The Ocean’s Mysterious Thiamine Deficiency

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cjm

cjm

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have you tried adding aspirin too?

I compiled research on aspercreme (read: "aspirin cream") that I'm gussying up for posting (I'm currently in the "there is no Pepe Silvia" phase). I'm obliged to start a separate thread shortly but I think you'll find it very interesting. COX-1 inhibition often takes the blame for adverse reactions but aspirin has a direct action that has been neglected in literature discussion of oral supplementation. Slight tease here, since I don't know how many loose ends are hiding in my argument:

"NSAIDs can cause right dorsal colitis in horses. This colitis is characterized by necrosis, resulting in erosions and ulcers. Epithelial loss may be severe, with only regenerating, rounded islands of normal mucosa remaining. The massive edema of the denuded intestine causes rupture of the submucosa in an elongated diamond-like pattern. The mechanism of injury is direct by topical application (oral administration) and through inhibition of prostaglandin synthesis."

Oral administration is a misnomer. Therapeutic substrate delivery is always topical if it's not injected. It's just a different skin inside the body.
 

TheSir

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It would be a temporary boost in the requirement, because thiamine is a treatment for lead poisoning, in conjunction with vitamin C and calcium EDTA.
I think acute lead poisoning is different from chronic toxicity in which lead has been integrated into your physiology as a metabolic surrogate for absent minerals such as calcium. This is why while Lonsdale is able to get Parkinson's go into remission with megadosing thiamine, the patient will begin to regress back into the disease if the regimen is stopped. This is because the lead and the functional blockages have not gone anywhere. @mostlylurking is a living example of this phenomenon (not Parkinson's).
 

mostlylurking

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I think acute lead poisoning is different from chronic toxicity in which lead has been integrated into your physiology as a metabolic surrogate for absent minerals such as calcium. This is why while Lonsdale is able to get Parkinson's go into remission with megadosing thiamine, the patient will begin to regress back into the disease if the regimen is stopped. This is because the lead and the functional blockages have not gone anywhere. @mostlylurking is a living example of this phenomenon (not Parkinson's).
According to Dr. Lonsdale, thiamine will resolve lead poisoning. There's a transcript of the interview here. Here's part of it:
"SB: That’s great, and I also recall that TTFD I believe there were some studies you mentioned – or in some of your research where it had protective capabilities against lead and some heavy metals if I am recalling correctly?

DL: That’s correct. Yes. It’s interesting because thiamine actually the mechanism is not by any means clear, but it clears the lead through the liver. It goes through the bialary system. So the lead comes out in the stool. Not in the urine, and what people are looking for is lead in the urine and they should be looking for it in the stool if they use thiamine. Well of course nobody is using thiamine because they don’t know about it, but I would have loved to have got in touch with the people in Flint and tell them that the kids that have lead poisoning all they need is 100 milligrams of thiamine a day and that will ease the lead out of their systems."
-end paste-

According to other researchers, the most successful way to get lead out is to combine thiamine with EDTA IV chelation. But, the researchers doing the study may well have been looking for the lead in the urine, which is what is tested in an EDTA challenge test (EDTA IV, then a 24 hour urine collection afterwards). They compared the results of thiamine alone, EDTA alone, and the two administered simultaneously.

Dr. Costantini had more experience treating Parkinson's Disease patients with thiamine (around 4000 patients over a period of around 11 years); he used thiamine hcl, by injection and also oral doses. He provided his opinion about why the thiamine treatment wasn't a "cure" but did resolve the symptoms of Parkinson's.

from Dr. Costantini's FAQs: FAQ
After I am stable on the right dose of thiamine, what happens if I suddenly stop taking it?

Q: Once a person has established the correct dose ofthiamine / B-1 and is stable, including a good response to the Pull Test and agood reduction of symptoms, if this person suddenly suspends thiamine whathappens?

A . Nothing appreciable happens. The patient’s conditiondoes not change for 1-3 months.

This is because the attack of the disease, not opposed bythiamine, starts again, but it takes a long time before it damages the cellsagain before they are healed by thiamine.

We have numerous confirmations in this regard, so much sothat in Italy we used to suspend thiamine one week a month to avoid risks ofoverdose and give the impression of “freedom” to the patient.

Look at Alberto’s video on highdosethiamine.org(Dr. Costantini’s website): after two years of treatment, it was recorded withthe patient who had not had thiamine injections for three months.

After this period the symptoms begin to reoccur; the samedose of thiamine begins again and in a short time everything returns as beforethe suspension.
-end paste-

Here are some of Dr. Costantini's studies:
High-dose thiamine as initial treatment
for Parkinson’s disease
from this study:
"On the whole, we had a favourable response to thiamine. The
patient reported a robust improvement of the symptoms.
Compared with other available therapies, thiamine therapy was
associated with an equal improvement in motor function, as
assessed by reduced scores in the UPDRS.2 Responsiveness to
levodopa (required to exceed 25–30% reduction in the motor
part of the UPDRS) is a diagnostic criterion for PD.2 Moreover,
fatigue and pain have improved (likely thanks to the normalisation
of the muscular tone). The absence of blood thiamine deficiency
and the efficacy of high-dose thiamine in our patients
suggest that the symptoms of PD are the manifestation of a thiamine
deficiency likely due to a dysfunction of the active transport
of thiamine inside the cells or due to structural enzymatic
abnormalities. In other words, we believe that the motor and
non-motor symptoms of PD could derive from a chronic thiamine
deficiency which is composed by:
1. Severe focal thiamine deficiency that could determine a progressive
dysfunction and selective neuronal loss in the substantia
nigra pars compacta and in other centres that are
typically hit in this disease.
2. Mild thiamine deficiency in all other cells that could lead the
cells to a suffering state and the presence of fatigue. Fatigue
could be the true systemic symptom of the disease. In our
opinion, the primary cause of PD is less expressed in all
other cells where the disease determines a mild thiamine
deficiency that causes fatigue and related disorders.3
Moreover, a dysfunction of intracellular thiamine transport
was described for genetic diseases characterised by mutations in
thiamine-transporter genes.9–11 A number of in-born errors of
metabolism have been described in which clinical improvements
can be documented following administration of pharmacological
doses of thiamine, such as thiamine-responsive megaloblastic
anaemia and Wernicke’s like encephalopathy.9–11 Genetic disorders
of thiamine metabolism that lead to neurological disease
can be treated with large doses of thiamine.12
The exact mechanism of thiamine responsiveness in these
patients is unknown.
In any case, the injection of high doses of thiamine was effective
in reversing all symptoms, suggesting that the abnormalities in
thiamine-dependent processes could be overcome by diffusion mediated
transport at supranormal thiamine concentrations.
Furthermore, we believe that parenteral thiamine administration
may play an important role in restoring survivor neurons
and in limiting the progression of the disease because the dysfunction
of thiamine-dependent processes could be a primary
pathogenic pathway leading to the demise of dopaminergic and
non-dopaminergic neurons in PD
(figure 1).13 14
In literature, there is no mention of thiamine-related
adverse effects even at high doses and for very long periods of
time.15
In conclusion, we believe that this report represent an important
contribution to the subject; nonetheless, further experience
is necessary to confirm the present observations."

An open-label pilot study with
high-dose thiamine in Parkinson’s disease

Long-Term Treatment with High-Dose

Thiamine in Parkinson Disease:
An Open-Label Pilot Study
 
Last edited:

Apple

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So, what 's the best natural source of thiamine ?
I see that pork is really top source but I rarely eat it.
 

David PS

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So, what 's the best natural source of thiamine ?
I see that pork is really top source but I rarely eat it.
thiamin-b1-foods-printable.png
 

A-Tim

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So, what 's the best natural source of thiamine ?
I see that pork is really top source but I rarely eat it.
I like to eat oranges as my main source of B1. Assuming wikipedia is correct, 100g of orange has 0.087mg of B1. Assuming the target is 1.1-1.2mg p/day, if you were aiming to get all your B1 from a single source (unlikely), that is 1.3kg of oranges p/day.

Oranges are cheap and available all year round where I live. I find them tasty and they have other benefits as discussed on the forums. Since B1 is heat sensitive, usually you'll lose some B1 in other foods that are cooked. Oranges are eaten raw - so no B1 loss. No anti-nutrients in fruit - so absorption isn't going to be inhibited. It wouldn't surprise me that if you got the bulk of your B1 from oranges that the rda is effectively lower.

The main risk here would be if you get an excess of a nutrient from this amount of oranges. The likely culprit would be vitamin c. There is some risk it could interfere with copper absorption, or that it de-loads copper from ceruloplasmin. Chris Masterjohn explains below. You could mitigate this risk by having slightly fewer oranges p/day.

 

peter88

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So, what 's the best natural source of thiamine ?
I see that pork is really top source but I rarely eat it.
Lean pork. Seems like countries that thrive on refined carbs (mostly white rice) eat pork.
 
OP
cjm

cjm

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Messages
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Location
Baltimore, MD
I think acute lead poisoning is different from chronic toxicity in which lead has been integrated into your physiology as a metabolic surrogate for absent minerals such as calcium. This is why while Lonsdale is able to get Parkinson's go into remission with megadosing thiamine, the patient will begin to regress back into the disease if the regimen is stopped. This is because the lead and the functional blockages have not gone anywhere. @mostlylurking is a living example of this phenomenon (not Parkinson's).

Interesting. Thanks for making that distinction.
 
OP
cjm

cjm

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Joined
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Messages
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Location
Baltimore, MD
I like to eat oranges as my main source of B1. Assuming wikipedia is correct, 100g of orange has 0.087mg of B1. Assuming the target is 1.1-1.2mg p/day, if you were aiming to get all your B1 from a single source (unlikely), that is 1.3kg of oranges p/day.

Oranges are cheap and available all year round where I live. I find them tasty and they have other benefits as discussed on the forums. Since B1 is heat sensitive, usually you'll lose some B1 in other foods that are cooked. Oranges are eaten raw - so no B1 loss. No anti-nutrients in fruit - so absorption isn't going to be inhibited. It wouldn't surprise me that if you got the bulk of your B1 from oranges that the rda is effectively lower.

The main risk here would be if you get an excess of a nutrient from this amount of oranges. The likely culprit would be vitamin c. There is some risk it could interfere with copper absorption, or that it de-loads copper from ceruloplasmin. Chris Masterjohn explains below. You could mitigate this risk by having slightly fewer oranges p/day.


Something I learned recently is that oranges are slightly copper "deficient" (compared to carbohydrate content, I believe) and can/should be balanced with something like pomegranate or pineapple. @electricsematic has posted about this and has a wild blog. But point granted, they are a B1 and otherwise all around nutrient powerhouse.
 

Regina

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I bathed in ~50 grams last night for 30 minutes. I went from 5 grams to 12 to 26 to 51 per bath over the course of a week. My tub is small, ~40 gallons. My nerves are coming alive.
Incredible. Thx for the update.
 
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I bathed in ~50 grams last night for 30 minutes. I went from 5 grams to 12 to 26 to 51 per bath over the course of a week. My tub is small, ~40 gallons. My nerves are coming alive.
thank you for explaining this!
 

Mathgirl

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I tried a magnesium and Thaimine bath. Sooo Relaxing. Felt great afterwards. 700mg Thiamine HCL and about 1/4 cup of magnesium chloride flakes
 

A-Tim

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Something I learned recently is that oranges are slightly copper "deficient" (compared to carbohydrate content, I believe) and can/should be balanced with something like pomegranate or pineapple. @electricsematic has posted about this and has a wild blog. But point granted, they are a B1 and otherwise all around nutrient powerhouse.
Thanks, I'll take a look.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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