HCG or Clomid DURING your cycle ?

[Gunsmith]

Any of you guys ever run clomid during your cycle? i had a guy ask me why i use HCG instead of clomid , he said he actualy had less shut down and faster recovery just taking clomid at 50mg ed throughout his cycle

you guys ever try that ?

 

[Ehren]

Works great, IMO. Big A recommended it and I tried it and liked the results a lot.

There's a thread running on it at the moment, here:

http://www.professionalmuscle.com/f...le-forum/59689-incredible-shrinking-nads.html

 

[Thebigone]

Im on hrt but still use 250iu hcg 2x per week when on real hrt and when on cycle 500iu 2x per week. I usually take clomid at a low dose of 25mg ED for about a month 3x or so per year. Just a month and then 3 or 4months off then add it again,etc.. honestly i dont know why. I feel maybe it boosts sperm count back a little.I do notice when im on it I bust more of a nut, orgasm feels way better(kinda like when on proviron). But i get awful acne on it and very very emotional.

 

[Thebigone]

Im actually curious to try real tribestane when on cycle. Not the stuff you can buy, the real stuff. I hear it kinda acts like proviron in a way and increases sperm count and ejaculate volume.

 

[Ehren]

I like Tribestan or a good Trib supplement during cycle or in PCT.

When Im shut down it seems to work wonders with Clomid. When Im off for a long time, it doesn't seem to do shit.

 

[dabeast75]

yeah Bro, Clomid is great while on cycle and I will never go without it again. I already mentioned this on the thread that Ehren referred to. I use it at 50mgs EOD, and 50mgs ED while on PCT. When taking it daily I do notice a few more sides, the occasional night sweats and acne. The acne is manageable, but still noticable (only on back and shoulder area). Nolvadex does the same to me.

 

[LBJK88981]

Any of you guys ever run clomid during your cycle? i had a guy ask me why i use HCG instead of clomid , he said he actualy had less shut down and faster recovery just taking clomid at 50mg ed throughout his cycle

you guys ever try that ?

I would not advocate taking clomid while on cycle. It will cause more harm than good. HCG is not a bad idea but it only addresses half of the problem (when referring to the physiologic feedback loop that causes suppression). Look into Naltrexone. With androgens (not as much with progestins), this can literally prevent HPTA shutdown. If anyone would like, I can talk about how.

-Alex

 

[Nssca]

I would not advocate taking clomid while on cycle. It will cause more harm than good. HCG is not a bad idea but it only addresses half of the problem (when referring to the physiologic feedback loop that causes suppression). Look into Naltrexone. With androgens (not as much with progestins), this can literally prevent HPTA shutdown. If anyone would like, I can talk about how.

-Alex

Id like to hear your opinions, please.

 

[LBJK88981]

Id like to hear your opinions, please.

Sure. Instead of posting my opinions, let me post some data and references. This should provide a solid background for understanding how naltrexone and other u-opioid receptor antagonists can aid in preventing HPTA shut-down.

"Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA – The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?



A closer look –

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan, Proviron, Anavar or Masteron). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --



Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few point to consider -

For those who choose to embark on an opioid antagonist protocol several things should be considered.



Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)


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[PHIL HERNON]

Nice article

So......dont use tren, dont use deca.......use primo or var and proviron and masterone..........use aromasin or letrozole.......and use inj naltrexone at 40mg 2 times a week for 4-16 weeks but be aware that it could raise liver enzymes.....I know many guys wont do that.......but its great advice......now what about these mega dosers who want to turn pro? There really is no hope for shutdown........just think ahead and try to do your best.........use caber if u need it with tren or deca......clomid, hcg intermittently and for PCT.......good stuff

 

[minister]

where to get these products?

Anybody has any info about who would carry any of these 3 products, Naloxone, Naltrexone or Nalmefene?

 

[Mr Anderson]

Would like to know more about running clomid during a cycle.

I was going to HCG in my next cycle, but if i could get away with running clomid that would be better and cheaper for me.

 

[LBJK88981]

So......dont use tren, dont use deca.......use primo or var and proviron and masterone..........use aromasin or letrozole.......and use inj naltrexone at 40mg 2 times a week for 4-16 weeks but be aware that it could raise liver enzymes.....I know many guys wont do that.......but its great advice......now what about these mega dosers who want to turn pro? There really is no hope for shutdown........just think ahead and try to do your best.........use caber if u need it with tren or deca......clomid, hcg intermittently and for PCT.......good stuff

For moderate/mild users it works quite well. Heavy doses of androgens and/or progestins/strong aromatization will defeat the purpose for sure. I think that the "shut down" concerns are blown out of proportion. The medical community was never too concerned about the bodies ability to re-establish homeostasis after administration of exogenous hormones for whatever medical purpose...why should we be? Obviously if there are ways to speed up the process of recovery it would benefit a bodybuilder but there will always be some hesitation for me to recommend taking more drugs to counter the 'temporary' effects of other drugs etc etc.

Anybody has any info about who would carry any of these 3 products, Naloxone, Naltrexone or Nalmefene?

You will likely have a hard time finding given what they are commonly prescribed for....

Would like to know more about running clomid during a cycle.

I was going to HCG in my next cycle, but if i could get away with running clomid that would be better and cheaper for me.

There is really no purpose to runnign clomid during a cycle. If anything, an aromatase inhibitor like arimidex or letrozole could be useful for controlling estrogen levels while on cycle.

 

[Mr Anderson]

There is really no purpose to runnign clomid during a cycle. If anything, an aromatase inhibitor like arimidex or letrozole could be useful for controlling estrogen levels while on cycle.

I was going to be using it for keeping Testies going lol not for an anit E

Like when ppl use hcg while on cycle.

 

[LBJK88981]

I was going to be using it for keeping Testies going lol not for an anit E

Like when ppl use hcg while on cycle.

yes but keep in mind that clomid has some other effects on the body.. it is half estrogen/half estrogen antagonist, it's not great for your liver, lipids or eyes. To me, the drawbacks outweigh the benefits of using it on cycle. HCG is okay for maintaining testicular size on cycle. Aromatase inhibitors may help a bit too.

-Alex

 

[minister]

yes but keep in mind that clomid has some other effects on the body.. it is half estrogen/half estrogen antagonist, it's not great for your liver, lipids or eyes. To me, the drawbacks outweigh the benefits of using it on cycle. HCG is okay for maintaining testicular size on cycle. Aromatase inhibitors may help a bit too.

-Alex

I agree with Alex 100%, ppl pop clomid like if it's candy, what ppl should know about this very dangerous drug is, that there has been a few studies in which long term use of clomid at 50 mgs a day has been linked to cataracts, and liver tumors, and not just isolated incidents, a high percentage of women using clomid to fight breast cancer, end up with some type of liver tumor, at first doctors thought this was just the breast cancer spreading to the liver, but as they took a closer look more doctors are linking the use of clomid to the formation of new malignant cells in the liver. So take caution my friends. God bless you guys.

 

[jamco54]

There is also some thought of Clomid and teticular cancer...

Clomiphene Citrate (IARC Summary & Evaluation, Supplement7, 1987)


...but then again what doesn't cause cancer anymore.

 

[EDED]

did all the research on naltrexone,,,htere is no inj naltrexone, only oral,,,,,inj naloxone if you want to try

yo uwill feel like shit first of alll

second, old studies look VERY promising

new studies only show preserved frequency but amplitidue of LH/FSH pulsations are still down

i would rather do hcg during cycle, come off with test only tpared down, hcg and aromasin for one week, low dose clomid/nolva/igf or insulin afterwards for a month. that has better track record than the old news of naltrexone and the possibility of opposing the negative feedback, impossible.

also i ve tried naltrexone, sucked,

LDN, low dose naltrexone is another type of off lable protocol for diseases,,,for pct you would need alot,,,i was using LDN dose and felt like garbage,,,the latter protocol was the easiest ever PCT.

goodluck

 

[LBJK88981]

did all the research on naltrexone,,,htere is no inj naltrexone, only oral,,,,,inj naloxone if you want to try

yo uwill feel like shit first of alll

second, old studies look VERY promising

new studies only show preserved frequency but amplitidue of LH/FSH pulsations are still down

i would rather do hcg during cycle, come off with test only tpared down, hcg and aromasin for one week, low dose clomid/nolva/igf or insulin afterwards for a month. that has better track record than the old news of naltrexone and the possibility of opposing the negative feedback, impossible.

also i ve tried naltrexone, sucked,

LDN, low dose naltrexone is another type of off lable protocol for diseases,,,for pct you would need alot,,,i was using LDN dose and felt like garbage,,,the latter protocol was the easiest ever PCT.

goodluck

I agree. it really depends on the compounds used. The effectiveness of Naltrexone while on cycle is a direct function of the types, and secondarily, the amounts of compounds used. HCG is a good way to preserve part of the function of your HPTA, thus likely providing for a quicker recovery.

Alex