Childhood psychological function and obesity risk across the lifecourse: findings from the 1970 British Cohort Study



Psychological comorbidities of obesity are well recognised. However, the role of childhood psychological problems in the aetiology of later obesity has been little studied.


Secondary analyses of a national birth cohort (1970 British Cohort Study). Analysis: Logistic regression models to predict obesity risk at 26, 30 and 34 years related to hypothesised predictors: maternal and teacher reported child psychological function at 5 and 10 years (general behavioural, conduct, emotional or attentional/hyperactivity problems) and maternal psychological function.


General behavioural problems at age 5 years increased the risk of obesity at 30 and 34 years. Persistence of these problems through childhood further increased the obesity risk. Inattention/hyperactivity at 10 years similarly increased risk of obesity at 30 years (adjusted odds ratios (AOR) 1.3). Chronic conduct problems at 5 and 10 years also increased the obesity risk at 30 years (AOR 1.6 (1.1, 2.4) P<0.05). Childhood emotional disorders and maternal psychological function were not associated with adult obesity.


Children with early and persistent behavioural problems, particularly conduct problems, hyperactivity and inattention in early and mid-childhood are at an increased risk of obesity in adult life. The promotion of child and adolescent mental health and well-being may form an important part of future obesity prevention strategies. The promotion of healthy eating and activity should form part of secondary prevention and management strategies for children with disruptive behaviour disorders.


Approaches to prevent and treat obesity have focused appropriately on modifications of environmental factors, the so-called obesogenic environment, and attempts to modify behaviours related to diet and activity.1, 2 Given that psychological factors are important in mediating between individuals, families and their environment, the implications of psychological function for obesity risk and prevention have been relatively neglected.

The literature is dominated by cross-sectional and short-term longitudinal studies. Life-course studies of the trajectories of psychological function and obesity from childhood to adulthood have not been undertaken. Evidence of the importance of childhood psychological function for later obesity appears strongest for depression, with a positive association in adolescent females,3, 4, 5, 6 but not males.3, 4, 6 Early behavioural problems appear to increase risk of adult obesity,7, 8 but it is unclear which behavioural phenotypes increase risk. Attention-deficit hyperactivity disorder has been associated with an increased body mass index (BMI) in clinical studies,9, 10 but not in longitudinal population studies.8, 11

The mechanisms by which childhood psychological dysfunction influence later BMI are unclear. Given that family environment factors including socioeconomic status are amongst the strongest predictors of adult obesity,12 family factors such as parental psychological function may have an important role, although this has not been studied. We used longitudinal data from a national birth cohort to explore the risk of adult obesity related to impaired child and maternal psychological function in childhood.

Materials and methods

The 1970 British Cohort Study (BCS70) offers an opportunity to study psychological function from early childhood and its association with obesity through to adult life, and enables the study of parental psychological function and BMI alongside that of their offspring.

We used data from the BCS70 to examine the hypotheses that impaired childhood psychological function increases risk of obesity later in the life course, and that this relationship was in part mediated by impaired parental psychological function in childhood.

BCS70 is an ongoing, multidisciplinary longitudinal study that follows up children born in Great Britain in the week 5–11 April 1970. A total of 16 567 babies born in England, Wales and Scotland were enrolled in a birth cohort and followed up at 5 (n=12 981), 10 (14 350), 16 (11 206), 26 (8654), 29–30 (10 833) and 34 years (9316). Additional people born in the same week who migrated into Great Britain or who were identified subsequently were added to the cohort. We obtained data from various surveys of the BCS70 from the UK Data Archive, University of Essex and supporting information and code for cleaning the databases, and deriving summary variables from the Centre for Longitudinal Studies, London. Table 1 shows cohort retention rates. Owing to poor data quality and small sample size, we chose not to include the data collected in the 1986 sweep when subjects were 16-years old.

Table 1 Characteristics of participants across BCS70 sweeps according to key factors under study

Childhood data

Height but not weight was measured at 5 years by the health visitor. At 10 years, height was measured by school medical staff with a standardised technique and recorded to the nearest 0.1 cm (or 0.25 inch). Weight was measured in underclothes with a beam balance and recorded to the nearest 0.1 kg (or 0.25 pound). BMI z score at 10 years was calculated from height and weight with the revised UK 1990 growth reference.13 Obesity at age 10 was defined as BMI >95th percentile on UK 1990 growth charts.

Behaviour at 5 and 10 years was measured using teacher and parent reports, based on validated questionnaires including a 19-item parent-completed report derived from the Rutter Parent Scale.14, 15 Factor analysis by Golding15 suggests that these 19-items fall into three groups of interest: conduct problems, emotional problems and hyperactivity. We have defined subjects with scores 1 s.d. above the mean as having problems in each of the areas described. Cognitive ability was assessed at 10 years by completion of the British Ability Scales; age-appropriate T-scores for each subscale and mean T-score were calculated using reference norms appropriate for 1980.16

Hyperactive symptoms were further assessed using an abridged Conners Parent Scale derived from the Conners Rating Scale,17, 18, 19 consisting of 19 out of the original 93 questions. High scorers are defined as having scores 1 s.d. above the mean. Teachers completed the 53-item Social Development Scale at 10 years, derived from the Conners Teacher Rating Scale20 and the Rutter Teaching Scale.21 Factor analysis enables us to derive two scales: conduct problems/impulsive/hyperactive and attention deficit.22 High scorers are defined as having scores 1 s.d. above the mean.

Maternal psychological well-being was assessed at 5 and 10 years using the Malaise Inventory, developed by Rutter et al.14 and based on the Cornell medical index. It consists of a 15-question scale for psychological symptoms and an 8-question subscale for somatic symptoms. High scorers are defined as having scores >7, representing the 81st percentile,23 close to +1 s.d. Paternal data on psychological function were not available.

Socioeconomic status was assessed by father's self-report of current occupation and maternal educational achievement.

Adult data

Height and weight were obtained by confidential self-report at ages 26, 29–30 and 34–35 years and BMI was calculated. Obesity was defined as BMI28.5 kg/m2, as population-based data from a contemporary cohort of UK adults found that obese adults under-report their BMI by approximately 1.5 kg/m2.24

Socioeconomic status was assessed by participant's occupation in adult life.

Retention rates

As loss to follow-up of those with significant psychopathologies or obesity in childhood would present a threat to validity for our planned analysis, we investigated subject retention rates according to the different measures of psychopathology, socioeconomic status and obesity.

Table 1 shows the demographic, BMI and psychological characteristics of participants in childhood and then across subsequent sweeps. For each factor, the number and proportion are shown at baseline and then the proportion in each subsequent sweep, allowing assessment of potential differential loss to follow-up. There was no additional loss to follow-up amongst those who were obese in childhood. There was minimal additional attrition of subjects with psychological problems in mid-childhood (10 years), more so in those with problems at 5 years. Both maternal psychological problems and high self-esteem at 10 years were associated with minimally reduced attrition in adult surveys.


BCS70 data were analysed in Stata 10 (Stata Corp, College Station, TX, USA). For each measure of psychopathology, rates of obesity amongst high scorers and normal scorers were compared using the χ2-test. Odds ratios for risk of obesity were then calculated using logistic regression and reported with 95% confidence intervals. At 10 years, odds ratios were calculated for risk of obesity related to each childhood psychological status variable, adjusted for gender, socioeconomic status in childhood, childhood cognitive ability and birthweight, together with BMI of both parents and maternal education level. Height was also included, as BMI is not entirely independent of height.

Models were then derived for risk of obesity at 26, 30 and 34 years related to each childhood psychological status variable, adjusted for childhood socioeconomic status, birthweight, parental BMI when the subject was aged 10 years, childhood cognitive ability and the participant's height and social class at the appropriate adult survey. Analyses in the adult surveys were also adjusted for BMI at 10 years, so that associations between childhood psychological function and adult obesity were independent of childhood BMI status.

The impact of timing and chronicity of psychological problems within childhood on later obesity was examined using Rutter's Behaviour Scores, available at both age 5 and 10 years. Models for later obesity were derived as above, examining the impact of the age at which problems were present (that is, at 5 or 10 years, or both) and the duration of problems (that is, in nil, 1 or 2 surveys).


Data were available on psychological function at 5 years (Rutter's scale) in 12 432 patients. For these analyses, data on BMI were also available in 9661 at 10 years (being 67% of the sample at 10 years), 5732 (66%) at 26 years, 8466 (78%) at 30 years and 7356 (79%) at 34 years.

Table 2 shows the associations of psychological factors at 5 and 10 years with obesity at 10 years. It shows the proportions that are obese by status (high scorer or normal) for each childhood psychological variable, together with adjusted odds ratios (AOR) for risk of obesity. At 5 years, emotional problems were associated with lower risk of obesity at 10 years, with a trend for general behavioural problems to also be associated with lower risk (P=0.07). Maternal psychological problems at either 5 or 10 years were not associated with obesity at 10 years of age.

Table 2 Associations of psychological factors at 5 and 10 years with obesity at 10 years

Table 3 shows the associations of psychological factors at 5 and 10 years with obesity at 26, 30 and 34 years. For each adult survey, the Table shows the proportions that are obese by status (high scorer or normal) for each childhood psychological variable, together with AOR for risk of obesity. At 5 years, general behavioural problems and hyperactivity, as measured using Rutter's scales, appeared to increase the absolute prevalence of obesity by 3–5% consistently across each survey, with conduct problems increasing by a similar margin in the 30- and 34-year surveys. After adjustment, total problems were significantly predictive of obesity at 30 and 34 years, with conduct problems and hyperactivity predictive at 30 years.

Table 3 Associations of psychological factors at 5 and 10 years with obesity at 26, 30 and 34 years

The association of psychological factors at 10 years with later obesity was more complex. Maternal report of attentional and hyperactivity problems predicted obesity across all adult surveys. Teacher report of conduct/impulsivity/hyperactivity problems predicted obesity at 30 and 34 years, and teacher report of attentional problems predicted obesity at 34 years. Hyperactivity, as measured on the Rutter scale, is associated with adult obesity, only at 26 years. As maternal psychological status was not associated with offspring obesity risk, either in childhood or in adult life, we did not undertake further mediator analyses.

We examined the importance of age and duration of psychological morbidity by examining the association of Rutter's scores at 5 and 10 years, with obesity at 30 and 34 years. Problems at one survey only, whether 5 or 10 years, were not associated with later obesity. In contrast, adult obesity was associated with persistent behavioural problems across both childhood surveys; AOR for obesity at 30 years were 1.9 (95% CI 1.3, 2.7) for general behavioural problems, 1.6 (1.1, 2.4) for conduct problems and 1.5 (1.1, 2.0) for hyperactivity. Similar AOR were seen at 34 years (data not shown).


These data are the first to examine the associations between obesity across the life course and a range of behavioural and psychological variables in early and mid-childhood, as well as measures of maternal psychological health.

We found a striking and consistent association of general psychological problems in childhood, particularly hyperactivity and attentional problems, with adult obesity. These associations were independent of childhood BMI and were largely consistent for both 5- and 10- year surveys, and across maternal and teacher report. Further, associations were seen with both discrete measures of attention and hyperactivity, and with composite measures of disruptive behaviour that tapped into conduct problems and impulsivity as well as hyperactivity. Greatest risk of obesity was associated with persistent psychological problems across childhood, with problems in early childhood appearing to confer a greater risk than problems in later childhood. For disruptive behaviours such as conduct, attentional and hyperactivity problems, these associations emerged only after childhood and were of similar magnitude (odds ratios of 1.3–1.5) across the adult surveys. In contrast, emotional problems in childhood initially showed an inverse association with obesity in childhood, which changed to a positive association of general childhood problems with obesity in adult life. We found no evidence that maternal psychological problems were associated with obesity risk in offspring, in either childhood or adolescence.

These data suggest that strategies to improve the population child and adolescent mental health should form part of obesity primary prevention strategies. In children with disruptive behaviour disorders, secondary prevention and management strategies should include promotion of healthy eating and activity to prevent later obesity.

Comparison with the literature

Our finding that general behaviour problems, particularly when persistent across childhood, increased risk of adult obesity, confirms previous reports from cross-sectional25 and limited longitudinal8 studies. Both show similar magnitude of increased risk of obesity in children with behavioural problems: AOR 3.08 (95% CI 1.3–7.29) in cross-sectional analysis of 8–11-year olds25 and AOR 3.30 (95% CI: 1.4–7.8) at 21 years, if behavioural problems were present at both 5 and 14 years.7 Both show a higher magnitude of risk than our cohort, possibly because of the differences in the population, duration of the study or period during which the populations were being monitored.

We found that conduct problems increased risk of adult obesity by approximately 40–60%, particularly when present early in childhood or persistently throughout childhood. This finding extends that of one short longitudinal study, which showed that young people with conduct problems aged 14 years had AOR 2.14 of obesity at 22 years.26 In contrast, Bardone et al.27 demonstrated that girls with conduct problems at 15 years have a lower risk of obesity at 21 years and Mustillo et al,11 in a study limited to childhood and adolescence, reported no association between chronic conduct disorder and adolescent obesity, although they noted that disruptive behaviour in the form of oppositional defiant disorder did increase the risk of obesity approximately 2.5-fold.

Our finding that attention deficit and hyperactivity problems increased risk of later obesity by 30–40%, particularly when persistent through childhood, supports observations from clinical reports.9, 10 However, previous longitudinal studies limited to adolescence and early adulthood have reported no association.8, 11 These differences may lie in the shorter follow-up of previous longitudinal studies, as we found that these associations only emerged after childhood. Alternatively, this may reflect the use of different case definitions in previous studies and different study populations.


Psychological dysfunction in childhood may affect body mass regulation through changes in appetite and eating behaviours, other lifestyle mechanisms or through biological pathways. Obesity and serious mental illnesses frequently co-occur in adults,28 potentially through similar mechanisms.

Appetite disturbance is common in many psychological conditions, from compulsive overeating in addictive disorders29 to poor appetite in depression.30 Mental health problems are often associated with chronic stress, and there is early evidence that stress is associated with increased reward eating, particularly of calorie dense foods, although mechanisms remain unclear.31

In terms of lifestyle mechanisms, it is possible that psychological dysfunction in the child may reduce adherence to lifestyle behaviours related to healthy diet and activity levels, thus leading to obesity. This may be particularly true of disruptive disorders, and fits with our findings that conduct, attentional and hyperactivity problems are most strongly linked with later obesity. Our finding that associations between psychological problems and obesity emerge after childhood is consistent with the transfer of control of diet and lifestyle from the parent to the offspring during the teenage years. Such obesogenic factors are likely to accumulate over the life course.

The association between attentional problems and hyperactivity and later obesity appears counterintuitive, given that higher activity levels protect against obesity.32 However, a number of mechanisms have been hypothesised to explain this association. Impulsiveness may result in binge eating leading to obesity;33 compulsive eating may act to help the person compensate for the frustration associated with attentional and organisational difficulties.34 Attention-deficit hyperactivity disorder and obesity may share common underlying biological mechanisms.35 The reward deficiency syndrome has been described,36 characterised by insufficient dopamine-related natural reward resulting in the use of unnatural rewards such as substance use, risk taking and eating. Levitan et al.37 hypothesised a common biological dysfunction of the 7R allele of DRD4 associated with dopamine dysfunction in prefrontal attentional areas and brain circuits involved in the reward pathways. Alterations in brain-derived neurotropic factor have also been implicated in animal models38 but not in humans.39

We found that emotional problems in early childhood reduced the risk of obesity in later childhood but not in adult life. Mechanisms for this are likely to relate to appetite suppression, common in childhood affective problems,40 or to neglect or deprivation, which may reduce access to food but also downregulate41 or upregulate appetite.42

Strengths and limitations

The BCS70 is a unique data set in that it contains a detailed and diverse set of measures of child and maternal mental health, BMI across the life course and a broad range of data on known risk factors for obesity that might confound associations under study. Further, it combines relatively contemporary data on child mental health from the 1980s with the ability to track obesity into adult life. The BCS70 has high retention rates, low loss to follow-up of disadvantaged groups and minimal attrition of those with childhood psychological problems or those with childhood obesity. Importantly, we were able to adjust adult analyses for BMI in childhood; identified associations between childhood psychological function and adult obesity were independent of baseline childhood BMI. This has allowed us to undertake the only life course study of psychological function and obesity, and the only study to include data from multiple adult surveys.

We controlled our analyses for a broad range of potential confounding factors including childhood and adult socioeconomic class, maternal education and parental BMI, together with birth weight, height, sex and cognitive ability of the subjects. We examined the impact of childhood psychological function on adult obesity across three sequential cohorts. Although the association of childhood psychological function with obesity was most significant at age 30 years, the largest of the adult surveys, odds ratios were largely similar across the adult surveys, suggesting that differences in significance reflect variations in sample size and prevalence of obesity across the adult surveys.

Limitations include the inability to investigate the effects of ethnicity (owing to the limited ethnic diversity of the UK in the 1970s) and the limitations on detailed data collection inherent in large-scale epidemiological studies. The use of self-report data for BMI in adulthood is well accepted for epidemiological studies,43 and we lowered the BMI threshold for obesity to take account of known reporting errors.44, 45 Psychological function was assessed by report from multiple informants (parents and teachers) using validated mental health screening instruments in use in the 1970s and 1980s. These instruments allow us to identify those with likely significant problems, but have limited comparability with modern diagnostic instruments and do not allow us to accurately identify those with disorder level problems. For similar reasons, we were unable to examine the association of depression in childhood with later obesity. Although we adjusted for a range of potential confounding factors, given the complex aetiology of obesity, we cannot exclude residual confounding as the explanation of some findings.


Children with early and persistent behavioural problems, particularly conduct problems, hyperactivity and inattention in early and mid-childhood are at an increased risk of obesity in adult life, independent of childhood BMI, socioeconomic status or cognitive ability. The promotion of child and adolescent mental health and well being may form an important part of future obesity prevention strategies. The promotion of healthy eating and activity should form a part of secondary prevention and management strategies for children with disruptive behavioural disorders.


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White, B., Nicholls, D., Christie, D. et al. Childhood psychological function and obesity risk across the lifecourse: findings from the 1970 British Cohort Study. Int J Obes 36, 511–516 (2012).

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  • child
  • adult obesity risk
  • childhood psychological function
  • epidemiology

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