Micronutrient Deficiency

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In older people at risk of nutritional compromise, micronutrient supplementation deserves special attention, in order to forestall the development of micro-nutrient deficiency (Table 6). The clinical features of established vitamin deficiency are well recognized. The first recourse in the management of micro-nutrient deficiencies should be the provision of a well-balanced diet. In the presence of a functioning gastrointestinal tract, an adequate diet containing the recommended daily allowance of each micronutrient effectively prevents and corrects deficiency states. However, the failure to consume the required amount of food may warrant the use of oral pharmacological micronutrient supplements. Vitamin B12 deficiency may be considered unique in this regard as, traditionally, replacement therapy has been administered parenterally. However, available evidence suggests that food-cobalamin deficiency may be the most common cause of vitamin B12 deficiency in older adults. In this condition cobalamin cannot be extracted from ingested food, although free coba-lamin is readily absorbed as absorptive function is normal and intrinsic factor is present in adequate quantities. Thus, in persons with vitamin B12 deficiency resulting from food-cobalamin deficiency, repletion may be adequately achieved by oral replacement therapy.

There is a rising trend toward dietary supplementation with pharmaceutical preparations containing large doses of vitamins and minerals, based on conclusions drawn from the results of several studies. Available evidence derived from human and animal studies indicates that antioxidant micronutrients, mainly vitamins A, C and E, may play a role in boosting immunity, preventing neoplastic disease, and preventing or retarding the progression of several degenerative diseases, such as atherosclerosis. Vitamins E and C have also been shown to reduce low-density lipoprotein (LDL) cholesterol levels and increase high-density lipoprotein (HDL) levels, in addition to lowering fasting plasma insulin levels and improving insulin efficiency. Epidemiological studies have suggested a protective role for antiox-idants such as vitamin C, vitamin E, ^-carotene, and glutathione in macular degeneration and cataracts. Nevertheless, evidence derived from other epidemio-logical studies suggests that antioxidants may lack significant benefit. Studies are ongoing in an attempt to resolve this controversy.

In older adults reduced cutaneous synthesis and enteric absorption of vitamin D increases the risk of vitamin D deficiency. Reduced renal responsiveness to parathormone is an added risk factor. At least 500IUday~1 of vitamin D are required to prevent significant osteoporosis in postmenopausal women. Institutionalized patients with reduced exposure to sunlight are at higher risk of vitamin D deficiency due to reduced cutaneous synthesis. The role of calcium supplementation in the prevention of osteoporosis is also well accepted. Additional evidence suggests that inadequate dietary calcium consumption may play a role in the genesis of colorectal cancer and hypertension.

Table 6 Vitamins: recommended daily allowances (RDAs) and clinical features of deficiency states

RDA

Deficiency states

Vitamin A

600-700 mg

Decreased immunity to infections, xerophthalmia, night blindness

Niacin

12-16 mg

Pellagra (dermatitis, dementia, diarrhea), glossitis, cheilosis

Pyridoxine

1.6-2 mg

Dermatitis, delirium, peripheral neuropathy, glossitis

Riboflavin

1.1-1.3mg

Glossitis, cheilosis, normochromic anemia

Thiamin

0.8-0.9 mg

Beriberi, Wernicke's encephalopathy, Korsakoff's psychosis

Cyanocobalamin

5 mg

Megaloblastic anemia, optic atrophy, peripheral neuropathy, subacute combined degeneration of the cord, dementia

Ascorbic acid

40 mg

Hyperkeratosis, petechial hemorrhages, mucosal bleeding, lethargy

Vitamin D

10 mg

Osteomalacia, osteoporosis

Vitamin E

8-10 mg

Peripheral neuropathy, ataxia, hemolytic anemia

Folate

200 mg

Megaloblastic anemia, cognitive dysfunction

Vitamin K

65-80 mg

Spontaneous hemorrhage, hypothrombinemia

NE, niacin equivalent; RE, retinal equivalent.

NE, niacin equivalent; RE, retinal equivalent.

Currently, the safety of large pharmacological doses of micronutrient supplements in humans remains to be established. In spite of this, a considerable proportion of the older population consumes large doses of these supplements as a primary preventive health measure. The risk of long-term supplementation with high doses of micronutrients, particularly in the presence of age-related changes, cannot be ignored, and few studies have addressed this issue specifically. Due caution must be exercised, even with the use of micronutrients such as vitamin D and calcium where clinical benefits have been clearly established. The complications of over-enthusiastic calcium and vitamin D supplementation include hypercalcemia, nephrocalcinosis, milk-alkali syndrome, ectopic calcification, and rebound gastric acidity. Calcium supplementation may also chelate iron compounds and precipitate iron deficiency. With regard to vitamin A, available data have identified an increase in absorption and reduced peripheral clearance of this vitamin in older adults, therapy increasing the risk of vitamin A toxicity. Similarly, older persons on long-term iron therapy, particularly in the absence of proven iron deficiency, are at increased risk for the development of secondary hemochromatosis.

On the basis of existing evidence, the use of pharmacological doses of vitamin and mineral supplements is probably best restricted to low-potency supplements and reserved for persons with established micronutrient deficiency who are unable to eat an adequate diet. Close monitoring of such patients for adverse effects is mandatory.

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