text:
الرئيسية Nature, Nurture, and Psychology
Nature, Nurture, and Psychology
Robert Plomin
G is for Genes: The Impact of Genetics on Education and Achievement
Kathryn Asbury, Robert Plomin
genetic1026
behavioral600
behavioral genetics299
genes292
influences280
plomin247
alcoholism194
siblings187
heritability172
variance165
traits152
fulker142
defries137
disorders136
environmental influences135
rutter134
nurture125
correlations117
quantitative104
trait103
reared91
genetic and environmental90
sibling90
molecular89
shared environmental87
mcgue87
phenotype86
reading disability86
analyses85
psychopathology84
genotype83
eaves83
familial83
linkage83
genetically82
estimates82
gottesman79
behavioral geneticists73
nonshared72
dna72
inheritance71
genetic influences70
Introduccion a la literatura infantil (Serie Ensayos sobre literatura infantil) (Spanish Edition)
Roman Lopez Tames
语言: spanish
Methods of Teaching Chemistry
Stephan Forster
Evolution of the NatureNurture Issue in the History
of Psychology
Gregory A. Kimble
ne of the earliest "experiments" on the nature-nurture issue dates
to the 13th century, when Frederick 11, King of Germany,
wanted to find out what kind of speech and what manner of speech children
would have when they grew up if they spoke to no one beforehand. So he
had foster mothers to suckle the children, to bathe and wash them, but in
no way to prattle with them, or to speak with them, for he wanted t o learn
whether they would speak the Hebrew language, which was the oldest, or
Greek, or Latin, or Arabic, or perhaps the language of their parents, of
whom they had been born. But he labored in vain because the children all
died. For they could not live without the petting and joyful faces and loving
words of their foster mothers. (Stone & Church, 1973, p. 104)
Three centuries later, the Mogul emperor Akbar, a descendant of
Tamerlane and Genghis Khan, reared children in isolation to discover
whether their natural religion would be Hinduism, the Christian faith, or
some other creed. But this experiment was also a failure: It only produced
deaf mutes (Broadhurst, 1968). The implicit assumption in these so-called
experiments was that environment contributes more than inheritance to
human talents: Experience has the power to hide the inborn nature of an
Early Dominance of Environmentalism
The environmental emphasis continued when the philosophical ancestors
of psychology discussed the origins of knowledge. For example, the British empiricist John Locke (1690/ 1979) answered the nature-nurture question this way in a much-quoted passage from his An Essay Concerning
Human Understanding:
Let us suppose the mind to be, as we say, white paper, void of all characters,
without any ideas:-How comes it to be furnished? Whence comes it by
that vast store which the busy and boundless fancy of man has painted on
it with an almost endless variety? Whence has it all the materials of reason
and knowledge? To this I answer, in one word, from experience.
Later on, support for environmentalism came from science. For example, Helmholtz (see Southwell, 1924-1925) held that any aspect of
perception that can be modified by experience must be the product of
experience. He concluded that, by this criterion, only the quality and
intensity of sensation are innate. Primitive consciousness is a pandemonium of sights, sounds, and all the other sensations, differentiated only
by these fundamental properties. How does perception create an environment made up of objects with coherence? A reasoning-like process
called unconscious inference constructs a perceptual world from the data
of the senses.
Meanwhile,Bell (1811/ 1948) and Magendie (1822) had independently
discovered the structural and functional independence of sensory and
motor neurons in the spinal cord, thus setting the stage for an environmental interpretation of acts as well as percepts. In 1860 the Russian
physiologist Sechenov (see 1935) stated the position forcefully: "The real
cause of every human activity lies outside man" (p. 334), and "...999/1,000
EVOLUTION OF NATURE-NURTURE
of the contents of the mind depends on education in the broadest sense,
and only 1/1,000 depends on individuality" (p. 335). But these statements
were less colorful than that made by Watson (1924):
Give me a dozen healthy infants and my own specified world to bring them
up in, and I'll guarantee to take anyone at random and train him to become
any kind of specialist I might select-doctor, lawyer, artist, merchant-chief,
and yes, even beggar and thief, regardless of his talents, penchants, tendencies, abilities, vocations and race of his ancestors. (p. 104)
The Beginnings of Behavioral Genetics
More than half a century before Watson's (1924) proclamation, Charles
Darwin (1859) and Gregor Mendel (1866) had sown the seeds of a genetic
revolution. In his theory of evolution, Darwin described three requirements for the occurrence of that process: (a) heredity (offspring resemble
their parents), (b) variation (although similar, offspring differ), and (c)
selection (the fittest variants survive, the unfit perish in the struggle for
existence).
Mendel's (1866) studies of genetics provided the details of the first
of Darwin's three requirements. Mendel contributed the distinction between phenotype (observable characteristics of organisms) and genotype
(underlying genetic makeup) and provided the laws of segregation (a
genotype consists of pairs of genes, one allele from each parent) and
independent assortment (the genes for traits are separate: inheriting wavy
hair does not make it more likely that a person's hair will be blonde or
red or black) and the concepts of dominance and recessiveness (dominant
genes gain phenotypic expression whether an organism has one or two
of them; recessive genes are expressed only if the individual receives one
from each parent). Mendel's work was lost until the beginning of the 20th
century and went largely unnoticed in psychology until later. Beginning
with William James (1890), Darwin's theory became the model for the
school of functionalism in psychology, which held that the adaptive value
of responses preserves those that survive the slings and arrows of outrageous fortune, just as it preserves the fittest of a species.
GREGORY A. KIYBLE
Hereditary Genius
Darwin (1859) proposed that evolution selects for mental traits as well
as anatomical structures, and Francis Galton (1869) argued for the
inheritance of the traits that lead to human eminence. To obtain the evidence for that conclusion, Galton began by identlfying eminent scientists,
judges, authors, musicians, military leaders, statesmen, and (despite the
popular opinion that "the children of religious parents frequently turn out
badly" [ 1869,p. 2581) theologians. He then searched biographies and other
records to obtain data like those summarized in Table 1. Using the most
eminent person in each family as a referent, this table presents percentages of relatives, who were eminent themselves, in four clusters representing decreasing closeness of relationship. The corresponding decrease
in percentages of eminent relatives makes the case for heritability.
Studies of the genealogies of defective families carried the genetic thesis
to the other end of the continuum of intellect. One of these was a study
of the Jukes family (Dugdale, 1877), which came to the attention of New
York state officials when they discovered that six of the Jukes were in
prison at the same time in just one county. A detailed genealogical survey,
Blood Relationship and Eminence
Nature of relationship
Great grandson
Great uncle
Great nephew
First cousin
More remote relationships
Eminent relatives (%)
which covered seven generations and about 750 Jukeses, revealed that
the family had cost the state over $1.5 million through crime, pauperism,
and vice. A second study was that of Martin Kallikak (Goddard, 1921), a
revolutionary soldier who had fathered two lines of offspring, one that
began with an illicit mating with a tavern maid who was thought to be
retarded, and the other with a woman of at least average intelligence
whom he married 2 years later. Over several generations, the first line
produced many cases of apparent mental retardation; the second line had
Environmentalism Undaunted
The conclusion sometimes drawn from these data was that intelligence
is inherited. Although these studies were suggestive, carried out without objective tests, the hypothesis that they were studies of intelligence,
instead of motivation or personality, is risky. More important, in all of
these studies, good or bad genes, good or bad environments, and good
or bad outcomes went together. It is possible that the environment, not
inheritance, causes eminence or incompetence. Because of its history,
psychology had a preference for environmentalist interpretations, a preference that received support from other studies.
The Wild Boy of Aveyron
Among the earliest of these studies was that of the French physician Jean
Itard (1807/1932), who undertook the task of training Victor, the so-called
"wild boy of Aveyron." When captured in the woods, Victor was 12 or 13
years old. He could not speak and only shrieked and grunted. He crouched
and trotted like a beast and, even when still, swayed back and forth
incessantly. Dirty and naked, indifferent and inattentive, he subsisted on
roots and raw potatoes. Itard believed that the boy had become retarded
as a result of social isolation. By supplying Victor with the necessary
experiences, he hoped to reverse the process. Itard did manage to teach
Victor to discriminate objects by sight, touch, and taste; to connect objects
to abstract symbols; to write a few words; and eventually to respond
positively to affection. Although Itard was never able to educate Victor
to the point of normalcy, the success he did achieve encouraged the
conclusion that mental development depends on environmental opportunity.
The Indian missionary J. A. L. Singh (Singh & Zingg, 1942) discovered a
second case of wild children. In his missionary tours, Singh became intrigued with stories of a "man-ghost" living in a nearby jungle and went
to locate him. The man-ghost habitat to which Singh was taken turned
out to be an abandoned white-ant mound that wolves had turned into a
den with numerous entrances and exits. The missionary had a shooting
stand erected and watched the den with field glasses. On October 9,1920,
his patience was rewarded: Two female wolves and two wolf cubs came
out of the den, followed by a hideous looking creature with a human body
and a head so covered with a ball of hair that only the sharp contour of
a human face was visible. Close behind this creature came a second
smaller one.
Eight days later, the two man-ghosts were captured. They proved
to be girls, one about 1.5 years old and the other about 8 years old, who
had been nurtured by the wolves. They were reported as having sharp,
piercing eyes and being more vicious than the wolf cubs with whom they
were taken. Their captors named them Amala and Kamala. Amala, the
younger child, died about a year later, having shown few signs of developing human capabilities. Kamala lived in the missionary orphanage for
almost 9 years.
During this period, Kamala changed from something more animal
than human into a recognizable child. Initially she ran on all fours, lapped
her food rather than using her hands for eating, showed a preference for
raw meat, and seemed more attracted to the farm animals than to the
human inhabitants of the orphanage. Her only vocalizations were peculiar
howling sounds that she often made at night, apparently to announce her
presence in a certain location. However, Kamala gradually learned to eat
using her hands, and she developed a taste for nutrients that she had
previously rejected. She learned to walk, first on her knees and then
eventually in an upright manner. Her savagery dissipated, and she developed an affection for certain people. She began to notice colors and
seemed to prefer red. Her crowning achievement was the acquisition of
a vocabulary of about 30 understandable words. Kamala died on November 11, 1929, after a long illness. What she had accomplished in her years
of human contact and the fact that her improvement was accelerating at
the time she died lent credence to an environmental interpretation of her
initial deficits.
Joint Contribution
Again, although these studies were suggestive, they did not provide a
convincing argument for the environmental determination of intellect
because the defects of the feral children might have been genetic; they
might have been abandoned in the first place because they were retarded.
Facts that can have either an environmental or a hereditary interpretation
obviously cannot decide between the two. Now about a century of more
formal research has shown that both factors are important.
Four Faces of the Issue
The nature-nurture issue may be the most pervasive in psychology, but
in different settings, it goes by different names. First, in the fields of
sensation and perception it is the nativism-empiricism issue. Second, in
developmental psychology it is maturation versus learning. Third, in learning and cognition it is a premise of environmental equipotentiality versus
a principle of biological preparedness. Fourth, in differential psychology
it is heredity versus environment as the determiner of human variation.
Perception: Nativism Versus Empiricism
All of the human senses are functional at birth. Soon thereafter, infants
have the ability to perceive the psychologically primary colors (Borstein,
Kessen, & Weiskopf, 1976), visual depth (Gibson & Walk, 1960), the location of auditory stimuli in space (Wertheimer, 1961), the contours of
the human face (Fantz, 1961), emotional expression (Field, Woodson,
Greenberg, & Cohen, 1982), and the human form in motion (Cutting,
1981)-all of which provide powerful arguments for a nativistic contribution.
But on the side of empiricism, William James (1890) knew that the
senses are educable:
[ W]e have the well-known virtuosity displayed by the professional buyers
and testers of various kinds of goods. One man will distinguish by taste
between the upper and the lower half of a bottle of old Madeira. Another
will recognize, by feeling the flour in a barrel, whether the wheat was grown
in Iowa or Tennessee. (p. 509)
As might be expected from these positive contributions of experience, sensory deprivation has negative effects. Humans have occasionally
lost their sight at an early age and, later on, regained it. One such individual, who was studied by Gregory and Wallace (1963), had color vision
when his sight was restored, but his depth perception was very bad; he
lacked most of the visual illusions and knew that a "blur" in front of him
must be a human face only because it talked and because he knew that
speech came from faces. Several decades of research have converged on
the conclusion that a learned coordination of sight and bodily motion is
critical to the development of visual perception (Held & Hein, 1963;Stratton, 1897).
Development: Maturation Versus Learning
The history of maturation versus learning is a history of the discovery
that abilities that offhandedly seem to be learned depend on biological
maturation. In a classical study, Coghill (1929) demonstrated that the
development of locomotion in the salamander is a maturational process
involving sequences (proximodistal, cephalocaudal, and mass actiondifferentiation) that depend on neural growth. Even earlier, Carmichael
(1926) did an experiment to show that experience has little or nothing
to do with the process. He kept salamander tadpoles in a chemical solution
that prevented movement, during the period when swimming normally
appears. When removed from the solution at the end of that period, they
swam almost immediately, unaffected by the lack of practice.
Soon there were demonstrations that Coghill's (1929) sequences
appear in the development of such human skills as walking and grasping
(Shirley, 1931),and in a study similar to Carmichael's (1926), Dennis (1940)
showed that confining Hopi children to a cradle-board for the first year
or so of life, which thus deprives them of exercise, does not postpone
the age of walking. It is apparent that what we informally call "learning
to walk" is largely maturation. The results of other studies suggest that
this conclusion applies in many contexts: emotional reactions (Bridges,
1932), smiling (Spitz & Wolf, 1946), and even language (Lenneberg, 1967).
Other studies began to hint that critical periods are important to the
interaction between maturation and learning. Imprinting in precocial birds
is most rapid during a brief age span when the animal is biologically ready
(Hess, 1958). Educational psychologists have known for years that a similar readiness is required for reading (Morphett & Washburn, 1931).
Learning and Cognition: Equipotentiality Versus Preparedness
Pavlov was an extreme environmentalist in the Sechenov tradition. He
favored what Seligman and Hager (1972) later called the "premise of
equipotentiality," the hypothesis that any response an organism can make
can be conditioned to any stimulus it can detect and that all of these
associations are formed with equal ease. Coupled with acceptance of
Lamarck's theory of the inheritance of acquired characteristics, this outlook was the basis for the Soviet belief that an entire population could
be trained to Marxist philosophy and that such an education could be
passed along to future generations (Kimble, 1967). Lamarckian theory did
not survive, but for a time, the premise of equipotentiality looked promising. The Russian laboratories produced many demonstrations of interoceptive conditioning, in which the conditioned and unconditioned stimuli
or responses were internal to the learner (Razran, 1961). American experimenters later added their support when they found evidence for the
learning of allergic reactions (Russell, Dark, Ellman, Callaway, & Peeke,
1984), resistance to the lethal effects of drug overdose (Siegel, 1984), and
analgesia (Maier, 1986).
Doubts about the ubiquity of conditioning arose when research began to show that inborn sympathies between certain stimuli and responses
modulate the process. Soon after Watson and Rayner (1920) demonstrated
the conditionability of fear in their experiment with "Little Albert," Valentine (1930) proposed a role for biological preparedness when he dis11
covered that such conditioning did not happen when the conditioned
stimulus was a pair of opera glasses rather than a rat. Later on, Garcia
and Koelling (1966) found, in rats, that aversions based on illness are easy
to condition to tastes but difficult or impossible to condition to sights or
sounds; they found that the reverse was true for shock-elicited avoidance
reactions.
The principle of preparedness also applies to instrumental learning,
a fact that is well known to animal trainers. For example, Breland and
Breland (1961) described a "dance" performed by a chicken in response
to the music from a juke box, which turned out to be little more than the
natural scratching pattern that chickens use in their search for food,
brought under stimulus control by reinforcement. Even language observes
the principle of preparedness. Although the importance of experience is
obvious from the fact that children learn their native tongues-instead
of Arabic or Hebrew, as King Frederick thought they might-biological
constraints are much in evidence. The neuroanatomy of aphasia proves
that language has specific representation in the human brain. Babies come
into the world with "wired-in" rudiments of linguistic competence. Their
babblings are the same the whole world over, even if they are born to
parents who are mute (Lenneberg, 1967). Furthermore, they discriminate
phonemes categorically (Eimas & Tartter, 1979) just as they do primary
Individual Differences: Heredity Versus Environment
The research that introduced psychology to the science of behavioral
genetics was Tryon's (1940) selective breeding study of maze learning.
Of all these studies of the nature-nurture issue, Tryon's was the only one
that dealt with individual differences in behavior. Tryon mated "mazebright" and "maze-dull" rats with others of the same kind for 21 generations. The members of the parent generation made about 14 errors in
19 trials on a complex maze. By the 7th generation, the progeny of the
maze-bright matings were making an average of about 8 errors; those
produced by the maze-dull matings were making approximately 18,which
thereby suggests that maze-learning ability is genetic. Hall (1951) obtained
similar evidence for the inheritance of fearfulness in rats, and Buss (1985)
made a convincing case that something like selective breeding goes on
with human beings because, contrary to a popular opinion, opposites do
not attract. People choose mates like themselves and, to the extent that
the similarities are genetic, pass them along to their children.
As happens in psychology, the behavioral genetic plot soon thickened. At the University of California, Berkeley, where Tryon did his pioneer investigation of the inheritance of maze talent, Krech, Rozenzweig,
and Bennett (1962) obtained evidence for a surprising environmental
influence: Rats reared in an "enriched" environment-in cages with other
rats and objects to manipulate and crawl on-developed heavier brains
and better problem-solving ability than did rats raised alone in an unfurnished, "impoverished" environment.
Further research with Tryon's rats exposed additional complexities.
Searle (1949) found that the superiority of Tryon's maze-bright rats disappeared when they were tested in other mazes. Moreover, by comparison
with the maze-dull rats, the maze-bright rats had a stronger hunger drive,
a lower level of spontaneous activity, and greater running speed-any of
which might have been responsible for their better performance on
Tryon's maze.
There are similar problems at the human level. What we call intelligence is actually a collection of cognitive abilities that are genetic, but
to varying degrees (Plomin, 1990). It seems certain that, if someone bred
a strain of humans who excelled on one cognitive ability, they would not
excel on others. The organization of human traits remains to be worked
out, and until it is, determining the effects of nature and nurture on
behavior will face the handicap that E. G. Boring once described-I can't
remember where-when he said that psychology might be more advanced
today if the giant in its history had been a Linnaeus instead of a Wundt.
The Issue at Mid-Century
When I was a student at Carleton College (1936-1940), psychology was
roughly half-way through this history. It understood that the naturenurture issue would not be settled in favor of one factor or the other and
that asking whether individual differences in behavior are determined by
heredity or environment is like asking whether the areas of rectangles
are determined by their height or width. The accepted wisdom was that
the right question was not "which?" but "how much?" But World War I1
began; for a decade, psychology was otherwise preoccupied, and there
was little progress on the problem. When it returned to normal business
at mid-century, it found learning theory in charge of scientific psychology.
Operating in the Watsonian tradition, it played down the importance of
genetic influences on behavior.
Common Themes and Variations
The basis for a constructive relationship between traditional psychology
and the emerging science of behavioral genetics was actually already
available because of the applicability to both disciplines of two powerful
ways of thinking, the first of which was R. A. Fisher's method of the
analysis of variance (ANOVA). The basic theorem of ANOVA is that the
total variance of phenomena is the sum of all variances produced by the
influences that control them (an "all-causes''variance) plus variance from
two sources of error: accidents of sampling and unreliability of measurement. Thus, in the most general case:
Skmi
S L Causes
Skrror,
where S2is variance.
The second powerful way of thinking is one that permeates psychology: Behavior is the consequence of relatively enduring potentials
for, and relatively more temporary instigations to, performance. A list of
commonly contrasted potentials and performances, together with their
instigators, in several different contexts makes this point (see Table 2).
The inclusion of genotype as a potential and phenotype as an outcomelike behavior in Table 2 underscores the fact that the table presents
a way of thinking-a metaphor or a model. In terms that are more concrete, it is useful to think that genetics provides individuals with a "potential potential" and that the environment determines the degree of "realized potential." The potentials of traditional psychology are these
realized potentials.
One implication of this model is that the all-causes variance can be
divided into component variances that are assignable to potential and
Nerve impulse
Classical learning theoretical
Skinnerian "nontheory"
Educational accomplishment
Dream content
--____
A Common Theme in Psychology
General pattern
Several Examples
Deep structure
Communicative need
Resting potential
Adequate stimulation
Stimulus (aboveibelow) criterion
Motivational minus inhibition
Reflex reserve
Environmental occasion
Environmental influence
Scholastic aptitude
Motivationistimulation
Latent content
"Dream work"
Trait anxiety
Releasing stimulus
Action-specific energy
"Hit"/"miss"
Operant response
Manifest content
State anxiety
Releasing reaction
instigation. Leaving aside for now the interactions among them, the following equation describes the simplest possible way in which these specific influences might work together:
Stotal
SLential
Sfnstigation
Skrror.
Accounting for Variance in Behavioral Genetics
When the concepts of polygenic inheritance (many genes contribute to
phenotypic variations in a trait) and norm of reaction (a genotype is a
repertoire of different phenotypes that can appear in different environments) found their way into psychology, the stage was set for a parallel
accounting from a genetic point of view. In this approach, total variance
in behavior is phenotypic variance, and in the simplest case for which
phenotypic variance is the sum of variances attributable to genes, environment, and error, the formula becomes:
Sknotypic
S?;met,c
SLmxnnental
+ S&ror*
This equation also implies another, which defines a "coefficient of
heritability" (h2),the fraction of total variance that is genetic variance:
The similarities between Equations 2 and 3 suggest that it might be
useful to look for other parallels between traditional experimental psychology and behavioral genetics.
The simplest experiments with outcomes that are treated to an
ANOVA often manipulate conditions that have their hypothetical effect
on either a potential or an instigator. An experiment that compares the
recall of two groups of participants who learn materials with deep or
superficial processing theoretically manipulates a potential, that is, the
knowledge acquired by the participant (Table 2). An experiment on encoding specificity, which shows that participants can recall that knowledge better in the context in which they learned it than in a different one,
manipulates one type of instigation. The analysis for these experiments
begins by dividing total variance on recall into two components: betweengroups variance, which is attributable to the effects of the independent
variable, and within-groups variance, the variance of individuals in the
same conditions. Because instigation does not vary in one experiment
and because potential does not vary in the other, these variances drop
out of the equations:
Now, moving to behavioral genetics, the beginning assumption of
that science is that the total phenotypic variance of a trait is the sum of
variances contributed by genes, environment, and error:
Behavioral genetics then proceeds to analyses that are parallel to
those just described. It divides genetic variance into two components:
additive polygenic variance and nonadditive variance, which is contributed by dominance and epistasis. As a reminder, dominance is a genetic effect that occurs at one genetic locus; epistasis refers to the fact
that, in some cases, the products of genes at one locus depend on genes
at others. Additive variance is like a main effect: The more genes an
organism has for a trait, the greater the phenotypic value of that trait.
Nonadditive variance is like within-groups variance (the error variance)
in an ANOVA: Individuals with the same additive genotype may vary in
nonadditive inheritance.
Also in step with traditional psychology, behavioral genetics divides
environmental variance into shared and nonshared components. All children in a family share the same environment to the extent that, on the
average, parenting in their family differs from that in other families. The
result, across families, is a between-families variance like the betweengroups variance in the results of an experiment. There is also a withingroups variance. Parents do not treat all their children in exactly the same
way. The result is nonshared environmental variance, which accounts for
more variation in behavior than does shared environmental variance. Two
equations describe the relationships:
S T ~ t a (rcnctic
- SAdditive
lEnvironrnrnt
(,enetic
Sionadditive
S i h a r e d Envlronrnrntal
Genetir
+ Stonshared
Enwronrnental.
As is well known, however, the variables that control behavior interact, and therefore, the equation must be longer:
S$<rtal
SLtential
Sinstigation
S&otrntlal
x In5tlgation)
+ S k i t h i n <,roups- (13)
In the behavioral genetics version of this formula, the interaction is
a genotype-environment interaction:
S$hcnotvpic
Skenrtlc
+ Sknwronrncntal +
StGenetic x Ennronrnental)
s!&c,r.
The interaction term in this equation is a measure of the variance
that occurs because the environment that is optimal for individuals with
one genotype may not be optimal for others: The education that is best
for a gifted child will not be the best for a child who is retarded. Experimental psychology acknowledges a similar interaction when it treats
individual differences as moderator variables that interact with other
independent variables. The best-known example is the history of research
showing that, although arousal (sometimes anxiety) may facilitate performance on a simple task, it may impede performance on a complex
one. Psychometric psychology calls its variation on that theme traitsituation interaction. In this case, individual differences are independent
variables, and different environments are moderator variables.
Finally, to complete the catalog of parallels, behavioral geneticists
have found that people tend to live in environments that match their
inherited potential. The infant who has potential academic giftedness is
apt to have parents who are bright themselves and who provide a stimulating environment. Such youngsters are often identified as gifted and
offered special educational opportunities. If such opportunities are not
offered, then the gifted child may seek them out. These gene-environment
correlations make it impossible to assign causality for behavior to heredity or environment. When that happens in experimental psychology
(i.e., when the effects of experimental treatments cannot be interpreted
because subjects in experimental conditions differ systematically), the
effect is called confounding.
Quantitative Behavioral Genetics
When Galton was assembling his data on hereditary genius, the idea of
correlation occurred to him. He passed the thought along to his follower
and biographer, Karl Pearson, who invented the product-moment correlation coefficient (r).Applied to data for pairs of people who differed
in blood relationship, this correlation coefficient became a standard tool
in the science of behavioral genetics. Analyses of such data soon revealed
that environment and heredity both contribute to these correlations. In
the case of I&, for example (see chapter 3, this book), their values parallel
the closeness of relationship of individuals whose scores are correlated,
which is an argument for genetics. However, the following argue for
environment: (a) When similarly related people who live together are
compared with those who live apart, the correlations for the people who
live apart are lower than those for the people who live together, and (b)
when unrelated people live together, their IQs are positively correlated.
Behavioral geneticists have developed quantitative measures of these influences.
Estimating the Contributions
of Heredity and Environment
These measures come from a variety of behavioral genetics methods, of
which I shall describe just one-the twin method. This method compares
the correlations of measures obtained on identical (monozygotic [MZ])
twins, who have 100%of their genes in common, and fraternal (dizygotic
[DZ]) twins, who share only 50% of their genes.
Data obtained with the twin method yield one formula for h2:
For example, if the correlations were 0.85 for MZ twins and 0.60 for
DZ twins, and both groups of twins were reared together, the formula
becomes:
h2 = 2(0.85
Z(0.25)
This formula requires four comments. First, although the fraction of
variance accounted for by a correlation coefficient is usually r2,in the
case of kinship correlations, it is just r (Jensen, 1971). Thus, correlations
of 0.85 for MZ twins and 0.60 for DZ twins would mean that those percentages of the variance in their IQs are accounted for by the joint environmental and genetic influences that come together in those relationships. Second, on the practical assumption that the environments of MZ
and DZ twins are similar, the difference between the correlations reflects
the genetic contribution. Third, the doubling of that difference is necessary
to assess the magnitude of the genetic contribution because the covariance of DZ twins, with 50% of their genes in common, includes only half
of the genetic influence. Fourth, it is important to recognize that coefficients of heritability, as is true of every statistic, are subject to sampling
error; the values of h2 obtained in different studies are varied.
Behavioral genetic research has now demonstrated an influence of heritability in many areas of psychology, including intelligence and its components, school achievement, organic dementia (Alzheimer's disease,
Huntington's chorea, alcoholism), what once was called "functional"
psychopathology (schizophrenia, the affective disorders, anorexia nervosa, panic disorder), traits of personality (extraversion-introversion,
emotionality-neuroticism), attitudes (conservatism-traditionalism), delinquency-criminality, and vocational interests (Plomin, 1990).These discoveries have powerful implications, not just for the nature-nurture problem, but for social policy and ow attitudes toward social issues.
Environment Accounts for the Majority of Variance
Estimates of the magnitude of the influence of genetics suggest that
inheritance accounts for something like 35% of the variance in this broad
range of human traits and tendencies, more for cognitive abilities and
less for traits of personality. These data mean that, on one hand, an
influence of this magnitude cannot be ignored-in psychology it is rare
for an experimentally manipulated variable to account for that much
variation-but, on the other hand, the answer to the nature-nurture question appears to be that environment is more important.
High Heritability Does Not Mean That Environment Has No Effect
Even if the coefficient of heritability for a trait is 1.0, environment can
have a large effect; but it will be the same for everyone. There can be no
gene-nvironment interaction because genetics accounts for all the variance. Over the centuries, something of that sort seems to have happened
to human height, for which the coefficient of heritability is about 0.90.
Better child care and nutrition have produced a substantial, but very
general, increase in the height of the population. As exhibits in American
museums often demonstrate, the clothing and beds used by early English
colonists would be much too small for Americans today.
Heritability Within Groups Is Not the
Same as Heritability Between Groups
Coefficients of heritability are extremely sensitive to the populations on
which they are based. Measures obtained on one population (e.g., race)
cannot be generalized to other populations or to differences between
populations. Such differences are phenotypic differences. There may or
not be genotypic differences, and if there are, they may favor either group.
Psychology and the world at large could have been spared much bitter
controversy if they had understood that it is important to distinguish
between within-groups and between-groups heritability. The coefficients
of heritability discussed in this chapter are fractions of the variance within
populations that are genetic. Although there is a coefficient of betweengroups heritability, which potentially provides a measure of the fraction
of differences between the means of groups that is genetic, it presently
is of no use because its calculation requires measures that, so far, are
not available (McClearn & Denies, 1973).
The nature-nurture issue in psychology is older than psychology itself.
A decade or so before Wilhelm Wundt set up his laboratory in Leipzig in
GREGORY A. KlMBLE
1879, Sechenov (1935) and Galton (1869), respectively, had already pronounced the environmentalist and hereditary agendas. In the century
and more since then, events have conspired to hide the fact that, going
their separate ways, the sciences of Sechenov and Galton have arrived
at similar destinations. The scope of psychology expanded. Modern Galtonism deals with topics that range from artistic aptitude to zoophilia;
modern environmentalism, in the Sechenov tradition, studies everything
from absolute thresholds to zero-sum games. Obsession with the details
of such phenomena makes the common content of psychology hard to
detect. Instead, war is waged over the content and method of psychology.
Perhaps the time has come to declare a cease-fire in the battles, to
look for commonalities in psychology, and to explore the possibility that
peace may be inherent in the consensus that we find. In the area of
content, most psychologists agree that psychology is the science of behavior, before some of them go on to say that it also is the science of
something more, like "mind," "brain," "mental processes," "human potential," or "experience." In the area of method, the question is that of
what it means to be a science. Of the many answers that are available,
the one that seems best to embrace the diversity of psychology comes
from behavioral genetics. The several sciences of psychology are all in
the business of accounting for the variance in behavior. The following
two formulae, which were presented earlier, will serve as reminders of
the argument:
Skta,
Phcnotypir
= Skxential
- S?;cnptic
Sknwronmottal
S&i-or
S&ror
In their prototypical versions, traditional psychology and behavioral
genetics are identical in structure. A break-down of these general equations shows that the resemblance is more than just skin-deep. It would
be easy to demonstrate that other psychological specialists accept these
formulae. In their actual operations, they are more alike than is ordinarily
Bell, C. (1948). Idea of a new anatomy of the brain: Submitted for the observation of his
friends. Reprinted in W. Dennis (Ed.), Readings in the history of psychology. New
York: Appleton-Century-Crofts. (Original work appeared in 1811)
Borstein, M. H., Kessen, W., & Weiskopf, S. (1976). The categories of hue in infancy. Science,
191,201-202.
Breland, K., & Breland, M. (1961). The misbehavior of organisms. American Psychologist,
16, 681-684.
Bridges, K. M. B. (1932). Emotional development in early infancy. Child Development, 3,
Broadhurst, P. L. (1968). Genetics. In D. L. Sills (Ed.), International encyclopedia of the
social sciences p o l . 6, pp. 96-102). New York: Macmillan.
Buss, D. M. (1985). Human mate selection. American Scientist, 73, 47-51.
Carmichael, L. (1926). The development of behavior in vertebrates experimentally removed
from the influence of external stimulation. Psychological Review, 33, 51-58.
Coghill, G. E. (1929). Anatomy and the problem of behavior. New York: Macmillan.
Cutting, J. E. (1981). Coding theory adapted to gait perception. Journal of Experimental
Psychology: H u m a n Perception and Pe?fonnance, 7, 71-87.
Darwin, C. (1859). On the origin of species by means of natural selection or the preservation of favoured races in the struggle for life. New York: Appleton.
Dennis, W. (1940). The effect of cradling practices upon the onset of walking in Hopi
children. Journal of Genetic Psychology, 56, 77-86.
Dugdale, R. L. (1877). The Jukes: A study in crime, pauperism, disease and heredity. New
York: Putnam.
Eimas, P., & Tartter, V. (1979). On the development of speech perception: Mechanisms and
analogies. In H. W. Reese & L. Lipsett (Eds.), Advances in child development and
behavior (Vol. 13). New York: Academic Press.
Fantz, R. L. (1961). The origins of form perception. Scientijic American, 204, 66-72.
Field, T. M., Woodson, R., Greenberg, R., & Cohen, D. (1982). Discrimination and imitation
of facial expressions by neonates. Science, 218, 179-181.
Galton, F. (1869). Hereditary genius: An inquiry into its laws and consequences. London:
Macmillan.
Garcia, J., & Koelling, R. A. (1966). Relation of cue to consequence in avoidance learning.
Psychonomic Science, 4 , 123-124.
Gibson, E. J., & Walk, R. D. (1950). The visual cliff. Scientific American, 202, 2-9.
Goddard, H. H. (1921). The Kallikak family: A study in the heredity of feeblemindedness.
New York: Macmillan.
Gregory, R. L., & Wallace, J. G. (1963). Recovery from early blindness: A case study.
Experimental Psychological Society Monographs (No. 2).
Hall, C. S. (1951). The genetics of behavior. In S. S. Stevens (Ed.), Handbook of experimental
psychology. New York: Wiley.
Held, R., & Hein, A. (1963). Movement-produced stimulation in the development of visually
guided behavior. Journal of Comparative and Physiological Psychology, 56,
Itard, J. M. G. (1932). The wild boy of Aveyron. New York: Appleton-Century. (Original
work published in 1807)
James, W. (1890). Principles of psychology. New York: Holt.
Jensen, A. R. (1971). Note on why genetic correlations are not squared. Psychological
Bulletin, 75, 223-224.
Kimble, G . (1967). Foundations of conditioning and learning. New York: AppletonCentury-Crofts.
Krech, D., Rozenzweig, M. R., & Bennett, E. L. (1962). Relations between brain chemistry
and problem-solving among rats raised in enriched and impoverished environments.
Journal of Comparative and Physiological Psychology, 55, 801-807.
Lenneberg, E. (1967). Biological foundations of language. New York: Wiley.
Locke, J. (1979). A n essay concerning h u m a n understanding (P. H. Nidditch, Ed.). New
York: Oxford University Press. (Original published in 1690)
Magendie, F. (1822). Experiences sur fonctions des racines des nerfs rachidiens [Experiments on the functions of the roots of the spinal nerves] Journal de Physioloyie
Experimentale et Pathologique, 2 , 276-279.
Maier, S. F. (1986). Stressor controllability and stress-induced analgesia. Annals of the New
York Academy of Sciences, 467, 55-72.
McClearn, G. E., & DeFries, J. C. (1973). Introduction to behavioral genetics. San Francisco:
Freeman.
Mendel, G. J. (1866). Versuche uber Pflanzen-Hybriden [Research on hybrid plants]. Verhandlungen des Natuqorshunden in Breuen, 4,3-47.
Morphett, M. V., & Washburn, C. (1931). When should children begin to read? Elementarg
School Journal, 31,496-503.
Plomin, R. (1990). Nature and nurture: A n introduction to behavioral genetics. Belmont,
CA: Brooks-Cole.
Razran, G. (1961). The observable unconscious and the inferable conscious in Soviet psychology: Introceptive conditioning, semantic conditioning, and the orienting reflex.
Psychological Review, 68, 81-147.
Russell, M., Dark, K. A., Ellman, G., Callaway, E., & Peeke, H. V. (1984). Learned histamine
release. Science, 225, 734-735.
Searle, L. V. (1949). The organization of hereditary maze brightness and maze dullness.
Genetic Psychology Monographs, 39,279-325.
Sechenov, I. M. (1935). Collected works. Moscow: State Publishing House.
Seligman, M. E. P., & Hager, J. L. (1972) Biological boundaries of learning. New York:
Appleton-Century-Crofts.
Shirley, M. M. (1931). The f i r s t two years of life: A study of twenty-five babies (Vol. 1).
Minneapolis: University of Minnesota Press.
Siegel, S. (1984). Pavlovian conditioning and heroin overdose: Reports by overdose victims,
Bulletin of the Psychonomic Society, 22, 428-430.
Singh, J. A. L., & Zingg, R. M. (1942). Wolfchildren and feral m a n . New York: Harper &
Row.
Southwell, J. P. C. (Ed.). (1924-1925). Helmholtz's treatise on physiological optics (Vols.
1-3). New York: Optical Society of America.
Spitz, R. A., & Wolf, K. M. (1946). The origin of the smiling response. Genetic Psychology
Monographs, 34,71-75.
Stone, L. J., & Church, J. (1973). Childhood and adolescence. New York: Random House.
Stratton, G. M. (1897). Vision without inversion of the retinal image. Psychological Review,
4,341-360.
Tryon, R. C. (1940). Genetic differences in maze-learning in rats. Yearbook of the National
Society f o r the Study of Education, 39, 111-119.
Valentine, C. W. (1930). The innate bases of fear. Journal of Genetic Psychology, 37,
Watson, J. B. (1924). Behaviorism. New York: Norton.
Watson, J. B., & Rayner, R. (1920). Conditioned emotional reactions. Journal of Experimental Psychology, 3, 1-14.
Wertheimer, M. (1961). Psychomotor coordination of auditory and visual space at birth.
Science, 134, 1692.
Behavioral Genetics: The Last
Century and the Next
Gerald E. McClearn
he purpose of this chapter is to sketch the history of the field of
behavioral genetics in the century since the founding of the American Psychological Association ( M A ) and forecast the next century. In
any field of science, the latter part of this assignment would be daunting.
In genetics, given the explosive growth of knowledge the field has been
experiencing, predicting even next week's main events is hazardous. Behavioral genetics, having drawn its theories and techniques from the parent discipline of genetics with some lag time, is not much more predictable
than that. I think, however, that I can discern some current developments
the general course of which can be conjectured. These guesses may constitute at least a peek through the curtain into the future.
In dealing with the past history of the field, there is little to be gained
here by extensive citation of the evidence for genetic influence on this
or that behavioral phenotype. Reviews and textbooks are readily available
to provide details of this kind (e.g., Plomin, DeFries, & McClearn, 1990).
In this limited space, I present some generalities about the range of behavioral properties investigated from the genetics perspective, and I cite
a few specific examples. In the main, however, I wish to trace the unfolding
of the ideational base of the field and indicate the relevance of that base
to the parent discipline of psychology.
A useful starting point might be to consider what the participants
of the first APA meeting in 1892 might have talked about if the issue of
heredity and behavior had come up for discussion. The specific body of
thought on inheritance of behavioral attributes available to these conferees might have included some speculations from the ancient Greek philosophers, who recorded thoughts on this as on all other matters; a vague
appreciation shared with the population at large that behavioral properties
"run in families"; Dugdale's (1877) sociological study on the Jukes family;
and a few other topics. But, the conversation almost certainly would have
been dominated by the more recent work of Francis Galton. Twenty-three
years before the first APA meeting, Galton (1869) published his volume,
Hereditary Genius, in which he examined the relatives of eminent persons and found that these relatives included a greater number of individuals of high mental ability than could be accounted for by chance. Seventeen years before APA's first meeting, Galton (1876) published "The
History of Twins as a Criterion of the Relative Powers of Nature and
Nurture," which established an alliterative phrase that, with a very heavy
burden of accumulated meaning and emotion, still exists. Just 9 years
previously (Galton, 1883), in his Inquiries Into H u m a n Faculty and Its
Development, Galton concluded:
There is no escape from the conclusion that nature prevails enormously
over nurture when the differences of nurture do not exceed what is commonly to be found among persons of the same rank of society and in the
same country. (p. 241)
Galton is well known to have been an inveterate counter and measurer, and throughout his career, he made many contributions to the
definition, measurement, and evaluation of behavioral traits. Even so, the
taxonomic status of psychology of his time was necessarily primitive by
current standards. For example, the "ability" that Galton evaluated was
based largely on reputation and unsystematic report, and the concept
appears intolerably vague to the modern observer.
The concepts of inheritance were only slightly less vague. By "nature," Galton meant whatever was transmitted between generations, but
it was far from clear what the nature of that hereditary material was or
what the rules of its transmission were. The prevailing theory of heredity
that was available as a thinking tool for Galton (and still, years later, for
the hypothetical APA founders) was the pangenesis theory of Darwin
(1859), which was featured in his theory of evolution. Briefly, this theory
postulated that some representation of body parts coalesced in germ cells
and formed the essence of the hereditary material. There were two aspects
to this theory (and other similar theories as well), which turned out to
be wrong. The first was that the hereditary influences received from
parents merged or blended in the offspring. The result of this blending
would be that the hereditary material passed on by an individual would
be different from that which contributed to that individual. Such blending
should constitute a great leveling, with everyone's genetic make-up ultimately approaching a common condition. An abiding and unresolved puzzlement was the maintenance of population variability, which remained
apparently unchanged over many generations. The second incorrect aspect of the theory was the presumption that environmental influences on
the body parts would change their representation in the germ cells and
would thus be transmissible to offspring.
Much of the available scientific literature comprised listings of outcomes of particular crosses, without generality. The results were complex,
and as Lush (1951) described the situation, the students of heredity at
the time APA was founded, and for quite some time to come, operated
with two vague rules: (a) like begets like, and (b) like does not always
beget like.
Mendelian Genetics
A new paradigm, destined to transform the life sciences, had actually
been published by a monk named Gregor Mendel (1866) 27 years before
the founding of APA. Mendel had examined a number of dichotomous
traits in the pea plant. The results of various matings were explained by
hypothesizing discrete hereditary elements, which occurred in pairs, with
one member of each pair having been provided to an organism by each
of its parents. These elements (later to be named genes) could exist in
alternate states (later to be named alleles). There was no "blending" (the
elements retained their characteristic nature regardless of what their
partner element was). Furthermore, evidence mounted that the elements
were buffered from the vagaries of specific environmental circumstances
to which the organism was exposed. Thus, an individual would pass on
to a particular offspring either one of the two alleles it possessed for each
gene, and the transmitted allele would be in the same state when it "left"
the individual as it was when it "entered'it. The maintenance of variability
in succeeding generations was no longer an enigma.
Figure 1 represents some principal features of the Mendelian
schema. Of fundamental importance is the distinction made between the
hereditary material and the observable characteristics. Note that the genotype is on the X axis and that the phenotype is on the Y axis (these
terms were introduced many years after Mendel's original proposal). Assuming the simplest case of two allelic forms for a gene, the possible
genotypes can be represented by aa, Aa, or AA, for example. These
possibilities can be quantified by considering the number of A alleles in
the phenotype-0, 1, or 2. The phenotype can take one of two values, for
example small and large. The classic relationship shown in Figure 1 between genotype and phenotype is a nonlinear, step-function relationship
in which possession of either one or two A alleles has the same phenotypic
consequence. This relationship is described as one of dominance: The A
allele is dominant to the recessive a allele. Later research demonstrated
that some genes could display other types of relationships, including the
additive one shown in Figure 2. In this relationship, the possessor of one
each of the allelic types is intermediate in phenotype, which imposes a
requirement for trichotomous rather than dichotomous classification. This
3-point scale presages an important later development-a system for dealing with phenotypes represented on a continuous scale (discussed later).
Number of A elements
Relationship between three genotypes and two discrete levels of phenotypic expression in a hypothetical additive Mendelian condition (A =
dominant allele; a = recessive allele )
The Mendelian model powerfully improved on its predecessors in
giving clear predictions of the consequences of different matings. Regrettably, however, Mendel's results and the interpretations of them remained largely unnoticed by the biological community until 1900, when
they were "rediscovered' by several investigators nearly simultaneously.
The intellectual climate was now receptive, and an explosion of research
effort ensued. The Mendelian model was found to apply to a large number
of diverse phenotypes. In the enthusiasm of the time, the fit of model to
data was sometimes forced, and some extravagant claims were made.
Behavioral phenotypes were among those targeted in the early days, and
Mendelian fits were attempted (and claimed) for nomadism, pauperism,
Relationship between three genotypes and three discrete levels of phenotypic expression in a hypothetical dominantirecessive Mendelian condition (A = dominant allele, a = recessive allele )
licentiousness, prostitution, alcoholism, and other characteristics that
were of top concern to the reformists of the day.
As research progressed, rigor increased in conceptualization and
measurement of phenotypes and in statistical methods and standards.
Many of the early claims are now just historical curiosities. Perhaps the
most prognosticative outcomes were in the general area of mental retardation, then called feeble-mindedness. The results of early studies that
dealt with a conglomerate of conditions were unclear. Differential diagnosis was foreshadowed in the mid-1930s when FBlling and colleagues
(see FBlling, M o b , & Ruud, 1945) identified a biochemical anomaly in
one type of retardation, and it was soon shown that this disease-phenylketonuria (PKU)--obeyed Mendelian rules.
Mendelian genetics has continued to the present as a powerful research interest. Many single-gene conditions have been identified in humankind, which demonstrates clearly that human beings, as well as plants
and experimental and domesticated animals, are subject to Mendelian
inheritance. A recent compilation (McKusick, 1992) describes over 2,300
single genes that have been assigned to specific chromosomes and at
least as many that have been tentatively identified. Many of these conditions involve anomalies of one kind or another, and over 100 of them
involve some degree of mental retardation. Other supposed single-gene
conditions of interest to behavioral scientists include some sensory anomalies such as color blindness, deafness, and ability to taste certain substances. A particularly dramatic condition is Huntington's disease in which
symptoms of neurological dysfunction, depression, and cognitive impairment first appear typically in the 3rd to 5th decades of life.
One avenue of modern research has focused strongly on attempts
by sophisticated segregation analysis to demonstrate that a Mendelian
gene underlies some condition and through linkage analysis to find the
location of that gene on the chromosomes. Some spectacular successes
have been recently attained, as in the case of Huntington's disease (Gusella et al., 1983) and muscular dystrophy (Davies et al., 1983). There have
been disappointments in the attempts to show Mendelian laws at work
in manic-depressive illness and in schizophrenia, however (McGuffin,
Owen, & Gill, 1992; see also Gottesman, chapter 12). To understand one
possible reason for these failures requires a return to the early days of
the century and an entirely different tradition of studying inheritance.
Biometrical Investigation of Inheritance
Regression and correlational analyses, now ubiquitous and commonplace
tools in psychological investigation, were invented in the context of research on inheritance by Galton, Karl Pearson, and their colleagues. The
phenotypes in which this school was interested generally were continuously distributed. "Ability" and "temperament" were seen as existing in
differing degree, not as the dichotomies for which Mendelian analysis
was appropriate. Regression and correlation were, of course, admirably
suited for describing the resemblance of relatives on these continuously
distributed traits. In general, it was observed for a variety of phenotypes
that resemblance increased as a function of the closeness of the biological
relationship-parents resembled offspring more than aunts and uncles
resembled nephews and nieces, and so on. Of particular relevance to
behavioral genetics was a study of siblings by Pearson (1904) that compared the inheritance of behavioral ("psychical") properties (e.g., teachers' ratings of vivacity, assertiveness, introspection, popularity, conscientiousness, temper, ability) and physical ones (e.g., health, eye color,
cephalic index). The average sibling correlation was slightly more than
0.50 for each class of traits, and Pearson concluded:
We are forced, I think literally forced, to the general conclusion that the
physical and psychical characters in man are inherited within broad lines
in the same manner, and with the same intensity. (p. 156)
A dispute, one of the most animated in the history of science, ensued
between the biometricians and the Mendelians. The Mendelians were
demonstrating, at least to their own satisfaction, the general applicability
of the Mendelian rules; the biometricians dismissed the Mendelian outcomes as special cases applicable only to abnormalities. A landmark
contribution by Ronald Fisher (1918) resolved the issue. Briefly, Fisher
proposed a model in which a large number of genes, each acting in a
Mendelian manner, had an individually small effect on a common phenotype. The collective influence of these myriad "polygenes" (a term coined
much later) would be to generate an essentially continuous distribution,
susceptible to the statistical analyses of the biometricians. The field of
quantitative genetics emerged from this fusion of Mendelian and biometrical genetics. Much of the subsequent elaboration and expansion of
the basic model occurred in agriculture, with an enormous beneficial
effect on the world's capacity to produce food. Because of the general
predilection of behavioral geneticists for continuously distributed phenotypes, quantitative genetics gradually came to occupy a central role in
the conceptualization of the field.
The Differential Model
The essence of the quantitative genetic approach is the decomposition
of the measured variance of a phenotype into components representing
genetic and environmental sources of influence. The fundamental expression of this perspective is given by the relationship
VP = V G
VE,
in which the measured variance of the phenotype (Vp) is considered to
be a linear composite of terms representing genetic variance (V,) and
environmental variance (VE). These principal categories are capable of
further subdivision, and interaction and covariance terms make for more
complicated expressions in many applications of the analytic model.
Those interested should consult Falconer (1989). The inclusion of environmental influence is of critical importance. Indeed, because environmental and genetic influences are given equal billing in the model, the
conventional term quantitative genetics seems inappropriate and, indeed,
misleading. For some time, and with practically no success, I have encouraged the term differential model as being more appropriate. This
differential model is so different from the "hereditarian" view so often
mistakenly attributed to behavioral genetics that it is worth some explication.
First, note that the model applies to genes that are "segregating" in
the population. That is to say, it applies to those genes that contribute to
individual differences among individuals within a species, not those that
contribute to differences between species. There are undoubtedly many
genes that all human beings have in common in an invariant allelic state.
A subset of these will also be shared with other primates, and a subset
of these with other mammals, and so on. Those genes for which alternative
allelic states are compatible with life provide the genetic basis for individuality. Estimates of the number of these segregating genes in human
beings typically range from 50,000 to 100,000.
An extremely important aspect of the model is the great power of
a polygenic system to generate variability. With several tens of thousands
of segregating genes, there is a truly awesome capability of sexual re-
production to generate individuality at the genetic level. As applied to
human beings, all who are not members of an identical twin pair or similar
multiple birth will have a unique genotype, never assembled before in the
entire history of our species.
Just as each individual has a unique genotype, each individual also
experiences a unique environmental history. It is important to note the
breadth of definition of environment in this context. The term embraces
everything not encoded in the genetic material and ranges from intimate
intracellular chemical milieus to peer group influences.
Different study designs allow various compartments of environmental and genetic influence to be estimated. One frequently presented statistic is heritability, which is the proportion of the measured variance
due to genetic differences among individuals in a studied population. In
keeping with the even-handedness of the differential model, many investigators also, or alternatively, report environmentality, which is 1 minus
heritability. Each of these measures is merely a descriptive statistic, not
a statement of eternal verities. They estimate the state of affairs of a
particular population with a particular gene pool in a particular array of
environments. The answer could well be different in a different population
or in different environmental circumstances. Note particularly that neither
the genetic influence nor the environmental influence can be estimated
without the other.
The principal tactics used to generate the data for such analyses
include the measurement of resemblance of family members, twins, and
adoptees in human studies and the use of inbred strains and selective
breeding in experimental animals. The logic involved is fairly straightforward, although the detailed application can be algebraically complex.
For example, any departure of the resemblance of identical twins from
perfect similarity must be due to environmental sources; the excess similarity of identical twins over fraternal twins can, with certain assumptions, be attributed to the fact that identical twins are genotypically identical and that fraternal twins share only half of their segregating genes,
like ordinary siblings; the resemblance of an adoptive child and an adoptive parent should reflect effects of rearing environment, as should re-
semblance between children separately adopted into the same home; and
so on.
In the case of animals, inbreeding generates genetic homogeneity
within each strain. Each animal within an inbred strain is essentially
genetically identical to each other within the strain, and strains differ
from each other. Thus, within-strains variance is due to environment, and
between-strains variance is due to genetic factors. Generations derived
by crossing unlike inbred strains permit further detailed estimates of
variance components.
Selective breeding is an unambiguous demonstration of the efficacy
of genes. Animals with like phenotype are mated together. For example,
those with high values are mated together to begin a "high" line, and a
contrasting "low" line is generated by mating of animals with low values.
If genotype is totally unrelated to phenotype, then the selection will be
ineffective. If the means of the lines diverge over repeated generations
of selection, then it is proof positive of a genotypic influence over the
phenotype, and the rate of divergence can be interpreted to estimate the
relative contributions of genes and environment.
With Fisher's insight and the subsequent development of the quantitative genetic (i.e., "differential") theory, all of the ingredients were
present for a declaration of peace in the intellectual war of the naturenurture controversy. Some scholars did in fact declare the war over, but
for a variety of reasoncdetailed discussion of which would require much
more space than available here-many segments of the behavioral and
social sciences were reluctant to accept genes into the realm of their
explanatory principles. To some extent, at least, this reluctance was based
on an assumption that things were either "genetic" or "environmental"
(remember nature versus nurture!). Furthermore, if something were genetic, then it was assumed to be unalterable. Thus, evidence of change
in a behavioral phenotype under altered environmental conditions, such
as training, for example, was often taken as proof that the phenotype
could not be genetic. The differential model makes it clear that it is not
a case of nature or nurture. Genes and environment coact. It is not necessary to choose sides. As for genetics representing unalterable fate, the
example of PKU is particularly instructive. In this classical Mendelian
condition, reseachers devised an environment (a nutritional environment,
it happens) that ameliorates substantially the mental retardation.
The differential model has been applied with vigor to a great variety
of behavioral phenotypes. The index of Plomin et al. (1990) includes
ability, activity, aggressive behavior, aggressive conduct disorder, alcoholism, Alzheimer's disease, amaurotic idiocy, anorexia nervosa, antisocial personality disorder, anxiety neurosis, attention deficit disorder, attitudes, avoidance behavior, and avoidance learning-just in the As. At
one time, the demonstration of a genetic influence in a behavioral phenotype was noteworthy (and, per se, publication-worthy). Now, it is almost
a foregone conclusion that some degree of heritability will be found; the
issue is its magnitude. It is similarly expected that there will be environmental influence. Indeed, it is becoming clear that avery powerful strategy
for investigating environmental factors is to use a genetic (differential)
design of some sort (e.g., Plomin et al., 1990). An important guide to
search for specific environmental factors can be derived from the estimation of the relative importance of the anonymous categories of shared,
nonshared, and prenatal environments, for example.
Mechanisms of Heredity
Mendel's elements were clearly hypothetical variables, but before long,
the early genetics research began to identlfy physical aspects of their
existence. First, it was observed that the Mendelian processes of genes
paralleled the processes of intranuclear structures called chromosomes.
Evidence rapidly accumulated that genes resided in particular places on
these chromosomes, and detailed microscopic study gave some intimations about what they were like (e.g., their average size), and the basis
was laid for the construction of the linear maps that permit the location
of particular genes. Just as there were these hints as to what genes were,
there were also some hints as to what they did. It was shown that at least
some genes seemed to be involved in the generation of enzymes, and the
conviction gradually grew that maybe that is what all genes did. Thus,
halfway through MAS 1st century, there was some very hard-won em38
BEHAVIORALGENETICS
pirical information and theory about gene structure and function, but the
prospect of clear understanding of the nature of the gene seemed very
remote, indeed.
In midcentury, an intellectual bombshell exploded, with the theory
of Watson and Crick (1953a, 1953b). The result was a breathtaking series
of major discoveries that have not only transformed biology but, with an
impact comparable to that of the Copernican and Darwinian revolutions,
also altered humankind's view of itself and its place in the scheme of
things. So well have the basic terms suffused society that public media
often no longer feel it to be necessary even to define the abbreviations
DNA and RNA.
The basic dogma is that DNA is the repository of the genetic information. That information is coded as a series of bases. The hereditary
information in the DNA is copied onto RNA by a complementation process. The RNA participates with certain intracellular structures to produce
polypeptides, which compose proteins; these proteins include structural,
transport, and catalytic proteins (enzymes). Enzymes are specially critical
in facilitating the chemical reactions of life. It became clear that different
allelic forms of a gene were due to different sequences of the bases in
the DNA, which result in different sequences of amino acids in the protein,
which might, as a consequence, alter functional properties.
Until quite recently, behavioral genetics has been an onlooker and
cheerleader for molecular genetics. The principal consequence of the
molecular revolution for behavioral genetics has been that we now have
a plausible answer to the question of how genes can possibly influence
labile behavior. It is a reductionist explanation: Genes influence the proteins that are critical to the functioning of the organ systems that determine behavior. Thus, two sets of beliefs are involved. First is that the
nervous system, endocrine system, sensory systems, musculature, and so
on each separately, and collectively, influence behavior. This is the stuff
of biopsychology, the interface between physiology, biochemistry, and
behavior. Second is the belief that allelic differences of genes influence
these anatomical systems and their function. This is the area of molecular
and physiological genetics. If the theories and databases of these domains
are accepted, then it is not surprising that genes can influence behavior.
It would be absolutely astonishing if they could not!
Simple graphic representations are useful in illustrating some important principles. In Figure 3 is displayed a network of organ systems
and processes leading to two phenotypes, P1 and P2. The Gs indicate a
genetic influence on each element in the network. Two considerations
merit attention. First, each of the phenotypes is influenced by multiple
genes. This, of course, is the basic differential model. Second, through
branching pathways, particular genes may influence more than one phenotype. This phenomenon is named pleiotropy and translates into genetic
correlation and comorbidity. The differential model is such that neither
genetic nor environmental factors alone suffice for explanation. Figure 4
makes this point by indicating that each process is also susceptible to
A representation of genetic
(P = phenotype.)
(G)influence on elements in a causal network.
A representation of environmental (E) influence on elements in a causal
network. (P = phenotype.)
environmental influence, and environmental analogs to polygeny and
pleiotropy are clearly implied: multiple influences and manifold effects.
The network of influences (causal field or causal matrix, if you prefer)
shown also suggests a rationalization of single-gene influence. In the
differential model, the Mendelian outcome is a limiting case in which the
allelic configuration of a single gene accounts for such a large part of the
variance that other genes and environment can, for most practical purposes, be ignored. In the network model presented in Figure 4,that outcome can be understood as a gene participating in a bottleneck in the
The model shown is both ridiculously symmetric and pathetically
simplified. The true complexity of, say, biochemical processes is enormously greater. A gesture to the true world is made in Figure 5 , which
Representation of a network of influences on several phenotypes (P) 11lustrating pleiotropy, polygeny, and other bases for correlations involving
phenotypes.
expands the causal field to embrace two more phenotypes and many
more elements in the matrix (with genetic and environmental factors
understood to be operative on all elements). The point of this figure is
to illustrate better the implications of multiple pathways leading to phenotypic expression. These multiple pathways may be the explanation of
the rarity of single-gene effects in the complex behaviors that are the
focus of behavioral genetics interest.
One of the attributes of complex biological systems such as suggested here is that they are controlled or regulated. Although the arrows
in the figures suggest simple unidirectional causality, real systems would
be replete with feedback systems providing homeostatic regulation. Newtonian causality considerations become inadequate, and notions of circular or network causality will be required for more complete comprehension of the operation of any such network.
A major result from these considerations is that researchers are
freed from the old notion that "genes are fate." If the environment is
operating on the same causal field that mediates genetic influence, then
compensation or remediation through environmental intervention is
clearly reasonable to seek. The most vivid success story to date is that
of PKU, and its example is encouraging even for polygenically influenced
phenotypes. Enormous research efforts will obviously be required to identlfy the elements in any particular causal field and characterize their
interrelationships. In many cases, the effort would be more than justified,
and the dramatic recent advances in structural modeling applied to quantitatively distributed phenotypes has given us a grand strategy for the
analysis.
Developmental Behavioral Genetics
It is perfectly apparent that a newborn resembles its parents less than it
will when it is grown. Something about genetic influence happens developmentally. In a prescient remark about genetic change, Galton (1876)
noted:
It must be borne in mind that the divergence of development, when it occurs,
need not be ascribed to the effect of different natures, but it is quite possible
that it may be due to the appearance of qualities inherited at birth, though
dormant. (p. 402)
Indeed, Galton's first study of twins investigated the extent to which twin
resemblance changed during development (Galton, 1876). This phenomenon has been carefully described for intellectual function. For example,
one study (Honzik, 1957) showed a dramatic increase in the correlation
between a child's I& and maternal education from about 0.05 at 2 years
of age to about 0.35 at 6 years of age. The finding of increased heritability
for cognitive ability has consistently been found in childhood (Fulker,
Denies, & Plomin, 1988) and, recently, in the last half of the life span in
which heritability reaches 80% (Pedersen, Plomin, Nesselroade, & McClearn, 1992; see also McGue et al., chapter 3). A s only one example in
the domain of temperament, the correlation of identical twins with respect
to activity level was found to increase from about 0.30 to about 0.58
between 3 and 24 months of age (Matheny, 1983; see also Plomin &
Nesselroade, 1990).
Another indication that there are developmental timing aspects to
genetic effects is provided by genetic diseases with late onset. The classic
case of this sort is the condition of Huntington's disease, in which the
onset is typically in young or middle adulthood.
There was a flowering of developmental genetics in the 1950s, featuring both single genes, particularly genes with lethal effects (e.g., Hadorn, 1955), and polygenic systems (e.g., Waddington, 1957). This line of
research was overtaken by the excitement of molecular genetics discoveries, and the molecular perspective on development has become a torrid
research area today.
A major event in the molecular approach was the demonstration in
microorganisms that genes could be turned on and turned off. In fruit fly
larvae, where chromosomes are particularly advantageous for microscopic study, it was subsequently discovered that in a critical developmental period there were visible manifestations of sequencing of activity
of different genes on different chromosomes. These and similar observations have given rise to a field of study of regulatory genes-genes that
control other genes (see MacLean, 1989, for a particularly accessible
treatment of gene regulation).
This field of investigation greatly enriches the perception of genetic
influence. Not only may researchers contemplate the consequences of
the differences among individuals in genotype, but they may also consider
intraindividual genetic differences. Although it is clear that individuals
get all of their genetic information at conception, only parts of the total
set are used by different organ systems, and different parts are called
into play at different times. From this perspective, development involves
programmatic change in what might be called the effective genotype.
Whereas many genes are undoubtedly operating from the beginning and
many others function for a while and then fade away, others heed their
call to perform at some specific life stage, are locked on, and function
from then on to the end; and still others put in brief appearances at critical
developmental periods. (An interesting conjecture is that senescing genes
may exist, which get turned on late in life.)
The control and regulation of genes is far from completely understood. The corpus of knowledge grows at a prodigious rate, however, and
it is easy to predict that profound new insights into development will be
the outcome of the current high interest in the field.
Behavioral genetics is increasingly using developmental genetics perspectives, with special journal issues (Plomin, 1983) and monographs
(Hahn, Hewitt, Henderson, & Benno, 1990; Plomin, 1986) testlfying to the
current prominence of the developmental orientation within behavioral
genetics.
As a summary, if the human genome could be visualized, a picture
would be presented of an organism proceeding through its lifetime with
programmed species-typical changes in effective genotype-changes in
the array of genes that are turned on at a particular time. These changes
are slow in relation to the life span and are unlikely to proceed at a
uniform rate. The rate may be relatively greater in infancy than in later
childhood, for example, and adolescence must mark particularly rapid
change in effective genotype. For these changes, the differential model
is an analytic tool of choice: It can partition interindividual variance, most
appropriately among individuals at the same general stage in their speciestypical trajectory.
The easy part of peeking into the future is to forecast more of the same.
More and more behavioral phenotypes will be described, and their components of variance will be estimated with increasing precision by increasingly sophisticated statistical models. It will increasingly be seen
that genetic methods are invaluable for researchers who are interested
in detecting, characterizing, and estimating the importance of effects of
environment. For an expanding number of behavioral phenotypes, insights
will be won into the physiological, anatomical, and biochemical mechanisms that mediate the genetic influence. Indeed, genetic methods will
likely come to suffuse the reductionist study of mechanisms of behavior.
Studies in developmental behavioral genetics, in the main, have been
characterized by quantitative perspectives. Increasing emphasis on molecular developmental genetics perspectives in the study of behavioral
development is easily predictable.
Application of the quantitative genetic model in behavioral genetics
has principally attended to the proximal input variables (the hypothesized
plural genes of small effect) and the distal output variables (the measured
behavioral phenotypes), with relatively little concern about the intervening variables. It is possible to imagine that each of the polygenes makes
its contribution to the final phenotype through the same simple causal
path, but the more complex scenarios suggested earlier (Figure 5) are
probably more veridical for complex behavioral attributes in general. That
is to say, the intervening variables from genes to behavior are likely to
constitute complex systems. The study of the properties of complex systems and application to various scientific disciplines (including behavior;
see Ford, 1987) has expanded prodigiously in recent years. As Murphy
and colleagues have pointed out in a series of incisive articles (e.g., Murphy & Berger, 1988; Murphy & Trojak, 1986), the principles of complex
systems have important implications for quantitative genetic research.
With considerable confidence about the event, but less about the rate at
which it will occur, I predict that complex-systems thinking will become
an integral part of the differential model (McClearn, 1993; McClearn &
Plomin, in press).
In a distinctly different approach, the intermediates between genes
and behavior will be opened to investigation with powerful techniques.
Until recently, researchers have been able to deal with two types of genes:
the sledge-hammer, Mendelian genes and the puny polygenes. It has long
been recognized that in the multiple gene situation there may be a whole
continuum of effect size. Some genes may exert enough influence to be
detectable if rather heroic efforts are made to locate them. Because of
the rapid increase in molecular markers of location on chromosomes,
plant geneticists recently began development of techniques for efficient
identification of chromosomal regions containing such quantitative trait
loci (QTL), and variants of these methods have now been adapted to
animal research (Plomin, 1990). The approach should work as well for
behavioral phenotypes as for any other class of phenotypes. QTL have
already been tentatively identified with respect to various aspects of
alcohol-related behavior (McClearn, Plomin, Gora-Maslak, & Crabbe,
1991) and other behavioral phenotypes (Plomin, McClearn, Gora-Maslak,
& Neiderhiser, 1991). Prospects now seem bright of identlfying, within a
polygenic system, a number of specific genes that collectively account
for a substantial part of the genetic variance component estimated by the
differential model.
Lifting the veil of anonymity for at least some of the genes that
influence the complex systems of behavioral phenotypes will offer grand
opportunities for the merging of molecular and quantitative genetics theories and methods. The way will be opened for application of the whole
molecular genetic armamentarium in the elucidation of mechanism in
polygenic systems. Furthermore, an unparalleled bridge may be generated
between research with animal models and that with human beings. The
fact that, for segments of chromosomes, the order of genes is the same
in man and other animals offers prospects that identification of QTL in
laboratory animals will point to specific areas of the human genome for
location of the homologous human gene.
Finally, I suggest that the attention of behavioral geneticists may be
drawn increasingly to the notion of intraindividual changes in effective
genotype. The idea of developmental changes in arrays of effective genes,
discussed earlier, opens the door to consideration of other possible types
of alteration of composition of the genetic team on the field of play.
A rapidly growing body of literature describes the effects of certain
long-term environmental circumstances on the types and amounts of RNA
present in certain organs. The nutritional environment provides many
useful examples. With appropriate dietary manipulations in rats, for example, variations have been shown in the amount of liver RNA for malic
enzyme (Katsurada, Iritani, Fukuda, Noguchi, & Tanaka, 1987), glucose6-phosphate dehydrogenase (Fritz & Kletzien, 1987; Tomlinson, Nakayama, & Holten, 1987), aldolase (Munnich et al., 1985), apolipoprotein E
(Kim et al., 1989), and L-type pyruvate kinase (Munnich et al., 1984; Weber
et al., 1984). These observations relate, of course, to the well-known
phenomenon of enzyme induction. The specific observations on RNA are
particularly pertinent to the present topic.
Other recent evidence in rats relates repeated immobihation stress
expression of genes for adrenal catecholamine biosynthetic enzymes:
tyrosine hydroxylase and dopamine Phydroxylase (McMahon et al., 1992).
Mild footshock stress in rats has been shown to increase expression of
the c-fos gene in the brain (Smith, Banerjee, Gold, & Glowa, 1992). Of
special relevance to behavioral science is that the conditioned stressor
alone (tone previously associated with footshock) is also effective in
increasing this gene expression in certain parts of the brain (Smith et al.,
It is irresistible to contemplate the effects of short periods of stress.
For example, a single immobilization stress episode has been shown to
increase tyrosine hydroxylase (McMahon et al., 1992). It is unlikely that
this represents a lower limit to the temporal grain in which gene+nvironment interactions take place. It may well be that such interactions
occur on the temporal scale appropriate for the processes of neurotransmitter production, reuptake, and disposition. So my momentary effective
genotype in certain brain regions may be fluctuating as I formulate these
arguments, and so may the reader's. There may lie herein a promising
research area bridging behavioral genetics and neuroscience.
Some Family Notes
Behavioral genetics, it may be said, has had an uneasy childhood. For
much of its existence, its parent discipline of genetics hasn't paid any
attention to it. If the geneticists who engaged in the furiously paced search
for the molecular basis of heredity paused at all to notice behavioral
scientists, then it was to express astonishment that anyone would be so
unwise as to select such messy phenotypes for study. However, more
complex systems have recently emerged within genetics as challenges
for the future (Bodmer, 1986). It is not impossible that some behavioral
phenotypes will be attractive targets in this new emphasis.
The other parent, psychology, has known of behavioral genetics but
has often appeared to wish to disown its offspring. Recent recognition
perhaps means that some merit is now seen in the child. Some of its
cousins and stepsiblings have come to like it in recent years and now
welcome it warmly. Some have even joined the child. Some remain suspicious, some say "Who?",and some pick up their plates and move away
as the child approaches the picnic table. So it goes!
All of the relatives in psychology should be assured that the behavioral genetics child is as interested as they are in the family businesthe understanding and explanation of behavior-and just as excited about
what lies ahead in the next century.
Bodmer, W. F. (1986). Human genetics: The molecular challenge. Cold Spring Harbor
Symposia on Quantitative Biology, 51, 1-14.
Darwin, C. (1859). On the origin of species by means of natural selection or the preservation of favoured races in the struggle f o r life. New York: Appleton.
Davies, K. E., Pearson, P. L., Harper, P. S., Murray, J. M., O'Brien, T., Sarfrazi, M., & Williamson, R. (1983). Linkage analysis of two cloned DNA sequences flanking the
Duchenne muscular dystrophy locus on the short arm of the human X chromosome.
Nucleic Acids Research, 11, 2303-2305.
Falconer, D. S. (1989). Introduction to quantitativegenetics (3rd ed.). Essex, UK: Longman
Scientific & Technical.
Fisher, R. A. (1918). The correlation between relatives on the supposition of Mendelian
inheritance. Transactions of the Royal Society of Edinburgh, 52, 399-433.
FQlling,A., Mohr, 0. L., & Ruud, L. (1945). Oligophrenia phenylpyrouvica: A recessive
syndrome in man. Norske VidenskapslAkademi I Oslo, Matematisk-Naturvidenskapelig h'lasse, 13, 1 4 .
Ford, D. L. (1987). Humans as self-constructing living systems. Hillsdale, NJ: Erlbaum.
Fritz, R. S., & Kletzien, R. F. (1987). Regulation of glucose-6-phosphate dehydrogenase by
diet and thyroid hormone. Molecular and Cellular Endocrinology, 51, 13-17.
Fulker, D. W., Denies, J. C., & Plomin, R. (1988). Genetic influence on general mental
ability increases between infancy and middle childhood. Nature, 336, 767-769.
Galton, F. (1876). The history of twins as a criterion of the relative powers of nature and
nurture. Royal Anthropological Institute of Great Britain and Ireland Journal, 6,
Galton, F. (1883). Inquiries into h u m a nfaculty and its development. London: Macmillan.
Gusella, J. F., Wexler, N. S., Conneally, P. M., Naylor, S. L., Anderson, M. A., Tanzi, R. E.,
Watkins, P. C., & Ottina, K. (1983). Apolymorphic DNA marker genetically linked to
Huntington's disease. Nature, 306, 234-238.
Hadorn, E. (1955). Developmental genetics and lethal factors. New York: Wiley.
Hahn, M. E., Hewitt, J. K., Henderson, N. D., & Benno, R. (Eds.). (1990). Developmental
behavioral genetics. New York: Oxford University Press.
Honzik, M. P. (1957). Developmental studies of parent-child resemblance in intelligence.
Child Development, 28, 215-228.
Katsurada, A,, Iritani, N., Fukuda, H., Noguchi, T., & Tanaka, T. (1987). Influence of diet on
the transcriptional and post-transcriptional regulation of malic enzyme induction in
the rat liver. European Journal of Biochemistry, 168, 487491.
Kim, M. H., Nakayama, R., Manos, P., Tomlinson, J. E., Choi, E., Ng, J. D., & Holten, D.
(1989). Regulation of apolipoprotein E synthesis and mRNA by diet and hormones.
Journal of Lipid Research, 30, 663-671.
Lush, J. L. (1951). Genetics and animal breeding. In L. C. Dunn (Ed.), Genetics in the 20th
century (pp. 493-525). New York: Macmillan.
MacLean, N. (1989). Genes and gene regulation. London: Edward Arnold.
Matheny, A. P., Jr. (1983). A longitudinal twin study of stability of components from Bayley's
infant behavior record. Child Development, 54, 356360.
McClearn, G. E. (1993). Genetics, systems, and alcohol. Behavior Genetics, 23, 223-230.
McClearn, G. E., & Plomin, R. (in press). Strategies for the search for genetic influences
in alcohol-related phenotypes. In H. Begleiter & B. Kissin (Eds.), Alcohol and alcoholism. London: Oxford University Press.
McClearn, G. E., Plomin, R., Gora-Maslak, G., & Crabbe, J. C. (1991). The gene chase in
behavioral science. Psychological Science, 2, 222-229.
McGuffin, P., Owen, M., & Gill, M. (1992). Molecular genetics of schizophrenia. In J. Mendlewics & H. Hippius (Eds.), Genetic research in psychiatry (pp. 25-48). New York:
Springer-Verlag.
McKusick, V. A. (1992). Mendelian inheritance in m a n (10th ed.). Baltimore: Johns Hopkins University Press.
McMahon, A., Kvetnansky, R., Fukuhara, K., Weise, V. K., Kopin, I. J., & Sabban, E. L. (1992).
Regulation of tyrosine hydroxylase and dopamine Phydroxylase mRNA levels in rat
adrenals by a single and repeated immobilization stress. Journal of Neurochemistry,
58, 2124-2130.
Mendel, G. J. (1866). Versuche uber Pflanzen-Hybriden [Research on hybrid plants]. Verhandlungen des Natu$orshunden in Breuen, 4, U 7 .
Munnich, A., Besmond, C., Darquy, S., Reach, G., Vaulont, S., Dreyfus, J-C., & Kahn, A. (1985).
Dietary and hormonal regulation of adolase B gene expression. Journal f o r Clinical
Investigation, 75, 1045-1052.
Munnich, A., Marie, J., Reach, G., Vaulont, S., Simon, M. P., & Kahn, A. (1984). I n vivo
hormonal control of L-type pyruvate kinase gene expression. Journal of Biological
Chemistry, 259, 10228-10231.
Murphy, E. A., & Berger, K. R. (1988). An approach to the genetics of physiological homeostasis. In B. S. Weir, E. E. Eisen, M. M. Goodman, & G. Namkoong (Eds.),
Proceedings of the Second International Conference on Quantitative Genetics (pp.
283-296). Sunderland, MA: Sinauer Associates.
Murphy, E. A., & Trojak, J. L. (1986). The genetics of quantifiable homeostasis: I. The general
issues. American Journal of Medical Genetics, 24, 159-169.
Pearson, K. (1904). On the laws of inheritance of man: 11. On the inheritance of the mental
and moral characters in man, and its comparison with the inheritance of the physical
characters. Biometrika, 3, 131-190.
Pedersen, N. L., Plomin, R., Nesselroade, J. R., & McClearn, G. E. (1992). A quantitative
genetic analysis of cognitive abilities during the second half of the life span. Psychological Science, 3, 34W53.
Plomin, R. (1983). Developmental behavioral genetics. Child Development, 54, 25g259.
Plomin, R. (1986). Development, genetics, and psychology. Hillsdale, NJ: Erlbaum.
Plomin, R. (1990). Role of inheritance in behavior. Science, 248, 183-188.
Plomin, R., Denies, J. C., & McClearn, G. E. (1990). Behavioral genetics: A primer (2nd
ed.). New York: Freeman.
Plomin, R., McClearn, G. E., Gora-Maslak, G., & Neiderhiser, J. (1991). Use of recombinant
inbred strains to detect quantitative trait loci associated with behavior. Behavior
Genetics, 21, 99-116.
Plomin, R., & Nesselroade,J. R. (1990). Behavioral genetics and personality change. Journal
of Personality, 58, 191-220.
Smith, M. A., Banerjee, S., Gold, P. W., & Glowa, J. (1992). Induction of c-fos mRNA in rat
brain by conditioned and unconditioned stressors. Brain Research, 578, 135-141.
Tomlinson, J. E., Nakayama, R., & Holten, D. (1987). Repression of pentose phosphate
pathway dehydrogenase synthesis and mRNA by dietary fat in rats. Journal of Nutrition, 118, 40W15.
Waddington, C. H. (1957). The strategy of the genes. New York: Macmillan.
Watson, J. D., & Crick, F. H. C. (1953a). Genetical implications of the structure of deoxyribonucleic acid. Nature, 171, 964-967.
Watson, J. D., & Crick, F. H. C. (1953b). Molecular structure of nucleic acids: A structure
for deoxyribose nucleic acids. Nature, 171, 737-738.
Weber, A,, Marie, J., Cottreau, D., Simon, M.-P., Besmond, C., Dreyfus, J.-C., & Kahn, A.
(1984). Dietary control of adolase B and L-type pyruvate kinase mRNAs in rat. Journal
of Biological Chemistry, 259, 1798-1802.
of Cognitive Ability:
A Life-Span Perspective
Matt McGue, Thomas J. Bouchard, Jr., William G. Iacono, and
David T. Lykken
ince the time of Francis Galton, the nature-nurture controversy has
\Jbeen virtually synonymous with debate on whether genetic factors
influence I&. Although there stdl may be some who would reduce the
debate to questioning the specifics of individual studies, it appears that
the issue has been resolved for the vast majority of psychologists. Snyderman and Rothman (1990) recently surveyed psychologists' beliefs
about intelligence and reported that over 90%of those responding agreed
that I& was, at least in part, heritable. This modern consensus, a clear
reversal of opinion from the 1950s and 1960s, is a direct result of the
substantial body of research compiled by behavioral geneticists over the
past 50 y e a r s a corpus that unequivocally implicates genetic factors in
the development of I&.
The preparatim of this chapter was supported, i n part, b y U S . Public Health Servicegrants AGO6886
and DAO5147. The chapter i s bused, i n part, m a paper presented at the centennial meeting of the
American Psychological Association i n Washington, DC, August 1992.
McGUE E l AL.
In 1981, Bouchard and McGue (1981) published an update of the
classic Erlenmeyer-Kimling and Jarvik (1963) review of familial studies
of intelligence. In this update, they summarized results from over 100
separate studies reporting over 500 familial I& correlations on over
100,000pairs of relatives. Some of the more significant results from this
review are given in Table 1. When taken in aggregate, twin, family, and
adoption studies of I& provide a demonstration of the existence of genetic
influences on I& as good as can be achieved in the behavioral sciences
with nonexperimental methods. Without positing the existence of genetic
influences, it simply is not possible to give a credible account for the
consistently greater I& similarity among monozygotic (MZ) twins than
among like-sex dizygotic (DZ) twins, the significant I& correlations among
biological relatives even when they are reared apart, and the strong association between the magnitude of the familial I& correlation and the
degree of genetic relatedness. The correlations summarized in Table 1
also strongly implicate the existence of environmental influences: The
correlation among reared-together MZ twins is less than unity; biological
Average Familial IQ Correlations ( R )
MZ twins
DZ twins
Parent-offspring
-~
Average R
Reared-together biological relatives
~-
Reared-apartbiological relatives
Parent-offsorina
Reared-together nonbiological relatives
Nore MZ = monozygottc, DZ = dtzygotic R was determined using sample-size-weighted
average of z transformations Adapted from "Familial Studies of Intelligence A Review" by
T J Bouchard. Jr , and M McGue 1981, Science. 250, p 1056, copyright 1981 by the American
Association for the Advancement of Science, adapted by permission
GENETICS OF COGNITIVE ABILITY
relatives who were reared together are more similar than biological relatives who were reared apart; and there is a significant correlation between the IQs of nonbiologically related but reared-together relatives.
In 1990, Chipeur, Rovine, and Plomin (1990) sought to estimate the
extent to which I& variability was associated with genetic, shared environmental, and nonshared environmental factors by fitting biometric
models to the aggregate data summarized by Bouchard and McGue (1981).
They found that a relatively simple biometric model fit the combined I&
data and yielded an estimate of 51% for the percentage of I& variance
associated with genetic factors (i.e., the heritability). Happily, their estimate of I& heritability fell midway between the estimates advocated by
some of the more strident partisans in the debate. Chipeur et al. also
reported that shared environmental influences (i.e., environmental factors
that are shared by individuals reared in the same home and thus contribute
to their similarity) accounted for anywhere from 11%to 35%, depending
on the particular relationship involved (i.e., siblings vs. DZ vs. MZ twins).
The balance of I& variance, from 14%to 38%of the total, was apportioned
to nonshared environmental influences (i.e., environmental factors that
are not shared by reare