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Pyruvate dehydrogenase function depends on thiamine (B1)

Asklipia

Senior Member
Messages
999
I have just received the results of our vitamin D test.
Over the last year, the weather has been horrible, and for other reasons we have not been in the sun at all. No vitamin D supplementation either.
Vitamin D 25-OH D3 :
for me last year 29, last week 35
for DH last year 28, last week 17

We both take the same supplements, but he does not take so much thiamine.
For both of us, it is impossible to find a symptom in the list provided by the laboratory for their statistics.

Maybe thiamine does something good to the vitamin D.
 

JasonUT

Senior Member
Messages
303
Any new experiences with Lipothiamine or Allithiamine? I am about to embark on the Lonsdale protocol for repleting Thiamine using Lipothiamine, magnesium and B-complex.

The paradox that he speaks of scares me. Like others I seem to be very sensitive to supplements and meds.
 

JasonUT

Senior Member
Messages
303
Another line of thought for me is that B vitamins are extremely sensitive to light. Blue light I learnt at school (maybe wrong? That was 50 years ago... ) destroys thiamin. A lot of lights inside the house and computer screens etc emit blue light. Outside UV and inside blue light, maybe it does take thiamin supplementation several times a day in small doses to feel normal.

@Asklipia Do you have any more background or research on this thought?
 

Asklipia

Senior Member
Messages
999

JasonUT

Senior Member
Messages
303
@Asklipia
@Chocolove

Lonsdale Protocol:
  1. Slowly titrate Lipothiamine from 50 mg to as much as 400 mg per day in divided doses. Differs by patient. I don't know how you decide the correct upper dose or titration rate.
  2. Take multi and B-complex
  3. At least 300 mg of magnesium.
Mg and B1 study by Lonsdale - Link
Lonsdale Testing - Link
Paradox 1 - Link
Paradox 2 - Link

I'd love to hear more stories about allithiamine and lipothiamine if there are any out there.

I tried searching for UV and blue light connection to Thiamine, but was not very successful. Maybe my googling skills aren't that good.
 

Asklipia

Senior Member
Messages
999
@JasonUT
I did a bit more googling for you, and found these lines in the new book by Dr Lonsdale & Dr Marrs, just published last week at Elsevier "Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition"
In page XV of the introduction
"We know from history (9) that a group of Japanese workers would develop the first symptoms of beriberi together when suddenly exposed to sunlight. This observation had misled the early investigators who were trying to elucidate the cause of this ancient scourge that had affected people for thousands of years. Because several individuals succumbed to the first symptoms of the disease concurrently, they concluded that the cause was a mysterious infection. Since we now know that the disease is caused by thiamine deficiency, we have to conclude that the exposure to the ultraviolet light acted as a stress factor and precipitated the disease in marginally malnourished individuals."
(9) Inouye K, Katsura E,. Etiology and pathology of beriberi. In : Shimazono N, Katsura E, editors, Thiamine nd beriberi, Tokyo: Igaku Shoin Ltd, 1965, p. 1-28.
 

Asklipia

Senior Member
Messages
999
More of the same, p. 2:
Of considerable interest to us today is that the peak incidence of beriberi occurs in August and September evry year. Although the reason for this is obscure, it might have been associated with the stress of ultraviolet light. For example, factory workers would take their lunch between factory buildings. If the sun came round so that it shone into the corridor between the buildings, some workers would show the first signs of the disease. When the underlying cause became known, it had to be concluded than the sun"s rays would stress them sufficiently to initiate the symptoms in individuals who were in a state of hitherto asymptomatic marginal malnutrition.
 

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
https://www.ncbi.nlm.nih.gov/pubmed/20385653/

Brain. 2010 May;133(Pt 5):1342-51. doi: 10.1093/brain/awq069. Epub 2010 Apr 12.
Powerful beneficial effects of benfotiamine on cognitive impairment and beta-amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice.
Pan X1, Gong N, Zhao J, Yu Z, Gu F, Chen J, Sun X, Zhao L, Yu M, Xu Z, Dong W, Qin Y, Fei G, Zhong C, Xu TL.
Author information
1
Department of Neurology, Zhongshan Hospital & Shanghai Medical College, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.
Abstract
Reduction of glucose metabolism in brain is one of the main features of Alzheimer's disease. Thiamine (vitamin B1)-dependent processes are critical in glucose metabolism and have been found to be impaired in brains from patients with Alzheimer's disease. However, thiamine treatment exerts little beneficial effect in these patients.

Here, we tested the effect of benfotiamine, a thiamine derivative with better bioavailability than thiamine, on cognitive impairment and pathology alterations in a mouse model of Alzheimer's disease, the amyloid precursor protein/presenilin-1 transgenic mouse. We show that after a chronic 8 week treatment, benfotiamine dose-dependently enhanced the spatial memory of amyloid precursor protein/presenilin-1 mice in the Morris water maze test.

Furthermore, benfotiamine effectively reduced both amyloid plaque numbers and phosphorylated tau levels in cortical areas of the transgenic mice brains. Unexpectedly, these effects were not mimicked by another lipophilic thiamine derivative, fursultiamine, although both benfotiamine and fursultiamine were effective in increasing the levels of free thiamine in the brain. Most notably, benfotiamine, but not fursultiamine, significantly elevated the phosphorylation level of glycogen synthase kinase-3alpha and -3beta, and reduced their enzymatic activities in the amyloid precursor protein/presenilin-1 transgenic brain.

Therefore, in the animal Alzheimer's disease model, benfotiamine appears to improve the cognitive function and reduce amyloid deposition via thiamine-independent mechanisms, which are likely to include the suppression of glycogen synthase kinase-3 activities.

These results suggest that, unlike many other thiamine-related drugs, benfotiamine may be beneficial for clinical Alzheimer's disease treatment.

PMID: 20385653
DOI: 10.1093/brain/awq069
 

JasonUT

Senior Member
Messages
303
@Asklipia
@Chocolove

Thanks for the research. It's fascinating.

I started getting brain fog and headaches 20 years ago when I started college. I moved to a new city, started drinking alcohol, coffee, ate junk food in the dorm cafeteria, and had to apply my brain at a level I wasn't accustomed to. Interestingly, most of my brain fog and headaches were the worst in the summer time.

It seems that all of the items above can be linked to thiamine deficiency. Perhaps I was inducing a low level thiamine deficiency 20 years ago, but it took some stressful triggering event in 2014 to send me into a "functional" thiamine deficiency?

Supplementing with 20 mg of Thiamine Mononitrate and 46 mg sublingual cocarboxylase did not change my thiamine status at all per labs. I am hoping that some TTFD, Allithiamine, Lipothiamine, Benfotiamine, and/or Sulbutiamine will make a difference. There seems to be a huge debate on which Thiamine form is best. I am going to start with Lipothiamine and cross my fingers.

Some of my prior Thiamine research can be found here, here, here, and here.
 
Last edited:

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
@JasonUT You may also be interested in: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609887/
Mol Cell Neurosci. Author manuscript; available in PMC 2014 Jul 1.

Published in final edited form as:
Mol Cell Neurosci. 2013 Jul; 55: 17–25.
Published online 2012 Sep 13. doi: 10.1016/j.mcn.2012.09.001
PMCID: PMC3609887
NIHMSID: NIHMS431588
Abnormal Thiamine-Dependent Processes in Alzheimer’s Disease. Lessons from Diabetes
Gary E. Gibson,*,1 Joseph A. Hirsch,1 Rosanna T. Cirio,1 Barry D. Jordan,1 Pasquale Fonzetti,1 and Jessica Elder2
 

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
Perhaps I was inducing a low level thiamine deficiency
Do you drink coffee or tea or perhaps have another source of tannins?

https://medlineplus.gov/druginfo/natural/965.html
Thiamine
Are there interactions with herbs and supplements?

Areca
Areca (betel) nuts change thiamine chemically so it doesn't work as well. Regular, long-term chewing of betel nuts may contribute to thiamine deficiency.
Horsetail
Horsetail (Equisetum) contains a chemical that can destroy thiamine in the stomach, possibly leading to thiamine deficiency. The Canadian government requires that equisetum-containing products be certified free of this chemical. Stay on the safe side, and don't use horsetail if you are at risk for thiamine deficiency.
Are there interactions with foods

Coffee and tea
Chemicals in coffee and tea called tannins can react with thiamine, converting it to a form that is difficult for the body to take in. This could lead to thiamine deficiency. Interestingly, thiamine deficiency has been found in a group of people in rural Thailand who drink large amounts of tea (>1 liter per day) or chew fermented tea leaves long-term. However, this effect hasn't been found in Western populations, despite regular tea use. Researchers think the interaction between coffee and tea and thiamine may not be important unless the diet is low in thiamine or vitamin C. Vitamin C seems to prevent the interaction between thiamine and the tannins in coffee and tea.
Seafood
Raw freshwater fish and shellfish contain chemicals that destroy thiamine. Eating a lot of raw fish or shellfish can contribute to thiamine deficiency. However, cooked fish and seafood are OK. They don't have any effect on thiamine, since cooking destroys the chemicals that harm thiamine.
 

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
Perhaps I was inducing a low level thiamine deficiency
@JasonUT If you soak your nuts you can remove most tannins.

Oh!... ah, er... Would that it were that easy. :redface: Um, soaking TREE nuts, beans and sprouts in salty water removes the tannins, phytic acid and other chemical weapons plants use to keep us from digesting them. (Well, at least you will remember this tip. ;):)

Details:
http://www.buzzle.com/articles/foods-that-contain-tannins.html
http://www.thenourishinggourmet.com...ped-my-digestion-learn-in-3-simple-steps.html
http://www.wikihow.com/Soak-Nuts

Soak in small batches you will eat immediately. Otherwise dehydrate a bulk quantity to prevent mold and other nasties from growing.
 

JasonUT

Senior Member
Messages
303
@Chocolove

Great info on tannins. Apparently, Apple Cider Vinegar contains tannins. I was using it for salad dressing. I can't win.

I guess I'll need to abstain for now until I get this Thiamine deficiency figured out.
 

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
@JasonUT
Lonsdale Protocol:
  1. Slowly titrate Lipothiamine from 50 mg to as much as 400 mg per day in divided doses. Differs by patient. I don't know how you decide the correct upper dose or titration rate.
  2. Take multi and B-complex
  3. At least 300 mg of magnesium.

There are other thiamine antagonists in food that are stable despite heat. There are lists of thiamine antagonists/antivitamins, as well as agonists/synergists.

For instance:
https://quizlet.com/6340036/vitamins-and-minerals-agonistantagonist-flash-cards/
This particular source lists Mg (magnesium as an agonist.) For this reason I don't take thiamine within a few hours of magnesium as the result would be as if I hadn't taken thiamine: no absorption.

However, having enough magnesium onboard in one's system is absolutely critical since it is required as a co-factor by the enzymes that utilize thiamine in the body. Otherwise the thiamine is simply not utilized and is as effective as flushing it down the loo from what I've read.

The enzymes transketolase, pyruvate dehydrogenase (PDH) and alpha-ketoglutarate dehydrogenase (α-KGDH) all require thiamin as a cofactor in order to function in carbohydrate metabolism... Transketolase is important in the pentose phosphate pathway. PDH and α-KGDH function in biochemical pathways that result in the generation of adenosine triphosphate (ATP), which is a major form of energy for the cell...
Impaired thiamin utilization:
Magnesium... is required for the binding of thiamin to thiamin-using enzymes.
From: https://thiamine.askdefine.com/

Note that magnesium deficiency is a common problem that it make take several months to replete.
Furthermore, because magnesium is subject to slow equilibration between serum and the intracellular spaces and tissues (eg, bone, red blood cells, muscle), the serum magnesium level may appear artificially high if measured too soon after a magnesium dose is administered. Large magnesium depletion requires sustained correction of the hypomagnesemia...
From:http://emedicine.medscape.com/article/2038394-treatment#d10

On top of that, the elderly and others are prone to poor digestion and absorption issues which may in part be alleviated by consumption of enzymes, pepsin and Betaine HCL, prebiotics (fibers - the food of your good gut microbes) and reintroduction of the good gut microbe strains often wiped out by broad spectrum antibiotics.

Thus we end up sometimes using injections, IVs, transdermal (skin) applications, rather than oral supplements or food to alleviate deficiencies. I am wary of IVs and the dumping of huge amounts of nutrients into a weakened body fearing that it may collapse in the effort to do everything at once with such neglected body machinery. I've heard and read accounts of that happening. I try the go slow and titrate slowly up to notice and address problems as they occur.

Like others I seem to be very sensitive to supplements and meds.

Noting that your Lonsdale protocol recommends titrating up, I am encouraged that you will catch budding problems before they overwhelm you.

Thank you very much for joining us and taking the time and effort to share your results. :hug: