Article

A Nested Case-Control Study of Plasma 25-Hydroxyvitamin D Concentrations and Risk of Colorectal Cancer

Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Bldg 2, Boston, MA 02115, USA.
CancerSpectrum Knowledge Environment (Impact Factor: 15.16). 08/2007; 99(14):1120-9. DOI: 10.1093/jnci/djm038
Source: PubMed

ABSTRACT Low vitamin D status has long been implicated in colorectal carcinogenesis. We investigated this relationship in a nested case-control study within the Health Professionals Follow-up Study (HPFS), a large ongoing study of male health professionals living in the United States.
Between 1993 and 2002, 179 colorectal cancer patients were diagnosed and matched to 356 control subjects by age and by month and year of blood collection. Results were also pooled with previously published results from the Nurses' Health Study (NHS) cohort, a large female cohort. Conditional logistic regression was used to analyze the association between plasma 25-hydroxyvitamin D [25(OH)D] and colorectal cancer, and pooled estimates were calculated using the method of DerSimonian and Laird. All statistical tests were two-sided.
In the HPFS, we observed a non-statistically significant inverse association between higher plasma 25(OH)D concentration and risk of colorectal cancer and a statistically significant inverse association for colon cancer (highest versus lowest quintile: odds ratio [OR] = 0.46, 95% confidence interval [CI] = 0.24 to 0.89; P(trend) = .005). After pooling the results from the HPFS and NHS, higher plasma 25(OH)D concentrations were statistically significantly associated with decreased risks of both colorectal cancer (highest versus lowest quintile, OR = 0.66, 95% CI = 0.42 to 1.05; P(trend) = .01) and colon cancer (highest versus lowest quintile, OR = 0.54, 95% CI = 0.34 to 0.86; P(trend) = .002). Inverse associations with plasma 25(OH)D concentration did not differ by location of colon cancer (proximal versus distal), but the number of patients was small and none of the associations was statistically significant. Opposite relationships between plasma 25(OH)D levels and risk of rectal cancers were found among men (positive) and women (inverse).
Our data provide additional support for the inverse association between vitamin D and colorectal and, in particular, colon cancer risk.

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    • "Fortunately, in the case for vitamin D's effect on colorectal cancer, evidence from epidemiological studies in individuals has been largely supportive. The majority of observational studies of serum 25(OH)D concentration or oral vitamin D intake [20] [21] [22] [23] [24] [25] [26] found significant, inverse relationships between vitamin D and risk colorectal cancer. While most studies have focused on the relationship between vitamin D and incidence of colorectal cancer, only a few studies have investigated the possible relationship between serum 25(OH)D status and colorectal cancer survival rates. "
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    ABSTRACT: To determine whether a higher serum 25-hydroxyvitamin D [25(OH)D] concentration at diagnosis is associated with longer survival of colorectal cancer patients. A meta-analysis was performed of studies of the relationship between 25(OH)D and mortality of patients with colorectal cancer. A random-effects model was used to calculate a pooled hazards ratio. Homogeneity was evaluated through a DerSimonian-Laird test. Higher serum concentrations of 25(OH)D were associated with lower mortality in patients with colorectal cancer. Patients in the highest quintile of 25(OH)D had 37% lower mortality from colorectal cancer compared to those in the lowest quintile of 25(OH)D (pooled odds ratio=0.63, p<0.0001). Dose-response curves showed lower hazard ratios for mortality with higher serum 25(OH)D through at least 40ng/ml. There were no exceptions. Higher serum 25(OH)D was associated with lower mortality of patients with colorectal cancer. These results suggest that colorectal cancer patients with deficient levels of serum 25(OH)D should have their levels restored to a normal range (30-80ng/ml). This could be done with regular testing of serum 25(OH)D to be confident that an adequate serum level is being maintained. Additional studies would be worthwhile to evaluate confounding or the possibility of reverse causation. Copyright © 2014. Published by Elsevier Ltd.
    The Journal of Steroid Biochemistry and Molecular Biology 12/2014; 148. DOI:10.1016/j.jsbmb.2014.12.010 · 4.05 Impact Factor
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    • "Fortunately, in the case for vitamin D's effect on colorectal cancer, evidence from epidemiological studies in individuals has been largely supportive. The majority of observational studies of serum 25(OH)D concentration or oral vitamin D intake [20] [21] [22] [23] [24] [25] [26] found significant, inverse relationships between vitamin D and risk colorectal cancer. While most studies have focused on the relationship between vitamin D and incidence of colorectal cancer, only a few studies have investigated the possible relationship between serum 25(OH)D status and colorectal cancer survival rates. "
    [Show abstract] [Hide abstract]
    ABSTRACT: To determine whether a higher serum 25-hydroxyvitamin D [25(OH)D] concentration at diagnosis is associated with longer survival of colorectal cancer patients. A meta-analysis was performed of studies of the relationship between 25(OH)D and mortality of patients with colorectal cancer. A random-effects model was used to calculate a pooled hazards ratio. Homogeneity was evaluated through a DerSimonian-Laird test. Higher serum concentrations of 25(OH)D were associated with lower mortality in patients with colorectal cancer. Patients in the highest quintile of 25(OH)D had 37% lower mortality from colorectal cancer compared to those in the lowest quintile of 25(OH)D (pooled odds ratio=0.63, p<0.0001). Dose-response curves showed lower hazard ratios for mortality with higher serum 25(OH)D through at least 40ng/ml. There were no exceptions. Higher serum 25(OH)D was associated with lower mortality of patients with colorectal cancer. These results suggest that colorectal cancer patients with deficient levels of serum 25(OH)D should have their levels restored to a normal range (30-80ng/ml). This could be done with regular testing of serum 25(OH)D to be confident that an adequate serum level is being maintained. Additional studies would be worthwhile to evaluate confounding or the possibility of reverse causation.
    The Journal of Steroid Biochemistry and Molecular Biology 12/2014; · 4.05 Impact Factor
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    • "The anticell differentiation effect has been correlated with cancer epidemiology. Recently, serum vitamin D levels have been found to be inversely associated with many malignancies, including breast cancer [4], head and neck cancer [5], colon cancer [6], prostate cancer [7], and pancreatic cancer [8]. In a systemic review and meta-analysis, it was found that there was a moderate inverse association between 25-hydroxy vitamin D [25(OH)D] concentrations and total cancer incidence and mortality [9]. "
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    ABSTRACT: Vitamin D and its analogues are widely used as treatments by clinical nephrologists, especially when treating chronic kidney disease (CKD) patients with secondary hyperparathyroidism. As CKD progresses, the ability to compensate for elevations in parathyroid hormone (PTH) and fibroblast growth factor-23 and for decreases in 1,25(OH)2D3 becomes inadequate, which results in hyperphosphatemia, abnormal bone disorders, and extra-skeletal calcification. In addition to its calciotropic effect on the regulation of calcium, phosphate, and parathyroid hormone, vitamin D has many other noncalciotropic effects, including controlling cell differentiation/proliferation and having immunomodulatory effects. There are several immune dysregulations that can be noted when renal function declines. Physicians need to know well both the classical and nonclassical functions of vitamin D. This review is an analysis from the nephrologist's viewpoint and focuses on the relationship between the vitamin D and the immune system, together with vitamin's clinical use to treat kidney diseases.
    01/2014; 2014:105456. DOI:10.1155/2014/105456
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