Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 346

An inadequate supply of vitamin B2, vitamin B6, folate, and/or vitamin B12 can cause hyperhomocysteinemia. Homocysteine is a sulfur‐containing amino acid considered an independent risk factor for cardiovascular diseases. Prospective studies also suggest a correlation between elevated homocysteine and dementia and osteoporotic fractures. Supplementation with folate and less so with cobalamin or pyridoxine demonstrated a reduction in serum homocysteine. Homocysteine‐lowering B vitamins have been mostly unsuccessful in reducing the incidence of CVD, osteoporosis, and AD progression.⁴⁷

Vitamin B2 contributes to hyperhomocysteinemia but is generally not considered a high‐risk nutrient in elderly people consuming sufficient dairy products. Vitamin B2 is high in nuts, almonds, whey, blueberries, feta cheese, and corn flour.

Vitamin B6 comprises various derivatives of pyridine, including pyridoxine, pyridoxal, and pyridoxamine. There are many dietary sources, and therefore dietary deficiency is rare. Vitamin B6 deficiency usually occurs in association with other water‐soluble vitamins. Deficiency may result from alcoholism, malabsorption, and other factors such as dialysis. Medication may act as a pyridoxine antagonist. Plasma pyridoxal‐5 phosphate is used to assess vitamin B6 status.

Folate represents a group of related pterion compounds; more than 35 forms of the vitamin are found naturally. In addition to plant sources, the various dietary sources include liver and other organ meats. Folate is sensitive to degradation by excessive heat from cooking.³⁰ Causal factors in addition to poor intake and absorption are atrophic gastritis, excessive alcohol intake, smoking, and use of some drugs.

Vitamin B12 is a group of cobalamin compounds with a corrin ring and a cobalt atom in the centre. Vitamin B12 is available only from animal foods. In the SENECA study, ~25% of the participants had a low vitamin B12 status: in some, 25% plasma cobalamin levels were <260 pmol l⁻¹ and plasma methylmalonic acid (MMA) >0.32 μmol l⁻¹.⁷ These levels could be only partly explained by insufficient dietary intake or atrophic gastritis. Pernicious anaemia, terminal ileal resection, bacterial overgrowth, and use of specific drugs are other possible causes of a deficiency state.

Vitamin C (ascorbic acid) is an essential water‐soluble vitamin widely found in fruits and vegetables. Unfortunately, this vitamin is readily lost from foods during storage and preparation. Such losses may account for about 50% of the potential vitamin content in the total diet. For Dutch and Danish diets, such vitamin C losses amounted to ~45% of the diet’s vitamin C content; consequently, ~30% of the subjects had too‐low intake.³¹ The absorption of the vitamin seems not to be affected by age. Low vitamin C levels have been associated with, in addition to classical deficiency signs, increased risk of coronary artery disease and senile cataract. The mechanism behind it is most likely the antioxidant properties of vitamin C. The brain has a remarkable demand for vitamin C: cerebral spinal fluid (CSF) levels are three to four times higher than that seen in plasma. This concentration gradient is maintained even though humans are completely dependent on the diet for vitamin C. Vitamin C is transported into the brain from blood by the sodium‐dependent vitamin C transporter at the choroid plexus. The higher CSF‐to‐plasma ratio of vitamin C is associated with slower cognitive decline in AD; however, breakdown of the blood‐brain barrier may cripple the brain’s ability to sustain high vitamin C concentration, a phenomenon associated with AD decline.^48–50

Vitamin A is a family of molecules containing different functional groups on a cyclohexenyl group and includes retinol, retinal, retinoic acid, and retinyl ester. Dietary sources are mainly retinyl esters provided by animal‐derived foods. Plant foods supply vitamin A as carotenoids such as β‐carotene, α‐carotene, and β‐cryptoxanthin. Vitamin A is of worldwide concern as a risk nutrient but has not been observed as a specific problem for elderly people, probably due to lower requirements in old age.³² An exception might be the observations of very low intakes in some ethnic groups in Asia.⁸

Vitamin D (calciferol) is a group of lipid‐soluble compounds with a four‐ringed cholesterol backbone. Vitamin D can be synthesized through adequate sunlight exposure to the skin. In most cultures, about one‐third of the vitamin D requirements can be obtained from a diet of fish, meat, and milk fat; the remainder has to be synthesized. Due to limited sunlight exposure and a fourfold reduced capacity of the skin to produce vitamin D, deficiencies occur, especially in homebound elderly people. Nevertheless, in the relatively healthy older European participants of the SENECA study, 40% had serum hydroxyvitamin D levels below 30 nmol l⁻¹,⁷ and this latter standard is below the currently proposed level of at least 50 nmol l⁻¹.³³ Vitamin D supplementation results in decreased bone loss and fracture rate in both older men and women. More recent trials also indicate an improvement of sarcopenia and a decrease in falls.