As of lately, there has been a lot of debate and a rise in the suggested use of AI's in PCT. So I want to shed a little light on the subject in layman's terms so that everyone can understand and make the choice that most appropriately fits their needs. Its hard to read these scientific journals and understand without a good background in science itself. My goal is to put the info out there as it is and let the debates begin!!!!!
First lets define each:
SERM- Selective Estrogen Receptor Modulator- are a class of compounds that act on the estrogen receptor. A characteristic that distinguishes these substances from pure receptor agonists and antagonists is that their action is different in various tissues, thereby granting the possibility to selectively inhibit or stimulate estrogen-like action in various tissues. Clomid and Nolvadex are examples of these.
Mode of Action for SERM
Estrogenic compounds span a spectrum of activity ranging from:
1) Full agonists (agonistic in all tissues) such as the natural endogenous hormone estrogen
2) Mixed agonists/antagonistics (agonistic in some tissues while antagonist in others) such as tamoxifen (a SERM)
3) Pure antagonists (antagonistic in all tissues) such as fulvestrant (ICI-182780).
The mechanism of mixed agonism/antagonism may differ depending on the chemical structure of the SERM, but, for at least for some SERMs, it appears to be related to (1) the ratio of co-activator to co-repressor proteins in different cell types and (2) the conformation of the estrogen receptor induced by drug binding, which in turn determines how strongly the drug/receptor complex recruits co-activators (resulting in an agonist response) relative to co-repressors (resulting in antagonism). For example, the prototypical SERM tamoxifen acts as an antagonist in breast and conversely an agonist in uterus. The concentration of steroid receptor co-activator 1 (SRC-1; NCOA1) is higher in uterus than in breast, therefore SERMs such as tamoxifen are more agonistic in uterus than in breast. In contrast, raloxifene behaves as an antagonist in both tissues. It appears that raloxifene more strongly recruits co-repressor proteins and consequently is still an antagonist in the uterus despite the higher concentration of co-activators relative to co-repressors.
AI- Aromatase inhibitors- are a class of drugs used in the treatment of breast cancer and ovarian cancer in postmenopausal women. AIs may also be used off-label to treat or prevent gynaecomastia in men. Aromatase is the enzyme which synthesizes estrogen. As breast and ovarian cancers require estrogen to grow, AIs are taken to either block the production of estrogen or block the action of estrogen on receptors. Arimidex and Aromasin are examples of these.
Mode of Action for AI
Aromatase inhibitors work by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens by a process called aromatization. As breast tissue is stimulated by estrogens, decreasing their production is a way of suppressing recurrence of the breast tumor tissue. The main source of estrogen is the ovaries in premenopausal women, while in post-menopausal women most of the body's estrogen is produced in peripheral tissues (outside the CNS), and also a few CNS sites in various regions within the brain. Estrogen is produced and acts locally in these tissues, but any circulating estrogen, which exerts systemic estrogenic effects in men and women, is the result of estrogen escaping local metabolism and spreading to the circulatory system.
WOW! Now what does this mean? The historical use of the SERM was to treat breast cancer in woman and as studies went on their was a group of non responders so the need for another medicine to treat was needed. That how AI’s came into the picture.
The pathophysiology is they do the same thing in reducing conversion of estrogen but they travel different neuro paths to do it and the AI’s bind stronger to receptor significantly reducing the estrogen, more so, over the SERM’s which bind a little weaker and allow a little more conversion.
I think it's based on the individual’s history with a PCTs and how his body rebounds with estrogen whether it is necessary or not. Blood work without the AI involved with the PCT will give you a reliable baseline to compare to by adding AI to your next PCT and doing blood work and making a reliable comparison because the numbers don’t lie in the labs. I plan to do this very exact thing that I have wrote about for my own personal experience so that I may speak with more authority on the subject with concrete evidence. Although, at this moment the studies back the claims of it being beneficial to the PCT. Now that I have given u the information. I hoped I helped you in better understanding this. Let’s have some fun and start the great debate….