low dose of clomid
- 09-03-2008, 08:53 AM
low dose of clomid
hey guys im currently on day 16 of my pct with just nolva and my balls still do not seem like they have returned to normal off of my pp/sd bridge.. would it be benefical if i waited another week and still don't see any progress to take a low dose of clomid, maybe 50 or 100 grams.. Also would that help for sex drive.. i was thinking about cialis but i dont want my body to become dependent on that, as it will only work when i take it but not permently thanks
- 09-06-2008, 08:31 PM
09-07-2008, 06:43 PM
use clomid, 50 mg a day and run an ai. no need for nolva in a pct does nothing to stimulate lh function. next time use hcg and then clomid. also run an ai. for some reason this board loves nolva only pct. this is not an effective pct as u are now finding out.
09-07-2008, 07:01 PM
Nolva is superior over Clomid for the simple reason that it’s a pure anti-estrogen at the hypothalamus. It will stimulate LH at a lower dose than Clomid everytime, and provide a higher testosterone boost than Clomid, everytime.
Clomid can get the job done, but it’s not as efficient as nolva. Clomid has a 50% mixture of zuclomiphene and enclomiphene. Enclomiphene is the primary anti-estrogen responsible for the effects you want [eg, boosting testosterone] However, the estrogenic zuclomiphene is the estrogenic isomer that causes the emotional side-effects, suppressed sex drive, and desensitization of the pituitary, which is why it can partly inhibit Testosterone production – sorta like taking 2 steps forward, and 1 step back. [also why you have to take twice as much for the same effect as Nolva]
My point is, you’re not going to get any better results from the Clomid, and it may even inhibit your results.
How long was the cycle anyway?
09-07-2008, 07:03 PM
09-07-2008, 07:06 PM
09-07-2008, 11:55 PM
im going to give sustain alpha a try from PP it has great reviews of people having an increased libido from the natural test boost.. well see how this goes..
09-08-2008, 12:19 AM
Steroids with Michael Scally, M.D. #1 - Clomid, Nolvadex, hCG, PCT and HPTA Normalization
Clomiphene is a synthetic derivative an estrogen. Clomid is a mixed agonist/antagonist for the estradiol receptor. Tamoxifen is a pure estradiol receptor antagonist. Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.
Perusal of the literature thus indicates that clomiphene acts in several ways in the human male; (a) due to its similarity of structure to stilbesterol it binds with receptor sites in the hypothalamus and pituitary, (b) It stimulates gonadotrophin secretion by acting on the hypothalamo-hypophyseal system, (c) the inhibitory effects of high levels of circulating estrogens (produced under the influence of clomiphene) on hypothalamo-hypophyseal axis are possibly prevented by its potent antiestrogenic behaviour. The result of these varied effects of clomiphene is an overall increase in gonadotrophin and estrogen secretion and accounts for their increase under clinical conditions.
09-08-2008, 12:33 PM
09-08-2008, 01:33 PM
Michael Scally is incorrect in his assertion that estrogen increases pituitary response to GnRH.
Estrogen only sensitizes the pituitary in females. It has the opposite effect in males. Consider the below abstracts.
Again, clomid is less effective than nolvadex, and will only inhibit nolvadex’s effectiveness.
Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback
F. J. Hayes, et al.
J. Clin. Endocrinol. Metab., September 1, 2000; 85(9): 3027 - 3035.
Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.
Winters SJ, Troen P.
J Clin Endocrinol Metab. 61:842–845 (1985)
LH and FSH response to synthetic LHRH after consecutive administration of clomiphene citrate in normal males. Hashimoto T, et al.
J Clin Endocrinol Metab. 41:1110–1112. (1975)
Modulation of pituitary responsiveness to exogenous LHRH by an estrogenic and an anti-oestrogenic compound in the normal male.
Dhont M, et al.
Clin Endocrinol (Oxf). 5:175–180 (1976)
09-08-2008, 01:34 PM
09-08-2008, 01:41 PM
09-08-2008, 03:03 PM
09-08-2008, 05:46 PM
09-08-2008, 06:31 PM
09-08-2008, 09:07 PM
CLOMID mimics the effects of GnRH.........that is, it stimulates the pituitary to produce LH/FSH........that's how it "kick starts" the pituitary gland.
ESTROGEN shuts down the HYPOTHALAMUS (shuts off the GnRH that stimulates the Pituitary to release LH/FSH).................when you stop estrogen production via 6-oxo (or any aromatase inhibitor), you release that negative feedback and GNRH increase, LH/FSH increase, and Testosterone production from the testicles increases.
NOLVADEX doesn't have a profound effect on the HYPOTHALAMUS. All it does is block estrogen receptors......
09-08-2008, 09:43 PM
I think your missing the point here...
Your right about Clomid being an anti-estrogen at the hypothalamus and stimulating LH & FSH.
However, Clomid has an estogenic action at the pituitary, thus it reduces the pituitary’s ability to respond to GnRH – which down-regulates the pituitary’s ability to produce LH & FSH. [part of the reason why it takes 2x a much clomid to be as effective as nolva]
Nolva is an anti-estrogen at the hypothalamus AND pituitary, thus it stimulates LH & FSH more efficiently than clomid.
09-08-2008, 09:54 PM
09-09-2008, 12:30 PM
120mg/day - week 1
120 mg/day -week 2
60mg/day week 3
30mg/day week 4
wouldnt that make more sense than a flat dosage all the way through the PCT so the body can learn to work for itself slowly as opposed to going 'cold turkey' after 4 weeks of PCT?
Again, thanks for the help
09-09-2008, 12:58 PM
09-11-2008, 05:41 AM
09-11-2008, 02:34 PM
09-11-2008, 02:36 PM
09-11-2008, 02:38 PM
09-11-2008, 04:17 PM
once again ....
this is what i asked palumbo, his answer in bold...
The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment).
As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.
dave how do you feel about this written by william Llewellyn
Since CLOMID is essentially mimics the hypothalamic hormone, GnRH, it makes sense that taking CLOMID would decrease pituitary sensitivity to naturally released GnRH because there's TOO MUCH "SIGNAL" around. However, the CLOMID is still doing the job of turning ON the pituitary and causing the release of LH/FSH (as is evident by the fact that testosterone levels increase in response to Clomid).
These simple facts are the exact reason that suggest taking an AROMATASE INHIBITOR and CLOMID in the PCT period.
The reason that NOLVADEX makes the pituitary more sensitive to naturally produced hypothalamic GnRH is that it blocks estrogen receptors on the hypothalamus and thus removes the NEGATIVE FEEDBACK HORMONE (Estrogen) from inhibiting the hypothalamus from producing GnRH.
If the experimenters had introduced an AROMATASE INHIBITOR like ARIMIDEX, they would have noticed lower serum estrogen AND higher pituitary sensitivity to GnRH as well since the estrogen was removed from the equation. (
i hardly see raloxofen used, but of the other 3, can you give a breakdown of what they do and where their estrogenic/anti estrogenic activities are observed, which are better during and post cycle, and why you chose it? which on stimulates what area (pituitary, hypothalmus or both) which one is favored for increease in testosterone?
maybe if you dont do it on here, maybe a write up in MD, because it seems soo controversial, and people use a combo of 2 and really cant seem to choose or find better evidence with one is better then the other.
Nolva, Clomid, and Torem
Going back to my original PCT recommendations:
(1) Aromatase inhibitors are taken throughout the PCT (whether you use ARIMIDEX or my TESTOSTOLYZE) to block estrogen formation.
(2) HCG (an LH/FSH mimicking agent) is taken to turn the testicles back ON and cause they to produce testosterone
(3) Clomid is started once the HCG is stopped. Clomid mimics the Hypothalamic hormone GnRH; therefore, it will turn the Pituitary back ON.
*** Once the testicles and pituitary is re-stimulated, we're good to go! The hypothalamus merely responds to levels of estrogen. When they're high, it stops producing GnRH.........when estrogen is low, it cranks out more GnRH.
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