"Nolvadex is believed to be the best anti-estrogen drug on the market today, and is by far the most popular.Nolvadex doesn't reduce gains from taking steroids. It does reduce water retention, a common side effect experienced by steroid users. So while it may appear to reduce gains it actually takes away a side effect."
"Clomid is the antiestrogen of choice for improving recovery of natural testosterone production after a cycle, improving testosterone production of endurance athletes, and is also effective in reducing risk of gynecomastia during a cycle employing aromatizable steroids."
So which is better : Nolva or Clomid?
Its kinda funny you ask this question because I was reading up on this...
So lets get the basics down:
Clomid: 2-[p(2-chloro1,2-diphenylviny)phenoxy] triethylamine citrate
Clomid(fda apporved) is used as the first fertility drug a couple will be introduced to if you can not get pregnant.femailes take it induce ovulation and asses ovarion function and the likelihood that a woman can still produce viable eggs.
Clomid use for men with low sperm counts due to genectic factors or after years of anabolic steriods drug abuse.Clomid influences the way the estrogen hormone, estradiol, influences three other hormones. Clomid can cause gynecomastia, so from that standpoint, you need to watch not only your testosterone levels, but also your estradiol.Clomid produces more sper count...
Anti-estrogens are drugs which act to reduce estrogenic activity in the body. This can be done either by reducing the amount of estrogen, or by reducing the activity of whatever estrogen is present.
Competitive aromatase inhibitors, such as Cytadren, Arimidex, and probably Proviron, bind to the same binding site on the aromatase enzyme that testosterone does. By doing this, they allow less testosterone to bind to aromatase. So, less testosterone is converted to estradiol (estrogen).
Here’s an important thing: the effectiveness of competitive inhibitors decreases as the amount of the normal substrate increases. Suppose that you had equal amounts of inhibitor and normal substrate in the blood, and they bound to the enzyme equally well. Then the inhibitor would at any moment be taking up half the sites that the normal substrate otherwise would, so it would reduce conversion rate by 50%. But if the amount of substrate is increased 10 times while the amount of inhibitor remains the same, then the inhibitor would be out-competed by the more numerous substrate molecules. It would therefore be rather ineffective.
For example, with more testosterone molecules available, and similar binding strengths, the enzyme will mostly bind testosterone. It will then mostly be working to produce estrogen. To obtain the 50% reduction we had before, then the amount of inhibitor would also have to be increased 10 times.
To be really effective, the inhibitor must either be present in higher concentration than the normal substrate, or must bind more tightly.
With Cytadren or Proviron, it takes quite a lot of inhibitor to out-compete high testosterone levels. With Arimidex, rather little, even 1 mg/day, can be sufficient because it binds so strongly.
The other general approach is estrogen receptor antagonism. If a molecule binds strongly to a hormone receptor, but does not activate that receptor and makes it unresponsive to the normal hormone, then it is a receptor antagonist. Clomid (clomiphene) and Nolvadex (tamoxifen) follow this approach. These drugs are very similar structurally. They are both what are called triphenylethylenes, and are not steroids. The differences are relatively minor, but seem to affect an important characteristic of these compounds: drug metabolism.
Both tamoxifen and clomiphene are metabolized to other related compounds which can be estrogenic or anti-estrogenic. Both act as estrogens in bone tissue, perhaps after metabolism, which is a very useful property for female patients, for whom these drugs are usually intended. (Otherwise, an anti-estrogen could lead to osteoporosis.) Tamoxifen seems particularly prone to acting as an estrogen in the liver, which may account for reduced IGF-1 levels seen when this drug is taken.
Users generally seem to agree that when tamoxifen is used, gains are a little less than what otherwise would be expected. (Let’s not take this too far though: many people have made great gains while using tamoxifen as an anti-estrogen. And it’s always hard to say what "would" have been the case if a drug had not been included.) I’ve heard nothing but good about clomiphene, though.
Proviron, an anabolic steroid, is particularly interesting. I suspect that it not only acts as an antiaromatase but in an unknown DHT-like anti-estrogenic manner. This might involve estrogen receptor downregulation for example. In any case, aromatase inhibition and/or Clomid don’t seem to give the same effect on appearance and muscle hardness as when Proviron is included.
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