[Marcy]

Thanks Lotus. I'm thinking I might add the hops back in. I'm continuing to have nice, steady growth with E2 and spiro, but hops has always held a special vibe. Your thoughts and research are MUCH appreciated

[Lotus]

Greetings BN,

I've made some discoveries about obesity and breast growth, ( my interpretation though ) that could shed some light on some stalled growth. The following study's demonstrate that obesity reduces estrogen receptor alpha ( ER-a, the boob growth receptor)........its kinda like the receptor disappears when being overweight, or/ the hormones aren't finding the cell receptor(s). In other words, reducing weight (bellies) initiates more ER-a receptor bioavailability.



ERα absence causes adipocyte hyperplasia and hypertrophy, insulin resistance, and glucose intolerance in both sexes.

http://www.ncbi.nlm.nih.gov/m/pubmed/11070086/

The full paper
http://m.pnas.org/content/97/23/12729.full


You're welcome Marcy

[pom19]

Greetings BN,

I've made some discoveries about obesity and breast growth, ( my interpretation though ) that could shed some light on some stalled growth. The following study's demonstrate that obesity reduces estrogen receptor alpha ( ER-a, the boob growth receptor)........its kinda like the receptor disappears when being overweight, or/ the hormones aren't finding the cell receptor(s). In other words, reducing weight (bellies) initiates more ER-a receptor bioavailability.



ERα absence causes adipocyte hyperplasia and hypertrophy, insulin resistance, and glucose intolerance in both sexes.

http://www.ncbi.nlm.nih.gov/m/pubmed/11070086/

The full paper
http://m.pnas.org/content/97/23/12729.full


You're welcome Marcy

----------------------------------------------
Hi Lotus, does that mean fat people have less breast growth and smaller boobs? Thanks, POM

[Billie]

Lotus do you do Yoga? I learned to meditate and do yoga at the Chopra Center.

[Lotus]

Hi Lotus, does that mean fat people have less breast growth and smaller boobs? Thanks, POM

It appears that the reduction (or absence) of ERalpha causes adipocyte hyperplasia, hypertrophy, insulin resistance, and glucose intolerance in both sexes (as stated).

In other words, exercise improved the sensitivity of ER-a, and obesity keeps breast growth to a minimum (if any) other than adding fat with increased obesity.

[rachel-rache]

Is HOPS (8-pin) here different than hops? Also, in Lotus's post of choosing one of each, how come there is no PM mentioned as one of the estrogens. Isn't it really strong? Thanks

[Lotus]

Lotus do you do Yoga? I learned to meditate and do yoga at the Chopra Center.

Sorry I don't practice yoga, tia chi is a different story though.

[Lotus]

Is HOPS (8-pin) here different than hops? Also, in Lotus's post of choosing one of each, how come there is no PM mentioned as one of the estrogens. Isn't it really strong? Thanks

8-pin ( known as " Prenylnaringenin " ) is a flavonoid.......a phytoestrogen in HOPS. In relation to PM, dexoymiroestriol (in PM) has been identified as stronger than HOPS in a few studies, (probably stronger at ER-a over ER-b), I believe we have posted a study or two about it though, still needs verifying.

As mentioned, HOPs is 70x stronger in ER-b (beta) binding than estradiol....

[pom19]

Hi Lotus, does that mean fat people have less breast growth and smaller boobs? Thanks, POM

It appears that the reduction (or absence) of ERalpha causes adipocyte hyperplasia, hypertrophy, insulin resistance, and glucose intolerance in both sexes (as stated).

In other words, exercise improved the sensitivity of ER-a, and obesity keeps breast growth to a minimum (if any) other than adding fat with increased obesity.

--------------------------------------------
Thanks Lotus.

[Lotus]

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.