Veteran's Consensus Statement on Post-Cycle Recovery - Page 2

archive_Mr. Nobody · 07-10-2003, 07:55 PM

O.k let me expalin my thinking here:

H C G is used to bring back the testicles by supplying exo LH

Clomid is used to jumpstart the HP and force LH production...it has been my experience (through blood tests on myself and some friends as well as other posts on here) that LH is low and stayed low after a cycle for a long time (8 weeks in my case)

Morning dbol is used to fill the gap of no androgens
Androgel...same as morning dbol, however I think the LH suppression is inconclusive (http://anabolicfitness.infopop.net/2...86#8963019286). Furthermore, androgel may suppress via aromatisation to E only. Arimidex could fix that. Arimidex is used not to increase test, its used to keep the added androgens and emerging test production from disrupting the HPTA. But if in doubt, lets take A-gel out.

Somebody said herbs. It has been my experience that all herbal supps were shit. I have tried trib, avena, carao, horny goat weed, maca.....(propably forgot a few)...and looking back, none were worth the bottle they came in.

And yes I agree it is a cycle, its a cycle to get from your cycle to homeostasis.....if you read the whole CS, you will see that 8 weeks off of everything is the minumum time recommended and that blood tests are a must to assess when the next cycle may be started.

At the beginning I said hormonal analysis is the best method to acertain the degree of recovery program necessary. We can sit here and argue about those values, but like said above w/o blood test its all assumptions. And I assumed the worst case scenario and wrote the program for that.

BTW: I was afraid that we would not agree on anything.....test recovery is very much uncharted territory....

Disclaimer:
Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner.
The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice.

[This message was edited by Mr. Nobody on 07-10-2003 at 10:16 PM.]

nandi12 · 07-10-2003, 08:09 PM

Re: Buffering

We had a very lengthy discussion of this at CEM a while back, if you don't mind me linking to my board. The thread is too long to reproduce.

http://www.cuttingedgemuscle.com/For...&threadid=1772

I've exchanged several emails with Torsten (who really is a published medical researcher) about this and he has a program outlined in the thread.

Because I am too cheap to buy the buffering agents he recommends, I have been using what the studies typically use: about 10 grams per day each of NaHCO(3) and KHCO(3). The NaHCO(3) is almost free (baking soda) and the KHCO(3) can be bought cheaply by the kilo of half kilo from chemical supply houses.

My diet is low in sodium anyway so I don't think I am getting an excess from the NaHC0(3)

As a side benefit, the buffering has cured my acid reflux and I no longer have to spend $60 a month on Nexium.

nandi12 · 07-10-2003, 08:21 PM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>O.k let me expalin my thinking here:

H C G is used to bring back the testicles by supplying exo LH

Clomid is used to jumpstart the HP and force LH production...it has been my experience (through blood tests on myself and some friends as well as other posts on here) that LH is low after a cycle.<HR></BLOCKQUOTE>

I agree 100% This is where Bill L is a little mistaken. LH is not high immediately after you quit. It takes many weeks for it to reach higher than baseline levels in an attempt to force the testes into producing more testosterone. We need the clomid for a jumpstart. For example, in Alen et al, baseline LH was 6.8 U/L. At the end of the 12 week cycle it had fallen to 4.7 U/L. (Other studies have shown much greater suppression). Four weeks after that it was still low at 5.2 U/L. It was not until 3 months after quitting that it was above baseline at 8 U/L. Who wants to wait that long for natural LH to climb to prebaseline levels?

archive_macrophage69alpha · 07-10-2003, 08:30 PM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>Originally posted by nandi12:

Basically in my earlier thread I cited a couple of studies that showed post cycle that estrogen is depressed because testosterone is depresssed, and low test means low estrogen since the bulk of our estrogen comes from test aromatization. <HR></BLOCKQUOTE>

only in cases where aromatase is not elevated... ie (one of the more common examples) in older men even with low serum test estrogen levels can be elevated.

are you sure that you want to "just say no" to use of aromatase inhibitors post cycle?
J Clin Endocrinol Metab. 2001 Oct;86(10):4887-94. Related Articles, Links

Inhibition of P450 aromatase enhances gonadotropin secretion in early and midpubertal boys: evidence for a pituitary site of action of endogenous E.

Wickman S, Dunkel L.

University of Helsinki, Hospital for Children and Adolescents, FIN-00029 Helsinki, Finland. sanna.wickman@helsinki.fi

In early pubertal boys, E concentrations are very low. We studied the role and site of action of endogenous E in the regulation of gonadotropin secretion in early and midpubertal boys by inhibiting the action of E with a potent and specific P450 aromatase inhibitor, letrozole. A total of 35 boys who were referred to us because of suspicion of delayed puberty were included in the study. The boys were in either early or midpuberty, and they composed 3 groups: 10 boys did not receive any treatment, 12 boys received T alone, and 13 boys received T and letrozole. In the untreated group during the 5-month follow-up, no changes were observed in 17beta-E2, T, basal gonadotropin, or inhibin B concentrations or in the GnRH-induced gonadotropin responses. In the T-treated group during the 5-month treatment, the T concentration increased by 55% (P < 0.05), and the 17beta-E2 concentration increased by 130% [P < 0.02). Concurrently, basal gonadotropin concentrations were suppressed, but the GnRH-induced gonadotropin responses and the inhibin B concentration remained unchanged. In the T- plus letrozole-treated group during the 5-month treatment, an increase in T concentration of 606% was observed [P < 0.001), but the 17beta-E2 concentration remained unchanged. The changes in the 17beta-E2 concentration within 5 months in the untreated and the T- plus letrozole-treated groups were different [P < 0.02), indicating significant inhibition of endogenous E synthesis during letrozole treatment. During the T plus letrozole treatment, basal gonadotropin concentration, the GnRH-induced LH response, and inhibin B concentration increased, and the GnRH-induced FSH response did not change significantly. Serum nocturnal gonadotropin pulses were determined in 5 boys treated with T and in 5 boys treated with T plus letrozole. In the T- plus letrozole-treated group, the nocturnal LH pulse amplitude increased, and the LH pulse frequency and interpulse interval remained unchanged. In conclusion, in early and midpubertal boys, suppression of the action of E by the P450 aromatase inhibitor increased LH concentration, LH pulse amplitude, and the GnRH-induced LH response, which indicates that in boys during early and midpuberty, endogenous E regulates LH secretion at the site of the pituitary.

MP

archive_macrophage69alpha · 07-10-2003, 08:31 PM

1: J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):437-43. Related Articles, Links

Inhibition of estrogen biosynthesis and its consequences on gonadotrophin secretion in the male.

Bhatnagar AS, Muller P, Schenkel L, Trunet PF, Beh I, Schieweck K.

Department of Research and Development, Pharmaceuticals Division CIBA-GEIGY Limited, Basel, Switzerland.

Of the gonadal steroids in the male, testosterone is the most important regulator of gonadotrophin secretion. However, whether testosterone affects gonadotrophin secretion directly or whether it must first be aromatized to estrogens is controversial. We have reported extensively on the endocrine and anti-tumor effects of the non-steroidal aromatase inhibitors CGS 16949A and CGS 20267 in adult female rats. In these animals, both inhibitors potently and selectively inhibit estrogen biosynthesis. Thus these agents can be effectively used in studying estrogen-dependent processes. CGS 16949A was administered for 14 days to adult male rats, over a dose range which in females suppresses estradiol and elevates LH. In male rats a suppression of estradiol was seen, however, there was no significant effect on either serum LH or on the weights of androgen-dependent organs. CGS 16949A, when administered to healthy men at a dose of 1 mg b.i.d. for 10 days, causes a significant fall in plasma estradiol and significant elevations of plasma FSH and testosterone. Dose-dependent suppression of serum estradiol and an increase in serum testosterone and LH are seen after administration of single oral doses of CGS 20267. These results indicate that in the male rat, inhibition of aromatization of testosterone to estrogens does not influence gonadotrophin secretion whereas in men the negative feedback exerted by testosterone on gonadotrophin secretion is dependent on the aromatization of testosterone to estrogens.

MP

archive_Flash · 07-10-2003, 08:36 PM

...and nootropics.

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>The Role of Anti-estrogens

It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.
<HR></BLOCKQUOTE>

No Bill. The test:estro ratio is precisely why we want an aromataze inhibitor. None of his argument shows me the "little value in using anti-estrogenic drugs". He's lumping competitors and enzyme inhibitors together and thats a mistake. Besides, Arimidex is cool.

archive_macrophage69alpha · 07-10-2003, 08:43 PM

btw- as this is an ongoing travesty... clomifin and nolvadex are NOT ANTI-ESTROGENS.. they are SERMS.. selective Estrogen Receptor Modulators.. they can both "activate" and "block" the ER.. dependent on tissue..(as well as the serm- of which these are but two among many) and in some tissues they have high and some low affinity.. (some virtually none)

MP

archive_the truth · 07-10-2003, 10:57 PM

Nolva isn't getting a lot of mention as an adjuctive tool in recovery. I believe in using clomid, arimidex and nolva post-cycle. I am a big believer in the use of nolva along w/ ari, although it probably wouldn't be useful for me to list my exact protocol here as it changes a bit with each cycle.

I do use d-bol while beginning clomid therapy and taper the d-bol down into a bridge over a two-week course (I only use clomid for 2 weeks, as I respond very well to it). I'll use nolva during that time and add arimidex and finish up with just arimidex and d-bol.

archive_TonyDelk · 07-10-2003, 10:58 PM

Right MP. As I originally wrote in one of my edits to Mr. N, Clomid's role is two fold.

A selective agonist in bone tissue and in helping to improve lipid profiles and an antagonist in the hypothalamus and breast tissue.

Not that it matters anymore, but Bill L's theories and arguments have been attacked by Raymond Scruggs in many of my detailed discussions with him. Actually Animal's theories(part of which are incorporated in this CS)are much more acceptable to Dr Scruggs than anything Bill L has said or written.

I've sent an email to my old buddy Bill Roberts and hopefully we'll have his take on this topic as well.

TD

archive_Mr. Nobody · 07-11-2003, 05:43 AM

Holy cow, my head is spinning. Guys, tell me what needs to be changed to have Consensus:
So far I have:

Take out Androgel since it may be detrimental to the HPTA (inconclusive at the least)

Take out Bromocriptine since it very likely is not needed and has too many negative sides (what about dostinex). MP, somewhat a Bromo advocate, may need to address this as well.

Add in nootropics at the very end......I remember thinking about that. I had done some limited research about nootropics and their impact on hormone production and was convinced of their usefulness (Dr. Mark might agree here)

What else?

Bjaarki, help me here, lol

Disclaimer:
Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner.
The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice.

archive_Bjaarki · 07-11-2003, 05:59 AM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR> Bjaarki, help me here, lol <HR></BLOCKQUOTE>

No need for my help, bro. You and the other knowledgable brothers are doing fine. You're moving toward consensus. Keep doing what you're doing, everyone.

Bjaarki

... Then, do what you have to do.

bigboy · 07-11-2003, 07:24 AM

I have something to add and it is hearsay but makes some sense logically. When coming to the end of the cycle I was told to take 4-5 days off from lifting. Still do aerobics and eat clean. But let the body recover from all of the stress it has been under but do this while still using, bot after the cycle. An example would be at the end when doing say 2 weeks of prop take the last 5 days of prop and stay away from the gym. Then go to the basic movement routine with cessation of drugs and all advice as listed above.... I have not tried this but I am coming off a 9 weeker next week and will be using all of this advice. What do you guys think? Does that make sense? I guess the goal is to really get the body anabolic and prepared for the swings in hormones, moods, etc...

Again, this is gym talk and I have nothing to support or deny it.

DaMan · 07-11-2003, 09:08 AM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>Originally posted by Mr. Nobody:
Holy cow, my head is spinning. Guys, tell me what needs to be changed to have Consensus:
So far I have:

Take out Androgel since it may be detrimental to the HPTA (inconclusive at the least)

Take out Bromocriptine since it very likely is not needed and has too many negative sides (what about dostinex). MP, somewhat a Bromo advocate, may need to address this as well.

Add in nootropics at the very end......I remember thinking about that. I had done some limited research about nootropics and their impact on hormone production and was convinced of their usefulness (Dr. Mark might agree here)

What else?

Bjaarki, help me here, lol

_Disclaimer:
Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner.
The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice._<HR></BLOCKQUOTE>

re dostinex - i used it on-cycle and the first three weeks off and it has DEFINITELY helped with wood/sexdrive, especially on/off fina. no sides for me.

re nootropics - i cycled without (once) and after that with piracetam, hydergine, dmae and choline. i will NEVER do a recovery stack w/o nootropics again, period. ever. without any science to back it up i HIGHLY recommend it. my bloodwork (free and total test) came back HIGHER than it did pre-cycle my last two cycles. this was at least three months after the last shot of prop so i'm pretty sure it's not any remaining estered test in my system. doc was amazed btw.

harddtime · 07-11-2003, 09:55 AM

daman,what doses did you do those nootropics at?

- harddtime

SteveDFW · 07-11-2003, 10:32 AM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>Originally posted by Mr. Nobody:
_Veterans’ Consensus Statement on Post-Cycle Recovery_

_A r i m i d e x_
A powerful aromatize inhibitor shall be part of every cycle. For testosterone recovery it is used to keep the testosterone/ estrogen balance in favor of testosterone. It is also of help to keep any additionally occurring estrogen from dbol and Androgel low to none. Studies have shown a 54% increase of testosterone in eugonadal patients
Week 1-10: ½-1mg ed

[This message was edited by Mr. Nobody on 07-10-2003 at 01:01 PM.]<HR></BLOCKQUOTE>

Can letro be substituted for arimidex?

archive_Iron God · 07-12-2003, 07:45 AM

This topic is assuming we actually come off gear.

archive_Mr. Nobody · 07-12-2003, 08:48 AM

I have no experience with letro. However, anecdotal evidence suggest a possible link between this anti-e and loss of libido.......not something we want post cycle

Alright, seems like we have hit an intermission here, I am still waiting for more direction from our more edumacated members.....and those that were contacted by Ulter to participate

Disclaimer:
Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner.
The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice.

archive_Ulter · 07-12-2003, 10:13 AM

This will probably take a while to complete. Especially this time of year when the boards are empty. It's not a race so let's take our time.

Rattle · 07-13-2003, 05:46 PM

Great Work Guys- this post contains a lot of useful information and is organised, well written and easy to read. Keep up the good work!

w_llewellyn · 07-14-2003, 08:10 AM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>Originally posted by Flash:

No Bill. The test:estro ratio is precisely why we want an aromataze inhibitor. None of his argument shows me the "little value in using anti-estrogenic drugs". He's lumping competitors and enzyme inhibitors together and thats a mistake. Besides, Arimidex is cool.<HR></BLOCKQUOTE>

The point I was making is that ELEVATED E is not suppressing gonadotropins post cycle (no TRUE post cycle estrogen rebound). If you thought I meant you never need anti-estrogen/AI's I think you are misreading the article. I am saying that these drugs are not going to have a significant impact on LH. If you read my article, I even recommend a combination of HCG and Nolvadex.

w_llewellyn · 07-14-2003, 08:14 AM

<BLOCKQUOTE class="**-ubbcode-quote">quote:<HR>Originally posted by macrophage69alpha:
btw- as this is an ongoing travesty... clomifin and nolvadex are NOT ANTI-ESTROGENS.. they are SERMS.. selective Estrogen Receptor Modulators.. they can both "activate" and "block" the ER.. dependent on tissue..(as well as the serm- of which these are but two among many) and in some tissues they have high and some low affinity.. (some virtually none)

MP<HR></BLOCKQUOTE>

Enough whining. Everyone knows they are SERMs. Not every little detail needs to be explained in every article that mentions Nolvadex or Clomid. "Anti-estrogen" is a fully sufficient description unless you want to get into an indepth discussion of its partial agonistic and antagonistic activity. Geez you are a pedantic twit sometimes.

07-10-2003, 08:21 PM	#28 (permalink)
nandi12 Junior Member Join Date: Feb 2002 Posts: 16 Rep Power: 4969	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>O.k let me expalin my thinking here: H C G is used to bring back the testicles by supplying exo LH Clomid is used to jumpstart the HP and force LH production...it has been my experience (through blood tests on myself and some friends as well as other posts on here) that LH is low after a cycle.<HR></BLOCKQUOTE> I agree 100% This is where Bill L is a little mistaken. LH is not high immediately after you quit. It takes many weeks for it to reach higher than baseline levels in an attempt to force the testes into producing more testosterone. We need the clomid for a jumpstart. For example, in Alen et al, baseline LH was 6.8 U/L. At the end of the 12 week cycle it had fallen to 4.7 U/L. (Other studies have shown much greater suppression). Four weeks after that it was still low at 5.2 U/L. It was not until 3 months after quitting that it was above baseline at 8 U/L. Who wants to wait that long for natural LH to climb to prebaseline levels?

07-10-2003, 08:30 PM	#29 (permalink)
archive_macrophage69alpha Senior Member Join Date: Dec 2000 Posts: 1,101 Rep Power: 6942	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>Originally posted by nandi12: Basically in my earlier thread I cited a couple of studies that showed post cycle that estrogen is depressed because testosterone is depresssed, and low test means low estrogen since the bulk of our estrogen comes from test aromatization. <HR></BLOCKQUOTE> only in cases where aromatase is not elevated... ie (one of the more common examples) in older men even with low serum test estrogen levels can be elevated. are you sure that you want to "just say no" to use of aromatase inhibitors post cycle? J Clin Endocrinol Metab. 2001 Oct;86(10):4887-94. Related Articles, Links Inhibition of P450 aromatase enhances gonadotropin secretion in early and midpubertal boys: evidence for a pituitary site of action of endogenous E. Wickman S, Dunkel L. University of Helsinki, Hospital for Children and Adolescents, FIN-00029 Helsinki, Finland. sanna.wickman@helsinki.fi In early pubertal boys, E concentrations are very low. We studied the role and site of action of endogenous E in the regulation of gonadotropin secretion in early and midpubertal boys by inhibiting the action of E with a potent and specific P450 aromatase inhibitor, letrozole. A total of 35 boys who were referred to us because of suspicion of delayed puberty were included in the study. The boys were in either early or midpuberty, and they composed 3 groups: 10 boys did not receive any treatment, 12 boys received T alone, and 13 boys received T and letrozole. In the untreated group during the 5-month follow-up, no changes were observed in 17beta-E2, T, basal gonadotropin, or inhibin B concentrations or in the GnRH-induced gonadotropin responses. In the T-treated group during the 5-month treatment, the T concentration increased by 55% (P < 0.05), and the 17beta-E2 concentration increased by 130% [P < 0.02). Concurrently, basal gonadotropin concentrations were suppressed, but the GnRH-induced gonadotropin responses and the inhibin B concentration remained unchanged. In the T- plus letrozole-treated group during the 5-month treatment, an increase in T concentration of 606% was observed [P < 0.001), but the 17beta-E2 concentration remained unchanged. The changes in the 17beta-E2 concentration within 5 months in the untreated and the T- plus letrozole-treated groups were different [P < 0.02), indicating significant inhibition of endogenous E synthesis during letrozole treatment. During the T plus letrozole treatment, basal gonadotropin concentration, the GnRH-induced LH response, and inhibin B concentration increased, and the GnRH-induced FSH response did not change significantly. Serum nocturnal gonadotropin pulses were determined in 5 boys treated with T and in 5 boys treated with T plus letrozole. In the T- plus letrozole-treated group, the nocturnal LH pulse amplitude increased, and the LH pulse frequency and interpulse interval remained unchanged. In conclusion, in early and midpubertal boys, suppression of the action of E by the P450 aromatase inhibitor increased LH concentration, LH pulse amplitude, and the GnRH-induced LH response, which indicates that in boys during early and midpuberty, endogenous E regulates LH secretion at the site of the pituitary. MP __________________ MP

07-10-2003, 08:31 PM	#30 (permalink)
archive_macrophage69alpha Senior Member Join Date: Dec 2000 Posts: 1,101 Rep Power: 6942	1: J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):437-43. Related Articles, Links Inhibition of estrogen biosynthesis and its consequences on gonadotrophin secretion in the male. Bhatnagar AS, Muller P, Schenkel L, Trunet PF, Beh I, Schieweck K. Department of Research and Development, Pharmaceuticals Division CIBA-GEIGY Limited, Basel, Switzerland. Of the gonadal steroids in the male, testosterone is the most important regulator of gonadotrophin secretion. However, whether testosterone affects gonadotrophin secretion directly or whether it must first be aromatized to estrogens is controversial. We have reported extensively on the endocrine and anti-tumor effects of the non-steroidal aromatase inhibitors CGS 16949A and CGS 20267 in adult female rats. In these animals, both inhibitors potently and selectively inhibit estrogen biosynthesis. Thus these agents can be effectively used in studying estrogen-dependent processes. CGS 16949A was administered for 14 days to adult male rats, over a dose range which in females suppresses estradiol and elevates LH. In male rats a suppression of estradiol was seen, however, there was no significant effect on either serum LH or on the weights of androgen-dependent organs. CGS 16949A, when administered to healthy men at a dose of 1 mg b.i.d. for 10 days, causes a significant fall in plasma estradiol and significant elevations of plasma FSH and testosterone. Dose-dependent suppression of serum estradiol and an increase in serum testosterone and LH are seen after administration of single oral doses of CGS 20267. These results indicate that in the male rat, inhibition of aromatization of testosterone to estrogens does not influence gonadotrophin secretion whereas in men the negative feedback exerted by testosterone on gonadotrophin secretion is dependent on the aromatization of testosterone to estrogens. MP __________________ MP

07-10-2003, 08:36 PM	#31 (permalink)
archive_Flash Senior Member Join Date: Sep 2001 Posts: 1,683 Rep Power: 6972	...and nootropics. <BLOCKQUOTE class="-ubbcode-quote"><font size="-1">quote:</font><HR>The Role of Anti-estrogens It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether)**. We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs. <HR></BLOCKQUOTE> No Bill. The test:estro ratio is precisely why we want an aromataze inhibitor. None of his argument shows me the "little value in using anti-estrogenic drugs". He's lumping competitors and enzyme inhibitors together and thats a mistake. Besides, Arimidex is cool. __________________ SELF ASSEMBLY REQUIRED

07-10-2003, 08:43 PM	#32 (permalink)
archive_macrophage69alpha Senior Member Join Date: Dec 2000 Posts: 1,101 Rep Power: 6942	btw- as this is an ongoing travesty... clomifin and nolvadex are NOT ANTI-ESTROGENS.. they are SERMS.. selective Estrogen Receptor Modulators.. they can both "activate" and "block" the ER.. dependent on tissue..(as well as the serm- of which these are but two among many) and in some tissues they have high and some low affinity.. (some virtually none) MP __________________ MP

07-10-2003, 07:55 PM	#26 (permalink)
archive_Mr. Nobody Senior Member Join Date: Nov 2000 Posts: 5,080 Rep Power: 11861	O.k let me expalin my thinking here: H C G is used to bring back the testicles by supplying exo LH Clomid is used to jumpstart the HP and force LH production...it has been my experience (through blood tests on myself and some friends as well as other posts on here) that LH is low and stayed low after a cycle for a long time (8 weeks in my case) Morning dbol is used to fill the gap of no androgens Androgel...same as morning dbol, however I think the LH suppression is inconclusive (http://anabolicfitness.infopop.net/2...86#8963019286). Furthermore, androgel may suppress via aromatisation to E only. Arimidex could fix that. Arimidex is used not to increase test, its used to keep the added androgens and emerging test production from disrupting the HPTA. But if in doubt, lets take A-gel out. Somebody said herbs. It has been my experience that all herbal supps were shit. I have tried trib, avena, carao, horny goat weed, maca.....(propably forgot a few)...and looking back, none were worth the bottle they came in. And yes I agree it is a cycle, its a cycle to get from your cycle to homeostasis.....if you read the whole CS, you will see that 8 weeks off of everything is the minumum time recommended and that blood tests are a must to assess when the next cycle may be started. At the beginning I said hormonal analysis is the best method to acertain the degree of recovery program necessary. We can sit here and argue about those values, but like said above w/o blood test its all assumptions. And I assumed the worst case scenario and wrote the program for that. BTW: I was afraid that we would not agree on anything.....test recovery is very much uncharted territory.... Disclaimer: Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner. The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice. [This message was edited by Mr. Nobody on 07-10-2003 at 10:16 PM.]

07-10-2003, 08:09 PM	#27 (permalink)
nandi12 Junior Member Join Date: Feb 2002 Posts: 16 Rep Power: 4969	Re: Buffering We had a very lengthy discussion of this at CEM a while back, if you don't mind me linking to my board. The thread is too long to reproduce. http://www.cuttingedgemuscle.com/For...&threadid=1772 I've exchanged several emails with Torsten (who really is a published medical researcher) about this and he has a program outlined in the thread. Because I am too cheap to buy the buffering agents he recommends, I have been using what the studies typically use: about 10 grams per day each of NaHCO(3) and KHCO(3). The NaHCO(3) is almost free (baking soda) and the KHCO(3) can be bought cheaply by the kilo of half kilo from chemical supply houses. My diet is low in sodium anyway so I don't think I am getting an excess from the NaHC0(3) As a side benefit, the buffering has cured my acid reflux and I no longer have to spend $60 a month on Nexium.

07-10-2003, 10:57 PM	#33 (permalink)
archive_the truth Senior Member Join Date: Feb 2001 Posts: 579 Rep Power: 6276	Nolva isn't getting a lot of mention as an adjuctive tool in recovery. I believe in using clomid, arimidex and nolva post-cycle. I am a big believer in the use of nolva along w/ ari, although it probably wouldn't be useful for me to list my exact protocol here as it changes a bit with each cycle. I do use d-bol while beginning clomid therapy and taper the d-bol down into a bridge over a two-week course (I only use clomid for 2 weeks, as I respond very well to it). I'll use nolva during that time and add arimidex and finish up with just arimidex and d-bol.

07-10-2003, 10:58 PM	#34 (permalink)
archive_TonyDelk Senior Member Join Date: Nov 2000 Posts: 749 Rep Power: 6636	Right MP. As I originally wrote in one of my edits to Mr. N, Clomid's role is two fold. A selective agonist in bone tissue and in helping to improve lipid profiles and an antagonist in the hypothalamus and breast tissue. Not that it matters anymore, but Bill L's theories and arguments have been attacked by Raymond Scruggs in many of my detailed discussions with him. Actually Animal's theories(part of which are incorporated in this CS)are much more acceptable to Dr Scruggs than anything Bill L has said or written. I've sent an email to my old buddy Bill Roberts and hopefully we'll have his take on this topic as well. TD __________________ “One Begins to Mistrust Clever People when Embarrassed by their Presence” Friedrich Nietzsche

07-11-2003, 05:43 AM	#35 (permalink)
archive_Mr. Nobody Senior Member Join Date: Nov 2000 Posts: 5,080 Rep Power: 11861	Holy cow, my head is spinning. Guys, tell me what needs to be changed to have Consensus: So far I have: Take out Androgel since it may be detrimental to the HPTA (inconclusive at the least) Take out Bromocriptine since it very likely is not needed and has too many negative sides (what about dostinex). MP, somewhat a Bromo advocate, may need to address this as well. Add in nootropics at the very end......I remember thinking about that. I had done some limited research about nootropics and their impact on hormone production and was convinced of their usefulness (Dr. Mark might agree here) What else? Bjaarki, help me here, lol Disclaimer: Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner. The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice.

07-11-2003, 05:59 AM	#36 (permalink)
archive_Bjaarki Senior Member Join Date: Nov 2000 Posts: 3,673 Rep Power: 13468	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR> Bjaarki, help me here, lol <HR></BLOCKQUOTE> No need for my help, bro. You and the other knowledgable brothers are doing fine. You're moving toward consensus. Keep doing what you're doing, everyone. Bjaarki ... Then, do what you have to do. __________________ First, say to yourself what you would become. Then, do what you have to do.

07-11-2003, 07:24 AM	#37 (permalink)
bigboy Senior Member Join Date: Nov 2000 Posts: 1,170 Rep Power: 7047	I have something to add and it is hearsay but makes some sense logically. When coming to the end of the cycle I was told to take 4-5 days off from lifting. Still do aerobics and eat clean. But let the body recover from all of the stress it has been under but do this while still using, bot after the cycle. An example would be at the end when doing say 2 weeks of prop take the last 5 days of prop and stay away from the gym. Then go to the basic movement routine with cessation of drugs and all advice as listed above.... I have not tried this but I am coming off a 9 weeker next week and will be using all of this advice. What do you guys think? Does that make sense? I guess the goal is to really get the body anabolic and prepared for the swings in hormones, moods, etc... Again, this is gym talk and I have nothing to support or deny it.

07-11-2003, 09:08 AM	#38 (permalink)
DaMan Senior Member Join Date: Aug 2001 Posts: 735 Rep Power: 6078	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>Originally posted by Mr. Nobody: Holy cow, my head is spinning. Guys, tell me what needs to be changed to have Consensus: So far I have: Take out Androgel since it may be detrimental to the HPTA (inconclusive at the least) Take out Bromocriptine since it very likely is not needed and has too many negative sides (what about dostinex). MP, somewhat a Bromo advocate, may need to address this as well. Add in nootropics at the very end......I remember thinking about that. I had done some limited research about nootropics and their impact on hormone production and was convinced of their usefulness (Dr. Mark might agree here) What else? Bjaarki, help me here, lol _Disclaimer: Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner. The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice._<HR></BLOCKQUOTE> re dostinex - i used it on-cycle and the first three weeks off and it has DEFINITELY helped with wood/sexdrive, especially on/off fina. no sides for me. re nootropics - i cycled without (once) and after that with piracetam, hydergine, dmae and choline. i will NEVER do a recovery stack w/o nootropics again, period. ever. without any science to back it up i HIGHLY recommend it. my bloodwork (free and total test) came back HIGHER than it did pre-cycle my last two cycles. this was at least three months after the last shot of prop so i'm pretty sure it's not any remaining estered test in my system. doc was amazed btw.

07-11-2003, 09:55 AM	#39 (permalink)
harddtime Senior Member Join Date: Jul 2001 Posts: 736 Rep Power: 6145	daman,what doses did you do those nootropics at? - harddtime __________________ - harddtime

07-11-2003, 10:32 AM	#40 (permalink)
SteveDFW Member Join Date: Apr 2003 Posts: 55 Rep Power: 4170	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>Originally posted by Mr. Nobody: _Veterans’ Consensus Statement on Post-Cycle Recovery_ _A r i m i d e x_ A powerful aromatize inhibitor shall be part of every cycle. For testosterone recovery it is used to keep the testosterone/ estrogen balance in favor of testosterone. It is also of help to keep any additionally occurring estrogen from dbol and Androgel low to none. Studies have shown a 54% increase of testosterone in eugonadal patients Week 1-10: ½-1mg ed [This message was edited by Mr. Nobody on 07-10-2003 at 01:01 PM.]<HR></BLOCKQUOTE> Can letro be substituted for arimidex?

07-12-2003, 07:45 AM	#41 (permalink)
archive_Iron God Senior Member Join Date: Nov 2000 Posts: 1,291 Rep Power: 7178	This topic is assuming we actually come off gear.

07-12-2003, 08:48 AM	#42 (permalink)
archive_Mr. Nobody Senior Member Join Date: Nov 2000 Posts: 5,080 Rep Power: 11861	I have no experience with letro. However, anecdotal evidence suggest a possible link between this anti-e and loss of libido.......not something we want post cycle Alright, seems like we have hit an intermission here, I am still waiting for more direction from our more edumacated members.....and those that were contacted by Ulter to participate Disclaimer: Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage, use nor condone the use of any illegal substances or the use of legal substances in an illegal manner. The information discussed is strictly for entertainment purposes only and shall not take the place of qualified medical advice.

07-12-2003, 10:13 AM	#43 (permalink)
archive_Ulter Senior Member Join Date: Nov 2000 Posts: 15,388 Rep Power: 21828	This will probably take a while to complete. Especially this time of year when the boards are empty. It's not a race so let's take our time. __________________

07-13-2003, 05:46 PM	#44 (permalink)
Rattle Junior Member Join Date: May 2003 Posts: 24 Rep Power: 4057	Great Work Guys- this post contains a lot of useful information and is organised, well written and easy to read. Keep up the good work! __________________ ----------------------------------------- Strength does not come from winning. Your struggles develop your strengths. When you go through hardships and decide not to surrender, that is strength. ~ Arnold Schwarzenegger

07-14-2003, 08:10 AM	#45 (permalink)
w_llewellyn Junior Member Join Date: May 2003 Posts: 6 Rep Power: 4087	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>Originally posted by Flash: No Bill. The test:estro ratio is precisely why we want an aromataze inhibitor. None of his argument shows me the "little value in using anti-estrogenic drugs". He's lumping competitors and enzyme inhibitors together and thats a mistake. Besides, Arimidex is cool.<HR></BLOCKQUOTE> The point I was making is that ELEVATED E is not suppressing gonadotropins post cycle (no TRUE post cycle estrogen rebound). If you thought I meant you never need anti-estrogen/AI's I think you are misreading the article. I am saying that these drugs are not going to have a significant impact on LH. If you read my article, I even recommend a combination of HCG and Nolvadex.

07-14-2003, 08:14 AM	#46 (permalink)
w_llewellyn Junior Member Join Date: May 2003 Posts: 6 Rep Power: 4087	<BLOCKQUOTE class="**-ubbcode-quote"><font size="-1">quote:</font><HR>Originally posted by macrophage69alpha: btw- as this is an ongoing travesty... clomifin and nolvadex are NOT ANTI-ESTROGENS.. they are SERMS.. selective Estrogen Receptor Modulators.. they can both "activate" and "block" the ER.. dependent on tissue..(as well as the serm- of which these are but two among many) and in some tissues they have high and some low affinity.. (some virtually none) MP<HR></BLOCKQUOTE> Enough whining. Everyone knows they are SERMs. Not every little detail needs to be explained in every article that mentions Nolvadex or Clomid. "Anti-estrogen" is a fully sufficient description unless you want to get into an indepth discussion of its partial agonistic and antagonistic activity. Geez you are a pedantic twit sometimes.