I have been on B1 injections for 3 months now (100 mg weekly). I have no idea if this dose is suitable for me. But one question is haunting me - why is it so important to find just the right dose? Why not take a very high dose and let the excess be excreted anyway? I hope this is not a stupid question
Best wishes! Mojca
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narcisa956
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What forum members have reported who are using or testing HDT/B-1 and so has Dr. Costantini, is that a dose that is too high will very frequently cause a worsening of existing PD symptoms and in some cases, new symptoms may appear that have not previously been experienced. Overall, PD symptoms seem to worsen at too high of a dose.
Thank you. That works. It is therefore important to clarify that, within a reasonable safety band , excess B1 is excreted, but above a certain level it can cause adverse events
Have you checked your serum magnesium status? If you're not noticing much difference, in the least be sure that you're not deficient in Mg since it is a required co-factor. Magnesium L-Threonate is a good form to try to cross the BBB.
The reason why the correct amount (of anything) is important involves the understanding of methylation metabolism, but incorrect balance because of malnutrition (or SNPs/epigenetics/toxins) can lead to high level of homocysteine (b6, b9 and b12 involved, an inflammatory biomarker) and among other things affect glycine (inhibitory neurotransmitter & a buffer of excess methyl groups, used by SAM->SAH). If you end up exhausting nutrients and the available methyl groups (CH3 - needed for the synthesis of creatine, phosphatidylcholine, etc) that starts/stops any gene/enzymatic reactions, it causes backups/jams in the cycle and you could also end up wasting glycine (esp if deficient in b2, choline or due to excess b3/b9 metabolism), and dysregulation of dopamine (COMT methylation), histamine (need methyl donor SAM and NAD+ to be metabolized), etc. B1 is used as an important cofactor (a spark) of most enzymatic reactions in the Krebs cycle for ATP required for methylation involving all Bs and other nutrients/minerals (including the important magnesium, zinc, copper, etc).
The result of imbalance of various reactions in the simplest relevant explanation will involve a no reaction or possible increased inflammation (back/joint/muscle pain), decreased detox, and worsening of PD symptom, but not permanent if because of short run B1 overdose. This is the reason why it's also important to identify/address any nutritional gap.
Too high of a dose made me jittery, kept me awake and made my dyskinesia worse. Some members have reported high blood pressure from too high of a dose and some others have also reported feeling jittery. It may not be "harmful" but it may make you feel bad.
Excess histamine in result of induced undermethylation (not enough methyl donors left after ramped up B1 metabolism and nutrient shortage) can affect the circadian rhythms (sleep/wake cycle) and cause insomnia, jitter, rash, allaergies, GERD, etc. Low glycine (because this transsulfuration synthesis through cysteine takes a backseat to SAM availability and dependent on adequate methylation) also affects sleep, inflammation, and detoxification (glycine is needed for glutathione). Blood pressure regulation can get compromised if left deficient in CH3 and magnesium that controls potassium (or deficient in K). If dopamine reuptake activity (esp if left excess of b3 that inhibits sirtuin thus increases DAT transport) dominates the amount available (compounded by deficient CH3 for dopamine synthesis from tyrosine), you’re left with lesser of the NT and feel worse.
Thiamine has been known and used for more than a hundred years to solve "beri beri", and also in emergency rooms to solve alcohol problems. Its pharmacokinetics and its effects have been widely studied. Here's a study of how b1 behaves in blood. You will also find interesting the amount of studies in references especially point 31 , 32 if I am not mistaken.
It’s also important to keep in mind that some people have compromised active transport activity of thiamine especially if they’ve been deficient for a while. That is why a high dose therapy is needed for the passive transport so that absorption could occur, and if the transketolase enzyme activity slowly gets restored for the active transport(for some this doesn’t happen), you can reduce the amount of the dosage eventually. I assume this is why Dr. C started his patients at as high as 2-4g oral dosage to begin with, monitor symptoms, and adjust per individual. You can also opt for TTFD since it does not depend on the transport enzymes to cross the BBB.
Answer: you can have side effects or potential toxic interactions or mutatiins that affect your processing to the bad. Also see Sharon's recent comment that's worth researching.
Also per rescuema comment a couple days ago now looking into TTFD.
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