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    Nutritional Genetics Part 4: Diseases B
    Nutritional Genetics Part 4: Diseases B
    Nutritional Genetics Part 4: Diseases B
    Ebook137 pages1 hour

    Nutritional Genetics Part 4: Diseases B

    By Ronald Steriti

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    About this ebook

    Nutritional Genetics is a very brief review of nutrition and genetics with a summary the published research, primarily from PubMed.
    Part 1 is an introduction, beginning with DNA damage and repair, nutrigenomics, nutrigenetics and epigenetics, genetic testing. It also contains sections on vitamins and nutrients and metabolism. Part 2 describes nutritional genetics lab tests.
    Parts 3 to 6 have sections on diseases. Part 3 includes Eyes, Ears, Respiratory, Cardiology, and Vascular diseases. Part 4 includes Gastrointestinal, Liver and Gallbladder, Pancreas, Thyroid, Urology, Gynecology, Obstetrics, and Men. Part 5 includes Neurology, Dermatology and Immunology. Part 6 includes Musculoskeletal, Hematology, Oncology, Psychiatry and Miscellaneous.

    Nutritional Genetics 4 - Diseases B

    Gastrointestinal
    1. Aphthous Stomatitis
    2. Celiac Disease
    3. Crohn’s Disease
    4. Gastritis
    5. Helicobacter pylori
    6. Ulcerative Colitis

    Liver and Gallbladder
    7. Cirrhosis of the Liver
    8. Fatty Liver (Steatosis)
    9. Gallstones (Cholelithiasis)
    10. Hepatitis, Autoimmune
    11. Hepatitis, Viral
    12. Wilson's Disease

    Pancreas
    13. Diabetes Type 1
    14. Diabetes Type 2
    15. Insulin Resistance

    Thyroid
    16. Grave’s Disease
    17. Hashimoto's Thyroiditis

    Urology
    18. Chronic Renal Failure

    Gynecology
    19. Cervical Dysplasia
    20. Endometriosis
    21. Menopause
    22. Polycystic Ovary Syndrome
    23. Postmenopausal
    24. Postmenopausal Osteoporosis
    25. Premenstrual Dysphoric Disorder

    Obstetrics
    26. Gestational Diabetes
    27. Miscarriage (Early Pregnancy Loss)
    28. Preeclampsia
    29. Pregnancy-Associated Hypertension
    30. Recurrent Pregnancy Loss

    Men
    31. Benign Prostatic Hyperplasia (BPH)
    32. Erectile Dysfunction
    33. Gynecomastia, Male
    34. Infertility, Male

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 23, 2016
    ISBN9781310592454
    Nutritional Genetics Part 4: Diseases B
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Book preview

      Nutritional Genetics Part 4 - Ronald Steriti

      Chapter 1. Aphthous Stomatitis

      MTHFR (C677T, A1298C)

      The study included 188 patients affected by RAS and 200 healthy controls. The genotype and allele frequencies of C677T mutation showed statistically significant differences between RAS patients and controls (p = 0.002 and p = 0.0004, respectively). After stratifying RAS patients according to clinical characteristics of oral ulcers, a significant association was observed between C677T mutation and number of oral ulcers of RAS patients (p = 0.006). A high association between MTHFR gene C677T mutation and RAS was observed in the present study. Also number of oral ulcers was found to be associated with MTHFR C677T mutation in RAS patients. (Kalkan et al., 2014)

      Serotonin Transporter Gene (5-HTTPLPR)

      Sixty-nine consecutive subjects affected by minor and major forms of RAS and 70 healthy volunteers were genotyped at 5-HTTLPR. The chi-square test was used for statistical analysis. A significant increase in the genotype of SS (P = 0.05) and of the allele S (P = 0.04) in the group of RAS were observed. RAS patients have a tendency to show polymorphism associated with anxiety-related traits. (Victoria et al., 2005)

      Interleukin-1β

      Sixty-two consecutive subjects affected by minor and major forms of RAS and 62 healthy volunteers were genotyped at IL-1beta (+3954). The chi-squared test was used for statistical analysis. A significant increase in the high production of IL-1beta genotype CT was observed in the group with RAS (P = 0.01). After stratifying RAS patients according to the mean number of lesions per episode, a significant difference was only observed between patients with >or=3 lesions in each episode and control. There is an increased frequency of polymorphism associated with high IL-1beta production in RAS patients. (Guimaraes et al., 2006)

      Interleukin-1β and TNF-alpha

      Sixty-four consecutive subjects affected by minor and major forms of RAS and 64 healthy volunteers were genotyped. A significant increase in the IL-1beta and TNF-alpha heterozygous genotypes were associated with an increased risk of RAS development (OR 2.40 and 3.07, respectively), in the multivariate model. Polymorphisms of high IL-1beta and TNF-alpha production were associated with an increased risk of RAS development. (Guimaraes et al., 2007)

      Interleukin-4 VNTR

      The study included 145 unrelated patients with a clinical diagnosis of RAS and 150 unrelated healthy controls. The distribution of genotype and allele frequencies of IL4 gene intron 3 VNTR polymorphism was statistically different between RAS patients and control group (p<0.0001 and p<0.0001, respectively) P2P2 genotype and P2 allele were also found to be protective with a lower risk for susceptibility to RAS (p<0.0001). The results of this study suggest that intron 3 VNTR polymorphism in the IL4 gene is associated with RAS susceptibility in Turkish population. (Kalkan et al., 2013)

      Interleukin-6 572G>C and 174G>C

      184 RAS patients and 150 healthy controls were included in the study. The genotype frequencies of -572G>C polymorphism showed statistically significant differences between RAS patients and controls (p = 0.01). Frequencies of GG + GC genotypes and G allele of -572G>C polymorphism were found higher in RAS patients (p = 0.0001, OR 10.8, 95 % CI 2.79-70.5; p = 0.0008, OR 2.06, 95 % CI 1.35-3.17, respectively). The genotype frequencies of -174G>C polymorphism also showed statistically significant differences between RAS patients and controls (p < 0.0001). Frequencies of GG genotype and G allele of -174G>C polymorphism were found higher in RAS patients (p < 0.0001, OR 4.87, 95 % CI 3.06-7.85; p < 0.0001, OR 3.82, 95 % CI 2.64-5.59, respectively). GG-GG combined genotype and G-G haplotype of -174G>C to -572G>C loci were also significantly higher in RAS patients (p < 0.0001 and p = 1.5 x 10(-8), respectively). After stratifying clinical and demographical characteristics of RAS patients according to IL-6 gene polymorphisms, an association was observed between family history of RAS and -174G>C polymorphism (p = 0.011). Susceptibility effects of both IL-6 gene -572G>C and -174G>C polymorphisms for RAS were observed. (Karakus et al., 2014)

      Nitric Oxide Synthase (NOS)

      Eighty-three Jordanian recurrent aphthous stomatitis patients and 83 age, gender and ethnically matched controls were genotyped for three NOS2 single-nucleotide polymorphisms, rs10459953, rs1060822 and rs2297518. Chi-squared analysis was used to compare the allele frequencies and genotypes. RESULTS: There was a significant association between recurrent aphthous stomatitis and inheritance of single-nucleotide polymorphism rs2297518 (P = 0.006). Although no direct association was demonstrated between rs10459953 or rs1060822 and recurrent aphthous stomatitis, a strong linkage disequilibrium was identified between rs1060822 and rs2297518. Inheritence of a NOS2 single-nucleotide polymorphism rs2297518 is associated with increased risk of recurrent aphthous stomatitis in a Jordanian population. (Karasneh et al., 2011)

      References

      Guimaraes, A. L., et al. (2006), ‘Association of interleukin-1beta polymorphism with recurrent aphthous stomatitis in Brazilian individuals’, Oral Dis, 12 (6), 580-83. PubMedID: 17054771

      Guimaraes, A. L., et al. (2007), ‘Investigation of functional gene polymorphisms IL-1beta, IL-6, IL-10 and TNF-alpha in individuals with recurrent aphthous stomatitis’, Arch Oral Biol, 52 (3), 268-72. PubMedID: 17052682

      Kalkan, G., et al. (2013), ‘Association between interleukin 4 gene intron 3 VNTR polymorphism and recurrent aphthous stomatitis in a cohort of Turkish patients’, Gene, 527 (1), 207-10. PubMedID: 23756192

      Kalkan, G., N. Karakus, and S. Yigit (2014), ‘Association of MTHFR gene C677T mutation with recurrent aphthous stomatitis and number of oral ulcers’, Clin Oral Investig, 18 (2), 437-41. PubMedID: 23665953

      Karakus, N., et al. (2014), ‘Effects of interleukin (IL)-6 gene polymorphisms on recurrent aphthous stomatitis’, Arch Dermatol Res, 306 (2), 173-80. PubMedID: 23982631

      Karasneh, J. A., et al. (2011), ‘Association between recurrent aphthous stomatitis and inheritance of a single-nucleotide polymorphism of the NOS2 gene encoding inducible nitric oxide synthase’, J Oral Pathol Med, 40 (9), 715-20. PubMedID: 21481004

      Victoria, J. M., et al. (2005), ‘Serotonin transporter gene polymorphism (5-HTTLPR) in patients with recurrent aphthous stomatitis’, J Oral Pathol Med, 34 (8), 494-97. PubMedID: 16091117

      Chapter 2. Celiac Disease

      HLA Genotyping

      HLA-DQ2 protein encoded by HLA-DQA1*05 and DQB1*02 alleles is found in 90-95% of CD patients. All of the remaining patients carry HLA-DQ8 protein encoded by HLA-DQA1*03 and DQB1*03:02 alleles. Specific HLA-DQ genotypes define different risk for CD incidence. Presence of susceptible HLA-DQ genotypes does not predict certain disease development, but their absence makes CD very unlikely, close to 100%. (Stanković et al., 2014)

      HLA testing is a practical and valuable test for most patients in whom initial evaluation for CD is inconclusive. A negative HLA result usually obviates the need for further celiac testing including endoscopy and gluten challenge. (Pallav et al., 2014)

      Plasminogen

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