Accumulating data suggest that vitamin K (K) insufficiency may contribute to osteoporosis development by causing by causing increased bone turnover. However, currently available data do not permit definitive conclusions to be drawn regarding a role of K in bone metabolism. Much of the evidence implicating K in bone health utilizes measurement of serum undercarboxylated osteocalcin (ucOC) as a sensitive indicator of K status. When ucOC elevation is used to define K inadequacy, insufficiency is extremely common. However, whether this """"""""insufficiency has skeletal relevance, or if elevated ucOC concentration is simply a surrogate for generalized inadequate nutrition, is unknown. To clarify the role of K insufficiency in skeletal health, we propose a 14 month, prospective, randomized, double-blind, placebo controlled trial of K1 supplementation in 226 postmenopausal women. We hypothesize that K1 supplementation reduces skeletal turnover. To test this hypothesis we will use a K1 dose (1000 mcg/day) that produces maximal reduction in serum ucOC. Our specific objective is to assess skeletal turnover by measuring serum osteocalcin, bone specific alkaline phosphatase, and N-telopeptides of type l collagen, as well as urinary pyridinoline and deoxypyridinoline. If K insufficiency causes high bone turnover, a known risk factor for low bone mass and osteoporotic fracture, the recommended K intake should be increased and K1 supplementation become part of standard preventative medical care.
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