Unit 20: Health Flashcards
NEED TO BELONG
- For our evolutionary ancestors, group
living served as a multi-purpose tool for
coping with survival challenges - E.g., protection against predators &
hostile conspecifics - Exclusion from the group meant
heightened vulnerability to threat and
greater risk of death
SOCIAL RELATIONSHIPS &
MORTALITY RISK
- Meta-analysis of 148 studies (N=308,849) assessing mortality as a function of social
relationships (e.g., having social support, marital status, integration in social networks) - Participants from North America, Europe, Asia & Australia
- Participants followed on average for 7.5 years
- Average effect size OR (odds ratio) = 1.50
– 50% increased likelihood of survival as a function of stronger social relationships
Results held across age, sex, initial health
status, follow-up period, and cause of death
OBJECTIVE VS. SUBJECTIVE ISOLATION
- Many early epidemiological studies focused on objective measures of
social isolation
– Frequently operationalized as being unmarried, living alone,
infrequent contact with family & friends, not participating in
organizations/clubs/religious groups - Being alone =/= feeling alone
- Loneliness is the subjective feeling of social isolation
– Discrepancy between desired and actual levels of social contact - Social loneliness = dissatisfaction with size of social network
- Emotional loneliness = lacking support & affection
LONELINESS & HEALTH OUTCOMES
- Emotional, rather than social, loneliness is
associated with poorer psychological health (major
depressive disorder, generalized anxiety disorder)
– Suggests the two constructs are dissociable; yet
not always distinguished in research - Loneliness is linked to increased all-cause mortality
risk & negative physical health outcomes—e.g.:
– Coronary heart disease and stroke
– Cognitive decline & dementia
– Decreased immunity
LONELINESS & COLD SYMPTOMS
* Experimental study
* Design
– Healthy participants completed measures of loneliness
and objective social isolation (social network size)
– Administered nasal drops containing a common cold
virus and quarantined for 5 days
* Results
– Loneliness, but not objective social isolation, predicted
greater cold symptoms
MARITAL QUALITY & HEALTH OUTCOMES
* Low marital quality (low marital satisfaction, negative attitude towards partners,
hostile behaviour) is also linked to heightened risk of mortality & negative health
outcomes
– Worse self-rated health
– Cardiovascular disease and metabolic syndrome (cluster of risk factors for CVD—e.g.,
high blood pressure, insulin resistance)
– Peptic ulcers
– Slower recovery post-surgery
HOW DO SOCIAL RELATIONSHIPS
AFFECT OUR HEALTH?
TWO MODELS OF SOCIAL SUPPORT
* Stress buffering model = close relationships protect health by buffering (mitigating)
the effects of external stressors
* Main effects model = close relationships exert direct effect on health outcomes
regardless of levels of external stress
* Both likely play a role in the association between relationships and health
HEALTH BEHAVIOURS
* Social control hypothesis = interactions with family &
friends motivate healthier behaviours
– E.g., being married associated with engaging in
health-promoting behaviours like exercise whereas
loneliness predicts physical inactivity
* May rely on unhealthy coping strategies (e.g.,
drinking, drug use) when dealing with social stressors
or lacking social support
* But association between relationships & health
persists even when controlling for (un)healthy
behaviours
PHYSIOLOGICAL MECHANISMS
* The presence or absence of positive social connection may directly tap into and
physiological systems that shape health and disease
– Autonomic nervous system
– Hypothalamic-pituitary-adrenal (HPA) axis
– Immune system
* Broadly, these systems help maintain body’s homeostatic balance (stable internal
environment) in the face of internal and external challenges (stressors)
– Stressor = anything that knocks (or threatens to knock) homeostasis out of balance
AUTONOMIC NERVOUS SYSTEM
Division of the nervous system that carries
involuntary commands to your organs, blood
vessels, and glands
Two branches:
* Sympathetic nervous system
– Energy mobilization; ”fight or flight” response
* Parasympathetic nervous system
– Energy conservation; “rest and digest”
response
HYPOTHALAMIC-PITUITARY-ADRENAL
(HPA) AXIS
* Cascade of events that culminates in the release of the
hormone cortisol from adrenal glands
– Mobilizes glucose reserves for energy, increases
conversion of proteins and fats
– Inhibits insulin production to prevent glucose storage
– Increases blood pressure ensuring adequate blood flow
IMMUNE SYSTEM
* Detects and eliminates harmful invaders such as bacterial
or viral pathogens
* Also detects and responds to tissue damage
* Highly complex, several components including
– Inflammatory response = rapid, nonspecific immune
defense against infection and tissue damage
– Antiviral response = more specific response tailored to
viruses
INFLAMMATORY RESPONSE
* Orchestrated by chemical messengers called proinflammatory cytokines
– Set of physiological changes—e.g., increasing blood flow to infected tissue,
increasing blood vessel permeability
– Also trigger a set of behavioural changes that help promote survival & recovery
(sickness behaviours)
* Sleepiness, lethargy, withdrawal, reduction in various kinds of activity (exploration,
social, sexual)
* Sickness behaviours help by conserving energy, may also reduce risk of
predation/attack while vulnerable
HEALTH IMPLICATIONS
* When functioning optimally, these systems facilitate adaptive coping with threats and
maintain health, but with sustained activation may begin to see dysregulation leading to
disease
* Feedback mechanisms become impaired—e.g.,
– Cortisol normally inhibits inflammation but prolonged exposure to cortisol and proinflammatory cytokines may increase glucocorticoid resistance of immune cells, leading
to chronic inflammation
* Chronic inflammation implicated in development of cancer, heart disease, diabetes,
neurodegenerative disorders, & depression
* Chronic activation of the sympathetic system can lead to the buildup of plaque on arterial
walls à increased risk of a heart attack
BRAIN-IMMUNE SYSTEM CONNECTION
- Why might social factors like loneliness or connection influence systems designed to
deal with physical threats, like the immune system? - Responses to challenges are proactive, not simply reactive—anticipate and prepare for
potential threats
– Earlier response facilitates adaptive coping - The immune system “talks to the brain” to gather information about environmental
conditions & expected threats - Social disconnection poses risk to survival (increased risk of predation, wounding,
infection)
– May respond by upregulating proinflammatory activity - At the same time, decreased risk of viral infection
– Downregulation of antiviral response - Among older adults, both objective social isolation and feelings of loneliness predict
higher levels of proinflammatory activity coupled with decreased antiviral response
REAL WORLD AND LABORATORY SOCIAL STRESSORS
REAL WORLD
* Across the lifespan, social stressors have been linked to greater inflammation—e.g.:
– Children (<8 years old) exposed to social stressors (parental separation, abuse) show
elevated markers of inflammation 2 and 7 years later
– Adolescents who report having more negative social interactions with friends and
family members (e.g., rejection) showed higher levels of inflammatory activity
– College students who reported experiencing more negative and competitive social
interactions on a daily basis showed higher levels of inflammation
– Older adults who recently lost a spouse had 1.5 x levels of inflammatory activity than
controls
* Feelings of loneliness are also related to other markers of physiological stress,
including elevated cortisol levels and increased blood pressure
LABORATORY SOCIAL STRESSORS
* Trier Social Stress Test (TSST)
– Combines elements of uncontrollability and social evaluation (situation where the
self could be negatively judged by others)
* Ps who completed the TSST in front of an evaluative panel (vs. a control non-social
evaluative condition) showed larger increases in cortisol and proinflammatory activity
from pre- to post-stress
– Additionally, immune cells of Ps from the social evaluative condition showed
decreased sensitivity to suppressive effects of glucocorticoids
* Ps who show more social pain-related neural reactivity to social exclusion (Cyberball)
showed larger increases in inflammation following TSST
* Other studies have evaluated effects of conflict discussions in couples
– Increase in systemic inflammation following conflict discussion in high- but not lowhostility couples
STRESS-BUFFERING
- Current experiences and history of social support affect
magnitude of physiological responses to stressors - E.g., preparing with romantic partner or receiving written
supportive messages from partners buffers cortisol
response to the TSST - Anxiously & avoidantly attached individuals show stronger
cortisol responses during lab stressors
COGNITIVE MECHANISMS:
STRESS APPRAISALS
* Social factors may also impact the way we THINK about potential stressors, which in
turn influences the stress response
* Cognition plays a role in triggering, amplifying, and reducing stress responses
* Most reactive to stressors when we perceive them as uncontrollable & exceeding our
coping capabilities
* Through history of positive interactions with caregivers, securely attached individuals
learn that stressors are manageable, that they are capable, and that others can be
relied on
COGNITIVE MECHANISMS:
THREAT DETECTION
* Current and former social conditions influence social threat detection
* Loneliness is associated with heightened threat vigilance
– E.g., in modified emotional Stroop task, lonely participants, relative to nonlonely
participants, showed greater Stroop interference specifically for negative social
relative to negative nonsocial words
* Anxiously attached individuals exhibit readiness to perceive threat & have high access
to threat-related cognitions even in positive contexts
– E.g., exhibit higher levels of cortisol and lower levels of heart rate variability (measure
of PNS activation) when asked to imagine being cared for by another person
SENSITIVITY TO THREAT & REWARD
* Experimental inflammatory challenge: administration of bacterial toxin (endotoxin)
that triggers an immune response
– Increases in depressed mood, feelings of social disconnection & sensitivity (e.g., “I feel
overly sensitive around others”), loneliness
– Greater neural reactivity in pain- and threat-related brain regions (e.g., dACC,
amygdala) in response to negative social evaluation & threatening social faces
* Larger increases in proinflammatory cytokines à greater neural reactivity
– BUT, also increased neural reactivity in reward-related brain regions (e.g., ventral
striatum) in response to social rewards (e.g., pictures of loved ones, positive social
feedback) but not non-social rewards (money)
* Also greater desire to be with close others
TYING IT ALL TOGETHER
- Relationships matter for our health
– Quality may be more important than quantity - Likely due to a combination of intertwined behavioural, cognitive, and physiological factors
- General theme: feelings of loneliness or social disconnection put us in “self-preservation
mode”
– Heightened HPA axis activity
– Altered immune gene expression & increased inflammation
– Hypervigilance for social threat
– Poorer sleep
– Depressive symptomatology, reduced social exploration
