Nice primer
the sad part is that this post was even necessary

indeed. have you been on the IIFYM fb page?



hahah, naw, when i did my paper last year on hypertrophy i reviewed a LOT of studies...was kinda sad how little valuable research we have on hypertrophy..

Yeah. I was thinking of posting it on there but I'm not sure.
Most people (that I see) tend to agree with the article anyway though..

And hah, that's very true.

"Effects of Long Term Supplementation of Anabolic Androgen Steroids on Human Skeletal Muscle"

http://www.plosone.org/article/infodoi10.1371journal.pone.0105330

fuk, idk why some links error
just google the title and it'll be the first result from PLOS

This post was edited by Balla on Sep 13 2014 03:51pm

Have you done any research on thermal nociception?
Currently doing a research paper on withdrawal and thermal nociception with rats. >.<

Not really
are you referring to hypersensitive thermal nociception in drug withdrawal? For instance from opioids?

My research involves alcohol consumption & withdrawal.
Measuring thermal nociception at various times including when and when not in withdrawal.

There's only 2 things I know that I've read about
that the hyperalgesia in withdrawal is mediated by PKC/PKC isoforms
and that theophylline antagonized that sensitive effect from alcohol withdrawal
e: that's interesting though. Wish I could do something in research neuroscience related now. I'm stuck with immunology/microbiology.. not too bad but not my interest either

This post was edited by Balla on Sep 13 2014 05:51pm

"The Anabolic Androgenic Steroid Nandrolone Decanoate Disrupts Redox Homeostasis in Liver, Heart and Kidney of Male Wistar Rats"

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0102699

- it increased NADPH oxidase levels & activity in the heart and liver
- it decreased catalase and superoxide dismutase in the liver
- it decreased catalase in the kidney
- it reduced thiol residues

This essentially means that DECA administration increases oxidative damage via concomitant increase in production of the superoxide radical and a decrease in the activity of a couple of different endogenous antioxidants.

This study basically gives some mechanistic insight into exactly how AAS use can contribute to tissue damage that is sometimes seen

Maybe I'm wrong for even thinking like this, however, perhaps this implies that small doses.. such as slightly above normal levels (obviously normal levels imply, but maybe SLIGHT supraphysiological levels would be best), it would induce a mitohormetic response, augmented lifespan/longevity via these same outlined mechanisms. This study and a study cited in this paper note that the ROS prod is overproduced w/ respsect to the activity of the antioxidant systems.. however, smaller amounts of ROS signaling and general body stressors and can often induce mitohormesis, whereby your body becomes more robustly stress resistant by ramping up antioxidant defense capacities through a positive ROS signaling. This could also explain why men that go on TRT-esque doses most often become healthier.

My hypothesis may be supported by a few studies too:

"Testosterone increases renal anti-aging klotho gene expression via the androgen receptor-mediated pathway."
http://www.ncbi.nlm.nih.gov/pubmed/25163025

&

"The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System"
http://www.jbc.org/content/early/2014/07/18/jbc.M114.567321

Thus, testosterone - androgen receptor interaction signaling induces expression of the anti-aging gene/protein Klotho.. and Klotho is known to exert much of its protective and longevity benefitting effect through the redox system, the same one that is disrupted in the study from very high doses. Notwithstanding, perhaps the positive effects of AAS/testosterone are mediated most optimally, already, at the normal physiological level.

Welcome to the dark side m9