Department of Pediatrics (M.M., V.S., J.M., O.S., J.T., R.H.), University of Turku, 20520 Turku, Finland and Turku University Hospital, 20520 Turku, Finland; Immunogenetics Laboratory (J.I.), University of Turku, 20520 Turku, Finland; Department of Clinical Microbiology (J.I.), University of Eastern Finland, 70211 Kuopio, Finland; Department of Pediatrics (R.V.), University of Oulu, 90014 Oulu, Finland and Oulu University Hospital, 90029 Oulu, Finland; Department of Virology (H.H.), University of Tampere, 33520 Tampere, Finland; Fimlab Laboratories (H.H.), Pirkanmaa Hospital District, 33520 Tampere, Finland; Children's Hospital (M.K.), University of Helsinki and Helsinki University Central Hospital 00029 Helsinki, Finland; Diabetes and Obesity Research Program (M.K.), University of Helsinki, 00014 Helsinki, Finland; Folkhälsan Research Center (M.K.), 00290 Helsinki, Finland; Department of Pediatrics (M.K.), Tampere University Hospital, 33521 Tampere, Finland; and Department of Physiology (J.T.), University of Turku, 20520 Turku, Finland.
J Clin Endocrinol Metab. 2014 Nov;99(11):E2353-6. doi: 10.1210/jc.2014-1455. Epub 2014 Jul 25.
In Finland the world-record for the highest incidence of type 1 diabetes has risen steeply over the past decades. However, after 2006 the incidence rate has plateaued. We showed earlier, that despite the strong genetic disease component, environmental factors are driving the increasing disease incidence.
Since vitamin D intake has increased considerably in the country since 2003, we analyzed how serum 25-hydroxyvitamin D (25[OH]D) concentration changed over time in healthy children, and the timely relation of these changes to disease incidence.
DESIGN, SETTING AND PARTICIPANTS: The birth cohort of the Finnish Type 1 Diabetes Prediction and Prevention project was used to explore longitudinal changes in serum 25-hydroxyvitamin concentrations. The sampling period was limited to children born from 1994 to 2004, with serum samples collected during 1998-2006 in the Turku area, Southwest Finland (60 °N).
25(OH)D concentrations were measured every 3-6 months from birth, ages ranging from 0.3 to 12.2 years (387 subjects, 5334 measurements).
Serum 25(OH)D concentrations were markedly lower before 2003 than after (69.3 ± 1.0 nmol/L vs 84.9 ± 1.3 nmol/L, respectively, P < .001) in both genders. The mean difference between the periods was 15.7 ± 1.3 nmol/L (P < .001). Importantly, the frequency of children with low serum 25(OH)D levels (< 50 nmol/L) was reduced to almost half from 2003 (37.3% vs 69.9 %; P < .001). Similarly, severe vitamin D deficiency (<25 nmol/L) also decreased (2.7% vs 7.7%; P = .005). In addition, we detected higher 25(OH)D concentrations in young children (< 2 years) as compared to older children, which is explained by higher vitamin D intake in this group.
We provide evidence that an increase in circulating concentrations of 25(OH)D shows a delayed temporal association with leveling off of type 1 diabetes incidence in Finland after 2006.
在过去几十年中，芬兰的 1 型糖尿病发病率一直呈急剧上升趋势。然而，自 2006 年以来，发病率已趋于平稳。我们之前曾表明，尽管 1 型糖尿病具有很强的遗传疾病成分，但环境因素正在推动疾病发病率的上升。
自 2003 年以来，芬兰的维生素 D 摄入量大幅增加，因此我们分析了健康儿童的血清 25-羟维生素 D（25[OH]D）浓度随时间的变化情况，以及这些变化与疾病发病率的及时关系。
设计、地点和参与者：芬兰 1 型糖尿病预测和预防项目的出生队列用于探索血清 25-羟维生素浓度的纵向变化。采样期仅限于 1994 年至 2004 年出生的儿童，血清样本于 1998-2006 年在芬兰西南部图尔库地区（60°N）采集。
从出生开始，每 3-6 个月测量一次 25（OH）D 浓度，年龄从 0.3 至 12.2 岁（387 名受试者，5334 次测量）。
无论性别如何，2003 年前的血清 25（OH）D 浓度均明显低于 2003 年后（分别为 69.3±1.0 nmol/L 和 84.9±1.3 nmol/L，P<0.001）。两个时期之间的平均差异为 15.7±1.3 nmol/L（P<0.001）。重要的是，血清 25（OH）D 水平低（<50 nmol/L）的儿童比例从 2003 年开始几乎减半（37.3%对 69.9%；P<0.001）。同样，严重的维生素 D 缺乏症（<25 nmol/L）也有所减少（2.7%对 7.7%；P=0.005）。此外，我们发现年龄较小的儿童（<2 岁）的 25（OH）D 浓度高于年龄较大的儿童，这是由于该组的维生素 D 摄入量较高所致。
我们的研究结果表明，25（OH）D 循环浓度的增加与芬兰 1 型糖尿病发病率在 2006 年后趋于平稳之间存在延迟的时间关联。
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