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Geriatric nutrition: Nutritional issues in older adults

Geriatric nutrition: Nutritional issues in older adults
Authors:
Christine Ritchie, MD, MSPH
Michi Yukawa, MD, MPH
Section Editors:
Kenneth E Schmader, MD
David Seres, MD
Deputy Editor:
Jane Givens, MD, MSCE
Literature review current through: Dec 2022. | This topic last updated: Aug 09, 2021.

INTRODUCTION — Changes associated with normal aging increase nutritional risk for older adults. Aging is characterized by diminished organ system reserves and weakened homeostatic controls. Data from studies of acute hospitalization in older adults suggest that up to 71 percent are at nutritional risk or are malnourished [1]. Malnutrition is associated with increased mortality risk [2].

Nutritional needs of older adults are determined by multiple factors, including specific health problems and related organ system compromise; an individual's level of activity, energy expenditure, and caloric requirements; the ability to access, prepare, ingest, and digest food; and personal food preferences.

This topic will discuss assessment of nutrition in the older adult, as well as the etiology, evaluation, and treatment of weight loss, overnutrition, and specific common nutrient deficiencies. Related issues of geriatric health maintenance and nutritional assessment are discussed separately. (See "Geriatric health maintenance" and "Approach to the patient with unintentional weight loss" and "Dietary assessment in adults" and "Vitamin intake and disease prevention".)

TERMINOLOGY — Although often used interchangeably, malnutrition and undernutrition are not synonymous. Malnutrition refers to a broader concept, which, according to the World Health Organization, encompasses undernutrition as well as overweight conditions and obesity [3]. However, in this topic, malnutrition will be used synonymously with undernutrition.

DIAGNOSTIC CRITERIA FOR MALNUTRITION — The following criteria for the diagnosis of malnutrition have been recommended in a consensus statement from the Academy of Nutrition and Dietetics (Academy) and the American Society for Parenteral and Enteral Nutrition (ASPEN) in 2012 [4]:

Two or more of the following six characteristics:

Insufficient energy intake

Weight loss

Loss of muscle mass

Loss of subcutaneous fat

Localized or generalized fluid accumulation that may mask weight loss

Diminished functional status as measured by handgrip strength

New criteria were introduced in 2018 from the Global Leadership Initiative on Malnutrition (GLIM). The GLIM was established in order to develop a global consensus on the identification and diagnostic criteria for malnutrition to facilitate comparison of malnutrition prevalence, treatment, and outcomes [5]. The new criteria include an appreciation of the role of acute and chronic inflammation, which is not represented in the International Classifications of Diseases 10th revision (ICD-10) codes.

The diagnosis requires the combination of at least one phenotype and one etiologic criteria:

Phenotype criteria – Non-volitional weight loss, low body mass index (BMI), or reduced muscle mass.

Etiologic criteria – Reduced food intake or absorption, or underlying inflammation due to acute disease/injury or chronic disease.

After making the diagnosis of malnutrition, a more comprehensive assessment of nutritional status can be performed by dietitians or nutritionists, who can develop individualized care and treatment plans.

MALNUTRITION PREVALENCE — The prevalence of malnutrition in older adults is dependent upon the population studied, varying by geography, age distribution, and living situation.

A review of results of the Mini Nutritional Assessment (MNA) across settings and countries in Europe, the United States, and South Africa found the prevalence of malnutrition among 4507 older adults (mean age 82.3, 75.2 percent female) was 22.8 percent [6]. Highest rates were in the rehabilitation setting (50.5 percent) and lowest among community dwellers (5.8 percent). Over one-third of hospitalized older adults (38.7 percent) in this study met the criteria for malnutrition.

In a 2016 meta-analysis on malnutrition in various health care settings (mostly in Europe), including data from 240 studies and over 110,000 persons, rates of malnutrition were: outpatients, 6.0 percent (95% CI, 4.6-7.5); hospital, 22.0 percent (95% CI, 18.9-22.5); nursing homes, 17.5 percent (95% CI, 14.3-20.6); long-term care, 28.7 percent (95% CI, 21.4-36.0); rehabilitation/sub-acute care, 29.4 percent (95% CI, 21.7-36.9) [7].

SCREENING FOR NUTRITIONAL STATUS — Elements of screening include measuring weight, calculating weight loss, and utilizing screening tools.

Weight — Serial measurements of body weight offer the simplest screen for nutritional adequacy and change in nutritional status in older adults.

Obtaining periodic body weights may be challenging, particularly in frail patients. A chair or bed scale that is regularly calibrated may be needed for patients who cannot stand on an upright balance beam scale. Low body weight is defined as <80 percent of the recommended body weight (table 1).

Weight loss — Studies suggest that weight loss in older adults, especially if it is not volitional, is predictive of mortality [2,8,9]. Loss of as little as 5 percent of weight over a three-year period is associated with increased mortality among community-dwelling older adults [10].

Weight loss for those with a body mass index (BMI) below 30 likely poses a greater mortality threat to older adults than not losing weight or of having a BMI of 25 to 30 [11]. However, obesity (BMI ≥30) continues to have a negative impact on morbidity and mortality in older adults. The relative benefit of intentional weight loss in obese older adults with osteoarthritis, impaired activity tolerance, diabetes mellitus, and coronary heart disease, especially when combined with exercise, is becoming increasingly apparent [12-14].

Weight loss is considered to be clinically significant with the following parameters [15]:

≥2 percent decrease of baseline body weight in one month

≥5 percent decrease in three months, or

≥10 percent in six months

In the long-term care setting, a clinically significant weight-loss episode is defined by the long-term care Minimum Data Set (MDS) as loss of 5 percent of usual body weight in 30 days, or 10 percent in six months [16].

Screening tools — A number of screening tools have been developed for identifying older adults at risk for poor nutrition. The two screening tools in the highest quartile for sensitivity (>83 percent) and specificity (>90 percent) were the MNA (SF) and the MST [17]. The MNA is used most often by nutritionists. The most commonly used screening tools include those listed below:

The Nutritional Risk Screening (NRS) 2002 has two components: a screening assessment for undernutrition and an estimate for disease severity. Undernutrition is estimated with three variables: BMI, percent recent weight loss, and change in food intake [18]. Disease severity ranges from a score of zero (for those with chronic illnesses or a hip fracture) to three (for those in the intensive care unit [ICU] with an APACHE score of 10). In hospitalized patients, the NRS 2002 showed a sensitivity of 39 to 70 percent and a specificity of 83 to 93 percent when compared with the Mini Nutritional Assessment and the Subjective Global Assessment [17].

The Simplified Nutrition Assessment Questionnaire (SNAQ), a four-item screener, was tested in community-dwelling older adults and long-term care residents [19]. In those populations, it had a sensitivity and specificity of 81.3 and 76.4, and 88.2 and 83.5 percent, respectively, for identification of older persons at risk for 5 and 10 percent weight loss, respectively (figure 1).

SCREEN II (Seniors in the Community: Risk Evaluation for Eating and Nutrition) is a 17-item tool that assesses nutritional risk by evaluating food intake, physiological barriers to eating (difficulty with chewing or swallowing), weight change, and social/functional barriers to eating. The tool has excellent sensitivity and specificity, as well as interrater and test/retest reliability [20]. An eight-question abbreviated version of SCREEN II is also available [21].

The Malnutrition Universal Screening Tool (MUST) incorporates BMI, weight loss in three to six months, and anorexia for five days due to disease. When neither height nor weight is available, the midarm circumference and subjective assessment of physical characteristics, such as very thin, can be used instead. It is commonly used in the United Kingdom and is particularly sensitive for recognition of protein energy undernutrition in hospitalized patients [22].

The Malnutrition Screening Tool (MST) was developed for use in acutely hospitalized patients and also validated for use in cancer patients (average age 57 to 60 years, range 15 to 89) [23]. It asks two simple questions: "Have you been eating poorly because of a decreased appetite?" and "Have you lost weight recently without trying?" The sensitivity of the MST in hospitalized patients ranges from 74 to 100 percent with a specificity of 76 to 93 percent when compared with the Subjective Global Assessment.

The Mini Nutritional Assessment (MNA) consists of a global assessment and subjective perception of health, as well as questions specific to diet, and a series of body measurements [24]. It has been widely validated and is predictive of poor outcomes [25-27]. The Mini Nutritional Assessment-Short Form (MNA-SF) uses six questions from the full MNA and can substitute calf circumference if BMI is not available. A validation study demonstrated good sensitivity compared with the full MNA [28].

MALNUTRITION — Compared with younger adults, undernutrition in older individuals is both more common and may have greater impact on outcomes, including physical function [29], health care utilization [30], and length of stay for surgical hospitalizations [31,32]. Inadequate energy intake is common in hospitalized older adults, with increased risk associated with poor appetite, higher body mass index (BMI), diagnosis of infection or cancer, delirium, and need for assistance with feeding [33]. Some studies suggest that older adults are less able to adapt to underfeeding. One study found that, following a period of experimental underfeeding, older adults experienced less frequent hunger than younger adults and did not regain the total amount of weight they had lost when allowed to consume food freely for six months while, on average, younger adults regained all their lost weight [34]. By contrast, a similar study did not demonstrate age differences in ad libitum intake, anthropometric indices, gastric emptying rate, and cholecystokinin levels in blood after a period of underfeeding and then consumption of food freely [35].

The lack of ability to compensate for periods of low food intake due to illness or other difficulties can result in long-term, persistent weight changes, especially when combined with social, medical, or psychological factors that can negatively impact body weight.

Involuntary weight loss may be driven by a variety of factors, including:

Inadequate dietary intake

Appetite loss (anorexia)

Disuse or muscle atrophy (sarcopenia)

Inflammatory effects of disease (cachexia)

or a combination of these factors.

Inadequate dietary intake — There are multiple causes of weight loss due to inadequate nutrient intake. These include social (eg, poverty, isolation), psychological (eg, depression, dementia), medical (eg, edentulism, dysphagia), and pharmacologic issues.

Social factors — Social factors contributing to weight loss include:

Increased likelihood of isolation at mealtimes. One-third of persons over 65 and one-half over 85 live alone, which typically decreases food enjoyment and calorie intake. Several studies have demonstrated that older adults who eat in the presence of others consume more than those who eat alone [36,37].

Financial limitations affecting food acquisition. A greater proportion of older adults live near the poverty line, compared with the general population. Individuals with fixed incomes may use money previously spent on food for medications and other needed items.

Medical and psychiatric factors — The most important medical and psychiatric causes of weight loss in older adults are malignancy and depression.

Malignancy was identified as the cause for weight loss in 9 percent of older patients in a study of medical outpatients, and was second to depression as the most frequent identifiable cause of undernutrition [38]. In another study of unexplained weight loss in 45 ambulatory older adults, the most common identified cause for weight loss was depression (18 percent), again followed by malignancy (16 percent) [39]. A third report found cancer, predominantly of the gastrointestinal tract, as a cause of weight loss in 36 percent of the 154 patients evaluated [40].

Depression and dysphoria are common in older adults and often remain unrecognized and undertreated. Depression is an important cause of weight loss in the subacute care and nursing home settings, as well as in older patients in the community. In a chart review of 1017 medical outpatients, for example, depression was the cause of weight loss in 30 percent of the older patients, compared with only 15 percent in younger patients [38]. (See "Diagnosis and management of late-life unipolar depression".)

Dysphagia is present in approximately 7 to 10 percent of the older adult population [41] and has a negative effect on energy intake [42]. Dysphagia occurs in approximately one-half of patients with acute first-ever stroke [43] or with Parkinson disease [44]. Oropharyngeal dysphagia may occur due to stroke, Parkinson disease, amyotrophic lateral sclerosis, Zenker's diverticula, and other motility or structural disorders. Esophageal dysphagia can be due to motility problems (eg, achalasia, diffuse esophageal spasm, scleroderma) and structural issues. (See "Approach to the evaluation of dysphagia in adults".)

Other important medical etiologies to consider include:

Endocrine disorders (hyperthyroidism, new onset diabetes mellitus)

End-organ disease (congestive heart failure, end-stage kidney disease, chronic obstructive pulmonary disease, hepatic failure)

Gastrointestinal disorders (celiac disease, ischemic bowel, inflammatory bowel disease, pancreatic insufficiency, peptic ulcer disease, gastroesophageal reflux disease)

Infections (tuberculosis)

Rheumatologic disorders (polymyalgia rheumatica, rheumatoid arthritis)

Neurologic conditions (Parkinson disease, chronic pain)

Alzheimer disease (especially among those with behavioral and psychological symptoms) [45]

Drug or alcohol dependence

Medication side effects (digoxin, opioids, serotonin-reuptake inhibitors, diuretics, and topiramate)

Additionally, medical or dental conditions in older adults may impair the ability to eat. Paralysis from stroke, severe arthritis, hand tremors, and dementia may lead to routine need for feeding assistance from others.

Chewing difficulty and oral pain puts older adults at risk for poor intake. In a study of noninstitutionalized older adults, being edentulous doubled the risk for significant weight loss over a one-year period, after adjusting for sex, income, age, and baseline weight [46]. In a separate analysis of 992 older adults in the Laussane 65+ cohort study, those with oral pain and chewing problems had higher odds of being frail; oral pain was also associated with weight loss and low hand grip [47].

Physiologic factors — Physiologic factors associated with weight loss include age-related decrease in taste and smell sensitivity, delayed gastric emptying, early satiety, and impairment in the regulation of food intake.

Age raises the threshold for odor detection and lowers perceived odor intensity [48]. The number of taste buds remains constant, but thresholds for recognition of salt and other specific tastes increase. Impaired taste and smell likely alter the cephalic phase of digestion, affecting learned associations between the taste and smell of food with signals involved in meal initiation, volume of food intake, and meal termination.

Decrease in the rate of gastric emptying in older adults may result in prolonged antral distension with reduced hunger and increased satiety [49].

Aging may influence production of, and/or central nervous system sensitivity to, several digestive hormones thought to be involved in satiety. Glucagon, glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), leptin, and ghrelin are peripheral satiety signals and appear to be less well-detected by the brain with increased age [50].

Causes of impaired regulation of food intake include decreased stimulatory effects of neurotransmitters involved in appetite (eg, opioids, neuropeptide Y, the orexins and ghrelin) and increased sensitivity to the inhibitory effects of corticotropin-releasing factor, serotonin, and cholecystokinin.

Anorexia — Anorexia, the decrease in appetite, in older adults is influenced by multiple physiological changes. Food intake gradually diminishes with age [51]. Much of the intake reduction in early old age is an appropriate response to decreased energy needs due to reduced physical activity, decreased resting energy expenditure (REE), and/or loss of lean body mass.

Changes in taste and smell lead to a decreased desire to eat and early satiety develops with age, related to gastrointestinal changes and gastric hormone changes, as discussed above. (See 'Physiologic factors' above.)

Appetite regulation is further affected by illness, drugs, dementia, and mood disorders. In 292 older adults from assisted living facilities or senior centers, fair to poor emotional well-being was most closely associated with poor appetite (odds ratio [OR] 5.60, 95% CI 2.60-12.07) [52]. In a study of 526 older Italians, the prevalence of anorexia was 21 percent and was more common in those living in institutional settings, with impairment of Instrumental Activities of Daily Living (IADL) and fewer residual teeth [51].

Cachexia — Cachexia has been defined as a "complex metabolic syndrome associated with underlying illness, and characterized by loss of muscle with or without loss of fat mass" [53]. It is associated with increased morbidity. Anorexia, inflammation, insulin resistance, and increased muscle protein breakdown are frequently associated with cachexia.

Cachexia is distinct from starvation, age-related loss of muscle mass (see 'Sarcopenia' below), or psychiatric, intestinal, or endocrinologic causes of weight loss. Cachexia involves many dysregulated pathways, leading to an imbalance between catabolism and anabolism. Because of the presence of underlying inflammation and catabolism, cachexia often is resistant to nutritional intervention. Despite the evidence supporting inflammation as an essential mechanism for cachexia, antiinflammatory medications or drugs targeting cytokines have not demonstrated beneficial effects [54]. Potential drugs such as thalidomide, selective cyclooxygenase (COX) inhibitors, w3-fatty acids like eicosapentaenoic acid, and anti-tumor necrosis factor (TNF) agents have shown variable efficacy in treating cachexia [54]. The cause of cachexia is multifactorial, and thus treatment should be multimodal, including the use of a combination of an appetite stimulant and an agent promoting muscle protein synthesis [55].

Cachexia usually occurs in the setting of underlying illness involving a cytokine-mediated response. Such illnesses include cancer, end-stage kidney disease, chronic pulmonary disease, heart failure, rheumatoid arthritis, and acquired immunodeficiency syndrome (AIDS).

Proinflammatory cytokines commonly involved in cachexia include interleukin (IL)-1, IL-6, and TNF-alpha (TNF-a) [56,57]. These cytokines promote myofibrillar breakdown by activating the ubiquitin proteasome pathway. In addition, release of cortisol and adrenergic hormones stimulated by cytokines can increase fat oxidation, fat atrophy, insulin resistance, hypermetabolism, and fatigue [55].

In a study of older Framingham Heart Study participants, levels of insulin-like growth factor (IGF)-1 and muscle mass decreased, whereas IL-6 levels increased, with age [58]. These changes appear to occur even in the absence of overt disease, suggesting that a subclinical inflammatory process may be part of normal aging. Although elevated proinflammatory cytokines (especially IL-1, IL-6 and TNF-a) are commonly seen in older adults, levels are higher in those with cachexia.

Sarcopenia — Sarcopenia is a syndrome characterized by the loss of muscle mass, strength, and performance [59-61]. Low muscle mass is defined as a decrease in appendicular muscle mass two standard deviations below the mean for young healthy adults [62], and is usually measured by DEXA or bio-electrical impedance in clinical practice. Unlike cachexia, sarcopenia does not require the presence of an underlying illness. Also, whereas most people with cachexia are sarcopenic, most sarcopenic individuals are not considered cachectic [63]. Sarcopenia is associated with increased rates of functional impairment, disability, falls, and mortality [64]. The causes of sarcopenia are multifactorial and can include disuse, changing endocrine function, chronic diseases, inflammation, insulin resistance, and nutritional deficiencies [61].

Sarcopenia was identified in 53 to 57 percent of men, and 43 to 60 percent of women, over the age of 80 in one study [65]. Loss of muscle mass, accompanied by decreased muscle strength, can occur in overweight individuals (sarcopenic-obese), as well as in normal and underweight individuals.

Causes of sarcopenia include endocrine changes, activation of proinflammatory cytokines, reduced alpha motor units in the spinal cord, decreased physical activity, and suboptimal protein intake.

Reductions in testosterone and estrogen that accompany aging appear to accelerate the development of sarcopenia [66]. Relative deficiencies of estrogen and testosterone contribute to muscle catabolism and promotion of catabolic cytokines such as IL-1 and IL-6 [34]. Furthermore, testosterone inhibits myostatin, stimulates myoblast, and increases satellite cells within muscle. Testosterone replacement may increase muscle mass, but studies have not demonstrated similar benefit for estrogen replacement [67-69]. Selective androgen receptor modulators (SARM), such as enobosarm, are a promising potential treatment for sarcopenia. A phase II trial of enobosarm in healthy older adults led to increases in lean body mass and improvement in stair climbing [70].

Insulin resistance increases with age. Insulin inhibits muscle breakdown and the reduction of insulin action on muscle may contribute to muscle catabolism [71].

Physical activity declines with age. In the United States, 28 to 34 percent of adults aged 65 to 74 and 35 to 44 percent of adults ages 75 or older are inactive [72]. Inactivity exacerbates ongoing muscle loss [73] and increases proportion of body fat mass [74].

Inadequate protein intake can also contribute to sarcopenia and decreased function. A prospective cohort study found that adults aged 70 to 79 with protein intake ≤0.8 g/kg/day (the Recommended Dietary Allowance [RDA]) were at greater risk of developing mobility limitations over six years of follow-up than those with protein intake ≥1.0 g/kg/day [75].

EVALUATION OF WEIGHT LOSS — Recommendations vary on the degree of weight loss, and the period of time for weight loss, that should prompt clinical investigation. One commonly accepted definition for clinically important weight loss is loss of 4 to 5 percent of total body weight over 6 to 12 months [2]. Unintentional weight loss should lead to clinical concern regardless of whether the patient is overweight at baseline. Whether or not intentional weight loss is of concern remains a matter of some speculation.

Initial evaluation — The following steps are suggested in the initial evaluation of an older person who is noted to have lost weight, or for whom concern is raised about weight loss by the patient, family members, or caregivers.

Document the weight loss. While it is important to note objective evidence of weight loss from recorded serial weights over time, this information is often not available.

Body fat and lean muscle mass may be estimated using bioelectrical impedance or anthropometric measures such as mean upper arm circumference (MUAC) or mid-arm circumference. MUAC measures the circumference of the left upper arm at the mid-point between the tip of the shoulder and the tip of the elbow (olecranon process and the acromion). MUAC of less than 22 cm for women and 23 cm for men are suggestive of chronic energy deficiency. Although suggestive of malnutrition, it is unclear whether MUAC predicts mortality and morbidity. The MUST screening tool uses mid-arm circumference measures.

Bioelectrical impedance measures are available for use with wheelchair- and bedbound patients, although bioelectrical impedance is significantly influenced by hydration status.

Evaluate appetite and dietary intake. Determining if there has been a change in hunger and satiety may provide more clinically revealing information than performing a formal dietary recall. Patients should be questioned regarding appetite, their dietary intake in relation to their usual pattern, the number of meals they consume per day, portion size, snacks between meals, if and when they feel full during their meal, and whether the patient likes what they are eating. The Subjective Global Assessment (SGA), Mini Nutritional Assessment (MNA), and Simplified Nutritional Appetite Questionnaire (SNAQ) all evaluate aspects of dietary intake in this way (see 'Screening tools' above). A more formal dietary intake assessment can be obtained with a dietetic consult.

Perform a complete history, including oral symptoms, and physical examination, including a complete oral examination. As a baseline, we suggest laboratory evaluation for evidence of metabolic or inflammatory disease, to include a basic chemistry profile including glucose and electrolytes, thyroid-stimulating hormone (TSH), complete blood count (CBC), and C-reactive protein (CRP) if cachexia is suspected. Chest and plain abdomen radiographs may be considered. Although studies describing the causes of involuntary weight loss have routinely performed chest radiographs and abdominal films, there is no clear evidence of their value. Order additional studies based on suspicion of underlying disease from the patient's history and examination.

Those with no localizing findings and with normal complete blood count, biochemical profile, or chest and plain abdomen radiographs have been considered by some to have isolated involuntary weight loss [76]. In one series, a little more than one-third of patients were ultimately diagnosed with a malignancy. Multivariate analysis found the strongest predictors of neoplasm in the setting of isolated involuntary weight loss were age >80 years, white blood cell count >12,000/mm3, serum albumin <3.5 g/dL, serum alkaline phosphatase > 300 IU/L, and serum lactate dehydrogenase (LDH) >500 IU/L. These authors recommend CBC, erythrocyte sedimentation rate (ESR), serum albumin, liver function studies, LDH, and abdominal ultrasound.

Subsequent evaluation — There are no clear guidelines for how to proceed in the assessment of a patient with weight loss and negative initial findings. The diagnostic yield of a thoracic/abdominal/pelvic computed tomography (CT) examination to assess for occult or metastatic malignant disease has not been determined. Incidental findings are common, the studies are costly, and may be inappropriate in patients who are frail or who have multiple comorbidities.

In the absence of evidence-based recommendations, we suggest ordering a thoracic/abdominal/pelvic CT scan with and without contrast for the patient with significant ongoing weight loss. Magnetic resonance imaging (MRI) may be ordered as an alternative when intravenous (IV) contrast cannot be administered, assuming there are no contraindications; patients with chronic kidney failure should not be given gadolinium. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

Upper gastrointestinal endoscopy is indicated for patients with early satiety.

Colonoscopy is not indicated in the evaluation of weight loss unless the patient simultaneously has signs of gastrointestinal blood loss, as colon cancer does not usually induce weight loss or cachexia unless there is obstruction or extensive metastases [77,78].

TREATMENT OF WEIGHT LOSS — When an underlying cause of weight loss is identified, such as depression, a medical illness, or inability to chew food, it is obviously important to treat the condition. In addition, nutritional repletion should be provided to restore the patient to a target weight, with recognition that weight correction in the older population is less readily accomplished than in younger people.

The Council for Nutritional Clinical Strategies in Long-Term Care has developed an evidence-based approach to nutritional surveillance and management for patients in long-term care [79]. Treatment recommendations are based on common reversible causes of malnutrition, as described by the acronym "MEALS ON WHEELS" (table 2). Likewise, the American Academy of Home Care Physicians has developed guidelines for unintended weight loss in home care patients [80].

Data from studies of acute hospitalization in older patients suggest that up to 71 percent are at nutritional risk or are malnourished [1]. One randomized trial found that individualized nutritional management by a dietitian (involving one visit during hospitalization and three home visits subsequent to discharge) resulted in improved scores on the Mini Nutritional Assessment (MNA) and higher albumin levels in the intervention group, compared with controls [81]. Decreased mortality rates at six months were also found (3.8 versus 11.6 percent for intervention and controls respectively), although high study dropout rates and issues with randomization allocation may have impacted this finding.

Calorie and protein requirements — Calorie needs (the estimated energy requirement [EER]) can be calculated in older adults using the following equations [82]:

For women: 354.1 – (6.91 x age [y]) + PAC x (9.36 x weight [kg] + 726 x height [m]).

For men: 661.8 – (9.53 x age [y]) + PAC x (15.91 x weight [kg] + 539.6 x height [m]).

The Physical Activity Coefficient (PAC) is determined as follows:

Sedentary PAC = 1.0

Low activity PAC = 1.12

Active PAC = 1.27

Very active PAC = 1.45

Protein needs do not appear to change significantly with age, although studies evaluating protein intake in older adults have shown wide variation in optimal protein requirements. A meta-analysis of data from 19 studies of nitrogen balance in older adults found no significant effect of age on the amount of protein required per kilogram of body weight [83].

The Institute of Medicine has determined that the Recommended Dietary Allowance (RDA) for protein for adults 51 years of age and older is 0.80 g/kg body weight/day [84]. However, subsequent studies indicate that protein intake above 0.08 g/kg body weight/day is protective of appendicular lean mass and preservation of handgrip strength and decreases the risk of functional disability [85-87].

Inadequate food intake — If the patient's food intake is inadequate:

Lift dietary restrictions whenever possible. In one study, undernutrition (average weight loss >1 pound per month, serum albumin <3.5 g/dL) was associated with dietary restrictions [88]. Fifty-nine percent of the patients with weight loss and 75.2 percent of those with hypoalbuminemia were on some type of dietary restriction.

In older, nutritionally high-risk adults with diabetes, regular monitoring of blood glucose and adjustment of medication is preferable to dietary restriction or even a "no concentrated sweets" prescription. The short-term substitution of a regular diet for a diabetic diet increased calorie consumption and did not cause gross deterioration of glycemic control in a study of chronic care patients with type 2 diabetes [89].

Make sure that feeding or shopping assistance is available, if appropriate. In a crossover controlled trial of feeding assistance in nursing home residents at risk of weight loss, those in the intervention group showed a significant increase in daily caloric intake and either maintained or gained weight, whereas those in the control group lost weight. Feeding assistance was resource-intensive and required an average 37 more minutes of staff time per meal [90]. Social work support may be important if inadequate finances are contributing to poor intake.

Assure that meals and foods meet individual tastes. Suggest offering foods that fit the patient's ethnic or regional preferences.

Consider ways to supplement the patient's diet. Increase the nutrient density of food. For example, increase protein content by adding milk powder, whey protein (found in many health food stores), egg whites, or tofu. Increase fat content by adding olive oil (or other "good fat") in preparation of sauces, fresh or cooked vegetables, and grains or pasta. If weight does not improve, offer daytime snacks between meals.

Give a daily multivitamin and mineral supplement until the cause of inadequate intake is determined.

Consider a liquid dietary supplement. (See 'Nutritional supplements' below.)

Nutritional supplements — A meta-analysis evaluated 55 randomized trials of nutritional supplements containing protein and energy to prevent malnutrition in older, high-risk patients [80]. Studies were generally judged to be of poor quality, due to lack of blinding and intent to treat analysis. The trials evaluated supplements providing between 175 and 1000 additional kcal/day and between 10 and 36 grams protein/day. Most subjects (45 percent) were hospitalized for stroke; 16 percent were community-based and 10 percent were in long-term care facilities.

Nutritional supplementation resulted in modest improvement in percentage weight change (weighted mean difference 1.75 percent, 95% CI 1.2 to 2.3), with slightly greater weight increase in patients at home or in long-term care. Overall mortality was reduced in the groups receiving nutritional supplement, compared with control, but there was no mortality impact for patients living at home, and no improvement in functional status. The greatest mortality impact was found in hospitalized undernourished patients who were 75 years or older and who received supplements with higher calorie content. Complication rates were lower for hospitalized patients who received supplementation, but there was no change in hospital length of stay.

In another meta-analysis, there was some evidence that volitional nutrient support (VNS) improved survival among malnourished geriatric patients [91]. Findings were significant for low-quality trials; two high-quality trials found benefit for VNS in this population, but the difference from control did not reach statistical significance. In a systematic review including 32 trials for a total of 4137 older adults, multi-nutrient supplements improved chair rise time and handgrip strength [92].

A randomized crossover trial of amino acid supplements in 41 sarcopenic older adults demonstrated increases in whole-body lean mass at 6 and 12 months. This study also demonstrated that supplementation led to improved nutrition as reflected by Mini Nutritional Assessment (MNA) scores, improved albumin levels, decreased scores for depression measured by the Geriatric Depression Scale (GDS), and better hand grip strength [93]. More studies are needed in the sarcopenic geriatric population before amino acid supplementation can be generally recommended in clinical practice [94].

Appetite stimulants — Use of appetite stimulants (orexigenics) may be considered, but with caution. There are few studies of use of these medications in the older population with weight loss and failure to thrive. There is inadequate information to determine the appropriate use of orexigenics in older adults with cachexia. If used, they should be used as a trial and evaluated for any benefit before continuing stimulants. The complex interplay between inflammation, catabolism, and nutritional substrate in cachexia demands multimodal interventions that address all three elements.

Megestrol acetate — Megestrol acetate, a progestational agent, has been shown to yield weight gain in patients with anorexia and cachexia. Megestrol acetate has demonstrated some weight gain and improved appetite in patients with cancer or acquired immunodeficiency syndrome (AIDS) cachexia [95-97].

In a randomized trial, megestrol acetate 800 mg daily for 12 weeks improved appetite and sense of wellbeing in a group of nursing home residents. However, weight gain was not found to be significant (>4 lbs) until three months after treatment [98]. Weight gain was more prominent in residents with elevated cytokine concentrations.

There are significant adverse effects of megestrol acetate. Patients should be monitored for edema and worsening of congestive heart failure, impaired function of the corticoadrenal axis [99], deep venous thrombosis [100], and muscle weakness. The use of megestrol in older adult nursing home residents has been associated with increase in all-cause mortality without increase in weight [101]. Due to these adverse effects, the 2015 Beer’s criteria list megestrol acetate as potentially inappropriate for patients 65 years and older [102]. We suggest that this medication should only be considered in older adults with cancer or AIDS cachexia for a limited trial to stimulate appetite.

Dronabinol — Dronabinol has been shown to improve appetite in patients with AIDS [103]; it was not as effective as megestrol in patients with advanced cancer [104]. Dronabinol has not been well-studied in older adults [105,106], although one nonrandomized trial showed that dronabinol may be useful for anorexia, weight gain, and behavior problems in patients with advanced Alzheimer disease who were refusing food [105]. Dronabinol has significant central nervous system side effects, limiting its use for most older adult populations.

Mirtazapine — Mirtazapine, an antidepressant that leads to more weight gain than selective serotonin reuptake inhibitor (SSRI) antidepressants, is commonly used for management of depression and weight loss in older adults. However, few studies have been specifically performed to evaluate its impact on weight among older adults with weight loss. Two studies in nursing home residents did not show conclusive benefit for mirtazapine over other non-tricyclic antidepressants [107,108]. However, a retrospective study in patients with Alzheimer disease and weight loss found that patients treated with mirtazapine for three months gained an average of 2 kg compared with baseline [109].

Ghrelin mimetics (growth hormone secretagogues) — Ghrelin is an endogenous growth hormone secretagogues (GHS) that has been shown to stimulate appetite and increase fat-free mass. Two randomized trials of GHS in healthy older adults demonstrated increases in lean mass (average gain of 1.6 kg), and improvements in strength and function compared with placebo [110,111]. One trial of capromorelin also found a gain in functional abilities (eg, tandem gait distance and stair-climbing) [110]. Further trials are necessary to assess the benefit and safety of GHS in the treatment of older adults with sarcopenia, cachexia, or weight loss. Adverse effects of ghrelin mimetics include hyperglycemia, dizziness, and nausea.

OVERNUTRITION — The National Heart, Lung, and Blood Institute clinical guidelines define overweight as a body mass index (BMI) of 25 to 29.9 and obesity as a BMI of 30 or greater [112,113]. For older adults, BMI and weight may not be reliable indicators of overweight or obesity in older populations, where normal weight may reflect loss of muscle mass rather than decreased adiposity. There is no consensus on the best method of measurement of obesity in older patients [114].

For the population as a whole, higher body weights are associated with increase in all-cause mortality, as well as morbidity related to hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, and endometrial, breast, prostate, and colon cancers.

However, several studies suggest that the relationship of overweight or obesity to mortality declines over time [115]:

Data from the Longitudinal Study of Aging found that a relatively high BMI (30 to 35 for women and 27 to 30 for men) was associated with minimal excess risk for mortality in adults older than 70 years of age [116].

A longitudinal study of over 500,000 adults in the United States found a decrease in the association of obesity with cardiovascular disease mortality over time [117].

Data from several other long-term observational studies, including the Cardiovascular Health Study [118,119], the Medicare Current Beneficiary Surveys [120], and the National Long Term Care Survey [121] have also found that being overweight does not increase mortality risk for people age 65 years and older.

A few studies suggest that being overweight as an older adult is associated with increased mortality:

In a study of men 60 to 79 years in the United Kingdom, mortality was not increased for overweight or obese participants as defined by BMI [122]. However, mortality risk was increased with increasing waist circumference and with BMI, when data were corrected for differences in mid-arm muscle circumference. These findings suggest that cardiorespiratory fitness and muscle mass may play an important role in the relationship between BMI and mortality.

Another report found a U-shaped pattern in women ≥65 years of age, comparing mortality across weight quintiles, with lower mortality for women in the middle 3 quintiles [123]. A J-shaped pattern for BMI and mortality was demonstrated in another study of adults, predominantly men, over age 60 [124]. In this study, BMI in the overweight range was protective.

Although the mortality risk of obesity may lessen with age, there are still metabolic and functional benefits to weight loss in obese older adults. Increasing obesity in older adults is associated with new or worsening disability [120], and weight loss can improve physical function, blood glucose and cholesterol levels, and quality of life [125,126]. Recommendations to lose weight should be individualized to the risk profile of particular patients. Those who are experiencing significant adverse effects associated with obesity (such as pain from osteoarthritis, obstructive sleep apnea, poor mobility, and falls) should be encouraged to pursue cautious weight loss. Few randomized controlled clinical trials have shown that diet and exercise combination can lead to successful weight loss and improve cardiometabolic risk factors and physical function for obesity older adults without adverse effects [14,127,128], but only in the context of regular exercise and appropriate calcium and vitamin D supplementation. Negative outcomes associated with weight loss in overweight older adults include loss of muscle mass and decrease in bone mineral density; both of these may be mitigated with regular exercise and vitamin D supplementation [129-132].

Sarcopenic obesity is a combination of age-related muscle atrophy and increase in adiposity, and this condition have been associated with increased mortality rate and greater risk for falls and cognitive impairment [133,134]. Several clinical trials of high-protein weight-loss diets have demonstrated success in weight loss while preserving lean mass and function [135,136]. Porter Starr et al randomized 67 obese older adults (BMI mean 36.9 ± 6.3) to normal weight loss diet and high-protein weight-loss diet for six months. Both groups lost significant weight loss, but the high-protein diet group improved their Short Physical Performance Battery score compared with the control group [137].

MICRONUTRIENT DEFICIENCIES IN OLDER ADULTS

Vitamin B12 deficiency — The prevalence of B12 deficiency in older adults ranges between 10 and 20 percent [138]. Some persons with low normal serum B12 levels may in fact be deficient, with resultant neurologic, psychological, or hematologic disease [139]. The diagnosis may need to be made by measurement of methyl malonic acid, which is elevated with B12 deficiency. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".)

In the past, a majority of B12 deficiencies were thought to result from intrinsic factor deficiency. It is now known that approximately 15 percent of older adults (>60 years) poorly absorb protein-bound B12 [140]. This is a result of malabsorption of the food-protein-B12 complex in the stomach, related to gastric achlorhydria and often associated with atrophic gastritis [140]. This may be consequent to current or past Helicobacter pylori infection.

Concern had been raised that folate fortification of foods may mask macrocytic anemia in those with vitamin B12 deficiency. However, a study using National Health and Nutrition Examination Survey (NHANES) data for older adults in the post-folate fortification years found that those with B12 deficiency and higher folate levels were more likely to be anemic and to have cognitive impairment than patients with normal folate levels [141].

Given the high prevalence of B12 deficiency and the ease and safety of treatment, some have advocated routinely screening adults over the age of 65 with a serum vitamin B12 assay [142]. However, this policy has not been endorsed in formal screening guidelines for the geriatric population.

Patients with B12 deficiency can generally be treated with oral B12 and may benefit from increasing the intake of B12 in food [143]. Because B12 malabsorption is common in older adults, with potentially significant effects of vitamin B12 deficiency on the nervous system, individuals >51 years of age should take supplements containing vitamin B12, or eat fortified food products. It is prudent to advocate a daily intake of 10 to 15 mcg [144]. For food cobalamin malabsorption-induced B12 deficiency, ongoing therapy with 1000 mcg per day of oral crystalline cyanocobalamin may correct serum vitamin B12 levels and yield adequate hematological responses [145].

Vitamin D deficiency — Lack of sun exposure, impaired skin synthesis of pre-vitamin D, and decreased hydroxylation in the kidney with advancing age contribute to marginal vitamin D status in many older adults [146]. In addition, dietary vitamin D intake is often low in older subjects. It has been estimated that approximately one-half of older women consume less than 137 international units/day of vitamin D from food, and nearly one-quarter consume less than 65 units/day [147]. However, the US Preventive Services Task Force (USPSTF) concluded that screening for vitamin D levels in asymptomatic adults to improve health outcomes lacks sufficient evidence [148]. A large trial, VITAL (Vitamin D and Omega A-3 Trial), is underway to investigate the efficacy of vitamin D supplementation on the prevention of cancer and cardiovascular diseases [149].

Inadequate vitamin D status has been linked with muscle weakness, functional impairment, depression, and increased risk of falls and fractures [150-152]. An observational study in a large integrated health care system found an association between low vitamin D and increased prevalence of diabetes, hypertension, hyperlipidemia, and peripheral vascular disease [153]. A meta-analysis found an association between low vitamin D levels and increased all-cause mortality as well as cardiovascular disease-related mortality and cancer mortality [154]. Lower serum 25-hydroxyvitamin D concentrations in older persons have also been associated with a greater risk of future nursing home admission [155]. Patients with vitamin D insufficiency may also have relative hypocalcemia and high serum parathyroid hormone (PTH) concentrations; this secondary hyperparathyroidism can be attenuated by the administration of vitamin D supplements [156-158]. Some studies have indicated an association between low vitamin D and certain cancers, such as colorectal cancer [159].

Many older adults will have low levels of serum of 25-hydroxyvitamin D levels (<20 ng/mL or 50 nmol/L). Older individuals at higher risk for vitamin D deficiency include those who are institutionalized, homebound, have limited sun exposure, obesity, dark skin, osteoporosis, or malabsorption. Monitoring of serum levels of 25-hydroxyvitamin D (25-OHD) is recommended for those at high risk, with the goal of achieving levels ≥30 ng/mL. Testing at three to four months following initiation of vitamin D supplements, if needed, should be done to assure that the target has been achieved. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)

A combination of exercise and vitamin D supplementation is associated with increase in muscle mass and improvement in function among older adults living in a community [160,161]. Therefore, increased consumption of dietary sources of vitamin D should be encouraged in all older adults. In 2010, the Institute of Medicine (IOM) released a report on dietary intake requirements for calcium and vitamin D for normal healthy persons [162]. The Recommended Dietary Allowance (RDA) of vitamin D for adults through age 70 years is 600 IU, with the RDA increasing to 800 IU after age 71. (See "Overview of vitamin D", section on 'Requirements'.)

Vitamin D supplementation with cholecalciferol (vitamin D3) in doses of 600 to 800 IU daily is suggested for individuals with serum 25OHD level in the range of 20 to 30 ng/mL. Some individuals may need higher doses. Regimens for vitamin D supplementation for those with serum 25OHD levels <20 ng/mL are discussed separately. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Dosing'.)

Inadequate intake of calcium — Calcium nutrition is strongly influenced by age. The efficiency of calcium absorption from the gastrointestinal tract decreases significantly after age 60. Individuals between 70 and 90 years of age absorb approximately one-third less calcium than do younger adults. Osteoporosis affects more than 10 million people in the United States and causes more than 1.5 million fractures within that population each year [163].

Given the impact of calcium deficiency on cortical bone loss, the adequate intake reference value for Ca for those >51 years of age was increased from 800 (1989 RDA) to 1200 mg/day. Food sources of calcium and available calcium supplements are shown in tables (table 3 and table 4).

Multivitamin supplementation — Whether multivitamin (MVI) supplementation should be routinely recommended to older adults remains a source of some controversy and confusion. Many older adults use MVI supplements. In the 1999 to 2000 National Health and Nutrition Examination Survey (NHANES), 35 percent of adults in the United States used multivitamin-multimineral supplements (MVM) and older adults were more likely than younger groups to use them (odds ratio [OR] 1.7, 95% CI 1.3-2.2) [164]. In a longitudinal cohort study of predominantly White older women, the use of dietary supplements increased significantly between 1986 and 2004 (from 63 to 85 percent of women reporting use of at least one supplement daily) [165].

MVM supplementation has been recommended for older adults who are more likely to have compromised nutritional status (such as those in the long-term care setting), to help achieve recommended intakes of certain micronutrients [166]. Available evidence, however, provides only weak support for this practice:

In a study of 263 older adults attending senior centers, nutrient intake was estimated from dietary recalls and reported use of MVM supplementation [167]. Subjects who reported taking MVM were calculated to have improved intakes of vitamins E, D, B6, folic acid, and calcium but were likely to exceed the Tolerable Upper Limit for niacin, folic acid, and vitamin A.

In a study of 4384 adults 51 years of age and older, supplements improved the nutrient intake of older adults. After accounting for the contribution of supplements, 80 percent or more of users met the estimated average requirement (EAR) for vitamins A, B6, B12, C, and E as well as for folate, iron, and zinc, but not for magnesium. However, some supplement users, particularly men, exceeded Tolerable Upper Intake Levels for iron and zinc and a small percentage of women exceeded the Tolerable Upper Intake Level for vitamin A [168].

A few studies have suggested that MVM might reduce the incidence of infections, and upper respiratory tract infections in particular. In a systematic review of eight randomized trials of multivitamins and mineral supplements primarily involving older adults, three studies found that MVM reduced the number of days spent with infection by 17.5 (95% CI 11-24), but analysis of four studies showed no impact on the infection rate [169]. In an 18-month randomized trial involving 763 institutionalized older adults from 21 long-term care facilities, there was no statistically significant difference in the rate of infections in the supplement and placebo groups [170].

In a cohort study of 38,772 older women followed for over 20 years with a mean age of 61.6 at baseline, supplementation with daily multivitamins was associated with a small increase in total mortality (hazard ratio [HR] 1.06, 95% CI 1.02-1.10) [165].

Therefore, routine supplementation with multivitamins and minerals is not indicated to reduce infections in frail older adults and is likely not beneficial unless it is clear that the older adult is not meeting his or her micronutrient needs due to low overall intake. The 2006 National Institutes of Health (NIH) Consensus Conference on the use of MVM found evidence insufficient to recommend for or against the use of MVMs to prevent chronic disease for the United States population in general [171].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Healthy diet in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Vitamin B12 deficiency and folate deficiency (The Basics)")

SUMMARY AND RECOMMENDATIONS

Involuntary weight loss – The involuntary loss of more than 5 to 10 percent of an older person's usual weight during one year is an important clinical sign associated with increased risk for mortality. Weight loss should thus be met with concern and prompt a search for the cause. (See 'Introduction' above.)

Causes of involuntary weight loss – Involuntary weight loss is generally related to one or a combination of four conditions: inadequate dietary intake, appetite loss (anorexia), muscle atrophy (sarcopenia), or inflammatory effects of disease (cachexia). (See 'Weight loss' above.)

Inadequate dietary intake may relate to social, psychological, medical, and physiologic issues. Depression is the most prevalent associated condition in several studies, with cancer as the second most common cause. (See 'Inadequate dietary intake' above.)

Proinflammatory cytokines are common in older adults and are particularly elevated in patients with cachexia. Sarcopenia is often related to a reduction in testosterone and estrogen and increase in insulin resistance. (See 'Cachexia' above and 'Sarcopenia' above.)

Evaluation – Evaluation of weight loss should include serial weight measurements, dietary or appetite assessment, history, physical examination, and screening laboratory studies (complete blood count [CBC], chemistry profile, thyroid studies). Additional studies should be based on findings of the initial evaluation and may include upper gastrointestinal endoscopy for patients with early satiety or thoracic/abdominal/pelvic computed tomography (CT) scan for patients with unexplained ongoing weight loss. (See 'Evaluation of weight loss' above.)

Treatment – Treatment should be directed at the underlying cause (ie, treatment for depression) as well as dietary modification. Nutritional restrictions should be lifted; patients with diabetes may do well with a regular diet and adequate monitoring. High-calorie foods should be provided.

We suggest providing oral nutritional supplementation for patients who do not regain weight with adjustments in meal preparation and diet (Grade 2B). We suggest not treating patients with appetite stimulants (megestrol acetate or dronabinol) due to marginal benefit and potential side effects (Grade 2B). (See 'Nutritional supplements' above and 'Appetite stimulants' above.)

Overnutrition - Mortality risk in people over age 70 is not significantly impacted by an elevated body mass index (BMI) in the 25.0 to 29.9 range. Advice regarding weight loss for the overweight older person should be tailored to the individual, assessing the impact of excess weight on their quality of life, and should include the need for regular exercise. (See 'Overnutrition' above.)

Micronutrient deficiencies

Vitamin B12 deficiency – Vitamin B12 deficiency affects approximately 15 percent of people >60 years in the United States and most commonly relates to malabsorption of food-protein-B12 complexes. Oral B12 supplements, 1000 mcg daily, can usually correct B12 deficiency in the older adult. Daily intake of B12 10 to 15 mcg, by supplement or fortified products in the diet, is recommended for individuals >50 years. (See 'Vitamin B12 deficiency' above.)

Vitamin D and calcium deficiency – Vitamin D deficiency is also common in the older population. Vitamin D supplements or fortified foods should supply 600 to 800 IU of vitamin D per day for older adults. Additionally, 1200 mg/day of elemental calcium should be provided daily. (See 'Vitamin D deficiency' above and 'Inadequate intake of calcium' above.)

  1. de Luis D, Lopez Guzman A, Nutrition Group of Society of Cstilla-Leon (Endocrinology, Diabetes and Nutrition). Nutritional status of adult patients admitted to internal medicine departments in public hospitals in Castilla y Leon, Spain - A multi-center study. Eur J Intern Med 2006; 17:556.
  2. Wallace JI, Schwartz RS, LaCroix AZ, et al. Involuntary weight loss in older outpatients: incidence and clinical significance. J Am Geriatr Soc 1995; 43:329.
  3. World Health Organization. What is malnutrition? 2016. www.who.int/features/qa/malnutrition/en (Accessed on June 06, 2019).
  4. White JV, Guenter P, Jensen G, et al. Consensus statement: Academy of Nutrition and Dietetics and American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition). JPEN J Parenter Enteral Nutr 2012; 36:275.
  5. Jensen GL, Cederholm T, Correia MITD, et al. GLIM Criteria for the Diagnosis of Malnutrition: A Consensus Report From the Global Clinical Nutrition Community. JPEN J Parenter Enteral Nutr 2019; 43:32.
  6. Kaiser MJ, Bauer JM, Rämsch C, et al. Frequency of malnutrition in older adults: a multinational perspective using the mini nutritional assessment. J Am Geriatr Soc 2010; 58:1734.
  7. Cereda E, Pedrolli C, Klersy C, et al. Nutritional status in older persons according to healthcare setting: A systematic review and meta-analysis of prevalence data using MNA®. Clin Nutr 2016; 35:1282.
  8. Wannamethee SG, Shaper AG, Lennon L. Reasons for intentional weight loss, unintentional weight loss, and mortality in older men. Arch Intern Med 2005; 165:1035.
  9. Gregg EW, Gerzoff RB, Thompson TJ, Williamson DF. Intentional weight loss and death in overweight and obese U.S. adults 35 years of age and older. Ann Intern Med 2003; 138:383.
  10. Newman AB, Yanez D, Harris T, et al. Weight change in old age and its association with mortality. J Am Geriatr Soc 2001; 49:1309.
  11. Locher JL, Roth DL, Ritchie CS, et al. Body mass index, weight loss, and mortality in community-dwelling older adults. J Gerontol A Biol Sci Med Sci 2007; 62:1389.
  12. Bales CW, Buhr G. Is obesity bad for older persons? A systematic review of the pros and cons of weight reduction in later life. J Am Med Dir Assoc 2008; 9:302.
  13. Shea MK, Houston DK, Nicklas BJ, et al. The effect of randomization to weight loss on total mortality in older overweight and obese adults: the ADAPT Study. J Gerontol A Biol Sci Med Sci 2010; 65:519.
  14. Villareal DT, Chode S, Parimi N, et al. Weight loss, exercise, or both and physical function in obese older adults. N Engl J Med 2011; 364:1218.
  15. Zawada ET Jr. Malnutrition in the elderly. Is it simply a matter of not eating enough? Postgrad Med 1996; 100:207.
  16. Health Care Financing Administration. Long Term Care Facility Resident Assessment (RAI) User's Manual, Minimum Data Set, Version 2, Eliot Press, Natick, MA 1999.
  17. Skipper A, Ferguson M, Thompson K, et al. Nutrition screening tools: an analysis of the evidence. JPEN J Parenter Enteral Nutr 2012; 36:292.
  18. Kondrup J, Rasmussen HH, Hamberg O, et al. Nutritional risk screening (NRS 2002): a new method based on an analysis of controlled clinical trials. Clin Nutr 2003; 22:321.
  19. Wilson MM, Thomas DR, Rubenstein LZ, et al. Appetite assessment: simple appetite questionnaire predicts weight loss in community-dwelling adults and nursing home residents. Am J Clin Nutr 2005; 82:1074.
  20. Keller HH, Goy R, Kane SL. Validity and reliability of SCREEN II (Seniors in the community: risk evaluation for eating and nutrition, Version II). Eur J Clin Nutr 2005; 59:1149.
  21. Tools can be purchased from Professor Heather Keller, RD, PhD. Contact hkeller@uoguelph.ca.
  22. Stratton RJ, King CL, Stroud MA, et al. 'Malnutrition Universal Screening Tool' predicts mortality and length of hospital stay in acutely ill elderly. Br J Nutr 2006; 95:325.
  23. Ferguson M, Capra S, Bauer J, Banks M. Development of a valid and reliable malnutrition screening tool for adult acute hospital patients. Nutrition 1999; 15:458.
  24. MNA Mini nutritional assessment. Available at: www.mna-elderly.com (Accessed on November 11, 2010).
  25. Charlton KE, Kolbe-Alexander TL, Nel JH. The MNA, but not the DETERMINE, screening tool is a valid indicator of nutritional status in elderly Africans. Nutrition 2007; 23:533.
  26. Sieber CC. Nutritional screening tools--How does the MNA compare? Proceedings of the session held in Chicago May 2-3, 2006 (15 Years of Mini Nutritional Assessment). J Nutr Health Aging 2006; 10:488.
  27. Vellas B, Guigoz Y, Garry PJ, et al. The Mini Nutritional Assessment (MNA) and its use in grading the nutritional state of elderly patients. Nutrition 1999; 15:116.
  28. Kaiser MJ, Bauer JM, Ramsch C, et al. Validation of the Mini Nutritional Assessment short-form (MNA-SF): a practical tool for identification of nutritional status. J Nutr Health Aging 2009; 13:782.
  29. Shen HC, Chen HF, Peng LN, et al. Impact of nutritional status on long-term functional outcomes of post-acute stroke patients in Taiwan. Arch Gerontol Geriatr 2011; 53:e149.
  30. Baumeister SE, Fischer B, Döring A, et al. The Geriatric Nutritional Risk Index predicts increased healthcare costs and hospitalization in a cohort of community-dwelling older adults: results from the MONICA/KORA Augsburg cohort study, 1994-2005. Nutrition 2011; 27:534.
  31. Leandro-Merhi VA, de Aquino JL, Sales Chagas JF. Nutrition status and risk factors associated with length of hospital stay for surgical patients. JPEN J Parenter Enteral Nutr 2011; 35:241.
  32. Lelli D, Calle A, Pérez LM, et al. Nutritional Status and Functional Outcomes in Older Adults Admitted to Geriatric Rehabilitations: The SAFARI Study. J Am Coll Nutr 2019; 38:441.
  33. Mudge AM, Ross LJ, Young AM, et al. Helping understand nutritional gaps in the elderly (HUNGER): a prospective study of patient factors associated with inadequate nutritional intake in older medical inpatients. Clin Nutr 2011; 30:320.
  34. Roberts SB. Regulation of energy intake in relation to metabolic state and nutritional status. Eur J Clin Nutr 2000; 54 Suppl 3:S64.
  35. Winkels RM, Jolink-Stoppelenburg A, de Graaf K, et al. Energy intake compensation after 3 weeks of restricted energy intake in young and elderly men. J Am Med Dir Assoc 2011; 12:277.
  36. de Castro JM, Brewer EM. The amount eaten in meals by humans is a power function of the number of people present. Physiol Behav 1992; 51:121.
  37. Locher JL, Robinson CO, Roth DL, et al. The effect of the presence of others on caloric intake in homebound older adults. J Gerontol A Biol Sci Med Sci 2005; 60:1475.
  38. Wilson MM, Vaswani S, Liu D, et al. Prevalence and causes of undernutrition in medical outpatients. Am J Med 1998; 104:56.
  39. Thompson MP, Morris LK. Unexplained weight loss in the ambulatory elderly. J Am Geriatr Soc 1991; 39:497.
  40. Rabinovitz M, Pitlik SD, Leifer M, et al. Unintentional weight loss. A retrospective analysis of 154 cases. Arch Intern Med 1986; 146:186.
  41. Achem SR, Devault KR. Dysphagia in aging. J Clin Gastroenterol 2005; 39:357.
  42. Keller HH. Malnutrition in institutionalized elderly: how and why? J Am Geriatr Soc 1993; 41:1212.
  43. Mann G, Hankey GJ, Cameron D. Swallowing disorders following acute stroke: prevalence and diagnostic accuracy. Cerebrovasc Dis 2000; 10:380.
  44. Edwards LL, Quigley EM, Pfeiffer RF. Gastrointestinal dysfunction in Parkinson's disease: frequency and pathophysiology. Neurology 1992; 42:726.
  45. Guérin O, Andrieu S, Schneider SM, et al. Characteristics of Alzheimer's disease patients with a rapid weight loss during a six-year follow-up. Clin Nutr 2009; 28:141.
  46. Ritchie CS, Joshipura K, Silliman RA, et al. Oral health problems and significant weight loss among community-dwelling older adults. J Gerontol A Biol Sci Med Sci 2000; 55:M366.
  47. Kamdem B, Seematter-Bagnoud L, Botrugno F, Santos-Eggimann B. Relationship between oral health and Fried's frailty criteria in community-dwelling older persons. BMC Geriatr 2017; 17:174.
  48. Rolls BJ. Do chemosensory changes influence food intake in the elderly? Physiol Behav 1999; 66:193.
  49. Horowitz M, Maddern GJ, Chatterton BE, et al. Changes in gastric emptying rates with age. Clin Sci (Lond) 1984; 67:213.
  50. Parker BA, Chapman IM. Food intake and ageing--the role of the gut. Mech Ageing Dev 2004; 125:859.
  51. Donini LM, Poggiogalle E, Piredda M, et al. Anorexia and eating patterns in the elderly. PLoS One 2013; 8:e63539.
  52. Engel JH, Siewerdt F, Jackson R, et al. Hardiness, depression, and emotional well-being and their association with appetite in older adults. J Am Geriatr Soc 2011; 59:482.
  53. Evans WJ, Morley JE, Argilés J, et al. Cachexia: a new definition. Clin Nutr 2008; 27:793.
  54. Rolland Y, Onder G, Morley JE, et al. Current and future pharmacologic treatment of sarcopenia. Clin Geriatr Med 2011; 27:423.
  55. Ali S, Garcia JM. Sarcopenia, cachexia and aging: diagnosis, mechanisms and therapeutic options - a mini-review. Gerontology 2014; 60:294.
  56. Martinez M, Arnalich F, Hernanz A. Alterations of anorectic cytokine levels from plasma and cerebrospinal fluid in idiopathic senile anorexia. Mech Ageing Dev 1993; 72:145.
  57. Oldenburg HS, Rogy MA, Lazarus DD, et al. Cachexia and the acute-phase protein response in inflammation are regulated by interleukin-6. Eur J Immunol 1993; 23:1889.
  58. Roubenoff R, Harris TB, Abad LW, et al. Monocyte cytokine production in an elderly population: effect of age and inflammation. J Gerontol A Biol Sci Med Sci 1998; 53:M20.
  59. Roubenoff R. Origins and clinical relevance of sarcopenia. Can J Appl Physiol 2001; 26:78.
  60. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 2010; 39:412.
  61. Janssen I. The epidemiology of sarcopenia. Clin Geriatr Med 2011; 27:355.
  62. Baumgartner RN, Waters DL, Gallagher D, et al. Predictors of skeletal muscle mass in elderly men and women. Mech Ageing Dev 1999; 107:123.
  63. Muscaritoli M, Anker SD, Argilés J, et al. Consensus definition of sarcopenia, cachexia and pre-cachexia: joint document elaborated by Special Interest Groups (SIG) "cachexia-anorexia in chronic wasting diseases" and "nutrition in geriatrics". Clin Nutr 2010; 29:154.
  64. Janssen I. Influence of sarcopenia on the development of physical disability: the Cardiovascular Health Study. J Am Geriatr Soc 2006; 54:56.
  65. Lindle RS, Metter EJ, Lynch NA, et al. Age and gender comparisons of muscle strength in 654 women and men aged 20-93 yr. J Appl Physiol (1985) 1997; 83:1581.
  66. Joseph C, Kenny AM, Taxel P, et al. Role of endocrine-immune dysregulation in osteoporosis, sarcopenia, frailty and fracture risk. Mol Aspects Med 2005; 26:181.
  67. Szulc P, Duboeuf F, Marchand F, Delmas PD. Hormonal and lifestyle determinants of appendicular skeletal muscle mass in men: the MINOS study. Am J Clin Nutr 2004; 80:496.
  68. Kenny AM, Dawson L, Kleppinger A, et al. Prevalence of sarcopenia and predictors of skeletal muscle mass in nonobese women who are long-term users of estrogen-replacement therapy. J Gerontol A Biol Sci Med Sci 2003; 58:M436.
  69. Wittert GA, Chapman IM, Haren MT, et al. Oral testosterone supplementation increases muscle and decreases fat mass in healthy elderly males with low-normal gonadal status. J Gerontol A Biol Sci Med Sci 2003; 58:618.
  70. Dalton JT, Barnette KG, Bohl CE, et al. The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy elderly men and postmenopausal women: results of a double-blind, placebo-controlled phase II trial. J Cachexia Sarcopenia Muscle 2011; 2:153.
  71. Rasmussen BB, Fujita S, Wolfe RR, et al. Insulin resistance of muscle protein metabolism in aging. FASEB J 2006; 20:768.
  72. US Department of Health and Human Services. Healthy People 2010, 2nd ed. Government Printing Office; US Department of Health and Human Services, Washington, DC.
  73. Rantanen T, Era P, Heikkinen E. Physical activity and the changes in maximal isometric strength in men and women from the age of 75 to 80 years. J Am Geriatr Soc 1997; 45:1439.
  74. Kyle UG, Morabia A, Schutz Y, Pichard C. Sedentarism affects body fat mass index and fat-free mass index in adults aged 18 to 98 years. Nutrition 2004; 20:255.
  75. Houston DK, Tooze JA, Garcia K, et al. Protein Intake and Mobility Limitation in Community-Dwelling Older Adults: the Health ABC Study. J Am Geriatr Soc 2017; 65:1705.
  76. Hernández JL, Riancho JA, Matorras P, González-Macías J. Clinical evaluation for cancer in patients with involuntary weight loss without specific symptoms. Am J Med 2003; 114:631.
  77. Buccafusca G, Proserpio I, Tralongo AC, et al. Early colorectal cancer: diagnosis, treatment and survivorship care. Crit Rev Oncol Hematol 2019; 136:20.
  78. Holtedahl K, Hjertholm P, Borgquist L, et al. Abdominal symptoms and cancer in the abdomen: prospective cohort study in European primary care. Br J Gen Pract 2018; 68:e301.
  79. Thomas DR, Ashmen W, Morley JE, Evans WJ. Nutritional management in long-term care: development of a clinical guideline. Council for Nutritional Strategies in Long-Term Care. J Gerontol A Biol Sci Med Sci 2000; 55:M725.
  80. Milne AC, Avenell A, Potter J. Meta-analysis: protein and energy supplementation in older people. Ann Intern Med 2006; 144:37.
  81. Feldblum I, German L, Castel H, et al. Individualized nutritional intervention during and after hospitalization: the nutrition intervention study clinical trial. J Am Geriatr Soc 2011; 59:10.
  82. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Institute of Medicine and National Acadamies Press 2005. Available at: http://www.nal.usda.gov/fnic/DRI//DRI_Energy/energy_full_report.pdf (Accessed on August 14, 2012).
  83. Rand WM, Pellett PL, Young VR. Meta-analysis of nitrogen balance studies for estimating protein requirements in healthy adults. Am J Clin Nutr 2003; 77:109.
  84. Panel on Macronutrients, Panel on the Definition of Dietary Fiber, Subcommittee on Upper Reference L. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients), The National Academies Press, Washington, DC 2005.
  85. Sahni S, Mangano KM, Hannan MT, et al. Higher Protein Intake Is Associated with Higher Lean Mass and Quadriceps Muscle Strength in Adult Men and Women. J Nutr 2015; 145:1569.
  86. McLean RR, Mangano KM, Hannan MT, et al. Dietary Protein Intake Is Protective Against Loss of Grip Strength Among Older Adults in the Framingham Offspring Cohort. J Gerontol A Biol Sci Med Sci 2016; 71:356.
  87. Bradlee ML, Mustafa J, Singer MR, Moore LL. High-Protein Foods and Physical Activity Protect Against Age-Related Muscle Loss and Functional Decline. J Gerontol A Biol Sci Med Sci 2017; 73:88.
  88. Buckler DA, Kelber ST, Goodwin JS. The use of dietary restrictions in malnourished nursing home patients. J Am Geriatr Soc 1994; 42:1100.
  89. Coulston AM, Mandelbaum D, Reaven GM. Dietary management of nursing home residents with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1990; 51:67.
  90. Simmons SF, Keeler E, Zhuo X, et al. Prevention of unintentional weight loss in nursing home residents: a controlled trial of feeding assistance. J Am Geriatr Soc 2008; 56:1466.
  91. Koretz RL, Avenell A, Lipman TO, et al. Does enteral nutrition affect clinical outcome? A systematic review of the randomized trials. Am J Gastroenterol 2007; 102:412.
  92. Veronese N, Stubbs B, Punzi L, et al. Effect of nutritional supplementations on physical performance and muscle strength parameters in older people: A systematic review and meta-analysis. Ageing Res Rev 2019; 51:48.
  93. Rondanelli M, Opizzi A, Antoniello N, et al. Effect of essential amino acid supplementation on quality of life, amino acid profile and strength in institutionalized elderly patients. Clin Nutr 2011; 30:571.
  94. Solerte SB, Gazzaruso C, Bonacasa R, et al. Nutritional supplements with oral amino acid mixtures increases whole-body lean mass and insulin sensitivity in elderly subjects with sarcopenia. Am J Cardiol 2008; 101:69E.
  95. Pascual López A, Roqué i Figuls M, Urrútia Cuchi G, et al. Systematic review of megestrol acetate in the treatment of anorexia-cachexia syndrome. J Pain Symptom Manage 2004; 27:360.
  96. Berenstein EG, Ortiz Z. Megestrol acetate for the treatment of anorexia-cachexia syndrome. Cochrane Database Syst Rev 2005; :CD004310.
  97. Ruiz Garcia V, López-Briz E, Carbonell Sanchis R, et al. Megestrol acetate for treatment of anorexia-cachexia syndrome. Cochrane Database Syst Rev 2013; :CD004310.
  98. Yeh SS, Wu SY, Lee TP, et al. Improvement in quality-of-life measures and stimulation of weight gain after treatment with megestrol acetate oral suspension in geriatric cachexia: results of a double-blind, placebo-controlled study. J Am Geriatr Soc 2000; 48:485.
  99. Reuben DB, Hirsch SH, Zhou K, Greendale GA. The effects of megestrol acetate suspension for elderly patients with reduced appetite after hospitalization: a phase II randomized clinical trial. J Am Geriatr Soc 2005; 53:970.
  100. Kropsky B, Shi Y, Cherniack EP. Incidence of deep-venous thrombosis in nursing home residents using megestrol acetate. J Am Med Dir Assoc 2003; 4:255.
  101. Bodenner D, Spencer T, Riggs AT, et al. A retrospective study of the association between megestrol acetate administration and mortality among nursing home residents with clinically significant weight loss. Am J Geriatr Pharmacother 2007; 5:137.
  102. By the American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc 2015; 63:2227.
  103. Beal JE, Olson R, Laubenstein L, et al. Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 1995; 10:89.
  104. Jatoi A, Windschitl HE, Loprinzi CL, et al. Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: a North Central Cancer Treatment Group study. J Clin Oncol 2002; 20:567.
  105. Volicer L, Stelly M, Morris J, et al. Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer's disease. Int J Geriatr Psychiatry 1997; 12:913.
  106. Wilson MM, Philpot C, Morley JE. Anorexia of aging in long term care: is dronabinol an effective appetite stimulant?--a pilot study. J Nutr Health Aging 2007; 11:195.
  107. Mihara IQ, McCombs JS, Williams BR. The impact of mirtazapine compared with non-TCA antidepressants on weight change in nursing facility residents. Consult Pharm 2005; 20:217.
  108. Goldberg RJ. Weight change in depressed nursing home patients on mirtazapine. J Am Geriatr Soc 2002; 50:1461.
  109. Segers K, Surquin M. Can mirtazapine counteract the weight loss associated with Alzheimer disease? A retrospective open-label study. Alzheimer Dis Assoc Disord 2014; 28:291.
  110. White HK, Petrie CD, Landschulz W, et al. Effects of an oral growth hormone secretagogue in older adults. J Clin Endocrinol Metab 2009; 94:1198.
  111. Nass R, Pezzoli SS, Oliveri MC, et al. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Ann Intern Med 2008; 149:601.
  112. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998; 158:1855.
  113. Bales CW, Porter Starr KN. Obesity Interventions for Older Adults: Diet as a Determinant of Physical Function. Adv Nutr 2018; 9:151.
  114. Kalish VB. Obesity in Older Adults. Prim Care 2016; 43:137.
  115. Donini LM, Savina C, Gennaro E, et al. A systematic review of the literature concerning the relationship between obesity and mortality in the elderly. J Nutr Health Aging 2012; 16:89.
  116. Allison DB, Gallagher D, Heo M, et al. Body mass index and all-cause mortality among people age 70 and over: the Longitudinal Study of Aging. Int J Obes Relat Metab Disord 1997; 21:424.
  117. Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific excess deaths associated with underweight, overweight, and obesity. JAMA 2007; 298:2028.
  118. Diehr P, Bild DE, Harris TB, et al. Body mass index and mortality in nonsmoking older adults: the Cardiovascular Health Study. Am J Public Health 1998; 88:623.
  119. Diehr P, O'Meara ES, Fitzpatrick A, et al. Weight, mortality, years of healthy life, and active life expectancy in older adults. J Am Geriatr Soc 2008; 56:76.
  120. Wee CC, Huskey KW, Ngo LH, et al. Obesity, race, and risk for death or functional decline among Medicare beneficiaries: a cohort study. Ann Intern Med 2011; 154:645.
  121. Kulminski AM, Arbeev KG, Kulminskaya IV, et al. Body mass index and nine-year mortality in disabled and nondisabled older U.S. individuals. J Am Geriatr Soc 2008; 56:105.
  122. Wannamethee SG, Shaper AG, Lennon L, Whincup PH. Decreased muscle mass and increased central adiposity are independently related to mortality in older men. Am J Clin Nutr 2007; 86:1339.
  123. Dolan CM, Kraemer H, Browner W, et al. Associations between body composition, anthropometry, and mortality in women aged 65 years and older. Am J Public Health 2007; 97:913.
  124. Sui X, LaMonte MJ, Laditka JN, et al. Cardiorespiratory fitness and adiposity as mortality predictors in older adults. JAMA 2007; 298:2507.
  125. Villareal DT, Apovian CM, Kushner RF, et al. Obesity in older adults: technical review and position statement of the American Society for Nutrition and NAASO, The Obesity Society. Am J Clin Nutr 2005; 82:923.
  126. Ard JD, Gower B, Hunter G, et al. Effects of Calorie Restriction in Obese Older Adults: The CROSSROADS Randomized Controlled Trial. J Gerontol A Biol Sci Med Sci 2017; 73:73.
  127. Messier SP, Mihalko SL, Legault C, et al. Effects of intensive diet and exercise on knee joint loads, inflammation, and clinical outcomes among overweight and obese adults with knee osteoarthritis: the IDEA randomized clinical trial. JAMA 2013; 310:1263.
  128. Messier SP, Loeser RF, Miller GD, et al. Exercise and dietary weight loss in overweight and obese older adults with knee osteoarthritis: the Arthritis, Diet, and Activity Promotion Trial. Arthritis Rheum 2004; 50:1501.
  129. Villareal DT, Banks M, Sinacore DR, et al. Effect of weight loss and exercise on frailty in obese older adults. Arch Intern Med 2006; 166:860.
  130. Villareal DT, Fontana L, Weiss EP, et al. Bone mineral density response to caloric restriction-induced weight loss or exercise-induced weight loss: a randomized controlled trial. Arch Intern Med 2006; 166:2502.
  131. Verreijen AM, Verlaan S, Engberink MF, et al. A high whey protein-, leucine-, and vitamin D-enriched supplement preserves muscle mass during intentional weight loss in obese older adults: a double-blind randomized controlled trial. Am J Clin Nutr 2015; 101:279.
  132. Mason C, Tapsoba JD, Duggan C, et al. Effects of Vitamin D3 Supplementation on Lean Mass, Muscle Strength, and Bone Mineral Density During Weight Loss: A Double-Blind Randomized Controlled Trial. J Am Geriatr Soc 2016; 64:769.
  133. Zamboni M, Rubele S, Rossi AP. Sarcopenia and obesity. Curr Opin Clin Nutr Metab Care 2019; 22:13.
  134. Tolea MI, Chrisphonte S, Galvin JE. Sarcopenic obesity and cognitive performance. Clin Interv Aging 2018; 13:1111.
  135. Weijs PJM, Wolfe RR. Exploration of the protein requirement during weight loss in obese older adults. Clin Nutr 2016; 35:394.
  136. Josse AR, Atkinson SA, Tarnopolsky MA, Phillips SM. Increased consumption of dairy foods and protein during diet- and exercise-induced weight loss promotes fat mass loss and lean mass gain in overweight and obese premenopausal women. J Nutr 2011; 141:1626.
  137. Porter Starr KN, Pieper CF, Orenduff MC, et al. Improved Function With Enhanced Protein Intake per Meal: A Pilot Study of Weight Reduction in Frail, Obese Older Adults. J Gerontol A Biol Sci Med Sci 2016; 71:1369.
  138. Pennypacker LC, Allen RH, Kelly JP, et al. High prevalence of cobalamin deficiency in elderly outpatients. J Am Geriatr Soc 1992; 40:1197.
  139. Lindenbaum J, Savage DG, Stabler SP, Allen RH. Diagnosis of cobalamin deficiency: II. Relative sensitivities of serum cobalamin, methylmalonic acid, and total homocysteine concentrations. Am J Hematol 1990; 34:99.
  140. Andrès E, Affenberger S, Vinzio S, et al. Food-cobalamin malabsorption in elderly patients: clinical manifestations and treatment. Am J Med 2005; 118:1154.
  141. Morris MS, Jacques PF, Rosenberg IH, Selhub J. Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification. Am J Clin Nutr 2007; 85:193.
  142. Stabler SP. Screening the older population for cobalamin (vitamin B12) deficiency. J Am Geriatr Soc 1995; 43:1290.
  143. Kuzminski AM, Del Giacco EJ, Allen RH, et al. Effective treatment of cobalamin deficiency with oral cobalamin. Blood 1998; 92:1191.
  144. Food and Nutrition Board, Institute of Medicine. Vitamin B12. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B-6, Vitamin B-12, Pantothenic Acid, Biotin, and Choline, National Academy Press, Washington, DC 1998.
  145. Andrès E, Kaltenbach G, Noblet-Dick M, et al. Hematological response to short-term oral cyanocobalamin therapy for the treatment of cobalamin deficiencies in elderly patients. J Nutr Health Aging 2006; 10:3.
  146. Holick MF, Matsuoka LY, Wortsman J. Age, vitamin D, and solar ultraviolet. Lancet 1989; 2:1104.
  147. MacLaughlin J, Holick MF. Aging decreases the capacity of human skin to produce vitamin D3. J Clin Invest 1985; 76:1536.
  148. LeFevre ML, U.S. Preventive Services Task Force. Screening for vitamin D deficiency in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015; 162:133.
  149. Manson JE, Bassuk SS, Lee IM, et al. The VITamin D and OmegA-3 TriaL (VITAL): rationale and design of a large randomized controlled trial of vitamin D and marine omega-3 fatty acid supplements for the primary prevention of cancer and cardiovascular disease. Contemp Clin Trials 2012; 33:159.
  150. Milaneschi Y, Shardell M, Corsi AM, et al. Serum 25-hydroxyvitamin D and depressive symptoms in older women and men. J Clin Endocrinol Metab 2010; 95:3225.
  151. Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, et al. Effect of Vitamin D on falls: a meta-analysis. JAMA 2004; 291:1999.
  152. Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int 2005; 16:1425.
  153. Anderson JL, May HT, Horne BD, et al. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and incident events in a general healthcare population. Am J Cardiol 2010; 106:963.
  154. Schöttker B, Jorde R, Peasey A, et al. Vitamin D and mortality: meta-analysis of individual participant data from a large consortium of cohort studies from Europe and the United States. BMJ 2014; 348:g3656.
  155. Visser M, Deeg DJ, Puts MT, et al. Low serum concentrations of 25-hydroxyvitamin D in older persons and the risk of nursing home admission. Am J Clin Nutr 2006; 84:616.
  156. Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency. Lancet 1998; 351:805.
  157. Need AG, O'Loughlin PD, Morris HA, et al. The effects of age and other variables on serum parathyroid hormone in postmenopausal women attending an osteoporosis center. J Clin Endocrinol Metab 2004; 89:1646.
  158. Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr 2005; 135:317.
  159. Theodoratou E, Tzoulaki I, Zgaga L, Ioannidis JP. Vitamin D and multiple health outcomes: umbrella review of systematic reviews and meta-analyses of observational studies and randomised trials. BMJ 2014; 348:g2035.
  160. Aoki K, Sakuma M, Endo N. The impact of exercise and vitamin D supplementation on physical function in community-dwelling elderly individuals: A randomized trial. J Orthop Sci 2018; 23:682.
  161. Antoniak AE, Greig CA. The effect of combined resistance exercise training and vitamin D3 supplementation on musculoskeletal health and function in older adults: a systematic review and meta-analysis. BMJ Open 2017; 7:e014619.
  162. Institute of Medicine. Report at a Glance, Report Brief: Dietary reference intakes for calcium and vitamin D, released 11/30/2010. http://www.iom.edu/Reports/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D/Report-Brief.aspx (Accessed on December 01, 2010).
  163. America's bone health: The state of osteoporosis and low bone mass in our nation, National Osteoporosis Foundation, Washington, DC 2002.
  164. Radimer K, Bindewald B, Hughes J, et al. Dietary supplement use by US adults: data from the National Health and Nutrition Examination Survey, 1999-2000. Am J Epidemiol 2004; 160:339.
  165. Mursu J, Robien K, Harnack LJ, et al. Dietary supplements and mortality rate in older women: the Iowa Women's Health Study. Arch Intern Med 2011; 171:1625.
  166. Johnson KA, Bernard MA, Funderburg K. Vitamin nutrition in older adults. Clin Geriatr Med 2002; 18:773.
  167. Weeden A, Remig V, Holcomb CA, et al. Vitamin and mineral supplements have a nutritionally significant impact on micronutrient intakes of older adults attending senior centers. J Nutr Elder 2010; 29:241.
  168. Sebastian RS, Cleveland LE, Goldman JD, Moshfegh AJ. Older adults who use vitamin/mineral supplements differ from nonusers in nutrient intake adequacy and dietary attitudes. J Am Diet Assoc 2007; 107:1322.
  169. El-Kadiki A, Sutton AJ. Role of multivitamins and mineral supplements in preventing infections in elderly people: systematic review and meta-analysis of randomised controlled trials. BMJ 2005; 330:871.
  170. Liu BA, McGeer A, McArthur MA, et al. Effect of multivitamin and mineral supplementation on episodes of infection in nursing home residents: a randomized, placebo-controlled study. J Am Geriatr Soc 2007; 55:35.
  171. NIH State-of-the-Science Panel. National Institutes of Health State-of-the-science conference statement: multivitamin/mineral supplements and chronic disease prevention. Ann Intern Med 2006; 145:364.
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