Disclaimer: This is an article about the history and philosophy of psychiatry. It is not meant and should not be used as advice on how to treat depression. If you feel symptoms of depression, please consult a specialist.
Incidence of depression is increasing. One explanation is that aspects of our modern lives are responsible. Loss of in person connections, fast paced and sometimes bewildering communication, the increase in temporary and insecure work. A British Prime Minister who seemingly can’t tell whether he is at a party or in a meeting. Henry Maudsley wrote, “an increase of (depression) is a penalty which an increase of our present civilisation necessarily pays.” Maudsley  wrote this in 1867 but he could have written it today. And he used the word ‘insanity’ rather than ‘depression’, but the point is the same. Are we driving ourselves insane? And have we been doing so for over a hundred years? To understand this, we need to understand how we came to think of ourselves as depressed.
Depression through the ages 
Historically, sadness was divided into ‘sadness with cause’, and ‘sadness without cause’, also known as melancholia. Melancholia was considered a medical disorder because there was no apparent reason for the person’s symptoms. This distinction has a long history, going all the way back to Hippocrates and Aristotle.
The early 10th
century Arabic physician Ishaq ibn Imran defined melancholia as “irrational, constant sadness and dejection” but noted that “the loss of a beloved child or an irreplaceable library can release such sadness and dejection that melancholy is the result.” The implied existence of non-beloved children and the equating of beloved children with libraries are interesting side issues. In the 19th
century, Mercier defined melancholia as “a disorder characterised by a feeling of misery which is in excess of what is justified by the circumstances in which the individual is placed.” This makes sense intuitively. If my irreplaceable library is burned to the ground I will be very sad, despondent, and have little interest in doing things. This is different from waking up one day and having those same feelings without an apparent cause. These early thinkers believed that melancholia had some physical cause, such as a misalignment of the humours.
Historically, sadness was divided into ‘sadness with cause’, and ‘sadness without cause’, also known as melancholia.
Freud (1856-1939) attempted to understand depression by uncovering hidden desires and motivations, rather than physical imbalances, but nevertheless maintained the traditional distinction. He wrote:
Although grief involves grave departures from the normal attitude to life, it never occurs to us to regard it as a morbid condition and hand the mourner over to medical treatment. We rest assured that after a lapse of time it will be overcome, and we look upon any interference with it as inadvisable or even harmful. (Freud, Mourning and Melancholia)
On the other side of the fence, Kraepelin (1856-1926) advocated a behavioural approach to psychology. For him, the focus should be symptoms, not hidden urges, and he used these to classify mental disorders. In a break with those before him, he moved away from just describing the major symptoms of mental disorders in favour of looking at patterns of symptoms over time. Those of us who are pretty sure that we never wanted to have sex with our parents might naturally have some sympathy with this approach. Kraepelin did agree with most of his forebears that the context within which patients exhibited symptoms was critical to understanding whether they were disordered or not. Kraepelin’s influence can be traced down the years into the American Psychiatric Association’s DSM, which provides diagnostic criteria for all mental disorders, based on symptoms.
The first version of the DSM (Diagnostic and Statistical Manual of Mental Disorders) was published in 1952. It listed 106 mental disorders, including homosexuality. The DSM II, published in 1968, listed 182 disorders. The third edition appeared in 1980 after a thorough revision because concerns had been raised that different psychiatrists came to different conclusions when diagnosing the same patient. The approach taken for DSM III harked back to Kraepelin, in that groups of symptoms were taken to indicate underlying pathology and Freudian inspired approaches were abandoned. It listed 265 diagnoses.
Very few doctors pull out a copy of the DSM when patients come to them with symptoms of depression. Instead, they use questionnaires, such as this one, used in the UK:
Over the last two weeks, how often have you been bothered by any of the following problems?
- Little interest or pleasure in doing things?
- Feeling down, depressed, or hopeless?
- Trouble falling or staying asleep, or sleeping too much?
- Feeling tired or having little energy?
Depression in the DSM
DSM III broke with prior understanding of depression. It was based on symptoms, rather than symptoms relative to potential triggers. As is clear from the questionnaire above, no mention is made of triggering events, or occurrences that might explain sleeplessness or low mood.
People with symptoms of depression should not be diagnosed as having depression if they had suffered the recent loss of a loved one.
However, until the DSM 5 in 2013, the criteria for diagnosing someone with depression did still retain a nod to the ‘sadness with cause’ and ‘sadness without cause’ distinction. This is because it exempted people from a diagnosis of depression for two months after the death of a loved one. In other words, people with symptoms of depression should not be diagnosed as having depression if they had suffered the recent loss of a loved one. Why just death you might wonder? Losing a job, family breakup, or the destruction of an irreplaceable library might have similar effects. But according to the DSM these would be classified as instances of depression, not normal reactions to unhappy circumstances. The depression exemption was removed in DSM 5.
Why does it matter how people are classified? It matters because a diagnosis usually leads to treatment of some sort, and the belief that there is something wrong with us. Either that our brain chemistry is out of balance, or that we are thinking about the world in ways that are making us miserable.
Treatments for depression have changed dramatically over time. In the 1940s, patients, mostly those in hospitals, began to be treated with electroconvulsive therapy. The first drugs targeting depression specifically appeared in 1958. These drugs appeared to work, and depression began to be understood as resulting from an imbalance in brain chemistry.
If depression is responsive to CBT, can it really result from a chemical imbalance in the brain?
The other option for treating depression is with therapy rather than, or sometimes alongside, drugs. Cognitive Behavioural Therapy (CBT) is the most common therapy in the UK and it has its origins in the 1960s when Aaron Beck wondered whether depression did not result from outside stressors but from our inability to cope with these stresses — because we have faulty beliefs that we are helpless or unworthy. Initial trials of CBT were successful. But this raised a question: If depression is responsive to CBT, can it really result from a chemical imbalance in the brain?
Prozac arrived in 1985 and tipped the balance back toward the chemical imbalance explanation. It was seen as safer than previous drugs, seemingly very effective and was very widely prescribed. In 1997, anti-depressants were marketed direct to US citizens, highlighting the chemical imbalance that could be cured by drugs.
An epidemic of depression
Between the end of World War II and the 1960s, depression was rare, partly because feelings of despondency and sadness were believed to result from anxiety. But by the 1970s it became a much more common diagnosis. To some extent this resulted in a change in classification of patients from anxiety to depression.
A WHO report also suggested that incidence of depression was much higher than usually supposed. How did this happen? People hadn’t often been assessed using questionnaires about their mental health before. These questionnaires asked people how they felt, not why they might be having these feelings. By the time of the DSM III in the 1970s, all reference to life story, background and triggering factors were dropped in favour of a checklist of symptoms. Depression became common. Even those not prone to conspiracy theory also note the enormous profits available to drug companies from selling drugs targeting common conditions.
Where does this leave our original question? Are our lives making us depressed?
People have always responded to their experiences, both good and bad. We have always felt sad when we suffer setbacks and disappointments. However, in the past, this would not necessarily have led us to believe we are depressed. If we continued to feel sad long after our disappointment had passed, we would have been more inclined to think that something might be wrong.
People have always responded to their experiences, both good and bad. We have always felt sad when we suffer setbacks and disappointments.
If we are categorised as depressed we will usually be offered drugs, CBT, or both. In the first case, our feelings are attributed to a chemical imbalance; in the second, due to faulty ways of thinking. But the old distinction between sadness with cause and sadness without cause allows us to challenge this. Insecure working patterns and social isolation are not making us sick, requiring treatment focussed on us. Insecure working patterns and social isolation are bad for us. The problem and the cure are not wholly within us, but outside of us. These are the things that need to change. Our negative mental states may be warranted, and reasonable; a sign that we are responding in an appropriate way to our environment.
Needless to say, there are many good therapists and doctors out there and we shouldn’t hesitate to get professional help if we need it.
 Anne Harrington: Mind Fixers.
 The historical overview is based on: Allan V Horwitz & Jerome K Wakefield: The Loss of Sadness – How Psychiatry Transformed Normal Sorrow into Depressive Disorder.
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Catherine Greene is a Research Associate at the Centre for Philosophy of Natural and Social Science at the London School of Economics. Her research interests are the philosophy of finance and social science. Before studying for a PhD she had a career in finance and still consults an ethics and investment strategy. More information is available at www.catherinegreene.co.uk
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