Re: elevated oral cancer risk in ALDH-deficient populations—I asked our dentech advisor Dr. Justin Merritt about it, and he said approximately,

The acetaldehyde cancer risk they describe is legit for AFR populations. However, connecting that risk to Lumina-derived ethanol production is where the argument becomes suspect.

Their argument is that a cariogenic diet (ie, sugar-rich) might produce sufficient ethanol in the mouth from Lumina to trigger local acetaldehyde production that damages the local epithelium; that the admittedly small total amounts of ethanol produced by Lumina might yield high local concentrations of acetaldehyde in the adjacent epithelium.

Firstly, S. mutans does not colonize the epithelium. It lives almost exclusively on enamel. The total surface area in the mouth that it could realistically inhabit is exceptionally small, unless Lumina can live in places that S. mutans generally does not. Other oral strep species overwhelmingly occupy the majority of epithelial surfaces of the mouth, which effectively restricts S. mutans to the teeth. This means that any miniscule quantities of ethanol produced by Lumina on enamel would be diluted by saliva before ever reaching the epithelium. Likewise, if other coinhabiting microbiota convert Lumina ethanol to acetaldehyde, this too would be diluted by saliva before reaching the epithelium.

Or, if one argues that Lumina could float around in saliva and affect oral epithelium by producing ethanol, I think this would be a dubious argument as well. Firstly, bacteria in saliva are transient, as they get swallowed. Secondly, the numbers just don't add up in my mind. The saliva of people with extreme caries risk have 10^6 CFU/ml S. mutans detectable in saliva. At that concentration of bacteria (which is already quite rare), one could not even visibly detect turbidity in liquid. That shows how few S. mutans are present relative [to] the large volume of the mouth (i.e., it's a pretty small quantity of ethanol production potential and even this level would only persist when sugar levels are high in saliva). S. mutans generally can only achieve high concentrations of bacteria in those specific places you tend to see caries develop, like the pit and fissures of the molars or interproximally.

The article makes a logical argument, but I suspect the actual risk is nowhere even close to what they propose. There are a number of estimates and guesses included in the article that may not pan out in reality. Fundamentally, the risks associated with Lumina-derived ethanol is miniscule compared to normal ethanol consumption. Is it possible that one who abstains from alcohol consumption could still be at risk due to Lumina ethanol production? I suppose it is possible, but I find it extremely unlikely.

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