I use a dry dilution method. It's not highly precise, but I think it's adequate. I use maltodextrin as the diluent. Corn starch would work too. In particular, I might empty the contents of 12 50 mg capsules into a tablespoon and then top it off to level with the maltodextrin. Mix thoroughly and it is ready to go. There are small measuring spoon sets that go from 1/64 tsp to 1/4 tsp by factors of two. I use the 1/16 tsp spoon to get a nominal dose of 12.5 mg.
Yep, that's going to be difficult. Did you order it or did a doctor prescribed that amount?
A pill cutter.
A pill cutter would be a good idea if there were pills. Capsule cutters might be a better idea but they'd create a mess and I don't think they exist.
Yes, the doctor prescribed that amount. I don't think he put much thought into it. We didn't really talk about dosages at my appointment. I just was curious to try it. I looked at everyone's dosages after the fact and saw most people take 12.5 mg.
Most healthcare providers these days, appointments are rushed, care now is triage in an overburdened healthcare system.
Same with me, I have 12.5mg at home because I was going to do a re-start to get my wife pregnant but she ended up getting pregnant anyways on TRT+HCG. I've been curious to see what taking 12.5mg of Clomid on top of my TRT regiment would be.
GnRH is negatively regulated at the hypothalamus by androgens and estrogens. The latter are most likely stronger.
Because estrogens are a significant source of negative feedback at the hypothalamus, (en)clomiphene is an effective stimulant of GnRH signaling. It's only under TRT that the negative feedback of long-lasting androgens commonly overrides the stimulatory capacity of SERMs.
I'm thinking about trialing enclomiphene soon; what I generally see from online user reports is that people have low testosterone levels overall (backed by bloods), then hop on (en)clomiphene, and they tend to report higher total testosterone after weeks of trial,
It is actually heightened sensitivity to estradiol at the pituitary or hypothalamus that can produce secondary hypogonadism. The SERM dulls this sensitivity by antagonizing the receptors. That is, the feedback is negative, so when reduced it yields a positive effect, a significant increase in LH.
Even if such upregulation occurs, the effect is clearly swamped by the SERM. That is, at typical doses, concentrations of the SERMs are more than enough to antagonize some additional estrogen receptors.
Ok, main rationale for switching is I've been on a 300mg sublingual DHEA daily regimen for about five months as a hormonal optimization plan.
ok, however upon enclomiphene discontinuation, lower pituitary LH signaling (from pituitary higher ER e2 sensitivity from the SERM), would possibly lead to lower LH intratesticular conversion amount to testosterone, therefore ending up with less serum e2 to go around overall to bind to e2 receptors in the brain, which might then be compensated by the higher brain ERs sensitivity from the upregulation consecutive to the antagonist actions from enclomiphene on those receptors (I read about enclomiphene at least affecting ER receptors at pituitary and hypothalamus, don't know exactly what other brain ERs should enclomiphene be binding to).
You have concocted quite an elaborate narrative here. In practice, when people stop enclomiphene, their levels quickly revert back to their original baseline. Any receptor sensitivity changes that may have been caused by enclomiphene do not endure.
