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Objective: A functional interaction between Catechol-O-Methyltransferase (COMT) Val158Met and methylenetetrahydrofolate reductase (MTHFR) C677T has been shown to differentially affect cognition in patients with schizophrenia and healthy controls; the effect of COMT Val158Met x MTHFR interaction on resilience to stress in patients and controls remains to be examined. Method: A total of 98 patients with non-affective psychotic disorder and 118 controls were genotyped for MTHFR C677T, MTHFR A1298C, and COMTVal158Met. Daily life reactivity to stress, modelled as the effect of daily life stress on psychotic experiences, was measured using the experience sampling method (ESM). Results: The MTHFR C677T genotype moderated the interaction between COMT Val158Met genotype and stress in patients (P

Objective: This study tested the hypothesis that stress-reactivity may represent an intermediary phenotype underlying positive psychotic symptoms. It was examined whether: (i) stress-reactivity clusters within families of psychotic patients and (ii) stress-reactivity in relatives cosegregates with positive symptoms in patients. Method: The sample consisted of 40 patients and 47 siblings of these patients. The Experience Sampling Method (ESM - a structured diary technique) was used to measure stress-reactivity. Positive symptoms in patients were measured with the Comprehensive Assessment of Symptoms and History. Results: Within-trait, cross-sib associations showed a significant association between stress-reactivity in the patient and stress-reactivity in their siblings. Significant cross-trait, cross-sib associations were established showing a significant association between positive psychotic symptoms in the patient and stress-reactivity in the sibling. Conclusion: The findings show familial clustering of increased stress-reactivity, suggesting common aetiological influences, probably both genetic and environmental, underlying stress-reactivity in the siblings and patients. In addition, the results underscore the hypothesis that increased stress-reactivity is an unconfounded mechanism of risk underlying the positive symptoms of psychotic disorders.

Epidemiological research has shown that stressful environmental factors can play an aetiological role in the development of psychosis. However, the mechanism underlying the link between stress and psychosis is still not fully understood. In this article it is argued that the interaction between stressful environmental factors and epigenetic factors can bring about psychological and biological changes. Both types of change can be referred to as 'sensitisation'. The underlying mechanism of sensitisation can be interpreted on the one hand as cognitive misinterpretations (psychological sensitisation) and on the other hand as altered dopaminergic neurotransmission (biological sensitisation). Both of these deviations can facilitate the onset and persistence of psychotic symptoms. With the help of epidemiological research at psychometric level sensitisation can be quantified as (i) stress-induced persistence (indicating continuous sensitisation) of the normally transient expression of subclinical psychotic experiences during adolescence and early adulthood and as (ii) the increased risk of transition from gradually more persistent subclinical psychotic experiences to a clinical psychotic disorder.

Translational Developmental Psychiatry 5, e547 (2015). doi:10.1038/tp.2015.37, Published by Co-Action Publ., Stockholm [u.a.]

Although excessive exposure to stress is one of the hazards of modern life, it is unclear what effect exposure to stress has on the brain. This thesis focuses on measuring the effects stress has on dopaminergic neurotransmission in the brain. Subjects were exposed to experimental stress (a difficult calculation task) and the levels of daily life stress were measured. The main conclusion was that low levels of dopamine in the brain measured during exposure to stress predicted an increased sensitivity to stress and psychological symptoms caused by stress. High levels of dopamine had a protective effect against stress. This information can contribute to the development of pharmacological interventions for stress-related psychological symptoms.