Thankyou Mary Kate…

Increased Fasting Insulin
Increased Insulin Resistance
Increased Testosterone
Increased Androstenedione
Increased LH
Increased LH/FSH ratio
Increased LH pulse frequency
Increased TNF-alpha
Increased DHEAS
Increased C-Reactive Protein
Increased Homocysteine
Increased Prolactin
Increased blood sugar
Increased Triglycerides
Increased MMP-2 and MMP-9
Increased Granulosa Cell VEGF
Increased 5 alpha-reductase activity
Increased Estrone (E1)
Increased Estrone/Estradiol (E1/E2) ratio
Increased ACTH
Increased Plasminogen Activator Inhibitor type 1 (PAI-1)
Increased Nuclear transcription factor kappa beta (NF-KappaB) activation
Increased insulin receptor serine phosphorylation
Increased melatonin production
Increased aldosterone
Increased serum neopterin levels
Increased Interleukin-6
Increased Interleukin-18
Increased Anti-mullerian hormone

Decreased Glutathione
Decreased SHBG levels
Decreased Antioxidant status
Decreased D-Chiro-Inositol
Decreased Magnesium
Decreased FSH
Decreased Hypothalamic sensitivity
Decreased Ghrelin
Decreased GnRH pulse generator sensitivity to inhibition by estradiol and progesterone
Decreased progesterone in early luteal phase
Decreased GH (other studies say GH is increased)
Decreased insulin receptor tyrosine phosphorylation
Decreased nitric oxide production

Lipolytic Catecholamine Resistance

Possible Adrenal insufficiency
Possible insufficient central beta-endorphin inhibition
Possible increased Progesterone
Possible increased LDL Cholesterol
Possible decreased HDL Cholesterol

There is conflicting evidence for some of the features listed above. Everyone will have different features and symptoms. Many women will not have high blood sugar, for example. That may come in later stages after insulin resistance takes its toll.

As one study put it: “Polycystic ovary syndrome describes a conformational ovarian state that may be the final common manifestation of several pathogenic pathways.”

These features share many features in common with diabetes and hyperinsulinemia.