Continuing the discussion from Thiamin, Vitamins and Derrick Lonsdale:
Thanks again for the informative and detailed reply. One small comment for now:
I googled a bit for TTFD and came across a post, which I didn’t realize immediately realize was written by Lonsdale. Quote:
Although the arrangement of the atoms is different from the thiamine diagram, the important thing to notice is that the thiazole ring (right side) has been opened, creating a disulfide, including what is known as a prosthetic attachment (the part attached to the disulfide). A disulfide is easily reduced (S-S becomes SH) when the molecule comes into contact with the cell membrane. The result is that the prosthetic group is removed and left outside the cell. The remainder of the molecule passes through the cell membrane into the cell. The thiazole ring closes to provide an intact thiamine molecule in the cell. It is inside the cell where thiamine has its activity and so this is an important method of delivering it to where it is needed. It is this ability to pass through the lipid barrier of the cell membrane that has caused allithiamine to be called fat-soluble. It only refers to this ability, however. It is soluble in water and can be given intravenously.
This “fat solubility” is extremely important because dietary thiamine has to be attached to a genetically determined protein, known as a transporter, to gain entry to cells. There are known to be diseases where the transporter is missing. Affected individuals have thiamine deficiency that does not respond to ordinary thiamine and are usually misdiagnosed. Therefore, a disulfide derivative that does not need the transporter is a method by which thiamine can be introduced to the cell when the transporter is missing. There is no difference between allithiamine and thiamine from a biological activity standpoint. It is this ability to pass the active vitamin through the cell membrane into the cell that provides the advantage.
I performed animal and clinical studies with thiamine tetrahydrofurfuryl (TTFD) for many years and found it to be an extremely valuable therapeutic nutrient. Any disease where energy deficiency is the underlying cause may respond to TTFD, unless permanent damage has accrued. Dr. Marrs and I believe that energy deficiency applies to any naturally occurring disease, even when a gene is at fault. For example, Japanese investigators found that TTFD protected mice from cyanide and carbon tetrachloride poisoning, an effect that was not shown by ordinary thiamine (Fujiwara, M. Absorption, excretion and fatal thiamine and its derivatives in the human body. In Shimazono, N, Katsura, E, eds. Beriberi and Thiamine. (pp 120-121) Tokyo, Igaku Shoin Ltd. 1965). They exposed a segment of dog’s intestine, disconnected it from its nerve supply and found that one of the disulfide derivatives stimulated peristalsis (the wavelike movement of the intestine). It is more than likely that TTFD could be used safely in patients with post operative paralysis of the intestine (paralytic ileus).
Sounds like he thinks using TTFD specifically can make an importance difference in certain cases, though knowing whether one falls into the category of potential beneficiaries of TTFD versus a different form of thiamine would require way more knowledge than I have. I will likely try reading his book.