Department of Social and Preventive Medicine, School of Public Health and Health Professions, University at Buffalo, 270 Farber Hall, Buffalo, NY 14214-8001, USA.
Am J Clin Nutr. 2010 May;91(5):1324-35. doi: 10.3945/ajcn.2009.28908. Epub 2010 Mar 10.
It is unclear how well surrogate markers for vitamin D exposure (eg, oral intake of vitamin D and estimates of sunlight exposure), with and without consideration of other potential predictors of 25-hydroxyvitamin D [25(OH)D] concentrations, similarly rank individuals with respect to 25(OH)D blood concentrations.
The objective was to determine how much variation in serum 25(OH)D concentrations (nmol/L) could be explained by a predictive model with the use of different vitamin D surrogate markers (latitude of residence, mean annual regional solar irradiance estimates, and oral sources) and other individual characteristics that might influence vitamin D status.
A random sample of 3055 postmenopausal women (aged 50-70 y) participating in 3 nested case-control studies of the Women's Health Initiative Calcium plus Vitamin D Clinical Trial was used. Serum 25(OH)D values, assessed at year 1 (1995-2000), and potential predictors of 25(OH)D concentrations, assessed at year 1 or Women's Health Initiative baseline (1993-1998), were used.
More than half of the women (57.1%) had deficient (<50 nmol/L) concentrations of 25(OH)D. Distributions of 25(OH)D concentrations by level of latitude of residence, mean annual regional solar irradiance, and intake of vitamin D varied considerably. The predictive model for 25(OH)D explained 21% of the variation in 25(OH)D concentrations. After adjustment for month of blood draw, breast cancer status, colorectal cancer status, fracture status, participation in the hormone therapy trial, and randomization to the dietary modification trial, the predictive model included total vitamin D intake from foods and supplements, waist circumference, recreational physical activity, race-ethnicity, regional solar irradiance, and age.
Surrogate markers for 25(OH)D concentrations, although somewhat correlated, do not adequately reflect serum vitamin D measures. These markers and predictive models of blood 25(OH)D concentrations should not be given as much weight in epidemiologic studies of cancer risk.
目前尚不清楚维生素 D 暴露的替代标志物（例如，维生素 D 的口服摄入量和估计的阳光暴露量），以及是否考虑到 25-羟维生素 D [25(OH)D]浓度的其他潜在预测因素，在多大程度上可以类似地对 25(OH)D 血浓度进行个体排序。
本研究旨在确定使用不同的维生素 D 替代标志物（居住地纬度、平均年区域太阳辐射估计值和口服来源）和其他可能影响维生素 D 状态的个体特征，预测模型可以解释多少血清 25(OH)D 浓度（nmol/L）的变异。
使用参加妇女健康倡议钙加维生素 D 临床试验的 3 项嵌套病例对照研究的随机抽样 3055 名绝经后妇女（年龄 50-70 岁）。在第 1 年（1995-2000 年）评估血清 25(OH)D 值，并在第 1 年或妇女健康倡议基线（1993-1998 年）评估 25(OH)D 浓度的潜在预测因素。
超过一半的女性（57.1%）的 25(OH)D 浓度不足（<50 nmol/L）。居住地纬度、平均年区域太阳辐射和维生素 D 摄入量的 25(OH)D 浓度分布差异很大。25(OH)D 预测模型解释了 25(OH)D 浓度变异的 21%。在调整采血月份、乳腺癌状态、结直肠癌状态、骨折状态、参加激素治疗试验以及随机分配到饮食修改试验后，预测模型包括食物和补充剂中的总维生素 D 摄入量、腰围、休闲身体活动、种族-民族、区域太阳辐射和年龄。
25(OH)D 浓度的替代标志物虽然有些相关，但并不能充分反映血清维生素 D 测量值。在癌症风险的流行病学研究中，这些标志物和 25(OH)D 血浓度的预测模型不应给予同等重视。
