For many decades, sugars have been the dietary constituents receiving the most attention in relation to their effects on dental caries. Frequently, however, there is little relationship between the amount of sugar in a food and its ability to induce caries. Therefore, it is clear that constituents in the diet can influence the ability of plaque to lower the pH of sugar solutions. For instance, replacing sugar in foods with xylitol, sorbitol, saccharin, or aspartame may lead to a reduction in the incidence of dental caries. All these sugar substitutes are non-cariogenic, and some may possess cariostatic properties. The presence of arginine-rich proteins in the diet may provide a ready source of this amino acid, which is the substrate for the arginine deiminase pathway which can result in a rapid elevation of plaque pH values. Proline can act as an acceptor for protons from lactate in the Stickland reaction. This is a major but much-neglected metabolic pathway in dental plaque. The presence of fat in experimental diets has been shown to affect their cariogenicity. The effects have been ascribed to enhanced clearance of sugars from the mouth. It is also conceivable that several fatty acids express a potent antibacterial effect. The presence of calcium and phosphorus has been shown to influence the cariogenicity of foods; the effect, however, is restricted to the food containing the minerals. Evidence suggests that pyridoxine (vitamin B6) may exert a cariostatic effect by enhancing decarboxylation activity in dental plaque. It is clear that sugar alone is not the sole determinant of whether food is cariogenic. Furthermore, myriad substances may hinder or enhance the caries-promoting properties of sugars in the diet.