Capella University Causes of Depression Analysis By successfully completing this assignment, you will demonstrate your proficiency in the following course

Capella University Causes of Depression Analysis By successfully completing this assignment, you will demonstrate your proficiency in the following course competencies and assignment criteria:
Competency 1: Apply information literacy and library research skills to obtain scholarly information in the field of psychology.

Provide the APA citations for two scholarly articles that support a position on the causes of depression.

Competency 2: Apply psychological principles to topics in psychology.

Identify the arguments each author uses to support his or her point of view and the quality of the evidence used to support the arguments.

Competency 3: Analyze scholarly information and research findings through critical thinking to solve problems in the field of psychology.

Describe the authors’ points of view and purpose in writing each article.
Identify multiple assumptions that the authors make.
Describe each author’s conclusions in the article and the implications of those conclusions.

Competency 4: Apply ethical principles and standards to topics in psychology.

Explain the ethical implications of the research and findings.

Competency 5: Communicate in a manner that is scholarly, professional, and consistent with expectations for professionals in the field of psychology.

Write in a manner that is scholarly in tone, easy to follow, and free from grammatical and spelling errors.

For this assignment, you will analyze two scholarly research articles concerning the causes of depression. To help you with your position and arguments for the Unit 5 debate discussion and Unit 6 paper on the causes of depression, select two articles that relate to the side you will take in the debate.The worksheet is similar to the article analysis you completed in Unit 2. In addition to the elements of purpose, point of view, assumptions, arguments, and evidence, for this worksheet, you will provide APA references and consider the inferences, conclusions, and implications of the findings from the research.You may select one article from the debate resources in this unit’s studies. You will choose the second article from the Capella library. If you do not find an article that you would like to use in the debate resources list, you may choose two from the Capella library:
After selecting and reading your articles, complete the Causes of Depression Issue Analysis Worksheet.
Submit a draft of your worksheet to SafeAssign and revise your work as needed.
Finally, submit your worksheet to your instructor for grading. Causes of Depression Issue Analysis Worksheet
Causes of Depression Issue Analysis Worksheet
Purpose: The Causes of Depression Analysis Worksheet’s purpose is to guide your steps in analyzing the resources from the
resource list in the Unit 4 studies and Capella Library regarding the cause of depression from the perspective you have chosen to
research. This worksheet will lead you through the research process by providing a systematic way to analyze the resources you
have chosen to research. As you review resources, you will use the worksheet to analyze the authors’ positions on the issue and the
arguments they present to support their positions. To fill out the worksheet, work your way down through the analysis components for
each individual article and record your analysis for each component in the cell under the title of the article you are reviewing. You will
submit your Causes of Depression Analysis Worksheet to the Unit 4 assignment.
Learner Name:
Name of Perspective:
Causes of Depression Research Articles
Analysis Components
APA reference for article:
APA reference for article:
The main purpose of this article is:
[State as accurately as possible the
author’s purpose for writing the article.
What is the author’s position or point of
view?]
The main arguments that the author
is making are: [Determine the main
arguments the author makes to support
their position.]
The evidence or facts the author
1
Causes of Depression Issue Analysis Worksheet
uses in this article to support their
arguments are: Identify the facts, data,
or resources the author uses to support
his or her argument.
The main conclusion[s] and
inference[s] in this article are:
[Identify the key conclusions the author
comes to and presents in the article.]
The main assumptions underlying
the author’s thinking are: [Think about
what the author is assuming to be true
and what might be questioned. To
expand on this statement, you will need
to think about the larger context of the
topic.]
If we accept the author’s line of
reasoning, the implications are: [What
consequence does the author’s
argument have on our understanding of
current research and theory?]
If we reject the author’s line of
reasoning, the implications are:
[What consequence does rejecting the
author’s argument have on our
understanding of current research and
theory?]
The ethical implications of the
research and findings are:
[What ethics were addressed in the
research, or what ethics would need to
be addressed in implementing the
research findings?]
2
Causes of Depression Issue Analysis Worksheet
3
Journal of Child Psychology and Psychiatry 51:6 (2010), pp 734–744
doi:10.1111/j.1469-7610.2010.02205.x
Genetic and environmental influences on the
transmission of parental depression to
children’s depression and conduct disturbance:
an extended Children of Twins study
Judy L. Silberg, Hermine Maes, and Lindon J. Eaves
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human and Molecular Genetics, Virginia
Commonwealth University, Richmond, VA, USA
Background: Despite the increased risk of depression and conduct problems in children of depressed
parents, the mechanism by which parental depression affects their children’s behavioral and emotional
functioning is not well understood. The present study was undertaken to determine whether parental
depression represents a genuine environmental risk factor in children’s psychopathology, or whether
children’s depression/conduct can be explained as a secondary consequence of the genetic liability
transmitted from parents to their offspring. Methods: Children of Twins (COT) data collected on 2,674
adult female and male twins, their spouses, and 2,940 of their children were used to address whether
genetic and/or family environmental factors best account for the association between depression in
parents and depression and conduct problems in their children. Data collected on juvenile twins from
the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate
child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated
using the statistical program Mx. Results: The most compelling model for the association between
parental and juvenile depression was a model of direct environmental risk. Both family environmental
and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions: These findings illustrate how a genetically mediated behavior such as parental
depression can have both an environmental and genetic impact on children’s behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic
liability influences both parental depression and juvenile conduct disturbance, implicating child
conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary,
our analyses demonstrate differences in the impact of parental depression on different forms of child
psychopathology, and at various stages of development. Keywords: Children of Twins, parental
depression, juvenile depression, conduct disturbance, genetic risk, family environment.
It has been well established that a family history of
depression is an important predictor of emotional
and behavioral problems in children (Merikangas,
Prusoff, & Weissman, 1988; Beardslee, 1996; Harrington, 1996; Kim-Cohen, Caspi, Rutter, Tomas, &
Moffit, 2006; Pilowsky et al., 2008). Despite convincing evidence for parent to offspring transmission, the processes by which parental depression
increases children’s risk are not yet fully understood.
Psychosocial theories postulate that impaired
parenting best accounts for the inter-generational
link between mother’s depression and children’s
psychopathology (Johnson, Cohen, Kasen, Smailes,
& Brook, 2001; Elgar, Mills, McGrath, Waschbusch,
& Brownridge, 2007). Depressed mothers have been
described as more inconsistent, insensitive, inattentive, and less psychologically available to their
children (Cox, Puckering, Pound, & Mills, 1987;
Goodman & Brumley, 1990; Burt et al., 2005).
A depressogenic parenting style characterized by
hostility, irritability, and enmeshment (Parker,
Conflict of interest statement: No conflicts declared.
Tupling, & Brown, 1979) has been shown to be a
significant risk factor for children (Weissman &
Paykel, 1974; Radke-Yarrow, 1998; Hammen et al.,
1987) and lack of parental warmth and overprotectiveness are predicted by a history of depression (Kendler, 1996). Given the pervasive difficulties
experienced by depressed parents in providing an
optimal rearing environment, it is not clear whether
the problems exhibited in the children are a unique
consequence of the parent’s depression or a consequence of the myriad parenting factors associated
with it. Moreover, despite psychosocial theories
suggesting the risk to children is environmental,
it has yet to be shown unequivocally whether
children’s behavioral and emotional problems arise
from the direct environmental impact of parental
treatment or through some form of genetic mediation. It is possible that certain aspects of the
so-called parental environment are not truly
environmental, but indicators of genetic risk that is
transmitted from parents to their offspring. Studies
showing that recurrence and severity of maternal
depression, and not necessarily its timing, are most
2010 The Authors
Journal compilation 2010 Association for Child and Adolescent Mental Health.
Published by Blackwell Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA
Genetic and environmental influences on the transmission of parental depression
predictive of children’s depression coincide with
genetic models of risk (Halligan, Murray, Martins, &
Cooper, 2007; Hammen, Burge, & Adrian, 1991). On
the other hand, the effect of negative maternal
behavior is most pronounced when it is associated
with a current depressive episode (Lovejoy, Graczyk,
O’Hare, & Neuman, 2000). A recent series of intervention (Pilowsky et al., 2008) and adoption studies
(Tully, Iacono, & McGue, 2008) do suggest the risk is
environmental.
To directly test whether parental depression represents a genetic and/or family environmental risk
factor for children’s depression and conduct problems we analyzed data from a large population
sample of children of adult monozygotic (MZ) and
dizygotic (DZ) twins. The study of the Children of
Twins (COT) is a powerful strategy for disaggregating
the nature of transmissible effects between parents
and their children (Heath, Kendler, Eaves, & Markell, 1985; Truett et al., 1994; Silberg & Eaves, 2004).
Specifically, we sought to determine whether the
impact of parental depression and children’s
depression and conduct disorder are due to the
sharing of genes, the provision of a high-risk environment, or both.
The logic of the Children of Twins design is as
follows: a child is as alike genetically to the MZ
co-twin as to the biological parent, with a 50%
correlation for their additive genetic effects, but is
provided a direct rearing environment only by the
biological parents. This has three implications:
1 The difference in association between the child and
the MZ twin parent and the child and his/her
aunt/uncle provides a direct estimate of the nongenetic interaction between parental behavior and
risk to childhood behavioral and emotional disorders.
2 The difference in association between children
and their parents’ MZ co-twin versus children
and their DZ aunt/uncle is a simple test of the
inter-generational transmission of hereditary
factors.
3 The co-twins of the MZ parent as compared to DZ
co-twins represent indices of the long-term
behavioral consequences of genes whose effects
may initially be expressed in the nieces and
nephews in childhood.
Methods
Ascertainment
Informed consent for the study was obtained from the
Institutional Review Board at Virginia Commonwealth
University (IRB# 2127). After screening for eligibility for
the Children of Twins study, 7407 twins from the MidAtlantic Twin Registry (MATR) were selected for possible
inclusion in the study. Of the 3343 twins that were
eligible and we were able to contact, data was obtained
735
on 83% of the individual twin families (n = 2774). The
resulting sample was comprised of 1043 complete twin
pair families having at least one child. Of these, 354
were monozygotic female twin pairs, 144 monozygotic
male, 225 dizygotic female, 98 dizygotic male, and 222
opposite sex twin pairs. Data from incomplete families
were used for estimating the association across generations and between spouses, critical parameters in the
Children of Twins model (see Figure 1). In addition to
the nearly 2700 male and female twins that agreed to
participate, data has been collected on 1639 spouses/
partners of the twins, and 2940 of their children (1608
of the children provided self ratings). The total number
of parent–child and avuncular–child dyads in MZ and
DZ twins is shown in Table 2.
Zygosity determination
Zygosity was assigned to each pair based on questionnaire responses using an algorithm developed for an
intersecting sample who had also been genotyped for
multiple microsatellite markers (Kendler & Prescott,
2006).
The Virginia Twin Study of Adolescent Behavioral
Development (VTSABD)
The Virginia Twin Study of Adolescent Behavioral
Development (VTSABD) is a population-based, multiwave, prospective study of 1412 male and female
juvenile twin pairs between the ages of 8 and 17. The
study was originally designed to elucidate the relative
influence of genetic and environmental factors on the
most common forms of childhood psychopathology.
Details concerning the ascertainment, participation
rates, and assessment protocol are available in
numerous publications (Hewitt et al., 1997; Eaves
et al., 1997; Simonoff et al., 1997). The twin data
from the VTSABD were included in the present study
to estimate any child-specific genetic and environmental effects on depression and conduct disturbance. For the purpose of elucidating the causes of
depressive and conduct disturbance symptoms in the
twin children most comparable in age to the children
in the COT study, we used data from the first wave of
the VTSABD study.
Assessment of parental and child depression and
child conduct disturbance
As part of a telephone interview, twins and their spouses were asked to report on depressive symptoms
experienced during the past 3 months using a shortened version of the Mood and Feelings Questionnaire
(MFQ; Angold et al., 1985). The children were also
asked to rate depressive symptoms presenting in the
past 3 months, using the same protocol used for evaluating depression in their parents. The ratings of conduct problems were obtained via maternal report using
the Rutter ‘A’ scale (Rutter, Tizard, & Whitmore, 1970).
These identical instruments were used to generate the
twin correlations for depression and conduct disturbance and the data for model fitting for the VTSABD
sample.
2010 The Authors
Journal compilation 2010 Association for Child and Adolescent Mental Health.
736
Judy L. Silberg, Hermine Maes, and Lindon J. Eaves
f
r
E
A
C
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S1
1
r
A
g
C
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E
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e
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w
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T1
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Figure 1 Children of Twins Model (COT). All latent and measured variables are assumed to be standardized to unit
variance to simplify the derivation of expected correlations between relatives. Note that there is assumed to be no
residual variance on the parentally derived shared environment (F) because differences are assumed to be explained
entirely by regression on parental phenotype. The effects of Mendelian segregation, however, contribute residual
variance in life-course-persistent genetic effects (A) which explains a proportion 1 – ½ (1 + g2m) of the total variance
in A. Key to symbols: T1 = Twin 1, T2 = Twin 2, S1 = Spouse of Twin 1, S2 = Spouse of Twin 2, O1 = Offspring of Twin
1, O2 = Offspring of Twin 2, A = additive genetic effects expressed in both adults and children (‘life course persistent’), A’ = residual additive genetic effects specific to children (‘juvenile limited’), C = shared environmental effects
adults, C’ = shared environmental effects on children explained by parental phenotype, C’ = residual, juvenile specific, shared environmental effects in twins and siblings, E = adult unique environmental effect
Data analysis
Familial correlations. The causes underlying the
transmission of risk from parent’s depression to their
children’s behavior (whether genetic and/or environmental) is based upon the pattern of association
between the phenotypes of MZ and DZ twin parents,
their co-twins, spouses, and children. To establish a
baseline for decomposing the intergenerational association between parental depression and depression and
conduct problems in the children, the correlations both
within and across generations for each behavior were
estimated for MZ and DZ twins using SAS (SAS Institute, 2000). These included the MZ and DZ parent–
offspring correlations between parental depression and
juvenile depression and conduct disturbance, and the
correlations between children’s depression and conduct
behavior and depression in their parents’ co-twin – the
child’s aunt or uncle. To elucidate the causes of adult
depression and depression and conduct in childhood,
the twin correlations for MZ and DZ COT twins and MZ
and DZ juvenile twins from the VTSABD were also
estimated.
Structural equation modeling. We adopt a more
rigorous approach for disaggregating the effect of the
shared family environment from any genetic liability
transmitted from parent to child using the Children of
Twins model shown in Figure 1. The model is based
upon the familial association between depression in MZ
and DZ twin pairs, their spouses, and their children’s
depression and CD, fitted using the statistical program
Mx (Neale, Boker, Xie, & Maes, 2003). The model
includes twins of an adult pair, T1 and T2, their spouses, S1 and S2, and a child from each twin family, offspring 1 (O1) and offspring 2 (O2) (up to 3 children were
included in the model). To take account of the possible
effect of age, gender, and sample origin these variables
were regressed out and the models fitted to the residual
raw data.
The basic unreduced model incorporates a number of
potentially important genetic and environmental sources of variation. In many respects, it is an extension of
the well-known ‘ACE’ model for the resemblance
between twins (see, e.g., Neale & Cardon, 1994; Eaves
et al., 1997) which recognizes that differences in a trait
may be due to the additive genetic effects, A, shared or
‘common’ environmental effects, C, and individualspecific within-pair environmental influences, E. However, this basic model is extended in several directions
(see Figure 1) to take into account developmental differences between adults and juveniles, and to represent
alternative theories about the influence of parents on
their children. (Note that there are many equivalent
parameterizations of the same basic model. Some
alternatives are being explored in anticipation of revisions of the Mx platform.)
Firstly, we recognize that different genes may affect
the phenotype in adults (adult twins and their spouses)
and juveniles (the children of twins). The model allows
for genes, represented by the latent variables ‘A’ in
Figure 1, that have effects that persist over the life
course. Although their effects may persist, through
development, the phenotype may be different in adults
and children. This difference is captured in the model
by specifying separate parameters, g and d, for the path
2010 The Authors
Journal compilation 2010 Association for Child and Adolescent Mental Health.
Genetic and environmental influences on the transmission of parental depression
from life-course-persistent genetic effects, A, to adult
and juvenile measures respectively. Genetic theory (see,
e.g., Neale & Cardon, 1994) predicts that the regression
of the additive genetic effects on juveniles on those of
their parents is ½. Not all genetic effects are life-course
persistent. Some, represented by A’ in Figure 1, are only
expressed in juveniles and do not contribute to adult
variation. The effect of these juvenile-limited genetic
effects is denoted by the path b in the figure. Since these
juvenile-genetic specific effects do not contribute to the
adult phenotype, their correlation between relatives (q
in the figure) is 1 in juvenile MZ twins, ½ in juvenile DZ
twins and siblings, ¼ in the (juvenile) offspring of MZ
twins (biologically half-siblings) and 1/8 in the offspring
of DZ twins (first cousins).
Secondly, we include parameters for the individual, unique, environmental effects, E, on adults and
juveniles.
Finally, the model involves parameters to account for
the shared environment, C, of adult and juvenile twins
and siblings. We assume that some of these effects
persist over the life course and affect the phenotype of
both adults (C) and juveniles (C’). Some, C’, are
assumed to be juvenile-specific. A critical feature of the
current model and data set is its ability to identify some
aspects of the non-genetic effect of parents on the
environment of their offspring and to separate these
direct environmental effects of parents from any
secondary correlation due to the genetic correlation
between generations. In this case, we assume that all
the life-course-persistent effects of the juvenile shared
environment may be traced t…
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