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Effect of vitamin D deficiency and replacement on endothelial function in asymptomatic subjects. Tarcin O, Yavuz DG, Ozben B, Telli A, Velioglu Ogunc A, Yuksel M, Toprak A, Yazici D, Sancak S, Deyneli O, Akalin S. J Clin Endocrinol Metab. 2009 Jul 7. [Epub ahead of print] PMID: 19584181 doi:10.1210/jc.2008-1212 Conclusions: This study shows that 25(OH)D deficiency is associated with endothelial dysfunction and increased lipid peroxidation. Replacement of vitamin D has favorable effects on endothelial function. Vitamin D deficiency can be seen as an independent risk factor of atherosclerosis. Hypovitaminosis D associated endothelial dysfunction may predispose to higher cardiovascular disease in the winter.

Endothelial-Vasoprotective Effects of High-Density Lipoprotein Are Impaired in Patients With Type 2 Diabetes Mellitus but Are Improved After Extended-Release Niacin Therapy. Sorrentino SA, Besler C, Rohrer L, Meyer M, Heinrich K, Bahlmann FH, Mueller M, Horváth T, Doerries C, Heinemann M, Flemmer S, Markowski A, Manes C, Bahr MJ, Haller H, von Eckardstein A, Drexler H, Landmesser U. Circulation. 2009 Dec 21. [Epub ahead of print] PMID: 20026785 doi: 10.1161/CIRCULATIONAHA.108.836346 Conclusions-HDL from patients with type 2 diabetes mellitus and metabolic syndrome has substantially impaired endothelial-protective effects compared with HDL from healthy subjects. ER niacin therapy not only increases HDL plasma levels but markedly improves endothelial-protective functions of HDL in these patients, which is potentially more important.

Conjugated linoleic acid impairs endothelial function. Taylor JS, Williams SR, Rhys R, James P, Frenneaux MP. Arterioscler Thromb Vasc Biol. 2006 Feb;26(2):307-12. Epub 2005 Dec 8. PMID: 16339498 CONCLUSIONS: A CLA isomeric mixture had at most modest effects on adiposity and worsened endothelial function. On the basis of these results, the use of the isomeric mixture of CLA as an aid to weight loss cannot be recommended

Egg consumption and endothelial function: a randomized controlled crossover trial. Katz DL, Evans MA, Nawaz H, Njike VY, Chan W, Comerford BP, Hoxley ML. Int J Cardiol. 2005 Mar 10;99(1):65-70. PMID: 15721501 Conclusion: Short-term egg consumption does not adversely affect endothelial function in healthy adults, supporting the view that dietary cholesterol may be less detrimental to cardiovascular health than previously thought

The two faces of endothelial nitric oxide synthase in the pathophysiology of atherosclerosis. Kawashima S. Endothelium. 2004 Mar-Apr;11(2):99-107. Review. PMID: 15370069 DOI: 10.1080/10623320490482637

"Quality of HDL differs in diabetics but improves with niacin therapy December 22, 2009 | Michael O'Riordan Hannover, Germany - A small study published this week hints that the effects of HDL cholesterol differ in healthy patients from those with diabetes mellitus [1]. HDL cholesterol in individuals with diabetes has impaired endothelial protective functions compared with the HDL from healthy subjects, although treatment with extended-release niacin can improve these endothelial protective effects, according to researchers. Publishing their findings online December 21, 2009 in Circulation, lead investigator Dr Sajoscha Sorrentino (Hannover Medical School, Germany) and colleagues write that because recent HDL-raising intervention studies have yielded mixed results, "circulating HDL-cholesterol levels alone likely do not represent an adequate measure of therapeutic efficacy, and indexes of HDL functionality are urgently needed for assessment of the potential of HDL-targeted therapies to exert vasoprotective effects." Speaking with heartwire, senior investigator Dr Ulf Landmesser (University of Zürich, Switzerland), said the results have implications for clinical research. "We have to understand that we can't look only at the HDL levels in the plasma, but we need to look at the quality," he said. "The quality of the HDL is not the same in different patients. This is very important for targeting HDL as a treatment. Second, niacin therapy is a promising way not only to raise HDL but also to improve the quality; it is a good treatment option, especially if the larger outcomes data are positive.""

The effect of omega-3 FAs on tumour angiogenesis and their therapeutic potential. Spencer L, Mann C, Metcalfe M, Webb M, Pollard C, Spencer D, Berry D, Steward W, Dennison A. Eur J Cancer. 2009 Aug;45(12):2077-86. Epub 2009 Jun 1. Review. PMID: 19493674 Omega-3 fatty acid (omega-3 FA) consumption has long been associated with a lower incidence of colon, breast and prostate cancers in many human populations. Human trials have demonstrated omega-3 FA to have profound anti-inflammatory effects in those with cancer. In vitro and small animal studies have yielded a strong body of evidence establishing omega-3 FA as having anti-inflammatory, anti-apoptotic, anti-proliferative and anti-angiogenic effects. This review explores the evidence and the mechanisms by which omega-3 FA may act as angiogenesis inhibitors and identifies opportunities for original research trialling omega-3 FAs as anti-cancer agents in humans. The conclusions drawn from this review suggest that omega-3 FAs in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found principally in oily fish have potent anti-angiogenic effects inhibiting production of many important angiogenic mediators namely; Vascular Endothelial Growth Factor (VEGF), Platelet-Derived Growth Factor (PDGF), Platelet-Derived Endothelial Cell Growth Factor (PDECGF), cyclo-oxygenase 2 (COX-2), prostaglandin-E2 (PGE2), nitric oxide, Nuclear Factor Kappa Beta (NFKB), matrix metalloproteinases and beta-catenin

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

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.

Inositols prevent and reverse endothelial dysfunction in diabetic rat and rabbit vasculature metabolically and by scavenging superoxide. Nascimento NR, Lessa LM, Kerntopf MR, Sousa CM, Alves RS, Queiroz MG, Price J, Heimark DB, Larner J, Du X, Brownlee M, Gow A, Davis C, Fonteles MC. Proc Natl Acad Sci U S A. 2006 Jan 3;103(1):218-23. Epub 2005 Dec 22. PMID: 16373499 doi: 10.1073/pnas.0509779103

The postprandial effect of components of the Mediterranean diet on endothelial function. Vogel RA, Corretti MC, Plotnick GD. J Am Coll Cardiol. 2000 Nov 1;36(5):1455-60. PMID: 11079642

Aspirin-triggered lipoxin A4 blocks reactive oxygen species generation in endothelial cells: a novel antioxidative mechanism. Nascimento-Silva V, Arruda MA, Barja-Fidalgo C, Fierro IM. Thromb Haemost. 2007 Jan;97(1):88-98. PMID: 17200775 DOI: 10.1160/TH06-06-0315

Lipoxin A4: anti-inflammatory and anti-angiogenic impact on endothelial cells. Baker N, O'Meara SJ, Scannell M, Maderna P, Godson C. J Immunol. 2009 Mar 15;182(6):3819-26. PMID: 19265161 doi:10.4049/jimmunol.0803175

Z. Papoutsi, E. Kassi, I. Chinou, M. Halabalaki, L. A. Skaltsounis and P. Moutsatsou (2008). Walnut extract (Juglans regia L.) and its component ellagic acid exhibit anti-inflammatory activity in human aorta endothelial cells and osteoblastic activity in the cell line KS483. British Journal of Nutrition, 2008 Apr, 99 , pp 715-722 PMID: 17916277 doi:10.1017/S0007114507837421

Hypertension, endothelial dysfunction and cardiovascular risk] Nitenberg A. Arch Mal Coeur Vaiss. 2006 Oct;99(10):915-21. Review. French. PMID: 17100143

Oral administration of both tetrahydrobiopterin and L-arginine prevents endothelial dysfunction in rats with chronic renal failure. Yamamizu K, Shinozaki K, Ayajiki K, Gemba M, Okamura T. J Cardiovasc Pharmacol. 2007 Mar;49(3):131-9. PMID: 17414224 doi: 10.1097/FJC.0b013e31802f9923

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.