Journal of Inflammatory Bowel Diseases & Disorders

Anti-inflammation refers to the ability of a medicine to help fight pain and unwanted or abnormal immune system reactions by reducing inflammation. Nonsteroidal Anti-inflammatory Drugs (NSAIDs) mitigate torment by balancing the cyclo Oxygenase (COX) enzyme. On its own, COX catalyst blends prostaglandins, making aggravation. In entire, the NSAIDs keep the prostaglandins from truly being orchestrated, diminishing or taking out the irritation and coming about torment.

Anti-microbial Resistance happens when microorganisms (like microscopic organisms, organisms, infections, and parasites) change and are yet ready to develop, in any event, when they are presented to antimicrobial prescriptions that are intended to execute or restrict their development.

The etiology of Inflammatory Bowel Diseases (IBD), which comprise predominantly of two types as Crohn's infection and ulcerative colitis, is at this point unclear. Nonetheless, increasingly more proof shows gut microflora has a significant influence in starting and keeping up the mucosal provocative reaction in IBD.

Inflammatory Bowel Disease (IBD) is a challenging medical condition that is driven by various genetic and environmental factors. Therapeutic opportunities for this disease remain limited due to the lack of in-depth understanding of the pathogenetic mechanisms and actionable targets driving the disease. Analysis of telomere dysfunctional mice and patients with genetic defects in telomere maintenance unexpectedly revealed phenotypes mirroring those observed in IBD. Molecular characterization of this model identified a pathway driven by telomere DNA damage-mediated activation of the ATM/cABL/YAP1 pathway, which directly regulates genes central to IBD pathogenesis and amenable to therapeutic intervention. This review summarizes the evidence correlating telomere dysfunction with IBD and colitis-associated cancer and proposes therapeutic opportunities for such inflammatory conditions targeting this newly identified pathway.

In the past 20 years, a gastro-intestinal complex has emerged that has been tentatively linked to Small Intestinal Bacterial Overgrowth (SIBO). The symptoms of constipation or diarrhea, bloating and distress, even to the level of cachexia have been presumed to be from bacterial overgrowth of methane producing Achaea bacteria including Methanobacteriales oralis and Methanobacteriales smithii. However, the SIBO symptom complex that was initially reported to be responsive to rifaximin and neomycin antibiotic therapy has subsequently become more and resistant leaving both patients and treating physicians in a quandary. The author was asked to consult on 18 patients whom had disruptive gastrointestinal symptoms, positive SIBO breathe test and repeated failure to respond to courses of primarily rifaximin therapy. These patients were overwhelming female and fell into the newly described field of Gender Specific Medicine (GSM). The biomarker for decreased bioavailable testosterone is the Free Androgen Index (FAI) in both sexes. Serum dysregulation included the gambit of hormonal assays: hypothyroidism, Hashimoto’s thyroiditis, menopause, male hypogonadism, adrenal fatigue and low levels of vitamin D3 (Cholecalciferol). These patients had an unexpected high incidence of gastrointestinal autoimmunity including pernicious anemia, hyperchlorhydria per the Heidelberg test and autoimmune gastritis. Treatment was naturopathic, non-gonadal hormonal and when all else failed, in systemic anabolic hormone replacement, patient improvement did not reach the 75 percent threshold required in the study. Therefore, the protocol of mixed anabolic steroid replacement was initiated subsequently.