Benfotiamine

Benfotiamine Common Name

Benfotiamine

Top Benefits of Benfotiamine

  • Supports energy metabolism*
  • Supports antioxidant defenses*
  • Supports brain function*
  • Supports the protection of organs and systems*

What is Benfotiamine?

Benfotiamine is a lipid derivative of thiamine (vitamin B1). Unlike the commonly used forms of vitamin B1 used in dietary supplements (thiamine HCL) and food fortification (thiamine mononitrate), which are water-soluble, benfotiamine is fat-soluble (i.e., dissolves in fat). This makes it more bioavailable, which results in higher levels of thiamine in peripheral tissues such as muscle, brain, liver, and kidney.(1) In these and other peripheral tissues, benfotiamine has the same functions as other sources of thiamine. These include playing a central role in the metabolism of sugars, proteins, and fats, and is instrumental in several important processes needed to make cellular energy.

Neurohacker’s Benfotiamine Sourcing

Benfotiamine is a fat-soluble derivative of vitamin B1 (thiamine). It can produce higher tissue levels of thiamine in peripheral tissues than water-soluble forms of thiamine.(2) 

Benfotiamine is additive with Thiamine—both have vitamin B1 activity. But, because of FDA labeling regulations, benfotiamine can not be listed on labels as having a daily value or contributing to vitamin B1 activity.

Benfotiamine sourcing is focused on identifying and purchasing from a reputable supplier and ensuring the benfotiamine is NON-GMO, gluten-free and vegan.

Benfotiamine Dosing Principles and Rationale

In general, we use a dose of benfotiamine that’s been shown to support metabolism of sugars through the key pathways where thiamine activity is critical (glycolysis and pentose phosphate pathway). This doses provides substantial thiamine activity in peripheral tissues. In general, benfotiamine has increased vitamin B1 activity in peripheral tissues like the brain, heart, liver, and muscles, but wouldn’t be expected to have as much activity in the stomach or intestines. If our formulation targets brain function, we don’t combine benfotiamine with thiamine HCL. If our formulation’s goal is to support all tissues (including stomach and intestines) we combine a small amount of thiamine HCL with benfotiamine. This captures the increased bioavailability in peripheral tissues that benfotiamine offers, while also getting the stomach/intestine vitamin B1 support from the thiamine HCL.

Benfotiamine Key Mechanisms 

Energy metabolism

  • Supports energy generation (ATP production) from carbohydrate metabolism (3)
  • Upregulates glucose oxidation (4)

Cofactor in the pyruvate dehydrogenase complex

  • Thiamine pyrophosphate (TPP) is required as a cofactor in the E1 subunit of the pyruvate dehydrogenase (PDH) complex (3)
  • TPP is essential for the generation by the PDH complex of acetyl-CoA, used in the citric acid cycle to generate ATP (3)
  • TPP is essential for the generation by the PDH complex of nicotinamide adenine dinucleotide (NADH), required for the production of ATP (3)

Cofactor in the citric acid cycle

  • TPP is required as a cofactor in the alpha-ketoglutarate dehydrogenase reaction of the citric acid cycle (conversion of alpha-ketoglutarate to succinyl-CoA) (3)
  • TPP is essential in propagating the citric acid cycle to generate ATP (3)

Cofactor in the pentose phosphate pathway

  • TPP is required as a cofactor in the transketolase reaction of the pentose phosphate pathway (PPP) (3)
  • The PPP provides nicotinamide adenine dinucleotide phosphate (NADPH), used in several biochemical pathways such as in steroid, fatty acid, amino acid, neurotransmitter, and glutathione synthesis (3)
  • The PPP provides ribose-5-phosphate, an essential building block in nucleic acids (3)
  • Ribose-5-phosphate can enter the non-oxidative phase of the PPP where transketolase and TPP help transform ribose-5-phosphate back into glycolysis intermediates (such as glucose-6-phosphate) (3)

Antioxidant defenses

  • Participates in the synthesis of NADPH to be used in the recycling of the antioxidant glutathione (GSH) (3)
  • Replenishes glutathione levels (5, 6)
  • Downregulates oxidative stress (7–9)

Brain function

  • Essential for the production by the pyruvate dehydrogenase complex of acetyl-CoA used for the production of acetylcholine (3)
  • The alpha-ketoglutarate dehydrogenase reaction of the citric acid cycle reaction has a role in maintaining glutamate and gamma-aminobutyric acid (GABA) levels (3)

Protection of organs and systems

  • Supports the metabolism of sugars and protects from the accumulation of advanced glycation end-products (AGEs) (7, 9–14)
  • Protects cardiac structure and function (6, 9, 10, 15)
  • Protects vascular structure and function (7, 12, 16–18)
  • Protects kidney structure and function (13, 14)

REFERENCES

1. Scientific Opinion of the Panel on Food Additives and Nutrient Sources added to Food (ANS), The EFSA Journal. 864, 1–31 (2008).
2. D. Loew, Int. J. Clin. Pharmacol. Ther. 34, 47–50 (1996).
3. D. A. Bender, in Nutritional Biochemistry of the Vitamins (Cambridge University Press, 2003), pp. 148–171.
4. D. A. Fraser et al., Genes Nutr. 7, 459–469 (2012).
5. S. Wu, J. Ren, Neurosci. Lett. 394, 158–162 (2006).
6. A. F. Ceylan-Isik, S. Wu, Q. Li, S.-Y. Li, J. Ren, J. Appl. Physiol. 100, 150–156 (2006).
7. A. Stirban et al., Diabetes Care. 29, 2064–2071 (2006).
8. U. Schmid, H. Stopper, A. Heidland, N. Schupp, Diabetes. Metab. Res. Rev. 24, 371–377 (2008).
9. R. Katare et al., Cardiovasc. Res. 97, 55–65 (2013).
10. H. Ma et al., J. Cell. Mol. Med. 13, 1751–1764 (2009).
11. N. Karachalias, R. Babaei-Jadidi, C. Kupich, N. Ahmed, P. J. Thornalley, Ann. N. Y. Acad. Sci. 1043, 777–783 (2005).
12. H.-P. Hammes et al., Nat. Med. 9, 294–299 (2003).
13. L. P. Kihm et al., J. Am. Soc. Nephrol. 22, 914–926 (2011).
14. N. Karachalias, R. Babaei-Jadidi, N. Rabbani, P. J. Thornalley, Diabetologia. 53, 1506–1516 (2010).
15. R. G. Katare et al., Circ. Heart Fail. 3, 294–305 (2010).
16. Y. Du, A. Kowluru, T. S. Kern, Am. J. Physiol. Regul. Integr. Comp. Physiol. 299, R1610–7 (2010).
17. V. Marchetti et al., Diabetes. 55, 2231–2237 (2006).
18. A. Stirban et al., Int. J. Vasc. Med. 2012, 968761 (2012).

*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.