Common Cures and treatments for Gyno

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No I think swagger jacker is more fitting, look it up on YouTube. It's by Cameron.
Just listened to it :) regarding that, I had mentioned in the very first post after the first correction that I spread the information (or, spread the correction I should say) but I assumed Austinite didn't want every prohormone starter seeking him out for advice, I know I myself get tired of the PM's sometimes... of course I don't mind helping where I can, but sometimes peace too is good. What I'm getting at is I assumed he preferred anonymity, since he didn't mention anything. But I've since then cited the works, so there's no issue. The only reason I made these "threads" or informative tid-bits in the first place is to clear out my own PM box on these forums, as well as contribute the knowledge, this way everyone knows what I know and doesn't have to ask me for every tiny detail.

Not justifying my actions; I've learned from my mistakes, simply explaining what truly is the case
 
Lol. Not sensitive at all, funny mostly. But, it's pretty disheartening when conversing with someone who admittedly does not draw for panels, unable to verify legitimacy of compounds and doesn't grasp the journey through metabolic pathways. I get diagnosed with sensitive. You have to admit its pretty funny. Makes you wonder why multiple urologists never diagnosed me as such. Doesn't it?

The best part of all this is that you said you collected all your info from forums. (A prohormone forum) but you never thought to actually research any of the info until you met someone who knows a little about this stuff. I saw the other forums and I understand that you're used to getting a pat on the back from members who don't question anything.

Anywho... I'm always happy to fact check, I have a strong background you'll be able to reference soon. I only ask that in your ventures, try to play devils advocate properly, as being objective for the sake of being objective gets redundantly silly. :)

I'm sorry brother, please excuse the ignorance, I truly did enjoy the discussion and thanks again for sharing your knowledge and viewpoints
 
and information/data supplied by you (however without proper acknowledgment) that foaster great debate and education.
Just to clarify, this information/data that's supplied by me (the actual written out parts) are all parts I wrote out of my own insight and experience, minus the videos and the links that I provided, and the stuff that I actually quoted.... so the article on expectation, and the little tid-bit on muscle mass retention, and the original OP (tho, obviously I had help from 2 forums and months of experience and answering questions before I decided to tackle explaining all this stuff) is just own insight from what I learned from around the whole block so far

To me personally, I don't care if it's cited, copied, or spread to every part of the world without citing "biggiesmallz"... because that's just a fictional internet name to me anyway, the essential point for me is that the proper understanding gets to where it's needed, not that my name is tagged to something I said or wrote, so maybe that's where we're having the rub. In any case happy to be here and glad to contribute what I can, will certainly cite the stuff that's not mine, and if I simply don't know the source from which it originated will gladly point that out as well
 
DO serms not often posses agonist and antagonist estrogenic activity? The agonist effects desireable and the antagonist not? Hmmm

Jimi, just for clarification, what exactly did you mean by this, in what ways are they agonists and in what ways are they antagonists (before I go spouting off crap and misusing information again:) )? Thanks brother

given;
agonist = binds with and interacts with the receptor. estrogen is an estrogen receptor agonist.

antagonist= binds with, and has limited to zero interaction with the receptor. serms are a estrogen receptor antagonist.
 
Jimi, just for clarification, what exactly did you mean by this, in what ways are they agonists and in what ways are they antagonists (before I go spouting off crap and misusing information again:) )? Thanks brother

given;

Agonist binds and exerts estrognic effects (to varying degrees-which is key) , Antagonist essentially "blocks"e receptor in the case of serms. They do both selectively. IE: they block recptor in brests tissue - awesome for gyno. They can exert SMALL e effects in bone in some cases - e is essential ffor bone mineral density etc. Its a fine line however suffice it to say crashing e2 is imprudeet and necessary to cure gyno IN 99.9% of all cases if you try to use an Aromatase inhibitor (AI). A serm is def the best option. Raloxifene binds to e receptor in brest tissue strongerr than any other serm, followed by tamox and closely by toermifen. Making them the clear cut choice for gyno reversal, clearly the safest and most prudent.
 
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My understanding;
Maybe Jimi had it backwards (the agonist and antagonist bit) which is where the confusion is;

As an antagonist, which is the desireable function, SERMs bind to and block the interaction of estrogen receptors with estrogen, which is how we prevent/reverse gyno formations with SERM treatment.

But as an agonist, (albeit indirectly) they stimulate HPTA production to test production, which leads to more test aromatizing to estrogen, so indirectly raising circulating estrogen, which would be the undesirable effect for the purposes of gyno treatment (and hence the suggestion to regulate this with mild Aromatase inhibitor (AI) use where needed)

Right? thanks (or am I not understanding this properly?)
DO serms not often posses agonist and antagonist estrogenic activity? The agonist effects desireable and the antagonist not? Hmmm
 
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either with a serm, or an Aromatase inhibitor (AI), you are going to have estrogen rebound, it is inevitable from the hormonal disruption you are causing in your body.

one could either use a serm post Aromatase inhibitor (AI) to prevent estrogen rebound sides
Which goes in accord with Austinite's suggestion of using Aromatase inhibitor (AI) on cycle for preventive measure if needed, and then just following up with a SERM PCT

or a Aromatase inhibitor (AI) post serm in an attempt to control estrogen an level things off.

dr mike scally doesn't recommend the use of an aromatase inhibitor (last I checked) in his power pct plan, an he is a expert in this field.
Which goes in accord with my suggestion of using a mild Aromatase inhibitor (AI) (even something like 6-oxo should work, or low-dosed aromasin) post-SERM treatment where needed (which can only really be varified by bloodwork) in an attempt to stabilize estrogen balance from any SERM-induced raise in circulating estrogen, where applicable.

So, no one's wrong or right, seemingly it's just different approaches at the same issue. Thanks for all of your guys' input, much appreciated
 
Agonist binds and exerts estrognic effects (to varying degrees-which is key) , Antagonist essentially "blocks"e receptor in the case of serms. They do both selectively. IE: they block recptor in brests tissue - awesome for gyno. They can exert SMALL e effects in bone in some cases - e is essential ffor bone mineral density etc. Its a fine line however suffice it to say crashing e2 is imprudeet and necessary to cure gyno IN 99.9% of all cases if you try to use an Aromatase inhibitor (AI). A serm is def the best option. Raloxifene binds to e receptor in brest tissue strongerr than any other serm, followed by tamox and closely by toermifen. Making them the clear cut choice for gyno reversal, clearly the safest and most prudent.

Yes in my first post i can see where I mixed it up by not fully expalining, in my follow up above it is right on the money. HOWEVER some agonist effects are good. like with clomid in pct my friend. It takes YEARS to understand this. I respect your quest for knowledge but perhaps read more type just a little less till a complete grasp is at hand. None the less the agonist effects are not all bad. Good discussion.
 
Yes in my first post i can see where I mixed it up by not fully expalining, in my follow up above it is right on the money. HOWEVER some agonist effects are good. like with clomid in pct my friend. It takes YEARS to understand this. I respect your quest for knowledge but perhaps read more type just a little less till a complete grasp is at hand. None the less the agonist effects are not all bad. Good discussion.

Thanks brother, I understand that I will probably never understand the full intricacies and full ins and outs of all of this hormonal signaling, I just wanna take some drugs, grow a little, repair some physical damage, preferably safely and side-effect free or as limited as I can get it, and move on my way; no desire to be a steroid scholar but it does take some relatively complex understanding just to even attempt a successful cycle.

 
I did mean to ask tho; I've noticed a lot of people claim clomid gives them a high level of emotional moodiness in a lot of cases... now I'm wondering; is this related to it's agonist effect on estrogen (the indirect rise of circulating E)?? So, would taking a mild Aromatase inhibitor (AI) get rid of this emotional moodiness sensitivity? Or is that just a characteristic of clomid use? Any thoughts would be highly appreciated, thanks
 
I did mean to ask tho; I've noticed a lot of people claim clomid gives them a high level of emotional moodiness in a lot of cases... now I'm wondering; is this related to it's agonist effect on estrogen (the indirect rise of circulating E)?? So, would taking a mild Aromatase inhibitor (AI) get rid of this emotional moodiness sensitivity? Or is that just a characteristic of clomid use? Any thoughts would be highly appreciated, thanks

Hard to say, hard to pinpoint as not all experience this. It could be but I dont think an Aromatase inhibitor (AI) alongside is the answer. That can in not way be definitively stated. I used clomid for years. Way before ai's and for pct solo. Clomid on cycyle to prevent gyno (yup that's what we did back then) and clomid solo for pct and only got some lethargy during pct. Took pct at night before bed. Minimal sides-prob related more to hormone fluctuation than the drug itself. But thats just me....
 
For the heck of it...

Script:

View attachment 554537


Pre-Letrozole at 100mcg:

View attachment 554538


10 days of letrozole + 7 days after discontinuing... (meaning it was at zero for several days):

View attachment 554539


This is at 12.44 body fat using a bodpod assessment.

Just for the heck of it :)

W.H.B said:
If I recall correctly, the study quoting 100mcg of Letrozole causing undetectable levels of estrogen, was not a sudy on men. In my mind it renders that study useless for our purposes. I will have to check and make for certain though.

There are a few studies that have been done on obese hypogaonadal men. The dosages of Letrozole ranged from 2.5mg/week to something like 17mg or more per week. I don't believe any of these dosing protocols caused undetectable levels of estrogen in the men. Of course, a leaner man would most likely require 2.5mg/week or less.

My interest in Letrozole started when Bill Roberts posted about Anastrozole causing stomach problems in those taking it. In the past year I have been having stomach issues that I could not for the life of me figure out the source of. Well, long story short, I stopped the Anastrozole and I have not had any issues for a while.

I have not used Letrozole while on cycle as of yet, but am currently using it off cycle at 2.5mg/week. The liquid formula I am using is dosed at 2.5mg/mL and one mL is equal to 54 drops. I take eight drops per day. I have not had any issues that would indicate signifigantly low estrogen levels. I have just successfully come off after being on for nearly seven months, and believe that the Letrozole has really helped with recovery. I will post about this some soon though, as I would like to comment on my experince for everyone.

I will try and find the links to the studies I mentioned and post them here. I don't think Letrozole is the severe estrogen killer everyone believes it to be. If I can buy one bottle of Letrozole and have it last me nearly a year, than I could save a lot of money and my stomach. I will be experimenting with Letrozole on cycle soon, but have to get through the three bottles of Anastrozole I already have.

Here is the infamous study where estrogen levels were reduced to undetectable levels. The problem is the dose of Letrozole is not given. This guy could have been given 100mg/day for all we know. If anyone has been in contact with the Weill Medical College of Cornell University and knows the dose used, I would love to know.
Aromatase inhibition, testosterone, and seizu... [Epilepsy Behav. 2004] - PubMed - NCBI
W.H.B said:
Here is one using 2.5mg/day in HIV-infected men with raised estradiol and low sexual desire. The reseachers stated that there were no adverse events from the medication. I would take that to mean that estrogen levels stayed within normal range. I do not have access to the full text, If anyone does I would like to know if that is true.
Letrozole versus testosterone. a single-center pil... [J Sex Med. 2007] - PubMed - NCBI
W.H.B said:
Here we have a study involving severely obese men with hypogonadotropic hypogonadism. The doses used ranged from 7.5 to 17.5mg/week. None of the men had estrogen levels out of the normal range after six weeks of treatment.
Letrozole normalizes serum testosterone ... [Diabetes Obes Metab. 2005] - PubMed - NCBI
W.H.B said:
Here is another involving obese men with hypogonadism. This one used 2.5mg/week of Letrozole. None of the test subjects were out of the normal range after six months of treatment.
Letrozole once a week normalizes serum test... [Eur J Endocrinol. 2008] - PubMed - NCBI

Google ninja comes through on the clutch :) That quote+studies taken from;
TESTOSTERONE NATION | Letrozole Dosing - Page 1

(mod feel free to remove T-nation link if want plz, was just making a point that letro, in some cases, can indeed be used effectively without crushing E2)
 
Why don't you start speaking for yourself instead of copying and pasting crap from T-Nation that is from 2008? Honestly man, you haven't shared a single thing that stems from your own mind. I'm not even sure how you're not embarrassed by such poor interaction and mind-stimulatory ability? Why can't you do your own research instead of bouncing from board to board, pasting my comments (as if it were yours), and then coming back with a collection of posts from various forums?

Enough is enough man. You're being passive aggressive and becoming more of a nuisance than anything.

Unlike yourself and likely everyone that has cited these abstracts, I've actually read the complete studies and can debunk all of your theories. Abstracts never list details. Vital details that would render your personal conclusions ineffectual. I'm really just not motivated to teach you anything else because I'm talking to 1000 different personalities within one man. Look into my post history, I love nothing but a challenge and enjoy nothing more than to learn and assist others. This is becoming nonsensical theatrics.

We have both agreed to disagree, so keep the peace and move along. Otherwise you're merely a mischief-maker.
 
- Osteoporosis (weakened bones) ; (long-term low levels)
- Fatigue
- Lethargy
- Skin quality diminishes
- Depression
- Poor sense of wellbeing & poor quality of life
- Anxiety & panic attacks
- Depression
- Erectile dysfunction
- Loss of balance/instability/dizziness
- Respiratory related concerns
- Irritability
- Low libido
- Insomnia

There is no denying the dose. You can attempt to debunk the ideology all day long, but until you've been prescribed, the efforts are fruitless, while appreciated. The leading testosterone therapy endocrinologist and urologists avoid letrozole as an e2 control method for a reason. Letrozole was never, not once mentioned in any of the seminars at ENDO2011, 2012 or 2013. Not one time.

I am the biggest devil's advocate, especially with physicians. This one, I can't challenge. Too many doctors and far too much evidence lead me to now only believe, but to understand how this compound works. (the real compound). It's damaging to mineralocorticoids and disruptive to isoprenos on the way to steroid-genesis pathway.

It takes many years to understand a compound and its metabolites, I assure you, I wouldn't be able to make an assessment based on no experience and a few reads on the internet.
^^From what I understand, those side effects are common when menopausal women use Letrozole to treat breast cancer (to the extreme dibilitating end); but I don't see that it's THAT significant of an impact, if responsibly used, on male physiology; especially guys who are gear-enhanced (which is the only real time one would even consider this med)

I read the rest of your quote tho, after the list of symptoms, and I have to agree with you that without tracking bloodwork progress one should probably not use it, otherwise there is every chance of irresponsible and abusive utility. In any case, honestly put, I'm just trying to get to the actual bottom of the truth behind what relative application of letrazole is safe and what is not. I'm getting mixed feedback from what you are suggesting as far as it's "power" and effect is concerned, versus what other very experienced (decades+) members are saying regarding it's use. So i'm trying to find the golden thread in the middle, the only study that I've actually seen referencing the 100mcg letrozole as fully incapacitating to aromatase process was again the one mentioned above from the T-nation link.

So you see my dilemma; it's not that I'm here to stir up your shit, or even degrade or disrespect your statements, I do truly value your input because you seem to be honest about what you know and everything makes perfect sense from a medical perspective, I'm just trying to dial in the proper relative application and effects of letro. So, either you're getting top-shelf nanomite letro that'll put anyone on their keester, or the effects of letrozole vary by individual response, or a combination of both. I just want you to clearly understand I'm not here to get into a pissing contest, since your experience clearly overshadows my own (and even if it didnt, I still wouldn't want a pissing match), I just want to understand the truth, simple as that.


edit-also as far as "using your statements as my own" I have yet to make a reply with your information where it wasn't specifically quoted as yours (outside of the threads I simply can't edit anymore since you've made the mention that you wanted quotations, but then I've mentioned that all of this information stemmed from you as the original source, just FYI)
 
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I guess I've answered my own question in a roundabout way thanks to your help; in the end it all boils down to try it and see for yourself, with bloodwork verification. Thanks again for your time brother, and again I'm sorry if I created any disturbance, the goal was to gain basic understanding; nothing more, nothing less. Thanks again for your time, generous input, and most of all, patience :) Take care
 
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