Effects of Methionine Loading on the Behavior of Schizophrenic Patients

Brune, Guenter G.; Himwich, Harold E.

doi:10.1097/00005053-196205000-00007

Cited by 110 publications

(22 citation statements)

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“…For example, methionine treatment was shown in the 60s to aggravate schizophrenia (Brune and Himwich, 1962; Israelstam et al, 1967). Similarly, there might be questions raised as to the impact of folate supplementation during pregnancy and beyond.…”

Section: Epigenetic Contributions To Mental Healthmentioning

confidence: 99%

Diet and the epigenetic (re)programming of phenotypic differences in behavior

2008

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Phenotypic diversity is shaped by both genetic and epigenetic mechanisms that program tissue specific patterns of gene expression. Cells, including neurons, undergo massive epigenetic reprogramming during development through modifications to chromatin structure, and by covalent modifications of the DNA through methylation. There is evidence that these changes are sensitive to environmental influences such as maternal behavior and diet, leading to sustained differences in phenotype. For example, natural variations in maternal behavior in the rat that influence stress reactivity in offspring induce long-term changes in gene expression, including in the glucocorticoid receptor, that are associated with altered histone acetylation, DNA methylation, and NGFI-A transcription factor binding. These effects can be reversed by early postnatal crossfostering, and by pharmacological manipulations in adulthood, including Trichostatin A (TSA) and L-methionine administration, that influence the epigenetic status of critical loci in the brain. Because levels of methionine are influenced by diet, these effects suggest that diet could contribute significantly to this behavioral plasticity. Recent data suggest that similar mechanisms could influence human behavior and mental health. Epidemiological data suggest indeed that dietary changes in methyl contents could affect DNA methylation and gene expression programming. Nutritional restriction during gestation could affect epigenetic programming in the brain. These findings provide evidence for a stable yet dynamic epigenome capable of regulating phenotypic plasticity through epigenetic programming.

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Section: Epigenetic Contributions To Mental Healthmentioning

confidence: 99%

Diet and the epigenetic (re)programming of phenotypic differences in behavior

2008

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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%

“…Furthermore, on the basis of the other symptomatology which was observed, the investigators, as a mie, found it difficult to decide whether they were observing a toxic psychosis, as suggested by Kakimoto et al (1967), an acute exacerbation of schizophrenic psycho pathology, as suggested by Antun et al (1971b), or a syndrome combining the features of both, as suggested by Brune and Himwich (1962a).…”

Section: Methionine Toxicitymentioning

confidence: 99%

Transmethylation Hypothesis of Schizophrenia: Methionine and Nicotinic Acid

Nestoros¹,

Ban²,

Lehmann³

1977

Int Pharmacopsychiatry

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“…Also the 'pseudostimulation' effect of tranquilliser withdrawal is not allowed for. Results obtained by Brune and H imwich [1962a] using betaine cannot be explained by the thiol group precursor hypothesis, since betaine, a methyl donor, is not a thiol group percursor.…”

Section: Mao Vs and The Feeding Of Methionine To Schizophrenicsmentioning

confidence: 86%