The current study examined the association of childhood BP and its determinants in a nationally representative sample of Canadian children and adolescents. We found that obesity was positively associated with SBP, but not with DBP (except in adolescent boys among whom obesity was associated with higher DBP). We observed that obese adolescents had an average of 7.6
mmHg higher SBP than that of normal weight adolescents. BMI had the strongest effect on BP among obese children and adolescents. Less physically active adolescent boys had higher SBP (3.9
mmHg) and DBP (4.9
mmHg) than physically active boys. FHH in young girls and adolescent boys was strongly associated with increases in both SBP and DBP. Both family income and parental education played independent roles on BP in young children.
Based on the first national physical measures survey, we reported that the prevalence of childhood hypertension and pre-hypertension was at 2-3
%, which is significantly lower than other Canadian studies, in which prevalence of hypertension was reported at 7.4
% and 14
]. However, it is difficult to compare across studies because of differences in age, study populations (i.e. rural resident) and variability in BP measurement methods. Our results do seem to be in line with those studies with repeated BP measurements [25
], suggesting the importance of standardizing BP measures. Our observations that BMI or obesity is consistently associated with increasing SBP are consistent with a series of studies performed on various populations, though some studies also observed the effect of BMI on DBP [2
]. The mechanism underlying the association between obesity and hypertension is poorly understood. Sorof et al. proposed that obesity-induced hypertension may be mediated in part by sympathetic nervous system hyperactivity, which is partly manifested by increased heart rate and BP variability [6
]. This possibility is supported by our data that heart rate is positively associated with BP, especially among children, and that a significant difference in heart rate was observed in the obese compared with nonobese groups (data not shown). Most research has focused on SBP because it is a strong predictor of arterial stiffness and many other cardiovascular risks growing into adulthood [11
]. Our results support the close association between SBP and obesity, reinforcing the importance of maintaining a healthy weight for optimal SBP during childhood. In addition to substantial increases in SBP, we found markedly higher DBP in obese adolescent boys. This might be explained by evidence of early atherosclerosis at autopsy and ultrasound findings of the carotid artery, in which severely obese children, especial boys, display arterial stiffness and increased diastolic wall stress, indicating adverse changes in vascular health that could be the culprit for the increases in both SBP and DBP [27
Furthermore, our results show that BMI has the strongest effect on BP among obese children and adolescents. Rosner et al. proposed that there may be a different effect of BMI on BP depending on the differing levels of fatness among various ethnic groups [12
]. Our result are consistent with a recent study by Tu et al. who found that there is a marked intensification of the influence of adiposity on BP when children reach the categories of overweight and obese [28
]. Moreover, the differing effect of BMI on both SBP and DBP may well be explained by some intervention studies. One such study by Rocchini et al. demonstrated that weight loss among obese adolescents changed the BP distribution from right skewed to no difference from the general population; however, they did not examine the effect on BP of weight loss among normal weight adolescents [29
]. Further intervention research involving normal weight children would provide more insights into this discussion. While mechanisms underlying these differences are still being researched, recent evidence also indicates that the adipose tissue-derived hormone, leptin, may be a potentially important mediator in linking the effect of adiposity on BP [28
]. Our results do suggest that small reductions in weight among obese children may lead to reductions in their BP.
The present study observed an inverse association between physical activity and SBP and DBP in adolescent boys. A number of observational and intervention studies have investigated associations between PA and BP in children and adolescents. Kelley et al. combined the results of 12 randomized trials and concluded that PA leads to a small but statistically significant reduction in BP [30
]. Using accelerometer-measured PA data from the NHANES, Mark et al. described a modest dose–response relation of total PA and moderate-to-vigorous intensity PA with hypertension [31
]. Leary et al. found a similar inverse association between total PA and SBP; however, when they compared the volume (duration and frequency) versus the intensity (vigorousness) of PA, they found that moderate to vigorous PA did not further reduce BP beyond the reduction achieved by a higher volume of PA, suggesting the volume of PA may be more important than the intensity of PA in reducing BP [15
]. Since PA levels defined in the CHMS did not distinguish between the volume and intensity of PA, we were unable to assess their individual effects on BP. Nevertheless, our study identified inactive or moderately active adolescent boys as at risk of increased SBP and DBP, suggesting that PA should be intensified to mediate the negative effect on BP of other risk factors, and be promoted particularly for girls as evidence suggests that girls are less likely to participate in moderate to vigorous PA than boys [32
]. Current clinical guidelines recommend that vigorous PA such as participation in competitive sports should only be limited in the presence of uncontrolled stage 2 hypertension, which is above 99th
percentile for gender, age and height [7
Research shows that both genetic and environmental factors significantly influence BP and the development of hypertension during childhood [17
]. Our results show that the strength of associations between BMI and BP was not modified by the presence of FHH. What our cross-sectional study was unable to address, however, is whether children with FHH are more susceptible to elevated BP due to increased BMI or decreased PA; more research is needed to explore effects of other risk factors in the presence of FHH so that targeted intervention can be designed for this genetically predisposed population. Interestingly, in future studies, increases in environmentally induced high blood pressure may serve to mask the association of blood pressure risk and genetic factors, for which FHH is a proxy.
Finally, the inverse relationship of post-secondary parental education with SBP in children, especially girls, is similar to previous findings in which BP in girls was related to socioeconomic variables in addition to anthropometric factors [33
]. However, living in a low income family situation did not appear to increase risk of high BP, and was even associated with lower BP in children in this study. While some recent epidemiological studies from western developed countries have pointed that SES is inversely associated with childhood obesity, evidence on the relationship of SES with BP in childhood is limited [18
]. Howe et al. in a recent study indicated important socioeconomic inequalities in obesity and cardiovascular risk factors including childhood BP in children; however, the SES indicator used in their study was maternal education [34
]. In Canada, findings on SES and its relation with childhood obesity are conflicting [35
]. In fact, we have noticed in our data that prevalence of obesity is lower in the lowest income (9.6
%) than middle to high income groups (13.9
%). With ongoing data collection for the next cycle of the CHMS, more studies with larger survey samples, detailed information on SES and inclusion of more variables (i.e. dietary, psychological factors) are expected to verify our findings.
The present study has several strengths. First, the CHMS is a high quality survey with standardized BP measurement for a nationally representative sample. Second, the sample of children aged 6 to 17
years was large enough to achieve sufficient statistical power to assess the independent effects of multiple variables. Limitations of our study include the cross-sectional survey design, which does not allow us to make casual inferences about BP and its determinants. However, reverse causation is unlikely. Another limitation is related to oscillometric measured BP, which may have underestimated DBP when compared with the US reference data using auscultatory method. However, the accuracy of the device has been validated by the company for its use in adults and children, and checked regularly by comparing with a T tube connected mercury sphygmomanometer for comparable readings for SBP and DBP [37
]. Finally, dietary factors have been important in the prevention and treatment of hypertension in adults, especially intakes of sodium and potassium [39
]. However, measures estimating these nutrient intakes are no available in cycle 1 of the CHMS.