The American journal of clinical nutrition · 9 authors, 4 centres
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This large, multi-country analysis found weak and inconsistent correlations between inflammation biomarkers (CRP and AGP) and vitamin D levels (25(OH)D) in preschool children and women of reproductive age. The prevalence of vitamin D deficiency did not show a clear linear trend across inflammation levels. Therefore, adjusting for these inflammation markers is not recommended when estimating population vitamin D deficiency prevalence.
**Background:** Vitamin D deficiency is a global public health concern, but it is unclear whether inflammation alters 25(OH)D concentrations, potentially biasing prevalence estimates. The Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRINDA) project previously recommended adjusting iron and vitamin A biomarkers for inflammation, but evidence for vitamin D was lacking. This study aimed to determine whether CRP and AGP correlate with 25(OH)D in preschool children (PSC) and females of reproductive age (FRA).
**Methods:** Cross-sectional data from six nationally representative surveys (Afghanistan 2013, Cambodia 2014, Pakistan 2011, UK 2014, USA 2006, Vietnam 2010) were analyzed. The sample included 9,880 PSC (6–59 months) and 14,749 nonpregnant FRA (15–49 years). Serum 25(OH)D, CRP, and AGP were measured using various laboratory methods. Inflammation was defined as CRP >5 mg/L or AGP >1 g/L. Weighted rank correlation coefficients were calculated to assess associations between inflammation biomarkers and 25(OH)D, accounting for complex survey design. The prevalence of vitamin D deficiency (<30 nmol/L) was plotted by CRP and AGP deciles. Stratification by BMI category was performed for FRA.
**Key Results:** Correlations between CRP/AGP and 25(OH)D were weak and mostly non-significant. For PSC, correlation coefficients between CRP and 25(OH)D ranged from −0.04 (Afghanistan) to 0.08 (Vietnam), and between AGP and 25(OH)D from 0.01 (Pakistan) to 0.05 (Cambodia). For FRA, CRP–25(OH)D correlations ranged from −0.11 (UK, p=0.02) to 0.14 (Vietnam, p=0.002), and AGP–25(OH)D correlations from −0.05 (Cambodia) to 0.01 (Afghanistan). Only three FRA surveys (UK, USA, Vietnam) showed statistically significant but small correlations. The prevalence of vitamin D deficiency (<30 nmol/L) varied across CRP and AGP deciles without a clear linear trend. BMI stratification revealed some significant correlations in specific subgroups (e.g., negative in overweight UK women, positive in normal-weight US women), but overall patterns were inconsistent.
**Clinical Implications:** The weak and inconsistent associations between inflammation biomarkers and 25(OH)D indicate that adjusting for CRP or AGP is not necessary when estimating population prevalence of vitamin D deficiency in PSC and FRA. This simplifies vitamin D assessment in national surveys and avoids unnecessary adjustments that could introduce bias. However, the findings are limited to these population groups and may not apply to clinical settings or other age groups. Future research should explore other inflammatory markers and longitudinal designs to better understand the vitamin D–inflammation relationship.