Journal of the National Cancer Institute Advance Access originally published online on May 27, 2008
JNCI Journal of the National Cancer Institute 2008 100(11):827-828; doi:10.1093/jnci/djn042
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Published by Oxford University Press 2008.
CORRESPONDENCE |
Response: Re: Prospective Study of Vitamin D and Cancer Mortality in the United States
Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD (DMF, BIG); National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, MD (ACL); AstraZeneca International, Wilmington, DE, formerly with Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD (SCC)
Correspondence to: D. Michal Freedman, PhD, Division of Cancer Epidemiology and Genetics, National Cancer Institute, EPS Rm 7036, 6120 Executive Blvd, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892-7238 (e-mail: mf101e{at}nih.gov).
We appreciate the opportunity to address comments by Garland et al. and Grant regarding our recent publication on vitamin D and cancer mortality. Garland et al. contend that we should have highlighted as "important" our finding of a statistically significantly lower risk of breast cancer mortality in women with higher (
62.5 nmol/L) levels of 25(OH)D and that we were incorrect to examine the linear trend in breast cancer mortality risk, which we determined was not statistically significant. As we said in the paper, we felt that it would be unwise to draw strong inferences about the categorical comparison, given the small number of cases involved (ie, a total of only 28 cases, with only eight in the higher category). Because of the necessarily arbitrary cut-point between the two categories (<62.5 and 62.5 nmol/L), we maintain that it was useful to examine the statistical significance of the trend in risk related to continuous incremental changes in serum vitamin D level. Also, given the small number of cases, we had low power to characterize specifically the dose–response relationship between serum vitamin D levels and breast cancer mortality risk in our data. Moreover, the study of breast cancer risk cited by Garland et al. as evidence of a threshold effect is a single study of breast cancer incidence risk, was interpreted by its authors as raising only "the possibility" of a threshold (1), and was evaluated using a linear trend across quintiles.
In his letter, Grant does not question the methods in our analysis; rather, he concludes that other studies, principally ecologic studies with neither individual vitamin D nor UV-B exposures, are more persuasive. Grant, however, does not acknowledge a major problem with ecologic designs––the inability to adjust for confounders at the individual level––or that this limitation could have contributed to spurious results. There is a need for additional studies with large numbers of 25(OH)D samples to help clarify the relationship between vitamin D and cancer risk.
REFERENCES
1. Bertone-Johnson ER, Chen WY, Holick MF, et al. Plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D and risk of breast cancer. Cancer Epidemiol Biomarkers Prev. (2005) 14(8):1991–1997.
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Del.icio.us What's this?
J Natl Cancer Inst 2008 100: 826.
J Natl Cancer Inst 2008 100: 826-827.
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