[Lotus]

Hi there, I'm still very new to this all but I've consistently experimenting for about a year and half now with low doses, staying safe while researching and also trying to nail down exactly what I want out of all this.

From a health standpoint, a low risk plan sounds ideal to try, but what kind of time frame for noticeable changes would you expect with it?

Thanks for all the info, Lotus.

Hi there Marshallen, (nice to meet you):

That's a good approach @ being cautious. The lower risk plan is of course not risk free, nothing is as I'm sure you well know. 

The human body does an amazing job at trying to correct an out of balance system, it's referred to as Hemostasis (keeping your body at its familiar set points). A reference would be starting NBE and adding anti-androgens. The body recognizes that T (testosterone) is going bankrupt, the hypothalamus sends a message to the pituitary and BAM, the signal is sent to LH (luteinizing hormone) to produce T in target tissues...like to the testes and other target tissues. It's called negative feedback loop.

This is just a cursory explanation, as we go further down this rabbit hole we'll touch on other aspects of this (e.g. SHBG sex hormone binding globulin). A study shows high levels of SHBG act as an estrogen amplifier while keeping T in the basement. 

Getting back on track...when this happens T will shoot into the stratosphere compensating for the loose of T. So, you'll hear people say " dang...PM is making me so horny". This is temporary, it'll correct itself because we're retraining T to shut up and sit back. The technical explanation would look like a Supraphysiologic does of T at first. Other examples of this are akin to feeling euphoric at first when trying PM or E2. It's short lived, that's because T is trying to re-establish Hemostasis. 

I was explaining this in another thread as to when a doctor would prescribe intramuscular testosterone injections to a man who has low T. In this example the man (who's probably older) with a higher BMI (body mass index) would see most of that T injection convert to E (estrogen) by way of the aromatase enzyme...until it could re-establish Hemostasis. 

Sorry marshallen, I had to lay all that out in order to bring into focus the lower risk plan. 

Phytoestrogens are nonsteroidal. For example, they can act as estrogen agonists, antagonists, or partial agonists/antagonists. Which basically means an agonists is pro estrogenic, while antagonists are anti-estrogenic, and then the partial agonist/antagonist phytoestrogens can't make up they're damned minds up lol...genistein is like a partial agonist/antagonist, yeah that's right, genistein is a swinger.

Estriol, estradiol cream(s) are bioidentical hormones, phytoestrogens are structurally similar. While bioidentical hormone cream may be weaker than straight HRT therapy it's still stronger than most all phytoestrogens. Then only exception would be if miroestrol/deoxymiroestrol in PM (pueraria mirifica) are biologically active, in which case they've got a stronger binding affinity over estradiol. In this diagram below estradiol is pro ER-α while phytoestrogens are ER-β, 

Bioidentical hormones are pro ER-α, while phytoestrogens are ER- ER-α is pro breast growth while ER-β are more protective in the role of antagonists.


The time frame for growth?, hard to say. Some folks are fast metabolizers while others are slow metabolizers. Systemic inflammation is a key factor that slows growth, and the way I see it, some phytoestrogens compound inner body inflammation...classic examples of that are fatigue, low energy and pink fog. 
 
Hope this helps, good luck.