Cycling is important. For one to mimic what the body is doing, and another to keep sensitization (so much of what is said is generally correct). Perhaps increasing the three hormones at once is also another route to go. It is possible that PM has two (or 3) hormonal effects, (based on anecdotal evidence of its effects) but I'm uncertain of this (still it could be cycled to improve its hormonal effect).
I'm not certain if an antagonist blocks receptors, but it does deactivate them while simultaneously sensitizes them. Too much of an antagonist (an overload) causes the opposite and also desensitize it, perhaps such as how (small amounts of) DHT by itself is this potent and stops growth.
From the last chart, it showed that an antagonist and agonist had mid range effects. There is a balance of sensitizing vs activation of receptors that needs to be found, so the (weak) antagonist and agonist working together might possibly be beneficial.
It is important to cycle (or possibly use together) effects of progesterone, estrogen and prolactin, which the body already does. Cycling with DHT is most counterproductive. It's less counterproductive to cycle weaker androgens, except to aromatase T into estrogens.
Dehydro forms of progesterone could also desensitize receptors, but theoretically be less inhibiting than DHT, since progesterones cause growth, while androgens don't cause mammary growth at all.
It's like a math puzzle to figure out how much to activate a receptor while balancing sensitization. Perhaps the functions that inhibit DHT also have to be cycled, or taken a break from.
I'm not certain if an antagonist blocks receptors, but it does deactivate them while simultaneously sensitizes them. Too much of an antagonist (an overload) causes the opposite and also desensitize it, perhaps such as how (small amounts of) DHT by itself is this potent and stops growth.
From the last chart, it showed that an antagonist and agonist had mid range effects. There is a balance of sensitizing vs activation of receptors that needs to be found, so the (weak) antagonist and agonist working together might possibly be beneficial.
It is important to cycle (or possibly use together) effects of progesterone, estrogen and prolactin, which the body already does. Cycling with DHT is most counterproductive. It's less counterproductive to cycle weaker androgens, except to aromatase T into estrogens.
Dehydro forms of progesterone could also desensitize receptors, but theoretically be less inhibiting than DHT, since progesterones cause growth, while androgens don't cause mammary growth at all.
It's like a math puzzle to figure out how much to activate a receptor while balancing sensitization. Perhaps the functions that inhibit DHT also have to be cycled, or taken a break from.