A series of prospective cohort studies have shown that people who are shorter in middle- and older-age experience an increased risk of future coronary heart disease (CHD).[1
] While several biologically plausible mechanisms for this effect have been advanced, the importance of one of the principal artifactual explanations – reverse causality due to shrinkage – remains largely unresolved.[1
] That is, the early stages of disease, which are undetectable at study entry, could lead to reductions in height and increase risk of coronary heart disease, thus generating the observed inverse stature-CHD associations.
Three observations provide mixed support for the reverse causality explanation. First, if reverse causality is generating the inverse relation between height with CHD in cohort studies, the magnitude of any height-CHD gradient should diminish over time. This is because individuals with sub-clinical disease at study entry would be expected to die in the earlier stages of follow-up, so contributing a declining proportion of person years to the risk set. In reports from studies with between 20[2
] and 36[3
] years of follow-up, the absence of a height-CHD effect provides some support for reverse causality. In a second approach, student populations who had their height assessed at University enrolment in early adulthood, when this measurement can largely be regarded as being pre-morbid and therefore pre-shrinkage, were followed for mortality experience. These studies, in contrast, showed greater height was associated with reduced CHD risk[4
] so failing to support the reverse causality explanation.
The third observation comes from studies that have examined the relation between components of height – trunk and leg length – and future CHD.[6
] With the trunk, but not the leg length, being subject to shrinkage due to osteoporotic vertical collapse, an inverse association of the former but not the latter with CHD would be anticipated if reverse causality was a likely explanation for the inverse overall height-CHD association. The finding that leg length was, in fact, the component of height that showed the strongest inverse relation with CHD provides evidence against the reverse causality explanation,[6
] although this is not a universal finding.[8
With height measured on only one occasion in these published analyses, none of the three approaches directly explores, nor quantifies, reverse causality due to shrinkage. In the only study of which we are aware to examine the relation of height loss between two time points and subsequent CHD, there was a suggestion of increased risk in older men undergoing the greatest degree of shrinkage.[9
] We further examine the relation of height loss with later CHD in participants in a prospective cohort study who had their height measured on two occasions. In doing so, we provide the first examination of CHD and height loss in women who typically experience a greater degree of decline in physical stature over time than men.[10