NEW RESEARCH: Researchers working with mice have just discovered a possible new cause of PCOS. Read about it on the News & Research tab here: http://mypcos.info/1/news-research/elevated-oestrogen-in-utero/
Polycystic Ovarian Syndrome is really a misnomer. The development of cysts on the ovaries is actually only a symptom of the disease, rather than being a cause. Current research indicates that the root cause of PCOS is actually Insulin Resistance (IR).
Insulin Resistance
Ordinarily, when a person ingests carbohydrates, they are broken down in the intestines by various enzymes into sugars which are then absorbed into the bloodstream. This triggers the pancreas to secrete insulin, which acts like a key to unlock the doorway for the sugar to enter the cells and provide energy.
Sometimes, as in PCOS, the cells become resistant to the insulin and the body needs to produce much higher than usual levels of insulin before the cells notice that there is sugar to be taken up.
When there is excess insulin in the blood stream it causes the theca cells in the ovaries to produce testosterone without any other communications to tell it to stop.
In women with PCOS, this cellular resistance to insulin may be due to a deficiency of a metabolite of one of the B-group vitamins, inositol, specifically called d-chiro inositol.
DCI is involved in the insulin signalling pathway through it’s attachment to a phosphoglycan where it then attaches to the outside of the cell, awaiting an enzyme which is produced when insulin binds to it’s receptor on the cell. This enzyme cleaves the bond between the cell and both d-chiro inositol phosphoglycans or DCI-IPGs and myoinositol phosphoglycans or MYO-IPGs so that they can enter the cells where they communicate chemically with the cell, telling it to perform various functions.
DCI-IPG tells the cell to burn or store the sugar for energy. MYO-IPG tells the theca cells in the ovaries to produce testosterone. When DCI-IPG is missing from this loop there is no way to tell the ovaries to stop producing testosterone, as insulin levels tend to remain high, continuously freeing MYO-IPG.
