Wednesday, January 30, 2008

good mood= intuition + good mood = psychosis?

I recently blogged about how good mood may lead to diminishing of working memory and I have blogged in the past regarding how good mood + intuitive thinking styles may lead to Magical thinking.

Now there appears a new study that shows that good mood, in and of itself, may lead to more reliance on Intuition or conscious gut feelings while making decisions. DeVries et al use the Iowa Gambling Task to ascertain whether an experimental manipulation (watching 2.5 minutes happy or sad clips) affected the performance on the IGT, in the window (20 to 40 cards from start) when the participants were using the conscious gut feeling or intuition to form their decisions . What they found was that a good or happy mood made the people rely more on their intuitive or conscious gut feelings vis-a-vis controls and the negative mood had the opposite effect of making them more deliberative. This was reflected in respectively good and poor performance on the second block of trial in the two affect cases . I present below the abstract of the study.

The present research aimed to test the role of mood in the Iowa Gambling Task . In the IGT, participants can win or lose money by picking cards from four different decks. They have to learn by experience that two decks are overall advantageous and two decks are overall disadvantageous. Previous studies have shown that at an early stage in this card-game, players begin to display a tendency towards the advantageous decks. Subsequent research suggested that at this stage, people base their decisions on conscious gut feelings. Based on empirical evidence for the relation between mood and cognitive processing-styles, we expected and consistently found that, compared to a negative mood state, reported and induced positive mood states increased this early tendency towards advantageous decks. Our results provide support for the idea that a positive mood causes stronger reliance on affective signals in decision-making than a negative mood.

I tend to put this in a broader context and it is apparent to me that good mood leads to more reliance and usage of intuitive thinking styles. this may even be mediated by the fact that working memory deficits associated with good mood prevent a deliberative approach to problem solving and instead favors an affective driven or intuitive approach. Taken together this implies that good mood leads to more intuitive thinking and decision making style. However, we have seen earlier that good mood and an intuitive thinking style are a dangerous mixture and lead to Magical thinking styles. Taken together this would mean that good mood induces a positive runaway process that causes more reliance on intuitive thinking which causes more
Magical thinking style and ultimately the good mood spirals upwards from good mood to Mania to full blown psychosis. I am excited by these linkages as they may provide additional points of attack where one can address the cognitive factors behind Mania / Psychosis and lead to additional therapeutic paradigms. How about you? Does this correlation and causation form Mood to Intuition to Magical thinking excite you too?

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Tuesday, January 29, 2008

Psychosis and Autism as Diametrical Disorders of the Social Brain: converging evidence!!

Readers of this blog will be familiar with my model of Autism/ Schizophrenia and I recently found an online article by Crespi et al that elegantly summarizes the theory that autism and Schizophrenia are on a continuum of phenotypic variations related to cognition and the social brain.

I will be using images and text from that article heavily, so go ahead and read the original article too, which is very well-written and thought provoking.

The Authors contend that autism and schizophrenia are on a continuum where cognition is concerned with Autistics leaning towards mechanistic cognition, while schizophrenics leaning towards mentalistic cognition. This should be a familiar story to readers of this blog.

They discuss the various contrasting features of Autism and Schizophrenia. They contend that Autism is made up of three dimensions: language and communication difficulties, social reciprocity difficulties and creative or imaginative difficulties (which they term as repetitive and restricted behavior) .

They contrast this with the psychotic spectrum in which they include the three corresponding dimensions as Unipolar depression, bipolar disorder and Schizophrenia.

They then go ahead and list a variety of evidence from studies of growth, development, neuroanatomy, cognition, behavior, and epidemiology for diametric phenotypes in autism and psychosis. I reproduce below the table (click to enlarge - the tables are a must read!!) which highlights salient differences in phenotypes:

The authors have their own theory (which seems very plausible to me) regarding why Autism and Schizophrenia are diametrically opposite. This they contend is due to evolutionary arms race between the child and mother for scarce resources mediated by maternal and paternal imprinting genes.

They do a brilliant job of describing their theory so I quote from them:

Further hints that imprinted genes may have something to do with autism and psychosis come from the finding that autistics have heavier birth-weight(especially males) while schizophrenics are lighter – just as you would expect if paternal genes were more prominent in autism. Again, more paternal and/or less maternal genetic influence is sometimes implicated in cancer(another form of over-growth) and here the striking finding is that schizophrenics have less cancer than autistics despite the fact that the former smoke much more. Again, there is evidence that autistics by contrast to psychotics show early brain growth at the expense of the mother.

The article's discussion is enlightening as it also throws light on other previous researchers who have hypothesized along similar lines. Alas The Mouse Trap doesn't get a mention, But Nettle , regarding whom I have blogged before gets a mention.

Our hypothesis can be conceptualized at two interacting levels: (1) the diametric architecture of autistic and psychotic-spectrum conditions (Badcock 2004), and (2) the underpinnings of this structure in dysregulated genomic imprinting. A diametric structure to autism and schizophrenia has been considered for some traits before: thus, Abu-Akel (1999) and Abu-Akel & Bailey (2000) suggested that autism and schizophrenia represent extremes on a continuum of theory of mind skills from hypodevelopment to hyper-development, Frith (2004b) described 'under-mentalizing' in autism and 'over-mentalizing' in schizophrenia, and Nettle (2006) anticipated an autism psychosis spectrum in noting that “autistic traits are in many ways the converse of the unusual experiences component of schizotypy”. However, most previous research on autism and psychosis has considered the disorders to be etiologically unrelated (or has considered the negative symptoms of schizophrenia in terms of autism), although both disorders are believed to be underlain by dysregulated development of the social brain (Broks 1997; Emery 2000; Burns 2004, 2006). By our hypothesis, autism and psychosis represent extremes on continua of human cognitive architecture from mechanistic to mentalistic cognition, with balanced cognition at the center (Figure 4). Each set of conditions is extremely heterogeneous but also highly convergent, in that diverse genetic, epigenetic and environmental effects can generate similar cognitive phenotypes (Happé 1994, p. 2; Keverne 1999; Seeman et al. 2005; Badcock & Crespi 2006; Happé et al.2006). These striking convergences are mediated, in our view, by the dynamics of social brain development, with under-development in autistic conditions and hyperdevelopment in psychotic conditions (Badcock 2004), Further tests of this hypothesis should focus on assessing the breadth and depth of diametric phenotypic structure to autistic and psychotic spectrum conditions, and testing for tradeoffs between mentalistic and mechanistic thought and ability.

I am thrilled to see my theory also being investigated in parallel and worked on by distinguished scientists and am grateful for the scientific work going in this area. I am sure we will soon see more research supporting my thesis.

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Monday, January 28, 2008

good mood= compromised working memory?

A recent study mentions that when people are in good mood, they are likely to choose from amongst the first of the options presented, if asked to choose on the run. However, if they are asked to withhold evaluation till all the alternatives are presented, then they chose the last item presented.

A new study in the February issue of the Journal of Consumer Research people finds that consumers in a good mood are more likely than unhappy consumers to choose the first item they see, especially if all the choices are more or less the same.

The researchers also found that when happy consumers were asked to withhold judgment until all options were presented, they tended to prefer the last option they saw.

To me this appears very much like the recency and primacy effects. Their working memory is so much compromised , due to their good mood that they resort to the heuristics of recency/ primacy to determine their decisions.

The above theory may seem outrageous at first glance, but there are studies suggesting that people are bad decision makers when in good mood and that working memory compromise may be the underlying factor.

A good mood may be bad for people faced with problem-solving tasks that demand a high degree of logical thought and planning, according to a study.

Researchers say the brain may be too busy retrieving "feelgood" memories to enhance the positive mood to focus fully on the task in hand. Someone in a neutral mood can devote themself solely to problem solving, they argue.

According to Mike Oswald, when in good mood, good memories are brought into consciousness and this intrudes with the limited working memory thus temporarily incapacitating it.

Dr Oaksford, who will receive the BPS Spearman Medal today for his work on human reasoning, said that the positive mood state may be affecting the brain's capacity for "working memory" - a space devoted to thinking, planning, and problem solving - as good memories are being retrieved at the same time.

"It is like a having a blackboard to work your problems out on but your memory is writing on that blackboard at the same time," he said

This compromising of working memory due to good mood may also explain the working memory deficits found in those suffering from Mania/ psychosis. This may also underlie their jumping to conclusions sort of thinking as they pick the first alternative that comes to mind. Also this may explain their irritable and impatient mood, where they just go for decision making without withholding judgment as the first option itself seems promising and does not get critical evaluation. The direction may even be reverse- due to irritability and good mood (manic style) associations, one may choose the first alternative and this may appear like the primacy effect. However the directionality may be it seems evident that good mood comes accompanied with bad decisions. If the relation is exclusively that of working memory overrode with primacy and recency heuristics we can devise better decision making guidelines for those suffering from Mania.

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Thursday, January 24, 2008

Auitsm, Valproate and Mania/Psychosis

There is a new open source journal available called Frontiers in Neuroscience , and in the first edition there is an article expounding autism as an Intense world syndrome. It is a very intriguing article that claims amongst other things that autistics have very rich local neural circuitry (perhaps in lieu of sparse global circuitry) and this may be the reason why they have rich modular cognitive abilities like memory etc. I am tempted to contrast this with Schizophrenia/ psychosis where there may be more global processing of information. But before my main thesis an abstract of the paper.

Autism is a devastating neurodevelopmental disorder with a polygenetic predisposition that seems to be triggered by multiple environmental factors during embryonic and/or early postnatal life. While significant advances have been made in identifying the neuronal structures and cells affected, a unifying theory that could explain the manifold autistic symptoms has still not emerged. Based on recent synaptic, cellular, molecular, microcircuit, and behavioral results obtained with the valproic acid (VPA) rat model of autism, we propose here a unifying hypothesis where the core pathology of the autistic brain is hyper-reactivity and hyper-plasticity of local neuronal circuits. Such excessive neuronal processing in circumscribed circuits is suggested to lead to hyper-perception, hyper-attention, and hyper-memory, which may lie at the heart of most autistic symptoms. In this view, the autistic spectrum are disorders of hyper-functionality, which turns debilitating, as opposed to disorders of hypo-functionality, as is often assumed. We discuss how excessive neuronal processing may render the world painfully intense when the neocortex is affected and even aversive when the amygdala is affected, leading to social and environmental withdrawal. Excessive neuronal learning is also hypothesized to rapidly lock down the individual into a small repertoire of secure behavioral routines that are obsessively repeated. We further discuss the key autistic neuropathologies and several of the main theories of autism and re-interpret them in the light of the hypothesized Intense World Syndrome.

The authors use the valproate model of autism for their discussion and it is a well established mouse model of autism. In this model, mother rats are given valproate during pregnancy and the children later had autistic syndromes and were developmentally retarded. There is also some literature documenting a linkage between fetal valproate syndrome and autism.

Rodier et al. have reported that, in a rat model for teratogen exposure, the administration of valproic acid in early development induces morphological brainstem pathology similar to changes sometimes observed in autism. Alterations in the distribution of serotonergic neurons in brain, suggestive of abnormal neuronal differentiation and migration, have also been observed in the animal model. Further work in rats has shown that the prenatal challenge with valproic acid induces behavioral changes, including delayed maturation, decreased social exploration, deficits in sensorimotor gating, and repetitive, stereotyped responses in an open field. In mice, exposure to valproic acid while in utero leads to behavioral retardation and regression during neonatal and juvenile development

Thus from the above discussion it is apparent that exposure to valproic acid has something to do with autism. It is to be noted that valproic acid/ sodium valproate is a well-known anti-convulsant that is also given in bipolar disorder as a mood stabilizer. Now readers of his blog will be familiar with my model of autism , whereby I stress the opposite polarity to schizophrenia/ psychosis. I believe that what we witness in Autism is the converse of what we witness in psychosis. Both are pathological states, but one with too much reality orientation (including not attributing agency to fellow humans/ animals) while other too much fantasy orientation (with tendency towards anthropomorphism). Also while autistics may be the proverbial detail-oriented missing forest for the trees sort of people, schizophrenics are more meaning-and-big-picture-obsessed people with possibly more hyper-active and hyper-plastic global neural circuitry as opposed to what is hypothesized in autistic intense world syndrome.
I also consider bipolar and schizophrenia to be closely related and am not surprised that while lack of valproic acid is used to treat the bipolar psychosis and the bipolar condition; an exposure to the same teratogen during pregnancy ( a critical developmental window ) may have the opposite effect of leading to the opposite disorder like autism. To me this valproic acid linkage proves further that autism and schizophrenia/ psychosis are opposite of each other.

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Friday, January 18, 2008

The Five Moral Foundations

Jonathan Haidt studies Morality and he , with Joseph and Graham, has discovered what he calls the five major moral foundations or ethical areas of concern. A Steven Pinker article that is doing the rounds these days introduces these as follows :

The exact number of themes depends on whether you’re a lumper or a splitter, but Haidt counts five — harm, fairness, community (or group loyalty), authority and purity — and suggests that they are the primary colors of our moral sense. Not only do they keep reappearing in cross-cultural surveys, but each one tugs on the moral intuitions of people in our own culture. Haidt asks us to consider how much money someone would have to pay us to do hypothetical acts like the following:

In a Science Magazine article Haidt originally listed these scenarios as follows and requested that we do a though experiment as to how much money someone would need to give us to perform the following acts (the first act is relatively amoral, while the second presents a moral dilemma) :

  • Stick a pin into your palm.
  • Stick a pin into the palm of a child you don't know.

  • Accept a plasma screen television that a friend of yours wants to give you. You know that your friend got the television a year ago when the company that made it sent it, by mistake and at no charge, to your friend.
  • Accept a plasma screen television that a friend of yours wants to give you. You know that your friend bought the TV a year ago from a thief who had stolen it from a wealthy family.

  • Say something slightly bad about your nation (which you don't believe to be true) while calling in, anonymously, to a talk-radio show in your nation.
  • Say something slightly bad about your nation (which you don't believe to be true) while calling in, anonymously, to a talk-radio show in a foreign nation.

  • Slap a friend in the face (with his/her permission) as part of a comedy skit.
  • Slap your father in the face (with his permission) as part of a comedy skit.

  • Attend a performance art piece in which the actors act like idiots for 30 min, including failing to solve simple problems and falling down repeatedly on stage.
  • Attend a performance art piece in which the actors act like animals for 30 min, including crawling around naked and urinating on stage.
As one can easily see from ones responses, the second of the set of questions appears to be morally reprehensible, though the category to which it belongs and the moral intuitions which guide our reaction to the underlying dilemma is different in each case. for the child-pricking-with-needle scenario we are focussed on harm avoidance and rely on empathy; while in the artists-running-naked we are more moved by our intuitions on what is aesthetically pure and sanctimonious.

Haidt also believes that these moral foundations have different evolutionary roots: while harm and fairness may rely on evolutionary mechanisms of kin selection and reciprocal altruism respectively, the other dimensions like ingroup/ loyalty may be due to group selection acting at group levels. The other foundations like respect for authority and desire for purity may have their own evolutionary mechanisms:

If I asked you to define morality, you'd probably say it has something to do with how people ought to treat each other. Nearly every research program in moral psychology has focused on one of two aspects of interpersonal treatment: (i) harm, care, and altruism (people are vulnerable and often need protection) or (ii) fairness, reciprocity, and justice (people have rights to certain resources or kinds of treatment). These two topics bear a striking match to the two evolutionary mechanisms of kin selection (which presumably made us sensitive to the suffering and needs of close kin) and reciprocal altruism (which presumably made us exquisitely sensitive to who deserves what). However, if group selection did reshape human morality, then there might be a kind of tribal overlay (—a coevolved set of cultural practices and moral intuitions—that are not about how to treat other individuals but about how to be a part of a group, especially a group that is competing with other groups.

In my cross-cultural research, I have found that the moral domain of educated Westerners is narrower—more focused on harm and fairness—than it is elsewhere. Extending a theory from cultural psychologist Richard Shweder, Jesse Graham, Craig Joseph, and I have suggested that there are five psychological foundations, each with a separate evolutionary origin, upon which human cultures construct their moral communities . In addition to the harm and fairness foundations, there are also widespread intuitions about ingroup-outgroup dynamics and the importance of loyalty; there are intuitions about authority and the importance of respect and obedience; and there are intuitions about bodily and spiritual purity and the importance of living in a sanctified rather than a carnal way. And it's not just members of traditional societies who draw on all five foundations; even within Western societies, we consistently find an ideological effect in which religious and cultural conservatives value and rely upon all five foundations, whereas liberals value and rely upon the harm and fairness foundations primarily.

To me, these five moral foundations fit beautifully with the five factor models that I have been considering. Harm being more physically rooted, fairness/ justice more subjectively rooted; ingroup/ loyalty more rooted in interactions between group members; respect/authority more socially rooted; while purity/sanctity more individualistically rooted.

Also this framework is broadly compatible with Kohlberg's moral development theory, with harm based reasoning predominating at stage I and so on. To elaborate:

  1. Stage 1 thinking is marked by Obedience and Punishment Orientation. This orientation clearly relies on Harm based reasoning to discern morality of acts- whether harm is caused by the cats and whether the results (including punishment ) would be harmful.
  2. Stage 2 thinking is marked by Individualism and Exchange. This exchange mentality is typical of those advocating reciprocal altruism or those who emphasize fairness and the golden rule.
  3. Stage 3 thinking is marked by Good Interpersonal Relationships. this reasoning is marked by emphasis on good relationships within a ingroup and loyalty to it and all its members.
  4. Stage 4 thinking is marked by Maintaining the Social Order. Here respect of authority is clearly evidenced as one wants to respect the authority inherent in the social order.
  5. Stage 5 thinking is marked by Social Contract and Individual Rights . Here the purity/ sanctity dimension is more prominent and one focuses on the purity, sanctity and inalienability of human rights. These rights are sort of divine.

I am excited to see how these five major moral foundations could still be under evolutionary selection and thus, we may not even be aware of the processes by which the later stage mechanisms work. While the evolutionary earlier kin selection and reciprocal altruism are well understood, we are still evolving the other traits and hence no clear mathematics for that yet in place- hence we are baffled by group selection or deny that other dimensions like purity/sanctity have anything to inform on moral matters. That may just be due to the fact that western morality is still not developed to higher stages of Morality as compared to other civilizations (or for that matters liberals less developed than conservatives? ). I am sure that there would be three more qualitatively different moral foundations taking the eventual number to eight moral foundations, but we must first appreciate the five moral foundations better before we move up and broaden the moral horizons.

Lastly let me briefly mention the relationship of these five major foundations to emotions. It has been found in studies that people respond with disgust (expressions) when confronted with an immoral act belonging to purity/sanctity dimension. They respond with contempt if they witness moral transgressions in respect/ ingroup dimensions and react with anger while witnessing transgressions of harm/ justice dimension. Thus, we may even relate these five moral foundations with the primary affects. But that is food for a later post!

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Wednesday, January 09, 2008

Dissociable areas of memory (in MTL): Two or three?

There has been some discussion in memory literature as to whether familiarity / novelty detection and recollection (contextual recognition of a stimulus or episodic recall) are independent processes or are the same processes, but only the memory strength varies.

In 2006, an fMRI study came around that showed that there were three dissociable areas in MTL that were associated with familiarity, novelty and recollection detection.

There have been indications that recollection, familiarity, and novelty involve different medial temporal lobe subregions, but available evidence is scarce and inconclusive. Within the medial temporal lobes (MTLs), they found a triple dissociation among the posterior half of the hippocampus, which was associated with recollection, the posterior parahippocampal gyrus, which was associated with familiarity, and anterior half of the hippocampus and rhinal regions, which were associated with novelty. Furthermore, multiple regression analyses based on individual trial activity showed that all three memory signals, i.e., recollection, familiarity, and novelty, make significant and independent contributions to recognition memory performance.

This appeared to be the established dogma to me, till I came across this new PNAS paper, which again strives to swing the pendulum back in favor of memory strengths and a single process for recollection and familiarity/novelty detection. The authors found that while a distinct group of neurons in hippocampus and anygdala was responsible for novelty and familiarity detection, recollection could just be ascertained by the strength of the neural firing of these groups of neurons. Here is the abstract of the study:

Episodic memories allow us to remember not only that we have seen an item before but also where and when we have seen it (context). Sometimes, we can confidently report that we have seen something (familiarity) but cannot recollect where or when it was seen. Thus, the two components of episodic recall, familiarity and recollection, can be behaviorally dissociated. It is not clear, however, whether these two components of memory are represented separately by distinct brain structures or different populations of neurons in a single anatomical structure. Here, we report that the spiking activity of single neurons in the human hippocampus and amygdala [the medial temporal lobe (MTL)] contain information about both components of memory. We analyzed a class of neurons that changed its firing rate to the second presentation of a previously novel stimulus. We found that the neuronal activity evoked by the presentation of a familiar stimulus (during retrieval) distinguishes stimuli that will be successfully recollected from stimuli that will not be recollected. Importantly, the ability to predict whether a stimulus is familiar is not influenced by whether the stimulus will later be recollected. We thus conclude that human MTL neurons contain information about both components of memory. These data support a continuous strength of memory model of MTL function: the stronger the neuronal response, the better the memory.

PNAS has made the article freely available, so go have a look. This is what they discuss:

We analyzed the spiking activity of neurons in the human MTL during retrieval of declarative memories. We found that the neural activity differentiated between stimuli that were only recognized as familiar and stimuli for which (in addition) the spatial location could be recollected. Further, we found that the same neural activity was also present during behavioral errors, but with reduced amplitude. This data are compatible with a continuous signal of memory strength: the stronger the neuronal response, the better the memory. Forgotten stimuli have the weakest memory strength and stimuli that are only recognized but not recollected have medium strength. The strongest memory (and thus neuronal response) is associated with stimuli that are both recognized and recollected.

One methodological flaw of the current study is that it didn't take the earlier studies showing triple dissociation into account and did not differentiate between MTL neurons based on their location within hippocampus/ amygdala. If they had distinguished based on the location, they might have found some neurons that were selectively coding for recollection. In absence of such observations I find it hard to concur that recollection is not an independent process from familiarity/ novelty detection. Recollection involves binding the familiarity/ novelty cues with other neuronal cues in MTL like neurons that code for time and place . It may be that the current study completely missed out on those integrator neurons.

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Monday, January 07, 2008

Depression, Dreaming and Rehearsal learning

We all know that depression is marked by an increase in REM Sleep or dreaming and their are various theories of why this increased dreaming may be a root cause of depression itself. One theory posits that having too much dreams or emotional negativity even while sleeping (most dreams have negative content) may lead to maintenance of downward spiral of depressive cognitive and emotional style. Another theory posits that having too much negative dreams may lead us to get exhausted and the morning weariness found in depression is due to this fact.

I'll not comment regarding the purported mechanism and causal direction of link between depression and dreaming. Suffice it to note few pertinent facts:

  • Depressives dream 3 -4 times more than normal people.
  • Most Anti-depressants cause REM sleep to be suppressed and this may underlie their therapeutic action or may just be a side-effect.
  • There is mixed evidence as to whether REM sleep is also altered in Mania (although a decrease in REM sleep is not mentioned in literature- if anything REM increases just like in depression)

Now I'll like to highlight an important experiment conducted by Wisconsin Madison scientists. They deprived rats of REM sleep and found that such rats became idiots in terms of survival sense and failed all standard test of survival. I'll first describe the procedure and their results and then theorize:

What happens when a rat stops dreaming? In 2004, researchers at the University of Wisconsin at Madison decided to find out. Their method was simple, if a bit devilish. Step 1: Strand a rat in a tub of water. In the center of this tiny sea, allot the creature its own little desert island in the form of an inverted flowerpot. The rat can swim around as much as it pleases, but come nightfall, if it wants any sleep, it has to clamber up and stretch itself across the flowerpot, its belly sagging over the drainage hole.

In this uncomfortable position, the rat is able to rest and eventually fall asleep. But as soon as the animal hits REM sleep, the muscular paralysis that accompanies this stage of vivid dreaming causes its body to slacken. The rat slips through the hole and gets dunked in the water. The surprised rat is then free to crawl back onto the pot, lick the drops off its paws, and go back to sleep—but it won't get any REM sleep.

Step 2: After several mostly dreamless nights, the creature is subjected to a virtual decathlon of physical ordeals designed to test its survival behaviors. Every rat is born with a set of instinctive reactions to threatening situations. These behaviors don't have to be learned; they're natural defenses—useful responses accrued over millennia of rat society.

The dream-deprived rats flubbed each of the tasks. When plopped down in a wide-open field, they did not scurry to the safety of a more sheltered area; instead, they recklessly wandered around exposed areas. When shocked, they paused briefly and then went about their business, rather than freezing in their tracks the way normal rats do. When confronted with a foreign object in their burrow, they did not bury it; instead, they groomed themselves. Had the animals been out in the wild, they would have made easy prey.

The surprise came during Step 3. Each rat was given amphetamines and tested again; nothing changed. If failure to be an effective rat were due to mere sleep deprivation, amphetamines would have reversed the effect. But that didn't happen. These rats weren't floundering because they were sleepy. Something else was going on—but what?

To me it seems that what is happening in these dream-deprived rats is an unlearning of learned helplessness paradigm. In learned helplessness, one stops exploring the environment and becomes extremely cautious. Learned helplessness is an extremely influential theory of depression and I have blogged about it previously. In the dream-deprived rats something exactly the opposite is happening - they are becoming more exploratory and sort of unlearning the basic survival instincts .

To me all this seems to nicely fit together. Dreams may be instrumental in rehearsal learning and when the rat (or human) has been repeatedly exposed to inescapable shocks (unavoidable stress), then it may lose the desire to explore not only in the real world, but also in the dream world - the primary purpose of which is to generate alternative strategies to previously un-encountered negative situations. When one loses or fails to find creative solutions to the inescapable situations, one falls in a negative dream loop whereby one fails to explore adequately new strategies or to reassess the environment in light of new evidences. Instead as one has failed to find creative solutions earlier, one;s dreams become pre-occupied with failure- and with each failure prompts more vigorous search for answers in the dream -thus leading to more REM sleep. Also, as REM sleep is required for thus maintaining the new (unhealthy) associations hence as long as adequate REM sleep is available one stays stuck with the learned negative associations and the learned helplessness.

SSRIs and other anti-depressants , by blocking the REM sleep , may be providing one additional step whereby dreaming stops for some duration and the synapses that underlie negative associations (that were constantly strengthened during dreams) are given time to naturally become weak. Thus events no longer have automatic negative connotations, but can be appraised afresh with a new outlook. This may be one putative mechanism of how anti-depressants work. This may also explain why anti-depressants take so much time to become effective. When dreaming stops, the unlearning doesn't happen in a day- the weakening of associations would take weeks and months to materialize and have an effect.

Cognitive - behavioral theory may also be working on the level of dreams and it would be interesting to note how much dreaming is reduced and brought to normal levels as CBT starts showing effects.

The behavior of the dream deprived rat seems almost manic- unconcerned with survival and unnecessarily risk-taking. One experiment that can be conducted is to first induce learned helplessness in rats (by exposing them to unavoidable shocks) and then dream-deprive them as per the above methodology. If dream-deprivation restores the normalcy in rats and removes the depressive symptomatology we have a new theory of how depression works. This is not a difficult experiment to do and can be easily performed. I'm sure it will lead to positive results. I look forward to hearing from some readers of this blog as to how the experiment actually went (I myself am in no position to conduct such experiments). Do let me know via comments the experimental results- even if they are negative.

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Friday, January 04, 2008

Depression not only has bland taste but bland sense of smell too

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.

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.

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Wednesday, January 02, 2008

pretend play = creating new worlds?

Edge asks a question each year to prominent scientists and there question this year was "What have you changed your mind about and why?". Well, they didn't invite me to answer that question (not yet :-) , so I wont force my thoughts on the readers of this blog; but instead would like to highlight one of the answers (by Alison Gopnik).

She mentions that she though earlier that pretend play (and related to that the adult fiction reading/creation) was a spandrel and had no evolutionary significance. Now she thinks that the capacity for pretend play is necessary for imagination to develop whcih is necessary for creating new worlds. I, to say the least, am firmly entrenched in the view that treats pretend play as of fundamental importance to development and it is heartening to get support from a prominent psychologist.

I reproduce below the response of Alison in its entirety. (emphasis added by me)

Imagination is Real

Recently, I've had to change my mind about the very nature of knowledge because of an obvious, but extremely weird fact about children - they pretend all the time. Walk into any preschool and you'll be surrounded by small princesses and superheroes in overalls - three-year-olds literally spend more waking hours in imaginary worlds than in the real one. Why? Learning about the real world has obvious evolutionary advantages and kids do it better than anyone else. But why spend so much time thinking about wildly, flagrantly unreal worlds? The mystery about pretend play is connected to a mystery about adult humans - especially vivid for an English professor's daughter like me. Why do we love obviously false plays and novels and movies?

The greatest success of cognitive science has been our account of the visual system. There's a world out there sending information to our eyes, and our brains are beautifully designed to recover the nature of that world from that information. I've always thought that science, and children's learning, worked the same way. Fundamental capacities for causal inference and learning let scientists, and children, get an accurate picture of the world around them - a theory. Cognition was the way we got the world into our minds.

But fiction doesn't fit that picture - its easy to see why we want the truth but why do we work so hard telling lies? I thought that kids' pretend play, and grown-up fiction, must be a sort of spandrel, a side-effect of some other more functional ability. I said as much in a review in Science and got floods of e-mail back from distinguished novel-reading scientists. They were all sure fiction was a Good Thing - me too, of course, - but didn't seem any closer than I was to figuring out why.

So the anomaly of pretend play has been bugging me all this time. But finally, trying to figure it out has made me change my mind about the very nature of cognition itself.

I still think that we're designed to find out about the world, but that's not our most important gift. For human beings the really important evolutionary advantage is our ability to create new worlds. Look around the room you're sitting in. Every object in that room - the right angle table, the book, the paper, the computer screen, the ceramic cup was once imaginary. Not a thing in the room existed in the pleistocene. Every one of them started out as an imaginary fantasy in someone's mind. And that's even more true of people - all the things I am, a scientist, a philosopher, an atheist, a feminist, all those kinds of people started out as imaginary ideas too. I'm not making some relativist post-modern point here, right now the computer and the cup and the scientist and the feminist are as real as anything can be. But that's just what our human minds do best - take the imaginary and make it real. I think now that cognition is also a way we impose our minds on the world.

In fact, I think now that the two abilities - finding the truth about the world and creating new worlds-are two sides of the same coins. Theories, in science or childhood, don't just tell us what's true - they tell us what's possible, and they tell us how to get to those possibilities from where we are now. When children learn and when they pretend they use their knowledge of the world to create new possibilities. So do we whether we are doing science or writing novels. I don't think anymore that Science and Fiction are just both Good Things that complement each other. I think they are, quite literally, the same thing.

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