Marriage and Family Therapy: Health and Illness Class
Paragraph 1:List 5-7 key points from the reading that could serve as a reference for a session working with the family of a child with an illness. Use bullet points and complete sentences.
Paragraph 2:Zubatsky and Mendenhall (2018) discuss MedFT’s need to remain sensitive to the myriad of emotions and mentalities that diabetic patients and their families express when approaching family collaboration. They also note the influence of diversity on conceptualization of illness and ‘habitudes,’ including traditional foods that may be harmful to the patient’s health. How can a family be guided to form ‘habitudes’ that benefit their relative with diabetes, themselves, and future children, while honoring their cultural values?
Paragraph 3:The review of family relational stress and pediatric asthma article introduces the Biobehavioral Family Model as a multilevel systemic biopsychosocial model. One of the concepts of this model is the family emotional climate which refers to the “intensity and valence of emotional exchange” within families. In addition, Rolland describes the potential for high levels of emotional reactivity of family members to illness. Knowing that individuals and cultures express emotions differently, how would you assess and address emotional reactivity and emotional climate in a family in a culturally sensitive way?
Reading:
Mendenhall, T., Lamson, A., Hodgson, J., & Baird, M. (Eds.) (2018). Clinical Methods inMedical Family Therapy. Springer. Chapter 3 & 11 • Rolland, J. (2018). Helping Couples and Families Navigate Illness and Disability: AnIntegrated Approach ISBN 9781462534951 Chapter 7 & 11 Review of Family Relational Stress and Pediatric
Asthma: The Value of Biopsychosocial Systemic
Models
BEATRICE L. WOOD*
BRUCE D. MILLER*
HEATHER K. LEHMAN†
Asthma is the most common chronic disease in children. Despite dramatic advances in
pharmacological treatments, asthma remains a leading public health problem, especially
in socially disadvantaged minority populations. Some experts believe that this health gap
is due to the failure to address the impact of stress on the disease. Asthma is a complex disease that is influenced by multilevel factors, but the nature of these factors and their interrelations are not well understood. This paper aims to integrate social, psychological, and
biological literatures on relations between family/parental stress and pediatric asthma,
and to illustrate the utility of multilevel systemic models for guiding treatment and stimulating future research. We used electronic database searches and conducted an integrated
analysis of selected epidemiological, longitudinal, and empirical studies. Evidence is substantial for the effects of family/parental stress on asthma mediated by both disease management and psychobiological stress pathways. However, integrative models containing
specific pathways are scarce. We present two multilevel models, with supporting data, as
potential prototypes for other such models. We conclude that these multilevel systems
models may be of substantial heuristic value in organizing investigations of, and clinical
approaches to, the complex social–biological aspects of family stress in pediatric asthma.
However, additional systemic models are needed, and the models presented herein could
serve as prototypes for model development.
Keywords: Family; Stress; Asthma; Biopsychosocial; Epigenesis; Health Disparities
Fam Proc 54:376–389, 2015
T
his paper reviews the literature focusing on how family stress may affect pediatric
asthma, with the goal of furthering understanding of the complex biopsychosocial and
social systemic nature of mind–body connections in physical disease. We briefly define
asthma, and its pathogenesis, triggers, and prevalence. The main body of the paper
focuses on an analysis and integration of the family relational stress and asthma literature organized by an overarching systems framework. We present two specific systemic
socio-psycho-biological models: one focusing on the impact of social stress on child asthma
by way of prenatal stress, and one focusing on specific family relational patterns as they
impact child emotional stress, and asthma. The models are presented as prototypes of the
kind of modeling we believe would foster theory development in stress-related illness by
engaging a systemic biopsychosocial perspective. To illustrate how such modeling might
*Psychiatry and Pediatrics, University at Buffalo, Buffalo, NY.
†
Allergy and Immunology, Woman and Children’s Hospital of Buffalo, Buffalo, NY.
Correspondence concerning this article should be addressed to Beatrice Wood, Psychiatry and Pediatrics, University at Buffalo, WCHOB, 219 Bryant Street, Buffalo, NY 14222. E-mail: bwood@buffalo.edu.
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WOOD, MILLER, & LEHMAN
be taken further, an integrated biosocial-family model is presented. Clinical implications
are discussed and directions for future research suggested.
BACKGROUND
Asthma is a chronic inflammatory disorder of the airways associated with airway
hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest
tightness, and coughing. Mechanisms of airway constriction include immune/inflammatory and cholinergic/vagal pathways, which are complexly interrelated. Episodes are associated with airflow obstruction that is reversible either spontaneously or with treatment.
Symptoms may be triggered by viral infections, exercise, exposure to allergens or irritants
(e.g., cigarette smoke), and emotions.
Prevalence of current asthma in 2011 for children under 18 has been estimated at 9.6%
(Bloom, Cohen, & Freeman, 2011). Morbidity and mortality of asthma remain problematic,
despite advances in pharmacological treatments. Some experts point to compromised
adherence and disease management as an explanation and others believe that the contribution of stress in asthma morbidity is underestimated, not well understood, and therefore
not adequately addressed in treatment.
RELATIONS BETWEEN FAMILY/PARENTAL STRESS FACTORS AND
PEDIATRIC ASTHMA
Family and asthma relations are complex with mutually causal pathways of effect.
Figure 1 offers an overarching framework to organize the review and consideration of
these complex interrelations. Subsequent sections will present findings addressing these
pathways of effects.
FIGURE 1. Relations between Family Function and Child Asthma.
Pediatric Asthma Affects the Family
In addition to the socioeconomic and life event stressors that impact on a family,
asthma can also be a stressor. It contributes to economic hardship, demoralizes caregivers,
causes family conflict, and disrupts routines. Asthma-related stressors have shown cumulative quadratic effects on caregiver quality of life (Everhart, Fiese, & Smyth, 2008).
Maternal depressive symptoms are elevated (Bartlett et al., 2004; Shalowitz et al., 2006),
and fathers are also vulnerable. In inner-city samples of children with asthma, 43% of
mothers and 32% of fathers scored in the depressed range on the Beck Depression Inventory (Lim, Wood, Miller, & Simmens, 2011; Waxmonsky et al., 2006). The disruptive
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impact of child asthma on parents and families in turn affects the child’s asthma by
impairing family management of the disease, and by impacting asthma disease through
stress-related pathways.
Family and Parental Stress Affect Asthma by Compromising Disease Management
Poor disease management as indexed by the Family Asthma Management System Scale
has been associated with increased asthma morbidity in children (Celano et al., 2010;
Fiese, Wamboldt, & Anbar, 2005). Family stress and conflicts can interfere with adherence
by affecting how well a family monitors a child’s symptoms and makes treatment decisions
(Bender, Milgrom, & Apter, 2003; Chen, Bloomberg, Fisher, & Strunk, 2003). Studies also
show that parents who are less vigilant due to being stressed or depressed are more likely
to allow their asthma-prone children to be exposed to cigarette smoke, viruses, or other
agents that exacerbate asthma (Leiferman, 2002).
Disruption in family routines caused by the stress of child asthma can also contribute
to impaired asthma management and poor disease control (Schreier & Chen, 2010), but
team-based management strategies and cohesive family climate promote adherence
(Fiese, Foley, & Spagnola, 2006; Fiese et al., 2005). A recent study using baseline data
from the School-Based Asthma Therapy Trial showed that families with more asthma routines had better adherence with preventive medications and less exposure to environmental triggers (Peterson-Sweeney, Halterman, Conn, & Yoos, 2010).
There is evidence that maternal negative affect contributes to worse asthma through
both nonadherence and psychobiologic stress pathways. In a longitudinal study of lowincome African-American children, Celano et al. (2010) reported an association between
caregiver depression and worse adherence. However, Bender and Zhang showed that
while negative affect predicted increased symptom scores, nonadherence did not explain
the relationship between negative affect and symptom scores. Furthermore, parent negative affect did predict prednisone bursts (which indicate asthma exacerbations) even when
controlling for level of adherence (Bender & Zhang, 2008).
Family and Parental Stress Affect Pediatric Asthma Onset through Psychobiologic
Pathways
In a longitudinal study of children at genetic risk for asthma, family distress (maternal
depression, inadequate spousal support) when infants were 3 weeks old was associated
with asthma onset at age 3 (Mrazek et al., 1999). A large cohort study (n = 14,000) of children not at risk for asthma enrolled in the Manitoba (Canada) Health Services insurance
plan showed that maternal distress (episodic mood disorders, anxiety, dissociative and
somatoform disorders, adjustment and depressive disorders) and pharmacy records of psychotropic medication prescriptions were strongly related to increase in offspring asthma
at age 7 (Kozyrskyj et al., 2008). Another study, focusing on inner-city African-American
families, demonstrated a prospective relationship specifically between maternal depressive symptoms and child asthma symptoms (Otsuki et al., 2010). In a prospective birthcohort study, parental stress was identified as a predictor of wheezing in infancy (Wright,
Cohen, Carey, Weiss, & Gold, 2002), associated with increased IgE expression, allergeninduced lymphocyte proliferation, and cytokine profiles in infants predisposed to atopy
and asthma (Wright et al., 2004). Milam showed a similar effect in a cohort study (California Child Health Study) which showed a stronger effect in boys (Milam et al., 2008). Nonstressed healthy family functioning may buffer children who are genetically at risk for
asthma. A study of at-risk children demonstrated that children in families with interactions marked by emotional engagement and organization when the children were
18 months old had a significantly lower risk for continuing atopic illness at age 3 (Gustafswww.FamilyProcess.org
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son, Kjellman, & Bjorksten, 2002). As disease management cannot be a factor affecting
onset of disease, findings from these studies suggest direct psychobiological effects of
family relational stress on asthma.
Evidence is mounting in support of contributions of parental stress to child asthma
through gene–environment interactions mediated by epigenetic mechanisms. (Epigenesis
refers to functionally relevant modifications of the genome, which do not involve a change
in the nucleotide [DNA] sequence. Such modifications are elicited by environmental
factors, and have profound effects on phenotypic outcomes.) A prospective cohort study
(California Children’s Health Study) of 2,497 children aged 5–9 years with no history of
asthma or wheeze at study entry (2002–2003) showed that if parents were chronically
stressed, their offspring were more susceptible to the effects of pollution and in utero
tobacco smoke on the development of asthma (Shankardass et al., 2009).
An additional pathway by which parental stress affects children’s asthma may be by
prenatally transmitted vulnerability to stress, through epigenetically altered stress
response systems. Evidence from animal and human research indicates that hypothalamic–pituitary–adrenal (HPA) functioning and other stress pathways may be altered by
in utero stress and early caregiving experiences, through epigenetic mechanisms (Curley,
Jensen, Mashoodh, & Champagne, 2011; Franklin et al., 2010; Wright, 2007, 2011). The
alteration of these stress pathways in offspring could have a profound effect on asthma by
making the offspring relatively stress-sensitive, thus rendering them vulnerable to the
effects of stress on their asthma.
One problem with the current gene 9 environment and epigenetic research is that
parental stress is vaguely defined and is examined isolated from the social and family context. This limitation renders the findings difficult to apply to clinical interventions. Models
are required to guide more contextual research on the effects of gene–environment
research in asthma. Such models need to encompass social and family stressors and protective factors. We will present such a model later in this paper.
Effect of Social Determinants on Asthma: A Developmental Biopsychosocial
Systems Model
There is abundant evidence that health disparities are due to multiple factors, many of
which are social and emotional stressors, as well as factors that interfere with access to
health care and disease management. Health disparities are defined as differences
between demographic groups in the overall rate of disease incidence, prevalence, morbidity, mortality, or survival (McQuaid, 2008). Low socioeconomic minority children experience differentially high morbidity and mortality from asthma (Bender, Milgrom, Rand, &
Ackerson, 1998; Celano et al., 2010; McQuaid, Walders, Kopel, Fritz, & Klinnert, 2005).
The underlying causes of these disparities are complex and not well understood (Apter &
Casillas, 2009; Canino, McQuaid, & Rand, 2009; Valet, Perry, & Hartert, 2009). KoinisMitchell et al. (2007) propose the use of a multidimensional cumulative risk index to
conceptualize the variety of factors. Canino et al. (2009) propose a multilevel framework
to advance research and clinical practice, including health care policies and regulations,
operation of the health care system, provider/clinician-level factors, social/environmental
factors, and individual/family attitudes and behaviors.
Wright (2009) claims that health disparities are due in large measure to the effects that
unrelenting poverty and disadvantaged social status have on parent and family emotional
well-being. For families, the external stress of social and economic circumstances may
exceed parental capacity for adaptive coping, thus causing chronic high levels of parental
stress, anxiety and depression, and, at times, parental discord and conflict. Research cited
above demonstrates how these factors affect asthma in children.
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Social disadvantage has even been shown to have prenatal effects which influence atopy
and asthma in offspring. One study of an urban pregnancy cohort demonstrated an association among maternal SES, prenatal stress and increased cord blood IgE levels, and
repeated wheeze in the offspring (Sternthal, Coull, Chiu, Cohen, & Wright, 2011). These
and other human and animal studies suggest that maternal prenatal stress may result in
programming of the infant’s HPA axis in a manner that renders them vulnerable to atopy
and subsequent asthma (Bagot & Meaney, 2010; Curley et al., 2011). Prenatal effects may
thus have underestimated, yet dramatic, effects on asthma onset and outcomes in socially
disadvantaged populations, but research to date is limited by lack of organizing models.
Wright proposes a specific socio-psycho-biological model in which prenatal maternal
stress plays a central role (Wright, 2011). Wright notes that a crucial focus for asthma
research is identifying mechanisms responsible for health disparities across economic and
racial/ethnic groups. She proposes that psychosocial stress considerations are of significant relevance in this regard. Specifically she claims that in addition to examining the
impact on asthma of environmental toxins that are prevalent in impoverished neighborhoods, it is also essential to consider social “toxins” as equally important. Wright points
out that ecological perspectives note that individual health risks have multilevel determinants, importantly including the social context. For example, chronic stress brought about
by social disadvantage is influenced by the characteristics of the families, homes, and communities in which they live. Trauma, community and interpersonal violence, other negative life events (job loss, family dissolution), racism, and discrimination all contribute to
the context of stress that typifies social disadvantage and health disparities.
Wright advocates examining these effects in a developmental perspective, noting that
for asthma it is relevant that immune and lung development occur largely in utero and
during early childhood. Thus, an important step toward identifying children at risk for
asthma is characterizing mechanisms that lead to and maintain early predisposition to
atopy and asthma. Wright regards stress as an important developmental programming
agent. Specifically stress may result in biobehavioral states, for example, PTSD, anxiety,
and depression, which can have long-lasting neurobiological effects that are relevant for
the development of physical diseases such as asthma. From a developmental perspective,
she notes that disturbed regulation of maternal stress systems may cause nonoptimal
early childhood caregiving experiences or negative long-lasting in utero effects on offspring stress regulation systems (Wright, 2011).
Wright has developed a specific multilevel model to organize future investigation that
takes social “toxins” into account (see Figure 2). In this model, social stressors such as
trauma, violence, discrimination, racism, and other negative life events cascade in their
effect by altering prenatal physiological processes in the mother. These in turn alter the
programming of stress pathways in the offspring (including disrupted autonomic/HPA
axes reactivity to stress, and immunomodulation). These alterations render the offspring
more susceptible to toxic (physical and social) environmental effects, culminating in atopy,
asthma (in genetically predisposed offspring), and compromised lung function (see
Figure 2; Wright, 2011).
The studies reviewed above and Wright’s model take an important step in explaining
how social factors influence disease process in asthma, by specifying socio (SES, community, racial stress), psychological (prenatal stress), and biological (atopy, asthma) parameters, along with pathways by which social stress cascades to effect physiological processes
influencing disease process. This research provides strong rationale for the importance of
addressing social stress in developing asthma prevention approaches. However, Wright’s
model does not consider the potential moderating effect of family with regard to the impact
of social stress on the mother and child. Nor does it posit specific aspects of family function
that may be key in this regard. The Biobehavioral Family Model, described below, is an
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FIGURE 2. Conceptual Model for Stress-Induced Perinatal Programming of Asthma, Atopy, and Lung
Function (Adapted from Wright, 2011).
empirically tested model that could be integrated with Wright’s model to address this limitation and thus extend the model’s heuristic value and clinical application.
The Biobehavioral Family Model (BBFM): A Biopsychosocial Systems Model of
Family Stress and Protection
The BBFM is a multilevel systemic biopsychosocial model, positing reciprocal pathways
of effect (Wood, 1993; Wood et al., 2008). This model rests upon assumptions of the interdependence of relational, emotional, and biological processes consistent with the current
“social neuroscience” paradigm (Cacioppo, 1994). The BBFM posits that family emotional
climate, quality of parent–parent relations, parent–child relational security, and biobehavioral reactivity are processes that influence one another and collectively either buffer or
potentiate psychobiological processes contributing to disease activity in stress-related illnesses (see Figure 3; Wood, 1993; Wood et al., 2008). This model is not a model of family
dysfunction, but rather a model that can explain how family relational stress reverberates
in the family plus how family relational support can buffer or protect the individuals and
family from external stressors, such as those described above in Wright’s model (Wright,
2011). The dimensional nature of the model provides for both stressful and protective
effects. It is constructed of four continua: family emotional climate, parental relationship
quality, parent–child relational security, and biobehavioral reactivity. Family process
characterized by the positive ends of each continuum would buffer the effects of stress
(internal and external) on the child, whereas family process characterized by the negative
ends of the continua would transmit internal family stress and exacerbate external stress
for the child. The dimensions are defined as follows.
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FIGURE 3. The Biobehavioral Family Model (Wood, 1993; Wood et al., 2008).
Family emotional climate refers to the overall intensity and valence of emotional
exchange. It colors all aspects of family relationship and therefore is likely a key factor
contributing to emotional status and outcomes in family members. Negative family emotional climate includes hostility, criticism, verbal attacks, etc., and is similar to the criticism construct of Expressed Emotion (EE; Brown & Rutter, 1966). Positive aspects include
warmth, affection, support, affirmation, kindness, etc. Family emotional climate is characterized by the intensity and balance of negative and positive emotional exchange among
family members. This balance or imbalance can be construed as reflecting one aspect of
family-level stress regulation or dysregulation. If the balance is skewed toward negative
emotional exchange, then family relational process produces or escalates stress dysregulation. If the balance is skewed toward positive emotional exchange, then family relational
process protects or buffers family members from the effects of stressors (internal and
external), thus regulating stress.
Parental relationship quality refers to parent–parent interaction patterns that include
mutual support, understanding, and adaptive disagreement (respectful and resolving)
versus hostility, rejection, and conflict. Parental discord contributes to negative family
emotional climate, contributes to parent–child relational insecurity and negative parenting, and thus stresses the child. Positive parental relationships contribute to positive family emotional climate and promote parent–child relational security and positive parenting,
which can buffer children from stress (see Figure 3).
Parent–child relational security is a construct related to attachment. Insecure parent–
child relations produce stress in the child or exacerbate the effect of family or external
stress on the child. Secure parent–child relationships can buffer a child from family and
external stress.
“Biobehavioral reactivity,” the pivotal construct linking family emotional processes with
biological and disease processes, is conceptualized as the degree or intensity with which an
individual responds physiologically, emotionally, and behaviorally to emotional challenge
(Boyce, 1992; Jemerin & Boyce, 1992). Biobehavioral reactivity reflects the ability of the individual to regulate stress and arousal, and is physiologically mediated by activation of stress
pathways, including the HPA, sympathetic adrenal medullary, and autonomic systems
(ANS). Biobehavioral reactivity is presumed to be influenced by innate tendencies toward
emotional and physiological reactivity (Kagan, Reznick, & Snidman, 1988; Suomi, 1987), and
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by external influences, particularly by patterns of attachment and caregiving (Calkins, 1994;
Cassidy, 1994; Field, 1994). The BBFM posits that if the family relational patterns are supportive, then the child’s biobehavioral reactivity will be moderate and well regulated and thus
the effects of stress on the child’s disease process will be buffered. If family relational patterns
are stressful, the child will be biobehaviorally dysregulated, and family and external stress
will have direct effects on disease processes by way of psychobiologic stress pathways.
Various stress-related diseases may be negatively impacted by high biobehavioral reactivity by way of altered or dysregulated stress pathways (Wood, Klebba, & Miller, 2000).
In asthma, anxiety and depression have been implicated in potentiating disease activity
through dysregulated stress pathways. Anxiety and depression are also considered prime
examples of maladaptive biobehavioral reactivity and emotion dysregulation (Kovacs,
Joormann, & Gotlib, 2008), characterized in part by altered ANS activation (Lehrer, 1998;
Miller, 1987). When applied to asthma the BBFM posits that child anxiety and depression
mediate, via dysregulated stress pathways, the effect of family and external stress on the
child’s disease processes.
Laboratory-based family interaction studies have tested the BBFM in child asthma.
Findings demonstrated that the chronic stress of negative family emotional climate, parental depression, parental conflict, insecure parent–child relationship, and negative parenting
predict child anxiety and depression, which in turn are associated with increased asthma
disease activity (Lim, Wood, & Miller, 2008; Lim et al., 2011; Wood et al., 2006, 2007,
2008). The child’s anxiety and depression may impact the asthma disease process through
asthma-relevant altered immune function (Chen & Miller, 2007) and autonomic dysregulation (Miller, Wood, Lim, Ballow, & Hsu, 2009). Thus, the results of these studies are suggestive that the BBFM may be useful in specifying family-psycho-biological pathways by which
family relational stress impacts child physiological well-being and disease. Furthermore,
the findings suggest that the BBFM, as a dimensional model, may be used to examine how
family function may moderate the impact of social stress on child asthma.
The Integration of the BBFM into Wright’s Socio-psycho-biological Model of the
Effects of Prenatal Maternal Stress on Child Asthma
Wright’s model does not address the factors which may determine the extent to which
external social, economic, and cultural stressors will cause maternal stress in the pregnant mother. It is clear that some pregnant mothers experience great stress under compromising socioeconomic conditions, but some do not. Models are needed to explain when
mothers are resilient and when they are psychophysiologically compromised by external
stress while pregnant. We propose that adaptive family relationships will buffer the
effects of external stress on the pregnant mother, whereas maladaptive family relationships will exacerbate the effects of external stress. The BBFM proposes specific family
relational dimensions by which the effects of stress on the mother may be either buffered
or exacerbated, depending on which end of the dimensions family relations operate.
The integrated model proposes that family function at the positive ends of dimensions of
the BBFM model will buffer the pregnant mother from external stressors, whereas function
at the negative ends will add to the external stress and exacerbate the stress effect in the
pregnant mothers. Thus, BBFM family function will moderate the effect of external stressors on maternal stress (see Figure 4 for the integrated Wright–BBFM model).
More explicitly, we propose that a warm family emotional climate, secure internal
attachment models within the pregnant mother, and good relationship quality between
the pregnant mother and an intimate partner, and between the pregnant mother and
other family members, will buffer the effect of external socioeconomic stress on the pregnant mother (Woods, Priest, & Roush, 2014). In contrast, hostile family emotional climate,
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FIGURE 4. Wright–BBFM Integrated Heuristic Model.
insecure maternal attachment, compromised partner and family relationships will fail to
buffer, and even exacerbate, the effect of external stressors on the pregnant mother.
Good BBFM family functioning would likely have positive effects on the pregnant
mother’s appraisal of demands and coping capabilities, decreasing the effects of stressors,
whereas negative BBFM functioning would distort the appraisal of demands and coping
capabilities, thus exacerbating the stress on the pregnant mother. This exacerbated stress
would increase prenatal mother’s biobehavioral (physiological) reactivity altering the maternal endocrine system, and autonomic nervous system reactivity, which, in turn, would alter
the neurodevelopmental programming of stress pathways in the offspring (including disrupted autonomic/HPA axes reactivity to stress, and immunomodulation). These alterations
would render the offspring more susceptible to atopic/allergic responses to toxic (physical
and social) environmental effects, thus placing the child at risk for asthma (see Figure 4).
Thus, BBFM-defined family relational processes would moderate the effects of stressors
on maternal biobehavioral/physiological reactivity and thus either undermine or protect
development of normal stress pathways and neuroendocrine, autonomic, and immune
function in the child.
This integrated model has not been tested, but is presented as a prototype of the kind of
multilevel biopsychosocial model that may enhance theory-building and innovative
research that is directly relevant to prevention and clinical intervention strategies.
CLINICAL IMPLICATIONS
The research and modeling reviewed herein has direct clinical implications. Clinicians
may be referred children with asthma for many reasons, sometimes for help in managing
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the disease because they have intractable asthma, or because of poor compliance, or
because the asthma health care provider has noted emotional distress in the child or family. Sometimes a child is referred from outside the medical system because of emotional
distress, but the distress may be importantly related to asthma. Therefore, when any child
or adolescent is seen for emotional distress, it is important to assess for co-occurring
asthma (or other stressful chronic illness). The illness may play an important role in the
child’s distress.
The first step in being helpful to children with any chronic physical illness and their
families is to acknowledge the potential stress and impact that the child’s illness has on
the family. This step is easy. However, it is unlikely that families, or even their physicians,
are fully aware of the research indicating that stress impacts asthma and other chronic illnesses. It is important, therefore, to clarify how stress can impact illness, by disrupting
optimal management, and, in addition, to point out that almost any disease is made worse
by the direct effects of stress on the disease. This then opens the opportunity for sensitive
inquiry as to possible chronic social and family relational stressors, and/or life events
which may challenge the ability to manage the illness or emotionally stress the child.
The BBFM directs the clinician to observe the emotional climate in the family. Is it
hostile, warm, depressed, anxious, a mix of those? Are some members more emotionally
compromised than others? What about the emotional climate between the adult parental
caregivers? Are the attachment relationships among family members secure and supportive? Is there secure attachment between the parent and the patient, or have there been
ruptures in parent–child attachment due to life circumstances or deterioration of relationship through conflict? If relationships are troubled it is important to examine and address
the source of the trouble, helping the family to engage in repair and forgiveness processes
if indicated.
BBFM findings support the importance of being aware of the possibility of parental
depression which may show itself in a variety of ways, for example, missed appointments,
poor asthma management, negative affect such as pessimism, irritability, anxiety, hopelessness, lack of pleasure, and in distressed relationships with partner and children.
Depression and anxiety in the parent are accompanied by biobehavioral reactivity, which
can undermine relationships by evoking conflict and causing ruptures in attachment
security between parents, and between parent and the asthmatic child. Depression in the
parent may also directly stress the child by causing them to worry about the safety and
well-being of the parent, and about whether the parent can take care of them.
If depression in one or both parents seems possible, it is important to evaluate the parent(s) specifically for depression and to incorporate treatment for their depression into the
intervention approach. Attention to stressed parental relationships may also be necessary
as part of overcoming the depression. Parenting is likely to be compromised for parents
who are depressed, and if the parent’s depression is chronic or repetitive, then the parent–
child attachment processes may be dysfunctional or disrupted. Treating the parental
depression and addressing the attachment ruptures (Diamond, Diamond, & Levy, 2014) is
essential to improve family emotional climate and to reduce high levels of child stress (and
even depression) which is accompanied by high biobehavioral reactivity which may potentiate disease activity. Care should be taken so as not to have the depressed parent feel to
blame for their child’s difficulties. Rather, language that conveys the resonance of suffering that impacts everyone in the family is more compassionate and acceptable to families.
Family systems-based intervention is essential in addressing the mutually exacerbating effects of parental depression, distressed family relationships, and negative parenting.
However, this does not mean that all sessions include all family members. Instead, the
BBFM helps identify what dimensions of relationship need attention, and the manner in
which the intervention is approached will depend upon various theoretical preferences
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and practical considerations. Adolescents, in particular, and parental dyads often require
their own private attention. At times, it is also most effective to have sessions with just
the parent–child dyad in which attachment ruptures or stress has occurred. All work with
subsystems requires knowledge and sensitivity to the family relational system as a whole
so as not to have unintentional negative effects. (For an example of BBFM guided treatment of an adolescent with asthma see Theodoratou-Bekou, Andreopoulou, Andriopoulou,
& Wood, [2012].) Wright’s prenatal model and research indicate the crucial role that prevention could play in alleviating prenatal and postnatal stress in mothers of children at
risk for asthma. Research guided by both the BBFM and Wright’s models suggests the
value of family-strengthening interventions (McHale & Lindahl, 2011) as preventative
measures for socially disadvantaged families at risk for genetic transmission of asthma,
or for children with early onset of wheezing. Family-strengthening can also be valuable
during the course of a child’s asthma, particularly if they have difficult to control asthma.
The integrated Wright–BBFM model described above may also guide in a similar way
specific family relational interventions aimed at buffering the pregnant mother from
transmitting stress reactivity and asthma vulnerability to their children. Potentially, such
interventions may be valuable to other epigenetically influenced chronic child diseases as
well.
DIRECTIONS FOR FUTURE RESEARCH
Rationale and initial findings of epigenetic and gene–environment interaction focusing
on parental stress and child diseases argue compellingly for further research in this area.
One limitation in the research to date is the identification of specific measurable and
mutable family relational factors for the “environment” aspect of the research. Models
such as the BBFM could serve a useful purpose in this research. For example, the interaction effect of BBFM family functioning (e.g., family climate, quality of parenting, parent–
child attachment, biobehavioral reactivity) on asthma-related genes could be examined as
predictors of asthma onset or disease morbidity.
Wright’s model similarly proposes specific socio-psycho-neurobiological mechanisms
and pathways that can organize and specify prenatal research aimed at prevention. The
integrated Wright–BBFM model offers a solid heuristic foundation for future research in
this area. For example, this model offers a rationale for intervention studies aimed at modifying patterns of parental depression and stressful family relations both pre- and postnatally. Such studies could test the causal contribution of family relational stress to asthma
outcomes, as well as the buffering effect of adaptive family relational function on asthma.
The modeling and research on co-parenting offers an excellent evidence-based intervention paradigm in which to effect these changes (McHale, Waller, & Pearson, 2012).
SUMMARY
This review of the research literature suggests that family/parental stress influences
pediatric asthma, and does so through disease management, adherence, and psychobiologic pathways. The effects of family turmoil on asthma disease management are well
established and recognized. The direct psychobiological effects of external social and family relational stress are beginning to receive increasing support and recognition. However,
most research is limited by lack of systems models which integrate biological, psychological, and social factors in the same heuristic model.
The integrated Wright–BBFM model presented above is illustrative of a potential “family” of systems models that could be of substantial heuristic value in organizing multilevel
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WOOD, MILLER, & LEHMAN
investigation promoting understanding and treatment of the complex biopsychosocial phenomenon of asthma and other stress influenced diseases as well.
It is our hope that the modeling approaches demonstrated in this paper will inspire
more multilevel systemic modeling, research, and treatment approaches to ultimately
reduce the prevalence, morbidity, and mortality in all kinds of stress-related emotional
and physical illnesses for children, adolescents, and adults.
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