abnormality. Many older people fail to make the
reference values for vitamin D, but the synthesis of
vitamin D
3
(cholecalciferol) by the action of sunlight
(UVL with a wavelength of 290–310 nnm) on the skin
contributes some two-thirds of the vitamin D stores.
Standard household glass prevents the passage of any
therapeutic wavelength of UVL, and housebound and
institutionalized patients are particularly susceptible
to vitamin D deficiency. Subtle degrees of vitamin D
deficiency lead to secondary hypoparathyroidism, in-
creased bone turnover and osteoporotic fractures.
Common dietary sources of vitamin D include eggs,
cheese, margarine (fortified with vitamins D and A),
and oily fish. Randomized controlled trials of dietary
supplementation with 17.5 mg (700 IU) and 20 mg
(800 IU) of vitamin D and 500 mg of calcium per
day show a reduced incidence of hip and other
nonvertebral fractures, whereas 10 mg (400 IU) of
vitamin D does not reduce the fracture rate. There is
considerable evidence for using vitamin D and cal-
cium supplements in the vulnerable elderly, provided
overdosage is avoided. Exposure to sunlight, even
diffuse sunlight, is also to be encouraged.
0011 Water-soluble vitamin C is readily destroyed during
food preparation and storage, and the COMA recom-
mendation of 40 mg does not take this into account.
The delay between preparation and delivery to the
patient in hospital or nursing home or of meals on
wheels to the person at home is often sufficient
to substantially reduce the vitamin C content. Meals
on wheels are reported to have lost some 90% of the
vitamin C content by the time of delivery. Older
people eat vegetables more regularly than young
adults, but elderly men who live alone have diets
poor in vitamin C-rich foods such as fresh green vege-
tables and fruit. Scurvy is uncommon, but chronic
mild deficiency is not infrequent and may play a role
in atherogenesis and stroke. The inverse correlation
between plasma fibrinogen concentration and serum
ascorbate levels suggests that vitamin C supplemen-
tation may be cardioprotective.
0012 Vitamin A intake is very variable, but needs tend to
decrease with age, as absorption may be increased,
whilst plasma clearance is delayed. However, it is
often difficult to be certain whether homeostasis is
achieved, or whether subclinical vitamin A states are
common and unrecognized. Failure of dark adapta-
tion is a well-recognized vitamin A deficiency phe-
nomenon, but dryness of the eyes and perifollicular
hyperkeratosis are uncommon deficiency manifest-
ations in the Western World. In some third world
countries, vitamin A deficiency is the commonest
cause of blindness. The potential benefit of the anti-
oxidant properties of vitamin A and the closely related
b-carotene have yet to be established.
0013Thiamin (vitamin B
1
) intake is closely related to
energy consumption. Older people generally eat
breakfast (‘something to eat within 2 hours of rising’),
and this commonly includes cereals and fortified
cereals containing adequate thiamin. If disease or
institutionalization impairs energy consumption,
thiamin intake may be deficient. Alcoholism may
give rise to confabulation and short-term memory
impairment (Korsakoff’s psychosis) due to associated
thiamine deficiency or, more rarely, Wernicke’s
encephalopathy – acute confusion, ataxia, and
opthalmoplegia. Acute postoperative delirium is not
improved by large parenteral doses of the vitamin B
group of vitamins. Any associated low plasma thia-
mine concentration may be an epiphenomenon.
0014Pyridoxine (vitamin B
6
) and folate are important
cofactors for the metabolism of homocysteine, and
both vitamins independently lower raised homocys-
teine levels, thought to play a key role in atherogen-
esis. The Nurse Health Study found that a long-term
intake of 3 mg of vitamin B
6
and/or at least 400 mgof
folate per day have a favorable impact on CHD. In
the Framingham Study, 20% of elderly subjects had
folate and vitamin B
6
levels below the recommended
intake.
0015Folic acid in its conjugated form (predominantly
polyglutamate) is present in a wide variety of food,
especially green leafy vegetables, kidney, and liver.
Hydrolysis of the polyglutamate to monoglutamates
is necessary for absorption in the small intestine.
Folate deficiency may be due to several causes, with
inadequate intake the most common, often aggra-
vated by prolonged cooking, which destroys the
vitamin. Disease that impairs absorption (e.g., gluten
enteropathy or ileal resection) or increases metabolic
demand (e.g., vitamin B
12
deficiency, the leukemias,
myelofibrosis, hemolytic anemia, sideroblastic ane-
mia) may result in deficiency. A number of drugs (e.g.,
trimethoprim, methotrexate, triamterene) inhibit con-
version of folate to tetrahydrofolate, which is the main
storage and metabolically active form of the vitamin.
The anticonvulsants, phenytoin, primidone, and
phenobarbitone, and the antibiotic, nitrofurantoin,
may also result in folate deficiency, but the underlying
mechanism has not been firmly established. Defective
DNA synthesis through the purine and pyrimidine
pathways following chronic dietary folic acid defi-
ciency or drug-induced activity gives rise to a megalo-
blastic anemia. Provided that vitamin B
12
deficiency is
not present, treatment with as little as 200 mg daily of
oral folic acid is rapidly effective. In practice, pharma-
cological doses of 1–5 mg daily are used. Folinic acid
(Leukovorin), a form of tetrahydrofolate, is preferable
if the deficiency is due to folate antagonist drugs. The
COMA recommendation of 200 mg per day isadequate
2030 ELDERLY/Nutritional Management of Geriatric Patients