kineticz
Member
tara said:kineticz said:'Refined sugar favors conversion of tryptophan to serotonin causing a relative dopamine deficiency and acetylcholine deficiency, which causes disturbances in movement and memory'
I just read this page. It looks as though he attributes to estrogen insufficiency some symptoms thant Peat seems to attribute to estrogen excess and/or progesterone deficiency (eg menopausal hot flashes). Since this is Peat's area of particular expertise, I'm inclined to go on Peat's model so far.
He refers to refined sugars a few times on that page. I didn't read further about his approach, but I'm guessing the point about refined sugar for him would be the lack of sufficient accompanying micronutrients, eg potassium, magnesium, B-vitamins, to aid in its efficient metabolism? I think Peat is also keen on supplying adequate micronutrients, though he does seem to think it can be done alongside some limited refined sucrose, when better sugar sources are not available.
I guess excessive refined sugars without adequate B-vitamins, potassium, magnesium etc could be expected to cause some problems.
In my honest experience, having estrogen, especially E2, below 10, is not desirable. It is making my recovery problematic because I am prone to excessive cortisol downregulating my testosterone production. Low E2 is also not good for liver enzymes.
For some people such as myself, low E2 can make recovery very difficult, since it maximises adrenaline, reduces the dopamine conversion to norephiprene (hence lowers ACTH - ACTH is a key signal for pregnenolone), and causes dry skin and hair. Peat says estrogen limits mitochondria respiration, but in my view that is desirable at least in the short term as you don't want excess mitochondria with low energy input and low thyroid. It just seems to increase prolactin and therefore cortisol directly independent of ACTH. He also says that estrogen promotes glycolysis - I thought this was desirable over lipolysis.
This is why I was hesitant at first to join the forum and accept Peat's views. He is anti-ACTH and anti-E2, but I am low in both and this has maximised my free fatty acids, and dug a great big hole for myself. In his studies and claims, he presents an adamant view that ACTH and estrogen are the bad guys, but he neglects to point out that:
a) for many people, having normal estrogen is actually key to fixing their issues at it regulates the free form of thyroid hormone and does promote better neurotransmitter management than having low ACTH, low pregnenolone and low estrogen.
b) While thyroid regulates all hormonal cascades, it does not do this equally. And having high LH and low ACTH is NOT desirable, but can happen when you lower E2 too much and the gonads are upregulated, diverting cholesterol away from the adrenals and making adrenal mitochondria suffocated by fatty acids in their attempt to maintain function in deficient pregnenolone. Low E2 can and does in my case increase LH. High LH when you are hypothyroid and your adrenals are smothered in fatty acids is a very BAD situation.
c) Prolactin in hypothyroidism, can be high even with low estrogen, due to catabolism and serotonins/prolactin's independent stimulation of cortisol. He says ACTH does this, but I don't believe this, as ACTH stimulates pregnenolone and should not be minimised. Excess thyroid and adrenal signals that cannot keep up will not be resolved purely by taking pregnenolone. It can actually increase fatty acids.
d) Cortisol is required for T3 to work.
Adrenals are always most important before the gonads and even the thyroid. Estrogen's stimulation of norephiprene allows the adrenals to strengthen whilst estrogen binding thyroid and adrenaline allows pregnenolone to recoup.
My prolonged pregnenolone use and aromatase blockers sent me near suicidal.
All I'm saying is, in the link I posted above, the theory of estrogen deficiency and progesterone excess, as shown by my blood results, is spot on.
Progesterone will attenuate the cortisol pathway and reduce the DHEA pathway in hypothyroidism, whereas a relatively higher estrogen will promote neurotransmitters, promote DHEA if resources allow, and slow down your thyroid while you work on your nutrients etc. Adding thyroid to relatively high progesterone when ACTH is already at full stretch and pregnenolone is low is not wise. E2, to a large extent, prevents this risk.