It is a deficiency of trehalase, the small intestine enzyme that splits trehalose into its two glucose units. Without enough of it the sugar is not absorbed, so it passes to the colon, ferments and draws water in, producing the same bloating, wind and diarrhoea that lactose does in lactose intolerance. The mechanism is closely analogous. It is rare in most populations but notably common among Greenlandic Inuit, where estimates run to roughly ten to fifteen per cent. The most common real world trigger is mushrooms, which are naturally high in trehalose.

A hypothesis was published in Nature in 2018 proposing that the wider use of dietary trehalose helped two hypervirulent Clostridioides difficile ribotypes become dominant, because those strains metabolise trehalose efficiently. It got a great deal of coverage. It has also been substantially challenged since, on the grounds that realistic dietary trehalose concentrations in the gut are far lower than the experiments used and that the timing of the ribotype spread does not line up neatly with trehalose adoption. The honest position is that this is a contested hypothesis rather than an established risk, and it is not a reason to avoid trehalose in food.

For structure rather than sweetness, since it is only about forty five per cent as sweet as sugar. Trehalose is exceptionally good at protecting cell membranes and proteins through freezing and drying, which is the same property that lets resurrection plants and tardigrades survive dehydration. In practice that means it keeps frozen desserts smooth, stops dried and freeze dried foods collapsing, protects the texture of frozen seafood and surimi, and reduces staling in baked goods. If you see it on a label it is almost always there as a texture stabiliser.