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Estrogen, Progesterone, And Aldosterone


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http://jp.physoc.org/content/589/4/975.full

Progesterone enhances adrenergic control of skin blood flow in women with high but not low orthostatic tolerance

This article put a lot of pieces of my puzzle together for me.

For those that haven't read it yet ------keep in mind that men also have progesterone and it's important for things such as healthy bones amongest other things in the body. I've often questioned the balance in men with POTS with testerone and estrogen ----when maybe it may be the balance between estrogen and progesterone.

This made sense with me in the fact that I had a complete hysterectomy. I was NOT able to use progesterone as it would GIVE me hot flashes and make me an emotional mess. I didn't do real well with additional estrogen of E1 or E2 ---but I do fine with E3 which is the milder estriol form. Because of having endometriosis - they figured out that estrogen triggers the growth of the tissues that attach to places in the abdomen and causes bleeding of them during menses. They also have discovered that endometriosis is connected to mast cell disorders. Interesting that this study shows an increase in prostanoids with progesterone administration and it also increases COX which causes vasoconstriction. I have been saying forever that I'm overly constricted and need more NO that will help with vasodilation. This study shows there is a connection between NO and COX and the effects of vasodilation/vasoconstriction. Interestingly enough, mast cells release prostaglandins and this is one thing that we try to suppress with mast cell treatment. (Although, some with MCAS find that blocking COX-1 with aspirin and creating a slow degranulation with aspirin - helps them. This will cause a slower degranulation and then you don't have a "dumping" situation with a mast cell release. From what I've read all NSAIDS will cause a mast cell degranulation. I personally, can not take the aspirin.)

This explains so much for me ---the need to vasodilate and have more NO. Hormones not agreeing with me despite having a complete hysterectomy and replacement not being helpful ---except for estriol which is a mild estrogen. (And this I can't use often or I get an estrogen excess problem.) And it even may explain why with me having high NE, this would explain why supplementation with PE made my symptoms worse. It increase NE ---and I need less of that not more.

Amazing how things start to fall into place after awhile.

Thanks for the link Rama!

Issie

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When i had my infertillety testing i know i was low in some stuff. But not sure what. I had my adsterol and renin levels taken two years ago. They where both very low. The doctors had no explanations for it.

I am very sure that hormones have a bigg part of my problems. Cos my pots symtoms, and a lot of the others goes Whit the sycle.

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The mechanism of increased venous tone has been
clearly associated with an enhanced generation of
prostaglandin F2 in human veins, by the group
of Berti in Milano [21]. Aescin, at concentrations
of 103 M or lower resulted in a clear increase of
contractility in human isolated saphenous veins. This
activity was lost after exposure to indomethacin, with
complete recovery of aescin’s activity 120 min after
removal of the anti-inflammatory agent. Assay of the
prostaglandin like material released by the saphenous
vein during incubation in the presence of aescin, clearly
established the presence of prostaglandin like material,
later identified as PGF2 [21] (Fig. 3). Increased PGF2
depends either on the activation of phospholipases or
of other acylhydrolases, and from stimulation of -keto
reductase, the enzyme converting PGE2 to PGF2 present
in many tissues and particularly in veins.The mechanism of increased venous tone has been
clearly associated with an enhanced generation of
prostaglandin F2 in human veins, by the group
of Berti in Milano [21]. Aescin, at concentrations
of 103 M or lower resulted in a clear increase of
contractility in human isolated saphenous veins. This
activity was lost after exposure to indomethacin, with
complete recovery of aescin’s activity 120 min after
removal of the anti-inflammatory agent. Assay of the
prostaglandin like material released by the saphenous
vein during incubation in the presence of aescin, clearly
established the presence of prostaglandin like material,
later identified as PGF2 [21] (Fig. 3). Increased PGF2
depends either on the activation of phospholipases or
of other acylhydrolases, and from stimulation of -keto
reductase, the enzyme converting PGE2 to PGF2 present
in many tissues and particularly in veins.

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um, so indomethacin is anti inflammatory. prostaglandin F2 stops production of progesterone??? are you saying that pots and anti-inflam's conflict? that mcad isn't related? I don't get it

I know Angela ---I asked him about this earlier and I still am not sure what he's getting at here. I'm sure it's something good --but, my brain isn't computing it. Rama!!! Can you explain your line of thinking here?

Issie

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