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

[IRQ_001]

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

anything you can add with regards to arimidex? Can you please provide the studies you referred to?

 

[IRQ_001]

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.

Doc, would you be able to confirm some of the findings so far?

 

[ApeShitFuckJacked]

Yes it's because of the metabolites..a study was posted in another thread a few weeks ago. It suggest that 100mg shot of deca suppresses HPTA function for a little longer than I have stated. I believe it's around 50 days.

The exact time is not concrete but from what I've seen I believe 40 days is reasonable.

40-50 days is going to give you the best chance at recovery but I lean toward the lower end because HPTA suppression is very limited at 40 days out and with this pct protocol your first two weeks are shooting HCG which is suppressive of LH anyway.

 

[IRQ_001]

Yes it's because of the metabolites..a study was posted in another thread a few weeks ago. It suggest that 100mg shot of deca suppresses HPTA function for a little longer than I have stated. I believe it's around 50 days.

The exact time is not concrete but from what I've seen I believe 40 days is reasonable.

40-50 days is going to give you the best chance at recovery but I lean toward the lower end because HPTA suppression is very limited at 40 days out and with this pct protocol your first two weeks are shooting HCG which is suppressive of LH anyway.

When you say suppressed, do you mean the length of period before you can start PCT? If so, 40 days is hardly a suppression compared to test E where you are suppressed for a little over a month. If this is the case, I say Deca's widely known massive gains out weigh the relatively longer suppression period to Test E. If I'm mistaken, how long does test E supress you for? I don't know what I'm missing.... why do people say they can't seem to recover for months???

 

[ApeShitFuckJacked]

Because it is roughly 40 days after only 100mg is in your system.

For example if you shot 400mg deca a week for a period of 4 weeks or more you would have the equivalent of roughly 800mg of deca in your blood.

Therefore you would have to wait 21 days plus another 40 or more. That's over two months.

And I calculated this with a 7 day half life not a possible 12 day half life.

It could easily take much longer.

 

[Dr JIM]

Jim

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.

According to this study (a journal source is missing) a 15% reduction of igf occurred? Compared to what: The "older patients" in the study, the younger age cohort. Placebo group etc. Was this change a relative or absolute reduction?

Was this "decline" statistically significant if so what was the p value because with only ten patient it would need to be much lower than 0.05, imo.

Lastly although there are many similarities between letro and anastrozole such as moa, their half life and dosage are quite different. Asaf how many bb are using 2.5 mg a day of letro?

Very few ime. Why? In part because it significantly reduces all estrogens in a similar manner and because complete clearance is not achieved for as many as 60 days.


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.

 

[msanchez]

What about with Test E, ASFJ?

Many successful users have told me that an "estimate" to start is roughly 14 days after last injection after a 8-12 week cycle. Obviously, this can change person-to-person, but I wasn't too sure where the 14 days came from.

 

[IRQ_001]

Because it is roughly 40 days after only 100mg is in your system.

For example if you shot 400mg deca a week for a period of 4 weeks or more you would have the equivalent of roughly 800mg of deca in your blood.

Therefore you would have to wait 21 days plus another 40 or more. That's over two months.

And I calculated this with a 7 day half life not a possible 12 day half life.

It could easily take much longer.

I just did the calculation using the calculator. The calculator is assuming a half-life of about 10 days for Deca. According to the answer of using 400mg deca vs 400mg Test E, the difference is only 10 days. If this is the case, stack Deca with Test E and stop it two weeks prior to last injection as normally advised and voila!!! no?

PCT Calculator | Post Cycle Therapy Calculator

 

[IRQ_001]

What about with Test E, ASFJ?

Many successful users have told me that an "estimate" to start is roughly 14 days after last injection after a 8-12 week cycle. Obviously, this can change person-to-person, but I wasn't too sure where the 14 days came from.

Bro, drop the two week advice... as per earlier responses, the start of PCT is also dose dependant and therefore varies. Use the calc below for a more precise answer.

In the case of 500mg per week, PCT should start about three weeks post last injection. in the case of 250mg per week, PCT can start two weeks post last injection.

PCT Calculator | Post Cycle Therapy Calculator

 

[joe0035]

Bro, drop the two week advice... as per earlier responses, the start of PCT is also dose dependant and therefore varies. Use the calc below for a more precise answer.

In the case of 500mg per week, PCT should start about three weeks post last injection. in the case of 250mg per week, PCT can start two weeks post last injection.

PCT Calculator | Post Cycle Therapy Calculator

Gentlemen I am really enjoying this thread and BRAVO!!! A thought I come from the old long ester school, Lets put deca a side for a sec. Since coming back I have read most of what you are talking about and ran different cycles ideas and the how and whens of pct using half lives and the pct calculator and the one thing I came up with is in the old days access to compounds was more limited so was pct knowledge but know days why would someone do a whole long ester cycle in the first place??? Take the basic test cycle, why run it the full 12 weeks lets say when you could switch the last couple weeks to prop allowing test e to clear finish the cycle and begin recovery SO MUCH FASTER!!! Now thoughts I have had on this is, well given Scally's hcg then clomid/nolva guide line how does the hcg blast period fall in the prop scenario, and if thats the way we go would lets say lower dose hcg 250mg x 2 a week in the last few weeks to restore testicular volume then stop with the last week of test p allow the same hcg benift and allow us to get to that magic number to start pct with clomid/nolva MUCH sooner and hopefully full recovery quicker and with more gains kept?

 

[ApeShitFuckJacked]

Of course letrozole and Adex are different but the MOA is the same as you stated therefore I believe the effect on cross talk between estrogen and igf-1 levels would be similar.

 

[ApeShitFuckJacked]

HCG blast period still would begin once Ex test is at 50mg.

And yes pct can be started much sooner when propping out of a cycle because the half life is significantly shorter. I'm would do this on all my cycles.

If you really want to maximize gains and keep TT levels higher with a shorter wait period you could switch from test e to test p 3 weeks before cycle ends then switch to TNE 1 week before cycle ends.

Wait Time between last injection and pct would be only 2 days!!!

 

[CensoredBoardsSuck]

According to this study (a journal source is missing) a 15% reduction of igf occurred? Compared to what: The "older patients" in the study, the younger age cohort. Placebo group etc. Was this change a relative or absolute reduction?

Was this "decline" statistically significant if so what was the p value because with only ten patient it would need to be much lower than 0.05, imo.

Lastly although there are many similarities between letro and anastrozole such as moa, their half life and dosage are quite different. Asaf how many bb are using 2.5 mg a day of letro?

Very few ime. Why? In part because it significantly reduces all estrogens in a similar manner and because complete clearance is not achieved for as many as 60 days.

I believe this is the study ASJF cited. A link to the full study is below.

• In young men, aromatase inhibition resulted in presumably lower fasting glucose levels, and markedly lower insulin and IGF1 levels. These findings corroborate with those of Wickman et al. who reported decreased insulin levels, correlating with changes in IGF1 levels, in boys treated long-term with T plus letrozole (9). By contrast, 2 years administration of letrozole to younger peripubertal boys did not improve insulin sensitivity (HOMA) (10). In line with our results in elderly men, Dougherty et al. found no changes in insulin sensitivity (HOMA) in elderly men with mild hypogonadism after 12 weeks of aromatase inhibition (anastrozole 1?mg daily or 2?mg weekly) (11).

• Together with our data, these observations might suggest that short-term effects of aromatase inhibition on glucose and lipid metabolism could be due to effects on GH and IGF1 metabolism, as endogenous estrogens are known to stimulate secretion of these hormones (13) and effects of IGF1 on glucose metabolism are well established (14). This could also explain the discrepant effects of aromatase inhibition in young versus elderly men, since IGF1 metabolism is known to decrease with ageing (15). However, 10-week administration of anastrozole (1?mg/day) to eight healthy men did not affect insulin, glucose, or lipid levels, despite decreasing IGF1 concentrations (16), nor were lipid levels affected in another study (17). In this regard, possible differences between studies might be explained by the higher aromatase-inhibiting potency of letrozole as compared with anastrozole (18). However, age-specific effects cannot be excluded, since despite similar changes in both of our age groups after active intervention, younger men presented higher absolute levels of FT and FE2 as compared with elderly men, both before and after treatment and in line with the well-known age-related changes in sex steroid levels. In addition, there is evidence for a decreased number of androgen receptors, and thus androgen sensitivity, in various tissues in elderly men (5). Taken together, age-specific effects may, at least partly, explain our divergent findings between young and elderly men.

Eur J Endocrinol. 2009 Mar;160(3):397-402.
Short-term aromatase inhibition: effects on glucose metabolism and serum leptin levels in young and elderly men. Short-term aromatase inhibition: effects on... [Eur J Endocrinol. 2009] - PubMed - NCBI
Lapauw B1, T'Sjoen G, Mahmoud A, Kaufman JM, Ruige JB.

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.

CONCLUSIONS: Short-term aromatase inhibition appears to affect glucose metabolism in young men, and lipid metabolism, including leptin secretion, in young and elderly men. Furthermore, the short period of exposure suggests that these changes might be mediated by direct effects of sex steroids rather than by changes in body composition.
Short-term aromatase inhibition: effects on glucose metabolism and serum leptin levels in young and elderly men

 

[Dr JIM]

Oh come on now ASSF your brighter than that!

Because when discrepancies occur in the literature as you suggest, yet I am unable to confirm, you need to present more than "I think" as evidence.

Nope one first needs to critically review that citation which deviates from the norm, YOURS, to compare and contrast the elements of each study in an effort to explain the differences in outcome. Perhaps after this is completed, extrapolation to a larger cohort of users, BB in this instance, would be possible.

Incidentally the ONLY PLACE I've located statements that ANY AI lowers IGF is on BB forums! Consequently ABSENT A PEER REVIEWED CITATION, it makes me curious what are their sources?,

Finally I believe, as do many Endo's, Adex is probably the "best" overall AI, for a variety of reasons. In that regard you have yet to present evidence which justifies or supports the contrary viewpoint of your original statement that, AMIRIDEX LOWERS IGF by 28% and should NOT BE USED FOR AT ALL THAT REASON.

Regards
JIM

 

[Dr JIM]

Damn you CBS arg! After I just commented I could not locate it!

Thx, I'll look it over!

 

[IRQ_001]

HCG blast period still would begin once Ex test is at 50mg.

And yes pct can be started much sooner when propping out of a cycle because the half life is significantly shorter. I'm would do this on all my cycles.

If you really want to maximize gains and keep TT levels higher with a shorter wait period you could switch from test e to test p 3 weeks before cycle ends then switch to TNE 1 week before cycle ends.

Wait Time between last injection and pct would be only 2 days!!!

Ape, why 50mg? why not 100mg? How did you come to this conclusion?

Also for switching from Test E to to Test P, lets say i go on a 10 week cycle of test E at 750mg/wk where I would inject 375mg every sunday and wednesday. When do I inject my first test P shot and what would be the concentration every other day thereafter for three weeks?

 

[CensoredBoardsSuck]

This study was cited by the one ASJF posted. Again, a link to the full paper is below.

• In the testosterone-plus-placebo-treated group, the insulin concentration did not change, but in the testosterone- plus-letrozole-treated group, the concentration decreased during letrozole treatment, suggesting an improvement in insulin sensitivity in the latter group. It is noteworthy that insulin concentrations decreased during letrozole treatment, despite a more than 5-fold higher increase in the mean testosterone concentration in this group. This finding indicates that an increase in the concentration of androgens during puberty does not contribute significantly to the development of insulin resistance in boys.
  
  
  
  
• Since no pubertal increases in IGF-I or IGFBP-3 concentrations were observed during letrozole treatment, the decrease in insulin concentrations during letrozole treatment may have been due to the suppression of GH secretion. This suggestion is further supported by the finding that the changes in insulin concentration correlated positively with the changes in IGF-I concentration. These observations suggest tight regulation of glucose–insulin homeostasis by GH in pubertal boys. Thus, a decrease in insulin sensitivity in boys during adolescence may result from the increasing action of GH; this has previously been demonstrated in groups of adolescents composed of both sexes (2–5, 7).

Eur J Endocrinol. 2002 Mar;146(3):339-46.
The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor. The role of sex steroids in the regulation ... [Eur J Endocrinol. 2002] - PubMed - NCBI
Wickman S1, Saukkonen T, Dunkel L.

Abstract

OBJECTIVE: Our purpose was to study the sex steroid-mediated changes in serum insulin and lipid concentrations in boys during puberty.

DESIGN AND METHODS: We treated boys with constitutional delay of puberty either with testosterone plus placebo or with testosterone plus an aromatase inhibitor, letrozole, which inhibits the conversion of androgens to oestrogens. We demonstrated previously that during treatment with testosterone plus letrozole the increase in testosterone concentration was more than 5-fold higher than during treatment with testosterone plus placebo. The concentrations of 17beta-oestradiol, IGF-I and IGF-binding protein-3 increased during testosterone-plus-placebo treatment, but during testosterone-plus-letrozole treatment the concentrations remained unchanged. These divergent changes in the two groups enabled us to study the effects of sex steroids and GH on insulin sensitivity and lipid concentrations.

RESULTS: The insulin concentration in the testosterone-plus-placebo-treated group did not change. In contrast, in the testosterone-plus-letrozole-treated group, the concentration decreased during letrozole treatment, indicating improved insulin sensitivity. Changes in insulin and IGF-I concentrations within 12 and 18 months were correlated. In the testosterone-plus-placebo-treated group, the high-density lipoprotein cholesterol concentration did not change but in the testosterone-plus-letrozole-treated group the concentration decreased. The concentrations of low-density lipoprotein cholesterol (LDL-cholesterol) and triglycerides did not change in either of the groups.

CONCLUSIONS: The findings indicate that androgens do not directly alter insulin sensitivity in boys during puberty. In contrast, the observations suggest tight regulation of glucose--insulin homeostasis by GH in boys at this stage. Furthermore, our findings indicate that sex steroids do not significantly participate in the regulation of serum concentrations of LDL-cholesterol or triglycerides in boys during early and mid-puberty.

The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor

 

[ApeShitFuckJacked]

Dr. I'm sorry but you need to go back through my statements I admitted to quoting an article written by L Rea. on decrease in igf-1 through use of arimidex which I did not fact check.

Therefore I immediately receded the entire statement and corrected the figure which was 18% reduction.

Upon doing my own research I concluded that I could not say either way if it lowered or raised igf-1 levels because of the study I cited.

I used the phrase "I think" as it is meant to be used not as evidence to back up a claim (I had already discredited the L. Rea article I cited ) I was only speculating a possible correlation between the letrozole study I cited and Adex. There was no hidden agenda of proving my original statement was correct. I believe this is what your referring to?

I'm not trying to imply you are wrong in any way by citing this study and questioning the study cbs cited, rather that my statement about inconclusive evidence was not a sad attempt at covering up a mistake I had made in citing the L Rea article. I admitted to that and did my best to find legitimate evidence to prove or disprove the article and upon doing so found I was not able to give a definitive answer.

Again at this point I have still receded my original statement on Adex. I'm not trying to back this statement in any way shape or form.

 

[ApeShitFuckJacked]

That being said I believe a study conducted in young men is much more accurate for our purposes than studies conducted in pubertal boys and women.

 

[ApeShitFuckJacked]

I came to 50mg conclusion based on the fact 100mg shot generally puts TT at about 800ng/dl

Therefore 50mg should put TT between 400-500ng/dl
(The conversion ratio lessens as doses increase therefore 50mg may be a little over 400)

This is a good environment to begin pct IMO clomid and nolva will still have a significant effect at this point and you are more likely to not allow your TT to fall below 300ng.

As for the test prop I would start the first injection on the day you would inject your test e approximately 4wks (your using 750mg not 500mg) before you plan to end your cycle. The first week should be half dose you were previously on. 2nd week 3/4 dose and from there full dose.

You don't want to spike your test levels. You could play with it and get the exact increase in mg day by day but that seems a bit excessive to me. This will be very effective and much simpler.