Effects of Vitamin D on Cardiovascular Risk and Oxidative Stress.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing mechanisms and associations without systematic review methodology or primary data
PubMed 36771474 · doi:10.3390/nu15030769
What was done
This narrative review examined literature on the biological mechanisms, observational associations, and clinical context linking vitamin D metabolism to cardiovascular disease, metabolic syndrome, type 2 diabetes mellitus, and oxidative stress.
What was found
The abstract provides no numerical data, effect sizes, or participant numbers. It describes mechanistic pathways through which 25-hydroxyvitamin D and calcitriol downregulate renin expression, suppress renin-angiotensin-aldosterone system activity, lower parathyroid hormone and aldosterone levels, and reduce systemic inflammatory mediators. It notes that optimal supplementation doses and sex-specific cardiovascular endpoints are not yet established.
Why it matters
It outlines endocrine and anti-inflammatory pathways that may explain observed associations between vitamin D deficiency and cardiometabolic disorders.
Limits
As a narrative review, it presents no primary data, quantitative synthesis, or systematic search strategy. Biological plausibility and observational links described do not establish causal clinical efficacy or optimal dosing.
Cited by
- supports The final stage of converting vitamin D into its active form requires functioning kidneys.