[Dynseli]

Discussion continued from http://www.breastnexus.com/showthread.php?tid=17416&page=20

Good find (by Lotus): http://www.ncbi.nlm.nih.gov/books/NBK26896/ NIH book, circa 2002. 'Carrier Proteins and Active Membrane Transport'

[Dynseli]

From Wikipedia, 'Sex hormone-binding globulin'

"the relative binding affinity of various sex steroids for SHBG is dihydrotestosterone (DHT) > testosterone > androstenediol > estradiol > estrone.[2]"

"SHBG is produced mostly by the liver"

"SHBG has both enhancing and inhibiting hormonal influences. It decreases with high levels of insulin, growth hormone, insulin-like growth factor 1 (IGF-1), androgens, prolactin and transcortin. High estrogen, and thyroxine cause it to increase."

"Conditions associated with high or low levels

SHBG levels are decreased by androgens, administration of anabolic steroids,[17] polycystic ovary syndrome, hypothyroidism, obesity, Cushing's syndrome, and acromegaly. Low SHBG levels increase the probability of Type 2 Diabetes.[18] SHBG levels increase with estrogenic states (oral contraceptives), pregnancy, hyperthyroidism, cirrhosis, anorexia nervosa, and certain drugs. Long-term calorie restriction of more than 50 percent increases SHBG, while lowering free and total testosterone and estradiol. DHEA-S, which lacks affinity for SHBG, is not affected by calorie restriction.[19] Polycystic Ovarian Syndrome is associated with insulin resistance and excess insulin lowers SHBG, which increases free testosterone levels.[20]

In the womb the human fetus has a low level of SHBG allowing increased activity of sex hormones. After birth, the SHBG level rises and remains at a high level throughout childhood. At puberty the SHBG level halves in girls and goes down to a quarter in boys.[1] he change at puberty is triggered by growth hormone, and its pulsatility differs in boys and girls. In pregnant women in the last two thirds of pregnancy the SHBG level escalates to five to ten times the usual level for a woman. A hypothesis is that this protects against the effect of hormone produced by the fetus.[1]

Obese girls are more likely to have an early menarche due to lower levels of SHBG.[1] Anorexia or a lean physique in women leads to higher SHBG levels, which in turn can lead to amenorrhea.[1]"

[Dynseli]

I had this in a draft in another thread, however I will list it here too.

Soy isoflavones have also been shown in several studies to elevate SHBG levels and to be mildly anti-estrogenic. High serum-High serum levels of estrogen also trick the brain into thinking that enough testosterone is being produced, further slowing its natural production. 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 that the gonads require to produce testosterone. High estrogen can thus shut down the normal testicular production of testosterone. A further complication of excess estrogen is that it increases the body's production of sex hormone-binding globulin (SHBG). SHBG binds free testosterone in the blood and makes it unavailable to cell receptor sites. The solution to this problem is to block the conversion of testosterone to estrogen.

This is why herbs that raise LH are useful. They seem to raise LH without causing negative feedback for androgen production. There might be negative feedback for LH production, but these can also be upregulated by herbs or by normal body functions. The adrenal glands also produce T. Androgen production just needs to be raised a few times, then it levels, that is enough to make estrogens. Testosterone doesn't need to keep being raised. Once its raised the body is already producing a level but higher level of testosterone. That is more than enough for conversion.

Estrogen dominance could already mean high T which both cause excess body hair, long and uncomfortable menstruation, tuberous breasts, etc... Here aromatase and raising LH are useful. What if prolactin and progestins raise AR sensitivity? Does estrogen shut down AR, does it upregulate it, or both? AR= androgen receptors

I've read that aromatase lowers prolactin in males (lacking), increased progesterone will cause an increase of prolactin. Increased estrogen levels can also stimulate increased prolactin levels. Prolactin stimulates the glandular tissue in the male breast. This is what causes the lactation and other gyno-like symptoms. The main control hormone for prolactin release is dopamine. Estrogens, and to a lesser extent progestins, can increase sensitivity of prolactin, but not necessarily increase levels.

Raising SHBG should up-regulate free T, which doesn't sound good for green tea at this point, I dunno, more searching I guess. The more exogenous testosterone that enters your body the more SHBG will be produced, its our own body's reaction or mechanism to maintain homeostasis. Definitely E shuts production of T down, which conventional thinking says that's what the mtf regime should be. Now the study I listed earlier from France says that enzymes play a role in raising E levels, and that's done through (not sure how much though) free T, or should we say bio-AVIABLE T.

about carrier proteins, copied from: http://www.breastnexus.com/showthread.php?tid=21168

[Dynseli]

estrogen doesn't increase serum prolactin, it lowers it. Estrogen increases prolactin Receptor sensitivity. Meaning the receptor responds more to less estrogen.

[Lotus]

estrogen doesn't increase serum prolactin, it lowers it. Estrogen increases prolactin Receptor sensitivity. Meaning the receptor responds more to less estrogen.

During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold.

On another note:

Excessive estrogen in circumstances of deficient progesterone induces a decrease in receptor sensitivity. One of progesterone's functions is to restore the normal sensitivity of estrogen receptors. When progesterone is restored, estrogen receptor sensitivity is restored also.

[Dynseli]

During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold.

I don't think that's how it goes.
During pregnancy, it's the placenta that raises progesterone sky high, to prevent a miscarriage. Progesterone=the pregnancy hormone. Now, progesterone from the placenta signals the pituitary to release more prolactin. Progesterone is the dominant hormone during pregnancy, and prolactin is secondary

Prolactin is stimulated by the baby breastfeeding, which also stops menstruation. When the baby is no longer breastfed, the menstrual cycle returns to normal. Here prolactin influences progesterone to also rise. Prolactin is the dominant hormone during breastfeed, and its function is breastfeeding. The reason for this is, the mother doesn't need to seek partners while nursing her child.

Both prolactin and progesterone lower estrogens. And estrogens lower both prolactin and progesterone.

If you meant [During pregnancy, high circulating concentrations of '''progesterone''' increase prolactin], that sounds more right, but I'm not sure by how much.

Excessive estrogen in circumstances of deficient progesterone induces a decrease in [estrogen] receptor sensitivity. One of progesterone's functions is to restore the normal sensitivity of estrogen receptors. When progesterone is restored, estrogen receptor sensitivity is restored also.

Clarified estrogen receptor. The rest is right.

[Lotus]

During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold.

I don't think that's how it goes.
During pregnancy, it's the placenta that raises progesterone sky high, to prevent a miscarriage. Progesterone=the pregnancy hormone. Now, progesterone from the placenta signals the pituitary to release more prolactin. Progesterone is the dominant hormone during pregnancy, and prolactin is secondary

Prolactin is stimulated by the baby breastfeeding, which also stops menstruation. When the baby is no longer breastfed, the menstrual cycle returns to normal. Here prolactin influences progesterone to also rise. Prolactin is the dominant hormone during breastfeed, and its function is breastfeeding. The reason for this is, the mother doesn't need to seek partners while nursing her child.

Both prolactin and progesterone lower estrogens. And estrogens lower both prolactin and progesterone.

If you meant [During pregnancy, high circulating concentrations of '''progesterone''' increase prolactin], that sounds more right, but I'm not sure by how much.

Excessive estrogen in circumstances of deficient progesterone induces a decrease in [estrogen] receptor sensitivity. One of progesterone's functions is to restore the normal sensitivity of estrogen receptors. When progesterone is restored, estrogen receptor sensitivity is restored also.

Clarified estrogen receptor. The rest is right.

That's directly from http://wikipedia.org/wiki/Prolactin


During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold. However, at the same time, estrogen, as well as progesterone, inhibit the stimulatory effects of prolactin on milk production. It is the abrupt drop of estrogen and progesterone levels following delivery that allows prolactin — which temporarily remains high — to induce lactation.

After childbirth, prolactin levels fall as the internal stimulus for them is removed. Sucking by the baby on the nipple then promotes further prolactin release, maintaining the ability to lactate. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland cause increased prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down: Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed.

[Dynseli]

That's directly from http://wikipedia.org/wiki/Prolactin
...
During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold.

its progesterone, not estrogen. Wikipedia gets things wrong. Someone probably thought progesterone was an estrogen, and its not. Verification would be needed.

summarized from britannica, the corpus luteum is the temporary organ which produces progesterone, this progesterone, signals the pituitary gland to release prolactin, which also tries to hold on to the egg. [This is a loop, a reinforced signal]. If the egg (corpus luteum) is not fertilized, it stops producing progesterone, the pituitary gets this message, and stops raising prolactin. Progesterone and prolactin were putting estrogen's effects on hold.

The unfertilized egg is released, through menstruation, because of estrogen. If the egg is fertilized, this produces more progesterone. The pituitary and the placenta signal strongly in a loop to protect the baby from being aborted through menstruation.

I also know that estrogen lowers both prolactin and progesterone.

The rest of the quote seems correct.

[BonitaDDs]

Yes estrogen rises during pregnancy too but the hormones do vary at different times during pregnancy are you saying that's not true?
But only some women grow bigger breasts in pregnancy so that's interesting others end up smaller after.
I don't know I'm not much into to science part of nbe

[Dynseli]

There's probably some estrogen during pregnancy. It's prolactin and progesterone that are way higher. I just disagree with that quote, because it conflicts with everything else.

These are the levels of progesterone and prolactin during pregnancy.
http://www.nlm.nih.gov/medlineplus/ency/...003714.htm
http://www.nlm.nih.gov/medlineplus/ency/...003718.htm