Posts tagged Depression (mood)
Regular readers of The Mouse Trap will be familiar with my obsession with knowing how nature is carved at its joints or in other words what are the natural categories or basic kinds.
This translates into thinking a lot about what are the fundamental drives, basic emotions and personalty traits and what taxonomic system of mental illness is most reflective of underlying fundamental nosological differences.
While synthesizing the work of others, has great value, and one derives many valuable theoretical insights based on such musings; there is nothing better than finding empirical studies that shed some light on such matters.
For example, I have argued that one set of disorders that arise form emotional polarity of fear/interest is Anxiety disorders and Obsession disorders. When fear is disproportional/ inappropriate to circumstances, it leads to anxiety; when interest is disproportional/ inappropriate it leads to Obsession. Fear and interest though opposed are two separate constructs as per the first tenet of positive psychology that good is not the absence of bad.
Similarly, the set of disorders that arise form sadness/ Joy polarity is depressive disorders and manic disorders. I am deliberately using plural form while defining depressive/ manic disorders as they contain sub-types – as we will soon see in the case of depression.
Now while depression is characterized by excessive low affect (sadness), one way to conceive Mania is as having excessive energy; the opposite of manic symptoms thus might be conceived of as fatigue or anergia. Anxiety is of course marked by excess anxiety while Obsession is too much interest; a possible opposite of obsession may be anhedonia– a sort of disinterest or apathy.
Now, its common to find depression and anxiety disorders comorbid with each other and just like treating bipolar as well as schizophrenia under one umbrella of psychosis, one may conceivably treat depression/ anxiety / anergia and anhedonia under a common nomenclature- in this case that of depression.
But we are perhaps getting ahead of ourselves. Lets backtrack a bit and go straight to this new study that found four neural subtypes of depression.
Basically, Liston and colleagues, used resting state fMRI to look at the functional connectivity of depressed patients and developed an algorithm to predict who has depression and who does not have in a sample consisting of both depressed patients and healthy controls. They found abnormal functional connectivity in frontostraital and limbic systems in teh depressive patients.
They also used clustering techniques to find that their depressive subset of patients clustered around two dimensions- one of which they called anxiety dimension and the other anhedonia. When one takes into account that there could be 2×2 = 4 combinations of anxiety and anhedoinia they found that their patients neatly clustered in those four quadrants.
If you note in the figure 1f accompanying the article,
- cluster 1 subjects have low scores on anhedonia and high scores on anxiety
- cluster 2 subjects have neither anxiety nor anhedonia
- cluster 3 have high anhedonia but low anxiety
- cluster 4 have both high anxiety and high anhedonia
The authors note that all subjects had low mood (sadness, hoplessness, helplessness) and that is why they were classified as depressed patients in the first place. The core depressive signature was also associetd with anergia and anhedonia with majority of patients showing these symptoms across all subtypes.
They also found slightly different neural signatures for all the four subtypes. For eg. cluster 1 & 4 characterized by high anxiety had reduced frontoamygdalar connectivity, linking it with fear circuit. Cluster 3 & 4 were associated with hyper connectivity between thalamic and frontostriatal networks and had high anhedonia and psychomotor retardation associated with them. And cluster 1 & 2 had reduced connectivity between anterior cingulate and orbitofrontal coretx involved in reward and incentive salience and guess what they showed anergia or fatigue.
To me it seems apparent that what we are seeing here are different effects of low mood, anxiety, anhedonia and anergia playing out as four clusters.
Cluster 3 I would classify as primarily anehdoina related; cluster 4 as primarily anxiety related; cluster 1 may be thought of as anergia related and clusetr 2 as pure depression or low mood related.
If my hunches are true we should find similar subdivisions in diagnosed anxiety disorders, obsessive disorders , manic disorders too. Of course that is an empirical fact to be proved.
Today I will approach the problem of depression, but from a particular vantage point – that steeped in cognitive theory and informed by the work of Martin Seligman.
There have been other views about depression- a psychoanalytical one whereby depression was deemed as rage turning upon inwards and directed towards the self; and a biomedical one whereby depression is considered a disease of the brain/body- imbalances in neurotransmitters etc. . Seligman rejects both models and considers depression (even clinically defined) as just the other extreme of response to loss etc. This is important to note as unipolar depression, clinically defined, is usually considered a type rather than a degree phenomena, i.e. people in depressive phase are qualitatively different from those who are not clinically depressed as per the prevalent model.However, note that even Seligman considers the mild form of depression as distinct from sadness.
The theory of depression that Seligman and colleagues came up with is based on his famous experiments with dogs whereby experimental dogs were subjected to uncontrollable mild shocks while the control dogs either received no shocks or shocks that they could stop and control. When the dogs who were subjected to uncontrollable shocks were placed in anew chamber whereby they could escape shocks by climbing over a low barrier, they sat passively. They had learned or internalized that nothing they do with respect to shocks makes the shocks go away and had even generalized it to new situations when things were actually under their control. Also the feelings of helplessness reflected in many diverse behaviors like less aggressiveness or exploration etc and was sort of generalized across situations too. So not only the experimental dogs made permanent attributions about their lack of control, but also pervasive attributions and thus became depressed.
Seligman and colleagues designed and executed similar experiments with rats and also humans. Using these experiments they were able to create a model of depression. That model of depression requires different things to come together, but typically as its called learned helplessness model of depression, the focus has been on the learned helplessness following a loss of control.
The different components of the model, when explicated, have different implications for treatment/ prevention. To start with before the process can start one has to have loss of control – if our environments provided more opportunity for control over our experiences and in general if people learned to feel more in control of their life, despite losses and all, then the chain stops at its beginning itself. While some losses are inevitable, say loss of loved one, other losses like pink slips can be minimized and then no matter what the loss is , one can choose one’s own attitude towards the loss – the last of human freedom’s as per Frankl.
Once loss/ dejection/rejection/ loss of control has happened, almost all of us will temporarily become helpless. However, becoming helpless is not same as becoming mildly depressed too. For some of us who have a habitual pessimistic explanatory style, in terms of seeing the negative events in our lives as being permanent and pervasive, the learned helplessness turns into momentary , mild depression. We have sad affect, disturbed sleeping, eating etc. However, for those who have optimistic explanatory styles, we re-bounce from the learned helpless and do not become depressed. So changing the habitual explanatory style is another intervention opportunity.
Finally, the mild and momentary depression become full-fledged clinical unipolar depression, when the symptoms continue for 2 weeks or more and as per Seligman this happens when one adds a ruminating thinking style to the mix. Thus a person who has a pessimistic style and also keeps thinking about his own thoughts is more likely to get clinically depressed. Again , if we can prevent or reduce rumination we can prevent the clinical variant.
Cognitive behavioral therapy , which has been found to be quite effective for depression, has been shown to work on some of these aspects increasing optimistic explanatory style and challenging negative automatic thoughts but probably can be augmented by focusing on preventing rumination and story-editing techniques to re-frame issues of loss and control.
In the end, in my view depression has complex roots – some steeped in biology and temperament, while others due to environmental stressors and our reactions to them. A clearer understanding of the learned helplessness model of depression is likely to aid in therapy.