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n-3 Fatty acids and cardiovascular disease: actions and molecular mechanisms. Torrejon C, Jung UJ, Deckelbaum RJ. Prostaglandins Leukot Essent Fatty Acids. 2007 Nov-Dec;77(5-6):319-26. Epub 2007 Dec 3. Review. Erratum in: Prostaglandins Leukot Essent Fatty Acids. 2008 Feb;78(2):157. PMID: 18060753 In conclusion, a growing body of evidence, encompassing human to cellular and molecular studies are defining the roles for n-3 FA as bioactive agents for reducing the risks of and treating CVD.

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

Vitamin D toxicity redefined: vitamin K and the molecular mechanism. Masterjohn C. Med Hypotheses. 2007;68(5):1026-34. Epub 2006 Dec 4. PMID: 17145139 doi:10.1016/j.mehy.2006.09.051

Yukihisa TANAKA, Takashi OHKUBO, Nobuo FUKUDA and Hidehiko HIBINO, "Effect of Molecular Forms on Distribution of Docosahexaenoic Acid into Organs in Mice", J. Oleo Sci., Vol. 52, 89-97 (2003) .

Medicinal mushroom modulators of molecular targets as cancer therapeutics. Zaidman BZ, Yassin M, Mahajna J, Wasser SP. Appl Microbiol Biotechnol. 2005 Jun;67(4):453-68. Epub 2005 Feb 23. Review. PMID: 15726350 DOI: 10.1007/s00253-004-1787-z

Vitamin D: the alternative hypothesis. Albert PJ, Proal AD, Marshall TG. Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12. Review. PMID: 19393200 Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.

In the field of molecular biology, the peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes.[1] PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism (carbohydrate, lipid, protein), and tumorigenesis[2] of higher organism.

A popular vitamin supplement is being advertised with claims that are demonstrably untrue, as revealed by research published in the open access journal BMC Pharmacology. Benfotiamine is a synthetic derivative of thiamine (vitamin B1). It is marketed heavily as a dietary supplement using a selection of unsubstantiated, 'not-quite-medical' claims that tend to characterize this field. A large part of this campaign has been built around the belief that benfotiamine is lipid-soluble and, therefore, more physiologically active. Scientific research led by Dr Lucien Bettendorff of the Center for Cellular and Molecular Neurobiology at the University of Liège, Belgium, has entirely disproved these claims.

"ScienceDaily (Nov. 30, 2009) - Universitat Autònoma de Barcelona (UAB) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps boost the production of the brain's stem cells -neurogenesis- and strengthens their differentiation in different types of neuron cells. The research revealed that mice fed an LMN diet, when compared to those fed a control diet, have more cell proliferation in the two areas of the brain where neurogenesis is produced, the olfactory bulb and the hippocampus, both of which are greatly damaged in patients with Alzheimer's disease. These results give support to the hypothesis that a diet made up of foods rich in these antioxidant substances could delay the onset of this disease or even slow down its evolution. The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology"

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

"Hi! This is Amy Proal. I wrote the article referenced at the start of the thread about vitamin D. Dr. Marshall is not concerned with vitamin D toxicity. Rather his molecular modeling research has clarified the actions of the two vitamin D metabolites 25-D and 1,25-D. The Vitamin D Receptor (VDR) is a fundamental receptor of the body - it controls the expression thousands of genes, as well as the activity of the innate immune system and the antimicrobial peptides. If you think of the VDR as a switch, 25-D (which is a corticosteroid) turns it off (inactivates it) and 1,25-D turn it on (activates it). What is commonly believed among vitamin D researchers is that if people supplement with extra vitamin D it will be converted into 1,25-D and activate the VDR. Unfortunately, Marshall's work revealed that the type of vitamin D derived from supplements and sun remains, for the most part, in it's precursor form 25-D. This means that the extra vitamin D we get from fortified food products and supplements is turning the VDR off, not on. That causes a decrease in immune function and gene transcription."

Metabolic effects of conjugated linoleic acid in humans: the Swedish experience. Riserus U, Smedman A, Basu S, Vessby B. Am J Clin Nutr. 2004 Jun;79(6 Suppl):1146S-1148S. PMID: 15159248 CONCLUSIONS CLA and specifically the isolated isomers are interesting model fatty acids for studies of the effects of (structural differences of) unsaturated fatty acids in humans. Today, there is no clear indication for human use of CLA concentrates. The possible importance of the small reduction of body fat after supplementation with the commercially available CLA products, without evidence of an associated improvement in the metabolic profile, has to be weighed against the apparent reduction of HDL cholesterol and an increased lipid peroxidation. The possible health consequences of prolonged treatment periods are at present unknown. Human supplementation with high doses of the trans-10,cis-12 CLA isomer should be avoided while awaiting further information on possible effects and side effects. However, it cannot be excluded that future studies could point to clinical applications, eg, as a result of antitumorigenic properties or as a tool to prevent weight gain. This possibility certainly requires more research to increase the understanding of the mechanisms behind the effects of CLA and specific CLA isomers on a molecular level. More controlled studies in defined populations are needed, as are controlled studies for comparisons of the effects of different and well-defined (mixtures of) isomers and human studies of longer duration to secure long-term effects and safety.

"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University. They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol. They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."

"In an article published in the December 29, 2005, issue of the journal Cell, the researchers report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production. Importantly, the scientists showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells. "We have discovered a mechanistic explanation for beta cell failure in response to a high-fat diet and obesity, a molecular trigger which begins the chain of events leading from hyperglycemia to insulin resistance and type 2 diabetes," said Jamey Marth, a Howard Hughes Medical Institute investigator at the University of California, San Diego (UCSD). Marth and first author Kazuaki Ohtsubo at UCSD collaborated on the studies with researchers from the Kirin Brewery Co. Ltd., and the University of Fukui, both in Japan."

The litchi benefits have been tried and proven in countries such as China and India and have also been well documented in ancient Chinese books. They contain many nutrients and vitamins that help to fight against various diseases as well as being a treatment for skin care, child growth and strengthening the body.
Tetra Pak Juice of Litchi fruit contains 66 calories per 100 g, comparable to that in the table-grapes. It has no saturated fats or cholesterol, but composes of good amounts of dietary fiber, vitamins, and antioxidants.
Oligonol is a low molecular weight polyphenol found abundantly in litchi fruit. Oligonol has several anti-oxidant and anti-influenza virus actions. It also helps to improve blood circulation, reduces weight and protects the skin from harmful UVA rays.
Litchi, like citrus fruits, is an excellent source of vitamin C; 100 g fresh fruits provide 71.5 mg or 119% of daily-recommended value. Studies suggest that consumption of fruits rich in vitamin C helps the human body develop resistance against infectious agents and scavenge harmful, pro-inflammatory free radicals.
Litchi is a very good source of B-complex vitamins such as thiamin, niacin, and folates. These vitamins are essential since they function by acting as co-factors to help the body metabolize carbohydrates, protein, and fats.
Litchi also carries a very good amount of minerals like potassium and copper. Potassium is an important component of cell and body fluids help control heart rate and blood pressure; thus, it offers protection against stroke and coronary heart diseases. Copper is required in the production of red blood cells.some Health Benefits Of Litchi are
Cancer, Heart Disease, Aids digestion, Maintains healthy bones, Vitamin C, Oligonol, Vitamin B, Weight loss, Improves skin conditions.

n vivo assessment of herb-drug interactions: possible utility of a pharmacogenetic approach? Tomlinson B, Hu M, Lee VW. Mol Nutr Food Res. 2008 Jul;52(7):799-809. Review. PMID: 18618477DOI: 10.1002/mnfr.200700454

Why "Vitamin D" is not a hormone, and not a synonym for 1,25-dihydroxy-vitamin D, its analogs or deltanoids. Vieth R. J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):571-3. PMID: 15225841 doi:10.1016/j.jsbmb.2004.03.037

An evaluation of the vitamin D3 content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D?\nLu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF.\nJ Steroid Biochem Mol Biol. 2007 Mar;103(3-5):642-4. Epub 2007 Jan 30.\nPMID: 17267210 \ndoi:10.1016/j.jsbmb.2006.12.010 \n