Ulcerative colitis, a debilitating condition, has long been shrouded in mystery. Conventional wisdom pointed to immune system abnormalities as the root cause, but emerging evidence challenges these long-standing beliefs. Let’s delve into this groundbreaking revelation: the true origin of ulcerative colitis.
Auto Immune of Inflammatory?
Historically, the predominant theory surrounding ulcerative colitis suggested an immune system malfunction. Yet, there’s no concrete evidence to support this assumption. Recent studies have illuminated a compelling alternative theory: an excess of hydrogen peroxide, secreted by the cells lining the inner surface of the colon, is the key instigator of this condition.
Two critical studies corroborate this hypothesis. The first, published in GUT, proposes a “radical induction” theory. It posits that the initial event in ulcerative colitis is an increased generation of hydrogen peroxide from mitochondria, mainly within the colonic epithelial cells. This surge in hydrogen peroxide production subsequently triggers all pathogenic events that follow.
A second study in the American Journal of Physiology-Gastrointestinal and Liver Physiology extends this theory. It suggests that excessive hydrogen peroxide, generated initially in the epithelial cells, recruits other nonimmune cells, furthering its production and transmural diffusion, leading to neuromuscular dysfunction.
Why H2O2 ?
Now, where does this excess hydrogen peroxide come from? It’s a normal by-product of cellular metabolism. However, when produced in excess, it leaks from the colonic epithelial cells, acting as a powerful signal that attracts white blood cells (neutrophils) into the colon’s inner lining, causing inflammation and ulcerative colitis.
The treatment developed in light of this theory focuses on eliminating the excess hydrogen peroxide in the colon. When hydrogen peroxide ceases to attract white blood cells into the colon, the result is a significant reduction in ulcerative colitis symptoms.
Contrary to traditional approaches that focus on altering or suppressing the immune response, the hydrogen peroxide theory provides a new perspective. Treatment guidelines based on the immune system’s presumed role are not evidence-based and can lead to unnecessary complications. For instance, chronic immune suppression can mask the underlying buildup of genotoxic cellular hydrogen peroxide in the colon. This not only increases the prevalence of colonic cancer but also necessitates surgeries in up to 30% of patients due to treatment failure.
While expert consensus statements suggest immune abnormalities as the widely accepted cause of ulcerative colitis, they do not change the fact that there is no substantial evidence supporting this notion. In fact, expert opinions hold the lowest quality of evidence, ranking lower than case studies and mechanistic studies.
In summary, individuals with ulcerative colitis do not exhibit immune system abnormalities as the root cause. Instead, excess hydrogen peroxide production by the colonic epithelium takes center stage. Treatment strategies aimed at restoring hydrogen peroxide levels to normal have led to significant relief and healing. It’s time to reevaluate the decades-long pursuit of an immune system anomaly as the cause of ulcerative colitis.
The Treatment of Ulcerative Colitis by Detoxing H2O2 from Intestional Membrane Tissue.
This groundbreaking discovery opens a new chapter in understanding and treating ulcerative colitis, offering hope to patients and their families. However, as established organizations remain resistant to this paradigm shift, the onus lies with the patients themselves. Joining forces to form a research organization that is open to new ideas may be the key to finally curing this chronic condition.
In the end, science will be the ultimate judge of these theories. What remains highly concerning is the lack of interest and failure of established organizations to explore new possibilities that might lead to a cure for ulcerative colitis. It’s time for a fresh perspective on this devastating condition.