[Lotus]

You sure answered my question. We are so fortunate to have such a researcher on our staff- <3 POM

Thanks Pom, I like answers, . What's your opinion about that DHT theory?, I might be missing something here, it's worth a open discussion to find more answers, or like I said, someone with better math skills.

i think it would be ideal that somewhere in the near future of NBE we'd see a breakdown of herbs, e.g.

Time of release (standard/sublingual delivery)
Concentrations for maxium therapeutic effect
Steroid pathway of the particular herb


And of course, charts and graphs, (cause their purdy) I don't think that's too unreasonable expectation right?.

[pom19]

You sure answered my question. We are so fortunate to have such a researcher on our staff- <3 POM

Thanks Pom, I like answers, . What's your opinion about that DHT theory?, I might be missing something here, it's worth a open discussion to find more answers, or like I said, someone with better math skills.

i think it would be ideal that somewhere in the near future of NBE we'd see a breakdown of herbs, e.g.

Time of release (standard/sublingual delivery)
Concentrations for maxium therapeutic effect
Steroid pathway of the particular herb
And of course, charts and graphs, (cause their purdy) I don't think that's too unreasonable expectation right?.

----------------------------------------------------------------------
Nothing is impossible and:

Hope is being able to see that there is light despite all of the darkness. Desmond Tutu

POM

[froger]

What I would want to know is how to limit DHT enough to grow breasts but not enough to lose erections. I know I don't have the answer because so far erections haven't stopped or even slowed for me in the two years since I started. I have had growth and some different fat allocation (hate to say redistribution), but not as much as I think I can achieve. I think I ideally if you can reduce DHT, leave some remain to do what it does, then backdoor convert the rest you may come close to the best of both worlds.

[Lotus]

What I would want to know is how to limit DHT enough to grow breasts but not enough to lose erections. I know I don't have the answer because so far erections haven't stopped or even slowed for me in the two years since I started. I have had growth and some different fat allocation (hate to say redistribution), but not as much as I think I can achieve. I think I ideally if you can reduce DHT, leave some remain to do what it does, then backdoor convert the rest you may come close to the best of both worlds.

Froger,

Option #1

I think we could walk the line with something like Finasteride and 25mg to 50mg of DHEA, androstenedione and DHEA are pro-aromatase. If estradiol is higher taking DHEA will go to aromatase, and whatever T is left over by Finsateride still on the table could get the lobido going. It's possible this action could be applied by reishi?, or using something like EFA's (essential fatty acids) epo or borage, which is about 85% ant DHT.


Option #2

Spiro- Although I'm less certain about this approach, meaning:

*Spiro displaces estrogen from SHBG, which lowers free estrogens
*Blocks tetosterones synthesis
*Binds to estrogen receptors (don't know which one yet)

option #3

cAMP or cyclic adenosine monophosphate is another possible NBE tool. Imo cAMP ties into fatty acids, or in large part how cAMP delivers FA's to hormones. In other words increasing blood flow to the receptors increase their bioavailability. Forilskin comes to mind, but quite honestly I think fatty acids work quite the same way.

cAMP is a second messenger important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.

Yes it's the same response seen from Forskolin-, but I believe there's other options besides forskolin though, which good luck finding the real thing.......to be continued (searching)

[Lotus]

What I would want to know is how to limit DHT enough to grow breasts but not enough to lose erections. I know I don't have the answer because so far erections haven't stopped or even slowed for me in the two years since I started. I have had growth and some different fat allocation (hate to say redistribution), but not as much as I think I can achieve. I think I ideally if you can reduce DHT, leave some remain to do what it does, then backdoor convert the rest you may come close to the best of both worlds.

Froger,

Option #1

I think we could walk the line with something like Finasteride and 25mg to 50mg of DHEA, androstenedione and DHEA are pro-aromatase. If estradiol is higher taking DHEA will go to aromatase, and whatever T is left over by Finsateride still on the table could get the lobido going. It's possible this action could be applied by reishi?, or using something like EFA's (essential fatty acids) epo or borage, which is about 85% ant DHT.


Option #2

Spiro- Although I'm less certain about this approach, meaning:

*Spiro displaces estrogen from SHBG, which lowers free estrogens
*Blocks tetosterones synthesis
*Binds to estrogen receptors (don't know which one yet)

option #3

cAMP or cyclic adenosine monophosphate is another possible NBE tool. Imo cAMP ties into fatty acids, or in large part how cAMP delivers FA's to hormones. In other words increasing blood flow to the receptors increase their bioavailability. Forilskin comes to mind, but quite honestly I think fatty acids work quite the same way.

cAMP is a second messenger important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.

Yes it's the same response seen from Forskolin-, but I believe there's other options besides forskolin though, which good luck finding the real thing.......to be continued (searching)

Sup' BN members,

I think we have more options, we'll call them scientific possibilities at point, because the science is there.

25% of estrogens are synthesized in the testes, however....., testosterone production is a 30:1 ratio over estrogen. So.....when that testosterone production is lowered what happens?, that ratio improves. We can further teak (turn up) that estrogen signal (production), here's how:

high concentrations of FSH-follicle stimulating hormone signal and cyclic AMP (known as) cAMP (cyclic adenosine monophosphate) increase estrogen biosynthesis in the testes.

E1-estrone- the weaker estrogen is synthesis in adipose tissue (breast) by aromatase by way of androstenedione (pathway), this weaker production is similar to what PM does, IMO it isn't enough.

Concerning DHT, that fact is no matter what we do or try they'll be DHT production somewhere (adrenal DHT shows up even after castration).

I made this point before, I think if DHT shows up, we force it to ER-beta and deactivate it. In other words, and it seems crazy to even suggest this, but.......if we give DHT a "free pass" to protien synthesis, we force its immediate exvacuatioin to estrogen receptor beta, we might be tipping the scales. At least that's the indication of what happens in the testes, we're just helping it along faster.

a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

[/quote]

[Railgun]

Hi Lotus,

sorry to intrude your thread. I hope you don't mind that i wanted to ask you three things.

1. Do you know of any herbs or supplements that might be benefitial to take with a synthetic HRT (DIY)?

* 200mg Spironolactone (100mg in the morning, 100mg in the evening; always directly after a meal - since it should improve spiro's effectiveness)
* 4mg Estradiol Hemihydrate (sublingually; 2mg mornings, 2mg evening)
* 5mg Finasteride (Proscar) (1x mornings; on empty stomach)

i'm already taking these supplements
* 2000mg fishoil (~ 700mg omega-3; 240mg DHA; 360mg EPA) - 1000mg mornings; 1000mg evening
* 1000IU/25mcg Vitamin D-3 (mornings)
* 50mg Iron; 120mg Vitamin C; 300mg Magnesium; 1.4mg Vitamin B1/B2; 1.4mg Vitamin B6/B12; 50ug Biotin; 200ug folic acid; 16mg niacin; 12mg Vitamin E; 9mg beta-carotin (all midday)

I regained my libido after 3 month (currently at 6) with this regimen. So i guess my testosterone might still be too high, but the earliest date i can check my levels is in august. My chest is still way below an european A-Cup (i'm at 8cm/3.15in difference to underbust), while my female relatives all have full C or Ds.
My weight currently is at 76kg (167.55) and didn't change the last 6 months. I'm 192cm (6.4'') tall.

2. Is there a specific reason you take 600mg of calcium every day?
I'm currently avoiding it since it interacts with L-Thyroxin (which i take due to my thyroid hypofunction).

3. According to this site: http://www.poliquingroup.com/articlesmul...load_.aspx @ 6) "Improve Estrogen Metabolism By Promoting the C-2 Pathway" it says that
"The C-2 pathway produces very weak estrogenic activity and is termed “good” estrogen. In contrast, the C-16 pathway produces robust estrogenic activity and promotes tissue damage that leads to cancer.

Key nutrients for supporting the C-2 pathway are EPA fish oils, phytoestrogens, and of special importance, B vitamins and a substance called DIM. The B vitamins, particularly B6, B12, and folic acid promote the C-2 pathway. B6 is also known to decrease gene activity once estrogen is bound to a receptor, meaning this vitamin can inhibit cell damage and cancer development."

so if i guess correctly promoting the C-2 pathway for a transsexual like me might be contra-productive. On the other hand i'm taking my estrogens sublingually, so most of it should go directly to the bloodstream and not through the metabolization pathway, so i don't have to cut down my vitamin intake, correct?
Vitamin B6 on the other hand sounds awful, but 1,4mg usually shouldn't matter against the pure quantity of 4mg estradiol.
Am i overseeing something?


I'm again sorry to intrude, but i've been lurking this forum for about 3 years now and you're the person with the most knowledge about the endocrine system and alternative feminization regimes (non-synthetic) i know of. ^.^;

kind regards
Anna

[Lotus]

Hi Lotus,

sorry to intrude your thread. I hope you don't mind that i wanted to ask you three things.

Hi Railgun, (either your ex-military type or you like blowing stuff up for the helluva it, lol),

Let me first just say this, (my own personal opinion), there's a medium ground between NBE/HrT, and some may say it's a cardinal sin to cross the proverbial boundaries, in my mind, not so anymore. Honestly, it's splitting hairs, I've seen enough and posted enough research (check it all) to see both sides of the pros/cons. What both sides miss is not more ER stimulation, but more gene expression. Look, you can stimulate estrogen receptors all day long and still not gain an advantage. In other words, some E2 will make it past the cell membrane surface into the cytoplasm and "not" move into the nucleus for nuclear binding, it's either not the right fit or its degraded, protein expression is lost. For instance, some Xenoestrogens bind to receptors are cause damage (cancers, over expression, aka-estro dominance). Improving the bioavailability of both is a good strategy. I've reported that EFA's are a carrier protein, in particular palmitate (also in skin application, estrogen receptors are favorable using a carrier, [palmitoleic]). Sorry if this gets technical here, intracellular cAMP production and the promoter-specific expression of mRNA coding for CYP19 equals aromatase, aka-gene expression.

That's part of what limits both productions, plus we don't include enough E1/E2 in the presence of progesterone. You will find it rare that anyone suggests the dual expression on a regular basis, oh sure progestin is prescribed with HrT, IMO it has to be bio-identical, and some Hrt programs already have it. However, it should be applied to the breasts, e.g. applying PM or E2 gel w/paraben free bio-identical PC, I'd even go a step further and say add coconut oil to this procedure.

One other thing I see as a possibility is forcing DHT into ER-b, in other words deactivate DHT. I think I shared that discussion (hypothesis) on the anti-androgen page. Also, nitric oxide synthase modulates lipolysis in adipocyte (builds breast tissue).

I've hijacked my own thread, sorry Railgun, I do have some suggestions on herbs for Hrt, I'll get to it in a minute, RL is calling.

[Lotus]

Hi Lotus,
1. Do you know of any herbs or supplements that might be benefitial to take with a synthetic HRT (DIY)?

1 cup of green tea daily
2 hard boiled eggs (organic) for the luecine content, helps estrogen receptor alpha.
1 cucumber (organic, if possible), skin peeled and w/pepper (aromatase, and 5 ar)
You can put the coconut oil (organic) on the eggs,

These all help synthesize estrogen better.



L-Lysine: While L-Lysine is NOT a DHT blocker, it may make DHT blockers more effective. Researchers have found that adding a supplementation of L-Lysine can make drugs like Propecia more effective. Since propecia is a DHT inhibitor, as all the natural products mentioned here, the addition of a L-Lysine supplement can make these products also more effective. Studies has shown that L-Lysine combined with a DHT inhibitor can for example promote hair growth in people suffering from androgenetic alopecia.

Essential Fatty Acids
In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546

Evening Primrose Oil- massage, Fibrocystic breast pain, treats hot flashes, relieves PMS symptoms, relieves Eczema, hormone balance, fights breast tumors and diabetes. Reports have GLA-Gamma-Linolenic Acid as helping with RA and arthritis, diabetic neuropathy, ADHD and CFS (chronic fatigue syndrome). And UPDATED to include it being an inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to DHT, (DHT is bad for BOOB GROWTH).

Coconut Oil- Makes connective tissues stronger, superb antioxidant, neutralizes free radicals and slowing down aging, aids in breast feeding, nature's richest source of MCFAs. 5 ar inhibitor, aromatase

[Lotus]

Hi Lotus,

1. Do you know of any herbs or supplements that might be benefitial to take with a synthetic HRT (DIY)?

i'm already taking these supplements
* 2000mg fishoil (~ 700mg omega-3; 240mg DHA; 360mg EPA) - 1000mg mornings; 1000mg evening
* 1000IU/25mcg Vitamin D-3 (mornings)
* 50mg Iron; 120mg Vitamin C; 300mg Magnesium; 1.4mg Vitamin B1/B2; 1.4mg Vitamin B6/B12; 50ug Biotin; 200ug folic acid; 16mg niacin; 12mg Vitamin E; 9mg beta-carotin (all midday)

Ok, good coverage there,

I regained my libido after 3 month (currently at 6) with this regimen.

Interesting, probably from the Finasteride.

So i guess my testosterone might still be too high, but the earliest date i can check my levels is in august.

Possibly, it takes a while before Finas (3-6 months) and spiro kick in.

My chest is still way below an european A-Cup (i'm at 8cm/3.15in difference to underbust), while my female relatives all have full C or Ds.

That's encouraging.

My weight currently is at 76kg (167.55) and didn't change the last 6 months. I'm 192cm (6.4'') tall.

That's cool, plenty of tall girls here at BN.

2. Is there a specific reason you take 600mg of calcium every day?
I'm currently avoiding it since it interacts with L-Thyroxin (which i take due to my thyroid hypofunction).

Given your height/weight and assume low bmi, your metabolism is most likely efficient at eliminating E. And that's in part with the addition of dim.

Long term use of PM was a concern in this animal study of the parathyroid,
1,000 mg/day decreased serum parathyroid hormone and calcium levels
http://www.drugs.com/npp/pueraria.html#ref40

https://www.jstage.jst.go.jp/article/jrd...9/_article

[Lotus]

3. According to this site: http://www.poliquingroup.com/articlesmul...load_.aspx @ 6) "Improve Estrogen Metabolism By Promoting the C-2 Pathway" it says that
"The C-2 pathway produces very weak estrogenic activity and is termed “good” estrogen. In contrast, the C-16 pathway produces robust estrogenic activity and promotes tissue damage that leads to cancer.

Key nutrients for supporting the C-2 pathway are EPA fish oils, phytoestrogens, and of special importance, B vitamins and a substance called DIM. The B vitamins, particularly B6, B12, and folic acid promote the C-2 pathway.

This is true, exercise, hydration and reducing stress and inflammation are absolutes too.

DIM is Diindolylmethane. It is an anticarcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, although the atomic compositions of the two substances are quite different. Taken together with our published reports of the estrogen agonist activities of DIM, the present results establish DIM as a unique bifunctional hormone disrupter. To our knowledge, DIM is the first example of a pure androgen receptor antagonist from plants.
http://www.jbc.org/content/278/23/21136.full

B6 is also known to decrease gene activity once estrogen is bound to a receptor, meaning this vitamin can inhibit cell damage and cancer development."

Please point this out in related research. Reducing xenoestrogens from our daily life can prevent cell damage, go organic, stop using plastic (yeah, right lol).

so if i guess correctly promoting the C-2 pathway for a transsexual like me might be contra-productive. On the other hand i'm taking my estrogens sublingually, so most of it should go directly to the bloodstream and not through the metabolization pathway, so i don't have to cut down my vitamin intake, correct?
Vitamin B6 on the other hand sounds awful, but 1,4mg usually shouldn't matter against the pure quantity of 4mg estradiol.
Am i overseeing something?

I think you're missing progesterone. Don't go with synthetic progestin, instead choose bio-identical paraben free progesterone.

I'm again sorry to intrude, but i've been lurking this forum for about 3 years now and you're the person with the most knowledge about the endocrine system and alternative feminization regimes (non-synthetic) i know of. ^.^;

kind regards
Anna

I dunno bout that, , we have plenty of people who know what's up, I just post a lot.


If your gonna do DIY lets talk about it, granted, we all know it's not the recommended way, everybody condones it, you assume the risk. Hopefully you know about the dangers of buying overseas meds and the health risks involved. Ok then..........

Sublingual delivery reduces the risk of hepatic injury, DVT and other vascular conditions, (doesn't eliminate mind you).

Risk factors for venous and arterial thrombosis
http://www.ncbi.nlm.nih.gov/pmc/articles...09-120.pdf


* 4mg Estradiol Hemihydrate (sublingually; 2mg mornings, 2mg evening)

The binding rate of E2 isn't as strong as people think, but sublingual E2 inside of an hour has a 26 fold increase and 9 fold increase of E1. It's also noted that E2 continued to circulate 2.5 fold during the week of the trail, suggesting that E2 will still be active for at least a week..

Sublingual absorption of micronized 17beta-estradiol

Abstract
The sublingual absorption rates, the sustained effects, te biologic activity, and the metabolism of micronized 17beta-estradiol (E2) were measured in 10 postmenopausal women. E2 (0.5 mg) was administered in a single sublingual dose to five of the patients. An alternate-day schedule with the same dosage was used for the other five patients. In the single-dose study, a twenty-six fold increase in serum E2 and a ninefold increase in serum estrone (E1) concentrations were observed 1 hour after the sublingual deposition of E2 (0.5 mg). Serum concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were significantly decreased within 6 hours. The rise in E2 was early and peaked in the first 2 hours. The rise in E1 was slower and progressive, reaching its maximum thirteenfold increase at 4 hours, and remained two and one half times the baseline of 29 pg/ml at 24 hours, whereas E2 returned to the baseline level of 24 pg/ml. When micronized E2 was given in a dosage of 0.5 mg sublingually every other night, increased circulating levels of estrogens continued to be elevated at a minimum two and one-half fold baseline level for the week of study.
PMID 6786097 [PubMed - indexed for MEDLINE]

________________________

* 5mg Finasteride (Proscar) (1x mornings; on empty stomach)

I'd split Finasteride into two doses, Finasteride's half life is about 4-5 hours.

Finasteride modestly increases serum testosterone (T), estrone (E1), and estradiol (E2). Aka-it increases libido, acne, and oily skin, just FYI, or be on the look out, lol. I have Finasteride as a slight aromatase modifier, 22%.

finasteride blocks the conversion of testosterone to dihydrotestosterone (DHT) and of androstenedione to 5α-androstanedione-3,17-dione, which also leads to the reduction of DHT.

I'll pick this up tomorrow, phew, that was a big list though, I'm still not done yet, I'm tired. have a good night.