[basedandfempilled]

Does it make any sense to cycle something like Reishi mushroom by going off for a week or should you only cycle estrogen and progesterone supplementation? I saw on one thread someone recommending to cycle the DHT blocker as well, but that does not make any sense to me. In what way would having increased DHT for a week mimic a womans cycle?

[Karen Hart]

Depending on how closely one wants to mimic the female cycle... there is a slight rise in testosterone between the end of the follicular phase and the beginning of the luteal phase. It starts a few days before day 14, where it peaks, and then begins to recede over the next 2 or 3 days. To mimic that, one would have to stop their AA a couple of days before day 14 and then resume the AA a couple of days after.

I wouldn't worry about it too much. In fact, I would not worry about it at all... and I am the one who was exploring that concept!
I was not recommending it, I was basically posing the question... suppose someone wanted to mimic the female cycle as closely as possible?
Testosterone IS involved in that cycle. It is not nearly as dominant as estrogen or progesterone but it is there.
The question is, is the small rise of testosterone worth considering in regard to NBE?

Further, I commented that this idea of 2 days before and 2 days after was pure guess work at best but this may allow that small hump in T level, maybe not. How long does the AA persist and at what level? How long does it take to get back to "normal" when reinitiated? Without daily T level testing, one would never know what effect it would be having. For this reason, I say, don't worry about it.

Karen 

[BlackButterfly]

For someone born male there isn't any real "need" to cycle DHT blockers; 
however trying to block DHT can be compared to playing whack-a-mole, your body can adapt over time to find a way round the blocker (unless you use prescription meds), so you may need to "cycle" between more than one AA to keep the things under control; DHT levels can also vary with the time of year (rutting season ), so at times you may need to vary the dose or use something stronger.

Get to know your own body and how it responds, then you can use the minimum needed to achieve what you want.

[Lotus]

Does it make any sense to cycle something like Reishi mushroom by going off for a week or should you only cycle estrogen and progesterone supplementation? I saw on one thread someone recommending to cycle the DHT blocker as well, but that does not make any sense to me. In what way would having increased DHT for a week mimic a womans cycle?

Hi baseandfempilled, welcome to BN, 

trying to block DHT can be compared to playing whack-a-mole

Hmm, this a coincidence… I made the whack-a-mole statement years ago in happyme's (bobbie) DHT thread.

Trying to block DHT is like playing "whack a mole", it finds different pathways for docking (binding)

In my experience, Reishi and Green Tea are an effective combination for NBE. The anti-androgens in both have strong anti-cancer fighting properties that block DHT production. Androgens (& DHT) production doesn't take a break, so cycling anti-androgens seems pointless… unless you've suppressed them enough to below female range then I'd say you might be able to skip a day. And following (or mimicking) the female menstrual cycle and approach when used with NBE (or HRT) doesn't make sense either because we don't have ovaries, in other words it's pointless.
There's additional information to address when dealing with androgen production like the negative feedback loop and how it relates to extreme androgen production and how it relates when first starting any NBE/HRT production. 
If you're planning on using HRT meds I've provided two anti-androgens to consider. 
Bicalutamide and Dutasteride are used in HRT programs, and their side effects are listed below. Bica doe
Hammerer P, Manka L (2019). "Androgen Deprivation Therapy for Advanced Prostate Cancer". Urologic Oncology. Springer International Publishing. pp. 255–276. doi:10.1007/978-3-319-42623-5_77. ISBN 978-3-319-42622-8. Bicalutamide is the most widely used antiandrogen in the treatment of prostate cancer. [...] Common side effects [of bicalutamide] include breast enlargement, breast tenderness, hot flashes, and constipation as well as feminization and changes in mood and liver as well as lung toxicity; monitoring of liver enzymes is recommended during treatment (Schellhammer and Davis 2004).

Adverse events of bicalutamide, such as hot flushes (9.2% vs 5.4%), decreased libido (3.6% vs 1.2%), impotence (9.3% vs 6.5%) and abnormal liver function tests (3.1% vs 1.7%), Wellington K, Keam SJ. Bicalutamide 150mg: a review of its use in the treatment of locally advanced prostate cancer. Drugs. 2006;66(6):837-50. doi: 10.2165/00003495-200666060-00007. Erratum in: Drugs. 2006;66(15):1987. PMID: 16706554.

The two predominant naturally occurring androgens are testosterone (T) and dihydrotestosterone (DHT). DHT is the more potent androgen in vivo and in vitro. All androgen-responsive genes are activated by androgen receptor (AR) bound to either T or DHT and it is believed that AR is more transcriptionally active when bound to DHT than T. The two classes of antiandrogens, presently available, are the steroidal derivatives, all of which possess mixed agonistic and antagonistic activities, and the pure non-steroidal antiandrogens of the class of flutamide and its derivatives.

Singh SM, Gauthier S, Labrie F. Androgen receptor antagonists (antiandrogens): structure-activity relationships. Curr Med Chem. 2000 Feb;7(2):211-47. doi: 10.2174/0929867003375371. PMID: 10637363.

Reduced sperm (quite possibly permanently). Dutasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of luteinizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lower T can have a strong impact on libido, lower Total T (& freeT) can affect penis size too. I have found success in using testosterone cream or gel applied directly on the penis, if used correctly (1x per week). It doesn't impact T levels like you'd think because the application is absorbed directly to penile skin. What T does get into the bloodstream is negligible. Results vary, I can say the application has a definite impact on libido and penis size and girth. 

Adrenal DHT has some impact, SRS would make them more apparent though.
Long term?, imo it's a top tier anti-androgen. I wouldn't use it just for NBE unless you seek the kinda of results as in hrt. My experience with dutasteride was approximately 12 months. Though my hrt doctor (Dr. Powers) put me on dutasteride two days a week recently because my DHT went up a bit from my last blood test. However, the rise in my DHT had no impact on my estradiol (or my free E2 percentage @ 2.0% which is considered optimal).
Dutasteride: A Review of Current Data on a Novel Dual Inhibitor of 5 Reductase 
http://www.ncbi.nlm.nih.gov/pmc/articles...4_0203.pdf
Dutasteride: How Does It Work?

DHT synthesis is catalyzed intracellularly by 5 reductase types 1 and 2 enzymes. Dutasteride is the first dual inhibitor of both 5 reductase isoenzymes. This leads to near-complete suppression of serum DHT—more than 90%, compared with the 70% seen with finasteride. Type 2 5 reductase is the predominant isoform in normal prostate and in BPH tissues. Type 1 5 reductase is present in BPH tissue in lower quantities, but it predominates in prostate cancer cell lines and seems to be over-expressed in some prostate cancers. Theoretically, the greater suppression of DHT arising from the dual 5 -reductase inhibition could result in greater efficacy than is observed in selective type 2 inhibition, and this dual inhibition could prevent type 1–mediated synthesis of DHT.

Take care, L. 

[basedandfempilled]

"In my experience, Reishi and Green Tea are an effective combination for NBE."

Could you explain why you should combine the two rather than using just one? Do they do different things?

[BlackButterfly]

My comment came from personal experience; I'd also recommend trying several (over time) to see what the affects (good and bad) are on your system, then decide what best suits what you want to achieve (and your life style).

[Lotus]

Here's just a few notes on why taking GTE is important. I'll post information on Red Reishi tomorrow and why taking RR with GTE is important in one's program.

I'd keep both, GTE @ 2x per day. Count on gte to do other things beside inhibit DHT, there's the whole Sirtuin 1 research that increases longevity thing...plus other benefits too. RR has longevity properties too, I'm digging into that research though. But you can cut back on the RR while using both.

Green Tea-(updated version 2017):

promotes aromatase, increases GABA, promotes estrogen and estrogen gene target receptor (pS2) and PR-progesterone, modifies signaling transduction pathways, antioxidant (relieves oxidative stress & reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols EGCG Epigallocatechin 3-gallate-inhibits DHT and are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance, anti-androgen (inhibits DHT), stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream, Green Tea displaces estradiol in SHBG, making a higher bioavailability of E2 (in the blood) benefiting delivery to target tissues. I believe green tea acts like a generic herbal version of Spironolactone.


If you'd like more information about " steroidal and natural lactones " see here:
http://www.breastnexum.com/showthread.php?tid=17436&pid=194280&highlight=Lactones#pid194280

http://www.sciencedirect.com/science/art...1714000056
New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate ☆

Highlights
•
Many biological actions of EGCG are mediated by specific mechanisms other than its well-known antioxidant properties.
•
EGCG is a pro-oxidant per se in some biological contexts.
•
EGCG directly interacts with cell surface membrane proteins and specific known receptors.
•
Treatment of cells with EGCG regulates specific intracellular signaling pathways and transcription.
•
Specific biological actions of EGCG are regulated in a concentration-dependent manner.
Abstract
Green tea is rich in polyphenol flavonoids including catechins. Epigallocatechin 3-gallate (EGCG) is the most abundant and potent green tea catechin. EGCG has been extensively studied for its beneficial health effects as a nutraceutical agent. Based upon its chemical structure, EGCG is often classified as an antioxidant. However, treatment of cells with EGCG results in production of hydrogen peroxide and hydroxyl radicals in the presence of Fe (III). Thus, EGCG functions as a pro-oxidant in some cellular contexts. Recent investigations have revealed many other direct actions of EGCG that are independent from anti-oxidative mechanisms. In this review, we discuss these novel molecular mechanisms of action for EGCG. In particular, EGCG directly interacts with proteins and phospholipids in the plasma membrane and regulates signal transduction pathways, transcription factors, DNA methylation, mitochondrial function, and autophagy to exert many of its beneficial biological actions.

I guess you are saying that it is more important to squash the more potent DHT than whatever level of inhibition of aromatase is caused by Silybin? Also about the other thing you mentioned: how does its inactivation of P450 3A4 and inhibiting of Glucuronidation affect NBE? Thanx.

Exactly, squash DHT by multiple means (pathways) and we'd see better gains.

Re: Glucuronidation- think of Glucuronidation as a process to eliminate toxins (to detoxify) from tissues, (via excretion). see this attached study below as an example of using glucuronidation. As we know, GTE inhibits DHT.......it's all relative lol.

Free Radic Res. 2004 Sep;38(9):1025-31.
Glucuronidation of the green tea catechins, (-)-epigallocatechin-3-gallate and (-)-epicatechin-3-gallate, by rat hepatic and intestinal microsomes.
Crespy V1, Nancoz N, Oliveira M, Hau J, Courtet-Compondu MC, Williamson G.
Author information


Abstract
The flavonoids (-)-epigallocatechin-3-gallate (EGCg) and (-)-epicatechin-3-gallate (ECg) are major components of green tea and show numerous biological effects. We investigated the glucuronidation of these compounds and of quercetin by microsomes. Quercetin was almost fully glucuronidated by liver microsomes after 3 h, whereas ECg and ECGg were conjugated to a lesser extent (12.2 +/- 0.2 and 7.5 +/- 0.2%, respectively). The intestinal microsomes also glucuronidated quercetin much more efficiently than ECg and EGCg. Although the rates were lower than quercetin, intestinal microsomes exhibited higher activity on the galloyl group of ECg and EGCg compared to the flavonoid ring, whereas hepatic glucuronidation was higher on the flavonoid ring of EGCg and ECg compared to the galloyl groups. The low glucuronidation rates could partially explain why these flavanols are present in plasma as unconjugated forms.

Polyphenols (specifically Green Tea) promotes aromatase, anti-oxidation, estrogen, modifies signaling transduction pathways, relieves oxidative stress (reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance.

Green Tea - stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream. Why is this important? 95-98% fatty acids are bound in the bloodstream (just like hormones are), we needed something that displaces hormones and fatty acids, looks like green tea is up for the task.

Green tea raises growth hormones (theanine in tea raises GABA), even at resting.
Determination of theanine, GABA, and other amino acids in green, oolong, black, and Pu-erh teas with dabsylation and high-performance liquid chromatography.
Syu KY, et al. J Agric Food Chem. 2008.
Show full citation
Abstract
Dabsyl chloride (dimethylaminoazobenzene sulfonyl chloride), a useful chromophoric labeling reagent for amino acids and amines, was developed in this laboratory in 1975. Although several methods have been developed to determine various types of amino acids, a quick and easy method of determining theanine, GABA, and other amino acids has not been developed in one HPLC system. In this paper are analyzed the free amino acid contents of theanine and GABA in different teas (green tea, black tea, oolong tea, Pu-erh tea, and GABA tea) with a dabsylation and reverse phase high-performance liquid chromatography (HPLC) system coupled with a detector at 425 nm absorbance. Two reverse phase columns, Hypersil GOLD and Zorbax ODS, were used and gave different resolutions of dabsyl amino acids in the gradient elution program. The data suggest that the tea source or the steps of tea-making may contribute to the theanine contents variations. High theanine contents of high-mountain tea were observed in both green tea and oolong tea. Furthermore, the raw (natural fermented) Pu-erh tea contained more theanine than ripe (wet fermented) Pu-erh tea, and the GABA contents in normal teas were generally lower than that in GABA tea.
PMID 18652476 [PubMed - indexed for MEDLINE]

Green Tea displaces estradiol in SHBG, making a higher bioavailability of E2 (in the blood) benefiting delivery to target tissues. As said before, green tea raises SHBG and free's E2 (blood serum), I really believe it acts like a generic herbal version of Spirolactone.

Green Tea Epigallocatechin-Green tea (camellia)-Reduce's the conversion of free testosterone into DHT and also raises SHBG (sex-hormone-binding-globulin). Also is for breast cancer prevention, reduces visceral fat.

In this study (animal) aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P n< 0.05, and 285.5 +/- 82.9% of control in vAT,

That's 60.6% in subcutaneous fat and 82.9% in visceral fat.

Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue.

Abstract
Green tea (GT) and its components have been shown to possess antiobesity properties and the corresponding mechanisms of action are being investigated, given the epidemic proportions of obesity incidence. In the current work, we used 12-mo-old male Wistar rats to test the effect of 6 mo of treatment with GT as the sole drinking beverage (52.8 +/- 6.4 mL/d) on adipose tissue (AT). AT aromatase expression was determined by Western blotting, plasma concentrations of 17beta-estradiol and testosterone were determined by RIA, and adipocyte size determined by measuring diameter in tissue sections. Proliferation and apoptosis were also assessed by Ki67 immunostaining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, respectively. Evaluations were made in subcutaneous (sc) AT and visceral (v) AT. Body weight increased over time in both groups (P < 0.001), but the increase was more pronounced in controls (P < 0.001) and food and fluid intake did not influence that effect. At the end of the experiment, aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P < 0.05, and 285.5 +/- 82.9% of control in vAT, P < 0.01). AT of GT-treated rats had a higher percentage of proliferating cells (204.1 +/- 19.5% of control in scAT, P < 0.01, and 246.6 +/- 50.2% of control in vAT, P < 0.01) and smaller adipocytes (78.3 +/- 1.7% of control in scAT, P < 0.001, and 87.9 +/- 3.2% of control in vAT, P < 0.05). GT also increased the number of apoptotic cells in vAT (320.4 +/- 21.9% of control; P < 0.001). These results suggest new mechanisms for GT on body weight and highlight its potential benefit to prevent or treat obesity and the metabolic syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/18936213#

The polyphenols (EGCG) in green tea absolutely inhibit DHT, (and in pharma strength I might add). Polyphenols inhibit 5 alpha reductase type 1. Dutasteride inhibits type 1 & 2 @ about 93%, effective but carries risk. Red clover, genistein (others too) inhibit type 2 (5 ar).

Green tea protects the prostate and also lowers PSA levels too, which is why I'd still take it.

Btw,

Green tea can increase a steady state expression level of pS2 and PR mRNA, which mRNA conveys genetic information from DNA to the ribosome (in other words-synthesis).

pS2-is an estrogen target gene
PR-is progesterone receptor

Epigallocatechin gallate induces the steady state mRNA levels of pS2 and PR genes in MCF-7 breast cancer cells.
C Mohan C Manjegowda, Gauri Deb, Anil M Limaye

Abstract
Investigations using in vitro and in vivo models of breast carcinogenesis have demonstrated anti-neoplastic activity of the green tea polyphenol, epigallocatechin gallate (EGCG). Although a number of molecular targets of EGCG have been identified, its impact on the expression of estrogen target genes is not completely understood. Here, we examined the mRNA expression levels of two estrogen target genes, namely Trefoil Factor 1 (pS2) and Progesterone Receptor (PR) in MCF-7 cells treated with EGCG. We observed that treatment with 40 microM EGCG, which caused only 20% decrease in cell viability, resulted in increased steady state expression levels of pS2 and PR mRNA. This suggests that EGCG may exert its biological activities, at least in part, by influencing the expression of estrogen target genes

Further benefits of Green Tea

EGCG plays an important role in lipid metabolism in whole body physiology as well as at the cellular level.

EGCG directly interacts with plasma membrane proteins and phospholipids which stimulate intracellular signaling pathways. In addition, EGCG is transported to intracellular compartments, cytosol, mitochondria, lysosome, and nucleus where it mediates additional biological actions.

Effect of green tea on metabolic and hormonal aspect of polycystic ovarian syndrome in overweight and obese women suffering from polycystic ovarian syndrome: A clinical trial
https://www.jehp.net//article.asp?issn=2...st=Tehrani

EGCG Inhibits Proliferation and Induces Apoptosis Through Downregulation of SIRT1 in Nasopharyngeal Carcinoma Cells

Shisheng Jiang et al. Front Nutr. 2022.
Abstract

Epigallocatechin-3-gallate (EGCG), a frequently studied catechin in green tea, has been shown to be involved in the anti-proliferation and apoptosis of human nasopharyngeal carcinoma (NPC) cells. However, the underlying molecular mechanism of the apoptotic effects of EGCG has not been fully investigated. Recent literature emphasized the importance of Sirtuin 1 (SIRT1), an NAD+-dependent protein deacetylase, in regulating cellular stress responses, survival, and organismal lifespan. Herein, the study showed that EGCG could significantly inhibit cell proliferation and promote apoptosis of 2 NPC (CNE-2 and 5-8F) cell lines. Moreover, it was also found that SIRT1 is down-regulated by EGCG, and the SIRT1-p53 signaling pathway participates in the effects of EGCG on CNE-2 and 5-8 F cells. Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC.

[wee2er]

Lotus you are an absolute gem, thank you.
Since going on HRT I had forgotten about GTE and RR, will get back on my green tea and order up some RR.

[Kay Lady]

Another thanks to you Lotus!!!
 Kay

[LisaM]

Such a great source of information, would like to see something about dosage and duration of effect (half life) though, especially for those of us who choose capsules rather than  cups of tea/powder.