Return to Main Page

Benfotiamine: Negotiating the fates of glucose‡

By Kelly Heim, Ph.D

As the principal fuel for cellular energy, glucose is essential for life. Like all nutrients, its abundance in cells must be maintained within healthy limits. With long-term ramifications extending to every organ-system, the body’s ability to handle glucose is a cornerstone of good health. When addressing glucose homeostasis in the clinic, establishing both short-term and long-term objectives can presage sustainable, systemic wellness. While numerous modalities exist for acute, postprandial glycemic control, the long-term health of glucose-sensitive tissues remains a critical consideration.

Throughout our lives, the nervous system, blood vessels, kidneys, and retinal epithelia, depend on a healthy balance of glucose to maintain normal function. When glucose is not utilized for energy, it is subject to a divergent fate that serves no energetic purpose. In a reaction known as glycosylation, glucose attaches to proteins to form advanced glycation end products (AGEs). In clinical practice, a familiar example is hemoglobin HbA1c, which serves as a biomarker of long-term glycemic control. HbA1c coexists with other AGEs arising from glucose derivatives and assorted proteins. Collectively, AGEs influence many aspects of tissue health through cytokine formation, redox balance and protein function.1

Glycosylation is part of the normal aging process. While consistent glycemic management offers the most powerful protection, more aggressive support may be indicated for peripheral nerve comfort and proper functioning of the vasculature. For these individuals, methylation cofactors, such as folate, vitamin B6 and vitamin B12 can offer significant benefit within several months.2 Thiamin, or vitamin B1, can deliver support in as little as 3 to 6 weeks.‡3-9

The body readily converts thiamin to the coenzyme thiamin diphosphate (TDP), a critical cofactor for the enzyme transketolase (Figure 1). Transketolase commits AGE precursors to alternative pathways that metabolize them to useful energetic intermediates. Animal and human studies have demonstrated protection of nerves and blood vessels as a result of this healthy metabolic shift.‡1,3-9

NewsCapsFigure 1. Thiamin readily converts to thiamin diphosphate (TDP), a cofactor for the enzyme transketolase (TK).  TK diverts AGE precursors to alternative metabolic pathways.‡

 

Contrary to initial expectations, neural and vascular protection with thiamin was modest, owing to the inherently poor bioavailability of thiamin. However, in 1997, researchers compared the bioavailability of thiamin with its lipid soluble analog, benfotiamine. Plasma levels following benfotiamine supplementation were 5-fold greater than levels attained with thaimin.10 In red blood cells, thiamine levels were 3.5 to 14.8 times higher in subjects receiving benfotiamine. Subsequent studies corroborated this remarkable pharmacokinetic performance. Measurable vascular and neurological outcomes were both clinically and statistically significant within 3 to 6 weeks at doses ranging from 200-600 mg per day.‡3-9

In any clinical context, benfotiamine repletes cellular thiamin more readily than the water-soluble form of the vitamin. BenfoMax provides 200 mg of BenfoPure® benfotiamine per capsule for vascular, nerve, retinal and renal applications. MethylAssist combines 75 mg BenfoPure® with the methylation cofactors Metafolin® L-5-methyltetrahydrofolate (L-5-MTHF), vitamin B12 (methylcobalamin), and activated vitamin B6 for cardiovascular and neurological applications. As part of a comprehensive approach to glycemic control, these new options deliver ingredients with excellent tolerability at clinically validated doses for the most reliable and sustainable support.‡

References

  1. Balakumar P, Rohilla A, Krishan P, et al. The multifaceted therapeutic potential of benfotiamine. Pharmacol Res. 2010, 61(6):482-488.
  2. Farvid MS, Homayouni F, Amiri Z, Adelmanesh F. Improving neuropathy scores in type 2 diabetic patients using micronutrients supplementation. Diabetes Res Clin Pract. 2011, 93(1):86-94.
  3. Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003, 52(8):2110-2120.
  4. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003, 9(3):294-249.
  5. Haupt E, Ledermann H, Köpcke W. Benfotiamine in the treatment of diabetic polyneuropathy–a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther. 2005, 43(2):71
  6. Winkler G, Pál B, Nagybéganyi E, et al. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999, 49(3):220-224.
  7. Fraser DA, Hessvik NP, Nikolić N, et al. Benfotiamine increases glucose oxidation and downregulates NADPH oxidase 4 expression in cultured human myotubes exposed to both normal and high glucose concentrations. Genes Nutr. 2012, 7(3):459-469.
  8. Schupp N, Dette EM, Schmid U, et al. Benfotiamine reduces genomic damage in peripheral lymphocytes of hemodialysis patients. Naunyn Schmiedebergs Arch Pharmacol. 2008, 378(3):283-91.
  9. Stracke H, Gaus W, Achenbach U, et al. Benfotiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study. Exp Clin Endocrinol Diabetes. 2008, 116(10):600-5.
  10. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol. 1997, 52(4):319-20.