So for now procaine is the best bet?
But, we are. Iām sure Awor is reading these papers and forwarding whatās important to his doctors. I know he has another treatment coming up soon and Iām sure heāll let us know when he has something important to tell us. Also, Dr. Jacob seems very interested in this idea. Iāve only been injecting Procaine so far but Iām also willing to do the IV treatments if I can get Jacobs or Shippen onboard with the idea.
Much thanks to Oscar and Mariobros for your research and keeping this thread interesting. This is by far our best shot at treatment.
It is also true that other genes involved in the correct function of the cell may be methylated which can interfere with the functioning of the androgen receptor.
boston332, I think it unlikely either will give you procaine by IV. I find it surprising you even got injections. Look at this website for adverse effects of using decetabine another demethylating agent ( dacogen.com/PI.aspx ). If you where to become seriously ill I imagine that they could lose their medical licence or suffer other professional or criminal consequences. I realise that they can prescribe āoff labelā but this isnt even close to their feild of medicine, neither are oncologists or cellular biologists with a speciality in epeginetics or experimental demethylising techniques.
Also these websites give an idea of the administration of procaine necessary;
cancerres.aacrjournals.org/content/63/16/4984.full#sec-16 (Procaine paper)
Not sure what that means but this is the method used to administer Decetabine for example.
dacogen.com/PI.aspx (Decetabine = Dacogen)
dacogen.com/hcp/LinkedFiles/Patient_Ed_Brochure.pdf (Patient Brochure, page 14 especially)
The side effects of these demethylating agents can be managed with good monitoring. Neutropenia and thrombocytopenia can be corrected if necessary. You should monitor anyone who takes demethylating agents but if this is appropriate treatment it is a risk worth taking. Hopefully this wonāt deter the post fin docs.
Just a quick question to do with procaine. Is procaine amide also a demethylating agent? It has a longer half life of up to 3hours and can be taken orally.
Nice summary of various substances relevant to epigenetic research, some already mentioned but still worth a look.
sigmaaldrich.com/life-science/epigenetics/bioactive-small-molecules.html
Procainamide Is a Specific Inhibitor of DNA Methyltransferase 1*
Procainamide has been shown to inhibit DNA methyltransferase activity and reactivate silenced gene expression in cancer cells by reversing CpG island hypermethylation. We report here that procainamide specifically inhibits the hemimethylase activity of DNA methyltransferase 1 (DNMT1), the mammalian enzyme thought to be responsible for maintaining DNA methylation patterns during replicationā¦Because many reports have strongly linked DNMT1 with epigenetic alterations in carcinogenesis, procainamide may be a useful drug in the prevention of cancer.
Curcumin is a potent DNA hypomethylation agent
Note: Curcumin = Turmeric (Indian Spice)
Abstract
Molecular docking of the interaction of curcumin and DNMT1 suggested that curcumin covalently blocks the catalytic thiolate of C1226 of DNMT1 to exert its inhibitory effect. This was validated by showing that curcumin inhibits the activity of M. SssI with an IC50 of 30 nM, but no inhibitory activity of hexahydrocurcumin up to 100 Ī¼M. In addition, curcumin can induce global DNA hypomethylation in a leukemia cell line.
How could Awor succeed in convincing the doctors to make a guinea pig of him? It is often impossible to be prescribed just complete blood testing, or some drug, how could it be possible to try such an experiment? If so, why donāt cancer patients ask their doctors to try experiments with them, based on the numerous āpromisingā treatments (including this demethylation theory) talked about in the numerous scientific publications?
Awor has done alot of ground work and has had one procaine treatment with his doctors. If you know the right people you can get it done. But it has to be in a controlled environment. I.v. procaine is not the most risky thing ever done but it does have it risks and things need to be done in order to minimise them.
Cancers are a different ball game to post drug persistent side effects. They are more variables as to how cancer progresses. Remedying the silent genes in cancer isnāt necessarily the cure for cancer. It may help but until proven benefits there are better treatments for them. Also it seems it is more preventative than curative in cancer as if the cancer is already present unsilencing the gene wonāt make it go away.
There are no better treatments for us it seems unless you prescribe to the TRT theory.
The problem is we regularly see a new breakthrough theory, with just one people having real success, and of course an enormous risk. Yesterday, it was GHB, or T3 treatment, today demethylation (and I donāt think demethylation or thyroid were a part of the GHB curing effect, at the time the theory was deep REM sleep). What else tomorrow? Heroin? Coke?
It seems the formula for a PFS ācureā is: nearly forbidden, difficult to find, and only administrable in a very specific way drug with enormous side effects (including death) but possibly the only chance to be cured. Itās every time the same pattern.
I really hope demethylation is the key, but past stories made me very skeptical. 
There is a huge difference. The procaine treatment originates from the theory: āif the demethylation theory is correct, then procaine will workā. With GHB the idea was: āI canāt sleep, therefore Iāll use GHBā and luckily GHB fixed him (ithappens). Taking GHB was not justified by a theory, it was just a lucky try.
In other words, GHB (like clomid or TRT) address some problem we have (likely a consequence of a deeper root problem), while Procaine addresses a possible root problem.
m_81, I understand your point, it makes sense, but this can be either way: a theory gives the idea to try something, or a success gives birth to a theory. In the first case, the theory sounds great and nearly evident, but there is no concrete success to validate it, in the latter case, there is only one success, and all the other people experiment failure.
We already had a theory about a root problem and its cure that seemed the most logical explanation: viewtopic.php?f=27&t=2262
On the paper, I donāt think I have seen a theory making more sense. Unfortunately, nobody succeeded in the long term with that method.
However, I sure hope IāM WRONG, and Iām eagerly waiting for good Awor news 
I dont think Awor is saying he is cured by a long shot. I believe he is in the right ballpark and on the right track here. This EXPLAINS why DHT treatment alone doesnt cure us. Alot of research yet to done. For instance, how to target the correct gene. Stay tuned. Iām sure when Awor has something important to share with us heāll let us know.
Y-C iām not really sure what point youāre trying to make - that we should all just give up and accept this situation? The thing that is different about this theory is that it addresses the problem in a scientific manner, there are studies posted here that specifically point to pharmaceutical drugs causing persistent side effects through hypermethylation.
Yes, other theories in the past have turned out to be false prophets, but that doesnāt mean they were necessarily a waste of time. By eliminating other possible causes for our symptoms (hormone imbalance, low DHT etc) it allows us to move on and look at new theories. It doesnāt matter how many times we get it wrong, we only have to be right once.
Trichostatin A causes selective loss of DNA methylation in Neurospora
Abstract
Both DNA methylation and hypoacetylation of core histones are frequently associated with repression of gene expression. Possible connections between these processes were investigated by taking advantage of genes controlled by methylation in Neurospora crassa. Trichostatin A (TSA), a potent inhibitor of histone deacetylase, derepressed a copy of hph that was repressed by DNA methylation which resulted from repeat-induced point mutation (RIP) acting on sequences flanking hph. Derepression by TSA was comparable to derepression by the inhibitor of DNA methylation, 5-azacytidine. TSA treatment also repressed an allele of am whose expression depends on methylation of an adjacent transposon, Tad. DNA methylation in the hph and Tad/am regions was greatly reduced by TSA treatment. TSA also caused hypomethylation of other methylated alleles of am generated by RIP. In contrast, TSA did not affect methylation of several other methylated genomic sequences examined, including the nucleolar rDNA and the inactivated transposon Punt RIP1. Several possible models are discussed for the observed selective demethylation induced by TSA. The implication that acetylation of chromatin proteins can directly or indirectly control DNA methylation raises the possibility that connections between protein acetylation and DNA methylation result in self-reinforcing epigenetic states.
Very interesting study.
Dihydro-5ā-azacytidine (DHAC) restores androgen responsiveness in androgen-insensitive prostate cancer cells.
Abstract
INTRODUCTION: The androgen resistance of some prostate cancer patients may be due to transcriptional inactivation of the androgen receptor (AR) gene catalyzed by cytosine DNA methyltransferase.
MATERIALS AND METHODS: To determine if an inhibitor of cytosine DNA methyltransferase, 5,6-dihydro-5ā-azacytidine (DHAC), can restore the androgen sensitivity in androgen-insensitive human prostate carcinoma cell lines in vitro, we cultured androgen-insensitive (PC3, DU-145, and TSUPrl) and androgen-responsive (LNCaP) cells with subcytotoxic concentrations (< or = IC50) of DHAC for 14 days followed by exposure to dihydrotestosterone (DHT) or to hydroxyflutamide for 7 days.
RESULTS AND CONCLUSIONS: Only DHAC-treated DU-145 cells showed growth stimulation by 10(-11) to 10(-9) M DHT and a partial inhibition by 10(-5) and 10(-6) M hydroxyflutamide. However, since DU-145 is the only cell line tested that is known to have a hypermethylated AR promoter, the observed effects may be due to a partial demethylation of the AR by DHAC. Our data provide an evidence that cytosine DNA methyltransferase inhibitors can restore androgen responsiveness in androgen-refractory tumor cells, which are then sensitive to growth inhibition by antiandrogens.
Inactivation of the human androgen receptor gene is associated with CpG hypermethylation in uterine endometrial cancer.
Treatment with 5-aza-2ā-deoxycytidine restored AR expression in all of the UEC cell lines that showed no AR expression before treatment. This study is the first to report that the possible mechanism of AR inactivation in endometrial cancer is through hypermethylation of the AR gene CpG islands.
DNA methylation in the androgen receptor gene promoter region in rat prostate cancers.
RESULTS: AR mRNA expression was not detected in any of the rat prostate cancers or cancer cell lines tested by Northern blot analysis. Higher levels of methylated CpGs were observed in PLS20 than PLS10 or 30. Demethylation treatment by 5-aza-2ā-deoxycytidine restored AR mRNA expression in PLS20. The CpGs suggested to be responsible for AR expression in rat prostate cancer were found to be located -9 and -1 nucleotides upstream of the transcriptional initiation site. All of the examined rat prostate and seminal vesicle cancers demonstrated hypermethylation at these CpG sites. CONCLUSIONS: These data clearly demonstrate that aberrant hypermethylation in the AR promoter region may play a critical role in AR expression in rat prostate cancers.