Pang Yao1, Liang Sun1, Ling Lu1, Hong Ding2, Xiafei Chen3, Lixin Tang3, Xinming Xu4, Gang Liu1, Yao Hu1, Yiwei Ma1, Feijie Wang1, Qianlu Jin1, He Zheng1, Huiyong Yin1, Rong Zeng5, Yan Chen1, Frank B Hu6, Huaixing Li1, Xu Lin1. 1. Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and. 2. Department of Nutrition and Food Hygiene, School of Public Health, Xinjiang Medical University, Urumqi 830011, China. 3. Huadong Hospital Affiliated with Fudan University, Shanghai 200040, China. 4. High School Affiliated to Fudan University, Shanghai 200433, China; and. 5. Key Laboratory of Systems Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and University of the Chinese Academy of Sciences, Shanghai 200031, China. 6. Departments of Nutrition and Epidemiology, Harvard T.H. Chan School of Public Health, Harvard University, Boston, Massachusetts 02115.
Abstract
Context: Little is known about how genetic and nongenetic factors modify responses of vitamin D supplementation in nonwhite populations. Objective: To investigate factors modifying 25-hydroxyvitamin D [25(OH)D] and bioavailable 25(OH)D [25(OH)DBio] responses after vitamin D3 supplementation. Design, Setting, Participants, and Intervention: In this 20-week, randomized, double-blinded, placebo-controlled trial, 448 Chinese withvitamin D deficiency received 2000 IU/d vitamin D3 or placebo. Main Outcome Measures: Serum 25(OH)D, vitamin D-binding protein (VDBP), parathyroid hormone (PTH) and calcium were measured, and 25(OH)DBio was calculated based on VDBP levels. Six common polymorphisms in vitamin D metabolism genes were genotyped. Results: Between-arm net changes were +30.6 ± 1.7 nmol/L for 25(OH)D, +2.7 ± 0.2 nmol/L for 25(OH)DBio, and -5.2 ± 1.2 pg/mL for PTH, corresponding to 70% [95% confidence interval (CI), 62.8% to 77.2%] net reversion rate for vitamin D deficiency at week 20 (P < 0.001). Only 25(OH)DBio change was positively associated with calcium change (P < 0.001). Genetic factors (GC-rs4588/GC-rs7041, VDR-rs2228570, and CYP2R1-rs10741657; P ≤ 0.04) showed stronger influences on 25(OH)D or 25(OH)DBio responses than nongenetic factors, including baseline value, body mass index, and sex. An inverse association of PTH-25(OH)D was demonstrated only at 25(OH)D of <50.8 (95% CI, 43.6 to 59.0) nmol/L. Conclusions: Supplemented 2000 IU/d vitamin D3 raised 25(OH)D and 25(OH)DBio but was unable to correct deficiency in 25% of Chinese participants, which might be partially attributed to the effect of genetic modification. More studies are needed to elucidate appropriate vitamin D recommendations for Asians and the potential clinical implications of 25(OH)DBio.
RCT Entities:
Context: Little is known about how genetic and nongenetic factors modify responses of vitamin D supplementation in nonwhite populations. Objective: To investigate factors modifying 25-hydroxyvitamin D [25(OH)D] and bioavailable 25(OH)D [25(OH)DBio] responses after vitamin D3 supplementation. Design, Setting, Participants, and Intervention: In this 20-week, randomized, double-blinded, placebo-controlled trial, 448 Chinese with vitamin D deficiency received 2000 IU/d vitamin D3 or placebo. Main Outcome Measures: Serum 25(OH)D, vitamin D-binding protein (VDBP), parathyroid hormone (PTH) and calcium were measured, and 25(OH)DBio was calculated based on VDBP levels. Six common polymorphisms in vitamin D metabolism genes were genotyped. Results: Between-arm net changes were +30.6 ± 1.7 nmol/L for 25(OH)D, +2.7 ± 0.2 nmol/L for 25(OH)DBio, and -5.2 ± 1.2 pg/mL for PTH, corresponding to 70% [95% confidence interval (CI), 62.8% to 77.2%] net reversion rate for vitamin D deficiency at week 20 (P < 0.001). Only 25(OH)DBio change was positively associated with calcium change (P < 0.001). Genetic factors (GC-rs4588/GC-rs7041, VDR-rs2228570, and CYP2R1-rs10741657; P ≤ 0.04) showed stronger influences on 25(OH)D or 25(OH)DBio responses than nongenetic factors, including baseline value, body mass index, and sex. An inverse association of PTH-25(OH)D was demonstrated only at 25(OH)D of <50.8 (95% CI, 43.6 to 59.0) nmol/L. Conclusions: Supplemented 2000 IU/d vitamin D3 raised 25(OH)D and 25(OH)DBio but was unable to correct deficiency in 25% of Chinese participants, which might be partially attributed to the effect of genetic modification. More studies are needed to elucidate appropriate vitamin D recommendations for Asians and the potential clinical implications of 25(OH)DBio.
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