Written by Gail S.
Genes do not act alone and neither does
the environment. Genes and the environment frequently act together. They may
correlate with each other or interact. These two relationships are quite
different and must be distinguished in order to understand their mechanisms.
correlations can be mistaken for gene × environment interactions and must be
separated. It has been hypothesized that there are three forms of
The first is referred to
as passive and occurs when a child’s genetic background and environment come
from one source — that of the parents. For example, adolescents may exhibit
aggressive behavior as a result of both inheriting genes that predispose them to
aggression and growing up in an environment in which their parents exhibit
aggression, making the two factors difficult to separate.1
The second is reactive,
in which genetically influenced behavior induces a certain type of environment.
For example, a genetic predisposition to shyness may make an adolescent less
responsive to peer overtures, resulting in isolation that leads to further
inhibition, again making it difficult to disentangle the environmental and genetic
components of the behavior.1
Active correlation is
hypothesized to occur when adolescents pick their environments based on their
genetic predispositions.1 For example, an adolescent who is
predisposed to antisocial behavior may seek out peers who are like-minded with
whom to engage in criminal acts.
In all cases, it is hard
to tease apart the genetic and environmental influences.
We now understand that
people with different genotypes respond differently to the same environment. In
other words, 2 or 20 people may be exposed to the same environment, and all may
react differently. For example, we know there are multitudes of risk factors
for criminal behavior (such as severe child abuse), but many people — in
fact, the majority — who are exposed to this risk factor will not commit a
crime. Sociological theories do not explain why the same environment can
produce such disparate results, but biosocial criminology can show that one
explanation for the disparity is the closely interwoven relationships between
genetic and environmental factors.5
"Gene x environment interactions" explain why some people who experience terribly adverse environments never commit crimes and why some others who experience a nurturing environment do commit crimes.
Frequently, there is an
interaction between a person’s genetic makeup and the environment experienced.
This occurs when an individual’s particular genotype is sensitive or vulnerable
to environmental factors; individuals with different genotypes will react
differently to different environmental triggers.1 In other words,
the effect the environment will have on an individual’s behavior depends on
genetic makeup, and the effect an individual’s genetic makeup will have on
behavior depends on the environment experienced.6 This is referred
to as gene × environment interactions, or G × E interactions. It is this
interaction that explains why some people who experience terribly adverse
environments never commit crimes and why some others who experience a nurturing
environment do commit crimes. If an individual does not have a genetic
predisposition toward criminal behavior, that person may never commit a crime,
even when faced with environmental adversity. If an individual does have a
genetic predisposition for criminal behavior but does not experience a
triggering environment, then that person too may never exhibit criminal
behavior. It is only when an individual has both a genetic predisposition and
experiences an adverse or triggering environment that the risk for criminal behavior
is high.6 However, although the existence of both increases risk, it
still does not guarantee a criminal outcome. Moreover, both genetic and
environmental risk factors act in gradients, with both increasing and
ameliorating risk, and there are many individual and interacting effects within
both genetic and environmental influences, all of which serve to moderate or
amplify behavior. Although the focus of most biosocial studies is to determine
the etiology of behavior and identifying risk factors, such studies also
identify protective factors. In particular, understanding G × E interactions
allows us to recognize protective environments that will prevent a risky
genotype from being expressed and so can inform intervention and prevention
There are a multitude of
examples of G × E interactions that are now being studied. One example is seen
in the development of schizophrenia and bipolar disorder. Numerous studies have
shown both environmental and genetic causes for these psychiatric disorders,
and a large number of genes have been implicated, with each contributing only a
small level of susceptibility.2
More recently a G × E
interaction has been proposed, and a large number of studies have looked at
genetic interactions with a range of environmental factors. In a review of such
studies, the majority considered variation in genes that code for
catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF),
and FK506-binding protein (FKBP5).2 COMT is an enzyme that breaks
down a number of substances in the body, such as some neurotransmitters and
certain drugs, and is implicated in several psychiatric disorders.7
BDNF is involved in growth and survival of brain neurons.8 FKBP5 is
a binding protein that regulates steroid receptors, and methylation of the gene
is thought to moderate the effects of genetic and environmental risk factors
for psychiatric diseases.9 Most of these studies found significant
interactions between certain alleles of these genes and cannabis use, as well
as early-life stress or childhood trauma, which increased risk for
schizophrenia and bipolar disorder, although there were far fewer studies on
bipolar disorder. A few studies also found some interactions between the
alleles and infectious diseases, birth complications, and season of birth.2
In attempting to
understand the underlying mechanisms of the complex G × E interactions that
underlie the expression of criminal or antisocial behavior, a number of
hypotheses, or models, have been developed, based on the proposed different
methods in which genetic polymorphic risk factors increase or decrease
susceptibility to unfavorable environments.6
1. Diathesis stress
The diathesis stress
model assumes that a genotype (involving many polymorphisms or different risk
alleles) confers risk and will lead to an extremely adverse outcome if the
individual is exposed to a negative environment. However, in a good environment
the outcome will not be as negative or may not occur at all.10 This
model stresses the adverse environment and its effects on a risky genotype that
is vulnerable to environmental triggers, resulting in antisocial behavior.6
This model, therefore, states that the fundamental causes of antisocial
behavior are environmental triggers.11
The diathesis stress model states that the fundamental causes of antisocial behavior are environmental triggers.
For example, several
studies have shown that genetic risk factors for antisocial behavior are
potentiated in the presence of parental conflict. In a study of over 1,300 twin
pairs aged 17 years, genetic risk for externalizing behaviors was greatly
exacerbated by increased environmental adversity and parental negativity,12
and similarly, in a study of 720 families genetic risk factors for antisocial
behavior had much greater influence when parents were negative or less
affectionate.13 This is perhaps the most common model used to
explain G × E interactions. The social control model is very similar to the
diathesis stress model but highlights the presence or absence of social
resources rather than an adverse environment as the trigger.11 For
example, high cigarette taxation has been found to reduce the genetic influence
on developing a smoking habit, which is considered to be a form of social
The bioecological model
states that genetic effects are only expressed in a positive environment and are
restricted and not expressed in a negative environment.10 In other
words, this model suggests that, in some situations, genetic risk factors may
reach their highest dominance in the absence of an adverse environment.14
An example of the bioecological model is parent-child conflict, in contrast to
parent-adolescent conflict, which is believed to fit the diathesis stress
model. In a U.S. study of 500 pairs of twins, shared environment was many times
more influential on antisocial behavior in children with high levels of parental
conflict than in those with low levels of conflict, but conversely, genetic
factors were much more significant in the development of antisocial behavior in
children with low levels of parental conflict.14
The bioecological model states that genetic effects are only expressed in a positive environment and are restricted and not expressed in a negative environment.
susceptibility suggests that certain genes or polymorphic genotypes do not
simply confer risk, but instead represent a type of gene plasticity or a level
of malleability to the environment, which may have negative or positive
outcomes.10,15(p885) In other words, a child with a risky genotype
who is exposed to a negative environment will have a very high risk for a bad
outcome, but if that same child with a risky genotype was placed in a more
positive environment, the child may have an even more positive outcome than a
child without the risky genotype.1
The differential susceptibility model focuses less on the adverse environment and looks more at an individual’s susceptibility to the effects of environment.
This model focuses less
on the adverse environment and looks more at an individual’s susceptibility to
the effects of environment. For example, certain genes involved in
neurotransmitter production and function (DRD4 and 5HTTLPR, which we will
explore in Chapter 9) are considered to be plasticity alleles.11(p716)
Studies have shown that individuals who possess certain alleles of these genes
(the 7R allele in DRD4 and the shorter allele in 5HTTLPR) are not only
significantly more likely to be aggressive when exposed to extremely adverse
environmental conditions but also significantly less likely to be aggressive in
extremely favorable environments.16
In a study of carriers
of the risk allele for another dopaminergic gene, DRD2, adolescents who were
homozygous for this allele were much more likely than those who were
heterozygous or homozygous for a non-risk allele to exhibit very seriously
antisocial behavior if they were raised in a family that was not close, but
they were substantially less likely to exhibit such behavior when raised in a
close family, which supports differential susceptibility.11
This model is important
because it suggests that we should not just focus on adverse or non-adverse
environments but also consider the entire range of environments, as it indicates
that normal or usual environments would not provoke any antisocial response
even in those with risky genotypes.11 Belsky argued that risk
alleles should instead be considered plasticity alleles and that individuals
with higher numbers of plasticity alleles are more likely to be impacted, either
positively or negatively, by an environment than individuals with lower numbers
of plasticity alleles. Therefore, G × E interactions, in this model, are the
result of the same environment having a different effect on people, depending
on the number of plasticity genes they possess.15,17
4. Social distinction
A less referenced model
is the social distinction model, which is quite different because it does not
suggest that the environment triggers a genotype to act in a certain way.
Genetic factors are only identifiable in the most favorable environments.11
For example, in a study on the relationship between the e4 allele of the
apolipoprotein, or APOE, gene (which increases the risk of developing Alzheimer’s
disease) and cognitive functioning in elderly people, the allele appeared to be
risky for individuals living in organized, well-kept environments but less
risky for those living in social disorder.18 The authors of this
study referred to this as non-causal G × E interaction.
The social distinction model does not suggest that the environment triggers a genotype to act in a certain way. Genetic factors are only identifiable in the most favorable environments.
5. Social push model
The social push model
focuses on the differences between normal and abnormal social environments, rather
than adverse environments, and suggests that genetic factors are relevant in
normal environments, but in extreme environments, the social environment
“pushes” the phenotype, so the genotype has less relevance.11 For
example, heritability of body mass index is highest in adolescents enrolled in
schools with normal body size expectations, but heritability is lower in
schools in which body mass index extremes are normal, as the environment is
driving the trait and the genotype cannot differentiate between individuals.11
The social push model suggests that genetic factors are relevant in normal environments — but in extreme environments, the social environment “pushes” the phenotype, so the genotype has less relevance.
intervention strategies, it is very important to consider G × E interactions;
most intervention strategies fail to recognize that individuals with particular
genetic risks may respond better to changes in environmental risks.6
This can also confound studies, as individuals with certain genotypes may be
more likely to participate in an experimental intervention treatment, thus biasing
the results, which would not indicate the efficacy for individuals with a
different genotype. Therefore, in order to truly understand the genetic and
environmental influences, randomized experiments are required in which
participants are not allowed to self-select.
For example, a study of
440 African American families in Georgia assessed the efficacy of
family-centered interventions on behaviors such as delinquency, substance
abuse, and unsafe sexual practices in relation to the families’ genetic makeup.19
The genotype that the authors considered involved the transporter gene for the
neurotransmitter serotonin, which we will consider in detail in Chapter 9. A
particular allele for this gene, referred to as the shorter allele, has been
shown to increase risky behavior, so the authors used a randomized experiment
to determine whether youth who had the shorter allele would be more or less
likely to exhibit risky behavior if they participated in the intervention program.
The results showed that risky behavior was higher in youth with the shorter
allele and that youth who had the at-risk genotype and did not participate in
the intervention program were twice as likely to exhibit risky behavior in
comparison with at-risk youth who did participate or youth not at risk.19
A significant interaction was seen between the genotype and treatment.19
In a follow-up study,
the researchers looked at older adolescents in the same intervention program to
see whether another neurotransmitter gene, the dopamine D4 receptor gene,
regulated the effect of the program on substance abuse.20 The
results showed that genetic risk increased substance abuse, but when broken
down by sex, the relationship held true only in males. There was also a G x E interaction
for males only,20 supporting the differential susceptibility model,
as high-risk youth were found to be particularly susceptible to risk, both
genetically and environmentally, but at the same time were also more
susceptible to prosocial protective environments such as those provided by the
Understanding G × E
interactions will help us better identify the most important environmental factors
that influence antisocial behavior and so will inform future intervention
strategies. Genetically informed studies can identify personality and risk
factors that are particularly amenable to intervention and result in behavioral
changes.6 These studies also show the types of individuals that are
most likely to benefit from intervention and at which developmental stage treatment
should be aimed.6
Anderson earned a BSc (Honors) in zoology from Manchester
University, England, and a Masters of Pest Management and PhD in medical and
veterinary entomology from Simon Fraser University. Her specialty is forensic
entomology, the use of insects in death investigations. Anderson is one of only
three board-certified forensic entomologists in Canada. She is a Professor in
the School of Criminology at Simon Fraser University, Burnaby, British
Columbia, Canada, holds a Burnaby Mountain Endowed Professorship, and is also
undergraduate director and co-director of the Centre for Forensic Research and
a forensic consultant to the Royal Canadian Mounted Police (RCMP) and municipal
police across Canada. Her work has been featured on many television programs on
networks including Discovery Channel, Planet Education, History Channel,
Knowledge Network, and CBC. She was a recipient of Canada’s “Top 40 under 40
Award” in 1999, a YWCA Women of Distinction Award for Science and Technology in
1999, and the Simon Fraser University Alumni Association Outstanding Alumni
Award for Academic Achievement in 1995. She was listed in Time magazine
as one of the top five innovators in the world, this century, in the field of
Criminal Justice in 2001 and received the Derome Award from the Canadian
Society of Forensic Sciences. In 2014, she received the Dean’s Medal for
Academic Excellence, and, in 2015, she was listed as one of the six most
influential scientists in British Columbia. In 2017, she received the American
Academy of Forensic Sciences Pathology and Biology Section Award for
Achievement in the Life Sciences.
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