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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS enriched foods, such as, fermented vegetables (sauerkraute) and milks (kefirs) are used to improve the status of human microbiota. However, research has shown human microbiota are resilient and may be resistant to change with probiotic supplements having the smallest effect on global microbiota change (1%) followed by specific diet strategies (5%). The largest effect on microbiota composition in the human intestine is through microbial transplantation (up to 100%)[33]. Thus far, gut microbiota seem to be quite stable and are easily restored, so even the small effect of probiotic supplementation has not been shown to last long [34, 35]. Microbial transplantation has shown the greatest effect on restoring gut microbiota. With further research, microbial transplantation may become the therapy of choice to restore a healthy gut [36]. Celiac disease is a partially inherited, life-long intolerance to gluten. The disease was traditionally defined as a gastrointestinal malabsorption disorder but we know recognize that manifestations of the disease are highly variable [37]. It is most certainly an inflammatory-related disorder in which gliadins, toxic peptides in gluten, pass through the epithelial barrier of the intestine generating an immune response that cascades into an inflammatory reaction guided by CD4+T cells bound to HLA DQ2 and HLA DQ8 molecules on antigen presenting cells[38]. The major environmental factor in celiac disease, gluten, found in wheat, barley and rye; was identified 60 years ago when Dr. W.K. Dicke published a paper that described the improvement of symptoms in celiac children when wheat, rye and oat flour had limited availability in the diet, during World War II. Approximately 1% of the global population has received a celiac disease diagnosis (current estimates), for which positive serum antibodies and an intestinal biopsy indicative of villous atrophy are required. However, many celiacs remain undiagnosed; some of whom are likely to have silent disease in which gastrointestinal 18 symptoms are absent, or other less obvious manifestations; such as neurologic symptoms or dermatitis herpetiformis[38]. Alleles that comprise the HLA DQ2 and 8 phenotypes associated with celiac disease susceptibility were identified over 30 years ago; and celiac disease does not develop unless an individual possesses one of various combinations of these alleles. However, 40% of the population has these genetic markers, and the contribution of the HLA genes to the genetics of celiac disease is less than 50% [39]. The additional contribution to disease manifestation could be additional, unidentified gene x gene interactions or environmental interactions, such as excessive gluten intake over a prolonged period of time. Genome Wide Association Studies (GWAS) have been conducted to examine additional genetic contributors to disease susceptibility and manifestations. Data have been collected on thousands of celiac patients and controls to compare non-HLA SNP frequencies. Approximately 39 non-HLA celiac disease risk loci have been identified, including multiple genes of obvious immunological functioning [40]. Since individuals with celiac disease are at risk of developing other autoimmune diseases, there is a particular interest in genes shared by autoimmune diseases and celiac disease. Thirty one unique genetic loci have been identified of which 14 are shared between celiac disease and rheumatoid arthritis. These shared genes are also implicated in T cell antigen presentation[41]. It is a common misconception that we wake up one day and have a chronic disease. The body needs to go through a period of progressive dysfunction first, that will ultimately result in disease diagnosis if it is not rectified. For individuals with celiac disease, a life-long, gluten free diet can prevent the development of other auto-immunities, however, quality of life is lower, 2012
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS despite following a gluten free diet. Thus, it is important we address these issues earlier with better, more comprehensive testing and a greater understanding of some of the changes occurring at an earlier phase of an individual’s health trajectory. Large data sets of genomics, metabolomics, transcriptomics, proteomics, and nutrient biomarker data that crossover ethnicities and geographic regions are needed to account for natural differences in genotype prevalence and environmental influence in order to continue to see scientific progress in nutritional genomics research. Genome wide association studies (GWAS) that cross over continents have been conducted and more are in progress to account for this need. Additionally, researchers such as Jim Kaput are pushing for more international research nodes to participate in and harmonize research protocols to allow for ease of data sharing. The Human Variome Project (HVP) is a worldwide effort to identify all gene variations in the human genome associated with phenotypic variability and human disease risk. Kaput et al., 2010, proposed a collaboration between the HVP and the nutritional genomics research community to harmonize and systematize their research efforts to ensure crossbenefit of novel data and results [42]. Advances in systems biology and genomics research are increasing the feasibility to assess the mechanistic effects of micronutrients on metabolism. As a result, a central repository of micronutrient data has been developed for scientific researchers to submit and access data, that will aid in further harmonizing and advancing nutritional genomics research efforts [43]. The micronutrient project ensures the environmental impact of nutrition is accounted for consistently on an international level. In the near future, data access will change in order to meet the growing needs of nutritional genetics and systems biology research and may 19 be partially fueled by the wants and needs of individuals with chronic disease desiring the opportunity to get closer to an understanding of the root cause of their health issues. Enterprises, such as Patients Like Me (www.patientslikeme.com), the Personal Genome Project (www.personalgenomes.org) , and mandatory data collection in clinical practice, will become part of the health routine and experience for the researcher and the patient. Is systems biology, of which nutritional genomics is a part, forming a scientific bridge between Western medicine/nutrition and Ancient Eastern traditions? While it is early to formulate this opinion from the scientific literature, there is some evidence to suggest this is the precise direction we are heading. In Chinese medicine, rheumatoid arthritis (RA) fits into the Bi-syndrome grouping, meaning blockage or obstruction. The Bi-syndromes are caused by pathogenic factors categorized as heat, cold, dampness and wind; and are identified by patient inquiry, palpation, pulse and the tongue’s appearance. Since RA therapy in Western medicine can lack effectiveness with lots of individual variation present; it can be frustrating for the medical practitioner and the patient. Differences have been identified between RA Cold and Heat patients that can be defined through unique symptomatology (to Western medicine), gene expression and metabolic profiling. Heat patients with RA tend to exhibit more apoptosis, while Cold patients seem to exhibit a better response to biomedical combination therapy., This information will hopefully lead to more personalized therapy [44]. Additionally, common RA symptoms evaluated through Western medical practice (joint pain, swelling, and stiffness) do not contribute to a greater understanding of significant variation amongst patients. In order to categorize RA patients with traditional Chinese medicine Bisyndromes, significant symptoms include the following: panting, shortness of breath and aversion to cold to define the Cold syndrome; and 2012
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