HCG during cycle; Clomid, Nolvadex, and Clenbuterol as PCT?

[Ironbender]

I was advised by one of the posters here that I can use HCG towards the end of the cycle or simply means within the cycle. And he seems right after doing my research. Now, I would like to know if anyone ever used Clomid (100 mg, then 50 mg) and Nolvadex (20 mg) with Clenbuterol (2 weeks on, 2weeks off, 2 weeks off)?

 

[Dr JIM]

What would be the objective for alternating the SERMS or adding Clen

 

[Ironbender]

What would be the objective for alternating the SERMS or adding Clen

To help me dry out after all the water retention from T-C and Dbol.

 

[Dr JIM]

The half life of Dbol is about ONE day consequently any fluid retention should have resolved before you start PCT. Moreover any volume overload from T-C or Dbol will be quite limited if an AI is included in your cycle. Furthermore Novladex has AGONIST activity in some folks mimicking the effects of elevated estrogen. Lastly since Clen is a beta agonist it's effect on volume status would be minimal.

 

[Ironbender]

The half life of Dbol is about ONE day consequently any fluid retention should have resolved before you start PCT. Moreover any volume overload from T-C or Dbol will be quite limited if an AI is included in your cycle. Furthermore Novladex has AGONIST activity in some folks mimicking the effects of elevated estrogen. Lastly since Clen is a beta agonist it's effect on volume status would be minimal.

So what do you suggest for me to use in my PCT?

 

[Ironbender]

BTW Doc I didn't use an AI during my cycle. I hope you can tell me what should I use. Thanks.

 

[Dr JIM]

When will your cycle end?

 

[Ironbender]

When will your cycle end?

My last injection of Test C will be on December 29 doc. I'm on my 7th week now. I just used T-C and Dbol. And I think it's settled in the other thread that for a first cycle it's better to use just one oral. So I will stick with Dbol and let go of Anavar or Winny.

 

[Dr JIM]

1)Acquire some Hcg and start 250 IU QOD,
2) If you've never used Hcg before have an AI on hand because the E-2 sides can be a problem for some.
3) Around week 1-3 start HCG 1000-2500IU QOD and continue until Clomid therapy begins at week five ( the amount and duration will depend the degree of testicular atrophy and AAS cycle dosing)
3) Clomid should be used for PCT after HCG has turned your family jewels into mountain oysters, around week 4-6 AFTER your cycle has ENDED with a loading dose of 200-300mg the 50-100mg QD. Labs (TT, E-2, LH) should be obatined 6 weeks into, that's 10-12 weeks after your cycle has ended PCT.
4) These are rough numbers and dates so you have an idea of what it's about AND what you need to PURCHASE ASAP! I'll look back on your cycle and provide more exacting dates and doses

 

[Donzi]

My last injection of Test C will be on December 29 doc. I'm on my 7th week now. I just used T-C and Dbol. And I think it's settled in the other thread that for a first cycle it's better to use just one oral. So I will stick with Dbol and let go of Anavar or Winny.

Why run dbol if u are trying to dry out. ?? I run HCG as part of TRT. will also hit it mid cycle and PCT just at diff, iu.. Anavar will keep u nice and lean while allowing u to increase LBM.

 

[Jimmyinkedup]

1- start hcg now - 250iu - 2x/week -run it up to pct. Have an ai on hand as was mentioned. You should be using one anyway . estrogen should be maintained at normal clinicla levels even when on cycle.
2- PCT nolva and clomid clomid 70/35/35/35 nolva 40/20/20/20
3- dont run ai in pct..run it up to pct
4- low dose clen is fine in pct but get ketotifen so you can run it entire pct and not 2on / 2 off ...

 

[Dr JIM]

The laboratory determination of E-2 levels is NOT routinely obtained DURING a cycle because treatment (lowering of E-2) is essentially only indicated when SIGNS and SYMPTOMS of an elevated level occur. Consequently, since aromatase activity AND E-2 receptor "responsiveness" is quite individualized, routine prophylaxis using an AI is simply not warranted. Additionally, there is NO evidence based on existing research or clinical outcome measures, that combining two SERMS affords any additional benefit compared to using one exclusively and only servers to complicate PCT. This is particularly relevant since Clomid has been shown to possess more central E-2 antagonist activity than Tamoxifen, and the literature is replete with studies involving Clomid's use for the treatment of male hypogonadotropic hypogonadism, compared to Tamo where the citations are very few.
Using Clen or any other beta agonist is not contraindicated during PCT, but it will NOT have any direct effect on physiologic free water, because of an increased E-2.
Lastly using both HCG and an AI "up to PCT" will NEGATE (because of increased TT levels via competitive inhibition) the E-2 antagonistic effects of SERMS! Simply put TT must be less than and remain around 200-4000ng/dl for the lowering benefits of E-2 (as perceived physiologically within the pituitary by SERM use) to be optimized. Therefore roughly five half lives should pass before PCT is initiated and for Arimidex that's THREE WEEKS and for HCG it's ONE WEEK.
In my experience "supplementing" those substances which increase TT, is by far the most common causation of PCT failure! Bottom line, a lowered Testosterone is the price we must all must pay for cycling and effective recovery.

 

[Jimmyinkedup]

The laboratory determination of E-2 levels is NOT routinely obtained DURING a cycle because treatment (lowering of E-2) is essentially only indicated when SIGNS and SYMPTOMS of an elevated level occur. Consequently, since aromatase activity AND E-2 receptor "responsiveness" is quite individualized, routine prophylaxis using an AI is simply not warranted. Additionally, there is NO evidence based on existing research or clinical outcome measures, that combining two SERMS affords any additional benefit compared to using one exclusively and only servers to complicate PCT. This is particularly relevant since Clomid has been shown to possess more central E-2 antagonist activity than Tamoxifen, and the literature is replete with studies involving Clomid's use for the treatment of male hypogonadotropic hypogonadism, compared to Tamo where the citations are very few.
Using Clen or any other beta agonist is not contraindicated during PCT, but it will NOT have any direct effect on physiologic free water, because of an increased E-2.
Lastly using both HCG and an AI "up to PCT" will NEGATE (because of increased TT levels via competitive inhibition) the E-2 antagonistic effects of SERMS! Simply put TT must be less than and remain around 200-4000ng/dl for the lowering benefits of E-2 (as perceived physiologically within the pituitary by SERM use) to be optimized. Therefore roughly five half lives should pass before PCT is initiated and for Arimidex that's THREE WEEKS and for HCG it's ONE WEEK.
In my experience "supplementing" those substances which increase TT, is by far the most common causation of PCT failure! Bottom line, a lowered Testosterone is the price we must all must pay for cycling and effective recovery.

Perhaps you should discuss with Dr Scally ...since just about everything you said contradicts his years of experience and the advice and consul he gives reversing steroid induced andropause.
I agree clomid has much more data supporting its use in a pct scenario - mostly compliments of guay et al ....but when Scally explains the potential benefits of combining the 2 serms and having done clomid only pct vs comid/tamox and recovering better using both ..I say use both.
Clen is not to reduce h20 during pct. What it is good for doing is helping to offset catabolism , especially in a caloric surplus. So it has a place in pct if one so desires.
Also let me get this straight ..the presence of anastrozole will hinder your recovery? Why 5 half lives and not just the active life of the compound ? Especially with a type 2 ai like anastrozole. Ill just cut to the chase...are you being for real with you "competitive inhibition" statement? Seriously? WTF do you think anastorzole wil do to endogenous t levels while exogenously introduced test is still present and clearing the system? Not a damn thing.
Have you ever done a pct Dr Jim ?

 

[Dr JIM]

1) If using two SERMS is beneficial, since their mechanisms if action are IDENTICAL and there is no evidence to support using the combination tell me what the reasons are? (I suspect you MAY be confusing the combination of two AI's, such as a steroidal and non- steroidal, which may be beneficial in certain instances)
2) Essentially all of the "anticatabolic" effects from beta agonists are theoretical performed on rodents and are void of MEASURABLE
human efficacy, otherwise all BB would use them to improve "mass".
3) The "active life" of a compound metabolically is determined by IT'S SERUM CONCENTRATION and based on KNOWN PHARMACOKENETICS FIVE HALF LIVES had been WELL established at the end point where the concentration above baseline (3%) is no longer metabolically relevant (or is measurable using standard techniques)
4) It's obvious from the question regarding "competitive inhibition" your arguing about a physiologic process which is VERY common in hormonal regulation, yet for which your understanding is quite limited. Should you choose to debate me or anyone else on the forum do so respectfully, intelligently and without resorting to profanity as means of emotional catharsis.
Nonetheless in spite of your offhanded gratuitous commentary I will ATTEMPT to explain CI to you and others whom are interested
Let's establish some know physiologic fact first;
1) Lowered testosterone OR estrogen levels INCREASE LH secretion
2) Incereased testosterone OR estrogen levels DECREASE LH secretion
3) LH, GnRh, Tedtostetone and E-2 receptors exist to varied degrees it the surface of the Pituitary and Hypothalmus.
4)Neural-hormonal pathways interconnect the pituitary receptors (TE,GnRH,LH) and similarly form pathways between the pituitary and hypothalamic receptor. (testosterone, estrogen, LH and GnRH) receptors
All of these receptors use structures called Ligands which allow binding of various substrate hormones or the secretealogs LH and GnRH.
Because of these differing receptors and their connections when one hormone attaches to a receptor it may INHIBIT the binding of another or vice versa, this process is referred to as COMPETITIVE INHIBITION.
Consequently when a SERM is used, it prevents E-2 binding and the pituitary SENSING lowered estrogen levels increases LH production. However as mentioned earlier, increased. testosterone levels decrease LH levels resulting in a net effect of ZERO through competitive inhibition.
I'd like to believe you know the answer to the last question posed; "What do I believe AI's will do to endogenous TT levels while exogenous T is exiting the system? Unequivocally they will increase T levels, and you I hope you actually know that!

 

[Jimmyinkedup]

1) If using two SERMS is beneficial, since their mechanisms if action are IDENTICAL and there is no evidence to support using the combination tell me what the reasons are? (I suspect you MAY be confusing the combination of two AI's, such as a steroidal and non- steroidal, which may be beneficial in certain instances) 1-Clomiphene is a mixture of the trans (enclomiphene) and cis (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor[74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor. 2- "Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen, it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor bind*ing sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondar*ily gonadal sex hormones. " Dr Michael Scally
2) Essentially all of the "anticatabolic" effects from beta agonists are theoretical performed on rodents and are void of MEASURABLE
human efficacy, otherwise all BB would use them to improve "mass". Care to explain this: More evidence for anabolic properties of albuterol

Aviat Space Environ Med. 2004 Jun;75(6):505-11

Albuterol helps resistance exercise attenuate unloading-induced knee extensor losses.

Caruso JF, Hamill JL, Yamauchi M, Mercado DR, Cook TD, Keller CP, Montgomery AG, Elias J.

Exercise Physiology Laboratory, University of Nevada, Reno, NV, USA.

john-caruso@utulsa.edu

INTRODUCTION: While resistance exercise (REX) attenuates knee extensor (KE) mass and strength deficits during short-term unloading, additional treatments concurrently administered with REX are required to reduce the greater losses seen with longer periods of unloading. METHODS: To determine whether Albuterol helps REX attenuate unloading-induced KE losses, two groups of subjects strength trained their left thigh three times per week, and otherwise refrained from ambulatory and weight-bearing activity for 40 d while receiving a capsule dosing treatment (Albuterol, placebo) with no crossover. A third group served as unloaded controls (CTRL). On days 0, 20, and 40, the following data were collected from the nonweight-bearing (left) thigh: cross-sectional area (CSA); integrated electromyography (IEMG); and concentric and eccentric KE strength measures. Thigh CSA was estimated using anthropometric methodology. IEMG was used to provide root mean square (RMS) values from submaximal (100 nm) and maximal isometric contractions. Concentric and eccentric strength were measured from eight-repetition unilateral leg press sets. RESULTS: Repeated-measures mixed-factorial 3 x 3 ANCOVAs with day 0 values as a covariate showed group by time interactions for concentric and eccentric total work (CTW, ETW). Tukey's post hoc test showed REX-Albuterol evoked significant (p < 0.05) day 40 CTW and ETW gains vs. within-group day 0 and within-time REX-placebo and CTRL values. By days 20 and 40, CTRL subjects incurred significant decrements. CONCLUSIONS: Albuterol augmented the effects of REX to increase CTW and ETW. Research identifying possible mechanisms responsible for such changes, as well as the safety of REX-Albuterol administration in other models, is warranted.


Perhaps Albuterol is more aptly classified as an ergogenic aid rather than an anabolic compound. One could go to Pub Med and search under something like "Albuterol strength" but w/o quotation marks. It seems to improve strength and endurance at therapeutic doses according to several studies. The data in humans for clen in this regard are pretty scanty.

Likewise a search under something like "Albuterol fat" shows it promotes lioplysis.

So IMO it is superior to clen for both strength gains and fat loss.

It also seems to improve the cholesterol profile in normal men:

"Significant alterations (P < or = .02) were observed in total cholesterol ([TC] -9.1% +/- 2.5%), low-density lipoprotein cholesterol ([LDL-C] -15.0% +/- 2.9%), and high-density lipoprotein cholesterol ([HDL-C] +10.4% +/- 3.2%) concentrations, as well as the TC/HDL-C (-17.4% +/- 2.6%) and LDL-C/HDL-C (-22.9% +/- 2.4%) ratios." (1)

And I don't know what the one person was drinking, but I've been playing with different concentrations, and a 4 mg/ml solution, which is in the therapeutic range used by a number of studies, is essentially tasteless.

(1) Metabolism. 1996 Jun;45(6):712-7

Effects of oral Albuterol on serum lipids and carbohydrate metabolism in healthy men.

Maki KC, Skorodin MS, Jessen JH, Laghi F.

3) The "active life" of a compound metabolically is determined by IT'S SERUM CONCENTRATION and based on KNOWN PHARMACOKENETICS FIVE HALF LIVES had been WELL established at the end point where the concentration above baseline (3%) is no longer metabolically relevant (or is measurable using standard techniques)
4) It's obvious from the question regarding "competitive inhibition" your arguing about a physiologic process which is VERY common in hormonal regulation, yet for which your understanding is quite limited. Should you choose to debate me or anyone else on the forum do so respectfully, intelligently and without resorting to profanity as means of emotional catharsis.
Nonetheless in spite of your offhanded gratuitous commentary I will ATTEMPT to explain CI to you and others whom are interested
Let's establish some know physiologic fact first;
1) Lowered testosterone OR estrogen levels INCREASE LH secretion
2) Incereased testosterone OR estrogen levels DECREASE LH secretion
3) LH, GnRh, Tedtostetone and E-2 receptors exist to varied degrees it the surface of the Pituitary and Hypothalmus.
4)Neural-hormonal pathways interconnect the pituitary receptors (TE,GnRH,LH) and similarly form pathways between the pituitary and hypothalamic receptor. (testosterone, estrogen, LH and GnRH) receptors
All of these receptors use structures called Ligands which allow binding of various substrate hormones or the secretealogs LH and GnRH.
Because of these differing receptors and their connections when one hormone attaches to a receptor it may INHIBIT the binding of another or vice versa, this process is referred to as COMPETITIVE INHIBITION.
Consequently when a SERM is used, it prevents E-2 binding and the pituitary SENSING lowered estrogen levels increases LH production. However as mentioned earlier, increased. testosterone levels decrease LH levels resulting in a net effect of ZERO through competitive inhibition. Yo utoallty did not take into consideration the dosge of hcg i recommended...it is 1/3 that hcg montherapy patients would use - makes a big diff huh?
I'd like to believe you know the answer to the last question posed; "What do I believe AI's will do to endogenous TT levels while exogenous T is exiting the system? Unequivocally they will increase T levels, and you I hope you actually know that! Since an ai increases test via effects re: negative feedback (which you demonstrated above you are familiar with) which is essentially moot when a subject is shut down due the presence of exogenous test this makes absolutely no sense what so ever- just like the majority of your points above - which i why i didnt bother to respond. You understanding of physiology is excellent - your understanding of the administration of exogenous test and the ancillaries effects that are administered alongside it and how they impact one another is strongly lacking.

BTW - That wasnt my last question...my last question was "Have you ever even done a pct Dr Jim ?

 

[Dr JIM]

The improved "endurance and or performance" observed with beta agonists is the result of increased perfusion and oxygenation rather than an "anticatabolic" or anabolic effect as you have suggested. ANY HUMAN STUDIES?

AI's have dual effects, FIRST; they decrease the conversion of testosterone into estrogen. SECOND; the lowered E-2 (as mentioned earlier) increases the secretion of LH which will enhances gonadal testosterone production. Admittedly this will have a limited effect on endogenous production UNLESS HCG is also used which is what you suggested should be done "HCG AND an AI should be used until PCT IS BEGUN", NOT, because the endogenous testosterone levels achieved often exceed 500ng/dl (depending upon dose of each) which may limit the effectiveness of SERMs!

Lastly the effect of Clomid's isomers have on it's efficacy is dependent upon THREE FACTORS
1) which Estrogen receptor (Alpha or Bets) is being referenced
2) E-2 concentration
3) Clomiphene concentration
Consequently the assertion that one isomer is more or less agonistic/antagonistic than the other remains controversial and contingent which study is cited.
I will cite a few references both pro and con in my next post.

 

[Jimmyinkedup]

The improved "endurance and or performance" observed with beta agonists is the result of increased perfusion and oxygenation rather than an "anticatabolic" or anabolic effect as you have suggested. ANY HUMAN STUDIES? No just real world experience...you? Only because Im being lazy as I have seen studies in fact ..There is an extensive read....im trying to recall ...hmm "actions of beta adrenergic agonists on muscle and adipose tissue"" - good read...goggle it... we can all remain open to learning right?

AI's have dual effects, FIRST; they decrease the conversion of testosterone into estrogen. SECOND; the lowered E-2 (as mentioned earlier) increases the secretion of LH which will enhances gonadal testosterone production. Admittedly this will have a limited effect on endogenous production UNLESS HCG is also used which is what you suggested should be done "HCG AND an AI should be used until PCT IS BEGUN", NOT, because the endogenous testosterone levels achieved often exceed 500ng/dl (depending upon dose of each) which may limit the effectiveness of SERMs! Which as I very accurately pointed out you failed to take into account the very low dosage of hcg I recommended...which you have now conveniently ignored twice...which makes your contention in response to my advice totally inapplicable.

Lastly the effect of Clomid's isomers have on it's efficacy is dependent upon THREE FACTORS
1) which Estrogen receptor (Alpha or Bets) is being referenced
2) E-2 concentration
3) Clomiphene concentration
Consequently the assertion that one isomer is more or less agonistic/antagonistic than the other remains controversial and contingent which study is cited.
I will cite a few references both pro and con in my next post. As I said ..I'll stick with Scally and real world experience..but hey at least your coming around a bit and admitting there may very well be some well founded prudence to this line of thought.

So again..Have you ever done a pct ?

 

[Dr JIM]

YEP, I did overlook your homeopathic dose of HCG (A WHOPPING 250IU) to be "run up to PCT" (YOUR QUOTE NOT MINE), lol! Please feel free to quantify the apt gonadal recovery (steroidogenesis) with that dose considering the typical dose approximates FIVE THOUSAND IU.PER WEEK, (one twentieth of the standard dose)? Moreover the another complication you will now create by adding an AI "until PCT is started" is hypo-estrogenemia from uninhibited adrenal excretion and the continued impediment of the Aromatase enzyme.
Regarding the isomeric forms of Clomiphene, since estrogen Beta receptors are uniformly antagonistic yet Alpha receptors are both agonists/antagonists (3). The tissue they are located in becomes a primary determinant of which effect will predominate. For example breast E-2 Alpha receptors are exhibit antagonistic activity while uterine Alpha receptors are E-2 agonist. The former is useful for the treatment in breast cancer while the latter is associated with an increased incidence of uterine CA. Moreover since the receptors within the HTPA are overwhelmingly Beta (2) the net effect from any SERM will be antagonistic AND because be Alpha agonist activity can be overcome by increasing Clomid concentrations (1) (which is why I select a relatively high dose of Clomiphene during PCT) the effect of differing isomers is minimized if not eliminated, IMO based on this evidence.
I've included a couple of SERM articles for those apparently not quite as "lazy" (one of many excuses I've heard for someones INABILITY to locate supporting references for the comments they make, AS I HAVE DONE) as yourself noting some of the differences between Clomid and Tamoxifen, used for MALE hypogonadism and infertility respectively.

 

[Jimmyinkedup]

YEP, I did overlook your homeopathic dose of HCG (A WHOPPING 250IU) to be "run up to PCT" (YOUR QUOTE NOT MINE), lol! Please feel free to quantify the apt gonadal recovery (steroidogenesis) with that dose considering the typical dose approximates FIVE THOUSAND IU.PER WEEK, (one twentieth of the standard dose)? Moreover the another complication you will now create by adding an AI "until PCT is started" is hypo-estrogenemia from uninhibited adrenal excretion and the continued impediment of the Aromatase enzyme.
Regarding the isomeric forms of Clomiphene, since estrogen Beta receptors are uniformly antagonistic yet Alpha receptors are both agonists/antagonists (3). The tissue they are located in becomes a primary determinant of which effect will predominate. For example breast E-2 Alpha receptors are exhibit antagonistic activity while uterine Alpha receptors are E-2 agonist. The former is useful for the treatment in breast cancer while the latter is associated with an increased incidence of uterine CA. Moreover since the receptors within the HTPA are overwhelmingly Beta (2) the net effect from any SERM will be antagonistic AND because be Alpha agonist activity can be overcome by increasing Clomid concentrations (1) (which is why I select a relatively high dose of Clomiphene during PCT) the effect of differing isomers is minimized if not eliminated, IMO based on this evidence.
I've included a couple of SERM articles for those apparently not quite as "lazy" (one of many excuses I've heard for someones INABILITY to locate supporting references for the comments they make, AS I HAVE DONE) as yourself noting some of the differences between Clomid and Tamoxifen, used for MALE hypogonadism and infertility respectively.

You cant even read..its 250iu - 2x/week - for a total of 500. Its around 1/3 the standard weekly hcg monotherapy dose...another fyi. Save you rhetoric...as i said earlier while you have knowledge of physiology....your knowledge of exogenous hormones , their interaction with ancillaries , and proper recovery using said ancillaries is less than up to par to be advising ...much less condescending.
Read that info i told you to google? Learn anything yet doc? Stick around.
BTW How did your last pct go ?
Your talking to guy in his 40's that uses the very procedure I outlined , whose off cycle stabilized test levels were in the high 600's last time I got blood work. I know a successful pct protocol ...so does Scally - you obviously do not. Spout off all the rhetoric you want..you wanted to look like you know your shit , you now dont wanna admit you very well may be wrong ...so you keep posting. Knock it off you pompus arrogant wanna be. Do you even work out? Seriously? Ever done a steroid? A pct ? Ever treated someone for steroid induced andropause?

 

[Dr JIM]

Ok 500IU weekly that's one tenth not a thrid, moreover since the half life is 24 hours, after three-four days the HCG level will approximate 25-12% which is fully inadequate. Through this process:
1) I've looked up the Beta agonist information previously which is WHY I know there's study supporting anabolic activity in humans!
2) I've answered your question about why FIVE HALF LIVES are important.
3) I explained the importance of hormonal competitive inhibition as it applies to PCT
3) AI's were discussed to enhance your vague understanding of their effects on E-2 and testosterone both during and after a cycle
4) I've provided rationale for my initial statement regarding SERM's and whether there is evidence to support their combined use in PCT.
In summary I've REBUTTED EACH AND EVERY ONE OF YOUR ORIGINAL ASSERTIONS and throughout this process the only thing you have done is to RELY ON OTHERS, as a scapegoat for your LIMITED FUND OF KNOWLEDGE, and ADMIT YOUR LAZY. Well you have certainly have convinced me of the latter, LMAO!