13th International Symposium of The Institute for Functional Medicine S 134 Managing Biotransformation: The Metabolic, Genomic, and Detoxification Balance Points Hyman Mark Hyman, MD, is editor in chief of Alternative Therapies in Health and Medicine, medical editor of Alternative Medicine, the Art and Science of Healthy Living, and the author of several books. He is also on the Board of Advisors and faculty of Food as Medicine, Center for Mind Body Medicine, Georgetown University School of Medicine, and on the Board of Directors and faculty of the Institute for Functional Medicine, as well as collaborating with the Harvard Medical School’s Division for Research and Education in Complementary and Integrative Medicine. Obesity is not a single clinical disorder. Obesity is a complex chronic illness resulting from the interplay among genetics, environment, and lifestyle. Emerging scientific concepts provide a new basis for understanding the multiple causes of obesity as well as the underlying mechanisms involved in weight dysregulation. While most obesity can be effectively treated for compliant patients, using a focused lifestyle intervention based on a whole-foods, low-glycemicload, phytonutrient-rich diet combined with exercise and stress management, there are patients who do not respond predictably to normally successful interventions. A novel hypothesis linking environmental and internal toxins to disruptions of key mechanisms involved in weight regulation may explain treatment resistance in obesity. The key biological systems involved in obesity (and all diseases) that are altered by toxins are the neuro-endocrine-immune system, and mitochondrial energetics and redox status. Obesity provides an illustrative example of new navigational tools for diagnosis and therapy of chronic illness based on a paradigm that focuses not on disease or symptoms, but on cause and mechanism. This new framework and methodological approach can be applied to any chronic disease and provides an opportunity to integrate fragmentary scientific discoveries into a cohesive whole that creates a new clinical roadmap. This paper will explore a novel hypothesis that links obesity and toxins; we will discuss how one particular disease and the effect of one underlying cause can create a clinically relevant, holographic view of physiology. Alterations in thyroid metabolism and receptor function, central appetite dysregulation, inflammation’s influence on insulin and leptin resistance, impaired mitochondrial oxidative metabolism, and oxidative-stress-mediated effects via nuclear factor kappa B (NFκB) are all mechanisms by which toxins create alterations in metabolism and finely-tuned weight regulatory mechanisms. These systems are not discrete entities but systems in the true sense of the word – interlocking, interactive, dynamic, overlapping networks of biochemical and physiological informational spheres of functional relationships. Multiple patterns of genetic, physiological, and biochemical dysfunction are linked to obesity, including genetic polymorphisms, inflammation, mitochondrial dysfunction, oxidative stress, neuro-endocrine-immune dysfunction, especially autonomic disturbances involving the hypothalamic-pituitary-adrenal axis, nutritional deficiencies or excesses, and toxins. The nature, causes, and remediation of obesity can be seen through the prism of any one of these patterns. The focus here will be on how toxins mediate their influence through all these mechanisms.
Xanya Sofra Weiss
Xanya Sofra Weiss
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