Post Cycle Therapy

I don't see a compelling reason not to run a SERM to at least ensure restart @ t he pituitary.
I do tend to think a lot of PCT protocols are far too heavy and ig nore a lot of secondary hormonal aspects. Concerns about SERM toxicity tend to b e overblown (by companies trying to tell you not to take them, conveniently igno ring the 40x difference in glucoronidation rates between rats and humans, which is what processes the carcinogenic 4-OH intermediate metabolites), though I stil l don't think tamoxifen is a particularly good idea. I'll just say it in the interest of harm reduction - the most important part of PCT is preventing testicular LH receptor expression degradation in the first pla ce by using physiological amounts of hcg any time while your system has supraphy siological levels of androgens. This has myriad positive effects, and provides a base of testosterone from which the body is free to convert to appropriate leve ls of estrogen and DHT. This prevents many of the issues associated with oral on ly runs - namely, estrogen rebound induced gyno. Additionally, any substances that may increase prolactin need to be mitigated wi th a dopamine agonist to avoid expressing androgen receptors at the pituitary an d causing a harder shut down on the pituitary side of the axis. Once androgen le vels are below baseline in recovery, taking something to raise PRL (fenugreek, D AA) actually speeds recovery time, due to the delta being seen more strongly @ t he pituitary/hypothalamus side. This is similar to the method of action of SERMs , since SERMS block the action of sex hormones @ the pituitary and hypothalamus without strongly activating them. The exception being clomiphene which has 2 isomers, enclomiphene and zuclomiphen e - because this has a mixed pro-estrogenic and anti-estrogenic action (differin g at the pituitary and hypothalamus in fact), it tends to spur restarts more str ongly because it does NOT as rapidly increase testosterone levels as toremifene or tamoxifen. However, it allows the fundamental machinery to become more respon sive to sex hormones and LH in comparison with the other SERMs. All SERMs lower IGF-1, which harms gains retention, although raloxifene and tore mifene show the least impact. Raloxifene has a high affinity for the breast rece ptor and not much else, and isn't a good candidate for PCT. Toremifene has very low breast affinity, and so it should not be used without being in concert with an aromatase inhibitor. Remember, there is no good way to keep all the gains from the use of anything su praphysiological (paging bb6kid), and if you're planning on maintaining any semb lance of general health, you need to have a brief period of low sex hormone to r estart the brain's side of the endocrine equation.
-Do you believe a SERM is always necessitated -Me, Coop, Neuron and Andy spoke about this on Get Ripped I have no idea who those people are I don't see a good reason to ever not run a SERM, given that recovery times from a hormonal standpoint with them have been shown time and again to be normal wit hin 1-2 months, instead of 4-6 for more minimalistic protocols (if baseline func tionality is ever recovered). I think in most cases barring shutdown at the test icular level a person would recover from exogenous androgen use in much longer t ime period. A SERM that didn't lower IGF-1 at all would be ideal. That's honestly the worst aspect of them. I kind of wonder if something like Daidzein would counteract it.
-Basically, from milder runs, DAA/AI post cycle and HCG intra would be sufficien t. I don't know enough about the stimulatory action of DAA on the anterior pituitar y to comment. I don't see a point in increasing the risk of not recovering. If t hey're increasing AI dosage anyway, IGF-1 production will be suppressed regardle ss by the decrease in estrogen.
-Josh (Illa) ran a cycle with Nolva than a cycle with DAA/AI/HCG and his recover y time was just as fast. Mind you both were mild cycles That doesn't surprise me, but I still wouldnt trust this to be the case for ever yone's biochemistry and all cycles. The fact that you only get to fuck up ONCE w ithout large consequences makes me say that anyone bothering should go with what 's proven. Subjectively I would expect a PCT without SERMs to retain more gains. However, i f you're blocking the sensing of androgens at the pituitary, you can simply run a SARM to combat that. Can't say that of a SERM-less PCT IMO ANd yes I'm going to delete all this shit, so don't worry about it

Post Cycle Therapy

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I don't see a compelling reason not to run a SERM to at least ensure restart @ t he pituitary.

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