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Coming Off Deca

murmp3

New member
I will soon be coming off an 7 week cycle of deca in which I ran it at about 300mg throughout cycle. I am definetly getting some clomid, do you think it is necessary to get on an anti-e
 
murmp3 said:
I will soon be coming off an 7 week cycle of deca in which I ran it at about 300mg throughout cycle. I am definetly getting some clomid, do you think it is necessary to get on an anti-e
I would also get some HCG as Deca shuts your Hpta down harder than any othe Anabolic and can reek serious havoc on your libido
 
I would also get some HCG as Deca shuts your Hpta down harder than any othe Anabolic and can reek serious havoc on your libido


Well... It is really about how tightly that AAS binds to the androgen receptor when it comes to suppression. I would say there are a couple that rank higher than deca including tren.

If you are going to use HCG post- cycle, my recommendation would be to use Nolvadex instead of Clomid. They are similar in terms of stimulating GnRH secretion, but Nolvadex has been shown to be superior in combating gynecomastia, which is a common occurance as a result of HCG use.
 
Jguns said:

but Nolvadex has been shown to be superior in combating gynecomastia.

This is an interesting statement. Do you have this referenced somewhere?

Nolva and clomid are almost identical structurally. From a dosage perspective, nolva is more efficient (i.e. it takes less to exert desired effects), but clomid, dosed accordingly, should be as efficient as nolva because it is, for all intensive purposes, the same thing. I know I've used clomid to fight dbol gyno.

My understanding is that the misconception amongst bb circles that nolva is more efficient at gyno than clomid was purely based on the way the drugs were originally marketed by the pharmeceutical companies. (i.e. they were marketed for very different purposes -- one fertility, one breast tissue cancer -- even though they are nearly the same drug)

With all of this said, I'd still pick nolva as I believe it is a more efficient drug...

P.S. Not trying to be inflammatory, just trying to figure out if my understanding is flawed...
 
jThis is an interesting statement. Do you have this referenced somewhere?

Nolva and clomid are almost identical structurally. From a dosage perspective, nolva is more efficient (i.e. it takes less to exert desired effects), but clomid, dosed accordingly, should be as efficient as nolva because it is, for all intensive purposes, the same thing. I know I've used clomid to fight dbol gyno.

My understanding is that the misconception amongst bb circles that nolva is more efficient at gyno than clomid was purely based on the way the drugs were originally marketed by the pharmeceutical companies. (i.e. they were marketed for very different purposes -- one fertility, one breast tissue cancer -- even though they are nearly the same drug)

With all of this said, I'd still pick nolva as I believe it is a more efficient drug...

P.S. Not trying to be inflammatory, just trying to figure out if my understanding is flawed...

No problem.. Actually Rolaxiphene is the most effective at treating gyno, but I don't know anyone that carries it.

As for Nolva vs. Clomid.. they are close but studies suggest that nolva is better at stimulating LH release:
Effects of estradiol and some antiestrogens (clomiphene, tamoxifen, and hydroxytamoxifen) on luteinizing hormone secretion by rat pituitary cells in culture.

Emons G, Ortmann O, Thiessen S, Knuppen R.

Primary pituitary cell cultures from adult female rats were incubated for 4 or 24 h with various concentrations of estradiol (E2) or the antiestrogens (AE) tamoxifen (TMX), 4-hydroxytamoxifen (OH-TMX), and clomiphene citrate (CC). The luteinizing hormone (LH)-response of these cultures to gonadotrophin releasing hormone (GnRH) was monitored. Treatment for 4 or 24 h with high concentrations (10(-5) M) of the AE significantly decreased the GnRH-induced LH-release by the gonadotrophs. The negative E2-effect, which is observed in this model after 4 h was enhanced and the positive E2-effect, which occurs after 24 h, was completely reversed into a negative effect by these high AE-concentrations. Treatment of pituitary cells with increasing concentrations of E2 (10(-13)-10(-6) M) or AE (10(-12)-10(-5) M) for 24 h led first to a dose dependent increase of the LH-response to 5 X 10(-10) M GnRH. At higher E2- or AE-concentrations this positive effect was lost, resulting in bell shaped dose-response curves. The following maximal effective concentrations (EDmax) were found: E2 = 10(-10) M, OH-TMX = 10(-9) M, CC = 10(-7) M, TMX = 10(-6) M. Incubation of pituitary cells for 24 h with concentrations of AE near their EDmax and stimulation with increasing concentrations (10(-11)-10(-7) M) of GnRH resulted in significant increases of LH-secretion over a wide range of GnRH-concentrations. It is concluded that AE possess marked intrinsic activities on pituitary LH-secretion: at extremely high concentrations they suppress the GnRH-induced release of the gonadotrophin. At lower concentrations they increase the pituitary LH-response to GnRH in a manner which is qualitatively indistinguishable from that of E2.


Comparison of tamoxifen with danazol in the management of idiopathic gynecomastia.

Ting AC, Chow LW, Leung YF.

Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Pokfulam.

Idiopathic gynecomastia, unilateral or bilateral, is a common physical finding in normal men. Successful treatment using tamoxifen (antiestrogen) and danazol (antiandrogen) has recently been reported. We compared the efficacy of tamoxifen and danazol in the treatment of idiopathic gynecomastia. We reviewed the clinical records of patients with idiopathic gynecomastia presenting to the Department of Surgery, University of Hong Kong, between August 1990 and September 1995. Medical treatment with either tamoxifen (20 mg/d) or danazol (400 mg/d) was offered and continued until a static response was achieved. The treatment response was compared. Sixty-eight patients with idiopathic gynecomastia were seen in the Breast Clinic. The median age was 39.5 years (range, 13-82), with a median duration of symptoms of 3 months (range, 1-90). The median size was 3 cm (range, 1-7). Twenty-three patients were treated with tamoxifen and 20 with danazol. Complete resolution of the gynecomastia was recorded in 18 patients (78.2%) treated with tamoxifen, whereas only 8 patients (40%) in the danazol group had complete resolution. Five patients, all from the tamoxifen group, developed recurrence of breast mass. In conclusion, hormonal manipulation is effective in the treatment of patients with idiopathic gynecomastia. Although the effect is more marked for tamoxifen compared with danazol, the relapse rate is higher for tamoxifen. Further prospective randomized studies would be useful in defining the role of these drugs in the management of patients with idiopathic gynecomastia.



In one study using Clomid for gynecomastia the clomid treated group had less of a rate of recovery, and it took longer to treat. Still, clomid has not proven to be an effective method for treatment while nolvadex has.



"Clomiphene citrate 100 mg daily was used to treat 28 boys with pubertal gynaecomastia. Six failed to complete the course and of the remaining, 14 (64%) responded within 6 months of commencement of therapy. LH, FSH, testosterone and oestradiol levels rose during therapy. It is suggested that clomiphene affects gynaecomastia locally as an anti-oestrogen."

The effect of clomiphene citrate on pubertal gynaecomastia.

LeRoith D, Sobel R, Glick SM.
 
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Thanks for digging out those studies :)

On the surface it would appear that there's about a 14 percent difference between the two (which is significant, but not dramatic), however, several things I noticed right away:

The tamoxifen group had idiopathic gynecomastia, the clomiphene group had pubertal gynaecomastia -- I wonder if this makes for a fair comparison.

Also, the tamoxifen group's median age was 39.5, the clomiphene group's age was unspecified, but said boys with pubertal gyno, so maybe 16 -19 year olds? If this is true, the clomiphene group would have higer test levels, and as a result, higher estrogen levels than the tamoxifen group -- which could effect treatment and remission rates...

Then dosage -- the tamoxifen group took 20 mg/day; the clomiphene group took 100 mg/day. Llewellyn has drawn a comparison that 20 mg of nolva = 150 mg of clomiphene. If this is true, the clomiphene group was not being treated with the same effective dosage...

Also, the clomiphene study was done with only 22 "boys" -- about a third of what the tamoxifen group was comprised of. The smaller group could lead to less reliable data.

I wonder what it would look like if two like groups went head to head -- one with 20 mg/day tamoxifen and the other with 150 mg/day of clomiphene?

Either way, interesting stuff...
 
The tamoxifen group had idiopathic gynecomastia, the clomiphene group had pubertal gynaecomastia -- I wonder if this makes for a fair comparison.

I don't think it makes a difference. Gynecomastia is initiated by a coordinated effort of pituitary and ovarian hormones, as well as local mediators. Although estrogens and progestogens are vital to breast tissue growth, they are ineffective without anterior pituitary hormones . Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development.
Both pathological gyno and pubertal gyno have the same underlying cause being due to either decreased production of androgens or increased aromatization of circulating androgens, thus increasing the estrogen to androgen ratio. Pretty much, any cause of estrogen excess from overproduction to peripheral aromatization of androgens can initiate the cascade to breast development.

The problem with the clomid study was that the sample size was much smaller, and they don't specify exactly what the "responding" means. It could just mean that there was a reduction in tissue size, but no resolution. Also, the time frame was much longer, at six months. Even if we took Llewellyn's word that 20 mg of nolva equals 150 Mg of clomid ( and I have no idea how he came up with that). Six months is still a much longer time than the tamoxifen study, if only to see a difference. When I battled gyno, I used 80 MG of nolva per day and stayed on cycle, I saw almost complete resolution in less then 5 weeks.
 
Fair enough. There's still a lot out there to interpret and discover eh?

I've completely replaced clomid with nolva as it is. Used it on my last cycle for post-recovery (following Llewellyn's conversion rate; I don't remember how he came up with that -- there is an article somewhere, I'll see if I can't dig it up again). Did exactly what clomid would have done, but with less moodiness (to be fair, inositol and 5htp were utilized this time to combat post-cycle depression; carao and maca were also part of the post-cycle recovery regime).
 
Seven weeks on deca at 300mg? what was the reason for this cycle. when i finish a deca only cycle i inject a little test suspension for about 5 days followed by 10000 hcg. I no longer waist my money on nolvadex or clomid. Left nip a little itchy sometimes, but thats it. No problems with recovery.........
 
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