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量化肥胖流行期间基因对体重指数的影响:来自 HUNT 研究的纵向发现。

Quantifying the impact of genes on body mass index during the obesity epidemic: longitudinal findings from the HUNT Study.

机构信息

Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Postboks 8905, 7491 Trondheim, Norway

Department of Paediatrics, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.

出版信息

BMJ. 2019 Jul 3;366:l4067. doi: 10.1136/bmj.l4067.

DOI:10.1136/bmj.l4067
PMID:31270083
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6607203/
Abstract

OBJECTIVES

To study the trajectories of body mass index (BMI) in Norway over five decades and to assess the differential influence of the obesogenic environment on BMI according to genetic predisposition.

DESIGN

Longitudinal study.

SETTING

General population of Nord-Trøndelag County, Norway.

PARTICIPANTS

118 959 people aged 13-80 years who participated in a longitudinal population based health study (Nord-Trøndelag Health Study, HUNT), of whom 67 305 were included in analyses of association between genetic predisposition and BMI.

MAIN OUTCOME MEASURE

BMI.

RESULTS

Obesity increased in Norway starting between the mid-1980s and mid-1990s and, compared with older birth cohorts, those born after 1970 had a substantially higher BMI already in young adulthood. BMI differed substantially between the highest and lowest fifths of genetic susceptibility for all ages at each decade, and the difference increased gradually from the 1960s to the 2000s. For 35 year old men, the most genetically predisposed had 1.20 kg/m (95% confidence interval 1.03 to 1.37 kg/m) higher BMI than those who were least genetically predisposed in the 1960s compared with 2.09 kg/m (1.90 to 2.27 kg/m) in the 2000s. For women of the same age, the corresponding differences in BMI were 1.77 kg/m (1.56 to 1.97 kg/m) and 2.58 kg/m (2.36 to 2.80 kg/m).

CONCLUSIONS

This study provides evidence that genetically predisposed people are at greater risk for higher BMI and that genetic predisposition interacts with the obesogenic environment resulting in higher BMI, as observed between the mid-1980s and mid-2000s. Regardless, BMI has increased for both genetically predisposed and non-predisposed people, implying that the environment remains the main contributor.

摘要

目的

研究挪威五十年间体重指数(BMI)的变化轨迹,并评估肥胖环境对 BMI 的影响是否存在遗传易感性差异。

设计

纵向研究。

地点

挪威特隆赫姆郡的一般人群。

参与者

118959 名年龄在 13-80 岁之间的人参加了一项基于人群的纵向健康研究(特隆赫姆健康研究,HUNT),其中 67305 人纳入了遗传易感性与 BMI 之间关系的分析。

主要观察指标

BMI。

结果

肥胖症在挪威的发病率从 20 世纪 80 年代中期到 90 年代中期开始上升,与较年长的出生队列相比,20 世纪 70 年代以后出生的人在年轻成年时的 BMI 就明显更高。在每个十年的所有年龄段,BMI 在遗传易感性最高和最低五分之一之间存在显著差异,并且这种差异从 20 世纪 60 年代到 2000 年代逐渐增加。对于 35 岁的男性,最具遗传易感性的人比最不具遗传易感性的人在 20 世纪 60 年代的 BMI 高 1.20kg/m(95%置信区间 1.03-1.37kg/m),而在 20 世纪 20 年代则高 2.09kg/m(1.90-2.27kg/m)。对于同龄的女性,BMI 的相应差异分别为 1.77kg/m(1.56-1.97kg/m)和 2.58kg/m(2.36-2.80kg/m)。

结论

本研究提供了证据表明,遗传易感性的人患更高 BMI 的风险更大,并且遗传易感性与肥胖环境相互作用导致 BMI 升高,如 20 世纪 80 年代中期至 2000 年代中期所观察到的那样。无论如何,遗传易感性和非遗传易感性的人的 BMI 都有所增加,这意味着环境仍然是主要的影响因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/2b4c33c5249c/bram047949.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/fc210fb7cfda/bram047949.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/aba6b8e38f26/bram047949.f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/2b4c33c5249c/bram047949.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/fc210fb7cfda/bram047949.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/aba6b8e38f26/bram047949.f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c6/6607203/2b4c33c5249c/bram047949.f3.jpg

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