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Boy! the trouble with trying to offer souces is that this is my fourth
attempt to send this to the list and it's rejected because it's too long.

Since a few people objected to the connection between celiac and
schizophrenia I am sending this study on the topic to the list. It should
be well documented enough for anyone other than those who do not consider
the Internet as an adequate source. It is too long for the list so I'm only
sending the first sixth, and I have used asterisks to mark some
interesting parts. I would be willing to send full copies to individuals if
there are not too many requests.

There are also some very interesting observations about
celiac disease itself. Pardon some of the typos.

Also, when I said in a recent post that the Irish have more celiac than
other ethnic groups, I invited anyone who knew better to let me know if I
was wrong. One member did send me a strongly reasoned argument against that
point of view, and she promises me a more complete version later that I can
post to the net. The argument is strong and I am swayed, but still not
quite convinced. Perhaps I will be when the complete version arrives. -vance

Malabsorption and Delinquency

A PSYCHOBIOLOGICAL STUDY OF DELINQUENTS (Chapter 3)
GEORGE VON HILSHEIMER, 1977
A way the hypothalamic choreographer might be deranged is by malabsorption
syndrome. If this suggestion is valid it directly leads to some simple
therapeutic guidelines and implications for inexpensive
and productive research. Malabsorption might result from:
constitutional inadequacy; failure of intestinal flora; some variant of
celiac disease;(Salvadori, 1976) other food intolerances, especially to
cow's milk;
toxins - e.g., lead or manganese, or even so common a substance as
granulated cane
sugar; psychosocial stress. Malabsorption would result in:
proteinurias caused by toxic processing in the gut and imbalances of
protein intake; vitamin dependencies, also resulting from toxic by-products
and poor uptake, especially in the new born; lipidosis; mineral imbalance,
especially deficiencies of zinc; ascorbic acid depletion; reactive
allergies and other immune dysfunctions. I suggest that malabsorption
syndrome is a whole complex of metabolic
disorders which interact with psychosocial stress, infection, allergies and
endocrine disorders. Malabsorption is a stressor in itself. Malabsorption
is associated with high levels of circulating adrenocortocotrophic hormone
(ACTH) and with high levels of acetylcholine (ACh). ACTH and ACh are in
turn associated with modes of learning
which are characterized by poor habituation (the animals do not learn or
unlearn well), by high levels of avoidance, by efficient escape
conditioning, by neophobia and by poor instrumental conditioning. The
experimental evidence suggests that children with malabsorption will often
be similar in their electrophysiological and conditioning patterns to
animals with lesions to the hypothalamus and to the
hippocampus. (Di Sant'Agnese & Jones, 1962.)

Background
The term "malabsorption syndrome" describes the symptoms caused by impaired
intestinal absorption of nutrients. This syndrome characteristically causes
diarrhea, seatorrhea, weakness, weight loss, vitamin deficiencies and
hematologic abnormalities to appear. The onset of this syndrome may be
sudden or insidious. A thorough review of the condition is found in
Losowsky, Walker and Kellerer (1974). Celiac disease, and adult celiac
disease (also known as nontropical sprue), carbohydrate intolerance and
pancreatic deficiency may also be considered in a differential diagnosis.
Many authors have remarked on the similarity of the symptoms of sprue and
celiac disease to schizophrenia (Dohan, 1969). Abnormal levels of
hydrochloric acid in the stomach are associated with hysteria and neurosis
(Hepler, 1970). The classic celiac syndrome is said to occur in about one
case in every two thousand patients seen by pediatricians, and there is a
similar frequency of nontropical sprue in adults.

My own experience is that many physicians are reluctant to diagnose celiac
disease and that the variability of its frequency as a diagnosis may be
even greater than that among expert clinicians diagnosing diabetes from
laboratory results (viz. from 2 to 76%. Jarrett & Keen (1976)).
Wheat or Gluten Sensitivity
Hemmings (1976) reports that circulating blood is flooded with foreign
protein after meals when many large molecular weight breakdown products
invade the blood stream. He says that 60% of bovine immmunoglobulin (Ig) G
labelled with radioiodine is recovered as breakdown products from rat
tissue eight hours after feeding; and that 46% of alpha-gliadin is
recovered as breakdown prdoucts 24 hours after feeding. Alpha-gliadin is
complexed in serum, which suggests it may directly interfere with the
biochemistry of the body. Alpha-gliadin is the active toxic fraction of
gluten in celiac disease (Baker, 1975). Giadin digest causes at least third
grade toxic effects in all cells tested (lung, intestine, adrenal, kidney
and carcinoma of the larynx) within five hours in celiac patients and in
normal controls.
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Oral papain seems to protect against the toxic effect of gluten (Messer &
Baume, 1976). Jellife and Jellife (1976) indicate that the gut is "open"
and absorbs markedly more large molecule products in the first six months
of life than later.
***************************************
Cow's milk fed babies consequently have less competent immune systems, more
allelrgy and high risk for lipid abnormalities than breat fed babies who
are subtantially protected from these effects. The lymphocites from celiac
patients react specifically to a subfraction of gluten; similar immune
responses are seen in other diseases (Gowand & McGregor, 1965). Scott and
Losowsky (1975) in an extensive review found celiac disease to be
associated with many other diseases, particularly autoimmune disorders, or
immune deficiency diseases, hypo- and hyperthyroidism, myxedemic madness,
and elevated ACTH and ACh. Hypoglycemia is frequently associated with celiac
disease.
*******************************
Celiac syndrome may appear quite late in life (Hamilton et al, 1976); may
present without jejunal anomalies in the first biopsy, and the tolerance
for gluten may be high. The disease may be stimulated by an abnormally high
intake of grain products (Sewell & Blenkinsopp, 1976). Gluten's effect is
similar to that of plant lectin and may act as a lectin due to cell
abnormality. Gluten sensitivity has been seen as a sequel to viral
infection, and then may be progressive. The first degree
relatives of celiac patients have changes in jejunal cells similar to
celiacs at a frequency 300 times that of the general population (Weiser &
Douglas, 1976).

Both soya meat and bread extracts cause severe cytotoxicity (whole-meal
bread is less toxic than white); but serum abolishes cytotoxicity.  Soy
lectin does not appear to be cytotoxic but wheat lectin causes cell
rounding and a toxicity distinctively different from that of gluten and
bread (Freed & Cooper, 1977).  The lymphocites of celiac patients show a
marked increase in DNA synthesis after in vitro incubation with a
subfraction of gluten which is not shown by the cells of controls.  This
results in an immune sensitization (Sikora et al, 1976).  Alpha-tocopherol
deficiency may be seen in patients with the impaired fat oabsorption of
celiac disease.  The effect of Vitamin E's protection against toxins may be
lost in these cases (Binder, 1965).  This is also true for Vitamin D, and
consequently, severe problems of bone metabolism are often encountered
(Losowsky et al, op cit).  The efficiency of the absorption of nutrition in
the gut is strongly affected by the balance of nutrients and by the
presence of benign microorganisms which assist in absorption and proudce
essential vitamins (Scrimshaw & Young, 1976; Rettger et al, 1935).  In an
extensive survey Dohan (op cit) concludes that some schizophrenias may be
due to wheat or to gluten intolerances.  Singh and Kay (1976a, b) gave
either gluten or a soy placebo to schziphrenics in a double-blind,
cross-over study.  The gluten caused regression in those patients who were
least responsive to tranquilizers.  The authors argue that since
anticholinergics cause regression in schizophrenics who are most responsive
to tranquilizers, then the effect of gluten is clearly different from the
effect of the anticholinergics and gluten's pathway of action may be an
immune, allergic or toxic reaction.  The side effects from neuroleptic
tranquilizers were no different during the gluten and gluten-free periods
of the study.
***********************************
Proteinurias
During stress reactions the gut is passively permeable for many substances
which are normally rejected. For example, oral adrenalin and histamine are
toxic to an animal under stress but are not normally toxic. Horse serum,
given by mouth, is sensitizing when an animal has first been stressed, but
normally it is not.

Endogenous metabolites which do not normally produce immune reactions will
do so under stress (Selye, 1950).  It is well known that excessive
concentrations of amino acids in the blood are highly toxic to the central
nervous system (CNS) in certain inborn errors of metabolism; but toxicity
caused by dietary imbalance may occur without an inborn error (Dodge et al,
1975).  More than 20 studies reviewed by Dodge and his colleagues indicte
that monsodium glutamate produces lesions of the hypothalamus and that
pyridoxine buffers this effect.  Eating disproportionate amounts of amino
acids may provoke metabolic difficulties which mimic inborn errors of
metabolism(Clark, 1965).  (CRUELLY CROPPED HERE)