Collected 1995 Net Articles by Dr. Kalle Reichelt

Copyright by Michael Jones, Bill Elkus, Jim Lyles, and Lisa Lewis 1995, 1996, 1997 - All rights reserved worldwide.

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Table of Contents

1. Intestinal permeability in schizophrenia
2. Trace amount of protein in milk.
3. Diet and mental disease.
5. Schizophrenia and diet
6. Gluten, casein and behaviour
7. Ear infections, allergy, autism & gluten
8. Behaviour and gluten
9. Downs syndrome and gut permeability
10. Dietary proteins in mothers milk
11. Copious stools.
12. Soy intolerance


Dr. Kalle Reichelt
Pediatric Research Institute
N-0027 Oslo, Norway
Tel: +47 22 86 90 45
Fax: +47 22 86 91 17
E-mail: Kalle Reichelt,

Dr. Reichelt has been researching the impact of gluten intolerance on
certain individuals with developmental delays. Most of the following is
from the mailing list. It is copyright Michael
Jones, Bill Elkus, Jim Lyles, and Lisa Lewis 1995 - All rights
reserved worldwide.


Subject: Intestinal permeability in schizophrenia
Date:    3 Jan 1995    9:19 AM

The data on this are conflicting and have been studies using different

1:  Wood NC et al (1987) Brit j psychiat 150:853-856 used the
cellobiose/mannitol test and found increased permeability in chronic
schizophrenics in 11 out of 32 patients.

2: Lambert MT et al (1989) Brit J psychiat 155,619-622.: used Chromium
labelled EDTA and found no difference in 12 schizophrenic patients, 12
patients in remission and normals.

3. We do however, all take up trace amounts of intact protein after a meal
(see eg. Husby S et al (1985) Scand J Immunol 22:83-92) so that a decreased
breakdown of fragments of these proteins could easily lead to accumulation.
One molecule of gluten contains 15 opioid sequences (Fukudome and Yoshikawa
(1991) FEBS Letters 296:107-111) and even 2.5 nanomoles of protein per ml
blood could therefore cause an "avalanche" of peptides being formed.  The
more so because peptidase defects regularly cause peptiduria (Watanabe Y et
al (1993) Res Comm Chem Pathol Pharmacol 81:323-350; Abassi Z et al (1992)
metabolism 41:683-685; Blau N et al (1980) J Inherit metab Dis 11 (Suppl 2)
240-242). Peptidura is of course a sign of hyperpeptidaemia. We do not
really need increased uptake to get into trouble although that would
accelerate the process and if sufficiently large it could overwhelm even
normal breakdown capacity. That there is gut to blood to mother milk
transport of intact food proteins is illustrated by papers where intact
antigens were found in mothers milk (Axellson I et al (1986) Acta paed Scand
75:702-707; Kilshaw PJ and Cant AJ (1984) Int Arch Allergy Appl Immunol
75:8-15; Troncone R et al (1987) Acta paed Scand 76:453-456; Stuart CA et al
(1984) Clin Allergy 14:533-535)

4. We all have IgG antibodies to food proteins indicating uptake of
immunologically active proteins in trace quantities. In schizophrenia IgG
antibody increases against gluten have been reported (Dohan FC et
al (1972) Biol Psychiat 5:127-131; Hekkens W Th et al (1980) in Biochemistry
of schizophrenia and Addiction (edit: Hemmings G) Lancaster, MTP press; Rix
KJB et al (1985) PSYCHOL MED 15:347-354). Increased IgE antibodies to food
proteins were also found in schizophrenics (Sugerman AA et al (1982) Annal
Allergy 48:166-171). Ashkenazi A et al (1979) Amer J psychiat 136:1306-1309:
found that leukocytes reacted to a fraction of gluten in a fashion
intermediate between coeliac disease and normal controls.

Finally we have (Reichelt Kl and LandmarkJ (1994) Biol psychiat: in press)
found IgA antibody increases in schizophrenics diagnosed after DSM III and
sex and age matched controls. These IgA antibodies were mainly against
gliadin, gluten, lactoglobulin and casein.

Unfortunately it is extremely difficult to finance research into diet and
psychoses. Neuropharmacology has become very dominant for obvious reasons .
The dismal state of the patients and their social integration in many cases
clearly makes more research an urgent matter.



)A question was raised: Can a baby receive gluten through breast milk?

Dr. Kalle Reichelt, a Norweigan researcher, has cited several articles as 
evidence that dietary proteins in general, and gluten/gliadin specifically, 
can be transfered to a breast-fed baby:

The following is from a post written by Reichelt to another internet
discussion group:

) proteins can be demonstrated in mothers milk (3-6) as intact
) proteins. This could easily therefore take place also during pregnancy.

)3: Kilshaw PJ and Cant AJ (1984) The passage of maternal dietary
) protein into human breast milk. Int Arch Allergy and Appl
)Immunol 75:8-15.

)4: Axelsson I, Jacobsson I, Lindberg T, and Benediktsson B (1986)
) Bovine lactoglobulin in human milk. Acta Paed Scand 75:702-707.

)5: Stuart CA, Twiselton R, Nicholas M and Hide DW (1984) Passage
) of cow's milk protein in breast milk. Clin Allergy 14:533-535.

) 6:Troncone R, Scarcella A, Donatiello A, Cannataro P, Tarabusco A and
)  Auricchio S (1987) passage of gliadin into human breast milk .
) Acta paed Scand 76:453-456.

)From Dr. Reichelt in reply to my post yesterday, in which I wondered whether
the amounts of gluten in mother's milk is significant:

Subject: Trace amount of protein in milk.
Date     9 Mar 1995    4:38 PM

It should be stressed that the amount are small. However, the point is that
even trace amounts can be important because if the proteins are not properly
broken down peptides will accumulate. After all the uptake of proteins from
the gut into blood has also been demonstrated: Husby et al (1985) passage of
undegraded dietary antigen into the blood of healthy adults. Scand j Immunol

Other references in brief :
Bloch KJ et al (1979) gastroenterology 77:1039-1044.
Thomas et al (1974) Immunology 27:631-639.
Walker WA et al (1974) gastroenterol 67: 531-550.

Because gluten contains at least 15 opioid sequences per molecule (Fukudodme
S-I and Yoshikawa M (1991) Opioid peptides derived from wheat gluten: Their
isolation and characterization. FEBS Letters 296:107-111.)  It is therefore
clear that one molecule could theoretically give 15 opioids. This means that
trace amount of peptide could quickly become very important.
Cheers                          Tiny


Subject: Diet and mental disease.
Date:    8 May 1995 16:10:20 +0200

Ratatat wrote in reply to the letter above (by the same subject):

)I read somewhere the the French Revolution was blamed on temporary mass
)schizophrenia brought on by the gluten in the bread that the peasants ate
)- some sort of fungus that had grown in it due to poor storage.

Hi. The big threat to grain eaters in Europe used to be alkaloids from
certain fungal toxins in grains collectively known as ergot alkaloids and
ergotamines. They cause epidemics of peripheral gangrene of the limbs. I
do not have any data on schizophrenia in this context, although ergot
alkaloids have been used to treat migraines and enhance delivery in
obstetrics. In much of the balkans they also have fungal toxins that cause
kidney and liver problems. (This is found in most countries where modern
antifungal spraying is not economically feasible). Also in periods of
starvation (esp war) Lathyrism caused by neurotoxin from chickling peas is
well known.

However, there is a precedent for excitotoxic amino acid like compounds
from food causing Central nervous disease in certain pacific islands such
as Guam with vastly increased incidence. The Chamorros of the marianas and
micronesia ate the seed of a false sago plant Cycas Circinnalis, from which
the compound beta-N Oxalamio-L -alanine could be isolated. This causes
amyotrophic lateral scelerosis, parkinsonism and Alzheimer -type dementia 
with considerable frequency (1,2)

1: Lewin R (1987) Environmental hypothesis for brain diseases strengthened
by new data. Science 237:483-484.
2:Spencer PS et al (1987) Guam amyotrophic lateral Sclerosis -Parkinsonism
-Dementia linked to a plant excitant neurotoxin.Science 237:517-522. 

All the best   Cheers



Subject: ADDHA.
Date:    26 May 1995 05:36:59 PM

Just a few references to diet and hyperactivity syndrome.
1: Egger J et al (1985) Controlled oligoantigenic treatment of the
hyperkinetic syndrome. The Lancet. March 9th:540-544.
2:Kaplan SJ et al (1989) Dietary replacement in preschool-aged hyperactive
boys. Pediatrics 83:7-17.
3: Egger J et al (1992) Controlled trial of hyposensitisation with
food-induced hyperkinetic syndrome. The Lancet 339:1150-1153.
4:Carter CM et al (1993) Effects of a few food diet in attention deficit
disorder. Arch Dis Child 69:564-568.
5: Marshall  (1989) Attention deficit disorder and allergy: A neurochemical
model of the relationship between illnesses. Psychol Bulletin 106: 434-446.
Furthermore high intake of low roughage (purified) carbohydrates cause
rapid increases in blood sugar followed by rapid insulin increase and
subsequent steep fall. This is prevented by high fiber additions concomitant
with carbohydrate intake. It is possible to have an overshoot with
postprandial hypoglycemia.
This is more common in habitually violent offenders in Finland.
Virkkunen M (1982)) Reactive hypoglycemia tendency among habitually violent
offenders. Neuropsychopharmacol 8:35-40.

Finally we have found peptide increases (possibly
phosphorylated/glycosylated?) in Hyperkinesia. (Hole K et al (1988)
Attention deficit disorders: A study of peptide-containing urinary
complexes. J develop behav Pediatrics. 9:205-212.).

It should also be noted that concentrated glucose can increase the
paracellular uptake in the gut. That is also more protein and peptides can
be taken up.

Ref: Pappenheimer JR and Madara JL (1993) Role of active transport in
regulation of junctional permeability and paracellular absorption of
nutrients by intestinal epithelia. in Istonic transport in leaky Epithelia
(Alfred benzen Symposium) Munksgaard, Copenhagen: pp 221-232.

Hope this may be of some use to at least some parents.

Cheers                          Tiny


Subject: Schizophrenia and diet
Date:    22 Jun 1995 11:00 AM

On 20 Jun 1995, Stephen Ronan ( wrote:
Re: Schizophrenia

)Gayle Kennedy wrote:
)) confusion and irrational anger, I keep wondering if the celiac diet would
)) be of any use to persons with schizophrenic symptoms....
)As far as I know the first person to suggest a possible link between
)schizophrenia (or a subset thereof) and gluten consumption was Dr. F.
)Curtis Dohan. Dohan graduated from medical school of the University of
)Pennsylvania in 1932. He was chief of the endocrine section of the William
)Pepper Laboratory at Penn from 1947 to 1966 and served on the medical
)faculty until 1975. About twenty-five years after first presenting his
)hypothesis, Dohan died in November 1991.
)"'The day before he died, we got a paper from a scientist in Norway,
)_Evidence and Arguments for Schizophrenia as a Dietary Disease_ and it was
)the last thing I read to him' said his wife Marie. That night, she got as
)far as Page 5. He died the following morning." (Philadelphia Inquirer, Nov
)14, 1991).
)I presume the Norwegian scientist was Dr. Kalle Reichelt...
)(Dr. Reichelt, incidentally, has given permission for his postings to be
)freely redistributed.) We are fortunate that he is pursuing his research
)regarding gluten, since NIMH has largely neglected this approach ever
)since conducting a rather minor intramural study of 8 patients about 15
)years ago (Potkin et al).
)The gluten apparently implicated in a subset of schizophrenia is protein
)found in the cereal grains wheat, rye, barley and oats.
)When some other people eat this gluten, the little, finger-like villi (that
)stick up from the inner walls of the small intestine, and wave around, and
)absorb food) get severely flattened and damaged and therefore cannot
)absorb food normally. It is not well understood how exactly the gluten
)causes the damage.
)People with that particular type of reaction to gluten are diagnosed as
)having something called celiac syndrome. A malabsorption of food with
)symptoms of diarrhea and fatty stools, and failure to thrive and grow at
)normal rates are often the symptoms first noticed in children with celiac
)syndrome. Fairly often doctors miss the diagnosis.  When successfully
)diagnosed, people with celiac syndrome are advised to eliminate all gluten
)and dairy from their diets and when they do so, it is usually the case
)that the villi in their small intestine recover and their digestion
)In the 1960's, F. Curtis Dohan MD came to believe that in regions where
)gluten consumption is common, the rate not only of celiac syndrome but
)also schizophrenia is substantially higher than in places where gluten
)consumption is absent (e.g., where people rely on sweet potato, rice or
)millet rather than wheat, rye, barley or oats).
)Subsequent research, including experiments by others involving biopsies,
)led Dohan to conclude that people diagnosed as schizophrenic did _not_
)typically have the same reaction to gluten as people with celiac syndrome.
)They did not have the same type of damage to the villi of the small
)intestine. He thought that the genetic basis might be related but
)different. He eventually came to believe that a gluten-sensitive subset of
)schizophrenics were processing gluten and the casein in dairy foods in a
)way that exposed their brains to certain very potent psychoactive
)substances that are now known to exist in those foods.
)In his initial published clinical trial, at a V.A. hospital, Dohan tried
)removing gluten and dairy from the diets of people diagnosed as
)schizophrenic while they were on a locked admitting ward.  They went back
)on a regular gluten-containing diet once they moved to the open wards. Of
)those on the gluten-free diet on the locked ward, 80% were on that ward
)and the gluten-free diet for 10 days or less.
)Other people diagnosed as schizophrenic who went through the same wards
)were kept on a high-gluten diet while on the locked ward instead of a
)gluten- and dairy-free diet.
)The people at the V.A. hospital who were on the gluten-free diet while on
)the locked ward were discharged almost twice as quickly as those who were
)on the high-gluten diet.  "The average time until discharge for the
)discharged CFMF [cereal-free, milk-free] patients (77 days) was 55 percent
)of that of the discharged HC [high cereal] patients (139 days)."
)The abstract of Dohan's article about this research read as follows (Am J
)Psychiatry 130:6 June 1973):
)"Routinely treated schizophrenics, who on admission were randomly assigned
)to a diet free of cereal grains and milk while on the locked ward, were
)discharged from the hospital about twice as rapidly as control patients
)assigned to a high-cereal diet. Wheat gluten secretly added to the
)cereal-free diet abolished this effect..."
)Dohan's study involved about 110 subjects, roughly half of whom were on
)the CFMF diet for at least a short while. As I recall (and I'm not
)positive), Dohan himself was not 'blind' to who was getting each diet,
)though facility staff were.
)Subsequently, Singh and Kay conducted a study that was reported in Science
)in January, 1976. Their article's abstract stated: "Schizophrenics
)maintained on a cereal grain-free and milk-free diet and receiving optimal
)treatment with neuroleptics showed an interruption or reversal of their
)therapeutic progress during a period of 'blind' wheat gluten challenge.
)The exacerbation of the disease process was not due to variations in
)neuroleptic doses. After termination of the gluten challenge, the course
)of improvement was reinstated. The observed effects seemed to be due to a
)primary schizophrenia-promoting effect of wheat gluten."
)In the Singh/Kay study, "Three of the patients were diagnosed as paranoid,
)four as catatonic, and seven as hebephrenic schizophrenics." [BTW, my
)impression has been that that people whose symptoms include very high
)levels of muscular tension (catatonia) and a giddy silliness (once known
)as hebephrenia) have tended to be most likely of all to improve via
)gluten-free diets. Then again, that info may be of limited value since the
)medicines typically used these days interrupt or preclude much catatonic
)symptomatology and the "hebephrenic" diagnosis disappeared.]
)As reported in the American Journal of Psychiatry 135: 1417-1418, 1978,
)Rice et al. began a study with 21 patients diagnosed as schizophrenic (5
)schizo-affective, 11 paranoid, and 5 chronic undifferentiated type). Five
)patients dropped out. The 16 patients who completed the study had a mean
)of 9 years of hospitalization and a mean age of 38.
)Potkin et al. (see below) cited the Rice study as involving: "16
)chronic schizophrenic patients treated with neuroleptics who were on a
)normal diet and challenged with gluten and subsequently were on a
)gluten-free, milk-free diet. In this study, 1 patient, who had been
)hospitalized for 14 years, became more agitated, uncooperative, and
)paranoid with the gluten load. This patient and another patient, who had
)been hospitalized for 13 years, substantially improved on the gluten-free
)diet. The latter patient improved to the degree that she could be
)discharged to the care of her family." No similar gains from a gluten-free
)diet were found among others in the study.
)In Am. J. Psychiatry 138:9, September 1981 Potkin et al. reported on their
)own experiment, which involved 8 patients -- "3 were subcategorized as
)being paranoid and 5 as chronic undifferentiated" (pg. 1209). These people
)were provided a relatively high-gluten diet for a month or two and a
)gluten- and dairy-free diet for two or three months, with their condition
)in the final two weeks of each of these periods compared. No significant
)difference in symptoms during the two diets was found.
)NIMH lost interest. Hope you haven't and don't...
)Steve Ronan

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 conclude:

a) That both urinary peptide excretion and rating scales (Comprehensive
Psychopathological 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, amino acid 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 cochromatographs 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
casomorphin (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
WE think therefore that it is important to be gluten/gliadin free and
milk protein 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 of 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 measurable 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 to 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 welcome here to learn by doing.
Finally it should be stressed that opioids do have maturation inhibitory
effects in rat brain (10), which would fit Crows (2) data quite nicely.

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. Psychiat 7:39-42
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 Psychiat 37:410-413.
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


Subject: Gluten, casein and behaviour
Date:    14 Jul 1995 15:46:35 +0200

Jason Kennerly asked:

)       - can gluten intolerance cause a forboding feeling that there is a 
)'conspiracy' working against you or causes you support, obsessiveness, or 
)lack of insight? Can it cause feelings of persecution, the sense that 
)things somehow pertain to you or your close friends and reletives? Can it 
)make someone display symptons of paranoid-type schizophrenia?

It is of course very difficult to make follow the effect of gliadin,
gluten and casein derived peptides and their specific effects on the
brain. However, the fact that opioids from exogenous proteins can be
isolated from patients (1,Reichelt et al submitted), and that other
peptides found in urine and dialysis fluid from patients (2,3) also causes
behavioural changes in animal models, makes it possible that paranoid
ideation and persecutory feeling could well be human correlates of the
behaviour changes noted in animals (2,3). We cannot do such experiments on
humans although they have been carried out before the advent of ethical
committees. Thus prof R Heath in New Orleans injected a serum prep on
volunteering prisoners called tarexein. They definitely demonstrated
schizoid behaviour. (I have seen the videos myself).
We have effect on schizophrenics on diet (blind) (4) which agrees with
some publications (5,6) but not with others. I think the negative
experiments were run for too short an interval. A dietary casein and gluten
free diet would need 1/2 to one year to be certain. In autistic children we
do also find a clearcut effect of diet run over 4 years (1).
However, if it is correct that you drink tons of coffee, this could in
itself be the cause. This is because caffeine act as a CNS stimulatory
agent causing higher arousal which again makes you more introverted. If the
doses are very large borderline conditions may develop and the world by
seeming strange causes paranoid ideation to explain the changed perception
of the world. See Prof Eysencks many paperbacks on psychology. Amphetamine
has the same effect (bad trips) in introverted persons. In Hyperkinetic
children where the attention related CNS centres show lower activation,
they go from extreme extroversion and become normalized. Treating epileptic
children with the drugs available often causes a iatrogenic hyperactivity
(ADD) syndrome because of increased CNS inhibition. This is a clinical
problem which is difficult but unavoidable.

1:Reichelt Kl et al (1991) Brain Dysfunct. 4:308-319.
2:Hole K et al (1979) Neuroscience 4:1883-1893.
3:Drysdale A et al (1982) Neuroscience 7:1567-1574  
4:Reichelt KL et al (1990) J Ortomol Med 5:223-239
5:Singh MM and Kay (1976) Science 191:401-402.
6:Vlissides DN et al (1986) Brit J psychiat 148:447-452 (some cases, not all)
Right now I do not have time for more references, but we can get back to
that later.


Subject: ear infections, allergy, autism & gluten
Date:    19 Jul 1995

Jack Challem, Editor of The Nutrition Reporter (TM) newsletter, wrote:

)       I'm sure you'll hear a lot of opinions. But I'll point to you to a
)specific journal citation that confirmed what people have been saying for
)years. The fundamental cause of ear infections is allergy, which causes fluid
)retention in the ear, which creates a great breeding ground for bacteria. The
)most common allergens for small children are milk and wheat.

)Nsouli TM, "Role of food allergy in serious otitis media," Annals of Allergy,
)September 1994;73:215-219.

This is quite interesting because the IgA antibodies formed in the gut are
transported to all mucous membranes in the body and may react with
appropriate antigens. Because intact antigens are taken up into the blood
postprandially (1) and we have also demonstrated increased levels of IgA
antibodies to gluten, gliadin and casein in some autistic patients (2,3); I
can easily see a possible connection, where all mucosal membranes are
irritated by the circulating antigen reacting with deposited IgA
1: Husby S et al (1985) Scand J Immunol 22:83-92.
2: Reichelt Kl et al (1990) J Applied Nutr. 42:1-11
3: Reichelt KL et al (1994) Develop Brain Dysfunct. 7:71-85


Subject: Behaviour and gluten
Date:    1 Sept 1995

Classic works on autistic symptoms in coeliac disease have been published
(1) and also depression (2). But of course not in all (is there ever
something that applies to all?)

It is extremely relevant that we find very high IgA antibodies against food
proteins in Downs syndrome (3). The effect of food proteins are also
manifest from our data on diet and autism (4).

Furthermore a series of neurological conditions have been related to gluten
intolerance. Thus spinocerebellar degeneration, neurological symptoms,
cerebellar syndromes and degeneration of the CNS have all been
implicated (5-8). Gluten provocation in young children with coeliac disease
can cause long lasting EEG (Electroencephalographic) changes in spite of
normal vitamin levels (9). In adults gluten intolerance, occipital
calcifications and a parietal epilepsy have been found (10).

Finally it is important that proteins which contain many eg. exorphin
sequences such as gluten where there are 15 per molecule (11), even trace
amounts may cause problems when the break down is decreased or intestinal
uptake increased swamping even normal digestive capacity.
Animal model of extreme relevance because monoamine changes are similar to
those described in human coeliac patients by Hallert (2) is that carried
out in Canada by Thibeault (12). Cats usually do not eat gluten.

1: Asperger H (1961) Die Psychopathologie des Coeliakiekranken Kindes. Ann
Paediatr. 197:146-151.
2: Hallert C et al (1982) psychic disturbances in adult coeliac disease
III.reduced central monoamine metabolism and signs of depression. Scand J
Gastroenterol. 17:25-28.
3: Reichelt Kl et al (1994) Increased levels of antibodies to food proteins
in Downs syndrome. Acta Paediat Japon. 36:489-492.
4: Reichelt Kl et al (1994) Nature and consequences of hyperpeptiduria amd
bovine casomorphin found in autistic syndromes. Develop brain Dysfunct.
5: Ward ME et al (1985) Celiac Disease and Spinocerebellar Degeneration
with Normal Vitamin E status. Neurology 35:1199-1201.
6: Cooke WT et al (1966) Neurological disorders associated with adult
coeliac disease. Brain 89:683-722.
7: Finelli PF et al (1980) Adult coeliac disease presenting as cerebellar
syndrome. neurology 30:245-249.
8: Kinney HC et al (1982) Degeneration of the central nervous system
associated with coeliac disease. J Neurol Sci 5:9-22.
9: Paul KD et al (1985) EEG-Befunde bei Zoeliakikrnaken Kinderen in
Abh{ngigheit der Ern{hrung. Z Klin med 40:707-709.
10: Gobbi G et al (1992) Coeliac disease, epilepsy and cerebral
calcifications. Lancet 340:439-443.
11: Fukudome Si and Yoshikawa M (1991) Opioid peptides derived from wheat
gluten: their isolation and characterization. FEBS Lett 296:107-111.
12: Thibault L et al (1988) Changes in serum amino acids content and
dopamine-beta-hydroxylase and brain neurotransmitter interaction in cats
fed casein with and without gluten. J Clin Biochem Nutr. 4:209-221.
13: Zagon IS and McLaughlin PJ (1987) Endogenous opioid systems regulate
mcell proliferation in the developing rat brain. Brain res 412:68-72

Conclusion: Because gluten can cause neurological problems it is not
strange at all that it may also give behavioural problems. The opposite
would be improbable.
We believe (4) that the mediators of these problems are peptides and
specifically exorphins that do have inhibition of nerve development as one
of their effects (13).


Subject: Downs syndrome and gut permeability
Date:    11 Sept 1995

Many Downs syndrome children have very high levels of IgA and also IgG
antibodies to food proteins (1,2) even if most of these do not have
endomycium antibodies and a normal gut lining. We have interpreted this as
indicating increased gut permeability but in most cases not a coeliac
condition. There is an inverse relationship between the size of the
children and the level of these antibodies (1). Apparently also Downs
syndrome with autism is more frequent than expected (3). I have four
children with this combined state so far.
It also is very relevant that Shattock found peptide increases in the
urine of such patients (4).
We also find substantial peptide increases in coeliacs (Reichelt et al
submitted) and thus confirming data published on increases in hydrolysis
released amino acids in the urine of coeliacs. (5)
1:Kanavin \ et al (1988) Immunological studies of patients with Downs
syndrome. Acta Med Scand 224: 474-477.
2:Reichelt KL et al (1994) Increased levels of antibodies to food proteins
in Down syndrome. Acta paediat Japon. 36: 489-492.
3:Howlin P et al (1995) The recognition of autism in children with Down
syndrome - implications for intervention and some speculations about
pathology. develop Med and Child neurol. 37: 398-414.
4:Shattock P et al (1990) Role of neuropeptides in autism and their
relationships with classical neurotransmitters. Brain Dysfunct 3: 328-346.
5:Klosse JA et al (1971) An automated chromatographic system for the
combined analysis of urinary peptides and amino acids. Clin Chim Acta 42:


Subject: dietary proteins in mothers milk
Date:    28 Sept 1995  08:23:24 am

It has been clearly established that bioactive and significant amounts of
protein and peptides are taken up from the gut (1,2).
It is therefore not suprising that the same proteins can be measured in
mothers milk (3-6). This has been done by immunological technique and also
demonstration that the proteins are not fragments of the precursors by
electrophoresis on acrylamide gels. Gliadin proteins see ref 6.
That this mechanism may have serious consequences is illustrated by the
many papers relating peptide fragments of milk proteins and the induction
of antibodies that destroy the beta-cells (insulin producing cells) and
cause diabetes mellitus (7-9). Certain epilepsy is also related to gluten

1: Gardner MLG (1994) Absorption of intact proteins and peptides. in Physiol
of gastrointestinal Tract 3rd edit (edit: LR Johnson) Raven press, NY 
2: Gardner MLG and Stffens K-J (eds)(1995) Absorption of orally adminsitered
enzymes. Springer Verlag, Berlin, Heidelberg.
3: AxelssonI et al (1986) Bovine bveta-lactoglobulin in human milk. Acta
Paed Scand 75: 702-707.
4: Kilshaw PJ and Cant AJ (1984) The passage of maternal dietary protein
into human breast milk. Int Arch Allergy and Appl Immunol 75:8-15.
5: Stuart Ca et al (1984) Passage of cow's milk protein in breast milk. Clin 
Allergy 14: 533-535.
6: Troncone R et al (1987) Passge of gliadin intio human breast milk. Acta
paediat Scand. 76: 453-456.
7: Karjalainen J et al (1992) Bovine albumin peptide as possible trigger  of
insulin-dependent diabetes mellitus. New Eng J Med 327: 302-307.
8: Martin JM et al (1991) Milk protein in the etiology of insulin-dependent
diabetes mellitus (IDDM) Ann Med 23: 447-452.
9: Virtanen SM et al (1994) Diet, cow's milk protein antibodies and the risk
of IDDM in Finnish children. Diabteologica 37: 381-387.
10: Gobbi G et al (1992) Coeliac disease, epilepsy and cerebral
calcifications. The Lancet 340: 439-443.


Subject: Copious stools.
Date:    20 Oct 1995  9:34 AM

I would like to draw your attention to a paper which highlights exactly
autism and large stools. Shattock P (1988) Autism: possible clues to the
underlying pathology.-2. A parent's view. in Aspects of Autism: Biological
Research (edit: Wing L) Gaskell/The national autistic society (ISBN 0-902241
25 7) pp 11-18.
Intensive diet and combined with training as described by Prof I Lovaas, Los
Angeles can still train patients to compensate for lost opportunity.


Subject: Soy intolerance
Date:    21 Oct 1995  09:21:04 +0100

Toril Myrtveit (toril.myrtveit@FYS.UIO.NO) wrote:

)I just went to a week-end cooking course (for g/c-free foods), where I
)learned that most people with casein intolerance didn't tolerate soy either.
)(no soy-milk, no soy-margarine, no soy sauce,...) This was all new to me.
)Supposedly, the soy-intolerance is due to the caseinates being similar in
)soy and cow-milk. Sounds wacko to me, and there was no medical experts there
)to explain why this should be so.

The evidence for this is very dubious. Sometimes when children are allergic
(IgE mediated) to milk their antibodies may cross react with soy bean
proteins. (Therefore if we are not satisfied with the progress of children
on gluten & casein free diet, soy protein has been removed too. I do not
find any definite effect of this.)
Exorphins have not been found from soy-proteins. The only bioactive
peptides found so far are antioxidant peptides from Soybean
beta-Conglycinin (1), and an immunomodulating peptide (2).
All proteins do give rise to peptides during uptake from the gut, and if
not broken down or otherwise increased they may inhibit the break down of
other dietary and also endogenous peptides. The reason for this has been
extensively discussed (3), and is due to peptides generally being good
peptidase inhibitors.
Therefore increasing the intake of peptidases (not proteinases) in
enterosoluble capsules like those from papaya would be a good idea.
Preliminary data look promising.

1: Chen H.M et al (1995) Structural analysis of antioxidative peptides
from Soybean Beta-Conglycinin. j Agricult and Food Chem 43: 574-578.
2: Yamauchi F and Suetsuna K (1993) Immunological effects of dietary
peptide derived from soybean protein. J Nutr Biochem 4: 450-457.
3: LaBella FL et al (1985) Administration of peptides inhibit the
degradation of enodgenous peptides. The dilemma of distinguishing direct
from indirect effects. Peptides 6: 645-660.
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