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> confusion and irrational anger, I keep wondering if the celiac diet would
> be of any use to persons with schizophrenic symptoms....

In May, I posted the material below to the mailing lists SCHIZOPH and
SCHIZ-L and I would be glad for any comments/corrections/suggestions from
members of this list. My regrets to those subscribed to both lists.

By the way, George and Gayle, I notice that you have a Cornell mailing
list. Perhaps you might want to be in contact with T. Colin Campbell who
works/teaches there.  Please feel free to forward this message to him. As
you may know, he has coordinated an acclaimed study of diet in China. I
think that it would be extremely useful if he were able to analyze his
collected data to determine the relative frequency of schizophrenia in
regions that rely on rice in comparison to those that have a wheat-based
diet.

- Steve
Ronan [log in to unmask]

*************************

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
normalizes.

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    [log in to unmask]