Studies

A Neurotrophic Agent Provides a Novel MOA (Mechanism of Action)

Neurotrophic refers to nutrition for the nerves. The ingredients in Pre-DX provide nutritional management of endothelial dysfunction associated with numbness, tingling, and burning sensations in diabetes patients with neuropathy. It offers a neurotrophic benefit by improving endothelial dysfunction and maintaining blood flow in the vessels that carry important nutrients and oxygen to the peripheral nerves.

Pre-DX is composed of the bioactive forms of essential B vitamins along with other agents that reduce inflammation and oxidative stress and are critical for peripheral nerve health.

Science:

  1. Pre-DX helps regenerate BH4, a cofactor for eNOS to convert L-arginine into nitric oxide
  2. Nitric oxide is diffused into the smooth muscle cells
  3. Smooth muscle cells dilate, and blood flow is increased

 

 

 

 

 

 

Ingredients:

L-methylfolate (folate) Methylcobalamin & Hydroxocobalamin (vitamins B12) Pyridoxal 5’ phosphate (vitamin B6), N-Acetyl Cysteine (NAC), Alpha Lipoic Acid, Vitamins C, D, E, B1, B2, B3, Pantothenic Acid, Zinc, Selenium, Copper.

Benefits:

Nitric oxide synthesis, myelin synthesis, neurotransmitter synthesis

Nitric Oxide Benefits 

 

The endothelium (the thin layer of cells that line the interior surface of blood vessels) helps maintain blood flow by producing a substance called nitric oxide. Nitric oxide signals the blood vessels to relax corresponding with improved blood flow to peripheral nerves. Studies have shown that endothelial cells produce twice as much nitric oxide in the presence of L-methylfolate.

Maintaining blood flow in the small blood vessels is critical for peripheral nerves to maintain their normal functions, such as peripheral nerve repair and regeneration. This includes production of the myelin sheath, a fatty substance that protects the nerve fibers. Research has demonstrated a significant increase in epidermal nerve fiber density after 6 months of L-methylfolate compared to baseline; further research is ongoing.

 

3rd Party COA 

 * COA on File -

For more information email info@pre-dx.com for a copy

* The studies listed below DO NOT have Pre-DX in them but use the same ingredients such as L-methylfolate, Methylcobalamin & Hydroxocobalamin (B12), Pyridoxal 5' phosphate (B6) and additional ingredients to increase methylation cycle. Pre-DX does not make a claim to cure diseases but addresses specific symptoms from a nutritional perspective.

1. CDC. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US Department of Health and Human Services, CDC; 2011.

2. Knowler WC, Barrett-Conner E, Fowler SE, et al; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393–403.

3. Geiss LS, James C, Gregg EW, et al. Diabetes risk reduction behaviors among U.S. adults with prediabetes. Am J Prev Med 2010;38:403–9.

4. CDC. National Health and Nutrition Examination Survey. Atlanta, GA: US Department of Health and Human Services, CDC; 2012.

5. Herman WH, Smith PJ, Thompson TJ, et al. A new and simple questionnaire to identify people at increased risk for undiagnosed diabetes. Diabetes Care 1995;18:382–7.

6. Mayer-Davis EJ, Dabble D, Lawrence JM, et al. Risk factors for type 2 and gestational diabetes. In: Venkat Narayan KM, Williams D, Gregg EW, Cowie C, eds. Diabetes public health: from data to policy. New York, NY: Oxford University Press; 2011:33–63.

7. American Diabetes Association. Standards of medical care in diabetes—2013. Diabetes Care 2013;36:S11–66.

8. Selvin E, Steffes MW, Gregg E, Brancati FL, Coresh J. Performance of A1C for the classification and prediction of diabetes. Diabetes Care 2011;34:84–9.

9. CDC. Increasing prevalence of diagnosed diabetes—United States and Puerto Rico, 1995–2010. MMWR 2012;61:918–21.

10. Clarke, R., Daly, L., Robinson, K., Naughten, E., Cahalane, S., et al. 1991.  Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med 324:1149–1155.

11. Homocysteine Studies Collaboration.  2002. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA. 288:2015–2022.

12.  Guilliams, T.G.  2004.  Homocystiene – a risk factor for vascular diseases:  Guidelines for Clinical Practices.  JANA.  7(1):11-24.

13. Wulffele, M.G., Kooy, A., Hehert, P., Bets, D., Octerop, J.C., Borger van der Burg, B., et al.  2003.  Effects of short-term treatment with metformin on serum concentration of homocysteine, folate and vitamin B12 in type 2 diabetes mellitus:  a randomized, placebo-controlled trial.  J Int Med.  254:455-463.

14. Scaglione, F.1. Panzavolta, G. 2014. Folate, folic acid and 5-methyltetrahydrofolate are not the same thing Xenobiotica. 44(5):480-8.

15. Lambie, D.G., Johnson, R.H. 1985. Drugs and folate metabolism. Drugs. 30(2):145-55.

16.  Amilburu, A., Idoate, I., Ponz, F., Larralde, J.  2002. Inhibition of intestinal absorption of 5-methyltetrahydrofolate by fluoxetine.  J. Phys. Biochem.  57(2):71-79.

17. Ruscin, J.M., Page, R.L. 2nd, Valuck, R,J, 2002. Vitamin B(12) deficiency associated with histamine(2)-receptor antagonists and a proton-pump inhibitor.  Ann Pharmacother. 36(5):812-6.

18. Cai, W., Yin, L.,Yang, F., Zhang, L., Cheng, J. 2014. Association between Hcy levels and the CBS844ins68 and MTHFR C677T polymorphisms with essential hypertension. Biomed Rep. 2(6):861-868.

19. Heifetz, E.M., Birk, R.Z. 2014.  MTHFR C677T Polymorphism Affects Normotensive Diastolic Blood Pressure Independently of Blood Lipids. Am J Hypertens. Aug 27. Epub ahead of print.

20. Nazki, F.H.,  Sameer, A.S., Ganaie, B.A.  2014.  Folate:  metabolism, genes, polymorphisms and the associated diseases.  Gene. 533(1):1-20.

21. Khandanpour, N., Willis, G., Meyer, F.J., Armon, M.P., Loke, Y.K., Wright, A.J., et al.  2009. Peripheral arterial disease and methylenetetrahydrofolate reductase (MTHFR) C677T mutations: A case-control study and meta-analysis. J Vasc Surg. 49(3):711-8.

22. Yigit, S., Karakus, N., Inanir, A. 2013. Association of MTHFR gene C677T mutation with diabetic peripheral neuropathy and diabetic retinopathy. Mol Vis. 2013 Jul 25;19:1626-30.

23. Niu, W., Qi, Y. 2012. An updated meta-analysis of methylenetetrahydrofolate reductase gene 677C/T polymorphism with diabetic nephropathy and diabetic retinopathy. Diabetes Res Clin Pract. 95(1):110-8

24. Maeda, M, Fujio, Y., Azuma. J. 2006. MTHFR gene polymorphism and diabetic retinopathy. Curr Diabetes Rev.2(4):467-76.

25. Sun, J., Xu, Y., Zhu, Y., Lu, H., Deng, H., Fan, Y., et al. 2003. The relationship between MTHFR gene polymorphisms, plasma homocysteine levels and diabetic retinopathy in type 2 diabetes mellitus. Chin Med J (Engl). 116(1):145-7.

26. Simões, MJ., Lobo, C., Egas, C., Nunes, S., Carmona, S., Costa, MÂ., et al.  2014. Genetic Variants in ICAM1, PPARGC1A and MTHFR Are Potentially Associated with Different Phenotypes of Diabetic Retinopathy. Ophthalmological. 232(3):156-62.

27. Tanaka, K., Nakayama, T., Yuzawa, M., Wang, Z., Kawamura, A., Mori, R., et al. 2011.

28. Liu, H.H., Shih, T.S., Huang, H.R., Huang, S.C., Lee, L.H., Huang, Y.C. 2013.  Plasma homocysteine is associated with increased oxidative stress and antioxidant enzyme activity in welders. Scientific World Journal. 2013:370487.

29. Faraci, F.M., Lentz, S.R.  2003.  Hyperhomocysteinemia, oxidative stress and cerebral vascular dysfunction. Stroke. 35:345-347

30. Rodrigo, R., Passalacqua, W., Araya, J., Orellana, M., Rivera, G. 2003. Implications of oxidative stress and homocysteine in the pathophysiology of essential hypertension.  J Cardiovasc Pharmacol. 2003 Oct;42(4):453-61.

31. Pushpakumar, S., Kundu, S., Sen U.  2014.  Endothelial dysfunction:  The link between homocysteine and hydrogen sulfide.  Curr Med Chem.  21:3662-3672.

32. Fohr, I.P., Prinz-Langenohi, Bronstrup, A., Bohlmann, A.M., Berthoid, H.K., Pietrzik, K. 2002. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 75(2):275-82.

33. Prinz-Langenohl, R., Brämswig, S., Tobolski, O., Smulders, Y.M., Smith, D.E., Finglas, P.M., Pietrzik, K. 2009.  [6S]-5-methyltetrahydrofolate increases plasma folate more effectively than folic acid in women with the homozygous or wild-type 677C–>T polymorphism of methylenetetrahydrofolate reductase. Br J Pharmacol. 158(8):2014-21.

34. Smith, D.E., Hornstra, J.M., Kok, R.M., Blom, H.J., Smulders, Y.M. 2013. Folic acid supplementation does not reduce intracellular homocysteine, and may disturb intracellular one-carbon metabolism. Clin Chem Lab Med. 51(8):1643-50.

35. van Guldener, C., Stehouwer, C.D. 2001. Homocysteine-lowering treatment: an overview. Expert Opinion on Pharmacotherapy 2 9):1449–1460.

36. Hustad, S., Midttun, O, Schneede, J., Vollset, S.E., Grotmol, T., Ueland, P.M. 2007.  The Methylenetetrahydrofolate reductase 677->T polymorphism as a modulator of a B vitamin network with major effects on homocysteine metabolism. Am J Hum Genet. 80(5):846-855.

37. García-Minguillán, C.J., Fernandez-Ballart, J.D., Ceruelo, S., Ríos, L., Bueno, O., Berrocal-Zaragoza, M.I., et al.  Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine. 2014. Genes Nutr.9(6):435.

38. Hustad, S., Ueland, P.M., Vollset, S.E., Zhang, Y., Bjørke-Monsen, A.L., Schneede, J. 2000. Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clin Chem. 46(8 Pt 1):1065-71.

39. McNulty, H., Dowey le, R.C., Strain, J.J., Dunne, A., Ward, M., Molloy, A.M., et al. 2006. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism. Circulation.113:74-80.

40. Gariballa, S.E, Forster, S.J., Powers, H.J. 2012. Effects of mixed dietary supplements on total plasma homocysteine concentrations (tHcy): a randomized, double-blind, placebo-controlled trial. Int J Vitam Nutr Res.;82(4):260-6.

41. Amer, M., Qayyum, R.  2014. The relationship between 25-hydroxyvitamin D and homocysteine in asymptomatic adults.  J Clin Endocrinol Metab. 99(2):633-8.

42. Eloranta, J.J., Zair, Z.M., Hiller, C., Hausler, S., Stieger, B., Kullak-Ublick, G.A.  2009. Vitamin D3 and its nuclear receptor increase the expression and activity of the human proton-coupled folate transponder. Molecular Pharmacology. 76(5):1062-1071.

43. Heidarian, E., Amini, M., Parham, M., Aminorroaya, A.  2009. Effect of zinc supplementation on serum homocysteine in type 2 diabetic patients with microalbuminuria.  Rev Diabet Stud. 6(1):64-70.

44. Huang, R.F.S., Huang, S.M., Lin, B.S., Hung C.Y., Lu, H.T.  2002.  N-Acetylcysteine, Vitamin C and Vitamin E Diminish Homocysteine Thiolactone-Induced Apoptosis in Human Promyeloid HL-60 Cells.  J Nutr.  132(8):2151-2156.

45. Slyshenkov, V.S., Dymkowska, D., Wojtczak, L. 2004. Pantothenic acid and pantothenol increase biosynthesis of glutathione by boosting cell energetics.  FEBS Letters 569(1-3):169-172.

46. Lukienko, P.I., Mel’nichenko, N.G.,  Zverinskii, I.V., Zabrodskaya, S.V. 2000. Antioxidant properties of thiamine, Bulletin of Experimental Biology and Medicine. 130(9);874–876.

47. Takahashi, K., Newburger, P.E., Cohen, H.J. 1986.  Glutathione peroxidase protein. Absence in selenium deficiency states and correlation with enzymatic activity.  J Lin Invest. 77(4):1402-1404.

48. Scaglione, F.1. Panzavolta, G. 2014. Folate, folic acid and 5-methyltetrahydrofolate are not the same thing,  Xenobiotica. 44(5):480-8.

49. Lambie, D.G., Johnson, R.H. 1985. Drugs and folate metabolism. Drugs. 30(2):145-55.

50. Amilburu, A., Idoate, I., Ponz, F., Larralde, J.  2002. Inhibition of intestinal absorption of 5-methyltetrahydrofolate by fluoxetine.  J. Phys. Biochem.  57(2):71-79.

51. Sobczyńska-Malefora, A., Harrington, D.J., Lomer, M.C., Pettitt, C., Hamilton, S., Rangarajan, S., Shearer, M.J. 2009.  Erythrocyte folate and 5-methyltetrahydrofolate levels decline during 6 months of oral anticoagulation with warfarin. Blood Coagul Fibrinolysis. 20(4):297-302.

52. Ruscin, J.M., Page, R.L. 2nd, Valuck, R,J, 2002. Vitamin B(12) deficiency associated with histamine(2)-receptor antagonists and a proton-pump inhibitor.  Ann Pharmacother. 36(5):812-6.

53. Wicken, B., Bamforth, F., Li, Z., Zhu, H., Ritvanen, A., Redlund, M., et al.  2003.  Geographical and ethnic variation of the 677C>T allele of 5,10 methylenetetrahydrofolate reductase (MTHFR): findings from over 7000 newborns from 16 areas world wide.  J Med Genet. 40:619-625.

54. Jacques, P.F., Bostom, A.G., Williams, R.R., Ellison R.C., Eckfeldt, J.H., Rosenberg, I.H., et al. 1996. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation 1996. 93:7-9.

55. Rosen, R.  2000.  Genetic modulation of homocysteinemia.  Semin Thromb Hemost.  26(3):255-61.

56. Zittoun, J., Tonetti, C., Bories, D., Pignon, J.M., Tulliez, M. 1998. Plasma homocysteine levels related to interactions between folate status and methylenetetrahydrofolate reductase: a study in 52 healthy subjects. Metabolism. 47(11):1413-8.

57. Faraci, F.M., Lentz, S.R.  2003.  Hyperhomocysteinemai, oxidative stress and cerebral vascular dysfunction. Stroke. 35:345-347

58. Rodrigo, R., Passalacqua, W., Araya, J., Orellana, M., Rivera, G. 2003. Implications of oxidative stress and homocysteine in the pathophysiology of essential hypertension. J Cardiovasc Pharmacol. 2003 Oct;42(4):453-61.

59. Fohr, I.P., Prinz-Langenohi, Bronstrup, A., Bohlmann, A.M., Berthoid, H.K., Pietrzik, K. 2002. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 75(2):275-82.

60. Prinz-Langenohl, R., Brämswig, S., Tobolski, O., Smulders, Y.M., Smith, D.E., Finglas, P.M., Pietrzik, K. 2009.  [6S]-5-methyltetrahydrofolate increases plasma folate more effectively than folic acid in women with the homozygous or wild-type 677C–>T polymorphism of methylenetetrahydrofolate reductase. Br J Pharmacol. 158(8):2014-21.

61. Smith, D.E., Hornstra, J.M., Kok, R.M., Blom, H.J., Smulders, Y.M. 2013. Folic acid supplementation does not reduce intracellular homocysteine, and may disturb intracellular one-carbon metabolism. Clin Chem Lab Med. 51(8):1643-50.

62. Lim, H.S., Heo, Y.R. 2002. Plasma total homocysteine, folate, and vitamin B12 status in Korean adults. J Nutr Sci Vitaminol (Tokyo). 2002. 48(4):290-7.

63. Chen, K.J., Pan, W.H., Yang, F.L., Wei, I.L., Shaw, N.S., Lin, B.F. 2005. Association of B vitamins status and homocysteine levels in elderly Taiwanese. Asia Pac J Clin Nutr. 2005;14(3):250-5.

64. van Guldener, C., Stehouwer, C.D. 2001. Homocysteine-lowering treatment: an overview. Expert Opinion on Pharmacotherapy 2 9):1449–1460.

65. Homocysteine Lowering Trialists’ Collaboration, Clinical Trial Service Unit, Radcliffe Infirmary, Oxford, UK. 2000. Lowering blood homocysteine with folic acid-based supplements: meta-analysis of randomised trials. Indian Heart J. 52(7 suppl):S59-S64.

66. Hustad, S., Midttun, O, Schneede, J., Vollset, S.E., Grotmol, T., Ueland, P.M. 2007.  The Methylenetetrahydrofolate reductase 677->T polymorphism as a modulator of a B vitamin network with major effects on homocysteine metabolism. Am J Hum Genet. 80(5):846-855.

67. García-Minguillán, C.J., Fernandez-Ballart, J.D., Ceruelo, S., Ríos, L., Bueno, O., Berrocal-Zaragoza, M.I., et al.  Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine. 2014. Genes Nutr.9(6):435.

68. Hustad, S., Ueland, P.M., Vollset, S.E., Zhang, Y., Bjørke-Monsen, A.L., Schneede, J. 2000. Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clin Chem. 46(8 Pt 1):1065-71.

69. McNulty, H., Dowey le, R.C., Strain, J.J., Dunne, A., Ward, M., Molloy, A.M., et al. 2006. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism. Circulation.113:74-80.

70. Gariballa, S.E, Forster, S.J., Powers, H.J. 2012. Effects of mixed dietary supplements on total plasma homocysteine concentrations (tHcy): a randomized, double-blind, placebo-controlled trial. Int J Vitam Nutr Res.;82(4):260-6.

71. Amer, M., Qayyum, R.  2014. The relationship between 25-hydroxyvitamin D and homocysteine in asymptomatic adults.  J Clin Endocrinol Metab. 99(2):633-8.

72. Abdel-Azeim, S., Li, X., Chung, L.W., Morokuma, K. 2011. Zinc-homocysteine binding in cobalamin-dependent methionine synthase and its role in the substrate activation: DFT, ONIOM, and QM/MM molecular dynamics studies. J Comput Chem. 32(15):3154-67

73. Heidarian, E., Amini, M., Parham, M., Aminorroaya, A.  2009. Effect of zinc supplementation on serum homocysteine in type 2 diabetic patients with microalbuminuria.  Rev Diabet Stud. 6(1):64-70.

74. Huang, R.F.S., Huang, S.M., Lin, B.S., Hung C.Y., Lu, H.T.  2002.  N-Acetylcysteine, Vitamin C and Vitamin E Diminish Homocysteine Thiolactone-Induced Apoptosis in Human Promyeloid HL-60 Cells.  J Nutr.  132(8):2151-2156.

75. Slyshenkov, V.S., Dymkowska, D., Wojtczak, L. 2004. Pantothenic acid and pantothenol increase biosynthesis of glutathione by boosting cell energetics.  FEBS Letters 569(1-3):169-172.

76. Lukienko, P.I., Mel’nichenko, N.G.,  Zverinskii, I.V., Zabrodskaya, S.V. 2000. Antioxidant properties of thiamine, Bulletin of Experimental Biology and Medicine. 130(9);874–876.

77. Takahashi, K., Newburger, P.E., Cohen, H.J. 1986.  Glutathione peroxidase protein. Absence in selenium deficiency states and correlation with enzymatic activity.  J Lin Invest. 77(4):1402-1404.

78. Scaglione, F.1. Panzavolta, G. 2014. Folate, folic acid and 5-methyltetrahydrofolate are not the same thing,  Xenobiotica. 44(5):480-8.

79. Lambie, D.G., Johnson, R.H. 1985. Drugs and folate metabolism. Drugs. 30(2):145-55.

80. Amilburu, A., Idoate, I., Ponz, F., Larralde, J.  2002. Inhibition of intestinal absorption of 5-methyltetrahydrofolate by fluoxetine.  J. Phys. Biochem.  57(2):71-79.

81. Sobczyńska-Malefora, A., Harrington, D.J., Lomer, M.C., Pettitt, C., Hamilton, S., Rangarajan, S., Shearer, M.J. 2009.  Erythrocyte folate and 5-methyltetrahydrofolate levels decline during 6 months of oral anticoagulation with warfarin. Blood Coagul Fibrinolysis. 20(4):297-302.

82. Ruscin, J.M., Page, R.L. 2nd, Valuck, R,J, 2002. Vitamin B(12) deficiency associated with histamine(2)-receptor antagonists and a proton-pump inhibitor.  Ann Pharmacother. 36(5):812-6.

83. Wicken, B., Bamforth, F., Li, Z., Zhu, H., Ritvanen, A., Redlund, M., et al.  2003.  Geographical and ethnic variation of the 677C>T allele of 5,10 methylenetetrahydrofolate reductase (MTHFR): findings from over 7000 newborns from 16 areas world wide.  J Med Genet. 40:619-625.

84. Jacques, P.F., Bostom, A.G., Williams, R.R., Ellison R.C., Eckfeldt, J.H., Rosenberg, I.H., et al. 1996. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation 1996. 93:7-9.

85. Rosen, R.  2000.  Genetic modulation of homocysteinemia.  Semin Thromb Hemost.  26(3):255-61.

86. Zittoun, J., Tonetti, C., Bories, D., Pignon, J.M., Tulliez, M. 1998. Plasma homocysteine levels related to interactions between folate status and methylenetetrahydrofolate reductase: a study in 52 healthy subjects. Metabolism. 47(11):1413-8.

87. Faraci, F.M., Lentz, S.R.  2003.  Hyperhomocysteinemai, oxidative stress and cerebral vascular dysfunction. Stroke. 35:345-347

88. Rodrigo, R., Passalacqua, W., Araya, J., Orellana, M., Rivera, G. 2003. Implications of oxidative stress and homocysteine in the pathophysiology of essential hypertension. J Cardiovasc Pharmacol. 2003 Oct;42(4):453-61.

89. Fohr, I.P., Prinz-Langenohi, Bronstrup, A., Bohlmann, A.M., Berthoid, H.K., Pietrzik, K. 2002. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 75(2):275-82.

90. Prinz-Langenohl, R., Brämswig, S., Tobolski, O., Smulders, Y.M., Smith, D.E., Finglas, P.M., Pietrzik, K. 2009.  [6S]-5-methyltetrahydrofolate increases plasma folate more effectively than folic acid in women with the homozygous or wild-type 677C–>T polymorphism of methylenetetrahydrofolate reductase. Br J Pharmacol. 158(8):2014-21.

91. Smith, D.E., Hornstra, J.M., Kok, R.M., Blom, H.J., Smulders, Y.M. 2013. Folic acid supplementation does not reduce intracellular homocysteine, and may disturb intracellular one-carbon metabolism. Clin Chem Lab Med. 51(8):1643-50.

92. Lim, H.S., Heo, Y.R. 2002. Plasma total homocysteine, folate, and vitamin B12 status in Korean adults. J Nutr Sci Vitaminol (Tokyo). 2002. 48(4):290-7.

93. Chen, K.J., Pan, W.H., Yang, F.L., Wei, I.L., Shaw, N.S., Lin, B.F. 2005. Association of B vitamins status and homocysteine levels in elderly Taiwanese. Asia Pac J Clin Nutr. 2005;14(3):250-5.

94. van Guldener, C., Stehouwer, C.D. 2001. Homocysteine-lowering treatment: an overview. Expert Opinion on Pharmacotherapy 2 9):1449–1460.

95. Homocysteine Lowering Trialists’ Collaboration, Clinical Trial Service Unit, Radcliffe Infirmary, Oxford, UK. 2000. Lowering blood homocysteine with folic acid-based supplements: meta-analysis of randomised trials. Indian Heart J. 52(7 suppl):S59-S64.

96. Hustad, S., Midttun, O, Schneede, J., Vollset, S.E., Grotmol, T., Ueland, P.M. 2007.  The Methylenetetrahydrofolate reductase 677->T polymorphism as a modulator of a B vitamin network with major effects on homocysteine metabolism. Am J Hum Genet. 80(5):846-855.

97. García-Minguillán, C.J., Fernandez-Ballart, J.D., Ceruelo, S., Ríos, L., Bueno, O., Berrocal-Zaragoza, M.I., et al.  Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine. 2014. Genes Nutr.9(6):435.

98. Hustad, S., Ueland, P.M., Vollset, S.E., Zhang, Y., Bjørke-Monsen, A.L., Schneede, J. 2000. Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clin Chem. 46(8 Pt 1):1065-71.

99. McNulty, H., Dowey le, R.C., Strain, J.J., Dunne, A., Ward, M., Molloy, A.M., et al. 2006. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism. Circulation.113:74-80.

100. Gariballa, S.E, Forster, S.J., Powers, H.J. 2012. Effects of mixed dietary supplements on total plasma homocysteine concentrations (tHcy): a randomized, double-blind, placebo-controlled trial. Int J Vitam Nutr Res.;82(4):260-6.

101. Amer, M., Qayyum, R.  2014. The relationship between 25-hydroxyvitamin D and homocysteine in asymptomatic adults.  J Clin Endocrinol Metab. 99(2):633-8.

102. Abdel-Azeim, S., Li, X., Chung, L.W., Morokuma, K. 2011. Zinc-homocysteine binding in cobalamin-dependent methionine synthase and its role in the substrate activation: DFT, ONIOM, and QM/MM molecular dynamics studies. J Comput Chem. 32(15):3154-67

103. Heidarian, E., Amini, M., Parham, M., Aminorroaya, A.  2009. Effect of zinc supplementation on serum homocysteine in type 2 diabetic patients with microalbuminuria.  Rev Diabet Stud. 6(1):64-70.

104. Huang, R.F.S., Huang, S.M., Lin, B.S., Hung C.Y., Lu, H.T.  2002.  N-Acetylcysteine, Vitamin C and Vitamin E Diminish Homocysteine Thiolactone-Induced Apoptosis in Human Promyeloid HL-60 Cells.  J Nutr.  132(8):2151-2156.

105. Slyshenkov, V.S., Dymkowska, D., Wojtczak, L. 2004. Pantothenic acid and pantothenol increase biosynthesis of glutathione by boosting cell energetics.  FEBS Letters 569(1-3):169-172.

106. Lukienko, P.I., Mel’nichenko, N.G.,  Zverinskii, I.V., Zabrodskaya, S.V. 2000. Antioxidant properties of thiamine, Bulletin of Experimental Biology and Medicine. 130(9);874–876.

107. Takahashi, K., Newburger, P.E., Cohen, H.J. 1986.  Glutathione peroxidase protein. Absence in selenium deficiency states and correlation with enzymatic activity.  J Lin Invest. 77(4):1402-1404.

 

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 *These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.