), so at times you may need to vary the dose or use something stronger.(29-03-2024, 07:42 PM)basedandfempilled Wrote: [ -> ]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?
(30-03-2024, 10:26 AM)BlackButterfly Wrote: [ -> ]trying to block DHT can be compared to playing whack-a-mole
(04-01-2016, 09:58 PM)Lotus Wrote: [ -> ]Trying to block DHT is like playing "whack a mole", it finds different pathways for docking (binding)
(16-02-2016, 02:11 AM)Lotus Wrote: [ -> ]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.Take care, L.
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.
(12-02-2023, 07:11 AM)Lotus Wrote: [ -> ]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.
(10-02-2023, 02:26 AM)Lotus Wrote: [ -> ](15-03-2017, 06:06 PM)Lotus Wrote: [ -> ]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
(30-01-2015, 09:08 PM)Lotus Wrote: [ -> ]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.
(30-12-2016, 11:22 PM)Lotus Wrote: [ -> ](29-12-2016, 10:08 PM)Atom Wrote: [ -> ]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.
(30-01-2015, 07:27 PM)Lotus Wrote: [ -> ]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.
(11-06-2016, 10:46 PM)Lotus Wrote: [ -> ]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.
(10-05-2016, 08:14 PM)Lotus Wrote: [ -> ]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]
(28-04-2016, 09:34 PM)Lotus Wrote: [ -> ]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.
(06-02-2016, 01:14 AM)Lotus Wrote: [ -> ]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.
(24-01-2015, 10:47 PM)Lotus Wrote: [ -> ]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#
(13-02-2016, 09:01 PM)Lotus Wrote: [ -> ]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.
(18-08-2015, 07:04 PM)Lotus Wrote: [ -> ]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
(31-01-2015, 10:18 PM)Lotus Wrote: [ -> ]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.
(30-01-2015, 08:20 PM)Lotus Wrote: [ -> ]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.
Kay