Zero sex drive post sustanon cycle:<

[bigbench]

Man, this is now the biggest potato poTOTo discussion yet. Many of us (myself included) have said that nolva stimulates the HPTA. Now, the reason that is said, is because we have to post about the same thing in almost every other post. They are not asking the MECHANISMS of how it does so. Just asking if nolva works for PCT so a breif sentence is all that is needed vs writing a paragraph ed. Also, depending on what defition of stimulate you want to refer to and how you intepret it (ie: Def- To increase temporarily the activity of (a body organ or part)). Also, look it it backwards. Would your HPTA be stimulated if you didnt take Nolva? No! But the BIGGEST reason, is because no where did anyone say that nolva DIRECTLY stimulates the HPTA. Causing a negative feedback is an INDIRECT stimulation.
So guys, we ALL know what the hell Nolva does and we all have valid points so lets just love one another and drop this crap

 

[jasthace]

Man, this is now the biggest potato poTOTo discussion yet. Many of us (myself included) have said that nolva stimulates the HPTA. Now, the reason that is said, is because we have to post about the same thing in almost every other post. They are not asking the MECHANISMS of how it does so. Just asking if nolva works for PCT so a breif sentence is all that is needed vs writing a paragraph ed. Also, depending on what defition of stimulate you want to refer to and how you intepret it (ie: Def- To increase temporarily the activity of (a body organ or part)). Also, look it it backwards. Would your HPTA be stimulated if you didnt take Nolva? No! But the BIGGEST reason, is because no where did anyone say that nolva DIRECTLY stimulates the HPTA. Causing a negative feedback is an INDIRECT stimulation.
So guys, we ALL know what the hell Nolva does and we all have valid points so lets just love one another and drop this crap

But we have'nt finished Aromasin yet ,which is a suicidal 3rd Gen AI, that is good on the lipids and endocrine system and is much better and MORE effective then Nolva or Adex.
Can we do that now BB? Oh go on??

 

[bigbench]

Lol, always keeping things light bro!

 

[Conciliator]

Ok
But then if we were to state in the same specific terms the effect of AAS,we would not be able to say that anabolic/androgenic steroids stimulate protein synthesis and glycogen retention.
We'd have to say the they stimulate gene regulation which in turn stimulates cell up regulation,
More specifically the steroid receptor complex activates transcription of transcriptional factors and aporepressors that then function in the transcription of active transport proteins specific to amino acids and glucose.

No, that's not the same thing. Following your analogy above, you'd have to say that pressing the gas pedal in a car doesn't "stimuate" speed because, because it's opening gas flow into the engine, with an indirect effect on speed. So what? That's still stimulation. Even though there's a chain of events, a mechanism of action, it's a positive one. Steroids are agonists of the androgen receptor. They are activiating it, or "stimulating" it, and stimulating the subsequent effects on protein synthesis.

 

[Conciliator]

Man, this is now the biggest potato poTOTo discussion yet. Many of us (myself included) have said that nolva stimulates the HPTA. Now, the reason that is said, is because we have to post about the same thing in almost every other post. They are not asking the MECHANISMS of how it does so. Just asking if nolva works for PCT so a breif sentence is all that is needed vs writing a paragraph ed. Also, depending on what defition of stimulate you want to refer to and how you intepret it (ie: Def- To increase temporarily the activity of (a body organ or part)). Also, look it it backwards. Would your HPTA be stimulated if you didnt take Nolva? No! But the BIGGEST reason, is because no where did anyone say that nolva DIRECTLY stimulates the HPTA. Causing a negative feedback is an INDIRECT stimulation.
So guys, we ALL know what the hell Nolva does and we all have valid points so lets just love one another and drop this crap

Actually, I think that most people here do NOT know "what the hell Nolva does." I think that most people who say that Nolva "stimulates" LH output are not sure what they're talking about.

It's not hard to decribe things correctly in one sentence, like I did earlier in this thread: "nolva blocks estrogen at the pituitary, reducing negative feedback, so that GnRH can better stimulate LH"

To say nolva "stimulates" something is to imply that it's an agonist at the HPTA. It's not. It's an antagonist. It doesn't stimulate anything. It blocks estrogen so that GnRH can provide a stimulus, with less inhibition, and thus a greater output of LH.

You say "Causing a negative feedback is an INDIRECT stimulation." First of all, negative feedback (in this case, from estrogen), is INHIBITION. When you block that effect, you're removing the inhibition. You are not stimulating anything. If you didn't have GnRH to stimulate LH output, taking a SERM would do absolutely nothing. It's like sitting in a car that's not moving and saying that if you take your foot off the brake, it will stimulate speed. It does not. It removes inhibition of speed, which makes no difference without an actual stimulus (the gas).

 

[BBC3]

OK Conciliator, here we go again.....

One point is that the HTPA is not Directly involved period.

The nolva competes for the receptor "Site", where ever that may be..... Hence this means that the estrogen circulating in your body can not affect the tissues that have the concentrations of estrogen receptors!!?!?!? Because the "slot is already filled". So to speak. There is already a car parked in the spot. The estrogen must then move on and look for another. Keep in mind. NOLVA COMPETES. It did not say dominate! Hence different dosages. Add more Nolva and you render more parking spots full. At 40mgs (even 20mgs) you have pretty much a max effective dose, speaking in peak plasma concentrations that is. This is the most you can cram in there for the buck. If 40mgs aint filling enought parking spots at this point, your going to have to use alternate means.

The Primary difference in Nolva and Arimidex is VERY SIGNIFICANT. With Nolva, your blood is still packed with heavy estrogens, free or not, to do as they please where they have other effects on the body, both good or bad. And there are plenty of E's just waiting to find that receptor that has not yet been occupied by a Nolva. With a SHITLOAD of estrogen produced and active in the system, you might even find that the "E's" are comming along and just booting the nolvas from the spots and taking them over regardless, or beating the nolva to the recpetors. Am I right?? Get it??? . Hence, sometimes it works, sometimes it don't..... With Arimedex you are stopping the actuall aromitization from ever occuring. this puts a whole different twist on things. It is much more effective in getting estrogen out of the picture by this means. Infact, 80-90% removed in as little as 2 weeks. BUT isn't this kinda creepy. Think of all the other processes in your body that require estrogen. For one, Conciliator's Boobs might shrink up and go away!! But dont worry, that clitoral enlargement can not be reversed. You are safe there.. It really makes me wonder if and "AI" or Aromitase Inhibitor, AKA Arimidex is safe long term. The shades of action by this drug I fear are much more encompassing. Kinda all or nothing. Correct me if I am wrong...

 

[BBC3]

I meant Pituitary not HTPA. So dont even go there with that weak ass shot in asshole. I am pretty sure we are argueing the same point, however, it is you who is using terms incorrectly.

OK Conciliator, here we go again.....

One point is that the HTPA is not Directly involved period.

The nolva competes for the receptor "Site", where ever that may be..... Hence this means that the estrogen circulating in your body can not affect the tissues that have the concentrations of estrogen receptors!!?!?!? Because the "slot is already filled". So to speak. There is already a car parked in the spot. The estrogen must then move on and look for another. Keep in mind. NOLVA COMPETES. It did not say dominate! Hence different dosages. Add more Nolva and you render more parking spots full. At 40mgs (even 20mgs) you have pretty much a max effective dose, speaking in peak plasma concentrations that is. This is the most you can cram in there for the buck. If 40mgs aint filling enought parking spots at this point, your going to have to use alternate means.

The Primary difference in Nolva and Arimidex is VERY SIGNIFICANT. With Nolva, your blood is still packed with heavy estrogens, free or not, to do as they please where they have other effects on the body, both good or bad. And there are plenty of E's just waiting to find that receptor that has not yet been occupied by a Nolva. With a SHITLOAD of estrogen produced and active in the system, you might even find that the "E's" are comming along and just booting the nolvas from the spots and taking them over regardless, or beating the nolva to the recpetors. Am I right?? Get it??? . Hence, sometimes it works, sometimes it don't..... With Arimedex you are stopping the actuall aromitization from ever occuring. this puts a whole different twist on things. It is much more effective in getting estrogen out of the picture by this means. Infact, 80-90% removed in as little as 2 weeks. BUT isn't this kinda creepy. Think of all the other processes in your body that require estrogen. For one, Conciliator's Boobs might shrink up and go away!! But dont worry, that clitoral enlargement can not be reversed. You are safe there.. It really makes me wonder if and "AI" or Aromitase Inhibitor, AKA Arimidex is safe long term. The shades of action by this drug I fear are much more encompassing. Kinda all or nothing. Correct me if I am wrong...

 

[bigbench]

Actually, I think that most people here do NOT know "what the hell Nolva does." I think that most people who say that Nolva "stimulates" LH output are not sure what they're talking about.

It's not hard to decribe things correctly in one sentence, like I did earlier in this thread: "nolva blocks estrogen at the pituitary, reducing negative feedback, so that GnRH can better stimulate LH"

To say nolva "stimulates" something is to imply that it's an agonist at the HPTA. It's not. It's an antagonist. It doesn't stimulate anything. It blocks estrogen so that GnRH can provide a stimulus, with less inhibition, and thus a greater output of LH.

You say "Causing a negative feedback is an INDIRECT stimulation." First of all, negative feedback (in this case, from estrogen), is INHIBITION. When you block that effect, you're removing the inhibition. You are not stimulating anything. If you didn't have GnRH to stimulate LH output, taking a SERM would do absolutely nothing. It's like sitting in a car that's not moving and saying that if you take your foot off the brake, it will stimulate speed. It does not. It removes inhibition of speed, which makes no difference without an actual stimulus (the gas).

Bro, your kind of proving my point. Again, writing everything you just did will get old saying it over and over again. Trust me, im not arguing with you. Just saying, unless someone asks the process of how Nolva works, you dont HAVE to go into all that. Also, INDIRECT means an action (in a chain of events) is set forth that causes a secondary action to take place. So yes, it does INDIRECTLY stimulate. Nolva is taken (action)- blocks estrogen (action)- causes negative feedback. These are ALL DIRECT ACTIONS OF NOLVA. What happens next? The inhibition causes GnRH to stimulate LH (action). This is a secondary action brought about by the actions of Nolva. So again, it IS AN INDIRECT ACTION

 

[solo47]

Actually, I think that most people here do NOT know "what the hell Nolva does." I think that most people who say that Nolva "stimulates" LH output are not sure what they're talking about.

It's not hard to decribe things correctly in one sentence, like I did earlier in this thread: "nolva blocks estrogen at the pituitary, reducing negative feedback, so that GnRH can better stimulate LH"

IOW, the end result of ingesting Nolvadex may be to cause the production of the luteinizing hormone that in turn stimulates the Leydig cells to produce Testosterone?

It's certainly more accurate to speak the way you suggest but unnecessary as long as the end result is known. Semantics. You're supposedly the Conciliator, so be conciliatory and not pedantic. The shorthand we've been using will suffice for the limited understanding of most gear-using bodybuilders.

Solo

 

[BBC3]

I believe I am in sync with you here. I think there is plenty of estrogen there in the first place, regarding detection. I just always assumed that the nolva simply does not stimulate test production worth a shit, maybe mildly at best. I have heard that clomid is much more effective and can bring HTPA online in as little as two weeks (150mgs and wean down). FOr whatever reason, idont know, maybe it has a better or more direct effect on the pituitary..?? I have also see some of my sources change their position on this recently. I have never needed or been big into any of them, however that is about to change as I am growing concerned with estrogen more so by day.

Regarding depression and, night crys, etc. I have also thought that this was only due to the "practical zeroing out of test levels" and only E remaining, at whatever level is present. If it outweighs the test, you bottom out, and that sucks. I experienced this once after comming off a 6 month test only heavy cycle cold turkey. There was a period of a week some 4-5 weeks down the road that really sucked. We are talking day cries. Turned out my test level was 65.. It came back of course. All the way up to my natural level of a smashing 302!!!!

Also, I never really thought of Adex and a testosterone stimulator either.
I am guessing it is the weakest of the three when it comes to stimulation of the HTPA. Regardless there are going to be LH reception problems in the nuts if there has not been any HCG maintenance. Then you have failed restarts. you know, the ones where the guy comes off the hard long 16-20 week cycle that included some Deca. He states he popped a couple of 2500iu blasts at the end of the cycle prior to clomid and nolva, completes 6-8 weeks of pill protocal, and then when he thinks he is done his titties start hurting again. Well, maybee he should have pinned that 1000iu shot every 4 weeks?!?!?!? I dont know.

When anyone says "PCT", I think of a blast of drug therapy designed to bring the body back on line as soon as possible.
Arimidex = maintenance and emergency save.
clomid = primary pct after hcg (4 weeks)
nolva = final 2-3 weeks insurance to get the clomid out and give everthing time to stabilize. Also good for cycle maintenance. Cant wait to try on this one...

I understand that are other agents out there "Carbergoline" (for progesterone) , and letro etc. I dont yet havae the full rundown on them. I am looking into them as I am getting reqady to incorporate Deca for the first time.

anyway, YES BRANG, I agree with you thoughts. I think Conciliator is there, just mis-stepping a bit...

Wooo! this is one of my favorite subjects!

So, just to rephrase this:
Nolva does NOT stimulate the HPTA directly (it can't right?). It simply blocks the receptor at the pituitary and the breast tissue receptors (amoung others possibly).
The LH and FSH production is due to the secondary effect of Pitutary not detecting the estrogen as it slowly builds up because the receptors are blocked.

Is that correct?
That has been my understanding of Nolva's action, which conflicts with many expert opinions.

If the above is correct, then i don't understand why PCT cannot be done well with an AI like Arimidex to prevent estrogen from building up (as natural Test comes back online) rather than binding to the Pitutary receptors.
Seems like just another way to skin a cat to me. Both prevent the detection of Estrogen, one by preventing Estrogen being created(Arimidex) and the other by hiding the estrogen that is there from the Pituitary..

Perhaps the use of Nolva is some of the reason that some people say they get depressed during PCT - its not that they have no Test, its that they have TOO much Estrogen!
I'm a beliver in prevention is better than cure. Therefore and AI should be better than a SERM for some respects of PCT.

A common argument against Arimidex for PCT is that Estrogen will be low due low Testosterone at the end of cycle so an AI will be ineffective (as there is nothing to arimatize).
But this is the same even if your using Nolva, it can't block what is not there, right?!

As natural Test comes back online the AI will be there to prevent aromatization just as Nolva would be there to block the receptor.
And, if Nolva is NOT stimulating the HPTA directly (it cannot, that's not how SERM or a negative feedback loop works - my understanding) then what's it doing when there is no Test to aromatize? Sweet-fuck-all i imagine..

It seems to me that an AI would work equally well as Nolva, as both achieve the same end result but via different mechanisms.
I concede that AI has less than positive effects on lipid profile(I have read this but haven't looked into it at any length) and from what i have read Nolva has positive effects? Or is this just more internet dogma?

Thoughts? Comments? Abuse?

I just want to learn!

regards,
- b

 

[Conciliator]

OK Conciliator, here we go again.....

One point is that the HTPA is not Directly involved period.

The nolva competes for the receptor "Site", where ever that may be..... Hence this means that the estrogen circulating in your body can not affect the tissues that have the concentrations of estrogen receptors!!?!?!? Because the "slot is already filled". So to speak. There is already a car parked in the spot. The estrogen must then move on and look for another. Keep in mind. NOLVA COMPETES. It did not say dominate! Hence different dosages. Add more Nolva and you render more parking spots full. At 40mgs (even 20mgs) you have pretty much a max effective dose, speaking in peak plasma concentrations that is. This is the most you can cram in there for the buck. If 40mgs aint filling enought parking spots at this point, your going to have to use alternate means.

The Primary difference in Nolva and Arimidex is VERY SIGNIFICANT. With Nolva, your blood is still packed with heavy estrogens, free or not, to do as they please where they have other effects on the body, both good or bad. And there are plenty of E's just waiting to find that receptor that has not yet been occupied by a Nolva. With a SHITLOAD of estrogen produced and active in the system, you might even find that the "E's" are comming along and just booting the nolvas from the spots and taking them over regardless, or beating the nolva to the recpetors. Am I right?? Get it??? . Hence, sometimes it works, sometimes it don't..... With Arimedex you are stopping the actuall aromitization from ever occuring. this puts a whole different twist on things. It is much more effective in getting estrogen out of the picture by this means. Infact, 80-90% removed in as little as 2 weeks. BUT isn't this kinda creepy. Think of all the other processes in your body that require estrogen. For one, Conciliator's Boobs might shrink up and go away!! But dont worry, that clitoral enlargement can not be reversed. You are safe there.. It really makes me wonder if and "AI" or Aromitase Inhibitor, AKA Arimidex is safe long term. The shades of action by this drug I fear are much more encompassing. Kinda all or nothing. Correct me if I am wrong...

What do you mean the pituitary is not directly involved? Of course it is. You say "nolva competes for the receptor 'Site', where ever that may be." Apparently, you don't know where the estrogen receptors are that you're trying to block. I'll tell you. They're in the pituitry. So you can bet your sweet ass that the pituitary is directly involved.

Second, it's not the "HTPA", it's the HPTA. The "P" in there stands for pituitary... which is directly involved in the recovery of your H-P-T Axis.

Thrid, when you say "At 40mgs (even 20mgs) you have pretty much a max effective dose" you're talking about maximal saturation. That has nothing to do with "peak plasma concentrations", which can go much higher with higher doses.

Fourth, you don't need to explain to me in kindergarten terms what the difference is between a SERM and an AI. I know how they work, and judging from your comments about the pituitary, you're a little confused about it..

Fifth, you say "With Nolva, your blood is still packed with heavy estrogens." Packed with heavy estrogens? First of all, WTF is a "heavy estrogen"? Second, estrogen is formed when testosterone aromatizes. When you don't have much testosterone, you won't have much estrogen either (hint: after a cycle). Your blood is NOT packed with estrogens when you take Nolva during PCT. Quite the contrary. So when you ask "Am I right??" The answer is, no, you are not right. There is not an excess of "heavy estrogens" (watever the hell that's supposed to mean) during recovery.

Surprisingly, I agree with you at the end when you talk about all the "processes in your body that require estrogen." That's why I've been repeating that SERMS have an advantage over AIs. They act like estrogen in several tissues where you want estrogen. In contrast, AI's are much more "all or nothing", you're right. They don't have a dual effect like SERMS do (antiestrogens in some tissues and pro-estrogens in others).

 

[Conciliator]

Bro, your kind of proving my point. Again, writing everything you just did will get old saying it over and over again. Trust me, im not arguing with you. Just saying, unless someone asks the process of how Nolva works, you dont HAVE to go into all that. Also, INDIRECT means an action (in a chain of events) is set forth that causes a secondary action to take place. So yes, it does INDIRECTLY stimulate. Nolva is taken (action)- blocks estrogen (action)- causes negative feedback. These are ALL DIRECT ACTIONS OF NOLVA. What happens next? The inhibition causes GnRH to stimulate LH (action). This is a secondary action brought about by the actions of Nolva. So again, it IS AN INDIRECT ACTION

No, you're still not getting it. I'm not proving any of your points.

We're not talking about "INDIRECT", we're talking about "INHIBITOR." An inhibitor does not having anything to do with stimulation. An inhibitor is an antagonist, not an agonist. Does taking your foot off the brake in a parked car "indirectly stimulate" anything having to do with speed? No. Pressing the gas does, and only pressing the gas.

You say "Nolva is taken (action)- blocks estrogen (action)- causes negative feedback." This is incorrect. You must not understand what is going on. Nolva does not cause negative feedback, it BLOCKS negative feedback That's why you take it. To block the inhibition of LH production that comes (as negative feedback) from estrogen. Nolva does not "indirectly stimulate" anything. GnRH is the only thing that stimulates LH output here. Estrogen interferes with that. When you remove estrogen, you are not stimulating anything. You are removing the inhibition, so that the GnRH can better stimulate LH release.

 

[Conciliator]

IOW, the end result of ingesting Nolvadex may be to cause the production of the luteinizing hormone that in turn stimulates the Leydig cells to produce Testosterone?

It's certainly more accurate to speak the way you suggest but unnecessary as long as the end result is known.

I agree the distinction is unnecessary when all you care about is the final effect on LH. However, I think it's completely misleading to people (like brang) who are trying to understand what exactly is going on.

Semantics.

I agree. Words mean things. In my opinion, to "stimulate" means to act as an agonist, unlike Nolva's mechanism of action. If you want to use simple terminology, I think you'd be better off (and more accurate) saying Nolva "promotes" LH release or "aids in the production" of LH.

You're supposedly the Conciliator, so be conciliatory and not pedantic. The shorthand we've been using will suffice for the limited understanding of most gear-using bodybuilders.

My user name doesn't mean I'm a pacifist. It means I help "reconcile" people with their mistakes

 

[Conciliator]

I believe I am in sync with you here. I think there is plenty of estrogen there in the first place, regarding detection. I just always assumed that the nolva simply does not stimulate test production worth a shit, maybe mildly at best. I have heard that clomid is much more effective and can bring HTPA online in as little as two weeks (150mgs and wean down). FOr whatever reason, idont know, maybe it has a better or more direct effect on the pituitary..?? I have also see some of my sources change their position on this recently. I have never needed or been big into any of them, however that is about to change as I am growing concerned with estrogen more so by day.

At the hypothalamus, both nolva and clomid are strong anti-estrogens. This makes both of them useful for PCT, blocking negative feedback at the hypothalamus and increasing GnRH levels. However, at the pituitary, nolva is anti-estrogenic (increasing LH output for a given amount of GnRH), whereas clomid actually exerts a weak estrogenic effect (reducing LH output for a given amount of GnRH). Based on the reseach, I think Nolva is the stronger anti-estrogen when it comes to the HPTA, making it a better choice for PCT.

Also, I never really thought of Adex and a testosterone stimulator either. I am guessing it is the weakest of the three when it comes to stimulation of the HTPA. Regardless there are going to be LH reception problems in the nuts if there has not been any HCG maintenance. Then you have failed restarts. you know, the ones where the guy comes off the hard long 16-20 week cycle that included some Deca. He states he popped a couple of 2500iu blasts at the end of the cycle prior to clomid and nolva, completes 6-8 weeks of pill protocal, and then when he thinks he is done his titties start hurting again. Well, maybee he should have pinned that 1000iu shot every 4 weeks?!?!?!? I dont know.

I agree with you here. I think that hCG taken during a cycle will do much, much more for recovery than SERMS will after a cycle (though both would be optimal).

 

[bigbench]

No, you're still not getting it. I'm not proving any of your points.

We're not talking about "INDIRECT", we're talking about "INHIBITOR." An inhibitor does not having anything to do with stimulation. An inhibitor is an antagonist, not an agonist. Does taking your foot off the brake in a parked car "indirectly stimulate" anything having to do with speed? No. Pressing the gas does, and only pressing the gas.

You say "Nolva is taken (action)- blocks estrogen (action)- causes negative feedback." This is incorrect. You must not understand what is going on. Nolva does not cause negative feedback, it BLOCKS negative feedback That's why you take it. To block the inhibition of LH production that comes (as negative feedback) from estrogen. Nolva does not "indirectly stimulate" anything. GnRH is the only thing that stimulates LH output here. Estrogen interferes with that. When you remove estrogen, you are not stimulating anything. You are removing the inhibition, so that the GnRH can better stimulate LH release.

Bro, you have to realize that im AGREEING with you on these things. Not trying to argue. Your point is that one should be more descriptive and the other is its ok to make a general statement of the cause and effect. The way its said is (like Solo said) Semantics. Next time, I will choose my words more carefully and be PRECISE instead of making it easier to understand. Both are opinions though so neither one can be wrong.
But the other point, again, Nolva DOES INDIRECTLY STIMULATE LH. LH is stimulated by GnRH ONLY because Nolva was taken. Its not a direct action, but it would not have occured if Nolva was not taken. Its the SECONDARY action or......INDIRECT action. There is nothing to argue on that point as its a fact. Going back to the car does not make sense. I understand what your trying to say with it being an inhibitor. But if a car was on a level ground and not moving and you took the foot off the brake, then nothing happens. There has to be a chain of event set forth to even have the need to apply the brakes first. Hell, if I gave a girl some alcohol, INHIBITED her (lowered her inhibition) and convinced her to cheat on her. Now that, I COULD say I had a dierect effect on that. But if the boyfriend finds out and goes and hits the guy. Well, I didnt DIRECTLY cause that, but I sure as hell set forth the chain of events that had that as an end result. I know, not as analytical as your analogy, but its still funny . But yes brother, I AM agreeing with you. We just have different views

 

[Oxygen]

Goodness !!! it seems to me that you'll never learn "agree to disagree" concept when you can't accept to meet midway,,

Anyhow, back to my problem, please all of you read & help.. I am getting what you can call dull pain/ache in my right testicle (I think), it has been persistent for about 2-3 days now, the slight pain/discomfort travels along my groin,, I can't really tell where is the specific source but its more likely the right testicle as I said,,,I read elsewhere that this could happen during pct sometimes & it could be a good sign that testicle is recovering/getting bigger ? I had the same thing before when I increased my nolvadex dose to 40mg/day, but then when I ran out of it & therefore had to stop, the pain had gone,,,,

now what could be triggering this pain? how long should I wait before seeing an urologist? should I continue with my regimen or stop?

my regimen:

1mg/day adex
activate xtreme
dhea 25mg

 

[jasthace]

Goodness !!! it seems to me that you'll never learn "agree to disagree" concept when you can't accept to meet midway,,

I think we'll all had a bit of a laugh about this thread along the way

Anyhow, back to my problem, please all of you read & help.. I am getting what you can call dull pain/ache in my right testicle (I think), it has been persistent for about 2-3 days now, the slight pain/discomfort travels along my groin,, I can't really tell where is the specific source but its more likely the right testicle as I said,,,I read elsewhere that this could happen during pct sometimes & it could be a good sign that testicle is recovering/getting bigger ? I had the same thing before when I increased my nolvadex dose to 40mg/day, but then when I ran out of it & therefore had to stop, the pain had gone,,,,

now what could be triggering this pain? how long should I wait before seeing an urologist? should I continue with my regimen or stop?

Have you had constant pain for 2-3 days now ,or coming and going {not so much coming I expect}
I think its normal to get the occasional dull ache in a testi,but cant recall having it for any great length of time.
I remember having quite a vivid pain at one stage on cycle,I just presumed it was part of the shutting down experience.
Have you had any more blood tests yet?
I realise that may post has'nt offered you the answers that you want and need,but with out the blood tests,it's like trying to park your car in the dark.{with the handbrake on!}

 

[Oxygen]

Have you had any more blood tests yet?
I realise that may post has'nt offered you the answers that you want and need,but with out the blood tests,it's like trying to park your car in the dark.{with the handbrake on!}

you are right, but shouldn't I stop taking adex so that I get a better/clearer idea about my hormons levels ? to my knowledge that adex slightly affects LH, FSH & increases T levels as well.

so should I take test now or stop adex first & wait for say 1-2 weekst?

 

[jasthace]

you are right, but shouldn't I stop taking adex so that I get a better/clearer idea about my hormons levels ? to my knowledge that adex slightly affects LH, FSH & increases T levels as well.

so should I take test now or stop adex first & wait for say 1-2 weekst?

Blood tests should be done after completion of pct so yes best to come clean before getting the bloods.
Anymore improvements downstairs?
You have made a positive improvement with your latest pct stack,keep going with that for a couple of weeks before trying anything else

 

[Conciliator]

But the other point, again, Nolva DOES INDIRECTLY STIMULATE LH. LH is stimulated by GnRH ONLY because Nolva was taken. Its not a direct action, but it would not have occured if Nolva was not taken. Its the SECONDARY action or......INDIRECT action. There is nothing to argue on that point as its a fact.

No, it is not a fact that "nolva indirectly stimulates LH." Nor is it a fact that LH is stimulated by GnRH "ONLY because nolva was taken." LH is stimulated by GnRH either way, with or without nolva, just with differing amounts of inhibition. Since the anaolgy to a stopped car is not working, let's try again. Imagine a car that's moving at 40 mph. Assume you're pressing the gas down and at the same time pressing the brake, so you have both some stimulation of speed and some inhibition of speed.

Now say you press harder on the gas and go up to 50. Have you decreased inhibition? No. The brake hasn't changed. Have you increased the stimulus for speed? Yes. There's more gas going to the engine.

Now say you ease up on the brake a little and your speed goes up to 60. Have you increased the stimulus for speed? NO, you haven't. The gas, the stimulus, has not changed. What you did was decrease inhibition from the brakes. You need to realize that the brakes do not ever stimulate speed. All they do is stimulate breaking. And when you remove the breaks, with something like nolva, you are NOT stimulating anything. You're just removing inhibition.

Without a stimulus, an inhibitor of negative feedback (like nolva or removing the brakes) will not do anything. They do not stimulate. They are not agonists. They won't have any effect at all unless something that actually does stimulate (like GnRH or a gas pedal) is present.