This cohort study evaluates the associations of excessive dietary sodium with all-cause and cause-specific mortality among predominantly low-income Black and White US residents.
Abstract
IMPORTANCE
Epidemiologic evidence regarding the outcomes of dietary sodium intake on mortality remains limited for low-income individuals, particularly Black people.
OBJECTIVE
To investigate the associations of excessive dietary sodium with all-cause and cause-specific mortality among predominantly low-income Black and White Americans.
DESIGN, SETTING, AND PARTICIPANTS
This cohort study included participants aged 40 to 79 years from the Southern Community Cohort Study who were recruited at Community Health Centers in 12 southeastern states from 2002 to 2009. Analyses were conducted between March 2022 and June 2023.
EXPOSURES
Dietary sodium intake was assessed using a validated food frequency questionnaire at baseline.
MAIN OUTCOMES AND MEASURES
Multivariable-adjusted Cox regression was used to estimate hazard ratios (HRs) and 95% CIs for mortality outcomes (all-cause, cardiovascular disease [CVD], coronary heart disease [CHD], stroke, heart failure, cancer, and other) associated with sodium intake. Nonlinear associations and population-attributable risk (PAR) of the mortality burden associated with excess sodium were further assessed.
RESULTS
Among the 64 329 participants, 46 185 (71.8%) were Black, 18 144 (28.2%) were White, and 39 155 (60.9%) were female. The mean (SD) age at study enrollment was 51.3 (8.6) years for Black participants and 53.3 (9.3) years for White counterparts. Mean (SD) dietary sodium intake was 4512 (2632) mg/d in Black individuals and 4041 (2227) mg/d in White individuals; 37 482 Black individuals (81.2%) and 14 431 White individuals (79.5%) exceeded the current dietary recommendations of 2300 mg/d. During a median (IQR) follow-up of 13.8 (11.3-15.8) years, 17 811 deaths were documented, including 5701 from CVD. After adjustment for potential confounders, in Black individuals, HRs per 1000-mg increase in daily sodium intake were 1.07 (95% CI, 1.03-1.10) and 1.08 (95% CI, 1.02-1.14) for deaths from total CVD and CHD, respectively; while in White individuals, the corresponding HRs were 1.08 (95% CI, 1.02-1.14) and 1.13 (95% CI, 1.03-1.23). No significant associations were found for cancer mortality. PAR estimates suggest that sodium intake above the recommended threshold may account for 10% of total CVD, 13% of CHD, and 30% of heart failure deaths in this low-income southern population.
CONCLUSIONS AND RELEVANCE
In this cohort study of 64 329 low-income Americans, nearly 80% of study participants consumed sodium exceeding the current recommended daily amount, which was associated with 10% to 30% of CVD mortality. Public health programs targeted to reduce sodium intake among this underserved population may be beneficial.
Key Points
Question
How is sodium intake associated with mortality outcomes among low-income Black and White Americans?
Findings
This cohort study of 64 329 Americans from the Southern Community Cohort Study found that approximately 80% of low-income Black and White Americans exceeded the recommended daily intake of sodium, which was associated with 10% to 30% of cardiovascular disease mortality.
Meaning
These findings suggest that approaches to lower sodium intake among underserved populations need to be established as the primary public health priority.
Introduction
Sodium is an essential nutrient for normal physiologic function, but excessive intake is associated with adverse health outcomes.1,2 For health promotion and disease prevention, the 2020 to 2025 Dietary Guidelines for Americans recommend less than 2300 mg of sodium per day.3 Most US adults, however, consume 3400 mg per day, which far exceeds the body’s needs.4
Excessive sodium consumption has been linked to elevated blood pressure, a major risk factor for cardiovascular disease (CVD),1,2 and can directly affect multiple target organs and tissues, including the brain, heart, kidneys, and bones, contributing to increased mortality hazards.5,6,7,8 A report from the National Health and Nutrition Examination Survey (NHANES) found 46% higher CVD mortality among people with high sodium diets.9 In another NHANES study, high sodium intake accounted for the largest portion of estimated diet-related cardiometabolic deaths among Americans.10 A meta-analysis of 25 prospective studies reported a 16% increase in all-cause mortality associated with high sodium intake.11 A cohort study of elderly Americans also found higher mortality among those who exceeded the recommendation, although statistical significance disappeared after adjustment for confounders.12 Epidemiologic evidence to date supports the mortality burden due to excessive sodium intake.2,13 Nevertheless, this burden remains overlooked in marginalized populations, especially Black Americans and individuals with low socioeconomic status (SES), who consume more high-sodium foods than others.14
In this cohort study of low-income Black and White Americans, we explored the racial and socioeconomic differences in daily sodium consumption. Furthermore, we investigated the associations of sodium intake with all-cause and cause-specific mortality (ie, CVD and its subtypes, cancer, and other diseases) and estimated the burden of mortality attributable to excess dietary sodium among this underserved population.
Methods
Study Population
This study is based on the Southern Community Cohort Study (SCCS), a prospective cohort to investigate the root causes of longstanding racial and ethnic disparities in health.15,16 With written informed consent, approximately 85 000 adults aged 40 to 79 years were recruited in 12 southeastern US states (Alabama, Arkansas, Florida, Georgia, Kentucky, Louisiana, Mississippi, North Carolina, South Carolina, Tennessee, Virginia, and West Virginia) from 2002 to 2009. About 86% of study participants were recruited at Community Health Centers (CHCs) that provide primary health care services to low-income individuals, who form the basis of the current study. A baseline survey was performed to collect self-reported information on sociodemographics, lifestyle, diet, and medical history. Among participants enrolled at CHCs, we excluded participants who reported implausible energy intake (<600 or >8000 kcal/d) or who had invalid follow-up information. Participants who self-reported a race other than Black or White were excluded due to their small sample size. The SCCS protocol was approved by the institutional review boards at Vanderbilt University Medical Center and Meharry Medical College. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline for cohort studies.
Exposure Assessment
Dietary data were collected using a food frequency questionnaire (FFQ) at baseline. The SCCS FFQ, containing 89 food items, was developed to capture the usual diet for Black and White Americans living in the southeastern US.17,18 Intakes of total energy, macronutrients, and micronutrients, including sodium, were estimated using the US Department of Agriculture Food Composition Databases.19 The overall validity of the FFQ was evaluated using correlation coefficients between FFQ and multiple 24-hour dietary recalls: 0.59 to 0.83 for macronutrients and 0.43 to 0.81 for micronutrients.19 In this study, dietary sodium intake was classified into 5 categories: the recommended level (<2300 mg/d), above recommendation by up to 50% (2300-3450 mg/d), more than 50% to 100% or less (3451-4600 mg/d), more than 100% to 200% or less (4601-6900 mg/d), and over 200% (>6900 mg/d).
Outcome Ascertainment
The survival status was ascertained by linking the Social Security Administration and the National Death Index through December 31, 2019. Underlying causes of death were defined using the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision: total CVD, I00-I99; coronary heart disease (CHD), I20-I25; stroke, I60-I69; heart failure, I50-I50.9; cancer C00-C97; and other diseases excluding external causes.
Statistical Analysis
Baseline characteristics across dietary sodium intake were compared using the χ2 test and the generalized linear model. Multivariable Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% CIs for all-cause and cause-specific mortality, using the recommended level as the reference. Additionally, HRs and 95% CIs per 1000-mg increase in daily sodium intake were evaluated. Follow-up time was treated as the time scale, calculated as total years from the date of enrollment to the date of death or censoring (ie, loss-to-follow-up or latest follow-up). The global goodness-of-fit test with Schoenfeld residuals found no violation against the proportional hazards assumption. All analyses were conducted separately among Black and White individuals, given the potential racial differences. Under the conceptual framework established from the literature review (eFigure in Supplement 1), factors for adjustment were chosen based on their association with sodium intake and mortality, including age at enrollment (years), sex (men or women), education (completed up to high school or completed beyond high school), annual household income (<$25 000 or ≥$25 000), marital status (married or living alone), medical insurance (no or yes), smoking status (never, former, or current with ≤20 or >20 pack-years), physical activity (sex-specific tertiles of total metabolic equivalent hours), alcohol consumption (none, ≤28, or >28 g/d of ethanol in men; none, ≤14, or >14 g/d in women), body mass index (BMI, calculated as weight in kilograms divided by height in meters squared; <30 or ≥30), total energy intake (kcal/d), and healthy eating index (score).20 Missingness (mostly <1%) was handled with imputation using median or mode values of nonmissing covariates. Potential nonlinear associations between sodium intake and mortality were assessed by using restricted cubic spline regression, with the reference as 2300 mg/d of sodium and 3 knots fitted at the 5th, 50th, and 95th percentiles. Stratified analyses were conducted, and interactions between sodium intake and strata variables were tested by the likelihood ratio test using the multiplicative interaction term. Population attributable risks (PARs) and corresponding 95% CIs were calculated with the following equation21:
| PAR = [P × (RR−1)]/{[P × (RR−1)]+1}, |
where P was the prevalence of dietary sodium intake, and RR was the relative risk (adjusted HRs in the current analyses).
A series of sensitivity analyses were performed by adjusting for history of hypertension or CVD and comorbidity index, excluding the first 2 years of observation, excluding individuals with history of CVD, and adopting competing risk models. All statistical analyses were conducted using SAS version 9.4 (SAS Institute), between March 2022 and June 2023. A 2-sided P value less than .05 was considered statistically significant.
Results
This study included 64 329 participants with a mean (SD) age at study enrollment of 51.3 (8.6) years for Black participants and 53.3 (9.3) years for White counterparts; 46 185 (71.8%) were Black, 18 144 (28.2%) were White, 39 155 (60.9%) were female, and 82.8% reported annual household income less than $25 000. The mean (SD) dietary sodium intake was 4512 (2632) mg/d for Black participants and 4041 (2227) mg/d for White participants. Those with the lowest income level (annual household income <$15 000) consumed more sodium each day, with a mean (SD) 4593 (2695) mg/d for Black individuals and 4145 (2314) mg/d for White individuals (eTable 1 in Supplement 1). Sodium consumption exceeded the current 2300 mg/d recommendation in 37 482 (81.2%) and 14 431 (79.5%) Black and White adults, respectively; these individuals were more likely to be young, male, less educated, lower earners, current smokers, and heavy alcohol drinkers (Table 1). When stratified by race (eTable 2 in Supplement 1), Black individuals with a history of CVD were less likely to fall into the high salt intake group, but their White counterparts showed no differences in sodium intake. In addition, Black individuals appeared to show lower educational attainment, earned less, lived without a partner, drank heavily (more than 28 g/day for men or more than 14g/day for women), high energy intake (mean 2703 kcal/day for black individuals vs. 2309 kcal/day for White individuals), and were more likely to have obesity, hypertension, and diabetes than White individuals (eTable 3 in Supplement 1).
Table 1. Baseline Characteristics of Study Participants.
| Baseline characteristics | Dietary sodium intake, No. (%), mg/da | P value | ||||
|---|---|---|---|---|---|---|
| <2300 (n = 12 416) | 2300-3450 (n = 16 109) | 3451-4600 (n = 12 651) | 4601-6900 (n = 13 729) | >6900 (n = 9424) | ||
| Enrollment age, mean (SD), y | 53.7 (9.2) | 53.1 (9.1) | 51.9 (8.7) | 50.7 (8.3) | 48.8 (7.2) | <.001 |
| Race | ||||||
| Black Americans | 8703 (70) | 10 917 (68) | 8943 (71) | 10 073 (73) | 7549 (80) | <.001 |
| White Americans | 3713 (30) | 5192 (32) | 3708 (29) | 3656 (27) | 1875 (20) | |
| Sex | ||||||
| Men | 2496 (20) | 4453 (28) | 4912 (39) | 7252 (53) | 6061 (64) | <.001 |
| Women | 9920 (80) | 11 656 (72) | 7739 (61) | 6477 (47) | 3363 (36) | |
| Education | ||||||
| Completed up to high school | 8251 (66) | 10 315 (64) | 8357 (66) | 9282 (68) | 6749 (72) | <.001 |
| Completed education beyond high school | 4165 (34) | 5794 (36) | 4294 (34) | 4447 (32) | 2675 (28) | |
| Annual household income | ||||||
| <$15 000 | 7465 (60) | 9337 (58) | 7618 (60) | 8533 (62) | 6220 (66) | <.001 |
| ≥$15 000 to <$25 000 | 2661 (22) | 3562 (22) | 2807 (22) | 3044 (22) | 2046 (22) | |
| ≥$25 000 to <$50 000 | 1539 (12) | 2148 (13) | 1569 (12) | 1591 (12) | 912 (10) | |
| ≥$50 000 | 751 (6) | 1062 (7) | 657 (6) | 561 (4) | 246 (2) | |
| Marital status | ||||||
| Married or living with a partner | 3927 (32) | 5635 (35) | 4321 (34) | 4358 (32) | 2466 (26) | <.001 |
| Living aloneb | 8489 (68) | 10 474 (65) | 8330 (66) | 9371 (68) | 6958 (74) | |
| Medical insurance | 7634 (61) | 9763 (61) | 7326 (58) | 7362 (54) | 4580 (49) | <.001 |
| Smoking status | ||||||
| Never | 5365 (43) | 6417 (40) | 4471 (35) | 4003 (29) | 2315 (25) | <.001 |
| Former | 2982 (24) | 3845 (24) | 2808 (22) | 2639 (19) | 1430 (15) | |
| Current with ≤20 pack-years | 2351 (19) | 3190 (20) | 2953 (23) | 3899 (28) | 3358 (36) | |
| Current with >20 pack-years | 1718 (14) | 2657 (16) | 2419 (19) | 3188 (23) | 2321 (25) | |
| Physical activityc | ||||||
| Low | 4955 (40) | 5791 (36) | 4221 (33) | 4317 (31) | 2447 (26) | <.001 |
| Middle | 4062 (33) | 5473 (34) | 4261 (34) | 4342 (32) | 2871 (30) | |
| High | 3399 (27) | 4845 (30) | 4169 (33) | 5070 (37) | 4106 (44) | |
| Alcohol consumptiond | ||||||
| None | 7257 (58) | 8559 (53) | 6056 (48) | 5662 (41) | 3256 (35) | <.001 |
| Moderate | 3996 (32) | 5656 (35) | 4539 (36) | 4887 (36) | 3296 (35) | |
| Heavy | 1163 (9) | 1894 (12) | 2056 (16) | 3180 (23) | 2872 (30) | |
| Body mass index, mean (SD) | 31.3 (7.5) | 31.2 (7.6) | 30.7 (7.7) | 29.8 (7.5) | 28.8 (7.3) | <.001 |
| Healthy eating index, mean (SD) | 60.5 (13.0) | 58.8 (12.4) | 56.6 (11.8) | 55.1 (10.8) | 54.2 (9.3) | <.001 |
| Disease history | ||||||
| Hypertension | 7660 (62) | 9694 (60) | 7151 (57) | 7168 (52) | 4363 (46) | <.001 |
| CVD | 1601 (13) | 2073 (13) | 1498 (12) | 1644 (12) | 1014 (11) | <.001 |
| Cause of death, No. | ||||||
| All causes | 3264 | 4331 | 3456 | 4011 | 2749 | NA |
| Total CVD | 1089 | 1392 | 1117 | 1227 | 876 | NA |
| Cancer | 736 | 942 | 796 | 944 | 614 | NA |
| Other diseases | 1233 | 1730 | 1299 | 1489 | 956 | NA |
Abbreviations: CVD, cardiovascular disease; NA, not applicable.
Mean (SD) intake was 4512 (2632) mg/d among Black individuals and 4042 (2227) mg/d among White individuals.
Included individuals who never married and those who were separated, divorced, widowed, or single.
Defined by tertiles of the total metabolic equivalent of task hours per week.
Defined as nondrinkers, 0 g/d; moderate drinkers, more than 0 but 28 or less g/d for men or more than 0 but 14 or less g/d for women; and heavy drinkers, more than 28 g/d for men or more than 14 g/d for women.
During a median (IQR) follow-up of 13.8 (11.3-15.8) years, 17 811 deaths were documented, including 5701 from CVD (2216 from CHD, 905 from stroke, 470 from heart failure, and 2110 from other), 4032 from cancer, and 6707 from other diseases. Compared with the recommended level of less than 2300 mg/d, higher sodium intake was associated with increased mortality (Table 2; eTable 4 in Supplement 1). Multivariable-adjusted HRs associated with intake greater than 6900 mg/d in Black individuals were 1.32 (95% CI, 1.07-1.63) for total CVD, 1.48 (95% CI, 1.05-2.09) for CHD, and 1.27 (95% CI, 1.04-1.56) for other diseases; for White individuals, HRs were 1.48 (95% CI, 1.04-2.10) for total CVD and 10.99 (95% CI, 3.04-39.76) for heart failure. In Black individuals, after adjustment for potential confounders, a 1000-mg increase in daily sodium intake was associated with a 3% higher risk of death from all-cause, 7% higher risk from total CVD (HR, 1.07; 95% CI, 1.03-1.10), 8% higher risk from CHD (HR, 1.08; 95% CI, 1.02-1.14). In White individuals, a 1000-mg increase in daily sodium intake was associated with an 8% higher risk from total CVD (HR, 1.08; 95% CI, 1.02-1.14), 13% higher risk from CHD (HR, 1.13; 95% CI, 1.03-1.23), and 55% higher risk of death from heart failure. Significant interactions between sodium intake and race were found for all-cause (P for interaction <.001), total CVD (P for interaction = .01), and heart failure mortality (P for interaction = .03).
Table 2. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake.
| Causes of death | No. of participants (No. of deaths) | Hazard ratio (95% CI) by dietary sodium intake, mg/da | 1000-mg/d increment | P for interactionb | ||||
|---|---|---|---|---|---|---|---|---|
| <2300 | 2300-3450 | 3451-4600 | 4601-6900 | >6900 | ||||
| All-cause | ||||||||
| Black Americans | 46 185 (12 256) | 1 [Reference] | 1.02 (0.96-1.08) | 1.08 (1.01-1.15) | 1.10 (1.01-1.19) | 1.21 (1.07-1.36) | 1.03 (1.01-1.05) | <.001 |
| White Americans | 18 144 (5555) | 1 [Reference] | 1.06 (0.97-1.15) | 0.98 (0.89-1.09) | 1.13 (1.00-1.27) | 1.09 (0.91-1.32) | 1.01 (0.98-1.04) | |
| Total CVD | ||||||||
| Black Americans | 46 185 (4112) | 1 [Reference] | 1.00 (0.90-1.10) | 1.10 (0.98-1.23) | 1.11 (0.96-1.27) | 1.32 (1.07-1.63) | 1.07 (1.03-1.10) | .01 |
| White Americans | 18 144 (1589) | 1 [Reference] | 1.09 (0.94-1.27) | 1.03 (0.85-1.24) | 1.18 (0.94-1.48) | 1.48 (1.04-2.10) | 1.08 (1.02-1.14) | |
| CHD | ||||||||
| Black Americans | 46 185 (1480) | 1 [Reference] | 0.96 (0.81-1.14) | 1.21 (1.00-1.46) | 1.21 (0.96-1.53) | 1.48 (1.05-2.09) | 1.08 (1.02-1.14) | .33 |
| White Americans | 18 144 (736) | 1 [Reference] | 1.05 (0.83-1.32) | 1.04 (0.79-1.37) | 1.16 (0.83-1.62) | 1.35 (0.80-2.28) | 1.13 (1.03-1.23) | |
| Stroke | ||||||||
| Black Americans | 46 185 (701) | 1 [Reference] | 0.95 (0.75-1.21) | 0.88 (0.66-1.16) | 0.99 (0.71-1.37) | 1.10 (0.67-1.80) | 1.11 (1.03-1.20) | .39 |
| White Americans | 18 144 (204) | 1 [Reference] | 1.12 (0.73-1.72) | 1.13 (0.66-1.92) | 1.64 (0.86-3.16) | 1.17 (0.39-3.54) | 1.02 (0.86-1.21) | |
| Heart failure | ||||||||
| Black Americans | 46 185 (354) | 1 [Reference] | 1.15 (0.84-1.59) | 1.07 (0.72-1.59) | 1.06 (0.65-1.74) | 1.29 (0.60-2.79) | 1.11 (0.98-1.26) | .03 |
| White Americans | 18 144 (116) | 1 [Reference] | 1.00 (0.56-1.77) | 1.24 (0.60-2.54) | 2.50 (1.05-5.93) | 10.99 (3.04-39.76) | 1.55 (1.20-2.01) | |
| Cancer | ||||||||
| Black Americans | 46 185 (2878) | 1 [Reference] | 0.92 (0.82-1.04) | 1.02 (0.89-1.16) | 1.04 (0.89-1.22) | 1.05 (0.82-1.33) | 1.00 (0.96-1.03) | .18 |
| White Americans | 18 144 (1154) | 1 [Reference] | 1.16 (0.97-1.39) | 1.19 (0.96-1.49) | 1.39 (1.06-1.81) | 1.30 (0.85-1.98) | 0.99 (0.93-1.06) | |
| Other diseases | ||||||||
| Black Americans | 46 185 (4444) | 1 [Reference] | 1.13 (1.03-1.25) | 1.12 (1.00-1.25) | 1.17 (1.03-1.34) | 1.27 (1.04-1.56) | 1.04 (1.01-1.07) | .32 |
| White Americans | 18 144 (2263) | 1 [Reference] | 1.03 (0.91-1.17) | 0.96 (0.82-1.12) | 1.02 (0.85-1.24) | 0.81 (0.60-1.10) | 0.97 (0.92-1.01) | |
Abbreviations: CHD, coronary heart disease; CVD, cardiovascular disease.
Adjusted for age, sex, education, income, marital status, medical insurance, smoking status, physical activity, alcohol consumption, body mass index, total energy intake, and healthy eating index.
Tested by the likelihood ratio test, comparing models with and without the multiplicative interaction term of sodium intake (continuous) × race.
In stratified analyses (Figure 1), overall association patterns between excess sodium intake and total CVD mortality in Black individuals appeared to be more evident among never-smokers than among ever-smokers (P for interaction = .002): multivariable-adjusted HRs for more than 6900 mg/d vs less than 2300 mg/d were 1.67 (95% CI, 1.11-2.52) for never smokers, 1.08 (95% CI, 0.66-1.76) for former smokers, 1.26 (95% CI, 0.87-1.83) for current smokers with 20 or fewer pack-years, and 1.30 (95% CI, 0.84-2.01) for current smokers with more than 20 pack-years. Meanwhile, White individuals with a history of CVD showed over 2-fold increased CVD mortality in relation to sodium intake more than 6900 mg/d, but no association was observed in their CVD-free counterparts: HRs for more than 6900 mg/d vs less than 2300 mg/d, 2.37 (95% CI, 1.29-4.33) and 1.16 (95% CI, 0.75-1.80), respectively (P for interaction = .02). Restricted cubic spline analyses suggested that the association between dietary sodium intake and total CVD mortality follows a near linear dose-response pattern in both Black and White individuals (Figure 2). No significant dose-response associations were observed for any other mortality outcomes. The overall PAR associated with exceeding 2300 mg of dietary sodium per day was approximately 10% for total CVD mortality, 13% for CHD mortality, and about 30% for heart failure mortality in our underserved population (Figure 3). The sodium-mortality associations were not changed in sensitivity analyses, indicating the robustness of our findings (eTable 5, eTable 6, eTable 7, eTable 8, and eTable 9 in Supplement 1).
Figure 1. Total Cardiovascular Disease Mortality in Relation to Dietary Sodium Intake: Subgroup Analysis by Baseline Characteristics.
Hazard ratios (HRs) and 95% CIs for more than 6900 mg/d vs less than 2300 mg/d were estimated after adjustment for age, sex, education, income, marital status, medical insurance, smoking, physical activity, alcohol consumption, body mass index, total energy intake, and healthy eating index. Living alone included individuals who never married and those who were separated, divorced, widowed, or single. Physical activity was categorized by tertiles of the total metabolic equivalent of task hours per week. Alcohol consumption was defined as nondrinkers, 0 g/d; moderate drinkers, more than 0 but 28 or less g/d for men or more than 0 but 14 or less g/d for women; and heavy drinkers, more than 28 g/d for men or more than 14 g/d for women. Interaction was tested by the likelihood ratio test, comparing models with and without the multiplicative interaction term of sodium intake (continuous) × each stratum variable. Error bars represent the 95% CIs.
Figure 2. Dose-Response Association of Dietary Sodium Intake With Total Cardiovascular Disease Mortality.
Solid lines represent the hazard ratios and shaded areas represent the 95% CIs. The reference was set at 2300 mg/d, with 3 knots fitted at the 5th, 50th, and 95th percentiles. Participants with the highest 1% of sodium intake were excluded to reduce the noise of extreme outliers. All models were adjusted for age, sex, enrollment source, education, income, marital status, medical insurance, smoking, physical activity, alcohol consumption, body mass index, total energy intake, and healthy eating index.
Figure 3. Population-Attributable Risk (PAR) for Cause-Specific Mortality by Dietary Sodium Intake Among Low-Income Black and White Americans.
The calculated PARs represent a value of 0 if they were negative for mortality outcomes. Error bars represent the 95% CIs for the population-attributable risk estimates. CHD indicates coronary heart disease; CVD, cardiovascular disease; PAR, population-attributable risk.
Discussion
In this cohort study of low-income Black and White Americans, we found approximately 80% of study participants exceeded current guidelines for sodium intake of 2300 mg or less per day. The average daily intake was 4512 mg in Black Americans and 4041 mg in White Americans—much higher than the average estimate of 3400 mg/d among the general US adult population.4 Excessive sodium intake was associated with increased hazards of mortality, mainly due to CVD-related deaths, after adjusting for potential confounders, including behavior factors and dietary quality. PAR analyses suggest that excessive dietary sodium may be responsible for approximately 10% of total CVD deaths and about 30% of heart failure deaths in this low-income population.
High sodium intake can promote oxidative stress, endothelial dysfunction, and increased arterial stiffness22 and further lead to an imbalance in immune homeostasis and a persistent proinflammatory state,23,24,25,26 all of which are significant predictors of CVD and hypertension. The Dietary Approaches to Stop Hypertension (DASH) diet sodium trial demonstrated blood pressure decreases with reduction in sodium intake,27 as well as improvements in vascular endothelial function.28 Given the biological connection between high sodium intake and blood pressure in left-ventricular hypertrophy,29 it was hypothesized that the harmful effects of excess sodium would be further intensified among hypertensive individuals, particularly Black people who have significantly higher rates of hypertension than other populations.30 However, in the current study, we found no evidence of effect modification by hypertension in the sodium-CVD mortality association. Furthermore, additional adjustments for history of CVD and hypertension did not change the primary associations. These findings suggest that high sodium diets may confer detrimental health consequences beyond their effects on hypertension.
The role of dietary sodium in increasing the risk of death, particularly from CVD, has been consistently reported. A meta-analysis of 23 cohort studies and 2 follow-up studies of randomized clinical trials reported a 16% increase in all-cause mortality associated with high sodium intake and a 9% risk reduction associated with low sodium intake.11 The third NHANES study showed 20% higher all-cause mortality per 1000-mg increase in daily sodium intake.9 Also, diets high in sodium were associated with an increased risk of congestive heart failure among overweight Americans31 and an increased risk of death among patients diagnosed with ambulatory heart failure.32 Meanwhile, a 10-year follow-up study of 2642 elderly Americans found nonsignificant positive associations between consuming more than 2300 mg/d of sodium and all-cause mortality, incident CVD, or incident heart failure.12 Another systematic review and meta-analysis showed that sodium intake was positively associated with deaths from CHD (RR, 1.32; 95% CI, 1.13-1.53) and stroke (RR, 1.63; 95% CI, 1.27-2.10), but null associations were found for all-cause mortality or incident CVD and CHD.33 It is worth noting that low-SES individuals and Black adults are disproportionately exposed to low-quality diets and have a higher risk of premature death than others14,34; however, they are relatively underrepresented in epidemiologic studies on this matter to date. Findings from the current study of predominantly low-income Black and White Americans not only demonstrated their substantially higher exposure to excessive sodium intake, but provided compelling evidence of the association between excessive sodium and CVD-related deaths in this underserved population.
Large amounts of dietary sodium intake from processed/restaurant foods have been documented in the US for several decades.35 Also, snacking raises sodium overconsumption dramatically, especially among individuals with the lowest income, uneducated people, and Black individuals.36 In the same vein, our findings affirmed that (1) Black Americans consumed more sodium than White Americans with the same SES; and (2) individuals with lower SES appeared to eat an even greater quantity of sodium overall, regardless of race. It is noteworthy that low-income Black Americans consumed almost double the recommended amount of sodium (4512 mg/d vs 2300 mg/d). The average sodium intake in our low-income cohort exceeded that of general US adults (3400 mg/d)4 by 19% for White individuals and 33% for Black individuals. It is imperative to emphasize that low-income communities exhibit a higher concentration of fast-food restaurants and convenience stores with limited healthy food options, particularly in areas where racial and ethnic minorities are overrepresented37,38; this contributes to higher sodium exposure in these underserved groups. Economic barriers and unfavorable nutrition environments, including food insecurity and a lack of access to nutritious foods, are significant determinants of poor diet quality, including excessive sodium intake.37 Providing accessible healthy diet resources and increasing knowledge on the potential harms associated with high sodium intake would be the first steps in reducing racial, ethnic, and socioeconomic disparities in everyday diets and health outcomes.
Our PAR findings suggest that excessive sodium was likely responsible for about 10% to 30% of CVD-related deaths among underserved Americans. Although causality cannot be inferred from a single observational study like ours, a study using US nationally representative data reported that high sodium accounted for the largest number of estimated diet-related cardiometabolic deaths in 2012 (9.5% of all cardiometabolic deaths),10 particularly deaths from CHD (10.2% of CHD deaths). These findings highlight that dietary sodium reduction can be one of the most effective strategies for improving cardiovascular health. Of note, our study found a significant effect modification by race for the sodium–CVD mortality association, with higher risk estimates seen among low-income White individuals than their Black counterparts. This heterogeneity might be attributable to the complex and multidimensional nature of racial diversity. Race is a sociological construct with the potential to influence physiological mechanisms that regulate health-influencing factors through certain variations in dietary composition, lifestyle habits, and levels of psychosocial stress experienced by Black and White individuals.39 Indeed, the baseline characteristics of our study participants significantly differed across races, potentially accounting for the observed racial difference in the sodium-CVD mortality association. Given racial disparities in CVD-related disorders linked to race-specific daily dietary patterns,40 it is possible that differences in nutrient composition (eg, potassium, fiber, and so forth) between Black and White people may impact the sodium-CVD mortality association. Further investigation focusing on social determinants of nutrition beyond sodium is necessary to tackle racial, ethnic, and socioeconomic disparities in health outcomes.
This prospective investigation enabled us to address associations of dietary sodium intake with mortality outcomes among low-income Black and White Americans, who are disproportionately exposed to excessive sodium intake. Our large sample size, long-term follow-up, and a wide range of detailed baseline information allowed for in-depth analyses in consideration of subgroup differences and comprehensive adjustments for CVD risk factors and confounders, as well as evaluations of the mortality burdens attributable to excessive sodium intake among underserved Americans. As our study participants have similar SES backgrounds and comparable access to medical care, we had the unique opportunity to evaluate potential racial differences in sodium and mortality associations with minimum confounding from SES.
Limitations
Study limitations should be noted. First, we could not measure sodium intake using objective methods, such as 24-hour urine13,41 or blood samples.25 Because we estimated dietary sodium intake based on FFQ data only, measurement errors in estimating sodium intake might exist.42 Such exposure misclassification is likely to be nondifferential given our prospective study design, leading to an underestimated risk. Second, sodium intake was assessed only at baseline; thus, dietary changes over time were not captured. Third, despite the important interplay between sodium and potassium in controlling CVD-related conditions,39 we could not address the impact of potassium intake on the sodium-mortality association, which calls for future comprehensive investigations. Fourth, despite our extensive adjustments for established CVD risk factors and potential confounders, we cannot exclude the possibility of residual confounding. Additionally, the treatment effects of comorbid conditions could not be controlled due to a lack of information. Fifth, the possible misclassification of underlying causes of death is another concern. Specific causes of death are often imprecisely captured in the death registry, and some reported causes, such as heart failure, could reflect multiple underlying causes. Additionally, small sample sizes included in some subgroup analyses, eg, heart failure mortality, might result in risk estimates that were not statistically significant or less reliable.
Conclusions
In this cohort study of low-income Black and White Americans, we found that over 80% of this underserved population did not adhere to the current dietary guidelines for sodium intake, despite substantial public health efforts to lower sodium intake in Americans during recent decades. High sodium intake appeared to account for about 10% to 30% of CVD-related deaths among them. Developing effective dietary modification strategies tailored to this marginalized population is urgently needed to promote health and prevent ever-increasing health disparities in the US.
eTable 1. Dietary Sodium Intakes by Educational Attainment and Annual Household Income
eTable 2. Baseline Characteristics of Study Participants by Race
eTable 3. Baseline Characteristics of Study Participants: Black Americans vs White Americans
eTable 4. Race-Specific Deaths Across Dietary Sodium Intake
eTable 5. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Further Adjusting for History of Hypertension and Cardiovascular Disease
eTable 6. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Excluding First 2 Years of Follow-up
eTable 7. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Excluding Individuals With History of Cardiovascular Disease
eTable 8. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Further Adjusting for Comorbidity Index
eTable 9. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Competing Risk Analysis
eFigure. Conceptual Framework for Research Questions
Data Sharing Statement
References
- 1.World Health Organization . Guideline: sodium intake for adults and children. 2012. Accessed December 18, 2018. https://www.ncbi.nlm.nih.gov/books/NBK133309/ [PubMed]
- 2.Mozaffarian D, Fahimi S, Singh GM, et al. ; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group . Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014;371(7):624-634. doi: 10.1056/NEJMoa1304127 [DOI] [PubMed] [Google Scholar]
- 3.U.S. Department of Agriculture and U.S. Department of Health and Human Services . Dietary guidelines for Americans, 2020-2025. 9th edition. 2020. Accessed December 17, 2018. https://www.dietaryguidelines.gov/
- 4.Brouillard AM, Kraja AT, Rich MW. Trends in dietary sodium intake in the United States and the impact of USDA guidelines: NHANES 1999-2016. Am J Med. 2019;132(10):1199-1206.e5. doi: 10.1016/j.amjmed.2019.04.040 [DOI] [PubMed] [Google Scholar]
- 5.Farquhar WB, Edwards DG, Jurkovitz CT, Weintraub WS. Dietary sodium and health: more than just blood pressure. J Am Coll Cardiol. 2015;65(10):1042-1050. doi: 10.1016/j.jacc.2014.12.039 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Kong YW, Baqar S, Jerums G, Ekinci EI. Sodium and its role in cardiovascular disease—the debate continues. Front Endocrinol (Lausanne). 2016;7:164. doi: 10.3389/fendo.2016.00164 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Morrison AC, Ness RB. Sodium intake and cardiovascular disease. Annu Rev Public Health. 2011;32:71-90. doi: 10.1146/annurev-publhealth-031210-101209 [DOI] [PubMed] [Google Scholar]
- 8.Whelton PK, Appel LJ, Sacco RL, et al. Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American Heart Association sodium reduction recommendations. Circulation. 2012;126(24):2880-2889. doi: 10.1161/CIR.0b013e318279acbf [DOI] [PubMed] [Google Scholar]
- 9.Yang Q, Liu T, Kuklina EV, et al. Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2011;171(13):1183-1191. doi: 10.1001/archinternmed.2011.257 [DOI] [PubMed] [Google Scholar]
- 10.Micha R, Peñalvo JL, Cudhea F, Imamura F, Rehm CD, Mozaffarian D. Association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA. 2017;317(9):912-924. doi: 10.1001/jama.2017.0947 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Graudal N, Jürgens G, Baslund B, Alderman MH. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens. 2014;27(9):1129-1137. doi: 10.1093/ajh/hpu028 [DOI] [PubMed] [Google Scholar]
- 12.Kalogeropoulos AP, Georgiopoulou VV, Murphy RA, et al. Dietary sodium content, mortality, and risk for cardiovascular events in older adults: the Health, Aging, and Body Composition (Health ABC) Study. JAMA Intern Med. 2015;175(3):410-419. doi: 10.1001/jamainternmed.2014.6278 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.O’Donnell M, Mente A, Rangarajan S, et al. ; PURE Investigators . Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371(7):612-623. doi: 10.1056/NEJMoa1311889 [DOI] [PubMed] [Google Scholar]
- 14.de Mestral C, Mayén AL, Petrovic D, Marques-Vidal P, Bochud M, Stringhini S. Socioeconomic determinants of sodium intake in adult populations of high-income countries: a systematic review and meta-analysis. Am J Public Health. 2017;107(4):e1-e12. doi: 10.2105/AJPH.2016.303629 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Signorello LB, Hargreaves MK, Blot WJ. The Southern Community Cohort Study: investigating health disparities. J Health Care Poor Underserved. 2010;21(1)(suppl):26-37. doi: 10.1353/hpu.0.0245 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Signorello LB, Hargreaves MK, Steinwandel MD, et al. Southern community cohort study: establishing a cohort to investigate health disparities. J Natl Med Assoc. 2005;97(7):972-979. [PMC free article] [PubMed] [Google Scholar]
- 17.Buchowski MS, Schlundt DG, Hargreaves MK, Hankin JH, Signorello LB, Blot WJ. Development of a culturally sensitive food frequency questionnaire for use in the Southern Community Cohort Study. Cell Mol Biol (Noisy-le-Grand). 2003;49(8):1295-1304. [PubMed] [Google Scholar]
- 18.Schlundt DG, Buchowski MS, Hargreaves MK, Hankin JH, Signorello LB, Blot WJ. Separate estimates of portion size were not essential for energy and nutrient estimation: results from the Southern Community Cohort food-frequency questionnaire pilot study. Public Health Nutr. 2007;10(3):245-251. doi: 10.1017/S1368980007258574 [DOI] [PubMed] [Google Scholar]
- 19.Signorello LB, Munro HM, Buchowski MS, et al. Estimating nutrient intake from a food frequency questionnaire: incorporating the elements of race and geographic region. Am J Epidemiol. 2009;170(1):104-111. doi: 10.1093/aje/kwp098 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Yu D, Sonderman J, Buchowski MS, et al. Healthy eating and risks of total and cause-specific death among low-income populations of African-Americans and other adults in the southeastern United States: a prospective cohort study. PLoS Med. 2015;12(5):e1001830. doi: 10.1371/journal.pmed.1001830 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Benichou J. Methods of adjustment for estimating the attributable risk in case-control studies: a review. Stat Med. 1991;10(11):1753-1773. doi: 10.1002/sim.4780101113 [DOI] [PubMed] [Google Scholar]
- 22.Edwards DG, Farquhar WB. Vascular effects of dietary salt. Curr Opin Nephrol Hypertens. 2015;24(1):8-13. doi: 10.1097/MNH.0000000000000089 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Amara S, Tiriveedhi V. Inflammatory role of high salt level in tumor microenvironment (Review). Int J Oncol. 2017;50(5):1477-1481. doi: 10.3892/ijo.2017.3936 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013;496(7446):518-522. doi: 10.1038/nature11868 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Yi B, Titze J, Rykova M, et al. Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study. Transl Res. 2015;166(1):103-110. doi: 10.1016/j.trsl.2014.11.007 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Wu C, Yosef N, Thalhamer T, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. 2013;496(7446):513-517. doi: 10.1038/nature11984 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Sacks FM, Svetkey LP, Vollmer WM, et al. ; DASH-Sodium Collaborative Research Group . Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med. 2001;344(1):3-10. doi: 10.1056/NEJM200101043440101 [DOI] [PubMed] [Google Scholar]
- 28.Jablonski KL, Racine ML, Geolfos CJ, et al. Dietary sodium restriction reverses vascular endothelial dysfunction in middle-aged/older adults with moderately elevated systolic blood pressure. J Am Coll Cardiol. 2013;61(3):335-343. doi: 10.1016/j.jacc.2012.09.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Kupari M, Koskinen P, Virolainen J. Correlates of left ventricular mass in a population sample aged 36 to 37 years. Focus on lifestyle and salt intake. Circulation. 1994;89(3):1041-1050. doi: 10.1161/01.CIR.89.3.1041 [DOI] [PubMed] [Google Scholar]
- 30.Muntner P, Carey RM, Gidding S, et al. Potential U.S. population impact of the 2017 ACC/AHA high blood pressure guideline. J Am Coll Cardiol. 2018;71(2):109-118. doi: 10.1016/j.jacc.2017.10.073 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK. Dietary sodium intake and incidence of congestive heart failure in overweight US men and women: first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Arch Intern Med. 2002;162(14):1619-1624. doi: 10.1001/archinte.162.14.1619 [DOI] [PubMed] [Google Scholar]
- 32.Arcand J, Ivanov J, Sasson A, et al. A high-sodium diet is associated with acute decompensated heart failure in ambulatory heart failure patients: a prospective follow-up study. Am J Clin Nutr. 2011;93(2):332-337. doi: 10.3945/ajcn.110.000174 [DOI] [PubMed] [Google Scholar]
- 33.Aburto NJ, Ziolkovska A, Hooper L, Elliott P, Cappuccio FP, Meerpohl JJ. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013;346:f1326. doi: 10.1136/bmj.f1326 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Fulgoni VL III, Agarwal S, Spence L, Samuel P. Sodium intake in US ethnic subgroups and potential impact of a new sodium reduction technology: NHANES Dietary Modeling. Nutr J. 2014;13(1):120. doi: 10.1186/1475-2891-13-120 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Jacobson MF, Havas S, McCarter R. Changes in sodium levels in processed and restaurant foods, 2005 to 2011. JAMA Intern Med. 2013;173(14):1285-1291. doi: 10.1001/jamainternmed.2013.6154 [DOI] [PubMed] [Google Scholar]
- 36.Dunford EK, Poti JM, Popkin BM. Emerging disparities in dietary sodium intake from snacking in the US population. Nutrients. 2017;9(6):610. doi: 10.3390/nu9060610 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Kris-Etherton PM, Petersen KS, Velarde G, et al. Barriers, opportunities, and challenges in addressing disparities in diet-related cardiovascular disease in the United States. J Am Heart Assoc. 2020;9(7):e014433. doi: 10.1161/JAHA.119.014433 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Hilmers A, Hilmers DC, Dave J. Neighborhood disparities in access to healthy foods and their effects on environmental justice. Am J Public Health. 2012;102(9):1644-1654. doi: 10.2105/AJPH.2012.300865 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Kurtz TW, DiCarlo SE, Pravenec M, Morris RC Jr. No evidence of racial disparities in blood pressure salt sensitivity when potassium intake exceeds levels recommended in the US dietary guidelines. Am J Physiol Heart Circ Physiol. 2021;320(5):H1903-H1918. doi: 10.1152/ajpheart.00980.2020 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Howard G, Cushman M, Moy CS, et al. Association of clinical and social factors with excess hypertension risk in black compared with White US adults. JAMA. 2018;320(13):1338-1348. doi: 10.1001/jama.2018.13467 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Mente A, O’Donnell M, Rangarajan S, et al. Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality: a community-level prospective epidemiological cohort study. Lancet. 2018;392(10146):496-506. doi: 10.1016/S0140-6736(18)31376-X [DOI] [PubMed] [Google Scholar]
- 42.Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129(9):981-989. doi: 10.1161/CIRCULATIONAHA.113.006032 [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
eTable 1. Dietary Sodium Intakes by Educational Attainment and Annual Household Income
eTable 2. Baseline Characteristics of Study Participants by Race
eTable 3. Baseline Characteristics of Study Participants: Black Americans vs White Americans
eTable 4. Race-Specific Deaths Across Dietary Sodium Intake
eTable 5. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Further Adjusting for History of Hypertension and Cardiovascular Disease
eTable 6. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Excluding First 2 Years of Follow-up
eTable 7. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Excluding Individuals With History of Cardiovascular Disease
eTable 8. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Further Adjusting for Comorbidity Index
eTable 9. All-Cause and Cause-Specific Mortality in Relation to Dietary Sodium Intake: Competing Risk Analysis
eFigure. Conceptual Framework for Research Questions
Data Sharing Statement