Data are from 30,372 individuals comprising 102,583 data points (). Each cohort was overlapped to some extent by at least one other cohort with data at a similar age. The birth dates of the cohorts spanned the years 1918 to 1992, and BP data were collected over a 29-y period from 1979 to 2008 (). The oldest T-07 cohort (1932/1933) and the HAS and CaPS cohorts had the highest proportion of individuals working in manual occupations () and were more likely to be from the manual social classes in childhood, reflecting secular changes in the UK labour market. WHII is predominantly a white collar cohort, with less than 10% employed in manual occupations and none in classes IV and V.
Number of participants and median age (years) at each wave in each population-based cohorts, stratified by sex.
Cohort information and baseline characteristics by sex.
The prevalence of individuals on HypRx was similar in men and women, rising sharply from ~40 y (). For example, in the T-07 1932/1933 cohort, 13% were on medication at 55 y, and 62% at 75 y. For a given age, treatment was more prevalent in the more contemporary cohorts, although the pattern of uptake with age was consistent across cohorts. also shows the observed distribution of SBP with age in each cohort. The distribution widened with age in both sexes from the fourth to seventh decade, as illustrated by comparing waves 1 to 3 between the T-07 1952/1953 and 1932/1933 cohorts where the same measurement device was used.
Observed SBP and prevalence of antihypertensive therapy.
Unadjusted SBP Life Course Trajectories
shows the predicted mean SBP trajectories and annual SBP change estimated from the unadjusted models in each cohort, while shows the coefficients for the age effects from these models. The steepest rises in SBP were in adolescence, reaching 5.2 mm Hg per year (95% CI: 5.1, 5.3) in ALSPAC boys and 3.6 mm Hg per year (95% CI: 3.5, 3.8) in ALSPAC girls from 14 to 15 y. From 15 to 30 y, the annual rate of change decreased in T-07 men from 0.9 mm Hg per year (95% CI: 0.6, 1.1) at age 15 y to 0.2 mm Hg per year (95% CI: −0.0, 0.4) at age 35 y. In T-07 women there was a relatively stable linear increase of 0.5 mm Hg per year (95% CI: 0.4, 0.6) from 15 to 35 y. In both men and women, there was then evidence of a midlife SBP acceleration beginning at ~35 y, and reaching a velocity of ~1.0 mm Hg per year by age 50 in both the T-07 1952/1953 and NSHD cohorts. The rate of SBP change reached a midlife peak at 55 y of 1.5 mm Hg per year (95% CI: 1.1, 1.9) in men and 1.4 mm Hg per year (95% CI: 1.1, 1.8) in women of the T-07 1932/1933 cohort. SBP increases then slowed and eventually began to decline at age 65, 66, and 70 y in the CaPS, HAS, and T-07 1932/1933 male cohorts, respectively, and at 77 y in the T-07 1932/1933 female cohort. SBP was already declining by age 65 y in the HAS female cohort. Compared to the population-based cohorts, SBP remained lower through midlife in the WHII occupational cohort, and the midlife acceleration in SBP occurred later (). For example, at age 60 y, mean SBP in WHII was 17.5 mm Hg and 15.5 mm Hg lower than that of the T-07 1932/1933 cohort for men and women, respectively, and reached a velocity of 1 mm Hg per year at age 75 y in men and 65 y in women, compared with 50 y in the other cohorts.
Predicted SBP from unadjusted models.
Regression coefficients (standard errors) for the fixed effects from the main unadjusted multilevel models displayed in .
We carried out several post hoc analyses to investigate possible reasons for the deceleration and decline seen in the older cohorts. An underestimation of the effect of HypRx was unlikely to have caused an artefact in the patterns we observed in old age (see Text S1
). Excluding individuals who had ever taken HypRx in order to capture the trajectories in a healthy untreated sub-group explained a large part of the declining pattern observed at older ages (see Text S4
). For example, in the T-07 1932/1933 cohort, the SBP of this non-medicated group continued to rise in a linear manner through old age, and in CaPS, the average untreated trajectory continued to rise for a longer period in later life and reached a plateau rather than exhibiting decline as in the primary analyses including treated individuals. The additional exclusion of those individuals who had suffered a myocardial infarction in this cohort further emphasised this plateau. Survivor bias (i.e., survival of those who are most healthy and least prone to common causes of premature mortality such as CVD) was unlikely to explain the general declining pattern of SBP, as the average trajectory of those who were still alive at the last wave of measurement still showed a deceleration and decline in the older population-based cohorts (see Text S4
BMI Adjusted Trajectories
ALSPAC children were taller than the T-07 1972/1973 cohort at baseline when compared on the UK 1990 growth scale (+0.28 z and +0.16 z in ALSPAC versus T-07 boys and girls, respectively; ). The median BMI (UK 1990 z-score) was similar in these cohorts, but individuals in the upper centiles of ALSPAC had a larger BMI than those in the upper centiles of T-07 1972/1973 (). At age 15 y, SBP in ALSPAC was ~10 mm Hg higher than in T-07. Adjusting the SBP trajectory to the UK 1990 growth reference made little difference to this cohort difference ().
Observed BMI (kg/m2) in each cohort.
BMI increased through adult life in all cohorts, with steeper rises seen in early to mid adulthood (20 to 50 y) (). Adjusting the SBP trajectory for BMI at each age in each cohort appeared to slow some of the SBP rise seen between 30 and 40 y, but the biggest impact of the BMI adjustment was on the intercept, shifting each cohort's mean SBP trajectory downwards (). shows the association between BMI and SBP in each cohort. Among adult cohorts there was a suggestion that the association was largest at 50 to 60 y.
Predicted mean SBP and velocity after adjusting for BMI.
Table 5 Association (β) between concurrent BMI (per z-score increase in UK 1990 growth reference units in cohorts where data collection began in childhood or adolescence and per kilogram/metre2 in adult cohorts) and SBP (millimetres of mercury) in each (more ...)
shows the sex differences in SBP in each cohort. The pattern of these differences was unaffected by adjustment for BMI (unadjusted not shown). From age 7 to 12 y, ALSPAC girls had a slightly higher SBP; boys caught up by age 13 and then overtook girls such that by age 15 y the mean SBP in boys was 5.0 mm Hg higher (95% CI: 4.5, 5.6). Similar sex differences were seen at age 15 y in the T-07 1972/1973 cohort. The maximum sex difference occurred at age 26 y (+8.2 mm Hg in men, 95% CI: 6.7, 9.8) in the T-07 1972/1973 cohort. Women experienced steeper early adulthood and midlife rises, and by the sixth decade there was no evidence of a sex difference in SBP in the T-07 1932/1933 cohort. However, in the HAS cohort, women had a higher SBP from 64 to 72 y, and men had a higher SBP from age 72 y. The pattern of sex difference in WHII followed the trends in the population-based cohorts.
Mean sex difference in SBP (men minus women) (in millimetres of mercury) and 95% CIs.