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Over acidity has been studied by many scientists as you will see here. You can help prevent the negative side effects by eating plenty of green foods and drinking green alkalizing drinks Excessive dietary intake of protein with consequent increase in metabolic acid production result in compensatory mechanisms that lead to progression of kidney stones, bone disease, renal disease and a catabolic state. Chronic metabolic acidosis is a process whereby an excess acid load is placed on the body due to excess acid generation or diminished acid removal by normal homeostatic mechanisms. Excessive meat ingestion and aging are two clinical conditions often associated with chronic metabolic acidosis. The body's homeostatic response to this pathology is very efficient. Therefore, the blood pH is frequently maintained within the "normal" range. However, these homeostatic responses engender pathologic consequences such as nephrolithiasis, bone demineralization, muscle protein breakdown and renal growth.

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.

Mechanisms underlying the biphasic effect of vitamin K1 (phylloquinone) on arterial blood pressure.\nTirapelli CR, Resstel LB, de Oliveira AM, Corrêa FM.\nJ Pharm Pharmacol. 2008 Jul;60(7):889-93.\nPMID: 18549675 \nDOI: 10.1211/jpp.60.7.0010\n

Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Pérez-Castrillón JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Dueñas A. Am J Cardiol. 2007 Apr 1;99(7):903-5. Epub 2007 Feb 8. PMID: 17398180 In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels. The mechanism by which atorvastatin increases vitamin D levels is related to inhibition of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. Cholesterol is synthesized from 7-dehydrocholesterol, which is also a precursor of vitamin D3. For this reason, we initially observed a statistically significant relation between total cholesterol and vitamin D. HMG-CoA enzyme reductase is key to the synthesis of cholesterol, whereas ultraviolet radiation causes the formation of 25-hydroxyvitamin D. Inhibition of the enzyme may increase levels of 7-dehydrocholesterol and increase the synthesis of 25-hydroxycholecalciferol, thereby increasing vitamin D levels,10 although we observed no relation between lower cholesterol and increased vitamin D. In addition, 25-hydroxyvitamin D has been shown to inhibit HMG-CoA enzyme reductase activity in in vitro studies.11 A greater concentration of vitamin D could increase enzymatic inhibition, acting in synergy with the statin in decreasing total cholesterol.

ScienceDaily (Aug. 25, 2009) - Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why. They have found that diabetics deficient in vitamin D can't process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.

Rapid appearance of resolvin precursors in inflammatory exudates: novel mechanisms in resolution. Kasuga K, Yang R, Porter TF, Agrawal N, Petasis NA, Irimia D, Toner M, Serhan CN. J Immunol. 2008 Dec 15;181(12):8677-87. PMID: 19050288

Resolvin D1, protectin D1, and related docosahexaenoic acid-derived products: Analysis via electrospray/low energy tandem mass spectrometry based on spectra and fragmentation mechanisms. Hong S, Lu Y, Yang R, Gotlinger KH, Petasis NA, Serhan CN. J Am Soc Mass Spectrom. 2007 Jan;18(1):128-44. Epub 2006 Oct 19. PMID: 17055291 doi:10.1016/j.jasms.2006.09.002    

Identification of endogenous resolvin E1 and other lipid mediators derived from eicosapentaenoic acid via electrospray low-energy tandem mass spectrometry: spectra and fragmentation mechanisms. Lu Y, Hong S, Yang R, Uddin J, Gotlinger KH, Petasis NA, Serhan CN. Rapid Commun Mass Spectrom. 2007;21(1):7-22. PMID: 17131464

Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Zhang H, Wei J, Xue R, Wu JD, Zhao W, Wang ZZ, Wang SK, Zhou ZX, Song DQ, Wang YM, Pan HN, Kong WJ, Jiang JD. Metabolism. 2009 Sep 3 doi:10.1016/j.metabol.2009.07.029 Liver function was improved greatly in these patients by showing reduction of liver enzymes. Our results confirmed the activity of BBR on InsR in humans and its relationship with the glucose-lowering effect. Together with our previous report, we strongly suggest BBR as an ideal medicine for T2DM with a mechanism different from metformin and rosiglitazone.

A recent study showed for the first time that refined carbohydrates can trigger food cravings many hours later, not through psychological mechanisms - a favourite food is just so tasty, you need to keep eating - but through biological effects on the brain. Read the full article.

"Cancer lies dormant in all of us," he wrote in his new book, "Anticancer: A New Way of Life" (Viking, $25.95). "But our bodies are also equipped with a number of mechanisms that detect and keep such (defective) cells in check." Cancer rears its ugly head when things get out of balance, Servan-Schreiber said in an interview. And that can happen if the bad guys that promote the growth of cancer cells (tobacco, excessive alcohol, excessive sugar, hydrogenated fats, environmental pollutants) outnumber the good guys that support our natural defenses (cancer-fighting phytochemicals found in fruits, vegetables, herbs and teas; physical activity; and stress management techniques). But conventional treatment, while indispensable, focuses on a single target: destroying cancer cells. Doctors rarely address the other side: teaching patients how to fortify themselves using nutrition, exercise and stress-management techniques to create an inhospitable environment for cancer.

Vitamin C and cancer revisited. Frei B, Lawson S. Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11037-8. Epub 2008 Aug 5. PMID: 18682554

ScienceDaily (Nov. 25, 2008) - Researchers at the University of Toronto, Faculty of Medicine, Toronto, Canada, have discovered that adiponectin, a protein secreted from adipocytes, is a metabolic link that can explain, in part, the known positive relationship between obesity and both bone mineral density and reduced susceptibility to fractures.

Use of vitamin D in clinical practice. Cannell JJ, Hollis BW. Altern Med Rev. 2008 Mar;13(1):6-20. PMID: 18377099 The recent discovery--from a meta-analysis of 18 randomized controlled trials--that supplemental cholecalciferol (vitamin D) significantly reduces all-cause mortality emphasizes the medical, ethical, and legal implications of promptly diagnosing and adequately treating vitamin D deficiency. Not only are such deficiencies common, and probably the rule, vitamin D deficiency is implicated in most of the diseases of civilization. Vitamin D's final metabolic product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone that targets more than 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. One of the most important genes vitamin D up-regulates is for cathelicidin, a naturally occurring broad-spectrum antibiotic. Natural vitamin D levels, those found in humans living in a sun-rich environment, are between 40-70 ng per ml, levels obtained by few modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to make the diagnosis and to assure treatment is adequate and safe. Three treatment modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B (UVB) radiation, and vitamin D3 supplementation. Treatment of vitamin D deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin D per day should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng per mL. In those with serious illnesses associated with vitamin D deficiency, such as cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other illnesses, doses should be sufficient to maintain year-round 25(OH)D levels between 55 -70 ng per mL. Vitamin D-deficient patients with serious illness should not only be supplemented more aggressively than the well, they should have more frequent monitoring of serum 25(OH)D and serum calcium. Vitamin D should always be

WEST LAFAYETTE, Ind. - Researchers have uncovered new evidence suggesting factors other than genes could cause obesity, finding that genetically identical cells store widely differing amounts of fat depending on subtle variations in how cells process insulin. Learning the precise mechanism responsible for fat storage in cells could lead to methods for controlling obesity. "Insights from our study also will be important for understanding the precise roles of insulin in obesity or Type II diabetes, and to the design of effective intervention strategies," said Ji-Xin Cheng, an assistant professor in Purdue University's Weldon School of Biomedical Engineering and Department of Chemistry. Findings indicate that the faster a cell processes insulin, the more fat it stores.

Floyd Chilton and colleagues wanted to examine whether theses fatty acids might have other effects, and developed a dietary intervention strategy in which 27 healthy humans were fed a controlled diet mimicking the w6/w3 ratios of early humans over 5 weeks. They then looked at the gene levels of immune signals and cytokines (protein immune messengers), that impact autoimmunity and allergy in blood cells and found that many key signaling genes that promote inflammation were markedly reduced compared to a normal diet, including a signaling gene for a protein called PI3K, a critical early step in autoimmune and allergic inflammation responses. This study demonstrates, for the first time in humans, that large changes in gene expression are likely an important mechanism by which these omega fatty acids exert their potent clinical effects