The Unsilenced Science

Blacks with Bullets Embedded in Bone

noreply@blogger.com (nooffensebut) — Fri, 02 Dec 2011 23:10:00 +0000

nce upon a time, a people now known as African Americans left plantations of slavery to live in relative peace among white people. Unfortunately, the mean, villainous whites schemed systems of organized crime that allowed them to enrich themselves into tranquil opulence, while they excluded the African Americans from their illegal get-rich connivances. Amidst their impoverishment, the African Americans experienced a psychological transformation that forced many of them to become violent criminals. The End.

This story emerges from the works cited by Steven Pinker in his bestselling, and possibly Pulitzer Prize-winning book, The Better Angels of Our Nature. Pinker writes,

Figure 3-14 shows the rates for two cities in which black-on-black and white-on-white homicides can be distinguished. The graph reveals that the racial disparity in American homicide has not always been with us.

Here is the figure:

He cites Eric Monkkonen’s Murder in New York City, which says,

Essentially, crime was more profitable for whites, whereas even in crime, discrimination blocked the more lucrative opportunities for African Americans and encouraged more violent, destructive offenses.

Pinker’s characterization of homicide data is another example of his distortions on matters pertaining to race and violence. See my previous post on how Pinker flubbed his summary of the decades of research on the best understood violence gene, including his citation of a copy-and-paste error. Much of his data for New York City in the above graph, including all years of equal homicide rates, comes from American History by Randolph Roth, who plotted a similar graph shown below and made clear that the data plotted actually do not represent known intraracial homicide assailants, but just homicide victims.

In fact, Roth further qualified the data for Philadelphia:

It may prove that blacks accounted for a greater proportion of homicide perpetrators than victims in Philadelphia, but determining that will require more data, including a tally of blacks and whites killed in riots. Blacks committed homicide there at over twice the rate whites did, 1839-1846, according to indictment records (6.5 per 100,000 adults per year versus 2.7), because they were more likely to commit both intraracial and interracial homicide. It may be that Philadelphia’s antiblack riots, the disfranchisement of blacks in Pennsylvania, and increased competition with whites for unskilled jobs were beginning to take their toll.

Roger Lane also questioned Philadelphia’s homicide victimhood data because coroners’ records “proved unreliable.” Coroners frequently failed to indicate that a death was a homicide. Ted Robert Gurr thought this problem might exist in other American cities of that era, but no one had bothered to check as Lane had done in Philadelphia.

Roth did provide actual estimates of New York City homicides, which doubled the very small racial gap in victimization. For Philadelphia, Pinker was not clear whether and for what years he made use of Roth’s data. Roth estimated that, from 1839 to 1846, Philadelphia’s African-American rate of homicide victimization was 28 percent higher than that of whites.

Monkkonen provided some context for the period of purported New York City homicide racial equality. First, he advised caution about the quality of the data. “Even though we can outline this demographic history of black New Yorkers, we cannot yet establish precise population measures… Thus, any construction of rates with at-risk denominators must be understood as estimates.” How unfortunate that this important historic moment of violence equality was so poorly documented.

Generalizing New York City to the rest of America has other complicating factors. Monkkonen offered estimates that suggest that racial homicide equality resulted from enormous white ethnic inequality. “My best estimate for the decade centered on 1860,” he wrote, “sets the Irish homicide rate at 37.5 per 100,000 adult males, the German rate at 15.7, and the black rate at 32.” About half of New York City’s population was immigrant in 1860. It is ironic that Pinker is allowing the violent tendencies of New York Irish-American immigrants to characterize the behavior of American whites in general because English Americans took to calling them “white Negroes.”

Lastly, the age demographics of these groups differed. In 1850, Irish immigrant males in New York City were 19 percent more likely to be in the potentially more violent age range of 16 to 45 than African-American men, and, despite being half as homicidal, German immigrant men were 73 percent more likely than African-American men to be in that age range. Monkkonen does not entirely attribute the eventual growth of a large racial homicide gap to poverty because New York City experienced a massive growth of young black men, such that in 1940 only 19 percent of African-American New York City men in this age range were born there.

Another recently published study, which Pinker did not consider, about this period described a qualitative distinction of racial patterns of violence. Last year, Carlina de la Cova published the first large-scale analysis of its kind, reviewing 651 male cadavers “of low socioeconomic status born between 1825 and 1877” from Cleveland, St. Louis, and Washington DC. Though these remains are apparently not of homicide victims, they do offer evidence of racial differences in violence from that era, but only among the poor, as none owned property, and most were transient. Thus, the study should bias towards exaggerating white delinquency with a sample more unrepresentative of whites than African Americans.

Although fully 92 percent of all cadavers had skeletal fractures, in every category of fracture, whites had more. The smallest differences were for injuries that were most plausibly from serious fights. 50 percent of whites had cranial fractures, compared to 48 percent of African Americans. 44.8 percent of whites had nasal fractures, compared to 42.3 percent of African Americans. Differences for vertebrae fracture rates were much greater, at 72.7 percent for whites and 35.8 percent for African Americans. De la Cova considered osteoporosis as a possible explanation. She noted that African Americans have less osteoporosis, greater bone mass, denser cortical bone, and lower bone resorption. Indeed, black people have greater bone mineral density from infancy, and hormonal levels contribute to such racial differences, even in childhood,. (Recall that the media accused research oncologist Kathy Albain of “racial medical profiling” for discovering that racial disparities in cancer mortality remain only in cancers related to sex hormones after accounting for zip code.) Of course, skin color affects the pathways of the hormone vitamin D. De la Cova checked for an influence of osteoporosis and age of death, but that negative result does not negate the fact that black people have stronger bones even in comparisons of whites and blacks without osteoporosis. This seems to extend to tooth loss, which de la Cova also utilized in her attempt to support differing rates of fighting. Even in the present-era National Health and Nutrition Examination Survey-III, in which whites were better educated, white people still had a higher rate of tooth loss than African Americans and Mexican Americans. In fact, having less education was significantly associated with tooth loss in white people, but not African Americans and Mexican Americans.

Even so, de la Cova points to historical accounts of popular and “ritualized” pugilism among poor white men to settle disputes and protect their “honor,” which logically might play less of a role in the violent behavior of a systematically oppressed minority.

On the other hand, black men comprised all eight of the gunshot wounds, most having a bullet embedded in a bone. Though this was a small number of the cadavers, historical accounts and African-American newspaper advertisements also reflected a gun-oriented African-American culture. Perhaps their early association with guns made fistfights an untenable means of resolving conflicts.

The US Census Bureau did not start tracking crime until 1880, and despite being a minority, African Americans were receiving 54 percent of unlawfully concealed weapons charges and 75 percent of exhibiting a deadly weapon charges and were committing 83 percent of shootings, 85 percent of stabbings, 48 percent of manslaughter homicides, and 43 percent of murders.

Perhaps the best argument for an era of relative homicide equality would be the well-documented, enormous widening of the racial homicide gap in the years that followed. Gurr provided an illustrative graph of this for Washington DC.

Here is Jeffrey Adler’s homicide graph for Chicago when African Americans were a tiny minority of the population.

Societal changes can influence patterns of violence, and these years certainly qualified as profoundly transformative for African Americans. However, given that African Americans have higher allele frequencies than whites of all or (debatably) nearly all identified violence genes, anyone who advertises a distant past of black peaceableness deserves an inspection of their data. I suggest this should even be so for a beloved Harvard celebrity professor.

Adler, Jeffrey S. 2006. First in Violence, Deepest in Dirt: Homicide in Chicago, 1875-1920. Cambridge, Mass.: Harvard University Press.

De La Cova C (2010). Cultural patterns of trauma among 19th-century-born males in cadaver collections. American Anthropologist, 112 (4), 589-606 PMID: 21132946

Gurr, T. (1981). Historical Trends in Violent Crime: A Critical Review of the Evidence Crime and Justice, 3 DOI: 10.1086/449082

Hui SL, Dimeglio LA, Longcope C, Peacock M, McClintock R, Perkins AJ, & Johnston CC Jr (2003). Difference in bone mass between black and white American children: attributable to body build, sex hormone levels, or bone turnover? The Journal of clinical endocrinology and metabolism, 88 (2), 642-9 PMID: 12574194

Jimenez M, Dietrich T, Shih MC, Li Y, & Joshipura KJ (2009). Racial/ethnic variations in associations between socioeconomic factors and tooth loss. Community dentistry and oral epidemiology, 37 (3), 267-75 PMID: 19302573

Lane, Roger. 1979. Violent Death in the City: Suicide, Accident, and Murder in Nineteenth-Century Philadelphia. Cambridge, Mass.: Harvard University Press.

Monkkonen, Eric H. 2001. Murder in New York City. Berkeley: University of California Press.

Pinker, Steven. 2011. The Better Angels of Our Nature: Why Violence Has Declined. New York, New York: Viking Penguin.

Roth, Randolph. 2009. American Homicide. Cambridge, Mass.: Harvard University Press.

The Education Bubble

noreply@blogger.com (nooffensebut) — Mon, 24 Oct 2011 23:02:00 +0000

Occupy Wall Street protests are drawing more attention to the Education Bubble. Since I coined the phrase, “Education Bubble,” I thought that I should repost my YouTube video about it. I originally posted this on May 4th, 2006, two years before Charles Murray published Real Education and three years before articles about the bubble began appearing in mainstream publications like The Chronicle of Higher Education and The Economist. Wikipedia claims that Bill Bennett originated the concept, but his editorial in 1987 did not use the phrase, and, of course, could not relate it to the series of economic bubbles that have occurred since.

The idea has really caught fire recently. PayPal founder Peter Thiel created a grant to encourage young people to skip college and start a business. He joined Murray in an Intelligence Squared debate on the subject. On Friday, comedian Bill Maher endorsed the existence of an education bubble on his HBO program, which elicited the typical, kneejerk reaction from liberal columnist Thomas Friedman to pump more money into educating more students. Friedman wants another GI Bill, but we did have a Post-9/11 GI Bill.

In order for credentials to have solid value, they must be a precious resource (to the extent that educational benefit bolsters zero-sum competitiveness), represent value added, and represent a quality of enduring merit. Because one often associates education with intelligence, and IQ tends to hold a stable value throughout an individual’s adulthood, one way to strengthen education’s value would be to make it more closely approximate IQ through stiffer admission policies or more challenging coursework. This also begs the question of whether allowing IQ testing in hiring would not be more efficient and, thereby, allow education to fill a different niche. Columnists like Friedman like to emphasize the role of education in teaching skills, but many skills do not necessarily endure as IQ and perhaps perseverance can. After the dot-com bubble burst and many engineers and computer scientists lost jobs, I recall James Fallows suggesting that graduates be able to purchase skills insurance so that their heavy investment does not crash when their particular set of specialized skills becomes obsolete. Maher quotes Fareed Zakaria in repeating the clichéd complaint about America’s paucity of engineers, but why should young people invest in advanced high-technology skills when someone as experienced and intelligent as Warren Buffett does not even feel confident in betting some money in high-technology companies. Even if the modern “information age” economy demands a more educated populace, there is no other age in which everyday folks had more access to cheap or free knowledge without needing to earn college credits in the process. Books are now available via illegal downloads as music has been for years, and bookstores are closing down permanently. Higher education is too expensive to constantly retrain workers, but tests could inexpensively verify knowledge or abilities.

What I find most ironic about the Education Bubble is that a liberal like Maher would endorse it without seeing that nearly any implication of it endorses politically incorrect concepts like IQ and the limitations of the well-meaning societal intervention that higher education is. All of this discussion is a high-wire act over the issue of race. It might not be “nice” to talk about race honestly, but racial disparities in IQ, SAT scores, and college majors are constants with profound economic impacts. Any reform will stir racial controversies with new disparities. Businesses cannot use straight IQ tests for reasons of race, alone. Can we afford our racial consensus?

Kill Popular Science

noreply@blogger.com (nooffensebut) — Thu, 13 Oct 2011 12:04:00 +0000

Steven Pinker’s new book, “The Better Angels of Our Nature,” is out, and the reception reminds me of an album release from a trendy band during the 1990’s. I must beg my readers’ forgiveness for writing this very preliminary review for a book that I have not finished because the subject matter is so important. Most reviews and buzz for this book center on Pinker’s observations about the decline of violence and the advance of enlightened views. Pinker has been speaking about this phenomenon for years, and many facets of it are apparent in my own lifetime, such as the utter metamorphosis of public consensus regarding homosexuality. The book has a number of fascinating graphs that speak to the changes, and I have little reason to critique his central thesis, other than to say that I am not sure the trend entirely represents genuine progress. For example, I suspect that he could have placed a graph of the decline of fat jokes alongside his graphs of the decline of racial prejudices. While society has improved control over physical aggression, the obesity epidemic proves that indiscipline still finds expression. In fact, when one considers the growing acceptance of “alternative”—excuse me, “integrative” medicine, one can see how the triumph of enlightened tolerance can coincide with a lax shrug off of reason and scientific rigor.

Though I perused the tome in the modern cursory version of the word’s contradictory meanings, I gave special attention to the latter chapters, particularly chapters 8 and 9 on the nature of violence, itself, which has been one of my obsessions. That discussion concerns the overriding paradox of this work. How could this man, who wrote The Blank Slate to passionately declare that we are not and that behavior is part heredity, reconcile with a belief that societal evolution pushed radical behavioral modification? I regret to say that this was a serious weakness of an otherwise well-reasoned exposition.

First let me stress that I do not see Pinker’s observations as fundamentally opposed to the revolution taking place in biosocial criminology and genetic psychiatry. On the contrary, making aggression anomalous likely accentuates the role of genetics and biology in what deserves to be considered a veritable behavioral disease. What science really calls into question is whether historic trends justify extrapolation, and from what I can tell, Pinker has dodged such speculation. To illustrate his handling, the book contains extensive discussion of how the secular rise in IQ, known as the Flynn effect, could be reducing violence, but I found no mention of the evidence for subsequent plateauing. Then again, my hope is that the research on the genetics of violence, which I attempt to elucidate, could help channel efforts to find new ways, including pharmacological developments, to sustain aggression’s decline.

Judging by Pinker’s treatment of the subject, my message is not getting out. He dismissed research on monoamine oxidase A (MAOA) using a study with which my regular readers are all too familiar.

[A]n association between the gene and aggression has not been found in non-European populations, perhaps because they have evolved other ways of regulating their catecholamine levels. (Genes often act in networks regulated by feedback loops, so in populations in which a particular gene is less effective, other genes may step up their activity to compensate.) For now, the Warrior Gene theory is staggering around with possibly fatal wounds.

Nice try. Pinker is referencing the Widom and Brzustowicz paper that combined men and women to compare “whites” to “non-whites.” Gender was not controlled, and that white sample was 33% female. Non-whites were 38% female, but women were far more represented among non-white subjects with the low-activity, 3-repeat allele. For the subjects with the 3-repeat allele, which is the allele considered most impacted by the environmental trigger, whites were 24% female, and non-whites were 43% female. Antisocial behavior in women, but not men, is mediated by the epigenetic methylation of MAOA as well as a newly discovered second promoter that actually has more effect in women than the alleles mentioned. Also, of course, MAOA is located on the X chromosome. Women have two copies, which helps explain why even the radical Brunner-syndrome mutation that completely disables the gene does not seem to affect the behavior of women. It can be nice to have a spare.

Pinker seems to have received his introduction to this subject through the New Zealand Maori controversy, in which Rod Lea had to make amends for allegedly saying that the Maori are prone to criminality. Thus, Pinker is completely unaware that studies have found that MAOA influences aggression in non-whites. Weder et al found that the gene-environment association of MAOA and aggression held for a 58-subject sample of African-American and biracial children. Kevin Beaver’s research also helps support this association. His 2009 study on MAOA’s effect on gang membership and weapon use included African Americans. His 2010 study on African-American men and violence used a genetic index that included MAOA and four other genes that affect catecholamine levels.

At least claiming that MAOA does not affect non-white people fits a politically correct agenda of raising the self-esteem of minorities who feel the burden of a violent stereotype. What would you think of Steven Pinker if he spread a complete falsehood that could label a group of people genetically violent without any scientific basis whatsoever?

[T]he low-activity version of the gene is even more common in Chinese men (77 percent of whom carry it), and the Chinese are neither descended from warriors in their recent history nor particularly prone to social pathology in modern societies.

I previously debunked this, but I guess I must do so, again. A study by Lu et al found that 42 Taiwanese men, or 55% of their 77-subject control sample, had the 3-repeat allele of MAOA. Lea and Chambers copied the information incorrectly. Then, an editorial against MAOA research by a doctoral student repeated the falsehood. Now, Pinker has immortalized this slander against Chinese people in a bestselling book. The actual allele frequency given by Lu et al matches the allele frequency found for Asians in subsequent research, which is not higher than that of other groups besides white people. Pinker, like so many others, conflated the 3-repeat allele with the 2-repeat allele as the “low-activity allele,” even though the 2-repeat allele doubles the association with violence without needing an environmental trigger. The 2-repeat allele accounts for 4.7% of African-American MAOA genes and 0.00067% of Asian MAOA genes (assuming that the only Chinese control subject with the allele did not have mixed ancestry). Not only does this bogus insult create a new stereotype for Chinese people, but the numbers error reinforces an old generalization, as all four guilty parties were white boys. (Chinese people, when you buy my neighborhood, recall that I personally sent Pinker a corrigendum request.)

Herein lies the problem with popular science. Steven Pinker is a Harvard professor who previously chastised Malcolm Gladwell for misspelling “igon value.” Pinker’s new book encompasses a prodigious collection of disparate lines of evidence. Even so, he dismissed a vital segment of potentially life-saving research using biased sources that were motivated at least in one case by racial politics. When Dr. Phil stumbled through his television show episode on the warrior gene, he made mistakes and showed his ignorance, but he did not bring an entire field of study into disrepute. However, when Malcolm Gladwell or Stephen Jay Gould call IQ testing an “ice flow” or decry its “reification,” it has consequences for science. Gladwell and Pinker inhabit a pantheon of respected liberal thinkers whose influence reverberates throughout academia. Their stature alone can transform an ignorant statement into an authoritative observation. Their superficial summations can leave a lasting imprint on another’s life’s work, as they bring along a vast audience of comparative ignoramuses to boo rogue points of view (not unlike a daytime talk show).

Widom CS, & Brzustowicz LM (2006). MAOA and the "cycle of violence:" childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological psychiatry, 60 (7), 684-9 PMID: 16814261

Weder N, Yang BZ, Douglas-Palumberi H, Massey J, Krystal JH, Gelernter J, & Kaufman J (2009). MAOA genotype, maltreatment, and aggressive behavior: the changing impact of genotype at varying levels of trauma. Biological psychiatry, 65 (5), 417-24 PMID: 18996506

Beaver KM, DeLisi M, Vaughn MG, & Barnes JC (2010). Monoamine oxidase A genotype is associated with gang membership and weapon use. Comprehensive psychiatry, 51 (2), 130-4 PMID: 20152292

Kevin Beaver, Ashley Sak, Jamie Vaske, & Jessica Nilsson (2010). Genetic risk, parent–child relations, and antisocial phenotypes in a sample of African-American males Psychiatry Research, 175 (1-2), 160-164

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

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

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

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

Girls Versus Boys: The Final Battle

noreply@blogger.com (nooffensebut) — Sun, 09 Oct 2011 14:26:00 +0000

SAT data provide an exciting reservoir of information thanks to extremely large sample sizes with detailed demographic data over a number of years. I previously graphed SAT scores by race and showed that the score gap between White people and African Americans greatly narrowed until the early 1990’s and that Asian Americans have been improving their SAT scores, unlike other groups. Now, I shall present how men and women compare for each racial group.

In 1966, William Petersen coined the phrase “model minority” to recognize the accomplishments of Japanese Americans. Liberals revised the label to “model minority myth,” which imparts elements of bitter sneering and jealousy, but the original compliment has never been truer for the SAT results of Asian Americans. Asian-American women appear to be advancing even faster than their male counterparts. Recent years have brought declines in the standard deviation gaps between Asian-American men and women on the math and critical reading (formerly “verbal”) sub-tests.

May all the trees that died for treatises on the eroticization of Asian women and the emasculation of Asian men rest in peace. With that said, I shall add my Asian Female Fit Hypothesis: Asian women are able to progress faster than other demographic categories because they transcend gender roles and expectations, in contrast with White women.

Though White women did slightly improve last year on the math SAT sub-test relative to White men, that was mostly due to a slight drop in the male score. Numerous factors could be discouraging academic progress for White women, particularly in math and the hard sciences. White women, as a group, might not place as high a priority on accomplishment in mathematics. Perhaps they see math as leading to career tracks that are less enjoyable or that would earn an income that would intimidate male suitors. Perhaps they associate math with demanding but financially rewarding careers, and some of them feel that only men should have to fill such a demanding provider role. Advanced math coursework and preparation could have a culture that is unappealing to White women. Also, a common view argues that women feel displaying intelligence makes them less attractive to men. For both young men and women, distractions can hurt academic performance, but perhaps White women are more preoccupied by them than White men.

I suggest that Asian-American women are able to transcend such barriers better than White women. Asians, in general, have a higher average IQ and tend to perform especially well on the SAT math sub-test. This advantage could give Asian women a confidence with mathematics above some threshold that makes further study more enjoyable and less intimidating. Another commonly held view is that Asian women are more amenable, perhaps owing to Confucian values, to relationships with studious men with whom they would come more in contact. I think that men actually do appreciate intelligent women, and the cultures of professions steeped in mathematics, like engineering, are so lacking in female representation that Asian women on such professional paths might be finding a comfortable niche. I also propose that Asian women have the advantage of simple beauty.

At first, one might think that physical attractiveness has nothing to do with mathematics skill, but beauty and fashion have a profound effect on the self-esteem of young women and can become a demanding preoccupation. Many Asian women have a simple beauty that does not really require makeup or hair treatments in modern American culture. Most Asian women whom I have known also seem to be naturally thin without exercising. A recent large meta-analysis of genome-wide association studies found three important loci for body fat percentage. According to the HapMap database, two of the alleles associated with increased body fat are far more common in White and Black people than in Chinese and Japanese people. The third allele is somewhat more common in Japanese and Chinese people, but the study found that this allele was associated with body fat percentage in Europeans, not in people from Northern India.

Allele Frequencies of loci that increase body fat percentage:

FTO:
White – 46.0%
Chinese – 13.9%
Japanese – 18.6%
African-American – 46.5%
Nigerian Yoruban – 45.2%
Mexican-American – 20.7%
Native-American – 25.2%

IRS1:
White – 41.8%
Chinese – 10.0%
Japanese – 6.8%
Nigerian Yoruban – 64.3%

SPRY2 (increased body fat percentage in Europeans, not Northern Indians):
White – 27.7%
Chinese – 48.1%
Japanese – 45.0%
African-American – 14.0%
Nigerian Yoruban – 18.4%
Mexican-American – 35.3%
Native-American – 48.5%

African-American women also are closing their gap with African-American men on the SAT math sub-test, but scores for Black people, as a whole, are declining, and the gap with White people seems to be slightly widening, as I previously discussed. Still, African-American women are the only demographic to consistently outperform their male counterparts on the SAT critical reading sub-test. On the newer writing sub-test, all demographics have a female advantage, but African Americans have the largest gender gap, and it is growing. Ever since the writing sub-test began in 2006, African-American women have had a consistent total raw score advantage over African-American men, and they are the only group of women to ever do so. Although it might be declining, the Hispanic male advantage over Hispanic women lies at the other end of the spectrum.

In conclusion, whether you are a dumb blonde, a dragon lady who is good at math, a troubled Black man, or a macho Mexican, the SAT reinforces the offensive stereotype that is right for you.

Kilpeläinen TO, Zillikens MC, Stančákova A, Finucane FM, Ried JS, Langenberg C, Zhang W, Beckmann JS, Luan J, Vandenput L, Styrkarsdottir U, Zhou Y, Smith AV, Zhao JH, Amin N, Vedantam S, Shin SY, Haritunians T, Fu M, Feitosa MF, Kumari M, Halldorsson BV, Tikkanen E, Mangino M, Hayward C, Song C, Arnold AM, Aulchenko YS, Oostra BA, Campbell H, Cupples LA, Davis KE, Döring A, Eiriksdottir G, Estrada K, Fernández-Real JM, Garcia M, Gieger C, Glazer NL, Guiducci C, Hofman A, Humphries SE, Isomaa B, Jacobs LC, Jula A, Karasik D, Karlsson MK, Khaw KT, Kim LJ, Kivimäki M, Klopp N, Kühnel B, Kuusisto J, Liu Y, Ljunggren O, Lorentzon M, Luben RN, McKnight B, Mellström D, Mitchell BD, Mooser V, Moreno JM, Männistö S, O'Connell JR, Pascoe L, Peltonen L, Peral B, Perola M, Psaty BM, Salomaa V, Savage DB, Semple RK, Skaric-Juric T, Sigurdsson G, Song KS, Spector TD, Syvänen AC, Talmud PJ, Thorleifsson G, Thorsteinsdottir U, Uitterlinden AG, van Duijn CM, Vidal-Puig A, Wild SH, Wright AF, Clegg DJ, Schadt E, Wilson JF, Rudan I, Ripatti S, Borecki IB, Shuldiner AR, Ingelsson E, Jansson JO, Kaplan RC, Gudnason V, Harris TB, Groop L, Kiel DP, Rivadeneira F, Walker M, Barroso I, Vollenweider P, Waeber G, Chambers JC, Kooner JS, Soranzo N, Hirschhorn JN, Stefansson K, Wichmann HE, Ohlsson C, O'Rahilly S, Wareham NJ, Speliotes EK, Fox CS, Laakso M, & Loos RJ (2011). Genetic variation near IRS1 associates with reduced adiposity and an impaired metabolic profile. Nature genetics, 43 (8), 753-60 PMID: 21706003

Intelligence

noreply@blogger.com (nooffensebut) — Sun, 18 Sep 2011 08:39:00 +0000

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

The SAT in Red, White, and Brown

noreply@blogger.com (nooffensebut) — Sun, 18 Sep 2011 07:07:00 +0000

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.

Attack of the Warrior Gene Babies!

noreply@blogger.com (nooffensebut) — Tue, 13 Sep 2011 20:07:00 +0000

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

Pulling the Empty Chair on Dr. Kevin Beaver

noreply@blogger.com (nooffensebut) — Wed, 07 Sep 2011 05:12:00 +0000

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.

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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?

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

noreply@blogger.com (nooffensebut) — Fri, 02 Sep 2011 23:09:00 +0000

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.

A Picture is Worth a Thousand Blogs

noreply@blogger.com (nooffensebut) — Wed, 31 Aug 2011 05:13:00 +0000

I have been meaning to write a blog post as a generic response to every not very smart genetics blogger who thinks he or she is smart because he or she wrote that there is no single gene for something. The only thing holding me back has been that I do not want to seem too angry because I am a nice guy in real life. You see, according to them, a behavior like having a fit of rage is so complex that it must be molded by thousands of genes, each only supplying the slightest tincture of that immense complexity. My response had been to say, “What about Brunner syndrome?” Brunner syndrome causes fits of rage and is the product of just one gene. They instantly become indignant (fit of rage?) because Brunner syndrome is rare. That is true, but it proves that one rare gene can drive a “complex behavior,” so why can’t a few somewhat uncommon genes cause the somewhat uncommon behavior of violent delinquency? Or three genes and crime:

Meet Towelie, the IQ Test of the Future

noreply@blogger.com (nooffensebut) — Sat, 27 Aug 2011 18:57:00 +0000

Popular culture warrants serious study. Take, for example, the 1991 movie Boyz N the Hood from the short-lived black-whining-drama genre. The film was almost universally praised despite its predictability and clichés. A major plot point hinged upon the SAT test, which used to stand for Scholastic Aptitude Test before it stood for Scholastic Assessment Test before it officially did not stand for anything. The omniscient, two-dimensional father figure in the movie gave us a pat summary of the SAT and IQ tests. “Most of those tests are culturally biased to begin with. The only part that is universal is the math.” However, data from the College Board disproves his assumption.

Below is the Black-White SAT score gap in standard deviations using College Board data that is available online from 1996 onwards and some additional data that Herrnstein and Murray obtained and published in The Bell Curve.

So, the “universal” math portion of the test produces a larger gap than the “culturally biased” verbal portion. The gap has clearly shrunk since the mid-70’s but is now flat and might even be slightly increasing. This could mean that racial egalitarianism has reached diminishing returns in Black college preparedness. When the pool of participants increases, it tends to create downward pressure on SAT scores because the proportion of people attending college is increasing and adding students who would not have been prepared to go to college in previous eras. To test whether the growth of Black SAT participation is responsible for the lack of decline in the Black-White SAT gap, I added a bar graph for the percentage increase of Black participants minus the percentage increase of White participants.

This shows that the percentage of Black people taking the SAT has been increasing faster than the White percentage, but the size of these increases do not seem to clearly coincide with changes in the gap. Compare this to the gaps between Asians and Whites.

Asians are also taking the SAT at a more accelerated participation rate, but their scores are also improving relative to Whites. They have reached parity with Whites on the verbal and written tests, while their math performance is increasingly surpassing that of White students. Consequently, the notion that cultural bias influences scores would be more logical in support of the conclusion that the strong performance of Asians is not yet at their potential, rather than the conclusion that Black students are suffering from such a bias.

Perhaps in response to such data and the attention brought to it by the bestseller status of The Bell Curve, egalitarian psychologists proposed a concept in 1995 called “stereotype threat,” the idea that internalized stereotypes in test takers undermine performance. My initial reaction to this notion was that the egalitarians were making a desperate reach for an untestable hypothesis for the sake of plausible deniability. However, it appears that this notion has led to an interesting array of research and a number of applications besides the Black-White score gap. They also traded relevance and subtlety to attain testability. After all, implying insults to black students before a test is not exactly standard proctoring procedure.

Now that the evidence for a high heritability for intelligence is stronger with corroborating lines of evidence, it is clear that the future of IQ testing will jettison the test experience altogether. In other words, the future of IQ testing will be examination of its physical underpinnings, including but not limited to genetic tests. A recent “debate” of two YouTube personalities featured an egalitarian who copied the questions from an inquirer speaking with controversial University of Western Ontario scientist JP Rushton. In the interview, the Black Al Jazeera journalist Rageh Omaar asked Rushton, “What then are the genes that determine intelligence? What are they? Can you name them?” The question was probably disingenuous, since it is easy enough to find out that genetic studies show no powerful IQ loci. However, the more up to date reply would be that naming most of them is possible if one has time because a recent study of 600,000 single nucleotide polymorphisms showed that they account for 51% of fluid intelligence. The study was not an exhaustive examination of human genome variation because there are many more differences yet to be studied in the many less common single nucleotide polymorphisms, as well as copy number variants and variable number of tandem repeats. A more detailed understanding could come from studies like the one being led by University of Oregon scientist Steve Hsu, who is developing a genome-wide association study of people with an intelligence level of about three standard deviations above the mean (an IQ of 145) or higher. Tellingly, his study is supported by a third-world country that has a serious need for reform of its own scientific establishment. I would suggest that fear of understanding the genetics of IQ plays a role in the potential for China to overtake America in this area.

Unlike twins studies, genome-wide association studies would advance race realism because probably most IQ variants affect IQ in all humans who have them, and the distribution of these variants in not likely to be geographically uniform.

Therefore, the future of the popular critique of IQ will be less Boyz N the Hood and more Gattaca. In Gattaca, a space flight company surreptitiously obtains genetic information from its employees, making the film a depiction of a horrific dystopia in which unhealthy people are prevented from being astronauts. IQ geneticists need an equally powerful pop culture icon to humanize their research.

After the popping of the dot-com bubble, much speculation and excitement turned to nanotechnology. Drugs would be programmed to target pathology with no fear of side effects. Plates would be programmed to tell us about food content. Computers would be woven into garments. Self-replicating nanobots would perfect manufacturing and become a new type of pollution. Enter Towelie. Towelie first appeared on the program South Park ten years ago. He is an RG-100 Smart Towel designed by Tynacorp with a computer chip and a programmed “TNA” to sense a person’s body moisture, beat the average person at chess, and become a weapon of mass destruction, should he fall into the wrong hands. None of this mattered to the boys of South Park because they were busy trying to find their stolen Okama GameSphere, which Stan’s mom bought for “only $399.99.” (All in all, that is fairly useful advice for the computer industry, considering that it is coming from a cartoon.) I would nominate Towelie to be the mascot for tomorrow’s IQ tests. Towelie clones would isolate DNA from hair or skin cells, decode the genome, run an IQ gene algorithm, and wirelessly transmit an IQ range estimate. All liberal handwringing about IQ validity would be moot. If only we could get Towelie to lay off the weed.

Community College Debate Resolves Issue of Race

noreply@blogger.com (nooffensebut) — Wed, 24 Aug 2011 16:52:00 +0000

(Part one of a continuing series.)

After millennia of controversies, passions, and subjugation, the issue of race was resolved over the weekend when a chain-smoking man with the equivalent of an associate degree won an over three-hour BlogTV debate against a former white nationalist who is part African-American. The winner of the debate, who goes by the pseudonym “Skeptical Heretic,” successfully used a debating style that was a cross between James Carville and Tony Soprano, despite a limited grasp of the primary subject, race and IQ. (This lack of proficiency was revealed in previous videos in which he confused anti-IQ polemicist Richard Nisbett with The Bell Curve co-author Charles Murray and the neo-conservative think tank, the American Enterprise Institute, with the eugenics science non-profit, the Pioneer Fund.) Nevertheless, his opponent’s exacerbated pauses with Al Gore-like sighs signaled to the approximately 300 viewers that the contest was decided, and doctors and scientists alike would no longer feel confident studying biological racial differences. Research oncologist Kathy Albain could not be reached for comment at the time of this writing, but presumably her groundbreaking investigations of the genetics of racial disparities in cancer mortality will be immediately shuttered.

Much of the victor’s case expectedly rested upon on the common linguistic argument of the continuum fallacy applied to race with the conclusion often summarized as “race is a social construct.” Anticipating this tact, I asked Heretic prior to the debate whether his disbelief in race extended to Neandertals. As I previously reported, Neandertals bore children with early non-African humans, and now people finally have access to a blood test that answers the eternal question, “Am I more Neanderthal than Ozzy Osbourne?” Thus, I was using the famous reductio ad absurdum argument to take his reductionist claims to their logical conclusion: Neandertals did not exist as a distinct group. Humanity is one! In fact, Heretic’s other major line of attack, which is commonly referred to as Lewontin’s fallacy, also has a rendition that applies to the distinction between humans and Neandertals, as University of Wisconsin-Madison professor John Hawks observed, “there are some human genes for which two human copies taken at random are more different from each other than one of them is from the Neandertal.”

To my inquiry, Heretic responded that Neandertals are not “established as an individual species or as a subspecies of modern mand [sic]. Right now, from what I can tell, the jury is still out, partially due to the mitochondrial observations.” For those unfamiliar, he is referring to the study by Green et al in 2008 that proved that humans and Neandertals do not share mitochondrial DNA. However, Neandertals cannot be a separate species by the classical definition of the term because Green et al in 2010 proved that Neandertals do share nuclear DNA with humans. I am not sure which deserves more blame for such a notable human as Heretic disowning his Neandertal relatives, public education or science reporting. Ironically, he cited a study to deconstruct race that also raised concerns about subspecies classifications for their “arbitrariness of criteria.”

During the debate, Heretic also disputed the validity and heritability of IQ. He never gave any indication that he had ever read a genome-wide association study on the topic (the first of which will celebrate its tenth anniversary next month) and admitted after the debate that he had not read Davies et al, which proved a week prior that fluid intelligence has a “lower bounds” narrow-sense heritability in a Scottish population of at least 51%. (For the record, I personally left him a link to this study several days before the debate.)

Perhaps racial political correctness deserves a more qualified public intellectual. However, I plan to make analysis of his case a continuing series for the simple reason that it was bad enough to be good.

The Politically Incorrect Guide to Weight Loss

noreply@blogger.com (nooffensebut) — Tue, 23 Aug 2011 07:00:00 +0000

Don’t try this at home.

Currently I have something important in common with British welfare mother Susanne Eman. We are both watching our weight. She is doing so in order to more than double her mass such that she will weigh over 1,600 pounds and be the heaviest human in history. I, on the other hand, have the more modest goal of losing 40 pounds. I was pretty skinny most of my life, but after college my weight gradually rose until my BMI entered the low overweight range. I have been surprised at my success so far, so I thought I would share my tips and some provocative science.

1. Love yourself, but do not accept your weight.

I have heard physiological arguments for fat acceptance. I do not doubt that weight has a complex endocrine regulation, and as obesity spreads, genetics influences who becomes obese first. However, personal psychology is what allows this shocking spread of obesity in America, which the CDC has illustrated with this animated map.

People tell themselves many excuses to relax their weight control expectations. Among these excuses are shifting blame to bad genes, previous pregnancy, or advancing age. I could help them by citing some additional causes of obesity. Race, work hours, stress, sleep, smoking, and various drugs affect weight. Some think that Helicobacter pylori eradication increased ghrelin production, and, thereby, obesity. Two adenoviruses have been linked to obesity, but obesity primarily spreads like a virus because relaxation of weight control expectations is normative. Such was the conclusion of a 32-year Harvard study, which found that obesity increases the obesity risk of others in a social network to three degrees of separation. Geographical distance had no effect, so the influence was exerted by having knowledge of one’s associates becoming obese, not living in the same place.

Nothing better illustrates the truth of that study as the incredible success of Singapore’s “Trim and Fit” (TAF) program, which lasted from 1992 to 2007 and decreased childhood obesity from 14% to 9.5%. After its end, childhood obesity rose to 12%. Why would such a successful program come to an end? TAF received substantial criticism for using peer pressure to motivate children to lose weight and for stigmatizing children. A pair of studies (only one of which appears to have actually been published) claimed that TAF drove children to have eating disorders. Briefly, I should mention how remarkable the hysteria over anorexia nervosa is, given what we know about how rare and how heritable it is.

Another example of this dynamic is the success of fat acceptance in promoting obesity among African-American women. Whereas a third of non-Hispanic white women are obese, most non-Hispanic African-American women are obese, but they think they are thinner than they are and are more satisfied with their size. This has forced the usually politically correct public health researchers to advocate “multifaceted intervention” to dispel these “overly optimistic beliefs.”

Clearly the feminist fat-acceptance movement is destroying lives, so I would be remiss to not thank Michelle Obama for her campaign against obesity. I find it very strange that conservatives have joined radical feminists in criticizing her just because she happens to be married to a Kenyan Muslim.

2. Buy a digital scale.

I had a spring scale that grossly underestimated my weight. Family practice doctors typically use balance beam scales, but those are expensive and less convenient than a simple digital scale. Digital scales are so precise that I can immediately see the consequences of my actions. If I overindulge at a meal, it shows. Water loss from a heavy workout shows. This feedback is great for overcoming a sense of weight inertia.

3. Do not play sports.

It should not surprise that the country with the largest sports market has the highest obesity rate. Of course, some people have improved health from playing sports, but I would advise against it for several reasons. First of all, I have met so many people who suffer from obesity and its co-morbidities and are helpless to do meaningful exercise due to an old sports injury. Australian researchers determined that, over a 2-week period, 5% of participants will have a sports injury. Injury prevents physical activity in 20% of 18-to-59-year-olds and 40% of those over 60. Sports injuries, therefore, contribute to obesity, which aggravates injuries. Many turn to prescription painkillers to mask the pain, leading to a downward spiral of opioid tolerance and addiction.

For those who avoid injury, sports can lead to obesity in other ways. American football actually encourages weight gain to produce massive players. In fact, many sports emphasize muscularity or other athletic qualities as more important that cardiovascular endurance. Sports participation is associated with excess alcohol consumption, which can cause obesity. Also, the mentality of sports deprives exercise of spontaneity. As people age, the infrastructure of organized sports leaves their lives, and they let their bodies go. Finally, sports create winners and losers. Those who repeatedly lose will feel discouraged from continuing, and those who always win might not feel a need to push themselves further.

4. Run instead.

When someone takes my pulse, they initially panic before they remember to ask me if I am a runner because runners have slow heart rates. Since heart disease is America’s number-one mass murderer, I find it comforting to know that my heart is not working too hard.

I suppose I should support the need for exercise, itself, before I further try to sell running. The straw-man critique of exercise, laid out last year in The Guardian, is that exercise alone does not reduce weight because people tend to compensate or reward themselves with additional calories or time of inactivity. So, while some might react to such an article by thinking that exercise is worthless, the studies it cited actually called for coupling exercise with dietary changes and increasing exercise intensity. One of the studies actually emphasized health benefits to exercise other than weight loss, including improved blood pressure and reduced abdominal fat.

So, here is my case for running. Running might be difficult for some people in inhospitable climates, but for the rest of us, it is a simple, time-efficient means to a lifelong exercise regime. Running is also a fun, stress-relieving activity that allows one time to think. At the end of a run, I have a renewed sense of well-being.

My routine is a 6-mile distance that allows me to minimize contact with traffic while still reaching a park for water, restroom access, and equipment suitable for toning exercises like pull-ups. USA Track and Field allows you to create a route map and measure its distance or look at others’ maps, which can include markers for water fountains.

I realize that some people believe in swimming because it puts less strain on joints, but I have heard conflicting data on whether running really is bad for joints. Running is certainly good for bone strength, but, above all, I think running is more conducive to an intense, enjoyable workout. When I swim, I am tempted to just have fun rather than do laps, and I cannot lose myself as I can running because I would bump my noggin.

5. Music helps.

I do not believe in sweating to the oldies, folk, jazz, country, or Rebecca Black. If you decide to take up running, I challenge you to channel your inner Kurt Cobain. I would place the motivation and enjoyment that music provides as a more important component to running than shoe type, and some forms of music have great artistic merit but do not fit a running habit. I generally prefer two styles of running music: energetic release music and runner’s high music. For the former, I need the uninhibiting verve of punk-inspired angst anthems and mechanized industrial torture devices. I look for the atmospheric and sublime in the latter, like a good Radiohead song or an electronic instrumental tapestry. Of course, every athletic badass has a secret pop smash hit somewhere on his mp3 player.

I would recommend Bluetooth headphones for running, rather than earbuds. Some mp3 players do not support Bluetooth without an adapter, but Insignia used to make decent Bluetooth mp3 players, which can be bought used for very little.

6. Do not run marathons.

I know a number of very healthy people who strongly believe in running marathons. Some run so many marathons that preparing for them is their typical running regimen. I do not share this enthusiasm for marathons because I think these push some people to treat running like an occasion for an accomplishment, rather than a steady exercise habit. Some studies show that marathon running is perfectly safe, but one MRI study found evidence of cartilage damage.

7. Exercise controlled shopping.

I have a sweet tooth. I love rich foods. Therefore, I am keenly aware that will power starts at the supermarket. Many people who struggle with their weight unfortunately decorate their homes with bright advertisements for unhealthy snacks on the sides of bulk packages. Instead of conditioning oneself to sugar highs like Pavlov’s dog, one should shop to bolster will power by purchasing fruit and sugar-free gum.

8. Do not overthink dieting.

Debates over diet types among advocates with vested interests are startlingly ugly. Any diet that truly decreases calorie intake will facilitate weight loss, and I think most people have a decent conception of the difference between healthy and unhealthy foods. Whole grains are better than refined. Soda increases weight, and I cannot understand why anyone ever drinks it. Fish is a good source of healthy fats. My problem with dieting plans is that they make people obsess about eating and create an illusion that picking the right diet will make weight loss easy. Eat less. Focus on something other than food.

9. Skip meals.

I believe in skipping meals because it has been helping me lose weight, but I am aware that nutritional studies warn against skipping meals and suggest benefits from small, frequent meals. These studies might be flawed by poor reporting of eating habits. The important factor is overall calorie intake and nutritional value. If breakfast is one’s most healthy meal, then skipping it could cause weight elevation, especially if one compensates with a larger dinner. I think a lot depends on how a person can best control his or her own appetite. I have found that by not eating for extended periods, hunger pangs decrease in intensity. People who let their bodies go will often develop diabetes, which requires them to control their blood sugar, making meal-skipping infeasible.

Why Lose Weight?
An extension of the fat acceptance movement is the contrarian view that weight is not important for health. This view flies in the face of recent progress in calorie restriction research, such as a new study that showed that calorie restriction lowers core boy temperature, which is believed to promote longevity. However, most people would not want to join the Calorie Restriction Society. A new study seemed to support the contrarian view when it found few lifestyle differences between a control group and people who have lived past 95. Although overweight women were significantly more likely to have longevity, long-lived men and women tended to not be obese, and if more men over 95 were in the study, perhaps their increased likelihood of being normal weight would have reached significance. A second recent study corroborated that weight control is especially important for men. In fact, optimal male body mass index for reduced mortality was lower than the threshold of being overweight.

Finally, I think it is worth confronting the masculine ideal of the husky, thick-necked man. Some men might have a substantial neck circumference due to heavy muscularity, but that criticism is just as valid for body mass index. I think neck thickness is more associated with masculinity among the lower classes. Doctors are now considering neck circumference as an alternative to body mass index as an indicator of cardiovascular health.

Why YouTube Sucks

noreply@blogger.com (nooffensebut) — Fri, 19 Aug 2011 13:34:00 +0000

Before I started blogging here, I created videos on YouTube. It was kind of fun, and I was proud of the results. At the time, YouTube advertised videos by using a snapshot of the video exactly in the middle, so I created a video detailing the scientific evidence that lesbianism is likely to not be biological in the way that male homosexuality is biological, but I advertised it as relating to a famous bisexual celebrity, Tila Tequila. The result was that about 70,000 people saw my video, and while no one did much to debate me on the science, I did have some interesting discussions with lesbians, and I may have convinced a few to question their sexuality again. Actually, I prefer to remember it as the time I reduced the world’s lesbian population by about 70,000. Another accomplishment of mine was that I think I coined the phrase “education bubble” in a video I created in 2007 or 2008 about higher education. Some anonymous people started asking me for my sources just prior to series of mainstream journalist pieces speculating about the possibility of a higher education bubble. Such a bubble could have a profound impact on our economy and our society.

Most of my work on YouTube came to an end when I posted a video series on the genetics of black violence. Certainly it is a provocative title and subject, but the video contained nothing that I would consider legitimately controversial. It consisted almost entirely of direct quotations from peer-reviewed scientific literature on dopamine genes and monoamine oxidase A (MAOA). One person gave me feedback that it was too difficult to follow for this reason, but I wanted to help educate the public without using sources that anyone could impugn. I have taken pains in all of my work to not only cite science directly, but also to rely on scientists whose motivations and politics are not lambasted as are those of, for example, University of Western Ontario researcher J Philippe Rushton. For entertainment value and to highlight or counter the opposing viewpoint, I peppered the video with excerpts from liberal documentaries and television programs, including parts of the movie Bowling for Columbine by Michael Moore. Now, YouTube is wholly owned by Google, and all of the studies I used can be accessed through Google Scholar. However, YouTube saw fit to remove my video. More to the point, YouTube removed me. My “channel,” all of my videos, and every single comment that I posted on any video anywhere on YouTube immediately vanished forever. In response, I reposted each of the three parts of the genetics of black violence video on three separate channels using a mix of L’s and I’s for channel names to complicate anyone’s attempt to remove these again. Those videos remain on YouTube and have received over 27,000 views, which is not bad for a hidden, extensive scroll of esoteric scientific jargon read by a computerized voice.

The view that YouTube tried to snuff out has become a burgeoning subfield of criminology, called biosocial criminology, which recently received a panel discussion at the annual National Institute of Justice conference, to which the New York Times chose to draw attention. In less academically rigorous news, the MAOA gene became the star of a sensational National Geographic documentary and an episode of the Dr. Phil television program.

What is obvious and hardly needs mentioning is that, even without the extreme, draconian censorship, YouTube would still have a dimwitted milieu. It is dominated by those with enough free time to express themselves in video format and with the kind of career prospects that do not demand anonymity when approaching taboo subjects. Two such individuals plan to stage a live debate this weekend on race and IQ, and I can only expect wreckage. YouTube comments, in particular, tend to be dominated by idiotic insults, forcing the video owners to choose between joining in the censorship or allowing endless bickering that would drive away anyone with a three-digit IQ.

A Pretty College Girl Promotes Race Realism

noreply@blogger.com (nooffensebut) — Thu, 18 Aug 2011 18:56:00 +0000

The intellectual bastion of YouTube has been rocked by a shocking discovery: a pretty, young woman who believes in race. Anti-racists fumbled nervously in damage-control mode, as they attempted to persuade the YouTube community that this woman was not, in fact, attractive, her videos notwithstanding. They further explained that if too many hot women became Sarah Palin-like activists for such a paradigm, the outcome would be forced sterilizations and genocidal atrocities.

The weakness of the ten’s arguments only further evinced the fact that she was indeed a hottie unaccustomed to the rigors of needing to persuade with words. She flicked her hair as she asked races to move into separate countries, which immediately resulted in a ten-point approval bump for segregation, according to Rasmussen.

After the initial shock, anti-racists put together a list of talking points about races not being real, except for the Neandertal race, or something. Anyway, about a third through her video she tilted her head and smiled in a very feminine manner. I shall be live-blogging her interview on CNN’s Piers Morgan Tonight.

The Genetics of Violence

noreply@blogger.com (nooffensebut) — Wed, 17 Aug 2011 06:26:00 +0000

This page will serve as a permanent index of all of my writings and videos on the genetics of violence and biosocial criminology.

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

Deus ex Machina Genetics – January 8, 2010

No Amore for MAOA from Maori – January 8, 2010

Epistemology & Endocrinology – January 8, 2010

The Racial Controversy of a Violent Gene – March 4, 2011

Revealed: “nooffensebut” is Walter Ward, Floridian retiree. – March 6, 2011

A Picture is Worth a Thousand Blogs – August 30, 2011

Pulling the Empty Chair on Dr. Kevin Beaver – September 6, 2011

Attack of the Warrior Gene Babies – September 13, 2011

Kill Popular Science – October 13, 2011

The Genetics of Black Violence – May 26, 2009

Part 1

Part 2

Part 3

Smart People are Educated, Greedy, Sexist Bigots

noreply@blogger.com (nooffensebut) — Wed, 20 Jul 2011 16:08:00 +0000

The brilliant and irascible science blogger, Razib Khan, has conducted a thorough survey of his readers, in which 367, by my count, reported their IQ scores. The mean reported IQ was shockingly high at 133. The survey also provides data on a range of interesting views. For instance, he questioned whether “biologically derived behavioral differences” between sexes and “human races” are “trivial,” “very modest,” “somewhat significant,” or “very significant,” which I assigned values from one to four in said order. As shown here, the smartest participants were more likely to consider racial and sex differences important.

Intelligence did not seem to affect immigration attitudes.

Intelligence also did not impact body mass index.

Likewise, though his readers were overwhelmingly liberal on social issues, the intelligence of the survey takers did not affect their reported liberalism on a scale from zero to ten.

Economic issues, on the other hand, seemed to evoke a conservative streak from the super-smart.

As expected, smarter people were better-educated, and this was the strongest association that I have found so far.

The second-strongest association that I discovered was the fact that smarter readers had been following his blog for more years.

This might be a point of pride for Khan, but it could also be a confounding variable. Could it be that Khan’s blog is a source of racism exposure, despite his own minority status and his readers’ professed liberal social beliefs? Are smart people especially impressionable to prolonged exposure to racism? Or are smart people sexist bigots because … they are smart?

Everything You Ever Wanted to Know About Black Women with Herpes, and More!

noreply@blogger.com (nooffensebut) — Tue, 07 Jun 2011 13:27:00 +0000

I think it is safe to say that herpes is the funniest venereal disease. A sexually-transmitted infection that is mortifying but not mortiferous seems tailor-made for the age of Failblog. On the other hand, many are unaware that herpes rarely can be fatal. A mother can transmit herpes to her infant at birth. The consequences of this neonatal herpes infection can include meningitis, pneumonia, and death. A herpes infection can also facilitate HIV transmission. Medication can manage genital herpes, but no cure exists because the virus hides in the nervous system.

Such an indelible marker risks spreading forbidden knowledge about human behavior and population differences. One mantra of the collection of clichéd falsehoods collectively named “political correctness” is that sexually transmitted diseases do not discriminate. However, if The Man injected most black women with a drug that caused itchy genital sores, would it not be fair to accuse The Man of discrimination? Well, the US Centers for Disease Control reported last year that the National Health and Nutrition Examination Survey (NHANES) results showed that herpes is so racist that almost half of black women and girls aged 14 to 49 have it. To be exact, 48% (with a 95% confidence interval from 44.1% to 52.0%) of these women are seropositive for herpes simplex virus 2 (HSV 2) genital herpes. In contrast, only 15.9% of non-Hispanic white women have it.

Hate Graph. (Turn Away!)
Now, as funny and relatively benign as this incredibly common condition usually is, I would not want to engage in a discussion that seems to mock anyone’s actual serious suffering. I feel compassion for those with this disease and truly hope for a cure and a vaccine. Nevertheless, the reaction to the NHANES results is instructive about the meaning of the word stereotype and left-wing resistance to science.

Take the reaction of The Root, which was started by Henry Louis Gates, Jr., the black Harvard professor who infamously accused a police officer of racial profiling because the officer wanted to ask him some questions after Gates broke into his own residence. Writing for The Root, Sheree Crute quoted Dr. David Malebranche of Emory “whose research focuses on STDs in African Americans” as saying, “This means that they have been exposed to the herpes virus, but it does not mean that these women have actually developed the disease or have active herpes. In fact, they may never develop active herpes.” What brilliant medical advice! Yes, ma’am, you have been exposed to herpes, but you do not have the disease. The virus is inside your body. You can infect others. Fortunately, you only have the disease at the various times that painful blisters appear on your privy parts. Feel free to live life as if nothing happened. Actually, Dr. Malebranche, two previous small studies determined that 56% of genital herpes transmissions, in one, or 69% in the other, occur without active symptoms. A person who contracts the herpes virus without yet having symptoms sheds the virus and has a 20% chance of being contagious at any given time. More than 4 out of 5 cases of genital herpes caused by herpes simplex virus 2 are undiagnosed possibly due to a lack of symptoms, according to the CDC study.

Dr. David J. Malebranche
Black Herpes Expert

Dr. Malebranche’s dubious logic feeds a black community that is hungry for denial. Danielle Canada, writing for “HipHopWired,” repeated his quotation and added that “people were shocked and outraged” by what the CDC report “seemed to say.” This forced the CDC to write to “HipHopWired” directly, saying, “We at CDC want to make it clear that CDC has not changed its position…” and “We also want to make it clear that Dr. David Malebranche … is not a CDC physician or representative…” Another delusion was offered by a British black woman named Susan Onyejiuwa, who noted that “the report actually says that 16 percent of the total American population have herpes, and of these 16 percent, 48 percent of people fall under the African-American female category.” The “false report” that 48% of black women have herpes worries Onyejiuwa because it conveys a sense that “it would be best to keep away” from black women, she says. If she were correct that 48% of the 16% of Americans with herpes are black women, then the percentage of the black women in the study who have HSV2 genital herpes would be much higher—63%. Based on her delusion, Onyejiuwa started an online petition against the CDC study. Think of all the lives that we could have saved if we had only thought to petition against epidemiologists when the AIDS epidemic began in the 1980s.

These people are all partly right in that it is not true that 48% of black women have herpes. This is because the CDC study only examined the prevalence of genital herpes caused by herpes simplex virus 2. Genital herpes is also caused by herpes simplex virus 1 (HSV1), the cold-sore virus. Thus, the true percentage of black women with genital herpes, an incurable sexually transmitted infection, is considerably more than half. Doctors tend to associate HSV1 only with cold sores of the mouth, but as oral sex has become more common, so has genital herpes caused by HSV1. Between 1992 and 2006, the percentage of new incidences of genital herpes in straight women attributable to HSV1 rose from 31% to 45%. There is sparse and contradictory evidence regarding the proportions of HSV1 and HSV2 in black people. A study from Seattle found that white people with herpes were almost four times more likely than “nonwhite” people to have herpes caused by HSV1, and black people in a 1998 study were less likely than white people to report having had oral sex. However, nonwhite people in Seattle are more likely to be Asian than black, and data on herpes infection rates among Asian Americans are nowhere to be found. Also, a 1992 study of unmarried adults in high-risk San Francisco neighborhoods found that both HSV1 and HSV2 were more common in black people than white people, especially HSV1 with 76% of black women being HSV1 positive compared to 43% of white women.

Black denialism of unflattering science is, of course, not limited to the herpes epidemic. Among African Americans, conspiracy theories about HIV and AIDS have become mainstream with deadly consequences. In spite of the recent shocking revelations about US involvement in the deliberate infection of 1,300 Guatemalan prisoners and mental patients with syphilis and gonorrhea and the failure of the Tuskegee syphilis study to offer African Americans penicillin when it was identified as the standard of care, black denialism of science is ignorant and belaboring such scandals probably kills far more than those actual transgressions by encouraging conspiracy beliefs about HIV prophylaxis and treatment. A 2005 survey determined that 48% of black people think HIV is a man-made virus, 53% think a cure exists that is being kept from the poor, 16% think the US government created AIDS to control black people, 7% consider HIV treatments to be poison, and 4% of black men believe that doctors intentionally infect condoms with HIV. Having AIDS-related conspiracy beliefs makes black men significantly less likely to consistently use condoms.

Ironically, when black activists or liberals decide to reject science that makes them feel uncomfortable, they often accuse it of being “pseudoscience,” regardless of the poverty of scientific evidence in support of their own dogma. One is reminded of the quarrel that arose when then-Harvard president, Larry Summers, tried to explain some possible reasons why Harvard math and science professors are less likely to be women. One reason, he offered, was that men have a higher standard deviation that results in more men among the very high and very low ability levels. National Organization for Women President Kim Grady characterized this notion as suggesting that “women are inferior.” MIT biology professor Nancy Hopkins expressed a similar misunderstanding that he meant that women have a genetic predisposition against math and engineering. I cannot quite remember whether I first learned about standard deviation in high school or middle school, but for these women to reveal their math ignorance in their attempts to defend the mathematics skills of women betrays just the sort of thoughtlessness and lack of self-awareness that seems particular to political correctness.

Revealed: “nooffensebut” is Walter Ward, Floridian retiree.

noreply@blogger.com (nooffensebut) — Mon, 07 Mar 2011 07:14:00 +0000

As an experiment, I submitted my last blog to Taki’s Magazine. You can judge the result for yourself. Their use of a scarred Rwandan above the title, “The Thug Gene?” was an interesting choice, I guess. Renaming MAOA seems unnecessary to me, since it was already widely known as “the warrior gene,” and ABC News also renamed it “the gangsta gene.” Likewise, yours truly has a new moniker:

“Walter Ward is a retired biology teacher. He lives in Florida and has eight grand children [sic].”

For the record, none of that is the case. I would prefer not to reveal my identity at this time, but lying, especially when the identity so easily fits a dismissible stereotype, seems counterproductive.

A couple edits to the essay changed my meaning. The article now claims that less than 1% of the whites in Rosenberg et al had the 2-repeat allele of MAOA. Just to be clear and precise, that study claimed that 2% of whites had alleles other than 3-repeats or 4-repeats, but it did not detail the exact percentage with 2-repeats for whites or African Americans. Also, the article now claims that there were four men included in the 14 total “afflicted” with Brunner syndrome, who also “escaped having the syndrome.” What I wrote was that these four had the mutation but not the syndrome. As I re-examine the only paper to mention these men, I see that there is some ambiguity as to whether they were included in the total 14, but they did not have a diagnosis by the standard of the Diagnostic and Statistical Manual of Mental Disorders (DSM, the Bible of psychiatry).

Overall, I was impressed that the editors at least wanted to check my sources. I wish they had been so careful when Michelle Malkin attacked the First Lady’s attempts to promote breastfeeding with the flippant and apocryphal claim that “the health advantages of bosom over bottle are short-lived.” Malkin gets an official pass from me though because she is soooooo gorgeous. What can I say? I recently became a very dirty, old man.

The Racial Controversy of a Violent Gene

noreply@blogger.com (nooffensebut) — Fri, 04 Mar 2011 14:35:00 +0000

Journalism, like any art form, has genres. There is a popular celebrity-fall-from-grace genre. There is the up-and-coming cable-television-political-commentator-zings-opposing-network-political-commentator genre. One particularly controversial genre is the scientists-discover-the-fill-in-the-blank-gene genre, with usually superficial and forgettable entries. However, I would submit that there is at least one gene for something, and it concerns one of society’s ugliest controversies, the stereotype of the black male thug.

I am referring to a gene called monoamine oxidase A, or MAOA. This gene produces an enzyme that breaks down the neurotransmitters that activate many of the brain’s circuits. Back in the 1990’s, scientists discovered a mutation of MAOA that completely turns it off. The result is called Brunner syndrome, which only 14 related men have been known to have (plus animal models). What makes this extremely rare mutation so important is that it proves that MAOA really is a violent delinquency gene. A man with Brunner syndrome is what expert psychiatrists refer to as “a bad guy.” Five of these men were arsonists. Some of the men were rapists or attempted killers. Inexplicably, four men with the mutation somehow escaped having the syndrome, but for men with the mutation, those are not good odds. Nevertheless, out of the approximately three-and-a-half-billion men in the world, 14 really are not that many. Trust me, your neighbor—the one with the motorcycle—is probably not one of them. In conclusion, out of sight, out of mind.

Then came the 2000’s. The MAOA gene has a portion with repeated segments of DNA. This section of the gene is called a promoter because having more repeats increases the amount of enzyme that the gene produces (with a rare, debatable exception). After a 2002 study found that having three repeats together with having suffered child abuse is somewhat associated with violent tendencies, a flood of follow-up research ensued, and MAOA was relabeled “the warrior gene.” This version of the gene and one with four repeats are the most common versions, or alleles. These studies always had a few people with neither the 3-repeat nor the 4-repeat allele. A small number only had 2-repeats. The scientists decided that having 2-repeats in the promoter is sort of like having 3-repeats, so they invented the term “MAOA-L.” (“L” stands for low. Pretty clever, huh?) However, a pair of studies in 2008 found that the 2-repeat allele is associated with twice the rate of violence without child abuse coming into the equation. This allele is less powerful than Brunner syndrome but far more common.

Two small studies gave hints that the especially dangerous 2-repeat allele might be more common among African Americans. One study wrote that 6% of their non-white (but probably mostly African-American) male subjects had this allele. The other had 5 of 37 (14%) African-American men possessing “rare MAOA alleles.” Those percentages are remarkable given that studies of white men have suggested that 1% or fewer have this gene.

If a single gene could offer some explanation as to why African-Americans commit roughly five times as many violent crimes per capita as whites, then wouldn’t studying it potentially save countless lives and deserve a Nobel Prize? After all, even a case of Brunner syndrome was effectively treated for a period with an antipsychotic. Well, at long last, Reti et al determined that 0.5% of white MAOA genes and 4.7% of African-American MAOA genes are this 2-repeat allele, almost a ten-fold difference.

Calculating Violence

Hopefully, for the sake of improved diagnosis and treatment, a small number of genes like MAOA greatly influence societal problems like violent delinquency. However, some studies suggest that the genetics of behavior is spread diffusely among many genes. Science must also examine the complex web of gene-environment, gene-hormone, and gene-gene interactions. As the price of decoding genomes declines, it will become easier to develop software that analyzes standardized behavioral and developmental metrics and multiple gene elements for sundry associations.

Consider the study Beaver et al from about one year ago. This was a study of African-American men and five violence genes that reached the shocking conclusion that a crude genetic index of these genes predicted adult violent delinquency better than a detailed measure of the quality of the men’s childhood relationship with their respective mothers. This finding is all the more impressive given how unimpressive the gene index was. Each allele was assigned a point. A 2-repeat allele of MAOA was worth the same as a 3-repeat allele of MAOA and the same as an allele of another gene that had limited evidence of impacting violent behavior. Also, MAOA is on the X chromosome, meaning that these men only had one copy, unlike the other genes, which come in pairs. So, apparently having a 2-repeat allele was actually worth only half as much as each pair of the other genes. This study could be improved upon by follow up research that weights the genes differently using a computer program that could compare multitudinous reiterations to determine the optimum weights.

The Case for Maturity in Ethics

After following research on the genetics of violence for years now, I am convinced that the various alleles of MAOA affect violent behavior in white men and black men. Thus, the differing frequencies of these alleles might contribute to the differing rates of violent crime. I am sensitive to the fact that this line of research could reinforce unfair judgments that all black men are dangerous, but the 2-repeat allele of MAOA illustrates that a gene might contribute to a racial disparity in violent behavior even though most black men do not have said allele. If it is an important violence gene, then maybe targeted treatments can be created that will be more likely to help African-American men and bring American society closer to equality. In other words, medical and scientific ethics should be informed by both the improved standards of moral responsibility since the end of the eugenics era and a mature, realistic appreciation of the coming genetics era.

Neandertal Miscegenation

noreply@blogger.com (nooffensebut) — Sat, 05 Jun 2010 01:35:00 +0000

I like to imagine science as the mind’s eye for the human collective. We became more fully conscious when we realized that Earth is not the center of the universe, that species evolved from shared ancestors, and that human activities alter the atmosphere and climate. Each epiphany, in its own way, disturbed our kind’s self-image. Add to that list the recent discovery that non-African humans are the product of human and Neandertal admixture. In one respect, this underlines what Luigi Luca Cavalli-Sforza called the most important difference in the human gene pool, the genetic Yarlung Zangbo Canyon between Africans and non-Africans. Then again, to discover in their family tree a race once universally considered an inferior species must be lowering the serum testosterone levels of my fellow supra-Saharans. If he were still alive, the politically correct paleontologist, Stephen Jay Gould, would have cause to reconsider the merits of genocide, for he wrote in his 1980 book, The Mismeasure of Man:

"The world might have been ordered differently. Suppose, for example, that one or several species of our ancestral genus Australopithecus had survived—a perfectly reasonable scenario in theory, since new species arise by splitting off from old ones (with ancestors usually surviving, at least for a time), not by the wholesale transformation of ancestors to descendants. We—that is, Homo sapiens—would have faced all the moral dilemmas involved in treating a human species of distinctly inferior mental capacity. What would we have done with them—slavery? extirpation? coexistence? menial labor? reservations? zoos?"

Well, at least we get a choice, right? To be fair, Australopithecus inhabited an entirely different genus. A common definition of species for organisms that reproduce sexually is the group of organisms that would be capable of producing fertile offspring with another member of the group. By that definition, Neandertals are not a separate species. If one categorizes them as a race, they would be a more distant race than any currently in existence, but that distance lends itself to some startling statements, such as a new application of Lewontin’s fallacy, as told by University of Wisconsin—Madison professor John Hawks:

"If you compare humans with other humans today, we differ by about one base pair out of a thousand. So, we’re between ten and twenty times more similar to each other, compared to what we are with chimpanzees. So, if you think about this in terms of years, we think that we divided from chimpanzees—our population split from them something like five-million years ago. Well, that means that humans, on average—two human genes split from each other, in ancestry, something like 500,000 years ago. If you look at us and Neandertals, they’re different from us by just a shade more than we’re different from each other, so that if you compare their genes and our genes, it looks like about maybe 800,000 years is the average. However, that’s recent enough that there are some human genes for which two human copies taken at random are more different from each other than one of them is from the Neandertal."

Hawks is referring to an estimate of the average divergence of autosomal DNA sequences between Neandertals and modern humans of 825,000 years. One should not confuse this with the timing of the populations diverging between 270,000 and 440,000 years ago. The overall genomes of modern humans and Neandertals are 99.84% identical, and only 78 protein-altering DNA changes separate Neandertals from the whole of modern humanity. In the study’s supplement, divergence is calculated not only for Neandertals, but also for a French person, a Han Chinese person, a Papua New Guinean, a Yoruban from West Africa, and a San person from Southern Africa. Here are the autosomal DNA divergence values calculated from a standard ratio of Neandertal-to-human distance over half of the chimpanzee-to-human distance:

French: 8.00
Han: 8.45
Papuan: 9.32
Yoruban: 9.43
San: 10.32
Neandertal: 12.67

This data would seem to suggest a genetic distance spectrum from Europeans to Neandertals with Africans closest to the Neandertals. That is an erroneous conclusion. This data made use of a reference human genome consisting of the DNA of an African-American who is genetically 50% white and 50% African. The numbers are composite autosomal divergences. For the European regions of autosomal DNA, shown below, the values are similar. However, the Neandertal divergence is slightly less, in accordance with the conclusion that Neandertals and non-Africans share 13 regions of DNA or an average of 2% of DNA from mixing.

French: 7.03
Han: 7.69
Papuan: 8.61
Yoruban: 9.27
San: 10.08
Neandertal: 12

The data for the African regions of autosomal DNA, below, look far more confusing. The Yoruban individual was actually not significantly closer to the African regions of DNA than the European regions, and the San person was even slightly (not significantly) closer to the European regions. Africa is the most genetically diverse region of the world. Perhaps its wealth of genetic diversity provided for such a manifestation of Lewontin’s fallacy.

French: 9.28
Han: 9.59
Papuan: 10.14
Yoruban: 9.17
San: 10.19
Neandertal: 13

Part of what makes this revelation so fascinating is its challenge to politically correct notions of race and the out-of-Africa anthropological model. Indeed, Green et al cite an estimate by Wall et al that non-Africans have 14% archaic ancestry. The implication is that the remainder of this archaic ancestry came from some other ancient primate population.

Equally intriguing is how Green et al inadvertently pits a traditional anthropocentrism against taboo, but perhaps commonly held, views of racial supremacy. Now, one should not consider the evidence of intimate relations between Neandertals and the ancestors of non-Africans a comeuppance. Obviously, "neanderthal" became an epithet on par with "cretin" or "jerk." On Razib Khan’s blog, one of the many co-authors of Green et al saw fit to defend Neandertals. "… I see no reason to think that they were not as smart as us."

Suppose the Neandertals were in some meaningful sense an inferior race. At least in a Darwinian sense, leaving a mere 1-to-4% of their genome is an underwhelming legacy. (Actually, Hawks says that each non-African has a different makeup of Neandertal DNA, and Green et al found that when the reference genome European regions were closest to Neandertal DNA, they diverged from the genome of Craig Venter, who is of European descent. Therefore, it is unclear to me exactly what percentage of Neandertal DNA collectively exists today in humans. Plus, Hawks thinks that it is still possible that Africans also have some Neandertal DNA that the study could not detect. That would result in a higher calculation of Neandertal ancestry for both Africans and non-Africans.) Even such a small percentage is a sufficient legacy to discredit the neurotic meme of racial supremacists/nationalists/separatists that impurity is abominable. Many possibilities could explain why so little Neandertal DNA remains in humanity, including natural selection. This leads to one useful argument against the supremacist meme: a Mendelian model.

White supremacists obsess over the dominance of certain phenotypes. Therefore, imagine that a population of brown-eyed individuals completely pair off with a population of blue-eyed individuals, and assume brown eyes are a phenotype with Mendelian complete dominance. There. In a single generation, all blue-eyed people vanish. But don’t cry, because they all passed their DNA onto a generation of brown-eyed heterozygotes. Statistically, about a quarter of the third generation will have blue eyes. Since blue eyes are so superior to brown, the forth generation will consist entirely of the blue-eyed.

Natural selection depends upon context or environment, which leads to a second argument, that of the inevitability of change. Skin color is a perfect example of environmental adaptation. The genes that influence human skin tone appear to be relatively few, and skin-expressed genes comprised the most common genetic differences between modern humans and Neandertals. If white people lost the ability to attain sufficient dietary folic acid, those who live in sunny climates would probably gradually evolve darker, melanin-pigmented skin. Even an otherwise inferior race of Neandertals could have had adaptations to the colder environs that they inhabited. Mixing and millennia may have allowed the non-Africans to absorb such advantages without ultimately losing advantageous African phenotypes.

One counterargument to consider is that holding off on mixing or preserving a differentiating subspecies could allow for further differentiation of some possible value. The process of natural selection is not teleological. Rather, evolution proceeds in whichever direction is immediately advantageous. Genetic separation helps to create a diversity of abilities and biological strategies. Moreover, often evolving in a distant environment leads to adaptations with nearly universal applicability. Just ask the brown tree snake, which immigrated to and now overruns the island of Guam, causing millions of dollars in damages each year. Invasive species cause damages in the United States worth $120 billion annually.

Animal predators as invasive species can devastate an ecosystem. However, a study by Sax and Gaines found that plant invasions of island ecosystems have actually doubled the amount of species diversity. Likewise, when two human populations come in contact, a gradient of mixing can result that creates a more complex form of diversity. Of course, it is hard to argue that leaving tiny segments of their DNA in the human genome was an adequate hedge against extinction for Neandertals. In fact, Harvard geneticist George Church hopes to bring them back from the dead. Nevertheless, the process of evolution did somehow work against these beings. The ethics and logistics of humanity guiding its own evolution receives surprisingly little analysis either from the scientists who might develop new means or from racialists who might possess the will.

With as much impact as humans have on the environment, of course they can shape the forces of evolution, but evolution will never stop. Even with the sprawling health care industry presumably treating hyperlipidemia and hypertension, humans are evolving to have lower cholesterol and systolic blood pressure, according to a recent study by Byars et al. The fact that humans are also evolving to be shorter and fatter may beg the label "dysgenics." However, such oversimplification flies in the face of a study by evolutionary psychologist Satoshi Kanazawa. He found that very liberal individuals have a nearly 12-IQ-point advantage and that atheists have a 6-IQ-point advantage. Monogamous men, but not women, have an IQ advantage, and that says it all. IQ allows one to overcome instinct. Liberal inclinations and abandonment of traditional beliefs can often come with personal costs. Liberals might sacrifice to help unrelated poor people. Atheists might miss opportunities for fellowship. Rather than higher IQ proving the evolutionary superiority of liberals and atheists, these associations may suggest that some height of IQ reduces biological fitness. However expedient blaming the welfare state for the apparent plateau of the Flynn effect in industrialized societies may seem, the context in which high IQ is actually genetically beneficial may be more limited than one might intuit.

The true meaning of the new understanding of Neandertals is that race is simultaneously more real and less important than the previous paradigm led some to believe. Racial purity is neither necessary nor sufficient to preserve the qualities by which some judge races, civilizations, and individuals. Those qualities would include intelligence, peaceableness, functional family values, productivity, and so forth. Nevertheless, race-realism has an important place in modern intellectual thought not only because race is real, but also because leftists have used racial disparities to discount these qualities and to discount the role of genetics in the formation of those qualities. Still, preserving human exceptionalism from fading into the background of natural selection is a cause more extreme and more just than the fancy to preserve any race.

Epistemology & Endocrinology

noreply@blogger.com (nooffensebut) — Fri, 08 Jan 2010 19:40:00 +0000

     How does one really know anything? As I have been researching genetic racial differences, I have frequently reencountered the dilemmas of scientific knowledge, such as the meanings of certainty and consensus. The skeptic Marcello Truzzi has been credited with originating the phrase "extraordinary claims require extraordinary proof." He actually defined extraordinary claims as being "revolutionary in their implications for established scientific generalizations already accumulated and verified." In that sense, skeptical claims also bear a burden of proof.
     Currently, the so-called Climategate scandal is receiving substantial attention from race realist bloggers. Skepticism can serve science well, but this particular movement has a clear political and financial constituency, and the climate science debate in the decades ahead could reach such an obvious conclusion that a veil of shame might extend to movements associated with global warming skepticism. Race realism science should stand on its own without its reception depending on unrelated causes. After all, race realism owes most of its taboo nature to World War II and Hitler rather than empirical disfavor.
     Therefore, I would like to briefly offer my own assessment of climate science before I detail the science of racial endocrinology, which could ultimately serve as the focal point of scientific understanding of racial differences. Though I must confess to the limitations of my knowledge of global warming research, I am cynical about global warming skeptics latching onto phenomena like El Niño or sun activity to repeatedly prophesy that the end is not nigh, as if they are Jehovah's Witnesses in reverse. In fact, I distinctly recall (though I cannot find a transcript) that Rush Limbaugh on his old television show interpreted the albedo effect of cooling caused by Mount Pinatubo's eruption as "Mother Nature" reversing global warming. How ironic that a conservative would employ the Gaia hypothesis to suggest that a living Earth would take it upon herself to negate human environmental impact. Even as skeptics attribute warming to a myriad of causes other than human activity, they refuse to accept that a temperature trend could have noise. Instead, they consider the record temperatures of 1998 as marking the year of complete reversal of global warming, which is not apparent from this graph:

     Even if all of that data is scientific fraud, no one seems to be disputing the rise of greenhouse gases or the greenhouse effect, itself. Therefore, even if anthropogenic global warming has not happened thus far, the greenhouse effect would presumably eventually overtake other influences on the climate.

     The fickleness of American public opinion on the matter seems to be contingent on gradients, much like support for the wars in Iraq and Afghanistan. How do things seem to be going? How soon and how bad will things get? What can be accomplished and at what cost? I, myself, felt relief when Archer et al placed radical positive feedback on global temperature escalations from a potential oceanic methane "belch" on the time scale of "millennia or longer." Then, Jain and Juanes detailed a mechanism by which methane could rise from the ocean much faster than previously thought. Methane is a more potent greenhouse gas than carbon dioxide.
     The Climategate scandal demonstrates politically correct liberals, who happen to be climate scientists, behaving like politically correct liberals. I consider it a greater scandal that the right wing has allowed the left wing to steal the cause of ecology. Even the Nazis had a green wing.

Polyglutamine Expansion Size Matters
     One link between race realism and environmentalism has been the alternative moniker "human biodiversity." As imperfect or imprecise as race realism may seem, I consider it superior to this pretentious ingratiation. It reminds me of atheists who demand that they be called "brights." Besides, every Seinfeld fan knows that one may not choose one's own nickname. As far as liberals are concerned, anyone who thinks independently about diversity is just a fascist white supremacist, anyway. Even worse, "human biodiversity" sounds prescriptive. I think it is fine if race realism informs one's views of interracial mixing—or global warming, for that matter. However, race realism science neither cares whom one marries nor what one drives. It just is.
     Author Steve Sailer explored the topic of interracial marriage in his 1997 National Review essay "Is Love Colorblind?" In particular, he offered his thoughts about the startling gender disparities of interracial marriage, pointing out that "on average, black men tend to appear slightly more and Asian men slightly less masculine than white men, while Asian women are typically seen as slightly more and black women as slightly less feminine than white women." Readers welcomed his insights by calling him "racist," "white supremacist," and a "typical white male" for peddling "age-old racial stereotypes," "prejudice," and "ignorance." If the media had reported the latest science on racial differences, Mr. Sailer would not have needed to postulate so modestly, and his oppugners could have skipped a self-induced hypertensive episode.
     Masculinity, of course, owes much to male hormones collectively called androgens. The level of expression of those androgens depends not only on the concentration of those hormones in the blood but also on the nature of the androgen receptor. At one end of the androgen receptor gene, which is alternatively labeled AR or NR3C4, there are varying amounts of the trinucleotide repeats CAG and GGC. The 1994 in vitro study by Chamberlain et al found that fewer CAG repeats caused increased transactivation of the receptor (meaning that the receptor became more activated to increase gene expression). Choong et al uncovered an association between fewer CAG repeats and higher amounts of receptors. In 1995, Irvine et al identified a 2.1-fold increased prostate cancer risk from having both fewer than 22 CAG repeats and not having the protective 16-repeat GGC allele. They surmised that the increased transactivation increased prostate cell proliferation, which "is known to promote tumorigenesis." They also produced the two tables below, showing African Americans to be the possessors of the alleles with the highest transactivation.

     Thus, African Americans average 18.5 CAG repeats, whites average 21, and Asians average 21.9. These results parallel both the prevalence of prostate cancer by population and Rushton's Rule, in which whites tend to be between the extremes of blacks and Asians. Sartor et al and Sasaki et al replicated these results. Edwards et al found such racial differences and also determined that the high rate of homozygosity in African Americans likely resulted from selection pressure.
     Genetic racial differences in the androgen receptor can give rise to disease susceptibility and trait disparities in the absence of racial differences in hormone levels. Research seems divided on the effects of CAG and GGC repeats on the actual baseline testosterone levels. Likewise, not all studies have found significantly higher baseline testosterone levels in African Americans, but Roney et al elicited transient salivary testosterone spikes that those other studies overlooked by developing an ingenious laboratory technique: expose men to young, attractive, and flirtatious women. Although the men scored the average of these women’s beauty a 5.83 on a scale from one to seven, the study failed to publish photographs. Nevertheless, men with fewer CAG repeats produced stronger testosterone responses to these ladies.
     This study also found that higher baseline cortisol suppressed testosterone increases with a beta coefficient equal to that of having more CAG repeats. Cortisol suppresses testosterone production, per Sapolsky and Dong et al.

Just How Nice is Sugar & Spice?
     Cortisol research has actually become a Holy Grail for politically correct liberals and people who make "alternative" or "integrative" medicine their hobby. The "central dogma," as one study put it, of cortisol research has been that stress is bad, and cortisol is a bad stress hormone. However, some research suggests that low cortisol or flattening of the daily circadian cycle of cortisol levels may be worse than high cortisol levels. DeSantis et al and Ukkola et al have found that African Americans have lower cortisol than whites. Liberals want to link this stress hormone to racism, which they presume is detrimental to the African-American psyche and physical well-being. Some research suggests that glucocorticoid hormones like cortisol affect memory processing and, therefore, cognition. Liberals also hope that cortisol stress response to discrimination will explain the higher rate of preterm births among African Americans. Two studies gave equivocal but arguably supportive results for this hypothesis. However, Lu and Chen failed to link preterm birth to stressful events other than "traumatic" events like becoming homeless or physical fights. Cohen et al also failed to link a higher level of evening cortisol to reported discrimination. DeSantis et al made much of the new evidence linking poor health outcomes to lower cortisol and the African Americans' considerably lower morning cortisol levels shown on the graph below. However, they also acknowledged the twin study by Bartels et al, showing a 60% heritability to morning cortisol levels. Hence, they turned their focus to a modestly higher evening cortisol level in African Americans, since this is apparently not heritable.

     This flip-flopping on the cortisol "central dogma" reminds me of the black-white suicide paradox. As an undergraduate, I came across some speculation as to why the universal oppressors, white males, have much higher suicide rates than the universal victims, black men. As author David Lester wrote, "The low rates of suicide in Africans in general, and African Americans in particular, may represent an African worldview which accepts suicide only in the very last resort in the face of extreme stress, an attitude consistent with the Afrocentric optimal psychology proposed by Myers and others." White men commit suicide more because they are prisoners to their own privileged status, which they must escape through suicide or bungee jumping. By the time I matriculated into medical school, the African-American male suicide rate was accelerating. The professors cited those startling statistics as further evidence of the oppression of the black man, while neglecting to mention that white men still had a higher suicide rate.

     Beginning with the 2004 Wust et al study on the effects of glucocorticoid receptor alleles on cortisol levels, progress in understanding cortisol heritability at the molecular level is slowly coming to fruition. Now, a new study by Way and Taylor has found that the short allele of 5-HTTLPR causes increased cortisol responses to a perceived social threat provided by the Trier Social Stress Test. As I previously mentioned, about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans possess this short allele. Also, a new study by Armbruster et al found that the 7R allele of DRD4 causes lower cortisol responses and that this allele interacted with the long allele of 5-HTTLPR to lower cortisol response to social stress. Beaver et al determined that African-Americans have significantly more 7R alleles than whites. The possibility that low cortisol levels in African Americans could be partly genetic has important implications for research on the genetics of violence. As I previously pointed out, the violence gene MAOA has a glucocorticoid and androgen response element, through which cortisol can up-regulate and testosterone can down-regulate MAOA enzyme levels. Sjoberg et al proved that higher testosterone levels increased aggressive tendencies in males with the 3R allele that is the most common MAOA allele in black people but did not increase aggression in males with the 4R allele that is the most common MAOA allele in whites.
     To summarize, African Americans have fewer CAG repeats in the androgen receptor gene, which somehow increases testosterone spikes. Higher testosterone decreases MAOA enzyme levels in those with the 3-repeat allele. Plus, androgen receptor alleles with fewer CAG repeats beget more androgen receptor activity. These receptors translocate to the cell nucleus and down-regulate the MAOA gene. African Americans likely have a significant genetic component to their lower baseline cortisol levels and lower cortisol spikes in response to threats. This further allows higher testosterone levels and decreases MAOA levels directly. Lower MAOA enzyme levels increase aggressive behavior, as my previous blog posts explain. These racial hormonal differences help to answer the black-Asian MAOA paradox: somehow Asians are much less inclined towards delinquent violence despite possessing about the same proportion of the 3R allele of MAOA. Greater prevalence of the 2R allele in black people cannot entirely explain the difference.
     The puzzle pieces are fitting together. One might predict based on this synthesis that fewer CAG repeats would correlate with aggression. Indeed, in 2008 Rajender et al determined that male control subjects average 21.19 repeats, rapists average 18.44 repeats, murderers average 17.59 repeats, and men who murder after they finish raping average 17.31 repeats. The shortest repeat lengths are associated with a higher degree of violence, earlier criminal records, verbal aggression, assertive personalities, extraversion, neuroticism, and self-transcendence (mystical tendencies), according to Cheng et al, Jonsson et al, and Westberg et al. Fewer GGC repeats are associated with aggression, impulsivity, promiscuity, and early menarche, according to Comings et al. A new study by Manuck et al localized the neural effects of shorter CAG repeat polymorphisms to the ventral amygdala, and previous research by Buckholtz et al found that the 3-repeat allele of MAOA is associated with increased amygdala activation.

Estrogen Poisoning
     Endocrinology studies a fascinating and complex web of hormonal interactions. Testosterone and cortisol decrease sex hormone-binding globulin (SHBG). SHBG, in turn, binds testosterone, which stimulates the hypothalamus to produce gonadotropin-releasing hormone, which acts on the pituitary gland to release follicle-stimulating hormone and luteinizing hormone. These hormones cause testicular aromatase to convert testosterone to estradiol. Studies show that young black men have higher SHBG than young white men. Specifically, I am referring to Abdelrahaman et al, Winters et al, Ross et al, Wright et al, and Gapstur et al (revealed only in a personal communication to Abdelrahaman et al). Black men have higher estradiol levels than white men, according to Morrison et al, Wright et al, and Rohrmann et al. The higher estradiol levels in black men have implications for bone mass, cardiovascular health, and, yes, violent behavior. Since estradiol decreases MAOA enzyme levels, one would expect higher estradiol levels to increase aggressive tendencies.
     By studying the plasma content of 214 twin pairs, Meikle et al calculated a 38% heritability for estradiol and a 62% heritability for SHBG. When Ahn et al published "the first comprehensive characterization of genetic variation in the sex steroid pathway" this past summer, I became somewhat disappointed that it could not definitively explain racial hormone disparities. Their supplement offered a list of 874 single nucleotide polymorphisms (SNPs) from 37 genes with p-values and beta coefficients for their effects on SHBG, testosterone, estradiol, and androstanediol-glucuronide (which converts testosterone to the more potent androgen dihydrotestosterone). To get a rough idea of how this data might relate to racial differences in hormones, I created graphs with p-values as the independent variable (making the graph most trustworthy towards the left side) and with the accumulative sums of beta coefficients multiplied by the allele prevalences for each population the dependent variable. In other words, the amount the graph rises with increasing uncertainty depends on both how common the more active alleles are in that group and how much effect that allele has on the hormone (or SHBG) concentration in blood. I calculated prevalences for whites, blacks, Chinese people, and Japanese people by combining all relevant populations in the HapMap database. Since the study population consisted entirely of white men, I expected a bias towards higher levels in whites, for whom these SNPs were selected and the beta coefficients were determined. In fact, each graph produced exactly that result with the exception of estradiol, shown below. The line for black people jumps above that of whites due to the adenine (A) allele of rs2687105 in the gene CYP3A4. The significance of this is questionable, as I have found no studies of breast or prostate cancer that found any correlation for this SNP. CYP3A4 produces an enzyme that mostly metabolizes testosterone but can also metabolize estrogen. Other variants of this gene may play a role in racial disparities in prostate and breast cancer.

Sweet and Noble It is to Die for One’s Meme
     Surely, everyone can comprehend that they will not wake up tomorrow and read the morning paper headline, "Cancer Cured!" The fight against cancer is incremental with multiple simultaneous strategies. One strategy would be to individually customize pharmacology based on decoded DNA. Every day you take the pill that is perfect just for you. Unfortunately, this approach is in its infancy. A superior approach to just waiting for this science to mature would be ethnopharmacology, in which drug approval is categorized for specific populations based on probability of benefit for individuals. Since different populations tend to have different medically-relevant allele frequencies, doctors could prescribe drugs based on the probability that the patient is like others in his or her ethnic group.
     The US Food and Drug Administration has already done this for BiDil, which was just a combination of existing approved generic drugs. It might not surprise that a drug created for improved compliance would help African Americans more given the new study by Roth et al, showing that African Americans had worse medical literacy (29% had adequate short test of functional health literacy in adults [S-TOFHLA] scores versus 58% of whites) and more medication-related problems, despite taking fewer medications. After poor sales, NitroMed stopped marketing BiDil and sold it to JHB Pharmaceuticals.

     In July, the Journal of the National Cancer Institute published a nearly 20,000-subject study, which sought to determine whether race affects cancer mortality independent of socioeconomic status. The "provocative aspect" of the study's conclusion was that the only cancers that have higher mortality for black people are the "sex-specific cancers (breast, ovarian, and prostate)." Apparently not knowing where they were supposed to stop, the authors continued that "one explanation for our findings might be that there are hormonal factors . . . that differ by race." Kathy Albain led the study. An accompanying editorial by Otis Brawley of the American Cancer Society decried "racial medical profiling," reminding the reader that race "is not a scientific categorization and is a construct rejected by anthropologists." Then, Catherine Elton wrote a tract in Time magazine that would have seemed like a slander that Dr. Albain is racist had it not included the disclaimer "no one is accusing authors like Albain of racism." Elton is a recipient of an exclusively female fellowship "to focus exclusively on human rights journalism and social justice issues."
     Progress in racial endocrinology may require braving (and possibly proving) a muck of the most offensive and sexualized stereotypes in order to better treat some of the most common and deadly cancers, (not to mention the disease of violence). I am hopeful in that I expect that we shall accomplish this before the methane belch ends our pitiful existence.

No Amore for MAOA from Maori

noreply@blogger.com (nooffensebut) — Fri, 08 Jan 2010 19:38:00 +0000

      It would be easier for me to keep up with the latest celebrity deaths if there were not such accelerating developments in genetics of violence research.
      Here in the US, most liberals seem to have made up their minds that they are the true defenders of science against the evil forces of the religious right. However, in some parts of the world, liberals have clued into the fact that science threatens some of their own presumptions. With regard to the genetics of violence, New Zealand liberals are standing up for the Maori, New Zealand’s most violent ethnic group, against a specter of a scientific right. It seems to have begun with a 2006 interview with Dr. Rod Lea about the fact that about two-thirds of Maori have the moderately violence-associated 3-repeat allele of MAOA.
      “Obviously, this means they are going to be more aggressive and violent and more likely to get involved in risk-taking behaviour like gambling,” he reportedly said. “It is controversial because it has implications suggesting links with criminality among Maori people. I think there is a link. It definitely predisposes people to be more likely to be criminals and engage in that type of behaviour as they grow older.”
      Seven months later, The New Zealand Medical Journal featured two essays that presented no new evidence. Rather, the first by Merriman and Cameron merely criticized the assumption that a genetic association found in whites can be applied to other racial groups. The second was co-written by Dr. Lea, himself. This essay attacked the anonymous journalist who conducted the 2006 interview for distortion, “misquotes,” “misunderstandings,” “misconception,” and “negative media hype.” This essay declared that their “research agenda” “does not involve investigation of aggressive traits in Maori or any other population.” Furthermore, “the extrapolation and negative twisting of this notion by journalists or politicians to try to explain non-medical antisocial issues like criminality need to be recognised as having no scientific support whatsoever and should be ignored.”
      That anyone could fail to see violent criminality as a medical issue should give emergency room doctors pause. Genetic or not, understanding this issue has life-and-death consequences. The most extreme manifestation of MAOA dysfunction, Brunner syndrome, revealed the value of dexamethasone treatment in raising MAOA levels in female carriers. Research in mice showed the potential of the experimental drugs Fenclonine, ketanserin, and tetrabenazine to lower neurotransmitter levels to normal levels. At the very least, at-risk youth could alter their diets because they may have excess tyramine from chocolate, red wine, or cheese, and restricting the amino acids phenylalanine and tryptophan could lower neurotransmitter levels without drugs.
      The point made by Merriman and Cameron was a reference to a study by Widom and Brzustowicz, which was recently echoed in an essay by G Raumati Hook, who compared Preimplantation Genetic Diagnosis to Nazi eugenics. I previously pointed out how the Widom and Brzustowicz paper hid their data on African Americans because it probably showed that the extremely violence-inductive MAOA 2-repeat allele is not so rare in African Americans. Another conclusion of Widom and Brzustowicz was that maltreated white males demonstrate greater lifetime aggression if they have the 3-repeat allele rather than the 4-repeat allele, but that this is not the case for non-whites. Here again, they drew a deceptive conclusion by hiding their data. They found that white females with 3R alleles did not have higher lifetime aggression, only higher juvenile aggression. This parallels other research such as Sjöberg et al (2007) that suggest the MAOA 3-repeat allele does not increase female aggression. When Widom and Brzustowicz reported on the effect of MAOA in “non-whites,” they only gave data on men and women in combination. Their entire sample was only 39% non-white, and their non-white sample of 3-repeat allele subjects was 57% male, compared to 76% of white 3-repeat allele individuals. (2-repeat allele subjects were excluded from analysis.) It is also questionable what conclusions can be determined from the presumably diverse group of only 35 non-white men with the 3-repeat allele. Perhaps the results would have been different if the six non-white men with the 2-repeat allele were included. Nevertheless, the conclusion that a gene would behave differently in different races is a remarkable break from the traditional politically-correct assumption that race is a mere social construct. However, their conclusion about MAOA in non-whites was contradicted by studies by Weder et al and Beaver et al.

      It would be difficult to overstate how intense the research focus on MAOA has become. I took the time to create a table that summarizes just the evidence comparing the 3-repeat allele to the 4-repeat allele in their effect on aggressive behavior. Even many of the scientists who study it seem to be missing the big picture, so I color-coded each study. Red studies either showed that the 4-repeat allele was more associated with aggression or that the difference was not statistically significant. Blue studies showed a significant association between the 3-repeat allele and aggression either with or without childhood maltreatment as a precipitating factor, at least in men. Purple studies had debatable results.
      Some points can be drawn from this table. One is that MAOA has bucked the trend of early studies’ positive findings giving way to negating studies, which has been common among gene associations that did not bear out. Another is that aggression is just one manifestation of antisocial behavior, which could explain why many such studies found no association. Yet another is how the pace of research has increased over the years.

      The table also illustrates the importance of the gene-environment combined effect on aggression, in which childhood maltreatment is also factored. Here is the same table with just those studies investigating this effect. It was originally discovered by Caspi et al, who spent decades interviewing and observing their subjects to discover maltreatment. The other studies that came out so quickly afterwards did not have time to investigate so thoroughly, and their outcomes when they successfully replicated Caspi et al tended to be less robust.

      Here is the table with only studies of adult males. Those studies that are still red are either just not quite statistically significant or have explanatory qualifiers. Thus, there really should be no question that MAOA is a violence gene even with the relatively modest difference between the 3-repeat allele and the 4-repeat allele.

      Now, MAOA is probably not the only gene that affects violent behavior, even if it is the most important gene for this. Reif et al found that the short allele of 5-HTTLPR enhanced the aggression effect of the 3-repeat allele of MAOA. Reif et al did not find a “main effect” of 5-HTTLPR alone on aggression, but a few other studies have. In the case of MAOA, the 3-repeat allele is much more common in Africans and Asians than in whites, but for 5-HTTLPR, the short allele is found in about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans. This should serve as a warning to watch out for any gangs of violent Asians on their way home from the library. In truth, Retz determined that the short allele only increased violence 5%. Plus, Patkar et al failed to find an effect of the short allele on aggression in African Americans, suggesting that the gene could have different effects in different races. (See above, regarding the novel consensus that race is not a social construct.)
      Genetics research is rapidly moving humanity towards an understanding of violence that is complex and, for some, deeply offensive. Sadly, as violent crime claims 17,000 lives per year in the US alone, some progressives are aligning themselves against progress.

Deus ex Machina Genetics

noreply@blogger.com (nooffensebut) — Fri, 08 Jan 2010 19:32:00 +0000

Since I began speaking out about the genetics of violence, the entire field of genetics has reached a tipping point of high stakes and high drama. The stakes are that this field, which I would characterize as being presided over to some extent by ivory tower liberals, may be on the verge of proving once and for all that black people have a greater genetic predisposition to violence, or the field may wipe away this evidence along with a couple of decades of knowledge from gene association studies.

Prior to this scientific cataclysm, I received some interesting feedback from a presentation on the genetics of black violence that I created. When the blog Half Sigma reported on the recent study that associated gang violence with the 3-repeat allele in the promoter of the violence gene MAOA, the readers immediately wanted to know about racial prevalences of the alleles. Henry Harpending, the famous researcher who has studied recent human evolution and who co-wrote a new book with Gregory Cochran, pointed to the Sabol et al study, which determined that two-thirds of white people have the 4-repeat allele that is not associated with violent behavior and that 60% of African-Americans and Asian-Americans have the more violence-associated 3-repeat allele.

As one of the few studies of MAOA that lays out such racial prevalences, this study is quite an enigma to me. One might expect a study of nearly 1,500 subjects to more accurately reflect reality than smaller studies, but the study apparently discovered no subjects with the 2-repeat allele, which has a markedly greater association with violence than the 3-repeat allele that has received so much attention. Other studies, like one of 1,100 American males by Guo et al, found that 1% of American males possess this allele. MAOA is on the X chromosome, of which females have two, giving the Sabol et al study well over 2,000 chromosomes to examine. Therefore, I would have expected about 20 or so chromosomes to have the 2-repeat allele, instead of none.

I point all this out because Harpending, for one, relied on Sabol et al to describe the allele frequency of the MAOA promoter in black people. Other studies have replicated the allele frequency of Sabol et al for white males, always with about 1% having the 2-repeat allele. However, two smaller studies offered evidence of a significant proportion of black people having the 2-repeat allele. After I showed the Half Sigma readers my video, someone who goes by the pseudonym, Nanonymous, drew my attention to an important hidden fact about one of the two smaller studies. It was the study by Widom and Brzustowicz, detailing prevalences of rare MAOA alleles, including the 2-repeat allele. The study considered one of its major findings to be a lack of an association between violence and the 3-repeat allele just in non-whites, but it only had 98 non-white male subjects. Then, it claimed to re-analyze the data just for black subjects with “no change in the results.” We do not receive any hints as to how many of the 98 non-whites are black. However, as Nanonymous pointed out, some of the subjects in this 2006 study also took part in a 1989 study by Widom. That study did not look at genetics, but it did reveal that its 1,575 subjects were 67% white and 31% black, leaving just 2% for other groups. For the 2006 study, just over 600 agreed to undergo DNA analysis out of the original 1989 cohort plus 1,196 additional subjects. They were 60.9% non-Hispanic white and 39.1% “non-white.” Having successfully covered up the proportion who are black, Widom and Brzustowicz felt comfortable revealing that 6% of the non-white men had the ultra-violent 2-repeat allele, and none had the other rare alleles. In 2006, Rosenberg et al found that 5 of 37 (13.5%) African-Americans had rare MAOA alleles, which was corroborated by a greater frequency of associated rare haplotypes of the MAOA gene, itself. In general, Africans would be expected to have more rare alleles because non-Africans descend from only a subset of the African population.

Then, the earth shook. Risch et al published a meta-analysis on the association between depression risk and the interaction of stressful life events and a serotonin transporter gene. They went beyond disproving this association to indicting the whole enterprise of candidate gene association studies. Then, they suggested that delinquency “may not even be under strong genetic influence” and specifically attacked the use of MAOA gene testing in forensics, referring to it as one of the “nonreplicated genetic associations.” The influential genetics blog, Gene Expression, picked up the story, with the writer known as P-ter declaring that the majority of gene association studies, including that of MAOA, are likely wrong. He later posted that correct associations found in genome-wide association studies tend to require thousands or tens of thousands of subjects, making studies with just hundreds of subjects essentially worthless. P-ter singled out for criticism Avshalom Caspi, the researcher who first published an association study for the serotonin transporter gene and depression and who first published an association study comparing the MAOA 3- and 4-repeat alleles’ influence on violent delinquency. “[E]verything he’s published is probably wrong,” P-ter sneered.

I was the first to comment, and I conveyed my shock. “So, I guess you don’t believe in Brunner syndrome, either,” I said. Brunner syndrome was first identified in 1993 as a point mutation that caused complete MAOA deficiency, and it is associated with aggressive outbursts, arson, attempted rape, and exhibitionism. P-ter tried to deny that the existence of Brunner syndrome is sufficient to lend credence to the influence of the promoter alleles. I reminded him that the MAOA Caspi et al study was not a study of the 2-repeat allele (since only one subject had it), and this allele has consistently shown a greater association with violence than the 3-repeat allele. Therefore, MAOA expression has a continuum from Brunner syndrome, to the 2-repeat allele, to the 3-repeat allele, and, finally, to the 4-repeat allele. However, P-ter may be right that the many other phenotypes studied in association with the MAOA promoter may be disproved.

I did my own review of the scientific literature that specifically sought to replicate the Caspi et al study of the 3- and 4-repeat alleles of MAOA in white males. Twelve total studies sought to replicate the study in one manner or another. Only three of these had unequivocally non-significant results. Confirmatory studies raised questions about the methods of those studies, such as the narrow definition of the environmental exposures. A study by Sjoberg et al found an association between the 3-repeat allele of MAOA and aggression when testosterone levels are high. Thus, even though this study did not try to replicate Caspi et al, it gives additional indirect support by using an aggravating environmental exposure (testosterone), which can be objectively measured. All told, the studies that looked at the interaction between the 3- versus 4-repeat allele genotype and maltreatment had a combined sample size of over four-thousand white male subjects. Granted, a serious meta-analysis would exclude some studies. Kim-Cohen et al attempted a meta-analysis, but it included its own cohort, and rather than look at an outcome of aggression in that cohort, it noted an association with composite mental health problems, and ADHD, in particular.

During the discussion on the Gene Expression blog, the Australian researcher, Daniel MacArthur, first hedged, “As for MAOA: I wouldn’t bet my house on this not turning up in [a] well-powered GWAS [genome-wide association study] for violent behaviour (as P-ter predicts), but I’d say the odds of this happening are much better than 50%.” He later conceded “that the evidence for an association between the VNTR [variable number of tandem repeats] variant and antisocial behaviour is substantially more consistent than most of these associations. This may well be one of the rare cases of genuine associations.…” I am pleased if a rank amateur, like myself, can help to convince a group of researchers not to glibly dismiss the past seven years of research on a gene for violent delinquency just due to an embarrassing failed association in the study of depression. I noticed that the original study on Brunner syndrome found that dexamethasone treatment increased MAOA expression of female carriers of the mutation. I really believe that this line of research will save lives. I was also happy to see contributions to the discussion from writers that I admire like Steve Sailer and Gregory Cochran.

This may indeed be a watershed moment that will lead to far more skepticism of future candidate gene association studies. Hopefully, replication studies will become more standardized. I look forward to reading any potential large genome-wide association studies for violent delinquency. P-ter envisioned that such studies would uncover multitudes of genes with each having very small effects. However, I agree with Cochran that violent behavior can be biologically advantageous. Plus, I have long been intrigued by the possibility of “master genes” or other ways of coordinating evolutionary change, so that life can adapt to changing environments.

I also think that it is important to be mindful of the politicization of science. Much of the articulation in the popular press of the notion that race is a social construct that I have come across was actually in the defense of the Human Genome Diversity Project. This project has sought to decode the genomes of all the diverse branches of our human race. However, some activists tried to shut it down out of a fear that biological weapons against specific peoples would result. Therefore, the defense that there, in fact, is no one gene for being black was put forth. Furthermore, as MAOA demonstrates, genetic racial differences are almost always just disparities of allele frequencies. Even so, those differences are enough to cause hysteria. Consider this statement at the end of Ellis and Nyborg’s study of racial differences in testosterone levels: “scientists should be on guard against even the hint of any misuse of research findings in this area.” I suppose it is a sort of misuse of science for one to childishly berate a group of people and identify with a “superior” group to compensate for one’s own inadequacies. The irony is that this statement was followed by an acknowledgement for the help given by J. Philippe Rushton, a scientist well-known for his courageous disregard for suppressive sensitivities concerning everything from brain size to penis length.

Other examples of science politicization abound. Last year, the blogger known as "gc" was concerned that the Obama administration might censor human biodiversity science. Harpending responded that he received an invitation from the National Human Genome Research Institute to attend a workshop about the ethics of researching and publishing evidence of natural selection in humans. Another example is how Bruce Lahn seemed to be under pressure when he decided to forswear IQ-related genetics research. Now I am wondering if the actions taken in the Widom and Brzustowicz study and the gratuitous linking to the MAOA-aggression association by Risch et al were further examples.

The Gene Expression blog has been an invaluable ally of human biodiversity research. The writers are highly intelligent freethinkers. The fact that some of them have some liberal-leaning views and were early supporters of Howard Dean is no more an incongruity with their race realism than is the Christian faith of Steve Sailer and Charles Murray. It would only help this line of research to make it a little more acceptable in polite (that is, liberal) company. On the other hand, I am noticing eroding anonymity for certain writers, which could be a problem for them because liberal academia, I believe, is their home. (Full disclosure: nooffensebut is not my real name.)

If, somehow, MAOA promoter alleles should ever be proven meaningless, as P-ter suggested they would be, I shall follow the scientific ideal described by Richard Dawkins in The Root of All Evil. I shall rejoice at having been proven wrong, such that scientific truth is advanced. Thankfully, we all believe in science.

Why I am a Supremacist

noreply@blogger.com (nooffensebut) — Fri, 08 Jan 2010 19:31:00 +0000

During medical school, The Spirit Catches You and You Fall Down by Anne Fadiman was required reading. This is the story of a little Hmong girl with epilepsy. Her refugee parents preferred traditional folk remedies to Western medicine. Consequently, the child developed mental retardation. At one point, the state took custody of the child because her parents kept rejecting medical advice. Throughout the book, Fadiman laid out how the arrogance of the doctors created barriers between the medical community and the Hmong community. She also extolled cultural relativism and faith healing and endorses patient referrals to shaman priests. The book was right to advocate for a diplomatic approach to practicing medicine through cultural sensitivity and employment of the Kleinman questions. However, I am thankful that the medical establishment has discarded her oppressive cultural permissiveness. Recently, several high-profile, tragic stories have drawn attention to the ironically-named practice of “faith healing.” In one case of particularly outrageous horror, 16-year-old Neil Beagley died painfully from bladder constriction. Catheterization, a procedure so simple that many people perform it on themselves multiple times each day, would have saved his life. His parents were charged with negligent homicide.

Just as one does not choose one’s race or one’s parents, one does not choose to be brought up in a religion or culture that disallows modern medicine. Therefore, if a physician believes that the welfare of a child under his or her care absolutely depends upon an intervention which the parents oppose for religious reasons, that physician is ethically bound to treat. 90% of court decisions favor physicians in such disputes, and Prince vs. Massachusetts found that parents may not “make martyrs of their children.”

Therefore, I would like to dissent from a seemingly disingenuous defensive posture that some white nationalists and other race realists take by declaring myself a supremacist. I am at least a supremacist of Western allopathic medicine. Furthermore, some of my values have absolute applicability. Granted, I use “absolute” in a relative sense. I am not seeking to refute the whole post-modernist movement, as Edward O. Wilson once tried. Nevertheless, within the limited confines of modern human civilization, I dedicate myself to the Enlightenment, including science, medicine, and the appropriate employment of technology. Not only am I a supremacist, but I am also a conniving, swindling supremacist, in that I want Western medicine to suck the very the life from every folk, Chinese, or “complimentary” medicinal treatment. If acupuncture is any better than placebo shams, I want a big pharmaceutical company to find out why, put it in a pill form, and get filthy rich in the process.

Self-described race realist, Jared Taylor, with all due respect, seems to be playing a game. His American Renaissance Web site updates daily with media headlines and accompanying, often clever and sardonic subheadings that unclothe racial angles. Rather than expound on white culture and heritage, Taylor is confronting black people and immigrants. I vaguely remember a few cheap shots, and I think some failures in the white community could deserve similar ridicule, but basically I agree. I think white Americans have legitimate grievances with our black community, such as their rate of violent crime, and we are right to defend standards like the SAT against them. I do not currently feel aggrieved towards, say, Nepalese people. In other words, whites are right, except when we are not. We stand for some things that are greater than ourselves. Still, Taylor wishes to back away from moral judgments and to affirm unconditional love for whites, as his people and his family.

Reading these reports might give white people a sense of pride. However, it is also possible that non-white people might acquaint themselves with this information and agree. Some of them might be inspired to bring change to their own ethnic community. Others might develop a fondness for white people and wish to assimilate into a white society more so. Many persuasive arguments remonstrate against immigration law relaxation, for instance, and for those reasons, I oppose it, as well. Yet, saving one’s worst rancor for those non-whites who most admire whites seems maladroit to me.

For all the accomplishments of white people, non-white people also develop ideas and tools, and it has been our Western tradition to engage in trade and even some cultural exchange. Japan understood the value of such exchange, and they adopted American Total Quality Management, to the long-term detriment of the US auto industry. Francis Galton understood the value of trade. He felt that Chinese people made better trade partners than Africans, so he wanted to Sinicize Africa. China has successfully adopted Western science, and I just discovered that Richard Lynn has a new book, which predicts Chinese ascendence on the order of the Roman Empire due to their adoption of something like Western eugenics. Jared Taylor has paralleled his own fight against immigration to the Dalai Lama’s protestations against Chinese settlement in Tibet. Considering China’s enormous investments in Tibet, I think a race realist should admire this spread of Western standards of living.

I reject the generic humanities professor’s stock straw man for racial realism. I am not an incurious, belligerent curmudgeon who must define “Us” by defining the “Other.” I am aware of Robert Putnam’s inadvertent discovery that diversity is not necessarily a strength, but I also understand a basic truism that diversity is not always the same. The experience of diversity from working with fellow physicians feels different from experiencing diversity by living near the Rio Grande. (In fact, Putnam’s figures show high levels of trust in diverse Silicon Valley.) For those who disagree with me, I suggest a “big tent” approach. Race realism is also about science, understanding the human condition, and finding cures by acknowledging biological differences. Jared Taylor should continue to forgo sowing discord with those race realists who lack the agenda of sowing discord.