I have not heard anything that would contraindicate Vitamin B1 (thiamin / thiamine) with respect to Prostate Cancer, and I have heard that it can protect against Chemo related nerve damage.
Does anyone else have any information, comments, opinions, links, or questions about Vitamin B1?
Here's an interesting paper [1].
Definitions:
... Antinociception - the action or process of blocking the detection of a painful or injurious stimulus by sensory neurons
... PAP - prostatic acid phosphatase -"an enzyme produced by the prostate. It may be found in increased amounts in men who have prostate cancer" (Wiki)
"... our study highlights an obligatory role for PAP in the antinociceptive effects of thiamine and phosphorylated thiamine analogs, and suggests a novel phosphatase-independent function for PAP."
-Patrick
[1] pubmed.ncbi.nlm.nih.gov/231...
Prostatic acid phosphatase is required for the antinociceptive effects of thiamine and benfotiamine
Julie K Hurt 1 , Jennifer L Coleman, Brendan J Fitzpatrick, Bonnie Taylor-Blake, Arlene S Bridges, Pirkko Vihko, Mark J Zylka
Affiliations expand
PMID: 23119057 PMCID: PMC3485352 DOI: 10.1371/journal.pone.0048562
Free PMC article
Abstract
Thiamine (Vitamin B1) is an essential vitamin that must be obtained from the diet for proper neurological function. At higher doses, thiamine and benfotiamine (S-benzoylthiamine O-monophosphate, BT)-a phosphorylated derivative of thiamine-have antinociceptive effects in animals and humans, although how these compounds inhibit pain is unknown. Here, we found that Prostatic acid phosphatase (PAP, ACPP) can dephosphorylate BT in vitro, in dorsal root ganglia (DRG) neurons and in primary-afferent axon terminals in the dorsal spinal cord. The dephosphorylated product S-benzoylthiamine (S-BT) then decomposes to O-benzoylthiamine (O-BT) and to thiamine in a pH-dependent manner, independent of additional enzymes. This unique reaction mechanism reveals that BT only requires a phosphatase for conversion to thiamine. However, we found that the antinociceptive effects of BT, thiamine monophosphate (TMP) and thiamine-a compound that is not phosphorylated-were entirely dependent on PAP at the spinal level. Moreover, pharmacokinetic studies with wild-type and Pap(-/-) mice revealed that PAP is not required for the conversion of BT to thiamine in vivo. Taken together, our study highlights an obligatory role for PAP in the antinociceptive effects of thiamine and phosphorylated thiamine analogs, and suggests a novel phosphatase-independent function for PAP.
"Prostatic acid phosphatase is required for the antinociceptive effects of thiamine and benfotiamine"
1. I thought benfotiamine was thiamine
2. I thought benfotiamine / thiamine healed nerves as opposed to just block nerve pain.
3. Do I understand this to mean that the more active your prostate cancer the more effective is the benfotiamine / thiamine?
I commented recently that I had seen B1 touted by Dr Berg as a remedy, or at least helpful, with sleep apnea. Search 'B1 and sleep apnea' on youtube. Any comments on this claim?
sciencedaily.com/releases/1...
That's good to know -- too much B1 is a danger. BTW, that 'Dr' Berg is a chiropractor touting all sorts of supplements.
en.wikipedia.org/wiki/Benfo...
Benfotiamine (rINN, or S-benzoylthiamine O-monophosphate) is a synthetic S-acyl derivative of thiamine (vitamin B1) that sold as a medication or dietary supplement to treat diabetic neuropathy. Combination drugs with pyridoxine or cyanocobalamin are also marketed.
Benfotiamine was developed and invented in Japan then reported internationally by Wada, Takagi, Minakami et al. in 1961.[1]
Uses
Benfotiamine is primarily marketed as an over-the-counter drug to treat diabetic neuropathy;[2] clinical trials results are mixed, finding it mildly useful or no different from placebo.[3][4]
Adverse effects
There is little published data on adverse effects;[5] in one study of a combination drug of benfotiamine, pyridoxine, and cyanocobalamin, around 8% of people taking the drug experienced nausea, dizziness, stomach ache and weight gain.[5]
Pharmacology
Benfotiamine is more bioavailable than thiamine salts,[6] providing higher levels of thiamine in muscle, brain, liver, and kidney.[5]
Benfotiamine is dephosphorylated to S-benzoylthiamine by ecto-alkaline phosphatases present in the intestinal mucosa, and is then hydrolyzed to thiamine by thioesterases in the liver.[7]
Benfotiamine mainly acts on peripheral tissues through an increase in transketolase activity.[7][5][8]
Chemistry
Benfotiamine is a synthetic S-acyl Vitamin B1 analogue; its chemical name is S-benzoylthiamine O-monophosphate.[9] Benfotiamine is a lipid derivative of thiamine vitamin. It has very low solubility in water or other aqueous solvents.[7]
Society and culture
As of 2017, benfotiamine was marketed as a pharmaceutical drug in Argentina, Bosnia & Herzegowina, Bulgaria, Colombia, Czech Republic, Estonia, Georgia, Germany, Hong Kong, Hungary, India, Indonesia, Japan, Latvia, Lithuania, Poland, Portugal, Romania, Serbia, Slovakia, Slovenia, Russian Federation, Taiwan, and Vietnam under the following brand names: Benalgis, Benfogamma, Benforce, Benfotiamina, Biotamin, Biotowa, Milgamma, and Vilotram.[10]
It was also marketed in some jurisdictions as a combination drug with cyanocobalamin as Milgamma, in combination with pyridoxine as Milgamma, in combination with metformin as Benforce-M, and with thiamine as Vitafos.[10]
Research
Benfotiamine has been studied in laboratory models of diabetic retinopathy, neuropathy, and nephropathy.[11] As of 2015 there had been one clinical study of benfotiamine in diabetic nephropathy.[12]
Administration of benfotiamine may increase intracellular levels of thiamine diphosphate, a cofactor of transketolase,[11] and based on metabolic theories of Alzheimer's disease, it has been studied in preclinical models of Alzheimer's disease.[13][clarification needed] If proven to be effective in humans, as it was shown in mouse models, the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of Alzheimer's disease progression.
Hi Nal, why oil soluble Benafotamide rather than water soluble Benfotiamine which I am taking ? I’d read that in low doses B-1 can actually promote cancer tumor growth but couldn’t find the source of these claims. I intend to follow your advice on this and other supplements because it’s very confusing with the advice, dosing etc. My neuropathy is not bad but as I age I am sure it will be bigger issue. Thanks
ncbi.nlm.nih.gov/pmc/articl...
Hmmm But it doesn't refer to any particular type of cancer.
That is less than ideal.
Thanks I’ll review…
Nal, I will run this by my MO. I've read that some people have GI tract issues with Alpha-Lipoic acid so I'll watch out for that. Toe, feet neuropathy is the fire I'm trying to put out. Like other people have described it's like having a pillow under the top part of your foot. Many Thanks!
I'm in Arlington, VA with snow on the ground and I'm jealous. Love fresh fish and great weather. Do you recommend people see a Naturopathy practitioner for aPC? For both the disease and side effects (including medication SE's) it seems they may have some good complimentary treatments. Anyway, enjoy the sun....Appreciate it, Cheers!
Just to clarify.
The B1 (in whatever form taken) is helpful to prevent neuropathy, but can't really help dead nerves.
The B1 does have potential to aggravate prostate cancer if over used.
R-Lipoic Acid helps the neuropathy benefits of B1, but unlike B1, would not be expected to aggravate prostate cancer, though it may have other adverse issues if overused.
Did I capture what you said accurately?
Lol, I was assuming the oil soluble, but I did want to get into those weeds.
Just trying to clarify that, with respect to prostate cancer only, the R-Lipoic Acid won't aggravate it, but overdoing the B1.
Yet they do work together.
Just wanted to make sure I was understanding you properly.
ncbi.nlm.nih.gov/pmc/articl...
>75 times rda appears to be helpful slowing cancer growth.
12-75 times rda appears to contribute to cancer growth.
Thiamine is the water soluble B1 form. Benfotiamine is the fat soluable form. The 1998 early study conflicts with newer data. Low B1 status is correlated with high PCa risk but we are all beyond that stage here having confirmed PCa diagnosis.
The study @GeorgeGlass references appears to be in vitro.
The only thing I can conclude from everything I could find is megadoses (seen reports up to several grams) don't appear to have any safety risk, at least I couldn't find any.
In-vivo study on Benfotiamine seems to have potential but they haven't determine the right dose.
sciencedirect.com/science/a...
It seems concludion is:
a) deficiciency = PCa risk and defficiency as as a side effect from treatment, is bad for cancerby activating the transcription factor p53
b) moderate doses are bad 12-75 time RDA per what george said or even higher per below.
c) mega doses have anti-cancer potential but there are no human studes. Doses like 2500X RDA according to this study. That would be what, close to 3 grams?
pubmed.ncbi.nlm.nih.gov/114...
I believe I saw a study about breast cancer where the dosages where in the 200-500mg range of thiamine that had anti-cancer effects but can't find it.
The substances with U shape curve responses, or I guess in this case it's a n shaped curve?
I'm not certain I understood all that, but thank you.
TL; DR version of my novel-length comments:
Based on in-vivo and rat studies, it is probably best to avoid Thiamine (B1) supplementation unless blood tests confirm you have a severe deficiency in which case I would think the best strategy is to take the bare minimum amount of B1 to correct it to the lowest level not cosidered deficient.
Theoretically if you took 300-600mg of Benfotiamine a day it may slow cancer but I think it's a bit risky, as shown in the rat study the cancer grew faster during the period where they were no longer deficient but not say, for lack of better word, at the "over saturated" level. Most supplements (other than 300+ mg Benfotiamine) I hypothesize would put you in that middle "well sufficient" level which can help the cancer grow (or at least it did in rats.)
If one could consistently take mega-doses of fat soluble Benfotiamine, you're basically rolling the dice it can help without any human clinical trials. (Although that's the case for a lot of nutraceuticals)
ncbi.nlm.nih.gov/pmc/articl...
"Vitamin B1 supplementation has a duality of effects on cancer cell survival and proliferation. At low to moderate doses, thiamine has been shown to support cancer cell proliferation."
B1 is good for neuropathy that you can get from diabetes and chemo.
That's a good point. The benefits in that case may outweigh any potential risk on the PCa side of things. I believe if you maintained daily high dose of Benfotiamine, you could get those benefits while potentially hindering the PCa. It's just that there are no human clinical studies to confirm that yet.
I'm going to go ahead and post a direct comprehensive reply to this as my recent research has by eyebrows raised on the potential of lyophilic thiamine (aka Benfotiamine.) I'm not giving medical advice but I know a lot of people here are open to trying things and watch if there's a change in their PSA kinetics. Things like Sulforphane (broccoli seed extract), melatonin, green tea extract (ECGC), curcumin, etc etc etc. These and others have some study data and anecdotal reports but it appears Benfotiamine use relating to cancer has relatively much less data (especially recent data) compared to these other more well-known substances, and I can find no anecdotal reports from Prostate Cancer patients.
To summarize what the data so far shows (read all the info yourself to confirm), low to medium doses of Thiamine (Vitamin B1) can possible accelerate cancer progression. However all data I have seen so far shows that high-dose Thiamine, especial the lyophilic form (fat-soluble) Benfotiamine, has anti-cancer effects. Here are is all the published data I've found that appears relevant starting with the most compelling evidence first.
Anyone considering trying this should probably read all the information on Examine.com to understand all the different possible effects:
examine.com/supplements/vit...
More specific studies related to cancer (some already referenced previous but including them for reader convenience):
> Thiamine mimetics sulbutiamine and benfotiamine as a nutraceutical approach to anticancer therapy
"The chemotherapeutic effectiveness of benfotiamine translated in vivo where its administration reduced tumor growth in a subcutaneous xenograft model of HCT 116 cells. To our knowledge, this is the first in vivo evidence for the anticancer effect of a commercially available thiamine analog. Highlighting the therapeutic safety of benfotiamine, no systemic toxicity was observed following bolus pharmacologic doses (250 mg/kg) administered via IP injection every second day. This supports the tolerability of daily benfotiamine administration (600–900 mg/day) that has previously been demonstrated in clinical trials for diabetic nephropathy"
sciencedirect.com/science/a...
> High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate
"Our findings suggest that high dose thiamine reduces cancer cell proliferation by a mechanism similar to that described for dichloroacetate."
ncbi.nlm.nih.gov/pmc/articl...
> The effect of thiamine supplementation on tumour proliferation. A metabolic control analysis study
"Thiamine supplementation in doses between 12.5 and 250 times the recommended dietary allowance (RDA) for mice were administered starting on day four of tumour inoculation. We observed a high stimulatory effect on tumour growth of 164% compared to controls at a thiamine dose of 25 times the RDA. This growth stimulatory effect was predicted on the basis of correction of the pre-existing level of thiamine deficiency (42%), as assayed by the cofactor/enzyme ratio. Interestingly, at very high overdoses of thiamine, approximately 2500 times the RDA, thiamine supplementation had the opposite effect and caused 10% inhibition of tumour growth. This effect was heightened, resulting in a 36% decrease, when thiamine supplementation was administered from the 7th day prior to tumour inoculation. Our results show that thiamine supplementation sufficient to correct existing thiamine deficiency stimulates tumour proliferation as predicted by MCA. The tumour inhibitory effect at high doses of thiamine is unexplained and merits further study."
(10% and 36% don't seem very impressive [to me] though)
pubmed.ncbi.nlm.nih.gov/114...
The Effects of Thiamine on Breast Cancer Cells
"Conclusions: The treatment of MCF7 breast cancer cells with 1 μg/mL and 2 μg/mL of thiamine for 24 h significantly reduced their proliferation. This reduction is associated with a reduction in glycolysis and activation of the PDH complex in breast cancer cells."
ncbi.nlm.nih.gov/pmc/articl...
> Prostatic acid phosphatase (PAP) is required for the antinociceptive effects of thiamine and benfotiamine
(my main takeway on this one is that PAP is increased in men with Prostate Cancer - it is unclear to me if this is to a lesser degree though after prostatectomy?)
pubmed.ncbi.nlm.nih.gov/231...
Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamin derivative
"Biokinetic data, measured as area under the curve and maximal concentration in plasma and hemolysate after ingestion, demonstrated a significantly improved bioavailability from the lipophilic derivative despite an ingested dose of only 40% as compared with the water-soluble salt. A superior cellular efficacy of benfotiamine was also concluded from the short-term stimulation of the thiamin-dependent transketolase activity in erythrocytes."
pubmed.ncbi.nlm.nih.gov/177...
Examining the full publication, by my math, 27 mg (not 40) Benfotiamine is equivalent to 100 mg Thiamine supplement based on the Plasma AUC numbers. Even greater difference based on Hemosylate AUC)
sci-hub.se/https://doi.org/...
> Pharmacokinetic study of benfotiamine and the bioavailability assessment compared to thiamine hydrochloride
"The transformation process of benfotiamine to thiamine produced large amount of hippuric acid. No accumulation of hippuric acid was observed after multiple-dose of benfotiamine."
pubmed.ncbi.nlm.nih.gov/243...
* My Personal Opinion *
Based on the data, it appears high-dose Benfotiamine is safe as multiple studies used doses in the range of 300-900mg and at least one study with 1,200 mg and I saw a reference to using 4,000 mg. This is not to say there are potential side effects related to stomach issues or rash but there's no indication of anything very serious.
One study mentions up to 75 times the RDA can promote cancer another referencing a mouse RDA that 2500 times was needed. This is where the challenge is, determine the dosage that is effective. Until a trial is run or we start seeing anecdotal reports this is going to be a best guess.
I could have sworn I read a paper/study that made the conclusion that a minimum of 200 or 300 mg was needed. I think that was Thiamine. That would be 166 to 250 times the RDA. I think to be conservative one might assume you need at least 500 times the human male RDA. That would be 600 mg of the water soluble form which would be approximately equivalent to (even using the very conservative 40% bioavailability figure) 240 mg Benfotiamine.
Yet we have people commonly taking 600-900 mg Benfotiamine for other purposes. So to me, as long as there were no side effect, to error on the side of caution to make sure the dose was high enough, I'd take 600-1000 mg a day Benfotiamine probably divided into two doses
First time I hit the reply character max.
To continue, 900mg Benfotiamine = at least the equiv of 2,250mg water-soluble Thiamine = 1,875 times the RDA - pretty close to the study citing the 2500 times mouse RDA.
Would someone out there do a human subject study regarding Prostate Cancer! I guess for now, it's up to any of us to try it if they choose. No MO is going to be able to give any clear answer I would suspect aside from the general high-dose safety profile if they are up on Vitamin B.
I did manage to find one article involving Benfotiamine use in a leukemia patient which is quite interesting.
ncbi.nlm.nih.gov/pmc/articl...
"We recently reported that in a patient with AML who was ineligible for standard chemotherapy due to his advanced age and because he had dementia, chronic renal disease and angina pectoris, the number of peripheral blasts decreased dramatically after receiving monotherapy with oral benfotiamine that was being given to treat low levels of vitamin B1. In that particular patient, leukemia cells became virtually undetectable by 20 days after the initiation of benfotiamine therapy without causing tumor lysis syndrome (Sugimori 2013: 75th annual meeting JSH, PS-2-35). Although the patient eventually died due to leukemia regrowth, we hypothesized that a relation may exist between benfotiamine intake and the transient leukemia remission observed in that patient. In the present study, we report evidences indicating that benfotiamine may have therapeutic potential against AML. Our mechanistic studies suggest that benfotiamine inhibits leukemic cell growth by triggering paraptosis cell death."
Prostate cancer 
Metastatic prostate cancer 
caught prostate cancer?
