Stress and Anxiety Biological Psychology PDF

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Summary

This lecture discusses stress and anxiety from a biological psychology perspective. It explores cognitive and physiological responses to stress, including the concept of the reactivity hypothesis and how stress can impact health. The presentation further elaborates on the prolonged activation model and its impact on the body, examines case studies to better understand the nature of the stress response and factors associated with it, and relates these concepts to concepts of social support and optimism.

Full Transcript

Stress and Anxiety Biological Psychology Dr. Dounya Schoormans Cathy, 42 years - Mother of two girls - Has rheumatoid arthritis (RA) since she was 31 - RA has been stable, yet a few months ago she experiences more symptoms - Currently getting a divorse John, 24 years -...

Stress and Anxiety Biological Psychology Dr. Dounya Schoormans Cathy, 42 years - Mother of two girls - Has rheumatoid arthritis (RA) since she was 31 - RA has been stable, yet a few months ago she experiences more symptoms - Currently getting a divorse John, 24 years - Student at UCLA - Has eczema since he was 10 - Symptoms fluctuate over time - Current outbreak - In a few days he has to take a major exam What do Cathy and John have in common? 5 Outline of this lecture 6 Why stress has physiological effects ▪ The cognitive representation of a threat causes a ‘fight-or-flight’ response ▪ Followed by a cascade of biological events ▪ Starting in the brain ▪ Inducing peripheral stress responses such as increases in heart rate, blood pressure, and stress hormones (cortisol) 7 The Reactivity Hypothesis Physiological response Stressor 1 Stressor 2 TIME --> Days/weeks ▪ Classical theoretical understanding: stressful events are accompanied by physiological responses, which, if frequent and intense, may cause bodily harm ▪ However, mostly weak and inconsistent support for this hypothesis ▪ Does not account for prolonged increased physiological activity 8 From Reactivity to the Prolonged Activation Model ▪ The prolonged activation model ‘Physiological activity during stressful events (i.e., stress reactivity) will only become a critical health threat when it is sustained long after these events, or when physiological activity is already present in anticipation of these events, sometimes even far before them.’ 9 The Prolonged Activation Model Worry, rumination, perseverative thinking Anticipation Slow Recovery Physiological response Stressor 1 Stressor 2 TIME ----------> Days/weeks 10 The Role of Continuing Stressful Thoughts: Perseverative Cognition ▪ To explain prolonged activity, the perseverative cognition hypothesis is formulated. Two core arguments: 1. Recovery of the autonomic nervous system after a physical stressor (e.g. running up a staircase) is much faster than from most psychological stressors 2. Human brain looks backwards and forwards: ruminating about the past and worrying about the future ▪ Unique to human beings ▪ Humans make mental representations of stressors, long before, and long after these events occur or are believed to occur → perseverative cognition (PC) Physiological and Psychological Profile of perseverative cognition Physiological profile Psychological profile Decreased heart rate variability Hyper vigilance to threat and failure to habituate to harmless stimuli Decreased prefrontal cortex activity Impaired cognitive functioning on tasks demanding delayed responding and executive functions Increased amygdala activity Lack of inhibitory behavior Altered immune function Denial and avoidant coping style Increased blood pressure Increased neuroticism Excess and prolonged cortisol Decreased conscientiousness responsivity Pupil dilation Lack of perceived control Greater levels of anxiety, depression, and hostility Input of the stress response Internal stressors (vagus nerve) Somatosensory stressors (skin and muscles) Painful stressors Emotional stressors Cognitive input Fight or flight response http://www.youtube.com/watch?v=j_04kcsIuJk Outline of this lecture 15 Complex network of signalling Immune system CNS Endocrine system http://www.nlm.nih.gov/medlineplus/brainandnerves.html http://www.nlm.nih.gov/medlineplus/immunesystem.html http://www.nlm.nih.gov/medlineplus/endocrinesystem.html 16 Complex network of signalling Sympathetic Nervous System (SNS) See www.youtube.com/watch?v=dOYOdJG0E0s for an overview of the nervous system http://lh6.ggpht.com/- VnH4IvnIbGE/UXuOJ1PrOCI/AAAAAAAAFt0/gKn68ggdcWw/s1600- h/parasympathetic%252520and%252520symapathetic%252520nerve%25255 B12%25255D.jpg Complex network of signalling Immune system CNS Endocrine system http://www.nlm.nih.gov/medlineplus/brainandnerves.html http://www.nlm.nih.gov/medlineplus/immunesystem.html http://www.nlm.nih.gov/medlineplus/endocrinesystem.html Complex network of signalling http://www.nlm.nih.gov/medlineplus/endocrinesystem.html Endocrine system Stress hormones HPA - axis HPA Grow and appetite CRH hormone Metabolism; Glucose storage; Learning and memory Schematic HPA-axis 21 Complex network of signalling Immune system CNS Endocrine system http://www.nlm.nih.gov/medlineplus/brainandnerves.html http://www.nlm.nih.gov/medlineplus/immunesystem.html http://www.nlm.nih.gov/medlineplus/endocrinesystem.html Effect of stress hormones Cortisol - stimulates lymphocyte maturation (+) - regulates inflammatory responses - promotes catechalomine release (+) Physiological response when life is in danger When survival is not threatened can lead to poor immune functioning Outline of this lecture 24 Homeostasis vs allostasis 25 Homeostasis vs allostasis 26 Outline of this lecture 27 Does stress has an effect on our health? And if so, how? Why is the durration of a stressor important when it comes to the effect of the stressor on one’s health? Effect of stress Upregulates on immune system (+) natural immunity, rises in the number of neutrophils and NK cells -> Preparation for infection or injury Downregulates (-) both natural and specific immunity Clinical relevance Clinical relevance Wound healing A model for studying the immune function, as the immune system is involved in wound healing. Wound healing – Example - 11 dental students - 3.5mm biopsy wound was made inside their mounth - Once wounds were made during vacation, once before exams Marucha et al. (1998) Psychosomatic medicine Wound healing – Example Wound healing – Example Marucha et al. (1998) Psychosomatic medicine Wound healing – Example Wound healing – Example Could the difference between ‘vacation’ and ‘exam’ be the result of different stress levels? Wound healing – Example Wound healing – Example Marucha et al. (1998) Psychosomatic medicine How are positive psychological factors related to health? Clinical relevance * Social support * Optimism Social support - example 73 HIV seropositive gay men were assessed for concealment of being gay, social support, depression and CD4-counts CD4 is a major predictor of prognosis in HIV Ullrich et al., 2003 Social support - example Philip et al., 2003 Clinical relevance * Social support * Optimism Wound healing – Example Is optimism positively or negatively related to health? Optimism Optimism is positively correlated to cellular immunity in controllable, brief and straightforward situations Optimism is inversely correlated with cellular immunity in uncontrollable, chronic and complex situations The latter may derive from optimists’ over- engagement in tasks, even if complex, they cannot ‘give up’ Segerstrom, 2005 In sum.. In sum Studies show that stress can have negative effects on our health (wound healing, colds/infections) Studies show that some psychological factors can be protective (social support and optimism) Segerstrom, 2005 Anxiety - (mal)adaptive? 46 Today’s lecture 47 GABA-A receptor 48 Anxiety and GABA Anxiety is too much activity in certain parts of the brain. GABA leads to CL- transportation into the cell making the cell more negative or hyperpolarized therefore less likely to generate action potential Thus inhibition of the neuron, less activity = less anxiety. 49 Indirect impact at the GABA receptor via the benzodiazepine binding site, Allosteric modulation of GABA via benzodiazepine by various drugs: effects can be positive (agonist) facilitating activity or negative (inverse agonist) inhibiting activity 50 Agonist: Benzodiazepine + GABA * Benzodiazepine + GABA enhance inflow of CL- * Cell is more negative, action potential is less likely * Inhibition of neuron, anxiety is reduced 51 Antagonist: flumazenil + GABA * Blocking the benzodiazepine binding site by flumazenil * Solely GABA binding will result in CL- induction (less then with benzodiazepines together) Flumazenil * There is no change in CL- inflow, no effect on anxiety 52 Indirect impact at the GABA receptor via the benzodiazepine binding site, Allosteric modulation of GABA via benzodiazepine by various drugs.. : effects can be positive (agonist) facilitating activity or negative (inverse agonist) inhibiting activity * Another drug attaches to the benzodiazepine binding site * GABA binding together with this inverse agonist results in a reduction in CL- induction * Cell is less negative, action potential is more likely * Less inhibition of neuron, anxiety is INDUCED 53 Full versus partial (inverse) agonist Full (inverse) agonist Partial (inverse) agonist 54 Response for each category CL- inflow 55 Barbiturates and benzodiazepines 56 Outline of this lecture 57 Serotonine Depression Anxiety Given the involvement of serotonine in both disorders a partial agonist when treating anxiety is benifical. 58 Outline of this lecture 59 Noradrenaline Alpha-2 adrenoceptors Blockage: increases release of noradrenaline Stimulation: decreases release of noredrenaline 60 In sum… 61

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