Comprehensive Guide to PCT

[ApeShitFuckJacked]

Maintaining the dosage will produce a greater LH and FSH response. In some people these dosages may be more than what is needed to achieve the maximal response but in others it is warranted.

When all is said and done there is no harm in using higher dosages than needed so you might as well air on the side of caution.

The pct you posted would still be very effective in many users but the one I have posted will be more effective in more users.

 

[illuminatty]

Very nice write up ape. I'm in the midst of my test e cycle and I decided to bump it up to 500mg.

I do have hcg on hand, but I'm hesitant to use as my friend used it and broke out in cystic acne.

I will do the standard clomid and tamoxifen

 

[Mike Oxbig]

Very nice write up ape. I'm in the midst of my test e cycle and I decided to bump it up to 500mg.

I do have hcg on hand, but I'm hesitant to use as my friend used it and broke out in cystic acne.

I will do the standard clomid and tamoxifen

Using an AI in conjunction with hCG can help with the E2 sides.

 

[Michael Scally MD]

Using an AI in conjunction with hCG can help with the E2 sides.

Actually, does an AI decrease the E2 from hCG?
Obviously, a loaded question.

 

[ApeShitFuckJacked]

^^^^Si

Mike knows his pct so his suggestions are almost always identical to mine.

Hope you continue answering questions on this thread.

 

[ApeShitFuckJacked]

It decreases the amount of aromatization that occurs thus combating the increase in e2 due to the proportional increase in TT stimulated by HCG.

Hah

Your loaded questions are no match for me.

 

[Mike Oxbig]

Actually, does an AI decrease the E2 from hCG?
Obviously, a loaded question.

To the best of my knowledge the cause of the increased TT doesn't impact the effectiveness of the AI at reducing aromatization?

Is that not the case?

 

[Michael Scally MD]

Actually, does an AI decrease the E2 from hCG?
Obviously, a loaded question.

It decreases the amount of aromatization that occurs thus combating the increase in e2 due to the proportional increase in TT stimulated by HCG.

Hah

Your loaded questions are no match for me.

Actually, no! AIs do NOT work on the hCG induced increase in E2.

 

[ApeShitFuckJacked]

What!!!!

Damnit I lose again

 

[Mike Oxbig]

Actually, no! AIs do NOT work on the hCG induced increase in E2.

Interesting. They appear to work on elevated TT induced by SERMs/real LH, why does substituting hCG with real LH render AIs ineffective?

 

[ApeShitFuckJacked]

Why do they not work?

I am very interested.

 

[ApeShitFuckJacked]

Does this imply that the TT produced from HCG converts to e2 absent of aromatase enzyme?

 

[Michael Scally MD]

Why do they not work?

I am very interested.

Does this imply that the TT produced from HCG converts to e2 absent of aromatase enzyme?

From my reading it is believed to be the inability of the AI to cross the testes/blood barrier. The testes, like the brain, has a special cell structure that prevents many meds from passing. I will find the cite, but what still troubles/perplexes me is the study was not on this claim.

 

[ApeShitFuckJacked]

I'm confused on why HCG would differ from natural test production because it has been shown that AI works on endogenous test production.

This is implying that all aromatization occurs within the testes when testosterone Is produced through HCG.

Why would this not also be the case with natural LH induced test production.

What is the mechanism that makes aromatization occur only within the testes as opposed to natural production?

 

[ApeShitFuckJacked]

This is starting to make less and less sense to me.

Why would aromatization not occur outside the testes when using HCG?

HCG has been shown to raise TT levels in circulating blood.

Therefore the mechanism by which the AI is rendered ineffective cannot be attributed to the inability of the AI to pass the blood barrier in the testes.

UNLESS...

All aromatization from HCG produced test occurs within the testes prior to its release into the bloodstream.

This is the only way your prior explanation can be correct...IMO

 

[ApeShitFuckJacked]

I'm so confused I just repeated my questions twice lol. Refer to the first post my question is articulated better and more simply.

 

[Michael Scally MD]

I have found the following statement that AIs are unable to prevent testicular aromatization. Further support is seen by the escape patient.

Moreover, AIs are not able to inhibit the testicular production of estrogen, which account for 20% of the circulating estrogen.

In Table 1, the patient was on Exemestane with the result the HPTA became very "stimulated." The response was abnormally high E2 level.

One patient (patient 1) had a large increase in E2 level [330 pmol/L], which was associated with an increase in FSH (27.5 mIU/ml) and LH (13.6 mIU/ml) levels.

Doyen J, Italiano A, Largillier R, Ferrero JM, Fontana X, Thyss A. Aromatase inhibition in male breast cancer patients: biological and clinical implications. Annals of Oncology 2010;21(6):1243-5. Aromatase inhibition in male breast cancer patients: biological and clinical implications

Background: The role of aromatase inhibitors (AIs) and their impact on estradiol (E2) levels remain unknown in male breast cancer (MBC) patients.

Patients and methods: MBC patients with metastatic disease and those treated with AIs were selected from the breast cancer database of the Centre Antoine-Lacassagne (Nice, France). Sex hormone levels were retrospectively assessed on serum samples from our institutional serum bank.

Results: Fifteen patients entered the study. Two patients (13%) had complete response, four patients (27%) had partial response, two patients (13%) had stable disease and seven patients (47%) had progressive disease. The median progression-free survival and overall survival were 4.4 months [95% confidence interval (CI) 0.1–8.6] and 33 months (95% CI 18.4–47.6), respectively. All assessable patients (n = 6) had E2 levels less than the lower limit of the assay during AI treatment. Among them, three had partial response, one had stable disease and two had progressive disease. A large increase in follicle-stimulating hormone, luteinizing hormone and E2 levels was observed in one responding patient at progression.

Conclusions: AIs are active in MBC patients. This activity is correlated with a significant reduction in E2 levels. Secondary resistance is in part related to a deleterious feedback loop resulting in a significant increase in substrate for aromatization.

 

[ApeShitFuckJacked]

I'm sorry I need more information to apply this to HCG.

Does all aromatization of HCG induced testosterone occur in the testes?

If so than your original statement is supported by this evidence.

 

[Michael Scally MD]

I'm sorry I need more information to apply this to HCG.

Does all aromatization of HCG induced testosterone occur in the testes?

If so than your original statement is supported by this evidence.

As the hCG induced production of E2 is typically a small percent an AI will still help control. It is a bit of trivia unless you have MBC.

 

[Michael Scally MD]

On MBC, it would be of some interest to see if a GnRH agonist and AI are administered for the "escape" type patient.