Lens ageing as an indicator of tissue damage associated with smoking and non-enzymatic glycation--a twin study

With ageing the long-lived proteins of the human lens undergo denaturation by non-enzymatic glycation. The denaturated proteins are fluorescent, a property that can be assessed in vivo by fluorometry. Our aim was to examine the relative contribution of hereditary and environmental effects on the accumulation of fluorescent compounds in the lens.

We examined 59 monozygotic and 55 dizygotic healthy twin pairs recruited from a population-based register of twins. Lens autofluorescence was measured on the undilated eye. All subjects underwent an OGTT and information on smoking habits was obtained. The genetic and environmental effects were estimated by structural equation modelling.

Lens autofluorescence was related to age (R(2)=53%), current glucose homeostasis (R(2)=10%) and smoking habits (R(2)=10%). After adjusting for these factors, interindividual variation in lens autofluorescence was statistically attributable to hereditary factors by approximately 28% as well as shared environment by 58% and non-shared environment by 14%. The hereditary factor seems not to be linked to a genetic predisposition to diabetes.

The correlation in lens fluorescence was greater in monozygotic twins than dizygotic twins indicating a genetically predetermined susceptibility for the accumulation of fluorophores in the lens, the relative importance of which was found to increase with age. Since fluorophore formation in the lens is attributable to non-enzymatic glycation our results support that genetic characteristics to some degree determine the susceptibility to glycation related diabetes complications and ageing processes.