MINDFULNESS TRAINING: SPECIFIC INTERVENTION OR PSYCHOLOGICAL PANACEA?

The paper by Brewer et al. [1] is based upon the assumption that there are common underlying mechanisms for depression and substance use disorders and the ambition is to provide a theoretical, clinical and neurobiological perspective that can frame the conceptualization and treatment of co-occurring depression and substance use disorders. The main starting point for this task is the meditation technique ‘mindfulness training’ (MT), which is claimed to have been shown to reduce problems related to depression as well as substance use disorders, and hence can be considered as a major candidate for intervention vis-à-vis co-occurring depression and substance use disorders. Although there is no doubt whatsoever that MT constitutes an interesting intervention which currently seems to be used as a possible remedy for an ever-growing number of health and behavioural problems, it can also be argued that the authors overstate their case in the sense that their argumentation lacks a critical stance concerning some of the circumstances that are presented in support of their perspective on MT.

A considerable weight of the authors' arguments in favour of MT as a first-rate candidate for the treatment of co-occurring depression and substance use disorders rests on the claim that MT de facto has produced results that show efficacy. However, in a fairly recent review on the effects of MT on depression, it was quite clear that when active control groups were used, no statistically significant reduction in depression could be found. Positive results were attained only when waiting lists or treatment as usual (TAU) groups were used as controls [2]. In a similar vein, the results from studies on the improvement in substance use disorders after exposure to MT are derived generally from comparisons with non-active control groups (with one exception). Given the fact of the close connection between the ‘outcome equivalence paradox’ and the use of active (bona fide) control groups [3,4], the idea of specific MT mechanisms is undermined.

Because MT is used for an extremely broad spectrum of health and behavioural problems [5], with quite different characteristics compared to depression and substance use disorders such as, for example, hypertension and cardiovascular diseases, it seems somewhat unlikely that MT would be effective for depression and substance use disorders due to ‘commonalities in regional brain dysfunction’ ([1], p. 1702). Instead it seems reasonable to assume that the possible mechanisms of action of MT are most likely to be of a wide-ranging nature. Given the broad implementation of MT, the apparent focus on the co-occurrence of the specific diagnoses of depression and substance use disorders, and the possibility of specific underlying neurobiological mechanisms, stands out to a certain extent as an overly narrow perspective.

The subheading of the paper is ‘What can we learn from the brain?’, which can be said to be consistent with the content inasmuch as the prospect of connecting dysfunction in specific brain regions with identified symptoms in both depression and substance abuse disorders is a major theme in the paper. A long list of references concerns findings from the use of functional magnetic resonance imaging (fMRI) identifying regions and structures of the brain that have a bearing on depression and substance use disorders. However, in this case one also has the impression that the authors are unwilling to look critically at the evidence that supports their ambition to provide a neurobiological underpinning for the effects of MT on depression and substance use disorders. The interpretation of brain activation maps is by no means a straightforward task due to the complex neuronal interconnections in the brain, which make it difficult to decide whether the identification of activity in a given part of the brain is primary or secondary to activity in some other part [6]. As pointed out by Kalant [7], there are good reasons to believe that neurobiology will never be able to tell us all that we need to know about addiction and we would be well advised to refrain from developing reductionist models of addiction.

Declaration of interest

None.