This chapter addresses the following Geriatric Fellowship Curriculum Milestones: #25, #72
Describe the important interrelationship between diet and physical activity in maintaining or restoring lean body mass (LBM) and the resulting effects this interaction has on total body mass in older adults.
Describe the changes in body composition that occur over the adult lifespan and what physiologic, dietary, lifestyle, and disease factors are responsible for these changes.
Describe the changing prevalence of obesity among older adults and be able to assess the impact of excess weight on the health status of older patients.
Advise older adults about what constitutes an optimal diet and the advisability of using nutrient supplements given their health status.
Key Clinical Points
With advancing age, the ratio of fat to total body mass increases regardless of whether total body weight increases or remains constant.
Although skeletal muscle mass generally declines with advancing age, the rate of decline in healthy individuals is highly dependent on the individual’s habitual level of physical activity and the quality of his/her diet.
Although the impact of excess weight (ie, body mass index [BMI] > 25 kg/m2) on long-term survival is highly controversial, there is a strong direct relationship between the level of obesity and the risk of developing disabling chronic diseases such as severe osteoarthritis, type 2 diabetes, and heart disease.
There is no evidence of benefit for any micronutrient supplement in healthy older adults who do not have a documented deficiency of the given nutrient or a condition that places them at high risk for the development of such a deficiency. Supplements of vitamins and minerals do not prevent or treat cardiovascular disease (CVD), cancer, or dementia.
Vitamin and mineral supplements, above the recommended upper limit (UL), increase adverse health outcomes. The Institute of Medicine (IOM) provides evidence-based guidelines for recommended dietary intakes of vitamins and minerals for most individuals.
Laboratory blood tests of serum proteins (such as albumin and prealbumin) are indicators of inflammatory status, disease severity, and morbidity risk, rather than nutritional status.
Throughout life, nutrition is an important determinant of health, physical and cognitive function, vitality, overall quality of life, and longevity. The quantity and variety of available foods, as well as the meaningfulness of the social interactions provided by meals, are important to psychological well-being. The composition of the diet and the amount that is consumed are strongly linked to physiologic function. When a well-balanced diet is not maintained, malnutrition may develop with consequent detrimental effects on health and well-being.
Malnutrition can have many manifestations. As outlined in Chapter 35, a diet that is deficient in one or more required nutrients (eg, calories, protein, minerals, fiber, or vitamins) can lead to a state of nutritional deficiency. The greater the magnitude and duration of the nutritional deprivation and the more fragile the individual, the more likely nutritional deficits will produce noticeable body compositional changes, functional impairments, or overt disease. Even borderline dietary deficiencies can have important health consequences such as producing subtle organ system impairments, diminished vitality, or increasing the individual’s susceptibility to disease. Protein and protein-energy undernutrition are two of the most common, frequently unrecognized, and potentially serious forms of nutritional deficiency. The prevalence of these conditions is particularly high among chronically ill older individuals and those in hospitals, nursing homes, and other institutional settings. Although there is a complex interrelationship between nutrition, disease, and clinical outcomes, protein and protein-energy undernutrition appear to be significant contributors to disease-related morbidity and mortality in these populations.
At the other end of the spectrum, the persistent consumption of excess quantities of one or more nutrients can have similar untoward consequences. Forms of malnutrition that result from excess consumption include hypercholesterolemia, hypervitaminosis, and obesity. Obesity is the most common nutritional disorder of advanced age in western societies with a high prevalence among noninstitutionalized free-living older adults. Many obese older individuals have other nutritional disorders. Among chronically ill or functionally debilitated obese older individuals, protein undernutrition is a common, serious, and frequently unrecognized problem that can develop for many reasons including an imbalanced diet, disease, and inactivity.
Recognizing and maintaining an optimally balanced diet is an important challenge, particularly as individuals age. The challenge is particularly great for older people who already are malnourished, especially if they have nutritional disorders that developed earlier in life, such as obesity, osteoporosis, or protein undernutrition. Even healthy individuals often fail to maintain an optimal diet due to lack of knowledge, resources, or willpower. The process of aging can introduce other factors including acute and chronic disease, physical disabilities, social isolation, use of multiple medications, depression, impaired cognitive ability, and dysregulation of appetite control that may contribute further to poor eating habits and the development or exacerbation of nutritional disorders. In turn, inappropriate dietary intake and poor nutritional status can impact the progression of many acute and chronic diseases such as coronary heart disease (CHD), cancer, stroke, diabetes, and osteoporosis, which are among the 10 leading causes of death in the United States. Approximately two-thirds of all deaths within the United States are due to diseases associated with poor diets and dietary habits.
Assessing diet quality of the older people is critical to addressing issues relevant to their health and nutritional status. Such an assessment must be based on knowledge of what constitutes a balanced diet for a given individual. The goal of this chapter is to identify an approach to nutrition evaluation and management that takes into account the unique needs, limitations, and desires of each older individual. The chapter examines the interrelationship between nutrition, activity, disease burden, and health outcomes and then focuses on age-related changes in body composition and appetite regulation that effect nutritional status and nutrient requirements. The chapter includes discussion of both undernutrition and obesity as well as specific dietary considerations for optimal health.
THE INTERRELATIONSHIP BETWEEN NUTRITION, ACTIVITY, AND DISEASE
Although nutrition is a vital component of good health, it cannot be evaluated in isolation. The relationship between nutrient intake and health is influenced by other factors, most notably activity level, disease burden, and advancing age. A basic understanding of these interrelationships is essential in order to assess the potential benefits and limitations of nutritional interventions.
Nutrition and physical activity are closely linked, each having vitally important and interacting effects on body composition, functional ability, and well-being. The balance between nutrient intake and physical activity is particularly important in determining muscle mass and strength, body fat content and distribution, and bone density and resilience. A detailed description of the importance of physical activity in these relationships is provided in Chapter 115.
To preserve existing muscle mass and strength, it is necessary to maintain both an adequate level of physical activity and a balanced diet that includes sufficient protein, energy, vitamins, and minerals to meet metabolic demands and prevent negative nitrogen balance (as discussed in detail below). It is not known precisely what level of physical activity is needed to prevent loss of existing muscle mass and strength in older adults. However, even a week or two of bed rest or similar degrees of activity restriction can result in noticeable loss of muscle mass, strength, and function even when the diet is adequate and the individual is otherwise healthy. In one study of 12 healthy, moderately active older adults, 10 days of voluntary total bed rest resulted in a 16% loss of strength and a 6% loss of skeletal muscle mass from the lower extremities. Muscle biopsies indicated that muscle protein synthesis declined 30%. Despite the provision of a diet containing the recommended dietary allowance for protein, the participants remained in negative nitrogen balance throughout the study. In contrast, fat mass did not change. The combination of inadequate diet and inactivity can result in an even more rapid loss of muscle. In contrast, overfeeding does not prevent muscle atrophy associated with inactivity and may exacerbate the functional consequences since the excess nutrients are converted to fat.
Consumption of a protein meal stimulates muscle protein synthesis. However, nutrition alone has never been demonstrated to be an effective method of repleting muscle mass, improving strength, or increasing endurance in frail older individuals who have experienced a recent loss of weight. Efforts at repletion should focus on both increasing nutrient intake and exercise. Based on studies of healthy older men, the combination of progressive resistance muscle strength training and a high-protein diet (containing up to 1.6 g of protein/kg body weight/day) may be the most effective method of improving muscle mass. The role of special formula amino acid supplements has yet to be determined.
Exercise and nutrition also play a critical role in maintenance of optimal bone density and strength. As discussed in Chapter 118, the nutrient needs of bone include the correct balance of protein and energy and adequate intake of vitamins and minerals, especially vitamin D and calcium. The importance of exercise for optimal bone health is also described in Chapter 115. Bed rest and weightlessness are associated with a rapid decline in bone mineral density (BMD). Consequently, osteopenia can develop despite an optimal diet if exercise or other weight-bearing activities are not adequate. Because of its apparent beneficial effects on BMD, exercise should be combined with an appropriate diet for both prevention and treatment of osteoporosis and fracture-related disability.
Having both direct and indirect effects on numerous metabolic processes within muscle, bone, and adipose tissues, exercise has a major impact on how nutrients are utilized by the body during health and illness. By inducing an increase in the mass and metabolic capacity of muscle, exercise effects energy expenditure, glucose metabolism, and size of protein reserves in a manner that counteracts some of the effects of aging and thus has important nutritional implications for individuals as they grow older. Total energy expenditure (TEE) represents the sum of basal energy expenditure, postprandial thermogenesis, and the energy expenditure of activity. Muscle represents not only the primary source of energy expenditure during physical activity, it is also the primary contributor to basal energy expenditure, which may represent 50% to 80% of TEE. With advancing age, there is a parallel decline in muscle mass and both basal and total daily energy expenditure that may be partially or fully accounted for by the fact that people tend to become more sedentary as they grow older.
Exercise-induced increases in muscle size and protein content result in greater body protein reserves, which can be critical to survival during episodes of nutritional deprivation that usually accompany profound physiologic stress such as trauma, sepsis, or other acute disease. Such physiologic insults trigger an acute inflammatory response that causes ketogenesis to be suppressed, leaving glucose as the primary energy source available to the body. The problem is invariably compounded by reduced nutrient intake that results as a consequence of the anorexia and gastrointestinal tract dysfunction induced by the inflammatory response. With nutrient intake suppressed, gluconeogenesis becomes the predominant source of glucose. Since the substrate for gluconeogenesis is provided by catabolism of skeletal muscle, LBM becomes an important determinant of survival. Once LBM falls below a critical level, the chance of surviving a serious acute illness diminishes dramatically. Studies conducted within the Warsaw Ghetto, hospital intensive care units, and other settings suggest that a loss of greater than 40% of baseline lean mass is incompatible with life. Indeed, very few healthy people have a LBM that is less than 70% of the mean for that of adults aged 20 to 30.
In addition to inducing muscle hypertrophy, exercise also affects insulin sensitivity and glucose disposal directly and plays a synergistic role with diet in maintaining a healthy weight and a sense of well-being. These effects of exercise can be important adjuncts to good nutrition in the prevention and treatment of hypertension, diabetes, and osteoporosis.
There is a complex interrelationship between nutrition, health status, and clinical outcomes. Although a full discussion of this topic is beyond the scope of this chapter, it is important to emphasize several key points. First, nutrient requirements and the ability to metabolize select nutrients are influenced by many disease states. In addition, many diseases compromise the older individual’s ability to consume adequate amounts of all nutrients. This can occur through a number of mechanisms including disease-induced suppression of appetite, alteration of the normal swallowing mechanism, maldigestion or absorption, or loss of self-feeding ability.
The detrimental effects of disease on nutrient metabolism often become more pronounced with advancing age. This is particularly true of the many acute and chronic diseases that induce an inflammatory response, including acute and chronic infections, congestive heart failure, chronic pulmonary disease, cancer, end-stage renal disease, and rheumatoid arthritis. As described in detail in Chapter 4, with advancing age, the inflammatory response often becomes dysregulated as indicated by persistently elevated serum concentrations of proinflammatory cytokines and other inflammatory mediators including interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and possibly IL-8 and others. IL-1, IL-6, and TNF-α all contribute to the loss of skeletal muscle, fat tissue, and bone mass that characterizes inflammation-associated cachexia. Although anorexia is almost always a contributing factor, the inflammation-induced loss of fat and lean mass is often refractory to nutrition support. Through a number of different mechanisms, proinflammatory cytokines create a state of muscle hypercatabolism by suppressing muscle protein synthesis and/or accelerating muscle protein breakdown independent of dietary factors.
Since these potentially deleterious effects of disease can be difficult to predict, older individuals with one or more acute or chronic health problems should have frequent reassessments of their nutritional status and their nutritional care plan revised as necessary. Although nutrient intake may not be adequate to completely reverse inflammation-induced catabolism, a low nutrient intake will accelerate the development of cachexia. Optimally, good nutritional care should be part of the overall plan of medical intervention aimed at treating the underlying pathology as well as addressing protein and energy deficits. Although a number of specific nutrients are being studied to determine their value in counteracting inflammation-induced loss of LBM, there is not yet adequate evidence that any given dietary supplement is more effective than current standard dietary or nutrition support practices.
AGE-RELATED CHANGES THAT AFFECT NUTRITION
Changes in Body Composition
With advancing age, there are significant changes in body composition that affect the nutritional needs of the individual. Weight increases steadily on average from age 30 to 60 years due primarily to an increase in total body fat. After age 60, weight usually stabilizes, and then begins to decline. Improved survival of nonobese individuals during middle age and cohort effects may account for some of the decline in weight with age. However, weight maintenance becomes increasingly difficult in the advanced years of life. The incidence as well as the potential causes of weight loss increase with age, particularly beyond age 75.
Regardless of whether or not weight changes, advancing age is characterized by a progressive loss in LBM, a relative increase in fat mass, and a redistribution of fat from peripheral to central locations within the body. These changes generally begin in the third decade and increase at an accelerated rate after age 65. This late accelerated phase may be a threshold effect brought about by the loss of lean body mass and the increased prevalence of chronic disease in old age. The loss of lean body mass consists predominantly of skeletal muscle, particularly type II or fast twitch fibers. Central lean body mass, such as the liver and other splanchnic organs, is relatively preserved. Muscle mass may decline by up to 45% between the third and eighth decade of life (Figures 34-1 and 34-2). The quality of muscle may also change. With advancing age, there is a gradual infiltration or replacement of muscle by fat, as has been documented by computerized tomography. Even accounting for body size, height, and other aspects of body composition, fatty infiltration into muscle is associated with symptomatic functional decline, poorer physical function, and change in strength. The loss of muscle mass with age may be greater in men than women, but this remains controversial.
Declining muscle mass with increasing age. (Data from Janssen I, Heymsfield SB, Wang ZM, Ross R. Skeletal muscle mass and distribution in 468 men and women aged 18-88 yr. J Appl Physiol. 2000;89:81–88.)
Cross-sectional computed tomography images of the mid-thighs of a younger and an older woman demonstrating the decline in muscle mass and relative increase in fat mass with age.
The loss of muscle mass with age appears to be the result of multiple interrelated factors including age-related changes in metabolism, function, or structure of organ tissues, disease, medical therapeutics, heritability, and behavior and lifestyle choices of the individual. Notable age-related changes that appear to contribute to loss of muscle include a progressive loss of alpha motor units in the spinal column, a diminution in the intrinsic muscle protein synthetic capacity, and a decline in the production of multiple hormones including testosterone, estrogen, and the insulin-like growth factors. The decline in the intrinsic muscle protein synthetic capacity parallels and may be causally related to a loss of mitochondrial adenosine triphosphate (ATP) production with advancing age. The declines in nutrient consumption and activity level that often accompany advanced age are possibly modifiable contributors to the loss of muscle mass. Many diseases accelerate the age-related decline, particularly degenerative diseases of the central nervous system (CNS) and those affecting any part of the motor pathway. An accelerated loss of muscle mass can occur when a serious illness requires treatment with steroids or other anti-anabolic drugs or is accompanied by low nutrient intake and the need for prolonged bed rest. In all individuals, the loss of muscle mass with age is closely linked with a reduction in muscle strength and exercise capacity, which contribute to the development of functional impairments and disability. The loss of muscle mass and exercise capacity is also linked to the development of coronary artery disease, diabetes mellitus, and other diseases that contribute further to the decline.
In parallel with the loss of LBM, there is an increase in the relative amount and the distribution of body fat with advancing age. Between the second and ninth decades of life, the percentage of body weight that is fat increases by 35% to 50% in females and to an even greater extent in males. Whether or not total body weight changes, intra-abdominal (visceral) fat increases quantitatively and proportionally more than peripheral fat mass. In females, the accumulation of intra-abdominal fat accelerates at menopause and represents primarily a shift from peripheral sites. In males, the increase in intra-abdominal fat with age represents primarily an increase in total body fat mass. For a given waist circumference, older adults have greater visceral fat than young adults, and men have greater visceral and less subcutaneous fat than women.
Changes in Appetite and Energy Intake Regulation
Maintenance of a stable weight requires a steady balance between nutrient intake and energy expenditure. With advancing age, the metabolic, neural, and humoral pathways that normally maintain this delicate balance by regulating appetite and hunger begin to lose their compensatory responsiveness to changes in energy demands. Psychological, socioeconomic, and cultural influences and numerous disease processes further contribute to the dysregulation. From the third to seventh decade of life, these factors integrate to create an imbalance usually favoring a tendency toward weight gain and increased fat deposition, at least in societies where food is plentiful and the physical demands of life are light. However, after age 70, the risk of losing weight increases steadily with each year of survival. Loss of body weight correlates with low dietary energy intake, which is common among both the healthy and frail older adults. The late-life weight decline is associated with many chronic conditions that increase risk of death in old age, including Alzheimer disease.
Pathophysiologic changes that lead to loss of taste, smell, and appetite with advancing age
Numerous pathologic and age-related physiologic changes contribute to the difficulty older people have maintaining a balance between metabolic needs and nutrient intake. The look, smell, taste, and texture of food all contribute to the desirability of a meal and can serve to stimulate or inhibit further consumption. Normal sensory systems are therefore necessary for the full enjoyment of food and are important regulators of nutrient intake. The abilities to smell and taste food are particularly important. The aroma of food can serve as a powerful appetite stimulant. After food enters the mouth, aromatic substances released from the food circulate up through the nasopharynx to the olfactory cleft where they enhance taste. The sensations of smell and taste add to the pleasure of eating while serving as chemosensory signals for food digestion by triggering salivary, gastric, pancreatic, and intestinal secretions. The texture, temperature, and quantity of food in the mouth also contribute to the hedonic qualities of a meal and serve to promote further consumption.
Thus, deterioration in sight, olfactory function, taste sensation, or ability to feel the temperature and texture of food in the mouth can have a deleterious effect on eating habits and the likelihood of maintaining an adequate diet. This becomes an important concern with advanced age. Even healthy older individuals experience a modest deterioration in their ability to detect odors and to differentiate one odor from another. There is a similar pattern to the loss of taste. Much greater losses in taste and smell occur in association with medication usage and other health-related concerns. Table 34-1 contains a representative listing of medications that can cause appetite suppression and a loss of olfactory function and taste sensation. Poor oral health and many diseases that decrease mastication, salivary flow, or ability to swallow can also lead to deterioration in taste and smell and adversely affect appetite. The grinding and mixing of food with saliva play important roles in the release of volatiles and in bringing substances in contact with taste receptors, while swallowing movements are essential to pump the released volatiles up to the olfactory cleft where they are perceived.
TABLE 34-1CLASSES OF MEDICATIONS THAT CAN SUPPRESS APPETITE AND ALTER OLFACTORY FUNCTIONa ||Download (.pdf) TABLE 34-1 CLASSES OF MEDICATIONS THAT CAN SUPPRESS APPETITE AND ALTER OLFACTORY FUNCTIONa
Antihypertensives and other cardiac medications
Bronchodilators and other asthma medications
Drugs for the treatment of parkinsonism
In addition to the special senses, there are various neural and humoral pathways within the gut that may change with advanced age and possibly contribute to the inability of many older individuals to adequately regulate food intake. There are also large numbers of hormones and other gut-derived substances that are thought to influence appetite and food metabolism as shown in Table 34-2. It is theorized that the age-related changes in some or all of these substances may adversely affect food intake in older adults.
TABLE 34-2HORMONES AND CHEMICALS THAT MAY PLAY A ROLE IN APPETITE AND OBESITY ||Download (.pdf) TABLE 34-2 HORMONES AND CHEMICALS THAT MAY PLAY A ROLE IN APPETITE AND OBESITY
Cholesterol and other lipid fractions
Gastrin-releasing peptide (GRP)
Glucagon-like peptide 1 (GLP-1)
Glucose-dependent insulinotropic polypeptide (GIP)
Nonesterified fatty acids (NEFAs)
Sex hormone—binding globulin (SHBG)
Vasoactive intestinal polypeptide (VIP)
Psychological, Socioeconomic, and Cultural Influences on Appetite
After the seventh decade of life, the importance of psychological, socioeconomic, and cultural factors to maintaining an adequate diet increases. Depression is a highly prevalent, frequently unrecognized, and potentially treatable cause of a poor appetite and must always be considered when evaluating an older patient who is losing weight. A correct diagnosis is often difficult to make, particularly when the older individual suffers from other medical problems or dementia. Similarly, bereavement is associated with a lack of appetite. Poverty, lack of education, limited mobility, feeding dependency, and social isolation are also important risks. In healthy adults eating alone may be associated with a lower energy intake than when eating with others. The presence of family and close friends leads to greater nutrient intake than eating with less familiar individuals. Within institutional settings, particularly nursing homes, physical environment and ambience within the dining areas are known to affect appetite. Interventions to ameliorate the dining experience within nursing homes can improve nutrient intakes and promote weight gain. Therapeutic diets (eg, low salt or low cholesterol) are frequently prescribed in nursing homes, often to residents who are losing weight, even though they may add little or nothing to disease management. For these reasons, the American Dietetic Association in collaboration with the Centers for Medicare and Medicaid Services, Pioneer Network, and others published a position statement suggesting that use of therapeutic diets in nursing homes be restricted.
Definition and Prevalence
Obesity is defined as an unhealthy accumulation of body fat, which leads to a higher risk of medical illness and premature death. Although not ideal, BMI and waist circumference are the most widely utilized metrics for classifying overweight and obesity. Both are easily obtained and highly validated measures. BMI is calculated as body weight in kilograms divided by height in meters squared (kg/m2), while waist circumference is a direct measure obtained halfway between the iliac crest and the lower anterior ribs, with the individual standing, and at the end of expiration.
The definition of body weight categories does not currently vary by age or race. Normal weight is considered to be a BMI between 18.5 and 25; overweight, a BMI of 25 to less than 30; and obesity a BMI of 30 or more. Waist circumference is used as an index of central/abdominal adiposity and is clinically useful in further categorizing an individual based on cardiometabolic risk. Traditionally, abdominal obesity is defined as a waist circumference greater than or equal to 89 cm (35 in) for women and greater than or equal to 102 cm (40 in) for men. As with BMI, there is controversy as to whether different reference ranges should be used depending on age and ethnicity. While overweight consistently increases morbidity risk in old age, the data on mortality are less consistent, suggesting that guidelines for both BMI and waist circumference should be liberalized for older individuals.
Based on National Health and Nutrition Examination Survey (NHANES) data and current definitions, obesity is highly prevalent among older adults, especially the young old (ie, individuals between the age of 65 and 80). The variability in rates of obesity by race, gender, and age is shown in Figure 34-3. In all race-by-gender groups, the prevalence declines steadily with each decade of life after age 70. In part, this may be a cohort effect. Reflecting trends for the nation as a whole, prevalence rates of obesity in older adults increased significantly between 1999 and 2010, especially among males (Figure 34-4). It was only among the oldest-old, those age greater than 80, that the prevalence remained stable during this time.
Prevalence of obesity among adults aged 65 and more, by sex and race and ethnicity: United States, 2007–2010. (National Center for Health Statistics Data Brief No. 106, September 2012, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services.)
Trends in the prevalence of obesity among adults aged 65 and more, by sex: United States, 1999–2010. (National Center for Health Statistics Data Brief No. 106, September 2012, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services.)
Potential Benefits and Adverse Consequences of Obesity
There is controversy regarding the potential benefits and adverse consequences of being overweight or obese after age 65. Potential benefits include protection against bone fractures and a possible survival advantage, at least for select populations of older adults. The lower fracture risk associated with obesity is related to several factors. As a result of their increased fat mass, obese older adults place more stress on their bones and convert more androstenedione to estrone than do slimmer individuals of similar age. Both of these factors contribute to the increased BMD in obese older adults. Fat also can serve as a cushion to protect against the impact of a fall, creating further protection against bone fractures.
Assessing the impact of weight on survival in old age is more complex. The numerous studies and meta-analyses that have examined this relationship in older adult populations have produced inconsistent results. Overweight and obese older adults may have a survival advantage during periods of protracted illness, an effect thought to be the result of their greater energy and protein reserves. In general, obesity is associated with greater lean mass; during periods of catabolic stress, the fat and lean mass serve as a functional nutritional reserve.
The impact of obesity on survival in the general population of community-residing older adults is less clear. Most population-based studies that have examined the relationship between weight categories and survival in older adults have identified a “J-shaped” relationship between BMI and all-cause mortality (Figure 34-5). The higher mortality associated with a BMI less than 18.5 is generally consistent across studies. However, this does not necessarily indicate that older adults who have been slender all of their lives are at increased risk of mortality. The high all-cause mortality associated with a low BMI probably reflects the fact that many of the older adults in this weight group had previously lost weight due to disease. However, low protein reserves, whether the result of weight loss or a thinner body habitus, may be the critical factor that is contributing to risk of death in older adults with a low BMI.
Data from the National Institutes of Health-AARP cohort aged 50 to 71 years-old and followed for a maximum of 10 years. Men (left) and women (right) shown by smoking status in relation to their current body mass index (BMI). Risks for never smokers are thought to most accurately estimate risk because they remove the effect of smoking on body weight and risk of death. Data adjusted for age, race or ethnic group, level of education, alcohol consumption, and physical activity.
Due to the heterogeneity of study results, it is also unclear what range of BMI is optimal for survival and at what level of obesity all-cause mortality risk begins to increase. Mortality risk appears to be lowest for older adults who are overweight (BMI, 25–30) or even moderately obese (BMI, 30–35), and mortality risk is similar for obese older adults as for age-matched adults who are in the normal weight category. However, when different methodologic approaches are used, which in some cases include controlling for cohort mortality and age-related survey selection bias, all-cause mortality increases in direct relationship with BMI in the range of 25 to greater than 40. Further complicating the issue, mortality risk in old age may relate more to fat distribution than total body mass. For any given body weight, mortality risk increases with increasing waist circumference, or more specifically, increasing intra-abdominal or visceral fat mass as measured by modern imaging modalities. Although waist circumference is strongly correlated with intra-abdominal fat mass, the two metrics are not the same. The relative contribution of mid-abdominal subcutaneous fat to waist circumference varies considerably among older adults. Thus, direct measures of intra-abdominal fat are more powerful indictors of cardiovascular (CV) risk. However, the mortality risk associated with obesity after controlling for intra-abdominal fat mass is also controversial. Given the many uncertainties about the impact of obesity on overall survival, it is important to consider what other effects excess weight has on the health of older adults.
The impact of obesity on overall health, functional status, and quality of life in older adults is more certain. Overweight in old age is associated with the same risks for disease as in younger populations, and it also exacerbates many age-associated diseases (Table 34-3). The higher risk of disease associated with obesity may result as a consequence of the detrimental metabolic effects of excess body fat and/or the adverse mechanical consequences of obesity. With regard to the latter effects, the relative excess in total body weight to muscle mass leads to osteoarthritis and other disabling conditions while increasing the work required to perform many activities of daily living. The result is a lower functional reserve, chronic pain, and an increased risk of disability. Some heavier individuals have relatively less muscle mass than expected on the basis of size, a situation described as sarcopenic obesity; for these individuals, the risk of disability is especially high.
TABLE 34-3DISORDERS DIRECTLY CAUSED OR EXACERBATED BY OBESITY ||Download (.pdf) TABLE 34-3 DISORDERS DIRECTLY CAUSED OR EXACERBATED BY OBESITY
Atherosclerotic cerebrovascular disease and stroke
Hypoventilation/obstructive sleep apnea
Coronary heart disease
Peripheral vascular disease
Varicose veins/venous insufficiency
Type 2 diabetes
Fatty liver diseases
Various forms of cancer
Degenerative disease of large joints
Degenerative disc disease
The metabolic effects of fat are mediated by a variety of hormones and proteins termed adipokines that are produced and secreted by the adipocytes. The adipokines include leptin, angiotensin, resistin, adiponectin, plasminogen-activator inhibitor 1, and proinflammatory cytokines such as IL-6 and TNF-α. When produced in excess quantities, particularly by visceral fat, these adipokines can have adverse health effects. Obesity is strongly linked to the development of numerous life-threatening diseases such as diabetes, heart disease, stroke, and multiple types of cancer. The adipokines appear to be the causal link between obesity and such diseases. They may play a role in the development of obesity-associated high blood pressure, dyslipidemia, and glucose intolerance, all of which are CV risk factors. The adipokines may also produce insulin resistance, which is seen with higher levels of intra-abdominal fat even in the absence of overt overweight. Intramuscular fat may also contribute to metabolic abnormalities or functional impairments that are mediated by adipokines. Many of the apparent adverse metabolic effects of excess body fat are inadequately studied. In postmenopausal women, overweight and weight gain are associated with risk of breast cancer, and with poorer outcomes for the cancer; overweight also appears to increase the risk of colon cancer. The potential mechanisms that causally link excess fat to these disease outcomes are being investigated.
Because of its many adverse effects on health, obesity is a major risk factor for functional disability with advancing age. Any disease or age-related process that leads to deterioration in central or peripheral nervous system, cardiopulmonary, or musculoskeletal function can contribute to disability. As stated above, obese older adults are at higher risk than age-matched nonobese individuals for developing many of the chronic disabling diseases prevalent among older adults. As a result of these diseases or the treatments required for their control, obese older adults are far more likely to develop physical impairments or disabilities than are other older adults. Obesity also makes it more challenging to obtain the needed level of care when disabled, all of which can lead to a deterioration in quality of life. For these reasons, interventions specifically targeting obesity are sometimes appropriate in older adults.
Interventions Targeting Obesity
Given the increased risk of disability associated with obesity, controlled weight loss may be an appropriate therapeutic option for select older adults with weight-related problems. Short-term clinical trials in older people show that appropriate interventions can lead to moderate weight loss resulting in improvements in cardiovascular risk factors (such as hypertension, insulin resistance, and metabolic syndrome) and other select clinical outcomes. However, there is a concern that weight loss in older adults could produce more long-term adverse than beneficial results. In fact, there is a strong association between weight loss in older adults and an increased risk of subsequent adverse clinical outcomes such as hospitalization and death. Even among studies that tried to differentiate between voluntary and involuntary weight loss, there were conflicting results as to the risks associated with purported (ie, self-reported) intentional weight loss. Furthermore, when dietary restriction is the primary mechanism for weight loss, the loss of fat is accompanied by loss of both LBM (particularly skeletal muscle mass) and BMD. Although the percentage loss from each of these tissue compartments with dieting is the same in old and young adults, the adverse consequences can be much greater in older people who have low functional reserves and high fracture risk. For this reason, a primary focus of any weight loss intervention in older adults has to be on preserving or improving LBM and BMD. The only approach to date that has proven successful in accomplishing this dual-purpose goal is the combination of an energy-restricted, normal- to high-protein diet with moderate to intense exercise. In obese older adults diet and exercise together can lead to clinically meaningful improvements in key metabolic parameters, physical performance, self-reported physical function, and quality of life; the beneficial effects are greater and the loss of both BMD and LBM less than with either intervention alone. To attain these benefits, only moderate weight loss (in the range of 10%) is required. The target of the weight loss should be improvement in the target weight-related health condition.
Although randomized, highly controlled trials provide strong evidence of benefit, little is known about how best to achieve these results with obese older adults in routine clinical settings. Efforts to increase physical activity and to decrease caloric intake are the best options for older adults, as surgical and pharmacologic options are limited, untested, and generally much riskier. In the absence of relevant long-term clinical trial data on outcomes with weight reduction, advice on weight loss should be guided by symptoms related to the overweight, anticipated short-term health benefits, and the general level of health status of the patient.
To be considered a candidate for a weight loss program, an obese older adult needs to have a weight-related problem that is likely amenable to weight loss plus the motivation to commit to the necessary lifestyle changes that are required to meet program goals. In order to have any lasting benefits, changes in dietary habits and level of physical activity need to be maintained long term. Such a vigorous program would likely require the individual patient to be relatively healthy.
Components of a Weight Loss Program for Older Adults
Upon committing to a weight loss program, an older adult should undergo a careful medical evaluation, which should include a detailed history and physical examination and a very careful assessment of the potential risks and benefits of both exercise and diet. American College of Sports Medicine guidelines should be used to assess the risks of exercise and need for more detailed diagnostic testing such as cardiac stress tests. Successful programs generally include an assessment of the individual’s insight, motivation, and readiness to make the necessary lifestyle changes. Using motivational interviewing or other techniques, the individual’s personal goals should be illuminated and a personalized intervention strategy devised that includes short- and long-term goals and timelines. Support from, or co-participation by family and significant others can be critical to success.
Ideally, both the dietary and exercise interventions need to be consistent with the individual’s lifestyle, abilities, interests, and personal goals. When an established program is not available to which the individual can be referred, input and support from a multidisciplinary team of professionals are crucial. Such a team may include a dietitian/nutritionist, physical therapist, nurse, physician, social worker, or other health professionals. The diet should include adequate protein and micronutrients and only moderate energy restriction (eg, 500–800 kcal/day) with the goal of 1 to 2 lb of weight loss in a week. The exercise intervention should include a combination of endurance and progressive-resistance muscle strength training. Inclusion of flexibility exercises is advisable, but the benefits of these exercises are not established. The types of exercises incorporated in the personalized plan will need to be predicated on availability of resources, facilities, and equipment and the individual’s living environment. The ideal exercise program is one that is conducted in a setting that is safe, accessible, and appropriately equipped and involves activities the individual likes doing. For many older adults, this would necessitate that the exercise program be home-based and require little equipment. Nearly all diet/exercise programs formally investigated have been supervised, institution-based programs, which represent a major access barrier for many older adults.
Once an obese older adult starts an exercise/weight loss program, the quality and frequency of follow-up support become crucial. Early in the intervention, frequent follow-up is often needed, but the intervals between contacts can be gradually extended once the individual demonstrates an acceptable trajectory of success. Follow-up can be accomplished by recurring clinic visits, phone calls, or any of a variety of electronic means. These follow-up visits can be used to monitor progress (eg, checking exercise and weight logs), provide ongoing support and assistance to deal with setbacks and barriers to success, and guidance in advancing exercise intensity or setting new goals. The level of involvement of a nurse or other appropriately trained health professional in the follow-up assessments needs to be determined based on the medical complexity of the participant.
NUTRIENT REQUIREMENTS TO MAINTAIN HEALTH
Daily energy requirements per kilogram of body weight generally decline with age, dropping as much as 33% between the third and ninth decade of life. Male gender and chronic disease are associated with a greater rate of decline. However, a decrease in energy requirements with age occurs even among those who remain healthy. The primary reason for this decline is the loss of muscle mass that is nearly universal with advanced age. Muscle is much more metabolically active than adipose tissue. As muscle mass is lost, the ratio of fat to lean mass increases leading to a greater drop in the resting or basal metabolic rate (BMR) than predicted by the decrease in total body mass. Since BMR generally accounts for 60% to 75% of TEE, the end result of the muscle loss is a significant decline in TEE and thus energy requirements.
A second mechanism accounting for the decline in energy requirements with age is a decrease in physical activity. Energy expenditure of physical activity (EEA) generally declines with age to the same extent as BMR, accounting for about 15% to 35% of TEE in the majority of older adults. However, EEA can range from 5% in those who are bedridden to 50% in highly active, physically fit older adults. Lifestyle plays a big role in determining physical activity energy expenditure of older people, just as it does in those who are younger. Although the increased prevalence of chronic disabling disease accounts for some of the decline in physical activity with advancing age, even healthy older adults tend to be more sedentary that younger individuals.
Some chronic conditions may result in an increased TEE, although this remains controversial. Individuals with Alzheimer disease who constantly pace would fall into this category, as would individuals with a constant tremor. Even when an individual appears to be rather sedentary, their EEA may be greater than expected, particularly if they have certain disabilities such as a neurologic disorder or amputation. These conditions sometimes result in a loss of neuromuscular energy efficiency and thus exceptional levels of energy expenditure while completing even basic activities of daily living.
The decline in energy requirements with advancing age means that older persons need to consume less food in order to maintain their weight and customary activity level. This places the older individual at risk of developing protein and micronutrient deficiencies, since requirements for other nutrients may not decrease as much as energy. Consequently, it is important that older individuals increase their activity level and change their diet to protein- and micronutrient-rich foods.
Because of the paucity of high-quality nutrition studies with adequate representation from older age groups, current recommendations for protein intake do not differentiate adults over the age of 65 from those who are younger. The latest (2005) version of the recommended dietary intake (RDI) for protein, released by the Food and Nutrition Board and the Institute of Medicine, is 0.8 g/kg body weight/day for both men and women over age 19. However, the question of whether protein requirements change appreciably with advancing age continues to be debated. Based on their interpretation of available data, some contend that the recommended protein intake for older adults should be 1.0 to 1.25 g/kg/day. Given the variability in estimates of protein requirements in older adults, it may not be possible to resolve this controversy until better measurement techniques become available.
Factors that influence the protein requirements of older individuals
The protein requirements of an individual can change with time, being influenced by age, nonprotein content of the diet, activity level, medications, and health status. The energy content of the diet is particularly important. The protein intake required to maintain nitrogen balance increases with decreasing energy intake. Carefully conducted metabolic studies of healthy young males indicate that nitrogen balance cannot be attained at any protein intake when total energy intake is less than 126 kJ/kg (30 kcal/kg). Although comparable data are not available for individuals over the age of 65, the importance of energy intake in older individuals is well recognized. A negative energy balance usually precipitates a negative nitrogen balance, especially in individuals who are ill or who have a low level of activity. Whether progressive resistance muscle strength training, alone or in combination with a high protein diet, can prevent loss of LBM in older individuals during periods of voluntary caloric restriction and weight loss is being investigated. As a general rule, protein requirements increase with high levels of activity such as sustained high-intensity exercise.
Many disease states and medications can induce a catabolic state for protein by altering the normal balance between protein synthesis and degradation. Older individuals who are both confined to bed and have an injury, infection, or another acute inflammatory condition are at particularly high risk of developing a profoundly negative nitrogen balance that can lead to a rapid loss of LBM, particularly skeletal muscle mass. High doses of corticosteroids can have a similar effect. The amount of protein that needs to be consumed in order to minimize loss of LBM and optimize recovery from such disease states is often difficult to determine. In general, older hospitalized patients who are acutely ill or recovering from major surgery or trauma warrant a protein intake of 1.5 g/kg of body weight/day unless they have a condition that necessitates protein restriction such as renal or hepatic insufficiency. Chronically ill and bedridden older residents of long-term care institutions are likely to have similarly high protein requirements. Whether one source of protein is better than another in meeting the nutrient needs of older adults is controversial. Although it is generally recognized that all older adults should consume a diet that provides adequate quantities of all essential amino acids, there is otherwise little consensus as to the importance of the dietary protein source. Several animal and laboratory-based human studies suggest that protein or amino acid supplements containing high concentrations of branched-chain amino acids such as leucine may be more effective than other dietary proteins in stimulating muscle protein synthesis, particularly in sedentary or chronically ill older adults. However, other studies refute these findings.
Fat serves as a key source of energy and essential fatty acids as well as a vehicle for transporting fat-soluble vitamins. Even when obesity and elevated cholesterol or triglycerides are a concern, fat intake should not fall below 10% of total energy requirements in order to allow for adequate absorption of fat-soluble vitamins (A, D, E, K), and to ensure that the requirements for the essential fatty acids are met. There are two main types of essential fatty acids, the omega-6 series, derived from linoleic acid (eg, arachidonic acid and γ-linoleic acid), and the omega-3 series, that could be derived from α-linolenic acid (from plant sources) or contained in certain cold water fish (eg, eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]). The essential fatty acids are required for the synthesis of cell membrane phospholipids and eicosanoids, which include prostaglandins, leukotrienes, and hydroxy acids. Cell membrane phospholipids influence the biomechanical properties of the membranes and their membrane-bound receptors. The eicosanoids, derived predominantly from arachidonic acid and EPA, serve many functions including modulation of inflammation and host defenses. It is currently recommended that intake of the omega-6 linoleic acids be at least 1% of total food energy.
Clinical deficiency of these essential fatty acids is rarely seen in adults since Western diets generally provide 8 to 15 g/day and adipose tissue provides a reserve of 0.5 to 1 kg. Omega-6 fatty acids are abundant in many of the foods common to the average American diet including most vegetable oils, nuts, cereals, seeds, and legumes. When a deficiency does develop, it is usually a result of profound cachexia or extensive small bowel disease or necrosis and the inadequate provision of nutrition support. Although current recommendations call for the omega-3 derivatives of α-linolenic acid to be at least 0.2 % of total food energy, many nutritionists suggest higher intakes due to their beneficial effects on lipid metabolism. Oils from a variety of cold water fish species including halibut, mackerel, herring, and salmon are potentially high in the omega-3 fatty acids. Currently, nutritional labeling does not indicate the amount of omega-3 fatty acids that is contained in fresh fish; farm-raised fish may have more or less omega-3 fatty acids than wild caught fish, depending on the food they are fed. Many omega-3 fatty acid supplements are available commercially, but these provide varying amounts of marine-based EPA and DHA. There is inadequate evidence that these supplements provide the same benefits as consuming fish. α-Linolenic acid, which serves as a precursor of EPA, is also a polyunsaturated omega-3 fatty acid, and is found primarily in plant products such as soybeans, canola oil, flaxseed oil, and walnut oil. However, it is controversial as to how effectively humans can convert α-linolenic acid to EPA; as little as 10% of α-linolenic acid may be converted to EPA.
The optimal fat intake for older adults needs to be determined on an individual basis. Although CHD remains the number one killer of older Americans, the importance of dietary fat after the age of 65 remains controversial. It is not known whether fat- and cholesterol-restricted diets have any beneficial effects in reducing CHD mortality in this age group. In fact such diets may have detrimental consequences, especially in those who are having problems maintaining their weight. Therefore, it seems prudent to limit fat intake only in healthy older individuals who otherwise would not be adversely affected by such dietary restrictions.
Increasing the ratio of monounsaturated and polyunsaturated fat to saturated fat, without changing total fat intake, may be beneficial in some situations. For this reason, some experts support the use of the Mediterranean-style diet, which promotes the use of olive oil, tree nuts and peanuts, fatty fish, seafood, and white meat, and discourages intake of red and processed meats. Concern has also been raised about the use of partially hydrogenated fats rich in trans fatty acids, as these products may have an adverse effect on lipid metabolism. Although more study is needed before any special diet can be recommended, it is probably prudent to emphasize the use of natural fats derived from vegetable oils (predominantly monounsaturated), nuts, and fish while reducing those from animal products and avoiding foods containing trans fatty acids. However, these guidelines may not be applicable to frail older individuals, especially those who are losing weight involuntarily, have a BMI less than 20, or have disease conditions limiting their nutrient intake. Since fats have twice the energy content per gram as carbohydrates and protein, a diet high in fat may be necessary for such frail older individuals in order to meet their maintenance energy requirements or to replete deficits. Restricting the types of foods these individuals consume may have only detrimental consequences.
Recommendations for carbohydrate content of the diet are generally based on two considerations, the source of the carbohydrates and the energy requirements of the individual. Ideally, food sources should be rich in fiber (see section on Fiber Content of Diet later) and provide primarily complex carbohydrates rather than simple sugars. The amount of carbohydrates that should be included in the diet is usually determined by default. The energy, protein, and fat requirements of the individual are determined first. Carbohydrate requirements are then determined by subtracting the amount of energy supplied by protein and fat from the total energy requirements. Since protein requirements represent approximately 15% of the total energy content of the diet and fat ideally should be less than 30%, carbohydrates usually represent 55% to 70% of the total. When carbohydrates are totally excluded from the diet, energy requirements of the body are partially met by the incomplete oxidation of fatty acids, which leads to ketosis and may cause lethargy and depression. This ketosis also contributes to anorexia, which is part of the appeal of low-carbohydrate weight loss diets. To prevent ketosis, at least 50 to 100 g of carbohydrates should be consumed each day.
Although fluid requirements do not change appreciably with age in adults, people over the age of 65 have a reduced ability to regulate their fluid intake and are much more likely than young adults to become dehydrated when their health status or environment changes. Aging is associated with a decline in the intensity of the thirst response to fluid deprivation, a delay in correcting the resulting increase in serum osmolarity, and a reduced ability of the kidneys to concentrate the urine despite an increase in serum vasopressin concentration. Urine output increases with age by two- to threefold over younger adults as urine concentrating ability declines. Chronic disease and injuries that cause a deterioration of cognitive or physical function increase the risk of dehydration further by altering the perception of thirst, reducing the ability to express the desire for water, or diminishing the capability to access and drink adequate amounts of fluids. When an acute febrile illness occurs in an older individual who is already physically or cognitively impaired, life-threatening dehydration can develop rapidly. This scenario occurs with alarming frequency in nursing homes. The failure of many health care providers, family members, and personal aid assistants to recognize the risk factors and early warning signs of dehydration contributes to the danger that a frail older individual will become severely dehydrated. Many older adults themselves do not recognize their risks and may inappropriately restrict their fluid intake, sometimes as a method of controlling incontinence.
Care must be taken to prevent dehydration by recognizing those at highest risk, especially older individuals with cognitive and physical deficits, swallowing problems, ongoing weight loss, diarrhea, fever, or poorly controlled diabetes, or receiving enteral feeding, diuretics, or laxatives. Although there is no DRI for water, the minimum daily intake for inactive adults in moderate climates is estimated to be between 1 and 3 L/day; a reasonable target is roughly 30 mL/kg/day for most healthy older adults. Requirements increase with fever, activity, or prolonged exposure to elevated environmental temperatures. Prolonged exposure to elevated environmental temperatures, such as may occur during heat waves, may also precipitate profound dehydration. Those at high risk for developing dehydration should be given set prescriptions for fluid intake and have their fluid intake monitored closely. Whenever hydration status is in doubt, the subject should be weighed, orthostatic blood pressure reading recorded, and serum electrolytes, urea nitrogen, and creatinine checked. Blood pressure readings should be compared to baseline values as many frail older adults have significant orthostasis even when fully hydrated. In some settings, it may also be appropriate to monitor urine output. Skin turgor is not a reliable indicator of hydration status and should not be used as such in the care of older subjects. Patients, family, and all health care staff, especially in nursing homes, need to be trained to recognize the importance of maintaining an adequate fluid intake at all times, and to carefully monitor intake if there is a change in mental status, activity level, or health status, or if fluid requirements increase, as occurs during heat waves.
Dietary fiber is derived from structural components of plant cell walls and consists of plant polysaccharides and lignin, which are resistant to digestion by intestinal enzymes. Many professional health organizations recommend a diet containing 20 to 35 g of fiber a day or 10 to 13 g dietary fiber per 1000 kcal consumed. Although dietary fiber may be associated with health benefits including a decreased rate of certain forms of cancer, diabetes, heart disease, and obesity, the average American diet is very low in fiber with consumption usually in the range of only 10 to 15 g daily.
There are two general categories of dietary fiber: water-insoluble fibers, such as cellulose, hemicellulose, and lignin; and water-soluble fibers, such as gum and pectin. Each category of fiber has a somewhat different spectrum of beneficial effects. Both types lower the energy density of the diet. The added bulk also has a short-term satiety effect, which helps control appetite and prevent overconsumption. Water-insoluble fiber has the further effect of holding water within the intestinal contents, which results in an increased fecal bulk, a decreased gut transit time, and a lower intraluminal pressure within the colon. These properties of water-insoluble fiber make it an important dietary component since it reduces constipation and may help to prevent the formation of colonic diverticula. Sources of insoluble fiber include fruits, vegetables, dried beans, wheat bran, seeds, popcorn, brown rice, and whole grain products such as breads, cereals, and pasta. About two-thirds to three-fourths of the dietary fiber in typical mixed-food diets is water insoluble. There are many excellent web sites that provide tables listing the soluble and insoluble fiber content of foods (eg, http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/high-fiber-foods/art-20050948, https://www.wehealny.org/healthinfo/dietaryfiber/fibercontentchart.html, https://www.prebiotin.com/resources/fiber-content-of-foods/. Accessed February 9, 2016.).
Water-soluble fiber increases the viscosity of intestinal contents, prolongs gut transit time, and decreases the rate of small intestinal absorption of carbohydrates and bile acids. These effects may have important physiologic implications that can be used to advantage clinically. By slowing the rate of carbohydrate absorption, a very high soluble-fiber diet can be effective in reducing the postprandial surge in the serum glucose, which may be beneficial in the treatment and prevention of diabetes. Through its effects on bile acid absorption, soluble fibers can lower total cholesterol and low-density lipoprotein (LDL) cholesterol by 3% to 10%. There is an inverse association between the total dietary fiber intake and the rate of fatal and nonfatal myocardial infarctions; several meta-analyses demonstrate that higher intake is also associated with decreased all-cause mortality. Most of these effects of soluble fibers were demonstrated using fiber concentrates. Comparable amounts of fiber can be obtained from food sources, such as apples, oranges, pears, peaches, grapes, vegetables, seeds, oat and rice bran, dried beans, oatmeal, barley, and rye. Diets that are high in fiber from food sources also provide essential micronutrients and nonnutritive compounds such as xenobiotics, antioxidants, and phytoestrogens that may have important health-promoting consequences.
As a general rule, a diet rich in fresh fruits, vegetables, legumes, and whole-grain products is recommended. As portrayed in the USDA Choosemyplate.gov, this should include two cups of fruit, 2 1/2 cups of vegetables, and 6 oz of grains each day (Figure 34-6). Since most fruits and vegetables contain less than 2 g/serving total fiber and most refined grain products contain less than 1 g/serving, legumes, whole grains, and cereal brans should be substituted for other foods whenever possible in order to increase the amount of both kinds of fiber. Supplementing the diet with any of the commercially available concentrated fiber sources may be necessary, especially in frail older people. Concentrated sources of dietary fiber may also be helpful in the treatment of chronic constipation when a limited variety of food is available or the amount of food consumed is inadequate. A large increase in fiber over a short period of time may result in bloating, diarrhea, gas, and general discomfort. It is important to add fiber gradually over a period of several weeks to avoid abdominal problems. Fiber supplements should always be taken with adequate fluid in order to avoid worsening constipation.
ChooseMyPlate.gov, U.S. Department of Agriculture, Center for Nutrition Policy and Promotion, June 2, 2011, USDA Center for Nutrition Policy & Promotion (CNPP), http://choosemyplate.gov/. Accessed February 9, 2016.
Between 1997 and 2011, the Food and Nutrition Board of the US National Research Council revised the dietary reference intakes (DRIs), which updated the earlier RDAs for vitamins and minerals. The DRIs include separate intake recommendations for adults aged 51 through 70, and for adults older than 70 years. There are not enough scientific data to calculate requirements for all micronutrients, and any person with a medical disorder may need more or less than the DRI for some nutrients. Table 34-4 lists the recommended intakes for various vitamins, as well as the recommended tolerable upper intake limits (ULs). Intakes of micronutrients that are lower than the UL usually pose little risk for toxic side effects in healthy people. The UL allows patients and health care workers to understand possible risks if large amounts of vitamins and minerals are consumed. Understanding and consuming the DRI for vitamins and minerals reduces the risk for classic deficiency disorders (like scurvy, pellagra, beriberi, etc), but the ideal intake of vitamins and minerals needed for optimum health, which may be higher than the DRIs or ULs, remains controversial. Changes to the DRIs are often contentious, and they can have major medicolegal and financial implications for fortified foods and the supplement/health food industry.
TABLE 34-4ADULT DIETARY REFERENCE INTAKES AND TOLERABLE UPPER LIMITS FOR SELECTED VITAMINS AND MINERALS ||Download (.pdf) TABLE 34-4 ADULT DIETARY REFERENCE INTAKES AND TOLERABLE UPPER LIMITS FOR SELECTED VITAMINS AND MINERALS
|VITAMIN OR MINERAL ||RECOMMENDED DAILY INTAKEa ||TOLERABLE UPPER LIMIT |
|Vitamin A (retinol) || |
900 μg (males)
700 μg (females)
|3000 μg |
|Vitamin D || |
600 IU (age 9–70)
800 IU (age > 70)
|4000 IU |
|Vitamin E || |
22 IU (natural vitamin E)
33 IU (synthetic vitamin E)
|1500 IU |
|Vitamin K || |
80 μg (males)
65 μg (females)
|Vitamin B1 (thiamin) || |
1.2 mg (males)
1.1 mg (females)
|Vitamin B2 (riboflavin) || |
1.3 mg (males)
1.1 mg (females)
|Niacin (nicotinamide) || |
16 mg (males)
14 mg (females)
|Vitamin B6 (pyridoxine) || |
1.7 mg (males)
1.3 mg (females)
|100 mg |
|Vitamin B12 (cobalamin) ||2.4 μg ||b |
|Folic acid (folate) ||400 μg ||1000 μg |
|Vitamin C (ascorbic acid) || |
90 mg (males)
75 mg (females) (increase by 35 mg for smokers)
|2000 mg |
|Calcium ||1000–1200 mg ||2000 mg |
|Selenium ||55 μg ||400 μg |
Vitamin and mineral supplementation
Many older adults, including those who are healthy and living independently as well as those who are frail, ill, or institutionalized, are at risk for micronutrient deficiencies. Several population-based nutritional surveys demonstrate that community-dwelling older adults commonly consume as little as 50% of the RDAs for many vitamins. These findings reflect the fact that even healthy adults do not consistently consume recommended amounts of fortified dairy products, fruits, and vegetables. Risk factors for poor intake, adverse drug-nutrient interactions, and nutrition-related diseases all increase as a function of age, and clinical (and subclinical) deficiencies of vitamins and minerals become more likely, particularly once frailty and the need for institutionalization occurs. The micronutrients most commonly deficient include vitamins C, D, E, B12, thiamine (B1), and folic acid, and the minerals calcium, magnesium, and zinc. Because of this, many nutritionists recommend that older adults add a daily, iron-free, general vitamin and mineral supplement supplying the DRI for most micronutrients to their diets, although evidence in support of benefit from this recommendation is lacking. Studies of multivitamin supplementation in noninstitutionalized people have found no benefit in reducing cardiovascular or cancer risk. It also remains unclear as to whether intakes of individual micronutrients above the DRI in selected populations are beneficial. High intakes of some micronutrients (such as vitamins A, D, and pyridoxine) are well known to cause toxicity, which may be so subtle and nonspecific that the harmful effects may not be easily diagnosed. High supplemental intakes of other vitamins or provitamins (like vitamin E and β-carotene), which had been thought to be risk free, have now been associated with adverse health consequences. Older adults should be counseled not to exceed the tolerable upper intake limits (see Table 34-4) for vitamin intake and to disclose all vitamin and mineral supplement use whenever medications are reviewed by any health professional. Vitamin and mineral supplementation should not substitute for an overall program of healthy nutrition (eg, high fruit, vegetable and whole grain intake and reduced saturated and trans fat intake).
Low-serum vitamin B12 levels become more common with aging, and about 10% to 15% of older adults have vitamin B12 deficiency. Thus, low levels do not represent normal aging. Pernicious anemia, an autoimmune disorder causing decreased gastric intrinsic factor production, is a rare cause of deficiency in the older adult. Cobalamin deficiency in older adults is more commonly due to malabsorption of cobalamin in foods, usually due to atrophic gastritis and hypochlorhydria (Table 34-5); supplemental B12 in crystalline form is not affected by atrophic gastritis and continues to be well absorbed. Stomach acid helps to remove the vitamin from food and make it bioavailable. There may be other causes for deficiency in older adults that are not yet known. Disorders that interfere with enterohepatic absorption (such as ileal disease or surgery) will lead to deficiency more rapidly than low intake because the high efficiency of enterohepatic vitamin B12 reabsorption will be impaired, and the vitamin lost in the stool.
TABLE 34-5CAUSES OF VITAMIN B12 DEFICIENCY ||Download (.pdf) TABLE 34-5 CAUSES OF VITAMIN B12 DEFICIENCY
Atrophic gastritis and hypochlorhydria
Chronic antacid use (histamine-2 blockers, proton pump inhibitors)
Diseases of the small intestine and terminal ileum: Crohn disease, sprue, malabsorption syndromes
Helicobacter pylori infection
Parasitic infections of the small bowel (eg, fish tapeworm)
Bacterial overgrowth syndromes
Acquired immune deficiency syndrome (AIDS) and AIDS treatment (eg, zidovudine)
Vitamin B12 deficiency can present clinically with two relatively independent disorders. There is a hematologic disorder that causes macrocytosis and anemia. And there is a neurologic disorder that can cause a peripheral neuropathy, including paresthesias and numbness; spinal column lesions, including loss of vibration and position sense, sensory ataxia, limb weakness, orthostatic hypotension, and plantar extensor responses; and neuropsychiatric symptoms. These signs and symptoms of vitamin B12 deficiency are nonspecific and common in many older adults with comorbid disorders. When there are several possible causes for the neurologic signs and symptoms, vitamin B12 supplementation is usually accompanied by disappointing, small measurable neurologic or behavioral improvement. The older the patient is and the more profound the signs and symptoms are, the less likely is the recovery. However, some patients may respond, especially if deficiency is relatively recent. Since patients with more severe hematologic signs often have less neurologic impairment, and vice versa, it is important to consider vitamin B12 deficiency even if the patient lacks macrocytosis and anemia. Thus, screening all older adults for vitamin B12 deficiency should be considered, and supplementation of all deficient patients is recommended.
Many patients with “low normal” vitamin B12 serum levels (< 350 pg/mL) have measurable biochemical abnormalities, including elevated methylmalonic acid (MMA) (> 270 nmol/L) levels, which improve with supplementation. Although these patients often appear to be asymptomatic, it is probable that borderline serum vitamin B12 levels represent an early preclinical deficiency state. If this is the case, current laboratory norms for vitamin B12 are too low since they may not identify patients with early deficiency. Secondary tests for low B12 status are also nonspecific; for example, MMA may also be elevated with renal failure, and homocysteine levels are also affected by folate and vitamin B6 status. Other tests for vitamin B12 deficiency, such as methylcitric acid or holotranscobalamin levels, may prove better (when used with vitamin B12 blood levels) but are not yet readily available.
An approach to screening for vitamin B12 deficiency, and treatment guidelines are presented in Table 34-6. Intramuscular or oral replacement is most common; alternative formulations (such as nasal gels) are more costly and have not been rigorously tested. There is no scientific basis for prescribing vitamin B12 supplementation as a general tonic, and it is not recommended.
TABLE 34-6EVALUATION AND TREATMENT OF VITAMIN B12 DEFICIENCY IN OLDER ADULTS ||Download (.pdf) TABLE 34-6 EVALUATION AND TREATMENT OF VITAMIN B12 DEFICIENCY IN OLDER ADULTS
Screen with a determination of serum vitamin B12 level any older adult who is frail, has macrocytosis or neutrophil hypersegmentation with or without anemia, has peripheral neuropathy or a gait disorder, or has otherwise unexplained neuropsychiatric symptoms.
Any patient with a vitamin B12 serum level less than 200 pg/mL (150 pmol/L) can be considered to have a deficiency. A serum level between 200 and 350 pg/mL (150–260 pmol/L) indicates a borderline deficiency.
Most older adults with a B12 deficiency can be treated with supplementation without further investigation. Only in rare cases is it essential to prove that an older patient has pernicious anemia by testing for antibodies to intrinsic factor or performing a Schilling test. Assessing for infection by Helicobacter pylori is an additional option.
Most older adults with a borderline deficiency can also be treated with supplementation. If it is necessary to obtain further biochemical evidence that a borderline serum vitamin level represents a significant deficiency, the methylmalonic acid (MMA) level (serum or urine) can be determined before and after treatment. (An elevated MMA level should fall to normal with correct treatment.) Assessing for infection by H pylori is an additional option.
All patients with possible symptoms of vitamin B12 deficiency should receive parenteral supplementation. This can be accomplished by giving several intramuscular shots (1000 μg) within several days to weeks and then continuing supplementation indefinitely with monthly injections. Any healthy patient whose deficiency was found incidentally and is otherwise asymptomatic can be given a trial of oral supplementation with 1 mg daily. These patients should have their serum vitamin B12 level reassessed in a month to affirm absorption, and periodic (once or twice yearly) screening thereafter.
Folate deficiency is associated with general malnutrition (particularly that accompanying alcohol abuse), or with specific folate antagonists, such as methotrexate, phenytoin, sulfasalazine, primidone, phenobarbital, and triamterene. Like vitamin B12 deficiency, it can present as a megaloblastic macrocytic anemia. Folate supplementation alone may improve the macrocytosis and anemia in vitamin B12 deficiency, without correcting the ongoing neurologic disorder of vitamin B12 deficiency, and may even cause a more rapid neurologic/cognitive deterioration. However, in patients with normal B12 status, high folate intake is associated with protection from cognitive impairment. Although measures of both vitamin B12 and folate status are often included in the evaluation of macrocytosis, low folate is a rare cause of this disorder. Fortification of grains with folic acid began in the United States in 1998 and has reduced the incidence of neural tube defects in developing fetuses. It was feared that this fortification (about 100 μg folate/day) would mask vitamin B12 deficiency, although this has not been proven. Consumption of a diet rich in fruits and vegetables, along with fortified grains, continues to be recommended as the best source for folic acid, but folate in supplements is more bioavailable.
Folate status may be assessed by measuring serum folate if dietary intake (diet or vitamin supplementation) has not recently changed, or with erythrocyte (RBC) folate levels if there has been a recent change in diet (as after hospital admission). Homocysteine levels can be elevated in folic acid deficiency, but may also increase with renal insufficiency, and with vitamin B12 or B6 deficiency.
Vitamin D plays a critical role in maintenance of normal bone health (see Chapter 118). There is evidence that vitamin D has many other physiologic functions beyond those related to bone and calcium metabolism, but the clinical implications of these effects are controversial. Vitamin D receptors are present on many different cell types and through these receptors, vitamin D can play a regulatory role in a number of physiologic processes such as insulin production, myocardial contractility, B and T lymphocyte function, thyroid-stimulating hormone (TSH) secretion, muscle contractility and growth, and CNS function. Vitamin D levels are directly correlated with many clinically important indicators of health and well-being in older adults including muscle strength and mass, physical performance, and the risk for age-related macular degeneration, periodontal disease, and mortality. Although research findings are inconsistent, there is evidence that vitamin D supplementation decreases the risk for falls and fractures in certain high-risk populations such as institutionalized older women. There are ongoing investigations to determine whether supplementation of the diet with vitamin D or vitamin D analogues decreases the risk for other diseases such as diabetes mellitus, inflammatory bowel disease, congestive heart failure, colon and prostate cancers, multiple sclerosis, and rheumatoid arthritis.
The risk of developing vitamin D deficiency increases with advancing age. In humans, vitamin D can be obtained from the diet or manufactured de novo in the skin in response to UV-B light exposure. Both sources of vitamin D can be compromised in older adults. Sunlight is usually the source of UV-B exposure. The capability of the skin to manufacture vitamin D when exposed to unfiltered sunlight decreases with advancing age. Older adults also get less sun exposure than when young; even when outdoors, older adults tend to shield themselves from the sun using clothing, topical sunscreens, or other means. Indeed, such sun protection should be advised to reduce the risk of skin cancer in this population. Sunscreens alone can reduce skin production of vitamin D by as much as 95%. Dark skin pigmentation also reduces the amount of vitamin D produced by the skin in response to sun exposure; this partially accounts for the higher prevalence of low vitamin D levels in blacks compared to whites. The season of the year is also important. In many parts of the United States, the skin makes very little vitamin D during winter.
Although many foods serve as a source of vitamin D (Table 34-7), older adults may not be able to consume enough of these foods to meet their requirements for this nutrient. A cup of fortified milk or fortified orange juice is supposed to contain about 100 IU of vitamin D, although the actual concentration can vary dramatically depending on the quality standards of the manufacturer. Fatty fish, particularly salmon, also have vitamin D, although the amount available in farmed salmon is less certain. Certain diseases and medications can also contribute to the development of a deficiency by decreasing the body’s stores or increasing requirements for vitamin D. These include medications such as certain antiepileptic drugs and glucocorticoids, and any disease that causes fat malabsorption or renal failure (glomerular filtration rate [GFR] < 60 mL/min).
TABLE 34-7DIETARY SOURCES OF VITAMIN D ||Download (.pdf) TABLE 34-7 DIETARY SOURCES OF VITAMIN D
|SOURCE ||TYPE a ||AMOUNT |
|Salmon ||D3 ||600–1000 IU per 3.5 ozb |
|Sardines and Tuna ||D3 ||300 IU per 3.5 oz serving |
|Cod liver oil ||D3 ||400–1000 IU per tsp |
|Shiitake mushrooms ||D2 || |
100 IU per 3.5 oz fresh
1600 IU per 3.5 oz dried
|Fortified milk ||D3 ||100 IU per 8 oz |
|Fortified cereals ||D3 ||100 IU per serving |
Vitamin D status is best assessed by measuring blood levels of 25(OH)D. With chronic kidney disease, a parathyroid hormone (PTH) level would also be important since conversion of 25(OH)D to 1,25(OH)D is often impaired. Serum calcium, ionized calcium, phosphate, alkaline phosphatase, and 1,25(OH)D levels do not adequately identify vitamin D deficiency. There is general consensus that a 25(OH)D level less than 10 ng/mL (25 nmol/L) represents a frank deficiency state. However, the level of vitamin D necessary for optimum health is uncertain. Although some experts feel that a blood level of 25(OH)D less than 20 ng/mL (50 nmol/L) should be used to define a deficiency state, others suggest that blood levels should be much higher, in the range of 30 ng/mL (75 nmol/L) to 60 ng/mL (150 nmol/L). A vitamin D level less than 30 ng/mL is found in as many as 75% of community-living older adults. The health benefits of using vitamin D supplements to achieve levels greater than 30 ng/mL in this population are unproven. Vitamin D is available in two forms, ergocalciferol (vitamin D2) that comes from plant sources and cholecalciferol (vitamin D3) that is of animal origin. Vitamin D2 may be used for fortification, but vitamin D3 is more potent in raising 25(OH)D levels for longer periods of time, especially in older adults. Thus, vitamin D3, the form made naturally from sunlight exposure to skin, is the preferred supplemental form. The Institute of Medicine (2011) recommends daily intake of 600 IU vitamin D3 for healthy adults below age 70 and 800 IU (20 μg) D3 for healthy adults above age 70. Not all older adults can meet these requirements from food sources. Older adults with conditions that place them at increased risk of vitamin D deficiency may require higher intakes of vitamin D and should probably take vitamin D supplements. Vitamin D deficiency [ie, 25(OH)D ≤ 20 ng/mL] can be treated with 1000 to 2000 IU D3 daily. This is the safest and most evidence-based approach. Alternatively, an oral dose of 50,000 IU of D2 can be consumed weekly for 8 weeks. After 8 weeks, further therapy should be guided by results of 25(OH)D, PTH, and calcium levels.
The value of routine screening of healthy older adults with 25(OH)D levels is highly controversial, as there is little consensus about who should consume vitamin D supplements and what is the optimal dose. The US Preventive Services Task Force (USPSTF) (2013) reports that there is insufficient evidence to recommend vitamin D and calcium supplementation for the primary prevention of fractures in pre- and postmenopausal women, and men. The USPSTF (2012) did find evidence to support vitamin D (averaging 800 IU for 12 months) supplementation (and exercise and physical therapy) to prevent falls (but not fractures) in high-risk community-dwelling adults aged 65 and older. Otherwise, decisions should be made on a case-by-case basis recognizing that there is limited evidence on which to base any given recommendation.
From adolescence onwards, both men and women should consume between 1000 and 1200 mg of elemental calcium daily, unless there are unique nutrition requirements. Many older adults consume far less than this amount. In addition, calcium absorption declines with age and varies depending on dietary source. A cup of milk or yogurt contains about 300 mg of calcium. Green vegetables contain some calcium, but they also contain other phytochemicals that interfere with calcium absorption. Therefore calcium bioavailability from vegetables may be limited. Because of dietary limitations or other factors, many older adults are unable to consistently obtain the recommended intake of calcium from natural sources and may need to take calcium supplements. Some brands of orange juice and candy now contain added calcium, which can add to dietary sources of this element. Calcium is also available in pill form. Calcium carbonate is least expensive, but should be consumed with food (although high-fiber foods may reduce absorption somewhat). Some other formulations, such as calcium citrate, are better absorbed but may cost more, and have less calcium per pill. Calcium supplements can increase constipation in some individuals. Persons who develop calcium oxalate kidney stones should not drastically limit their calcium intake from foods, as dietary calcium can bind with and reduce food oxalate absorption and decrease risk of stone formation. Observational studies have identified a possible association between calcium supplementation and increased risk for CVD. Until this issue is clarified, emphasis should be placed on maximizing calcium intake from food sources.
SPECIFIC DIETARY CONSIDERATIONS FOR OPTIMAL HEALTH
Although numerous vitamins have been linked to cognitive decline with advancing age and to the pathogenesis of Alzheimer disease, most of this evidence is from observational studies. For example, there are associations between dietary intake of foods high in carotenoids and a diminished risk of cognitive impairment. A theorized mechanism by which carotenoids may preserve cognitive function is by decreasing small vessel disease in the brain. Similarly, an association between neurocognitive dysfunction (including cognitive impairment without dementia, Alzheimer disease, and vascular dementia) and elevated plasma homocysteine has been identified, which suggests a potential role for folate and B vitamins in preserving cognitive function with advancing age. These findings highlight the potential importance of maintaining a well-balanced diet, but do not provide evidence of benefit of using supplements containing these particular vitamins. Likewise, there is an association between 25 (OH)D serum levels and cognitive function. However, there is no evidence that vitamin D supplementation improves cognition or delays further cognitive decline.
As stated previously, it is known that B12 deficiency can lead to a deterioration of multiple structures within the CNS. The investigation of reversible causes for dementia has routinely included the assessment of folic acid and vitamin B12 status. Vitamin B12 deficiency can cause neuropsychiatric symptoms, including delirium manifesting as slowed thinking, depression, confusion, memory loss, and poorer language comprehension and expression that is difficult to differentiate from early Alzheimer disease. Low serum folate is associated with atrophy of the cerebral cortex, perhaps as a result of hyperhomocysteinemia. Among nondemented persons over 75 years of age, those with low levels of either vitamin B12 or folate had increased risk for developing Alzheimer disease over 3 years. There are very rare case reports of neuropathy associated with folate deficiency. Slowed mental processing, including poorer performance on mental status testing, and depressive symptoms (particularly impaired motivation and social withdrawal) have been described in patients with folic acid deficiency. While deficiency of vitamin B12 is common in frail older adults with cognitive disorders, vitamin B12 (or folic acid) supplementation almost never affects the course of slowly progressive cognitive decline. The effectiveness of B12 replacement therapy to reverse the neurologic pathology may relate to timing of diagnosis and treatment.
One multicenter randomized, controlled trial found a small but significant effect of vitamin E supplementation (2000 IU/day of α-tocopherol) in slowing functional decline and decreasing caregiver burden in older adults with mild to moderate Alzheimer disease. Whether vitamin E supplementation should become a standard of care for this patient population will needed to be determined, weighing the potential benefits and harms of such a policy. There is no evidence that other nutritional supplements, including multivitamins, have a clinically significant effect on preserving cognition.
Nutrition and Cardiovascular Disease and Cancer
There is a growing body of evidence that nutrition plays an important role in CVD prevention. Diets that are low in saturated fat, contain poly- and monounsaturated fatty acids, and include an abundance of fruits and vegetables are associated with a reduced risk of cardiovascular events. A number of dietary regimens fall into this category including the so called Mediterranean diet, which reduced major CV events in persons at high CV risk. The Mediterranean diet emphasizes olive oil, tree nuts and peanuts, fresh fruits and vegetables and legumes, fatty fish and seafood, and white meat, and less commercial bakery goods, pastries, and red and processed meats. The benefits of the various types of oils, especially those containing poly- and monounsaturated omega-3 essential fatty acids, have already been discussed. Various theories have been formulated to explain the beneficial effects of increased consumption of vegetables and fruits. These include the fact that many vegetables and fruits are low in saturated fats and contain ample amounts of vitamins, dietary fiber, and plant polyphenols, which represent a large group of natural antioxidants. In addition to their antioxidant properties, polyphenols elicit several interesting effects in animal models and in vitro systems; they trap and scavenge free radicals, regulate nitric oxide, decrease leukocyte immobilization, induce apoptosis, inhibit cell proliferation and angiogenesis, and exhibit phytoestrogenic activity. Whether these properties of polyphenols are important in human nutrition or contribute to the role of fruits and vegetables in CVD protection remains to be determined.
Antioxidants have also been promoted as protective for cardiovascular disease. The rate of cardiac death is lower in people who consume a diet rich in the antioxidant vitamins and minerals, particularly vitamins E and C, and carotenoids. High levels of serum carotenoids are associated with a lower risk of periventricular white matter lesions on magnetic resonance imaging (MRI), particularly in smokers. These findings are difficult to interpret as diets rich in antioxidants are also higher in fiber and lower in cholesterol and saturated fat, and people who consume large amounts of fruits and vegetables, or who take vitamin supplements often have healthier lifestyles. Meta-analyses of randomized clinical trials for primary prevention of cardiovascular disease have not confirmed a beneficial effect of any vitamin, antioxidant mineral, or fish oil supplement. In fact, increased morbidity or mortality was found with the use of supplemental β-carotene, vitamin E, and selenium; high supplemental vitamin E may increase risk for hemorrhagic stroke and all-cause mortality.
An indirect association between the concentration of antioxidants in the diet (which typically includes diets high in fruits and vegetables) and lower cancer rates has been observed. Similar to studies of antioxidants and CVD, it is difficult to determine whether these findings are due to the antioxidant nutrients themselves or to other reasons. There is currently no convincing evidence that any vitamin, mineral, or antioxidant supplementation prevents cancer.
It is very likely that people with cancer or other serious illnesses will try alternative therapies, including megavitamin and mineral supplements, and herbal or folk remedies. Although it is generally thought that the toxicity of antioxidant vitamins and most B vitamins is low for intakes below the UL, there is increasing evidence of potential harms. Some of this evidence has come from intervention trials which have reported an increased incidence of lung cancer in high-risk patients treated with β-carotene supplements, an association between selenium supplementation and skin cancer, and an increased incidence of prostate cancer in men who took vitamin E. Folic acid supplementation has been linked to an increased risk for colon cancer. Certain subgroups, like smokers, persons with uncontrolled hypertension, and those with other risk factors for the development of cancer appear to be at higher risk for such adverse effects. These risks should be discussed proactively with patients so that they can have the best information available to make their decisions and toxic side effects can be prevented. Tolerable ULs should not be exceeded.
Nutrition and Age-Related Eye Diseases
Evidence to support a protective effect of individual vitamin and mineral supplements on age-related eye diseases is conflicting. The Age-Related Eye Disease Study (AREDS) found a slight reduction in progression (not prevention) of age-related macular degeneration (AMD) using a combination of higher-dose vitamins C and E, β-carotene, zinc, and cupric oxide. In the AREDS2 study, the addition of omega-3 fatty acids (DHA and EPA), and/or lutein and zeaxanthin (macular xanthophylls), and removal of β-carotene, did not decrease AMD progression. The AREDS2 supplementation also did not reduce the risk of cardiovascular disease in the older adult participants. Observation studies have identified an association between dietary antioxidant content and a lower risk of age-related cataracts. However, there is also no evidence that regular high doses of antioxidant vitamin and mineral supplements are effective in preventing cataracts.
ASSESSMENT OF NUTRITIONAL STATUS
Initial Screening Assessment
The risk of developing one or more nutritional disorders increases as a function of age, paralleling the age-associated increase in the prevalence of disease and disability that are often causally related to the development of protein, energy, and micronutrient deficiency states as well as obesity. Prevention and early intervention are the best approaches to keeping older individuals optimally nourished because many forms of malnutrition, particularly protein and energy undernutrition, are very difficult to reverse.
Providers should routinely screen their older patients to determine if they have or are at risk of developing nutritional problems. Ideally this should be done as part of a general health maintenance program that is automatically scheduled at least annually and whenever there is a change in the patient’s health state. Like other screening instruments, the nutritional screen should use simple criteria, be relatively easy to complete, have relatively low attendant costs, and provide a valid assessment of nutritional risk with a reasonable degree of sensitivity and specificity. Components of the screening evaluation can be self-administered, completed by associate staff, or gleaned from other assessments including a routine history and physical examination. Individuals identified by the screen to be at risk of having or developing nutritional disorders should be scheduled for a more in-depth assessment.
For the purpose of the initial screening assessment, older individuals who have experienced a recent deterioration in their socioeconomic or health status should be considered at risk for the development of subsequent nutritional problems. For this reason, it is important to carefully assess for new health concerns and change in socioeconomic status as part of a nutritional screening assessment. Since many older individuals facing financial hardship do not volunteer this information, it is always important to assess whether financial resources are inadequate to meet living expenses, including the purchase and preparation of an appropriate variety and quantity of foods. When the older person is dependent on others for meal preparation or feeding assistance, the resources, health status, and dedication of the caregivers become important. Caregiver neglect and other forms of abuse can pose serious threats to nutritional health and often require careful vigilance to identify. The nutritional screen should also look for psychological stressors that can have a detrimental effect on nutritional status, particularly the loss of a spouse or other family members. Older individuals should always be evaluated for depression since this is a common cause of nutritional deterioration in this age group. Alcohol and drug abuse are serious but frequently unrecognized problems that can cause a variety of nutritional disorders. Screening for alcohol abuse with the University of North Carolina CAGE questionnaire or a similar instrument can be included as part of the nutritional assessment.
Other known risk factors for the development of nutritional problems include a recent deterioration in physical or cognitive function and a change in the number or type of medications prescribed. The effects that these disabilities can have on appetite and food intake have been described previously. The list of medications that can adversely affect nutrient intake is very long. As a general rule, any drug that is being taken should be considered suspect when nutrient intake declines, especially when the individual is having other health problems. Many drugs produce subtle side effects that older individuals may tolerate when feeling well. However, these same side effects, which may include alterations in appetite, taste sensation or salivary secretion, nausea, constipation, diarrhea, or a depressed sensorium, can contribute to the development of anorexia during periods of ill health. Swallowing problems can also adversely affect nutrient intake. Although patients with dysphagia classically present with the complaint of choking or coughing during meals or when consuming liquids, the signs and symptoms are often far more subtle and can include only food avoidance necessitating a high index of suspicion, and a comprehensive dysphagia evaluation, to make the diagnosis. As mentioned previously, older patients who are hospitalized due to an acute illness or surgical problem are at very high risk of developing nutritional deficits prior to discharge. Prolonged bed rest, acute inflammation, and inadequate nutrient intake, which are common during hospitalization, rapidly lead to the depletion of both lean and total body mass placing the older patient at high risk for subsequent mortality. For this reason, any acute hospitalization should be recognized as a nutritional risk factor and prompt a more in-depth assessment.
A careful weight history, possibly the most important and specific component of the nutrition screen, should be obtained from all older patients. If prior weights are available from the medical record, these should be utilized since patients often provide inaccurate accounts of their weight history. A weight loss of 5% or more within the prior 6 months or 10% or more within the prior 3 years should be considered indicative of a potentially serious nutritional problem unless the weight fluctuation can be ascribed with certainty to alterations in fluid balance. There is a clear and direct correlation between the amount of weight that is lost and an increased risk of subsequent mortality (Figure 34-7). This is true even if the older individual states that they voluntarily lost the weight. Voluntary weight loss in frail older adults has the same adverse implications as involuntary weight loss. This probably relates to the fact that few older individuals are successful in their efforts to volitionally lose weight and to keep the weight off while healthy. Voluntary weight loss is probably the result of underlying pathology in many older individuals.
The relationship between the amount of weight that was lost in the previous year and the estimated risk of mortality within the subsequent year. Based on a study of 750 patients aged 65 and older discharged from an acute-care hospital.
As part of the general physical examination, a weight and height should be obtained. If significant kyphosis or scoliosis is present, the patient’s estimate of peak adult height can be utilized for current height. From the weight and height measurements, the patient’s BMI, weight as a percentage of ideal, and weight as a percentage of usual weight can be calculated using standard formulas. Signs of dry skin, thinning hair and nails, and other dermatologic findings are very nonspecific and probably of no value in the nutritional assessment other than indicating the need for careful review of appetite and eating patterns. Since poor oral health may contribute to the development of nutritional problems, a careful oral examination is indicated.
Comprehensive Nutritional Assessment
Although poor reliability limits their usefulness for monitoring change over time, anthropometric measurements provide a prognostically important assessment of an older individual’s nutritional status when skillfully obtained. Whereas skinfold measurements (biceps, triceps, suprailiac, subscapular, and mid-thigh) provide a rough indication of the adequacy of subcutaneous fat stores, arm and arm muscle circumferences are indicators of both muscle mass and subcutaneous fat. There is an inverse correlation between both types of anthropometric measurements and an increased risk of subsequent mortality. Values below the 10th percentile for age for any of these measures should prompt a careful assessment of both nutrient intake and functional status or activity level.
Neither BMI nor the skinfold measurements are good measures of total body fat mass if there is significant intra-abdominal fat accumulation, as often occurs with advanced age. Waist circumference and the waist-to-hip ratio are reasonably useful indicators of abdominal fatness. These measurements can be obtained easily in most clinical settings and provide a useful indication of nutritional status when viewed in conjunction with the other anthropometric measures. A waist-to-hip ratio greater than 1.0 in males and 0.8 in females or a waist circumference greater than 40 in (102 cm) in males and greater than 35 in (88 cm) in females are indicators of central obesity and an increased risk of diabetes and cardiovascular disease.
Although serum albumin, transferrin, prealbumin, and cholesterol are commonly utilized as indicators of nutritional status, considerable caution must be exercised when interpreting the results of these serum measurements. With advancing age, it becomes increasingly difficult to differentiate the interrelated effects of natural aging, disease, and nutritive state on the physiologic processes that determine the serum concentrations of these substances. Consequently, random determinations may have marginal clinical value. However, when used to supplement other data, these measurements often provide valuable clues as to the patient’s overall health status, which influences nutritional risk and prognosis. Interpretation of these measures is aided by knowledge of what physiologic and pathologic factors influence their serum concentration.
A random serum albumin, interpreted without regard to clinical context, has low sensitivity and specificity and only limited clinical utility as a nutritional indicator. While albumin synthesis decreases by 30% to 50% after only 24 to 48 hours of protein and energy deprivation, there may be little change in the serum albumin concentration even after a much more prolonged period of fasting in an otherwise healthy individual. During periods of inadequate nutrient intake, a decreased rate of albumin degradation and mobilization of albumin from the extravascular space may contribute to the maintenance of a normal serum albumin concentration. For these reasons, albumin is not a very sensitive screening test for early stages of nutritional deterioration. Conversely, a low albumin concentration has low specificity as an indicator of protein-energy undernutrition. Acute and even chronic subclinical inflammation and other disease conditions are usually the primary contributors to the development and maintenance of a low serum albumin. Although in healthy individuals serum albumin has a half-life of approximately 20 days, during periods of acute physiologic stress (such as major surgery or sepsis), the serum concentration can decline by up 30 g/L within a few days. This effect on the albumin concentration is probably mediated by cytokines (such as tumor necrosis factor and interleukin-6) that are believed to increase vascular permeability to albumin. The concentration of albumin is normally much greater within the intravascular compared to the extravascular space (35–50 g/L compared to ~ 10 g/L). With inflammation induced changes in vascular permeability, there is a rapid loss of the normal concentration gradient between the intra- and extravascular space and an apparent sequestration of albumin in extravascular sites. These same cytokines also suppress albumin synthesis and may trigger an increased rate of albumin degradation with a resultant drop in the serum concentration to 25 g/L or less. Prolonged hypoalbuminemia can also develop in association with advanced liver disease (cirrhosis), severe congestive heart failure, nephrotic syndrome, and protein-losing enteropathies. When these conditions are not present, a persistently low serum albumin probably represents ongoing inflammation and is associated with a high risk of adverse outcomes, including death. The independent effect of nutritional deprivation on low albumin is unclear. Since it is not currently possible to differentiate the effects of inflammation from those of nutritional deprivation, a low albumin indicates only that the patient is at risk for being undernourished. Unexplained hypoalbuminemia should trigger a more in-depth evaluation of the patient to identify other evidence of protein-energy undernutrition and to determine whether nutrient intake is adequate. Serum albumin does not increase rapidly with refeeding and should not be utilized as an indicator of the adequacy of nutritional support.
Prealbumin and the Prealbumin–Retinol-Binding Protein Complex
Although it has limited specificity as a nutritional indicator, prealbumin may respond to changes in nutrient intake if there is no persistent inflammation or other active disease processes that are keeping the serum levels suppressed. Prealbumin can be used to monitor for change in a patient’s clinical status and to identify risk for the development of nutritional deficits. Despite its name, prealbumin is not a precursor to albumin. Its more descriptive name is transthyretin, because it transports both thyroxine and retinol (vitamin A). In health, prealbumin has a half-life of 2 to 3 days and a much smaller volume of distribution compared to albumin. Like albumin, prealbumin and the prealbumin–retinol-binding protein complex are negative acute-phase reactants. In response to systemic inflammation, liver production declines and the serum concentration drops rapidly. Low levels are also found in association with end-stage liver disease, iron deficiency, and nutrient deprivation. Renal failure (which results in a decreased catabolism of both prealbumin and retinol-binding protein by the kidney) and high-dose steroid therapy are associated with elevated prealbumin concentrations. Because of its relative short half-life, prealbumin is more sensitive to changes in nutrient intake and disease activity than is albumin. The serum concentration begins to drop after 3 to 5 days of very low nutrient intake in an otherwise healthy individual and can decline by 50% or more subsequent to a major physiologic insult. In the latter case, the nadir value is usually reached within 3 to 5 days and corresponds to the period of maximal negative nitrogen balance. With resolution of the inflammatory process, the serum concentration will climb rapidly to the normal range if nutrient intake is adequate. A rising prealbumin correlates with positive nitrogen balance. This fact can be used to advantage to assess the adequacy of nutrition support. Failure of the serum concentration to increase by at least 20 mg/L in 1 week is considered an indication of inadequate nutrient intake and/or ongoing inflammation and should prompt a careful assessment of the patient and the nutrient regimen being employed.
Assessment of nutrient intake
Although frequently difficult to obtain, a detailed nutrient intake assessment is often the most critically needed part of the nutritional assessment. In the outpatient setting where both over- and undernutrition may be a concern, a 24-hour recall or a 3-day food intake diary can be effective tools for estimating nutrient intake and identifying where dietary modifications need to be made, especially if a dietitian or comparably skilled health care provider gives the patient and the family adequate instructions on how to collect the needed data. The employment of more accurate methods of measuring nutrient intake is often especially necessary within hospitals and nursing homes.
Unfortunately, many older patients are maintained throughout their hospitalization on nutrient intakes that are far less than their estimated maintenance energy requirements. Contributing to the problem, the attending health care team often overestimates how much food the older patient is consuming. In one study, over 20% of nonterminally ill older hospitalized patients had an average daily nutrient intake while hospitalized that was less than 50% of their maintenance energy requirements. This lack of adequate nutrient intake was associated with a significant deterioration in protein-energy nutritional status by discharge and a sevenfold increased risk of mortality. Low nutrient intake may be an even more widespread problem within nursing homes. Only by carefully monitoring each older individual’s nutrient intake during their institutional stay can this problem be recognized. However, resources are often not available to support monitoring efforts at the required level of intensity. For this reason, careful selection of older individuals to be monitored is essential. Within the hospital setting, older patients who are not recovering as rapidly as expected, have been placed on clear liquids or nothing by mouth for more than 24 hours, have a persistently low serum prealbumin, or are unexpectedly losing weight, should have their nutrient intake measured each day until they resume an adequate diet. A dedicated team of appropriately trained staff members may be needed to perform this daily nutrient intake assessment, since accuracy often suffers when the regular nursing and dietary staff performs this function. Within extended care facilities, any resident experiencing an acute illness, change in mental status, loss of weight, or decline in functional status should have their nutrient intake monitored in a similar fashion.
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