Hi all
A short backround on me:
I have pcos and on 2000mg metformin - helped for normalisation of my weight - now 55kg from 75kg and acne
Always used herbs which helped for my testosterone excess problems
SP & inositol At the moment
I am sure that im low estrogen, long follicular phase (ovulate late) low body fat on butt and hips and thighs
Generous bust in tubular shape which rounded out somewhat through pregnancy breaat feeding and herbs
Would like more help on rounding boobs and adding fat to butt hips and thighs and breasts have lost much volume due to weight loss
Any help would be much appreciated!!
Thank u
I've honestly noticed MUCH bigger bottom half growth with flaxseed oil, DHA, and Fenugreek than anything on top. These will help to fill them out though. You should also try massaging liquid Flaxseed oil topically on your breasts and butt. MSM is also reported to round out breasts and cause growth when taking large amounts. Initially you're going to want to start small on what you ingest because you'll only be able to absorb a small amount at first. The rest will be expelled or show up as acne.
With any supplements, you're going to need a multi to absorb too.
Most importantly, drink plenty of water and get plenty of rest for maximum growth.
Walnut oil, macadamia nut oil, coconut oil (both external & internal) would be better. Add progesterone type herbs for side branching growth aka - the rounding of breast. A healthy regime (mix) of omega 3's (chia seeds, fish oil, cod liver oil & 6's (evening primrose/borage oil/hempseed oil) add protection and growth cycles.
Vitex and red clover are good in the first half, though they're quite versatile for the whole cycle, (mid cycle-break 3-5 days)
LH and probably FSH during follicular phase raise androgens; this is supposed to raise estrogens too, but this is secondary. Androgens are believed to cause PCOS. Estrogens can only be formed from Androgens, through aromatase. There being less prolactins and progesterone than estrogens could explain breast shape. It looks like there is high LH, high androgens, lower estrogens, and even lower prolactin levels during follicular.
I think aromatase, prolactin and progesterone herbs together during menstruation and luteal would be good. Lack of prolactin is causing the extended periods, and lack of aromatase explains PCOS and high androgen levels. There may also be too much LH herbs. The proportion has to be right.
Thank you everyone who took the time To reply to me
Blood test did show high LH and extremely low FSH
Ok so good herbs would be agnus castus, oil massage, aromatase...would that be a combo of peony root and spearmint?
I took soooo much saw palmetto, like 5000mg that my thighs did enlarge, but i had terrible dry skin and low mood..most low estrogen symptoms....do you guys think to much SP can lower aromatase?
Im now on 1000mg sp hoping to get levels right again somewhat
Also when i took progesterone i had a terrible reaction, about 10 yrs ago....just felt super PMS X 1000
I will try again now im bit more balanced
Saw Palmetto and Spearmint raise LH. I believe chasteberry (vitex) raises LH too, while raising progesterone. Spearmint is also an aromatase, but I don't think it aromatases as much as it raises LH which raises Androgens. Raising LH also lowers prolactin and progesterone.
Chasteberry normalizes the luteal phase because of its contradicting effects of raising LH, and progesterone, which each normally lower each other.
Saw palmetto is supposed to lower DHT through the prostate, but I don't know if it has an effect on the female prostate. Decreasing 5alpha-reductase (that creates DHT) during the last week of luteal isn't too good, because it lowers dihydroprogesterones which helps the brain deal with PMS. In other words Saw Palmetto doesn't work during the luteal phase.
Was FSH measured throughout the cycle or only at a certain time. Because FSH is supposed to be low at certain times.
Wow its complicated!
They measured on cycle day 4 and FSH was less than one quarter of the lowest range, it was 0. Something, almost non existant...
What does this mean?
I know high fsh is ovaries running out of supplies but very low FSH? And LH was almost 3 times the normal range....this was before metformin. I havent had time to retest...had 2 young kids and little bro had lueakemia so had no time to worry about myself ... As my periods were coming monthly and acne had cleared, i asumed all was well
But now that kids are in school and bro has recovered im concentrating on getting myself better
That answers my question. I don't remember exactly but some of the above herbs raise LH and lower FSH, while others raise both FSH and LH.
I'm not sure what it means except there's low FSH. I think limiting LH herbs to once every once in a while. Aside from finding which ones lower FSH; then limiting LH herbs because their effects are a big deal; maybe adaptogens and eating eggs. Focus more on aromatase instead of LH for estrogenic properties. High LH perfectly explains a lot; too much androgens and not enough conversion into estrogens, while there being even less prolactin and progesterone balance than estrogen.
It's good that everyone is doing better.
I remembered, prolactin and progesterone both lower LH. Above I've mentioned lack of prolactin causing extended periods. Also a suggestion above to use progesterone herbs was correct. Adding prolactin herbs is also helpful. Phyto-progesterones do their action weakly and by raising prolactin, but serum progesterone won't raise during follicular. So prolactin, aromatase and progesterone herbs together during menstruation should be good.
I don't think I'd limit progesterone and estrogen together anymore, this is possibly why we don't see a balanced growth. Expand the possibilities beyond conventional science, that's when see a whole new dimension of NBE. Controlling androgens first, there are precursor hormones after all.
Progesterone and estrogen E2 (together) in-quote-"induced proliferation that resulted in sidebranching and alveologenesis," but E+P treatment produced more proliferation sooner and extensive sidebranching and alveologenesis. The exact amounts of E2 (estradiol) and progesterone weren't given. In other words having progesterone combined with E2 produces side-branching of the breasts (outward growth),
function of progesterone receptor isoforms in normal adult mouse mammary gland.
Aupperlee MD1, Haslam SZ.
Author information
Abstract
In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2'-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2'-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion.
These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.
http://www.ncbi.nlm.nih.gov/pubmed?filte...%5Bauth%5
Estrogen's concentration in a particular tissue depends on many things,
including its affinity or binding strength for components of that tissue, relative to its affinity for the blood; the activity in that tissue of the aromatase enzyme, which converts androgens to estrogen activity of glucuronidase enzyme, that converts water-soluble estrogen glucuronides into the oil soluble active forms of estrogen; and the sulfatases and several other enzymes that modify the activity and solubility of the estrogens. The "
estrogen receptors," proteins which bind estrogens in cells, are inactivated by progesterone, and activated by many physical and chemical conditions.
Recently I've been reading articles from a PhD of biology named Ray Peat, here's a few paragraphs from his articles.
Quote:polyunsaturated fats and prostaglandins stimulate the expression of aromatase, the enzyme that synthesizes estrogen, aspirin decreases the production of estrogen.
Quote: The amount of estrogen in tissue is decreased when progesterone is abundant. In the absence of progesterone, tissues retain estrogen even when there is little estrogen circulating in the blood.
Quote:Estrogen is produced in many tissues by the enzyme aromatase, even in the breast and endometrium, although these are considered "target tissues" rather than endocrine glands. Aromatase increases with aging.
Quote:Estrogen is inactivated, mainly in the liver and brain, by being made water soluble by the attachment of glucuronic acid and/or sulfuric acid.