biggiesmallz
New member
Just listened to itNo I think swagger jacker is more fitting, look it up on YouTube. It's by Cameron.

Not justifying my actions; I've learned from my mistakes, simply explaining what truly is the case
Just listened to itNo I think swagger jacker is more fitting, look it up on YouTube. It's by Cameron.
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.![]()
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 farand information/data supplied by you (however without proper acknowledgment) that foaster great debate and education.
DO serms not often posses agonist and antagonist estrogenic activity? The agonist effects desireable and the antagonist not? Hmmm
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;
DO serms not often posses agonist and antagonist estrogenic activity? The agonist effects desireable and the antagonist not? Hmmm
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 PCTeither 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 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.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.
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.
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
Steroidology.com
Uncovering the truth about bodybuilding
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.
Aromatase inhibition, testosterone, and seizu... [Epilepsy Behav. 2004] - PubMed - NCBIW.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.
Letrozole versus testosterone. a single-center pil... [J Sex Med. 2007] - PubMed - NCBIW.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 normalizes serum testosterone ... [Diabetes Obes Metab. 2005] - PubMed - NCBIW.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 once a week normalizes serum test... [Eur J Endocrinol. 2008] - PubMed - NCBIW.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.
^^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)- 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.