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Bullying victimization in childhood predicts inflammation and obesity at mid-life: a five-decade birth cohort study

  • R. Takizawa (a1) (a2), A. Danese (a1) (a3) (a4), B. Maughan (a1) and L. Arseneault (a1)

We aimed to test whether childhood bullying victimization increases risk for age-related disease at mid-life using biological markers including inflammation and adiposity, independent of other childhood risk factors and key adult variables.


The present study was a 50-year prospective longitudinal birth cohort study of all births in Britain in 1 week in 1958. Exposure to bullying was assessed prospectively when participants were aged 7 and 11 years (27.7% occasionally bullied; 14.6% frequently bullied). Blood inflammation biomarkers [C-reactive protein (CRP) and fibrinogen] and adiposity [body mass index (BMI) and waist:hip ratio] were measured at age 45 years.


Participants who had been frequently bullied in childhood showed increased levels of CRP at mid-life [β = 0.07, 95% confidence interval (CI) 0.04–0.10] and higher risk for clinically relevant inflammation cut-off [CRP > 3 mg/l: 20.4% v. 15.9%, odds ratio (OR) = 1.35, 95% CI 1.12–1.64]. Women who were bullied in childhood had higher BMI than non-bullied participants and were at increased risk of being obese (BMI ≥ 30 kg/m2: occasionally bullied: 26.0% v. 19.4%, OR = 1.45, 95% CI 1.18–1.77; frequently bullied: 26.2% v. 19.4%, OR = 1.41, 95% CI 1.09–1.83). Findings remained significant when controlling for childhood risk factors (e.g. parental social class; participants’ BMI and psychopathology in childhood) and key adult variables (e.g. adult social class, smoking, diet and exercise).


Bullied children show increases in risk factors for age-related disease in middle adulthood, independent of co-occurring childhood and adult risks. Given the high prevalence of bullying victimization in childhood, tackling this form of psychosocial stress early in life has the potential of reducing risk for age-related disease and its associated burden.

Corresponding author
* Address for correspondence: L. Arseneault, Ph.D., MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, Box Number P080, De Crespigny Park, London SE5 8AF, UK. (Email:
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