Maybe what we really need is a sort of Phytotestosterone type thing - a compound which ould fool the endocrine system into believing that there is too much T of all sorts floating around. This would then shut down the production process

M x

Maybe what we really need is a sort of Phytotestosterone type thing - a compound which ould fool the endocrine system into believing that there is too much T of all sorts floating around. This would then shut down the production process

M x

Hi Miranda,

Essentially that's already happening,

High serum levels of estrogen also trick the brain into thinking that enough testosterone is being produced, further slowing the natural production of testosterone. This happens when estrogen saturates testosterone receptors in the hypothalamus region of the brain. The saturated hypothalamus then stops sending out a hormone to the pituitary gland to stimulate secretion of luteinizing hormone, which the gonads require to produce testosterone. High estrogen can thus shut down the normal testicular production of testosterone



As estrogen levels increase with age, testosterone cell stimulation may be locked in the "off" position, thus reducing sexual arousal and sensation and causing the loss of libido so common in aging men.

http://www.dcnutrition.com/miscellaneous/Detail.CFM?RecordNumber=475

Remember in the first post of the thread this statement:


Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol E2)


The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).


.02% of E is converted by the enzyme aromatase, this small percentage can be misleading, estradiol is 100 more potent at the receptor sites then T, that means T needs to balance at the same level to have the same affinity.



Although naturally-occurring estrogens circulate in the blood largely bound to sex hormone-binding globulin and albumin, only unbound estrogens enter target tissue cells. This statement is explaining Free E, exactly the same principle as FREE T and that also means E-receptors.

Below is what I'm talking about if anybody would like some supported info:

Testosterone-derived estradiol production by male endothelium is robust and dependent on p450 aromatase via estrogen receptor alpha.
http://www.springerplus.com/content/2/1/214

Let me throw a spanner in the works .
Since it is the pituitary gland that sends signals for production of various hormones and also signals for balancing any unbalances .

I was watching a health program where this guy's breast ( albeit small ) was producing milk , he was diagnosed by the doctor pituitary gland malfunction for which this guy had treatment .

So here is me thinking maybe we at NBE could look at manipulating the pituitary gland . As by doing that you are tackling the source rather than end product.

Is my logic correct ?

Well yes ,

Your logic is correct and assuming that the pituitary regulates homeostasis (control) over the endocrine, it's the master gland.

But that condition is called prolactinoma-its a benign tumor of the pituitary gland that produces a hormone called prolactin. It is the most common type of pituitary tumor. Symptoms of prolactinoma are caused by too much prolactin in the blood (hyperprolactinemia) or by pressure of the tumor on surrounding tissues.

The improper hormonal balance, or thyroiditis is big problems for NBE'ers, also cortisol in older bio-males has a great affect in the whole enzymatic (Aromatase) response if that's what you meant.

Aarrrggg cortisol that dreaded stuff I had so much off when I was overworking that it ruined my teeth and my eczema went bezerk .

Sorry to hear that myboobs, I think NBE isn't easy on dental work btw.


I have been experimenting a Progesterone FG/HOPs program. Progesterone upon topical application is immediately active when released into the bloodstream. It is also a strong DHT blocker and boosts sensitivey to other herbs. I'll just say that aerola expansion is crazy if only temporary, but we'll see.




_______________________________________________________________
Men produce 3mg to 10mg of T per day, and of that 4% gets converted to DHT and .02% gets converted to estrogen, (estradiol E2)

The prostate converts 95% of T to DHT by 5 alpha reductase, ( 5ar).

.02% of E is converted by the enzyme aromatase, this small percentage can be misleading, estradiol is 100 more potent at the receptor sites then T, that means T needs to balance at the same level to have the same affinity.

Now, in bio-males, if we increase E, some E receptors will, in turn, cause decreased T production, right?

If we decrease T (through AAs), in contrast, are there some T receptors that won't be activated that would normally suppress E production, leading to increased E levels?

A related question: in bio-males, are there any sources of E other than by aromatase conversion of T?

Michelle

Now, in bio-males, if we increase E, some E receptors will, in turn, cause decreased T production, right?

If we decrease T (through AAs), in contrast, are there some T receptors that won't be activated that would normally suppress E production, leading to increased E levels?

A related question: in bio-males, are there any sources of E other than by aromatase conversion of T?

Michelle

Hi Michelle,
What we discussed in a private conversation, in which I stated that lowering your T will cause the body to increase E to maintain a total amount of sex hormone was misleading.

Lotus can correct me, as needed, but the fact is that the only way that E2 (estradiol) is formed in a bio-male is through aromatization which occurs in various tissues of the body including adipose (fatty) tissue. If one's testosterone level is reduced, the amount of estrogen produced also is reduced, but not as drastically. So men with low T will also likely have lower than normal E. What does change, however, is the ratio of T to E. As the T/E ratio drops, the available E has a greater effect because there's less T to overcome, thus secondary female sex characteristics (e.g. breast enlargement, increased body fat, etc.) are realized.

On the other hand, if we increase E exogenously by taking PM, for example, the hypothamus and pituitary glands will detect it and signal the testes to produce less testosterone. Thus, PM has the effect of an anti-androgen even though it is not classified as one.

If you aggressively drive down your T with AAs (not PM mind you), your E level will also drop below normal. That is not a good thing as I understand it. For example, it can lead to severe osteoporosis.

Please, if I'm off base with this explanation, I'd like someone to correct me. On the other hand, if I'm correct, please confirm.

Clara

Now, in bio-males, if we increase E, some E receptors will, in turn, cause decreased T production, right?

Yes, Increased E shuts down (blocks off) your T receptors, essentially making them inactive.

If we decrease T (through AAs), in contrast, are there some T receptors that won't be activated that would normally suppress E production, leading to increased E levels?

I think your saying that if we prevent T from turning into Dht through 5-ar (5 alpha reductase) it will turn it into E, if so that's correct.

A related question: in bio-males, are there any sources of E other than by aromatase conversion of T?

Not that I'm aware of (we'd need ovaries) bio-males produce .02 mg 0f E daily from Aromatase and for bio-females it's virtually the same for their production of T per day (.05 mg).

Thanks for the brain teasers!


Sorry Clara, just saw your post!

Thanks very much, Clara and Lotus! That's exactly the kind of analysis I was trying to work through!

Michelle

Sorry Clara, just saw your post!

No problem, Lotus, because you clear up an important point for me....

I think your saying that if we prevent T from turning into Dht through 5-ar (5 alpha reductase) it will turn it into E, if so that's correct.

What you are saying here is that it IS possible for a bio-male to increase his estrogen level by using anti-androgens only, if done in such a way as to block the conversion of testosterone into DHT. Aromatase will then convert more of the available T to estrogen. That tells me that taking Spearmint Leaf, which has the effect of binding up free T making in unavailable for use by either 5-alpha reductase or aromatase, is not the best approach to increase your estrogen short of taking an estrogenic herb like PM. Better to take SP, Pygeum or one of the other AAs that target 5-alpha reductace.

Thank you, Lotus, you are a dear.

Clara

Sorry Clara, just saw your post!

No problem, Lotus, because you clear up an important point for me....

I think your saying that if we prevent T from turning into Dht through 5-ar (5 alpha reductase) it will turn it into E, if so that's correct.

What you are saying here is that it IS possible for a bio-male to increase his estrogen level by using anti-androgens only, if done in such a way as to block the conversion of testosterone into DHT. Aromatase will then convert more of the available T to estrogen. That tells me that taking Spearmint Leaf, which has the effect of binding up free T making in unavailable for use by either 5-alpha reductase or aromatase, is not the best approach to increase your estrogen short of taking an estrogenic herb like PM. Better to take SP, Pygeum or one of the other AAs that target 5-alpha reductace.

Thank you, Lotus, you are a dear.

Clara

Clara, I think you're reading my mind! That was going to be my next question, the effect of spearmint vs the other AAs.

I think Lotus might have even mentioned PC as a DHT blocker; is that true?