Samenvatting literatuur Affective Science
Week 1.
Artikel 1.
A Heuristic for Developing Transdiagnostic Models of Psychopathology: Explaining Multifinality and
Divergent Trajectories (Nolen-Hoeksema, Watkins)
Problem: Current transdiagnostic models, however, have difficulty simultaneously explaining the
mechanisms by which a transdiagnostic risk factor leads to multiple disorders (i.e., multifinality) and
why one individual with a particular transdiagnostic risk factor develops one set of symptoms while
another with the same transdiagnostic risk factor develops another set of symptoms (i.e., divergent
trajectories).
Goal: In this article, we propose a heuristic for developing transdiagnostic models that can guide
theorists in explicating how a transdiagnostic risk factor results in both multifinality and divergent
trajectories. We also (a) describe different levels of transdiagnostic factors and their relative
theoretical and clinical usefulness, (b) suggest the types of mechanisms by which factors at 1 level
may be related to factors at other levels, and (c) suggest the types of moderating factors that may
determine whether a transdiagnostic factor leads to certain specific disorders or symptoms and not
others (distal and proximal).
Theoretical background:
Approaches focused on transdiagnostic processes have a number of theoretical and clinical
advantages over disorder-specific approaches. First, there is growing agreement that the
heterogeneous disorders in our current diagnostic system are each made up of dysfunctional
versions of processes that vary along continua in the general population.
Second, transdiagnostic approaches can help us understand the comorbidity between disorders.
Third, if a transdiagnostic factor is causally related to two or more disorders, then assessment and
training could more parsimoniously focus on these factors than on the large number of discrete
disorders currently in the DSM.
Intermediate phenotypes: are conceived as neurocognitive and affective processes, such as learning,
memory, attention, stress sensitivity, and emotional reactivity that are causally linked to the
development of symptoms
Endophenotypes: are intermediate phenotypes that are heritable (erfelijk)
Multifinality refers to the process by which certain environments, experiences, or characteristics
increase risk for a number of different types of psychopathology in children or adults—for example,
stress is associated with multiple disorders
Similarly, transdiagnostic processes generally have not addressed phenotypic plasticity, wherein the
pattern of symptoms morphs across the life course, often unpredictably, especially during the
transitions through childhood and adolescente into adulthood.
,Distal risk factors contribute to disorders only through mediating proximal risk factors. Proximal risk
factors directly influence symptoms relative to distal risk factors. Distal and proximal risk factors lead
to multiple disorders (i.e., multifinality), which are comorbid (indicated by dashed lines). Moderators
interact with proximal risk factors to determine which specific disorder individuals will experience
(i.e., to determine divergent trajectories)
Distal factors: environmental and congenital biological variables relatively distal to observable
symptoms of disorders. Two categories:
1. The first is environmental context factors, such as parental psychopathology, a history of
sexual or physical abuse, and other traumatic events. These are what Hammen (1991, 2005)
labels independent stressors because they are not caused by the individual experiencing
them (e.g., the death of a spouse), and dependent stressors, which the individual may have
played a role in creating (e.g. interpersonal conflict)
2. The second category of distal risk factors consists of congenital biological abnormalities,
principally genetic abnormalities and congenital abnormalities in brain function or structure
(caused by genetic abnormalities or early brain injuries
,Proximal factors: within-person variables that are more proximal to symptoms of disorders.
Thus, proximal risk factors are operationalized as those intrapersonal risk factors that (a) directly
precede symptoms (relative to distal risk factors), and/or (b) directly influence symptoms. Proximal
risk factors are more often modifiable than distal risk factors, but being modifiable is not a criterion
for proximal risk factors. 3 Categories:
1. The first category is biological factors leading to potentially maladaptive emotional, cognitive,
or behavioural tendencies.
2. The second category of proximal transdiagnostic risk factors is basic cognitive deficits or
biases in information processing such as attentional biases or working memory deficits,
which are consistently and strongly linked to several psychopathologies
3. A third category of proximal transdiagnostic risk factors is stable psychological individual
difference factors reflecting the tendency to adopt particular styles of responding to
situations, such as a pessimistic attributional style, emotion regulation tendencies like
chronic suppression, or personality characteristics such as neuroticism or negative affectivity.
Distal risk factors may lead to proximal risk factors via at least three mechanisms/processes
- First, distal risk factors may shape responses to the environment
- Second, distal factors could shape individuals’ beliefs, schemas, and self-images to create
proximal factors
- Third, classical and operant conditioning, modelling, and observational learning are likely to
play roles in linking distal and proximal risk factors
Moderators: determine what particular symptoms proximal transdiagnostic risk factors will lead to in
a given individual. Create symptoms by 3 categories:
1. The first category of moderators is conditions that raise certain themes or concerns that
proximal factors then act upon
2. A second category of moderators is conditions that operate on proximal transdiagnostic risk
factors to shape them into disorder-specific responses through modelling, observational
learning, and reinforcement.
3. The third group of moderators is biological or environmental characteristics that change the
sensitivity to and reinforcement value of internal and external stimuli. It is important to note
that changes in reinforcement value can occur for both the processes of positive
reinforcement, which refers to responses that are followed by the presentation of a stimulus
that increases the chance of that behavior occurring (typically onset of a pleasant stimulus),
and negative reinforcement, which refers to the removal of a stimulus that increases the
chance of the behavior occurring (typically removal of something aversive)
Authors: We suggest that by confining moderators to environmental and biological factors as we do,
we reduce the potential for circularity and increase the potential explanatory power of a
transdiagnostic model.
Critical distinctions between distal risk factors and moderators are (a) their temporality relative to
proximal risk factors and psychopathology and (b) how they exert their causal effects. Distal risk
factors precede proximal risk factors and psychopathology in time; moreover, distal risk factors are
conceived as causes of proximal risk factors; proximal risk factors, in turn, cause psychopathology
(i.e., are mediators between distal risk factors and psychopathology). Moderators have their effects
by interacting with and acting on existing proximal risk factors and thus follow them in time or are
concurrent with them; however, moderators precede and have causal effects on psychopathology.
Proximal risk factors explain comorbidity and multifinality, that is, the mechanisms by which one
process leads to multiple comorbid disorders. Moderators explain how individuals with that proximal
risk factor develop specific disorders—that is, their divergent trajectories.
, Limitations:
- A major limitation of this heuristic is that it is new and has not been directly tested
- A second limitation of our heuristic is that it is likely to be too simplistic
- Third, the heuristic has not specified the potential role of developmental factors in the
effects of risk factors and moderators, although we believe that developmental processes are
important
Artikel 2.
Emotion, Emotion Regulation, and Psychopathology: An Affective Science Perspective (Gross,
Jazaieri)
Outline: In the first section of this article, we define emotion and emotion regulation. In the second
and third sections, we present a simple framework for examining emotion and emotion regulation in
psychopathology. In the fourth section, we conclude by highlighting important challenges and
opportunities in assessing and treating disorders that involve problematic patterns of emotion and
emotion regulation.
Difficulty in characterizing psychiatric disorders with emotions and emotion on regulation due to: the
heterogeneity of emotion-related processes, as well as the considerable divergence in definitions of
emotion and emotion regulation (Gross & Barrett, 2011). Another difficulty is the tremendous
heterogeneity within psychiatric disorders.
In addition, uncertainty prevails regarding the causal role of emotion and emotion-regulation
difficulties. similar phenomena are characteristic of multiple emotions.
Emotional reactivity: as emotions arise they typically involve loosely coupled experiential,
behavioural, and physiological responses: One feels, behaves, and mounts whole-body responses
Emotion regulation occurs when one activates—either implicitly or explicitly—a goal to influence the
emotion-generative process.
- Intrinsic/intrapersonal (regulating one’s own emotions)
- Extrinsic/interpersonal (regulating someone else’s emotions)
3 important common factors for adaptive regulation:
- Awareness (as well as the context in which they are occurring) enhances both the range of
available strategies and the flexibility with which one uses them
- Goals; what one means to achieve include increasing or decreasing the magnitude or
intensity of emotion experience, expression or physiology
- Strategies; specify the means
Week 1.
Artikel 1.
A Heuristic for Developing Transdiagnostic Models of Psychopathology: Explaining Multifinality and
Divergent Trajectories (Nolen-Hoeksema, Watkins)
Problem: Current transdiagnostic models, however, have difficulty simultaneously explaining the
mechanisms by which a transdiagnostic risk factor leads to multiple disorders (i.e., multifinality) and
why one individual with a particular transdiagnostic risk factor develops one set of symptoms while
another with the same transdiagnostic risk factor develops another set of symptoms (i.e., divergent
trajectories).
Goal: In this article, we propose a heuristic for developing transdiagnostic models that can guide
theorists in explicating how a transdiagnostic risk factor results in both multifinality and divergent
trajectories. We also (a) describe different levels of transdiagnostic factors and their relative
theoretical and clinical usefulness, (b) suggest the types of mechanisms by which factors at 1 level
may be related to factors at other levels, and (c) suggest the types of moderating factors that may
determine whether a transdiagnostic factor leads to certain specific disorders or symptoms and not
others (distal and proximal).
Theoretical background:
Approaches focused on transdiagnostic processes have a number of theoretical and clinical
advantages over disorder-specific approaches. First, there is growing agreement that the
heterogeneous disorders in our current diagnostic system are each made up of dysfunctional
versions of processes that vary along continua in the general population.
Second, transdiagnostic approaches can help us understand the comorbidity between disorders.
Third, if a transdiagnostic factor is causally related to two or more disorders, then assessment and
training could more parsimoniously focus on these factors than on the large number of discrete
disorders currently in the DSM.
Intermediate phenotypes: are conceived as neurocognitive and affective processes, such as learning,
memory, attention, stress sensitivity, and emotional reactivity that are causally linked to the
development of symptoms
Endophenotypes: are intermediate phenotypes that are heritable (erfelijk)
Multifinality refers to the process by which certain environments, experiences, or characteristics
increase risk for a number of different types of psychopathology in children or adults—for example,
stress is associated with multiple disorders
Similarly, transdiagnostic processes generally have not addressed phenotypic plasticity, wherein the
pattern of symptoms morphs across the life course, often unpredictably, especially during the
transitions through childhood and adolescente into adulthood.
,Distal risk factors contribute to disorders only through mediating proximal risk factors. Proximal risk
factors directly influence symptoms relative to distal risk factors. Distal and proximal risk factors lead
to multiple disorders (i.e., multifinality), which are comorbid (indicated by dashed lines). Moderators
interact with proximal risk factors to determine which specific disorder individuals will experience
(i.e., to determine divergent trajectories)
Distal factors: environmental and congenital biological variables relatively distal to observable
symptoms of disorders. Two categories:
1. The first is environmental context factors, such as parental psychopathology, a history of
sexual or physical abuse, and other traumatic events. These are what Hammen (1991, 2005)
labels independent stressors because they are not caused by the individual experiencing
them (e.g., the death of a spouse), and dependent stressors, which the individual may have
played a role in creating (e.g. interpersonal conflict)
2. The second category of distal risk factors consists of congenital biological abnormalities,
principally genetic abnormalities and congenital abnormalities in brain function or structure
(caused by genetic abnormalities or early brain injuries
,Proximal factors: within-person variables that are more proximal to symptoms of disorders.
Thus, proximal risk factors are operationalized as those intrapersonal risk factors that (a) directly
precede symptoms (relative to distal risk factors), and/or (b) directly influence symptoms. Proximal
risk factors are more often modifiable than distal risk factors, but being modifiable is not a criterion
for proximal risk factors. 3 Categories:
1. The first category is biological factors leading to potentially maladaptive emotional, cognitive,
or behavioural tendencies.
2. The second category of proximal transdiagnostic risk factors is basic cognitive deficits or
biases in information processing such as attentional biases or working memory deficits,
which are consistently and strongly linked to several psychopathologies
3. A third category of proximal transdiagnostic risk factors is stable psychological individual
difference factors reflecting the tendency to adopt particular styles of responding to
situations, such as a pessimistic attributional style, emotion regulation tendencies like
chronic suppression, or personality characteristics such as neuroticism or negative affectivity.
Distal risk factors may lead to proximal risk factors via at least three mechanisms/processes
- First, distal risk factors may shape responses to the environment
- Second, distal factors could shape individuals’ beliefs, schemas, and self-images to create
proximal factors
- Third, classical and operant conditioning, modelling, and observational learning are likely to
play roles in linking distal and proximal risk factors
Moderators: determine what particular symptoms proximal transdiagnostic risk factors will lead to in
a given individual. Create symptoms by 3 categories:
1. The first category of moderators is conditions that raise certain themes or concerns that
proximal factors then act upon
2. A second category of moderators is conditions that operate on proximal transdiagnostic risk
factors to shape them into disorder-specific responses through modelling, observational
learning, and reinforcement.
3. The third group of moderators is biological or environmental characteristics that change the
sensitivity to and reinforcement value of internal and external stimuli. It is important to note
that changes in reinforcement value can occur for both the processes of positive
reinforcement, which refers to responses that are followed by the presentation of a stimulus
that increases the chance of that behavior occurring (typically onset of a pleasant stimulus),
and negative reinforcement, which refers to the removal of a stimulus that increases the
chance of the behavior occurring (typically removal of something aversive)
Authors: We suggest that by confining moderators to environmental and biological factors as we do,
we reduce the potential for circularity and increase the potential explanatory power of a
transdiagnostic model.
Critical distinctions between distal risk factors and moderators are (a) their temporality relative to
proximal risk factors and psychopathology and (b) how they exert their causal effects. Distal risk
factors precede proximal risk factors and psychopathology in time; moreover, distal risk factors are
conceived as causes of proximal risk factors; proximal risk factors, in turn, cause psychopathology
(i.e., are mediators between distal risk factors and psychopathology). Moderators have their effects
by interacting with and acting on existing proximal risk factors and thus follow them in time or are
concurrent with them; however, moderators precede and have causal effects on psychopathology.
Proximal risk factors explain comorbidity and multifinality, that is, the mechanisms by which one
process leads to multiple comorbid disorders. Moderators explain how individuals with that proximal
risk factor develop specific disorders—that is, their divergent trajectories.
, Limitations:
- A major limitation of this heuristic is that it is new and has not been directly tested
- A second limitation of our heuristic is that it is likely to be too simplistic
- Third, the heuristic has not specified the potential role of developmental factors in the
effects of risk factors and moderators, although we believe that developmental processes are
important
Artikel 2.
Emotion, Emotion Regulation, and Psychopathology: An Affective Science Perspective (Gross,
Jazaieri)
Outline: In the first section of this article, we define emotion and emotion regulation. In the second
and third sections, we present a simple framework for examining emotion and emotion regulation in
psychopathology. In the fourth section, we conclude by highlighting important challenges and
opportunities in assessing and treating disorders that involve problematic patterns of emotion and
emotion regulation.
Difficulty in characterizing psychiatric disorders with emotions and emotion on regulation due to: the
heterogeneity of emotion-related processes, as well as the considerable divergence in definitions of
emotion and emotion regulation (Gross & Barrett, 2011). Another difficulty is the tremendous
heterogeneity within psychiatric disorders.
In addition, uncertainty prevails regarding the causal role of emotion and emotion-regulation
difficulties. similar phenomena are characteristic of multiple emotions.
Emotional reactivity: as emotions arise they typically involve loosely coupled experiential,
behavioural, and physiological responses: One feels, behaves, and mounts whole-body responses
Emotion regulation occurs when one activates—either implicitly or explicitly—a goal to influence the
emotion-generative process.
- Intrinsic/intrapersonal (regulating one’s own emotions)
- Extrinsic/interpersonal (regulating someone else’s emotions)
3 important common factors for adaptive regulation:
- Awareness (as well as the context in which they are occurring) enhances both the range of
available strategies and the flexibility with which one uses them
- Goals; what one means to achieve include increasing or decreasing the magnitude or
intensity of emotion experience, expression or physiology
- Strategies; specify the means
