Posts tagged psychosis

The Creativity-dopamine (b)linkage: more brains and bonkers connections

rh?zom?ng Cam?ra?Obscura pl?ats . .
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Creativity is certainly different from intelligence; it is usually gauged as the ability to make novel and useful unique contributions to a field. Creativity itself is not a unified construct but can be broken into convergent creativity (involving more focused approach) and divergent creativity (involving more widening and loosening of associations).

It has been evident for quite some time that there is a connection between insanity (especially bipolar/schizophrenia spectrum) and creativity , especially as evidenced by the creative bent of schizotypal people. See for example this article covering a recent study that looks at exactly the same issue. However, most of these studies rely on a unitary construct of creativity that does not do full justice to the correlations that could be found if convergent and divergent creativity was distinguished and effect of intelligence was factored out. The new study by Hommel, B. does just that.

Schizophrenia/psychosis as many will know from their elementary neuroscience knowledge is associated with dopamine dysfunction; specifically it is believed that high baseline dopamine levels are there in schizophrenics/psychotics. So it was not unreasonable for Hommel et al to hypothesize that dopamine should have some relation with creativity possible higher dopamine associated with high creativity. However, dopamine has shown an inverse U relation for many other factors and thus they were cautious and tried to fit both linear and quadratic graphs to their data. But we are moving ahead of ourselves. Before they could find the underlying relation between dopamine and creativity, they had to measure these things accurately.

They measured dopamine using Eye Blink Rate (EBR): that is how many time you blink in a minute. For creativity , they measured Convergent Creativity using a remote association task (don’t go by the name …the task has only one answer and measures convergent thinking) . for eg. a subject is given three words (say time, hair, stretch) and have to come up with a word that is commonly related to all three (answer: long) . this reliably measures creativity but of he convergent type. For Divergent thinking , they administered the Alternate Uses task (AUT),a task that requires one tocome up with novel uses of everyday objects like brick, toothpaste etc. The responses to AUT were further coded for fluency (how easily one could come up with alternatives measured by total no. of responses) , flexibility(the number of different categories used or how remote the mind wandered) and elaboration (the level of detail surrounding the use). They also measured fluid intelligence using Raven’s progressive matrices.

They then conducted experiments (administered the tests to subjects) , collected data and analyzed the results. The main findings of interest to us is that they found a inverse u shaped relation between dopamine (EBR) and flexibility dimension fo divergent thinking. This effect was present even when the effect of intelligence was factored out. thus both low dopamine, as well as too much dopamine is detrimental to flexible divergent thinking/creativity and schizotypals , placed precariously between normals and psychotics are best placed to be the most creative as they presumably have the optimum dopamine levels. the authors also argue that schizophrenics dopamine levels should not be brought down indiscreetly by using anti-psychotics (which reduce dopamine levels) but they should be brought in the optimum range of dopamine functioning. this obviously has immense importance and treatment implications. No wonder creative people feel stiffed when on anti-psychotics- their dopamine levels are being brought down way too much.

The other interesting finding was that dopamine (EBR) was negatively ad linearly related to convergent thinking. Thus, it is evident that convergent creativity and divergent creativity are different constructs and while dopamine has a complex quadratic relationship with divergent thinking, that with convergent thinking is linear though not very comforting. It seems that as dopamine levels increase the ability to narrow focus diminishes and this would be concordant with other studies linking dopamine to ADHD for example.

Overall, a view of how brains and bonkers are two sides of the same coin is emerging and it is exciting to note that many previous inconsistencies in literature around this issue may have to do with not differentiating and decomposing creativity into its many components and not looking for inverse u shaped effects.

Chermahini SA, & Hommel B (2010). The (b)link between creativity and dopamine: Spontaneous eye blink rates predict and dissociate divergent and convergent thinking. Cognition PMID: 20334856

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Creativity-psychosis linkage via reduced white matter /myelination
I have been following, and am passionate about, the positive psychology movement for quite some time, but was surprised to discover that there was something called positive neuroscience also in place. I recently came across this new scientist article about the research paper of Rex Jung et al and was pleased to discover that Jung was working on the frontier of applying latest in neuroscience research to Positive brain states and substrates like that involved in creativity.

The article is in PLOSOne, an open access journal and is lucidly written , so you should go and read it now. I’ll anyway like to summarize their study results. First a bit of background about creativity psychopathology linkage.

Some research reports positive correlations between various definitions of creativity and a diagnosis of psychopathology [1], [2], [3], [4]. Other studies report that psychopathology is rarely, if ever, associated with creative insight, capacity, or productivity [5]. When artists are studied more carefully, certain personality characteristics appear to reside upon a continuum of both normal behavior and psychopathology. For example, creative expression in the visual arts and poetry has been linked with the overlapping personality traits of schizotypy and Openness to Experience (Openness), and particularly to self-reports of “unusual experiences” and “unconventional nonconformity”, but not the “introvertive anhedonia” characteristic of schizophrenia [6].

This is inline with what we have been covering at mouse trap regarding association of creativity with the psychotic spectrum especially the creativity that is artistic or revolutionary in nature rather than scientific and methodical in nature. This is how the authors distinguish between types of creativity inline with my views that one type of creativity is autistic (cognitive) in nature while the other is psychotic (emotional) and these are on a continuum.

First, there does not exist one “creativity”; rather, this construct is hypothesized to reside upon a continuum between cognitive (i.e., scientific) and emotional (i.e., artistic) behavioral domains [41], [42]. Thus, when comparing scientists and artists directly, researchers have found lower lifetime rates of psychopathology for: 1) scientists compared to artists, 2) natural scientists compared to social scientists, 3) nonfiction writers compared to fiction writers and poets, and 4) formal artists compared to “expressive” artists [3], [4], [43]. These findings have led researchers to hypothesize a hierarchical structure of creativity across disciplines [42], which echoes the notions of “paradigmatic” (i.e., a fundamental model of events) versus “revolutionary” (i.e., rejection of doctrines) approaches as applied to the sciences [44]. The benefits of working within the lines of a given field appear to be lower levels of psychopathology; alternately, individuals with lower levels of psychopathology may be attracted to such endeavors. Similarly, there is increasing evidence that the cost of “revolutionary” approaches to creative endeavors, whether it is in the arts or sciences, may be associated with increased levels of psychopathology although, again, causative links are weak at best.

So that fits in with broader creativity/ psychopathology linkage, but to get back to the current study the authors had already established earlier that performance on Divergent Thinking (DT) (a measure of creativity) “exhibited significant inverse relationships with both cortical thickness in frontal lobe regions and metabolite concentration of N-acetyl-aspartate (NAA) in the anterior cingulate cortex in normal young subjects “. Thus, some theoretical relationship between creativity and underlying brain circuitry in the frontal reagion was available a priori. Also, research by other researchers has already established that ” Both schizophrenic and bipolar patients have been shown to have reduced fractional anisotropy (FA) in the anterior thalamic radiation [12], [13] and uncinate fasciculus [14] within frontal brain regions. Similarly, reduced FA was observed within the uncinate fasciculus of a cohort with schizotypal personality disorder, providing strong support for the hypothesis that similar neural phenotypes may not result in full-blown clinical symptoms [15]. Finally, in normal subjects, the Neuroregulin-1 (NRG1) single nucleotide polymorphisms (SNP’s) SNP8NRG243177 and SNP8NRG221533 were found to predict lower FA in the left anterior thalamic radiation [16]. As NRG1 has been found to predict higher risk of schizophrenia [17], [18] and bipolar disorder [19], and is linked with axonal myelination and migration [20], these authors hypothesize a mechanistic link between NRG1 within the anterior thalamic radiation and risk for psychotic disorders [16].”

Thus, from the above it is easy to see that there should be a inverse relationship between Fractional Anisotropy (a construct related to myelination of axons) in the frontal regions and creativity if one assumes that creativity and psychopathology are related and are on one end of a continuum. And this inverse relationship between creativity and FA is exactly what they found:

Our results suggest a convergence between a cognitive measure of divergent thinking, a personality measure of Openness, and a white matter integrity measure within the inferior frontal lobes. We found that normal young subjects with lower levels of FA within predominantly left inferior frontal white matter (i.e., regions overlapping the uncinate fasciculus and anterior thalamic radiation) scored higher on the CCI; similarly subjects with lower levels of FA within the right frontal white matter (i.e., regions overlapping the uncinate fasciculus and anterior thalamic radiation) scored higher on self-reported measures of Openness. These two regions of white matter overlap with those reported by other researchers who found lower FA in both schizophrenia and bipolar disorder [13], [14], [30].

They could also nail the reduced FA to reduced myelination as radial diffusion was affected more than axial diffusion. As reduced myelination has been shown as a diatheisis for psychosis, this fits in with previous research linking risk factors common to psychosis and creativity.

Whereas more neural resources are often associated with higher intellectual capacity in a parieto-frontal network of brain regions [39], studies in DT appear to suggest that less is often better in a different network of brain regions, particularly fronto-cingulate-subcortical networks linked via white matter loops [40].

One can speculate that frontal region, more concerned with executive control , when with reduced activity or functional connectivity , may not inhibit the other brain regions that much, and may thus lead to flowering of inherent creativity and cross-talk amongst different brain regions. On the other hand too much white matter/ gray matter in this region may lead to too much control and leave little room for flexibility and creativity.

However, while lower FA is commonly seen in diseases where both cognition and white matter integrity are impaired (e.g., Traumatic Brain Injury, Schizophrenia, Alzheimer’s disease) [45], [46], [47], evidence is accumulating that higher FA in particular brain regions may also be associated with clinical disorders including post-traumatic stress disorder [48], obsessive-compulsive disorder [49], panic disorder [50], synaesthesia [51], and Williams syndrome [52].

It is interesting to note that enhanced FA is associated with clinical disorder of Williams syndrome, which is associated with Autism; on the other end of continuum, reduced FA in particular brain region is associated with psychosis proneness, thus providing another convergent linkage of autism and psychosis as opposites.

Jung, R., Grazioplene, R., Caprihan, A., Chavez, R., & Haier, R. (2010). White Matter Integrity, Creativity, and Psychopathology: Disentangling Constructs with Diffusion Tensor Imaging PLoS ONE, 5 (3) DOI: 10.1371/journal.pone.0009818

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Am happy, will seek novelty; am sad, will stick with familiar

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I have earlier written about the entrepreneurial roller-coaster and how when entrepreneurs are in a happy mood, they focus on long-term vision related creativity; while when they are in negative mood they focus on the task at hand. I had also tried to relate this to prevention and promotion focus and weave it in the narrative of preventive focus as depressive and promotion focus as being manic in nature.

Another bit of research extends the thesis and adds to our knowledge base. This new article by Winkielman et al suggest that people in sad mood tend to value familiarity whereas those in a happy mood are more open and welcoming of novelty.

Here is the abstract of the study:

People often prefer familiar stimuli, presumably because familiarity signals safety. This preference can occur with merely repeated old stimuli, but it is most robust with new but highly familiar rototypes of a known category (beauty-in-averageness effect). However, is familiarity always warm? Tuning accounts of mood hold that positive mood signals a safe environment, whereas negative mood signals an unsafe environment. Thus, the value of familiarity should depend on mood. We show that compared with a sad mood, a happy mood eliminates the preference for familiar stimuli, as shown in measures of self-reported liking and physiological measures of affect (electromyographic indicator of spontaneous smiling). The basic effect of exposure on preference and its modulation by mood were most robust for prototypes (category averages). All this occurs even though prototypes might be more familiar in a happy mood. We conclude that mood changes the hedonic implications of familiarity cues.

The authors reasoning is as follows:

Happy or sad mood signal the safety of the environment.

Much psychological research points out that one signal of environmental safety or danger is an individual’s mood (e.g., Clore, Schwarz, & Conway, 1994; Schwarz, 2002). Bad mood signals a problem, tuning individuals toward safety concerns, whereas good mood signals that an environment is benign. Tuning accounts assume that mood adjusts cognitive and affective reactions so that they best serve the individual in the specific context.

In a safe environment, one can experiment or value novelty. In an unsafe environmental it makes sense to stick to tried and proven things.

After all, familiarity is only a heuristic cue to safety. Thus, as with any heuristic cue, its validity and hedonic meaning vary by context (Hertwig, Herzog, Schooler, & Reimer, 2008). Specifically, the familiarity-positivity link should depend on whether individuals are tuned toward safety concerns. Familiarity should be valued in an unsafe environment, but less so in a benign environment (e.g., Bornstein, 1989). Analogously, in a strange city a familiar face elicits a warm glow, whereas locally the same face prompts a yawn. Numerous studies (and parents) have observed that in unsafe environments infants are neophobic, but in safe settings, they are less so (Shore, 1994). Similarly, in multiple species, stress increases neophobia, whereas comfort reduces it.

Thus they hypothesize that sad mood should lead to mare liking for familiarity while happy mood should lead to novelty preference. They do some clever experimentation and get exactly the same result.

To me this is extension of promotion focus is expansive, is happy, is creative and long-term, and is novelty preferring versus prevention focus is restrictive, is sad, is focused on the task at hand, and is familiarity preferring. In other words people in safe environments having promotion focus are manic while those in unsafe environments and having prevention focus are depressive.

Another finding that struck out from the current paper was that the (false) memory for prototype was increased in positive mood condition. This is congruent with the fact that the promotion focus / mania condition has a more narrative focus that tries to weave a narrative around things and remembers a gist rather than is accuracy based and tries to recall the exact events. thus, I believe the risk of delusions and hallucinations magnifies as one goes deep into promotion focus / mania and starts weaving narratives and having false prototypical memories of events/happenings.

de Vries, M., Holland, R., Chenier, T., Starr, M., & Winkielman, P. (2010). Happiness Cools the Warm Glow of Familiarity: Psychophysiological Evidence That Mood Modulates the Familiarity-Affect Link Psychological Science DOI: 10.1177/0956797609359878

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Autism and Schizophrenia: proof from comparative genomics

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I have blogged extensively about the Autism and Schizophrenia as opposites on a continuum theory. I remember first putting this theory in words in an article 3 yrs back on the mouse trap titled Autism and Schizophrenia: the two cultures. That 2006 article, in turn, was inspired by Daniel Nettle’s 2005 article in Journal of Research in Personality where Nettle had also proposed the dichotomy and that paper helped crystallize my thoughts on the subject, a theory which I had been building on my own and now supported by someone like Nettle who I respect a lot. Important to note that at that time I was blissfully unaware of Badcock or Crespi and their work. It is to the credit of Badcock that he had published in 2006 his own theory of Autism and Schizophrenia as opposites on a continuum based on parental imprinting of genes and proposed a mechanism. Crespi I guess got involved in Badcocks’s efforts later on and gave it more experimental and theoretic grounding. I firts became aware of Badcock and Crespi’s work in early 2008.

The wider world became aware of the Autism/Schizophrenia dichotomy sometime in late 2008 (November 2008) . at that time too, I was a little disappointed because most of the coverage did not mention Daniel Nettle, who I think should be credited for this work and line of reasoning too. As a consolation, some reports did mention Chris Frith who has also been partly supporting the thesis.

I wanted to give a historical perspective, because I am sure the recent Crespi article would be grabbed on by mainstream media and the pioneers Chris Frith/Nettle perhaps overlooked- but to me they too are heroes for having come up with such profound early insights. this is not to discredit teh work of Badcock and Crespi- they are doing a thorough job of convincing the skeptics and delineating the exact mechanism and genetics involved.

While we are on the topic of historical perspective , let me also pat myself on the back. In May 2008, a study came out that de novo Copy Number Variations’s (CNVs) were quite high in schizophrenics and they are in the same region as that for autistics who also have high CNVs in the same region. While some took that result to imply that Schizophrenia and Autism are same and are not different, I persisted and proposed a mechanism, whereby they could still be opposites : To quote:

Now as it happens previous research has also found that CNVs are also found to a higher extent in autistics. Moreover, research has indicated that the same chromosomal regions have CNVs in both Autism and Schizophrenia. To me this is exciting news. Probably the chromosomal region (neurexin related is one such region) commonly involved in both schizophrenia and autism is related to cognitive style, creativity and social thinking. Qualitatively (deletions as opposed to duplications) and quantitatively (more duplications) different type of CNVs may lead to differential eruption of either Schizophrenia or Autism as the same underlying neural circuit gets affected due to CNVs, though in a different qualitative and quantitative way.

Now one and half year later Crespi et al report the results of their study which has found exactly the same- that is, if deletions in some locus lead to autism, duplications lead to schizophrenia and vice versa. That to me is clinching evidence of my thesis. Who says Science does not happen on blogs- I proposed something to flow as a consequence of theory and exactly the same thing is found as per the hypothesis. I feel vindicated and emotional to some extent. Loves labor has not been lost to deaf ears.

Let us then return to the new and latest study that has sort of proven that Autism and Schizophrenia are opposites, genetically. Crespi et al, report in the latest PNAS edition that comparative genomics leads to that conclusion. What Crespi et al did was look at theCNV s and the locus whee CNV in both Autism and Schizophrenia are involved and sure enough they found the pattern I had proposed. I’ll now quote from the abstract and the article extensively:

We used data from studies of copy-number variants (CNVs), singlegene associations, growth-signaling pathways, and intermediate phenotypes associated with brain growth to evaluate four alternative hypotheses for the genomic and developmental relationships between autism and schizophrenia: (i) autism subsumed in schizophrenia, (ii) independence, (iii) diametric, and (iv) partialoverlap. Data from CNVs provides statistical support for the hypothesis that autism and schizophrenia are associated with reciprocal variants, such that at four loci, deletions predispose to one disorder, whereas duplications predispose to the other. Data from single-gene studies are inconsistent with a hypothesis based on independence, in that autism and schizophrenia share associated genes more often than expected by chance. However, differentiation between the partial overlap and diametric hypotheses using these data is precluded by limited overlap in the specific genetic markers analyzed in both autism and schizophrenia. Evidence from the effects of risk variants on growth-signaling pathways shows that autism-spectrum conditions tend to be associated with upregulation of pathways due to loss of function mutations in negative regulators, whereas schizophrenia is associated with reduced pathway activation. Finally, data from studies of head and brain size phenotypes indicate that autism is commonly associated with developmentally-enhanced brain growth, whereas schizophrenia is characterized, on average, by reduced brain growth.These convergent lines of evidence appear most compatible with the hypothesis that autism and schizophrenia represent diametric conditions with regard to their genomic underpinnings, neurodevelopmental bases, and phenotypic manifestations as reflecting under-development versus dysregulated over-development of the human social brain.

Copy Number Data. Rare copy-number variants (CNVs) at seven loci, 1q21.1, 15q13.3, 16p11.2, 16p13.1, 17p12, 22q11.21, and 22q13.3 (Tables S1 and S2), have been independently ascertained and associated with autism and schizophrenia in a sufficient number of microarray-based comparative genomic hybridization (aCGH) and SNP-based studies to allow statistical analysis of the frequencies of deletions versus duplications in these two conditions (Table 1, Tables S3–S9). For five of the loci (1q21.1, 16p11.2, 16p13.1, 22q11.21, and 22q13.3), specific risk variants have been statistically supported for both autism and schizophrenia using case-control comparisons, which allows direct evaluation of the alternative hypotheses in Fig. 1. One locus (16p13.1) supports a model of overlap, and four loci support the reciprocal model, such that deletions are associated with increased risk of autism and duplications with increased risk of schizophrenia (16p11.2, 22q13.3), or deletions are associated with increased risk of schizophrenia and duplications with increased risk of autism (1q21.1, 22q11.21). For 1q21.1 and 22q11.21, contingency table analyses also indicate highly significant differences in the frequencies of deletions compared with duplications for the two disorders, such that schizophrenia is differentially associated with deletions and autism with duplications. By contrast, for 16p11.2 and 22q13.3 such analyses show that autism is differentially associated with deletions and schizophrenia with duplications.


I cannot cut n paste the table, but a look at the table clears all doubts. They also look at gene association data and come to a similar conclusion ruling out model A (autism, subsumed in schizophrenia) or model B (autism and schizophrenia are independent of each other).

Models 1C (diametric) and 1D (overlapping) both predict broad overlap in risk genes between autism and schizophrenia, and do not necessarily predict an absence or paucity of genes affecting one condition but not the other. In theory, these models can be differentiated by using data on specific risk alleles for specific loci (such as single-nucleotide polymorphisms, haplotypes, or genotypes), which should be partially shared under the overlapping model but different under the diametric model. For the genes DAO, DISC1, GRIK2, GSTM1, and MTHFR, the same allele, genotype, or haplotype was associated with both autism and schizophrenia, and for the genes AHI1, APOE, DRD1, FOXP2, HLA-DRB1, and SHANK3, alternative alleles, genotypes, or haplotypes at the same loci appear to mediate risk of these two conditions (SI Text). For the other genes that have been associated with both conditions, heterogeneity in the genetic markers used, heterogeneity among results from multiple studies of the same genes, and the general lack of functional information preclude interpretation in terms of shared or alternative risk factors.

Models of autism as a subset of schizophrenia (Fig. 1A), and autism and schizophrenia as independent or separate (model 1B), can be rejected with some degree of confidence, but models involving diametric etiology (model 1C) or partial overlap (model 1D) cannot be clearly rejected. Taken together, most of the data and analyses described here appear to support the hypothesis of autism and schizophrenia as diametric conditions, based primarily on the findings that reciprocal variants at 1q21.1, 16p11.2, 22q11.21, and 22q13.3 represent statistically-supported, highly-penetrant risk factors for the two conditions (Table 1), and that for a number of genes, alternative alleles or haplotypes appear to mediate risk of autism versus schizophrenia.
Additional lines of evidence supporting the diametric hypothesis, from previous studies of autism and schizophrenia, include:

  • 1. Data showing notable rarity of familial coaggregation of autism with schizophrenia (38), in contrast, for example, to strong patterns of co-occurance within pedigrees of schizophrenia, schizoaffective disorder, and bipolar disorder (39).
  • 2. Psychiatric contrasts of Smith-Magenis syndrome with Potocki-Lupski syndrome (due to the reciprocal duplication at the Smith-Magenis locus), Williams syndrome with cases of Williams-syndrome region duplication, and Klinefelter syndrome with Turner syndrome, each of which tends to involve psychotic-affective spectrum phenotypes in the former syndrome, and autistic spectrum conditions in the latter (5, 40).
  • 3. Effects of autism and schizophrenia risk alleles on common growth-signaling pathways, such that autism has been associated with loss of function in genes, such as FMR1, NF1, PTEN, TSC1, and TSC2 that act as negative regulators of the PI3K, Akt, mTOR, or other growth-signaling pathways (41–45), whereas schizophrenia tends to be associated with reduced function or activity of genes that up-regulate the PI3K, Akt, and other growth-related pathways (46–49).
  • 4. Increased average head size, childhood brain volume, or cortical thickness in individuals with: (i) idiopathic autism (50–53), (ii) the autism-associated duplications at 1q21.1 (17) and 16p13.1 (32) and the autism-associated deletions at 6p11.2 (31), and (iii) autism due to loss of function (or haploinsufficiency) of FMR1 (54), NF1 (55), PTEN (56) and RNF135 (57). By contrast, reduced average values for brain size and cortical thickness, due to some combination of reduced growth and accelerated gray matter loss, have been demonstrated with notable consistency across studies of schizophrenia (58–62), and such reduced head or brain size has also been associated with the schizophrenia-linked CNVs at 1q21.1 and 22q11.21 (17, 63, 64), and with deletions of 16p13.1 (65).

I am more than pleased with these results. Badcock too is. You can read his comments here. What about you? What would it take to convince you? 🙂

Crespi, B., Stead, P., & Elliot, M. (2009). Evolution in Health and Medicine Sackler Colloquium: Comparative genomics of autism and schizophrenia Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0906080106

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Logos Vs Mythos: Autism Vs Schizophrenia

I recently came across this TED talk by Devdatt Patnaik, A chief Belief Officer in an Indian industry group and was fascinated by his description of the distinction between logos based ‘the’ world which is objective, logical, universal, factual and science based and mythos based ‘my’ world which is subjective,emotional, personal, belief-based and mythological in nature. while ‘the’ world tries to answer ‘how’, ‘my’ world tires to answer ‘why’.

To me the same is true of Autism and Psychosis dichotomy. While autistic frame of reference is rooted in ‘the’ world – trying to apply a science based approach even to the mind and mental; the psychotic frame of reference becomes detached from ‘the’ world and is totally enamored by the subjective depths of ‘my’ world -attributing mental properties to physical things too.

Devdatt, later on goes to contrast East Vs West Myths and here at the second order , though we are talking of mythos and not of logos and are in the psychotic/mythic world , we see a difference in focus, between the eastern traditions and the western traditions. While the east is portrayed as more spiritual and renunciation-believing in multiple lives and thus multiple chances; the west is depicted as more materialistic and ambitious and believing in one and only life and thus believing in only one chance of redemption -and though this dichotomy may be simplistic it does bring into focus the fact that the cultures do differ profoundly.

The difference between cultures and mythologies, and the people shaped from them thereof, is important in light of a new study , for eg., that demonstrates that most of the behavioral research is carried on with WEIRD people! WEIRD stands for Western, Educated, Industrial, Rich and Democratic subjects and the paper claims that these WEIRD subjects are outliers and not representative of the general population. If much of the scientific and psychological research is done on WEIRD subjects (which is a fact) and if WEIRD are not representative of the population (which seems reasonable given the differences in culture and the ability of culture to shape people) , than that raises a more serious questions on the results of behavioral studies than the voodoo correlations paper raised questions about the fMRI studies.

Devdutt, though seems to be slightly biased towards Indian culture, but the TED talk is worth a watch. And you may also find one of my earlier post relating Indian culture,religion, and Autism, Schizophrenia quite pertinent here.

Do you think Devdutt is right when he stresses differences in cultures and myths? If so, do you think Culture shapes people? and if so do you believe with Norenzayan et al that if we just do studies based on WEIRD subjects, our results are not representative but skewed. Lot of questions to think about!

Joseph Henrich, Steven J. Heine, & Ara Norenzayan (2009). The Weirdest People in the World? Behavioral and Brain Sciences

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