I don't get it.

from: http://www.craigsams.com/pages/tobac.html:
WHAT ARE ACETYLCHOLINESTERASE INHIBITORS?


• The chemical that transmits nerve impulses from one nerve ending to the next is acetylcholine - once it has transmitted a nerve impulse it has done its job and is no longer needed so it is broken down by an enzyme called acetylcholinesterase and recycled.

• Solanine (or tomatine from tomatoes) slows the production of this acetylcholinesterase, so acetylcholine isn't broken down as fast as it's being produced.

• Acetylcholine builds up causing a 'traffic jam' of stimulation at the receptor nerve endings.

• The nerve endings become overstimulated

• This overstimulation can lead to muscle weakness, muscle twitching, hypertension, increased intestinal contractions and increased secretions of tear, sweat, saliva, gastric and intestinal glands.

• All nightshade foods contain solanine, a strong acetylcholinesterase inhibitor.
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Yet, studies done regarding dementia are using acetylcholinesterase inhibitors because with dementia (and Down Syndrome) there isn't enough acetylcholine in the brain.
 
So does Kaiden have an adequate supply of acetylcholine, and the nightshades were inhibiting acetylcholinesterase, thereby causing a buildup of acetylcholine in his brain?  Or did he not have enough acetylcholine . . . which doesn't really make sense because then you would think a bigger supply of acetylcholinesterase inhibitors would help - as with the dementia studies.  Yet we all know what happens: Kaiden + nightshades = seizures and impaired cognitive function.  Not that he isn't still delayed developmentally . . . but the astounding progress he has made since being nightshade free would make one think that he didn't have enough acetylcholinesterase, and too much choline.  But when I began giving him choline supplements, he didn't get worse, he developed further.
 
There is so much to this, I wonder if I'll ever figure this whole thing out.