Nutritional Genetics Part 5: Diseases C
()
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
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.
Read more from Ronald Steriti
A Brief Introduction to Naturopathy and Naturopathic Medicine Rating: 4 out of 5 stars4/5Ballroom Rhythms for Musicians and Dancers Rating: 4 out of 5 stars4/5Nutritional Genetics Part 4: Diseases B Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 9: Gynecology Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 13: Dermatology Rating: 5 out of 5 stars5/5Complementary and Alternative Medical Lab Testing Part 7: Endocrine Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 14: Immunology Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 1: Introduction Rating: 0 out of 5 stars0 ratingsGreat Health Quotes Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 19: Miscellaneous Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 3: Diseases A Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 12: Neurology Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 16: Hematology Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 2: Respiratory Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 1: EENT (Eyes, Ears, Nose and Throat) Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 5: Gastrointestinal Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 2: Labs Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 4: Vascular Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 8: Urology Rating: 3 out of 5 stars3/5Complementary and Alternative Medical Lab Testing Part 3: Cardiology Rating: 1 out of 5 stars1/5Nutritional Genetics Part 6: Diseases D Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 15: Musculoskeletal Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 10: Obstetrics Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 18: Psychiatry Rating: 5 out of 5 stars5/5Complementary and Alternative Medical Lab Testing Part 11: Men Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 17: Oncology Rating: 0 out of 5 stars0 ratings
Related to Nutritional Genetics Part 5
Related ebooks
Nutritional Genetics Part 6: Diseases D Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 2: Labs Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 3: Diseases A Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 8: Urology Rating: 3 out of 5 stars3/5Complementary and Alternative Medical Lab Testing Part 7: Endocrine Rating: 0 out of 5 stars0 ratingsEpigenetics in Human Disease Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 14: Immunology Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder Rating: 0 out of 5 stars0 ratingsComplementary and Alternative Medical Lab Testing Part 12: Neurology Rating: 0 out of 5 stars0 ratingsNutritional Genetics Part 1: Introduction Rating: 0 out of 5 stars0 ratingsPractical Nutrigenomics: a guide to setting up your personalised nutrition service Rating: 4 out of 5 stars4/5Nutritional Modulation of Neural Function Rating: 0 out of 5 stars0 ratingsMethylation Madness: Insight into the Biochemical and Personal Lives of Hypermethylators Rating: 0 out of 5 stars0 ratingsFix Your Genes to Fit Your Jeans: Optimizing Diet, Health and Weight Through Personal Genetics Rating: 0 out of 5 stars0 ratingsNonvitamin and Nonmineral Nutritional Supplements Rating: 0 out of 5 stars0 ratingsNutrition and Genomics: Issues of Ethics, Law, Regulation and Communication Rating: 3 out of 5 stars3/5Nutrition and Functional Foods in Boosting Digestion, Metabolism and Immune Health Rating: 0 out of 5 stars0 ratingsThe Secret of Long Life Is Personalized, Like Nutrigenomics Rating: 0 out of 5 stars0 ratingsMitochondrial Metabolism: An Approach to Disease Management Rating: 0 out of 5 stars0 ratingsModern Medicine for Modern Times: The Functional Medicine Handbook to Prevent and Treat Diseases at their Root Cause Rating: 0 out of 5 stars0 ratingsNutrigenetics: Applying the Science of Personal Nutrition Rating: 4 out of 5 stars4/5Personalized Epigenetics Rating: 3 out of 5 stars3/5Breast Cancer: Melatonin Helps to: Prevent Cancer, Avoid Drug Resistance, Stop Metastasis Rating: 0 out of 5 stars0 ratingsDecipher Your Labwork - CBC: Functional Medicine Rating: 1 out of 5 stars1/5Cholesterol Cure: Heal Naturally, Without Medication Rating: 0 out of 5 stars0 ratingsDiet-Microbe Interactions in the Gut: Effects on Human Health and Disease Rating: 5 out of 5 stars5/5Root Cause Rating: 5 out of 5 stars5/5Amino Acids: A Practical Guide Rating: 0 out of 5 stars0 ratingsMolecular Nutrition and Diabetes: A Volume in the Molecular Nutrition Series Rating: 3 out of 5 stars3/5
Wellness For You
The Big Book of 30-Day Challenges: 60 Habit-Forming Programs to Live an Infinitely Better Life Rating: 4 out of 5 stars4/5The Little Book of Hygge: Danish Secrets to Happy Living Rating: 4 out of 5 stars4/5The Emperor of All Maladies: A Biography of Cancer Rating: 5 out of 5 stars5/5The Subtle Art of Not Giving a F*ck: A Counterintuitive Approach to Living a Good Life Rating: 4 out of 5 stars4/5How Not to Diet: The Groundbreaking Science of Healthy, Permanent Weight Loss Rating: 4 out of 5 stars4/5When the Body Says No Rating: 5 out of 5 stars5/5Thinner Leaner Stronger: The Simple Science of Building the Ultimate Female Body Rating: 4 out of 5 stars4/5Bigger Leaner Stronger: The Simple Science of Building the Ultimate Male Body Rating: 5 out of 5 stars5/5Why We Sleep: Unlocking the Power of Sleep and Dreams Rating: 4 out of 5 stars4/5How Am I Doing?: 40 Conversations to Have with Yourself Rating: 5 out of 5 stars5/5Outsmart Your Brain: Why Learning is Hard and How You Can Make It Easy Rating: 4 out of 5 stars4/5Glucose Revolution: The Life-Changing Power of Balancing Your Blood Sugar Rating: 5 out of 5 stars5/5Summary of Anna Lembke's Dopamine Nation Rating: 4 out of 5 stars4/5The Illustrated Easy Way to Stop Drinking: Free At Last! Rating: 4 out of 5 stars4/5Deep Nutrition: Why Your Genes Need Traditional Food Rating: 4 out of 5 stars4/5The Lost Book of Simple Herbal Remedies: Discover over 100 herbal Medicine for all kinds of Ailment Inspired By Barbara O'Neill Rating: 0 out of 5 stars0 ratingsThe Wim Hof Method: Activate Your Full Human Potential Rating: 5 out of 5 stars5/5The Happiness Makeover: Overcome Stress and Negativity to Become a Hopeful, Happy Person Rating: 4 out of 5 stars4/5Muscle for Life: Get Lean, Strong, and Healthy at Any Age! Rating: 4 out of 5 stars4/5The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally Rating: 4 out of 5 stars4/5Summary of Lindsay C. Gibson's Adult Children of Emotionally Immature Parents Rating: 5 out of 5 stars5/5The Secret Language of Your Body: The Essential Guide to Health and Wellness Rating: 5 out of 5 stars5/5Childhood Disrupted: How Your Biography Becomes Your Biology, and How You Can Heal Rating: 4 out of 5 stars4/5Herbal Healing for Women Rating: 4 out of 5 stars4/5
Reviews for Nutritional Genetics Part 5
0 ratings0 reviews
Book preview
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