A Debate on the Causes of Depression

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Question Description

A Debate on the Causes of Depression

Before beginning, please read the complete instructions for this debate.

Statement of the Problem

A single cause of depression has not been identified; however, there is evidence to suggest the potential for a variety of causes stemming from different psychological perspectives. For example, the biological perspective suggests that depression is a result of family history (that is, a genetic link), a chemical imbalance in the brain (for example, depletion of the neurotransmitter serotonin), a specific medical condition (for example, underactive thyroid), or even increased levels of hormones (for example, cortisol—a stress hormone). The cognitive-behavioral perspective suggests that depression is directly influenced by faulty thinking such as low self-esteem, negative outlook on the world and the future, learned helplessness (that is, a perceived lack of control that leads to giving up), and influences based on one's gender, race, socioeconomic status, levels of social support and stress, or other environmental events (for example, divorce).

Based on your research into the causes of depression from your assigned perspective, debate the following:

  • Which comes first: Does a biochemical imbalance, medical condition, or change in hormone level cause changes in mood and faulty thinking, which leads to depression? Or do changes in mood and faulty thinking cause a biochemical imbalance, which then leads to depression?

Discussion Instructions

For this debate, you will:

  1. Post your original position statement.
  1. Respond with counterarguments to the original postings of two other learners.
  1. Respond with a rebuttal to each counterargument offered to your position statement.

Each time you post, you are expected to support your position, counterargument, or rebuttal with evidence from research. Remember to use APA citations and references to give proper credit to authors of information used to support your arguments.

Discussion Standards

In order to keep the discussion focused and clear, everyone will adopt a specific standard for their responses as follows:

  • Position statement: Position statements should include a discussion of the issue, a detailed description of the perspective, and three individual arguments you have developed to support your position. The standard for posting your position statement is as follows:
  • Subject line: Position Statement – Your Name.
  • Message box:
  • Describe the issue.
  • Describe the perspective you are championing.
  • Describe three arguments with evidence from research to support arguments for your perspective.
  • Counterargument: Post at least two counterarguments to opposing learners' positions. Each argument should include at least one piece of evidence to support it. The standard for posting your counterargument is as follows:
  • Subject line: Counterargument – Your Name.
  • Message:
  • Describe your counterargument to the stated position.
  • Provide at least one piece of evidence to support your counterargument.
  • Rebuttals: After you have posted counterarguments to the opposing perspective, go back to your original post and see who has posted counterarguments to your position and arguments. Provide a rebuttal to each counterargument posed by your classmates. The standard for posting your rebuttal is as follows:
  • Subject: Rebuttal – Your Name
  • Message:
  • Details of your refutation (rebuttal) to the counterargument.
  • Provide at least one piece of evidence to support your rebuttal.

To understand how this discussion will be graded, review the scoring guide.

Resources

Unformatted Attachment Preview

Learner Name: Debate Preparation and Summary Worksheet To prepare for the debate in Unit 5, use this worksheet to synthesize what you have learned from your research on the causes of depression. Complete Section 1 Debate Preparation to organize your position, arguments, and evidence for the debate. You will then complete Section 2 Debate Summary following the debate, and will turn the full worksheet in at the end of the Unit 6 for grading as a summary of the debate. Section 1 - Debate Preparation • Your Position Statement In the space below, construct a position statement that reflects your perspective on the cause of depression. Your position should include the following: • A description of the perspective you are taking (either biological or cognitive behavioral). • Write your position statement. • A brief summary of each argument that you will present to support your position (you should construct three arguments for your position). • Your Summary of the Arguments that Support Your Position and the Evidence From Research to Support Those Arguments. (Please include appropriate in-text citations for your evidence and then include the full reference in the reference list - #5 below). Include evidence from research for each argument. Supporting Argument 1: Evidence, example, illustration 1: Evidence, example, illustration 2: Evidence, example, illustration 3: Supporting Argument 2: Evidence, example, illustration 1: Evidence, example, illustration 2: Evidence, example, illustration 3: Supporting Argument 3: Evidence, example, illustration 1: Evidence, example, illustration 2: Evidence, example, illustration 3: Add additional supporting arguments as needed. (If you have more than three arguments, place them in the same format as the others here): Section 2 - Debate Summary • Counter Arguments to Your Position and Your Rebuttals – With what counter arguments did others challenge your position? How did you reply to challenge their counter arguments (these are your rebuttals). What opponents said to counter your arguments (paraphrase your understanding of their counter arguments—do not copy and paste them). Your rebuttals to the counter arguments that they made to you or could have made to you based on their positions. (Please cite any sources you used): Note: If you did not receive any counter arguments directly to your post, think about counter arguments presented to your peers that could also apply to yours. You may also use counter arguments that you have read in the literature. • Summary and Conclusion Section (use this section as a way to summarize the debate) • From the information from above, in one or two well-developed paragraphs, summarize in your own words the counter arguments opposing your position: • In one or two well-developed paragraphs, summarize your rebuttals to the counter arguments that opposed your position: • Write a statement and conclusion of why your position is the most valid and reasonable: • APA Reference List – Journal articles go in the following format: Author last name, initials of first and middle names (if provided). (Year of publication). Title of the article. Title of the Journal, volume(issue), page numbers. doi number if the article has one. Example of a reference for a journal article: Klassen, R. M., Perry, N. E., & Frenzel, A. C. (2012). Teachers’ relatedness with students: An underemphasized component of teachers’ basic psychological needs. Journal of Educational Psychology, 104(1), 150–165. doi: 10.1037/a0026253 Use this area below to format the references you used in the debate. References Journal of Abnormal Psychology 2013, Vol. 122, No. 2, 339 –352 © 2013 American Psychological Association 0021-843X/13/$12.00 DOI: 10.1037/a0031994 Rumination as a Mechanism Linking Stressful Life Events to Symptoms of Depression and Anxiety: Longitudinal Evidence in Early Adolescents and Adults Louisa C. Michl and Katie A. McLaughlin Kathrine Shepherd Boston Children’s Hospital, Harvard Medical School Kent State University This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Susan Nolen-Hoeksema Yale University Rumination is a well-established risk factor for the onset of major depression and anxiety symptomatology in both adolescents and adults. Despite the robust associations between rumination and internalizing psychopathology, there is a dearth of research examining factors that might lead to a ruminative response style. In the current study, we examined whether social environmental experiences were associated with rumination. Specifically, we evaluated whether self-reported exposure to stressful life events predicted subsequent increases in rumination. We also investigated whether rumination served as a mechanism underlying the longitudinal association between self-reported stressful life events and internalizing symptoms. Self-reported stressful life events, rumination, and symptoms of depression and anxiety were assessed in 2 separate longitudinal samples. A sample of early adolescents (N ⫽ 1,065) was assessed at 3 time points spanning 7 months. A sample of adults (N ⫽ 1,132) was assessed at 2 time points spanning 12 months. In both samples, self-reported exposure to stressful life events was associated longitudinally with increased engagement in rumination. In addition, rumination mediated the longitudinal relationship between self-reported stressors and symptoms of anxiety in both samples and the relationship between self-reported life events and symptoms of depression in the adult sample. Identifying the psychological and neurobiological mechanisms that explain a greater propensity for rumination following stressors remains an important goal for future research. This study provides novel evidence for the role of stressful life events in shaping characteristic responses to distress, specifically engagement in rumination, highlighting potentially useful targets for interventions aimed at preventing the onset of depression and anxiety. Keywords: rumination, stress, internalizing symptoms, depression, anxiety & Frederickson, 1993; Nolen-Hoeksema, Parker, & Larson, 1994), heightened risk for new onsets of major depression (Abela & Hankin, 2011; Just & Alloy, 1997; Nolen-Hoeksema, 2000; Robinson & Alloy, 2003), and greater chronicity of depressive episodes (Robinson & Alloy, 2003). Rumination is also associated with elevated risk for anxiety symptomology (Fresco, Frankel, Mennin, Turk, & Heimberg, 2002; Harrington & Blankenship, 2002; Mellings & Alden, 2000; Nolen-Hoeksema, 2000; NolenHoeksema & Morrow, 1991). In addition, experimentally inducing rumination in distressed individuals prolongs both depressed and anxious mood compared with inducing distraction (Blagden & Craske, 1996; McLaughlin, Borkovec, & Sibrava, 2007; NolenHoeksema et al., 1993). Despite the fact that rumination is among the most robust risk factors for depression and anxiety (Aldao, Nolen-Hoeksema, & Schweizer, 2010), we know very little about the factors that predict the development of a ruminative response style. Identifying such factors would not only improve our understanding of the etiology of a ruminative response style but also have important implications for designing preventive interventions. One factor that may increase engagement in rumination is the experience of stress, that is, social and environmental circumstances that require psychological Rumination involves repetitive and passive focus on the causes and consequences of one’s symptoms of distress without engagement in active coping or problem solving to alleviate dysphoric mood (Nolen-Hoeksema, 1991). Numerous studies suggest that the tendency to ruminate is associated prospectively with increases in depressive symptoms (Nolen-Hoeksema & Davis, 1999; NolenHoeksema, Larson, & Grayson, 1999; Nolen-Hoeksema, Morrow, Louisa C. Michl, Boston Children’s Hospital, Harvard Medical School; Katie A. McLaughlin, Department of Pediatrics & Psychiatry, Boston Children’s Hospital, Harvard Medical School; Kathrine Shepherd, Department of Psychology, Kent State University; Susan Nolen-Hoeksema, Department of Psychology, Yale University. Louisa C. Michl is now at the Department of Psychology, University of Rochester. We are deeply saddened that Susan Nolen-Hoeksema passed away before this article went to press. In addition to being a tremendous scholar, she was an inspiring, generous, and insightful collaborator. We will miss her terribly. Correspondence concerning this article should be addressed to Katie A. McLaughlin, 21 Autumn Street, Boston, MA 02115. E-mail: katie .mclaughlin@childrens.harvard.edu 339 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 340 MICHL, MCLAUGHLIN, SHEPHERD, AND NOLEN-HOEKSEMA and physiological adaptation over time by the organism (Monroe, 2008). The stress process involves a dynamic interaction between the organism and environment that changes over time in response to external challenges, perceptions of those challenges, and the coping resources that are activated following social and environmental challenges (Monroe, 2008). Conceptual models regarding the etiology of rumination argue that the experience of stressful life events might lead to rumination not only about those events but also about many areas of an individual’s life (NolenHoeksema, 1994; Nolen-Hoeksema et al., 1999). The current report examines this possibility. Control theories (Carver & Scheier, 1981; Martin & Tesser, 1996) provide the most direct explanation for how stressful experiences might lead to rumination (cf. Watkins, 2008). Negative events can create discrepancies between goals or desired states and one’s current state and lead to rumination about how to reduce such discrepancies (Carver & Scheier, 1981; Martin & Tesser, 1996). For example, receiving an unexpectedly low grade on a term paper may create a discrepancy with a student’s goal of doing well in a course, which in turn leads to rumination about this discrepancy. If the rumination leads to resolution of the discrepancy (e.g., the student decides the course is too difficult and decides to drop it), then the rumination will stop. If the discrepancy cannot be resolved, the individual may continue to ruminate about it. Uncontrollable or chronic stressors may be especially likely to lead to rumination because they create discrepancies between the individual’s current state and his or her goals or desired states (e.g., happiness) that cannot be resolved (Watkins, 2008). Indeed, one study of bereaved adults found that those who reported greater chronic stress showed increased rumination over time (NolenHoeksema et al., 1994). Similarly, in an experience sampling study of individuals facing stigma-related stressors due to race or sexual orientation, engagement in rumination was higher on days when stigma-related stressors were experienced (Hatzenbuehler, NolenHoeksema, & Dovidio, 2009). Stress may also induce rumination by undermining selfregulation, or the capacity to engage in self-control over one’s behavior (Baumeister, Gailliot, DeWall, & Oaten, 2006; Inzlicht, McKay, & Aronson, 2006). Limited regulatory abilities may impair an individual’s ability to engage in problem solving or active coping and increase the likelihood of engagement in rumination. Indeed, various studies have shown that active coping strategies such as problem solving are negatively correlated with rumination (see review by Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008). A variety of other cognitive mechanisms might also increase the likelihood of rumination following stressful life events, including attention to negative thoughts and feelings, autobiographical memory for previous negative events, and negative self-schema activation (Scher, Ingram, & Segal, 2005; Segal & Ingram, 1994). Slavich’s psychobiological theory of depression (Slavich, O’Donovan, Epel, & Kemeny, 2010) provides an additional conceptual framework linking experiences of stress—particularly interpersonal stressors involving social rejection—to engagement in rumination. This theory proposes that social rejection stressors elicit a coordinated pattern of cognitive, emotional, and neurobiological responses that culminate in heightened risk for depression (Slavich, O’Donovan, et al., 2010). In particular, social rejection is associated with activa- tion in brain regions involved in emotional awareness and emotion regulation (Beauregard, Lévesque, & Bourgouin, 2001; Lane et al., 1998; Ochsner & Gross, 2005; Slavich, Way, Eisenberger, & Taylor, 2010; Somerville, Heatherton, & Kelley, 2006) that are activated during self-reflection (Johnson et al., 2006). Thus, brain regions that are sensitive to social rejection stressors are also centrally involved in the core selfreflective process that underlies rumination, suggesting a potential neurobiological mechanism linking interpersonal stressors to increased engagement in rumination. Like rumination, stressful life events consistently predict the onset of major depression and anxiety disorders (Brown, 1993; Hammen, 2005; Kendler, Hettema, Butera, Gardner, & Prescott, 2003; Kendler, Karkowski, & Prescott, 1999), and it is possible that rumination represents a mechanism that explains the relationship between stress exposure and the onset of internalizing psychopathology. Early studies with individuals who had experienced stressors such as a natural disaster (Nolen-Hoeksema & Morrow, 1991) or bereavement (Nolen-Hoeksema et al., 1994) found that those who were prone to ruminate had more severe and longer periods of negative mood following these events than those not prone to ruminate. However, these studies did not directly examine rumination as a mechanism linking stress to internalizing symptoms. More recently, evidence from an experience sampling study suggested that engagement in rumination partially mediates the association between negative life events and negative affect (Moberly & Watkins, 2008). Similarly, rumination was found to mediate the relationship between stigma-related stressors and psychological distress (Hatzenbuehler et al., 2009). Yet, the extent to which rumination explains the association between stressful events and symptoms of psychopathology is not well understood. The purpose of the current study was twofold: (a) to examine the role of self-reported stressful life events as a predictor of changes in rumination over time, and (b) to determine whether rumination is a mechanism linking self-reported stressful life events to subsequent increases in symptoms of depression and anxiety. We expected that self-reported stress exposure would be associated prospectively with increases in rumination, such that individuals reporting greater stress exposure would show greater increases in rumination over time than those reporting less stress exposure. We additionally predicted that increases in rumination following self-reported exposure to stress would mediate the relationship between reported stressful life events and increases in symptoms of depression and anxiety over time. To evaluate these hypotheses, we examined the association between self-reported stressful life events, rumination, and symptoms of depression and anxiety in two longitudinal studies: one using a school-based sample of early adolescents and one based on a community sample of adults. Finally, given substantial gender differences in rumination (Nolen-Hoeksema, 1991) and in the prevalence of symptoms of depression and anxiety beginning in adolescence (Hankin et al., 1998; NolenHoeksema & Girgus, 1994; Twenge & Nolen-Hoeksema, 2002), we examined whether the relationships between self-reported stressful life events, rumination, and symptoms of depression and anxiety varied by gender. STRESS AND RUMINATION Study 1 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Method Participants and procedure. Adolescents were recruited from the total enrollment of two middle schools (Grades 6 – 8) in central Connecticut that agreed to participate in the study, excluding students in self-contained special education classrooms and technical programs who did not attend school for the majority of the day. The schools were located in a small urban community (metropolitan population of 71,538). Schools were selected for the study on the basis of demographic characteristics of the school district and their willingness to participate. The parents of all eligible children (N ⫽ 1,567) in the participating middle schools were asked to provide active consent for their children to participate in the study. Parents who did not return written consent forms to the school were contacted by telephone. Twenty-two percent of parents did not return consent forms and could not be reached to obtain consent, and 6% of parents declined to provide consent. Adolescent participants provided written assent. The overall participation rate in the study at baseline was 72%. The baseline sample included 51.2% (n ⫽ 545) boys and 48.8% (n ⫽ 520) girls. Participants were evenly distributed across grade level (mean age ⫽ 12.2 years, SD ⫽ 1.0). The race/ethnicity composition of the sample was as follows: 13.2% (n ⫽ 141) non-Hispanic White, 11.8% (n ⫽ 126) non-Hispanic Black, 57.3% (n ⫽ 610) Hispanic/Latino, 2.3% (n ⫽ 24) Asian/Pacific Islander, 0.2% (n ⫽ 2) Native American, 0.8% (n ⫽ 9) Middle Eastern, 9.4% (n ⫽ 100) biracial/multiracial, and 4.2% (n ⫽ 45) other racial/ethnic groups. Several students (n ⫽ 8, 0.8%) did not provide information on race/ethnicity. Twenty-seven percent (n ⫽ 293) of participants reported living in single-parent households. The participating middle schools reside in a predominantly lower socioeconomic status community, with a per capita income of $18,404 (Connecticut Department of Education, 2006, based on data from 2001). School records indicated that 62.3% of students qualified for free or reduced lunch in the 2004 –2005 school year. There were no differences across the two schools in demographic variables. Two additional assessments took place after the baseline assessment. Of the participants who were present at baseline, 221 (20.8%) did not participate at the Time 2 assessment, and 217 (20.4%) did not participate at the Time 3 assessment, largely due to transient student enrollment in the district. Over the 4-year period from 2000 to 2004, 22.7% of students had left the school district (Connecticut Department of Education, 2006). Participants who completed the baseline but not both follow-up assessments (n ⫽ 1,065) were more likely to be girls, ␹2(1) ⫽ 6.85, p ⬍ .01, but did not differ in grade level, race/ethnicity, or being from a single-parent household (ps ⬎ .10). Participants who did not complete at least one of the follow-up assessments did not differ from participants who completed all three assessments on levels of rumination or symptoms of depression or anxiety symptoms at baseline (ps ⬎ .10). Participants completed study questionnaires during their homeroom period. All questionnaires used in the present analyses were administered at Time 1 and Time 3, and the rumination measure was additionally administered at Time 2. Four months elapsed 341 between the Time 1 (November 2005) and Time 2 (March 2006) assessments, and 3 months elapsed between Time 2 and Time 3 (June 2006) assessments. This timefra ...
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steffveny
School: Purdue University

Hey there. It was great working on the order and I look forward to working with you again
Hey there. It was great working on the order and I look forward to work with you again. You can use this final document as its more refined

Learner Name:
Debate Preparation and Summary Worksheet
Section 1 - Debate Preparation


Your Position Statement


Description of the perspective

Many researchers associate the causes of depression to biochemical characteristics
like chemical, hormonal imbalance and medical condition or cognitive behavioral in
nature where depression is associated with low self-esteem, stress and social
support or influences of environmental, gender, socio-economic status. Although
both factors are associated with depression, cognitive-behavioral factors come first
and they trigger the biochemical imbalances associated with causing depression. A
dearth of research studies attribute depression with stress and rumination which are
cognitive factors influenced by social environment, social support and exposure to
stressful events.


Position Statement

I believe depression is caused mainly by the cognitive behavioral factors like
stressful environment, lack of social support, self-evaluation which then trigger
biochemical imbalances resulting in depression.


Summary of Arguments

The causes of depression are greatly cognitive because of three main reasons.
Firstly, lack of a strong support structure because affects self-evaluation which
subsequently leads to depression. Secondly, exposure to stressful events leads to
discrepancies between ones goals and reality which can lead to rumination and
depression. Stress can also interpersonal stressors affect brain regions responsible for
emotio...

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