Methionine Effects on Chronic Schizophrenics

Park, Lee C.; Baldessarini, Ross J.; Kety, Seymour S.

doi:10.1001/archpsyc.1965.01720340018003

Cited by 71 publications

(8 citation statements)

References 17 publications

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“…18 There is an extensive literature documenting impaired methionine metabolism in schizophrenia. Studies by Kety and his colleagues found that methionine supplementation could precipitate an acute psychotic episode in many schizophrenic patients, while it had no effect in normal individuals, 19,20 a finding which has been replicated many times (for a review see reference 21 ). Moreover, the rate of whole body methionine metabolism in people with schizophrenia (including untreated individuals) is reduced to less than one-third that of controls.…”

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confidence: 96%

D4 dopamine receptor-mediated phospholipid methylation and its implications for mental illnesses such as schizophrenia

et al. 1999

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Keywords: receptors; G protein-coupled; phospholipid methylation; methionine; folic acid; membrane fluidity; purines; de novo synthesis Schizophrenia is a complex psychiatric disorder affecting approximately 1% of the population worldwide with a typical onset between the late teens and midthirties, often in the absence of significant prodromal psychiatric symptoms.1 Decades of research have yielded many theories on the origin of schizophrenia, although none provides a satisfying mechanistic explanation. Logically, dysfunctional neurotransmission is the most widely held theory, and specific abnormalities involving dopaminergic, 2 glutamatergic, 3 GABAergic 4 and nicotinic cholinergic 5 signaling have been proposed. Of these, the 'Dopamine Hypothesis' is dominant, based largely on the recognized therapeutic efficacy of drugs which block D2-like dopamine receptors (ie D2, D3 and D4 receptors), although their specific mechanism of benefit and the importance of individual receptor subtypes remains unclear. The D4

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confidence: 96%

D4 dopamine receptor-mediated phospholipid methylation and its implications for mental illnesses such as schizophrenia

et al. 1999

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“…F. Linder on the occasion of his 65th birthday. genic amines or other transmitter substances (20,21,23) than to disorders in oxidative brain metabolism in schizophrenic reactions. Only a small number of measurements of cerebral blood flow (CBF), oxygen and glucose consumption of the brain in patients with schizophrenia have been performed, mostly about 20 years ago.…”

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confidence: 99%

Blood Flow and Oxidative Metabolism of the Brain in Patients with Schizophrenia

Hoyer¹,

Oesterreich²

1975

Psychopathology

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55 patients with schizophrenia were divided into three groups according to the clinical symptoms: (1) productive schizophrenias, i.e. patients with hallucinations, catatonic excitation and stupor; (2) paranoia and schizophrenia simplex, and (3) non-productive schizophrenias, i.e. patients with schizophrenic defects and hebephrenia. Total cerebral blood flow (CBF) and the rates of cerebral oxygen, carbon dioxide, glucose and lactate metabolism were investigated. Patients with productive schizophrenias displayed a significant increase in CBF (to an average of 101.4 ml/l00 g min), CMR oxygen (to an average of 6.26 ml/100 g min) and CMR glucose (to an average of 12.11 mg/100 g min), i.e. CBF and CMR oxygen nearly doubled and CMR glucose more than doubled in comparison with normal findings. In patients with paranoia and schizophrenia simplex CBF and oxidative metabolism did not vary much and were within the normal range. Non-productive schizophrenias showed a significant decrease in CBF (to an average of 36.7 ml/100 g min), CMR oxygen (to an average of 2.20 ml/100 g min) and CMR glucose (to an average of 3.86 mg/100 g min) in comparison with both other groups of schizophrenias and the group of healthy young men. The results demonstrated variations in CBF and oxidative metabolism of the brain in patients with distinct types of schizophrenia. It was possible to find a correlation between the mental state of the psychosis on the one hand and CBF and metabolism on the other. The high CBF and metabolic rates of the brain in productive schizophrenias might be due to disturbances in the cerebral metabolism of biogenic amines.

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“…This clinical phenomenon has been confirmed in ten studies by several independent groups of investigators and it has not been, so far, contradicted by anyone (Pollin et al, 1961;Brune and Himwich, 1962a;Alexander et al, 1963;Berlet et al, 1965b;Haydu et al, 1965;Park et al, 1965;Kakimoto et al, 1967, Ananth et al, 1970Jus et al, 1970;Antun et al, 1971b; also see reviews by Wyatt et al, 1971 andCohen et al, 1974). In their review of the ten methionine loading studies, Cohen et al (1974) revealed that 62 of 107 (57.9%) chronic schizophrenic patients given methionine, alone or in combination with a MAOI, manifested one or more of the following: auditory Pollin et al (1961) observed that methionine loading alone (without MAOI) for 1 week did not produce any behavioral changes in 3 chronic schizophrenic patients.…”

Section: Methionine Loadingmentioning

confidence: 76%