Quote (Afficionado @ Oct 21 2014 09:25pm)

I haven't quite finished this as it is over 400+ comments with MANY studies cited, however, I would strongly suggest HNF read it.

It is valuable information presented in an entertaining to read fashion.

However, Hahn has got to be one of the most irritating people...he argued like a child..

https://www.facebook.com/FredrickHahn/posts/10152399056907864

Quote (Balla @ Oct 24 2014 09:06pm)

"Regulation of skeletal muscle energy/nutrient-sensing pathways during metabolic adaptation to fasting in healthy humans"

http://ajpendo.physiology.org/content/early/2014/09/17/ajpendo.00215.2014

Waiting to get the full text..

However, assuming it holds up, I'm quite disappointed in no change in AMPK activity. That's one of the biggest factors I predicated much of a fasting stance around. I feel almost dishonest if this is completely true and even after 24hrs it doesn't really change activity.
Regardless, I'd still tout fasting as a great mediator of health & longevity via mitohormesis. Despite lack of AMPK signaling, FoxO, Sirt1 and I'm assuming factors such as NRF2 are still indeed increased, which does culminate in a hormetic response, thus still highly beneficial. I suppose fasting still has most of the beneficial effects I've touted on, it just doesn't have AS robust an effect in terms of inhibiting lipid & cholesterol synthesis, insulin-independent glucose uptake, etc.

Quote (Balla @ Sep 16 2014 07:16pm)

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

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