It isn’t the sugar that damages your teeth

What actually causes a cavity

Sometimes our teeth feel furry after eating or drinking something sugary. That coating is plaque, a film of bacteria living on the tooth surface. Those bacteria feed on sugar, and the waste product they make from it is acid, mostly lactic acid.

It is the acid that does the damage. When the pH at the tooth surface falls far enough, the mineral in tooth enamel begins to dissolve. Repeated often enough, that becomes a cavity. The sugar itself is inert. It is the bacterial fermentation of sugar that produces the acid, and the acid that attacks the tooth.

Dr Coy’s conclusion follows directly from this. If the damage requires fermentation, then a sugar that mouth bacteria cannot ferment cannot cause it, however sweet it tastes. The useful question is not how sweet a sugar is, but whether the bacteria in the mouth have the enzymes to break it down.

This is the same reasoning that runs through the rest of his work. Fermentation, and the lactic acid it produces, is the thread connecting his research on teeth to his research on metabolism and on cancer cell behaviour. The mouth is simply the place where it is easiest to observe.

Three sugars, three reasons bacteria can’t ferment them

Each of the three works for a different chemical reason, which is what makes the argument checkable rather than merely plausible.

Isomaltulose:

The bond is wrong. Isomaltulose is made of exactly the same two sugars as table sugar, glucose and fructose. The only difference is how they are joined. In sucrose, that bond is cleaved very quickly by digestive enzymes. In isomaltulose it is a different linkage, and it is broken down slowly. Mouth bacteria have no enzyme that can cleave it at all, so they cannot get at the sugar inside, and they cannot produce acid from it. The same slow linkage is why isomaltulose releases glucose into the blood gradually rather than all at once.

Tagatose:

It passes through. Only a small part of tagatose is absorbed in the small intestine. Oral bacteria cannot convert it into the acids that attack enamel. Much of what is eaten reaches the colon, where gut bacteria including bifidobacteria ferment it and produce the short-chain fatty acid butyrate, a fuel source for the cells lining the intestine.

Galactose:

The pathway is closed. Galactose is not available to the fermentation metabolism that produces lactic acid, so the bacteria cannot make acid from it. Studies have looked at this directly. A 2020 study in Archives of Oral Biology reported that galactose regulates biofilm growth of oral streptococci, the bacteria responsible for plaque. An earlier German study, published in 1989, reported an anticaries effect for galactose. Dr Coy’s interest in it follows from both: a sugar that neither feeds the acid-producing bacteria nor supports the biofilm they live in.

What is formally authorised:

For two of these three sugars, the effect on tooth mineralisation is an authorised health claim in Great Britain. The authorised wording is fixed and must be used exactly as follows:

Consumption of foods/drinks containing tagatose or isomaltulose instead of other sugars contributes to the maintenance of tooth mineralisation.

This applies where the food or drink does not lower plaque pH below 5.7 during consumption and for up to 30 minutes afterwards.

Regulators elsewhere have reached the same conclusion independently. In 2003 the United States Food and Drug Administration issued a final rule authorising a health claim for tagatose and dental caries.