The Evolution of Anti-Social Behavior in a Cooperative Species

Humans and primates have evolved to be highly social species who tend to live in groups. Being social is evolutionarily beneficial, meaning it has benefits for both reproductive and survival reasons (PBS 2001, Dunbar 1998). Human and primate social networks are very complicated and require a lot of cognitive and empathetic skills to be able to function in these species’ social groups. The social brain hypothesis, first proposed by British anthropologist Robin Dunbar, explains the increase in neocortex size as an adaptation to more complex social networks.

People have struggled to explain how humans can be both altruistic and cooperative, and selfish and uncooperative, and why some people are more selfish and uncooperative than others. Evolution would seem to favor selfishness, but humans generally tend to be more altruistic and empathetic than other species, including primates. Research in human cooperative behavior does not always leave a place for the small proportion of humans whose antisocial behaviors are their main means of survival and the main way they interact with others. They are classified as having antisocial behaviors and are often referred to as sociopaths and psychopaths. Still, they are thought of as exceptions to typical human behavior. While antisocial personality disorders are exceptional in their dependence on cheating behavior for survival, they are not complete anomalies in human evolution. Most humans evolved to have a social brain, but antisocial personality disorder is a disorder of the social brain. This small minority of humans found cheating behaviors to be an evolutionary stable strategy. Today, environmental influences continue to be a major factor in allowing inherited antisocial personality disorder genes to be expressed.

The gene-culture co-evolution theory has linked behavior and social learning with genetics in a way that was not previously considered in evolution research. This theory has generated a lot of research into how humans evolved to be cooperative rather than just learned how to be cooperative. The gene-culture co-evolution theory, often applied to altruism, hypothesizes that early human groups favored certain characteristics and behaviors that were unique to their group culture. Those cultural variations created natural selection pressures to favor individuals who conformed to those traits (Laland 2003). Therefore, the cultural selection of traits affected the transmission of certain genes from one generation to the next. Simultaneously, genetic changes in populations influenced culture. For example, in places where dairy farming is common, adults produce the enzyme necessary to digest milk—lactase. It is believed that dairy farming occurred before some adults could produce lactase, allowing Holden and Mace to conclude that the rise of dairy farming influenced the evolution of lactase production. Recognizing the influence of both culture and genetics has been very important to explaining how human social networks have evolved to function as they do now.

Gene-culture coevolution can be combined with two motivations for cooperation or selfishness, from neuroeconomic theory, to explain how humans evolved to be cooperative. The neuroeconomic motivations for behavior, presented in the book “Neuroeconomics of Prosocial Behavior” by Carolyn Declerck and Christophe Boone, are “self-enhancement” and “group inclusion”. Humans need other humans to survive, as inclusion in a group provides for physical and emotional needs. Cooperative behaviors are favored when they benefit the individual or when they will lead to being accepted in a group. Gene-culture coevolution is part of the group inclusion motivation of cooperation. Since humans know groups favor cooperative individuals, learning to behave in ways that benefit the group, such as sharing resources, helps an individual gain the trust of a group and all the benefits that come with that trust, while also influencing the behavior genes that the individual will pass to its offspring. However, for certain individuals for whom their environment encourages uncooperative behavior, different genes could potentially be selected for, according to this theory.

Group inclusion and self-enhancement are neutral motivations that do not always favor cooperative behavior. Using these motivations, the decision to use cooperative versus selfish behaviors is influenced by the reward of one behavior over another and by the social environment. The “prisoner’s dilemma” can illustrate this point (“Game Theory” article; “Prisoner’s Dilemma” article). If the possibility of your partner in crime betraying you could mean a death sentence for you, the cost of staying silent (group cooperation) is too high and the personal reward of betraying (self-enhancement) is more appealing. If you have a very trusting relationship with your partner and the punishment for neither of you betraying the other is a year in prison, then cooperation for the sake of self-enhancement (your life) and group inclusion (your relationship with your partner), would be a favorable behavior. From this example, we can conclude that trust and the type of reward for a certain behavior are key factors in influencing cooperation versus self-enhancement.

Navigating human social networks in a way that balances both individual and group inclusion motivations requires a very complex skill set. The social brain hypothesis explains brain size expansion in primates and humans as an adaptation to navigate larger and more complex social networks (Dunbar, 1998). There is a strong positive correlation between social group size and neocortex size in primates (Dunbar, 2009). This correlation has been applied to other species, but is not always as strong. The neocortex contains the neural networks for cognitive processes essential to social interaction, such as consciousness and reasoning. Expanding the neocortex allows for the possibility of “mind reading”, a skill that allows us to predict how others may react to a situation or how another individual feels.

Anti-social disorders have created a niche in which cheating behavior is a sustainable means of survival, by exploiting social networks built on trust and altruism. At this point, it is important to distinguish how psychopaths differ from sociopaths and how these two disorders are different from other types of anti-social behaviors in conditions such as autism. We generally do not talk about autistic anti-social behaviors in the same way we talk about psychopaths and sociopaths.

Autistic antisocial behavior is a result of decreased connectivity in brain regions associated with social functions (Gotts, 2012). People with autism are not able to exploit trust and empathy the way the other two disorders do (Samenow, 2014). Sociopaths and psychopaths are antisocial personality disorders without autism (Samenow, 2014). Both display similar behavioral characteristics, including inability to empathize with others, extreme risk-taking, lack of remorse, deceitfulness, and a tendency to behave violently or participate in criminal behaviors (Bonn, 2014; NICE Clinical Guidelines, 2010). Psychopathic behavior is mainly due to genetic factors, and the childhood environment has a minimal effect on preventing the behavior. About 10% of cases of ASPD are considered psychopaths (Hare et al., 2000). Sociopathic behavior, on the other hand, is highly influenced by a childhood environment. Sociopaths have genetic predispositions to violent and impulsive behavior, and their childhood experiences provide an environment that encourages those genes to be expressed. These two pathways that explain the development of these two different types of antisocial disorders as a product of evolutionary influences were first proposed in a 1995 article, “The Sociobiology of Sociopaths,” by Linda Mealy. While psychopathic and sociopathic behavior are created by different mechanisms, they both have genetic components that affect their expression, and they exploit the same niche in human societies. So, for the purpose of this paper, I will refer to these two disorders generally as antisocial personality disorders (ASPD).

Linda Mealy’s influential 1995 article, “The Sociobiology of Sociopaths,” presents an evolutionary model of how cheating behavior or antisocial behavior, as it is referred to in humans, can be a stable method of survival and the two pathways that lead to the development of two types of ASPD. Her model for the evolution of ASPD has two possible pathways, resulting in what Mealey calls primary or secondary sociopaths. Primary sociopaths’ behavior is entirely based on genetic causes, and the environment does little to curb or suppress the behaviors, while secondary sociopaths have genetic tendencies for antisocial behaviors, and an unhealthy childhood environment encourages the expression of these behaviors. It is essential to note that this article met much criticism for Mealey’s primary and secondary sociopath categories instead of calling them psychopaths and sociopaths. However, her analysis and arguments about the stability of ASPD strategies for survival are generally well received (Walsh, Wu).

While altruistic and cooperative behaviors are one example of evolutionarily stable strategies for survival and reproduction in human groups, having such a large population gives way to genetic diversity and the possibility for a variety of evolutionarily stable strategies. The evidence that ASPD has genetic links has been shown in many adoption and twin studies. Most studies on ASPD behavior focus on criminal behavior, and adoption studies have been an important piece of evidence that ASPD has a genetic link. Children of sociopaths and criminals who have been adopted have a higher rate of criminal behavior compared to other adopted children. ASPD genetically linked traits are passed down and expressed in small quantities in a population. A 2005 meta-analysis of 100 twin studies found 50% of the variance in anti-social behavior was due to genetic factors (Moffit 2005). Their status as a minority in the population makes taking advantage of trust and altruistic behaviors in other people an evolutionarily stable strategy (Young 2012). Mealy argues that for individuals who struggle to find a mate because they were unattractive, less socially adept, or intelligent, developing cheating strategies would be a viable way to compete with other individuals who are not disadvantaged (Mealy 1995).

A number of studies of criminal behavior spanning 60 years have found that between 50 and 70% of violent crimes are committed by 5-6% of a given population, suggesting that the carrying capacity for cheating or anti-social behavior is stable when it remains in this proportion of the population (Walsh, Wu 2008). However, if too many people start using cheating behaviors for reproductive or survival advantages either because they had some genetic predisposition or started copying the behavior of other cheaters, then the strategy becomes unstable and the population of cheaters must be reduced (Walsh, Wu 2008). This is where punishment and empathetic cruelty can be introduced, and ASPD may actually be helpful.

Empathetic cruelty is a characteristic of antisocial personalities that can benefit the social group because it discourages cheating behavior and keeps the population of cheaters at a sustainable size. Punishment is a way that cheating behavior can be discouraged. However, the human brain’s theory of mind or mind reading ability, which allows us to feel what another person feels such as pain or sadness, can make punishment a difficult task to carry out. Lack of empathy is a commonly cited trait of anti-social personality disorders. However, empathetic cruelty may be a better description. Empathetic cruelty is when a person receives pleasure from punishing another. Taking pleasure in punishing bypasses a person’s theory of mind that stops them from inflicting the punishment.

To a certain extent, all people have the capacity for empathetic cruelty. We guiltily take pleasure in a successful person’s misfortune and mistakes. However, guilt is the key component that keeps most of us from acting with no remorse or empathy, like psychopaths or sociopaths. People with anti-social personality disorders have the ability to bypass the emotional barrier created by theory of mind (Mealey 1995). Imaging studies have found that people with diagnosed ASPD have similar levels of arousal to emotionally linked words such as “mother,” “death,” and “cancer” as they do to neutral words such as “apple” or “cup.” To receive the same amount of neurological arousal, people with ASPD participate in risky or extreme behaviors. While empathetic cruelty has allowed people to commit horrible acts, the capacity to punish more easily has helped maintain order in human groups and discouraged widespread cheating behavior.

There is still some uncertainty as to whether changes to certain brain structures associated with anti-social behavior have a genetic cause. However, a 2008 review paper by neurocriminologist Adrian Raine, known for his work neuroimaging murderers’ brains, supports the hypothesis that genes are at play in causing impairments to the social brain. This is because the reduction in grey matter volume in the pre-frontal cortex of patients with diagnosed anti-social personality disorder could not be correlated with any environmental factors such as head injuries, child abuse, or substance abuse. The review paper also created a model that found “90% of the variance in grey matter” in the prefrontal cortex was due to genetic factors (Raine 2008).

The social brain is an important tool for functioning in human groups, but genetics and environment affect the expression of genes resulting in an impaired social brain in people with anti-social personality disorder. ASDP has been linked to structural and neurochemical changes that affect the social brain. Seven genes are both linked to anti-social and aggressive behavior and affect brain structure and chemistry. MAOA is a well-studied example of a gene that codes for an enzyme that breaks down serotonin. When this gene is not expressed, studies have found that mice tend to be more aggressive. Studies in humans with family histories of anti-social personality disorders have also found that MAOA expression is decreased in people with ASPD. Decreased MAOA expression is associated aggression, violence, and impulsivity (Brunner 1993, Guo 2008, Raine 2008). Males with decreased expression of the MAOA gene have an 8% reduction in volume of brain structures (amygdala, anterior cingulate, and ventral prefrontal cortex) that are important to emotion.

The MAOA gene is just one example of a gene that is associated with structural changes in the brain. The pre-frontal cortex is an area associated with both emotional and cognitive processes, and damage or reduction to grey matter in this brain structure has been linked to anti-social behaviors such as aggression. Imaging studies of people with ASPD have found an 11% reduction in pre-frontal grey matter. However, people with brain injuries to certain regions, particularly the pre-frontal cortex, can also provide insight into how brain structure is related to anti-social behavior. Patients with damage to the ventral prefrontal cortex often display anti-social-like behaviors including reduced emotional expression and detection, and poor decision-making.

Environment is an important factor that influences a person’s likelihood of acting on anti-social behavior tendencies, particularly for sociopaths. A majority of cases of ASPD are considered sociopathy rather than psychopathy, and environmental factors are the main contributing factor. Social environment is known to affect gene expression. The gene-culture co-evolution hypothesis suggests that social environments can affect the selection of certain genetic traits. Just as early humans created selective pressures for cooperative, social traits, long-term exposure to violent, hostile environments for many generations could select for anti-social, aggressive personality traits as a means of survival. Today, poverty and abusive childhood experiences are strongly linked to the development of sociopathic behaviors. Experiences in violent environments affect the developing brain and can train a person to be on high alert for threats and to respond to potential threats more aggressively than most people (Walsh, Wu 2008).

Numerous studies show the interaction between environment and genetics in encouraging the expression of ASPD. (Multiple studies have looked at this.) Generally, these studies, which involve people separated from parents with diagnosed ASPD and adopted into homes of various family environments, conclude that negative environments – such as those with marital problems between parents, drug abuse, and child abuse – can encourage ASPD expression.

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