"What a pain killer does is occupy the sodium/potassium pump and prevents the active transport of Na+ from within the axon chambers after the neuron has fired. This slows the influx of K+ and Cl- wich leaves the neuron unable to fire for longer periods of time. If the neuron can't fire, it can't send a message of pain. If it can't send the messsage, the brain doesn't know that there is injury or trama. The stronger the pain killer, the more it prevents the actions of the sodium/potassium pump and the more it prevents the pain sensations."
STEW, what pain killers work through this mechanism? Narcotics work through opioid receptors, which reduce substance P release. There maybe indirect alteration of the Na/K channels, but it is not through direct inhibition of the channels.
"The same is true for anabolic steroids. The further the levels get from your normal baseline, the harder you liver works to metabolise them. Whenever the levels are remaining high for a long time, eventually the liver becomes so efficient that it is destroying/breakign down the AS before the androgen even has a chance to bind to its appropriate receptors and elicit its anabolic response. It does this in an effort to get levels to return to baseline. Thus, higher and higher dossages must be used in order to have the same response that one once had for low dosses."
Hepatic breakdown of hormones most likely increases (I have not seen any research), but I seriously doubt that it is a primary reason for decreases in activity. And in no way would the liver be able to remove hormones from the system at the rate you are suggesting.
Cell signalling and signal transduction processes are still vastly uncharted territories in molecular biology, and are most likely the areas that we will find the answers to why steroids reduce activity over time. More than not, the cells find a way to decrease activity through one or more minor pathway.