I mostly agree with this, but I think it’s also wrong in a couple of places.
Crohn’s disease is not a spondyloarthritis! (and neither is psoriasis, ulcerative colitis, or acute anterior uveitis). As the name suggests, spondyloarthritides are arthritides (i.e. diseases principally of joints—the ‘spondylo’ prefix points to joints between vertebrae); Crohn’s a disease of the GI tract.
I think this is just restating the hypothesis, that Crohn’s shares (most of) its pathophysiology with the spondyloarthritides… Which is a well-known open possibility. The incidence of Crohns is >10% in people with AS and vice versa. They share heredity, HLA-B27. Apparently 2⁄3 of those with AS also have silent gut signs [1].
Also, I think the following is off the mark:
Although these are imperfect, if the person behind the project doesn’t have credentials in a relevant field (bioinformatics rather than gastroenterology, say), and/or a fairly slender relevant publication record, and scant/no interest from recognised experts, these are also adverse indicators. (Remember the nobel-prize winner endorsed Vit C megadosing?)
Note that the author did manage to co-author his latest piece with an ophthalmologist/rheumatologist with a professorship in inflammation research and 20k cites.
Overall, the parts of the objection that I agree most with are i) that it seems very unlikely that one or two fungi would be implicated with all of these 14 various diseases, and that treating the fungus would cure the inflammatory disease (rather than the fungus just acting as an initial trigger), and ii) that there are mistakes, especially semantic ones, and especially on malassezia.org (as opposed to in the papers), with some of the medical science.
The interesting questions seems to me to be whether an overconfident-seeming author could nonetheless be correct about the minimal prediction that some antifungals would work well in at least Crohn’s disease. I don’t yet see why this is <1% likely.
I mostly agree with this, but I think it’s also wrong in a couple of places.
I think this is just restating the hypothesis, that Crohn’s shares (most of) its pathophysiology with the spondyloarthritides… Which is a well-known open possibility. The incidence of Crohns is >10% in people with AS and vice versa. They share heredity, HLA-B27. Apparently 2⁄3 of those with AS also have silent gut signs [1].
Also, I think the following is off the mark:
Note that the author did manage to co-author his latest piece with an ophthalmologist/rheumatologist with a professorship in inflammation research and 20k cites.
Overall, the parts of the objection that I agree most with are i) that it seems very unlikely that one or two fungi would be implicated with all of these 14 various diseases, and that treating the fungus would cure the inflammatory disease (rather than the fungus just acting as an initial trigger), and ii) that there are mistakes, especially semantic ones, and especially on malassezia.org (as opposed to in the papers), with some of the medical science.
The interesting questions seems to me to be whether an overconfident-seeming author could nonetheless be correct about the minimal prediction that some antifungals would work well in at least Crohn’s disease. I don’t yet see why this is <1% likely.
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996322/
2. https://www.ncbi.nlm.nih.gov/pubmed/29675414, https://en.wikipedia.org/wiki/James_T._Rosenbaum
Hi Ryan, Thanks for double checking Seke’s impact numbers. Could you help me draft the impact phrase, I’m afraid of getting it wrong again.