Stress Networks
- The entire brain is involved in responding to stress
- Stress networks: highly connected brain structures that are activated when real –or- imagined threats to an individual are perceived
responses in the network usually initiated by amygdala - things such as memory, perception etc, all connected and activate the network.
heightened activity (in sympathetic network) result in stress response. all these networks talk together and work together, when stressful experience, networks start to produce more energy (heart rate, respiration, etc), body tries to calm these down through coping behavior. if we didn't have a stress network we would basically die = nothing would alarm us or push us to change in the face of threat.
amygdala = signals that something is stressful. not part of ANS or stress response, but it is like a light switch - light turning on is the stress response –> the amygdala is what presses the switch for the light response
nervous systems have evolved over time.
initial importance: create responses to things such as pain, hunger, thirst, etc.
over time, multicelullar organisms develop networks for more advanced functions –> behavioral pursuits became part of evolutionary selection process. brain evolved to points where evolution selected for specific behavioral pattterns
“multidirectional communication” –> more complex human brain
take away: evolution created my complex brain.
stress can even be enforced from imagination/thoughts, this complexity is what makes field of stress and coping so interesting and challenging.
Autonomic nervous system
nervous system when talking about stress and coping, we are interested in ANS
endocrine system also important in stress and coping
- Main parts of the human nervous system
- Central Nervous System (CNS)
- Peripheral Nervous System (PNS)
- Autonomic Nervous System (ANS)
- Sympathetic Nervous System
- Parasympathetic Nervous System
- Somatic Nervous System (SNS)
sympathetic activates to RELEASE energy, parasympathetic work to STORE energy - work in pretty much counter-reactive way.
Sympathetic Nervous System
- Flight/fight
- Energy resources are shifted - energy shifted towards fleeing response.
- Signals adrenal glands (Endocrine system becomes important)
signals to release cortisol etc –> hormones signals cardiovascular/respiratory/muscuskeletal towards fleeing (increase HR, increase oxygen distribution, more breathing/oxygen, gastrointestinal (increase blood-glucose levels = more energy available)
role of parasympathetic = to turn the stress response off and get body back in calm tempo.
problem: system is built for EXTERNAL threatening systems, but many problems today are PSYCHOLOGICAL = we can’t FLEE them. –> continually triggers the system –> we need to figure out a way to decrease them.
important to note than even if sympathetic is the important one to stress response, the CNS regulates this, as it overall regulated ANS (and CNS is the one that recognizes stressor). ANS will not be turned on if not CNS says “oh crap this is a stressful situation”
- Direct psychological system in the body
- Fast response system
Endocrine system
- HPA Axis – this is a very important part!!
- Hypothalamic-Pituitary Adrenal Axis
- Hypothalamus signals the pituitary glands to produce hormones to trigger the adrenal glands to increase cortisol production – help increase energy fuels to body.
chronic stress distorts communication between immune system and HPA axis.
HPA is turned on usually through amygdala, amygdala signals hypothalamus, which gets the system going.
Without triggering from CNS, the HPA activity isn’t happening.
Stress and the Immune System
Prolonged stress can cause:
immunosuppression (e.g. by decreasing baseline leukocyte numbers (white blood cells) and through alteration in regulatry T-cells)
immunopathology (e.g. autoimune disease - we don’t need to know it is type 2 cytokine response, just know there are different cell responses - but know its a certain cell response, where the body attacks itself)
acute stress can cause:
Immunoprotection = e.g. vaccination (stresses you out, but does so in a way that increase body’s acute stress reaction)
Immunopathology from acute stress: e.g. allergic reaction
chronic stress is the problem, not so much acute.
short term fight/flight stress response is a fundamental defense mechanism. (enhance survival, incl immune system)
immunosuppresion: turning “down” the immune system
imunopathology = turning “on” somethign that is bad.
immunesystem = we turn it up when some kind of sickness, like a radio we turn up to hear nice music better.
immunopathology: e.g. autoimmune disease = we turn UP for negative function, e.g. a radio starts to get “itchy” and annoying.
stress increases vulnerability to infection - may trigger autoimmune diseases and inflammation-based diseases. = immunopathology
BUT stress can also enhance immune functioning
studies: short duration stress make a re-distribution of immune cells –> boost immune system where they end up in.
modern medicine: vaccinations: something we do, it is a stressor to our body. Surgery also a stressor, and injuries too. So we send immune “system” to parts exposed to stress to boost regeneration there. These acute stressors are likely to be more immune-enhancing, increase protection of the body. having a surgery = stressor = body has automatic response, stress response turns on, more white bloodcells to the area = more regenration and healing.
but a body can OVERRESPOND = autoimmune disease (body attacks itself, basically) = problem in chronic stress.
INDIVIDUAL DIFFERENCES ARE IMPORTANT (e.g. resiliency - can affect your transition between acute and chronic stress, and how fast you can get back to a “maintenance” level.
Double Hit Hypothesis
take away: psychological stress may be an important factor, in the “halfway mark” between a genetic disposition, and disease development - the “triggering factor”
double hit = more focused on (negative) health OUTCOMES (as effect of genetics and trigger)
Warner and Schapira, 2003
• Genetic predisposition plus environmental trigger increases vulnerability
• hypothesis: your genetic predisposition, coupled with environmental stressor, makes some individuals more susceptible to disease - whether your genetics are “triggered”
• e.g. we know schizophrenia is to some degree genetic –> idea that the environment triggers it.
• not a new idea, but resurgence around 2003.
- Caspi and Colleagues
- 2002: reported risk of conduct disorder and antisocial traits varied by a polymorphism - polymorphism (genetic variation) in MAOA gene
- = risk of having conduct disorder dependent on genetic variation in gene PLUS maltreatment in childhood. if maltreatment = more variation in gene = more conduct disorder
- 2003: impact of childhood maltreatment and stressful life events on depression differed by genotype
genetic predisposition, what does that mean? = A person can be predispositioned towards 1) harmful stress response, or towards 2) a negative health outcome.
Lazarus and Folkman (1984) (in relation to double hit hypothesis)
• Hypothesized that the genetic factors could influence the process of stress
specifically argued that impact of stress on health effects may very well depend on your genetics.
Question: predispotistion to negative stress reaction, or specific health outcome? = really both.
Emphasized overall genetic influence on PROCESS of stress.
what are their SPECIFIC argument was: impact of stress on the physiological response to a stressor, could be based on your genetic background.
difference from double hit hypothesis: they are VERY similar in what they propose.
double hit = more focused on negative health OUTCOMES.
lazarus = more focused on PROCES of stress (rather than the OUTCOME)
they are not DIFFERENT, they both look at genetics and environment.
A Systematic Review of Genetic Influences on Coping - • Dunn, S.H. & Conley, Y. P. (2015).
Purpose • Summarize published literature • Assess those studies • Identify key findings • Summarize current state of knowledge • Propose future directions of research
19 studies were reviewed (as only 19 fit their definitions) of 850 studies
• Two categories
• 9 studies address heritability of coping
• used twin pairs
• heritability estimates varied a lot across studies - possibly due to methods of phenotoping + definition of coping (varied)
• 10 studies focused on candidate genes to explore
Heritability of Coping:
• Used twin pairs as subjects
• Estimate of heritability varied considerably across studies
• Greatest heritability estimates were for nonadditive genetic factors (interactions among genes)
- great heritability for john henryism
Candidate Gene-Control
• Used self-report measurements of coping
• Candidate genes either had a central nervous system function or a role in susceptibility to risk factors for cardiovascular disease
• certain genes associated with more disengagement / emotion type coping. found interactions between e.g. genes and anger?
Main problem identified in the study: there is no consensus regarding instruments for phenotype coping. Consistency is essential within a single genetic study and when trying to compare two or more genetic studies.
there is lack of research in the area = more research needs to happen, but despite this lack of research overall conclusion = support for role of genetics in COPING behaviors. - but larger and more well-designed studies are needed.
–> possibly basis for biological interventions, e.g. gene therapy.
• John Henryism
- “A form of coping that involves attempts to actively cope with stress regardless of insurmountable odds”
- often coping found in black americans – for racial discrimination, coping “requires” that you persistently try to overcome the circumstances, even if they are not exactly in your favor – this has substantial physical consequences.
- John Henryism (JH) is a strategy for coping with prolonged exposure to stresses such as social discrimination by expending high levels of effort which results in accumulating physiological costs
Origin: from story of black american, in an endless fight against a machine (or something like that), causing great health distress, ultimately resulting in his death. (but he kept fighting despite the odds)
John henryism is basically perseverance - its just the name for the COPING relying on perseverance.
with john henryism specifically, can we consider it perseverance under racial discrimination (high effort of coping under conditions of racial discrimination –> can ultimately lead to negative health effects)
Epigenetics
- The study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNS sequence.
- changes in epigenome does NOT affect DNA directly. what it is, is an added layer above and beyond DNA. These added layer effects how DNA sequences are read, and what are the EXPRESSED (might be different form what was intended by the gene)
Epigenetic mechanisms = what leads to different gene expressions.
important thing to know for this class: external factors (e.g, childhood maltreatment) can influence, through the processes noted in slide) can affect how your DNA is read, and through reading process, change how genes are expressed, potentially changing your coping response, and these gene EXPRESSIONS might be heritable
• DNA
- Deoxyribonucleic acid
- It is a molecule found in almost all cells in the body
- Double helix
- forms chromosomes
- Chromosomes are subdivided into genes
- 4 types of nitrogen bases:
- 46 chromosomes in single cell.
- if your chromosomes were all taken out and stretched, they would be about 2 m long. what happens in cells, DNA molecules are clustered around proteins (histones) –> compaction varies across cell types (= different cells with different functions, and these can be read for replication)
Epigenetic mechanisms
= what leads to different gene expressions.
complex gene-environment interactions = more ways for causing changes.
in contrast to genome sequence which doesn’t change, epigenetic regulation is the response to a range of external things going on, which influence internal cell functioning (how DNA is expressed) – e.g. drugs, diet, social environment.
- DNA Methylation
- Chemical marking of the DNA sequence
- methyl groups added to molecule, changing how cell is being read - does not alter DNA sequence. effect of methylation depends on when it is happening, and the location of it.
- Really turns the gene expression on or off when chemical attaches to the gene.
- Histone Modification
- Chemical tagging of histone proteins (molecular tool by which gene expression levels are controlled)
- Increase/decrease transcriptional properties, influence what is READ in the process.
- It loosens or tightens the DNA string’s “wrap” around the histone protein, the loose the string = the more gene expression.
DNA Methylation
- Chemical marking of the DNA sequence
- methyl groups added to molecule, changing how cell is being read - does not alter DNA sequence. effect of methylation depends on when it is happening, and the location of it.
- Really turns the gene expression on or off when chemical attaches to the gene.
Histone Modification
- Chemical tagging of histone proteins (molecular tool by which gene expression levels are controlled)
- Increase/decrease transcriptional properties, influence what is READ in the process.
- It loosens or tightens the DNA string’s “wrap” around the histone protein, the loose the string = the more gene expression.
Weaver et al., (2004) study
- Series of animal studies (rats)
- Levels of handling, included licking and grooming by rat mothers, altered the methylation and acetylation patterns within the hippocampus resulted in lower levels of circulating stress hormones
- Cross fostering caused pups to acquire an epigenetic pattern that was consistent with the mothering style of the foster mother
- Low handling rats that received drugs to induce epigenetic changes similar to regular handled ones including lower stress hormone levels
what to know: this is one of the defining studies within the field of epigenetics:
they did a bunch of animal studies.
what they found: epigentic impact on stress (circulating stress hormone) if you took an animal in a lower nurturing environment to a more nurturing environment, there was a change in epigenetics.
if you administered a drug, it also helped.
Showed that within animals at least, thre are epigenetics going on in regards to stress = changing environment can change outcomes + providing an injection of drugs/medication ALSO made a positive change
positive change = lower amonts of stres hormone circulating.
Epigenetics and Depression - Clark, P., Rosenblat, J. D., Brietzke, E., Pan, Z., Lee, Y., Cao, b., Zuckerman, H., Kalantarova, A., & McIntyre, R.S. (2019)
- Review of literature
- A number of genes have been studied
Take away: environmental stress and childhood adversity can alter biological systems through epigenetics. e.g related to major depressive disorders
STRESS AND HEALTH: Psychological, Behavioral, and Biological Determinants - paper (the long one)
from class:
know that the stress response can become maladaptive in chronic stress, and enhanced stress hormone with chronics stress and supress immune activity.
don’t worry about cell types or a lot of the details.
we have covered the gist of it in the presentations
we’ll cover a lot of the rest next week
Critical Factors (for stress and the immune system)
- Duration
- Acute or chronic
- Acute stress experiences = can enhance immune responses. surgery = stressor = white blood cells flow to area = beneficial
- chronic = decrease immune cell number and function. and can dysregulate immune function, by dysregulating immune responses.
- don’t need to know celltype, but know chronic stress can promote inflammation and “turn on” harmful cells.
- Leukocyte distribution
- the white blood cells! immune enhancing for whatever parts of the body the leukocytes are sent to. mostly to the skin (combating infections from wounds etc) –> deficits in other parts (where it is then immune suppresive - stress helps send white blood cells to specific places, but harmful as it leaves other places “unprotected”
- Physiological versus Pharmacological concentration
- differential effects: of stress hormones for phys vs pharmaco. endogenous hormones: hormones produced in body: in normal concentration = immune-enhancing effects. if concentration too high, or SYNTHETIC hormones = immune-depressing effects.
- main take away: if endogenous concentration too high or too low, but too high is where we are more concerned in regards to stress = immune suppressing.
- It matters if endogenous (made within body) or synthetic.
- important: concentration! endogenous hormones within normal concentrations are immune-enhancing –> can get to a point where they are PHRAMACOLOGICAL (too high levels) or they are SYNTHETIC they will be immune suppressing.
- Timing
- timing of stressor: and how long it lasts: also have impact. = it is the same as duration.
- acute = immune enhancing.
- immune suppressing on later states (longer term stress)
- if stress and hormones occur EARLY and SHORTER = better. of hormones occur LATER (after stressor is gone) = worse. and if stress is LONGER = bad.
• Duration refers to how long the stressor itself if causing stress whereas timing is referring to when the immune function occurs (i.e. shortly after the stressor or after some time has passed)
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Topic 1 - definitions and models24
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Topic 2 - biological aspects19
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Topic 3 - psychological aspects21
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Topic 4 - individual and social factors27
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Topic 10 - academic stress8
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Topic 7 - Resilience13
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Topic 11 - Interventions13
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Topic 9 - occupational stress24
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Topic 6 - Multicultural Perspectives – Part 216
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Topic 8 - PTSD21
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Topic 5 - Multicultural perspectives - part 110
