I believe that personal experience is just as important as medical studies. I wanted to post something supporting my opinion, not because I want ot be right but simply to point out I wasn't talking from broscience. Now the funny thing is this, there are studies out there that will claim the exact opposite meaning that hcg should be used during cycle and not after. For the sake of a good old fashion on-line pissing contest, I suggest you try one method first and if that doesnt work well for you, try the other.
I have no reason to be right here, after trying both methods I know what works for me. One method had me feeling like crap for weeks and the other method didnt. Now there are lots of variables here, like compunds used, duration of said compounds, hell even diet and rest can play a factor.
Research results on reversal HPTA
Objective:
Although shown to be effective for their intended medical treatment, AAS have been shown to induce hypogonadotropic hypogonadism in adult males. The medical literature is conflicting in the reports of spontaneous return and long-term suppression of gonadal suppression post AAS usage. This observational study documents the treatment protocol of HCG, clomiphene citrate, and tamoxifen in returning hormonal function to normal post AAS usage. Design:
Five HIV-negative males age 27-49, weighing 77-100 kg, with serum total testosterone levels below 240 ng/dL and luteinizing hormone (LH) levels below 1.5 mIU/mL were considered for this observational study. All five patients were administered the treatment protocol.
Methods:
Treatment consisted of combination therapy which included concurrent administration of (a) Human Chorionic Gonadotropin, (b) Clomiphene Citrate and (c) Tamoxifen Citrate for a standard duration of 45 days. This protocol was repeated with every patient until serum LH and total testosterone values reached normal ranges.
Results:
All five patients were considered eugonadal by normal laboratory reference ranges by the conclusion of treatment. Average serum total testosterone rose from 98.2 to 692.8 ng/dL (p<.001) while the average serum LH rose from an average undetectable value of less than 1.0 to 7.92 mIU/mL (p<.0008).
Conclusions: Although the treatment protocol of HCG, clomiphene citrate, and tamoxifen proved beneficial in reversing AAS induced hypogonadotropic hypogonadism, future controlled studies need to be performed to confirm the beneficial effects of this combined pharmacotherapy in returning HPGA functioning to normal.
Key Words- anabolic-androgenic steroids, clomiphene, HCG, tamoxifen, testosterone, HIV
INTRODUCTION
Testosterone and testosterone analogues, anabolic-androgenic steroids
(AAS), have long been used in the athletic community for improving lean muscle tissue and strength. A positive correlation has been shown with testosterone to include:
increased protein synthesis resulting in lean muscle tissue development (Bhasin et al, 1996; 1997; Hervey et al, 1981; Tenover, 1992),
enhanced sexual desire (libido) (Schiavi et al, 1991),
increased muscular strength (Bhasin et al, 1996; 1997; Hervey et al, 1981; Sih et al, 1997),
increased erythropoiesis (Bhasin et al, 1997; Evans & Amerson, 1974; Sih et al, 1997; Tenover, 1992),
a possible positive effect on bone development (Anderson et al, 1996; 1997; Baran et al, 1978; Tenover, 1992),
improved mental cognition and verbal fluency (Alexander et al, 1998), and male masculinizing characteristics (Starr & Taggart, 1992).
Recently, however, clinicians have recognized the potential benefits of their use in the treatment of various disorders and ailments. Numerous studies have discussed the use of AAS in the treatment of HIV-associated conditions (Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al, 1999; Van Loan et al, 1999), hypogonadism (Bhasin et al, 1997; Davidson et al, 1979; Rabkin et al, 1999; Sih et al, 1997; Snyder et al, 2000; Tenover, 1992; Wagner & Rabkin, 1998; Wang et al, 2000), impotence (Carani et al, 1990; Carey et al, 1988; Klepsch et al, 1982; Lawrence et al, 1998; McClure et al, 1991; Morales et al, 1994; 1997; Nankin et al, 1986 Rakic et al, 1997; Schiavi et al, 1997), burn victims (Demling et al, 1997), various anemia’s (Doney et al, 1992; Gascon et al, 1999; Hurtado et al, 1993; Stricker et al, 1984), deteriorated myocardium (Tomoda, 1999), glucose uptake (Hobbs et al, 1996), continuous ambulatory peritoneal dialysis (CAPD) (Dombros et al, 1994), alcoholic hepatitis (Bonkovskyet al 1991; Mendenhall et al, 1993), hemochromatosis (Kley et al, 1992) and prevention of osteoporosis (Anderson et al, 1996; 1997; Baran et al, 1978; Behre et al 1997; Hamdy et al, 1998; Prakasam et al, 1999).
While AAS have proven effective in cases of lean muscle wasting conditions (HIV/AIDS), this class of medicines is not without their inherent problems. AAS have been shown to induce hypogonadotropic hypogonadism (Alen et al, 1987; Bhasin et al, 1996; Bijlsma et al, 1982; Clerico et al, 1981; Jarow & Lipshultz, 1990; Strawford et al, 1999; Stromme et al, 1974). This condition typically results from an abnormality in the normal functioning of the hypothalamic-pituitary-gonadal axis (HPGA), usually from a negative feedback inhibition of one of the hormone secreting glands, causing a cascading unbalance in the rest of the axis. Possibly resulting from a physiological abnormality (i.e. mumps orchitis, Klinefelters syndrome, pituitary tumor) or as an acquired result of exogenous factors (i.e. androgen therapy, AAS administration). Clerico et al (1981) found a dramatic suppression of serum gonadotropin levels in athletes given methandrostenelone, suggesting a direct action of AAS on the hypothalamus. Similar results of suppressed gonadotropins have been found in patients supplementing solely testosterone (Bhasin et al, 1996; Marynick et al, 1979; Strawford et al, 1999; Tenover, 1992). Case report studies discussed a 36-year old male competitive bodybuilder and a 39-year old father, each using various AAS regimens over extended periods of time, who showed a blunted response to GnRH stimulation tests (Jarow & Lipshultz, 1990). One particular study administered 600 mg of nandrolone decanoate to 30 HIV-positive males over twelve weeks (Sattler et al, 1999). The results made no reference to LH or testosterone levels. The lack of gonadotropin measurement is puzzling as the data showed 12 of 30 subjects experienced testicular shrinkage, implying Leydig cell dysfunction and suppressed testosterone levels. Other studies using AAS have also shown no reference to LH or FSH levels but suppressed values are expected in each case (Bagatell et al, 1994; Behre et al, 1997; Sheffield-Moore et al, 1999; Tricker et al, 1996).
Declining, or suppressed, circulating testosterone levels as a result of either pathophysiological or induced hypogonadal conditions can have many negative consequences in males. Declining levels of testosterone have been directly linked to a progressive decrease in muscle mass (Mauras et al, 1998), loss of libido (Schiavi et al, 1991), decrease in muscular strength (Balagopal et al, 1997; Mauras et al, 1998) impotence (Rakic et al, 1997), oligospermia or azoospermia (Vermeulen & Kaufman, 1995), increase in adiposity (Mauras et al, 1998) and an increased risk of osteoporosis (Wishart et al, 1995).
While some research suggests that the hormonal axis will spontaneously return to normal shortly after cessation of testosterone administration (Knuth et al, 1989), documented cases have taken up to 2 ½ years to return to normal (Jarow & Lipshultz, 1990). This case of a 39-year old male who previously used AAS was found to have low serum testosterone levels (6nmol/L, range 14 to 28 nmol/L) 2 ½ years after his last administration of the drugs (Jarow & Lipshultz, 1990). For most men, suffering with diminished libido, impotence, depression, fatigue, muscle atrophy, and infertility for 2 ½ years is not a pleasant option. Other androgen or anabolic steroid induced cases of hypogonadotropic hypogonadism have taken 6 months (Gazvani et al, 1997; Wu et al, 1996), 8 months (Gazvani et al, 1997), 10 months (Boyadjiev et al, 2000), 12 months (Schurmeyer et al, 1984), and 18 months (Gazvani et al, 1997) to finally return to eugonadal status.
The individual use of human chorionic gonadotropin (HCG), clomiphene citrate, and tamoxifen citrate in the treatment of testicular sub-function and gonadotropin suppression, respectively, is well documented. HCG has been shown to significantly improve gonadal function in hypogonadotropic hypogonadal adult males (Barrio et al, 1999; Burgess & Calderon, 1997; Cisternino et al, 1998; D’Agata et al, 1982; 1984; Dunkel et al, 1985; Kelly et al, 1982; Ley & Leonard, 1985; Liu et al, 1988; Martikainen et al, 1986; Okuyama et al, 1986; Ulloa-Aguirre et al, 1985; Vicari et al, 1992). Studies using clomiphene citrate to induce endogenous gonadotropin production in males found significant improvements in LH and FSH values after treatment (Bjork et al, 1977; Burge et al, 1997; Guay et al, 1995; Landefeld et al, 1983; Lim & Fang, 1976; Ross et al, 1980; Spijkstra et al, 1988). Tamoxifen citrate has also been found to produce a profound increase in serum LH levels as well as improved semen and sperm quality (Gazvani et al, 1997; Krause et al, 1985; Lewis-Jones et al, 1987; Wu et al, 1996).
As HCG’s effect is centralized at the Leydig cells of the testicles, clomiphene citrate and tamoxifen citrate act upon the hypothalamic-pituitary region in stimulating gonadotropin production. Tamoxifen, a nonsteroidal antiestrogen, and clomiphene citrate, a nonsteroidal ovulatory stimulant, compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary and allowing gonadotropin production to resume normally. The normal operation of both the testicular and hypothalamic-pituitary regions is crucial in returning HPGA function to normal. Returning one component of the axis to normal without concurrently returning the other would sabotage and inhibit the operation of the entire HPGaxis. It was with this understanding that HCG was eventually combined with clomiphene citrate and tamoxifen as attempted therapy to reverse gonada function in hypogonadotropic hypogonadal males.
In accordance with previous studies, each medication was used individually, and along with HCG, in initial trials. The simultaneous use of clomiphene citrate and tamoxifen was determined through preliminary use of clomiphene citrate and tamoxifen individually. It was discovered that although both clomiphene citrate and tamoxifen met with some success, when combined together they achieved a more significant increase in gonadotropin production. This clinical outcome resulted in the combination therapy of HCG, clomiphene citrate and tamoxifen.
