In this prospective cohort study, females and males with overweight/obesity in childhood or adolescence were more likely than their peers without overweight/obesity to develop hypertension between ages 20 and 35. Importantly, our results show that empirically derived phenotypes of childhood and adolescent overweight/obesity had differential risks of incident hypertension in young adulthood. Among both females and males, the risk of developing hypertension was higher for those in the “early puberty”, “mothers with obesity”, and “high weight concerns” phenotypes compared to the risk of hypertension for overall overweight or obesity, indicating the importance of using empirically derived phenotypes when assessing risks of disease. Additionally, among females, the highest risks were observed among those in the “early puberty” and “mothers with obesity” phenotypes while those in the “high weight concerns” phenotype had the greatest risks of developing hypertension among males. In both sexes, participants in the “mixed” phenotypes had the lowest risks. Previous studies assessing obesity phenotypes in children have focused primarily on associations between phenotypes characterized by dietary and physical activity behaviors and weight status.35, 36 Our results demonstrate that there is additional heterogeneity of risk among people with obesity with other clinically discernable characteristics.
There are multiple established risk factors for hypertension in adulthood, including elevated blood pressure in childhood37, 38 and age at menarche.39, 40 Females with an early age at menarche are more likely to develop both obesity and hypertension.41 Some of the increase in risk of elevated blood pressure is mediated by obesity. However, the increased risk is not entirely explained by the body composition changes that accompany pubertal development in women. Even after adjusting for changes in body composition and BMI, women with an early age at menarche have an increased risk of hypertension in adulthood, compared to their peers with average or late age at menarche.42, 43 Another potential mechanism through which early age at menarche might act is via longer duration of exposure to high levels of estrogen, which has been found to increase the risk of developing hypertension.44, 45
Weight concerns are a highly prevalent source of chronic stress for many individuals in the US, yet relatively few studies have examined the associations between weight concerns and the development of hypertension.46–49 Most of the previous research has been among females or samples that were predominantly female. We observed that participants in the high weight concerns phenotype were more likely to develop hypertension in young adulthood compared to those without overweight/obesity in childhood or adolescence. High weight concerns, potentially due to internalized weight bias and perceived weight discrimination, can generate a chronic stress response leading to increased cortisol secretion.50, 51 Furthermore, previous studies have also found an obesity-independent relationship between hypertension and binge eating, which can increase oxidative and inflammatory responses.23, 52 Those physiological arousal processes have been linked to the development of hypertension.53, 54 Our findings suggest that males with obesity and weight concerns are at a substantially elevated risk of developing hypertension.
There is a strong association between parental and offspring weight status that persists into mid-adulthood.55 In addition, independent of BMI and waist circumference, parental history of hypertension is associated with increased odds of hypertension.41, 56–58 Because obesity is a strong risk factor for the development of hypertension, it is essential to tease apart whether the association between family history and the development of hypertension is independent of weight status. Few studies have considered both family history of hypertension and obesity. Dormanesh et al. found a family history-related elevation in risk of hypertension above and beyond the contribution of BMI.59 The association reflects a genetic propensity of hypertension, as well as non-genetic factors, such as shared lifestyle.56, 60 Our findings showing strong associations between the mothers with obesity phenotype and incident hypertension are consistent with those of Dormanesh and colleagues.
There are numerous strengths to our study, including using a large community-based sample of participants residing across all regions of the US. Second, by assessing obesity phenotypes between 9–19 years and assessing incident hypertension between 20–35 years, our study provides evidence for the temporal ordering of obesity phenotypes in childhood and adolescence and incident hypertension in young adulthood. Third, we were able to adjust our models for potential confounding variables including physical activity and diet that are often not measured in detail in other studies. Finally, given that previous studies have mostly used BMI cutoffs alone to study the association between childhood obesity and hypertension in adulthood, our study expands the literature by showing significant associations between obesity phenotypes characterized by psychological, behavioral, and familial factors and incident hypertension.
There are several limitations that warrant consideration. First, incident hypertension was self-reported, which may lead to some underestimation and misclassification of the outcome. Second, the homogeneity of our sample may limit the generalizability of our results to primarily White or economically advantaged populations. Third, some participants who were eligible for inclusion into the study were missing data on incident hypertension in adulthood and were excluded, which may result in selection bias if exclusion was related to overweight/obesity in childhood or adolescence and hypertension in young adulthood. Lastly, there is a potential for residual confounding due to other potential confounders not included in the models, including family history of hypertension.
Despite these limitations, our results offer strong support for examining the health consequences of obesity separately by obesity phenotypes rather than combining all people with obesity into a heterogenous group, which is the approach taken in most research. If these results are replicated prospectively, it may be valuable for clinicians to increase hypertension surveillance in young adults with obesity sub-phenotypes that increase risk.