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I have to say that is the topic about which effective information is most lacking. What little expertise I have suggests that licorice is very effective as an anti-androgen. I take that as verified by mainstream sites like Web Md telling you not to take it if you have erectile disfunction. Its problem is that it has harmful side effects, and you should not stay on it for more than a month. Still, you can rotate from Licorice to a combination of other less effective anti androgens-I do use Red Reishi, Vitex and Saw Palmetto when off licorice.
I would hesitate to say I am a big success, but I can say that I have seen surprising (to me, at least) growth in 4 months, for an old girl. I have added 2 inches in bustline since September, 2014 using this basic program with PM and bio identical estrogen creams.
I do hate how opaque this market is, but that is the price of it being a "food" versus a "drug."
Christine
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(20-01-2015, 03:05 AM)Lenneth Wrote: any ideas on Reishi Dosages? (Liquid Extract)
2x a day for mild androgen expression (1 dropper full each)
3x a day for excess DHT expression, considering how many target sites DHT affects, (which is about a nearly 100% conversion in some tissues).
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(20-01-2015, 06:27 AM)Lotus Wrote: (20-01-2015, 03:05 AM)Lenneth Wrote: any ideas on Reishi Dosages? (Liquid Extract)
2x a day for mild androgen expression (1 dropper full each)
3x a day for excess DHT expression, considering how many target sites DHT affects, (which is about a nearly 100% conversion in some tissues).
Feck me !! I thought I finished college 30 yrs ago !! All that chart is woosh over head
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Ah, no worries.
it took me a while to realize that estrogens and androgens compete inside the same receptor cell (called the cytoplasm). Even more confusing is that sometimes an androgen will bind to its receptor but not get activated, scientist are unsure why.
But the affinity is towards estradiol, for the most part these hormones must be in the free form for synthesis (you remember the 2% that gets delivered from SHBG/albumin).
And new research has determined there's a few more androgens, although I won't confuse you with them just yet lol.
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My have times changed. 16 yrs ago everyone was worried about Y2K. OMG.... LOL. Just what to do for JUST boobs. hehehehehe
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So true ia,
But the more you look into these thing you start to understand some links, for instance,
Something called "intercellular pathways" or in other words how hormones travel to the receptors. A visual always helps me see the process, and this one does explain in some detail compared to others I've seen.
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(20-01-2015, 10:50 PM)Lotus Wrote: So true ia,
But the more you look into these thing you start to understand some links, for instance,
Something called "intercellular pathways" or in other words how hormones travel to the receptors. A visual always helps me see the process, and this one does explain in some detail compared to others I've seen.
Sod it ! I am gona award professorship to lotus . As his research is unbeatable though most of it goes over this dumbo's head
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*blinks* Ok... I have a fairly high IQ and I am generally scientifically minded and all that just caused brain fog. *taps skull a few times* Is anybody in there, there.. there... there....
Guess nobody is home between my ears anymore.
~E
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(21-01-2015, 05:18 AM)ElainMoria Wrote: *blinks* Ok... I have a fairly high IQ and I am generally scientifically minded and all that just caused brain fog. *taps skull a few times* Is anybody in there, there.. there... there....
Guess nobody is home between my ears anymore.
~E
No hope for dumbo like me than
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(13-01-2015, 07:44 PM)Lotus Wrote: Ok, but it may not make much sense,
It's like deconstructing a model (call it a airplane model) that someone else built, only you're working in reverse to deconstruct right. Same applies here, you see a study that states 5 alpha reductase is reduced in the liver, now maybe this study was for cancer research or something similar. Let's take one of these studies,
Role of human type 3 3alpha-hydroxysteroid dehydrogenase (AKR1C2) in androgen metabolism of prostate cancer cells.
Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family, which are present in most tissues of the body, and play important roles in hormone synthesis and breakdown (including estrogen and testosterone synthesis and metabolism), cholesterol synthesis, and vitamin D metabolism. Cytochrome P450 enzymes also function to metabolize potentially toxic compounds, including drugs and products of endogenous metabolism such as bilirubin, principally in the liver.
AKRs are involved in the development and progression of many cancers, as well as chemotherapeutic drug resistance. AKR1B1 and AKR1B10 are overexpressed in tumors, such as liver, breast, and lung cancer. Several AKRs (AKR1A1, AKR1B10, and AKR1C1-3) are involved in tobacco-carcinogenesis, but they also catalyze the detoxication of nicotine derived nitrosamino ketones. In addition, AKR1C1-3 enzymes play a key role in the regulation of proliferative signaling in hormone dependent cancers.
So what they did in this study was to cut off the androgen synthesis to the receptors using another steroid , Four human aldo-keto reductases (AKRs) that belong to the AKR1C subfamily function in vitro as 3-keto-, 17-keto- and 20-ketosteroid reductases or as 3alpha-, 17beta- and 20alpha- hydroxysteroid oxidases to varying degrees. By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.
In English, I want to find the link to activate AKR1c in the liver to shut off the androgen receptors therefore DHT never gets activated, simple right?.
Cha-Ching, found it.
Regulates access of 5alpha-DHT to the androgen receptor.
Abstract
Pairs of hydroxysteroid dehydrogenases (HSDs) govern ligand access to steroid receptors in target tissues and act as molecular switches. By acting as reductases or oxidases, HSDs convert potent ligands into their cognate inactive metabolites or vice versa. This pre-receptor regulation of steroid hormone action may have profound effects on hormonal response. We have identified the HSDs responsible for regulating ligand access to the androgen receptor (AR) in human prostate. Type 3 3alpha-hydroxysteroid dehydrogenase
(aldo-keto reductase 1C2, aka-AKR acts solely as a reductase to convert 5alpha-dihydrotestosterone (DHT), a potent ligand for the AR (K(d)=10(-11)M for the AR), to the inactive androgen 3alpha-androstanediol (K(d)=10(-6)M for the AR); while RoDH like 3alpha-HSD (a short-chain dehydrogenase/reductase (SDR)) acts solely as an oxidase to convert 3alpha-androstanediol back to 5alpha-DHT. Our studies suggest that aldo-keto reductase (AKRs) and SDRs function as reductases and oxidases, respectively, to control ligand access to nuclear receptors.
http://www.ncbi.nlm.nih.gov/pubmed/17223255