Abstract
Dr Andrews repeats succinctly the issues raised by Professor Parker's initial commentary [1]. However, simple repetition of the statement that there is a ‘lack of demonstrated efficacy of antidepressant treatments in major depression’ doesn't make it true. When the evidence has been reviewed in Australasia [2], [3], and elsewhere in the world [4], the overall efficacy of antidepressant medications in persons with major depression has been accepted. As described previously [5], within patients with major depression antidepressant response does indeed vary according to other factors such as illness severity, age, age-of-onset, duration of illness, concurrent features (e.g. psychotic features) or other comorbid medical or psychological factors.
Contrary to Dr Andrew's assertion, such variations in treatment (and placebo) response, and prognosis, within diagnostic categories are well recognized in trials of persons with other psychological and medical conditions. Obvious examples include responses to medications of persons with acute onset versus chronic schizophrenia or early versus later phases of dementia. Similarly, patients who have had myocardial infarcts have different outcomes depending on whether they have comorbid diabetes mellitus. From a methodological point of view, there are also specific reasons as to why severity predicts better treatment response in antidepressant trials, particularly when a 50% improvement in Hamilton depression rating scale scores has been accepted as the benchmark for efficacy [4].
The more appealing aspect of Dr Andrew's correspondence is his proposition that ‘major depression’ be replaced by the notion of ‘clinical depression’. Presumably this is the depression that clinicians recognize easily and the illness for which they go on to provide specific treatments. Dr Andrews implies that this category can be readily differentiated from other clinical states (e.g. ‘anxiety’) and normal human emotions (e.g. ‘unhappiness’). Unfortunately, he provides us with no specific diagnostic criteria, no evidence of interrater reliability (always a challenge for new diagnostic systems in psychiatry), no evidence of cross-sectional or longitudinal differentiation from anxiety disorders nor controlled trial evidence to support his assertion that this diagnostic grouping is any better than ‘major depression’ at predicting specific treatment response. Potential validation against other external genetic, familial, neurobiological, psychological, social or longitudinal features is not discussed. Many would argue that ‘major depression’ developed largely from the concept of ‘clinical depression’ and was an active attempt to move away from the unhelpful previous systems (e.g. ‘reactive’ versus ‘endogenous’ depression).
There is also no doubt that many specialist clinicians feel that the criteria for various depressive disorders, including ‘major depression’, have shifted too far in recent years in favour of dimensional, epidemiological and population-health perspectives [1]. However, there is little doubt that we will continue to see a rapid move away from such historic and categorical diagnostic systems, even though they continue to occupy the pages of this Journal [1], [5] and to persist in specialist and academic mental health centres. After all, the main population-based rewards for the better treatment of depressive disorders in Australia (including falling suicide rates) have come from work outside the specialist sector [6], [7].
Importantly, the push to diagnostic systems based on better understanding of genuine developmental [8] or aetiological [9] paths is now clear. To date, these categories do not match easily with those historic or existing clinical concepts derived from specialist practice. Potentially, such systems will not only have greater validity but will also be of greater value from both a population health and a clinical perspective. That is, if valid, they should lead to more precise illness prevention, clinical interventions and prognostic statements.