Vitamin B1 / Thiamine deficiency increases serotonin in the brain

Mauritio

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This study finds that a vitmain B1 (thiamine ) deficiency causes an increase of serotonin in several brain areas . Although they avoid to use the word increase (they use "affects") in the abstract, the full study shows that this is what happened .
They also found that the thiamine defiicient mice showed ataxia, goosebumps amd paresis.
They administered the thiamine antagonist phyrithiamine to the rats in order to create a deficiency.


"A strong increase in yellow fluorescence, indi-
cating an increase in 5-HT, was observed in the RD cells of pyrithiamine-treated animals. "

"There was a significant (P < 0.01) increase in both 5-HT and 5-HIAA in the RC (raphe centralis), RD (raphe dorsalis), LC (locus coeruleus)
and ST (striata), in 5-HIAA only in RM (raphe
magnus) and Hyp. (hypothalamus), and in 5-HT
only in SN (substantia nigra). "
 
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Elie

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Nice find.
I wonder though to what degree are these rodent studies relevant to humans?
 

Ben.

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With all the thiamin threats and findings we have ... i wonder what is causing the thiamin deficiency in the first place? ( i doubt it is a lack of food containing thiamin)

Assimilation issue? Environmental toxins like glyphosate? Gut microbiome dysbiosis? Genetic damage/mutations?

I fear that future generations might need copious amounts of supplemental vit b1 and b3 to function normaly if we dont get to find the root causes.
 

Sergey

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With all the thiamin threats and findings we have ... i wonder what is causing the thiamin deficiency in the first place? ( i doubt it is a lack of food containing thiamin)

Assimilation issue? Environmental toxins like glyphosate? Gut microbiome dysbiosis? Genetic damage/mutations?

I fear that future generations might need copious amounts of supplemental vit b1 and b3 to function normaly if we dont get to find the root causes.
Quite likely fungi and/or some bacterial species. When grain feeding induces ruminal acidosis in cows thiamine content in their ruminal fluid drops to almost zero. It wipes out thiamine dependant flora and, it seems, thiamine producing flora too.
While methanogenic archaea and fungi thrive.

When thiamine is supplemented normal fermentation pattern and flora profile is restored, and methane output drops.

It seems that overconsumption of starch drives growth of archaea which are quite efficient in displacing many “good” species. And being very resistant to most antimicrobials, they can stay unaffected by antibiotics etc.
They are however susceptible to attacks from
L. Reureri, especially when carbs and polysaccharides are limited.
Almost forgot, omega-3 pufa seem to kill methanogenic archaea too.
 
Last edited:

Elie

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With all the thiamin threats and findings we have ... i wonder what is causing the thiamin deficiency in the first place? ( i doubt it is a lack of food containing thiamin)

Assimilation issue? Environmental toxins like glyphosate? Gut microbiome dysbiosis? Genetic damage/mutations?

I fear that future generations might need copious amounts of supplemental vit b1 and b3 to function normaly if we dont get to find the root causes.
In this particular study they used a thaimin antagonist.
 
OP
Mauritio

Mauritio

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There is a connection between EMFs and thiamine.
"The mitochondrial dysfunction and oxidative stress induced by EMF no doubt increase thiamine requirements."
How does thiamine relate to EMF-hypersensitivity and brain cell dysfunction?

And irradiated food.
"Thiamin and vitamin C are the most radiation-sensitive vitamins"
http://www.foodirradiation.org/pages/Stewart/Woodside.pdf
Thanks for sharing !
On cronometer b1 is always one of the vitamins I'm the lowest in . Supplementation might be necessary a this point, especially when fungal toxins, radiation, etc. use up or destroy b1.
 

YourUniverse

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Quite likely fungi and/or some bacterial species. When grain feeding induces ruminal acidosis in cows thiamine content in their ruminal fluid drops to almost zero. It wipes out thiamine dependant flora and, it seems, thiamine producing flora too.
While methanogenic archaea and fungi thrive.

When thiamine is supplemented normal fermentation pattern and flora profile is restored, and methane output drops.

It seems that overconsumption of starch drives growth of archaea which are quite efficient in displacing many “good” species. And being very resistant to most antimicrobials, they can stay unaffected by antibiotics etc.
They are however susceptible to attacks from
L. Reureri, especially when carbs and polysaccharides are limited.
Almost forgot, omega-3 pufa seem to kill methanogenic archaea too.
Supplementing thiamine can kick start a thiamine-promoting/sparing cycle?
 

Ben.

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Supplementing thiamine can kick start a thiamine-promoting/sparing cycle?

Dr. Gominak who treats her insomnia patients with b50 complex and vitamin d based on that asumption claims that too.

Supplementing b vitamins until you have colonized the gutmicrobiome so the body is sustaining itself with the proper bugs. I think she mentions that in a couple of interviews.
 

Sergey

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Supplementing thiamine can kick start a thiamine-promoting/sparing cycle?
I don’t know. Probably. Its like when complex system has reached certain stable state, it will stay there until some destabilisation happens which pushes it to another stable state. Absence of thiamine consuming/degrading microbes probably blocks some important chains of cross feeding in the gut, and when some of it is restored innate rebalancing does the rest. I believe that often very little help is needed and such self organising systems as we are, will do the rest.
As long as I remember methanogenic archaea with accompanying fungi creates some kind of dead-end microbiology, interrupts cross feeding and enjoys this empty niche. In cows this is caused by too much starch and corrected by removing starch, giving thiamine, etc.
I had great initial reactions to thiamine, but even after experimenting with all its forms and doing things a-la Lonsdale could not achieve resolution of the most weird symptoms. There are many unanswered questions about paradoxical reactions and what they really mean etc. Now I believe is that the core might be presence of thiamine degrading flora not even in the small gi, but in oesophagus, mouth, and sinuses. Thinking of it, they, especially oesophagus, are such great niches for bugs - constant flow of nutrients (sweets, drinks, soups, stocks, liquid supplements, coffee) and no antimicrobial would stay there for a long time. All those stories about eradicated sibo coming back etc..
Easy to see why candida’s most favourite site after large intestine is oesophagus. And why fasting has sometimes so miraculous effects on overall health.
 

cjm

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Sci-Hub | Sleep and indolamine alterations induced by thiamine deficiency. Brain Research, 248(2), 275–283 | 10.1016/0006-8993(82)90585-6

"INTRODUCTION

Thiamine-deficient animals have been used as an experimental model to simulate symptoms of Wernicke's encephalopathy and Korsakoff's psychosis resulting from malnutrition or alcoholism. In these diseases, ataxia, myoclonic seizure and loss of retrograde and anterograde memory are the most important neurological findings.

Post-mortem examinations of brains from patients suffering these conditions have shown symmetrical lesions in the paraventricular regions of the thalamus and hypothalamus, mamillary bodies, the periaqueductal regions of the midbrain, the floor of the fourth ventricle and the anterior lobe of cerebellum (particularly in the vermis). 'Memory alterations' following thiamine deficiency have been also observed together with histological changes in the raphe nuclei, spinal and medullary central grey substances, cerebellum and mamillary nuclei.

Thiamine deficiency is now established as the causative factor of most of these symptoms. Further, a loss of indolamine-labeled cerebellar mossy fibers and of parallel fiber-like systems, but not of diffuse axon inputs, has been reported z. These alterations agree with biochemical findings of decreased [3H]5-HT uptake in cerebellar synaptosomal fractions from the thiamine-deficient brain, and it is speculated that these changes in cerebellar indolamines may be related to the generation of ataxia.

The relationship between 5-HT and myoclonic seizure has already been recognized in man and several studies have also been done in animals. The main results published indicate that thiamine deficiency prevents autoradiographic labeling in almost all indolamine neurons and their processes in the midbrain and medulla. In thiamine-deficient animals only a few dystrophic cells with hypertrophied axons are seen. The periaqueductal regions of spinal cord, medulla, midbrain and diencephalon, the mamillary nuclei, habenular nuclei and cerebellum are the most severely affected.

Additional correlative autoradiographic studies performed after intraventricular infusion of radioactive 5-HT demonstrated and underlined the loss of labeling of the so called 'synaptic-serotoninergic axons' in the cerebellum and also in the brainstem and diencephalon of thiamine deficient animals.

Pyrithiamine treatment induced a significant increase in the ratio of 5-HIAA to 5-HT in all brain regions with the exception of the cerebral cortex. Part of this increase in 5-HIAA was shown to be due to impairment of active transport of this 5-HT metabolite out of the brain.

Recent studies with thiamine-deficient rats have also suggested an increase in the in vivo turnover of 5-HT and/or an impaired effiux of 5-HIAA from the brain.

Pyrithiamine apparently induced an increase in endogenous 5-HIAA in the medulla and pons simultaneously with the onset of neurological signs, and both parameters could be reversed by thiamine administration.

Further, a functional role of the serotonergic system in the regulation of the sleep and waking states has been demonstrated TM. The most significant results supporting this hypothesis have been obtained with PCPA-treated animals, which demonstrated a severe insomnia (reversed by injection of D,L-5-HTP), and with electrolytic destruction of the raphe system, resulting in a marked insomnia.

The studies described here were undertaken in order to investigate alterations of the sleep and waking cycle in parallel with variations of 5-HT metabolism after thiamine deficiency."
 

meatbag

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Motif

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no, I've accidentally used two bottles of the mononitrate form before. Get the HCL version, I've been using this brand the past week and half and it's great. B1 and B3 are 2 of my favorite supplements
Vitamin B1 Powder Thiamine HCl USP Grade

I've noticed benefits from using higher amounts; like 1000-1500mg-Thiamine Is A Carbonic Anhydrase Inhibitor As Effective As Acetazolamide
What effects do you feel from it?

Cool, then I’ll get the now one and after that like i said I will use yeast
 

Korven

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Quite likely fungi and/or some bacterial species. When grain feeding induces ruminal acidosis in cows thiamine content in their ruminal fluid drops to almost zero. It wipes out thiamine dependant flora and, it seems, thiamine producing flora too.
While methanogenic archaea and fungi thrive.

When thiamine is supplemented normal fermentation pattern and flora profile is restored, and methane output drops.

It seems that overconsumption of starch drives growth of archaea which are quite efficient in displacing many “good” species. And being very resistant to most antimicrobials, they can stay unaffected by antibiotics etc.
They are however susceptible to attacks from
L. Reureri, especially when carbs and polysaccharides are limited.
Almost forgot, omega-3 pufa seem to kill methanogenic archaea too.

Interesting ideas. I'm not sure how much we can extrapolate from these studies but grain feeding in cows seems to reliably induce thiamine deficiency through several mechanism = high lactate (Thiamine status, metabolism and application in dairy cows: a review - PubMed):

"As the co-enzyme of pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows. Apart from feedstuff, microbial thiamine synthesis in the rumen is the main source for dairy cows. However, the amount of ruminal thiamine synthesis, which is influenced by dietary N levels and forage to concentrate ratio, varies greatly. Notably, when dairy cows are overfed high-grain diets, subacute ruminal acidosis (SARA) occurs and results in thiamine deficiency. Thiamine deficiency is characterised by decreased ruminal and blood thiamine concentrations and an increased blood thiamine pyrophosphate effect to >45 %. Thiamine deficiency caused by SARA is mainly related to the increased thiamine requirement during high grain feeding, decreased bacterial thiamine synthesis in the rumen, increased thiamine degradation by thiaminase, and decreased thiamine absorption by transporters. Interestingly, thiamine deficiency can be reversed by exogenous thiamine supplementation in the diet. Besides, thiamine supplementation has beneficial effects in dairy cows, such as increased milk and component production and attenuated SARA by improving rumen fermentation, balancing bacterial community and alleviating inflammatory response in the ruminal epithelium."

Does the same thing happen in humans who eat too much grain/starch?
 
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Mauritio

Mauritio

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Interesting ideas. I'm not sure how much we can extrapolate from these studies but grain feeding in cows seems to reliably induce thiamine deficiency through several mechanism = high lactate (Thiamine status, metabolism and application in dairy cows: a review - PubMed):

"As the co-enzyme of pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows. Apart from feedstuff, microbial thiamine synthesis in the rumen is the main source for dairy cows. However, the amount of ruminal thiamine synthesis, which is influenced by dietary N levels and forage to concentrate ratio, varies greatly. Notably, when dairy cows are overfed high-grain diets, subacute ruminal acidosis (SARA) occurs and results in thiamine deficiency. Thiamine deficiency is characterised by decreased ruminal and blood thiamine concentrations and an increased blood thiamine pyrophosphate effect to >45 %. Thiamine deficiency caused by SARA is mainly related to the increased thiamine requirement during high grain feeding, decreased bacterial thiamine synthesis in the rumen, increased thiamine degradation by thiaminase, and decreased thiamine absorption by transporters. Interestingly, thiamine deficiency can be reversed by exogenous thiamine supplementation in the diet. Besides, thiamine supplementation has beneficial effects in dairy cows, such as increased milk and component production and attenuated SARA by improving rumen fermentation, balancing bacterial community and alleviating inflammatory response in the ruminal epithelium."

Does the same thing happen in humans who eat too much grain/starch?
White polished rice can do that.
 
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