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    Malabsorption and Delinquency - A Psychobiological Study Of Delinquents


    Scott Adams

    George Von Hilsheimer, 1977


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    (Celiac.com 06/12/2000) 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 - 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 SantAgnese & Jones, 1962.)...

    ...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. However, one authority (Hodgkin, 1973) reported seeing only one case of celiac disease and no sprue in ten years on a British National Health Service with 2500 patients. 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)...

    ...Consequences of Malabsorption:

    • The ecology of the gut would be poor;
    • Imbalances in blood chemistries and developmental anomalies would indicate neonatal and fetal nutritional inadequacy;
    • The adrenal glands would be depleted;
    • The immune system would be over reactive...

    ...Evidence for Malnutrition in Middle Class Delinquents

    Summarizing the preliminary reports reviewed above and looking at my delinquents in their light suggest that compared to other children:

    • Delinquents are more often products of unfortunate pregnancies;
    • They suffer more pregnancy and birth complications;
    • They are seldom breast fed;
    • They have more colic and other early indications of GI distress and food intolerance;
    • They are often victims of celiac syndrome and other inborn errors of metabolism;
    • They are early addicted to diets high in sugar and refined carbohydrates;
    • They have poor absorption of food deficient intestinal flora, and slow transit times for food products moving through their guts;
    • They have thiamin, pyridoxine and pantothenic acid deficiencies as neonates.

    These facts suggest that delinquents are at high risk for unusual CNS development, CNS damage, poor continuing synthesis of CNS amino acids and neural transmitters, and are extremely vulnerable to derangements of the immune and allergy systems...

    ...Criminal, felon (schizophrenics), and chronic patients had the greatest evidence of malabsorption syndrome of all the subjects, who generally evidenced malabsorption. Felon (schizophrenic) had lower hair Cu than (schizophrenic) patients who were not actively delinquent...

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  • About Me

    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

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  • Related Articles

    Scott Adams
    The following was written by Dr. Kalle Reichelt who is a leading celiac disease researcher at the Pediatric Research Institute in Oslo, Norway. Please direct any questions regarding this article to him at: K.L.Reichelt@rh.uio.no
    What most people ignore is that both peptides and trace (biologically significant amounts) amounts of proteins are taken up across the gut mucosa (1,2). Because one molecule of gluten contains at least 15 opioid sequences it is quite clear that this could cause a problem. Increased peptide excretion is found in the urine of celiacs before treatment (3) (Reichelt et al in prep). This is confirmed by a series of papers that demonstrate intact food proteins in mothers milk (4-7). A Canadian group has confirmed that gluten does change a brain enzyme and monoamine levels in cats (8). Their findings a significant even though cats are not gluten eating animals. There is increasing evidence that components from food can indeed cause serious psychiatric (9-12) and neurological (13-16) diseases. Even rheumatoid arthritis may have a link to food proteins (17), and it well established that stress increases gut permeability. Nobody denies the possibility of reactive depression, but there is little reason why this could not be made worse by dietary factors. Because antibodies are indeed induced by peptides it may even be so that dietary peptides by mimicry to endogenous cell surface peptide sequences, may be responsible for many autoimmune diseases (18).
    References:
    Gardner MLG (1994) Physiology of the gastrointestinal tract. Edit: LR Johnson. Raven press 3rd edit. pp 1795-1820. Husby S et al (1985) Scand J Immunol 22:83-92. Klosse JA et al (1972) Clin Chim Acta 42:409-422. Kilshaw PJ and Cant AJ (1984) Inter. Arch Allergy Appl Immunol 75:8-15. Axelsson I et al (1986) Acta paed Scand 75:702-707. Stuart CA et al (1984) Clin Allergy 14:533-535. Troncone R et al (1987) Acta paed Scand 76:453-456. Thibault L et al (1988) J Clin Biochem Nutr. 4:209-221. Hallert C et al (1982) Psychic disturbances in adult celiac disease III.Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol 17:25-28. Singh MM and Kay SR (1976) Wheat gluten as a pthogenic factor in schizophrenia. Science 191:401-402. Dohan FC and Grasberger JC (1973) relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Amer J Psychiat 130:685-686. Reichelt KL et al (1990) The effect of gluten free diet on glycoprotein attached urinary peptidee excretion and behaviour in schizophrenics. J Orthomol Med 5:223-239. Gobbi G et al (1992) Celiac disease, epilepsy and cerebral calcifications. The Lancet 340:439-443. Paul K-D et al (1985) EEG-Befunde Zoeliakikranken Kindern in Abh{ngigkkeit von der Ern{hrung. Z Klin Med 40:707-709. Kahn A et al (1987) Difficulty of initiating sleep associated with cows milk allergy in infants. Sleep 10:116-121. Hadjivassiliou M et al (1996) Does cryptic gluten sensitivity play a part in neurological illness? The Lancet 347:369-371. Kjeldsen-Kragh J et al (1991) Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. The Lancet 338:899-902. Karjalainen J et al (1992) Bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. New Eng J Med 327:302-307.

    Scott Adams
    Celiac.com 09/01/2002 - Patients with celiac disease are 20 times more likely than the general population to have epilepsy and often have associated cerebral and cerebellar calcifications imaged by CT and MRI. Depression, dementia, and schizophrenia are all also common in persons with untreated celiac disease. Cerebellar degeneration with resulting ataxia (gluten-associated ataxia) is a known entity in Europe, and the National Institutes of Health (NIH) is currently recruiting subjects with ataxia to examine them for gluten sensitivity and celiac disease. Focal white matter lesions in the brain recently have been reported to occur in children with celiac disease and are thought to be either ischemic in origin as a result of vasculitis or caused by inflammatory demyelination. Parents of children with celiac disease have reported behavioral changes such as irritability, separation anxiety, emotional withdrawal, and autistic-like behaviors that all seemed to improve on a GFD. Although not scientifically validated, the GFD is now also being advocated for children with autism by several groups. Whether or not children with autism are at a higher risk for celiac disease or celiac children have a higher incidence of autism remains to be proven. However, children with Down syndrome, who often have autistic-like behaviors, are at higher risk for celiac disease. It has been hypothesized that gluten may be broken down into small peptides that may cross the blood-brain barrier and interact with morphine receptors, leading to alterations in conduct and perceptions of reality.
    The serologic tests can be divided into 4 different types of antibodies: antigliadin (AGA), antireticulin, antiendomysium (AEA), and antitissue transglutaminase (tTG). Each antibody varies widely in its sensitivity, specificity, and positive and negative predictive values (Table 2).
    Table 2 (from Pietzak et al, 2001, compiled data from multiple studies)

    Test Sensitivity Specificity PPV NPD AGA IgG 57-100 42-98 20-95 41-88 AGA IgA 53-100 65-100 28-100 65-100 AEA IgA* 75-98 96-100 98-100 80-95 Guinea pig tTG† 90.2 95 Human tTG† 98.5 98 * Patients older than 2 years of age.
    † IgG +IgA antibodies.

    The AEA IgA immunofluorecent antibody is an excellent screening test for celiac disease, with both a high sensitivity and specificity. This antibody was discovered in the early 1980s and rapidly gained use as part of a screening celiac panel by commercial laboratories in combination with AGA IgG and AGA IgA. Its major drawbacks are that it may be falsely negative in children under the age of 2 years, in patients with IgA deficiency, and in the hands of an inexperienced laboratory. Also, the substrate for this antibody was initially monkey esophagus, making it expensive and unsuitable for screening large numbers of people. Recently, the human umbilical cord has been used as an alternative to monkey esophagus. However, the subjective nature of the AEA assay may lead to false-negative values and unacceptable variability between laboratories.
    Because tTG had been first described as the autoantigen of celiac disease in 1997, it has been used to develop innovative diagnostic tools. The tTG IgA ELISA test is highly sensitive and specific, using either the commercially available guinea pig tTG or human recombinant tTG. The tTG assay correlates well with AEA-IgA and biopsy. However, it represents an improvement over the AEA assay because it is inexpensive and rapid (30 minutes), is not a subjective test, and can be performed on a single drop of blood using a dot-blot technique. Therefore, this test is ideally suited for mass screenings and in the future could be performed in the general practitioners office, much like the now routine finger-stick hematocrit.
    For the reasons outlined above, the IgA class human anti-tTg antibody, coupled with the determination of total serum IgA, currently seems to be the most cost-effective way to screen for celiac disease. AEA should be used as a confirmatory, pre-biopsy test, whereas AGA determinations should be restricted to the diagnostic work-up of younger children and patients with IgA deficiency, using the guidelines in Table 3.
    Table 3
    Probability of celiac disease based on three antibodies in combination
    AEA IgA AGA IgA AGA IgG Interpretation + + + Celiac disease 99% probable + - + probable + + - Celiac disease probable + - - Celiac disease probable - + + Celiac disease less likely* - - + Celiac disease less likely* - + - Celiac disease less likely - - - Celiac disease very unlikely+ * If patient is IgA sufficient: AGA IgG > 100 warrants work-up of enteropathy.
    + If patient is on a gluten-containing diet.
    Celiac disease: AEA, antiendomysium antibodies: AGA, antigliadin antibodies.

    Scott Adams
    American Journal of Psychiatry 163:521-528, March 2006
    Celiac.com 03/14/2006 – Danish researchers have found yet another link between celiac disease and schizophrenia. In a large epidemiologic study the researchers looked at 7,704 Danish people who were diagnosed with schizophrenia between 1981 and 1998, including their parents, and matched them to comparison control subjects. The data linkage required that the autoimmune disease be diagnosed before the diagnosis of schizophrenia. The researchers found that patients with a history of an autoimmune disease had a 45% increased risk for schizophrenia, and nine autoimmune disorders were indicators of a higher prevalence for schizophrenia when compared to the controls. The researchers conclude: “Schizophrenia is associated with a larger range of autoimmune diseases than heretofore suspected. Future research on co-morbidity has the potential to advance understanding of pathogenesis of both psychiatric and autoimmune disorders.”

    Jefferson Adams
    Celiac.com 02/13/2013 - A team of researchers wanted to determine whether levels of immunoglobulin G (IgG) were associated with a later diagnosis of a non-affective psychotic disorder.
    The researchers included H. Karlsson, Å. Blomström, S. Wicks, S. Yang, R.H. Yolken, and C. Dalman. They are affiliated with the Department of Neuroscience at the Karolinska Institute in Stockholm, Sweden.
    To accomplish their goal, the team analyzed archival dried blood spots taken from newborns in Sweden between 1975 and 1985 with verified register-based diagnoses of non-affective psychoses made between 1987 and 2003 and comparison subjects matched on sex, date of birth, birth hospital, and municipality.
    The team reviewed samples from a total of 211 case subjects and 553 comparison subjects who agreed to take part in the study. They pulled data for factors associated with maternal status, pregnancy, and delivery from the Swedish Medical Birth Register.
    They used enzyme-linked immunosorbent assay to analyze the results for levels of IgG directed at gliadin (a component of gluten) and casein (a milk protein) in eluates from dried blood spots. They then calculated odds ratios for levels of IgG directed at gliadin or casein for non-affective psychosis.
    Comparison subjects associated with non-affective psychosis showed levels of anti-gliadin IgG (but not anti-casein IgG) above the 90th percentile of levels observed (odds ratio=1.7, 95% CI=1.1-2.8).
    This connections was not affected by differences in maternal age, immigrant status, or mode of delivery. They also found that gestational age at birth, ponderal index, and birth weight were not associated with maternal levels of anti-gliadin IgG.
    From their study, they concluded that high levels of anti-gliadin IgG in the maternal circulation are associated with an elevated risk for the development of a non-affective psychosis in offspring.
    They point out that more research is needed to identify the mechanisms underlying this association in order to develop preventive strategies.
    Source:
    Am J Psychiatry. 2012 Jun;169(6):625-32. doi: 10.1176/appi.ajp.2012.11081197.

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    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
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    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
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    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.