Abstract
Several lines of evidence suggest that schizophrenia, a severe mental illness characterized by delusions, hallucinations and thought disorder is associated with accelerated aging. The free radical (oxidative stress) theory of aging assumes that aging occurs as a result of damage to cell constituents and connective tissues by free radicals arising from oxygen-associated reactions. Schizophrenia has been associated with oxidative stress and chronic inflammation, both of which also appear to reciprocally induce each other in a positive feedback manner. The buildup of damaged macromolecules due to increased oxidative stress and failure of protein repair and maintenance systems is an indicator of aging both at the cellular and organismal level. When compared with age-matched healthy controls, schizophrenia patients have higher levels of markers of oxidative cellular damage such as protein carbonyls, products of lipid peroxidation and DNA hydroxylation. Potential confounders such as antipsychotic medication, smoking, socio-economic status and unhealthy lifestyle make it impossible to solely attribute the earlier onset of aging-related changes or oxidative stress to having a diagnosis of schizophrenia. Regardless of whether oxidative stress can be attributed solely to a diagnosis of schizophrenia or whether it is due to other factors associated with schizophrenia, the available evidence is in support of increased oxidative stress-induced cellular damage of macromolecules which may play a role in the phenomenon of accelerated aging presumed to be associated with schizophrenia.
Highlights
Several lines of evidence suggest that schizophrenia, a severe mental illness characterized by delusions, hallucinations and thought disorder is associated with accelerated aging
Schizophrenia, a severe mental illness characterized by delusions, hallucinations and thought disorder has been proposed to be associated with accelerated aging [4, 5], implying that whole-body agingrelated physiological and structural changes appear at an earlier age in schizophrenia patients compared with the general population
Metabolic abnormalities that are associated with aging, such as elevated pulse pressure, diabetes, low testosterone and low bone mass, are more prevalent in schizophrenia patients compared to age-matched controls [4, 14, 15, 16, 17] and these findings provide additional support for accelerated aging in schizophrenia
Summary
A number of findings in the schizophrenia literature support the hypothesis of accelerated aging in the disorder One such finding is the 10-25-year reduction in life expectancy (three-fold higher mortality rates) in schizophrenia patients when compared with the general population [9]. There is evidence to suggest an accelerated rate of aging-related brain volume reduction in patients with schizophrenia compared to healthy controls [12, 13]. Metabolic abnormalities that are associated with aging, such as elevated pulse pressure (the difference between systolic and diastolic blood pressure), diabetes, low testosterone and low bone mass, are more prevalent in schizophrenia patients compared to age-matched controls [4, 14, 15, 16, 17] and these findings provide additional support for accelerated aging in schizophrenia. The original view of Harman was probably too simplistic in that ROS/RNS may not just function stochastically (as assumed by Harman) but there is evidence indicating that ROS/RNS function as specific signaling molecules under both physiological and pathophysiological conditions and increased protein oxidative damage during the aging process maybe a targeted rather than a stochastic phenomenon [8, 35, 37]
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