Health & Medicine

What Exactly Creates a Sociopath?

Sociopathy is blamed on a warrior gene, on an abusive childhood or on a damaged brain. This page sets each explanation against what twin studies, genetic studies, maltreatment research and brain imaging measured.

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Before the evidence

None of the studies below measures "sociopathy." They measure antisocial personality disorder, psychopathy, conduct disorder, or antisocial behaviour, and these are four different things. Every figure below is labelled with what it actually measured. Whether anything can treat the condition is a separate question, covered in Can Sociopaths Be Fixed?

The short answer

No single cause. Antisocial personality disorder (ASPD), the diagnosis behind the word sociopath, has several known influences and no known single cause. In twin studies, genes account for 38% to 51% of the differences between people in antisocial behaviour and ASPD, spread across many variants of small effect. Childhood maltreatment goes with nearly twice the odds of antisocial behaviour in adulthood, compared with peers who were not maltreated. But twin studies disagree on how much of that is cause.

What the word sociopath refers to

Sociopathy is not a diagnosis in today's psychiatric manual, the Diagnostic and Statistical Manual of Mental Disorders (DSM). The manual's first edition, in 1952, did list a "sociopathic personality disturbance", one form of which was the "antisocial reaction". The words sociopath and psychopath were often used interchangeably.

The diagnosis the word maps to is antisocial personality disorder (ASPD). The current manual, DSM-5-TR, requires a pervasive pattern of disregard for and violation of the rights of others since age 15. The pattern must show in at least three of seven ways: repeated unlawful behaviour, deceitfulness, impulsivity, irritability and aggressiveness, reckless disregard for safety, consistent irresponsibility, and lack of remorse. The person must be at least 18, with evidence of conduct disorder that began before age 15. The criteria are mainly about behaviour, such as crime and irresponsibility.

In the United States, 4.3% of adults have had ASPD at some point in their lives, according to the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-III). It interviewed 36,309 adults face to face in 2012 and 2013. The rate was 6.4% among men and 2.4% among women.

The survey's authors note that 4.3% falls within the 3% to 5% of earlier US surveys. Because the survey covered households and some group quarters, not prisons, they think it likely underestimates. A Cochrane review of psychological treatments for ASPD says most studies put it at 2% to 3% of the general population.

Conduct disorder is the childhood diagnosis, and ASPD cannot be diagnosed without evidence of it before age 15. Most children with conduct disorder do not go on to develop ASPD. StatPearls, a clinical reference, says nearly 25% of girls and 40% of boys diagnosed with conduct disorder eventually do.

NESARC-III, which asked adults about their childhood, gives a much higher figure. In that 2012-13 survey, 1,600 respondents met the ASPD criteria. Only 154 had conduct disorder without going on to ASPD. So about nine in ten of the adults who recalled conduct disorder also met the adult criteria.

Psychopathy is a related construct, measured with the Hare Psychopathy Checklist-Revised rather than diagnosed from the DSM. It adds interpersonal and emotional traits, such as a lack of empathy, grandiosity and shallow affect, to the behaviour that ASPD describes. The overlap runs one way. Most people who meet the criteria for psychopathy also meet those for ASPD, but most people with ASPD do not meet the criteria for psychopathy.

The popular split, that psychopaths are born and sociopaths are made, has a scholarly version in the psychologist David Lykken's 1995 book The Antisocial Personalities. His publisher's summary describes sociopaths as people whose failure of socialization "can be attributed largely to incompetent or indifferent rearing". It says fearlessness, one of the heritable traits the book reviews, seems to be one basis for primary psychopathy.

As a division of causes, the split does not fit the evidence. A 2018 review of 24 studies found psychopathic traits modestly to highly heritable. A 2022 meta-analysis of 47 studies found a moderate link between psychopathy and childhood physical abuse, emotional abuse and neglect. Antisocial behaviour, as the sections below show, is also partly heritable and also linked to maltreatment.

Heritability

Twin and adoption studies find a moderate genetic contribution to antisocial behaviour. A 2002 meta-analysis by Rhee and Waldman pooled 51 twin and adoption studies. Its best-fitting model divided the variation between people as the table shows.

Shares of the variation between people in antisocial behaviour, in Rhee and Waldman's best-fitting model
Influence	Share of the variation
Additive genetic influences	32%
Nonadditive genetic influences	9%
All genetic influences, the two above together	41%
Shared environment	16%
Nonshared environment, the experiences unique to each person	43%

Twin studies of antisocial personality disorder (ASPD) itself give figures in the same range. A 2017 study interviewed 2,794 Norwegian twins with a structured diagnostic interview. The single factor that the seven ASPD criteria share had a heritability of 51%. Its 95% confidence interval ran from 40% to 67%. An earlier study of the same Norwegian twin panel found a heritability of 38% for ASPD traits.

Heritability describes variation within a population, not a share of any one person. A heritability of 51% does not mean genes caused half of anyone's condition. It means that in the population studied, about half the variation between people was due to genetic differences.

In both studies, experiences unique to each person accounted for about as much of the variation as genes did. In Rhee and Waldman's meta-analysis that was 43% against 41%. In the Norwegian twins it was 49% against 51%, and that share also takes in measurement error.

Studies of DNA itself find much smaller figures. A 2022 genome-wide study by Tielbeek and colleagues pooled 85,359 people from 28 samples. It found one region linked to antisocial behaviour, in an intron of the FOXP2 gene. All the common variants it measured explained 3.4% of the variation in the data of the study's own consortium and 7.7% in its combined analysis. In a separate set comparing people diagnosed with disruptive behaviour disorders with controls, the estimate was 24.8%.

The authors describe antisocial behaviour as highly polygenic. Each variant that contributes has a small effect, so a score built from all of them still explains only a small share of antisocial behaviour.

The warrior gene

On its own, variation in the monoamine oxidase A (MAOA) gene, nicknamed the "warrior gene", has only a modest link with antisocial behaviour. The gene makes an enzyme that breaks down the neurotransmitters dopamine, norepinephrine and serotonin. A common variant in the gene's promoter region lowers the enzyme's activity. This low-activity variant is the one studied in connection with antisocial behaviour.

A 2014 meta-analysis by Ficks and Waldman found the gene's promoter variants significantly associated with antisocial behaviour across studies. But the size of the association varied widely between studies, and the authors called the role of such common variants modest. The low-activity variant is common: 37% of the males in the original 2002 study of the variant and childhood maltreatment carried it.

What the research supports is narrower and more conditional: in males, a common gene variant appears to change how much harm childhood maltreatment does. The 2002 study, by Caspi and colleagues, followed 442 males of a New Zealand birth cohort, the Dunedin study, to age 26. Childhood maltreatment predicted antisocial outcomes more strongly among those with the low-activity variant. In that study the variant had no effect by itself.

Only 12% of the male cohort had both the low-activity variant and a history of maltreatment. Those males accounted for 44% of the cohort's violent convictions. Among the severely maltreated boys who carried the low-activity variant, 85% developed some form of antisocial behaviour.

A 2014 meta-analysis by Byrd and Manuck tested this across 20 male cohorts and confirmed it. Early adversity predicted antisocial outcomes more strongly for the low-activity variant, and the effect was specific to maltreatment rather than adversity in general. Across 11 female cohorts, the variant did not change the effect of early adversity as a whole. For maltreatment alone, a weak effect ran the other way, stronger in women with the high-activity variant. In women, the pattern has not been established.

Single studies agree only partly. Byrd and Manuck pooled 12 later studies of maltreatment in men. Of those, 6 found the effect at the usual level of significance, a one-tailed p value below .05. Studies of this kind, testing one candidate gene against one environment, replicate poorly as a field. A 2011 review of the first decade of such research in psychiatry found 96% of first studies significant, against 27% of the attempts to replicate them.

Childhood maltreatment and other early factors

Childhood maltreatment has a measured but modest link with later antisocial behaviour. A 2018 meta-analysis by Braga, Cunha and Maia pooled 14 prospective studies of 20,946 people followed into adulthood. Compared with peers who were not maltreated, maltreated young people had nearly twice the odds of antisocial behaviour as adults, an odds ratio of 1.96. The 95% confidence interval ran from 1.42 to 2.71.

For later violence, a 2020 meta-analysis by Fitton, Yu and Fazel found an odds ratio of 1.8 and called the increase in risk modest. It pooled 18 prospective studies of 39,271 people.

Prospective studies follow people forward from childhood, but they cannot by themselves separate the effect of maltreatment from what a family passes on. Twin studies try to, and they disagree. A Swedish study of 18,083 adult twins compared those who reported maltreatment with unrelated people. Twins who reported maltreatment had nearly twice the odds of a violent conviction (odds ratio 1.98). Compared with their own twin who had not been maltreated, the odds ratio fell to 1.18, which was not statistically significant.

The Swedish authors concluded that maltreatment was a weak causal risk factor for adult violent offending, with substantial confounding by genes or family environment. A study of 1,116 twin pairs at ages 5 and 7 pointed the other way. It found that physical maltreatment appeared to play a causal role in children's antisocial behaviour.

For antisocial personality disorder (ASPD) itself, as opposed to antisocial behaviour, the evidence is thinner. A 2021 umbrella review by Solmi and colleagues found only five meta-analyses of risk factors for personality disorders that met its criteria. No risk factor for ASPD had evidence of class I, II or III, its strongest grades; six met class IV. That does not mean maltreatment is irrelevant, since the meta-analyses of antisocial behaviour above find a link.

Smoking in pregnancy shows how hard such causes are to pin down. A 2006 meta-analysis found its link with children's later deviant or criminal behaviour statistically significant but small, and sensitive to how studies were done. A 2013 study using adoption and in vitro fertilisation (IVF) designs found the link with conduct problems held even among children reared by mothers genetically unrelated to them. A 2022 review said findings on conduct disorder need more research using genetically sensitive designs.

Other features of family life are linked too. Erratic, coercive and punitive parenting puts boys at risk of conduct disorder, antisocial personality symptoms and violent offending, as Caspi and colleagues summarised the earlier research.

Twin studies also separate the environment that siblings share from experiences that differ between them. The shared environment shows up in conduct disorder: a 2013 study of 2,769 male twins in Virginia found one shared-environment factor, linked to covert acts such as stealing. In the Norwegian twin studies of adult ASPD it did not show up at all, and the environment's share came entirely from experiences that differ between twins.

The brain

Imaging studies find differences between groups. A 2009 meta-analysis by Yang and Raine pooled 43 structural and functional imaging studies of antisocial, violent and psychopathic individuals. It found reduced prefrontal structure and function, with an overall effect size (Cohen's d) of -0.60. The differences were localised to the right orbitofrontal cortex, the right anterior cingulate cortex and the left dorsolateral prefrontal cortex.

A 2023 meta-analysis by Tully and colleagues pooled 23 studies of young people with disruptive behaviour disorders and adults with antisocial personality disorder (ASPD) or psychopathy. Compared with healthy controls, these groups had smaller total grey matter (an effect size of -0.6) and smaller amygdalas (-0.89).

None of this establishes a cause. The studies compare groups at one point in time, so they cannot show whether a brain difference came before the behaviour or after it. Yang and Raine wrote that their meta-analysis "underscores the critical need for longitudinal imaging studies".

Substance use is one possible explanation. In the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-III), 83.6% of adults with ASPD had had a substance use disorder, against 32.5% of adults with no antisocial syndrome. A 2019 pooled analysis of 3,240 people linked dependence on any of five substances to lower volume or thickness in regions including the medial orbitofrontal cortex. But Yang and Raine found that the prefrontal effect did not differ significantly between studies with and without comorbid disorders such as substance abuse.

The samples are small and mixed. Yang and Raine's 43 studies held 789 antisocial individuals between them. Of those individuals, 83.9% were male. Each meta-analysis pools several groups under one label.

Tully and colleagues also found total grey matter more variable in the antisocial groups than in controls. They say the finding suggests a key role for this variability in how these disorders diverge.

The verdict: what the evidence shows

No single cause has been found. Genes, childhood experience and the brain all show up in the evidence on antisocial behaviour and on antisocial personality disorder (ASPD), the diagnosis behind the word sociopath. None has been shown to produce it alone.

The genetic part is real but spread across many genes: twin studies trace 38% to 51% of the differences between people to genes, and no single gene explains them. Childhood maltreatment goes with nearly twice the odds of antisocial behaviour in adulthood, compared with peers who were not maltreated. But twin studies disagree on how much of that link is cause. The brain differences come from comparing groups at one point in time, which cannot show which came first.

Five claims, against the evidence

Claim"Psychopaths are born, sociopaths are made."

Not supportedLike antisocial behaviour, psychopathy is linked to both genes and childhood maltreatment. A 2018 review of 24 studies found psychopathic traits modestly to highly heritable, and a 2022 meta-analysis linked psychopathy to childhood abuse and neglect.

Claim"It's in the genes."

PartlyTwin studies trace 38% to 51% of the differences between people in antisocial behaviour and antisocial personality disorder (ASPD) to genes. But a 2022 genome-wide study of 85,359 people found only one linked region, and many variants each with a small effect.

Claim"A 'warrior gene' causes violence."

Not shownOn its own, variation in the monoamine oxidase A (MAOA) gene has only a modest link with antisocial behaviour. In males, its low-activity variant appears to change how much harm childhood maltreatment does, a finding later single studies support only in part.

Claim"Childhood abuse causes it."

Partly supportedIn prospective studies, maltreated young people had nearly twice the odds of antisocial behaviour as adults, compared with peers who were not maltreated (odds ratio 1.96). Twin studies disagree on how much of that link is cause rather than family background.

Claim"Sociopaths have damaged brains."

Correlation onlyOn average, antisocial groups show reduced prefrontal structure and function, and smaller amygdalas, than controls. The studies compare groups at one point in time, so they cannot show which came first.

What would change this conclusion

This article concludes that:

twin studies trace 38% to 51% of the differences between people in antisocial behaviour and antisocial personality disorder to genes, spread across many variants with no single gene behind them;
childhood maltreatment goes with nearly twice the odds of antisocial behaviour in adulthood, compared with peers not maltreated, but twin studies disagree on how much of that link is cause;
the brain differences found in antisocial groups have not been shown to come before the behaviour.

These conclusions would be falsified by:

• A genome-wide study that finds one variant, or a few, accounting for most of the genetic share that twin studies find

• Large twin or sibling studies of adult antisocial behaviour that agree on whether maltreatment's link survives comparison within families

• Longitudinal imaging studies that scan children before antisocial behaviour begins and find that the brain differences come first

Sources

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Cite this article TruthBased.org. "What Exactly Creates a Sociopath?" Updated October 2026. https://www.truthbased.org/what-exactly-creates-a-sociopath