Objective: The prevalence of obesity and consequently the risk for cardiovascular diseases(CVD) increases dramatically worldwide. It has been suggested that increased serum levels of interleukin-18(IL18), reflecting systemic inflammation, could be the missing link between obesity and increased cardiovascular risk. We hypothesized that obese individuals show increased IL18 levels and that this would be accompanied by increased subclinical atherosclerosis (non-invasively determined) in our population-based cohort.

Methods & Results: We measured IL18, waist, and subclinical atherosclerosis with a panel of non-invasive measurements of atherosclerosis(NIMA) in 1517 participants of the Nijmegen community. We determined intima-media thickness(IMT), pulse wave velocity(PWV), pulse wave analysis and ankle-brachial index(ABI). IL18(pg/ml) was higher in men(128.7±69.2) compared to women(114.2±68.7) but IL18 was not different between participants with(129.3±74.0) and without prevalent CVD(120.2±68.6). Participants with a high waist (4^th quartile, gender specific) had higher IL18 levels than those with a low waist(1^th quartile)(125.9±77.9 versus 117.2±61.0). The increase in IL18 was accompanied by an increase in subclinical atherosclerosis, as reflected by a lower ABI (1.09 versus 1.11), a thicker IMT(0.86 versus 0.83 mm) and increased arterial stiffness, as reflected by an increased PWV(10.3 versus 9.6 m/s) and an increase in all derived central pressure parameters.

Conclusion: In our population-based cohort obesity, as reflected by an increased waist circumference, was accompanied by increased IL-18 levels and an increase in non-invasively determined subclinical atherosclerosis. Our data support the hypothesis that the increased CVD risk in obesity might be caused by increased inflammation, although prospective studies are needed to conclude on causality of this relation.