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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS Two primary arms of the immune system are the cytotoxic (Th-1) and humoral (Th-2) arms, where ‚Th‛ denotes thymus, an organ thought to contribute to educating the Tcells. The cytotoxic arm is involved in cell-to-cell defenses, where the immune cell acts directly against the pathogen. The humoral immune response is antibody mediated. The immune system is modulated in part by the endocrine system.(23) The balance of the cellular and humoral arms of the immune system is regulated in part by the hormonal environment with testosterone, DHT, DHEA and DHEA-S favoring a shift toward cellular (Th1 immunity) and glucocorticoids, estrogens, and catecholamines favoring a shift toward the humoral, or antibody producing, (Th2) arm of the immune system. Gut Biome and the Immune System 70-80% of the immune system cells are located around the gastrointestinal tract. There is evidence that the gut flora act to educate the immune system in self-recognition during the early years of life, as the gut environment changes in relationship to the foods that are eaten.(20) The balance of organisms in the gut therefore influence the immune activity within the gut, setting the stage for health or disease. The gut biome is very responsive to changes in diet, hormones, and stress and can shift in its balance of flora, the implications of which are not well understood.(22) This is an emerging science and is only included here to bring an awareness to the reader that there is a sophisticated and complex relationship between the organisms living within the gut, the human immune response, and the health of the human organism.(21) Evolution of sensitivity Food Sensitivity as an Immune Phenomena Consider that the development of food sensitivity is an evolutionary process; it is not likely a sudden or isolated event. The development of food sensitivity involves the exposure of the immune cells to food antigens, which requires the breakdown of multiple 76 2012 steps in human anatomy and physiology. You learned about these steps in isolation in the preceding paragraphs. Now we will tie these concepts together to help you understand how the process might develop. In order for food sensitivity to develop, the immune system must be exposed to food antigen. Food antigen is essentially poorly digested food. When optimal digestion has occurred, food has been broken down into its basic macronutrient components as it passes through the digestive tract. Furthermore, in order for the immune system to ‚see‛ a food antigen requires the gut barrier to be permeable to the contents of the digestive tract, a concept referred to as intestinal hyper-permeability. Poor digestion alone may not lead to the development of significant food sensitivity if there is adequate integrity of the enterocyte lining. In contrast, ensuring optimal digestion beginning with the choice of foods and how they are eaten may play a role in preventing or minimizing the development of food sensitivity if the patient has a problem with the barrier of the enterocyte layer, or a ‚leaky gut.‛ The bacterial environment within the gut could be a starting point for the establishment of food sensitivity as well. Gut floral imbalances and overgrowth (termed dysbiosis) can lead to a pro-inflammatory environment within the gut. This inflammatory state may increase the degree of intestinal permeability, setting the stage for prolonged exposure of the immune cells to the intestinal contents. Dysbiosis The human microbiota is undergoing intensive study. The Human Microbiota Project which began in 2007 as an extension of the Human Genome Project is intended to understand the role of human microbial communities in human health.(28) The gut biome alone contains up to 100 trillion organisms of approximately 500 to 1000 species. The term dysbiosis refers to an abnormal, or imbalanced, growth of organisms in the digestive tract that may lead to such issues as poor digestion, malabsorption, intestinal hyper-permeability, inflammation, and other problems in various systems of the body. Dysbiosis may be caused by the growth of a specific pathogen or the overgrowth or absence of a commensal organism. These organisms likely play a
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS very significant role in our health, the details of which will be determined over time. Some functions of the organisms which live in the human gut include synthesis of vitamins (such as B6 and Vit K), detoxification, and metabolization of fats. Given the tremendous number of species present within the gut, it is not clear what balance or ratio of certain species is optimally beneficial, or if this concept is even legitimate.(29) Certainly, there are organisms that act pathologically at a certain colony growth number; there may be organisms that are simply present and innocuous, and there may be organisms that act within the host in such a way that even small numbers can create imbalances that lead to symptoms and ultimately disease processes. Intestinal Permeability Understanding food sensitivity is only relevant if there is an impact on the health of the individual. Indeed, it is important to understand that food sensitivity has little to do with helping clients with symptoms such as diarrhea, bloating, and dyspepsia; rather, these symptoms are a reflection of an underlying inflammatory process, originating at the level of the gut, and being mediated by the immune system. This process can involve both the innate (nonspecific) and acquired (educated) arms of the immune system. The innate immune system is designed to recognize and destroy foreign invaders in a general way and does not require previous exposure to the pathogen or antigen. The acquired immune system responds based on its memory of previous exposure to a foreign pathogen. The endothelial cells and the integrity of the ‚tight junction‛ between them is responsible for providing the physical separation between the contents of the digestive tract and the immune cells.(30) It is known that a wide variety of conditions can cause a loss of tight junction control and allow macromolecules and intestinal flora entry into the body. A reduction in tight junction integrity is seen in acute stress, extreme exercise, sleep deprivation, and exposure to gluten. It is likely that some degree of intestinal permeability is necessary to establish food sensitivity, as this would 77 2012 be the predominate mechanism to expose the immune system to food antigen. Gluten can trigger hyper-permeability Is Gluten sensitivity the same as Celiac Disease? Much media and healthcare attention has focused on celiac disease and sensitivity to gluten, therefore healthcare providers and patients have a higher level of awareness regarding this issue. The following is a brief overview of celiac disease and gluten sensitivity; please see the extensive work of Alessio Fasano, MD for in-depth research on the topic. Although there is overlap between celiac disease and gluten sensitivity, it is important to understand that current thinking places them as two distinctly different entities, both with clinical implications.(24) Celiac Disease and gluten sensitivity may have overlapping symptomatology, but the immune system likely deals with the environmental trigger gliadin, in a different way, due in part to the underlying physiologic response dictated by the individual’s genetics (25), gut flora and metabolic environment. What is Celiac Disease? Celiac disease is an autoimmune enteropathy triggered by gliadin. It is the only treatable autoimmune disease, responding to a gluten free diet.(26) The prevalence of Celiac Disease (CD) has doubled every 15 years since 1974 and it is now clear that Celiac Disease can develop at any age. The prevalence of CD in not-at-risk groups in the US was found to be 1:133; whereas the prevalence was 1:22 in first-degree relatives of CD patients.(25) There is evidence that in the CD individual, gliadin binds to and triggers a chemokine receptor on the gut enterocyte, ultimately causing the release of zonulin. Zonulin in turn interferes with the skeletal structure of the cell, leading to a weakening of the intercellular tight junctions.(23) This is referred to as intestinal hyper-permeability (‚leaky gut‛) and may allow passage of gliadin and other antigens access to the body’s innate immune system.(26) The innate immune cells initially respond to this foreign material, creating an inflammatory cascade. Over time,
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