Hypertension, Sodium and Sleep A Toolkit for Clinicians
2 Contents 5 Hypertension at a Glance 6 The Relationship Between Sodium Intake and Hypertension 7 The Relationship Between Sleep and Hypertension 8 Why Sodium Matters in Hypertension and Cardiovascular Health 9 Practical Sodium Reduction Strategies Clinicians Can Use in Routine Care 11 Sleep as a Modifiable Risk Factor in Hypertension 12 The Sodium–Sleep Connection: Counseling Patients on Overlapping Lifestyle Factors 12 Improving Sleep Duration to Support Blood Pressure Control 13 Incorporating Sleep Screening Into Personalized Hypertension Care Plans 14 Key Takeaways 15 References Jazz Pharmaceuticals, Inc. is proud to support the American Heart Association’s Hypertension, Sodium and Sleep Professional Education Initiative. Contributing Authors Younghoon Kwon, MD, MS, FACC, is a cardiologist at University of Washington. He is one of the few cardiologists who is formally trained and board-certified in sleep medicine. Given this background, he has special interests in the interface of sleep and cardiovascular health. His work in physiological monitoring of sleep in patients with cardiovascular risks has been supported by various funding agencies. He is passionate about exploring novel therapies and innovative avenues to help mitigate cardiovascular risks and improve outcomes in patients with cardiovascular disease through improving sleep. He is an active member of both the American Heart Association and the American Academy of Sleep Medicine. Disclosures: Consultant: iRhythm Technologies, Inc. Paola Rosas, MD, PhD, is an assistant professor in the College of Pharmacy at the University of Illinois Chicago. Dr. Rosas investigates the molecular and metabolic mechanisms that drive cardiometabolic heart disease. Her work integrates cardiac signaling, metabolism and the gut–heart axis to identify new therapeutic strategies that improve cardiac function and advance the treatment of cardiovascular disease. Disclosures: Nothing to disclose Mark É Czeisler, MD, PhD, is a resident physician in the Department of Medicine at Brigham and Women’s Hospital and clinical fellow in medicine at Harvard Medical School. Dr. Czeisler has conducted research in sleep and circadian biology, spanning from characterizing the neuroanatomy of the central mammalian circadian pacemaker to largescale epidemiologic studies. Currently in training with aspirations to pursue clinical cardiology, he has increasingly focused on the role of digital health technologies in studying and improving cardiovascular health and performance. Disclosures: Consultant: Nychthemeron, LLC
3 A Toolkit for Clinicians Hypertension, Sodium and Sleep Billy Caceres, PhD, RN, FAHA, FAAN, FPCNA, is a nurse scientist and assistant professor at the Columbia University School of Nursing. His research program uses biobehavioral approaches to identify and intervene on psychosocial stressors that influence cardiovascular and sleep health across the lifespan. Dr. Caceres has led groundbreaking research that has increased understanding of contributors to cardiovascular and sleep health among minoritized populations, including sexual and gender minority adults and people of color. He is a fellow of the American Heart Association and the American Academy of Nursing. Disclosures: Nothing to disclose Christopher C. Imes, PhD, RN, is an associate professor in the School of Nursing and faculty member of the Center for Sleep and Circadian Science at the University of Pittsburgh. His areas of research include sleep and cardiovascular disease, sleep and shift work, and interventions to improve multidimensional sleep health. Disclosures: Grant/Contract: Shadyside Hospital Foundation, University of Pittsburgh Marie-Pierre St-Onge, PhD, CCSH, FAHA, is the founding director of the Center of Excellence for Sleep & Circadian Research at Columbia University Irving Medical Center. Her NIHfunded research focuses on the impact of sleep, circadian rhythms and diet on cardiometabolic health. Dr. St-Onge has led multiple American Heart Association scientific statements on sleep, meal timing and cardiometabolic risk and was director of the American Heart Association’s Go Red for Women Strategically Focused Research Center. Disclosures: Consultant: American Pistachio Growers, Lindus Health, Nestle HealthCare Nutrition Inc. Data And Safety Monitoring: Harvard University Grant/Contract: American Pistachio Growers, California Walnut Commission, Dairy Management, National Institutes of Health Other: Simon & Schuster Virend K. Somers, MBChB, DPhil, is a cardiologist and Mayo Clinic Investigator in the Department of Cardiovascular Diseases at Mayo Clinic in Rochester, Minnesota, where he holds the Alice Sheets Marriott Professorship. His translational research focuses on the integration of sleep, cardiometabolic regulation and vascular biology, with funding from the NIH and the American Heart Association. Disclosures: Consultant: Axsome Therapeutics, GEM Health, iRhythm Technologies, Inc., Jazz Pharmaceuticals Inc., Mineralys Therapeutics Gift/Other: Medtronic (Research equipment to Mayo Clinic) ZOLL Medical Corporation (Research equipment to Mayo Clinic) Grant/Contract: National Institutes Health (Paid to Mayo Clinic) Other: Sleep Number Advisory Board Janet Mullington, PhD, is professor of neurology at Harvard Medical School and director of the Clinical Research Center at Beth Israel Deaconess Medical Center. She leads a research team that investigates sleep and circadian science, bridging human neuroscience, cardiovascular health and the role of sleep in host defense. Her interdisciplinary studies have explored the links between sleep and changes in heart rate variability, blood pressure regulation and physiological regulatory processes that contribute to cardiovascular risk. Through her interdisciplinary research, Dr. Mullington has advanced understanding of how optimizing sleep can promote heart health. Disclosures: Grant/Contract: Brigham and Women’s Hospital, Duke Clinical Research Institute, NYU Langone Medical Center Lee A. Surkin, MD, FACC, FCCP, FASNC, FAASM, is a triple board-certified physician in Cardiovascular Disease, Nuclear Cardiology and Sleep Medicine. He has been in clinical practice since 1997 and is the founder of the American Academy of Cardiovascular Sleep Medicine. Dr. Surkin focuses on prevention, early detection and integrated care to support cardiovascular and sleep health. Disclosures: Consultant: Jazz Pharmaceuticals Inc. Relationship disclosures within the past 24 months: The American Heart Association is committed to ensuring balance, independence, objectivity and scientific rigor in its certified educational activities. All faculty, planners and contributors in a position to control the content for a Heart-sponsored activity are required to disclose to the activity audience any financial relationships regardless of the amount during the prior 24 months with (1) the manufacturer(s) of any ineligible company product(s) and/or interest(s) of ineligible companies regardless of relation to the content of the activity and (2) any ineligible company supporters of the activity. When an unlabeled use of a commercial product or an investigational use not yet approved for any purpose is discussed during an educational activity, the faculty must disclose that the product is not labeled for the use under discussion or that the product is still investigational.
4 Publisher’s Note Hypertension, Sodium and Sleep: A Toolkit for Clinicians is published by Ascend Media. 401 SW Ward Road, Suite 210, Lee’s Summit, MO 64081 © 2026 American Heart Association, Inc., a 501(c)(3) not-for-profit. All rights reserved. Unauthorized use prohibited. All references and data are as of June 2026.
A Toolkit for Clinicians Hypertension, Sodium and Sleep 5 Modifiable Risk Factors The persistent burden of hypertension and inadequate blood pressure control are influenced by common modifiable risk factors through diet and/or medication.4,5 These include, but are not limited to: Hypertension remains one of the most actionable determinants of cardiovascular morbidity and mortality. Sodium exposure — derived from both diet and medications — is a clinically meaningful and fully modifiable driver of elevated blood pressure and long-term cardiometabolic risk. Emerging evidence also highlights sleep health as an underrecognized contributor to sodium sensitivity and abnormal nocturnal blood pressure regulation. Integrating sodium assessment, medication review and sleep screening offers clinicians an immediate opportunity to uncover reversible contributors to poor blood pressure control. Hypertension is a persistent elevation in arterial blood pressure. The 2025 American Heart Association/American College of Cardiology High Blood Pressure Guideline categorizes blood pressure across a spectrum of increasing severity, with elevated blood pressure as 120 to 129 mm Hg systolic and <80 mm Hg diastolic; stage 1 hypertension as 130 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic; and stage 2 hypertension as ≥140 mm Hg systolic or ≥90 mm Hg diastolic.36 Hypertension imposes excessive force on arterial walls, increasing the risks of cardiovascular disease if untreated. U.S. Epidemiology In the United States, the prevalence of hypertension (defined as ≥130/80 mm Hg or use of antihypertensive medication) among adults was 47.7% between August 2021 and August 2023, increasing markedly with age, from 23.4% in those aged 18-39, to 52.5% in those aged 40-59, and 71.6% for those aged ≥60 years.2 Individual awareness of having hypertension has been stable, at approximately 60%. More than half of affected adults receive antihypertensive therapy, and only about one in five achieve guidelinerecommended control (<130/80 mm Hg), highlighting substantial gaps across the awareness, treatment and control cascade.2 Hypertension at a Glance z stroke and heart failure risk 13% z ischemic heart disease risk 8% z cardiovascular mortality 5% A 5 mm Hg reduction in systolic blood pressure significantly lowers cardiovascular risk:3 Mean arterial pressure (MAP) is the average blood pressure within the arteries during a cardiac cycle and is calculated as: diastolic blood pressure + 1/3 (systolic blood pressure − diastolic blood pressure). Where CO = heart rate (HR) × stroke volume (SV), and SV is modulated by preload (venous return/blood volume), afterload (arterial resistance) and contractility. MAP = Cardiac Output (CO) × Total Peripheral Resistance (TPR) Among these modifiable risk factors, excessive sodium intake plays a central role in blood pressure regulation. Mechanisms include extracellular volume expansion that increases preload and cardiac output (CO), increased total peripheral resistance (TPR) and endothelial dysfunction.6,7 excessive sodium through diet and/or medication obesity physical inactivity alcohol/ tobacco use x suboptimal adherence to blood pressure therapy poor sleep quality poor dietary food choice CO TPR Mean Arterial Pressure (MAP) x =
The magnitude of blood pressure reduction achieved with sodium reduction can be comparable to that observed with first‑line antihypertensive therapies in some populations, underscoring sodium exposure as a high‑impact, clinically actionable target. Dietary sodium intake is difficult to validly capture through questionnaires and often is missing other sources of sodium, such as medications. The gold-standard method of estimating sodium intakes in individuals is from 24-hour urinary sodium excretion.6,8 Close to four decades ago, the Intersalt Cooperative Research Group noted a significant linear association between sodium excretion and blood pressure.9 More recently, a study of more than 100,000 adults from 18 countries showed a positive linear association between urinary sodium excretion and blood pressure.10 This relationship was stronger with higher sodium levels, in people with hypertension, and as age increased. In contrast, higher potassium excretion was associated with lower blood pressure, and this effect was strong in people with hypertension and increased age.10 The DASH‑Sodium Trial remains one of the most influential studies demonstrating the effect of sodium intake on blood pressure and cardiovascular risk. In this randomized trial, adults with elevated blood pressure were assigned to either a typical American diet or the DASH diet and exposed to three different sodium levels (high, medium, low). The study showed a clear, dose‑dependent relationship: Lower sodium intake resulted in significant reductions in blood pressure and estimated 10‑year ASCVD risk. Notably, the greatest benefit was observed when low sodium intake was combined with the DASH dietary pattern, yielding a –14.1% reduction in estimated cardiovascular risk, reinforcing the synergistic effect of dietary quality and sodium restriction.11,12 The original DASH trial and its sodium‑reduction extension further clarified the independent and additive roles of diet and sodium. The DASH diet alone — rich in fruits, vegetables, and low‑fat dairy — produced meaningful reductions in systolic blood pressure (approximately 5.5 mm Hg). However, when sodium intake was further reduced, blood pressure declined even more substantially, particularly among individuals with stage 1 hypertension. These findings established that while overall dietary pattern is important, sodium reduction provides an additional and clinically significant benefit, especially in higher-risk populations.11,12 More recently, the 2023 JAMA Sodium Crossover Trial provided rigorous, contemporary evidence supporting these earlier findings. In this controlled feeding study of adults aged 50–75 (including both normotensive and hypertensive individuals), participants transitioned between high- and low-sodium diets. The results showed that reducing sodium intake led to an average decrease of 8 mm Hg in systolic blood pressure, with nearly three-quarters of participants experiencing a measurable reduction. Importantly, the magnitude of this effect was comparable to that of firstline antihypertensive medications, underscoring sodium reduction as a potent, nonpharmacologic intervention.13 Taken together, these landmark studies consistently demonstrate a causal and graded relationship between sodium intake and blood pressure, with lower sodium intake leading to meaningful reductions in hypertension and cardiovascular risk. They also highlight that dietary strategies combining sodium restriction with healthful eating patterns (such as DASH) provide the greatest benefit. This body of evidence forms the foundation for current clinical guidelines recommending sodium reduction as a central component of hypertension prevention and management.11,12,13 6 The Relationship Between Sodium Intake and Hypertension Due to these studies, it is now well accepted that reducing sodium intake is important for dietary management of hypertension.
7 A Toolkit for Clinicians Hypertension, Sodium and Sleep This creates a reinforcing cycle in which sleep disruption and hypertension perpetuate one another, highlighting the importance of recognizing and treating sleep disorders as part of comprehensive blood pressure management strategies.15 The relationship between sleep and blood pressure is also bidirectional. Elevated nocturnal blood pressure can lead to pressure natriuresis and nocturia, resulting in sleep fragmentation and repeated awakenings. The Relationship Between Sleep and Hypertension Epidemiological evidence demonstrates a strong association between sleep health and blood pressure regulation, with both insufficient and disrupted sleep contributing to an increased risk of hypertension. Short sleep duration and poor sleep quality are linked to sympathetic nervous system activation and impaired nocturnal blood pressure dipping, all of which promote elevated cardiovascular risk. Observational data further suggest that sleep disturbances and short sleep duration are associated with a higher incidence of hypertension, particularly in women, even after adjustment for lifestyle and cardiometabolic factors.14,15,16 Sleep disorders contribute to hypertension risk through distinct but overlapping mechanisms. Obstructive sleep apnea (OSA) is strongly associated with hypertension and resistant hypertension, driven by intermittent hypoxia, oxidative stress and sustained sympathetic activation, resulting in increased vascular tone and abnormal blood pressure regulation. Other disorders, including insomnia, are associated with chronic hyperarousal and heightened cardiometabolic risk. The prevalence and risk of developing cardiovascular, cardiometabolic and renal comorbidities has also been shown to be elevated in individuals with narcolepsy and idiopathic hypersomnia compared with those without these conditions.34,35 Across these conditions, disruption of normal sleep patterns contributes to nocturnal hypertension phenotypes, which are strongly linked to adverse outcomes.17,18,19 Sleep insufficiency is an important contributor to cardiometabolic risk, acting through behavioral and metabolic pathways such as increased caloric intake, higher sodium consumption and accumulation of visceral adiposity. These changes contribute to elevated blood pressure and may also worsen coexisting sleep disorders such as OSA. Sodium-related fluid retention and redistribution during sleep can promote upper airway narrowing and exacerbate sleep-disordered breathing, further compounding hypertension risk.17,18,20
8 Sodium Is a Key, Modifiable Driver of Blood Pressure Excess sodium intake plays a central role in the development and progression of hypertension. Evidence from epidemiologic studies and randomized clinical trials demonstrates a direct, dose-dependent relationship between sodium intake and blood pressure.6,11,12 z Higher sodium intake is associated with higher blood pressure z Lower sodium intake leads to meaningful reductions in blood pressure Excess sodium intake is also associated with increased cardiovascular risk. Observational data suggest that each 1,000 mg increase in daily sodium intake is associated with approximately an 18% increase in cardiovascular events, highlighting the clinical importance of sodium reduction for both blood pressure control and Why Sodium Matters in Hypertension and Cardiovascular Health Clinical Considerations The magnitude of blood pressure reduction with sodium intake may vary based on patient characteristics. Greater reductions are often observed in: z Older adults z Individuals with hypertension z Patients with obesity or metabolic disease Some individuals may exhibit greater blood pressure responsiveness to sodium intake, often referred to as salt-sensitive blood pressure (salt-sensitive BP). Salt sensitivity refers to a physiological tendency in which blood pressure changes significantly in response to sodium (salt) intake. Individuals with salt-sensitive BP may experience a notable rise in blood pressure when consuming a higher sodium diet and a reduction in blood pressure when sodium intake is lowered.8 However, salt sensitivity is not typically used to guide routine clinical decision-making, and current guidelines recommend sodium reduction broadly rather than targeting specific subgroups.1 long-term cardiovascular health.21 Most Adults Exceed Recommended Sodium Intake Average sodium intake in the United States is approximately 3,400 mg per day, exceeding the American Heart Association recommended maximum of 2,300 mg per day.21 This excess contributes to: z High prevalence of hypertension z Suboptimal blood pressure control across populations Sodium Reduction Is Effective Across Populations Reducing sodium intake is a foundational, evidencebased strategy for both prevention and management of hypertension.11,12,13 z Lowers blood pressure in individuals with and without hypertension z Produces consistent effects across diverse populations z May achieve reductions comparable to first-line antihypertensive therapies in some individuals Clinical Takeaways1 1 2 3 Sodium reduction is a core component of guideline-directed hypertension management. Recommendations apply to all adults, not just select populations. Clinicians should routinely: { Assess sodium intake from diet and medications { Counsel patients on practical strategies to reduce sodium intake { Reinforce sodium reduction as part of overall cardiovascular risk reduction
9 A Toolkit for Clinicians Hypertension, Sodium and Sleep Converting Sodium to Salt and Salt to Sodium Fundamental to reducing sodium and salt intake is understanding how salt relates to recommended daily consumption of sodium and knowing the relationship between salt (sodium chloride) and sodium. To figure out how much sodium is in a given amount of salt, divide the salt amount by 2.5 because salt consists of 40% sodium and 60% chloride by weight. On the other hand, to convert recommended sodium intake to salt consumption, multiply sodium by 2.5.23 Some practical conversions are listed below: z 1,000 mg (1 g) of sodium = 2,500 mg (2.5 g) of salt z 2,300 mg of sodium (recommended daily limit) = 5,750 mg (5.8 g) of salt z 1,500 mg of sodium (ideal target to prevent or treat hypertension) = 3,750 mg (3.8 g) of salt1 This unit conversion is also important for understanding the sodium content of medications. In the United States and Canada, medication labels and scientific publications typically report sodium content in milligrams, whereas some countries report salt (sodium chloride) content in grams. For example, a medication containing 1,500 mg of sodium is equivalent to approximately 3,750 mg (3.8 g) of salt, an amount that is consistent with guideline recommended targets to prevent or treat hypertension.23 For practical purposes, it is also important to recognize that 1 teaspoon of table salt contains approximately 2,330 mg to 2,400 mg of sodium, which corresponds to the recommended daily upper limit of sodium intake.23 Practical Sodium Reduction Strategies Clinicians Can Use in Routine Care Within this context, sodium reduction and sleep optimization represent first-line, nonpharmacologic levers that can meaningfully improve blood pressure control — particularly in patients with early-life onset conditions, cumulative risk or unexplained treatment resistance. Unlike fixed risk factors, sodium exposure is fully modifiable and directly influenced by clinical decision-making and patient counseling.1,15 To summarize, the clinical implications of hypertension are difficult to overstate, particularly given its often silent progression and cumulative end organ damage over time. Unlike fixed or nonmodifiable risk factors, hypertension is both measurable and treatable, and a large body of randomized trial evidence demonstrates that lowering blood pressure meaningfully reduces stroke, myocardial infarction, heart failure, kidney disease progression and mortality.3 Importantly, effective management is achievable through a combination of well-established nonpharmacologic strategies such as sodium reduction, weight optimization and behavioral interventions focused on sleep, diet and physical activity, together with a broad range of proven pharmacologic therapies. This makes hypertension one of the most impactful and actionable targets in cardiovascular risk prevention. z all-cause mortality 13% z major cardiovascular disease events 20% z coronary heart disease events 17% z stroke events 27% z heart failure events 28% Every 10 mm Hg reduction in systolic blood pressure significantly reduces the risk of:3 Even more modest blood pressure reduction, by as little as 5 mm Hg on average, can lead to making meaningful gains in the prevention of incidents or recurrent cardiovascular disease.3 Extensive evidence supports the association between blood pressure lowering approaches and improved health outcomes. Findings from a systematic review and meta analysis of studies comprising more than 600,000 adults indicate that across a range of different baseline blood pressure levels and patient groups:22
10 Sodium in Medications Sodium-containing medications represent an overlooked and often cliniciancontrolled source of chronic sodium exposure. In patients requiring long-term pharmacotherapy, medications can contribute substantial sodium loads that may approach or exceed recommended daily intake, potentially undermining blood pressure control even when dietary recommendations are followed.24,25 Medications, including those obtained over the counter, prescribed for oral use or intravenous medications and even those used as colonoscopy preparations, can contain significant amounts of sodium.24,25 Over-the-counter medications that are effervescent formulations may have especially high sodium content. These include effervescent vitamin supplements (average of 378 mg/tablet), effervescent pain/cold medications including effervescent acetaminophen (approximately 450 mg/dose), and effervescent alendronate (650 mg/tablet). Some liquid antacids may have up to 400 mg/day of sodium at recommended dosing. Omeprazole/sodium bicarbonate has between 300 mg and 400 mg of sodium per dose, but standard omeprazole has minimal sodium.24,25 Certain gastrointestinal and bowel‑preparation medications may contribute clinically meaningful sodium exposure, particularly with repeated use or in individuals with hypertension or salt sensitivity. When available, lower‑sodium alternatives should be considered as part of comprehensive sodium assessment. High sodium oxybate formulations used to treat narcolepsy can contribute to substantial medication‑derived sodium exposure. At higher therapeutic doses, nightly sodium intake from high-sodium oxybates may exceed 1,500 mg at the highest recommended dose, approaching or surpassing recommended daily sodium limits, which may adversely affect blood pressure control when used chronically for a lifelong condition. The lower‑sodium formulation of twice‑nightly oxybate contains approximately 92% less sodium — about 1,500 mg less per night at the maximum approved dose — and has been associated in a single-arm switch study with significant reductions in 24‑hour ambulatory blood pressure six weeks after switching from higher‑sodium twice‑nightly formulations. Observational data also suggest a higher risk of incident hypertension among users of high‑sodium oxybate compared with noninitiators, underscoring the clinical relevance of medication‑related sodium burden.24,25 Intravenous medications, including certain antibiotics, may contribute clinically meaningful sodium exposure, particularly with repeated dosing or in patients with hypertension or salt sensitivity. Medication‑related sodium exposure should be considered as part of comprehensive sodium assessment. Sodium in Foods Sodium in foods is generally found as an added ingredient for preservation in processed foods. Most natural food sources are low in sodium with lowest levels found in fruits and vegetables, legumes and whole grains. Animal products, such as eggs, meats, and seafood contain sodium, with seafood obtained from saltwater (for example, mussels, shrimp, sardines) containing higher amounts. Canning foods and curing meats involve the addition of salt for preservation and flavor enhancement and thus these processes increase the food’s sodium content. Clinicians can encourage individuals to buy no-salt-added or low-sodium versions and rinse foods prior to use or consumption as effective strategies to reduce sodium intake.23 Patients should also be aware of “hidden” sources of sodium, such as breads and baked goods, ice cream and prepared frozen entrées. Comparing food labels, which are required to display the food’s sodium content, is essential in making the most healthful choice. Since sodium is ubiquitous in the modern food supply, patients should be discouraged from adding salt at the table to stay within the sodium intake limits. According to the American Heart Association, this should be <2,300 mg/day; ideally, <1,500 mg/day.1 Intravenous medications Gastrointestinal preparations Sodium oxybate formulations Over-the-counter medications Medication-related sodium exposure may contribute meaningfully to total sodium intake and is an important consideration in the prevention and management of hypertension. 24
A Toolkit for Clinicians Hypertension, Sodium and Sleep 11 Sleep as a Modifiable Risk Factor in Hypertension z Inconsistent sleep–wake patterns over time, an aspect of sleep regularity and timing, are associated with increased prevalence of hypertension.26 z Longer sleep onset latency, a component of sleep quality, may be associated with hypertension in both men and women after adjustment for age, educational level, body mass index, smoking, alcohol use, sitting time and other sleep variables.28 z Short sleep duration is associated with higher blood pressure and increased prevalence of hypertension.14,29 z Long sleep duration may also be associated with higher blood pressure and hypertension, although findings across studies are mixed likely due to residual confounding.29 Several sleep health dimensions are associated with increased blood pressure and hypertension risk. Sleep is multidimensional. Although a standard definition of multidimensional sleep health has yet to be established, common modifiable sleep dimensions include regularity/rhythmicity, satisfaction/ quality, alertness/sleepiness, timing, efficiency, duration, disturbed sleep and sleep architecture.15 Sleep duration, an indicator of sleep health, was added to the American Heart Association’s concept of cardiovascular health creating the Life’s Essential 8.27 z Disturbed sleep is an underrecognized contributor to blood pressure dysregulation. Individuals with sleep disorders characterized by disrupted nighttime sleep, such as obstructive sleep apnea (OSA) and narcolepsy, are at increased risk of developing hypertension.17,20,37 z Other primary sleep disorders, which may increase hypertension risk through hyperarousal and autonomic dysregulation, include restless legs syndrome, narcolepsy, idiopathic hypersomnia and REM sleep behavior disorder. Although these conditions have been associated with alterations in nocturnal blood pressure regulation, data linking these conditions directly to hypertension remains limited.20 z Multidimensional sleep health composite scores, which integrate multiple sleep dimensions into a single measure, demonstrate that better overall sleep health is associated with lower hypertension risk and lower systolic and diastolic blood pressure.17
12 z Increased sodium intake and disturbed sleep have been found to be separately associated with increased risk of hypertension. However, research in the past decade has demonstrated that sodium intake and sleep are connected through several biological processes including, but not limited to, regulation of blood pressure, fluid balance and sleep-related physiology.6,14 z Recent studies have shown that higher sodium intake is associated with poorer sleep quality and shorter sleep duration across populations.30 z Higher sodium intake may also contribute to sleep disruption through effects on fluid balance, including increased nocturnal urination. Frequent nighttime urination can fragment sleep by interrupting sleep periods and deeper stages of sleep.6 z Sodium intake may also influence sleep through its effects on fluid balance and overnight fluid redistribution, which can affect sleep quality and contribute to sleep-related disturbances.6 z In analyses of data from the U.K. Biobank, researchers found that in a sample of more than 500,000 adults aged 40–69 years, those who reported more frequent addition of salt to foods had a higher risk of developing OSA during a median follow-up of 12.3 years, even after accounting for a number of demographic, behavioral and clinical factors.31 z In patients with hypertension, higher urinary sodium excretion (an indirect measure of sodium intake) has been associated with greater severity of sleepdisordered breathing, supporting a role for sodium-related fluid shifts in overnight respiratory physiology.32 z Interventional studies have also demonstrated that reducing sodium intake or fluid volume can improve sleep-related breathing disturbances. In a randomized trial of men with obstructive sleep apnea (OSA), participants assigned to sodium restriction or diuretic therapy had significant improvements in OSA severity after one week compared with placebo, indicating that sodiumrelated fluid shifts influence sleep and blood pressure regulation.32 z Although further research is needed to fully characterize the bidirectional relationship between sodium intake and sleep, existing mechanistic, epidemiologic and interventional evidence is sufficient to support clinical action. Integrating sodium reduction and sleep optimization into hypertension care offers an immediate opportunity to address converging modifiable risks and improve long‑term cardiovascular outcomes. The Sodium–Sleep Connection: Counseling Patients on Overlapping Lifestyle Factors Improving Sleep Duration to Support Blood Pressure Control Hypertension management has traditionally focused on diet, physical activity, weight and pharmacotherapy, which are all core components of blood pressure management. Yet sleep represents a frequently overlooked and modifiable determinant of blood pressure regulation. Short sleep duration, poor sleep quality and OSA are independently associated with incident hypertension and resistant hypertension.14,17 Given the associations linking short sleep duration with increased risk of hypertension and adverse cardiovascular outcomes in epidemiological studies, and the physiological evidence that short sleep is associated with increased blood pressure in experimental settings, several behavioral interventional studies have been designed to increase sleep duration in children and adults.14,29 Methods for increasing sleep duration have been tested and involve adherence to changes in scheduling of the bed period and often include multiple behavioral strategies to increase sleep time. These approaches have been shown to increase total sleep time, although evidence still remains limited.29 Research investigating the efficacy of sleep extension as an intervention to lower blood pressure in otherwise healthy adults is in its early phases. Some studies have shown initial promise, and others are ongoing.14 More work is needed to delineate target populations and appropriately designed interventions to facilitate the manipulation of sleep in personalized blood pressure management.
13 A Toolkit for Clinicians Hypertension, Sodium and Sleep Incorporating Sleep Screening Into Personalized Hypertension Care Plans Incorporating structured sleep screening into routine hypertension care may help clinicians identify reversible contributors that may otherwise blunt treatment response, especially given evidence that treating sleep impairments (e.g., OSA) can confer benefits for blood pressure management.33 Checklist for sleep screening Obtain a history of sleep health (for example, sleep duration, satisfaction with sleep, sleep timing) Routine sleep screening using brief tools (e.g., the STOP‑BANG for OSA risk) and, where appropriate, wearables may be particularly relevant among individuals at higher risk for sleep disorders:1,17 { Resistant hypertension (similar to contemporary recommendations to screen for primary aldosteronism) { Nondipping or reverse dipping patterns on ambulatory monitoring { Atrial fibrillation or other arrhythmias { Irregular sleep schedules (such as shift workers)
14 6. Small reductions in systolic blood pressure (5–10 mmHg) yield large clinical benefits. These changes significantly reduce the risk of stroke, coronary heart disease, heart failure and cardiovascular death — highlighting the clinical value of identifying reversible contributors such as poor sleep and excess sodium.3 7. Excess sodium raises blood pressure through multiple physiologic mechanisms. Volume expansion, increased cardiac output, elevated peripheral resistance, endothelial dysfunction and altered nocturnal blood pressure regulation may contribute to sodium-driven hypertension.6 8. Salt sensitive BP is common and clinically relevant. Approximately 25% of the general population — and more than 50% of individuals with hypertension — exhibit salt sensitive BP, with higher prevalence among older adults, individuals who are Black and those with obesity, chronic kidney disease or metabolic syndrome. Importantly, sodium intake matters for those with and without salt sensitive BP.8 Integrating Sleep and Sodium Into Hypertension Care 9. Obstructive sleep apnea is strongly associated with resistant hypertension, and treatment can improve blood pressure control. Continuous positive airway pressure (CPAP) therapy produces modest but clinically meaningful blood pressure reductions, particularly in patients with uncontrolled or resistant hypertension.17,33 10. Routine sleep screening can be an important part of hypertension evaluation. Screening is especially important for patients with resistant or nocturnal hypertension, nondipping patterns, atrial fibrillation, obesity, hypersomnolence symptoms or shift work exposure. 11. Integrating sleep optimization, sodium reduction and medication review can help identify reversible drivers of suboptimal blood pressure control. Personalized care plans that address sleep health alongside dietary and pharmacologic sodium sources offer actionable opportunities to improve hypertension management and reduce long term cardiovascular risk. Key Takeaways What Clinicians Can Act on Today 1. Sleep is a modifiable and under-addressed determinant of blood pressure control. Short sleep duration, irregular sleep timing, poor sleep efficiency and sleep disorders — particularly obstructive sleep apnea — are independently associated with increased hypertension risk, resistant hypertension and adverse cardiovascular outcomes.17 2. Sleep disorders may amplify sodium-related blood pressure elevations. Conditions such as obstructive sleep apnea and hypersomnolence disorders are associated with abnormal nocturnal blood pressure patterns, heightened salt sensitivity and poorer blood pressure control, potentially magnifying the effects of excess sodium exposure.17,20 3. Medication-derived sodium is a clinician-controlled source of chronic sodium exposure. Effervescent tablets, antacids, high sodium oxybate, some analgesics and antibiotics can contribute ≥1 g/ day of additional sodium — an amount that may meaningfully raise blood pressure and cardiovascular risk, particularly in patients with hypertension or salt sensitivity.24 4. Dietary and medication sodium sources should be assessed together — not separately. Most adults already consume substantially more sodium than recommended from diet alone (~3,400 mg/day vs <2,300 mg/day; ideally <1,500 mg/day).21 Chronic medication use may further increase total sodium exposure, in some cases rivaling or exceeding dietary contributions, making sodium reduction through diet alone insufficient for many patients.24 Why Sleep and Sodium Matter for Blood Pressure 5. Hypertension affects nearly half of U.S. adults and remains a leading modifiable driver of cardiovascular, kidney and cerebrovascular disease. Even modest improvements in blood pressure control can translate into substantial reductions in morbidity and mortality.2 1 2 3 4 5 6 7 8 9 10 11
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