Nolvadex VS Clomid?

[maxgear]

Anti-Estrogen Usage to Protect Your Physique and Your Physiology
Nolvadex VS Clomid?
Nolvadex
Nolvadex is one of the most well known anti-estrogens. It is also one of the oldest and most popular medications for breast cancer victims, which is the text book clinical use for this drug. Nolvadex is actually a weak estrogen and will bind to the estrogen receptor. The receptor is then occupied and when the normal and stronger estrogen floats by the receptor, it has no where to “park”. This is what we have defined as the classic second line inhibitor. Second line, because we are allowing estrogen to be produced, we are just blocking it at the receptor. For male usage, nolvadex is a good drug of choice to use for ant-bloating and to control gyno if you are not particularly susceptible to these estrogenic side effects. If you are not and just need minor control, 20mg per day is probably enough to keep the majority of water off and your nips from being sensitive. If you are susceptible, you may need a stronger ant-estrogen, or may need to combine nolvadex with another anti-estrogenic drug, or may need a much higher dosage of nolvadex (probably closer to 40mg/day).
There is some literature out there that states nolvadex having better leutinizing (testosterone stimulating) properties than clomid. This is with respect to post cycle recovery and jump starting your natural testosterone. Personally, amongst all my friends and colleagues, I have not found this to be true. With respect to post cycle recovery of natural testosterone production clomid is definitely more effective.
Clomid
As we’ve stated above, clomid is more effective at restoring natural testosterone production. Everything you read about these two drugs seems to offer the same info. I will afford you with something different. For anti-estrogen protection, nolvadex is probably a little stronger. Its chemical structure makes for a slightly more potent anti-estrogen.
I have yet to see any quality literature which describes the affinity for either drug at the estrogen receptor. Clomid after all, is also a weak estrogen. Another term used to classify clomid and nolvadex is “competitive inhibitor”. They are so called due to the fact that they are weak estrogens and actually bind to the receptor. By doing this they are competing for the “parking spot” in the receptor, thereby occupying the space when the truer, stronger estrogen comes along. Its like being at the local mall and having someone pull around the isle, cut you off and take your spot. In a sense they just “competed” with you for your spot and “inhibited” you from taking it. Got it? Good. See this stuff is simple, my fellow friends and athletes.
The literature also fails to describe exactly why clomid works more efficiently as a leutinizer. Even in the medical literature, the drug is primarily used for fertility purposes for both males and females. This means clomid has value in stimulating the pituitary in both men and women. Clomid is used on a five day course in order to stimulate ovulation in the female in order to enable fertilization. There is not a fertility doctor in the world that doesn’t know what clomid is. It is a drug that has always been in their toolbox. Part of the reason is, it works. The literature is less extensive for fertility cases in the male but know that it is indeed used for this purpose. Now, as much as I am all for underground self taught knowledge, we have to hand it to the medical professionals for specific cases. For example, if nolvadex were a better leutinizer, it would be the drug of choice in fertility clinics for stimulating ovulation in the female and for aiding fertility and motility of sperm in the male. Simple fact is that this is not the case. Save your self time and frustration by using a medically time tested drug for your post cycle recovery of testosterone. For recovery of your natural test, use clomid.

Share with my brothers!

[macedog24]

This gives some insite on ai 's and serms .
When looking to control Estrogen, we have two choices. These are SERMS and AI's. SERM is an acronym for Selective Estrogen Receptor Modulator, and AI is an acornym for Aromatase Inhibitor.

SERM's:
Let's take a look at what SERM's do and our SERM options. SERM's, by definition, compete for the space that Estrogen binds to. This receptor is then full and cannot accept the estrogen and therefore cannot produce the effects of estrogen. Some of the more popular SERM's are: Clomiphene Citrate (Clomid), Tamoxifen (Nolvadex), Toremifene Citrate (Fareston), and Raloxifene hydrochloride (Evista).

AI's:
Now let's look at some of the AI's and how they work. AI's, by definition, prevent aromatizable steroids from converting to Estrogen via the aromatase enzyme. Some are more effective than others. Some of the more popular ones are: Anastrozole (Arimidex), Aromasin (Exemestane), and Letrozole (Femara).

So what are some facts and uses of the different SERM's and AI's?

Well, some AI's take time to build up blood levels and therefore need to be utilized for a certain time before they are effective, whereas SERM's go to work immediately.

SERM's:

Clomid: Usually dosed from 25-300 mgs depending on the desired effect, is both effective during a cycle for estrogen sides and post cycle for support of natural Testosterone levels. While it has been claimed that Clomid "stimulates" production of LH and therefore of testosterone, in fact Clomid's activity is achieved not by stimulation of the hypothalamus and pituitary, but by blocking their inhibition by estrogen.

Clomid is a mixed estrogen aganoist/antagonist (activator/blocker) which, when bound to the estrogen receptor, puts it in a somewhat different conformation (shape) than does estradiol. The estrogen receptor requires binding of an estrogen or drug at its binding site and also the binding of any of several cofactors at different sites. Without the binding of the cofactor, the estrogen receptor is inactive.

Different tissues use different cofactors. Some of these cofactors are able to bind to the estrogen receptor/Clomid complex, but others are blocked due to the change in shape. The result is that in some tissues Clomid acts as an antagonist -- the cofactor used in that tissue cannot bind and so the receptor remains inactive -- and in others Clomid acts as an agonist (activator), because the cofactors used in that tissue are able to bind. Clomid is an effective antagonist in the hypothalamus and in breast tissue. It is an effective agonist in bone tissue, and for improving blood cholesterol.

Clomid also has the property of reducing the adverse effect of exercise-induced damage of muscle tissue. This is very significant for endurance athletes but is not very significant, if at all significant, with reasonable weight training. Clomid does not perceptibly affect gains of the weight trainer either favorably or adversely in my experience.

It should also be noted that Clomid seems to have estrogenic effects on mood, causing some slight depression or moddiness. It can also effect eyesight by causing it to seem blurry. No this isn't from crying while listening to James Blunt CD's. LOL

Nolva: Usually dosed from 10-100 mgs, Nolva is best dosed at 20-40 mgs. It has a certain affinity for binding to breast tissue receptors that Clomid doesn't. It can significantly raise Testosterone levels. However, it can reduce IGF-1 levels. It is commonly said that Nolva can accomplish at 20 mgs what Clomid can at 150mgs. Something to keep in mind. Nolva does not decrease the bodies LH response to LHRH like Clomid can. It can reduce the blood levels of Arimidex and Letro rendering them less effective. It does not affect Aromasin.

Evista: Evista is a second-generation SERM. It is approved by the FDA for this use in women. Although it bears structural and mechanistic similarities to other SERMs which have been approved either as fertility drugs (Clomid) or Breast Cancer medication (Nolvadex), it has not been approved for either of those uses. Ralixofene exerts its effects by antagonizing the estrogen receptor in some tissues, and agonizing it in others. In this way, certain estrogenic pathways are activated and others are blockaded. It seems to exert estrogenic effects on blood lipids, reducing LDL and total cholesterol, as well as estrogenic effects on bone, improving density.

It would also appear to exert anti-estrogenic effects in breast tissue, displacing the traditional effects of estrogen, effectively helping prevent breast cancer in postmenopausal women. Evista only raises Testosterone by about 20%, much less than Nolva. Common Evista doses are 30-150 mgs. It is better utilized during a cycle versus being used in PCT.

Toremifene: Usually dosed around 60 mgs, some dose it up to 240 mgs. Its androgenicity:estrogenicity ratio is 5x that of Nolvadex. It is prescribed to female patients for breast cancer and has shown a high affinity for bonding to the Estrogen receptors in the breast tissue. Male patients treated with toremifene citrate 80 mg compared to placebo demonstrated statistically significant increases in bone mineral density in the lumbar spine, hip, and femur skeletal sites. It decreased the risk by up to 50%. Toremifene citrate 80 mg treatment compared to placebo also resulted in a decrease in total cholesterol, LDL, and triglycerides, and an increase in HDL. There were also statistically significant improvements in gynecomastia. This data are from an ongoing study of men receiving treatment for ADT (androgen depravation therapy). These men are receiving ADT for advanced prostate cancer. ADT removes much of the testosterone and estrogen in the body which helps the prostatic cancer cells grow. So these men were suffering from side effects from reduced estrogen and testosterone in the body. Some studies have even suggested that Torm doesn't regulate progesterone receptors and we may see in the future the possibility of using it with 19-nors.

Some possible side effects include the risk of stroke, pulmonary embolism, and cataracts.

A typical PCT of Toremifene only would be similar to this:
Week 1: 120mg ED
Week 2: 90mg ED
Week 3: 60mg ED
Week 4: 30mg ED

AI's:

Arimidex: A-dex, seems to be the aromatase inhibitor of choice. Usually doesed from 0.25 - 3.0 mg it is effective even when not used every day. 0.5mgs per day can get rid of up to 50% estrogen.

Aromasin: Aromasin is usally doesed from 20-50 mgs per day. It can raise blood testosterone by 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20%! It can suppress estrogen by 65-80%. It's a third generation Aromatase Inhibitor just like A-dex and Letro, but unlike these A-dex and Letro, it is a Type I inhibitor. Whats the difference in a Type I and II inhibitor? Well, Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs.

Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs�?�both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI's.

In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis.

Now, on the other hand, competitive inhibitors, called type II AI's, reversibly bind to the active enzyme site, and one of two things can happen: 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect. The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors.

Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don�??t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin.

Letro: Letrozole is currently the most powerful aromatase inhibitor available. It has been shown to reduce estrogen levels by 98% or more. Intravenous administration of Letrozole lowered Estrogen by 46% in the young men tested, and 62% in the elderly subjects. Because estrogen is part of the negative feedback loop of the HPTA, Letrozole (and other anti-estrogens) are able to raise testosterone in male subjects. Letrozole was studied in men, and found to significantly increase LH levels to a 339 and 323% in the young and the elderly, respectively and Testosterone by 146 and 99%, respectively.

Letrozole was also able to produce a peak LH response to Gonadatropin Releasing Hormone equal to a 152 and 52% increase from baseline in either young or older men, respectively. In a similar study 0.02 mg of Letrozole increased testosterone by 45% after 2 days. That same twenty micrograms of Letrozole was also enough, in one study done on men, to reduce estrogen levels by roughly a third. Letrozole has a 2-4 day half-life, and it needs to be taken for up to 60 days to get a steady blood plasma level. Letro is best dosed from 0.125-2.5 mgs depending on the desired effect.

[JohnDoe]

Good info brothers thanks for the posts!

[Mountain-Man]

Nice I'm a nolva man myself well when I did pct

[Thaistick]

Toremifene was my favorite back when I still did PCT. The nocturnal emissions were a surprise. That and spontaneously busting a nut when I saw an attractive woman.

[macedog24]

Toremifene was my favorite back when I still did PCT. The nocturnal emissions were a surprise. That and spontaneously busting a nut when I saw an attractive woman.

Toremifene is my favorite. 2 days my balls felt like cantaloupes.
Also, i love the fact you can use it with any a.i. letro,arimidex or Aromasin. Nolva , you can not do this,I <_you shouldn't run nolva w/ letro or arimidex. It reduces their effectiveness by up to 60%

[PAiN]

Very informative thread brothers!

[maxgear]

Thanks, i will post more nice info with my bro! LOL

[Aahl]

for pct i go for clomid and low dose aromasin . Nolvedex makes feel like crap. great info btw

[Tbrotherx]

I'd rather just use aromasin/raloxifene tbh . Nolvadex reduces igf which is not good.

[Trenagade]

Awesome thread!!! I having been researching clomid. I need to get my sperm levels up. I'm slightly shut down. Starting HCG next 1000ius a week for 3 months. Hopefully that will get me back to normal so my wife and I can have our last child.

[old fart]

Nice info...

[HoRRorT]

Great info brothers!!

[Hatebreed]

Ive only ever used clomid post cycle. never tried it as estrogen contoll. But I can say I do as a rule of thumb run novaldex 20mg daily throught any cycle with test or aromatiseable gear.

[Skinnyblack]

Thanks for sharing the info brother. Some really great info here.

[Xraytek]

Thanks for the info

[Apple]

Thanks for your post.

[11B410thMTN]

Thanks for post


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