Module 02 MAOA Gene and Crime Research PDF

Preview

Summary

module 2 pt 3 summary ...

Description

Module 02: MAOA Gene and Crime Research Shelley Brown: OK, welcome, everyone. Welcome back to Module 2 for Psychology 3402, Criminal Behavior, Biological and Evolutionary Theories of Crime. In today's section, we're going to focus on molecular explanations or correlates of criminal behavior. Thus far, we focused on evolutionary perspectives that have been used to explain crime. Those real distal species-level perspectives that have been used to explain human behavior as well as criminal behavior. We've also focused on twin and adoption studies, so we know from the twin adoption research that, yes, there is a genetic component that accounts for criminal conduct. It's about 40%. 40% of the variance in whether people engage in crime or not. Can be attributed to our genetic makeup. We don't know what part of our genes is accounting for it. Those twin and adoption studies don't tell us exactly what the genetic mechanisms are, just that there's something in our DNA that makes us more likely to engage in crime. 40% of the variance is attributable to genes. And 60% is attributable to the environments. So, a couple case studies here to introduce this notion that something about a specific gene, the molecular level, can be used to explain aggression and violence. And I'm going to talk about two specific case studies. These are real cases from the United States. The first one involves Stephen Mobley in 1995. He was a man from Georgia, I believe. He was quite violent. He had committed a string of violent robberies. And he committed an actual murder. It was very tragic. He murdered a college student who was working at night as a manager of a Domino's Pizza. It was a very gratuitous homicide, execution style homicide. Very sad, very tragic. During the trial, Stephen's lawyer tried to bring up this genetic defense. Something called MAOA gene. Or an MAOA deficiency. MAOA stands for monoamine oxidase. So, the defense was trying to argue, you know what? Stephen's got this gene, this MAOA genetic deficiency that caused him to be violent. It causes him, predisposes him to aggression, violence. He can't help himself. It's in his DNA. This is the first time that this notion of your genes being responsible for how you act in a violent sense. That's the first time it was raised in a court of law. However, essentially, the trial judge said uh-uh. There's some evidence out there, but it's way too early to render any causal conclusions. Essentially, the trial judge, said the science is in its infancy. It's way too early to say, yes, this was causally related. Or

predisposed Steven to his violence. And subsequently, Mobley was executed in 2005 for his crimes. Now, let's fast forward to 2009, to a case involving Bradley Waldroup. He was a man from Tennessee, I believe. He was estranged from his wife. Quite a brutal estrangement. He was intoxicated. He goes to his wife's cabin, or wherever she is staying. The wife is there with her friend. Bradley wants to take the children away from the wife. There's an altercation that ensues. Bradley brutally murders the wife's friend and almost murders his wife. He's convicted of murder, or he's charged with murder and attempted murder. In this trial, again, it's discovered through genetic testing that Bradley, just like Stephen, he had this MAOA deficiency. Again, we haven't talked about this. All we know is that there's research showing that this particular gene is somehow linked to increases in violence and aggression. In this case, however, the judge ruled yes. OK? This was a mitigating factor in Bradley's case. Therefore, he shouldn't be convicted of murder. Instead his murder and attempted murder charge, well, murder charge, in particular, was reduced to manslaughter, on the grounds that he suffered from this MAOA deficiency. Now, let's just try to unpack what this MAOA gene deficiency or hypothesis actually is all about. So, this particular gene is fundamentally responsible for metabolizing neurotransmitters in our brain. Those things that transfer chemical or transfer electrical impulses through our nerve cells, throughout the brain. There's three main ones that this particular gene is responsible for metabolizing. Norepinephrine, right? The fight or flight response or transmitter. Serotonin, predominantly associated with mood regulation, behavioral inhibitions. And then, of course, dopamine, the pleasure center of the brain. OK? So, this gene is responsible for metabolizing these three types of neurotransmitters. Now, what is important to realize is for this particular gene, there's two versions, if you will, or two morphs of this gene, that occur in the population. Just naturally. There's a low and a high activity version. In the same way, in the general population, we have different morphs for eye colors. We have blue eyes. We have brown eyes. We have hazel eyes. You're not a mutant if you have hazel eyes. It's a naturally occurring phenomena in the environment. So, it's important to take away from this particular gene is that there's two versions. And they both occur naturally in the environment. A low activity version and something dubbed a high activity version. What's important to realize, it's the low activity version that's been linked with aggression and violence. Not the high activity version. And another point I want to make

is that this particular gene is on the X chromosome. All right? We're not going to talk about this right now. But I do want you to think what that means for explaining, potentially, gender differences in crime. OK? If this particular gene is X linked, what does that potentially mean for explaining gender differences in crime? Why men engage in way more crime and way more overt violence than their female counterparts. So, low activity version is linked to aggression and violence. So, I'm going to highlight one main study that tells us a lot about the role of this gene and criminal violence and anti-social conduct. Now, there's been lots of other research in labs with mice and correlational studies, showing a clear association between that gene and aggression. However, this is a really solid study. Caspi et al., 2002. This is one of the seminal studies in developmental criminology. They followed up 1037 kids, right from birth all the way into adulthood in a small town in New Zealand. And it's just a beautiful study. They had multiple waves. It's a longitudinal study. Remember longitudinal? It occurs over time. They had multiple ways of data collection. At birth, they interview the mom. They get all kinds of data. Then a year later, they get more data from the mom about all kinds of things. Physical developments, well-being, all kinds of things. They interview as the participants get older. They're using different sources of collateral information, as there may teenagers. Right? They're looking at police records and so forth. It's a great study. Multi-wave study to see what risk factors are predicting different outcomes over time. So, this study gets a gold star. Many studies have been published from this particular dataset. But in this case, I'm going to highlight one study. Here was the research question. How does the low activity version of the MAOA gene interact with childhood maltreatment to predict different types of anti-social behavior and anti-social personality? So, they wanted to know, OK, we've got these people. We did genetic testing on them. We know whether they have the low version or the high version of this gene. We know how much maltreatment they experienced. They either experience none, maybe they experienced some or severe. We know that. We know their maltreatment history, right? Abused, not abused. Whether they have the low or high version of the gene. And then, we also know whether they got diagnosed with conduct disorder as a kid. Did they evidence antisociality? We also know whether they acted violently, whether they have convictions for violence. We've got all of this data. Their analysis? This is what they found. There was no main effect for the gene. What does that mean? Having the low activity version or the high activity version in no way influenced the probability of whether a person got labeled having conduct disorder, got labeled having antisocial personality

disorder, or that they were more apt to engage in violence. OK? No effect for the gene alone. However, there was a strong main effect for childhood maltreatment. Childhood maltreatment predicted whether or not somebody was likely to be labeled conduct disorder. To have antisocial personality disorder. Or to engage in future violence. OK? Very important, these findings. Most importantly, though, was that there was an interaction between the gene and whether or not the person was maltreated as a child. And here it is. I wrote it out on the slide, so it's really clear. What was the nature of the interaction? People who had the low activity version of the gene. When they that low, they're at risk- they're predisposed with that low activity version, and they were also exposed to severe maltreatment. Those two variables in combination, the interaction of those two things, dramatically increased the odds of subsequent violent offending, conduct disorder, and whether or not they'd be labeled an antisocial personality disorder person. As an aside, as you can tell, this may be a little frustrating. But researchers, when we're studying phenomena, we operationalize our constructs, in this case, crime, differently. Right? We have different labels, different ways of measuring things. Just important to keep that in mind. In this case, the researcher had a couple different definitions of crime or antisociality. Here's the last slide for this section. And it shows you, vividly, the nature of the interaction that I'm talking about. OK? So, on the Y-axis, we have the percent of youth who were diagnosed with conduct disorder. And we're graphing that percentage as a function of the gene variant, whether it was low activity or high activity. The three bars clustering on the left are people who had the low activity version. The bars on the right are those that fell into the high activity version. Remember, it's the low activity version that's been linked to aggression. And then, of course, the bars. The different colors represent the degree of maltreatment. All right. Green represents high, severe levels of maltreatment. Blue is none. And red is probable. So, what you can see, who's at greatest risk for being labeled conduct disorder? It is those who had the low activity version of the gene and also were subject to severe maltreatment. Almost 80% of that group were diagnosed with conduct disorder. versus, for example, I don't know, 40% of those with the high activity version, who were also exposed to severe maltreatment. Huge interaction. Gene plus low activity version of the gene plus severe maltreatment dramatically escalates the odds that you're going to, in this case, be labeled with conduct disorder....