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Answering Common “Criticisms” of the Theory of African American Offending
4150 words
Introduction
Back in September I published an article arguing that since the theory of African American offending (TAAO) makes successful novel predictions and hereditarian explanations don’t, that we should accept the TAAO over hereditarian explanations. I then published a follow-up arguing that crime is bad and racism causes crime so racism is bad (and I also argued that stereotypes lead to self-fulfilling prophecies which then cause the black-white crime gap). The TAAO combines general strain theory, social control theory, social disorganization theory, learning theory, and low self control theory in order to better explain and predict crime in black Americans (Unnever, 2014).
For if a theory makes successful novel predictions, therefore that raises the probability that the theory is true. Take T1 and T2. T1 makes successful novel predictions. T2 doesn’t. So if T1 and T2 both try to explain the same things, then it’s only logical to accept T1 over T2. That’s the basis of the argument against hereditarian explanations of crime—the main ones all fail. Although some attempt at a theory has been made integrating hereditarian explanations (Ellis’ 2017 evolutionary neuroandrogenic theory), it doesn’t make any novel predictions. I’ve recently argued that that’s a death knell for hereditarian theories—there are no novel predictions of any kind for hereditarianism.
But since I published my comparison of the successes of the TAAO over hereditarian explanations, I’ve come across a few “responses” and they all follow the same trend: “What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?” or “So blacks don’t have agency?” or “Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?” or “What about IQ and it’s relationship to crime?” or “What control groups are there for TAAO studies?” or “The black-white crime gap was lower during Jim Crow, how is this possible if the TAAO is true?” or “Unnever and Gabbidon are just making excuses for blacks with their TAAO” or “The so-called ‘novel predictions’ you reference aren’t novel at all.” I will answer these in turn and then provide a few more novel predictions of the TAAO.
“What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?“
For some reason, TAAO detractors think this is some kind of knock-down questions for the TAAO and think that they disprove it. These are easily answered and they don’t threaten the theory at all.
For one, the theory of AFRICAN AMERICAN offending is irrelevant places that… Aren’t America. It’s a specific theory to explain why blacks commit crime at a higher rate IN AMERICA, therefore other countries are irrelevant. There would need to be a specific theory of crime for each of those places and contexts. So this question doesn’t hurt the theory. So going off of the first question, the answer to the second question also addresses it—it’s a theory that’s specifically formulated to explain and predict crime in a certain population in a certain place.
For two, why would a theory that’s specifically formulated to explain crime using the unique experiences of black Americans matter for other American groups? Blacks went through 400 years of slavery and then after that went through segregation and Jim Crow, so why would it mean anything that other groups face discrimination but then don’t have higher rates of crime compared to the average? Since the theory has specific focus on understanding the unique experiences and dynamics of crime in the black American population, it’s obvious that asking about other groups is just irrelevant. Other racial and ethnic groups aren’t the primary focus—since it aims to address historical and contemporary factors that lead to higher crime in the black American population. It’s in the name of the theory—so why would other racial groups matter? Unnever and Gabbidon (2011: 37) even explicitly addressed this point:
Our work builds upon the fundamental assumption made by Afrocentists that an understanding of black offending can only be attained if their behavior is situated within the lived experiences of being African American in a conflicted, racially stratified society. We assert that any criminological theory that aims to explain black offending must place the black experience and their unique worldview at the core of its foundation. Our theory places the history and lived experiences of African American people at its center. We also fully embrace the Afrocentric assumption that African American offending is related to racial subordination. Thus, our work does not attempt to create a “general” theory of crime that applies to every American; instead, our theory explains how the unique experiences and worldview of blacks in America are related to their offending. In short, our theory draws on the strengths of both Afrocentricity and the Eurocentric canon.
“So blacks don’t have agency?”
The theory doesn’t say that blacks lack agency (the capacity to make decisions and choices) at all. What the theory does say is that systemic factors like racism, socioeconomic disparities, and historical and contemporary marginalization can influence one’s choices and opportunities. So while individuals have agency, their choices are shaped by the social context they find themselves in. So if one has a choice to do X or ~X but they physical CAN’T do X, then they do not have a choice—they have an illusion of choice. The TAAO acknowledges that choices are constrained by poverty, racism, and social inequity. So while blacks—as all humans do—have agency, some “choices” are constrained, giving the illusion of choice. Thus, constraints should also be considered while analyzing why blacks offend more. This, too, is not a knock-down question.
“Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?”
Over the years I’d say I’ve done a good job of arguing against hereditarian theories of crime. (Like testosterone increasing aggression and blacks having higher levels of testosterone, the AR gene, and MAOA.) They’re just not tenable. The genetic explanation makes no sense. (Talk about disregarding agency…) But one response is that we could find some as-of-yet-to-be-discovered genes, gene networks, or neurohormonal influences which explain the higher crime rates in black Americans. This is just like the “five years away” claim that hereditarians love to use. We just need to wait X amount of years for the magic evidence, yet five years never comes since five years away is always five years away.
“What about IQ and it’s relationship to crime?”
Of course the IQ-ists love this question. The assumption is that lower IQ people are more likely to commit crime. So low is means more crime and high IQ means less crime. Ignoring the fact that IQ is not a cause of anything but an outcome of one’s life experiences, we know that the correlation between IQ and crime is -0.01 within family (Frisell, Pawitan, and Langstrom, 2012). So that, too, is an irrelevant question. The relationship just isn’t there.
“What control groups are there for TAAO studies?”
Other than the first question about why don’t other groups who experience racism commit more crime and what about blacks in other countries, this one takes the cake. The TAAO doesn’t need control groups in TAAO tests since it focuses specifically on understanding the unique factors that contribute to crime in America. So instead of comparing different racial or ethnic groups, the TAAO seeks to identify and analyze specific historical, social, and systemic factors which shape the experiences and behaviors of black Americans within the context of American society.
“The black-white crime gap was lower during Jim Crow, why? How is this possible if the TAAO is true?”
Between 1950 and 1963, non-whites made up 11 percent of the US population, 90 percent of which were black. In 1950 for whites the murder rate was 2 to 3 deaths per 100,000 while for non-whites the rate was 28 deaths per 100,000 (28 times the US average) which then fell to 21 per 100,000 in 1961 which was still about 8 times that of the white murder rate while the rate raised again between 1962 and 1964 (Langberg, 1967). Langan (1992) showed a steady increase in the incarcerated black population from 1926 (21 percent) to 1986 (44 percent). But demographic factors account for this, like increases in the sentencing of blacks, the increase in the black population, and increase on black arrest rates—furthermore, there is evidence for increased discrimination between 1973 and 1982 that would explain the 70s-80s incarceration rates (Harding and Winship, 2016). Harding and Winship also showed that differential population growth can account for one-third of the increase in the prison population difference while the rest can be accounted for by differences in sentencing and arrest rates between 1960 and 1980. So the black population increased more in states that had higher incarceration rates. Nonetheless, the TAAO isn’t supposed to retroactively explain trends.
Therefore, the disparity between whites and blacks remained, even pre-1964. This question, too, isn’t a knockdown for the TAAO either. These questions that are asked when one is provided with the successful novel predictions of the TAAO are just cope since hereditarian explanations don’t make novel predictions and their explanations fail (like the ENA theory).
“Unnever and Gabbidon are just making excuses for blacks with their TAAO.”
This is not what they’re doing with their theory at all. A theory is a well-substantiated explanation of some aspect of the natural word that’s based on observation, empirical data, and evidence. They provide testable hypotheses that can be empirically tested. They also make predictions based on their proposed explanations. Predictive capacity is a hallmark of scientific theories. And it’s clear and I’ve shown that the TAAO makes successful novel predictions. Therefore the ability of a theory to make predictions—especially risky and novel ones—lends credibility to the validity of the theory.
The claim that the TAAO is a mere excuse for black crime is ridiculous. Because if that’s true, then all theories of crime are excuses for criminal activity. The TAAO should be evaluated on its predictive power—it’s ability to make successful novel predictions. Claims that the theory is a mere “excuse” for black crime is ridiculous, especially since the theory makes successful novel predictions. It’s clearly a valuable framework for understanding black crime in America.
“The so-called ‘novel predictions’ you reference aren’t novel at all”
We need to understand what the TAAO actually is. It’s a theory of crime that considers the African American “peerless” worldview. “Peerless” means “incomparable.” They have the worldview they do due to the 400 years of slavery and oppression like Jim Crow laws and segregation. Therefore, to explain black crime we need to understand the peerless African American experience. That’s a main premise of the theory. So the TAAO has one main premise, and it’s from this premise that the predictions of the TAAO are derived.
The peerless worldview of African Americans This premise recognizes the unique historical, contemporary, social, and cultural experiences of African Americans including their experiences of racial discrimination, social marginalization, and racial identity. This premise, then, lays the key groundwork for understanding black crime. This core premise of the TAAO then centers the theory within the context of the African American experience. Each of the predictions below are derived from the core premise of the TAAO—that of the peerless worldview of African Americans without relying on the predictions as premises used for the construction of the theory. Each of the predictions follows from the core premise, and they reflect how the African American experiences of racial discrimination, social marginalization and racial identity influence their likelihood of experiencing racial discrimination. Unnever and Gabbidon gave many arguments and references that this is indeed the case. The predictions, then, weren’t used as premise to construct the TAAO but they indeed are derived from—indeed they emerge from—the foundational experiences of African Americans and then serve as testable hypotheses which are derived from that understanding.
Thus, the predictions follow from the TAAO and they are derived from the foundational premise of the TAAO, without being used in the construction of the theory itself, qualifying as novel predictions according to Musgrave (1988): “a predicted fact is a novel fact for a theory if it was not used to construct that theory — where a fact is used to construct a theory if it figures in the premises from which that theory was deduced” and Beerbower: “the purpose of science is to enable accurate predictions and that, in fact, science cannot actually achieve more than that...The test of an explanatory theory, therefore, is its success at prediction, at forecasting. This view need not be limited to actual predictions of future, yet to happen events; it can accommodate theories that are able to generate results that have already been observed or, if not observed, have already occurred...it must have some reach beyond the data used to construct the theory“
More novel predictions of the TAAO
Therefore, since the TAAO has success in its predictions and hereditarian ones don’t (they don’t even make any novel predictions), it’s only rational to accept the theory that makes successful novel predictions over the one that doesn’t. The only reason one would accept the hereditarian explanations over the TAAO is due to bias and ignorance (racism), since the TAAO is a much more robust theory that actually has explanatory AND predictive power. So the issue here is quite clear—since we know the causes of black crime due to the successful novel predictions that the TAAO generates, then there are clear and actionable things we can do to try to mitigate the crime rate. This is something that hereditarian theories don’t do, most importantly because they don’t make any novel predictions. Since the TAAO makes successful risky novel predictions—predictions that, if they didn’t hold, they would then refute the theory—and since the predictions hold, then the theory is more likely to be true than not. The TAAO not only accommodates, but it makes predictions, and we can’t say the same for hereditarianism.
The issue is that so-called “race-neutral” theories of crime need to assume that racial discrimination isn’t a cause of black American offending because this would then limit it only to black Americans. Therefore race-neutral theories of crime don’t have the same predictive and explanatory power as a race-centric theory of crime—which is what the TAAO is. It’s clear that: the TAAO makes successful novel predictions, the predictions aren’t used as premises in the TAAO, the TAAO is a race-centric, country-specific theory of crime (and not a general theory of crime), racism and stereotypes don’t explain offending for non-African Americans, the theory doesn’t say that blacks lack agency, IQ doesn’t explain crime within families, and cope from hereditarians that one day we will find genes or neurohormonal influences which lead to crime in black Americans is just cope. It’s clear that the TAAO is the superior theory of crime because it does what scientific theories are supposed to do: successfully predict novel facts of the matter, something that hereditarianism just does not do which is why I’m justified in calling it a racist movement. Basically since there are unique characters of a demographic that require perspectives that are solely related to that group, then we need group-centric theories of crime due to the unique experiences of thsg group, and this is what the TAAO does.
Now that I’ve answered common criticisms of the TAAO, I have a few more successful novel predictions of the theory. In my original article I cited 3 novel predictions, how they followed from the theory, and then the references that confirmed the predictions:
(Prediction 1) Black Americans with a stronger sense of racial identity are less likely to engage in criminal behavior than black Americans with a weak sense of racial identity. How does this prediction follow from the theory? TAAO suggests that a strong racial identity can act as a protective factor against criminal involvement. Those with a stronger sense of racial identity may be less likely to engage in criminal behavior as a way to cope with racial discrimination and societal marginalization. (Burt, Simons, and Gibbons, 2013; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019)
(Prediction 2) Experiencing racial discrimination increases the likelihood of black Americans engaging in criminal actions. How does this follow from the theory? TAAO posits that racial discrimination can lead to feelings of frustration and marginalization, and to cope with these stressors, some individuals may resort to committing criminal acts as a way to exert power or control in response to their experiences of racial discrimination. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019)
(Prediction 3) Black Americans who feel socially marginalized and disadvantaged are more prone to committing crime as a coping mechanism and have weakened school bonds. How does this follow from the theory? TAAO suggests that those who experience social exclusion and disadvantage may turn to crime as a way to address their negative life circumstances. and feelings of agency. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016)
(Prediction 4) Black people who experience microaggreesions and perceive injustices in the criminal justice system are more likely to engage in serious and violent offending. How does this follow from the theory? Experiences of racial discrimination and marginalization can lead to negative emotions like anger and depression among black people. These negative emotions, which are then exacerbated by microaggreesions and perceptions of injustice in the criminal justice system, may increase the likelihood of engaging in serious and violent offending as a coping mechanism or means of asserting power. But, again, those with a stronger racial identity may be more resilient to the effect of discrimination (Isom, 2015).
(Prediction 5) Black Americans who perceive a lack of opportunity for socioeconomic advancement due to systemic barriers are more inclined to engage in criminal activity as a means of economic survival and social mobility. How does this follow from the theory? Perceptions of limited opportunities and systemic injustices can drive individuals to engage in criminal behaviors as a response to inequality (Vargas, 2023).
The fact that the TAAO generates these novel and successful predictions is evidence that we should accept the theory.
We also know that perceptions of criminal injustice predict offending (Bouffard and Piquero, 2013), we know that blacks are more likely than whites to perceive criminal injustice (Brunson and Weitzer, 2009) and we know that there are small differences among blacks and their perception of criminal injustice (Unnever, Gabbidon, and Higgins, 2011). So knowing this, more blacks should offend, right? Wrong. The vast majority of blacks don’t offend even though they share the same belief about the injustices of the criminal justice system. So how can we explain that? “Positive ethnic-racial socialization buffers the effect of weak school bonds on adolescent substance use and adult offending” (Gaston and Doherty, 2018). So the discrimination that black Americans have erodes their trust in social institutions like the school system, and then these weakened school bonds then increase the risk of offending.
Supporting a major tenet of TAAO and prior research on the protective ability of ethnic-racial socialization, the analyses showed that Black males who received positive ethnic-racial socialization messages in childhood develop resilience to the criminogenic effect of weak school bonds and face a lower risk for offending over the life course. (Gaston and Doherty, 2018)
One factor that is salient in the TAAO is racial subordination. We know that black people don’t commit crime because they are black, but we know that their offending is related to socio-environmental context like poverty, bad schools (while racism and stereotypes weaken school bonds blacks have, which makes them more likely to offend), broken families, and lead exposure (Butler, 2010) of which the TAAO addresses. We also know that there is no such thing as a “safe” level of lead exposure and that the relationship between lead and crime is robust and replicated across different countries and cultures. We also know that blacks were used as an experiment of sorts, where they were knowingly exposed to lead paint in subsidized homes.
This environmental racism (Washington, 2019), then, is another aspect of the racial subordination of blacks. And from 1976 to 2005, blacks were 7 times more likely than whites to commit murder. The fact of the matter is, the black-white murder gap has been large for over 100 years. And in discussing environmental racism, Unnever and Gabbidon (2011: 188) are explicit about the so-called genetic hypothesis of crime: “We want to be perfectly clear that our argument in no way is related to the thesis that there is a genetic cause to African American offending.” Therefore, this question doesn’t strike the heart of the TAAO and is just an attempt at evading the successful novel predictions the theory generates.
Conclusion
I’ve shown that the common “criticisms” of the TAAO are anything but and are easily answered. I then gave more successful predictions of the TAAO. It’s quite clear that one should accept the TAAO over hereditarian explanations. We also know that black isolation is a predictor of crime as well—even in 1996 blacks accounted for over 50 percent of murders and two-thirds of robberies (Shihadeh and Flynn, 1996). In 2020, blacks were six times more likely to be arrested for murder than whites. We also know that the belief by blacks in the violent stereotype predicts their offending and their adherence to the stereotype predicts crime and self control (Unnever, 2014). Therefore, a kind of stereotype threat arises here and has effects during police encounters like wkth height (Hester and Gray, 2018)(Najdowski, Bottoms, and Goff, 2015; Strine, 2018; Najdowski, 2012, 2023) , with one argument that race stereotypes track ecology, not race, (Williams, 2023) (just like for IQ; Steele and Aronson, 1995; Thames et al, 2014). We know that stereotype threats weaken school bonds and that weakened school bonds are related to offending, therefore we can infer that stereotype threats lead to an increase in crime (Unnever and Gabbidon, 2011).
Unnever and Gabbidon were quite clear and explicit in their argument and the hypotheses and predictions they made based on their theory. So when tested, if they were found not to hold then the theory would be falsified. But the theories held under empirical examination. Unnever and Gabbidon (2011: 98) were explicit in their theory and what it meant:
Put simply, we hypothesize that the probability of African American offending increases as blacks become more aware of toxic stereotypes, encounter stereotype threats, and are discriminated against because of their race. Our theory additionally posits that these forms of racism impact offending because they undermine the ability of African Americans to develop strong ties with conventional institutions. The extant literature indicates that stereotype threats and personal experiences of racial discrimination negatively impact the strength of the bonds (attachment, involvement, commitment) that black students have with their schools (Smalls, White, Chavous, and Sellers, 2007; Thomas, Caldwell, Faison, and Jackson, 2009). And, the research is clear; weak social bonds increase the probability of black offending (Carswell, 2007).
The worldview shared by black Americans is a consequence of the experience they and their ancestors had in America. This then explains their offending patterns, and why they commit more crime than whites. The socio-historical context that the TAAO looks to explain black crime is robust. Since the TAAO is successful in what it sets out to do, then, I wouldn’t doubt that there should be other race-centric theories of crime that try to explain and predict offending in those populations. The empirical successes of the TAAO’s predictions attest to the fact that other theories of crime for other races would be fruitful in predicting and explaining crime in those groups.
Hereditarians dream of having a theory that enjoys the empirical support that the TAAO has. The fact that the TAAO makes successful novel predictions and hereditarianism doesn’t is reason enough to reject hereditarian explanations and accept the TAAO. Accepting a theory that makes novel predictions is rational since it speaks to the theory’s predictive power. So by generating predictions that were previously unknown or untested and them confirming them through empirical evidence, the theory therefore shows its ability to predict and anticipate real-world phenomena. This then strengthens confidence in the theory’s underlying principles which provides a framework for understanding complex phenomena. Further, the ability of a theory to make such predictions suggests that the theory is robust and adaptable, meaning that it’s capable of accommodating new data while refining our understanding over time.
Hereditarians would love nothing more than to reduce black criminality to their genes or hormones, but reality tells a different story, and it’s one where the TAAO exists and makes successful novel predictions.
Race, Racism, Stereotypes, and Crime: An Argument for Why Racism is Morally Wrong
2300 words
Introduction
(1) Crime is bad. (2) Racism causes crime. (C) Thus, racism is morally wrong. (1) is self-evident based on people not wanting to be harmed. (2) is known upon empirical examination, like the TAAO and it’s successful novel predictions. (C) then logically follows. In this article, I will give the argument in formal notation and show its validity while defending the premises and then show how the conclusion follows from the premises. I will then discuss two possible counter arguments and then show how they would fail. I will show that you can derive normative conclusions from ethical and factual statements (which then bypasses the naturalistic fallacy), and then I will give the general argument I am giving here. I will discuss other reasons why racism is bad (since it leads to negative physiological and mental health outcomes), and then conclude that the argument is valid and sound and I will discuss how stereotypes and self-fulfilling prophecies also contribute to black crime.
Defending the argument
This argument is obviously valid and I will show how.
B stands for “crime is bad”, C stands for “racism causes crime”, D stands for racism is objectively incorrect, so from B and C we derive D (if C causes B and B is bad, then D is morally wrong). So the argument is “(B ^ C) -> D”. B and C lead to D, proving validity.
Saying “crime is bad” is an ethical judgement. The term “bad” is used as a moral or ethical judgment. “Bad” implies a negative ethical assessment which suggests that engaging in criminal actions is morally undesirable or ethically wrong. The premise asserts a moral viewpoint, claiming that actions that cause harm—including crime—are inherently bad. It implies a normative stance which implies that criminal behavior is wrong or morally undesirable. So it aligns with the idea that causing harm, violating laws or infringing upon others is morally undesirable.
When it comes to the premise “racism causes crime”, this needs to be centered on the theory of African American offending (TAAO). It’s been established that blacks experiencing racism is causal for crime. So the premise implies that racism is a factor in or contributes to criminal behavior amongst blacks who experience racism. Discriminatory practices based on race (racism) could lead to social inequalities, marginalization and frustration which would then contribute to criminal behavior among the affected person. This could also highlight systemic issues where racist policies or structures create an environment conducive to crime. And on the individual level, experiences of racism could influence certain individuals to engage in criminal activity as a response or coping mechanism (Unnever, 2014; Unnever, Cullen, and Barnes, 2016). Perceived racial discrimination “indirectly predicted arrest, and directly predicted both illegal behavior and jail” (Gibbons et al, 2021). Racists propose that what causes the gap is a slew of psychological traits, genetic factors, and physiological variables, but even in the 1960s, criminologists and geneticists rejected the genetic hypothesis of crime (Wolfgang,1964). However we do know there is a protective effect when parents prepare their children for bias (Burt, Simons, and Gibbons, 2013). Even the role of institutions exacerbates the issue (Hetey and Eberhardt, 2014). And in my article on the Unnever-Gabbidon theory of African American offending, I wrote about one of the predictions that follows from the theory which was borne out when it was tested.
So it’s quite obvious that the premise “racism causes crime” has empirical support.
So if B and C are true then D follows. The logical connection between B and C leads to the conclusion that “racism is morally wrong”, expressed by (B ^ C) -> D. Now I can express this argument using modus ponens.
(1) If (B ^ C) then D. (Expressed as (B ^ C) -> D).
(2) (B ^ C) is true.
(3) Thus, D is true.
When it comes to the argument as a whole it can be generalized to harm is bad and racism causes harm so racism is bad.
Furthermore, I can generalize the argument further and state that not only that crime is bad, but that racism leads to psychological harm and harm is bad, so racism is morally wrong. We know that racism can lead to “weathering” (Geronimus et al, 2006, 2011; Simons, 2021) and increased allostatic load (Barr 2014: 71-72). So racism leads to a slew of unwanted physiological issues (of which microaggressions are a species of; Williams, 2021).
Racism leads to negative physiological and mental health outcomes (P), and negative physiological and mental health outcomes are undesirable (Q), so racism is morally objectionable (R). So the factual statement (P) establishes a link between negative health outcomes, providing evidence that racism leads to these negative health outcomes. The ethical statement (Q) asserts that negative health outcomes are morally undesirable which aligns with a common ethical principle that causing harm is morally objectionable. Then the logical connection (Q ^ P) combines the factual observation of harm caused by racism with the ethical judgment that harm is morally undesirable. Then the normative conclusion (R) follows, which asserts that racial is morally objectionable since it leads to negative health outcomes. So this argument is (Q ^ P) -> R.
Racism can lead to stereotyping of certain groups as more prone to criminal behavior, and this stereotype can be internalized and perpetuated which would then contribute to biased law enforcement and along with it unjust profiling. It can also lead to systemic inequalities like in education, employment and housing which are then linked to higher crime rates (in this instance, racism and stereotyping causes the black-white crime gap, as predicted by Unnever and Gabbidon, 2011 and then verified by numerous authors). Further, as I’ve shown, racism can negatively affect mental health leading to stress, anxiety and trauma and people facing these challenges would be more vulnerable to engage in criminal acts.
Stereotypes and self-fulfilling prophecies
In his book Concepts and Theories of Human Development, Lerner (2018: 298) discusses how stereotyping and self-fulfilling prophecies would arise from said stereotyping. He says that people, based on their skin color, are placed into an unfavorable category. Then negative behaviors were attributed to the group. Then these behaviors were associated with different experience in comparison to other skin color groups. These different behaviors then delimit the range of possible behaviors that could develop. So the group was forced into a limited number of possible behaviors, the same behaviors they were stereotyped to have. So the group finally develops the behavior due to being “channeled” (to use Lerner’s word) which is then “the end result of the physically cued social stereotype was a self-fulfilling prophecy” (Lerner, 2018: 298).
From the analysis of the example I provided and, as well, from empirical literature in support of it (e.g., Spencer, 2006; Spencer et al., 2015), a strong argument can be made that the people of color in the United States have perhaps experienced the most unfortunate effects of this most indirect type of hereditary contribution to behavior–social stereotypes. Thus, it may be that African Americans for many years have been involved in an educational and intellectual self-fulfilling prophecy in the United States. (Lerner, 2018: 299)
This is an argument about how social stereotypes can spur behavioral development, and it has empirical support. Lerner’s claim that perception influences behavior is backed by Spencer, Swanson and Harpalani’s (2015) article on the development of the self and Spencer, Dupree, and Hartman’s (1997) phenomenological variant of ecological systems theory (PVEST). (Also see Cunningham et al, 2023). Spencer, Swanson and Harpalani (2015: 764) write:
Whether it is with images of the super-athlete, criminal, gangster, or hypersexed male, it seems that most of society’s views of African Americans are defined by these stereotypes. The Black male has, in one way or another, captured the imagination of the media to such a wide extent that media representations create his image far more than reality does. Most of the images of the Black male denote physical prowess or aggression and downplay other characteristics. For example, stereotypes of Black athletic prowess can be used to promote the notion that Blacks are unintelligent (Harpalani, 2005). These societal stereotypes, in conjunction with numerous social, political, and economic forces, interact to place African American males at extreme risk for adverse outcomes and behaviors.
A -> B—So stereotypes can lead to self-fulfilling prophecies (if there are stereotypes, then they can result in self-fulfilling prophecies). B -> C—Self-fulfilling prophecies can increase the chance of crime for blacks (if there are self-fulfilling prophecies, then they can increase the chance of crime for blacks. So A -> C—Stereotypes can increase the chance of crime for blacks (if there are stereotypes, then they can increase the chance of crime for blacks). Going back to the empirical studies on the TAAO, we know that racism and stereotypes cause the black-white crime gap (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019), and so the argument by Spencer et al and Lerner is yet more evidence that racism and stereotypes lead to self-fulfilling prophecies which then cause black crime. Behavior can quite clearly be shaped by stereotypes and self-fulfilling prophecies.
Responses to possible counters
I think there are 3 ways that one could try to refute the argument—(1) Argue that B is false, (2) argue that C is false, or (3) argue that the argument commits the is-ought fallacy.
(1) Counter premise: B’: “Not all crimes are morally bad, some may be morally justifiable or necessary in certain contexts. So if not all crimes are morally bad, then the conclusion that racism is morally wrong based on the premises (B ^ C) isn’t universally valid.”
Premise B reflects a broad ethical judgment which is based on social norms that generally view actions that cause harm morally undesirable. My argument is based on consequences—that racism causes crime. The legal systems of numerous societies categorize certain actions as crimes since they are deemed morally reprehensible and harmful to individuals and communities. Thus, there is a broad moral stance against actions that cause harm which is reflected in the societal normative stance against actions which cause harm.
(2) Counter premise: C’: “Racism does not necessarily cause crime. Since racism does not necessarily cause crime, then the conclusion that racism is objectively wrong isn’t valid.”
Premise C states that racism causes crime. When I say that, it doesn’t mean that every instance of racism leads to an instance of crime. Numerous social factors contribute to criminal actions, but there is a relationship between racial discrimination (racism) and crime:
Experiencing racial discrimination increases the likelihood of black Americans engaging in criminal actions. How does this follow from the theory? TAAO posits that racial discrimination can lead to feelings of frustration and marginalization, and to cope with these stressors, some individuals may resort to commuting criminal acts as a way to exert power or control in response to their experiences of racial discrimination. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019)
(3) “The argument commits the naturalistic fallacy by inferring an “ought” from an “is.” It appears to derive a normative conclusion from factual and ethical statements. So the transition from descriptive premises to moral judgments lacks a clear ethical justification which violates the naturalistic fallacy.” So this possible counter contends that normative statement B and the ethical statement C isn’t enough to justify the normative conclusion D. Therefore it questions whether the argument has good justification for an ethical transition to the conclusion D.”
I can simply show this. Observe X causing Y (C). Y is morally undesirable (B). Y is morally undesirable and X causes Y (B ^ C). So X is morally objectionable (D). So C begins with an empirical finding. B then is the ethical premise. The logical connection is then established with B ^ C (which can be reduced to “Harm is morally objectionable and racism causes harm”). This then allows me to infer the normative conclusion—D—allowing me to bypass the charge of committing the naturalistic fallacy. Thus, the ethical principle that harm is morally undesirable and that racism causes harm allows me to derive the conclusion that racism is objectively wrong. So factual statements can be combined with ethical statements to derive ethical conclusions, bypassing the naturalistic fallacy.
Conclusion
This discussion centered on my argument (B ^ C) -> D. The argument was:
(P1) Crime is bad (whatever causes harm is bad). (B)
(P2) Racism causes crime. (C)
(C) Racism is morally wrong. (D)
I defended the truth of both premises, and then I answered two possible objections, both rejecting B and C. I then defended my argument against the charge of it committing the naturalistic fallacy by stating that ethical statements can be combined with factual statements to derive normative conclusions. Addressing possible counters (C’ and B’), I argued that there is evidence that racism leads to crime (and other negative health outcomes, generalized as “harm”) in black Americans, and that harm is generally seen as bad, so it then follows that C’ and B’ fail. Spencer’s and Lerner’s arguments, furthermore, show how stereotypes can spur behavioral development, meaning that social stereotypes increase the chance of adverse behavior—meaning crime. It is quite obvious that the TAAO has strong empirical support, and so since crime is bad and racism causes crime then racism is morally wrong. So to decrease the rate of black crime we—as a society—need to change our negative attitudes toward certain groups of people.
Thus, my argument builds a logical connection between harm being bad, racism causing harm and moral undesirability. In addressing potential objections and clarifying the ethical framework I ren, So the general argument is: Harm is bad, racism causes harm, so racism is morally wrong.
The Theory of African American Offending versus Hereditarian Explanations of Crime: Exploring the Roots of the Black-White Crime Disparity
3450 words
Why do blacks commit more crime? Biological theories (racial differences in testosterone and testosterone-aggression, AR gene, MAOA) are bunk. So how can we explain it? The Unnever-Gabbidon theory of African American offending (TAAO) (Unnever and Gabbidon, 2011)—where blacks’ experience of racial discrimination and stereotypes increases criminal offenses—has substantial empirical support. To understand black crime, we need to understand the unique black American experience. The theory not only explains African American criminal offending, it also makes predictions which were borne out in independent, empirical research. I will compare the TAAO with hereditarian claims of why blacks commit more crime (higher testosterone and higher aggression due to testosterone, the AR gene and MAOA). I will show that hereditarian theories make no novel predictions and that the TAAO does make novel predictions. Then I will discuss recent research which shows that the predictions that Unnever and Gabbidon have made were verified. Then I will discuss research which has borne out the predictions made by Unnever and Gabbidon’s TAAO. I will conclude by offering suggestions on how to combat black crime.
The folly of hereditarianism in explaining black American offending
Hereditarians have three main explanations of black crime: (1) higher levels of testosterone and high levels of testosterone leading to aggressive behavior which leads to crime; (2) low activity MAOA—also known in the popular press as “the warrior gene”—could be more prevalent in some populations which would then lead to more aggressive, impulsive behavior; and (3) the AR gene and AR-CAG repeats with lower CAG repeats being associated with higher rates of criminal activity.
When it comes to (1), the evidence is mixed on which race has higher levels of testosterone (due to low-quality studies that hereditarians cite for their claim). In fact, two recent studies showed that non-Hispanic blacks didn’t have higher levels of testosterone than other races (Rohrmann et al, 2007; Lopez et al, 2013). Contrast this with the classical hereditarian response that blacks indeed do have higher rates of testosterone than whites (Rushton, 1995)—using Ross et al (1986) to make the claim. (See here for my response on why Ross et al is not evidence for the hereditarian position.) Although Nyante et al (2012) showed a small increase in testosterone in blacks compared to whites and Mexican Americans using longitudinal data, the body of evidence shows that there is no to small differences in testosterone between blacks and whites (Richard et al, 2014). So despite claims that “African-American men have repeatedly demonstrated serum total and free testosterone levels that are significantly higher than all other ethnic groups” (Alvarado, 2013: 125), claims like this are derived from flawed studies, and newer more representative analyses show that there is a small difference in testosterone between blacks and whites to no difference.
Nevertheless, even if blacks have higher levels of testosterone than other races, then this would still not explain racial differences in crime, since heightened aggression explains T increases, high T doesn’t explain heightened aggression. HBDers seem to have cause and effect backwards for this relationship. Injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). If the hereditarian hypothesis on the relationship between testosterone and aggression were true, then we would see the opposite finding from what Tricker et al and O’Connor et al found. Thus this discussion shows that hereditarians are wrong about racial differences in testosterone and that they are wrong about causality when it comes to the T-aggression relationship. (The actual relationship is aggression causing increases in testosterone.) So this argument shows that the hereditarian simplification on the T-aggression relationship is false. (But see Pope, Kouri and Hudson, 2000 where they show that a 600 mg dose of testosterone caused increased manic symptoms in some men, although in most men there was little to no change; there were 8 “responders” and 42 “non-responders.”)
When it comes to (2), MAOA is said to explain why those who carry low frequency version of the gene have higher rates of aggression and violent behavior (Sohrabi, 2015; McSwiggin, 2017). Sohrabi shows that while the low frequency version of MAOA is related to higher rates of aggression and violent behavior, it is mediated by environmental effects. But MAOA, to quote Heine (2017), can be seen as the “Everything but the kitchen sink gene“, since MAOA is correlated with so many different things. But at the and of the day, we can’t blame “warrior genes” for violent, criminal behavior. Thus, the relationship isn’t so simple, so this doesn’t work for hereditarians either.
Lastly when it comes to (3), due to the failure of (1), hereditarians tried looking to the AR gene. Researchers tried to relate CAG repeat length with criminal behaviors. For instance, Geniole et al (2019) tried to argue that “Testosterone thus appears to promote human aggression through an AR-related mechanism.” Ah, the last gasps to explain crime through testosterone. But there is no relationship between CAG repeats, adolescent risk-taking, depression, dominance or self-esteem (Vermeer, 2010) and the number of CAG repeats in men and women (Valenzuela et al, 2022). So this, too, fails. (Also take look at the just-so story on why African slave descendants are more sensitive to androgens; Aiken, 2011.)
Now that I have shown that the three main hereditarian explanations for higher black crime are false, now I will show why blacks have higher rates of criminal offending than other races, and the answer isn’t to be found in biology, but sociology and criminology.
The Unnever-Gabbidon theory of African American criminal offending and novel predictions
In 2011, criminologists Unnever and Gabbidon published their book A Theory of African American Offending: Race, Racism, and Crime. In the book, they explain why they formulated the theory and why it doesn’t have any explanatory or predictive power for other races. That’s because it centers on the lived experiences of black Americans. In fact, the TAAO “incorporates the finding that African Americans are more likely to offend if they associate with delinquent peers but we argue that their inadequate reinforcement for engaging in conventional behaviors is related to their racial subordination” (Unnever and Gabbidon, 2011: 34). The TAAO focuses on the criminogenic effects of racism.
Our work builds upon the fundamental assumption made by Afrocentists that an understanding of black offending can only be attained if their behavior is situated within the lived experiences of being African American in a conflicted, racially stratified society. We assert that any criminological theory that aims to explain black offending must place the black experience and their unique worldview at the core of its foundation. Our theory places the history and lived experiences of African American people at its center. We also fully embrace the Afrocentric assumption that African American offending is related to racial subordination. Thus, our work does not attempt to create a “general” theory of crime that applies to every American; instead, our theory explains how the unique experiences and worldview of blacks in America are related to their offending. In short, our theory draws on the strengths of both Afrocentricity and the Eurocentric canon. (Unnever and Gabbidon, 2011: 37)
Two kinds of racial injustices highlighted by the theory—racial discrimination and pejorative stereotyping—have empirical support. Blacks are more likely to express anger, exhibit low self-control and become depressed if they believe the racist stereotype that they’re violent. It’s also been studied whether or not a sense of racial injustice is related to offending when controlling for low self control (see below).
The core predictions of the TAAO and how they follow from it with references for empirical tests are as follows:
(Prediction 1) Black Americans with a stronger sense of racial identity are less likely to engage in criminal behavior than black Americans with a weak sense of racial identity. How does this prediction follow from the theory? TAAO suggests that a strong racial identity can act as a protective factor against criminal involvement. Those with a stronger sense of racial identity may be less likely to engage in criminal behavior as a way to cope with racial discrimination and societal marginalization. (Burt, Simons, and Gibbons, 2013; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019)
(Prediction 2) Experiencing racial discrimination increases the likelihood of black Americans engaging in criminal actions. How does this follow from the theory? TAAO posits that racial discrimination can lead to feelings of frustration and marginalization, and to cope with these stressors, some individuals may resort to committing criminal acts as a way to exert power or control in response to their experiences of racial discrimination. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019)
(Prediction 3) Black Americans who feel socially marginalized and disadvantaged are more prone to committing crime as a coping mechanism and have weakened school bonds. How does this follow from the theory? TAAO suggests that those who experience social exclusion and disadvantage may turn to crime as a way to address their negative life circumstances. and feelings of agency. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016)
The data show that there is a racialized worldview shared by blacks, and that a majority of blacks believe that their fate rests on what generally happens to black people in America. Around 38 percent of blacks report being discriminated against and most blacks are aware of the stereotype of them as violent. (Though a new Pew report states that around 8 in 10—about 80 percent—of blacks have experienced racial discrimination.) Racial discrimination and the belief in the racist stereotype that blacks are more violent are significant predictors of black arrests. It’s been shown that the more blacks are discriminated against and the more they believe that blacks are violent, the more likely they are to be arrested. Unnever and Gabbidon also theorized that the aforementioned isn’t just related to criminal offending but also to substance and alcohol abuse. Unnever and Gabbidon also hypothesized that racial injustices are related to crime since they increase the likelihood of experiencing negative emotions like anger and depression (Simons et al, 2002). It’s been experimentally demonstrated that blacks who perceive racial discrimination and who believe the racist stereotype that blacks are more violent express less self-control. The negative emotions from racial discrimination predict the likelihood of committing crime and similar behavior. It’s also been shown that blacks who have less self-control, who are angrier and are depressed have a higher liklihood of offending. Further, while controlling for self-control, anger and depression and other variables, racial discrimination predicts arrests and substance and alcohol abuse. Lastly the experience of being black in a racialized society predicts offending, even after controlling for other measures. Thus, it is ruled out that the reason why blacks are arrested more and perceive more racial injustice is due to low self-control. (See Unnever, 2014 for the citations and arguments for these predictions.) The TAAO also has more empirical support than racialized general strain theory (RGST) (Isom, 2015).
So the predictions of the theory are: Racial discrimination as a contributing factor; a strong racial identity could be a protective factor while a weak racial identity would be associated with a higher likelihood of engaging in criminal activity; blacks who feel socially marginalized would turn to crime as a response to their disadvantaged social position; poverty, education and neighborhood conditions play a significant role in black American offending rates, and that these factors interact with racial identity and discrimination which then influence criminal behavior; and lastly it predicts that the criminal justice system’s response to black American offenders could be influenced by their racial identity and social perceptions which could then potentially lead to disparities in treatment compared to other racial groups.
Ultimately, the unique experiences of black Americans explain why they commit more crime. Thus, given the unique experiences of black Americans, there needs to be a race-centric theory of crime for black Americans, and this is exactly what the TAAO is. The predictions that Unnever and Gabbidon (2011) made from the TAAO have independent empirical support. This is way more than the hereditarian explanations can say on why blacks commit more crime.
One way, which follows from the theory, to insulate black youth from discrimination and prejudice is racial socialization, where racial socialization is “thoughts, ideas, beliefs, and attitudes regarding race and racism are communicated across generations (Burt, Lei, & Simons, 2017; Hughes, Smith, et al., 2006; Lesane-Brown, 2006) (Said and Feldmeyer, 2022).
But also related to the racial socialization hypothesis is the question “Why don’t more blacks offend?” Gaston and Doherty (2018) set out to answer this question. Gaston and Doherty (2018) found that positive racial socialization buffered the effects of weak school bonds on adolescent substance abuse and criminal offending for males but not females. This is yet again another prediction from the theory that has come to pass—the fact that weak school bonds increase criminal offending.
Doherty and Gaston (2018) argue that black Americans face racial discrimination that whites in general just do not face:
Empirical studies have pointed to potential explanations of racial disparities in violent crimes, often citing that such disparities reflect Black Americans’ disproportionate exposure to criminogenic risk factors. For example, Black Americans uniquely experience racial discrimination—a robust correlate of offending—that White Americans generally do not experience (Burt, Simons, & Gibbons, 2012; Caldwell, Kohn-Wood, Schmeelk-Cone, Chavous, & Zimmerman, 2004; Simons, Chen, Stewart, & Brody, 2003; Unnever, Cullen, Mathers, McClure, & Allison, 2009). Furthermore, Black Americans are more likely to face factors conducive to crime such as experiencing poor economic conditions and living in neighborhoods characterized by concentrated disadvantage.
They conclude that:
The support we found for ethnic-racial socialization as a crime-reducing factor has important implications for broader criminological theorizing and practice. Our findings show the value of race-specific theories that are grounded in the unique experiences of that group and focus on their unique risk and protective factors. African Americans have unique pathways to offending with racial discrimination being a salient source of offending. While it is beyond the scope of this study to determine whether TAAO predicts African American offending better than general theories of crime, the general support for the ethnic-racial socialization hypothesis suggests the value of theories that account for race-specific correlates of Black offending and resilience.
…
TAAO draws from the developmental psychology literature and contends, however, that positive ethnic-racial socialization offers resilience to the criminogenic effect of weak school bonds and is the main reason more Black Americans do not offend (Unnever & Gabbidon, 2011, p. 113, 145).
Thus, combined with the fact that blacks face racial discrimination that whites in general just do not face, and combined with the fact that racial discrimination has been shown to increase criminal offending, it follows that racial discrimination can lead to criminal offending, and therefore, to decrease criminal offending we need to decrease racial discrimination. Since racism is due to low education and borne of ignorance, then it follows that education can decrease racial attitudes and, along with it, decrease crime (Hughes et al, 2007; Kuppens et al, 2014; Donovan, 2019, 2022).
Even partial tests of the TAAO have shown that racial discrimination related to offending and I would say that it is pretty well established that positive ethnic-racial socialization acts as a protective factor for blacks—this also explains why more blacks don’t offend (see Gaston and Doherty, 2018). It is also know that bad (ineffective) parenting also increases the risk for lower self-control (Unnever, Cullen, and Agnew, 2006). Black Americans share a racialized worldview and they view the US as racist, due to their personal lived experiences with racism (Unnever, 2014).
The TAAO and situationism
Looking at what the TAAO is and the predictions it makes, we can see how the TAAO is a situationist theory. Situationism is a psychological-philosophical theory which emphasizes the influence of the situation and its effects on human behavior. It posits that people’s actions and decisions are primarily shaped by the situational context that they find themselves in. It highlights the role of the situation in explaining behavior, suggests that people may act differently based on the context they find themselves in, situational cues which are present in the immediate context of the environment can trigger specific behavioral responses, suggests that understanding the situation one finds themselves in is important in explaining why people act the way they do, and asserts that behavior is more context-dependent and unpredictable and could vary across different situations. Although it seems that situationism conflicts with action theory, it doesn’t. Action theory explains how people form intentions and make decisions within specific situations, basically addressing the how and why. Conversely, situationism actually compliments action theory, since it addresses the where and when of behavior from an external, environmental perspective.
So the TAAO suggests that experiencing racial discrimination can contribute to criminal involvement as a response to social marginalization. So situationism can provide a framework for exploring how specific instances of environmental stressors, discrimination, or situational factors can trigger criminal behavior in context. So while TAAO focuses on historical and structural factors which lead to why blacks commit more crime, adding in situationism could show how the situational context interacts with historical and structural factors to explain black American criminal behavior.
Thus, combining situationism and the TAAO can lead to novel predictions like: predictions of how black Americans when faced with specific discriminatory situations, may be more or less likely to engage in criminal behavior based on their perception of the situation; predictions about the influence of immediate peer dynamics in moderating the relationship between structural factors like discrimination and criminal behavior in the black American community; and predictions about how variations in criminal responses to different types of situational cues—like encounters with law enforcement, experiences of discrimination, and economic stress—within the broader context of the TAAO’s historical-structural framework.
Why we should accept the TAAO over hereditarian explanations of crime
Overall, I’ve explained why hereditarian explanations of crime fail. They fail because when looking at the recent literature, the claims they make just do not hold up. Most importantly, as I’ve shown, hereditarian explanations lack empirical support, and the logic they try to use in defense of them is flawed.
We should accept the TAAO over hereditarianism because there is empirical validity, in that the TAAO is grounded in empirical research and it’s predictions and hypotheses have been subject to empirical tests and they have been found to hold. The TAAO also recognizes that crime is a complex phenomena influenced by factors like historical and contemporary discrimination, socioeconomic conditions, and the overall situational context. It also addresses the broader societal issues related to disparities in crime, which makes it more relevant for policy development and social interventions, acknowledging that to address these disparities, we must address the contemporary and historical factors which lead to crime. The TAAO also doesn’t stigmatize and stereotype, while it does emphasize the situational and contextual factors which lead to criminal activity. On the other hand, hereditarian theories can lead to stereotypes and discrimination, and since hereditarian explanations are false, we should also reject them (as I’ve explained above). Lastly, the TAAO also has the power to generate specific, testable predictions which have clear empirical support. Thus, to claim that hereditarian explanations are true while disregarding the empirical power of the TAAO is irrational, since hereditarian explanations don’t generate novel predictions while the TAAO does.
Conclusion
I have contrasted the TAAO with hereditarian explanations of crime. I showed that the three main hereditarian explanations—racial differences in testosterone and testosterone caused aggression, the AR gene, and MAOA—all fail. I have also shown that the TAAO is grounded in empirical research, and that it generates specific, testable predictions on how we can address racial differences in crime. On fhe other hand, hereditarian explanations lack empirical support, specificity, and causality, which makes it ill-suited for generating testable predictions and informing effective policies. The TAAO’s complexity, empirical support, and potential for addressing real-world issues makes it a more comprehensive framework for understanding and attempting to ameliorate racial crime disparities, in contrast to the genetic determinism from hereditarianism. In fact, I was unable to find any hereditarian response to the TAAO, so that should be telling on its own.
Overall, I have shown that the TAAO’s predictions that Unnever and Gabbidon have generated enjoy empirical support, and I have shown that hereditarian explanations fail, so we should reject hereditarian explanations and accept the TAAO, due to the considerations above. I have also shown that the TAAO makes actionable policy recommendations, and therefore, to decrease criminal offending, we thusly need to educate more, since racism is borne of ignorance and education can decrease racial bias.
Nutrition and Antisocial Behavior
2150 words
What is the relationship between nutrition and antisocial behavior? Does not consuming adequate amounts of vitamins and minerals lead to an increased risk for antisocial behavior? If it does, then lower class people will have commit crimes at a higher rate, and part of the problem may indeed be dietary. Though, what kind of data is there that lends credence to the idea? It is well-known that malnutrition leads to antisocial behavior, but what kind of effect does it have on the populace as a whole?
About 85 percent of Americans lack essential vitamins and minerals. Though, when most people think of the word ‘malnutrition’ and the imagery it brings along with it, they assume that someone in a third-world country is being talked about, say a rail-thin kid somewhere in Africa who is extremely malnourished due to lack of kcal and vitamins and minerals. However, just because one lives in a first-world country and has access to kcal to where they’re “not hungry” doesn’t mean that vitamin and mineral deficiencies do not exist in these countries. This is known as “hidden hunger” when people can get enough kcal for their daily energy needs but what they are eating is lower-quality food, and thus, they become vitamin and nutrient deficient. What kind of effects does this have?
Infants are most at risk, more than half of American babies are at-risk for malnutrition; malnutrition in the postnatal years can lead to antisocial behavior and a lower ‘IQ’ (Galler and Ramsey, 1989; Liu et al, 2003; Galler et al, 2011, 2012a, 2012b; Gesch, 2013; Kuratko et al, 2013; Raine et al, 2015; Thompson et al, 2017). Clearly, not getting pertinent vitamins and minerals at critical times of development for infants leads to antisocial behavior in the future. These cases, though, can be prevented with a good diet. But the preventative measures that can prevent some of this behavior has been demonized for the past 50 or so years.
Poor nutrition leads to the development of childhood behavior problems. As seen in rat studies, for example, lack of dietary protein leads to aggressive behavior while rats who are protein-deficient in the womb show altered locomotor activity. The same is also seen with vitamins and minerals; monkeys and rats who were fed a diet low in tryptophan were reported to be more aggressive whereas those that were fed high amounts of tryptophan were calmer. Since tryptophan is one of the building blocks of serotonin and serotonin regulates mood, we can logically state that diets low in tryptophan may lead to higher levels of aggressive behavior. The role of omega 3 fatty acids are mixed, with omega 3 supplementation showing a difference for girls, but not boys (see Itomura et al, 2005). So, animal and human correlational studies and human intervention studies lend credence to the hypothesis that malnutrition in the womb and after birth leads to antisocial behavior (Liu and Raine, 2004).
We also have data from one randomized, placebo-controlled trial showing the effect of diet and nutrition on antisocial behavior (Gesch et al, 2002). They state that since there is evidence that offenders’ diets are lacking in pertinent vitamins and minerals, they should test whether or not the introduction of physiologically adequate vitamins, minerals and essential fatty acids (EFAs) would have an effect on the behavior of the inmates. They undertook an experimental, double-blind, placebo-controlled randomized trial on 231 adult prisoners and then compared their write-ups before and after nutritional intervention. The vitamin/mineral supplement contained 44 mg of DHA (omega 3 fatty acid docosahexaenoic acid; plays a key role in enhancing brain structure and function, stimulating neurite outgrowth), 80 mg of EPA (eicosapentaenoic acid; n3), and 1.26 g of ALA (alpha-linolenic acid), 1260mg of LA (linolic acid), and 160mg of GLA (gamma-Linolenic acid, n6) and a vegetable oil placebo. (Also see Hibbeln and Gow, 2015 for more information on n3 and nutrient deficits in childhood behavior disorders and neurodevelopment.)
Raine (2014: 218-219) writes:
We can also link micronutrients to specific brain structures involved in violence. The amygdala and hippocampus, which are impaired in offenders, are packed with zinc-containing neurons. Zinc deficiency in humans during pregnancy can in turn impair DNA, RNA, and protein synthesis during brain development—the building blocks of brain chemistry—and may result in very early brain abnormalities. Zinc also plays a role in building up fatty acids, which, as we have seen, are crucial for brain structure and function.
Gesch et al (2002) found pretty interesting results: those who were given the capsules with vitamins, minerals, and EFAs had 26.3 percent fewer offenses than those who got the placebo. Further, when compared with the baseline, when taking the supplement for two weeks, there was an average 35.1 percent reduction in offenses compared to the placebo group who showed little change. Gesch et al (2002) conclude:
Antisocial behaviour in prisons, including violence, are reduced by prisons, are reduced by vitamins, minerals and essential fatty acids with similar implications for those eating poor diets in the community.
Of course one could argue that these results would not transfer over to the general population, but to a critique like this, the observed effect of behavior is physiological; so by supplementing the prisoners’ diets giving them pertinent vitamins, minerals and EFAs, violence and antisocial behavior decreased, which shows some level of causation between nutrition/nutrient/fatty acid deprivation and antisocial behavior and violent activity.
Gesch et al (2002) found that some prisoners did not know how to construct a healthy diet nor did they know what vitamins were. So, naturally, since some prisoners didn’t know how to construct diets with an adequate amount of EFAs, vitamins and minerals, they were malnourished, though they consumed an adequate amount of calories. The intervention showed that EFA, vitamin and mineral deficiency has a causal effect on decreasing antisocial and violent behavior in those deficient. So giving them physiological doses lowered antisocial behavior, and since it was an RCT, social and ethnic factors on behavior were avoided.
Of course (and this shouldn’t need to be said), I am not making the claim that differences in nutrition explain all variance in antisocial and violent behavior. The fact of the matter is, this is causal evidence that lack of vitamin, mineral and EFA consumption has some causal effect on antisocial behavior and violent tendencies.
Schoenthaler et al (1996) also showed how correcting low values of vitamins and minerals in those deficient led to a reduction in violence among juvenile delinquents. Though it has a small n, the results are promising. (Also see Zaalberg et al, 2010.) These simple studies show how easy it is to lower antisocial and violent behavior: those deficient in nutrients just need to take some vitamins and eat higher-quality food and there should be a reduction in antisocial and violent behavior.
Liu, Zhao, and Reyes (2015) propose “a conceptual framework whereby epigenetic modifications (e.g., DNA methylation) mediate the link between micro- and macro-nutrient deficiency early in life and brain dysfunction (e.g., structural aberration, neurotransmitter perturbation), which has been linked to development of behavior problems later on in life.” Their model is as follows: macro- and micro-nutrient deficiencies are risk-factors for psychopathologies since they can lead to changes in the epigenetic regulation of the genome (along with other environmental variables such as lead consumption, which causes abnormal behavior and also epigenetic changes which can be passed through the generations; Senut et al, 2012; Sen et al, 2015) which then leads to impaired brain development, which then leads to externalizing behavior, internalizing behavior and autism and schizophrenia (two disorders which are also affected by the microbiome; Strati et al, 2017; Dickerson, 2017).
Clearly, since the food we eat gives us access to certain fatty acids that cannot be produced de novo in the brain or body, good nutrition is needed for a developing brain and if certain pertinent vitamins, minerals or fatty acids are missing, negative outcomes could occur for said individual in the future due to lack of brain development from being nutrient, vitamin, and mineral deficient in childhood. Further, interactions between nutrient deficiencies and exposure to toxic chemicals may be a cause of a large amount of antisocial behavior (Walsh et al, 1997; Hubbs-Tait et al, 2005; Firth et al, 2017).
Looking for a cause for this interaction between metal consumption and nutrient deficiencies, Liu, Zhao, and Reyes (2015) state that since protein and fatty acids are essential to brain growth, lack of consumption of pertinent micro- and macro-nutrients along with consumption of high amounts of protein both in and out of the womb contribute to lack of brain growth and, at adulthood, explains part of the difference in antisocial behavior. What you can further see from the above studies is that metals consumed by an individual can interact with the nutrient deficiencies in said individual and cause more deleterious outcomes, since, for example, lead is a nutrient antagonist—that is, it inhibits the physiologic actions of whatever bioavailable nutrients are available to the body for us.
Good nutrition is, of course, imperative since it gives our bodies what it needs to grow and develop as we grow in the womb, as adolescents and even into old age. So, therefore, developing people who are nutrient deficient will have worse behavioral outcomes. Further, lower class people are more likely to be nutrient deficient and consume lower quality diets than higher, more affluent classes, though it’s hard to discover which way the causation goes (Darmon and Drewnowski, 2008). Of course, the logical conclusion is that being deficient in vitamins, minerals and EFAs causes changes to the epigenome and retards brain development, therefore this has a partly causal effect on future antisocial, violent and criminal behavior. So, some of the crime difference between classes can be attributed to differences in nutrition/toxic metal exposure that induces epigenetic changes that change the structure of the brain and doesn’t allow full brain development due to lack of vitamins, minerals, and EFAs.
There seems to be a causal effect on criminal, violent and antisocial behavior regarding nutrient deficiencies in both juveniles and adults (which starts in the womb and continues into adolescence and adulthood). However, it has been shown in a few randomized controlled trials that nutritional interventions decrease some antisocial behavior, with the effect being strongest for those individuals who showed worse nutrient deficiencies.
If the relationship between nutrition/interaction between nutrient deficiencies and toxins can be replicated successfully then this leads us to one major question: Are we, as a society, in part, causing some of the differences in crime due to how our society is regarding nutrition and the types of food that are advertised to our youth? Are people’s diets which lead to nutrient deficiencies a driving factor in causing crime? The evidence so far on nutrition and its effects on the epigenome and its effects on the growth of the brain in the womb and adolescence requires us to take a serious look at this relationship. That lower class people are exposed to more neurotoxins such as lead (Bellinger, 2008) and are more likely to be nutrient deficient (Darmon and Drewnowski, 2008; Hackman, Farrah, and Meaney, 2011) then if they were educated on which foods to eat to avoid nutrient deficiencies along with avoiding neurotoxins such as lead (which exacerbate nutrient deficiencies and cause crime), then a reduction in crime should occur.
Nutrition is important for all living beings; and as can be seen, those who are deficient in certain nutrients and have less access to good, whole, nutritious food (who also have an increased risk for exposure to neurotoxins) can lead to negative outcomes. These things can be prevented, it seems, with a few vitamins/minerals/EFA consumption. The effects of sleep, poor diet (which also lead to metabolic syndromes) can also exacerbate this relationship, between individuals and ethnicities. The relationship between violence and antisocial behavior and nutrient deficiencies/the interaction with nutrient deficiencies and neurotoxins is a great avenue for future research to reduce violent crime in our society. Lower class people, of course, should be the targets of such interventions since there seems to be a causal effect—-however small or large—on behavior, both violent and nonviolent—and so nutrition interventions should close some of the crime gaps between classes.
Conclusion
The logic is very simple: nutrition affects mood (Rao et al, 2008; Jacka, 2017) which is, in part, driven by the microbiome’s intimate relationship with the brain (Clapp et al, 2017; Singh et al, 2017); nutrition also affects the epigenome and the growth and structure of the brain if vitamin and mineral needs are not met by the growing body. This then leads to differences in gene expression due to the foods consumed, the microbiome (which also influences the epigenome) further leads to differences in gene expression and behavior since the two are intimately linked as well. Thus, the aetiology of certain behaviors may come down to nutrient deficiencies and complex interactions between the environment, neurotoxins, nutrient deficiencies and genetic factors. Clearly, we can prevent this with preventative nutritional education, and since lower class people are more likely to suffer the most from these problems, the measures targeted to them, if followed through, will lower incidences of crime and antisocial/violent behavior.
Does Playing Violent Video Games Lead to Violent Behavior?
1400 words
President Trump was quoted the other day saying “We have to look at the Internet because a lot of bad things are happening to young kids and young minds and their minds are being formed,” Trump said, according to a pool report, “and we have to do something about maybe what they’re seeing and how they’re seeing it. And also video games. I’m hearing more and more people say the level of violence on video games is really shaping young people’s thoughts.” But outside of broad assertions like this—that playing violent video games cause violent behavior—does it stack up to what the scientific literature says about it? In short, no, it does not. (A lot of publication bias exists in this debate, too.) Why do people think that violent video games cause violent behavior? Mostly due to the APA and their broad claims with little evidence.
Just doing a cursory Google search of ‘violence in video games pubmed‘ brings up 9 journal articles, so let’s take a look at a few of those.
The first article is titled The Effect of Online Violent Video Games on Levels of Aggression by Hollingdale and Greitemeyer (2014). They took 101 participants and randomized them to one of four experimental conditions: neutral, offline; neutral online; (Little Big Planet 2) violent offline; and violent online video games (Call of Duty: Modern Warfare). After they played said games, they answered a questionnaire and then measured aggression using the hot sauce paradigm (Lieberman et al, 1999) to measure aggressive behavior. Hollingdale and Greitemeyer (2014) conclude that “this study has identified that increases in aggression are not more pronounced when playing a violent video game online in comparison to playing a neutral video game online.”
Staude-Muller (2011) finds that “it was not the consumption of violent video games but rather an uncontrolled pattern of video game use that was associated with increasing aggressive tendencies.” Przybylski, Ryan, and Rigby (2009) found that enjoyment, value, and desire to play in the future were strongly related to competence in the game. Players who were high in trait aggression, though, were more likely to prefer violent games, even though it didn’t add to their enjoyment of the game, while violent content lent little overall variance to the satisfactions previously cited.
Tear and Nielsen (2013) failed to find evidence that violent video game playing leads to a decrease in pro-social behavior (Szycik et al, 2017 also show that video games do not affect empathy). Gentile et al (2014) show that “habitual violent VGP increases long-term AB [aggressive behavior] by producing general changes in ACs [aggressive cognitions], and this occurs regardless of sex, age, initial aggressiveness, and parental involvement. These robust effects support the long-term predictions of social-cognitive theories of aggression and confirm that these effects generalize across culture.” The APA (2015) even states that “scientific research has demonstrated an association between violent video game use and both increases in aggressive behavior, aggressive affect, aggressive cognitions and decreases in prosocial behavior, empathy, and moral engagement.” How true is all of this, though? Does playing violent video games truly increase aggression/aggressive behavior? Does it have an effect on violence in America and shootings overall?
No.
Whitney (2015) states that the video-games-cause-violence paradigm has “weak support” (pg 11) and that, pretty much, we should be cautious before taking this “weak support” as conclusive. He concludes that there is not enough evidence to establish a truly causal connection between violent video game playing and violent and aggressive behavior. Cunningham, Engelstatter, and Ward (2016) tracked the sale of violent video games and criminal offenses after those games were sold. They found that violent crime actually decreased the weeks following the release of a violent game. Of course, this does not rule out any longer-term effects of violent game-playing, but in the short term, this is good evidence against the case of violent games causing violence. (Also see the PsychologyToday article on the matter.)
We seem to have a few problems here, though. How are we to untangle the effects of movies and other forms of violent media that children consume? You can’t. So the researcher(s) must assume that video games and only video games cause this type of aggression. I don’t even see how one can logically state that out of all other types of media that violent video games—and not violent movies, cartoons, TV shows etc—cause aggression/violent behavior.
Back in 2011, the Supreme Court case Brown vs. Entertainment Merchants Association concluding that since the effects on violent/aggressive behavior were so small and couldn’t be untangled from other so-called effects from other violent types of media. Ferguson (2015) found that violent video game playing had little effect on children’s mood, aggression levels, pro-social behavior or grades. He also found publication bias in this literature (Ferguson, 2017). Contrary to what those say about video games causing violence/aggressive behavior, video game playing was associated with a decrease in youth crime (Ferguson, 2014; Markey, Markey, and French, 2015 which is in line with Cunningham, Engelstatter, and Ward, 2016). You can read more about this in Ferguson’s article for The Conversation, along with his and others’ responses to the APA who state that violent video games cause violent behavior (with them stating that the APA is biased). (Also read a letter from 230 researchers on the bias in the APA’s Task Force on Violent Media.)
How would one actually untangle the effects of, say, violent video game playing and the effects of such other ‘problematic’ forms of media that also show aggression/aggressive acts towards others and actually pinpoint that violent video games are the culprit? That’s right, they can’t. How would you realistically control for the fact that the child grows up around—and consumes—so much ‘violent’ media, seeing others become violent around him etc; how can you logically state that the video games are the cause? Some may think it logical that someone who plays a game like, say, Call of Duty for hours on end a day would be more likely to be more violent/aggressive or more likely to commit such atrocities like school shootings. But none of these studies have ever come to the conclusion that violent video games may/will cause someone to kill or go on a shooting spree. It just doesn’t make sense. I can, of course, see the logic in believing that it would lead to aggressive behavior/lack of pro-social behavior (let’s say the kid played a lot of games and had little outside contact with people his age), but of course the literature on this subject should be enough to put claims like this to bed.
It’s just about impossible to untangle the so-called small effects of video games on violent/aggressive behavior from other types of media such as violent cartoons and violent movies. Who’s to say it’s not just the violent video games and not the violent movies and violent cartoons, too, that ’cause’ this type of behavior? It’s logically impossible to distinguish this, so therefore the small relationship between video games and violent behavior should be safely ignored. The media seems to be getting this right, which is a surprise (though I bet if Trump said the opposite—that violent video games didn’t cause violent behavior/shootings—that these same people would be saying that they do), but a broken clock is right twice a day.
So Trump’s claim (even if he didn’t outright state it) is wrong, along with anyone else who would want to jump in and attempt to say that video games cause violence. In fact, the literature shows a decrease in violence after games are released (Ferguson, 2014; Markey, Markey, and French, 2015; Cunningham, Engelstatter, and Ward, 2016). The amount of publication bias (also see Copenhaver and Ferguson, 2015 where they show how the APA ignores bias and methodological problems regarding these studies) in this field (Ferguson, 2017) should lead one to question the body of data we currently have, since studies that find an effect are more likely to get published than studies that find no effect.
Video games do not cause violent/aggressive behavior/school shootings. There is literally no evidence that they are linked to the deaths of individuals, and with the small effects noted on violent/aggressive behavior due to violent video game playing, we can disregard those claims. (One thing video games are good for, though, is improving reaction time (Benoit et al, 2017). The literature is strong here; playing these so-called “violent video games” such as Call of Duty improved children’s reaction time, so wouldn’t you say that these ‘violent video games’ have some utility?)
Lead, Race, and Crime
2500 words
Lead has many known neurological effects on the brain (regarding the development of the brain and nervous system) that lead to many deleterious health outcomes and negative outcomes in general. Including (but not limited to) lower IQ, higher rates of crime, higher blood pressure and higher rates of kidney damage, which have permanent, persistent effects (Stewart et al, 2007). Chronic lead exposure, too, can “also lead to decreased fertility, cataracts, nerve disorders, muscle and joint pain, and memory or concentration problems” (Sanders et al, 2009). Lead exposure in vitro, in infancy, and in childhood can also lead to “neuronal death” (Lidsky and Schneider, 2003). While epigenetic inheritance also plays a part (Sen et al, 2015). How do blacks and whites differ in exposure to lead? How much is the difference between the two races in America, and how much would it contribute to crime? On the other hand, China has high rates of lead exposure, but lower rates of crime, so how does this relationship play out with the lead-crime relationship overall? Are the Chinese an outlier or is there something else going on?
The effects of lead on the brain are well known, and numerous amounts of effort have been put into lowering levels of lead in America (Gould, 2009). Higher exposure to lead is also found in poorer, lower class communities (Hood, 2005). So since higher levels of lead exposure are found more often in lower-class communities, then blacks should have higher blood-lead levels than whites. This is what we find.
Blacks had a 27 percent higher concentration of lead in their tibia, while having significantly higher levels of blood lead, “likely because of sustained higher ongoing lead exposure over the decades” (Theppeang et al, 2008). Other data—coming out of Detroit—shows the same relationships (Haar et al, 1979; Talbot, Murphy, and Kuller, 1982; Lead poisoning in children under 6 jumped 28% in Detroit in 2016; also see Maqsood, Stanbury, and Miller, 2017) while lead levels in the water contribute to high levels of blood-lead in Flint, Michigan (Hanna-Attisha et al, 2016; Laidlaw et al, 2016). Cassidy-Bushrow et al (2017) also show that “The disproportionate burden of lead exposure is vertically transmitted (i.e., mother-to-child) to African-American children before they are born and persists into early childhood.”
Children exposed to lead have lower brain volumes as children, specifically in the ventrolateral prefrontal cortex, which is the same region of the brain that is impaired in antisocial and psychotic persons (Cecil et al, 2008). The community that was tested was well within the ‘safe’ range set by the CDC (Raine, 2014: 224), though the CDC says that there is no safe level of lead exposure. There is a large body of studies which show that there is no safe level of lead exposure (Needleman and Landrigan, 2004; Canfield, Jusko, and Kordas, 2005; Barret, 2008; Rossi, 2008; Abelsohn and Sanborn, 2010; Betts, 2012; Flora, Gupta, and Tiwari, 2012; Gidlow, 2015; Lanphear, 2015; Wani, Ara, and Usmani, 2015; Council on Environmental Health, 2016; Hanna-Attisha et al, 2016; Vorvolakos, Aresniou, and Samakouri, 2016; Lanphear, 2017). So the data is clear that there is absolutely no safe level of lead exposure, and even small effects can lead to deleterious outcomes.
Further, one brain study of 532 men who worked in a lead plant showed that those who had higher levels of lead in their bones had smaller brains, even after controlling for confounds like age and education (Stewart et al, 2008). Raine (2014: 224) writes:
The fact that the frontal cortex was particularly reduced is very interesting, given that this brain region is involved in violence. This lead effect was equivalent to five years of premature aging of the brain.
So we have good data that the parts of the brain that relate to violent tendencies are reduced in people exposed to more lead had the same smaller parts of the brain, indicating a relationship. But what about antisocial disorders? Are people with higher levels of lead in their blood more likely to be antisocial?
Needleman et al (1996) show that boys who had higher levels of lead in their blood had higher teacher ratings of aggressive and delinquent behavior, along with higher self-reported ratings of aggressive behavior. Even high blood-lead levels later in life is related to crime. One study in Yugoslavia showed that blood lead levels at age three had a stronger relationship with destructive behavior than did prenatal blood lead levels (Wasserman et al, 2008); with this same relationship being seen in America with high blood lead levels correlating with antisocial and aggressive behavior at age 7 and not age 2 (Chen et al 2007).
Nevin (2007) showed a strong relationship between preschool lead exposure and subsequent increases in criminal cases in America, Canada, Britain, France, Australia, Finland, West Germany, and New Zealand. Reyes (2007) also shows that crime increased quicker in states that saw a subsequent large decrease in lead levels, while variations in lead levels within cities correlating with variations in crime rates (Mielke and Zahran, 2012). Nevin (2000) showed a strong relationship between environmental lead levels from 1941 to 1986 and corresponding changes to violent crime twenty-three years later in the United States. Raine (2014: 226) writes (emphasis mine):
So, young children who are most vulnerable to lead absorption go on twenty-three years later to perpetrate adult violence. As lead levels rose throughout the 1950s, 1960s, and 1970s, so too did violence correspondingly rise in the 1970s, 1980s and 1990s. When lead levels fell in the late 1970s and early 1980s, so too did violence fall in the 1990s and the first decade of the twenty-first century. Changes in lead levels explained a full 91 percent of the variance in violent offending—an extremely strong relationship.
[…]
From international to national to state to city levels, the lead levels and violence curves match up almost exactly.
But does lead have a causal effect on crime? Due to the deleterious effects it has on the developing brain and nervous system, we should expect to find a relationship, and this relationship should become stronger with higher doses of lead. Fortunately, I am aware of one analysis, a sample that’s 90 percent black, which shows that with every 5 microgram increase in prenatal blood-lead levels, that there was a 40 percent higher risk of arrest (Wright et al, 2008). This makes sense with the deleterious developmental effects of lead; we are aware of how and why people with high levels of lead in their blood show similar brain scans/brain volume in certain parts of the brain in comparison to antisocial/violent people. So this is yet more suggestive evidence for a causal relationship.
Jennifer Doleac discusses three studies that show that blood-lead levels in America need to be addressed, since they are related strongly to negative health outcomes.Aizer and Curry (2017) show that “A one-unit increase in lead increased the probability of suspension from school by 6.4-9.3 percent and the probability of detention by 27-74 percent, though the latter applies only to boys.” They also show that children who live nearer to roads have higher blood-lead levels, since the soil near highways was contaminated decades ago with leaded gasoline. Fiegenbaum and Muller (2016) show that cities’ use of lead pipes increased murder rates between the years o921 and 1936. Finally, Billings and Schnepnel (2017: 4) show that their “results suggest that the effects of high levels of [lead] exposure on antisocial behavior can largely be reversed by intervention—children who test twice over the alert threshold exhibit similar outcomes as children with lower levels of [lead] exposure (BLL<5μg/dL).”
A relationship with lead exposure in vitro and arrests at adulthood. The sample was 90 percent black, with numerous controls. They found that prenatal and post-natal blood-lead exposure was associated with higher arrest rates, along with higher arrest rates for violent acts (Wright et al, 2008). To be specific, for every 5 microgram increase in prenatal blood-lead levels, there was a 40 percent greater risk for arrest. This is direct causal evidence for the lead-causes-crime hypothesis.
One study showed that in post-Katrina New Orleans, decreasing lead levels in the soil caused a subsequent decrease in blood lead levels in children (Mielke, Gonzales, and Powell, 2017). Sean Last argues that, while he believes that lead does contribute to crime, that the racial gaps have closed in the recent decades, therefore blood-lead levels cannot be a source of some of the variance in crime between blacks and whites, and even cites the CDC ‘lowering its “safe” values’ for lead, even though there is no such thing as a safe level of lead exposure (references cited above). White, Bonilha, and Ellis Jr., (2015) also show that minorities—blacks in particular—have higher rates of lead in their blood. Either way, Last seems to downplay large differences in lead exposure between whites and blacks at young ages, even though that’s when critical development of the mind/brain and other important functioning occurs. There is no safe level of lead exposure—pre- or post-natal—nor are there safe levels at adulthood. Even a small difference in blood lead levels would have some pretty large effects on criminal behavior.
Sean Last also writes that “Black children had a mean BLL which was 1 ug/dl higher than White children and that this BLL gap shrank to 0.9 ug/dl in samples taken between 2003 and 2006, and to 0.5 ug/dl in samples taken between 2007 and 2010.” Though, still, there are problems here too: “After adjustment, a 1 microgram per deciliter increase in average childhood blood lead level significantly predicts 0.06 (95% confidence interval [CI] = 0.01, 0.12) and 0.09 (95% CI = 0.03, 0.16) SD increases and a 0.37 (95% CI = 0.11, 0.64) point increase in adolescent impulsivity, anxiety or depression, and body mass index, respectively, following ordinary least squares regression. Results following matching and instrumental variable strategies are very similar” (Winter and Sampson, 2017).
Naysayers may point to China and how they have higher levels of blood-lead levels than America (two times higher), but lower rates of crime, some of the lowest in the world. The Hunan province in China has considerably lowered blood-lead levels in recent years, but they are still higher than developed countries (Qiu et al, 2015). One study even shows ridiculously high levels of lead in Chinese children “Results showed that mean blood lead level was 88.3 micro g/L for 3 – 5 year old children living in the cities in China and mean blood lead level of boys (91.1 micro g/L) was higher than that of girls (87.3 micro g/L). Twenty-nine point nine one per cent of the children’s blood lead level exceeded 100 micro g/L” (Qi et al, 2002), while Li et al (2014) found similar levels. Shanghai also has higher levels of blood lead than the rest of the developed world (Cao et al, 2014). Blood lead levels are also higher in Taizhou, China compared to other parts of the country—and the world (Gao et al, 2017). But blood lead levels are decreasing with time, but still higher than other developed countries (He, Wang, and Zhang, 2009).
Furthermore, Chinese women, compared to American women, had two times higher BLL (Wang et al, 2015). With transgenerational epigenetic inheritance playing a part in the inheritance of methylation DNA passed from mother to daughter then to grandchildren (Sen et al, 2015), this is a public health threat to Chinese women and their children. So just by going off of this data, the claim that China is a safe country should be called into question.
Reality seems to tell a different story. It seems that the true crime rate in China is covered up, especially the murder rate:
In Guangzhou, Dr Bakken’s research team found that 97.5 per cent of crime was not reported in the official statistics.
Of 2.5 million cases of crime, in 2015 the police commissioner reported 59,985 — exactly 15 less than his ‘target’ of 60,000, down from 90,000 at the start of his tenure in 2012.
The murder rate in China is around 10,000 per year according to official statistics, 25 per cent less than the rate in Australia per capita.
“I have the internal numbers from the beginning of the millennium, and in 2002 there were 52,500 murders in China,” he said.Instead of 25 per cent less murder than Australia, Dr Bakken said the real figure was closer to 400 per cent more.”
Guangzhou, for instance, doesn’t keep data for crime committed by migrants, who commit 80 percent of the crime in this province. Out of 2.5 million crimes committed in Guangzhou, only 5,985 crimes were reported in their official statistics, which was 15 crimes away from their target of 6000. Weird… Either way, China doesn’t have a similar murder rate to Switzerland:
The murder rate in China does not equal that of Switzerland, as the Global Times claimed in 2015. It’s higher than anywhere in Europe and similar to that of the US.
China also ranks highly on the corruption index, higher than the US, which is more evidence indicative of a covered up crime rate. So this is good evidence that, contrary to the claims of people who would attempt to downplay the lead-crime relationship, that these effects are real and that they do matter in regard to crime and murder.
So it’s clear that we can’t trust the official Chinese crime stats since there much of their crime is not reported. Why should we trust crime stats from a corrupt government? The evidence is clear that China has a higher crime—and murder rate—than is seen on the Chinese books.
Lastly, effects of epigenetics can and do have a lasting effect on even the grandchildren of mothers exposed to lead while pregnant (Senut et al, 2012; Sen et al, 2015). Sen et al (2015) showed lead exposure during pregnancy affected the DNA methylation status of the fetal germ cells, which then lead to altered DNA methylation on dried blood spots in the grandchildren of the mother exposed to lead while pregnant.—though it’s indirect evidence. If this is true and holds in larger samples, then this could be big for criminological theory and could be a cause for higher rates of black crime (note: I am not claiming that lead exposure could account for all, or even most of the racial crime disparity. It does account for some, as can be seen by the data compiled here).
In conclusion, the relationship between lead exposure and crime is robust and replicated across many countries and cultures. No safe level of blood lead exists, even so-called trace amounts can have horrible developmental and life outcomes, which include higher rates of criminal activity. There is a clear relationship between lead increases/decreases in populations—even within cities—that then predict crime rates. Some may point to the Chinese as evidence against a strong relationship, though there is strong evidence that the Chinese do not report anywhere near all of their crime data. Epigenetic inheritance, too, can play a role here mostly regarding blacks since they’re more likely to be exposed to high levels of lead in the womb, their infancy, and childhood. This could also exacerbate crime rates, too. The evidence is clear that lead exposure leads to increased criminal activity, and that there is a strong relationship between blood lead levels and crime.
Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012)
2100 words
Rushton et al have kept me pretty busy over the last year or so. I’ve debunked many of their claims that rest on biology—such as testosterone causing crime and aggression. The last paper that Rushton published before he died in October of 2012 was an article with Donald Templer—another psychologist—titled Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? (Rushton and Templer, 2012) and they make a surfeit of bold claims that do not follow. They review animal studies on skin and fur pigmentation and show that the darker an animal’s skin or fur, the more likely they are to be aggressive and violent. They then conclude that, of course (it wouldn’t be a Rushton article without it), that the long-debunked r/K ‘continuum’ explains the co-variation between human populations in birth rate, longevity, violent crime, infant mortality and rate and acquisition of AIDS/HIV.
In one of the very first articles I wrote on this site, I cited Rushton and Templer (2012) favorably (back when I had way less knowledge of biology and hormones). I was caught by biases and not knowing anything about what was discussed. After I learned more about biology and hormones over the years, I came to find out that the claims in the paper are wrong and that they make huge, sweeping conclusions based on a few correlations. Either way, I have seen the error of my ways and the biases that lead me to the beliefs I held, and when I learned more about hormones and biology I saw how ridiculous some of the papers I have cited in the past truly were.
Rushton and Templer (2012) start off the paper by discussing Ducrest et al (2008) who state that within each species studied, darker-pigmented individuals of said species exhibited higher rates of aggression, sexuality and social dominance (which is caused by testosterone) than lighter-pigmented individuals in that same species. They state that this is due to pleiotropy—when a single gene has to or more phenotypic effects. They then refer to Rushton and Jensen (2005) to reference the claim that low IQ is correlated with skin color (skin color doesn’t cause IQ, obviously).
They then state that in 40 vertebrate species that within each that the darker-pigmented members had higher levels of aggression and sexual activity along with a larger body size, better stress resistance, and are more physically active while grooming (Ducrest, Keller, and Roulin, 2008). Rushton and Templer (2012) then state that this relationship was ‘robust’ across numerous species, specifically 36 species of birds, 4 species of fish, 3 species of mammals, and 4 species of reptiles.
Rushton and Templer (2012) then discuss the “Validation of the pigmentation system as causal to the naturalistic observations was demonstrated by experimentally manipulating pharmacological dosages and by studies of cross-fostering“, citing Ducrest, Keller, and Roulin (2008). They even state that ‘Placing darker versus lighter pigmented individuals with adoptive parents of the opposite pigmentation did not modify offspring behavior.” Seems legit. Must mean that their pigmentation caused these differences. They then state something patently ridiculous: “The genes that control that balance occupy a high level in the hierarchical system of the genome.” Though, unfortunately for their hypothesis, there is no privileged level of causation (Noble, 2016; also see Noble, 2008), so this is a nonsense claim. Genes are not ‘blueprints’ or ‘recipes’ (Oyama, 1985; Schneider, 2007).
They then refer to Ducrest, Keller and Roulin (2008: 507) who write:
In this respect, it is important to note that variation in melanin-based coloration between human populations is primarily due to mutations at, for example, MC1R, TYR, MATP and SLC24A5 [29,30] and that human populations are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.
This quote, however, seems to be ignored by Rushton and Templer (2012) throughout the rest of their article, and so even though they did a brief mentioning of the paper and how one should be ‘cautious’ in interpreting the data in their study, it seems like they just brush it under the rug to not have to contend with it. Rushton and Templer (2012) then cite the famous silver fox study, where tame foxes were bred. They lost their dark fur and became lighter and, apparently, were less aggressive than their darker-pigmented kin. These animal studies are, in my useless when attempting to correlate skin color and the melanocortin system in the modulation of aggressive behavior, so let’s see what they write about human studies.
It’s funny, because Rushton and Templer (2012) cite Ducrest, Keller, and Roulin (2008: 507) to show that caution should be made when assessing any so-called differences in the melanocortin system between human races. They then disregard that by writing “A first examination of whether melanin based pigmentation plays a role in human aggression and sexuality (as seen in non-human animals), is to compare people of African descent with those of European descent and observe whether darker skinned individuals average higher levels of aggression and sexuality (with violent crime the main indicator of aggression).” This is a dumb comparison. Yes, African nations commit more crime than European nations, but does this mean that the skin color (or whatever modulates skin color/melanocortin system) is the cause for this? No. Not at all.
There really isn’t anything to discuss here, though, because they just run through how different African nations have higher levels of crime than European and East Asian nations, how blacks report having more sex and feel less guilty about it. Rushton and Templer (2012) then state that one study “asked married couples how often they had sex each week. Pacific Islanders and Native Americans said from 1 to 4 times, US Whites answered 2–4 times, while Africans said 3 to over 10 times.” They then switch over to their ‘replication’ of this finding, using the data from Alfred Kinsey (Rushton and Bogaert, 1988). Though, unfortunately for Rushton and Bogaert, there are massive problems with this data.
Though, the Kinsey data can hardly be seen as representative (Zuckerman and Brody, 1988), and it is also based on outdated, non-representative, non-random samples (Lynn, 1989). Rushton and Templer (2012) also discuss so-called differences in penis size between races, too. But I have written two response articles on the matter and shown that Rushton used shoddy sources like ‘French Army Surgeon who contradicts himself: “Similarly, while the French Army surgeon announces on p. 56 that he once discovered a 12-inch penis, an organ of that size becomes “far from rare” on p. 243. As one might presume from such a work, there is no indication of the statistical procedures used to compute averages, what terms such as “often” mean, how subjects were selected, how measurements were made, what the sample sizes were, etc” (Weizmann et al, 1990: 8).
Rushton and Templer (2012) invoke, of course, Rushton’s (1985; 1995) r/K selection theory as applied to human races. I have written numerous articles on r/K selection and attempts at reviving it, but it is long dead, especially as a way to describe human populations (Anderson, 1991; Graves, 2002). The theory was refuted in the late 70s (Graves, 2002), and replaced with age-specific mortality (Reznick et al, 2002). Some of his larger claims I will cover in the future (like how r/K relates to criminal activity), but he just goes through all of the same old motions he’s been going through for years, bringing nothing new to the table. In all honesty, testosterone is one of the pillars of Rushton’s r/K selection theory (e.g., Lynn, 1990; Rushton, 1997; Rushton, 1999; Hart, 2007; Ellis, 2017; extensive arguments against Ellis, 2017 can be found here). If testosterone doesn’t do what he believes it does and the levels of testosterone between the races are not as high as believed/non-existent (Gapstur et al, 2002; read my discussion of Gapstur et al 2002; Rohrmann et al, 2007; Richard et al, 2014. Though see Mazur, 2016 and read my interpretation of the paper) then we can safely disregard their claims.
Rushton and Templer (2012: 6) write:
Another is that Blacks have the most testosterone (Ellis & Nyborg, 1992), which
helps to explain their higher levels of athletic ability (Entine, 2000).
As I have said many times in the past, Ellis and Nyborg (1992) found a 3 percent difference in testosterone levels between white and black ex-military men. This is irrelavent. He also, then cites John Entine’s (2002) book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It, but this doesn’t make sense. Because he literally cites Rushton who cites Ellis and Nyborg (1992) and Ross et al (1986) (stating that blacks have 3-19 percent higher levels of testosterone than whites, citing Ross et al’s 1986 uncorrected numbers)—and I have specifically pointed out numerous flaws in their analysis and so, Ross et al (1986) cannot seriously be used as evidence for high testosterone differences between the races. Though I cited Fish (2013), who wrote about Ellis and Nyborg (1992):
“These uncorrected figures are, of course, not consistent with their racial r- and K-continuum.”
Rushton and Templer (2012) then state that testosterone acts like a ‘master switch’ (Rushton, 1999), implicating testosterone as a cause for aggression, though I’ve shown that this is not true, and that aggression causes testosterone production, testosterone doesn’t cause aggression. Testosterone does control muscle mass, of course. But Rushton’s claim that blacks have deeper voices due to higher levels of testosterone, but this claim does not hold in newer studies.
Rushton and Templer (2012) then shift gears to discuss Templer and Arikawa’s (2006) study on the correlation between skin color and ‘IQ’. However, there is something important to note here from Razib:
we know the genetic architecture of pigmentation. that is, we know all the genes (~10, usually less than 6 in pairwise between population comparisons). skin color varies via a small number of large effect trait loci. in contrast, I.Q. varies by a huge number of small effect loci. so logically the correlation is obviously just a correlation. to give you an example, SLC45A2 explains 25-40% of the variance between africans and europeans.
long story short: it’s stupid to keep repeating the correlation between skin color and I.Q. as if it’s a novel genetic story. it’s not. i hope don’t have to keep repeating this for too many years.
Rushton and Templer (2012: 7) conclude:
The melanocortin system is a physiological coordinator of pigmentation and life history traits. Skin color provides an important marker placing hormonal mediators such as testosterone in broader perspective.
I don’t have a problem with the claim that the melanocortin system is a physiological coordinator of pigmentation, because it’s true and we have a great understanding of the physiology behind the melanocortin system (see Cone, 2006 for a review). EvolutionistX also has a great article, reviewing some studies (mouse studies and some others) showing that increasing melatonin appears to decreases melanin.
Rushton and Templer’s (2012) make huge assumptions not warranted by any data. For instance, Rushton states in his VDare article on the subject, J. Phillipe Rushton Says Color May Be More Than Skin Deep, “But what about humans? Despite all the evidence on color, aggression, and sexuality in animals, there has been little or no discussion of the relationship in people. Ducrest & Co. even warned that genetic mutations may make human populations not exhibit coloration effects as consistently as other species. But they provided no evidence.” All Rushton and Templer (2012) do in their article is just restating known relationships with crime and race, and then attempting to implicate the melanocortin system as a factor driving this relationship, literally off of a slew of animal studies. Even then, the claim that Ducrest, Keller, and Roulin (2008: 507) provide no evidence for their warning is incorrect, because before they stated that, they wrote “In this respect, it is important to note that variation in melanin-based coloration between human populations is primarily due to mutations at, for example, MC1R, TYR, MATP and SLC24A5 [29,30]. . .” Melanin does not cause aggression, it does not cause crime. Rushton and Templer just assume too many things based on no evidence in humans, while their whole hypothesis is structured around a bunch of animal studies.
In conclusion, it seems like Rushton and Templer don’t know anything about the physiology of the melanocortin system if they believe that pigmentation and the melanocortin system modulates aggression and sexual behavior in humans. I know of no evidence (studies, not Rushton and Templer’s 2012 relationships with crime and then asserting that, because these relationships are seen in animals, that it must mean that the melanocortin system in humans modulates the relationships too) for these assertions by Rushton and Templer (2012). The fact that they think that restating relationships between crime and race, country of origin and race, supposed correlations with testosterone and crime and blacks supposedly having higher testosterone than whites, among other things, shows that the proposed relationships are caused by the melanocortin system and Lift History Theory shows their ignorance of the human physiological system.
Musings on Testosterone and Race
1500 words
People don’t understand the relationship between testosterone, aggression, and crime. People hear the sensational media stating that testosterone causes crime, aggression, and anger. However, I have written numerous articles on this blog on the true nature of testosterone, what it’s really needed for and why we need it in high amounts. I’ve mused a lot on this hormone, which is one of my favorites to discuss due to the numerous misconceptions surrounding it.
Which way does causation run in regard to prisoners and their testosterone level?: heightened testosterone > aggression > violence or aggression > heightened testosterone > dominance > possibility (not necessarily, as I have written myself in the past) of violence.
People may use animal studies in support of their contention that testosterone causes aggressive behavior. However, for reasons I have discussed in the past, animal models only show avenues for future research and do not necessarily mean that this is the case for humans (as Mazur, 2006 point out). I don’t use animal studies. They’re good for future research, but to use them as evidence for causation in humans doesn’t make sense.
People may cite Dabbs et al showing that the more violent prisoners had higher levels of testosterone and therefore conclude that higher levels of testosterone drive the violent crime that they commit, however it is much more nuanced than that.
Does being a violent criminal raise testosterone or are violent people more likely to have high testosterone? Dabbs never untangles this; they just showed a correlation, which is small as evidenced by my other citations.
Testosterone is, as evidenced by numerous studies, related to dominance and dominance contests, however, during these dominance contests “a killing is rarely the outcome of a violent dominance contest” (Mazur, 2006: 25). Therefore, this throws a wrench in the testosterone-causes-crime hypothesis.
Some individuals may state that these dominance contests then lead to violence, however, as Mazur (2006) puts it: “Heightened testosterone is not a direct cause of male violence.”
Other animals assert dominance violently but we, necessarily, do not.
Mazur (2006) states that dominance contests rarely escalate to murder. Mazur also states that dominance contests also lead to increased T for the winners and decreased T for the losers, and these contests also don’t necessarily lead to murder/violent behavior. There is a feedback loop with high T causing behavior and behavior causing high T (Mazur, 2006) while this feedback loop may lead to “lethal effects” (Mazur and Booth, 2008).
It’s worth noting that Mazur seems to advocate for ‘testosterone-depressing drugs’. He concludes:
There are strong linkages between macro-level culture and the physiology of
individuals. We may find solutions to some of our social problems by altering these linkage.
Macro-level culture being white culture, black culture, Asian culture, etc.
The physiological differences are due to the preparation for dominance contests. So, his hypothesis goes, the culture of dominance among young black men with no education is why their T is so high. That low education was also associated with low education lends credence to the claim that this is changeable.
However, in his newer article on education, low testosterone and blacks he advocates for more sensible solutions (attempting an environmental change). I don’t know about you but I have big problems with using FDA/Big Pharma drugs to ‘reduce societal problems’, and it seems that Mazur has changed his view there. Mazur (2016) writes:
If high T does facilitate the high violence rate among young black men, there would be a troubling policy question of what, if anything, to do about it. Any notion of a medical or pharmaceutical fix, rather like prescribing Ritalin for hyperactivity, would reek of race-based chemical castration and should be regarded as outside the pale. However, social interventions might be workable and ethically acceptable.
I have railed against measures like this in the past, since proposing measures to attempt to ‘decrease crime through supposedly decreasing one of the main “causes”‘ is very Brave New World-ish, and I am highly against those measures. Social interventions are, in my view, the more sensible measures to undertake.
In regard to low education and testosterone, this same relationship was noticed by Assari, Caldwell, and Zimmerman (2014) where they note that testosterone was not associated with aggression in men, but low education was, which Mazur (2016) replicates, showing that blacks of the same age group with more education had lower levels of testosterone when compared to age-matched blacks. Mazur (2016) cites one study in support for his contention that education can decrease aggressive behavior (Carre et al, 2014)
The correlation is there, I agree. let’s take the middle value of .11 between Archer, Graham-Kevan, and Davies, 2005 at .08; and Book, Starzyk, and Quinsey, 2001 .14. So testosterone explains 3 percent of the the relationship with aggression. Not high at all.
Great evidence against the testosterone-causes-aggressive-behavior hypothesis are data on the Yanomami. About 50 percent of Yanomami men meet their deaths by other Yanomami men. So the Yanomami must have testosterone levels through the roof, right? Wrong. De Lima et al (2015) write:
We observed that Yanomamis present lower levels of testosterone (414 ng/dL) in relation to other ethnic groups (502/512 ng/dL), but still within normal limits (350-1000 ng/dL).
(Note that these values for “normal limits” changed, going into effect at the end of July.)
The Yanomami with an extremely high murder rate with nowhere near a modern society have T levels on the lower end of our range. So….. The Yanomami example is direct evidence against the assertion of testosterone directly causing crime, as some people assert (it is even evidence against an indirect cause). The evidence of the Yanomami having testosterone levels near our lower range is direct evidence against the testosterone/crime hypothesis. Clearly, other variables drive the high violence rate in this society that are not testosterone. More interestingly, these people have had little contact with Western societies, and their T levels are still low compared to ours despite constantly being vigilant for threats from other Yanomami.
Most dominance contests do not end violently in the first-world, there is numerous evidence to attest to this fact. So with the low correlation between testosterone and aggression (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005), along with dominance contests rarely ending in murder/violent crime, then there are way more factors influencing these phenomena.
So the feedback loop goes: Testosterone rises in expectation of a challenge which then, after the dominance contest (which doesn’t always necessarily lead to violence), it affects both individuals differently depending on whether or not they won or lost that dominance contest and these values then persist over time if the dominance contests continuously end up the same.
Let’s say, for argument’s sake, that testosterone is a large cause for aggressive behavior in lower-educated blacks, what should be done about it? Mazur cites evidence that behavioral interventions seem to work to decrease violent behavior during certain circumstances (Carre et al, 2014), so that is a good way to lower violence in populations that have low education.
So heightened testosterone does lead to dominance which then facilitates a dominance contest between two individuals which does not necessarily lead to crime and aggressive, violent behavior (this outcome is rare in dominance contests among “higher primates” [Mazur’s words]) so, therefore, while testosterone does facilitate dominance contests, it rarely leads to violence in our species. Therefore, testosterone does not cause aggressive behavior and crime, but it does cause dominance which, for the most part, do not always result in violent, aggressive, murderous behavior.
I’ve shown that Mazur replicated other analyses that show that testosterone and aggressive behavior are related to lower education. Testosterone wasn’t associated with aggressive behavior in Assari, Caldwell, and Zimmerman’s (2014) study, and, as Mazur (2016) replicates, low education was. So one way to end this relationship is to educate people, as shown by Carre et al (2014), and with this education, crime will begin to fall. Heightened testosterone is not a direct cause of male violence.
(Note: I also believe that other factors such as sleep and depressed nutrition play a factor in crime, as well as racial differences in it. See Birch, 1972; Liu et al, 2003; Liu et al, 2004; Walker et al, 2007; Galler et al, 2011, 2012a, 2012b; Spratt et al, 2012; Gesch, 2013; Kuratko et al, 2013; Waber et al, 2014; Raine et al, 2015; Thompson et al, 2017 for more information, I will cover this in the future. I’m of course not daft enough to believe that no genetic differences between individuals/populations are the cause of a lot of crime between them, however, as I have laid out the case in regard to testosterone and MAOA numerous times, these two explanations for both individual differences in crime as well as racial differences in crime leave a lot to be desired. Other genetic factors, of course, influence these differences, however, I am only worried about refuting the popular notions of ‘testosterone and MAOA, the ‘warrior gene” cause crime. The relationship is a lot more nuanced as I have provided mountains of evidence for.)
Sex Differences in Aggressive Behavior and Testosterone
1700 words
Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
…
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
MAOA, Race, and Crime: A Simple Relationship?
2400 words
When I first got into HBD back in 2012, one of the first things I came across—along with the research on racial IQs from Rushton, Lynn, Jensen et al—was that the races differed in a gene called MAOA-L, which has a frequency in Caucasians at .1 percent (Beaver et al, 2013), 54 percent in Chinese people (Lu et al, 2013; 56 percent in Maoris (Lea and Chambers 2007) while about 60-65 percent of Japanese people have the low-frequency version of this gene (Way and Lieberman, 2007).
So if these ethnies have a higher rate of this polymorphism and it is true that this gene causes crime, then the Chinese and Japanese should have the highest rates of crime in the world, since even apparently the effect of MAOA and violence and antisocial behavior is seen even without child abuse (Ficks and Waldman, 2014). Except East Asian countries have lower rates of crime (Rushton, 1995; Rushton and Whytney, 2002). Though, Japan’s low crime rate is relatively recent, and when compared with other countries on certain measures “Japan fares the same or worse when compared to other nations” (Barberet 2009, 198). This goes against a lot of HBD theory, and I will save that for another day. (Japan has a 99 percent prosecution rate, which could be due to low prosecutorial budgets; Ramseyer and Rasmusen, 2001. I will cover this in the future.)
The media fervor—as usual—gave the MAOA gene the nickname “the warrior gene“, which is extremely simplistic (I will have much more to say on ‘genes for’ any trait towards the end of the article). I will show how this is a very simplistic view.
The MAOA gene was first discovered in 1993 in a Dutch family who had a history of extreme violence going as far back as the 1890s. Since the discovery of this gene, it has been invoked as an ultimate cause of crime. However, as some hereditarians do note, MAOA only ’causes’ violence if one has a specific MAOA genotype and if they have been abused as a child (Caspi et al, 2002; Cohen et al, 2006; Beaver et al, 2009; Ferguson et al, 2011; Cicchetti, Rogosch, Thibodeau, 2012;). People have invoked these gene variants as ultimate causes of crime—that is, people who have the low-expressing MAOA variants are more likely to commit more crime—but the relationship is not so simple.
Maoris are more four times more likely to have the low-expressing gene variant than Europeans, the same holding for African Americans and Europeans (Lea and Chambers, 2007).
There is, however, a protective effect that protects whites (and not non-whites in certain cases) against antisocial behavior/violent attitudes if one has a certain genotype (Widom and Brzustowicz, 2006), though the authors write on page 688: “For non-whites, the effect of child abuse and neglect on the juvenile VASB was not significant (beta .08, SE .11, t 1.19, ns), whereas the effect of child maltreatment on lifetime VASB composite approached significance (beta .13, SE .12, t 1.86, p .06). For non-whites (see Figure 2), neither gene (MAOA) environment (child abuse and neglect) interaction was significant: juvenile VASB (beta .06, SE .28, t .67, ns) and lifetime VASB (beta .01, SE .29, t .14, ns).” So as you can see, there are mixed results. Whites seem to be protected against the effect of antisocial behavior and violence but only if they have a certain genotype (which implies that if they have the other genotype, then if abused they will show violent and antisocial behavior). So, we can see that the relationship between MAOA and criminal behavior is not as simple as some would make it out to be.
MAOA, like other genetic variants, of course, has been linked to numerous other traits. Steven J. Heine, author of the book DNA is Not Destiny: The Remarkable and Completely Misunderstood Relationship Between You and Your Genes:
However, any labels like “the warrior gene” are highly problematic because they suggest that the this gene is specifically associated with violence. It’s not, just as alleles from other genes do not only have one outcome. Pleiotropy is the term for how a single genetic variant can influence multiple different phenotypes. MAOA is highly pleiotropic: the traits and conditions potientially connected to the MAOA gene invlude Alzheimer’s. anoerxia, autism, body mass index, bone mineral density, chronic fatigue syndrome, depression, extraversion, hypertension, individualism, insomnia, intelligence, memory, neuroticism, obesity, openness to experience, persistence, restless leg syndrome, schizophrenia, social phobia, sudden infant death syndrome, time perception and voting behavior. (59) Perhaps it would be more fitting to call MAOA “the everything but the kitchen sink gene. (Heine, 2017: 195)
Something that I have not seen brought up when discussions of race, crime, and MAOA come up is that Japanese people have the highest chance—even higher than blacks, Maoris, and whites—to have the low repeat MAOA variant (Way and Lieberman) yet have lower rates of crime. So MAOA cannot possibly be a ‘main cause’ of crime. It is way more complex than that. “However intuitively satisfying it may be to explain cultural differences in violence in terms of genes“, Heine writes, “as of yet there is no direct evidence for this” (Heine, 2017: 196).
Numerous people have used ‘their genes’ in an attempt to get out of criminal acts that they have committed. A judge even knocked off one year off of a murder’s sentence since he found the evidence for the MAOA gene’s link to violence “particularly compelling.” I find it “particularly ridiculous” that the man got less time in jail than someone who ‘had a choice’ in his actions to murder someone. Doesn’t it seem ridiculous to you that someone gets less time in jail than someone else, all because he may have the ‘crime/warrior gene’?
Aspinwall, Brown, and Tabery (2012) showed that when evidence of a ‘biomechanic’ cause of violence/psychopathy was shown to the judges (n=191), that they reduced their sentences by almost one year if they were reading a story in which the accused was found to have the low-repeat MAOA allele (13.93 to 12.83 years). So, as you can see, this can sway judges’ perception into giving one a lighter sentence since they believe that the evidence shows that one ‘can not control themselves’, which results in the judge giving assailants lighter sentences because ‘it’s in their genes’.
Further, people would be more lenient on sentences for criminals who are found to have these ‘criminal genes’ than those who were found to not have them (Cheung and Heine, 2015). Monterosso, Royzman, and Schwartz (2010) also write: “Physiologically explained behavior was more likely to be characterized as “automatic,” and willpower and character were less likely to be cited as relevant to the behavior. Physiological explanations of undesirable behavior may mitigate blame by inviting nonteleological causal attributions.” So, clearly, most college students would give a lighter sentence if the individual in question were found to have ‘criminal genes’. But, if these genes really did ’cause’ crime, shouldn’t they be given heavier sentences to keep them on the inside more so those with the ‘non-criminal genes’ don’t have to suffer from the ‘genetically induced’ crime?
Heine (2017: 198-199) also writes:
But is someone really less any responsible for their actions if his or her genes are implicated? A problem with this argument is that we would be hard-pressed to find any actions that we engage in where our genes are not involved—our behaviors do not occur in any gene-free zones. Or, consider this: there actually is a particular genetic variant that, if you possess it, makes you about 40 times more likely to engage in same-sex homicides than those who possess a different variant. (66) It’s known as the Y chromosome—that is, people who possess it are biologically male. Given this, should we infer that Y chromosomes cause murders, and thus give a reduced sentence to anyone who is the carrier of such a chromosome because he is really not responsible for his actions? The philosopher Stephen Morse calls the tendency to excuse a crime because of a biological basis the “fundamental psycholegal error.” (67) The problem with this tendency is that it involves separating yout genes from yourself. Saying “my genes made me do it” doesn’t make sense because there is no “I” that is independent of your genetic makeup. But curiously, once genes are implicaed, people see, to feel that the accused is no longer fully in control of his or her actions.
Further, in the case of a child pornographer, one named Gary Cossey, the court said:
The court predicted that some fifty years from now Cossey’s offense conduct would likely be discovered to be caused by “a gene you were born with. And it’s not a gene you can get rid of.” The court expressed its belief that although Cossey was in therapy, it “can only lead, in my view, to a sincere effort on your part to control, but you can’t get rid of it. You are what you’re born with. And that’s the only explanation for what I see here.”
However, this judge punished Cossey more severely due to the ‘possibility’ that scientists may find ‘genes for’ child pornography use in 50 years. Cossey was then given another, unbiased judge, and was given a ‘more lenient’ sentence than the genetic determinist judge did.
Sean Last over at The Alternative Hypothesis is also a big believer in this so-called MAOA-race difference that explains racial differences in crime. However, as reviewed above (and as he writes), MAOA can be called the “everything but the kitchen sink gene” (Heine, 2017: 195), as I will touch on briefly below, to attribute ’causes’ to genes is not the right way to look at them. It’s not so easy to say that since one ‘has the warrior gene’ that they’d automatically be violent. Last cites a study saying that even those who have the MAOA allele who were not abused showed higher rates of violent behavior (Ficks and Waldman, 2014). They write (pg. 429):
The frequency of the ‘‘risk’’ allele in nonclinical samples of European ancestry ranges from 0.3 to 0.4, although the frequency of this allele in individuals of Asian and African ancestry appears to be substantially higher (*0.6 in both groups; Sabol et al. 1998).
So, why don’t Asians have higher rates of crime—along with blacks—if MAOA on its own causes violent and antisocial behavior? Next I know that someone would claim that “AHA! TESTOSTERONE ALSO MEDIATES THIS RELATIONSHIP!!” However, as I’ve talked about countless times (until I’m blue in the face), blacks do not have/have lower levels of testosterone than whites (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Though young black males have higher levels of testosterone due to the environment (honor culture) (Mazur, 2016). So that canard cannot be trotted out.
All in all, these simplistic and reductionist approaches to ‘figuring out’ the ’causes’ of crime do not make any sense. To point at one gene and say that this is ‘the cause’ of that do not make sense.
One last point on ‘genes as causes’ for behavior. This is something that deserves a piece of its own, but I will just provide a quote from Eva Jablonska and Marion Lamb’s book Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life (Jablonska and Lamb, 2014: 17; read chapter one of the book here; I have the nook version so the page number may be different):
Although many psychiatrists, biochemists, and other scientists who are not geneticists (yet express themselves with remarkable facility on genetic issues) still use the language of genes as simple causal agents, and promise their audience rapid solutions to all sorts of problems, they are no more than propagandists whose knowledge or motives must be suspect. The geneticists themselves now think and talk (most of the time) in terms of genetic networks composed of tens or hundreds of genes and gene products, which interact with each other and together affect the development of a particular trait. They recognize that whether or not a trait (a sexual preference, for example) develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule, and the environment in which an individual develops.
So to say that those who have low-functioning MAOA variants have an ‘excuse’ as to why they commit crime is incorrect. I know that most people know this, but when you read some people’s writings on things like this it’s like they think that these singular genes/polymorphisms/etc cause these things on their own. In actuality, you need to look at how the whole system interacts with these things, and not reduce whole complex physiological systems to a sum of its parts. This is why implicating singular genes/polymorphisms as explanations for racial differences in crime does not make sense (as can be seen with the Japanese example).
To reduce behaviors simply to gene X and not look at the whole system does not make any sense. There are no ‘genes for’ anything, except a few Mendelian diseases (Ropers, 2010). Stating that certain genes ’cause’ X, as I have shown does not make sense and, wrongly, in my opinion, gives criminals less of a sentencing since judges find stuff like this ‘very compelling’. If that’s the case, why implicate any murderer? ‘Their genes made them do it’, right? Though, things are not that simple to implicate one gene as a cause for crime or any other complex behavior; in this sense—like for most things to do with the human body—holism makes way more sense and not reductionism. We need to look at how these genes that are ‘implicated’ in criminal behavior interact with the whole system. Only then can we understand the causes of criminal behavior. Looking at singular genes impedes us from figuring out the true underlying reasons why people commit crime.
Remember: we can’t blame “warrior genes” for violent crime. If someone does have a ‘genetic predisposition to crime’ from the MAOA gene, then wouldn’t it make more sense to give them more time? Though, the relationship is not so simple as I have covered. So to close, there is no ‘simple relationship’ between race, crime and MAOA. Not in the way that other hereditarians would like you to believe. Because if this relationship were so simple, then East Asians (Chinese, Japanese) would have the highest rates of crime, and they do not.
NotPoliticallyCorrect 