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CHAPTER 2
HEREDITARY INFLUENCES ON DEVELOPMENT
OUTLINE
I.
Principles of Hereditary Transmission
Determining how one’s genotype, the genetic endowment that an individual inherits, is
expressed as a phenotype, or the ways in which a person’s genotype is expressed in observable
or measurable characteristics
A.
B.
C.
Genetic material
1.
Conception is the moment of fertilization, when a sperm penetrates an ovum,
creating a zygote, the single cell formed at conception from the union of a sperm
and an ovum
2.
Chromosome is a threadlike structure made up of genes; humans have 46
chromosomes in the nucleus of each body cell
3.
Genes are the hereditary blueprints for development that are transmitted
unchanged from generation to generation
4.
Deoxyribonucleic acid or DNA is the long, double-stranded molecules that
make up chromosomes
Growth of the zygote and production of body cells
1.
Mitosis is the process in which a cell duplicates its chromosomes and then
divides into two genetically identical daughter cells
The germ (or sex) cells
1.
Production of gametes through meiosis
a. Meiosis is the process in which a germ cell divides, producing gametes
(sperm or ova) that each contain half of the parent cell’s original
complement of chromosomes; in humans, the products of meiosis
contain 23 chromosomes.
2.
Crossing over is a process in which genetic material is exchanged between pairs
of chromosomes during meiosis.
Box 2.1 – Focus on research: Crossing over and chromosome segregation during meiosis
3.
4.
Hereditary uniqueness
a.
Independent assortment is the principle that each pair of chromosomes
segregates independently from all other chromosome pairs during
meiosis
Multiple births
a.
Monozygotic (or identical) twins develop from a single zygote that
later divides to form two genetically identical individuals
Chapter 2
b.
D.
E.
II.
Dizygotic (or fraternal) twins result when a mother releases two ova at
roughly the same time and each is fertilized by a different sperm,
producing two zygotes that are genetically different
Male or female?
1.
Autosomes are the 22 pairs of human chromosomes that are identical in males
and females
1.
X chromosome is the longer of the two sex chromosomes; normal females have
two X chromosomes, whereas normal males have only one
2.
Y chromosome is the shorter of the two sex chromosomes; normal males have
one Y chromosome, whereas females have none
What do genes do?
1.
At the most basic level, genes call for the production of amino acids
2.
Genes also guide cell differentiation
3.
Some genes regulate the pace and timing of development
4.
Environmental factors influence how genes function in several ways
a.
At the intracellular level, a molecular gene-environment interaction
occurs
b.
At the extracellular level, a cellular gene-environment interaction occurs
c.
At the level of the external environment, both experience-expectant
(experienced by all humans) and experience-dependent (experienced by
some humans) interactions may occur
How Are Genes Expressed?
A.
Single-gene inheritance patterns are a pattern of inheritance in which one allele
dominates another so that only its phenotype is expressed
1.
Simple dominant-recessive inheritance is a pattern of inheritance in which one
allele dominates another so that only its phenotype is expressed
a.
Allele is an alternative form of a gene that can appear at a particular site
on a chromosome
b.
Dominant allele is a relatively powerful gene that is expressed
phenotypically and masks the effect of a less powerful gene
c.
Recessive allele is a less powerful gene that is not expressed
phenotypically when paired with a dominant allele
d.
Homozygous indicates having inherited two alleles for an attribute that
are identical in their effects
e.
Heterzygous indicates having inherited two alleles for an attribute that
have different effects
f.
Carrier is a heterozygous individual who displays no sign of a recessive
allele in his or her own phenotype but can pass this gene to offspring
Box 2.2 – Applying research to your life: Examples of dominant and recessive traits in
human heredity
2.
Codominance
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Hereditary Influences on Development
a.
B.
III.
Codominance is a condition in which two heterozygous but equally
powerful alleles produce a phenotype in which both genes are fully and
equally expressed
b.
Sickle-cell anemia is a genetic blood disease that causes red blood cells
to assume an unusual sickle shape and to become inefficient at
distributing oxygen
3.
Sex-linked characteristic is an attribute determined by a recessive gene that
appears on the X chromosome; more likely to characterize males
Polygenic inheritance
1.
Polygenic trait is a characteristic that is influenced by the action of many genes
rather than a single pair
Hereditary Disorders
A.
B.
C.
D.
Congenital defects are is present (though not necessarily apparent) at birth; such defects
may stem from genetic and prenatal influences, or from complications of the birth
process
Chromosomal abnormalities
1.
Abnormalities of the sex chromosomes
2.
Abnormalities of the autosomes
b.
Down syndrome is a chromosomal abnormality (also known as trisomy21) caused by the presence of an extra 21st chromosome; people with
this syndrome have a distinctive physical appearance and are moderately
to severely retarded
Genetic abnormalities
1.
Mutation is a change in the chemical structure or arrangement of one or more
genes that has the effect of producing a new phenotype
Predicting, detecting, and treating hereditary disorders
1.
Predicting hereditary disorders
a.
Genetic counseling is a service designed to inform prospective parents
about genetic diseases and to help them determine the likelihood that
they would transmit such disorders to their children
i.
Fragile X syndrome is an abnormality of the X chromosome
caused by a defective gene and associated with mild to severe
mental retardation, particularly when the defective gene is
passed from mother to child
2.
Detecting hereditary disorders
a.
Amniocentesis is a method of extracting amniotic fluid from a pregnant
woman so that fetal body cells within the fluid can be tested for
chromosomal abnormalities and other genetic defects
b.
Chorionic villus sampling (CVS) is an alternative to amniocentesis in
which fetal cells are extracted from the chorion for prenatal tests; CVS
can be performed earlier in pregnancy than is possible with
amniocentesis
c.
Ultrasound is a method of detecting gross physical abnormalities by
scanning the womb with sound waves, thereby producing a visual
outline of fetus
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Chapter 2
3.
Treating hereditary disorders
a.
Phenylketonuria (PKU) is a genetic disease in which the child is
unable to metabolize phenylalanine; if left untreated, it soon causes
hyperactivity and mental retardation
b.
Germline gene therapy is a procedure, not yet perfected or approved
for use with humans, in which harmful genes would be repaired or
replaced with healthy ones, thereby permanently correcting a genetic
defect
Box 2.3 – Applying research to your life: Ethical issues surrounding treatments for
hereditary disorders
IV.
Hereditary Influences on Behavior
A.
B.
Behavioral genetics is the scientific study of how a genotype interacts with the
environment to determine behavioral attributes such as intelligence, personality, and
mental health
Methods of studying hereditary influences
1.
Heritability is the amount of variability in a trait that is attributable to hereditary
factors
2.
Selective breeding experiment is a method of studying genetic influences by
determining whether traits can be bred in animals through selective mating
3.
Family studies
a.
Kinship is the extent to which two individuals have genes in common
b.
Twin design is a study in which sets of twins that differ in zygosity
(kinship) are compared to determine the heritability of an attribute
c.
Adoption design is a study in which adoptees are compared with their
biological relatives and their adoptive relatives to estimate the
heritability of an attribute, or attributes
4.
Estimating the contribution of genes and environment
a.
Concordance rates are the percentage of cases in which a particular
attribute is present for one member of a twin pair if it is present for the
other
b.
Gene influences
i.
Heritability coefficient is a numerical estimate, ranging from
.00 to +1.00, of the amount of variation in an attribute that is due
to hereditary factors
c.
Nonshared environmental influence (NSE) is an environmental
influence that people living together do not share that should make these
individuals different from one another
d.
Shared environmental influence (SE) is an environmental influence
that people living together share that should make these individuals
similar to one another
e.
Myths about heritability
i.
They cannot tell us whether we inherited a trait
ii.
They apply only to populations, never individuals
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Hereditary Influences on Development
iii.
C.
D.
E.
V.
They refer only to a particular trait displayed by a particular
population under particular environmental circumstances
iv.
Heritable traits can be modified by environmental influences
Hereditary influences on intellectual performance
1.
As children mature, genes seems to contribute more to individual differences in
IQ
2.
Both twin studies and adoption studies support this conclusion
Hereditary contributions to personality
1.
Core dimensions genetically influenced
a.
Introversion/extroversion: the opposite poles of a personality
dimension, where introverts are shy, anxious around others, and tend to
withdraw from social situations, and extroverts are highly sociable and
enjoy being with others.
b.
Empathic concern is a measure of the extent to which an individual
recognizes the needs of others and is concerned about their welfare
2.
How much genetic influence? Personality traits appear to be moderately
heritable
3.
Which aspects of environment influence personality?
4.
Measuring the effects of nonshared environments
5.
Do siblings have different experiences because they have different genes?
a.
Children raised in the same home generally do not have the same
personality
b.
Even within the same home, environmental differences can occur due to
gender (sons treated differently than daughters) or birth order (firstborns
treated differently than later born children)
Hereditary contributions to behavior disorders and mental illness
1.
Schizophrenia is a serious form of mental illness characterized by disturbances
in logical thinking, emotional expression, and interpersonal behavior
2.
Bipolar disorder is a psychological disorder characterized by extreme
fluctuations in mood
3.
Neurotic disorder is an irrational pattern of thinking or behavior that a person
may use to contend with stress or to avoid anxiety
4.
Although there are genetic predispositions for mental illness, it usually takes a
number of stressful experiences to trigger it
Theories of Heredity and Environment Interactions in Development
A.
B.
C.
Canalization is genetic restriction of phenotype to a small number of developmental
outcomes; a highly canalized attribute is one for which genes channel development along
predetermined pathways, so that the environment has little effect on the phenotype that
emerges
Range-of-reaction principle is the idea that genotype sets limits on the range of
possible phenotypes that a person might display in response to different environments
Genotype/environment correlations
1.
Passive genotype/environment correlations reflect the notion that the rearing
environments biological parents provide are influenced by the parents’ own
genes, and hence are correlated with the child’s own genotype
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Chapter 2
2.
D.
IV.
Ethological and Evolutionary Viewpoints
A.
B.
C.
D.
VII.
Evocative genotype/environment correlations reflect the notion that our
heritable attributes affect others’ behavior toward us and thus influence the
social environment in which development takes place
3.
Active genotype/environment correlations reflect the notion that our
genotypes affect the types of environments that we prefer and seek out
4.
How do genotype/environment correlations influence development?
a.
The relative influence of these different types of correlations changes
over the lifespan, with active correlations taking on greater influence as
the child matures
5.
Separated identical twins
Contributions and criticisms of the behavioral genetics approach
1.
Genes and environment interact to influence development
2.
Critics point out this is more a descriptive overview than a well-articulated
explanation
Assumptions of classical ethology
1.
Ethology is the study of the bioevolutionary basis of behavior and development
with a focus on the survival of the individual
2.
All animal species are born with biologically programmed characteristics that
evolved as a result of natural selection (an evolutionary process, proposed by
Charles Darwin, stating that individuals with characteristics that promote
adaptation to the environment will survive, reproduce, and pass these adaptive
characteristics to offspring; those lacking these adaptive characteristics will
eventually die out)
Ethology and human development
1.
Critical period is a limited time span during which developing organisms are
biologically prepared to display adaptive patterns of development, provided they
receive the appropriate input
2.
Sensitive period is period of time that is optimal for the development of
particular capacities, or behaviors, and in which the individual is particularly
sensitive to environmental influences that would foster these attributes
Modern evolutionary theory is the study of the bioevolutionary basis of behavior and
development with a focus on survival of the genes
Contributions and criticisms of the ethological viewpoint
1.
Present view of child as a biological creature
2.
Difficult to test, and cultural learning may overshadow innate evolutionary
mechanisms
Applying Developmental Themes to Hereditary Influences on Development
A.
B.
C.
D.
The Active Child
Nature and Nurture Interactions in Development
Qualitative and Quantitative Changes in Development
The Holistic Nature of Child Development
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Hereditary Influences on Development
LECTURE 2-1: HEREDITY AND ENVIRONMENT AS CO-DETERMINERS OF
DEVELOPMENTAL OUTCOMES
This text identifies four basic developmental themes. One was the nature-nurture controversy over whether
people are primarily the product of environment or of their heredity and biological predispositions. Today,
behavior geneticists emphasize how heredity and environments interact to determine developmental
outcomes. Chapter 2 explores the mechanisms of heredity and reviews our current understanding of how
heredity and environment work together to determine both physical and behavioral characteristics.
This interactionist view is more in line with reality, and students will benefit from seeing examples of that.
These examples all illustrate a basic tenet of genetics: a variety of phenotypes are possible for each
genotype. How broad a variety will depend on the degree of canalization of the trait (Waddington’s notion)
or, put differently, the range of reaction (Gottesman’s notion). According to Gottesman and others, genetics
sets the upper and lower limits on the possible variations. All characteristics show variation. Environment
does not change genetic makeup, but differentially selects one of several potentials. Examples help students
see how wide a range of phenotypes is possible for a given genotype.
Example 1: Physical Changes at Adolescence
Pubertal changes provide a very striking example of the interaction of heredity and environment. They
illustrate the notion that there are a variety of possible outcomes given a particular genetic makeup, while at
the same time, some limits are set by heredity. In this example, environment refers to an internal
environment, the cell environment. The cell environment changes with pubertal increases in levels of
androgens and estrogens. The genes do not change, but there are dramatic changes in physical
characteristics. All that has changed is the chemical makeup of the cell environment, yet the difference in
outcome is striking if you compare the physical appearance of a 16-year-old girl to pictures of her at age
nine.
Example 2: Graying at 40
Similarly, when adults begin to get gray hair in their 40s, they have not undergone genetic mutation, but
some changes have occurred in the chemical makeup of the cell environment that influences hair color.
In both Examples 1 and 2, note that there are some limits set by heredity for what outcomes can occur. The
hormones may set in action the physical changes that occur during adolescence, but heredity will have
something to say about what the ultimate height of the girl will be, the size of the girl’s breasts, the timing of
menarche, etc. The full range of outcomes is not possible for all genotypes. The unique genetic makeup of
an individual determines what particular range of outcomes will be possible. Similarly, in the hair color
example, chemical changes associated with the aging process set graying into action, but there are limits in
the possible outcomes. We do not see too many people with green or purple hair as they age (maybe blue,
though—out of a bottle!). We see shades of gray, silver, and white. Heredity plays a role in the commonality
we see across individuals in physical and behavioral outcomes and also plays a role in the individuality we
see, likewise for environment.
Example 3: Himalayan Rabbit
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Chapter 2
A particularly striking example of the interaction of heredity and environment comes from an experiment
with Himalayan rabbits. Temperature has been found to exert considerable influence on the fur color of
these rabbits. Himalayans are typically white except for the extremities, nose, and ears. We can turn any part
black, however, by shaving the area and applying ice. If the area is kept cold, the fur will grow back black
where there once was white fur. We could create a very interesting rabbit (with patterns). The potential for
either black pigmentation or no pigmentation (white) is present in every cell all the time. Which potential is
released apparently depends on environmental conditions (specifically, temperature). White to black is quite
a range of reaction. Note here again that the options are constrained—no red, purple, or green fur has
resulted from the application of cold.
Example 4: IQ and Gottesman’s Range of Reaction Notion
Note: This example can be used with Activity 2-7 and Handout 2-1. Handout 2-1 provides a graphic
representation of the hypothetical outcomes for IQ test score when (a) heredity is the sole determining factor
(top graph), (b) environment is the sole determining factor (middle graph), and (c) heredity and environment
interact as Gottesman suggests (bottom graph).
The examples so far have illustrated the interactive role of heredity and environment in determining
physical characteristics. Students will enjoy extending this thinking to behaviors as well, particularly
looking at Gottesman’s notion as applied to IQ. It may help to begin by reviewing the evidence for heredity
and environment separately, and then work toward a discussion of the interaction of these features and the
complexity of it.
Evidence for Role of Heredity in Determining IQ

Kinship studies reveal that the closer the kinship, the higher the correlation (e.g., r = .47 for
siblings reared together, but r ranges from .72 to .91 for identical twins)

IQs of identical twins reared apart are more strongly correlated than the IQs of fraternal
twins reared together.

The correlation between the IQs of adopted children and their biological parents has been
found to be greater (r = .49) than the IQ correlation between adopted children and their
adoptive parents (r = .29).
Evidence for Role of Environment

IQs of biologically unrelated children who grow up in the same home are more strongly
correlated (r = .34) than are the IQ scores of unrelated children living in different homes (r
= .01).

IQ scores of African-American adoptees reared by middle-class Caucasian parents were 20
points higher than the IQs of comparable children raised by African-American parents.

Disadvantaged children show IQ gains after participation in compensatory education
programs, but these gains are lost if the stimulation necessary to maintain intellectual
development is not continued.
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Hereditary Influences on Development

Genetically normal children reared by feebleminded mothers show dramatic drops in IQ
because these mothers are unable to provide the intellectual stimulation needed to promote
development past the early elementary level.

Children who have extended illnesses that prevent normal experiences promoting
intellectual development will often show marked gains in IQ after their health permits
normal interaction with a normally stimulating environment.

The IQs of identical twins reared in different homes having similar environments are
strongly correlated (r = .75 to .91). Identical twins reared in very different environments
have been found to differ by as much as 24 points, and the correlations are much lower (as
low as r = .26).
Gottesman’s Model
Both heredity and environment clearly influence IQ test performance. How can their joint contribution best
be conceptualized? Gottesman has formulated a useful conceptual model.
1.
There is a range of possible IQ outcomes for each genotype. Have students consider four genotypes:

Genotype A ranges from 78 to 165

Genotype B ranges from 68 to 125

Genotype C ranges from 40 to 75

Genotype D ranges from 20 to 38
Note: the wide range of reaction (outcomes) that Gottesman includes in his schematic for some
genotypes is compatible with the finding that as many as 15 percent of a sample followed from age
2 to 18 years changed over 40 IQ points (McCall et al., 1973).
2.
We can say that, for each genotype, there is a “ceiling” on how much IQ test performance can
improve under the most favorable conditions and a performance “floor” below which an individual
of that genotype is unlikely to fall.
3.
Note that the Gottesman model provides a clear way of explaining why we can say very little about
a person’s potential (their genotype) knowing only their IQ test scores. If we open up a file and read
that an individual’s IQ score is 78, we can conclude nothing about this child’s potential. This child
could be a Genotype C in an enriched environment and operating near the top limit of potential, or
could be a Genotype A in a restricted environment. Ask students to discuss the implications of
educational placement based on IQ scores.
4.
Gottesman’s model shows us that if two individuals or groups are found to differ by 20 IQ points,
we really cannot conclude anything about genotype or potential unless we can assume these
individuals or groups have experienced equally favorable or equally unfavorable environmental
stimulation. (Note: Gottesman’s model is useful for explaining why concluding that the difference
between the IQ scores of African Americans versus Caucasians reflects genetic differences is
unwarranted—we cannot assume equal favorableness of environment for both racial groups.)
43
Chapter 2
LECTURE 2-2: PKU and TAY-SACHS AS ILLUSTRATIONS OF HEREDITY-ENVIRONMENT
INTERACTION
Note: Use separately or as an extension of Lecture 2-1. Use Handouts 2-2a and 2-2b with this lecture
PKU—Phenylketonuria, a Treatable Recessive Genetic Disease
The condition PKU provides a powerful example of the practical importance of understanding how heredity
and environment interact to determine outcomes. Discovery of this interaction has made the difference
between normal and subnormal intelligence for hundreds of children afflicted with the condition.
Environmental intervention early in life can “block” the expression of this disorder.
How does the recessive gene for PKU exert its influence?
PKU is short for phenylketonuria, a condition resulting from a genetically-transmitted inability to produce
an enzyme. This enzyme, called phenylalanine hydroxylase, is necessary to metabolize phenylalanine (a
substance found in many foods) into a usable substance, tyrosine. Tyrosine is an amino acid, one of the
constituents of protein. Tyrosine is important for normal formation of thyroxine (a hormone) and
epinephrine (a neurotransmitter). It is also important for the formation of pigment for the skin and hair. In
the absence of the necessary enzyme to convert phenylalanine into tyrosine, a toxic build-up of pyruvic acid
results, which is damaging to the central nervous system, particularly the developing one. If nothing is done
to counter the build-up, the result is severe mental disability (mean IQ is about 40 for children untreated).
How is this genetic disorder treated?
Environmental intervention can counter the effects of the inherited inability to convert phenylalanine into
tyrosine—that intervention is diet therapy. If infants are started on a diet low in phenylalanine during the
first weeks of life, these children will not suffer severe damage to the nervous system and the resulting
disability, and will have IQs in the normal range. Research suggests that there may be some deficits
remaining that are not detected by IQ testing. Welsch, Pennington, Ozonoff, Rouse, and McCabe (1990)
report evidence that executive functions carried out in the prefrontal areas were impaired in a diet-controlled
group of PKU children. They suggest that even mild elevations in phenylalanine blood levels can result in a
lowering of dopamine and other amines essential for normal intellectual functioning.
Most foods contain some protein and, hence, phenylalanine. Nutritional therapy requires strict adherence to
a very restrictive diet that excludes or restricts intake of milk, meat, and most other normal protein sources.
Even normal pastas and breads are too high in protein for these children. To fulfill their nutritional
requirements while restricting phenylalanine, a special formula called Lofenalac has been developed for
infants. After age three, a preparation called Phenyl-free is given along with natural foods that are low in
phenylalanine, such as fruit ices instead of ice cream, low-protein spaghetti with tomato sauce instead of
spaghetti with meatballs, and jelly sandwiches with low-protein bread instead of peanut butter and jelly
sandwiches. The child must learn at an early age which are the YES foods and which are the NO ones and
how to assume responsibility for food management. Diet therapy used to be discontinued when children
started school or, more recently, at around age 10, however, some nutritionists now think that individuals
with PKU benefit from a phenylalanine-restricted diet throughout their lives, not just during the periods of
greatest brain development (Trahms, 1984).
What have we learned from PKU about the way heredity and environment work to affect outcomes?
44
Hereditary Influences on Development
What is of particular interest in the case of PKU is that, by learning how environment (diet) and heredity
(genetic abnormality in enzyme production) interact, it has been possible to help these children. To ensure
that children who need help will be identified early, PKU testing is mandatory in most states a few days
after birth. PKU provides a good illustration of the broad range of IQ scores (outcomes) that are possible
given a particular genetic makeup—from IQs of 20 to 120!—depending on environment (diet, in this case).
To use Gottesman’s terminology, that is a wide range of reaction.
Addendum: further evidence of the interactive influence of heredity and environment
An even more striking example of the wide range of possible reaction is evident when we look at the IQs of
the children of PKU mothers. A pregnant PKU woman may be carrying a genetically normal child (PKU is
a recessive trait) who we would expect to have normal IQ. However, if the PKU mother’s diet is not
carefully controlled during pregnancy, the levels of unconverted phenylalanine can get high enough to
damage the developing fetus, resulting in cardiac defects, retarded growth, mental disability, and
microcephaly. The possibility exists that a genetically normal baby can be normally intelligent or mentally
disabled, depending on the degree of control of the mother’s phenylalanine blood levels. Clearly, neither
heredity nor environment is key. They work in an interactive fashion to determine outcomes, and the range
of outcomes is quite broad.
Resources
Trahms, C. (1984). Nutritional care for children with metabolic disorder. In M. Krause & L. K. Mahan
(Eds.), Food, Nutrition, and Diet Therapy. Philadelphia: Saunders.
Verp, M. S. (1993). Genetic counseling and screening. In C. Lin, M. S. Verp, & R. E. Sabbagha (Eds.), The
high-risk fetus: Pathophysiology, diagnosis, management. New York: Macmillan.
Welsh, M., Pennington, B., Ozonoff, S., Rouse, B., & McCabe, E. (1990). Neuropsychology of early-treated
phenylketonuria: Specific executive function deficits. Child Development, 61, 1697–1713.
Tay-Sachs, a Not-Yet-Treatable Recessive Genetic Disease
Tay-Sachs is another example of a recessive genetic disorder. But unlike PKU, the disease is fatal: TaySachs children die by three to five years of age. There is no known therapy. Tay-Sachs newborns appear
normal, but symptoms emerge by about four to eight months of age:

Severe brain damage

Enlargement of head

Seizures

Blindness, deafness; reddish spot on retina

Increasing delays in development

Increasing unresponsiveness to parents and environment
How is Tay-Sachs transmitted?
Tay-Sachs is a recessive disorder, which means that both parents must be carriers for a Tay-Sachs child to
be born. If both parents are carriers, then their chances are 1 in 4 with each pregnancy that a Tay-Sachs child
will be born. See Handout 2-2b for illustration. (Note: same type of diagram can illustrate PKU
transmission as well, a similarity that may need to be pointed out to students.)
How many people carry this recessive gene?

1 in 150 in the general population

1 in 30 in the Jewish population
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Chapter 2
Actual occurrence rate?

1 in 300,000 in the general population

1 in 3,600 of Ashkenazic Jews (of Eastern European origins)
How does the presence of the recessive gene for Tay-Sachs exert its influence?
Tay-Sachs children lack a vital enzyme called HEX A. This enzyme is essential in breaking down a fatty
material called ganglioside (GM2) in brain cells. The build-up begins prenatally and reaches a potentially
harmful level around six to eight months of age. In normal infants, the HEX A enzyme has begun to break it
down by then, preventing any damage to the brain. In Tay-Sachs infants, the GM2 continues to build,
eventually causing the symptoms mentioned above. The result is fatal. See Handout 2-2b for an illustration
of the normal brain cell and the Tay-Sachs brain cell.
Point to Make
The mechanism of genetic transmission is through physiological functioning. In this case, the result of
abnormal physiology is brain deterioration and the death of the child. This example, like PKU, provides
concrete illustration of a way that heredity actually produces its effects on behavior. It also opens the way
for a discussion of how knowing the mechanism of influence stimulates and directs research efforts for an
intervention that will prevent the build-up of GM2 and the fatal outcome for Tay-Sachs children.
Understanding that genetic makeup affects physiology, which in turn affects physical and behavioral
outcomes, takes some of the mystery out of the notion of genetically transmitted diseases and/or
characteristics.
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Hereditary Influences on Development
LECTURE 2-3: SCARR ON UNDERSTANDING INDIVIDUAL DIFFERENCES
Note: lecture coordinates with Handouts 2-3a and 2-3b and Activity 2-4.
Sandra Scarr’s 1991 presidential address to the biennial meeting of the Society for Research in Child
Development (also in Child Development, 63, 1–19) can provide the basis for an extension of the material in
the text on individual differences. Her address evoked strong reactions (see Baumrind, 1993; Jackson, 1993)
and illustrated the ongoing controversy about the relative contribution of heredity and genetics and the
debate over the emphasis many behavior geneticists place on the genetic contribution to individual
differences. The heated reaction occurs because of the apparent threat of a strongly hereditary position on
the effectiveness of interventions or attempts to optimize development. A discussion of the question, “What
does evidence for a role of heredity imply regarding the potential for interventions to be effective?” is
relevant to students’ roles as the policy makers and voters of tomorrow. As was evident in the responses to
the publication of The Bell Curve in 1994, this issue is not just academic; how individuals interpret evidence
of a genetic contribution can have far-reaching social policy ramifications.
Suggestion
Start the class with excerpts from Murray and Herrnstein’s controversial book The Bell Curve and examples
of reactions in the media (e.g., Newsweek, Oct. 24, 1994, pp. 52–62) as a way of illustrating the implications
of the heredity-environment debate for social policy. Most psychologists would argue that there is no reason
for a debate—both factors influence outcomes in an interdependent fashion. Nevertheless, any mention of
heredity playing a role still triggers the erroneous assumption in the public mind that hereditary influence
implies no room for change. Some scientists have fueled that misconception. Scarr has provided some fuel
to the debate by making comments to the effect that environmental characteristics (including parenting)
cannot cause predictable outcomes in individuals.
Scarr’s 1992 Presidential Address and Child Development Article
Scarr and McCartney’s theory of genotype/environment interaction is presented in the text and helps to
capture some of the ways that genotype works indirectly to influence an individual’s experience. In her
address, Scarr further elaborated on the theme of her research of the prior 25 years—the notion that
organisms and environments combine to produce human development. Some points that Scarr made in her
address:
1.
Cross-cultural research clearly demonstrates that the environmental variation within our species
affects normal development. The children within each society, however, grow up to be individually
different—a reflection of the influence of the child’s genotype on development.
Scarr presented a path model illustrating the causal role of both genes and environments on
enduring phenotypes. She elaborated on environment, showing how enduring phenotypes vary in
actual expression depending on developmental context (home, school, etc.), and on the transitory
situation (school party, football game, family dinner, etc.). This is an important notion, not unlike
Bronfenbrenner’s conceptualization of various levels of environmental influence—mesosystem,
exosystem, and macrosystem. She has incorporated into the model the fact that a particular
genotype and rearing condition do not add up to a single phenotype but rather to an array.
Expressed phenotype also depends on the characteristics of the environment at the moment.
47
Chapter 2
Suggestion
Prepare transparencies from Figures 2, 3, and 4 in the Scarr article (Child Development, 1992, pp.
6–8) to illustrate her theory of how different levels of genetics and environment influence
behavioral development and expression.
2.
An important contention of Scarr’s theory is that the genetic uniqueness of individuals results in the
creation of unique environmental experiences by these individuals. The manner in which genetic
makeup influences environment is stated in three propositions:

Proposition 1: There are three kinds of genotype/environment effects: passive,
evocative, and active (summarized in Chapter 2 and used for Activity 2-4 below).

Proposition 2: With development, genotype/environment effects become decreasingly
passive and increasingly active. As children become increasingly able to choose their own
friends, activities, and interests, self-selected niches (active genotype influence) become a
stronger influence than the parent-provided (passive genotype influence) environment.
People tend to choose work, home, and recreational settings that match their personal
characteristics. For example, a withdrawn or unsociable person is not likely to seek
employment as a car salesperson or as a sales representative for a book company.

Proposition 3: As a necessary corollary of Proposition 2, Scarr maintained that genetic
differences become more potent determiners across development as individuals
become increasingly capable of and responsible for making their own environments.
For example, children who do not possess characteristics that allow them to thrive in the
public school environment have little choice but to stay there until high school. At that
point, more options are available, and students begin to sort themselves among them. Some
choose advanced placement classes, some take college preparatory programs, some
gravitate toward vocational-technical programs, some choose work-study, and others
emphasize sports, debate, drama, or band and do as little academic work as possible to
maintain eligibility and keep their parents placated. After high school, even more options
open up—postal worker, mechanic, truck driver, secretary, gardener, ski instructor,
professional athlete, librarian, bartender, and more. The diversity of options allows young
adults much more opportunity to actively niche-pick than they had in childhood.
This model differs from the more traditional conceptualization that environmental variations are the
causes of the individual variations we observe in phenotypes. In the triarchic theory of experience,
Scarr argued that variations in environment are best understood as products of parental and child
characteristics, not as causes of their unique characteristics.
Scarr strongly emphasized that individuals differ in how they encode and experience their
environments and that variations in encoding are evident at various points in their development. For
example, all the families in a neighborhood may subscribe to the same daily newspaper, all have
access to the local public library, and all have a television set. In those ways, their environments are
identical. Yet, how those identical environmental features affect each family and each individual
will depend on each person’s unique genetic makeup. People who read well and easily are more
likely to read the newspaper, spend more time in leisure reading, and make use of the library. What
each chooses to read in the newspaper or for pleasure reading will depend on the person’s
48
Hereditary Influences on Development
individual characteristics. Not only will the individual who is a capable reader select more and
different reading material than someone with different capabilities, but the voracious reader also
will evoke different reactions from others. Others who enjoy reading will respond positively, while
those who do not may find the voracious reader boring. During childhood, adults will typically
respond positively unless a child is reading a novel at an inappropriate time (e.g., during math or
music class, during meals or chore time) or is reading Playboy instead of Wind in the Willows or the
Tolkien trilogy.
3.
Throughout her address and the 1992 article, Scarr emphasized that environmental variations do
exist, as suggested by traditional developmental theory. She also agreed with Plomin and Thompson
(1987), that considerable environmental variance is contributed by nonshared environmental
influences (i.e., those environmental characteristics that are not common for all family members).
For example, only the oldest child of two has the experience of being the firstborn, or being age 10
when the parents are ages 33 and 37, or of having a younger sibling. Scarr argued, however, that the
unique characteristics of an individual’s environment are due less to circumstantial factors such as
those just noted and more to (a) the differences in opportunities actively selected or ignored by the
individual, and (b) the differences in responses the individual evokes from others.
Scarr maintained that the developmental data simply do not support the view that particular
environmental characteristics can cause predictable outcomes in individuals. For example, the
correlations between parenting practices and behavior outcomes are not very high. Children adopted
into the same family do not turn out to be clones of each other. Not all children reared with a
depressed mother show depressed behavior. Not all abused children become aggressive adolescents.
The data do not support the view that “common family and larger context have common
influences.” Even when children are genetically related (and especially when they are not), Scarr
maintained that there is ample evidence that they respond in unique ways to common experiences
and may even create unique experiences.
4.
Scarr further argued that this lack of one-to-one correspondence between common environment and
outcomes should alleviate some of the concern and guilt parents often feel about not being perfect.
Parents go into the parenting role assuming that if they do A, B, and C and do not do E, F, and G,
that their children will turn out with the characteristics they desire. Scarr maintained that children
will turn out in a particular way with a relatively wide range of parenting behaviors simply because
of who those children are genetically. Basically, Scarr argued that a wide range of circumstances
will foster normal development and that parenting in some specific way will not necessarily mold a
child to be something that he or she is not. Children who are not receiving parenting and
environmental supports within the range normal for the species (i.e., those who are malnourished,
deprived of stimulation, or abused) can benefit from a change in their environments. However, she
suggested that parenting that falls within the normal range will be “good enough” parenting to
support normal development and the emergence of the child’s genetic potential physically,
cognitively, socially, and otherwise. The result may not always be to the parents’ liking; sometimes
children take an undesirable trajectory despite parenting that falls within the normal range.
Interventions in such cases may have only temporary and limited effects according to Scarr and
others (e.g., Clarke & Clarke, 1989).
49
Chapter 2
Responses to Scarr
Two articles were published in reaction to Scarr’s address, one by Baumrind (1993) and one by Jackson
(1993).
Baumrind (1993) takes strong exception to Scarr’s notion that the “average expectable environment” is
“good enough.” She argues that the “details of socialization patterns are crucial to an understanding of
normal and deviant development,” and “what parents do or fail to do crucially affects their children’s
development” (p. 1299). Baumrind supports her view by citing evidence showing that parenting over and
above “good enough” parenting results in more positive outcomes for children. Baumrind objects to Scarr’s
pessimistic view of interventions or “better than good enough” parenting efforts. In Baumrind’s view, there
are simply too many studies showing that quality of rearing environment matters. She argues that Scarr has
relied too heavily on heritability analyses to support her views. Heritability analyses have, in Baumrind’s
view, overestimated the role of genetic factors (e.g., identical twins reared in different environments are
typically not reared in radically different environments, inflating the correlation). Baumrind expresses
concern that Scarr’s emphasis on “good enough” parenting as all that is requisite for normal development
will lead to a parental and societal abdication of responsibility to provide optimal environments for
development—not out of malice but out of a sense of disempowerment. After all, if it doesn’t really matter
what I do as a parent, why should I spend the extra money to send my child to a private school, provide a
tutor for a struggling young student, or give up my bowling night to go to a school open house?
Jackson is an African-American researcher who expresses concern for the negative implications of Scarr’s
views on interventions, particularly for African-American children. Jackson questions the adequacy of the
evidence Scarr uses to support her theory of genotype/environment effects, arguing, for example, that
reliance on biracial adoptive studies may not be appropriate. Scarr’s work has not adequately acknowledged
the potentially confounding of adoptive status, of being an African-American or biracial child reared in a
Caucasian home, or of being a twin. Neither adoptees nor twins are typical individuals reared in “typical”
environments unless one assumes that adoptees are treated no differently than biological children or that
having a twin does not affect a child’s experience (a point Baumrind makes as well). Of considerable
concern to Jackson (as well as to Baumrind) is the pessimism of Scarr’s theory with respect to the
effectiveness of interventions or of high-quality care. Jackson and Baumrind both present several studies
that challenge Scarr’s pessimism regarding the effectiveness of intervention.
Scarr’s Response to Baumrind and Jackson
50
Hereditary Influences on Development
Scarr’s response to her critics comes in the form of an elaboration of the theory presented in her presidential
address. In addition, she acknowledges the importance of instruction for specific, nonuniversal skills, citing
the differing levels of mathematical knowledge across cultures as a function of different cultural practices.
Scarr also acknowledges that sometimes interventions have effects on development that are quite large. She
emphasizes that the behavior genetics view does not mean that behavior is intractable. To say that much of
human development is programmed to unfold under a wide variety of “good enough” environments does not
preclude the possibility of raising the mean. Scarr concludes her response by cautioning psychologists not to
be blind to the role of heredity in the name of humanitarianism.
Resources
Baumrind, D. (1993). The average expectable environment is not good enough: A response to Scarr. Child
Development, 64, 1299–1317.
Clarke, A. M., & Clarke, A. D. B. (1989). The later cognitive effects of early intervention. Intelligence, 13,
289–297.
Jackson, J. F. (1993). Human behavioral genetics, Scarr's theory, and her views on interventions: A critical
review and commentary on their implications for African American children. Child Development, 64,
1318–1333.
Plomin, R., & Daniels, D. (1987). Why are children in the same family so different from one another?
Behavioral and Brain Sciences, 10, 1–60.
Plomin, R., & Thompson, R. (1987). Life-span developmental behavior genetics. In P. B. Baltes, D. L.
Featherman, & R. M. Lerner (Eds.), Life-span development and behavior (Vol. 8, pp. 111–123).
Hillsdale, NJ: Erlbaum.
Scarr, S. (1992). Developmental theories for the 1990s: Development and individual differences
(Presidential Address). Child Development, 63, 1–19.
Scarr, S. (1993). Biological and cultural diversity: The legacy of Darwin for development. Child
Development, 63, 1–19.
51
Chapter 2
LECTURE 2-4: THE IMPACT OF THE SAME ENVIRONMENT IS NOT THE SAME FOR ALL
INDIVIDUALS
Use with Handout 2-4.
A particularly powerful example of the point that genetic factors set limits on the way environment affects
behavior is found in a study by King and Eleftheriou (1959) with deer mice. (It is necessary to use animals
rather than people for this demonstration to achieve experimental control over environmental factors.) In
this study, King and Eleftheriou compared the effect of an experience, systematic handling, on two
subspecies of deer mice (bairdii and gracilis).
Half of the gracilis and half of the bairdii deer mice experienced 10 minutes of daily handling from ages
three to 25 days old (in an automatic handling machine to control for experimenter bias or the possibility of
the handler responding differentially to subspecies differences in reactions to the handling); the other half of
each subspecies remained in their home cages and were not exposed to the handling.
Experimental Environment (handled)
Genotype 1 gracilis (Gs)
Control Environment (nonhandled)
Genotype 1 gracilis (Gs)
Genotype 2 bairdii (Bs)
Genotype 2 bairdii (Bs)
What might we expect handling to do? For most young animals, handling is frightening initially. Frightened
animals tend either to freeze in place or become frantic and urinate and defecate. Deer mice (like pet kittens,
puppies, hamsters, rabbits, etc.) become less afraid and more docile as they become habituated to the
handling. This habituation effect typically transfers to other contexts. Knowing this, the experimenters
looked at how the Gs and Bs reacted in an open-field situation, a situation that is moderately stressful for
most animals. When assessed at 79 days of age, these questions were of interest:

Would the two subspecies differ in their reactions to that environment? That is, would the control
Bs and Gs differ in how many squares of the gridded floor that they crossed?
Results: Control Bs were much more active than the control Gs in the open field, indicating a
“baseline” subspecies difference in boldness. Control Bs also learned more quickly to avoid shocks
than did Control Gs. Clearly, genetic makeup affected phenotype.

Would one subspecies be more active in the open field than the other after experiencing the
handling? Would the subspecies differ in how quickly it learned to avoid the shock?
Results: On the open-field test, the handled Bs increased their activity level considerably compared
to control Bs, while handled Gs crossed even fewer squares than control Gs. On the shock
avoidance learning tasks, handled Gs performed better than control Gs in learning to avoid shocks.
In contrast, handled Bs performed less well than control Bs. Again, the effects were in opposite
directions.
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Hereditary Influences on Development
The early handling experience did not just have an effect that differed in magnitude for the two
subspecies—it actually had an opposite effect! A treatment that increased activity in one subspecies
decreased it in the other; a treatment that facilitated learning for one subspecies interfered with learning for
the other. (Sound familiar, parents? Does what worked well with one child sometimes fail miserably with
the other, or make things worse?) The results of the King and Eleftheriou study are a clear demonstration
that the response to a given experience may differ with genotype; i.e., not everyone responds the same way
to the same treatment because genetic factors set limits on the way environment can affect behavior.
Resource
King, J. A. & Eleftheriou, B. E. (1959). Effects of early handling upon behavior in two subspecies of deer
mice, peromyscus maniculatus. Journal of Comparative and Physiological Psychology, 52, 82–88.
53
Chapter 2
LECTURE 2-5: EXPERIENTIAL CANALIZATION
To balance off the emphasis on genetic factors of the other lecture suggestions, consider discussing
Gottlieb’s (1991) Developmental Psychology paper. Like Scarr, Gottesman, Plomin, and others, Gottlieb
argues that outcomes are not the result of purely genetic or maturational forces. He emphasizes the role of
environment to a greater extent. In fact, he argues that canalization may reflect the influence of environment
as much as heredity. Some characteristics (e.g., intelligence) may show stronger canalization during infancy
and the preschool years because experience is more common across children during that period than later. It
is possible that early intelligence is much more open to variation than we typically observe.
Resource
Gottlieb, G. (1991). Experiential canalization of behavioral development: Theory and commentary.
Developmental Psychology, 27, 4–13.
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LECTURE 2-6: THE DNA REVOLUTION
The 50th anniversary of the discovery of DNA was in 2003, and there were a number of very good
celebrations. The following resources can assist you in preparing a lecture on various aspects of the
discovery.
Nature provides a website, containing news, features and web specials celebrating the historical,
scientific, and cultural impacts of the discovery of the double helix.
http://www.nature.com/nature/dna50/
Here is the original paper, from James Watson and Francis Crick, published in Nature on April 25, 1953
http://www.nature.com/nature/dna50/watsoncrick.pdf
It was Rosalind Franklin’s photograph of the double helix that was responsible for the discovery of the
structure of DNA. Franklin has often been overlooked; she didn’t share the Nobel Prize for the discovery
because she died of ovarian cancer at age 37. You can hear an interview, from NPR, with author Brenda
Maddox about the role of Rosalind Franklin.http://www.npr.org/programs/atc/features/2002/oct/darklady/index.html
National Public Radio News produced a special series of short programs on The DNA Revolution.
http://www.npr.org/news/specials/dnaanniversary/index.html
55
Chapter 2
STUDENT ACTIVITIES
ACTIVITY 2-1 DETERMINANTS OF SIMILARITIES AND DIFFERENCES
This is a good activity to assign before a lecture on the interaction of heredity and environment. Ask
students to speculate on what factors might have contributed to making them the way they are in terms of
such characteristics as sociability, aggression, personality characteristics, temperament, and intelligence.
List them on the board or on an overhead projector and discuss to what extent they reflect heredity,
environment, or an interaction of the two. Activity 2-1 can be used as a lead-in to make the following points:
Point A: The assumptions we make about what factors lay behind our characteristics are not always
supported by scientific evidence. For example, some students may have listed parental and experiential
factors as lying behind your sociability, your lack of aggression, or your personality characteristics. Others
may have attributed your level of intelligence to genetic factors. The evidence presented in the text, and that
will be presented in class, indicates that the factors you identified do play a role, but the evidence strongly
suggests that all human characteristics are determined by the combined influence of heredity and
environment. It is not consistent with current evidence to attribute most human characteristics to either one
or the other. (Evidence could be described at this point or students could be referred to the text.)
(Option: insert Lecture 2-1 here. The question could be raised at this point: How can the interaction of
heredity and environment be best conceptualized? The notions of canalization and range of reaction could
be presented or students could be referred to the text.)
Point B: Heredity has been shown to play an important role in all of the characteristics mentioned as part of
Activity 2-1 (sociability, aggression, personality, temperament, and intelligence). You might well ask: Just
how has a role been determined? How is it possible to determine to what extent a characteristic is heritable?
(Methods for estimating hereditary influences can be reviewed at this point, or students can be referred to
the text.)
Point C: Twin studies have shown that identical twins reared apart are more similar than fraternal twins
reared together on many characteristics. How can the remarkable similarities between identical twins reared
in different environments be explained solely based on shared genes? (Discuss Scarr and McCartney’s
notions of evocative and active genotype/environment correlations.)
ACTIVITY 2-2 CREATE A ZYGOTE
Assign to be due on the day you will go over this material in class or in place of lecture material on this
topic.
This activity asks students to answer questions about cell division and parental genetic contributions and
then draw a magnified picture of the chromosome pairs for a single-cell zygote. They are asked to use
different colors to indicate the mother’s and father’s contributions and to identify the sex chromosomes with
an arrow and label. The purpose of the activity is to actively engage students in processing some of the
material at the beginning of Chapter 2 and to stimulate questions about the mechanisms of genetic
transmission and about how the gene exerts its influence.
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Hereditary Influences on Development
ACTIVITY 2-3 UNDERSTANDING GENETIC TRANSMISSION
This activity relates to the text material on transmission of characteristics through single-gene-pair
inheritance. Present two problems to help students understand the possible outcomes that can occur from
various parental genotypes. Problem 1: ask how a couple who is intellectually normal could have a child
with PKU and potential cognitive deficits (to illustrate the possible outcomes of two heterozygous parents).
Problem 2: ask whether the offspring of a woman who is a carrier for cystic fibrosis and normal male are at
risk for cystic fibrosis (to illustrate the possible outcomes of one heterozygous and one homozygous parent,
neither of whom displays the trait).
ACTIVITY 2-4 SCARR AND MCCARTNEY’S PASSIVE, EVOCATIVE, AND ACTIVE
GENOTYPE/ENVIRONMENT CORRELATIONS
Coordinates with Lecture 2-3 and Handouts 2-3a and 2-3b.
This activity can be used as a cooperative group activity or an individual take-home activity. Either before
or after discussing Scarr and McCartney’s theory of genotype/environment interactions, ask students to
generate examples from their own lives of each type of gene influence discussed by Scarr: passive,
evocative, and active. Then have them discuss whether the example they have given is consistent with the
developmental trends in the influence of each of the three types of influence shown in Figure 2.16, or ask
them to discuss why one would expect the developmental trends in Figure 2.16. Use Handouts 2-3a and 23b for brief definitions of passive, evocative, and active influences. Consider projecting Figure 2.16 using a
document camera or through PowerPoint. Display it during the pair/small-group activity or after to serve as
a focus for the discussion.
Scarr, S. & McCartney, K. (1983). How people make their own environments: A theory of
genotype/environment effects. Child Development, 5, 424–435.
ACTIVITY 2-5 USING THE INTERNET: PATTERNS OF GENETIC TRANSMISSION
Ask students to use the Internet to learn more about the principles of genetic transmission. This activity
provides students with problem sets and tutorials that expand their knowledge of monohybrid crosses and
sex-linked inheritance. Then have them apply those to a genetically transmitted behavioral or physical
characteristic of their choosing (e.g., cystic fibrosis, muscular dystrophy, phenylketonuria, Tay-Sachs,
hemophilia, diabetes, Graves disease, schizophrenia, depression, Alzheimer’s disease, Huntington’s chorea,
etc.), or a chromosomal disorder (e.g., Down syndrome, Fragile X syndrome, supermale syndrome) and find
out the following:
1.
How is the disorder transmitted, how severe is it, and what is the likelihood of occurrence in
relatives?
2.
Can the abnormality be detected prenatally?
3.
Is there any known treatment for the disorder, and, if so, what does it involve?
Students may want learn more about a disorder that has occurred in their own family. When discussing this
topic, some points to make include the following.
57
Chapter 2
Point A: Not all offspring of a parent who displays or carries a genetic disorder will display or carry
the disorder.
Point B: Not all genetically predisposed individuals will display a characteristic (ever or in all contexts).
For example, one may have an identical twin with schizophrenia or diabetes but may not display the same
disorder him/herself. For many disorders, the concordance rate in identical twins has actually been found to
be quite low. How can this be explained? Gottesman and Bertelsen (1989) and Scarr (1992) argue that a
genotype may be unexpressed under some environmental conditions and overexpressed in others. Some
environmental conditions, particularly stressful ones, are more likely to trigger the expression of genotypes
for abnormal behavioral and physical disorders. Scarr argues that, if the environment is outside the speciesnormal boundaries, expression of the genotype for a disorder is more likely to occur. Abnormal behavior or
a physical disorder may continue because an important component of their environment (often the parents’
unhealthy responses) remains consistent, eliciting abnormal behavior.
Note: in his book Leaving Home (1980), one of Haley’s main theses was that, to help an addicted, “mad,” or
apathetic youth begin to engage in productive behavior that will eventually allow for his/her leaving home
and leading an independent life, parents must demand normal behavior. He argued that often the parents’
marital problems “hook” a child into behaving abnormally as a way of holding the marriage and family
together. Haley described therapy strategies designed to help parents work together as a unit to provide the
environmental catalyst for normal and increasingly independent behavior. Haley’s therapy orientation is
very compatible with the theoretical position that Scarr takes in her presidential address and the 1992 Child
Development article—variations in phenotype may be expressed in different contexts by the same
individual. This orientation is a particularly appealing one because it does not “condemn” an individual who
carries the genotype for a disorder or who has been symptomatic at one point of his/her life to always being
“abnormal.” If abnormal or stressful environmental situations become normalized (e.g., by the parents
reconciling or making the decision to live separate lives), so should the youth’s behavior and health.
The perspective on genotype/environment interaction espoused by Gottesman and Bertelsen and by Scarr
helps our understanding of why there is so much individual variability in when and whether individuals
display abnormal behavior or physical symptoms. It is typically when stressors reach a sufficient level that
the abnormal pattern is released/expressed. For example, some individuals with a genetic predisposition for
Graves disease (a hyperthyroid condition) may display symptoms in the late elementary years, during
adolescence, or, more commonly, between 20 and 40 years of age. Others might not display the symptoms
until much later in life. For each, the emergence of symptoms tends to follow a period of exposure to
abnormally high environmental stress (e.g., family conflict, unusually high job stress, an unsupportive
teacher at school, etc.).
Resources
Gottesman, I. I. & Bertelsen, A. (1989). Confirming unexpressed genotypes for schizophrenia. Archives of
General Psychiatry, 46, 867–872.
Haley, J. (1980). Leaving home: The therapy of disturbed young people. New York: McGraw-Hill.
Scarr, S. (1992). Developmental theories for the 1990s: Development and individual differences. Child
Development, 63, 1–19.
ACTIVITY 2-7 APPLYING GOTTESMAN’S RANGE OF REACTION NOTION
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Hereditary Influences on Development
As a lead-in or conclusion to a presentation of Gottesman’s range of reaction principle (e.g., Lecture 2-1),
ask students to turn to Figure 2.15 in the text. This figure presents the hypothetical reaction ranges for the
intellectual performances of three children. Ask students to answer the following questions.
Question 1: Suppose that you are a teacher and have been given IQ information on a new student, Jamie.
You have been told that his IQ score is 100. Assume that you have no additional information about Jamie at
the moment, that is, you know nothing about the home environment, past educational experience, language
spoken in the home, etc. What can be concluded about the child’s genotype/genetic potential with respect to
IQ test performance? Which student in Handout 2-1 is Jamie most similar to genetically?
(Note: it is not possible to determine whether Jamie is more similar to Juan or Tony in Handout 2-1
knowing only the IQ score. Have students try to articulate scenarios under which Jamie would resemble
each of the three children.)
Question 2: Now suppose that you have been told that Erica has an IQ of 75 and Ben has an IQ of 100. Can
we confidently conclude that Erica is genetically inferior to Ben with respect to intellectual potential,
knowing only the IQ scores? Explain your answer using the Gottesman model.
(Note: students should conclude that they cannot draw the conclusion that Erica has lower genetic potential
in the absence of information about the favorableness of the environment these children have been reared in.
If Erica has been reared in a very restricted environment and Ben in a highly enriched one, it is within the
realm of possibility that Erica actually has the greater potential.)
ACTIVITY 2-8 ETHICS OF EMBRYO DESIGN
http://ublib.buffalo.edu/libraries/projects/cases/genetics/genetic_selection.html
A case study from the collection through the National Center for Case Study Teaching in Science, this
dilemma case, originally developed by Julia Omarzu for a course in developmental psychology, is based
on the true story of Jack and Lisa Nash, whose daughter Molly was born with a rare genetic disorder,
Fanconi anemia. By having another child with specific genetic markers, the Nashes hoped to cure Molly
using stem cells from the new baby’s umbilical cord blood. Students learn about developmental disorders
and consider the ethical issues of genetic manipulation and fertility treatments.
Questions for the case include both factual information and critical thinking about ethics. The questions can
be modified to fit the needs of the individual class.
59
Chapter 2
WEB RESOURCES
How Cells Divide: Mitosis versus Meiosis: http://www.pbs.org/wgbh/nova/baby/divi_text.html
This companion site to the Nova program, 18 Ways to Have a Baby, provides a flash presentation on the
processes of mitosis and meiosis.
Human Genome Project:
http://www.ornl.gov/sci/techresources/Human_Genome/education/education.shtml
The Education page of the official site for the Human Genome Project offers images, webcasts, and
presentations suitable for use in the classroom.
Journey into DNA: http://www.pbs.org/wgbh/nova/genome/dna.html#
This companion site to the Nova program, Journey into DNA, allows the visitor to examine DNA on 15
different levels.
Learn.Genetics: http://learn.genetics.utah.edu/content/begin/traits/
This website from the University of Utah’s Genetic Science Learning Center has a wealth of information
and teaching resources and interactive learning objects on topics related to genetics.
American Association for Klinefelter Syndrome Information and Support: http://www.aaksis.org
National Fragile X Foundation: http://www.fragilex.org/html/home.shtml
Trip-lo X Syndrome: http://www.triplo-x.org
Turner Syndrome Society of the U.S.: http://www.turnersyndrome.org/
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Hereditary Influences on Development
VIDEO SUGGESTIONS
Birth Defects: Causes and Prevention (Films for the Humanities and Sciences, 10 min., 1990) Describes
both genetic and environmental causes of birth defects.
Brave New Babies (Penn State Audio-Visual Services, 48 min., 1982) An introduction to genetic
engineering.
Different Strokes: Nurture and Human Diversity (Insight Media, 30 min. 2006) Discusses the ways in
which nature and nurture affect an individual’s growth, ranging from prenatal environment to peer
groups to cultural factors.
Frontiers of Science: Genetic Testing—Clinical and Ethical Issues (Penn State Audio-Visual Services,
101 min., 2001) Explores the role of genetic counseling in understanding the impact of DNA
technology on patients.
Heredity and Environment: Beginnings of a Baby (Insight Media, 29 min., 2011) Describes basic
mechanisms of heredity and discusses the joint role of heredity and environment in determining
human characteristics and development.
Phenylketonuria (Films for the Humanities and Sciences, 29 min., 2000) Explores diagnostic methods,
including the Guthrie test. The biochemistry and metabolic pathways are traced, and interviews are
provided with both dietary experts and patients about the complications of dealing with PKU in
pregnancy.
Prenatal Testing: A Mixed Blessing (Films for the Humanities and Sciences, 51 min., 1995) Follows four
couples through the process of an initial screening indicating some risk for Down syndrome, the
decision to have an amniocentesis or not, and the final decisions they made.
The Human Genome: Traits, Disorders, and Treatments (Insight Media, 30 min. 2005) Examines
genetic disorders such as sickle-cell anemia, Huntington’s disease, and hemophilia. Explores
polygenic inheritance and environmental influences on gene expression.
To Build Our Future (Penn State Audio-Visual Services, 60 min., 1982) A film on genetic counseling.
61
Chapter 2
HANDOUTS
Handout 2-1: Understanding Gottesman’s Range of Reaction Notion
Handout 2-2a and 2-2b: Understanding PKU and Understanding Tay-Sachs
Handout 2-3a and 2-3b: Scarr’s Triarchic Theory of Individual Differences and Three Ways
Genotype Influences Environment
Handout 2-4: King and Eleftheriou Deer Mice Study: Different Responses to the Same Experience
62
Handout 2-1: UNDERSTANDING GOTTESMAN'S RANGE OF REACTION NOTION
Text Figure 2.15
Handout 2-2a: UNDERSTANDING PKU
NORMAL PHYSIOLOGY
normal diet
containing
phenylalanine
functioning
+
enzyme
phenylalanine
hydroxylase

essential
amino acid
tyrosine

normal
brain
ABNORMAL PHYSIOLOGY
normal diet
containing
phenylalanine
+
(lack enzyme)
 pyruvic acid
+
(lack enzyme)
 no pyruvic 
acid buildup

mental
disability
THERAPY
diet low in
phenylalanine
no mental
disability
Handout 2-2b: UNDERSTANDING TAY-SACHS
Q:
What is the likelihood that offspring of parents who are both carriers of the
Tay-Sachs gene will be born with Tay-Sachs?
A:
Chances are one in four for each pregnancy.
Father
Normal
Tay-Sachs
Normal
Mother
Tay-Sachs
Q:
What is the mechanism of influence of the recessive gene for Tay-Sachs?
A:
Lack of enzyme (HEX A)  buildup of fat (ganglioside/GM2) in cells
Handout 2-3a: SCARR’S TRIARCHIC THEORY OF INDIVIDUAL DIFFERENCES
The genetic uniqueness of individuals results in the creation of unique environmental experiences for and
by these individuals.
1.
Genotype influences environment in three ways:

Passive gene influences

Evocative gene influences

Active gene influences
2.
With development, genotype/environment influences become decreasingly passive and
increasingly active.
3.
Genetic differences become more potent determiners across development as individuals become
increasingly capable of and responsible for making their own environments.
In the Scarr model, variations in environment are believed to be best understood as products of parental
and child characteristics, rather than as causes of their unique characteristics.
Based on Scarr, S. (1992). Child Development, 63, 1–19.
Handout 2-3b: THREE WAYS GENOTYPE INFLUENCES ENVIRONMENT
1.
Passive Genotype/Environment Correlations:
Athletic parents provide athletic opportunities (environmental influence) and contribute athletic
genes to child (genetic influence).
Examples:
2.
Evocative Genotype/Environment Correlations:
Attractive, happy children receive more favorable reactions than less attractive or moodier
children.
Examples:
3.
Active Genotype/Environment Correlations:
Individuals select activities that are compatible with their genetic predispositions
Examples:
Handout 2-4: KING AND ELEFETHERIOU DEER MICE STUDY (DIFFERENT
RESPONSES TO THE SAME EXPERIENCE)
Experimental Environment (daily handling days 3–25)
Genotype 1: Gracilis (Gs)
Genotype 2: Bairdii (Bs)
Control Environment (no handling)
Genotype 1: Gracilis (Gs)
Genotype 2: Bairdii (Bs)
Question 1: Would the two subspecies differ in their reactions when assessed in an open-field situation?
In a learning situation?
Results: Control Bs were much more active and learned faster than the control Gs, indicating a “baseline”
subspecies difference.

Control Gs crossed fewer squares on the open-field task than Control Bs

Control Gs learned at a considerably slower rate than Control Bs
Question 2: Would handling differentially affect the two subspecies’ reactions in an open-field situation?
On a learning task?
Results: Effects were in opposite directions for the two subspecies.

Handled Bs crossed more squares and learned at a slower rate than Control Bs

Handled Gs crossed fewer squares and learned at a faster rate than Control Gs
Conclusion: The response to a particular experience may differ with genotype (i.e., not everyone
responds the same way to the same treatment or practices).
WHY? Because genetic makeup sets limits on the way/extent to which environment affects behavior.