Major conscious and unconcoscious processes in the brain

Today I plan to touch upon the topic of consciousness (from which many bloggers shy) and more broadly try to delineate what I believe are the important different conscious and unconscious processes in the brain. I will be heavily using my evolutionary stages model for this.

To clarify myself at the very start , I do not believe in a purely reactive nature of organisms; I believe that apart from reacting to stimuli/world; they also act , on their own, and are thus agents. To elaborate, I believe that neuronal groups and circuits may fire on their own and thus lead to behavior/ action. I do not claim that this firing is under voluntary/ volitional control- it may be random- the important point to note is that there is spontaneous motion.

1. Sensory system: So to start with I propose that the first function/process the brain needs to develop is to sense its surroundings. This is to avoid predators/ harm in general. this sensory function of brain/sense organs may be unconscious and need not become conscious- as long as an animal can sense danger, even though it may not be aware of the danger, it can take appropriate action - a simple 'action' being changing its color to merge with background. 
   
2. Motor system:The second function/ process that the brain needs to develop is to have a system that enables motion/movement. This is primarily to explore its environment for food /nutrients. Preys are not going to walk in to your mouth; you have to move around and locate them. Again , this movement need not be volitional/conscious - as long as the animal moves randomly and sporadically to explore new environments, it can 'see' new things and eat a few. Again this 'seeing' may be as simple as sensing the chemical gradient in a new environmental.
3. Learning system: The third function/process that the brain needs to develop is to have a system that enables learning. It is not enough to sense the environmental here-and-now. One needs to learn the contingencies in the world and remember that both in space and time. I am inclined to believe that this is primarily pavlovaion conditioning and associative learning, though I don't rule out operant learning. Again this learning need not be conscious- one need not explicitly refer to a memory to utilize it- unconscious learning and memory of events can suffice and can drive interactions. I also believe that need for this function is primarily driven by the fact that one interacts with similar environments/con specifics/ predators/ preys and it helps to remember which environmental conditions/operant actions lead to what outcomes. This learning could be as simple as stimuli A predict stimuli B and/or that action C predicts reward D .
4. Affective/ Action tendencies system .The fourth function I propose that the brain needs to develop is a system to control its motor system/ behavior by making it more in sync with its internal state. This I propose is done by a group of neurons monitoring the activity of other neurons/visceral organs and thus becoming aware (in a non-conscious sense)of the global state of the organism and of the probability that a particular neuronal group will fire in future and by thus becoming aware of the global state of the organism , by their outputs they may be able to enable one group to fire while inhibiting other groups from firing. To clarify by way of example, some neuronal groups may be responsible for movement. Another neuronal group may be receiving inputs from these as well as say input from gut that says that no movement has happened for a time and that the organism has also not eaten for a time and thus is in a 'hungry' state. This may prompt these neurons to fire in such a way that they send excitatory outputs to the movement related neurons and thus biasing them towards firing and thus increasing the probability that a motion will take place and perhaps the organism by indulging in exploratory behavior may be able to satisfy hunger. Of course they will inhibit other neuronal groups from firing and will themselves stop firing when appropriate motion takes place/ a prey is eaten. Again nothing of this has to be conscious- the state of the organism (like hunger) can be discerned unconsciously and the action-tendencies biasing foraging behavior also activated unconsciously- as long as the organism prefers certain behaviors over others depending on its internal state , everything works perfectly. I propose that (unconscious) affective (emotional) state and systems have emerged to fulfill exactly this need of being able to differentially activate different action-tendencies suited to the needs of the organism. I also stick my neck out and claim that the activation of a particular emotion/affective system biases our sensing also. If the organism is hungry, the food tastes (is unconsciously more vivid) better and vice versa. thus affects not only are action-tendencies , but are also, to an extent, sensing-tendencies.
5. Decisional/evaluative system: the last function (for now- remember I adhere to eight stage theories- and we have just seen five brain processes in increasing hierarchy) that the brain needs to have is a system to decide / evaluate. Learning lets us predict our world as well as the consequences of our actions. Affective systems provide us some control over our behavior and over our environment- but are automatically activated by the state we are in. Something needs to make these come together such that the competition between actions triggered due to the state we are in (affective action-tendencies) and the actions that may be beneficial given the learning associated with the current stimuli/ state of the world are resolved satisfactorily. One has to balance the action and reaction ratio and the subjective versus objective interpretation/ sensation of environment. The decisional/evaluative system , I propose, does this by associating values with different external event outcomes and different internal state outcomes and by resolving the trade off between the two. This again need not be conscious- given a stimuli predicting a predator in vicinity, and the internal state of the organism as hungry, the organism may have attached more value to 'avoid being eaten' than to 'finding prey' and thus may not move, but camouflage. On the other hand , if the organisms value system is such that it prefers a hero's death on battlefield , rather than starvation, it may move (in search of food) - again this could exist in the simplest of unicellular organisms.

Of course all of these brain processes could (and in humans indeed do) have their conscious counterparts like Perception, Volition,episodic Memory, Feelings and Deliberation/thought. That is a different story for a new blog post!

And of course one can also conceive the above in pure reductionist form as a chain below:

sense-->recognize & learn-->evaluate options and decide-->emote and activate action tendencies->execute and move.

and then one can also say that movement leads to new sensation and the above is not a chain , but a part of cycle; all that is valid, but I would sincerely request my readers to consider the possibility of spontaneous and self-driven behavior as separate from reactive motor behavior. 

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Child Psychology: The Mouse Trap turns 3

The Mouse Trap turns 3 today. It was exactly three years and 334 posts earlier that the Mouse Trap was born. The Mouse Trap has indeed learnt to walk on its own and has also developed adequate linguistic skills in the meantime. The toddler years are all but over, as it now becomes more playful and enters play age of early childhood. Already people are demanding that it not be developmentally delayed, but start indulging in rich imaginative pretend play with topics being requested like symbolic interactionsim and social epistemology.

Some stock taking and reality check is in store. The wiki page on toddler lists the following last milestones for 25-36 months and I hope the Mouse trap is doing fine. To recap:

1. Speaking in sentences: Hopefully the strands of mouse trap blog posts now form more cohesive sentences (like the theme of autism-psychosis, stage theories etc) and are not disjointed phrases and one-off utterances.
2. Ability to be independent to primary care giver: I hope that the reader partcipation has increased and with more reader participatory initiatives like Skribit suggestions, Google FriendConnect etc., the Mouse Trap is able to become more and more independent of its primary caregiver, that is me, and instead make deep attachments with other secondary caregivers like its prized readers and subscriber base.
3. Easily learns new words, places and people's names: Hopefully as the Mouse trap matures, it is learning to expand its horizons and foraying into topics left hitherto untouched; with better reader connect features , like twitter/Frinedfeed etc it is surely remembering peoples names and where they come form!
4. Anticipates routines: The mouse trap hopefully has learnt to anticipate the routine articles and topics that its readership likes to read and is doing a decent job on that score. do suggest your topics if the mouse trap doesn't anticipate them!
5. Toilet learning continues : Once th emouse trap might have been suffering from blogorrehea, but now it knows that passing motion (posting articles) once a week is adequate enough an dthat one should write a article only when one is full of it! There does exist scope for more routinized daily motion passing though!!
6. Plays with toys in imaginative ways: I am experimenting a lot with social media (my favorite web 2.0 toy) so as to engage more readers in a conversation. If you have any imaginative ideas of how to play with this toy, do let me know!!
7. Attempts to sing in-time with songs: Hopefully, the mouse trap has learnt to sing in tune with the zeitgeist of the day; though here I believe Mouse trap more has an original, unsynchronised with others voice and singing profile. Hope to change that and be more in sync with what others in the science blogosphere are singing (but definitely not the atheism/evolution debate which just bores me)

So, the Mouse trap is just about doing fine. It has been consistently featured in wikio top 100 science blogs, is amongst the top 5 blogs in India as ranked by Indiblogger.in, has a google page rank of 6 and has a subscriber base of close to 450 dedicated RSS feed subscribers, besides those that visit it daily on web via search. Also , the twitter followers of @sandygautam are increasing steadily and have reached 450 and the rate at which they are growing it seems they'll grow way beyond the Mouse trap feed subscribers. With micro-blogging and twitter/ FriendFeed, I have found a new way to share links and ideas and deepen conversations and connect with my readers, that was not possible with just the Mouse Trap.



I would also like to take this opportunity to encourage all feed subscribers to join me at twitter (@sandygautam) to keep up to date on links that I don't find exciting enough to write a blog post about or do not have much to add to, but which still are related to theme of what I write about and would make for a good read and need to be shared. I would also encourage new as well as veteran readers and subscribers, just for today,  to visit the mouse trap blog on the web and not in their feed readers (to celebrate its B'day, you are invited to the party at the web) so that they can become familiar with new social media tools I have put together on the Mouse Trap blog, like the 'recommended by readers' widget, the 'top posts by PostRank' widget or the 'suggest topics to write' widget.

Lastly as a primary caregiver, though my investment in the mouse trap has been more and my pride consequently in its progress has been immense; I must also thank all the other caregivers like you , the reader, or the peers like the other science blogs that have provided a safe and playful environment in which the Mouse Trap could flower or learn by peer play/ imitation learning. You all are a part and parcel of the Mouse Trap blog, so thanks everyone and take pride in your child's development and maturation and now that it becomes more independent come forward and supplant the primary caregiver and let it achieve its full potential! Amen!

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Children not mini-adults, at least in cognitive control

A predominant, but unstated, thinking that biases many research paradigms is the assumption that children are just mini-adults with less well developed mechanisms than adults, but fundamentally using and relying on the same unitary cognitive mechanisms as the adults use. this has proven time and again wrong, and better psychologists now agree that children view the world in a fundamentally different manner from adults. I have covered some research in the past that showed for example that while differentiating between two color hues (categorical color perception), children show a more right hemisphere domination (non-verbal); while adults rely on Left hemisphere (verbal knowledge). Over development the RH processes are shadowed by the maturing LH verbal process, as far as it relates to Categorical Perception.

This recent PNAS article , by none other than the famed Chris Catham of the Developing Intelligence fame, is an effort in the same direction, showing that children use a different mechanism than adults when it comes to using cognitive control. while Adults use a more proactive cognitive control, the children rely on a reactive cognitive control. The authors do a good job of describing the proactive and reactive cognitive control so over to them:

Although sometimes derided as ‘‘creatures of habit,’’ humans develop an unparalleled ability to adaptively control thought and behavior in accordance with current goals and plans. Dominant theories of cognitive control suggest that this flexibility is enabled by the proactive regulation of behavior through sustained inhibition of inappropriate thoughts and actions , the active biasing of task-relevant thoughts, or construction of rule-like representations. Theories of the developmental origins of cognitive control converge in positing that children engage these same proactive processes, but in a weaker form, with less strength or stability , less resistance toward habitual responses, or degraded complexity.
...
However, children can be notoriously constrained to the present, raising the possibility that the temporal dynamics of immature cognitive control are fundamentally different from that of adults. Specifically, we hypothesized that young children may show ‘‘reactive’’ as opposed to ‘‘proactive’’ context processing , characterized by a failure to proactively prepare for even the predictable future and a tendency to react to events only as they occur, retrieving information from memory as needed in the moment. For lack of age-appropriate methods, the possibility of this qualitative developmental shift has not been directly tested.

They also describe the paradigm used beautifully so again quoting from the article:

In the AX-CPT, subjects provide a target response to a particular probe (‘‘X’’) if it follows a specific contextual cue (‘‘A’’). Nontarget responses are provided to other cue–probe sequences (‘‘A’’ then ‘‘Y,’’ ‘‘B’’ then ‘‘X,’’ or ‘‘B’’ then ‘‘Y’’), each occurring with lower probability than the target pair. This asymmetry in trial type frequency is critical for revealing distinct behavioral profiles for proactive versus reactive control. Proactive control supports good BX trial performance at the expense of AY trials. Maintenance of the ‘‘B’’ cue supports a nontarget response to the subsequent ‘‘X’’ probe; however, maintenance of the ‘‘A’’ cue leads to anticipation of an X and thus a target response (due to the expectancy effect cultivated by the asymmetry in trial type frequencies), which can lead to false alarms in AY trials . Reactive control leads to the opposite pattern. The preceding cue is retrieved when needed, that is, in response to ‘‘X’’ probes but not to ‘‘Y’’ probes. Such retrieval renders BX trials vulnerable to retrieval-based interference; the lack of such retrieval on AY trials means that false alarms are less likely in this case. Similarly, proactive control should lead to increased delay-period effort, whereas reactive control should lead to increased effort to probes.

What they found was consistent with their hypothesis. The reaction time data, the effort data gauged from puppilometry, the speed-accuracy trade off data all pointed to the fact that children used a reactive cognitive control mechanism while adults used a proactive cognitive control mechanism. This what they conclude:

By dissociating proactive and reactive control mechanisms in children, our findings call into question a previously untested assumption of developmental theories of cognitive control, that is, relative to young adults, weaker but qualitatively similar control processes guide the task performance of children. Of course, children and even infants may be capable of sustaining context representations over shorter delays than the 1.2 s used here, but such limited proactive mechanisms would seem unlikely to strongly influence most behaviors.

Further research is needed to determine the processes that drive the developmental transition from reactive to proactive control. This qualitative shift could reflect genuinely qualitative changes, for example, in metacognitive strategies that allow children to engage proactive control. Alternatively (or additionally), the underlying mechanisms for this qualitative shift could be continuous. For example, the gradual strengthening of task-relevant representations could allow proactive control to become effective, thus supporting a shift in the temporal dynamics of control. In any case, the developmental progression to be addressed is a shift from reactive to proactive control rather than merely positing incremental improvements with development.

I think these are steps in the right direction; I lean towards a stage theory account of development so am supportive of a dramatic developmental stage whereby reactive cognitive control mechanisms are replaced by proactive ones, although both strategies may be available to the critical age children equally. However, it may be the case that the neural architecture for proactive CC develops late (just like linguistic CP) and overrides the default reactive CC circuit. that dominance of Proactive CC over reactive CC to me should mark an important developmental stage.

Thanks Chris, for your wonderful blog posts and this paper!



Chatham, C., Frank, M., & Munakata, Y. (2009). Pupillometric and behavioral markers of a developmental shift in the temporal dynamics of cognitive control Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0810002106

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SES and the developing brain

I have written about poverty/SES and its effects on brain development/IQ earlier too,and this new review article by Farah and Hackman in TICS is a very good introduction to anyone interested in the issue.

The article reviews the behavioral studies that show that SES is correlated with at least the two brain systems of executive function and language abilities.It also review physiological data that shows that even when behavioral outcomes do not differ ERP can show differential activation in the brains of people with low and middle SES , thus suggesting that differences that may not be detected on behavioral measures may still exist. They also review (f)MRI data that shows no structural differences in the brains of low and middle SES children, but definite functional differences.they also review experimental manipulation of social status in labarotaories, and show how those studies also indicate that SES and executive function are correlated.

They then turn to the million dollar question of the direction of causality and for this infer indirectly based on the SES-IQ causal linkages.

What is the cause of SES differences in brain function? Is it contextual priming? Is it social causation, reflecting the influence of SES on brain development? Alternatively, is it social selection, in which abilities inherited from parents lead to lower SES? Current research on SES and brain development is not designed to answer this question. However, research on SES and IQ is relevant and supports a substantial role of SES and its correlated experience as causal factors.

Slightly less than half of the SES-related IQ variability in adopted children is attributable to the SES of the adoptive family rather than the biological. This might underestimate environmental influences because the effects of prenatal and early postnatal environment are included in the estimates of genetic influence. Additional evidence comes from studies of when poverty was experienced in a child's life. Early poverty is a better predictor of later cognitive achievement than poverty in middle- or late-childhood, an effect that is difficult to explain by genetics. SES modifies the heritability of IQ, such that in the highest SES families, genes account for most of the variance in IQ because environmental influences are in effect at ceiling in this group, whereas in the lowest SES families, variance in IQ is overwhelmingly dominated by environmental influences because these are in effect the limiting factor in this group. In addition, a growing body of research indicates that cognitive performance is modified by epigenetic mechanisms, indicating that experience has a strong influence on gene expression and resultant phenotypic cognitive traits . Lastly, considerable evidence of brain plasticity in response to experience throughout development indicates that SES influences on brain development are plausible.

Differences in the quality and quantity of schooling is one plausible mechanism that has been proposed. However, many of the SES differences summarized in this article are present in young children with little or no experience of school , so differences in formal education cannot, on their own, account for all of the variance in cognition and brain development attributable to SES. The situation is analogous to that of SES disparities in health, which are only partly explained by differential access to medical services and for which other psychosocial mechanisms are important causal factors .

The last point is really important and can be extended. Access to health services for low SES people may be a reason why , for eg, more schizophrenia incidence is found in low SES neighbourhoods. which brings us to the same chicken-and-egg question of the drift theory of schizophrenia- whether people with schizophrenia drift into low SES or low SES is a risk factor in itself. Exactly this point was brought to my attention when I was interacting with a few budding psychiatrists recently, this Martha Farah theory about the SES leading to lower IQ/ cognitive abilities. It is important to acknowledge that low SES not only leads to left hypo-frontality (another symptom of schizophrenia), schizophrenia is supposed to be due to lessened mylienation and again nutritional factors may have a role to play; also access to health care, exposure to chronic stress and lesser subjective feelings of control may all be mediating afctors that lead low SS to lead to schizophrenia/ psychosis.Also remember that schizophrenia is sort of a devlopmenetal disorder.

Well, I digressed a bit, but the idea is that not only does low SES affect 'normal' cognitive abilities, it may even increase the risk for 'abnormal' cognitive abilities that may lead to psychosis, and his effect of SES on IQ/cognitive abilities/ risk of mental diseases is mediated by the effect of SES on the developing brain. I have already covered the putative mechanisms by which SES may affect brain development, but just to recap, here I quote from the paper:

Candidate causal pathways from environmental differences to differences in brain development include lead exposure, cognitive stimulation, nutrition, parenting styles and transient or chronic hierarchy effects. One particularly promising area for investigation is the effect of chronic stress. Lower-SES is associated with higher levels of stress in addition to changes in the function of physiological stress response systems in children and adults. Changes in such systems are likely candidates to mediate SES effects as they impact both cognitive performance and brain regions, such as the prefrontal cortex and hippocampus, in which there are SES differences.

We can only hope that the evil of low SES is recognized as soon as possible and if for nothing else, than for advancing science, some intervention studies are done that manipulate the SES variables in the right direction and thus ensure that the full cognitive potential of the children flowers.



HACKMAN, D., & FARAH, M. (2009). Socioeconomic status and the developing brain Trends in Cognitive Sciences, 13 (2), 65-73 DOI: 10.1016/j.tics.2008.11.003

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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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The stage theories: are they all fiction?

I normally do not like to thrash articles or opinion pieces, but this article by Michael Shermer, in the Scientific American, has to be dealt with as it as masquerading as an authoritative debunking by one of the foremost skeptics in one of the most respected magazines. Yet, it is low on science and facts and is more towards opinions, biases and prejudices.

Shermer, from the article seems to be generally antagonistic to stage theories as he thinks they are mere narratives and not science. The method he goes about discrediting stage theories is to lump all of them together (from Freud's' theories to Kohlberg's theories), and then by picking up on one of them (the stages of grief theory by Kubler-Ross) he tries to discredit them all. This is a little surprising. While I too believe (and it is one of the prime themes of this blog) that most of the stage theories have something in common and follow a general pattern, yet I would be reluctant to club developmental stage theories that usually involve stages while the child is growing; to other stage theories like stages of grief, in which no physical development is concurrent with the actual stage process, but the stages are in adults that have faced a particular situation and are trying to cope with that situation. In the former case the children are definitely growing and their brains are maturing and their is a very real substrate that could give rise to distinctive stages; in the latter case the stages may not be tied so much to development of the neural issue; as much they are to its plasticity; the question in latter case would be viz does the brain adapt to losses like a catastrophic news, death of loved one etc by reorganizing a bit and does the reorganizing happen in phases or stages. The two issues of childhood development and adult plasticity are related , but may be different too. With adult neurogenisis now becoming prominent I wont be surprised if we find neural mechanisms for some of these adult stages too, like the stages of grief, but I would still keep the issues different.

Second , assuming that Shermer is right and that at the least the stage theory of grief, as proposed by Kubler-Ross is incorrect; and also that it can be clubbed with other stage theories; would it be proper to conclude that all stage theories were incorrect based on the fact that one of them was incorrect/ false. It would be like that someone proposed a modular architecture of mind; and different modules for mind were proposed accordingly; but on of the proposed modules did not stood the scrutiny of time( lets say a module for golf-playing was not found in the brain); does that say that all theories that say that the brain is organized modularity for at least some functions are wrong and all other modules are proved non-existent. Maybe the grief stages theory is wrong, but how can one generalize from that to all developmental stage theories, many of them which have been validated extensively (like Paiget's theories) and go on a general rant against all things 'stages'!!

Next let me address another fallacy that Shermer commits; the causal analogy fallacy: that if two things are analogous than one thing is causing other , when in fact no directional inference can be drawn from the analogical space. He asserts that humans are pattern-seeking, story-telling primates who like to explain away there experiences with stories or narratives especially as it provides a structure over unpredictable and chaotic happenings. Now, I am all with Shermer up till this point and this has been my thesis too; but then he takes a leap here and says that this is the reason we come up with stage theories. Why 'stage' theories? Why not just theories? any theory, in as much as it is an attempt to provide a framework for understanding and explication is a potential narrative and perhaps anyone that tries to come up with a theory is guilty of story-telling by extension. The leap he is making here, is the assumption that story-telling is a 'stage' process and a typical story follows a pattern, which is, unfolding of plot in distinct stages.

Now, I agree with the leap too that Shermer is making- a narrative is not just any continuous thread of yarn that the author spins- it normally involves discrete stages and though I have not touched on this before, Christopher Brooks work that delineated the eight basic story plots also deals with the five -stage unfolding of plot in all the different basic story plots. so I am not contesting the fact that story-telling is basically a stage process with distinct stages through which the protagonist pass or distinct stages of plot development; what I am contesting is the direction of causality. Is it because we have evidence of distinct stages in the lives of individuals, and in general, evidence for the eight-fold or the five-fold stages of development of various faculties, that our stories reflect distinct stages as they unfold and the mono myth has a distinct stage structure; or is it because our stories have structures in the form of stages, that the theories we develop also have stages? I believe that some theorizing in terms of stages may indeed be driven by our desire to compartmentalize everything into eight or so basic stages and environmental adaptive problems we have encountered repeatedly and which have become part of our mythical narrative structure; but most parsimoniously or mythical narrative structure is stage bound, as we have observed regularities in our development and life that can only be explained by resorting to discrete stages rather than a concept to continuous incremental improvement/ development/ unfolding.

Before moving on, let me just give a brief example of the power of stage theories and how they can be traced to neural mechanisms. I'll be jumping from the very macro phenomenon I have been talking about to the very micro phenomenon of perception. One can consider the visuomotor development of a child. Early in life there is a stage when the oculomotor control is mostly due to sub cortical regions like superior colliculus and the higher cortical regions are not much involved (they are not sufficiently developed/ myelinated) . The retina of eye is such that the foveal region is underdeveloped; and all this combination means that infants are very good at orienting their eyes to moving targets in their peripheral vision, but are poor at colour and form discrimination. Also, they can perform saccades first, the capability to make antisaccades develops next and the capacity to make smooth pursuit movement comes later. There are distinct stages of oculomotor control that a child can move through and this would definitely affect its perception of the world. (for example on can recognize an disicrimintae based on form first and color later as the visual striated areas for these mature in that order. In sort, there are strong anatomical, physiological and psychological substrates for most of the developmental stage theories.

Now let me address, why Shermer, whom I normally admire, has taken this perverse position. It is because his Skeptic magazine recently published an article by Russell P. Friedman, executive director of the Grief Recovery Institute in Sherman Oaks, Calif. (www.grief-recovery.com), and John W. James, of The Grief Recovery Handbook (HarperCollins, 1998), which tried to debunk an article published by JAMA that found support for the five stage grief theory. Now, that Skeptic article had received a well-deserved thrashing by some reputed blogs, see this world Of Psychology post that exposes many of the holes in Friedman and James' argument, so possibly out of desperation Shermer though why not settle the scores and expose all stage theories as pseudoscience. Unfortunately he fails miserably in defending his publication and we have seen above why!

Now, let us come to the meat of the controversy: the stages of grief theory of Kubler-Ross for which the Yale group found evidence and which the Skeptics didn't like and found the evidence worth criticizing. I have read both the original JAMA paper and the skeptic article and see some merits to both side. In fact I guess the stance that Friedman et al have taken I even agree with to an extent, especially their decoupling of stages of grief from stages of dying person/ stages of adjustment to catastrophic death. Some excerpts:

IN 1969 THE PSYCHIATRIST ELIZABETH KÜBLER-ROSS wrote one of the most influential books in the history of psychology, On Death and Dying. It exposed the heartless treatment of terminally-ill patients prevalent at the time. On the positive side, it altered the care and treatment of dying people. On the negative side, it postulated the now-infamous five stages of dying—Denial, Anger, Bargaining, Depression, and Acceptance (DABDA), so annealed in culture that most people can recite them by heart. The stages allegedly represent what a dying person might experience upon learning he or she had a terminal illness. “Might” is the operative word, because Kübler-Ross repeatedly stipulated that a dying person might not go through all five stages, nor would they necessarily go through them in sequence. It would be reasonable to ask: if these conditions are this arbitrary, can they truly be called stages?

Many people have contested the validity of the stages of dying, but here we are more concerned with the supposed stages of grief which derived from the stages of
dying.

During the 1970s, the DABDA model of stages of dying morphed into stages of grief, mostly because of their prominence in college-level sociology and psychology courses. The fact that Kübler-Ross’ theory of stages was specific to dying became obscured.

Prior to publication of her famous book, Kübler-Ross hypothesized the Five Stages of Receiving Catastrophic News, but in the text she renamed them the Five Stages of Dying or Five Stages of Death. That led to the later, improper shift to stages of grief. Had she stuck with the phrase catastrophic news, perhaps the mythology of stages wouldn’t have emerged and grievers wouldn’t be encouraged to try to fit their emotions into non-existent stages.

I wholeheartedly concur with the authors that it is not good to confuse stages that a dying person may go through on receiving catastrophic death of terminal illness, with grief stages that may follow once one has learned of a loss and is coping with the loss(death of someone, divorce of parents etc); in the first case the event that is of concern is in the future and would lead to different tactics, than for the latter case when the event is already in the past and has occurred. thus, as rightly pointed by the authors, denial may make sense for dying people - 'the diagnosis is incorrect, I am not going to die; I have no serious disease.'; denial may not make sense for a loos of a loved one by death, as the vent has already happened and only a very disturbed and unable to cope person would deny the factuality of the event (death). but this is a lame point; in grief (equated with loss of loved one), they stage can be rightly characterized as disbelief/dissociation/isolation, whereby one would actively avoid all thoughts of the loved one's non-existence and come up with feelings like 'I still cannot believe that my mother is no longer alive' . Similarly My personal view is that while anger and energetic searching of alternatives may be the second stage response to catastrophic prospective forecast; the second stage response to a catastrophic news (news of a loss of loved one) would be more characterized by energized yearning for the lost one and an anger towards the unavoidable circumstances and the world in general that led to the loss.

The third stage is particularly problematic; in dying people it makes perfect sense to negotiate and bargain, as the event has not really happened ('I'll stop sinning, take away the cancer); but as rightly pointed out by the authors it doesn't make sense for events that have already happened.while many authoritative people have substituted yearning for the third stage in case of grief , I would propose that we replace that with regret or guilt. I know this would be controversial; but the idea is a bargaining of past events like 'God, please why didn't you take my life, instead of my young son' ; it doesn't make sense but is a normal stage of grieving - looking for and desiring alternative bad outcomes ('I wish I was dead instead of him'. The other two stages depression and acceptance do not pose as much problems, so I'll leave them for now. suffice it to say that becoming depressed / disorganized and then recovering/ becoming reorganized are normal stages that one would be expected to go through.

What I would now return is to their criticism of Kubler-Ross. They first attack her saying her evidence was anecdotal and based on personal feelings then , instead of correcting this gross error and themselves providing statistical and methodological research results, present anecdotal evidence based on their helping thousands of grieving persons.

Second they claim, that this stage based theories cause much harm; but I am not able to understand why a stage based theory must cause harm and , for all their good intentions, I think they are seriously confused here. On the one hand they claim (for eg in depression section) that stages lead to complacency:

It is normal for grievers to experience a lowered level of emotional and physical energy, which is neither clinical depression nor a stage. But when people believe depression is a stage that defines their sad feelings, they become trapped by the belief that after the passage of some time the stage will magically end. While waiting for the depression to lift, they take no actions that might help them.

and on the other hand they claim that labeling something causes over reactivity and over treatment:

When medical or psychological professionals hear grievers diagnose themselves as depressed, they often reflexively confirm that diagnosis and prescribe treatment with psychotropic drugs. The pharmaceutical companies which manufacture those drugs have a vested interest in sustaining the idea that grief-related depression is clinical, so their marketing supports the continuation of that belief. The question of drug treatment for grief was addressed in the National Comorbidity Survey published in the Archives of General Psychiatry,Vol. 64, April, 2007). “Criteria For Depression Are Too Broad Researchers Say—Guidelines May Encompass Many Who Are Just Sad.” That headline trumpeted the survey’s results, which observed more than 8,000 subjects and revealed that as many as 25% of grieving people diagnosed as depressed and placed on antidepressant drugs, are not clinically depressed. The study indicated they would benefit far more from supportive therapies that could keep them from developing full-blown depression.

Now, I am not clear what the problem is - is it complacency or too much concerns and over-treatment. And this argument they keep on repeating and hammering down - that stages do harm as them make people complacent that thing swill get better on its own and no treatment is needed. I don't think that is a valid assumption, we all know that many things like language develop, but their are critical times hen interventions are necessary for proper language to develop; so too is the case with grieving people, they would eventually recover, but they do need support of friends and family and all interventions, despite this being 'just a phase'. I don't think saying that someone would statistically go away in a certain time-period eases the effects one if feeling of the phenomenon right now. An analogy may help. It is statistically true, that on an average, within six months a person would get over his most recent breakup and start perhaps flirting again; that doesn't subtract from the hopelessness and feelings of futility he feels on teh days just following the breakup and most of the friends and family do provide support even though they know that this phase will get over. Same is true for other stages like stages of grief and the concerns of authors are ill-founded.

The concerns of the author that I did feel sympathetic too though was the stage concept being overused in therapy and feelings like guilt being inadvertently implanted in the clients by the therapists.

Grieving parents who have had a troubled child commit suicide after years of therapy and drug and alcohol rehab, are often told, “You shouldn’t feel guilty, you did everything possible.” The problem is that they weren’t feeling guilty, they were probably feeling devastated and overwhelmed, among other feelings. Planting the word guilt on them, like planting any of the stage words, induces them to feel what others suggest. Tragically, those ideas keep them stuck and limit their access to more helpful ideas about dealing with their broken hearts.

Therapists have to be really careful here and not be guided by pre-existing notions of how the patient is feeling. they should listen to the client and when in doubt ask questions, not implicitly suggest and assume things. That indeed is a real danger.

Lastly the criticism of stages/ common traits vs individual differences and uniqueness have to be dealt with. the claim that each grieves uniquely is not a novel claim and I do not find it lacking in evidence too. It is tautological. But still some common patterns can be elucidated and subsumed under stages. These stages are the 'normal' stages with enough room for individual aberration . I think there has to be more tolerance and acceptance of the 'abnormal' in general - if someone directly accepts and never feels and denial he too is abnormal - but one we readily accept as a resilient persons; the other who gets stuch at denial has to be shown greater care and hand-holded through the remaining stages to come to acceptance.

In the end I would like to briefly touch on the Yale study that reignited this controversy. Here is the summary of An Empirical Examination of the Stage Theory of Grief by Paul K. Maciejewski, PhD; Baohui Zhang, MS; Susan D. Block, MD; Holly G. Prigerson, PhD.

Context The stage theory of grief remains a widely accepted model of bereavement adjustment still taught in medical schools, espoused by physicians, and applied in diverse contexts. Nevertheless, the stage theory of grief has previously not been tested empirically.

Objective To examine the relative magnitudes and patterns of change over time postloss of 5 grief indicators for consistency with the stage theory of grief.

Design, Setting, and Participants Longitudinal cohort study (Yale Bereavement Study) of 233 bereaved individuals living in Connecticut, with data collected between January 2000 and January 2003.

Main Outcome Measures Five rater-administered items assessing disbelief, yearning, anger, depression, and acceptance of the death from 1 to 24 months postloss.

Results Counter to stage theory, disbelief was not the initial, dominant grief indicator. Acceptance was the most frequently endorsed item and yearning was the dominant negative grief indicator from 1 to 24 months postloss. In models that take into account the rise and fall of psychological responses, once rescaled, disbelief decreased from an initial high at 1 month postloss, yearning peaked at 4 months postloss, anger peaked at 5 months postloss, and depression peaked at 6 months postloss. Acceptance increased throughout the study observation period. The 5 grief indicators achieved their respective maximum values in the sequence (disbelief, yearning, anger, depression, and acceptance) predicted by the stage theory of grief.

Conclusions Identification of the normal stages of grief following a death from natural causes enhances understanding of how the average person cognitively and emotionally processes the loss of a family member. Given that the negative grief indicators all peak within approximately 6 months postloss, those who score high on these indicators beyond 6 months postloss might benefit from further evaluation.

I believe they have been very honest with their data and analysis. They found peak of denial, yearning, anger , depression and acceptance in that order. I belie they could have clubbed together anger and yearning together as the second stage as this study dealt with stages of grief and not stages of dying and should have introduced a new measure of regret/guilt and I predict that this new factors peak would be between the anger/yearning peak and depression peak.





Thus, to summarize, my own theory of grief and dying (in eth eight basic adaptive problems framework) are :

Stage theory of dying (same as Kubler-Ross):

1. Denial: avoiding the predator; as the predator (death ) cannot be avoided , it is denied!!
2. Anger/ Searching: Searching for resources; an energetic (and thus partly angry)efforts to find a solution to this over looming death; belief in pseudo-remedies etc.
3. Bargaining/ negotiating: forming alliances and friendships: making a pact with the devil...or the God ...that just spare me this time and I will do whatever you want in future.
4. Depression: parental investment/ bearing kids analogy: is it worth living/ bringing more people into this world?
5. Acceptance: helping kin analogy: The humanity is myself. even if I die, I live via others.

Stage theory of grief (any loss especially loss of a loved one)

1. Disbelief: Avoiding the predator (loss) . I cant believe the loss happened. Let me not think about it.
2. Anger/ Yearning: Energetic search for resources (reasons) . Why did it happen to me; can the memories and yearning substitute for the loved one?
3. Bargaining/ regret/ guilt: forming alliances and friendships: Could this catastrophe be exchanged for another? could I have died instead of him?
4. Depression: parental investment/ bearing kids analogy : is it worth living/ bringing more people into this world?
5. Acceptance: helping kin analogy: Maybe I can substitute the lost one with other significant others? Maybe I should be thankful that other significant persons are still there and only one loss has occurred.

Do let me know your thoughts on this issue. I obviously being a researcher in the stages paradigm was infuriated seeing the Shermer article,; others may have more balanced views. do let me know via comments, email!!



Paul K. Maciejewski, PhD; Baohui Zhang, MS; Susan D. Block, MD; Holly G. Prigerson, PhD (2007). An Empirical Examination of the Stage Theory of Grief JAMA, 297 (7), 716-723

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Blog Action Day: Poverty and IQ: from the archives

Well, today is blog action day 2008, and the topic for today is Poverty.

I am afraid I will be posting one of my old posts today: a post relating Poverty and SES to IQ and I am also publishing some relevant comments as the comment length generally exceeded the article length:-):

The post, comments and my response to comments are as follows; I would love to rekindle debate on SES/Poverty and IQ again and am looking for more discussions. Also please check out this earlier post on the simillar poverty and IQ topic:

Original Post: Is low IQ the cause of income inequality and low life expectancy or is it the other way round?

As per this post from the BPS research digest, Kanazawa of LSE has made a controversial claim that economic inequality is not the cause of low life expectancy, but that both low life expectancy and economic inequality are a result of the low IQ of the poor people. The self-righteous reasoning is that people with low IQ are not able to adapt successfully to the stresses presented by modern civilization and hence perish. He thinks he has data on his side when he claims that IQ is eight times more strongly related to life expectancy, than is socioeconomic status. What he forgets to mention(or deliberately ignores) is growing evidence that IQ is very much determinant on the socioeconomic environment of its full flowering and a low IQ is because of two components- a low genetic IQ of parent plus a stunted growth of IQ/intelligence due to impoverished environment available because of the low socio-economic status of the parents.

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. Also discussed there, is the fact that the modern civilization as a whole has been successful in archiving the sate of socioeconomic prosperity that is sufficient for the full flowering of inherent genetic IQ of a child and as such the increments in IQ as we progress in years and achieve more and more prosperity (the Flynn effect) has started to become less prominent. This fact also explains the Kanazawa finding that in 'uncivilized' sub-Saharan countries the IQ is not related to life expectancy, but socio-economic status is. although, he puts his own spin on this data, a more parsimonious ( and accurate) reason for this is that in the sub-Saharan countries, even the well -of don't have the proper socio-economic conditions necessary for the full flowering of IQ and thus the IQ of both the well-off and poor parents in these countries is stunted equally. Thus, the well-off (which are not really that well-off in comparison to their counterparts in the western countries) are not able to be in any more advantageous position (with respect to IQ) than the poor in these countries. The resultant life expectancy effect is thus limited to that directly due to economic inequality and the IQ mediated effect of economic inequality is not visible.

What Kanazawa deduces from the same data and how he chooses to present these findings just goes on to show the self-righteous WASP attitude that many of the economists assume. After reading Freakonomics, and discovering how the authors twist facts and present statistics in a biased manner to push their idiosyncratic theories and agendas, it hardly seems surprising that another economist has resorted to similar dishonest tactics - shocking people by supposedly providing hard data to prove how conventional wisdom is wrong. Surprisingly, his own highlighting of sub-Saharan counties data that shows that life-expectancy is highly dependent on socio-economic conditions in these countries is highly suggestive of the fact that in cultures where the effects og economic inequality are not mediated via the IQ effects, economic inequality is the strongest predictor of low life expectancy.

Instead of just blaming the people for their genes/ stupidity, it would be better to address the reasons that lead to low IQs and when they are tackled, directly address the social inequality problem , as in the author's own findings, when IQ is not to blame for the low life expectancy, the blame falls squarely on economic inequality (as in the sub-Saharan countries data) .

7 comments:

Asterion said...

First of all, I beg you pardon for my limited english.
I find quite interesting your findings. But there could be an issue which limits the reasoning: how the IQ is meassured? or what does it really meassures? Does it really defines how smart or clever a person is?
I think there must be a lot of denounces about it. So, I think it's important to recognize the limits of this aproach based on IQ meassurment limitants. Of course, there could be a reference in your and Kanazawa's articles (I have not seen none of them).
All of this is beacuse I have met childs quite smarts living in the poorest zones of my city (Bogotá,
Colombia), I would say all of them seems to be quite smart, at least form my point if view. They are all really quick undertanding abstract problems and linking things. I think they have a strong capability to analize any situation. So, if you are able to meassure their IQ using problems wich need, for instance, to apply Phitagora's theorem, surelly they will be in trouble. So I think education could explain better economic inequalities and, thus, low life expentacy.
I never have explored this issue, so I would thank you refering me to some relevant literature related. Even telling me if I am quite wrong or not.

Always learning...


Sandy G said...

Hi Julian,

I appreciate your thoughtful comments. It is true that intelligence consists of a number of factors (as large as 8-10 broad factors), and is also differentiated as crystallized(Gc) and fluid (Gf); but for most analysis a concept of a general underlying common factor , spearman's g, is taken as reflective of intelligence and measured by the IQ scores.

In this sense, IQ/g does reflect how clever or smart a person is, but success/outcome in life is affected by other factors like motivation, effort, creativity etc.

I agree that many children in impoverished environments are quite smart, but you would be surprised to discover how providing an enriched environment to them, at their critical developmental periods,would have resulted in lasting intelligence gains. They are smart, but could have been smarter, if they had the right socioeconomic environment. On the other hand, an average child from well-to-do family would be able to maximally develop its inherent capabilities and thus stand a stronger chance than the poor smart child, whose capabilities haven't flowered fully.

Cultural bias in IQ measures have been found in the past, but the field has vastly improved now and these biases are fast disappearing leading to more accurate and valid cross-cultural comparisons.

The key to remember here is that poor socio-economic condition affects longevity via multiple pathways- one of them is direct by limiting access to good health care and nutrition, but there are also indirect effects mediated by , as you rightly pointed, education (poor people get less education and not vice versa) and also intelligence.

Garett Jones said...

Two words: East Asia.

If bad social and economic outcomes were the key driver of low IQ, then we'd expect East Asians to have had low IQ's back when they were poor--say, back in the 50's and 60's. Check out Table 4 of my paper (page 28) to see if that's the case...

http://mason.gmu.edu/~atabarro/iqprodprelim.pdf

Guess not. So, East Asians have been beating Causasians on IQ tests (on average) for as far back as we have data. You can get more historical data along these lines from Lynn's (2006) book, Race Difference in Intelligence.

And one can go even further back if you look at brain size, which correlates about 0.4 with IQ. Asian brains have been well-known to be larger than Caucasian brains for as long as folks have been measuring both of them. Hard to fit that in with WASP-driven science...

So simple reverse causality surely plays some role, but it can't explain East Asia.....

Sandy G said...

Hi Garret,

Thanks for dropping by and commenting.

I guess we agree on more things, than we disagree on. For example, in section IID of your paper, you concur with my explanation of Flynn effect that it is most probably due to the increase in living conditions and due to environmental factors enabling the full flowering of potential. Environment can and does have a strong disruptive negative effect, though it only has a limited positive enabling effect (no amount of good environment can give you an intelligence that is disproportionate to what your genes endow on you; but even minor lack of right environmental inputs or toxins, can lead to dramatic stunted achievement of that potential intelligence).

Also, it is heartening to note, that early on in your paper you take the position that your paper will not settle genetic vs environmental debate on IQ, but would only provide evidence that national IQ is a good indicator of ntaional productivity.

I have no issue with the same and agree that if one disregards the process by which adult stable IQs are archived, then the stable adult IQ that has been archived would be a very good predictor of productivity and economic status (in a free market environment where other conditions re not adversely affecting success). There is no qualms with the causal relation between a better IQ leading to better SES, in a fair world.

What I do strongly disagree with is the assumption that low IQ is solely dependent on genetic factors. Bad socio-economic factors are the key drivers of low IQ- especially in situations where the socio-economic status is so low that it does'nt guarantee access to basic amenities of life like proper nutrition/ health care.

It is interesting to note that poor SES would cause stunted growth of IQ, and due to the causal relation between IQ and SES would lead to less productivity and lower income, thus maintaining or even aggravating the low SES. This is the downward vicious cycle from which it is very hard to emerge. This type of economy and culture would definitly have lower IQ than what could have been achieved in the right conditions. The sub-saharan countries that Kanazawa used in his study, match this pattern and some of the African countries National IQ (as per data appendix in your paper) viz. Kenya: 72, south afric: 72, ghana : 71 confirms to this pattern).

The opposite observation, that a spiraling economy should radically lead to high IQs is not reasonable, as the circle is vicious only in the downward direction. Monumental leaps in SES would not lead to dramatic effects in IQ, if the earlier SES levels were just sufficient to ensure that no negative effects of environment come into play. The Flynn effect is a tribute to the fact that high jumps in SES (above the base level) only lead to small incremental changes in IQ.

Another thing to keep in mind is that when the SES to low IQ causal link is suggested it is only for the achievement of the stable adult IQ and instrumental during the critical childhood developmental periods. Although, environmental toxins do have the capability to adversely affect IQ during adulthood, and there is emerging evidence for plasticity and neurogenesis in adulthood, a simpler and reasonably model is whereby adult IQ is stable and not much affected by SES changes (either up or down) once it has been stabilized. Thus, even if some positive effects of rising SES have to be observed, they would be observable only in children exposed to that SES and not in the IQ of the rest of the adult population, that has already acheived a stable IQ.

Thus, I do not agree with your explanation of the east Asian example. To me the data set appears to be very limited ( no IQ results before the 1950's; no data sets for the same country or population over time) and even if we assume that only after the 1980s the SES of these countries rose above the minimal needed SES, we still do not have the data for the IQ of children born under theses SES condition, to proclaim that ther eis no rise in IQ.

Further, it is quite plausible that productivity is dependent on many other factors than IQ, some of which are directly related to SES independent of IQ. Given a base level of SES, in which the East Asians had managed to develop their inherent genetic IQ to the fullest, the SES may still not be good enough to convert that IQ advantage to productivity. For example, a given household that has sufficient SES to provide good nutrition and health care, and thus ensure that its children archive their full IQ potentiality, may still not have enough resources to send them to a good school (or any school for that matter), may lack access to basic infrastructure support which handicaps the utilization of its intelligence and so on. Thus despite having the human capital, lack of the more prosaic monetary capital, may prevent them from archiving their full productivity. Thus, IQ may increase first to the maximal achievable level and only then SES increase dramatically.

It would be interesting to turn the East Asian example on its head and beg the question that if IQ is the definitive causal relation leading to SES , how do you explain the anomaly that despite high IQ's in 1950s (or for that matter Asian big brain since time immemorial) he East Asian countries did not have the corresponding productivity levels or SES. You might counter by saying that IQ -> SES causal link is mediated by factors like free markets, reforms etc to ensure that proper economic conditions are in place etc etc and only if these ideal market conditions are in place then only IQ predicts SES.

To that my simple counter-argument would be that SES -> IQ causal link also works but only in conditions when the SES is below the base level and that SES would not predict IQ absolutely. Given the same optimal SES in differnet countries, different cultures (which have different genetic pools) will have different IQ levels based on their inherent genetic capabilities.
As per this the IQ of east asians can be explained as either arising from the fact that they have already archived the SES required for full flowering; or that they still have to archive their highest IQ levels and their IQ levels are genetically vastly superior and may show more rise in future.

From Anecdotal evidence I can tell you that an average Indian has far more intelligence and creativity potential that the average IQ of 82 would suggest; most of the high SES families that have archived that high IQ migrate to US/ west and archive high SES there.
What brings down the national average is the sad fact that still a lot of Indians live below the poverty line - living in sub-optimal SES conditions that leads them to have low IQ' than what their genes or genetic makeup would suggest.

Looking forward to a fruitful discussion.
PS: Despite the tone of my original mail, I have high regards for economists in general and people like Amartya sen, Kahnman and Traversky in particular.

12:31 PM
Anonymous said...

Interesting blog entry. Has the author of it actually read the paper he is criticizing? I noticed that it costs $15 online. If not, is the author of the blog certain that the statistical methods employed by Kanazawa do not take his complaints into account implicitly? One hopes that the author is not criticizing a peer-reviewed scientific paper without having read it.

Sandy G said...

Dear Anonymous,

It would be better if, after having read the paper (otherwise by your own high standards you wouldn't have defended an article without having read it first), you would be kind enough to tell the readers of this blog how Kanazawa has taken the effects of low SES-low IQ developmentally mediated effect in consideration in his study.

You are correct in guessing that I haven't read the article (I believe in free access; so neither publish nor read material that is not freely available). I'll welcome if you or someone else could mail me the relevant portions or post them on this blog (under fair use).

As for invoking authority covertly by referring to peer-review in a prestigious journal, I would like to disclose that I haven't taken a single course or class in psychology- either in school or college- so if authority is the determinant: you can stick to reading articles in scholarly journals by those who have doctoral degrees. Blogs are not for you. Otherwise, if you believe more in open discussions and logical arguments, lets argue on facts and study method weaknesses etc and rely more on public-review to catch any discrepancies.

What I could gather from the abstract was that "The macro-level analyses show that income inequality and economic development have no effect on life expectancy at birth, infant mortality and age-specific mortality net of average intelligence quotient (IQ) in 126 countries". I take this to mean, that SES has no effect on longevity , if the effects of IQ are factored out. the 'if' is very important. This a very perverse position. This assumes that longevity is due to IQ and if IQ mediated difference in longevity data is factored out, the effcets on longevity of SES are negligible. This depends on an a priori assumption that longevity is primarily explained by IQ; and only after taking its effects into consideration, we need to look for an effect of SES on longevity.

What prevents the other, more valid and real interpretation : that SES predicts longevity and that there is little effect of IQ on longevity net of SES. Here the variation in longevity is explained by SES and after taking that into account, it would be found that, independent of IQ as a consequent of SES, IQ by itself would have little effect on longevity. the same set of data leads to this interpretation, because IQ and SES are related to a great degree and both are also related to longevity. It is just a matter of interpretation, that which is the primary cause and which an effect.


To take an absurd position, I can argue that longevity predicts/ causes both SES and IQ and reverse the causal link altogether. One can take a theoretical stand, that if people live longer , we have more labor force, blah, blah,blah... so more prodcutivity so better SES; further longevity menas that there are more wise old folks in the society and as IQ is mostly deterinmed by social influences (I do not subscribe to this, I am just taking an absurd position to show the absurdity of Kanazawa position), hence longevity of the population(more wise men) causes high IQs.

Also, please note that the above conclusion is only for the macro data he has. That interpretation is independent of his micro level data that found that self-reported health was more predicted by IQ than by SES. That micro data has nothing to do with the interpretation of the macro data. Again I don't know where he got the micro data, but I'm sure that would be a developed world population sample.
I am somewhat familiar with the macro data on which he is basing such claims, and there I do not see any reason to prefer his interpretation over other more realistic interpretations.

In the future, lets discuss merits of arguments, and not resort to ad hominem attacks over whether someone is qualified to make an argument or not. (in my opinion, by reading an abstract too, one can form a reasonable idea of what the arguments and methodologies employed are, and is thus eligible to comment)

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