In our societies, the proportions of elderly people and of obese individuals are increasing. Both factors are associated with high health-related costs. During obesity, many authors suggest that it is a high chronic intake of added sugars (HCIAS) that triggers the shift towards pathology. However, the majority of studies were performed in young subjects and only a few were interested in the interaction with the ageing process. Our purpose was to discuss the metabolic effects of HCIAS, compare with the effects of ageing, and evaluate how deleterious the combined action of HCIAS and ageing could be. This effect of HCIAS seems mediated by fructose, targeting the liver first, which may lead to all subsequent metabolic alterations. The first basic alterations induced by fructose are increased oxidative stress, protein glycation, inflammation, dyslipidaemia and insulin resistance. These alterations are also present during the ageing process, and are closely related to each other, one leading to the other. These basic alterations are also involved in more complex syndromes, which are also favoured by HCIAS, and present during ageing. These include non-alcoholic fatty liver disease, hypertension, neurodegenerative diseases, sarcopenia and osteoporosis. Cumulative effects of ageing and HCIAS have been seldom tested and may not always be strictly additive. Data also suggest that some of the metabolic alterations that are more prevalent during ageing could be related more with nutritional habits than to intrinsic ageing. In conclusion, it is clear that HCIAS interacts with the ageing process, accelerates the accumulation of metabolic alterations, and that it should be avoided.
Keywords: AGE advanced glycation endproducts; APP β-amyloid precursor protein; Aβ β-amyloid; CRP C-reactive protein; ChREBP carbohydrate-response element-binding protein; DNL de novo lipogenesis; HCIAS high chronic intake of added sugars; IR insulin receptor; IRS insulin receptor substrate; JNK c-Jun N-terminal kinase; NAFLD non-alcoholic fatty liver disease; ROS reactive oxygen species; SOD superoxide dismutase; SREBP sterol regulatory response element-binding protein; Ageing; Fructose; Inflammation; Insulin; Lipids; Liver; Oxidative stress.