Fetal and childhood growth and hypertension in adult life
Fetal and childhood growth and hypertension in adult life
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DOI：
10.1161/01.hyp.36.5.790
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发表时间：
2000-11-01
期刊：
影响因子：
8.3
通讯作者：
Barker, D
中科院分区：
文献类型：
--
作者：
Eriksson, J;Forsén, T;Barker, D
低出生体重和高血压之间的联系已被广泛复制。关于儿童期的生长如何改变低出生体重的影响，人们知之甚少。我们报告了1924-1933年间出生于芬兰赫尔辛基的7086人队列中1958名接受高血压治疗的男性和女性的胎儿和儿童期生长情况。与预期的一样，患有高血压的男性和女性出生时体重较低（P = 0.002），出生时身长也较短（P = 0.02）。出生后，他们经历了加速增长，因此，7岁时，他们的身高和体重接近平均水平。在同步回归中，出生时的身长和身高对高血压有统计学意义，尽管有相反的影响（出生时的身长P = 0.003，7岁时的身高P = 0.009）。出生后生长加速与儿童生活条件改善有关。那些后来同时患上高血压和2型糖尿病的儿童，而不是单纯的高血压，在出生时胎盘尺寸和身体尺寸都很小，他们出生后的加速生长持续了7年以上。我们认为，高血压可能起源于子宫内生长迟缓，随后由于良好的生活条件而加速出生后的生长。胎儿生长迟缓导致肾脏和其他组织中的细胞数量永久性减少，随后的加速生长可能导致对这种有限细胞群的过度代谢需求。
The association between low birth weight and raised blood pressure has been extensively replicated. Little is known about the way childhood growth modifies the effects of low birth weight. We report on the fetal and childhood growth of 1958 men and women who received treatment for hypertension and belong to a cohort of 7086 people born in Helsinki, Finland, during 1924-1933. As expected, the men and women who developed hypertension had low birth weight (P = 0.002), They were also shorter in body length at birth (P = 0,02). After birth they experienced accelerated growth, so that by 7 years their heights and weights were approximately average. In a simultaneous regression, both birth length and tall height had statistically significant although opposing effects on hypertension (P = 0.003 for birth length and 0.009 for height at 7 years). Accelerated postnatal growth was associated with better childhood living conditions. Children who later developed both hypertension and type 2 diabetes, rather than hypertension alone, had small placental size as well as small body size at birth, and their accelerated postnatal growth continued beyond 7 years. We suggest that hypertension may originate through retarded growth in utero followed by accelerated postnatal growth as a result of good living conditions. Retarded fetal growth leads to permanently reduced cell numbers in the kidney and other tissues, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass.