A Debate on the Causes of DepressionBefore 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: Post your original position statement. Respond with counterarguments to the original postings of two other learners. 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 Discussion Participation Scoring Guide. G.R.E.A.T. Discussions and Feedback With Checklist.




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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
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

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.
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
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
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
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.
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.
Study 1
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This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
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
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
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
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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