One source of confusion that impedes our comparison across studies concerns the terminology used to describe metabolic disorders.1The insulin resistance syndrome occurs when tissues become unresponsive to the effects of insulin and can selectively affect insulin's actions on the muscle, liver, adipose tissue, endothelium, or brain. It is typically accompanied by compensatory hyperinsulinemia in the periphery, which has independent deleterious effects. Insulin resistance is thought to be the underlying cause of metabolic syndrome, diabetes, and vascular disorders such as hypertension and cardiovascular disease for most patients (Table). It may thus be considered a core syndrome that increases the risk of AD and VaD. Our ability to study the mechanistic relationship of insulin resistance to AD and VaD is hampered, however, by the complexity of its measurement. The hyperinsulinemic-euglycemic clamp, a method in which a standard dose of insulin is infused with dextrose, is the criterion standard,2but is time and labor intensive. The integrated area under the curve for insulin during oral glucose tolerance testing has been proposed as an acceptable surrogate.3The homeostasis model assessment for insulin resistance, which is based on fasting insulin and glucose values, correlates well with the hyperinsulinemic-euglycemic clamp,3is relatively low in cost, and is computationally straightforward.