Professor Ronan McCarthy, at Brunel University of London’s Antimicrobial Innovations Center, and his team have found that saccharin shows surprising power to overcome antibiotic resistance:
“Saccharin breaks the walls of bacterial pathogens, causing them to distort and eventually burst, killing the bacteria. Crucially, this damage lets antibiotics slip inside, overwhelming their resistance systems.”
[…]
The international team found that saccharin both stops bacterial growth and disrupts DNA replication and stops the bacteria from forming biofilms—sticky, protective layers that help them survive antibiotics.
They also created a saccharin-loaded hydrogel wound dressing that, in tests, outperformed market-leading silver-based antimicrobial dressings currently used in hospitals.
“This is very exciting,” Prof McCarthy added. “Normally it takes billions of dollars and decades to develop a new antibiotic. But here we have a compound that’s already widely used, and it not only kills drug-resistant bacteria but also makes existing antibiotics more effective.
“Artificial sweeteners are found in many diet and sugar-free foods. We discovered that the same sweeteners you have with your coffee or in a ‘sugar-free’ drink could make some of the world’s most dangerous bacteria easier to treat.”
What does saccharin do to benign bacteria?
The paper says it’s apparently already well known that saccharine is not good for the gut microbiome:
It’s interesting to have another example of antibiotic resistance / biofilms, though.
I’ve wondered if biofilms, quorum sensing, and other complex microbial community dynamics — which are critical to their survival in difficult environments like hospitals — are the reason antibiotic resistance doesn’t become universal; perhaps antibiotics exist because they primarily damage or are involved in the community dynamics, and so bacteria are put on the horns of a dilemma if they try to become resistant to every antibiotic.
Gwern is correct; saccharin is mildly bad for gut bacteria, but usually not so bad as to generate noticeable symptoms unless coupled with antibiotics.
While it’s a lot more complicated than this, you can get a rough impression of why by just comparing the structure of with saccharin (bi-cyclic “gamma-lactam” with sulfur (as sulfone) at the alpha position) with the original “sulfa drugs” (sulfa = “sulfonamide”) and the penicillin-family antibiotics (bi-cyclic “beta-lactam” with sulfur at the beta position).
Saccharin is both a lactam and a sulfonamide and sulfur-containing lactams and things close in structure to sulfonamides in general tend to inhibit DHPS which doesn’t usually kill bacteria but makes it so they can’t grow or multiply and the numbers will end up shrinking as they expire.
Penicillin was discovered just slightly earlier than the sulfa drugs, but the big advantage of sulfa drugs is that they could be artificially chemically synthesized at quantity and relatively easily even with 1930s tech. While it’s technically possible to do a total synthesis of penicillin, it’s completely impractical compared to just having brewing giants vats of microorganisms making it for us, which is how it’s done to this day.