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Neil C. Binkley

Neil C. Binkley, M.D.

Assistant Professor
Department of Medicine & Primate Research Center
Rm 2245 Medical Science Center
608-262-0788
nbinkley@wisc.edu

Emphasis Group:
Human Nutrition

Principal Research Interest:
Vitamin K Insufficiency and Osteoporosis

Research Summary:
Osteoporosis is a common disease in which the bones become weak such that fractures occur with normal activities. It is a multifactorial illness caused by calcium and vitamin D inadequacy, inactivity, estrogen deficiency, and a multitude of other factors including advancing age. We are currently evaluating the possibility that unappreciated vitamin K inadequacy may contribute to what is currently accepted as "age-related" bone loss.

A small body of literature suggests that vitamin K insufficiency becomes common with advancing age. Furthermore, functional vitamin K deficiency is produced by the widely prescribed anticoagulant, warfarin. It is well understood that vitamin K plays a critical role in blood coagulation, but less well appreciated that three vitamin K dependent proteins exist in bone. It is possible that these proteins function to regulate calcium balance. As such, a deficiency of vitamin K could cause dysfunction of these proteins and contribute to bone loss and subsequent fractures.

We are currently evaluating the frequency with which "subclinical" vitamin K insufficiency occurs in a normal population. In addition, in collaboration with Dr. J. Suttie, we are assessing the effect of dietary vitamin K insufficiency and vitamin K insufficiency induced by warfarin on bone mass accumulation and subsequent loss in rodents. We are also involved in human clinical trials and will soon begin, in collaboration with Dr. F. Scheuning, head of bone marrow transplantation, to evaluate the effect of bone marrow transplantation upon the skeleton. While organ transplantation and the agents required to prevent rejection lead to bone loss and fractures, this potential complication of bone marrow transplantation has received little evaluation. We will initially document changes in bone density and turnover and subsequently assess whether or not therapeutic agents prevent the anticipated bone loss.


Representative Publications

Przybelski N, Binkley N. (2007) A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function.  Archives of Biochemistry and Biophysics, 460:202-205.

Binkley N, Novotny R, Krueger D, Kawahara-Baccus T, Daida YG, Gemar D, Lensmeyer G, Hollis B, Drezner MK.  (2007) Low vitamin D status despite abundant sun exposure.  J Clin Endocrinol Metab, 92:2130-2135.

Binkley N, Krueger D, Engelke J, Suttie JW.  (2007) Long-term warfarin treatment does not alter skeletal status in male rhesus monkeys. J Bone Miner Res, 22:695-700.

Hollis BW, Wagner CL, Drezner MK, Binkley NC. (2007) Circulating vitamin D3 and 25-hydroxyvitamin D in humans:  An important tool to define adequate nutritional vitamin D status.  J Steroid Biochem Mol Biol, 103:631-634.

Binkley N.  Does low vitamin D status contribute to "age-related" morbidity? J Bone Miner Res, in press.