Vitamin D and Phosphate Interactions in Health and Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review / book chapter describing physiological mechanisms without primary empirical data
PubMed 35288871 · doi:10.1007/978-3-030-91623-7_5
What was done
Narrative review summarizing the physiological mechanisms and endocrine feedback loops between vitamin D (specifically 1,25(OH)2D), inorganic phosphate, fibroblast growth factor 23 (FGF23), and parathyroid hormone (PTH) in healthy and diseased states.
What was found
The interaction of 1,25(OH)2D with its receptor increases intestinal calcium absorption efficiency to 30–40% and phosphate absorption to nearly 80%. High phosphate levels suppress vitamin D activation and stimulate PTH release, while elevated FGF23 reduces vitamin D synthesis. In vitamin D deficiency, impaired calcium absorption triggers elevated PTH, which stimulates 1,25(OH)2D production and causes excessive urinary phosphate wasting. No original empirical data or statistical comparisons are reported.
Why it matters
It outlines the biological mechanisms connecting vitamin D and phosphate regulation to clinical outcomes such as chronic kidney disease, cardiovascular calcification, rickets, and osteomalacia.
Limits
This is an overview chapter/narrative review without a systematic search protocol, new clinical data, patient cohorts, or quantitative statistical testing.
Cited by
- supports High levels of vitamin D increase the intestinal absorption of both dietary calcium and phosphorus.