Is Folate inhibiting Thiamine (B-1) ?

[aquariusgirl]

I am sorry....but do we kniw why this B1dependent enzyme PDH goes down or gets blocked ?whats depleting the B1? Tnx

 

[Gondwanaland]

I am sorry....but do we kniw why this B1dependent enzyme PDH goes down or gets blocked ?whats depleting the B1? Tnx

Good question with many possible answers. Glycation? MMP-9?

 

[aquariusgirl]

So we don't know?

 

[alicec]

I am sorry....but do we kniw why this B1dependent enzyme PDH goes down or gets blocked ?whats depleting the B1? Tnx

Fluge and Mella showed there is an upregulation of pyruvate kinases which inhibit PDH. The reason for this is presently unknown.

 

[tango]

Sheep study that shows copper influences level of blood thiamine

http://pubs.aic.ca/doi/abs/10.4141/cjas91-096

Thank you! I think this could be relevant for me.

I got dysautonomia after taking progesterone and followed that with a stint on the Walsh protocol and high doses of Zinc. I'm coming to the conclusion that thiamine deficiency could be a factor in my dysautonomia (Marrs and Lonsdale have written a very expensive book on the subject) and it appears that both progesterone and Zinc could have contributed to interfering with both thiamine stores and my body's ability to convert thiamine to active forms and transport it where needed.

 

[liverock]

@alethea

only the western medical complex weren't in the back pocket of the drug companie$ perhaps we'd be seeing more serious research into Alzheimer's & thiamine ..... B1 being necessary for pyruvate / Krebs / citric acid cycle and Az being akin to a kind of loss of glucose metabolism in the brain .... Makes even an English major go Hmmmmmmm.......
Sulbutiamine looks highly promising but seems to build tolerance and lose efficacy in just a matter of days. Is there a way around this? https://www.amazon.com/Sulbutiamine...8&qid=1501049799&sr=1-4&keywords=sulbutiamine

Don't despair, these are before and after pet scans of the brains of patients after Benfotiamine was used in a small scale recent Alzheimer's trial.
( red&yellow show highest active areas)

A bigger trial using higher patient numbers is in progress and still recruiting.

http://knowledgeofhealth.com/put-stop-to-insanity-of-alzheimers-disease-treatment/#more-1633

 

[tisho23]

After reading thie link ......on this thread about the sheep ..I took my B1 & my MITOSYNERGY copper together. Seems to work,...early days though .....& suddenly I want folate....well isn't that cool?


I suspect that the copper transporter in the gut is deregulated or down regulated.

Hello. Can you please share more about the Cu+Thiamine ? How was it different thatn the straight thiamine? What else did you notice except the folate cravings Thanks

 

[Eastman]

More on benfotiamine and Alzheimer's, albeit on mice.

Benfotiamine Treatment Activates Nrf2/ARE Pathway and is Neuroprotective in a Transgenic Mouse Model of Tauopathy

Abstract

Impaired glucose metabolism, decreased levels of thiamine (vitamin B1) and its phosphate esters, and downregulated activity of thiamine-dependent enzymes, such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase have been linked to Alzheimer’s disease (AD). Thiamine-deficient mice exhibit increased amyloid deposition, tau hyperphosphorylation, and oxidative damage1. Experimental evidence has shown that benfotiamine (BFT), a synthetic S-acyl derivative of thiamine, rescued cognitive deficits and reduced amyloid burden in APP/PS1 mice2. We investigated whether BFT confers neuroprotection against tau phosphorylation and the generation of neurofibrillary tangles (NFTs) ‒ which causes frontotemporal dementia in humans ‒ in a mouse model of tauopathy. Exposure to BFT resulted in increased lifespan, behavioral improvement, reduced and glycated tau and NFTs, and prevented neuronal death in P301S transgenic (TG) mice. In addition, BFT administration significantly ameliorated mitochondrial dysfunction, attenuated oxidative damage, and decreased the expression of several pro-inflammatory mediators, consistent with a possible activation of the Nrf2/ARE neuroprotective pathway. Accordingly, we found that BFT (but not thiamine) triggers the expression of Nrf2/ARE-dependent genes in wild-type (WT) but not in Nrf2-deficient fibroblasts. Our findings suggest that BFT is a promising therapeutic agent for the treatment of tauopathies.

But back on topic.

Effects of a Folic Acid 5 Mg Daily Intervention on Markers of Vitamin B Status and Kynurenine Pathway

Abstract
Background

In Brazil, most folic acid (FA) containing supplements contain 5 mg FA. This dose is usually prescribed for patients with chronic hemolytic anemia and for women planning pregnancy. The effects of high FA doses on vitamin B1, B2 and B6 status including the kynurenine pathway are still unclear.

Aims

To assess the effects of a daily intervention with 5 mg FA in healthy subjects on vitamins B1, B2 and B6 serum marker status and serum concentration ok kynurenines.

Material and Methods

Thirty health subjects participated in a 5 mg/day FA intervention. Blood samples were obtained at baseline (D0) and after 45 (D45) and 90 days (D90) of intervention. We assessed serum concentrations of vitamin B6 (pyridoxal-5'-phosphate (PLP), pyridoxal (PL) and 4-pyridoxic acid (PA)), vitamin B2 (riboflavin and flavin mononucleotide (FMN)) and vitamin B1 vitamers (thiamine and thiamine monophosphate (TMP)), as well as tryptophan, kynurenine and several metabolites of tryptophan catabolism in the kynurenine pathway (3-hydroxykynurenine (HK), kynurenic acid (KA), anthranilic acid (AA), xanthurenic acid (XA), 3-hydroxyanthranilic acid (HAA), picolinic acid (Pic) and quinolinic acid (QA)) using LC-MS/MS. PA ratio (PAr) was calculated by PA/(PLP + PL). All variables were normalized by Box-Cox transformation. Comparisons were performed by repeated-measures ANOVA.

Results

Concentrations of all vitamin B6 vitamers (PLP, PL and PA), as well as PAr, were similar at baseline and D45 and D90 of FA intervention. No differences were found among serum vitamin B2 vitamers (riboflavin and FMN) after FA intervention. However, a trend for a decrease in serum TMP concentrations was observed at D90 (P = 0.054). No changes in serum tryptophan and all serum kynurenine pathway metabolites were observed after intervention with FA compared with baseline, except for AA, which was higher at D45 and D90 than baseline (P < 0.001).

Conclusion

Our data suggest that daily use of 5 mg FA by healthy subjects may interfere with vitamin B1 status markers. In addition, serum AA increased with FA intervention, which suggest that the use of high dose FA supplements might affect the kynurenine pathway.

 

[Saint George]

Can anyone comment on Andy cutlers views on TTFD here: (taken from onibasu wiki)

link: http://onibasu.com/wiki/TTFD

• Cutler speculates the hepatoxic effect of TTFD comes from the tetrahydrofurfuryl when it separates and becomes a mercaptan (single thiol). Due to its toxicity there is no reason to use it - http://onibasu.com/archives/am/106469.html

• TTFD does not have two sulfhydrl groups, it has a disulfide bond, not effective as mercury chelators - http://onibasu.com/archives/am/56724.html

• Disulfide bonds do not capture inorganic or organic mercury. If TTFD becomes a dimercaptan (dithiol, two sulfhydryls), it doesn't stay intact - http://onibasu.com/archives/am/106524.html

• Why Cutler thinks the real adverse reaction rate is around 20% or higher, based on multiple populations. Explains how sample bias results in TTFD advocates (specifically Derek Lonsdale) understating adverse reaction rates. Adverse reactions generally relate to liver issues (liver damage) - http://onibasu.com/archives/am/101501.html

• No clear benefit to using TTFD, Lonsdale's own data shows no increased heavy metal excretion, and plenty of risks - http://onibasu.com/archives/am/101623.html

• No reason to use TTFD as a Vitamin B1 alternative. Benfotiamine is a much better choice - http://onibasu.com/archives/am/116173.html

• Analysis of Lonsdale's paper showing that the data cannot support the conclusions - http://onibasu.com/archives/am/116222.html and http://onibasu.com/archives/am/120510.html

• Benfotiamine is already phosphorylated once, thiamine needs to be phosphorylated twice in the body to be useful. Phosphorylating is not easy for the body so benfotiamine has an advantage over thiamine. TTFD needs to be phosphorylated twice. Regression from using TTFD is consistent with liver damage but not all kids show elevated liver enzymes - http://onibasu.com/archives/am/116239.html

He seems to argue against Derek lonsdale, a big proponent of ttfd, and cautions supplementing with ttfd due to its heptotoxic effects. He suggests benfotiamine as a better alternative.

On another note, I am using source naturals b1 sublingual to help with my current beri-beri. I have noticed that it has raised my serum levels of b1, but does not alleviate the neuropathy associated with beriberi as much as the benfotiamine does.

Can you tell me why Allithiamine / TTFD would possibly be harmful to the liver? That doesn't make much sense and your source has virtually zero information and there are no other online sources I can find that describe thiamine or TTFD having any negative effects on the liver?

 

[dannybex]

Can you tell me why Allithiamine / TTFD would possibly be harmful to the liver? That doesn't make much sense and your source has virtually zero information and there are no other online sources I can find that describe thiamine or TTFD having any negative effects on the liver?

@alicec basically answered this on the previous page. And worth noting in her answer is this quote:

"Cutler has advanced the theory that the reason for the adverse reaction is the toxicity of the tetrahydrofurfuryl group. He weaves this in to his own narrative and pet theories by claiming the presence of a free thiol is the issue."

Also worth noting is the fact that Cutler died from atherosclerosis and hypertension in 2017 at only 60 years old. Not trying to bash the man at all, but just pointing out the fact that there's a long, long history of health gurus dying surprisingly young -- and Cutler was unfortunately one of the latest. These people are often looked at almost as 'gods' -- and their words taken as fact -- when in fact of course they're only human.

http://cutlersuccessstories.weebly.com/andy-cutler-legacy.html

 

[dannybex]

Also, this study showed that allithiamine helped patients with Wernicke's encephalopathy, which can sometimes be due in part to liver problems. I couldn't find anything that suggested TTFD causing liver problems.

https://www.jstage.jst.go.jp/article/jnsv1973/22/Supplement/22_Supplement_63/_article/-char/ja/

 

[Saint George]

I usually have mildly elevated liver enzymes with my blood work, in part due to lifestyle amongst some SNPs. Thiamin HCL has done nothing to raise my functional B1 status, and I have been feeling so much better on either benfotiamine or allithiamine (both seem to work). Thus, I was excited by these fat soluble solutions at their ability to help correct blood sugar drops. When I read the comment about possible liver damage, it was very disheartening.

Thanks @dannybex !