[Lotus]

Green tea, vitamin D, coconut oil, genistien (tricky one though), horny goat weed, licorice root, white peony, cAMP, the hormone Leptin are all pro-aromatase. I believe FSH (follicle stimulating hormone) is also pro-aromatase, this technique is only to be used by someone who knows the ways of the force lol, (it does take skill though)

These pro-aromatase herbs/hormone up-regulates the synthesis to estrogen anywhere from 2 to 45 fold, (listed in FAQ aromatase, my program page).

LanaG, licorice is used in short duration (2-3 weeks), and if your adernals are fine I'd suggest backing it down to 2x per day.

Don't forget vitamin C.......which helps NBE metabolism. Eat walnuts, 3-4 pieces a day to a 1/4 cup, or some peanuts. Greek yogurt helps with growth hormones. Nbe isn't set and forget it, take NBE 4x daily to match the release of hormones.

There's a lot more to NBE and even hrt, these threads could offer more suggestions.

Good luck

Hrt Pharmacokinetics (which lists the half-life of E2, anti-androgens, metabolism, using NBE with HrT, etc).
http://www.breastnexus.com/showthread.php?tid=23606
Breast Growing guide 101
http://www.breastnexus.com/showthread.php?tid=24358
FAQ-Aromatase
http://www.breastnexus.com/showthread.php?tid=19581


There's one other thing you'll need LanaG, (without it breast growth will be listed)

what's your guess?

[LanaG]

Posted by Sillygirl37 - Today 02:19 PM
Lana G, I know you said you had feelings of being TG, but what is your ultimate goal on this journey? I'm only asking because I like to believe that finding the most direct route to success is the road to finding happiness. Of course, resources and money not withstanding.

Sillygirl37, I am not sure of my goal, but I am sure I want to start, if that makes anysense. I think I will have to sort some things out along the way

[LanaG]

Posted by Lotus - Today 04:31 PM
Green tea, vitamin D, coconut oil, genistien (tricky one though), horny goat weed, licorice root, white peony, cAMP, the hormone Leptin are all pro-aromatase. I believe FSH (follicle stimulating hormone) is also pro-aromatase, this technique is only to be used by someone who knows the ways of the force lol, (it does take skill though)

These pro-aromatase herbs/hormone up-regulates the synthesis to estrogen anywhere from 2 to 45 fold, (listed in FAQ aromatase, my program page).

LanaG, licorice is used in short duration (2-3 weeks), and if your adernals are fine I'd suggest backing it down to 2x per day.

Don't forget vitamin C.......which helps NBE metabolism. Eat walnuts, 3-4 pieces a day to a 1/4 cup, or some peanuts. Greek yogurt helps with growth hormones. Nbe isn't set and forget it, take NBE 4x daily to match the release of hormones.

There's a lot more to NBE and even hrt, these threads could offer more suggestions.

Good luck Smile

There's one other thing you'll need LanaG, (without it breast growth will be listed)

what's your guess?

Lotus thank you so much!

Should the coconut oil be unrefined or refined?

I am taking vitamin C, D, E, A and Calcium supplements
As for the Licorice, I have only used that for the past 10 days or so and plan on stopping taking it by this Friday since my BO and PC will be arriving on Thursday (I had been using SP prior)

My plan starting Friday (besides Vitamins A, B, C, D, E and Calcium) is BO, Pituitary extract, Goats Rue, Fenugreek, Spearmint and Wild Yam.

Lotus, my guess on the one other thing is "Whey Protein". Is that the correct guess?

LanaG

[Lotus]

Posted by Lotus - Today 04:31 PM
Green tea, vitamin D, coconut oil, genistien (tricky one though), horny goat weed, licorice root, white peony, cAMP, the hormone Leptin are all pro-aromatase. I believe FSH (follicle stimulating hormone) is also pro-aromatase, this technique is only to be used by someone who knows the ways of the force lol, (it does take skill though)

These pro-aromatase herbs/hormone up-regulates the synthesis to estrogen anywhere from 2 to 45 fold, (listed in FAQ aromatase, my program page).

LanaG, licorice is used in short duration (2-3 weeks), and if your adernals are fine I'd suggest backing it down to 2x per day.

Don't forget vitamin C.......which helps NBE metabolism. Eat walnuts, 3-4 pieces a day to a 1/4 cup, or some peanuts. Greek yogurt helps with growth hormones. Nbe isn't set and forget it, take NBE 4x daily to match the release of hormones.

There's a lot more to NBE and even hrt, these threads could offer more suggestions.

Good luck Smile

There's one other thing you'll need LanaG, (without it breast growth will be listed)

what's your guess?

Lotus thank you so much!

Should the coconut oil be unrefined or refined?

I am taking vitamin C, D, E, A and Calcium supplements
As for the Licorice, I have only used that for the past 10 days or so and plan on stopping taking it by this Friday since my BO and PC will be arriving on Thursday (I had been using SP prior)

My plan starting Friday (besides Vitamins A, B, C, D, E and Calcium) is BO, Pituitary extract, Goats Rue, Fenugreek, Spearmint and Wild Yam.

Lotus, my guess on the one other thing is "Whey Protein". Is that the correct guess?

LanaG

Coconut oil needs to be "virgin organic", in fact all oils should be unrefined. Man made oils lack the nutritional prolife of unrefined. Synthetic oils cause inflammation, free radical damage.

You know what?, you already have what I was asking about......PC, my bad lol. (Sorry)

Growth hormone is a good choice though. Whey protein would be ok. Personally I'm looking for an Organic Pea protein. But, cottage cheese is a quick protein punch, tuna (1-2 cans a week) salmon is also great for NBE. Source organic fruits and veggies. Peanuts (boiled) has the same resveratrol as in red wine and genistien (aromatase).

PC, applied directly to breasts (thinly applied) 1/4 teaspoon is about 20 to 25 mg. I would advise to use PC at bedtime. I think this will help two fold, PC is also an anti-androgen, that's 1 (number 2) is helping with growth hormone released in the first two hours of sleep, PC helps with sleep.

If you have an estrogenic cream use it when applying PC. Make sure it's less then the amount of PC you use. PC combined with E2 (phytoestrogen in this scenario) stimulates more tissue growth than if used separately....(paper posted in Hrt pharmacokinetics thread). It takes about 15 minutes for PC to dry. Don't put PC on the areolas, it will produce brown spots (freckles).

[LanaG]

Lotus, thank you so much for the guide on Coconut oil and PC/PM cream.

I am getting some PM cream also, I was wondering if/how they could be used together.

Until the BO and PC arrive Thursday, I am going to keep going with what I have.

I am also organize my plan, my diet and my exercise regime. My main concern is I want to lose ~20-30 lbs. So I am concerned that may work against me.

- Lana

[Lotus]

Lotus, thank you so much for the guide on Coconut oil and PC/PM cream.

I am getting some PM cream also, I was wondering if/how they could be used together.

- Lana

Ok, since you asked..........get ready.


Btw, weight loss?, adding a fitness plan to NBE can be very beneficial as opposed to just weight loss. HIIT (High intensity interval training) increases growth.......which fuels NBE......(you'll find that info using the search option).

[Lotus]

I posted a few studies that introduced prolactin and E2 simultaneously, which they worked synergistically (what a mouthful lol). The same is held true about introducing progesterone and E2.

And for that reason it (imo) explains the essence of how the combo birth control works, (2 hormone release).

In terms of a cycle its best to gain back stability, the fatigue is (can be) from an increase in prolactin.

There's other ways (things) to make add-ons but I wouldn't until you get PRL in order, first.

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?filters=&orig_db=PubMed&cmd=Search&term=148%2A%5Bvolume%5D%20AND%202290%5Bpage%5D%20AND%202007%5Bpdat%5D%20AND%20Aupperlee%20MD%5Bauth%5D

Prolactin stimulates breast growth in the presence of high estrogens, progesterone and estrogen stimulate growth too, and from what I've seen (still needs to be verified) pharma progestins up-regulate IGF-1. However, imo peptides look very promising.




Hormone-Dependent Mammary Gland Development

Hormone-dependent mammary gland development occurs after puberty and results in ductal elongation; recurrent estrous cycles in adulthood trigger side branching; pregnancy enhances side branching and induces alveolo- genesis with lactational differentiation followed by involution at weaning (Brisken 2002). In the late fifties, a series of experiments defined the minimal hormonal requirements for mammary gland development in mice (Nandi 1958) and rats (Lyons 1958). Endocrine ablation was achieved by surgically removing the major sources of reproductive hormones from mature females, the ovaries, which secrete estrogens and progesterone, the pituitary gland, a major source of growth hormone (GH) and prolactin (Prl), and for some experiments the adrenal glands, which release cortisol and precursors of sex steroids (see Fig. 1). Hormone replace- ment in hormone-deprived animals established that additive and sequential treatment with 17-b-estradiol, progesterone, and prolactin in conjunction with cortisol and GH can recapitulate mammary gland development.

http://www.ncbi.nlm.nih.gov/pmc/articles...003178.pdf

I almost forgot, I have this one of kind study (2006?) on mtf's that proved progesterone and E2 promoted tissue growth, I'll put it up asap, (when I find it lol).

The study was from 2000, not '06.

Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
Kanhai RC1, Hage JJ, van Diest PJ, Bloemena E, Mulder JW.
Author information
Abstract
The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature. We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation. To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer. The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast. In men treated with nonprogestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs. Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes. Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast. Orchidectomy does not contribute to this. Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.

Here's the full paper, or view the PDF as listed on the site.
http://journals.lww.com/ajsp/Fulltext/20..._of.9.aspx

Interesting this..about P.

''Your breasts needs progesterone as well as estrogen to grow. It is progesterone that activates estrogen receptors so that estrogen can bind to them. Progesterone is also the hormone responsible for building up fat stores in the breast.''

Absolutely true, the combined therapy is like a bio-directional response, for instance free T (the bio-active T) decreases by two-fold by the combined E and progesterone.

The effect of combined oral contraception on testosterone levels in healthy women: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/24082040

The current literature review and meta-analysis demonstrates that COCs decrease circulating levels of total T and free T and increase SBHG concentrations. Due to the SHBG increase, free T levels decrease twice as much as total T. The estrogen dose and progestin type of the COC do not influence the decline of total and free T, but both affect SHBG. The clinical implications of suppressed androgen levels during COC use remain to be elucidated.

Another similar study states a higher result from staggering dosages (orally). Imo this suggests a cyclic approach to lower androgens. Which btw androstenedione is the androgen culprit in GG's........not DHT.

contraceptives containing ethinylestradiol and gestodene or norgestimate upon androgen parameters and serum binding proteins.

Abstract
The effect of a triphasic oral contraceptive containing ethinylestradiol and gestodene (EE/GSD) on various serum hormonal parameters was compared with that of a monophasic formulation containing 35 micrograms ethinylestradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth and twelfth treatment cycle. There was no significant difference in the influence on any hormonal parameter between both formulations. Both EE/GSD and EE/NGM caused a time-dependent suppression of serum dehydroepiandrosterone sulphate (DHEA-S) by 20-30% (p < 0.01) and a reduction of 5 alpha-androstane-3 alpha, 17 beta-diol glucuronide by 50-60% (p < 0.01) during each treatment cycle, while androstenedione levels were reduced by 25% (p < 0.01). There was also a significant decrease in the levels of total testosterone by 30-35% (p < 0.01) and free testosterone by 60% (p < 0.01), while sex hormone-binding globulin (SHBG) was increased by 200-240% on days 11 and 21 (p < 0.01). During the pill-free interval the SHBG levels were reduced to a certain degree but remained elevated by 100% as compared to the pretreatment values. The serum levels of corticosteroid-binding globulin (CBG) which is known to be influenced only by the estrogenic component of combination pills, increased significantly by 170% (p < 0.01) during each treatment cycle. During the pill-free interval of 7 days, the CBG levels decreased but were still elevated by 90-100% as compared to the control cycle. Similarly, the serum levels of cortisol were significantly elevated by 110-140% (p < 0.01) during treatment with both preparations. The results demonstrate a profound suppression of androgen levels and peripheral androgen metabolism.

I think we just busted the freaking door wide open.

Lotus, As you know I have never managed to grow an after reading this article I understood that cortisol was the culprit - I did a blood test and indeed the cortisol was really high.

So basically I increased Oestro with my high cortisol and everything went in my belly.
From the article and the blood test, I also understood that I my oestro is higher that my progesteron (based on my body shape)

So here is what I decided to do:

1/ Increase oestro with fenugreek/fennel in the first part of my cycle

2/ and just PC in the second half.

3/ I will drink Spearmint tea to decrease testosterone during the whole cycle

4/ Cut out coffee, and curb my carb consumption, meditate more to take care of the cortisol levels

5/ Massage 2x day

6/ Lift weight 3x week


What do you think about this programme ? Should I take fenugreek throughout the month ?

Thanks

NLH,

I like this plan, keep a watch on sodium and starch. Fenugreek can be taken all cycle, I'd go slow though, maybe take a few days off (day 16-19).

From the blog: (thanks for the link again, it's great info).

There are two type of adrenergic receptors. Alpha adrenergic receptors and beta adrenergic receptors. The alpha receptors slow fat release and beta receptors speed fat release. To keep this straight in your head think “A” for “anti-burn” and “B” for “burn”.

Stubborn fat has more alpha receptors
Stubborn fat has less beta receptors
Stubborn fat stores more fat and releases less of it under the influence of insulin
Stubborn fat has less blood flow through it
Hormones that increase HSL activity and/or inhibit LPL activity stimulate fat release
Hormones that decrease HSL activity and/or stimulate LPL action encourage fat storage
Calories matter too. It is impossible to store fat regardless of hormonal action in a low calorie state and it is unlikely to lose fat if you are in calorie excess
Stubborn fat is stubborn not because it can’t be released, but rather because it releases fat much more slowly compared to less stubborn fat.
The sex steroids (estrogen, progesterone and testosterone) have receptors in fat tissue and play an important role in HSL/LPL activity as well as impact alpha versus beta receptor number and activity
http://www.metaboliceffect.com/how-to-lo...ps-thighs/

High sodium diet was associated with increased urinary cortisol and its metabolites. Also, HS diet was associated with HT, insulin resistance, dyslipidaemia and hypoadiponectinaemia, even when adjusting by confounding variables. Further, we observed that high salt intake, IR and higher cortisol metabolites, alone or combined in a clinical simple model, accurately predicted MetS status, suggesting an additive mechanism in obesity-related metabolic disorders.

High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/23594269


High-Salt Diet May Boost Cortisol
Eating a diet high in sodium increased levels of cortisol and other metabolites, potentially giving rise to metabolic syndrome, researchers found.
http://www.medpagetoday.com/Endocrinolog...logy/39256

The other things I would look at would be GTE-green tea extract with a cyclic amp cAMP (second messenger) supplement which supports cellular function, actually intracellular communication. Forskolin is one of the types, although imo other cAMP supplements exist. CoQ10 is similar imo, so is the intent of PGE2, Prostaglandins. These help get rid of that stubborn middle, and can help reshape the waist, the ELEL is example of doing just that.

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),


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.

polyunsaturated fats and prostaglandins stimulate the expression of aromatase, the enzyme that synthesizes estrogen, aspirin decreases the production of estrogen.

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.

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.

Estrogen is inactivated, mainly in the liver and brain, by being made water soluble by the attachment of glucuronic acid and/or sulfuric acid.

An androgen antagonist (anti-androgen) can broadly be defined as any compound that has the biological effect of blocking or suppressing the action of male sex hormones such as testosterone within the human body. DHT blocks the conversion of aromatase (bad for breast growth).
____________________________________________________________________

Reishi-reishi mushrooms significantly reduced levels of 5-alpha reductase, preventing conversion of testosterone into the more potent DHT. High levels of DHT are a risk factor for conditions such as benign prostatatic hypertrophy (BPH), acne, and baldness.

White Peony--Estrogenic, blocks 5ar and pro-aromatase - Strong.
A compound found in white peony inhibits the production of testosterone and promotes the activity of aromatase, which converts testosterone into estrogen.

Spearmint-anti-androgenic properties reduce the level of free testosterone in the blood, while leaving total testosterone and DHEAS unaffected.


Green Tea Epigallocatechin-Green tea (camellia)-Reduce's the conversion of free testosterone into DHT and also raises SHBG (sex-hormone-binding-globulin).


Pygeum-include phytosterols that inhibit the production of dht. Pygeum also reduce's prolacting levels and block the accumulation of cholesterol in the prostate. Prolactin increase's the uptake of testosterone by the prostate. Pygeum reduces the levels of DHT in the blood and reduces the number of sites where the dht can attach.


Saw palmetto-Saw palmetto-Beta-sitosterol is a natural alpha-adrenergic receptor blocker. Prevents DHT from accumulating in prostate tissue that would otherwise cause excessive cell growth and inflammation. The plant steroids in saw palmetto also act on progesterone receptors, an action that causes a reduction in estrogen levels.


DIM is Diindolylmethane-It is an anti carcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, Taken with estrogen agonist, activities of DIM are seen as an hormone disrupter. DIM is the first example of a pure androgen receptor antagonist from plants.


Nettle Root--Binds to SHBG (hormone that binds to excess hormones by decreasing hormone levels), and decreases 5ar and aromatase. Taking this tends to increase estrogen and testosterone. Would need to be taken with a pro-aromatase, and maybe estrogen.


Chinese Skullcap Inhibits the 5alpha-reductase enzyme-
Baicalein has been shown to inhibit the 5alpha-reductase enzyme, which converts testosterone to dihydrotestosterone (DHT). DHT is strongly associated with the development of prostate enlargement (benign prostatic hyperplasia) and prostate cancer. As such, baicalein is reported to be potentially useful for the prevention and/or treatment of androgen-dependent (testosterone-driven) disorders, including prostate enlargement and prostate cancer.


Licorice (Glycyrrhiza glabra)-Anti-androgenic and activates alpha and beta estrogen receptors and blocks 5-ar - Strong, but take in moderation!
Use with extreme caution

-For most disorders: Take 200 mg standardized extract in pill form three times a day, or 20 to 45 drops, three times a day, of a 1:5 tincture. (The 1:5 tincture represents one part herb is soaked in five parts liquid


Pumpkin Seed Oil: Has been demonstrated to inhibit DHT formation through the inhibitory effect on 5-alpha-reductase activity. Pumpkin seed oil breaks down DHT via the liver.


Emu Oil: Research has shown that emu oil contains a high level of linolenic acid which further research has shown to be an efficient antiandrogen. Linolenic acid is a potent 5 alpha reductase inhibitor and may be usefull in the treatment of disorders related to the hormone Dihydrotestosterone. Linolenic Acid has been suggested to be of use in the disorders such as benign prostratic hyperplasma, acne androgenetic alopecia and hirsuitism.


Even though it's not an AA it's worth mentioning because of its interaction.

L-Lysine: While L-Lysine is NOT a DHT blocker, it may make DHT blockers more effective. Researchers have found that adding a supplementation of L-Lysine can make drugs like Propecia more effective. Since propecia is a DHT inhibitor, as all the natural products mentioned here, the addition of a L-Lysine supplement can make these products also more effective. Studies has shown that L-Lysine combined with a DHT inhibitor can for example promote hair growth in people suffering from androgenetic alopecia.


Considering the potential to block DHT and increase aromatase adding fatty acids makes sense, only don't forget a fitness plan.

Anti-androgenic activity of fatty acids.

In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546

Evening Primrose Oil- massage, Fibrocystic breast pain, treats hot flashes, relieves PMS symptoms, relieves Eczema, hormone balance, fights breast tumors and diabetes. Reports have GLA-Gamma-Linolenic Acid as helping with RA and arthritis, diabetic neuropathy, ADHD and CFS (chronic fatigue syndrome). And UPDATED to include it being an inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to DHT, (DHT is bad for BOOB GROWTH).

Coconut Oil- Makes connective tissues stronger, superb antioxidant, neutralizes free radicals and slowing down aging, aids in breast feeding, nature's richest source of MCFAs. 5 ar inhibitor, aromatase



________________________________________

Reishi (Ganoderma lucidum)
Red reishi, commonly known as LingZhi in Chinese, is a mushroom thought to have many health benefits. In a research study exploring the anti-androgenic effects of 20 species of mushrooms, reishi mushrooms had the strongest action in inhibiting testosterone (3). That study found that reishi mushrooms significantly reduced levels of 5-alpha reductase, preventing conversion of testosterone into the more potent DHT. High levels of DHT are a risk factor for conditions such as benign prostatatic hypertrophy (BPH), acne, and baldness.

White Peony (Paeonia lactiflora)
Chinese peony is a widely grown ornamental plant with several hundred selected cultivars. Many of the cultivars have double flowers with the stamens modified into additional petals. White peony has been important in traditional Chinese medicine and has been shown to affect human androgen levels in vitro. In a 1991 study in the American Journal of Chinese Medicine Takeuchi et al described the effects of paeoniflorin, a compound found in white peony that inhibited the production of testosterone and promoted the activity of aromatase, which converts testosterone into estrogen (7). To date, there have been no studies that translate or explore the clinical effects.

Chaste Tree (Vitex agnus-castus)
Chaste tree (or chasteberry) is a native of the Mediterranean region and is traditionally used to correct hormone imbalances. In ancient times, it was believed to be an anaphrodisiac, hence the name chaste tree. Clinical studies have demonstrated effectiveness of medications produced from extract of the plant in the management of premenstrual syndrome (PMS) and cyclical mastalgia (14). The mechanism of action is presumed to be via dopaminergic effects resulting in changes of prolactin secretion from the anterior pituitary. At low doses, it blocks the activation of D2 receptors in the brain by competitive binding, causing a slight increase in prolactin release. In higher concentrations, the binding activity is sufficient to reduce the release of prolactin (15).

Reduction in prolactin levels affects FSH and estrogen levels in females and testosterone levels in men. There is as yet no information regarding its efficacy in endocrine disease states such as PCOS, however, one small-scale study has demonstrated this prolactin reducing effect in a group of healthy males, and the implication is that it could be of use in mild hyperprolactinemia (16, 17). One could also theorize that it could be refined for use as a male contraceptive, because testosterone reduction should reduce libido and sperm production. This topic is further explored in a review by Grant & Anawalt (18).



http://www.ncbi.nlm.nih.gov/pmc/articles...10-497.pdf

http://endometabol.com/?page=article&article_id=3644

Aromatase is way more useful than I thought. It kills two birds with one stone: reducing androgens which directly inhibit breast size, and it makes estrogens. One example is the effectiveness of aromatase to cause major gynecomastia. Aromatase-inhibitors do the opposite. LH, androgen, or dhea may not even be necessary. Many times, LH increases on its own based on feedback or everyday foods. I hypothesize that topical aromatases may be highly effective. I wonder if topical tea tree and lavender are aromatases.

5-alpha-reductase-inhibitors are useful for preventing testosterone conversion into the more inhibiting DHT. Aromatase reduces the amount of testosterone available to turn into DHT.

Liver health is very important, first of all for overall health, and secondly it uses the enzyme 16a-OHase to break down estradiol into the more bioavailable estriol. Does Milk thistle support this function?

Aromatase mostly takes care of estrogens. There are also progestogens and prolactin.

Ok Lovely, you've got me thinking, here's something to ponder: (a theoretical powerhouse aromatase formula, lol)........

Add oats to your program because it down-regulates SHBG and up-regulates free testosterone, then add an aromatase booster (WP), a 5 ar-inhibitor (PSO, reishi, etc), DHEA (low dose) to up-regulate hormones (btw, maca upregulates dhea).

This study makes makes me go off into the deep end, and now I'm on the curve.

http://www.ncbi.nlm.nih.gov/pubmed/23416106
Interaction of Androst-5-ene-3β,17β-diol and 5α-androstane-3β,17β-diol with estrogen and androgen receptors: a combined binding and cell study.


Androst-5-ene-3β,17β-diol (ADIOL) and 5α-androstane-3β,17β-diol (3β-DIOL), metabolites of dehydroepiandrosterone (DHEA) and dihydrotestosterone (DHT), respectively, are known to possess estrogenic properties. To better understand their hormonal action and roles in the proliferation of breast cancer (BC) cells, we studied their binding to sex-hormone receptors in estrogen receptor (ER)-positive (ZR-75-1 and T-47D) and ER-negative (MDA-MB-231) human BC cells. The results demonstrated that estradiol (E2), ADIOL and 3β-DIOL stimulated the proliferation of ZR-75-1 and T-47D cells, but had no effect on ER-negative cells. In the presence of estradiol, ADIOL and 3β-DIOL inhibited the estrogen-stimulated BC cell growth. This inhibition was counteracted by anti-androgens, which were unable to affect the ADIOL and 3β-DIOL stimulatory effects in E2-free medium. On the other hand, in the presence of tamoxifen, ADIOL and 3β-DIOL showed an additional anti-proliferative activity on hormone-sensitive BC cells compared with tamoxifen treatment alone. These results are similar to previous reports obtained using MCF-7 cells, which confirmed that ADIOL and 3β-DIOL stimulated estrogen-dependent BC cell growth via ERs, but inhibited growth via androgen receptors (ARs). Several steroids bind to both ER and AR in a different preference and degree, i.e. E2>estrone (E1)>ADIOL>3β-DIOL>testosterone (T)>DHT for ER and DHT>T>3β-DIOL>ADIOL>E1>E2 for AR. The relative binding affinities of ADIOL, 3β-DIOL, and E2 corresponded well to their respective potential in stimulating cell proliferation of ZR-75-1 and T-47D cells in our results. The intrinsic relationship between cell proliferation effects and binding affinities for receptors of several steroids was revealed here by a combined binding and cell study. This article is part of a Special Issue entitled 'Synthesis and biological testing of steroid derivatives as inhibitors'.

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Or even further:

Low-Dose DHEA Increases Androgen, Estrogen Levels in Menopause

Dec. 12, 2003 — Low-dose dehydroepiandrosterone (DHEA) administration increases adrenal hormone plasma levels in early and late menopause, according to results of a prospective case study published in the December issue of Fertility and Sterility.

"Although DHEA supplementation is not yet considered a medical treatment, this steroid has been demonstrated to induce specific metabolic effects and to increase both androgen and estrogen plasma levels in postmenopausal women," write Alessandro D. Genazzani, MD, PhD, and colleagues from the University of Modena in Italy.

The Italian team selected 20 healthy, postmenopausal patients, age 50 to 65 years, who were not using hormone replacements, for the 12-month prospective study. All patients received an ultrasound examination and a mammogram before the start of the study to exclude organic disease.

Dr. Genazzani and colleagues divided patients by age into two groups: early (aged 50-55 years, n = 10, group A) who were two to three years postmenopausal; and late (aged 60-65 years, n = 10, group B) who were five or more years postmenopausal. Five of the women were mild smokers.

All patients took 25 mg/day DHEA supplementation for 12 months. Every three months throughout the trial period, the investigators evaluated patients and drew blood samples to determine plasma levels of LH, FSH, E 2, DHEA, DHEAS, androstenedione (A), testosterone, dihydrotestosterone, progesterone, 17 alpha-hydroxyprogesterone (17-OHP), allopregnanolone, estrone (E1), sex-hormone binding globulin (SHBG), cortisol (F), beta-endorphin, growth hormone (GH), and insuline-like grown factor-1 (IGF-1).

Investigators also conducted a transvaginal ultrasound examination in each patient before and after 6 and 12 months of treatment to evaluate endometrial thickness. In addition, the researchers administered a Kupperman questionnaire to evaluate subjective vasomotor and psychological symptoms before and after 3, 6, and 12 months of therapy.

Younger postmenopausal subjects (group A) demonstrated higher levels of DHEA, DHEAS, testosterone, and beta-endorphin levels than older subjects ( P < .05). Significant changes in endocrine levels were observed with therapy. DHEA treatment eliminated endocrine differences observed between the two groups at baseline.

Testosterone and dihydrotestosterone plasma levels, and plasma E 1 and E 2 levels increased significantly and progressively in both groups. Investigators found no changes in SHBG concentrations in either group despite significant changes in A and E plasma concentrations. Allopregnanolone and beta-endorphin concentrations significantly increased in both groups.

Cortisol F plasma levels progressively decreased throughout the study. Both groups also experienced significantly reduced LH and FSH plasma levels. GH and IGF-1 levels significantly increased in both groups. Supplementation did not induce changes in endometrial thickness.

At baseline, group A had higher values for subjective vasomotor disturbances and psychological disturbances than group B, whereas the latter had a higher score for psychological variables. Scores significantly improved in both groups during therapy.

"The present study demonstrates the efficacy of low-dose DHEA administration of endocrine and psychoneuroendocrine parameters in early and late menopause and confirms that a low-dose DHEA supplementation increases adrenal androgens plasma levels (mainly DHEA and DHEAS), which are significantly impaired during menopause," Dr. Genazzani and colleagues write.

"These data support and confirm that DHEA must be considered a valid compound and drug for [hormone therapy] in postmenopausal women and not just a 'dietary supplement,' " they add.

Fertil Steril. 2003;80:1495-1501

Many times, LH increases on its own based on feedback or everyday foods. I hypothesize that topical aromatases may be highly effective. I wonder if topical tea tree and lavender are aromatases.

Hmm, good question and point, applying Borage oil could work too, tea tree was listed in a study if I remeber, they reported Gyno in young men (or boys?). lavender sounds promising.

Liver health is very important, first of all for overall health, and secondly it uses the enzyme 16a-OHase to break down estradiol into the more bioavailable estriol. Does Milk thistle support this function?

Aromatase mostly takes care of estrogens. There are also progestogens and prolactin.

Agreed, liver health and NBE ultimately go hand in....well, you know what I mean. I'm sure you've heard about E getting absorbed back into the system before elimination and possibly causing toxic and unwanted effects. Milk Thistle and Dandelion root help with healthy E metabolism.
Comparative Measurements of Serum Estriol, Estradiol, and Estrone in Non-pregnant, Premenopausal Women: A Preliminary Investigation

http://www.anaturalhealingcenter.com/doc...trogen.pdf

[LanaG]

Lotus, wow.. that was a long but helpful read. Thank you!

[Eloise]

Welcome, Lana. It may take a few days, maybe a few weeks, or possibly a few years to process that info Lotus unloaded on you. Read it. Learn it. Implement it. But, perhaps most importantly and tisk-tisk Lotus (I am just teasing ) for not saying so, but experiment. Experiences with PM and herbs differ person-to-person. What may work for one person here may not work at all for another. If you take anything, initially, away from what Lotus just gave you, it is that this process (and it is a process) isn't an Easy Bake Oven where you put in some pills and presto! boobies. I wish it were that easy. Unfortunately it is not. This is not to say you can't just pop a few PM's and sprout in a few months. You can and that is entirely up to you. But the people here (past and present) that have had really good success have invested time researching and were/are constantly experimenting. Welcome again and happy growing!