BIOLOGICAL FACTORS

SECTION OVERVIEW

1. Behavioral Genetics: The intergenerational

influences
2. cNS (conceptual Nervous System) models
3. Brain Injury
LEARNING OBJECTIVES
1. Understand the concepts of heritability and
environmental effects.
2. Become familiar with the logic of adoption studies
and twin studies, as well as their limitations.
3. Examine research evidence addressing the relative
contribution of genetic and environmental
contributors to antisocial behavior.
BEHAVIORAL GENETICS
A quantitatively oriented science that attempts to
estimate the relative contributions of both heritable
and environmental factors to human behavior.
Francis Galton (cousin of Charles Darwin) was
among the first to study the heritability of non-
physical phenotypic features.
Some traits (e.g., eye color) are determined by single
genes. The expression of one phenotype over the
other results from dominance or incomplete
dominance.
Characteristics of interest to psychologists are
generally polygenic. I.e., influenced by multiple genes.
For example, intellectual functioning can be influences
by genes that regulate neurotransmitter function,
cerebral morphology, blood flow, etc.
DOES THIS IMPLY DETERMINISM?
No!
But we are born with predispositions and a variety of
talents, weaknesses, etc.
Other than in extreme cases, this does not imply
absolute control by our genes.
This is often true in physical medicine also. Eg.,
diabetes can be highly debilitating but exercise,
healthy diet, and sometimes medication can
dramatically offset those effects.
HERITABILITY: THE CONTRIBUTION OF GENES

Heritability, or h2, is formally defined as the ratio of

genetic variance to phenotypic variance.
More simply, what proportion of the observed
trait’s expression can be chalked up to genetic
factors.
Since it’s a proportion, it can range from 0 (no
identified genetic contribution) to 1 (all variance
is genetically based).
Please take note: Heritability estimates:

Give us an idea of how important genes are to the

expression of a given trait.
Are based on whole populations. They are not
specific to individuals.
May vary from one population to another.
Are heavily dependent on the measurement
approaches used to assess a given trait.
WHAT’S VARIANCE?
Technically it’s a statistical term, s2, defined as:

s2 = Σ (xi – xavg)2 / n – 1

So really it quantifies the amount of ‘spread’ in a given

population WRT some variable such as intelligence,
criminality, height, etc.
When we use this term it’s often in the context of
accounting for individual or group differences.
Can be great or small.
This concept isn’t restricted to discussions of
criminality. The expression of virtually any
psychological variable or construct can be examined in
this way.
Buss (1995): h2 is never 0 in psychology.
Recall genotype refers to the alleles possessed by an
individual organism.
Phenotype refers to the manifested characteristics of
that organism.
Polygenic Determination:
Several genes contribute to the expression of a
certain characteristic.
Eg., Physical factors affecting intelligence include…
blood flow
neurotransmitters
cerebral morphology
many more.
Each of these, in turn, may be polygenically
influenced.
IS H2 CONSTANT OVER TIME?
No. Since the total variance (degree of variability) in
any trait can change, so can h2.
Therefore, to say that genetic variance affects a
characteristic does not limit environmental effects.
This is about genetic differences between one
organism to another, not about nature vs. nurture.
 WHAT ELSE IS THERE BESIDES H2?
Environment Effects (c2 and e2).
This can be broken down further:
Shared Environment (c2): Those aspects encountered
by all members of a certain group. Eg., full siblings
raised by their biological parents share exposure to
the same set of parents. Siblings reared apart do
not.
Other examples?
Non-Shared (e2): Encountered uniquely. Eg., your
peer group, the fight you had in grade 4, your
gender and age.
ASIDE: WHAT ABOUT EPIGENETICS?
The study of changes in the expression of genes that
do not result from alterations in the sequence of the
genetic code. (APA)
Some genes are “switched on” or “switched off” in
response to some environmental factors, which
could include certain stressors such as trauma.
DNA methylation, occurs when molecules called
methyl groups attach to certain pieces of DNA,
which can affect a gene's expression.
(There are other mechanisms also)
SLC6A4: Serotonin (5-HT) transporter gene - lower
levels of 5-HT are associated with increased
aggression. (Wang et al, 2012) Hypermethylation
essentially contributes to lower 5-HT synthesis.
OXTR: Oxytocin transporter gene (related to
empathy and emotional regulation)
MAO-A promoter: Monoamineoxidase promoter –
initiates transcription, which is the first step in
expression. Hypermethylation is associated with
increased aggression and ASPD.
DRD1: Dopamine receptor gene – more methylated in
aggressive boys (Provencal et al., 2014) and girls
(Guillemin et al., 2014). May be related to relatively
lower executive functioning and cognition.
PLEASE NOTE…

Our understanding of the epigenetics of antisocial

behaviour is still very much in its infancy.
The exact mechanisms are not fully understood.
Most of the information on the previous slide is
about association, not causation.
MORE ABOUT VARIANCE: BACK TO H2, E2,
AND C2
A GREY AREA
Obviously, there are differences in the quality of
interaction between individuals and otherwise shared
environments that moderate environmental effects on
behavior. These are correctly placed in the non-shared
category.
Eg., Mom is closer to your younger sister and
spends more time with her. Though you have the
same mother, the influences she exerts on your
behavior are likely to be different than those she
exerts on your younger sister. This refers to your
evocative style.
BUT WHAT DOES THIS CONTRIBUTE TO OUR
UNDERSTANDING OF CRIME?
We can exploit the fact that certain sibling pairs vary
in their degree of genetic similarity.
MZ twins: Genetically identical.
DZ twins: Share half their genetic constitution (on
average).
Non-twin sibs: Also share half their genetic
constitution (on average).
Since some siblings are reared apart, and others
together, we have a “pre-built” way to examine the
effects of environmental diversity
TWIN STUDIES
Raine (1993) completed a meta-analysis of 13 twin
studies.
Results:
Concordance DZ: 20.6 %
MZ: 51.5 %
Objection: Gene effects are confounded with
environment effects.
H2 REVISTED

 h2 can be estimated by examining the difference in

correlation between MZ and DZ twins.

h2 = 2(rMZ – rDZ)
Eg., DiLalla & Gottesman (1989)

rMZ = 0.87
rDZ = 0.72

From those values:

h2 = 2(0.87 – 0.72)
= 2(0.15)
= 0.30
In fact, that’s a pretty typical estimate of h2 where
criminality is concerned.
Lykken (1995) wrote that:
 h2 estimates fall into the (0.30 to 0.40) range.
 c2 estimates fall around 0.30 but decrease
dramatically over the lifespan (to about 0.05) as e2
and h2 increase.
Why?
Parental control/influence decreases
Total variability increases
h2 is much higher for ‘component’ traits like
fearlessness, aggressiveness, IQ, impulsivity, sensation
seeking.
ADOPTION STUDIES: ANOTHER APPROACH

Intended to separate heritability from environmental

effects.
Strategy 1: Follow children adopted from criminal
families. Compare conviction rates with non-adopted
controls.
Hutchings & Mednick (1975) followed 1145 males
(ages 30 - 44) and 1145 non-adopted controls.
16.2 % of adoptees had convictions.
8.9 % of controls had convictions.
Problem: While this addresses h2 it neglects e2.
Strategy 2: (A variant). Follow children adopted from,
and into, both criminal and non-criminal families.
Compare conviction rates.
Eg., Mednick et al, 1986.
Parental convictions
Biological Adoptive Sons Difference
no no 13.5%
no yes 14.7 1.2%
yes no 20.0 6.5%
yes yes 24.5 -- 3.3%
OBJECTIONS TO ADOPTION STUDIES
Adoptive homes are more alike than others (r = 0.30).
Tend to be affluent (higher SES)
Carefully screened
This decreases variability to well below random levels.
These effects would artificially suppress e2 estimates if a
researcher was working under the assumption that r =
0.
I.e., would lead to the conclusion that a higher
proportion of observed variance stems from
heritable contributors.
CONCLUSIONS
Genes play a significant role in the expression of
criminal behavior.
Environment plays a significant role too.
Criminal behavior is best understood in terms of the
interaction between genetic and environmental
factors.
CONCEPTUAL NERVOUS SYSTEM (CNS)
MODELS
LEARNING OBJECTIVES

1. Review neuropsychological models of human

motivation.
2. Understand their application to the study of
criminal behavior.
CONCEPTUAL NERVOUS SYSTEM (CNS)
MODELS
What is a cNS model?
Theory about the functioning of the CNS (Central
Nervous System) based on, and able to
accommodate existing data.
Can be based on both psychological and physical
properties.
May emphasize different aspects of functioning. In
AS behavior, sensation seeking, aggression, failure to
learn from certain types of experience.
 AMONG THE FIRST…
Eysenck (1967, 1981)
Based on ARAS levels. Assumed high level of between-
subject variance. (Ascending Reticular Activating System)
 Receives input from most major sensory systems
 Involved in sleep-wake transitions and level of cortical arousal
Assumed to influence more fundamental processes.
(learning, motivation, etc.)
Differences in ARAS activity are genetically determined.
Results in differences along the orthogonal dimensions
of I-E, P, and N.
ARAS
THREE-FACTOR MODEL
Stable (N)

Psychoticism (P)

I E

Unstable (N)
I-E, P, and N influence pre-disposition (personality),
and therefore one’s tendency to engage in criminal
behavior.
They are moderator variables.
Same physiological characteristics can lead to
different behaviors
Eg., Lykken (1982)

Low ARAS Antisocial Criminal

(limited fear)
Altruistic Heroic
Eysenck & Eysenck have presented evidence that
prisoners score higher on measures of N and P than
controls, though the greatest hypothesized differences
(I-E) were small.
MORE RECENTLY
Gray’s Model. Based on septohippocampal system
(SHS).
Model deals with organism’s responses to
conditioned stimuli.
BAS: Behavioral Activation System (approach)
BIS: Behavioral Inhibition System (avoidance)
NAS: Non-specific Arousal System
BAS and BIS operate on basis of reciprocal inhibition.
Both can increase NAS
BAS is sensitive to (activated by cues) for reward and
active avoidance.
BIS is activated by cues for punishment and non-
reward. Also serves to re-focus attention toward
other cues.
NAS modulates the intensity of behaviors triggered by
both systems.
HOW DOES THIS EXPLAIN CRIMINAL
BEHAVIOR?
Criminals are seen as having an imbalance.
BAS activity predominates.
BIS fails to inhibit goal-oriented behavior in the
presence of certain cues (including socialized values).
The model fits well with experimental findings such
as…
deficient passive avoidance learning
high aggressiveness
low anxiety (low EDR)
impulsivity
CONCLUSION

cNS models attempt to relate physiology to

personality and behavior.
Better models (eg., Eysenck, Gray) appear to
accommodate a number of key findings well, and
incorporate learning history.
Eysenck: Three factor theory
Gray: Dynamic processes.
BRAIN INJURY
LEARNING OBJECTIVES
1. Examine possible consequences of brain injury
from a broad perspective that considers cognition,
inhibition, and emotional regulation.
2. Apply the above to an understanding of criminal
conduct.
3. Dispel a common misunderstanding about the
mechanism of effect that brain injury may have on
aggression.
BRAIN INJURY
At times, traumatic brain injury (TBI) or the onset of
illness will mark the emergence of highly antisocial,
aggressive behavior.
Sometimes in a previously peaceful, law-abiding
individual.
More frequently in someone that showed those
tendencies at a lower level beforehand.
PHINEAS GAGE
RECONSTRUCTION
BY RATIU ET AL
(2005)
(RIGHT)

NB: SOME DOUBT

HAS ARISEN AS THE
NATURE OF HIS
PERSONALITY
CHANGES
PHINEAS GAGE
EXAMPLES
agitation
irritability
short-temper
failure to discontinue harmful, maladaptive
behavior (perseveration)
obsessions
confusion/frustration
compromised insight/abstraction
Actual outbreaks of aggression attributable to TBI are
not that common (about 11% of patients).
Tends to be unfocused when it occurs.
No real underlying reasoning or planning.
Most likely in acute phase of injury.
Not clearly related to severity of injury (95% are
mild or moderate (Miller & Jones, 1985).
May be secondary consequences to frustration over
poor memory, low mood, lost abilities.
Tolerance of exogenous substances often lowered.
More typically threats are uttered, or language
becomes vulgar and/or threatening.
WHAT IS THE MECHANISM OF EFFECT?
Depends on which brain areas are affected by injury.
Frontal Lobes:
Higher executive functioning and inhibition.
Most common site of injury.
Two patterns emerge (Miller, 1990):
Lethargic, apathetic, indifferent (diffuse)
Impulsive/aggressive (orbital-frontal).
Some knowledge gleaned from lobotomy patients.
DR. FREEMAN PERFORMING TRANSORBITAL
LOBOTOMY – LATE 1940’S

George Washington University, Gelman Library

NEUROTOME PATH
Limbic System:
Deep mid-brain structures. Eg., amygdala and
hippocampus.
Involved in emotional regulation as well as memory
consolidation.
Humans with damage in those areas are often
highly emotional. Fear can switch to anger very
quickly.
A number of case studies record high levels of
aggression in previously peaceful patients.
Often there is elaborate planning, so it can’t be
entirely impulsive.
Temporal Lobe Epilepsy:
Fast, spike-like activity (localized seizures) in EEG
recordings over the temporal lobes is sometimes
accompanied by increased risk for aggression. May
be followed by confusion and limited recall. (see
next slide)
Neurotransmitters and Testosterone:
All are essential, and none are specifically
connected to level of aggression. That said…
Testosterone levels in males is positively
correlated with aggression.
NE and ATCH levels are sometimes elevated in
bipolar disordered patients.
EEG BURSTS
CONCLUSION
Most physiological correlates of increased aggression
likely have an indirect effect.
Reduced inhibition.
Frustration over cognitive difficulties
Reduced problem solving effectiveness
Pre-morbid personality remains an important
predictor.
A few types of TBI may be more directly related.