The Relationships between Intestinal Permeability and Target Antibodies for a Spectrum of Autoimmune Diseases.

The worldwide prevalence of autoimmune diseases that have limited treatment options and preventive strategies is rapidly rising. There is growing evidence that the microbiota and the integrity of the intestinal barrier play a role in autoimmune diseases. The potential to evaluate intestinal barrier integrity for susceptible individuals and to determine whether restoring intestinal junction integrity impacts autoimmune diseases is an important area of research that requires further attention. In the intestinal permeability model of autoimmune diseases, the breakdown of the intestinal tight junction proteins (zonulin/occludin) allows bacteria, toxins, undigested dietary proteins, and other antigens to pass into the lumen, thereby increasing the number of inflammatory reactions and the activation of immune cells throughout the body. In this study, we investigate the relationship between zonulin/occludin antibodies, which are used to determine intestinal permeability, with autoantibodies used to diagnose autoimmunity. Our investigation may identify significant levels of circulating autoantibodies in human subjects with intestinal permeability compared to those without intestinal permeability. Furthermore, we identified that significant positive linear correlations between serum occludin/zonulin antibodies and circulating autoantibodies could be used to determine autoimmune diseases.

TENS and EMS Treatment for Diabetic Peripheral Neuropathy.

Context: Diabetic peripheral neuropathy (DPN) is a common complication occurring in both type 1 and type 2 diabetics. DPN may result in foot ulceration or lower-limb amputation. Objective: This case was undertaken to evaluate the efficacy of ReBuilder® therapy in the treatment of diabetic peripheral neuropathy. Methods: The case report is based on 3 selected patients, 2 males and 1 female. Each patient continued being managed by his/her primary care physician. No changes to allopathic medicine or diet were advised by our team. In addition to the allopathic therapy, we added ReBuilder® therapy, low level light therapy, vibration therapy and supplementation. The treatment period ranged from 17 to 20 weeks. Conclusion: The data presented here show promise for future, larger, controlled studies on the use of ReBuilder® devices for the treatment of diabetic peripheral neuropathy pain.

The Use of Personalized Functional Medicine in the Management of Type 2 Diabetes: A Single-Center Retrospective Interventional Pre-Post Study.

Background: There is a subgroup of patients with type 2 diabetes (T2D) in whom traditional treatment does not work well. Traditional management of T2D does not address the autoimmune component seen in a subgroup of patients with T2D. Primary Study Objective: We sought to evaluate the effectiveness of using a personalized functional medicine (PFM) approach to managing T2D. Methods/Design: Patient files from 2010 to 2015 were culled for patients previously diagnosed with T2D and their deidentified data regarding medications and T2D biomarker test results were compiled. A total of 35 patients were contacted for permission to use their deidentified data for the purposes of this article. Of 35 patients, 11 provided written consent. Setting: All participants had entered a single, private, integrative medicine clinic based in Maryland, USA. Participants: The patient group consisted of 5 women and 6 men; age 50 to 77 years. Each patient was taking an antidiabetic medication and had reached a plateau in recovery, or wanted to reduce their medication intake. Allopathic physicians were retained by patients undergoing PFM treatment. Intervention: After a thorough intake history was completed, necessary specimens were collected for analysis. Once test results were reviewed to identify nutrient deficiencies, intestinal dysbiosis, hormone imbalances, chemical burden and food immune reactivities, a personalized plan was developed for each individual patient. Each patient was retested appropriately during treatment. Treatment lasted from 2 to 10 months based on the patients' goals. Primary Outcome Measures: The effectiveness of the PFM approach was measured by the reduction in medication needed to manage T2D and improvement in T2D biomarkers. Results: At the end of PFM treatment, 6 patients were completely off T2D-related medications, and 5 had their doses reduced by 50%. Diabetes biomarkers improved: glucose decreased by an average of 78.36 mg/dL and hemoglobin A1c (HbA1c) was lowered by an average of 2.71%. Conclusion: In individuals not well-managed using traditional protocols, the PFM approach should be considered as an adjunct therapy.

Plant and human aquaporins: pathogenesis from gut to brain.

Corn, soybean, spinach leaf, and tomato aquaporins have been shown to share homology with human aquaporin-4, which is abundantly expressed by brain astrocytic endfeet. Thus, antibodies formed against the dietary aquaporins may potentially cross-react with brain aquaporin, leading to blood-brain barrier permeability and setting the stage for neuroautoimmunity and neurodegeneration. Here, we review the role of aquaporins in plants and humans in maintaining a healthy organism and mechanisms by which dietary aquaporins may contribute to neurological disorders. We include clinical data on the correlation between four real-world, dietary aquaporin and five neurological tissue antibodies. Our findings showed the percent of neurological tissue antibody production increased with the number of positive food aquaporins. Of the four food aquaporins, spinach was the most common reactive. Of the neurological tissues assessed, tubulin was the most common positive. Patients with antibody reactivity to dietary aquaporins may consider abstaining from the aquaporin-containing food in order to prevent neurological tissue damage.

The Gut-Brain Axis: Autoimmune and Neuroimmune Disorders.

No Abstract Available.

The onset of enhanced intestinal permeability and food sensitivity triggered by medication used in dental procedures: a case report.

Enhanced intestinal permeability and food sensitivity are two of the many proven causes of gastrointestinal disorders. This present report describes a woman with no previous gastrointestinal (GI) complaints, who underwent dental root canal, bone graft, and implant procedures. Postsurgery she experienced an allergic reaction to the combined medications. In the weeks that followed, she presented with multiple food intolerances. Four weeks after the final dental procedure, she was assessed serologically for mucosal immune function, salivary, and blood-gluten reactivity, intestinal permeability, and other food sensitivities. Compared to her test reports from two months prior to her first dental procedure, the patient's results showed high total secretory IgA (SIgA) and elevated salivary antibodies to alpha-gliadin, indicating abnormal mucosal immunity and loss of tolerance to gluten. Her serologic assessments revealed immunoglobulin G (IgG) and IgA antibodies to a range of wheat/gluten proteins and peptides, gut bacterial endotoxins and tight junction proteins. These test results indicate gut dysbiosis, enhanced intestinal permeability, systemic gluten-reactivity, and immune response to other dietary macromolecules. The present case suggests that patients who experience severe allergic or pseudoallergic reactions to medication should be assessed and monitored for gut dysfunction. If left untreated this could lead to autoimmune reactions to self tissues.

The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II.

Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. Here we describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. Through the recruitment of inflammatory infiltration neutrophils and the activation of matrix metalloproteinases, IL-17, a cytokine secreted by Th17 cells, contributes to blood-brain barrier breakdown and the subsequent attraction of macrophages and monocytes into the nervous system. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics, N-acetyl-cysteine, α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration.

The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part I.

CD4(+) effector cells, based on cytokine production, nuclear receptors and signaling pathways, have been categorized into four subsets. T-helper-1 cells produce IFN-γ, TNF-ß, lymphotoxin and IL-10; T-helper-2 cells produce IL-4, IL-5, IL-10, IL-13, IL-21 and IL-31; T-helper-3, or regulatory T-cells, produce IL-10, TGF-ß and IL-35; and the recently discovered T-helper-17 cell produces IL-17, IL-17A, IL-17F, IL-21, IL-26 and CCL20. By producing IL-17 and other signaling molecules, Th17 contributes to the pathogenesis of multiple autoimmune diseases including allergic inflammation, rheumatoid arthritis, autoimmune gastritis, inflammatory bowel disease, psoriasis and multiple sclerosis. In this article, we review the differential regulation of inflammation in different tissues with a major emphasis on enhancement of neuroinflammation by local production of IL-17 in the brain. By understanding the role of pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting Th17 and associated cytokine activities and signaling pathways to repair the intestinal and blood-brain barriers for their patients with autoimmunities, in particular, those with neuroinflammation and neurodegeneration.

The Role of Th17 in Neuroimmune Disorders: A Target for CAM Therapy. Part III.

Abundant research has mapped the inflammatory pathways leading to autoimmunity and neuroinflammatory disorders. The latest T helper to be identified, Th17, through its proinflammatory cytokine IL-17, plays a pathogenic role in many inflammatory conditions. Today, healthcare providers have a wealth of anti-inflammatory agents from which to choose. On one hand, pharmaceutical companies market brand-name drugs direct to the public and physicians. Medical botanical knowledge, on the other hand, has been passed down from generation to generation. The demands for natural healing therapies have brought corresponding clinical and laboratory research studies to elucidate the medicinal properties of alternative practices. With a variety of options, it can be difficult to pinpoint the proper anti-inflammatory agent for each case presented. In this review, the authors highlight a vast array of anti-inflammatory medicaments ranging from drugs to vitamins and from botanicals to innate molecules. This compilation may serve as a guide for complimentary and alternative healthcare providers who need to target neuroinflammation driven by Th17 and its inflammatory cytokine IL-17. By understanding the mechanisms of anti-inflammatory agents, CAM practitioners can tailor therapeutic interventions to fit the needs of the patient, thereby providing faster relief from inflammatory complaints.