scholarly journals Childhood social class and adult adiposity and blood-pressure trajectories 36–53 years: gender-specific results from a British birth cohort

2010 ◽  
Vol 66 (6) ◽  
pp. 512-518 ◽  
Author(s):  
Bjørn Heine Strand ◽  
Emily T Murray ◽  
Jack Guralnik ◽  
Rebecca Hardy ◽  
Diana Kuh
Author(s):  
David Bann ◽  
Meg Fluharty ◽  
Rebecca Hardy ◽  
Shaun Scholes

ObjectiveTo evaluate whether socioeconomic inequalities in blood pressure (BP) have changed from 1989 to 2016—a period in which average BP levels declined and the detection and treatment of high BP increased.DesignRepeated observational studies.Setting3 nationally representative British birth cohort studies—born in 1946, 1958, and 1970—and 21 nationally representative cross-sectional studies (Health Survey for England 1994 to 2016, HSE).Participants147,775 participants with BP outcomes at age 42-46 years (cohorts) or 25 years and over (HSE).Main outcome measureAbsolute differences in systolic BP (SBP) by educational attainment (cohorts and HSE) and early life social class (cohorts).ResultsIn both datasets, lower education was associated with higher SBP, with similar absolute magnitudes of inequality across the studied period. Differences in SBP by education (Slope Index of Inequality) based on HSE data were 3.0mmHg (95% CI: 1.8, 4.2) in 1994 and 4.3mmHg (2.3, 6.3) in 2016. Findings were similar for diastolic BP (DBP) and survey-defined hypertension. Cohort data suggested that disadvantage in early and adult life had cumulative independent associations with BP: cohort-pooled differences in SBP were 4.9mmHg (3.7, 6.1) in a score combining early life social class and own education, yet were 3.4mmHg (2.4, 4.4) for education alone. In both datasets, inequalities were found across the SBP distribution—below and above hypertension thresholds—yet were larger at the upper tail; in HSE, median SBP differences were 2.8mmHg (1.7, 3.9) yet 5.6mmHg (4.9, 6.4) at the 90th quantile.ConclusionSocioeconomic inequalities in BP have persisted from 1989 to 2016, despite improved detection and treatment of high BP. To achieve future reductions in BP inequalities, policies addressing the wider structural determinants of high BP levels are likely required—targeting detection and treatment alone is unlikely to be sufficient.


The Lancet ◽  
2003 ◽  
Vol 362 (9391) ◽  
pp. 1178-1183 ◽  
Author(s):  
Rebecca Hardy ◽  
Diana Kuh ◽  
Claudia Langenberg ◽  
Michael EJ Wadsworth

BMC Medicine ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
David Bann ◽  
Meg Fluharty ◽  
Rebecca Hardy ◽  
Shaun Scholes

Abstract Background High blood pressure (BP) is a key modifiable determinant of cardiovascular disease and a likely determinant of other adverse health outcomes. While socioeconomic inequalities in BP are well documented, it remains unclear (1) how these inequalities have changed across time, given improvements over time in the detection and treatment of high BP (hypertension); (2) whether BP inequalities are present below and above hypertension treatment thresholds; and (3) whether socioeconomic position (SEP) across life has cumulative effects on BP. We sought to address these gaps using evidence from two complementary sources: birth cohort and repeated cross-sectional datasets. Methods We used three British birth cohort studies—born in 1946, 1958, and 1970—with BP measured at 43–46 years (in 1989, 2003, and 2016), and 21 repeated cross-sectional datasets—the Health Survey for England (HSE), with BP measured among adults aged ≥ 25 years (1994–2016). Adult education attainment was used as an indicator of SEP in both datasets; childhood father’s social class was used as an alternative indicator of (early life) SEP in cohorts. Adjusting for the expected average effects of antihypertensive medication use, we used linear regression to quantify SEP differences in mean systolic BP (SBP), and quantile regression to investigate whether inequalities differed across SBP distributions—below and above hypertension treatment thresholds. Results In both datasets, lower educational attainment was associated with higher SBP, with similar absolute magnitudes of inequality across the studied period. Differences in SBP by education (Slope Index of Inequality) based on HSE data were 3.0 mmHg (95% CI 1.8, 4.2) in 1994 and 4.3 mmHg (2.3, 6.3) in 2016. Findings were similar for diastolic BP (DBP) and survey-defined hypertension. Inequalities were found across the SBP distribution in both datasets—below and above the hypertension threshold—yet were larger at the upper tail; in HSE, median SBP differences were 2.8 mmHg (1.7, 3.9) yet 5.6 mmHg (4.9, 6.4) at the 90th quantile. Adjustment for antihypertensive medication use had little impact on the magnitude of inequalities; in contrast, associations were largely attenuated after adjustment for body mass index. Finally, cohort data suggested that disadvantage in early and adult life had cumulative independent associations with BP: cohort-pooled differences in SBP were 5.0 mmHg (3.8, 6.1) in a score combining early life social class and own education, yet were 3.4 mmHg (2.4, 4.4) for education alone. Conclusion Socioeconomic inequalities in BP have persisted from 1989 to 2016 in Britain/England, despite improved detection and treatment of high BP. To achieve future reductions in BP inequalities, policies addressing the wider structural determinants of high BP levels are likely required, particularly those curtailing the obesogenic environment—targeting detection and treatment alone is unlikely to be sufficient.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Amaraporn Rerkasem ◽  
Sarah E. Maessen ◽  
Antika Wongthanee ◽  
Sakda Pruenglampoo ◽  
Ampica Mangklabruks ◽  
...  

AbstractWe examined the associations between caesarean section (CS) delivery and cardiovascular risk factors in young adults in Thailand. Participants were 632 offspring from a birth cohort in Chiang Mai (Northern Thailand), born in 1989–1990 and assessed in 2010 at a mean age of 20.6 years, including 57 individuals (9.0%) born by CS and 575 born vaginally. Clinical assessments included anthropometry, blood pressure (BP), carotid intima-media thickness, and fasting blood glucose, insulin, and lipid profile. Young adults born by CS had systolic BP (SBP) 6.2 mmHg higher (p < 0.001), diastolic BP 3.2 mmHg higher (p = 0.029), and mean arterial pressure (MAP) 4.1 mmHg higher (p = 0.003) than those born vaginally. After covariate adjustments, SBP and MAP remained 4.1 mmHg (p = 0.006) and 2.9 mmHg (p = 0.021) higher, respectively, in the CS group. The prevalence of abnormal SBP (i.e., pre-hypertension or hypertension) in the CS group was 2.5 times that of those born vaginally (25.0% vs 10.3%; p = 0.003), with an adjusted relative risk of abnormal SBP 1.9 times higher (95% CI 1.15, 2.98; p = 0.011). There were no differences in anthropometry (including obesity risk) or other metabolic parameters. In this birth cohort in Thailand, CS delivery was associated with increased blood pressure in young adulthood.


2011 ◽  
Vol 51 (5) ◽  
pp. 583-591 ◽  
Author(s):  
Alexandros Heraclides ◽  
Gita D. Mishra ◽  
Rebecca J. Hardy ◽  
Johanna M. Geleijnse ◽  
Stephanie Black ◽  
...  

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Mingyu Zhang ◽  
Tiange Liu ◽  
Guoying Wang ◽  
Jessie P Buckley ◽  
Eliseo Guallar ◽  
...  

Background: In utero exposure to metals lead (Pb), cadmium (Cd), and mercury (Hg) may be associated with higher childhood systolic blood pressure (SBP), while trace elements manganese (Mn) and selenium (Se) may have protective, antioxidant effects that modify metal-SBP associations. No study has examined how in utero co-exposure to these metals affect offspring SBP. Objectives: To examine the individual and joint effects of in utero exposure to Cd, Pb, Hg, Mn, and Se on offspring SBP. Methods: We used data from the Boston Birth Cohort (enrolled 2002-2013). We measured metals in maternal red blood cells collected 24-72 hours after delivery. We calculated child age-, sex-, and height-specific SBP percentile per 2017 American Academy of Pediatrics guidelines. We used linear regression models to estimate associations of each metal, and Bayesian kernel machine regression (BKMR) to examine metal co-exposures, with child SBP between 3 to 15 years of age. Results: Our analytic sample comprised 1194 mother-child pairs (61% Black, 20% Hispanic). Hg and Pb were not associated with child SBP. Se and Mn were inversely associated with child SBP: each log2(Se) and log2(Mn) increment was associated with a 6.23 (95% CI: 0.96-11.51) and a 2.62 (95% CI: 0.04-5.20) percentile lower child SBP, respectively. BKMR models showed similar results ( Panel A ). While Cd was not overall associated with child SBP, there was an antagonistic interaction between Cd and Mn (P-interaction = 0.036): the association of Mn and lower child SBP was stronger with higher levels of Cd ( Panel B ). Consistent with this finding, in utero exposure to cigarette smoke (a major source of Cd) modified the association of Mn and child SBP: among children born mothers who smoked cigarette in pregnancy, each log2(Mn) increment was associated with a 10.09 (95% CI: 2.15-18.03) percentile lower SBP ( Panel C ). Conclusion: Optimizing in utero Se levels, as well as Mn levels in pregnant women who had high Cd or smoked during pregnancy, may protect offspring from developing high BP during childhood.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Quaisar Ali ◽  
Yonnie Wu ◽  
Tadashi Inagami ◽  
Tahir Hussain

Angiotensin II acting via Angiotensin II type 2 receptors (AT2Rs) is believed to be protective against blood pressure increase and affects renal function under pathophysiological condition. Recently we have observed that stimulation of AT2Rs in male obese Zucker rats has shifted the two opposing arms of renin angiotensin system (RAS) i.e. ACE-Ang II-AT1 vs ACE2/Ang-(1-7)-Mas. Evidence suggests that estrogen regulates RAS, including AT2R in female mice. We hypothesized that AT2R has a gender specific regulation of RAS. In the present study, we investigated the role of AT2Rs in regulating RAS components in male and female mice. Kidney cortex from AT2R knockout (AT2RKO) male and female mice and wild type (WT) with similar background (C57BL/6) of 20 weeks of age were used in the study. The cortical ACE expression (ng ACE/μg tissue) was significantly increased in AT2RKO mice (3±0.02) compared to WT males (1.9±0.02). LC/MS analysis of cortical tissue revealed that Ang II was also significantly increased in AT2RKO mice (WT: 31±3, AT2RKO: 47±3 fmoles/mg tissue). Deletion of AT2R significantly increased AT1R (204%, 204 of 100) expression and had no effect on renin activity compared to WT males. The cortical expression of ACE2 activity (WT: 113±8, AT2RKO: 40±11, RFU/min), Ang-(1-7) levels (WT: 7.3±1.4, AT2RKO: 3±0.8 fmoles/mg tissue) and Mas receptor (AT2RKO: 54±15, % of WT) was significantly decreased in AT2RKO males compared to WT. The cortical expression of the AT2R and MasR was 2-fold greater in WT females compared to WT male. The renin activity (WT: 32±2, AT2RKO: 21±0.3, RFU/min) and MasR expression (WT: 187.5±55, AT2KO: 47±9) was significantly decreased in AT2RKO females compared to the female WT. Interestingly, Ang-(1-7) level (WT: 5.7±0.7, AT2RKO 2.6±0.7 fmoles/mg tissue) was decreased but no changes in ACE or ACE2 activity was observed in AT2KO females compared to their WT, suggesting a role of non-ACE2 pathway. This study suggests that AT2R regulates ACE/ACE2 ratio-Ang II-AT1R expression negatively only in males, whereas in females, it regulates Ang-(1-7) potentially via non-ACE2 pathway. Such changes indicate a gender specific mechanisms potentially associated with AT2R-mediated regulation of renal function and blood pressure control.


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