Medically Reviewed by: Nicole Anne Vergara, RD
New research shows that, as vitamin D levels increase to normal levels, systemic inflammation—often caused by a deficiency of the nutrient—declines.
However, changes in vitamin D levels did not appear to affect CRP levels.
In an interview with Medscape Medical News, Professor Elina Hypponen—an author of the study and a professor in nutritional and genetic epidemiology at Adelaide University’s Australian Centre for Precision Health–said: “This is the first study of its kind, and the first to show that the well-known relationship between vitamin D status and CRP is at least in part driven by vitamin D.”
“Given that the serum CRP level is a widely used biomarker for chronic inflammation, these results suggest that improving vitamin D status may reduce chronic inflammation, but only for people with vitamin D deficiency,” Hypponen and his colleagues have reported their findings in the journal International Journal of Epidemiology.
Vitamin D’s Association with CRP in ‘L-Shaped’ Manner
Nutritional factors are known to influence an individual’s body chemistry and can play a part in causing systemic inflammation.
However, recent research has suggested that the relationship between vitamin D and C-reactive protein (CRP), a protein measured to detect inflammation, is not as strong as originally thought.
The authors performed a Mendelian randomization analysis, using data from a cohort of 294,970 unrelated participants in the UK Biobank—the largest cohort to date with measured serum 25(OH)D concentrations.
Overall, the average 25(OH)D concentration was 50.0 nmol/L (range 10–340 nmol/L). 11.7% (34,403 people) had concentrations of <25nmol/L—which is considered deficient.
There is an inverted “U”-shape relationship between genetically predicted serum 25(OH)D, and C-reactive protein (CRP)—a marker of inflammation—which shows that CRP levels sharply decrease as 25OHD concentrations rise to normal.
However, the relationship between vitamin D and anger was only significant among participants with low levels of 25-hydroxyvitamin D (<25 nmol/L), reaching a plateau at about 50 nmol/L—generally considered an adequate level.
Further stratified Mendelian randomization analyses confirmed an inverse association between serum 25(OH)D in the deficiency range (but not with higher concentrations of vitamin D), and CRP.
On the other hand, neither linear nor non-linear Mendelian randomization analysis revealed a relationship between blood CRP levels and 25(OH)D levels.
The authors write that the results “indicate that improvement in vitamin D status in the deficient range could lower systemic low-grade inflammation and potentially minimize the risk or severity of chronic disorders with an inflammatory component.”
The most significant drops in CRP are seen when the most severe vitamin D insufficiency is corrected, according to Hypponen.
According to Hypponen, who spoke with Medscape Medical News, “those with severe insufficiency will notice the largest advantages from boosting concentrations.”
When participants in our trial attained the National Academy of Sciences-recommended cut-off of 50 nmol/L (for vitamin D sufficiency), a significant portion of the effect was realized.
Pro-Hormonal Capacity of Vitamin D
According to the authors, the anti-inflammatory effects of serum vitamin D may be due to its pro-hormonal capacity to affect immune cells that express vitamin D receptors, including monocytes, B cells, T cells, and antigen-presenting cells.
In fact, cell studies have demonstrated that active vitamin D can boost the synthesis of IL-10, an anti-inflammatory cytokine, while inhibiting the production of pro-inflammatory cytokines like TNF-alpha, interleukin (IL)-1b, IL-6, IL-8, and IL-12.
Accordingly, adequate vitamin D concentrations may help prevent obesity-related inflammation-related complications as well as lower the risk or severity of chronic illnesses like cardiovascular disease, diabetes, autoimmune diseases, neurodegenerative conditions, and others that have an inflammatory component.
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Previous Studies Couldn’t Determine The Impact Of The Deficiency
The authors point out that while the previous studies only used a standard linear Mendelian randomization method and could not completely rule out the possibility of a “threshold effect” specific to vitamin D deficiency, the current findings contradict those earlier studies and show no causal effect of 25(OH)D on CRP.
“In fact, it makes sense to assume that increasing vitamin D status would only be important in
a vitamin D deficit, when any additional additions could be unnecessary and, in the case of supplementation, potentially hazardous, “They compose.
The authors note that the method has also recently been used in research showing an adverse effect of vitamin D deficiency on cardiovascular disease (CVD) risk and mortality, which would not be visible using the standard linear Mendelian randomization approach. However, the nonlinear Mendelian randomization approach used in the current study allows for better detection of the association.
Hypponen underlined that the current findings support broader studies that shows supplementation with vitamin D provides little to no benefit for healthy individuals who are not deficient in the vitamin.
In a press release, Hypponen stated, “We have frequently observed evidence for health benefits for boosting vitamin D concentrations in patients with very low levels, but there appears to be little to no benefit for others.”
These results emphasize the need to prevent clinical vitamin D deficiency and offer more proof of the extensive impacts of hormonal vitamin D, she continued.