12-07-2012, 02:48 PM
Hi Karen,
When you look at it from a distance, that's more or less correct. However, if you look at the mechanics of it, I don't believe weak phyto-estrogens are all that bad.
A low binding affinity just means a phyto-estrogen comes off the receptor more easily. So let's pick my number of 20. If the binding affinity of 8-PN is 20 times lower than that of estradiol, it just means 8-PN leaves the receptor 20 times easier than estradiol.
This has consequences:
1) a 20 times lower dose of estradiol will have the same effect as a given dose of 8-PN
2) at equal doses, of all the occupied receptors, 95 % have estradiol on them, and 5 % have 8-PN on them.
This means that 95 % of the work will be done by the receptors that have estradiol on them. What the 5 % receptors with 8-PN on them do, doesn't really matter in the first place. So your conclusion that the best NBE strategy is upping estradiol by cutting down DHT (and not taking too much progestogens), is correct.
Actually, the 8-PN on the receptors sets in motion the same chain of events in the cell as the estradiol does. Those events will eventually lead to cell growth and/or division. Steroids that bind to the estrogen receptor without setting that chain of events in motion, are not estrogens. They are anti-estrogens.
I really believe that the story you read many times on the forum, that if you have only so many receptors, you would prefer to have them occupied by strong phyto-estrogens, is just echoing sales talk from vendors of strong phyto-estrogens. If you take two phyto-estrogens together, the one with the lower binding affinity will just occupy a smaller portion of the receptors, at equal dose. So if you take ten times more of a phyto-estrogen with a ten times lower binding affinity, both phyto-estrogens will contribute equally to your growth.
In scientific literature, a "weak" phyto-estrogen is not necessarily a phyto-estrogen with a low binding affinity. The term is also used for phyto-estrogens that are selective for the estrogen receptor β (ERβ). ERβ is the receptor found in skin cells, while ERα is in breast cells. Genistein and daidzein from soy are selective for ERβ. So soy gives you smooth skin. Daidzein is digested to equol, which is selective for ERα. So people who have the right bacteria in their intestines, may also grow breasts on soy.
The bacteria that digest daidzein to equol are partly the same bacteria that digest isoxanthohumol from hops to 8-PN. So if you keep them busy with lots of soy, they will produce less 8-PN. That's why cosupplementation of hops and soy is slightly less effective than using either hops or soy alone. You need to adjust the doses upward by say 30 % to compensate for that effect.
The above is my understanding of the literature. I don't want to pretend to know it all, though. I have quite a few questions too:
- Why doesn't anyone seem to grow on SP alone?
- Soy users generally have excellent skin, but why do many have no breasts?
- Why is there no literature on women who have no boobs because they have been consuming a dietary or environmental anti-estrogen for too long?
- Why do some transition regimes insist on adding a progestin?
- Why don't gym rats take anti-estrogens instead of aromatase inhibitors?
- Why do we lose size when we stop phyto-estrogens, if gynecomastia are so hard to get rid of?
When you look at it from a distance, that's more or less correct. However, if you look at the mechanics of it, I don't believe weak phyto-estrogens are all that bad.
A low binding affinity just means a phyto-estrogen comes off the receptor more easily. So let's pick my number of 20. If the binding affinity of 8-PN is 20 times lower than that of estradiol, it just means 8-PN leaves the receptor 20 times easier than estradiol.
This has consequences:
1) a 20 times lower dose of estradiol will have the same effect as a given dose of 8-PN
2) at equal doses, of all the occupied receptors, 95 % have estradiol on them, and 5 % have 8-PN on them.
This means that 95 % of the work will be done by the receptors that have estradiol on them. What the 5 % receptors with 8-PN on them do, doesn't really matter in the first place. So your conclusion that the best NBE strategy is upping estradiol by cutting down DHT (and not taking too much progestogens), is correct.
Actually, the 8-PN on the receptors sets in motion the same chain of events in the cell as the estradiol does. Those events will eventually lead to cell growth and/or division. Steroids that bind to the estrogen receptor without setting that chain of events in motion, are not estrogens. They are anti-estrogens.
I really believe that the story you read many times on the forum, that if you have only so many receptors, you would prefer to have them occupied by strong phyto-estrogens, is just echoing sales talk from vendors of strong phyto-estrogens. If you take two phyto-estrogens together, the one with the lower binding affinity will just occupy a smaller portion of the receptors, at equal dose. So if you take ten times more of a phyto-estrogen with a ten times lower binding affinity, both phyto-estrogens will contribute equally to your growth.
In scientific literature, a "weak" phyto-estrogen is not necessarily a phyto-estrogen with a low binding affinity. The term is also used for phyto-estrogens that are selective for the estrogen receptor β (ERβ). ERβ is the receptor found in skin cells, while ERα is in breast cells. Genistein and daidzein from soy are selective for ERβ. So soy gives you smooth skin. Daidzein is digested to equol, which is selective for ERα. So people who have the right bacteria in their intestines, may also grow breasts on soy.
The bacteria that digest daidzein to equol are partly the same bacteria that digest isoxanthohumol from hops to 8-PN. So if you keep them busy with lots of soy, they will produce less 8-PN. That's why cosupplementation of hops and soy is slightly less effective than using either hops or soy alone. You need to adjust the doses upward by say 30 % to compensate for that effect.
The above is my understanding of the literature. I don't want to pretend to know it all, though. I have quite a few questions too:
- Why doesn't anyone seem to grow on SP alone?
- Soy users generally have excellent skin, but why do many have no breasts?
- Why is there no literature on women who have no boobs because they have been consuming a dietary or environmental anti-estrogen for too long?
- Why do some transition regimes insist on adding a progestin?
- Why don't gym rats take anti-estrogens instead of aromatase inhibitors?
- Why do we lose size when we stop phyto-estrogens, if gynecomastia are so hard to get rid of?