Posts tagged depression

Manic Depressive Leaders in a Time of Crisis

S. Nassir Ghaemi, in his book, A First Rate Madness: Uncovering the links between  Leadership and Mental Illness, makes a case for the fact that while ‘normal’ leaders are good in times of stability and peace; in times of crisis, mentally ill or mentally abnormal people make for better leaders.

He does this via historical analysis of leaders like Gandhi, Martin Luther King jr, Franklin D. Roosevelt, Winston Churchill, Abraham Lincoln etc. Some of these leaders he classifies as being predominantly depressive, others as manic while the rest as being of bipolar proclivity. In the book he writes:

The depressed person is mired in the past; the manic person is obsessed with the future. Both destroy the present in the process.

He lists four traits that distinguish a manic/depressive leader from other normal leaders: Empathy, ResilienceCreativity and Realism! I can easily map these to the ABCD dimensions: empathy is an Affective trait (the ability to feel emotions), resilience is more about Behaviors (bouncing back from failures), creativity is related to Cognition (ability to think in a divergent manner) while realism can be linked to Desire/Dynamism (do we do realistic assessments).

He claims, and I find that claim very attractive and true, that depressive people typically are better at empathy and realism, that is, they have heightened empathy and realism as compared to the normal population; in a similar vein, manic people are typically better at creativity and resilience than the normal population.

If one views depression and mania  as somewhat opposed to each other. at least on on some dimensions, it goes without saying that depressive people may be less creative (they are typically stuck in ruts)/resilient (they often cant cope and sometime stake the extreme step of suicide); similarly, in a manic phase, people may be less realistic (may even become psychotic losing touch with reality)/ empathetic (may not be able to get inside the head of others).

While a depressive or manic phase may be debilitating, the relatively ‘normal’/symptom free period may confer advantages on depressives, manics or bipolars by making them leverage their resilience, creativity, realism and empathy, especially to tide over crisis.

Why should it be the case that in normal periods a ‘normal’ leader may help, but in a crisis only an ‘abnormal’ leader may be able to rise to the occasion? The answer lies in evolution and genetic diversity. Consider moths that are generally gray in color, but some are darker (closer to black) while some others lighter (white in color) . The majority gray moths are the ‘normal’ moths, while the minority black and white are abnormal ones. Now these moths are exquisitely adapted to their environments, and typically gray moths will flourish. However if the area has suddenly become polluted such that darker color moths are now less easier to detect than the gray moths by the predators, then dark moths will thrive at the cost of  light moths.

A similar analogy can be applied to humans. Normal leaders are adapted to stable conditions; while in times of crisis, more atypical brains may suffer greater advantage.

So next time you select a leader, be mindful of whether its a change/crisis situation or a stable situation; if a crisis/ change situation, you may do well to do some reverse discrimination and select a mentally ill/ abnormal person as a leader!!

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

Down in a hole
Image by ParanoidMonk via Flickr

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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

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stress and neurogenesis: the orchid -dandelion effect

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Orchid
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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 coeruleusnorepinephrine 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.

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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

Am Manic, will focus; Am sad, will drift

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Lucky Guy Happy Gal... :-)
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Attention can be focused or it can be diffused. Attentional focus has been shown to be affected by mood or affect; with positive affect leading to a broadening of attentional focus;  and negative affect, in general been shown to be associated with a narrowing of focus.

However, Gable and Harmon-Jones argue that emotion or affect is not a uni-dimensional construct, but has at least two dimensions: affective valence- i.e. whether it is felt as pleasurable or dis-pleasurable; and motivational  direction- i.e. the action tendency to approach or avoid in pursuit of a preventive/promotional goal.

Much work on emotions has emphasized that they have a number of underlying dimensions. Two dimensions that have received considerable attention are affective valence, the felt pleasure or displeasure, and motivational direction, the action tendency associated with a particular emotional state—approach or withdrawal. Approach motivation refers to an urge or action tendency to go toward an object, whereas withdrawal motivation refers to an urge or action tendency to move away from an object.

They also argue that much of the extant literature on emotion-attention linkage has focused on emotional valence alone, with just one type of motivational direction, and thus has not clarified the (in)dependent role of valence and motivational direction as regards to attention.

Thus, for e.g., the finding that positive emotions lead to  broadening of attention is focused on such research as emotions of joy, contentment etc that are low in approach motivation and are emotions felt after the goal has been reached.

Similarly, the research that has found that negative emotions lead to narrowing of focus have relied on emotions such as fear, anger etc that are high in withdrawal motivation and are pre-goal.

I believe, it is important to step back a little here and go back to our conception of happiness-ennui (mental well-being) continuum and sadness-mania (mental illness) continuum. Another way to conceptualize them is to see sadness having negative valence and low withdrawal motivation – it is passive; mania as having positive valence and high approach motivation- mania is characterized by immense desire for a goal and is pre -goal. Happiness is post goal emotion and is characterized by positive valence and low approach motivation- you have already reached the goal and do not need to exert much efforts in goal directed activity; ennui/boredom/listlessness is negative in valence and has high withdrawal motivation- it is pre-goal- a search for a worthwhile goal.

Another way to make the difference stark is employ the terminology of Berridge et al: happiness is related to liking and the opioid system; while mania is related to wanting and the dopamine system.  Depression/sadness  is related to disliking /feeling pain while ennui/boredom is related to dreading the outcome/feeling anxious (nothing to do and hence life is useless/meaningless!..anxiety but existential anxiety). Berridghe et al have shown that wanting/liking and dreading/disliking differ and have different neural and neurochemichal correlates.

To become a little philosophical, the wanting/disliking  mental illness continuum leading to mania or depression in extremes is to be avoided (thus the dictum of all religions to shun desire/ be stoic) while the happiness-ennui/boredom/existential anxiety system is more preferable where you focus on liking positive outcomes and dreading negative/neutral ones. While the former, to paraphrase Freud,  is the hysterical misery at worst, the latter is common unhappiness at worst.

But anyway that was long detour. Lets get back to the studies by Gable et al.

In the first study, the authors showed that motivational direction was relevant and was the reason behind the positivity-broadening of attentional focus effect. they showed that positive emotions lead to broadening of attention only in low approach motivation condition; but when the positive emotion had high approach motivation (emotions like desire. engagement etc), the positive affect lead to narrowing of focus.

Now a brief detour into methodology: the attentional focus is usually measured using local-global tasks whereby it is determined whether one is paying attention to global features or local features of an ambiguous/mixed stimuli. For eg, the most popular of these consists of a global big H made up of smaller (say 5 in number) F’s and then determining whether the subject notices the global H or the local F. Details can be seen in the Gable papers which are open access.

Now the authors found robust support for their hypothesis that it is the motivational direction and not affective valence that determines the attentional focus. They also relate it to adaptivity.

Positive affects, particularly those low in approach motivation, suggest a comfortable, stable environment and allow for a broadening of attention and cognition, which may serve adaptive functions (Carver, 2003; Fredrickson, 2001). However, broadening does not occur when positive affects are high in approach motivation. Such positive affects often encourage specific action tendencies, such as tenacious goal pursuit, and an associated reduction in attentional breadth. This reduced attentional breadth may prove adaptive, as it assists in obtaining goals.

They also extend these finding to negative affects and depression etc and I can easily relate them to earlier work I have covered regarding the danger or safety of environment and promotional/ preventive focus:

Together with past research, the present research supports the idea that low- and high-approach-motivated positive affect produce opposite effects on attentional breadth. It is possible that the intensity of withdrawal motivation exerts similar attentional effects; that is, low-withdrawal-motivated negative affect may cause broadening, whereas high-withdrawal-motivated negative affect may cause reduction in breadth. Indeed, such an interpretation would fit with past research. For example, individuals with depression, a low-intensity motivation, are more creative than nondepressed individuals (Andreasen, 1987) and show broadening of attention and memory (von Hecker & Meiser, 2005). In the case of low-motivated negative affects such as sadness and depression, “a more open, unfocused, unselective, low-effort mode of attention would prove not deficient but, on the contrary, beneficial” (von Hecker & Meiser, 2005, p. 456), as one disengages from a terminally blocked goal and becomes open to new possibilities (Klinger, 1975). The past research that found negative affect caused decreased attentional breadth may have evoked negative affective states that were high in withdrawal motivation (e.g., fear; Gasper & Clore, 2002).

This brings me to their current paper , aptly titled , The Blues Broaden, but the Nasty Narrows, that found exactly the effect hypothesized above that sadness/depressive mood was related to broadening of attention, while disgust, a negative emotion with high withdrawal motivation was related to narrowing of focus. they also found that the effect of negative emotion was mediated by arousal which could stand as a proxy for motivational direction.

These two experiments revealed that the relationship between negative affect and attentional precedence is more complex than commonly thought. In line with past theory and evidence, Experiment 2 demonstrated that negative affect caused a narrowing of attention. However, this narrowing occurred only when negative affect was high in motivational intensity. When negative affect was low in motivational intensity, in Experiment 1, it caused a broadening of attention. These results are consistent with the idea that the effect of emotion on local/global precedence is not due to negative versus positive affect, but is instead due to motivational intensity. Positive and negative affects of low motivational intensity broaden attention, whereas positive and negative affects of high motivational intensity narrow attention.

To me this is sufficient, clinching and converging proof of the theories I have been trying to develop with regards to emotions (specifically mania, depression, happiness and despair) and make clear that there are at least two dimensions to happiness/sadness and mental well being/illness constructs. Perhaps if we start liking what we have and stop coveting or wanting more, we have a philosophical, religious, as well as now a psychological, blueprint for how to lead the good life and how to avoid a living hell.

Gable, P., & Harmon-Jones, E. (2010). The Blues Broaden, but the Nasty Narrows: Attentional Consequences of Negative Affects Low and High in Motivational Intensity Psychological Science, 21 (2), 211-215 DOI: 10.1177/0956797609359622
Gable, P., & Harmon-Jones, E. (2008). Approach-Motivated Positive Affect Reduces Breadth of Attention Psychological Science, 19 (5), 476-482 DOI: 10.1111/j.1467-9280.2008.02112.x

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Chronic stress, neurogenesis and depression

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Diagram of hippocampal regions in a rat brain....
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Chronically stressful life events have been shown to lead to depression. Chronic stress leads to hyperactivity of HPA axis leading to more glucocorticoids (cortisol) in the human body. This excess cortisol in term is proposed to underlie the affective symptoms of depression. Also, depressive people have been found to have up to 20% smaller hippocampal volume, and a recent theory is gaining ground that depression is due to reduced neurogenesis. Even if the entire spectrum of depressive symptoms is not due to reduced neurogenesis and atrophied or smaller hippocampus, at least the cognitive symptoms of depression are largely due to this.

I stumbled upon a commentary by Robert Sapolsky that although is 10 years old, but I still found interesting and worth bringing to notice of my dear readers. In it Sapolsky looks at a study by Czeh et al that found evidence linking reduced proliferation in dentate gyrus and a shrunken hippocampus to depressive stress as modeled by psycho-social stress paradigm in tree shrew. Also, they found that an antidepressant, tianeptine, reversed the effects of stress by restoring proliferation and hippocampus size and thus reversing symptoms of depression. However the level of glucorticiods were still higher, after anti-depressant treatment, and thus it is apparent that anti-depressants work downstream of stress induced increase in glucorticoids.

Sapolsky believes that the data support either of models presented in figure 1A or figure 1B i.e. the increased glucocrticoids can lead to shrinkage of hippocampus directly or through their effect on affective symptoms. I believe figure 1C is also possible and its not necessarily incompatible with 1A or 1B and that increased stress may lead to increased cortisol- may lead to reduced neurogenesis may lead to shrinkage of hippocampus and which may in turn lead to affective and cognitive symptoms.

An alternative to reduced neurogenesis/ proliferation theory is the dendritic atrophy/ neurotoxicity theory that posits that shrinkage of hippocampus is due to cell death/ white matter loss. This again is a possibility but the evidence in favor of reduced neurogenesis is growing and becoming strong by the day.

Overall the new paradigms in depression research that look beyond serotonin or mono amine imbalance is a welcome trend and hopefully would lead to better interventions and prevention strategies and not just better pharmaceutical innovations. Its time one realized the rile chronic stress play sin depression and how that can be easily prevented to reduce the mental health burden.

Sapolsky, R. (2001). Depression, antidepressants, and the shrinking hippocampus Proceedings of the National Academy of Sciences, 98 (22), 12320-12322 DOI: 10.1073/pnas.231475998
Czeh, B. (2001). Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine Proceedings of the National Academy of Sciences, 98 (22), 12796-12801 DOI: 10.1073/pnas.211427898

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