Abstract
We identified demographic, lifestyle, and clinical factors associated with vitamin D status among breast cancer survivors. The vitamin D prediction model may be a useful surrogate of circulating 25-hydroxvitamin D (25(OH)D) concentrations when this measure was not available. We included a total of 216 Korean breast cancer survivors aged 21–79 years who had been diagnosed with stage I to III primary breast cancer and had breast cancer surgery at least 6 months before enrolment. We used linear and logistic regressions to identify determinants for the plasma 25(OH)D concentrations and vitamin D insufficiency (plasma 25(OH)D concentration < 50 nmol/L). We observed that 48.85% of breast cancer survivors had a plasma 25(OH)D concentration less than 50 nmol/L. We identified the following determinants for plasma 25(OH)D concentrations: time since diagnosis (β = −0.005 for 1 month increment), supplementary vitamin D intake (β = 0.06 for 10 μg/day increment), season of the blood draw (β = 0.35 for summer; β = 0.32 for fall; β = 0.26 for winter vs. spring), smoking status (β = 0.28 for former vs. never), use of any supplement (β = −0.35 for non-use vs. use), and the parity number (β = −0.30 for three or more vs. one) were associated with the plasma 25(OH)D concentrations. In addition to the aforementioned variables, body mass index (BMI) was associated with the prevalence of vitamin D insufficiency. We identified the determinants for the plasma 25(OH)D concentrations among Korean breast cancer survivors. Future studies are needed to investigate the role of vitamin D in the progression of breast cancer among Korean breast cancer survivors.
Highlights
Vitamin D from diet and supplements and from synthesis in the skin is first metabolized to25-hydroxyvitamin D (25(OH)D) in the liver and further metabolized to 1,25-dihydroxyvitaminD (1,25(OH)2D) by 1-α-hydroxylase in the kidney and other tissues
We aimed to develop a predicted 25(OH)D score and identify the demographic, lifestyle, and clinical factors associated with vitamin D status among breast cancer survivors
When we included all of these determinants in the multivariate linear regression models (Adjusted R2 = 0.33); we identified that time since diagnosis (β = −0.005 for 1 month increment), supplementary vitamin D intake (β = 0.06 for 10 μg/day increment), season of the blood draw (β = 0.35 for summer; β = 0.32 for fall; β = 0.26 for winter vs. spring), smoking status (β = 0.28 for former vs. never), use of any supplement (β = −0.35 for non-use vs. use), the parity number (β = −0.30 for three or more vs. one), and the centre (β = −0.30 for centre 2 vs. 1; β = −0.36 for centre 3 vs. 1) were associated with the plasma 25(OH)D concentrations (Table 2)
Summary
Vitamin D from diet and supplements and from synthesis in the skin is first metabolized to25-hydroxyvitamin D (25(OH)D) in the liver and further metabolized to 1,25-dihydroxyvitaminD (1,25(OH)2D) by 1-α-hydroxylase in the kidney and other tissues. Vitamin D from diet and supplements and from synthesis in the skin is first metabolized to. The actions of 1,25(OH)2D are receptor mediated, and vitamin D receptors are present in normal and malignant breast tissues [1]. Increasing the vitamin D concentrations has been suggested to decrease the risk of breast cancer [2,3]. Carcinogenesis-related functions of vitamin D include an increase in cellular differentiation, T-cell mediated immunity, cell-cycle arrest, and apoptosis and a decrease in proliferation, invasiveness, and metastasis [1,4,5,6,7]. The vitamin D status in the circulation is determined by exogenous sources from dietary and supplemental intake, endogenous production through synthesis in the skin, and the activities of vitamin D metabolic enzymes [9,10]
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