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.