Low acetylcholine? Dysautonomia?

[mostlylurking]

Awesome thank you! I think so too I will increase my milk. I’m at 200mg of Benfothiamine and 100mg of TTFD. I think I will to to 300mg of Benfothiamine and maybe start experimenting again with thiaminHCL as an addition, like you said at least 30min after a meal. Or I will raise TTFD further..

I think that experimentation is very important. However, it is good to try to keep it as simple as possible. Changing more than one thing at a time can make things very confusing. When you have a response (positive or negative) it will be more difficult to figure out what caused it.

A few days ago, I tried a 100mg sublingual thiamine mononitrate pill. I did get a noticeable response from it that I had not noticed from my usual 1gram thiamine hcl 2Xday for a long time. I've read that the 100mg sublingual is comparable to a 100mg injection of thiamine hcl because neither of these have to get absorbed via the gut. The difficulty for me is trying to work out how often to take the sublingual. The amount of thiamine hcl I've been taking (2 grams/day) equals to one 100mg injection of thiamine hcl per week. I decided I shouldn't take the 100mg sublingual everyday because that would probably be too much and I'd get negative effects. So I skipped the next day and took nothing. The next morning, I woke up with severe inflammation which I had not experienced in 18 months. So I took my one gram of thiamine hcl and the inflammation disappeared in about an hour. So for now I've decided that I'm just going to continue taking the 1gram of thiamine hcl 2Xday and not pursue the sublingual thiamine.

 

[exile]

Dr. Costantini warns about taking thiamine hcl with anything other than water. Fruit juice will cancel out the benefit. Coffee and tea block thiamine; I avoid both. I space anything with sugar (including carbs) at least 30 minutes before and after the thiamine intake. I space taking my thyroid med and my thiamine at least an hour apart.

I think it would be a good idea to read as much as you can about thiamine. Dr. Lonsdale and Dr. Chandler Marrs have written/said that many times the improvement from supplementing with thiamine can take months. Dr. Costantini's work pointed to using the amounts of thiamine hcl he writes about on his website (link above in my last post) because this is what works for Parkinson's Disease. I found it helpful to watch the patients' videos to see their massive improvement.

Do you have any idea where the zinc overload you have came from? Zinc blocks copper and you need copper. The zinc overload is concerning. I follow Ray Peat's advice and eat shellfish once a week to get my trace minerals. I read somewhere that high dose thiamine will deplete manganese so I used maple syrup for a manganese source for maybe six months. It tasted really good! I wound up giving myself a manganese overload via the maple syrup. Manganism is something to be avoided. I'm better now since I gave up the maple syrup (sob).

Aggravated effects of coexisting marginal thiamine deficits and zinc excess on SN56 neuronal cells - PubMed

<span><b>Objectives:</b> Zinc excitotoxicity and thiamine pyrophosphate deficiency (TD) are known pathogenic signals contributing to mechanism of different encephalopathies through inhibition of enzymes responsible for energy metabolism such as pyruvate dehydrogenase, aconitase or ketoglutarate...

pubmed.ncbi.nlm.nih.gov

"Objectives: Zinc excitotoxicity and thiamine pyrophosphate deficiency (TD) are known pathogenic signals contributing to mechanism of different encephalopathies through inhibition of enzymes responsible for energy metabolism such as pyruvate dehydrogenase, aconitase or ketoglutarate dehydrogenase. The aim of this work was to investigate whether subclinical Zn excess and TD, frequent in aging brain, may combine yielding overt neuronal impairment.Results: Clonal SN56 cholinergic neuronal cells of septal origin were used as the model of brain cholinergic neurons, which are particularly susceptible to neurodegeneration in the course of Alzheimer's disease, hypoxia and other dementia-linked brain pathologies. Neither subtoxic concentration of Zn (0.10 mM) nor mild 20-25% TD deficits alone caused significant negative changes in cultured cholinergic neurons viability and their acetyl-CoA/acetylcholine metabolism. However, cells with mild TD accumulated Zn in excess, which impaired their energy metabolism causing a loss of neurons viability and their function as neurotransmitters. These negative effects of Zn were aggravated by amprolium which is an inhibitor of thiamine intracellular transport.Conclusion: Our data indicate that TD may amplify otherwise non-harmful border-line Zn excitotoxic signals yielding progress of neurodegeneration."

also this one: Protection of Cholinergic Neurons against Zinc Toxicity by Glial Cells in Thiamine-Deficient Media - PubMed
"Brain pathologies evoked by thiamine deficiency can be aggravated by mild zinc excess. Cholinergic neurons are the most susceptible to such cytotoxic signals. Sub-toxic zinc excess aggravates the injury of neuronal SN56 cholinergic cells under mild thiamine deficiency. The excessive cell loss is caused by Zn interference with acetyl-CoA metabolism. The aim of this work was to investigate whether and how astroglial C6 cells alleviated the neurotoxicity of Zn to cultured SN56 cells in thiamine-deficient media. Low Zn concentrations did not affect astroglial C6 and primary glial cell viability in thiamine-deficient conditions. Additionally, parameters of energy metabolism were not significantly changed. Amprolium (a competitive inhibitor of thiamine uptake) augmented thiamine pyrophosphate deficits in cells, while co-treatment with Zn enhanced the toxic effect on acetyl-CoA metabolism. SN56 cholinergic neuronal cells were more susceptible to these combined insults than C6 and primary glial cells, which affected pyruvate dehydrogenase activity and the acetyl-CoA level. A co-culture of SN56 neurons with astroglial cells in thiamine-deficient medium eliminated Zn-evoked neuronal loss. These data indicate that astroglial cells protect neurons against Zn and thiamine deficiency neurotoxicity by preserving the acetyl-CoA level."

There are recommendations online that chelation therapy will reduce zinc levels. I just want to include a heads up about info I've read that the chelating physician should always determine the patient's thiamine status before chelating because if there is a thiamine deficiency the chelation can result in death. I was chelated in 2014 for lead poisoning (EDTA by IV) and was probably thiamine deficient (nobody bothered to check). It didn't kill me but I did get rheumatoid arthritis and almost had to go into assisted living because I couldn't take care of myself. I did recover with increased thyroid medication and b vitamins, including thiamine hcl.

I take magnesium glycinate, about 1200mg/day which equals to around 600mg magnesium. I consume orange juice and bananas for the potassium. I salt my food to taste for the sodium. I take about 90mg niacinamide and 90mg riboflavin 4Xday. I drink milk for the calcium. I do take some other things but I don't think they pertain to the high dose thiamine hcl I take.

I take 1 gram of thiamine hcl 2Xday. I'm following Dr. Costantini's protocol. According to what he's written and based on my weight my dose should have been 2.5 grams/day. However, when I tried that dose, I experienced shooting electrical zapping pains in my thighs that night when I went to bed. So I reduced my dose back down to the 2 grams/day. I do not experience any negative symptoms at this dose. However there was a period of adjustment early on when I started this high dose. It turned out that my electrolytes were low so I increased my salt intake.

How to know when to stop thiamine supplementation: Dr. Costantini advises his Parkinson's Disease patients to go off of the thiamine hcl for a while after taking it for maybe 6 months. I think this is to show the patient and their family that they really do need to keep taking the thiamine because after maybe 2 months the Parkinson's Disease symptoms come back. Dr. Costantini has written that he has had some patients taking high dose thiamine hcl for as long as 7 years with no ill effects.

Would taking thiamine hcl in the morning 30 minutes prior to be breakfast be fine as far as you know?

 

[mostlylurking]

Would taking thiamine hcl in the morning 30 minutes prior to be breakfast be fine as far as you know?

Yes, I think so. 30 minutes should be enough time for the thiamine hcl to get out of the stomach, into the small intestine, and be absorbed through the intestinal wall.

 

[exile]

Yes, I think so. 30 minutes should be enough time for the thiamine hcl to get out of the stomach, into the small intestine, and be absorbed through the intestinal wall.

Ok thanks. I had been taking some in oj/water at breakfast, but I will give it the taking it as you say. Have you ever done a blood test for b1 or are they don’t have them/are not useful?

 

[mostlylurking]

Ok thanks. Have you ever done a blood test for b1 or are they don’t have them/are not useful?

Information on blood testing is here: Thiamine Deficiency Testing: Understanding the Labs- Hormones Matter

 

[Bart1]

I think that experimentation is very important. However, it is good to try to keep it as simple as possible. Changing more than one thing at a time can make things very confusing. When you have a response (positive or negative) it will be more difficult to figure out what caused it.

A few days ago, I tried a 100mg sublingual thiamine mononitrate pill. I did get a noticeable response from it that I had not noticed from my usual 1gram thiamine hcl 2Xday for a long time. I've read that the 100mg sublingual is comparable to a 100mg injection of thiamine hcl because neither of these have to get absorbed via the gut. The difficulty for me is trying to work out how often to take the sublingual. The amount of thiamine hcl I've been taking (2 grams/day) equals to one 100mg injection of thiamine hcl per week. I decided I shouldn't take the 100mg sublingual everyday because that would probably be too much and I'd get negative effects. So I skipped the next day and took nothing. The next morning, I woke up with severe inflammation which I had not experienced in 18 months. So I took my one gram of thiamine hcl and the inflammation disappeared in about an hour. So for now I've decided that I'm just going to continue taking the 1gram of thiamine hcl 2Xday and not pursue the sublingual thiamine.

Yeah if you’re doing well on only hcl, I would probably stick with that, healing is taking place.

I considered going to hcl because it seems to cause the least issues for most people, but I tried once dropping the TTDD and I immediately feel terrible, so it’s doing something positive I guess..

 

[mostlylurking]

Yeah if you’re doing well on only hcl, I would probably stick with that, healing is taking place.

I considered going to hcl because it seems to cause the least issues for most people, but I tried once dropping the TTDD and I immediately feel terrible, so it’s doing something positive I guess..

I'm 72 so I'm at the age where poor absorption of thiamine hcl in the gut happens (hence the 2 grams/day) so I wanted to find out if the sublingual would be a better way for me to go. It's more complicated/confusing than I first thought. But I do have it to fall back on if the oral hcl stops working and I find myself in trouble again.

 

[Bart1]

I'm 72 so I'm at the age where poor absorption of thiamine hcl in the gut happens (hence the 2 grams/day) so I wanted to find out if the sublingual would be a better way for me to go. It's more complicated/confusing than I first thought. But I do have it to fall back on if the oral hcl stops working and I find myself in trouble again.

Are you taking a B-complex in addition to the thiamin? You could try improving your gut. Taking things to tighten the junctions for instance, like Bacillus Coagulans, PQQ, Saccharomyces Boulardii, Butyrate etc

 

[mostlylurking]

Are you taking a B-complex in addition to the thiamin? You could try improving your gut. Taking things to tighten the junctions for instance, like Bacillus Coagulans, PQQ, Saccharomyces Boulardii, Butyrate etc

I'm pretty sure my gut is doing pretty well. I've got a long history of gut disbiosis, leaky gut, SIBO, and I'm strongly gluten sensitive so I know what the symptoms are. I've also been diagnosed with rheumatoid arthritis. But for the past 18 months I've got the inflammation under control and I'm doing pretty well. The thiamine hcl has gotten the gut issues normalized. I'm not a fan of fiddling with the gut bacteria. I've been in trouble before; the high dose thiamine normalized my gut bacteria after a disastrous reaction to prescription Bactrim antibiotic. I was messed up for months because of the Bactrim which killed off the gut bacteria and also blocked my thiamine function.

I take riboflavin, niacinamide, thiamine, and biotin separately; I'm not currently relying on a b-complex, mainly because they all seem to have too much b-6 for me.

Thiamine Acquisition Strategies Impact Metabolism and Competition in the Gut Microbe Bacteroides thetaiotaomicron - PubMed

Thiamine (vitamin B₁) is an essential cofactor for all organisms. Humans primarily acquire thiamine through their diet, and thiamine deficiencies have adverse neurological effects. However, the role gut microbes play in modulating thiamine availability is poorly understood, and little...

pubmed.ncbi.nlm.nih.gov

How Low Thiamine Can Thin Villi: Old Research Rediscovered and its Clinical Significance in Celiac Disease

What was the trigger for celiac disease, of course gluten played a part, but what in my past history put me over the edge? What had changed? Did the doctors know so little about the trigger for celiac disease that it was only now becoming clinically identifiable?

www.celiac.com

Effect of dietary thiamin deficiency on intestinal functions in rats - PubMed

The effect of dietary thiamin deficiency has been studied on intestinal functions and chemical composition of brush border membranes in rats. Intestinal uptake of glucose, glycine, alanine, and leucine was significantly stimulated in thiamin deficiency compared to pair-fed control group. Studies...

pubmed.ncbi.nlm.nih.gov

Got SIBO? Here's why you need to get your thiamine status checked!

Small intestinal bacterial overgrowth (SIBO) is classified according to the types of gasses produced by microflora occupying the upper gut. The two types of gases are hydrogen, and methane. However, a new classification has emerged based on relatively recent findings which is characterized by...

www.eonutrition.co.uk

 

[Bart1]

I'm pretty sure my gut is doing pretty well. I've got a long history of gut disbiosis, leaky gut, SIBO, and I'm strongly gluten sensitive so I know what the symptoms are. I've also been diagnosed with rheumatoid arthritis. But for the past 18 months I've got the inflammation under control and I'm doing pretty well. The thiamine hcl has gotten the gut issues normalized. I'm not a fan of fiddling with the gut bacteria. I've been in trouble before; the high dose thiamine normalized my gut bacteria after a disastrous reaction to prescription Bactrim antibiotic. I was messed up for months because of the Bactrim which killed off the gut bacteria and also blocked my thiamine function.

I take riboflavin, niacinamide, thiamine, and biotin separately; I'm not currently relying on a b-complex, mainly because they all seem to have too much b-6 for me.

Thiamine Acquisition Strategies Impact Metabolism and Competition in the Gut Microbe Bacteroides thetaiotaomicron - PubMed

Thiamine (vitamin B₁) is an essential cofactor for all organisms. Humans primarily acquire thiamine through their diet, and thiamine deficiencies have adverse neurological effects. However, the role gut microbes play in modulating thiamine availability is poorly understood, and little...

pubmed.ncbi.nlm.nih.gov

How Low Thiamine Can Thin Villi: Old Research Rediscovered and its Clinical Significance in Celiac Disease

What was the trigger for celiac disease, of course gluten played a part, but what in my past history put me over the edge? What had changed? Did the doctors know so little about the trigger for celiac disease that it was only now becoming clinically identifiable?

www.celiac.com

Effect of dietary thiamin deficiency on intestinal functions in rats - PubMed

The effect of dietary thiamin deficiency has been studied on intestinal functions and chemical composition of brush border membranes in rats. Intestinal uptake of glucose, glycine, alanine, and leucine was significantly stimulated in thiamin deficiency compared to pair-fed control group. Studies...

pubmed.ncbi.nlm.nih.gov

Got SIBO? Here's why you need to get your thiamine status checked!

Small intestinal bacterial overgrowth (SIBO) is classified according to the types of gasses produced by microflora occupying the upper gut. The two types of gases are hydrogen, and methane. However, a new classification has emerged based on relatively recent findings which is characterized by...

www.eonutrition.co.uk

Thanks for the links. Interesting how it helped your gut, I'm hoping the same will happen for me.

Have you looked at the desert harvest b complex without b6 ? I don't know if you tolerate or want the other b's but that's at least a b complex without b6. b6 problems are also tied to thiamin defiency right ?

I have hemochromatosis and I theory I have is that thiamin is heavily involved in that and maybe riboflavin too. If one is deficient in thiamin, magnesium becomes deficient as well and I saw studies also on this forum that a magnesium will cause iron to accumulate. My iron overload seems to be more extreme the last couple of years and I think it's caused by the thiamin deficiency.

 

[mostlylurking]

Thanks for the links. Interesting how it helped your gut, I'm hoping the same will happen for me.

Have you looked at the desert harvest b complex without b6 ? I don't know if you tolerate or want the other b's but that's at least a b complex without b6. b6 problems are also tied to thiamin defiency right ?

I have hemochromatosis and I theory I have is that thiamin is heavily involved in that and maybe riboflavin too. If one is deficient in thiamin, magnesium becomes deficient as well and I saw studies also on this forum that a magnesium will cause iron to accumulate. My iron overload seems to be more extreme the last couple of years and I think it's caused by the thiamin deficiency.

My husband had an overload of iron a while back. He used to donate blood twice a year. I don't think it was a genetic thing; more likely he had the problem because he's a welder. I had a high ferritin level for a year or so, the same time I became aware of my thiamine problem. Chelation therapy would chelate iron out, but you'd need to find someone who actually knows what they're doing. They are supposed to verify a person's thiamine status before chelating them because chelating someone with a thiamine deficiency can result in death.

I just took a look at the desert harvest b complex; it's got b-5 plus silicon dioxide in it. I reacted badly to b-5 one time. I did some research on it; it is supposed to facilitate the release of fat into the bloodstream. I think I reacted badly because of probable stored PUFA. I had not yet found Ray Peat's work so my diet wasn't the best; too much olive oil.

Regarding iron and thiamine: thiamine deficient people are more susceptible to iron getting in the brain because thiamine is required to maintain the integrity of the blood/brain barrier. Thiamine is also needed to maintain the integrity of the permeability of the gut.

 

[Bart1]

My husband had an overload of iron a while back. He used to donate blood twice a year. I don't think it was a genetic thing; more likely he had the problem because he's a welder. I had a high ferritin level for a year or so, the same time I became aware of my thiamine problem. Chelation therapy would chelate iron out, but you'd need to find someone who actually knows what they're doing. They are supposed to verify a person's thiamine status before chelating them because chelating someone with a thiamine deficiency can result in death.

I just took a look at the desert harvest b complex; it's got b-5 plus silicon dioxide in it. I reacted badly to b-5 one time. I did some research on it; it is supposed to facilitate the release of fat into the bloodstream. I think I reacted badly because of probable stored PUFA. I had not yet found Ray Peat's work so my diet wasn't the best; too much olive oil.

Regarding iron and thiamine: thiamine deficient people are more susceptible to iron getting in the brain because thiamine is required to maintain the integrity of the blood/brain barrier. Thiamine is also needed to maintain the integrity of the permeability of the gut.

Yes I have had numerous iron chelations, but as of late I don't tolerate it anymore and I guess your right it could be dangerous now. I try to manage it now by doing milk fasts for a couple of days (only drinking milk).

B5 is an important one.It serves as a direct precursor for CoA/acetyl-COA. It got tons of studies with Parkinsons. I read a post from Elliot somewhere stating that for some people who do not respond well to high dose thiamin, they could need b5 first. Maybe you don't need it, have you tried different versions ? Also he said something like high dose thiamin could "waste" this vitamin in the beginning, so that would show up high in urine (excretion). He said he had numerous patients of his who were helped by it.

Interesting about the blood/brain barrier. And I didn't now bout the gut permeability!

 

[mostlylurking]

Yes I have had numerous iron chelations, but as of late I don't tolerate it anymore and I guess your right it could be dangerous now. I try to manage it now by doing milk fasts for a couple of days (only drinking milk).

B5 is an important one.It serves as a direct precursor for CoA/acetyl-COA. It got tons of studies with Parkinsons. I read a post from Elliot somewhere stating that for some people who do not respond well to high dose thiamin, they could need b5 first. Maybe you don't need it, have you tried different versions ? Also he said something like high dose thiamin could "waste" this vitamin in the beginning, so that would show up high in urine (excretion). He said he had numerous patients of his who were helped by it.

Interesting about the blood/brain barrier. And I didn't now bout the gut permeability!

You may not be able to tolerate chelation anymore because of a thiamine deficiency. I'm pretty sure that the reason why I had such a negative effect the last time I was chelated (for lead poisoning) was because of a thiamine deficiency. I wound up with rheumatoid arthritis from it but now that has completely gone away.

I reacted so badly to the b-5 pill that my doctor prescribed for me that I was messed up for 48 hours. It was a 500mg b-5 pill. I don't ever want to go through that again. Since I'm doing well, maybe I get enough via my diet. Here's hoping....

 

[Bart1]

You may not be able to tolerate chelation anymore because of a thiamine deficiency. I'm pretty sure that the reason why I had such a negative effect the last time I was chelated (for lead poisoning) was because of a thiamine deficiency. I wound up with rheumatoid arthritis from it but now that has completely gone away.

I reacted so badly to the b-5 pill that my doctor prescribed for me that I was messed up for 48 hours. It was a 500mg b-5 pill. I don't ever want to go through that again. Since I'm doing well, maybe I get enough via my diet. Here's hoping....

wow! Yes I will definitely be carefull. As for b5, very interesting that you felt so messed up. Might be because it can deplete biotin ? I actually starting to feel similar, I was high dosing b5 for a couple of days and in the beginning felt great but now not so much

 

[mostlylurking]

wow! Yes I will definitely be carefull. As for b5, very interesting that you felt so messed up. Might be because it can deplete biotin ? I actually starting to feel similar, I was high dosing b5 for a couple of days and in the beginning felt great but now not so much

I remember that I took it in the morning and was OK all day. The problem happened at 2:00am when I woke up with extremely high adrenaline and felt horrible. I spent an hour or so online researching the issue and found a scientific article that said that b-5 increases something (I've forgotten the name) that causes fatty acids to be released from storage. I did not take a second pill but the same thing happened the next night so it took 48 hours to clear my system. This was around 2015 when I was researching a lot and reading a lot of Ray Peat articles. I was pretty sure that my body fat was toxic, my lead toxicity was high, and it was not a good idea to encourage the release of free fatty acids; I still think it's good to keep fatty acids in storage and that niacinamide helps do that. The body stores toxins in the fat; PUFA becomes concentrated in the fat because even fat cells don't want to burn it because it is toxic.

This doctor was mainly focused on weight loss and tried to push a keto diet on me. She put all her patients on weight loss meds. I wasn't there to lose weight; I was there because she was the only doctor in town who would prescribe Armour desiccated thyroid and I had lost my doctor who had put me on it (the state stripped him of his license). He was a good doctor, just a little strange and paranoid about keeping his patients' records; he only kept hard copies, never computerized them. He prescribed vitamins a lot and I remember he would examine patients' blood with a dark field microscope. My blood showed I had a serious problem with leaky gut so he put me on deglycyrrhizinated licorice and golden seal (if memory serves) for 3 months, which helped a lot. The State raided his office and shut him down.

Here's some info about b-5: Pantothenic acid as a weight-reducing agent: Fasting without hunger, weakness and ketosis

 

[Bart1]

I remember that I took it in the morning and was OK all day. The problem happened at 2:00am when I woke up with extremely high adrenaline and felt horrible. I spent an hour or so online researching the issue and found a scientific article that said that b-5 increases something (I've forgotten the name) that causes fatty acids to be released from storage. I did not take a second pill but the same thing happened the next night so it took 48 hours to clear my system. This was around 2015 when I was researching a lot and reading a lot of Ray Peat articles. I was pretty sure that my body fat was toxic, my lead toxicity was high, and it was not a good idea to encourage the release of free fatty acids; I still think it's good to keep fatty acids in storage and that niacinamide helps do that. The body stores toxins in the fat; PUFA becomes concentrated in the fat because even fat cells don't want to burn it because it is toxic.

This doctor was mainly focused on weight loss and tried to push a keto diet on me. She put all her patients on weight loss meds. I wasn't there to lose weight; I was there because she was the only doctor in town who would prescribe Armour desiccated thyroid and I had lost my doctor who had put me on it (the state stripped him of his license). He was a good doctor, just a little strange and paranoid about keeping his patients' records; he only kept hard copies, never computerized them. He prescribed vitamins a lot and I remember he would examine patients' blood with a dark field microscope. My blood showed I had a serious problem with leaky gut so he put me on deglycyrrhizinated licorice and golden seal (if memory serves) for 3 months, which helped a lot. The State raided his office and shut him down.

Here's some info about b-5: Pantothenic acid as a weight-reducing agent: Fasting without hunger, weakness and ketosis

Interesting, I have had adrenalin too from it I think, although it also did some positive things. I have high mercury and lead. Thanks for the info!

 

[mostlylurking]

Interesting, I have had adrenalin too from it I think, although it also did some positive things. I have high mercury and lead. Thanks for the info!

I have high mercury and lead too. I found some interesting info about thiamine for heavy metals.

I'll paste my notes here for you:
thiamine and heavy metals quotes

Thiamine (2–4 mg/kg per day, SC) alleviates clinical manifestations and reduces tissue deposition of lead. Combined Ca-EDTA and thiamine treatment appears to produce the most beneficial response. Lead Poisoning in Animals - Toxicology - Merck Veterinary Manual

Lead induced thiamine deficiency in the brain decreased the threshold of electroshock seizure in rat

Thiamine supplementation reversed these signs and decreased the brain lead concentration in the lead treated group. The results from the present study suggest that the increased seizure susceptibility induced by lead intoxication in rats may be mediated at least in part through the changes of thiamine status.



Thiamine and zinc in prevention or therapy of lead intoxication: Thiamine and zinc in prevention or therapy of lead intoxication - PubMed

Thiamine, zinc or their combination given through gastric gavage were investigated for their ability to prevent or treat experimental lead toxicity in rats. Simultaneous dietary supplementation with thiamine plus zinc was found to be the most effective way of reducing the lead-induced inhibition of delta-aminolevulinic acid dehydratase activity in blood, urinary, excretion of delta-aminolevulinic acid and accumulation of lead in blood, liver and kidney. Prevention was more effective than post-lead exposure treatment which may be due mainly to the decrease in the absorption of lead in the gastro-intestinal tract in the presence of thiamine and/or zinc.



Eating to Block Lead Absorption | NutritionFacts.org

Intake of certain nutrients has been associated with lower lead levels in the body. For example, women with higher intake of thiamine, also called vitamin B1, tended to have lower blood lead levels, and the same was found for lead-exposed steel workers—and not just with thiamine, as “content of dietary fiber, iron, or thiamine intake each correlated inversely with blood lead concentrations in workers…” The thinking is that the fiber might glom onto the lead and flush it out of the body, the iron would inhibit the lead absorption, and the thiamine may accelerate lead removal through the bile. So, researchers suggest that eating lots of iron, fiber and especially thiamine-rich foods “may induce rapid removal and excretion of the lead from the tissues.” But thiamine’s never been put to the test by giving it to people to see if their lead levels drop. The closest I could find is a thiamine intervention for lead-intoxicated goats.



Thiamin (vitamin B1) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential

Thiamin (vitamin B1) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential:

The purpose of this study was to evaluate the effects of thiamin on lead (Pb) poisoning in cattle. Fifteen Holstein male calves were divided into three groups: Group I served as controls, Group II calves were dosed orally with 5 mg Pb acetate/day/kg of body wt, and Group III calves were dosed similarly with Pb and with 100 mg/day/calf of thiamin hydrochloride, subcutaneously. Calves were treated daily for 20 days. None of the control or Pb plus thiamin-treated calves showed clinical signs of poisoning and no deaths occurred. However, four of five Pb-treated calves showed signs of Pb poisoning and two died during the study. Tissues from both groups receiving Pb contained significantly higher (p < 0.01) concentrations of Pb than tissues from control calves. However, tissues from calves receiving Pb plus thiamin contained 2 to 10 times less Pb than tissues from calves receiving only Pb. The Pb concentrations in liver, kidney, and blood from thiamin-treated calves remained below confirmatory levels associated with Pb poisoning; while Pb concentrations in the same tissues from calves dosed only with Pb were within the range considered diagnostic of Pb poisoning. On the other hand, δ-aminolevulinic acid dehydratase activity in erythrocytes was decreased 70% from pretreatment levels in both groups receiving Pb. Thus, thiamin appeared to have no protective effect on the ability of Pb to inhibit this enzyme. But in the tissues analyzed, thiamin interacted with Pb in some way to prevent tissue accumulation, thus preventing clinical signs and death. These results suggest that therapeutic doses of thiamin may be of value in the prevention and treatment of Pb poisoning in cattle, and in other animals or humans exposed to high environmental levels of Pb.



Thiamine reduces tissue lead levels in rats: mechanism of interaction - BioMetals

Lead (Pb) toxicity has been a serious concern in industrialized societies because of its association with functional deficits in nervous, haematopoietic and renal systems. Several studies have shown beneficial effects of thiamine on Pb toxicity. It is speculated that Pb chelation by thiamine may be a possible mechanism. However, the exact nature of these interactions remained elusive. In the present study we have characterized the interaction of Pb with thiamine using UV–Vis as well as fluorescence spectroscopic methods and studied the effect of thiamine treatment on blood and tissue Pb levels during simultaneous or post-exposure to Pb in rat model. The spectroscopic studies revealed that Pb interacts with the pyrimidine ring of thiamine, leading to its solubilization at physiological pH. Further, thiamine reduced the Pb levels in blood, kidney and bone during both simultaneous and post-exposure Pb treatment. Interestingly, thiamine appears to prevent the accumulation of Pb in bone during simultaneous treatment. Together these results suggest that pyrimidine ring of thiamine mediates its interaction with Pb, leading to the prevention of its accumulation and/or increased clearance from tissues.

Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on dead toxicity

Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on dead toxicity

Calcium disodium ethylenediaminetetracetate (CaNa2EDTA; Versenate) was more effective than thiamine (vitamin B1) in enhancing the urinary excretion of lead, reducing tissue lead and restoring lead induced biochemical alterations in rats. However, the combination of CaNa2EDTA and vitamin B1 enhanced the beneficial effect of CaNa2EDTA in lead intoxication and was particularly effective in reducing the brain concentration of lead.

more: thiamine and heavy metals, including iron overload:

https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12146

quote: We hypothesize that excess iron, that is, brain iron overload (BIO), is a highly relevant pathway leading to cognitive deterioration in individuals with AUD. We further hypothesize thiamine depletion, a common concomitant feature in AUD patients, to be a key stimulus for BIO, as thiamine deficiency disrupts the integrity of the blood-brain barrier (BBB), enabling iron from the circulation to enter the brain in an uncontrolled manner.



Vitamin B1 Deficiency a Key Factor in the Development of Alcohol-Related Dementia - Neuroscience News

quote: A common consequence of chronically high alcohol consumption is a decline in cognitive function, which can even progress to full-blown dementia. However, we do not yet fully understand how alcohol damages the brain. A research group led by Stephan Listabarth from MedUni Vienna’s Department of Psychiatry and Psychotherapy, Division of Social Psychiatry, has now developed a hypothesis whereby iron deposits in the brain – resulting from alcohol-induced vitamin B1 deficiency – can be regarded as key factors in cognitive decline. The work has now been published in the leading journal “Alzheimer’s and Dementia”.



Chelation Therapy in Medicine - Hormones Matter

quote: Because of a sick cow, a farmer had called a veterinarian who had recognized the symptoms of thiamine (vitamin B1) deficiency. When given an injection of the vitamin the symptoms in the cow had disappeared but they had subsequently returned and the veterinarian was asked to come again. Thinking this was a strange recurrence, the doctor had the presence of mind to search the field where the cow had been grazing. He had found an old trunk in a corner of the field that was partly covered with lead paint and which the cow had been licking. Lead has a sweet taste and the veterinarian concluded that this was the cause of the thiamine deficiency. In a study using rats, calcium disodium EDTA was more effective than thiamine in enhancing the urinary excretion of lead in restoring lead induced biochemical alterations. However, the combination of the drug and thiamine enhanced the beneficial effect and was particularly effective in reducing the brain concentration of lead.

In lead loaded sheep the combination of EDTA and thiamine administration was better than EDTA or thiamine given singly. It was concluded however that thiamine, even by itself, does increase lead excretion via bile and urine, a beneficial effect that has not been followed up since. The influence of dietary protein deficiency on the effects of exposure to lead or its combination with copper was investigated in rats.

Thiamine Saves — Mercury Free Kids

I am adding to this list a high body burden of mercury.
Amalgam (mercury) dental fillings.

Thiamine has a sulfur molecule in it, and mercury having an affinity for sulfur will tear the Thiamine compound apart to bind with that sulfur molecule.

 

[Bart1]

I have high mercury and lead too. I found some interesting info about thiamine for heavy metals.

I'll paste my notes here for you:
thiamine and heavy metals quotes

Thiamine (2–4 mg/kg per day, SC) alleviates clinical manifestations and reduces tissue deposition of lead. Combined Ca-EDTA and thiamine treatment appears to produce the most beneficial response. Lead Poisoning in Animals - Toxicology - Merck Veterinary Manual

Lead induced thiamine deficiency in the brain decreased the threshold of electroshock seizure in rat

Thiamine supplementation reversed these signs and decreased the brain lead concentration in the lead treated group. The results from the present study suggest that the increased seizure susceptibility induced by lead intoxication in rats may be mediated at least in part through the changes of thiamine status.



Thiamine and zinc in prevention or therapy of lead intoxication: Thiamine and zinc in prevention or therapy of lead intoxication - PubMed

Thiamine, zinc or their combination given through gastric gavage were investigated for their ability to prevent or treat experimental lead toxicity in rats. Simultaneous dietary supplementation with thiamine plus zinc was found to be the most effective way of reducing the lead-induced inhibition of delta-aminolevulinic acid dehydratase activity in blood, urinary, excretion of delta-aminolevulinic acid and accumulation of lead in blood, liver and kidney. Prevention was more effective than post-lead exposure treatment which may be due mainly to the decrease in the absorption of lead in the gastro-intestinal tract in the presence of thiamine and/or zinc.



Eating to Block Lead Absorption | NutritionFacts.org

Intake of certain nutrients has been associated with lower lead levels in the body. For example, women with higher intake of thiamine, also called vitamin B1, tended to have lower blood lead levels, and the same was found for lead-exposed steel workers—and not just with thiamine, as “content of dietary fiber, iron, or thiamine intake each correlated inversely with blood lead concentrations in workers…” The thinking is that the fiber might glom onto the lead and flush it out of the body, the iron would inhibit the lead absorption, and the thiamine may accelerate lead removal through the bile. So, researchers suggest that eating lots of iron, fiber and especially thiamine-rich foods “may induce rapid removal and excretion of the lead from the tissues.” But thiamine’s never been put to the test by giving it to people to see if their lead levels drop. The closest I could find is a thiamine intervention for lead-intoxicated goats.



Thiamin (vitamin B1) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential

Thiamin (vitamin B1) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential:

The purpose of this study was to evaluate the effects of thiamin on lead (Pb) poisoning in cattle. Fifteen Holstein male calves were divided into three groups: Group I served as controls, Group II calves were dosed orally with 5 mg Pb acetate/day/kg of body wt, and Group III calves were dosed similarly with Pb and with 100 mg/day/calf of thiamin hydrochloride, subcutaneously. Calves were treated daily for 20 days. None of the control or Pb plus thiamin-treated calves showed clinical signs of poisoning and no deaths occurred. However, four of five Pb-treated calves showed signs of Pb poisoning and two died during the study. Tissues from both groups receiving Pb contained significantly higher (p < 0.01) concentrations of Pb than tissues from control calves. However, tissues from calves receiving Pb plus thiamin contained 2 to 10 times less Pb than tissues from calves receiving only Pb. The Pb concentrations in liver, kidney, and blood from thiamin-treated calves remained below confirmatory levels associated with Pb poisoning; while Pb concentrations in the same tissues from calves dosed only with Pb were within the range considered diagnostic of Pb poisoning. On the other hand, δ-aminolevulinic acid dehydratase activity in erythrocytes was decreased 70% from pretreatment levels in both groups receiving Pb. Thus, thiamin appeared to have no protective effect on the ability of Pb to inhibit this enzyme. But in the tissues analyzed, thiamin interacted with Pb in some way to prevent tissue accumulation, thus preventing clinical signs and death. These results suggest that therapeutic doses of thiamin may be of value in the prevention and treatment of Pb poisoning in cattle, and in other animals or humans exposed to high environmental levels of Pb.



Thiamine reduces tissue lead levels in rats: mechanism of interaction - BioMetals

Lead (Pb) toxicity has been a serious concern in industrialized societies because of its association with functional deficits in nervous, haematopoietic and renal systems. Several studies have shown beneficial effects of thiamine on Pb toxicity. It is speculated that Pb chelation by thiamine may be a possible mechanism. However, the exact nature of these interactions remained elusive. In the present study we have characterized the interaction of Pb with thiamine using UV–Vis as well as fluorescence spectroscopic methods and studied the effect of thiamine treatment on blood and tissue Pb levels during simultaneous or post-exposure to Pb in rat model. The spectroscopic studies revealed that Pb interacts with the pyrimidine ring of thiamine, leading to its solubilization at physiological pH. Further, thiamine reduced the Pb levels in blood, kidney and bone during both simultaneous and post-exposure Pb treatment. Interestingly, thiamine appears to prevent the accumulation of Pb in bone during simultaneous treatment. Together these results suggest that pyrimidine ring of thiamine mediates its interaction with Pb, leading to the prevention of its accumulation and/or increased clearance from tissues.

Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on dead toxicity

Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on dead toxicity

Calcium disodium ethylenediaminetetracetate (CaNa2EDTA; Versenate) was more effective than thiamine (vitamin B1) in enhancing the urinary excretion of lead, reducing tissue lead and restoring lead induced biochemical alterations in rats. However, the combination of CaNa2EDTA and vitamin B1 enhanced the beneficial effect of CaNa2EDTA in lead intoxication and was particularly effective in reducing the brain concentration of lead.

more: thiamine and heavy metals, including iron overload:

https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12146

quote: We hypothesize that excess iron, that is, brain iron overload (BIO), is a highly relevant pathway leading to cognitive deterioration in individuals with AUD. We further hypothesize thiamine depletion, a common concomitant feature in AUD patients, to be a key stimulus for BIO, as thiamine deficiency disrupts the integrity of the blood-brain barrier (BBB), enabling iron from the circulation to enter the brain in an uncontrolled manner.



Vitamin B1 Deficiency a Key Factor in the Development of Alcohol-Related Dementia - Neuroscience News

quote: A common consequence of chronically high alcohol consumption is a decline in cognitive function, which can even progress to full-blown dementia. However, we do not yet fully understand how alcohol damages the brain. A research group led by Stephan Listabarth from MedUni Vienna’s Department of Psychiatry and Psychotherapy, Division of Social Psychiatry, has now developed a hypothesis whereby iron deposits in the brain – resulting from alcohol-induced vitamin B1 deficiency – can be regarded as key factors in cognitive decline. The work has now been published in the leading journal “Alzheimer’s and Dementia”.



Chelation Therapy in Medicine - Hormones Matter

quote: Because of a sick cow, a farmer had called a veterinarian who had recognized the symptoms of thiamine (vitamin B1) deficiency. When given an injection of the vitamin the symptoms in the cow had disappeared but they had subsequently returned and the veterinarian was asked to come again. Thinking this was a strange recurrence, the doctor had the presence of mind to search the field where the cow had been grazing. He had found an old trunk in a corner of the field that was partly covered with lead paint and which the cow had been licking. Lead has a sweet taste and the veterinarian concluded that this was the cause of the thiamine deficiency. In a study using rats, calcium disodium EDTA was more effective than thiamine in enhancing the urinary excretion of lead in restoring lead induced biochemical alterations. However, the combination of the drug and thiamine enhanced the beneficial effect and was particularly effective in reducing the brain concentration of lead.

In lead loaded sheep the combination of EDTA and thiamine administration was better than EDTA or thiamine given singly. It was concluded however that thiamine, even by itself, does increase lead excretion via bile and urine, a beneficial effect that has not been followed up since. The influence of dietary protein deficiency on the effects of exposure to lead or its combination with copper was investigated in rats.

Thiamine Saves — Mercury Free Kids

I am adding to this list a high body burden of mercury.
Amalgam (mercury) dental fillings.

Thiamine has a sulfur molecule in it, and mercury having an affinity for sulfur will tear the Thiamine compound apart to bind with that sulfur molecule.

Wow thank you so much! Thiamin is really amazing! Lots of reading to do

 

[mostlylurking]

Wow thank you so much! Thiamin is really amazing! Lots of reading to do

You're welcome. I've found thiamine to be very helpful; I want to share the info.

 

[cs3000]

You're welcome. I've found thiamine to be very helpful; I want to share the info.

thanks, full text link for the 1st one THIAMINE IMPROVES LEAD-INDUCED NEUROTOXICITY IN RATS: BEHAVIORAL, BIOCHEMICAL AND STRUCTURAL ASSESSMENT

(Interesting how brain serotonin went up 2x in the lead intoxicated rats, which they associated with the increased anxiety, and also lowered GABA, which both were close to normal baseline in the thiamine group, ~1g human dose used. other human study showed increased lead excretion at 100mg. this also mentions how lead can deplete iron and skew tryptophan levels high, where the other one says correcting thiamine deficiency can prevent iron overload too so helps to balance both ends by the looks of it). did not fully prevent all brain lesions but prevented all severe lesions, and most moderate lesions.