Dysfunctional Families

Family communication quality: not every study finds a significant difference
Liem (1974): parents’ instructions to 11 sons with schizophrenia vs 11 without
Result: instructions were no more disordered in the schizophrenia group

Apparent communication difficulties: parents may adapt to their child’s existing communication style
Reverse causality: communication problems may be an effect
Implication: weakens a simple claim that communication caused the disorder

Furthermore: Koopmans (1997)
Incidental variations: communication may change during family disruption
Parent’s own pathology: another possible source of double-bind messages
Alternative origins: several processes could generate the same pattern

True origins unclear: double binds do not isolate a single cause
Conflicting evidence: limits generalisation of the theory
Judgement: family patterns may be relevant without being a proven primary cause

The child’s existing communication difficulties may alter parental communication. The observed family pattern could be an effect of the disorder rather than its initial cause.

1. Firstly: conflicting conclusions
Family communication quality: not every study finds a significant difference
Liem (1974): parents’ instructions to 11 sons with schizophrenia vs 11 without
Result: instructions were no more disordered in the schizophrenia group
2. Liem’s alternative explanation
Apparent communication difficulties: parents may adapt to their child’s existing communication style
Reverse causality: communication problems may be an effect
Implication: weakens a simple claim that communication caused the disorder
3. Furthermore: Koopmans (1997)
Furthermore: Koopmans (1997)
Incidental variations: communication may change during family disruption
Parent’s own pathology: another possible source of double-bind messages
Alternative origins: several processes could generate the same pattern
4. Therefore: causal foundation
True origins unclear: double binds do not isolate a single cause
Conflicting evidence: limits generalisation of the theory
Judgement: family patterns may be relevant without being a proven primary cause

Vaughn & Leff (1976): relapse assessed within nine months
High-EE relatives: 53% relapsed
Low-EE relatives: 12% relapsed

Family emotional climate: may influence vulnerability to relapse
Clinical implication: family environment can matter after treatment
Key distinction: relapse after onset ≠ initial causation

McCreadie & Phillips (1998): did not find higher subsequent 6-to-12-month relapse rates in high-EE homes
Contradiction: high EE is not a universal predictor across studies

May contribute: one factor influencing relapse
Not sole or exclusive: other personal; biological & treatment factors may also matter
Judgement: use expressed emotion as a risk-related factor; not an inevitable outcome

Relapse is a return or worsening of illness after improvement. Initial onset is the first emergence of the disorder. Evidence linking family emotional climate with relapse does not establish the initial cause.

1. Secondly: supporting research
Vaughn & Leff (1976): relapse assessed within nine months
High-EE relatives: 53% relapsed
Low-EE relatives: 12% relapsed
2. What this supports
Family emotional climate: may influence vulnerability to relapse
Clinical implication: family environment can matter after treatment
Key distinction: relapse after onset ≠ initial causation
3. However: inconsistent prediction
McCreadie & Phillips (1998): did not find higher subsequent 6-to-12-month relapse rates in high-EE homes
Contradiction: high EE is not a universal predictor across studies
4. This suggests a qualified role
May contribute: one factor influencing relapse
Not sole or exclusive: other personal; biological & treatment factors may also matter
Judgement: use expressed emotion as a risk-related factor; not an inevitable outcome

Shared family unit: contains shared environment AND biological relatedness
Communication difficulties & high EE: do not automatically identify the original cause

Family relationships: may increase stress
Trigger vs underlying cause: stress may act on pre-existing vulnerability
Diathesis-stress = predisposition + environmental stressor

SWGPGC / PGC (2014)
108 genetic loci: associated with schizophrenia
Genetic predisposition: supports a biological contribution
Risk is probabilistic: association does not mean every carrier develops schizophrenia

Family dysfunction: may serve as the environmental stressor
Already vulnerable individuals: stress may help trigger onset
Judgement: genetic & family explanations can complement each other

Diathesis-stress combines a predisposition with an environmental stressor. Vulnerability is the pre-existing susceptibility; a trigger may help precipitate onset in an already vulnerable person.

1. Finally: alternative explanation
Shared family unit: contains shared environment AND biological relatedness
Communication difficulties & high EE: do not automatically identify the original cause
2. Psychosocial trigger
Family relationships: may increase stress
Trigger vs underlying cause: stress may act on pre-existing vulnerability
Diathesis-stress = predisposition + environmental stressor
3. SWGPGC / PGC (2014)
SWGPGC / PGC (2014)
108 genetic loci: associated with schizophrenia
Genetic predisposition: supports a biological contribution
Risk is probabilistic: association does not mean every carrier develops schizophrenia
4. Integrated conclusion
Family dysfunction: may serve as the environmental stressor
Already vulnerable individuals: stress may help trigger onset
Judgement: genetic & family explanations can complement each other