Increased Risk Of Hypertension Research Articles

Air pollution from agricultural fires increases hypertension risk

In many parts of the developing world, farmers widely use deliberate fires to burn vegetation and clear land to plant crops. These agricultural fires, however, are known to be associated with health costs due to increased air pollution. We contribute to underpinning the associated health cost estimates by studying the effects of these fires on hypertension risk. Despite being one of the leading causes of mortality globally, there is little direct evidence on how hypertension risk changes with exposure to pollution from agricultural fires. To overcome common data and empirical challenges in this setting, we match blood pressure readings from nearly 784,000 individuals across India with satellite data on 1.2 million agricultural fires, wind direction realizations, and local ambient air pollution. We find that the incidence of hypertension increases by 1.8% for each standard deviation increase in the number of upwind fires observed one day before the blood pressure readings. We find that the impact is stronger among older males, smokers, individuals that were already on blood pressure medication, and individuals belonging to socially marginalized groups. Our estimates suggest that agricultural fires in India lead to hypertension-related additional mortality, associated with USD 9 billion annually in costs.

Night Shift Work, Genetic Risk, and Hypertension

ObjectiveTo perform a prospective cohort study to investigate whether night shift work is associated with incident hypertension and whether this association is modified by genetic susceptibility to hypertension because evidence on the association between night shift work and hypertension is insufficient. MethodsA total of 232,665 participants of UK Biobank who were recruited from 2006 to 2010 and observed to January 31, 2018, were included in this study. A Cox proportional hazards model with covariate adjustment was performed to assess the association between night shift work exposure and hypertension risk. We constructed a polygenic risk score (PRS) for genetic susceptibility to hypertension, which was used to explore whether genetic susceptibility to hypertension modified the effect of night shift work. The robustness of the results was assessed by sensitivity analysis. ResultsNight shift workers had a higher hypertension risk than day shift workers, which increased with increasing frequency of night shift work (Ptrend<.001). The association was attenuated but still remained statistically significant in the fully adjusted model. We explored the joint effect of night shift work and genetic susceptibility on hypertension. Permanent night shift workers with higher hypertension PRSs had higher risk of hypertension than day workers with low PRSs. ConclusionNight shift work exposure was associated with increased hypertension risk, which was modified by the genetic risk for hypertension, indicating that there is a joint effect of night shift work and genetic risk on hypertension.

Change in Body Mass Index and Attributable Risk of New-Onset Hypertension Among Obese Living Kidney Donors.

To examine whether body mass index (BMI) changes modify the association between kidney donation and incident hypertension. Obesity increases hypertension risk in both general and living kidney donor (LKD) populations. Donation-attributable risk in the context of obesity, and whether weight change modifies that risk, is unknown. Nested case-control study among 1558 adult LKDs (1976-2020) with obesity (median follow-up: 3.6 years; interquartile range: 2.0-9.4) and 3783 adults with obesity in the Coronary Artery Risk Development in Young Adults (CARDIA) and Atherosclerosis Risk in Communities (ARIC) studies (9.2y; interquartile range: 5.3-15.8). Hypertension incidence was compared by donor status using conditional logistic regression, with BMI change investigated for effect modification. Overall, LKDs and nondonors had similar hypertension incidence [incidence rate ratio (IRR): 1.16, 95% confidence interval (95% CI): 0.94-1.43, P =0.16], even after adjusting for BMI change (IRR: 1.25, 95% CI: 0.99-1.58, P =0.05). Although LKDs and nondonors who lost >5% BMI had comparable hypertension incidence (IRR: 0.78, 95% CI: 0.46-1.34, P =0.36), there was a significant interaction between donor and >5% BMI gain (multiplicative interaction IRR: 1.62, 95% CI: 1.15-2.29, P =0.006; relative excess risk due to interaction: 0.90, 95% CI: 0.24-1.56, P =0.007), such that LKDs who gained weight had higher hypertension incidence than similar nondonors (IRR: 1.83, 95% CI: 1.32-2.53, P <0.001). Overall, LKDs and nondonors with obesity had similar hypertension incidence. Weight stability and loss were associated with similar hypertension incidence by donor status. However, LKDs who gained >5% saw increased hypertension incidence versus similar nondonors, providing support for counseling potential LKDs with obesity on weight management postdonation.

Bevacizumab for advanced ovarian cancer treatment. A GRADE based approach

&#x0D; Background: in advanced ovarian cancer, over the last 10 years no studies have demonstrated more appropriate therapeutic options compared to the current standard Carboplatin-Paclitaxel (Cb-P) regimen. Two phase III randomized studies (GOG-218 36 and ICON-7 37) have recently demonstrated the efficacy of bevacizumab (recombinant monoclonal antibody that binds with a high affinity to VEGF-A) in adjunct to Cb-P, with 12-15 months maintenance treatment.&#x0D; Methods: the quality of evidence provided was assessed by the use of the GRADE method. Each outcome (deemed to be essential for the purpose of evaluation of the intervention) was assessed to express the degree of confidence in the entity of the beneficial and/or harmful effects of the intervention. Thus, limitations in the quality of conducting the studies (risk of bias), direct applicability/relevance of results to the target population, and precision of results were taken into account.&#x0D; Results: the GOG-218 and the ICON7 study (high-risk subgroup) demonstrated with MODERATE confidence an improvement in critical outcomes PFS and OS, with an absolute reduction of 96 (GOG-218) – 103 (ICON-7) episodes of progression, and 40 (GOG-218) – 135 (ICON-7) deaths per 1 000 patients. A marked increase in risk of hypertension of Grade ≥3 was observed, with an absolute increase of 59 episodes per 1 000 patients in the ICON-7 study, and 157 episodes in the GOG-218 study, respectively, the majority of which were controlled by means of appropriate treatment. The increased risk of other adverse events considered was negligible.&#x0D; Conclusions: the positive effects produced should be viewed as taking prevalence over the negative effects (FAVOURABLE benefit/harm ratio).&#x0D;

Increased hypertension risk for the elderly with high blood levels of strontium and lead.

Hypertension has long been recognized as the global health burden. Heavy metal pollution may be one of the environmental risk factors of hypertension. However, the association remains unclear. We studied the levels of aluminum (Al), vanadium (V), manganese (Mn), arsenic (As), selenium (Se), strontium (Sr), barium (Ba), titanium (Ti), lead (Pb) and cobalt (Co) in whole blood, and the relationship between trace element exposure and hypertension in the elderly community-based Chinese population. A total of 1013 participants from the west of Anhui Province in China were consecutively enrolled in this study in 2016. The general sociodemographic characteristics, lifestyles, disease history and physical examination information were collected by face-to-face survey and physical examination. The levels of ten trace elements were determined by inductively coupled plasma mass spectrometry (ICP-MS). Multivariable logistic regression model was used to assess the association of trace element exposure with the risk of hypertension. Results showed that the odds ratio of hypertension in the highest quartile was 1.811 (95% CI 1.175-2.790, P trend = 0.005) and 1.772 (95% CI 1.121-2.800, P trend = 0.022), respectively, after adjusting for potential confounders, as compared with the lowest quartile of blood Pb and Sr levels.

Physiological Mechanisms of Hypertension and Cardiovascular Disease in End-Stage Kidney Disease.

In this article, we summarize recent advances in understanding hypertension and cardiovascular disease in patients with end-stage kidney disease. Factors such as anemia, valvular and vascular calcification, vasoconstrictors, uremic toxins, hypoglycemia, carbamylated proteins, oxidative stress, and inflammation have all been associated with the progression of cardiovascular disease in end-stage kidney disease but the causality of these mechanisms has not been proven. The high risk of cardiovascular mortality has not improved as in the general population despite many advancements in cardiovascular care over the last two decades. Mechanisms that increase hypertension risk in these patients are centered on the control of extracellular fluid volume; however, over-correction of volume with dialysis can increase risks of intradialytic hypotension and death in these patients. This review presents both recent and classic work that increases our understanding of hypertension and cardiovascular disease in end-stage kidney disease.

Childhood Violence Exposure Predicts High Blood Pressure in Black American Young Adults

To test the impact of childhood adversity, including community violence exposure, on hypertension risk in Black American young adults to understand what risk factors (eg, prenatal factors, later exposures) and ages of adversity exposure increased hypertension risk. The study included 396 Black American participants with data from prenatal, birth, and age 7-, 14-, and 19-year visits. At age 19years, individuals with blood pressure (BP) measures >120mmHg systolic and/or >80mmHg diastolic were classified as having high blood pressure (HBP), and those with BP <120/80mmHg were classified as normal. Associations between prenatal and birth risk factors; childhood adversity at age 7, 14, and 19years; age 19 body mass index (BMI); and both systolic and diastolic BP at age 19 were tested using logistic regression models. Age 19 BMI was positively associated with systolic and diastolic HBP status at age 19. Controlling for all covariates, community violence exposure at age 7 and 19years was associated with 2.2-fold (95% CI, 1.242-3.859) and 2.0-fold (95% CI, 1.052-3.664) greater odds of systolic HBP, respectively, at age 19years. Prenatal risk, birth risk, and other dimensions of childhood adversity were not associated with HBP in this cohort. Childhood community violence exposure is a significant risk factor for HBP in young adults. As Black American children typically experience more community violence exposure than other American children, our results suggest that racial disparities in childhood community violence exposure may contribute to racial disparities in adult hypertension burden.

0204 Sleep Irregularity Is Associated with Increased Risk of Hypertension: Data From Over Two Million Nights

Abstract Introduction Sleep irregularity has been associated with worse cardio-metabolic health compared to regular sleep, but prior studies have been limited in sample size and have assessed sleep irregularity by actigraphy or questionnaires over a relatively short duration (~ 14 days). The current study investigated associations between sleep regularity and hypertension in a large, global sample over multiple months. Methods Data from 12,300 participants (aged 18-90 years) who used an under-mattress sleep device and a portable blood pressure monitor between July 2020 and March 2021 were included in this study. Sleep duration regularity was assessed as the standard deviation via device-assessed total sleep time. Sleep timing regularity was assessed as the standard deviation in sleep onset time and in sleep midpoint. Logistic regressions controlling for age, sex, BMI, and mean total sleep time were conducted to investigate potential associations between sleep regularity and hypertension. Results Participants were typically middle-aged (Mean ± SD; 50 ± 12 years) and predominantly male (12% females). Each participant had ~180 nights of recordings and ~70 blood pressure entries. There were 2,499 cases of hypertension defined as SBP&amp;gt;140 and/or DBP &amp;gt;90mmHg (20% of the sample). Across total sleep time quartiles, high sleep duration irregularity was consistently associated with a 9 to 15% increase in hypertension risk. A 38-minute increase in sleep midpoint irregularity was associated with an 11% (1.11 [1.03, 1.20]) increase in hypertension risk, independent of mean total sleep time and mean sleep midpoint. Similarly, a ~31-minute increase in sleep onset time irregularity was associated with a 29% increased risk of hypertension (1.29 [1.18, 1.42]). Conclusion These novel findings provide insight into the potential important impact of sleep irregularity on cardiovascular health. Further assessment of day-to-day fluctuations in sleep duration and timing for potential effects on next-day blood pressure and other cardiovascular health outcomes are warranted. Support (If Any) This was an unfunded investigator-initiated study. De-identified data were provided by Withings for unrestricted investigator-led analysis. PE serves as a consultant for Withings.

Association between cadmium and lead co-exposure, blood pressure, and hypertension: a cross-sectional study from northwest China

Cadmium (Cd) and lead (Pb) co-exposure have been inconsistently associated with blood pressure (BP) and hypertension (HTN). This cross-sectional study included 309 participants who completed a health examination and had blood Cd (Cd-B) and Pb (Pb-B) levels measured. The association between Cd, Pb, and their combined exposure levels, with systolic (SBP) and diastolic blood pressure (DBP) and HTN was evaluated using models which were stratified according to sex, age, BMI, and smoking habit categories. The results found both increasing Cd-B and Pb-B were associated with elevated SBP and DBP in the overall population. In addition, increases in Cd-B and Pb-B were also associated with increased risk of HTN in overall and stratified models. Moreover, compared with the low exposure group, co-exposure to high levels of Cd and Pb was associated with increased SBP (β = 10.95, 95% CI: 5.69, 16.21), increased DBP (β = 5.09, 95% CI: 1.53, 8.66), and increased HTN risk (OR = 2.45, 95% CI: 1.15, 5.21) in the overall model, and above results were different in the stratified model. This study provides evidence of an association between Cd and/or Pb exposure levels, BP, and HTN. However, the significance of this association differed according to sex, age, BMI, and smoking habit. Highlights Cadmium/lead exposure is associated with elevated blood pressure and hypertension. Cadmium and lead co-exposure increased blood pressure in a dose-dependent manner. Results revealed differences according to sex, age, BMI, and smoking habit category. Health oversight should be implemented for residents with high heavy metal exposure.

The Impact of Occupational Noise on Hypertension Risk: A Case-Control Study in Automobile Factory Personnel.

BackgroundMany epidemiological studies have investigated the relationship between occupational noise and hypertension, but with conflicting findings. This study aimed to assess the relationship between occupational noise exposure and the risk of hypertension.MethodsA case-control study was conducted to explore hypertension predictors, and then sensitivity analysis was performed based on propensity score matching (PSM). Data were collected from participants' annual physical examinations and occupational noise exposure measurements. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression analysis. A restricted cubic spline (RCS) function was used to fit the dose-effect relationship.Results500 cases and 4,356 controls were included in the study. Multivariate logistic regression showed that an increase in the level of occupational noise [range 68–102 dB(A)] of 1 dB(A), corresponded to an increase in hypertension risk of 8.3% (OR: 1.083, 95% CI: 1.058–1.109). Compared to the first quartile, the risk of hypertension in the fourth quartile was 1.742 (95% CI: 1.313–2.310). After applying PSM to minimize bias, we obtained a population of 500 cases and 1,000 controls. Noise level was significantly associated with the risk of hypertension. In addition, the RCS curve showed the risk of hypertension was relatively stable until a predicted noise level of around 80 dB(A) and then started to increase rapidly afterward (Pnonlinear = 0.002).ConclusionsOccupational noise exposure was significantly associated with hypertension risk and there was a positively correlated dose-response relationship.

Assessment of Future Hypertension Risk by Sex Using Combined Body Mass Index and Waist-to-Height Ratio.

Background: Body mass index (BMI) and the waist-to-height ratio (WHtR) are widely used anthropometric indices of obesity to predict cardiovascular risks. However, the usefulness of combining WHtR and BMI values to predict hypertension risk by sex has not been well elucidated. Methods and Results: This cohort study enrolled 45,921 participants (mean [±SD] age 53.8±10.5 years; 47.0% men) without hypertension from among those undergoing annual health checkups. Participants were divided into 4 categories based on median BMI and WHtR values, and the 5-year incidence of hypertension was assessed for both sexes using logistic regression analysis. Mean (±SD) BMI and WHtR values were 23.5±3.1 kg/m2 and 0.50±0.05, respectively, in men and 22.4±3.3 kg/m2 and 0.53±0.06, respectively, in women. Among the women, those with high BMI and low WHtR had an increased risk of hypertension compared with those with low BMI and low WHtR (odds ratio [OR] 1.37, P<0.001); however, the same result was not found in men (OR 1.14, P=0.080). In both sexes, the incidence of hypertension was higher among participants with low BMI and high WHtR than among those with low BMI and low WHtR (men: OR 1.26, P<0.001; women: OR 1.15, P=0.048). Conclusions: Using WHtR and BMI together provides a better hypertension risk assessment. Among men, those with a high BMI had no increased hypertension risk when WHtR was low.

Does severe subacute noise exposure increase risk of new onset hypertension beyond conventional risk factors? A 30 000 person-years cohort study.

Objectives:Previous studies mostly focused on the relationship between chronic environmental noise exposure and hypertension but the effects of subacute (under 4 years) exposure with severe (>85 dB) noise exposure on clinical level hypertension have not been explored. This study aimed to reveal the association between severe noise exposure and hypertension.Methods:The severe noise exposure group was recruited from a Common Data Model conducted for the Korean Participants Health Examination from January 2014 to December 2017. The use of antihypertensive drug and/or blood pressure of at least 140/90 mmHg was defined as new onset clinical hypertension. A multivariate Cox proportional hazard model was implemented to estimate hazard ratios and 95% confidence intervals (CI) by adjusting covariates including demographic, lifestyle, and other chemical exposure factors. Time-dependent Cox analysis and Landmark analysis were further performed as a sensitivity analysis.Results:During the 29 332 person-years follow-up with 12 412 participants of the entire cohort, new onset hypertension occurred in 1222 participants. The findings showed that severe noise exposure was associated with an increased risk of hypertension incidence in the entire cohort [final model hazard ratio 1.28 (95% CI 1.11–1.47)]. Other covariates did not attenuate the association after adjusting age and sex. Time-dependent Cox and Landmark analysis also showed significant results [hazard ratio 1.60 (95% CI 1.38–1.85) and hazard ratio 1.33 (95% CI 1.13–1.57)].Conclusion:Severe noise with subacute exposure is significantly associated with hypertension development. Further studies should be implemented to clarify whether severe exposure to noise could be an important risk factor for hypertension.

Replication of European hypertension associations in a case-control study of 9,534 African Americans.

ObjectiveHypertension is more prevalent in African Americans (AA) than other ethnic groups. Genome-wide association studies (GWAS) have identified loci associated with hypertension and other cardio-metabolic traits like type 2 diabetes, coronary artery disease, and body mass index (BMI), however the AA population is underrepresented in these studies. In this study, we examined a large AA cohort for the generalizability of 14 Metabochip array SNPs with previously reported European hypertension associations.MethodsTo evaluate associations, we analyzed genotype data of 14 SNPs for their associations with a diagnosis of hypertension, systolic blood pressure (SBP), and diastolic blood pressure (DBP) in a case-control study of an AA population (N = 9,534). We also performed an age-stratified analysis (>30, 30≥59 and ≥60 years) following the hypertension definition described by the 8th Joint National Committee (JNC). Associations were adjusted for BMI, age, age2, sex, clinical confounders, and genetic ancestry using multivariable regression models to estimate odds ratios (ORs) and beta-coefficients. Analyses stratified by sex were also conducted. Meta-analyses (including both BioVU and COGENT-BP cohorts) were performed using a random-effects model.ResultsWe found rs880315 to be associated with systolic hypertension (SBP≥140 mmHg) in the entire cohort (OR = 1.14, p = 0.003) and within women only (OR = 1.16, p = 0.012). Variant rs17080093 associated with lower SBP and DBP (β = -2.99, p = 0.0352 and - β = 1.69, p = 0.0184) among younger individuals, particularly in younger women (β = -3.92, p = 0.0025 and β = -1.87, p = 0.0241 for SBP and DBP respectively). SNP rs1530440 associated with higher SBP and DBP measurements (younger individuals β = 4.1, p = 0.039 and β = 2.5, p = 0.043 for SBP and DBP; (younger women β = 4.5, p = 0.025 and β = 2.9, p = 0.028 for SBP and DBP), and hypertension risk in older women (OR = 1.4, p = 0.050). rs16948048 increases hypertension risk in younger individuals (OR = 1.31, p = 0.011). Among mid-age women rs880315 associated with higher risk of hypertension (OR = 1.20, p = 0.027). rs1361831 associated with DBP (β = -1.96, p = 0.02) among individuals older than 60 years. rs3096277 increases hypertension risk among older individuals (OR = 1.26 p = 0.0015), however, this variant also reduces SBP among younger women (β = -2.63, p = 0.0102).ConclusionThese findings suggest that European-descent and AA populations share genetic loci that contribute to blood pressure traits and hypertension. However, the OR and beta-coefficient estimates differ, and some are age-dependent. Additional genetic studies of hypertension in AA are warranted to identify new loci associated with hypertension and blood pressure traits in this population.

Trans-ethnic Mendelian-randomization study reveals causal relationships between cardiometabolic factors and chronic kidney disease.

BackgroundThis study was to systematically test whether previously reported risk factors for chronic kidney disease (CKD) are causally related to CKD in European and East Asian ancestries using Mendelian randomization.MethodsA total of 45 risk factors with genetic data in European ancestry and 17 risk factors in East Asian participants were identified as exposures from PubMed. We defined the CKD by clinical diagnosis or by estimated glomerular filtration rate of <60 ml/min/1.73 m2. Ultimately, 51 672 CKD cases and 958 102 controls of European ancestry from CKDGen, UK Biobank and HUNT, and 13 093 CKD cases and 238 118 controls of East Asian ancestry from Biobank Japan, China Kadoorie Biobank and Japan-Kidney-Biobank/ToMMo were included.ResultsEight risk factors showed reliable evidence of causal effects on CKD in Europeans, including genetically predicted body mass index (BMI), hypertension, systolic blood pressure, high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein(a), type 2 diabetes (T2D) and nephrolithiasis. In East Asians, BMI, T2D and nephrolithiasis showed evidence of causality on CKD. In two independent replication analyses, we observed that increased hypertension risk showed reliable evidence of a causal effect on increasing CKD risk in Europeans but in contrast showed a null effect in East Asians. Although liability to T2D showed consistent effects on CKD, the effects of glycaemic phenotypes on CKD were weak. Non-linear Mendelian randomization indicated a threshold relationship between genetically predicted BMI and CKD, with increased risk at BMI of >25 kg/m2.ConclusionsEight cardiometabolic risk factors showed causal effects on CKD in Europeans and three of them showed causality in East Asians, providing insights into the design of future interventions to reduce the burden of CKD.

Influence of serum ferritin combined with blood cadmium concentrations on blood pressure and hypertension: From the Korean National Health and Nutrition Examination Survey

BackgroundPrevious studies have suggested that cadmium (Cd) exposure and serum ferritin levels may influence the development of hypertension. ObjectiveWe evaluated whether the association between blood Cd levels and the development of hypertension could be modified by serum ferritin levels in a representative sample of the adult population of South Korea. MethodsWe used data from the Korean National Health and Nutrition Examination Survey (2008–2012), a nationally representative, cross-sectional, population-based study. We included 5752 adults aged 19 years and older who had records of blood Cd and ferritin levels and blood pressure measurements. Multiple logistic regression was used to examine the association between Cd exposure and the development of hypertension, as well as the modifying effects of serum ferritin. ResultsMen had higher levels of serum ferritin, and women had higher levels of Cd. Smoking in men was significantly associated with high blood pressure and risk of hypertension. Significantly fewer women were smokers, and the combination of abnormal serum ferritin levels and high Cd levels was significantly associated with high systolic blood pressure [odds ratio (OR) = 2.11; 95% confidence interval (CI) = 1.04–4.28], high diastolic blood pressure (OR = 2.07; 95% CI = 1.04–4.12), and increased hypertension risk (OR = 1.83; 95% CI = 1.03–3.25) in women who never smoked. ConclusionsOur results provide further evidence that individuals with abnormal serum ferritin levels should limit their exposure to Cd to prevent hypertension.

Bisphenol A, S, and F exposure, ESR1/2, CAT, and eNOS genetic polymorphisms, and the risk of hypertension

While bisphenol A (BPA) exposure was inconsistently associated with hypertension risk, little is known about whether its alternatives bisphenol S and F (BPS and BPF) have similar hypertensive effects. Furthermore, epidemiologic studies on the genetic susceptibility to the hypertensive effects of bisphenols are scarce. We conducted a case-control study in 439 pairs of hypertension cases and matched controls. Urinary bisphenols concentrations were measured to characterize the internal exposure levels. The genotyping of ESR1/2, CAT, and eNOS was performed by a multiplex fluorescent polymerase chain reaction. BPA exposure was positively associated with hypertension risk. Carriers of rs2234693 C allele in ESR1 were associated with increased hypertension risk. Significant associations of BPA exposure with increased hypertension risk were suggested in individuals with the major allele of rs1256049 in ESR2, rs769214 in CAT, and rs1799983 in eNOS. Besides, rs4755374 in CAT might modify the association of BPA exposure with hypertension risk. Individuals with specific genotypes in ESR1/2, CAT, and eNOS might be more susceptible to the hypertensive effects of BPA.

A prospective study of multiple sleep dimensions and hypertension risk among white, black and Hispanic/Latina women: findings from the Sister Study.

Poor sleep is associated with increased hypertension risk, but few studies have evaluated multiple sleep dimensions or investigated racial/ethnic disparities in this association among women. We investigated multiple sleep dimensions (sleep duration, inconsistent weekly sleep patterns, sleep debt, frequent napping and difficulty falling or staying asleep) and hypertension risk among women, and determined modification by age, race/ethnicity and menopausal status. We used data from the Sister Study, a national cohort of 50 884 women who had sisters diagnosed with breast cancer in the United States enrolled in 2003-2009 and followed through September 2018. Of 33 497 women without diagnosed hypertension at baseline (mean age ± standard deviation: 53.9 ± 8.8 years; 88.7% White, 6.4% Black and 4.9% Hispanic/Latina), 23% (n = 7686) developed hypertension over a median follow-up of 10.1 years [interquartile range: 8.2-11.9 years]. Very short, short or long sleep duration, inconsistent weekly sleep patterns, sleep debt, frequent napping, insomnia, insomnia symptoms as well as short sleep and exploratory cumulative poor sleep score were associated with incident hypertension after adjustment for demographics factors. After additional adjustment for lifestyle and clinical factors, insomnia [hazard ratio = 1.09, 95% confidence interval (95% CI): 1.03-1.15] and insomnia symptoms plus short sleep (hazard ratio = 1.13, 95% CI: 1.05-1.21) remained associated with incident hypertension. These associations were stronger in younger (age<54 vs. ≥54 years) and premenopausal vs. postmenopausal women (all P-interaction < 0.05). Associations did not differ by race/ethnicity (all P-interaction > 0.05). Thus, screening for multiple sleep dimensions and prioritizing younger and premenopausal women may help identify individuals at high risk for hypertension.

Birth Weight and Adult Obesity Index in Relation to the Risk of Hypertension: A Prospective Cohort Study in the UK Biobank.

Objectives: To investigate the association between birth weight and the risk of hypertension, and to examine the interaction between birth weight and the adult obesity index.Methods: We included 199,893 participants who had birth weight data and no history of hypertension at baseline (2006–2010) from the UK Biobank. A multivariate cubic regression spline was used to visually explore the dose-response relationship. Multivariate Cox proportional hazard regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).Results: We observed a nonlinear inverse association between birth weight and hypertension. The risk for hypertension decreased as birth weight increased up to approximately 3.80 kg. Compared with the participants with the fourth quintile of birth weight (3.43–3.80 kg), those with the first quartile of birth weight (<2.88 kg) were associated with a 25% higher risk of hypertension [HR 1.25; 95% CI (1.18–1.32)]. In addition, the participants with birth weight <2.88 kg and body mass index ≥30 kg/m2 had the highest risk [HR 3.54; 95% CI (3.16–3.97); p for interaction <0.0001], as compared with those with birth weight between 3.43–3.80 kg and body mass index between 18.5–25.0 kg/m2. These associations were largely consistent in the stratified and sensitivity analyses.Conclusion: Our findings indicate that lower birth weight is nonlinearly correlated with higher risk of hypertension, and birth weight between 3.43–3.80 kg might represent an intervention threshold. Moreover, lower birth weight may interact with adult obesity to significantly increase hypertension risk.

Internalized Shame and Social Stress-Induced Blood Pressure Patterns among Young Black Women.

The increasing prevalence of hypertension among young Black women warrants further exploration of hypertension risk factors in this population. Social cognitive pathways that increase hypertension risk have been understudied among Black women. Shame, an emotional response to social evaluative threats, may be important to understanding the contribution of social emotions to hypertension risk. The current study examined the association of internalized shame on systolic (SBP) and diastolic blood pressure (DPB) patterns of reactivity and recovery in a sample of Black women. Black women (N=32) aged 18-22 were recruited from a public university in August 2019 and January 2020. Participants completed the Internalized Shame Scale, Self-Esteem subscale, and the Perceived Stress Scale. All participants completed the Trier Social Stress Test (TSST) and subsequent blood pressure readings were recorded at baseline and 1 min, 15 min, 30 min, 45 min, and 60 min post-TSST. Two separate repeated measures ANOVAs examined time and group effects of low shame (ISS score ≤ 39.9) vs high shame (ISS score ≥ 40) on blood pressure reactivity patterns. A significant effect of shame on DBP responses to the TSST was observed (P=.020). DBP for women in the low shame group peaked immediately following the TSST relative to baseline (M =81.2 mm Hg vs M =72.2 mm Hg) and remained stable during 60-minute recovery. DBP for women in the high shame group did not peak until 45 min post-TSST relative to baseline (M =84.2 mm Hg vs M =68.0 mm Hg) only slightly decreasing at 60 min post-TSST. These results highlight the need to further examine the role of shame on hypertension risk among young Black women.

GENETICALLY, DIETARY SODIUM INTAKE IS CAUSALLY ASSOCIATED WITH SALT-SENSITIVE HYPERTENSION RISK IN A COMMUNITY-BASED COHORT STUDY: A MENDELIAN RANDOMIZATION APPROACH

Objective: Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). Design and method: We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1,282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Results: Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR = 0.356, 95% CI = 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR = 2.114, 95% CI = 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Conclusions: Our findings suggest that dietary sodium intake may be causally associated with hypertension risk.