Cooper C, Eriksson J G, Forsén T, Osmond C, Tuomilehto J, Barker D J
The MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, UK.
Osteoporos Int. 2001;12(8):623-9. doi: 10.1007/s001980170061.
Although measures to enhance bone mineralization during childhood and adolescence are widely incorporated into preventive programmes against osteoporotic fracture, there are no published data directly linking growth rates in childhood with the risk of later hip fracture. We addressed this issue in a unique Finnish cohort in whom birth and childhood growth data were linked to later hospital discharge records. This permitted follow-up of 3639 men and 3447 women who were born in Helsinki University Central Hospital between 1924 and 1933, who went to school in Helsinki and still lived in Finland in 1971. Body size at birth was recorded and an average of 10 measurements were obtained of height and weight throughout childhood. We identified 112 subjects (55 men and 57 women) who sustained a hip fracture during 165 404 person-years of follow-up. After adjustment for age and sex in a proportional hazards model, we identified two major determinants of hip fracture risk: tall maternal height (p < 0.001) and a low rate of childhood growth (height, p = 0.006; weight, p = 0.01). The hazard ratio for hip fracture was 2.1 (95% CI 1.2-3.5) among men and women born to mothers taller than 1.61 m, when compared with those whose mothers were shorter than 1.54 m. The ratio was 1.9 (95% CI 1.1-3.2) among those whose rate of childhood height gain was below the lowest quartile for the cohort, compared with those whose growth rate was above the highest quartile. The effects of maternal height and childhood growth rate were statistically independent of each other, and remained after adjusting for socioeconomic status. The patterns of childhood growth that predicted future hip fracture differed between boys and girls. In boys, there was a constant deficit in height and weight between ages 7 and 15 years among those later sustaining fractures; in girls, there was a progressively increasing deficit in weight but a delayed height gain among those later sustaining fractures. This epidemiologic study provides the first direct evidence that a low rate of childhood growth is a risk factor for later hip fracture. Whether reduced growth rate is a consequence of childhood lifestyle, genetic background or intrauterine hormonal programming, the data support measures to optimize childhood growth as part of preventive strategies against osteoporotic fracture in future generations.
尽管在儿童期和青春期增强骨矿化的措施已广泛纳入预防骨质疏松性骨折的计划中,但尚无公开数据直接将儿童期的生长速度与日后髋部骨折的风险联系起来。我们在一个独特的芬兰队列中研究了这个问题,该队列中出生和儿童期生长数据与后来的医院出院记录相关联。这使得对1924年至1933年在赫尔辛基大学中心医院出生、在赫尔辛基上学且1971年仍居住在芬兰的3639名男性和3447名女性进行了随访。记录了出生时的身体尺寸,并在整个儿童期平均进行了10次身高和体重测量。我们确定了112名受试者(55名男性和57名女性),他们在165404人年的随访期间发生了髋部骨折。在比例风险模型中对年龄和性别进行调整后,我们确定了髋部骨折风险的两个主要决定因素:母亲身高较高(p<0.001)和儿童期生长速度较低(身高,p = 0.006;体重,p = 0.01)。与母亲身高低于1.54米的人相比,母亲身高高于1.61米的男性和女性发生髋部骨折的风险比为2.1(95%CI 1.2 - 3.5)。与生长速度高于队列最高四分位数的人相比,儿童期身高增长速度低于队列最低四分位数的人发生髋部骨折的风险比为1.9(95%CI 1.1 - 3.2)。母亲身高和儿童期生长速度的影响在统计学上相互独立,并且在调整社会经济地位后仍然存在。预测未来髋部骨折的儿童期生长模式在男孩和女孩之间有所不同。在男孩中,后来发生骨折的人在7至15岁之间身高和体重持续不足;在女孩中,后来发生骨折的人体重逐渐增加不足,但身高增长延迟。这项流行病学研究提供了首个直接证据,即儿童期生长速度较低是日后髋部骨折的一个风险因素。无论生长速度降低是儿童期生活方式、遗传背景还是宫内激素编程的结果,这些数据都支持将优化儿童期生长作为预防后代骨质疏松性骨折策略的一部分的措施。