The diagnosis of the clinical illness of depression, in the absence yet of reliable biological markers, is therefore still based exclusively on symptoms, and not signs. One consequence of this ambiguity is that the dividing line between depression and other kinds of psychological states remains blurred. For example, while some contend depression is a categorical concept, others regard it as existing on a continuum with normal functioning.
To complicate matters even further, cross-cultural specialists have argued that each culture has varying criteria for describing everyday misery, and distinguishing this from abnormal unhappiness. Yet despite the shaky assumptions on which diagnosis and the central concept is built, surveys of depression producing dramatic results have increasingly guided thinking and public policy.
Major depression was cited by the World Health Organization as the fourth main cause of burden of disease in the world in 1990, and it is projected that by 2020 it will then occupy first place in developing countries, and third place in developed ones. Depression is second only to hypertension as the most common chronic condition encountered in Western general medical practice. Despite its prevalence, depression is not taken seriously by governments and health departments, according to campaigners, perhaps because it is seen as relatively innocuous. Yet depression is also a killer, through suicide and other related conditions like alcoholism and drug addiction.
It is estimated that between 40 and 60 per cent of those who commit suicide were suffering from serious clinical depression. Worldwide, suicide is among the top ten causes of death for individuals of all ages, and is the leading cause of death for those under 35.
A very important issue for primary care medicine is that over half of those who commit suicide have seen a physician within the previous 3 months, and 20 per cent of elderly suicides have done so within 24 hours. They may have complained about depression, but more commonly their symptoms (insomnia, weight loss, lack of energy, pain, loss of interest in life, anxiety, irritation, loss of concentration, appetite loss, loss of pleasure, psychomotor retardation) were not seen as part of a psychiatric disturbance, so assessment about suicide was not made. Primary care physicians seem to miss the diagnosis of major clinical depression about 50 per cent of the time. Only 25–30 per cent of those who commit suicide are even under the care of any mental health professional.
So not only is depression common and a killer, it is also frequently missed and misdiagnosed by clinicians. For example, it is estimated that 20–25 per cent of cancer patients suffer often unrecognized and untreated long-term depression, a condition that can make life miserable in the physically unwell. Given that the majority diagnosed with clinical depression can be effectively treated with one form of treatment or another (psychological, pharmacological, or a combination) it is now important that healthcare professionals routinely assess and offer treatment for depression.
Another problem with diagnosis is that there are probably several distinct types of depression, like seasonal affective disorder, where the depression has a strong seasonal component, and atypical depression, where weight gain and increased appetite are a feature. There are also a group of disorders that are commonly thought to be part of the affective spectrum, and include eating disorders, addictions, anxiety problems, obsessive–compulsive disorder, and cycling mood disorder. Another difficulty with the cluster of symptoms used to diagnose depression is that while the 'morning-worse' pattern is commonly mentioned, researchers have, however, also identified an 'evening-worse' pattern of mood. This pattern is sometimes thought to be associated with milder depressive symptoms, and may characterize chronic dysthymia rather than clinical depression.
According to one of the main diagnostic manuals used in psychiatry, the Diagnostic and Statistical Manual of Mental Disorders, 4th edn. (DSM-IV) published by the American Psychiatric Association, there are four other symptoms besides depression that must be present before 'major depression' can be diagnosed. So it seems that depression is not simply a state of low mood, but a syndrome comprising mood problems, psychomotor changes, and a variety of bodily and biological disturbances. All of these changes may be present, but none, including oddly enough depressed mood, is essential to the diagnosis.
The dominant paradigm at the moment is to view depression as a biological condition, and accumulating research uncovers strong links with other physical problems. For example, depression significantly increases the risk of mortality following myocardial infarction, and there also appears to be a link between depression and the later onset of dementia. The most likely possibilities for this association are: (i) depression can be an early prodrome of dementia, (ii) depression brings forward the clinical manifestation of dementing diseases, and (iii) depression leads to damage to the hippocampus through a glucocorticoid cascade.
It is this link between depression and structural brain changes that has proved one of the most revolutionary recent findings and current theories focus on the recent discoveries of decreases in various brain structure volumes, including in particular the hippocampus, in depression and anxiety-related conditions. It would now appear that neuron loss is linked to major depression. One theory is that glucocorticoids, the adrenal steroids secreted during stress, may play a contributing role to any such neuron loss.
However, it is also possible that biological differences found in the depressed could be due to genetics, and available data suggests that genes may account for over 50 per cent of the observed correlation between neuroticism and symptoms of anxiety and depression. But little is still known about the genes responsible, though much research activity centres on genes for neurotransmitters implicated in depression like serotonin and noradrenaline. Both the brain serotonergic and noradrenergic systems appear to have a role in suicide, mood disorders, aggression, and alcoholism.
A clear genetic influence in suicide has also been established and appears to operate via mechanisms not necessarily related to the genetics of depression, but implicating impulsivity as a mediating factor.
Yet if depression is common and has a genetic component this has also guided recent thinking towards the idea that it might have played a role in our evolutionary history. Depression may be maladaptive to the individual, but adaptive to the species. For example, it may be that in small bands of ancestral human hunter–gatherers, when a member lost her or his mate, the survival of the tribe was enhanced by the reduced food intake of the remaining member of the pair via depression or death. The genes enhancing a depressive reaction to loss would be carried by close kin of a depressed individual, and the enhanced survival of those kind would promote the increase of the depressogenic genes in the population.
The fact that suicide is partly genetic can also be explained with 'suicide as altruism' reconciling self-destructive behaviour with the 'selfishness' of the gene, thus clearing the way for an evolutionary hypothesis of depression which takes into account the associated increase in mortality. Suicide, paradoxically enough, potentially therefore enhances the likelihood of survival of the individual's genes.
In contrast to these generally currently favoured evolutionary perspectives on depression, psychoanalytic perspectives are less momentarily fashionable, though they continue to play an important role in psychotherapy for depression. Freud noted that the pathological depressed state is always unconscious, summing up his thoughts on depression with the famous sentence: 'The shadow of the object falls over the ego.' Psychodynamic drives involved in depression include, according to Freud, the central importance of aggression turned against the self when intensely ambivalent object investments are lost. Also implicated are the role of the superego in this self-directed aggression, the split in the self revealed in the superego's attack on the ego, and the fusion of another part of the self with an internalized object as the victim of that attack.
More recent psychodynamic formulations emphasize attachment and mourning for loss of major attachment figures perhaps predisposed to by earlier attachment formation difficulties during early childhood. There is an obvious possible convergence between genetic and psychological explanations if attachment difficulties via personality disorder could be shown to have a partial genetic basis.
While it is clear that genes cannot account for the whole story of depression, the relationship between life events and depressed mood is not simple. Though life events account for a reliable and significant portion of the variance of depressed mood, about 10 per cent in some studies, it is not usually large enough to attribute the cause of depressed mood to life events. Another complicating factor is that negative life events themselves seem to be partially heritable, possibly due to passing on poor life management skills within a family.
The latest thinking emphasizes the importance of 'life management' so that it is not what bad things happen to you that predict depression, but how you think about them, heralding the current dominance of the 'cognitive' approach. Cognitive processes of various types are presumed to represent vulnerabilities to development of depressive symptoms, and the current favourites are the holding of especially high standards, the tendency to be self-critical after failure, plus the tendency to generalize from a single failure to the broader sense of self-worth. There is indeed evidence that cognitive styles like 'generalization' and 'self-criticism' interact with adverse events to predict subsequent depressive symptoms.
These cognitive theories arose out of the Learned Helplessness paradigm, which is one of the few to integrate cognitions, emotions, and biology in depression. The model depended on identifying a particular class of animal behaviours as equivalent to an apparently discrete emotional state in humans. Animals when placed in a situation where they could not escape a negative consequence appear to give up trying and exhibit what looked like an animal equivalent of human depression. Faced by observation that depressed patients often claim excessive responsibility for the misfortunes in life, the theory was then modified to include an attributional component.
According to the revised learned helplessness theory, depression therefore occurs when an individual experiences negative events as uncontrollable, but also attributes them to causes which are internal to the self, stable over time, and global in their impact of areas of the individual's life. Subsequent research indicated that depressed people on the whole did make the expected attributions for negative events, but much less clearly indicated that attributions, especially of internality, were trait vulnerability markers for depression as the theory expected.
However, life event research appears most fruitful when explaining why women are at greater risk of depression, one of the most consistent findings in psychiatric epidemiology. There is little evidence to suggest this is a measurement artefact, or that men develop alternative, more externalizing, disorders to depression. If anything, women are more likely to experience and express anger about life events. Consistent with an explanation based on gender differences of roles, women appear only at greater risk of depression following an event involving children, housing, and reproduction, and then only when there were clear gender differences in associated roles. It seems likely that women's greater risk of depression is a consequence of gender differences in roles, which lead to differences in the experience of life events.
Sociologically inclined researchers have also emphasized the importance of social support as providing a buffer for women when facing stress, and explaining why more isolated women are prone to depression. Men appear on the other hand to be more prone to depression secondary to goal frustration.
However, an alternative to these sociological accounts is a more biological perspective which argues that depression is commoner in women because they are more prone to post-natal depression and menstrual mood problems as a direct result of their hormonal differences to men. It has indeed been found that around 10–20 per cent of women experience an episode of depression during the first 2–3 months after delivery. Maternal depression is important, and vital not to miss, because occurring so early in the infant's life it may affect the child's psychological development, with significant intellectual deficits as a result.
Perhaps the biggest future advance will not need to await the revealing of biological markers for depression, but instead the more widespread teaching of effective coping skills to populations before they experience adverse life events, so heralding an age when depression is prevented rather than merely diagnosed and treated.
(Published 2004)
— Raj Persaud
- Bibliography
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- Brown, G. W., and Harris T. (1978). Social Origins of Depression.
- Healy, D. (1997). The Anti-Depressant Era.
- Mendels, J. (1970). Concepts of Depression.
