There is increasing evidence that consumption of polyphenol and phenolic-rich foods and beverages have the potential to reduce the risk of developing diabetes type 2, with coffee a dominant example according to epidemiological evidence. One of the proposed mechanisms of action is the inhibition of carbohydrate-digesting enzymes leading to attenuated post-prandial blood glucose concentrations, as exemplified by the anti-diabetic drug, acarbose. We determined if the phenolic, 5-caffeoylquinic acid, present in coffee, apples, potatoes, artichokes and prunes, for example, and also selected free phenolic acids (ferulic acid, caffeic acid and 3,4-dimethoxycinnamic acid), could inhibit human salivary α-amylase and rat intestinal maltase activities, digestive enzymes involved in the degradation of starch and malto-oligosaccharides. Using validated assays, we show that phenolic acids, both free and linked to quinic acid, are poor inhibitors of these enzymes, despite several publications that claim otherwise. 5-CQA inhibited human α-amylase only by <20% at 5 mM, with even less inhibition of rat intestinal maltase. The most effective inhibition was with 3,4-dimethoxycinnamic acid (plateau at maximum 32% inhibition of human α-amylase at 0.6 mM), but this compound is found in coffee in the free form only at very low concentrations. Espresso coffee contains the highest levels of 5-CQA among all commonly consumed foods and beverages with a typical concentration of ~5 mM, and much lower levels of free phenolic acids. We therefore conclude that inhibition of carbohydrate-digesting enzymes by chlorogenic or phenolic acids from any food or beverage is unlikely to be sufficient to modify post-prandial glycaemia, and so is unlikely to be the mechanism by which chlorogenic acid-rich foods and beverages such as coffee can reduce the risk of developing type 2 diabetes.