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Melatonin’s Paradox: Study Reveals Contradictory Impact on Gut Inflammation in IBD, Highlighting Unforeseen Consequences

“The utilization of melatonin as a potential treatment for inflammatory bowel disease (IBD) has garnered interest due to its role in modulating immune response,” stated a recent study published in the journal Microorganisms. However, the study presented contradictory results regarding the effectiveness of melatonin in treating IBD.

In a mouse model of IBD, melatonin was found to exacerbate gut inflammation and delay recovery during remission. Surprisingly, these effects were attributed to changes in the composition of the gut microbiota. Dr. Cristina Ribeiro de Barros Cardoso, a professor at the University of Sao Paulo in Brazil and one of the study authors, cautioned against the assumption that melatonin is harmless, stating, “It’s a hormone and can help regulate sleep… but our study shows that people should be careful about taking hormone supplements.”

Dr. Shilpa Ravella, a gastroenterologist at Columbia University Medical Center, echoed this sentiment, emphasizing the need for caution when using long-term supplements for chronic diseases. She highlighted the potential unknown effects of seemingly harmless supplements, which are often inadequately regulated.

Inflammatory bowel disease is characterized by chronic inflammation in the gastrointestinal tract, encompassing conditions such as Crohn’s disease and ulcerative colitis. Individuals with IBD experience alterations in the diversity and abundance of gut bacteria, with harmful microorganisms increasing while beneficial ones decrease.

The gut microbiota play a crucial role in the development and maintenance of the intestinal immune system. Dysregulation of the gut microbiota in IBD contributes to an inflammatory environment and tissue damage in the digestive system. Although immunosuppressive drugs and anti-inflammatory antibodies are common treatments for IBD, some individuals do not respond to these therapies and may require surgery.

Given melatonin’s ability to modulate immune responses, researchers have investigated its potential as a treatment for IBD symptoms. Melatonin, primarily synthesized in the pineal gland, regulates the circadian rhythm and is often used as a sleep aid. However, it is also produced in specific cells in the intestines, suggesting its importance in the digestive tract.

While some preliminary studies suggest beneficial effects of low-dose and short-term melatonin use in IBD patients, there is evidence indicating that chronic melatonin use could worsen inflammation.

To explore the impact of melatonin on IBD progression and remission, researchers induced colitis in mice using dextran sulfate sodium (DSS). Melatonin administration during DSS treatment exacerbated colitis severity, increased inflammatory markers in the blood and intestines, and prolonged the recovery phase. Additionally, melatonin altered the composition of the gut microbiota, increasing certain bacterial species associated with inflammation and reducing those linked to intestinal health.

Notably, when the researchers depleted the gut microbiota with antibiotics before inducing colitis, remission occurred more rapidly, and systemic and gut inflammation decreased. These findings suggest that the adverse effects of melatonin on gut inflammation may be mediated by the gut microbiota.

Dr. Ravella stressed the limitations of the study, as it was conducted in mice and may not directly translate to humans. Furthermore, previous literature has suggested the potential benefits of melatonin in treating inflammation and intestinal diseases. She also highlighted the connection between sleep loss and increased inflammation, emphasizing melatonin’s primary use as a sleep regulator.

In summary, the study raises caution regarding the use of melatonin supplements for IBD treatment. While further research is needed to establish the implications in humans, it underscores the delicate interaction between hormones, immune function, and the gut microbiota in the context of IBD.