Introduction

Hypertension, a global threat to human health, substantially increases the risk of cardiovascular diseases and is a prominent contributor to mortality with more than 1 billion cases [1, 2]. Along with the improvement in the social economy and the aging of the population, the incidence of hypertension is rising at an alarming rate. In China, the prevalence of hypertension is 23.2% [3], while in the United States, the situation may be even more critical [4]. Notably, recent studies have also shown that high BP in adolescents and children is also a worrisome concern [8, 25, 26]. As we all know, hypertension is a multifactorial disorder involving the combined effect of environment and genes with an unsatisfactory controlling rate [10, 11]. Continuing to explore the etiology of hypertension, especially in adolescence and childhood, has significant implications for preventing disease progression and improving global health. Low body weight, an indicator of congenital development dysplasia or an adverse intrauterine environment, has recently been thought to be widely implicated in high blood pressure and other cardiovascular diseases [27, 28].

Barker et al. [29] first proposed the hypothesis of birth weight and later cardiovascular risk in adulthood. A large number of subsequent studies also confirmed the conclusions of the predecessors [30,31,32,33]. A Mendelian randomized study aimed at elucidating complex underlying biological mechanisms further corroborated previously published work [30]. The study identified a causal relationship between low birth weight and susceptibility to cardiovascular disease and diabetes, independent of adult obesity or high blood pressure. Recently, studies have further indicated that birth weight had a negative relationship with blood pressure, and low birth weight might lead to the risk of late increased blood pressure in adulthood [12,13,14, 28, 34, 35]. In agreement with earlier findings, the negative correlation between birth weight and SBP was also uncovered in children and adolescents even after adjusting for other relevant confounders, including the mother's age when born that may possess an elevation in blood pressure in the present study.

The following underlying mechanism may be involved in the reverse relationship between birth weight and blood pressure. Firstly, low birth weight caused by fetal dysplasia is a significant cause of increased blood pressure in later life. Low birth weight is considered an essential surrogate indicator of a poor and adverse intrauterine environment [36, 37]. Later, scholars advanced this theory to integrate the critical role of the kidney, indicating that the decrease in the number of nephrons at birth was a significant cause for diseases such as hypertension and coronary heart disease in adolescents and adulthood [12, 16, 38, 39]. In 2003, the kidney collected by Hughson M et al. [40] through autopsy confirmed that people with low birth weight had fewer nephrons, providing further evidence for the reverse association between birth weight and blood pressure. In addition, the developmental origin theory may further explain the negative relationship between birth weight and blood pressure, which believed that cardiovascular diseases originate from intrauterine development, not just traditional acquired [41].

Nevertheless, some studies have questioned the relationship between birth weight and blood pressure, and some scholars even draw contradictory conclusions [15,16,17, 42]. Inadequate adjustment of related variables and nonrepresentative study samples are the main reasons that may contribute to discrepant results [43]. Our research object is the nationally representative NHANES, and after adjusting BMI, weight, height, waist circumference, and common risk factors for high blood pressure such as FBG and blood lipids, this negative correlation between birth weight and SBP still exists. Moreover, we performed a subgroup analysis of different groups, and the same conclusions could be drawn.

Previous findings have revealed that birth weight was identified to be associated inversely with DBP in adults [12] and adolescents [44]. This negative correlation, conversely, has not been replicated in children and adolescents in the current research. Our findings suggested a nonidentical relationship between birth weight and DBP, which may imply that the influence of birth weight on DBP may be the result of a combination of multiple factors, including growth restriction in utero and acquired factors. Similar to our findings, an analysis of data from a census in six major urban areas in China showed that birth weight did not influence DBP [16]. Since China is a predominantly agricultural country, the objects of this study mainly collected from urban areas without rural regions, so the sample may not be nationally representative. The NHANES data used in our research is a typical nationally representative database based on demographic characteristics. We found this nonlinear relationship between birth weight and DBP and that the effect persisted after adjusting for potential confounding factors. Unlike SBP, DBP is not affected by birth weight, highlighting different potential mechanisms behind high SBP and high DBP in the young [16, 45]. As a result, more animal models and clinical studies are required to explain this relationship between birth weight and DBP in our observations.

In addition, we found that among participants at the age of 13 to 15 years and Mexican Americans, there was an inverted U-shaped and inverted J-shaped relationship between birth weight and blood pressure. Furthermore, these trends were not observed in those younger than 13, which may be related to different physical growth manner after the age of 13, such as changes in adolescent hormones, which requires further confirmation. Previous studies have found that different groups of people had different responses to blood pressure. For example, Keller G et al. [46] analyzed 10 patients with essential hypertension who died unexpectedly and found that White had significantly fewer nephrons. Our cross-sectional study found that birth weight and DBP formed a reverse J-shaped relationship in Mexican Americans. Specifically, when the birth weight was less than 105 oz, the effect on DBP was little. While the birth weight was greater than 105 oz, the diastolic blood pressure decreased by 1.06 mmHg for every ounce increase in birth weight. Additionally, our study also implies that for those aged 13 to 15, a birth weight less than 105 oz may contribute to an elevation in blood pressure.

To conclude, the current study identified that birth weight was negatively related to SBP but not significantly related to DBP in children and adolescents aged 8 to 15 during the NHANES 2007–2018. However, we observed an inverted U-shaped association between birth weight and DBP, with low and high levels being related to lower DBP in individuals aged 13 to 15. In addition, our current study indicates a reverse J characteristic curve between birth weight and DBP in Mexican Americans. It is well known that even a slight rise in blood pressure can increase the long-term risk of target organ damage and cardiovascular disease. Therefore, it is imperative to tease out the etiology of hypertension in the young and find potential preventive measures. Our findings have a number of profound implications in clinical practice. In the first place, our research supports the view that using precision medical measures to improve prenatal nutrition and growth to intervene in low-weight fetuses may improve cardiovascular fitness in adulthood. Secondly, for infants with low birth weight, standardized monitoring of blood pressure and timely intervention, such as nutrition and diet adjustments, may help reduce the risk of hypertension, exceptionally high SBP. Lastly, birth weight has different effects on DBP for different groups of people, suggesting that targeted intervention measures should be taken rather than generalizations.

Nevertheless, this study still has the following primary deficiencies. First, this is a cross-sectional study, and the birth weight data reported by the agency may have some recall bias. Second, there is a lack of dynamic information regarding the impact of birth weight on adolescents' blood pressure. Finally, the absence of data about underlying confounding factors such as gestational age, puberty development, physical activities, and other unidentified prognostic factors was another flaw of the study. Our findings should be interpreted with caution, given the above limitations. Prospective studies examining infants and tracking their blood pressure in adulthood to verify the causal effect of birth weight on hypertension are imperative and urgent.