Mineral requirements of elderly people1

Transcription

1 Review Articles Mineral requirements of elderly people1 Richard J Wood, Paolo M Suter, and Robert M Russell ABSTRACT Poor mineral nutrition reported in elderly peopie is attributed in large part to low dietary intake. Evaluation of the adequacy of mineral nutriture is limited for several minerals because of inadequate methods for assessing mineral status. In addition, there is a general lack of information about mineral nutriture and metabolism in very old people (> 85 y). Given these reservations, the 1989 recommended dietary allowance (RDA) for iron, zinc, and selenium appears adequate for elderly people, as does the estimated safe and adequate daily dietary intake (ES- ADDI) recommendation for copper. In contrast, the current RDAS for calcium and magnesium and the ESADDI for chromium need careful reevaluation. Current recommendations for calcium may be too low, whereas those for magnesium and chromium may be higher than necessary. For phosphorus, iodine, manganese, fluoride, and molybdenum the available data are insufficient to make a critical judgement about the appropriateness of the dietary recommendations for elderly people. Am J C/in Nutr 1995;62: KEY WORDS Minerals, elderly people, geriatrics, dietary requirements, nutrition, RDA INTRODUCTION Increasing attention is being paid to the relation between nutrition and health, particularly regarding the possible linkages between nutrition and the development of chronic disease. Elderly people are a rapidly growing segment of the US population. In 1960, < 1 of 10 people in the United States was aged 65 y (1); by the year 2030 it is estimated that 1 in 4 of the population will be elderly (2). The most rapidly growing segment of the population is the group > 75 y of age (3). It is therefore appropriate that we put increased emphasis on the relation between nutrition and health in elderly people and better understand their nutrient requirements. Several factors may potentially increase the risk of mineral deficiency in elderly people (4). Alterations in appetite can be brought on by various medications and changes in taste and smell sensitivities in elderly people. Difficulties in chewing because of poor-fitting dentures or oral health problems or difficulties in swallowing can also limit food and nutrient intakes. Aging is also associated with changes in endocrine status as well as in gastrointestinal and renal physiology, which could alter the requirements of some minerals. The Food and Nutrition Board of the National Academy of Sciences has established recommended dietary allowances (RDAs) for the maintenance of good nutrition of practically all healthy people in the United States, where it felt an adequate database of information existed (5, 6). In addition, it recently established recommended ranges of dietary nutrient intakes, the so-called estimated safe and adequate daily dietary intakes (ESADDIs) for some nutrients, for which the information base was less complete. For minerals, adults have been divided into two age categories: y and 51 y. However, it is uncertain that the mineral needs of a 25-y-old person are the same as for a 5 1-y-old person or that the needs of a 5 1-y-old person are the same as for a 90-y-old person. Specific RDAS for minerals (ie, for calcium, phosphorus, magnesium, iron, zinc, iodine, and selenium) have been set for older adults (aged 51 y). ES- ADDIs have been established for all adults for the minerals copper, manganese, fluoride, chromium, and molybdenum. Assessment of the overall mineral nutriture of the elderly population from the available literature is complicated for several reasons. Difficulties are present in defining appropriate population samples that represent various strata of the elderly population, which can be confounded by undetected disease and use of medications. In addition, for several minerals the database of controlled metabolic studies in elderly people is either quite limited or nonexistent. Furthermore, although mmeral intake data among elderly people are reviewed in this paper, the accuracy of many of these estimates in free-living populations is suspect because of limitations of food-intakeassessment methods in elderly people, and the limitations in the completeness and accuracy of mineral values in various foodcomposition tables. Thus, interpretation of mineral intake data must be done with caution, especially for some trace elements. Biochemical assessment of mineral status for many minerals is notoriously unreliable. The preponderance of studies has measured mineral concentrations in serum or plasma, despite questions of the validity of this approach for several minerals, 1 From the Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, and the Department of Medicine, Medizinische Poliklinik, University Hospital, Zurich. 2 The contents of this publication do not necessarily reflect the views or policies of the US Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. 3 Supported by a grant from the United States Department of Agriculture, Agricultural Research Service under contract #53-3K06-5-1O. 4 Address reprint requests to RJ Wood, Laboratory Chief, Mineral Bioavailability Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, 71 1 Washington Street, Boston, MA 0211!. Received March 1, Accepted for publication March 9, Am J Clin Nutr 1995;62: Printed in USA American Society for Clinical Nutrition 493

2 494 WOOD ET AL eg, magnesium, zinc, and copper. Some studies have measured mineral concentrations in other specimens (eg, red or white blood cells, saliva) or metalloenzyme concentrations when appropriate, but the number of subjects considered was rather small. Mineral-balance studies have served as the gold standard for assessing mineral requirements. However, homeostatic adaptation can severely limit the usefulness of this approach, eg, for assessment of magnesium and phosphorus needs. Innovative approaches to assessing mineral status are clearly needed. The objective of this paper is to review what is currently known about the mineral nutriture of elderly people and to draw preliminary conclusions about the appropriateness of the 1989 RDAs for minerals in old people (6). Although there is increasing interest in linking recommended mineral intakes to the prevention of specific diseases in elderly people, our present knowledge in this area for most minerals is quite limited. Thus, our focus in this paper will be mainly on evaluation of the RDAs from the perspective of preventing mineral deficiency states from occurring. CALCIUM The 1989 RDA for calcium remains unchanged from the 1980 value: 800 mg (20 mmol) for men and women in the age category 5 1 y (5, 6). The RDA subcommittee based the 1989 RDAs on estimates of obligatory losses of mg Ca/d ( mmol Ca/d) and an estimated calcium absorption rate of 30-40% (6). This is in contrast with the recommendation of 1500 mg Ca/d (37.5 mmol Ca/d) for postmenopausal women, put forth by the 1984 National Institutes of Health (NIH) Consensus Conference on Osteoporosis (7). Moreover, the 1994 NIH Consensus Development Panel on Optimal Calcium Intake recently recommended 1000 mg Ca/d (25 mmol Ca/d) for adult men and estrogen-sufficient women < 65 y of age, and 1500 mg Ca/d (37.5 mmol Ca/d) for both men and women aged 65 y (8). In humans there is an age-related decrease in calcium absorption and an impaired ability to increase calcium absorption efficiency when eating a low-calcium diet (9, 10). Similarly, old rats show decreased calcium absorption compared with younger control animals (1 1-13). In part, this decreased absorption may be due to an impaired renal production of 1,25- dihydroxyvitamin D [1,25(OH)2D1 with advancing age and/or an age-related resistance of the intestine to the action of 1,25(OH)2D (13-16). Heaney and Recker (17) found the mean fractional absorption of calcium in women who are 12 mo postmenopausal and eating 802 ± 419 (i ± SD) mg/d (20 ± 10.5 mmol/d) to be 0.27 (ie, 25% absorption efficiency) (17). Moreover, the fractional absorption of calcium is lower in postmenopausal osteoporotic women than in postmenopausal women without osteoporosis (18, 19). The question of whether age-related declines in gastric acidity affect calcium bioavailability was addressed in a study by Knox et al (20). These investigators show a reduced calcium bioavailability in subjects with a high fiber intake. However, they found no effect of the presence or absence of acid on the bioavailability of calcium from the meal. Thus, they concluded that the presence of atrophic gastritis in elderly people would not affect calcium absorption in the fed state. A similar conclusion was reached by Serfaty-Lacrosniere et al (21) in human subjects made hypochlorhydric by treatment with the proton pump inhibitor omeprazole. Seminal studies of calcium balance in pre- and postmenopausal women by Heaney et al (22) showed that premenopausal women and estrogen-treated postmenopausal women achieve calcium balance at a calcium intake of 1000 mg Ca/d (25 mmol Ca/d), whereas, estrogen-deficient postmenopausal women need 1500 mg Ca/d (37.5 mmol Ca/d) to achieve calcium balance. Milk and milk-based products supply about one-half of the dietary calcium intake of elderly people (23). Calcium consumption varies widely among elderly people, depending on the particular populations studied. In several studies, the proportion of elderly people ingesting less than two-thirds of the RDA ranges from 19% to 40% for males and from 35% to 43% for females (24-28). From the Food and Drug Administration (FDA) Total Diet Study of 1982 to 1986, it is estimated that the mean dietary intake of calcium in women y old was 507 mg (12.7 mmol), and in men it was 670 mg (16.8 mmol) (29). In arriving at a calcium requirement for elderly people, it is worthwhile to consider the effect of calcium intakes on bone mineral loss. Most calcium-intervention studies (using supplemental doses ranging from 500 to 2000 mg/d; mmol/d) have shown at least some positive effects on slowing or preventing bone mineral loss at specific bone sites (forearm, spinal column, and/or total skeletal bone) (30-34) and on lowering circulating parathyroid hormone concentrations (34, 35). However, the threshold concentration at which calcium intakes is optimized is not well documented in elderly people. In a review of 12 studies that used calcium supplements alone, Cumming (30) concluded that the greatest effect of supplemental calcium in slowing bone mineral loss in elderly women occurred in those with habitually low dietary intakes of calcium (30). Dawson-Hughes et al (36) found that postmenopausal women with dietary calcium intakes of about half of the RDA lost significantly greater bone from the spine than did postmenopausal women with dietary intakes approximating the RDA or greater. Moreover, Andon et al (37) in a cross-sectional analysis of 131 postmenopausal women showed lower bone mmeral density of the lumbar spine in women with dietary calcium intakes below 600 mg/d (15 mmol/d) than in those with intakes above this amount. In a study that most directly addresses a threshold effect, Dawson-Hughes et a! (34) investigated 301 postmenopausal women in a 2-y prospective, double-blind, placebo-controlled, randomized study. Half of the women had dietary calcium intakes less than half the RDA and half had dietary intakes of calcium ranging from 400 to 650 mg/d (10 to 16.2 mmol/d). Supplemented women received an additional 500 mg Ca/d (12.5 mmol/d). These investigators found that in the group of late (ie, 6 y since the start of menopause) postmenopausal women who ingested < 400 mg Ca/d (< 10 mmol/d) in their diets, a 500-mg (12.5-mmol) calcium citrate and malate supplement, which boosted their total calcium intake to 800 mg Ca/d (20 mmol Ca/d), prevented bone mineral loss from the spine, femoral neck, and radius. No beneficial effect of supplementation could be seen in the postmenopausal women with higher initial dietary calcium intakes (ie, mg/d; mmol/d). In contrast, beneficial effects of calcium supplementation ( mg/d; mmol/d) on postmenopausal bone loss were recently reported in two separate

3 MINERAL REQUIREMENTS OF ELDERLY PEOPLE 495 studies done in women with dietary intakes of > 650 mg Ca/d (> 16.2 mmol Ca/d) (38, 39). In a study by Aloia et al (38), calcium supplementation at 1700 mg/d (42.5 mmol/d) resulted in retardation of bone loss from the entire skeleton and the femoral neck. Average calcium intake in this study was higher than in the subjects studied by Dawson-Hughes et al (34), with only 25% of volunteers having intakes < 400 mg/d (< 10 mmol/d). Note that vitamin D supplements (400 IU/d; 10 Wd) were also given to all participants of the study by Aloia et al (38), and this may have increased the response to the calcium supplement. Similarly, a recent calcium supplementation study from France conducted in very old women (average age 84 y) showed a significant decrease in the rate of bone loss in the hip and a reduction in the number of hip fractures occurring in elderly women receiving a combination of 1200 mg (30 mmol) Ca and 800 IU (20 jig) vitamin D daily compared with control subjects receiving a double placebo (40). The independent need for increased vitamin D and calcium in elderly people needs additional research. Chevalley et al (41) reported an additional benefit from calcium supplementation on femoral bone mineral density and vertebral fracture rate in vitamin D-replete elderly subjects. In summary, many elderly people ingest inadequate amounts of calcium in their diets. Although an age-related decrease in calcium absorption has been shown, this may be related to poor vitamin D status. Exact estimates of the amount of calcium needed to prevent bone mineral loss in elderly women are not possible from the data available. Additional studies that address a threshold effect of calcium, between 800 and 1500 mg Ca/d ( mmol/d), against bone mineral loss are needed, both with and without vitamin D supplementation. More studies are also needed to examine the effects of exercise on rates of bone loss in elderly people, which would modulate calcium need. Recently, Nelson et al (42) found that high-intensity strength training had significant beneficial effects on bone mineral density of the femur neck and lumbar spine in postmenopausal women. It does appear that calcium intakes more than the current RDA may be beneficial to reduce bone mineral loss in healthy postmenopausal women, especially loss of bone at the hip, which is of enormous public health significance. Thus, it is prudent to concur with the recommendation of the recent NIH Consensus Development Panel on Optimal Calcium Intakes (8): 1000 mg Ca/d (25 mmol/d) for both elderly men and estrogen-sufficient women up to age 65 y, and 1500 mg/d (37.5 mmol/d) for all estrogen-deficient women and both men and women older than 65 y. Even greater amounts of calcium may be required in the medical management of women who are already osteoporotic, in view of a possible calcium absorption defect in these women and a need to support an increase in bone mass. However, because high calcium intakes may interfere with the absorption of iron and other minerals from the diet (43-47), additional research in the area of potential negative mineralmineral interactions is needed. Potential beneficial effects of high calcium intakes on various other health-related measures, eg, reduced blood pressure or decreased risk of colon cancer, in different populations may prove important for future RDA committees to consider, although for now the available data are insufficient. MAGNESIUM The 1989 RDA for magnesium for adults of both sexes is 4.5 mg/kg body wt, which translates into 350 mg/d for a reference 76-kg male and 280 mg/d for a 62-kg female (6). The 1989 RDA for women is slightly lower than the 1980 RDA of 300 mg/d (5). Because of technical limitations, such as the inability to measure long-term rates of magnesium turnover as a result of the short half-life of radioactive 28Mg and the relatively high natural abundance of usable stable isotopes, magnesium requirements have been based on findings from metabolic balance studies. The current RDA for magnesium was estimated from data gathered from short-term balance studies done in mostly young adult subjects. The amount of published experimental data relevant to determining magnesium needs in elderly people is quite small, and information concerning the mineral needs of the oldest subjects (age > 85 y) is practically nonexistent (4). The prevalence of various chronic diseases is increased in the older population and low magnesium intake or magnesium deficits are purported to be linked to the pathogenesis of a variety of disease states (48), including ischemic heart disease (49), hypertension (50-53), osteoporosis (54), glucose intolerance (55), diabetes (56), and stroke (57). Moreover, several diseases and/or prescribed medications can alter magnesium metabolism (48). Surveys of older subjects with illnesses show a significant proportion with apparent magnesium depletion (58). A study of 381 unselected hospitalized elderly patients (mean age 80 y) in long-term care facilities in France revealed that 10% had abnormally low serum magnesium and 21% had abnormally low erythrocyte magnesium (59). Diets high in unrefined grains and vegetables are high in magnesium (6). Magnesium intake apparently varies little with age between 14 and 65 y of age, according to the direct diet analysis of the FDA Total Diet Study (29). In this study, females aged 14-16, 25-30, and y consumed selfselected diets containing 194 mg/d (8.1 mmol/d), 189 mg, d (7.9 mmol/d), and 187 mg/d (7.8 mmol/d), respectively; males in the same age categories consumed 297 mg/d (12.4 mmol/d), 294 mg/d (12.3 mmol/d), and 250 mg/d (10.4 mmol/d), respectively. Older women and men, therefore, like younger adults consume on average dietary magnesium intakes about twothirds of the current RDA. Similar estimates of average magnesium intakes have been found in several surveys. For example, the average intake of magnesium in the United States has been estimated from the US Department of Agriculture Nationwide Food Consumption Survey ( ) to be 280 mg/d (11.7 mmol/d) for males and 225 mg/d (9.4 mmol/d) for females older than 65 y (60). In a survey of free-living elderly people in Boston, aged y, the median dietary intake for males was 253 mg/d (10.5 mmol/d) and for females 210 mg/d (8.8 mmol/d) (28). Forty-three percent of the males and 36% of the females had magnesium intakes less than two-thirds of the RDA. This finding is similar to magnesium intakes reported from elderly participants in the Baltimore Longitudinal Study of Aging (61). However, despite the apparent widespread consumption of less than recommended intakes of magnesium, there is no compelling evidence that magnesium deficiency is prevalent in either young or older adults in the United States (62, 63). This observation suggests that the current RDA for magnesium in adults is too high.

4 496 WOOD ET AL Although the data are scant, there is little information available that suggests significant age-related changes in intestinal or renal magnesium handling that would alter dietary magnesium needs in elderly compared with younger adults. Intestinal magnesium absorption efficiency has been shown to decline only slightly with age (64). Little or no information is available on any other age-related changes in magnesium metabolism in elderly people, especially the very old. As with other mineral nutrients, magnesium bioavailability can be influenced by several dietary components. In humans, high magnesium intakes do not affect calcium absorption (65). In contrast, at least in rats, high calcium intakes can inhibit magnesium absorption (66). It is unknown whether aging affects the efficiency of the renal magnesium conservation mechanism during low dietary magnesium intakes. Moreover, elderly patients receiving diuretic therapy may be at increased risk of magnesium deficiency because of increased urinary magnesium loss (58). Estimating magnesium requirements in humans based solely on the achievement of whole-body balance during dietary magnesium restriction is difficult because of the compensating ability of the kidney. In humans with normal kidney function, a severe restriction of dietary magnesium results in the reduction of urinary magnesium losses to < 6 mg/d (0.25 mmol/d) within < 1 wk of magnesium restriction (48). Although there is considerable debate about the accuracy and sensitivity of various measures of magnesium status (67), there is no evidence that widespread magnesium deficiency is common in elderly people in the United States. For example, serum magnesium concentrations of a representative sampling of the US population between 17 and 74 y of age obtained during the First National Health and Nutrition Examination Survey (NHANES I) show no age-associated change in this measure of magnesium status (62). However, because only a small fraction of body magnesium is found in plasma (48), it has been argued that the magnesium content of other tissues, such as erythrocytes, leukocytes, bone, or skeletal muscle would more accurately reflect intracellular magnesium concentrations and body stores (68). A comparison of red blood cell and mononuclear cell magnesium showed no significant difference in magnesium status due to aging (69). Cancellous bone magnesium from the iliac crest was measured in a sample of 88 healthy men and women between the ages of 20 and 90 y, who died suddenly (70). No significant correlation was observed between bone magnesium concentration and age in these apparently healthy subjects. In conclusion, there is no indication based on available information that the current RDA for magnesium of 350 mg/d (14.6 mmol/d) for adult males and 280 mg/d (11.7 mmol/d) for females is not sufficient to meet the needs of the healthy older adult population. Given the chronically low magnesium intakes in the elderly population and the lack of evidence of impaired magnesium status, the RDA for magnesium needs to be reevaluated. IRON The 1989 RDA for iron for adults aged > 51 y is 10 mg/d (0.18 mmol/d) for both men and women. No change in the RDA for this older age group was made from the previous 1980 RDA recommendation (5). The RDA for women of this age group is lower than that for younger women (15 mg/d; 0.27 mmol/d) and represents the reduced dietary iron needs of females after menopause because of the cessation of monthly iron losses in the menses. Studies measuring radiolabeled iron loss from circulating red blood cells in adult men aged y found a daily rate of endogenous iron loss of 14 pg/kg body wt (0.25 mol/kg; 0.02 mmol/79 kg; 1.1 mg/79 kg) (71). Heme and nonheme forms of iron in the diet are absorbed in the intestine by different mechanisms. On average 40% of the iron in animal tissues is found in the highly bioavailable heme-iron form; all of the remaining iron in animal tissue and the iron found in vegetables is nonheme iron. In contrast with heme iron, the absorption of nonheme iron can be enhanced or inhibited by various substances found in food. The absorption of nonheme iron in the diet can vary up to 10-fold depending on the dietary content of inhibiting and enhancing factors (6, 72). Thus, changes in dietary patterns in elderly people, such as a reduction in meat (ie, heme iron) consumption (73) or an increased consumption of iron inhibitors (4), eg, dietary fiber, can alter dietary iron bioavailability. Of additional potential importance to iron absorption in elderly people is the reduction in gastric acidity commonly associated with aging (74). Ageassociated hypochlorhydria, or reduced gastric acidity due to chronic use of antacids or other acid-lowering medications, can impair intestinal iron absorption (74). Iron is present in the diet in both heme and nonheme forms and these two types of iron are absorbed by different pathways in the intestine (75). Hemeiron absorption is not influenced by gastric acid (76). Nonheme iron can be present as either ferric or ferrous iron. Hypochlorhydria only influences the bioavailability of ferric iron in the diet; an acid environment in the stomach and upper small intestine is believed necessary to maintain the less-soluble ferric iron in solution until it reaches the absorptive sites on the duodenal mucosa (74). However, in a population study of elderly Bostonians aged y, Krasinski et al (77) found no difference in iron status (serum iron and serum ferritin) in subjects with hypochlorhydria. The literature supporting an effect of aging on iron absorption is scant and contradictory (78). It is well known that there exists an inverse relation between iron stores and the efficiency of iron absorption (75). Some of the different findings regarding aging and iron absorption may be due to measuring iron absorption in populations with highly variable iron status (78). Heme-iron absorption is apparently not affected by aging (79). In addition, nonheme-iron absorption, measured by using a stable iron isotope, was 8% in both healthy young and elderly men fed a semipurified formula diet (80). Information about iron absorption and homeostasis in very old (> 85 y) individuals is lacking. Several recent studies have provided information on the amount of iron consumption in various elderly populations. NHANES II reported an average iron intake in persons older than 55 y to be 14 mg/d (0.25 mmol/d) in men and 10.4 mg/d (0.19 mmol/d) in women (73). Similarly, median daily dietary iron intakes in free-living male and female subjects aged 60 to 90 y in the Boston Nutritional Status Survey were 14 mg (0.25 mmol) and 11 mg (0.20 mmol), respectively (81). None of the male subjects in that study and only 3% of the female subjects had iron intakes less than two-thirds of the 1989 RDA. A slight decrease with age in mean dietary iron intake was

5 MINERAL REQUIREMENTS OF ELDERLY PEOPLE 497 observed in men, whereas no change in mean dietary iron intake was observed in women. Among the participants (n = 564) of the Baltimore Longitudinal Study of Aging (61), 10% of the women older than 50 y consumed less than two-thirds of the RDA for iron. In general, the median intake of iron in the US elderly population appears to equal or exceed the current RDA for iron of 10 mg/d (0.18 mmol/d) (73). An important consideration in determining whether the current dietary iron consumption is appropriate in elderly people is whether excessive body iron accumulation occurs. It has been suggested that excess iron may act as a pro-oxidant, increasing free radical damage to tissues and increasing the risk of disease. Some surveys have reported that serum ferritin concentrations, an index of body iron stores, increase with age in elderly men (82, 83), although others have not found this relation (84, 85). No relation between age and plasma ferritin was evident from multiple-regression analysis in the elderly population studied in the Boston Nutritional Status Survey (86). These studies are suspect, however, because they did not control for the presence of inflammation, which could confound interpretation because it is more prevalent in elderly people and can elevate serum ferritin (87, 88). In a population of healthy elderly people aged y, chosen not to be suffering from inflammation (erythrocyte sedimentation rate < 40 mm/h or a blood leukocyte count < 1 1 X 109Th) or certain conditions or diseases known to alter serum ferritin concentrations, no relation between age and serum ferritin was observed (88). This observation is important because it suggests that aging alone does not result in marked accumulation of iron in the body. In the NHANES II survey, evidence of frank iron overload (based on both elevated age-adjusted serum ferritin and the percentage of transferrin saturation or serum iron) was 0.2% in adults aged y (89). However, these cases of excess body iron stores probably reflect individuals who are homozygous for the hereditary hemochromatosis gene, because population studies have found that the homozygous condition occurs with a frequency of 3 in 1000 (75). Individuals who are heterozygous for this iron-loading gene are much more common, representing as much as 10% of populations of white northern European derivation (90), and thus could represent a significant public health concern. However, a recent Canadian study has shown that most heterozygotes for the hereditary hemochromatosis gene have a normal serum ferritin and transferrin saturation and do not have evidence of excessive iron overload, as assessed directly by hepatic iron concentration (91). Persons who are homozygous for the hemochromatosis gene, who have a genetic predisposition to marked iron overload, are at increased risk of developing a variety of chronic diseases, including heart disease and cancer. Concern has also been raised about the relation between increased iron consumption in the general population and the development of certain chronic diseases. Recently, a study done in middle-aged men in Finland reported a positive relation between total iron intake, serum ferritin, and the risk of acute myocardial infarction (92). A preliminary report, however, from the United States (93) did not confirm the relation between serum ferritin and the incidence of heart disease. Heme (ie, meat-derived) iron, but not total dietary iron intake, was associated in another study with an increased risk of fatal coronary disease and nonfatal myocardial infarct in men (94). Iron status has also been implicated in carcinogenesis (95), but the relation remains controversial (96). Additional research concerning whether progressive body-iron accumulation occurs in elderly people, the role of dietary factors in iron status of elderly people, and possible linkages between iron status and chronic disease risk is warranted. The subject of iron nutriture in elderly people was recently reviewed by Johnson et al (96). Few normative data about the iron status of elderly people older than 75 y are available. NHANES II did not survey people older than 74 y. However, this problem is being rectified in the NHANES III survey, which will be completed in Anemia can be quite preyalent in elderly people because as many as 24% of elderly people seeking medical care can be anemic (97, 98). Most of this anemia, however, is not due to iron deficiency but rather to the presence of chronic diseases, such as cancer and rheumatoid disease. The relation between inflammation and anemia was explored in a subset of the data from NHANES I conducted between 1971 and The prevalence of anemia in men aged y was observed to be 2-4% for men without evidence of inflammation [erythrocyte sedimentation rate (ESR) < 20 mm/h] compared with 9-78% for men with inflammation (ESR > 30 mm/h) (87). Estimates of iron deficiency in the elderly US population are 1-6% (96). Diagnosis of iron deficiency [on the basis of abnormal findings in two of three iron indexes: mean corpuscular volume (MCV), transferrin saturation, and erythrocyte protoporphyrin concentrations] in white men indicates that the frequency of iron deficiency increases by fivefold from 0.7% to 3.5% between the fourth and eighth decades. In contrast, in white, nonpregnant women the prevalence of iron deficiency was reduced from 6.5% in women aged y to 2.7% in women aged y. However, the prevalence of iron deficiency in certain groups of elderly people can be quite substantial. For example, in elderly Hispanic women iron deficiency exceeds 7%, whereas the prevalence of iron deficiency in poor elderly people is about two- to threefold higher than that in elderly people that are not poor (96). Measurement of serum ferritin is a good indicator of iron status. However, because serum ferritin concentrations can be elevated as a result of inflammation, interpretation of this iron-status index in elderly people could be confounded by the increased prevalence of inflammatory diseases in this population (87). Normative ranges for serum ferritin in elderly people need more investigation. Usually a serum ferritin value of 12 j.lg/l is used as a cutoff to indicate depleted iron stores (89). Questions have been raised about the adequacy of this benchmark value for detecting iron deficiency in elderly people (99, 100). For example, Guyatt et al (99) reported that two-thirds of the patients presenting with anemia in a community hospital setting had no stainable iron in their bone marrow despite apparently normal serum ferritin concentrations (18-45 gfl). Similar conclusions were made by Holyoake et al (100), who studied the relation between stainable bone marrow iron and serum ferritin in a series of consecutive new referrals to a geriatric unit. They found that 84% of the subjects with serum ferritin concentrations between 12 and 45 g/l had no detectable stainable iron, suggesting that most elderly patients with serum ferritin concentrations in this range have iron deficiency. This finding was not influenced by patients with chronic inflammatory diseases. Additional research to define appropriate age-sensitive values for iron indexes is needed, because the

6 498 WOOD ET AL findings of Guyatt et al (99) and Holyoake et al (100) suggest that a substantial portion of elderly people could be at risk of iron deficiency. In 530 free-living elderly women studied in the Boston Nutrition Status Survey, 1 of 4 had a serum ferritin concentration < 45 g/l (81). In light of some uncertainty concerning age-associated iron accumulation in healthy elderly people and appropriate normative values for measures of iron stores in elderly people, it is our belief that the current RDA for iron should not be altered. More research in this area is clearly needed. ZINC In 1989 the RDA for zinc for individuals aged 51 y remained the same as the 1980 RDA for men (15 mg/d; 0.23 mmol/d), but was lowered from 15 mg/d (0.23 mmol/d) to 12 mg/d (0.18 mmol/d) for women to reflect average sex differences in body weight (5, 6). The zinc requirement for adults is based on results of zinc-balance studies, and estimates of endogenous losses and zinc bioavailability from food (6). Several studies show that zinc absorption efficiency is decreased in elderly people. Zinc absorption measured with stable zinc isotope techniques was only 17-21% in elderly people compared with 31-39% in young people (101, 102). Similarly, zinc absorption estimated from plasma appearance of zinc over time after a 25-mg oral zinc load has been significantly lower in older people (aged > 60 y) compared with younger adults (103). However, Couzy et al (104) reported that fractional zinc absorption did not differ significantly between young (24-40 y) and elderly (70-83 y) men eating a meal containing either a low or high amount of phytic acid, an important inhibitor of zinc absorption. Moreover, old age (67-83 y) apparently does not impair the ability of the intestine to increase the efficiency of zinc absorption in response to the ingestion of a low-zinc diet (1.6 mg/d; 0.02 mmol/d) (101). The data that show a possible age-associated reduction in intestinal zinc absorption are in contrast with results of studies of aged rats. In Ussing chambers, duodenal intestinal tissue from 24-mo-old rats showed an increased transport of zinc compared with that in the intestine from 3- or 12-mo-old rats (105). Although Turnlund et al (102) found impaired zinc absorption in elderly men aged y compared with younger men (22-30 y), they found no difference in zinc balance between the two age groups. Their results thus suggested a lower zinc requirement for elderly men. Possible explanations for this could be lower lean body mass, exercise, and ejaculation frequency in the older men. Zinc absorption and balance data for young and elderly women are not available, but should be gathered in future studies. Diets rich in phytate and fiber are known to depress zinc absorption (106), but the role of milk and calcium intake as a potential inhibitor of zinc absorption is controversial (44, 46, 47, 107, 108) and needs additional study in light of current recommendations that elderly people increase their calcium intakes (8). This is a particularly important issue in elderly people because zinc intakes tend to be lower than those currently recommended and any adverse effect on dietary zinc bioavailability could increase the risk of zinc deficiency. Milk and milk-based products are a major source of calcium and zinc in the diet of elderly people, contributing 50% of daily calcium intake and 16% of zinc intake (23), and it is likely that increased low-fat milk consumption will be encouraged to augment calcium intakes in this age group in an attempt to promote bone health. Besides milk and milk-based products, the other important food source of zinc in the diets of elderly people is meat (23). As mentioned above, dietary zinc intakes by elderly people are much less than the present RDAs, and parallel a decline in energy consumption in this age group. Among elderly Canadians, 66% of males are ingesting < 7.2 mg ( mmol) Zn/d, and 72% of females are ingesting < 5.4 mg (0.08 mmol) Zn/d ( 24). In this study, no consistent relation was found between dietary zinc intake and plasma zinc concentrations, although 18% of the population had a serum zinc value < 1 1 tmolth. In the Boston Nutritional Status Survey, median dietary zinc intakes in free-living elderly males and females were 1 1 mg/d (0.17 mmol/d) and 9 mg/d (0.14 mmol/d), respectively (28). The overall prevalence of low serum zinc values (< 10.8,tmol) in the Boston study was quite low. Plasma zinc was positively correlated with zinc intake and negatively correlated with age in multiple-regression analysis (109). Various other surveys have similarly shown low dietary intakes of zinc among healthy elderly people, ranging from 5.8 to 12.8 mg/d (0.09 to 0.20 mmol/d) ( ), and high percentages (57-90%) of elderly people taking in < 15 mg (0.23 mmol) Zn/d ( 28, 29, 112, 113). In these surveys, mean serum zinc values range from 10.8 to 14.6 mol/l among healthy elderly people, and from 10.5 to 11.3 j.tmol/l among institutionalized or housebound elderly people (24, 1 10, 1 1 1, ). Although plasma or serum zinc concentrations are not ideal indicators of zinc status, there is presently no agreement about what is a better indicator or better combination of indicators. Polymorphonuclear leukocyte concentrations of zinc decrease in experimental zinc depletion and have been found to correlate well with muscle zinc (117, 118) but not with plasma zinc (116). Among hospitalized elderly people aged y, 27% were found to have polymorphonuclear leukocyte zinc concentrations below a reference standard for healthy elderly people. Salivary concentrations of zinc also do not correlate with plasma concentrations, but have been reported to increase with age (1 19). Saltzman et al (120) in a cadaver study found little correlation between blood and total body burden of zinc, and reported no correlation between total body zinc and age. A second cadaver study found evidence for an accumulation of liver zinc with age (121). More reliable indicators of zinc status are needed before definitive statements can be made about zinc nutriture in elderly people. Because zinc nutriture may affect immunocompetence, there has been some interest in correlating zinc intake and blood concentrations with immune function in elderly people (112, 122, 123). For example, in an elderly hospitalized group of patients with marginal zinc status, zinc supplementation (20 mg/d; 0.31 mmol/d) resulted in increased serum thymulin (124). In contrast, in an interesting study by Bogden et al (123), supplementation of elderly people aged y with 15 mg (0.23 mmol) Zn/d, resulted in no change in the mononuclear or polymorphonuclear leukocyte concentrations after mo. Moreover, delayed dermal hypersensitivity was suppressed in the group receiving zinc along with a multivitamin-mineral supplement (without zinc) compared with the group receiving the multivitamin-mineral supplement (without zinc) alone, sug-

7 MINERAL REQUIREMENTS OF ELDERLY PEOPLE 499 gesting a possible negative impact of zinc supplementation on the immune status of elderly people. In contrast, another study by the same research group (125) showed that a daily vitaminmineral supplement that included 15 mg (0.23 mmol) Zn increased the immune response in elderly people. Excessive zinc intakes may have other negative effects, however. For example, zinc supplementation at mg/d ( mmol/d) for 12 wk has been reported to lower serum highdensity-lipoprotein cholesterol (126). In view of the above evidence, it appears that the present RDAS for zinc for elderly people are generous. However, until better measures of zinc status are available and used in population studies of elderly people, the present RDAS are justifiable. SELENIUM The RDA for selenium in the United States was first established in Because of the lack of specific data on selenium requirements of elderly people, the same recommendation is made for adults aged 51 y as for younger adults: 70 pg/d (889 nmol/d) for men and 55 j.g/d (699 nmol/d) for women (6). The selenium requirement has been based primarily on plasma glutathione peroxidase activity responses to graded selenium supplementation in adult men in China with low selenium status (6). Age-related changes in the absorption and metabolism of selenium have not been described. Whether age-related changes in renal function affect the urinary excretion of selenium is controversial ( ). It is likely that poor selenium intake is responsible for the lower measures of selenium status found among elderly people (129, 130). However, Abdulla et al (131) found no difference in selenium intakes in young (20-55 y) compared with healthy elderly adults aged > 65 y by analysis of duplicate meals. Seafood, kidney, liver, and to a lesser extent other meats are good dietary sources of selenium; the concentration of selenium in food can vary according to geographic location as a function of the soil content of selenium (6). However, little information is available concerning relative selenium bioavailability from different foods. Most studies on selenium intake have used food tables that are unreliable and/or incomplete. Thus, calculated dietary selenium intake can only be considered a crude estimate of actual intake. Several studies have shown lower serum or plasma selenium concentrations in adults aged 60 y than in younger adult age groups (127, 129, ). Although some studies have reported a decrease in serum selenium concentrations throughout adulthood (133, 138), the decrease is more marked between the ages of 65 and 90 y ( ) compared with subjects aged y. A study among healthy Finnish males aged y reported that 3-4% of the subjects had low serum selenium concentrations (< 46.tg/L; 582 nmol/l), whereas 45-52% of the subjects had serum selenium concentrations in the borderline range (46-69 jg/l; nmol/l) (142). Some investigators have not been able to show a relation between age and plasma and/or red blood cell selenium concentrations (137, 143). However, the selenium concentrations in fingernails and/or toenails have been reported to decline with age (127, 137). In a Greek study, selenium in hair and fingernails and selenium excretion in morning urine were lower in elderly subjects than in younger subjects (127). Bunker et al (144) reported that healthy free-living elderly people aged y living in the United Kingdom have higher whole blood and plasma selenium concentrations than do housebound elderly subjects of the same age, and this difference was attributed to lower selenium intakes in the housebound group (: 37.5 p.g/d; 475 nmol/d) compared with the free-living group (: 64.7 p.g/d; 819 nmol/d) (144). The daily selenium intake was directly and significantly correlated with selenium balance in both groups of elderly people, but despite the low selenium intakes among the housebound group, they remained in positive balance. It is interesting that in this study there was no difference found in whole-blood glutathione peroxidase activity between the housebound and normal groups. Although selenium is part of the body s antioxidant defense mechanism, it is uncertain whether selenium intakes that are higher than the current RDA would provide any additional beneficial effect in the prevention of chronic diseases, such as cancer or cardiovascular disease ( ). Data that have related selenium nutriture to atherogenesis and cancer are not consistent and may be confounded by other nutritional factors, such as vitamin E status (138, ). Moreover, smoking may affect measures of selenium status in that smokers show reduced glutathione peroxidase activity in platelets compared with nonsmokers (144). This finding could be explained by lower selenium intakes in smokers (151), although other mechanisms may also be operative (132). The amount of dietary selenium exposure needed to cause chronic poisoning in humans is not known with certainty. In China, dietary exposure of 5 mg/d (63 p.mol/d) in seleniferous regions is associated with changes in fingernails and hair loss (152), and a single case report of thickened but fragile nails and a garlic odor in dermal secretions were reported by this group in a person consuming 1 mg sodium selenite/d (12.7 p.mol/d) for > 2 y (6). Although selenium status may be low in some elderly groups, it appears to be related to low selenium intake. Additional research is needed, however, concerning selenium nutriture and status in very old people (> 85 y). Given that positive selenium balance is evident in elderly subjects consuming less than the current RDA for selenium, it appears that the 1989 RDA for selenium is sufficient to meet the needs of elderly people. COPPER No RDA for copper has been set because of uncertainties about its requirement in humans. The current ESADDI for copper for all adults, including elderly people, is mg/d ( jmol/d) (6), which encompasses a larger range than was previously recommended in 1980 (5). There is no change in copper absorption with age (80, 101, 153). In adults aged y there is a sex difference in copper absorption, with females showing a higher absorption. However, this sex difference in absorption disappears in older women, possibly because of changes in estrogen status (153). A study by August et al (101) suggests that elderly people aged 71 ± 6 y increase their efficiency of copper absorption when consuming low-copper diets. In younger (20 ± 1 y of age) subjects they found no significant change in copper absorption when a low-copper diet was fed. Older men have a faster copper turnover (ie, shorter biological half-life) with aging, and

8 500 WOOD ET AL the turnover is faster than in older women (153). In men, the biological half-life of copper is 24 d at age y, 16 d at age y, and 13 d at age y. In contrast, in women the corresponding turnover values are 19 d at all three ages. Organ meats, especially liver, are the richest dietary sources of copper, followed by seafood, nuts, and seeds (6). Little is known about copper intake in elderly people. Sixty percent of the menus provided by Food Services for the Elderly in Washington State contained less than recommended amounts of dietary copper (154). Several other groups also reported typically low copper contents in the diets of elderly people (111, 131, 153, 155). Little information about copper bioavailability from different foods is available; however, various dietary factors are known to influence copper availability, including dietary fiber, ascorbic acid, and excessive zinc intakes (6, 156). Bunker et al (157) reported that elderly people can maintain copper balance with a mean daily copper intake of 20.1 jtmol (1.28 mg/d). As with many trace minerals, it is difficult to accurately assess copper status. In some studies, plasma or serum copper concentrations have been shown to increase with age (153, ). Similar results have been reported in mice (165). However, Johnson et al (153) reported increasing plasma copper concentrations only until the age of 60 y and thereafter a decline. These investigators found a parallel increase in the activity of cytochrome c oxidase in platelets and mononuclear leukocytes up to age 60 y, but platelet activity then declined in older subjects (153). Copper concentrations in hair (119, 166, 167) and saliva (1 19) decline with age. In the Boston Nutrition Status Survey, multiple-regression analysis showed a decrease in serum copper of 0.90 jmol/l per decade with age in females aged 60 to > 90 y, after correction for serum proteins, medications, and various other factors (168). Women at all ages, however, show higher plasma copper concentrations than men (153). In two studies, plasma and whole-blood copper concentrations were lower in free-living healthy elderly than in housebound ill elderly people, probably because sick housebound people have higher ceruloplasmin concentrations (1 13, 168). In another study, no clear age trends could be found for ceruloplasmin (153). Moreover, when leukocyte copper concentrations are used as an index, lower copper concentrations have been shown in housebound elderly people than in free-living elderly people (1 13, 169). In an autopsy study a comparison of tissue copper from elderly (mean age 80 y) and young healthy accident victims (mean age 29 y) showed lower copper concentrations in elderly people s heart tissue, whereas in skeletal muscle, liver, and kidney, no age difference in copper concentrations could be found (121). Aging has not been associated with significant changes in copper metabolism that would influence the copper requirement, and copper balance can be maintained in elderly people at dietary copper intakes less than the current minimum recommended amounts. Thus, the present ESADDI for copper appears adequate for elderly people. CHROMIUM Because of the lack of accurate methods to assess chromium status, it is difficult to estimate chromium requirements (6). An ESADDI for chromium between 50 and 200 g/d ( mol/d) has been tentatively recommended for adults of all ages by the 1989 RDA subcommittee (6). This recommendation is identical to the previous recommendation in 1980 (5). Data on chromium in food are scarce and unreliable. Several studies conducted in elderly people have reported chromium intakes below the current recommended range (1 1 1, ). Moreover, it seems quite difficult, especially for elderly people, to obtain the recommended amounts of chromium from diet alone. Based on available dietary data of typical intakes by adults, it has been estimated that 3000 kcal (12.6 Mi) would have to be eaten to obtain the minimum suggested amount of chromium of 50 g/d (0.96 p.mol/d) (173). Median energy intakes reported for elderly men aged 60 to > 90 y in the Boston Nutritional Status Survey were 1871 kcal (7.8 MJ), whereas in elderly women the median intake was 1468 kcal (6.1 MJ). Moreover, essentially all of the subjects studied ingested < 3000 kcal (12.6 MJ)/d (81). In view of the low energy intakes in elderly people, the ingestion of recommended amounts of chromium from food alone is unlikely. Consideration of the apparent unreasonableness of the current chromium recommendation for the elderly population should therefore be given strong consideration by future RDA committees. Offenbacher et al (170) reported that two elderly subjects (aged 62 and 66 y) could maintain positive chromium balance despite chromium intakes of 37 p.g/d (0.71 pmol/d), which is below the lower limit of the ESADDI. This report agrees with an earlier balance study in elderly subjects aged y reported by Bunker et al (171). A subsequent report by Bunker and Clayton (111) found that both free-living and housebound elders could maintain apparent positive chromium balance at chromium intakes about one-half the lower recommended limit. Chromium acts as a cofactor for insulin and is required for the maintenance of normal glucose and lipid metabolism in animals and probably in humans (6, 174). In view of these proposed physiological functions, chromium nutriture has been assessed by measuring glucose tolerance. In one study, chromium supplementation, 200 j.g/d (3.84 mol/d) as chromium chloride, in elderly people aged > 65 y led to an improvement in glucose tolerance (175). However, such improvement has not been universally reported (176). Several older studies show that most elderly people can respond to chromium supplementation with improved glucose tolerance (172). Conflicting reports in this area may be due to variability in the study populations. In many studies the response of a younger age group was not evaluated; thus it is uncertain whether this possible effect of chromium supplementation is limited to elderly people who may have compromised chromium status or whether the apparent effect of chromium in these situations represents an acute pharmacological effect on glucose metabolism. Chromium supplementation has also been shown to affect blood lipids and is thus regarded as a possible modulating cofactor for normal lipid metabolism. Chromium supplementation, 250 pg/d (4.8 mol/d) as chromium chloride, induced a decrease in very-low-density lipoproteins cholesterol and an increase in high-density-lipoprotein cholesterol with no change in total cholesterol in subjects (aged 63 ± 14 y) with non-insulin-dependent diabetes mellitus (176). Similar findings were reported by others (177, 178). Whether chromium nutritional status is important in atherogenesis is unknown.

9 MINERAL REQUIREMENTS OF ELDERLY PEOPLE 501 The effect of age on body chromium is uncertain. An autopsy study comparing ill elderly subjects (mean age 80 y) admitted to a geriatric service with healthy young subjects (mean age 29 y) killed in accidents showed an apparent accumulation of chromium in muscle, liver, kidney, and especially heart tissue of the older subjects (121). Other sources suggest that tissue chromium decreases with age (6). Animal data suggest a decrease in cellular chromium with age (179). Although it is certainly desirable to optimize glucose tolerance and lipid profiles in elderly people, tentative recommendations for this group do not appear to be possible with diet alone. Because chromium balance in older adults can be achieved at dietary chromium concentrations <50 g/d (<0.96 j.mol/d) and no clearly defined chromium deficiency syndrome has been described in older adults, the current recommended lower limit for dietary chromium appears to be set too high and should be reevaluated. OTHER MINERALS Insufficient data on the intake, metabolism, and status of phosphorus, iodine, manganese, fluoride, and molybdenum in elderly people are available to adequately assess the validity of current dietary recommendations for these minerals in the older population. Additional research is needed. CONCLUSION Except for calcium, surprisingly little information is available concerning the mineral requirements of elderly people. Mineral nutriture of elderly people is a subject that should be an ongoing area of investigation that applies new and more sensitive measures of mineral status. Additional research also needs to be done to evaluate whether various biochemical cutoff values for commonly used measures of mineral nutriture are appropriate for the older population. Moreover, the possible linkage between nutriture of various minerals and the development or treatment of chronic disease needs special attention in this population. Our review of mineral needs in elderly people suggests that the 1989 RDA for several minerals needs reevaluation. In our opinion, estimates of dietary calcium needs in elderly people are too low, whereas dietary recommendations concerning minimum magnesium and chromium intakes are higher than necessary. Current recommendations for zinc, iron, copper, and selenium are appropriate given our current information in elderly people. Finally, there is insufficient information available to judge the adequacy of dietary recommendations for elderly people concerning phosphorus, iodine, manganese, fluoride, and molybdenum. 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