[tanysquirrel]

Seminal vesicles and urinary bladder as sites of aromatization of androgens in men

http://www.academia.edu/23896195/Seminal..._specimens

http://www.fasebj.org/content/27/4/1342.full

https://en.wikipedia.org/wiki/Seminal_vesicle

aromatization of bladder only:
http://www.ncbi.nlm.nih.gov/pubmed/20412431

this puts an understanding on why women pee more than men?

other interesting info:
https://www.researchgate.net/publication...ia_in_Mice
http://humrep.oxfordjournals.org/content/20/12/3481.short?cited-by=yes&legid=humrep;20/12/3481
more research needed.

[tanysquirrel]

prickly pear 'cactus' flowers for enlarged prostate- dht inhibitor? or just a diuretic?

http://www.herbamed.com/Portals/0/articles/Opuntia.pdf

http://www.vibrantlife.com/?p=118

[tanysquirrel]

interesting re: Pueraria mirifica

worth the read :
http://www.multibriefs.com/briefs/acam/A...eisher.pdf

" strong anti-mutagenic properties  anti-carcinogenic effects, esp. among breast cancer and colon cancer lines  relatively safe control of perimenopausal and postmenopausal symptoms, i.e., vasomotor instability, hot flashes, night sweats, and mood changeability, similar to effects exhibited by conjugated equine estrogens, but without the toxicity  prevention and improvement of osteopenia and osteoporosis in both sexes  significant improvement of blood lipid and cholesterol levels  enhanced function of the endothelial lining of blood vessels  cardiovascular protective properties  prevention and reduction of prostate hyperplasia  prevention and reduction of erectile dysfunction  mammogenic effects, i.e., natural promotion of enlargement, toning and firming of the female breasts, by stimulating healthy, breast gland fibroblastic activity'- this would explain why some people maintain erections on it or they come back?

more: Current scientific research recognizes that there are two types of estrogen cell surface receptors, the alpha receptor (ERa) and beta receptor (ERb). ERa affects classical, estrogen sensitive tissues, e.g., breasts, uterine endometrium, ovarian stromal cells, male testes and vas deferens, and the hypothalamus in the brain. Whereas, ERb affects non-classical, estrogen sensitive tissues, e.g., brain, bone, heart, lungs, kidneys, intestinal mucosa, and vascular endothelium in both sexes.
Excessive ERa stimulation can lead to breast cancer and other estrogen-dependent cancers. Competitive inhibition of ERa receptors by phytoestrogens, via blocking the binding of the stronger, estrogenic hormones, i.e., estrone and estradiol, can help protect against the development of estrogen-dependent cancers of the breast, uterus, ovaries and prostate. This is the physiochemical basis for the anti-carcinogenic effect of soy isoflavones, and various other naturally occurring phytoestrogens.
Phytoestroegns from various plant sources may either activate or inhibit ERa and/or ERb receptors. Miroestrol and deoxymiroestrol in Pueraria preferentially powerfully stimulate ERb receptors, and inhibit ERa receptors. Miroestrol and its derivatives are known to be approximately 3,000 times more potent than soy isoflavones with respect to estrogen receptor effects.
ERb stimulation in the brain has been shown to protect neuronal cells from injury and death from excitotoxins, e.g., MSG. ERb stimulation in the prostate gland helps protect against hyperplasia, and reduce symptoms of benign enlargement of the prostate.
Pueraria mirifica may constitute a new class of safe, non-toxic, effective, hormonal therapeutic support as natural, Selective Estrogen Receptor Modulators (SERMs), with estrogen agonist activity in certain tissues and antagonist activity in others, which help balance hormonal function, and possess significant, anti-aging, protective properties for estrogen sensitive tissues in both men and women.'

so it is my understanding,that.. in activating the ERb , your are creating the negative feedback loop in the hypothalamus, leading to the aromatization of testosterone? since the ERb have to do with brain barrier and such.. according to this article, PM inhibits the ERa activity, which has to do with the breasts directly.. so it would seem that the PM is a "backdoor" method of getting the endocrine system to feminize the biomale? So its not adding breasts by estrogen, its telling the body to convert T into E.. am I wrong?

[tanysquirrel]

interesting article on receptors:
http://gettingstronger.org/2010/10/chang...-setpoint/

[tanysquirrel]

interesting: ottoman aphrodisiac : Mesir macunu

available on Amazon $13.99

http://www.al-monitor.com/pulse/original...siacs.html#

https://en.wikipedia.org/wiki/Mesir_macunu

herbs in "paste" :
Allspice (Yeni bahar) (Pimenta dioica)
Alpina officinarum root (Havlican koku) (Alpina officinarium)
Anise (Anason) (Anisum vulgare)
Black cumin (Corek otu) (Nigella sativa)
Black Myrobalan (Kara halile) (Terminalia nigra)
Black pepper (Karabiber) (Piper nigrum)
Buckthorn (Topalak or Akdiken) (Nerprun alaterne)
Cardamon (Kakule) (Elettaria cardamomum)
Cassia (Hiyarsenbe) (Cassia)
Chebulic myrobalan (Kara halile) (Terminalia chebula)
China root (Cop-i cini) (Smilax china)
Cinnamon (Tarcin) (Cinnamomum verum)
Cloves (Karanfil) (Syzygium aromaticum)
Coconut (Hindistan cevizi) (Cocos nucifera)
Coriander (Kisnis) (Coriandum sativum)
Cubeb (Kebabe) (Cubebae fructus)
Cumin (Kimyon) (Cuminum cyminum)
Dried orange blossom (Portakal cicegi)
Fennel (Rezene) (Foeniculum vulgare)
Galingale (Havlican) (Alpinia officinarum)
Ginger (Zencefil) (Zingibar officinalis)
Iksir sugar (Iksir sekeri)
India blossom (Hindistan cicegi)
Java Pepper (Kuyruklu biber) (Piper cubeba)
Licorice extract (Meyan bali) (Glycyrrhiza uralensis fisch)
Licorice root (Meyan koku) (Glycyrrhiza glabra)
Mastic (Cam sakizi) (Mastichum)
Millet (Hintdarisi) (Pennisetum glaucum)
Myrrh (Murrusafi) (Commiphora Molmol)
Muskroot (Sumbul) (Adoxa moschatellina)
Mustard seed (Hardal tohumu) (Brassica nigra)
Orange peel (Portakal kabugu)
Rhubarb (Ravend) (Rheum Palmatum)
Saffron (Safran) (Crocus Orientalis)
Citric acid (Limon tuzu)
Senna (Sinameki) (Cassia senna)
Turmeric (Zerdecal) (Curcuma domestica)
Udulkahr (Udulkahir)
Vanilla (Vanilya) (Vanilla planifolia)
Woad (Civit) (Isatis)
Yellow myrobalan (Sari halile) (Fructus myrobalani

[tanysquirrel]

another very good article on Natural phytoestrogens and such:

http://www.hormoneimbalanced.com/plantestrogen.html

I found this part particularly interesting, however the whole article should be read:

Coffee


Coffee is a known phytoestrogen that makes my patients with breast cysts worse. Even decaffeinated coffee makes premenstrual bloating and breast tenderness worse. The caffeine may also keep the liver busy so that it cannot excrete estradiol and other xenoestrogens. One Bringham Young University study showed that 2 cups of coffee per day would increase estradiol by 70 percent.

[tanysquirrel]

interesting article as well as health ideas

for the transgender person:
http://www.ohlonecenter.org/research-pap...ant-folks/

[tanysquirrel]

https://en.wikipedia.org/wiki/Genistein
"Several studies have shown that both ERs and PPARs influenced each other and therefore induce differential effects in a dose-dependent way. The final biological effects of genistein are determined by the balance among these pleiotrophic actions"

https://en.wikipedia.org/wiki/Peroxisome...d_receptor

"The function of PPARs is modified by the precise shape of their ligand-binding domain (see below) induced by ligand binding and by a number of coactivator and corepressor proteins, the presence of which can stimulate or inhibit receptor function, respectively"

so it seems that ER's are co dependent with PPARs or symbiotic. may need to do further research on PPAR's to upregulate ER's availability to phytoestrogens.

more research needed

[Lotus]

https://en.wikipedia.org/wiki/Genistein
"Several studies have shown that both ERs and PPARs influenced each other and therefore induce differential effects in a dose-dependent way. The final biological effects of genistein are determined by the balance among these pleiotrophic actions"

https://en.wikipedia.org/wiki/Peroxisome...d_receptor

"The function of PPARs is modified by the precise shape of their ligand-binding domain (see below) induced by ligand binding and by a number of coactivator and corepressor proteins, the presence of which can stimulate or inhibit receptor function, respectively"

so it seems that ER's are co dependent with PPARs or symbiotic. may need to do further research on PPAR's to upregulate ER's availability to phytoestrogens.

more research needed

Hi BN,

Red Clover is beneficial for NBE. If you don't know what PPAR (peroxisome proliferator-activated receptor), you should. (Info supplied below).


red clover extract: a putative source for simultaneous treatment of menopausal disorders and the metabolic syndrome.
Mueller M1, Jungbauer A.
Author information

Abstract
OBJECTIVE:
Currently, red clover extract is used to treat menopausal disorders as an alternative to classic hormone therapy. Several human and animal studies have attributed hypolipidemic, hypoglycemic, or antiatherosclerotic effects to red clover extract or isoflavones. This study was designed to determine the peroxisome proliferator-activated receptor (PPAR) gamma activation by red clover extract.
DESIGN:
The PPARgamma binding affinities and the transactivation activities of red clover extracts, isoflavones, and their metabolites were analyzed. The presence of specific substances in the extracts was proved by high-performance liquid chromatography/electrospray ionization/mass spectrometry.
RESULTS:
The red clover extracts and the compounds genistein and biochanin A were potent PPARgamma ligands and activators. Several metabolites exerted higher binding affinities or transactivational activities than their precursor molecules. 6-Hydroxydaidzein exerted a more than 100-fold higher binding affinity than its precursor daidzein. The maximal transactivational activity of 6-hydroxydaidzein and 3'-hydroxygenistein exceeded even that of rosiglitazone, a known PPARgamma agonist. Equol and O-desmethylangolensin showed an approximately fivefold higher binding affinity and, in the case of O-desmethylangolensin, a fourfold higher PPARgamma agonistic activity than the precursor. The daily dose of Menoflavon forte, a widely used red clover extract for treatment of menopausal disorders, provides theoretically 15% to 30% of the daily recommended dose of rosiglitazone. Considering the more active metabolites formed, activity must be higher in vivo.
CONCLUSIONS:
This study shows that red clover extracts, the major compounds, and especially several main metabolites exert significant PPARgamma binding and transactivational activity. Red clover extract, which is currently used for treating menopausal disorders, could be simultaneously used for ameliorating the metabolic syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/18724264



peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
Schoonjans K1, Staels B, Auwerx J.
Author information

Abstract
The three types of peroxisome proliferator-activated receptors (PPAR), termed alpha, delta (or beta), and gamma, belong to the nuclear receptor superfamily. Although peroxisome proliferators, including fibrates and fatty acids, activate the transcriptional activity of these receptors, only prostaglandin J2 derivatives have been identified as natural ligands of the PPAR gamma subtype that also binds thiazolidinedione antidiabetic agents with high affinity. PPARs heterodimerize with retinoic X receptor (RXR) and alter the transcription of target genes after binding to response elements or PPREs, consisting of a direct repeat of the nuclear receptor hexameric DNA recognition motif (PuGGTCA) spaced by 1 nucleotide (DR-1). Upon activation by fatty acids (FAs) and drugs that affect lipid metabolism, PPARs control the expression of genes implicated in intra- and extracellular lipid metabolism, most notably those involved in peroxisomal beta-oxidation. PPARs partially mediate the inductive effects of fibrates and fatty acids on high density lipoprotein (HDL) cholesterol levels by regulating the transcription of the major HDL apolipoproteins, apoA-I and apoA-II. The hypotriglyceridemic action of fibrates and certain fatty acids also involves PPAR and is constituted of: 1) increased hydrolysis of plasma triglycerides due to induction of LPL and reduction of apoC-III expression; 2) stimulation of cellular fatty acid uptake and conversion to acyl-CoA derivatives due to increased expression of genes for fatty acid transport protein and acyl-CoA synthetase; 3) increased peroxisomal and mitochondrial beta-oxidation; and 4) decreased synthesis of fatty acids and triglycerides and decreased production of very low density lipoprotein (VLDL). Hence, both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL particles contribute to the hypolipidemic effect of fibrates and fatty acids. Finally, PPARs appear to be involved in differentiation processes because activation of PPAR gamma 2 triggers adipocyte differentiation and stimulates expression of several genes critical to adipogenesis. It is suggested that PPARs are key messengers responsible for the translation of nutritional and pharmacological stimuli into changes in gene expression and differentiation pathways.
PMID: 8725145 [PubMed - indexed for MEDLINE] Free full text

[Lotus]

PUFA have been known for nearly 40 years to uniquely suppress lipid synthesis. PUFA, particularly n-3, accomplish this by coordinating an upregulation of lipid oxidation and a downregulation of lipid synthesis. In other words, PUFA function as metabolic fuel “repartitioners.” Such fuel repartitioning may protect cells against the accelerated rates of apoptosis reportedly observed with excessive triglyceride accumulation (12, 25). PUFA exert their effects on metabolic pathways by governing the DNA binding activity and nuclear abundance of select transcription factors responsible for regulating the expression of genes encoding key regulatory proteins of lipid and glucose metabolism. With respect to their role in fatty acid oxidation, PUFA increase the fatty acid oxidative capacity of tissues through their ability to function as ligand activators of PPAR-α and thereby induce the transcription of several genes encoding proteins affiliated with fatty acid oxidation. On the other hand, PUFA suppress lipid synthesis by inhibiting transcription factors that mediate the insulin and carbohydrate control of lipogenic and glycolytic genes. In this regard, PUFA rapidly generate an intracellular signal that immediately suppresses the proteolytic release-

Molecular mechanism for polyunsaturated fatty acid regulation of gene transcription
http://ajpgi.physiology.org/content/281/4/G865