Androgen desensitization:
I think this might be due to the specificity of binding between the two hormones DHT and T.
Testosterone binds and dissociates faster than DHT to the AR. Which means there will be more occurance of binding incidents.
Since your body isn’t used to so much binding to the AR it desensitizes the receptors and reduces receptor formation. Its comparable to drug tolerance
(Infor on drug tolerance here. erowid.org/ask/ask.php?ID=1794)
I don’t know if everyone has receptor desensitization or not but.
I think that you can resensitize receptors of chemicals by promoting use of an antagonist of the receptor. An antagonist is a drug which acts as a competative inhibitor of the receptor site. These competative inhibitors do not form a ligand-protein complex with the AR and also do not produce a signal when bound to the receptor.
This type of interferance with the androgen receptor might cause a resensitization of the receptor to DHT and testosterone by increasing the amount of AR’s and increasing the signals they produce when androgen hormones bind to them.
here is another link to an explaination of drug addiction and withdrawl symptoms:
utexas.edu/research/asrec/dopamine.html
Neurons can become sensitized or desensitized to dopamine
One important aspect of drug addiction is how cells adapt to previous drug exposure.
For example, long-term treatment with dopamine antagonists increases the number of dopamine receptors. This happens as the nervous system tries to make up for less stimulation of the receptors by dopamine itself. Likewise, the receptors themselves become more sensitive to dopamine. Both are examples of the same process, called sensitization.
I’ve told golf(add numbers here) that saw palmetto is such an antagonist. It apparently has an ability to reduce signaling in the prostate by up to 50%
Studies in the lab haven’t proven with consistant results if saw palmetto extract causes 5aR inhibition or not. It may be because of genetics, may be faulty test results, I have no idea. I know some studies have shown that it produces no reduction in serum DHT, other studies have shown that it reduces DHT in the prostate, some studies saying it reduces serum DHT up to 20% and so on so forth.
Just a theory, any thoughts?