IQ in childhood and atherosclerosis in middle-age: 40 Year follow-up of the Newcastle Thousand Families Cohort Study
Introduction
Findings from extended follow-up of a series cohort studies initiated in childhood reveal an association between lower childhood IQ scores and raised coronary heart disease (CHD) events in middle- and older-age [1], [2], [3], [4], [5], [6], [7]. These effects do not appear to be due to reverse causality or confounding. Despite these concordant reports of the IQ-CHD association, explanations for it remain unclear. One suggestion is that established behavioural (smoking, diet, heavy alcohol intake, physical inactivity) [8], [9], [10], [11] and cardiometabolic (obesity, metabolic syndrome) [12], [13], [14] CHD risk factors, which are also related to IQ, lie on the pathways linking IQ with CHD, although this appears to be only partially the case [2].
Further insight into the mechanisms by which IQ is associated with CHD is limited by the use of clinical CHD outcomes, such as fatal and non-fatal myocardial infarction, which occur late in the natural history of the disease. Atherosclerosis, the most significant pathology giving rise to CHD, is characterised by a thickening of the artery wall [15]. The degree of atherosclerosis can be determined using a range of methods including carotid-wall intima-media thickness (IMT) [15] and ankle brachial index [16], both of which offer predictive validity for coronary events [17], [18] and other relevant outcomes such as stroke [19] and dementia [20]. In the only prospective study of which we are aware, IQ in early adulthood was inversely related to ankle brachial index [21], a marker of atherosclerosis, but this was a study of men who were recruited from the US army, so raising concerns regarding the generalisability of the results. Accordingly, we used the Newcastle Thousand Families Study, a general population-based study of men and women to further examine the relationship between IQ between in childhood and IMT ascertained in middle-age.
Section snippets
Material and methods
The Newcastle Thousand Families Study is a prospective birth cohort study of all 1142 children (583 males, 559 females) born in May and June 1947 to mothers then residing in the city of Newcastle upon Tyne, UK [22], [23]. In 1958, the children sat the so-called ‘11-plus’ examination, a standard IQ-type test widely used in English schools at that time for the purposes of educational selection from primary to secondary education [24]. The full range of tests taken included the Moray House Tests
Results
Of the 412 individuals who attended the screening examination and returned the questionnaires at the age 49–51 years, 278 (67.6%; 127 men, 151 women) had complete data relevant to these analyses. There was no marked nor statistically significant difference in mean childhood IQ and IMT between those with complete data and those excluded owing to missing data (mean childhood IQ, excluded 100.6 vs. included 100.4, p = 0.12; mean IMT, excluded 0.80 vs. included 0.86, p = 0.08).
In the group of 278
Discussion
In this prospective cohort study, having a higher overall childhood IQ, and higher scores on tests of English and arithmetic were significantly associated with lower IMT at age 50 in both men and women. On controlling for selected confounding or mediating variables, the strength of these associations were essentially unchanged in men but increased in women. To our knowledge, only one previous paper has examined the association between early life cognition and later life atherosclerosis [21]. In
Significance
This is only the second paper to examine the association between childhood intelligence and atherosclerosis in adulthood and the first to examine this in a population sample using intima-media thickness. It has shown that those of lower childhood intelligence may be at higher risk of atherosclerosis in adulthood. In this study there was a suggestion of partial mediation by intermediary risk factors, although, importantly, none of these appeared to completely account for the IQ-IMT association.
Sources of funding
BAR, GDB, CRG and IJD are members of The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (G0700704/84698). Funding from the BBSRC, EPSRC, ESRC and MRC is gratefully acknowledged. David Batty was a Wellcome Trust fellow during the early preparation of this manuscript.
Disclosures
None.
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