[Ronn]

iron game,

Outside of AR down regulation (which part one of the above article clearly questions if my memory serves), I think another way of perceiving the “stall” or “plateau” one usually hits after long term use of AAS is the basic biological inclination towards homeostasis.

As we know, add an extraneous source of androgens and the hypothalamus reacts by slowing or stopping the pituitary’s production of GNRH and LH (in order to lower the blood levels). By doing so, the body has also eliminated it primary means to maintain homeostasis through it’s own production of steroidal compounds (such as progesterone, the estrogens, cortisol, and aldosterone—this latter hormone being an often overlook cause of bloat during cycles).

Therefore, it begins converting the extraneous testosterone (note I’m addressing only non-DHT derived AAS at this juncture) in to other compounds, the best know of which would be estrogens and DHT. Variations in individual response dictate what pathway(s) will be primarily activated.

As we know, some people are “inclined” towards gyno (as I happen to be having had adolescent onset gyno when I was younger). The aromatase enzymes convert the circulating test in estrogen in order to maintain homeostasis. Now, it doesn’t necessarily follow that those pro to gyno are aromatizing more test into estro, it simply means their breast tissue is more susceptible to higher estrogen concentrations—we’re all losing some test to estrogen (which isn’t so bad, estrogen does have many positive effects on the body). Therefore, it not to far fetched a conclusion that the longer test levels are kept abnormally high, the more efficient the body will get in aromatizing it. Thereby eventually diminishing some the positive effects of the AAS. And lets remember, when we “stall out” on a cycle, we don’t go back to are “un-supplemented” state—we just stop growing. Usually maintaining what we’ve gained…homeostasis.

Another player in the gane is the 5alpha reductase enzyme, Type 1 5-alpha-reductase is found primarily in the skin and Type 2 5-alpha-reductase is found primarily in the prostate and inner sheath of the hair follicle. As well all know, some people are prone to ance and/or hair loss while on cycle—this is a clear indicator that the DHT conversion is taking place (and the lack of symtoms is not an indication of the lack of 5AR response, but merely an individuals lack of response to DHT). Again, the end result in longer cycles is homeostasis and a “platue.”

Finally we have Sex hormone-binding globulin (SHBG). Normally 60-80% of our circulating test is bound to SHBG and rendered ineffectual to bodily tissue. About 20% is attached to albumin—which can leave as little as 10% of our test “free”—or has high as 30%. Now we can begin to see what some guys are natural “twice as big as me.” So logic would seem to indicatehat if in normal circumstances the body holds most of it’s test in check, homeostasis dictates an increased production of SHBG to compensate.

Now, this is an N=1 antidotal observation, but I’ve found adding Proviron (which has a very strong affinity to SHBG) towards the end of the cycle can get me going again. Don’t get me wrong, it’s not like adding in dbol, but I see progress begin again.

Unfortunately, I can’t find some articles I’ve had that discus how the body can actually break down testosterone to “reproduce” other steroidal agents as well (like aldosterone), so I can really spell out that process for you. But hopefully it’s sufficient to say from what I have outlines, homeostasis’s is a much better explanation for the “stall” one has in longer cycles than AR down regulation.

Hope that helps,

Ronn