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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Addiction and Incentive Saliance

Readers of this blog will be aware that I support and am sympathetic more towards the incentive-saliance theory of dopamine rather than the reward-prediction theory of dopamine. The incentive salience theory of dopamine has been elaborated on by Berride and Robinson and I have touched upon that previously in my posts.

It was heartening to note that Daniel Lende, a co-author of one of the blogs I admire, Neuroanthropology, has research interests in the same incentive salience paradigm and had been doing an anthropological study of Colombian teens with regards to addiction and how the drug-users themselves describe their condition from the inside. He has been featured in a recent Scientific American interview and I would recommend reading the article in its entirety. He also has a three part series on his blog on the same topic.

Amongst other things, he notes that there are three parts to addiction (and dopamine's role in addiction):

First was the emphasis that researchers placed on “wanting.” I was lucky in Colombia; addicted adolescents often described their experiences as “querer más y más,” to want more and more. Second, dopamine affects shifts in attention, which meant that some adolescents couldn’t focus on anything else when they knew an opportunity to consume was about to come along. Third, adolescents described a sense of being pushed toward something—an urge that rose up without conscious desire.

In other words the possible role for dopamine in addiction may be related to 1) conscious wanting 2) shifts in attention 3) un/subconscious urge or compulsive craving. Of course he also mentions the importance of cultural symbols and how they affect drug use.

He has also developed an eight-point scale for assessing addictive urges (craving and compulsive involvement scales) and the scale is available in both English and Spanish. Hope it spurs more research and is widely used.

A must read for those of us, who are too focussed on dopamine and the disease mode, when it comes to addiction.

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Encepahlon #58 now Out: Decide to read it now!!

The 58th edition of Encephalon, is now available at the Highlight Health blog. This decision making edition that implores you to take stock of your needs, preferences, values and emotions to arrive at a decision to read and appreciate the best in last fortnight's brain blogging, is very ably hosted and presented by Walter.

The articles I liked in particular were a comprehensive review of  gender differences in aging by Chris at Ouroboros; an article on whether, to what extent and at what age do fetuses start feeling/ experiencing pain by Paul at the Combining Cognits blog; a review  of gender differences in depression and its treatment by Dr Shcok; and various other interesting articles like the five-clover luck theory by David at ScienceBase or the bullies get kick out of seeing pain of others deconstruction by the the Neurocritic. There is more available including reports on psychopathy, multi-tasking, addiction etc, so rush on to the original Encephalon edition for more stimulating posts.

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Goals of Psychology and major persoanlity theory groupings

I recently came across the All Psych  website which I found to be a very good resource for anyone interested in Psychology.  I was reading the Personality synopsis section and was struck by the goals of psychology delineated there :

Psychology is the study of thoughts, emotions, and behavior, and their interaction with each other and the world. There are five basic goals of psychology:

1. Describe – The first goal is to observe behavior and describe, often in minute detail, what was observed as objectively as possible

2. Explain – While descriptions come from observable data, psychologists must go beyond what is obvious and explain their observations. In other words, why did the subject do what he or she did?

3. Predict – Once we know what happens, and why it happens, we can begin to speculate what will happen in the future. There’s an old saying, which very often holds true: "the best predictor of future behavior is past behavior."

4. Control – Once we know what happens, why it happens and what is likely to happen in the future, we can excerpt control over it. In other words, if we know you choose abusive partners because your father was abusive, we can assume you will choose another abusive partner, and can therefore intervene to change this negative behavior.

5. Improve – Not only do psychologists attempt to control behavior, they want to do so in a positive manner, they want to improve a person’s life, not make it worse. This is not always the case, but it should always be the intention.

To me the five major goals of psychology follow the five general stages that I usually talk about:  The first stage in my analysis of disparate phenomenons begins with it being descriptive and focused on clearly delineating the phenomenon under study and is generally biological. The second stage usually tries to find the impulses or reasons behind the phenomenon and is more related to explaining causes for the phenomenon and is generally related to motivation. The third stage  is usually concerned with development of phenomenon such that we can get some basic predictive properties in the mundane real world and is generally related to outward behavior. The fourth stage is usually focussed on how the phenomenon can be kept in check and is generally related to social dimensions (conformity and peer pressures). The fifth stage is usually related to how the phenomenon sort of gets a unique personal flavor and is generally related to individualistic and individuation dimensions.

Now, as an example I will try to make a case that though all the major theoretical approaches in personality psychology make use of all the stages and have as their goal all the five goals as delineated above; some of them are more focussed on one particular goal/ stage and thus are characterized by that goal/ stage.

Let me briefly review the major theoretical approaches to personality psychology below in the light of this framework:

1. Trait / Biological approaches to personality: I believe it is fair to group the biological and trait theories under the same group as the major feature of these theories is to outline the number of factors that can be used to describe a personality adequately. They are primarily descriptive in nature. One can argue that biological theories also explain the traits in terms of underlying biological markers; but that is juts begging the question one level down. Why does neurotransmitter system A over activation lead to this observable trait? They just describe the higher trait in terms of a lower biological phenomenon and are very good at descriptive level; but they lack explanatory powers.
2. Psycho dynamic/ Psychoanalytical theories:  These theories, the most famous being that of Freud, try to explain the personality and are totally obsessed in trying to find reasons for all and sundry observable phenomenon including accidental slips of tongues.  these are very good at explanatory levels, but not very good at other levels like predicting personality from childhood experiences or even in adequately describing the personality structure. They are more focussed on dynamics and less on structure. 
3. Behavioristic/ behavior genetics theories: These theories , the most famous being Skinnerian theories are most concerned with predicting behavior based on past experiences/ learning. These are the S-R or CS-CR theories and operant theories; the primary motivation not being to either describe or to explain personality; but just to predict how a behavior can be predicted given a personality (previous behavioristic learning).  Thus the primary focus on the ability to predict phenomenon and applications too limited to situations and traits that can lead to predictability.  
4. Social learning/ Cognitive theories: These theories like that  of Bandura, Beck etc are more concerned with how personality can be ingrained or learned and controlled. Both Bandura's bobo doll experiments as well as CBT point to the direction and focus of these approaches: what are the right conditions of personality formation and how that process can be controlled either by providing right role models/ environments conducive to social learning or by changing our cognitive schema. The action has moved away from describing or explaining or predicting to controlling how a good and socially acceptable personality can be formed/ learned.
5. Existential - Phenomenological theories:  These theories, like that of Maslow, are more concerned with how to improve one's personality. The focus is on flows, self-actualization, self-transcendence or whatever. One has moved away from mere description, analysis, prediction or control to actually thinking about what is a good personality and how to attain it; hence the primary focus on finding meaning; finding full potential and on improvement and positive psychology

I am sure there are other approaches to personality that I have not covered here- like the evolutionary theories; but than what else are the next three stages for, if not to make room for more such approaches!!

Do let me know if you disagree that the major approaches to personality theory follow a patterns and sort of stages and are primarily concerned with one primary goal at the cost of the other.

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The Mouse Trap is in the WIKIO 100 Top Science Blogs!!

I would like to thank all the readres of this blog, especially those who have linked to my posts or commented here; as a result of their patronage the humble Mouse Trap blog has made it to the top 100 Science blogs list maintained by none other than Wikio. It is a great honor to share the same space as that of BPS research digest, Cognitive Daily, Sharp Brains, Mixing Memory and  Developing Intelligence, to name a few of my admired blogs. I note that my ranking is 93 and prone to slip from the top 100 list next time; that doesnt bother me- this recognition, even if not sustained, but for one time only, acts as  a booster to motivate and spur towards more and more quality blogging.  

Thanks again to all the readers.

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Encephalon 57 now out

The latest edition of Encephalon is now up at the Mind Hacks blog. It is a very good collection of neuro articles and there is lot of good stuff to drool at.
I especially liked the Neurocritic article on correlation between the spontaneous activity in fMRIs and slow wave EEG signals- we know that it is an important phenomenon, but what all this spontaneous activity signifies is still unclear. I also like Pure Pedantry commentary on the finding that tow subregions of dlPFC are implicated in hypothesis-generation. He raises important points regarding what three conditions a brain area should show before we jump to concluding that that area is indeed responsible for a particular function.

There is plenty of other interesting stuff including A Michael Posner interview, a report on selectively erasing memories in mice and a controversial post on whether more gesture usage implies slower linguistic learnings and capabilities in children; so head on to the Encephalon and get your kicks!

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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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Autism and Schizophrenia: a minicolumnar deficit?

It has been my long standing thesis that Autism and Schizophrenia are opposite poles on a continuum; and the most recent evidence I would like to allude to is the mini columnar structure and abnormalities associetd with it in both the diseases. 

Let me at the outset, say that I am not an expert on mini-columns and hardly understand them, so would be glad if somebody corrected me or pointed out errors in the analysis.

First let me report on Schizophrenia from an abstract of a paper titled Mean cell spacing abnormalities in the neocortex of patients with schizophrenia by M Casanova et al

It has been postulated that the prefrontal cortices of schizophrenic patients have significant alterations in their interneuronal (neuropil) space. The present study re-examines this finding based on measurements of mean cell spacing within the cell minicolumn. The population studied consisted of 13 male schizophrenic patients (DSM-IV criteria) and 13 age-matched controls. Photomicrographs of Brodmann's areas 9, 4 (M1), 3b (S1), and 17 (V1) were analyzed with computerized image analysis to measure parameters of minicolumnar morphometry, i.e., columnarity index (CI), minicolumnar width (CW), dispersion of minicolumnar width (VCW), and mean interneuronal distance (MCS). The results indicate alterations in the mean cell spacing of schizophrenic patients according to both the lamina and cortical area examined. The lack of variation in the columnarity index argues in favor of a defect postdating the formation of the cell minicolumn.

To simplify the terms, I assume that CI relates to number of minicolumns in the neocortical broadmann area under consideration; CW is generally refered to as the width of the minicolumns i.e how big a particular minicolumn is , VCW I presume is related to how widely are the minicolumns themselves spaced from each other ie. the distance between two mini-columns and the last MCS is related to how densely neurons are packed within a mini-column.

Now for Schizophrenia, what I could find on the net, seems to suggest that they have reduced MCS as compared to controls i.e the neurons of schizophrenics are more densely packed within a mini-column as compared to controls .  Also, it was found that the density was greatest in core region and lesser so in the outer neuropil region of the mini-column.

An  opposite pattern is observed in Autism. Here is the abstract of article titled: Disruption in the inhibitory architecture of the cell minicolumn: implications for Autisim. by M Casanova et al again: 

The modular arrangement of the neocortex is based on the cell minicolumn: a self-contained ecosystem of neurons and their afferent, efferent, and interneuronal connections. The authors' preliminary studies indicate that minicolumns in the brains of autistic patients are narrower, with an altered internal organization. More specifically, their minicolumns reveal less peripheral neuropil space and increased spacing among their constituent cells. The peripheral neuropil space of the minicolumn is the conduit, among other things, for inhibitory local circuit projections. A defect in these GABAergic fibers may correlate with the increased prevalence of seizures among autistic patients. This article expands on our initial findings by arguing for the specificity of GABAergic inhibition in the neocortex as being focused around its mini- and macrocolumnar organization. The authors conclude that GABAergic interneurons are vital to proper minicolumnar differentiation and signal processing (e.g., filtering capacity of the neocortex), thus providing a putative correlate to autistic symptomatology.

Now the above clearly shows that the Autistics have an increased interneuronal space in mini-columns as opposed to normals and thus have lesser density of neurons within a minicolumn. However, they have more number of minicolumns to make up for this so that overall the number of neurons in the Broadmann area remains the same or the overall neuronal density does not differ. 

We can extend the results in other directions and hypothesize that 

1) Autistics will have increased no. of mini-columns, narrower mini-columns, narrowly spaced minicolumns and decreased neuronal density within a mini0-column as compared to controls.

2) Scchizophrenics will have lesser no. of minicolumns, wider mini-columns, widely spaced minicolumns and increased neuronal density within a mini-column as compared to controls.

Some of the above hypothesis is already supported and the rest may be in press/ under lab trials. 

What this means for in cognitive terms and how this translates to autistic and schizophrenic behaviour is another issue that I may address later (once I understand more of this minicolumn stuff!!)

D Buxhoeveden (2000). Reduced interneuronal space in schizophrenia Biological Psychiatry, 47 (7), 681-682 DOI: 10.1016/S0006-3223(99)00275-9

M CASANOVA, L DEZEEUW, A SWITALA, P KRECZMANSKI, H KORR, N ULFIG, H HEINSEN, H STEINBUSCH, C SCHMITZ (2005). Mean cell spacing abnormalities in the neocortex of patients with schizophrenia Psychiatry Research, 133 (1), 1-12 DOI: 10.1016/j.psychres.2004.11.004

Manuel F. Casanova, Daniel Buxhoeveden, Juan Gomez (2003). Disruption in the Inhibitory Architecture of the Cell Minicolumn: Implications for Autisim The Neuroscientist, 9 (6), 496-507 DOI: 10.1177/1073858403253552

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