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From:
Bill Elkus <[log in to unmask]>
Date:
Thu, 22 Jun 1995 14:40:44 EDT
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<<Disclaimer:  Verify this information before applying it to your situation.>>

A guest post from Kalle Reichelt, MD, PhD (in reply to the recent posts on
this topic)

Hi.
I would like to draw your attention to a wee paper from us (1) on diet and
schizophrenia ,where we followed completely blind 10 semichronic (not the
best starting point) male schizophrenics for 1 year. We could conlcude :

a) That both urinary peptide excretion and rating scales (Comprehensive
Pyschopathological rating scale and Whitaker Index of schizophrenic
thinking) as well as clinical state improved slowly on diet, with regression
in those off.  This was a crossover study.

b) It is not unreasonable that changes will be slow because the kidneys are
efficient peptide, aminoacid and protein preserving organs.

c) The trophic changes in brain in schizophrenia  established
macroscopically and microscopically in a great many publications the last
10 years, would take time to correct if at all possible. Probably not
completely being maturational defects to some extent ( 2).There is also the
problem of an optimal timing for maturation of nerve cells as demonstrated
in the visual cortex. This means that experiments on chronic cases is a poor
way to test the hypothesis. Fairly fresh cases would be ideal.

We have recently been able to demonstrate the presence of at least 5 (five)
peptides with opioid activity in urines and dialysis fluid from
schizophrenics that react to antibodies against bovine casomorphin 1-8.One
of these cochromatogrpahs and has the same amino acid composition as bovine
casomorphin 1-8.(Reichelt submitted ; as in autists (3)).The very fulminant
psychosis seen in post-partum psychosis seems to be mediated by human
casomoprhin (4) and demonstrates that such peptides do have access to the
Central nervous system (CNS).
Furthermore IgA antibodies against gliadin .beta-lactoglobulin and casein
are increased in male schizophrenics (5)indicating a connection.NB: The
biopsies were normal so that this is not coeliac disease, but a state with
increased transmucosal protein/peptide transport. After all uptake in small
amounts of intact protein and peptides is well documented (see earlier
communications)
WE think therefore that it is important to be gluten/gliadin free and
milkprotein free if diet is to be used.The more so because gliadinomorphin
and casomorphin are very similar and gliadinomorphin is part of the coeliac
disease peptide B3142(6)
Gliadinomorphin : Y-P-Q-P-Q-P-F
Casomorphin(b)    Y-P-F-P-G-P-I etc.
There are a series og gluten derived opioids too. This is one of the
reasons why we remove both protein sources in autistic syndromes too
(2,7,8)with  again long term but clearly measureable effects and regression
in all who quit diet.
The paper that was read to Dohan  has been changed to : Can schizophrenia be
reasonably explained by Dohan s hypothesis on genetic interaction with a
dietary peptide overload? . It is hard ot get this published because it goes
against the present trends. However, I think it extremely important so I
keep trying ( I am of course rather partial to the hypothesis which makes
it difficult).
I find it remarkable that given the complete lack of aetiology directed
treatment that  a proper clinical trial should be so difficult to
establish.After all also an American has published data along these lines (9)
using our old urine screening assay.Our new technique based on Shattocks
groups work in the UK but changed a little( Reichelt in prep) is of course
available to anyone who is interested.It is fast and with fewer false
positives.They are also wellcome here to learn by doing.
Finally it should be stressed that opiods do have maturation inhibitory
effects in rat brain (10),which would fit Crows(2) data quite nicely .
References
1: Reichelt KL et al (1990) The effect of a gluten free diet on
glycoprotein associated urinary peptide excretion in schizophrenia J Ort
Mrd 5: 223-239.
2:Crow T(1994) Aetiology of schizophrenia .Current Opin.Psychiat7: 39-42
3:Reichelt Kl et al (1991) The probable etiology and possible treatment of
childhood autism . Brain Dysfunct. 4:308-319.
4:Lindstr|m LH et al (1984) CSF and plasma beta-casomorphin-like opioid
peptides in post-partum psychosis. Amer.j psychiat. 141:1059-1066.
5: Reichelt Kl and Landmark J (1995) Specific IgA antibody increases in
schizophrenia. J Biol Psychiat37:410-413.
6. Wieser H et al (1984) Amino-acid sequence of the coleiac active peptide
B 3142. Z Lebensmittel Untersuch Forsch 79:3371-3376.
7:Knivsberg A-M et al (1990) Dietary intervention in autistic syndromes.
Brain Dysfun.3:315-327.
8: Knivbserg A-M et al (1995) Autistic syndromes and diet .A four year
follow-up study of 15 subjects. Scand J Educat. Res : In press (accepted)
9: Cade R et al (1990)The effects of dialysis and diet in schizophrenia
Psychiatry: A World prespective 3:494-500.
10:Zagon IS and Mclaughlin PJ (1987) Endogenous opioid systems regulate
cell proliferation in the developing rat brain .Brain Res 412:68-72

K. Reichelt
Pediatric Research Institute
N-0027 Oslo, Norway
Tel: +47 22 86 90 45
Fax: +47 22 86 91 17
E-mail: [log in to unmask]

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