Are Anabolic Steroids That Bad?

[golder]

Interesting, it all sounds a bit overrated is the vibe I’m getting, the modified forms that is.

How much Test did you use? Did you use an aromatase inhibitor?

Have you ever tried procaine or Novocaine with them?

Do the caines pair well with test? I’ve not read anything on this, could you share some bits with us? Thanks!

 

[Drareg]

Do the caines pair well with test? I’ve not read anything on this, could you share some bits with us? Thanks!

I don’t know, my thinking is the caines demethylate therefore should allow more transcription to occur, I think the historical methylation patterns are rigidly fixed, the steroid lifts some of it but the deeper priming is still there, what causes this is your inheritance from your parents.
When most gear heads default to genetics I think the above process is closer to the truth which potentially would allow for a little more expression, the methylation at certain levels won’t change because this is dangerous, your bodies structure once fully grown limits change because of energetic capacitance issues, like overload, that’s why too much demethylation can kill you.

Ramdom

 

[golder]

I don’t know, my thinking is the caines demethylate therefore should allow more transcription to occur, I think the historical methylation patterns are rigidly fixed, the steroid lifts some of it but the deeper priming is still there, what causes this is your inheritance from your parents.
When most gear heads default to genetics I think the above process is closer to the truth which potentially would allow for a little more expression, the methylation at certain levels won’t change because this is dangerous, your bodies structure once fully grown limits change because of energetic capacitance issues, like overload, that’s why too much demethylation can kill you.

Ramdom

Solid reasoning. I know this is off-the-cuff and extremely unscientific, but if you were pairing say procaine/lidocaine alongside a cycle, what dosage/frequency would you use to theoretically try to allow more transcription to occur.

 

[Drareg]

Solid reasoning. I know this is off-the-cuff and extremely unscientific, but if you were pairing say procaine/lidocaine alongside a cycle, what dosage/frequency would you use to theoretically try to allow more transcription to occur.

This I don’t know, I would start with a small dose without the caines to gauge the effect, then add the caines with same dosage, Haidut’s diamant is a potent hdac inhibitor, this is based on my experience, when using other substances I notice it does potentiate the effect.

I found this, this is used as a demethylating agent, I’m not sure about its overall safety though.

decitabine​

Decitabine - Wikipedia

en.wikipedia.org

This study claims that using decitabine and stanozolol creates a better effect for MDS patients.

Stanozolol improves the progression-free survival of patients with high-risk myelodysplastic syndrome after decitabine treatment - PubMed

It is unknown whether adding stanozolol to decitabine for maintenance can further improve progression-free survival (PFS) and overall survival (OS) after effective decitabine treatment in patients with high-risk myelodysplastic syndrome (MDS). Patients newly diagnosed with high-risk MDS who...

pubmed.ncbi.nlm.nih.gov

It is unknown whether adding stanozolol to decitabine for maintenance can further improve progression-free survival (PFS) and overall survival (OS) after effective decitabine treatment in patients with high-risk myelodysplastic syndrome (MDS). Patients newly diagnosed with high-risk MDS who achieved at least partial remission after 4 cycles of decitabine (20 mg/m2 days 1-5) were selected. In total, 62 patients (median age 66 years) were enrolled, of whom 21 were treated with stanozolol and decitabine for maintenance, and 41 were treated with decitabine alone. The median number of cycles for maintenance treatment was 6 (2-11) and 5 (2-12) for the stanozolol and control groups, respectively (p > 0.05). PFS in the stanozolol group was significantly longer than in the control group (15.0 vs 9.0 months, hazard ratio

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= 0.35, 95%CI: 0.19-0.63, p = 0.0005), whereas OS was not significantly prolonged in the stanozolol group (21.0 vs 15.0 months, HR = 0.73, 95%CI: 0.39-1.37, p = 0.33). The proportion of patients with severe neutropenia during maintenance treatment in the stanozolol group was lower than in the control group (76.2% vs 95.1%, p = 0.039). In conclusion, adding stanozolol to decitabine after effective decitabine treatment can prolong PFS and reduce the severity of neutropenia for patients with high-risk MDS

 

[Drareg]

Another interesting study on decitabine in prostate cancer

Epigenetic modulation of AR gene expression in prostate cancer DU145 cells with the combination of sodium butyrate and 5'-Aza-2'-deoxycytidine - PubMed

The androgen receptor (AR) plays an essential role in the development and progression of prostate cancer. Castration-resistant prostate cancer (CRPC) is a consequence of androgen deprivation therapy. Unchecked CRPC followed by metastasis is lethal. Some CRPCs show decreased AR gene expression...

pubmed.ncbi.nlm.nih.gov

The androgen receptor (AR) plays an essential role in the development and progression of prostate cancer. Castration-resistant prostate cancer (CRPC) is a consequence of androgen deprivation therapy. Unchecked CRPC followed by metastasis is lethal. Some CRPCs show decreased AR gene expression due to epigenetic mechanisms such as DNA methylation and histone deacetylation. The aim of this study was to epigenetically modulate the methylated state of the AR gene leading to targeted demethylation and AR gene expression in androgen-independent human prostate cancer DU145 cell line, representing the CRPC model with very low or undetectable AR levels. The cell treatment was based on single and combined applications of two epigenetic inhibitors, sodium butyrate (NaB) as histone deacetylases inhibitor and 5'-Aza-2'-deoxycytidine (Aza-dC) as DNA methyltransferases inhibitor. We found that the Aza-dC in combination with NaB may help reduce the toxicity of higher NaB concentrations in cancer cells. In normal RWPE-1 cells and even stronger in cancer DU145 cells, the combined treatment induced both AR gene expression on the mRNA level and increased histone H4 acetylation in AR gene promoter. Also activation and maintenance of G2/M cell cycle arrest and better survival in normal RWPE-1 cells compared to cancer DU145 cells were observed after the treatments. These results imply the selective toxicity effect of both inhibitors used and their potentially more effective combined use in the epigenetic therapy of prostate cancer patients.

 

[Drareg]

Using debitabine again-

Androgen receptor DNA methylation regulates the timing and androgen sensitivity of mouse prostate ductal development - PubMed

Androgen receptor (AR) signaling initiates mouse prostate development by stimulating prostate ductal bud formation and specifying bud patterns. Curiously, however, prostatic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days. This study's objective was to...

pubmed.ncbi.nlm.nih.gov

Androgen receptor (AR) signaling initiates mouse prostate development by stimulating prostate ductal bud formation and specifying bud patterns. Curiously, however, prostatic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days. This study's objective was to test the hypothesis that DNA methylation controls the timing and scope of prostate ductal development by regulating Ar expression in the urogenital sinus (UGS) from which the prostate derives. We determined that Ar DNA methylation decreases in UGS mesenchyme during prostate bud formation in vivo and that this change correlates with decreased DNA methyltransferase expression in the same cell population during the same time period. To examine the role of DNA methylation in prostate development, fetal UGSs were grown in serum-free medium and 5 alpha dihydrotestosterone (DHT) and the DNA methylation inhibitor 5'-aza-2'-deoxycytidine (5AzadC) were introduced into the medium at specific times. As a measure of prostate development, in situ hybridization was used to visualize and count Nkx3-1 mRNA positive prostatic buds. We determined that inhibiting DNA methylation when prostatic buds are being specified, accelerates the onset of prostatic bud development, increases bud number, and sensitizes the budding response to androgens. Inhibition of DNA methylation also reduces Ar DNA methylation in UGS explants and increases Ar mRNA and protein in UGS mesenchyme and epithelium. Together, these results support a novel mechanism whereby Ar DNA methylation regulates UGS androgen sensitivity to control the rate and number of prostatic buds formed, thereby establishing a developmental checkpoint.

 

[Brandin]

hey I won't dodge this question, and I know most people will think it's a stupid answer but I want to be BIG. that simple

What many people dont talk about is the fact that one gets dopamine hits from looking at aesthetic people. If you think that being big looks good its a logical reason. It feels awesome to see people who look amazing. Now when someone is so big that its freaky its instead entertaining in a good way.