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Stress & Coping Week 6 Notes

by: Freddi Marsillo

Stress & Coping Week 6 Notes PSYC 3199

Marketplace > George Washington University > Psychology > PSYC 3199 > Stress Coping Week 6 Notes
Freddi Marsillo
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These notes cover what we learned this past week in class.
Psychology of Stress and Coping
Class Notes
Psychology, stress
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This 14 page Class Notes was uploaded by Freddi Marsillo on Monday October 10, 2016. The Class Notes belongs to PSYC 3199 at George Washington University taught by Howe in Fall 2016. Since its upload, it has received 3 views. For similar materials see Psychology of Stress and Coping in Psychology at George Washington University.

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Date Created: 10/10/16
Stress & Coping Week 6 10/11/16 12:08 AM Stress and Genes What’s a gene? • Chromosomes • 2 nucleotides form a base pair • Genes (sequences of nucleotides with defined beginning and end) What role do genes play? • Templates for making proteins The whole genome • Chromosomes: 23 • Base pairs: ~3,200,000,000 o Almost all of these are the same for all humans o Percent that show variation across humans: 0.1% • These make up protein-coding genes: ~20,000 How do genes vary for different people? • Allele: gene from one parent (we have two alleles of each gene) • So we have two copies of each gene, and those could be the same or different • Polymorphisms: different forms of the same gene • Two main types o Copy number variations (CNVs): some genes have different numbers of base pairs ▯ Due to copy “errors” during evolution ▯ So you might inherit two longer genes, two shorter genes, or a longer and a shorter gene o Single nucleotide polymorphisms (SNPs): genes also differ at a single base pair ▯ Due to mutations and repair processes ▯ Common: occur around 1 for every 300 nucleotides ▯ Most have little impact, but some can What are the effects of having different forms of a gene? • Often, nothing: SNPs most frequently occur on DNA that is between genes • Occasionally, can lead to different patterns of protein production, which in turn can shape processes involving those proteins Could variation in genes be associated with differences in stress response? • Similar to Bolger & Zuckerman’s differential reactivity model • Does exposure to stressor have different effects for people with different gene variants? • Also known as gene-environment interaction Vulnerability or “Diathesis”? • Diathesis: an underlying vulnerability that is apparent only in the face of a “provoking agent” • Stress-Diathesis Framework: effects of stressors are intensified when a diathesis is present • So, are there “vulnerability genes” that act as a diathesis? Serotonin Transporter • Serotonin: neurotransmitter released into the synaptic cleft, involved in firing of neurons • Serotonin is “implicated” in emotion regulation • Serotonin transporter (SERT): protein that “cleans up” serotonin in the synaptic cleft after a neuron fires; recycles it • Reuptake of serotonin implicated in control of depression and anxiety, mainly through the effects of Selective Serotonin Reuptake Inhibitors (SSRIs) as medication for severe mood problems Genetics of SERT Serotonin transporter gene (also called SLC6A4) – encodes for the serotonin transporter protein Polymorphisms in the gene • The promoter section of the gene (5-HTTLPR) can come in two different versions, long or short • The long version is more efficient in the production of SERT • You have two copies, so three different possible patterns o LL: high efficiency (less SERT) o SL: moderate efficiency o SS: low efficiency (more SERT) Is this a vulnerability gene? Three types of studies to address this question • Field studies measuring stressors and depression or anxiety • Laboratory studies using challenges and studying negative affect • Trials of prevention programs All three collect biological samples (saliva, blood) and genotype them Field Studies • Follow a large sample of people over time • Assess who is exposed to major stressful events • Study whether reactions differ for those people with different polymorphisms The Dunedin longitudinal study One of the first to use this approach • Conducted in Dunedin, NZ – Caspi & Moffet, 2003 – looked at stress and genetic diathesis together • Followed large cohort of kids annually from birth • Measured stressors, and then later depression in early adulthood • Looked at response curves for different genetic groups Unemployment as a stressor • 426 recently unemployed • Stressors following job loss • Genotyped for 5-HTTLPR • Assessed “internalizing” (anxiety, depression, anger) o Howe et al (2013) Summary of field studies Sharpley (2014): 81 studies • Early stressors (abuse) • Current stressors Findings: • Significant overall G by E effect • But some studies found nothing, and others found opposite effects Evidence for “crossover” effects: so not simple vulnerability pattern Lab Study • Select people with different polymorphisms • Have them engage in a standard challenge situation • Look for changes in stress response system • Example: Hariri & Holmes, 2006 o Track amygdala activation in fMRI o Expose people to “provocative stimuli” o Evaluate whether different people have different reactivity Lab studies: summary • Evidence for serotonin transporter gene associated with stress response to immediate challenge including: o Cortisol reactivity o Negative attention bias o Fear extinction o Amygdala response • BUT, two caveats: o Effects in amygdala response research have faded over time (i.e. more recent studies show weaker or no effects) o The s/s pattern is associated with better responses to positive environments Example: Fox et al • Risk mechanism: biased attention to negative stimuli • Protective mechanism: biased attention to positive stimuli • Training to modify attention bias Microtrial of attention bias modification • Elaine Fox and colleagues (2011) • Stratified random assignment, based on prescreening of 5-HTTLPR, to: o ABM for positive bias o ABM for negative bias Doesn’t fit the idea of “vulnerability gene” Also found in primate research – Steve Suomi: studies macaque and rhesus monkey development Effects of attachment In Suomi’s studies, serotonin transporter gene in monkeys is associated with: • Deficits in early behavioral functioning • Deficits in serotonin metabolism • Extreme aggression • Excessive alcohol consumption But, only among monkeys who experienced insecure early attachment (Barr et al, 2004) Boyce: Susceptibility to Context Thomas Boyce: suggests this may reflect genetic influence on susceptibility to both harmful and nurturing contexts • Under adversity: higher rates of disease, disorder • Growing up in low-stress, supportive social environments: lower rates than less reactive peers • Suomi finds that monkeys with a polymorphism are more likely to become leaders than those with a polymorphism when raised by a “super-mom” • Swedes refer to “dandelion” and “orchid” children Evidence for susceptibility gene rather than just vulnerability gene? Prevention trials • Identify children or adolescents at increased risk due to stressful circumstances • Randomly assign to prevention programs • Study whether preventive effect differs for those with different polymorphisms Example: SAAF • Strong African American Families (SAAF) program for rural poverty- level families • Randomized trial of parenting program • Tested effects on later problem behavior (Brody et al, 2009) • “Genetically at-risk” did better • Very few studies of this type From individual genes to gene systems • Most effects of individual genes are very small • Does combining multiple genes involved in similar physical systems help? • Multiple risk genes in SAAF study (Brody et al, 2013) Multiple susceptibility genes? • Van Izjendoorn et al (2014) recently reviewed 19 studies with several genes from serotonin and dopamine systems: o All showed evidence for differential susceptibility to positive interventions Can stress influence genes? Turning genes off and on • Epigenetics: studying how genes are turned off and on • Methylation: methyl groups attach to genes, block their functioning o This is why you don’t have noses growing out of your stomach o Early, including prenatal experience leads to methylation of genes as well Stress and Methylation Berghol et al (2011) • Identified people with and without socioeconomic disadvantage in childhood and adulthood from 1958 cohort • Collected blood and assessed whole-genome methylation • Found that child disadvantage associated with substantial methylation, adult disadvantage was not Can we influence methylation? • Long-term follow-up of SAAF (Beach et al, 2016) o Studied gene (OXTR) involved in oxytocin: hormone and neurotransmitter ▯ Associated with down-regulation of stress-response system o Assessed methylation of OXTR that has been associated with lowered production of oxytocin o Also looked at whether people with different alleles serotonin transporter gene responded differently Results • SAAF effects on substance use initiation at 13 varied by serotonin transporter gene (5-HTTLPR) • Early substance use initiation associated with OXTR methylation at age 20, again moderation by 5-HTTLPR There’s evidence that methylation can be altered • But complex path through substance use, and depending on other genes Might this explain long-term effects of early stressors on later stress response? Prenatally (animal studies): • Maternal glucocorticoids cross placental barrier • Evidence that maternal stress in pregnancy may lead to reduced methylation of gene that promotes CRH o Higher expression of CRH in mouse offspring o Higher endocrine responses to stress as well Post-natally • Evidence for substantial changes in methylation after exposure to early economic adversity • Early economic adversity predicts methylation of depression-related SNPs, particularly in those carrying the s/s serotonin transporter alleles (Beach et al, 2014) • Preventive interventions may influence methylation Stress and chromosomes: the telomere story • Telomeres: caps at the end of chromosomes that protect from deterioration • Telomeres shorten with age, and this is associated with disease risk Telomeres and Stress • Telomere length associated with exposure to racial discrimination in African American men (Chae et al, 2014) • Family-based program blocks association of earlier harsh parenting with later reductions in telomeres in young African American men (Brody et al, 2014) Putting it all together Summary • Genetic story is complex • Evidence that stressors may turn health-related genes off or on after exposure to stress • Also that stressors may contribute to degradation of telomeres • Evidence that genetic polymorphisms can alter effects of stressors • But the same polymorphism can increase vulnerability or protect against it, depending on other factors (such as secure attachment and social support) • Genes and environment intertwine in many complex ways: no simple “genetic vulnerability” Can stress kill you? Physiological regulation • To regulate: to keep in balance; to adjust to some standard or requirement o Maintain within a range o Often essential for physiological “parameters” Example: Regulation of Sodium • When happens when your system goes outside normal range? • Hyponatremia: too little o Imbalance in plasma blood concentration of sodium, defined as when concentration falls below 135mmol/L o Too much water in the blood o Effects: confusion, diminished reflexes, convulsions, stupor, coma, death. Even when treated, can leave brain damage, particularly in cerebellum Example: Regulation of Sodium • Hypernatremia: too much o When plasma sodium concentration goes above 157mmol/L o Dehydration o Effects, convulsions, coma, death Regulation of sodium-water balance • Eating, drinking, exercising, sweating all change amount of water or sodium • Body must respond dynamically to keep these in balance o i.e. within a restricted range Homeostasis • Process of returning to same state after some perturbation • Homeostasis involves negative feedback control: parameter is compared to setting, and action taken when deviation from the setting is exceeded in either direction Back to sodium for a minute • As sodium concentration changes, adrenal glands secrete hormone, aldosterone o This in turn affects kidney function: when to hold sodium in the body rather than releasing it into urine, or when to release it o This adjusts concentration in blood What does this have to do with stress? • Hans Selye • Introduced the idea of general adaptation syndrome General Adaptation Syndrome Short term: • Body is responsive to stressors, which lead to physiological or behavioral stress response designed to ready the body for action • If stressor goes on too long, leads exhaustion • Once stressor is over, physiological systems return to normal levels • Homeostatic response Long term: • “Wear and tear model”: Each episode of stressor and stress response, particularly if it is severe, leads to some small wear on the system, with these accumulating over time • This accumulation leads to damage and chronic disease Some problems with the GAS theory • 1) Physiological systems have many feedback loops, not just one o This would be like having many thermostats with somewhat different settings connected to many heaters and air conditioners Sodium Besides kidney function change, other systems involved include: • Mucous membranes in mouth, nose and eyes can dry out • Thirst sensations lead to intake of water • Sweat glands operate to reduce water volume • Release of arginine vasopressin (AVP) will increase; and veins and arteries will constrict to maintain blood pressure with a smaller blood volume Stress Response: Multiple Feedback Loops • No single adaptation response o Several brain systems o Several body systems • These systems influence each other Some problems with the GAS theory • 2) Longer-term adaptation to stressors may actually change the “target” levels of the physiological processes o Like the setting on the thermostat slowly goes down if the room is heated and cooled too many times Effects of sleep deprivation on rats’ sleep patterns (nREM delta from EEG) • When forced to stay awake 20 hours, then allowed to sleep 4 hours, % of time in nREM jumps to compensate • Over five days of sleep deprivation, compensation declines • During recovery period, with no deprivation, system appears to have a new “setting” Some problems with the GAS theory • 3) Long-term adaptation to stressors may even disrupt the regulatory process itself, leading to loss of body ability to maintain system parameters within normal operating ranges o Like the high-low range on the thermostat slowly gets wider and wider if the room is heated and cooled too many times Example: “brittle” diabetes • Fluctuations in blood glucose levels, normally kept in acceptable range through insulin balance o Normal range: 70-140 From Homeostasis to Allostasis • Homeostasis: a state of physiological equilibrium (body regulates its own temperature, for example) • Allostasis: (from Karlamangla et al, 2006) o Dynamic regulatory process, with continuous adaptation of physiology in response to challenge o Not simple homeostasis, because multiple feedback systems are involved across multiple physiological systems Allostasis and Stress • Longer-term stress exposure and adaptation may actually change the internal targets (reset the thermostats) • Long-term adaptation may even disrupt the regulatory process itself, leading to loss of body ability to maintain system parameters within normal operating ranges Summary of stages in an allostatic process • 1) Body responds to stressors • 2) Stress response involves multiple organ systems, with multiple feedback loops, and multiple “targets” or set points • 3) If stressor is relatively short, homeostasis occurs • 4) If stressor is longer or more repetitive, the reactions of the organ systems themselves can change, as set points change • 5) Over time, system can lose the ability to maintain important parameters within normal operating range • 6) Resulting in physiological damage to organ systems Allostatic Load • Allostatic Load: (definition from Karlamanga et al, 2006) o The total accumulation of stress response dysregulation across multiple physiological systems o Hypothesized to mediate the effects of stressors on long-term health Hypothesis: Health Effects of Allostatic Load Exposure to stressors ▯ overall physiollgical dysregulation ▯ damage to organ systems ▯ chronic disease Why? What are the mechanisms? • What, exactly, is dysregulated in the face of stressors? • How does dysregulation lead to “damage”? • How are particular patterns of damage associated with specific diseases? 10/11/16 12:08 AM 10/11/16 12:08 AM


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