Personalized Nutrition

1 - Cover [Seite 1]
2 - Contents [Seite 6]
3 - List of Contributors [Seite 8]
4 - Preface [Seite 12]
5 - Opportunities and Challenges in Nutrigenetics/Nutrigenomics and Health [Seite 22]
5.1 - Why Nutrigenetics/Nutrigenomics? [Seite 22]
5.2 - Opportunities [Seite 23]
5.3 - Challenges [Seite 25]
5.4 - How to Deal with the Challenges [Seite 27]
5.5 - References [Seite 27]
6 - Genome-Wide Association Studies and Diet [Seite 29]
6.1 - Monogenic Disorders and Complex Disease [Seite 30]
6.2 - Enabling Technologies in GWAS [Seite 31]
6.3 - GWAS: Why Are They Important? [Seite 31]
6.4 - Use of Gene Chips and GWAS Datasets in Personalized Health Predictions [Seite 32]
6.5 - Gene-Diet Interactions: Crohn's Disease [Seite 33]
6.6 - Acknowledgments [Seite 34]
6.7 - References [Seite 34]
7 - Copy Number Variation, Eicosapentaenoic Acid and Neurological Disorders [Seite 36]
7.1 - Ethyl-EPA [Seite 36]
7.2 - Huntington's Disease [Seite 37]
7.3 - Myalgic Encephalomyelitis [Seite 38]
7.4 - Conclusions [Seite 39]
7.5 - References [Seite 39]
8 - Nutrigenetics: A Tool to Provide Personalized Nutritional Therapy to the Obese [Seite 42]
8.1 - Observational Studies Evidencing Gene-Nutrient Interactions on Weight Gain [Seite 43]
8.2 - Intervention Studies Concerning Genetic Modification Effects on Weight Loss and Maintenance [Seite 46]
8.3 - Nutritional Studies Concerning Gene-Dependent Effects on Obesity-Related Manifestations [Seite 49]
8.4 - Conclusions [Seite 51]
8.5 - References [Seite 51]
9 - Xenobiotic Metabolizing Genes, Meat-Related Exposures, and Risk of Advanced Colorectal Adenoma [Seite 55]
9.1 - Materials and Methods [Seite 56]
9.2 - Results [Seite 57]
9.3 - Discussion [Seite 59]
9.4 - Acknowledgments [Seite 62]
9.5 - References [Seite 64]
10 - Strategies to Improve Detection of Hypertension Genes [Seite 67]
10.1 - Subject Selection [Seite 68]
10.2 - Selecting an Intervention [Seite 69]
10.3 - Study Time Windows [Seite 69]
10.4 - Tissue versus Central Phenotype Measurement [Seite 70]
10.5 - Intervention Studies [Seite 72]
10.6 - Improving Genome-Wide Association Results [Seite 73]
10.7 - Summary [Seite 74]
10.8 - Acknowledgments [Seite 74]
10.9 - References [Seite 75]
11 - Diet, Nutrition and Modulation of Genomic Expression in Fetal Origins of Adult Disease [Seite 77]
11.1 - Epidemiology [Seite 78]
11.2 - Experiments of Nature [Seite 79]
11.3 - Cancer Risk and Early Life [Seite 80]
11.4 - Growth and Development [Seite 81]
11.5 - Size and Body Composition at Birth [Seite 83]
11.6 - Developmental Plasticity [Seite 84]
11.7 - Animal Models [Seite 84]
11.8 - Epigenetics and Cancer [Seite 88]
11.9 - Conclusion [Seite 88]
11.10 - References [Seite 90]
12 - Choline: Clinical Nutrigenetic/Nutrigenomic Approaches for Identification of Functions and Dietary Requirements [Seite 94]
12.1 - Challenges for Clinical Nutrigenetics/Nutrigenomics [Seite 94]
12.2 - Other Considerations before Undertaking Clinical Nutrigenetics/Nutrigenomics [Seite 96]
12.3 - Prototype Experiment in Nutrigenetics/Nutrigenomics: Studies on Choline Deficiency [Seite 96]
12.4 - Choline Metabolism [Seite 96]
12.5 - Consequences of Dietary Choline Deficiency in Humans [Seite 97]
12.6 - Genetic Variation in Dietary Requirements for Choline [Seite 99]
12.7 - Choline and Neural Development [Seite 99]
12.8 - Choline Deficiency Alters Gene Expression via Epigenetic Mechanisms [Seite 100]
12.9 - Long-Lasting Consequences of Prenatal Choline Availability [Seite 100]
12.10 - Implications for Human Brain Development [Seite 101]
12.11 - Acknowledgments [Seite 101]
12.12 - References [Seite 101]
13 - Dietary Polyphenols, Deacetylases and Chromatin Remodeling in Inflammation [Seite 105]
13.1 - Polyphenols: An Overview [Seite 106]
13.2 - Modulation of Inflammation by Polyphenols [Seite 106]
13.3 - Deacetylases and Inflammation [Seite 108]
13.4 - Modulation of Deacetylases by Dietary Polyphenols [Seite 109]
13.5 - Conclusions [Seite 112]
13.6 - Acknowledgments [Seite 113]
13.7 - References [Seite 113]
14 - Dietary Manipulation of Histone Structure and Function [Seite 116]
14.1 - Use of Histone Deacetylase Inhibitors in Cancer Prevention [Seite 117]
14.2 - Dietary Inhibitors of Histone Deacetylases [Seite 118]
14.3 - Future Directions and Conclusions [Seite 120]
14.4 - Acknowledgments [Seite 121]
14.5 - References [Seite 122]
15 - Changes in Human Adipose Tissue Gene Expression during Diet-Induced Weight Loss [Seite 124]
15.1 - Obesity [Seite 124]
15.2 - Obesity Treatment [Seite 125]
15.3 - Adipose Tissue [Seite 125]
15.4 - Expression Profiling of Human Adipose Tissue during Diet-Induced Weight Loss [Seite 126]
15.5 - Serum Amyloid A Expression in Human Adipose Tissue and Association with Metabolic Disease [Seite 129]
15.6 - CIDE Family [Seite 130]
15.7 - A Local Activin B Signaling System in Adipose Tissue? [Seite 131]
15.8 - Conclusions [Seite 132]
15.9 - Acknowledgments [Seite 132]
15.10 - References [Seite 132]
16 - Toxicogenomics and Studies of Genomic Effects of Dietary Components [Seite 136]
16.1 - Reference Materials and Methods to Improve and Monitor Laboratory Proficiency in Microarray Assays [Seite 137]
16.2 - Identification of Factors that Increase Biological Noise in Gene Expression Studies [Seite 138]
16.3 - Phenotypic Anchoring to Supply a Biological Context for Interpreting Gene Expression Data [Seite 140]
16.4 - Reference Sets that Aid in the Interpretation of Adverse versus Adaptive Effects [Seite 141]
16.5 - Conclusions [Seite 142]
16.6 - Disclaimer [Seite 142]
16.7 - References [Seite 142]
17 - Dietary Methyl Deficiency, microRNA Expression and Susceptibility to Liver Carcinogenesis [Seite 144]
17.1 - Materials and Methods [Seite 145]
17.2 - Results and Discussion [Seite 146]
17.3 - Disclaimer [Seite 150]
17.4 - References [Seite 150]
18 - Redox Dysregulation and Oxidative Stress in Schizophrenia: Nutrigenetics as a Challenge in Psychiatric Disease Prevention [Seite 152]
18.1 - Redox/Glutathione Dysregulation Is a Vulnerability Factor in Schizophrenia [Seite 155]
18.2 - Pathophysiological Mechanisms [Seite 157]
18.3 - Developmental Animal Models with Redox Dysregulation [Seite 159]
18.4 - Therapeutic and Preventive Perspectives [Seite 162]
18.5 - Conclusion [Seite 167]
18.6 - Acknowledgments [Seite 167]
18.7 - References [Seite 167]
19 - Nutrigenomics and Agriculture: A Perspective [Seite 175]
19.1 - Genomic Prediction in Dairy Cows [Seite 175]
19.2 - Dietary Guidance [Seite 176]
19.3 - Discussion [Seite 178]
19.4 - References [Seite 180]
20 - Opportunities and Challenges in Nutrigenetics/Nutrigenomics: Building Industry-Academia Partnerships [Seite 181]
20.1 - The Challenge before Us [Seite 181]
20.2 - Accelerated Learning Curves [Seite 181]
20.3 - Professional Development and Building Networks [Seite 184]
20.4 - Sharing Science [Seite 184]
20.5 - Anatomy of a Partnership Model in Molecular Nutrition [Seite 184]
20.6 - Final Thoughts [Seite 188]
20.7 - Disclosures [Seite 188]
20.8 - References [Seite 189]
21 - Tailoring Foods to Match People's Genes in New Zealand: Opportunities for Collaboration [Seite 190]
21.1 - Role of Genetics in CD in New Zealand [Seite 190]
21.2 - Modeling Genetic Variation in Human CD Populations in vitro [Seite 192]
21.3 - Estimating the Role of Diet in CD [Seite 193]
21.4 - Animal Models of IBD [Seite 194]
21.5 - Double-Blind Placebo Controlled Human Clinical Trials [Seite 194]
21.6 - Data Management and Integration [Seite 195]
21.7 - Acknowledgments [Seite 195]
21.8 - References [Seite 195]
22 - Author Index [Seite 197]
23 - Subject Index [Seite 198]