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Naturopathic Medicine and the Prevention and Treatment of Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Gluten consumption may not only contribute to inflammation in the arteries, but may lead to inflammation in the intestines as well. In a landmark study of The Lancet, Dr. Alessio Fasano discovered an intestinal protein called zonulin elevated in people with celiac disease. In the small intestine, regardless of if someone has celiac or non-celiac gluten sensitivity, zonulin induces tight junction disassembly, which leads to an increase in intestinal permeability.19 In other words, gluten consumption can cause leaky gut syndrome. The intestines become inflamed, and “leaky” contents of the intestinal tract including bacterium and undigested food proteins are allowed to pass through the intestinal epithelium into the bloodstream. Chronically, this can lead to an overactivation of the immune system that may set the stage for auto-immune disease and other chronic inflammatory conditions.20 Surprisingly, even individuals who do not have celiac disease are susceptible to zonulin elevations. Gliadin, one of the proteins found in gluten, can trigger zonulin release temporarily regardless of whether someone has celiac disease or not.21 Therefore, all of us are susceptible to the increased intestinal permeability due to gluten consumption.
Bacterial Infections in Atherosclerosis
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Emil Kozarov, Ann Progulske-Fox
Importantly, the abundant evidence accumulated so far points at infections (often of periodontium) as a contributing factor for CVD. Periodontitis provides an “open gate” to the circulation for entry of oral bacteria into the bloodstream, allowing them to activate the host inflammatory response in the direction of atherogenesis (i.e., atheroma formation, maturation, and exacerbation) (Reyes et al., 2013). Similarly, the “leaky gut” syndrome can deliver intestinal species to a new, systemic location, inducing inflammation (Figure 5.1 shows the multiple way the infections contribute to chronic inflammation, including atherogenesis).
Predictive Biomarkers in Personalized Laboratory Diagnoses and Best Practices Outcome Monitoring for Musculoskeletal Health
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
When routine wear-and-tear is not repaired, the integrity of the extracellular connective tissue scaffolding is impaired [38]. Increase in tissue permeability ensues, setting the stage for AI. This can be provoked by a variety of external or internal antigens perceived as foreign that preoccupy the immune system with excess defense burden [39]. Initially, this increase in tissue permeability results in the entry of larger plasma proteins and platelets, dendritic cells, and lymphocytes all seeking to induce repair, i.e., to “put things right” [40]. Fibromyalgia is a classic example. Leaky gut syndrome is another common clinical term for incomplete repair. Too often, the lack of essential nutrients and/or excess defense burdens on the immune system prevent repair of cells from being completed [41].
Mechanisms and Methods to Understand Depressive Symptoms
Published in Issues in Mental Health Nursing, 2022
Sameena F. Sheikh-Wu, Kathryn S. Gerber, Melissa D. Pinto, Charles A. Downs
Leaky-gut syndrome, increased permeability of intestinal mucosa, occurs in inflammatory bowel diseases (e.g., Crohn’s and celiac disease), gastrointestinal tract cancer, and associated cancer treatment (e.g., radiation). The leaky gut result is the movement of bacteria, toxins, and small molecules into the bloodstream, which then induces a systemic inflammatory response (Obrenovich, 2018). A healthy gut epithelium is a tight barrier in which transport proteins regulate macromolecules concentrations, and concentrations of bacteria, toxins, and small molecules are tightly regulated. The translocation of bacteria, toxins, and small molecules induce a peripheral pro-inflammatory response, including increased levels of cytokines, such as IL-1, IL-1β, interferon-α, C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) (Cooper et al., 2018; Miller et al., 2013; Swardfager et al., 2016).
Lack of Efficacy of the Neutropenic Diet in Decreasing Infections among Cancer Patients: A Systematic Review
Published in Nutrition and Cancer, 2020
Venkataraghavan Ramamoorthy, Muni Rubens, Sandeep Appunni, Anshul Saxena, Peter McGranaghan, Emir Veledar, Ana Viamonte-Ros, Nancy Shehadeh, Adeel Kaiser, Rupesh Kotecha
An open question is whether preventing leaky gut syndrome to limit microbial transit may be more effective than reducing the overall microbial content of food. This question has merit since gut permeability remains a hallmark pathway for bacteremia (5), with most cases of sepsis arising from commensal organisms already on or within the body (10). Preclinical data suggests that increasing dietary fat may enhance the barrier properties of gastrointestinal mucus (35). Butyrate, a short-chain fatty acid, promotes colonocyte proliferation and healing through growth factor induction (36). Butyrate is a major energy source for enterocytes and maintains epithelial integrity for antimicrobial defense through epigenetic effects on DNA methylation and histone acetylation (37). Phase III data in colitis suggests that phosphatidylcholine, a major constituent of biological membranes, and readily available in egg yolks, improves intestinal injury and may be beneficial in neutropenia (38). Conversely, limitation of anti-nutrients that enhance intestinal permeability may also be advantageous for neutropenic patients. Gliadin, the main fraction of wheat gluten responsible for the intestinal damage in celiac disease, increases gut permeability to macromolecules (39). This impact on mucosal integrity is observable irrespective of the presence of autoimmunity.
Going gluten free in non-celiac autoimmune diseases: the missing ingredient
Published in Expert Review of Clinical Immunology, 2018
Aaron Lerner, Ajay Ramesh, Torsten Matthias
Several potential mechanisms can be envisioned for the beneficial place of the nutritional therapy, applying GFD in those non-celiac, celiac-associated Ads, or extra-intestinal manifestation of celiac disease [3–5,7,10]. Starting from the vast genetic background shared by many of those ADs, going through the evolutionary changes of the wheat with its increased gluten content and gluten itself become more immunogenic and toxic. The multiple systemic and cellular side effects of gluten described above and its intestinal permeability effect resulting in break of the functional integrity of the tight junction might represent additional autoimmune inducing mechanisms. In the intestinal lumen, gluten peptides are preferred substrates for post translational modification thus decreasing its tolerogenic properties. Noteworthy are the facts that gluten affects the microbiome and the microbiota/dysbiota ratio composition and diversity are characteristic to some of those ADs. The leaky gut syndrome, the plethora of the intestinal-originated pro-inflammatory immune cells and cytokines shared by those conditions, and the last decades increased consumption of deleterious industrial-processed food additives that might drive autoimmunity can add each one to progression of gluten-driven autoimmunogenesis.