Sunday, September 18, 2011


This page will serve as a permanent index of all of my writings on intelligence and psychometrics.

The Post-Racial Era is Over – January 8, 2010

Smart People are Educated, Greedy, Sexist Bigots – July 20, 2011

Meet Towelie, the IQ Test of the Future – August 27, 2011

The SAT’s Cohen’s d & the Topography of IQ Denialism – September 2, 2011

The SAT in Red, White, and Brown – September 18, 2011

Girls Versus Boys: The Final Battle – October 9, 2011

Racial Amplitudes of Scholastic Aptitude – April 11, 2012

The SAT Bell Curve – April 25, 2012

Just Say No Limit: Trayvon, Dextromethorphan, Marijuana, and MAOA – July 5, 2012

The Hispanic Asian Flynn Effect – August 5, 2012

Genes Dealt Made Asians Svelte – September 10, 2012

The SAT Zombie Apocalypse – September 29, 2012

Arthur Jensen & JP Rushton – November 1, 2012

Inscrutable Voters – December 6, 2012

Scientists Rediscover the Violence Gene, MAOA-2R – December 30, 2012

The SAT-ACT Score Map – June 10, 2013

Black Suits, Gowns, & Skin: SAT Scores by Income, Education, & Race – October 24, 2013

Parents’ Income Poorly Predicts SAT Score – July 4, 2014

Merit’s Liquidity – October 18, 2014

The SAT in Red, White, and Brown

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The College Board just released another year’s set of SAT results, and Steve Sailer’s blog took notice of the results and the posts that I have recently made on the subject. I try to emphasize science over conjectured analysis on this blog so that my readers can feel some confidence in the knowledge they gain here. Interpreting the SAT is complicated by many factors, including the various tweaks and reforms that the College Board has instituted and the changes in the examinee populations. However, using standard deviations should help in making group comparisons because the students are experiencing the same changes. I have tried to address the differences in demographic groups’ increased participation. In general, every group is increasing their participation more than White people. Here is a graph of each group’s increased participation from the year prior:

When one sees the raw-score graphs below, the trend of Asian advancement is obvious, which exposed the anxieties of many White people in the discussions that I saw. Analysis of the data ultimately becomes a Rorschach test of disposition towards Asian cultures. Clearly, SAT scores are revealing strengths that will serve Asians well wherever meritocracy is allowed. A common reaction from some White people to this data is to try to introduce nuance and critical analysis to emphasize flaws in Eastern societies. I think it is reasonable to conclude that every culture has its flaws, which is a strong argument for cultural exchange. However, I believe that those who are trying to champion these arguments just want to explain away Asian accomplishments to convince Whites that they are superior or at least have enough good points to raise the stock value of racial separation. I have yet to see anyone address the fact that such illustrations could have universal appeal. How does one convince the world that a group of people, like White people, is a nice group without also convincing them that the group is also a nice group to be around? Apparently, White nationalists are trying to posture that every group is nice, but only when each is separate, and mixed groups do not count. I think I can make a stronger case that the success of Asians on the SAT proves that testing is not White-supremacist. In fact, as tuition rates grow, tests are less elitist than education and, therefore, more indicative of important characteristics other than privilege.

Here is the updated graph of the Asian-White score gaps in standard deviations.

Here is the updated graph for the Black-White score gaps.

I have not given much discussion on this blog to people who self-identify as having Hispanic ethnicity or those of Native-American ancestry. I think these can be confusing designations for my purposes because I am interested in genetic research, and such groups have significant ancestral overlap, just as many American White people can claim a fraction of Native-American heritage. I find that these minority groups do not receive as much attention in the scientific literature, probably partly for this reason. Native American SAT scores are based on a relatively small and fluctuating sample size, so I caution against drawing strong conclusions from this graph.

I compiled the three Hispanic groups that the SAT delineates into a single population. The Hispanic sample has grown significantly, so an increasing gap might not surprise. However, I would have expected more changes to the verbal/critical reading score gap, either improvement from acculturation and language mastery or a worsening gap from continued immigration of young non-native speakers. Instead, the math score gap has changed more and seems to have converged with the verbal score gap. I could hypothesize that changes made to the SAT caused it to become a more g-loaded exam like an IQ test because general intelligence is a component of both exam sub-tests. This is a hypothesis that could be tested by re-assembling an older version of the test.

However, the Educational Testing Service’s principal measurement statistician Neil Dorans claimed that the 1995 recentering of the test explains this. “[O]n the original [SAT mathematical] scale, scores below 400 were compressed and scores between 400 and 700 were stretched out…. Hispanic students are 40 points higher at the median on SAT M than on SAT V on the original scale, whereas they have the same median (945) for both SAT M and SAT V on the recentered scale. Thus, the major effect of recentering for Hispanic students was to bring SAT V scores in line with SAT M scores and place both sets of scores closer to the midpoint of the score reporting scale.” He also credited recentering with bringing Asian-American SAT verbal scores “more in line with” SAT math scores. However, recentering was supposed to make each group “appear closer to average on SAT M than they appeared on the original scale,” making Asians, Whites, and men “appear less above average” and do the reverse for Black people, Hispanics, and women, without changing the “rank orderings of individuals.” I wonder if this is why the College Board does not make reports from before the recentering available to the general public. If one ignores the raw score graphs and examines the standard deviation numbers compared to White examinees that are published for Black examinees back to 1986 and for Hispanics back to 1992, one can see that the gaps between Whites and these minorities grew. Perhaps an increased sense of competitive urgency motivated White examinees more after 1995.

Any questions one might still have can be answered with a shrug. Dorans insisted we heed a heedless take on the SAT. “To believe that one set of scales represents ‘truth’ is to reify the score scales in a way that scores on general intelligence tests were reified during the first half of the twentieth century.” Then, he provided a reference to The Mismeasure of Man by Stephen Jay Gould.

Tuesday, September 13, 2011

Attack of the Warrior Gene Babies!

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The so-called “warrior gene” is the reason babies have tantrums. And you thought it was creamed spinach. Okay, I lied. Actually, the first study on the effects of monoamine oxidase A (MAOA) on infants determined that the 3-repeat allele decreases behavioral regulation in Chinese baby girls. Crying was a controlled factor because it could represent fear rather than baby rage. Behavioral regulation was measured by gaze aversion from a menacing toy gorilla. Believe it or not, the inability to do this is associated with childhood externalizing behaviors like fighting and hitting.

The only significant main effect of MAOA was in the girls, which was fodder for interesting discussion of the gender differences and developmental component of the gene’s expression. MAOA is subject to epigenetic methylation, but mostly just in women. The vast majority of that methylation seems to have already occurred by age 5, according to Wong et al. Increased methylation gives women more symptoms of alcohol and nicotine dependence but not antisocial personality disorder, according to Philibert et al. The warrior gene concerns a VNTR (variable number tandem repeat) promoter, but another study by Philibert et al recently discovered a second VNTR that seems to have a greater effect on antisocial personality disorder in women (but not men) than the heavily studied VNTR, and both VNTR influence MAOA methylation in women. The fact that the sex hormones testosterone and estradiol affect MAOA expression should also enter any thorough discussion of sex differences in the warrior gene. Such increasingly complex factors involved in MAOA expression in women are modifying a long-held view that MAOA does not affect women even when it is completely shut off in Brunner syndrome. Or as Dr. Phil put it, “[the warrior gene] is more rare in women, of course” which is not actually true, but at least he is trying.

Speaking of hormones, over the past decade many studies have examined the effects of testosterone and cortisol on aggression. One study determined that testosterone and cortisol even affect the militancy and aggression of Palestinians. Oddly, this research has never seemed to cross paths with research on the proven effects of testosterone and cortisol on MAOA expression. However, scientists have identified a gene-gene interaction between the androgen receptor and glucocorticoid receptor genes, so these might be violence genes just like MAOA, DAT1, DRD2, DRD4, and 5-HTTLPR.

Getting back to the study on babies, this new data also helps clarify the allele frequencies in Asians. I now count a nearly 1,500 cumulative allele sample size among those Asian subjects, predominantly Chinese, for whom selection bias does not apply, and 54% are the warrior gene, which I consider the three-repeat allele (although the much less common 2-repeat allele is also included under this label). This is not much different from that of African Americans, but nearly five percent of African American men have the more violent 2-repeat allele, compared to only one allele of Asian control subjects in the seven studies that I counted. A 2009 editorial that was included in a series of attacks on MAOA research as a reaction to the Rod Lea/Maori controversy claimed Chinese people have the highest warrior gene allele frequency of any ethnic group. That was based on an uncorrected error in The New Zealand Medical Journal that switched the number of subjects (77) with the percentage with the three-repeat allele (55%) from the study by Lu et al. One would think that researchers who study warriors would be more careful.

Zhang M, Chen X, Way N, Yoshikawa H, Deng H, Ke X, Yu W, Chen P, He C, Chi X, & Lu Z (2011). The association between infants' self-regulatory behavior and MAOA gene polymorphism. Developmental science, 14 (5), 1059-1065 PMID: 21884321

Zhou Q, Hofer C, Eisenberg N, Reiser M, Spinrad TL, & Fabes RA (2007). The developmental trajectories of attention focusing, attentional and behavioral persistence, and externalizing problems during school-age years. Developmental psychology, 43 (2), 369-85 PMID: 17352545

Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, Moffitt TE, & Mill J (2010). A longitudinal study of epigenetic variation in twins. Epigenetics : official journal of the DNA Methylation Society, 5 (6), 516-26 PMID: 20505345

Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A (2008). MAOA methylation is associated with nicotine and alcohol dependence in women. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B (5), 565-70 PMID: 18454435

Philibert RA, Wernett P, Plume J, Packer H, Brody GH, & Beach SR (2011). Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder. Biological psychology, 87 (3), 366-71 PMID: 21554924

Victoroff J, Quota S, Adelman JR, Celinska B, Stern N, Wilcox R, & Sapolsky RM (2011). Support for religio-political aggression among teenaged boys in Gaza: part II: neuroendocrinological findings. Aggressive behavior, 37 (2), 121-32 PMID: 21274850

Chen S, Wang J, Yu G, Liu W, & Pearce D (1997). Androgen and glucocorticoid receptor heterodimer formation. A possible mechanism for mutual inhibition of transcriptional activity. The Journal of biological chemistry, 272 (22), 14087-92 PMID: 9162033

Sue Z. Sabol, Stella Hu, & Dean Hamer (1998). A functional polymorphism in the monoamine oxidase A gene promoter Human Genetics, 103 (3), 273-279 : 10.1007/s004390050816

Ono H, Shirakawa O, Nishiguchi N, Nishimura A, Nushida H, Ueno Y, & Maeda K (2002). No evidence of an association between a functional monoamine oxidase a gene polymorphism and completed suicides. American journal of medical genetics, 114 (3), 340-2 PMID: 11920860

Lu RB, Lee JF, Ko HC, Lin WW, Chen K, & Shih JC (2002). No association of the MAOA gene with alcoholism among Han Chinese males in Taiwan. Progress in neuro-psychopharmacology & biological psychiatry, 26 (3), 457-61 PMID: 11999895

Rosenberg S, Templeton AR, Feigin PD, Lancet D, Beckmann JS, Selig S, Hamer DH, & Skorecki K (2006). The association of DNA sequence variation at the MAOA genetic locus with quantitative behavioural traits in normal males. Human genetics, 120 (4), 447-59 PMID: 16896926

Wang TJ, Huang SY, Lin WW, Lo HY, Wu PL, Wang YS, Wu YS, Ko HC, Shih JC, & Lu RB (2007). Possible interaction between MAOA and DRD2 genes associated with antisocial alcoholism among Han Chinese men in Taiwan. Progress in neuro-psychopharmacology & biological psychiatry, 31 (1), 108-14 PMID: 17007976

Lee SY, Hahn CY, Lee JF, Huang SY, Chen SL, Kuo PH, Lee IH, Yeh TL, Yang YK, Chen SH, Ko HC, & Lu RB (2010). MAOA interacts with the ALDH2 gene in anxiety-depression alcohol dependence. Alcoholism, clinical and experimental research, 34 (7), 1212-8 PMID: 20477771

Patrick-Michael Whittle (2009). Darwinism and the nature of Māori MAI Review

Lea R, & Chambers G (2007). Monoamine oxidase, addiction, and the "warrior" gene hypothesis. The New Zealand medical journal, 120 (1250) PMID: 17339897

Tuesday, September 6, 2011

Pulling the Empty Chair on Dr. Kevin Beaver

I laughed out loud when Bill O’Reilly walked out of an interview with Terry Gross in 2003. The NPR Ombudsman, Jeffrey Dvorkin, rebuked her for conducting an “empty chair interview” after O’Reilly left by asking the questions that he did not let her finish. I had never heard of the term “empty chair interview” before that instance, and while it seems to be a violation of journalist ethics, Gross never apologized to my knowledge, and NPR played the occurrence, even though it was not live.

Well, I have decided to release this empty chair interview with Dr. Kevin Beaver, PhD. Dr. Beaver is a famous criminologist at Florida State University and the author and co-author of numerous published studies and academic texts on biosocial criminology. Mainstream media outlets frequently seek comments from him whenever news breaks about the genetics of violence, and I have cited his research from the beginning of this blog. I briefly shared an email exchange with him that was always cordial and professional, and I requested that he answer a list of questions about his research and this field of study for me to post here. Without objecting to the questions, he refused to answer the questions after seeing this blog because he could not endorse the views contained therein. As a man who spent the greater part of my life getting educated at liberal institutions, I completely understand and sympathize, and I expected this response. I hope that nothing I write ever harms his career or research. Perhaps noting his unwillingness to be associated with this blog will convince whichever would-be detractors he might have that he is well-intentioned and a team player.

I have listed the questions I posed to him below with added links to provide additional background. It is worth a read because I premised the questions with some quick summary points of some of the accomplishments and controversies of the research, where I suspect the research might be going, and criticisms I have of Dr. Beaver’s own research methodologies. I welcome any critical comments of my journalistic ethics or otherwise. Of course, many differences exist between this post and the NPR example that I mentioned. First of all, I am not a journalist, and I am not remunerated as Gross is. Secondly, my questions are more informative and required more research than Gross reading from People magazine. Lastly, Dr. Beaver received a copy of all questions and is exercising his prerogative to not respond at all.

In defense of the blog, itself, I do not consider my writings to be mean-spirited or racist. In fact, I have on multiple occasions made an effort to debunk the views of those whom I would label as “white nationalists.” I make no apologies for confronting the pseudo-controversies regarding the validity of IQ, the usefulness of “race” in medical research, and, indeed, the inherently sensitive subjects that Dr. Beaver broaches in his work. In each case, I see a matter of life-and-death importance, and I shall expound on that characterization in future posts. I think a fair assessment of this blog would label it the least radical of the many “human biodiversity” or “race realist” sites. Among these I would include Gene Expression, which carries the imprimatur of Discovery Communications and the Unz Foundation. Its author, Razib Khan, regularly interviews noted academics and authors, and his status seems undiminished by his somewhat outside-the-traditional-mainstream takes on eugenics and whether egalitarian policies should end due to the high heritability of IQ. Oh, and I have never called any of my commenters a “retard.”

Perhaps a savvy reporter will review this page next time before seeking a sound bite from Dr. Beaver. If not, I am glad that I brought these unrequited inquiries to a researcher’s attention, and I insist on interpreting the reticence as a testament to the need for a blog titled The Unsilenced Science.

A June New York Times article that quoted you also mentioned a forensic science panel on creating a genetic database during the first day of the National Institute of Justice conference. How can we obtain more information about the panel discussion? Are minutes available? Will the database allow public viewing?

The New York Times article said that you agreed with the view that “hundreds or thousands of genes” contribute to aggressive behavior as is the case for many complex behaviors. Why should we consider aggression a complex behavior?

Does this view discourage you from studying small numbers of genes, as you have been doing?

The only genome-wide association study of which I am aware related to psychopathy was Viding et al, “In search of genes associated with risk for psychopathic tendencies in children: a two-stage genome-wide association study of pooled DNA.” Are you aware of other such studies that have or will be published?

Do you have any plans to participate in making a genome-wide association study?

Viding et al did not find major genetic loci for psychopathic tendencies in children. Do you expect that aggressive behavior has no especially important genetic loci?

It is my understanding that genome-wide association studies cannot address VNTR components. Therefore, they would not compare the most studied variants of genes like MAOA. How should we reconcile research of such genes with studies like Viding et al?

Do you see any kind of study like a genome-wide association study actually taking VNTR into account in the future?

In your studies of MAOA, you used the convention of including the 2-repeat and 3-repeat alleles in the category MAOA-L, but Guo et al “The integration of genetic propensities into social-control models of delinquency and violence among male youths” and Guo et al “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity” found that the 2-repeat allele had twice as much effect on violent delinquency as either the 3-repeat or 4-repeat alleles and that the 2-repeat allele had more effect than the dopamine genes DAT1 and DRD2. How do you justify following the MAOA-L convention rather than studying the 2-repeat allele separately?

In your study “Genetic risk, parent-child relations, and antisocial phenotypes in a sample of African-American males” you studied MAOA and four autosomal genes. You created an index with the maximum score of 9. Is it correct, therefore, that the X-chromosome MAOA allele was counted as equal to only one allele of an autosomal pair of alleles? Would not the hemizygosity of the X-chromosome allow for increased impact of its alleles?

Why did you decide to not calculate constants to differentially weight genes in this study, as you suggested be studied in the discussion?

Table 4 showed a statistically significant p-value for your genetic index affecting adult violent delinquency but not for parent-child relations. Why did you not highlight this finding in the abstract? Is it wrong to view this as evidence that “nature” has more impact than “nurture”?

According to Scopus, only five studies have cited this study, and all five were by you and your research team. Do you have any thoughts regarding why so few other researcher teams are currently building upon your work?

Why did you decide to exclude the genes MAOA and 5-HTTLPR from the genetic index that you created in “The association between genetic risk and contact with the criminal justice system in a sample of Hispanics”?

According to my PubMed searches, research on MAOA and aggression or antisocial personality disorder has been published at a slower rate since about the time that you started publishing studies on the subject. Have you noticed this, and, if so, do you have any thoughts on the matter?

Much of the research on MAOA seemed to be in response to the Caspi et al study “Role of genotype in the cycle of violence in maltreated children.” His team published a similar study on 5-HTTLPR and depression, which seemed to produce a backlash against all candidate gene research as evidenced by Risch et al “Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression.” The Uher et al study “Serotonin transporter gene moderates childhood maltreatment’s effects on persistent but not single-episode depression: replications and implications for resolving inconsistent results” seemed to try to counter this sentiment in press reports. Have you noticed that this back-and-forth has had any impact on how your candidate gene research is received?

Is violent behavior a disease?

A disproportionate number of studies on MAOA and antisocial personality disorder were negative (Saito et al, Koller et al, Parsian et al, Lu et al, and Prichard et al). Why should antisocial personality disorder be a focus of genetic research? Should not the aggression or impulsive criteria of antisocial personality disorder be considered separately in genetic studies?

Why have you never studied the genetics of intermittent explosive disorder?

Do you see the Diagnostic and Statistical Manual of Mental Disorders (DSM) as adequate in addressing these subjects?

Have you been in contact with anyone regarding the shaping of DSM-V?

Other studies (Chakrovorty and Halbreich, Chevillard et al, Gundlah et al, Klaiber et al, Luine et al, Ma et al, Ou et al, Redmond et al, Sjoberg et al, and Smith et al) suggest MAOA interacts with the hormones testosterone, estradiol, and cortisol. Why have you chosen to not include hormonal factors in your research? Could not an index that includes multiple aggression-associated genes, hormone levels, and hormone receptor genetic alleles produce more powerful results?

Fowler et al “Brain monoamine oxidase A inhibition in cigarette smokers” found that smoking lowers brain MAOA. Why have you not included smoking status as a factor in your studies—or have I missed you doing so?

You appeared in the National Geographic documentary on MAOA. Have you seen the completed version, and would you care to comment on it?

When this documentary came out, the Dr. Phil program also dedicated an episode to MAOA. Have you seen that, and would you care to comment on it?

You opposed the decision by an Italian court to reduce the sentence of Abdelmalek Bayout, but the testimony of Dr. William Bernet helped do something similar for Bradley Waldroup in Tennessee. Did Dr. Bernet act irresponsibly?

What steps would you recommend that our criminal justice system take regarding exculpatory genetic evidence of this sort?

Should the insanity defense be expanded or contracted based on your research?

How, if at all, have the controversies associated with biosocial criminology impeded your work?

Prior to your research on MAOA, some studies and editorials cited Widom and Brzustowicz “MAOA and the ‘cycle of violence:’ childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior” that questioned “the suitability of using the MAOA promoter VNTR polymorphism as a proxy for MAOA levels in non-white populations” based on a comparison between whites and non-whites of unrevealed ethnic proportions and without taking gender into account. Would you say that your research has upset the potential for racial harmony on this issue and made studying the genetics of violence more difficult?

Are you familiar with the controversy surrounding Dr. Rod Lea, the New Zealand scientist who was quoted as saying that his research on MAOA “has implications suggesting links with criminality among Maori people”? Do you have an opinion on how he or the media acted during that controversy?

In general, Asian societies like Japan have low rates of violent crime, but East Asians have higher rates of violence-associated alleles, including the 3-repeat allele of MAOA, the short allele of 5-HTTLPR, and the 10R allele of DAT1. Do those facts seem contradictory to you, or do you see a possible explanation?

Chiao and Blizinsky in “Culture-gene coevolution of individualism-collectivism and the serotonin transporter gene” suggested that culture evolves with specific alleles to prevent side effects like depression in those with the short allele of 5-HTTLPR. Do you have thoughts on this hypothesis, and have you considered conducting research related to culture-gene coevolution and aggression?

Has the decline in crime rates made your work in biosocial criminology more or less challenging and in what ways?

What plans do you have for future research on the genetics of aggression?

Are there additional candidate genes that you would like to include in future research?

Are you planning on studying or have interest in searching for individuals with Brunner syndrome?

Friday, September 2, 2011

The SAT’s Cohen’s d & the Topography of IQ Denialism

In the comments of my previous post about IQ and the SAT, Chuck11 helpfully pointed me to the formula for pooled variance to make the appropriate calculation for Cohen’s d and a collection of data points for the Black-White SAT gap beginning in 1987. I do wish that the College Board would simplify everything by releasing all of their reports online, so that I would not need to rely on texts like this and The Bell Curve. The Bell Curve did not use pooled variance for the data they provided in 1976, 1980, 1991, and 1993, so I shall not combine their data with this new data. In general, SAT data show high standard deviations for Asians, “other,” and “no response,” and show low standard deviations for Black people and Mexican-American people. Using Cohen’s d with pooled variance had little effect on the Asian-White graph, but the Black-White SAT graph of the math subtest now looks more dramatic, and the new data reveals the inflection point of the early 1990s more clearly, during which a steep gap decline pivoted to the rising trend that we have seen mostly since. The SAT revamp of 2005 seemed to rapidly shrink the verbal test Black-White gap, but it grew back.

One commenter seemed to want to know the raw score differences, so I shall also post them, even though this is not a typical presentation of this sort of data.

My first blog post mentioned how I think it is odious to compare and that race realists have been too obsessed with IQ. The recent genome-wide association study, Davies et al, has certainly helped convince me that we are living in an important era for IQ research. Also, I am finding it increasingly offensive for educated, otherwise reasonable people to continue to deny the existence and validity of IQ. Henry Louis Gates, Jr. once expressed the view that the IQ and race controversies can make black people feel shut out of intellectualism. I sympathize with this view, but I can also see that many liberal white people use the racism critique as a cudgel against intellect, itself. In fact, the enemies of IQ actually seem to have disparate views. Some think IQ is not real. Others question its importance. Stephen Jay Gould had an autistic child and seemed to support IQ testing as a means of separating the “retarded” from the “normal.” He also gave some recognition to genius when he referred to “the company of Newton and Einstein.” However, he was reincarnated as Malcolm “igon value” Gladwell, who promised us that “once someone has reached an IQ of somewhere around 120, having additional IQ points doesn’t seem to translate into any measurable real-world advantage.” There you have it: liberal America’s favorite author says that George W. Bush has an IQ fit for a genius. The hardest part of defending IQ is figuring out where IQ’s enemies hid the goal posts.