I've been doing research on homocysteine -- high levels of this are associated with PCOS, along with heart disease, IBS, birth defects and depression.
It seems to me that homocysteine may explain why some PCOS cysters have too much hair, some too little, and some have both problems.
Here's where I got most of my information -- I'm not a doctor, and this is just my guess at what this might mean -- feel free to point out if I've misunderstood something:
http://www.homocysteine.net/pages/ho.../abouthcy.html
So basically, when everything works right, when you digest food, your body turns it into the correct chemicals, and your brain and your tummy are happy, and you get the benefit of what you've eaten. When things go wrong, you get high homocysteine levels and lots of trouble.
So, the body has basically three different ways of converting homocysteine into what your body needs:
1 - Using B12 and folic acid, your stomach "remethylates" homocysteine into the SAM that makes your body happy;
1a - a subset of this, your body uses betaine in your liver and kidney tissues to remethylate the homocysteine;
2 - The remaining homocysteine is converted in the trans-sulphuration pathway to cysteine in two reactions requiring vitamin B6 as a co-factor. Cysteine is a precursor to glutathione, the major cellular redox buffer.
SO, maybe we PCOS chicks divide down in which way our body CAN'T process the homocysteine --
-- where something is wrong in the trans-sulpheration pathway, our bodies don't get sulphur somehow, and lack of sulphur is known to cause hairloss.
-- where something is wrong with the body's use of B12 or folic acid or stomach acids, the remethylation process goes awry, and hormones get messed up, and hair growth in the wrong place occurs.
--where both pathways are messed up, we get both sets of symptoms.
That middle one I can speak to from experience -- when I radically increased folic acid supplementation, my hirsutism lessened substantially, which makes me think that high homocysteine levels caused it, since lowering those levels helped it.
If you look at the main link at homocysteine.net, it talks about how 10-20% of the population has a "variation of the gene for enzymes involved in the homocysteine metabolism" which "results in decreased enzyme activity and causes moderately increased tHcy. The impact on tHcy is, however, dependent on folate status and tHcy can generally be normalised by increased folate intake."
I also relate to this, as I've always had the strangest stomach in the world -- it'd make sense that I've got a problem with stomach enzymes.
I'm continuing to do research on this, but I thought I'd post this much to see if the brilliant cysters here have any thoughts on whether this might be a feasible explanation of what's up.