“…Upper intestinal lesions related to autism have also been reported (Horvath et al, 1999;Torrente et al, 2002), and increased low molecular gut permeability in autism is known (D'Eufemia et al, 1996). It has been suggested that the latter could be due to decreased sulphation of aminoglycans in the gut (Waring and Ngong, 1993), but peptidase defects or inhibition also increases gut uptake of peptides (Mahe et al, 1989). Late onset autism could also be caused by introduction of gluten containing foods from about 6 months and onwards.…”
Section: Early and Late Onset Subtypesmentioning
confidence: 96%
“…We all take up peptides (Gardner, 1994) and proteins (Husby et al, 1984;Gardner, 1994) from the gut and inhibition of peptidases increases the uptake (Mahe et al, 1989). These dietary proteins can be demonstrated in mothers' milk (Kilshaw and Cant, 1984;Troncone et al, 1987).…”
Opioid peptides derived from food proteins (exorphins) have been found in urine of autistic patients. Based on the work of several groups, we try to show that exorphins and serotonin uptake stimulating factors may explain many of the signs and symptoms seen in autistic disorders. The individual symptoms ought to be explainable by the properties and behavioural effects of the found peptides. The data presented form the basis of an autism model, where we suggest that exorphins and serotonin uptake modulators are key mediators for the development of autism. This may be due to a genetically based peptidase deficiency in at least two or more peptidases and, or of peptidase regulating proteins made manifest by a dietary overload of exorphin precursors such as by increased gut uptake.
“…Upper intestinal lesions related to autism have also been reported (Horvath et al, 1999;Torrente et al, 2002), and increased low molecular gut permeability in autism is known (D'Eufemia et al, 1996). It has been suggested that the latter could be due to decreased sulphation of aminoglycans in the gut (Waring and Ngong, 1993), but peptidase defects or inhibition also increases gut uptake of peptides (Mahe et al, 1989). Late onset autism could also be caused by introduction of gluten containing foods from about 6 months and onwards.…”
Section: Early and Late Onset Subtypesmentioning
confidence: 96%
“…We all take up peptides (Gardner, 1994) and proteins (Husby et al, 1984;Gardner, 1994) from the gut and inhibition of peptidases increases the uptake (Mahe et al, 1989). These dietary proteins can be demonstrated in mothers' milk (Kilshaw and Cant, 1984;Troncone et al, 1987).…”
Opioid peptides derived from food proteins (exorphins) have been found in urine of autistic patients. Based on the work of several groups, we try to show that exorphins and serotonin uptake stimulating factors may explain many of the signs and symptoms seen in autistic disorders. The individual symptoms ought to be explainable by the properties and behavioural effects of the found peptides. The data presented form the basis of an autism model, where we suggest that exorphins and serotonin uptake modulators are key mediators for the development of autism. This may be due to a genetically based peptidase deficiency in at least two or more peptidases and, or of peptidase regulating proteins made manifest by a dietary overload of exorphin precursors such as by increased gut uptake.
“…Almost ten to arrive in the cardiovascular system after gastrointestinal digestion of milk or milk products in more than years later, Renlund and colleagues 82 for the first time succeeded in demonstrating by use of chemical negligible amounts-at least not in adult animals or humans; enzymatic degradation in the intestinal wall and physical methods one of these peptides, b Hcasomorphin, (1)(2)(3)(4)(5)(6)(7)(8) in the milk from a woman with and in the blood appear to prevent it. [88][89][90] The situation looks different in newborn animals, postpartum psychosis, i.e., under in vivo conditions. i.e., presumably also in the human neonate as well Pharmacological Characteristics of Synthetic b-Casomorphin Analogues.…”
“…Ces résultats ont permis d'affirmer l'existence non seulement de récepteurs des~-casomorphines du côté sereux de la muqueuse intestinale, mais ils accréditent aussi l'hypothèse selon laquelle il existerait un mécanisme de régulation dont une des facettes serait la dégradation transépithéliale des fJ-casomorphines naturelles. Mahé et al (1988) ont montré que cette dégradation était principalement l'oeuvre de la dipeptidylpeptidase IV. En effet, le blocage de l'activité de cette enzyme par le di-isopropylfluorophosphate (DFP) permettait à de la morphiceptine placée du côté luminal d'une chambre de Ussing de réduire le courant de court-circuit et de stimuler l'absorption des ions Nat et CI-.…”
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