As mentioned in the article, there's also studies where it may improve things. This particular one is a mouse model with induced DSS colitis, which I kind of wi

As mentioned in the article, there's also studies where it may improve things. This particular one is a mouse model with induced DSS colitis, which I kind of wish would be erased from methodology forever across literature. Not only is it mice rather than humans, but it is focused on replicating the end symptoms without mirroring the underlying causes. For example, what if IBD/Crohn's had to do with decreased gut melatonin production, leading to bacterial changes in the gut leading to autoimmune attacks leading to gut inflammation/ulcerations? Without replicating the casual factors, simply inducing ulcerations using a chemical agent without also replicating the autoimmune attack isn't very helpful. And anecdotally, my own disease is in complete remission with a surprisingly light medical treatment particularly after comparing dietary interventions inducing remission in two meta-analyses and finding the one key shared factor was reduction in processed sugars and introducing the same in my own diet. But that's with me taking 20mg of melatonin for a sleep disorder. And when my sleep is disturbed too much (as occurs if I don't have the melatonin to use), the resulting physical stress can sometimes induce small flares. In my own experience and in having looked at studies looking at melatonin use in human IBD patients, I'm fairly skeptical of the findings in the DSS mouse study are enough that anyone with sleep issues helped by melatonin should avoid it. Especially given there's a 2-fold increase in risk of disease activity in humans with poor sleep: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659204/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659204/