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      Toxins, Toxicity, and Endotoxemia: A Historical and Clinical Perspective for Chiropractors

      review-article
      , DC, MS *
      Journal of Chiropractic Humanities
      National University of Health Sciences
      Detoxification, Toxicity, Toxins, Endotoxin, Endotoxemia

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          Abstract

          Objective

          The purpose of this commentary is to review the notion of toxicity in the context of chiropractic practice.

          Discussion

          The belief that body toxicity is the cause of disease has been promoted for thousands of years. Prior to the emergence of the chiropractic profession, the medical profession embraced the notion that the body becomes “toxic,” requiring detoxification interventions or surgery. The legacy of body toxicity within the chiropractic approach to patient care began with Daniel David Palmer. Today, some sectors within the medical and chiropractic professions continue to embrace the concept of body toxicity and the related need to engage in detoxifying treatments. The most common areas of focus for detoxification are the intestines and liver; however, the nature of the toxicity in these organs has yet to be defined or measured. In contrast, diet-induced systemic bacterial endotoxemia is a measureable state that is known to be promoted by a diet rich in sugar, flour, and refined oil. This suggests that bacterial endotoxin may be a candidate toxin to consider in the clinical context, as many common conditions, such as obesity, metabolic syndrome, diabetes, interstitial cystitis, depression, and migraine headache, are known to be promoted by endotoxemia.

          Conclusion

          A diet rich in refined sugar, flour, and oils may induce proinflammatory changes within intestinal microbiota that lead to systemic, low-grade endotoxemia, which is a common variety of “toxicity” that is measurable and worthy of research consideration. Introducing a diet to reduce endotoxemia, rather than attempting to target a specific organ, appears to be a rational clinical approach for addressing the issue of toxicity.

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          Most cited references77

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          Inflammation and cardiovascular disease mechanisms.

          The traditional view of atherosclerosis as a lipid storage disease crumbles in the face of extensive and growing evidence that inflammation participates centrally in all stages of this disease, from the initial lesion to the end-stage thrombotic complications. Investigators now appreciate that narrowing arteries do not necessarily presage myocardial infarction and that simply treating narrowed blood vessels does not prolong life. Although invasive approaches such as angioplasty and coronary artery bypass will remain necessary in some cases, we now understand that at least some of the cardiovascular benefits attributable to medical treatment and lifestyle modification (diet and physical activity) may result from reductions in inflammatory processes.
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            The effects of diet on inflammation: emphasis on the metabolic syndrome.

            Reducing the incidence of coronary heart disease with diet is possible. The main dietary strategies include adequate omega-3 fatty acids intake, reduction of saturated and trans-fats, and consumption of a diet high in fruits, vegetables, nuts, and whole grains and low in refined grains. Each of these strategies may be associated with lower generation of inflammation. This review examines the epidemiologic and clinical evidence concerning diet and inflammation. Dietary patterns high in refined starches, sugar, and saturated and trans-fatty acids, poor in natural antioxidants and fiber from fruits, vegetables, and whole grains, and poor in omega-3 fatty acids may cause an activation of the innate immune system, most likely by an excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. The whole diet approach seems particularly promising to reduce the inflammation associated with the metabolic syndrome. The choice of healthy sources of carbohydrate, fat, and protein, associated with regular physical activity and avoidance of smoking, is critical to fighting the war against chronic disease. Western dietary patterns warm up inflammation, while prudent dietary patterns cool it down.
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              Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

              Activation of the Toll-like receptor 4 (TLR4) complex, a receptor of the innate immune system, may underpin the pathophysiology of many human diseases, including asthma, cardiovascular disorder, diabetes, obesity, metabolic syndrome, autoimmune disorders, neuroinflammatory disorders, schizophrenia, bipolar disorder, autism, clinical depression, chronic fatigue syndrome, alcohol abuse, and toluene inhalation. TLRs are pattern recognition receptors that recognize damage-associated molecular patterns and pathogen-associated molecular patterns, including lipopolysaccharide (LPS) from gram-negative bacteria. Here we focus on the environmental factors, which are known to trigger TLR4, e.g., ozone, atmosphere particulate matter, long-lived reactive oxygen intermediate, pentachlorophenol, ionizing radiation, and toluene. Activation of the TLR4 pathways may cause chronic inflammation and increased production of reactive oxygen and nitrogen species (ROS/RNS) and oxidative and nitrosative stress and therefore TLR-related diseases. This implies that drugs or substances that modify these pathways may prevent or improve the abovementioned diseases. Here we review some of the most promising drugs and agents that have the potential to attenuate TLR-mediated inflammation, e.g., anti-LPS strategies that aim to neutralize LPS (synthetic anti-LPS peptides and recombinant factor C) and TLR4/MyD88 antagonists, including eritoran, CyP, EM-163, epigallocatechin-3-gallate, 6-shogaol, cinnamon extract, N-acetylcysteine, melatonin, and molecular hydrogen. The authors posit that activation of the TLR radical (ROS/RNS) cycle is a common pathway underpinning many “civilization” disorders and that targeting the TLR radical cycle may be an effective method to treat many inflammatory disorders.
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                Author and article information

                Contributors
                Journal
                J Chiropr Humanit
                J Chiropr Humanit
                Journal of Chiropractic Humanities
                National University of Health Sciences
                1556-3499
                December 2016
                03 September 2016
                : 23
                : 1
                : 68-76
                Affiliations
                National University of Health Sciences, Pinellas Park, FL
                Author notes
                [* ]Corresponding author: David R. Seaman, DC, MS, SPC-Health Education Center, 7200 66th St N, Pinellas Park, FL 33781. Tel.: +1-727-803-6129.SPC-Health Education Center7200 66th St NPinellas ParkFL33781 dseaman@ 123456nuhs.edu
                Article
                S1556-3499(16)30001-8
                10.1016/j.echu.2016.07.003
                5127911
                27920621
                b819436f-86b8-40e5-9207-eb30b9404fc4
                Copyright © 2016 by National University of Health Sciences.
                History
                : 30 March 2016
                : 29 June 2016
                : 26 July 2016
                Categories
                Original Article

                Complementary & Alternative medicine
                detoxification,toxicity,toxins,endotoxin,endotoxemia
                Complementary & Alternative medicine
                detoxification, toxicity, toxins, endotoxin, endotoxemia

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