Running a SERM+SARM Cycle - decreases suppression?

This might be a controversial topic, and one that doesn’t make much sense on the outset, but after seeing a couple of blood logs of folks running a SERM during cycle I decided to take a look at it: my starting hypothesis is that the rise in LH that SERMs provide (or by another mechanism) will help counter the decline in testosterone, and thus suppression will not be an issue. I think this is worth proving or disproving one way or another. Let me also lead with a disclaimer - I'm taking a big leap here, making speculation that I hope to prove or disprove. It's quite possible that my logic or science is bad as a result of dealing with the unknown. As always, I welcome your input and critique.

First, some definitions

Follicle-stimulating hormone (FSH) is a glycoprotein gonadotropin secreted by the anterior pituitary in response to gonadotropin-releasing hormone (GnRH) released by the hypothalamus. The pituitary gland also secretes luteinizing hormone (LH), another gonadotropin… FSH and LH bind to receptors in the testis and ovary and regulate gonadal function by promoting sex steroid production and gametogenesis.

In men, LH stimulates testosterone production from the interstitial cells of the testes (Leydig cells). FSH stimulates testicular growth and enhances the production of an androgen-binding protein... This androgen-binding protein causes high local concentrations of testosterone near the sperm.

Basically, FSH and LH are both gonadotropins. Both help kick off the production of testosterone, FSH a little more indirectly than LH.

We often state that SARMs have no impact on LH and FSH. That’s not strictly true because, well, they do. It would be more correct to say that SARMS have no significant impact, but an impact is surely there. As evidence, I submit the Ostarine pre and post bloods from 2011, where LH fell by about 20%, depending on the dose. It’s not significant, especially when compared to steroids where LH will become undetectable. Such a relatively small change might even be considered within a margin of error, if it didn't come up repeatedly in SARM studies. When writing the ‘Ostarine, or Kegels In A Bottle’ article, I noticed this and filed it away for later as a clue to follow up later on this same subject.

As exhibit 2 of evidence, I present a 2004 and 2005 study on S4 which found that LH and FSH were suppressed in rats at 3mg/kg/day.

Assuming I have convinced you of the LH and FSH suppressing ability of SARMs, limited as it may be, let’s look at the role of a SERM. Quick level set on what a SERM is:

Compounds that modulate estradiol levels in these clinical conditions are referred to as selective estrogen receptor modulators (SERMs)... In a certain subset of infertile men, particularly those with hypogonadism, or those who have a low serum testosterone to estradiol ratio, there is some evidence suggesting that SERMs... can reverse the low serum testosterone levels or the testosterone to estradiol imbalance and occasionally improve any associated infertile or subfertile state.

A SERMs role is to increase luteinizing hormone (LH) and follicle-stimulating hormone (FSH) that will increase testosterone when coming from a suppressed state:

(SERMs) work as estrogen antagonists at the level of the pituitary gland and thus stimulate the release of luteinizing hormone and follicle-stimulating hormone, which in turn drive both the steroidogenic and spermatogenic functions of the testes.

How SARMs lower testosterone while LH & FSH are still at detectable levels (albeit slightly lower) is at this point unknown. But by using a SERM, LH & FSH are preserved and thus testosterone should be higher. Or something else is going on. And it might just work: 1. /u/NatureFreakLS experienced an INCREASE in testosterone on his SARM + Clomid cycle. 2. /u/gargalese decreased suppression while on SARM + Torem cycle.

There are a ton of gaps in this hypothesis. If this were a journal article, it’s where I would say ‘further study is necessary’, and it’s absolutely true. For example, are all SERM’s equal? Can /u/NatureFreakLS results be replicated or is it just a freak (couldn’t resist) accident?

Don’t let anyone confuse this with PCT. PCT, in my mind, is still unnecessary (see here for more details), partly because of the 14 day half-life of tamoxifen (as an example) and the 4 weeks necessary to achieve steady blood levels… at which point most users have already discontinued their therapy. If you’re going to use a SERM, what I am arguing here is that it might be done alongside the compound, or preferably not at all. SERMs have side effects. Some can be very unpleasant, like temporarily losing the ability to get Mr. Happy to respond to direct stimulation.

So, with that said, I’d like to gather more data here from the PEDsR and PEDs member base. Folks that are reading this, if you’re willing to run a SERM + SARM cycle, get pre and post bloods and tell me about your cycle details, I’d like to get a larger sample size than the n=2 that I have right now, and either prove or disprove this hypothesis.