Believe it or not, your body is producing poisons at this very moment. And while they may be a natural part of aging, they’re also very, very damaging. In fact, advanced glycation end products (AGEs)—toxic molecules formed through a series of haywire reactions between sugar, proteins and lipids—are directly involved in just about every disease of aging imaginable.1–11
Research shows that, among diabetics, AGEs are the main culprit behind aging that’s accelerated a full 20 to 40 years faster than non–diabetics—taking the form of conditions like arterial plaque and hardening of arteries, kidney disease, retinopathy and peripheral nerve damage.12 But even non–diabetics need to watch out for these dangerous byproducts, as your levels only increase with age, and pave the way to any number of other serious diseases—including Alzheimer’s disease, arthritis and macular degeneration.
The good news is that there’s a way to block and even reverse the damage these AGEs can cause—and a single B vitamin may be your secret weapon.13
In recent years, scientists have discovered that benfotiamine—a synthetic, fat–soluble form of thiamine, or vitamin B1—is a potent AGE blocker. In fact, clinical studies show that this form of the vitamin is as much as 430 percent more bioavailable than its water–soluble counterpart, which has a modest absorption rate of only four to six percent.14–16
This superior absorption rate offers one reason for the powerful protection benfotiamine offers against AGEs—a benefit that’s been borne out in a number of animal and human studies. In one study, for example, researchers found that type 1 diabetics given 600 mg of benfotiamine daily experienced a 40 to 62 percent drop in just four weeks of levels of carboxymethyllysine (CML) and methylglyoxal — two predominant AGEs implicated in Alzheimer’s disease, blood vessel complications and atherosclerosis.17
Further trials show that supplementing with benfotiamine can also significantly reduce pain associated with diabetic neuropathy (that is, peripheral nerve damage), while helping to regulate heartbeat—results that don’t correspond to standard B–complex supplementation.18–19 And finally, animal studies suggest that benfotiamine offers critical protection against diabetic retinopathy, too.
In a 36–week study of three groups of rats—two of which were diabetic or hyperglycemic, along with one set of healthy controls—researchers found that rats receiving benfotiamine had retinas as healthy as controls by the end of the study. Those diabetic rats that did not receive benfotiamine, however, suffered severely damaged retinal blood vessels as a result.20
The bottom line: Even if you’re already taking a B–complex, adding an additional daily dose of benfotiamine—readily available in capsule form through Vitamin Research Products—can provide a critical extra layer of protection against AGE damage at any age.
References:
1.Metz T et al. Pyridoxamine, an inhibitor of advanced glycation and lipoxidation reactions: a novel therapy for treatment of diabetic complication. Arch Biochem Biophys 2003, 419:41–49.
2. Anderson M, Heinecke J. Production of N–epsilon–(carboxymethyl)–lysine is impaired in mice deficient is NADPH oxidase. Diab 2003, 52:2137–43.
3. Zieman S, Kass D. Advanced glycation end product cross–linking: pathophysiologic role and therapeutic target in cardiovascular disease. Congest Heart Fail 2004, 10:144–49.
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10. Nagariaji R. et al. Pyradoxamine inhibits alpha–dicarbonyl–www.ed modifications of lens proteins in diabetic rats. Invest Ophthalmol Vis Sci 2002, 43:E–abstract 2382.
11. Alderson N et al. The AGE inhibitor pyridoxamine inhibits lipemia and development of renal and vascular disease in Zucker obese rats. Kidney Int 2003, 63:2123–33.
12. Karachalias N et al. Accumulation of fructosyl–lysine and advanced glycation end products in the kidney, retina and peripheral nerve of streptozotocin–induced diabetic rats. Biochem Soc Trans 2003, 31:1423–25.
13. Babaei–Jadidi R et al. Prevention of incipient diabetic neuropathy by high–dose thiamine and benfotiamine. Diab 2003, 52:2110–20.
14. Woelk H et al. Benfotiamine in treatment of alcoholic polyneuropathy: an 8–week randomized controlled study (BAP I study). Alcohol Alcoholism 1998, 33:631–38.
15. Frank T et al. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfotiamine. Eur J Clin Pharmacol 2000, 56:251–57.
16. Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther 1998, 36:216–21.
17. Lin J et al. Benfotiamine inhibits intracellular formation of advanced glycation end products in vivo. Diab 2000, 49 (suppl 1): A143.
18. Sadekov R. et al. Diabetic polyneuropathy treatment by milgamma–100 preparation. Zh Nevrol Psikhiatr Im S S Korsakova 1998, 98:30–32.
19. Simeonov S et al. Therapeutic efficacy of “Milgamma” in patients with painful diabetic neuropathy. Folia Med (Plovdiv) 1997, 39:5–10.
20. Hammes H et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med 2003, 9:294–99.
