+ 1 SERM during cycle
So we've been discussing this proposed theory over at AM about having a serm on cycle to keep the HPTA and testes alive. So far the general consensus has been that it's a good theory, or at least one good enough to give it a try, and that with small amount of compounds; ie. 400mg primo e, or 25mg anavar, ones HPTA would remain fully active and you don't need a test base. Also consistent use of serms on fully suppressive cycles like test have also shown to keep LH/FSH in normal levels through the whole cycle.
These are some of the proposed key points:
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"SERMs are inverse agonists at hypothalamic ER-alpha receptors. This is the only plausible explanation of why SERMs can maintain LH/FSH on cycle. SERMs aren't merely blocking E2 from binding to ER-alpha, they're actually causing a reverse of whatever impulse flow E2 produces."
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SERMs mostly block ERa and activeate ERb.
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Torem is the best serm to use on cycle: "Clomid is stronger, but torem is much, much cleaner (doesn't really elevate SHBG, no occular toxicity, doesn't lower T3, very protective of the prostate, doesn't lower IGF-1, seems to possess some degree of androgenicity on its own, is basically side effect-free for most users, very very favorable effects on lipids and other cardiovascular health markers, MUCH more potent E2 control to the point where an AI isn't needed on any cycle)."
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If taking a serm on cycle you don't need an ai: "E2 levels mean nothing if the E2 cannot bind to a receptor because it's being blocked by a SERM. A SERM allows you to manage E2 without having to tinker with anything. Pop the SERM -- done. E2 is completely controlled and balanced. Not too much, not too little."
"At full saturation doses they bind to every receptor The "selective" part means they block ER-a and stimulate ER-b. The action is selective, not the binding. " -
There are countless studies on serms, with patients being on them for YEARS without any major side effects. Matter of fact the cancer patient taking them, usually get more positive outcomes from taking them then negatives. Nolvadex is proven to help with type 2 diabetes, I want to say torem is proven to reduce LDL, plus all them have pro fertility benefits.
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Nolva and torem do not desensitise pituitary's sensitivity to GnRh, the opposite is actually true. Larger doses of clomid however have been proven to desensitise.
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The typical IGF1 reduction when using serms is of no concern. Firstly bc most aas increase IGF1 and secondly, 20% really isn't much to have an impact.
So what do you guys think? The discussion there has seemingly hit an end with people getting ready to try this out on their next cycle. Torem has been voted as the best serm for the job as it's the least toxic or not toxic at all.
EDIT:
Let me make my self clear: I am not advocating this theories, I have copy pasted this from post of other AM members. I think it's an interesting discussion, especially bc nobody gave any concrete negative comments about it. All the negative comments were just bro science and/or just straight up refusal on the grounds of "this is not how it's done". But no concrete science based opinions against it.
I would really like if somebody that has a greater knowledge on pharmacokinetics and/or is a scientist, an endo, a trt doc, etc. chimes in and helps to create a constructive debate. Thanks.
Also I'm not saying PCT is not needed. Especially with longer esters like cyp, ent... The pct it self however might have less mg of a serm in it because the body is already saturated with it, so no need for a loading phase like 20/20/10/10 but rather just 10/10/10/10. Keep in mind, serms have a long half life and nolva even with a small dose of 10mg should fully saturate all ER's over the time of the cycle...
Again I have no idea if this theories are true or false, Im just looking for opinions. Regards
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The brain is the control, not your receptors. The brain notices you have a high level of a hormone so the brain shuts down your testes, no amount of serms or other things will tell your brain to turn back on the faucet while it sees a high level and since test flows through your blood the brain sees it. Maybe if you cut your head off or find a way to make the brain think you have low t in your blood, maybe then it will keep the faucet on. The brain is constantly trying to balance.
SHCM - selective head cutting modulator...
Still in some people it works and in some it doesn't. Somebody proposed this: "There may very well be a genetic polymorphism in hypothalamic E2 receptors that causes this to work in some but not others. That would explain the mixed results... "
The same people bashing this question probably use hcg lol the question is a better one than most will appreciate. I have tested this with a high binding affinity AAS. It doesnt work. I got my bloods, no fsh lh, my estro crashed. The SERMs don't defeat the negative feedback loop completely. I used clomid and nolv together and seperately. No bueno. The negative feedback loop isnt as simple an on/off switch as people think. In fact, its a hair trigger off switch.
However what can work is something that actually creates enough test/estro to keep you functional such as consistant high hcg doses with very low test or just very low test. I use hcg BUT my fsh and lh are still non existent according to my bloods. Could you use a serm or hcg to allow a very mild steroid to work without shutdown? Yeah probably an oral dht one that has a very low binding affinity for the androgen receptors in skeletal muscle such as proviron. But... whats the point in that? There is no point in that.
To your points:
1. Nobody truly knows what happens at receptor level. So say my endo books. None mention 'impulse flow' wtf?!
3. Who are YOU to say what best for me? Nobody. Fact is i tolerate clomid perfectly well and it is efficacious.
"to the point where an AI isn't needed on any cycle" - whoever said that might actually be trying to hurt you! Take enough hcg and you make estrogen that can create mammory glands and will raise prolactin and make milk. Have fun.
4. Delete this please. It is a lie and will hurt someone. A 3g testo cycle will give you estrogenic sides wherever the serm doesnt act and will MULTIPLY the estrogenic action of serm where it does act as ab estrogen.
You understand serms are estrogen analogues as well as the opposite?
Tnx for a serious reply! It's nice to hear some good arguments.
Yeah, that's what was speculated, small dht cycles, like primo e or anavar. For me at least, the point I see in such cycles is cutting. A 12 week cut or a 12 week slow (really slow) bulk. Of course the amount of aas that one needs to grow or retain mm will largely depend on their desensitisation to aas and their FFMI. For some it might be nice for others not so much...
No idea what impulse flow means. I'll try and google it.
This is the study that says that clomid in larger doses desensitises pituitary to gnrh. It was done however in vitro so take it with a grain of salt. https://www.ncbi.nlm.nih.gov/m/pubmed/6781360/
If clomid works for you than by all means take it. I think the text wasn't commanding you to do anything
What do you mean by ab estrogen?
Yes I do
And thanks for posting your own results on using a serm on cycle! It's interesting, for some it works but for some it doesn't. Probably depends on a lot of factors; how much mg of aas are you taking, your pituitary's "healt", your ledyig cells health, etc. I've read from a lot of guys who are on trt, that when they took a serm, there balls came back to life. Also did tests to see where there LH was, and it was in range.
I was sceptical a lot about this theory, it seems to good to be true in some respects. Mostly on the total control of estrogen, as you also clearly pointed out.
This is just a pile of shit. Sorry..all of it is based on the theory of retardation. Serms are the new miracle grow that contain unicorn sperm. 5% per ml.
Obviously hes dumb...
RustyhookerIts a retread. Promoting another websites bogus ideas to get drama. His last attempts failed. Lets watch him cycle.
https://www.eroids.com/forum/steroids-qa/steroid-cycles/first-ostarine-c...
https://www.eroids.com/forum/steroids-qa/pct-anti-estrogens/normal-lh-ze...
I'm curious why you didn't use a SERM when you did your ostarine cycle , zero TT
Hi! Thanks for reading my "cycle log". I didn't try this theory because I didn't know about it at the time. And even if I did, I probably wouldn't have tried it as I wanted to see how just Ostarine works, how it effects the HPTA bc it's touted so often as being lightly suppressive. And in the end I saw how it works but unfortunately the liver toxicity was to much for me. If liver enzymes were ok I would have added a test base to the cycle and continued with it. I had it ready, but now it's waiting for a next run...
RustyhookerMight quit promoting some am site and research. Estro will cause issues if raised. Just because tits didnt form does not mean theres no sides.
Your theories dont hold water imo.
https://www.eroids.com/forum/steroids-qa/pct-anti-estrogens/normal-lh-ze...
Your last theory crashed. I dont believe youre 32. Looks like youre playing with fire and have a very short health expectancy
Hi! Thanks for insulting me... I guess.
Firstly, this are not my theories and I am not in a position to advocate them. I just think it's interesting, especially as nobody had anything substantial to say against it. And in substantial I mean science based comments. All the negative comments it got were all just bro science or just down right refusal due to the fact that "everybody knows" that this is not how it's done. So nothing concrete.
I'm hoping for somebody that knows more about pharmacokinetics or is a doctor, a scientist could present some good info. And without a condescending tone.
And just for debates sake, If all the ER receptors are saturated by the serm, and by all I mean all, not just in the breast, what does it mater how much e2 is floating in your plasma? Secondly, if serms are also inverse ER agonists, this means that they are activating the ER's and you wont have low e2 symptoms. This is at least how I understand it. Also the S in SERM's stands for selective. Which means they don't attach the same to ER alpha and ER beta. Anyway... Constructive and scientific opinions are welcomed.
Regarding "my" last theory crashing, what do you mean? A 20% drop of IGF1 seems significant to you? Or you don't think aas raise IGF1? Tnx
RustyhookerYour theory crashed. Its bunk.
Igf drop 20% to who? Your measurements or just jargon you found?
Aromasin pct, proven to raise igf.
Estro and what does it matter? You really know jackshits. Estro effects everything in your body. Not just the receptors youre selecting. Thats about as smart as crashing estro so that its not a worry. Estro balance is part of your hormonal axis. All these hormones also effect your thinking/mind as well. You cant just scratch the surface to find gold.
Insult you? If youre that thin skinned, this isnt the place for you.
Using serms on cycle is redonculous. You also list pct therapy on cycle as the best. Smh....
Nah I'm not thin skinned mate. It's just that your demeanour is hostile for no reason and it's off putting, that's all.
To answer your questions or statements. Again, this are not my theories, are you even reading what I wrote?
20% IGF1,... yeah I just farted that out my stupid little juvenile brain. This info is from research done on tamoxifen. Off course I didn't just make this up. And the fact that you don't know this is making me doubt your age now.
Regarding estro, again did you even read what I wrote?? If ALL receptors are taken by a serm. ALL. Do you understand what all means? Are you implying that e2 binds to other receptors as well? I would gladly read up on that literature if you can provide it off course. And if it would make you feel more at ease just use a frekin Ai with it if you wish.
Again, why is using serms on cycle ridiculous?? I am up for a discussion, just please substantiate your claims with more backing than "it's redonculous". Tnx
RustyhookerJump in and run cycles your way. Prove your outcomes. Simple.
If it was correct, you wouldnt be posting bs from a different site. Youd be on cycle and stayed with that website. Fact is that youre uneducated.
Just the fact alone that I am asking for other peoples opinions implies I need information, doesn't it? So why so blatantly attack? Obviously if I wanted to do something like this, if I was 100% sure about it, I wouldn't be asking anything would I? I would just create a cycle log and be done with it. Or yet again, with the amount of hostility that has been presented by other members from just me trying to get a debate going... why even try. Fu*k this. God damn it, this thread is totally senseless, it's like nobody has actually read what I've wrote and people just go in attack mode. Don't really know why I am even trying anymore to create a sensible debate... Have a good one
RustyhookerYoure good at trolling.
We don’t debate bullshit...
I think you’re smart enough to know that no one is going to agree with you. If you spend any time at all looking around and researching you will notice that everyone agrees that test is your base.
Yes I definitely know there will be lots of negative and down putting comments on this topic. It's just a debate I'm interested in as the comments over at AM are really compelling and there have been quite a lot of anecdotal evidence that it works.
I know test is your base but with lighter cycles it might not be if a serm can help.
Also if having a serm on a really suppressive cycle like test + tren + oral, etc. keeps your LH/FSH in normal ranges and thus keeps your testes up and running, the recovery would be much quicker and easier. Also the damage done to the leydig cells, specifically apoptosis of the cells from regular shutdown bc of cycling would maybe be totally mitigated. Thus eliminating the need for HCG and it's sides.
I'm no doctor though and this is all just speculation on my part and furthering the debate on the topic.
400 mgs of primo? No test? What’s exactly do you think your going to get out of that?
That was just a suggestion. A user over at AM said he ran 25mg clomid on 12 week cycle of 400mg primo e and 50mg dbol. He kept his TT at 450 during the whole cycle.
400mg primo on a 12 week run can have results. It would depend however on your level of desensitisation to AAS off course and on your FFMI. A natty or a "half natty" would gain on it probably. A seasoned 250lbs veteran probably not so much
My self I'm planing 400mg primo for a 10 week cut. 5 to 6 pounds cut.
I guarentee youll have better results on 500 mgs of test only. Dont shut your body down over something someone said on a conputer. I would pct either way.
Not saying a PCT isn't needed and I'm not saying that 400mg primo is the best bang for buck choice. Did I imply or say this at one point? No I didn't
There is a chance 400mg primo on it's own wouldn't shut down. But I'm not saying I want to get shut down. I would either use a TRT dose of test as a base or try the serm on cycle theory. I think that with such a light dose of a not heavy suppressive compound this might just work. There are others who have done it and it worked nicely.
I didn't want this to be a debate about my cutting cycle. But so you don't try to discredit me further; I will have test prop and cyp at hand if suppression goes out of hand. Also I am not looking for a recomp, just something that will help me keep my mass while on a small cut, that I want to do slowly and carefully. SERM is taken in PCT, especially with longer esters that take time to clear from the system. But as the body will already be fully saturate by the serm there is no need for a "loading" phase of pct, ie. no need for 20/20/10/10 but probably just 10/10/10/10... I will do bloods on a bi or tri-weekly basis. This is an experiment, no need to take it personally. I'm sure the info provided from it will help the community.
Do you want to grow or just play with theorys ? Stay with time proven methods. -2 because I think your trolling.
Well... I'm lost for words... Good luck to you