Depressive disorders have become the leading cause of disability worldwide and a major contributor to the overall global burden of disease. Prospective epidemiological studies show that depression may affect about half of the population up to late adulthood. But what is a depressive disorder, why is it so prevalent and how should we address this epidemic in both practice and research?
Before the introduction of DSM-III in 1980, it was differentiated between endogenous (melancholic) depression, a rare but severe and persistent form of depression, and exogenous (reactive) depression, a frequent, but milder and transitory emotional reaction to stressful life events. With the advent of DSM-III, both diagnostic categories were lumped together to form the new heterogeneous diagnosis of major depression. The low diagnostic threshold of this arbitrary catch-all construct, in combination with an increased sensibility for the diagnosis due to aggressive drug company marketing and public awareness campaigns, has contributed to the current overdiagnosis of depression in primary care and a widespread medicalisation of unhappiness.
The recent increase in depression diagnoses and antidepressant prescriptions suggests that emotional reactions to socio-economic hardship are increasingly treated as medical conditions. Although certainly unpleasant and burdensome, emotions such as sadness, despair and sorrow are not necessarily symptoms of brain pathology, but rather normal reactions to severe but common life stressors. Except perhaps for some cases of endogenous (melancholic) depression, the vast majority of current major depression diagnoses are not indicative of inherited brain disorders. We should thus not be surprised that there is no specific and consistent aberration in brain functions related to major depression and no candidate genes for major depression. Moreover, polygenic risk scores derived from genome-wide association studies explain at best 1–3% of the variance in the risk of major depression. Just as falling in love, winning at the lottery and professional success makes us happy, loss of a beloved person, financial problems and career failures make us unhappy. In contrast to genetic and neurobiological factors, socio-environmental risk factors, including in particular maltreatment and stressful life events, are thus strongly and consistently related to the occurrence of depression.
Some might argue that it’s largely irrelevant, whether depression diagnoses capture normal reactions to adverse circumstances of life or rather inherited brain pathologies, the only thing that would matter is that people receive a medical explanation for their suffering and professional help. In my view, such a vindication misses the larger societal picture. Medicalising ordinary life, that is, labelling normal emotional reactions to severe life stressors as mental disorders distract from fundamental societal problems. Instead of addressing the root causes of this depression epidemic, specifically, poverty, inequality, discrimination and criminality, people suffering from social grievance receive a medical diagnosis and treatment for an alleged brain disorder. We don’t cure the ills of society; we merely treat its victims. From a public health perspective, such an approach is doomed to failure.
The increased public perception of depression as an inherited brain disorder that requires primarily drug treatment had unexpected adverse consequences. Research has shown that biomedical explanations have possibly contributed to an increase in stigma towards people with mental health problems. And although the prescription of antidepressants has massively increased over the last three decades, it reduced the prevalence (and burden) of depression, not a bit. Moreover, healthcare resources are inherently limited. The massive economic costs due to the ever-increasing (mis)diagnosis and (over)treatment of depression in primary care imply that money is missing elsewhere, for instance for population-wide social interventions (such as interventions targeting income inequality, criminality and unemployment). In accordance, in a recent report for the United Nations, it was stated that: ‘Mental health policies and services are in crisis – not a crisis of chemical imbalances, but of power imbalances… There is now unequivocal evidence of the failures of a system that relies too heavily on the biomedical model of mental health services, including the frontline and excessive use of psychotropic medicines, and yet these models persist.’
The situation is no different in science, where the vast majority of funds were invested in genetic and neurobiological research. Leading experts such as the former NIMH director Dr Insel repeatedly claimed that mental disorders are brain disorders and that academic psychiatry should be a clinical neuroscience discipline. Fortunately, a growing minority of psychiatrists now question such an indiscriminate and reductionist focus on the neurobiological bases of mental disorders. The biological research paradigm has not advanced clinical practice, that is, the identification, prevention and treatment of mental disorders. Even Dr Insel, one of the most fervent promoters of biological psychiatry, recently admitted in an interview: ‘I spent 13 years at NIMH really pushing on the neuroscience and genetics of mental disorders, and when I look back on that I realise that while I think I succeeded at getting lots of really cool papers published by cool scientists at fairly large costs – I think $20 billion – I don’t think we moved the needle in reducing suicide, reducing hospitalisations, improving recovery for the tens of millions of people who have mental illness.’
There is an epidemic of depression in developed Western nations because normal emotional reactions to adverse socioeconomic conditions are increasingly labelled as medical illness. This has led to a massive medicalisation of unhappiness, that is, overdiagnosis of depression and overprescribing of antidepressants. Intense sadness, despair and sorrow undeniably can be very burdensome and painful, but they are part of the human experience. Except possibly in endogenous melancholic depression, there is no scientific evidence that depression episodes are the result of (inherited) brain pathology. Instead of medicalising individual reactions to adverse living conditions, we should primarily intervene at the community level and try to combat the root causes of depression, in particular socio-economic hardship. Prescribing evermore antidepressants will not cure the ills of society.
Dr Michael Hengartner is a Senior Lecturer at Zurich University of Applied Sciences. His research interest encompasses social psychiatry and clinical psychology.
