Thursday, February 08, 2018

So what would a bio-criminology justice system look like?

People associated with American Renaissance
Richard Spencer is in the front row wearing a tan suit.

They pay Steve Sailer to write racist bullshit.
In 1997 John Paul Wright co-authored a paper, along with his doctoral advisor Francis T. Cullen, Crime and the Bell Curve: Lessons from Intelligent Criminology which states:
(Charles) Murray repeatedly informs interviewers that he simply is being a good social scientist who is conveying unpleasant truths that can be ignored only at the nation's long-term peril (see also DeParl 1994; Murray and Herrnstein 1994). 
At least with regard to crime, we claim otherwise; Murray's social science is misleading, and his message is erroneous. He needs a boost in his criminological intelligence. The apparent persuasiveness of The Bell Curve, which Murray coauthored with the late Richard Herrnstein, is that it purports to show that IC has powerful and largely immutable effects across a range of behaviors. If "cognitively disadvantaged," a person is going to commit crimes, fail at school, be unemployed, end up on welfare, produce illegitamet kids, and be a lousy citizen. But if these effects do not in fact exist, or if these effects are in fact amenable to reversal, then the foundation on which Herrnstein and Murray's (1994) thesis is built crumbles. 
In 2012 Wright co-authored a paper along with Beaver, Boutwell, Barnes, DeLisi, and Vaughan called Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior which associates African-American criminality with a higher instance of the 2-repeat allele among blacks.
Analyses revealed that African-American males who carried the 2-repeat allele were, in comparison with other African-American male genotypes, significantly more likely to be arrested and incarcerated. Additional analyses revealed that African-American male carriers of the 2-repeat allele scored significantly higher on an antisocial phenotype index and on measures assessing involvement in violent behaviorsover the life course. 
They admit that their subjects self-reported their "race" but say:
Since prior research has revealed that the distribution of the 2-repeat allele varies by race (e.g., Reti et al., 2011; Widom & Brzustowicz, 2006), the analysis begins by examining the allelic distributions by race. As Table 1 shows, the 2-repeat allele was carried by 0.1% of Caucasian males and by 5.2% of African-American males. To check the consistency of these estimates, all of the analyses were recalculated using self-reported race instead of interviewer-rated race. Importantly, research has revealed that self-reported race correlates almost perfectly with race identified via genetic markers (Tang et al., 2005). 
The Tang et al. they are pointing to is the 2005 study concerning micro satellite markers Genetic structure, self-identified race/ethnicity, and confounding in case-control association studies. Its abstract says this:
We have analyzed genetic data for 326 microsatellite markers that were typed uniformly in a large multiethnic population-based sample of individuals as part of a study of the genetics of hypertension (Family Blood Pressure Program). Subjects identified themselves as belonging to one of four major racial/ethnic groups (white, African American, East Asian, and Hispanic) and were recruited from 15 different geographic locales within the United States and Taiwan. Genetic cluster analysis of the microsatellite markers produced four major clusters, which showed near-perfect correspondence with the four self-reported race/ethnicity categories. Of 3,636 subjects of varying race/ethnicity, only 5 (0.14%) showed genetic cluster membership different from their self-identified race/ethnicity. On the other hand, we detected only modest genetic differentiation between different current geographic locales within each race/ethnicity group. Thus, ancient geographic ancestry, which is highly correlated with self-identified race/ethnicity--as opposed to current residence--is the major determinant of genetic structure in the U.S.
Once again we have the problem with genetics and race. Co-author Neil Risch says they used US Census categories for race, which is an obvious social construction. They identify four races in this case, white, black, Hispanic and East Asian.

We've already discussed the issue  in this evo-psycho bros series with self-identified whites being as much as 1/8 black and the average African American being almost a quarter white. And so clearly a lot of genetic information is missed by the study by forcing people to be one "race" when they are usually not.

There is also the issue of Hispanic being identified as a race, as Razib Khan can tell you:

So there's no clear establishment of genetic ethnicity in the 2005 microsatellite markers study. Everybody was shoved into one of four buckets regardless of what the 326 microsatellites indicated.

Therefore, what "black" means in all these studies is:
  • descendants of primarily West African ethnicity;
  • who were enslaved by whites and who have on average almost one-quarter white ancestry due to slave-rape; 
  • who are identified as "black" even when they have obvious European ancestry, thanks to social custom (one-drop rule);
  • And subsequent to slavery have suffered mistreatment as "blacks" by the white majority from lynching to segregation.
That's a very specific group of people and calling them "African" American tells almost nothing about this group of people. And this group of people tells you almost nothing about the genetics of an entire continent.

Thanks to 23andme we know approximately how much European ancestry turns a "black" into a "white" - 87.5%. What was once considered completely black thanks to the one-drop rule and identified as "octoroon."

But in addition to the problems of genetic/race uncertainty, there is also room for doubt about the 2-repeat allele of the MAOA gene issue.

The evo-psycho bros don't have much motivation to explain themselves clearly, especially since obfuscation is mostly their friend. It not only hides - usually - their contempt for African Americans but it covers the weaknesses in their methodologies.

Locating weaknesses in methodologies hidden by poor writing is a big part of what technical writers in IT do. Which may be why I'm going through this exercise instead of journalists, who have mostly avoided it, in spite of the controversial nature of the topic.

Luckily there are some scientists who do write clearly. Dr. Aaron Gardner with a BSc (Honours) in Genetics published on his blog: The Warrior Gene: 5 common myths debunked.


The Genetics of MAOA

MAOA is interesting as changes in its activity don’t relate to individual SNPs, rather they are driven by changes in its promoter region. All genes have a promoter region, which sit upstream of the gene in the DNA sequence and this is the location where polymerase proteins bind and begin to read through the gene.
Within the promoter of MAOA is a region of DNA known as a variable number tandem repeat or VNTR. VNTRs are small sequences of DNA which can be repeated a variety of times, which gives rise to the 2R or 3R terminology you may have seen around MAOA. 2R means that there are two repeat sequences in the VNTR, 3R three repeat sequences and so on. This is important as the number of repeats has a big impact on how well MAOA is “read” by the polymerase protein. When the gene is not read as efficiently not as much MAO-A is produced meaning the breakdown of neurotransmitters is also reduced [R]. It is this lack of MAO-A enzyme activity which is thought to lead to increased aggressive behaviour [R].
Myth 3: The aggressiveness associated with the “warrior gene” is caused by SNPs.
Fact: Changes in MAOA function are actually linked to alterations in the VNTR located in the promoter region.
I’ve summarised the common repeats below and how they impact on the efficiency of MAOA reading and thus MAO-A activity. 3.5R and 4R variants are thought of as normal, with 2R variants having the most reduced function and 3R and 5R variants sitting between. As such the 2R, 3R and 5R types are sometimes referred to as MAOA-L meaning low activity [RR].
The number of repeats within the MAOA VNTR has a big impact on transcription efficiency and subsequently MAO-A activity [RR].

What effect do changes in MAOA VNTR have on aggressiveness?

Low activity of MAO-A is thought to drive increased aggressiveness. But if you look at the table above you can see the 3R  form of MAOA is actually very common. I don’t know about you but upwards of 30% of the population being overly aggressive sounds very high.
So lets look at the data; the 2R, 3R and 5R variants which show reduced MAO-A enzyme activity have been linked with increased aggressiveness in a variety of studies [RR]. So far the hypothesis seems to be holding together.
But! all these reports come with a very large caveat. Whilst they do show that the MAOA-L forms are associated with increased aggression, having an MAOA-L form does not mean that someone will be aggressive, there are numerous other factors associated, with the most important thought to be early life abuse [R]. 
Simply put, whilst some people with the 2R, 3R and 5R variants were more aggressive, there were lots of people who also had these variants who weren’t more aggressive. The associations only appeared when a large enough population was studied, and this suggests that there are lots of other factors which are also influencing how aggressive we are, not just MAOA. Some studies have failed to find a link between MAOA and aggression [R].

I'm sure "lots of other factors" influencing aggression is not what the bio-criminology bros want to hear since it's so much easier to just assume there's a genetic marker for aggression related to African ethnicity.

Now with all this uncertainty about racial identification and the uncertainty surrounding a "warrior gene" you might expect the evo-psycho bros to be less assertive in their claims of what it all means for society at large. But if you expected that you don't know the evo-psycho bros.

Much like its sister web site, the book Conservative Criminology: A Call to Restore Balance to the Social Sciences by John Paul Wright and Matt DeLisi contains much ranting about liberals. They are angry because liberals won't let them make racist claims without criticism.
We have also published papers that have clearly violated the liberal ethos of academia. Our work, along with the work of our friend and colleagues, has examined the rather important role of genetic influences on human behavior, including criminal behavior (Beaver et. al, 2013b; DeLisi et al, 2014), and various traits such as impulsivity and low self-control (DeLisi et al., 2010; Wright et al, 2012). 
Indeed, we and our colleagues have been instrumental in creating an arm of criminological study called “biosocial criminology.” 
So what would a "biosocial criminology" justice system look like? Maybe something like this...
(The DEFENSE attorney addresses Kevin WRIGHT, the prosecution's expert witness.)
Mr. Wright, as an expert in racial criminology -  
That's biosocial criminology.
Right. Mr. Wright, you say black people are more likely to commit crime because of their genetic background.
That is what the science says. It's all in The Bell Curve.  
And what makes you so sure my client is a member of the black "race"?

As Steven Pinker told us, race is real. There is a black race and a white race. And other races.
How many races are there? 

Objection. Irrelevant. 

Would it interest you to know that my client has a mixed ethnicity of 40% White, 10% Pacific Islander, 15% Native American and only 35% African? And so he is not even half African.
As we learn in Bio-criminology 101: If it looks African, it is African.

I've mentioned the paper A social science without sacred values written by Bo and Ben Winegard earlier in this series, but only in reference to how they misrepresented what Larry Summers said at the NBER conference on diversity in STEM careers.

The Summers reference is part of the main argument of the paper, the problem of liberal mental bias.

Although they are not at all worried about conservative mental bias they admit, perhaps inadvertently, that it exists:
One, researchers have consistently complained that stereotypes are inaccurate, unjust, and maladaptive products of a biased social brain (see Jussim, 2012). However, it turns out that many stereotypes are actually remarkably accurate. Because many stereotypes are about talent, skill, and personality inequalities among social groups, this line of research, according to Duarte et al., was not surprisingly initiated by a conservative social scientist, Clark McCauley (McCauley & Stitt, 1978). That is, liberal researchers were not interested in discovering that stereotypes were accurate because that would violate a sacred liberal narrative about equality. 
They believe that while liberals avoid exploring stereotypes because of their "sacred liberal narrative about equality" on the other hand conservatives actively seek to research stereotypes in order to confirm they are correct - stereotypes are "remarkably accurate."

Presumably to honor the sacred conservative value of inequality.

Which gives us some insight into why, in spite of the flimsiness of the evo-psycho bros methodology designed to demonstrate the innate criminality and lower intelligence of blacks, they rush to tell the world about their weak findings. Without shame.

The Winegard brothers have so little concern for the possibility that conservatives are influenced by their political positions that although they discuss the persecution Charles Murray has endured, they don't mention the connection between The Bell Curve and the white supremacist organization the Pioneer Fund.

More about that next.