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Vitamin D is a hormone that is produced when sunlight is absorbed by the skin. Vitamin D insufficiency has been recognized as a problem in areas where sun exposure is limited, especially in the wintertime. In addition, the more pigmented the skin is, the less capable it is of utilizing sunlight to make vitamin D. Vitamin D plays an important role in helping the body absorb calcium and in building strong bones. It has also been shown to improve muscle function in the elderly. As we get older, our vitamin D levels in the blood go down and this may increase the risk for falls and fractures. If we can improve vitamin D status as we age, we may be able to improve muscle strength and decrease the risk of falls and fractures.
The long-term goal of this project is to develop strategies for the prevention of osteoporotic fractures in African Americans. Most intervention studies have excluded African Americans because of the erroneous belief that osteoporosis is not a major health problem in this population. In fact, the incidence rate of hip fracture in blacks is 50% of the rate in whites. Since longevity is increasing in the black population, osteoporotic fractures will become an even greater problem for this ethnic minority in the future. Furthermore, morbidity and mortality from osteoporotic fractures is greater in blacks. The elderly require higher intake of vitamin D to prevent bone loss resulting from secondary hyperparathyroidism. Calcium with sufficient vitamin D supplementation may decrease fractures in elderly white populations as a result of reduction in bone loss and falls (improved physical performance). The only fracture intervention study to include African Americans—the Women's Health Initiative—used an inadequate dose of vitamin D (400 IU), a dose unlikely to achieve the vitamin D status proposed by U.S. experts: serum 25 hydroxyvitamin D [25(OH)D] concentration above 75 nmol/L. No calcium/vitamin D intervention studies on fall prevention or physical performance have included African Americans.
As a result of increased skin pigmentation, blacks synthesize less vitamin D from sun exposure. As a result, serum 25(OH)D levels are often in the "insufficient" range. This is accompanied by secondary hyperparathyroidism, but adult blacks have a relative skeletal resistance to PTH, so that they have lower bone turnover. They also have more efficient renal conservation of calcium starting in childhood. Addition of vitamin D3 to a calcium-sufficient African American postmenopausal population does not prevent bone loss. The calcium/vitamin D requirements of black adults may be lower than white adults through midlife. However, the elderly require more vitamin D to produce the higher 25(OH)D levels required to overcome the hyperparathyroidism associated with aging. The skeleton of elderly African Americans appears to be susceptible to the increasing parathyroid hormone levels of old age. Bone loss accelerates and bone turnover markers increase in elderly African Americans just as in whites. The specific aims of this project are to determine if dietary supplementation with calcium/vitamin D will safely reduce bone loss and bone turnover and improve physical performance in elderly African Americans. We will enroll 250 African American women in a four-year vitamin D3 intervention trial where serum 25(OH)D will be maintained at an optimum level above 75 nmol/L. Adequate calcium intake will be ensured. Functional markers of vitamin D including bone density, serum PTH, and bone turnover will be measured. The NIH Conference on Vitamin D and Health in the 21st Century, September 5-6, 2007 concluded that research in this population is a high priority.
Allocation: Randomized, Control: Placebo Control, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Prevention
Vitamin D 3, placebo
Winthrop University Hospital
Not yet recruiting
Winthrop University Hospital
Published on BioPortfolio: 2014-08-27T03:12:32-0400
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A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.
A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.
A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)
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