Biological Pathways Linking
Social Environment to
Health
Routes for biological embedding
Everything interconnected, so hard to establish a
beginning. Somewhat arbitrarily:
1.
2.
3.
4.
Embodiment & epigenetics
Endocrine system – hormonal messengers
Limbic system emotions, meaning and learning
The autonomic nervous system, closely linked to
endocrine system & hormone secretions
5. Immune system
6. Life course perspective.
Part 1
EMBODIMENT & EPIGENETICS
‘Embodiment’
• The processes whereby our physical bodies incorporate
traces of lived experiences (+ & -).
• Ecosocial & life course perspective; bodies as active
agents in adaptation
• Brain & mind involved: neural substrates of our
learning (body memory); driving becomes automatic…
• Culturally learned bodily expression of emotions
• Neuroses & psychological effects of trauma
• Social embodiment = patterned responses to
situations: reinforce social bonds: smiling, reach out a
hand in greeting
• Shaped epigenetically - environment modifies gene
expression (rather than changing the genes
themselves) to modify phenotype.
Genotypes, Phenotypes & Plasticity
• Genes code for proteins, building blocks for
everything we will discuss
• Variants of genes (alleles) lead to diversity
• Expression of a gene is strongly influenced by
environment
How does a genotype express a
phenotype?
• Transcription
– Portion of DNA unravels
– Messenger RNA (mRNA) created from part of DNA
– mRNA exits nucleus into cytoplasm of the cell
• Translation
– Transfer RNA (tRNA) uses mRNA’s information to create proteins
– Using amino acid materials from our diet (e.g. essential ones) or
manufactured in the cell
• Proteins used in most structures, and also functions
throughout the body. E.g. many hormones are built from
proteins
From DNA to Protein
Strings of
3 DNA nucleotides
= 1 Codon
1 of 20 Amino Acids
Assembled into peptide
Protein
Proteins
• More than 50% of dry weight in most cells
• Drive and regulate all bodily processes
PROTEIN
TYPES
Structural
Storage
Transport
Receptors
Contractile
Defensive
Hormonal
Enzymatic
Genes “act” via the proteins they code for
Factors Influencing Phenotype
1. Dominance
2. Polygenic Inheritance
– Multiple genes involved
3. Environment (epigenetics)
The observable
physical or
physiological
trait
Side-bar: Genetic disorders
• Important, but not the main focus today.
• Dominant genetic disorders; rare. E.g.,
– Huntington’s
– Hemophilia
• Polygenetic; you inherit genes that predispose
you to the disorder; will not necessarily get it.
– Diabetes
– Asthma
– Breast cancer, etc.
3. Environment
• Environment influences gene action in many
ways:
– Proteins must use elements from the environment
to build structures
– Influences gene regulation (temperature, light,
nutrients, toxins, stress, etc.)
– Demonstrated in genetically identical plants, twin
studies (e.g., Tim Spector)
Genetics: Phenotypic plasticity
• A critical idea is that of “phenotypic plasticity,”
which refers to the capacity of a single
genome to produce a range of physically or
functionally adaptive traits.
– For example, fetuses that experience poor
maternal nutrition adapt by incorporating energysaving metabolic changes that anticipate a postnatal environment that is also characterized by
food scarcity. These children often become obese.
Nature via Nurture
• Changing thinking over relative contributions of
genes and environment
• Biological determinism wrong: genes provide a
range of phenotypic possibilities
• Epigenetics
• The combination of genetics and epigenetics
blends evolutionary and developmental biology.
This has been termed ‘evo-devo’: the one leads to
invariant outcomes and the other to individual
differences.
Epigenetics
• Our cells contain full DNA code, but produce only cells
of their own type. Cookbook & recipe metaphor.
• DNA transcription & translation regulated by
‘supervisory’ enzymes which determine type, amount
& timing of protein produced
• Enzyme regulation influenced by many factors,
including environment.
• Epigenetics studies these mechanisms, which lead to
persistent changes in gene activities and effects, but
without changing DNA base sequences
Epigenetic mechanisms
• DNA string is long & is tightly wound on ‘spools’. To be
transcribed the relevant section needs to be unwound.
• The spools are made of histone proteins; these can
change shape to allow or forbid access. Enzymes
control this, in a dynamic balancing act of promoting &
inhibiting access, e.g.
– Methylation tightens the DNA & impedes transcription
– Acetylation loosens the bonds.
• These enzymes are influenced by internal milieu,
including health, stress levels, chemical exposures, etc.
• A critical point is that the methylation can be lasting, so
that early exposures & experiences (including in utero)
can lead to lifelong changes in gene expression.
• It can also be passed on to offspring.
Epigenetic influences
• Gene-environment interactions are especially relevant at sensitive
periods of infant and child development. We carry alleles that can
be turned on or off via environmental triggers.
• Birth cohort studies increasingly showing links between child
experiences and later life sickness. For example:
– There is a genetic polymorphism in the monoamine oxidase A
(MAO-A) promoter region of the genome, which seems to
contribute to aggression. The Dunedin birth cohort study
showed that a low activity allele in association with severe
maltreatment in childhood led to antisocial outcomes in 85% of
males.
– British 1958 birth cohort study studies methylation of 20,000
genes by categories of SES. Methylation more closely linked to
childhood SES than to adult (N Borghol, 2012).
Genetics and Behaviour
• Evidence that genes influence behaviour
– “Innate” behaviours we observe in many different
species
– Changes to biological structures, such as brain
areas, may lead to change in behaviour
– Behaviours of closely related species, e.g. humans
and chimpanzees
• Behaviours are highly complex traits, and
likely involve many genes
Example: Tobacco Use
• Nicotine binds to nicotinic-acetylcholine receptors in
the brain, which in turn modulate release of dopamine
• The gene CHRNA4 codes for one subunit of the
nicotine receptor
– There are several different forms of this gene
• Feng et al 2004 found a form of the gene
to be protective against nicotine addiction
Genetics may influence susceptibility
to nicotine-addiction
Part 2:
ENDOCRINE SYSTEM
The Endocrine System
• Made up of all hormone-secreting
cells in the body: glands
• Secrete directly into bloodstream
(vs. exocrine glands)
• Internal communication system between brain
and body (complementary to nervous system)
• Maintains homeostasis and long-term control
– Regulates slower processes than nervous system
(e.g., growth, stress response)
Hormones
“A substance produced by one tissue and
transported to another tissue where it induces
a specific physiological response.”
• More than 50 known human hormones
• Grouped into 3 classes:
– Peptides (short chains of amino acids)
– Amines
– Steroids (lipids
derived from
cholesterol)
Hormone Action
• Hormones trigger
actions in specific
target cells
• These have receptor molecules that hormones
bind to (lock & key analogy)
• Steroid hormones act inside the cell, while
peptide and amine hormones bind with
receptors on the cellular membrane
• Binding changes the shape of the receptor,
eliciting a chemical/physiological response
Action of Steroid Hormones
• Steroids can enter cell since they are lipids and
can cross the cellular membrane
Action of Non-Steroid Hormones
• Peptides and amines cannot cross the cell
membrane
• Bind to receptor on membrane,
causing chemical signal
(second messenger)
inside the target cell
Homeostasis and Regulation
• Negative feedback regulates secretion of
almost every hormone
• Most elements of the internal environment are controlled by
hormones which have simple, negative-feedback relations with the
products or processes that they regulate (e.g., blood glucose &
insulin). A disturbance in a process stimulates hormonal secretion:
the hormone corrects the disturbance so removing the stimulus for
its own secretion.
• This occurs without neural involvement.
• But hormones are also controlled by the brain, via the autonomic
nervous system, sympathetic & parasympathetic branches. E.g.,
pancreas, kidneys & adrenal glands all linked to ANS.
• The hypothalamus also secretes hormones (ACTH, oxytocin, GH and
a dozen others). These act on numerous organs. Hence, controls
occur via local, neural and neural-hormonal pathways.
• Why? In part so that the body can respond in anticipation of
metabolic fluctuations. E.g. anticipatory insulin release in
anticipation of food. In part so that the brain can exert overriding
control, ‘resetting the thermostat’.
• Individual variability in hormone secretion:
Some people are habitual low excretors of
hormones; others are higher.
• Secretion has also been studied in relation to
coping styles, showing that when
characteristic coping approach fails hormone
secretions change abruptly. (Sterling & Eyer)
Part 3:
LIMBIC SYSTEM
Structure
• Part of the brain that translates ideas and affects into
feelings and emotions
• Connects to frontal lobes (‘thinking brain’) and also to
endocrine system
• The limbic system is closely connected to organs of
perception (olfaction; memory) and plays a role in
appraisal of the environment and hence in interpreting
the stressfulness of a threat. It seems to be involved
in processing the meaning of perceptions.
• Comprises an upper and lower circuit, which connect
the neocortex (thinking brain) to parts of the
endocrine system
The Limbic System
Functions
• Upper circuit appears to be involved in feeling
states, while the lower circuit is involved in
emotional states specific to survival (flight or
fight response)
• Functions include:
– Olfaction
– Arousal, motivation, etc.
– Regulation of homeostasis through the autonomic and
endocrine systems
– Coding in laying down new memories
– Emotional responses, learning and higher control over
exchanges between the body and the external world
through emotions
The Limbic System
• Loosely defined
• About the size of
a walnut (larger
in women than
men)
• Evidence on
functions comes
from braindamaged animals
and people
• Amygdala
– Receives sensory information from other regions
– Organization of emotional information
– Role in memory (damage results in amnesia for
non-procedural memories)
– Connected to olfactory bulb – memory of odours
is strong
– Stimulation causes aggression, damage leads to
passivity and lack of reaction to fearful stimuli
• Hippocampus
– Involved in converting short-term memory
(things in your mind) into long-term memory
– Damage prevents formation of new memories
• Thalamus
– A relay station that channels sensory impulses
from the nervous system to appropriate parts of
the cerebral cortex.
– Links “thinking brain” with sensory and
emotional areas
– Damage results in emotional apathy
• Hypothalamus
– Linked to pituitary gland – the master gland and
thereby the endocrine system. The pituitary releases
hormones related to growth, reproduction,
metabolism
– Important in homeostatic regulation (the body’s
thermostat)
– Regulates drives (hunger, thirst, sex), autonomic
nervous system (stress response), aggressive behaviour
– Plays a central role in the stress response via secreting
CRH, which causes the pituitary to secrete ACTH,
which stimulates the adrenal medulla to release
epinephrine. The “HPA” (see below).
Together, these structures:
• Are connected to organs of perception (olfaction;
memory) and play a role in appraisal of the
environment and hence in interpreting the
stressfulness of a threat
• Are involved in processing the meaning of
perceptions
• Set emotional tone & add emotional dimensions to
stress perception: fear, anger, anxiety
• Store emotional components of memory
• Facilitate bonding: damage prevents animals from
bonding with young
• Regulate motivation and drive via orchestrating the
SAM and HPA responses (see below).
The brain system for appraising threats
• Limbic system:
– Adds emotional dimensions to stress perception: fear,
anger, anxiety
– Especially centered in the hypothalamus
Part 4:
NEURO-ENDOCRINE PATHWAYS
Overview of structures involved
Nervous system
Central nervous
system (CNS)
Brain
(See next
slide)
Peripheral nervous
system (PNS)
Spinal cord
Autonomic nervous
system (ANS)
Somatic nervous
system
(involuntary muscles)
(voluntary muscles)
Parasympathetic
Sympathetic
(conserves energy;
undertakes ‘housekeeping’)
(mobilizes & expends energy;
prepares for fight or flight)
Divisions of the autonomic nervous system
How do the Nerves work?
SYNAPSES
Note idea of synaptic
memory: well-used
pathways.
Others are disused &
may store emotions &
hidden memories
Neurotransmitters
• Dopamine
o Natural Amphetamine
o Motor coordination, cognition, mood, attention and learning,
metabolism (BP, MR, digestion) – positive reinforcement
• Serotonin (Peripheral & Central NS)
o Provides a healing, nourishing, satisfied feeling in the body –
allows you to sleep naturally, enjoy time and think rationally
• GABA
o Chief inhibitory neurotransmitter
o Relaxation, anti-anxiety, involved in endorphin production
• Acetylcholine
o Cognition, memory, arousal
o Deficiency = lower creativity, learning
ANS structure: Adrenal Glands
Adrenal glands
• On top of the kidneys
• Two parts:
– Outer covering (cortex)
– Inner part (the medulla)
• Both parts secrete stress hormones
• These perform complementary roles
in up- and down-regulation.
Adrenals
Stress response: SAM & HPA
Operates via two interrelated systems:
• SAM (Sympathetic-adrenomedullary – the
medulla)
• HPA (hypothalamic-pituitary-adrenocortical
– the cortex).
• These balance each other
• Both are triggered by the hypothalamus
SAM
• Adrenal medulla (the inner part)
releases hormones epinephrine
(adrenaline) and norepinephrine
• Epinephrine Stimulates rapid
mobilization of metabolic resources:
increased heart rate, increased rate of
respiration, inhibition of digestive
system, release of glucose, increased
alertness, etc.
• "Rapid response"
HPA
• Hypothalamus secretes corticotropin-releasing
hormone (CRH)  pituitary, stimulates release of
adrenocorticotropic hormone (ACTH)  adrenal
cortex, stimulates release of glucocorticoid (GC)
& mineralocorticoid (MC) hormones.
• These form a “back-up response"; slower effect
– Cortisol involved in regulating metabolism, immune
response, and general homeostasis.
– Protein & fat are metabolized into glucose; this
suppresses immune response; raises BP
• Receptors = GRs and MRs
• Targets the brain
• Also changes gene expression
GR and MR Receptors
• The glucocorticoids from HPA bind to specific
mineralocorticoid (MR) or glucocorticoid (GR)
receptors on the target organs.
• GRs mediate most of the stress response; MRs
mediate basal responses such as regulating
neurotransmitters, BP, circadian rhythm
• GR effects therefore often oppose MR effects. This
leads some to argue that vulnerability to stress is
affected by the ratio of GR to MR receptors and their
activation
• Such ratios set by gene expression, susceptible to
epigenetic influences.
Function
• Normal homeostasis (body temperature, etc) is
maintained within relatively narrow limits.
• By contrast, the stress response maintains
homeostasis over a far wider range of adaptive
circumstances, and in responding to challenges.
• This is 'allostasis': achieving stability through
change.
• It occurs via the 'stress response'.
Anabolism & Catabolism
• The hormones suppressed during arousal are ones that
promote synthetic or "anabolic" processes requiring
energy.
– Anabolic processes include energy storage, growth, synthesis of
proteins, repair, and surveillance against infectious agents &
malignant cells.
• Most of the hormones that increase during arousal are
ones that promote degradative or "catabolic" processes
directed at the immediate mobilization of energy.
– Epinephrine, growth hormone, glucagon, and cortisol all
promote carbohydrate, fat, and protein breakdown.
• The effects of this shift in overall hormonal pattern is all the
more powerful because each hormone has multiple effects
that reinforce the others.
HPA: Animal evidence
• Evidence from rodent models shows that infant rearing modifies
activation of HPA response.
• For example, when a mother rat grooms her offspring this stimulates
the development of GR receptors, which therefore allows more
efficient control of HPA system activation.
• This epigenetic effect illustrates how neurobiology can be modified
by social experience in critical periods of infant development.
• Pups reared by nurturing mothers, yet which are given freedom to
explore, become more stress resilient. The ratio of their GR : MR
receptors is different from rat pups that experienced maternal
separation.
• This epigenetic mechamism involves methylation of a region of DNA
that regulates HPA axis function, and also higher-order executive
functions in the brain.
Weiss & Rats under stress
• Rats received electric shocks & got ulcers.
• 4 factors predicted level of ulceration:
– If warned by a buzzer that shock was coming, ulcers lessened.
Unpredictable = bad.
– Rats with control over shock (by pressing a level) had fewer
ulcers.
– Reinforcement: a signal that the control behavior was correct
led to fewer ulcers.
– Demand level: if rat had to press lever several times fast, ulcers
were worse.
• (Weiss J. Sci Am 1971; 226: 104)
Human evidence
• Humans in insecure relationships show elevated cortisol and heart rate in
response to HPA activation: i.e., their stress reaction is prolonged.
• Children who receive supportive care appear to have reduced stress
responses "that may buffer or protect the developing brain and result in a
more stress-resilient child." (Gunnar & Quevedo)
• Studies of Romanian orphans: after neglect during the first 6 mos. in
orphanages, children tended to become high cortisol reactors and to
suffer profound social-emotional, as well as cognitive, developmental
disturbances that persist at least into early adolescence.
• "Responsive caregiving allows children to elicit help by expressing negative
emotions, without triggering the endocrine component of the stress
response": plausibly a modified limbic system reaction.
• Infants lacking maternal attachment show more reactive HPA and less
adaptive behaviors.
Summary
• "Stress reactivity is better understood as the result of
intertwined biological and psychological processes that
ultimately ensure an organism's survival."
• "There is a cost to frequent physiological adjustments
(allostatic load)"
• “One of the most interesting findings emerging from the
research ... is that in the absence of supportive care,
stressors experienced during sensitive periods of
development can ... leave permanent imprints in the
neural substrate of emotional and cognitive processes.
... the nervous system of mammals carries their singular
epigenetic history and expresses it in unique but
predictable ways”.
Reference: Gunnar M, Quevedo K. The neurobiology of stress and
development. Annu Rev Psychol 2007; 58: 145-173.
Social Status & Physiological Responses
• Sapolsky (1997): baboons of higher rank had greater
cortisol suppression, suggesting more effective
glucocorticoid negative feedback
• Steptoe & Marmot: cardiovascular reactivity is generally
greater in lower SES individuals
• Lupien et al. (2000): lower SES children had higher salivary
cortisol levels than higher SES children
• Cohen et al. (2006): higher SES associated with lower
levels of cortisol and epinephrine, independent of race, age,
gender and body mass
• Allostatic load is a representation of how the cumulative
wear and tear of life conditions can undermine host
resistance.
Part 5:
IMMUNE SYSTEM
How could psychological factors
influence immunity and disease?
Psychological characteristic or state
CNS innervations
Hormonal response
Behavioral change
Immune change
Disease susceptibility
Stressful events
Coping
Smoking
Poor dietary
habits
poor sleeping
Cohen et al, Ann Rev Psychol, 1996
Immune Response
• Immune response elicited when foreign substance
enters body
• Two types:
– Innate or Non-specific:
• Called non-specific because the same response occurs regardless
of the foreign material that enter the body
• Characterized by inflammation reaction
– Acquired or specific:
• Tailored to specific pathogens that enter the body.
• Characterized by antibodies, T-cells (T-lymphocytes), and B-cells
(B-lymphocytes)
Innate or Non-specific immunity
(Note skin & mucous membranes = first line of defence)
• Bacterium or virus enters body through wound (or other route)
• Damaged cells release histamine resulting in increased blood flow
and temperature: Pain, redness, swelling
• Platelets released from bloodstream to clot blood at wound site
• Complement System: proteins that cause pores in microorganism to
open so that fluids and salts enter, causing cell to burst
• Neutrophils migrate to site and kill bacteria by phagocytosis (Link to
YouTube video and another)
• Macrophages remove pathogens by phagocytosis and release
hormones called cytokines
• Cytokines attract T-cells and B-cells to site and activate them.
Acquired or Specific Immunity
Mnemonics: Antibody = anti foreign body (the good guys).
Antigen = antibody generators; generates an immune response
(the bad guys)
• Pathogens such as bacteria and viruses have unique proteins
on their surfaces called antigens.
• After phagocytosis, cytokines signal T-cells and B-cells.
• Cytotoxic T-cells bind to infected cells and release chemicals
that kill the pathogen
• Suppressor T-cells then inhibit immune response when no
longer needed
• Helper T-cells assist in B-cell growth; B cells make the
antibodies …
Acquired or Specific Immunity (2)
• … B-cells develop into either antibody-producing cells
or memory cells.
• Antibodies are matched to the pathogenic antigen.
They kill the pathogenic cells in a variety of ways:
• Secondary immune response: Memory cells remain in
the body after the pathogen is eliminated. If a
pathogen presenting the same antigen enters the body
again, the immune response will be much faster and
stronger than it was the first time.
• Vaccines work by introducing an inactivated virus into
the body that elicits an immune response and causes
memory cells to develop for that virus.
How can psychosocial state affect
immunity?
How does this affect health?
• Cytokines are hormones released by macrophages to attract and
activate other immune cells.
• Pro-inflammatory cytokines such as interleukin-6 (IL-6) promote
inflammation.
• Anti-inflammatory cytokines such as IL-10 decrease the immune
response.
• Anxious and depressed moods increase the production of proinflammatory cytokines [2], [3].
• IL-6 promotes the production of C-reactive protein, which is a risk
factor for myocardial infarction [4].
Conclusions
• No question that psyche, CNS and
immunity are interrelated
• Psychological factors alters the immune
system
• Effects of psychological factors on cancer
onset or progression intermediated by the
immune system is a question that remains
unanswered
Part 6:
LIFE COURSE
Sensitive Periods hypothesis
• Limited spans of developmental time when specific brain systems
and the cognitive, emotional, or behavioral capacities they subserve
are maximally receptive to environmental tuning and input.
• These allow both mundane and extraordinary experiences to get
under the skin at critical times to affect biological function and
hence perhaps alter life course trajectories.
• Sensitive periods in brain and biological development start in the
prenatal period, reach a peak in the first few years of life, and
continue at a declining rate throughout childhood and adolescence.
– E.g., learning a second language best up to age 7
– Age of parental divorce is critical for impact on the children
– E.g., epigenetic influences on rat gene that codes for
establishment of glucocorticoid receptors; linked to anxiety in
the pup.
Life Course
• Barker: exposures in utero lead to phenotypic
adaptations (e.g. short stature or early
menarche); these may entail lifelong
susceptibilities
• = Developmental Origins of Health and Disease,
or DOHaD
• Boyce: Social subordination, even in the very
young, is associated with heightened
cardiovascular, autonomic, and adrenocortical
responses to stress and with disproportionately
higher rates of chronic medical conditions and
injuries.
Hertzman & Boyce
• Opportunities for biological embedding link closely to
sensitive periods in the development of neural
circuitry.
• Social environments and experiences get under the
skin early in life, and do so in ways that affect the
course of human development.
• Epigenetic regulation is the best example of operating
principles relevant to biological embedding.
• Heart disease, diabetes, obesity, depression, substance
abuse, school success, premature mortality, disability
at retirement, accelerated aging and memory loss all
have social determinants in early life
Hertzman & Boyce (2)
• Social causation is nonlinear and is nested within complex,
dynamic accumulations of exposures over time, with
interactions among multiple causal factors, and disease
occurrence that is a nonlinear function of exposure.
• Social causation implicates symbolic processes. The
psychosocial determinants of disease uniquely traffic in the
meaning and affective valences of life experience.
• Social causation is nonspecific, unlike traditional
epidemiology that links singular causes with singular
outcomes. “Adverse social conditions yield broad,
pluripotential pathogenicity rather than focal, specific
morbidities.”
Hertzman & Boyce (3)
• Life experiences involve mundane, rather than
exceptional, exposures: cf. the weathering metaphor.
• Physical and emotional abuse in childhood create
serious health consequences, but it is often the less
memorable but far more prevalent misfortunes of
childhood that become embedded in neural circuitry
and produce the vulnerabilities of adult life.
• Social causation is iterative and recursive: it involves
repeated, self-amplifying exposures over time.
Developmental bio-programming
• Hertzman & Boyce: examples of biological embedding:
– Early sensory stimulation activates genes in different parts of the brain
to differentiate neuron functions and establish sensory pathways.
– Sensory pathways, in turn, influence the development of neural
pathways within the brain and other biological pathways, including the
immune and endocrine systems.
– Maternal attachment & stimulation drives the development of neural
pathways that help the baby’s brain become attuned to its immediate
environment: without attachment (grooming in primates, licking in
rats) these pathways do not develop.
– Child’s attachment to mother is critical; lack of early signaling of
attachment can lead to failure to set up the reactions of positive
attachment in the HPA and brain of the child. This deficit makes the
child will be at risk of missing significant social cues.
– Negative reinforcement loop: lack of response to social cues can make
the child hard to relate to; this, in turn, can lead to deterioration of the
child’s immediate social environment, making it more stressful.
Biological reactivity
• From early in life, ∼15% of children are more highly
biologically reactive to their immediate social context than
others are.
• The effects of being highly reactive biomedical outcomes are
bivalent: they can be protective in some contexts and riskaugmenting in others.
• Those who are biologically sensitive to context are distributed
across social strata, but the less privileged will tend to find
themselves in risk-augmenting contexts, whereas those from
more privileged backgrounds will tend to find themselves in
protective environments.
Prefrontal cortex
• Biological incorporation of executive function:
– Hertzman reports experimental studies of attention
varying by SES: higher SES kids seem able to focus
their attention and to be less distractable.
– Lower SES kids tended to pay attention to irrelevant
stimuli in a distraction experiment. This was then
linked to higher cortisol secretions.
• Linked to the relative instability & chaos of early
childhood environment, which varied by SES.