Reply to Dr. Lonsdale

Townsend Letter for Doctors and Patients, August-Sept, 2004 by Traj P.S. Nibber

That benfotiamine is indeed taken up by cells and tissues more avidly than either thiamine itself or other allithiamines is demonstrated not only by the many clinical and experimental studies which clearly show the superiority of benfotiamine to thiamine in correcting diabetic nerve and kidney dysfunction, but also by direct pharmacokinetic studies documenting its higher accumulation and retention within cells and tissues after both oral and intravenous administration (which latter eliminates the confounding factor of absorption in the GI), and its especially selective incorporation into neural tissue. On these points, see studies reviewed by Loew (2); see also many subsequently-published original investigations. (3,8-12) In the present context, Greb and Bitsch's study (12) is of special interest, because it compared benfotiamine to TTFD (which Dr. Lonsdale appears to favor) and thiamine disulfide. These investigators found that benfotiamine was more bioavailable and bioactive than the other two supplements, not only in increasing plasma thiamine levels, but also in raising levels within red blood cells and in increasing biological activity as assessed by absolute transketolase activity.

Finally, Dr. Lonsdale states that "The prosthetic group from BTMP has not, to my knowledge, been studied" and that this bears on benfotiamine's ability to assist in the excretion of heavy metals. In fact, both sides of this issue have been addressed, both in studies evaluating the metabolism of benfotiamine itself and of its first metabolite, S-benzoylthiamine, (4,13) and in a study directly showing that benfotiamine increases excretion of tissue cadmium stores. (14)

I trust that this information satisfactorily addresses Dr. Lonsdale's questions. Extensive information on benfotiamine is also available on our website at www.AOR.ca.

References

1. Stracke H, Lindemann A, Federlin K. A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.

2. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.

3. Hilbig R, Rahmann H. Comparative autoradiographic investigations on the tissue distribution of benfotiamine versus thiamine in mice. Arzneimittelforschung. 1998 May;48(5):461-8.

4. Ziems M, Netzel M, Bitsch I. Biokinetic parameters and metabolism of S-benzoylthiamine-O-monophosphate. Biofactors. 2000;11(1-2):109-10.

5. Centerwall BS, Criqui MH. Prevention of the Wemicke-Korsokoff syndrome: a cost-benefit analysis. N Engl J Med. 1978 Aug 10;299(6):285-9.

6. Price J, Theodoros MT. The supplementation of alcoholic beverages with thiamine--a necessary preventive measure in Queensland? Aust NZ J Psychiatry. 1979 Dec;13(4):315-20.

7. Loew D. Development and Pharmacokinetics of Benfotiamine In Gries FA, Federlin K. Benfotiamin in the Therapy of Polyneuropathy. New York: Georg Thieme Verlag, 1998; 19-27.

8. Karpov LM, Rozanov Ala, Filippova TO. Characteristic features of 35S-benzoylthiamine monophosphate in albino mice. Vopr Med Khim. 1986 Jul-Aug; 32(4):136-9.