There is evidence that supports the existence of an altered co- metabolic pathway of methionine in inflammatory bowel disease (IBD) patients. For example, the fecal metagenome of ileal Crohn’s disease (CD) patients exhibits a significant increase in genes related to cysteine and methionine metabolism compared with that in healthy subjects.39 Additionally, fecal sulfur-containing compounds (such as MT, DMS, methyl propyl sulfide, and methyl-2-propenyl disulfide) are significantly lower in CD patients compared with that in healthy subjects, whereas H2S production is higher.40,41 Interestingly, Dawiskiba et al. reported that serum DMSO2 is significantly lower in IBD patients (24 UC and 19 CD patients) compared with that in healthy controls.42 It is therefore possible that these intestinal diseases are associated with both a disruption of microbial methionine degradation as well as the host detoxification pathways (discussed in Section 4.2) that reshape the sulfur-compound distribution in the host metabolic profile.