Hypertension is an extremely common problem in older individuals, with the National Health and Nutrition Examination Survey (NHANES) finding that 44% of whites and 60% of blacks aged 65 to 74 years have a blood pressure in excess of
160/95 mmHg.1 The prevalence of hypertension is increasing with the increasing prevalence of obesity, and this increase was particularly noticeable from 1990 to 2000.2 Both the Framingham Study and the Chicago Stroke Study have shown that untreated hypertension in older individuals is strongly associated with an increased risk of stroke and cardiovascular disorders.3 Studies such as the Systolic Hyperten-sion in the Elderly Program (SHEP) have shown that lowering blood pressure has decreased the occurrence of stroke.4 Thus, nutritional interventions that would lower the prevalence of hypertension in older individuals could have a major impact on the health status of this group.
In younger patients, being overweight has been linked to hypertension, and with age there is an increase in body fat. Malnourished patients in nursing homes often display a marked amelioration of preexisting hypertension. These findings suggest that excess weight could contribute to hypertension in older individuals.
Epidemiologic studies have long suggested a relationship between hypertension and salt intake. Luft et al.5 suggested that 25 to 30% of individuals over 40 years of age may display sodium-sensitive blood pressure responses. A difference of 100 meq/day in sodium intake is associated with a 3- to 6-mm difference in systolic blood pressure.6 It has been suggested that older individuals (mean age, 85 years) are especially sensitive to the effects of a high-salt diet on blood pressure.7 This increased sensitivity may be secondary to the reduced rate of urinary sodium excre-tion in older individuals. It would appear prudent to suggest that most elderly should FIGURE 3.1 Pictorial representation of the world record for the 1-mile run.
04:19.2
avoid adding table salt to their food and should not use excessive salt for cooking.
Some drinking water is particularly high in salt; tap water should not exceed 20 mg of sodium per liter. When the sodium content of tap water is particularly high, consideration should be given to drinking and cooking with bottled water. However, severe sodium restriction should be avoided wherever possible in older individuals, as it can result in unpalatable food and the development of malnutrition. It also can lead to severe postural hypotension.8 There is some evidence that long-term use of very low sodium diets may actually lead to an increased mortality.9
Low calcium intake has been associated with increased arterial pressure,10 and high calcium intakes ameliorate systolic hypertension.11 A meta-analysis found that many older individuals have a suboptimal calcium intake. In view of the putative protective effects of high calcium intake on bone (vide infra), it seems reasonable to liberalize calcium intake to 1 to 1.5 g in subjects 50 years of age or older in the hope that it will also result in a lower blood pressure.
Both low potassium and magnesium are associated with increased blood pres-sure, and administration of these ions produces a small decrease in blood pressure.12,13 Insulin resistance is associated with hypertension, and persons with insulin resistance have increased salt sensitivity.14 Consuming one or two alcoholic drinks a day is associated with a lower blood pressure than seen in persons who do not drink.15 Greater consumption of alcohol is associated with hypertension. A meta-analysis showed that 3.7 g of fish oil produced a small reduction in blood pressure.16
Overall, geriatric hypertension appears to have a relatively strong relationship to diet; a lifetime of moderate salt and caloric intake, as well as an adequate calcium intake, appears to be a prudent preventive medicine approach. The Trial of Non-Pharmacologic Intervention in the Elderly (TONE) showed that over a 4-year period of sodium reduction and weight loss, 23% of patients did not need medications to control their blood pressure compared to 7% in the usual-care group.17 In view of the high cost of antihypertensive medications, careful dietary intervention in older subjects (mild salt restriction or added calcium intake) may represent the most prudent approach to the management of borderline elevations in blood pressure. This approach is particularly relevant in the “stroke belt” of the southern U.S., where NHANES III showed this region to have the highest salt and lowest potassium, calcium, and magnesium intakes.18
3.1.2 OSTEOPENIA
The development of osteoporosis and subsequent fractures is a major cause of morbidity in postmenopausal Caucasian females. Clearly, the first approach to pre-vention is measurement of bone mineral density and appropriate bisphosphonate therapy in severely osteopenic persons. In addition, there is reasonable epidemiologic evidence linking the development of type II (age-related) osteopenia to lifetime calcium intake.19 Studies in Hong Kong have suggested that subjects with a calcium intake below 400 mg/day are particularly at risk for the development of osteoporosis and hip fractures.20 Osteoporosis is more prevalent in subjects with lactose intoler-ance, which leads to poor intake of dairy products and thus calcium, and in subjects with malabsorption syndromes, again suggesting a role for dietary calcium in bone
protection. For these reasons, it seems appropriate to suggest a total calcium intake of the order of 1 to 1.5 g/day.
The role of vitamin D deficiency in the pathogenesis of hip fractures in individ-uals over 70 years of age is rapidly emerging.21 A number of factors make older individuals at risk for developing vitamin D deficiency. These include decreased dietary intake, decreased sun exposure, the use of sunscreen to prevent recurrent skin cancer, impairment of the ability of ultraviolet light to produce cholecalciferol in older skin, decreased conversion of 25(OH) vitamin D to 1,25(OH) vitamin D by the kidney, and decreased intestinal reception for vitamin D. Studies from Israel have suggested that even elderly subjects living in high-sun-exposure areas can develop vitamin D deficiency.22 A longitudinal study over 14 years showed that even very healthy older persons living in New Mexico had declines in their 25(OH) vitamin D levels.23 Elderly in institutions appear to be particularly vulnerable to developing vitamin D deficiency, which increases their chances of having a hip fracture. For this reason, all institutionalized older subjects should receive 800 IU of vitamin D daily. If this is given, calcium levels need to be checked regularly to avoid the development of unrecognized hypercalcemia. A placebo controlled study of 3270 healthy ambulatory women aged 84 ± 6 years who were supplemented with 1.2 g of elemental calcium and 800 IU of vitamin D daily for 18 months produced a 43% decrease in hip fracture.24 Recent studies have supported the need to have vitamin D levels of at least 30 mg/dl.
3.1.3 CHOLESTEROL
Is it rational to have embarked on a national campaign to lower cholesterol? McCor-mick and Skrabanek25 have argued that future generations will look back at the era of population interventions to reduce coronary artery disease with disbelief and contempt for the epidemiologic analysis that supported these political actions. Alter-natively, Fries et al.,26 although accepting that cholesterol reduction is unlikely to reduce mortality, have cogently argued that, at least in some populations, reduction in cholesterol may compress morbidity by reducing morbid cardiovascular events.
Thus, in the Helsinki Heart Study trial, for example, there was a 37% reduction in nonfatal coronaries.26 In addition, it is possible but not proven that such prevention may reduce medical expenditures. Thus, it would appear still reasonable to pursue cholesterol reduction vigorously in high-risk groups, such as those with a previous myocardial infarction or those subjects with a strong family history of atherosclerotic heart disease. The cholesterol level at which intervention should begin is uncertain, although values above 300 mg/dl would certainly warrant attention. For the best overall mortality target, levels of cholesterol should probably be in the range of 200 to 220 mg/dl in subjects under 65 years of age. One study suggested that, even in subjects with a mean age of 82 years, a total cholesterol greater than 250 mg/dl and a high-density lipoprotein cholesterol less than <35 mg/dl remain indicators of subsequent coronary events.27 However, in other studies a high total cholesterol was associated with longevity,28 and in a study of 3572 men aged 71 to 93 years, persons with the lowest quartile had a higher all-cause mortality than those in the highest quartile.29 However, there is no evidence that routine intervention in subjects over
65 years of age has any benefit on mortality or mental or function status.30 In addition, the Women’s Health Initiative could show no major health benefits of a low-fat diet.31–33 It is now recognized that small, dense low-density lipoprotein (LDL) is easily absorbed and oxidized by blood vessels. This is in contrast to large, foamy LDL, which is not atherogenic and found in high amounts in many centenarians.
Treatment of elevated cholesterol levels in older persons requires understanding that all LDL is not bad. In view of these facts—that major interventions in diet in older subjects may result in malnutrition—it seems reckless to attempt to alter the cho-lesterol content of diets in the populations over 70 years of age. In addition, animal and human studies have suggested that lowering cholesterol may result in cognitive impairment.34,35
3.1.4 FISHAND FISH OILS
Greenland Eskimos, despite their high fat intake, have a low prevalence of athero-sclerosis and develop acute myocardial infarction at 10% the rate of Danes or North Americans. The difference is explained by the quality of fats ingested, with the Eskimos ingesting high qualities of omega-3 fatty acids derived mainly from seals and whales, whereas the other populations eat more saturated fats and omega-6 fatty acids.
These epidemiologic findings have led to the suggestion that polyunsaturated fatty acids, such as eicosopentanoic and docoscipentanoic acid, may decrease cor-onary artery disease both by decreasing platelet adhesiveness and by lowering tri-glycerides and, to a lesser extent, low-density lipoprotein cholesterol.36 As these fatty acids are the predominant fat in fish, eating a high-fish diet may also prove protective against heart disease. Population studies have suggested that eating fish regularly may reduce atherosclerotic disease.37 Mortality from coronary artery disease was 50% lower among those who consumed fish than among those who did not. At present, no large population trials showing the efficacy of raw fish oils over a prolonged period have been published. Because of the increased bleeding tendency produced by fish oil ingestion, intake of excess fish oil should be avoided in older subjects. However, there would appear to be minimal risk and potentially some benefit of increasing fish consumption to three or four times per week. Other poly-unsaturated fatty acids, as seen in the Mediterranean diet, may be equally effective.
3.1.5 CANCER
Approximately half of all the new cancers in the U.S. can occur in individuals over the age of 65 years. Gastrointestinal, prostate, and breast cancer are responsible for over half the cancers in patients over 60 years of age. Although the cancer incidence rises with age, it begins to decrease in those 85 to 90 years of age. The concept that diet can modulate the prevalence of cancer is not a new one. In 1933, Morison and Orr38 suggested that cancer in betel nut chewers was less prevalent in those with high vitamin A intake. In the same year, Stocks and Karn39 found that high intake of whole-meal bread, vegetables, and fresh milk was associated with a decrease in cancer incidence at multiple sites.
Animal studies have suggested that food restriction reduces the cancer rate.40 Further, feeding high-fat diets to animals induces breast and colon cancers. Human epidemiologic studies support the increased occurrence of carcinoma of the colon and breast in subjects on high-fat diets.41 However, recent large prospective studies have considerably weakened the support for a major role of fat intake independent of calories as a major pathogenic factor in breast and colon cancer.42 There is stronger evidence to support a relationship between aggressive prostate cancer and fat intake.43 There is a 15% increase in colon cancer for each 100-g increase in red meat44 and a 30% increase in prostate cancer in high-red-meat eaters.45 This may be due to N-nitrose compounds formed from nitrogenous residues in red meat. Vegetarian groups, such as the Seventh Day Adventists, have a low occurrence of carcinoma of the colon, which could be related to low fat intake, the effect of lack of meat, or, most likely, the increased fiber in the diet. Numerous animal and human studies have supported the protective effect of dietary fiber against the development of colon cancer.
Iron deficiency has been associated with hypopharyngeal cancers in women.46 Iodine deficiency predisposes to thyroid cancer.47 Aflatoxin, from Aspergillus flavus, is a contaminant of peanuts and cereals in some situations and has been associated with hepatoma.48 In Japan, eating bracken fern is associated with a five-fold increase in esophageal cancer.49
Epidemiologic studies have suggested a decrease in lung cancer in subjects with high intakes or serum levels of beta-carotene or vitamin A.50 Vitamin A ingestion can lead to hypercalcemia by cathespin D activation and release of parathormone.
For this reason, supplementation with vitamin A is never recommended. In the Alpha-Tocopherol Beta-Carotene (ATBC) trial, there was no association with lung cancer but a 34% lower incidence of prostate cancer in heavy smokers.51 Long-term use of folate supplementation reduced the risk of colon cancer by approximately 40%.52
Low selenium levels in the blood have been associated with an increase in cancer incidence.53 The combination of low selenium and low vitamin E levels seems to be highly predictive of increased risk, especially for gastrointestinal cancers.54 Countries with high selenium levels in the soil, such as Venezuela, have much lower colon carcinoma rates than do those with lower selenium levels in the soil, such as the U.S. Overall, there is mounting evidence that selenium deficiency may predispose to the development of cancer.
Unfortunately, diets that protect against some cancers are associated with an increase in prevalence of cancers at other sites. For example, cereal cultures, such as those of Japan and Southeast Asia, have a high prevalence of stomach and esophageal cancer, whereas the incidence of breast, colon, and prostate cancers is decreased. Meat-eating cultures, such as the U.S., show exactly the opposite cancer pattern. Table 3.1 summarizes some of the known dietary influences on cancer.
3.1.6 EXERCISE
There is mounting evidence that moderate exercise can prolong the life span.55 Exercise is associated with salutary effects on the cardiovascular system, bone, and muscle. The strengthening of muscle and bone may decrease the incidence of hip fracture. In addition, evidence in both animal56 and human57 studies suggests that
exercise is associated with a decrease in cancer. Recent studies have shown that exercise produces an acute increase in nature killer (NK) cell activity, most probably secondary to the release of beta-endorphin from the pituitary gland.58 NK cells are responsible for scavenging circulating tumor cells. Thus, there is now a biochemical basis for the cancer-protective effect of moderate exercise.
Overall, it would seem that mild to moderate exercise can produce myriad ben-eficial effects when introduced at almost any age. This includes decreased brain atrophy, improved memory, and decreased depression. In older individuals, the exer-cise program should be tailored to the individual’s capacity. All exerexer-cise programs should consist of endurance, resistance, balance, flexibility, and posture elements.
3.1.7 LIFE EXTENSION
Since Ponce de Leon set out from Puerto Rico in search of the fountain of youth, only to discover Florida instead (in view of the senior migration to Florida, he might be considered to have been at least partially successful in his quest), many humans have craved a magic potion that would prolong their life span. Books and magazines on life extension have proved to be particularly successful with the lay public.
Although clearly this author joins with Fries59 in feeling that we should spend more time searching for ways to compress morbidity, it is nevertheless appropriate to review briefly dietary studies on life extension.
Numerous animal studies in many species from Drosophila to rodents have demonstrated that dietary restriction leads to a prolongation of life span.60 Dietary restriction seems to be most effective when calories are restricted by approximately 25%. However, dietary restriction is not capable of extending life in rotifers.61 No single macronutrient appears to be specifically responsible for the life span extension.
The mechanism by which mild caloric deprivation enhances life span is uncertain, with theories ranging from a reduction in free radical generation or tissue glycation to a delay in thymic involution. There is relatively strong support for the growth TABLE 3.1
Potential Dietary Influences on Cancer
Cancer Effects of Nutrients
Lung Decreased prevalence with increased beta-carotene, vitamin A, carrots, and green leafy vegetable intake
Esophageal Increased rates with high bread or bracken from consumption
Stomach Increased risk with dried salty fish consumption; decreased risk with vegetable and fruit consumption
Pancreas Increased risk with butter, fried and grilled meal; decreased risk with raw fruits, vegetables, and vitamin C
Colon Increased risk with pasta, rice, and cereals; decreased risk with vegetables, fiber, selenium, and vitamin C
Hypopharyngeal skin cancers
Increased risk with iron deficiency; decreased risk with selenium consumption
hormone/insulin-like growth factor 1 (IGF-1) hypothesis. Caloric restriction appears to work by increasing the silent information regulator 2 (SIR2) or its mammalian ortholog (Sirt).62 SIR2 is an NAD-dependent deacetylase. Besides altering histone deacetylation, Sirt also suppresses p53 and Foxo medicated apoptons and inactivates the proapoptotic factor, BAX. Sirt1 also decreases insulin, growth hormone/IGF-1, and leptin and increases adiponectin. It should be realized that such studies as these can be interpreted as demonstrating that overnutrition is not good for an animal, rather than demonstrating an effect of undernutrition per se. There is an attempt to develop caloric restriction mimetics, such as 2-dioxyglucose, to produce the bene-ficial effects of caloric restriction.63
Attempts to prove that the spartan existence increases life span led to searches for long-lived human populations. Three such populations were putatively identi-fied—the Georgians in Russia, the Afghans in the Khyber Pass, and the people of Villacabamba in Ecuador. After much excitement concerning the ability of these individuals to live high-quality lives on a frugal diet, it rapidly becomes obvious that the great ages attained by these individuals were more closely linked to their inability to count correctly, rather than to their dietary and exercise habits. The longest-documented human life span is 122 years in a French woman. The most long lived population in the U.S. is in Hawaii, hardly a group of people who follow a spartan nutritional existence. Caloric restriction in rhesus monkeys lowers body temperature and energy expenditure, but also causes an increased loss of bone from the hip.64–66 Attempts at caloric restriction in humans show a decrease in body temperature, oxidative stress, cholesterol, triglycerides, fasting glucose and insulin, c-reactive protein, and carotid artery intema media thickness.67–69
One theory of aging proposes that the generation of free radicals causes tissue damage and ultimately death. If this is true, then one would expect that intake of
One theory of aging proposes that the generation of free radicals causes tissue damage and ultimately death. If this is true, then one would expect that intake of