[The First Aria]

I understand what inactivate means, but I am no chemist. Which, if any, herb or supplement will do this w/out running serious risk?

[BestBreasts]

Hi 34,

EPO should've given you swelling, help elimate DHT and help synthesize aromatase. Biotin will also help with FAS (fatty acid synthase). Omega 3's will help reduce inflammation, if you've got too much omega 6's you'll see (or get) unnecessary inflammatory response. Too much PGE2 (prostaglandin) in response from inflammation pushes this response ratio, in other words.....stop growth potential.

Imo balance the omegas, (stop the EPO for 2 weeks) add in omega 3 (chia seeds) 2-3 grams daily. After 2 weeks add coconut oil, 1-2 tablespoons daily. Drop the PSO, there's enough 5 ar inhibitor in EPO once you add it back.

I think you have the right components, it's just missing a few essentials, (e.g. growth hormone). Here's what I mean:

Effects of growth hormone on adipose tissue.

Abstract
Physiological effects of growth hormone (GH) extend beyond the stimulation of linear growth. These include important metabolic effects upon adipose tissue. GH affects both proliferation and differentiation of preadipocytes, although this varies between clonal cell lines and preadipocyte cultures. Both preadipocytes and mature adipocytes possess specific GH receptors. GH may mediate its actions via these receptors, but some effects are indirectly mediated through the GH-mediated secretion of insulin-like growth factor-I (IGF-I) within adipose tissue. GH promotes lipolysis via inhibition of lipoprotein lipase, which hydrolyzes triglycerides in the circulation to make them available for triglyceride accumulation in adipose tissue. GH also stimulates hormone sensitive lipase (HSL), the rate-limiting step for release of stored triglyceride in adipocytes (lipolysis). As GH becomes utilized for various "non-growth" concerns (see Figure 1), awareness of the metabolic effects on adipocytes is important to understand the clinical effects seen with GH therapy.
http://www.ncbi.nlm.nih.gov/pubmed/11086655

_______________________

This website below gives an excellent summary on how to go about proceeding:

Stimulating the Body’s Production of Human Growth Hormone
http://www.bodybuildingforyou.com/articl...uction.htm

I'll post other info on inducible nitric oxide synthase, and how it modulates lipolysis in adipocytes (The basis for building breast tissue), really interesting stuff.
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iaboy and gamer, what's (a) the simple explanation of inactivating DHT?, (i dunno) picture a free loading uncle named DHT, hey lol, work with me! .....all he does is sponge off you...eats you out of house and home.......solution.....drop kick his ass to the curb while he's sleeping...(oh yeah!!, you forgot to tell him it's also trash day).

Now he's......I-N-A-C-T-I-V-E (sorry, it's the best I got today).

Thank you oh so very much for responding Lotus!!!!! xoxox

I will stop the PSO altogether, and go on a break w/ EPO, and switch over to chia seeds & coconut oil like you said!!

I do work out on a consistent basis, get my veggies and sleep like that article said for the Growth Hormone....not sure if there is a vitamin/supplement that will help.... i'll just start PM again in a couple of months ..seems like the best GH lol (=

thanks again!!! <3

[Lotus]

Here's some interesting research about Finasteride. The ironic part was that I found the commentary after this particular statement peaked my interest after investigating the study.

"When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels."

Testosterone down-regulates the levels of androgen receptor mRNA in smooth muscle cells from the rat corpora cavernosa via aromatization to estrogens.

Lin MC, Rajfer J, Swerdloff RS, Gonzalez-Cadavid NF.

Department of Surgery, UCLA School of Medicine, Torrance 90509.

Androgens down-regulate the levels of androgen receptors (AR) and AR mRNA in the penis and prostate of castrated rats, and are assumed to cause their decrease during sexual maturation in the penile smooth muscle of intact rats. In order to determine whether these effects occur directly at the target cell level, and to what extent they are due to testosterone (T) or to their metabolites, we have measured AR mRNA in cultures of smooth muscle cells from the adult rat corpora cavernosa treated in vitro with sex steroids. T at high concentrations (100 nM) acted like dihydrotestosterone (DHT) in increasing moderately the levels of AR mRNA in both proliferating and contact-inhibited cells. However, when conversion of T to DHT was blocked by the 5-alpha reductase inhibitor finasteride, the levels of AR mRNA were considerably down-regulated by T (10-500 nM), particularly in the contact-inhibited cells. Finasteride by itself was inactive. These effects in both types of cultures were inhibited by platelet derived growth factor (PDGF) (20 ng/ml), a growth factor that up-regulates AR mRNA levels, and by fadrozole (100 nM), an aromatase inhibitor of the T/estrogen conversion. Estradiol (50 nM) was even more potent than T in decreasing AR mRNA levels. With the exception of PDGF none of the treatments affected significantly cell growth, as measured by DNA synthesis and content. Our results indicate that it is possible to modulate in vitro AR mRNA levels in the penile smooth muscle cells, and that under normal conditions DHT and T act as moderate up-regulators. When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels. We assume that the in vivo AR down-regulation in the penile smooth muscle by androgens is an indirect effect mediated by a paracrine or endocrine mechanism elicited in another tissue.
PMID: 8499343 [PubMed - indexed for MEDLINE]

-Using finasteride will block conversion of testosterone to DHT
-Using finasteride will increase testosterone(temporary I believe) and estradiol levels
-increase in Estradiol and Testosterone(?) down regulate AR mRNA
-the low DHT level caused by using finasteride, which blocks the conversion of testosterone to DHT, will prevent the increase of AR mRNA in both proliferating and contact-inhibited cells.

So there are some problems with finasteride:

1)low DHT which prevents the increase AR mRNA due to DHT. Does this mean that androgen receptors can't increase, that DHT can't bind to AR?

2)high estradiol due to testosterone not being converted to DHT because of finasteride, but being aromitized to estradiol which down regulates AR mRNA. What does this mean exactly? Less androgen receptors?

3)finasteride blocks conversion of testosterone to DHT. DHT is important for maintaining NOS(nitric oxide/vasodilation if I am correct) activity in the penile corpus cavernosum.

Furthermore I remember reading somewhere that DHT is also antiestrogenic. DHT can compete with estrogen for the same receptor. Also that the ratio of androgens to estrogen is very important.

So by using finasteride which blocks conversion of T to DHT which makes estradiol levels increase we are changing the ratio of androgens to estrogen causing gynecomastia.

http://www.hairlosstalk.com/interact/sho...and-Dr-Lin

I like the lively conversations from the hair-loss forum

[spanky]

I recently took note of warnings about 5 alpha reductase inhibitors possibly being associated with more aggressive prostate cancers.

http://www.drugs.com/fda/5-alpha-reducta...12977.html

Has there been further research to counter the warnings? I have been faithfully taking reishi for many months, but maybe there are risks that I should be taking into account.

[Lotus]

I recently took note of warnings about 5 alpha reductase inhibitors possibly being associated with more aggressive prostate cancers.

http://www.drugs.com/fda/5-alpha-reducta...12977.html

Has there been further research to counter the warnings? I have been faithfully taking reishi for many months, but maybe there are risks that I should be taking into account.

Hi Spanky, I did some checking, the main point would be to monitor your health with a PCP and get regular PSA screenings while on 5 ar therapy. There are other therapies discussed besides using 5 ar inhibitors, Reishi is an herbal remedy that's been used for a long time (ancient), and of course other herbals like SP, green tea, etc.

Questions and Answers: 5-alpha reductase inhibitors (5-ARIs) may increase the risk of a more serious form of prostate cancer

On June 9, 2011, the U.S. Food and Drug Administration (FDA) informed the public of new safety information for drugs called 5-alpha reductase inhibitors (5-ARIs). Men who take these drugs may have an increased risk of being diagnosed with a more serious form of prostate cancer (high-grade prostate cancer). The Warnings and Precautions section of the labels for all FDA-approved 5-ARIs have been revised to include information about this risk.
The following questions and answers address potential issues raised by this safety information.
Q1. What are 5-alpha reductase inhibitors (5-ARIs)?
Q2. What is high-grade prostate cancer?
Q3. Why have the labels of all 5-alpha reductase inhibitors (5-ARIs) been revised?
Q4. What data are available on this safety issue?
Q5. Why is the labeling of Propecia being changed when this drug was not included in either study?
Q6. Does FDA believe the benefits of 5-alpha reductase inhibitors (5-ARIs) still outweigh their risks for the approved indications?
Q7. What should men do if they are currently taking 5-alpha reductase inhibitors (5-ARIs)?
Q8. How should men taking 5-alpha reductase inhibitors (5-ARIs) be screened for prostate cancer?
Q9. Are there other medications to treat benign prostatic hyperplasia (BPH) or male pattern baldness?

http://www.fda.gov/Drugs/DrugSafety/ucm258358.htm



Hyperplasia Medications Do Not Increase Mortality In Men With Prostate Can

http://www.healthylivingmagazine.us/Articles/9107/

Dr. William D. Figg, from the National Cancer Institute, Bethesda, Maryland, and Dr. Ian M. Thompson, from the University of Texas Health Science Center at San Antonio, Texas wrote a commentary related to this report. Dr. Figg told Reuters Health by email, "These data should ease the concern of some urologists who have patients that need a 5-ARI, that it is safe to prescribe and that those patients are not at an increased risk of developing high-grade aggressive types of prostate cancer."

"I think the FDA should clearly re-evaluate the warning '5-alpha reductase inhibitor may increase the risk of a more serious form of prostate cancer' (Here: http://1.usa.gov/1yNWbgG), " Dr. Figg said.

Utility of 5-alpha-reductase inhibitors in active surveillance for favourable risk prostate cancer
http://www.ncbi.nlm.nih.gov/pmc/articles...12-450.pdf


American Urological Association Symptom Index - Topic Overview
http://www.webmd.com/urinary-incontinenc...c-overview

It's a interactive questionnaire that can help you determine how bad your urinary symptoms are and check how well your treatment is working.

________________________________

Serum estrogen levels and prostate cancer risk in the prostate cancer prevention trial: a nested case–control study
http://www.ncbi.nlm.nih.gov/pmc/articles...e_9787.pdf

[spanky]

Thanks, Lotus. I appreciate the research.

The comments of Drs. Figg and Thompson are partuclarly encouraging. I used to get PSA tests done every year or two, but after all of the jawboning done in favor of "watchful waiting" rather than aggressive monitoring and treatment, I discovered that the my doctors is less favorably disposed to testing. Perhaps they are influenced by health care insurers who are less inclined to pay for testing if there is not a clear treatment path that the medical community agrees upon.

I think I will continue to take my reishi, drink my green tea, and cross my fingers.

[Lotus]

Thanks, Lotus. I appreciate the research.

The comments of Drs. Figg and Thompson are partuclarly encouraging. I used to get PSA tests done every year or two, but after all of the jawboning done in favor of "watchful waiting" rather than aggressive monitoring and treatment, I discovered that the my doctors is less favorably disposed to testing. Perhaps they are influenced by health care insurers who are less inclined to pay for testing if there is not a clear treatment path that the medical community agrees upon.

I think I will continue to take my reishi, drink my green tea, and cross my fingers.

Yup, I agree. And healthy humans don't turn a profit in the "for profit" money market..

[spanky]

Forgive me if this link has been posted before. It provides some interesting information about a protocol involving both white peony (Paeonia lactiflora) and chasteberry (Vitex agnus-castus), including its effect on androgen levels.

http://www.promedics.ca/site/downloads/P...20PCOS.pdf

[Lotus]

Forgive me if this link has been posted before. It provides some interesting information about a protocol involving both white peony (Paeonia lactiflora) and chasteberry (Vitex agnus-castus), including its effect on androgen levels.

http://www.promedics.ca/site/downloads/P...20PCOS.pdf

Great find spanky,

I'd say it's in-line with what we've been saying about having WP, Vitex in NBE programs, thanks.

[Trixy]

Would anyone be willing to do a bit of a summary on the most noteworthy anti-androgens, their primary effects, important side effects and (roughly) recommended safe doses? A kind of pros vs cons for some of the more common AAs would be awesome.

I get that I could probably scrape this sort of information by reading through this thread, but seriously, it's 71 pages... I'd be grateful if someone who's been following this thread (or has knowledge on natural AAs from elsewhere) would write a kind of overview, or if such an overview already exists then direct me to it. Thanks in advance. <3