hgh and igf during pct??

[db006]

i know igf is good during this period, but what about gh?? my pct will consist of nolva, clomid, femara, and bromo, for roughly six weeks. i know i read a few things about nolva making gh useless, is that true?? what kind of doses would i want to use if were to use them during my pct? and what is the bottom line for the best time of the day to take your igf?

 

[Pinnacle]

Nolv is said to reduce IGF levels.Actually all Anti's...

Secondly,your PCT protocol is overkill.Femara and bromo together?


I like IGF for PCT.It worked well for me.If you are going to run HGH as well.You'll need to start with it at least 2 mos prior to PCT so it will have started to kick in.

~Pinnacle~

 

[Pinnacle]

Posted by LMR at AR.com

SERM/AI Definition

--------------------------------------------------------------------------------

Selective Estrogen Receptor Modulator (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex).

Aromatise Inhibitor (AI) Aromatase inhibitors exhibit a very different mechanism of action than SERM’s. Aromatase inhibitors prevent the conversion of androgens into estrogen in fat, muscle, breast, and brain. ex: Anastrazole (brand name Arimidex). FEMARA (letrozole tablets).

NOTE: Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes.

Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary.

by William Llewellyn


SERM:
Clomid, stimulates the hypophysis to release more gonadotropin so that
a faster and higher release of follicle stimulating hormone aud
luteinizing hormone occurs. This results in an increase of the body's
own testosterone production. Clomid is a synthetic estrogen, however
it does also work as an anti-estrogen. How does it work? Because it is
a weak synthetic estrogen, it will bind to the estrogen receptor (ER)
and not cause any problems. At the same time the increase in estrogen
from steroids are blocked from attaching to the ER.

Nolvadex, is very comparable to Clomid, behaves in the same manner in
all tissues, and is a mixed estrogen agonist/antagonist of the same
type as Clomid. The two molecules are also very similar in structure.
It is not correct that Nolvadex reduces levels of estrogen: rather, it
blocks estrogen from estrogen receptors and, in those tissues where it
is an antagonist, causes the receptor to do nothing.

Cyclofenil, similar to HCG and Clomid in action. This drug is most
commonly used to increase endogenous testosterone levels after a cycle
in an attempt to avoid a hard crash while waiting for your hormone
levels to naturally balance. Similar to HCG and Clomid, cyclofenil
seems to quickly and effectively raise natural levels. Cyclofenil is
an estrogen that works as an anti-estrogen as well as a testosterone
booster.

AI:
Femara, (letrozole tablets) for oral administration contain 2.5 mg of
letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen
synthesis). Letrozole is a nonsteroidal competitive inhibitor of the
aromatase enzyme system; it inhibits the conversion of androgens to
estrogens.

Cytadren, (aminoglutethimide) at moderate doses, is a fairly effective inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the
production of all steroids), and at higher doses becomes an effective
inhibitor of desmolase. It is therefore useful when using aromatizable
steroids, though it is not the drug of choice for this purpose.

Aromasin, tablets for oral administration contain 25 mg of exemestane,
an irreversible, steroidal aromatase inactivator. Exemestane is
chemically described as 6-methylenandrosta-1,4-diene-3,17 -dione.

Anastrozole,(Arimidex) is the aromatase inhibitor of choice. The drug
is appropriately used when using substantial amounts of aromatizing
steroids, or when one is prone to gynecomastia and using moderate
amounts of such steroids. It is manufactured by Zenica Pharmaceuticals
and was approved for use in the United States at the end of Dec 1995.

Proviron, is also an estrogen antagonist which prevents the
aromatization of steroids. Unlike the antiestrogen Nolvadex which only
blocks the estrogen receptors (see Nolvadex) Proviron already prevents
the aromatizing of steroids. Therefore gynecomastia and increased water
retention are successfully blocked. Since Proviron strongly suppresses
the forming of estrogens no re-bound effect occurs.

Teslac,is unique in its effectiveness as an antiestrogen. Like
Proviron, it prevents the aromatizing process of the steroids from the
basis. Thus, Teslac prevents almost completely the introduction of more
estrogens into the blood and subsequent bonding with the estrogen
receptors.

6-OXO, contains a naturally occurring aromatase inhibitor that is devoid of any direct hormonal or prohormonal activity (androgenic or estrogenic). It is what science refers to as a "suicide inhibitor" of aromatase.

L-Dex, same as arimidex or anastrozole; known as an AI and popular on chemical supply sites. This is the name given on chemical supply sites instead of it's original name. L-Dex meaning "Liquidex".

There are a number of chemical research sites that sell liquid products similar to the above mentioned items. These products are the same but in liquid form such as liquid clomid, liquid nolva, liquid femera, and liquid arimidex.

Dosage's are usually adminstered by droppers but dosage amounts per ml differ from site to site.



Also, even though bodybuilders resort to these products in paranoia of the affects of estrogen. It is important to remember, estrogen is necessary and must be balanced not completely inhibited in the system. Below is an excellent reading about the necessity of estrogen.

To much is bad, but estrogen in moderation is priceless!
by William Llewellyn

Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

What does this all mean?
It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.

References
1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45

 

[Pinnacle]

Pheedno's PCT AT AR.com

--------------------------------------------------------------------------------

My post cycle therapy consists of a three compound administration which is designed so that there is a primary and secondary LH stimulator which both are maximizing potential early in the duration; with the primary being phased out in extended protocol. With the addition of an Aromatase Inhibitor, which makes the above possible, the individual will also endure less of an increase in Sex Hormone Binding Globulin, which allows free testosterone levels to reach base line at a much quicker pace. The individual will also see less of a problem in most cases with sexual libido as the bounding SHBG is controlled(to an extent). Below you will find my suggested bare minimum, as well as a sample of an extended protocol. Extended PCT protcol is cycle length dependant so the below is not the standard for all cycles


PCT for cycles 8-16wks:
Day 1-30- .25mg L-dex + 100mg Clomid + 20mg Nolva

Extended protocol sample for a 12+ month cycle:
Day 1-15_ .25mg L-dex + 100mg Clomid + 20mg Nolva
Day 16-45_.25mg L-dex + 75mg Clomid + 20mg Nolva
Day 46-65_.25mg L-dex + 20mg Nolva
Day 66-80_.25mg L-dex

Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur.
With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux
occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary. In the longer forms of PCT, the clomid will be phased out, leaving Nolva and L-dex

Arimidex(or L-dex)
Estrogen is the main inhibitence of restoring HPTA, and AI administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of PCT, since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis

 

[Pinnacle]

Tamox vs Clomid

Am J Physiol 1983 Feb;240(2):E125-30

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

Adashi EY, Hsueh AJ, Bambino TH, Yen SS.

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

__________________________________________________
_________

Br J Pharmacol 1978 Apr;62(4):487-93

Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.

Kurl RN, Morris ID.

1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.

__________________________________________________
__________

the following study was not available in my library, so i wasn't able to obtain the article or abstract. it may have to be purchased, so if someone is interested, here's the title and authors of the research.

Nippon Funin Gakkai Zasshi 1978 Oct;23(4):398-404

[The hormonal dynamics picture of tamoxifen treatment cases, in comparison of clomid treatment cases]

__________________________________________________
_______

Cochrane Database Syst Rev 2000;(2):CD000151

Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.

Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN.

 

[Pinnacle]

Case for Clomid

J Clin Endocrinol Metab 1985 Nov;61(5):842-5

Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.

Winters SJ, Troen P.

To examine the mechanism by which endogenous estrogens inhibit gonadotropin secretion in men, blood samples were drawn every 10 min for 12 h in five men before and at the completion of 3 weeks of treatment with the estrogen antagonist clomiphene citrate (50 mg twice daily). Samples were analyzed for LH and alpha-subunit by RIA. Clomiphene produced a 3-fold rise in circulating LH levels, which was associated with a 80% increase in pulse frequency and a 70% increase in pulse amplitude. Immunoreactive alpha-subunit secretion was also pulsatile before and after clomiphene treatment. Mean alpha-levels rose 70%, together with a 39% increase in pulse frequency and a 41% increase in pulse amplitude. Circulating testosterone and estradiol levels increased 2-fold and FSH levels increased 3-fold after clomiphene treatment. Insofar as each LH and uncombined alpha-subunit pulse reflects a LHRH secretory episode, our data indicate that endogenous estrogens tonically restrain the hypothalamic release of LHRH. From these results and those of previous studies, we conclude that estrogens as well as androgens are important in the testicular feedback inhibition of the hypothalamic oscillator that governs pulsatile gonadotropin secretion.


J Androl 1991 Jul-Aug;12(4):258-63

The effects of normal aging on the response of the pituitary-gonadal axis to chronic clomiphene administration in men.

Tenover JS, Bremner WJ.

Department of Medicine, University of Washington School of Medicine, Seattle.

Serum androgens decline with age in normal men, despite normal or elevated bioactive serum gonadotropins, suggesting that primary testicular dysfunction occurs with aging. The authors further assessed the question of age-related testicular dysfunction by evaluating whether raising serum gonadotropins above the normal serum range for an extended time in healthy elderly men might result in bringing their gonadal function to a level similar to that found in young adult men. Five elderly (65 to 85 years old) and five young adult men (26 to 33 years old) were given 50 mg of clomiphene citrate (CC) twice a day for 8 weeks to stimulate gonadotropin production. During that time, testosterone (T), non-sex hormone-binding globulin bound T, and estradiol increased significantly in both age groups, while serum inhibin increased significantly only in the young adult men. The increases in serum androgens with CC administration were significantly greater in the young adult men than in the elderly men. These hormone changes occurred in the setting of serum gonadotropins that increased significantly in both age groups, although there was a tendency for the elderly men to have a smaller increase in luteinizing hormone. Despite 8 weeks of stimulation of the pituitary-gonadal axis by CC administration, the elderly men demonstrated significantly diminished testicular responses compared with the young adult men. Sertoli cell function, as determined by inhibin production, was more diminished in the elderly men than was Leydig cell function. These data strengthen the hypothesis that normal aging in men is accompanied by a decline in testicular function.


Urology 1991 Oct;38(4):317-22

Possible hypothalamic impotence. Male counterpart to hypothalamic amenorrhea?

Guay AT, Bansal S, Hodge MB.

Section of Endocrinology, Lahey Clinic Medical Center, Burlington, Massachusetts.

Twenty-one men with erectile complaints who were found to have a low level of serum testosterone without a reciprocal elevation of the serum levels of luteinizing hormone were evaluated to identify whether the defect was of hypothalamic or of pituitary origin. Patients underwent a luteinizing hormone (LH)-follicle-stimulating hormone (FSH)-releasing hormone stimulation test that showed a normal but sluggish increase in LH and FSH levels, thus ruling out a pituitary defect and suggesting a suprapituitary abnormality. This was confirmed when, in response to clomiphene, patients had a normal increase in gonadotropin and testosterone levels. Although the basal as well as clomiphene and gonadotropin releasing hormone-stimulated levels of total testosterone and gonadotropins were identical in men less than and more than fifty years old, the elevation of free testosterone levels in response to clomiphene was higher in patients younger than fifty. This suggested that although the primary abnormality found in these patients is altered secretion of gonadotropin hormone-releasing hormone from the hypothalamus, an age-related decline in the responsivity of Leydig cells to LH may make it more manifest in older patients. Elevation of testosterone levels from a subnormal to a normal range in response to clomiphene administered for seven days suggests that the defect is functional and reversible and that the drug may be useful in treatment of sexual dysfunction in this group of patients.
Nephron 1993;63(4):390-4

Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.

Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P.

Department of Nephrology, Hospital Universitario Reina Sofia, Cordoba, Spain.

The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls (C). At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the

 

[Pinnacle]

Tamoxifen

nolvadex aka tamoxifen studies:

Arch Gynecol Obstet 1993;252(3):143-7

Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.

Sterzik K, Rosenbusch B, Mogck J, Heyden M, Lichtenberger K.

Abteilung Frauenheilkunde, Geburtshilfe der Universitat, Ulm, Germany.

Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had no significant effect (P > 0.05) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), or estradiol (E2). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.


Asian J Androl 2001 Jun;3(2):115-9

Effect of intermittent treatment with tamoxifen on reproduction in male rats.

Gill-Sharma MK, Balasinor N, Parte P.

Department of Neuroendocrinology, Institute for Research in Reproduction, ICMR, Parel, Mumbai, India. [email protected]

AIM: To identify the antifertility effect of intermittent oral administration of tamoxifen in male rat. METHODS: Tamoxifen was administered orally at a dose of 0.4 mg x kg(-1) x d(-1) with an intermittent regime for 120 days. Treated and control rats were mated with cycling female rats on days 60, 90 and 120 of treatment. The mated males were sacrificed and the weights of reproductive organs were recorded, and the serum levels of LH, FSH, testosterone and estradiol estimated by radioimmunoassay. In the female rats, the numbers of implantation sites, corpora lutea, and numbers of normal and resorbed foetuses were recorded on d 21 of gestation. The potency, fecundity, fertility index, litter size and post-implantation loss were then calculated. RESULTS: The fecundity of male rats was completely suppressed by tamoxifen while the potency was maintained at the control level. The fertility index was significantly decreased. No viable litters were sired. Post implantation loss, indicative of non-viable embryos, was observed but was not significantly increased above the control level. The weights of the testes, epididymides, ventral prostate and seminal vesicles were significantly reduced. The blood LH and testosterone levels were significantly decreased, but not FSH and estradiol. CONCLUSION: Intermittent oral tamoxifen administration completely suppressed the fecundity of adult male rats with reserved potency

 

[Pinnacle]

Case study showing benefit to FSH, LH, and testosterone from tamox- Notice administration duration

Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S

[see related articles]

PrintEmail
--------------------------------------------------------------------------------

Affiliation
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.

Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy. PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment. RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant. CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.

 

[Pinnacle]

Study on benefit of tamox-again pay attention to duration. Also notice levels were checked at 2wks-12wks, but it is not specified when increased levels of FSH, LH, and T were seen at maximized effect. Levels of T and FSH are only significant, with T at miniscuel proportions

Fertil Steril. 1983 May;39(5):700-3. Related Articles, Links


Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.

Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.

Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.

 

[db006]

thanks for that info bro. unfortunately, alot of it is way over my head. i have been using gh for 4 months now, and i want to stay on for at least a year. i just wanted to make sure i was going to be wasting it.

my pct protocol will go something like this......
1-2 femara 1.25mgs
1-2 clomid 300mgs, 200mgs, 100mgs for 10 days, 50mgs for 2 weeks
1-4 bromo 2.5mgs (prolatctin sensitive)
1-6 nolva 20mgs

this was suggested by my boy, i just wanted to get others suggestions. i will be getting his opinion as well about the gh.

all that medical mumbo jumbo aside, whats the verdict?

 

[dragonfire101]

Femara and bromo together

They can be taken together. Bromo is not a Aromatase inhibitor. It will regulate his prolactin levels and can be used also as a mild noortopic something Aromatase inhibitors or SERMS will not do.


foremenstane
bromo
clomid

would be the optional post cycle combo if one would want to use gh or igf-1 and not worry about lowering igf-1 levels since studies indicate foremestane actually raises it igf-1 levels.

 

[Pinnacle]

They can be taken together. Bromo is not a Aromatase inhibitor. It will regulate his prolactin levels and can be used also as a mild noortopic something Aromatase inhibitors or SERMS will not do.


foremenstane
bromo
clomid

would be the optional post cycle combo if one would want to use gh or igf-1 and not worry about lowering igf-1 levels since studies indicate foremestane actually raises it igf-1 levels.

I didn't mean to sound like they couldn't be used together.More like it's over kill.Letro(femara)would be sufficient.

From Hooker on AR.com
Letrozole

(Femara)

Letrozole is the chemical name of Novartis’ selective third generationAromatase Inhibitor (AI). This drug was developed to fight breast cancer by inhibiting the aromatization. It is usually used as a part of an aggressive treatment in post-menopausal women, to fight and reverse the spread of breast cancer after other treatments (such as Tamoxifen therapy) has failed. It’s probably the most efficient product on the market for this purpose currently (5) It is very similar in structure and action to it’s predecessor Arimidex.

Letrozole also does quite a few things which would be of interest to both bodybuilders and athletes. Firstly, it has been shown to reduce estrogen levels by 98% or greater(1). In at least one documented incidence, Letrozole reduced estrogen in the test subject to undetectable levels, and increased LH, FSH and SHBG (4). Clearly this is all of interest to bodybuilders, as less estrogen in the body means less chance of certain side effects such as water-retention, Gynocomastia, and acne. This makes Letrozole an appropriate choice for even the heaviest bulking or cutting cycles including harsh androgens. Also, if you are a competitive bodybuilder, Letrozole is a must have product for contest prep; no other Ancillary compound will produce a dry and tight look like Letro will.


An effective dose of Letrozole is .25-.5mg/day (I use .25mgs/day), but be forewarned, if you go over that amount, it can kill your sex drive. Also worth noting is that there's a rebound effect on your estrogen when you come off Letrozol. Maximum inhibition of the aromatase enzyme has been found to happen at doses as low as 100mcg! (2)

Letrozole's effects on serum lipids (cholesterol, both HDL and LDL) are, in the words of one researcher: "inconsistent. " Clearly, however, you’ll eventually suffer an impaired lipid profile and immune system if you keep your estrogen levels too low for too long. Your sex drive will also probably suffer from extraordinarily low levels of estrogen present.

As previously mentioned, Letrozole can be used to raise LH and FSH (which are hormones which signal your testes to produce more testosterone). It also, of course, will raise your testosterone levels (6) via this mechanism. Again, this is of interest to athletes and bodybuilders for obvious reasons. Letrozole, of course, can be used for post-cycle-therapy (PCT) to raise test levels, but for various reasons, Tamoxifen may be a better choice. Still, I have successfully used Letrozole for this purpose.

How good is this compared with Aromasin and Arimidex, it’s too other main rivals? Well, In non-cellular systems, letrozole is 2-5 times more potent than anastrozole and exemestane in its inhibition of the aromatase enzyme and activity, and in cellular systems it is 10-20x more potent! It also lasts quite a long time in your body,but takes awhile to get going… Letrozole has a whopping 2-4 day (!) ½ life, and you need to take Letrozole for 60 days to get a steady blood plasma level (8).

Those are impressive numbers, but here’s one of the most interesting things about Letrozole:

It may reduce/eliminate/reverse existing gynocomastia!

In a study conducted on mice (*no, I know it’s not perfect), gyno-like-changes in the mammary gland were totally destroyed ! Here’s a direct quote from that study:

“Our results also indicate aromatase overexpression-induced changes in mammary glands can be abrogated [destroyed] with very low concentrations of the aromatase inhibitor, letrozole.”(7)

In addition, I’ve used Letro to get rid of my own gyno, as has a friend of mine, and we both used it at a dose of 2.5mgs/day, tapering down to .25mgs/day, and then finally off….the gyno never returned in both our cases.

I’d say that this stuff is pretty great, considering its availability and cost (when you consider the fact that .25mgs/day is more than enough protection from estrogen-related sides on most cycles), not to mention it’s overall utility for a variety of functions (destroying gyno, preventing estrogenic sides, and for PCT).



References:
1. Clin Cancer Res. 2005 Apr 15;11(8):2809-21.
2. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
3. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5
4. Epilepsy Behav. 2004 Apr;5(2):260-3
5. Semin Oncol. 2004 Dec;31(6 Suppl 12):3-8.
6. Diabetes Obes Metab. 2005 May;7(3):211-5.
7. J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):27-34. Aromatase overexpression transgenic mice model: cell type specific expression and use of letrozole to abrogate mammary hyperplasia without affecting normal physiology.
8. (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.).

 

[ag-guys]

i know igf is good during this period, but what about gh?? my pct will consist of nolva, clomid, femara, and bromo, for roughly six weeks. i know i read a few things about nolva making gh useless, is that true?? what kind of doses would i want to use if were to use them during my pct? and what is the bottom line for the best time of the day to take your igf?

Never tried GH exclusive but had darn good IGF-1 results for PCT.

AG
www.ag-guys.com

 

[dr. livingstone]

Just stick with Nolvadex and IGF-1 for PCT. Nolvadex will not affect the effect of IGF-1 as in the case of HGH. HGH gets converted to IGF-1 in the liver and Nolvadex has a negative influence on this conversion.

Nolvadex is enough to restore the HPTA. Clomid has more side-effects and worse overall result and the addition of Femara will result in a level of estrogen that is to low.

You don't want to reduce the level of estrogen to much. It will mean that your HDL will get very low, which is (over a longer period) a very dangerous situation. Nolvadex works as an agonist in the liver and actually raises the level of HDL.

A low level of estrogen also has other side effects like impotence and reduced bone formation.
What is important to know for you at this moment is that your HPTA will actually restore sooner if the level of estrogen is low but not zero: so don't use the Femara.

 

[xcelbeyond]

You don't want to reduce the level of estrogen to much. It will mean that your HDL will get very low, which is (over a longer period) a very dangerous situation. Nolvadex works as an agonist in the liver and actually raises the level of HDL.

IMHO, getting your HDL and LDL back to normal is as important as HPTA. I'd avoid letrozole or anastrozole for this reason. Now I've heard exemestane does not have a negative effective on HDL but would definately be overkill for PCT.