Heres just a bit LINE:
Research is showing that Magnesium does not continue to raise Vitamin D levels over 30ng/ml but brings them back down when higher back to around that level. Magnesium was found to have a regulating effect, raising and lowering vitamin D levels based on the original starting baseline 25(OH)D levels. In those people who had a baseline 25-D level of 30 ng/ml or below, magnesium supplementation raised up their 25-D level as expected. However, In those who started out with higher 25-D baseline levels starting around 30 ng/ml (75 nmol/L) up to 50 ng/ml (125 nmol/L), magnesium supplementation LOWERED THEIR 25-D levels back down, not raised 25-D levels to even higher levels that some suggest is an optimal level (it appears its not according to many new research findings that needs to be reconsidered). Magnesium regulates vitamin D levels, low magnesium impedes your body's ability to utilize vitamin D, even when it's present or taken by supplementation. Magnesium deficiency shuts down the vitamin D synthesis and metabolism pathways.
https://www.sciencedirect.com/science/article/pii/S0002916522030581 Note that some groups among the population may do better with lower levels due to genetics.
The vitamin D binding protein (DBP) increased significantly after estrogen and there was a significant positive correlation between the plasma concentration of 1,25-(OH)2D (active Vitamin D) and DBP.
https://www.researchgate.net/public...strogen_on_Vitamin_D_Metabolism_in_Tall_Girls Unlike vitamin A, which facilitates the hepatic secretion of the retinol-binding protein, vitamin D sterols or other calciotropic hormones do not regulate the plasma Vitamin D binding protein (DBP) concentration. Its hepatic synthesis is estrogen dependent and is significantly increased during pregnancy and estrogen therapy.
https://www.sciencedirect.com/science/article/pii/B9780128000946000017 Estrogen conversion from testosterone is linked to cytochrome p450 enzymes requiring magnesium as a cofactor and can be lowered during inflammation states. Vitamin A is also needed which further needs zinc for its metabolism. So again can point to inflammation, zinc, vitamin A, or mag as other potential culprits rather than Vitamin D.
https://forums.phoenixrising.me/thr...eficiency-in-the-raw-datas.91176/post-2448637
Boron helps prevent the breakdown of vitamin D and increases the amount of available vitamin D in the body. Boron suppresses the activity of 24-hydroxylase encoded by CYP24A1, the microsomal enzyme primarily responsible for catabolism (breakdown) of 25(OH)D3 Another study mentioned that after only 1 week of boron supplementation of 6 mg/d all of the inflammatory biomarkers that were measured also decreased: (1) interleukin (IL) 6, from 1.55 pg/mL to 0.87 pg/mL; (2) high-sensitivity C-reactive protein (hs-CRP) by approximately 50%, a remarkable decrease, from 1460 ng/mL to 795 ng/mL; and (3) tumor necrosis factor (TNF-) by approximately 30%, from 12.32 to 9.97 pg/mL.
Levels of dihydrotestosterone, cortisol, and vitamin D increased slightly.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712861/ https://pubmed.ncbi.nlm.nih.gov/22100522/
Example: Retinoid X receptor requires Vitamin A. The RXR also forms a heterodimer with a number of other receptors (e.g., vitamin D and thyroid. hormone).
https://en.wikipedia.org/wiki/Peroxisome_proliferator-activated_recepto Vitamin D binds to its receptor (VDR) and dimerizes (combine with a similar molecule to form a dimer) with the retinoid X receptor (RXR), which is a retinoic acid (vitamin A) receptor. RXR is needed to activate the vitamin D receptor (VDR) and the Thyroid Hormone Receptor (THR) and peroxisome proliferator–activated receptor (PPARs).
Without sufficient vitamin A, vitamin D is unable to properly fulfill some of its functions related to the VDR. [In the cell, VDR binds 1,25(OH)2D, and the complex interacts with the retinoid X receptor to form a 1,25(OH)2D*VDR*retinoid X receptor heterodimer complex. This complex can bind vitamin D–responsive elements in the promoter regions of target genes.]
https://pubmed.ncbi.nlm.nih.gov/9790574/ https://link.springer.com/article/10.1007/s10552-004-1661-4 Zinc also is shown to be needed for VDR beyond its role with vitamin A metabolism.
Vitamin A and D also work in synergy throughout the body including for immunity which is compromised upon loss of Vitamin A, and that Retinoic Acid served to activate the T cells driving these responses.
https://www.medicalnewstoday.com/articles/219513#1
Chronic fructose intake decreases the active form of Vitamin D 1,25(OH)2D3 levels. Chronically high fructose intakes can decrease serum levels of 1,25(OH)2D3 in adult rodents experiencing no Ca2+ stress and fed sufficient levels of dietary Ca2+. This finding is highly significant because fructose constitutes a substantial portion of the average diet of Americans.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0093611
