What do methyl steroids and trib have to do with each other? Are you saying we should try trib or methyl steroids? My issues are mainly visual and I’m starting to believe it’s inflammation of the optic nerve. Had my eyes checked and my nerve/neurons in my eye are much less dense then they should be. Is there a risk to methyl steroids? I’m considering mayo as well.
This may be a stupid question, but a simple google search did not yield much. Is there any testing to determine brain inflammation?
Methylprednisolone is a DNA Methyltransferases Inhibitors
Now look what this article said : The use of specific inhibitors of DNMT might reactivate those genes and stop or even reverse the aberrant cell processes.
It mean that DNMT inhibitor can reactivate silence genes.
@axolotl, @awor, what do you think about this? Methyl steroids seem to be used from some neurological disorders like MS - you think this holds weight?
Please try to stay on topic.
This discussion of methylprednisone and autoimmunity has been moved from a topic focused on tribulus as a treatment method.
Even if you gradually build up a dose ? Accumulation doesn’t work in this occasion ?
Do you guys think the oral form would work? I bet it would be easier to get that
Not sure you can take dosages that high orally… I dunno. The small amount of googling I did on it sounded like it was a worse idea
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Let me explain you something, inflammation is always there, basically everything that we eat cause inflammation at cellular level.
This is my theory.
Finasteride have anti-inflammatory proprieties.
https://www.ncbi.nlm.nih.gov/pubmed/19007044
DHT is a pro-inflammatory.
DNMT1
DNA methylation -mediated gene silencing, DNMT1 also binds to several transcriptional inhibitors
Methylation at previously unmethylated sites is catalyzed by a DNA (cytosine-5)-methyltransferase, such as DNMT3a/b, and is commonly maintained by DNMT1, referred to as maintenance methyltransferase. Together, these enzymes guarantee that a substantial part of the genome is often methylated, leaving only regulatory elements like promoters and enhancers, as well as CpG-rich islands, in an unmethylated state (Lindroth and Park 2013). The hypermethylation state of DNA at the promoter is predominantly associated with gene silencing. There is also evidence pointing to multiple epigenetic modifications, including DNA methylation and various histone modifications, that can work synergistically or antagonistically (Lindroth and Park 2013).
My Theory
Our brain was accustom to the normal inflammation ( pre-finasteride), on finasteride inflamation goes very low and or brain get accustom to it very quickly, when we withdraw Finasteride inflamation rise + DHT rise and with it rise even more inflamation, our inmune system react through DNMT1 increasing inflamation casuing Methyliation of the CpG islands as result silencing SRD5A2 and maybe others genes involved in the same pathway. causing all the symptoms that we are feeling.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521964/
Note: The methylation of CpG islands results in stable silencing of gene.
The more I read and analyze it the more pieces come to fit.
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this guy already confirmed that methyl steroids did NOT treat his impotence. Also, I have had hallmark pfs symptoms for nearly two years and have went on corticosteroids twice and have had zero noticeable effect. just fyi
How do you explain the people like myself who took 1 or 2 pills and had an almost instant and extreme reaction?
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Methylprednisolone for sure don’t cure impotency,
What you do not still understand the issue here. The issue here is epigenetic and it is what Baylor still currently doing a research and Milano university is going to do another epigenetic research.
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this guy already confirmed that methyl steroids did NOT treat his impotence. Also, I have had hallmark pfs symptoms for nearly two years and have went on corticosteroids twice and have had zero noticeable effect. just fyi
The problem here is not to going on corticosteroids, the proble here is #1 dosage of corticosteroids and what type of corticosteroids, #2 you need to make sure that the used corticosteroids also have to cross the Blod Brain Barrier (BBB).
You guys come to a conclusion to quick and that’s why you never going to anywhere just acting like that.
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You have almost extreme reaction with two pills because we are not equals, our genes are different.
it explain perfectly why some peoples do not have reaction at all and never have the side effect. others take months or years to get the side effect.
because again the problem here is epigenetic.
The recovery also it going to be different, for example anonymous after Methylprednisolone came to play to fix his side 5 months later, epiegentic modification doesn’t come instantly.
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Preclinical and clinical data
suggest that depression is associated with the activation of the
immune system, which is manifested as inflammation [11,21].
There are suggestions that in the pathogenesis of depression in
patients, a key role is played by an increase in pro-inflammatory
cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and
tumor necrosis factor (TNFa) [27,29,30,38]. Cytokines are responsible for varied cells processes and also for the maintenance of
homeostasis in tissue. The production of cytokines increases in
cases of acute stress or inflammation. There is a suggestion that
depression is a chronic inflammation of structures in the central
nervous system responsible for emotions and mood [26]. It is
known that pro-inflammatory cytokines have a direct influence on
the nervous system and may cause disturbances in the functioning
of the brain, resulting in behavioral changes such as anhedonia,
which is one of the main symptoms of depression.
http://if-pan.krakow.pl/pjp/pdf/2014/1_22_ab.pdf
maybe they work by decreasing shbg and increasing dht transport??
20d
this guy already confirmed that methyl steroids did NOT treat his impotence. Also, I have had hallmark pfs symptoms for nearly two years and have went on corticosteroids twice and have had zero noticeable effect. just fyi
Yes you went on corticosteroids twice, but at what dosage ? and I believe that it is the key
You are very heavy saying always the same…
5α-Reductase Type 2 Regulates Glucocorticoid Action and Metabolic Phenotype in Human Hepatocytes
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