As with most good arguments, we don't know enough yet to settle the argument. Sadly neither Gale's typically lucid and logical text, nor Alberti and Zimmet's search to justify the widespread application of largely unhelpful measures confront the one issue that could validate the Metabolic Syndrome, however exactly defined. Does a single pathogenetic process promote the syndrome, with the phenotypic features varying with the background constitution, or do several different pathogenetic processes need to coincide? The authors agree that the syndrome's aetiology is unknown, and stating its 'underlying causes' to be obesity and sedentary lifestyle (Alberti and Zimmet) is superficial, when they both know that, placed in an arm-chair, they would rise up to act, and overfed they would be sated and reduce their intake. They will also have learnt that it's a minority of subjects who will follow long-term their wise recommendations to reduce adiposity by cutting energy intake and increasing its output. We don't yet know if there is something about the 'Metabolic Conformation' that leads to obesity and so decreased insulin sensitivity and liability to hypertension, or whether an associated obesity promotes insulin resistance and hypertension, hyperglycaemia and soon pancreatic islet-cell failure among the vulnerable. Just as the first chemical messengers were metabolites, so some metabolites would have been the first addictive substances, probably with the subject's phase of peak vulnerability pretty early in life. Therapy could be as arduous as detoxification from an addictive substance, but might benefit from being recognised as such. Prevention requires a better understanding of the entwined elements of Mother: Foetus and Child: and Familial nutrient movements.
Competing interests: None declared
Competing interests: No competing interests