"Epigenetics literally means "above" or "on top of" genetics.
It refers to external modifications to DNA that turn genes "on" or "off."
Table of contents
- Epigenetic Memories are Passed Down 14 Successive Generations, Game-Changing Research Reveals GreenMed Info Oct 2018
- See VitaminDWiki
- See also Web
- DNA tests are blind to epigenetic activations
- Amount of response to Vitamin D is passed on to future generations – May 2018
- In vivo response of the human epigenome to vitamin D: A Proof-of-principle study.
- VitaminDWiki pages with EPIGENETIC in title (16 as of June 2022)
Epigenetic Memories are Passed Down 14 Successive Generations, Game-Changing Research Reveals GreenMed Info Oct 2018
- “Genes Load the Gun, Environment Pulls the Trigger” (is Vitamin D a bullet-proof vest?)
- one dose of insecticide methoxychlor caused poor fertility for 4 generations of rats
- Cherry smell was given concurrently with electric shock. Rats two generations later still feared the cherry scent
- Thermal effects of environment passed on thru14 generations of nematode worms
- 5.8 X more likely to die in 15 year followup if low vitamin D and poor methylation – July 2018
- Stressors as a fetus or child can cause health problems in adult (perhaps via epigenetics) – Dec 2017
- Vitamin D Receptor – environment, genetics and epigenetics – May 2015
- Low vitamin D in pregnancy – epigenetic pancreas problems in offspring (mice) – May 2016
- Epigenetics of Multiple Sclerosis – March 2014
- Epigenetics, vitamin D, and Multiple Sclerosis
- Micronutrients, methylation, epigenetics, longevity podcast by Rhonda Patrick and Tim Ferriss - June 2015
- Vitamin D and the epigenome - April 2014
- Food allergies are associated with Vitamin D thru genes, etc. – March 2018
- Vitamin D Heritability: twin studies – 20 percent to 85 percent, GWAS 5 percent – Oct 2018
- Health problems that run in families are often associated with low vitamin D
- Hypothesis – less vitamin D results in faster aging – Nov 2017
- Regulation of the vitamin D receptor gene by environment, genetics and epigenetics = 2015 https://doi.org/10.1016/j.gene.2015.02.024
- Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging - Wimalawansa May 2019 PDF
- Vitamin D supplementation is associated with slower epigenetic aging PDF
- An Epigenetic Signature is Associated with Serum 25-Hydroxyvitamin D in Colorectal Cancer Tumors - July 2021 https://doi.org/10.1002/mnfr.202100125
- Epigenetic Aging in Early Life: Role of Maternal and Early Childhood Nutrition - Feb 2022 PDF
- Maternal vitamin D depletion alters DNA methylation at imprinted loci in multiple generations (mice) - 2016 PDF
- Epigenetics: Fundamentals
- "Epigenetics is the study of heritable changes in gene expression (active versus inactive genes) that do not involve changes to the underlying DNA sequence"
-  Download Epigenetics for Dummies - 2014 from VitaminDWiki
- Genetic and epigenetic factors influencing vitamin D status May 2018 10.1002/jcp.26216
- Epigenetics across the human lifespan 2014
- No - these tests look at the underlying DNA sequence, using technologies that are “blind” to the presence or absence of epigenetic marks on the DNA.
- There are some direct-to-consumer tests that look at epigenetic changes, but they’re specifically marketed as epigenetic tests.
- One company charges $1,500 Oct 2018
- Want to know when you’re going to die? MIT Review Oct 2018
Epigenetics +DNA predicts lifespan much better than DNA alone
DNA methylation-based measures of biological age: meta-analysis predicting time to death - Sept 2016
Life Epigenetics mentioned
Clew Medical uses AI to predict death in critical hospital situations
- Does not consider the reduction in ICU and Sepsis deaths due to Vitamin D
Vitamin D Genomics: From In Vitro to In Vivo.
Front Endocrinol (Lausanne). 2018 May 23;9:250. doi: 10.3389/fendo.2018.00250.
School of Medicine, Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
free PDF online
The vitamin D3 metabolite 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] is the exclusive high-affinity ligand of the vitamin D receptor (VDR), a transcription factor with direct effects on gene expression. Transcriptome- and epigenome-wide data obtained in THP-1 human monocytes are the basis of the chromatin model of vitamin D signaling. The model describes, how VDR's spatio-temporal binding profile provides key insight into the pleiotropic action of vitamin D. The transcription of some 300 primary target genes is significantly modulated through the action of genomic VDR binding sites in concert with the pioneer transcription factor PU.1 and the chromatin organizer CTCF. In parallel, the short-term vitamin D intervention study VitDbol (NCT02063334) was designed, in order to extrapolate insight into vitamin D signaling from in vitro to in vivo.
Before and 24 h after a vitamin D3 bolus chromatin and RNA were prepared from peripheral blood mononuclear cells for epigenome- and transcriptome-wide analysis. The study subjects showed a personalized response to vitamin D and could be distinguished into high, mid, and low responders. Comparable principles of vitamin D signaling were identified in vivo and in vitro concerning target gene responses as well as changes in chromatin accessibility.
In conclusion, short-term vitamin D supplementation studies represent a new type of safe in vivo investigations demonstrating that vitamin D and its metabolites have direct effects on the human epigenome and modulate the response of the transcriptome in a personalized fashion.
J Steroid Biochem Mol Biol. 2018 Jun;180:142-148. doi: 10.1016/j.jsbmb.2018.01.002. Epub 2018 Jan 6.
Carlberg C1, Seuter S2, Nurmi T3, Tuomainen TP3, Virtanen JK3, Neme A2.
In vitro cell culture studies showed that the hormonal form of vitamin D3, 1α,25-dihydroxyvitamin D3, significantly (p < 0.05) affects the human epigenome at thousands of genomic loci. Phase II of the VitDbol vitamin D intervention trial (NCT02063334) involved a proof-of-principle study of one individual, who was exposed three times every 28 days to an oral bolus (2000 μg) of vitamin D3. Blood samples were taken directly before each supplementation as well as one and two days after, chromatin was isolated from peripheral blood mononuclear cells without any further in vitro culture and at all nine time points epigenome-wide chromatin accessibility was assessed by applying FAIRE-seq (formaldehyde-assisted isolation of regulatory elements sequencing). The vitamin D3 bolus resulted in an average raise in 25-hydroxyvitamin D3 (25(OH)D3) serum concentration of 11.9 and 19.4 nM within one and two days, respectively. Consistently accessible chromatin was detected at 5205 genomic loci, the 853 most prominent of which a self-organizing map algorithm classified into early, delayed and non-responding genomic regions: 70 loci showed already after one day and 361 sites after two days significant (p < 0.0001) chromatin opening or closing. Interestingly, more than half of these genomic regions overlap with transcription start sites, but the change of chromatin accessibility at these sites has no direct effect on the transcriptome. Some of the vitamin D responsive chromatin sites cluster at specific loci within the human genome, the most prominent of which is the human leukocyte antigen region in chromosome 6. In conclusion, this study demonstrates that under in vivo conditions a rather minor rise in 25(OH)D3 serum levels is sufficient to result in significant changes at hundreds of sites within the epigenome of human leukocytes.
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