VitaSearch: The Experts Speak
Cardiovascular Disease and Vitamin D
Khanh Vinh Quoc Luong, M.D.
Vietnamese American Medical Research Foundation
14971 Brookhurst Street
Westminster, California 92683, USA
(714) 839-5898 / (714) 839-5989 (FAX)
lng2687765@aol.com

“Vitamin D and Cardiovascular Disease”
Curr Med Chem. 2006;13(20):2443-7. 45276 (1/2007)
Kirk Hamilton: Can you please share with us your educational background and current position?
Khanh Vinh Quoc Luong: I have my Medical Doctor degree from University of Kansas, School of Medicine at Kansas City, Kansas. I am a Scientific Fellow of the American College of Allergy, Asthma and Immunology, Fellow of the American College of Chest Physicians, Fellow of the American College of Physicians, Fellow of the American College of Endocrinology, Fellow of the American College of Nutrition, Fellow of the American Society of Nephrology, and member of the American Society for Bone and Mineral Research.
I have an appointment as a Clinical Associate Professor of Family Medicine at the University of Southern California, Keck School of Medicine, Los Angeles, California, and I am currently President of the Vietnamese American Medical Research Foundation, Westminster, California.
KH: What got you interested in studying the role of vitamin D and cardiovascular disease?
KQL: It has been noticed that the changing environment may cause diseases. There are many geographic and seasonal factors contributing to the development of both vitamin D deficiency and cardiovascular diseases (CVD).
KH: What is the hypothesized pathophysiology of how vitamin D might benefit cardio - vascular disease?
KQL: There was some evidence of a non-genomic action of vitamin D in cardiac muscle; 1,25-dihydroxyvitamin D3 (1,25OHD) involved in the activation of the 3’,5’-cyclic AMP pathway (Cell. Endocrinol. 1991, 82, 229), protein kinase A (J. Mol. Cell. Cardiol. 1998, 30, 225), protein kinase C (Cell Signal, 1994, 6, 531), β-adrenergic-sensitive signal transduction pathway (J. Mol. Cell. Cardiol, 1999, 31, 1095), and calcium channels (Mol. Cell. Endocrinol. 1991, 77, 67) that regulated calcium influx. 1,25OHD has been reported to down-regulate renin production in the kidney (J Clin Invest. 2002; 110:229-238), suggesting that 1,25OHD may have an influence on the blood pressure control.
KH: How do you assess for vitamin D? What is vitamin D deficiency, insufficiency and excess with regards to appropriate laboratory testing?
KQL: The typical biochemical features of vitamin D deficiency are hypocalcemia, hypophosphatemia, high level of alkaline phosphatase, and an increased plasma parathyroid hormone (PTH). Serum calcium and phosphorus values may occasionally be within the normal range in some cases. Indeed, the best way to assess for vitamin D status is measuring 25-hydroxyvitamin D3 (25OHD) serum levels. Many commercial laboratories have reported the lower limit of normal value for 25OHD to be between 10 and 15 ng/ml. There is no consensus on the ideal serum concentration of 25OHD. However, 25OHD levels needed to be at least 32.4 ng/ml to maximize intestinal calcium absorption (J Am Coll Nutr. 2003; 22:142-146). Excessive doses of vitamin D increased intestinal absorption of calcium, and lead to hypercalcemia and hypercalciuria.
KH: Who is at risk for vitamin D deficiency? What is the prevalence of vitamin D insufficien- -cy or deficiency?
KQL: The risk and prevalence of vitamin D deficiency increases significantly with age, season (especially winter time), latitude (away from the equator), and skin pigmentation.
KH: Would you define vitamin D’s role in cardiovascular disease prevention as minor or significant?
KQL: The relationship of vitamin D and cardiovascular diseases (CVD) has been discussed in the literature. Certainly, vitamin D has an important role in modulating CVD. However, further clinical trials for vitamin D in CVD are needed.
KH: Are there certain diseases related to cardiovascular disease that increase the risk to vitamin D insufficiency?
KQL: Diabetes mellitus has a high cardiovascular risk. The relationship between vitamin D and diabetes type 1 has been known previously. Baumgartl et al. (Diabetes Research, 1991; 16:145-148) reported that serum 25OHD levels measured at matched time points through -out the year are lower in patients with newly diagnosed type 1 diabetes compared to healthy controls. The high prevalence of hypovitaminosis D has been reported in female type 2 diabetics (Diabetes Care. 2001; 24:1496).
Sulimovivi and Roginsky (Acta Endocrinologica 1980; 93:346-350) examined the isolated microsomal liver in streptozotocin-induced diabetes in rachitic rats; they found that the conversion of vitamin D3 to 25OHD was significantly less than control animals.
KH: What is the significance of vitamin D receptors on the heart muscle?
KQL: In the cardiac myocyte, vitamin D enhances calcium transport across the plasma membrane by a mechanism resembling a receptor-mediated phenomenon (J Biol Chem. 1987; 262:2536). 1,25OHD through its receptor, vitamin D receptor (VDR), has important physiological effects, such as: calcium transport, cell growth, and differentiation. High-affinity receptors for 1,25OHD have been identified in both myocardial (J Mol Cell Cardiol. 1986; 18:67) and vascular smooth muscle (Calcif Tissue Int.1987; 41:112) cells, where 1,25OHD play a role in regulating proto-oncogene expression, cell growth, and mitogenesis (J Clin Invest. 1991; 87:1889 & Endocr Rev. 1989; 10:351).
KH: What role does genetics play with respect to vitamin D and cardiovascular disease?
KQL: Certain allelic variations in the vitamin D receptor may be of genetic risk for cardio -vascular disease. In a recent issue, Luong and Nguyen provided a summary of a genetic risk factor for both vitamin D deficiency and cardiovascular diseases (Current Medicinal Chemistry. 2006; 13:2443-2447).
KH: Is there an interplay between vitamin D and vitamin K and cardiovascular risk? Low levels of both are associated with cardiovascular disease and both play a role in bone (and calcium) metabolism which could effect calcification of the arteries?
KQL: Recent studies have suggested that concurrent use of menaquinone and vitamin D may substantially reduce bone loss. Adams and Pepping (Am J Health Syst Pharm. 2005; 62:1574-1581) reported that the phytonadione and menaquinone may be effective for prevention and treatment of osteoporosis and arterial calcification.
KH: How would you address the issue of vitamin D and cardiovascular disease risk? What would you like to see done with this topic for further clarification?
KQL: Further clinical trial would be needed.

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