Tamoxifen, Clomid, Toremifene and Rolaxifene. Which for what?

[elfin1mf]

both bolded items led me to think you said tamo increased igf,

This is interesting about protein binding, can you tell me more? Do other serms increase the protein binding?

I'd just like to clear a few things up...

Below are some facts regarding Tamoxifen , Clomid, Toremifene and Rolaxifene:


- Tamoxifen is NOT weak at restoring the HPTA, post cycle. Its as effective, perhaps more, than Clomid.

- Tamoxifen alone will restore HPTA function in around 6 weeks (sometimes less) at 20mg/ED. Thats what the data states. I'm not sure AAS user's should be using 40mg/ED of Tamoxifen. Thats a large dose for males IMHO. A smaller dose of 20mg/ED should be used for more lengthy peroids, rather than larger doses for shorter durations. There is also no evidence that states 40mg/ED is BETTER than 20mg/ED for HPTA restoration.

- Clomid is made up of 2 isomers:

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 peroids 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.


Few facts...

- 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. As shown in this study.

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

- When Clomid and Tamoxifen where compared in this study. 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.


So what about Toremifene and Rolaxifene...

In a recent study done on Tamox, Tore and Rolax comparing HPTA restoration. Tamoxifen can out on top. In 8 weeks, 20mg/ED of Tamoxifen increased LH from 4.54 to 7.73 and Test from 496.59 to 835.06. After two months, 60mg/day of Toremifene increased LH from 4.05 to 5.05 and Test from 496.59 to 709.79.

The Tore dose is low IMHO though. I've used far more. 120mg/ED for 7-14 days. Followed by 100mg/ED, then down to 60mg/ED over 3-4 weeks.

- Tore will increase pituitary sensitivity to GnRH, as Tamoxifen did. As discussed above.

- Rolax is fairly weak at restoring the HPTA. Its best used for treating gyno (Evista) and has the highest affinity for breast tissue out of the current SERMs. So it has its uses.

There is limited clinical data on both Tore and Rolax, but Tore increases lipid values more potently than most other SERMs and increases bone mineral density very well.

So what are your thoughts Swifto?

I dont think it matters what SERM(s) you choose for PCT. But go with either Clomid, Tore or Tamox. Using 2 would be a better choice IMHO. The data states Tamoxifen is better than Clomid in a head to head comparison. The data also states Tamoxifen is better than Toremifene and Rolaxifene in head to head comparisons...But take the doses into account.

The backbone of my PCT is Tore + Tamox 20mg/ED or Clomid 25mg/ED.

For gyno Rolax should be your first choice. Then Tamox and Tore. Clomid isnt the mose effective at fighting gyno.

All SERMs seem to increase IGF, imporve lipids and bone mineral density.

2nd Gen SERMs (Tore, Rolax) are safer than 1st Gen (Clomid, Tamox).

I hope this has shed more of a light in SERMs, their actions, uses and decide for youself what you use which for...

Sorry for making you feel uncomfortable, I was just hoping you had some info I could never find. I honestly spent months trying to read studies about serms and have found not too much to make me feel any better using clomid over tamo, so I just use tamo to avoid the clomid sides.