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PONTIFICIA UNIVERSIDAD CATÓLICA DE CHILE

FACULTAD DE CIENCIAS SOCIALES

ESCUELA DE PSICOLOGÍA

Bidirectional relationship between behavioral

activation and postpartum depressive symptoms: a

random intercept cross-lagged panel model

IVELISSE HUERTA GARCÍA

Profesores guía: Lydia Gómez-Pérez, Patricio Cumsille

Tesis presentada a la Escuela de Psicología de la Pontificia Universidad Católica de

Chile, como requisito para optar al grado académico de Magíster en Psicología de la

Salud

Mayo, 2021

Santiago, Chile

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PONTIFICIA UNIVERSIDAD CATÓLICA DE CHILE

FACULTAD DE CIENCIAS SOCIALES

ESCUELA DE PSICOLOGÍA

Bidirectional relationship between behavioral

activation and postpartum depressive symptoms: a

random intercept cross-lagged panel model

IVELISSE HUERTA GARCÍA

Profesores guía: Lydia Gómez-Pérez, Patricio Cumsille

Tesis presentada a la Escuela de Psicología de la Pontificia Universidad Católica de Chile,

como requisito para optar al grado académico de Magíster en Psicología de la Salud.

Tesis financiada por proyecto FONDECYT 1171727 “Predicting perinatal and postpartum

pain, physical health symptoms, and depressive symptoms among Chilean women”

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AGRADECIMIENTOS

Si bien esta tesis lleva mi nombre en la portada, esta no hubiese sido posible sin la

contribución de múltiples personas.

En primera instancia me gustaría comenzar por agradecer a mi familia, la cual me ha apoyado

incondicionalmente a través de este largo proceso. Gracias mamá y papá por impulsarme a

seguir mis estudios, por la paciencia e infinita confianza que han tenido en mi, por las mil

horas que han pasado escuchándome hablar sobre esta tesis, y por el amor que me han

otorgado. También me gustaría agradecer a mis hermanas, especialmente a mi hermana

Andrea que me ha motivado con sus llamadas y palabras de aliento, y a Carmen que me ha

brindado su apoyo y cariño cada paso del camino. Ustedes son el pilar que me han permitido

ser yo, y convertirme en la profesional que hoy soy.

Por otra parte, quiero darle las gracias a mi pareja Jinwoo. Gracias por creer en mí, alentarme

a lo largo de este trayecto, por comprenderme y amarme.

También quiero agradecer a de sobremanera a mis profesores guías Lydia Gómez-Pérez y

Patricio Cumsille por permitirme adherirme a su proyecto, aceptarme como tesista, y más

importantemente por su continuo esfuerzo, ayuda e interés. Tanto su trato profesional como

personal hacia mi persona no puede ser pasado por alto. Gracias por su cariño. Sin su apoyo

no hubiese sido capaz de realizar este trabajo. Por otra parte, debo agradecer a todos los

integrantes del equipo de investigación que facilitaron el desarrollo de esta tesis. A mis

compañeras de tesis Daniela Valenzuela y Javiera Ramírez quiero extenderles un

agradecimiento especial. Muchas gracias de corazón. Hacer esta tesis con ustedes ha sido una

experiencia inolvidable, y la ayuda desinteresada que me han otorgado en este proceso

realmente significa mucho para mí.

Muchas gracias a todas estas personas que hicieron de este trabajo posible.

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Índice

1. Resumen de tesis 7

2. Introducción a la Tesis 8

3. Artículo científico

a. Portada 10

b. Abstract en español 11

c. Abstract en inglés 11

d. Introducción 12

i. Definición de constructo y descripción de modelos conductuales

de depresión

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ii. Activación conductual y depresión 17

iii. Objetivos del estudio 19

e. Metodología

i. Participantes 20

ii. Procedimiento 20

iii. Instrumentos 22

iv. Análisis de Datos 23

f. Resultados

i. Características sociodemográficas y psicológicas 23

ii. Análisis estadístico

1. ANOVA de medidas repetidas de puntajes de activación

conductual

2. ANOVA de medidas repetidas sintomatologia depressiva

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3. Random Intercept Cross-lagged Panel Model de síntomas

depresivos y activación conductual

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g. Discusión 30

h. Referencias 33

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Índice de Tablas y Figuras

1. Figura 1 15

2. Figura 2 16

3. Figura 3 21

4. Tabla 1 24

5. Tabla 2 25

6. Figura 4 26

7. Figura 5 27

8. Figura 6 29

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Resumen de la Tesis

La presente tesis tiene por objetivo examinar la relación bidireccional entre los síntomas

depresivos postparto y la activación conductual de mujeres gestantes. Para esto se utilizaron

datos del proyecto FONDECYT 1171727 “Predicting perinatal and postpartum pain,

physical health symptoms, and depressive symptoms among Chilean women”. Los datos

corresponden a mediciones longitudinales en cuatro tiempos, esto es, entre las 32 y 37

semanas de embarazo, un mes, tres meses y seis meses postparto. Se realizó un modelo panel

de efectos cruzados con interceptos aleatorios (RI-CLPM, por sus siglas en inglés) para

evaluar esta relación. Los resultados indicaron que la relación entre síntomas depresivos

postparto y activación conductual es bidireccional, lo que apoya nuestra hipótesis.

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Introducción

La depresión postparto es una dificultad común en el puerperio. Esta potencialmente puede

generar síntomas depresivos persistentes, además de efectos secundarios a largo plazo en la madre,

su hijo y su relación.

Dado lo anterior, es fundamental intentar comprender mejor los factores que potencialmente

juegan un rol en el desarrollo y mantenimiento de la depresión posparto. Uno de estos factores

potenciales es la activación.

La activación es un concepto que surge de la terapia de activación conductual (AC) y puede

explicarse como un conjunto de comportamientos objetivo de tratamientos en el contexto de la

terapia de AC. Esto es, ya que se cree que la activación afecta tanto el inicio como el

mantenimiento de la depresión.

Algunas de las pruebas más convincentes que abogan por una fuerte relación entre la

activación y los síntomas depresivos son la abundante evidencia empírica con respecto a la

efectividad de la terapia de AC. Fuera del contexto de la terapia, hay pocos estudios que abordar

esta temática. Nuestro estudio pretende desenvolverse en este contexto, intentando superar algunas

de las limitaciones de estudios anteriores.

Por ello, el objetivo principal de este estudio es examinar la relación bidireccional entre los

síntomas depresivos postparto y la activación conductual de mujeres gestantes. La relevancia del

presente estudio radica en ser la primera vez que se estudia esta relación en el contexto perinatal,

una población importante a abordar dada las consecuencias de la depresión postparto tanto en las

mujeres como en sus bebés. Por lo demás es uno de los primeros estudios en explorar esta relación,

proveyendo sustento empírico a los supuestos teóricos de las terapias de Activación Conductual y

los modelos conductuales de la depresión. Adicionalmente, este estudio supera limitaciones de

estudios anteriores al utilizar un método estadístico más robusto y explorar longitudinalmente este

fenómeno.

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El estudio es de diseño longitudinal, considerando cuatro tiempos de medición, y una

muestra de 504 mujeres mayores de 18 años, sin presencia de dolor crónico, y sin dificultad para

comprender español.

En el presente documento expone en formato de artículo los antecedentes de la

problemática, una revisión bibliográfica de la literatura hasta la fecha, los objetivos del estudio, la

metodología utilizada, los resultados, la discusión, un listado de las referencias bibliográficas

utilizadas, y un anexo de la pauta de la primera entrevista. El formato de la tesis corresponde a un

artículo de extensión regular basado en las orientaciones propuestas por la revista Journal of

Abnormal Psychology, pues se pretende publicar en ella.

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Bidirectional relationship between behavioral activation and postpartum depressive

symptoms: a random intercept cross-lagged panel model

Ivelisse Huerta, Patricio Cumsille, & Lydia Gómez-Pérez

Pontificia Universidad Católica de Chile

Corresponding author's contact information: Lydia Gómez Pérez, lgomeze@uc.cl;

lydiagp2@gmail.com. Phone: +56 223544850. Escuela de Psicología. Facultad de Ciencias

Sociales, Pontificia Universidad Católica de Chile, Campus San Joaquín. Avda. Vicuña

Mackenna 4860, Macul, RM, Santiago, Chile.

Collate acknowledgements: we want to thank all the women that participated in the present

research as well as the reviewer of the paper for their time and insights. We also want to thanks to

the research assistants Camila Román, Catalina Esparza Benavente, Marcela Cortéz, Milagros

Bussio, Laura Rodríguez, Débora Martellanz, Mariela Bustamante, Daniela Valenzuela, Javiera

Ramírez, Magdalena Domeiko, Colomba Prado, and Daniella Gallardo who contributed to the data

collection.

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Resumen

Objetivo: evaluar la relación bidireccional entre síntomas depresivos postparto y puntajes de

activación conductual. Método: Mujeres embarazadas (N = 504) completaron una batería de

cuestionarios (incluidas la Escala de Depresión Postparto de Edimburgo y la subescala de

activación de la Escala de Activación Conductual para la Depresión) entre las 32 y 37 semanas de

gestación y, posteriormente, tres veces más al mes postparto, a los tres meses postparto, y a los

seis meses postparto. Se utilizó un análisis de modelo panel de efectos cruzados con interceptos

aleatorios (RI-CLPM, por sus siglas en inglés). Resultados y Conclusiones: El resultado del RI-

CLPM indicó que la relación entre los síntomas depresivos postparto y la activación conductual es

bidireccional. Este resultado es congruente con nuestra hipótesis, y adicionalmente nos permitió

observar que los síntomas depresivos postparto y la activación conductual no se predicen por igual.

Los síntomas depresivos postparto parecen ser predictor dominante de la activación conductual.

Palabras clave: postparto, depresión, activación conductual, RI-CLPM.

Abstract

Objective: to evaluate whether the relation between postpartum depressive symptoms and

behavioral activation scores is bidirectional. Method: Pregnant women (N = 504) completed a

battery of questionnaires (including the Edinburgh Postnatal Depression Scale and the Activation

subscale of the Behavioral Activation for Depression Scale) when they were between the 32 and

37 weeks of gestation, and subsequently at one, three, and six months after delivery. Data was

modelled using a Random Intercept Cross-lagged Panel Model (RI-CLPM). Results and

Conclusions: The RI-CLPM analysis indicated that the relationship between postpartum

depressive symptoms and behavioral activation is bidirectional. This result was in line with our

hypothesis and allowed us to further observe that postpartum depressive symptoms and behavioral

activation do not predict each other equally. Postpartum depressive symptoms are a dominant

predictor of behavioral activation scores.

Keywords: postpartum, depression, behavioral activation, RI-CLPM.

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Introduction

Depression is one of the most common manifestations of psychological distress worldwide

(World Health Organization, 2017), and Chile is no exception. According to the Chilean National

Health Survey, 6.2% of the population experiences depression, with a higher prevalence in women

(10.1%) than men (2.1%) (Ministerio de Salud, 2018). Major depression is particularly of concern

due to its high prevalence (9.0%) and its association with disability (Vicente, Kohn, Saldivia, &

Rioseco, 2007). Chilean studies rate unipolar depression as the second leading cause of disease

burden in the general population, accounting for 4.5% of the total disability-adjusted life years

(DALYs) (Ministerio de Salud – Pontificia Universidad Católica de Chile, 2008). Within

depressive disorders, postpartum depression (PPD) is a major public health concern.

PPD is considered to be a common complication of childbearing, with varying prevalence

across countries (Halbreich & Karkun, 2006). Nevertheless, prevalence estimates for perinatal

depressive disorders markedly differ depending on the definition of the disorder and the period

over which prevalence is determined. As for Chile, no recent studies of prevalence were found.

The only study found was that of Jadresic and Araya from 1995, which estimated prevalence at

35.7%.

More importantly, PPD is impactful due to the potential long-term side effects on the

mother, her child, and their relationship. Women with PPD may encounter difficulty coping with

daily life and parenting tasks, which may result in long-term persistent depressive symptoms

(Mendoza & Saldivia, 2015; Horowitz and Goodman, 2004). These complications can lead to

troubled mother-child relations that may prove to be detrimental to the child’s emotional,

behavioral and cognitive development (Mendoza & Saldivia, 2015; Murray & Cooper, 1997).

Many consider transition to parenthood to be a challenging and stressful life event (Simpson,

Rholes, Campbell, Tran, & Wilson, 2003), as it is a complex process characterized by both

personal and familial changes that require an important adjustment. Taking care of a baby can

result in profound changes in an individual’s lifestyle, generating changes in recreational time,

sleep patterns, relationships and even identity (Epifanio, Genna, De Luca, Roccella, & La Grutta,

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2015), intimately affecting women’s pattern of behavior. Untreated maternal depression also puts

mothers at a higher risk for smoking, alcohol or substance abuse, and physical, emotional, or sexual

abuse when compared to non-depressed mothers (Fitelson, Kim, Baker, & Leight, 2010). Given

the above, attempting to better comprehend the factors that potentially play a role in the

development and maintenance of postpartum depression is fundamental. One of these potential

factors is activation (Kanter, Manos, Bowe, Baruch, Busch, Rusch, 2010; Dimidjian et al., 2017).

Construct Definition and Overview of Behavioral Models of Depression

Activation is a concept that emerges from Behavioral Activation (BA) therapy, a highly

effective evidence-based treatment for depression that stems from behavioral theories (Kanter et

al., 2010; Dimidjian, Barrera, Martell, Muñoz, Lewinsohn, 2011). While BA therapy is utilized in

a wide range of settings, therefore not exclusively to treat PPD, there is recent evidence suggesting

its effectiveness for this group (Dimidjian et al., 2017). Activation is a key subset of behaviors that

is targeted by BA treatments, as it is thought to affect both the onset and the maintenance of

depression (Dimidjian et al., 2011). It can be defined as the performance of actions or activities

directed towards personal goals and the accomplishment of important functional activities (Kanter

et al., 2010). It is crucial to understand that activation does not refer to the number of activities

carried out, nor if they were pleasant or enjoyable, but rather the perception that the behaviors we

carry out allow for functional performance in life (Kanter et al., 2010). While many researchers

have contributed to both our understanding of depression from a behavioral standpoint, as well as

the development of BA treatments as we know them today, to limit the scope of the present study,

we will mainly work around the framework provided by Peter Lewinsohn and colleagues.

Lewinsohn is a key author that pioneered the development of behavioral theories of depression,

and even though he does not specifically emphasize activation as a concept in his models, it is a

popular construct utilized to partially measure disrupted behavior in clinically depressed

individuals coursing BA treatments. Disrupted automatic behaviors and emotional responses ard

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considered a central aspect of the model. To further understand the relationship between activation

and Lewinsohn’s models, we will expand on his theoretical propositions below.

The first theoretical behavioral model of depression proposed by Lewinsohn and Shaffer

in 1971, explained that depressive symptoms are developed and maintained due to a decrease in

response-contingent positive reinforcement (RCPR) of healthy behaviors. They speculated that

this relationship was not linear, but circular. In other words, when RCPRs decrease, depressive

symptoms increase, which in turn, cause the individual to put himself in situations that do not

allow for RCPRs of healthy behaviors to occur, leading to either more depressive symptoms or

maintained depressive symptoms (Lewinsohn & Shaffer, 1971). RCPRs can be understood as

events that increase the frequency of a behavioral response, where the response is dependent or

conditioned by the event itself. Lewinsohn explained that the total amount of RCPRs experienced

by an individual depends on three factors: (1) the number of potentially reinforcing events for an

individual, (2) the availability of such events in the environment, and (3) the ability the individual’s

capacity to obtain such reinforcement from the environment. For example, a person with multiple

hobbies will probably have a larger pool of potentially reinforcing events compared to someone

who lacks them. While quantity is important, accessibility is as well. If our hobby-loving

individual is a wine connoisseur but doesn’t have the financial means to enjoy a glass of wine

occasionally, the chance of RCPRs decreases as well. Finally, if the individual is not proficient at

obtaining the reinforcements from the environment even if they are present (i.e., he/she is passive

or has a negative attitude), the possibility that RCPRs occur is diminished. (Dimidjian et al., 2011).

To summarize, Lewinsohn and Shaffer’s first model asserts that a decrease in RCPR leads to an

increase in depressive symptoms (Figure 1).

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Figure 1

Diagram of Lewinsohn’s 1971 Behavioral Model of Depression

Note. Figure retrieved from “The origins and current status of behavioral activation treatments for

depression” by Dimidjian, S., Barrera, M., Martell, C., Muñoz, R., and Lewinsohn, P., 2011, Annual

Review of Clinical Psychology, 7(1), 1-38. Copyright 2011 by Annual Reviews.

As Lewinsohn continued to study depression, he realized his first model oversimplified

depression and its causes. His views began to broaden as new emerging empirical evidence

appeared, and, in 1985, he proposed a second version of the model: the integrative model (Figure

2). A critical assertion of the integrative model is that depression is a heterogeneous disorder that

presents itself with different levels of severity and symptom patterns, dysphoria being the most

common symptom experienced by depressed individuals. Depression can not only have different

forms of presentation but is also caused and influenced by a multitude of factors. The intention of

the integrative model was to highlight the multicausality, complexity and diversity of depression,

while still providing a framework that could summarize its intricate nature where dispositional

(i.e., genetics, behavior, cognitions, personality traits, etc.) and environmental factors meet in the

individual. A key concept that is incorporated into the model is the influence of environmental

stressors. These are considered the main, albeit not unique, triggers of the depressogenic process.

Stressors are any external stimulus or event that can cause stress to an organism (Centre for Studies

on Human Stress [CSHS], 2017). The model dictates that the degree in which a stressor produces

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depression is intimately related to the degree in which an individual’s automatic behavior and

emotional response are affected. At the same time, disrupted automatic behavior and emotional

response are associated with decreases in positive reinforcement and increases in avoidant

behavior. This, in turn, is linked to an increase in negative self-consciousness, such as self-

criticism and negative expectations, that lead to states of dysphoria and depression. It culminates

in emotional, behavioral, cognitive, somatic, and interpersonal consequences. This whole process

is influenced by predisposing individual characteristics, and, akin to the first model, is circular.

Poor emotional, cognitive and behavioral states negatively impact individual’s predisposing

characteristics (i.e., resilience, history of past depression, etc.), reduce their ability to cope in the

face of stressful events, influencing their ability to respond functionally, which can aggravate

depressive symptoms (Dimidjian et al., 2011). The integrative model provides a much more

comprehensive theory compared to its predecessor.

Figure 2

Diagram of Lewinsohn’s 1985 Integrative Model of Depression

Note. Figure retrieved from “The origins and current status of behavioral activation treatments for depression”

by Dimidjian, S., Barrera, M., Martell, C., Muñoz, R., and Lewinsohn, P., 2011, Annual Review of Clinical

Psychology, 7(1), 1-38. Copyright 2011 by Annual Reviews.

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Behavioral Activation Research and Considerations

As stated previously, activation is a construct that alludes to the performance of actions

and activities that aim to satisfy personal goals and complete important activities aligned with such

goals (Kanter et al., 2010). A decrease in activation can be considered a partial measure of

disrupted behavior and emotional response, as lower rates of RCPR can be explained by decreased

activation and increased avoidance (Chen, Liu, Rapee, & Pillay, 2013; Collado, Castillo, Maero,

Lejuez, & MacPherson, 2014; Wagener, Bayens, & Blairy, 2016, as cited in Krings, Bortolon,

Yazbek, & Blairy, 2021). Researchers have undertaken a multitude of randomized controlled trials

that show that activation and depression are linked. Some of the most compelling pieces of

evidence that advocate for the strong relationship between activation and depressive symptoms are

the abundant empirical evidence regarding the effectiveness of BA therapy (Ekers, Webster, Van

Straten, Cuijpers, Richards, & Gilbody, 2014; Mazzucchell, Kane, & Rees, 2009; Cuijpers, Van

Straten, & Warmerdam, 2007). The effectiveness of BA therapy indicates that there is a definite

overlap between activation levels and depression severity, but this does not automatically assert a

causal relationship. While BA Therapy certainly targets activation intensively, it does not

exclusively work on activation. Other factors might be playing an important role in the

effectiveness of the therapy, such as a variety of skills training interventions, contingency

management, or procedures targeting avoidance and verbal behavior (Kanter et al., 2010). In other

words, BA therapy has set empirical grounds to state that these factors are related, but does not

provide a full picture of this relationship, as this relationship has not been studied extensively

outside the context of therapy.

In a longitudinal study, Santos, Leonard, Puspitasari, Cook and Riemann (2019) evaluated

if behavioral activation is a plausible mechanism of change for depressive symptoms. Akin to other

studies on effectiveness of therapy, they observed increases in activation and decreases in

depressive symptomatology throughout the course of treatment. But more importantly, through the

use of growth curve modeling, they were able to observe that changes in activation predict the

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quadratic rate of change of depression, while the linear change in depression significantly

predicted activation.

The effectiveness of BA therapy is not the only kind of evidence that asserts a robust

relationship between decreased activation and increased depressive symptoms. A few researchers

have studied the relationship outside of the context of treatment as well.

In a correlational cross-sectional study, Wagener, Baeyens, and Blairy (2016) studied the

influence of activation on different depressive symptoms (such as sadness, self-dislike, pessimism,

loss of pleasure, loss of energy, past failure, etc.) on adults (n = 1169) recruited from adult

communities or mental health care facilities, considering potential gender discrepancies. Their

findings suggest that activation is negatively correlated with most depressive symptoms present in

both genders, but regression coefficients showed symptom probability differed by gender, where

men exhibited more pessimism, feelings of punishment, loss of energy, concentration difficulty,

sense of past failure, and loss of pleasure. In short, their findings align with the theory that

behavioral activation and depressive symptoms are indeed related. The greatest limitation of this

study is its cross-sectional design which does not allow to infer a causal relation between these

variables. Future research with longitudinal designs is necessary to better evaluate the relationship

between behavioral activation and depressive symptoms. A longitudinal design would allow us to

distinguish if the pattern of associations is stable or varies in time, as well as determine the

differences between within and between-subjects, and assess the bidirectionality of the

relationship.

The only longitudinal study found that attempted to empirically establish a temporal

relationship between BA and depressive symptomatology is that of Shudo, Yamamoto, and Sakai

(2017). Its objective was to examine whether activation and avoidant behavior played a role in the

development of depression. The participants were undergraduate students (n=129), who answered

the same survey at two different times (T1, T2) over an 8-week time interval. The Behavioral

Activation Scale for Depression-Short Form (BADS-SF) was used to measure activation and

avoidance, while the Center for Epidemiological Studies – Depression Scale (CES-D) was used to

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measure depressive symptoms. The results indicated that activation at T1 was negatively

associated with depression at T1, but that activation was not a predictor of depression at T2. This

finding seems to indicate that low levels of activation are a symptom concurrent with depression

but not a predictor of future depression.

Even though the Shudo et al. (2017) study concluded that activation does not predict

depressive symptoms, their study has some important limitations. For example, the sample selected

was a group of undergraduate students without a standardized and uniform stressor. As previously

stated, Lewinsohn posits that a meaningful stressful life event is a common trigger of reduced

activation and increased depressive symptoms (Dimidjian et al., 2011). Another limitation is the

lack of extended follow-up, as data was only collected twice. To evaluate the form of change of

variables, current methodological guidelines for longitudinal research suggest a minimum of three

measurements (Kehr & Kowatsch, 2015). These limitations, together with the fact that, to our

knowledge, only two previous studies have examined the association between behavioral and

depressive symptoms outside of the context of treatment, suggest the need to further investigate

the relationship between behavioral activation and depressive symptoms.

Study Overview

To comprehend the nature of the present study, we would like to highlight how

Lewinsohn’s theory establishes stressors as main triggers of the depressogenic process, and the

role of disruptive automatic behaviors as precursors of the process leading to increased depressive

symptoms. In the present study, behavioral activation was considered a partial measure for

disruptive behavior and emotional response that can occur due to pregnancy and transition to

parenthood. Pregnancy and transition to parenthood were regarded as tangible and predictable life

stressors. From this perspective, pregnant women are a suitable population to study the relationship

between behavioral activation and depressive symptoms.

Accordingly, the main goal of this study was to examine the relationship between BA and

depressive symptoms in women going through pregnancy and transition to parenthood. More

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specifically, we first aimed to describe the changes of behavioral activation between the prepartum

period, 1-month, 3-months, and 6-months postpartum, as well as the changes in depressive

symptomatology during the same period in a sample of Chilean women. Secondly, we evaluated

the bidirectionality of the relationship between behavioral activation and postpartum depressive

symptoms longitudinally.

For the first aim, we expected a significant decrease of BA levels between the prepartum

and postpartum period, as our participants were all subjected to a life stressor, as well as a

significant increase in depressive symptomatology. As for our second aim, we expected to observe

an inverse bidirectional relationship between the activation scores and depressive symptoms, as,

according to Lewinsohn, disrupted behavioral and emotional responses lead to an array of changes

that culminate in depression. This depressive state further disrupts the individual’s behavioral and

emotional response, making their relationship cyclical and bidirectional.

Method

Participants

This study used data collected in a larger FONDECYT project titled “Predicting perinatal

and postpartum pain, physical health symptoms, and depressive symptoms among Chilean

women”, a prospective pregnancy-pain related longitudinal study. Women (n=504) who were 32

to 36 weeks pregnant were recruited from obstetrics and gynecology services, more specifically at

a health network service in the Santiago Metropolitan area in Chile. Exclusion criteria included

being younger than 18 years old, having trouble speaking Spanish, presence of chronic pain before

pregnancy, and non-viability of the fetus.

Recruitment and procedure

The method of recruitment to this study consisted of research assistants approaching and

inviting women to participate while they waited to be attended to by their physician. Alternatively,

they were introduced to the study by a nurse or doctor or volunteered to participate in the study

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after encountering poster advertisements posted in the waiting rooms. To avoid participants feeling

pressured to take part in the study, a structured verbatim speech was designed.

The design consisted of four interviews: an initial face-to-face interview at 32 to 36 weeks

of pregnancy, and three follow-up phone calls at 1-month, 3-months, and 6-months postpartum

(Figure 3). Once the individual decided to participate, a more detailed explanation of the study was

provided and a consent form was signed. The first interview was conducted immediately after

consent was given. All interviews were oral questionnaires. The first interview took 40 to 60

minutes to answer, while the follow-ups took 25 minutes to answer approximately. Research

assistants, all of which were trained master level psychologists, took care of explaining the study

to the participants, oversaw the informed consent process, and led both the initial interview and

the follow-ups. Finally, participants were given gift cards after the completion of each interview,

10.000 CLP after the first assessment, and 5.000 CLP for each telephone follow-up.

Figure 3

Temporal Flowchart of the Study’s Design Procedure

Time 1

n = 504

CH

ILD

BIR

TH

Time 2

n = 419

Time 3

n = 437

Time 4

n = 418

Prepartum at 32 to 36 weeks of

pregnancy

1-month

postpartum

3-months

postpartum

6-months

postpartum

Face-to-face

40 to 60 min assessment

Phone call

25 min assessment

Phone call

25 min assessment

Phone call

25 min assessment

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Instruments

Descriptive statistics. Age, marital status, occupational status, education, household

income, history of psychological disorders, and treatment for depression at the time of

enrollment were assessed.

Edinburgh Postnatal Depression Scale (EPDS). To assess prenatal and postpartum

depressive symptoms, we used the validated Chilean version of the Edinburgh Postnatal

Depression Scale (Jadresic, Araya, Jara, 1995). Despite this scale being designed to

measure postpartum depression, there is evidence supporting the use of this scale during

pregnancy as well (Vega-Dienstmaier et al., 1997). The Chilean Health Ministry

(Ministerio de Salud, 2014), as well as other Chilean researchers (Mendoza & Saldivia,

2015), recommend using the EPDS to detect depression during pregnancy and postpartum.

The questionnaire contains 10 items rated on a four-point scale, scores ranging from 0 to

3, with a total potential score ranging from 0 to 30 points. The score of 12 is categorized

as the cut-off point for postpartum depression, where the higher the score indicates a greater

severity of depressive symptoms. The internal consistency for the EPDS in our sample

was estimated by Cronbach’s α = .84.

Behavioral Activation for Depression Scale—Activation Subscale (BADS-A). To

assess behavioral activation, we used the subscale “A” of the validated Spanish version of

the Behavioral Activation for Depression Scale (Barraca, Pérez-Álvarez, Bleda, 2011).

Originally, the BADS is a 25-item scale consisting of 4 subscales that assess activation,

avoidance/rumination, work/school impairment, and social impairment (Kanter, Mulick,

Busch, Berlin, & Martell, 2007). Subscale “A” contains 7 items rated on a seven-point

scale, with individual scores ranging from 0 to 6 and a total score ranging from 0 to 42.

Higher scores suggest higher levels of activation. The internal consistency for the BADS-

A in our sample was estimated by Cronbach’s α = .85.

23

Data Analysis

All analyses were executed in R Version 3.6.1 (R Core Team, 2019). To accomplish the first

specific aim of our study, we used repeated measures ANOVA to estimate if there were significant

changes in BA scores throughout the prepartum and postpartum period. For the second specific

aim, we estimated a random-intercept cross-lagged panel analysis (RI-CLPM). RI-CLPM is a

relatively new, statistical analysis that overcomes the limitations of simple cross-lagged models

(Hamaker, Kuiper, & Grasman, 2015). It aims to analyze bidirectional relationships at a within-

person level. It is able to achieve this result because it statistically accounts for an individual's

time-invariant trait-like differences at the between-person level (Hamaker, Kuiper, & Grasman,

2015). Hence, to explore the directionality of the relationship between BA and depressive

symptoms, and to infer a causal relation between the variables, we used RI-CLPM analysis.

Missing data was handled using full-information maximum likelihood, considering all available

data points.

Results

Descriptive Statistics

Descriptive statistics are presented in Table 1. Participants were on average 31.19 (SD=5.3)

years old, with over half possessing university degrees and living under high income households.

The participants of our study were fairly representative when compared to pregnant women from

the metropolitan area of Santiago. Differences were found in both educational level and marital

status, where our sample presented higher educational level and were married in greater proportion

(Instituto Nacional de Estadísticas de Chile, 2019).

Clinical characteristics measured longitudinally at the prepartum, 1-month postpartum, 3-

months postpartum, and 6-months postpartum phases are summarized in Table 2. Reported

activation scores were relatively high, while depressive symptoms were moderately low

throughout the prepartum and postpartum periods. The percent of women who exceeded the

24

established clinical cutoff score on the EPDS consistently increased throughout time, the

maximum percent being found at 6-months postpartum.

Table 1

Demographic and Clinical Characteristics of the Sample

Characteristic n = 504

Age, years, mean (SD)

Marital Status, N (%)

Single

Cohabitation with partner

Married

Divorced

Widowed

Occupational Status, N (%)

Student

Full-time employee

Part-time employee

Unemployed

Maternity leave

Sabbatical

Education Level, N (%)

< High school

High school

Technical degree

University

Postgraduate

Household Income, N (%)

Less than 200,000 CLP

200,000 to 500,000 CLP

500,001 to 800,000 CLP

800,001 to 1,200,000 CLP

1,200,001 to 1,700,000 CLP

1,700,001 to 3,000,000 CLP

More than 3,000,001 CLP

Past psychological disorders, N (%)

Major depression

Other mood disorders

Treatment for depression at enrollment, N (%)

Psychotherapy

Pharmacological

31.19 (5.3)

1 (0.19%)

128 (25.54%)

191 (38.12%)

176 (35.12%)

5 (0.99%)

37 (7.35%)

54 (10.73%)

23 (4.76%)

29 (5.76%)

288 (57.25%)

17 (1.19%)

8 (1.59%)

54 (10.75%)

115 (22.91%)

268 (53.38%)

57 (11.35%)

3 (0.60%)

52 (10.32%)

70 (13.89%)

103 (20.44%)

111 (22.02%)

119 (23.61%)

41 (8.13%)

134 (26.80%)

101 (20.12%)

35 (7.03%)

19 (4.00%)

25

Table 2

Observed Behavioral Activation and Depressive Symptoms

Measure

Prepartum

(n = 504)

1-month postpartum

(n = 419)

3-months postpartum

(n = 437)

6-months postpartum

(n = 418)

BADS-A, mean (SD)

EPDS, mean (SD)

34.78 (6.42)

5.70 (4.50)

30.57 (8.81)

5.71 (4.64)

33.56 (8.35)

5.55 (4.98)

32.73 (8.96)

5.74 (5.32)

Note. BADS-A = Behavioral Activation for Depression Scale ⎯ Activation subscale; EPDS = Edinburgh Postnatal

Depression Scale

Statistical Analysis

Observation of BA trends. A repeated measures ANOVA was conducted to compare activation

scores obtained by pregnant women at 32 to 37 weeks prepartum, 1-month postpartum, 3-months

postpartum, and 6-months postpartum. Prior to estimating the repeated measures ANOVA,

Mauchly’s sphericity test indicated that the assumption of sphericity was met (χ2(5) = 5.23, p =

.388), therefore we proceeded with the analysis. The results showed that there was a difference

between activation scores at different time points (F(3, 678) = 16.61, p < .001). To determine how

periods differentiated from each other in function of time, we opted for a trend analysis.

Polynomial contrasts suggest that there is a significant cubic trend (F(1, 226) = 37.64, p < .001),

represented in Figure 4. Post hoc analysis with Bonferroni correction revealed that not all

measurements had significant differences. These results revealed that not all measurements had

significant differences. Scores at 1-month postpartum significantly differed from all other

measurements, and prepartum scores were significantly different from those at 6-months

postpartum. In other words, BA levels don’t follow a linear trend, and mothers do not seem to fully

recover to their prepartum state 6-months after delivery.

26

Figure 4

Comparison Line graph with 95 confidence intervals of behavioral activation (BA) scores

between prepartum, 1-month postpartum, 3-months postpartum, and 6-months postpartum

Note. Matching letters indicate no significant differences between those time periods

were found. Original scale ranges from 0 to 42 points.

Observation of depressive symptoms. A repeated measures ANOVA was conducted to compare

depressive symptoms scores obtained by pregnant women at 32 to 37 weeks prepartum, 1-month

postpartum, 3-months postpartum, and 6-months postpartum. Prior to estimating the repeated

measures ANOVA, Mauchly’s sphericity test indicated that the assumption of sphericity was

A

B AC C

27

violated (χ2(5) = 16.727, p = .005), therefore a Huynh-Feldt correction was applied (𝜀 =.978). The

results showed that there was no significant difference in depressive symptoms scores between

waves (F(2.935, 1012.439) = 1.212, p < .304).

Figure 5

Comparison Line graph with 95 confidence intervals of depressive symptoms scores

between prepartum, 1-month postpartum, 3-months postpartum, and 6-months postpartum

Note. Matching letters indicate no significant differences between those time periods were found. Original

scale ranges from 0 to 30 points. International cutoff score is 12 points. National cutoff score is 9 or 10 points.

A A A A

28

Relationship between depressive symptoms and BA scores. To examine the directionality of

the relationship between depressive symptoms and BA scores, the data was analyzed utilizing RI-

CLPM. Nested models were tested, where the autoregressive parameters for both behavioral

activation and depressive symptoms were restricted, as well as the cross-lagged parameters. The

more restrictive and parsimonious model was chosen, as chi-square comparisons established that

it was not different from the initial model (∆χ2 = 14.789, ∆df = 10, p = .140). The model fit to the

data was adequate; χ2(25) =105.088, p < .001, CFI=0.915, TLI=0.904, RMSEA = 0.085, and

significant bidirectional associations were found between depressive symptoms and BA scores.

Autoregressive and cross-lagged parameter estimates are presented on Figure 6. The

autoregressive parameters of behavioral activation suggest there is no intra-individual stability

(unstandardized β = 0.156, SE = 0.097, p = .109), implying that previous levels of activation do

not predict future activation scores. On the other hand, the autoregressive parameters for

depressive symptoms presented low intra-individual stability (unstandardized β = 0.276, SE =

0.078, p < .001), meaning that previous depressive symptoms somewhat predict future depressive

symptoms. Autoregressive parameters obtained using the RI-CLPM are low due to the inclusion

of the random intercept that controlled for trait-like activation levels; therefore, all stability was

accounted for in a trait-like factor. As for the cross-lagged parameters, the analysis indicated an

inverse relationship, where BA scores inversely predicted within-person changes of depressive

symptoms (unstandardized β = -0.089, SE = 0.034, p = .008), and depressive symptoms inversely

predicted within-person changes of BA scores (unstandardized β = -0.523, SE = 0.114, p < .001).

The standardized β values allow us to conclude that not only are these constructs reciprocally and

inversely related, but the magnitude of the coefficient seems to suggest that depressive symptoms

are a dominant predictor of BA scores of women undergoing perinatal pregnancy and postpartum.

Given this, we decided to run a second RI-CLPM where we restricted the model even further with

the intention of forcing it to be symmetrical. In this way, if the goodness of fit of the symmetrical

model is significantly worse, the parameters behave asymmetrically. The model fit for the

symmetric bidirectional relationship model was less adequate (χ2(15) = 90.280, p < .001,

29

CFI=0.926, TLI=0.861, RMSEA = 0.102), and chi-square comparisons revealed a statistically

significant difference between the model fits (∆χ2 = 16.319, ∆df = 1, p < .001), making our

asymmetrical model a better fit to our data. In other words, results suggest that the effect of

depressive symptoms on BA scores is larger than that of BA scores on depressive symptoms.

Lastly, there was a moderate to high inverse correlation (not presented in Figure 6) between trait-

like depressive symptoms and trait-like behavioral activation (r(25, n=504) = -0.518, p = .012).

Figure 6

Random Intercept Cross-Lagged Panel Model of Behavioral Activation (BA) and Depressive

Symptoms (DS)

Note. All standardized coefficients are in parenthesis. Dashed lines indicate non-significant coefficients. All

coefficients shown are significant p < .001. Estimated covariance between residuals of variables at the within-person

level represented as the relationship between e1. Trait-like depressive symptoms and trait-like behavioral activation

are not present in the figure.

30

Discussion

The aims of the current study were to describe the changes in BA levels, as well as changes

in depressive symptoms, throughout the prepartum and postpartum period, and to examine the

bidirectional relationship between BA levels and prepartum/postpartum depressive symptoms. As

mentioned previously, for our first aim we expected a significant decrease of BA levels between

the prepartum and postpartum period, as our participants were all subjected to a life stressor. The

results were mostly in line with our hypothesis of a significant decrease in behavioral activations

scores, but also suggested a more complex trajectory than stipulated as scores drop at 1-month

postpartum and tend to recover in the following measurements. On the other hand, we expected an

increase in depressive symptoms, but no significant change was observed between waves. This

can be attributed to the fact that our participants are overall a sample of healthy women to begin

with.

As for our second aim, we expected to observe an inverse bidirectional relationship

between behavioral activation scores and depressive symptoms. Our findings indicate that, as

Lewinsohn suggested, the relationship between behavioral activation and depressive symptoms is

bidirectional, albeit asymmetrical. Future research that delves into the mechanisms of behavioral

activation and depressive symptomatology should consider further analysis considering the

possible asymmetric relationship between these constructs. On the other hand, the autoregressive

parameters revealed that previous levels of behavioral activation do not predict within-person

changes of future behavioral activation levels. This is unlike Shudo and colleagues’s (2017) results

where they found that behavioral activation is a predictor of future changes in behavioral activation

and might be explained by the fact that RI-CLPM accounts for the stable invariant trait behavioral

activation levels in our participants. Autoregressive parameters for depressive symptoms indicated

that previous depressive symptoms directly predict future within-person changes in depressive

symptoms. This coincides with the abundant existing literature on the important predictive power

of prior depression over future depressive symptoms (Tram & Cole, 2006; Lewinsogn, Zeiss &

31

Duncan, 1989), which has also been observed to be true in the postpartum context (Guintivano,

Manuck & Meltzer-Brody, 2018).

Some of the strengths of the present study are that it’s the first study to explore the

bidirectional relationship between activation scores and depressive symptoms longitudinally.

While other studies have considered a relationship between activation and depressive symptoms,

none had assessed the bidirectional relationship between them previously. It is also the first study

of its kind in the perinatal context, an important population to address given the consequences of

postpartum depression on both women and their offspring. Additionally, in a more practical sense,

this study provides further support for the early screening protocol of postpartum depression,

already available in our healthcare system (Ministerio de Salud, 2014). It also provides support for

modifications of behavioral activation as a mechanism of change for postpartum depression, as it

is also evidenced by the effectiveness of behavioral activation therapy in this context (Dimidjian

et al., 2017). The study also contributes additional evidence for the theoretical behavioral models

of depression proposed by Lewinsohn. Finally, several limitations of previous studies were

overcome by including a stressor, addition of longitudinal waves, and selecting a more current and

robust statistical analysis.

Some limitations of this include the fact that the sample is not entirely representative of

pregnant women in Santiago, therefore it would be important to replicate this study with a more

representative sample or, alternatively, a contrasting population such as pregnant women with

lower income and educational level. Additionally, avoidance and response-contingent positive

reinforcements were not considered for this study, when they are both heavily targeted by

Behavioral Activation Therapy. Control variables such as social support, disrupted sleep, and

parental stress were also not contemplated. Better understanding of the mechanisms that might be

playing a role in the development, maintenance, and treatment of postpartum depression is key to

continue improving both preventive and curative alternatives to postpartum depressive

symptoms. Future studies should consider accounting for avoidance, response-contingent positive

32

reinforcements, as well as common psychosocial factors that affect postpartum depressive

symptomatology.

Overall, the findings of this study contribute to the growing literature surrounding

behavioral models of depression, providing support for an asymmetric bidirectional relationship

between depressive symptoms and behavioral activation in the peripartum period.

33

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