Thoughts never stop. You think at least 6000 thoughts during your waking hours. Constant processing of data from both your inner world and the outer world – even minute details that you might not consciously register – generates thoughts.
Unless you’re concentrating on something, thoughts switch 6-7 times over 1 minute, and each thought creates a corresponding fleeting micro-mood. If you’ve had an unproductive, lousy morning it could be because the average of these micro-moods has kept your mood below the baseline-neutral one that you usually bring to work.
Your thoughts stay focused if you’re in problem-solving mode, or totally immersed in something, or meditating, and your mood remains stable. Otherwise, they come and go like puffs of wind and you go through finely nuanced mood changes that give a particular colour to the ‘I’ of the moment, like flag colours of different countries that are shone on monuments like the Eiffel Tower to mark an occasion.
Or, moods are like visible shifting sands on the beach, thoughts like invisible gusts of wind that cause the waves that shift the sands.
Sadness is a mood. It is a biologically designed response, like pain. It tells you that something hurts inside you. You can’t always trace the feeling back to a particular thought because the link between the thought-clip and the mood-clip often disappears instantly.
You might self-diagnose depression because you see no obvious reason for you to be sad. Actually, feeling blue, being in a funk, being down in the dumps, being in the doldrums, feeling low – describe these passing bouts of sadness better. They happen to everyone.
Sadness is the tube of black paint nestled in the midst of greens, browns, blues, reds, yellows and whites in the box. Mixed with any other colour in a small amount, it adds depth. Too much of it smothers the other colour out of existence. Nevertheless, it belongs on your emotional palette and underlines the importance of someone or something in your life. It is also the basis of necessary emotions like empathy and compassion.
Sadness is physiological, i.e. feeling sad is a normal response to a sad situation, unlike depression, which is pathological. We shouldn’t brand a patient with a label that signifies a ‘disorder’ when he has cause to be sad. Every low mood is not depression. But since ‘depression’ is used interchangeably with ‘sadness’ in common parlance, it is compromised as a diagnostic term, though it’s still in use.
Depression, unlike sadness, doesn’t tell you something is wrong, but falsely makes you feel something is terribly wrong, because it takes away your insight. It’s like too much black paint. The visceral howl that escapes when a patient chokes out, “Why can’t I be like everyone else? Why can’t I just be happy? It’s so-o-o-o hard . . . ” comes from the depths of her being. Her misery is agonizing as she fights to understand how and when the dark abyss yawned open in her inner world.
This is depression, not sadness. It is closest to the grief of bereavement, a deep sorrow mixed with a sense of irrevocable loss. Here, it’s the loss of the Self that used to be a happy, normal girl before the bouts of black moods set in.
According to DSM-5 criteria, Major Depressive Disorder is diagnosed if sadness has been present for more than two weeks, there has been a loss of interest or pleasure in most activities, physical exhaustion, inability to think clearly, marked changes in appetite, weight and sleep pattern, feelings of worthlessness and guilt, recurrent thoughts of death and suicide. At least five of these, along with the sad mood, have to be present.
So, intense sadness lasting over two weeks and adversely affecting a patient’s ability to deal with day-to-day activities, eat, sleep, work and engage with the world as expected, qualifies for a diagnosis of Major Depressive Disorder and is to be treated accordingly.
In practice, the DSM has to be used along with clinical judgment and common sense, and the context in which depression has occurred must be taken into account to plan sensible treatment.
Sadness and depression are not synonyms. Sadness lies within the normal range of human emotions and doesn’t need medicines, except perhaps a dose of a mild sedative if there’s accompanying anxiety, insomnia or crying spells. Whereas, depression often benefits from antidepressants – they take the edge off melancholy, reduce anxiety, bring a little clarity to thought, and improve sleep. They are given for only a few months unless depression persists over time.
Depressed people need to return to normal and we have to use all available resources to help them along. Medicines may not be effective all the time, but we need to get what use we can out of them.
That’s not all. The probable trigger, the circumstances in which the episode originated, the course it took, coping strategies used, have to be examined for treatment to be complete, and to find ways to recognize and limit the effects of future episodes. Resilience is built into the human mental make-up, and most people process the experience and find ways to make sense of it, and therapy might help tap into that natural resilience.
The DSM-5 criteria for the diagnosis of Major Depressive Disorder are not set in stone. They get revised every few years based on current research in the domains of genetics, epigenetics, stress (hypothyroid-pituitary-adrenal stress response), neurological biomarkers, neuromodulators, individual variables, and psychic and social processes.
Here are a few representative references from research articles on depression, but please note, they are only by people working in the field of mental illness. People in other fields like Philosophy, Sociology, Evolutionary psychology, Psychological anthropology and Religion have their own take on why people get depressed. And I think every individual has his own theory too!
There are 227 possible ways to meet the symptom criteria for major depressive disorder.
The current criteria for major depression have been criticized for the heterogeneity of the clinical syndrome they define. The genetics and neurobiology underlying the depressive disorder still remain largely unknown.
Diagnoses, like many psychological terms, are concepts that refer not to fixed behavioural or mental states but to complex apprehensions of the relationship of a variety of behavioural phenomena with the world.
Rosenman and Nasti, 2012
Neuroticism, morning cortisol, frontal asymmetry of cortical electrical activity, reward learning and biases of attention and memory have been proposed as endophenotypes for depression.
Goldstein and Klein, 2014
Neuroimaging studies have identified that anhedonia, a core feature of major depressive disorder, is associated with dysfunction in reward and cognitive control networks.
Liang Gong, 2018
Links between specific depressive symptoms and areas of the brain have been identified, for example, crying with fusiform gyrus, irritability and loss of interest with hippocampus, worthlessness with cingulate gyrus.
Hilland et al, 2020
Data-driven studies have identified biological subtypes of major depressive disorder based on clinical features, biological variables, disturbed neurotransmitter levels, medication response, inflammation, and weight gain.
But here’s the thing. One group’s research often contributes only one little fact to the existing body of literature on a subject. It might not have an immediate application, or none at all, ever. It’s like how water has been discovered on the moon and on Mars – so what are we going to do about it? For the moment, nothing. Maybe future generations will.
Depression needs a tighter definition to be useful as a diagnostic term. It is the outer manifestation of many different processes. Two examples:
- Many people respond with a low mood to reduced ambient light, a condition called Seasonal Affective Disorder caused by a process that leads to decreased serotonin levels in the brain. This sort of depression, then, comes from somewhere else, not directly from thoughts.
- Then, there’s depression associated with low motivation, a lack of interest in chasing goals, apparently because of low dopamine levels. This is controlled by the limbic system in the brain, so emotions influence the endocrine system and the autonomic nervous system first, then the person uses thought to figure out why he does not particularly want what he is supposed to, and gets depressed.
As the current diagnostic criteria are based on symptoms and not the yet-unknown cause of depression we use the diagnosis of Major Depressive Disorder to address symptoms. This way, the patient can get his life back on track to an extent.
So ‘depression’ has been reduced to the status of ‘cough’ or ‘fever’. Without knowing the cause of a cough or a fever, the only treatment given is a dose of cough syrup or an antipyretic rather than an appropriate antibiotic.
For depression, it is a course of an antidepressant, which is like giving a course of a broad-spectrum antibiotic because there’s no lab available to run a culture and sensitivity test – not the best, but a fair chance that it will help. This is not the ideal way to treat a life-wrecking condition.
We are constantly looking for ways to define and diagnose depression, but we aren’t anywhere close to giving an irrefutable statement of what it is. Medicines and therapy are the best we’ve got at present, imperfect though they both are. Tracing the history of depression from Melancholia to Depressive Disorder through the centuries shows that it has been a fraught journey, and still is.