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Project X (hrt)

H jannet,

Recent blood showed normal (healthy) ranges, and believe me.....a lot was tested. My thyroid has been an issue though (for a long time actually). So naturally, my immune is always a concern, thus the need to have antioxidants, anti-inflammatories, Vitamins, minerals, etc.

Currently my E2 dosage is at 4mg, as I've shown in the previous post, that's all I take. My doctor has ordered a battery of tests (EKG, blood work, X-ray) all normal as I stated. There's no way I'd risk losing my doc, it took two years to find her. She says stay the course, I say ok,

Now I will say this, the freeT is at 1%, and bioT is 24.5%. E2 levels in my blood is indicative of the SHBG results.

In essence, I'm taking less hormones than before and getting better results, fwiw.
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well if it makes you feel better.. ALL of us here stare at your boobs.Tongue  Because its your avatar Tongue Big Grin
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(19-04-2016, 10:03 PM)Lotus Wrote:  
(13-04-2016, 08:09 PM)spanky Wrote:  Here's an article on some research involving effect of diets high in medium chain fatty acids such as caprylic acid on LDL as compared to diet high in oleic acid.

http://ajcn.nutrition.org/content/79/4/564.full


Spanky,

Oddly enough, while I was at looking MCFA's (caprylic acid and others) I stumbled upon that dutasteride contains medium chained fatty acids, (see below).

Dutasteride, a synthetic 4- azasteroid compound, is an antiandrogen with the chemical name (5a, 17β) -N- [2, 5 bis (trifluoromethyl) phenyl] -3- oxo-4-azaandrost -1-ene- 17- carboxamide. Dutasteride is indicated for the treatment of symptomatic benign prostate hyperplasia (BPH) in men with enlarged prostate glands. Dutasteride, a synthetic 4-azasteroid compound is a selective inhibitor of the type 1 and type 2 isoforms of steroid 5a-reductase, an intracellular enzyme that converts testosterone to 5a-dihydrotestosterone. The empirical formula of Dutasteride is C27H30F6N2O2. Dutasteride is a white to off-white colored powder and stable under ordinary conditions. The melting point is 245°C - 245.5°C.

Dutasteride is soluble in ethanol (44 mg/mL), methanol (64 mg/mL), and polyethylene glycol 400 (3 mg/mL), but it is insoluble in water. Dutasteride has a partition coefficient, Log P = 5.609 ± 0.618.

[0003] Commercially available soft gel capsule formulations (e.g., Avodart®, which is produced by Glaxo Smithkline Pharmaceuticals), is a soft gelatin capsule used in the treatment of BPH, which contains 0.5 mg dutasteride dissolved in a mixture of

mono/diglycerides of caprylic/capric acid (Capmul MCM) (349.5mg) and butylated hydroxytoluene (0.035mg). However, the manufacture of soft gel capsules is a slow and burdensome process, and therefore the manufacture of soft gel capsules is cost intensive and inefficient. [0004] Consequently, there is a need for improved hard gel capsule formulations that reduce manufacturing costs, while maintaining the bioavailability and stability of the soft gel dosage forms.

SUMMARY

[0005] According to one embodiment, a liquid-filled hard gel capsule pharmaceutical formulation is provided. The liquid-filled hard gel capsule formulation comprises a non- emulsified mixture disposed in a hard capsule shell, wherein the non-emulsified mixture comprises about 0.1 to about 5% by weight of at least one active pharmaceutical ingredient, about 50 to about 95% by weight medium chain triglycerides, and about 5 to about 25% by weight medium chain mono/diglycerides, wherein the medium chain triglycerides and medium chain mono/diglycerides are present at a ratio by weight of from about 10: 1 to about 5: 1.

[0006] According to another embodiment, another liquid-filled hard gel capsule pharmaceutical formulation is provided. The liquid- filled hard gel capsule pharmaceutical formulation comprises a non-emulsified mixture disposed in a hard capsule shell, wherein the non-emulsified mixture comprises about 0.1 to about 5% by weight of at least one active pharmaceutical ingredient; about 50 to about 95% by weight long chain triglycerides; and about 5 to about 25% by weight medium chain mono/diglycerides, wherein the long chain triglycerides and medium chain mono/diglycerides are present at a ratio by weight of from about 10: 1 to about 5: 1.

http://www.google.com/patents/WO2013074205A1?cl=en

Caprylic Capric Triglycerides
http://www.ingredientstodiefor.com/item/...rides/464/

Thanks for the find, Lotus. Could it be why some report breast growth as a side effect of dutasteride? In any event, it sounds like not a very large amount of medium chain triglycerides.

Boobs for Peace!
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(19-04-2016, 04:30 PM)christmas Wrote:  Looks like Lotus is the new Cheryl1989 for everybody to aspire to.
Keep it up!

Lol thanks, (and for the encouragement), Wink I think Cheryl is a league of her own no?, definitely a legend though, wonder what she's up to these days?.

Thanks again Xmas, (I'm honored)......hey, making boobies and beauty is no small task, so, all the credit to the gals/guys who are on the hot pursuit to achieve the result, (much respect to all). Tongue


(20-04-2016, 12:16 AM)spanky Wrote:  Thanks for the find, Lotus. Could it be why some report breast growth as a side effect of dutasteride? In any event, it sounds like not a very large amount of medium chain triglycerides.

Boobs for Peace!

Spanky, I believe this to be true. I did dustas for 12 months as you know, I haven't noticed the rebound (motility) they state, I think its permanent imo. You're right about the MCFA's, I do think they're a carrier oil, for which makes the cell diffusion highly bioavailable.

Smile
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(21-04-2016, 06:36 PM)Lotus Wrote:  
(20-04-2016, 12:16 AM)spanky Wrote:  Thanks for the find, Lotus. Could it be why some report breast growth as a side effect of dutasteride? In any event, it sounds like not a very large amount of medium chain triglycerides.

Boobs for Peace!

Spanky, I believe this to be true. I did dustas for 12 months as you know, I haven't noticed the rebound (motility) they state, I think its permanent imo. You're right about the MCFA's, I do think they're a carrier oil, for which makes the cell diffusion highly bioavailable.

Smile

I hope you are referring only to semen motility, and not gastric! I didn't notice it on dutasteride alone, but when combined with EGCg, there was a distinct change in semen. Much clearer, thinner, and less of it. At my age and station in life, I am not so concerned with fertility or motility, unless there is some associated negative side effect I don't know about. One other side effect that may be all in my mind, but I feel like orgasms/ejaculation is slightly less pleasurable than before. While I haven't noticed any gastric changes, I would not want to risk it.
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Speaking of making beauty Rolleyes

Here's some useful workout routines for those who want a more feminine shape:

How to create a more feminine body from a male form
http://www.reneereyes.com/Crossdress%20S...se%20Tips/

Body Feminization Exercises Workout For Transsexuals (should be titled " for a trans-woman (women) no?,
I dunno lol.....whatever , the exercise part starts about half way through if you want to skip the lady talking (though I like the info).
https://m.youtube.com/watch?v=a_BOlHEbHZc

And just for the heck off it: Wink

Lower Testosterone Increase Estrogen Fast! For MTF! Transgender Subliminals Frequencies Hypnosis
https://m.youtube.com/watch?v=AKEYVh2DLNc
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Yes, (sorry spanky) I meant semen motility. In my case, dutas knocked off any production of those little guys, (that doesn't bother at this point in life either).

So, that tells me that inhibiting type I and type II long enough can put sperm motility at risk.........FYI for those who don't want to loose those guys.
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Some important info on adipose (fat).....repost from last year:

(30-12-2015, 05:15 AM)Lotus Wrote:  Hi BN,

A quick thanks to Marcy, Ella, Hannah, Pom , Eloise (omg thanks Big GrinTongue), Wendy, iaboy (no worries, post away), thank you again.........Cool

I keep going back to Leptin and how it can help benefit NBE. Additionally, "adipose" (fat) is also interwoven with a huge endocrine function, number #3 in my book. My apologies for the technical nature of this post, please plod along the best you can, Big Grin if you can grasp some of the basics of this (LEPTIN and adipose) you will undoubtedly be further along on how to adopt it into NBE. I will provide some of the broad strokes, (hopefully). RolleyesTongue may the Boobie Force be with you. Wink

Aromatization of Androgens by Human Abdominal and Breast Fat Tissue
Abstract
The ability of human abdominal, breast and axillary fat to convert androgens into estrogens was investigated by incubating labeled substrates in the presence of NADPH with a variety of cell preparations. The incubation products were subjected to phenolic partition, paper chromatography, methyl-ether formation, repeat chromatography and crystallization with cold carrier reference standards to constant specific activity. Androstenedione was converted to estrone and, to a lesser extent, to 17β-estradiol by crude homogenates, minces, fat-free particulate fractions (1,000–100,000 × g) and isolated fat cells obtained from abdominal, breast or axillary fat. Testosterone was found to be aromatized as actively as androstenedione, but in this case more 17 β-estradiol was formed than estrone. 19-Hydroxyandrostenedione2 also served as substrate, giving results similar to those obtained with androstenedione. Fat tissue obtained from cancerous breasts was found to be as active as normal breast fat (1–4 pg/g fat/90 min) and within the range found for abdominal fat (1–27 pg/g fat/90 min). In each case in which axillary fat was compared to breast fat from the same subject, the activity of the axillary fat was 5 to 10 times higher. The results indicate a possible role of adipose tissue as a significant extra-gonadal source of estrogens.[/b]
- See more at: http://press.endocrine.org/doi/abs/10.12...Mhqtw.dpuf


From the study below:

Several steroidogenic enzymes are expressed in adipose tissue including cytochrome P450-dependent aromatase , 3 -hydroxysteroid dehydrogenase (HSD), 3 HSD, 11 HSD1, 17 HSD, 7 -hydroxylase, 17 -hydroxylase, 5 - reductase, and UDP-glucuronosyltransferase 2B15 (71, 72). Given the mass of adipose tissue, the relative contribution of adipose tissue to whole body steroid metabolism is quite significant, with adipose tissue contributing up to 100% of circulating estrogen in postmenopausal women and 50% of circulating testosterone in premenopausal women.

Although the adrenal gland and gonads serve as the primary source of circulating steroid hormones, adipose tissue expresses a full arsenal of enzymes for activation, interconversion, and inactivation of steroid hormones.
http://www.iub.edu/~k662/articles/obesit...202004.pdf


Adipose Tissue as an Endocrine Organ

Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes, adipose tissue contains connective tissue matrix, nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor-1, proteins of the renin-angiotensin system, and resistin. Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders. This review presents an overview of the endocrine functions of adipose tissue. (J Clin Endocrinol Metab 89: 2548 –2556, 2004)
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The middle paragraph is profound imo, in other words, FAT has a mix of a few androgens, a couple co-regulators of hormones, pro growth hormone (IGF-1/insulin), a couple pro-estrogen factors..........and another regulator of how fat is mobilized (rather metabolized) aka P450 cytochrome family of enzymes. Key word here is mobilizing fat......you know lol, using our fat as an NBE supplement (that's absolutely free). Rolleyes



Several steroidogenic enzymes are expressed in adipose tissue including cytochrome P450-dependent aromatase , 3 -hydroxysteroid dehydrogenase (HSD), 3 HSD, 11 HSD1, 17 HSD, 7 -hydroxylase, 17 -hydroxylase, 5 - reductase, and UDP-glucuronosyltransferase 2B15 (71, 72).

Given the mass of adipose tissue, the relative contribution of adipose tissue to whole body steroid metabolism is quite significant, with adipose tissue contributing up to 100% of circulating estrogen in postmenopausal women and 50% of circulating testosterone in premenopausal women.

Although the adrenal gland and gonads serve as the primary source of circulating steroid hormones, adipose tissue expresses a full arsenal of enzymes for activation, interconversion, and inactivation of steroid hormones.
http://www.iub.edu/~k662/articles/obesit...202004.pdf
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(05-01-2016, 11:09 PM)Lotus Wrote:  I think we have an answer, Green Tea Extract- GTE inhibits prostate cancer by reducing the cell growth and blocks the androgen receptor. Green tea extract need to be @ 60-80% in EGCG polyphenols though. The dosage needs to be determined, recommend use is 2-3 capsules per day, I'm thinking it's slightly more (4-5?) from what this study says. Would this elimante the need for other anti-androgens?, possibly. Soooo- I see a good plan as follows: (though, it's up to you, it won't hurt my feelings). Wink

1-pro-estrogen source
1-pro-aromatase
Green tea extract (imo 4-5 caps per day)
1-growth hormone source
Add the standard healthy fats, exercise, massage, pumping, etc.

Quote: Epigallocatechin-3-gallate EGCG, the major polyphenolic constituent present in green tea, imparts antiproliferative effects against both androgen-sensitive and androgen-insensitive human PCA cells, and this effect is mediated by deregulation in cell cycle and induction of apoptosis. GTE is potent inhibitors of type 1 but not type 2 5α-reductase. (−)Epigallocatechin-3-gallate also inhibits accessory sex gland growth in the rat. These results suggest that certain tea gallates can regulate androgen action in target organs.



Quote: EGCG (green tea) acts as an antagonist of androgen function, similar to the pharmacological inhibitor Casodex, which was used as a control.


So what does this mean?,........it means green tea acts like a pro-pharma class of anti-androgens named Casodex, as in brand name Bicalutamide-aka, a pure antiandrogen used in the treatment of prostate cancer:

Bicalutamide
https://en.m.wikipedia.org/wiki/Casodex

Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer
The present study is one of the first few reports demonstrating the antiandrogenic action of a plant product and the first report showing the effect of EGCG, a naturally occurring polyphenol present in green tea, in inhibiting human prostate carcinoma cell growth. We have shown that EGCG effectively inhibits the transactivation functions and expression of AR by interfering with its stability as a result of decreased interdomain interaction (Fig. 5). We also showed that EGCG is a novel antagonisAR signaling, which can block AR-regulated gene expression and cell growth in human PCa cells. We thus suggest that EGCG could be developed as a chemotherapeutic agent against hormone-refractory PCa.

http://www.fasebj.org/content/25/4/1198.full
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