Laskarzewski P M, Khoury P, Morrison J A, Kelly K, Mellies M J, Glueck C J
Int J Obes. 1983;7(6):505-27.
Using the Princeton School District Family Study cohort, our specific aim was to estimate the prevalence of suspected familial ponderosity and leanness, to provide empirical risk estimates for the proportion of probands' first-degree relatives who were similarly affected, and to estimate the contributions of diseases, drugs and caloric intake to relative obesity and leanness. We studied 379 probands, 125 whites and 52 blacks from a random recall group, 147 whites and 55 blacks from a hyperlipidemic recall group. Suspected familial obesity and leanness were arbitrarily identified in those kindreds with at least two first-degree relatives in the same Quetelet index decile as the proband, top or bottom respectively. Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites. Suspected familial leanness was identified in 2.4 percent and 1.4 percent of random and hyperlipidemic recall whites and in 3.8 percent of randomly recalled blacks. Approximately twice as many as expected white first-degree relatives of top Quetelet index decile probands themselves had top decile Quetelet indices; approximately three times as many as expected first-degree relatives of bottom decile Quetelet index probands themselves had bottom decile Quetelet indices. Nineteen percent and 31 percent of top decile Quetelet index white probands from random and hyperlipidemic recall groups came from families where at least two other first-degree relatives were similarly obese; 18 percent and 20 percent of white random and hyperlipidemic recall group probands with bottom decile Quetelet indices had suspected familial leanness. Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus. Within-family clustering of hypertension was common in kindreds with suspected familial obesity and was absent in kindreds with suspected familial leanness. Marked within-family clustering of both obesity and leanness is useful diagnostically; therapeutic intervention to reduce obesity, to be most effective, should be family-wide in the many kindreds which share familial obesity.
利用普林斯顿学区家庭研究队列，我们的具体目标是估计疑似家族性肥胖和消瘦的患病率，为先证者中同样受影响的一级亲属比例提供实证风险估计，并估计疾病、药物和热量摄入对相对肥胖和消瘦的影响。我们研究了379名先证者，其中随机召回组有125名白人、52名黑人，高脂血症召回组有147名白人、55名黑人。在那些至少有两个一级亲属与先证者处于相同体重指数十分位数（分别为最高或最低）的家族中，任意确定疑似家族性肥胖和消瘦。在随机召回组和高脂血症召回组的白人中，分别有2.4%和6%观察到疑似家族性肥胖。在随机召回的白人中，有2.4%被确定为疑似家族性消瘦，高脂血症召回的白人中有1.4%，随机召回的黑人中有3.8%。体重指数十分位数最高的先证者的白人一级亲属中，自身体重指数处于最高十分位数的人数约为预期人数的两倍；体重指数十分位数最低的先证者的一级亲属中，自身体重指数处于最低十分位数的人数约为预期人数的三倍。随机召回组和高脂血症召回组中体重指数十分位数最高的白人先证者，分别有19%和31%来自至少有另外两个一级亲属同样肥胖的家庭；体重指数十分位数最低的随机召回组和高脂血症召回组白人先证者中，分别有18%和20%有疑似家族性消瘦。几乎所有有家族性肥胖或消瘦的受试者，其体型都没有明显的代谢或药理学解释。在疑似家族性肥胖的家族中，高血压的家族聚集现象很常见，而在疑似家族性消瘦的家族中则不存在。肥胖和消瘦在家族内的明显聚集在诊断上很有用；在许多存在家族性肥胖的家族中，为了使减肥治疗干预最有效，应该在全家族范围内进行。
