Very interesting. Got any references for this?
Well let me begin with saying that how can estrogen cause all these wonderful problems. Excessive estrogen increases lipid perioxadtion which is similar to that of alcohol. Excessive lipid perioxation will cause excessive ROS to be formed. All large amounts of ROS will cause the enzyme Methione synathse to be reduced and so there for production of methionne will be reduced since it can not be recycled from homocysteine and therefore Sam-e Levels drop and what sam-e is made gets divered to the CBS pathways and excessive bile is produced. Now we begin to have a build up of viole bile acid in the liver which complicates the situationeven more by spraying the walls of the intestines with bile acids causing severe inflamation. With excessive estrogen causing hypomethlation this results in a neurological deficiency the methylb-12 and folininc acid which it is highly docoumneted that people with folic acid and b-12 deficeincy are more prone to cancer. With lower production of Sam-e (undermethylation) the liver to fatty liver as well as diabetes, atherosclrosis, lack of hormonal binding to the receptors (still trying to find concrete eveidence of this, but strong theory need more info to back it up). Excessive estrogen causes hypomethylation due to the fact that process of methylation is what inactivates estrogen and over time this eventually drains the supply of methyl donors (sam-e, creatin, choiline, TMG) resulting in undermethylation and there for estrogen domaince. People with dybiosis of the bowel will have impaired estrogen metabilism due to the fact of lack of good bacteria in the intestinal tract. One function of intestinal bacteria is help to congugate estrogen to its not cacingagenic form. So there for possible in theory that people have normal estrodial levels and have dybiosis may not be able to metabolise the estrogen properly and end up with a higher percentage 16 alpha hydroxy estrone to 2 hydroxy estrone resulting in having hidden estrogen imbalnaces and never even knowing it.
To theory of estrogen inducing mitoconhriol dyfunction would be
1. increase lipid perioxiation depletes antioxident reserves
2. increase free radicals and oxidative stress shift homocystein pathways resulting in diversion to CBS vs b12/folate pathways resulting in fatty liver die to low sam-e production this fatty liver this will bog down the thyroid due to insufficent glycogen metabolism will be altered and conversion fron t4 to t3 would be reduced. With out t3, t2 can not be produced which is highly specified to fuel mitochondrion metabolism
3. to make this more complicated it is noted that women using estrogen need to be aware that it can cause a b-5 deficeincy which can alter mitocondrioal function to the fact that b-5 is the precursor to coenzyme A which is the first enterance into the kreb cycle. i am still resarching this and will take time to get concrete evidence to back my theories. Stil trying to find data on how intestinal flora can alter estrogen metabolism would be nice
Hypomethylation of DNA in estrogen-induced and -dependent hamster kidney tumors -- Lu et al. 9 (6): 925 -- Carcinogenesis
http://jncimono.oxfordjournals.org/cgi/content/full/
2000/27/113
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