PCT - Lets get it ironed out (Dr Scally?)

[ApeShitFuckJacked]

Also in ApeShits PCT a low dose of AI is used and extended out 1 week past cessation of clomid and Nolva.

This is used to combat high e2 levels that Nolva and clomid create. And also to prevent the e2 rebound. Which would in turn lower FSH and LH levels more quickly and to a greater extent after coming off the SERMs

I used 12.5mg Aromasin e3d

I believe this is a largely overlooked factor that people do not consider when planning PCT.

Now I'm done, my fingers hurt

Hope you fuckers are happy...

 

[BIGMESC]

1-2)
Arimidex is a poor choice as an AI for BB IMO

Arimidex lowers the anabolic hormone igf-1 by up to 26%

While letrozole and Aromasin
Raise igf-1 levels by 26% and 28% respectively.

Well shit I use Adex had not heard this before.
ASFJ do you have any studies on those numbers you could share.

 

[ApeShitFuckJacked]

It was a Bill Roberts article with what I thought were reputable references so I blindly accepted this as a fact.

Upon doing my own research I am not so certain this is the case. I recede that statement until I can confirm that it is or is not true.

 

[ApeShitFuckJacked]

Ok foot in mouth big time...I apologize the actual number was 18% and it was a think steroids article but it was not written by bill Roberts it was written by L. Rea.

Upon doing my own research findings are extremely inconclusive on the subject.

How do I post links?

 

[CensoredBoardsSuck]

It was a Bill Roberts article with what I thought were reputable references so I blindly accepted this as a fact.

Upon doing my own research I am not so certain this is the case. I recede that statement until I can confirm that it is or is not true.

J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8.
Short-term effects of anastrozole treatment on insulin-like growth factor system in postmenopausal advanced breast cancer patients. Short-term effects of anastrozole... [J Steroid Biochem Mol Biol. 2002] - PubMed - NCBI
Ferrari L1, Martinetti A, Zilembo N, Pozzi P, Buzzoni R, La Torre I, Gattinoni L, Catena L, Vitali M, Celio L, Seregni E, Bombardieri E, Bajetta E.

Abstract

Insulin-like growth factors (IGFs) play a fundamental role in cancer development by acting in both an endocrinal and paracrinal manner, and hormone breast cancer treatments affect the IGF system by modifying circulating growth factor levels. We evaluated total IGF-1, IGF-2, IGF binding protein (IGFBP)-1 and IGFBP-3 in the blood of 34 postmenopausal advanced breast cancer patients (median age 63 years, range 41-85) treated with anastrozole, a non-steroidal structure aromatase inhibitor (NSS-AI). The plasma samples were obtained at baseline, and after 2, 4, 8 and 12 weeks of treatment. The IGFs were quantitated by means of sensitive radioimmunoassays (RIAs). IGF-1 significantly increased during anastrozole treatment (baseline versus 12 weeks, P=0.031), IGF-2 showed a trend towards an increase, and IGFBP-1 constantly but not significantly decreased; IGFBP-3 did not seem to be affected at all. The anastrozole-induced changes in IGFs and IGFBP-1 appeared to be different in the patients receiving a clinical benefit from those observed in non-responders. We have previously shown that letrozole (a different type of NSS-AI) modifies blood IGF-1 levels, and the results of this study of the biological effects of anastrozole on the components of the IGF system confirm our previous observations.


J Cancer Res Clin Oncol. 2013 May;139(5):837-43.
Insulin-like growth factor 1 and musculoskeletal pain among breast cancer patients on aromatase inhibitor therapy and women without a history of cancer. Insulin-like growth factor 1 and mus... [J Cancer Res Clin Oncol. 2013] - PubMed - NCBI
Gallicchio L1, MacDonald R, Helzlsouer KJ.

Abstract

PURPOSE: Musculoskeletal pain is a common side effect of aromatase inhibitors (AIs), the adjuvant hormonal treatment of choice for postmenopausal estrogen-receptor-positive breast cancer. Although the pain is usually attributed to the estrogen depletion associated with AIs, not all women on AIs experience these symptoms. Thus, the goal of this study was to examine whether changes in the insulin-like growth factor (IGF) axis were associated with pain among women initiating AI therapy or a comparison group of women without a history of cancer.

METHODS: Data were analyzed from a cohort study of 52 breast cancer patients for whom AI therapy was planned and 88 women without a history of cancer. Questionnaire data on pain symptoms were collected, and blood was drawn at baseline (prior to AI therapy for patients) and 6 months after baseline. The blood samples were assayed for IGF-1 and IGF-binding protein-3 (IGFBP-3).

RESULTS: While results showed no statistically significant changes in any of the measures across time for either the breast cancer or the comparison group, increases in both IGF-1 concentrations and the IGF-1/IGFBP-3 ratio over the first 6 months of AI treatment were significantly associated with the onset or increase in musculoskeletal pain among the breast cancer patients. Associations between IGF-1, IGFBP-3, and the IGF-1/IGFBP-3 ratio and pain were not observed in the comparison group.

CONCLUSIONS: Although preliminary, findings from this study implicate the IGF axis in the development of AI-associated musculoskeletal pain and represent a first step in developing effective interventions to alleviate this side effect.

 

[ApeShitFuckJacked]

Yep I read this study cbs they also have a letrozole study that they mentioned and you bolded that shows similar increase.

But in young men the letrozole findings seem to contradict these findings in women.

Abstract

Objective To assess and compare the effects of short-term aromatase inhibition on glucose metabolism, lipid profile, and adipocytokine levels in young and elderly men.
Design and methods Ten elderly and nine young healthy men were randomized to receive letrozole 2.5?mg daily or placebo for 28 days in a crossover design.
Results Both in young and elderly men, active treatment significantly increased serum testosterone (+128 and +99%, respectively) and decreased estradiol levels (?41 and ?62%, respectively). Fasting glucose and insulin levels decreased in young men after active intervention (?7 and ?37%, respectively) compared with placebo. Leptin levels fell markedly in both age groups (?24 and ?25%, respectively), while adiponectin levels were not affected by the intervention. Lipid profile was slightly impaired in both groups, with increasing low density lipoprotein-cholesterol levels (+14%) in the younger age group and 10% lower levels of APOA1 in the elderly. A decline in IGF1 levels (?15%) was observed in the younger age group. No changes in weight or body mass index were observed in either young or old men.

I have a feeling that if this study were conducted with anastrozole findings would be bee similar as letrozole and arimidex are both type 2 aromatase inhibitors and function extremely similarly.

 

[ApeShitFuckJacked]

I'll keep researching but at this point it's too hard to say.

I apologize for quoting that L Rea article without fact checking it myself it's something I do not normally do and I feel pretty dumb for putting my trust in it.

 

[CensoredBoardsSuck]

I have a feeling that if this study were conducted with anastrozole findings would be bee similar as letrozole and arimidex are both type 2 aromatase inhibitors and function extremely similarly.

You could be right. It's not something I have any previous knowledge of.

 

[Dr JIM]

Based on the results of three studies I'm aware of both AI's, Anastrozole and Letrozole INCREASE IGF, while the SERMS Tamoxifen and Clomid, both DECREASE IGF.



Jim

 

[Dr JIM]

Sorry CBS I didn't see your post one hour ago, why is that

 

[CensoredBoardsSuck]

Sorry CBS I didn't see your post one hour ago, why is that

I like to fly under the radar.

 

[Dr JIM]

ASF
I've no doubt your referring to the two separate SERM NOT AI's!

Incidentally why do you state SERMS cause a RISE of E-2 SEPARATE of the increased TT.

Both SERMS cause the release of LH and FSH thereby RESTORING PHYSIOLOGIC gonadal TT secretion. The ratio of TT to E-2 is normative.

The rise in E-2 which occurs from the use of SERMS NOT disproportionate, which frequently occurs with HCG use.

Lastly NEITHER AI''s or SERM's cause "rebound".

That notion was concocted in the Golds gym on 6th Avenue in San Fran, Febuary 22nd 1998 at 12noon when two bros decided it "should be so".

The only thing that was missing, a means to propagate this garbage, they pondered briefly, shaking their head in unison; "that's what AAS forums ARE FOR" and quipped, "long live bro science and bro lore!!!

 

[Michael Scally MD]

Some good questions/posts, but unfortunately not within the Blue Collar Radio thread. https://thinksteroids.com/community/threads/134350403

If you wish for me to consider some topics for the broadcast, please post on that thread. If there are no objections, I will merge this thread with Blue Collar Radio later today.

Separately, I look to a TT 350+ with hCG as a marker for possible successful HPTA restoration. If less, I find the likelihood to be less. There is the importance of timing. This brings up the area of synchronization (GnRH Pulse Generator). This is the probable cause for a lower TT level in TRT with a higher baseline. Also, the reason tapering is a non-starter.

On hCG, there are very few times it should NOT be used for PCT (ASIH). It is an important part of ASIH treatment. Otherwise, one will experience a period of hypogonadism! As we all know, hypogonadism causes muscle loss. Why would anyone wish to experience this effect if avoidable.

 

[ApeShitFuckJacked]

Hey dr Jim good to see you here.

I was referring to the AI not SERMs and if you read the study I posted in young men the outcome seems to differ from previous studies conducted in women regarding igf-1 levels. And even more surprisingly Letrozole did not change igf-1 levels at all in older men. So we have three different outcomes with three different groups of people.

I like to control my estrogen while my t production is higher than normal which I assumed it would be on 2000iu HCG no? So I suggested that others should do the same as I only see benefits.

Also the rebound effect I was referring to was the elevated levels of estrogen that may cause Gyno after cessation of the SERM that is no longer protecting the breast tissue receptor sites.

I understand the ratio is relevant to the amount of T being produced but if T is higher than normal I believe estrogen should be controlled. I personally have an affinity for Gyno and take more precaution with estrogen levels than most.

I actually have puberty induced Gyno. It's not horrible but it's noticeable.

I did not mean to infer there was a skewed ratio of estrogen that is being produced. Only that when coming off the SERM e2 levels exceed that of normal production and protection at the receptor sites no longer exists.

 

[BIGMESC]

Bump
Hey all, you don't get an opportunity like this very often.

 

[ApeShitFuckJacked]

(When I use the term normal production I am referring to the specific users natural production not what is considered clinically in range levels.)

 

[ApeShitFuckJacked]

Bump.

 

[IRQ_001]

IRQ - please be carefull starting conversations like this one. I fear that you are going to expose us juicers. Society considers us 'wreckless meathead drug users' who have no respect for our own health. They look at us as idiots who think about nothing beyond how much we can bench press. Your attempts to gain and share knowledge about how to better and more safely use these substances may reveal us to be the cerebral, intelligent, forward thinkers that we are.

We don't want that, now.

We have to be honest with each other bro...there are a LOT of idiots out there that give the responsible among us a bad name.

 

[IRQ_001]

About the only question I don't believe he has addressed is the "optimal TT level" before PCT is begun.

Understandingly NO ONE likes the answer (< 200ng/DL, IMO) and some aimlessly choose to remain ignorant of it's importance by suggesting exogenous AAS are GTG up to, and including the PCT interval (for some).

Things like "low dose TT", "a weak oral like Var", "just bridging doses of AAS", etc come to mind.

Of course their rationale is "to diminish the reduction of gains achieved during a cycle"

Jim

Are you suggesting that <200ng/dl is the set mark for starting PCT? How did you come to this Jim?

 

[IRQ_001]

1-2) Pct wait Time is dose and compound dependent. Different compounds are more or less suppressive to the HPTA at equal doses therefore more half lives must pass in suppressive compounds before an environment for HPTA restoration can be achieved. In the case of testosterone Exogenous T levels should be equal to or less than 500ng/dl this is the equivalent of about 50-75mg of test.

3/6/7) After an optimal HPTA environment is reached HCG should be taken for two weeks 2000iu EOD Dr scally mentions that without a long AAS history 1000iu may be sufficient but I can find no reason not to lean on the side of caution and adopt the more aggressive protocol.

4) Clomid 100mg and Nolva 40mg taken for 4 weeks (first two are during administration of HCG)

5) Arimidex is a poor choice as an AI for BB IMO

Arimidex lowers the anabolic hormone igf-1 by up to 26%

While letrozole and Aromasin
Raise igf-1 levels by 26% and 28% respectively.

Everyone is different regarding their AI dosage. But I would recommend starting doses of 12.5mg ed aromasin and 1mg ed letrozole for 500mg of aromatizable AAS

You should confirm your dosage via blood test not by sensitive/insensitive nipples.

8) When using Deca HPTA suppression generally continues for around 35-40 days after 1 100mg shot of deca.

The half life of the parent hormone is 7-12 days. Pct should be started 40 days after enough half lives have past to reach 100 mg.

In some cases users experience HPTA suppression for longer periods.

I knew you'd come through...Thanks Bro!

The suggested PCT regime seems to contradict Bill Robert's approach where he says that hCG needs to be taken during cycle. This also seems to be the approach of many with successful recoveries. hmmmmm, any other opinions on this?

Noted about the dex but studies are not conclusive with regards to IGF (?) and the other suggestions have more sides from what I recall.

As for the Deca, why does it suppress the HPTA to that degree? It's half life is only three days more that of Test E. Is it related to Metabolites? If so, are there any studies that show that metabolites suppress HPTA (fkn Deca, it's driving me crazy)