Our findings are consistent with circulating Lp(a) being here the major confounder, in view of the inverse relationship between serum Lp(a) and fasting insulin[16,28] and because impaired fasting glucose (IFG) status in nondiabetic people without MetS is associated with a less adverse cardiovascular risk profile and reduced future coronary heart disease (CHD) risk.[28,29] Thus, low insulinemia may be a mediator of higher Lp(a) concentrations, or vice versa. Here, INS is linked to metabolic syndrome.