Archive for October, 2008

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!

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!!

ResearchBlogging.org

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

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!!)

ResearchBlogging.org
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

IQ and Religion: is the relation mediated by wealth and feelings of control?

Last week, on the blog action day, I re posted one of my earlier posts that questioned Kanazawa’s assertion that IQ causes Longevity (and implicitly that low IQ causes Poverty and not the other way round) and that SES has no effect on longevity net of IQ.  That has been thoroughly dealt with earlier and I will not readdress the issue; suffice it to say that I believe (and think that I have evidence on my side) that shows that in low SES conditions, a Low SES does not lead to full flowering of genetic Intelligence potential and is thus a leading cause of low IQ amongst low SES populations. This Low IQ that is a result of Low SES also gets correlated to longevity; again which would be largely explained by the low SES of the person. But as Low SES leads to less longevity and less IQ , a correlation between IQ and Longevity would also be expected. 

A similar issue has cropped up , this time with respect to religion or belief in God. It has been claimed that high IQ  causes atheism and that low IQ leads to superstition and belief in God. The result, this time by Lynn’s team is again correlational in nature and just like Kanazawa’s study partially relies on Macro-data i.e. mean IQ of a country and its mean religious belief scores.
The abstract of the paper goes like:
Evidence is reviewed pointing to a negative relationship between intelligence and religious belief in the United States and Europe. It is shown that intelligence measured as psychometric g is negatively related to religious belief. We also examine whether this negative relationship between intelligence and religious belief is present between nations. We find that in a sample of 137 countries the correlation between national IQ and disbelief in God is 0.60.

Now, BHA science group , has written a  very good rebuttal to this proposition and I urge readers to go and read the discussion there in full. 
For the sake of completeness, let me summarize the case against the hypothesis that high IQ causes atheism.
Problems with the macro data on which this analysis is made:  for countries that have about 100 (average) mean IQ, the correlation does not hold. The correlation is mainly an artifact of the fact that low mean IQ countries also have high religious belief (see accompanying figure) . We can, in my opinion, thus restrict the discussion to low (mean) IQ countries and try to explain whether its the Low mean IQ of their people that causes religiosity; or that high religiosity somehow leads to low IQ (a very counter-intuitive though indeed); or more plausibly that some other factor like SES/ feelings of control may be the underlying reason for both low IQ and high religiosity. 
Now, I have shown elsewhere that low SES causes low IQ and not the other way round; what remains to be shown is that low SES also causes religious faith. 
The latter part I’ll like to break in two parts: first , I believe that it is intuitive and there would be wealth of data showing that poverty or Low SES leads to fellings of helplessness or feelings of loss of control. Thus , the first assertion is that low mean SES in these countries, leads to the average person feeling less in control of his/her life and thus to feelings of loss of control.
The second part of the argument is that low feelings of control lead to religiosity/ superstition. Again I too have touched this before, but would right now like to point to this recent study that found that feelings of loss of control, lead to magical thinking/ superstitious belief and by extension (I am indeed taking a leap here) propensity towards religiosity. Of course we all know that religion is the opium of the masses (which are usaully poor) and rightly subdues the pwoerlessness and lack of control feelings that are otherwise unbearable.
 
Thus, I rest my case,  claiming that it is the low SES that leads to low IQ and high religious beliefs; the effect being mediated by nutritional/ enriched environmental factors in the former (IQ) case, while that of religion being mediated by feelings of control in the latter case. The actual correlation observed between IQ and religious faith , on the basis of low SES data , is at best spurious and due to the underlying low SES effects. 
  
 

ResearchBlogging.org

Richard Lynn, John Harvey, Helmuth Nyborg (2008). Average Intelligence Predicts Atheism Rates across 137 Nations Intelligence

J. A. Whitson, A. D. Galinsky (2008). Lacking Control Increases Illusory Pattern Perception Science, 322 (5898), 115-117 DOI: 10.1126/science.1159845

The Cognition and Culture website and blog

Those of you who are veterans in the cognitive blogosphere would remember the excellent AlphaPsy blog and how it had suddenly stopped posting and sort of ‘died’. The team, including Olivier and Hugo have now come back in their second reincarnation as a newly launched cognition and culture website with a blog and a news section.  I am excited and looking forward to reading some good stuff. Do sample the blog and I am sure you will be happy to add it to your blogrolls. 

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