Abstract

See related article, pp 237–242 The adage that correlation does not prove causation is a well-worn qualification in the scientific literature. As such, modern observational studies, rightly, are critiqued frequently for optimistic causal inferences, and yet, it is important to remember that the classical cardiovascular risk factors (including blood pressure) we take for granted were elegantly framed by the iconic Framingham Study in one of the first uses of observational epidemiology in the noncommunicable diseases setting. Observational studies can, therefore, provide important clues and lines of enquiry into the causes of disease. The underlying potential causes of arterial stiffness and hemodynamic changes, in large and small vessels, remain inadequately defined. Although the practical use of such measures in the clinical setting is still a matter of considerable debate, they are generally associated with future cardiovascular risk.1 In the work of Zachariah et al,2 it is interesting to return to the offspring studies of the original Framingham cohort and ask the question “can we identify potentially modifiable causes of age-related decline in arterial health?” The authors looked specifically at body mass index (BMI), fasting glucose, and …

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