“Growing from depression” is a short, easy read on the subject of the depressive experience and how to make best use of and grow from that experience. The book is written by Dr. Neel Burton, who is a psychiatrist as well as a philosopher, and an exceptionally good writer.
“If I had more time, I would have written a shorter letter” so wrote Pascal/ Twain and in case of Neel he seems to have spent enough time on this book, making it succinct yet easy to understand and follow by a layman.
The book is organized in four sections; one dealing with defining and delineating depression – an experience that is bound to affect us or our close family/friends once in the lifetime. Some estimates have put lifetime incidence of depression as high as 30 percent , which means we are either a sufferer or a caregiver at some point, thus the importance of the topic.
The second section deals with current treatments for depression, including CBT, ECT and antidepressants. Maybe in future editions newer treatments like Metacognitive therapy or rTMS/ DBS can be explored and elaborated at in depth.
The third section makes the meat of the book- its a self help section with bite sized chapters making one think aloud and get help growing from the depressive experience. Given that Neel is a philosopher, some chapters do digress a bit and become more philosophical/ at tangent with the main premise of the book, but overall the suggestions and elaboration is grounded in what we do indeed know about depression- including things like depressive realism.
The last section is related to mental health services and mental health law and has limited appeal to international audience as its focused and based around the UK health care system and the UK laws.
Overall, its a pretty good read and makes you realize that there is much that you can gain from the depressive experience- including wisdom as to how prevent a relapse by controlling daily stress, maintaining good daily habits like exercise etc.
I wish many more experts and scientists were able to break up from the jargon, and write a self help book for people at large. I am sure we all will be richer for that!
Buy the book here.
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.
I was reading ‘Depression’ by Aaron T Beck, who was instrumental in pioneering the treatment of depression with the cognitive behavioral approach, and was surprised to find that Beck had classified depressive symptoms in four buckets which correspond to the ABCD system.
For example, like the Affect, Behavior, Cognition and Drive (motivation) ABCD model, he parses depressive symptoms as either emotional manifestations, cognitive manifestations, motivational manifestations and vegetative and physical manifestations. A complete list of symptoms is given below:
- Dejected mood
Negative feelings toward self
Reduction in gratification
Loss of emotional attachments
Loss of mirth response
- Low self-evaluation
Self-blame and self-criticism
Distortion of body image
- Paralysis of the will
Avoidance, escapist, and withdrawal wishes
Vegetative and Physical Manifestations
While the world has moved beyond these models to the DSM V (although DSM IV-TR ) is still widely used) and its good to be up to speed regarding the latest diagnostics criteria for depression, this historical classification of symptoms to me proves once more the power of the ABCD conceptualization.
No, I am not speaking metaphorically. Quite literally,there has been accumulating evidence that sense are sharpened and have great acuity in mania while they are dulled in depression and the effects can be seen within the same individual over time as he/she suffers from manic/depressive episodes.
The latest study to add to this literature is by Bubl et al that found that depressive people’s brain registered lesser contrast than that registered by normal control brains when presented with same black and white images. They used pattern electroretinogram (PERG) to find whether the contrast gains registered by depressive retinas (those suffering from MDD) were different from those of controls and they found a strong and significant association with the severity of the depression.
I have covered earlier studies that found that sense of taste was compromised in depression (and enhanced in mania) and similarly that the sense of smell showed similar effects. Some snippets from the earlier posts:
What this means is that if you increase the amount of serotonin in the brain, then the capacity to detect sweet and bitter tastes is increased; if you increase noradrenaline levels those of detecting salty and bitter tastes is augmented; while a general increase in anxiety leads to better bitter taste detection. This also means that an anxiety state produces more bitter taste perception whereas a depressive state (characterized by low serotonin) is marked by bland sense of taste with marked inability to detect sweet and bitter tastes. A stressed state , marked by abundance of noradrenaline, would however lead to more salty and bitter taste perception.
In one of my earlier post on depression, I had commented on the fact that those suffering from depression have less sensitivity to sweet and bitter tastes and as such may compensate by eating more sugar thus leading to the well documented diabetes – depression linkage.
In a new study it has just been discovered that not only depressives have bland sense of taste, their sense of smell is also diminished and they may make compensations by using greater amounts of perfume. Overall it seems that those suffering from depression will have bland subjective experience of flavor(which is a combination of both smell and taste) and thus may even not really find what they eat to be tasty.
Further on, I speculate prophetically that blander vision will also be found:
To me, this is an important finding. To my knowledge no research has been done in other sense modalities (like vision), but there is every reason to think that we may discover a bland sense of vision in depression. Why do I surmise so? this is because there is extensive literature available regarding the manic state and how things seem ‘vivid’ during that state including visual vividness. If depression is the converse of Mania, it follows that a corresponding blandness of vision should also be observed in those who are clinically depressed.
We also know that in extreme or psychotic forms of Mania, auditory hallucinations may arise. I am not suggesting that hallucinations are equal to vividness, but I would definitely love to see studies determining whether the auditory sense is heightened in Mania (maybe more absolute pitch perception in Mania) and a corresponding loss of auditory absolute pitch perception in depression. If so found, it may happen that music literally becomes subdued for people with depression and they sort of do not hear the music present in everyday life!
Whether other sense like touch, vestibular/ kinesthetic , proprioception (a heightened sense of which may give rise to eerie out-pf-body experiences in Mania) are also diminished in depression is another area where research may be fruitful.
Of course I have also speculated about the others senses and would love to hear studies supporting/contradicting this thesis. But given that senses are attenuated in depression and exaggerated in mania the question remains why? Which brings me to the topic of this post- why is the world bleak /bland to a depressive and vivid for a manic?
This was also the question asked by Mark Changizi (@Mark_Changizi) on twitter with respect to this new study uncovered today and I replied that this may be due to broaden-and-build theory being applied to sensory domain or sensory gating phenomenon differentially acting in manic/ depressive states, while Mark was of the opinion that it might be the result of physiological arousal with arousal being the variable of interest controlling whether the sense remain acute or dull?
I do not see the two views necessarily contradictory and it may be that chronic affect per se activates arousal and that is the mediating variable involved in its effect on senses; and we can design experiments to resolve this by measuring the effect of state sadness/ happiness/arousal on visual acuity (if the effects of state manipulations are big enough); howsoever, I woudl like to elaborate on my broaden and build theory.
In the cognitive, psychological and psychosocial domains the broaden and build theory of positive affect is more or less clearly elaborated and delineated. I wish to extend this to the sensory domain. I propose that chronic positive affect signals to our bodies/brains that we can afford to make our attention more diffuse, let senses be perceived more vividly as we have more resources available to process incoming data; conversely in a chronic low affect state we might like to conserve resources by narrowing focus/ literally narrowing the range of sensory inputs/reducing the sensitivity of sense organs and pool those resources elsewhere.
I know this is just a hypothesis , but I am pretty convinced and would love to hear the results of experiments anyone conducts around this theory.
Bubl, E., Kern, E., Ebert, D., Bach, M., & Tebartz van Elst, L. (2010). Seeing Gray When Feeling Blue? Depression Can Be Measured in the Eye of the Diseased Biological Psychiatry, 68 (2), 205-208 DOI: 10.1016/j.biopsych.2010.02.009