Maternal height, childhood growth and risk of hip fracture in later life:: A longitudinal study
Maternal height, childhood growth and risk of hip fracture in later life:: A longitudinal study
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DOI：
10.1007/s001980170061
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发表时间：
2001-01-01
影响因子：
4
通讯作者：
Barker, DJP
中科院分区：
文献类型：
--
作者：
Cooper, C;Eriksson, JG;Barker, DJP
虽然在儿童和青少年时期加强骨矿化的措施已被广泛纳入预防骨质疏松性骨折的方案，但没有公布的数据将儿童时期的生长速度与以后髋部骨折的风险直接联系起来。我们在一个独特的芬兰队列中解决了这个问题，该队列的出生和儿童生长数据与后来的出院记录有关。这项研究对1924年至1933年出生于赫尔辛基大学中心医院的3639名男性和3447名女性进行了随访，他们在赫尔辛基上学，1971年仍住在芬兰。记录出生时的身体尺寸，并在整个童年期间获得平均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人年的随访中发生了髋部骨折。在比例风险模型中调整年龄和性别后，我们确定了髋部骨折风险的两个主要决定因素：母亲身高高（p < 0.001）和儿童生长速度低（身高，p = 0.006;体重，p = 0.01）。与母亲身高小于1.54英寸的人群相比，母亲身高大于1.61英寸的人群发生髋部骨折的风险比为2.1（95%CI 1.2-3.5）。儿童期身高增长率低于队列最低四分位数的儿童与增长率高于最高四分位数的儿童的比率为1.9（95%CI 1.1-3.2）。母亲身高和儿童生长速度的影响在统计学上相互独立，并在调整社会经济地位后保持不变。预测未来髋部骨折的儿童生长模式在男孩和女孩之间存在差异。在男孩中，有一个恒定的赤字，在7岁和15岁之间的那些后来持续骨折;在女孩中，有一个逐步增加的赤字，体重，但延迟的身高增长之间的那些后来持续骨折。这项流行病学研究提供了第一个直接证据，表明儿童生长速度慢是日后髋部骨折的危险因素。无论生长率降低是儿童生活方式、遗传背景还是宫内激素编程的结果，数据支持采取措施优化儿童生长，作为预防后代骨质疏松性骨折的预防战略的一部分。
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 in, when compared with those whose mothers were shorter than 1.54 in. The ratio was 1.9 (95% Cl 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.