A trend I’ve noticed is that the majority of members have abnormally elevated SHBG levels. For me this is the crux of the situation, as the only test results showing healthy free testosterone levels have been from members with no sexual side-effects.
Conventional theory behind high SHBG is that it’s an regulatory response to excessive estrogen. An attempt to limit aromatisation of testosterone by suppressing free testosterone.
I think there are other factors involved. There’s no evidence to support higher levels of estrogen in PFS suffers. Most of the tests on here are within the normal range, some slightly high but not enough to oppose testosterone and cause dysfunction. Instead, because it has a higher affinity to testosterone, SHBG amplifies the estrogenic effects rather than being driven by it.
Clinically, estrogen receptor antagonists (Tamoxifen, Clomid) stimulate SHBG. While estrogen receptor agonists (Tibolone) cause a downregulation in SHBG, freeing up testosterone. Other drugs have also been proven to stimulate SHBG. Anti-epileptic drugs in males and contraception in females. This happens at a hepatic (liver) level, but I’ve found no explanation as to how.
Males with premature balding have typically more free testosterone, so there’s nothing to support a genetic predisposition for higher SHBG levels either. Given that DHT steroids suppress SHBG, is it unreasonable to suggestion dht deprivation would cause this state? Perhaps long-exposure to exogenous DHT is needed to reset SHBG at a lower level, but it would need to be achieved without use of a SERM post-cycle for reasons described above. Maybe this is why AndroHard has yielded recoveries, as it provides the androgens without requiring a traditional PCT.