Sci Rep. 2018 Sep 14;8(1):14065. doi: 10.1038/s41598-018-32482-3.
Triantos C1, Aggeletopoulou I2, Kalafateli M2, Spantidea PI3, Vourli G4, Diamantopoulou G2, Tapratzi D2, Michalaki M5, Manolakopoulos S6, Gogos C7, Kyriazopoulou V5, Mouzaki A3, Thomopoulos K2.
Clipped from the PDF
Survival analysis:... ff genotype vs FF: HR = 0.22 95% CI (0.06–0.77), p = 0.018)
- Cirrhosis infection and death both associated with low vitamin D – June 2015
- Advanced liver cirrhosis death 6.3X more likely if extremely low vitamin D – Jan 2013
NOTE: Vitamin D Receptor restricts how much of the Vitamin D in the blood gets to the cells
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019
Vitamin D Receptor Activation can be increased by any of:
Resveratrol, Omega-3, Magnesium, Zinc, non-daily Vitamin D dosing, etc
Note: The founder of VitaminDWiki uses 10 of the 12 known VDR activators
Items in both categories Liver and Vitamin D Receptor are listed here:
- Liver Cirrhosis death is 4X more likely if poor Vitamin D Receptor – Sept 2018
- Non-alcoholic fatty liver disease and the Vitamin D Receptor – editorial Sept 2019
- Hepatitis B virus reduced by 5X the Vitamin D getting to liver cells in the lab – Oct 2018
- Perhaps a sunshine option for chronic liver disease – Nov 2013
- Liver and interactions with vitamin D deficiency - Review July 2013
From the web
Fibrosis is the first stage of liver scarring. When scar tissue builds up and takes over most of the liver, this is a more serious problem called cirrhosis (pronounced "sir-o-sis"). Scar tissue cannot perform any of the jobs of normal liver cells, and this causes a person with cirrhosis to slowly become ill.
Several polymorphisms in the vitamin D receptor (VDR) are associated with the occurrence of chronic liver disease. Here, we investigated the association between BsmI, ApaI, TaqI and FokI VDR polymorphisms and the severity of liver cirrhosis in relation to serum cytokine and lipopolysaccharide binding protein (LBP) levels and their role on survival in cirrhotic patients. We found that patients harboring the BB genotype had higher MELD score, and they were mainly at CP stage C; patients harboring the AA genotype had increased LBP, IL-1β and IL-8 levels, and they were mostly at CP stage C; TT genotype carriers had higher MELD score and they were mainly at CP stage C and FF genotype carriers had lower IL-1β levels when compared to Bb/bb, Aa/aa, Tt/tt and Ff/ff genotypes respectively. In the multivariate analysis ApaI, BsmI and TaqI polymorphisms were independently associated with liver cirrhosis severity. In the survival analysis, the independent prognostic factors were CP score, MELD and the FF genotype. Our results indicate that the ApaI, TaqI and BsmI polymorphisms are associated with the severity of liver cirrhosis, through the immunoregulatory process. Survival is related to the FF genotype of FokI polymorphism, imparting a possible protective role in liver cirrhosis.