Although remarkable advances have been made in the detection and management of mood disorders over the last decade, the increasing worldwide prevalence of depression continues to challenge researchers and clinicians alike. The World Health Organisation (WHO) has predicted that by 2030, depression will account for the highest level of disability accorded any physical or mental disorder in the world (WHO, 2008). In Australia, significant levels of depression affect approximately 20 per cent of adults either directly or indirectly during their lifetime, with almost twice as many women diagnosed with the disorder compared to men. Depression also runs in families, with risk of depression increasing with every first degree relative affected by the disorder. Up to 80 per cent of suicides are reported to be preceded by a mood disorder, and depression is associated with higher rates of death and disability from cardiovascular disease (Frassure-Smith & Lesperence, 1995), diabetes (Eaton, 2002) and cancer (Massie, 2004).
The social and economic costs of depression in Australia are staggering. Depression costs the Australian economy approximately $12.6 billion per year and accounts for up to six million working days of lost productivity (www.beyondblue.org.au), and there are significant personal and social costs to individuals and their families which are associated with depression. Associated anger and irritability play a role in family conflict, while high levels of anxiety and panic attacks may lead to heightened dependence on family members. In a substantial number of cases, risk of suicide also puts the family on high alert and can lead to high levels of stress amongst family members.
Longitudinal follow-up studies of people with depression have found that up to 50 per cent will recover within the first six months following treatment. However, approximately 10 per cent will experience a chronic course often lasting several years. Risk of relapse is also higher amongst those who continue to experience sub-clinical symptoms after recovering from an episode and who have had a history of depression. Other risk factors for relapse are a family history of depression, early age of onset for the first episode and ongoing life stressors.
Depression is associated with high levels of co-morbidity with other conditions such as anxiety disorders, substance abuse and eating disorders. It is frequently preceded by another physical or mental health problem, especially in adolescence and early adulthood, and this has led to controversy in conceptualising depression, either as part of a larger constellation of affective spectrum disorders or as a distinct clinical entity which frequently occurs in the context of other disorders. A related issue lies in the conceptualisation of depression as a dimensional or categorical construct. The DSM classification system and other conventional nosologies tend to regard all depressions along a continuum and only differing in symptom severity.
The Black Dog Institute has proposed an alternative hierarchical model of depression which includes three subtypes: psychotic, non-psychotic melancholic, and non-melancholic depression, as presented in Figure 1 (Parker & Manicavasagar, 2005). Each of these subtypes of depression may vary in severity along a continuum but each subtype is thought to support a unique ‘category’ of depression with its own pattern of symptoms, aetiology and illness course. In addition, the subtyping model asserts the involvement of dysfunction in specific neurotransmitter pathways which are responsible for the presentation of certain symptoms and features.
This subtyping model offers an alternative to the DSM-based dimensional model of depression and can help inform treatment choices. For example, both psychotic and melancholic depressions are thought to be primarily driven by faulty neurobiological processes and thus will respond best to medication as a first step. On the other hand, non-melancholic depression, which is thought to be driven by psychological factors such as personality styles and stress, will respond to psychological interventions as a first step, with adjunctive medication being prescribed if the response to treatment is slow or hampered by high levels of anxiety, poor sleep or ruminative thoughts.
A challenge for the future will be in assessing how these two models best account for comorbidity in depressive disorders and whether the subtyping model offers significant advantages in treatment outcomes.
Theories about the aetiology of unipolar depression have been dominated by biological formulations which stress the role of abnormal neurotransmitter pathways in its development and maintenance. Among the brain neurotransmitters involved in depression, serotonin (5-HT), noradrenalin (NA) and dopamine (DA; the monoamine neurotransmitter) remain the main ones which are also implicated in the regulation of sleep cycles, motivation and appetite. Recent theories about neurotransmitter dysfunction have asserted that abnormalities in receptor density and sensitivity results in changes in neurotransmitter availability. Other recent theories have implicated hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis in the development of depression. Overactivity of the HPA axis, which results in the over-production of stress hormones such as cortisol, affects the way in which monoamine neurotransmitters work in the brain. These are intriguing ideas that warrant further investigation for developing more targeted treatments in certain types of depression.
The down side of the ‘medicalisation’ of depression however has possibly contributed to claims of over-diagnosis and to the development of a range of medical ‘treatments’ for normal responses to stress in the context of routine life experiences. Whilst there is little doubt that genetics and biology can play a role in clinical depression (especially in expressions of more severe forms of the disorder), in the majority of cases the development of depression is due to a combination of biological, social, psychological and environmental factors. Aetiological models are increasingly attempting to integrate these factors and to identify vulnerabilities to depression in the context of stressful life events or stressful living environments.
The subtyping model proposed by the Black Dog Institute (Figure 1) has attempted to reconcile biological formulations with psychological theories about the aetiology of depression (Parker & Manicavasagar, 2005). This model acknowledges that all mood states are subsumed by neurotransmitter pathways and processes which for the most part are responding appropriately to external and internal events. In a minority of cases, estimated at around 10 per cent seen in clinical practice, faulty neurotransmitter processes (which may or may not have a genetic basis) dominate the aetiology of a mood disorder as seen in psychotic and non-psychotic melancholic depression. However, for the vast majority of depression presentations (up to 90 per cent in clinical practice), psychological processes are responsible for its development and these are grouped together as non-melancholic depression. As mentioned earlier, these psychological processes include personality styles which interact with life stressors. For example, an individual with an ‘anxious worrying’ personality style, who is prone to catastrophising and ruminating about events, and who would rate highly on measures of neuroticism, will also have greater vulnerability to non-melancholic depression, especially when confronted by several stresses by which they feel overwhelmed. Individuals with highly perfectionistic personality styles may become overwhelmed by stresses that compromise their ability to perform their tasks to their exacting standards. That, together with procrastination and ‘behavioural paralysis’ which are also hallmarks of a dysfunctional perfectionism, can exacerbate their initial distress and contribute to the downward spiral into a non-melancholic depression.
According to this model, over time, even depressions that have begun from purely psychological causes can result in significant neurobiological perturbations which require biological treatments in order to return to a normal level of functioning. As mentioned earlier, medication is also recommended in non-melancholic depression where symptoms interfere with the application of psychological interventions and/or cause undue distress. Similarly, predominantly biological depressions which have been treated with physical treatments may still require the use of psychological interventions especially as the depression begins to remit. Psychological interventions commonly used in the recovery phase of melancholic and psychotic depressions can include assertiveness training, family therapy, stress management techniques and psychoeducation.
Although the prevalence of depression is highest in people between the ages of 35 to 44 years (National Survey of Mental Health and Wellbeing of Adults, 1997), depression can and does affect people of all ages and from every strata of society. However, the presentation of depression varies according to age, from the moody adolescent who prefers to shut himself off from the family in his bedroom to the elderly aunt who has lost her husband and is feeling lonely and abandoned in her own home. In many cases, depression at either end of the age range is likely to be missed as patients do not always provide reliable or accurate information about their own level of symptomatology or functioning, and clinicians making the diagnosis have to decide whether an individual’s presentation is ‘normal’ for their age, emotional maturity and stage of life. From a clinical point of view, the assessment of severe depression, and possible depression in young people and in the elderly, should include supplementary information from a close relation or carer. In this way, more accurate assessment can help to inform suitable interventions that are tailored to the specific needs of each individual.
Several recent studies have demonstrated that for more severe depressions, a combination of both medical and psychological interventions is especially effective. However, for most non-melancholic depressions, psychological interventions alone are usually recommended at least as a first step. Ultimately though, choice of treatment should depend on how depression is conceptualised, patient characteristics, and on available evidence rather than on current treatment trends. Nor should treatment choice be entirely dependent on the clinician’s ‘preferred’ treatment.
For the more ‘biologically-based’ depressions, antidepressant medication is usually the first point of treatment. These include the tricylics (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin-noradrenalin reuptake inhibitors (SNRIs) and the monoamine oxidase inhibitors (MAOIs). There are also several new medications which do not easily fit the previous four classes of antidepressants, while antipsychotics are used to control psychotic symptoms in severe depressions. Antidepressant medications are thought to increase the availability of brain neurotransmitters and/or increase the sensitivity of receptors in the brain.
Other more recent developments in medical interventions for depression include: the use of repetitive transcranial stimulation (rTMS) which comprises the application of repeated, high-intensity magnetic pulses to the brain; vagus nerve stimulation which is thought to increase activity in the hypothalamus and amygdala regions of the brain; bright light therapy which affects levels of melatonin, serotonin and noradrenalin and which is especially useful in treating seasonal affective disorder; and electroconvulsive therapy (ECT) which is usually used in cases of severe and intractable biological depressions.
Psychological interventions, though not recommended to be used in isolation with severe forms of depression, are recognised as useful adjuncts to medication and other medical treatments. Such interventions in the acute phase usually comprise psychoeducation about depression and the use of medication, which in turn increases compliance, and basic cognitive and behavioural techniques depending on the level of cognitive processing impairments.
Some of the recent advances in treatments for depression have been in the psychological arena. Psychological interventions tend to be relatively short, usually comprising 12 to 20 sessions administered in either an individual or group format. Cognitive behaviour therapy (CBT) continues to be one of the most popular and well supported psychological interventions for depression (Gloaguen, Cottraux, Cucherat & Blackburn, 1998). Schema focussed therapy has also gained in popularity, but by far one of the most promising areas has been in the development of mindfulness-based cognitive therapy (MBCT) for preventing relapse (Segal, Williams & Teasdale, 2002) and in treating current depression (Manicavasagar, Parker & Perich, 2011). Further research is required to examine the effectiveness of MBCT compared to other psychological interventions for depression.
It is increasingly obvious, however, that apart from targeting the symptoms directly, there are a number of other interventions that are crucial to a successful outcome, including interpersonal skills training, goal setting, problem solving, family therapy and relationship counselling, drug and alcohol counselling, vocational guidance, anxiety and stress management techniques, and relapse prevention strategies. Multiple interventions are usually required throughout the ‘life-cycle’ of a depressive episode and for relapse prevention.
The advent of ehealth initiatives has led to the development of several online programs for various mental health problems, including depression. Most of them provide education about depression with varying degrees of specific psychological intervention such as mood monitoring and cognitive therapy (see for example ‘MoodGYM’ and ‘The Sadness Program’). The Black Dog Institute has developed a self-help program for depression, anxiety and stress called ‘myCompass’, which can be administered through mobile phone technology.
This program is currently under evaluation and will be available later this year. These ehealth initiatives are relevant for managing a mild to moderate level of non-melancholic depression and can be helpful for dealing with the aftermath of more severe biological depressions that have remitted. Psychologists and other health professionals can play an important role in directing their clients to use these programs as an adjunct to ongoing face-to-face treatment, monitor client progress while they engage in ehealth programs, and themselves participate in innovative ways to use online and mobile phone technology to facilitate collaboration between health professionals and to enhance client outcomes (see for example the Mood Assessment Program (MAP), an online diagnostic tool for clinicians). However, at this point, there is little doubt that in the treatment of severe and complex cases of depression, intensive psychological intervention will not be replaced by online or mobile phone technology.
An area that warrants further investment is in the field of depression prevention, particularly in young people. Several studies have demonstrated that targeted prevention programs for adolescents are far more effective than general interventions. This is an emerging area in which psychologists with specialised skills in working with at-risk adolescents and young people with sub-clinical symptoms could make a significant impact.
On the broader front, we need to question whether we are training and supervising enough psychologists and psychology interns in the recognition and management of depression. We also need to focus on preventative and resilience-building approaches in vulnerable populations in order to counter the increasing prevalence of depression and depression-related problems. To improve health outcomes, psychologists and other health professionals may need to become savvy in using the available range of technological and other advances in depression treatments – incorporating them into their clinical repertoires to ultimately tailor their interventions to their clients’ needs.
The author can be contacted at firstname.lastname@example.org.