[hannah]

Progesterone does two things, it is the precursor to androgens which are the precursors to estrogens, and it causes duct branching.

Because of body hair, it could be that progesterone is converted into androgens, and not enough of it is aromatized into estrogen.

Lumps can be from too much progesterone, or too much of another hormone. I hypothesize that too much duct branching without elongation can cause a lot of crowded tissue, but this doesn't explain lumps from too much estrogen, except for unhealthy cell growth.

If anyone is having these problems, avoid prolactin and progesterone herbs, like fenugreek, fennel. PM looks too risky. Fruits, vegetables, grains, vitamins, and green tea hopefully should help.

I hypothesize that aromatase/phytoestrogen such as tea tree, or lavender could help, but anyone with lumps, it is not worth the risk. Something such as lavender might help, or it might make things worse when a lump is already present. This study is worth reading, Epigenetic reactivation of estrogen receptor-α (ERα) by genistein enhances hormonal therapy sensitivity in ERα-negative breast cancer . They normally treat lumps with androgens.

As suggested above a cleanse sounds good.

So if the body hair comes from progesterone that is getting converted in androgens instead of aromatized in estrogen you should take an aromatizer? What are all the sorts of aromatizers available?
Do you also know what the possible side effects are from taking anti androgens?

[Dynseli]

So if the body hair comes from progesterone that is getting converted in androgens instead of aromatized in estrogen you should take an aromatizer?

For people without health problems, yes, and anti-reductase herbs are also useful here.

Generally, all serum estrogen comes from androgens. Aromatase can only help the body form estrogens from androgens. The ovaries do so much of creating androgens signaled by LH, and converting androgens into estrogen. Then PCOS is common with high androgens (perhaps more androgens than the ovaries are capable of aromatizing without help). Fatty tissue can also aromatize androgens, perhaps by herbs.

What are all the sorts of aromatizers available?

Peony, topical tea tree, and topical lavender. Those are the only herbal ones I'm familiar with. (mints too, but mints seem to raise androgens more than they aromatize them)

Do you also know what the possible side effects are from taking anti androgens?

There's a side effect from too much of anything that influences a hormone. Too much estrogens can desensitize certain tissue, or influence cancer; but it's the same with progesterone, and any other hormone. Balancing progesterone and estrogen helps counter each other's bad effects. Estrogen and progesterone receptors are in different reproductive tissue (ovum ducts, breasts, pituitary, neuro, follicles), which can sometimes cause tissue to grow or shrink if either hormone is by itself. Effects on the brain are behavioral, mostly the differences in women and men, and parents.

If its about issues in fibriotic breasts, I can only theorize, especially since I don't know what fibriotic tissue looks like. Estrogen could either alleviate it, or it could cause it to get worse. Both cases would possibly be due to growth, either by growing out to allow more space, or growing more in a fibriotic way.

progesterone causes branching like, <<<<<<< (pictorial of a branch)
estrogen allows more, <---<---<---< (spacing between branching)
If fibriotic breasts are mostly from too much clusters of branching with no space to spread out. Fibriotic breasts happen mostly during the luteal phase when progesterone is available. Then again, I don't know the effects of estrogens after fibriotic breasts have occured.

If you want an idea of what aromatase anti-androgens do, maybe look up finasteride for an idea (or educated guess). I'm against suggesting synthetics (and serums).

An Anti-DHT (anti-reductase) anti-estrogen would lower the effects of potent progestogens and DHT. These are oatmeal, pumpkin (squash) seed, palm fruits, pygeum, red reishi. Some of these noticeably remove a little bit of body hair.

Androgens have been used to lower breasts problems, but then again, I don't know how effective this is in various cases.

This is theory of what aromatase herbs do on fibriotic breasts, and I wish for everyone to be cautious and to not get hurt. There are a lot of facts supported by studies of what aromatase does too. I can't be too sure when it comes to what estrogen does on already fibriotic breasts.

Green tea is the only one I'd suggest for fibriotic breasts. It lowers DHT, reduces androgens effects, increases tissue metabolism, and it has a good reputation against breast problems.

[Lotus]

Progesterone restores estrogen receptor sensitivity to its original state. Progesterone also protects against the proliferate side of breast cancer in estrogen receptors. It also down regulates DHT through 5 alpha reductase. It has no feminzing effect. Progesterone in the presence of estrogen up-regulates side branching, and estrogen promotes the elongation of breasts. But......an odd spin is that progesterone down regulates it's own receptor.

[Lotus]

I like this response in a medhelp forum:

Best Answer

zouzi
Feb 22, 2012
To: cally44
Hi,
The causes of Fibroadenomas are not entirely known,but it is believed that it is associated with hormones fluctuations.For a suspected fibroadenoma mammograms are routinely performed for women age 30 and older.For women younger than age 30, the doctor may opt for a breast ultrasound instead of a mammogram to evaluate a breast lump.Radiation used during mammograms is about the same as a dental x-ray, and less than what is needed for a standard chest x-ray.So I don't see any reason to worry about that, since the radiation is minimal and the benefits far outweigh the risk.

Breast ultrasound has excellent contrast resolution,,but it lacks the detail of conventional mammography.Ultrasound is not usually used as a screening tool for breast cancer.Rather,it is used to investigate an abnormality detected by mammography.After all the tests required are studied and the radiologist is pretty sure that the lump in your breast has all the characteristics of a benign fibroadenoma,then there would be no need to remove the lump,because in many cases fibroadenomas could go away on their own within a few years.These benign breast tumors are known to increase in size and tenderness in relation to the menstrual cycles due to hormonal changes and are not related to breast cancer in any way.There are some reports stating that low fat, high fiber diets,limiting caffeine intake ( coffee,chocolate,colas) could decrease incidence of fibroadenoma.
When a Radiologist is certain that the lump is most likely a benign fibroadenoma,then he/she could recommend conservative management with regular follow up to make sure that there are no changes.However,if there is any concern,(mammogram or ultrasound cannot tell if a lump is cancerous or not) then a biopsy of the tumor has to be performed so that the tissue extracted can be examined by a pathologist to obtain a correct diagnosis.

[Dynseli]

It also down regulates DHT through 5 alpha reductase.

Regulation or (de)sensitization happens to receptors, not hormones AFAIK. Did you mean something else?

[Lotus]

It also down regulates DHT through 5 alpha reductase.

Regulation or (de)sensitization happens to receptors, not hormones AFAIK. Did you mean something else?

Nope, I didn't mean something else, the info below explains regulation.

Plasma levels of sex-hormone-binding globulin (SHBG) in man are known to be regulated up and down by oestradiol and testosterone.
http://www.ncbi.nlm.nih.gov/pubmed/2591057

DHEA upregulates the activity of 5AR (5-alpha-reductase) enzyme, which further converts testosterone to DHT. As a consequence, some women may experience a slight increase in hair loss, especially if their estrogen levels are low.
@ MedLine Plus

Hormonal regulation of hormone release involves a hormone binding to its receptor on an endocrine cell to regulate hormonal secretion. A hormone that stimulates hormone secretion is called a tropic hormone. Tropic hormones may also stimulate proliferation of endocrine cells.

The ACTH (adrenocorticotropic hormone (ACTH) receptor is a G-protein coupled receptor or seven-transmembrane domain protein. ACTH binding ultimately leads to stimulation of adenylyl cyclase and the production of the second messenger cyclic AMP (cAMP). cAMP causes cellular changes that ultimately lead to the activation of the enzymes involved in cortisol synthesis.

In some cases, hormones can inhibit hormone secretion. One key example is the peptide hormone somatostatin, which is a hypothalamic hormone that inhibits GH secretion. Another important example is negative feedback regulation in which hormones negatively regulate the secretion of their own tropic hormones.

http://courses.washington.edu/conj/bess/...monal.html

Why improving receptor sensitivity is important for NBE,


Regulation of hormone receptors is very important for a normal functioning cell. There are several ways a cell regulates its hormone receptors. Below is an outline of such regulatory functions

Regulating the expression of receptors - changing the number of receptors on the plasma membrane.
________________________________

1. Up regulation - increasing the number of receptors

2. Down regulation - decreasing the number of receptors

Mechanism:

-internalization - endocytosis of receptors

-modify transcription - inhibiting or stimulating transcription factors

-modify receptor half-life - adding groups to the receptors which will degrade them faster


Downregulation is the process by which a cell decreases the quantity of a cellular component, such as RNA or protein, in response to an external variable. An increase of a cellular component is called upregulation.

An example of downregulation is the cellular decrease in the number of receptors to a molecule, such as a hormone or neurotransmitter, which reduces the cell's sensitivity to the molecule. This phenomenon is an example of a locally acting negative feedback mechanism.

An example of upregulation is the increased number of cytochrome P450 enzymes in liver cells when xenobiotic molecules such as dioxin are administered (resulting in greater degradation of these molecules).

Most receptor agonists downregulate their respective receptor(s), while most receptor antagonists upregulate their respective receptor(s). The disequilibrium caused by these changes often causes withdrawal when the long-term use of a medication or drug is discontinued. However, the chronic use of certain receptor antagonists may also damage receptors faster than they upregulate.

Upregulation and downregulation can also happen as a response to toxins or hormones. An example of upregulation in pregnancy is hormones that cause cells in the uterus to become more sensitive to oxytocin.

An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response. Whereas an agonist causes an action, an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist.




Downregulation and upregulation

http://wikipedia.org/wiki/Downregulation...regulation
Question- what triggers tissue growth in order for NBE to work?

[Dynseli]

SHBG is a protein, and some proteins are/have receptors. So that can make sense that SHBG can be up/down-regulated. The other term of regulation isn't being used to the same meaning as de/re-sensitization of cell receptors. up/down regulation, also meaning (de)sensitization, is for hormone receptors, which are on proteins on cells.

5-alpha-reductase is an enzyme, but I'm unsure if it is a receptor or protein. It seems like 5AR is.

[hannah]

Progesterone restores estrogen receptor sensitivity to its original state. Progesterone also protects against the proliferate side of breast cancer in estrogen receptors. It also down regulates DHT through 5 alpha reductase. It has no feminzing effect. Progesterone in the presence of estrogen up-regulates side branching, and estrogen promotes the elongation of breasts. But......an odd spin is that progesterone down regulates it's own receptor.

Very interesting and helpful, Thank you very much Lotus. But I dont get the last part:
''But......an odd spin is that progesterone down regulates it's own receptor. ''
I dont know If I'm right but what I get from this is that if you take Progesterone-''cream,other stimulants'' your own natural progesterone will be down regulated, so create less progesterone?

[Lotus]

Progesterone restores estrogen receptor sensitivity to its original state. Progesterone also protects against the proliferate side of breast cancer in estrogen receptors. It also down regulates DHT through 5 alpha reductase. It has no feminzing effect. Progesterone in the presence of estrogen up-regulates side branching, and estrogen promotes the elongation of breasts. But......an odd spin is that progesterone down regulates it's own receptor.

Very interesting and helpful, Thank you very much Lotus. But I dont get the last part:
''But......an odd spin is that progesterone down regulates it's own receptor. ''
I dont know If I'm right but what I get from this is that if you take Progesterone-''cream,other stimulants'' your own natural progesterone will be down regulated, so create less progesterone?

Enzymes are definitely proteins. We know hormones can readily diffuse across cell membranes, but I think it's more beneficial for synthesis to have a carrier protein accompany it, in other words essential fatty acids. My first choice is coconut oil. We had a lengthy discussion about receptor up/down regulation, it's a good thread with attached research, take a look if you get time. Hannah, to answer your question, progesterone down regulation of its own receptor comes from the study below, as you can see PR also down-regulates estrogen receptor alpha and beta (ER-a & ER-b), sorry, but lol it's the techy stuff.


RECEPTOR REGULATION
http://www.breastnexus.com/showthread.php?tid=20747

REGULATION OF RECEPTOR NUMBERS


The half-life of steroid hormone receptors ranges from 2 to 4 hours for ERα 4 hours for AR, 7 to 10 hours for PR, and 19 hours for GR. The relatively long half-life of the steroid hormone receptors strongly suggests that the receptor proteins are recycled before eventual degradation.


Estrogen synthesis and signaling pathways during ageing: from periphery to brain
Steroid hormones generally autoregulate their receptor levels. Desensitization or downregulation of receptor numbers, measured by decreased ligand binding capacity, occurs in response to exposure to high levels of ligand and involves the reduction in receptor mRNA levels, decreasing the number of available receptors. The receptor gene may be negatively regulated by the hormonal ligand itself through its receptor protein interacting with specific HREs in the gene. Upregulation or self-priming may occur in an analogous fashion. Steroid hormones can regulate receptor levels for other hormones (e.g. E2 increases PR levels in estrogen-responsive tissues). Progesterone can downregulate its own receptors, as well as ERα and ERβ. This increase or decrease in receptor levels in homologous or heterologous regulation can be caused by alterations in receptor gene transcription or decay rates for receptor mRNA or protein. Binding of the cytosolic GR complex to very long 3'-untranslated regions of its receptor mRNA has been reported to cause premature degradation.
http://www.ncbi.nlm.nih.gov/pmc/articles...425860.pdf

[hannah]

Progesterone restores estrogen receptor sensitivity to its original state. Progesterone also protects against the proliferate side of breast cancer in estrogen receptors. It also down regulates DHT through 5 alpha reductase. It has no feminzing effect. Progesterone in the presence of estrogen up-regulates side branching, and estrogen promotes the elongation of breasts. But......an odd spin is that progesterone down regulates it's own receptor.

Very interesting and helpful, Thank you very much Lotus. But I dont get the last part:
''But......an odd spin is that progesterone down regulates it's own receptor. ''
I dont know If I'm right but what I get from this is that if you take Progesterone-''cream,other stimulants'' your own natural progesterone will be down regulated, so create less progesterone?

Enzymes are definitely proteins. We know hormones can readily diffuse across cell membranes, but I think it's more beneficial for synthesis to have a carrier protein accompany it, in other words essential fatty acids. My first choice is coconut oil. We had a lengthy discussion about receptor up/down regulation, it's a good thread with attached research, take a look if you get time. Hannah, to answer your question, progesterone down regulation of its own receptor comes from the study below, as you can see PR also down-regulates estrogen receptor alpha and beta (ER-a & ER-b), sorry, but lol it's the techy stuff.


RECEPTOR REGULATION
http://www.breastnexus.com/showthread.php?tid=20747

REGULATION OF RECEPTOR NUMBERS


The half-life of steroid hormone receptors ranges from 2 to 4 hours for ERα 4 hours for AR, 7 to 10 hours for PR, and 19 hours for GR. The relatively long half-life of the steroid hormone receptors strongly suggests that the receptor proteins are recycled before eventual degradation.


Estrogen synthesis and signaling pathways during ageing: from periphery to brain
Steroid hormones generally autoregulate their receptor levels. Desensitization or downregulation of receptor numbers, measured by decreased ligand binding capacity, occurs in response to exposure to high levels of ligand and involves the reduction in receptor mRNA levels, decreasing the number of available receptors. The receptor gene may be negatively regulated by the hormonal ligand itself through its receptor protein interacting with specific HREs in the gene. Upregulation or self-priming may occur in an analogous fashion. Steroid hormones can regulate receptor levels for other hormones (e.g. E2 increases PR levels in estrogen-responsive tissues). Progesterone can downregulate its own receptors, as well as ERα and ERβ. This increase or decrease in receptor levels in homologous or heterologous regulation can be caused by alterations in receptor gene transcription or decay rates for receptor mRNA or protein. Binding of the cytosolic GR complex to very long 3'-untranslated regions of its receptor mRNA has been reported to cause premature degradation.
http://www.ncbi.nlm.nih.gov/pmc/articles...425860.pdf

Okay, I dont want to be rude, But I'm outta time now. So I'll read this techy stuff tomorrow, ha ha. Maybe during daytime I'm a bit more fresh to understand this and read this over and over and over again.LOL. Thanks Loots!