A preliminary transcriptome analysis suggests a transitory effect of vitamin D on mitochondrial function in obese young Finnish subjects
Endocrine Connections , vol. 8 , no. 5 , pp. 559-570 . https://doi.org/10.1530/EC-18-0537
Einarsdottir , E , Pekkinen , M , Krjutskov , K , Katayama , S , Kere , J , Mäkitie , O & Viljakainen
- Genetics category listing has
326 items along with related searches
- Huntington disease patients – ALL had low vitamin D levels – Sept 2014
- 430 genes changed when 3,800 IU Vitamin D added in late second trimester – RCT May 2018
- Vitamin D during pregnancy – dramatic changes in both metabolism and genes – Feb 2017
- 5839 genes changed during pregnancy (many genes were related to Vitamin D) – Oct 2016
Overview Alzheimer's-Cognition and Vitamin D has the following summary
- FACT: Cognitive decline is 19X more likely if low vitamin D
- FACT: Dementia is associated with low vitamin D levels.
- FACT: Alzheimer’s Dementia 2.3X more likely in elderly if low vitamin D – Dec 2022
- FACT: Dementia is associated with low vitamin D - many studies
- FACT: Alzheimer's Disease is 4X less likely if high vitamin D
- FACT: Every single risk factor listed for Alzheimer's Disease is also a risk factor for low vitamin D levels
- FACT: Elderly cognition gets worse as the elderly vitamin D levels get even lower (while in senior homes)
- OBSERVATION: Reports of increased vitamin D levels result in improved cognition
- OBSERVATION: Alzheimer’s patients 3X more likely to have a malfunctioning vitamin D receptor gene – 2012
- OBSERVATION: Alzheimer's Disease has been seen to halt when vitamin D was added.
- OBSERVATION: Alzheimer’s is associated with all 7 of the genes which restrict vitamin D
- OBSERVATION: 39 vitamin D and Alz. or Cognition intervention trials as of Sept 2018
- OBSERVATION: 2 Meta-analysis in 2012 agreed that Alzheimer's Disease. associated with low vitamin D
- OBSERVATION: 50X increase in Alzheimer's while decrease in vitamin D
- OBSERVATION: Vitamin D reduces Alzheimer’s disease in 11 ways
- OBSERVATION: Alzheimer’s cognition improved by 4,000 IU of vitamin D
- OBSERVATION: Plaque removed in mice by equiv. of 14,000 IU daily
- OBSERVATION: DDT (which decreases Vit D) increases risk of Alzheimer's by up to 3.8X
- OBSERVATION: 2% of people have 2 copies of the poor gene reference: Alz Org
- OBSERVATION: Genes do not change rapidly enough to account for the huge increase in incidence
- FACT: Vitamin D is extremely low cost and has very very few side effects
- CONCLUSION: Everyone concerned about cognitive decline or Alzheimer's Disease should take vitamin D
- PREDICTION: By 2024 Omega-3 and high dose Vitamin D will be found to reverse Alzheimer's in humans
- As of 2018 that combination has worked well with Multiple Sclerosis, Sleep, and Cluster Headaches
There are 12+ Alzheimer’s meta-analyses in VitaminDWiki
There are 91+ Alzheimer’s studies in VitaminDWiki
- End of Alzheimer's video and transcript - June 2023
Dementia is associated with low vitamin D - many studies 50+
16+ studies in both categories Cognitive and Omega-3
The End of Alzheimer's and Dementia if adjust Vitamin D, B-12, Iron, Omega-3, etc.
Customizing the types of treatment to the individual results in reversing Alzheimer's
- Neuro problems (AD, PD, MSA) associated with poor vitamin D genes (CYP27A1, CYP27B1) – Sept 2022
- Lower vitamin D in blood causes Alzheimer's Disease (Mendelian gene analysis) – Dec 2019
- Alzheimer’s is associated with all 7 of the genes which restrict vitamin D from getting to tissues – Sept 2018
- 8 genes associated with both Alzheimer’s and lowish Vitamin D – May 2019
- Body may change gene activation if more Vitamin D is needed by tissue (Schiz. in this case) – Oct 2018
- Study concluded cognitive problems are not a result of low vitamin D (many studies disagree) Nov 2017
- Genes which reduce blood-level vitamin D increase the risk of Alzheimer’s disease – Dec 2016
- Less vitamin D generated from sunlight by schizophrenia patients – 2016
- Schizophrenia and vitamin D have latitude-related genes – Nov 2010
Objective: The effect of vitamin D at the transcriptome level is poorly understood, and furthermore, it is unclear if it differs between obese and normal-weight subjects. The objective of the study was to explore the transcriptome effects of vitamin D supplementation.
Design and methods: We analysed peripheral blood gene expression using GlobinLock oligonucleotides followed by RNA sequencing in individuals participating in a 12-week randomised double-blinded placebo-controlled vitamin D intervention study. The study involved 18 obese and 18 normal-weight subjects (of which 20 males) with mean (+/- s.D.) age 20.4 (+/- 2.5) years and BMIs 36 (+/- 10) and 23 (+/- 4) kg/m(2), respectively. The supplemental daily vitamin D dose was 50 mu g (2000 IU). Data were available at baseline, 6- and 12-week time points and comparisons were performed between the vitamin D and placebo groups separately in obese and normal-weight subjects.
Results: Significant transcriptomic changes were observed at 6 weeks, and only in the obese subjects: 1724 genes were significantly upregulated and 186 genes were downregulated in the vitamin D group compared with placebo. Further analyses showed several enriched gene categories connected to mitochondrial function and metabolism, and the most significantly enriched pathway was related to oxidative phosphorylation (adjusted P value 3.08 x 10(-14)). Taken together, our data suggest an effect of vitamin D supplementation on mitochondrial function in obese subjects.
Conclusions: Vitamin D supplementation affects gene expression in obese, but not in normal-weight subjects. The altered genes are enriched in pathways related to mitochondrial function. The present study increases the understanding of the effects of vitamin D at the transcriptome level.