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B.S., University of Southwestern Louisiana, Lafayette, Louisiana
Ph.D., University of Wisconsin at Madison
My laboratory has been conducting studies on factors affecting vitamin D status and on effects of vitamin D supplementation on cardiovascular disease. The relationship between salt-sensitivity and the vitamin D endocrine system has been characterized using the Dahl salt-sensitive rat as a model. High salt intake in this rat model results in hypertension, hyperparathyroidism, and hypovitaminosis D. The hypovitaminosis D is caused in large part by loss of protein-bound vitamin D metabolites into urine. High dietary vitamin D (cholecalciferol) during high salt intake optimized vitamin D status, but did not attenuate the hypertension of salt-sensitive rats. We concluded that low salt intake may be necessary to both maintain optimal vitamin D status and prevent hypertension in salt-sensitive individuals (26% of the normotensive USA population, 51% of the hypertensive USA population, higher prevalence in the Africa-American population). Since black and white female adolescents also lost vitamin D metabolites and vitamin D binding protein (s) into urine, we have concluded that urinary loss of vitamin D metabolites may be one cause of low vitamin D status, in addition to low dietary intake and decreased skin synthesis. We are interested in collaborating in clinical studies to test whether urinary loss of vitamin D metabolites limits the ability of supplemental vitamin D to optimize vitamin D status.
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