Week 11: Intervention for the kids of Bipolars

Question 1

What is cool about this intervention?

Answer 1

It puts what we know about risk factors in practice.

Question 2

Prevalence of major affective

disorders

Answer 2

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

Question 3

Why is depression so bad (2 things)

Answer 3

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

Question 4

The enigma of affective disorders

Answer 4

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

Question 5

Approaches to the problem of the

affective disorders

Answer 5

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

Question 6

Risk for psychopathology in offspring of

BD parents: Systematic review (n=973)

Answer 6

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

Question 7

More recent data:

Rates of affective disorders

Answer 7

Recent studies 15*56% OBD (for affective disorders

Concordia cohort 32%

Question 8

HPA axis and affective disorders

Answer 8

The HPA system is profoundly 
dysregulated in depression and bipolar 
disorder (Holsboer, 1995). 
–Problems at all levels!
• Most deficits disappear upon remission

Question 9

Methods: Salivary Cortisol

Answer 9

• 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

Question 10

HPA in Offspring of Bipolar Disorder vs control (via salivary cortisol)

Answer 10

Same pattern

Consistently higher

Question 11

Why high cortisol?

Answer 11

Exposed to more stress?
More sensitive to stress?
Biological marker of 
environmental or genetic 
risk? 
Parenting ?

Question 12

Early environmental sensitization

Answer 12

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.

Question 13

Parental structure may be

particularly important in the OBD

Answer 13

Parents who have consistent relationships with chilldren

E.g. have meal at the same time etc

This reduces stress

Question 14

Mean parenting practices in OBD

and control families

Answer 14

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)

Question 15

Cortisol rise following awakening

adolescence

Answer 15

Same pattern, higher release in OBD

Question 16

Cortisol response to psychosocial stress

Answer 16

Using the TSSR

Again, same relationship, similar pattern higher release in OBD vs control

Question 17

OBD as young adults

Answer 17

• 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

Question 18

REVIEW

Answer 18

• 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

Question 19

Reducing
Unwanted
Stress in the
Home

Overview

Answer 19

• 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

Question 20

Participants

Answer 20

• 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

Question 21

Design

Answer 21

Would be assessed at 4 time points

Intervention between T1 and T2

both control and intervention would be assessed

Question 22

Assessments

Answer 22

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

Question 23

Results: Primary outcomes

Answer 23

• Disappointing
• Internalizing symptoms
• Externalizing symptoms
• Salivary cortisol
– No robust treatment effect across the 4 time points

Question 24

Did RUSH improve the family

environment of the OBD?

Answer 24

• Family Environment Scale (FES; Moos et al, 1974)
– Organization subscale

Risk groups structure improved

Closer to control (maybe no longer stat sign different)

Question 25

Did changes in the home

environment benefit the OBD?

Answer 25

• Mediation analysis

The indirect effect (ab) of intervention predicting externalizing problems through the mediator, change in home organization, was significant (95% confidence
intervals: -6.3, -0.05)

Question 26

Did the RUSH program improve
parent-child interactions among OBD
dyads?

Answer 26

Parent-Child Interaction Paradigm (Stevenson-Hinde &
Shouldice, 1995; Deater-Deckard & O’Connor, 2000)
– Parental positivity
– Parental negativity
– Dyadic mutuality
– Inter-rater reliability, ICC= .81-.90

Question 27

Parent-Child Interaction Quality

Answer 27

Significant effects of RUSH
program on slope (linear),
from T1 to T2 and T1 to T4
for all three measures.

Parental negativity

Parental positivity

Dyadic mutuality

Question 28

Outcome: Parent-reported internalizing

problems

Answer 28

The indirect effect (ab) of intervention predicting parent-report child anxiety
through the mediator, change in parental negativity, was significant (95%
confidence intervals: 0.06, 5.51

Question 29

Conclusions

Answer 29

• Developed a prevention program from our
biobehavioural studies of the OBD.
• The RUSH program decreased child behavioral
and emotional problems when it effectively
changed the home environment and parent-child
interactions.
• Need to consider how to increase RUSH impact or
figure out which types of families should be
targeted
• Next phase is to conduct an RCT in a wider range
of offspring at risk for affective disorders.

Not everyone responded. Could be that non responders were not overpowered statistically by responders due to small sample size