<<Disclaimer: Verify this information before applying it to your situation.>> 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. ******************************** 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)