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INTRODUCTION The human body orchestrates countless integrated physiological interactions every moment of its existence. These physiological responses occur due to cellular messengers such as hormones. When hormonal imbalances exist, physiology [...]

The most common cause of infertility in the United States today is polycystic ovary syndrome (PCOS). (1), (2) PCOS is also the most common female hormone disorder in menstruating women. [...]

Functional Endocrinology Philosophy In order to truly understand the philosophy of functional endocrinology, we must first compare and contrast functional endocrinology to standard pathological-centered models. Secondly, we must compare the [...]

Evidence continues to increase linking autoimmunity and other complex diseases to the chemicals commonly found in our environment. Bisphenol A (BPA) is a synthetic monomer used widely in many forms, from food containers to toys, medical products and many others. The potential for BPA to participate as a triggering agent for autoimmune diseases is likely due to its known immunological influences. The goal of this research was to determine if immune reactivity to BPA has any correlation with neurological antibodies. BPA binds to a target enzyme called protein disulfide isomerase (PDI). Myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) are neuronal antigens that are target sites for neuroinflammation and neuroautoimmunity. We determined the co-occurrence of anti-MBP and anti-MOG antibodies with antibodies made against BPA bound to human serum albumin in 100 healthy human subjects. Correlation between BPA to PDI, BPA to MOG, BPA to MBP, PDI to MBP and PDI to MOG were all highly statistically significant ( P < 0.0001). The outcome of our study suggests that immune reactivity to BPA-human serum albumin and PDI has a high degree of statistical significance with substantial correlation with both MBP and MOG antibody levels. This suggests that BPA may be a trigger for the production of antibodies against PDI, MBP and MOG. Immune reactivity to BPA bound to human tissue proteins may be a contributing factor to neurological autoimmune disorders. Further research is needed to determine the exact relationship of these antibodies with neuroautoimmunities. Copyright © 2016 The Authors Journal of Applied Toxicology Published by John Wiley & Sons Ltd. [ABSTRACT FROM AUTHOR]

In spite of numerous research efforts, the exact etiology of autoimmune diseases remains largely unknown. Genetics and environmental factors, including xenobiotics, are believed to be involved in the induction of autoimmune disease. Some environmental chemicals, acting as haptens, can bind to a high-molecular-weight carrier protein such as human serum albumin (HSA), causing the immune system to misidentify self-tissue as an invader and launch an immune response against it, leading to autoimmunity. This study aimed to examine the percentage of blood samples from healthy donors in which chemical agents mounted immune challenges and produced antibodies against HSA-bound chemicals. The levels of specific antibodies against 12 different chemicals bound to HSA were measured by ELISA in serum from 400 blood donors. We found that 10% (IgG) and 17% (IgM) of tested individuals showed significant antibody elevation against aflatoxin-HSA adduct. The percentage of elevation against the other 11 chemicals ranged from 8% to 22% (IgG) and 13% to 18% (IgM). Performance of serial dilution and inhibition of the chemical-antibody reaction by specific antigens but not by non-specific antigens were indicative of the specificity of these antibodies. Although we lack information about chemical exposure in the tested individuals, detection of antibodies against various protein adducts may indicate chronic exposure to these chemical haptens in about 20% of the tested individuals. Currently the pathological significance of these antibodies in human blood is still unclear, and this protein adduct formation could be one of the mechanisms by which environmental chemicals induce autoimmune reactivity in a significant percentage of the population. Copyright © 2014. The Authors. Journal of Applied Toxicology Published by John Wiley & Sons Ltd. [ABSTRACT FROM AUTHOR]

The article presents a study which discusses the significance of the evaluation of serotonin deficiency, brain neurotransmitter serotonin and compounds that enhances serotonin and brain functions. It mentions that the lack of the substance in the body is a very common neurotransmitter imbalance and affirms that serotonin is produced in the peripheral nervous system that is associated with gastrointestinal motility. It affirms that high levels of serotonin can be fatal and toxic.

The article discusses research on the physiological aspects of nitric oxide and the specific influences of 3 Nitric Oxide Synthase (NOS) isomers including Neuronal NOS (nNOS), Inducible NOS (iNOS), and Endothelial NOS (eNOS). Research findings regarding consumption of pre-exercise nitric products are reported. Arginine and caffeine are said to be problematic ingredients because they cause elevated levels of inflammation-promoting iNOS.

The incidence of autoimmunity is growing rapidly worldwide. Many epidemiological studies have found environmental factors, such as toxic chemicals, to be a key factor in this rapid progression. Many mechanisms that can cause immune dysregulation and autoimmune reactivity from toxic chemical exposure to subsets of individuals with genetic susceptibility in immune regulatory genes have been identified. In susceptible genotypes, toxic chemicals can induce epigenetic expressions, bind to immune and endocrine receptors throughout the body and promote immune dysregulation, bind to nucleic acids and promote anti-nuclear autoimmunity, deplete antioxidant reserves, promote immune barrier degradation, induce lymphocyte dysregulation, and alter normal antigen presenting responses. This paper reviews the specific immunological pathways involved with environmental toxins and autoimmunity exposure., Competing Interests: Conflicts of Interest The author declares no conflicts of interest involved with this manuscript., (Copyright © 2024 InnoVision Professional Media Inc.)

The incidence of autoimmunity is growing rapidly worldwide. Many epidemiological studies have found environmental factors, such as toxic chemicals (persistent organic pollutants, toxic metals, solvents, endocrine disruptors), to be a key factor in this rapid progression. Numerous mechanisms have been identified that can cause immune dysregulation and autoimmune reactivity from toxic chemical exposure to subsets of individuals who have genetic susceptibility in immune regulatory genes. In susceptible genotypes, toxic chemicals can induce epigenetic expressions, bind to immune and endocrine receptors throughout the body and promote immune dysregulation, bind to nucleic acids and promote anti-nuclear autoimmunity, deplete antioxidant reserves, promote immune barrier degradation, induce lymphocyte dysregulation, and alter normal antigen-presenting responses. This paper provides a detailed review of the specific immunological pathways involved with exposure to environmental toxins and autoimmunity., (Copyright © 2021 InnoVision Professional Media Inc.)

Aim: To evaluate the measurement of zonulin level and antibodies of zonulin and other tight junction proteins in the blood of controls and celiac disease patients., Methods: This study was conducted to assess the variability or stability of zonulin levels vs IgA and IgG antibodies against zonulin in blood samples from 18 controls at 0, 6, 24 and 30 h after blood draw. We also measured zonulin level as well as zonulin, occludin, vinculin, aquaporin 4 and glial fibrillary acidic protein antibodies in the sera of 30 patients with celiac disease and 30 controls using enzyme-linked immunosorbent assay methodology., Results: The serum zonulin level in 6 out of 18 subjects was low or < 2.8 ng/mL and was very close to the detection limit of the assay. The other 12 subjects had zonulin levels of > 2.8 ng/mL and showed significant fluctuation from sample to sample. Comparatively, zonulin antibody measured in all samples was highly stable and reproducible from sample to sample. Celiac disease patients showed zonulin levels with a mean of 8.5 ng/mL compared to 3.7 ng/mL in controls ( P < 0.0001). Elevation of zonulin level at 2SD above the mean was demonstrated in 37% of celiac disease patients, while antibodies against zonulin, occludin and other tight junction proteins was detected in up to 86% of patients with celiac disease., Conclusion: Due to its fluctuation, a single measurement of zonulin level is not recommended for assessment of intestinal barrier integrity. Measurement of IgG and IgA antibodies against zonulin, occludin, and other tight junction proteins is proposed for the evaluation of the loss of intestinal barrier integrity., Competing Interests: Conflict-of-interest statement: Dr. Aristo Vojdani is the CEO and technical director of Immunosciences Lab., Inc.

Traumatic brain injury (TBI) is a leading cause of disability worldwide. One commonly overlooked effect of TBI is the disruption of the brain-gut axis, leading to gastrointestinal dysfunction. The brain-gut axis consists of the cortical areas of the insular cortex, cingulate, and hypothalamus that have bidirectional communication with the visceral enteric nervous system through afferent and efferent projections into the pontine vagal complex and nucleus tractus solitarius. Communication with the brain also occurs through messenger signals from the gut's microbiota, involving gut peptides, cytokines, and lipopolysaccharides. Disruption of the brain-gut axis from TBI can lead to a chronic, inflammatory, vicious sequela, involving both the brain and the gastrointestinal system, with both neuroregulatory and neuroimmunological loops.