Study Links Dietary Sodium Intake to Increased Atopic Dermatitis Prevalence, Severity

Excessive dietary sodium intake is associated with increased active atopic dermatitis (AD) and AD severity, according to a study published in JAMA Dermatology.¹

The researchers explained that lifestyle and environmental factors contribute to AD prevalence and activity. However, the roles of specific exposures that drive AD onset and persistence remain poorly understood. Therefore, identifying specific modifiable exposures is important to patients and their caregivers.²

A past study identified diet as a potential key contributor to AD onset and persistence.³ More specifically, fast food consumption resulted in a 20% increase in AD risk and a 70% increase in severe AD risk among adolescents. Therefore, excessive dietary sodium, which is common in fast food, may be connected to AD.

Data on this association are lacking, so the researchers conducted a cross-sectional study to investigate the potential link between higher levels of sodium consumption and AD prevalence, severity, and activity at the population level.¹

The researchers linked dietary sodium intake with active atopic dermatitis (AD) and increased AD severity. | Image Credit: EdNurg - stock.adobe.com

To conduct the study, the researchers used the UK Biobank, a population-based cohort with over 500,000 participants between the ages of 37 and 73 from the National Health Services across England, Wales, and Scotland.⁴ For each patient, they analyzed primary care records and data collected at an assessment visit between March 31, 2006, and October 1, 2010¹; at the assessment visit, patients underwent clinical measurements, completed questionnaires, and provided spot urine samples.

The primary exposure was 24-hour urinary sodium excretion, which represents approximately 90% of 24-hour dietary sodium intake. The researchers calculated each patient's 24-hour dietary sodium intake with the International Cooperative Study on Salt, Other Factors, and Blood Pressure (INTERSALT) equation, which considers body mass index, age, and urine concentrations of sodium, creatinine, and potassium.

Also, the primary outcome was AD. The researchers identified those with AD by using an algorithm that requires at least 1 relevant clinical Read code and 2 different dates of AD therapy prescriptions; they considered the latter of the 2 prescription dates as the AD diagnosis date. The researchers labeled patients with active AD if their diagnosis date was before their assessment visit and they had at least 1 clinical or prescription AD code within the 2 years before and after the urine sample collection date.

By default, they classified those with AD with mild AD. However, the researchers considered those who received at least 2 potent topical corticosteroid prescriptions, or a topical calcineurin inhibitor prescription, as having moderate AD; they classified those with a systemic immunotherapy prescription as having severe AD.

After adjusting for possible AD risk factors, like sex, age, and race, they used multivariable logistic regression models to examine the association between estimated grams of 24-hour urine sodium excretion, AD, and active AD. The researchers also used an ordinal logistic regression model to assess the association of estimated 24-hour urine sodium excretion and AD severity, adjusting for the same covariates.

They validated their findings by using publicly available data from the US-based National Health and Nutrition Examination Survey (NHANES). Within this database, AD was measured via self-report on patient surveys, and sodium intake was measured using 24-hour dietary recall questionnaires. The researchers used logistic regression models to estimate the association between AD and sodium intake, which they then compared with their UK Biobank findings.

Initially, the researchers identified 221,964 patients in the UK Biobank who completed a spot urine sample collection and had available primary health records. However, they excluded 6132 patients with missing data or negative INTERSALT values. Consequently, the study population consisted of 215,832 patients, the majority of which were female (54.3%) and White (95.2%); the mean (SD) age of the population was 56.52 (8.06) years. The researchers identified 10,839 patients (5.0%) who had AD, 4813 (44.4%) of whom they classified with moderate AD and 320 (3.0%) with severe AD; of this subpopulation, 1282 (11.8% of patients with AD) had active AD.

Additionally, the mean estimated 24-hour urine sodium excretion was 3.01 (0.82) g/day. Consequently, they found that a 1-g higher estimated 24-hour urine sodium excretion was associated with higher odds of AD (adjusted OR [aOR], 1.11; 95% CI, 1.07-1.14; P < .001), active AD (aOR, 1.16; 95% CI, 1.05-1.28; P < .001), and increasing AD severity (aOR, 1.11; 95% CI, 1.07-1.15).

Lastly, the validation cohort from NHANES consisted of 13,014 patients. Of this cohort, 1493 reported AD in the past year and 794 reported current AD. The mean dietary sodium intake was 3.45 (0.73) g. More specifically, the mean dietary sodium intake was 3.47 (0.61) g for those with current AD and 3.44 (0.74) g for those without. Like the UK Biobank results, a 1-g per day higher dietary sodium intake was significantly associated with higher current AD risk (aOR, 1.22; 95% CI, 1.01-1.47) and a marginally higher risk of AD in the past year (aOR, 1.14; 95% CI, 0.97-1.35).

The researchers acknowledged their limitations, one being using a single spot urine sample to estimate 24-hour urinary sodium excretion; this only captures the last 24 hours of dietary intake and is not the best measure of long-term sodium intake. Despite these limitations, the researchers suggested areas for future research based on their findings.

“Our study opens the potential for future studies on restriction of dietary sodium intake as an intervention for AD that would be cost-effective, low risk, and widely available,” the authors concluded.

References

1. Chiang BM, Ye M, Chattopadhyay A, Halezeroglu Y, Van Blarigan EL, Abuabara K. Sodium intake and atopic dermatitis. JAMA Dermatol. Published online June 5, 2024. doi:10.1001/jamadermatol.2024.1544

2. Kim RW, Barta K, Begolka WS, et al. Qualitative analysis of the impact of atopic dermatitis on caregivers. Br J Dermatol. 2022;187(6):1038-1041. doi:10.1111/bjd.21828

3. Ellwood P, Asher MI, García-Marcos L, et al. Do fast foods cause asthma, rhinoconjunctivitis and eczema? Global findings from the International Study of Asthma and Allergies in Childhood (ISAAC) phase three. Thorax. 2013;68(4):351-360. doi:10.1136/thoraxjnl-2012-202285

4. Sudlow C, Gallacher J, Allen N, et al. UK Biobank: an open access resource for identifying the causes of a wide range of complex diseases of middle and old age. PLoSMed. 2015;12(3):e1001779. doi:10.1371/journal.pmed.1001779