More than 20 years ago, the high prevalence of depressive
symptoms in patients with personality disorders led researchers
to explore the relationship between affective disorders and
borderline personality disorder by using phenomenological,
epidemiological, and biological approaches (1). As the number of
readily available biological tools was small, investigators used
the 1.0-mg dexamethasone suppression test (DST), which had been
found to demonstrate cortisol nonsuppression (postdexamethasone
cortisol level >5 μg/dl) in approximately 40%–60% of depressed
subjects. This test was used in studies of subjects with
personality disorders (primarily borderline personality
disorder) in an attempt to examine the biological interface
between affective disorder and personality disorder. The results
were equivocal and did not support the conclusion that
borderline personality disorder was biologically similar to
major depression (2). Over the past few decades, it has become
recognized that approximately 70% of individua