The Power of Peers: Hoe persoonlijke ervaringen met leeftijdsgenoten tot immuunsysteemactivatie kunnen leiden bij adolescenten

Matteo Giletta

Department of Developmental Psychology

Tilburg University

Social Relationships

Humans = Social species

Innate human need to belong

Peer Relations in Adolescence

Changes in social network Increased autonomy

Increased time spent with peers

Changes in quality of peer relations

Biological changes = Puberty Increased orientation (social motivation) toward peers

Increased peer sensitivity

Enhanced emotional and physiological responses to peers

Negative Peer Experiences and Health

Fatigue

Sleep problems

Adulthood Adolescence

Great Smoky Mountain Study

(Wolke et al., 2013)

British National Child Development

Study (Takizawa, 2014)

Underlying Processes

How do peer experiences has such enduring consequences on both mental and physical health?

Guiding theoretical frameworks

Biological embedding model (Miller et al., 2011) How does stress “get under the skin”?

Human social genomics Social signal transduction theory (Slavich & Cole, 2013)

Inflammation

Stress and Inflammation

Slavich & Cole, 2013

Social stress can trigger inflammatory responses

Social evaluative stressors

Upregulation proinflammatory genes

Downregulation antiviral and antibody-related genes

Conserved Transcriptional Response to

Adversity (CTRA; Cole, 2014)

Inflammation and Health

Slavich & Irwin, 2014

Consequences of elevated inflammation Physical health

Mental health

Depressive symptoms

Anxiety symptoms

Peripheral inflammation can reach the CNS

Inflammation in the CNS induces “sickness behaviors”

Inflammation alters the synthesis reuptake of monoamine and reduces availability of serotonin (Miller et al., 2009)

Peer relations and inflammation

? Immune Cell

Social-Evaluative Stressors Negative Peer Experiences

Peer Preference and Inflammation

Peer preference = (social) belonging to the peer group

Sociometric procedure Who do you like the most?

Who do you like the least?

Standardized like – dislike nominations

Peer preference Systemic

inflammation Internalizing symptoms

Marieke de Bruine

TRAILS Tracking Adolescents' Individual Lives Survey

604 Dutch adolescents (55% girls) from Tracking Adolescent Individual Live Survey (De Winter et al. 2005)

Peer preference

hsCRP

Internalizing symptoms

12 14 15 17 16 18 19 13 16 19

Results

Longitudinal effects of peer preference on internalizing symptoms via C-reactive protein

Peer preference CRP Internalizing symptoms T3

Internalizing symptoms T2

Internalizing symptoms T1

-.08*

.53***

.60***

-.060†

Χ2 = 46.387 Df = 21 RMSEA = .047 CFI = .960 TLI = .936 SRMR = .036

Conclusions

Peer preference and systemic inflammation Prospective effects (3 years later) using objective measurement

of social environment

Peer preference as index of social connection

Low peer preference = risk for survival

Inflammation and internalizing problems Systemic inflammation did not predict changes in internalizing

problems over time

To what extent and when does inflammation pose risk for internalizing problems?

Sensitization Hypothesis

0

1

2

3

4

5

6

7

8

Stress Stress Stress

Stre

ss r

esp

on

se

0

1

2

3

4

5

6

7

8

Stress Stress Stress

Stre

ss r

esp

on

se

Sensitization Hypothesis

Neuro-inflammatory sensitization (Slavich & Irwin, 2014)

Exposure to social stress may result in enhanced inflammatory responses to subsequent stressors

Lower levels of stress trigger inflammation

Proinflammatory phenotype (Miller et al., 2011)

Evidence concerning family adversity

Peer Victimization and Inflammation

Laboratory social stress

Acute inflammatory

responses

Peer victimization

Role of Cognitions

Individual differences in cognitive processes Expectations, perception and appraisal

of social situations

Perception of social threat is key to activate pathways to inflammation

Slavich & Cole, 2013

Diathesis-Stress Model

Laboratory social stress

Acute inflammatory

responses

Peer victimization

Cognitions

Negative cognitive style

Attribute negative events to internal, stable and global causes

Hopelessness

Project ARCH Adolescent Relationships, Coping, and Health

Participants 220 clinically-referred girls

14.71 years (SD = 1.29)

64% Caucasian, 24% African-American

Inclusion criteria 12-16 years old

History of mental health concerns in the two prior years

Caregiver available to participate

No active psychosis, mental retardation or pervasive developmental disorders

PI: Mitch Prinstein

Study Design

3 mth 6 mth 9 mth Baseline

Phone interviews

Interview and questionnaires

3 hours

Baseline saliva

20 min post-speech

30 min 40 min

Lab visit

Retention rate 80-91%

Speech task

Modified TSST (Kirschbaum et al., 1993)

Cytokines

Interview and questionnaires

3 hours

Baseline saliva

20 min post-speech

30 min 40 min Speech task

Pro-inflammatory cytokines Interleukin-6 (IL-6)

Interleukin-1β (IL-1β)

Tumor necrosis factor-α (TNF-α)

Measures

Baseline laboratory session

Questionnaire based-measures Peer victimization (overt, relational, and reputational; RPEQ; Prinstein

et al., 2001)

Hopelessness (HSC; Kazdin, Rodgers, & Colbus, 1986)

Negative cognitive style (ACSQ; Hankin & Abramson, 2002) 5 Interpersonal scenarios

Average across inferential styles about causes, consequences, and the self

Depressive symptoms (MFQ; Costello & Angold 1988)

Covariates Body mass index, medication, illness, caffeine intake

Measures

Follow-up assessment (9-months)

Semi-structured interview

Depressive symptoms (MFQ; Costello & Angold 1988)

Life stress assessment (Youth Life Stress Interview; Rudolph & Flynn, 2007)

Narrative of stressful life events between baseline and follow-up

“Objective coding” (coding teams) of severity scores for interpersonal and nonintepersonal stress

Latent Change Score Models

Outcome: cytokine responses to the social stress task

Latent Change Score Models

Outcome: cytokine responses to the social stress task

Latent Change Score Models

Outcome: cytokine responses to the social stress task

-0,5 -0,4 -0,3 -0,2 -0,1 0 0,1 0,2 0,3

Hopelessness

Negative cognitive style

Peer victimization

Pre-stress cytokine

Standardized coefficients

TNF-α

IL-1β

IL-6

***

*

*** ***

**

**

Giletta, Slavich, Rudolph, Hastings, Nock, & Prinstein (2018). Journal of Child Psychology and Psychiatry

Peer Victimization X Hopelessness

-0,2

-0,15

-0,1

-0,05

0

0,05

0,1

0,15

0,2

0,25

0,3

Low High

IL-6

ch

ange

s

Peer victimization

High Hopelessness

Low Hopelessness

Outcome: IL-6 responses to the social stress task

b = 0.71**

b = -0.01

Giletta et al. (2018). JCPP

Peer Victimization X Hopelessness

Outcome: IL-1β responses to the social stress task

-0,3

-0,2

-0,1

0

0,1

0,2

0,3

0,4

Low High

IL-1

β c

han

ges

Peer victimization

High Hopelessness

Low Hopelessness

b = 0.83***

b = -0.21

Giletta et al. (2018). JCPP

Peer Victimization X Hopelessness

Outcome: TNF-α responses to the social stress task

-0,25

-0,2

-0,15

-0,1

-0,05

0

0,05

0,1

0,15

0,2

Low High

TNF-

α c

han

ges

Peer victimization

High Hopelessness

Low Hopelessness

b = 0.32†

b = -0.57**

Giletta et al. (2018). JCPP

Supplementary Analysis

Robustness of findings

Identical results when adjusting for SES, BMI, family climate, recent illness, same-day caffeine intake, smoking, birth control and medication use

Consistency of findings

Results consistent across subtypes of peer victimization (overt, relational, and reputational)

Conclusions

Peer victimization enhances inflammatory stress responses

Key role of cognitive vulnerability Diathesis-stress model

Implications Biological embedding

Is inflammation a primary mechanism linking negative peer experiences to health?

Does inflammation predict depression?

Depressive symptoms

Stress-induced inflammation

Interpersonal stress

Linear Regressions

Outcome: Depressive symptoms at 9 months follow-up

0 0,1 0,2 0,3 0,4 0,5

Stress-induced inflammation

Interpersonal stress

Baseline depression

Standardized coefficients

TNF-α

IL-1β

IL-6*

*** ***

***

*** ***

***

TNF-α responses X Interpersonal Stress

0

0,2

0,4

0,6

0,8

1

1,2

Low High

Dep

ress

ive

sym

pto

ms

follo

w-u

p

Recent interpersonal stress

High TNF-α responses

Low TNF-α responses

b = 0.019***

b = 0.01†

IL-1β responses X Interpersonal Stress

0

0,1

0,2

0,3

0,4

0,5

0,6

0,7

0,8

Low High

Dep

ress

ive

sym

pto

ms

follo

w-u

p

Recent interpersonal stress

High IL-1β responses

Low IL-1β responses

b = 0.017***

b = 0.01

Supplementary Analysis

Noninterpersonal stress

No main effect

No interaction effects

Pre-stress cytokines

No main effect

No interaction effects

Conclusions

Inflammation as important factor in the development of depression in adolescence

Support different research lines

Peer Power Project

Ongoing multiwave study (N=200) examining the effects of

peer relations on inflammatory markers

Fall 2016

Spring 2017

Fall 2017

1st year high-school 2nd year high-school

Measures

Peer experiences (self- and peer-reported) Individual differences (rejection sensitivity, personality) Inflammation (C-reactive protein; cytokines; gene

expression)

Spring 2018

Retention rate > 85%

Peer Power Project

Developmental psychopathology perspective

Development Peer relations

Immune system

Development

Development

Adolescent behavior

Ongoing Project

5 times a day X 10 days

Phase 1 Phase 2

Questionnaire Peer nominations ESM

Phase 3

Peer experiences Individual differences

Laboratory social stressor

Spring 2019

Thank you!

m.giletta@uvt.nl

Mitch Prinstein (UNC)

George Slavich (UCLA)

Tineke Oldehinkel (Groningen University)

Marieke de Bruine

Lisa Schreuders