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    Nutritional Genetics Part 5: Diseases C
    Nutritional Genetics Part 5: Diseases C
    Nutritional Genetics Part 5: Diseases C
    Ebook123 pages1 hour

    Nutritional Genetics Part 5: Diseases C

    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 5 - Diseases C

    Neurology
    1. Alzheimer's Disease
    2. Amyotrophic Lateral Sclerosis
    3. Autism
    4. Cognitive Impairment
    5. Epilepsy
    6. Essential Tremor
    7. Headache
    8. Huntington's chorea
    9. Memory Loss
    10. Migraine
    11. Multiple Sclerosis
    12. Parkinson's Disease
    13. Transverse Myelitis

    Dermatology
    14. Alopecia
    15. Eczema
    16. Psoriasis
    17. Purpura
    18. Scleroderma and Systemic Sclerosis
    19. Vitiligo

    Immunology
    20. Autoimmune Disease
    21. Chronic Fatigue Syndrome
    22. Human Immunodeficiency Virus (HIV)
    23. Systemic Lupus Erythematosus

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 23, 2016
    ISBN9781311490292
    Nutritional Genetics Part 5: Diseases C
    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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      Nutritional Genetics Part 5 - Ronald Steriti

      Chapter 1. Alzheimer's Disease

      MTHFR (C677T, A1298C)

      A meta-analysis included 40 case-control studies with 4503 AD cases and 5767 controls. In subgroup analyses stratified by ethnicity, age of onset, and APOE ϵ4 status, significant increased AD risk was found in Asians, late-onset AD, and APOE ϵ4 carriers, but not in Caucasians, early-onset AD, and non-APOE ϵ4 carriers. The present meta-analysis suggested that the MTHFR is a candidate gene for AD susceptibility. The MTHFR C677T polymorphism may be a risk factor for AD in Asians, APOE ϵ4 carriers, and late-onset AD. (Peng et al., 2015)

      Forty-three Alzheimer's cases and 32 non-AD controls were genotyped for the 677C>T polymorphism. No significant differences in the frequencies of the MTHFR alleles or genotypes between AD cases and controls (P = 0.14) were identified. The 677T mutant allele was significantly overrepresented in AD cases compared to controls (OR = 2.22; P = 0.03). The 677T/T frequency was three times higher in AD patients than in controls, which could increase plasma homocysteine levels. Severe cases of AD were the most frequent in patients with the T/T genotype (11.6%). The effect of the MTHFR polymorphism on the risk of AD may be independent of homocysteine, vitamin B12, or even cholesterol levels. The MTHFR 677C>T polymorphism--especially the presence of one copy of the T allele--appears to confer a potential risk for the development of AD. The T/T genotype may contribute to hypercysteinemia as a sensitive marker. (Elhawary et al., 2013)

      A case-control study consisted of thirty-eight patients and 100 individuals without dementia constituted the control group. Genotyping of MTHFR polymorphisms was performed on patients and controls. Genetic analyses did not indicate a significant association between the MTHFR C677T mutation and AD (C/T: 63.15% versus 39%, p=0.087). However, the genotype prevalence of the missense variant MTHFR A1298C was significantly different between patients and controls (A/C: 55% versus 7%, p<10(-3)). The data suggest an association between the MTHFR A1298C mutation and AD; however, the MTHFR C677T mutation did not contribute to susceptibility for AD. The MTHFR A1298C polymorphism is a possible risk factor for Alzheimer's disease. (Mansouri et al., 2013)

      Vitamin D Receptor (VDR)

      A study included 108 AD patients (aged 73.7±8.6) vs 77 healthy volunteers (aged 64.5±7.8) in the Lower Silesian population. Frequency of allele A of ApaI in the control group was significantly higher vs AD patients (p<0.0177) in the Lower Silesian population. Furthermore the difference in the occurrence of allele t in TaqI and allele A in ApaI between AD patients vs the control group was significant (respectively p<0.0056, p<0.0140) in British Europeans. This observation may suggest that allele a of the ApaI polymorphism is a risk allele in AD Lower Silesian patients. We compared our results with those obtained for the population of British Europeans. In multivariate stepwise regression, allele A of ApaI was associated with 30% lower risk of AD (OR=0.70, p=0.0009) in total treated Polish and British populations. We did not observe similar results in Turkish and Iranian populations. This data suggest that the allele A VDR genotype of ApaI reduces AD risk, probably depending on ethnic origin and climatic conditions. (Laczmanski et al., 2015)

      A study compared 108 AD patients and 115 age-matched controls. The frequency of TaubF haplotype (alleles of TaqI, ApaI, Tru9I, BsmI and FokI, respectively), which was determined by analyzing 5 polymorphisms together, was significantly higher in the AD patient group, suggesting that this haplotype is a risk factor in AD. (Gezen-Ak et al., 2012)

      An association study included 492 late-onset AD cases and 496 controls. The strongest association was found at a promoter SNP rs11568820 (P = 9.1 x 10(-6), odds ratio (OR) = 1.69), which resides within the transcription factor Cdx-2 binding site and the SNP has been also known as CDX2. The risk-allele at rs11568820 is associated with lower VDR promoter activity (p < 10(-11)). The overexpression of VDR or vitamin D treatment suppressed amyloid precursor protein (APP) transcription in neuroblastoma cells (p < 0.001). We provide both statistical evidence and functional data suggesting VDR confers genetic risk for AD. (Wang et al., 2012)

      A study included 255 Alzheimer's disease (AD) cases and 260 cognitively screened elderly controls from the longitudinal cohort of the Oxford Project to Investigate Memory and Ageing (OPTIMA). The presence of each of the linked alleles, Apa1 T and Taq1 G, was associated with the risk of AD, particularly in people <75 years old: odds ratios >/=3.0 and p

      Apolipoprotein E (APOE2, APOE3, APOE4)

      A systematic review and meta-analysis included 14 cross-sectional studies identified in Pubmed from 1996 to 2014 (n=1628). POE varepsilon4 carrier status was associated with atrophic hippocampal volume (pooled SMD: -0.47; 95% CI -0.82 to -0.13; p=0.007) and increased cerebral amyloid positron emission tomography tracer (pooled SMD: 0.62, 95% CI 0.27 to 0.98, p=0.0006). APOE varepsilon4 was also associated with decreased cerebral metabolism, especially in right middle frontal gyrus. APOE varepsilon4 was associated with atrophic hippocampal volume in MRI markers, increased cerebral amyloid deposition and cerebral hypometabolism. Theses associations may indicate the potential role of the APOE gene in the pathophysiology of Alzheimer's disease. (Liu et al., 2015)

      A consecutive hospital-based autopsy series examined the relationship between apolipoprotein E (apoE) and Alzheimer's disease (AD). The study population included 99 patients (mean age 81 years) with AD-related neuropathological findings at death, and a control group of patients without neurodegenerative disease (n = 1429). Among patients with definite AD according to CERAD, 65 % were epsilon4 carriers, compared to 32 % among controls (p < 0.001). The risk of epsilon4 carriers to develop AD was higher (odds ratio = 4.65, p = 0.001) than for non-epsilon4 carriers. The amount of beta-amyloid deposition and neurofibrillary pathology differed significantly (p < 0.01) between the genotypes, with increasing densities from epsilon2 carriers to homozygous epsilon4 carriers. (Kumar et al., 2015)

      A study prospectively recruited 35 patients with AD (19 APOE4 carriers and 16 non-carriers), and 14 normal controls, then followed them for five years. Hippocampal comparison between APOE4 carriers and non-carriers with AD showed carriers had rapid changes in the head and body, while non-carriers had rapid changes in a small portion of the body. Cortical thickness comparison between APOE4 carriers and non-carriers with AD dementia showed carriers had rapid thinning in the lateral frontal, temporal, and parietal regions, while no region showed more rapid cortical thinning in non-carriers than in carriers. (Kim et al., 2015)

      Pooled estimates for APOE e4 carrier prevalence data were derived from 142 independent samples: 48.7% (95% CI: 46.5-51.0), and from 73 samples for

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