PKP Kap. 9

What role does biology play in personality psychology research?

Role: empirical foundation (≠ competing personality theory); provides scientific findings that every personality theory must explain; supports trait theories while expanding them through evolutionary psychology and neuroscience.

Core evidence: Phineas Gage → frontal cortex damage → intelligence/language/memory preserved; personality radically altered (responsible → impulsive, irresponsible) → specific brain systems contribute causally to personality.

Research focus: biological foundations of personality via: (1) Temperament, (2) Evolutionary psychology, (3) Behavioral genetics, (4) Mood, emotion & the brain, (5) Plasticity.

Describe temperament research.

Temperament: biologically based individual differences in emotional/motivational tendencies evident early in life (emotional reactivity; mood; arousal; self-soothing) → suggests biological origins before substantial social experience (but keep prenatal experience in mind for homosexual study!).

(A) Historical development: early taxonomy + causal explanations

• Hippocrates/Kant: four temperaments explained by bodily fluids (rejected);

• Gall: phrenology (correct: functional specialization; incorrect: isolated localization—brain functions via interconnected systems);

• Darwin: evolution + emotional expression → foundation for evolutionary psychology;

• Mendel: modern genetics;

• Kretschmer/Sheldon: body type → temperament/personality (weak empirical support; methodological flaws);

• Pavlov: nervous-system strength (maintaining functioning under high stimulation) + conditioned reflexes → precursor of biological stress reactivity.

(B) Modern longitudinal research:

• Thomas & Chess (NYLS):

  • (1) easy (adaptable; positive); (2) difficult (negative; poorly adaptable); (3) slow-to-warm-up (low reactivity; cautious)

  • → infant temperament predicts later adjustment (difficult → most problems; easy → fewest);

  • goodness-of-fit: optimal development depends on match between temperament and parenting (≠ universally optimal parenting).

• Buss & Plomin:

  • inherited dimensions: (1) emotionality; (2) activity; (3) sociability → stable across development; substantial genetic influence (especially MZ twins);

  • limitation: parental-report bias (e.g., overestimating twin similarity). → Shift toward biologically grounded temperament dimensions; influenced later trait models (Big Five); lacked direct biological measures.

• Kagan’s biological temperament model: objective laboratory observations (≠ parent reports);

  • (1) inhibited: fear; avoidance; restraint; physiological arousal to novelty vs. (2) uninhibited: curiosity; sociability; positive affect.

  • Hypothesis: high-reactive (!) infants → inhibited; low-reactive → uninhibited. 4-month testing: ~20% high-reactive; ~40% low-reactive; ~40% intermediate. Longitudinal follow-up (14 mo; 21 mo; 4.5 y; 8 y): substantial continuity (high-reactive → greater fear; HR/BP; less smiling/talking; low-reactive → confident/social).

  • Continuity ≠ determinism: (a) supportive, (b) non-overprotective parenting with (c) reasonable demands reduced fearful outcomes; BUT no high-reactive infant became consistently uninhibited; low-reactive → inhibited only rarely → inherited temperament biases developmental direction (predisposition ≠ destiny).

  • Biological mechanisms: high-reactive infants form distinct categorical group (~10% consistently inhibited; ≠ purely continuous dimension).

    • Amygdala: novelty/threat detection; frontal cortex: regulates amygdala/emotion. fMRI: inhibited at age 2 → greater amygdala activation to unfamiliar / novel (but not non-novel!) faces at ~20 y → long-term biological stability.

    • Animal knockout studies: stathmin gene influences amygdala functioning (gene present → greater fearfulness; absent → reduced fear). Limitations: amygdala ≠ fear center only (multiple functions); amygdala damage ≠ absence of emotion; novelty may activate amygdala more than fear; maternal social support moderates genetic prediction (high support weakens genetic risk) → biology provides predispositions expressed within developmental context; temperament retains built-in flexibility across life.

• Effortful control & conscience:

  • Rothbart: effortful control = suppress dominant response to perform adaptive/subdominant response (delay gratification; inhibit impulses).

  • → Kochanska: temperament × parenting → conscience (Freud’s superego analogue). Longitudinal behavioral measures (slow walking; whispering; delay candy) + observed parenting + later conscience tasks (cheating; obedient vs. naughty dolls).

    • Findings: authoritarian/high power assertion → ↓ effortful control; ↑ effortful control → ↑ later conscience; effortful control mediated parenting → conscience relation. → Moral development emerges from interaction of biologically based self-regulation and environmental experience (biology × parenting; mediation).

Describe the research in evolutionary psychology.

Evolutionary psychology: explains ultimate causes (why mechanisms evolved via natural selection for survival/reproductive success) ≠ proximate causes (current biological mechanisms producing behavior) // Main assumptions (Buss; Cosmides; Tooby; Pinker):

• (1) Personality = evolved psychological mechanisms solving recurrent ancestral adaptive problems.

• (2) Adaptations evolved in hunter-gatherer environments (modern mismatch possible; e.g., fat preference → obesity);

• (3) Domain-specific mechanisms (specific problems ≠ general traits; e.g., jealousy ≠ childcare; fear of ancestral threats ≠ general fear)

• (4) Mind = multiple specialized modules (social exchange; parenting; mating; exclusion…) ≠ single general processor. → Contrasts with trait theory (specialized adaptive mechanisms ≠ broad context-free traits).

  • Social exchange & cheating detection (Cosmides): reciprocal exchange repeatedly essential → cheating detection adaptive. Abstract logical reasoning (“if P then Q”) → poor performance; identical logic framed as social contract/cheating (e.g., taxes) → high accuracy. Replicated across literate/non-literate cultures → evidence for universal evolved module. Neuropsychology: frontal cortex/amygdala damage → normal general reasoning; impaired social-contract reasoning → specialized cognitive system for cooperative exchange.

  • Sex differences: Parental Investment Theory (Trivers): women invest more biologically (pregnancy; limited fertility; childcare); men face paternity uncertainty.

    • (1) Predictions: men prefer youth; physical attractiveness; chastity (reproductive value; paternity certainty); women prefer earning capacity; ambition; industriousness; protection/resources. Buss:>10,000 participants; 37 samples; 33 countries + islands;

      • → broad support (men consistently valued youth/attractiveness; chastity only moderate support; women valued financial resources/ambition).

    • (2) Jealousy hypothesis: men → sexual infidelity (paternity threat); women → emotional infidelity (resource threat).

      • → questionnaires supported predicted distress; physiological measures replicated; strongest effect for men with prior committed relationships (women: nonsignificant).

Evaluation/Criticism: universal evolutionary mechanisms predict cross-cultural consistency;

• Eagly & Wood: sex differences smaller in gender-equal societies (women ↓ emphasis on earning capacity; men ↓ emphasis on domestic skills) → supports biosocial model (biology × social roles) ≠ biological determinism.

• Miller et al.: men and women showed highly similar overall mate preferences.

• DeSteno; Harris: jealousy effects largely disappeared when replacing forced-choice methods (MCQ) with separate ratings/real experiences; both sexes responded more strongly to sexual infidelity; men generally reacted more strongly to sexual content BUUT regardless of infidelity (!)

• → Evolution contributes to behavior, but evidence for universal, hardwired sex differences is mixed/inconsistent; biology and social context jointly shape behavior.

Describe behavioral genetics research.

Behavioral genetics: investigates genetic contributions to individual differences (genes influence personality INDIRECTLY via biological development; ≠ genes for Extraversion/Neuroticism) // Methods:

• Selective breeding: experimentally breed animals for traits (e.g., fearfulness; alcohol responsiveness) → demonstrates genetic effects; manipulate environments experimentally (not possible in humans).

• Twin studies: MZ (~100% shared genes) vs. DZ (~50%; ordinary siblings); MZ > DZ similarity → genetic influence; MZ reared apart → isolates environmental effects. MZ reared apart: r ≈ .45–.50; nearly identical to MZ reared together → substantial genetic contribution.

• Adoption studies: compare adopted children with biological vs. adoptive relatives → biological resemblance = genetic effects; adoptive resemblance = environmental effects.

Heritability (h²): proportion of population variance attributable to genetic differences (remainder = environmental variance + residuals); population statistic (varies across traits/populations/environments; e.g., war ↓ h² by increasing environmental variation or different for different populations!); ≠ percentage of an individual’s trait caused by genes; h² = 0 possible despite genetic necessity (e.g., universal abilities with no person-to-person variation).

• Findings: personality moderately heritable (~40–50%); genetic influences across virtually all traits (Big Five; IQ; emotionality; activity; sociability; impulsivity; attitudes such as conservatism). Self-report limitation addressed by peer ratings → independent peer reports replicated Big Five genetic findings (slightly lower genetic estimates) → greater validity/generalizability across measures.

• (!) Caveats: (1) heritability ≠ immutability (environment can modify highly heritable traits); (2) heritability = nomothetic (population differences) ≠ idiographic (individual prediction); (3) genetics operate via gene × environment interactions, not genetic determinism; e.g. Molecular genetics: identifies specific genes underlying outcomes (≠ estimating overall h²).

  • MAOA study: high-activity allele buffered childhood maltreatment → lower antisocial behavior than low-activity allele.

  • Serotonin transporter study: low-serotonin variant + many stressful life events → higher depression risk; gene alone insufficient.

  • → Both demonstrate gene × environment interaction.

• Gene–environment interaction: genes and environment = inseparable partners (≠ nature vs. nurture).

  • Cooper & Zubek: maze-bright/maze-dull rats × enriched/impoverished environments → enrichment benefited genetically dull rats; deprivation mainly harmed genetically bright rats → same environment produces different outcomes depending on genotype.

  • Environmental influences: shared environment (makes siblings similar) vs. nonshared environment (makes siblings different).

    • Findings: shared family environment contributes little to personality; ~40% of variance reflects nonshared environment. Big Five: substantial heritability across all traits (Openness independent of IQ); multiple measures separated measurement error from nonshared environment; peer ratings largely replicated self-reports

    • Reiss: nonshared effects partly arise because genetically different children evoke different parental treatment.

Three gene–environment interactions:

1. Passive: same environment → different effects depending on genotype.

2. Evocative: genetically influenced traits evoke different responses from others.

3. Active: individuals increasingly select/create environments matching genetic predispositions.

Describe the research on brain systems.

Focus: identifies neural/biochemical mechanisms underlying personality (emotion; temperament; self; morality); biology = dynamic system (≠ fixed cause only).

• (!) Hemispheric asymmetry (Davidson): (L) left prefrontal → positive affect; enthusiasm; approach motivation; (R) right prefrontal → negative affect; distress; avoidance.

  • EEG: greater (L) left baseline activation → stronger positive emotions to pleasant films; greater (R) right activation → stronger negative emotions to unpleasant films.

  • Clinical evidence: depression → ↓ (L) left-anterior activity; left frontal damage → depression; (R) right frontal damage → mania;

  • distressed infants (maternal separation) → greater (R) right activation.

• Worry ≠ anxious arousal: worry shows relatively greater (L) left-frontal activation → distinct neural mechanisms (≠ single Neuroticism factor).

• Anger: despite negative valence → (L) left activation (approach/confrontation) → hemispheric asymmetry reflects approach vs. avoidance, not simply positive vs. negative emotion.

• Neurotransmitters & temperament:

  • (1) Dopamine: reward/reinforcement; learning; pleasure; approach; positive affect; energy; impulsivity; incentive motivation; excess → schizophrenia; deficit → Parkinson’s disease.

  • (2) Serotonin: mood regulation; emotional stability; impulsivity; aggression. Low serotonin → depression; anxiety; OCD; alcoholism; impulsive aggression; pessimism. SSRIs prolong serotonin action.

  • (3) Cortisol: stress hormone; adaptive acutely; chronic elevation → depression; memory impairment; inhibited children (Kagan) ↑ cortisol at age 5 (effect absent age 7).

  • (4) Testosterone: dominance; competitiveness; aggression // high testosterone promotes competitive/aggressive behaviour, while winning competitions (even coin tosses) increases testosterone and losing decreases it → bidirectional cause–effect relationship.

• Clark & Watson’s 3-factor temperament model → No one-to-one neurotransmitter–trait mapping; each transmitter influences multiple traits; personality reflects interacting biological systems. (A) Differentiation/localization: specialized brain regions vs.(B) organization/system: personality emerges from coordinated interaction of interconnected systems:

  • (A) PE (Positive Emotionality): Extraversion-like; energetic engagement; dopamine; left hemispheric activation.

  • (B) NE (Negative Emotionality): Neuroticism-like; threat sensitivity; emotional instability; low serotonin; right hemispheric activation; heightened amygdala responsiveness.

  • (C) DvC (Disinhibition vs. Constraint): self-regulation (≠ affective valence); high = impulsive; sensation-seeking; reward-driven; low = cautious; controlled; future-oriented; serotonin (primary) + dopamine + testosterone.

• Plasticity: biology both cause and effect of experience.

  • Monkeys: dominance ↑ serotonin; loss ↓ serotonin.

  • Testosterone: promotes competition and increases after winning (even coin tosses), decreases after losing.

  • Juggling study: 3 months learning → ↑ gray matter in motion-processing regions → adult brain structurally plastic.

  • SES study: lower socioeconomic communities → reduced serotonergic responsiveness (serotonin agonist; prolactin measured), independent of IQ/Big Five → environment alters neurobiology.

• Higher-level functions:

  • Self: fMRI; self-judgments (vs. Bush vs. perceptual judgments) → selective medial prefrontal cortex (mPFC; vgl. Rogers) activation → self-referential processing recruits specialized neural systems.

  • Morality: moral dilemmas activate emotion-related brain regions more than nonmoral reasoning → moral judgment integrates emotion + cognition (≠ purely rational).

2 Interesting studies:

• Stress & telomeres (Epel): telomeres = chromosome end caps shortening with cell division (biological aging marker). Higher perceived + objective stress (especially mothers of chronically ill children vs. normal/healthy ones) → significantly shorter telomeres (~9–17 years greater biological age) → chronic stress modifies cellular biology; strong evidence for biological plasticity.

• Prenatal environment: probability of male homosexuality ↑ with number of older biological brothers, independent of being raised together (!) → shared family environment excluded. Maternal immune hypothesis: successive male pregnancies trigger maternal immune response → altered prenatal environment → fetal brain development. → Prenatal biology contributes alongside genes and postnatal environment.

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