Social Science & Medicine 70 (2010) 1277–1284

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Social Science & Medicine

journal homepage: www.elsevier.com/locate/socscimed

Genotype–environment interaction and sociology: Contributions

and complexities
Jamie A. Seabrook a, *, William R. Avison a, b, c, d
a
Departments of Sociology and Paediatrics, The University of Western Ontario, 1151 Richmond Street, London, Ontario, Canada, N6A 3K7
b
Childrens Health Research Institute, Childrens Hospital, London Health Sciences Centre, 800 Commissioners Road East, London, Ontario, Canada N6C 2V5
c
Department of Epidemiology and Biostatistics, The University of Western Ontario, 1151 Richmond Street, London, Ontario, Canada, N6A 3K7
d
Lawson Health Research Institute, London Health Sciences Centre, London, Ontario, Canada

a r t i c l e i n f o a b s t r a c t

Article history: Genotype–environment interaction (GE) refers to situations in which genetic effects connected to
Available online 12 February 2010 a phenotype are dependent upon variability in the environment, or when genes modify an organism’s
sensitivity to particular environmental features. Using a typology suggested in the GE literature, we
Keywords: provide an overview of recent papers that show how social context can trigger a genetic vulnerability,
Genes compensate for a genetic vulnerability, control behaviors for which a genetic vulnerability exists, and
Environment
improve adaptation via proximal causes. We argue that to improve their understanding of social
Social environment
structure, sociologists can take advantage of research in behavior genetics by assessing the impact of
Medical sociology
Review within-group variance of various health outcomes and complex human behaviors that are explainable by
genotype, environment and their interaction. Insights from life course sociology can aid in ensuring that
the dynamic nature of the environment in GE has been accounted for. Identification of an appropriate
entry point for sociologists interested in GE research could begin with the choice of an environmental
feature of interest, a genetic factor of interest, and/or behavior of interest. Optimizing measurement in
order to capture the complexity of GE is critical. Examining the interaction between poorly measured
environmental factors and well measured genetic variables will overestimate the effects of genetic
variables while underestimating the effect of environmental influences, thereby distorting the interac-
tion between genotype and environment. Although the expense of collecting environmental data is very
high, reliable and precise measurement of an environmental pathogen enhances a study’s statistical
power.
Ó 2010 Elsevier Ltd. All rights reserved.

Genotype–environment interaction (GE) refers to situations in
which genetic effects connected to a phenotype are dependent
upon variability in the environment, or when genes modify an
organism’s sensitivity to particular environmental features
(Shanahan & Hofer, 2005). Although both genetic and environ-
mental factors play important roles in the causality of human
disease as well as complex human behaviours (e.g., problem
behaviours, health-related behaviours, motivation, psychopa-
thology), the combined interaction between genotype and envi-
ronmental factors is greater than their independent effects (Botto &
Khoury, 2001; Grigorenko, 2005; Shanahan & Hofer, 2005). This is
because assessment of only the separate contributions that genes
* Corresponding author.
E-mail addresses: jamie.seabrook@lhsc.on.ca, jseabroo@uwo.ca (J.A. Seabrook).
and environment make to a particular disease or human behaviour
distorts the estimates of how genes, the environment, and GE
contribute to disease or behavioural outcomes.
Despite the recognition that most complex human behaviours
and diseases evolve through GE, few empirical studies assessing
the interaction between genotype and environment have been
conducted (Shanahan & Hofer, 2005). While much sociological
research has focused on the impact that environment has had on
contributing to mental disorders (Schnittker, 2008), gene research
into mental disorders by contrast has largely ignored the contri-
butions that environmental factors have made (Moffitt, Caspi, &
Rutter, 2005). The assumption in much of genetic research that
direct paths will be found from gene to diseases has not been found
for complex psychiatric disorders (Caspi et al., 2003).
The discipline of sociology has traditionally been reluctant
about embracing other sources of explanation regarding social

0277-9536/$ – see front matter Ó 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.socscimed.2010.01.016
1278 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
behaviour and disease. For the most part, sociologists have
attempted to discredit and deny biological explanations about
human behaviour and disease, which has resulted in the majority of
sociologists knowing little about alternative causes of behaviour
(Udry, 1995). As Schnittker (2008: S235) notes, ‘‘Even among those
interested in genetic influence, most focus on interpreting herita-
bility appropriately, rather than examining the implications of
heritability for theories of environmental influence.’’
Only recently has there been an increased interest in sociology
about how genetic differences can explain individual outcomes of
interest to social scientists (Freese, 2008). In a recently published
article, Shanahan, Vaisey, Erickson, and Smolen (2008) argue that
given the expertise of sociologists in conceptualizing and
measuring social context, studies of GE can capitalize on the work
of sociologists in this area. Schnittker (2008) believes that
analyzing genes will reveal environmental complexity in such
a way that sociologists can more appropriately argue the impor-
tance of environment in research on well-being. Freese (2008) also
notes how attention to genetic differences will enhance under-
standing of the social mechanisms by which genetic differences
result in various behaviours.
Understanding GE may also improve methods of disease
prevention, and provide better treatment after a disease has been
diagnosed. Although there have been many recent unprecedented
discoveries in the genomics of such diseases as obesity, prostate
cancer, breast cancer, lymphoblastic leukemia, coronary heart
disease, and type 2 diabetes mellitus, the important question for
sociologists is how genetics can advance sociology assuming that
individuals do in fact differ in their genetic propensities for
complex human behaviour (Guo, Tong, & Cai, 2008).
After providing a basis for understanding sociological theories
on the causes and consequences of health disparities, we will
describe various genotype–environment interactions that have
been published from the 1990s to the present using a typology
which identifies ways in which the environment can moderate
genetic expression. We then conclude by highlighting some of the
complexities inherent in genotype–environment interaction
research. We argue that the life course perspective in sociology can
aid in ensuring that the dynamic nature of the environment in
genotype–environment interaction has been accounted for.
Sociological theories on health and illness
A core principle in sociology is that social experience affects the
psychological state of individuals. This social experience is derived
from what sociologists refer to as social structure and social inter-
action. The social structure is stratified in such a way that factors
such as socioeconomic status, gender, age, and the life course all
have mental health consequences for individuals. Thus, for
example, poverty has been a consistent risk factor for such mental
disorders as depression, antisocial personality, substance-use
disorders and anxiety disorders (Muntaner, Borrell, & Chung,
2007). Social interaction, on the other hand, involves social
exchanges between individuals that can be either positive or
negative. Research on social relationships has found that
unpleasant interactions between individuals perceived by a recip-
ient as unsupportive, critical, and demanding increase the likeli-
hood of mental illness, and that negative social interactions
influence mental health more so than do measures of social support
(Evans-Campell, Lincoln, & Takeuchi, 2007).
The founders of sociology were also effective in demonstrating
how individual attributes were a reflection of structural processes
and social arrangements. In his classic study on suicide rates, Emile
Durkheim showed how suicide resulted from deficiencies in social
integration (familial, religious, and political), in which individuals
felt isolated from one another (Horwitz, 2007). Durkheim called
these types of suicides egoistic suicides. He also found that too much
integration increased the likelihood of altruistic suicides because
individuals felt overwhelmed by social demands (Horwitz, 2007).
For Karl Marx, widespread alienation of humans from the
products they produce, from the natural world, other people, and
their own human nature, creates misery and has major negative
psychological consequences on individuals (Horwitz, 2007). This
alienation will persist, according to Marx, until private property is
abolished and communism emancipates the human essence.
Finally, Max Weber focused on explaining social action in its
historical context, and emphasized social values, culture, and
meaning of human action. These values are fundamentally social
because they motivate individuals and contribute to the meaning of
one’s existence (Horwitz, 2007). Further, Weber felt that the spread
of bureaucracy and technocratic ideas in modern society would
negatively impact psychological well-being, although he was not
explicit in his writing on this.
Given that biological and genetic determinants of behavior were
not well understood in the nineteenth century, Durkheim, Marx,
and Weber were more focused on how the mental health of indi-
viduals were shaped by their relationship to large-scale structural
processes. Contemporary theoretical and empirical work in soci-
ology continues to emphasize the importance of social stratification
and its subsequent impact on health disparities and behavioural
outcomes. The social causation hypothesis is based on the notion
that position in the social structure causes variations in health
outcomes (Turner, Wheaton, & Lloyd, 1995). These social causes of
health disparities, moreover, can be divided into proximate (life-
style) and fundamental causes, with the former including such
factors as diet, exercise, and hypertension. According to Link and
Phelan (1995), the problem with epidemiological research
emphasizing proximate risk factors is that it assumes that the
individual has the capability to control his or her fate. Instead, Link
and Phelan argue that it is important to contextualize risk factors by
understanding why some people are more likely to be exposed to
individually-based risk factors. Central to their argument is the
notion that there are more distal ‘‘fundamental causes’’ of disease,
such as socioeconomic status, race/ethnicity, gender and social
support, which determine the extent to which people are able to
adopt protective strategies and avoid risks that contribute to
differences in morbidity and mortality. Across a wide range of
illnesses and disease, people with higher levels of knowledge,
money, power, prestige and social connections are less likely to be
afflicted by disease (Chang & Lauderdale, 2009; Link & Phelan,
1995; Luftey & Freese, 2005). An important implication of this is
that the association between fundamental social causes and disease
will persist when health policy focuses its interventions on
reducing proximal causes of disease. The reason for this persistent
association is that resources are important causes of risk factors
and, henceforth, fundamental causes are associated with many
disease outcomes via multiple risk-factor mechanisms (Link &
Phelan, 1995).
While social causation examines the impact that social structure
has on causing health disparities, social selection posits that people
who have a physical and/or mental illness are more likely to
experience downward mobility throughout the life course (Turner
et al., 1995). In a study assessing the impact of marital transitions
and mental health, Wade and Pevalin (2004) found that separated,
divorced and widowed individuals had poorer mental health than
married persons, and that the rate of poor mental health among
people who experienced a marital disruption was higher than
married persons prior to the transition of the marital disruption,
thus providing evidence of both social causation and social selec-
tion, respectively. The evidence for social selection also appears
 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
strong, for example, in people with schizophrenia (Link & Phelan,
1995; Turner et al., 1995).
Differences in exposure to stress are also critical in under-
standing variations in health outcomes. Turner and Avison (2003)
show that there are social status differences in stress exposure
based on such factors as gender, race, and social class and that
differences in mental health are at least partially attributable to
systematic differences in stress exposure by people differentially
situated in the social structure. In other words, exposure to stress is
rooted in structural contexts, consistent with the social causation
hypothesis. For example, adolescents tend to experience more
stressful events than older people, and unmarried people report
higher occurrences of undesirable life events than do married
persons (Turner et al., 1995).
It seems clear that sociological theory and research has signifi-
cantly advanced our understanding of the ways in which social
structure and social experiences affect health. Udry (1995) has
argued persuasively that biological processes might also be usefully
integrated into sociological perspectives on health and illness.
We argue that to advance their understanding of social struc-
ture, sociologists can take advantage of research in behavior
genetics by assessing the impact of within-group variance of
various health outcomes and complex human behaviours that are
explainable by genotype, environment and their interaction.
Furthermore, the sociological study of genetic data can provide
insight on how the environment can mediate and moderate the
effect of genetic dispositions on stratification-related outcomes
(Shanahan et al., 2008). It is to genotype–environment interactions
that we now turn.
Genotype–environment interactions
The study of GE requires information on both genetic vulner-
ability as well as environmental factors because although a genetic
effect can influence the phenotype of an organism, this genetic
effect can be altered by environmental conditions. Genetic
vulnerability can be inferred from direct analysis of DNA sequence,
family history, and phenotype. Environmental factors are typically
measured using self-report through such methods as interviews,
questionnaires, direct measurement of participants, or records
(Hunter, 2005).
In their review of GE, Shanahan and Hofer (2005) propose
a typology identifying four ways by which environment moderates
gene expression. The authors assert that social context can trigger
a genetic vulnerability, compensate for a genetic vulnerability,
control behaviours for which a genetic vulnerability exists, and
improve adaptation via proximal causes.
Triggering interaction
A triggering interaction is a situation in which a genetic
vulnerability is only expressed in the presence of a particular
stressor or trigger (Shanahan & Boardman, 2009). Several exam-
ples exist in the literature demonstrating the triggering interaction
of social context to a genetic vulnerability. For example, Kendler
et al. (1995) examined the etiology of major depression by
assessing the interaction between genetic liability and stressful life
events in a population-based sample of female twins. The authors
found that for individuals at lowest genetic risk (monozygotic
twins with unaffected co-twins), the risk of onset of major
depression in the month of a severe stressful life event was 6.2%
compared to .5% in individuals at lowest genetic risk who did not
experience a severe stressful life event. However, for those at
highest genetic risk (monozygotic twins with affected co-twins), in
the month of a severe stressful life event, the risk of onset of major
1279
depression was 14.6%. Those individuals with the highest genetic
risk for the onset of major depression and who experienced
a severe stressful life event were therefore 2.4 times more likely to
have an onset of major depression than were individuals at the
lowest genetic risk and who did not experience a severe stressful
life event. The observation that some triggering interactions may
involve stressful life events suggests that the stress process para-
digm (Pearlin, 1989; Pearlin, Lieberman, Menaghan, & Mullan,
1981; Pearlin, Schieman, Fazio, & Meersman, 2005) may have an
important contribution to play in understanding certain gene–
environment interactions.
It is also useful to examine the long-term patterns of social risk
factors and their impact on depression. For example, adult children
of parental divorce not only have higher risk for depression, but
also have lower levels of socioeconomic status, and are more likely
to divorce and remarry (McLeod, 1991; O’Connor, Thorpe, Dunn, &
Golding, 1999; Ross & Mirowsky, 1999). Two studies further show
that the association between parental divorce and depression in
adulthood is largely explained by hostile parental conflict during
childhood as well as poor parent–child relations, particularly
neglect (Harris, Brown, & Bifulco, 1990; O’Connor et al., 1999).
Although these studies establish relationships between childhood
adversities and adult depression, perhaps more important is the
identification of pathways which contribute to these life course
adversities that were first experienced in childhood.
Taylor (1995: 67) uses the term ‘‘historical constructionism’’ to
connote that ‘‘science in the making is a process of agents building
by combining a diversity of components’’. He maintains that the
social origins of severe depression among women are the result of
a combination of social class, familial characteristics, psychological
factors, and possibly genetic vulnerability, all of which coexist
throughout the life course. Specifically, the loss of or prolonged
separation from the mother when the woman was a child, a severe
adverse event in the year prior to depression onset, the lack of
a caring partner, and persistently difficult living conditions are four
key factors identified in adult women with severe depression. What
Taylor advocates is that social, psychological and biological factors
which contribute to the origins of depression should not be thought
of as separate contributing causes, but rather causal links or path-
ways that build on each other. These increase the likelihood of
depression in later life among some women. Moreover, if depres-
sion is the result of a combination of heterogeneous components
that build on one another, this undercuts the conventional
dichotomy of characterizing a given outcome as either purely
genetic or purely environmental.
The growing interest in epigenetics is also relevant to any
consideration of GE research. In their informative review, Rutter,
Moffitt, and Caspi (2006) examine the role that epigenetic effects
may have in understanding the etiology of psychopathology.
Jaenisch and Bird’s (2003) classic work on the chemical bases of gene
expression demonstrated how methylation influenced this process.
This set the stage for a substantial growth in research focusing on the
ways in which environmental exposures might alter gene expres-
sion. Perhaps the most compelling work on epigenetic influences on
psychopathology has been a series of studies by Meaney and his
colleagues (Cameron et al., 2005; Champagne et al., 2004) in which
maternal behaviors of rats – nursing, licking, and grooming – affect
gene expression among offspring in the brain regions that control
defensive and reproductive behaviors.
It remains to be seen whether epigenetics research among
human subjects will be as fruitful. There are several methodological
and ethical obstacles to studying the epigenetics of human
psychopathology that may make it extremely difficult to generate
convincing results. Nevertheless, it is theoretically important and
intriguing to continue to think about the possibilities that
1280 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
environmental experiences and exposures might alter the expres-
sion of genes among humans.
Although sensitivity to stressful life events may be dependent on
an individual’s genetic makeup, less is known about whether
specific genes intensify or buffer the effects of stressful life events on
depression. In a prospective longitudinal study, Caspi et al. (2003)
found that a functional polymorphism in the promoter region of
the serotonin transporter (5-HTT) was found to alter environmental
life stress on depression. Specifically, those individuals with one or
two copies of the short allele of the 5-HTT promoter polymorphism
were more likely to be experience depressive symptoms, a diagnosis
of major depression, and suicide ideation or attempt in relation to
life stress when compared to individuals with two copies of the long
allele. What makes this finding unique from a sociological
perspective is that it found that the apparent link between stressful
life events and depression occurred almost exclusively in individuals
with one or two copies of the short allele of the 5-HTT promoter
polymorphism. As a result of this finding, Shanahan et al. (2008: 2)
argue that ‘‘the challenge then becomes the identification of social
psychological mechanisms by which the risky variant combines
with life events to increase depression’’.
Another example demonstrating the triggering interaction of
social context to a genetic vulnerability can be found in a recent
study assessing the role of genotype in the cycle of violence in
maltreated children. In this study, Caspi et al. (2002) examined the
impact of childhood maltreatment in males from birth to adulthood
to see why it is that some maltreated children experience antisocial
behaviour (conduct disorder, disposition toward violence, convic-
tions for violent offenses, and antisocial personality disorder
symptoms) in adulthood while others who were also maltreated in
childhood do not. Using a functional polymorphism in the
promoter of the monoamine oxidase A (MAOA) gene to charac-
terize genetic susceptibility to childhood maltreatment, the authors
found that severely maltreated males with low levels of MAOA
expression were more likely to develop antisocial problems in
young adulthood than were severely maltreated males with
a genotype demonstrating high levels of MAOA activity. The
authors suggest that high levels of MAOA are able to sufficiently
metabolize high levels of neurotransmitters. Thus, the association
between childhood maltreatment and antisocial behaviour in
young adulthood is conditional on the child’s MAOA genotype.
The impact of childhood deprivation, as measured by not having
enough food to eat because of poverty, has also been shown to
interact with genotype in research on alcoholism. For example, one
study revealed that among men having the high-risk GABRA2
genotype for alcohol dependence, the predicted probability of
being diagnosed with alcohol abuse was much higher for individ-
uals who experienced childhood deprivation compared to those
who did not (Pescosolido, Perry, Long, & Martin, 2008).
Social compensation
It is also possible to thwart the expression of a genetic vulner-
ability through a positive social context. Focusing on DRD2, a gene
on chromosome 11 (q23.1) which aids in the functioning of neural
circuits in the brain, Shanahan et al. (2008) found that although
DRD2 risk increases the likelihood of discontinuing education after
secondary school in both white and black boys, high parental
socioeconomic status, high parental involvement in school, and
attending a high quality school helps compensate for this rela-
tionship. Likewise, in a similar study assessing the role of mentors
and the likelihood of continuing education beyond secondary
school, Shanahan, Erickson, Vaisey, and Smolen (2007) found that
the negative relationship between DRD2 risk allele and the prob-
ability of continuing education beyond high school was fully
attenuated in both black and white boys by having a teacher who is
also a mentor.
Other recent evidence has shown how positive social environ-
ments can prevent the expression of a genetic vulnerability. Guo
et al. (2008) found that among white males, the 10R genotype in
the dopamine transporter gene (DAT1) is associated with higher
numbers of sexual partners relative to 9R/9R genotype. However,
even with the 10R genotype among males, there was a substantial
and negative relationship between those who attended church
services on a weekly basis and their total number of sexual partners.
Specifically, those who attended church on a weekly basis reported
60% fewer sexual partners than those who had never attend church
services or those who attended on an infrequent basis only.
Using data from the Collaborative Study of the Genetics of
Alcoholism (COGA), Pescosolido et al. (2008) found evidence for
a modest but significant increase in the likelihood of being diag-
nosed with alcohol dependence when having the GABRA2 gene
(OR ¼ 1.26, p < .01). Interestingly, however, it was only for men with
a high-risk genotype on GABRA2 that resulted in a higher probability
of alcohol dependence. That is, women had the same probability of
alcohol dependence whether or nor they had a high or low risk on
GABRA2, suggesting an important genotype-by-gender interaction.
It is also possible that other factors may help to explain this apparent
genotype-by-gender interaction. For example, gender differences in
alcohol dependence may be attributable to different messages that
males and females receive during adolescent socialization about
how they are supposed to behave. Research indicates that adoles-
cent females tend to receive messages about putting others first to
the exclusion of the self, while males learn about the importance of
putting one’s own interests first (Rosenfield, Lennon, & White,
2005). As a result of very different self-salient messages received
via socialization, males tend to respond to distress externally
whereas women are more likely to respond to distress by experi-
encing internalizing problems. Specifically, women tend to respond
to distress by experiencing depressive symptoms and anxiety, while
men are more predisposed to alcohol abuse and antisocial behaviour
(Rosenfield et al., 2005).
Another interesting finding in Pescosolido et al.’ study (2008)
was that the predicted probabilities of alcohol dependence were
much lower when individuals perceived themselves as having high
levels of social support from family members. This coincides with
other research that has shown the importance of perceived support
on positively affecting an individual’s adjustment, health, and well-
being (Hartwell & Benson, 2007). It also suggests a possible buff-
ering mechanism among those individuals at high risk on GABRA2
for alcohol dependence when they perceive themselves as having
high levels of family social support. In fact, in a context of strong
familial support, the increased probability of alcohol dependence
among men with the GABRA2 gene is virtually eliminated
(Pescosolido et al., 2008).
Social control
Whereas social compensation refers to avoiding low levels of
functioning as a result of an enriched environmental setting or the
absence of a stressor, the social control GE negates the genetic
expression of a diathesis as a result of social norms and structures
that limit people’s behaviour and choices (Shanahan & Boardman,
2009). Returning again to research on alcohol dependence,
Pescosolido et al. (2008) found that there was no difference in alcohol
dependence between women at a low or high risk for alcohol abuse.
Because of women’s lower alcohol tolerance, these findings can be
interpreted to demonstrate the effectiveness of social regulation in
curbing a genetic vulnerability to alcohol abuse. Similarly, Shanahan
and Hofer (2005) note that the suppressive effect of the ALDH2*2
 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
genotype in inhibiting alcoholism, coupled with higher prevalence of
this genotype among Jews, may be one reason why Jews drink less
than Caucasians. However, the authors suggest that the inhibitory
effect of ADH2*2 could be contingent on environment. For instance,
the effect of ADH2*2 in suppressing alcohol consumption was much
larger among Israeli Ashkenazi and Sephardic Jews than among
Russian Jews, the latter of whom were exposed to heavy drinking
prior to their immigration (Shanahan & Hofer, 2005).
Other examples of social control GE can be found. Providing
evidence showing that obesity has risen in the adult U.S. population
from 4% in the 1890s to almost 33% at the turn of the twenty-first
century, Martin (2008: S68) argues that the assertion from
behavioural genetics research that the intergenerational correla-
tion in weight is solely the result of genetic vulnerability does not
account for the social, technological, and economical changes
occurring over the last century, as well as the fact that underlying
genetic vulnerability could not have changed that dramatically in
such a short timeframe. Moreover, although Martin found that 74%
of the variation in body mass index could be accounted for by
genetic vulnerability, families’ behavioral and social characteristics
were also important. For example, even when adolescents had
a vulnerability to be obese, this expression was reduced when
adolescents ate three meals per day, were physically active, and
when their parents’ socioeconomic status was high.
Social enhancement
Finally, a GE enhancement interaction is one in which the
environment accentuates a ‘‘positive’’ genetic tendency (Shanahan
& Hofer, 2005). Using data from the white male DNA sample in the
National Longitudinal Study of Adolescent Health, Guo et al. (2008)
show that the protective factor of the 9R/9R genotype relative to the
Any10 R genotype depends on the percentage of adolescents in
school that have already had sex by the age of 16. For instance,
although adolescents with the 9R/9R genotype report only about
63% as many sexual partners as adolescents with Any10 R, this
protective factor is virtually lost once 50% of students have had sex
by age 16. If only 25% of students have had sex by age 16, those
adolescents with the 9R/9R genotype only report about one sexual
partner, while those with Any10 R have on average four sexual
partners. Thus we see the importance of school culture and its role
in interacting with genotype. Similarly, the protective effect of 9R/
9R is also conditional on cognitive ability. Interestingly, while
cognitive ability was not significantly associated with total number
of sexual partners, the protective effect of 9R/9R with respect to
lowers numbers of sexual partners was conditional on having
average to higher levels of cognitive ability.
In a study comparing twins and non-twin siblings, Rowe,
Jacobson, and Van den Oord (1999) report that the genetic poten-
tial for verbal intelligence is much greater among high-education
households than among low-education households. When the
average educational level of both parents exceeded high school, the
heritability of verbal intelligence was .74 among offspring
compared to only .26 when parents had less than a high school
education. The authors argue that heritability is much higher
among offspring of higher educated parents because the latter are
able to provide better proximal causes. These might include such
factors as greater parental involvement in their children’s educa-
tion or the opportunity for their children to attend a high quality
school (Shanahan et al., 2008).
Complexities of genotype–environment interactions
One important limitation in GE research has been the concep-
tualization and measurement of social context as a cross-sectional
1281
phenomenon. Although genes can be expressed at specific times
in development, a cross-sectional conceptualization and measure-
ment of social context does not capture the dynamic properties of
environment which determine the meaning of social experiences
(Shanahan & Hofer, 2005). Turner and colleagues (Turner & Avison,
2003; Turner et al., 1995) report that less than 10 percent of the
variance in indices of mental health and well-being can be accoun-
ted for by examination of life events. One reason that the magnitude
of the relationship between life events and distress is modest is
because stressful life events constitute only one dimension of
stressful experience. It may also be the case, however, that stressors
are contingent on prior, contemporaneous, and subsequent indi-
vidual experiences (Shanahan & Hofer, 2005). Insights from life
course sociology, therefore, can aid at ensuring that the dynamic
nature of the environment in GE has been accounted for.
The four types of GE – contextual triggering, social context
as a compensation, social control, and social enhancement are
also likely to differ in their meaning depending upon their
temporal qualities, synchronization across domains, and timing
in an individual’s life (Shanahan & Boardman, 2009). Childhood
and adolescence, for example, are crucial periods of risk for
mental health and illness. While such childhood traumas as
sexual abuse, physical abuse, parental death, and parental
divorce can have proximal effects on mental illness, they can
also have distal effects in that they are also significantly related
to mental disorders in middle and later adulthood (George,
2007). These childhood traumas and adversities therefore can
set trajectories of periods of mental illness throughout the life
course.
If substantial progress is to be made in GE research, it may be
important for scientists to develop fine-grained measures of social
and environmental experiences that can be precisely mapped. One
such promising approach is dynamic systems theory (DS). DS,
a mathematical language used to study how a system changes over
time, has been used to examine process-level accounts of system
behavior organization and structure (Granic & Hollenstein, 2003;
Granic & Lamey, 2002; Granic, Hollenstein, Dishion, & Patterson,
2003). Four principles central to the DS framework are the
discontinuous nature of change in developmental systems, the
emergence of novelty through self-organization processes,
changing patterns in real-time behavior and their relation to
changes in developmental patterns, and how increases in vari-
ability are representative of a less stable system and one that is
poised to change (Granic & Hollenstein, 2003). A relatively new
approach in DS studies under development in psychology is state
space grids. A state space is a topographical map that represents
many behavioral possibilities for a given system, and is a hypo-
thetical landscape of behaviors that have become stabilized over
development (Granic et al., 2003). Granic and Lamey (2002) used
state space grids to compare the diversity of mother–child inter-
actions in aggressive children exhibiting ‘‘pure’’ externalizing
behavior and those with ‘‘mixed’’ externalizing and internalizing
problems. The results revealed that although both of the ‘‘pure’’ and
‘‘mixed’’ dyads engaged in a permissive pattern (child hostile–
parent neutral/positive) during a problem-solving session, only the
mixed dyads became mutually hostile after a perturbation was
implemented. This suggests that changing interactional contexts
can reveal variability in behavioral outcomes. Furthermore,
although genetic influences likely play a role in the development of
subtypes of aggressive children, state space grids offer a strategy to
study heterogeneous, interactional processes between parents and
children, which in turn are associated with child psychopathology
development (Granic & Lamey, 2002). Thus, fine-grained
measurement of social interactions can be combined with genetic
information to estimate potential GE interactions more precisely.
1282 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
Another limitation in much GE research has been the study of
just one dimension of social context and a single indicator of
genetic risk (Grigorenko, 2005; Shanahan & Hofer, 2005). The
problem with such an approach is that it artificially minimizes the
effect of both contextual factors and genetic influence, resulting in
an oversimplification of interactions. It is likely that the majority of
mental illnesses and complex human behaviors depend on
a variety of combinations of genes, as well as multiple and alternate
interactions between environmental influences and genetic factors
(Grigorenko, 2005; Schooler, 2007; Shanahan & Hofer, 2005).
Indeed, one of the current controversies surrounding the value of
genome-wide association studies is that although more than 250
genetic loci have been identified between 2007 and 2009 in which
common genetic variants occur that are reproducibly related to
polygenic traits (Hirschhorn, 2009), only modest effect sizes of
common variants have been found, thus contributing to only
a small fraction of heritability (Goldstein, 2009; Hirschhorn, 2009;
Kraft & Hunter, 2009). Moreover, Goldstein (2009) argues that
genome-wide association studies will likely yield too many loci
resulting in the possibility of every gene in the genome be impli-
cated, with the end result being limited biological insights. Using
the term gene–environment correlation (rGE), which is the
tendency for people to experience particular social contexts that
are correlated with their genotype, Shanahan and Hofer (2005)
maintain that interpreting bivariate correlations between one
genotype and one contextual factor can be misleading given the
strong correlations that are often found between contextual vari-
ables. These correlated environmental variables co-occur and work
interactively and are more apt to provide a realistic view of context
given the complex nature through which environmental factors
moderate genetic expression. Thus, while rGE is often estimated
with a Pearson correlation coefficient to assess the strength and
direction of a linear relationship between two variables, in reality
the bivariate correlation does not address the dynamic processes
through which causal associations extend from genotype to context
to behaviour (Shanahan & Boardman, 2009).
Although the foregoing highlights some of the challenges and
limitations in previously conducted GE research, Shanahan and
Boardman (2009) have suggested ways to proceed in terms of
empirical research. Emphasizing the importance of studying social
context from a life course perspective, the authors recommend
ways to identify an entry point for purposes of analysis, and to
optimize measurement to capture complexity.
Beginning with identification of an entry point, Shanahan and
Boardman (2009) suggest the value of choosing a feature of envi-
ronmental interest, a genetic factor of interest, and/or behaviour of
interest. In evaluating environmental factors, it is important to
ensure that an environmental factor has a causal relationship with
the predicted behaviour, that there is considerable variability in
how people respond to the specific environmental factor and that
there is a plausible link between human biology and the environ-
ment. Likewise, if first identifying a genetic candidate or behaviour
of interest, life course sociologists would follow the same pattern as
those beginning with a feature of environmental interest – namely,
causality, variance, and plausibility.
Optimizing measurement in order to capture the complexity of
GE is also critical. For example, examining the interaction
between poorly measured environmental factors and well
measured genetic variables will overestimate the effects of genetic
variables while underestimating the effect of environmental
influences, thereby distorting the interaction between genotype
and environment. As Schooler (2007: 62) correctly notes, ‘‘Good
measurement requires good understanding of the processes being
measured and good understanding of such processes depends on
good basic research’’. This means that measurement of social
context should consider the dynamic properties of the environ-
ment, that longitudinal studies on the same subjects are essential,
that measures should be age-appropriate, and that social context
should be categorized as distal or proximal (Shanahan & Boardman,
2009).
Distal environmental factors include such influences as socio-
economic status, race/ethnicity and gender. These distal factors
determine the extent to which people are able to adopt protective
strategies and avoid risks that contribute to differences in
morbidity and mortality (Link & Phelan, 1995). Distal effects of
social disadvantage have profound consequences on children’s
mental health and disorder and evidence suggests that these distal
effects function through proximal parent–child relationships
(Avison, 1999; Moffitt et al., 2005). Avison (1999) argues that
studies of intergenerational transmission of mental illness that do
not consider distal social factors are more apt to overestimate the
effects of parental illness on the mental health of their children. He
also highlights the importance of careful measurement of such
environmental variables as social status, family processes, social
stressors, and psychosocial resources so that sociologists and
geneticists can more accurately estimate how much variance in the
intergenerational transmission of mental illness can be attributed
to genetic influences. According to Moffitt et al. (2005), proximal
environmental influences, which directly impact the individual
through social and physical exposures, are more ideal than distal
risk factors for studying GE interaction because they are more apt
to be eligible for pathogen status and to be included in biological
hypotheses which test their influence on neurobiological systems
that act as mediators of psychiatric symptoms.
Although the expense of collecting environmental data is very
high, reliable and precise measurement of an environmental
pathogen enhances a study’s statistical power. As sample size
depends on allele frequency, the magnitude of the interaction term,
and the strength of the relationship between an environmental
exposure and outcome, simulations have revealed 20-fold differ-
ences in sample size between unreliable versus reliable measure-
ments (Moffitt et al., 2005).
Finally, the study design of GE research is also very important.
Shanahan and Boardman (2009) insist that more effective retro-
spective measurement strategies are necessary. They argue that the
multifaceted nature of social context should be captured before the
commencement of data collection since recall bias can be particu-
larly challenging the farther back one is expected to remember.
Additionally, selection bias can be problematic when the use of
controls in case-control studies does not represent the population
from which the cases were drawn. For instance, if substantial
difference exists in the ethnicity between the cases and the
controls, differences in ethnicity will produce spurious relation-
ships with gene variants (Hunter, 2005).
Genetics and social change
Less than two decades ago, Lippman (1991, 1992) used the term
‘geneticization’ to refer to the interplay among genetics, medicine,
and culture. According to Lippman and others (Rothman, 1998;
Nelkin & Lindee, 1995; Shakespeare, 2006), as the public became
more aware of genetic research, relatively uncritical acceptance of
the promise of genetics and molecular biology to address problems
of disease, health, and ‘deviant’ behaviour resulted in changes in
cultural belief systems that stressed genetic determinism and
redefined individual identity in terms of DNA and genomics.
Although there has certainly been widespread public accep-
tance of the promise of the genetics revolution, other authors have
been somewhat more critical in their assessment of the concept of
geneticization. Hedgecoe (1998) has argued that there is little
 J.A. Seabrook, W.R. Avison / Social Science & Medicine 70 (2010) 1277–1284
evidence of the wholesale geneticization of society and suggests,
instead, that the assertion that genetics permeates society is largely
polemical. Instead, Hedgecoe (2001) suggests that a more nuanced
or ‘enlightened geneticization’ has emerged in which scientists
subtly give priority to genetic explanations of diseases such as
schizophrenia.
Others have drawn attention to the ways in which the concept of
geneticization may have considerable similarity to the process of
medicalization (Shakespeare, 2006; ten Have, 2001). In ten Have’s
view, geneticization may be a valuable cultural tool for focusing
public debate on the ethical and moral issues surrounding the use
of genetic knowledge. Shakespeare (2006) maintains that
commercial interests may see business potential in genetic diag-
nosis, gene therapy, and pharmacogenetics by providing an
incentive to promote the biological basis of human behaviors and
socially stigmatized diseases. Although the promotion of organic
and genetic causes of conditions may undermine the importance of
complex social causes of health and illness, it may work to remove
some of the blame that is often attributed to individuals with
various health conditions (Shakespeare, 2006).
More recently, Freese and Shostak (2009) have written exten-
sively on the interplay between genetics and social research. They
have made some perceptive comments with respect to genetici-
zation and the public belief in the importance of genetic causes.
They point out that a distinction can be made between genetici-
zation and genetic determinism and suggest that advances in the
study of gene–environment interactions and epigenetics may lead
social scientists to reconsider the concept of geneticization.
Freese and Shostak also argue that the public’s understanding of
genetics is somewhat more sophisticated than some observers have
suggested. Indeed, Shostak, Conrad, and Horwitz (2008) have
argued that the public opinion importantly affects the way in which
findings about genetic influences are interpreted. In a similar vein,
Phelan (2005) has shown that there is a complicated relationship
between genetic attributions of mental illness and stigma that is
difficult to disentangle.
All of these considerations suggest that the social and cultural
consequences of genetic research are likely to produce social and
cultural changes, especially in public beliefs and in discourse about
social and public health policy. Thus, advances in genetic research
seem destined to provide social scientists with a rich source of
research topics that range from epigenetics and gene–environment
interactions to the nature of geneticization and its consequences for
cultural belief systems.
Summary and conclusions
Genotype–environment interaction (GE) refers to situations in
which genetic effects connected to a phenotype are dependent
upon variability in the environment, or when genes modify an
organism’s sensitivity to particular environmental features. The
study of GE requires information on both genetic vulnerability as
well as environmental factors. Genetic vulnerability can be inferred
from direct analysis of DNA sequence, family history, and pheno-
type. Environmental factors are typically measured using self-
report through such methods as interviews, questionnaires, direct
measurement of participants, or records.
A triggering interaction occurs when a genetic vulnerability is
expressed in the presence of a stressor or trigger. Whereas social
compensation refers to avoiding low levels of functioning as
a result of an enriched environmental setting or the absence of
a stressor, the social control GE negates the genetic expression of
a diathesis as a result of social norms and structures that limit
people’s behaviour and choices. An enhancement interaction is one
in which the environment accentuates a ‘‘positive’’ genetic
1283
tendency. These four types of genotype–environment interaction
are likely to differ in their meaning depending upon their temporal
qualities, synchronization across domains, and timing in an indi-
vidual’s life.
Although there is likely a genetically heritable component to
most outcomes of interest to social scientists, sociologists can
uniquely show how genomic causation is a product of social
conditions (Freese, 2008). Unlike geneticists who primarily study
the main effects of genes, sociologists can benefit from genetic
information by investigating how social context and genotype
depend on one another. By doing so, we believe that sociologists
will develop a more thorough understanding of social context by
knowledge of its mediation and moderation effects of genetic
vulnerability on various health outcomes. Isolating genetically
distinct groups will also aid in understanding which social contexts
matter for those at high risk (Shanahan et al., 2008). Finally,
insights from life course sociology can aid at ensuring that the
dynamic nature of the environment in GE has been accounted for.
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