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Whittle et al. 10.1073/pnas.0709815105.

Supporting Information

Files in this Data Supplement:

SI Table 2
SI Table 3
SI Methods




Table 2. Means and SD of raw brain volumes and asymmetry measures, and tests for gender differences

Raw brain measure

Full sample

Males

Females

Gender difference: raw (corrected)

N

M (SD)

N

M (SD)

N

M (SD)

t

Whole brain

137

1303565.66 (109328.89)

74

1348941.2 (99720.42)

63

1250267.41 (95742.59)

-5.88***

Left amygdala

137

1895.79 (273.50)

74

1971.95 (272.10)

63

1806.33 (248.71)

-3.69** (-4.43**)

Right amygdala

137

1833.09 (283.30)

74

1886.41 (294.83)

3

1770.46 (257.54)

-2.43* (-2.82*)

OFC asymmetry

136

-622.65 (1616.72)

74

-783.11 (1516.10)

63

-438.97 (1715.49)

1.24 (1.23)

ACCL asymmetry

135

-649.97 (2590.05)

74

-949.82 (2534.31)

63

-307.29 (2630.58)

1.44 (1.43)

ACCP asymmetry

131

437.63 (2274.25)

74

449.61 (2203.09)

63

424.29 (2368.92)

-0.06 (-0.06)

Corrected, regional brain volume or asymmetry measure corrected for whole brain volume; OFC, orbitofrontal cortex; ACCL, anterior cingulate cortex (limbic); ACCP, anterior cingulate cortex (paralimbic). *, P < 0.05. **, P < 0.001; ***, P < 0.0001.





Table 3. Summary of hierarchical regressions predicting adolescent reciprocity of parental aggressive behaviors and duration of adolescent dysphoric behaviors with adolescent brain volume/asymmetry measures

 

N

ß

t

F

R2

DV: Adolescent aggressive given parent aggressive

Left amygdala

136

.174

1.909

3.643

.026

Left amygdala × gender

136

.161

1.298

1.686

.012

Right amygdala

136

.071

.800

.640

.005

Right amygdala × gender

136

.166

1.270

1.612

.012

OFC asymmetry

135

.104

1.200

1.439

.011

OFC asymmetry × gender

135

.017

.139

.019

.000

ACCL asymmetry

134

.084

.965

.932

.007

ACCL asymmetry × gender

134

.120

.954

.910

.007

ACCP asymmetry

130

-.169

-1.938

3.754

.028

ACCP asymmetry × gender

130

-.149

-1.216

1.477

.011

DV: duration of dysphoric behaviors

Left amygdala

136

.026

.285

.081

.001

Left amygdala × gender

136

.028

.213

.045

.000

Right amygdala

136

-.075

-.849

.721

.005

Right amygdala × gender

136

-.163

-1.251

1.565

.012

OFC asymmetry

135

.003

.031

.001

.000

OFC asymmetry × gender

135

-.059

-.489

.239

.002

ACCL asymmetry

134

-.065

-.737

.554

.004

ACCL asymmetry × gender

134

-.009

-.073

.005

.000

ACCP asymmetry

130

.090

1.031

1.064

.008

ACCP asymmetry × gender

130

.007

.055

.003

.000

These values are based on the model controlling for adolescent gender effects (not significant and hence not shown here); therefore, change in F and R2 values are displayed. DV, dependent variable; OFC, orbitofrontal cortex; ACCL, anterior cingulate cortex (limbic); ACCP, anterior cingulate cortex (paralimbic).





SI Methods

Recruitment and Screening Procedure. Adolescents and their families were recruited as part of an ongoing research program investigating the relationship between adolescent temperament, brain development, and risk for psychopathology. As part of the study, final-year primary school students (grade 6; aged 10-12 yr) across metropolitan Melbourne, Australia, were approached through their schools to take part in the study. Through this process, 2,479 students completed the revised Early Adolescent Temperament Questionnaire [EATQ-R (1)] in groups of 18-25 students in the classroom. Given that the main aim of the screening procedure was to provide a risk-enriched sample, EATQ-R scores were used to select a sample that was representative of scores across the full range of two higher-order temperament dimensions thought to confer risk for affective disorders: Negative Affectivity and Effortful Control. Equal numbers of male and female students were selected from each of the following ranges of scores on these dimensions: 0-1, 1-2, 2-2.5, and greater than 2.5 standard deviations above and below the mean. This produced a sample that showed relatively even distribution across each higher order temperament dimension, while maintaining the range of temperament scores evident in the larger sample. The sampling frame was constructed such that all students scoring in the extreme ranges of each temperament dimension were recruited. This resulted in a selected sample of 414 students.

Selected participants were invited to complete a diagnostic interview. Given that this broader study set out to prospectively investigate the role of emotion regulation as a vulnerability factor in the development of adolescent depression, only participants who had no current or past case-level depressive disorders were selected for the study. From the selected sample, 245 families consented to participate in the diagnostic interview. No differences between participants who agreed to the interview and those that declined were observed on temperament (Negative Affectivity (t[407] = 0.16, n.s.; Effortful Control (t[413] = -0.54, n.s.), gender (c2[1] = 0.34, n.s.), or socioeconomic status as defined by an index of neighbourhood social disadvantage (2), (t[405] = -1.00, n.s.).

All adolescents completing the diagnostic interview were invited to participate in neuroimaging and/or the family interactions task. Adolescents completing both of these research components did not differ significantly from those who ceased participation after the diagnostic interview in Negative Affectivity (t[242] = -.23, n.s.), Effortful Control (t[243] = - .20, n.s.), or gender (c2[1] = 3.11, n.s).

1. Ellis LK, Rothbart MK, Biennial Meeting of the Society for Research in Child Development, Minneapolis, MN, April 20-23, 2001, poster.

2. Vinson T (2004) Community Adversity and Resilience: The Distribution of Social Disadvantage in Victoria and NSW, the Mediating Role of Social Cohesion (Jesuit Social Services, Richmond, Victoria, Australia).





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