There is preliminary but biologically plausible evidence that sugar accelerates skin ageing through glycation, particularly with chronically elevated blood sugar levels. The mechanism is well described, but evidence from controlled experiments in healthy people is limited. In practical terms, this means that managing blood sugar levels and limiting heavily heat-processed foods are the most well-supported points of action, even though the exact benefit for the skin of healthy people has not yet been established.
Sugar accelerates skin ageing through a chemical process called glycation. In this process, glucose and fructose react spontaneously with proteins in the skin, particularly collagen and elastin. This produces advanced glycation end products, abbreviated as AGEs. These AGEs cross-link collagen fibres together, after which the body can barely repair them. The longer blood sugar levels remain elevated, the faster this process proceeds. This mechanism is well described biologically and is considered probably causal.
The accumulation of AGEs in the skin is associated in multiple review studies with wrinkles, reduced elasticity and a dull, yellowish skin tone. In addition, elevated AGE levels are linked to poorer wound healing, a reduction in the mechanical load-bearing capacity of the skin, and abnormalities in the small blood vessels. Many of these functional findings come from research in people with diabetes, in whom AGEs are strongly elevated. Direct intervention data in healthy people, where someone eats less sugar and their skin subsequently improves, are largely absent.
Not only sugar-rich foods but also the method of preparation plays a role. Grilling, frying and roasting produce considerably more AGEs in food than boiling or steaming. Whether those dietary AGEs make a clinically relevant difference to the skin of healthy people has not yet been proven, but it is a little-known and potentially relevant factor. UV radiation amplifies the glycation process on top of the effect of high sugar levels, although the precise magnitude of that combined effect in humans has not been quantitatively established.
A laboratory study using human skin cells showed that high fructose levels activated ageing markers, inhibited cell growth and slowed wound healing. This research was funded by Estee Lauder, which calls for caution in interpreting the findings. Furthermore, it is cell culture research: the fructose concentrations used may not be comparable to what skin cells experience under normal dietary intake. This is therefore not evidence that a glass of soft drink directly ages your skin cells.
Research has also been conducted into substances that might counteract AGE formation or its effects. The compound dihydromyricetin (a flavonoid from certain plants) improved skin elasticity in rats and showed effects in cell culture, but human data are entirely absent. Plant-based compounds such as hesperidin and rhamnose inhibited enzymes that break down skin structure in laboratory research. Whether that protection is achievable through diet or skincare products, and at what dosage, cannot be determined on the basis of the available studies.
All claims are based on PMID 20620757, 36364850, 38564405, 27224842, 40649936, 40507131 and 36838716. The mechanistic basis (AGE formation) is well described biologically. The clinical translation to visible skin ageing in healthy people rests largely on associative review studies and diabetes research, not on intervention trials. The fructose cell culture study (PMID 40649936) was funded by Estee Lauder.