Support for the Broken Window

Ed at Not Exactly Rocket Science has an important post  on research by Keizer and colleagues, which found support for the broken windows theory of crime spread. He dos a very good job of describing the broken window theory, the experiments of Keizer et al and how they show that disorder spreads like a virus, so I won't repeat all that here but urge you to go to his blog to get the complete lowdown.  

What I would like to highlight instead is that fact that this Broken window theory was brought to public focus by Malcolm Gladwell in The Tipping Point and subsequently the same theory was thrashed in Frekonomics by Dunbar and surprisingly Malcolm Gladwell had promoted and written an encouraging blurb for Freakonomics. You can read more on the controversy here . I obviously had disliked almost all the explanations in Freakonomics and believe that the book was more on trying to be controversial rather than offering new insights. I , on the other hand, have been sympathetic to Gladwell's writings and it is heartening to note that new research supports the old position that lawlessness spreads via small acts and it may be more important to take care of small, everyday acts of lawlessness than to focus on a few big problems like the cocaine addicts. I would just end with a brief note on Gladwell's new book Outliers, which is on my immediate reading list and I am pleased that he shares some of my thoughts about how SES affects outcomes in life (like IQ) and how we are creatures of circumstances.

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The Science Blog Meme

A meme, that started in Nature Networks  , has slowly gained momentum and as many science bloggers have participated, I think I might as well jump in.

1. What is your blog about?
It is definitely not about catching mice, though I sometimes regret why I chose this particular name from the available zillions. My blog is solely focussed and devoted to psychology and neurosceince; within them some pet themes keep emerging; it started with a focus on cognitive maps; another is the focus on stage theories; then still another is focus on Autism and Schizophrenia as diametrically opposed on a continuum.but I take pride in the fact that most reviewers of this blog have determined this blog to be focussed diffusely on disparate subjects.

2. What will you never write about?
about my day-to-day humdrum existence as I lack the capacity to make that sound interesting. Also I like to keep the personal separate from professional as far as possible.

3. Have you ever considered leaving science?
The question is a bit odd, as I am not a working scientist and my science focus is part-time; but leaving science as a hobby/ part-time vocation seems unthinkable - perhaps if all the applied uses of science have been exhausted I may think of leaving sceince; but till the time there is much to be discovered and applied in the real world; there is no parting company.

4. What would you do instead?
Social Work (though for some reasons I don't like the word..juts like the concept of working for the disadvantaged)/ Education and guidance---of course the assumption is that I have all the resources to enjoy my present lifestyle and only then in my free time instead of science do these things.

5. What do you think will science blogging be like in 5 years?
It should replace scince journalism even before that and might perhaps be replaced by somemore disruptive technologies. It would be more actual science and less reporting. The science would be prominent over the blogging part and both will happen collaboratively.

6. What is the most extraordinary thing that happened to you because of blogging?
In the real world, not much! In the online world, I met and befreinded many interesting, prominent and like-minded people. Overall, blogging provided me a much needed outlet for sharing all the knowledge/information that I was accumulating but finding no outlet for.

7. Did you write a blog post or comment you later regretted?
Yes, one or two blog posts I regret to have written. even today, I feel embarrassed when someone comments on them.


8. When did you first learn about science blogging?
I believe it must have been 3 years back; as soon as I learnt about that I started my own blog!!


9. What do your colleagues at work say about your blogging?
Not many at my work place read my blog or are aware of its existence; for those who are aware its more of a personal eccentricity and a freaky thing - though I have received some very positive feedback too from some; but most say it is incomprehensible and too technical for them (my workplace is not in a scientific setting/ concerned with psychology/ neuroscience)

10.Extra credit: are you able to write an entry to your blog that takes the form of a poem about your research?
I believe I am able, for I pride myself as the next big thing- an undiscovered poet/ creative writer that is just waiting for the right break; the bad part is that I maintain a dedicated creative writing blog , that is separate from my scientific blog, so have never mixed the too, so am not quite sure!!

Thats it folks! I love these memes, especially those that come without any tagging requirements!!

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Autism and Schizophrenia co-occurence

Socrates has raised an important point in one of the recent comments that if Autism and Schizophrenia are opposite poles , how do you explain their (rare) simultaneous co-occurrence?  This same question has been raised by other commentators (like Julia)  before and though I have responded in the comments, I'll like to highlight the earlier response here for the benefit of all readers. Here is one of my earlier responses to the prevalance of mCDD and I hope to stimulate some discussion on this:

One way to look at this (mCDD) would be to treat this as similar to mixed episodes in bipolar disorder. Here both symptoms of Mania and depression are present in the same individual though traditionally Mania and depression are thought of as opposite poles on a continuum. In effect though Autism and Schizophrenia/psychosis are opposite extremes, in some individuals both may be present. However, also note the differences form mixed episodes in bipolar; there the mixed state as well as mania and depression happen in the same individual over time; here the disorders itself are simultaneously present in the individual.

Another example I can think of is of recessive alleles for both disorder at the same gene locus. (lets for example consider that eye color is due to recessive alleles at the eye-color locus). Now suppose that recessive allele S confers risk of schizophrenia and N is the normal variant. so SS is schizophrenic; SN is on the continuum toward schizophrenia and normality, perhaps a schizotypal individual. Suppose also that recessive allele A at the same locus makes one susceptible to Autism (they are opposite poles so evidently should work on same locus / loci). Thus AA is autistic and AN is asperper's; now consider the rare scenario where one gets AS genotype ; in this case one might be asperger's and schizotypal; in rare scenario this may develop into full-blown child-onset schizophrenia and classified as PDD_NOS or McDD.

To test my theory one can see the frequencies of Autistic and Schizophrenics and also the McDD iondividuals. If there was no interaction, Autism and schizophrenia should be independently inherited and P(mcDD) = P(Autism) * p(schizophrenia) where P is probability of an individual in a population belonging to that disorder. As my theory predicts there should be some interaction (the gene locus is same), so P(mcDD) should be different from that calculated from above (though I lack the requisite math knowledge to come up with a good formula!)

 I believe I owe a bigger response to the questions raised, but I am hoping this to turn out as more of a conversation, then a one -sided defense of my pet theory,  and would encourage more and more readers to get involved and propose new and radical solutions to this conundrum that has been highlighted!  Also any statistics on the co-occurrence and individual occurrence and prevalence of Autism and schizophrenia would be more than welcome

 

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Decision-making research in autism and schizophrenia: Implications for each other

Today I would like to review two recent articles on decision-making: one concerned with autism or ASD and the other with Schizophrenia individuals. I would like to demonstrate how some of the findings fit in, in the larger context of Autism and Schizophrenia as diametrical poles on a continuum.

The first article is by Martino et al, and discusses a finding that those with ASD display more consistent and logical decision-making that is immune to framing effects.  Here is the abstract of the study:

The emotional responses elicited by the way options are framed often results in lack of logical consistency in human decision making. In this study, we investigated subjects with autism spectrum disorder (ASD) using a financial task in which the monetary prospects were presented as either loss or gain. We report both behavioral evidence that ASD subjects show a reduced susceptibility to the framing effect and psycho-physiological evidence that they fail to incorporate emotional context into the decision-making process. On this basis, we suggest that this insensitivity to contextual frame, although enhancing choice consistency in ASD, may also underpin core deficits in this disorder. These data highlight both benefits and costs arising from multiple decision processes in human cognition.

Here is the introduction:

Logical consistency across decisions, regardless of how choices are presented, is a central tenet of rational choice theory and the cornerstone of modern economic and political science. Empirical data challenge this perspective by showing that humans are highly susceptible to the manner or context in which options are cast, resulting in a decision bias termed the "framing effect". We have previously shown that the amygdala mediates this framing bias, a finding that highlights the importance of incorporating emotional processes within models of human decision making. An ability to integrate emotional contextual information into the decision process provides a useful heuristic in decision making under uncertainty. This is a factor that is likely to assume considerable importance during social interactions in which information about others is often incomplete, ambiguous, and not easily amenable to standard inferential reasoning processes.

In this study, we investigated the effect of contextual frame on choice behavior of individuals with autistic spectrum disorder (ASD). Autism is a neurodevelopmental disorder characterized by deficits in social interaction, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior, interests, and activities. From Kanner's earliest description, it has been recognized that individuals with ASD have a strong tendency to focus on parts rather than global aspects of objects of interest and are unable to integrate disparate information into a meaningful whole (weak central coherence theory).

We previously proposed that susceptibility to a framing bias reflects the operation of an affect heuristic. Here, we show that individuals with ASD, a condition characterized by marked behavioral inflexibility, demonstrate a decreased susceptibility to framing resulting in an unusual enhancement in logical consistency that is paradoxically more in line with the normative prescriptions of rationality at the core of the current economics theory. Furthermore, insensitivity in these subjects to a contextual framing bias was associated with a failure to express a differential autonomic response to contextual cues as indexed in skin conductance responses (SCRs), a standard measure of emotional processing. Our findings suggest that a more consistent pattern of choice in the ASD group reflects a failure to incorporate emotional cues into the decision process, an enhanced economic "rationality" that may come at a cost of reduced behavioral flexibility.

The experimental procedure used framing of gambles in terms of loss and gain and it is a well established paradigm that shows that normal people are risk-averse when the same gamble is framed in gain terms and risk-prone when the same gamble is framed in loss terms. Autistcis were not only more risk-averse in general , but their responses did not differ in relation to whether the frame was of loss or of gain. Thus, they were consistent in both the framing conditions. also , a measure fo their skin conductance did not show differential activation in the two frames of loss and gain; while the SCR of controls differed significantly. thus, teh authors conclude that it is the inability to take into account emotional information, that results in the consistent response of the autistics.Here is the discussion:

These findings suggest the ASD group fail to integrate emotional contextual cues into the decision-making process. This is evident both in a reduced behavioral susceptibility of a framing effect and an absence of a differential SCR response to our contextual manipulation. The concept that ASD individuals fail to integrate information across cognitive domains also informs the suggestion that an uneven profile of abilities and deficiencies in autistic individuals may reveal an imbalance in empathizing and systemizing behaviors (Baron-Cohen and Belmonte, 2005)

They discuss these findings in terms of the two-system theory of decision-making and here is what they have to say:

Recent theoretical accounts of decision making have put forward a "two-systems" model of human judgment (Evans, 2003). This view proposes that human decision making arises through a combination of intuitive and analytic processes. This model proposes that intuitive reasoning is rapid and capable of processing large amounts of information in parallel; however, it is prone to mistakes and strongly influenced by contextual emotional information (Kahneman, 2003). In contrast, analytical reasoning is more accurate but slow and computationally demanding. According to this view, the framing bias reflects an affect heuristic by which normal individuals incorporate a potentially broad range of additional emotional information into the decision process. In evolutionary terms, this mechanism may confer a strong advantage because such contextual cues may carry useful, even critical, information that dictates a rapid response. We propose that this ability is particularly crucial in a social context in that subtle contextual cues communicate knowledge elements (possibly unconscious) that allow optimal decisions to be made in uncertain environments (Stanovich and West, 2002).

In the context of the "two-systems" model of decision making described above, these results suggest that ASD individuals have an increased tendency toward the analytic type of decision making, attributable to impairment within their intuitive reasoning mechanisms. This interpretation would also support the empathizing-systemizing (E-S) theory of autism (Baron-Cohen and Belmonte, 2005). The E-S theory proposes that the imbalance between analytic and empathic behavior underlies both the impairment in social skills in ASD and their enhanced analytical skills. During the framing task, ASD subjects were better able to ignore biasing contextual information and isolate the critical information about the numerical value of the sure and risky options. This result is consistent with other experimental findings showing that ASD have enhanced attention for the task's details but reduced capacity to deal with the global aspect of the task as predicted by weak coherence theory (Frith and Happé, 1994).

Now, I am just overjoyed reading the above. It has always been my contention that Autistics use a more deliberate, rational approach to decisions while schizophrenics are at the opposite end relying on the intuitive part. I elaborated it in the form of Maximisers and Satisficers distinction that Barry Scwatrz has proposed and extended it to include exploration and exploitation in general. In short my thesis was, and remains, that autistics are more analytical while decision-making and schizophrenics more intuitive . the former does not take the context or frames into account while making decisions while the other takes into account too much context and is susceptible to too much framing effects.

If the above thesis is correct it leads to many testable predictions:

• 1) Schizophnrenics/ Schizotypal individuals should be more susceptible to framing effects and should show greater inconsistencies in decision-making under uncertainity as compared to controls.
  
• 2) They may also show more SCR variability when different frames of loss and gain are presented to them as compared to controls.
  
• 3) They may have higher baseline risk-prone behavior than controls in all conditions.
  
• 4) They may have higher activation in amygdala than controls as they use affect heuristic quite frequently while making decisions.
  

Part of this prediction may be satisfied by this decision-making and schizophrenia study by Ludwig et al  that found decision-making dysregulation in first episode Schizophrneia patients. Here is the abstract of the study:

Studies with chronic schizophrenia patients have demonstrated that patients fluctuate between rigid and unpredictable responses in decision-making situations, a phenomenon which has been called dysregulation. The aim of this study was to investigate whether schizophrenia patients already display dysregulated behavior at the beginning of their illness. Thirty-two first-episode schizophrenia or schizophreniform patients and 30 healthy controls performed the two-choice prediction task. The decision-making behavior of first-episode patients was shown to be characterized by a high degree of dysregulation accompanied by low metric entropy and a tendency towards increased mutual information. These results indicate that behavioral abnormalities during the two-choice prediction task are already present during the early stages of the illness.

The authors used the CT paradigm and it is important to explain that a bit here:

The purpose of the CT is to quantify decision-making characteristics based on the individuals’ sequential response patterns, which result from repeated selections of different alternatives associated with an uncertain outcome. Each subject received computerized instructions. The subject’s task is to predict on which side a stimulus (a car on the screen) will appear and select a response (to match up one of 2 figures shown on the screen) accordingly. The outcome is shown for 250 milliseconds after the subject has selected as response. A new trial begins immediately after the car has been displayed. The subject is not given any information about the sequence of the stimulus presentations, i.e., whether the stimulus is presented randomly or in any kind of order. Unbeknownst to the subjects, the location of the car shown is based on the subject’s response, i.e., the subject “correctly” predicts the location of the car in 64 trials. The basic measurements consist of the subject’s response, the presentation of the car and the latency of the response selection process, i.e., the time from the beginning of the trial to the pressing of the button. For the behavioral analysis, we used nonlinear methods— described elsewhere in detail (Paulus et al., 2001)—to obtain the following key measures:

Dysregulation: Dysregulation quantifies the range of response sequence entropies during the course of an experiment.A high dysregulation value indicates that the response sequences occurring during the experiment are characterized by botho¨perseverative tendencies“ and highly unpredictable or dynamically ”chaotic” strategies.

Metric entropy: Entropy measures the “sequential order” within sequences of responses. Whereas low entropy indicates that the response sequences are highly predictable, high entropy implies highly unpredictable response sequences. Thus, predictability is a collateral measure for the degree to which sequences of responses are based on a consistent internal strategy. However,this measure does not take into account the dependence of the response sequence on external stimuli, which is measured by the cross-mutual information (see below).

Mutual information: Mutual information quantifies the degree to which the previous response predicted the current response and provides a measure of the immediate influence of the past response on the decision in the current trial.

Cross-mutual information: Cross-mutual information quantifies the degree to which the previous location of the stimulus (presentation of the car on the LEFT or RIGHT hand side) is able to predict the current response. As opposed to entropy and mutual information, this measure quantifies the influence of external stimuli on the response sequences.

Switching probability: the probability of using the simple strategy RIGHT – LEFT.

Reaction time: the time between stimulus and response.

What they observed is summarized below:

As shown above in the results section, first-episode patients performing this decision-making test, irrespective of whether they were unmedicated or recently medicated, can be observed to have (a) more dysregulated behavior, (b) a reduced metric entropy, and (c) a tendency towards increased mutual information. As a specific response behavior (d), the patients used the switching strategy more intensely (switching between pushing the right and the left button). This study has supported our main hypothesis that decision-making dysfunctions are already present in first-episode schizophrenia (or SZ) patients.

I believe the results need some explanation, and I will stick my neck out here. More dysregulated behavior in my view, is due to the schizophrenic either trying too hard to remain consistent (when in self-aware frame of mind) or trying to be unpredictable (when in other-aware and being-watched frame of mind). The reduced metric entropy can be explained similarly . Tendency towards increased mutual information is quite informative in my view. It seems that the schizophenreic is working on the basis of an internal model and is ignoring external feedback: thus his reliance on previous response.I propose that an opposite pattern would be observed in Autistics with Autistics showing no or less mutual information, as they have poor self-models; but greater cross-mutual information , as they would base their decisions more on external stimuli or feedback.

Some other predictions, keeping in mind the autism is opposite of Schizophrenia theory are:

• 1) Autistcis should show lesser dysregulation and more rational behavior than even controls.
  
• 2) autistcis should show greater cross-mutual information than controls.
  
• 3) Autistcis may or may not show lesser mutual information.
  
• 4) Autistcis should use less switching strategy than controls.
  

All these are testable predictions and I hope someone out there tests these and lets me know!

B. De Martino, N. A. Harrison, S. Knafo, G. Bird, R. J. Dolan (2008). Explaining Enhanced Logical Consistency during Decision Making in Autism Journal of Neuroscience, 28 (42), 10746-10750 DOI: 10.1523/JNEUROSCI.2895-08.2008
Cattapan-Ludewig Katja; Ludewig Stephan; Messerli Nadine; Vollenweider Franz X; Seitz Antonia; Feldon Joram; Paulus Martin P (2008). Decision-Making Dysregulation in First-Episode
Schizophrenia The Journal of nervous and mental disease, 196 (2), 157-160

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Not Exactly Rocket Science : the book

Some of you may be familiar with Ed Yong's blog Not Exactly Rocket Science . He is an excellent writer and his blog postings are always well researched , readable and informative. I'm a a regular follower and can vouch for the quality of hits article length blog posts. For those of us , who like to do some off line quality reading, Ed has published his best blog posts in the form of a book that is currently available from Lulu. I encourage all of you to buy the book , either for yourself, or as a gift for a loved one: it will make for an excellent present!! While I feel happy for Ed, I wonder, if and when, can at least one of my articles appear in a book form; maybe openlab2008 is it; maybe I have to wait longer:-( Anyway, its happy to see that blog form is being recognized and I wish Ed and all prospective blogger-writers all the best!

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Better late than never: Mainstream media rises to Autism and Schizophrenia polarity

Readers of this blog will be familiar with two of my passionate theory building exercises- the first concerned with the eight stage developmental/ evolutionary stage theories and the second being the Autism and Schizophrenia /Psychosis as opposite poles on a continuum theory. While the first premise of stage theories was recently attached by Micaheal Shermer in Mainstream media of Scientific American; the other theory seems to have caught the fancy of Mainstream Media. Two days ago there were two articles by people I admire a lot, in magazines I admire a lot, that elucidated the Autism and Schizophrenia as opposite poles theory. The first was an article by Benedict Carrey in NYT and the second was an article by Carl Zimmer in Discover magazine. The two synchronous reporting are a result of a Baddock and Crespi article in Nature , this august. But the mainstream media, as always, is late to the party when compared with the blogosphere. 

I have been proposing and promoting the Autism and Schizophrenia as opposite poles argument since the inception of this blog, but the ideas crystallized about two year back based on work of Nettle. Since then I have found evidence from different quarters including Chris Frith and Baddock and Crespi. I covered the Baddock and Crespi original article (not the Nature opinion piece) about a year back, though it didn't find many takers at that time. I am glad that the same is finding acceptance now and is going mainstream. The Discover magazine article is really good and gives you some analysis of how gene imprinting works and how that may be instrumental in differential outcomes in the two cases of Autism and Schizophrenia and I recommend reading it as well as the NYT arcticle. If you want to read more about this theory, of course the first recommendation from me would be to read all the Mouse Trap articles labeled Autism or Schizophrenia or Psychosis. If you are more scientifically inclined, go read the original Baddock and Crespi paper amongst others. If you would just like to see the buzz in blogosphere and for some more context see the Mind Hacks article (that correctly mentions Chris Frith as a pioneer, but sadly does not mention efforts of Nettle in the same Autism-Schizophrenia model development) or see the Peter Cramer blog at In Practice from which I originally came to know of this mainstream media acceptance.

I hope that one day the eight stage model will also find the same sort of media acceptance and will lead to more stimulating work.

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Nominate The Mouse trap

If you like what you read here, you may like to nominate the Mouse Trap blog for either the Weblog Awards 2008 (category science) or submit one of your favorite articles from this blog  to the OpenLab 2008. The submissions links for both can be formed in the side bar on the blog, so please visit the blog (the links are not present in the RSS feeds)  and nominate the Mouse Trap or your other favorite psychology and science blogs and writings using the banners in the side navigation bar.

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Neurological correlates of Poverty

While people generally do not squirm on reading a headline claiming neural correlates of religion, god, trust, consciousness, political/ sexual orientation etc, I am sure the title neural correlates of Poverty would have lead to some uneasy shuffling around. How can poverty that is clearly a result of economic opportunities/ capabilities be reduced to brain? Are we claiming that low inherent IQ and the neural correlates thereof define and lead to poverty? Or is the claim instead that poverty leads to definite changes in the brain, which may lead to manifestation of low IQ and the sustenance of the vicious circle of poverty? The regular readers of the blog will know which side of the fence I am sitting on!

The blogosphere is normally abuzz with controversial topics like atheism, meaninglessness of evolution and race and gender differences(for eg.  in IQ) and people defend these sacred dictum doggedly, claiming that 'is' and 'ought' need not be confused, especially in a cold, logical science which deals with all facts and should not be guided by values. Yet, the same blogosphere generally silently ignores, or does not take a stand , when the 'is' and 'ought' are in sync and something morally significant is also found to be scientifically valid. Rather the apology for such facts is made very cautiously, with the spirit of not offending the people who have a different, and in my view, an inferior moral system.

I believe whenever people discuss poverty/SES, they have either of the two moral systems: first, the world is unfair and poor people are poor because of some external factors/ circumstances; addressing them may solve/ eliminate the problem of poverty;  and second: the world is fair (like an idealized free market) and if someone is poor they are due to either inherent internal flaws (bad genes) or maybe bad choices (they want to be poor/ are lazy and unindustrious etc); so the problem of poverty cannot/ should not be solved.  I subscribe to the first moral system and believe in interventions to solve the problem of poverty. I am glad to have scientific facts to my side and have been addressing these issues in a series of posts .

The latest impetus to write on the topic comes form reading Lehrer's post titled Poverty and the brain at the Frontal cortex and I am glad to have found a fellow blogger who doesn't mind speaking on such controversial topics and take a stand for 'is' that is in sync with 'ought'. It is an excellent post regarding how early interventions can help alleviate poverty and how a poor person suffers from the viscous circle of poverty by the mediating influence of brain and IQ.

Lehrer also mentions the work of Martha Farah (of Visual Agnosia fame whose earlier work was on vision) on the same and I recommend reading at least this article by Martha and colleagues, although many other invaluable gems are present on her site.

The article begins with an anecdotal reference to how Martha first became aware of the gravity of the issue, when she saw her babysitters / maids steeped in poverty and the low IQ and SES viscous circle. this resonates with me and I can easily relate to this as my child enjoys a lot of toys while our maid's children are faced with lack.

I would now quote extensively from the aforementioned article:

It seemed to me that children’s experience of the world is very different in low and middle SES environments. Most middle SES children have abundant opportunities to explore the world, literally, in terms of people met and places seen, and figuratively, in terms of the world of ideas. In contrast, low SES children generally have fewer interactions with the wider world and much of what they do experience is stressful. Basic research with animals has established the powerful effects of both environmental impoverishment and stress on the developing brain.

She then goes on to make out the case for NCC of poverty:

For the sake of exploring the cognitive neuroscience perspective on transgenerational poverty, and discovering what, if anything, it can contribute to correcting socioeconomic inequality, the first order of business is to ask whether socioeconomic status bears any straightforward relation to brain development. On the face of things it might seem unlikely that characteristics such as income, education and job status, which are typically used to estimate SES, would bear any systematic relationship to physiological processes such as those involved in brain development. It is, however, well established that SES affects physical health through a number of different causal pathways (Adler et al. 1994), many of which could play a role in brain development. It is also clear that poverty is associated with differences in brain function on the basis of the differences in standardized test performance cited earlier, as cognitive tests reflect the function of the brain. However, for a cognitive neuroscience approach to be helpful, the relations between socioeconomic status and the brain must be relatively straightforward and generalizable. The first question that my collaborators and I addressed was therefore: Can we generalize about the neurocognitive correlates of socioeconomic status? Once we have established the neurocognitive profile of childhood poverty, we can begin to test more specific hypotheses about causal mechanisms.

I will now digress a little from the main topic and introduce the five neurocognitive systems that Martha and colleagues have identified and how they tested some children from low and middle SES for finding their capabilities in these systems.

The children were tested on a battery of tasks adapted from the cognitive neuroscience literature, designed to assess the functioning of five key neurocognitive systems. These systems are described briefly here.

• The Prefrontal/Executive system enables flexible responding in situations where the appropriate response may not be the most routine or attractive one, or where it requires maintenance or updating of information concerning recent events. It is dependent on prefrontal cortex, a late-maturing brain region that is disproportionately developed in humans.

• The Left perisylvian/Language system is a complex, distributed system encompassing semantic, syntactic and phonological aspects of language and dependent predominantly on the temporal and frontal areas of the left hemisphere that surround the Sylvian fissure.

• The Medial temporal/Memory system is responsible for one-trial learning, the ability to retain a representation of a stimulus after a single exposure to it (which contrasts with the ability to gradually strengthen a representation through conditioning-like mechanisms), and is dependent on the hippocampus and related structures of the medial temporal lobe.

• The Parietal/Spatial cognition system underlies our ability to mentally represent and manipulate the spatial relations among objects, and is primarily dependent upon posterior parietal cortex.

• The Occipitotemporal/Visual cognition system is responsible for pattern recognition and visual mental imagery, translating image format visual representations into more abstract representations of object shape and identity, and reciprocally translating visual memory knowledge into image format representations (mental images).

Not surprisingly, in view of the literature on SES and standardized cognitive tests, the middle SES children performed better than the low SES children on the battery of tasks as a whole. For some systems, most notably the Left perisylvian/Language system and the Prefrontal/Executive system, the disparity between low and middle SES kindergarteners was both large and statistically significant.

Thus, they found, in a small group of children , that Language and Executive systems' performance differed in low and middle SES children and they were able to replicate this finding with a larger group of children too. This time they broke executive function further into components and found a finer granularity of how SES affects the brain:

As before, the language system showed a highly significant relationship to SES, as did executive functions including Lateral prefrontal/Working memory and Anterior cingulate/Cognitive control components and the Parietal/Spatial cognition system. With a more demanding delay between exposure and test in the memory tasks, we also found a difference in the Medial temporal/Memory system. Performance on the Parietal/spatial system tests also differed as a function of SES.

They also did some studies with older children and to summarize the results of all these studies in their own words:

In sum, although the outcome of each study was different, there were also commonalities among them despite different tasks and different children tested at different ages. The most robust neurocognitive correlates of SES appear to involve the Left perisylvian/Language system, the Medial temporal/Memory system (insofar as SES effects were found in both studies that tested memory with an adequate delay) and the Prefrontal/Executive system, in particular its Lateral prefrontal/Working memory and Anterior cingulate/Cognitive control components. Children growing up in low SES environments perform less well on tests that tax the functioning of these specific systems.

Next they look at the causal versus correlational nature of findings and if causal, then the directions of causality. It is this paragraph , that amazed me, for they seem to be apologetic for the fact that their findings are also ethically good ones.

Do these associations reflect the effects of SES on brain development, or the opposite direction of causality? Perhaps families with higher innate language, executive and memory abilities tend to acquire and maintain a higher SES. Such a mechanism seems likely, a priori, as it would be surprising if genetic influences on cognitive ability did not, in the aggregate, contribute to individual and family SES. However, it seems also seems likely that causality operates in the opposite direction as well, with SES influencing cognitive ability through childhood environment. Note that the direction of causality is an empirical issue, not an ethical one. The issue of whether and to what extent SES differences cause neurocognitive differences or visa versa should not be confused with the issue of whether we have an obligation to help children of any background become educated, productive citizens.

Then, quite important from this blog's point of view, they review the literature that supports SES to IQ direction of causality.

Cross-fostering studies of within- and between -SES adoption suggest that roughly half the IQ disparity in children is experiential (Capron & Duyme, 1989; Schiff & Lewontin, 1986). If anything, these studies are likely to err in the direction of underestimating the influence of environment because the effects of prenatal and early postnatal environment are included in the estimates of genetic influences in adoption studies. A recent twin study by Turkheimer and colleagues (2003) showed that, within low SES families, IQ variation is far less genetic than environmental in origin. Additional evidence comes from studies of when, in a child’s life, poverty was experienced. Within a given family that experiences a period of poverty, the effects are greater on siblings who were young during that period (Duncan et al. 1994), an effect that cannot be explained by genetics. In sum, multiple sources of evidence indicate that SES does indeed have an effect on cognitive development, although its role in the specific types of neurocognitive system development investigated here is not yet known.

Next they tried to tease out what specific SES related factors can affect the different neurocognitive systems. They list both physical and psychological factors that have been hypothesized and researched on in relation to SES and IQ.

Potential causes, physical and psychological

What aspects of the environment might be responsible for the differences in neurocognitive development between low and middle SES children? A large set of possibilities exist, some affecting brain development by their direct effects on the body and some by less direct psychological mechanisms. Three somatic factors have been identified as significant risk factors for low cognitive achievement by the Center for Children and Poverty (1997): inadequate nutrition, substance abuse (particularly prenatal exposure), and lead exposure.

As with potential physical causes, the set of potential psychological causes for the SES gap in cognitive achievement is large, and the causes are likely to exert their effects synergistically. Here we will review research on differences in cognitive stimulation and stress.

They then discuss the psychological factors, which they then investigated, in more detail.

One difference between low and middle SES families that seems predictable, even in the absence of any other information, is that low SES children are likely to receive less cognitive stimulation than middle SES children. Their economic status alone predicts that they will have fewer toys and books and less exposure to zoos, museums and other cultural institutions because of the expense of such items and activities. This is indeed the case (Bradley et al. 2001a) and has been identified as a mediator between SES and measures of cognitive achievement (Bradley and Corwyn 1999; Brooks-Gunn and Duncan 1997; McLoyd 1998). Such a mediating role is consistent with the results of neuroscience research with animals. Starting many decades ago (e.g., Volkmar & Greenough, 1972) researchers began to observe the powerful effects of environmental stimulation on brain development. Animals reared in barren laboratory cages showed less well developed brains by a number of different anatomical and physiological measures, compared with those reared in more complex environments with opportunities to climb, burrow and socialize (see van Praag et al 2000 for a review).

The lives of low SES individuals tend to be more stressful for a variety of reasons, some of which are obvious: concern about providing for basic family needs, dangerous neighborhoods, and little control over one’s work life. Again, research bears out this intuition: Turner and Avison (2003) confirmed that lower SES is associated with more stressful life events by a number of different measures. The same appears to be true for children as well as adults, and is apparent in salivary levels of the stress hormone cortisol (Lupien et al. 2001).

Why is stress an important consideration for neurocognitive development? Psychological stress causes the secretion of cortisol and other stress hormones, which affect the brain in numerous ways (McEwen 2000). The immature brain is particularly sensitive to these effects. In basic research studies of rat brain development, rat pups are subjected to the severe stress of prolonged separation from the mother and stress hormone levels predictably climb. The later anatomy and function of the brain is altered by this early neuroendocrine phenomenon. The brain area most affected is the medial temporal area needed for memory, although prefrontal systems involved in the regulation of the stress response are also impacted (Meaney et al. 1996).

They then go on to discuss how this information can be used to formulate mechanisms that mediate the effect of low SES on diffrent neurocognitive systems.

The latest phase of our research is an attempt to make use of the description of the SES disparities in neurocognitive development in testing hypotheses about the causal pathways. Drawing on our previous research that identified three neurocognitive systems as having the most robust differences as a function of SES (Perisylvian/Language, Medial temporal/Memory, and Prefrontal/Executive), we are now testing hypotheses concerning the determinants of individual differences in the development of these systems in children of low SES. Specifically, we are investigating the role of childhood cognitive stimulation and social/emotional nurturance (Farah et al. 2005; Childhood experience and neurocognitive development: Dissociation of cognitive and emotional influences).

They then describe an observational study of interaction between children and parents and how they assess the cognitive simulation an social/emotional nurturance using HOME assessment battery. What they found follows:

Children’s performance on the tests of Left perisylvian/Language was predicted by average cognitive stimulation. This was the sole factor identified as predicting language ability by forward stepwise regression, and one of three factors identified by backwards stepwise regression, along with the child’s gender and the mother’s IQ. In contrast, performance on tests of Medial temporal/Memory ability was predicted by average social/emotional nurturance. This was the sole factor identified as predicting memory ability by forward stepwise regression and one of three factors identified by backwards stepwise regression, along with the child’s age and cognitive stimulation. The relation between memory and early emotional experience is consistent with the animal research cited earlier, showing a deleterious effect of stress hormones on hippocampal development. Our analyses did not reveal any systematic relation of the predictor variables considered here to Lateral prefrontal/Working memory or Anterior cingulate/Cognitive control function. In conclusion, different aspects of early experience affect different systems of the developing brain. Cognitive stimulation influences the development of language, whereas social/emotional nurturance affects the development of memory but not language.

Here is what they conclude:

What are the implications for society of a more mechanistic understanding of the effects of childhood poverty on brain development? To different degrees, and in different ways, we regard children as the responsibility of both parents and society. Parents’ responsibility begins before birth and encompasses virtually every aspect of the child’s life. Society’s responsibility is more circumscribed. In the United States, for example, society’s contribution to the cognitive development of children begins at age 5 or 6, depending on whether public kindergarten is offered. The physical health and safety of all infants and children is a social imperative, however, well before school age. Laws requiring lead abatement in homes occupied by children exemplify our societal commitment to protect them from the neurological damage caused by this neurotoxin. Research on the effects of early life stress and limited cognitive stimulation has begun to show that these concomitants of poverty have negative effects on neurological development too, by mechanisms no less concrete and real. Thus, neuroscience may recast the disadvantages of childhood poverty as a bioethical issue rather than merely one of economic opportunity.

In my view the societal implications are far reaching, if low SES leads to lowered cognitive functioning, it becomes our duty to provide more cognitive stimulation and ensure that all children get sufficient social/ emotional nurturance so that their IQ can flower to its full potential.

I would have liked to end on this note, but cant help pointing that the five neurocognitive systems Martha has identified, to me seems to follow in stages, with the later systems maturing later :

1) Occipital/ visual : describe/ perceive the world/ self
2) Parietal/ spatial:explain the world/self (may be involved in consciousness)
3) Temporal/ Memory: predict the world/self
4) Frontal/ executive: control the world/ self
5) Sylvian/ Language: improve the world/ self


We all know that language abilities develop the oldest and vision is more or less developed at birth; also the fact that SES should affect the latter stages of neurocognitive systems also gels in. the fact that cognitive stimulation affects language and emotional/social nurturance affects memory to me also fits in.

Anyway whatever the implication sof this research for stage theories, they have far reaching and imprortanat implications for social policy and education.

Farah, M.J.,Noble, K.G. and Hurt, H. (2005). Poverty, privilege and brain development: Emprical findings and ethical implications. In J. Illes (Ed.) Neuroethics in the 21st Century. New York: Oxford University Press.

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