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Vitamin D: a Review of its Effects on Epigenetics and Gene Regulation.

Folia medica
January 1, 1970
Violeta Snegarova et al. (2 authors)
Journal ArticleReviewHuman Study
Study Details

Study Goal

The researchers aimed to review the role of vitamin D in epigenetics, gene regulation, and its ability to control oxidative stress in conjunction with antioxidants.

Results Summary

The study found that vitamin D deficiency increases the incidence and severity of oxidative stress-related disorders, and normalization of vitamin D levels may improve clinical outcomes by regulating epigenetic mechanisms and oxidative stress.

Population

General human population, with specific mentions of conditions like obesity, diabetes, hypertension, and autoimmune diseases.

Effective Dosage

Not specified

Duration

Not specified

Interactions

None mentioned

Extracted Claims (5)
InterventionDirectionEndpointPopulationDosageImpactClaim #
Vitamin D
neutral
several body systems other than the musculoskeletal system
-
-
has known beneficial effects on
#1
25 dihydroxy vitamin D [25(OH)2D] and 1,25-dihydroxyvitamin D [1,25(OH)2D]
neutral
human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses
human
-
are essential for
#2
hypovitaminosis D
increase
several age-related common diseases such as the oxidative stress-associated metabolic disorders
-
-
increases the incidence and severity of
#3
hypovitaminosis D
increase
obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases
-
-
increases the incidence and severity of
#4
normalization of serum 25(OH)D and tissue 1,25(OH)2D concentrations
increase
better cost-effective clinical outcomes
humans
-
are likely to promise
#5
Abstract

Vitamin D is a secosteroid hormone with known beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)2D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)2D] are essential for hu-man physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. In the present study we set out to review all available literature on vitamin D and the role it plays in epigenetics and gene regulation. We searched the PubMed/Medline electronic database for studies published in the English language up to January 2020. The Medical Subject Headings (MeSH) database was searched with the keywords 'vitamin D', 'DNA methylation', 'nutritional supplements', 'epigenome' and 'pregnancy'. Observational studies, supplementation studies, and meta-analyses dealing with the effect of vitamin D on epigenetics and gene regula-tion were included in the review. The obtained information from the databases such as PubMed, Google Scholar, and ResearchGate was analysed and summarized. We found that hypovitaminosis D increases the incidence and severity of several age-related common diseases such as the oxidative stress-associated metabolic disorders. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunc-tion with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentra-tions, are likely to promise better cost-effective clinical outcomes in humans. There is a strong reciprocity between the vitamin D system and epigenetic mechanisms. The vitamin D system is, on the one hand regu-lated by epigenetic mechanisms and, on the other hand, is involved in regulating epigenetic events.

Medical Subject Headings (MeSH)
DNADNA DamageEpigenesis, GeneticHumansOxidative StressVitamin DVitamin D DeficiencyVitamins
Study Links
Quality Scores
SafetyNot Assessed
Efficacy85/10
Quality78/10
Citation Metrics
Total Citations20
Citations/Year4.0
Relative Citation Ratio1.46
NIH Percentile64.1%
Research Impact Scores
APT Score0.75
Weight Score1.71
Normalized Score0.70
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