For ulcerative colitis: compensate for selenium deficiency!
Selenium deficiency is a common find in inflammatory bowel diseases. Recent studies emphasise that there is a benefit in selenium intake for these patients.
Why correcting this common deficiency can be important in IBD
- Selenium deficiency is more common in inflammatory bowel disease than in the general population and increases with disease activity.2
- In a controlled clinical trial of 100 patients, selenium supplementation as an adjunct to standard therapy led to remission and improved quality of life in active mild to moderate IBD.1
- According to current understanding, selenium can promote mucosal healing by immunomodulation, support the antioxidant system and probably contribute to an increase in protective intestinal bacteria.2
Standard therapy plus selenium significantly better than standard therapy alone in study
In a double-blind, randomised clinical trial, 50 ulcerative colitis patients received selenium supplementation (as selenomethionine, 200 µg/day) in addition to standard therapy, while 50 other patients received only standard therapy plus placebo.1
With selenium, disease activity and inflammation scores decreased significantly and the treated patients reported fewer symptoms. Specifically, after 10 weeks, SCCAI scores had decreased significantly (p < 0.001) in the selenium cohort. Clinical improvement (defined as a decrease of ≥ 3 from baseline) was seen in 38% of the selenium group (compared to only 6% on placebo), resulting in significantly improved quality of life. All patients in whom the disease went into remission (defined as SCCAI ≤ 2) were in the selenium cohort.
In addition, interleukin-17 concentrations decreased significantly with selenium. In contrast, there was no difference between the groups in terms of interleukin-10 levels.
How can the anti-inflammatory effects of selenium be explained?
Selenium is an essential micronutrient that is incorporated into proteins in the body. Selenoproteins are important for many functions, for example as thyroid hormones or antioxidant enzymes such as glutathione peroxidase.3 Selenium is needed for the biosynthesis of these enzymatically active proteins and thus contributes to the effective functioning of the antioxidant system and the immune defence.
Selenoproteins can inhibit inflammatory reactions and reduce oxidative stress. In animal models of UC, the anti-inflammatory properties of selenium can induce remission.2
A key feature of inflammatory bowel disease (IBD) is a change in the microbiome. Among other things, a study from Stanford documented a lack of protective bacterial taxa in patients with UC.4 Much of the research conducted in recent years indicates that beneficial bacteria could be the key to reversing the inflammatory cycle of IBD, as these produce anti-inflammatory substances.5 Selenium strengthens the protective microbiota, which indirectly supports treatment.2
Selenium may also help to prevent ulcerative colitis-associated colorectal cancer. Some studies suggest that selenium blocks important signalling pathways in tumour development that are described in this context.2 Further clinical studies would be desirable to better characterise the short- and long-term effects of selenium in active and inactive IBD.
- Khazdouz, M. et al. The effect of selenium supplementation on disease activity and immune-inflammatory biomarkers in patients with mild-to-moderate ulcerative colitis: a randomized, double-blind, placebo-controlled clinical trial. Eur J Nutr 62, 3125–3134 (2023).
- Ala, M. & Kheyri, Z. The rationale for selenium supplementation in inflammatory bowel disease: A mechanism-based point of view. Nutrition 85, 111153 (2021).
- [In German] "Stichwort - Selenoproteine und Selenosom." laborjournal.de/rubric/stichwort/stichwort/w_22_10.php.
- Bruce Goldman is a senior science writer in the Office of Communications Email him at. Stanford scientists link ulcerative colitis to missing gut microbes. News Center http://med.stanford.edu/news/all-news/2020/02/stanford-scientists-link-ulcerative-colitis-to-missing-gut-micro.html (2019).
- Chen, L. et al. NLRP12 attenuates colon inflammation by maintaining colonic microbial diversity and promoting protective commensal bacterial growth. Nat Immunol 18, 541–551 (2017).