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Biological Perspectives of Personality – Comprehensive Notes

Overview and Learning Objectives

By the end of this seminar on Biological Perspectives of Personality, students should be able to describe the basic roles of genetics and environment in relation to personality traits; critically evaluate the fundamental assumptions of the behavior genetics paradigm for explaining personality traits; explain the basic role of brain biochemistry on personality; and understand the basics of neural influences on personality traits. Key objectives include recognizing how genetics, environment, brain biochemistry, and neural processes interact to shape stable patterns of affect, cognition, desires, and behavior across individuals.

Biological Models

The biological (or medical) model underpins the biological perspective on personality. Biological processes relevant to personality include genetics, biochemistry, and brain structure. This model situates personality variation within physiological substrates, positing that differences in biological processes contribute to patterns of behavior and experience. The model emphasizes the continuity between biology and psychology, arguing that psychological traits have underlying biological mechanisms that can be studied empirically.

Behavior Genetics

Behavior genetics seeks to disentangle how much of personality variation is due to genetic factors versus environmental factors. The field aims to determine heritability, identify gene × environment interactions, and determine what aspect of the environment is most important (e.g., parent socialization or peer group influence). The goals include quantifying genetic influence, understanding how genes and environments interact, and clarifying how environmental contexts shape or constrain genetic predispositions.

Heritability

Heritability is defined as the proportion of observed individual variation in a trait that can be attributed to genetic effects. Important distinctions include: Phenotype (observable trait) versus Genotype (genetic constitution) and Environment as a source of variation.

Common Misconceptions

Common misunderstandings include: that heritability can be applied to single individuals; that heritability is constant across populations and time; and that heritability is a precise statistic for a trait in every individual. These misconceptions can mislead interpretations of what heritability means in practice.

Behavior Genetic Decomposition

Heritability studies decompose trait variation into genetic and environmental components, often summarized as A (additive genetic effects), C (shared environmental effects), and E (non-shared environmental effects, including measurement error). This decomposition helps researchers understand how much of the variance in a trait is attributable to each source, given a particular population and developmental stage.

Genetic Influence Estimates and Population Variability

Genetic influence estimates reflect the variability that exists in the studied population across genomes and environments. Heritability can vary across cultures and generations; it is age-dependent; and it is trait-dependent (i.e., not all traits are equally heritable). These nuances imply that heritability is not a fixed property of a trait, but a statistic contextualized by the population and time frame studied.

Practical and Theoretical Implications

Because heritability estimates depend on the range of environments present in a population, even highly heritable traits can show substantial environmental modulation. Conversely, a low heritability estimate does not imply that genetics is unimportant; it may reflect substantial environmental variation or gene–environment interplay.

Empirical Illustrations of Heritability Across Traits

A stylized ordering of published heritability estimates across a variety of traits shows substantial variability. For example, psychiatric conditions and some cognitive abilities tend to show high heritability, while certain behavioral traits may show moderate to high heritability depending on measurement and context. In many cases, laypeople’s estimates of genetic influence correlate with scientific estimates quite strongly (approximately r = 0.77), indicating a relatively good alignment between lay intuition and empirical findings on average.

Family Method and Shared Genetics

Family methods examine how genetic relatedness across relatives relates to trait similarity. Shared genetics vary across relative types:

  • Strangers – less than 1%
  • Cousins – 12.5%
  • Grandparents/Uncles/Aunts – 25%
  • Parents/Siblings/Fraternal twins – 50%
  • Identical twins – 100%
    These relationships form the basis of estimates about how much genetic similarity explains phenotypic similarity among relatives. The methods assume some level of equal environments and shared genetics to partition variance into genetic and environmental components.

Twin Method

Twin studies compare monozygotic (MZ) twins who share essentially 100% of their genes to dizygotic (DZ) twins who share about 50% of segregating genes. By comparing the degree of similarity between MZ and DZ twins, researchers estimate heritability. The heritability index is usually computed as:
h^2 = 2 \, (r{MZ} - r{DZ})

where $r{MZ}$ and $r{DZ}$ are correlations for the trait in MZ and DZ twins, respectively. This approach relies on the Equal Environments Assumption, which posits that MZ and DZ twins experience equally similar environments, so differences in similarity can be attributed to genetic factors.

Adoption Studies

Adoption studies examine both genetic and environmental influences by looking at adopted children and their biological and adoptive parents. They help separate genetic effects from environmental ones. Key findings often show positive correlations between adopted child and adoptive parent (environment) and between adopted child and biological parent (genetics), highlighting the roles of both genetic predispositions and environmental contexts in shaping traits.

Results from Twin Studies (Selected Illustrative Tables)

Loehlin & Nichols (1976) – 800 adolescent twin pairs

  • General Cognitive Ability: Identical twins h2 ≈ 0.86; Fraternal twins ≈ 0.62;
  • Special Cognitive Ability: Identical ≈ 0.74; Fraternal ≈ 0.52;
  • Personality Scales: Identical ≈ 0.50; Fraternal ≈ 0.28;
  • Ideals, Goals, and Interests: Identical ≈ 0.37; Fraternal ≈ 0.20;
  • Overall pattern shows genetic influence is stronger for cognitive abilities than for many personality facets, but genetic effects are evident across domains.

Tellegen et al. (1988) – Twins Reared Apart

Identical twins generally show higher correlations than fraternal twins across several personality domains, even when raised apart, suggesting robust genetic contributions to aspects of well-being, social potency, achievement, social closeness, stress reactivity, aggression, control, harm avoidance, traditionalism, absorption, and higher-order factors such as Positive Emotionality, Negative Emotionality, and Constraint.

Riemann et al. (1997) – German study (1,000 twin pairs)

Correlations within pairs varied by measure and informant source: Self-Report Extraversion
Identical Twins: 0.56; Fraternal Twins: 0.28; Self-Report Neuroticism: 0.53; Fraternal Twins: 0.13; Peer Ratings Extraversion: 0.40 (Identical) vs 0.17 (Fraternal); Neuroticism: 0.43 (Identical) vs -0.03 (Fraternal); Agreeableness and Conscientiousness also showed differing patterns, indicating both genetic and rater-based environmental contributions.

Johnson et al. (2008) – Meta-analysis

Neuroticism: Identical twins r ≈ 0.43 (N ≈ 26,698 pairs) vs Fraternal r ≈ 0.19 (N ≈ 40,890); Extraversion: r ≈ 0.50 (Identical, N ≈ 22,949) vs 0.17 (Fraternal, N ≈ 24,636); Openness: r ≈ 0.47 vs 0.23; Agreeableness: r ≈ 0.40 vs 0.22; Conscientiousness: r ≈ 0.47 vs 0.20.

Mednick et al. (1984) – Danish Registry on Criminal Behavior

Genetic influences on criminal behavior were evidenced, with correlations suggesting higher risk when biological parents were criminals compared to when adoptive parents were criminals. In a 2x2 table: biological parents criminal? Yes/No; adoptive parents criminal? Yes/No; the observed frequencies were: Yes/Yes: 24.5%; Yes/No: 14.7%; No/Yes: 20.0%; No/No: 13.5%.

Johnson et al. (2008) – Shared Environment (Adopted Siblings)

For example, Neuroticism: Adopted siblings r ≈ 0.00?; Extraversion: Adopted siblings r ≈ 0.13; Openness: Adopted siblings r ≈ 0.01; Agreeableness: Adopted siblings r ≈ 0.14; Conscientiousness: Adopted siblings r ≈ 0.13. These patterns highlight how shared environmental effects contribute variably across domains, with some traits showing modest shared environmental influences while others are more strongly governed by genetics or non-shared environment.

Shared vs Non-Shared Environment

Shared environment refers to environmental influences that make individuals raised in the same family more alike (e.g., SES, parental styles, home environment). Non-shared environment refers to influences that make individuals within the same family different (e.g., unique experiences, peer groups, different teachers, measurement error). The extent of shared environmental influence can be inferred from correlations among adopted siblings on a given trait, whereas non-shared environmental influence (including measurement error) can be inferred from correlations between identical twins raised apart.

Summary of Shared vs Non-Shared Environment

  • Shared Environment: Factors like SES, course of pregnancy, living environment, birth circumstances, relatives and acquaintances of the family, birth order, parental marriage quality, parental child preference, general family environment, peer associations, parental educational attainment, school class/cohort, accidents, illnesses. Some of these factors may or may not be shared for twins.
  • Non-Shared Environment: Unique experiences shaping individuals, contributing to differences among genetically identical individuals in the same family.

Non-Shared Environment as a “Free-Will Coefficient”?

A provocative perspective notes that even with identical genetics and similar environments, twin studies suggest substantial continuity in cognitive ability and education, with non-shared environment accounting for differences in non-cognitive traits. Harden (2021) summarizes that, if you rewound life with the same genetic and environmental starting point, you might diverge in some personality traits (e.g., extraversion, organization) and life outcomes, but you would likely be similar in cognitive ability, education, or risk for mental illness. This perspective emphasizes limits on free will when viewed through a twin-genetic lens and highlights the substantial role of non-shared experiences in shaping personality differences.

Criticisms of Behavior Genetics

  • Some argue that the twin method overestimates genetic variance due to interactions not accounted for and assumptions about equal environments.
  • Adoption studies can underestimate genetic variance due to restricted environmental variance within adoptive families.
  • Contrast effects in sibling pair assessments can inflate genetic estimates.
  • Shared parental similarities can confound estimates of shared genetic variance because parents’ own traits influence the family environment.
  • These criticisms motivate careful interpretation of heritability and call for triangulation with genotype data and more nuanced models of environment.

Genotype–Environment Correlation and Interaction

Genotype–Environment Correlation

Genotype–Environment Correlation (rGE) occurs when individuals with certain genotypes are more likely to be found in particular environments than others. Three types are commonly described:

  • Passive rGE: The child’s genotype correlates with family environment because parents’ genotypes (which are correlated with the child’s genotype) shape the environment.
  • Reactive (or Evocative) rGE: Individuals with certain genotypes evoke reactions from their environment that correlate with those genotypes.
  • Active rGE: Individuals with a certain genotype seek out and create environments that correlate with their genotype.

Genotype–Environment Interaction (G×E)

G×E refers to the idea that environmental variables affect individuals differently depending on their genotype, and genetic effects vary depending on the environment. Studies that examine combinations of genes and environments are needed to capture these interactive effects.

Ayoub et al. (2019)

Using N = 1,411 pairs of twins and their parents, the study found that 27% of variance in parental warmth and 45% of variance in parental stress were attributable to child genetic influences. This implies child genetics can influence parenting behavior and, in turn, parental warmth and stress through child personality traits such as agreeableness and conscientiousness, suggesting a bidirectional association between parenting behavior and child personality.

Genotype–Environment Interaction in a Developmental Context

G×E research emphasizes that individuals differ in sensitivity to environmental inputs. Some environments may exacerbate or mitigate genetic predispositions, and certain genes may confer vulnerability or resilience in response to environmental insults (e.g., maltreatment). A classic exemplar is Caspi, McClay, Moffitt, et al. (2002) showing MAOA gene variation moderating the effect of childhood maltreatment on later antisocial behavior.

Caspi et al. (2002) – MAOA Moderation of Maltreatment Effects

Dunedin Longitudinal Study

  • Sample: N ≈ 442 boys, followed from birth to adulthood.
  • Genetic variant: MAOA promoter polymorphism, with alleles conferring high or low MAOA expression (and thus different levels of monoamine oxidase A activity).
  • Environmental factor: Childhood maltreatment (3–11 years).
  • Outcome: Antisocial behavior (e.g., antisocial personality disorder indicators, number of convictions, ratings).
  • Hypothesis: The combination of alleles associated with low MAOA activity and exposure to severe childhood maltreatment increases risk for antisocial outcomes, whereas high MAOA activity confers resilience in the context of maltreatment.

Findings

  • Individuals with low MAOA activity who experienced severe maltreatment showed higher risk of antisocial outcomes compared to those with the high MAOA activity genotype or those not exposed to maltreatment.
  • The interaction suggests that the MAOA genotype moderates sensitivity to environmental insults, providing an example of a gene–environment interaction with long-term behavioral consequences.

Implications

  • This study illustrates how genetic variation can shape an individual’s susceptibility to environmental influences, linking biological mechanisms with developmental psychology and public health.
  • It supports a view of personality and behavior that integrates neural and neurochemical processes with environmental context, rather than attributing outcomes to genetics or environment alone.

Brain and Personality: Physiological Influences

Biochemical Influences

Neurons and neurotransmitters underpin neural signaling related to personality. Key neurotransmitters include:

  • GABA
  • Dopamine
  • Serotonin
  • Norepinephrine
    These biochemicals influence arousal, reward processing, mood regulation, and impulse control, thereby shaping personality traits and behavior.

Endocrine System and Hormones

The endocrine system integrates hormonal signaling with brain and bodily processes. Major components include:

  • Hypothalamus
  • Pineal gland
  • Pituitary gland
  • Parathyroid, Thyroid, Thymus glands
  • Adrenal glands
  • Liver, Kidney
  • Pancreas
  • Reproductive organs (Ovary in females; Testis in males) and, during pregnancy, Placenta
    Hormones released by these glands influence development, arousal, stress responses, and social and mating behaviors.

Prenatal Hormonal Exposure and Behavior

Prenatal hormones can influence behavior such as aggression, dominance, impulsivity, and social tendencies. Testosterone has been linked to aggression and impulsivity; oxytocin has associations with empathy and perspective taking. Hormonal milieu can thus bias later personality patterns and social behaviors.

Early Biological Theories and Mood/Arousal Regulation

Early formulations (e.g., Eysenck and ARAS concepts) linked cortical arousal to extraversion vs. introversion, where arousal levels influence emotional conditioning and trait patterns through neuromodulatory systems.

Eysenck’s Ascending Reticular Activation System (ARAS)

Explanations propose that cortical arousal levels influence extraversion/introversion via limbic system interactions and arousal of brain centers. The broader idea is that neural activation patterns contribute to emotional conditioning and personality traits.

The Limbic System and Brain Structures

Core limbic structures—the cingulate gyrus, thalamus, fornix, hypothalamus, amygdala, hippocampus, olfactory bulbs, mammillary bodies—mediate emotion, motivation, memory, and autonomic responses. The limbic system interacts with the prefrontal cortex to regulate behavior and emotional responses that underlie personality traits.

The Prefrontal Cortex and Executive Functioning

The Frontal Cortex

Executive functioning and response inhibition are central to self-control and planning, functions attributed to the prefrontal cortex. This region helps regulate behavior, plan actions, and control impulses, contributing to traits such as conscientiousness and impulse control.

Orbitofrontal Cortex (OFC)

The OFC is involved in decision-making, particularly when decisions depend on changing information and reward/punishment contingencies. The Somatic Marker Hypothesis (Damasio, 1994) posits that autonomic cues guide emotional decision-making via the OFC. Functions of the OFC include evaluating rewards, social decision-making, and integrating affective signals into choices.

Impulsivity and Neurotransmitter Systems

  • An overactive BAS (Behavioral Activation System) and underactive BIS (Behavioral Inhibition System) are associated with impulsivity and poor emotional regulation, linked to OFC dynamics.
  • An overactive FFFS (Fight-Flight-Freeze System) and underactive BIS can correspond to high Neuroticism and rigid thinking.
  • Dorsolateral prefrontal cortex involvement is associated with high Neuroticism and rigid, inflexible thinking patterns; this region may also be implicated in conscientiousness and cognitive control.

Hemispheric Asymmetry and Affective Style

Left vs. Right Hemisphere EEG Alpha Activity

Frontal EEG alpha power asymmetries have been linked with affective style: relatively greater left frontal activity (lower alpha power) has been associated with approach motivation and positive affect, whereas greater right frontal activity is linked to withdrawal motivation and negative affect.

Frontal Brain Symmetry and Affective Style

Longstanding research suggests stable individual differences in frontal asymmetry relate to temperament and affective style. Studies (e.g., Davidson and colleagues) show associations between frontal asymmetry and trait patterns such as Positive Emotionality/Extraversion and Negative Emotionality/Neuroticism.

Behavioral Systems and Personality: Gray’s Reinforcement Sensitivity Theory

Core Components

  • Behavioral Activation System (BAS) or Goal Attraction System (GAS): related to approach behaviors and responsiveness to reward.
  • Behavioral Inhibition System (BIS) or Goal Inhibition System (GIS): related to avoidance, conflict processing, and anxiety.
  • Fight-Flight-Freeze System (FFFS) or Goal Repulsion System (GRS): linked to aversive responses to threat and punishment.
    These systems constitute neurobiological substrates for motivational and emotional responses that shape personality.

Revised Theory and Neural Activation

Gray & McNaughton proposed refinements (Reinforcement Sensitivity Theory) that integrate neural circuits with behavioral tendencies. The FFFS/ BIS/GAS systems map onto distinct neural substrates, including limbic structures and prefrontal regions, with neuromodulators (e.g., serotonin, dopamine) modulating their sensitivity and balance.

Personality Neuroscience: Integrating Biology and Psychology

Overview

McNaughton (2020) argues for starting with evolutionary biology and conserved neural-level modulators when explaining personality constructs, especially basic emotions and related disorders. He suggests that neuromodulators influence personality constructs across metatraits and aspects, and that pharmacotherapy can temporarily alter personality by modulating neural systems. He contends that causal explanations should be anchored in neural-level mechanisms, with higher-order explanations invoked only when neural explanations fail to account for observed patterns.

Key Takeaways

  • Personality reflects coherent patterns in affect, cognition, desires, and behavior, anchored in neural-level factors.
  • Emotion systems are conserved across species and organized hierarchically; modulators at lower levels influence higher-order personality traits.
  • Neurotransmitters and hormones provide mechanisms linking neural activity to observed personality variability.
  • Interventions (e.g., serotonergic drugs, anxiolytics) can shift stability, neuroticism, and trait anxiety, illustrating neural-level influence on personality.

Nomenclature for Goal Control Systems (Table 2)

  • GAS: Goal Attraction System (Attractor; Appetitive/Proactive engagement); Activation associated with approach toward rewards.
  • GIS: Goal Inhibition System (Inhibition; Conflict resolution; Informative modulation); Activation associated with avoidance or conflict resolution.
  • GRS: Goal Repulsion System (Repulsor; Aversive/Withdrawal tendencies);
    Notes: These systems are fronto-limbic-hypothalamic and distinct from motor control; benzodiazepine receptor ligands can target GIS, while serotonin can modulate across multiple systems, shifting control from lower to higher levels of the system hierarchy.

Figure Concepts (From McNaughton, 2020)

  • Attraction and repulsion have different motivational gradients and are modulated by GAS and GRS, with GIS resolving conflicts between approaching and avoiding goals.
  • Individual differences in sensitivity to GAS (attraction) and GRS (repulsion) can alter trait expressions such as neuroticism via neural-level pathways.

Main Brain Regions Involved in Emotional and Behavioral Processing

  • Periaqueductal grey (PAG): Autonomic responses and defensive behaviors
  • Limbic system: Central to emotion processing
  • Amygdala: Fear and threat processing
  • Hippocampus: Memory formation and contextual processing
  • Prefrontal cortex (PFC): Executive control and decision making; regulation of limbic activity
  • Orbitofrontal cortex (OFC): Reward/punishment evaluation and decision making
  • Anterior cingulate: Conflict monitoring and error processing
  • Striatum: Reward processing and action selection
  • Other structures: Olfactory bulb, thalamus, hypothalamus, etc.
    Oversimplified neuroscience views emphasize the interplay among these regions in emotion, motivation, and behavior that contribute to stable personality patterns.

The Frontal Cortex and Executive Functioning

Frontal Cortex Roles

  • Executive functioning: planning, problem solving, sequencing, cognitive flexibility
  • Response inhibition: stopping or altering planned actions in response to changing circumstances

Orbitofrontal Cortex (OFC) Functions

  • Decision-making based on changing information and reward/punishment contingencies
  • Somatic Marker hypothesis: autonomic cues guide decision-making (gut feelings) via the OFC
  • OFC dysfunction has been associated with impulsivity and poor emotional regulation

Implications for Personality Traits

  • OFC and associated networks influence conscientiousness and emotional regulation.
  • Dorsolateral prefrontal cortex involvement relates to higher-order control and may relate to conscientiousness and neuroticism patterns when dysregulated.

Laterality and Emotional Processing

Left vs. Right Hemisphere and EEG Alpha Power

  • Alpha power differences between left and right frontal cortices relate to approach vs. withdrawal tendencies.
  • Left-dominant activity is often associated with positive affect and approach motivation; right-dominant activity with negative affect and withdrawal tendencies.

Frontal Brain Symmetry and Affective Style

  • Stable individual differences in frontal asymmetry predict affective style and susceptibility to mood variations.
  • Empirical work links frontal asymmetry to temperament, with links to Positive Emotionality/Extraversion and Negative Emotionality/Neuroticism.

Back to Personality: Linking Behavioral Systems and Neurobiology

Behavioral Activation System (BAS) / GAS

  • Related to approach behaviors and the processing of rewards.

Behavioral Inhibition System (BIS) / GIS

  • Related to avoidance, threat sensitivity, and anxiety.

Fight-Flight-Freeze System (FFFS) / GRS

  • Related to responses to threat and aversive stimuli.

Neural Correlates

  • Prefrontal cortex (inhibitory control), amygdala (emotional responses), ACC (conflict monitoring), OFC (reward/punishment evaluation), and limbic circuits interact to shape temperament and personality traits such as neuroticism, extraversion, conscientiousness, and impulsivity.

Practical and Ethical Implications

  • Recognition that personality traits have neural and genetic underpinnings does not negate agency; rather, it highlights how environments interact with biology to shape behavior.
  • Understanding G×E and rGE suggests that interventions could be tailored to individual neurobiological and environmental profiles, with implications for education, mental health, and social policy.
  • The limitations and criticisms of behavior-genetic methods emphasize the need for cautious interpretation and the integration of molecular genetic data and longitudinal designs.

Summary of Key Formulas and Figures

  • Heritability index:
    h^2 = 2 \big(r{MZ} - r{DZ}\big)

  • Shared vs Non-Shared Environment concepts and their operational Indicators:

    • Shared Environment: measures of environmental similarity contributing to trait similarity in relatives raised together.
    • Non-Shared Environment: environmental differences contributing to trait differences among relatives, including measurement error.

  • Foundational models and terms:

    • A: Additive genetic effects
    • C: Shared environmental effects
    • E: Non-shared environmental effects (including measurement error)

  • Key interactions and processes:

    • Genotype–Environment Correlation (rGE): Passive, Reactive, Active forms
    • Genotype–Environment Interaction (G×E): Differential genetic effects across environmental contexts

  • Representative empirical patterns (illustrative values from slides):

    • Twin correlations often show higher r for MZ than DZ twins across traits, with cognitive abilities typically showing higher heritability than some personality facets.
    • Meta-analytic patterns for Neuroticism, Extraversion, Openness, Agreeableness, and Conscientiousness show substantial genetic influence, but non-shared environment also contributes meaningfully across domains.

  • Caspi et al. (2002) MAOA study: interaction between a genetic variant (MAOA activity level) and childhood maltreatment predicting antisocial outcomes; illustrates a gene–environment interaction with long-term behavioral consequences.

  • Institutional examples: infancy to adulthood longitudinal studies (e.g., Dunedin study) using genetic markers and life-history data to parse development of antisocial outcomes.

Connections to Foundational Principles and Real-World Relevance

  • The material integrates core concepts from behavioral genetics, neurobiology, and developmental psychology, emphasizing how genetic predispositions and environmental contexts interact to shape stable personality patterns.
  • It prompts consideration of how neural circuits, neurotransmitter systems, and hormonal milieus scaffold individual differences in emotion regulation, motivation, social behavior, and cognitive control.
  • Practical implications include informing mental health interventions, educational strategies, and policies that account for both biological susceptibility and environmental modulation.
  • Ethically, the material invites reflection on determinism versus plasticity, the reliability of behavioral predictions based on biology, and how to balance biological explanations with respect for individual variation and autonomy.

Notes on Terminology and Conceptual Themes

  • Heritability is population- and context-specific; it does not apply to individuals and is not a fixed property of a trait.
  • Shared environmental effects can inflate or obscure estimates of genetic influence if not properly modeled, and vice versa for non-shared environmental effects.
  • Gene–environment interplay is crucial for understanding why individuals with similar genetic predispositions may diverge in personality outcomes based on their environments.
  • Neurobiological models of personality bridge psychology and neuroscience, offering mechanistic explanations for stable patterns of behavior and emotion.