Carbohydrates can destroy elastin and collagen, the major structural molecules of the skin, through non-enzymatic glycation, covalent linking of sugars to proteins, and the subsequent production of AGEs, advanced glycation end products.

The known mechanism by which carbohydrates cause oxidative stress is the activation of mitochondrial oxidative metabolism of glucose, resulting in the production of reactive oxygen species (ROS). In this case, ROS is produced by various enzymes in the mitochondrial respiratory chain: xanthine oxidase, lipoxygenase, cyclooxygenase, nitric oxide synthase, and peroxidase.

Elevated glucose levels are known to cause dermal connective tissue disruption, but galactose has received less attention. Galactose (especially D-galactose or D-gal) is a more powerful saccharifying agent than glucose and can induce oxidative stress.

Although skin abnormalities have not been identified as clinical manifestations of galactosemia, irregular glycation of collagen has been detected in the bones of patients with galactosemia, and high D-gal concentrations can induce skin cytotoxicity and aging-like skin changes.