Reply to BJ Boucher et al

Division of Clinical Epidemiology and Preventive Medicine
Department of Medicine
David Geffen School of Medicine
University of California, Los Angeles
924 Westwood Boulevard, Suite 335
Los Angeles, CA 90024
E-mail: kchiu{at}mednet.ucla.edu

Dear Sir:

We appreciate the comments from Boucher et al regarding our recent article (1), specifically with respect to the issue of a relation between serum 25-hydroxyvitamin D concentrations and the lipid profile. Because elevated C-reactive protein concentrations are associated with insulin resistance and the presence of the metabolic syndrome (2), the published data of Timms et al (3) on the relation between hypovitaminosis D and elevated C-reactive protein (r = –0.22, P = 0.031) in a sample of 146 subjects are in accord with our observation that hypovitaminosis D is associated with insulin resistance and the metabolic syndrome (1). Their unpublished observation of a positive correlation of serum 25-hydroxyvitamin D with both total cholesterol and apolipoprotein B and a negative correlation with triacylglycerols does not support the possibility of a relation between hypovitaminosis D and insulin resistance phenotypes.

We have no information regarding the concentrations of C-reactive protein, plasma metalloproteinase 9, and apoliproteins A1 and B in this sample. Because there were only 126 subjects in our multiracial sample, we focused on the whites, who were the largest racial or ethnic group in the sample (n = 56). The influence of 25-hydroxyvitamin D on fasting lipid profile is shown in Table 1. The results are highly similar to our published results (1). The negative association of serum 25-hydroxyvitamin D with both total and LDL cholesterol is in agreement with the association of hypovitaminosis D with insulin resistance and the metabolic syndrome. The 3 nonwhite ethnic groups in our sample were not large enough to have adequate power to detect the association. Although the association study provides no information on the cause-effect relation, hypovitaminosis D could be one of the culprits of insulin resistance.

View this table:
TABLE 1. Regression analysis of the effect of 25-hydroxyvitamin D on fasting lipid profile in the 56 whites in the study

REFERENCES

1. Chiu KC, Chu A, Go VL, Saad MF. Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction. Am J Clin Nutr 2004;79:820–5.
2. Rutter MK, Meigs JB, Sullivan LM, D'Agostino RB Sr, Wilson PW. C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham Offspring Study. Circulation 2004;110:380–5.
3. Timms PM, Mannan N, Hitman GA, et al. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM 2002;95:787–96.