Post by Moderator on Nov 9, 2003 12:05:29 GMT -5
From: fawnmarie42 (Original Message) Sent: 7/1/2003 10:00 PM
As many of you who have been following my psuedo-scientist/herbalist (was that it?) ramblings over the last couple of months are aware, I did a survey that anectodally showed that women using progesterone with their BE program did not progress unless they also used a topical preparation.
Working from the observation that most natural growth occurs when estrogen is high and progesterone is inhibited, I surmised that progesterone blocked the growth action of estrogen in the process.
Further research on my part, however, showed that progesterone does perform an important task and the glandular growth was higher during periods of both high estrogen and high progesterone - these concepts were in direct opposition with each other, and it has been bothering me for some time why medical studies showed higher glandular growth during times when both were high and present, where experience was showing otherwise. This has left me extremely frustrated and banging my head on nearby doorframes.
Women who used both progesterone and a topical did grow - though not as fast - and I assumed this was because topical (and targeted) application of estrogens overrode the affect of progesterone's interference (while keeping levels normalized throughout the rest of the body).
This has been driving me insane.
Well - I ran into some further research that might explain this contradiction. FINALLY! And I'd like to share it...
As you all know, breasts are made up of both glandular tissue and fat/connective tissue.
During the follicular phase, estrogen is dominant and this causes an increase of insulin resistance, and increase of A2 receptors and an increase of glutocorticoids - these are the hormones responsible for the storage of fat into the breast tissues. Some women experience their "high-point" during this phase - and it's my guess that these would be women with insulin resistance (i.e., PCOS or just older) and/or women who are well into involution (higher proportion of fat to glandular tissue), which would include older women and women who have not had a baby in some time.
During the luteal phase, progesterone is introduced and this causes replication and growth of glandular tissue - but it opposes two vital hormones that increase fat storage - cortisol and prolactin. While glandular growth is occurring, fat storage is at a minimum. Some women have enough glandular tissue and enough growth in this tissue during the luteal phase that it is at this time during that their cycle that the seem to have the most growth. (My off-handed guess would be that these are women under 30 or who have not had children at all, or have had one very recently, since there is significantly more gland to fat tissue in this population).
Okay - so what's the deal? Why did women using progesterone measure no growth, women using progesterone and topical grow a little, and women using no progesterone grow faster?
One thing I noticed was that it didn’t seem to matter WHAT they were using topical, EPO, phytoestrogens, or just massage with body lotion.
In the midst of more research today I found a bit of a clue.
"These results indicate that PRLR (prolactin receptors) are not only present on MEC (glandular tissue), but are also present in the mammary fat pad, consistent with findings that adipose tissue expresses RPLR and that L-PRLR tranduces a signal for PRL-stimulated lipogenesis (fat tissue growth)."
(Role of the stroma and extracellular matrix during mammary gland growth and development. R Hovey & B. Vonderhaar NIH MD 20892-1402)
What does that mean? Prolactin receptors in the "stroma" (supporting connective and fat tissue) stimulates fat storage around the glandular tissue.
Prolactin was the difference. Prolactin is produced by STIMULATION to the breasts – so it didn’t really matter what was being applied, the mechanical processed itself produced prolactin.
What inhibits prolactin? DOPAMINE!!!
Anectodal note – when I first embarked on BE this year, I had a lot of growth VERY fast. Thinking back – I also remember that I was taking wellbutrin at the time (trying to quit smoking). When did I stall out? When I STOPPED taking the wellbutrin in March!!! Wellbutrin BLOCKS dopamine!
So, what does this mean?
Prolactin is required for BE. What does this mean? Reduction of consumption of caffeine and nicotine! (Sorry Mom!) Both cause surges of dopamine.
I’m looking into further studies on prolactin and adipose tissue – and further asking myself if those of us who are further along into involution don’t wish to rethink progesterone. That’s another post.
Anyway – all the data will be available at the information website I’ve been working on, and once I get it up and running, ya’ll can take a look at it.
JEEZ - I forgot the most important point - being that progesterone blocks and inhibits prolactin and glutocorticoids - which is why only those who added massage (applying a topical) might had had levels of prolactin raised high enough to meet that of the added progesterone.
Did ANY of this make sense?
Another point being that those who used progesterone & massage grew slower because an increase of glandular tissue would not register as much in size as an increase in fat tissue, though it would increase firmness.
(Or did you all extrapolate that yourselves?)
Fawn
As many of you who have been following my psuedo-scientist/herbalist (was that it?) ramblings over the last couple of months are aware, I did a survey that anectodally showed that women using progesterone with their BE program did not progress unless they also used a topical preparation.
Working from the observation that most natural growth occurs when estrogen is high and progesterone is inhibited, I surmised that progesterone blocked the growth action of estrogen in the process.
Further research on my part, however, showed that progesterone does perform an important task and the glandular growth was higher during periods of both high estrogen and high progesterone - these concepts were in direct opposition with each other, and it has been bothering me for some time why medical studies showed higher glandular growth during times when both were high and present, where experience was showing otherwise. This has left me extremely frustrated and banging my head on nearby doorframes.
Women who used both progesterone and a topical did grow - though not as fast - and I assumed this was because topical (and targeted) application of estrogens overrode the affect of progesterone's interference (while keeping levels normalized throughout the rest of the body).
This has been driving me insane.
Well - I ran into some further research that might explain this contradiction. FINALLY! And I'd like to share it...
As you all know, breasts are made up of both glandular tissue and fat/connective tissue.
During the follicular phase, estrogen is dominant and this causes an increase of insulin resistance, and increase of A2 receptors and an increase of glutocorticoids - these are the hormones responsible for the storage of fat into the breast tissues. Some women experience their "high-point" during this phase - and it's my guess that these would be women with insulin resistance (i.e., PCOS or just older) and/or women who are well into involution (higher proportion of fat to glandular tissue), which would include older women and women who have not had a baby in some time.
During the luteal phase, progesterone is introduced and this causes replication and growth of glandular tissue - but it opposes two vital hormones that increase fat storage - cortisol and prolactin. While glandular growth is occurring, fat storage is at a minimum. Some women have enough glandular tissue and enough growth in this tissue during the luteal phase that it is at this time during that their cycle that the seem to have the most growth. (My off-handed guess would be that these are women under 30 or who have not had children at all, or have had one very recently, since there is significantly more gland to fat tissue in this population).
Okay - so what's the deal? Why did women using progesterone measure no growth, women using progesterone and topical grow a little, and women using no progesterone grow faster?
One thing I noticed was that it didn’t seem to matter WHAT they were using topical, EPO, phytoestrogens, or just massage with body lotion.
In the midst of more research today I found a bit of a clue.
"These results indicate that PRLR (prolactin receptors) are not only present on MEC (glandular tissue), but are also present in the mammary fat pad, consistent with findings that adipose tissue expresses RPLR and that L-PRLR tranduces a signal for PRL-stimulated lipogenesis (fat tissue growth)."
(Role of the stroma and extracellular matrix during mammary gland growth and development. R Hovey & B. Vonderhaar NIH MD 20892-1402)
What does that mean? Prolactin receptors in the "stroma" (supporting connective and fat tissue) stimulates fat storage around the glandular tissue.
Prolactin was the difference. Prolactin is produced by STIMULATION to the breasts – so it didn’t really matter what was being applied, the mechanical processed itself produced prolactin.
What inhibits prolactin? DOPAMINE!!!
Anectodal note – when I first embarked on BE this year, I had a lot of growth VERY fast. Thinking back – I also remember that I was taking wellbutrin at the time (trying to quit smoking). When did I stall out? When I STOPPED taking the wellbutrin in March!!! Wellbutrin BLOCKS dopamine!
So, what does this mean?
Prolactin is required for BE. What does this mean? Reduction of consumption of caffeine and nicotine! (Sorry Mom!) Both cause surges of dopamine.
I’m looking into further studies on prolactin and adipose tissue – and further asking myself if those of us who are further along into involution don’t wish to rethink progesterone. That’s another post.
Anyway – all the data will be available at the information website I’ve been working on, and once I get it up and running, ya’ll can take a look at it.
JEEZ - I forgot the most important point - being that progesterone blocks and inhibits prolactin and glutocorticoids - which is why only those who added massage (applying a topical) might had had levels of prolactin raised high enough to meet that of the added progesterone.
Did ANY of this make sense?
Another point being that those who used progesterone & massage grew slower because an increase of glandular tissue would not register as much in size as an increase in fat tissue, though it would increase firmness.
(Or did you all extrapolate that yourselves?)
Fawn