Category Archives: depression

Introducing GLEO: SandyG’s Positive Tetrad

Most of you would be familiar with Aaron Beck’s Cognitive Triad also known as the Negative Triad. To recap, a depressed person is characterized by negative views about the self, negative views about the world and negative views about the future.

Guilt, shame, worthlessness, not accepting the self are all aspects of negative views about the self, which I conveniently relabel as self-loathing. It can even be conceived that these self concepts are closer to a neurotic belief system.

Similarly, being pessimistic and having a sense of hopelessness, is what can be thought of as having negative views about the future. Learned helplessness, an explanatory model of depression, is more aligned with this aspect.

That leaves us with negative views about the world. Items that measure it include “No one values me” or “People ignore me all the time”; items that talk more about negative views about other people rather than world at large. Also we know that depression is characterized by rumination or repetitive negative brooding over the past. So my humble submission is that its better to break this negative views about the world into two components: one about negative views about other people and the other about negative views about the past/ present.

So, Cynicism or cynical hostility, which is characterized by cynicism, distrust, resentment, and suspicion, would be what is dysfunctional in depression as far as negative views about others is concerned. There is some evidence that high scores on cynical hostility raises the odds of being depressed 5 times the general population.

And that leaves us with the last of factors that affect depression: bitterness or negative views about the past/ present. There is an automatic negative tendency to see past as full of regrets and losses and missed opportunities and this leads to rumination and sustaining of sad mood and depression.

This however means that Beck’s triad is no longer a triad but has become a tetrad. This needs to be empirically verified but I’m sure it will be a useful construct.

Most important, from the perspective of this post is how we can flip these unconscious, negative automatic thoughts and replace them with positive automatic thoughts/ habits so as to immunize and buffer us against depression (and other disorders) . So with some fanfare I introduce SandyG’s Positive Tetard.

Self-esteem, self-efficacy, self worth, self acceptance etc are all positive processes and indicators that one has a positive view of self. Like the other three components of GLEO/Positive tetrad, these all can be developed and are state like/ trait like and not fixed in nature. Bandura for eg. has elaborated extensively on how self efficacy can be developed. Rosenberg similarly has focused on self-esteem. The E of GLEO comes from this component (self Esteem/Self Efficacy). Developing this buffers against self-loathing and is thus a protective factor.

Optimism (generalized expectancy as well as learned optimism) and hope (wills and ways) are positive processes and indicators that one has a positive view of future. Optimism interventions like Best possible future selves exercise leads to increase in optimism and again helps buffer against depression/ other disorders. The O in GLEO come from Optimism. This protective resource can again be built.

Love, compassion, kindness and altruism all come form a place where others are trusted and one has positive views about others. Interventions like loving-kindness mediation or random acts of kindness can increase the social support one feels and thus buffer against depression/ other disorders. The L in GLEO comes from Love. Other people matter and to build social support you have to start by trusting/ loving others.

That leaves us with the G in GLEO. It stands for Gratitude. Thankfulness, feeling blessed and grateful all lead to a positive view or interpretation of what has happened in the past or is continuing to happen in present. Gratitude interventions like counting your blessings or a gratitude visit leads to noticing and appreciating the good that has happened and continues to happen. This acts as a strong antidote to feelings of bitterness and buffers against depression.

Taking a bird’s eye view, sadness driven by ruminating on past events leads to depressive disorders and can be prevented by gratitude interventions. Fear driven by apprehension of future events leads to anxiety disorders and can be buffered against by optimism/ hope interventions. Anger driven by cynical hostility towards others leads to aggression(intermittent explosive disorder)/ conduct disorders and can be protected against by cultivating kindness/ compassion etc. Finally, disgust (with self ) that may be driven by self-loathing may lead to neuroses / impulsive and compulsive disorders (OCD, personality disorders etc) and can be prevented by developing self esteem, self compassion etc. I know this is slightly conjectural, but I have good reasons to extend this tetrad beyond depression.

Finally, how this new concept of GLEO/SandyG’s Tetrad compare to existing constructs like HERO/PsyCap and the ‘light triad‘ ?

HERO/PsyCap I believe is limited by its focus on work domain. It gets the Hope/Optimism and Self-Efficacy part right but stops short. Self-concept should include more things like self esteem and adding gratitude and love to the model makes it many fold strong and in a sense equivalent to my model as Luthans is explicit that PsyCap is state like and can be developed. However, I see of GLEO as more processes than as either trait like or state like.

‘Light Triad’ on the other hand is posited as opposed to the ‘dark triad’ and is more or less a personality trait construct. Perhaps, Cynicism is a milder and passive form of the dark triad and Love/compassion/altruism is the milder form of the light triad. I think of it in these terms, but I may be mistaken.

I am excited to unveil this model; does this resonate with you? Should we all cultivate GLEO as a path to glee and happiness?

Depression : Symptoms and Subtypes

Depression is one of the most common mental illness; as a matter of fact it has been said to be the common cold of mental disorders- almost everyone gets it one time or the other. ~57 million people, in India itself, are estimated to suffer from depression. However, depression thought currently diagnosed and classified as one entity,  is not a homogeneous illness in practice. There are different sub-types of depression.

But first lets recall the symptoms of depression. These I have drafted in ABCD terms for easy recall. Its also useful to think of symptoms as tings that are added to normal experience (the positive symptoms if you may) and things that are missing (the negative symptoms) – although this distinction is usually made in case of schizophrenia. Also important to remember is that at least 5 of the following symptoms need to be present for at least 2 weeks for a clinical diagnosis.

  1. Affective:  Presence of affect : Low mood or prolonged sadness is an affect that is present, and required for diagnosis of depression. The sad emotion is something that has been added.
  2. Affective : absence of affect: Typically one feels pleasure while doing small everyday activities like having a cup of coffee in the morning. A depressed person doe snot feel pleasure form such activities and suffers from Anhedonia – on the inability to experience pleasure. Here something has been taken away from the normal experience.
  3. Behavioral:  presence of behavior: Depression results in abnormalities in sleep, appetite and body weight. When excess sleep (hypersomnia) or excessive appetite or psychomotor agitation or weight gain appears that can be a symptom of depression.
  4. Behavioral:  absence of behavior: Depression results in abnormalities in sleep, appetite and body weight. When loss of sleep (insomnia ) or less appetite or psychomotor retardation or weight loss appears that can be a symptom of depression.
  5.  Cognitive: presence of thoughts/ beliefs: dysfunctional beliefs are present in depressed people including worthlessness and guilt. These thoughts do not make or dominate the normal thought repertoire of most people.
  6. Cognitive: absence of cognitive capacity: Depressed people are not able o think or concentrate; they are also indecisive. All these are cognitive capacities that are lacking or compromised as compared to normal folks.
  7. Drive: presence of motivation : Here I am tempted to put suicidal ideation and attempts: a drive to escape from life and end it. Something again not normally found in normal people, but a motivational force for the depressed person.
  8. Drive: absence of motivation: Anergia (loss of energy) and fatigue go here: one feels drained and unwilling and unable to do anything. Again normal people have decent amount of energy or drive  and this is somewhat deficient in the depressed person.

Now that we know what depression looks like, and how its diagnosed (above is as per DSM-5 criteria), what can we conjecture about the heterogeneous nature of depression?  One useful way to think about depression sub-types is to think of whether it is predominantly Affective in nature, or is it Behavioral or Cognitive or Motivational. Could this differentiate among meaningful sub-types?

For this it may make sense to refer to this paper [pdf] about which I blogged some time back. Please do read my blog or the original paper. The authors identified two dimensions of Anhedonia and Anxiety and identified four neural subtypes of depression. They replicated the four subtypes in Generalized Anxiety Disorder (GAD) too which is closely related to depression.

It is instructive to note that in that paper, that Anhedonia axis is affect related while Anxiety axis is more cognitive.  To me the four subtypes appear as equivalent to whether the predominant symptoms are affective (subtype 3), or whether they are behavioral (subtype 1?) or cognitive (subtype 4?) or motivational (subtype 2).

Irrespective of what the underlying subtypes may refer to, its clear that depression is heterogeneous and the better we identify and start treating the subtypes differently the better it will be for those suffering from depression.

Anxiety, Depression and the Internalizing Spectrum

Pathological mental health problems in children and young adults have been classified into externalizing (substance abuse, conduct disorder etc) and internalizing disorders (depression , anxiety etc). Today’s post will try to  work out the structure of this internalizing spectrum.

English: An anxious person

English: An anxious person (Photo credit: Wikipedia)

The first major difference, that is made in say DSM, is between Mood disorders (disturbance in mood) and Anxiety disorders (characterized by anxiety and avoidance behaviors) . However, Watson in this article (pdf) emphasizes that this classification is not proper and in many cases these disorder say depression (say MDD) and Anxiety (say Panic disorder) are co-morbid with each other.

To explain this as well as other genotypical and phenotypical findings, Watson has developed a structure of these ‘distress disorders’ – however the road was long, an intermediate stop was tripartite model of depression/anxiety.

According to this tripartite model (developed by Watson and Clark), both depression (MDD, dysthymia etc)  and anxiety disorders (phobia, panic etc) share a common non-specific factor called Negative Affect (NA) which is characterized by things like preponderance of negative emotions like sadness, fear, guilt, anger etc as well as irritability, difficulty concentrating etc.

Depressive disorders meanwhile are specifically characterized by lack of Positive Affect (PA), which means less emotions like happiness, interest etc, but also Anhedonia or inability to derive pleasure from earlier pleasurable experiences.  Anxiety disorders, on the other hand, are characterized by physiological hyper arousal (PH) (shortness of breath, dizzyness etc) .

This model however was also found wanting and replaced with an hierarchical integrative model, which posited that there was a generic non-specific factor of NA common to both anxiety and depressive disorders, and a lower order low PA factor characterizing depression and more specific multiple low order factors (instead of one PH hyperarousal factor) associated with the different types of anxiety disorders like panic/ agoraphobia, Phobia-specif stimuli, phobia social etc .

However , Watson further modified the structure and came up with this model shown below:   One broad factor of distress/NA; two specific factors of anxious-misery and fear and then further unique factor specific to individual diagnosis.

To summarize and also extending it a a bit,

  1. At top there is an internalizing spectrum and associated with it a non-specific NA factor.
  2. In middle there are four spectrum:-  a depressive spectrum , a Fear spectrum and a bipolar spectrum and an Obsessive compulsive spectrum.
  3. each of these can be further divided into discrete diagnosis along two factors/dimensions (I will not eb focusing too much on bipolar or OCD for the purposes of this post) :
    1. Depressive spectrum :
      1. group 1: MDD and dysthemia
      2. group 2: GAD and PTSD
    2. Fear Sepctrum
      1. group 1: Panic and agarophobia
      2. group 2: Phobia (specific stimuli) and Social Phobia
    3. Bipolar spectrum (bipolar I, II and cyclothymia)
    4. OCD

Lets focus more closely on Depressive and Fear Spectrum and try to see alignment with ABCD model. MDD/Dysthemia imho are mainly about mood or Affect;  GAD/PTSD are more Cognitive (reaming stuck in a thought loop) ; Panic/agorophobia more Physiological or Dynamic in nature and Phobia (both specific and Social) more Behavioral in nature (avoiding people, places and animals).

Each of these in turn splits into four factors; for ex PTSD splits into four factors- Dysphoria (A), Intrusions (C), Hyperarousal(D) and Avoidance (B). Similarly, recent research has shown that MDD is itself heterogeneous made up of four neural subtypes- one way to list those would be – marked primarily by Anhedonia (A), Anxiety (C) , Psychomotor retardation (D) and Fatigue (B) . Similar analysis should be possible for other discrete diagnosis.

For now, we will turn to the structure of Bipolar and OCD spectrum by analogy to dep/anxiety spectrum.

  1. Biploar spectrum:
    1. Euphoria (Affective)
    2. Flight of ideas (Cognitive)
  2. OCD spectrum
    1. Obsessions (Dynamic)
    2. Compulsions (Behavioural)

Within this OCD can be seen to be comprising  of four factors: Hoarding (A?) , Order and symmetry (C), Obsessions and Checking (D) and Washing and cleaning (B).

Another way to think about the depressive and anxiety spectrum is to say that Depression rgoup 1 is characterized by Low PA, depression group 2 by high PH; Fear group 1 by High PH and Fear group 2 by low PA. What distinguished Fear spectrum from Depression spectrum is the fact that much more variance is explained by High NA for depressive syndromes and only moderate variance explained by NA for Fear syndromes.

What do you think is missing from the above model? Where might it be wrong? where might it be correct? If correct what are the implications?

Goals and Depression

Striving towards meaningful goals is good for your well-being; even just having goals by themselves are indicative of well-being. This is an established dogma of positive psychology, so how can one argue that goals may be at the root of the experience called depression.

A framework that aims to throw some light on this is the dual-process Tenacious Goal Pursuit (TGP) and Flexible Goal Adjustment (FGA) theory as proposed by Brandstatdter and colleagues.

As per this framework, we all strive towards goals, but only goals that are meaningful (say goals which align with our self-identity) and attainable (we have self-efficacy beliefs and can figure out strategies to achieve the goals) lead to well-being. A goal that we find meaningful and are highly committed to, but which becomes unattainable due to either external circumstances or our internal capacities, may lead to depression.The depression, and the helplessness and rumination that accompany it, may paradoxically have the function of decreasing our commitment to the goal and releasing ourselves from that unattainable goal.

And here is where the TGP and FGA theory comes to the rescue. In view of internal or external obstacles, that is when you are not able to make progress towards meaningful goals, you may either try to change the situations or your actions to ensure that they are congruent to the goals and would thus be demonstrating an adaptive process of assimilation (not to be confused with Piaget’s use of assimilation) also known as Tenacious Goal Pursuit (TGP), or you may adjust your goals and ambitions to reflect the situations / your capacities using the process of accommodation also known as Flexible Goal Adjustment (FGA).

Now, lets backtrack a little and reflect on the many routes to happiness: some say its all in your head- that you just need to change your mindset/ perception of events and you can be happier;  others say that happiness is dependent on your situations and the actions that you take- you can and should cultivate happiness by activities and by changing your circumstances. Like all debates, like Nature-Nurture, the answer probably lies in the interaction and in-between. Haidt has famously claimed that happiness lies in-between, and I concur.

Similarly, sadness or depression may lie in your flexibility and tenacity of goal pursuits – while showing rigidity to a goal and not giving up may lead to sadness and depression, giving up too early or not being tenacious when circumstances could have been changed, may also lead to regret and sadness.

Bring Back My Happiness

Bring Back My Happiness (Photo credit: Wikipedia)

Its important to note that changing circumstances/ TGP etc are active processes; meanwhile changing mindset/ FGA are relatively passive processes, in that they happen in the background and not so much consciously.

That brings me to my major thesis: Depression is a disorder characterized by inability to use the adaptive process of FGA optimally. To me, Depression is a disorder of Behavior related to the Passive polarity of the ABCD Behavioral dimension. When one has a goal, to which one is committed, but is no longer attainable (and this may include an irreparable loss like bereavement ) then most people will use Flexible Goal Adjustment to come out of that state. However, the people with depression may be less able to use FGA and may remain committed to unattainable goals.

One of the evidence that comes to mind is, and for this you have to refer to my previous post about personality disorders and emotions,  that the passive pole of Behavior dimension in ABCD model is also associated with Dysthemic and borderline personalities and hypothesized to be associated with the Conscentiousness trait. Now, It does seem that there is some evidence that highly conscientious people who have high commitment to goals, also are more likely to get depressed following setbacks or adverse life events. This makes immense theoretical sense too.

One can also examine the Active pole of the Behavior dimension in ABCD model to gain equivalent insights. As I had mentioned in my last post, that is associated with personality disorders of Histroinic and Hypomanic personality disorders and likely associated with the trait Impulsive Sensation Seeking. Extending this joy/ happiness related dimension, all these are also likely to be associated with the active process of Tenacious Goal Pursuit; here it is instructive to note that a high score on Impulsive Sensation Seeking may prevent TGP from happening as the person may keep moving from one activity to the other; and extremes of this may lead to manic behavior. The high scores on Impulsive Sensation seeking leading to less TGP leading to full-blown mania, is similar in nature to high scores on Conscientiousness leading to less FGA leading to full-blown depression.

To me, this seems a novel and fruitful approach to think about and conceptualize depression- as an inability to give up goals that are no loner feasible. If we focus more on this aspect, perhaps we need to augment our talking therapies of CBT etc that focus on negative self-talk and also introduce safe spaces and experiences whereby people can indulge in Flexible Goal Adjustment and give up on goals that are no longer feasible and replace them with other more meaningful and attainable goals.

Growing From Depression

“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.

The Four Neural Sub-Types of Depression

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.

Anhedonia (The Graduate album)

Anhedonia (The Graduate album) (Photo credit: Wikipedia)

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.

Depression and its Antecedents

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.

English: Abraham Lincoln, the sixteenth Presid...

English: Abraham Lincoln, the sixteenth President of the United States. Latviešu: Abrahams Linkolns, sešpadsmitais ASV prezidents. ?????? / Srpski: ??????? ???????, ????????? ?????????? ?????????? ????????? ??????. (Photo credit: Wikipedia)

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.

Depressive symptoms

On the Threshold of Eternity

On the Threshold of Eternity (Photo credit: Wikipedia)

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:

Emotional Manifestations

  • Dejected mood
    Negative feelings toward self
    Reduction in gratification
    Loss of emotional attachments
    Crying spells
    Loss of mirth response

Cognitive Manifestations

  • Low self-evaluation
    Negative expectations
    Self-blame and self-criticism
    Indecisiveness
    Distortion of body image

Motivational Manifestations

  • Paralysis of the will
    Avoidance, escapist, and withdrawal wishes
    Suicidal wishes
    Increased dependency

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.

Why is the world vivid in mania, but bleak in depression?

Down in a hole
Image by ParanoidMonk via Flickr

ResearchBlogging.org
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.

and…

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

Enhanced by Zemanta

stress and neurogenesis: the orchid -dandelion effect

ResearchBlogging.org

Orchid
Image by santoshnc via Flickr

Chronic stress in mice leads to the ‘learned helplessness‘ model of depression in mice. Also, from studies in humans as well as other animals we know that chronic stress is a risk factor and cause for depression and this is mediated by the interactive effects of two stress related systems: “the neural substrate for the organism’s stress response comprises two anatomically distinct but functionally integrated circuits, the corticotropin-releasing hormone CRH system and the locus coeruleus–norepinephrine LC-NE system.”

The relation between cortisol level/ activity in the CRH/LE-NE system and stress related maladaptation is not simple , but the relationship is complex.

There are many theories of depression. A finding that has gained ground in recent years is the enhanced neurogenesis due to administration of anti-depressants and how the action of anti-depressants may be due to their enhancing neurogenesis effects.

However this new study in PNAS, conducted on mice,  casts doubt that the relation between stress/depression and neurogenesis is simple. It seems the relation is as complex as that between stress/depression and the cortisol levels.

I would first like to briefly summarize the findings of the study:

  • chronic stress paradigm used was that of social defeat (cohabitation with a socially dominant conspecific). 10 days of this social defeat were administered. this typically leads to social avoidance behaviors and these behaviors are correlated with other depressive phenotypes.
  • after 10 days when social avoidance (time interacting with a potential friendly con-specific) was measured it was found that about half the mice exhibited social avoidance and were sensitive to the stress; the rest of the half were ‘resilient’ and did not differ from control mice (not exposed to chronic social defeat) in their social avoidance.
  • all mice, both resilient and sensitive , showed decreased proliferation in subgranular zone (SGZ) for new cells immediately after stress exposure. This effect disappeared / normalised after 24 hrs.
  • Cell survival for cells created before stress exposure was not affected by stress exposure.
  • cell survival for neurons created 1 day after stress exposure was enhanced selectively for those mice that were susceptible or sensitive to stress, but was not enhanced for the resilient mice or the mice taken as a whole.
  • when the mice were irradiated, before stress exposure,  to prevent neurogenesis, then the social avoidance behavior, even in susceptible mice disappeared. It is thus evident that social avoidance is mediated by increased neurogenesis post-stress exposure in the susceptibel mice.

Overall, the results I believe are clearly in favor of conceptualizing the susceptible mice as ‘orchid’ mice – having enhanced tendency for neurogenisis following positive/negative events of interests. they are biologically sensitive to context and exhibit neurogenesis reactivity similar to stress reactivity shown by orchid children. Given a positive life experience the increased neurogenesis post-event helps in having happy memories and cognition s and better functioning; preponderance of negative life vents in contrast lead to more negative and longlasting cognitions and memories leading to reduced functioning. Of course the dandelion mice are resilient and not that much affected by chronic stress. However, they would also not be able to make best use of environment in good conditions.

The only hiccup I see in the whole scheme of things is the effect of anti-depressants on neurogenesis and my earlier theorizing that cells may die under repetitive stress and reduced or absent neurogenisis would be a prime factor in depression. However, the relation between neurogenesis and stress will be , I am sure, complex and needs to be settled empirically, rather than theoretically.  However one thing is clear, neurogenesis has a rpime role to play in depression , mediated perhaps by, chronic stress exposure and genetic diatheisis (orchid-dandelion effect).

I am excited and would love to hear of more papers that are addressing this new trend in depression – neurogenesis research keeping in mind the biological sensitivity to context thing too.

Reblog this post [with Zemanta]

Lagace, D., Donovan, M., DeCarolis, N., Farnbauch, L., Malhotra, S., Berton, O., Nestler, E., Krishnan, V., & Eisch, A. (2010). Adult hippocampal neurogenesis is functionally important for stress-induced social avoidance Proceedings of the National Academy of Sciences, 107 (9), 4436-4441 DOI: 10.1073/pnas.0910072107