Height, wealth, and health: An overview with new data from three longitudinal studies
Introduction
The characteristic of physical stature has been utilised for many years in the fields of economic history and development, anthropology, anthropometry and, more recently, epidemiology. Economists have typically regarded height as a marker of historical prosperity – one which conventional, contemporaneous indicators fail to capture – that may, in turn, reflect differences in health and longevity within and between countries. Anthropologists, on the other hand, have been more concerned with the influence of various nutritional privations on height.
Over the last two decades, epidemiologists have begun to take an interest in adult stature (Waaler, 1984, Walker et al., 1989, Gunnell, 2002, Batty et al., 2006a) as the volume of research into the early life origins of chronic disease, specifically cardiovascular disease, has increased exponentially. The use of stature in this manner has arisen out of the paucity of longitudinal studies which hold data on prospectively gathered early life factors and adult disease outcomes; that is, studies which follow population-based childhood groups for several decades through into middle- and older age when the majority of clinical events occur. Height, which may capture, amongst other insults, early life illness, socioeconomic disadvantage, sub-optimal nutrition, and psychosocial stress has the added advantage of varying little during adult years, although some “shrinkage” in trunk length owing to osteoporotic vertical collapse appears to occur (see later discussions).
Taking largely an epidemiological perspective, but aiming wherever possible to incorporate findings from the afore named fields, the objectives of this overview are fourfold: (a) to outline the major determinants of height, so providing an indication as to what exposures this characteristic may capture; (b) to review reports from large scale studies to summarise the relation between adult height and a range of disease outcomes – both somatic and psychiatric – with a particular emphasis on cardiovascular disease; (c) to discuss why these relationships may exist, in particular the role, if any, of socioeconomic position in explaining the apparent associations; and, finally, (d) to outline future research directions in this field. For the purpose of illustration, we introduce new data from other studies: the original Whitehall study of men (Reid et al., 1974), the second Whitehall study of men and women (Marmot and Brunner, 2005), and the Vietnam Experience Study of men (TCDCVES, 1987, Batty et al., 2008d).
Section snippets
Determinants of height
As evidenced by the classic studies demonstrating the predictive value of midparental height for offspring stature (Galton, 1885, Pearson and Lee, 1903), height is clearly under a large degree of genetic control. Indeed, estimates suggest that up to 80% of the phenotypic variation in height in a given population is determined by genetic factors (Carmichael and McGue, 1995, Silventoinen et al., 2003, Perola et al., 2007). However, for centuries it has also been recognised that environmental
Height as a determinant of chronic disease
Given that height may capture the afore-described pre-adult socioeconomic, nutritional, psychological, and infectious insults, it has been related to a series of morbidities to test the hypothesis that pre-adult exposures may have a long term impact on adult health. In the main, the outcomes considered have been all-cause mortality, cardiovascular disease – principally comprising coronary heart disease, stroke (including sub-types of haemorrhagic and ischaemic) – and cancer. A much smaller
Conclusions and future research directions
Although very few experimental studies have been conducted, there is good observational evidence to suggest that, while undoubtedly under a large degree of genetic control, height is also influenced by early life environmental factors, which include nutrition, psychosocial stress, chronic illness, and living circumstances. Height consistently reveals inverse relations with total mortality (weakly), CHD (more strongly) and possibly stroke, that appear to be robust to the adjustment of
Funding
The Medical Research Council (MRC) Social and Public Health Sciences Unit receives funding from the UK MRC and the Chief Scientist Office at the Scottish Government Health Directorates. David Batty is a Wellcome Trust Fellow (WBS U.1300.00.006.00012.01). Martin Shipley is supported by the British Heart Foundation, Mika Kivimaki by the Academy of Finland, and Rachel Huxley by a Career Development Award from the National Heart Foundation of Australia
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