PCT and older AAS users

[Pericles]

As discussed in various other posts (and yes, I may be considered a Dinosaur) I have used a pct protocol (before we even called it PCT) that always worked.

From the age of 30, to the age of 43, I successfully returned my HPTA to normalcy w/ a 2.5 to 3 week run of about 1.5 k IUs e2d (first shot was 5 days after a 100 mg shot of test). I would then run Clomid, at 150 mgs a day for 1 week along w/ 20 mgs of Nolva. I would then go to 100 mgs of Clomid for 5 or so days, then 50. I would run the Nolva dropping down to 10 mgs.

This protocol worked for many years, however the last time I tried (used to feel fairly normal 5-6 days after the introduction of SERMs) I was not responding to the serms.

I wonder if I am at the age where SERMS no longer work?

 

[Michael Scally MD]

Dare I say, LABS.

 

[Michael Scally MD]

Here is some food for thought. While in females, I am sure the same occurs in males.

Zhang X, Wang ZY. Estrogen Receptor-alpha Variant, ER-alpha36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity. Endocrinology. http://endo.endojournals.org/content/early/2013/03/29/en.2013-1116.abstract (Estrogen Receptor-? Variant, ER-?36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity)

Antiestrogens such as tamoxifen provided a successful treatment for ER-positive breast cancer for the past two decades. However, most breast tumors are eventually resistant to tamoxifen therapy. The molecular mechanisms underlying tamoxifen resistance have not been well established. Recently, we reported that breast cancer patients with tumors expressing high concentrations of ER-alpha36, a variant of ER-alpha, benefited less from tamoxifen therapy than those with low concentrations of ER-alpha36, suggesting that increased ER-alpha36 concentration is one of the underlying mechanisms of tamoxifen resistance. Here, we investigated the function and underlying mechanism of ER-alpha36 in tamoxifen resistance. We found that tamoxifen increased ER-alpha36 concentrations and tamoxifen-resistant MCF7 cells expressed high concentrations of ER-alpha36. In addition, MCF7 cells with forced expression of recombinant ER-alpha36 and H3396 cells expressing high concentrations of endogenous ER-alpha36 were resistant to tamoxifen. ER-alpha36 downregulation in tamoxifen-resistant cells with the shRNA method restored tamoxifen sensitivity. We also found tamoxifen acted as a potent agonist by activating phosphorylation of the AKT kinase in ER-alpha36 expressing cells. Finally, we found that cells with high concentration of ER-alpha36 protein were hypersensitive to estrogen; activating ERK phosphorylation at pM range. Our results thus demonstrated that elevated ER-alpha36 concentration is one of the mechanisms by which ER-positive breast cancer cells escape tamoxifen therapy and provided a rational to develop novel therapeutic approaches for tamoxifen resistant patients by targeting ER-alpha36.

 

[Pericles]

Oh, just noticed that I was not clear....1.5k IUs was of HCG.

No labs, but I have always been able to tell when my HPTA is up and running. Usually about 5-6 days after starting the Clomid/Nolva stack.

Another clear indicator is my ability to get wood.

 

[Pericles]

Here is some food for thought. While in females, I am sure the same occurs in males.

Zhang X, Wang ZY. Estrogen Receptor-alpha Variant, ER-alpha36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity. Endocrinology. http://endo.endojournals.org/content/early/2013/03/29/en.2013-1116.abstract (Estrogen Receptor-? Variant, ER-?36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity)

Antiestrogens such as tamoxifen provided a successful treatment for ER-positive breast cancer for the past two decades. However, most breast tumors are eventually resistant to tamoxifen therapy. The molecular mechanisms underlying tamoxifen resistance have not been well established. Recently, we reported that breast cancer patients with tumors expressing high concentrations of ER-alpha36, a variant of ER-alpha, benefited less from tamoxifen therapy than those with low concentrations of ER-alpha36, suggesting that increased ER-alpha36 concentration is one of the underlying mechanisms of tamoxifen resistance. Here, we investigated the function and underlying mechanism of ER-alpha36 in tamoxifen resistance. We found that tamoxifen increased ER-alpha36 concentrations and tamoxifen-resistant MCF7 cells expressed high concentrations of ER-alpha36. In addition, MCF7 cells with forced expression of recombinant ER-alpha36 and H3396 cells expressing high concentrations of endogenous ER-alpha36 were resistant to tamoxifen. ER-alpha36 downregulation in tamoxifen-resistant cells with the shRNA method restored tamoxifen sensitivity. We also found tamoxifen acted as a potent agonist by activating phosphorylation of the AKT kinase in ER-alpha36 expressing cells. Finally, we found that cells with high concentration of ER-alpha36 protein were hypersensitive to estrogen; activating ERK phosphorylation at pM range. Our results thus demonstrated that elevated ER-alpha36 concentration is one of the mechanisms by which ER-positive breast cancer cells escape tamoxifen therapy and provided a rational to develop novel therapeutic approaches for tamoxifen resistant patients by targeting ER-alpha36.

So, the Cliffs Note version is that people can develop a tolerance, reduced response, to Nolva. That makes sense. That is also why I have always gotten good results from Clomid, I only use it for short periods 2-3 times a year.

 

[Pericles]

Dare I say, LABS.

It takes the whole day to get into seeing him, and he is booked months ahead. I get labs twice a year.

It has been 5 days since my last shot of HCG (which also shuts down the HPTA) a month since last 100 mg shot of test, and have been taking fairly large amounts of serms (150-200 mgs of Clomid, 40 mgs of Nolva ed) starting 2 days after last shot of HCG.

I feel fairly good, have been training like an animal all week, except now I am taking 2 days off per week, cut my cardio to 3 days per week). I am still doing hardcore lifting for an hour, followed by some stretching/yoga. I then do 25 minutes on bags, doing abs between rounds . The difference now I that I am totally exhausted and don't bounce back the way I do on cycle. I do this routine MWF, and take Tue/Thursday off.

Although I feel good, Mister happy down there seems to have abandoned his post. No morning wood, or any desire to look at porn. I would estimate that my test has dropped to the 4-500 level or so. Interestingly, my lack of obsession w/ sex has freed up a great deal of my time and I am getting more done.

My goal right now is stay off a bit longer. Yes, I did a fairly large cycle, but I spent 3 weeks on fairly low test (300 first week, then 200 last 2 weeks). It has been almost 4 weeks since last 100 mg shot of test (and 4 days earlier, I did 100) so the test esters are 100% gone. I want to stay off for at least another week regardless of how I feel, and longer if the Serms are working (again, real easy to tell from Mr Happys' reports).

My Hematocrit is way down (42 from last labs...probably lower now) so things look good for my next cycle.

 

[DTdr2]

PS Labs Founder, care to comment on this for Pericles :banghead:

 

[Pericles]

PS Labs Founder, care to comment on this for Pericles :banghead:

He just needed for me to explain how I trained and competed w/ Arnold who had not competed in more then 20 years. Here is the explanation

You see my dear flounder, being the clever man that you are, were able to do the math and size up the discrepancy.

I didn't train w/ the 70's bodybuilding champ, I trained with the 90's version when Arnold was sent back in time to find some chick.....what was her name again...oh yea, her name was Sarah Connor The Arnold from the future was obsessed w/ her, after each set, he would sit up, look around the room and say "Sarah Connor?"

I swear man, I never met a guy so obsessed w/ some chick. I mean seriously, Arnold was the man, he could get any chick (even the maid). I was kind of disappointing, but I guess Sarah Connor must have given him his best blow job ever.

 

[Pericles]

No Terminator fans?

 

[DTdr2]

PS Labs Founder..." I'll be back"

 

[Pericles]

PS Labs Founder..." I'll be back"

Thank you...at least one person got the joke[)]

 

[BBC3]

But this would imply (as some have speculated in the past) that folks could indeed biologically compensate for the presence of an SERM via natural biological compensation methods. NOT ONLY, but that there could be a "rebound" period after SERM usage, and potentially even permanent? ( I doubt they go that far in review/results description).

We must also note that these studies apply to breast cancer conditions, further denoting the gravity of the extent and duration that these women involve themselves with these drugs - which makes a PCT look like a "flavor test". There must be a curve in response based on the time of CONTINUED SERM usage I have to speculate, and I bet that 1,,,,,,,,+1,,,+1,+1,,,,,1 (<) DOES NOT = Five...

Here is some food for thought. While in females, I am sure the same occurs in males.

Zhang X, Wang ZY. Estrogen Receptor-alpha Variant, ER-alpha36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity. Endocrinology. http://endo.endojournals.org/content/early/2013/03/29/en.2013-1116.abstract (Estrogen Receptor-? Variant, ER-?36, is Involved in Tamoxifen Resistance and Estrogen Hypersensitivity)

Antiestrogens such as tamoxifen provided a successful treatment for ER-positive breast cancer for the past two decades. However, most breast tumors are eventually resistant to tamoxifen therapy. The molecular mechanisms underlying tamoxifen resistance have not been well established. Recently, we reported that breast cancer patients with tumors expressing high concentrations of ER-alpha36, a variant of ER-alpha, benefited less from tamoxifen therapy than those with low concentrations of ER-alpha36, suggesting that increased ER-alpha36 concentration is one of the underlying mechanisms of tamoxifen resistance. Here, we investigated the function and underlying mechanism of ER-alpha36 in tamoxifen resistance. We found that tamoxifen increased ER-alpha36 concentrations and tamoxifen-resistant MCF7 cells expressed high concentrations of ER-alpha36. In addition, MCF7 cells with forced expression of recombinant ER-alpha36 and H3396 cells expressing high concentrations of endogenous ER-alpha36 were resistant to tamoxifen. ER-alpha36 downregulation in tamoxifen-resistant cells with the shRNA method restored tamoxifen sensitivity. We also found tamoxifen acted as a potent agonist by activating phosphorylation of the AKT kinase in ER-alpha36 expressing cells. Finally, we found that cells with high concentration of ER-alpha36 protein were hypersensitive to estrogen; activating ERK phosphorylation at pM range. Our results thus demonstrated that elevated ER-alpha36 concentration is one of the mechanisms by which ER-positive breast cancer cells escape tamoxifen therapy and provided a rational to develop novel therapeutic approaches for tamoxifen resistant patients by targeting ER-alpha36.