Understanding and explaining depression: from Karl Jaspers to Karl Friston
Throughout my career, I have had two main interests: working as a psychiatrist to help patients with major depression, and researching the neuroscience of depression with the aim of learning more about its etiology and response mechanisms to treatment. My clinical work has helped frame the questions of neuroscience, but in reality the research results have done little to advance my understanding of patients. The gap between these two components of my work as a physician and scientist has led me to reflect on why it exists (and why it seems so large) and to consider how it might be bridged.
There is an urgent need to learn more about depression and its treatment. Depression causes more disability than any other mental disorder and is a leading cause of disability throughout society. Despite this – and perhaps precisely because of this – the diagnosis remains controversial. Operationalized as Major Depressive Disorder (MDD), it is questioned regarding the breadth of its diagnostic scope, causes, and treatments.
Many of the arguments can be characterized as a contrast between two perspectives. On the one hand, it is argued that depression is an understandable reaction to the stresses and strains of contemporary life. It can be understood as a psychological response to social events rather than something that requires assessment, diagnosis and treatment (that is, it is not something that should be subjected to the medical model). Depression can be alleviated by addressing the social factors that caused it. If treatment is suggested, it should focus on psychological and lifestyle factors.
From another perspective, depression is explained to be due to abnormal brain processes, and many of its symptoms (fatigue, insomnia, loss of appetite, reduced sexual interest) suggest that it is clearly a physical cause. When severe, depression can have serious physical consequences, such as life-threatening dehydration and hunger. Treatments should rightly include medications that impact mood, and other biology-focused treatments could also be considered.
'Depression'
Depression has been a feature of the human experience since the beginning of recorded history, and we can assume that this has been the case before. Our current conceptualization of the disorder – MDD – emerged from the neo-Kraepelinian movement. The diagnostic scheme was first formulated in the 1970s by a group of research psychiatrists at Washington University in St. Louis, and the diagnosis gained authority with the publication of the Diagnostic and Statistical Manual of Mental Disorders (3rd edition; DSM-III). in 1980. The criteria for MDD were intended to provide an atheoretical approach to diagnosis, which contrasted with the psychoanalytic approach that prevailed in the mid-20th century. It was neo-Kraepelinian in the sense that it returned to the observational perspective favored by Emil Kraepelin and listed the symptoms associated with the disorder without basing them on etiological assumptions.
The diagnosis of MDD was criticized from the start. Initial attention focused on the way the diagnosis combined different forms of depression, thus circumventing the older diagnosis of melancholia. This was, according to Shorter (2007), “a nosological catastrophe from which the field has not recovered.” There has also been criticism of the breadth of the diagnosis, as it captures too many normal mood swings and pathologizes understandable reactions to life's difficulties.
Many people agree that the diagnostic criteria for depression and related disorders are flawed and have different ideas about how the diagnosis could be improved. However, the question arises: Can a categorization of mental illnesses adequately explain the variety of manifestations of psychological distress? One of the first critics of Kraepelin's approach was Karl Jaspersa German psychiatrist trained at the University of Heidelberg.
Karl Jaspers
Jaspers published the first edition of General Psychopathology in 1913, at the age of 30, for which he is best known. He then gave up psychiatry to pursue a career as a philosopher. He wrote it while studying psychiatry at the University of Heidelberg, in a psychiatric department that was still under Kraepelin's spell.
However, Jaspers was skeptical of Kraepelin's nosological approach and believed that psychiatry first needed to better understand its conceptual foundations. He developed descriptive psychopathology that focused on patient-reported experiences. He also developed a framework for how psychiatrists can identify the nature of a patient's psychological problems. His approach was based on the idea that psychiatry works at the interface between the natural sciences and the humanities. Although Jaspers believed that biological processes were important in the development of mental illness, he believed that humans could not be broken down into their component parts, as scientific explanations require. Humans are always holistic and complex, he argued, and are never fully captured by a single method of knowing.
Jaspers introduced the distinction between understanding and explanation into the way psychiatrists get to know their patients. On the one hand, the psychiatrist understands the patient's difficulties through his intuitive sense of the connections between the patient's psychological experiences and his psychosocial circumstances. The psychiatrist does this by empathizing with the patient's situation, drawing on his experience of having seen many patients who have had similar experiences. For example, you can understand why a patient's mood is low after the breakdown of a relationship and why he feels so depressed when he witnesses his ex-partner starting a relationship with another person. Jaspers called this “understanding.”
Psychiatrists also bring scientific knowledge into their interactions with their patients. The research results help to explain his symptoms: Jaspers referred to this knowledge as “explaining”. The psychiatrist could better understand his patient's experiences if he had research showing that depression arises from defective functioning of the serotonergic system, or from overactivity of the amygdala and medial prefrontal cortex, or because the patient has a neurotic personality style. This research was generated by studying patient populations. To do this, patients must be classified based on the diagnostic criteria they meet.
Jaspers worked at a time when biological theories were dominant: Kraepelin believed that mental illnesses arose from biological processes, and his nosology was partly an attempt to provide the basis for their discovery. While Jaspers also believed that biological processes were important, he felt that such explanations did not capture the complexity of our individual patients' experiences. The two ways we know (understand and explain) our patients approach the patient from different perspectives without ever meeting. “The situation,” said Jaspers (1959), “is analogous to exploring an unknown continent from opposite directions, where the explorers never meet because of the impenetrable land.”
This does not mean that the gap between the two cannot be narrowed by improving our explanations. While it is argued that understanding is intuitive and applies to the entire patient, we bring many aspects of our knowledge to this understanding, including basic information about culture, history, socioeconomic processes, etc. (Ghaemi, 2013). Our knowledge of biological processes can also contribute to our understanding and, with more coherent frameworks, improve our ability to understand our patients.
Nosology
Jaspers believed that nosological schemes had some function (e.g. to collect statistical data), but argued that any scheme that attempted to classify the complexities of individual patients into clear diagnostic pictures would ultimately fail. “A classification is always contradictory in theory and never completely agrees with the facts” (Jaspers, 1959).
The benefits that can arise from classifying natural phenomena were demonstrated by Linnaeus's classification of animals and plants. The success of his taxonomy rested on a fact about nature that he did not yet know at the time of its development. It is descent through natural selection that shapes the downward flow of families, genera, and species. His contemporaries compared Kraepelin's nosology with Linnaeus's taxonomy; although, as Jaspers (1959) noted, “[las enfermedades mentales] They do not resemble the plants that we can classify in a herbarium. Rather, the most uncertain thing is what a “plant” is – a disease.”
While Linnaeus's classification of the plant and animal kingdoms is celebrated, his taxonomy for his third kingdom, the minerals, is also not so outdated. His classification of minerals into rocks, ores, and deposits developed similarly to his taxonomy of animals and plants. However, because it is not subject to natural selection, its mineral taxonomy makes little sense today. Instead, we understand the geological world through a very different classification system: Mendeleyev's periodic table. Hacking (2013) proposes that we will one day understand mental illness using means currently unknown to us and similar to the relationship between the periodic table and Linnaeus's taxonomy.
A network approach
Jaspers understood that symptoms of depression and anxiety were present in different combinations in each individual as their different personalities interacted with their particular social circumstances. This is a perspective supported by network theories of mental disorders (Borsboom, 2017). This approach views symptoms as ends in themselves rather than manifestations of underlying disorders. Relationships between symptoms are observed in people over time, and by studying their time courses, conclusions can be drawn about the causal effect that one symptom has on another. For example, it can be observed that the presence of insomnia leads to a delayed onset of fatigue.
The network approach radically changes our usual approach to mental disorders, which assumes that symptoms are the observable manifestations of the disorders we describe in our nosological systems. Network theories suggest that there are no latent disorders underlying the symptoms. While the symptoms cluster in patterns that are not random, they do not cluster in a way that supports our diagnostic criteria. Mood-related symptoms are grouped with anxiety-related symptoms, and their categorization, for example into MDD and social anxiety disorder, is artificial and does not reflect natural categories.
The gap between the symptomatic presentation of patients and our nosological system is one reason that Jasper's explanation is not understood. Our diagnostic categories necessary for research do not fit the complex ideas of our patients and lead us to narrow our view of patients' difficulties (Ghaemi, 2013). If there are no latent disorders underlying our patients' symptoms – if there are only symptoms – then how do we explain what is happening to them?
The predictive brain