HCG throughout or at the end of cycle?

[dirtyluke1]

subq

 

[Rekrul]

..

Food for thought...

Quote:
J Clin Endocrinol Metab. 2005 May;90(5):2595-602. Epub 2005 Feb 15.

Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression.
Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK, Anawalt BD, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow JP.

Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA. [email protected]

Abstract
In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally, we determined the dose-response relationship between human chorionic gonadotropin (hCG) and ITT to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for 3 wk. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment. Baseline serum T (14.1 nmol/liter) was 1.2% of ITT (1174 nmol/liter). LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.
So HCG appears to a be a big help on cycle even and especially with a source of exogenous testosterone. And it has been used in patients with transient hypogonadotropic hypogonadism secondary to AAS use (not the best approach-what I would call post-cycle).

 

[needtogetaas]

lol... how is something being natural going to make it potentially less harmful? I mean If these substances don't have some sort of action then they are essentially useless.

Your argument is, that herbal supplement X is great because its 'natural' and that it triggers LH release and that HCG is bad because its not 'natural' and keeps your balls alive and you will become desensitized. Yet, there is a strong likelihood that you would become desensitized by the supposed LH release while using supplement X. Furthermore, you go on to say that you are going to be messing with feedback no matter what.

You assert that you are going to desensitize the testes by using 250-500 Iu a week of HCG(this is a 'natural' level) while ON vs hammering our testes with doses 5-10x at the end of our cycle. That to me makes absolutely no sense. The logic doesn't add up.

Like I was saying before, the ideal way is to keep your balls working and prime them for LH release, which is what supplement X would be great for. Your balls won't need a kick start if you had been using hcg throughout. All you are concerned with now, is your LH release.

The hypothalamus, upon realizing that blood levels of androgens are low releases Gonadotropin Releasing Hormone (GnRH). GnRH goes to the pituitary which takes this hormone as the stimulus to release Lutenising Hormone (LH). LH then goes to the testes and stimulates T production. HCG mimics LH however it is not LH!!!!!!!

The HCG would stimulate more T to be released. but during a cycle the hypothalamus would still "recognise" the increased level of androgens and still stop releasing GnRH which in turn would lead to the pituitary stopping your own natural production of LH.

This wouldn't matter so much whilst you were taking the HCG as this replaces the LH and so T production would continue whilst you kept taking the HCG. So although Hcg may prevent degeneration of the ladeg cells (remember that your own body isnt producing any LH or GnRH anymore!!! regardless ) As the hypothalamus recognizes outside sources of both androgens and LH now it will feather suppress its own production of LH and GnRH The problem is that whilst the pituitary has been lying dormant due to not receiving any GnRH from the Hypothalamus it atrophies (just like the testes do when not used).

Get it?


In a normal healthy male luteinizing hormone (LH) and follicle stimulating hormone (FSH) are sent from the brain (the pituitary) to stimulate the testes to make testosterone and sperm.

The release of LH & FSH from the pituitary is stimulated by Gonadotropin Releasing Hormone (GnRH) from the hypothalamus. The hypothalamus is stimulated to produce GnRH when it senses low levels of testosterone and estrogen.

(hypothalamus [GnRH] --- > pituitary [LH & FSH]--- >(hcg would be placed here if we placed it anywhere)---> testes [testosterone])


So although hcg may cause there to be less atrophie of the ladeg cells it in turn causes more atrophie of the pituitary.

7,8-Benzoflavone -- increases testosterone production by preventing the negative feedback of testosterone and estrogen on the hypothalamus through GABAergic modulation though. And although researchers are just beginning to understand how the GABAergic system regulates the hypothalamus and GnRH secretion its important to know that a lot more studies have been done and are getting done then you think.. On Natural ingredients!!! Like 7,8-Benzoflavone and other phytoserms one can find in products like forma-stanzol.


Now I am not saying that preventing the desensitization of the ladeg cells during a cycle is not a good thing. Because as we know No matter how much LH & FSH the brain secretes, the testes won't secrete testosterone if they are desensitized to LH & FSH. (remember, this can happen from too much, or not enough LH & FSH stimulation)


hCG’s effect is centralized at the Leydig cells of the testicles and stimulates hormone function at the testicular level but does not reverse hypothalamic-pituitary suppression. Adequate stimulation from pituitary gonadotropins is required for the Leydig cells of the testicles to function independently in the body’s normal hormone axis.

of course during a cycle there are natural compounds and products that work through different mechanisms to prevent complete shutdown with out feather suppressing pituitary some through GABAergic modulation and some through others like with hcgenerate.


Hcg is a synthetic "out side source" of a hormone. So for the sake of argument and layman's terms ( so that your self and everyone can grasp/wrap head around subject) I will brake things down and give them a names.

steroids,Hcg,drug serms, and just about anything manufactured by a pharmaceutical company that we have commonly used= Synthetic "out side source of the target hormone"

Now we will give things like hcgenerate,bridge,unleashed/post cycle a name. Natural "bio-identical hormone" or "Homeopathic hormones" but in reality they have many names and even medically excepted ones like Phyto-SERMs, phytochemicals, phytonutrients , phenolic compounds ,phytotherapy, blah blah blah and a whole slew of other terms..
But for now will use the terms Synthetic and bio-identical hormones.


See I am explaining it like this because this has a lot to do with the parts you are not understanding. Although this is not everything and many of the natural and or even OTC hormones in the products mentioned work through other mechanisms and ways of action. Not just in a bio-identical/Homeopathic hormone manner of action.

Bio-identical/Homeopathic hormones are plant-derived and identical to the body's hormones. They are naturally the exact same thing and or they cause "natural" production/suppression of the target hormone.

Synthetic hormones such as hcg or a drug like serm are similar but not identical to the body's hormones. Fethermore they are "always" a outside source of the parent/target hormone. Moreover through manipulation of the hormone cascade they can also be used to suppress the production of a target hormone in the hopes to facilitate the production of another. We use compounds like Hcg and or clomid often notwithstanding the fact These slight chemical shift create a mismatches between the body's receptors ,Parent hormones,sister hormones, and or governing hormone cascade.

Now don't pull out your pitch forks and torches just yet
I love my steroids,drugs,chemical enhancement just as much as the next guy and in fact IMO more bwahahahahaaaa . So lets not try and act like I am downing there use. On the contrary I just happen to be more of a nonconformist who believes that Both Natural and synthetic coexist synergisticly in many concomitant circumstances.

Now at times I think you are confusing Bio-Identical with Homeopathic . One naturally augments or reduces and the other Naturally replaces. Although all things considered Naturally replacing is often (but not always) the superior. This creates less of a problem in the way of mismatching, adverse reactions, or suppression then the chemical counterparts.

Weather Fadogia agrestis method of action is more of a Bio-Identical or a Homeopathic Is somewhat unfounded however its actions through what ever Natural Mechanisms is founded. Through both scientific and real world results/feed back.

Title: Aphrodisiac potentials of the aqueous extract of Fadogia agrestis (Schweinf. Ex Hiern) stem in male albino rats.
Author: Yakubu MT , Akanji MA , Oladiji AT
Source: Asian J Androl, 7(4): 399-404 2005


Abstract: AIM: To evaluate the phytochemical constituents and the aphrodisiac potential of the aqueous extract of Fadogia agrestis (Rubiaceae) stem in male albino rats. METHODS: The aqueous stem extract of the plant was screened for phytochemical constituents. Male rats were orally dosed with 18 mg/kg, 50 mg/kg and 100 mg/kg body weight, respectively, of the extract at 24 h intervals and their sexual behavior parameters and serum testosterone concentration were evaluated at days 1, 3 and 5. RESULTS: Phytochemical screening revealed the presence of alkaloids and saponins while anthraquinones and flavonoids are weakly present. All the doses resulted in significant increase in mount frequency, intromission frequency and significantly prolonged the ejaculatory latency (P 0.05) and reduced mount and intromission latency (P 0.05). There was also a significant increase in serum testosterone concentrations in all the groups in a manner suggestive of dose-dependence (P 0.05). CONCLUSION: The aqueous extract of Fadogia agrestis stem increased the blood testosterone concentrations and this may be the mechanism responsible for its aphrodisiac effects and various masculine behaviors. It may be used to modify impaired sexual functions in animals, especially those arising from hypotestosteronemia

http://www.elitefitness.com/forum/anabolic-steroids/hcgenerate-needto-does-again-691319.html
http://www.elitefitness.com/forum/bodybuilding-supplements/hcgenerate-716865.html
http://www.elitefitness.com/forum/anabolic-steroids/hcgenerate-sent-heaven-way-needto-707933.html
http://www.elitefitness.com/forum/anabolic-steroids/my-hcgenerate-experience-687243.html
http://www.elitefitness.com/forum/anabolic-steroids/hcgenerate-needto-707157.html
http://www.elitefitness.com/forum/bodybuilding-supplements/hcgenerate-689005.html
http://www.elitefitness.com/forum/a...ate-amazing-need-some-help-advice-711743.html
http://www.elitefitness.com/forum/a...w-hcgenerate-saved-yet-another-me-704063.html
http://www.elitefitness.com/forum/a...ate-solve-my-problems-710985.html#post9544455
http://www.elitefitness.com/forum/bodybuilding-supplements/wow-hcgenerate-powerful-699719.html
http://www.elitefitness.com/forum/bodybuilding-supplements/hcgenerate-year-round-695837.html
http://www.elitefitness.com/forum/bodybuilding-supplements/hcgenerate-review-695755.html
http://www.elitefitness.com/forum/bodybuilding-supplements/props-n2bm-hcgod-like-sex-720583.html
http://www.elitefitness.com/forum/a...perience-hcgenerate-formastanozol-722309.html

 

[Gym James]

I think using hCG for the last few weeks of your cycle sounds very reasonable. (Although I'm probably a few years late on helping you with this decision....)

Now to address all the other posts:

A lot of you guys have things straight -- but it seems that others are way off. I'll skip the HPTA axis explanation -- seems like everyone has got that down.

The most compelling evidence shows that a delay in the return to normal test levels post-cycle is not due to a deficiency of LH, but due to testicular atrophy/ unresponsiveness to LH. It's not the "signal" (LH) that is deficient, its the "factory" (testicles) that just can't handle the demand anymore because it was shut down for a good while. If you don't use it, you lose it. Realize, LH comes back quick ~ 3 weeks, but testosterone takes ~ 10 weeks. This favors the theory of testicular atrophy being the rate limiter, and NOT pituitary atrophy... Here's the evidence:

"... One of the most detailed views of what a post-cycle crash probably looks like comes from an investigation into testosterone enanthate.354 It involves a group of men that were given weekly injections (250 mg) for 21 weeks, a dose that admittedly does go beyond normal HRT use. Various hormones were measured each week during the study, and for more than 4 months after the medication was discontinued. A review of the data shows that at the start of the study, LH levels were suppressed in direct relation to the rise in testosterone (see Figure I). Once the steroid was withdrawn, however, there was a delay between the return towards normal LH production (which began to correct by the 3rd week) and testosterone (which took more than 10 weeks before noticeable correction). The above study suggests that one of the first things to happen after steroid cessation is that the brain recognizes testosterone levels are low again. This will cause GnRH and LH levels begin correcting fairly quickly. The substantial delay between this and an increase in testosterone levels is caused largely by testicular unresponsiveness to luteinizing hormone. After months of receiving extremely weak stimulation, they will have lost a substantial amount of mass (atrophied). This is a well-documented side effect of anabolic steroid use, even if a size difference may not be immediately visible in all cases. When LH levels begin surging back, the testes will initially be unable to handle the workload. This is expected to correct itself in time, but it may take many weeks for the testes to slowly restore to their original mass. With a good portion of the post-cycle recovery period actually being characterized by normal (even high) levels of LH, we must address recovery broadly if we expect it to be effective."

Here's the study: Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men.J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84





In Anabolics, Llewellyn mostly emphasizes the importance of hCG use as a PCT (starting during the last 2 weeks of your cycle), but he does give some good info on the use of hCG on-cycle:


"... administer Human Chorionic Gonadotropin throughout a steroid cycle, in an effort to avoid testicular atrophy and the resulting reduced ability to respond to LH stimulus. In effect, this practice is used to avoid the problem of testicular atrophy, instead of trying to correct it later on when the cycle is over. It is important to remember that the dosage needs to be carefully monitored with this type of use, as high levels of hCG may cause increased testicular aromatase expression (raising estrogen levels),771 and also desensitize the testes to LH.772 As such, the drug may actually induce primary hypogonadism when misused, greatly prolonging, not improving, the recovery window. Current protocols for the use of hCG in this manner involve administering 250 IU subcutaneously every 3rd or 4th day throughout the length of the steroid cycle. Higher doses may be necessary for some individuals, but st no point should exceed 500 IU per injection. These on-cycle hCG protocols were developed by Dr. John Crisler, a well-known figure in the anti-aging and hormone-replacement field, for use with his testosterone replacement therapy (TRT) patients. Although TRT is often administered on a long-term basis, testicular atrophy is a common cosmetic complaint of patients irrespective of the maintenance of normal androgen levels. Dr. Crisler’s hCG program is designed to alleviate this concern in a manner that is acceptable for longer-term use. For those interested in precisely timing their hCG shots in relation to a prescribed testosterone replacement program, Dr. Crisler recommends the following in his paper,“An Update to the Crisler hCG Protocol,” “…my test cyp TRT patients now take their hCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their hCG subcutaneously,and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required)… Those TRT patients who prefer a transdermal testosterone, or even testosterone pellets (although I am not in favor of same), take their hCG every third day.”




Llewellyn, William. Anabolics E-Book Edition (Kindle Locations 10973-10988). Molecular Nutrition. Kindle Edition.
^^Great Book downloaded to my PC for 10 bucks.
Llewellyn, William. Anabolics E-Book Edition (Kindle Locations 10973-10988). Molecular Nutrition. Kindle Edition.