Cardiovascular disease, the leading cause of premature death and disability in most western countries, has a well-established multi-factorial basis involving a complex interplay between genetic predisposition, environmental and personal risk factors – including systemic hypertension, diabetes mellitus, hyperlipidaemia, obesity and cigarette smoking – and more recently recognized mechanisms, including endothelial dysfunction [118], vascular inflammation [119] and leptin levels [104]. Here, LEP is linked to endothelial dysfunction.