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. 

  

 

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

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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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The Maudsely debates: anti-depressants and placebo

The Institute Of Psychiatry, London conducts Madusley debates on relevant psychiatric topics between distinguished psychiatrists and neuroscientists and also publishes them as a podcast. The most recent such debate consisted of the issue of whether anti-depressants are any better than Placebos in treating depression. There were knowledgeable arguments on both fronts and no matter what position you hold, hearing the debate would definitely enhance your knowledge about the issues involved.

I, for one, did not knew that anti-depressants worked by addressing the automatic and unconscious attention/ perception and memory biases. While I was aware that CBT worked top-down and affected cognitive biases and brain regions different from that areas affected by anti-depressants that presumably worked on neurotransmitter levels and bottom-up, the revelation that Goodwin's team had found that anti-depressants too work on biases, but unconscious ones, while CBT works on conscious ones, was new and enriching.

On the other hand I agree with many of the methodological issues raised by the speakers who claimed that anti-depressants were no good than placebos : the fact that the results lack 'clinical significance'; being psycho-active they are bound to have some effects and also the fact that the relief may be symptomatic due to 'drug' nature of anti-depressants and not specific and addressing the underlying disease, that the scale (HRSD) measuring depression may be not reflective of DSM criterion and may not be the best measure of disease severity; and I concur, but still think that the current generation of anti-depressants (other medicines) must be some good (over and above the good they bring by way of Placebo effect) especially since research has shown how they work (with a lag of few weeks before showing effects and by primarily inducing neurogenesis and affecting discrete brain areas) and how they are indeed effective at least in severely depressed people. Still all this should be taken with a pinch of salt- we have continuously been replacing outdated models of depression (like serotonin deficiency) by more and more accurate models (like neurogenesis). In my view we need to persist in that direction, though also having a healthy skepticism of what the drug companies might say and market new drugs and models for. Fortunately there are a host of unbiased pharmacists, neuroscientist and psychiatrist out there who are struggling with finding the most accurate model and the most accurate medication/ treatment like CBT for the same; so we don't need to despair. However, to blindly accepted all drugs (and models) , marketed by the Big Pharma, at their face value, and in clear evidence that they have not been proved effective beyond doubt, in clear evidence that negative finding have not been reported diligently and in view of the fact that at many time side -effects are glossed over, I would request not to be seduced overtly by the anti-depressants efficacy hype, but to moderate that with other known efficacious manes like exercise, CBT and yoga (all of which may be working by placebo effect themselves, but which definitely have lesser or no side-effects than anti-depressants. this of course does'nt mean that you give up your medicenes- at least not without consulting your psychiatrist- but supplementing them with other non-drug measures and reducing your reliance on the drugs- as they definitely have side-effects and may not be that efficacious as depicted in advertisements/ popular press.

Here is the summary of the talk from the IoP website:

Inspired by the recent media-frenzy at Prof Irving Kirsch?s research which suggested that antidepressants are no better than placebo, this Maudsley debate had an extremely good turnout.

Professor Kirsch gave us a run through of his research, in which he claimed to have found that there was a statistically significant benefit in the use of SSRIs over placebo - but that the difference was smaller than the standard of ?clinical significance? set down by the UK?s National Institute for Clinical Excellence (NICE) for all but the most depressed patients. His team also found that patients? response to placebo across all the trials was ?exceptionally large? - an indication of the complexity of the disorder. It was only the fact that the most severely depressed patients showed a much lower response to placebo that made the drug response clinically significant in this group of patients.

Against the motion, Professor Guy Goodwin argued that there were crucial flaws to the bounds that Kirsch had used to define clinical effectiveness. He pointed out that these criteria fail to contain an accurate description of depression, for example that they fail to mention persistent negative thoughts and other crucial symptoms that would be included in DSM IV.

For the motion, Dr Joanna Moncrieff alluded to the idea that there may be some sort of conspiracy of complacency and wishful thinking within the psychiatric profession as to the effectiveness of anti-depressants.

An impassioned speech against the motion was then given by Prof Lewis Wolpert. This was inspired by his own experiences of depression, which proved a powerful persuader as to the place that anti-depressants have in the treatment of severe depression.

Prior to the debate the audience were asked to vote which side of the argument they favoured. The leaning was overwhelmingly against the motion, perhaps not surprising in a room full of psychiatrists! After the speakers had made their points votes were recounted and a minority had changed their minds and had been swayed to support the motion. However those against the motion still had the majority.

The original article that sparked this debate is available online at PLOS Medicine, and I'm including the editor's summary below:

Background.

Everyone feels miserable occasionally. But for some people—those with depression—these sad feelings last for months or years and interfere with daily life. Depression is a serious medical illness caused by imbalances in the brain chemicals that regulate mood. It affects one in six people at some time during their life, making them feel hopeless, worthless, unmotivated, even suicidal. Doctors measure the severity of depression using the “Hamilton Rating Scale of Depression” (HRSD), a 17–21 item questionnaire. The answers to each question are given a score and a total score for the questionnaire of more than 18 indicates severe depression. Mild depression is often treated with psychotherapy or talk therapy (for example, cognitive–behavioral therapy helps people to change negative ways of thinking and behaving). For more severe depression, current treatment is usually a combination of psychotherapy and an antidepressant drug, which is hypothesized to normalize the brain chemicals that affect mood. Antidepressants include “tricyclics,” “monoamine oxidases,” and “selective serotonin reuptake inhibitors” (SSRIs). SSRIs are the newest antidepressants and include fluoxetine, venlafaxine, nefazodone, and paroxetine.

Why Was This Study Done?

Although the US Food and Drug Administration (FDA), the UK National Institute for Health and Clinical Excellence (NICE), and other licensing authorities have approved SSRIs for the treatment of depression, some doubts remain about their clinical efficacy. Before an antidepressant is approved for use in patients, it must undergo clinical trials that compare its ability to improve the HRSD scores of patients with that of a placebo, a dummy tablet that contains no drug. Each individual trial provides some information about the new drug's effectiveness but additional information can be gained by combining the results of all the trials in a “meta-analysis,” a statistical method for combining the results of many studies. A previously published meta-analysis of the published and unpublished trials on SSRIs submitted to the FDA during licensing has indicated that these drugs have only a marginal clinical benefit. On average, the SSRIs improved the HRSD score of patients by 1.8 points more than the placebo, whereas NICE has defined a significant clinical benefit for antidepressants as a drug–placebo difference in the improvement of the HRSD score of 3 points. However, average improvement scores may obscure beneficial effects between different groups of patient, so in the meta-analysis in this paper, the researchers investigated whether the baseline severity of depression affects antidepressant efficacy.

What Did the Researchers Do and Find?

The researchers obtained data on all the clinical trials submitted to the FDA for the licensing of fluoxetine, venlafaxine, nefazodone, and paroxetine. They then used meta-analytic techniques to investigate whether the initial severity of depression affected the HRSD improvement scores for the drug and placebo groups in these trials. They confirmed first that the overall effect of these new generation of antidepressants was below the recommended criteria for clinical significance. Then they showed that there was virtually no difference in the improvement scores for drug and placebo in patients with moderate depression and only a small and clinically insignificant difference among patients with very severe depression. The difference in improvement between the antidepressant and placebo reached clinical significance, however, in patients with initial HRSD scores of more than 28—that is, in the most severely depressed patients. Additional analyses indicated that the apparent clinical effectiveness of the antidepressants among these most severely depressed patients reflected a decreased responsiveness to placebo rather than an increased responsiveness to antidepressants.

What Do These Findings Mean?

These findings suggest that, compared with placebo, the new-generation antidepressants do not produce clinically significant improvements in depression in patients who initially have moderate or even very severe depression, but show significant effects only in the most severely depressed patients. The findings also show that the effect for these patients seems to be due to decreased responsiveness to placebo, rather than increased responsiveness to medication. Given these results, the researchers conclude that there is little reason to prescribe new-generation antidepressant medications to any but the most severely depressed patients unless alternative treatments have been ineffective. In addition, the finding that extremely depressed patients are less responsive to placebo than less severely depressed patients but have similar responses to antidepressants is a potentially important insight into how patients with depression respond to antidepressants and placebos that should be investigated further.

Irving Kirsch, Brett J. Deacon, Tania B. Huedo-Medina, Alan Scoboria, Thomas J. Moore, Blair T. Johnson (2008). Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration PLoS Medicine, 5 (2) DOI: 10.1371/journal.pmed.0050045

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Obesity and the dopamine connection

I had blogged previously regarding the obesity and dopamine connection and how obese people have been shown to have lesser dopamine receptors in the brain. The studies till now were correlational and there was a possibility that eating more food and the resultant obesity may be a cause and may play a part that decreases the dopamine receptors just like in addicted individuals(the addicted people also have less dopamine receptors).

However a new study by Stice and colleague in the latest Science edition has shown that the less number of dopamine receptors is a cause rather than a consequence of obesity. This they did by studying a genetic variation, A1 allele of the TaqIA restriction fragment length polymorphism , that leads to lesser number of dopamine receptors. They found that having this allele increased the risk for obesity and using FMRI they were also able to show that this was mediated by reduced dopamine signaling in the striatum.

Here is the abstract of the study:

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by the presence of the A1 allele of the TaqIA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (DRD2) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.

Now this should not be news to readers of this blog, because this was exactly what I had proposed in my earlier blog pots. Low number of dopamine receptors leading to lower dopamine rush, leading to overeating and obesity. It is heartening to see the same being confirmed; though we will need more evidence to settle the direction of causality.

E. Stice, S. Spoor, C. Bohon, D. M. Small (2008). Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele Science, 322 (5900), 449-452 DOI: 10.1126/science.1161550

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A gene implicated in operant learning finally discovered

Till now, most of the research on learning at the molecular level or LTP/TLD has focused on classical conditioning paradigms. To my knowledge for the first time someone has started looking at whether , on the molecular level, classical conditioning , which works by associations between external stimuli, is differently encoded and implemented from operant learning , which depends on learning the reward contingencies of one's spontaneously generated behavior.

Bjorn Brembs and colleagues have shown that the normal learning pathway implicated in classical conditioning, which involves Rugbata gene in fruit fly and works on adenylyl cyclase (AC) , is not involved in pure operant learning; rather pure operant learning is mediated by Protein Kinase C (PKC) pathways. This is not only a path breaking discovery , as it cleary shows the double dissociation showing genetically mutant flies, it is also a marvelous example fo how a beautiful experimental setup was convened to separate and remove the classical conditioning effects from normal operant learning and generate a pure operant learning procedure. You can read more about the procedure on Bjorn Brembs site and he also maintains a very good blog, so check that out too.

Here is the abstract of the article and the full article is available at the Bjorn Brembs site.

Learning about relationships between stimuli (i.e., classical conditioning ) and learning about consequences of one’s own behavior (i.e., operant conditioning ) constitute the major part of our predictive understanding of the world. Since these forms of learning were recognized as two separate types 80 years ago , a recurrent concern has been the
issue of whether one biological process can account for both of them . Today, we know the anatomical structures required for successful learning in several different paradigms, e.g., operant and classical processes can be localized to different brain regions in rodents [9] and an identified neuron in Aplysia shows opposite biophysical changes after operant and classical training, respectively. We also know to some detail the molecular mechanisms underlying some forms of learning and memory consolidation. However, it is not known whether operant and classical learning can be distinguished at the molecular level. Therefore, we investigated whether genetic manipulations could differentiate between operant and classical learning in dorsophila. We found a double dissociation of protein kinase C and adenylyl cyclase on operant and classical learning. Moreover, the two learning systems interacted hierarchically such that classical predictors were learned preferentially over operant predictors.

Do take a look at the paper and the experimental setup and lets hope that more focus on operant learning would be the focus from now on and would lead to a paradigmatic shift in molecular neuroscience with operant conditioning results more applicable to humans than classical conditioning results, in my opinion.



B BREMBS, W PLENDL (2008). Double Dissociation of PKC and AC Manipulations on Operant and Classical Learning in Drosophila Current Biology, 18 (15), 1168-1171 DOI: 10.1016/j.cub.2008.07.041

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Blog Action Day: Poverty and IQ: from the archives

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

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

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

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

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

A series of studies that I have discussed earlier, clearly indicate that in the absence of good socioeconomic conditions, IQ can be stunted by as large as 20 IQ points. Also discussed there, is the fact that the modern civilization as a whole has been successful in archiving the sate of socioeconomic prosperity that is sufficient for the full flowering of inherent genetic IQ of a child and as such the increments in IQ as we progress in years and achieve more and more prosperity (the Flynn effect) has started to become less prominent. This fact also explains the Kanazawa finding that in 'uncivilized' sub-Saharan countries the IQ is not related to life expectancy, but socio-economic status is. although, he puts his own spin on this data, a more parsimonious ( and accurate) reason for this is that in the sub-Saharan countries, even the well -of don't have the proper socio-economic conditions necessary for the full flowering of IQ and thus the IQ of both the well-off and poor parents in these countries is stunted equally. Thus, the well-off (which are not really that well-off in comparison to their counterparts in the western countries) are not able to be in any more advantageous position (with respect to IQ) than the poor in these countries. The resultant life expectancy effect is thus limited to that directly due to economic inequality and the IQ mediated effect of economic inequality is not visible.

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

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

7 comments:

Asterion said...

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

Always learning...


Sandy G said...

Hi Julian,

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

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

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

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

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

Garett Jones said...

Two words: East Asia.

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

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

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

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

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

Sandy G said...

Hi Garret,

Thanks for dropping by and commenting.

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

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

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

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

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

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

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

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

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

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

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

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

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

12:31 PM
Anonymous said...

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

Sandy G said...

Dear Anonymous,

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

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

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

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

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


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

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

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

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Magical thinking and feelings of control

A recent article in Science Magazine relates Magical thinking to feelings of control. It is an interesting paper and here is the abstract:

We present six experiments that tested whether lacking control increases illusory pattern perception,which we define as the identification of a coherent and meaningful interrelationship among a set of random or unrelated stimuli. Participants who lacked control were more likely to perceive a variety of illusory patterns, including seeing images in noise, forming illusory correlations in stock market information, perceiving conspiracies, and developing superstitions. Additionally, we demonstrated that increased pattern perception has a motivational basis by measuring the need for structure directly and showing that the causal link between lack of control and illusory pattern perception is reduced by affirming the self. Although these many disparate forms of pattern perception are typically discussed as separate phenomena, the current results suggest that there is a common motive underlying them.

More discussion of the studies can be found at Mind Hacks and Psychology Today Blog Brainstorm. 

To me, it is exciting that Magical thinking  and feelings of control are linked together. It is my thesis that Manic episodes and frank psychosis are marked by presence of Magical Thinking to a large and  non-adaptive degree.  Sometimes severe depression too causes Psychosis and I presume that Magical thinking in that case too may be increased. If so, one of the frameworks for understanding depression is that of learned helplessness paradigm , whereby mice are exposed to uncontrollable shocks and then do not even try to avoid the shocks , even after the external environment has changed and they could now possibly avoid them by correct behaviour. One explanation for psychosis in severe depression may be that feelings of lack of control rise to such a level that one starts indulging in Magical thinking and starts creating and seeing patterns that are not there and thus loosing touch with Reality. 

This raises another question of whether Manic psychosis may itself be due to the same stress and feelings of non-control, but this time not leading to Depression but Mania. We all know that bipolarity is a stress-diatheisis model and maybe whenever stress causes feelings of lack of control the bipolar people have a tendency to exaggerated magical thinking: When mood is good this may lead to Manic psychosis; while when mood is low the same magical thinking may lead to depressive psychosis. Does anyone know any literature on bipolar people being more magical thinkers? does the same reason also work well for them and endow them with creativity? Another related question would be whether bipolar people have more feelings of being out of control? And what about self-esteem, do those in Mania , who get psychosis, also suffer from lack of self-esteem and this is mediated by the role of self-esteem in protecting against magical thinking? 

    

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Language and intentionality

Michael Tomasello has a new book out titled " The origins of human communication" and the book seems to be promising, though has been a bit harshly reviewed at the Babel's Dawn. In it Tomasello proposes that a pre-requisite for language is 'a psychological infrastructure of shared intentionality'. It is based on Jean Nicod lectures and you can read a review here too.
What I am most interested is in this intentionality business. I have commented on orders of intentionality previously and this shared intentionality seems to fit the third order of intentionality that I proposed was necessary for communication.

But first for the premise of the book:

Tomasello opens his book with a consideration of the “infrastructure” that enables people to tell one another things. Apes do not have this infrastructure and the absence leads to scenes like this one:

A “whimpering chimpanzee child” is searching for its mother; the other chimps in the area are smart enough and social enough to recognize why the chimpanzee is whimpering; sometimes one of the chimps present will know where the mother is, and of course chimps have the physical ability to raise an arm point out the mother; even so, chimpanzees never help forlorn infants by pointing to the mother.

Why not?

There is a straightforward, Darwinian explanation for the ape’s mum’s-the-word behavior. Individuals don’t help non-kin. There is nothing in it for the informed adults to help the whimpering child of another. But Tomasello comes at the question from another perspective. Humans typically do help out whimpering children, even if the child is a stranger. An adult, happening upon a solitary, unknown, whimpering child is very likely to stop and ask what is wrong, take charge, and stick around until the problem is resolved. This activity strikes us as perfectly natural, normal behavior, even though it is contrary to so many of the rules in Darwin’s book. What, Tomasello wonders, is there about humans that makes such behavior easy and routine? His answer: “a psychological infrastructure of shared intentionality” [p. 12].

Thus, the premise is that pro-social behaviour and the shared intentionality underlying it are the pre-requisites for any meaningful language to evolve. And for this some tools are required.

The psychological tools Tomasello refers to are cognitive and emotional. The cognitive tools give us the understanding to engage in joint purposes and joint attention. The emotional tools provide us with the motivation for helping and sharing with others. These tools enable people to act together on a “common ground.”

Ebolles goes on further to speculate that this could be tied to Autistics' difficulty with language and I concur that the cognitive deficits related to intentionality as opposed to affective deficits empathy or mindblindness may be the roots of Autistics' language and communicative difficulties. We already know that they lack ToM to an extent and they also have communicative and social difficulties; might lack of shared intentionality, or intentionality at all or the lack of feeling of one has an intentional agent,  lie at the heart of the autism issue?

Immediately one can imagine all sorts of peculiarities that would arise in people who lack some part of these needs. Some people might have the prosocial motivation but not the cognitive ability to form a bird’s eye view. Perhaps autistic-spectrum disorder includes this difficulty. Others might have the cognitive ability, but not the prosocial motivation. There’s your sociopath, in a nutshell.

I think this common ground and 'infrastructure of shared intentionality' concept is awesome and I intend to read the book and review it soon on this blog. 

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