Serms

Keep in mind all 3 serms will work in favour of your liver (Agonists) since they are mild estrogens, like said earlier estrogen is good for your liver so adding a serm will always improve your hdl/ldl. All serms don?t lower estrogen in fact they will increase your total estrogen. They also block your estro in the nipple area, but similar to the binding AI?s once that estro gets released you rebound and you end up with even higher estro than before


Nolvadex/Tamoxifene

Agonist: Liver, uterus (female)
Antagonist: Breast/nipple

As I am sure you heard nolvadex reduces IGF-1 leves by 25% now that might seem like the biggest disadvantage ever but if you take into account that your liver is going to be healthier while you use it, it balances out the deduction of your igf-1 levels.

Nolvadex is more suited for pct purposes not on cycle therapy (oct) since it increases natural test levels by 60% and decreases igf-1 levels

Dosage on cycle: 20-40mg


Raloxifene/Evista

Agonist: Liver, bone (increases bone density like deca and is a recognised treatment for osteoporosis)
Antagonist: Breast/nipple (stronger than nolva for gyno)

Raloxifene doesn?t affect igf-1 levels whatsoever, also it increases bone density but does nothing for your tendons like deca does, so it might be a double edge sword if you are not using deca along side it since by having stronger bones and muscles chance for tendon injury is higher.

Raloxifene is the ideal AI for oct since its an agonist for your bones, doesn?t affect igf-1 levels and is perfectly safe to run with a 19nor. Raloxifene shouldn?t be used in pct since it raises natural test levels by 40% only, 20% less than nolvadex

Dosage on cycle: 60mg-120mg

Nolva vs Raloxifene for HGH/IGF-1

Objective: The aim was to compare the impact of raloxifene and tamoxifen on GH-IGF-I and gonadal axes in healthy men.

Design: We conducted a randomized, open-label crossover study.

Patients and Intervention: Ten healthy men were randomized to 2-wk sequential treatment with tamoxifen (10 and 20 mg/d) and raloxifene (60 and 120 mg/d), with a 2-wk intervening washout period.

Main Outcome Measures: We measured the GH response to arginine and circulating levels of IGF-I, LH, FSH, testosterone, and SHBG.

Results: Tamoxifen, but not raloxifene, significantly reduced IGF-I levels by 25 ? 6% (P < 0.01) and increased SHBG levels by 20 ? 7% (P < 0.05) at the higher therapeutic dose. There was a nonstatistically significant trend toward a reduction in the GH response to arginine with both SERMs. Both drugs significantly increased LH, FSH, and testosterone concentrations. The mean increase in testosterone (40 vs. 25%; P < 0.05) and LH (70 vs. 30%; P < 0.01) was significantly greater with tamoxifen than with raloxifene treatment.

Conclusions: Tamoxifen, but not raloxifene, reduces IGF-I levels. Both SERMs stimulate the gonadal axis, with tamoxifen imparting a greater effect. We conclude that in therapeutic doses, raloxifene perturbs the GH and gonadal axes to a lesser degree than tamoxifen.

Nolva vs Raloxifene for gyno

OBJECTIVES: To assess the efficacy of the anti-estrogens tamoxifen and raloxifen in the medical management of persistent pubertal gynecomastia. STUDY DESIGN: Retrospective chart review of 38 consecutive patients with persistent pubertal gynecomastia who presented to a pediatric endocrinology clinic. Patients received reassurance alone or a 3- to 9-month course of an estrogen receptor modifier (tamoxifen or raloxifene).
RESULTS: Mean (SD) age of treated subjects was 14.6 (1.5) years with gynecomastia duration of 28.3 (16.4) months. Mean reduction in breast nodule diameter was 2.1 cm (95% CI 1.7, 2.7, P <.0001) after treatment with tamoxifen and 2.5 cm (95% CI 1.7, 3.3, P <.0001) with raloxifene. Some improvement was seen in 86% of patients receiving tamoxifen and in 91% receiving raloxifene, but a greater proportion had a significant decrease (>50%) with raloxifene (86%) than tamoxifen (41%). No side effects were seen in any patients.
CONCLUSION: Inhibition of estrogen receptor action in the breast appears to be safe and effective in reducing persistent pubertal gynecomastia, with a better response to raloxifene than to tamoxifen. Further study is required to determine that this is truly a treatment effect.

Clomid

Agonist: Liver
Antagonist: Brest/nipple

Clomid is a really harsh drug it should be avoided at all costs, if you get the visual sides/blurry vision from clomid they stay for life! They are rare but do happen

Clomid should only be used in restart protocols imo by the supervision of a doctor. So if you want to start producing sperm again you will have to take hcg along with clomid for 9-12months straight. It has some use in pct but it can be completely avoided by using serms only or ideally nolvadex + aromasin

Some good info on clomid:

?Clomiphene is a mixed agonist/antagonist. This is due o the fact that clomiphene is composed of two isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). Enclomiphene is an estradiol receptor antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood, the net antagonist effect might be due to the composition being 70% trans (enclomiphene) and 30% cis (zuclomiphene). Tamoxifen is more of a strict antiestrogen, decreases the effect of estrogen in the body, and potentiates the action of clomiphene. This combination came about after 100s of clinical experience. - Michael Scally MD

So Tamoxifen is more of an antagonist, than Clomid is. Its better at blocking the ER than Clomid is. Clomid also seems to exert agonistic effects in parts of the brain that control emotion. That would explain why some turn into women on periods during there experiences with Clomid.

Tamoxifen is also made of slightly more isomers, the cis isomer of tamoxifen (inactive one) trans-tamoxifen and trans-4-OHT isomer.

- Clomid will double LH at 100mg/ED in 5-7 days and increase FSH by 20-50%. LH rises quickly post cycle, but not that quick.

- Clomid will raise enodgenous testosterone (total) by 146% after 3 months at 25mg/ED.

- Clomid at 100mg/ED will raise endogenous testosterone (total) by 268% after 8 weeks and free testosterone by 1,410% (Thats not a typo).

-Tamoxifen increased serum testosterone to 142% of baseline in only 10 days. It took 150mg/ED of Clomid to get the same 142% increase. After 6 weeks it raised testosterone and LH levels to an average of 183% and 172% of starting values.

Another thing to note after the above study is how sensitive the pituitary become to GnRH. The more sensitive the pituitary is to GnRH, the more LH it will produce. Tamoxifen increase pituitary sensitivity to GnRH and Clomid seemed to decrease it.

- Estrogen will decrease sensitivity to GnRH. It will not increase it. If estrogen were to increase the pituitary to GnRH it calleds "estrogen priming". Priming the pituitary to become more sensitive to GnRH. This happens in females, but not males. There is no evidence to suggest there is E priming in males.

- Tamoxifen is more an an antiestrogen than Clomid is. Both are SERM's and selective with agonistic/antagonistic effects in "selective" tissues. Both will block the ER in breast tissue. Both are agonists in the liver, which would explain the increase in IGF binding proteins and decrease in plasma IGF?

Dose while on cycle: 50mg eod some say it can substitute hcg but I haven?t tried that route way to many mental sides to use it on cycle imo