Group items tagged

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.

Giving saturated fat another chance. Saturated fat has long held a bad rep and been noted for its potential to contribute to cardiovascular disease. So you might understand why I was a bit skeptical of all the hype surrounding the supposedly miracle-working power of coconut oil, which is composed of saturated fatty acids. However, if there's one thing I have learned as a nutrition student, it is that research has the potential to change our views as we continue to expand our knowledge and make new discoveries. Coconut oil may prevent and alleviate disease. Both research and clinical studies have shown that MCFA may be useful in treating and preventing diseases such as diabetes, osteoporosis, virus-related dieases (mononucleosis, hepatitis C, herpes, etc.), gallbladder disease, Crohn's disease, and cancer. The smaller size of MCFA (compared to LCFA) allows them to be digested more easily, making them ideal for those suffering from digestive diseases. Coconut oil may assist in the absorption and retaining of calcium, thereby benefiting bones. Coconut oil has antimicrobial, antiviral, and antifungal properties. Lipid-coated bacteria and viruses contain a lipid coat which encloses their DNA among other cellular materials. When consumed by humans, coconut oil disrupts the lipid membrane, killing the pathogens without damaging the host or harming health-promoting intestinal bacteria. The antimicrobial properties stem from the monoglycerides and free fatty acids (mainly lauric acid and capric acid) that compose coconut oil.

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. Review. PMID: 19667164

"My goal is to gather the basic science and apply it to nutrition - NUTRIGENOMICS. What do I mean? How does what we eat signal our genes in the nucleus. By our food choices, we are sending different signals to our genes. High carbohydrate and high fructose intake signals it is summer time and winter is coming -- grow and store the energy (insulin). High fat, low carbohydrate diet with calorie restriction signals our genes that winter is here -- use the stored energy, repair the genes, and slow down growth (i.e. Sirt1/Foxo pathway). The Sirt1/FoxO1 pathway is important as it aids in repairing DNA. Damaged DNA can lead to uncontrolled cellular replication (i.e. cancers). The immune system (phagocytes) has a mechanism to remove old and unwanted cells called apoptosis (cellular death). "

"Summer vs Winter Mode: Explaining AMPK Last year I read an article which made a statement that has not left my mind. The statement went as follows: "You are only good as your mitochondria." In fact, the more a dwell into the details of human metabolism, the more I sense that this is true - especially with the metabolic syndrome. For those who are not familiar with the concept of mitochondria, they are the tiny energy factories within the cells that produce cellular energy through aerobic means (meaning oxygen). Mitochondria utilize oxygen to ultimately produce Adenosine Triphosphate or simply ATP. ATP relays energy by donating a phosphate bond resulting in Adenosine Diphosphate (ADP). Another phosphate release would entail Adenosine Monophosphate or AMP. ATP is one of the main sources of cellular energy in the body."

"Summer vs Winter Mode: Explaining AMPK Last year I read an article which made a statement that has not left my mind. The statement went as follows: "You are only good as your mitochondria." In fact, the more a dwell into the details of human metabolism, the more I sense that this is true - especially with the metabolic syndrome. For those who are not familiar with the concept of mitochondria, they are the tiny energy factories within the cells that produce cellular energy through aerobic means (meaning oxygen). Mitochondria utilize oxygen to ultimately produce Adenosine Triphosphate or simply ATP. ATP relays energy by donating a phosphate bond resulting in Adenosine Diphosphate (ADP). Another phosphate release would entail Adenosine Monophosphate or AMP. ATP is one of the main sources of cellular energy in the body

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. Review. PMID: 19667164

Age, stress, and poor nutrition can sap our immune system of its effectiveness. Influenza provides one example. During young adulthood, when the body can mount a robust immune response to this common virus, influenza is rarely fatal. Among the elderly, however, the virus is associated with significant rates of death and hospitalization (Nichol KL 2005). The impact of aging on the immune system is profound. As people age, a number of critical immune system components are reduced or slowed, including cellular response, response to vaccines, and antibody production. At the same time, susceptibilities to infection and cancer are increased. Some of this increased susceptibility to disease is linked to chronic inflammation, which is associated with many disorders of aging (Ershler WB et al 2000; Hamerman D 1999; Taaffe DR et al 2000).

PROYOUNG® GANO SPORE is 100% pure high potency Ganoderma Spore Powder which provides high antioxidants that helps to maintain an optimal immune system. The Ganoderma Spores are effcetive in maintaining healthy blood glucose levels and regulating cortisol levels.

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. PMID: 19667164

Did you know that cutting the florets into smaller pieces and the stems into thin slices and letting them sit for 5 to 6 minutes before cooking will enhance their cancer protective properties? Cutting broccoli into smaller pieces breaks the cells and activates an enzyme called myrosinase. The myrosinase converts some of the sulfur-containing chemicals found in broccoli (call glucosinolates) into other sulfur containing chemicals (called isothiocyanates) which research has shown to contain cancer preventive properties not found in the glucosinolates . Studies have actually pinpointed specific mechanisms, like changes in cellular genetic processes, which are involved in increasing cancer protection.

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.

Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations. Czernik M, Sroka J, Madeja Z, Czyz J. Cell Mol Biol Lett. 2008;13(3):327-38. Epub 2008 Feb 21. PMID: 18292973 DOI: 10.2478/s11658-008-0003-z This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

"5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.[1] It should not be confused with cyclic AMP-activated protein kinase (protein kinase A), which, although being of similar nature, may have opposite effects.[2]"

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.

"Coenzyme Q10 (also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ10 - pronounced like "ko-cue-ten" -, CoQ, Q10, or simply Q) is a 1,4-benzoquinone, where Q refers to the quinone chemical group, and 10 refers to the isoprenyl chemical subunits. This oil-soluble vitamin-like substance is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, generating energy in the form of ATP. Ninety-five percent of the human body's energy is generated this way.[1][2] Therefore, those o

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.

Coenzyme Q10. Bonakdar RA, Guarneri E. Am Fam Physician. 2005 Sep 15;72(6):1065-70. Review. PMID: 16190504 Coenzyme Q10 is a vitamin-like substance used in the treatment of a variety of disorders primarily related to suboptimal cellular energy metabolism and oxidative injury. Studies supporting the efficacy of coenzyme Q10 appear most promising for neurodegenerative disorders such as Parkinson's disease and certain encephalomyopathies for which coenzyme Q10 has gained orphan drug status. Results in other areas of research, including treatment of congestive heart failure and diabetes, appear to be contradictory or need further clarification before proceeding with recommendations. Coenzyme Q10 appears to be a safe supplement with minimal side effects and low drug interaction potential.

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 cognitive performance in adults: a systematic review. Annweiler C, Allali G, Allain P, Bridenbaugh S, Schott AM, Kressig RW, Beauchet O. Eur J Neurol. 2009 Oct;16(10):1083-9. Epub 2009 Jul 29. PMID: 19659751 DOI: 10.1111/j.1468-1331.2009.02755.x This systematic review shows that the association between serum 25OHD concentrations and cognitive performance is not yet clearly established. The inconclusive results of the reviewed studies could be due to methodology, types of the cognitive tasks used and/or the cellular mechanisms of vitamin D.