Stress responses ******* I have all the notes from the textbook in a file to use but need to alternative scholary sources

· What physiological changes occur in the brain due to the stress response?

· What emotional and cognitive effects might occur due to this stressful situation?

· Would the above changes (physiological, cognitive, or emotional) be any different if the same stress were being experienced by a person of the opposite sex or someone much older or younger than you?

· If the situation continues, how might your physical health be affected?

· What three behavioral strategies would you implement to reduce the effects of this stressor? Describe each strategy. Explain how each behavior could cause changes in brain physiology (e.g., exercise can raise serotonin levels).

· If you were encouraging an adult client to make the above changes, what ethical considerations would you have to keep in mind? How would you address those ethical considerations?

In addition to citing the online course and the text, you are also required to cite a minimum of two scholarly sources. Please see the Academic Resources section under Course Home to use the Argosy University online library to find appropriate scholarly sources. For reputable web sources, look for .gov or .edu sites as opposed to .com sites. Please do not use Wikipedia.

Your paper should be double-spaced, in 12-point Times New Roman font, and with normal 1-inch margins; written in APA style; and free of typographical and grammatical errors. It should include a title page with a running head, an abstract, and a reference page. The body of the paper should be at least 6 pages in length

Stress hormones increase blood pressure and have various other effects on the body that might not be adaptive over long periods.

Selye proposed the concept of the general adaptation syndrome to account for the effect of stress on the body

Currently, there are two primary systems for the classification of psychological disorders—The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) (American Psychiatric Association, 2013), and The International Statistical Classification of Diseases and Related Health Problems (ICD) (World Health Organization, 1992).

Major depressive disorder is characterized by a lowering of mood, energy, and activity that results in significant distress or impairment in life. There is much research focusing on imbalances in the monoamine neurotransmitters (dopamine, norepinephrine, and serotonin) in people suffering from depressive disorders

In the brain, the amygdala and the anterior cingulate cortex show structural and functional abnormalities in people with depression.

Bipolar disorder is characterized by an extremely elevated mood with increases in activity and energy (manic phase) followed by an equally low mood with decreases in activity and energy (depressive phase), resulting in significant distress or impairment. Typically, in people with bipolar disorder, the higher their manic phase, the lower the successive depressive phase will be

Anxiety disorders such as panic disorder, specific phobias, and social anxiety disorder feature a heightened autonomic nervous system response that is above and beyond what would be considered normal when faced with the object or situation that the person reacts to.

In general, anxiety disorders have been linked to underactive gamma-aminobutyric acid (GABA) in the brain, resulting in overexcitability of the amygdala and the anterior cingulate cortex. Additionally, genetic research shows that anxiety disorders demonstrate a clear pattern of genetic predisposition

Obsessive compulsive disorder is characterized by repetitive thoughts and behaviors that result in significant distress or impairment in life. Common obsession and compulsion pairings include contamination/washing, harm/checking, and perfectionism/ordering and hoarding. There is much research demonstrating the genetic inheritance of obsessive–compulsive disorder. While early research showed that dopamine and serotonin are involved in obsessive–compulsive disorder, recent research suggests that glutamate may also play an important role in the disorder. Obsessive–compulsive disorder seems to be mediated by overactivity in the orbitofrontal cortex

Medications for psychological disorders are often categorized by function:

· Some medications tend to decrease psychotic experiences, such as hearing voices and delusional thinking. These medications are called antipsychotics, and we discussed them in the earlier modules' lectures.

· Antidepressants are medications that reduce depression.

· Mood stabilizers are also frequently used for patients who experience depression and periodic emotional highs.

Antianxiety drugs reduce panic and anxiety. These medications are used together with psychotherapy or counseling. But, sometimes, these drugs are used by themselves.

Counseling is also recommended as a treatment for most psychological disorders, either alone or in conjunction with pharmacotherapy. While access to mental health care has been limited in the past, the Mental Health Parity and Addiction Equity Act, which went into effect in January 2010, has reduced barriers for those covered by group health insurance plans (US Department of Health and Human Services, 2010

fear has three important qualities: It is the easiest emotion to infer from behavior in various species; it plays an important adaptive function in motivating the avoidance of threatening situations; and chronic fear induces stress.

(Pinel 443)

Pinel, John P. Biopsychology, 8th Edition. Pearson Learning Solutions, 10/2010. VitalBook file.

It was apparent that the damage to Gage’s brain affected both medial prefrontal lobes, which we now know are involved in planning and emotion (see Machado & Bachevalier, 2006; Vogt, 2005).

(Pinel 443-444)

Darwin developed a theory of the evolution of emotional expression that was composed of three main ideas:

• Expressions of emotion evolve from behaviors that indicate what an animal is likely to do next.

• If the signals provided by such behaviors benefit the animal that displays them, they will evolve in ways that enhance their communicative function, and their original function may be lost.

• Opposite messages are often signaled by opposite movements and postures, an idea called the principle of antithesis.

(Pinel 444)

The first physiological theory of emotion was proposed independently by James and Lange in 1884. According to the James-Lange theory , emotion-inducing sensory stimuli are received and interpreted by the cortex, which triggers changes in the visceral organs via the autonomic nervous system and in the skeletal muscles via the somatic nervous system. Then, the autonomic and somatic responses trigger the experience of emotion in the brain.

(Pinel 444)

James and Lange argued that the autonomic activity and behavior that are triggered by the emotional event (e.g., rapid heartbeat and running away) produce the feeling of emotion, not vice versa.

(Pinel 444)

1915, Cannon proposed an alternative to the James-Lange theory of emotion, and it was subsequently extended and promoted by Bard. According to the Cannon-Bard theory , emotional stimuli have two independent excitatory effects: They excite both the feeling of emotion in the brain and the expression of emotion in the autonomic and somatic nervous systems. That is, the Cannon-Bard theory, in contrast to the James-Lange theory, views emotional experience and emotional expression as parallel processes that have no direct causal relation.

(Pinel 444-445)

biopsychological view. According to this view, each of the three principal factors in an emotional response—the perception of the emotion-inducing stimulus, the autonomic and somatic responses to the stimulus, and the experience of the emotion—can influence the other two

(Pinel 445)

In 1937, Papez (pronounced “Payps”) proposed that emotional expression is controlled by several interconnected nuclei and tracts that ring the thalamus

(Pinel 446)

key structures in this circuit, now known as the limbic system ( limbic means “border”): the amygdala, mammillary body, hippocampus, fornix, cortex of the cingulate gyrus, septum, olfactory bulb, and hypothalamus. Papez proposed that emotional states are expressed through the action of the other structures of the circuit on the hypothalamus and that they are experienced through their action on the cortex. Papez’s theory of emotion was revised and expanded by Paul MacLean in 1952 and became the influential limbic system theory of emotion.

(Pinel 446)

autonomic nervous system (ANS) in emotion has focused on two issues: the degree to which specific patterns of ANS activity are associated with specific emotions and the effectiveness of ANS measures in polygraphy (lie detection)

(Pinel 446)

The hypothesis that our facial expressions influence our emotional experience is called the facial feedback hypothesis .

(Pinel 448)

The subjects reported that the slides made them feel more happy and less angry when they were making happy faces, and less happy and more angry when they were making angry faces

(Pinel 448)

Most biopsychological research on emotion has focused on fear and defensive behaviors. Fear is the emotional reaction to threat; it is the motivating force for defensive behaviors. Defensive behaviors are behaviors whose primary function is to protect the organism from threat or harm. In contrast, aggressive behaviors are behaviors whose primary function is to threaten or harm.

(Pinel 450)

The fact that social aggression in many species occurs more commonly among males than among females is usually explained with reference to the organizational and activational effects of testosterone. The brief period of testosterone release that occurs around birth in genetic males is thought to organize their nervous systems along masculine lines and hence to create the potential for male patterns of social aggression to be activated by the high testosterone levels that are present after puberty.

(Pinel 452)

LeDoux and his colleagues began their search for the neural mechanisms of auditory fear conditioning by making lesions in the auditory pathways of rats. They found that bilateral lesions to the medial geniculate nucleus (the auditory relay nucleus of the thalamus) blocked fear conditioning to a tone, but bilateral lesions to the auditory cortex did not. This indicated that for auditory fear conditioning to occur, it is necessary for signals elicited by the tone to reach the medial geniculate nucleus but not the auditory cortex. It also indicated that a pathway from the medial geniculate nucleus to a structure other than the auditory cortex plays a key role in fear conditioning. This pathway proved to be the pathway from the medial geniculate nucleus to the amygdala. Lesions of the amygdala, like lesions of the medial geniculate nucleus, blocked fear conditioning. The amygdala receives input from all sensory systems, and it is believed to be the structure in which the emotional significance of sensory signals is learned and retained

(Pinel 453)

Several pathways (see Balleine & Killcross, 2006; LaBar, 2007) carry signals from the amygdala to brain-stem structures that control the various emotional responses. For example, a pathway to the periaqueductal gray of the midbrain elicits appropriate defensive responses (see Bandler & Shipley, 1994), whereas another pathway to the lateral hypothalamus elicits appropriate sympathetic responses.

(Pinel 453)

Environments, or contexts , in which fear-inducing stimuli are encountered can themselves come to elicit fear. For example, if you repeatedly encountered a bear on a particular trail in the forest, the trail itself would elicit fear in you. The process by which benign contexts come to elicit fear through their association with fear-inducing stimuli is called contextual fear conditioning .

(Pinel 453)

When the body is exposed to harm or threat, the result is a cluster of physiological changes that is generally referred to as the stress response—or just stress . All stressors (experiences that induce the stress response) produce the same core pattern of physiological changes, whether psychological (e.g., dismay at the loss of one’s job) or physical (e.g., long-term exposure to cold). However, it is chronic psychological stress that has been most frequently implicated in ill health (see Kiecolt Glaser et al., 2002; Natelson, 2004),

(Pinel 454)

Selye attributed the stress response to the activation of the anterior-pituitary adrenal-cortex system. He concluded that stressors acting on neural circuits stimulate the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary, that the ACTH in turn triggers the release of glucocorticoids from the adrenal cortex , and that the glucocorticoids produce many of the components of the stress response (see Erickson, Drevets, & Schulkin, 2003; Schulkin, Morgan, & Rosen, 2005). The level of circulating glucocorticoids is the most commonly employed physiological measure of stress.

(Pinel 455)

, stressors activate the sympathetic nervous system, thereby increasing the amounts of epinephrine and norepinephrine released from the adrenal medulla . Most modern theories of stress acknowledge the roles of both the anterior-pituitary adrenal-cortex system and the sympathetic-nervous-system adrenal-medulla system (see Gunnar & Quevedo, 2007; Ulrich-Lai & Herman, 2009).

(Pinel 455)

There is good evidence that all kinds of common psychological stressors—such as losing a job, taking a final exam, or ending a relationship—act like physical stressors.

(Pinel 455)

Stress responses are complex and varied, with the exact response depending on the stressor, its timing, the nature of the stressed person, and how the stressed person reacts to the stressor (e.g., Joëls & Baram, 2009; Miller, Chen, & Zhou, 2007; Smith, 2006).

(Pinel 455)

In the 1990s, there was an important advance in the understanding of the stress response (see Fleshner & Laudenslager, 2004). It was discovered that brief stressors produce physiological reactions that participate in the body’s inflammatory responses. Most notably, it was found that brief stressors produced an increase in blood levels of cytokines , a group of peptide hormones that are released by many cells and participate in a variety of physiological and immunological responses, causing inflammation and fever. The cytokines are now classified with the adrenal hormones as major stress hormones

(Pinel 455)

Responses to extreme stress tend to mask normal variations in the stress response, and it is difficult to relate the results of such studies to common human stressors (see Fleshner & Laudenslager, 2004; Koolhass, de Boer, & Buwalda, 2006).

(Pinel 455)

Interest in pathological effects of stress has increased as researchers have identified more and more psychosomatic disorders (medical disorders that have psychological causes). So many adverse effects of stress on health (e.g., in heart disease, asthma, and skin disorders) have been documented that it is now more reasonable to think of most, if not all, medical disorders as psychosomatic (Miller & Blackwell, 2006; Wargo, 2007).

(Pinel 456)

Gastric ulcers were one of the first medical disorders to be classified as psychosomatic. Gastric ulcers are painful lesions to the lining of the stomach and duodenum, which in extreme cases can be life-threatening. About 500,000 new cases are reported each year in the United States.

(Pinel 456)

Apparently, there is another factor that increases the susceptibility of the stomach wall to damage from H. pylori, and this factor appears to be stress. Gastric ulcers occur more commonly in people living in stressful situations, and stressors produce gastric ulcers in laboratory animals.

(Pinel 456)

The discovery that stress can increase susceptibility to infection led in the early 1980s to the emergence of a new field of research: psychoneuroimmunology —the study of interactions among psychological factors, the nervous system, and the immune system (see Fleshner & Laudenslager, 2004). Psychoneuroimmunological research is the focus of this subsection.

(Pinel 456)

Segerstrom and Miller found that the effects of stress on immune function depended on the kind of stress. They found that acute (brief) stressors (i.e., those lasting less than 100 minutes, such as public speaking, an athletic competition, or a musical performance) actually led to improvements in immune function.

(Pinel 458)

In contrast, chronic (long-lasting) stressors, such as caring for an ill relative or experiencing a period of unemployment, adversely affected the adaptive immune system. Stress that disrupts health or other aspects of functioning is called distress, and stress that improves health or other aspects of functioning is called eustress.

(Pinel 458)

Stress produces widespread changes in the body through its effects on the anterior-pituitary adrenal-cortex system and the sympathetic-nervous-system adrenal-medulla system, and there are innumerable mechanisms by which these systems can influence immune function.

(Pinel 459)

Conversely, cytokines, originally thought to be produced only by cells of the immune system, have been found to be produced in the nervous system (Salzet, Vieau, & Day, 2000). In short, the physiological mechanisms by which the nervous system and the immune system can interact are innumerable.

(Pinel 459)

people under severe stress often change their diet, exercise, sleep, and drug use, any of which could influence immune function. Also, the behavior of a stressed or ill person can produce stress and illness in others. For example, Wolf and colleagues (2007) found that stress in mothers aggravates asthmatic symptoms in their children; conversely, asthma in the children increases measures of stress in their mothers.

(Pinel 459)

The immune system seems to have many redundant components; thus, disruption of one of them may have little or no effect on vulnerability to infection.

• Stress-produced changes in immune function may be too short-lived to have substantial effects on the probability of infection.

• Declines in some aspects of immune function may induce compensatory increases in others.

(Pinel 459)

Early exposure to severe stress can have a variety of adverse effects on subsequent development. Children subjected to maltreatment or other forms of severe stress display a variety of brain and endocrine system abnormalities (Evans & Kim, 2007; Teicher et al., 2003)

(Pinel 459)

Also, early exposure to stress often increases the intensity of subsequent stress responses (e.g., increases the subsequent release of glucocorticoids in response to stressors).

(Pinel 459)

I hope you remember from earlier chapters that traits can be passed from parents to off-spring by epigenetic mechanisms—literally, epigenetic means “not of the genes.”

(Pinel 460)

Exposure to stress affects the structure and function of the brain in a variety of ways (see Rodrigues, LeDoux, & Sapolsky, 2009). However, the hippocampus is particularly susceptible to stress-induced effects. The reason for this susceptibility may be the particularly dense population of glucocorticoid receptors in the hippocampus (see McEwen, 2004).

(Pinel 460)

Stress has been shown to reduce dendritic branching in the hippocampus, to reduce adult neurogenesis in the hippocampus, to modify the structure of some hippocampal synapses, and to disrupt the performance of hippocampus-dependent tasks (see Sandi, 2004). These effects of stress on the hippocampus appear to be mediated by elevated glucocorticoid levels: They can be induced by corticosterone (a major glucocorticoid) and can be blocked by adrenalectomy (surgical removal of the adrenal glands)—see Brummelte, Pawluski, and Galea (2006), Gould (2004), and McEwen (2004).

(Pinel 460)

Cognitive neuroscience is currently the dominant approach being used to study the brain mechanisms of human emotion. There have been many functional brain-imaging studies of people experiencing or imagining emotions or watching others experiencing them. These studies have established three points that have advanced our understanding of the brain mechanisms of emotion in fundamental ways (see Bastiaansen, Thioux, & Keysers, 2009; Niedenthal, 2007):

• Brain activity associated with each human emotion is diffuse—there is not a center for each emotion. Think “mosaic,” not “center,” for locations of brain mechanisms of emotion.

• There is virtually always activity in motor and sensory cortices when a person experiences an emotion or empathizes with a person experiencing an emotion (see Figure 17.13).

• Very similar patterns of brain activity tend to be recorded when a person experiences an emotion, imagines that emotion, or sees somebody else experience that emotion.

(Pinel 461)

the activity observed in sensory and motor cortex during the experience of human emotions is now believed to be an important part of the mechanism by which the emotions are experienced. The re-experiencing of related patterns of motor, autonomic, and sensory neural activity during emotional experiences is generally referred to as the embodiment of emotions (see Niedenthal, 2007).

(Pinel 461)

The discovery that certain patterns of brain activity are observed on fMRI scans when individuals experience an emotion or watch somebody else experience the same emotion suggests that a mirror-like system might be the basis for human empathy (Fabbri-Destro & Rizzolatti, 2008; Iacoboni, 2009; Keysers & Gazzola, 2009; Oberman & Ramachandran, 2007).

(Pinel 461)

Emotion and cognition are often studied independently, but it is now believed that they are better studied as components of the same system (Phelps, 2004, 2006; Beer, Knight, & Esposito, 2006). The medial portions of the prefrontal lobes (including the medial portions of the orbitofrontal cortex and cingulate cortex) are the sites of emotion-cognition interaction that have received the most attention

(Pinel 462)

The medial prefrontal lobes have been hypothesized to monitor the difference between outcome and expectancy (Potts et al., 2006), to respond to personal choices that result in losses (Gehring & Willoughby, 2002), to predict the likelihood of error (Brown & Braver, 2005), to guide behavior based on previous actions and outcomes (Kennerly et al., 2006), and to respond to social rejection (Somerville, Heatherton, & Kelley, 2006). Which hypothesis is correct? Perhaps all are; the medial prefrontal lobes are large and complex, and they likely perform many functions. This point was made by Kawasaki and colleagues (2005).

(Pinel 462-463)

This confirms previous research linking the medial prefrontal lobes with negative emotional reactions, but it also shows that not all neurons in the area perform the same function—neurons directly involved in emotional processing appear to be sparse and widely distributed in the human brain.

(Pinel 463)

There is considerable evidence that emotional functions are lateralized, that is, that the left and right cerebral hemispheres are specialized to perform different emotional functions (e.g., Kim et al., 2004; Shaw et al., 2005)—as you learned in Chapter 16. This evidence has led to several theories of the cerebral lateralization of emotion (see Demaree et al., 2005);

(Pinel 463)

The right-hemisphere model of the cerebral lateralization of emotion holds that the right hemisphere is specialized for all aspects of emotional processing: perception, expression, and experience of emotion.

• The valence model proposes that the right hemisphere is specialized for processing negative emotion and the left hemisphere is specialized for processing positive emotion.

(Pinel 463)

the cortical localization of language processes varies substantially from person to person. Nevertheless, few studies of the neural mechanisms of emotion have focused on individual differences (see Leppänen & Nelson, 2009; Samanez-Larkin et al., 2008).

(Pinel 463-464)

Canli and colleagues (2002) used functional MRIs to compare the reactions of healthy participants who scored high on extraversion with those of healthy participants who scored high on neuroticism. These personality dimensions were selected because of their relation to emotion—people high on the extraversion scale have a tendency toward positive emotional reaction; people high on the neuroticism scale have a tendency toward negative emotional reaction. Although all the participants displayed increased activity in the amygdala when viewing fearful faces, only the extraverts displayed increased amygdalar activity when viewing happy faces.

(Pinel 464)

http://www2.byui.edu/CounselingCenter/Physiological%20Changes%20that%20Occur%20During%20the%20Stress%20Response%20(2).pdf d