Background: The relative contribution of childhood and pubertal body mass index (BMI) for the risk of adult colorectal cancer is not known. The aim of this study was to evaluate the independent associations for childhood BMI and pubertal BMI change with risk of colorectal cancer in men. Methods: We included 37,663 men born in 1946 to 1961 who had weight and height measured at 8 (childhood) and 20 (young adult age) years of age available from the BMI Epidemiology Study. Information on colorectal cancer was retrieved from the Swedish National Patient Register (257 cases of colon cancer and 159 cases of rectal cancer). Results: Childhood BMI at 8 years of age [HR, 1.19 per SD increase; 95% confidence interval (CI), 1.06–1.33], but not pubertal BMI change (HR, 1.02; 95% CI, 0.90–1.15), was associated with increased risk of colon cancer. Due to a significant interaction between childhood BMI and pubertal BMI change (P < 0.001), we stratified the analyses according to the median of pubertal BMI change. Childhood BMI was associated with risk of colon cancer in individuals with a pubertal BMI change above, but not below, the median (above: HR = 1.48, 95% CI, 1.26–1.74; below: HR = 0.95, 95% CI, 0.80–1.12). Neither childhood BMI nor pubertal BMI change was associated with rectal cancer. Conclusions: High childhood BMI was associated with increased risk of colon cancer only if it was followed by a pubertal BMI increase above the median. Impact: Further studies should evaluate prepubertal childhood BMI in relation to pubertal BMI change and BMI in middle age for the risk of colon cancer.

An inverse association between childhood body mass index (BMI; in kg/m²) and pubertal timing is well established for girls. Among boys, studies are scarce and the results inconclusive. We aimed to determine the association between childhood BMI and age at peak height velocity (PHV) in boys. We collected height and weight measurements between 6.5 and 22 y of age for boys born 1945–1961 (original cohort; n = 31,971; mean ± SD childhood BMI: 15.74 ± 1.41; age at PHV: 14.06 ± 1.11 y) and 1981–1996 (replication cohort; n = 1465; childhood BMI: 16.47 ± 2.06; age at PHV: 13.71 ± 1.08 y) attending schools in Gothenburg, Sweden, and examined at mandatory military conscription. Age at PHV was obtained from curve-fitting of measured heights with the use of a modified Infancy-Childhood-Puberty model. In the original cohort, childhood BMI was inversely associated with age at PHV (P < 0.001) and a significant quadratic term for childhood BMI (P < 0.001) indicated the nonlinearity of this association. Via piecewise linear regression, we identified a threshold for the association at a childhood BMI of 18.42. A significant inverse association was observed below (β: −0.17 y/BMI unit; 95% CI: −0.18, −0.16 y/BMI unit) but not above (β: 0.02 y/BMI unit; 95% CI: −0.03, 0.06 y/BMI unit) this childhood BMI threshold. For every unit increase in childhood BMI, age at PHV was ∼2 mo earlier up to the childhood BMI threshold. Similar results were observed in the replication cohort, demonstrating a significant inverse association below (β: −0.16; 95% CI: −0.21, −0.11) but not above (β: −0.03; 95% CI: −0.11, 0.05) the childhood BMI threshold. The identified threshold was close to the cutoffs for overweight at 8 y of age, and childhood BMI was inversely associated with age at PHV below but not above the overweight cutoffs. The present findings establish an inverse association between childhood BMI and pubertal timing in normal-weight but not overweight boys.

Aim: The aim of this study was to present prevalence data for overweight and obesity across school age in a large, recent, population‐based cohort of children in Gothenburg, Sweden.Methods: We included 66,807 children (48.5% girls) aged 5–18.9 years who had their height and weight measured in school health care 2015–2018. The BMI values were categorised according to the age‐dependent cut‐offs for overweight and obesity from the International Obesity Task Force (IOTF).Results: Overall, the prevalence of overweight and obesity for girls and boys was 18.1% and 18.0%, respectively. We observed increasing proportions of overweight (girls 11.5–17.1% and boys 8.4–17.4%) and obesity (girls 3.0–4.2% and boys 2.7–6.1%) with increasing age (p < 0.001 for trend in both sexes). Moreover, girls had higher prevalence of overweight during ages 5.0 to 8.9 years compared with boys (p < 0.001), while boys had higher prevalence of obesity 15.0–18.9 years compared with girls (p < 0.001).Conclusion: In conclusion, we demonstrate increasing prevalence of overweight and obesity across the entire school age range, as well as differences in prevalences between boys and girls, in a population‐based sample of 67,000 children in Gothenburg city, Sweden. Continuous monitoring of schoolchildren, together with effective preventive measures, is crucial to curb the obesity epidemic and its consequences.

Aims: Hospitalizations for heart failure among young adults and middle-aged individuals have increased. The aims of the present study were to evaluate the association between birth weight and risk of adult heart failure and the importance of change from low birth weight to overweight/obesity at young adulthood. Methods and results: We used the population-based body mass index (BMI) Epidemiology Study cohort Gothenburg (n = 35 659) with birth weight and young adult BMI (20 years) available from child healthcare records, school health records, and military conscription register for men born 1945–1961. The cohort includes all children who finished school, which was mandatory, in Gothenburg, Sweden. Information on heart failure diagnosis was retrieved from the National Patient Register and the Cause of Death Register (n = 415). In cox regression analyses, there was an inverse association between birth weight and risk of heart failure [hazard ratio (HR) 0.83 per standard deviation (SD), 95% confidence interval (CI) 0.76–0.90], and a direct association for young adult BMI (HR 1.48 per SD, 95% CI 1.36–1.61). Of note, individuals with birth weight in the lowest tertile, who were overweight/obese in young adulthood had a five-fold risk of heart failure (HR 4.95, 95% CI 3.36–7.31) compared with individuals in the middle birth weight tertile who were normal weight at 20 years. Conclusions: Birth weight was inversely associated with the risk of hospitalization due to heart failure. The combination of low birth weight and overweight/obesity in young adulthood results in excess risk of heart failure beyond that of low birth weight or young adult overweight/obesity separately. These findings indicate the need of a life course perspective in heart failure prevention and risk assessment.

Hematologic malignancies are common and the incidence is increasing. Adult obesity has been associated with hematologic malignancies (HM), but the importance of body mass index (BMI) in childhood and during puberty has not been evaluated. The aim of the present study was to evaluate the relative contribution of BMI and height in childhood and during puberty for the risk of adult HM. 37 669 men born in 1946 to 1961 who had weight and height measured at 8 (childhood) and 20 (young adult age) years of age available from the BMI Epidemiology Study were included in the study. Pubertal BMI change was calculated as BMI at 20 years of age minus BMI at 8 years of age. Information on HM was retrieved from Swedish registers (459 cases of HM). Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regressions. Childhood BMI (HR 1.11 per SD increase [95% CI 1.02-1.23]), but not pubertal BMI change, was associated with hematologic malignancies in a linear manner. Childhood BMI was, independent of childhood height, associated with the diagnostic entities Non-Hodgkin lymphoma (HR 1.14 [95% CI 1.00-1.30]) and its largest subgroup diffuse large B-cell lymphoma (HR 1.31 [95% CI 1.03-1.67]). Childhood height was associated with multiple myeloma (HR 1.30 [95% CI 1.04-1.64]) independent of childhood BMI. We conclude that childhood but not puberty is the critical developmental period regarding future risk of HM and we suggest that elevated childhood BMI is a determinant of Non-Hodgkin lymphoma and diffuse large B-cell lymphoma.