"These caries ecological concepts have been confirmed by recent DNA- and RNA-based molecular studies that have uncovered an extraordinarily diverse microbial ecosystem, where S. mutans accounts for a very small fraction (0.1%–1.6%) of the bacterial community implicated in the caries process.[20]"
Note the sudden conversion of "implicated in the caries process" to "cause caries".
"In recent years, the use of second-generation sequencing and metagenomic techniques has uncovered an extraordinarily diverse ecosystem where S. mutans accounts only for 0.1% of the bacterial community in dental plaque and 0.7–1.6% in carious lesions[14,15]."
But, importantly, the citation in the McGill article doesn't much support the original claim, and this citation chain could easily have bottomed out in a completely different set of results which didn't happen to lend some (weak) evidentiary support to the high-level claim.
Also importantly, this article is committing the sin of figuring out some reasons why a treatment might not be perfectly effective in all cases, and implicitly deciding that justifies ignoring any non-total benefits (i.e. cases where S. Mutans would have been counterfactually responsible for causing caries, that could be prevented). Questions that would have been appropriate, but were apparently uninteresting:
"Does this intervention also happen to chase out other acid-producing bacteria that fulfill a similar ecological niche as S. Mutans?"
"What percentage of caries cases would be prevented by chasing out just S. Mutans with this intervention, while leaving other acid-producing bacteria untouched?"
Likely this is because answers to those questions would not really have changed the bottom line. That bottom line was written by the "unanswered" safety concerns (reasonable in the abstract, less obviously reasonable in this specific case). All of the listed safety concerns have evidence pointing in various directions. Very little of that evidence is listed, probably because it's not in a format that's legible to scientific institutions. The article does note, earlier on, "The toxicity of this Mutacin-1140 compound had not been tested. What would be the consequences of millions of bacteria in the mouth releasing this compound? The answer wasn’t clear, even though the archetypal compound in the family Mutacin-1140 belonged to was known to be very safe." This is obviously relevant evidence about the safety of Mutacin-1140. _How much_ evidence? Unasked, unanswered. (I have no idea how predictive the safety of other compounds in the same family is of another unstudied compound in that family, I'm not a biologist. But this is not an _unanswerable_ question.)
(Marginal conflict of interest: I know the Lumina founder socially. I have no financial interest in that venture or any of his other ventures. I have not taken Lumina myself.)
The safety concerns sound circular in an almost Kafkaesque manner. From what I can tell, a strain of the bacteria was found in the wild that created less acid and seemed to lead to less carries. So people thought it needed to be safer, so they instead created a genetically modified version of the bacteria. But now it couldn’t even be tested in the wild because the “safer” version had so many unknowns that even letting people experiment with it would be dangerous, since it could potentially escape into the general population and hurt people (possibly escape through activities like kissing, the article states). But the earlier strain has been out there spreading in the population for decades/centuries already.
Why not just let people experiment on their own with the original low acid bacteria if they want? It’s already there in the wild. You’re already “painting your teeth” with different bacteria when you kiss people, so why not at least let some people pick which naturally occurring bacteria they can expose themselves to instead of letting it happen by random chance?
A lot of the hype about Lumina seemed to be goofy, but the hand wringing over “painting your mouth with bacteria!” is just as bad if not worse.
> From what I can tell, a strain of the bacteria was found in the wild that created less acid and seemed to lead to less carries
I think you're confused about which changes to the bacteria were natural and which were engineered. A strain in the wild was discovered that produced a weak antibiotic that it had also developed a resistance to, but it still had the original metabolic pathway that produced lactic acid. Researches took that strain and genetically modified it to produce ethanol instead of lactic acid, and then relied on the natural antibiotic-related mutations to get this strain to replace common S. Mutans in the oral microbiomes of test subjects.
The useful non-acidic property of the strain is entirely artificially introduced. The natural mutation in the wild just allowed for outcompeting and replacing bacteria that lack it. There would be no benefit from personally experimenting with the natural non-engineered strains.
If that strain produces ethanol and can colonize the guts, then it has the potential to cause the auto-brewery syndrome. That a good reason to be careful!
But why did they decide that? It seems to be a pretty clear example of the perfect being the enemy of the good.
1. Better bacteria is found in the wild, it might be able to significantly reduce cavities. People could be randomly passing it to others through kissing, and no one is concerned about it since it doesn't seem to be harmful.
2. It’s not given to people for replacement therapy because (as the article states) people decided that a replacement therapy “needs to meet a number of criteria."
3. Except meeting that criteria makes people think the replacement isn’t safe and shouldn’t be tried.
The article is saying “of course we needed to add X characteristics to the bacteria, they were necessary in order for it to be a good replacement” and then goes on to say “of course people shouldn’t be using the bacteria with X characteristics, X characteristics might be dangerous.”
I tracked down the chain of citations here. The directly cited article (https://www.nature.com/articles/sj.bdj.2018.81) says the following:
"These caries ecological concepts have been confirmed by recent DNA- and RNA-based molecular studies that have uncovered an extraordinarily diverse microbial ecosystem, where S. mutans accounts for a very small fraction (0.1%–1.6%) of the bacterial community implicated in the caries process.[20]"
Note the sudden conversion of "implicated in the caries process" to "cause caries".
The next step in the citation chain is https://www.cell.com/trends/microbiology/abstract/S0966-842X....
"In recent years, the use of second-generation sequencing and metagenomic techniques has uncovered an extraordinarily diverse ecosystem where S. mutans accounts only for 0.1% of the bacterial community in dental plaque and 0.7–1.6% in carious lesions[14,15]."
Now the claim is merely one of prevalence!
The next steps in the citation chain, https://karger.com/cre/article-abstract/47/6/591/85901/A-Tis... and https://journals.plos.org/plosone/article?id=10.1371/journal..., do seem to plausibly provide evidence that there are other mouth-colonizing bacteria which would perform the same function as S. Mutans when it comes to causing caries, such that fully eliminating S. Mutans probably wouldn't eliminate caries entirely.
But, importantly, the citation in the McGill article doesn't much support the original claim, and this citation chain could easily have bottomed out in a completely different set of results which didn't happen to lend some (weak) evidentiary support to the high-level claim.
Also importantly, this article is committing the sin of figuring out some reasons why a treatment might not be perfectly effective in all cases, and implicitly deciding that justifies ignoring any non-total benefits (i.e. cases where S. Mutans would have been counterfactually responsible for causing caries, that could be prevented). Questions that would have been appropriate, but were apparently uninteresting:
"Does this intervention also happen to chase out other acid-producing bacteria that fulfill a similar ecological niche as S. Mutans?"
"What percentage of caries cases would be prevented by chasing out just S. Mutans with this intervention, while leaving other acid-producing bacteria untouched?"
Likely this is because answers to those questions would not really have changed the bottom line. That bottom line was written by the "unanswered" safety concerns (reasonable in the abstract, less obviously reasonable in this specific case). All of the listed safety concerns have evidence pointing in various directions. Very little of that evidence is listed, probably because it's not in a format that's legible to scientific institutions. The article does note, earlier on, "The toxicity of this Mutacin-1140 compound had not been tested. What would be the consequences of millions of bacteria in the mouth releasing this compound? The answer wasn’t clear, even though the archetypal compound in the family Mutacin-1140 belonged to was known to be very safe." This is obviously relevant evidence about the safety of Mutacin-1140. _How much_ evidence? Unasked, unanswered. (I have no idea how predictive the safety of other compounds in the same family is of another unstudied compound in that family, I'm not a biologist. But this is not an _unanswerable_ question.)
(Marginal conflict of interest: I know the Lumina founder socially. I have no financial interest in that venture or any of his other ventures. I have not taken Lumina myself.)