Two main underlying deficits have been proposed in autism- one concerning an inactive or non-existent Theory of Mind module and another a tendency towards Weak Central Coherence. ToM defects reflect in the communicative, social and imaginative deficits seen in autistics; while the savant skills as well as restrictive and repetitive behavior (restricted repertoire of interests ;obsessive desire for sameness – islets of ability – idiot savant abilities – excellent rote memory – preoccupation with parts of objects ) are best explained by taking recourse to the Autism-as-a cognitive-style having weak Central Coherence argument. I’ve discussed the crucial aspects of both of these two dimensions in y series of posts on autism and psychosis and shown how they have to be seen on a continuum and more as deviation from the normal range with one end as autism and the other as psychosis. We also know that psychosis itself is two dimensional with one dimension being that of schizophrenic spectrum and the other the bipolar spectrum. Thus what I propose is that we start seeing Autism also as a two dimensional disorder with TOM defect subtype a mirror image of schizophrenia; while the Weak CC subtype a mirror image of bipolar or manic depressive phenotype. Here are autistic and psychotic features on these dimensions (from Autism, Happe, the autistic deficits and assets table):

• ordering behavioural pictures (Baron-Cohen et al. 1986) vs ordering mentalistic pictures understanding “see” (Perner et al. 1989)
• understanding “know” protoimperative pointing (Baron-Cohen 1989c) vs protodeclarative pointing sabotage (Sodian & Frith 1992)
• deception false photographs (Leekam & Perner 1991, Leslie & Thaiss 1992) vs. false beliefs recognising happiness and sadness (Baron-Cohen et al. 1993a)
• recognizing surprise object occlusion (Baron-Cohen 1992) vs. information occlusion
• literal expression (Happé 1993) vs. metaphorical expression
• elicited structured play (Wetherby & Prutting 1984)vs. spontaneous pretend play
• instrumental gestures (Attwood et al. 1988) vs. expressive gestures
• talking about desires and emotions (Tager-Flusberg 1993) vs. talking about beliefs and ideas
• using person as tool (Phillips 1993) vs. using person as receiver of information
• showing “active” sociability (Frith et al. 1994) vs. showing “interactive” sociability

It is also pertinent in this regard to revisit the question of co-occurrence of autism and schizophrenia. Happe maintains that psychois can only be relaibly seen in Asperge’s group who might have a late developing ToMm ability. To quote:

The higher incidence of psychiatric disorders in this group (asperger’s group) (Tantam 1991, Szatmari et al. 1989b) is well explained by this hypothesis. Depression will be more common since these people have greater insight into their own difficulties and their own feelings and thoughts. Positive symptoms of psychosis, such as hallucinations and delusions would be found only in Asperger’s syndrome cases by this account, if one takes Frith & Frith’s (1991) view of these symptoms as resulting from an “over-active” theory of mind. Asperger’s syndrome people, who gain theory of mind late and therefore abnormally, may be at high risk for having their theory of mind “go wrong”. On this hypothesis it would be impossible for a Kanner-type autistic person (who has no theory of mind) to show these psychotic or positive symptoms. In this sense (according to Frith & Frith’s theory) Asperger’s syndrome would be something of a midpoint between autism and (positive or florid) schizophrenia; while the former is due to a lack of theory of mind, and the latter due to over-active theory of mind, some people with Asperger’s syndrome may show both the scars of early lack and the florid symptoms of late acquired theory of mind working abnormally hard.

There is some preliminary evidence to support the suggestion that the term “Asperger’s syndrome” could meaningfully be restricted to those subjects with autism who have achieved some ability to think about thoughts. Ozonoff et al. (1991) found that their group labelled (perhaps arguably) as having Asperger’s syndrome did not show impairments relative to controls.

It is interesting to note the ‘over-active’ theory of mind reference to Frith and Frith. I could not locate that paper but came across another paper by Abu-akkel that propose over-active ToM as a mechanism of psychosis. There are also some full text related articles available online that may be of interest to the serious reader. As for me, it is heartening to note that others concur with the theory of autism and psychosis as opposites on a  continuum.

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I recently came across this TEDx video by David Logan talking about the five tribal stages and was glad on discovering another confirmation to my stage theoretic model. Dave along with King and Haleee have also written a book titled “Tribal Leadership” which summarizes their research, their tribal leadership model and how corporates and other organizations can move from one tribal stage to another.

As their theoretical background they have rhetorics, organizational theory and chaos theory and they view ‘culture as a self-correcting system of language’. This needs a bit of elaboration. What they mean is that the day to day language we use in our workplace or tribes and our relationships with other members of the tribes (behavior) is indicative of the stage at which the tribe is functioning. They explicitly dismiss all ‘cognitions, beliefs, attitudes, or other factors we cannot directly observe’ and in doing so and thus focusing solely on language and behavior are more in the behavioristic tradition, than grounding their tribes in a cognitive framework. Despite the resistance to cognitive framework, they do take recourse to developmental theory and Ken Wilbur’s spiral dynamics . However, their stages do seem to be good enough and are elaborated below:

1. stage 1: Despairing Hostility :“Life sucks”: If people at Stage One had T-shirts, they would read “life sucks,” and what comes out of their mouths support this adage. People at this stage are despairingly hostile, and they band together to get ahead in a violent and unfair world.
2. stage 2: Apathetic Victim: “My life sucks”: People in this cultural stage are passively antagonistic; they cross their arms in judgment yet never really get interested enough to spark any passion. Their laughter is quietly sarcastic and resigned. The Stage Two talk is that they’ve seen it all before and watched it all fail. A person at Stage Two will often try to protect his or her people from the intrusion of management. The mood that results from Stage Two’s theme, “my life sucks,” is a cluster of apathetic victims.
3. stage 3: Lone Warrior: “I’m great (and you’re not)”: People at Stage Three have to win, and for them winning is personal. They’ll outwork and outthink their competitors on an individual basis. The mood that results is a collection of “lone warriors,” wanting help and support and being continually disappointed that others don’t have their ambition or skill. Because they have to do the tough work (remembering that others just aren’t as savvy), their complaint is that they don’t have enough time or competent support.
4. stage 4 : Tribal Pride :“We’re great (and they’re not)”: A “we’re great” tribe always has an adversary— the need for it is hardwired into the DNA of this cultural stage. In fact, the full expression of the theme is “we’re great, and they’re not.” For USC football, the “you’re not” is usually UCLA (and in good years, whichever team is contending for the national championship). For Apple’s operating systems engineers, it’s Microsoft (although this is changing as Apple has moved to using Intel processors). Often, it’s another group within the company. A tribe will seek its own competitor, and the only one who has influence over the target is the Tribal Leader.The rule for Stage Four is this: the bigger the foe, the more powerful the tribe.
5. stage 5 :Innocent Wonderment: “Life is great”: Stage Five’s T-shirt would read “life is great,” and they haven’t been doing illicit substances. Their language revolves around infinite potential and how the group is going to make history—not to beat a competitor, but because doing so will make a global impact. This group’s mood is “innocent wonderment,” with people in competition with what’s possible, not with another tribe.

This fits with my own stage model pretty well: the first stage is pretty much about survival and safety and getting together to outsmart the cruel environment. The second stage is more personal and (non) motivational in nature. The third stage is about accomplishment and has an achievement focus. The fourth is the most tribal with social focus and a visible ‘enemy’ or competitor tribe. The fifth stage has an imaginative and innovative focus.

It is possible and desirable to move from one stage to other and Dave shows that nicely in his TEDx talk embedded below:

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A reader of this blog wrote to me recently regarding a series of posts I have written regarding IQ,SES and heritability, and I thought it would be good to share the comments with the rest of the mouse trap community and to delineate my position on the matter (and what I believe the studies show the relation is). First I’ll like to quote extensively from the comment (private mail):

Let me start with my belief that I think we share the same idea about IQ and its origins.
That is, genetics endows each and every person with a maximum IQ that can be achieved if and only if the environment is perfect for the development of this IQ.

Agreed!

Consequently, in identical twins, environment is the only cause of differences in IQ; IQ differences between persons that are not identical twins must be related to both environment and genes.

There are subtle nuances here. (no I’m not being pedantic, the importance of these will become clear in the course of this post). First if MZ twins are raised in the same family, they share the same genotype (A), they share the same ’shared environment’ (C), so the difference is due to the non-shared environmental factor (E) only. In case of DZ twins raised in the same family, they share half the genotype (A), they share the same shared environment (C) and the difference in say IQ, is due to both genotype (A) and non-shared environmental factors (E). Twin studies with MZ and DZ twins (and in some cases siblings, half-siblings etc ) raised in the same family are used to tease apart the contribution of shared environmental factor, as opposed to genetics and non-shared environmental factors and can be used to find at a broad level if the trait is highly ‘genetically’ heritable (correlation between MZ>>DZ>>siblings), has high ’shared environmental’ factors operating (MZ~DZ~sibling , but correlation still high) or is largely controlled by random non-shared environmental influences (low correlation in DZ/MZ/siblings). Please see accompanying Wikipedia figure.

Adoption studies are another method that is used to tease apart the shared environmental factors from genetic factors in calculating the heritability of a trait. Thus, even if correlation in MZ twin IQ is high, the effect could be due to shared environment factors (if say both MZ and DZ twin show similar correlation) , or it may be largely genetic (if MZ>>DZ when it comes to correlation between the trait in affected twins.

So it is necessary to qualify your statement: In identical twins, raised in the same family, , non-shared environment is the only cause of differences in IQ. IQ differences between persons that are not identical twins must be related to both shared environment , non-shared environment and genes.

I fully back up this citation:
“suffice it to say that I believe (and think that I have evidence on my side) that shows that in low SES conditions, a Low SES does not lead to full flowering of genetic Intelligence potential and is thus a leading cause of low IQ amongst low SES populations.”
In this case, I think that the problem starts only with your following comments; while you write “a leading cause”, I think that, by yourself, you mean “way more important than genetics”. If this is the case, would you explain to me why you think that?

Here goes. Consider a large sample of children in say low SES populations. IQ may be represented by a formula IQ= aA+cC+eE; where A reflects genotype, C shared environment and E non-shared environment. Here we are assuming no interaction of IQ with SES, so this equation (given values of a, c, e ) should hold for all SES data (both high as well as low SES cohort) . Unfortunately, life is not that simple, and one can not fit the same equation to low SES as well as high SES data set without changing the slopes of variables involved. Thus, Turkheimer and colleagues in two sets of studies have shown that there is an interaction of IQ and SES and there is direct affcet (SES mediated by s) and indirect interaction effects mediated via effects on A(a’), C(c’) and E(e’). Thus our equation becomes
IQ= sSES+(a+a’SES)A+(c+c’SES)C+(e+e’SES)E.
This equation, with suitable values of s, a, a’, c, c’, e and e’ now holds for all values of SES and IQ and the data fits nicely and can be interpreted. Remember that a+a’SES is sort of indicative of contribution of genetic factor to IQ and the proportion of variance due to genetic factor(at any given SES) can be found by squaring this and dividing this by sum of all other variances .
Var(A) =SQR(a+a?SES)
Similarly heritability or proportion of variance due to A :SQR(h)=SQR(a+a?SES)/(SQR(a+a?SES)*SQR(c+c?SES)*SQR(e+e?SES))

Turkheimer have plotted nice plot of their data which sows clearly that in LOW SES situations, the proportion of variance in IQ is largely due to shared environmental factors (C) , while in HIGH SES situations, the proportion of variance in IQ is largely due to genetic factors (A). the figures (in the free PDF available at Turkheimer’s side) is a must see to grasp the significance of this. I am quoting a bit from the paper:

Figure 3 shows the FSIQ variance accounted for by the three components, with 95% confidence intervals. In the most impoverished families, the modeled heritability of FSIQ is essentially 0, and C accounts for almost 60% of the variability; in the most affluent families, virtually all of the modeled variability in IQ is attributable to A.

Let us pause here and reflect on what this means. This means that in low SES families, IQ is independent of genotype and is mostly dependent on the SES status. Let us take some concrete examples. Say the mean IQ of low SES sample (income as a proxy for SES ranging from 1000-5000 rs p.a.; mean 2500 and variance 250)) is 80 with mean variance of 20. Thus, in this sample a typical child has IQ in range 80 +-20 or between 60 and 100. Suppose further that there are 5 alleles that confer differential advantage for IQ on a locus thus representing 5 genotypes, then having either of the genotype will essentially give us no predictive power to say whether the IQ of a particular sample is 80 or 60 or 100. Also, let us assume that there are 5 classes of C and they are highly correlated with SES. First class of C (is 1000-1500 SES range) and so on and so forth. Then knowing whjat kind of family (C) the child grew up in we could easily predict his IQ (if he is of class C where SES ranges from 1000-1500), his IQ is most probably 60. This is what I mean when I say that in low SES environments IQ is largely determined by environment and not by genetics. Now , I have taken a jump here and equated C with SES, but that is a justified leap in my opinion (more about that later).

What this also means is that given the right type of environment (say class C with SES in upper range of 3500-5000 rs p.a.) , all children (irrespective of their genotype (any 5 variants of genotype) can still achieve an IQ in the upper range , say 100 as the environment is the only predominant factor operating at this level and the impact of genetics is still not felt. Thus, if we do increase SES and provide the right C, then every child in this group can have mean IQ of 100.

Contrast this with the case at the upper end of the strata (SES). Here most of the variation in IQ is predominantly due to genetics (A) and shared environment C does not seem to play a big factor. Thus, knowing a genotype of a child has greater predictive power in this sample, than knowing his C (or family income or SES). Thus, evenif we provide a very enriched environment to all children (increase their C to the highest percentile), it would have no effect on increasing the mean IQ of the sample as now the IQ is mostly under genetic control.

This in a nutshell, is what I mean when I claim that low SES is the leading cause of low IQ in low SES families.

Before I rest, some objections might be readily apparent to a keen observer. First is the assumption inherent that SES and C are the same. I would like to propose here a new shared and universal sub-threshold environmental factor and would like to elaborate with a couple of examples. Let us say that those below poverty level do not have access to iodized salt and are thus prone to goiter and also mysteriously to low IQ as there is a module of brain (5 diff alleles at a particular locus leading to differences in abilities using this module) that needs iodine for its flowering and in absence of iodine, none of the alleles have any effect whatsoever- the module itself does not develop, so there are no questions of differences in ability or IQ due to differences in genotype etc. Now, given this state of affairs and also the fact that low SES families do not have access to iodine, when IQ is measured (then because of absence of this factor X), all children in this proband will have an IQ that does not measure abilities of this module (say this module adds 20 points of IQ) and thus all of them will have an IQ less by 20 points than was actually possible.Say the mean IQ measured is 80. Given the fact that some of the higher SES within this low SES group may have partial and sporadic access to iodine , the variance will be entirely environmental and no genetic variance would be found with some people having IQ close to 100 , who are in relatively upper start and have decent access to iodine. Contrast this the higher SES proband all of whom have access to iodized salt and thus can use their additional 20 points advantage on IQ tests. It would not be surprising if most of the variation here was genetic based on factor X allele) rather than due to income level or SES.

Another example to ruminate on is another universal and shared sub-threshold factor like having a golf course in the house. Let us assume that within higher SES group, this environmental enrichment factor plays a role, with some lower strata of higher SES (the middle class) not able to afford a golf course, while the higher higher SES strata (the upper class) abvle to afford a golf course and expose their children to them . Further, suppose that there is a module in the brains and genes switched on only if exposure to golf course takes place. Then within this higher SES group, what we will observe is that though the genetics plays a good role (due to factor X-iodine: remember, which is available to all in this group) ; still there would also be variation due to environment (golf course exposure) and that a full 20 points more can be added to all people of this group (with mean IQ 100 raising their IQ to 120), if all were exposed to a golf course and a intelligence-module-dependent-on-golf-course-exposure was allowed to develop. And on the higher end of IQ (and SES) what we would find is that most of the variance now is genetic (due to this golf-course module coming into play), while at the lower end, most of the variance is still environmental within this ‘high’ SES group.

If the above seems far fetched this is exactly what Turkheiemrs et al found in their follow up study focusing on mid to high SES children. I quote from it (again the pdf has beautiful figures and you should see them) :

Figure 2 illustrates the relations between income and genetic and shared environmental proportions of variance, as implied by the parameters estimated in Model 3. Genetic influences accounted for about 55% of the variance in adolescents’ cognitive aptitude and shared environmental influences about 35% among higher income families. Among lower income families, the proportions were in the reverse direction, 39% genetic and 45% shared environment. Although the shared environmental proportion of variance decreased with income, shared environmental variance per se did not decrease. The interactive effect was driven entirely by the increase in genetic variance. Genetic variance in cognitive aptitude nearly doubled from 4.41 in families earning less than $5000 annually to 8.29 in families earning more than $25,000 annually.

Our investigation supports our hypothesis that the magnitude of genetic influences on cognitive aptitude varies with socioeconomic status. This partially replicates the results presented by Turkheimer et al. (2003); however, no shared environmental interaction effects were demonstrable in the current study. Genetic influences accounted for about 55% of the variance in adolescents’ cognitive aptitude and shared environmental influences about 35% among higher income families. Among lower income families, the proportions were in the reverse direction, 39% genetic and 45% shared environment. This pattern is similar to the pattern seen in Turkheimer et al. (2003), although less marked.

So, I want you to pause here and grasp the significance of this- at every level of IQ-SES, there may be threshold factor that giverns whether IQ modules flower to full potential and this is the putative mechanism that leads to SES causing low or high IQ directional and causal relation. At each level, as the threshold factors become available,. more and more IQ starts coming under genetic control, but , and this is important, for jumps in IQ to take place , increasing SES (removing the sub-threshold conditions) is VERY important.

I mean “not following up on the ‘a leading cause’”, because in a later post, you write:
“Now, I have shown elsewhere that low SES causes low IQ”
Here, there is no mention of any other possible cause besides the environment anymore.

Yes, because as shown very strongly by Turkeihems and team , at low SES, shared environment/SES is the putative mechanism and genetics has no/negligible role to play. So for low SES, low SES causes low IQ. period.

in another post, you write
“A series of studies that I have discussed earlier, clearly indicate that in the absence of good socioeconomic conditions, IQ can be stunted by as large as 20 IQ points. ”
This same post also contained this citation “Children of well-off biological parents reared by poor/well -off adopted parents have Average IQ about 16 point higher than children of poor biological parents”
In my opinion, the latter would indicate the approximate range of genetic IQ differences for the samples in this study, while the former would indicate the approximate maximal environmental gain that can be hoped for in the environments that were encountered in these studies.

No they don’t. They talk about different SES groups, so as shown findings from one cannot be extrapolated to the other. In the low SES group, there is no genetic variation. We can thus not conclude that that (16 points diff.) is the ‘average’ genetic component taken the entire sample together. what one can say is that if mean IQ of high SES children was 100, the mean IQ of low SES children was 84 . Period. The difference is likely due to the fact, that the module X has not developed in low SES people (more later) .

Regarding the former, yes I agree that that is the maximum gain that one can hope for if all children of low SES were given the right environment (raised to high SES). Put another way, if mean IQ of poor/low SES children is 84 , then given the right conditions the mean of the low SES children can be raised to 104 (greater than high SES children’s mean .

As both of them do cover the same IQ range (10-20), the logical consequence for a broad statement on IQ and genetics seems therefore to be, that these studies may say that overall, IQ changes can be expected to be determined to approximately equal parts by genetics and environment, with environment being responsible for a typically larger part in low SES families, and genetics playing a relatively larger part in high SES families.

Agreed partially, but that glosses over the fact of sub-threshold universal shared environments and the fact that the role of genetic and environmental component varies with SES, an therefore an ideal statement would be IQ is under gentic controltolarge extent, but that gentics needs threshold environments to flower and thus the importance of environment component- not in explaining variance , but by its direct effect on IQ enabling/flowering.

This same post also contained this citation “Children of well-off biological parents reared by poor/well -off adopted parents have Average IQ about 16 point higher than children of poor biological parents”
In my opinion, the latter would indicate the approximate range of genetic IQ differences for the samples in this study, while the former would indicate the approximate maximal environmental gain that can be hoped for in the environments that were encountered in these studies.
As both of them do cover the same IQ range (10-20), the logical consequence for a broad statement on IQ and genetics seems therefore to be, that these studies may say that overall, IQ changes can be expected to be determined to approximately equal parts by genetics and environment, with environment being responsible for a typically larger part in low SES families, and genetics playing a relatively larger part in high SES families.
There also is this citation:
“The normal observation that identical twins belonging to well-off/middle class families have IQ rates similar as compared to fraternal twins, thus indicates that for children from well-off background (biological/adopted), the IQ (observed phenotype) is mostly due to genetic factors (underlying genotype) and environmental factors are not a big determinant.

The paradoxical observation that identical twins belonging to poor families have IQ rates as varying as compared to fraternal twins, should indicate that for children from poor background (biological/adopted), the IQ (observed phenotype) is mostly due to environmental factors and genetic factors (the underlying genotype ) are not a big determinant.”

These are extremely nice observations. I would be interested in the conclusions one might be tempted to draw from them. Reading the latter part of this sentence, one might come to the following conclusion (conclusion 1): “if in low-SES families the variations in IQ are largely determined by environmental factors, then providing a positive environment for the development of IQ would increase the IQ levels in these families impressively (up to 20 points; but, this is an up to value, means would be more interesting).”
While I completely agree with this thinking, one might also be tempted to draw the conclusion that (conclusion 2) “As IQ variations in low-SES families are largely due to environment, providing an IQ-stimulating environment in low-SES families might completely eliminate the IQ differences between low-SES families and high-SES families”
At the least, a non-cautious reader might understand your words as such. I am not sure whether you think that way or not. I would like to hear your opinion on that. I think that this citation “Children of well-off biological parents reared by poor/well -off adopted parents have Average IQ about 16 point higher than children of poor biological parents” provides an argument that precludes conclusion 2. It would rather say that (conclusion 3), ” providing a perfect IQ-stimulating environment for low-SES families as encountered in these studies, one should think that their offspring would achieve an IQ level that is 16 points lower than that of the offspring of high-SES families.”
I would like to hear your opinion on my conclusion 3.

I agree with conclusion 1. I also agree with conclusion 2 (not based on political correctness, but hard data). The paper on which these figures are based can be found here. The mean IQ of high SES persons is 113.5 and the mean IQ of low SES children is 98.00, thus a difference of ~16 points. The variation in IQ of high SES children raised in high SES families is 12.25; as shown this variance is likely due to genetics (say hundred percent is due to genetics); then changing the SES within the given range should have no effect on average IQ and it would remain 119 (for this high +/high+ group). On the other hand, the variance in low SES, reared by low SES families is 15.41 and mean is 92.40;thus if all were given enriched environment, their mean IQ would become 92.4+ 15.4 = ~ 108 . We still have a 10 point difference which can be accounted for by the fact that genetics had not come into play for low SES , low SES group yet and as genetics enters and increases the variance due to genetic flowering,, their IQ would be in the same league as high IQ/High IQ children.

So definitely the conclusion 3 is flawed- the difference would not be close to 16 points, but negligible, as the 16 points nowhere measures gentic difference in abilities, but reflects the genetic factor not yet active in low SES, due to improper environmental exposure.

I think that this is a rather important conclusion, as it tells us something about the differences in IQ that can be expected to exist between distinct population stratums (don’t know whether this is an appropriate word for what I try to say; I hope you understand what I mean).
If this is the ballpark of figures that we can expect between low-and high SES IQ differences, this would have important effects on future IQ-distributions. Population-wide stability of IQ-performance, if measured in a saturated environment (maximum stimulation of all members of society), can then only be achieved if all stratums of society have the same number of offspring per individuum. If low-SES families have more children, we have to expect that the 16-point lower IQ will decrease the whole-population IQ.
Here, the 16 points only apply to the sample as measured in your example; the true value of the saturated stratum-dependent-IQ together with stratum-dependent birthrates will determine the shift of the saturated IQ-distribution for the generations to come.

Do you agree with this point of view?

To use a very strong and negative connotation word, the above smacks of eugenics. And I wont comment further on this. Each according to his own philosophy, but beware that science does not support your conclusions. Instead of population controlling the poor, please try to elevate their vicious loop of undeserved poverty, low IQ and harmful stigma.

Turkheimer, E., Haley, A., Waldron, M., D’Onofrio, B., & Gottesman, I. (2003). Socioeconomic status modifies heritability of iq in young children Psychological Science, 14 (6), 623-628 DOI: 10.1046/j.0956-7976.2003.psci_1475.x

Harden, K., Turkheimer, E., & Loehlin, J. (2006). Genotype by Environment Interaction in Adolescents’ Cognitive Aptitude Behavior Genetics, 37 (2), 273-283 DOI: 10.1007/s10519-006-9113-4

Capron, C., & Duyme, M. (1989). Assessment of effects of socio-economic status on IQ in a full cross-fostering study Nature, 340 (6234), 552-554 DOI: 10.1038/340552a0

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What can one say about an article that explores self in terms of stage theories (5 stages that match my own stage theoretic framework), has references to infantile autism and paranoia , and even references Carol Dweck’s entity vs incremental intelligence theories and George Lakoff’s ‘idealized cognitive model‘- all focuses of this blog…Well I just love this article by Ulric Neisser titled ‘Five kinds of self-knowledge’. That artcile gives me an opportunity to integrate and synthesize many of the prominent threads of this blog in a coherent narrative.

Let me start with core thesis of Ulrich that there are at least five different types of selves that we gradually become aware of in developmental time frame. Because Ulrich does such a nice job of presenting his findings , I’ll quote at length from him.

The analysis to be presented here distinguishes among several kinds of self-specifying information, each establishing a different aspect of the self. These aspects are so distinct that they are essentially different selves: they differ in their origins and developmental histories, in what we know about them, in the pathologies to which they are subject, and in the manner in which they contribute to human social experience. Here, in capsule form, is the list:

•The ecological self is the self as perceived with respect to the physical environment: I am the person here in this place, engaged in this particular activity.
•The interpersonal self, which appears from earliest infancy just as the ecological self does, is specified by species-specific signals of emotional rapport and communication: I am the person who is engaged, here, in this particular human interchange.
•The extended self is based primarily on our personal memories and anticipations: I am the person who had certain specific experiences, who regularly engages in certain specific and familiar routines.
• The private self appears when children first notice that some of their experiences are not directly shared with other people: I am, in principle, the only person who can feel this unique and particular pain.
• The conceptual self or ’self-concept’ draws its meaning from the network of assumptions and theories in which it is embedded, just as all other concepts do. Some of those theories concern social roles (husband, professor, American), some postulate more or less hypothetical internal entities (the soul, the unconscious mind, mental energy, the brain, the liver), and some establish socially significant dimensions of difference (intelligence, attractiveness, wealth). There is a remarkable variety in what people believe about themselves, and not all of it is true.

Note the five stage model fitting perfectly to the T. The first stage marked by a sensory stage that is more defined in relation to the environment around. The second stage more subjective in nature and based on agentic conceptions of intersubjectivity- related to significant humans around and also valence and affect based. The third stage being ‘experiential ‘ in nature and marked by remembered/internalized activities with family playing a major role in its development. The fourth stage marked by hidden or private stage in which peers or social sphere plays a significant role- also the most traditional defintion and conceptualizations associated with a trait. The fifth, and for now the final, stage associated with abstracting and conceptualization and model-driven depending on culture and subject to cultural variations and also cognition based. Many of the stage features may not be readily apparent and map to the five forms of selves described above, but bear with me- they will become clearer as I elaborate on the selves and quote more from the article.

First let us take the ecological self: Neisser describes them in slightly technical and inaccessible terms of ‘optic flow’ and ‘looming’ -some difficult concepts to grasp but which basically focus on the fact that relative motion between eye(observation point) and the environment (say a wall) lead to this sense of an ecological self that is perceiving the immediate environment and also acting on it. Neisser discusses experiments with children in this context like the child when he closes his eyes claims that you cannot see him. See more below:

One surprising bit of evidence for the importance of optical flow for the ecological self comes from a phenomenon investigated by Flavell, Shipstead & Croft (1980). The phenomenon is amusing in its own right and has often been described: young children cover their eyes with their hands and say “You can’t see me!” Prior to the work of Flavell et al. (1980), this behavior was typically interpreted in Piagetian terms: since the child cannot see anything, s/he assumes that you can’t see anything either. Indeed, when these experimenters asked their eyes-covered subjects “Can I see you?”, most 2- and 3-year-olds answered No. Surprisingly, however, the same subjects answered Yes to many other questions about what the experimenter could see. “Can I see Snoopy (a doll located nearby)?” Yes. “Can I see your leg?” Yes. “Can I see your head?” Yes. These results show that “You can’t see me” does not reflect any egocentric misapprehension about other people’s seeing; rather, it is a clue to the speaker’s own conception of self. The child’s ‘me’—the entity to which the adult’s question “Can I see you?” refers—is evidently somewhere near the eyes. To be sure, that localisation is not precise: Flavell et al. got mixed results when they had their subjects cover only one eye, or stand behind a barrier with a hole in it so that nothing but an eye was visible. Nevertheless the implication seems clear: children locate the self at the point of observation, as specified by the optical flow field.

Important as it is, optical flow is by no means the only determinant of the ecological self. The self is an embodied actor as well as an observer; it initiates movements, perceives their consequences, and takes pleasure in its own effectivity. Infants love to look at their own hands in action, and they can distinguish their own moving legs, seen in real time on a TV screen, from the moving legs of another baby (Bahrick & Watson, 1985). Many theorists have noted the importance of agency in establishing a sense of self. I can cause changes in the immediately perceptible environment, and those objects whose movements and changes I can inevitably and consistently control are parts of me. This kind of self-perception is precisely time dependent and richly intermodal. I can see and feel what I do: the optical and kinesthetically-given structures that specify the consequences of movement are exactly synchronous, and both coincide with the efferent activity by which the action itself is produced. In general, then, the two principal aspects of the ecological self are defined by two distinguishable kinds of information. The existence of a perceiving entity at a particular location in the environment is most clearly specified by the optical flow field (though touch and hearing also contribute); the existence of a bounded, articulated and controllable body is specified not only by what we can see of it but by what we feel and what we can do6.
The ecological self does not always coincide with the biological body. In particular, anything that moves with the body tends to be perceived as part of the self—especially if its movements are self-produced. This principle applies most obviously to the clothes we wear. It is / who kick the soccer ball, though in fact its only contact is with my shoe; when you touch my shoulder you are touching me, even when a shirt and a jacket interpose between your fingers and my skin. These experiences have nothing to do with my ownership of the clothes. The same jacket is not part of my ecological self when it hangs in my closet, or when I am carrying it home from the cleaners; to touch it in such cases is not to touch me at all. What matters is not possession or contact but agency and co-ordinate movement. The same principle explains why the practised wearer of an artificial limb so naturally perceives it as a part of the self. Such wearers have not mistakenly come to believe that the limbs are flesh-and-blood parts of their bodies. On the contrary, their perceptions are exactly correct: to the extent that the motion of a limb is responsive to one’s intentions and is co-ordinated with movements of the point of observation, it belongs to the ecological self.

He also gives example of the colloquial use of identification with your car while you are driving one. He also claims that this self is present from birth and only refines a bit with experience. He believes phantom limbs and neglect are pathologies associated with this kind of self.

In summary, here are some of the characteristics of the ecological self:
• The self, like the environment, exists objectively; many of its characteristics are specified by objectively-existing information. That information allows us to perceive not only the location of the ecological self but also the nature of its ongoing interaction with the environment.
•Much of the relevant information is kinetic, consisting of structure over time. Optical structure is particularly important, but self-specifying information is often available to several perceptual modalities at once.
•The ecological self is veridically perceived from earliest infancy; nevertheless self-perception develops and can become more adequate with increasing age and skill.

Next we come to the inter personal self:

The interpersonal self is the self as engaged in immediate unreflective social interaction with another person. Like the ecological self, it can be directly perceived on the basis of objectively existing information. Again like the ecological self, most of the relevant information it is essentially kinetic, i.e. consists of structures over time. In this case, however, the information—and the state of affairs that it specifies—come into existence only when two (or more) people are engaged in personal interaction. If the nature, direction, timing, and intensity of one person’s actions mesh appropriately with the nature/direction/timing/intensity of the other’s, they have jointly created an instance of what is often called intersubjectivity. The mutuality of their behaviour exists in fact and can be perceived by outside observers; more importantly, it is perceived by the participants themselves. Each of them can see (and hear, and perhaps feel) the appropriately interactive responses of the other. Those responses, in relation to one’s own perceived activity, specify the interpersonal self.

Then he illustrates some mother-child cooing examples and elaborates:

These interactions illustrate what Trevarthen has called ‘primary intersubjectivity’. The participants respond to each other immediately and coherently, in both action and feeling; their reciprocal activities are closely co-ordinated in time. The result is a shared structure of action—a structure that both of the participants enjoy, and that neither of them could have produced alone. Indeed, the contributions of the individual partners would be useless and foolish if they occurred by themselves. An elegant experiment by Lynne Murray (Murray & Trevarthen, 1985) demonstrates this point. Mothers and their 6 to 12 week-old babies, actually in separate rooms, interacted via double closed-circuit television. Each partner saw and heard a fullface, life-size video image of the other, with appropriate eye contact being made. As long as the video presentation was ‘live’, this system allowed interaction to proceed normally: the babies looked intently at their mothers with open and relaxed mouth, slightly raised eyebrows, and other signs of interest. The first minute of live interaction comprised the control condition. It was recorded on videotape; the tape of the mother was then rewound and immediately replayed on the infant’s screen. This second (replay) minute comprised the experimental condition. Although what the infants saw and heard was identically the same in both conditions—the same mother, the same gestures, the same displays of affection—their responses were dramatically different. In the experimental condition, the babies who had been happy a minute ago now exhibited signs of distress: they turned away from the mother’s image, frowned, grimaced, and fingered their clothing.10. (A final control presentation ensured that they had not simply become tired of the situation itself.) The subjects’ distress during the replay was evidently produced by some kind of mismatch between their mothers’ responses and their own.
Murray’s study shows that infants in normal face-to-face interactions are not just picking up information about their partners; they actually perceive the ongoing intersubjective relationship. J. J. Gibson’s (1979) principle that all perceiving involves co-perception of environment and self applies also to the social environment and to the interpersonal self, i.e. the self that is established in these interactions. Just as the ecological self is specified by the orientation and flow of optical texture, so the interpersonal self is specified by the orientation and flow of the other individual’s expressive gestures; just as the ecological self is articulated and confirmed by the effects of our own physical actions, so the interpersonal self is developed and confirmed by the effects of our own expressive gestures on our partner.

These examples (Stern gives many others) show again that intersubjectivity is anemotional business: the two partners are obviously sharing an affect. Nevertheless,the ordinary vocabulary of the emotions is not adequate to describe what is going on. It is not just that both are ‘happy’ or ‘excited’, but that the mother is precisely matching the pattern and temporal contour of the infant’s activity with her own. Such ‘vitality affects’ (Stern, 1985) are specified by information in several sensory modalities: in visible movement, in the emphasis and modulation of the voice, in bodily contact. Their specification is so rich that they are readily perceived and shared, not only between mothers and infants but between any two individuals in social contact. The resulting experience is an immediate awareness of both the other person and the (interpersonal) self, as well as of the specific present relationship between them.

Now comes the important part. The claim that developmental failures at this stage are associated with autism. I would in parallel surmise that too much reliance on this intersubjective self should however dispose towards psychosis too.

The close parallels between ecological and interpersonal self-perception should not be allowed to obscure certain important differences. The successful achievement of intersubjectivity depends not only on the operation of the perceptual and motor systems but on some additional, specifically human mechanism that permits us to relate to members of our own species. The mechanism can fail, and it has often been suggested that the dramatic condition called infantile autism, characterised from the outset by a total lack of interest in relationships with people, results from just such a failure. Leo Kanner made this point explicitly in the paper that established autism as a diagnostic category: “We must, then, assume that these children have come into the world with innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handicaps” (1943, p. 250). Murray (1984) has recently presented a similar argument, and suggested that the effects observed in her double closedcircuit television paradigm may provide useful models for autism research.

Awareness of the interpersonal self is almost invariably accompanied by a simultaneous awareness of the ecological self. A wealth of information specifies their co-existence: I can see that the person to whom you are addressing yourself (the interpersonal me) is the very person who is located here, at this point of observation in this environment (the ecological me). For this reason, these two aspects of the self are rarely experienced as distinct. Such a separation can occur, however, if we attend exclusively to one class of information and ignore the other entirely. To attend only to ecological information structures, ignoring the interpersonal, is to treat another individual merely as a non-human object—perhaps to walk past him, or shove him aside, without engaging in any form of intersubjectivity. The opposite case can occur in very intimate personal contact, as between lovers or (as psychoanalysts have long suggested) between mothers and infants: one’s attention is so fully directed to the ongoing intersubjective experience that one does not pick up any ecological-self-specifying information at all. This does not mean that lovers and infants have no ecological selves, but only that there are moments at which those aspects of their selves may go unnoticed.

It is interesting to note that Neisser equates too much inetrsubjectivity with the obsession (or colloquial) madness involved in bond between lovers/ parents-child.

Next he analyzes the extended self:

The objectively-existing kinds of information considered so far—optical flow, effective movement, other people’s expressive gestures—specify only the present self. We can see what we are doing right now, and with whom, but how can we know what we did yesterday or last week? The answer, of course, is just that we remember, the information is in our own heads. The extended self is the self as it was in the past and as we expect it to be in the future, known primarily on the basis of memory.

He discusses amnesia as a pathology of thisslef and distinguishes between episodic memory and scripts involved at this stage.

Genuine remembering occurs when at least some information about the past is disentangled from the current situation. In many cases, that information is about my past, i.e. it is a record of some aspect of the extended self14. In remembering something that I did or experienced on some’other occasion—by remembering that I did it rather than merely how to do it—I necessarily became aware that my existence transcends the present moment. This can happen in two rather different ways. To the extent that what I recall is a unique and particular past event (say, presenting a colloquium talk at the University of Aberdeen in November 1987), I am having an episodic memory (Tulving, 1972). But to the extent that what I recall is a repeated and familiar routine (there is a script for colloquiua that includes arriving in town, talking to colleagues, being introduced, giving the talk, answering questions, etc.), I am using a general event representation (Nelson, 1986) or script (Schank & Abelson, 1977). Both kinds of memory contribute to the extended self. / am the person who gave that colloquium in Aberdeen: I am also a person who gives colloquium talks from time to time. While these two examples are certainly not among the most central components of my extended self (!), that self can be thought as a kind of cumulated total of such memories: the things I remember having done and the things I think of myself as doing regularly.

Recent studies show that episodic recall, like script knowledge, is in place by the age of three. A 2 \ -year-old child will often fail to remember the particular ‘target event’ that an interviewer first asks about, but s/he will usually have at least some fairly accurate memories that go back 3 or more months (Todd & Perlmutter, 1980; Fivush, Gray & Fromhoff, 1987). Despite these findings, I doubt that episodic memory contributes very much to the sense of self at this early age. Children under 3 years are not very interested in the past, even when they can recall it. They would much rather talk about something in the present—or play and not talk at all—then spend effort in remembering earlier experiences (Galotti & Neisser, 1982). That interest increases as the child come to realise the social significance of autobiographical recall, i.e. its potential for extending relationships beyond the present moment. The most important adaptive function of memory may be that it makes permanent interpersonal relations possible, and thus vastly strengthens the coherence of human groups (Neisser, 1988). Note that even rather sloppy memories can serve this purpose: my recall of a shared event must be close enough to yours to avoid bizarre discrepancies, but it need not be accurate in every detail. Unsurprisingly, this is just the level of mnemonic accuracy that people generally achieve.

I would like to pause here and reflect on the fact that in amnesia the intersubjective self is dysfunctional- that in my view should lead to problems at this level too. In particular because they do not appreciative the social subtleties that should guide the appropriate memory and scrips generation, they end up with too much detailed memory (savant abilities) and too rigrous scripts (repetitive and restrictive movements and interests). On the other hand too much intersubjectivity reliance in memory and scripts formation should lead to inaccurate and self-serving memories and scripts that are partly delusional and confabulatory.

The extended self becomes increasingly important as we grow older. Most adults develop a more or less standard life-narrative that effectively defines the self in terms of a particular series of remembered experiences. These accounts are continually being extended (and occasionally revised!), creating a narrative structure much like that of more formal autobiographies (Barclay, 1986). As in the case of social relationships, the memory that supports these narratives need not be highly accurate. It also need not deal in equal detail with every epoch of life. Recent studies suggest that elderly people have particularly rich and accessible memories for the period of adolescence and young adulthood.

Note also that how as we move up the developmental stages we move from agentic/experiential “I” to narrative ‘me’, the two types of selves I discussed recently in a different context.

Next he moves to the Private self:

Each of us has conscious experiences that are not available to anyone else. Some of these are the inner aspects of perception and action; others (dreams, for example) are quite independent of the individual’s actual present circumstances. These personal experiences are an important source of self-knowledge15. When are they first used for that purpose? While even the youngest children surely have a conscious mental life (including an awareness of the ecological and interpersonal selves!), I suspect that they do not yet take the immediacy of their experience as an important line of demarcation between themselves and the rest of the world. They do not need to: such a line already exists for them, established by ecologically available information. Although each of us certainly “dichotomizes the Kosmos in a different place,” as William James put it (1890, p. 290), we first do so by exterospection rather than by introspection.

We not only have private experience but remember it, recalling dreams we had last night or thoughts we had last week and thus augmenting the extended self. The importance of this contribution varies substantially from one person to another, perhaps in part because memory for mental experiences is relatively poor. Pains are notoriously difficult to recall; we remember that we were in pain, but cannot easily recapture the quality of the experience. Most people forget most of their dreams almost immediately.

Philosophers in the Western tradition—indeed, in many traditions—have often treated the private self as the only self worth knowing. Descartes is primarily responsible for the further claim that it is the only self we can be sure about, all other experiences being subject to error and delusion. I have argued, in contrast, that the ecological and interpersonal selves are perceived effectively and surely from the beginning of life. (This argument does not dispute the value of the private self, only its epistemiological priority.) In any case it is worth noting that individuals differ widely in the value and importance they attach to inner experience. This was roughly Jung’s original distinction between extraverts and introverts. In the extravert, ” . . . thinking is oriented by the object and objective data” (Jung, 1921/1971, p. 342), while introverted thinking ” . . . is neither determined by objective data nor directed to them; it is a thinking that starts from the subject and is directed to subjective ideas or subjective facts” (p. 344). These are essentially differences in the allocation of attention. All such forms of information and experience are available to everyone, but within the normal range they are not all equally noticed, equally used, or equally valued. Outside the normal range are the pathologies of the private self, which include obsessive thinking, repression and denial of feelings, multiple personality, and related conditions.

The private self to me is the most mundane and boring aspect of self- the “I think therefore I am” dictum.

Next we move on to the most interesting conceptual self:

Each of us has a concept of him/herself as a particular person in a familiar world. These self-concepts originate in social life, and so they vary widely across different societies and cultures. A few concepts of my own can serve as convenient examples: I am an American, a husband, and a professor. I assume that I have certain social obligations and political rights; that I have a liver and a spleen and a distinctive pattern of nuclear DNA; that I am a fast reader, poor at remembering names, and neither handsome nor ugly; that in general I do not think enough about the future consequences of my actions. Everyone could make such a list, and no two lists would be the same. Even the relevant dimensions need not be the same: a member of the Lohorung Rai in East Nepal would include the state of his Niwa (Hardman, 1981), and a medieval Englishman the state of his soul.

In the face of this complexity, it is useful to begin by considering concepts and categories of other kinds. What do we mean, for example, when we say that something is a ‘dog’? The so-called classical theory of concepts, which would claim that the class dog is defined by certain necessary and sufficient features, no longer seem adequate: it is too difficult to think of really definitive features, and those that do come to mind (e.g. ‘has four legs’) are just as hard to define as dog itself (Murphy & Medin, 1985). The classical theory also fails to explain the typicality effects discovered by Eleanor Rosch (1978); in most categories, some members function as ‘prototypes’ while others are more marginal. But category membership cannot just be a matter of similarity to the prototype either: besides the difficulty of defining ’similarity’, such a definition would miss the point that many categories, including dog, are conceptually all-or-none. (Any given animal either is or isn’t a dog.) These difficulties are resolved by realising that concepts do not stand alone: each is defined with reference to a network of others, i.e. to a theory.

Many linguists, philosophers, and psychologists have made this point (e.g. Lakoff, 1987; McCauley, 1987; Medin & Wattenmaker, 1987). To call something a dog is to assign it to a place in our theory of animals in general and dogs in particular, i.e. to assert that it occupies space, has internal organs, must eat or starve to death, is likely to behave in certain ways, is bigger than a mouse and smaller than an elephant, should be treated in a particular manner appropriate to dogs, had two parents who were dogs and will (if it becomes a parent) have puppies, etc. These beliefs are components (not all equally central) of our implicit theory of doghood—of what George Lakoff (1987) would call an ‘idealised cognitive model’. Children have such models quite early, at least where animals are concerned (Carey, 1985).

I love the references to Lakoff and am a firm believer in his other theory of conceptual metaphors. Next he talks about paranoia and how that may be a result of too much theorizing. This is fortunate reference I have found because just the other day CMB, a reader of this blog pointed that paranoia is hard to explain if we treat autism and schizophrenia as opposites and grant a role for opposing effects of Oxytocin. My reply was that oxytocin may be more a social hormone than a trust hormone and paranoia is more a excessive theorizing about others defect than a suspicion deficit.

These principles apply equally to the concept of self. My notion of what I am, like your notion of what you are, reflects a cognitive model embeded in a theoretical network. It too is based primarily on what I have been told, not only in the form of general cultural assumptions but also of communications addressed to me in particular. Like other concepts it tends to govern what I notice; in this case, what I notice about myself. Like other theories, it is not necessarily correct; all of us know people whose self-theories seem off the mark in certain respects. Nevertheless most self-theories do work fairly well, at least in areas where they make predictions about real experience. (Where this is not the case—e.g. in paranoia—we tend to classify them as pathological.) When Epstein (1973) proposed that psychologists should think of the self as a theory rather than as an independently-existing entity, he was talking about the conceptual self.

Next closely followed are references to Carol Dweck- another psychologist I just adore.

Although the self-concept can usefully be regarded as a single cognitive model, it usually comprises several more or less distinct sub-theories. Three of these deserve specific mention, although they cannot be considered in detail here. Role theories, which have been much studied by sociologists, are our own notions of how we fit into society: of what we should do and how we should be treated. They originate, I think, in children’s understanding of the scripts in which they participate; hence they are in place very early. Internal models, in contrast, concern or bodies and our minds. In modern Western culture, self-theories of the body (like my firm belief that I have an internal organ called the liver18) are mostly based on biology and medicine. Theories of the mind, in contrast, are the province of psychology, philosophy, and religion. Children are presented with these theories by the people around them, and do their best to interpret their own lives in terms of what they have been told. When and what they are told depends, of course, on the particular culture in which they are growing up.

Trait attributions are an important class of self-theories that straddle the boundary between social roles and internal models. We may believe, for example, that we are clever or stupid, handsome or ugly, fortunate or unlucky. Although these dimensions are essentially conventional—not all cultures classify along the same dimensions, or value them to the same extent—they can be of considerable importance. In this vein, Carol Dweck (1986) has shown that children’s beliefs about intelligence affect their actual performance in school. Those who believe that intelligence is a fixed quantity (and that they themselves are stupid) learn much less from school experience than those who have a self-concept that allows for intellectual growth and development. Although such attributions are acquired early, they are not impervious to change.

And thus he concludes talking about some tantalizing tangential thoughts on the perceived and felt unity of self, how we know our neighbors as ourselves , the ‘doer’ as opposed to ‘knower’ and admiring or despising oneself- all perhaps food for the next three stages (relational, reflexive/recursive/generative and integrative ) of self.

I enjoyed reading the article and would like to thank whole heartedly the ‘References wanted’ room on FrinedFeed and Kubke in particular, without whom I would have not had access to this lovely article.

Neisser, U. (1988). Five kinds of self-knowledge Philosophical Psychology, 1 (1), 35-59 DOI: 10.1080/09515088808572924

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Autism is a hard disorder to nail down genetically- single nucleotide polymorphisms (SNPs) or even multiple locus genetic effects are not able to account for the large genetic component to the disorder. In recent times, Copy number variations (CNVs) has come to the forefront of Autism research , suggesting that microdeletions, duplications etc may account for some cases. Another new , till now unsuspected mechanism that has recently been implicated in autism is epigenetic mechanism of increased methylation in promoter regions that has the effect of silencing/reducing the expression of genes involved to a certain extent. The recent study by Gregory et al, is just such a step in the right direction, which will hopefully bring us closer to the truth.

The study is available in full at BMC Medicine site and is accompanied by a must read commentary that explains a lot of things and puts the finding in context.

In a nutshell, the study authors used CNV determining methods to discover that a deletion of OXTR (oxytocin receptor) gene was presnet in an autistic subject and was not de novo , but the deletion was inherited from his mother. One of the affected siblings of the autistic subject, who too was autistic, on the other hand did not have a deletion, but had increased methylation of the OXTR. this led the study authors to revisit their genomics data and look at adta across all autistic subjects and controls and discover that indeed, in other autistics too the OXTR had increased methylation. Then they looked for expression of OXTR in peripheral blood cells and temporal cortex and found that indedd in autistics, as compared to controls, there was reduced expression of OXTR. This strongly suggest that the epigentic changes that lead to autism (the efffect of OXTR suppression) happen quite early in the devlopmenet and might happen in utero.

Before I elaborate on my take home from the study, there are some excerpts (as I know you didn’t read the originals)

Classic autism comprises a spectrum of behavioral and cognitive disturbances of childhood development. The core autism phenotype includes deficits in social interaction, language development and patterns of repetitive behaviors and/or restricted interests. The population prevalence of the spectrum of autism disorders is estimated to range between 1/300 [1] to 1/100 (http://www.nschdata.org/), with a male: female ratio of 4:1 [2,3]. The disorder has been shown to be highly heritable with the relative risk for siblings being approximately 2% to 8%, much higher than that of the general population [4]. To date, only a small percentage of autism cases (<10%) have been ascribed to single gene disorders such as fragile X syndrome, tuberous sclerosis [5] and Rett syndrome [6]. Numerous approaches including genetic linkage, genome-wide association, candidate gene association and gene expression analysis have been used to identify the additional genes
implicated in the development of autism [7,8]. However, the heterogeneous nature of autism and autism spectrum disorders has limited their success.

An additional approach to identify genes involved in autism is to characterize copy number variants (CNVs), that is, chromosomal deletions and duplications, that are known to be present within at least 5% of individuals with idiopathic autism [9]. Autism CNVs have been shown to involve almost all chromosomes [10,11], with the most frequently observed alteration localizing to chromosome 15q11-13 [12-23]. A number of different methods have been used to characterize autism related CNVs, including but not limited to, cytogenetic Gbanding [14,23,24], metaphase fluorescence in situ hybridization (FISH) [22], Southern blotting [18], loss of heterozygosity (LOH) analysis [15-17,19], quantitative polymerase chain reaction (PCR) [25] and, more recently, genotyping and representational oligonucleotide microarray analysis (ROMA) [26].
Here we describe the use of genome-wide tilepath microarrays and array comparative genomic hybridization (CGH) to identify CNVs in a dataset of 119 unrelated probands from multiplex autism families [27]. The genomic profiles of our autism dataset were compared to the array CGH profiles of 54 phenotypically normal individuals, to previously published CNVs present within the database of genomic variants [28] and to the Autism Chromosome Rearrangement Database (http://projects.tcag.ca/autism/). The most significant finding thus far from our analysis is a heterozygous deletion of the oxytocin receptor gene (OXTR) (MIM accession no.: 167055) in an individual with autism and his mother with putative obsessive-compulsive disorder (OCD). We further investigated the relationship between OXTR and autism by carrying out epigenetic analysis of the promoter region of OXTR. We show that the gene is hypermethylated in independent cohorts with autism as compared to controls, in both peripheral blood mononuclear cells (PBMCs) and the temporal cortex. Additionally, our analysis of expression levels of OXTR in the temporal cortex shows decreased levels of expression in individuals with autism as compared to controls matched for age and sex.

These data suggest that OXTR and the oxytocin signaling pathway play an important role in the etiology of autism and autism spectrum disorders and implicate epigenetic misregulation of OXTR in this complex disease.
…
Epigenetic control of autism susceptibility is a recent concept and most certainly a topic of great interest in the field. Over the past decade, researchers have uncovered suggestive links between epigenetics and autism, for example, autism is associated with duplications of 15q11-13 (especially maternally inherited), an imprinted region in the genome where DNA methylation status has been linked to Prader-Willi syndrome (PWS) and Angelman syndrome (AS) [66]; mutation within a gene that encodes a methyl-DNA-binding protein (MECP2, (MIM accession no.: 300005)) is the causative agent of Rett syndrome [67]; and mutation of this same gene has been associated with both autism and AS populations [55]. Nagarajan et al. have shown that 79% of autism cases have a decrease in MECP2 expression in the frontal cortex and that an increase in aberrant DNA methylation correlates with this decrease in MECP2 expression [68]. These data implicate epigenetic dysregulation as a mechanism for the development of autism and justify the examination of DNA methylation of autism candidate genes, such as OXTR identified in this study.

Now from the accompanying (more accessible) commentary:

The article by Gregory et al. published this month in BMC Medicine, reports on genomic and epigenetic alterations of OXTR, the gene encoding the receptor for oxytocin. The involvement of this gene was suggested by its deletion in an autistic patient. The subsequent analysis of a group of unrelated autistic subjects did not show an OXTR deletion, but rather hypermethylation of the gene promoter, with a reduced mRNA expression.

These findings address two major points of the current debate on the etiology and pathogenesis of autism: the role of oxytocin, known to be involved in modeling human behavior, and the possible involvement of epigenetic mechanisms. The nature of this epigenetic dysregulation is unknown but, if proved to be true, might explain the failure to identify sequence alterations in a host of candidate genes. Practical implications of these findings may be forthcoming, however not before extension and validation on a larger scale have confirmed their value.
..
The second issue raised by Gregory et al. deals with the epigenetic inhibition of OXTR expression in ASD. Such epigenetic modification, at least as reported so far, does not seem to be sequence based but rather of a different, as yet unknown nature. This might explain why researchers have been looking for decades for genetic mutations in ASD and yet have found almost none. An epigenetic mechanism would justify the ‘unusual’, non-Mendelian familial aggregations of ASD. In this respect, even the family with OXTR deficiency reported by Gregory et al. shows an unusual genotype-phenotype correlation, in that the same phenotype is caused by alterations of the same gene but due to different molecular defects (deletion versus hypermethylation).

Also, the possibility that in most ASD patients there might be an epigenomic instability is of interest in consideration of the fact that it has been shown that the epigenetic status in early fetal development can be reprogrammed by maternal behavior in a reversible way [34]. Therefore, other environmental factors, yet to be discovered, might also be able to reprogram the epigenotype of the embryo.

I hope the fact that epigenetic changes may happen during pregnancy line of reasoning does not lead to the harmful and without-any-basis vaccination is cause of autism arguments. On the other hand I had covered earlier how Autism is more likely if mother was exposed to valproate during pregnancy or the child soon after birth. What if valproate is instrumental in an epigenetic fashion in leading to more or less methylation and gene expression. It is well known that valproate and valporic acid is given as treatment for psychosis/bipolar. In a similar vein, I am inclined to stick my neck out and claim that in schizophrenics/psychotics , the OXTR should be more expressed : perhaps more methylation, duplications etc . However I am checked in my musings by these studies that claim that negative symptoms of schizophrneia may be associated with reduced oxytocin activity in the brain. Yet, all said and done I would like to see a study that analyzes for epigenetic mechanisms in schizophrneia especially at the OXTR locus. Although the negative symptoms like social withdrawal of schizophrenia may lead to the opposite hypothesis regarding schizophrenia and oxytocin correlation, I am inclined to believe that schizophrenics (at least those suffering from positive symptoms predominantly) are too much oxytocin guided , trusting and socially too much involved in others type of people.

Gregory, S., Connelly, J., Towers, A., Johnson, J., Biscocho, D., Markunas, C., Lintas, C., Abramson, R., Wright, H., Ellis, P., Langford, C., Worley, G., Delong, G., Murphy, S., Cuccaro, M., Persico, A., & Pericak-Vance, M. (2009). Genomic and epigenetic evidence for oxytocin receptor deficiency in autism BMC Medicine, 7 (1) DOI: 10.1186/1741-7015-7-62
Gurrieri, F., & Neri, G. (2009). Defective oxytocin function: a clue to understanding the cause of autism? BMC Medicine, 7 (1) DOI: 10.1186/1741-7015-7-63
Hat tip to @Boraz for tweeting about this study.

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I came across this study article today by Farb et al, that talks about two distinct neural networks in the brain that are involved in self-reference. To be fair, the networks are somewhat blurred and overlap in naive people, while in people who practice mindfulness meditation, the networks are more distinct and non-overlapping. My interest was piqued as I am a keen follower of default-brain network , which has been implicated in self-referential thinking and this article seems to at one point argue that the narrative self viz ‘me’ is grounded in default brain network, while the experiencer ‘I” has some other nearby related areas as the neural substrates.

But first let us clarify what we mean by ‘me’ and ‘I’. For this I would like to quote form a Gallagher article:

Ever since William James (1890) provided a catalogue of different senses of the self, philosophers and psychologists have been hard at work refining and expanding the possible variations of this concept. Supplementing James’ inventory of physical self, mental self, spiritual self, and the ego, Neisser (1988), for example, suggested important distinctions between ecological, interpersonal, extended, private, and conceptual aspects of self. More recently, reviewing a contentious collection of essays from various disciplines, Strawson (1999) found an overabundance of delineations between cognitive, embodied, fictional, and narrative selves, among others. It would be impossible to review all of these diverse notions of self in this short paper, so I have focused on several recently developed approaches that promise the best exchange between philosophy of mind and the other cognitive sciences. Because these approaches move in divergent theoretical directions they should help to convey the breadth of philosophical analysis on this topic. They can be divided into two groups that are focused, respectively, on two important aspects of self.

A first approach involves various attempts to account for a ‘minimal’ sense of self. If we strip away all of the unessential features of self, the intuition is that there is a basic, immediate, or primitive something that we are still willing to call a self. This approach leaves aside questions about the degree to which the self is extended beyond the short-term or ’specious’ present to include past thoughts and actions. Although identity over time is a major issue in the philosophical definition of personal identity, the concept of the minimal self is limited to that which is accessible to immediate and present self-consciousness. Non-philosophers have found that certain aspects of the minimal self are relevant to current research in robotics. Furthermore, aspects of the minimal self that involve senses of ownership and agency in the context of both motor action and cognition can be clarified by neurocognitive models (developed to explain pathologies such as schizophrenia) that suggest the involvement of specific brain systems (including prefrontal cortex, SMA, and cerebellum).

A second approach involves conceiving of the self in terms of narrative, a concept imported into the cognitive-science context by Dennett (1991) , but one which may have a more complex significance than indicated in Dennett’s account. The narrative self is extended in time to include memories of the past and intentions toward the future. It is what Neisser refers to as the extended self, and what Dennett calls a ‘nonminimal selfy’ self. Neuropsychological accounts of episodic memory or loss of memory can help to circumscribe the neurological underpinnings of the narrative self.

If you haven’t guessed by now, the minimal self is ‘I’: the doer , experiencer experiencing the immediate present; the narrative self is ‘me’ -an entity stretched in time and living as much in past and future as in the present. The study authors delineate the same as follows (note that they too start with William James reference):(* references removed)

Since William James’ early conceptualization, the ‘self ’ has been characterised as a source of permanence beneath the constantly shifting set of experiences that constitute conscious life. This permanence is often related to the construction of narratives that weave together the threads of temporally disparate experiences into a cohesive fabric. To account for this continuity, William James posited an explanatory ‘me’ to make sense of the ‘I’ acting in the present moment . Recently, progress has been made in characterizing the neural bases of the processes supporting William James’ ‘me’ in the form of ‘narrative’ self-reference , highlighting the role of the medial prefrontal cortices (mPFC) in supporting self awareness by linking subjective experiences across time . The mPFC has been shown to support an array of self-related capacities, including memory for self-traits , traits of similar others , reflected self-knowledge , and aspirations for the future . As such, cortical midline processes may be characterised as supporting narrative self-reference that maintains continuity of identity across time .

Narrative self-reference stands in stark contrast to the immediate, agentic ‘I’ supporting the notion of momentary experience as an expression of selfhood. Most examinations of self-reference ignore mechanisms of momentary consciousness, which may represent core aspects of self-experience achieved earlier in development and may have evolved in earlier animal species. Indeed, little is known about whether the neural substrates underlying momentary self-reference are one and the same, or distinct from, cortical midline structures supporting narrative experience. One hypothesis suggests that awareness of momentary self-reference is neurally distinct from narrative self-reference and is derived from neural markers of transient body states, in particular, right lateralised exteroceptive somatic and interoceptive insular cortices. In the present study, we examined this thesis.

In short using fMRI, they tried to find the different hypothesized neural networks underlying the two senses of self and did find evidence for clear segregation in those practicing mindfulness meditation. Their methodology however, is not fool proof and this they themselves note in their conclusions. Here are their findings:

Consistent with a theory of self-reference as mentalising, linguistically mediated and of higher order executive origin , participants engaged midline prefrontal cortices and a left lateralised linguistic-semantic network (inferior lateral PFC, middle temporal and angular gyri) during NF (narrative focus: ‘me’ condition). Demonstrating a default bias towards NF as previously revealed in ‘resting’ mind wandering states , relatively restricted reductions in the cortical midline network were found when attention was explicitly directed towards a moment-to-moment EF (experiential focus: ‘I’ condition) in novice participants with little training in this form of self-reflection. These individuals revealed increased left lateralised prefrontal-parietal activations during EF likely reflecting greater task-related linguistic processing that has been shown to be associated with decreased medial prefrontal recruitment .

So what they found was that a part of default network was engaged in ‘me’ condition; while task-related areas were recruited in “I” condition and appropriate task-related suppression of some part of default network observed. This effect was with naive subjects, but with those trained in mindfulness meditation, they observed a sort of double dissociation:

Following an intensive 8 week course in mindfulness meditation, during which individuals learn to develop the capacity to monitor moment-to-moment experience, EF resulted in a pronounced shift away from midline cortices towards a right lateralised network comprised of the ventral and dorsolateral PFC, as well as right insula, SII and inferior parietal lobule. Consistent with a dual-mode hypothesis of self-awareness, these results suggest a fundamental neural dissociation in modes of self-representation that support distinct, but habitually integrated, aspects of self-reference: (i) higher order self-reference characterised by neural processes supporting awareness of a self that extends across time and (ii) more basic momentary self-reference characterised by neural changes supporting awareness of the psychological present. The latter, represented by evolutionary older neural regions, may represent a return to the neural origins of identity, in which self-awareness in each moment arises from the integration of basic interoceptive and exteroceptive bodily sensory processes. In contrast, the narrative mode of self-reference may represent an overlearned mode of information processing that has become automatic through practice, consistent with established findings on training-induced automaticity.

To me this sounds interesting: If I had to stretch my neck and relate this to autism and schizophrenia , I would say that based on earlier coverage on this blog: Schizophrenics have a higher default brain activity and perhaps try to spin too much of a narrative. Perhaps they are the ones that would best benefit with mindfulness meditation trainings to calm their default ‘me’ and activate the ‘I’ also at relevant times. On the opposite side, one is all too aware of the here-and-now feeling of self that many autistics have- a direct and immediate perceptual relation with world. Perhaps, they too can benefit from some for of mindfulness meditation by learning to use the default brain network too at times – letting teh mind wander and spinning a tale (however fictional) about themselves.

Farb, N., Segal, Z., Mayberg, H., Bean, J., McKeon, D., Fatima, Z., & Anderson, A. (2007). Attending to the present: mindfulness meditation reveals distinct neural modes of self-reference Social Cognitive and Affective Neuroscience, 2 (4), 313-322 DOI: 10.1093/scan/nsm030
Gallagher, S. (2000). Philosophical conceptions of the self: implications for cognitive science Trends in Cognitive Sciences, 4 (1), 14-21 DOI: 10.1016/S1364-6613(99)01417-5

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The Society for Neuroscience(SfN) was formed 40 years ago and to commemorate the occasion, the journal of Neuroscience has made some review articles open-access. They are written by leading luminaries in their filed and are somewhat scholarly- though I found some of them pretty accessible too.

Two articles relate to reviewing memory research in the past 40 years and both are a pretty good read. The first is written by Larry Squire and gives you a broad overview of memory research. The second by Eric Kandel focuses more on the molecular aspects of memory formation- but is an excellent article and ends with 11 still unresolved questions for the next 40 years in the memory research.

There is another article by Marcus Raichle that I found pretty interesting, partly because of my continuing fascination with the default brain network and the intrinsic activity of the brain. this again is a very accessible article that brings one up to speed on the 40 yrs of imaging with special focus on the default brain network.

There are other retrospectives there including one on neurotransmitters so go to the source and enjoy the ride.

Hat Tip: Mind Hacks
Squire, L. (2009). Memory and Brain Systems: 1969-2009 Journal of Neuroscience, 29 (41), 12711-12716 DOI: 10.1523/JNEUROSCI.3575-09.2009
Kandel, E. (2009). The Biology of Memory: A Forty-Year Perspective Journal of Neuroscience, 29 (41), 12748-12756 DOI: 10.1523/JNEUROSCI.3958-09.2009
Raichle, M. (2009). A Paradigm Shift in Functional Brain Imaging Journal of Neuroscience, 29 (41), 12729-12734 DOI: 10.1523/JNEUROSCI.4366-09.2009

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