Glueck C J, Laskarzewski P M, Suchindran C M, Chambless L E, Barrett-Connor E, Stewart P, Heiss G, Tyroler H A
Circulation. 1986 Jan;73(1 Pt 2):I51-61.
Using data from Lipid Research Clinics study participants at visit 2 (3972 and 2346 adult men and women), we examined the hypothesis that parental mortality from cardiovascular disease (CVD) or cancer before age 60 predicts their adult progeny's lipid and lipoprotein levels. Weighted regression analysis was used to control for the potential effect of progeny's other CVD risk factors (age, systolic blood pressure, Quetelet index, cigarette smoking, and alcohol consumption), and to assess for the effect of progeny's parental cause-specific mortality status on progeny's lipids and lipoproteins. Nearly all of the statistically significant parent-progeny predictions were for sons. Paternal death from CVD before age 60 years was associated with significantly higher plasma total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels in sons and (at marginal significance) in daughters, when compared with those in reference progeny with paternal survival over age 60 or over age 75. Maternal death from CVD before 60 was associated with lower levels of high-density lipoprotein cholesterol (HDL-C) in sons. Paternal and maternal death from cancer before age 60 years were associated with higher triglyceride levels in adult sons than in sons whose parents had lived beyond ages 60 and 75. Paternal all-cause mortality before age 60 was associated with higher cholesterol and triglycerides in sons; maternal all-cause mortality before age 60 was associated with depression of HDL-C in sons. Familial aggregation of lipids and lipoproteins may account, in part, for familial aggregation of CVD. Knowledge of family history facilitates identification of progeny at higher risk for CVD by virtue of elevated cholesterol or LDL-C, or reduced HDL-C.
利用脂质研究临床中心研究参与者在第2次访视时的数据(3972名成年男性和2346名成年女性),我们检验了以下假设:60岁之前因心血管疾病(CVD)或癌症导致的父母死亡可预测其成年后代的脂质和脂蛋白水平。采用加权回归分析来控制后代其他CVD风险因素(年龄、收缩压、体重指数、吸烟和饮酒)的潜在影响,并评估后代父母特定病因死亡率状况对其脂质和脂蛋白的影响。几乎所有具有统计学意义的亲子预测都是针对儿子的。与父亲活到60岁以上或75岁以上的参照后代相比,60岁之前因CVD导致的父亲死亡与儿子血浆总胆固醇和低密度脂蛋白胆固醇(LDL-C)水平显著升高相关,女儿也有(边缘显著性)升高。60岁之前因CVD导致的母亲死亡与儿子高密度脂蛋白胆固醇(HDL-C)水平较低相关。60岁之前因癌症导致的父亲和母亲死亡与成年儿子的甘油三酯水平高于父母活到60岁和75岁以上的儿子相关。60岁之前父亲的全因死亡率与儿子的胆固醇和甘油三酯升高相关;60岁之前母亲的全因死亡率与儿子HDL-C降低相关。脂质和脂蛋白的家族聚集可能部分解释了CVD的家族聚集现象。了解家族病史有助于识别因胆固醇或LDL-C升高或HDL-C降低而患CVD风险较高的后代。