The review mapped evidence concerning workplace violence and harassment, recognized psychosocial stressors that can affect cardiovascular health, and their links with clinical hypertension and continuous blood pressure levels. Researchers followed the PRISMA Extension for Scoping Reviews, or PRISMA-ScR, framework. They searched 11 databases from inception through March 2026 and supplemented that search with Google Scholar screening and backward citation tracking of eligible studies.

The supplied abstract does not describe the workers’ locations, occupations or demographic characteristics, so the review’s findings should be understood as covering the populations represented in the included literature rather than all workers. Beyond the 10 consistently supportive studies, the remaining quantitative studies reported mixed findings, no clear association, or consistently inverse estimates. This variation was the central result of the review.

The authors identified heterogeneity across the evidence and methodological limitations that prevented them from drawing causal conclusions. Consequently, the available studies do not establish that workplace violence or harassment directly causes hypertension, nor do they establish a single uniform association across every population or analysis. Its findings indicate that some studies support a positive relationship between occupational violence or harassment and hypertension-related outcomes, while others do not show that pattern consistently.

The evidence therefore warrants attention as a potential occupational health concern, but the direction, strength and persistence of the association remain uncertain because the quantitative results are not uniform. The authors called for longitudinal studies that repeatedly assess both workplace violence and harassment exposure and blood pressure. Such research could help distinguish acute blood pressure responses from persistent changes and clarify the implications for occupational hypertension prevention.

Its overall conclusion is measured: workplace violence and harassment may be associated with hypertension and adverse blood pressure outcomes, but causal claims require stronger and more consistent evidence.

Subject of Research: Scoping review of workplace violence, harassment and hypertension-related outcomes

Article Title: Association between workplace violence and harassment and hypertension-related outcomes: a scoping review

Article References: Xu, S., Zhang, M., Li, K., Huang, Y., He, C., Tang, Y., Wang, X., & Zhang, Y. (2026). Association between workplace violence and harassment and hypertension-related outcomes: a scoping review. BMC Public Health. https://doi.org/10.1186/s12889-026-30008-5

Image Credits: AI Generated

DOI: 10.1186/s12889-026-30008-5

Keywords: workplace violence, workplace harassment, hypertension, blood pressure, occupational health, psychosocial stress, cardiovascular health, scoping review, longitudinal research, Association, between, workplace

The liver supplies the bulk of circulating AGT, but AGT found in peripheral tissues need not have come directly from the liver. It may instead be produced locally or arrive through vascular retention, glomerular filtration, barrier crossing or receptor-mediated uptake. These routes can differ in how much protein reaches a tissue and in the molecular forms available for signaling.

The review therefore treats tissue abundance as an incomplete indicator: even a high concentration of AGT does not reveal its source, delivery route or biological activity. Source-specific genetic experiments in mice offer the most detailed evidence that the liver contributes AGT to the kidney. By deleting AGT in defined cell populations and tracing cellular lineages, researchers can test causal links between a particular source and a target organ more precisely than measurements of circulating protein alone.

For most other proposed axes of interorgan communication, the available evidence does not provide that same granularity. The distinction matters because a pathway is not established merely because AGT and an organ response are observed together; a correlation does not identify where the protein originated or how it reached the tissue. The protein’s molecular state adds another layer.

Intact AGT and des(Ang I)AGT can have effects that differ from those of angiotensin II and, under some conditions, can oppose them. Enzymatic processing can therefore change the direction as well as the magnitude of a response. The review’s model consequently places AGT upstream of several possible outcomes, with its output shaped by the form in which it is present, its local accessibility, the reactions it undergoes and the receptors available to act on it.

Measuring total AGT alone cannot establish which molecular form is present or which pathway is being engaged. Human genetic loss-of-function studies provide strong evidence for two essential functions of AGT: renal morphogenesis and blood-pressure regulation. In contrast, observational cohorts and biomarker studies generally cannot establish the tissue origin of the measured protein or the route by which it reached its target.

Such human observations are valuable for identifying associations, but they must be separated from the source-specific causal circuits demonstrated in animal models. The findings also open a possible therapeutic path centered on suppressing AGT in hepatocytes. The review identifies zilebesiran and tonlamarsen as agents that target hepatocytes and can produce durable AGT suppression.

This approach could potentially ease treatment burden relative to conventional daily treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. That comparison represents a potential advantage rather than a demonstrated clinical benefit, and the review reports that solid cardiovascular and renal outcome data for AGT-suppressing treatment are still lacking. A major unresolved issue is the safety margin for lowering AGT.

The protein supports renal morphogenesis and blood-pressure regulation, while the review identifies renal self-regulation, fluid–electrolyte balance and pressor responses to physiological stress as functions that could be affected if suppression becomes too extensive. The slow offset of action associated with these agents may allow prolonged suppression, but it does not answer how much reduction is tolerable or whether the absence of cardiovascular and renal outcome data represents a limitation for clinical use. Overall, the review presents AGT as an upstream determinant with conditional effects rather than a ubiquitous interorgan signaling molecule.

Its influence depends on which organ produces it, how it reaches a target, whether it remains intact or is processed, and what receptor environment surrounds it. The evidence is strongest for a liver-to-kidney pathway in mice and for AGT’s genetic importance in human renal development and blood-pressure regulation. Applying that knowledge to therapy will require carefully separating established circuits from plausible pathways and recognizing that durable biochemical suppression, by itself, does not establish improved clinical outcomes.

Subject of Research: Tissue origins, molecular processing and therapeutic targeting of angiotensinogen in interorgan communication.

Article Title: Angiotensinogen as a molecular hub in interorgan communication

Article References: Zhou, J., Ye, X., Wang, Y., Hong, M., Rong, J., Wang, J., & Xu, Y. (2026). Angiotensinogen as a molecular hub in interorgan communication. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-09074-1

Image Credits: AI Generated

DOI: 10.1186/s12967-026-09074-1

Keywords: angiotensinogen, interorgan communication, liver-kidney signaling, renal morphogenesis, blood pressure, angiotensin II, hepatocyte targeting, zilebesiran, tonlamarsen, source-specific knockout, molecular, interorgan

The scale of the problem is substantial. The review reports that an estimated 2.5 billion adults worldwide were overweight in 2022, including more than 890 million living with obesity. High body mass index is associated with cardiovascular disease, diabetes, cancer and other conditions, and the review cites an estimated 3.7 million deaths linked to elevated BMI in 2021. In the United States, the proportion of adults with both obesity and hypertension increased from 39.6% in 2001 to 55.4% in 2023. Obesity-induced hypertension is a multifactorial phenotype involving sympathetic activation, altered renal sodium handling, renin-angiotensin-aldosterone system activation, insulin resistance, endothelial dysfunction and chronic inflammation. Yet peripheral mechanisms alone do not explain why blood pressure remains elevated in many people with obesity.

That unresolved component has drawn attention to central autonomic networks, especially the hypothalamic arcuate nucleus, paraventricular nucleus of the hypothalamus, nucleus tractus solitarius and rostral ventrolateral medulla. These regions integrate metabolic, hormonal and cardiovascular information. Leptin is a key signal in this process because its levels generally rise with fat mass and activate hypothalamic pathways that can increase sympathetic outflow and arterial pressure. The review describes a form of selective leptin resistance in obesity: leptin’s effects on appetite and energy expenditure may become impaired while its cardiovascular effects on sympathetic activity remain intact. Persistent activation of sympathetic pathways can increase vasoconstriction, heart rate and renal sodium reabsorption, supporting sustained elevations in blood pressure.

Astrocytes provide a possible connection between circulating signals and the neurons that control autonomic output. These abundant central nervous system glia regulate extracellular glutamate, buffer potassium, support neuronal energy metabolism, maintain the blood–brain barrier and couple neural activity to blood flow. Under obesogenic conditions, the review says, excess nutrients, circulating saturated fatty acids such as palmitic acid, adipokines and inflammatory mediators can induce astrogliosis in autonomic regions. Reactive astrocytes undergo structural and molecular changes, including increased glial fibrillary acidic protein expression and greater release of pro-inflammatory cytokines. The resulting environment is one of chronic neuroinflammation rather than a simple loss of supportive glial function.

Glutamate regulation may be one of the most consequential links between astrocyte reactivity and sympathetic activation. Glutamate is the main excitatory neurotransmitter in the central nervous system, and excitatory amino acid transporters rapidly remove it from the synaptic cleft. EAAT1 and EAAT2 are predominantly astrocytic, whereas EAAT3, EAAT4 and EAAT5 are primarily neuronal. Astrocytically captured glutamate is converted to glutamine, returned to neurons and converted back to glutamate, forming the glutamate–glutamine cycle. If EAAT2-dependent uptake is impaired, extracellular glutamate can accumulate, increasing neuronal excitability and potentially strengthening excitatory drive in cardiovascular control circuits. Astrocyte-derived gliotransmitters, including ATP and D-serine, may further influence synaptic transmission in those networks.

The proposed pathway also includes oxidative stress, mitochondrial dysfunction and inflammatory signaling inside astrocytes. Palmitic acid exposure has been associated in experimental systems with endoplasmic reticulum stress, impaired mitochondria, reactive oxygen species production and lipid accumulation. These cellular stresses can activate the IKKβ/NF-κB pathway, increasing cytokines such as TNF-α, IL-1β and IL-6. The review further links astrocyte-driven neuroinflammation with central renin-angiotensin-aldosterone system activation and reduced baroreflex sensitivity. Because astrocytes also participate in neurovascular coupling and blood–brain barrier maintenance, their dysfunction may allow additional inflammatory mediators and metabolic substrates to enter the brain, creating a cycle of inflammation and autonomic imbalance.

Some experimental results make the proposed connection more concrete, although they do not establish an obesity-specific causal mechanism. The review highlights single-nucleus RNA-sequencing work identifying distinct astrocyte populations in the rostral ventrolateral medulla of spontaneously hypertensive rats. Increased expression of contactin-associated protein-like 2, or Cntnap2, was associated with lower EAAT2 expression and reduced glutamate uptake; neuronal excitability, sympathetic outflow and blood pressure increased in the same model. This finding was not produced in an obesity model, and it remains unknown whether obesity causes comparable astrocyte-specific changes in that region or in other autonomic nuclei. Most other evidence comes from hypothalamic metabolic studies, cultured cells or hypertension models that are not specific to obesity. Human neuroimaging supports an association between obesity and hypothalamic gliosis, but there is little direct evidence of astrocyte dysfunction in human cardiovascular regulatory regions.

The review examines several possible intervention strategies while distinguishing laboratory compounds from established clinical therapies. Arundic acid has increased EAAT1 expression and glutamate uptake in experimental studies and has also reduced markers of oxidative stress, neuroinflammation and reactive astrogliosis. The review states that it is not yet commercially available and that much of the work has involved mice. Butein, a dietary flavonoid, and berberine have shown anti-inflammatory and antioxidant effects in experimental models that may be relevant to astrocyte dysfunction. These findings indicate biological activity, not demonstrated treatment of obesity-induced hypertension in people. Clinical studies have not established that either compound controls blood pressure through astrocyte-specific mechanisms.

GLP-1 receptor agonists present a more immediate question because semaglutide, liraglutide and tirzepatide are already used for weight reduction and can lower blood pressure in people with obesity. GLP-1 receptors occur in autonomic regions of the hypothalamus and brainstem, including the nucleus tractus solitarius, and have been reported on astrocytes. Experimental work suggests that GLP-1 signaling may reduce reactive gliosis and neuroinflammation. Yet central GLP-1 receptor activation has also increased sympathetic activity and heart rate in some settings. Researchers therefore do not know whether the blood-pressure effects of these drugs arise only from weight loss, from direct actions in autonomic circuits, or from weight-independent changes in astrocytic glutamate transport or inflammatory signaling.

Several gaps must be addressed before astrocytes can become a practical treatment target. It is unclear whether obesity-associated metabolic stress impairs EAAT2 before sympathetic activation and hypertension develop, whether astrocyte changes precede or follow elevated blood pressure during high-fat feeding, and whether astrocytes initiate inflammation or amplify signals from microglia, neurons, endothelial cells and peripheral immune cells. Sex differences also matter: experiments in male rodents dominate the literature, while studies of mouse and human astrocytes have found that palmitic-acid responses differ between females and males in glutamate–glutamine cycling, energy metabolism, oxidative stress and antioxidant pathways. Translation is further limited by the scarcity of direct evidence from the human paraventricular nucleus, nucleus tractus solitarius or rostral ventrolateral medulla. The review concludes that longitudinal blood-pressure telemetry, sympathetic-nerve recordings, cell-specific genetics, spatial transcriptomics and multi-omics approaches are needed to establish causality and identify astrocyte subpopulations that contribute to obesity-induced hypertension.

Subject of Research: The proposed contribution of astrocyte dysfunction to obesity-associated hypertension and sympathetic nervous system activation.

Article Title: Role of astrocytes in obesity-induced hypertension

Article References: Nanayakkara, D., Negron, C. P., & Subramanian, M. (2026). Role of astrocytes in obesity-induced hypertension. Frontiers in Neuroscience, 20, 1992730. https://doi.org/10.3389/fnins.2026.1992730

Image Credits: AI Generated

DOI: 10.3389/fnins.2026.1992730

Keywords: astrocytes, obesity-induced hypertension, sympathetic nervous system, glutamate transport, EAAT2, neuroinflammation, autonomic regulation, glial reactivity, blood pressure, metabolic dysfunction, Role, obesity-induced

The review examined 11 outcomes, including perceived or general stress, anxiety, depressive symptoms, fatigue, resting systolic and diastolic blood pressure, resting heart rate, blood cortisol and three heart rate variability indices. The interventions included aerobic exercise, high-intensity interval training, resistance training, sport-based training, yoga, qigong and multicomponent school programs, lasting from three weeks to 10 months. Comparators included usual physical education, usual activity, health or attention education, no-intervention and wait-list conditions. The studies covered 18 countries or regions. Outcome-specific analyses contained 4–15 studies and 90–3,157 participants, so each pooled result rested on a different and often limited body of evidence.

For perceived or general stress, seven studies produced a pooled standardized mean difference of Hedges’ g = −0.28, with a 95% confidence interval of −0.48 to −0.08 and p = 0.006. Negative values represented lower post-intervention stress scores in intervention groups. Heterogeneity was moderate, with I² = 49.9% and τ² = 0.030. The estimate remained statistically significant under an adjusted Knapp–Hartung method and when non-randomized studies were excluded, but it became non-significant when Ranjani and colleagues’ study was removed. The analysis therefore supports a possible benefit rather than demonstrating a robust, generalizable effect. This estimate was one of several statistically significant psychological results, and the review did not establish a clear hierarchy among them.

Physical activity interventions were also associated with lower depressive symptom scores in a synthesis of 13 studies. The primary pooled estimate was g = −0.53, with a 95% confidence interval of −1.04 to −0.02 and p = 0.041. Most individual estimates favored intervention groups, but their magnitude varied widely: I² reached 94.8% and τ² was 0.809, indicating substantial variation in the studies’ estimated effects. The result was statistically fragile. Its confidence interval crossed zero under modified Knapp–Hartung inference, it became non-significant after several individual studies were omitted, and it also depended partly on the inclusion of non-randomized evidence. Depressive symptoms are not a direct measure of stress and can have other determinants, so the finding cannot by itself establish improved stress regulation.

No statistically significant pooled effect was found for anxiety or fatigue. For anxiety, 15 studies yielded g = −0.34, but the 95% confidence interval ranged from −0.79 to 0.11, with p = 0.137 and very high heterogeneity of I² = 93.7%. The point estimate favored lower anxiety, yet the data did not show a clear overall difference. Fatigue was assessed in only four studies; its pooled estimate was close to no effect at g = −0.11, with a 95% confidence interval of −0.32 to 0.10. An estimated I² of zero did not establish that the studies were genuinely alike, because the number of contributing studies was too small to characterize heterogeneity reliably. These non-significant results indicate that the available evidence is insufficient to confirm an effect, not that exercise has been shown to have no effect.

On the physiological side, one pooled signal was a small reduction in resting systolic blood pressure. Ten studies produced g = −0.15, with a 95% confidence interval of −0.26 to −0.04 and p = 0.008. The direction remained negative when individual studies were removed, although some confidence intervals then crossed zero. The estimate also survived the modified Hartung–Knapp inference used in sensitivity analysis and restriction to randomized studies. This outcome received the review’s highest certainty rating, but that rating was still low because of risk-of-bias concerns and imprecision. The confidence interval included effects smaller and larger than the review’s 0.20-standard-deviation benchmark. A lower resting blood pressure may reflect a general cardiovascular adaptation to training rather than a changed response to psychological stress.

Resting diastolic blood pressure showed a larger pooled association, with g = −0.33, a 95% confidence interval of −0.64 to −0.01 and p = 0.041 across 10 studies. However, heterogeneity was substantial at I² = 90.5%, and statistical significance disappeared under modified Hartung–Knapp inference, after exclusion of non-randomized studies, and in leave-one-out analyses that removed several individual studies. An Egger regression also indicated possible small-study effects for this outcome, making publication bias a plausible explanation for some of the observed asymmetry. No significant changes were found in resting heart rate, blood cortisol, or two heart rate variability measures, RMSSD and SDNN. Blood cortisol, for example, had g = −0.07 and a 95% confidence interval of −0.80 to 0.67.

Heart rate variability was assessed through three separate indices. Across four studies, the LF/HF ratio yielded g = −0.43, with a 95% confidence interval of −0.80 to −0.05 and p = 0.028, indicating a lower ratio in intervention groups. Yet the finding was fragile: statistical significance was lost when any one of the four studies was omitted, when the analysis was restricted to randomized studies, and under modified Hartung–Knapp inference. LF/HF is influenced by both sympathetic and parasympathetic activity, and its traditional use as a direct index of “sympathovagal balance” has been increasingly questioned. The direction of change therefore cannot confidently be translated into better or worse autonomic regulation. Estimates for RMSSD, g = 0.03, and SDNN, g = 0.01, were both close to no effect, with confidence intervals that crossed zero.

The evidence base also had important methodological weaknesses. None of the randomized analytical entries was judged to have an overall low risk of bias: after consolidating entries from the same report, seven of 32 randomized studies were classified as high risk and 25 raised concerns. Common problems included insufficient detail about allocation concealment, intervention deviations, analysis populations and prespecification of results. All three non-randomized studies had serious overall risk of bias, including serious confounding. Psychological outcomes were commonly self-reported and participants were generally unblinded, creating the possibility that expectations could inflate apparent benefits. Missing data, baseline imbalances, selective reporting and inadequate information about intervention dose further limited confidence in the estimates. The analyses used unadjusted post-intervention comparisons, so residual differences between groups could influence the pooled results.

These limitations matter because psychological symptoms and resting physiological measurements are related to, but not specific to, stress. Cortisol varies with sampling time, sleep, acute stress and circadian rhythms; resting heart rate changes with age; and blood pressure and heart rate variability describe cardiovascular or autonomic state rather than reactions to a defined stressor. To measure stress reactivity and recovery, measurements would need to be taken during and after a standardized challenge. The review therefore cannot establish that physical activity produces a unified improvement in stress regulation, that subjective benefits are accompanied by physiological changes, or that the reverse relationship holds. Differences in age, activity type, intensity, frequency, session duration, intervention length, psychological instruments and measurement conditions may also explain why pooled effects varied, especially for anxiety and depressive symptoms.

Overall, the analysis provides tentative evidence that structured movement may help some young people feel less stressed and may modestly lower resting blood pressure. It does not establish a reliable effect on anxiety, fatigue, cortisol, resting heart rate, RMSSD or SDNN, and the apparent reductions in depressive symptoms, diastolic blood pressure and LF/HF depend on analytical choices or individual studies. Larger, well-designed randomized trials with clearly specified activity doses, standardized psychological and physiological measures, adequate follow-up and assessment during and after stressors are needed to determine which programs benefit which populations. Until then, the evidence supports physical activity as a plausible support for youth stress management, but it does not yet demonstrate a broad or uniform effect across psychological and physiological outcomes.

Subject of Research: Effects of physical activity interventions on stress-related psychological and physiological outcomes in children and adolescents

Article Title: The effects of physical activity interventions on stress-related psychological and physiological outcomes in children and adolescents: a systematic review and meta-analysis

Article References: Chen, L., Zhang, J., Wang, B., & Gao, Z. (2026). The effects of physical activity interventions on stress-related psychological and physiological outcomes in children and adolescents: a systematic review and meta-analysis. Frontiers in Psychology, 17, Article 2000159. https://doi.org/10.3389/fpsyg.2026.2000159

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DOI: 10.3389/fpsyg.2026.2000159

Keywords: physical activity, children, adolescents, stress, exercise, depressive symptoms, blood pressure, heart rate variability, cortisol, systematic review, meta-analysis, effects

Researchers recruited 225 participants from community health service centers affiliated with regional medical consortia between January and December 2025. All received the mobile health–enabled hierarchical diagnosis and treatment education program, delivered through the Shekangtong WeChat mini program. The program combined home blood pressure self-monitoring, personalized education, family doctor follow-up and specialist consultation pathways within the existing regional care network.

Participants were encouraged to record daily home blood pressure measurements, while tailored education on hypertension prevention, diet, physical activity and lifestyle modification was offered two to three times per week. Participants could consult family doctors through platform functions, with responses to health-related inquiries expected within 24 hours. Family doctors could also seek additional assessment or specialist support through the regional medical consortium pathway. Monthly online education and experience-sharing sessions were part of the program.

Among the 210 participants who completed both baseline and 12-month assessments, mean systolic blood pressure decreased from 145.35 ± 4.18 mmHg to 130.64 ± 5.62 mmHg. The mean difference was 14.71 mmHg, with a 95% confidence interval of 13.68 to 15.74 mmHg and p<0.001. Mean diastolic blood pressure decreased from 68.93 ± 4.85 mmHg to 60.73 ± 4.31 mmHg, a mean difference of 8.20 mmHg with a 95% confidence interval of 7.28 to 9.12 mmHg and p<0.001. Endpoint measurements were taken by trained research personnel using calibrated electronic sphygmomanometers, rather than derived from home readings.

The primary outcome, health-related quality of life measured with the EQ-5D-5L, also improved. Its mean utility value rose from 0.82 ± 0.13 at baseline to 0.94 ± 0.06 at follow-up, a mean difference of 0.12 (95% CI, 0.10 to 0.14; p<0.001). The mean EQ-VAS score increased from 74.16 ± 11.07 to 80.93 ± 8.03, a mean difference of 6.77 points (95% CI, 6.18 to 7.36; p<0.001).

The largest change among the five EQ-5D-5L dimensions was in anxiety/depression: the proportion reporting no problems increased from 68 of 210 participants, or 32.4%, to 178, or 84.8%, after false-discovery-rate correction (adjusted p<0.001). The authors emphasized that this item measures perceived health-related distress rather than diagnosing or treating clinical anxiety or major depression. Changes in mobility were also significant after correction, while changes in pain/discomfort, self-care and usual activities did not meet the corrected significance threshold.

Greater blood pressure reductions were associated with larger quality-of-life improvements. Systolic reductions correlated with changes in the EQ-5D-5L utility value (r=0.32; 95% CI, 0.21 to 0.43) and EQ-VAS score (r=0.25; 95% CI, 0.14 to 0.36). Diastolic reductions correlated with utility-value changes (r=0.28; 95% CI, 0.17 to 0.39) and EQ-VAS changes (r=0.22; 95% CI, 0.11 to 0.33); all reported p-values were below 0.001. These correlations represent associations, not evidence that blood pressure reduction caused the quality-of-life gains.

Implementation data were broadly consistent with feasibility over 12 months. The retention rate was 93.3%, as 210 of 225 enrolled participants completed follow-up, and participants uploaded home blood pressure measurements an average of 3.2 ± 1.4 times per week. No intervention-related adverse events were reported. However, standardized measures of adherence across all program components and formal intervention-fidelity assessment were not used, so engagement with blood pressure uploads could not establish the degree of exposure to the complete model.

The absence of a control group prevents causal attribution. Potential contributors to the observed changes include regression to the mean, the natural course of hypertension, concurrent lifestyle changes, participation-related behavior and broader changes in care. Medication use is another important limitation: baseline regimens were documented, but medication initiation, dose adjustment, discontinuation and adherence changes were not systematically tracked during follow-up. The study also excluded adults older than 70 and did not establish whether the improvements were sustainable, cost-effective or transferable to other healthcare settings. The authors therefore characterized the results as preliminary evidence of pre–post associations and called for controlled studies with concurrent comparison groups and more comprehensive measurement.

Subject of Research: Prospective evaluation of mobile health–enabled hierarchical hypertension care in Chinese adults aged 60–70

Article Title: Evaluation of a mobile health–enabled hierarchical care model for hypertension management and health-related quality of life among older adults: a prospective pre–post intervention study

Article References: Ma, X., Li, K., Zheng, D., Song, Y., Lin, J., & Chen, L. (2026). Evaluation of a mobile health–enabled hierarchical care model for hypertension management and health-related quality of life among older adults: a prospective pre–post intervention study. Frontiers in Public Health, 14, Article 1964536. https://doi.org/10.3389/fpubh.2026.1964536

Image Credits: AI Generated

DOI: 10.3389/fpubh.2026.1964536

Keywords: mobile health, hypertension, blood pressure, quality of life, older adults, hierarchical care, pre–post study, digital health, WeChat, Shenzhen, Evaluation, mobile

Physical activity was assessed using daily step counts recorded by Fitbit wearable devices. Baseline activity metrics were positively associated with the Gradual Onset Continuous Performance Task (Grad-CPT), Delay Discounting Task (DD-Task) and Flanker-Task. The reported regression coefficients were 0.31 for Grad-CPT (95% confidence interval [CI], 0.18 to 0.44), 0.05 for the DD-Task (95% CI, 0.04 to 0.07) and 0.26 for the Flanker-Task (95% CI, 0.17 to 0.35). The abstract did not report an association between baseline activity and the Multiracial Emotional Recognition Task.

Blood pressure measurements spanned 14 years, and baseline systolic blood pressure was negatively associated with DD-Task performance, with a regression coefficient of −0.01 (95% CI, −0.02 to −0.004). The abstract did not report corresponding results for diastolic blood pressure. A longitudinal k-means clustering analysis identified three activity groups with mean daily step counts of 5,108, 8,875 and 14,161. Participants in the two groups with more steps had higher scores than those in the lowest-step group on the DD-Task, Grad-CPT and Flanker-Task.

Cognition was assessed with the Grad-CPT, DD-Task, Multiracial Emotional Recognition Task and Flanker-Task. The available evidence is limited to the abstract, which does not provide full methodological details, participant characteristics, adjustment variables or model diagnostics. The findings therefore describe associations in this observational All of Us sample rather than causal effects or evidence that changing physical activity or blood pressure would improve cognitive performance.

Subject of Research: Observational associations of physical activity and blood pressure with cognitive performance in All of Us participants

Article Title: Physical activity and blood pressure as predictors of cognitive function in the all of us research program

Article References: Okusaga, O. O., Lin, Y.-S., & Atkinson, E. (2026). Physical activity and blood pressure as predictors of cognitive function in the all of us research program. Scientific Reports. https://doi.org/10.1038/s41598-026-74379-6

Image Credits: AI Generated

DOI: 10.1038/s41598-026-74379-6

Keywords: All of Us, physical activity, blood pressure, cognitive function, wearable step counts, Fitbit, observational study, k-means clustering, Physical, activity, blood, pressure

The research team searched PubMed, Web of Science, and the Cochrane Library from their inception to 6 February 2026, with additional searches of Scopus and Embase conducted on 17 August 2026. After screening more than 1,300 records, they identified 22 study reports representing 17 unique trials — 15 randomised and 2 non-randomised controlled trials — encompassing 588 unique participants. The clinical populations spanned hypertension, prediabetes, type 1 and type 2 diabetes, breast cancer, prostate cancer, and broader metabolic risk profiles. Participants ranged in age from roughly 14 to 67 years, and interventions ran from 8 weeks to 12 months, typically delivered two to three times per week at moderate-to-vigorous intensity, with net playing time between 7 and 45 minutes per session.

Methodologically, the analysis was more sophisticated than most in this field. Because some trials contributed multiple effect estimates — through multiple intervention arms, linked reports from the same cohort, or repeated measures of the same outcome — the authors used three-level random-effects meta-analyses that treated effect sizes as nested within trials. They then applied cluster-robust (CR2) variance estimation, clustering on the independent trial, to every outcome as a robustness check, and drew conclusions only where the two inferential procedures agreed. Certainty of evidence was rated with the GRADE framework, and prediction intervals were reported to show how variable the true effects might be across different settings.

The headline findings are striking for a group of patients often excluded from vigorous team sport. Recreational football was associated with significant improvements in cardiorespiratory fitness, with a standardised mean difference (SMD) of 0.70 for peak oxygen uptake (VO₂peak) and an even larger 1.43 for Yo-Yo Intermittent Endurance Test performance. Cardiovascular outcomes also improved: diastolic blood pressure fell (SMD −0.53), mean arterial pressure dropped (SMD −0.89), and resting heart rate showed the largest effect in the entire synthesis (SMD −1.01). In clinically interpretable units, the pooled mean differences amounted to roughly a 5 mmHg reduction in mean arterial pressure and a 5.7 beats-per-minute reduction in resting heart rate.

Body composition and blood lipids moved in the right direction too. Body fat percentage declined significantly (SMD −0.36), muscle mass increased modestly (SMD 0.22), and both triglycerides (SMD −0.56) and total cholesterol (SMD −0.69) fell. Notably, body weight, BMI, and waist circumference did not change significantly — a pattern the authors attribute to the insensitivity of scale-based measures to compositional change when fat is lost and lean tissue is gained, particularly in patients taking medications with weight-active effects. One prostate cancer trial, for example, reported a between-group lean body mass difference of about 0.7 kilograms after 12 weeks of football training in men undergoing androgen deprivation therapy.

The bone-health results tell a subtler story. Plasma osteocalcin, a marker of bone formation, rose significantly (SMD 1.07), and P1NP, another formation marker, increased under the primary analysis (SMD 1.28). Yet DXA-derived bone mineral density and content showed no significant changes, and the P1NP effect did not survive cluster-robust inference. The authors interpret this as evidence of early anabolic signalling in response to the mechanical loading of football — the jumps, turns, accelerations, and decelerations that small-sided games demand — without enough training exposure to produce measurable structural remodelling in older, clinically vulnerable cohorts. Bone turnover markers can respond within weeks, whereas density changes typically require longer and are most visible at mechanically loaded lower-limb sites.

Several seemingly positive findings proved fragile under scrutiny. Borderline effects on fat mass, systolic blood pressure, and LDL cholesterol were not retained under cluster-robust inference, and effects on body fat percentage, fat mass, muscle mass, systolic pressure, and LDL were sensitive to the assumed pre–post correlation used to derive change-score statistics. No significant pooled effects emerged for HbA1c, fasting glucose, fasting insulin, HDL cholesterol, or C-reactive protein. Across 27 outcomes, the statistical interpretation was unchanged for 22 under the robust procedure — but certainty of evidence was rated low to very low for most outcomes, and prediction intervals for several significant findings crossed zero, meaning the average benefit was not reproduced consistently across diagnoses and programmes.

On feasibility, the picture is encouraging but not uniform. Mean attendance across 13 independent trials was 82.7 percent, and mean attrition across 14 trials was 15.6 percent — respectable figures for exercise interventions in clinical populations, and consistent with the idea that the social structure, team affiliation, and sheer enjoyment of football help sustain engagement where solitary treadmill work often fails. Adverse events were summarised narratively because quantitative pooling was impossible: most reported events were musculoskeletal, including muscle soreness, strains, joint pain, and lower-limb injuries, with occasional serious injuries such as fibular fractures and Achilles tendon ruptures. Several trials noted that injuries clustered in the early phase of training, underscoring the importance of progressive exposure, warm-up, and qualified supervision.

The authors are explicit that these results should not be read as evidence that football can replace established exercise prescriptions or as a disease-specific therapy. The included populations differ enormously in pathophysiology, treatment burden, medication status, and baseline fitness, and the number of studies within any single diagnostic category was too small for firm conclusions. In hypertension, blood-pressure effects were inconsistent, particularly among patients already on antihypertensive medication, where residual headroom for further lowering may be limited. In diabetes, glycaemic outcomes were largely unchanged at the pooled level, plausibly because fasting indices and HbA1c are relatively insensitive to modest exercise effects in pharmacologically controlled patients. Cancer-related evidence came from small, highly selected samples with variable attendance.

Nevertheless, the synthesis marks a milestone for the ‘Football is Medicine’ platform, which has argued for years that small-sided games deliver a uniquely multimodal stimulus — cardiovascular, neuromuscular, and osteogenic load within a single session — that continuous aerobic training and isolated resistance exercise cannot match. The physiological profile is coherent: heart rates of 80 to 90 percent of maximum, repeated high-intensity efforts, and weight-bearing impacts together explain the concurrent gains in fitness, heart rate, body fat, and bone formation markers. For appropriately screened patients who prefer group-based, game-based activity and can participate safely under supervision, the authors conclude that recreational football may be considered a supervised adjunctive exercise option — particularly where cardiorespiratory fitness is the target. Adequately powered, diagnosis-specific trials with standardised reporting of training dose, adherence, and adverse events are the next step before football earns a formal place in the clinical exercise toolkit.

Subject of Research: Effects and feasibility of recreational football exercise in patients with chronic diseases

Article Title: Recreational football as medicine? A meta-analysis of its effects and feasibility in patients with chronic diseases

Article References: Wei, K., Chen, G., Wang, T., & Wang, B. (2026). Recreational football as medicine? A meta-analysis of its effects and feasibility in patients with chronic diseases. Frontiers in Public Health, 14, Article 1869982. https://doi.org/10.3389/fpubh.2026.1869982

Image Credits: AI Generated

DOI: 10.3389/fpubh.2026.1869982

Keywords: recreational football, meta-analysis, chronic disease, cardiorespiratory fitness, blood pressure, hypertension, type 2 diabetes, cancer survivors, bone health, exercise as medicine, body composition, feasibility

The trial, published in Pharmacology Research & Perspectives, addressed a stubborn clinical problem. Hypertension remains the most prevalent modifiable risk factor for cardiovascular disease, and bringing blood pressure under control with medication dramatically reduces that risk. Yet studies consistently show that 20 to 40 percent of cardiovascular risk persists in well-controlled hypertensive patients, a phenomenon researchers call residual risk. Scientists attribute this stubborn remainder to chronic inflammation, oxidative stress, endothelial dysfunction, arterial stiffness and genetic and epigenetic factors, including microRNA-21, a small regulatory RNA implicated in hypertensive vascular remodeling. Standard antihypertensive drugs do not fully neutralize these pathways, which is why nutraceuticals with antioxidant and anti-inflammatory properties have attracted attention as potential adjuncts.

Chios mastic was a plausible candidate. The resin contains characteristic triterpenes, notably masticadienonic acid and isomasticadienonic acid, and preclinical work has documented antioxidant, anti-inflammatory and cardioprotective effects. An earlier human study by Kontogiannis and colleagues reported an acute antihypertensive effect and hinted at mechanisms involving proteostasis, the cellular system that degrades oxidized and misfolded proteins, and the control of reactive oxygen species. The HYPER-MASTIC team hypothesized that sustained mastic supplementation might chip away at residual cardiovascular risk in treated hypertensive patients, and designed a double-blind, placebo-controlled, parallel-group trial to find out.

Between April 2022 and February 2024, the researchers enrolled 105 participants aged 40 to 80 with stable, well-controlled hypertension confirmed by 24-hour ambulatory monitoring. Volunteers were randomized to receive 1500 milligrams per day of mastic, 2800 milligrams per day, or matching placebo for three months. Blinding was unusually thorough: placebo tablets were identical in size and shape and were sprayed with mastic scent to preserve the illusion. Participants attended four study visits, during which the team measured 24-hour ambulatory peripheral and central blood pressure, pulse wave velocity as a gold-standard index of arterial stiffness, endothelial function via flow-mediated dilatation, carotid and femoral artery ultrasound, and echocardiographic cardiac function. Blood sampling tracked reactive oxygen species and proteasome activity in immune cells and red blood cells, and RNA sequencing captured transcriptomic changes in a predefined high-risk subgroup of 59 participants.

The primary result was unambiguous. Changes in 24-hour systolic and diastolic blood pressure, the trial’s primary endpoints, did not differ significantly between the mastic and placebo groups. The low-dose group showed some statistically significant within-group increases in pulse wave velocity and central blood pressure parameters, but these did not translate into significant time-by-group interactions, with the single exception of 24-hour central systolic pressure, where a trend toward an increase in the low-dose group emerged. Office diastolic pressure rose slightly in the high-dose group, and flow-mediated dilatation barely changed anywhere. In short, mastic conferred no additional short-term antihypertensive benefit in these patients.

Crucially, the researchers could rule out poor adherence as an explanation. Participants kept daily diaries, received biweekly follow-up calls, and, most persuasively, plasma levels of the mastic triterpenes masticadienonic and isomasticadienonic acid were measured objectively. These metabolites rose in the low-dose group and climbed roughly three-fold further in the high-dose group while remaining flat under placebo, confirming that participants were genuinely taking their supplements. The supplement was also well tolerated, with no serious adverse events reported across the three arms.

The molecular assays told a similar story of neutrality. Reactive oxygen species and proteasome activity in peripheral blood mononuclear cells and red blood cells showed no significant differences between groups at baseline or at three months, contrasting with the effects seen in earlier acute and experimental studies. The authors suggest this likely reflects a ceiling effect: participants whose blood pressure and metabolic risk factors were already well controlled simply carried a low inflammatory and oxidative burden, leaving little room for mastic to improve. This pattern echoes findings from other nutraceutical trials, including studies of quercetin and resveratrol, where blood pressure effects shrink or vanish in lower-risk populations, and from the earlier MAST4HEALTH trial, in which mastic improved metabolic and inflammatory markers most clearly in people with greater baseline cardiometabolic burden.

Where the trial did find something intriguing was at the level of gene expression. In the high-risk subgroup, defined by criteria such as elevated C-reactive protein, advanced age, chronic renal failure or residual blood pressure elevation, RNA sequencing of whole blood revealed a distinct set of differentially expressed genes after mastic supplementation compared with placebo. Only about one percent of altered genes overlapped between the mastic and placebo arms, with 141 genes uniquely changed by mastic. Functional enrichment analysis showed that the upregulated genes clustered in pathways governing tight junction organization and cellular adhesion, processes central to endothelial barrier integrity and vascular permeability that are disrupted in hypertension. The authors interpret this as evidence that mastic may support endothelial stability and vascular homeostasis even when it does not move the blood pressure needle, a mastic-specific biological effect supported by the absence of comparable transcriptomic changes under placebo. Complementary analyses from the same project also found modulation of microRNA-21, an epigenetic marker of vascular remodeling, particularly in relation to night-time blood pressure.

The investigators are careful about the caveats. The low-dose group was significantly younger than the placebo group and reported family history of hypertension more often, imbalances that were adjusted for statistically but that may have contributed to vascular variability. A three-month intervention may be too brief for gradual nutraceutical effects to emerge, and the well-controlled baseline state of the cohort itself limited the opportunity to detect additive benefits. The authors also emphasize that mastic was studied as a nutraceutical supplement and is not approved by regulators for treating hypertension or reducing cardiovascular risk, so patients should not view the resin as a substitute for prescribed therapy.

The takeaway from HYPER-MASTIC is a nuanced one that resists the simple narrative of a miracle supplement. Chios mastic, at 1500 or 2800 milligrams daily for three months, does not lower blood pressure in people whose hypertension is already well managed, and the trial’s rigorous design, objective adherence verification and comprehensive vascular phenotyping make that null result difficult to dismiss. Yet the resin’s ability to shift expression of genes involved in endothelial integrity in higher-risk patients suggests that its biological activity is real and may be most relevant where inflammatory and metabolic burden is greatest. The authors call for longer trials in higher-risk populations with integrated molecular and clinical endpoints to determine whether mastic’s transcriptomic fingerprints translate into fewer heart attacks and strokes. For now, the ancient resin of Chios remains what it has long been: a fascinating natural product with genuine biological activity, still awaiting proof that it can protect the cardiovascular system in the patients who need it most.

Subject of Research: Effects of Chios mastic gum supplementation on blood pressure and vascular biology in well-controlled hypertension

Article Title: Chios Mastic in Well‐Controlled Hypertension: Findings From the HYPER‐MASTIC Randomized Controlled Trial

Article References: Kalafati, I. P., Kyriazopoulou‐Korovesi, A.-A., Mentsiou‐Nikolaou, E., Papaioannou, M., Konstantaki, C., Angelidakis, L., Gianniou, D. D., Mikropoulou, E. V., Giardoglou, P., Valakos, D., Vatsellas, G., HYPER‐MASTIC Consortium, Andreadou, I., Manios, E., Halabalaki, M., Trougakos, I. P., Dedoussis, G. V., & Stamatelopoulos, K. (2026). Chios Mastic in Well‐Controlled Hypertension: Findings From the HYPER ‐ MASTIC Randomized Controlled Trial. Pharmacology Research & Perspectives, 14(6), Article e70322. https://doi.org/10.1002/prp2.70322

Image Credits: AI Generated

DOI: 10.1002/prp2.70322

Keywords: Chios mastic, hypertension, randomized controlled trial, cardiovascular risk, blood pressure, endothelial function, oxidative stress, nutraceutical, Pistacia lentiscus, RNA sequencing, arterial stiffness, residual cardiovascular risk

The research team assembled a retrospective cohort of 289 children between the ages of six and twelve who had been diagnosed with obesity at their hospital between March 2021 and March 2024. Rather than randomizing participants, the investigators compared two real-world pathways. One group of 162 children was enrolled in a family-centered comprehensive lifestyle intervention, a twelve-month multidisciplinary program that wove together dietary counseling, physical activity guidance, behavioral support, and medical monitoring, all delivered with the household as the unit of change. The remaining 127 children received routine guidance, the standard health education that most pediatric clinics dispense: advice sheets, brief counseling sessions, and periodic weigh-ins.

What distinguishes this study from the crowded field of pediatric weight-loss trials is the sheer breadth of its measurement battery. At baseline and again at the twelve-month follow-up, the researchers captured anthropometric data, full body composition, blood pressure, lipid profiles, glucose metabolism indices, inflammatory markers, liver function, uric acid, cardiovascular structure, and health-related quality of life. That last category, assessed with the Pediatric Quality of Life Inventory, is often an afterthought in cardiometabolic research. Here it was treated as a primary outcome, a deliberate choice that reflects a growing recognition in pediatric medicine that a child’s subjective wellbeing is not separable from their metabolic status.

The numbers, when they arrived, were strikingly consistent. Children in the family-centered program showed an adjusted mean difference in body mass index of minus 1.23 compared with the routine guidance group, with a 95 percent confidence interval running from minus 1.80 to minus 0.66. Waist circumference, a proxy for visceral adiposity that many researchers consider more prognostically meaningful than BMI itself, dropped by an adjusted 4.13 centimeters on average. Body fat percentage fell by 2.61 points. Each of these differences was statistically robust, with adjusted p-values below 0.001, and each moved in the direction that a decade of pediatric obesity literature would predict only from sustained, genuine behavioral change rather than measurement noise or regression to the mean.

But the story does not end at the tape measure. Systolic blood pressure in the intervention group was an adjusted 4.23 millimeters of mercury lower than in the comparison group. The homeostasis model assessment of insulin resistance, the workhorse index known as HOMA-IR that captures how hard the pancreas is working to keep blood glucose in check, improved by an adjusted 0.46 units. High-sensitivity C-reactive protein, the systemic inflammation marker that cardiologists track as a harbinger of atherosclerotic disease, fell by 0.57 milligrams per liter. Uric acid declined, lipid profiles shifted favorably, and the children reported a meaningfully better quality of life, with total PedsQL scores rising by an adjusted 4.73 points.

Perhaps most remarkable are the structural findings. The researchers documented improvements in cardiac structure and a reduction in carotid intima-media thickness, the thickness of the innermost layers of the carotid artery wall that ultrasound can measure noninvasively. In adult medicine, carotid intima-media thickness is treated as a window into early atherosclerosis, a disease process that typically takes decades to become clinically manifest. Finding that a twelve-month lifestyle intervention was associated with measurable favorable change in school-aged children suggests that the vascular consequences of childhood obesity are not merely a future risk to be managed but an active, ongoing process that responds to intervention in near real time. All of these secondary outcomes reached statistical significance at p below 0.05.

The mechanism, the authors argue, is baked into the design of the intervention itself. A six-year-old does not shop for groceries, plan meals, or decide whether the evening is spent on a screen or a soccer field. Conventional pediatric obesity counseling that addresses the child in isolation asks the least empowered member of the household to engineer her own environment, which is a bit like prescribing a diet to someone else’s pantry. A family-centered model instead treats the home as the therapeutic unit, aligning parents, siblings, and caregivers around shared changes in food, activity, and routine. The multidisciplinary structure, drawing on pediatric, endocrine, nutritional, and behavioral expertise over a full year, provides the scaffolding that single-visit advice cannot.

The quality-of-life result deserves particular attention because it complicates a persistent fear in pediatric weight management: that intensive intervention damages children’s self-image. In this cohort, the opposite occurred. Children whose families went through the program together reported better overall health-related quality of life, not worse, with the adjusted difference of 4.73 PedsQL points reaching significance at p equal to 0.002. The implication is that when lifestyle change is framed as a household project rather than a child’s personal failure, the psychological burden of intervention may transform into psychological benefit.

Honest caveats temper the enthusiasm, and the authors are careful to supply them. This was a retrospective, non-randomized study, which means families were not assigned to their groups by chance. It is entirely possible that households willing and able to commit to a twelve-month multidisciplinary program differed systematically from those that received routine guidance, in motivation, resources, health literacy, or baseline stability, and that these differences, rather than the intervention itself, drove part of the observed benefit. The authors state plainly that the findings should be interpreted as hypothesis-generating associations rather than causal effects. Adjusted analyses can narrow the gap between groups statistically, but they cannot manufacture the equivalence that randomization provides.

Even with that caution, the study lands at a consequential moment. Childhood obesity continues to climb globally, and the pharmacological options now arriving for adults are raising uncomfortable questions about lifelong medication in growing bodies. Against that backdrop, evidence that a structured, family-centered, non-pharmacological program can shift not just weight but insulin resistance, systemic inflammation, blood pressure, arterial wall thickness, and a child’s own reported wellbeing is a signal worth taking seriously. The next step, which this study’s authors implicitly invite, is the randomized trial that can separate the program’s effect from the families who choose it. If the associations hold, the prescription for pediatric obesity may turn out to be written not for the child at all, but for everyone who shares her dinner table.

Subject of Research: Family-centered lifestyle intervention for childhood obesity and cardiometabolic health

Article Title: Long-term effects of a family-centered comprehensive lifestyle intervention on body composition and cardiometabolic indicators in school-aged obese children aged 6–12 years

Article References: Lv, F., & Wang, Y. (2026). Long-term effects of a family-centered comprehensive lifestyle intervention on body composition and cardiometabolic indicators in school-aged obese children aged 6–12 years. BMC Pediatrics. https://doi.org/10.1186/s12887-026-07616-6

Image Credits: AI Generated

DOI: 10.1186/s12887-026-07616-6

Keywords: childhood obesity, family-centered care, pediatric health, cardiometabolic risk, body composition, insulin resistance, blood pressure, inflammation, quality of life, lifestyle intervention, retrospective study, BMC Pediatrics

The research team, led by Yan Gao, Yingjie Peng, and Yuanyuan Wang of Weifang Maternal and Child Health Hospital and collaborating institutions in Shandong, China, set out to answer a deceptively simple question: after accounting for how high someone’s blood pressure actually is, does knowing about a hypertension diagnosis matter for survival? The question matters because awareness is often treated as a key performance indicator in hypertension care. National surveys track the percentage of hypertensive adults who know their status, and screening programs celebrate rising awareness figures. But if awareness itself does not translate into lower mortality, the metric may be a weaker proxy for health benefit than commonly believed.

To investigate, the researchers turned to two of the most respected population-based cohort studies in the world. The first was the China Health and Retirement Longitudinal Study, known as CHARLS, which enrolled adults aged 45 and older with a baseline survey conducted in 2011 and 2012. The second was the US National Health and Nutrition Examination Survey, or NHANES, drawing on cycles conducted between 1999 and 2018. Both studies combine household interviews with physical examinations, meaning participants had their blood pressure actually measured by trained staff rather than merely self-reported. That combination of subjective awareness data and objective measurements is what made the analysis possible.

The analytic samples were substantial: 12,868 participants in CHARLS, of whom 12,640 contributed mortality follow-up, and 26,351 participants in NHANES. Hypertension awareness was defined strictly as a self-reported previous diagnosis of hypertension made by a physician or other health professional. Participants were then sorted into five mutually exclusive categories based on their awareness status and their baseline measured blood pressure: normotension, aware controlled hypertension, aware uncontrolled hypertension, unaware grade 1 hypertension, and unaware grade 2 to 3 hypertension. This classification scheme allowed the team to compare, for example, someone with severe but undiagnosed hypertension against someone with equally severe diagnosed hypertension, isolating the effect of awareness itself.

The two cohorts were analyzed independently using a broadly common analytical framework, a deliberate design choice that guards against pooling artifacts and allows each country’s data to speak with its own weighting and covariate adjustments. The researchers employed cohort-specific Cox proportional hazards models, the standard statistical tool for survival analysis, incorporating appropriate survey weights and adjusting for demographic, lifestyle, and clinical covariates such as age, sex, body mass index, smoking status, and relevant clinical markers. They also compared aware and unaware hypertension within the same blood pressure severity categories and modeled continuous systolic blood pressure in relation to mortality, providing both categorical and continuous views of the same underlying biology.

The headline results were striking in their consistency across two very different health systems. Compared with normotension, aware but uncontrolled hypertension was associated with higher all-cause mortality in both cohorts. In CHARLS, the hazard ratio was 1.53, with a 95 percent confidence interval of 1.26 to 1.85, meaning a roughly 53 percent higher risk of death during follow-up. In NHANES, the corresponding hazard ratio was 1.39, with a confidence interval of 1.28 to 1.52. Unaware severe hypertension, grade 2 to 3, showed similarly elevated risks: a hazard ratio of 1.58 in CHARLS and 1.50 in NHANES. In other words, a person walking around with dangerously high blood pressure faced substantially elevated mortality whether or not a doctor had ever told them they had the condition.

The more provocative finding emerged when the researchers compared aware and unaware participants within the same broad blood pressure severity categories. If awareness itself conferred a survival advantage, aware individuals should have fared better than unaware individuals with equivalent blood pressure. They did not, at least not consistently. Awareness status was not reliably associated with mortality across the two cohorts, and the pattern of results differed between China and the United States. When the team modeled systolic blood pressure as a continuous variable, mortality rose steadily with increasing systolic pressure in both countries, but evidence of an interaction between systolic pressure and awareness appeared in NHANES and not in CHARLS. Notably, the main phenotype associations did not differ significantly between the cohorts, underscoring that the core relationship between blood pressure severity and death was robust on both sides of the Pacific.

What might explain the inconsistency of awareness as a predictor? The authors are careful to frame their conclusions as observational, describing associations among baseline-defined phenotypes rather than causal effects of knowing one’s diagnosis. Awareness, after all, is only meaningful if it leads to treatment, and treatment only matters if it achieves control. A person diagnosed with hypertension who never fills a prescription, or whose medication fails to bring readings down, is physiologically little different from someone who was never diagnosed at all. The data appear to reflect that reality: the aware uncontrolled group fared about as badly as the unaware severe group, while the measured blood pressure categories told a coherent story in both nations. Awareness without control is, from the body’s perspective, a label rather than a protection.

The authors explicitly warn against a misreading of their work. These findings should not be interpreted as evidence that hypertension awareness itself is unimportant, they conclude. Detection remains the essential gateway to treatment, and untreated severe hypertension carried some of the highest mortality risks in the study. The correct lesson is more nuanced: screening programs that stop at diagnosis, without ensuring continued clinical follow-up and sustained blood pressure control, may be capturing the credit for awareness statistics while leaving the underlying lethal physiology untouched. The researchers emphasize that hypertension detection remains important and should be followed by continued clinical follow-up and sustained blood pressure control.

For policymakers, the study arrives at a moment when hypertension burdens are climbing in both aging China and the United States, and when digital screening initiatives promise to push awareness figures ever higher. The message embedded in these two cohorts is that the numbers on the cuff, not the words on a chart, are what the body registers. Public health systems that measure success by diagnosis rates alone may be optimizing the wrong variable. The true target, this research suggests, is sustained control, verified by measurement, for everyone whose blood pressure sits in the danger zone, whether or not they have ever heard a doctor speak the word hypertension.

Subject of Research: Association of hypertension awareness and blood pressure severity with all-cause mortality in Chinese and US population cohorts

Article Title: Hypertension awareness, blood pressure severity, and all-cause mortality: independent analyses of population-based cohorts in China and the United States

Article References: Gao, Y., Peng, Y., & Wang, Y. (2026). Hypertension awareness, blood pressure severity, and all-cause mortality: independent analyses of population-based cohorts in China and the United States. BMC Public Health. https://doi.org/10.1186/s12889-026-29908-3

Image Credits: AI Generated

DOI: 10.1186/s12889-026-29908-3

Keywords: hypertension, blood pressure, all-cause mortality, awareness, CHARLS, NHANES, systolic blood pressure, blood pressure control, Cox proportional hazards, epidemiology, public health, cohort study