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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.

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Taking a combination of vitamins B6 and B12 and folic acid appears to decrease the risk of age-related macular degeneration in women, according to a report in the February 23 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. Age-related macular degeneration (AMD) is a leading cause of vision loss in older Americans, according to background information in the article. Treatment options exist for those with severe cases of the disease, but the only known prevention method is to avoid smoking. Recent studies have drawn a connection between AMD and blood levels of homocysteine, an amino acid. High levels of homocysteine are associated with dysfunction of the blood vessel lining, whereas treatment with vitamin B6, vitamin B12 and folic acid appears to reduce homocysteine levels and may reverse this blood vessel dysfunction.

Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Chiu KC, Chu A, Go VL, Saad MF. Am J Clin Nutr. 2004 May;79(5):820-5. PMID: 15113720 Conclusions: The data show a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher risk of insulin resistance and the metabolic syndrome. Further studies are required to explore the underlying mechanisms.

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Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator. Pereira CV, Machado NG, Oliveira PJ. Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3. PMID: 18599498 doi: 10.1124/jpet.107.128017 The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study. Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs. In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.

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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

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

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