by which pathways does clomid work?

jacked1

New member
clomid was originally thought to stimulate production of LH and therefore stimulate the production of testoterone levels. now most believe this is not how it works. Can someone steer me to some scientific data that shows exactly what pathways clomid takes to boost test levels?
 
the reason I ask is, if clomid doesn't work like most believed for years and years, it may not be an effective (or as effective) post cycle therapy for certain cycles - depending on what gear was run. If this is true, HCG may be a needed ( or required) component in post cycle therapy in at the end of certain cycles.
 
CLomid works just like estrogen. It is an estrogen antagonist, which occupys the ER in the hypothalmus/pituitary axis preventing estrogen from shutting down secretion of LH/Fsh. It is a negative feedback system. The more estrogen which aromatises from testosterone, the less Lh/fsh released. High levels of test also directly cause suppression as well, but I can't tell you the exact mechanism. Some steroids do not aromatise into estrogen, for example primo, winstrol, oxandrolone, and even trenbolone. For these steroids clomid will not be as effective. Some of these steroids cause very little suppression such as primo, var, and stan, while others like tren are quite suppressive.

HCG - I personally believe should be administered on a weekly basis throughout the cycle, starting at the end of the third week (which is the point where suppression reaches the testicular level) - This will help maintain testicular size and function while on cycle. The dose I personally use is just 250iu every Sunday, but some use as much as 500 iu on a Saturday/ Sunday basis - this is Swale's protocol.

Recovery from htpa suppression seems to occur much more easily than recovery of testicular size and fuction post cycle, so a regular hcg protocol would be a good idea. For those who don't know, Hcg 'mimics' lutenizing hormone at the leydig receptors of the testes which stimulates spermotogenisis via the production of endogenous testosterone, which causes maturation of the sperm. Lh is secreted naturally by the htpa for this purpose.

There is a danger of using too much hcg at cycle's end which could cause receptor desensitivity at the leydig cells. This could slow down recover, in itself. I don't think it is wise to use more than 500 - 1000 iu of hcg at a time, for this reason.

One other thing to bear in mind is that Hcg is suppressive in itself. If there is exgenous Lh, no endogenous Lh will need to be secreted by the htpa. On top of that, hcg aromatises to estrogen - about 50%. It is possible to do hcg post cycle, stop and end up worse than before because of the extra estrogen in one's system, and over use of the hcg causing desensitization of the leydig receptors.

For that reason I recommend keeping the dosages injected at one time low - is that hcg has a 23 hr halflife. Also I suggest the use of femara while taking hcg - especially if post cycle. This will eliminate the aromatisation of estrogen, making pct easier on cessation of hcg therapy.
 
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