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    Nutritional Genetics Part 6: Diseases D
    Nutritional Genetics Part 6: Diseases D
    Nutritional Genetics Part 6: Diseases D
    Ebook129 pages1 hour

    Nutritional Genetics Part 6: Diseases D

    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 6 - Diseases D

    Musculoskeletal
    1. Ankylosing Spondylitis
    2. Fibromyalgia
    3. Gout
    4. Herniated Disc
    5. Osteoarthritis
    6. Osteoporosis
    7. Rheumatoid Arthritis
    8. Sarcopenia
    9. Sjögren Syndrome

    Hematology
    10. Hemochromatosis (Iron Overload)
    11. Iron Deficiency
    12. Platelets

    Oncology
    13. Bone Cancer
    14. Breast Cancer
    15. Colon Cancer
    16. Glioblastoma
    17. Leukemia, Acute
    18. Leukemia, Chronic
    19. Lymphoma
    20. Pancreatic Cancer
    21. Prostate Cancer
    22. Thyroid Cancer

    Psychiatry
    23. Attention Deficit Hyperactivity Disorder
    24. Anxiety
    25. Bipolar Affective Disorder
    26. Depression
    27. Post-Traumatic Stress Disorder
    28. Schizophrenia

    Miscellaneous
    29. Ageing
    30. Obesity

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 23, 2016
    ISBN9781310017056
    Nutritional Genetics Part 6: Diseases D
    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 6 - Ronald Steriti

      Chapter 1. Ankylosing Spondylitis

      MTHFR (C677T, A1298C)

      Fifty AS patients (mean age of 36.6 +/- 4.79 years) and 50 control subjects (36.34 +/- 4.72 years) were included in the study. Plasma homocysteine levels of AS patients and control group were also similar (14.26 +/- 9.96 vs. 11.81 +/- 5.53 mumol/L). Hyperhomocysteinemia was present in 11 subjects in patient group (22.0 %), while it was seen in 5 subjects in the control group (10.0 %). The MTHFR C677T genotype distribution was as follows: CC 31 (62 %), CT 14 (28 %), TT 5 (10 %) in AS patients. The mean carotid IMT values were also found to be similar between the groups. The most important factor influencing pHcy level was found as MTHFR 677TT genotype. We indicated no difference of atherosclerosis indices revealed by IMT values and pHcy levels AS patients and control subjects. But an association between MTHFR 677 gene polymorphism and pHcy levels was concluded, which may suggest that MTHFR 677 TT polymorphism may be a potential prognostic factor for cardiovascular disease in patients with AS. (Gecene et al., 2013)

      Vitamin D Receptor (VDR)

      In this study, 104 patients with AS (m/w 71/33, mean age 41+/-12 years) were investigated for their lumbar and femoral BMD by DEXA and in part by QCT measurements and compared to 54 healthy controls. In male AS patients, FokI genotypes were significantly associated with spinal but not with femoral BMD values ( P=0.01) as independent predictors of low BMD, which was also influenced by BMI, and inflammatory and pain indices. CRP and ESR values were also significantly associated with FokI genotypes. BMD in female patients showed no significant association with either FokI or BsmI genotypes of the VDR. This is the first evidence that the VDR gene may be involved in BMD differences, bone metabolism and inflammatory processes in ankylosing spondylitis. A possible interaction of the vitamin D system, cytokines and bone could define new diagnostic and therapeutic implications in ankylosing spondylitis. (Obermayer-Pietsch et al., 2003)

      References

      Gecene, M., et al. (2013), ‘Atherosclerosis in male patients with ankylosing spondylitis: the relation with methylenetetrahydrofolate reductase (C677T) gene polymorphism and plasma homocysteine levels’, Rheumatol Int, 33 (6), 1519-24. PubMedID: 23247802

      Obermayer-Pietsch, B. M., et al. (2003), ‘Vitamin D receptor initiation codon polymorphism, bone density and inflammatory activity of patients with ankylosing spondylitis’, Osteoporos Int, 14 (12), 995-1000. PubMedID: 14530911

      Chapter 2. Fibromyalgia

      MTHFR C677T and ACE

      This study included 200 FM patients and 190 healthy controls. There was a statistically significant relation between ACE polymorphism and FM (p<0.001, OR: 1.71, 95% CI: 1.28-2.27). However, this was not the case for ACE polymorphism and the clinical characteristics of the disease. There was also no statistically significant relation between MTHFR C677T mutation and FMS (p>0.05, OR: 1.20, 95% CI: 0.82-1.78), but dry eye and feeling of stiffness which are among the clinical characteristics of FMS were significantly related with MTHFR C677T mutation (p<0.05). (Inanir et al., 2015)

      Catechol-O-Methyl-Transferase (COMT)

      A meta-analysis revealed an association between fibromyalgia and the COMT Met/Met + Val/Met genotype in all study subjects (odds ratio (OR) 1.635, 95 % confidence interval (CI) 1.029-2.597, p = 0.037). (Lee et al., 2015)

      Another meta-analysis showed that the COMT gene val(158)met polymorphism was not associated with FM risk. (Zhang et al., 2014)

      The study included 379 FMS patients and 290 controls. The Met/Met genotype was significantly higher in FMS patients than healthy controls (p = 0.016). Pain sensitivity, measured by algometry, was statistically higher in patients with Met/Met genotype than the patients with Val/Val and Val/Met genotypes (p = 0.017). (Inanir et al., 2014)

      A total of 137 fibromyalgia patients were assessed and compared to 99 matched controls. Central sensitization (nociceptive flexion reflex <27 mA) was present in 95/134 (71%) patients. Among them, COMT p.Val158Met polymorphism displayed a significant linear genotype effect (P = .033), with the Met/Met (mean = 17.8 +/- 4.8 mA) and Val/Val (mean = 21.4 +/- 4.6 mA) subgroups at the opposite ends of the nociceptive flexion reflex threshold (Met/Met vs Val/Val P = .015) and the Val/Met subgroup (mean = 19 +/- 4.9 mA) in between (Val/Met vs Val/Val P = .041). (Desmeules et al., 2014)

      A study included 100 women with FMS diagnosed according to the American College of Rheumatology criteria. Women with FMS with the Met/Met genotype exhibited higher disability (F = 11.836; P < .001), anxiety (F = 13.385; P < .001), and depression (F = 6.931; P = .002) than those with Val/Val and Val/Met genotypes. (Fernandez-de-Las-Penas et al., 2012)

      Forty-five women with fibromyalgia (FM) were included. COMT genotype moderated the daily relations of both maladaptive coping processes and pain. FM women with the homozygous met/met genotype evidenced more pain on days when pain catastrophizing was elevated relative to heterozygous and homozygous val(158) carriers. FM women with the homozygous met/met genotype evidenced more pain on days when pain attention was elevated relative to those with the homozygous val/val genotype. (Finan et al., 2011)

      5-HT2A-Receptor Gene, T102C Polymorphism

      A study investigated the silent T102C polymorphism of the 5-HT2A-receptor gene in 168 FM patients and 115 healthy controls. Results showed a significantly different genotype distribution in FM patients with a decrease in T/T and an increase in both T/C and C/C genotypes as compared to the control population (Fisher's Exact test, two-sided, P = 0.008). However, the increase in allele-C102 frequency fell short of significance (P = 0.07). The pain score, being a self reported information on pain severity, was significantly higher in patients of the T/T genotype (Mann-Whitney U test, P = 0.028). This suggests that the T102-allele might be involved in the complex circuits of nociception. (Bondy et al., 1999)

      Monoamine Oxidase (MAO)

      One hundred and seven fibromyalgia patients and 90 unrelated healthy subjects were included into the study. Polymorphism of the MAO gene was: 1-1, 1-3, 3-3, 3-4. The allele 3 had a 2.7 to 4.8-fold increased transcription activity than the allele 1. The frequencies of the genotypes of the patients with FS and healthy controls were compared. Although no significant difference was found in genotypes of patients and controls (P = 0.0559), it is likely that allele 3 could be a more riskful factor for FS than allele 1 (P = 0.033). Fibromyalgia impact questionnaire was administered to FS group as well as control group. One of our findings is that, the patients whose genotype 3-3 may be mostly affected by the symptoms of FS. In conclusion, it seems plausible to say that MAOA-dependent metabolism of the biological amines may be partly related to high-activated MAO-A, allele 3, in the occurrence of FS among Turkish population. (Gursoy et al., 2008)

      References

      Bondy,

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