I am stuck on the simplicity and logic of PD being a symptom of a nutritional collapse with regard to thiamin. And while current studies continue to expound on the link between PD and diabetes, check out this article that says diabetes just might be caused by a thiamin deficiency:

http://link.springer.com/article/10....592-008-0042-y where it says:

"...Lack of thiamine or defects in its intracellular transport can cause a number of severe disorders. Thiamine acts as a coenzyme for transketolase (TK) and for the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism. In particular, TK is able to shift excess fructose-6-phosphate and glycerhaldeyde-3-phosphate from glycolysis into the pentose-phosphate shunt, thus eliminating these potentially damaging metabolites from the cytosol. Diabetes might be considered a thiamine-deficient state, if not in absolute terms at least relative to the increased requirements deriving from accelerated and amplified glucose metabolism in non-insulin dependent tissues that, like the vessel wall, are prone to complications. A thiamine/TK activity deficiency has been described in diabetic patients, the correction of which by thiamine and/or its lipophilic derivative, benfotiamine, has been demonstrated in vitro to counteract the damaging effects of hyperglycaemia on vascular cells..."

http://www.ncbi.nlm.nih.gov/pubmed/21564442:

"Abstract

Despite the targeting of traditional risk factors for cardiovascular disease, disease burden has not been completely eliminated. Thiamine is an essential cofactor in carbohydrate metabolism and individuals with diabetes are thiamine deficient. The pathophysiology of recognised complications of thiamine deficiency is similar to that underlying atherosclerosis and the metabolic syndrome, namely oxidative stress, inflammation and endothelial dysfunction. This review examines the mechanisms by which thiamine deficiency occurs in individuals with diabetes, how this deficiency leads to hyperglycaemic-induced damage, and the effect of thiamine replacement on vascular disease, endothelial function and oxidative stress. Thiamine administration can prevent the formation of harmful by-products of glucose metabolism, reduce oxidative stress and improve endothelial function. The potential benefit of long-term replacement in those with diabetes is not yet known but may reduce cardiovascular risk and angiopathic complications...."

I have to wonder why in the world every diabetic patient is not told to make sure they are getting a hefty dose of thiamine every day, but I have never heard of it ever being mentioned

Not only a connection between thiamin deficiency and diabetes, but also mitochondrial dysfunction, Alzheimer's, to name a few...

http://lpi.oregonstate.edu/infocenter/vitamins/thiamin/

Scroll down to the "Disease Prevention" (yes, it says prevention, not treatment) section and you see this under Diabetes:

:...In a randomized, double-blind pilot study, high-dose thiamin supplements (300 mg/day) were given for six weeks to hyperglycemic individuals (either glucose intolerant or newly diagnosed with type 2 diabetes). Thiamin supplementation prevented any further increase in fasting glucose and insulin levels compared with placebo treatment but did not reduce the hyperglycemia (36). However, one study suggested that thiamin supplementation might improve fasting glucose levels in type 2 diabetics in early stages of the disease (i.e., pre-diabetes or early diabetes) (37)...."

And under the "Disease Treatment" section they list Alzheimer's and have this to say, in part:

"...Thiamin deficiency has been linked to increased beta-amyloid production in cultured neuronal cells and to plaque formation in animal models (57, 58). These pathological hallmarks of AD could be reversed by thiamin supplementation, suggesting that thiamin could be protective in AD. Moreover, other disorders including mitochondrial dysfunction and chronic oxidative stress have been linked to both thiamin deficiency and AD pathogenesis and progression (9, 59). ..."

It seems that our ability to absorb nutrients from the gut declines with age naturally, which would explain why PD and Alz. used to be seen primarily in the elderly populations. http://www.jbc.org/content/142/1/239.full.pdf ("reduced function of the alimentary tract is a common attribute of thiamine deficiency...")

I am wondering whether, with with our lousy diet and rampant antibiotic use, we have wrecked our gut biome and ability to absorb critical nutrients, and thus see younger and more people suffering from the collective symptoms known as PD, dementia, Alz., etc. We know there is reduced glucose metabolism in Alz, it can actually be seen. Many brave scientists have been calling Alz. a third type of diabetes, a diabetes of the brain, and now it looks like more and more PD research is heading the same direction.

The link below is an excellent slideshow. Here are some highlights, but you really should go through it yourself, it's only 41 slides and very well done. It actually has slideshows on several vitamins, worth looking at. Here are some highlights from the thiamin slideshow, with regard to nerves:

1. thiamin it phosphorylates/activates a chloride channel in the nerve membrane (remember the PD calcium channel blocker drugs in trial not so long ago?) and

2. it appears to have a role in axonal conduction, PARTICULARLY with regard to serotoninergic and acetyl cholinergic neurons.

3. because the brain and heart use so much thiamin, they are most affected by a deficiency.

4. a deficiency means the brain cannot efficiently metabolize pyruvate normally and must go through an extra step using lactate first

5. insufficient thiamin translates into reduced regeneration of glutathione which increases oxidative stress

Many of these have been implicated in PD (and PD symptoms).

from: http://www.slideshare.net/namarta28/thiamine

Thiamine deficiency has been documented in adults with diabetes and in a single report of reversible encephalopathy in a child with diabetic ketoacidosis. In children who present with severe diabetic ketoacidosis, one of the most serious complications is cerebral edema of which the primary symptom may be encephalopathy. Thiamine deficiency in other disease states has been clearly linked with acute encephalopathy, but there are no data on thiamine status in children with diabetic ketoacidosis. This study describes the prevalence of thiamine deficiency in children with type 1 diabetes mellitus who present with diabetic ketoacidosis and are admitted to the ICU.

http://www.ncbi.nlm.nih.gov/pubmed/25560422

http://www.ncbi.nlm.nih.gov/pubmed/24550684

Thiamine Deficiency in Diabetes

https://www.youtube.com/watch?v=UNRaFjdeuZk

Thank you so much Lurking & Zanpar for all of these wonderful posts.

I, too, have been thinking so much about the possible thiamine connection - I've just been to busy lately to do any online digging on the subject. So I really appreciate that you've done it! It's all so interesting - especially the gut/absorption connection, and all the side effects of being deficient.

I've ordered a bottle of thiamine, I'm taking 250mg 2x per day. I'm not sure if this will be absorbed, but I'm giving it the experimental try!

Thank you!

I've been taking benfotiamine 250mg once per day for 2 days now and so far I've noticed that my restless leg seems to have disappeared. It's still too early to tell but so far so good. Thiamine didn't do anything for me for a week or so. Benfotiamine is fat soluable so it gets into cells and is absorbed much more than Thiamine.

Can you tell us how/where you got it? Is it OTC and if so, what brand? Hope your improvement continues

lef.org

Thanks. Best wishes to you as well.