[jannet.duff]

Here's what I've heard regarding this:

Anti-androgens are only risky if you are not taking some form of estrogen.

The harmful thing is having really low levels of all sex hormones, so if you get rid of your testosterone without raising your estrogen, you are in trouble.

If your blood chemistry is in the female range you should be fine. After all, females aren't at a higher risk for dementia as far as I know.

This study was conducted on people who were taking anti androgens for other health reasons. They were not on estrogen of any kind.

Yeah, you did point out the possibility of low testosterone to be a possible cause. I'd say that's very likely.

My gender doctor said that the trick is to lower active DHT and T.  But once you do that, you have to raise E to about 200.  Otherwise you do risk dementia as well as osteoporosis and other maladies.

Aso the higher your E, the less AA, your Going to need. From what I read, you need @ 400 to shut down your T completly, once your T has been shout down for @ 4 months you can begin to slowly lower your E to the 200 range.

How can I get my T to the point of no return? You have really peeked my interest I want to learn more now.

I am not sure there is an actual point of actual no return. I have read of transgender females of 3 years or more having to come off all HRT due to circumstances beyond their control, within a few months their "T" is back in full swing ( That's just "T" no viable swimmers )
Once you have had your "E" high enough to drop off "E", you can drop it down, but you still need it to keep "T" at bay.

[Stevenator.]

I'm curious why WP is considered to be so good. 
I've read a few times where there have been no studies on WP. 
And the only report, that I've read, is based on a report from China dated 1991. 

Thx

[BeautifulBambi]

Here's what I've heard regarding this:

Anti-androgens are only risky if you are not taking some form of estrogen.

The harmful thing is having really low levels of all sex hormones, so if you get rid of your testosterone without raising your estrogen, you are in trouble.

If your blood chemistry is in the female range you should be fine. After all, females aren't at a higher risk for dementia as far as I know.

This study was conducted on people who were taking anti androgens for other health reasons. They were not on estrogen of any kind.

Yeah, you did point out the possibility of low testosterone to be a possible cause. I'd say that's very likely.

My gender doctor said that the trick is to lower active DHT and T.  But once you do that, you have to raise E to about 200.  Otherwise you do risk dementia as well as osteoporosis and other maladies.

Aso the higher your E, the less AA, your Going to need. From what I read, you need @ 400 to shut down your T completly, once your T has been shout down for @ 4 months you can begin to slowly lower your E to the 200 range.

How can I get my T to the point of no return? You have really peeked my interest I want to learn more now.

I am not sure there is an actual point of actual no return. I have read of transgender females of 3 years or more having to come off all HRT due to circumstances beyond their control, within a few months their "T" is back in full swing ( That's just "T" no viable swimmers )
Once you have had your "E" high enough to drop off "E", you can drop it down, but you still need it to keep "T" at bay.

So I would have to keep taking BO to keep T down forever?

[jannet.duff]

My gender doctor said that the trick is to lower active DHT and T.  But once you do that, you have to raise E to about 200.  Otherwise you do risk dementia as well as osteoporosis and other maladies.

Aso the higher your E, the less AA, your Going to need. From what I read, you need @ 400 to shut down your T completly, once your T has been shout down for @ 4 months you can begin to slowly lower your E to the 200 range.

How can I get my T to the point of no return? You have really peeked my interest I want to learn more now.

I am not sure there is an actual point of actual no return. I have read of transgender females of 3 years or more having to come off all HRT due to circumstances beyond their control, within a few months their "T" is back in full swing ( That's just "T" no viable swimmers )
Once you have had your "E" high enough to drop off "E", you can drop it down, but you still need it to keep "T" at bay.

So I would have to keep taking BO to keep T down forever?

I would say yes, but I am not sure how BO works anyway, it's not something I ever looked into. I would very much doubt BO on its own is ever going to get your E in the 400s without taking an extra source of E..

[Lotus]

I'm curious why WP is considered to be so good. 
I've read a few times where there have been no studies on WP. 
And the only report, that I've read, is based on a report from China dated 1991. 

Thx

Here's a few WP studies collected (you'll find more using the BN search option).

Hi there BN, I don't expect everyone to follow where I'm going with this new research for BN, but basically a short explanation is that I've found addtiional info that White Peony inhibits prostate cancer (which mostly is androgen driven) along with treating many other illnesses. Though one particular find is that WP gives support for treating diabetes, though I find it to be from β-cells (or generation of β-cells) which is newer science (or on the horizon) for the treatment of diabetes (via stem cell technology). 

But.....by inhibiting cancer, WP inhibits androgens, though I think we'll see it (inhibiting androgens aka DHT) in a new light through the PI3K/Akt/mTOR signaling pathway. (more on that later).

I'll be posting additional info on β-cells and the pancreas......

Paeonilorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling
http://www.ncbi.nlm.nih.gov/pmc/articles...2-1471.pdf

PI3K/Akt/mTOR signaling is mediated by Paeoniflorin

mTOR signaling impacts most major cellular functions, e.g. PI3K mediates G1 cell cycle progression and cyclin expression through the activation of AKT/mTOR/p70S6K signaling pathway in the prostate cancer cells.
http://www.sciencedirect.com/science/art...1X03018734

Paeoniflorin (100mg/kg) and EGCG inhibit B lymphocyte (B cell) proliferation and induced B lymphocyte apoptosis. In conclusion, BAFF/BAFF receptor might regulate B cell anti-apoptosis through PI3K/Akt/mTOR pathway. 

BAFF/BAFF-R involved in antibodies production of rats with collagen-induced arthritis via PI3K-Akt-mTOR signaling and the regulation of paeoniflorin.
http://www.ncbi.nlm.nih.gov/pubmed/22760071


Rapid determination of paeoniflorin from Paeonia sinjiang K. Y. Pan. by rapid resolution liquid chromatography
A rapid, effective, binary reverse phase rapid resolution liquid chromatographic method has been developed for the determination of Paeoniflorin extracted from Paeonia sinjiang K. Y. Pan
http://www.ncbi.nlm.nih.gov/pmc/articles...rt=classic


Pro-apoptotic effect of epigallo-catechin-3-gallate on B lymphocytes through regulating BAFF/PI3K/Akt/mTOR signaling in rats with collagen-induced arthritis.
http://www.ncbi.nlm.nih.gov/pubmed/22760071


regeneration of pancreatic β-cells.
Minami K1, Seino S2.
Author information


Abstract
Newly generated insulin-secreting cells for use in cell therapy for insulin-deficient diabetes mellitus require properties similar to those of native pancreatic β-cells. Pancreatic β-cells are highly specialized cells that produce a large amount of insulin, and secrete insulin in a regulated manner in response to glucose and other stimuli. It is not yet explained how the β-cells acquire this complex function during normal differentiation. So far, in vitro generation of insulin-secreting cells from embryonic stem cells, induced-pluripotent stem cells and adult stem/progenitor-like cells has been reported. However, most of these cells are functionally immature and show poor glucose-responsive insulin secretion compared to that of native pancreatic β-cells (or islets). Strategies to generate functional β-cells or a whole organ in vivo have also recently been proposed. Establishing a protocol to generate fully functional insulin-secreting cells that closely resemble native β-cells is a critical matter in regenerative medicine for diabetes. Understanding the physiological processes of differentiation, proliferation and regeneration of pancreatic β-cells might open the path to cell therapy to cure patients with absolute insulin deficiency. 
KEYWORDS:


Brain Res. 2015 Aug 27;1618:149-58. doi: 10.1016/j.brainres.2015.05.035. Epub 2015 Jun 3.
Paeoniflorin attenuates Aβ1-42-induced inflammation and chemotaxis of microglia in vitro and inhibits NF-κB- and VEGF/Flt-1 signaling pathways.
Liu H1, Wang J2, Wang J3, Wang P4, Xue Y5.
Author information

Abstract
Alzheimer׳s disease (AD) is a neurodegenerative disease with elusive pathogenesis, which accounts for most cases of dementia in the aged population. It has been reported that persistent inflammatory responses and excessive chemotaxis of microglia stimulated by beta-amyloid (Aβ) oligomers in the brain may accelerate the progression of AD. The present study was conducted to explore whether paeoniflorin (PF), a water-soluble monoterpene glycoside isolated from the root of Paeonia lactiflora Pallas, could attenuate Aβ1-42-induced toxic effects on primary and BV-2 microglial cells in vitro. Our data showed that PF pretreatment inhibited Aβ1-42-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in rodent microglia. Also, the nuclear translocation of nuclear factor kappa B (NF-κB) subunit p65 and the phosphorylation of NF-κB inhibitor alpha (IκBα) in Aβ1-42-stimulated microglial cells were suppressed by PF administration. Moreover, PF treatment reduced the release of chemokine (C-X-C motif) ligand 1 (CXCL1) and chemokine (C-C motif) ligand 2 (CCL-2) from Aβ1-42-stimulated microglia. Additionally, application of PF inhibited the increases in vascular endothelial growth factor (VEGF) and VEGF receptor 1 (Flt-1) triggered by Aβ1-42, and resulted in a concomitant reduction in microglial chemotaxis. Restoration of VEGF was noted to counteract the inhibitory effect of PF, suggesting that PF mitigated Aβ1-42-elicited microglial migration at least partly by suppressing the VEGF/Flt-1 axis. In summary, in presence of Aβ1-42, PF pretreatment inhibited the excessive microglial activation and chemotaxis.

peony root extract has helped my areolas both in size and color. At least I think they have. If I don't do it once a day they def go back smaller.

Cool, 

White peony inhibits the 5 alpha reductase enzyme (from the conversion to DHT) in the sebaceous glands, which produces sebum. 

Thanks Elaine, good to hear from you.

I think lemon and orange peel could work too, try it. the fact they inhibit DHT (CYP17 inhibitor) makes sense too. 

In conclusion, we suggest in the present study that the supplementation with lemon polyphenols suppressed body weight gain and body fat accumulation by increasing the peroxisomal β-oxidation, which was likely mediated via up-regulation of the mRNA levels of PPARα in the liver. In addition, the levels of serum insulin, glucose and leptin were significantly improved by lemon polyphenols, thereby improving the insulin resistance. We suggest that a supplementation with lemon polyphenols may prevent or improve obesity and insulin resistance by modulating lipid metabolism and preventing metabolic syndrome as a representative, lifestyle-related cluster of diseases caused by an excessively high fat diet. 

Lemon Polyphenols Suppress Diet-induced Obesity by Up-Regulation of mRNA Levels of the Enzymes Involved in β-Oxidation in Mouse White Adipose Tissue
http://www.ncbi.nlm.nih.gov/pmc/articles...43-201.pdf

Have you seen this study?

Androgen Modulators from the Roots of Paeonia lactiflora (Paeoniae
Radix) Grown and Processed in Nara Prefecture, Japan
Kazuto W ASHIDA ,* , a Yoshiyuki I TOH , b Takashi I WASHITA , b and Kyosuke N OMOTO a

https://www.jstage.jst.go.jp/article/cpb...9_971/_pdf

We have thus isolated the first hormone modulators from
the roots of P. lactiflora. This is the first report of paeoni-
florin and albiflorin derivatives such as 1, 2, 4 and 5 showing
AR binding activity. Interestingly, compounds 6 and 7
showed no AR binding activity. The AR binding activity of
6-O-galloylalbiflorin (2) was much stronger than that of the
galloylpaeoniflorin derivatives (1, 5). These results suggested
that both the structure of albiflorin and the galloyl moiety
were important for 2 to show strong AR binding activity. Ad-
ditionally, 6-O-galloylpaeoniflorin (5) displayed the weakest
AR binding activity of the paeoniflorin derivatives (1, 4, 5).
The only structural differences between 2 and 5 are at C-4
and C-9, so the galloyl moiety of 2 might interact with the
carbonyl group of C-9 and/or the hydroxyl group of C-4.
It has been reported that 3 can inhibit growth of prostate
cancer LNCaP cells by two aspects including inhibition of 5-
a -reductase activity and expression of AR protein levels;
however, the AR binding activity of 3 has not been re-
ported. 12) We propose that 3 inhibits prostate cancer cell
growth partly by acting as an AR antagonist.
The AR binding activity of compound 3 was equivalent to
flutamide (IC 50 5.0 m M ), 13) which is in clinical use, and the
activity of compound 2 was also relatively strong. Additon-
ally, because Paeoniae radix was taken in long time as a
crude drug, compounds 2 and 3 might be candidates as safe,
natural AR antagonists.

That's a great find Atom, (thanks)

It looks like  6 -O-galloylalbiflorin and pentagalloylglucose acts like flutamide (a strong non-steroidal anti-androgen), but flutamide carries hepatic risks (toxicity). Aside from the health benefits of WP, the fact it inhibits human prostate cancer cells is a major find. 



So, in ovaries WP promotes aromatase, (I believe in the breasts too), inhibits DHT in sebum, inhibits prostate cancer cells, (which means it inhibits C17 @ CYP17 P450 enzyme, a strong anti-androgen. The lab dosage was 2 grams (I'll have to double check). Roots be king.

[Stevenator.]

Thank you Lotus.

[Stevenator.]

Thank you Lotus.

[Celestia Lane]

quote:
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. 


am i reading this right? it reduces estrogen? or is that a typo? assuming it is a typo, how much should i take daily to lower testosterone? the SP i have says take 2 capsules twice a day as a dietary supplement. each capsule is 450mg. or should i stop taking it all together to avoid an estrogen block?

[Emma Th3saurus]

It's not a typo Celestia, SP reduces both DHT and estrogen

[The First Aria]

quote:
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. 


am i reading this right? it reduces estrogen? or is that a typo? assuming it is a typo, how much should i take daily to lower testosterone? the SP i have says take 2 capsules twice a day as a dietary supplement. each capsule is 450mg. or should i stop taking it all together to avoid an estrogen block?

That's why Lotus suggest most people not to use SP.