Nick Glass
HRS 331
Dr. Isabelle Cherney
4 February, 2004
“The Central Nervous System,” excerpted from Ch. 3: Structure of the Nervous System
The central nervous system develops from a simple tubular structure to an almost
ineffably elaborate, yet still somewhat tubular structure. The brain, along with the other nervous
tissue, arises from the embryonic germ layer known as the ectoderm. The neural ectoderm
undergoes neurulation, thereby forming the neural tube. This neural tube then differentiates into
a collection of chambers.
These chambers, in concert with the four ventricles, undergo further maturation, during
which neural stem cells proliferate via symmetrical division. Later, after the establishment of
founder cells, their asymmetrically divided progeny migrate away from the ventricular zone to
the outer periphery of the growing brain. The outermost layer, or cortex, structurally and
functionally distinguishes humans from all other species. The cortex is populated with cells
transmitted along radial glia. Cortical development ceases at the point when founder cells
undergo apoptosis, i.e. programmed cell death.
As evolution would have it, the developing human brain generates a marked surplus of
neurons, which it must synaptically prune and kill off under the guidance of its chemical and
experiential milieus. With experience, the neurons and neuronal connections that survive
become stronger and more meaningful, eventually leading to neural maps which allow
interpretation of somatosensory and optic information, while other kinds of sensory input are
parsed through other circuitous pathways.
The human brain achieved its colossal size as a result of genetic duplication. The
duplicated genes are presumably master genes responsible for the delay in cessation of
symmetric division of founder cells. Interestingly, human founder cells continue symmetric
division for two days longer than chimpanzee founder cells, thus enabling 15% more cortical
growth. Apparently, this master timing gene is among those comprising the 1.2% genetic
difference between the two species.
Race and IQ, by Ashley Montagu. Chapter 11: Race and Intelligence, by Richard Lewontin
Lewontin equates “jensenism” to “Jansenism,” an officially condemned heretical doctrine
of “total depravity, irresistible grace, lack of free will, predestination, and limited atonement.”
“Jensenism” is the position of Arthur R. Jensen, a Berkeley professor of educational psychology.
His position is that compensatory investments in educating African-American children are
wasted because IQ arises foremost from genetic sources and not from modifiable environmental
ones.
Because of its latent racism and elitism, this position warrants careful examination. In
addition, the baiting introduction to his article similarly elicits examination of his position. Like
too many others, Jensen has apparently blamed nature for his view of human failures, thus
attributing scholastic failure to ontological instead of epistemological shortcomings. Jensen
argues that differences between cultures (and hence between culture-correspondent intelligences)
are genetically determined. Jensen proposes “g” to be the general, non-culture-specific factor for
which IQ tests validly and reliably probe. Contrary to Jensen’s premise, no such singular factor
necessarily exists in this case.
Jensen goes on to claim that in his preferred scheme of the world, “true merit” would
dictate the assortment of persons into occupational roles. From this claim we can infer that
Jensen believes real-world failure results from the lack of “true merit” held by a group of
students. At the same time, Jensen quite irresponsibly fails to admit the possibility that
educational psychologists have performed less than meritoriously in their educating of students.
Jensen then spends the bulk of his article trying to establish that IQ is developmentally stable and
that most of a population’s IQ variance is genetically based. Jensen then fallaciously concludes
that it is not worth trying to change IQ by training after age 8. A correct inference from the data
cited would have been that a child with a poor educational experience before age 8 is unlikely to
experience a more beneficial educational environment later in life.
Jensen reasonably argues that too little attention has been given to the contribution of
genetics to learning. He then unreasonably asserts that genetics– which he just admitted has an
insufficiently understood role in learning ability– has the principal role in learning ability. He
ostensibly asserts this because of “Galton, filial regression, mutant genes, a few major genes for
exceptional ability and assortative mating.” However, these considerations neither singly nor
jointly provide automatic or even probable grounds for normal distribution of intelligence in a
population. Nonetheless, Jensen maintains that normal distribution of intelligence, together with
unjustified context-remote quotes from Thorndike and other supposed authorities, is proof that
intelligence is primarily determined by genetic makeup.
Lewontin states that “Every character of an organism is the result of a unique interaction
between the inherited genetic information and the sequence of environments through which the
organism has passed during its development.” Jensen ignores the verified truth of this
declaration. Heritability (H) is commonly defined as “the ratio of the variance due to the
differences between the genotypes to the total variance in the population.” By this definition, H
can only be applied to a single trait in a single population with its characteristic allele frequencies
and environmental conditions. Because H calculations are based on woefully imprecise
approximations of both genetic and environmental relatedness, they tend to give false-positive
results. At any rate, studies involving twins, adoption, etc. have estimated H of IQ in different
human populations to be between .6 and .8. The preferred value, though, is irrelevant to Jensen’s
position. Assuming (1) the difference in mean IQ between black and white Americans of
“equalized” socio-economic status to be 11 points and (2) the H of IQ to be .8, Jensen concludes
nothing literally, but suggests furtively that most of the difference between the IQs of blacks and
whites is due to genes.
Jensen’s ultimate suggestion is erroneous because he confused H within a population
with H between multiple populations. “The genetic basis of the difference between two
populations bears no logical or empirical relation to the heritability within populations and
cannot be inferred from it,” states Lewontin. Consider the following example. Seeds of two
completely inbred strains of corn are potted. H of plant height is .0 under these circumstances
because of the genetic identity within a single seed population. But, the difference between the
means of the heights of the two lines will be completely genetical even though H is .0.
Conversely, when there are two varieties of stringently controlled environments, both hosting
genetically heterogeneous seeds, the variation in height within one environment will be totally
genetical (H=1). However, the deprived environment would give rise to much shorter plants,
even though their H would also be 1. In this case, H=1 in both populations, but the difference
between populations is totally due to the difference between their environments.
Jensen, in effect, argues that improving the environments of African-American children
could never result in equalizing their mean IQ with that of their most privileged EuropeanAmerican counterparts. Such conjecture is tantamount to saying that “changing the form of the
17th century gutter would not have a pronounced effect on public sanitation.”
Regardless of his scientific bankruptcy, Jensen apparently wants a society “in which the
‘race of life’ is ‘to get ahead of somebody’ and in which ‘true merit,’ be it genetically or
environmentally determined, will be the criterion of men’s earthly reward.” He is opposed by at
least one person (Lewontin) who wants “a society in which [everyone] can aspire to the fullest
measure of psychic and material fulfillment that social activity can produce.”
Human Genetics for the Social Sciences, by Gregory Carey. Ch. 18: Quantitative Genetics I
Quantitative, continuously distributed behavioral traits require a more complex analytic
approach than the simple Mendelian models that suffice for discrete traits. Sir Francis Galton,
Karl Pearson, Sir Ronald A. Fisher, and Sewell Wright have all been instrumental in advancing
our understanding of genetic principles and problems and how they impact social sciences.
I.
II.
Continuous Variation
A. Continuous Variation and a Single Locus
1. Genotypic (or “genetic”) value for a genotype is the average phenotypic
value for all individuals with that genotype.
2. There is variation around the genotypic value because of effects from the
environment and from other gene loci.
3. If the means of the three different genotypic values for a single locus
differ, the trait specified by that locus affects the phenotype.
4. The genotypic value for the heterozygote isn’t necessarily the average of
the two homozygotic genotypic values.
5. Since the three genotypes can have different frequencies, their
representative curves won’t always be of equal height.
6. The phenotypic distribution is the sum of the distributions for the three
genotypes.
7. We refer to these kinds of genes as Quantitative Trait Loci (QTL).
B. Continuous Variation and Multiple Loci
If two traits are being dealt with, there will be (3^2=) 9 normally distributed
genotypic curves.
Important Quantitative Concepts
A. Heritability and Environmentability
1. A given person’s genotypic value (G) for a certain trait is equal to the
mean phenotypic value of all the individuals with that phenotype in the
population.
2. The quantification of all the environmental experiences in a person’s life
yields his environmental value (E).
3. Heritability (H) can be defined as the square of the correlation
coefficient between genotypic values and phenotypic values.
4. Alternatively, H = the proportion (0≤H≤1) of phenotypic variance
attributable to or predicted by genetic variance.
5. Squaring the correlation between environmental values and phenotypic
values yields the environmentability (e) of the trait.
6. Environmentability is the proportion (0≤e≤1) of phenotypic variance
attributable to or predicted by environmental variance.
B. Genetic Correlations and Environmental Correlations
1. Simultaneous analysis of more than one phenotypic trait is termed
multivariate genetic analysis (MGA).
2. MGA provides the genetic correlation and the environmental correlation
among the two traits of interest.
3. The genetic correlation between two traits is the correlation between
their genotypic values: rg = corr(Gv, Gq).
4. Genetic correlation relates the extent to which the genotypic values for
one trait predict the genotypic values for the other.
5. The environmental analogue of rg is environmental correlation:
re = corr(Ev, Eq).
C. Gene-Environment Interaction
The idea of “gene-environment interaction” needs to be carefully defined in order
to be useful.
1. Common usage: Both genes and environment contribute to behavior.
2. Strict, scientific senses:
a. The actual relationship between the environment and a phenotype
depends on the genotype.
b. The actual relationship between a genotype and a phenotype depends
on the environment.
3. Example: difference in alcohol consumption between generations
a. Trends can be regarded loosely, or
b. They can be statistically analyzed:
Strict gene-environment interaction is indicated by intersecting (i.e.
non-parallel) regression lines representing one trait with respect to
the other within >1 group of subjects.
4. How Important Is Gene-Environment Interaction?
a. In the loose sense, it is always important.
b. In the strict sense, we don’t know yet.
D. Gene-Environment Correlation
1. Occurs when people with extreme genotypic values for a trait experience
environments with similarly extreme values for the trait.
2. Gene-environment (GE) correlation increases phenotypic variance.
3. GE correlation can be produced in several ways:
a. joint transmission of genes and environment within families
e.g. intelligent and intellectually inclined parents
b. self-selection of environments
People stick with behaviors that are intrinsically reinforced.
4. How important is GE correlation?
III.
IV.
There’s not enough data to know at this point. However, the
existence of both GE interaction and GE correlation is less
important than the specific mechanism generating the interaction
or correlation and the initial parameters of the situation.
The Twin and Adoption Methods
A. Family Correlations
1. It’s impossible to directly measure genotypic values for polygenic traits.
2. It’s hardly imaginable that all influential environmental factors could be
measured.
3. So we’re forced to rely on phenotypic correlations of dubious worth
because behavioral similarity may be caused by:
i.
shared genes
ii.
shared environments
iii.
combinations of i. and ii.
4. Therefore, researchers turn to the twin method.
B. The Twin Method: Rationale
1. Monozygotic (MZ) twins are genetically identical.
2. Therefore, any difference between them must be due to an
environmental difference.
3. Dizygotic (DZ) twins, a.k.a. fraternal twins, are genetically as alike (or
as different) as ordinary siblings.
C. The Twin Method: Assumptions
1. The Equal Environments Assumption
Environmental factors do not make MZ twins more similar than they
make DZ twins similar.
a. Violation of this assumption requires two occurrences:
i.
environmental factors treating MZ twins more similarly
than DZ twins
ii.
similarity in treatment making a difference in the
phenotype under study.
2. Results
The equal environments assumption meets the definition of a robust
definition, i.e. it might actually be violated, but the effect of violating the
assumption is so small that its estimates and substantive conclusions are
not altered.
D. The Adoption Method: Rationale
When parents adopt a genetically unrelated child, or when two adoptive children
are raised in the same family, similarities between the parents and adopted
child(ren) or between the biological children and the adopted child(ren) must have
to do with the environment.
E. The Adoption Method: Assumptions
1. Absence of selective placement that influences the trait in question
2. Representativeness of the adoptive families in spite of screening for
good mental health, probability of providing a good home, etc.
The Family Environment
A. Definitions of “Family environment” (FE)
V.
1. Social research (“substantive”) definition:
FE refers to the physical, psychological, and social state of the
household and the members within it.
2. Behavioral genetic research (“statistical”) definition:
FE consists of all those factors that make relatives similar on a
phenotype. E.g., living in the same neighborhood counts as FE. Plus,
nothing that doesn’t make relatives similar phenotypically counts as FE.
B. Definitions of nonfamily environment
1. Behavioral genetic research (“statistical”) definition:
Nonfamily environment is all those factors that make relatives different
from one another.
Comments on Heritability and Environmentability Estimation
A. H and E are measured in humans with only very limited accuracy—comparable to
simply guesstimating the air temp on a given day.
B. H and E are population concepts that apply only weakly to individuals.
C. H depends on the range of environments, and E depends upon the range of
genotypes.
D. H and E within populations are uninformative about differences between
populations.
More Experience = Bigger Brain
It is commonly believed that children need stimulation from their environments in order
to develop optimally from an intellectual and neural standpoint. Studies with dogs and birds
reinforced this notion, since brains from animals reared in enriched environments appeared more
complex, with more folds and fissures.
This line of research was resumed in the late 1960s and early 1970s, when the necessary
technology and interest coincided. The new studies were performed using rats, since rats are
small, inexpensive, relatively easy to breed and handle, and their cerebra could be examined and
measured with sufficient ease.
To test their hypothesis that animals raised in highly stimulating environs would exhibit
more robust brain growth and chemistry, Rosenzweig and his colleagues exhaustively controlled
their subjects and the conditions of their subjects. Specifically, three inbred (and therefore
virtually cloned) male pups were taken from litters and randomly assigned to one of three test
conditions. These three conditions were the normal lab cage along with the rest of the colony, an
“enriched” cage equipped with a variety of playmates and novel objects, and an “impoverished”
cage with no companions or objects with which to play. The rats spent from 4 to 10 weeks in
their assigned environment, after which their brains were dissected and the different sections of
interest measured, weighed, and biochemically tested for acetylcholinesterase (AChE).
The cerebral cortex of the enriched rats was heavier and thicker. The enriched rats also
showed greater AChE activity. Though the number of brain cells was comparable between the
two populations, the enriched rats developed larger neurons. In addition, the enriched rat brains
registered a higher ratio of RNA to DNA, indicating that they were synthesizing proteins more
vigorously. These results have been replicated many times, with the most consistent effect of
environmental enrichment being the ratio of the weight of the cortex to the weight of the rest of
the brain. The synapses of the enriched rats were also found to be 50 percent larger than those of
the impoverished rats.
These findings might help elucidate the relationship between malnutrition and
intelligence. An undernourished person is less likely to respond to certain environmental stimuli.
He or she may thereby miss out on commonly utilized opportunities for development.
Since this landmark study, others have demonstrated similar trends regarding brain use or
disuse and the ensuing cerebral atrophy or hypertrophy. Further light has also been shed on the
impact of emotional attachments and stress on brain development.