BMI increase through puberty and adolescence is associated with risk of adult stroke

Objective: To evaluate the contribution of prepubertal childhood body mass index (BMI) and BMI change through puberty and adolescence, 2 distinct developmental BMI parameters, for risk of adult stroke in men. Methods: In this population-based study in Gothenburg, Sweden, men born in 1945–1961 with information on both childhood BMI at age 8 and BMI change through puberty and adolescence (BMI at age 20–BMI at age 8) were followed until December 2013 (n = 37,669). Information on stroke events was retrieved from high-quality national registers (918 first stroke events, 672 ischemic stroke events [IS], 207 intracerebral hemorrhage events [ICH]). Results: BMI increase through puberty and adolescence (hazard ratio [HR] 1.21 per SD increase; 95% confidence interval [CI] 1.14–1.28), but not childhood BMI, was independently associated with risk of adult stroke. Subanalyses revealed that BMI increase through puberty and adolescence was associated with both IS (HR per SD increase 1.19; 95% CI 1.11–1.28) and ICH (HR per SD increase 1.29; 95% CI 1.15–1.46). High BMI increase during puberty was strongly associated with increased risk of adult hypertension (odds ratio per SD increase 1.35; 95% CI 1.32–1.39). Conclusions: BMI increase through puberty and adolescence is associated with risk of adult IS and ICH in men. We propose that greater BMI increases during puberty contribute to increased risk of adult stroke at least partly via increased blood pressure.

Adolescent weight gain confers long-term increased stroke risk Weighty matters Adult obesity has been consistently associated with risk of total, ischemic, and hemorrhagic stroke [1][2][3] ; however, the degree to which change in weight and body mass index (BMI) during late childhood and adolescence affects adult risk of stroke has remained uncertain. Understanding this relationship is of particular importance given the rising obesity epidemic during childhood and adolescence. Ohlsson et al. 4 in this issue of Neurology ® provide key data on the long-term increased risk of weight gain during puberty, and the detrimental effects of overweight and obesity during adolescence and early adulthood on adult stroke risk. The authors analyzed BMI from childhood (age 8) through early adulthood (age 20) and the change over that period with risk of subsequent stroke in 36,000 Swedish men using high-quality school and military BMI records as well as health system linkage data. Each BMI change of 2 kg/m 2 from age 8 to age 20 was associated with a 21% increased risk of total stroke in adulthood. Risk of intracerebral hemorrhage was increased by 28% for each 2 kg/m 2 change, while risk of ischemic stroke increased by 19%. Notably, BMI gain (2 kg/m 2 ) during puberty/adolescence was associated with a 35% increased risk of adult hypertension, a likely mediating factor.
Boys who were overweight at both age 8 and age 20, as well as those who became overweight by age 20, had increased risk of stroke compared to those with normal weights. However, importantly, boys who were overweight at age 8 but who achieved normal weight at age 20 did not have increased risk of stroke during adulthood. Strengths of this thoughtful study include direct measures of height and weight from school and military records and long-term stroke follow-up. One limitation is the lack of data on women.
This study highlights the importance of events during adolescence on the later risk of chronic diseases and provides a potential explanation for the recently reported uptick in stroke incidence in midlife. 5 Despite being the most dynamic period biologically and behaviorally in our life cycle, adolescence is a relatively quiescent time in medical surveillance, in part because the adolescent has fewer common childhood infections and fewer immunization requirements. This age group often falls between pediatric and adult medicine.
Over the last 3 decades, obesity has reached a pandemic level globally, affecting all ages, especially in the United States. In recent years, the upward trajectory in young children (ages 2-5) seems to have stabilized. 6 However, obesity rates in older children (ages 6-11) and adolescents (ages 12-19) have continued upward. Between 1988-1989 and 2014-2015, adolescents doubled their obesity prevalence from 10.5% to 20.5% while older children had a 1.5-fold (11.3%-17.4%) increase. Furthermore, extreme obesity quadrupled among adolescents from 2.6% to 9.1%; for older children, the change was from 3.6%-4.3%. Based on the data from Ohlsson et al., this exponential increase in obesity in adolescents portends serious health consequences later in life.
Although the factors behind these trends remain incompletely understood, tantalizing clues exist. A large 10-year cohort study showed a breathtaking decline in physical activity during adolescence, with a drop of 100% and 64% in the physical activity median scores in black and white girls, respectively. 7 Further, a 10-year follow-up in the same cohort demonstrated a clear inverse relationship between physical activity and BMI changes. 8 Black women also became heavier than white women, although both groups doubled their rates of obesity, to 37% for black women and 18% for white women by age 19. 9 The strong association between overweight status in early adulthood and BMI gain during adolescence and subsequent stroke risk offers one potential explanation for the recently reported dramatic risk in stroke rates among men and women in midlife (age 40-54). 5 Stroke prevalence among women aged 35-54 years tripled in the United States over the last 2 decades, corresponding to the rise in obesity rates. 5 The role of extreme obesity, especially during adolescence, remains to be explored. The study by Ohlsson et al. did not stratify risk ratios by degrees of obesity due to low prevalence in this cohort. The transitioning into extreme obesity during adolescence is a concern, especially given its high incidence. The data from Ohlsson et al. suggest a dose-response relationship between the degree of obesity and stroke risk. However, there might be a threshold level of obesity beyond which the relationship may change from linear to exponential. These hypotheses require further investigation; we commend Ohlsson et al. for a study that leads to these interesting hypotheses.
The report by Ohlsson et al. 3 demonstrates the critical import of changes in BMI during adolescence, an oft-overlooked phase of the life cycle. Importantly for public health implications, children who reduced their BMI to the normal range by age 20 had no longterm increased risk of stroke. These findings emphasize the need to target interventions for children and adolescents to prevent overweight and obesity in early adulthood and also reduce future cardiovascular morbidity. Battling childhood and adolescent obesity is the first step toward prevention of stroke and major adult chronic diseases.

STUDY FUNDING
No targeted funding reported.