Limits...
Vitamin D and C-Reactive Protein: A Mendelian Randomization Study.

Liefaard MC, Ligthart S, Vitezova A, Hofman A, Uitterlinden AG, Kiefte-de Jong JC, Franco OH, Zillikens MC, Dehghan A - PLoS ONE (2015)

Bottom Line: Vitamin D deficiency is widely prevalent and has been associated with many diseases.In conclusion, higher levels of Vitamin D are associated with lower levels of C-reactive protein.In this study we did not find evidence for this to be the result of a causal relationship.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands; Netherlands Institute for Health Sciences, Rotterdam, the Netherlands.

ABSTRACT
Vitamin D deficiency is widely prevalent and has been associated with many diseases. It has been suggested that vitamin D has effects on the immune system and inhibits inflammation. The aim of our study was to investigate whether vitamin D has an inhibitory effect on systemic inflammation by assessing the association between serum levels of vitamin D and C-reactive protein. We studied the association between serum 25-hydroxyvitamin D and C-reactive protein through linear regression in 9,649 participants of the Rotterdam Study, an observational, prospective population-based cohort study. We used genetic variants related to vitamin D and CRP to compute a genetic risk score and perform bi-directional Mendelian randomization analysis. In linear regression adjusted for age, sex, cohort and other confounders, natural log-transformed CRP decreased with 0.06 (95% CI: -0.08, -0.03) unit per standard deviation increase in 25-hydroxyvitamin D. Bi-directional Mendelian randomization analyses showed no association between the vitamin D genetic risk score and lnCRP (Beta per SD = -0.018; p = 0.082) or the CRP genetic risk score and 25-hydroxyvitamin D (Beta per SD = 0.001; p = 0.998). In conclusion, higher levels of Vitamin D are associated with lower levels of C-reactive protein. In this study we did not find evidence for this to be the result of a causal relationship.

No MeSH data available.


Related in: MedlinePlus

Results of Mendelian randomization analyses with the genetic risk scores in quartiles.Panel A: quartiles of the 25-hydroxyvitamin D genetic risk score in relation to C-reactive protein. P for trend = 0.056. Panel B: quartiles of the C-reactive protein genetic risk score in relation to 25-hydroxyvitamin D. P for trend = 0.374Error bars represent 95% confidence intervals.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4492676&req=5

pone.0131740.g002: Results of Mendelian randomization analyses with the genetic risk scores in quartiles.Panel A: quartiles of the 25-hydroxyvitamin D genetic risk score in relation to C-reactive protein. P for trend = 0.056. Panel B: quartiles of the C-reactive protein genetic risk score in relation to 25-hydroxyvitamin D. P for trend = 0.374Error bars represent 95% confidence intervals.

Mentions: The genetic risk scores for vitamin D and CRP were robustly associated with their respective phenotypes (S1 and S2 Figs). The 25-hydroxyvitamin D GRS explained 5.1% of the variation in serum 25-hydroxyvitamin D. The 25-hydroxyvitamin D GRS was not associated with lnCRP (n = 10,788, β = -0.018 per SD, p = 0.082). Moreover, there was no significant trend across the GRS quartiles (Fig 2). Associations of individual SNPs with lnCRP are shown in S5 Table. Among all, rs2282679 (GC: Vitamin D binding protein) was significantly associated with lnCRP (p = 0.027), however, after correcting for multiple testing this was no longer significant. The additional analysis that estimated the effect of the GRS for 25-hydroxyvitamin D on lnCRP in data of a CRP GWAS did not provide a significant result (p = 0.23). The CRP GRS explained 5.5% of the variation in lnCRP. We did not observe a significant association between the CRP GRS and serum 25-hydroxyvitamin D (n = 6,267, β = 0.001 per SD, p = 0.998). Similarly, after dividing the GRS in quartiles, there was no significant trend (Fig 2).


Vitamin D and C-Reactive Protein: A Mendelian Randomization Study.

Liefaard MC, Ligthart S, Vitezova A, Hofman A, Uitterlinden AG, Kiefte-de Jong JC, Franco OH, Zillikens MC, Dehghan A - PLoS ONE (2015)

Results of Mendelian randomization analyses with the genetic risk scores in quartiles.Panel A: quartiles of the 25-hydroxyvitamin D genetic risk score in relation to C-reactive protein. P for trend = 0.056. Panel B: quartiles of the C-reactive protein genetic risk score in relation to 25-hydroxyvitamin D. P for trend = 0.374Error bars represent 95% confidence intervals.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4492676&req=5

pone.0131740.g002: Results of Mendelian randomization analyses with the genetic risk scores in quartiles.Panel A: quartiles of the 25-hydroxyvitamin D genetic risk score in relation to C-reactive protein. P for trend = 0.056. Panel B: quartiles of the C-reactive protein genetic risk score in relation to 25-hydroxyvitamin D. P for trend = 0.374Error bars represent 95% confidence intervals.
Mentions: The genetic risk scores for vitamin D and CRP were robustly associated with their respective phenotypes (S1 and S2 Figs). The 25-hydroxyvitamin D GRS explained 5.1% of the variation in serum 25-hydroxyvitamin D. The 25-hydroxyvitamin D GRS was not associated with lnCRP (n = 10,788, β = -0.018 per SD, p = 0.082). Moreover, there was no significant trend across the GRS quartiles (Fig 2). Associations of individual SNPs with lnCRP are shown in S5 Table. Among all, rs2282679 (GC: Vitamin D binding protein) was significantly associated with lnCRP (p = 0.027), however, after correcting for multiple testing this was no longer significant. The additional analysis that estimated the effect of the GRS for 25-hydroxyvitamin D on lnCRP in data of a CRP GWAS did not provide a significant result (p = 0.23). The CRP GRS explained 5.5% of the variation in lnCRP. We did not observe a significant association between the CRP GRS and serum 25-hydroxyvitamin D (n = 6,267, β = 0.001 per SD, p = 0.998). Similarly, after dividing the GRS in quartiles, there was no significant trend (Fig 2).

Bottom Line: Vitamin D deficiency is widely prevalent and has been associated with many diseases.In conclusion, higher levels of Vitamin D are associated with lower levels of C-reactive protein.In this study we did not find evidence for this to be the result of a causal relationship.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands; Netherlands Institute for Health Sciences, Rotterdam, the Netherlands.

ABSTRACT
Vitamin D deficiency is widely prevalent and has been associated with many diseases. It has been suggested that vitamin D has effects on the immune system and inhibits inflammation. The aim of our study was to investigate whether vitamin D has an inhibitory effect on systemic inflammation by assessing the association between serum levels of vitamin D and C-reactive protein. We studied the association between serum 25-hydroxyvitamin D and C-reactive protein through linear regression in 9,649 participants of the Rotterdam Study, an observational, prospective population-based cohort study. We used genetic variants related to vitamin D and CRP to compute a genetic risk score and perform bi-directional Mendelian randomization analysis. In linear regression adjusted for age, sex, cohort and other confounders, natural log-transformed CRP decreased with 0.06 (95% CI: -0.08, -0.03) unit per standard deviation increase in 25-hydroxyvitamin D. Bi-directional Mendelian randomization analyses showed no association between the vitamin D genetic risk score and lnCRP (Beta per SD = -0.018; p = 0.082) or the CRP genetic risk score and 25-hydroxyvitamin D (Beta per SD = 0.001; p = 0.998). In conclusion, higher levels of Vitamin D are associated with lower levels of C-reactive protein. In this study we did not find evidence for this to be the result of a causal relationship.

No MeSH data available.


Related in: MedlinePlus