108 Biological Bases of Personality
neurotransmitters and enzymes like MAO that regulate them;
hormones like testosterone and cortisol; psychophysiological
characteristics such as augmenting/ reducing of the cortical
evoked potential; brain structure and physiology as assessed
by brain imaging methods in humans and lesion and stimula-
tion studies in other species; and molecular genetic studies
that link genes, biological mechanisms, and behavioral and
personality traits.
Simple-minded reductionism would expect one personal-
ity or behavioral trait to be associated with one brain struc-
ture, one neurotransmitter, one hormone, one physiological
pattern of reactivity, and one gene in both humans and other
animals. The chapter is organized by personality traits, but if
one reads across the traits it is clear that this neat kind of
phrenological isomorphism is not the rule. Evolution may
have shaped the nervous system around behavioral mecha-
nisms necessary for adaptation, but evolution did not select
for personality traits. The tendency to explore, forage, and ap-
proach novel but nonthreatening objects or creatures is part of
that adaptation and is important in survival, as is competitive
and defensive aggression, cooperation, and even altruism.
If we reverse direction and work up from the biological
mechanisms to the personality trait and behavioral levels
the fourfold classification at the top becomes blurred.
Monoamine reactivities, MAO, testosterone, cortisol, and re-
activity of cortical EPs to stimulus variation are related to so-
ciability and sensation seeking, impulsivity and aggression,
asocialization, neuroticism, anxiety, and inhibition, but in no
simple one-to-one manner. Low levels of serotonergic activ-
ity are related to both depression and impulsive aggression
producing both violent and impulsive homicides and sui-
cides, sometimes in the same person. Is it the impulsivity, the
aggression, or the neuroticism that is related to a serotonin
deficiency? High levels of testosterone are related to socia-
bility and social dominance, disinhibitory sensation seeking,
aggressivity, asocialization, and low levels to neuroticism
and agreeableness. Low levels of MAO are related to sensa-
tion seeking, impulsivity, asocial tendencies, and sociability.
Personality traits may be orthogonal, but biological traits
do not respect these boundaries. It is almost as if the func-
tional biology of the organism is organized around two basic
traits: approach (including sociability, impulsivity, sensation
seeking, and aggression) and inhibition/avoidance (or
neuroticism/anxiety at the personality trait level). The com-
parative psychologist Schneirla (1959) put this idea into a
postulate: “For all organisms in early ontogenetic stages, low
intensities of stimulation tend to evoke approach reactions,
high intensities withdrawal reactions” (p. 3). In evolved or
more mature organisms Schneirla used the terms “seeking”
and “avoidance” in place of “approach” and withdrawal.”
The latter terms convey the idea of reflexive or tropistic
mechanisms, whereas the former imply learned behavior.
Approach-withdrawal describes a basic dimension of tem-
perament and inhibition/shyness another in infant scales of
temperament. These individual differences in infants may
represent two biologically based dimensions found in other
species, and they may develop into more diffentiated charac-
teristics in adult humans.
Genetic dissection is one method of defining the bound-
aries of biological influence in traits. If both biological and
behavioral traits are included in biometric or molecular ge-
netic studies, the genetic covariance between the genetic and
the other two can be determined. Rarely are genetic, biologi-
cal, and behavioral traits all included in one study.
A biosocial approach cannot ignore the complex interac-
tions between biological traits and environmental experi-
ences. In both animals and humans the levels of the hormones
testosterone and cortisol influence behavioral interactions
with the environment but are in turn influenced by the out-
comes of these interactions. There is no reason to think that
similar interactions do not occur for the monoamine neuro-
transmitters. All of these systems are regulated by internal
mechanisms. For instance, if there is overactivity in a system,
regulators like MAO may catabolize the excess neurotrans-
mitter. There may be more trait stability in the regulator than
in the transmitter itself. After repeated experiences, however,
there may be changes in the activity of a biological system
that are relatively enduring if not irreversible. Environment
may even influence the effect of genes by affecting their
release. Given the constant interaction between the biological
and environmental pathways (Figure 4.1), reductionism of
one to the other is impossible. It would be like describing the
biological activity of the lungs in the absence of oxygen, the
digestive organs in the absence of food, or, using a more rel-
evant analogy, the brain in the absence of stimulation.
Psychology emerged from the biological sciences more
than a century ago, although its origins were forgotten by
those who wanted a science that would emulate physics
and those who wanted to cut all connections with the biolog-
ical sciences. Fifty years ago, when I entered the field, the
founder of behaviorism, Watson, had declared that the out-
come of personality was entirely a matter of life experience
(conditioning) and had nothing to do with genetics, and
Skinner had declared the irrelevancy of the brain in behavior.
Despite Freud’s own view that the mysteries of the psyche
would one day be understood in terms of biology, his follow-
ers advocated an environmental determinism that put the en-
tire weight of explanation on society, the family, and early
experience. These early prophets of our science are now his-
torical footnotes, and the science is more cognitive and
biosocial with new cross disciplines like cognitive neuro-
science emerging. The changes are in large measure due to