- Joined
- Apr 9, 2021
- Messages
- 1,718
Bill Roberts wrote extensively in Dan Duchaine's Dirty Dieting Newsletter (you may be able to find some free copies gathering electronic dust on the internet) about the presence (or lack thereof) of a sigmoidal S-curve in AAS dose/response (dose vs. ΔLBM), indicating that dose/response was, for some AAS, not modulated solely by the AR. This led him to a hypothesis that some AAS are synergistic. It comports with my own understanding. He was light-years ahead conceptually, but did err in his classifications, due merely to lack of identification of the mechanisms that confer synergy (e.g., aromatization as a discrete mitogenic & myogenic process; increased autocrine/paracrine IGF-I & satellite cell responsiveness; glucocorticoid modulation).The above means that the cells lining the inner wall of capillaries and the muscle cells involved in constricting and dilating blood vessels are responsive to testosterone and analogues causing blood vessels to constrict. Remember that your diastolic blood pressure is the outward force on your capillary walls. If those walls constrict (tighten) the pressure rises = hypertension. Makes meds like ARBs seem fairly uniquely useful to users of steroids.
Apoptosis (cell death) caused by reduction of electrolytes or electrolyte signaling to cell tissues. It's a push pull relationship. There is oxidative stress (oxidation) and antioxidant activity (why people take antioxidants). We need both. However, too great a shift to one or the other is not necessarily a good thing. But we know that excessive oxidation caused by many things including stress, training, environmental pollutants is not good. So people overdose the hell out of antioxidants (also not necessarily a good thing). There are free radicals and reactive oxygen species (ROS) that are produced inside cells. Also important in killing damaged or malfunctioning cells.
Mineralcorticoid Receptor (MR) but I don't need to explain why reduced Na (sodium) absorption is bad.
Here's an example of where oxidation is necessary. I intend to do a more in-depth write-up on glucocorticoids, adrenaline, and nor-adrenaline and AAS. This is actually a very complicated bodily process that is impossible to summarize in a few words. Get anxiety on steroids? That's from adrenaline. You get the idea.
The sigmoid function is a mathematical function and creates a curve that starts out relatively flat, rises steeply, then levels off. The curve resembles an "S" so it is called a S-curve. Put simply, this means that what are commonly considered weak steroids whose dose respondent curve is relatively weak until dosage is increased to where the AR and MR begin to be more saturated have a more pronounced effect which then levels off. As opposed to most AAS which just straight line right up the graph as dosage increases. This was new information to me. Not the calculus, but rather the S-curve with certain compounds.
The stronger the compound, the more heart stress. But what @Type-IIx typed above is a wealth of information and there's a lot to unpack there. This is great information for AAS users to know. He shoudn't be chastised for it. Jeeez....
The discussions and works of authorship surrounding AAS used to be scintillating, sophisticated, engaging. These days, apparently, there's less appetite for curiosity and independent learning. BuT eInStEiN cOuLd ExPlAiN iT mOrE sImPlE.