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Koch and Pasteur provided modern medicine with its primary model of disease – that it has a specific and organic cause. Treatment is generally developed from an understanding of that agent of causation. Generations of medical students have been taught the causes of disease in their pathology classes: genetic, infection, trauma and so on. But for some situations such a model is inadequate. The boundaries between normality and abnormality blur, and can be situational and dependent on when and where an individual lives. Persistence of intestinal lactase function was the co-evolutionary outcome when groups of Homo sapiens started herding cattle and using their milk for food.1 So while northern Europeans and some Africans see lactase intolerance as a disease, and the label implies as much, for much of humanity non-persistence of lactase activity is the evolutionary norm and of no significance in a world, historically at least, largely free of cows’ milk. So we have a problem in defining disease – the answer may indeed be contextual.
The “metabolic syndrome” is a term often given to a multisystem cluster of cardiovascular risk factors, including central obesity, glucose intolerance, dyslipidaemia and hypertension, associated with endothelial dysfunction and insulin resistance. The use of the term has been debated,2 3 in no small part because the failure to identify a single causative agent has suggested to critics that it is merely the accidental co-clustering of common abnormalities, and this uncertainty is reflected in the numerous and various definitions of the syndrome that are found in the literature. In this issue of the journal, Reinehr and colleagues use eight different definitions of metabolic syndrome to ascertain the prevalence of …
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