The role of H2o2 Dysregulation in Ulcerative Colitis.

The role of H2o2 Dysregulation in Ulcerative Colitis.

Ulcerative colitis (UC), a form of inflammatory bowel disease, is a chronic condition causing inflammation in the gastrointestinal tract. It often strikes individuals in their late adolescence or early adulthood, resulting in a lifelong struggle with symptoms like abdominal pain and bloody diarrhea. The global prevalence of UC has been on the rise, affecting millions of people worldwide and incurring substantial financial burdens. Current treatments are primarily focused on modulating the immune response, yet they are not curative and often lead to the need for surgical intervention.


In 2005, a groundbreaking theory emerged, challenging the conventional wisdom about UC. This theory suggests that excess hydrogen peroxide (H2O2) produced by colonic epithelial cells within the large intestine initiates the inflammation characteristic of UC. Unlike the long-standing belief in immune system abnormalities, this theory paves the way for a fresh perspective on the condition.


The Role of Hydrogen Peroxide


In the new model, UC development is linked to the diffusion of excess H2O2 through the cell membrane into the extracellular space. H2O2 possesses unique characteristics that enable it to damage tight junctional proteins in the colonic epithelium, facilitating bacterial penetration. Simultaneously, it attracts white blood cells into the colonic epithelium, leading to inflammation and eventually UC.


Support for this theory comes from studies revealing significantly elevated H2O2 levels in the mucosal lining of the large intestine before inflammation sets in, implying its causal role in UC. The reduction of H2O2 has been demonstrated to completely heal colonic inflammation in a significant percentage of patients with refractory UC. Moreover, experiments with animal models have induced inflammation mimicking human UC by introducing H2O2 into the colon.


This new perspective simplifies UC treatment. Rather than the complex array of treatment guidelines based on location and severity of inflammation, focusing on the reduction of colonocyte H2O2 provides a more streamlined approach. It also simplifies diagnosis, allowing for quantitative measurements of mucosal H2O2.


Challenges of Current Treatments


The conventional approach to UC often relies on immunosuppressive or immunomodulating drugs such as biologics, which can lead to remission but may mask the underlying H2O2-related oxidative stress. Prolonged use of these drugs can result in oxidative DNA mutations and an increased risk of colorectal cancer.



After nearly four decades of unresponsive disease, one patient’s experience suggests that long-term complete mucosal healing and remission can be achieved through the reduction of colonic H2O2. The evidence strongly supports the idea that UC is primarily caused by an excess of colonocyte hydrogen peroxide due to oxidative stress. Therefore, treatments aimed at restoring colonic redox homeostasis by reducing H2O2 should be considered as a primary approach before resorting to long-term immunosuppression or immune modulation.


In light of this compelling evidence, it is essential to rethink UC treatment strategies and consider alternative approaches that offer patients a path to complete healing and remission. This new perspective provides a ray of hope for individuals battling UC, offering a fresh outlook on a condition that has long been a source of suffering and uncertainty.


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