Reduced life expectancy is one of the main concerns in the treatment of schizophrenia. The size of reduction is a consistent phenomenon in studies across the oceans. It varies from 16–32 years (USA, Colton & Manderscheid 2006), 22–25 years (Finland, Tiihonen 2009) and 15–20 years (Nordic European countries, Wahlbeck 2011). Increased prevalence of cardiovascular risk factors has been shown to contribute significantly to increased mortality in schizophrenia (Osby 2001). Diabetes mellitus, a major age dependent cardiovascular risk factors, has been found to be ten times as prevalent in the relative young age between 30–39 years (Cohen 2006).

Hundred years ago Kraepelin coined the diagnostic entity ‘dementia praecox’ for what is currently called schizophrenia. In parallel we hypothesized a somatic process - with the provisional name of ‘premature ageing’ - to occur that would explain both these two phenomena at once, the increased prevalence of the age dependent disease diabetes and the premature death in schizophrenia. Advanced glycated endproducts (AGEs), endproducts of the metabolisation of glucose, have been shown, in the general Dutch population, to increase age-dependently (Koetsier 2010). We hypothesized the concentration of AGEs in schizophrenia tocorrespond that found in 20 years older general population. We present the results of the measurements in the first fifty patients.

The consequence fo the finding could be twofold. First theorethically, a confirmation of the concept premature ageing. Second a rpactical issue, that patients with schizophrenia should be considered and treated not according to their calendar age but to according to their biological age.