Associations of height, leg length, and lung function with cardiovascular risk factors in the Midspan Family Study

Abstract

Background: Taller people and those with better lung function are at reduced risk of coronary heart disease (CHD). Biological mechanisms for these associations are not well understood, but both measures may be markers for early life exposures. Some studies have shown that leg length, an indicator of pre-pubertal nutritional status, is the component of height most strongly associated with CHD risk. Other studies show that height-CHD associations are greatly attenuated when lung function is controlled for. This study examines (1) the association of height and the components of height (leg length and trunk length) with CHD risk factors and (2) the relative strength of the association of height and forced expiratory volume in one second (FEV₁) with risk factors for CHD. Subjects and methods: Cross sectional analysis of data collected at detailed cardiovascular screening examinations of 1040 men and 1298 women aged 30–59 whose parents were screened in 1972–76. Subjects come from 1477 families and are members of the Midspan Family Study. Setting: The towns of Renfrew and Paisley in the West of Scotland. Results: Taller subjects and those with better lung function had more favourable cardiovascular risk factor profiles, associations were strongest in relation to FEV₁. Higher FEV₁ was associated with lower blood pressure, cholesterol, glucose, fibrinogen, white blood cell count, and body mass index. Similar, but generally weaker, associations were seen with height. These associations were not attenuated in models controlling for parental height. Longer leg length, but not trunk length, was associated with lower systolic and diastolic blood pressure. Longer leg length was also associated with more favourable levels of cholesterol and body mass index than trunk length. Conclusions: These findings provide indirect evidence that measures of lung development and pre-pubertal growth act as biomarkers for childhood exposures that may modify an individual's risk of developing CHD. Genetic influences do not seem to underlie height-CHD associations.