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Life Extension Mix™ and Mitochondrial Energy Optimizer Now with Pyridoxamine

When sugars react with the body’s proteins, the result is the formation of non-functioning glycated structures called Advanced Glycation End Products.1 While glycation is a normal consequence of aging, it is far from desirable.2-5

The age-related reduction of visual acuity is a result, amongst other factors, of a lifetime of glycation reactions.6-8 Glycation is also associated with reduced arterial blood flow and long term kidney problems.9-11 The effect of glycation can be seen in the form of cross-linked proteins that accumulate in neurons, endothelial cells, eye lenses, and senescent skin.12-13

Collagen accounts for about a third of our total body proteins. Glycation-induced collagen cross-linking in vascular wall, skin, muscle, and organs throughout the body leads to the inelasticity of tissues that are characteristic of aging.14 Glycation in arterial walls appear to be an especially deleterious event, causing cross-linking of collagen molecules to each other and to circulating proteins. This leads to plaque formation and loss of vascular elasticity.

Similarity between cooked foods and aging

Glycation was first described in food products in the year 1912. When meat is cooked at high heat, particularly broiling and frying, rapid glycation or "browning" reactions occur as proteins interact with the sugars present. Advanced Glycation End Products (AGEs) from the diet can also be absorbed into our body, which make a significant contribution to the plasma and tissue pool of AGEs.

The same glycation process that takes place in cooked protein foods also happens at a slower rate to long-lived proteins of the body, such as collagen! This alarming phenomenon of our body slowly being cooked to death has motivated scientists to develop ways to block glycation reactions.

Anti-glycation nutrients

Life Extension members gained access to a validated anti-glycation agent when high-dose carnosine supplements first became available.15 Additional protection against glycation was shown in response to benfotiamine, a fat-soluble form of vitamin B1.16

For over a decade, however, governmental regulatory issues blocked access to one of the most important anti-glycation agents … a unique form of vitamin B6 called pyridoxamine.

You may wonder why supplementing with more than one anti-glycating agent is desirable. The direct answer is that there are many chemical processes involved in the formation of advanced glycation end products in the body.1-5, 17 By blocking multiple chemical “checkpoints” involved in glycation reactions, one can optimally slow this devastating degradation of our living proteins.

Pyridoxamine has been extensively studied and its multiple anti-glycation properties make it important to include in a science-based daily supplement program.17a, 18-20 Pyridoxamine has been added to two popular formulas that many Life Extension members use everyday as part of an anti-aging program!

Life Extension Mix™ Now with Pyridoxamine

A popular multi-nutrient formula long favored by Foundation members is Life Extension Mix. One reason so many people choose Life Extension Mix is the comprehensive blend of fruit and vegetable extracts it provides.

A unanimous recommendation of health experts is for Americans to consume more fruits and vegetables. Despite constant media publicity, the majority of us do not ingest enough of these plant foods each day.

Life Extension Mix provides 21 standardized fruit and vegetable extracts, along with high-potency vitamins, minerals and amino acids that form the cornerstone of a comprehensive health maintenance program. Life Extension Mix saves time and money by combining the most popular nutrients into one product, eliminating the need to take separate bottles of B-complex, vitamins C and E, minerals, and much more that would be required to achieve the same effects.The new Life Extension Mix contains 50 mg of pyridoxamine to help reduce glycation reactions in the body.

A keystone of a comprehensive supplement program, Life Extension Mix saves members money because it provides so many well-studied nutrients into one formula. If you are on a budget, the Life Extension Mix provides the best “cost-per-milligram” value.

With the addition of pyridoxamine, the new Life Extension Mix is now an even greater value. A complete description of the new Life Extension Mix formula.

Mitochondrial Energy Optimizer Now with Pyridoxamine

Some of the most serious consequences of aging occur with the onset of inflammation and mitochondrial energy depletion in our cells.21-25

All cells require healthy mitochondrial activity to perform life-sustaining metabolic processes.26 As mitochondrial function weakens, so does the vitality of organs such as the heart and brain, or in some cases, the entire body.27-32

Mitochondrial Energy Optimizer contains a new microencapsulated R-lipoic acid designed to provide optimal restoration of youthful mitochondria energy output, while guarding against the generation of toxic free radicals. R-lipoic acid is more effective than alpha lipoic acid 33-35 commonly sold by commercial supplement companies.

Mitochondrial Energy Optimizer contains only the superior “R” form of stabilized lipoic acid along with the most neurologically active form of the critical carnitine amino acid called acetyl-L-carnitine arginate.36-37

Low-level systemic inflammation is involved with virtually every undesirable consequence of aging. Mitochondrial Energy Optimizer provides the most potent flavonoid (luteolin) to suppress the type of persistent inflammatory reactions that most often occur as a result of “normal” aging.38-41

Anti-glycating nutrients such as high-dose carnosine and benfotiamine serve as a foundation for this advanced anti-aging formula. The new Mitochondrial Energy Optimizer contains 50 mg of pyridoxamine, making it the most comprehensive and cost-effective anti-glycation formulation anywhere.

References

1. DeGroot J. The AGE of the matrix: chemistry, consequence and cure. Curr Opin Pharmacol. 2004 Jun;4(3):301-5. Review.

2. Peppa M, Uribarri J, Vlassara H. Aging and glycoxidant stress. Hormones (Athens). 2008 Apr-Jun;7(2):123-32. Review.

3. Gasser A, Forbes JM. Advanced glycation: implications in tissue damage and disease. Protein Pept Lett. 2008;15(4):385-91.

4. Hyogo H, Yamagishi S. Advanced glycation end products (AGEs) and their involvement in liver disease. Curr Pharm Des. 2008;14(10):969-72. Review.

5. Susic D. Cross-link breakers as a new therapeutic approach to cardiovascular disease. Biochem Soc Trans. 2007 Nov;35(Pt 5):853-6. Review.

6. Gul A, Rahman MA, Salim A, et al. Advanced glycation end products in senile diabetic and nondiabetic patients with cataract. J Diabetes Complications. 2008 May 26. [Epub ahead of print]

7. Pawlak AM, Glenn JV, Beattie JR, et al. Advanced glycation as a basis for understanding retinal aging and noninvasive risk prediction. Ann N Y Acad Sci. 2008 Apr;1126:59-65.

8. Tezel G, Luo C, Yang X. Accelerated aging in glaucoma: Immunohistochemical assessment of advanced glycation end products in the human retina and optic nerve head. Invest Ophthalmol Vis Sci. 2007 Mar;48(3):1201-11.

9. Nazratun N, Mahmood AA, Kuppusamy UR, et al. Diabetes mellitus exacerbates advanced glycation end product accumulation in the veins of end-stage renal failure patients. Vasc Med. 2006 Nov;11(4):245-50.

10. Suliman ME, Stenvinkel P, Jogestrand T, et al. Plasma pentosidine and total homocysteine levels in relation to change in common carotid intima-media area in the first year of dialysis therapy. Clin Nephrol. 2006 Dec;66(6):418-25.

11. Sakata N, Imanaga Y, Meng J, et al. Increased advanced glycation end products in atherosclerotic lesions of patients with end-stage renal disease. Atherosclerosis. 1999 Jan;142(1):67-77.

12. Sell DR, Monnier VM. Conversion of arginine into ornithine by advanced glycation in senescent human collagen and lens crystallins. J Biol Chem. 2004 Dec 24;279(52):54173-84.

13. Ravelojaona V, Robert AM, Robert L. Expression of senescence-associated beta-galactosidase (SA-beta-Gal) by human skin fibroblasts, effect of advanced glycation end-products and fucose or rhamnose-rich polysaccharides. Arch Gerontol Geriatr. 2008 Jan 18.

14. Pageon H, Técher MP, Asselineau D. Reconstructed skin modified by glycation of the dermal equivalent as a model for skin aging and its potential use to evaluate anti-glycation molecules. Exp Gerontol. 2008 Jun;43(6):584-8.

15. Reddy VP, Garrett MR, Perry G, et al. Carnosine: a versatile antioxidant and antiglycating agent. Sci Aging Knowledge Environ. 2005 May 4;2005(18):pe12. Review.

16. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.

17. Nagai R, Fujiwara Y, Mera K, et al. Investigation of pathways of advanced glycation end-products accumulation in macrophages. Mol Nutr Food Res. 2007 Apr;51(4):462-7.

17a. Williams ME, Bolton WK, Khalifah RG, et al. Effects of pyridoxamine in combined phase 2 studies of patients with type 1 and type 2 diabetes and overt nephropathy. Am J Nephrol. 2007;27(6):605-14.

18. Padival S, Nagaraj RH. Pyridoxamine inhibits maillard reactions in diabetic rat lenses. Ophthalmic Res. 2006;38(5):294-302.

19. Waanders F, van den Berg E, Nagai R, et al. Renoprotective effects of the AGE-inhibitor pyridoxamine in experimental chronic allograft nephropathy in rats. Nephrol Dial Transplant. 2008 Feb;23(2):518-24.

20. Fujiwara Y, Kiyota N, Motomura K, et al. Some natural compounds enhance N epsilon-(carboxymethyl)lysine formation. Ann N Y Acad Sci. 2008 Apr;1126:152-4.

21. Szabó C. The pathophysiological role of peroxynitrite in shock, inflammation, and ischemia-reperfusion injury. Shock. 1996 Aug;6(2):79-88. Review.

22. Cuzzocrea S, Thiemermann C, Salvemini D. Potential therapeutic effect of antioxidant therapy in shock and inflammation. Curr Med Chem. 2004 May;11(9):1147-62. Review.

23. Vasto S, Carruba G, Lio D, et al. Inflammation, ageing and cancer. Mech Ageing Dev. 2008 Jul 10.

24. Müller-Werdan U. Inflammation and ageing. Z Gerontol Geriatr. 2007 Oct;40(5):362-5. Review.

25. Passos JF, von Zglinicki T, Kirkwood TB. Mitochondria and ageing: winning and losing in the numbers game. Bioessays. 2007 Sep;29(9):908-17.

26. Seidman MD, Khan MJ, Bai U, et al. Biologic activity of mitochondrial metabolites on aging and age-related hearing loss. Am J Otol. 2000 Mar;21(2):161-7.

27. Ames BN. Delaying the mitochondrial decay of aging. Ann N Y Acad Sci. 2004 Jun;1019:406-11.

28. Harman D. Free radical theory of aging: a consequences of mitochondrial aging. Age. 1983 6:86-94

29. Miquel J., Fleming JE. A two step hypothesis on the mechanisms of in vitro cell aging: cell differentiation followed by intrinsic mitochondrial mutagenesis. Exp Gerontol. 1984 19: 31-36

30. Shigenaga MK., Hagen TM., Ames BN., Oxidative damage and mitochondrial decay in aging. Proc Natl Acad Sci USA. 1994 91:10771-10778

31. Hagen TM., Yowe DL, Bartholomew JC., et al. Mitochondrial decay in hepatocytes from old rats: membrane potential declines, heterogeneity and oxidants increase. Proc Natl Acad Sci USA. 1997 94:3064-3069

32. Beckman KB., Ames BN., Mitochondrial aging: open questions. Ann NY Acad Sci. 1998; 854:118-127

33. Maitra I, Serbinova E, Tritschler HJ, et al. Stereospecific effects of R-lipoic acid on buthionine sulfoximine-induced cataract formation in newborn rats. Biochem Biophys Res Commun. 1996 Apr 16;221(2):422-9.

34. Hagen TM, Ingersoll RT, Lykkesfeldt J, et al. (R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate. FASEB J. 1999 Feb;13(2):411-8.

35. Hagen TM, Vinarsky V, Wehr CM, et al. (R)-alpha-lipoic acid reverses the age-associated increase in susceptibility of hepatocytes to tert-butylhydroperoxide both in vitro and in vivo. Antioxid Redox Signal. 2000 Fall;2(3):473-83.

36. Scorziello A, Meucci O, et al. Acetyl-L-carnitine arginine amide prevents beta 25-35-induced neurotoxicity in cerebellar granule cells. Neurochem Res. 1997 Mar;22(3):257-65.

37. Taglialatela G, Navarra D, Olivi A, et al. Neurite outgrowth in PC12 cells stimulated by acetyl-L-carnitine arginine amide. Neurochem Res. 1995 Jan;20(1):1-9.

38. Chen CY, Peng WH, Tsai KD, et al. Luteolin suppresses inflammation-associated gene expression by blocking NF-kappaB and AP-1 activation pathway in mouse alveolar macrophages. Life Sci. 2007 Nov 30;81(23-24):1602-14.

39. Harris GK, Qian Y, Leonard SS, et al. Luteolin and chrysin differentially inhibit cyclooxygenase-2 expression and scavenge reactive oxygen species but similarly inhibit prostaglandin-E2 formation in RAW 264.7 cells. J Nutr. 2006 Jun;136(6):1517-21.

40. Hougee S, Sanders A, Faber J, et al. Decreased pro-inflammatory cytokine production by LPS-stimulated PBMC upon in vitro incubation with the flavonoids apigenin, luteolin or chrysin, due to selective elimination of monocytes/macrophages. Biochem Pharmacol. 2005 Jan 15;69(2):241-8.

41. Kim JS, Jobin C. The flavonoid luteolin prevents lipopolysaccharide-induced NF-kappaB signaling and gene expression by blocking IkappaB kinase activity in intestinal epithelial cells and bone-marrow derived dendritic cells. Immunology. 2005 Jul;115(3):375-87.

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