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30 Day Reset Program References

NAD+ Gold® References https://www.quicksilverscientific.com/nadgoldreferences/

[1] Longo VD et al. Interventions to Slow Aging in Humans: Are We Ready? Aging Cell 14 (4): 497-510. View Abstract

[2] Fang EF et al. NAD (+) in aging: molecular mechanisms and translational implications. Trends Mol Med. 2017;23(10):899–916 View Abstract

[3] Wu, L et al. The elusive NMN transporter is found. Nat Metab 2019: 1; 8-9  View Full Paper

[4] Rajman L et al. Therapeutic potential of NAD-Boosting molecules: The in vivo evidence. Cell Metab. 2018 Mar 6;27(3):529-547. View Abstract

[5] Li W et al. NAD+ Content and Its Role in Mitochondria. Mitochondrial Regulation. 2014: 39–48 View Abstract

[6] Lee CF et al. Targeting NAD+ metabolism as interventions for mitochondrial disease. Sci Rep. 2019 Feb 28;9(1):3073. View Abstract

[7] Schultz MB et al. Why NAD+ Declines during Aging: It’s Destroyed. Cell Metab. 2016 June 14; 23(6): 965–966 View Full Paper

[8] Davila, A et al. Nicotinamide adenine dinucleotide is transported into mammalian mitochondria. Elife. 2018 Jun 12;7 View Full Paper

[9] Imai S. The NAD World 2.0: the importance of the inter-tissue communication mediated by NAMPT/NAD+/SIRT1 in mammalian aging and longevity control. NPJ Syst Biol Appl. 2016 Aug 18;2:16018 View Full Paper

[10] Massudi H et al. Age-associated changes in oxidative stress and NAD+ metabolism in human tissue PLoS One. 2012;7(7):e42357 View Abstract

[11] Zhu XH et al. In vivo NAD assay revels the intracellular NAD contents and redox state in healthy human brain and their age dependences. Proc. Natl. Acad. Sci. 2015; 112:2876–2881 View Full Paper

[12] Hershberger KA et al. Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases. Nat Rev Nephrol. 2017 Apr;13(4):213-225. View Full Paper

[13] Gross CJ et al. Digestion and absorption of NAD by the small intestine of the rat J Nutr. 1983 Feb;113(2):412-20. View Abstract

[14] Poljsak B. NAMPT-Mediated NAD biosynthesis as the internal timing mechanism: in NAD+ World, time Is running in its own way. Rejuvenation Res. 2018 Jun;21(3):210-224 View Abstract

[15] Tsubota, K. The first human clinical study for NMN has started in Japan. NPJ Aging Mech. Dis. 2016, 2, 16021 View Abstract

[16] Strait, JE. Scientists identify new fuel-delivery route for cells. Washington University School of Medicine. Available at: https://medicine.wustl.edu/news/scientists-identify-new-fuel-delivery-route-for-cells/ Accessed: 9-14-2019

[17] Mills KF et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metab. 2016: 24, 795–806. View Full Paper

[18] Anti-Aging compound in human clinical trial: will boosting NMN slow aging? Available at: https://hecmedia.org/posts/anti-aging-compound-in-human-clinical-trial-will-boosting-nmn-slow-aging-6/ Accessed 9-1-2019

[19] Guan Y et al. Nicotinamide Mononucleotide, an NAD+ precursor, rescues age-associated susceptibility to AKI in a sirtuin 1-dependent manner. J Am Soc Nephrol. 2017 Aug;28(8):2337-2352. View Full Paper

[20] Martin As et al. Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model.JCI Insight. 2017 Jul 20;2(14). View Full Paper

[21] Johnson S et al. NAD + biosynthesis, aging, and disease. F1000Res. 2018 Feb 1;7:132 View Full Paper

[22] Mills KF et al. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016; 24:795–806 View Full Paper

[23] Das A et al. Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging. Cell. 2018 Mar 22;173(1):74-89.e20 View Abstract

[24] Kathirvel E et al. Betaine improves nonalcoholic fatty liver and associated hepatic insulin resistance: a potential mechanism for hepatoprotection by betaine Am J Physiol Gastrointest Liver Physiol. 2010 Nov;299(5):G1068-77  View Full Paper

[25] Schmeisser K et al. Role of sirtuins in lifespan regulation is linked to methylation of nicotinamide. Nat Chem Biol. 2013;9(11):693–700. View Full Paper

[26] Bonkowski MS et al. Slowing ageing by design: the rise of NAD+ and sirtuin-activating compounds. Nat Rev Mol Cell Biol. 2016 November ; 17(11): 679–690 View Full Paper

[27] Kane AE et al. Sirtuins and NAD+ in the development and treatment of metabolic and cardiovascular disease. Circ Res. 2018 Sep 14;123(7):868-885. View Full Paper

[28] Sun WP et al. Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels. Clin Nutr, 2017. 36(4): p. 1136-1142 View Abstract

[29] Van der Meel R et al. Extracellular vesicles as drug delivery systems: lessons from the liposome field. J Control Release. 2014 Dec 10;195:72-85 View Abstract

[30] Yoshida M. Extracellular vesicle-contained eNAMPT delays aging and extends lifespan in mice. Cell Metab. 2019 Aug 6;30(2):329-342.e5 View Abstract

[31] Yoshino J et al. NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR. Cell Metab. 2018 Mar 6;27(3):513-528 View Full Paper

[32] Gaddipati R et al. Visceral adipose tissue visfatin in nonalcoholic fatty liver disease. Ann Hepatol. 2010;9(3):266–70. View Abstract

[33] Revollo JR et al. Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme. Cell Metab. 2007;6(5):363–75 View Full Paper

[34] Caton PW et al. Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated

[35] impairment of mouse islet function. Diabetologia. 2011;54(12):3083–92. View Abstract

[36] De Picciotto NE et al. Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice. Aging Cell 2016, 15, 522–530. View Full Paper

[37] Yoshino J et al. Nicotinamide mononucleotide, a key NAD (+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011;14(4):528–36 View Full Paper

[38] Uddin GM et al. Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice. Front. Pharmacol. 2016, 7, 258 View Full Paper

[39] Wei CC et al. Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway. Sci. Rep. 2017, 7, 717 View Full Paper

[40] Wang X et al. Nicotinamide mononucleotide protects against –amyloid oligomer-induced cognitive impairment and neuronal death. Brain Res. 2016, 1643, 1–9. View abstract

[41] Yao Z et al. Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease. Neurosci. Lett. 2017, 647, 133–140. View Abstract

[42] Hou Y et al. NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. Proc. Natl. Acad. Sci. USA 2018, 115, E1876–E1885 View Abstract

[43] Wei CC et al. NAD replenishment with nicotinamide mononucleotide protects blood-brain barrier integrity and attenuates delayed tissue plasminogen activator-induced haemorrhagic transformation after cerebral ischaemia. Br J Pharmacol. 2017 Nov;174(21):3823-3836 View Full Paper

[44] Gomes AP et al. Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell 2013; 155, 1624–1638.View Full Paper

[45] Stromsdorfer KL et al. NAMPT-Mediated NAD(+) biosynthesis in adipocytes regulates adipose tissue function and multi-organ insulin sensitivity in mice. Cell Rep. 2016 Aug 16;16(7):1851-60. View Abstract

[46] Camacho-Pereira J et al. CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab. 2016; 23:1127–1139 View Full Paper

[47] Lin JB et al. NAMPT-Mediated NAD(+) Biosynthesis Is Essential for Vision In Mice. Cell Rep. 2016; 17:69–85 View Full Paper

[48] Sheedfar F et al. Liver diseases and aging: friends or foes? Aging Cell. 2013 Dec;12(6):950-4 View Abstract

[49] Hamaguchi M. Aging is a risk factor of nonalcoholic fatty liver disease in premenopausal women.

[50] World J Gastroenterol. 2012 Jan 21;18(3):237-43 View Full Paper

[51] Day CR et al. Betaine chemistry, roles, and potential use in liver disease. Biochim Biophys Acta. 2016 Jun;1860(6):1098-106 View Abstract

[52] Zhao G et al. Betaine in inflammation: mechanistic aspects and applications.  Front Immunol. 2018 May 24;9:1070. View Full Paper

[53] Ueland PM et al. Betaine: a key modulator of one-carbon metabolism and homocysteine status.

[54] Clin Chem Lab Med. 2005;43(10):1069-75. View Abstract

[55] Craig SA. Betaine in human nutrition. Am J Clin Nutr. 2004 Sep;80(3):539-49. View Abstract


AMPK Charge+ References https://quicksilverscientific.com/ampkchargereferences 

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[2] Hardie DG, et al. Targeting an energy sensor to treat diabetes. Science. 2017; 357 (6350): 455-456.

[3] Foretz M and Viollet B. Activation of AMPK for a break in hepatic lipid accumulation and circulating cholesterol. EBio Medicine. 2018; 31: 15-16.  

[4] Tamargo-Gomez I, et al. AMPK: Regulation of metabolic dynamics in the context of autophagy. Int J Mol Sci. 2018; 19(12): 3812.

[5] Furman D, et al. Chronic inflammation in the etiology of disease across the life span. Nature Medicine. 2019; 25: 1822-1832.

[6] Jeon SM, et al. Regulation and function of AMPK in physiology and diseases. Exp Mol Med. 2016; 48: e245.

[7] Shirwany NA and Zou MH. AMPK in cardiovascular health and disease. Acta Pharmacol Sin. 2010; 31(9): 1075-1084.

[8] Ruderman NB, et al. AMPK, insulin resistance, and the metabolic syndrome. J Clin Investig. 2013.

[9] Seabright AP, et al. AMPK activation induces mitophagy and promotes mitochondrial fission while activating TBK1 in a PINK1-Parkin independent manner. FASEB J. 2020; 34(5): 6284-6301.

[10] Ruderman NB, et al. AMPK and SIRT1: a long-standing partnership? Am J Physiol Endocrinol Metab. 2010; 298(4): E751-E760.

[11] Pan H and Finkel T. Key proteins and pathways that regulate lifespan. J Biol Chem. 2017; 292(16): 6452-6460.

[12] Connell NJ, et al. NAD+ metabolism as a target for metabolic health: have we found the silver bullet? Diabetologia. 2019; 62(6): 888-899.

[13] Anton SD, et al. Flipping the metabolic switch: Understanding and applying health benefits of fasting. Obesity (Silver Spring).

[14] Fan W and Evans RM. Exercise mimetics: Impact on health and performance. Cell Metab. 2017; 25(2): 242-247.

[15] Dolinksy VW, et al. Improvements in skeletal muscle strength and cardiac function induced by resveratrol during exercise training contribute to enhanced exercise performance in rats. J Physiol. 2012; 590(Pt 11): 2783-2799.

[16] Konrad M and Nieman DC. Evaluation of quercetin as a countermeasure to exercise-induced physiological stress. antioxidants in sports nutrition. 2015.

[17] Kaeberlein M, et al. Substrate-specific activation of sirtuins by resveratrol. J Biol Chem. 2005; 280(17): 17038-17045.

[18] Park D, et al. Resveratrol induces autophagy by directly inhibiting mTOR through ATP competition. Sci Rep. 2016; 6: 21772.

[19] Grant R. Resveratrol increases intracellular NAD+ levels through the up-regulation of the NAD+ synthetic enzyme nicotinamide mononucleotide adenylyltransferase. Nature Precedings. 2010.

[20] Csiszar A, et al. Resveratrol induces mitochondrial biogenesis in endothelial cells. Am J Physiol Heart Circ Physiol.

[21] Sun H, et al. Berberine ameliorates blockade of autophagic flux in the liver by regulating cholesterol metabolism and inhibiting COX2-prostaglandin synthesis. Cell Death & Dis. 2018; 9: 824.

[22] Lee YS, et al. Berberine, a natural plant product, activates AMP-activated protein kinase with beneficial metabolic effects in diabetic and insulin-resistant states. Pharmacol & Ther. 2006; 55(8).

[23] Gomes AP, et al. Berberine protects against high fat diet-induced dysfunction in muscle mitochondria by inducing SIRT1-dependent mitochondrial biogenesis. Biochim Biophys Acta. 2012; 1822(2): 185-195.

[24] Rayamajhi N, et al. Quercetin induces mitochondrial biogenesis through activation of HO-1 in HepG2 Cells. Oxid Med Cell Longev. 2013; 2013: 154279.

[25] Li Y, et al. Quercetin, inflammation and immunity. Nutrients. 2016; 8(3): 167.

[26] Kim SG, et al. Quercetin-induced AMP-activated protein kinase activation attenuates vasoconstriction through LKB1-AMPK signaling pathway. J Med Food. 2018; 21(2): 146-153.

[27] Lewinska A, et al. AMPK-mediated senolytic and senostatic activity of quercetin surface functionalized Fe3O4 nanoparticles during oxidant-induced senescence in human fibroblasts. Redox Biol. 2020; 28: 101337.

[28] Van Deursen JM. Senolytic therapies for healthy longevity. Science. 2019; 364(6441): 636-637.

[29] Weng Z, et al. Quercetin Is more effective than Cromolyn in blocking human mast cell cytokine release and inhibits contact dermatitis and photosensitivity in humans. PLoS One. 2012; 7(3): e33805.

[30] Jiang K, et al. Silibinin, a natural flavonoid, induces autophagy via ROS-dependent mitochondrial dysfunction and loss of ATP involving BNIP3 in human MCF7 breast cancer cells. Oncol Rep. 2015; 33(6): 2711-2718.

[31] Lovelace ES, et al. Silymarin suppresses cellular inflammation by inducing reparative stress signaling. J Nat Prod. 2015; 78(8): 1990-2000.

[32] Ye Y, et al. 3,3′-Diindolylmethane induces anti-human gastric cancer cells by the miR-30e-ATG5 modulating autophagy. Biochem Pharmacol. 2016; 115: 77-84.

[33] Hornero RA, et al. The impact of dietary components on regulatory T cells and disease. Front Immunol. 2020; 11: 253.

[34] Shen Y, Honma N et al. Cinnamon extract enhances glucose uptake in 3T3-L1 adipocytes and C2C12 myocytes by inducing LKB1-AMPactivated protein kinase signaling. PLoS One. 2014 Feb 14;9(2):e8789

[35] Park KR, Nam D. β-Caryophyllene oxide inhibits growth and induces apoptosis through the suppression of PI3K/AKT/mTOR/S6K1 pathways and ROS-mediated MAPKs activation. Cancer Lett. 2011 Dec 22;312(2):178-88

[36] Mollazadeh H and Hosseinzadeh H. Cinnamon effects on metabolic syndrome: a review based on its mechanisms. Iran J Basic Med Sci. 2016; 19(12): 1258-1270.


QuintEssential® 3.3 References https://www.quicksilverscientific.com/hypertonicreferences/

[1] Holm NG, Anderson EM. Abiotic synthesis of organic compounds under the conditions of submarine hydrothermal systems: a perspective. Planet Space Sci 1995; 43(1-2): 153-9.

[2] He HZ, Li HB et al. Determination of vitamin B1 in seawater and microalgal fermentation media by high-performance liquid chromatography with fluorescence detection. Anal Bioanal Chem 2005; 383(5): 875-9.

[3] Litchfield CD, Hood DW. Microbiological assay for organic compounds in seawater. II. Distribution of adenine, uracil, and threonine. Appl Microbiol 1966; 14(2): 145-51

[4] Quinton, R. L’eau De Mer, Milieu Organique: Constance Du Milieu Marin Originel, Comme Milieu Vital Des Cellules, À Travers La Série Animale. Ulan Press. 2012

[5] Yoshizawa Y, Tanojo H et al. Sea water or its components alter experimental irritant dermatitis in man, Skin Res. Technol., 2001 (7): 36–39.

[6] Kimata H, Tai H et al.  Improvement of skin symptoms and mineral imbalance by drinking deep sea water in patients with atopic eczema/dermatitis syndrome (AEDS), Acta Med. (Hradec Kralove, Czech Repub.), 2002 (45): 2; 83–84.

[7] Tabary O, Muselet C et al. Reduction of chemokine IL8 and RANTES expression in human bronchial epithelial cells by a sea water derived saline through inhibited nuclear factor kB activation, Biochem. Biophys. Res.Commun., 2003 (309); 2: 310–316.

[8] Miyamura M, Yoshioka S et al. Difference between deep seawater and surface seawater in the preventive effect of atherosclerosis, Biol. Pharm. Bull., 2004; (27): 11;  1784–1787.

[9] Slapak I, Skoupá J et al Efficacy of isotonic nasal wash (seawater) in the treatment and prevention of rhinitis in children, Arch. Otolaryn gol. Head Neck Surg., 2008 (134); 1:  67–74.

[10] Yoshioka S, Hamada A et al. Pharmacological activity of deep-sea water: examination of hyperlipemia prevention and medical treatment effect. Biol Pharm Bull. 2003 Nov;26(11):1552-9.

[11] Armstrong LE, Ganio MS. Mild dehydration affects mood in healthy young women. J Nutr. 2012 Feb;142(2):382-8.

[12] Fadda R, Rapinett G. Effects of drinking supplementary water at school on cognitive performance in children. Appetite. 2012 Dec;59(3):730-7.

[13] Suhr JA, Hall J. The relation of hydration status to cognitive performance in healthy older adults.  Int J Psychophysiol. 2004 Jul;53(2):121-5.

[14] Lieberman HR. Hydration and cognition: a critical review and recommendations for future research. J Am Coll Nutr. 2007;26(5S)

[15] Paik IY, Jeong MH et al. Fluid replacement following dehydration reduces oxidative stress during recovery. Biochem Biophys Res Commun. 2009 May 22;383(1):103-7.

[16] Texas Heart Institute: Trace Elements: what they do and where to get them. Available at: https://www.texasheart.org/. Accessed June 1, 2019.

[17] Scotney B, Reid S. Body weight, serum sodium levels and renal function in an ultra-distance mountain run. Clin J Sport Med. 2015 Jul;25(4):341-6.

[18] Hoffman MD, Joslin J et al. Management of suspected fluid balance issues in participants of wilderness endurance events. Curr Sports Med Rep. 2017 Mar/Apr;16(2):98-102.

[19] Armstrong LE, Johnson EC et al. COUNTERVIEW: Is drinking to thirst adequate to appropriately maintain hydration status during prolonged endurance exercise? No. Wilderness Environ Med. 2016 Jun;27(2):195-8.

[20] Angier, N. The wonders of blood. Available at: https://www.nytimes.com/2008/10/21/science/21angi.html. Accessed June 1, 2019.

[21] Theocharis AD, Skandalis SS et al. Extracellular matrix structure. Adv Drug Deliv Rev. 2016 Feb 1;97:4-27.

[22] Pischinger, A. The Extracellular Matrix and Ground Regulation: Basis for a Holistic Biological Medicine. North Atlantic Books; 2007.

[23] Nabaa A, Clauser KR et al. The extracellular matrix: tools and insights for the “omics” era. Matrix Biol. (2016) 49; 10–24

[24] Gomez C, Deravi L. Self-assembling extracellular matrix proteins as materials for the condensation of silica nanostructures. RSC Advances 2016 (97) ra/c6ra20911d

[25] Silkin VA, Pautova LA et al. Drivers of phytoplankton blooms in the northeastern Black Sea. Mar Pollut Bull. 2019 Jan;138:274-28

[26] Litchman E, Klausmeier CA et al. The role of phytoplankton functional traits in structuring phytoplankton communities: scaling from cellular to ecosystem level. Ecol. Lett. 2007(10); 1170–1181

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Methyl Charge+ References https://www.quicksilverscientific.com/methylchargereferences/

[1] McKee SE et al. Effect of supplementation with methyl-donor nutrients on neurodevelopment and cognition: considerations for future research Nutrition Reviews, 2018 (75): 7:497-511 View Full Paper

[2] Williams AC et al. Nicotinamide, NAD(P)(H), and methyl-group homeostasis evolved and became a determinant of aging diseases: hypotheses and lessons from Pellagra. Curr Gerontol Geriatr Res. 2012;2012:302875. View Full Paper

[3] Longo VD et al. Interventions to Slow Aging in Humans: Are We Ready? Aging Cell 14 (4): 497-510. View Abstract

[4] Fang EF et al. NAD (+) in aging: molecular mechanisms and translational implications. Trends Mol Med. 2017;23(10):899–916 View Abstract

[5] Hershberger KA et al. Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases. Nat Rev Nephrol. 2017 Apr;13(4):213-225. View Full Paper

[6] Tasselli L et el. Methylation gets into rhythm with NAD(+)-SIRT1Nat Struct Mol Biol. 2015 Apr;22(4):275-76 View Abstract

[7] Aguilar-Arnal L et al. NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1.Nat Struct Mol Biol. 2015 Apr;22(4):312-8. View Full Paper

[8] Cantó C et al. NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell Metab. 2015 Jul 7;22(1):31-53. View Full Paper

[9] Kang-Lee YA et al. Metabolic effects of nicotinamide administration in rats. J Nutr. 1983 Feb;113(2):215-21. View Abstract

[10] Aksoy S et al. Human liver nicotinamide N-methyltransferase. cDNA cloning, expression, and biochemical characterization. J. Biol. Chem. 1994 269, 14835–14840.

[11] Li W et al. NAD+ content and its role in mitochondria. Mitochondrial Regulation. 2014: 39–48 View Abstract

[12] Lee CF et al. Targeting NAD+ metabolism as interventions for mitochondrial disease. Sci Rep. 2019 Feb 28;9(1):3073. View Abstract

[13] Pelizzola M. The DNA methylome. FEBS Lett. 2011 Jul 7; 585(13): 1994–2000. View Full Paper

[14] Moore LD et al. DNA methylation and its basic function. Neuropsychopharmacology. 2013;38(1):23–38.View Full Paper

[15] Szyf M. The role of DNA hypermethylation and demethylation in cancer and cancer therapy. Curr Oncol. 2008;15(2):72–75. View Full Paper

[16] Friso S et al. One-carbon metabolism and epigenetics. Mol Aspects Med. 2017 Apr;54:28-36. View Abstract

[17] Shames DS, Minna JD et al. DNA methylation in health, disease, and cancer. Curr Mol Med 7: 85-102View Full Paper

[18] gene in diet-induced nonalcoholic fatty liver disease-associated carcinogenesis. Toxicol Sci. 2019 May 14. pii: kfz110 View Full Paper

[19] Ligthart S et al. DNA methylation signatures of chronic low-grade inflammation are associated with complex diseases. Genome Biol. 2016 Dec 12;17(1):255 View Full Paper

[20] NIH U.S. National Library of Medicine, MTHFR gene. Genetics Home Reference Available at: https://ghr.nlm.nih.gov/gene/MTHFR Accessed 1-4-2020

[21] Castro R et al. 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C→T and 1298A→C mutations are associated with DNA hypomethylation. Journal of Medical Genetics 2004;41:454-458View Full Paper

[22] Hustad S et al. Riboflavin and methylenetetrahydrofolate reductase. Madame Curie Bioscience Database [Internet]. View Full Paper

[23] Pinto JT et al. Riboflavin. Advances in Nutrition 2016 (5):5;973-975 View Full Paper

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[26] Belardo A et al. The concomitant lower concentrations of vitamins B6, B9 and B12 may cause methylation deficiency in autistic children J Nutr Biochem. 2019 Aug;70:38-46. View Abstract

[27] Anderson OS e al. Nutrition and epigenetics: an interplay of dietary methyl donors, one-carbon metabolism and DNA methylation.J Nutr Biochem. 2012 Aug;23(8):853-9. View Full Paper

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H2 Elite References https://www.quicksilverscientific.com/h2elitereferences/

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[2] Sauer H, Wartenberg M et al. Reactive oxygen species as intracellular messengers during cell growth and differentiation. Cell. Physiol. Biochem. 2001 11, 173–186

[3] Liu H, Colavitti R et al. Redox-dependent transcriptional regulation. Circ. Res. 2005 97, 967–975

[4] Bjelakovic G. Meta-regression analyses, meta-analyses, and trial sequential analyses of the effects of supplementation with beta-carotene, vitamin A, and vitamin E singly or in different combinations on all-cause mortality: do we have evidence for lack of harm? PLoS One. 2013 Sep 6;8(9):e74558

[5] Apostolova N, Victor VM. Molecular strategies for targeting antioxidants to mitochondria: therapeutic implications. Antioxid Redox Signal. 2015 Mar 10;22(8):686-729

[6] Ohta, S. A multi-functional organelle mitochondrion is involved in cell death, proliferation and disease. Curr. Med. Chem. 2003 10, 2485–2494

[7] Turrens JF. Mitochondrial formation of reactive oxygen species. J. Physiol. (Lond.) 2003 552, 335–344

[8] Zhai X, Chen X et al. Lactulose ameliorates cerebral ischemia-reperfusion injury in rats by inducing hydrogen by activating Nrf2 expression Free Radic Biol Med. 2013 Dec;65:731-741

[9] Yu J, Zhang W. Molecular hydrogen attenuates hypoxia/reoxygenation injury of intrahepatic cholangiocytes by activating Nrf2 expression Toxicol Lett. 2015 Nov 4;238(3):11-9

[10] Hara F, Tatebe J et al. Molecular Hydrogen Alleviates Cellular Senescence in Endothelial Cells.Circ J. 2016 Aug 25;80(9):2037-46

[11] Qiang Ma. Role of Nrf2 in oxidative stress and toxicit. Annu Rev Pharmacol Toxicol. 2013; 53: 401–426.

[12] Itoh T, FujitaY et al. Molecular hydrogen suppresses FcepsilonRI-mediated signal transduction and prevents degranulation of mast cells. Biochem Biophys Res Commun. 2009;389(4):651–6

[13] Itoh T, Hamada N et al. Molecular hydrogen inhibits lipopolysaccharide/interferon gamma-induced nitric oxide production through modulation of signal transduction in macrophages. Biochem Biophys Res Commun. 2011;411(1):143–9

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