25 Forum Posts by "MH19870410"
24901miles, you know, I'm busy. Lot of works. I have read just briefly this thread. Mostly, I had focused mostly on Naronic posts because he seems to have more knowledge on this topic than the average of the forumers here or any where you will see.
It's not the first time I tell him that I suspect he fails to understand most of what he reads or cites. Again I don't really care. In fact, I don't know really what kind of games Naronic is playing around here. But it's a lot of fun. Indeed, he cites Whitherspoon et al. 2007 paper as a proof against Lewontin and his followers, meaning the "fact" that individuals of different races are more alike than are people within the same race. See Figure 1 below ?
Genetic Similarities Within and Between Human Populations
Figure 1C shows you what you need to know, the common allele frequencies between races, meaning the very fact that there is virtually no overlap between races when it comes to between-race comparison involving many thousands of loci. The more information you put in your genetic analyses, the more between-race overlap you should get especially when more unique alleles are used in the comparison analyses.
Thus the answer to the question ‘‘How often is a pair of individuals from one population genetically more dissimilar than two individuals chosen from two different populations?’’ depends on the number of polymorphisms used to define that dissimilarity and the populations being compared. The answer, wˆ, can be read from Figure 2. Given 10 loci, three distinct populations, and the full spectrum of polymorphisms (Figure 2E), the answer is wˆ ~= 0.3, or nearly one-third of the time. With 100 loci, the answer is ~20% of the time and even using 1000 loci, wˆ ~= 10%. However, if genetic similarity is measured over many thousands of loci, the answer becomes ‘‘never’’ when individuals are sampled from geographically separated populations.
What is shameful, really, is that today, we need empirical proof to establish that same-race persons are more alike among them than are people from different races. It's really a joke we need to prove it. White people are so laughable sometimes.
"I see people here talking about creativity. Jensen (1980) in Bias in Mental Testing covered that topic, read pages 353-355."
The link was a wrong one. I corrected it.
I read some more comments starting from the beginning of this thread, although briefly. Some comments need be invoked. While culture could influence IQ, it is not the same thing as g-score changes. Especially if we consider that g is unrelated with environment. See here.
Also, I know well that most hereditarians usually rely on transracial adoption and/or mixed race IQ, data that showed mixed-race to have scored intermediate to whites and blacks. While I think mixed race data do not support hereditarian model as such, because environmentalists could also say it is consistent with their own cultural models, so that the only use with mixed race data is to show it does not contradict hereditarian hypothesis rather than to say it confirms it, this said, I also believe that transracial adoption data is even less conclusive. Generally, you need a lot of longitudinal information about the adoptees and their adoptive parents. Locurto made such good comments on it. Given the all the evidence we have today (see here), my opinion is that either transracial adoption gives a very weak support for hereditarian against environmentalist, or either there is no clear winner because the data are somewhat inconsistent, with some studies that were found to be impossible to replicate, such as the Tizard study in which blacks score higher than mixed-race who themselves score higher than whites. Most of them lacked relevant informations about the adopted and biological parents (background, IQ) as well as longitudinal data on the adopted children. And all of them had very small samples, so that it is not easy to draw conclusions from them.
On the other hand, adoption gains found in the Capron/Duyme study is more interesting. And investigating the adoption gain with g-loadings is probably more informative than transracial adoption data, which are mostly uninformative. Jensen (1997) was able to show for instance that adoption gains were not related with g. Two limitations : small number of subtests, and small sample sizes. This needs replication, but if we believe Jensen's numbers, one can probably infer that adoption does not increase intelligence, and as such, these data are more informative than most misleading transracial adoption data ever known today.
I also see comments on how we could stimulate IQ through intervention and cultural/behavioral changes. As some say, behavior is partly heritable, but more important is that, as Locurto suggested, such environmental changes are unlikely to boost IQ substantially, unless there is a drastic change in environments, which hardly occurs. Theoretically, we could believe there is much room for substantial IQ gains (assuming there were equivalent to g-changes) but in reality, what we have is this :
To see what the policy implications might be, let us suppose that low- and high-SES homes in the French studies represented the 10th and 90th centiles in the quality of the home environment, respectively. If that were the case, what might be accomplished by moving children from very deprived homes (at the 2d centile, to make the example concrete) to very advantaged ones (98th centile)? ...
If adoption is one of the only affordable and successful ways known to improve the life chances of disadvantaged children appreciably, why has it been so ignored in congressional debate and presidential proposals? Why do current adoption practices make it so difficult for wouldbe parents and needy infants to match up? Why are cross-racial adoptions so often restricted or even banned? All these questions have political and social answers that would take us far outside our territory. But let it be said plainly: Anyone seeking an inexpensive way to do some good for an expandable number of the most disadvantaged infants should look at adoption.
The tough question about adoption involves the way the adoption decision is made. Governments should not be able to force parents to give up their children for any except the most compelling of reasons. Right now, the government already has the power (varying by state), based on evidence of neglect and abuse, which we do not advocate expanding. Instead, we want to return to the state of affairs that prevailed until the 1960s, when children born to single women - where much of the problem of child neglect and abuse originates - were more likely to be given up for adoption at birth.
The above passage is from The Bell Curve (pp. 412, 416). It is important because theoretical models need conditions not necessarily attainable in real life. As Herrnstein & Murray made it clear, these conditions are extremely difficult to satisfy. It's something some people here (e.g., AxTekk) obviously missed. If we remember Capron/Duyme adoption data, which show about 20 IQ points increase, as one would expect, those children were abused indeed before being adopted by high SES families. But even most blacks living in western countries never encountered such depressive environmental conditions. So, when scholars such as Nisbett rely on Capron/Duyme as a way of reducing BW IQ differences, we know where it gets wrong.
I see people here talking about creativity. Jensen (1980) in Bias in Mental Testing covered that topic, read pages 353-355.
I'm busy. So I will simply list some good references on the topic related to how brain is linked to intelligence. It's not all I have, but they are probably the most interesting.
The Parieto-Frontal Integration Theory (P-FIT) of intelligence: Converging neuroimaging evidence
Genetic Influences on Human Brain Structure: A Review of Brain Imaging Studies in Twins
Associations between cortical thickness and general intelligence in children, adolescents and young adults
A genetic analysis of brain volumes and IQ in children
A multivariate analysis of neuroanatomic relationships in a genetically informative pediatric sample
The neuroscience of human intelligence differences
Review of Twin and Family Studies on Neuroanatomic Phenotypes and Typical Neurodevelopment
Neuroanatomical correlates of intelligence
Common variants at 12q15 and 12q24 are associated with infant head circumference
There is also Rushton & Ankney 2009 paper, Whole Brain Size and General Mental Ability: A Review, but I don't think it's the most important among those listed here. Probably the most interesting number is the correlation between g-loadings and brain size. But this has been reported in Jensen (1998) first, and the MCV technique is not without its limits.
Naronic,
I see that your level on this topic as lower than I expected from when I read this thread for the first time. I can beat even when I'm sleeping. I'm disappointed.
You said : "Firstly the Flynn effect doesn't mean nothing because you think it’s secular and fails to raise a statistical artifact to your satisfaction"
And I ask : what's the point of repeating an argument I crashed once in my previous interventions ? What's the use ? This is not a reply.
You said :"G simply comes from the stipulation that people whom are good at one test tend to be good at them all, and vice versa, and it’s relevance only goes as far as it’s correlations and estimates."
In my previous comment, I cited this paper. No comment from you.
You said : "measurement in-variance (which we've already discussed can't explain 20 point jumps in IQ)"
As usual, you're being ridiculous. FE gains vanish entirely when using IRT scores to remove item bias. I told you before to read it.
You spew : "Another area which you seem not to get me (as shown by you linking to Sesardic's paper) is how heritablility works."
It's a fantastic argument. Also, I bet I know how heritability works, much better than you do (as shown by you linking to Ted Block's paper).
You said : "It's why 'heritability' tends to become unpredictable when SES comes into play with a lot of different studies reporting a lot of different heritabilities at both sides of the spectrum, as well as why it tends to 'increase with age'."
At the same time, evidence does not support this hypothesis. I said it in my very first intervention on this thread. But you still continue ignoring my comments.
For the increasing IQ heritability with age, as your entire previous paragraph suggests, you rely on G*E correlation. I pointed out to this article. No reply, as usual. GxE correlation as accounting for increasing heritability is not the only hypothesized model, and as such is unlikely to be tenable. See also Brant 2013 comment on it, in the discussion section.
You said : "Me citing ned block 'worries' you because it's old (sigh),"
But I never said it. Learn to read. Simply. The problems with Block is that some genetic analyses were not available at that time. So yes, you must learn to read, as evidenced here and there, if you people here want to see why I said his level of comprehension on this topic is weak.
You said : "This paper in question finding that some genes can account for 1% of variation in IQ."
So, that's why in their paper, the authors write :
Only 1% (approximately) of the variance was explained in the prediction analysis due to the individual SNP effects being very small and therefore estimated with much error, which detracts to a great extent from the accuracy (8–11%) of the prediction equation. Our finding that 40–50% of phenotypic variation is explained by all SNPs is fully consistent with the low precision of a predictor based upon a discovery sample of ~3500 individuals; estimation of the SNPs’ effects is different from prediction accuracy.
Also, from Chabris (2012) :
Following Davies et al. (2011), we then dropped individuals whose relatedness exceeded .025. Davies et al. reported that the approximately 550,000 SNPs in their data could jointly explain 40% of the variation in crystalized g (N = 3,254) and 51% of the variation in fluid g (N = 3,181). We applied the same procedure in our analysis of data from the STR sample in Study 3 and estimated that the approximately 630,000 SNPs in our data jointly accounted for 47% of the variance in g (p < .02), thus confirming the findings of Davies et al. (2011) in an independent sample. These and our other results, together with the failure to date of whole-genome association studies to find genes associated with g, are consistent with the view that g is a highly polygenic trait on which common genetic variants individually have only small effects.
From Plomin (2013) :
We found that DNA markers tagged by the array accounted for .66 of the estimated heritability, reaffirming that cognitive abilities are heritable.
GCTA has been used to estimate heritability as captured by genotyping arrays for height (Yang et al., 2010), weight (Yang, Manolio, et al., 2011), psychiatric and other medical disorders (Lee et al., 2012; Lee et al., 2011; Lubke et al., 2012), and personality (Vinkhuyzen, Pedersen, et al., 2012). GCTA was first applied to cognitive ability in a study of 3,500 unrelated adults, which yielded heritability estimates of .40 and .51 for crystallized and fluid intelligence, respectively (Davies et al., 2011). The GCTA estimate for general cognitive ability was .47 in a meta-analysis across three studies involving nearly 10,000 adults (Chabris et al., 2012) and .48 in a study of nearly 2 thousand 11-year-old children (Deary et al., 2012).
The GCTA results from these initial studies appear to account for a substantial portion of the heritability of general cognitive ability found in twin studies, which, as mentioned earlier, meta-analyses have found to be about .50.
You said : "you need to step your game up and stop giving me stupid non-responses and claiming a logistical high road you're not on."
I reply : speak for yourself. I commented nearly all these, as well the link you give here again. But no answers coming from you.
You said : "(highly unlikely given the studies that you ignored)"
I ignored nothing. You ignore everything. I told you not to rely on small samples, and provide instead a large review or meta-analysis that look for moderators. Yes, you're the one being silly.
You said : "It's not about G being unitary or not."
It is. Moronic replies won't get you anywhere. Hampshire rebuttal is entirely based on the hypothesis that g is biologically unitary, which needs not to be the case in fact. They ignore Jensen's work, like you ignore my replies. I provided my response to Hampshire in my first long intervention, and here again you make repeat it 2 times more, so 3 times in total.
So then, Naronic, it's the last time I reply to you. I already said I won't reply to you until you come up with answers. You are really stubborn. So that was my last reply. Thanks for nothing.
If people here want to debate with him, for what it worths, I won't be here to reply.
If you need further proof that g causes, say, academic achievement, you may be interested by Watkins & Canivez (2007). In their cross-lagged path analysis study, they were able to show that IQ influences education and not the reverse. Their model 2 (M2) in which each of the IQ latent factors at Time 1 had direct paths to the IQ latent factors and achievement latent factors showed the best fit to the data, while alternatives models (e.g., M3, which assumes direct path from achiev factor Time1 on both achiev factor and IQ factor at Time2). This is consistent with previous research, mentioned by Jensen (1980, pp. 336-337).
Related to this topic, you have Rindermann & Neubauer (2004) as well as Dasen Luo and co. (2003a, 2003b). Luo's papers are particularly interesting, in that they found (2003b) psychometric g, measured by Wisc (call it WISC-g), while correlated with Achievement (MAT variables), to be substantially mediated by processing speed (measured by CAT). In the 1rst paper (2003a), what you have is that CAT group factors are not important in predicting achievement (MAT), at the same time, the g derived from CAT (call it CAT-g) affects achievements measures essentially through the genetic paths, as assessed by the substantial chi-square changes in the models (see their table 8). All these are fully consistent with Jensen's hypothesis (see his 2006 book, Clocking the Mind). I should note as well that (Vock et al. 2011) basic cognitive processes could exert achievements outcomes through reasoning and divergent thinking, as can be seen from the fact that direct paths from mental speed to achiev. performance were not significant.
So if you ask whether or not we have proofs of causal link between IQ (g) and scholastic performance, I think it's safe to say : yes.
On the role of g in training success and job performance, you have Ree & Earles (1991, 1994). The title of the respective papers is self-explanatory. Psychomotor abilities do not have much validity beyond g, I must add. See Carretta & Ree (1997).
This said, about the videos poxpower has posted, it is not surprising that they are not interesting. First, if your english is limited, like mine, you wouldn't expect to hear everything very clearly. Second, is the fact that at a conference, you must summarize and condense as much as possible your findings. So, a lot of details are omitted. That's why I rarely see videos by now. It's useless. The most important portions of the academic papers are the method section and result section. These of course have been more or less omitted in such videos. Still related, you can see this video, debate Rushton/Suzuki. For the last one, you see how he uses fallacious arguments such as Lewontin's fallacy, discrimination hypotheses, and so on. I don't have need to debunk that again. I already covered this topic a lot on my blogs. You can also check the papers for yourself.
http://www.youtube.com/watch?v=i9FGHtfnYWY
@ Naronic :
I said earlier : "If you have time, read this article. If your time is short, then simply look at the Davies et al. (2011) study."
I forgot a link, now I fixed it.
I'll also reply to a comment of
@ AxTekk :
So you said :"No, this doesn't control for the racial/ cultural element. You need to control for this by having people visibly indistinguishable."
Two problems. First, absence of violation in measurement bias or similarity in developmental processes make this argument highly implausible. Second, when talking about nearly impossible empirical test, which I don't like because it cannot be testable and is thus by definition irrefutable, we can look somewhere else. Skin color for instance. Link here. It explains that for colorism hypothesis to be tenable, its effects must be present anywhere, meaning that skin-color based discrimination must be universal, e.g., at school, at work, even in sports, and, yes, everywhere else. And this must hold irrespective of gender, of course. But this is not the case in fact. For example, when controlling for SES and still other variables of interest, the link between skin color and earnings or education level within blacks disappear altogether. This is inconsistent with colorism because it posits that discrimination is prevalent irrespective of status, IQ, and else. In other words, it very looks like an hypothesis based discrimination solely based on physical appearance (e.g., skin color).
And, interestingly, skin color-IQ association does not hold within families, only between-families. Link here. Again, this renders discrimination hypotheses mostly untenable.
You said: "No matter what the topic, if all you have is correlational studies, you'll never get an academic consensus on the cause of a thing."
Of course you don't know this topic well. In fact, Jensen's default hypothesis is testable, unlike some environmental/cultural hypotheses by definition irrefutable. By using structural equation modelling, which disentangles genetic and environmental components and assess the fit of different competing models, such as default model, against purely genetic, or against purely environmental, or neither of them, as being the cause of racial differences. Jensen's The g Factor (pp. 464-467) explained briefly the subject.
I'm in a hurry, so I will come back later with more comments.
Naronic:
You said : "Genes code for proteins and are responsible for all the variation you see in people, but genes don’t “determine” much of anything on the macro scale which is why to this day we’re having so much trouble finding and replicating evidence of genes that substantially effect IQ or personality to degrees we find in between individuals."
You mention Chabris. The original paper is here. What it shows is that IQ is affected by a multitude of genes of extremely small effects and that the reasons as they speculate is because samples were not large enough, so you wouldn't expect to attain a high level of significance. But so, in what way it weakens the arguments about IQ heritability, I'm still wondering. On this topic, see also Plomin (2013), Trzaskowski (2013).
You said : "I’ve also pointed to another study that there’s a good chance IQ tests are probably not a good measure of innate intelligence so much as skills needed to succeed in a western society, there’s a lot we simply can’t know from correlations."
Well, and again, you provide no comment on measurement invariance tests which show that IQ scores are cross-culturally comparable. The paper Fractioning Human Intelligence is another silly one. The problem is the authors pretend that g must be unitary at a biological level, which is not necessary in fact. It's a shame they made such a mistake. I mean, when you debate IQ stuff, the least thing to be aware of, is obviously Jensen's work, in particular his 1998 book, The g Factor. So yes, Hampshire and co. completely ignored Jensen's earlier work and remark on this subject.
By way of comparison, there is that paper who showed that g can be edified as a causal higher-order factor, here. These authors managed to establish the causal role of g, which falsifies the common claims that IQ, or g, is a hollow entity. The only problem with that study is the sample size, which is not large, only modest (about 200). It needs to be replicated therefore.
You said :"Recent research has shown that African-American exhibit smaller total cerebral volume than Caucasians, although there were no statistically significant differences in total gray matter, total white matter, or ventricular CSF volumes, African Americans have a larger orbitofrontal cortex than Caucasians."
Assume it's right. Still, it does not mean that BW differences have no genetic component.
You said: "There’s also the stipulation that nerve conduction velocity can affect scores on IQ tests and G and there have been no statistical significant differences between blacks and whites"
And to which I reply : "sample size =50 blacks, 50 whites."
If so, does that give us a proof for an entirely non-genetic BW IQ gap component ? Of course not.
You said : "I direct you again to the link I think I’ve posted before
http://www.nih.gov/news/health/oct2011/nimh-26.htm"
I don't really understand why, from the beginning of this thread, you are continuing to cite this article ? How many times by the way ? Because I don't see where it shows that the B-W IQ difference has no genetic component whatsoever. I'll read this again later, because it's really a mistery why you're always referring to this. Regardless, the citation is not necessarily consistent with Out of Africa theory, contra the authors, and I don't give it even a slight credit. That book (read it 2 years ago) contains all the arguments you may want to check.
I noticed another link who refers to Gardner's multiple intelligence. You have your answer here.
You said : "No one component, or IQ, explained everything."
Yes, but this is actually a strawman. Who ever said that IQ explains everything ? Obviously, no one ever made this claim.
You said : "G simply refers to a person’s ability to be proficient at all cognitive tasks, it has no “reality” beyond that."
Refer to the above. And read also Gottfredson's article Why g Matters. g is also a function of complexity. When you are trying to train people, some will learn at a faster rate than others, regardless of experience and education level and still other background levels, gender, race, and some personality variables (e.g. Big Five), etc.
You said : "this rebuttal is also really stupid as this study involved anywhere up to 40,000 participants last I checked."
What are you talking about ? The Jaeggi study ? Or the Hampshire ? The first had n=70, the second n=16. So stop calling others stupid while in fact you're the one being silly.
By the way Naronic, would you try the next time to give some direct links to the studies you cite, instead of a mere link toward ScienceDaily, NIH or else ? Because these articles are not very helpful. They only provide a rather short summary of the study they are referring to. Some important details could be omitted, for instance, methods, tables, figures, and else. It's rather difficult to make a very technical comment on them when you don't provide the paper.
Naronic :
Too many articles. I'm busy. Although I read them, I will probably need to look again.
You said : "When we look at the brain and the environmental effects on it and then turn around and look at what correlates with “g” ... All that changes and responds pretty heavily with environment."
If I interpret it correctly, you argue that because brain correlates with g, and that brain responds to environmental influences, thus it can be inferred that Flynn effect (FE) gains are related with g. I'm sorry but it's a total nonsense. First, environment indices are found not to be related with g. I thought I already linked to that meta-analysis. As usual, you simply ignore all the evidence. Second, it doesn't answer the question of violation in measurement invariance. No inference is possible when measurement bias is detected in cohort comparison.
In this article that I pointed out in my previous post, there was a citation from Jensen, of course, that you failed to notice. It says that if FE gains were 'real' there should be a bias with respect to earlier cohorts in predictive validity of IQ with other variable (e.g., IQ vs. indices of economic status, achievement. etc.). As Jensen writes :
"If the IQs had increased in the later generation without reflecting a corresponding increase in functional ability, the IQ would markedly underpredict the performance of the earlier generation – that is, their actual criterion performance would exceed the level of performance attained by those of the later generation who obtained the same IQ. The IQ scores would clearly be functioning differently in the two groups. This is the clearest indication of a biased test – in fact, the condition described here constitutes the very definition of predictive bias. If the test scores had the same meaning in both generations, then a given score (on average) should predict the same level of performance in both generations. If this is not the case (and it may well not be), the test is biased and does not permit valid comparisons of “real-life” ability levels across generations."
It seems that IQ scores indeed maintained their predictive validity, so this would suggest hollow effect in the secular gains. See Williams (2013) interesting review of FE. Also, even when we accept the false idea that FE gains are on g, it does not mean it has something to do with BW differences. Wicherts (2004) says it doesn't because BW difference is measurement invariant, unlike cohort comparisons. Also, you should remember that B-W differences have not diminished, and must remained at about 1SD. Maybe the only exception I know if UK, where the BW gap is probably lower than 1SD, could be somewhere between 1 SD and 0.50 SD. Related to that topic, you could be interesting by LaGriffeduLion's article on BW gaps. The demonstration of how you can play and manipulate the statistical BW gap was impressive I must say.
You said : "this isn’t a response and doesn’t “refute” anything"
Stop cherrypicking my comments, would you ? This won't help defending your case, quite the contrary. And your comment is not a reply anyway. There is a ton of arguments I made earlier and to which you have simply ignored. Regardless, I already destroyed the arguments that environmental stress would account for a huge part of the BW gap, assuming of course that these environmental influences were totally independent of genetic influences. The post is here. I also linked to that blogpost. You never tried to comment it.
You said : "But if we really need an arrow of causality I direct you to http://www.nih.gov/news/health/may2012/ninds-23.htm"
That doesn't make sense to talk about causality if a relationship has not been established. Given Metzen (2012) meta-analyses, I'm not sure that environmental stress, malnutrition included, is related with g. About your link, anyway, it does not show that the causality does not work the other way as well. My suspicion is that causality could work both ways. Intelligent people would be more likely to avoid such stress.
You said : "The problem with heritability is one of semantics; heritability unlike what intuition would tell people does not measure genetic determination. For instance you can’t compare heritability between groups and environmental factors can also be heritable."
You cite Block's article "How heritability misreads about Race". It's sad because that article is extremely bad written. And all so wrong. He believes heritability would not be equal between races, yet the opposite happens (Rushton & Jensen, 2005, 2010). His claims is not supported by any evidence. Further, a great portion of the article is devoted to Ogbu's theory using the illustration based on Lewontin's plant analogy. Call it Theory X. As I mentioned earlier the very fact that measurement invariance holds with respect to IQ race differences makes the plant's analogy dubious. This is the more annoying because it is known that BW IQ gaps increase when SES levels increase, and Block uses Theory X to reject this fact.
Block also says that heritability is misleading because indirect estimates ignore GxE correlations. At the time when Block wrote this article, you may be right to pose the question, now we have a lot of strong evidence. The fact that you still refer to this article today makes me feel rather uneasy. If you have time, read this article. If your time is short, then simply look at the Davies et al. (2011) study.
Also, note that Sesardic (2005, for instance, see pp. 115-116) refuted Block a while ago in so many ways.
AxTekk :
You said : "This will of course effect people of every race, but there are unique and powerful factors that only affect the motivation of black people and Hispanic people quite uniformly. These are what I guess I refer to as the "x" factor."
If you read Rowe (1994), lubke (2003, pp. 551-553) and Jensen (1998, p. 456 and following) you see that it could be thought as the plant analogy (two plants growing in totally different environments) used once by the likes of Lewontin, Gould, and Flynn, among others. But yes, generally, your description would be more or less accurate, although I wouldn't have formulated it this way.
You said : "The point is that institutionalising people, removing their motivation and self worth creates deficits in cognitive ability (as tested psychometrically)."
Yes, I've read something like that. But this has nothing to do with g. There was no test of measurement invariance, or method of correlated vectors, or even a principal component analysis. So, as I said, it is rather inconclusive.
You said : "What the Rowe shows is that many developmental processes work the same between races, ie: If a white kid does drugs he'll become the same amount more aggressive as a Hispanic kid who does drugs. What it doesn't show is that all races are exposed to the same developmental processes equally ie: that there isn't something about Hispanic culture that will expose more Hispanic kids to doing drugs."
I'm not sure you really understand the study, assuming you have read it. Either way, if blacks and whites are subjected to different environments and/or to a different magnitude, the default hypothesis, more exactly, what Jensen termed it (see his book, page 418 and following), would have been rejected. Instead, Rowe et al. confirmed the default model. They found a statistically nonsignificant difference in causal processes. This was true for Hispanics vs whites or blacks vs whites. Rowe speculates one possible reason for identical developmental processes. Roughly, it's mass-media culture with all the things we could imagine. If, say, there is a racial difference in GxE interaction, this would reject the default hypothesis, because this would mean that even when blacks and whites were IQ-matched they would have attained that level of IQ through different developmental processes and thus through different environmental factors or influences.
Also, if by this comment, you also argue that blacks' heritability should be lower than whites', Jensen (1998) said earlier that they are quite similar. Rushton & Jensen (2005, 2010) made the same point, more recently.
AxTekk,
You said : "You can't understand numbers until you understand the world they refer to."
Let me ask you. Do you realize that you're totally off-topic here ? I don't think this sentence is relevant for you if you don't understand what these numbers were refering to. You seem to suggest there is no logic behind all those maths. If so, this is wrong. Researchers test hypothesis X against Y using the maths. So what you say does not make sense. Besides, you haven't answered to my requiries. You cite 3 papers. I found perhaps one of them, but this was clearly irrelevant to the topic under discussion. For the two other ones, nothing can be found.
You can indeed write a reply to my earlier posts, if you want. But I won't reply if you continue to talk like this. You see, if you had posted on my blogs using this ton, I would have banned you with no hesitation. If I was wrong about something, tell me then. But be polite.
poxpower,
If blacks and whites were matched for SES levels (which also encompass cultural differences between SES, that is, poor versus rich, and therefore, matching for SES also match for cultural influences), the IQ gaps diminish somewhat : -30% at most. See Herrnstein & Murray, The Bell Curve 1994, page 286. Jensen (1973) also says that after controlling for income gap, given a BW IQ gap of 15 points, there is a reduction of about 2.7 points. Some may argue that SES (education, income, occupation levels...) cannot account for all of the environmental effects possible. Therefore it is assumed that SES represents just a mere fraction of the totality of the environmental influences/effects. Even if that was true, the problem is that controlling for SES would also control for genetic variance. SES has a genetic component as well (see Jensen 1973). Thus, controlling for SES makes absolutely no sense. I don't really think environmentalists generally consider this argument.
With regard to motivation and test scores among schizophrenics, after a further google research, I found that paper (link) where Nisbet 1996 is briefly mentioned, but I can't access the paper itself. Concerning Foster Green 1992, google gives me nothing in particular.
[Not related to this subject, but Raven score gains are not related with g, as measurement invariance is violated. See here. Just to make sure there is no objection on this.]
AxTekk
You said : "The X-variable would also affect Hispanics, who have also been shown to suffer social consequences if they perform well on standardised tests and grow up with less cause for motivation (or perceiving there being less cause for motivation)."
It can. But as long as X does not affect (all) other ethnicities as well, it violates the so-called 'measurement invariance'. This means that g is not affected, put it simply.
You say :"So why did motivation affect the general abilities of schizophrenics in the studies I gave you?"
If you mean "Bellack 1990, Foster Green 1992, Nisbet 1996..." you provided no links. I only found the Bellack 1990. But I won't do all the work for you. Although I gave it a quick glance, I did not understand why you have even cited that paper in the first place unless it wasn't that paper. But given the text, there is no mention of g-loadings whatsoever. Not even measurement invariance.
You say : "I never suggested the depressive effects were not encountered among other races."
I'm wondering if you really understand what the "Theory X" implies. This theory says that some environmental/cultural variables affect some groups while leaving some others totally unaffected.
You say : "Please note I am also not suggesting that these disadvantages do not effect any white people, just that they affect black people (and hispanics) more in a roughly uniform manner."
This sentence is ambiguous. But the first part of it tends to say that some whites, although not all whites, may experience some kind of stereotypes as well. In other words, the X-variable affects one group but not another, and it acts not uniformly towards this stereotyped and depressed group, but has instead a heterogeneous effect. The problem, you see, is that "Theory X" implies that your 1) X-variables must exert an uniform effect, 2) affect some groups while leaving some others unaffected.
You say : "I can't help but feel like you're trying to have it both ways on this: groups don't exist in disadvantages to IQ, only individuals do but groups do exist in IQ differences."
That's not what you're thinking about. If you read Rowe's paper, the text says this :
This latter explanation features strongly in Ogbu's (1991) explanation of "involuntary" minorities' poor school achievement. He defined as involuntary those minorities brought into another society through slavery, conquest, or colonization. Because their incorporation into another society was imposed, the involuntary minority, according to Ogbu, develops a psychological identity in opposition to that of the mainstream culture. Members of an involuntary minority perceive institutionalized discrimination against them and therefore they lose faith in their ability to compete successfully in institutions such as schools. Although these minority parents may verbally value schooling as a means of social advancement, their lack of personal academic effort and success may undermine their exhortations. In these groups, young people may channel their energies away from conventional routes to success and into survival strategies of petty crime and other oppositional behavior. In their generally poor schools, they also see evidence of discrimination — that they are given less just because they are minorities. In overview, minority-unique experience with social discrimination may lead to their (relative) failure in schooling and later in conventional economic competition.
They were testing the hypothesis of unique developmental process. This was proven to be wrong. That's why my earlier citation says this : "There are two realms of variance, between and within groups; there is only one realm of development.".
I must add that the X-theory (or whatever we call it) has been debunked by Rowe (1994) as well. Shortly, they found the hypothesis of different causal process between blacks and whites to be untenable. This cannot be expected if black are affected by any depressive effects not encountered among other races/ethnicities.
Although the two-realms [group and individual] hypothesis is now . the received view of nature and nurture . . . it is implausible to suggest that the forces shaping the IQs of groups are different from those shaping the IQs of individuals; environmental and genetic factors can affect only individuals, one at a time. . . . There are two realms of variance, between and within groups; there is only one realm of development.
At 8/31/13 07:56 PM, AxTekk wrote: I'm not talking about stereotype like effects at all.
What the clinical psychologists I named were identifying were the effects of institutionalisation on cognitive testing. When a person loses motivation to perform well on a test, g related cognitive measures drop. ... Black Americans are generally raised with at least the perception that they have less opportunity than their white counterparts. They then suffer disparagement from their peers if they perform well on standardised tests, as part of the "acting white" phenomenon. ...
Well, this simply means you don't understand what you're talking about because the description you are giving me is totally a stereotype-like effect. The definite confirmation of it, is that you brought out the concept of "acting white" and X-variables effect that affect one racial group but not the others. So yes it's totally a stereotype-like effect. Anyway, motivation does not affect general abilities for the same reason anxiety does not affect general abilities. These are situational effects. Generally, comparison between blacks and whites with regard to IQ tests are measurement equivalent, meaning that strong inferences are possible, because measurement bias is absent. See Dolan (2000) or Lubke (2003, pp. 551-553) for a description.
AxTekk,
I don't really understand what you're trying to say (especially the first post). In Metzen's study 5, he correlates score differences owing to biological-environmental (variables) pressure with g-loadings. To test the Spearman effect, you can use a variety of techniques, MGCFA, principal component analysis, or the method of correlated vectors. Metzen uses the latter. The correlations were generally negative or approaching zero.
Generally, when studies assess the environmental effects on any given environmental factors on IQ, or even g, one thing must be done as well : controlling for confounding variables. For example, some believed that breastfeeding improve IQ. Der, Batty, Deary 2006 meta-analysis shows that controlling for mother's IQ, the effect is nil. The Nisbett 2012 paper Naronic is always citing, over and over again, says that it is difficult to believe. Still, the most recent paper on this subject, Breast milk and cognitive development-the role of confounders: a systematic review, located 84 studies, with breastfeeding having no impact on IQ when controlling for confounders. So, indeed, the topic is more complicated than most (environmentalists) would believe.
"This is thought to be (by all three of the above researchers and their teams, as well as big names Szasz and Bentall) because schizophrenics become institutionalised and lose hope."
Again I'm not sure about what you said. But if you are talking about stereotype-like effects, I must say that it violates measurement invariance, meaning that the effects are situational effects, affecting specific, not general abilities. See Wicherts et al. (2005), specifically, Study 1.
SmilezRoyale :
You write : "In fact the hereditarianism position doesn’t even demand that the gaps in IQs between populations be unbridgeable."
Of course not. Because it posits that given a certain heritability, IQ malleability has its limits. Assuming of course that there is a Jensen effect in those IQ gains. But regardless, you may want to read that paper relate to that topic on what intervention can do and cannot.
You write : "But I’m also wondering if you’re comfortable saying back a few posts ago that IQ is highly malleable ..."
A lot of people are not able to make the distinction between IQ changes and g changes. For instance, it's obvious from Metzen (2012) and Jensen (1997) that environmental effects on IQ are not necessarily equal to their effect on g itself.
Naronic :
You cite : But when the team did a statistical analysis for the strength of the correlations for each SNP, they found that even the strongest accounted for just 0.02 per cent of the total variation in educational attainment (Science, doi.org/mqw).
Can't read the article. Blocked or something. But here's a paper that is relevant to the topic in question.
Still a different stuff, but here's something interesting.
Effects of cis and trans Genetic Ancestry on Gene Expression in African Americans
And go to Figure 1.
And Naronic,
About the link you provided here, earlier, on the practice effect, I forgot to mention that the abstract says this : "
These gains reflect practice effects instead of genuine intellectual changes, which may lead to errors in clinical judgment."
Therefore, I don't understand why you are citing a paper to refute yourself. To repeat, practice effect is not g-loaded.
Talking about the heritability stuff, here's a relevent passage from The Bell Curve :
1. A brief refresher (see Chapter 4): A heritability of 60 percent (a mid-range estimate) says that 40 percent of the observed variation in intelligence would disappear if a magic wand wiped out the differences in those aspects of the environment that bear on intelligence. Given that variance is the standard deviation squared and that the standard deviation of IQ is 15, this means that 40 percent of 15² is due to environmental variation, which is to say that the variance would drop from 225 to 135 and the standard deviation would contract to 11.6 instead of 15 if all the environmental sources of variation disappeared.
86. A twenty-point swing is easily reconciled with a heritability of .6 for IQ. Suppose the high- and low-SES homes in the French studies represent the 90th and 10th centile of environmental quality, as the text says. A twenty-point swing in IQ from the 2d to the 98th centile of environmental quality would then imply that the standard deviation of home environment effects on IQ is 4.69. Squared, this means a variance of 22 attributable to home environment. But as we noted in note 1, a heritability of .6 implies that there is a variance of 225 – 135, or 90, attributable to environmental sources. The French adoption studies, in short, are consistent with the conclusion that about a quarter of environmental variance is the variance across homes (if our guesses about the adopting and biological home environments are not way off). Three-quarters of the environmental influence on intelligence must be uncorrelated with the family SES, according to the present analysis. Note again that the balance tips toward environmental factors outside families as being the more relevant than those provided by families in affecting IQ, as mentioned in Chapter 4.
This assumes of course that those IQ gains are g-loaded. If not, to begin with, you don't even need to formulate that argument.
Naronic
I left you a couple of days to develop your arguments. Sadly, there is nothing substantial to deal with, I'm afraid.
You write : "And I'm pretty sure I have a lot of links that contradict your views as well"
I doubt, since your level on this subject is pretty weak. See below.
You write : "I don't think it's too inconvenient that I ask you too extract your arguments from the sources you use"
So, that's your excuse for not replying. Forget it then. I consider that you lost. End of story.
You write: "There have been clear gains on most g loaded tests including wechsler scale."
Again, you don't understand what you say. This sentence is the proof. It's about the items or subtests g-loadings we are talking about when referring to r(d*g) with regard to Flynn Effect versus Jensen Effect. That's why you should read Nijenhuis (2007) meta-analysis. He found a perfect (true) negative correlation of -1.00 between secular gains and g-loadings. Also, it has been shown that all the variance across studies was definitely explained by the artifacts they have taken into account, meaning that the other dimensions on which the studies differ (e.g., age, IQ samples, test type) play absolutely no role in the differential Flynn effects and that all the variance was solely due to those artifacts.
The same conclusion can be found from Wicherts and Beaujean analysis that were presented briefly here. If measurement invariance does not hold this would mean 1/ different factors are being compared or 2/ the differences in the items or subtests in question are not due to common factors (g), or both. The effect is thus not g-loaded. See an illustration here.
You write : "when in many developing nations scores increase from anywhere between 5 to 20 points, and most of all these IQ scores have been going up on mostly tests that measure fluid g rather than crystallized g, you'd expect the opposite"
Well, no. See here for details. The test-retest effects violate measurement invariance, thus implying measurement bias, either coming from violation in 1) metric invariance or 2) scalar invariance. Violation of 1) means that measures different factors across groups. Violation of 2) means that items/subtests are of unequal difficulty across groups. The Spearman hypothesis would hold if measurement invariance level 3 is attained, meaning that scalar and metric invariance simultaneously hold. All this simply means that practice effects affect specific abilities rather than general abilities, meaning that the effect is hollow in g. Again, the literature has been summarized here and your quotation of James Flynn completely missed that point. Flynn effect is hollow, just like your arguments.
You write : "Also a little supplemental on evolutionary theories of iq"
Unimpressive. And I know that paper by the way. What Wicherts et al simply show is that evolutionary variables and environmental variables have different pattern of loadings in their principal component analysis, and that environmental variables form with national IQ a common cluster while evolutionary variables do not. As I mentioned before, this has been replied here (check the citation from Hassall & Sherratt 2011. You can continue to ignore the arguments presented there, but I will simply stop this conversation. It's time wasting for me.
Also, Wicherts and co mentioned that if you remove African countries, evolutionary hypotheses do not hold. Again, it is fallacious to remove African countries, because it also remove a lot of variation, thus attenuating the correlations. If Wicherts et al do not trust Lynn's data on African IQ, they can simply use their own estimates. Here's Templer (2010) "Can’t see the forest because of the trees" :
To omit the Black-African countries in considering the geographical distribution of HIV/AIDS is like omitting the Northwestern European countries in a study of Nobel laureates. Wicherts should have computed the IQ-HIV/AIDS correlation using the Black-African IQs of his choice. I re-computed the correlation extending generosity to Wicherts by assigning every Black-African country an IQ of 80. The correlation is -.41.
You write : "We also propose a complementary hypothesis that may explain some of the effects of infectious disease on intelligence. ... bla bla bla"
As mentioned before, the reply has been given here. I won't repeat it again. Or simply, I should perhaps drop this conversation. You simply have no arguments. It's crystal clear. You refuse to reply. I'm losing my time. Don't expect me to waste more time on you.
This aside, about one of your affirmations "You know what's also false, that “culture-only theories predict a zero relationship between heritability and group differences” but well get to that later." made out of thin air, I thought you would make a developed argument. Just like I thought you would reply to my earlier points. I was foolish to believe you were willing to provide anything substantial.
You said : "Not that this really matters because the metanarritive to this argument has already been set by multiple brain scans in animals. Impoverished environments severely limits neuronal growth, this is one of those findings you can't ignore.
You shouldn't generalize studies on animals to humans. Anyway, with regard to impoverished environment, here's what Jensen said in 1973.
I asked Dr Herbert Birch, a leading researcher in this field, for a rough estimate of the percentage of our population that might suffer a degree of malnutrition sufficient to affect IQ. He said he would guess ‘Not more than about 1 percent’ (personal communication, 19 April 1971). … Assume that all of the 1 percent of malnutrition in the U.S. population occurs within the Negro population; this would mean that approximately 9 percent of the Negro population suffers from malnutrition. Assume further that all 9 percent of this group afflicted by malnutrition has thereby had its IQ lowered by 20 points (which is the difference between severely malnourished and adequately nourished groups in South Africa – the most extreme IQ difference reported in the nutrition literature). Assuming the present Negro mean IQ in the U.S. to be 85, what then would be the mean if the 20 points of IQ were restored to the hypothetical 9 percent who had suffered from intellectually stunting malnutrition? It would be 86.70, or a gain of less than 2 IQ points as an outer-bound estimate.
But perhaps you don't know how he did the calculation. So I will tell you then. It's something like this :
100 – [(0.09*80) + (0.91*100)] = 100 – (7.2 + 91) = 100 – 98.2 = 1.8.
Where 0.09 is the percent of black people suffering from malnutrition in the US, 0.91 the percent of people not suffering, 80 is the IQ mean of starving people and 100 the IQ mean of non-starving people. But anyway, the 1.8 IQ loss is exaggerated because poor environments correlate with genotype. People are poor partly because they were not intelligent to begin with. That 1.8 point IQ loss is not additive in fact. Note, also, that the 20 IQ point deficit could be exaggerated as well. I remember clearly that Lynn saying the effect of poor nutrition causes a 10-point deficit. Such that africans will gain 10 points by moving from Africa to America. He speculates this because southern US blacks who don't have much white admixture (near zero) averaged an 80 IQ point mean.
You said : "mostly though the most non ignorable finding is the way infection rate becomes the best predictor of IQ across nations, making the hereditarian argument defeasible."
The Eppig 2010 study is simply another widely cited paper. Of course I know that one. But here again, you're wrong. It's a pretty weak argument. Please go there, and you will know why.
You said : "individuals are frequently more similar to members of other populations than to members of their own population."
Looks like a Lewontin fallacy, no ? The fact is that Lewontin's error is to look at the differences in the alleles of single genes instead of groups of genes unique to each race. Also, Sesardic (2005) dealt with that a while ago. I'm not sure about the exact page however because it's been a while, but you sure will figure out. This aside, I don't understand why you were talking about this. I never brought that subject.
In my earlier post, I forgot to comment on the Jaeggi et al. Here's what you need to know. Especially when you have so small sample sizes, you should better rely on meta-analysis, not on any single study. Because this is pure nonsense. Meta-analytic studies are based on real theory of data. That's why they are so useful to understand the variation of effect sizes between studies. Hunter & Schmidt talked a lot about it in their 2004 book. Before drawing any conclusion, you have to remove variance attributed to measurement error, sampling error, range restriction or enhancement, and unreliability. You can't do this by only citing one single study of any kind.
I also missed that, from Nisbett 2012 : "This reduction in the measured g gap occurred even though the magnitude of Black gains on Whites by subtest did not correlate highly with Wechsler subtest g loadings. This is scarcely surprising, because the g loadings of Wechsler subtests are very similar.". This is pure nonsense and it simple means Nisbett does not understand anything he says. Range restriction in g-loadings substantially reduces the observed correlation. You have to correct it. Again, read the Jensen's passage quoted here.
This aside, there was a ton of arguments of mine you have simply ignored. I will just wait.
Naronic,
When you quote Hanscombe 2012 for writing this : "In a UK-representative sample, the genetic effect on intelligence is similar in low- and high-SES families. Children’s shared experiences appear to explain the greater variation in intelligence in lower SES.". You are mistaken because you failed to noticed the numbers from Table 7. Just look carefully the pattern of their best-fitting model : "First, the only significant GxE interaction with SES index 1 found for g at age 10 (higher heritability in low-SES families) disappears with the more proximal measures of SES at ages 7 and 9. Second, the best fitting model indicates no interaction of any kind at three ages for SES index 1 (ages 3, 7, and 12), and for two ages for SES index 2 (ages 7 and 14). Third, moderation of the shared environmental component of g is indicated at four of eight ages for SES index 1, three of five ages for SES index 2, and four of four ages for SES index 3. Thus, the most consistent result across ages and across the three indices of SES is moderation of the influence of shared environment on children’s intelligence – an environment-environment interaction.". So there you go.
Next, look at Figure 7. You see that the A component does not really decrease at lower SES levels even if you look at the standardized values rather than the raw values. But the C component can increase at lower SES levels in fact because at low SES the E component decreases, not A. That's surely something you failed to grasp.
Also, here's how Hanscombe summarizes the finding in the discussion section : "we did not find evidence for the presence of such a gene-environment interaction across childhood and adolescence. At only one of the eight ages, age 10, did we find a significant moderation of the genetic contribution to IQ. However, the GxE interaction was in the opposite direction from that predicted by the environmental disadvantage hypothesis". Either ways, I'm not sure you really understand what the study is showing here.
Also, remember what Turkheimer said in his paper : "It would be naive, however, to interpret SES strictly as an environmental variable. Most variables traditionally thought of as markers of environmental quality also reflect genetic variability (Plomin & Bergeman, 1991). Children reared in low-SES households, therefore, may differ from more affluent children both environmentally and genetically (Gottesman, 1968), and the models we employed in this study do not allow us to determine which aspect of SES is responsible for the interactions we observed.". Of course, this is not something the likes of you would admit so easily, if you have even reported it in the first place.
When you quote Asbury & Plomin for saying this : "We conclude that GxE exists for verbal ability in early childhood and tends to be in the direction of greater heritability in high-risk environments.". I don't really understand because it's exactly what I said. That it countered Turkheimer's.
You quote Nisbett 201 : "A new analysis of the same dataset extending the analysis through age 14 (Hanscombe et al., 2012) has found significant interactions in the original direction for the environmental term. The investigators concluded that shared environmental experiences have greater impact on intelligence in low-SES families."
This isn't going anywhere because you haven't really read that paper, right ? I read it, and I can tell you that Nisbett is simply misreporting the findings of the paper. What the authors said is this : "First, shared environmental influence is found in both lower- and higher-SES families and the difference in shared environmental influence between them is modest. Second, shared environmental influences on IQ decline from childhood to adulthood so that these influences might not have an impact in the long run.". Perhaps Nisbett misread it, or he is dishonest. It doesn't really matter anyway.
Most importantly, you deliberately avoided the Brant 2013 study. It shows there is a higher heritability among low-IQ people. Obviously you have nothing to say on it.
Even if environmental variance becomes larger as SES decreases, or genetic variance larger as SES increases, it doesn't matter because the black white IQ gap increases with SES levels. Go here and there.
Naronic,
You said : "Hey, your links suck! Worship mine instead!! ... A user randomly named MH19870410 with an account younger than a day old comes along"
I'm very busy those days, and extremely tired, losing energy by posting blog articles, analysing data, and so on. If you want to discuss with me any further, you have to use another tone. That's the first and last time I tell you this. There won't be a next time. I hope you get that.
You said : "preferably actual studies and not links to blog-posts."
The problem, you see, is that those blog posts contain a lot of papers that contradict your views. You can invoke whatever excuse that fits you well, but you're simply in denial here. Anyway, do as you wish.
You said : a recent review of the literature found major gains with high g loaded tests, most notably Ravens progressive matrices formerly thought as "culture free",
Where to begin. That's an argument I have seen a million of times. That's quite unimpressive, to tell you the truth. Read Jensen (1998) here :
“These tendencies increase the chances that one or two multiple-choice items, on average, could be gotten “right” more or less by sheer luck. Just one additional “right” answer on the Raven adds nearly three IQ points”
Or Kaufman (2010a) as well :
The item type used in Similarities resembles the age-old questions that teachers have asked children in schools for generations. In contrast, matrices-type items were totally unknown to children or adults of yesteryear and remained pretty atypical for years. Over time, however, this item type has become more familiar to people around the world, especially as tests of this sort have been increasingly used for nonbiased assessment, including for the identification of gifted individuals from ethnic minorities. And, because Raven’s tests can be administered by nonpsychologists, these items tend to be more accessible to the public than are items on Wechsler’s scales, which are closely guarded because of the clinical training that is a requisite for qualified examiners. But go to any major bookstore chain, or visit popular websites, and you can easily find entire puzzle books or pages of abstract matrix analogies.
It is, therefore, difficult to evaluate gains on matrices tasks without correcting these gains for time-of-measurement effects. The power of this “time lag” variable was demonstrated by Owens in his groundbreaking longitudinal study of aging and intelligence. Owens (1953) administered the Army Alpha test in 1950 to 127 men, age 50, who had been administered the same test in 1919 at age 19, when they were freshmen at Iowa State University (initial N = 363). The study continued in 1961 when 96 of these men were tested again, at age 61 (Owens, 1966).
The 96 men tested three times improved in verbal ability between ages 19 and 50 followed by a slight decline from age 50 to 61. On nonverbal reasoning ability, they displayed small increments from one test to the next. However, Owens had the insight to also test a random sample of 19-year-old Iowa State freshmen on the Army Alpha in 1961 to 1962 to permit a time-lag comparison. He was able to use the data from the 19-year-olds to estimate the impact of cultural change on the obtained test scores. When Owens corrected the data for cultural change, the Verbal scores continued to show gains between ages 19 and 61; but what had appeared to be small increments in Reasoning were actually steady decreases in performance.
The time-lag correction may reflect real differences in mental ability (i.e., FE) as well as changes in test-taking ability and familiarity with a particular kind of task. The mere fact of large gains on a test such as Raven’s matrices over several generations, in and of itself, cannot be interpreted unequivocally as an increase in abstract reasoning ability without proper experimental controls. When Flynn has interpreted gain scores for groups of individuals tested generations apart on the identical Raven’s matrices items (e.g., Flynn, 1999, 2009a), he has not controlled for time-of-measurement effects.
And Kaufman (2010b) again :
I am not talking about practice effects, the kind of IQ gains that occur over an interval of weeks or months simply because of the experience of having taken the same test before. Rather, I am talking about a cohort effect, one that affects virtually everyone who is growing up during a specific era. In the 1930s, matrices tests were largely unknown and children or adults who would have been administered such tests would have found them wholly unfamiliar. A whole society would have performed relatively poorly on such test items because of their unusualness. By the 1950s, such tests would have been known by some, not many, and by the 1990s and 2000s, matrices tests and similar item styles proliferate and are accessible to everyone. Therefore, it is feasible that people would score higher on a Raven test from one generation to the next simply because the construct measured by the test would have been a bit different from one decade to the next. Such time-of-measurement or time lag cohort effects exert powerful influences in cross-sectional and longitudinal studies of IQ and aging (Kaufman, 2001b; Owens, 1966) and must be controlled when evaluating true changes in ability between early adulthood and old age.
These time lag effects include both instrumentation and real FE gains in IQ. It is the instrumentation aspect of cohort effects that needs to be controlled in FE studies to determine which aspect of the gain is “real” and which aspect concerns the familiarity of the test.
With regard to the decreasing BW difference over time, please note in the Dickens-Flynn 2006 paper that the decreasing gap holds only for the youngest samples. In adult samples, there is no reduction at all. They acknowledged this : "our data give a current IQ for blacks age 24 of 83.4 or exactly 1.1 SDs below whites." So this ends here.
At 8/6/13 04:34 PM, naronic wrote: As for reaction times, if you subscribe to Rushton's laughable theory that faster reaction times means higher IQ then blacks have the fastest reaction times
Deary, Ian J (2001)
Flynn (1991)
Pretty bad references, especially the Deary 2001. I had that book, named "Intelligence, A very short introduction". As the title suggests, yes, there is nothing very interesting there for those who already know this topic very well. It's a book for beginners, otherwise, buying that book is not useful. And what Deary says (p. 62 in the book you mentioned) about the supposedly low correlation between IQ and reaction time of 0.2, this is obviously wrong, and mainly explained by artifacts lowering this correlation, such as measurement error, range restriction and so on.
If you need better references that the ones you were citing, go there :
The g Factor
Clocking the Mind
This said, if you people around there really hate Richard Lynn for any reasons (or excuses) you are building, then so be it. I don't really care because I don't like the guy as well, and I'm not impressed by his works by any means. Anyway, you may rely instead on Heiner Rindermann, or Garett Jones. See below :
African cognitive ability: Research, results, divergences and recommendations
Relevance of education and intelligence for the political development of nations: Democracy, rule of law and political liberty
The impact of smart fractions, cognitive ability of politicians and average competence of peoples on social development
Cognitive Capitalism The Effect of Cognitive Ability on Wealth, as Mediated Through Scientific Achievement and Economic Freedom
IQ and Entrepreneurship: International Evidence
Will the Intelligent Inherit the Earth? IQ and Time Preference in the Global Economy
IQ in the Production Function: Evidence from immigrant earnings
Intelligence, Education, and Economic Growth: A Bayesian averaging of classical estimates (BACE) approach
Hey,
Someone linked to my blog, and so I came here. There's a lot wrong about hmm, a lot of things here, I have to admit. Nevertheless, there was a lot of references that need to be discussed.
For instance, instead of relying on Dickens & Flynn 2006 paper on the black-white decreasing gap, we should better look at this instead :
http://humanvarieties.org/2013/01/15/secular-changes-in-the-black-white-cognitive-ability-gap/
The fact is that even at age 3, the BW cognitive difference is more or less similar to the magnitude of the BW difference generally found in adulthood. Jason Malloy did a good job showing this :
http://humanvarieties.org/2013/05/26/the-onset-and-development-of-b-w-ability-differences-early-infancy-to-age-3-part-1/
With regard to the black white difference, it is well known that it is more pronounced on the more g-loaded items/subtests/tests. A meta-analysis published on that same blog shows this. A corrected correlation of g with heritability of around 0.70. The correlation between g and shared and nonshared environment is a negative one. Here's the link. If you have any question, ask it :
http://humanvarieties.org/2013/08/18/a-meta-analysis-of-jensen-effect-on-heritability-and-environmentality-of-cognitive-tests-using-the-method-of-correlated-vectors/
Generally, black white cognitive difference in the US does not violate measurement invariance (see Dolan 2000), meaning that it is not biased, so that the inference that B-W difference as a function of g-loadedness of tests for example using Jensen's MCV remains strong.
Someone here linked to an article that points to the Hampshire 2012 paper. Here's the counter :
http://humanvarieties.org/2013/04/03/is-psychometric-g-a-myth/comment-page-1/#comment-351
But regardless of the above linked comment, the article on psychometric g is worthy of reading and I highly recommend it.
Someone here, probably naronic, mentioned the Turkheimer over-cited 2003 paper. It is a shame that it keeps cited over and over again, in spite of all other papers showing the opposite. Here were some examples :
The Nature and Nurture of High IQ: An Extended Sensitive Period for Intellectual Development
Socioeconomic Status (SES) and Children’s Intelligence (IQ): In a UK-Representative Sample SES Moderates the Environmental, Not Genetic, Effect on IQ
Environmental moderators of genetic influence on verbal and nonverbal abilities in early childhood
Does Parental Education have a Moderating Effect on the Genetic and Environmental Influences of General Cognitive Ability in Early Adulthood?
There are a ton of papers who failed, besides, to show any significant GxE interaction effect, thus, countering the Turkheimer's conclusion. Here, from Educability and Group Differences :
<blockquote>One of the conceptually neatest methods for detecting one kind of G x E interaction, first proposed by Jinks and Fulker (1970, pp. 314-15), is applicable to our data on MZ twins reared apart. We can ask: Are different genotypes for intelligence equally affected by environmental advantages (or disadvantages)? In the case of genetically identical twins, any phenotypic difference between them reflects some environmental difference. One twin can be said to be environmentally advantaged and the other disadvantaged, relative to one another. While the phenotypic difference between the twins, |t1 – t2|, reflects only environmental effects, the average of their phenotypes, (t1 + t2)/2, reflects their genotypic value (plus the average of their environmental deviations). If this correlation is significantly greater than zero, we can claim a G x E interaction. A positive correlation would mean that genotypes for high intelligence are more susceptible to the influence of good or poor environments; a negative correlation would mean that genotypes for lower intelligence are more sensitive to the effects of environment. The correlation of IQ differences with IQ averages of the 122 MZ pairs is -0.15, which is not significantly different from zero. When measurement error is removed by using regressed true scores instead of the obtained IQs, the correlation falls to -0.04. Thus the twin data reveal no G x E interaction. This finding is consistent with Jinks and Fulker’s (1970) failure to find any evidence for a G x E interaction in their analysis of a number of studies of the heritability of intelligence.</blockquote>
For further replication, see here.
Concerning the relationship of the secular IQ gains (flynn effects) with g-loadings, see the below post :
Hollow Flynn Effect in Two Developing Countries and A Further Test of the Debatable Black-White Genetic Differences
Concerning childhood education, there is indeed some evidence that it could increase later IQ levels, but it is not the same thing as to say it increases g itself. Evidence points out that it is not the case, in fact. See Nijenhuis 2007 and especially Ritchie & Bates 2013. The latter shows that education while increasing your IQ does not cause any improvement in cognitive processing speed, meaning that those IQ gains were not generalizable, thus hollow with respect to g. This is generally the outcome of most test-retest effects.
