Are fat and sugar just as detrimental in old age?

Aging and poor nutrition are independent risk factors for the development of chronic disease. When young animals are given diets high in fat or sugar, they exhibit hallmarks of aging like mitochondrial dysfunction and inflammation, and also develop a greater risk for age-related disease. The same mitochondrial dysfunction and inflammation that progress with aging may also further predispose older individuals to dietary insults by fat and sugar. The purpose of this work is to review the most recent studies that address the impact of fat and sugar consumption on hallmarks of aging (mitochondrial dysfunction and inflammation). Findings from these studies show that obesogenic, high-fat diets can exacerbate age-related disease and hallmarks of aging in young animals, but high-fat diets that are non-obesogenic may play a beneficial role in old age. In contrast, high-sugar diets do not require an obesogenic effect to induce mitochondrial dysfunction or inflammation in young rodents. Currently, there is a lack of experimental studies addressing the impact of sugar in the context of aging, even though empirical evidence points to the detrimental effect of sugar in aging by contributing to a variety of age-related diseases. Fig. 1 Mitochondrial dysfunction and altered cellular communication (e.g. inflammation) progress with advancing age and increase the risk for age-related disease (ARD). Given the physiological changes that occur with age, the impact of high-fat (HFD) and high-sugar diets (HSD) may differ in later and earlier stages of life. HFD can promote the development of hallmarks of aging in young animals and can also exacerbate the risk for ARD when consumed at an old age. However, non-obesogenic high-fat diets may also reduce the risk for ARD in old age by acting on these hallmarks of aging. On the other hand, HSD promotes mitochondrial dysfunction and inflammation without necessarily inducing weight gain in young animals. Empirical evidence points to sugar as a major contributor to age-related disease and more experimental studies are needed to clarify whether aged individuals are more susceptible to its effects.