E2 control without AI'S
- Thread starter railrider
- Start date
cjw2021
Pro Bodybuilder
Is this spam?
MoparMuscle
Amateur Bodybuilder
Isn't Vitex and p5p an effective natural anti E or no? Typical dose of 1200-1800 for Vitex and 200-300mg for p5p
railrider
New member
I opted for the aromasin instead just not sure how on going to dose yet. I want to start out low so I don't crash my estrogen Again. I find many posts that this type of Aromatase inhibitor (AI) allow your body to still produce E1 the good estrogen and not E2 is there any fact to this.
MoparMuscle
Amateur Bodybuilder
Saw this on another forum and thought it was interesting:
"When it comes to this comparison its more about type of estrogen suppression as opposed to "strength". Arimidex is a VERY potent sulfatase inhibitor, which inhibits estrone. It is a moderately strong aromatase inhibitor (weak as compared to aromasin, AIFM or letrozole). This is fine for women with breast cancer who produce percentage wise very high levels of estrone (the weak estrogen), which can be converted to estradiol (the strong estrogen) via aromatase.
For men this is generally not very good, especially for men on testosterone replacement therapy (TRT) since sulfatase inhibitors have very little effect on exogenous testosterone. Actually its generally not a good thing since it nearly completely eliminates estrone, while still allowing estradiol. If you have a choice as a man, you want estrone (weak estrogen) with near total elimination of estradiol (strong). AIFM and aromasin do inhibit sulfatase, though to a lesser extent than the competitive inhibitors (dex and letro). They are both potent aromatase inhibitors and highly suppress estradiol. Since exogenous test converts to estradiol via aromatase, AIFM and aromasin are much better suited.
Lowest doses of letrozole completely suppresses glandular production of estrone(E1). while it generally takes higher end doses of exemestane(aromasin) to come close to doing this. Exemestane dose dependantly decreases estradiol and to a lesser extent estrone. Basically aromasin at low doses is mostly peripheral, which means blocking conversion of estrone, testosterone and other aromatic precursors to estradiol. Whereas because they are competitive inhibitors that have high permeability through tissue types, arimidex and letrozole have high affinity and saturation of tissues like testes and adrenals, where estrone is produced. They highly block synthesis of aromatase in those tissues at even lowest doses.
Though aromasin/exemestane can produce high level suppression, particularly in low estrogen producers as well as those that generally produce less aromatase. (genetics, followed by factors like age and bodyfat). Keeping in mind that there are many endogenous and exogenous regulators of aromatase...ie, dopaminergics tend to down regulate aromatase mRNA, thus synthesis (not block, down regulate) but their use may require a lesser dose of Aromatase inhibitor (AI) (of either kind) that you are used to."
"When it comes to this comparison its more about type of estrogen suppression as opposed to "strength". Arimidex is a VERY potent sulfatase inhibitor, which inhibits estrone. It is a moderately strong aromatase inhibitor (weak as compared to aromasin, AIFM or letrozole). This is fine for women with breast cancer who produce percentage wise very high levels of estrone (the weak estrogen), which can be converted to estradiol (the strong estrogen) via aromatase.
For men this is generally not very good, especially for men on testosterone replacement therapy (TRT) since sulfatase inhibitors have very little effect on exogenous testosterone. Actually its generally not a good thing since it nearly completely eliminates estrone, while still allowing estradiol. If you have a choice as a man, you want estrone (weak estrogen) with near total elimination of estradiol (strong). AIFM and aromasin do inhibit sulfatase, though to a lesser extent than the competitive inhibitors (dex and letro). They are both potent aromatase inhibitors and highly suppress estradiol. Since exogenous test converts to estradiol via aromatase, AIFM and aromasin are much better suited.
Lowest doses of letrozole completely suppresses glandular production of estrone(E1). while it generally takes higher end doses of exemestane(aromasin) to come close to doing this. Exemestane dose dependantly decreases estradiol and to a lesser extent estrone. Basically aromasin at low doses is mostly peripheral, which means blocking conversion of estrone, testosterone and other aromatic precursors to estradiol. Whereas because they are competitive inhibitors that have high permeability through tissue types, arimidex and letrozole have high affinity and saturation of tissues like testes and adrenals, where estrone is produced. They highly block synthesis of aromatase in those tissues at even lowest doses.
Though aromasin/exemestane can produce high level suppression, particularly in low estrogen producers as well as those that generally produce less aromatase. (genetics, followed by factors like age and bodyfat). Keeping in mind that there are many endogenous and exogenous regulators of aromatase...ie, dopaminergics tend to down regulate aromatase mRNA, thus synthesis (not block, down regulate) but their use may require a lesser dose of Aromatase inhibitor (AI) (of either kind) that you are used to."
maxxmill17
New member
Rail; please update..I have had E problems now for 2 years and kind of threw in the towel. I have bad reactions to a-dex and nolva. feel like shit and even my skin hurts (tought to explaine)..I have great libedo but tought to keep hard,sleep good luck unless i use xanex and started losing hair 1 yr ago 40 yrs old...I have .25 mg cap's of anastrozole my dr. had compounded I may try the small dose to see If i can get away with it without reaction (to be honest I has sat on my tavle for 3 months scared of reaction). my e stay around 48 on 140 mgs enanthate split 2x per week...thoughts thx
railrider
New member
I feel ya man. Controlling my estrogen levels has made testosterone replacement therapy (TRT) a bad experience for me. I've tried Aromasin now and I can't even find a sweet spot with it. It still gives me some of the same sides and I still have trouble with it crashing my E to much. This last 8 months I'd have one good day after an adjustment then 3 or 4 bad ones. I'm actually thinking of trying a restart program with nolvadex to get back to baseline. If the nolva gets me back to the upper 500's like clomid did before I started I'll taper of it to see if my levels hold and if they do I'll stay off testosterone replacement therapy (TRT) for good. I think my main issue is my body is telling me I'm trying to manipulate to much. I want to know what people did before AI's to control E2 sides. Cause to be honest when my E2 was at 47 with no Aromatase inhibitor (AI) I felt great mentally and physically with great results in the gym, but I had absolutely no sexual function and small flare ups. Would Nolva possibly block enough E2 give me back some libido with no AI? Because if I could have those levels and still be able to fuck on command I'd be a happy man.
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remember, tamox is not an Aromatase inhibitor (AI), so its not gonna lower any estrogen that's produced, its only gonna keep it from binding to the receptor. So no gyno essentially.
What dose are you using with Aromasin? And what sides are you talking about? Could you be in your head a little too much rail?
Aromasin to me is great because 12.5mg ED or EOD is a great dose, which won't crash E2 and will keep enough around without causing normal Aromatase inhibitor (AI) sides like letro does.
I've even gona E3D with it and been great.
railrider
New member
Well I started off at 3.125mg E3d cause I've crashed before and didn't want it to happen again. The sides I have are fatigue and swollen lymph nodes in my throat which are very uncomfortable I know it has to do with an embalance estrogen poisoning LOL. At that dose I started getting my morning wood back and had great libido for a few day's but had those sides. I upped the dose to 6.25 and that started to take away the swollen nodes and fatigue almost completely and then they start to return about the 2nd day after dose. But it also took away my morning wood and my libido isn't near as high I can still get it up but the sensation isn't near as good. So I'm not sure if a higher dose would be good for me or not.
Maybe I'm not dosing correctly and if I go to a higher dose the libido will get better with time. I don't know this has been haunting me for 8months now thats why I'm ready to throw in the towel.
Maybe I'm not dosing correctly and if I go to a higher dose the libido will get better with time. I don't know this has been haunting me for 8months now thats why I'm ready to throw in the towel.
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