HomeHypertensionVol. 79, No. 8Distinct Trajectories of Overweight During Childhood and Elevated Blood Pressure at Late Adolescence Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessEditorialPDF/EPUBDistinct Trajectories of Overweight During Childhood and Elevated Blood Pressure at Late Adolescence Zdenka Pausova Zdenka PausovaZdenka Pausova Correspondence to: Zdenka Pausova, MD, Departments of Physiology and Nutritional Sciences, Hospital for Sick Children, University of Toronto, Peter Gilgan Centre for Research and Learning, 686 Bay St, Rm. 10-9705, Toronto, ON M5G 0A4, Canada. Email E-mail Address: [email protected] https://orcid.org/0000-0002-7784-1380 Departments of Physiology and Nutritional Sciences, The Hospital for Sick Children, University of Toronto, Canada. Search for more papers by this author Originally published13 Jul 2022https://doi.org/10.1161/HYPERTENSIONAHA.122.18990Hypertension. 2022;79:1614–1616This article is a commentary on the followingExploring Overweight Risk Trajectories During Childhood and Their Associations With Elevated Blood Pressure at Late Adolescence: a Retrospective Cohort StudySee related article, pp 1605–1613Childhood and adolescence are periods of human development during which the initial stages of cardiovascular disease may emerge.1 They may also be periods when disease trajectories can still be altered and full-blown disorders prevented. Cohort studies suggest that adolescent obesity is a major risk factor for adult obesity—being obese as a 15- to 17-year adolescent increases the risk of being obese as an adult by 17.5-fold.2 Adolescent high blood pressure (HBP) is also a strong predictor of adult hypertension, as shown in the Bogalusa Heart Study (Figure).3 Critically, both childhood obesity and HBP are leading risk factors for adult atherosclerosis. Several studies have shown that carotid intima-media thickness measured at age 30 to 40 years correlates positively with body mass index and BP assessed in childhood.4-6In this issue, Wang et al7 conducted a longitudinal cohort study of 17 810 children (7 to 18 years of age) to identify trajectories of the overweight risk and their associations with the risk of HBP. All data were acquired during annual physical examinations taking place in elementary and high schools in the city of Zhongshan in China between 2005 and 2016. All measurements were done by medical staff according to standardized procedures, and only children with at least 8 annual examinations were included in the study. Overweight was defined as age- and sex-specific body mass index Z scores based on the growth reference from World Health Organization.8 Elevated BP was defined as 85th≤ systolic BP or diastolic BP <95th age- sex- and height-specific percentile for children <13 years old, and 120 mm Hg≤ systolic BP ≤129 mm Hg with diastolic BP <80 mm Hg for children ≥13 years. HBP was defined when either systolic BP or diastolic BP ≥95th age-, sex-, and height-specific percentile for children <13 years, and BP ≥130/80 mm Hg for children aged ≥13 years.The results of the Wang et al7 study provide strong evidence that overweight is a major risk factor for HBP in children and that the overweight-related risk of HBP increases with age during childhood and adolescence.9,10 The novelty of the study lies in the use of elegant group-based trajectory modeling, which identified 4 groups of children with distinct trajectories of overweight, labeled as constant low, low increasing, high decreasing, and constant high based on change in overweight status. Most children in the study demonstrated stable weight status (86.9% in constant-high and constant-low groups), but the 2 smaller groups (13.1% in low-rising and high-decreasing groups) changed the weight status during childhood. A significant increase in HBP risk was found in the low-rising group, which reached a similar level as that in the constant-high group. The trajectories of the 2 smaller groups intersected at about the age of 13 years, making it difficult to distinguish adolescents from the two groups and identify the ones who are at a higher risk for HBP and who would thus benefit from a closer follow-up and interventions.The study is noteworthy for its size and multiple yearly follow-ups between ages 7 and 18 years, which is a period of major body growth characterized by increasing body mass index and blood pressure. An additional strength of the study is the recruitment via schools, making the cohort representative of the local population. At the same time, results in this cohort may not be fully relevant to other populations; for example, the prevalence of overweight and obesity was only 14% in this cohort, which is about a half of the prevalence of overweight and obesity in North America.11 Additionally, the study did not account for potentially confounding effects of diet, physical activity, or stress, as these factors were not evaluated. The identified overweight trajectories and associated risk of HBP were similar in boys and girls, but without deep phenotyping, we do not know whether the underlying mechanisms are also similar between the two sexes; previous research suggests otherwise.12-15 It also remains to be studied what role age-related changes in sex hormones and body composition during puberty play. Future studies could also find out whether children with distinct body mass index trajectories might be identified early on using, for example, polygenic risk scores or blood biomarkers16,17; this would facilitate translation of the findings from this study to personalized (preventive) medicine.Download figureDownload PowerPointFigure. Overweight and high blood pressure track together from childhood to adulthood.Article InformationSources of FundingSupported by NIH (grant R01AG056726).Disclosures None.FootnotesThe opinions expressed in this article are not necessarily those of the American Heart Association.For Sources of Funding and Disclosures, see page 1615.Correspondence to: Zdenka Pausova, MD, Departments of Physiology and Nutritional Sciences, Hospital for Sick Children, University of Toronto, Peter Gilgan Centre for Research and Learning, 686 Bay St, Rm. 10-9705, Toronto, ON M5G 0A4, Canada. Email zdenka.[email protected]ca