We observed large differences in 20-year hypertension incidence across four US urban areas with 30–40% lower incidence in Chicago or Minneapolis compared with Birmingham. These differences were observed in blacks and whites, in men and women, and persisted after adjustment for major hypertension risk factors. Independent of geography and hypertension risk factors, blacks, particularly black women, had significantly higher rates of 20-year hypertension incidence. As hypertension incidence increased over time, racial differences also increased, whereas geographic differences persisted.
Although some7, 12, 13
but not all14
studies have shown greater hypertension prevalence or elevated BP incidence in the Southeastern US, few studies have assessed geographic differences in hypertension incidence over prolonged time periods. In one National Health and Nutrition Examination Surveys (NHANES I) analysis, region was not associated with incident hypertension between 1971 and 1984 for 14,235 adults aged 25–74 years perhaps owing to higher death rate, survival bias, masking of important geographic differences within the 4 large US census regions studied, and adjustment for diabetes, which may be on the causal pathway.14
Among younger adults, we found that differences in 20-year hypertension incidence between US cities were not fully accounted for by socio-demographic, behavioral, familial, and clinical correlates. Our findings are consistent with some26–28
but not all research17
showing geographic differences in BP even after adjusting for risk factors.
Potential causes of geographic differences in hypertension incidence include socioeconomic factors not captured by adjustment for education,29
dietary or lifestyle factors,30–32
or environmental-gene interactions.32
Our finding of a significant urine sodium/potassium*site interaction suggests that dietary sodium and potassium intake may modify the association between geography and hypertension incidence with greater effect in Minneapolis and Chicago; however, urine sodium/potassium was measured at year 5 only and the numbers in this sub-sample are small. Environmental exposures including air temperature33
and particulate air pollution34
may contribute to geographic differences with effect modification by obesity and genotypic or phenotypic indicators of systemic inflammation and oxidative stress.35
Given that geographic variations in BP appear at young ages,13, 27
differences in exposure to these or other potential risk factors may occur in early life.
Similar to some17
but not all18
research, we observed marked racial differences in hypertension incidence between US blacks and whites at middle age, in men and women, and after adjusting for major hypertension risk factors. A Baltimore study (n=377, mean age 44 years) may not have found racial differences because the participants had relatively high socioeconomic status, a factor associated with lower hypertension risk,29
most blacks were female (72%), most whites were male (73%), and follow-up was only 7 years.18
Our finding of some non-significant racial contrasts after adjusting for urine sodium/potassium in the sub-study may be due to decreased power or may reflect a true attenuation of the association between race-sex and hypertension incidence by dietary sodium and potassium intake. In addition, we found that black women had higher hypertension incidence after adjusting for baseline systolic BP; this masking of race-sex differences in hypertension by risk factors is consistent with prior research.36
Racial differences in hypertension incidence may result from racial differences in sympathetic reactivity to stress,37
cumulative effects of psychosocial factors and stress,38
responsiveness of the renin-angiotensin-aldosterone system,39
dietary or lifestyle factors,40
or environmental-gene interactions.41
We found striking BP increases in blacks compared to whites, and in women compared to men, changes supported by previous studies.18, 29
Given recent research showing that, among participants aged 7–16 years, boys had a greater increase in BP over 15 years than girls,41
our results suggest that sex trajectories in BP may vary from adolescence to young adulthood. Moreover, our observed race-sex trajectories in hypertension incidence may continue into middle-age, more so in disadvantaged subgroups.29
Our cohort includes four urban areas only and we used the baseline recruitment site for geographic assignment. Analyses including participants (80%) residing within 50 miles of their baseline recruitment site at year 20 produced similar results. Although the method for BP measurement changed from year 15 to year 20, results of analyses for cumulative 15-year hypertension incidence were similar. Despite high retention of the cohort, incomplete follow-up may bias our results; reassuringly, analyses that did not require the year 20 examination or that adjusted for the probability of missing variables did not change our results significantly. Although excluded participants had higher prevalence of hypertension risk factors than included participants, hypertension incidence was similar or lower in analyses which included many of the excluded participants, please see http://hyper.ahajournals.org
Geographic variations in hypertension management or anti-hypertension medication use could contribute to our observed differences; however, we focus on incident hypertension, thus our differences would have to be influenced by medical management preceding the diagnosis of hypertension. Further, geographic variations in anti-hypertensive medication use did not change results in a previous CARDIA analysis.13
Some factors (e.g., lifestyle, family history) were self-reported and subject to recall bias. Although BMI may predict hypertension less than measures of central obesity, we obtained similar results when we replaced BMI with waist circumference in models. Importantly, our lifestyle measures may not capture lifestyle factors adequately given that we observed site differences in diet and physical activity but these factors did not explain variations in hypertension incidence. Moreover, our findings of robust associations between hypertension incidence and physical activity or BMI in fully adjusted models confirm that exercise and weight management are important modifiable risk factors for hypertension.
Given that we do not fully understand the mechanisms of the demographic and racial differences we demonstrated, action-oriented recommendations based on our findings may be premature. Other large epidemiologic studies42, 43
are contributing to our understanding of the pattern of end-organ damage attributable to hypertension in older populations as mechanistic studies40, 44
of pathophysiology are being actively pursued. In the meantime, we believe that the groups known to be at highest risk of hypertension (e.g., black women in the South) need especially high surveillance and aggressive management of known hypertension risk factors, such as obesity.