kineticz
Member
haidut said:kineticz said:haidut said:kineticz said:The prolactin is caused by ACTH/Adrenal suppression. You spiked preg and/or DHEA higher than your basal metabolic rate will allow. This will make TRH and TSH rise.
Take some thyroid hormone instead for a while.
Hey kineticz, sorry for posting this to this thread but I could not find your other post that I was looking for. Didn't you say that DHEA suppresss the HPA axis? What do you think of this study?
http://www.ncbi.nlm.nih.gov/pubmed/17928160
That confirms what I have been saying, that in the conditions of hypothyroidism, excess adrenal steroids will spike your preg, dhea, cortisol, resulting in net adrenal suppression.
If I am reading this study right it says that the adrenal steroids like DHEA will spike ACTH and cortisol. How is that "adrenal suppression"? Am I missing something?
I do agree that DHEA and pregnenolone can make matters worse for hypothyroid people but I suspect that it would be due to this stimulation of ACTH and cortisol, not due to suppressing ACTH/cortisol. Also DHEA and maybe pregnenoloone can convert into estrogen and for hypo people that would be bad b/c estrogen directly suppresses the thyroid and induces fatty acid oxidation, which is bad in Peat-land.
In what capacity do you think estrogen can be good in such situation? I saw you said that with high estrogen you felt better and low estrogen made you tired and depressed, so I am wondering what mechanism you think is at play.
Thanks in advance.
In hypothyroidism, and in advanced stages of cortisol deficiency, norephiprene stimulates the adrenals via ACTH. My view is that it is much preferable to have norephiprene stimulate ACTH than to have serotonin and catabolism stimulate ACTH, because norephiprene activates all systems ready to absorb preg in small doses, and serotonin and catabolism will just result in excess free floating adrenal hormones that downregulate multiple metabolic pathways. Excess cortisol resulting from the addition of a spike in adrenal hormones and increased cortisol shown in the study will downregulate this protective norephiprene mechanism (cortisol has a negative feedback mechanism on norephiprene), leading to lower metabolic rate and increased fatty acid suffocation of the adrenal mitochondria, which results in depersonalisation as I have experienced.
Norephiprene as we know is a TRH and ACTH potentiator, which extracts deficient energy from the adrenal mitochondria which has the effect of minimising the risk of fatty acid and serotonin suffocation of the adrenal intake of LDL to form steroids. Due to norephiprene downregulation via excess adrenal hormones in hypothyroidism, serotonin will increase as a ratio of the stimulatory neurotransmitters, further exacerbating the issue of mitochondrial respiration.
The study also doesn't mention the thyroid or metabolic state of the test subjects. In a normal person, pregnenolone sparing will occur leading to increased DHEA, preg-s, and cortisol, which are all beneficial IF your cellular metabolic capacity is efficient and respiring clearly enough, since DHEA makes the sex hormones for gender vitality, and T3 requires sufficient cortisol aside from cortisol's many functions such as anti-inflammation.
My theory on the use of E2 to protect pregnenolone and therefore avoid depression and increased adrenaline is here:
viewtopic.php?f=3&t=6177&p=74169#p74401
In blood tests, my TSH would go down when my E2 went up, indicating a positive correlation between E2 and effective thyroid.
I have recently boosted estrogen using pueraria mirifica and licorice. My personality and zest for life are showing new signs I've never felt before.
In hypothyroidism, Peat shows that E2 raises ACTH. Other studies show E2 protects ACTH from responsiveness to stress, resulting in increased pregnenolone storage in the mitochondria, despite using fatty acids for this purpose. I am sure Peat also says E2 increases glycolysis somewhere, so not just lipolysis. So this combination of stimulating ACTH but modulating pregnenolone exhaustion and prolonging neurotransmitter synapse residue via MAO-I, I believe is crucial to my recovery.
So my theory is that E2, while not metabolically optimum or efficient, can have a protective role in adrenal mitochondria, because it helps to keep the ball in the adrenal's court, and through it's slowing of active thyroid hormone will reduce or slow the need for fatty acid liberation. Excess fatty acid liberation is the crux of aging and stress in the modern day.