RISCK is a multi-centre randomised controlled dietary intervention in subjects at increased risk of metabolic syndrome⁽Reference Jebb, Frost, Griffin, Lovegrove, Moore, Sanders and Williams¹⁾. The results are reported of measurements of vascular function from a substudy conducted on cohorts recruited at King's College London and Imperial College London. Altered vascular function is one of the hallmarks of metabolic syndrome⁽Reference Williams, Wheatcroft, Shah and Kearney²⁾. It is currently believed that the impaired vascular function is a consequence of increased production of reactive oxygen species that decrease the bioavailability of NO, a potent anti-atherogenic molecule with vasodilator, anti-platelet, anti-leucocyte and anti-proliferative actions(3). Following a 1-month run-in period on a diet high in SFA, measurements were made of: endothelial function using the flow-mediated dilatation (FMD) technique; endothelial-independent vasodilation following 25 μg sublingual glycerol trinitrate (GTN); aortic stiffness using the carotid–femoral pulse wave velocity (PWV); vascular tone using the digital volume pulse stiffness index (SI). Further measures were carried out following a 6-month dietary intervention with a SFA-rich diet similar to the run-in diet, a high-MUFA diet or a low-fat (LF) diet. The target intake for total fat was 38% energy (%E) for the SFA and MUFA diets and 28%E for the LF diets. The MUFA and LF diets were designed to reduce dietary SFA to 10%E with a planned MUFA intake of 18%E on the MUFA diet. The study had statistical power to detect a change of 1% in FMD. The results are shown in the Table.

Value was significantly different from that for the SFA treatment (Bonferroni's multiple comparison test):

* P<0.05.

The dietary intervention did not affect endothelium-dependent or -independent vasodilatation of the brachial artery as assessed by ultrasound. This finding suggests that the diets did not affect the production of NO. Large-artery stiffness as measured by PWV was not affected by treatment. However, there was a borderline-significant (P=0.05) difference between the SFA diet and the LF diet on SI, which although it is correlated with PWV is also an indicator of small-vessel reactivity. The findings of the present study do not support previous conclusions that a diet high in SFA impairs FMD by about 50% compared with high-MUFA or LF diets in healthy subjects.