study:Effect of SARM on hypogonadism induced muscular atrophy

[Luckfax]

Don’t think this is the complete text but interesting nonetheless, doesn’t say what type of SARM.
jcem.endojournals.org/cgi/reprin … 3560-a.pdf

[golf]

this is just a link to pay for an article… can you post it all?

[Luckfax]

Sadly not costs $$.

[golf]

well, this is a bit better - though still not all of it - and it doesnt mention sexual effects at all:

Glucocorticoids are the most widely used antiinflammatory drugs in the world. However, prolonged use of glucocorticoids results in undesirable side effects such as muscle wasting, osteoporosis, and diabetes. Skeletal muscle wasting, which currently has no approved therapy, is a debilitating condition resulting from either reduced muscle protein synthesis or increased degradation. The imbalance in protein synthesis could occur from increased expression and function of muscle-specific ubiquitin ligases, muscle atrophy F-box (MAFbx)/atrogin-1 and muscle ring finger 1 (MuRF1), or decreased function of the IGF-I and phosphatidylinositol-3 kinase/Akt kinase pathways. We examined the effects of a nonsteroidal tissue selective androgen receptor modulator (SARM) and testosterone on glucocorticoid-induced muscle atrophy and castration-induced muscle atrophy. The SARM and testosterone propionate blocked the dexamethasone-induced dephosphorylation of Akt and other proteins involved in protein synthesis, including Forkhead box O (FoxO). Dexamethasone caused a significant up-regulation in the expression of ubiquitin ligases, but testosterone propionate and SARM administration blocked this effect by phosphorylating FoxO. Castration induced rapid myopathy of the levator ani muscle, accompanied by up-regulation of MAFbx and MuRF1 and down-regulation of IGF-I, all of which was attenuated by a SARM. The results suggest that levator ani atrophy caused by hypogonadism may be the result of loss of IGF-I stimulation, whereas that caused by glucocorticoid treatment relies almost solely on up-regulation of MAFbx and MuRF1. Our studies provide the first evidence that glucocorticoid- and hypogonadism-induced muscle atrophy are mediated by distinct but overlapping mechanisms and that SARMs may provide a more effective and selective pharmacological approach to prevent glucocorticoid-induced muscle loss than steroidal androgen therapy.

[anonnn1]

Like anything, this is worth looking into.

If GTXI can get their Ostarine SARM approved for cancer, we maybe able to have doctors prescribe this to see if we can recover.

It’s a very promising drug.

I highly suggest we write a letter to GTXI and see if they would be interested in doing a experimental trial on us…What do you guys think?

[golf]

I suggest having a doctor do so, not yourself.

[anonnn1]

Yes i agree…I think we should shoot for awor’s demylination theory first and see how that works…trial/error…That’s all we can do…

[golf]

and you can always sample S4 if so inclined - as far as i know the effects only stay as long as your administering it however - not after you stop.

[Mew]

Yes i agree…I think we should shoot for awor’s demylination theory first and see how that works…trial/error…That’s all we can do…

It’s demethylation, not demylination. Two completely unrelated concepts, the latter of which has nothing to do with Awor’s theory.

[anonnn1]

Ok Mew.

[Mew]

Just for clarity’s sake.

[spstriken]

Don’t you Guys (Awor, Mew especially) think trying SARM is a good idea? If they give us desired results then our Receptors are not damaged and if not then yes they are damaged.
Awor what do you think?

I