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Addition of milk prevents vascular protective effects of tea. Lorenz M, Jochmann N, von Krosigk A, Martus P, Baumann G, Stangl K, Stangl V. Eur Heart J. 2007 Jan;28(2):219-23. Epub 2007 Jan 9. PMID: 17213230 doi:10.1093/eurheartj/ehl442 In conclusion, milk may counteract the favourable health effects of tea on vascular function. The finding that the tea-induced improvement of vascular function in humans is completely attenuated after addition of milk may have broad implications on the mode of tea preparation and consumption. In addition, it indicates that caution is warranted in the design of studies involving nutritional flavonoids.

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one type of pathology is considered a likely predictor of the other. This potentially causal relationship has led to the hypothesis that these conditions share core mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part I of this review summarizes current research linking vitamin D deficiency to cardiovascular disease, the physiological mechanisms underlying vitamin D's cardiovascular effects, and leading vitamin D researchers' recommendations for significantly higher supplemental doses of the pro-hormone. Part II reviews the vitamin K connection to cardiovascular disease; the ways in which vitamin D and vitamin K pair up to prevent inflammation, vascular calcification and osteoporosis; and the necessity of providing vitamin K along with vitamin D to preclude adverse effects associated with hypervitaminosis D, which include vascular and other soft tissue calcification.

Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Mills NL, Törnqvist H, Robinson SD, Gonzalez M, Darnley K, MacNee W, Boon NA, Donaldson K, Blomberg A, Sandstrom T, Newby DE. Circulation. 2005 Dec 20;112(25):3930-6. PMID: 16365212 doi: 10.1161/CIRCULATIONAHA.105.588962

Zittermann A, Schleithoff SS, Koerfer R. \nVitamin D and vascular calcification.\nCurr Opin Lipidol. 2007 Feb;18(1):41-6. Review.\nPMID: 17218831 [PubMed - indexed for MEDLINE

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one is considered a likely predictor of the other. This relationship has led to the hypothesis that these conditions share core pathophysiological mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part II, The Vitamin K Connection to Cardiovascular Health, reviews the ways in which vitamin K regulates calcium utlization, preventing vascular and soft tissue calcification while complimenting the bone-building actions of vitamin D, and also discusses vitamin K safety and dosage issues, and the necessity of providing vitamin K and vitamin A along with vitamin D to preclude adverse effects associated with hypervitaminosis D.

Vitamin K has been known as the coagulation vitamin, because of its role in the blood-clotting process. However, research over the last few decades has shown that the role of K Vitamins - and natural Vitamin K2, the menaquinones, in particular - has been greatly expanded. Of note, K Vitamins activity outside the liver is required for calcium utilization, the key factor in maintaining both bone and cardiovascular health.\n\nVitamin K2 helps to activate vitamin K-dependent proteins responsible for healthy tissues. In bone, it activates osteocalcin, a protein required to bind calcium to the mineral matrix, thus strengthening the skeleton. In circulation, Vitamin K2 participates in carboxylation of Matrix Gla Protein (MGP), the most potent inhibitor of arterial calcification known, lowering the risk of vascular damage.

NEW YORK (Reuters Health) May 29 - Supplementation with coenzyme Q10 (CoQ10) improves endothelial dysfunction in patients with type 2 diabetes on statin therapy, according to results of a study reported in the May issue of Diabetes Care. The vascular benefits of statins might be attenuated by inhibition of CoQ10 synthesis, Dr. Gerald T. Chew and colleagues from University of Western Australia, Perth, note in their report.

High dietary menaquinone intake is associated with reduced coronary calcification.\nBeulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT.\nAtherosclerosis. 2008 Jul 19. [Epub ahead of print]\nPMID: 18722618 \ndoi:10.1016/j.atherosclerosis.2008.07.010 \n

Vitamin K in the treatment and prevention of osteoporosis and arterial calcification.\nAdams J, Pepping J.\nAm J Health Syst Pharm. 2005 Aug 1;62(15):1574-81. Review.\nPMID: 16030366

Vitamin K is a fat-soluble vitamin. The "K" is derived from the German word "koagulation." Coagulation refers to the process of blood clot formation. Vitamin K is essential for the functioning of several proteins involved in blood clotting (1). There are two naturally occurring forms of vitamin K