Maybe the graph below helps you to understand the problem of both, salivary and serum morning cortisol for the detection of adrenal insufficiency.
The two populations (black AI ruled out; blue AI confirmed) simply can’t be separated by means of a static test such as the morning cortisol test (also not for other time points as the discriminative power is even lower). At t=0 (morning test before ACTH administration) about half of the population of subjects with AI ruled out overlaps with half of the population with confirmed AI. This problem is completely independently of the question whether cortisol can be accurately quantified or not.
Only at t=90 after ACTH the populations are sufficiently separated increasing sensitivity and specificity of the test.
The only conclusion which can be drawn from a morning salivary cortisol test is to rule AI out at a certain level (= high negative predictive value).
You are all in denial. It is a fact that exogenous AAS/ Testosterone use causes inhibition of both the HPTA and Adrenal (cortisol/DHEA-S) production.
I am having a good laugh at your claim of >99% of men on TRT don’t have a decrease in DHEA-S. It is guaranteed to decrease both cortisol and DHEA-S. The only question is the degree of the decreases for each. Again, MOST men that initiate TRT do so without first addressing other underlying health factors that start them off at a disadvantage and susceptible to poor adrenal status.
Cortisol synthesis and release is actually increased under TRT.
Circulating serum levels of DHEA and DHEAS are almost exclusively synthesized in the adrenals. There is no evidence that both hormones are reduced upon administration of exogeneous T.
Johann, you are wrong; Cortisol decreases on TRT.
However, ACTH does increase in response to the decreased cortisol levels.
"…the effect of testosterone in young men is to inhibit rather than augment the cortisol response to CRH stimulation. …recent data suggesting that testosterone suppresses stimulated cortisol secretion through its metabolite 3 β- androstanediol, which acts through ER β in the PVN, but not through ER alpha or the androgen receptor. The surprising finding in our study of increased ACTH during testosterone replacement, however, localizes the suppressive effects on cortisol to the periphery. A possible explanation for reduced stimulated cortisol in the face of increased ACTH is decreased adrenal sensitivity.In conclusion, we have shown that testosterone regulates CRH-stimulated HPA axis activity in men. Similar to findings in animal studies, CRH-stimulated cortisol was decreased during testosterone-replaced compared with hypogonadal conditions. The concomitant increase in ACTH suggests that the decrease in stimulated cortisol levels by testosterone or its metabolites is mediated at the level of the adrenal gland.
I am trying very hard to help this forum/community. Now, please stop arguing this issue with me. You are impeding the health of others that need to understand the impact of TRT on their adrenal status. Thank you.
It seems more like you can’t prove the things you’re saying to me. I am 100% sure you’re trying to help, but saying something is so doesn’t make it so. Post studies, research, something to prove your positions.
The study (Rubiniw et al, 2005) you are referencing used a CRH stimulation test to measure the responsiveness of the adrenals after 2 to 3 weeks of leuprolide shutdown of the HPTA +/- T substitution treatment in 10 young men.
The results demonstrated that, neither basal levels of cortisol nor urinary free cortisol levels differed between the groups.
Upon CRH stimulation cortisol levels were indeed reduced by about 10% in the T treatment group. The difference reached statistical significance, however given the very small sample size (total of 10 men, 5 in the placebo group and 5 in the T group) and the standard errors i would be very cautions in the interpretation of this finding.
While the study appears to be in agreement with rodent studies it is in disagreement with 2 more recent human studies and 1 study in rhesus monkeys.
Muniyappa et al, 2010 found no difference between 35 men assigned to two groups (T treated and non treated) in cortisol concentrations, diurnal rythm or any other related markers after 26 weeks of treatment. Noteworthy, the study was conducted in elderly men which would be significantly more susceptible to downregulation of the adrenals ‘productivity’ if there was any.
Knight et al 2017 studied the cortisol response to a social stressful situation in 120 men assigned to a T treatment group and a non T group. They found about 10% higher cortisol level post stress in the T group compared to the placebo group (Figure below).
@TRT_Phoenix - how about posting in the TRT Credentials thread so those you are trying to help have a little background about the person giving advice?
The general concensus here is don’t use the ai at all and only use hcg when trying to be fertile.
Is that 100mgX2 weekly for 200mg total, you gotta start somewhere, and that’s as good a place as any. Perhaps a bit on the higher side. If you wanted to be more conservative 75mgx2/week would be ok, but if it’d been me I’d probably just do the 200mg, but that’s just how I roll.
