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How do you use it for PCT (details, please)?I use it for PCT.
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How do you use it for PCT (details, please)?I use it for PCT.
Again does RALOX actually get rid of gyno or only reduce it while you are on it? Same question for LETRO?
How do you use it for PCT (details, please)?
Just picked sum up hope it works!!
I am using ralox right now, very little change, nipple is becoming more tender. Toremifene gave me almost instant reduction, not tender and cost is comparable. I have heard great things about toremifene and use with prolactin reduction. I know it affected the itching (gone) the hardness (became much more pliable), and tenderness (gone) in my unilateral gyno.
I am using ralox right now, very little change, nipple is becoming more tender. Toremifene gave me almost instant reduction, not tender and cost is comparable. I have heard great things about toremifene and use with prolactin reduction. I know it affected the itching (gone) the hardness (became much more pliable), and tenderness (gone) in my unilateral gyno.
Just got mine today . Well keep everyone updated! Starting tommarow 60mg till it goes away or till the bottle is empty!
If I was a hateful person I would flame blergs. Dumbest response I have ever seen.
There is this contention that glandular tissue develops out of nowhere, and then once it is developed it stays forever. That in itself is ridiculous. This gland which is always there in the nipple has many E2 receptors, and can be stimulated to grow due to receptor activation.
If you have real questions, use your copay and your mandated insurance, and get an endocrinologist to check you out. AAS, puberty, genetic or medication issues are really all about conversion of testosterone to due aromitization by CYT P450, or the abundance of estradiol in relation to test. DHT blocks estrogen from binding at the site, so if you knock your test down due to AAS, you knock down DHT that prevents activation of the glands that everyone has in their nipple. Likewise you remove estrogen through an AI, or you use a peptide that acts in the same way that DHT does and differentially binds to the site, then it atrophies from lack of stimulation.
Will it come back? If your hormonal imbalance is off, possibly. These SERMs don't act forever. AI does not permanently block estrogen, in fact there are many chances for rebounds. So back to square 1. Get your levels checked, have an endocrinologist talk with you about your numbers. If it can resolve naturally in a teen, there is no reason to believe it cannot resolve in an adult, your AAS cycle being likened to surges of test, aromatization, and your body trying to balance it out. It happens in babies that are breast feeding because of the hormones of mama. these systems are complex loops.
Good luck. BTW, I found toremifene to be a better SERM than ralox. It immediately stopped the itching, proliferation, and tenderness.
Please inform me about the parts I'm misinformed on. I'm no endo, I'm trying to piece this together from bro science and textbooks. I'm just a zoologist that has a few textbooks, and a lot of time, and unilateral gyno. So please enlighten me how pubertal gyno goes away, how its different than AAS derived and where my logic and misunderstandings have steered me afoul.
In my last reply I asked for sage advice from someone I thought had a wealth of personal information, and possibly personal experience with gynecomastia, and information of where my logic/information/understanding is off. I get in return, that I am misinformed, that half of what I say is wrong, that I am bashing, and I am looking more and more silly, and to explain how I think an AI works.
So... since I do have time to spoon feed: There are two classes of Aromatase Inhibitor, one that binds preferentially to aromatase, and one that is a suicidal inhibitor of aromatase. Both prevent aromatase from acting on test to convert into estrogen. No estrogen, means no proliferation of the gland. Develop= cell division and growth, I don't know where this swelling thing or women going through puberty came from. The fat deposits around mast cells in a breast, a breast is certainly not all gland. I never made those comparisons. I have never acted like I know it all, in fact the thread you are responding to was asking for information, hoping for some good sound advice, since I thought you may have personal experience, or be a repository of knowledge. You apparently have neither, you do however have enough time to tell me you don't have time to spoon feed me information, tell me I look silly, etc. If you had anything really backing your claims, except misunderstanding, and maybe a poor grip on the english language, I would have been happy to hear you.
I've tried AI Femara, and if it was real it did nothing except give me the side effects. I took Arimidex, nothing. I am taking Raloxifene, no real help. I took Toremifene, and it stopped hurting, and gynecomastia got smaller, with no rebound. That's my broscience. Everything else is what I have read, studied up on, and trying to process.
I wish everyone that is working to undo gyno, whether its from puberty, or from a mistake with anabolics. Let's get some good information from real trials.
I have been using ralox for almost 1.5 months, started at 100mg a day for three days, and then dialed down to 50mg a day since. Do you think AAS is appreciably different that pubertal gyno? I am not sure. I'm still on the torem bandwagon, I was using it at 60 mg/ day. Just in the day 2 when my nipple didn't hurt any more. I'm ordering the torem again. So much of these old threads are about use of DHEA, DHT, masteron, and competitive receptor site binders, and how balance of E2/test may be the culprit even when estrogen levels might be "normal". If there is no test, the ratios may be the cause. Tell me how you are doing
Toremifene will work but the fact is raloxifene has a much stronger binding affinity to the e receptor in breast tissue making it the best choice by a fairly significant margin. Tamox and torem are second and are fairly comparable when it come to binding affinity to said e receptor.
Perhaps (just a guess here) you were asked to explain about ai's since you inaccurately made a statement asking how long someone thought an ai would block estrogen when in fact ai's do not block estrogen at all.
Of course there are 2 predominant causes of gyno. High estrogen levels and an out of whack androgen/estrogen ratio. For our purposes when it comes to steroid use, the latter is rarely the culprit. Under other circumstances however the latter may in fact be the cause. The only way to really tell what the cause is would be blood work, which in my opinion is the mandatory first step in any case involving gyno.
Im not sure where the attitude or condescension is coming from but if you lose it I will be more than hay to have an intelligent conversation on the topic where everyone could possibly benefit. That being said if you are a jerk off to me, whether it be in a direct or a round a bout way, I wont share dick with you on the topic.
Fair enough??
My apologies to anyone that thought my condescension was aimed at them. StanG, you have been helpful, informative. My comment about AI may be misinformed and misinterpreted. By remove estrogen from the equation, doesnt the AI specifically prevent conversion into estrogen thus "removing" it from the equation of free circulation. I did not mean an interpretation that AI somehow binds to estrogen turning it into another compound. After using letro, my joints hurt, my skin looked haggard, and I had severe hot flashes. It seemed to drop the estrogen to 0 in my body. Does the estrogen circulating just bind and get used up? SHBP increase and bind it up? Again, my apologies to you, or anyone that felt the ire of my message was directed at them. Only one person using terms like spoon feeding and saying directly I don't know half of what I'm talking about, or calling me a know it all.
Thanks
It is just one of the last places or stores of bodyfat that your body uses to burn for energy in males. Chest and stomach.Hate to post this twice but does anyone know:
I am happy to report that I am seeing SIGNIFICANT reduction in the nipple that was so afflicted. No tenderness, no pain, the "puffy" look what I would liken to the concussion look where one nipple was over-sized in comparison is all resolving rapidly right now. I started a test booster, an epi clone, zinc, and another round of 60mg toremifene. I have my doubts about my ralox source, it was not CEM, and when the tenderness and definitive asymetrical look started occurring again, I promptly went to what seemed to help. I don't know if I am doing myself a service or a disservice with a prohormone that claims to reduce estrogen, does not convert, but will stop natural test production by my body temporarily. The immediate results are miraculous. This has been going on for about 9 months.
Any thoughts in the group about SARMs or if using ANY prohormones should be reconsidered in a good course of treating gyno? Prohormones may have been the reason this all started.