Week 11: Intervention for the kids of Bipolars Flashcards
What is cool about this intervention?
It puts what we know about risk factors in practice.
Prevalence of major affective
disorders
National Comorbidity Study -Replication (n=9282) Depression 16.2% Bipolar disorder 2.1% Sub-threshold BD 2.4%*
and the WHO has it at a massive disease burden
Why is depression so bad (2 things)
Prevalence
burden
The onset of it keeps getting younger with each passing generation
Among diseases, unique combination of –High prevalence –Early age of onset –High chronicity –High role impairment
The enigma of affective disorders
Efficacious treatments exist. They are widely available BUT
Still, prevalence
continues to
increase.
Cos we focus on adult depression and not the causes in childhood
Approaches to the problem of the
affective disorders
LONGITUDINAL PROSPECTIVE RESEARCH
HIGH RISK POPULATIONS
The issue is you cannot always find participants cos they’re comparatively rare so you focus on known long term risk populations
Risk for psychopathology in offspring of
BD parents: Systematic review (n=973)
Kids with parents wwith BPD have 16.2% rate of depression which is really high
26.5% all affective disorders
They also have 5.4% BPD which is way above normal
More recent data:
Rates of affective disorders
Recent studies 15*56% OBD (for affective disorders
Concordia cohort 32%
HPA axis and affective disorders
The HPA system is profoundly dysregulated in depression and bipolar disorder (Holsboer, 1995). –Problems at all levels! • Most deficits disappear upon remission
Methods: Salivary Cortisol
• Cortisol sampling in the natural environment 2-3 days, 6-7 samples / day • Cortisol response following awakening (CAR): awakening, \+ 30, + 60 minutes post awakening • Objective measures of compliance, using electronic monitoring of sampling
HPA in Offspring of Bipolar Disorder vs control (via salivary cortisol)
Same pattern
Consistently higher
Why high cortisol?
Exposed to more stress? More sensitive to stress? Biological marker of environmental or genetic risk? Parenting ?
Early environmental sensitization
Animal research has demonstrated that the HPA
axis is calibrated by the prenatal and postnatal
environment (Lupien et al, 2009)
• Human studies suggest that early environmental
adversity is associated with HPA sensitization
later in life.
Parental structure may be
particularly important in the OBD
Parents who have consistent relationships with chilldren
E.g. have meal at the same time etc
This reduces stress
Mean parenting practices in OBD
and control families
There is a significant difference between OPD and control families in terms of their structure, support and control
Structure and control, but not support, mediated the
relationship between risk status (having a parent with BD) and behavioral outcomes in children (Iacono et al, 2018)
Cortisol rise following awakening
adolescence
Same pattern, higher release in OBD
Cortisol response to psychosocial stress
Using the TSSR
Again, same relationship, similar pattern higher release in OBD vs control
OBD as young adults
• Re-assessed HPA functioning in the natural
environment, now at 20 years of age
• Does parental structure in middle childhood
predict HPA reactivity in young adulthood?
• Do change in HPA functioning predict the
development of depressive and anxiety symptoms?
Having a parent with BPD predicted the structure of the family (it was lower)
This predicted the amount of salivary cortisol (higher)
This in turn predicted the Current MDD/ANX symptoms
So the effect of BP in parents is mediated by structure and HPA activity
This has been replicated a lot
One study found an interaction between cortisol levels and the risk allele for HTTSLR (serotonin) made 7.6x more likely to have affective disorders or symptoms
REVIEW
• OBD are a high risk for developing
internalizing and externalizing problems, as
well as changes in the HPA axis
• Exposure to childhood stress and adversity in
the OBD might sensitizes the HPA axis
• Parental structure might mitigate these effects
Reducing
Unwanted
Stress in the
Home
Overview
• Twelve-week group intervention
• Weekly, 2-hour meetings; led by graduate-level co-therapists
• Separate sessions for parents and their children
• Draws on empirically-supported treatments for stress management and family-focused therapy for BD (Abramowitz,
2012; Miklowitz, 2011; Shapiro & Sprague, 2009; Kendal et al,
2006)
• Techniques to improve consistency and structure in the home
• Stress-management skills
• Parenting practices
• Coping skills for children
Participants
• Parents and their biological children aged 6-11 years
• 34 OBD (20 families) vs. 32 low-risk Control (25 families)
• Groups matched on child age, gender, ethnicity, and family
SES (p > .05)
• Age (M = 8 years, 2 months; SD = 1 year, 6 months)
• Gender (52% male, 48% female)
• SES (parental education = some college; mean annual
income = $40 000-60 000)
• Middle class, Caucasian, French Canadian
Design
Would be assessed at 4 time points
Intervention between T1 and T2
both control and intervention would be assessed
Assessments
Examples of Parent Measures • Mental Health Status (SCID) • Family Environment (HOME & FES) • Parent-Child Interactions (Etch-a-Sketch Paradigm) • Personality (NEO-PI-R) Examples of Child Measures • Mental Health Status (KSADS) • Neuropsychological Testing (NEPSY-II and ANT-C) • Psychopathology (BASC-II) • Salivary Cortiso
Results: Primary outcomes
• Disappointing • Internalizing symptoms • Externalizing symptoms • Salivary cortisol – No robust treatment effect across the 4 time points
Did RUSH improve the family
environment of the OBD?
• Family Environment Scale (FES; Moos et al, 1974)
– Organization subscale
Risk groups structure improved
Closer to control (maybe no longer stat sign different)
