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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.

Vitamin K epoxide reductase complex and vascular calcification: is this the important link between vitamin K and the arterial vessel wall? Spronk HM. Circulation. 2006 Mar 28;113(12):1550-2. Review. PMID: 16567578

Xu YC, Leung SW, Yeung DK, Hu LH, Chen GH, Che CM, Man RY. Structure-activity relationships of flavonoids for vascular relaxation in porcine coronary artery. Phytochemistry. 2007 Mar 27; [Epub ahead of print] PMID: 17395220 [PubMed - as supplied by pu

Amsterdam, The Netherlands, May 26, 2009 - There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases

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.

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

Research has uncovered the fact that vitamin K also plays a crucial role in maintaining bone health. It was found that the amount of vitamin K required to halt bone absorption leading to osteoporosis requires much greater intakes than that required for blood clot regulation. Further, it appears that bone and vascular tissue (like coronary arteries) maintain a preference for a different form of vitamin K than that required for blood clotting regulation. Rather than vitamin K1 needed for clotting, vitamin K2 is the form preferred by bones and arteries (Schurgers LJ et al 2001). It appears that much of the information generated over the years for vitamin K focused on the K1 form, ignoring the K2 form necessary for bone and vascular health. Normal deposition of calcium occurs only in bone and in teeth. Abnormal deposition of calcium in the body occurs in three places: the inner lining of the arteries of the body (the intima) that causes atherosclerotic plaque; the muscle layer of arteries ("medial calcification"); and heart valves. K2 appears to be the form of vitamin K responsible for controlling these phenomena.

C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. The Lancet, Early Online Publication, 22 December 2009 doi:10.1016/S0140-6736(09)61717-7 Interpretation CRP concentration has continuous associations with the risk of coronary heart disease, ischaemic stroke, vascular mortality, and death from several cancers and lung disease that are each of broadly similar size. The relevance of CRP to such a range of disorders is unclear. Associations with ischaemic vascular disease depend considerably on conventional risk factors and other markers of inflammation.

"Study highlights: * Ginkgo biloba doesn't prevent cardiovascular death, heart attacks or strokes, and should not be recommended as a way to prevent them. * Further research should explore its potential benefit to people with peripheral vascular disease. DALLAS, Nov. 24, 2009 - Ginkgo biloba didn't prevent cardiovascular death or major events such as heart attack and stroke in people age 75 and older, but the herb may affect peripheral vascular disease, according to research reported in Circulation: Cardiovascular Quality and Outcomes, a journal of the American Heart Association. "Surprisingly, Ginkgo was associated with a reduction in peripheral artery disease, but the number of patients was small. The difference was statistically significant," said Lewis H. Kuller, M.D., Dr.P.H., first author of the study and distinguished university professor of public health and professor of epidemiology at the University of Pittsburgh. Gingko biloba contains a class of nutrients - flavonoids - found in fruits, vegetables, dark chocolate and red wine, which are believed to offer some protection against cardiovascular events. "

Silver Line Hospital provide expert Endocrinologist for the treatment of sexual dysfunction disorder. We offer related treatments like hormone therapy, psychological therapy and diagnosis blood tests, sensory testing, vascular assessment

Inhibitions of vascular endothelial growth factor expression and foam cell formation by EGb 761, a special extract of Ginkgo biloba, in oxidatively modified low-density lipoprotein-induced human THP-1 monocytes cells. Liu HJ, Wang XL, Zhang L, Qiu Y, Li TJ, Li R, Wu MC, Wei LX, Rui YC. Phytomedicine. 2009 Jan 7. [Epub ahead of print] PMID: 19135347

Conclusions In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events. \n\nRosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.\nRidker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Study Group.\nN Engl J Med. 2008 Nov 20;359(21):2195-207. Epub 2008 Nov 9.\nPMID: 18997196

Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Prior IA, Davidson F, Salmond CE, Czochanska Z. Am J Clin Nutr. 1981 Aug;34(8):1552-61. PMID: 7270479 Two populations of Polynesians living on atolls near the equator provide an opportunity to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. The habitual diets of the toll dwellers from both Pukapuka and Tokelau are high in saturated fat but low in dietary cholesterol and sucrose. Coconut is the chief source of energy for both groups. Tokelauans obtain a much higher percentage of energy from coconut than the Pukapukans, 63% compared with 34%, so their intake of saturated fat is higher. The serum cholesterol levels are 35 to 40 mg higher in Tokelauans than in Pukapukans. These major differences in serum cholesterol levels are considered to be due to the higher saturated fat intake of the Tokelauans. Analysis of a variety of food samples, and human fat biopsies show a high lauric (12:0) and myristic (14:0) content. Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations.

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.

This site was established to provide visitors with comprehensive information about benfotiamine, a synthetic derivative of thiamine (vitamin B-1) which shows promise in treating a number of neurological and vascular conditions. Benfotiamine also appears to have beneficial anti-aging qualities, protecting human cells from harmful metabolic end products. Benfotiamine is not just for diabetics. Any population suffering from conditions brought about by unknown or inadvertent thiamine deficiencies should respond well to benfotiamine. Benfotiamine is emerging as the most effective of the thiamine compounds.

A compound found in vegetables like broccoli, cabbage and cauliflower, may protect arteries from disease by boosting a natural defence mechanism, says a new study from the UK. Researchers from Imperial College London (ICL) report that sulforaphane, a compound most widely associated with broccoli, may activate a protein called Nrf2 in arteries, according to findings published in Arteriosclerosis Thrombosis and Vascular Biology. While the protein is normally protective, in areas of arteries that are susceptible to disease the London-based researchers found that Nrf2 is inactive.

Prostacyclin (or PGI2) is a member of the family of lipid molecules known as eicosanoids.\nAs a drug, it is also known as "epoprostenol".[1] The terms are sometimes used interchangeably Prostacyclin (PGI2) chiefly prevents formation of the platelet plug involved in primary hemostasis (a part of blood clot formation). It is also an effective vasodilator. Prostacyclin's interactions in contrast to thromboxane (TXA2), another eicosanoid, strongly suggest a mechanism of cardiovascular homeostasis between the two hormones in relation to vascular damage.

Artemisinin (pronounced /ɑːtə'misinən/) is a drug used to treat multi-drug resistant strains of falciparum malaria. The compound (a sesquiterpene lactone) is isolated from the plant Artemisia annua. Not all plants of this species contain artemisinin. Apparently it is only produced when the plant is subjected to certain conditions, most likely biotic or abiotic stress. It can be synthesized from artemisinic acid.[1] The drug is derived from a herb used in Chinese traditional medicine, though it is usually chemically modified and combined with other medications. Artemisinin is under early research and testing for treatment of cancer, primarily by researchers at the University of Washington.[7][8] Artemisinin has a peroxide lactone group in its structure. It is thought that when the peroxide comes into contact with high iron concentrations (common in cancerous cells), the molecule becomes unstable and releases reactive oxygen species. It has been shown to reduce angiogenesis and the expression of vascular endothelial growth factor in some tissue cultures.