We examined Dohan's hypothesis that schizophrenia is associated with the absorption of "exorphins" contained in gluten and casein. In addition, because of the work of Reichelt et al. (Reichelt, K.L., Saelid, G., Lindback, J. and Orbeck, H. (1986) Biological Psychiatry 21:1279-1290) and Rodriguez et al. (Rodriguez, Trav, A.L., Barreiro Marin, R, Galvez, Borrero, I.M., del Olmo Romero-Nieva, F. and Diaz Alvarez, A. (1994) Journal of Nervous and Mental Disease Aug; 182(8): 478-479), we carried out similar studies on a group of children with autism. In both syndromes we found similar patterns of peptide containing peaks (Ninhydrin positive) after molecular screening with Sephadex G-15. Immunoglobulin assay of IgA and IgG against gliadin and casein in serum was done. High titer IgG antibodies to gliadin were found in 87% of autistic and 86% of schizophrenic patients and high titer IgG antibodies to bovine casein were found in 90% of autistic and in 93% of schizophrenic patients. High titer IgA antibodies to gluten or casein were found in 30% of children with autism while in schizophrenic patients 86% had elevated IgA antibodies to gluten and 67% to casein; some normal children and adults have these antibodies but only in trace amounts. When schizophrenic patients were treated with dialysis or a gluten-casein free diet, or both (Cade, R., Wagemaker, H., Privette, R.M., Fregly, M., Rogers, J. and Orlando, J. (1990) Psychiatry: A World Prespective 1: 494-500) peptiduria and Brief Psychiatric Rating Scores fell while abnormal behavior diminished. A gluten-casein free diet was accompanied by improvement in 81% of autistic children within 3 months in most of the behavior categories. Our data provide support for the proposal that many patients with schizophrenia or autism suffer due to absorption of exorphins formed in the intestine from incomplete digestion of gluten and casein.
Abstract-The aim of the present study was to assess our hypothesis that the renin-angiotensin system (RAS) is responsible for cold-induced hypertension and cardiac hypertrophy. Two groups of wild-type (WT) mice and 2 groups of angiotensinogen gene knockout (Agt-KO) mice (6 per group) were used. After blood pressures (BP) of the four groups were measured 3 times at room temperature (25°C), 1 WT and 1 Agt-KO group were exposed to cold (5°C). The remaining groups were kept at 25°C. BP of the cold-exposed WT group increased significantly in 1 week of cold exposure and rose gradually to 168Ϯ7 mm Hg by week 5, whereas the BP of the Agt-KO group did not increase until week 3. The cold-induced increase in BP (⌬BP) was decreased significantly in the Agt-KO mice (19Ϯ3 mm Hg) compared with that of the WT mice (61Ϯ5 mm Hg) by 5 weeks of exposure to cold. Both WT and Agt-KO groups had cardiac hypertrophy in cold to the same extent. Agt-KO caused a significant increase in nitric oxide (NO) production. Thus, the RAS may inhibit NO formation. Chronic cold exposure decreased NO production, which may be mediated partially by activation of the RAS. These results strongly support that the RAS plays a critical role in the development of cold-induced hypertension but not cardiac hypertrophy. Moreover, the role of the RAS in cold-induced hypertension may be mediated in part by its inhibition on NO production. [3][4][5]7,8 frequently that cold winter weather makes hypertension more severe in hypertensive patients and is associated with an increased incidence of stroke and myocardial infarction. Normal human subjects have seasonal variations in blood pressure, with higher pressure in winter. 9 -13 Donaldson et al, 2 after studying the relation between outdoor temperature and blood pressure in men in central London between 1986 and 1992, reported that cold exposure of normal life in winter is sufficient to induce significant and prolonged hypertension in the general population. Exposure of the bare face to cold could induce a significant elevation of systolic and diastolic blood pressure in normotensive subjects dressed in cold-protective clothing. 14 Thus, low environmental temperature is an important factor contributing to the high incidence of hypertension and the high cardiovascular mortality in cold (north) regions.Previous studies [15][16][17][18][19][20][21][22] from this laboratory have shown that chronic exposure of rats to mild cold (5°C or 41°F) induces hypertension including cardiac hypertrophy. This is presently the only "naturally occurring" form of experimentally induced hypertension that is induced without surgical intervention, administration of large doses of drugs or hormones, or genetic manipulation. Thus, it is important to understand fully the mechanism contributing to this unique model of hypertension because it is naturally occurring. It is notable that the elevated blood pressure of rats after 7 weeks of exposure to cold does not return to precold exposure level during 4 weeks after removal from cold. 23 Thus, a...
Upregulation of brain AT1 receptors plays a role in the development of cold-induced hypertension.
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