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There are a lot of theories circulating the community when it comes to SARM cycles, especially regarding PCT, SERMs ,Aromatase Inhibitors (AI’s), and what is necessary vs. unnecessary in regards to them.
There are theories as to why you should or shouldn’t PCT after a SARM cycle, and realistically nobody is correct or incorrect.
Basically, when you finish a cycle of suppressive compounds, your hormonal profile is left in a vulnerable state where you are extremely catabolic (prone to muscle loss and fat gain), and your physiological functions are likely impaired to a degree relative to your level of suppression (erection quality, mood, recovery rate, fatigue level, etc.).
This does not happen, for example, if you use the SARM + SERM protocol on a cycle.
The longer your body is left in a state with suppressed/shutdown Testosterone, the more time your body has to essentially deteriorate, and the longer you have to experience the crappy side effects that can occur from having abysmally low levels of Testosterone.
The point of PCT is to get your hormones back to normal much faster than your body would normally be capable of on its’ own.
SERMs vs Aromatase Inhibitors
The misunderstanding that SERMs, such as Tamoxifen Citrate (Nolvadex) and Clomifene (Clomid), serve to lower estrogen levels must first be addressed before delving into any further details.
Selective Estrogen receptor modulators (SERMs) belong to broader class of drugs known as anti-estrogens. The other subcategory of drug under the anti-estrogens category is known as aromatase inhibitors (AIs), such as Aromasin (Exemestane) and Arimidex (Anastrozole), Letrozole, Arimistane. AIs and SERMs make up anti-estrogens. Aromatase inhibitors differ greatly from SERMs in their action and how they deal with the issues of estrogen control.
SERMs serve to block the action of Estrogen at the receptor sites in breast tissue by occupying the receptor sites in place of Estrogen so that Estrogen itself cannot exert its effects there through receptor site binding. Conversely, SERMs will also act as Estrogens at receptor sites at other cells in other areas of the body (the liver, for example in Tamoxifen’s case). SERMs do not lower circulating levels of Estrogen in blood plasma. Aromatase inhibitors serve to do this by eliminating the production of Estrogen through binding to and disabling the aromatase enzyme, which is the enzyme responsible for the conversion (or aromatization) of androgens into Estrogen.
Post Cycle Therapy (PCT) On A SARM Cycle
SARMs are non-steroidal and do not convert into Estrogen.
However, you will still hear once and a while of a rare case of some guy getting gyno flareup while on a SARM only cycle, or a variety of other high Estrogen side effects.
This means they will suppress your natural testosterone levels.
To what extent they will do this is dependent on which compound you are using, the dose, the length of your cycle, and your individual propensity to suppression.
While some individuals could likely get away with no PCT at all and recover just fine, this is absolutely not the case for some others, and it would be far safer for everyone to just do a proper PCT regimen after any cycle.
The most common being Tamoxifen Citrate (Nolvadex), and Clomifene (Clomid).
Tamoxifen (Nolvadex) is specifically a non-steroidal SERM.
Tamoxifen might block the effect of Estrogen at the cellular level in certain tissues, it can enhance Estrogenic effects in other areas of the body. These can be positive effects as well as negative effects. Tamoxifen exhibits Estrogenic effects in the liver, for example, which for all intents and purposes is a positive effect, as its effects here result in a positive change in cholesterol profiles (something desired by many). The area of concern with Tamoxifen is particularly in breast tissue, where it serves to act as an anti-Estrogen in this area (and a very strong one at that).
Tamoxifen possesses other very desirable effect, such as its ability to increase circulating levels of endogenous gonadotropins Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH), and through this, increasing the endogenous production of Testosterone
In layman’s terms, Tamoxifen essentially acts as a ‘fake’ Estrogen that acts as a placeholder at the receptor sites in breast tissue. As a result, Estrogen cannot activate gene transcription in the cells there in order to formulate gynecomastia, and any existing Estrogen that has already bound to receptor sites will essentially be ‘forced’ out of the receptor sites by Tamoxifen which then occupies the receptor site instead.
The other primarily utilized purpose for Tamoxifen among bodybuilders and athletes is its ability to stimulate and increase the male production of endogenous Testosterone, as evidenced by many studies. It does so by acting on the pituitary and hypothalamus gland in the brain, and signaling an increase in production of FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone), which then signal the testes to produce Testosterone.
In this case, Tamoxifen is usually administered during PCT, which is immediately after SARMs cycle.
In this application of administration, 10 – 20mg per day of Tamoxifen per day for approximately 2 – 4 weeks. Studies have demonstrated that venturing higher than 20 – 40mg per day does not generate any significantly greater amount of Testosterone production.
The quickest and smoothest recovery will always be guaranteed by using the traditional PCT SERMs (Selective Estrogen Receptor Modulators) as opposed to over the counter products that are marketed as equivalent recovery agents, or turnkey all in one PCT products.
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