Lecture 10: Stress, Health Disparities, and Biopolitics

stressors and stress have a

cause and effect relationship

stress is hard to define in an objective way

it is a perceived experience - everyone reacts differently to stress depending on perception and lived experience

stress is linked to many

modern health problems

• CVD

• immune dysfunction

psychosocial stress affects neuroendocrine functions →

affects immune systems

reduced appetite under high stress can affect

nutritional status

stress is linked to

vulnerabilities

humans have evolved vulnerabilities to stress

• advanced cognition

• good memory

• complex social life

• ability to think about the future

all help plan ahead, adjust to environment, and build social bonds

humans’ evolved vulnerabilities can also

make them more vulnerable to psychological stress

stress can be adaptive and beneficial

exercise or training for health

“black box” between stress exposure and health outcomes

complex psychological and behavioral mechanisms that translate perceived or environmental stress into physical disease

importance of social gradients (differences in the microenvironment we grow up in)

• history has produced different types of conditions in which various people live

• different economic and political arrangements impact the environment, which impacts our bodies

income disparity

unequal distribution of household or individual income across a population

social status relates to

income and agency

perceived status has health effects

marketing can shape perceived status - we are not good enough; we need more, etc.

sense of belonging and social cohesion

influence how stress is experienced

• the same stressor can affect individuals differently depending on what factors are already influencing their lives, bodies, and minds

there was an old persistent idea that observed health disparities were related to individual inheritance, but they are now

understood as largely driven by unequal exposures to disease and stressors due to structural inequality

social construction of “race”

racialized health disparities

• can be harmful to attribute health differences to heritage rather than immediate conditions and social inequities

• who has more or less in a constructed notion - meaning making

if we don’t measure stress and embodied outcomes in all individuals, we will

under measure disease prevalence and health impacts on historically under-served pops and communities

stressor from social dimensions

can be embodied

stressors activate stress responses:

reactions to a perceived threat to our physical/psychological/function/survivial/reproductionl

types of stress responses

• active coping behaviors - conscious efforts to manage, reduce, or adapt to stressors

• physiological stress responses - automatic bodily reactions to perceived threats

two types of evolved stress responses

• stereotypical stress response - automatic, fixed physiological reactions that occur the same way across situations

• adaptive prediction - brain predicts needs and adjusts the body’s response based on context and past experience

stereotypical (normal changes within daily life)

the body undergoes episodic shifts during the day - ex. rising and setting of sun, changes in weather

• available energy

• cognition

• action

• maintenance

• growth

• pain

we cannot respond strongly to every small change or

we would be too reactive to function normally

• prevents wasting available energy or cognitive function

for every external input, there is a threshold, and

responses occur only when the threshold is reached

• ex. you do not start sweating until temp. goes up enough

most days, stress responses are activated _______ to maintain function within a normal range of changes

episodically

allostasis

outside normal range

homeostasis

normal range

episodic stress responses are often

related to what is detected (ex. range of change) rather than the stressor itself

expectation from one type of stress to another

there are expected ranges of normal stress responses (ex. sweat when it’s hot, feeling nervous when giving a speech)

body needs to maintain balance between

fail safe responses (hand on hot pan) vs reducing false positives (oversensitive, sensitization)

neuroendocrine system

neural + hormonal

autonomic nervous system

• parasympathetic - rest and relax

• sympathetic - fight or flight

fight or flight; adrenaline rush

• changes happen in awareness, sensitivity, CV, and pulmonary functions

  • raid response to threat

  • we like to “exercise” our nervous system - roller coasters, horror movies

neurosecretion of norepinephrine (noradrenaline): fast

cells will make their glucose avialble when there is adrenaline around

adrenal secretion of epinephrine (adrenaline): sustained

leads to metabolic shifts - you will start to burn energy and fats in the liver more quickly

adrenal secretion of epinephrine

• fight or flight response hormone

• sweating increases, bp and HR go up, etc.

Hypothalamus, pituitary, adrenal glands (HPA axis)

• corticotrophin-releasing hormone > corticotrophin > cortisol > wide effects:

  • glycogenolysis

  • gluconeogenesis

  • immune suppresion

• evens short term stress can cause changes (ex. DNA methylation)

chronic (long term stress responses)

• neural (excitability) + hormonal (an ovulation changes)

• moods and emotions

• negative effects are well-documented in humans and baboons

• when under chronic stress and threat, it becomes trauma, which can heighten the stress response

• war and conflict contexts can generate a wide range of stressors

evolved stress responses; mammals use

environmental cues to predict future condition and make developmental shifts accordingly to better handle anticipated threats

if a stressor comes to a fetus

• cues in early life that things are good → adaptively benefit from switching genes on and off to grow bigger and faster

• cues that environment is bad → shift genome activation patterns to conserving energy more (lower birth eight, smaller body size, early reproductive maturation)

• methylation and demethylation of DNA and RNA sites

natural selection has found ways to make use of early cues to “optimize” →

life history trade-offs

thrifty phenotype hypothesis

• nutrient signals program metabolism during development to help offspring adapt to their environment

• both nutritional and social stress is mothers can expose the fetus to elevated glucocorticoids through common pathways

• diseases can arise id there is a mismatch between developmental environment in utero and the environment outside utero later in life

example of thrifty phenotype hypothesis - early life nutritional stress

• may increase risk of obesity and diabetes → metabolism programmed for energy conservation

• may make individuals reach sexual maturation early so they can reproduce sooner, thus having less time to grow and not reaching a bigger body size (tradeoff between reproduction and growth)

• altered metabolism as an adaptive response in anticipation of famine, but the later life environment is resource-rich

early exposure to stress influence on HPA axis

• anxiety

• caring behaviors in life

early exposure to stress influence on rate of reproductive maturation

• life history tradeoffs

• change of pubertal timing

• early menarche - speeds ip life history reproduce early

early exposure to stress influence on social aspect

• childhood experience

• withdrawal

• hyperactivity

• etc.

early exposure to stress influence critical windows of development

environmental experiences are essential for development

Gluckman, Beedle, and Hanson 2009 - Life History response to developmental cues

• first 1000 days in utero and postnatal

• plasticity vs vulnerability

• life history traits (growth rate, timing or reproduction) are relatively plastic compared to other phenotypic traits

• current plasticity and developmental plasticity

• early-life cues “program” biological strategies, which can be adaptive - but may become maladaptive if the environment later differs

two types of environmental cue during development

• perceived optimal environment

• perceived threatening environment

perceived optimal environmental cue

• predicted benign life course

• investment for longevity

• commitment to repair

• tissue reserve (neuronal and nephron number)

• investment for large adult size in terms of bone mass and muscle growth

perceived threatening environment

• predicted uncertain life course

• adjustment to ensure survival at birth - smaller size(premature birth)

• altered reproductive strategy (early puberty)

• adjustments to resit a threatening and difficult environment (altered HPA axis and behavior, increases insulin resistance, propensity to store fat)

Sapolsky 2004 - Why Zebras Don’t Get Ulcers - general model of stress-related diseases

• repeated acute stress over time can make you move off an optimal baseline

• chronic activation of stress responses negatively impacts immune functions

Stress - Large brain and intelligence

• consciousness, language, memory

• scenario building vs unknowable future (feeling unsafe)

• communication of stressful scenarios to others (sharing traumas, cognitive stress)

• ability to call up stressful memories repeatedly

people are stressful

• expanded social network compared to earlier generations - social media, communication, complex

• material uncertainty, violence, deprivation, interpersonal conflicts, subordination, lack of support, care needs of others

novel environments are stressful

• chronic activation of stress responses is likely now more frequent

• ongoing social change, pressures/demands and network density - exams, tech

• few opportunities to act physically (run away or fight)

• large inequalities in economic and social status that amplify health differences

• large scale war, famine, loss of livelihood, and structural violence

• evolved social supports eroded and reduced traditional coping methods (ritual dancing, feasts, gatherings, elders, mentors, and psychological healers)

• stigma: you could be having a stress-related illness, but you don’t get to inhabit the sick role until recently

Sociopoitcal stress and its effects on mortality

1. Mateusz Zatonski, 2013: During Europe’s period of Cold War - higher male premature mortality in Eastern Europe and Central Asian Countries vs Western Euro Countries

2. CVD, cancer, stroke, suicide rates rose dramatically in Russia after the collapse of the USSR in 1991 and the collapse of the Roubles in 1998

health gradient

• stressors can stack up to create more and more health hazards

health gradient - layers of social stressors

• poverty

• poor housing

• unemployment

• inadequate food and nutrition

• lack of education

• environmental health hazards

health gradient - individually oriented preventive action

• often promoted, but does not help the individual overcome the social gradients and health erosion by structural challenges

Whitehall Studies (UK)

• British civil servants

  • universal healthcare access and low risk of exposure from work environment

• 4 fold disparity in adult mortality related to income/employment grade

• class gradients in all health indicators

• not explained by genetic predisposition or health effects on social mobility

• income differences were modest, suggesting pathway was social status

social inequality

• disparities in income and other status markers

• social effects observed even in rich countries where material needs satisfied most

death per 100,000 across low to high social classes in UK vs Sweden

• in both countries, deaths decrease as you go higher in social status

• differences are larger in British data compared to Swedish data

• might reflect larger social disparities in British society

life expectancy in the Americas - Murray, Christopher, et al., 2005

• persistent income, class, and racialized disparities in life expectancy

  • different life expectancies across 8 demographic groups within the US

  • related to race, ethnicity economic opportunities, healthcare investments

  • you have to recognize and adjust for different social gradient factors to improve national and global health

daily experiences of socially constructed categories (ex. race, caste, class, etc.)

affect stress and stress responses

Race concept (groups share genetic characteristics affecting health) is NOT supported

• biological evidence: % of human variation is arbitrary

• cultural evidence: race is a socially constructed category/variable - not the same as ethnicity

socially and historically constructed racial/social categories map to health disparities

• inequalities are embodied through stress → race becomes biology

• persistence of this contributes to social construction of race

positionally in analysis of health disparities

we would lose a lot of insight if we don’t look at at stress on different people, but we need better ways to measure it

social disparities →

health disparities