (ie, the risk for each increased BMI point decreases with age).10,13

There is also a debate about the definition of the ideal BMI in old age and whether the definition of obesity should be the same as in young individuals. In fact, it has been demonstrated that over-reliance on BMI as a marker of obesity may mask the change in body composition toward increasing fatness.14 The analyses of body composition and fat distribution may change the concepts of obesity in older persons and may help to elucidate the relationships between obesity, morbidity, and mortality in this population. The true nature of obesity and CMS in older persons may have been undervalued because of the reduced life expectancy of this population, the presence of comorbidities, and the concurrence of unintentional weight loss.15

Prognostic Power of CMS in Older Persons

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

There is still a question regarding which of the different CMS criteria may best apply to older individuals, since different CMS definitions may lead to different results on its association with cardiovascular risk. For example, a study in Germany found a CMS prevalence of 24%, 38%, and 46% among women and of 28%, 50%, and 57% in men, when classified according to NCEP ATP III, World Health organization (WHO), and International Diabetes Federation criteria, respectively. Of interest, the possibility of having an elevated C-reactive protein level was similar with the 3 definitions after adjusting for various confounders.16 Nevertheless, a recent meta-analysis of 21 studies indicates that individuals with CMS, according to the NCEP ATP III and WHO definitions, compared with those without, have increased mortality from all causes (relative risk [RR], 1.35) and from CVD (RR, 1.74) and an increased incidence of CVD (RR, 1.53), coronary heart disease (CHD) (RR, 1.52), and stroke (RR, 1.76).1

Several studies conducted specifically in older populations confirm that the presence of CMS is an important predictor of cardiovascular mortality in this age group. Data from the Cardiovascular Health Study17 showed a prevalence of CMS of 28.1% by NCEP ATP III and 21.0% by WHO criteria in participants aged 65 years or older who were free of CVD at baseline. The presence of CMS by the NCEP ATP III definition was an independent predictor of the occurrence of a cardiovascular event after 4.1-year follow-up (38% increased risk), even after adjustment for traditional cardiovascular risk factors and considering each individual domain of CMS.17 Furthermore, it appears that clustering of the multiple components of CMS has a greater impact on vascular damage than do individual parameters of the syndrome, interacting synergistically to impact vascular thickness and stiffness.18

In the Italian Longitudinal Study on Aging (ILSA),5 a population-based survey in a sample of 5632 individuals aged 65 to 84 years, the prevalence of CMS was 25.9% in nondiabetic men and 55.2% in nondiabetic women. In diabetic individuals, it was 64.9% and 87.1% in men and women, respectively. During the 4-year follow-up, nondiabetic men with CMS had a risk of CVD mortality that was 12% higher than those without CMS, whereas no significant differences were found in women.5

A recent 12-year follow-up study reported the association of NCEP ATP III-defined CMS with the progression of carotid intima-media thickness (IMT) in women aged 60 to 70 years. Among individuals without CMS at baseline, the increase in carotid IMT was greater in women who developed CMS during the 12-year period than in women who did not, after adjustment for several confounders.19 Another current study with a mean follow-up of 6.6 years corroborates that CMS and waist-to-hip ratio are independent predictors of cardiovascular outcomes in women aged 60 to 84 years.20

Waist Circumference in Old Age

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

Body composition changes with aging; fat mass increases and muscle mass and strength decrease.15 Hence, older individuals tend to have a greater proportion of fat than younger persons with the same BMI.21,22 Due to multiple age-related physiologic mechanisms, body fat distribution also changes with aging, with an increased risk of developing intra-abdominal fat deposit15,23 and of fat inside skeletal muscle23 and the liver.24 Waist circumference is a surrogate marker of visceral fat that correlates closely with intra-abdominal adiposity; waist circumference, independent of BMI or body weight, confers risk of the development of glucose intolerance/DM, HTN, dyslipidemia, and CVD.25,26 A waist circumference >102 cm in men and >88 cm in women has been shown to confer a 4.5- and 3.8-fold higher risk, respectively, of developing type 2 DM and a 4.2- and 2.8-fold higher risk of having at least 1 major cardiovascular risk factor.25 Analyses of NHANES III data showed that waist circumference is a significant predictor of obesity-related comorbidities for all categories of BMI, even after adjustment for age and other confounding variables.26 A very recent study demonstrated that visceral fat is an important site of secretion of the inflammatory mediator interleukin (IL) 6 in extremely obese participants, providing a potential mechanistic link between visceral fat and systemic inflammation in persons with abdominal obesity.27

Insulin Resistance in Old Age

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

The pathophysiology of CMS appears to be largely attributable to insulin resistance, with excessive flux of fatty acids implicated.28 If we consider the association of some of the features of CMS to insulin resistance, a study conducted in Sweden in persons aged 70 years at baseline and followed up for 10 years demonstrated that adjusted insulin sensitivity index measured by euglycemic insulin clamp predicted subsequent CHD.29 One standard deviation increase in the sensitivity index (adjusted for serum cholesterol, systolic blood pressure, fasting glucose, BMI, and smoking) decreased the risk of a CHD event by 18%.

An association of insulin resistance with a 40% reduction in mitochondrial oxidative and phosphorylation activity linked to an increased accumulation of fat in muscle and liver has been observed in older adults, supporting the notion that age-associated decline in mitochondrial function contributes to insulin resistance in late life.30 The reduction in mitochondrial adenosine triphosphate production in skeletal muscle with aging has been attributed to cumulative DNA oxidative damage, resulting in a reduced capacity of oxidative phosphorylation and, hence, insulin resistance.30 On the other hand, insulin has been shown to increase muscle mitochondrial biogenesis, an increase that is defective in type 2 DM and insulin-resistant individuals, such as older persons.31 Thus, it is difficult to determine whether muscle mitochondrial dysfunction causes or results from insulin resistance.

Leptin seems to be an important mediator of insulin resistance and not only a marker of adiposity in older individuals. A recent study demonstrated that leptin is significantly associated with insulin resistance evaluated by homeostasis model assessment as well as with fasting insulin and cholesterol levels after adjustments for age, body fat, and fat distribution in a cohort of 67- to 78-year-old women.32 Furthermore, even moderate weight loss improves body fat distribution, muscle lipid infiltration, insulin resistance, and leptin levels in older women.33

Low serum and intracellular magnesium (Mg) concentrations, increased Mg excretion, and low Mg intake have been found to be associated with the development of insulin resistance, type 2 DM, and CMS.34–36 Taking into account the role of Mg in glucose and insulin homeostasis, as well as in blood pressure and lipid metabolism, and the recently demonstrated relationship of hypomagnesemia to oxidative stress and inflammation,37 it cannot be excluded that alterations of Mg metabolism associated with aging38 may also contribute to the pathophysiology of insulin resistance and CMS in the older population. Of interest, serum magnesium status is an independent correlate of muscle performance in older persons,39 which may link the role of magnesium in skeletal muscle glucose/insulin homeostasis and associated CMS with the risk of sarcopenia and disability in older adults (see below).

Sarcopenic Obesity

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

A new entity has been proposed in older persons, so-called sarcopenic obesity, which has been linked to the increased production of inflammatory substances by the adipose tissue (ie, leptin, IL-6, tumor necrosis factor [TNF] α, IL-1α) known to alter insulin sensitivity, growth hormone secretion, and energy metabolism.8,40 Sarcopenia denotes the decline in muscle mass and strength that usually occurs as part of aging; it may occur even in the absence of a specific disease, but it is accelerated by the presence of chronic diseases.9,31 Its prevalence is estimated to range from 8.8% in women aged 65 to 75 years to 17.5% in men older than 75 years.9 Possible factors that may contribute to sarcopenia in old age include increased oxidative stress and proinflammatory cytokine levels; low growth hormone, insulin-like growth factor 1, and testosterone levels; malnutrition; reduced neurologic drive; peripheral vascular disease; and, of particular importance, immobility and lack of exercise.9,31 The loss of muscle mass and strength combined with the gain in abdominal fat may act synergistically to exacerbate metabolic disorders and to increase disability (Figure 1).8,15,40

image

Figure 1. Changes that occur during aging are major contributors to sarcopenia, abdominal obesity, insulin resistance, and the components of the cardiometabolic syndrome (CMS), leading to cardiovascular disease (CVD) and type 2 diabetes mellitus (DM). Reduced glucose disposal may occur because of reduced metabolically active muscle mass that may be based on increased cytokine production by the adipose tissue, promoting a sustained inflammatory state. ABD indicates abdominal; EXP, expenditure; HDL, high-density lipoprotein cholesterol; HTN, hypertension; IR, insulin resistance; TG, triglycerides.

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Several investigators have reported that body fat percentage is increasingly higher regardless of BMI, in older persons compared with young adults.14,21,22 Hence, BMI may not be a good estimator of fatness in old age. Conventional cutoffs for defining obesity based on BMI values may miscalculate the true prevalence of excess body fatness, leading to a wrong estimate of the risk for conditions, such as CVD, associated with obesity. Therefore, body fat percentage and distribution may be better risk predictors,15 as well as waist circumference, which correlates closely with intra-abdominal adiposity.25,26

An interesting study by Myers and colleagues41 demonstrated that exercise capacity is a more powerful predictor of mortality among men than other established risk factors for CVD. After adjustment for age, the peak estimated exercise capacity achieved during the exercise test was the strongest predictor of the risk of death among patients with or without CVD, compared with other risk factors including obesity: each increase of 1 metabolic equivalent in exercise capacity conferred a 12% improvement in survival. The absolute peak exercise capacity outperformed the percentage of age-predicted exercise capacity for both those with and without CVD. This applies to normal-weight, overweight, and obese individuals. The study by Myers and associates,41 among others, corroborates Darwin's concept of “survival of the fittest” that was controversial at his time but revolutionized the course of science. The notion that sarcopenic obesity may be a better predictor of disability than obesity,40 or that fatness per se is less important than fatness with low muscle mass, goes in the same direction. Accordingly, Katzmarzyk and colleagues42 have demonstrated that the positive trend of a higher BMI being associated with a higher risk of CVD and all-cause mortality is greatly attenuated after controlling for cardiorespiratory fitness. Therefore, regardless of body weight, cardiorespiratory fitness seems to be protective for premature mortality.

Sarcopenic obesity may be frequent and underestimated among older persons if the risk assessment takes into account only body weight or BMI. In a group of obese, frail older persons, although absolute fat-free mass (FFM) was greater than that in a group of sex- and age-matched, nonobese, frail persons with similar low scores on physical performance testing, the percentage body weight as FFM and muscle quality was lower in the obese older group and was associated with a poorer quality of life.43

Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

Does Muscle Loss Cause Fat Gain? Skeletal muscle, the largest insulin-sensitive tissue in the body, is fundamental to the metabolic dysregulation associated with obesity and physical inactivity, contributing to the development of CMS. It is likely that the decrease in muscle mass/strength and reduced endurance causes reduced physical activity in old age.8,9,31 Indeed, regarding the relationship between sarcopenia and physical activity, it is difficult to establish which comes first, because low mass and strength (ie, sarcopenia) may lead to reduced physical activity during aging, but reduction of physical activity may also lead to or worsen sarcopenia since there is evidence that both aerobic and resistance exercise programs stimulate muscle protein synthesis.44 A reduction in muscle mass and physical activity levels decreases total energy expenditure. This reduction in overall energy expenditure in older persons results in an increased prevalence of obesity, especially abdominal fat accumulation, with consequent insulin resistance, CMS, and increased CV death and other morbidities31 (Figure 1). A reduction in energy expenditure should only result in obesity if it is less than energy intake, however.

Does Fat Gain Cause Muscle Loss by Means of Inflammation? Pathways leading from obesity to the expression of CMS involve a number of metabolic risk factors, as well as adipokines, mediators of inflammatory response, thrombogenic and thrombolytic para-meters, vascular endothelial reactivity,45 and renin-angiotensin system activation.46 Potential mechanisms that contribute to reducing insulin signaling and action in skeletal muscle include adipose tissue expansion with recruitment of macrophages through various signals, including chemokines synthesized by adipocytes, such as CC chemokine ligand 2 (CCL2). Recruited macrophages are found mainly around apoptotic adipocytes. The augmented secretion of proinflammatory cyto-kines, particularly TNF-α and IL-6, synthesized by adipocytes and macrophages, along with diminished secretion of the protective adiponectin, might contribute to local and systemic chronic inflammation45 that may target skeletal muscle (Figure 2). Analyses of data from the Trial of Angiotensin Converting Enzyme Inhibition and Novel Cardiovascular Risk Factors (TRAIN)47 demonstrated a positive association of C-reactive protein and IL-6 with total fat mass and a negative association with lean mass; this suggests that obesity-associated inflammation may play an important role in the age-related process that leads to sarcopenia.

image

Figure 2. Adipose tissue is at present considered a component of both the endocrine and the immune systems. It synthesizes and releases adipokines such as adiponectin, leptin, and resistin as well as proinflammatory cytokines, such as tumor necrosis factor (TNF) α, and interleukin (IL) 6, and chemokines, such as CC chemokine ligand 2 (CCL2). Macrophages recruited after expansion of the adipose tissue may also release proinflammatory substances (resistin, IL-1β, TNF-α, IL-6, CCL2). All these inflammatory mediators may trigger sarcopenia (loss of skeletal muscle mass and strength) during the aging process.

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It has been proposed that TNF-α and adiponectin are antagonistic in stimulating nuclear transcription factor κB (NF-κB activation.45,48 Through this activation, TNF-α induces oxidative stress, which exacerbates low-density lipoprotein (LDL) oxidation, insulin resistance, HTN, endothelial dysfunction, and atherogenesis. Elevated free fatty acid, glucose, and insulin levels enhance NF-κB activation and, further downstream, modulate specific clinical manifestations of CMS.48 Oxidative stress induced by angiotensin II with increased production of nicotinamide adenine dinucleotide phosphate and consequent reactive oxygen species generation in skeletal muscle provides another mechanism for insulin resistance and CMS.46

Unger24,49 has proposed that a condition of leptin resistance may help to elucidate CMS. Leptin is a liporegulatory hormone that maintains intracellular homeostasis in the face of wide variations in caloric intake. Leptin deficiency or resistance is generally associated with triglyceride accumulation in nonadipose organs (eg, liver, muscle) related to the inability of leptin to activate adenosine monophosphate kinase in muscle.50 Rats tolerate a 60% fat diet because 96% of the fat excess is deposited in adipocytes. When leptin is absent or inactive, however, dietary fat surplus is deposited in nonadipose tissues, causing dysfunction (lipotoxicity) and cell death (lipoapoptosis). Hence, CMS may be the human equivalent of the lipotoxic syndrome of rodents.24,49

Is Fat Mass Gain or Fat Free Mass Loss the Main Determinant of Disability in the Elderly? Analyses from men and women aged 70 and older from NHANES III showed that women in the highest quintile for body fat percentage and women with a BMI ≥30 were twice as likely to report functional limitations than women in the comparison groups,51 which suggests that prevention of excessive body fat accumulation may reduce the likelihood of functional limitations in old age. Analogous results were obtained with data from the Cardiovascular Health Study,52 with a positive association between fat mass and disability. In this study, fat mass at baseline, adjusted for several confounders, predicted the occurrence of mobility-related disability 3 years later (odds ratio, 2.83 for women and 1.72 for men), supporting the urgency of avoiding high body fatness in old age to reduce disability.52 A recent report using data from the Duke Established Populations for Epidemiologic Studies of the Elderly (EPESE) showed that CMS is an independent and highly significant predictor of decline in mobility.53

A longitudinal study showed that sarcopenic obese persons in the community at baseline were 2 to 3 times more likely to report onset of disability associated with instrumental activities of daily living during follow-up than lean sarcopenic or nonsarcopenic obese persons and those with normal body composition. The RR for incident disability in sarcopenic obese persons was 2.63, adjusted for age, sex, physical activity level, length of follow-up, and prevalent morbidity.40 Hence, obesity seems to act synergistically with sarcopenia to maximize the risk of disability.

Implications for Treatment in Older Persons

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

The increased risk of type 2 DM and CVD in persons with CMS demands therapeutic attention for those at high risk. Studies on the effect of intentional weight loss in older adults are limited but suggest that even small amounts of weight loss (5%–10% of initial body weight) may be beneficial.33,54,55 A study conducted in obese older adults randomly assigned to diet and exercise therapy for 6 months or no therapy demonstrated that lifestyle intervention decreases multiple metabolic CHD risk factors simultaneously. Serum free fatty acids, C-reactive protein, and IL-6 decreased in the treatment group, and the incidence of CMS was decreased by 59%.54 Another study showed that weight loss can be achieved and sustained over a 6-month period in older obese persons with knee osteoarthritis through a combined dietary and exercise intervention; this leads to improvements in pain, disability, and performance accompanied by a decrease in IL-1 circulating level.55 Therefore, in older as well as in younger adults, intentional weight loss may help to prevent the adverse health consequences of obesity and derived CMS.

On the other hand, current data suggest that moderate to high levels of cardiorespiratory fitness provide protection against mortality in older women and men who are normal-weight, overweight, and obese.31 There is convincing evidence of aerobic exercise training in patients with CMS as a treatment strategy in adults56 and, recently, the results of the Lifestyle Interventions and Independence for Elders Pilot (LIFE-P) study57 demonstrated that an intervention of structured physical activity improves physical performance scores in a group of 70- to 89-year-old participants. Hence, clinicians and public health authorities should promote physical activity in older adults. Pharmacologic therapy might be considered when necessary for DM and CVD risk reduction.28

Conclusions

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References

The CMS is a complex condition most frequently observed in older adults. Considering the current and future demographic dynamics toward an aging world population, it is critical to consider treatment and realistic preventive efforts for CMS in older patients to avoid an epidemic of CMS and associated CVD.

The picture of CMS in the elderly is further complicated by the physiologic modifications in body composition and fat redistribution during aging; older adults are at higher risk for developing central obesity and sarcopenia or sarcopenic obesity, a condition in which obesity perhaps contributes to the genesis and acts synergistically with sarcopenia to maximize the risk of disability. Identification of older persons with sarcopenic obesity may be clinically relevant, although its definition and clinical consequences require further study. Nevertheless, obesity and sarcopenic obesity are major public health problems in the older population. Improvements in physical activity and diet are presumably the most effective public health interventions for these conditions. The concept of sarcopenic obesity may help to explain the complexity of the relationship between CMS and mortality/morbidity in mature adults.

References

  1. Top of page
  2. Abstract
  3. Prevalence of CMS in Older Populations
  4. Prognostic Power of CMS in Older Persons
  5. Waist Circumference in Old Age
  6. Insulin Resistance in Old Age
  7. Sarcopenic Obesity
  8. Biological Mechanisms of CMS and Sarcopenic Obesity in Older Adults
  9. Implications for Treatment in Older Persons
  10. Conclusions
  11. References