Martyn C N, Barker D J, Osmond C
Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital.
Lancet. 1996 Nov 9;348(9037):1264-8. doi: 10.1016/s0140-6736(96)04257-2.
People who have a low birthweight show increased death rates from coronary heart disease and a higher prevalence for its risk factors. These findings have led to the hypothesis that the disease is programmed in fetal life. The aim of this study was to explore whether risk of stroke in adult life was linked to impaired fetal growth.
We ascertained deaths from stroke and coronary heart disease in 13 249 men in two cohorts from Hertfordshire and Sheffield, UK. We related death rates from these disease to body size at birth, weight at 1 year, and to measurements of the mothers' pelvises.
Death rates from both stroke and coronary heart disease tended to be highest in men whose birthweight had been low. Standardised mortality ratios (SMRs) for stroke fell by 12% (95% Cl 1-22) and for coronary heart disease by 10% (6-14) between each of five groupings of increasing birthweight (< or = 5.5 lb, 5.6-6.5 lb, 6.6-7.5 lb, 7.6-8.5 lb, and > 8.5 lb). Mortality from stroke was most strongly associated with low birthweight in relation to head size, and low placental weight in relation to head size. These patterns of growth occurred in offspring of mothers with flat bony pelvises. The SMR in sons of these women was 184 (67-396) compared with 104 (78-138) in the remainder of the cohort. In contrast, mortality from coronary heart disease was associated with small head circumference, thinness or shortness at birth and an altered ratio of placental weight to birthweight.
Stroke may originate in poor nutrition during the mother's childhood, which deforms the bony pelvis and subsequently impairs her ability to sustain the growth of the placenta and fetus in late pregnancy. Coronary heart disease, on the other hand, seems to originate in adaptations made by the fetus to inadequate delivery of nutrients when it occurs for reasons other than failure of placental growth.
出生体重低的人冠心病死亡率增加,且其风险因素的患病率更高。这些发现导致了一种假说,即该疾病在胎儿期就已被编程。本研究的目的是探讨成年后中风风险是否与胎儿生长受损有关。
我们确定了来自英国赫特福德郡和谢菲尔德的两个队列中13249名男性的中风和冠心病死亡情况。我们将这些疾病的死亡率与出生时的体型、1岁时的体重以及母亲骨盆的测量值相关联。
出生体重低的男性中风和冠心病死亡率往往最高。在出生体重递增的五个分组(≤5.5磅、5.6 - 6.5磅、6.6 - 7.5磅、7.6 - 8.5磅和>8.5磅)中,中风的标准化死亡率(SMR)下降了12%(95%可信区间1 - 22),冠心病下降了10%(6 - 14)。中风死亡率与相对于头围的低出生体重以及相对于头围的低胎盘重量最密切相关。这些生长模式出现在骨盆扁平的母亲的后代中。这些女性儿子的SMR为184(67 - 396),而队列其余部分为104(78 - 138)。相比之下,冠心病死亡率与出生时头围小、消瘦或矮小以及胎盘重量与出生体重的比例改变有关。
中风可能源于母亲童年时期的营养不良,这使骨盆变形,随后损害了她在妊娠晚期维持胎盘和胎儿生长的能力。另一方面,冠心病似乎源于胎儿因胎盘生长失败以外的原因出现营养供应不足时所做出的适应性反应。