FYI
I posted some of the inquiries from this list to the autism list and here are
some of the replies:

Jackie,

I believe the link between the PST problem and the effect on the
neurotransmitters mentioned in your quote is in the effect of
cholecystokinin on those same neurotransmitters.  Serotonin and
cholecystokinin are mutually regulated and their receptors show up together,
but CCK only works right when sulfated.  PST doesn't work right either if it
is missing sulfate.

I'll amen the comment on vomiting.  My headaches immediately get better if I
vomit, but I'm not always that nauseated.  This probably also is a CCK
thing. The feeling is that nothing in your stomach is working at digesting
food...it just sits like a lump.  If CCK is sulfated and working properly,
then it will cause the pancreas and the gall bladder to release their
food-digesting goodies.  At times of low sulfation, such as probably occurs
twice a month in women when their estrogen is low (estrogen is sulfated,
too, and is known to regulate CCK), you would expect that digestion would be
poor, and that that could account for that "lump in the tummy" feel.  I've
also found that at times when I'm getting sick and headachey, I also tend to
get an unhappy tummy.

There are feedback mechanisms to the brain from the gut which regulate CCK,
but a study I read said that they traced radiolabelled sulfated CCK which
was introduced into circulation (via I.V., intranasally, or in the
peritoneum), and it showed up in places like the liver, kidney and
intestines, but it never showed up in the brain, where CCK also is found.(1)
Other studies talk about the involvement of the vagal nerve in carrying a
signal to the brain, and that may in turn help regulate brain CCK. One study
noticed that an effect of CCK was totally reversed by removing a vagal
nerve.(2) This probably offers some explanation for why brain (CNS)
serotonin and circulating serotonin can have opposite levels in autism,
which also might have to do with the different proportions of the two CCK
receptor types in the two regions.

Someone else also said:

>
>> I would be *very* interested to learn whether the PST enzyme is
>> itself sensitive to changes on the insulin/glucagon axis.
>> If so, this would be another *major* confirmation of the Ancient
>> Wisdom of paleodiet.

CCK is very involved with insulin because of its role of encouraging the
pancreas to release its stuff, and insulin levels in diabetic rats actually
change the expression of CCK receptors(3).  In fact, in diabetics, CCK's
usual effects in the heart are "diminished or abolished".  Somehow this also
involves the interaction of CCK with the alpha and beta-adrenergic systems
(the domain of the familiar beta-blocker)(4,5).  These interactions may
explain why diabetics have increased risk of heart attack.

Susan

1.  Curry SH; McCarthy D; Morris CF; Simpson-Heren L.  (1995) Whole body
autoradiography of CCK-8 in rats.  Regulatory Peptides, 55:2, pp. 179-88.

2.  Koyama S; Fujita T; Shibamato T; Matsuda Y; Uematsu H; JOnes RO. (1990)
Contribution of baroreceptor reflexes to blood pressure and sympathetic
responses to cholecystokinin and vasoactive intestinal peptide in
anesthetized dogs.  European Journal of Pharmacology, 175:3, pp. 245-51.

3.  Otsuki M; Williams JA.  (1983)  Direct modulation of pancreatic CCK
receptors and enzyme secretion by insulin in isolated pancreatic acini from
diabetic rats.  Diabetes, 32:3, pp. 241-6.

4.  Wisniewska RJ; Wisniewski K.  (1996)  Cholecystokinin (CCK) and
C-terminal fragments of CCK: effects of CCK-33, CCK-8 and CCK-4 in the
cardiovascular system of diabetic rats.  General Pharmacology, 27:2, pp.
399-405.

5.  Fiedorowicz RJ; Wisniewski K.  (1989)  Effects of cholecystokinin
(CCK-33) and its fragments, C-terminal octapeptide (CCK-8) and C-terminal
tetrapeptide (CCK-4) on the circulatory system of diabetic rats.  (Polish
Journal of Pharmacology and Pharmacy, 41:6, pp. 561-72.