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Project X (hrt)

(29-01-2021, 05:47 AM)Stevenator_too Wrote:  It’s good to have you back.

Smile  Frank and Gene light as feathers,  Cool

Love it.
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Lotus, we have communicated on a different thread and I greatly appreciate your help there. I have been on PM and SP only a short time. I am at the 1,000 mg dose of PM and 450 SP. Are you recommending that I get off the PM and go to the OTC Estriol/Estradiol cream. with Progesterone cream  and drop the PM and SP? I am 60, diabetic, Low-T and 30 to 40lbs overweght...though I want to drop more like 60. I am not looking for large breasts, but I would like them to look femine. I have moobs as it is LOL but those would likely go away with the weight loss. I would also like some fat redistribution to my hipps and thighs...for a more femmine booty.


I really do not want any Cardiovascular issues. My father had a serious blood clot in his groin and ultimately died of a heart attack. So I am cautious and willing to go slowly.


Therasa

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[Hi Diometres, 

Great questions. In past research (posted in this thread) I've learned there's more progesterone in glandular tissue and more prolactin in fat tissue. True, progesterone can store fat, but it's also catabolic to fat. And this statement seems paradoxical to me but progesterone stimulates ketones in the liver while storing glycogen...say what?. See the study below. I'll have check on progesterone cream studies and get back to you. On the range of progesterone in PC, it can vary for sure. Smokey Mountain I believe is 21mg per pump. Remember, skin absorption and liver metabolism are two of the biggest target tissue for hormone synthesis. PC inhibits DHT on the skin and in the breasts...it's bioidentical to progesterone. It's recommended you change up the location of application to prevent dermal fatigue. Let me know if I missed something. Btw, I like how you format your program thread
(28-06-2016, 12:08 AM)Lotus Wrote:  
" Progesterone stimulates deposition of body fat but had catabolic effects on protein metabolism. Provisional evidence is offered that the steroid may influence ketone body production by the liver as well. When these steroid actions are considered together, their most relevant expression appears to be the physiologic changes observed during normal pregnancy. " 

.......perfect. This tells (suggests) me an additional opportunity for progesterone in breasts. Progesterone stimulates fat deposition in breasts, but is catabolic of protein. Two things come to mind, increasing protein intake prior to progesterone application, and the other is having muscle depletion (isometrics) of breast tissue followed by cold therapy. 



Metabolic effects of progesterone.
Kalkhoff RK. Am J Obstet Gynecol. 1982.
Show full citation
Abstract
Progesterone has important effects on carbohydrate, lipid and protein metabolism. This steroid induced hyperinsulinemia, possibly by direct action on pancreatic islets, while promoting glycogen storage in the liver. Paradoxically, it antagonizes the effects of insulin on glucose metabolism in adipose tissue and skeletal muscle. Progesterone stimulates deposition of body fat but has catabolic effects on protein metabolism. Provisional evidence is offered that the steroid may influence ketone body production by the liver as well. When these steroid actions are considered together, their most relevant expression appears to be the physiologic changes observed during normal pregnancy. 

PIP: 

Parenteral progesterone injections into different mammalian species induce hyperinsulinemia, pancreatic islet hypertrophy, and exaggerated insulin secretion in vitro in response to glucose. The primary effect of progesterone by itself on carbohydrate metabolism appears to be the diversion of glucose utilization away from muscle and fat to other tissues, and the promotion of more storage of glycogen in the liver. On lipid metabolism, the 1 effect of progesterone is to favor storage of depot fat in adipose and breast tissue and to partially reduce the hypertriglyceridemic action of estrogens. On protein metabolism, it has been suggested that progesterone may have a catabolic action in man, and that the basic effects may be a lowering of several plasma amino acids and an increased total urinary nitrogen excretion without an associated aminoaciduria. On ketone body metabolism, progesterone partially suppresses the estrogen effect on liver triglyceride formation while promoting ketogenesis. The metabolic effects of progesterone are most relevant to pregnancy. The hormonal milieu of early to midgestation favors the stimulation of hyperphagia, pancreatic islet hypertrophy, hyperinsulinemia, and body fat and glycogen deposition. This period promotes maternal tissue accretion and weight gain. During the later half of pregnancy, progesterone acts simultaneously with prolactin and other hormones to prepare the breasts for lactation by promoting hyperinsulinemia and fuel storage and by helping to condition the liver in elaborating ketones more promptly to meet the demands of advancing pregnancy.

(11-12-2016, 08:02 PM)Lotus Wrote:  
Big GrinBlush Hi Steve, (and thanks).  

Here's something interesting, the study and (follow up study below) track prolactin production in human breasts tissue indicating adipose (fat tissue) creates more prolactin than glandular tissue. Prolactin in adipose is described as a circulating hormone. Note the 10 fold increase by day 10. So, progesterone lowers PRL and estradiol had no effect in this study.  

In other words, having more fat in your breasts would indicate a higher presence of prolactin, conversely, more glandular would indicate higher progesterone.....in theory (lol, just an opinion). Higher prolactin in men turns off the pituitary signal to make more T, and although estradiol is unaffected (in this study) one should believe it's keeping estradiol low.....aka- no boob growth. So if indeed prolactin is cyclic in nature, (peaks on day 10) the other nine days are optimal growth cycles for breasts......feel free to chime in. 


Prolactin expression and secretion by human breast glandular and adipose tissue explants.
Zinger M1, McFarland M, Ben-Jonathan N.
Author information


Abstract
Prolactin (PRL) is a 23-kDa hormone produced by the pituitary and extrapituitary sites. The main target of PRL is the breast, where it affects cellular growth, differentiation, and milk production. Recent evidence suggests that locally produced PRL plays a role in breast tumorigenesis. Our objective was to examine PRL synthesis/release in different tissues of the human breast and determine the effect of ovarian steroids. Breast tissue, obtained from women undergoing mastectomy or breast reduction, was separated into glandular (nonmalignant) and adipose explants and incubated for 10 d. Conditioned media were analyzed for PRL by a bioassay. PRL release from glandular explants decreased by 60% from d 1-3, followed by a 4-fold increase on d 10. PRL release from adipose explants was unchanged from d 1-3 and increased more than 10-fold by d 10. PRL gene expression, determined by RT-PCR, was low on d 0 and markedly increased on d 10 in both types of explants. De novo synthesis of PRL was confirmed by metabolic labeling. Progesterone suppressed PRL release from glandular explants without affecting adipose explants. Estradiol did not alter PRL release from either tissue. In conclusion, the human breast produces and releases bioactive PRL, with a higher release rate by adipose than glandular tissue. The time-dependent rise in PRL release suggests removal from inhibitory control. Progesterone may be one of the factors that suppresses PRL production in the glandular compartment, whereas the factor(s) that regulate adipose PRL are unknown. These data suggest an autocrine/paracrine role for PRL in human glandular and adipose breast tissue. 

Adv Exp Med Biol. 2015;846:1-35. doi: 10.1007/978-3-319-12114-7_1.
Prolactin (PRL) in adipose tissue: regulation and functions.
Ben-Jonathan N1, Hugo E.
Author information


Abstract
New information concerning the effects of prolactin (PRL) on metabolic processes warrants reevaluation of its overall metabolic actions. PRL affects metabolic homeostasis by regulating key enzymes and transporters associated with glucose and lipid metabolism in several target organs. In the lactating mammary gland, PRL increases the production of milk proteins, lactose, and lipids. In adipose tissue, PRL generally suppresses lipid storage and adipokine release and affects adipogenesis. A specific case is made for PRL in the human breast and adipose tissues, where it acts as a circulating hormone and an autocrine/paracrine factor. Although its overall effects on body composition are both modest and species-specific, PRL may be involved in the manifestation of insulin resistance. 
PMID: 25472532  DOI: 10.1007/978-3-319-12114-7_1

Progestogens and venous thromboembolism in menopausal women: an updated oral versus transdermal estrogen meta-analysis
P-Y Scarabin. Climacteric. 2018 Aug.
Show details

Full-text links
Cite

Abstract
Postmenopausal hormone therapy (HT) is a modifiable risk factor for venous thromboembolism (VTE). While the route of estrogen administration is now well recognized as an important determinant of VTE risk, there is also increasing evidence that progestogens may modulate the estrogen-related VTE risk. This review updates previous meta-analyses of VTE risk in HT users, focusing on the route of estrogen administration, hormonal regimen and progestogen type. Among women using estrogen-only preparations, oral but not transdermal preparations increased VTE risk (relative risk (RR) 1.48, 95% confidence interval (CI) 1.39-1.58; RR 0.97, 95% CI 0.87-1.09, respectively). In women using opposed estrogen, results were highly heterogeneous due to important differences between the molecules of progestogen. In transdermal estrogen users, there was no change in VTE risk in women using micronized progesterone (RR 0.93, 95% CI 0.65-1.33), whereas norpregnane derivatives were associated with increased VTE risk (RR 2.42, 95% CI 1.84-3.18). Among women using opposed oral estrogen, there was higher VTE risk in women using medroxyprogesterone acetate (RR 2.77, 95% CI 2.33-3.30) than in those using other progestins. These clinical findings, together with consistent biological data, emphasize the safety advantage of transdermal estrogen combined with progesterone and support the current evidence-based recommendations on HT, especially in women at high VTE risk.


Quote:
Transdermal E2 is effective at enlarging breasts and increasing feminizing subcutaneous fat, increasing sex hormone-binding globulin (although less than oral E/E2) and thus, decreasing free (active) T. However, transdermal E2 carries less increased risk for venous thromboembolism (VTE)
https://academic.oup.com/jcem/article/10...81/5270376
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Thanks for all the background information, Lotus!  Very informative.  And good to meet you too.


It's just Marshall btw, I was just getting into the myers-briggs personality types at the time I found this site, enfj is one of them.  Both that and exploring whether feminization, which I've been into pretty much all my life, were part of a drive for better health and happiness.


Yeah, you're definitely right about this not being without risks and the T-spikes when starting explains a lot of my experience.  It was initially very encouraging because I felt started feeling really good - horny too - when I started so it felt right for me, but headaches, muscle cramps, and fatigue set in pretty quickly.  That's why I've still been experimenting with what's right for me.


Sorry to pester you, but can you advise me in related question?


My goals are similar to Therasa's.  I want curves, hips, and an ass more than breast development, though I understand that breasts develop first and long before other meaningful fat redistribution.  I would also love a discreet, sensitive chest, and once I started getting some sensations in my chest, I've become more inclined to develop my breasts. It's wild to actually feel growing pains and sensitivity changes, but the negative health impacts, among personal factors, keep preventing me from making any real progress.  I also want to experience general feminization mentally/emotionally to figure if out if I should continue.  I'm 28 y/o, 6'5", ~245, ~29 BMI and don't want to risk permanent organ damage if this isn't for me.


I've recently narrowed down the other daily supplements I like and was going to start another experiment regimen soon when I saw your post:

500-2000mg PM

2000-4000mg White peony

3-10g maca

Green tea replace coffee


I tried saw palmetto but felt awful.  I still want my energy and vitality, so my thinking is to have a relatively low dose of PM, no anti-androgen, and instead promote aromatase to develop rather than dropping T.


At a passing glance, does this make sense?  Am I missing something or doing something stupid?  Finally, would this kind of regimen combine well with the low-risk one you posted?  I'd assume it would.


Thanks again for all the info you've provided already, I also previously have been reading your older posters about what everything is/does. And sorry for asking for like a review of my personal stuff. If this type of thing/goals have been discussed before, can you just point me in that direction?


Cheers

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(29-01-2021, 11:29 PM)Therasa Wrote:  


Lotus, we have communicated on a different thread and I greatly appreciate your help there. I have been on PM and SP only a short time. I am at the 1,000 mg dose of PM and 450 SP. Are you recommending that I get off the PM and go to the OTC Estriol/Estradiol cream. with Progesterone cream  and drop the PM and SP? I am 60, diabetic, Low-T and 30 to 40lbs overweght...though I want to drop more like 60. I am not looking for large breasts, but I would like them to look femine. I have moobs as it is LOL but those would likely go away with the weight loss. I would also like some fat redistribution to my hipps and thighs...for a more femmine booty.


I really do not want any Cardiovascular issues. My father had a serious blood clot in his groin and ultimately died of a heart attack. So I am cautious and willing to go slowly.


Therasa



Hi again Therasa,

Oh cool, we're the same age. Bioidentical hormones such as the creams previously discussed decreases the risk of DVT (does not eliminate the risk though). Do you have a weight loss plan?. I refer to fat redistribution as feminizing fat...because that's what it's doing. Given your risk factors and family history I am concerned about using PM. Has it caused any issues?.
Are you under a doctor's care? and if so have you thought about talking to them?. Apologies for all the questions. 

SP didn't agree with me, in fact I hated it lol. Are you taking metformin, finasteride or other meds?, if so please share. Drug interactions can derail breast growth depending on the medication...or potentiate them. Progesterone inhibits DHT, and breast tissue has androgens (and receptors) in them. Progesterone has a pathway to estradiol from androstenedione via aromatase. 
https://en.m.wikipedia.org/wiki/Steroidogenic_enzyme

I look forward to hearing from you. 
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(30-01-2021, 09:07 PM)Lotus Wrote:  Progesterone has a pathway to estradiol from androstenedione via aromatase. 

I would Progesterone has a pathway to estradiol from androstenedione via aromatase. 
https://en.m.wikipedia.org/wiki/Steroidogenic_enzyme

I thought you said you didn’t understand these stop-sign looking thingy things? 

I need to learn more about this pathway, given my love for, and questions about micronized progesterone. Thank you for your continued research, Lotus.
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(31-01-2021, 01:15 AM)Stevenator_too Wrote:  
(30-01-2021, 09:07 PM)Lotus Wrote:  Progesterone has a pathway to estradiol from androstenedione via aromatase. 

I would Progesterone has a pathway to estradiol from androstenedione via aromatase. 
https://en.m.wikipedia.org/wiki/Steroidogenic_enzyme

I thought you said you didn’t understand these stop-sign looking thingy things? 

I need to learn more about this pathway, given my love for, and questions about micronized progesterone. Thank you for your continued research, Lotus.

Lol, no it's the exact opposite...I understand them all to well.  Big Grin
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(30-01-2021, 06:05 AM)marshallenfj Wrote:  Thanks for all the background information, Lotus!  Very informative.  And good to meet you too.

You're welcome.

(30-01-2021, 06:05 AM)marshallenfj Wrote:  It's just Marshall btw, I was just getting into the myers-briggs personality types at the time I found this site, enfj is one of them.  Both that and exploring whether feminization, which I've been into pretty much all my life, were part of a drive for better health and happiness.

Awesome. Marshall...I love that name.

(30-01-2021, 06:05 AM)marshallenfj Wrote:  Yeah, you're definitely right about this not being without risks and the T-spikes when starting explains a lot of my experience.  It was initially very encouraging because I felt started feeling really good - horny too - when I started so it felt right for me, but headaches, muscle cramps, and fatigue set in pretty quickly.  That's why I've still been experimenting with what's right for me.

Well, now we know why this happens, it's just getting others the information. 

(30-01-2021, 06:05 AM)marshallenfj Wrote:  Sorry to pester you, but can you advise me in related question?
no worries here.


(30-01-2021, 06:05 AM)marshallenfj Wrote:  My goals are similar to Therasa's.  I want curves, hips, and an ass more than breast development, though I understand that breasts develop first and long before other meaningful fat redistribution.  I would also love a discreet, sensitive chest, and once I started getting some sensations in my chest, I've become more inclined to develop my breasts. It's wild to actually feel growing pains and sensitivity changes, but the negative health impacts, among personal factors, keep preventing me from making any real progress.  I also want to experience general feminization mentally/emotionally to figure if out if I should continue.  I'm 28 y/o, 6'5", ~245, ~29 BMI and don't want to risk permanent organ damage if this isn't for me.
that's understandable. 

(30-01-2021, 06:05 AM)marshallenfj Wrote:  I've recently narrowed down the other daily supplements I like and was going to start another experiment regimen soon when I saw your post:

500-2000mg PM

2000-4000mg White peony

3-10g maca

Green tea replace coffee

Green tea is good, it inhibits 5 alpha reductase type I & II, meaning it'll inhibit DHT in hair, prostate and other target tissue. 

(01-10-2020, 04:41 AM)Lotus Wrote:  
(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 needs 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 eliminate 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 a potent inhibitor 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 antagonisT 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



4-5 cups of green tea per day is a bit much, 2 cups per day is reasonable. And btw, EGCG is antiviral.


(30-01-2021, 06:05 AM)marshallenfj Wrote:  I tried to see palmetto but felt awful.  I still want my energy and vitality, so my thinking is to have a relatively low dose of PM, no anti-androgen, and instead promote aromatase to develop rather than dropping T.

Saw palmetto didn't work for me either. In order for aromatase to work testosterone needs to be inhibited, and here Green Tea can inhibit DHT. It doesn't reduce total T, it just blocks the receptors, thus Total T isn't really reduced because nearly all of T isn't really bioactive except 3-5%...and this small fraction is what's known as Free T. Estradiol works the very same way T works, meaning only 3-5% free estradiol is bioactive. This (E2-.estradiol) scenario is rarely talked about, but exists.

(30-01-2021, 06:05 AM)marshallenfj Wrote:  At a passing glance, does this make sense?  Am I missing something or doing something stupid?  Finally, would this kind of regimen combine well with the low-risk one you posted?  I'd assume it would.

It does make sense. The EGCG in green tea (per the study) used less than 1mg of EGCG (aka Epigallocatechin Gallate). I've used decaf green tea with 98% EGCG polyphenols, so I know it works. So, if inhibit  DHT the better chance of feminizing. You can always add a pro-aromatase to help the conversion of T to E. I can give you a list of pro-aromatase items. And there's one final approach to all this is just increasing SHBG (sex hormone binding globulin), that's right, SHBG has the potential to become a estrogen amplifier. I'm going to lay all that out, plus a few other exciting things asap. Oh, what meds do you take?. 


(30-01-2021, 06:05 AM)marshallenfj Wrote:  Thanks again for all the info you've provided already, I also previously have been reading your older posters about what everything is/does. And sorry for asking for a review of my personal stuff. If this type of thing/goals have been discussed before, can you just point me in that direction?
Cheers
.

My pleasure, that's awesome, you'll never know what you'll find in this threads archive unless you read it. Smile
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What are some good sources of progesterone, assuming no doctor to prescribe anything?

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SMOKEY MOUNTAIN NATURALS 


Big Grin
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