Sie sind auf Seite 1von 44

Behavioral Genetics

What is behavioral genetics?


[text provided by Joseph McInerney]

Sir Francis Galton (1822-1911) was the first scientist to study heredity and human behavior systematically.
The term "genetics" did not even appear until 1909, only 2 years before Galton's death. With or without a
formal name, the study of heredity always has been, at its core, the study of biological variation. Human
behavioral genetics, a relatively new field, seeks to understand both the genetic and environmental
contributions to individual variations in human behavior. This is not an easy task, for the following reasons.
• It often is difficult to define the behavior in question. Intelligence is a classic example. Is intelligence
the ability to solve a certain type of problem? The ability to make one's way successfully in the
world? The ability to score well on an IQ test? During the late summer of 1999, a Princeton
molecular biologist published the results of impressive research in which he enhanced the ability of
mice to learn by inserting a gene that codes for a protein in brain cells known to be associated with
memory. Because the experimental animals performed better than controls on a series of traditional
tests of learning, the press dubbed this gene "the smart gene" and the "IQ gene," as if improved
memory were the central, or even sole, criterion for defining intelligence. In reality, there is no
universal agreement on the definition of intelligence, even among those who study it for a living.
• Having established a definition for research purposes, the investigator still must measure the
behavior with acceptable degrees of validity and reliability. That is especially difficult for basic
personality traits such as shyness or assertiveness, which are the subject of much current research.
Sometimes there is an interesting conflation of definition and measurement, as in the case of IQ tests,
where the test score itself has come to define the trait it measures. This is a bit like using batting
averages to define hitting prowess in baseball. A high average may indicate ability, but it does not
define the essence of the trait.
• Behaviors, like all complex traits, involve multiple genes, a reality that complicates the search for
genetic contributions.
• As with much other research in genetics, studies of genes and behavior require analysis of families
and populations for comparison of those who have the trait in question with those who do not. The
result often is a statement of "heritability," a statistical construct that estimates the amount of
variation in a population that is attributable to genetic factors. The explanatory power of heritability
figures is limited, however, applying only to the population studied and only to the environment in
place at the time the study was conducted. If the population or the environment changes, the
heritability most likely will change as well. Most important, heritability statements provide no basis
for predictions about the expression of the trait in question in any given individual.

What indications are there that behavior has a biological basis?


[text provided by Joseph McInerney]

• Behavior often is species specific. A chickadee, for example, carries one sunflower seed at a time
from a feeder to a nearby branch, secures the seed to the branch between its feet, pecks it open, eats
the contents, and repeats the process. Finches, in contrast, stay at the feeder for long periods, opening
large numbers of seeds with their thick beaks. Some mating behaviors also are species specific.
Prairie chickens, native to the upper Midwest, conduct an elaborate mating ritual, a sort of line dance
for birds, with spread wings and synchronized group movements. Some behaviors are so
characteristic that biologists use them to help differentiate between closely related species.
• Behaviors often breed true. We can reproduce behaviors in successive generations of organisms.
Consider the instinctive retrieval behavior of a yellow Labrador or the herding posture of a border
collie.
• Behaviors change in response to alterations in biological structures or processes. For example, a
brain injury can turn a polite, mild-mannered person into a foul-mouthed, aggressive boor, and we
routinely modify the behavioral manifestations of mental illnesses with drugs that alter brain
chemistry. More recently, geneticists have created or extinguished specific mouse behaviors—
ranging from nurturing of pups to continuous circling in a strain called "twirler"— by inserting or
disabling specific genes.
• In humans, some behaviors run in families. For example, there is a clear familial aggregation of
mental illness.
• Behavior has an evolutionary history that persists across related species. Chimpanzees are our
closest relatives, separated from us by a mere 2 percent difference in DNA sequence. We and they
share behaviors that are characteristic of highly social primates, including nurturing, cooperation,
altruism, and even some facial expressions. Genes are evolutionary glue, binding all of life in a
single history that dates back some 3.5 billion years. Conserved behaviors are part of that history,
which is written in the language of nature's universal information molecule—DNA.

How is behavioral genetics studied?


[text provided by Joseph McInerney]

Traditional research strategies in behavioral genetics include studies of twins and adoptees, techniques
designed to sort biological from environmental influences. More recently, investigators have added the
search for pieces of DNA associated with particular behaviors, an approach that has been most productive to
date in identifying potential locations for genes associated with major mental illnesses such as schizophrenia
and bipolar disorder. Yet even here there have been no major breakthroughs, no clearly identified genes that
geneticists can tie to disease. The search for genes associated with characteristics such as sexual preference
and basic personality traits has been even more frustrating.
Genetics and molecular biology have provided some significant insights into behaviors associated with
inherited disorders. For example, we know that an extra chromosome 21 is associated with the mental
retardation that accompanies Down's syndrome, although the processes that disrupt brain function are not
yet clear. We also know the steps from gene to effect for a number of single-gene disorders that result in
mental retardation, including phenylketonuria (PKU), a treatable metabolic disorder for which all newborns
in the United States are tested.
In general, it is easier to discern the relationship between biology and behavior for chromosomal and single-
gene disorders than for common, complex behaviors that are of considerable interest to specialist and
nonspecialist alike. So the former are at the more informative end of a sliding scale of certainty with respect
to our understanding of human behavior. At the other end of the scale are the hard-to-define personality
traits, while somewhere in between are traits such as schizophrenia and bipolar disorder—organic diseases
whose biological roots are undeniable yet unknown and whose unpredictable onset teaches us about the
importance of environmental contributions, even as it reminds us of our ignorance.

What implications does behavioral genetics research have for society?


[text provided by Joseph McInerney and Mark Rothstein]

Researchers in the field of behavioral genetics have asserted claims for a genetic basis of numerous physical
behaviors, including homosexuality, aggression, impulsivity, and nurturing. A growing scientific and popular
focus on genes and behavior has contributed to a resurgence of behavioral genetic determinism—the belief
that genetics is the major factor in determining behavior.
Are behaviors inbred, written indelibly in our genes as immutable biological imperatives, or is the
environment more important in shaping our thoughts and actions? Such questions cycle through society
repeatedly, forming the public nexus of the "nature vs. nurture controversy," a strange locution to biologists,
who recognize that behaviors exist only in the context of environmental influence. Nonetheless, the debate
flares anew every few years, reigniting in response to genetic analyses of traits such as intelligence,
criminality, or homosexuality, characteristics freighted with social, political, and legal meaning.
What social consequences would genetic diagnoses of such traits as intelligence, criminality, or
homosexuality have on society? What effect would the discovery of a behavioral trait associated with
increased criminal activity have on our legal system? If we find a "gay gene," will it mean greater or lesser
tolerance? Will it lead to proposals that those affected by the "disorder" should undergo treatment to be
"cured" and that measures should be taken to prevent the birth of other individuals so afflicted?
There are several scientific obstacles to correlating genotype (an individual's genetic endowment) and
behavior. One problem is in defining a specific endpoint that characterizes a condition, be it schizophrenia or
intelligence. Another problem is in identifying and excluding other possible causes of the condition, thereby
permitting a determination of the significance of a supposed correlation. Much current research on genes and
behavior also engenders very strong feelings because of the potential social and political consequences of
accepting these supposed truths. Thus, more than any other aspect of genetics, discoveries in behavioral
genetics should not be viewed as irrefutable until there has been substantial scientific corroboration.

How do genes influence behavior?


No single gene determines a particular behavior. Behaviors are complex traits involving multiple genes that
are affected by a variety of other factors. This fact often gets overlooked in media reports hyping scientific
breakthroughs on gene function, and, unfortunately, this can be very misleading to the public.
For example, a study published in 1999 claimed that overexpression of a particular gene in mice led to
enhanced learning capacity. The popular press referred to this gene as "the learning gene" or the "smart
gene." What the press didn't mention was that the learning enhancements observed in this study were short-
term, lasting only a few hours to a few days in some cases.
Dubbing a gene as a "smart gene" gives the public a false impression of how much scientists really know
about the genetics of a complex trait like intelligence. Once news of the "smart gene" reaches the public,
suddenly there is talk about designer babies and the potential of genetically engineering embryos to have
intelligence and other desirable traits, when in reality the path from genes to proteins to development of a
particular trait is still a mystery.
With disorders, behaviors, or any physical trait, genes are just a part of the story, because a variety of genetic
and environmental factors are involved in the development of any trait. Having a genetic variant doesn't
necessarily mean that a particular trait will develop. The presence of certain genetic factors can enhance or
repress other genetic factors. Genes are turned on and off, and other factors may be keeping a gene from
being turned "on." In addition, the protein encoded by a gene can be modified in ways that can affect its
ability to carry out its normal cellular function.
Genetic factors also can influence the role of certain environmental factors in the development of a
particular trait. For example, a person may have a genetic variant that is know to increase his or her risk for
developing emphysema from smoking, an environmental factor. If that person never smokes, then
emphysema will not develop.

Where can I learn more about the genetics of different behavioral traits?
Online Mendelian Inheritance in Man (OMIM) is a large, searchable, up-to-date database of human genes,
genetic traits, and disorders. Each OMIM record contains bibliographic references and a summary of the
scientific literature describing what is known about a particular gene, trait, or disorder. The following
behavioral traits are included in OMIM. The six-digit number MIM number is used to uniquely identify each
record.
• Hand skill, relative (handedness): (139900)
• Hand clasping pattern: (139800)
• Arm folding preference: (107850)
• Ears, ability to move: (129100)
• Tongue curling, folding, or rolling: (189300)
• Musical perfect pitch: (159300)
• Novelty seeking personality trait: (601696)
• Stuttering: (184450)
• Tobacco addiction: (188890)
• Alcoholism: (103780)
• Homosexuality: (306995)
You also may want to search OMIM for behavioral traits not included in the list above. For step-by-step
instructions, see our OMIM Search Tutorial. For more detailed information, review the Help and FAQs
pages. For information on other databases of human genes, see the Gene and Protein Database Guide
available through Gene Gateway.

Behavioral Genetics Links


General Information
• University of Pennsylvania Behavioral Genetics Laboratory
• Virginia Institute for Psychiatric and Behavioral Genetics
o Behavioral Genetics A downloadable book and special supplement from AAAS and the
Hastings Center
o Genetics and Human Behaviour - Health feature from the BBC in the U.K.
o DNA & Behavior: Is Our Fate in Our Genes? - An overview of the science and social
implications of research in behavior genetics. From The DNA Files, last updated October
2001.
o Personality Traits: Nature and Nurture - Audio file of a radio program from SoundVision
Productions. From The DNA Files.
o Genes, Environment, and Human Behavior -- Educational module targeted to teachers
includes five student activities and extensive background information on the methods and
assumptions of behavioral genetics (2000).
Articles
o Toward Behavioral Genomics - Article from Science (February 2001).
o Learning About Addiction From the Genome - Article from Nature (February 2001).
o Caution urged for brain research on violence--from CNN (July 28, 2000)
o Judging Molecular Biology of Murder, Addictive Disorders, and Dementia - Meeting
proceedings, Human Genome News 11(1-2)
o Genes and Behavior: A Complex Relationship - Article by Joseph D. McInerney, Judicature
83, 112 (November-December 1999).
o The Impact of Behavioral Genetics on the Law and the Courts - Article by Mark A. Rothstein,
Judicature 83, 116 (November-December 1999).
o Recent Developments in Human Behavioral Genetics: Past Accomplishments and Future
Directions - Am. J. Hum. Genet. 60, 1265 (1997 ASHG Statement).
Associations
o Behavior Genetics Association
o Society of Behavioral Medicine
o International Society of Behavioral Medicine
o International Society for the Study of Behavioural Development
Books
• Behavioral Genetics in the Postgenomic Era, by Robert Plomin, John C. Defries, Ian Craig, and
Peter McGuffin, eds., and Jerome Kagan. 2002, 608 pp.
• Behavioral Genetics: The Clash of Culture and Biology by Ronald A. Carson and Mark A. Rothstein. 1999,
224 pp.
• Behavioral Genetics by Robert Plomin (Editor), John C. Defries, Gerald E. McClearn, Peter McGuffin. 2000, 4th
edition, 449 pp.
• Living With Our Genes: Why They Matter More Than You Think by Dean H. Hamer and Peter Copeland.
1999, 368 pp.
• Genetics of Mental Disorders: A Guide for Students, Clinicians, and Researchers by S.V. Faraone, M.T.
Tsuang, and D.W. Tsuang. Guilford Press (1999), 272 pp.

Behavioural genetics
From Wikipedia, the free encyclopedia
Behavioural genetics is the field of biology that studies the role of genetics in animal
behaviour. The field is an overlap of genetics, ethology and psychology (particularly
evolutionary psychology). Classically, behavioural geneticists have studied the heritability of
behavioural traits.

Francis Galton
In 1869, Francis Galton published the first empirical work in human behavioural genetics,
Hereditary Genius. Here, Galton intended to demonstrate that "a man's natural abilities are
derived by inheritance, under exactly the same limitations as are the form and physical
features of the whole organic world." Like most seminal work, he overstated his conclusions.
His was a family study on the inheritance of giftedness and talent. Galton was aware that
resemblance among familial relatives can be a function of both shared genes and shared
environments. Contemporary behavioural genetics studies special populations—in human
research, twins and adoptees and in animal research, specially bred strains and lines—to
separate genetic from environmental effects.
The initial impetus behind behavioural genetic research was to demonstrate that there were
indeed genetic influences on behaviour. In psychology, this phase lasted for the first half of the
20th century largely because of the overwhelming influence of behaviourism in the field. Later
behavioural genetic research focused on quantitative methods, and today there is a large
emphasis on applying techniques from molecular genetics to isolate individual genes that
influence behaviour. Currently, the largest branch of behavioural genetics is psychiatric
genetics which studies phenotypes such as schizophrenia, bipolar disorder, and alcoholism.
Recent trends in behaviour genetics has indicated an additional focus toward researching the
heritability of human characteristics typically studied in developmental psychology. For
instance, a major focus in developmental psychology has been to characterize the influence of
parenting styles of children. However, in most studies, genes are a confounding variable.
Because children share 50% of their genes with each parent, any observed effects of
parenting styles could be effects of having many of the same genes as a parent (e.g. harsh
aggressive parenting styles have been found to correlate with similar aggressive child
characteristics- is it the parenting or the genes?). Thus, behaviour genetics research is
currently undertaking to distinguish the effects of the family environment from the effects of
genes. This branch of behaviour genetics research is becoming more closely associated with
mainstream developmental psychology and the sub-field of developmental psychopathology
as it shifts its focus to the heritability of such factors as emotional self-control, attachment,
social functioning, aggressiveness etc..

References
 Carey, G. (2003) Human Genetics for the Social Sciences. Thousand Oaks, CA: Sage
Publications. [1]
 DeFries, J. C., McGuffin, P., McClearn, G. E., Plomin, R. (2000) Behavioral Genetics 4th
ED. W H Freeman & Co.
 Scott, J.P. and Fuller, J.L. (1965) Genetics and the Social Behavior of the Dog. University
of Chicago Press.
 Weiner, J. (1999) Time, Love, Memory : A Great Biologist and His Quest for the Origins of
Behavior. Knopf

Heredity Versus Environment: Twin, Adoption, and


Family Studies
Avi G. Haimowitz
Rochester Institute of Technology

A plethora of internal and external variables combine to create individual personalities,


behaviors, and psychopathologies supposedly unique to every human being. The argument of
genetic makeup versus environmental influences, however, has researchers working to
determine what really shapes us. Some say genotypes control how people think, feel, and
behave. Others believe it is the environment alone that is responsible for molding humans
into who they are. There is much unknown in this field, but the perusal and review of twin,
adoption, and family studies is a significant stepping stone in better understanding this topic.
Even today, the sole sculptor of human personality, behavior, and psychopathology remains
unknown; modern research indicates that a combination of biology and environment
constructs us all.

Studying how genes and our surroundings may or may not form the personalities, behaviors,
and psychopathologies of human beings is probably the most obvious way to approach the
argument of heredity versus the environment. It is often the tendency of humans to polarize
themselves and choose a specific side when a question like this is introduced. Despite this
common inclination, it is probably not the wisest method of deciphering the basis for the three
main variables that construct human beings; who is to say that a single factor is the source of
all our differences? It is more logical to examine the distinctions between biology and the
environment, and to figure out in what ways the two may intertwine to form the singular
entities that are our personas.
Because of this palpable meshing together of two variables, it is then plausible to establish what aspects of
personality are linked to genes, and what aspects most likely exist due to environmental leverage. It has been
said that heredity and the environment both contribute 50% to the makeup of an entire human being, but
much debate exists about specific percentages and the existence of higher percentages of one factor in
different age groups than others (Petrill et al., 2004). Some tactics that have been used in attempts to figure
out the many characteristics of human beings include adoption studies, family studies, and twin studies. A
review of different topics in human behavior and psychopathology, from human attitudes to the mental
disorder schizophrenia, is a beneficial way to broadly explore the argument. Loose conclusions may be
derived from these studies, but much more investigation needs to be done, both in creating new research
projects and in analyzing previous methodologies and results, before this argument has any potential of
being resolved.
Twin Studies
Twin studies are a vastly important tool in dissecting the nature versus nurture argument.
Identical twins, or monozygotic twins, are siblings whose genotypes are duplicates of each
other. They are most likely the best indicator of whether biology affects traits and
psychopathology in human beings. For example, if one twin has dark hair, then the other twin
has dark hair as well; this concept of identical genes would ideally distribute itself toward the
phenotypes of behavior and personality of identical twins (Plomin, DeFries, McClearn, &
Rutter, 1997).
Fraternal twins, or dizygotic twins, share exactly half their genes with each other. They are not as optimal as
identical twins for deciphering the degrees of genetic influence, but they are a very good basis for
comparison for identical twins. Fraternal twins are similar to first-degree relatives, except they are sure to
share the exact same age, as do identical twins. Twin studies usually rely on samples of identical and
fraternal twins; if biology has a greater hand than environment, then identical twins should behave or
possess psychopathology similar to each other more so than fraternal twins (Plomin et al., 1997). This is an
example of the heritability coefficient coming into play: the estimate of how much someone's specific trait in
comparison to other people's traits under one characteristic is attributable to genes (Olson, Vernon, Harris,
Aitken, & Jang, 2001). This coefficient ought to be higher in identical twins than in fraternal twins. Then
again, it is possible for identical twins to express different phenotypes (external expression of genetics) for
the same genotypes (genetic makeup). This is representative of their nonshared environments; even though
identical twins possess the same genetic makeup, they may go through different experiences throughout
their lives that shape their personality, behavior, and psychopathology in ways that make them unique
relative to each other (Hughes et al., 2005).
Attitudes
One particular study sought to determine the heritability of attitudes among twins, as well as
the genetic variables, such as intelligence, that could affect attitudes among pairs of twins. A
questionnaire was provided to the participants, in which they were asked to rate their
personality traits, physical abilities, and physical attractiveness. They were also asked to note
their academic achievements (Olson et al., 2001).
The results of the study showed that differences between attitudes of the participants were at least partially
correlated to genetic factors. It also showed that attitudes related to self-reported perspectives or to activities
were often correlated. For instance, the survey asked subjects to rate themselves on the trait of sociability.
That trait was correlated with 5 out of 6 attitude factors subjects had toward sociability. Attitudes toward
athleticism highly correlated with findings on self-reported athletic abilities.
The causal model was expressly supported in these findings, because athletic skill (the mediator), for
example, seemed to be linked with attitudes toward athleticism. Of course, this model is not without its
problems: one cannot assume that X is the cause of Y in every single situation. Case in point: attitudes
toward leadership seemed to be related to high self-ratings of physical attractiveness, sociability, and
aggressiveness. Because of these numerous factors, it is still not possible to always accurately assume direct,
singular relations between genetic traits and attitudes (Olson et al., 2001).
Interestingly, nonshared environment experiences between pairs of twins seemed to be the strongest cause of
attitude variances, overshadowing genetic predispositions as well as shared environment experiences (Olson
et al., 2001). Nonshared environment is a term used to refer to something in the environment that directly
affects one twin but does not impact the other at all (Van den Oord, Boomsma, & Verhulst, 2000). The study
did indicate that some nonshared environment experiences were very much connected to attitudes and self-
reports of physical characteristics and intelligence (Olson et al.). This study leads to further questions about
nonshared environments: why is it that different environments have so much effect on twins' behaviors and
personalities? And why are some attitudes apparently rooted in genetics, while others are not? As previously
stated, it is clear that much more research must be conducted on twins before any solid answers can be
found.
Theory of Mind
Mental states are made up of beliefs, intents, and desires. A child usually acquires a theory of
mind, which is the understanding that objects and situations can be falsely interpreted or
represented by their own mental states, by the age of four. The question for research here is:
between biology and environment, what accounts the most for the differences in how much
individual children vary in false-belief comprehension? It has been shown that children from
large families experience accelerated acquisition of theory of mind, but deaf children born to
hearing adults experience decelerated acquisition of theory of mind. This points to cultural
influences, and thus, to environmental influences. Inversely, children with the highly
transmissible disorder autism have also been found to possess impaired theory of minds, as
do girls with the chromosomal disorder Turner's syndrome. This points to genetic influences
(Hughes et al., 2005).
A study was created to investigate this topic, using both identical and fraternal twins. It measured
socioeconomic status, verbal ability, and more importantly, the theory of mind of each participant. The first
part of the test given to the subjects contained questions that examined their abilities to connect a mistaken
belief about a character in stories provided. The second part tested the subjects' abilities to make inferences
and their tendencies to attribute a false belief to a belief about characters within the provided stories (Hughes
et al., 2005).
Most of the variation between theory of minds of the pairs of twins resulted from nonshared environments.
The percentages of influence in decreasing order were attributed to shared environments, verbal abilities,
and then genetics. Families with twins are often highly charged with competitiveness, and the more the
families discuss conflicts, the more accelerated theory of minds tend to be. This emphasis on environmental
influences does outweigh genetic influences on the development of theory of minds in children, but it does
not outweigh genes' existence and role entirely (Hughes et al., 2005).
Genotype-Environment Interaction
A study was performed using a portion of the identical twins that participated in the Swedish
Adoption/Twin Study of Aging (Bergeman, Plomin, McClearn, Pederson, & Friberg, 1988). These
researchers were interested in the relations between phenotypes and genotypes of twins
reared apart, which was the experience of all the participants in the Swedish study. One twin's
phenotype should be the biggest indicator of the other twin's genotype, because the study
examined the experiences of pairs of twins who had been separated their whole lives
(Bergeman et al., 1988). If anything was similar about the pair, it ought to be correlated to
their shared genes, because they certainly did not share the same environment.
The study was designed to measure personality traits of extraversion and neuroticism among the twin pairs,
traits of impulsivity and monotony avoidance, and family environment and socioeconomic status. Using this
information, and taking into consideration that a study like this had never been done before, the researchers
came to three different conclusions in regards to genotype-environment interaction. Genotype-environment
interaction is a term used by many researchers in relation to twin studies, referring to the potential for people
with different genetic makeup to respond differently toward the same external situation (Bergeman et al.,
1988). This is an important concept in twin studies because genotype-environment interaction can also be
applied to how people with the same genotypes might respond to the same environment.
One particular genotype-environment, labeled Type I, indicates that the environment has more of an impact
on individuals with a genotype for low scores on a specific personality trait. Individuals who had low
genotypes for extraversion would also score low on extraversion if they perceived their families as high in
control or organization, as opposed to individuals who had high genotypes for extraversion. The latter
individuals expressed that high extraversion trait regardless of the perceived level of control or organization
of their respective families (Bergeman et al., 1988).
Type II genotype-environment interaction was essentially the opposite of Type I. Individuals who have
genotypes that cause them to score high on a specific trait were affected by their environments, while
individuals with genotypes that caused them to score lower were not affected by their environments. For
example, an individual who possesses a high genotype for impulsivity will have that trait increased if she or
he lives in a conflict-filled environment (Bergeman et al., 1988).
Finally, Type III genotype-environment interaction was a category only derived from the researchers' study
on mice; it was not derived from the Swedish twins. Type III genotype-environment interaction occurs when
the environment influences individuals with genotypes that cause them to score higher on traits as well as
individuals who have genotypes that cause them to score lower on traits. An environment high in parental
control, for example, will restrict the expression of a genotype, while a permissive environment will allow a
genotype to emerge as a strong phenotype (Bergeman et al., 1988).
Adoption Studies
A very significant portion of studying heredity and environmental effects on human traits and
psychopathology is devoted to adoption studies. Adoption studies are important because they
include two sets of factors that may account for differences in behavior, personality, and
psychopathology: biological parents and environmental parents. Of course, any links between
the biological parents and the child that is given away is usually explained by genetics, and
any links between the adoptive, or environmental parents, to the adopted child is usually
attributed to environment (Plomin et al., 1997).
Schizophrenia
The first adoption study performed on schizophrenia showed that family environment
contributes little to a child's risk for a disorder such as schizophrenia. This study was
performed through interviews of adopted-away children of biological mothers who suffered
from schizophrenia, and interviews of adopted children whose birth parents did not suffer
from any mental disorders. Several of the adopted away children of schizophrenic mothers
suffered from schizophrenia themselves, while the adoptees whose parents didn't have
schizophrenia also did not have schizophrenia themselves. This supports the theory that it
doesn't matter what specific environment a child is raised in; if its parent or parents suffer
from a mental disorder, the risk for suffering from the same disorder will be equal regardless
of if the child was raised with its biological parents or with its adoptive parents (Plomin et al.,
1997).
Another adoption study showed that a high percentage of proband adoptees, or adoptees whose birth parents
had schizophrenia, also suffered from chronic schizophrenia or displayed schizophrenic-like behaviors.
None of the control adoptees, or adoptees whose biological parents did not suffer from schizophrenia, had
schizophrenia themselves, and only a small percentage of them displayed schizophrenic-type symptoms. A
current study is also supporting these results, because a significant percentage of proband adoptees displayed
some psychotic symptoms, while only a small percentage of control adoptees displayed these types of
symptoms. This study also showed that the adoptees whose biological parents suffered from schizophrenia
had a higher likelihood of schizophrenia or other related disorders when the adoptive families were low
functioning. This speaks volumes for the genotype-environment interaction theory, because of the
expression of a genotype being linked to the type of rearing environment (Plomin et al., 1997).
Despite all of this information, it is still very much uncharted territory as to what explicitly causes
schizophrenia, and how it may or may not be expressed among adopted children. One of the main
difficulties subsists in the deficiency of knowledge on a gene that carries the disorder schizophrenia. It is
unknown whether such a gene exists, and doubly unknown to what degree this possible gene influences
these types of adoption studies (Loehlin, Willerman, & Horn, 1988).
Infant Shyness
An adoption study was conducted to disentangle the reasons behind why some infants are
open and responsive to attention right away, some take time to open up, and still yet, some
others are fearful and withdrawn. It is difficult to tell whether babies are shy because their
mothers are shy and thus do not take them out very much, or because the shy mothers pass
down their shyness traits. Measures of this study attempted to clarify the relationship
between the infants and adoptive and biological parental shyness, parental sociability, and
parental introversion-extraversion (Daniels & Plomin, 1985).
Adoptive parents were given questionnaires that asked them to rate their infants' shyness levels, and then to
rate themselves on the traits listed previously. It must be noted that the self-reported ratings of the biological
were performed before the birth of the infants, and the scoring of the infants' shyness were performed by the
adoptive parents when the babies were two years old. The results showed that in nonadoptive families, the
parents who reported high rates of shyness, low rates of sociability, and high rates of introversion also had
shy infants. This was also seen in adoptive families whose parents rated similarly, indicating that a
combination of home environment and genetics must come into play. One significant conclusion was made
in this study that was based on the fact that biological mothers rated high in shyness, and their adopted-away
babies were also shy. This strengthens the possibility of a genetic link overshadowing family environment,
but of course further research must be done (Daniels & Plomin, 1985).
Children's Adjustment to Divorce
A study was performed to investigate the possible connection between genetic factors and
children's adjustment to parental divorce. Interviews, questionnaires, and standardized tests
were administered to probands and their parents. Interviewers also rated the social behavior
of the probands at the time of their interviews (O'Connor, Plomin, Caspi, & DeFries, 2000).
Measures of the study included age of the probands at the time of separation and/ or divorce, self concept
(self-esteem) of the probands, social ability, academic ability, behavioral and/or emotional problems,
loneliness, and substance use. Of course, the type of adjustment processes that children from biological
families went through could be attributed to biology or environment, while adjustment for probands would
have had to be linked to environmental processes. The results showed that probands' adjustment to divorce
in terms of social ability, self-concept, and academic accomplishments were at least partially genetically
influenced, but that their psychopathology could be attributed to environmental factors (O'Connor et al.,
2000).
Antisocial Personality Disorder
Many studies have been composed to attempt to discover if children who are at risk for
antisocial personality disorder are more likely to develop symptoms in an adoptive family
environment, or if that environment will protect them from the disorder's development. It has
been shown through these various studies that antisocial personality disorder is, indeed, more
likely to present itself in adoptees that already have biological risk factors (at least one
biological parent had a background of criminality or antisocial personality disorder). The
adoptees that are born with no risk of developing the disorder do not usually develop it while
living in an adoptive environment. The adoptive family environment combining with the
preexisting biological risk seems to make antisocial personality disorder quite prevalent
among adoptees (Roth & Finley, 1998).
It was also found that adoptees experienced an even higher risk for antisocial personality disorder if both
their biological parents and their adoptive parents came from criminal backgrounds. However,
methodological problems exist with these kinds of studies because there are so many factors to consider. For
example, it has yet to be clarified whether this disorder is more likely to be carried through the biological
mother, or the biological father. Most of these adoption studies were conducted using only information from
the biological mother, and not the other half of the equation: the biological father. Information is also vague
regarding a criminal background as an instant checkmark for antisocial personality disorder in biological and
adoptive parents. It is often assumed that the existence of a biological parent's criminal background
immediately means that that parent has antisocial personality disorder, and also has definitely passed it down
to the adopted-away offspring. The problem is, it also cannot be assumed that the lack of a criminal
background points to a lack of the disorder itself (Roth & Finley, 1998).
Interpreting the results of adoption studies is very difficult for the aforementioned reasons, and it is also
challenging to make valid conclusions due to the fact that adoptees already display a higher rate of antisocial
personality disorder as compared to the general population. Ironically, the adoptive family environment is
often better in terms of care, education, stability, and health in comparison to families in the rest of the
population. Adopted-away children, however, are often placed in adoptive family environments similar to
their original, biological family environments. Genetic factors are thus "simulated" when the adoptive
family environment is similar to the biological environment (Rhee & Waldman, 2002). With all of these
discrepancies and uncertainties, it is undoubtedly a complex process to try to figure out what factor has the
most effect on the development of antisocial personality disorder.
Family Studies
Family studies are not as oft cited as twin and adoption studies, but nonetheless they are still
a valid and important piece in the puzzle of heredity versus the environment. Family studies
are mostly used to identify the degree of risk of relatives developing mental disorders that
other family members suffer from. Case-control family studies are employed, including
estimates of relative risk and population relative risk of a mental illness. Relative risk
compares how large the likelihood is that one relative of a person with a mental disorder will
also develop the disorder than the relative of a person with no mental disorder. Population
relative risk calculates approximately how much risk there is that the relatives of a person
suffering from mental illness will also be affected as opposed to relatives of a person who
does not suffer from any mental illness (Jang, 2005).
These kinds of studies are most often used to determine the risk of passing down mental disorders to
offspring within families. It must also be taken into consideration that these types of studies do not tangibly
express outside factors, such as family environment and culture. These studies are performed using
molecular genetic studies, where DNA is extracted from participants' blood samples and the correlation
between the DNA and the observed behavior is projected. The most common molecular genetic study is
called linkage analysis. This type of study tries to locate a specific gene on a chromosome in the human
body. If a gene for a particular mental illness is being searched for, researchers identify an already-
recognized gene on the chromosome and label that as a marker. That marker's location, and the location of
the actual diseased gene, is very important: the closer the two are, the higher the likelihood that the disease
and marker genes will be passed on together, or linked together (Jang, 2005).
Bipolar Disorder and Schizophrenia
Bipolar disorder and schizophrenia share many similarities, from the average age of onset to
the courses of the illnesses. Family studies, including molecular genetic studies, were
conducted to decipher how much overlap exists for the genetic risks for both these disorders
(Berrettini, 2000).
Studies carried out on bipolar disorder showed that first-degree relatives of people with bipolar disorder
suffered a higher risk for some related mental disorders including bipolar I disorder, bipolar II disorder,
schizoaffective disorder, and recurrent unipolar disorder. However, there was not an increased risk for
schizophrenia itself (Berrettini, 2000).
Studies carried out using first-degree relatives of people who suffered from schizophrenia showed similar
results. Those relatives were at higher risk for schizophrenia, schizoaffective disorder, and recurrent unipolar
disorder, but not for bipolar disorder. Interestingly enough, first-degree relatives of people who suffered
from both bipolar disorder and schizophrenia did experience higher risk for schizoaffective and recurrent
unipolar disorders. This indicates an overlap and suggests a possible partial overlap in familial risk for
bipolar disorder and schizophrenia (Berrettini, 2000). A larger-scaled study needs to be conducted before
this can be fully determined.
Suicide
Suicidal behavior is increased among relatives of suicide victims, but the singular cause of
this is unclear. A study was conducted to figure out if the cause for this increased risky
behavior was due to family heritability. It compared relatives of suicide victims with relatives
of demographically similar adolescents; both groups were examined for Axis I and II disorders,
histories of aggression, and histories of suicidal behavior (Brent, Bridge, Johnson, & Connolly,
1996).
First-degree relatives of suicide victims, also called suicide probands, had a greater likelihood of suicide
attempts, but it also has to be taken into consideration that they also had an increased risk of other
psychological disorders. The suicide probands who had high rates of aggression also had higher risk for
attempts at suicide. The increased risk for suicidal behavior in suicide probands, it was concluded from this
study, is probably a trait independent of Axis I and II psychiatric disorders (Brent et al., 1996).
Eating Disorders
Anorexia nervosa and bulimia often exist comorbid with other psychiatric disorders, such as
depression, anxiety, and obsessive-compulsive disorder. A study was performed to attempt to
figure out if eating disorders were comorbid through family genetics. Interviews of relatives of
eating disorder victims and best-estimate conclusions were conducted throughout the study.
Interviews of a control group, or a group of relatives whose family members did not suffer
from any eating disorders, were also carried out. The interviews determined whether the
eating disorder probands themselves had eating disorders, and whether they suffered from
mood, anxiety, substance abuse, and specific personality disorders (Lilenfield et al., 1998).
This study's results showed that eating disorder probands experienced a higher risk of eating disorders,
major depressive disorder, and obsessive-compulsive disorder. Substance abuse disorder was placed at
higher risk for bulimia probands than for anorexia probands, and obsessive-compulsive disorder was placed
at higher risk for anorexia probands than bulimia probands (Lilenfield et al., 1998).
It was concluded that there was definitely a link between people who suffered from eating disorders and
their relatives' risk for suffering from the same problems. A plausible connection between the probands' risk
for major depressive disorder, substance abuse disorder, and obsessive-compulsive disorder, however, could
not be proven. The only theory that could be somewhat supported was that the traits for obsessive-
compulsive disorder could cause a familial risk for anorexia (Lilenfield et al., 1998).
Conclusion
It is clear from the brief summaries provided on twin, adoption, and family studies that there
is no black or white answer to the age-old question of what contributes to human behavior,
personality, and psychopathology. In reviewing a multitude of twin, adoption, and family
studies broaching a large variety of topics, it is clear to see that the foundation for each
human being is diverse in structure. For some cases, genetics seem to dominate; in some
other cases, environment explains all. In still more situations, it is a strong combination of the
two factors that mold people to be who they are. This is a strong indicator that there will
never be an umbrella response to the question, and that personality and psychopathology
may always have to be rationalized on a case-by-case basis.

Peer Commentary

Nature Versus Nurture: Are We Really Born That Way?


Heather A. Blout
Rochester Institute of Technology
I read Haimowitz's article "Heredity Versus Environment: Twin, Adoption, and Family Studies." Her
conclusion of the heredity versus environment debate was very logical and I must at least partly agree.
Based on the current research, specifically the studies explained in the article, it seems that the only answer
to this debate may always have to be rationalized solely on a case by case basis. However, there has been
research that shines new light on the age-old debate.
The heritability coeffecient was casually mentioned in the discussion of twins and the number of genes that
they share. Haimowitz made it seem that it was a simple fact and was not subject to change. I, however,
strongly disagree. The heritability coefficient sounds like it answers the nature versus nurture question, but it
only scratches the surface. The answer to the question "Are traits caused by the environment or genetics?" is
usually both. Even a heritability coefficient of 1.0 does not mean that the environment cannot affect the trait,
which is what is implied by a coefficient of 1.0. She also mentioned the heritability coefficient in the
introduction to the topic of twin studies, but never related it to the studies. She should have either omitted
the topic from the paper or related it to the studies. If she connected the heritability coefficient to the studies,
then that might have provided more solid evidence from which to draw conclusions. The data could still be
refutible, but at least we would be able to attribute a specific amount of genetic cause for each study.
Personality was also transiently brushed upon in the paper, but I think that this is one of the most important
reasons for the existing nature versus nurture debate, because it directly relates to behavior. I thought the
three types of genotype-environment relations that were discussed were confusing and should have been
embellished a bit more. I think this idea is very important in reference to personality. It was not clear what
the results of the study actually were or what the frequencies of each type of relation were found to be in this
study. The types of personality did not have a clear connection with how the genotype-environment
interaction came into play. The conclusion arrived at was that when participants score low for a personality
trait, they are more suspceptible to environmental impact. However, the study did not further discuss
anything about how people obtain their personality traits. I also did not think that the results of the study
were ncessarily valid, because they derived the Type III interaction from mice as opposed to humans, like
the first two types. I do not feel that this is applicable to personality in humans.
Personality is a good example of a trait that has been studied in twins. Identical twins reared apart are far
more similar in personality than fraternal twins. These observations suggest that personality is heritable.
However, the environment must also be looked at. There are two kinds of environmental effects: shared
experiences and nonshared experiences. Although identical twins are genetically identical and share the
same family environment, identical twins raised together do not have identical personalities. These
differences must then be explained entirely by nonshared environmental effects.
I feel that disorders should be discussed in relation to the heredity-environment debate, because the better-
understood their causes are, the more efficiently and effectively they can be treated. One such disorder that
is currently being heavily researched is depression. Depression is very common, so it is important to
understand the relation between genetics and environment in depression. According to a recent twin study of
depression, the concordance between identical twins was the highest when compared to other familial
relationships (Kendler, Walters, & Truett, 1995). This implies that depression can largely be attributed to
genetics.
The nature versus. nurture debate is a highly sensitive topic for a lot of scientists and still creates passionate
opinions for one side or the other. Haimowitz briefly discussed in the conclusion that we may never know
the answer to the great gentic versus environment question. It seems that the answer we get will be
determined by the situation that we set up. There is no doubt that more studies will be conducted to inform
scientists more on the topic and maybe finally will create an umbrella response to the question of the effects
of heredity and environment on personality and psychopathology.

Peer Commentary

How Identical Twins Grow Up To Be Different


Caitlin M. Jones
Rochester Institute of Technology
In the paper, "Heredity Versus Environment: Twin, Adoption, and Family Studies," Haimowitz reviewed
relevant research regarding the debate over how personalities are shaped. This issue is surrounded by
contention between behavioral geneticists and personality researchers. As the author states, there is still
much unknown in this field to determine whether one side is right or wrong. But certainly, for those who
understand both sides of the debate, it seems possible that they are both right, and in fact there is a relation
between heredity and environment.
Although the author made good points and revealed the different methods for measuring heredity and
environmental influences, I wish to question one study mentioned. Haimowitz explained a study that was
conducted to determine the heritability of attitudes among twins. The researchers concluded that there was
variance between individuals on a number of the measured attitudes that could be traced to genetic factors
(Olsen, Vernon, Harris, & Jang, 2001). They also found that the nonshared environment contributed even
more variance within the sample. After reading the study, I became aware that the sample was an adult
population of monozygotic (MZ) and dizygotic (DZ) twins with an average age of 30.4 years (Olsen et al.,
2001). I realize that by this age twins should have countless experiences apart from one another, which could
account for the variance attributed to the non-shared environment. However, I do not agree with that
assumption and believe that the variance associated with the nonshared environment should not be so large.
Attitudes, beliefs, and norms are constructed during adolescence and made more concrete over time (Harris,
1995). This process of socialization most notably occurs through the contact that adolescents have with their
peer groups. The theory of group socialization posits that the peer group and other outside-the-home
socialization are responsible for shaping the personality of adolescents and teenagers (Harris, 1995). The
fact that siblings reared in the same home environment have very distinct personalities could be attributed to
each sibling's different peer groups. Now the question is, does this theory apply to twins as well?
For the most part, or at least from my experience, twins tend to stick together when they are in their
adolescent and teenage years. As a result of being together they would also share the same peer group.
Combining these ideas and the group socialization theory, it seems logical that if twins share the same peer
group then they would also share the same attitudes, beliefs, and norms. And if what we learn in our early
years becomes a part of our personality, how could twins have different attitudes, beliefs, and norms when
they are older?
This question seems to relate more to MZ twins than to DZ twins, because DZ twins are comparable to
normal siblings in that they only share half of their genes. Perhaps the variance is greater for the nonshared
environment because of the DZ twins, who are more apt to have different peer groups. Another explanation
could be that both MZ and DZ twins had individual life experiences that changed how they thought and
what they believed.
Even with these explanations, which are only guesses, I am still unsure why there was greater variance
across the sample for certain attitudes that were attributed to the nonshared environment. I am sure further
research could answer these questions.

Peer Commentary

Addictive Behaviors: Heredity or Environment?


Samantha P. Lumbert
Rochester Institute of Technology
For a commentary on Haimowitz's paper, "Heredity Versus Environment: Twin, Adoption, and Family
Studies," I thought it would be useful to examine the association of addictive behaviors in twins and the
connection to heredity and environment. Haimowitz devoted a section to schizophrenia under adoption
studies, and its link to heredity and environment. I thought that research on addictive behaviors with twins
would also be a worthwhile matter to explore in search for influences of genes and surroundings. A
fascinating article I discovered explored the question of whether smoking was connected with schizophrenia
itself, the treatment of the illness, or the mere vulnerability to the illness. To study this, the researchers used
two dozen people affected with schizophrenia, and their unaffected, healthy twins. Because of their genetic
similarity, the unaffected twins would clearly be susceptible to the illness. The researchers also used control
participants to compare with the results given by the twins. It was found that the unaffected twins had higher
daily rates of smoking than the controls, the schizophrenic and unaffected twins were more often
unsuccessful in attempts to quit than were the controls, and both types of twins reported more frequent,
negative symptoms following their successful attempt at quitting than did the controls. The study found
evidence to support that the addictive behavior of smoking is indeed linked to the susceptibility to
schizophrenia, rather than the illness itself (Lyons et al., 2002).
Another interesting study considered alcohol expectancies in twins. It was found that positive alcohol
expectancies shared by twins were mostly due to shared experiences, and a great part of the expectancies
were due to non-familial factors. This study demonstrated that positive attitudes towards consuming alcohol
are mostly a result of environmental factors (Slutske et al., 2002).
In her paper, Haimowitz also devoted a section to antisocial personality disorder; another article I examined
explored this disorder and its connection to another addictive behavior: gambling. The researchers found
that pathological gambling was highly associated with the antisocial behavior disorders of antisocial
personality disorder, child conduct disorder, and adult antisocial behavior. These behaviors appeared to be
explained mostly by genetic factors, suggesting that there is a genetic vulnerability for developing antisocial
behaviors which may also lead to addictive behaviors such as pathological gambling (Slutske, et al., 2001).
I believe that these three studies add an interesting perspective that considers addictive behaviors such a
smoking, alcohol consumption, and gambling, and their connection with psychological disorders in twin
studies. As was mentioned in Haimowitz's paper, there is no clear-cut explanation for whether these
behaviors are genetic or environmental, but studies indicate that some addictions appear to be mostly due to
genetics, whereas some attitudes toward addictive behavior are due to environment. Examination of heredity
versus environment regarding addictive behaviors would make an interesting addition to Haimowitz's paper.

Peer Commentary

Nature or Nurture: The Inexhaustible Debate


EmilyAnn A. O'Coin
Rochester Institute of Technology
The commonly disputed topic of nature versus nurture has been an ongoing deliberation that dates back to
Darwin. In "Heredity Versus Environment: Twin, Adoption, and Family Studies," Haimowitz exhibited
many compelling research findings that help us understand the roles that environment and genetics play;
however, I found that some of her studies held little relevance in the search for a "black and white" answer.
Although I agree that neither genetics nor environment is the sole determinant of how a person behaves or
develops schizophrenia, I am skeptical of particular ways in which Haimowitz claimed that this is true. One
issue that I am dubious toward is the topic of genotype-environment interaction. I am critical of the way
Haimowitz portrayed this material for several reasons. It is illogical when documenting the three types of
genotype-environment interaction to document a study that is not consistent with the people being tested.
The first two types discussed were based on studies from human twins, whereas the third type was
formulated based on research using mice. Humans and mice may not be correlated in a study that is
investigating extraversion, neuroticism, impulsivity, monotony avoidance, and family environment let alone
socioeconomic status. Despite the lack of an appropriate study, it is important to emphasize the usefulness of
identical twin (as opposed to fraternal twin) studies on this dimension because of the great degree of validity
associated with the results. Identical twins share 100% of their genetic information (as opposed to only 50%
in fraternal twins); therefore, any discrimination between the twins can be attributed to environmental
factors.
A further concept that I had difficulty accepting was the discussion of children's adjustment to divorce under
the topic of adoption studies. First, it is extremely difficult to validate a study basing its results on
information received at the time of an event (separation/divorce) without considering background
knowledge of the participants' attitudes and behaviors prior to the event. Without the awareness of how a
person behaved or socialized prior to the experience of parental separation/divorce, it is insufficient to base
conclusions on that person's personality after the often-upsetting event of experiencing a parental
separation/divorce. Although it is sufficient for Haimowitz to state that "the type of adjustment processes
that children from biological families went through could be attributed to biology or environment...," it is
completely inappropriate to assert that "...adjustment for probands would have had to be linked to
environment processes" without any valid arguments to purport this claim. One's genetic makeup provides
the potential for the development of behavior among individuals. The environment in which one develops
helps to shape the person that they become. Therefore, to argue that an adopted proband is affected by their
adopted parental separation or divorce, only due to the environmental factors that influenced their behavior
is groundless.
Schizophrenia has been widely researched in the attempt to determine whether environment or genetics
plays a more dominant role. Haimowitz reiterated the common knowledge that it is difficult to determine
what genetic factors influence such a disorder; therefore we can proclaim that environmental factors
inevitably contribute to the development of schizophrenia. However, I would like to expand upon this issue
by arguing that we cannot generalize that environmental factors--particularly in the case of adopted
probands--play a triggering role. "Perhaps because the overall size of the genetic effect is large, accounting
for about 80% of variance, definite environmental factors have been difficult to pin down. It has even been
suggested that 'the environment' consists entirely of epigenetic or stochastic phenomena that can never be
detected by standard epidemiological methods" (McGuffin, 2004, p. S192). It is indeed reasonable to argue
that environment is a contributing factor in schizophrenia. Nevertheless, we cannot measure the numerous
factors in varying environments that are conducive to schizophrenia, leaving us with the question as to
which type of environmental factors play a causal role.
Although there were several issues that I felt were not adequately demonstrated, there were several
significant points that Haimowitz presented. When breaking down the debate of nature versus nurture, it is
essential to incorporate practices that produce clear-cut results. The most essential contention recognized
was that of twin studies. If two identical twins were separated at birth and one twin developed schizophrenia
but the other did not, we could conclude that schizophrenia is strictly environmental. The percentages
associated with twin concordance rates cannot be disputed, thus making the choice of twin studies very
useful in the case of nature versus nurture.
I found most of Haimowitz's ideas for dissecting the deliberation of nature versus nurture to be very
intellectually stimulating. It was fitting to provide many different examples of research conducted under the
categories of twin, adoption, and family studies. However, there was very little supportive data that
contribute to this discussion in the examples of bipolar disorder, schizophrenia, or antisocial personality
disorder. In these studies, Haimowitz admitted that there was not enough research conducted or information
available to interpret the results. When discussing a topic that is so controversial, it is imperative that
research associated with compelling findings be presented, rather than research that did not provide enough
information to present a valid argument. If Haimowitz had presented her findings in a matter that supported
her conclusions rather than leaving room for ambiguity from research that was immaterial, a much stronger
argument would have been evoked.

Author Response

Drawing Conclusions From Behavior Genetics


Avi G. Haimowitz
Rochester Institute of Technology
I found all four of my peer commentaries very interesting. I was impressed by the concepts that they brought
up, and they made me think about ways I could have presented my paper in a more logical manner.
Blout said that she believed I should have touched on the topic of the heritability more, or otherwise have
completely omitted it from my paper. She made a good point here since I only briefly mentioned the term
and did not go into great detail on how it impacts research in twin studies. My only issue with Blout's
argument against the way I discussed the heritability coefficient is that she thought I made it seem like a
concrete fact. I do not believe I did; in fact, I described it for what it is: an estimate. I wrote that nonshared
environment does play a role in twins, which invalidates Blout's statement that I did not take environment
into consideration when mentioning the heritability coefficient.
It is also true I could have done a better job at explaining the study performed in relation to genotype-
environment interaction. I do not think, however, that it was pointless to include the information I did on the
third study done with mice; studies done using mice can often produce parallels explanations for human
behavior, or they can be precursors to studies performed using humans as the subjects. I understand Blout's
argument that personality often influences behavior, but I did not write this paper with the intent to cover
any specific component of what makes a human being; this is obvious with the varied topics I touched upon.
Blout seemed to contradict herself when she said that disorder should also be mentioned; if anything, I
discussed more mental disorders than I did aspects of personality itself.
Jones brought up a good point in her commentary, in which she questioned the study I discussed related to
attitude heritability in twins. She was dubious about the validity of attribuiting so much variability to
nonshared environment because the study was performed on adult twins rather than younger twins. I agree
that it is more difficult to pinpoint exactly how nonshared environment could have such a large effect if you
go by the assumption that most twins tend to share the same peer groups and thus obtain the same belief
systems and behaviors. However, we cannot state that as fact; it is not known in the study the history of each
pair of twins and how similar their upbringings were and how much of their social lives were shared with
one another. I believe that the authors of the study should have elaborated on this issue more, and I think
Jones' question is worth pursuing in a different study.
I would like to thank Lumbert for her fascinating summary of research done on addictive behaviors related
to behavior genetics. I was intruigued by the information she provided on a study done on gambling and its
correlates with antisocial personality disorder. That is one study I would have liked to include in my paper if
I had examined the topic of addictive behaviors in relation to the argument of heredity versus the
environment.
O'Coin's criticism of the study I discussed related to mice and genotype-environment interaction is similar
to the one made by Jones. I understand why she believes that study to be irrelevant to my paper, but research
is often done in stages, and I would have liked to have seen the results of that study done in its latter stages –
with humans, of course. I mentioned it in my paper because I thought it was worth broaching the topic, not
because I thought it was conclusive. I should have been more clear about that. O'Coin's comments on the
adjustment to divorce study surprised me, but when I re-read what she said I had to agree with her argument
that the conclusions made by myself based on the study did not really have any foundation in rationality.

References
Bergeman, C. S., Plomin, R., McClearn, G. E., Pederson, N. L., & Friberg, L. T. (1988). Genotype-
environment interaction in personality development: Identical twins reared apart. Psychology
and Aging, 3, 399-406.
Berrettini, W. H. (2000). Are schizophrenic and biological disorders related? A review of family and
molecular studies. Biological Psychiatry, 48, 531-538.
Brent, D. A., Bridge, J., Johnson, B. A., Connolly, J. (1996). Suicidal behavior runs in families: A controlled
family study of adolescent suicide victims. Archives of General Psychiatry, 53, 1145-1152.
Daniels, D., & Plomin, R. (1985). Origins of individual differences in infant shyness. Developmental
Psychology, 21, 118-121.
Harris, J. R. (1995). Where is the child's environment? A group socialization theory of development.
Psychological Review, 102, 458-489.
Hughes, C., Happé, F., Taylor, A., Jaffee, S. R., Caspi, A., & Moffitt, T. E. (2005). Origins of individual
differences in theory of mind: From nature to nurture? Child Development, 76, 356-370.
Jang, K. L. (2005). The behavioral genetics of psychopathology: A clinical guide. Mahwah, NJ: Erlbaum.
Kendler, K., Walters, E., & Truett, K. (1995). Heredity vs. environment in depression. Harvard Mental
Health Letter, 12, 5-8.
Lilenfield, L. R., Kaye, W. H., Greeno, C. G., Merikangas, K. R., Plotnicov, K., Pollice, C., Rao, R., Strober,
M., Bulik, C.M., & Nagy, L. (1998). A controlled family study of anorexia nervosa and bulimia nervosa:
Psychiatric disorders in first-degree relatives and effects of proband comorbidity. Archives of General
Psychiatry, 55, 603-610.
Loehlin, J. C., Willerman, L., Horn, J. M. (1988). Human behavior genetics. Annual Review of Psychology,
39, 101-134.
Lyons, M., Barr, J., Kremen, W., Toomey, R., Eisen, S., Goldberg, J., Faraone, S., & Tsuang, M. (2002).
Nicotine and familial vulnerability to schizophrenia: A discordant twin study. Journal of Abnormal
Psychology, 111, 687-693.
McGuffin, P., (2004). Nature and nurture interplay: Schizophrenia. Psychiatrische Praxis, 31, S189-S193.
O'Connor, T. G., Plomin, R., Caspi, A., & DeFries, J. C. (2000). Are associations between parental divorce
and children's adjustment genetically mediated? An adoption study. Developmental Psychology, 36, 429-
437.
Olson, J. M., Vernon, P. A., Harris, J. A., & Jang, K. L. (2001). The heritability of attitudes: A study of twins.
Journal of Personality and Social Psychology, 80, 845-860.
Petrill, S. A., Lipton, P. A., Hewitt, J. K., Plomin, R., Cherny, S. S., Corley, R., & DeFries, J. C. (2004).
Genetic and environmental contributions to general cognitive ability through the first 16 years of life.
Developmental Psychology, 40, 805-812.
Plomin, R., DeFries, J. C., McClearn, G. E., & Rutter, M. (1997). Behavioral genetics (3rd. ed.). New York:
Freeman.
Rhee, S. H., & Waldman, I. D. (2002). Genetic and environmental influences on antisocial behavior: A meta-
analysis of twin and adoption studies. Psychological Bulletin, 128, 490-529.
Roth, W. E., & Finley, G. E. (1998). Adoption and antisocial personality: Environmental factors associated
with antisocial outcomes. Child and Adolescent Social Work Journal, 15, 133-150.
Slutske, W., Cronk, N., Sher, K., Madden, P., Bucholz, K., & Heath, A. (2002). Genes, environment, and
individual differences in alcohol expectancies among female adolescents and young adults. Psychology of
Addictive Behaviors, 16, 308-317.
Slutske, W., True, W., Goldberg, J., Eisen, S., Xian, H., Lyons, M., & Tsuang, M., (2001). A twin study of
the association between pathological gambling and antisocial personality disorder. Journal of Abnormal
Psychology, 110, 297-308.
Van den Oord, E. J. C. G., Boomsma, D. I., & Verhulst, F. C. (2000). A study of genetic and environmental
effects on the co-occurrence of problem behaviors in three-year-old twins. Journal of Abnormal Psychology,
109, 360-372.

Winner of 2005 RIT Kearse Award for Writing

Genetic and Environmental Influences on Criminal


Behavior
Caitlin M. Jones
Rochester Institute of Technology

Criminal behavior has always been a focus for psychologists due to the age old debate
between nature and nurture. Is it the responsibility of an individual's genetic makeup that
makes them a criminal or is it the environment in which they are raised that determines their
outcome? Research has been conducted regarding this debate which has resulted in a
conclusion that both genes and environment do play a role in the criminality of an individual.
This evidence has been generated from a number of twin, family, and adoption studies as well
as laboratory experiments. Furthermore, the research has stated that it is more often an
interaction between genes and the environment that predicts criminal behavior. Having a
genetic predisposition for criminal behavior does not determine the actions of an individual,
but if they are exposed to the right environment, then their chances are greater for engaging
in criminal or anti-social behavior. Therefore, this paper will examine the different functions
that genetics and the environment play in the criminal behavior of individuals.

There is a vast amount of evidence that shows our criminal justice system is the new home
for individuals with psychological problems. Although this may seem like a solution to some, it
is creating a dilemma for our society. Once we label these individuals as criminals it creates a
stigma for those who may suffer from psychological problems. Certain psychological problems
have been shown to be heritable and if given the right circumstances, individuals with those
genes could find themselves engaging in criminal activity. Therefore, should society look
towards limiting the reproductive capabilities of individuals who suffer from certain
psychological problems to better society?
That same question was asked back in the late nineteenth and early twentieth centuries when the role of
genetics in crime was widely accepted (Joseph, 2001). Prominent researchers believed that genes were fully
responsible for criminal activity and that criminals could be identified by their physiological features. Along
with this information and the idea of a eugenics movement during the same time period, it was not
surprising to learn that acts of sterilization took place to rid society of “criminals, idiots, imbeciles, and
rapists" (Joseph, 2001, p. 182). This period was therefore marked with inhumane treatment and the belief
that genes were the sole reason behind criminal behavior.
Not long after the practices of controlled breeding, there was evidence to support the idea that the
environment also played an important role in crime. Early family studies were conducted that showed a
predisposition for criminal behavior as a result of inherited characteristics, but that an individual's
characteristics and personality could still be modified by the environment (Joseph, 2001). Although these
studies were void of high validity and reliability, it still raised the question of whether the environment can
also influence individuals to act in a criminal manner. The debate between genetics and environment
continues today with much more reliable research and data. Consequently, this paper will examine the
various roles in which both genes and environmental factors influence criminal behavior.
Definition and Measurement of Criminal Behavior
To fully understand the nature of how genes and the environment influence criminal behavior,
one must first know how criminal behavior is defined. Law in our society is defined by social
and legal institutions, not in biology (Morley & Hall, 2003). Therefore determining what
constitutes criminal behavior can envelope a wide variety of activities and for that reason,
researchers tend to focus on the wider context of antisocial behavior. Authors Morley and Hall
(2003), who have investigated the genetic influences on criminal behavior, point out three
different ways to define antisocial behavior. First is equating it with criminality and
delinquency, which both involve engaging in criminal acts. Criminality can lead to arrest,
conviction, or incarceration for adults, while delinquency is related to juveniles committing
unlawful acts (Rhee & Waldman, 2002). Information can be collected using court and criminal
records, as well as self report surveys to analyze the influences that were present. Secondly,
they advise individuals to define antisocial behavior is through criteria used to diagnose
certain personality disorders. More specifically, they mean those personality disorders, such
as Antisocial Personality Disorder, which is associated with an increased risk in criminal
activity. A final measure suggested for defining antisocial behavior is by examining personality
traits that may be influential in the criminal behavior of individuals. Traits such as
aggressiveness and impulsivity are two traits that have been investigated the most (Morley &
Hall, 2003). Further details of disorders and personality traits associated with criminal
behavior will be discussed later in the paper.
With regards to determining the effects the environment plays in criminal behavior there are fewer resources
available. Observational studies and reports submitted by parents are two sources, but not everyone agrees
on the validity of information collected from these sources. Three additional sources that most researchers
cite when gathering information about both genetic and environmental influences are twin, family, and
adoption studies (Tehrani & Mednick, 2000).
Twin, Adoption, and Family Studies
There has been great debate between researchers regarding the outcomes of twin, adoption,
and family studies. Some claim that these studies support the notion of a genetic basis to
criminal behavior (Tehrani & Mednick, 2000). On the other hand, some have concluded that
there is not enough evidence from these twin, family, and adoption studies to profess that
genetics do play a role in antisocial or criminal behavior (Lowenstein, 2003). To understand
why there are such conflicting opinions, one must first look at the available studies that have
been conducted.
Twin studies are conducted on the basis of comparing monozygotic (MZ) or identical twins and their rates of
criminal behavior with the rates of criminal behavior of dizygotic (DZ) or fraternal twins. Ordinarily these
studies are used to assess the roles of genetic and environmental influences. If the outcomes of these twin
studies show that there is a higher concordance rate for MZ twins than for DZ twins in criminal behavior,
then it can be assumed that there is a genetic influence (Tehrani & Mednick, 2000). A study conducted
looked at thirty two MZ twins reared apart, who had been adopted by a non-relative a short time after birth.
The results showed that for both childhood and adult antisocial behavior, there was a high degree of
heritability involved (Joseph, 2001). This study was of particular importance because it examined the factor
of separate environments. Another researcher studied eighty-five MZ and one hundred and forty-seven DZ
pairs and found that there was a higher concordance rate for the MZ pairs. Ten years later after checking
police records of these same twins, two other researchers concluded that there was a fifty-four percent
heritability of liability to crime (Joseph, 2001). Around the same time of the study just mentioned, two
researchers studied forty-nine MZ and eighty-nine DZ pairs, but found no difference in the concordance
rates. They concluded therefore that in respect to common crime, hereditary factors are of little significance
(Joseph, 2001). Many other twin studies have been conducted, but there is concern over the validity of those
studies and their ability to separate out the nature and nurture aspects; therefore other sources of information
should be examined.
Adoption studies are critical in examining the relationship that exists between adopted children and both
their biological and adoptive parents because they assume to separate nature and nurture. Studies have been
conducted that test for the criminal behavior of the adopted-away children, if their biological parents had
also been involved with criminal activity. In Iowa, the first adoption study was conducted that looked at the
genetics of criminal behavior. The researchers found that as compared to the control group, the adopted
individuals, which were born to incarcerated female offenders, had a higher rate of criminal convictions as
adults. Therefore this evidence supports the existence of a heritable component to antisocial or criminal
behavior (Tehrani & Mednick, 2000). Another study in Sweden also showed that if a biological background
existed for criminality, then there was an increased risk of criminal behavior in the adopted children. In
Denmark, one of the largest studies of adopted children was conducted and found similar results to the
previous studies. The defining feature of the Denmark study was that the researchers found a biological
component for criminal acts against property, but not for violent crimes (Joseph, 2001). Children whose
biological fathers had been convicted of property crimes were more likely to engage in similar behavior,
when compared to those biological fathers who had been convicted of violent crimes. According to an article
by Jay Joseph (2001), who studied all of the minor and major adoption studies, the majority of researchers
have found and agreed upon the non-significance of genes in violent crime. This reestablishes the findings
from the studies mentioned already in that there may be a genetic component to antisocial behavior or that
genes influence criminal behavior, but specifically for property offenses.
Family studies are the third type of instrument used to assess the relationship between genetics and
environmental influences on criminal or antisocial behavior. Research in this field has probably been the
least accepted by psychologists and other scholars because of the degree of difficulty in separating out
nature and nurture in the family environment. Children experience both the influence of their parents' genes
and also the environment in which they are raised, so it is difficult to assign which behaviors were
influenced by the two factors. Twin studies have this flaw, as stated earlier, but it is more prevalent in family
studies. An additional concern with family studies is the inability to replicate the results, therefore leading to
a small number of studies. Regardless of these drawbacks, one family study in particular should be
acknowledged for its findings.
Brunner, Nelen, Breakefield, Ropers, and van Oost (1993) conducted a study utilizing a large Dutch family.
In their study they found a point mutation in the structural gene for monoamine oxidase A (MAOA), a
neurochemical in the brain, which they associated with aggressive criminal behavior among a number of
males in that family (Alper, 1995). These males were reported to have selective MAOA deficiency, which
can lead to decreased concentrations of 5-hydroxyindole-3-acetic acid (5-HIAA) in cerebrospinal fluid.
Evidence suggests that low concentrations of 5-HIAA can be associated with impulsive aggression. These
results have not been confirmed in any additional family studies, which lead to a need for more studies to
determine if other families share similar results (Brunner et al., 1993). However, this one family study does
seem to suggest that genetics play an important role in antisocial or criminal behavior.
Neurochemicals in Criminal and Anti-Social Behavior
Neurochemicals are responsible for the activation of behavioral patterns and tendencies in
specific areas of the brain (Elliot, 2000). As seen in the Brunner et al. study, there have been
attempts to determine the role of neurochemicals in influencing criminal or antisocial
behavior. Included in the list of neurochemicals already cited by researchers are monoamine
oxidase (MOA), epinephrine, norepinephrine, serotonin, and dopamine.
Monoamine oxidase (MAO) is an enzyme that has been shown to be related to antisocial behavior.
Specifically, low MAO activity results in disinhibition which can lead to impulsivity and aggression (Elliot,
2000). The Brunner et al. study is the only one to report findings of a relationship between a point mutation
in the structural gene for MAOA and aggression, which makes the findings rare. However, there has been
other evidence that points to the conclusion that deficiencies in MAOA activity may be more common and
as a result may predispose individuals to antisocial or aggressive behavior (Brunner et al., 1993). MAO is
associated with many of the neurochemicals that already have a link to antisocial or criminal behavior.
Norepinephrine, serotonin, and dopamine are metabolized by both MAOA and MAOB (Elliot, 2000). While,
according to Eysenck (1996), MAO is related to norepinephrine, epinephrine, and dopamine, which are all
related to the personality factor of psychosis.
Serotonin is a neurochemical that plays an important role in the personality traits of depression, anxiety, and
bipolar disorder (Larsen & Buss, 2005). It is also involved with brain development and a disorder in this
system could lead to an increase in aggressiveness and impulsivity (Morley & Hall, 2003). As Lowenstein
(2003) states, “studies point to serotonin as one of the most important central neuro-transmitters underlying
the modulation of impulsive aggression" (p.72). Low levels of serotonin have been found to be associated
with impulsive behavior and emotional aggression. In addition, children who suffer from conduct disorder
(which will be discussed later), have also been shown to have low blood serotonin (Elliot, 2000). Needless
to say, there is a great deal of evidence that shows serotonin is related to aggression, which can be further
associated with antisocial or criminal behavior.
Dopamine is a neurotransmitter in the brain that is associated with pleasure and is also one of the
neurotransmitters that is chiefly associated with aggression. Activation of both affective (emotionally
driven) and predatory aggression is accomplished by dopamine (Elliot, 2000). Genes in the dopaminergic
pathway have also been found to be involved with Attention Deficit Hyperactivity Disorder (ADHD)
(Morley & Hall, 2003). In one study cited by Morley and Hall (2003), a relationship was found between the
genes in the dopaminergic pathway, impulsivity, ADHD, and violent offenders. Obviously, from this list of
neurochemicals it seems plausible that there is a genetic component to antisocial or criminal behavior.
Personality Disorders and Traits
Personality traits and disorders have recently become essential in the diagnosis of individuals
with antisocial or criminal behavior. These traits and disorders do not first become evident
when an individual is an adult, rather these can be seen in children. For that reason it seems
logical to discuss those personality disorders that first appear in childhood. Attention Deficit
Hyperactivity Disorder (ADHD), Conduct Disorder (CD), and Oppositional Defiance Disorder
(ODD) are three of the more prominent disorders that have been shown to have a relationship
with later adult behavior (Holmes, Slaughter, & Kashani, 2001).
ODD is characterized by argumentativeness, noncompliance, and irritability, which can be found in early
childhood (Holmes et al., 2001). When a child with ODD grows older, the characteristics of their behavior
also change and more often for the worse. They start to lie and steal, engage in vandalism, substance abuse,
and show aggression towards peers (Holmes et al., 2001). Frequently ODD is the first disorder that is
identified in children and if sustained can lead to the diagnosis of CD (Morley & Hall, 2003). It is important
to note however that not all children who are diagnosed with ODD will develop CD.
ADHD is associated with hyperactivity-impulsivity and the inability to keep attention focused on one thing
(Morley & Hall, 2003). Holmes et al. (2001) state that, “impulse control dysfunction and the presence of
hyperactivity and inattention are the most highly related predisposing factors for presentation of antisocial
behavior" (p.184). They also point to the fact that children diagnosed with ADHD have the inability to
analyze and anticipate consequences or learn from their past behavior. Children with this disorder are at risk
of developing ODD and CD, unless the child is only diagnosed with Attention Deficit Disorder (ADD), in
which case their chances of developing ODD or CD are limited. The future for some children is made worse
when ADHD and CD are co-occurring because they will be more likely to continue their antisocial
tendencies into adulthood (Holmes et al., 2001).
Conduct Disorder is characterized with an individual's violation of societal rules and norms (Morley & Hall,
2003). As the tendencies or behaviors of those children who are diagnosed with ODD or ADHD worsen and
become more prevalent, the next logical diagnosis is CD. What is even more significant is the fact that
ODD, ADHD, and CD are risk factors for developing Antisocial Personality Disorder (ASPD). This disorder
can only be diagnosed when an individual is over the age of eighteen and at which point an individual shows
persistent disregard for the rights of others (Morley & Hall, 2003). ASPD has been shown to be associated
with an increased risk of criminal activity. Therefore, it is of great importance that these early childhood
disorders are correctly diagnosed and effectively treated to prevent future problems.
Another critical aspect that must be examined regarding antisocial or criminal behavior is the personality
characteristics of individuals. Two of the most cited personality traits that can be shown to have an
association with antisocial or criminal behavior are impulsivity and aggression (Morley & Hall, 2003).
According to the article written by Holmes et al. (2001), antisocial behavior between the ages of nine and
fifteen can be correlated strongly with impulsivity and that aggression in early childhood can predict
antisocial acts and delinquency. One statistic shows that between seventy and ninety percent of violent
offenders had been highly aggressive as young children (Holmes et al., 2001). These personality traits have,
in some research, been shown to be heritable.
Environmental Influences
Thus far it has been established through research and various studies that genetics do
influence criminal or antisocial behavior. Researchers agree on the point that genes influence
personality traits and disorders, such as the ones just mentioned. However, researchers also
agree that there is an environmental component that needs to be examined. Environmental
influences such as family and peers will be discussed, as well as a look into the social learning
theory.
The family environment is critical to the upbringing of a child and if problems exist then the child is most
likely to suffer the consequences. We have seen the problems associated with a child who is diagnosed with
ADHD and how that can influence antisocial or criminal behavior. In relation to that, some researchers have
claimed that it is the family environment that influences the hyperactivity of children (Schmitz, 2003). The
researchers in this article specifically identify family risk factors as poverty, education, parenting practices,
and family structure. Prior research on the relationship between family environment and child behavior
characterizes a child's well being with a positive and caring parent-child relationship, a stimulating home
environment, and consistent disciplinary techniques (Schmitz, 2003). Families with poor communication
and weak family bonds have been shown to have a correlation with children's development of
aggressive/criminal behavior (Garnefski & Okma, 1996). Therefore it seems obvious to conclude that those
families who are less financially sound, perhaps have more children, and who are unable to consistently
punish their children will have a greater likelihood of promoting an environment that will influence
antisocial or delinquent behavior. Another indicator of future antisocial or criminal behavior is that of abuse
or neglect in childhood. A statistic shows that children are at a fifty percent greater risk of engaging in
criminal acts, if they were neglected or abused (Holmes et al., 2001). This has been one of the most popular
arguments as to why children develop antisocial or delinquent behaviors.
One additional research finding in the debate between genetic and environmental influences on antisocial or
criminal behavior has to deal with the age of the individual. Research seems consistent in recognizing that
heritability influences adult behavior more than environmental influences, but that for children and
adolescents the environment is the most significant factor influencing their behavior (Rhee & Waldman,
2002). As an adult, we have the ability to choose the environment in which to live and this will either
positively or negatively reinforce our personality traits, such as aggressiveness. However, children and
adolescents are limited to the extent of choosing an environment, which accounts for the greater influence of
environmental factors in childhood behaviors.
Another significant factor in the development of antisocial or delinquent behavior in adolescence is peer
groups. Garnefski and Okma (1996) state that there is a correlation between the involvement in an antisocial
or delinquent peer group and problem behavior. One of the primary causes as to why this occurs can be
traced back to aggressive behavior in young children. When children are in preschool and show aggressive
tendencies towards their peers, they will likely be deemed as an outcast. This creates poor peer relationships
and relegates those children to be with others who share similar behaviors. A relationship like this would
most likely continue into adolescence and maybe even further into adulthood. The similar tendencies of
these individuals create an environment in which they influence one another and push the problem towards
criminal or violent behavior (Holmes et al., 2001).
Social learning theory has been cited as way to explain how the environment can influence a child's
behavior. Using this theory to explain the aggressive or antisocial behavior of a child means that a child
observes aggressive behavior between parents, siblings, or both. As a result, the children believes that this
aggressive behavior is normal and can therefore use it themselves because they do not see the harm in acting
similar to their parents (Miles & Carey, 1997). As stated earlier, interaction between family members and
disciplinary techniques are influential in creating antisocial behavior. Using the social learning theory these
two factors are also critical in the development of aggression. Children who are raised in an aggressive
family environment would most likely be susceptible to experiencing a lack of parental monitoring,
permissiveness or inconsistency in punishment, parental rejection and aggression. The exposure to such high
levels of aggression and other environmental factors greatly influences and reinforces a child's behavior. A
significant point that should be known however is the fact that other research has supported the notion that
genetics do influence levels of aggression, which stands in opposition to the social learning theory (Miles &
Carey, 1997).
Gene-Environment Interactions
There are theories, however, concerning genetic and environmental influences, which seem to
suggest an interaction between the two and one such theory is the general arousal theory of
criminality. Personality psychologist Eysenck created a model based on three factors known as
psychoticism, extraversion, and neuroticism, or what is referred to as the PEN model
(Eysenck, 1996). Psychoticism was associated with the traits of aggressive, impersonal,
impulsive, cold, antisocial, and un-empathetic. Extraversion was correlated with the traits of
sociable, lively, active, sensation-seeking, carefree, dominant, and assertive. Finally,
neuroticism was associated with anxious, depressed, low self-esteem, irrational, moody,
emotional, and tense (Eysenck, 1996). Through research and surveys, Eysenck found that
these three factors could be used as predictors of criminal behavior. He believed this to be
especially true of the psychoticism factor and that measuring it could predict the difference
between criminals and non-criminals. Extraversion was a better predictor for young
individuals, while neuroticism was a better predictor for older individuals (Eysenck, 1996). An
important point about these factors and the personality traits associated with them is that
most of them have already been found to be heritable (Miles & Carey, 1997).
Understanding Eysenck's original model is critical to assessing the general arousal theory of criminality,
which suggests an interaction between factors. Research has shown that criminality is strongly correlated
with low arousal levels in the brain. Characteristics related to low arousal levels include lack of interest,
sleepiness, lack of attention, and loss of vigilance. Eysenck (1996) believed that these characteristics were
similar to the personality factor of extraversion. Individuals with low arousal levels and those who are
extraverts need to seek out stimulation because they do not have enough already in their brains. Therefore,
the premise of the general arousal theory of criminality is that individuals inherit a nervous system that is
unresponsive to low levels of stimulation and as a consequence, these individuals have to seek out the proper
stimulation to increase their arousal. Under this theory, the proper stimulation includes high-risk activities
associated with antisocial behavior, which consists of sexual promiscuity, substance abuse, and crime (Miles
& Carey, 1997). A significant fact that must be pointed out though is that not every individual with low
arousal levels or those who are extraverts will seek those high risk activities just mentioned. It takes the right
environment and personality to create an individual with antisocial or criminal tendencies and that is why
this theory can be considered to take into account both factors of genetic and environmental influences.
Conclusion
There cannot be enough possible evidence to conclude the point that genetics play the most
important role in the outcome or behavior of an individual. The opposing viewpoint of
environmental factors is not without its doubts either as to being the prominent factor
influencing antisocial or criminal behavior of an individual. In this paper, there is more
evidence supporting the genetics viewpoint, but that does not mean it is more important.
With the research and studies having numerous flaws and the inability to adequately separate
nature and nurture, there is still a great debate between genetic and environmental factors.
Researchers, however, have certainly come far in their progression, to the point where there is a large
consensus of the fact that genes do influence behavior to a certain extent. Although not as widely publicized,
it is the belief of the author that these same researchers also believe that environmental factors account for
what cannot be explained by genes. Therefore it seems obvious to reach the conclusion that an individual's
antisocial or criminal behavior can be the result of both their genetic background and the environment in
which they were raised.
One researcher has proposed a theory relating to sociopaths and their antisocial behavior. According to the
theory, a primary sociopath is lacking in moral development and does not feel socially responsible for their
actions. This type of sociopath is a product of the individual's personality, physiotype, and genotype. A
secondary sociopath develops in response to his or her environment because of the disadvantages of social
competition. Living in an urban residence, having a low socioeconomic status, or poor social skills can lead
an individual to being unsuccessful in reaching their needs in a socially desirable way, which can turn into
antisocial or criminal behavior. The first type of sociopath is dependent on their genetic makeup and
personality, while certain factors of the second type can also be heritable. Notwithstanding, the second type
has a greater dependence on environmental factors (Miles & Carey, 1997). Perhaps from this review of both
genetic and environmental factors, it seems clear to support the idea of the secondary sociopath type. An
individual can inherit certain genes and when combined with the right environmental factors can lead them
to engage in antisocial or criminal behavior.
Although not mentioned extensively in the text of the paper, there is a great need to try and identify those
individuals, especially children, who may become susceptible to certain disorders or personality traits that
can lead into antisocial, delinquent, or criminal behavior. Society should not try to imitate the era of
controlled breeding, but rather focus on the treatment and rehabilitation of those individuals in need. Certain
educational, environment enrichment programs have been shown to have a lasting effect on children if given
by a certain age (Raine, Mellingen, Liu, Venables, & Mednick, 2003). If more of these programs could be
developed, society could help prevent the future antisocial or criminal behavior of children.

Peer Commentary

Men Are Not the Only Criminals: Insights Into Criminal Behavior in
Women
Lisa C. Burt
Rochester Institute of Technology
Jones addressed how both genes and environment affect the outcomes and predispositions of criminals. This
paper goes into great detail on whether criminal behavior is in a person's genes or environment. Having a
genetic predisposition for criminal behavior and the right environment can definitely increase the likelihood
of criminal activity. Jones took criminal behavior further to describe actions relating to antisocial behavior.
This identification of an antisocial personality with criminal behavior leads to the idea that criminal mischief
is more prevalent in males. Although our justice system is heavily loaded with male criminals, women are
still part of the criminal "world."
It has been determined that men are much more physically violent than women. A few points are essential
when discussing women and violence. First, women should not be entirely eliminated from the spectrum of
criminality just because of their smaller predisposition toward aggression. Second, women are just as
capable as men of committing a violent act. Jones discussed how certain neurochemicals are associated with
criminal behavior. These neurochemicals might be more active in men, but women can still grow up in
environments in which certain tendencies are brought on.
Family environment is crucial in the development of a child's brain and personality. Genetics can only go so
far, and environment works to shape a child's mind after the child has left a mother's womb. Jones discussed
how poor communication and weak family bonds are correlated with the development of aggressive and
criminal tendencies. She also mentioned how a financially unstable family and child abuse or neglect are
associated with criminal behavior. Environment is important for a child to grow and develop into a normal,
prospering adult. Without proper nurturance, guidance, and support, no child, male or female, will learn
coping strategies, learn life skills, or grow up with a strong sense of right and wrong and respect other
people. Whether one is male or female, growing up in an environment in which one is beaten or neglected is
going to cause serious traumatic repercussions. The aggressive tendencies in males lead them to become
more aggressive in adulthood, which in turn is why they are more apt to commit violent crimes. Yet women
have been known to commit those same violent crimes, regardless of the prevalence relative to males--
women are capable of criminal behavior. Men have committed more crimes and are known to be more
violent, yet women should not be eliminated from the discussion. It has not been shown that genes or
environment alone determine criminal behavior, as Jones mentioned in her paper, so there should be no
reason why only men are mentioned, whether directly or by implication.

Peer Commentary

Criminal Behavior and Personality Disorders


Jeffrey C. Tatar
Rochester Institute of Technology
In addition to the research showing that the gene responsible for production of monoamine oxidase has a
possible link to criminality, some evidence has also shown a possible link between other genes. One area of
personality research in molecular genetics that has received a lot of attention is the trait of novelty-seeking,
and novelty seeking is a personality trait often associated with criminality. Research has indicated that the
single DRD4 gene may account for 10% of the genetic variance in relation to novelty-seeking (Sloan, 2000).
This conclusion is highly controversial because in subsequent studies there has been both replication of the
original findings, and failure to replicate in other studies. It seems most molecular genetic approaches in
relating heritability of personality characteristics such as criminality to a single gene frequently suffer from
failures in replication.
The author also proposed that some studies have demonstrated a genetic link between ADHD, CD, and ODD
and criminality. However, there are possible alternate explanations for a greater rate of criminality for those
who have suffered from these disorders that the paper failed to mention. It has been shown that people evoke
certain responses from their environment. It is plausible that children suffering from these disorders are
treated in a different manner than normal children due to the responses that they evoke, and it is because of
these environmental differences that they are more prone to criminal behavior. Say a child suffering from
ADHD is having problems in school, they may be placed in a remedial class in which there is a greater rate
of delinquency. This would be a very important environment difference that could contribute greatly to
future criminality. Other children may also socialize less with children with these disorders, which could
plausible lead to anti-social behavior.
While it is possible that in some cases the relationship between these disorders and criminality is not direct
byproduct of genes, but rather as a byproduct of the same environment. There have been studies on ADHD
in relation to a multitude of environmental factors, including everything from nutrition to environmental
toxins. For example, a studies have been done that indicate an increased time spent viewing television in
children was related to a decreased attention span and ADHD. There have also been studies showing a
relationship between television viewing and desensitization to violence, which could influence criminal
behavior. I am not proposing that it is watching TV that is the major factor in these disorders, or in
criminality, I am just trying to illustrate that perhaps there is some environmental factor that could influence
criminality as well as disorders such as ADHD.
In addition to ADHD, CD, and ODD, other disorders have shown to influence criminality as well. Studies
have shown that there is a higher occurrence of disorders such as schizophrenia, major depressive disorder,
bipolar disorder, just to name a few. It is possible that having these personality disorders gives one a greater
predisposition toward criminal behavior. A Swedish study found that the occurrence of major mental
disorders in prisoners to be 5%, as well as a 20% occurrence of personality disorders (Rasmussen, 1999).
Other studies have given different values for the occurrence, but in most cases the research agrees that there
is a much higher incidence of these mental disorders in those who commit crimes.
Genetics has shown to be a major factor in the occurrence of many of these disorders. There have been
studies that examine the rate of personality disorders such a schizophrenia, psychosis, and manic?depressive
illness in adopted children. We can hypothesize that if adopted children are more likely to suffer from such
disorders if their biological parents are or were afflicted, it would be indicative of a genetic basis for the
disorder. Research done by Leonard Heston in 1960 examined children of schizophrenic mothers that were
removed after birth and raised by foster parents. Out of a total of 47 children examined, Heston found that
nine of them were diagnosed with sociopathic personalities and antisocial behavior, and four of the 47
children developed schizophrenia. Heston also found behavioral abnormalities in many of the other children
(Eysenk, 1982). This study shows a significant increase in the rate of personality disorders in the progeny of
an affected parent, in comparison to population statistics on these mood disorders. In fact, when both parents
are affected by a personality disorder the rate of occurrence in their offspring is even higher.
Not only do adoption studies support a genetic basis for personality disorders that are shown to have a
relation to criminality, but twin studies as well. Statistics show a high concordance between identical and
non-identical twins for schizophrenia and manic depression. Analysis of the statistics clearly show the
genetic basis for these disorders: For schizophrenia the concordance in identical twins was 60%, compared
to only 10% in non-identical twins, and the normal frequency being 1% in northern European populations.
Similarly, manic depression showed a 70% concordance between identical twins, a 15% concordance
between non-identical twins, and again only a 1% frequency in the normal population (Russo & Cove,
1995). This research supports the theory that genetics play a crucial role in these personality disorders.

Peer Commentary

Criminality Is a Product of Genes and Environment


Maureen E. Wood
Rochester Institute of Technology
In considering the roles of genetics and environment on criminal behavior, or any behavior for that matter, I
think the best explanation is that there is a complex interaction between one's inherited traits and the
environment in which he or she lives. Although the idea of environmental influences seems rather intuitive,
regardless of knowledge regarding heredity and biological factors, it is surprising that some may have
considered criminal behavior to be solely a result of genetics. I propose that the debate of nature versus
nurture now is not whether genetics or environment influence behavior, but how complex the interaction
between these factors is.
Despite the relative lack of reliability and validity in twin, adoption, and family studies, they still provide
valuable insight into the roles of heredity and environment in criminal behavior. However, it seems that most
studies of this kind focus on the role of heredity in influencing behavior. It would be interesting to see
whether any studies with adopted children have examined the role of environment in criminal behavior.
Most adoption studies examine the correlation between criminality in the biological parents of adopted
children, but what about the correlation between the children and their adopted parents who are crucial to
their environment?
I agree with Jones that the influence of neurochemicals on criminal and antisocial behavior are indicative of
a genetic component to such behaviors. However, I think a more complete explanation of neurochemical
influences is that they reflect the complex interactions between genetics and environment. There is evidence
that the expression of genes is influenced by a wide variety of environmental factors. Therefore, it is very
possible that disorders relating to such chemicals as serotonin and dopamine could be caused by stressful
environmental situations. If environment affects the regulation of gene expression and, in turn, the activity
of neurotransmitters that modulate behavior, this kind of interaction may be a significant factor in the
development of criminal and antisocial behavior.
Jones's argument regarding the extent to which environmental and genetic factors influence antisocial and
criminal behavior in childhood versus adulthood seems somewhat incomplete. While it is true that adults
have more control of their environment than children, I do not think that children are necessarily affected
more by environment and adults are influenced more by heredity. Inherited traits provide the foundation by
which people are able to learn and respond to their environment. An adult's personality is the combination of
traits and learned behavior patterns that have been established throughout childhood. Thus, although it is
true that adults have more control over their current environment, I believe that they are still heavily
influenced by both their current environment and by past exposure to environmental factors.
The social learning theory is a good way to explain the influence of environment on antisocial behavior in
children, and does not necessarily have to oppose the notion of genetic influence on behavior as well.
Rather, it should be considered part of a larger theory or model that could describe how environment and
genetics interact. Eysenck's general arousal theory, which suggests such an interaction, could be modified to
encompass the social learning theory, providing a more complete model to explain how upbringing and
inherited traits interact to influence criminal behavior.
Overall, I agree with Jones's support of the idea of the secondary sociopath type. Genetics and
environmental factors are so intertwined, that it seems impossible to separate them in explaining how people
are caused to engage in criminal acts. Also I agree that it is important for society as a whole to take
responsibility in preventing the advent of criminal and antisocial behavior in children via programs to
provide children with healthy, enriching environments. A eugenic approach to preventing antisocial behavior
is immoral and impinges on human rights, but taking an active approach to ensure positive environmental
influences would be appropriate.

Author Response

Criminal Behavior: Those Affected, Other Causes, and Beyond


Caitlin M. Jones
Rochester Institute of Technology
I would like to thank those who wrote peer commentaries because there is obviously a lot of information that
was not covered in my paper but that should not be neglected. Overall, I think it is safe to say that the
majority believe that there are both environmental and genetic influences for criminal or antisocial behavior.
The information from the peer commentaries adds to this notion.
Burt discussed the inference that my paper was specifically addressing the male population as more
aggressive and consequently leading to criminal or antisocial behavior. I cannot disagree with this point,
because some of the studies referred to in the paper were conducted on males only, and most research points
to the male sex as more aggressive. It is important to know that women can be just as criminal in their
behavior, as Burt pointed out. An integral piece of information, however, is that although women commit a
large part of crimes, it is usually in the form of non-violent crimes.
Tatar first addressed the fact that there are other genes that may be associated with criminality, such as the
gene DRD4, which is associated with the personality trait of novelty seeking. As mentioned in my paper,
there is no single gene that is responsible for criminal or antisocial behavior, so I applaud the mention of
other genes. I also agree with Tatar that there are other environmental influences, such as how a child's
behavior or disorder can evoke certain responses from the child's environments. I believe this to be true, and
more research needs to be focused on how to treat or approach these children so that their behaviors do not
develop further into antisocial or criminal behavior. A topic that was omitted from my paper, which Tatar
also mentioned, was the heritability of personality disorders. This is an important topic, because some
personality disorders have been associated to a higher degree with criminal or antisocial behavior.
Wood believed that there is an interaction between environmental and genetic influences on criminal or
antisocial behavior. The point she brought up, with which I also agree, is how complex that interaction is.
With regard to the adoption studies, my research did not go far enough to report on the findings of adoptive
parents and their adopted children. I am positive that those adoption studies looked at that relation, and one
of the findings that might have resulted is that the environment in which the adoptive parents raise their
child has a significant influence, regardless of the genes inherited. Another point that Wood discussed was
the impact that environmental influences has on children and adults. I realize that the environment in which
one lives will always influence one, but the point I was making regarding children being more affected was
focused on peer influences as well as parents. Children are more susceptible to peer pressure and being
controlled by their parents, whereas adults have the ability to shape their own environments.

References
Alper, J. (1995). Biological influences on criminal behavior: How good is the evidence? British
Medical Journal, 310, 272-273.
Brunner, H. G., Nelen, M., Breakefield, X. O., Ropers, H. H., & van Oost, B. A. (1993). Abnormal behavior
associated with a point mutation in the structural gene for monoamine oxidase A. Science, 262, 578-580.
Elliot, F. A. (2000). A neurological perspective of violent behavior. In D. H. Fishbein (Ed.), The science,
treatment, and prevention of antisocial behaviors: Application to the criminal justice system (pp. 19-1 to 19-
21). Kingston, NJ: Civic Research Institute.
Eysenck, H. J. (1982). Personality, genetics, and behavior. New York: Praeger.
Eysenck, H. J. (1996). Personality and crime: Where do we stand? Psychology, Crime, & Law, 2, 143-152.
Garnefski, N., & Okma, S. (1996). Addiction-risk and aggressive/criminal behavior in adolescence:
Influence of family, school, and peers. Journal of Adolescence, 19, 503-512.
Holmes, S. E., Slaughter, J. R., & Kashani, J. (2001). Risk factors in childhood that lead to the development
of conduct disorder and antisocial personality disorder. Child Psychiatry and Human Development, 31, 183-
193.
Joseph, J. (2001). Is crime in the genes? A critical review of twin and adoption studies of criminality and
antisocial behavior. The Journal of Mind and Behavior, 22, 179-218.
Larsen, R. J., & Buss, D. M. (2005). Personality psychology: Domains of knowledge about human nature
(2nd ed.). New York: McGraw Hill.
Lowenstein, L. F. (2003). The genetic aspects of criminality. Journal of Human Behavior in the Social
Environment, 8, 63-78.
Miles, D. R., & Carey, G. (1997). Genetic and environmental architecture of human aggression. Journal of
Personality and Social Psychology, 72, 207-217.
Morley, K., & Hall, W. (2003). Is there a genetic susceptibility to engage in criminal acts? Australian
Institute of Criminology: Trends and Issues in Crime and Criminal Justice, 263, 1-6.
Raine, A., Mellingen, K., Liu, J., Venables, P., & Mednick, S. A. (2003). Effects of environmental
enrichment at ages 3-5 years on schizotypal personality and antisocial behavior at ages 17 and 23 years.
American Journal of Psychiatry, 160, 1627-1635.
Rasmussen, K., Storsaeter, O., & Levander, S. (1999). Personality disorders, psychopath, and crime in a
Norwegian prison population. International Journal of Law and Psychiatry, 22, 91-97.
Rhee, S. H., & Waldman, I. D. (2002). Genetic and environmental influences on antisocial behavior: A meta-
analysis of twin and adoption studies. Psychological Bulletin, 128, 490-529.
Russo, E., & Cove, D. (1995). Genetic engineering dreams and nightmares. New York: Freeman.
Schmitz, M. F. (2003). Influences of race and family environment on child hyperactivity and antisocial
behavior. Journal of Marriage & the Family, 65, 835-849.
Sloan, P. R. (2000). Controlling our destinies. Notre Dame, IN: University of Notre Dame Press.
Tehrani, J., & Mednick, S. (2000). Genetic factors and criminal behavior. Federal Probation, 64, 24-28.

DNA & BEHAVIOR

Is Our Fate in Our Genes?

The Topic In­Depth

by Sophia Koliopoulos (October 2001)

Since 1998, when  The DNA Files  first presented an  overview  of the science and social implications of 


research   in   behavior   genetics,  scientific   discovery   has   been   relatively   limited.  Instead,   commentary   has 
focused on the complex interplay of genetics and environment in affecting human behavior. 

Discussion has also emphasized the inherent difficulty in applying standard scientific techniques ­ such as 
the "experimental method" ­ when studying the genetic factors that influence human behavior. 

Further, experts continue to urge caution against using terms like "genetic" and "inherited," interchangeably 
with terms like "familial." While "genetic" and "inherited" involve the transfer of a trait from one generation 
to another by physical means like DNA, a "familial" trait simply occurs at a high rate within a particular 
family ­ a phenomenon that may due to biological factors, environmental influences, or a combination of the 
two.

Meanwhile, the reported discovery of a "gay gene" in 1993 continues to be challenged. Likewise, the "gene 
for"   or   "genes   for"   violence   or   particular  personality   traits  have   remained   no   more   than   theoretical 
possibilities. While specific genetic factors continue to be associated with  alcoholism  and other addictive 
behaviors, their exact contributions ­ and how this information could be used in mitigating the behaviors ­ 
are still unclear. 

Progress,   mainly   through   studies   of   twins,   has   also   been   made   in   identifying   genetic   factors   that   may 
influence the development of bipolar disorder. Still, scientists caution, no single genetic determinant for the 
condition exists ­ and environment plays a key role.

Yet the influence of one's genes on anti­social behavior gained increasing attention in the spring of 2001, as 
the  U.S. Supreme Court reversed the death sentence  of a mentally retarded man and the  Texas governor 
vetoed a bill which would have banned execution of such individuals. These events fueled the debate over 
executing the mentally retarded, some of whose abilities may be impaired by genetic conditions like Down 
syndrome, fragile X syndrome or certain non­syndromic genetic conditions.
DNA & Behavior: The Topic In­Depth

by Sally Lehrman 

(Originally published in November 1998)

To hear some behavioral geneticists talk, our genes hard­wire our personalities and the best thing to do is to 
get used to it. Sure, they say, the environment plays an important role, and people can make their own way in 
learning to cope with their genetic predispositions. But normal variations in personality characteristics such 
as thrill­seeking, worry, anger and addictive behavior all trace back to genetic roots, the behavioralists assert.

The   best­known   U.S.   researcher   in   this   field,   Dean   Hamer,   leapt  into   the   public   eye   in   1993   with   the 
announcement he had discovered "the gay gene." Since then, Hamer, a molecular geneticist at the National 
Cancer Institute, has become a lively spokesman for a new era of behavioral genetics. He commands large 
audiences enraptured by clues as to why they overeat, hate surprises, or sleep around. His controversial ideas 
are bolstered by a growing number of studies that seem to draw connections between physiological states and 
specific human behaviors.

Hamer and other scientists are leading a resurgence of interest in finding the biological roots of personality 
and behavior. "This is a tool for liberation, a scientific window into the soul. Yes, we are born with a certain 
genetic makeup. No, that doesn't mean we have no control over our lives," Hamer writes in his book, Living  
with Our Genes.

Hamer emphasizes that genes don't dictate a person's future; rather, they interact with each other, with the 
environment, and with an individual's response to these influences. It's hard to avoid linking genes with 
destiny, though, when talking about behavior. And it's easy to make leaps of logic when trying to make 
generalizations about personality characteristics. The history of behavioral genetics has been fraught with 
philosophical battles, scientific errors, and social and scientific debate. The field has provided fodder for 
class­, race­ and sex­based bigotry, and triggered alarms for those fighting discrimination. The media often 
report researchers' pronouncements uncritically, and have even repeated claims long disproven.

Could someone really be "born bad"? It's not nearly that simple. Researchers on all sides of the behavioral 
genetics debate emphasize that the link between a gene and a behavior is not the same as cause and effect. 
Bottom line: a gene does not make people do things. It doesn't code for emotions or thoughts. It may not 
even turn on or off without an instruction from its surroundings. Instead, a gene may trigger a whole cascade 
of biochemical events in the body, interact with environmental and developmental influences, and ­ together 
with these ­ increase the likelihood that you'll behave in a particular way.

Eugenics

The historical context of behavioral research makes it easy to see why it's a touchy subject today. In the early 
1900s,   American   scientists   used   Mendelian   concepts   of   inheritance   to   show   that   manic   depression, 
"criminality," "pauperism," "feeblemindedness," "shiftlessness" and various other socially harmful traits they 
identified were passed from generation to generation via genes. They drew from observations of laboratory 
mice   and   farm   animals   to   develop   theories   about   ways   to   abolish   mental   and   social   dysfunction   by 
manipulating human reproduction. 
Francis Galton, the cousin of evolution theorist Charles Darwin, had come up with the term "eugenics" ­ 
meaning "well­born" ­ in the late 19th century. A British population geneticist, Galton studied correlations 
among relatives to learn which aspects of social well­being ­ such as intelligence, birthrate and alcoholism ­ 
might be heritable. His American disciple, Charles B. Davenport, relied instead on the Mendelian framework 
of understanding inheritance through family pedigrees, but nevertheless eagerly picked up and promoted the 
philosophy of eugenics as a way to improve the quality of the human species and create a better future for 
everyone. 

He   and   his   colleagues   hunted   for   patterns   in   alcoholism,   so­called   criminality,   insanity,   and   other 
characteristics they believed might be passed down through families. In huge leaps of conjecture, they traced 
certain behavioral tendencies to particular races. For example, Davenport characterized Italians as drawn 
toward   crimes   of   personal   violence,   Greeks   as   slovenly,   and   Swedes   as   tidy.   Through   immigration 
restrictions, sterilization laws and related policies, these eugenicists hoped to excise social and economic 
problems   at   their   root.   By   1935,   thirty   states   had   passed   sterilization   laws   to   prevent   reproduction   by 
genetically "inferior" people. The United States led the drive; other countries took up similar activities.

The Nazis adopted and expanded upon American eugenic ideas to rationalize first mass sterilization, then 
extermination programs. The atrocities in Germany generally discredited the eugenics movement after the 
World War II era but didn't stamp out its ideology or its practice. Involuntary sterilizations continued in 
Alberta, Canada, for instance, until as recently as 1971, and in the state of Alabama until 1973. As of 1985, at 
least nineteen states still had laws permitting the sterilization of people with mental disabilities, according to 
physician and lawyer Phillip Reilly, who specializes in medical ethics at the Shriver Center in Waltham, 
Mass.

Today   you   can   still   find   people   who   support   eugenics   theories,   although   they   are   pretty   much   on   the 
periphery.   Most   scientists   working   in   the   behavioral   genetics  field   avoid   making   broad   statements   that 
connect particular populations to gene­based characteristics. Charles Murray and Richard Herrnstein, who 
made a case for a race­based gap in the inheritance of intelligence in their book  The Bell Curve, are a 
notable exception. The book has refueled concerns that discoveries of links between behavior and genes will 
undermine ideas of equality among people and lead to regressive social policies.

The Science

While behavioral genetics is beset on either side by grandiose claims and ardent detractors, there does seem 
to be growing consensus that heredity does play some role in human behavior. This doesn't mean geneticists 
agree that our genes set a course for individual behavior, or that nature has taken precedence over nurture. 
Debate over scientific and social issues related to the field rages on. 

Biological studies on behavior began with observations of similarities among family members that seemed 
to indicate the action of both shared genes and shared environment. In order to tease these apart, researchers 
turned to twin and adoption studies, which date back more than 70 years. The most famous of these is 
housed at the University of Minnesota Center for Twin and Adoption Research in Minneapolis, headed by 
Thomas J. Bouchard. Researchers there have examined more than 1,000 pairs of twins.

Identical twins share all of their genes (with some exceptions), while fraternal twins, on average, share only 
half. Identical twins come from the same fertilized egg, which splits into two. Fraternal twins develop from 
separate eggs, fertilized by different sperm. In order to estimate the influence of genes over a particular trait, 
researchers often try to compare shared behaviors between each of the two types of twins. The results aren't 
that easy to interpret, though, and can be misleading. Identical twins, for example, may be more often treated 
alike than fraternal twins, making genetic influence seem more important. So twin studies have focused 
especially on the behavioral similarities of identical twins raised apart as a way to try to identify the various 
influences. 

Researchers   use   the statistical results  of  twin comparisons  to develop  estimates of  "heritability,"   or   the 


variation   in   a   particular   trait   within   a   group   that   is   attributable   to   genes.   In   a   mathematical   sense, 
"heritability" represents the variance in an observed trait due to genes, divided by the total variance in the 
observed trait. Overall, twin studies specialists have estimated that genes account for 40­ to 60­percent of the 
variation in human psychological traits. But this kind of numerical summary implies a scientific certainty 
that doesn't exist. Sorting out the relationship between environmental and genetic factors into some measure 
of heritability is impossible, in part because of the interplay between the two, says Peter Schonemann, a 
psychologist at Purdue University, in a June 1994 issue of Science. Other critics point to problems in both 
the manner in which twin studies are performed and in the concept of heritability itself. 

Twin Controversies

The twin studies are a popular topic because of startling similarities that emerge between twins raised apart ­ 
siblings   with   seemingly   little   in   common   except   identical   genes:   flushing   the   toilet   twice,   sneezing   in 
elevators, and wearing cowboy hats, among other things. But, surprisingly, there may be explanations having 
little to do with genetics. For one thing, the sample of people studied might not accurately represent the 
broad population of twins. Those who volunteer for this kind of study probably have a special interest in 
being "twins." And individuals who share physical features are likely to be treated alike, and so may share 
developmental experiences. In effect, their looks create similar environments.

In her book The Nature Assumption, Judith Harris gives an example. Say two identical twins are both tall. 
Researchers have demonstrated that society tends to act toward taller people with more respect, attention and 
reinforcement, which then is likely to lead to greater self­esteem. When these twins fill out a personality test 
for behavioral geneticists, they'll both probably score high on extroversion and self­confidence ­ but not 
because of any "self­esteem" gene.

Adoption agencies add to the likelihood of a shared environment by attempting to match children with 
circumstances comparable to their original home, including economic status, religion, and cultural interests. 
On the other side of the equation, researchers may overestimate the common experiences of siblings raised 
together. Factors such as a child's birth order can cause big differences in his or her upbringing. 

Finally, the statistical assumptions made when calculating the frequency of differences between twins have 
been controversial. Even if the numbers do work out, it's important to keep them in perspective. They can't 
be interpreted to show the likelihood a parent will transmit a specific type of behavior to his or her offspring. 
Rather, they refer to populations as a whole at a given time. They also don't indicate some portion of a trait 
that is unchangeable or unaffected by environment. Families tend to think of "heritability" as the handing 
down of an intact behavior from parent to child like a baton, explains University of Illinois psychologist 
Scott Stoltenberg. But the technical definition refers more generally to the proportion of a trait in a particular 
population accounted for by genetic factors. 

Linkage Studies
DNA­based   techniques   have   allowed   more   specific   studies   of   genetic   influences   on   human   behavior. 
Geneticists identify people in families with a particular behavioral disorder such as manic depression, then 
look for sections of genes (genetic markers) that they all seem to share. They aim to narrow these results 
down to find markers very close to the targeted gene, and then its exact location. The researchers then test 
whether the gene's activity ­ or failure to act ­ seems to trigger the observed behavior. Finally, they look at 
the product made by the gene and try to determine its role. Ultimately, they hope to discover a way to lessen 
the effects of a malfunctioning gene.

Linkage analysis is a familiar tool in medical genetics. But the case for behavioral genetics today is haunted 
by   a   series   of   linkage   studies   in   the   late   1980s   that   traced   particular   behaviors   to   certain   genetic 
characteristics, then failed confirmatory tests by other scientists. Sometimes the researchers' claims were 
withdrawn   for   other   reasons.   While   behavioral   geneticists   have   recently   become   more   optimistic,   new 
discoveries still seem plagued by follow­up studies that appear to disprove their findings. Some critics say 
the problem is quite basic: they argue that the research is based on weak methodology and is an effort to add 
scientific weight to social beliefs. Others remain hopeful, pointing out that research on behavior is very 
complicated and difficult.

Animal Studies

Studies on mice have become a convenient way to investigate the genetic roots of behavior while controlling 
for the environment. Even though mice and humans may seem worlds apart in appearance and behavior, the 
mouse genome is very similar to ours; mouse researchers say the components are essentially the same, only 
arranged   in   different   order.   Mouse   breeders   have   learned   how   to   inactivate   certain   genes   and   create 
"knockout mice," which geneticists can then observe. In studies in France, for instance, mice without a 
particular receptor for serotonin showed more aggression toward other mice. In other research, mice missing 
the same neurotransmitter were unusually tolerant of and drawn to alcohol. Scientists at Johns Hopkins 
University   reported   in   1995   that   another   knockout   mouse   strain,   which   was   missing   a   gene   needed   to 
produce nitric oxide, was extremely aggressive.

Other   researchers   first   hunt   for   strains   of   mice   that   act   a   certain   way   and   then   start   looking   for   the 
responsible gene. Some rodent families crave alcohol; some seem to have superior learning capabilities. In 
theory, it's not vital that the mice mimic humans exactly. Once researchers identify a particular gene in mice, 
they can look for its counterpart in humans and check whether it has a similar effect. 

But even as scientists try to narrow in on the gene that's responsible for a behavior, they have begun to 
realize that it's hard to tease out just what it is they're studying. Mice that appeared predisposed to addiction 
because they kept returning to a morphine­laced drinking bottle, for example, turned out instead to hate the 
quinine  spiking  the alternate choice. Is  a rodent that strikes at another mouse on top of  its cage  more 
aggressive? Or is it more anxious, claustrophobic or sensitive to shadow? To add to the confusion, what 
looks like a measurable behavior could be the side effect of a physical characteristic. A mouse that seems to 
be aggressive, say, might have an unusually low physical pain threshold ­ and so be hurting, grumpy, and 
prone to strike others. 

Studies in People

Here are summaries of some key areas of behavioral research on humans: 
Alcoholism.   In   1990,   psychiatrist   Ernest   Noble   of   UCLA   and   pharmacologist   Kenneth   Blum   of   the 
University of Texas in San Antonio reported a strong association between alcoholism and one version of a 
gene that makes the dopamine D2 receptor. They found this particular gene variation, which they called A1, 
in more than two­thirds of 35 deceased alcoholics, compared to just one­fifth of the same number of non­
alcoholics. The gene builds a receptor on the surface of nerve cells that responds to dopamine, a chemical 
messenger in the brain's "pleasure center."

Their report followed a number of twin, family and adoption studies that pointed toward inheritance of a 
tendency toward drinking too much. But six months later, a team at the National Institute on Alcohol Abuse 
and Alcoholism said they could not find any such genetic difference between living alcoholics and non­
alcoholics. Four more groups followed with negative findings. Blum and Noble, however, stood by their 
hypothesis and medical geneticist David Comings of the City of Hope Medical Center in Duarte, California, 
agreed.   Together   they   pressed   their   case,   expanding   their   view   of   the   gene's   influence   to   a   variety   of 
compulsive disorders including cocaine addiction and obesity. They labeled it a "reward" gene associated 
with addictive behavior. 

"The   Gay   Gene".   In   the   summer   of   1993,   Dean   Hamer   announced   he   had   found   a   section   of   the   X 
chromosome  shared by gay brothers.  Hamer named the region Xq28, and declared it the first  concrete 
evidence that "gay genes" really do exist. The finding catapulted Hamer into the center of a heated debate 
over nature's role in the development of homosexuality. Some gays hailed the finding as a weapon against 
discrimination, since they believed it showed that their sexual orientation was not chosen. Others pointed to 
a history of shock treatments, aversion therapy, and brain surgery aimed at making gay men straight, and 
they predicted further discrimination.

Political debate aside, Hamer's findings had some problems. His team examined the X chromosomes of 40 
pairs of gay brothers and found that 33 pairs (or 82­percent) shared genetic markers in one region. Men who 
inherited some gene or genes in that section were predisposed to becoming gay, Hamer concluded. But 
Hamer didn't look at the chromosomes of any of the men's straight brothers; if any had matched in the same 
region, it would have hurt the significance of the similarities he found. Plus, the population he studied had 
been self­selected through ads in gay publications and so couldn't be considered a representative sample.

Five   years   later,   no   other   lab   has   confirmed   Hamer's   results.   George   Ebers,   a   neurogeneticist   at   the 
University of Western Ontario, studied 52 pairs of gay men but found no special link with the Xq28 region. 
Hamer did seem to confirm his own results in another 33 pairs of gay brothers: about 66­percent shared 
Xq28.   He   also   checked   heterosexual   brothers   and   lesbian   sisters   in   the   same   families   but   found   no 
association with the marker.

At first glance, an earlier twin study seems to support the idea of inheriting homosexuality. But a closer look 
at the 1991 work ­ which also had its methodological problems ­ shows a more complicated picture. Michael 
Bailey of Northwestern University and Richard C. Pillard of Boston University interviewed gay volunteers 
and found that in 52­percent of the identical twins they surveyed, both men were gay. As many as 22­percent 
of the fraternal twins they talked to also shared a homosexual orientation. Regular non­twin brothers, from 
whom you might expect similar results because they share the same amount of genes as fraternal twins (half 
of them), were both gay only 9­percent of the time. 

For the moment, then, it's impossible to say whether a "gay gene" (or genes) exists. Some critics of the hunt 
for  a  "gay  gene"  point to what they consider an essential flaw in the researchers'  assumptions.  Human 
sexuality is complicated, diverse, and often inconsistent ­ and so, they argue, can't be reduced to a simple 
series of orientations, biologically determined or not. 

Normal Personality. In January 1996, researchers from Israel and the United States separately reported 
what they called the first link between a gene and what's termed by psychologists a "normal" personality 
trait,   novelty­seeking.   People   with   this   characteristic   seemed   to   be   more   excitable,   adventurous,   and 
impulsive than others, based on their responses to personality tests. Researchers connected their behavior to 
a variant of a gene, called D4DR, that appeared to affect the way the body responded to dopamine, the brain 
chemical linked to pleasure. At least three studies since then, however, have failed to show an association 
between   the   gene   variation   and   novelty­seeking.   The   reasons   could   include   differences   in   personality 
measures, ethnicity, or errors in methodology ­ or just that the sample sizes were way too small. Dean 
Hamer, who led the U.S. studies, suggests that researchers have been measuring the wrong thing: the gene 
may instead have a strong effect on a happy outlook on life.

In November 1996, Hamer was part of a group that reported a gene that seemed to influence mood. One 
mutation in it appeared to induce self­confidence and good cheer. A different mutation seemed to predispose 
people  to  chronic  anxiety, as  measured by their own  assessment.  The gene regulates serotonin,  a  brain 
chemical   that   affects   people's   sense   of   well­being;   it   happens   to   be   the   same   brain   chemical   that   the 
antidepressant Prozac acts upon. The researchers, led by Klaus­Peter Lesch of the University of Wuerzburg 
in   Germany,   said   they   think   the   gene   accounts   for   about   4­percent   of   the   difference   in   anxiety   and 
cheerfulness   between people.  Hamer  says  the  gene may  also  be linked  to alcoholism and  smoking.   Of 
course, more studies are needed to test such claims. 

Violence. Efforts to uncover the biological roots of violence have long been a research pastime ­ and a focus 
of controversy. As with much of behavioral genetics, the heart of the problem has to do with how society 
uses the results. While the work could help explain differences in individuals across populations, it also 
could   stimulate   a   hunt   for   generalized   tendencies   that   could   be   assigned   to   a   particular   group.   Such 
expeditions   are   particularly   dangerous   because   of   the   difficulty   in   defining   the   characteristics   (or 
"phenotype") of a behavior like violence. Just as it's hard to sort out when self­defense shifts into aggression, 
the same behavior can be interpreted differently depending on the situation. Activities and attitudes that 
observers   condemn   as   unprovoked   violence   on   the   street   may   be   celebrated   as   patriotic   duty   on   the 
battlefield.

In April 1998, revelations about violence studies conducted on children in New York demonstrated the ways 
aggression   is   often   linked   broadly   to   heredity   ­   and   to   social   stereotypes.   Researchers   in   New   York 
administered the now­recalled diet drug fenfluramine to mostly low­income boys believed to have violent 
tendencies. Researchers hoped to find out whether the drug, which triggers the brain to release serotonin, 
could lessen aggression. Some of the boys had already been treated for attention­deficit disorder. But 100 
African American and Latino boys were chosen only because their older brothers had gotten into legal 
trouble.   Not   surprisingly,   the   researchers   were   widely   attacked   for   deeply   flawed   theoretical   and 
methodological assumptions ­ and for poor ethics in their study design.

Some   argue   that   genetics­based   research   on   violence   and   aggression   could   help   dispel   some   of   the 
stereotypes that lead to such studies. Others take the opposite point of view. In 1992, the National Institutes 
of Health funded a conference on genetic factors in crime. Many criticized the idea as racist in concept, 
believing that the focus on genetics masked an attempt to rationalize discriminatory criminal justice policies. 
Peter   Breggin,   director   of   the   Center   for   the   Study   of   Psychiatry   in   Bethesda,   Maryland,   organized   a 
campaign that convinced NIH to withdraw its plans.

Nevertheless,  in  1995 the conference went ahead at the University of  Maryland. Organizers insisted  its 


purpose was to challenge the notion that there could be a meaningful link between genetics and crime, given 
the   state   of   genetic   research   and   the   subjective   interpretation   of   "crime."   Protesters   didn't   buy   the 
explanation and condemned the meeting. 

At   a   gathering   in   London   that   same   year,   many   researchers   in   attendance   said   evidence   seemed   to   be 
growing for genetic influence on aggressive behavior as well as propensity for crime. But among other 
complaints, critics marveled at the lack of discussion of their hypotheses' social implications ­ especially in 
regard to race. In a 1996 review for the science journal Trends in Genetics, Jonathan Flint of the Institute of 
Molecular Medicine in Oxford, England, expressed alarm at the omissions: "Should we then expect those 
scientists who do manage to meet to discuss the genetics of crime to confront contentious issues? Or should 
we simply be astonished that they do not seem to notice that they are dealing with an explosive social 
problem?" The criminal justice system isn't waiting for the answers to be sorted out. In an August 1998 
interview with the journal Nature, Massachusetts state senator James Jajuga suggested that DNA collected 
from parolees could help to develop a "criminal" genetic profile and help law enforcement officers prevent 
relapse among offenders through education, drug therapy or counseling. 

Skeptics

By its nature, behavioral genetics touches on some very sensitive issues. Its historical link to eugenics has 
spurred some to argue on moral grounds against seriously pursuing such research. Others say there is little 
scientific basis to justify the field. In a 1997 article in the science journal Genetica, University of Western 
Ontario evolutionary biologist Robert Bailey summed up such a perspective. "As long as humans are not 
exposed to artificial selection and crossing experiments, behavior geneticists will be very limited in their 
ability to partition the effects of genes, the environment and ... their interaction on human behavior and 
cognitive ability," he said. 

Judicature
Genes and Justice
The Growing Impact of the New Genetics on the
Courts

November-December 1999 Vol 83(3)

The IMPACT of BEHAVIORAL GENETICS on


the LAW and the COURTS
by Mark A. Rothstein
The Human Genome Project, officially begun in 1990 and scheduled for completion between 2000 and
2003, has heralded a period in which genetic factors have been identified for numerous disorders. In
addition, researchers in the field of behavioral genetics have asserted claims for a genetic basis of numerous
physical behaviors, including homosexuality, aggression, impulsivity, and nurturing. A growing scientific
and popular focus on genes and behavior has contributed to a resurgence of behavioral genetic determinism
—the belief that genetics is the major factor in determining behavior. This could lead to grievous social
consequences.

Research in behavioral genetics has been extremely contentious. There are several scientific obstacles to
correlating genotype (an individuals genetic endowment) and behavior. One problem is in defining a specific
endpoint that characterizes a condition, be it schizophrenia or intelligence. Another problem is in identifying
and excluding other possible causes of the condition, thereby permitting a determination of the significance
of a supposed correlation. Much current research on genes and behavior also engenders very strong feelings
because of the potential social and political consequences of accepting these supposed truths. Thus, more
than any other aspect of genetics, discoveries in behavioral genetics should not be viewed as irrefutable until
there has been substantial scientific corroboration.

Flawed scientific theories can be refuted by more rigorous science. A more perplexing social quandary
involves the permissible societal response to legitimate discoveries in behavioral genetics. Undoubtedly,
there is some correlation between certain genes and behavioral traits. The only serious scientific dispute
concerns the overall degree of correlation and the applicability of genetic factors in a range of specific
behavioral traits. What, then, are the likely psychological, social, political, and legal consequences of such
correlations?

As an example, take the case of alcoholism. Several past and ongoing studies have explored whether there is
a genetic component of alcoholism.1 Assume such a component exists in some cases of alcoholism. Does
that mean that, as a society, we will be more or less tolerant of alcoholics, more or less inclined to mandate
genetic testing to detect a particular version of a gene or genes (called "alleles"), or more or less likely to
embrace a disease model for this behavior? On the one hand, it could be argued that the genetic component
decreases the moral taint attached to individuals with alcoholism.

On the other hand, the genetic, heritable nature of the disorder may increase the stigma, it may increase the
pressure for genetic screening for the particular allele, it may contribute to individuals feeling a sense of
resignation and a reluctance to enter treatment, and it may lead to disdain for individuals who, despite
knowledge of their genotype, continue to drink.

Similar issues are raised with regard to a possible genetic link to homosexuality. If we find a "gay gene,"
will it mean greater or lesser tolerance? My suspicion is that it will not change the way most people view
homosexuals. For individuals who are tolerant of homosexuals, it will reaffirm that the behavior is
physiologically based and does not represent moral depravity. For those less tolerant of homosexuality, it
will confirm their view that such individuals are "abnormal." It also could lead to proposals that those
affected by the "disorder" should undergo treatment to be "cured" and that measures should be taken to
prevent the birth of other individuals so afflicted.

Genetic determinism and the law

One consequence of new genetic research may be a resurgence of behavioral genetic determinism. If so, this
phenomenon would have major implications for the legal system. I have written elsewhere at length about
the effects of genetics on many areas of law, including employment, insurance, commercial transactions,
civil litigation, and privacy.2 Rather than discussing specific areas of the law in which behavioral genetics
may be important, I will discuss five general principles of law that help to frame the issues of behavioral
genetics and the law.

1. The law has established a unitary standard for determining an individual's legal duty. In both the
civil and criminal law, the lawfulness of an individual's conduct is determined by reference to the standard of
behavior of a reasonable person. The hypothetical reasonable person is not the average person or the average
juror, but the personification of a community ideal of reasonable behavior. This is an objective and largely
unitary standard.

The reasonable person standard, originally expressed as the "reasonable man" standard, was first applied to
negligence law in England in the middle of the nineteenth century. 3 The concept was soon adopted in the
United States.4 By the beginning of the twentieth century the gender-neutral "reasonable person" came into
use and is now used in every state. The reasonable person standard is often expressed as the reasonably
prudent person, or some similar terminology, all of which have the identical meaning. Thus, both plaintiffs
and defendants in civil negligence cases have the reasonableness of their conduct evaluated in terms of
whether it conforms to the standard of a reasonably prudent person under similar circumstances.

Although the law does not consider minor, individual variations in the character and abilities of the
individual in establishing the standard for evaluating conduct, there are some exceptions. Children are held
to the standard of a reasonable child of the same age. An individual's special talents or training also are
considered.

For example, in a medical malpractice case, the "standard of care" is that of a reasonably prudent physician
in good standing in the profession, or if the individual is a specialist, the reasonably prudent physician in a
certain specialty. If the individual has a physical impairment, the standard is the reasonably prudent person
with the same impairment, such as the reasonably prudent person with blindness. Note, however, that the
reasonable person standard generally has not been adjusted for mental impairments or behavioral
shortcomings. These matters historically were assumed to be impossible to assess accurately. Moreover,
excusing the conduct of people because of their asserted individual inability to conform to the reasonable
person standard was seen as an invitation to fraud.

The criminal law also recognizes a version of the reasonable person standard. Criminal negligence is defined
by reference to a reasonable person. In cases where a murder has been committed in a moment of passion, a
reasonable person standard is used to determine whether the circumstances would cause such a reaction. If
so, then the charge of murder is reduced to voluntary manslaughter.

The main rationales for the reasonable person standard are:

• the required conduct of the individual and the outcomes of cases are more predictable,
• having a unitary, objective standard allows individuals to have reasonable expectations
of the behavior of others,
• it is easy for juries to apply,
• it can adapt and change over time,
• it does not need detailed codification.

Inherent in the application of the reasonable person standard is that it is impossible to


determine the precise cognitive, physical, or behavioral abilities of the individuals in any given
legal proceeding. Notwithstanding this established legal principle, suppose precise evaluation
of individual characteristics were possible—or even were believed to be possible. Suppose an
expert witness on behavioral genetics were prepared to testify about the innate capability of a
specific individual in a civil or criminal proceeding. Would this matter? Should it?

Philosopher Dan Brock frames the issue in the following way. "If a person's genetic structure is a principal
cause of behavior and that genetic structure is completely beyond the individual's control, can an individual
justifiably be held responsible for the resultant behavior?"5 It is not clear whether or how behavioral genetic
discoveries and claims will affect the law's fundamental assumptions about individuals as responsible
agents. If the unitary standard were replaced with a more subjective standard, it would cause a significant
change in the law's view of the bounds of individual conduct.
2. The adversary system requires lawyers to present all possible arguments on behalf of their clients,
especially in criminal cases. The adversary system of adjudicating lawsuits was transported to the
American colonies from England. It can be traced to two Renaissance ideas: the attempt to use reason to
understand the world; and the concern for human dignity, whereby individuals on trial should have a wide
range of defenses available in attempting to avoid conviction.

The adversary system uses a partisan presentation of the evidence, a largely passive judge, a neutral jury,
and a structured trial format. The lawyer's role in both criminal and civil cases is not to determine the truth;
the truth will be decided by the impartial trier of fact—either the judge or jury. The lawyer's role is to be the
zealous advocate of the position of his or her client. Overreaching, implausible, or untruthful assertions by
either side are exposed through the cross-examination of witnesses and the presentation of contrary
evidence. Theoretically, this system not only uncovers the truth, but it results in popular support for the
judicial system because parties have a chance to present all of their arguments.

Trial lawyers are not merely permitted to be zealous advocates, they are required to be so by legal ethics.
The Model Rules of Professional Conduct provide that a lawyer "has a duty to use legal procedure for the
fullest benefits of the client's cause."6 The lawyer is duty bound to make any lawful argument in support of
the client's position "without regard to [the lawyer's] professional opinion as to the likelihood that the
construction will ultimately prevail," so long as the argument is not frivolous. In criminal cases, even
frivolous arguments may be asserted, the only limitation being that a lawyer may not offer perjured
testimony. During the post-conviction, sentencing phase of a criminal case, defendants are given even wider
leeway in presenting mitigating evidence.

Innovative scientific assertions come within the "zealous advocacy" principle in criminal cases. One
example involves the use of the post-partum psychosis defense in at least 12 U.S. cases in which mothers
were accused of murdering their infants. In most of the cases, the women were found not guilty by reason of
insanity or received light sentences, although it is not clear what weight, if any, was given the defense.
Premenstrual syndrome and post traumatic stress syndrome also have been asserted as defenses.

For many individuals, the zealous advocacy standard for presenting novel defenses was stretched to the
breaking point by the "Twinkie defense" in the murder trial of Dan White, a former San Francisco supervisor
charged with murdering Mayor George Moscone and supervisor Harvey Milk in 1978. At trial, forensic
psychiatrist Dr. Martin Blinder, then an assistant clinical professor at the University of San Francisco
Medical School, testified that the junk food eaten by White could have affected his decision to shoot the
victims. After White was convicted merely of voluntary manslaughter, the California Legislature amended
the penal code to limit defense attorneys' right to offer such evidence.

In civil cases, such as personal injury litigation, plaintiffs often have a difficult time proving causation—that
their injury was caused by the unlawful act of the defendant. Using what detractors have termed "junk
science" or "liability science," scientific experts have pushed the frontiers of scientific thinking in asserting
that, for example, a particular environmental exposure, pharmaceutical product, or medical device resulted
in a particular harm to the plaintiff.

Because of the adversary system, it is virtually certain that parties in both criminal and civil cases will assert
behavioral genetic arguments well before there is general support for such views in the scientific
community. These arguments are particularly appealing in criminal cases because they can be used to prove
that the defendant was compelled to commit the act by uncontrollable genetic factors.

3. Judges and juries have little, if any, expertise in evaluating scientific claims. If the adversary system
encourages—indeed demands—that lawyers zealously advocate unproven scientific theories on behalf of
their clients, the next important question is how will judges and juries view this evidence? By all indications,
both judges and juries are ill-prepared to evaluate the validity of novel scientific assertions, and juries are
likely to give too much credence to such arguments.
The initial problem faced by a lawyer in trying to introduce scientific evidence is persuading the court that
the proffered evidence is admissible. In an influential 1923 decision, Frye v. United States, the Court held
that scientific evidence is admissible if it is generally accepted as valid by the scientific community.

The so-called Frye-test lasted for 70 years, until the Supreme Court's 1993 decision in Daubert v. Merrell
Dow Pharmaceuticals, Inc. The Court held that Frye did not survive the enactment of the Federal Rules of
Evidence in 1975. Under the Federal Rules, judges cannot defer to the scientific community's acceptance of
the evidence in question. Instead, judges are required to make an independent determination of the reliability
and probative value of the evidence.

Judges must determine "whether the reasoning or methodology underlying the testimony is scientifically
valid." This is composed of four factors: (1) whether the theory or techniques can be or have been tested; (2)
the extent to which there has been peer review and publication of the theory or techniques; (3) the known or
potential error rate and the existence and maintenance of standards controlling the technique's operation; and
(4) the general acceptance of the methodology or technique in the scientific community.

Although there is some disagreement among judges and scholars, most believe that Daubert, at least in
theory, made it easier to get scientific evidence admitted into court. There is no dispute, however, that
Daubert made things more difficult for trial court judges. According to Judge Jack Weinstein of the United
States District Court for the Eastern District of New York:

Many federal judges believe Daubert made their lives more difficult. They are going to have to give a
more reasoned statement about why they are letting in evidence. They can't do it on a rubber-stamp
basis the way some of them did it in the past.... After all, we're not scientists. We're in strange territory
and we want to do the best we can.7

Although Daubert is not binding on state courts, many state courts have adopted the approach of requiring a
more active role for trial court judges in deciding admissibility. At the least, the new responsibilities have
caused state court judges to diversify their reading materials to include scientific works. Yet, according to
one state court judge, both trial and appellate judges "tend to have no particular training in statistical
analysis as it relates to scientific research, unless they worked through doctoral programs in science before
making the career switch to law."8 In fact, "they tend to be scientifically ignorant, which means they are not
acquainted, let alone conversant, with scientific practice or language."9 To increase the scientific acumen of
judges, state and federal court administrators have begun programs of scientific education as well as
publication of manuals on scientific evidence. It is not clear how successful these efforts have been.

If efforts are under way to educate judges about scientific methodology, no such efforts are being
contemplated with respect to jurors. Indeed, the Anglo-American tradition of a lay jury is based on the
premise that jurors should be average members of the community and they should not have special
expertise. Jurors with expertise in the matters at issue are generally dismissed during jury selection, because
lawyers are concerned that the other jurors will defer to the single knowledgeable juror, thereby negating the
whole purpose of a jury.

Jurors' lack of scientific expertise has resulted in a demonstrated inability to comprehend scientific evidence.
Nevertheless, several studies have documented that jurors tend to put great credence in expert testimony,
even though they do not understand it.10 A key factor is the persuasiveness of the expert presenting the
testimony.

Putting together the factors discussed above produces the following results. The adversary system demands
that lawyers introduce scientific evidence that may not have been rigorously tested, judges without scientific
expertise must decide whether the methodology and theories have a valid scientific basis, novel scientific
evidence is increasingly being found admissible, and juries often give great credence to the evidence even
though they usually do not understand it, so long as the expert appears knowledgeable. There is no reason to
believe that behavioral genetic information would not fit this pattern as well.
(Editor's note: Efforts to assist judges and juries with scientifically-complex material are discussed in several
articles in this issue—"Keeping the gate: the evolving role of the judiciary in admitting scientific evidence"
by Joseph T. Walsh; "Complex scientific evidence and the jury" by Robert Myers, et. al.; and "Educating
judges for adjudication of new life technologies" by Franklin Zweig and Diane E. Cowdrey.)

4. The law encourages risk-averse behavior. If lawyers are required by legal ethics and encouraged by
financial incentives to assert all possible claims for their clients, unproven scientific evidence increasingly is
admitted into evidence, and judges and juries generally lack the expertise to evaluate the evidence critically,
what are the effects? Obviously, one effect in personal injury litigation could be to establish the liability of a
particular defendant. Another potential consequence is to create a generalized state of risk aversion among
other possible defendants.

The concept of "defensive medicine" has been widely discussed. It is difficult to quantify the extent or the
effects of medical practices designed primarily to avoid malpractice litigation. Yet, this is merely one
manifestation of risk averse behavior caused by concern for tort liability. Other examples include companies
ceasing the manufacture of football helmets and the removal of diving boards from public swimming pools.
It took an act of Congress, the National Childhood Vaccine Injury Act, to ensure that there would be enough
pharmaceutical companies willing to produce vaccines.

In some instances of deleterious environmental health effects, such as those resulting from asbestos and
tobacco, the evidence of both industry culpability and causation are overwhelming and irrefutable. In other
instances, however, such as the harms allegedly resulting from bendectin and breast implants, the evidence
is less clear. Regardless of the scientific community's position on the evidence, the fear of liability often
motivates the actions of individuals, institutions, and companies.

Behavioral genetic information could lead to a wide range of risk-averse actions. To illustrate, in a 1994 case
a security guard at a Bon Jovi rock concert attempted to rape a 16-year-old patron under the stands. The girl
then sued the security company that employed the guard for negligent hiring. She alleged that had the
company done a background check, it would have discovered that the man had four prior convictions,
including one for second degree robbery. In reversing the trial court's granting of summary judgment for the
company, the appellate court observed that upon discovery of a prior robbery conviction, a prospective
employer would be on notice that the prospective employee had a propensity for violent behavior. (Carlsen
v. Wackenhut Corp., 1994.)

Would employers in the future have a duty to review medical records or conduct their own medical testing to
determine whether applicants had genetic indicators of an increased risk for violent behavior? Would it
violate the Americans with Disabilities Act or other laws to do so? If behavioral genetic tests were on the
market and their use by employers was not unlawful, it is possible that a jury might impose liability for
failure to use them, especially in light of the great harms that often befall the plaintiffs in such cases. If there
were a single case finding liability, it is easy to imagine other employers being pressured by insurers and the
public to require tests of school teachers, day care workers, police officers, home health care workers, and
numerous other employees.

It is also possible that behavioral genetic information could be required in other contexts besides
employment. For example, suppose a young camper at summer camp unexpectedly and deliberately hit
another camper in the head with a baseball bat, causing serious injury. Because statutory liability of parents
for the intentional torts of their children is quite limited, and because the child is unlikely to have adequate
assets to satisfy a judgment, a negligence action might be brought against the camp. Assuming the children
were adequately supervised, the injured child's lawyer might assert that had the camp required behavioral
genetic testing of all campers it would have learned that the aggressor child was predisposed to violent
behavior. It then could have refused to admit the child, thereby preventing the injury. If the injured child is
able to obtain a judgment, or even a settlement, then the risk-averse behavior for every other summer camp,
boarding school, college dormitory, and other entities might be to require a review of behavioral genetic test
results. Pressure to do so also could come from parents.
These are just two examples of possible liability avoidance measures that could be used for violent or
aggressive behavior. A similar response is also possible for asserted behavioral genetic associations
involving substance abuse, impulsivity, homosexuality, or other "predispositions."

5. The law has not done a good job of protecting medical privacy. The recognition of a legal right to
privacy is largely a twentieth-century development. In American law, the development has proceeded along
three separate lines: constitutional privacy, common law privacy, and statutory privacy. In none of these
areas, however, has the privacy and confidentiality of medical information been afforded adequate
protection.

The federal constitutional right to privacy is based on the Fourth, Fifth, and Fourteenth Amendments. This
right to privacy and related interests, such as liberty and autonomy, have been used to prohibit the
government from interfering with personal medical decisions, such as providing and withholding medical
treatment, procreation, contraception, and abortion. Federal constitutional rights protect against
governmental and not private interference, but a few state constitutions also contain privacy provisions
applicable to both the public and private sectors.

Even where federal constitutional law applies to protect privacy, the right to privacy is not absolute and
often is considered to be outweighed by other governmental interests. For example, New York enacted a
statute requiring that in filling all prescriptions for Schedule II drugs an official form must be completed,
including the name of the prescribing physician, dispensing pharmacy, drug and dosage, and the patient's
name, address, and age. The form is then filed with the state health department, where the information is
entered in a computer and stored for five years. In a unanimous decision, the Supreme Court held that the
statutory scheme was a legitimate effort to deal with the serious problem of drug abuse (Whalen v. Roe,
1977). Interestingly, the Court relied on the generally diminished privacy rights of patients to support the
view that the governmental intrusion was minimal.

Disclosures of private medical information to doctors, to hospital personnel, to insurance companies, and to public health agencies
are often an essential part of modern medical practice even when the disclosure may reflect unfavorably on the character of the
patient. Requiring such disclosures to representatives of the State having responsibility for the health of the community, does not
automatically amount to an impermissible invasion of privacy.

The second privacy law doctrine, common law invasion of privacy, may be applied to a variety of factual
situations. Indeed, the legal doctrine has evolved into four related torts: public disclosure of private facts,
intrusion upon seclusion, false light, and appropriation of name or likeness. The first two are especially
relevant to medical privacy.

To establish a claim for invasion of privacy based on public disclosure of private facts, the plaintiff must
show dissemination or "publication" of private matters (e.g. medical information) in which the public has no
legitimate concern so as to bring shame or humiliation to a person of ordinary sensibilities. Some parties,
such as employers, have been granted a qualified privilege to disclose certain facts deemed essential to their
business interests. For example, where work was disrupted at a nuclear power plant because of rumors that
the reason for an employee's illness at work was radiation exposure, a Mississippi court held that the
employer had a privilege to tell employees that the plaintiff was ill due to the effects of a hysterectomy
(Young v. Jackson, 1990).

The other important basis of invasion of medical privacy is intrusion upon seclusion. "One who intrudes,
physically or otherwise, upon the solitude or seclusion of another or his private affairs or concerns, is subject
to liability to the other for invasion of his privacy if the intrusion would be highly offensive to a reasonable
person."11 Individuals who are in a weaker economic position (e.g. employees, insurance applicants) often
are compelled to disclose or release medical information. They are often placed in a no-win situation, which
is not aided by the common law doctrine. If they refuse to supply information, even if they are discharged as
a result, the courts hold that their privacy has not been invaded. On the other hand, if they supply the
information, then they have consented to release of the information and there is no right to legal redress.
The third main legal method of protecting privacy is statutory. A variety of state and federal statutes attempt
to deal with one or more aspects of medical privacy. None of these laws provides adequate protection,
however. For example, in 1995 Oregon enacted the nation's first state law designed to protect the privacy of
genetic information. Subject to various exceptions, the law provides, among other things, that no person may
obtain genetic information from an individual without informed consent, no person may retain genetic
information without obtaining specific authorization, and no person may disclose genetic information
without specific authorization. A similar "procedural" law has been enacted in California.

What has been labeled "genetic privacy" legislation is, in reality, genetic security legislation. The laws only
prohibit the unauthorized collection, retention, or disclosure of genetic information. They have no effect on
the myriad instances in which individuals can be required to release genetic and other medical information
as a condition of employment, insurance, education, commercial transactions, and other matters.

There is no reason to expect that behavioral genetic information will be afforded greater privacy protection
than other forms of medical or genetic information. Some constitutional, statutory, or common law theories
may be applied to limit some overly intrusive inquiries or unnecessarily extensive disclosures. In general,
however, a wide range of substantive limitations in each specific area will need to be enacted to safeguard
the privacy of this information.

How will the law respond?

The law does not operate independently of culture, it follows culture. In the 1920s, when eugenics
dominated American scientific thinking, it also dominated American culture and American law. How will the
law respond to new discoveries in genetics, including behavioral genetics? To what level of legal scrutiny
will claims of behavioral genetics be subjected? How will proven associations of genetics and behavior
affect a range of legal doctrines related to privacy, autonomy, nondiscrimination, and societal opportunities?
How will unproven or outright bogus assertions be received by the courts?

Legislative and judicial responses to new genetic discoveries will have a major effect on whether we are
about to enter an unprecedented period of behavioral genetic determinism and, with it, social disruption, or
the promised enlightened era of genetic marvels. While history does not preordain the future, it certainly
reminds us of the stakes involved.

Mark A. Rothstein is Cullen Distinguished Professor of Law and director of the Health Law &
Policy Institute at the University of Houston Law Center.

This article has been adapted and excerpted from Mark A. Rothstein, Behavioral Genetic Determinism: Its
Effect on Culture and Law, in Behavioral Genetics: The Clash of Culture and Biology, 89-115. Ronald A.
Carson & Mark A. Rothstein, eds. (Johns Hopkins University Press 1999). Reprinted by permission of the
publisher.

1. Hamer and Copeland, Living with our Genes 144 (New York: Doubleday, 1998).
2. 2. See Rothstein, Genetic Secrets: A Policy Framework, in Rothstein, ed., Genetic Secrets: Protecting Privacy and
Confidentiality in the Genetic Era (New Haven: Yale University Press, 1997); Rothstein, Preventing the Discovery of
Plaintiff Genetic Profiles by Defendants Seeking to Limit Damages in Personal Injury Litigation, 71 Ind. L.J. 71 (1996);
The Use of Genetic Information for Nonmedical Purposes, 9 J.L. & Health 109 (1995); Rothstein, Genetics, Insurance,
and the Ethics of Genetic Counseling, in Friedman, ed., Molecular Genetic Medicine, vol. 2. (San Diego: Academic
Press, 1993); Genetic Discrimination in Employment and the Americans with Disabilities Act, 29 Hou. L. Rev. 23
(1992).
3. Blyth v. Birmingham Waterworks Co., 156 Eng. Rep. 1047 (1856); Vaughan v. Menlove, 132 Eng. Rep. 490 (1837).
4. See Holmes, The Common Law 108 (Boston: Little, Brown and Co., 1881)
5. Brock, The Human Genome Project and Human Identity, 29 Hou. L. Rev. 7, 16 (1992).
6. Model Rules of Professional Conduct, Rule 3.1, Comment 1.
7. Sherman, "Junk Science" Rule Used Broadly; Judges Learning Daubert, NatÕl L.J., Oct. 4, 1993, at 3
8. Gless, Some Post-Daubert Trial Tribulations of a Simple Country Judge: Behavioral Science Evidence in Trial Courts, 13
Behavioral Sci. & L. 261, 263 (1995).
9. Id.
10. Broyles, Taking the Courtroom into the Classroom: A Proposal for Educating the Lay Juror in Complex Cases, 64 Geo.
Wash. L. Rev. 714, 721-722 (1996).
11. Restatement (Second) of Torts §652B (1977).

Das könnte Ihnen auch gefallen