Crisler recommended transdermal over oral because it skips the first pass of the liver, which is responsible for much of the pregnenolone -> progesterone conversion; transdermal skips the first pass, seemingly increasing preg sulfate and the androgens more than prog and the progestins. Regardless, Crisler demonized prog purely on the basis that it's 'femininizing', which whilst true in excess, does not mean that men don't need optimal levels, nor does it mean maintaining levels within the physiological range for a healthy male will produce feminization. What dose of oral pregnenolone did you take? Some theorize that non-extended release forms can cause issues due to the sudden spike / drop from it's short half-life, so perhaps you could try a brand like nutricology. There are studies that show doses above 10mg can increase progesterone disportionately to the androgens, which may have been your issue. Conversely, there are many people on trt who see no increase at all in progesterone from preg (this was the case for me, presumably from HPTA-induced downregulation of specific enzymes in the steroid hormone cascade), or who find that pregnenolone supplementation produces side effects that are not repeated by taking progesterone directly, so your reaction could have just been something specific to the preg.
As far as how I plan to go about increasing cortisol: it'll probably be with some combination of preg, prog and dhea with thyroid. The ability of the adrenals to produce cortisol is thyroid-dependant, as T3 is required to drive cholesterol -> pregnenolone conversion in the mitochondria - and thus the production of all downstream steroids - which is why chronic, unaddressed hypothyroidism will usually lead to low cortisol, prog, dhea, testosterone, etc. Paradoxically, thyroid hormone requires the presence of the adrenal hormones to exert its own action, so trying to restore either one without the other is often unsuccessful. The key distinction here is that we're trying to restore the bodies ability to produce its own hormone, but taking hydrocortisone does the exact opposite by suppressing CRH/ACTH, and by-proxy, further inhibiting the body's own production of cortisol, preg, prog, dhea and their associated metabolites. Pregnenolone can serve as substrate upstream for cortisol without causing suppression to the HPA, but it also has many of its own actions independent of the conversion to cortisol that aid the body in supporting the increased thyroid function required to restore adrenal steroidogenesis.
In my view, the elevated prolactin is secondary to hypothyroidism and the associated increase in estrogen / serotonin it produces (thyroid function determines the rate at which estrogen is glucuronidated and subsequently excreted), so addressing it directly isn't something I'll be pursuing. I don't take trt anymore, but when I did, an aromatase inhibitor would reduce my prolactin as expected. However, this never produced the improvements in symptomatology that I'd have hoped, and I believe this is because the underlying physiological state that leads to one being prone to an excess of aromatization is more problematic than the absolute amount of estrogen, which is merely the manifestation, and not the problem itself. I don't deny that aromatase inhibitors do help some people, but very rarely are they the difference between feeling like shit and feeling 100% — which is expected, given the aforementioned. Aromatase inhibitors also have many issues of their own, some of which that go beyond solely the inhibition of aromatase.
I could be wrong, but addressing anything other than thyroid function (and also trying to identify the exact reason why thyroid function is impaired along with taking supplemental thyroid) is not addressing the real issue.
