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E2, Estradiol, Estrogen, Prolactin, Progesterone

Ivanhoe

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Is there a link or thread or someone kind enough to explain (without saying this has been posted, well I realize that everything I could ever need is on google however im looking for time saving here)

What the differences are, how aromatization works with the various estrogen isomers (im in the know for test into dht/androgen etc)

Is a SERM specifically targeting breast tissue, or all estrogen receptors in the body?

is an AI going to fuckup blood pressure/ LDL even with exogenous supraphys test levels concurrently?

Appreciate the help in advance.
Ive heard way too many contradictory things about this topic and Im starting to get a bit outraged(tren? Lol)
 

Old RhynoS

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Use the search bar. You're asking for quite a bit of info.
Serms block the receptor, AI kill the enzyme. Some serms prefer the breast tissue, some act systemically in the adipose.
AIS act on different pathways than test and can be harsh on your system, how they may effect you specifically no one knows.
Test can/will skew your lipid profile.
If you want research papers you will have to do your research.
 

Ivanhoe

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Use the search bar. You're asking for quite a bit of info.
Serms block the receptor, AI kill the enzyme. Some serms prefer the breast tissue, some act systemically in the adipose.
AIS act on different pathways than test and can be harsh on your system, how they may effect you specifically no one knows.
Test can/will skew your lipid profile.
If you want research papers you will have to do your research.
Thanks for the assistance. In terms of the test vs est ratio, i was thinking is it more a matter of balance between the two for lipid/cardiovascular sides or is it more related to total T and E independent of one another.

Ive got my miners hat on, digging for the motherlode
 

Old RhynoS

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Thanks for the assistance. In terms of the test vs est ratio, i was thinking is it more a matter of balance between the two for lipid/cardiovascular sides or is it more related to total T and E independent of one another.

Ive got my miners hat on, digging for the motherlode
I've not seen any studies relating to T and E and their effects on lipids as a they relate to eachother but you can have elevated lipids on a test cycle and still have E in range. Of course this can change drastically from cycle to cycle and person to person. That's why blood work is key.
 

Ivanhoe

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BigBen

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Serms, such as tamoxifen (nolvadex) and clomid, have both antagonistic and agonistic properties, depending on the particular tissue. Since men don't have a uterus, we can for the most part consider nolvadex a pure antagonist, in the tissue it does bind to. But that isn't all estrogen receptor sites. It's very complicated, and its best to just go the to practical applications for which these drugs are used.
 

Ivanhoe

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Serms, such as tamoxifen (nolvadex) and clomid, have both antagonistic and agonistic properties, depending on the particular tissue. Since men don't have a uterus, we can for the most part consider nolvadex a pure antagonist, in the tissue it does bind to. But that isn't all estrogen receptor sites. It's very complicated, and its best to just go the to practical applications for which these drugs are used.
thanks!!
 

Axon

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I have been spending hours reviewing the literature on PCT drugs, mainly Tamoxifen, Clomiphene and HCG. Below are some exerts from some of the studies.

Tamoxifen
  • Tamoxifen/Nolvadex is known to have a dual mechanism of action and affects estrogen receptors throughout the body, including those in the cardiovascular system and in bones. Its primary MOA is to compete with 17β-estradiol (E2) at the receptor site in breast tissue and to block the promotional role of E2 (Estradiol (E2) in males is produced from testosterone by aromatization) (Yu & Bender, 2001).
  • Most long terms studies (6-12months+) find the drug safe for use in men and women with most studies using a daily dose of 10-20mg ED/EOD.
    • Five RCTs have investigated the effect of tamoxifen on men with infertility, and the ages of the participants ranged between 18 and 44 years old (unspecified in two studies). These men (n = 321) were treated daily with 20 or 30 mg tamoxifen for 3–6 months. Three studies reported minimal or no side effects (AinMelk et al., 1987; Maier & Hienert, 1990; Cakan et al., 2009).
  • One study found 20 mg of tamoxifen daily effectively blocked the breast estrogen receptors and stimulated HPG axis recovery (Rahnema et al., 2014).
Clomid
  • "The HPG axis in males includes the hypothalamus, the anterior pituitary gland, and the testicles. Gonadotropin-releasing hormone (GnRH) is produced from the hypothalamus, which stimulates the production of LH and FSH in the anterior pituitary gland. LH and FSH released from the anterior pituitary promote the production of testosterone and spermatogenesis. Testosterone is then converted to estradiol by the aromatase enzyme. Estradiol in the normal physiological state exhibits part of the negative feedback mechanism on the reproductive axis by binding to the hypothalamus, which inhibits the continuous release of GnRH. Clomiphene (CC) competes with estradiol at the hypothalamic receptor level, specifically located on the anterior hypothalamus and hypophysis, which blocks the negative feedback mechanism and results in increased GnRH. Unlike testosterone, both compounds do not suppress the HPG axis, but actually lead to an increase in LH and FSH, which results in an increased production of intratesticular testosterone by the Leydig cells and the promotion of spermatogenesis (Herzog et al., 2020)".

Clomid Safety
  • Side effect reports include headache, dizziness, gynecomastia, and exacerbation of psychiatric illnesses. Despite these reports, CC is generally considered to be safe and well-tolerated (Wheeler et al., 2019).
  • Treatment has been associated with few adverse events. The most common adverse events reported are hot flushes and visual disturbances (Asch and Greenblatt, 1976; Adashi, 1996). Hot flushes occur in ~10% of patients (Jones and De Moraes-Ruehsen, 1965). Visual disturbances occur in <2% of patients (Asch and Greenblatt, 1976); while generally reversible, a few reports have suggested that the problem may be permanent (Purvin, 1995). (Goldstein et Al., 2000).
  • Taylor and Levine (2010) investigated the long-term safety and efficacy of CC versus testosterone gel and noted that CC did not significantly increase cholesterol, PSA, or hemoglobin.
  • Chandrapal et al. (2016) reported no effect of CC on PSA and hematocrit in their study of 77 patients on CC. (G1: 50mg ED, G2: 50mg EOD).

An old but interesting study by Vermeulen & Comhaire (1978) looking at Nolva vs Clomid
  • They looked at the hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
  • Results
    • Tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid).
    • Tamoxifen, 20 mg/day for 10 days saw a statistically significant increase in LH levels after 3 days of treatment, a plateau at 150% ± 20% (mean ± standard deviation) basal levels being reached after 6 days of treatment.
    • After Clomid treatment (50mg, 3x a day for 10 days), LHRH stimulation resulted in LH values constantly lower than before treatment, whereas FSH levels were constantly higher. Compared to treatment with tamoxifen, where levels of LH and FSH after LHRH stimulation were constantly higher than before treatment.
    • In comparison with clomiphene, tamoxifen has a much weaker intrinsic estrogenic activity, which in males might have a deleterious effect

I hope some of this info helped... My advice would be to find research databases like PubMed, Sciencedirect and Medline and search the individual drug itself. Most articles will include a brief mechanism of action, its interactions with other drugs and the overall effect it had on participants, both good and bad.
 

Ivanhoe

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I have been spending hours reviewing the literature on PCT drugs, mainly Tamoxifen, Clomiphene and HCG. Below are some exerts from some of the studies.

Tamoxifen
  • Tamoxifen/Nolvadex is known to have a dual mechanism of action and affects estrogen receptors throughout the body, including those in the cardiovascular system and in bones. Its primary MOA is to compete with 17β-estradiol (E2) at the receptor site in breast tissue and to block the promotional role of E2 (Estradiol (E2) in males is produced from testosterone by aromatization) (Yu & Bender, 2001).
  • Most long terms studies (6-12months+) find the drug safe for use in men and women with most studies using a daily dose of 10-20mg ED/EOD.
    • Five RCTs have investigated the effect of tamoxifen on men with infertility, and the ages of the participants ranged between 18 and 44 years old (unspecified in two studies). These men (n = 321) were treated daily with 20 or 30 mg tamoxifen for 3–6 months. Three studies reported minimal or no side effects (AinMelk et al., 1987; Maier & Hienert, 1990; Cakan et al., 2009).
  • One study found 20 mg of tamoxifen daily effectively blocked the breast estrogen receptors and stimulated HPG axis recovery (Rahnema et al., 2014).
Clomid
  • "The HPG axis in males includes the hypothalamus, the anterior pituitary gland, and the testicles. Gonadotropin-releasing hormone (GnRH) is produced from the hypothalamus, which stimulates the production of LH and FSH in the anterior pituitary gland. LH and FSH released from the anterior pituitary promote the production of testosterone and spermatogenesis. Testosterone is then converted to estradiol by the aromatase enzyme. Estradiol in the normal physiological state exhibits part of the negative feedback mechanism on the reproductive axis by binding to the hypothalamus, which inhibits the continuous release of GnRH. Clomiphene (CC) competes with estradiol at the hypothalamic receptor level, specifically located on the anterior hypothalamus and hypophysis, which blocks the negative feedback mechanism and results in increased GnRH. Unlike testosterone, both compounds do not suppress the HPG axis, but actually lead to an increase in LH and FSH, which results in an increased production of intratesticular testosterone by the Leydig cells and the promotion of spermatogenesis (Herzog et al., 2020)".

Clomid Safety
  • Side effect reports include headache, dizziness, gynecomastia, and exacerbation of psychiatric illnesses. Despite these reports, CC is generally considered to be safe and well-tolerated (Wheeler et al., 2019).
  • Treatment has been associated with few adverse events. The most common adverse events reported are hot flushes and visual disturbances (Asch and Greenblatt, 1976; Adashi, 1996). Hot flushes occur in ~10% of patients (Jones and De Moraes-Ruehsen, 1965). Visual disturbances occur in <2% of patients (Asch and Greenblatt, 1976); while generally reversible, a few reports have suggested that the problem may be permanent (Purvin, 1995). (Goldstein et Al., 2000).
  • Taylor and Levine (2010) investigated the long-term safety and efficacy of CC versus testosterone gel and noted that CC did not significantly increase cholesterol, PSA, or hemoglobin.
  • Chandrapal et al. (2016) reported no effect of CC on PSA and hematocrit in their study of 77 patients on CC. (G1: 50mg ED, G2: 50mg EOD).

An old but interesting study by Vermeulen & Comhaire (1978) looking at Nolva vs Clomid
  • They looked at the hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
  • Results
    • Tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid).
    • Tamoxifen, 20 mg/day for 10 days saw a statistically significant increase in LH levels after 3 days of treatment, a plateau at 150% ± 20% (mean ± standard deviation) basal levels being reached after 6 days of treatment.
    • After Clomid treatment (50mg, 3x a day for 10 days), LHRH stimulation resulted in LH values constantly lower than before treatment, whereas FSH levels were constantly higher. Compared to treatment with tamoxifen, where levels of LH and FSH after LHRH stimulation were constantly higher than before treatment.
    • In comparison with clomiphene, tamoxifen has a much weaker intrinsic estrogenic activity, which in males might have a deleterious effect

I hope some of this info helped... My advice would be to find research databases like PubMed, Sciencedirect and Medline and search the individual drug itself. Most articles will include a brief mechanism of action, its interactions with other drugs and the overall effect it had on participants, both good and bad.
This is a great pct summary with comparisons which are superb! Thanks a lot.

couple more questions I have, does high estrogen,estrodiol,progesteron all have positive muscle building effects, and can I assume water retention as a key indicator of dosing AI or AEs?
 
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