In a study of adults, an increase of 1 g in estimated 24-hour urinary sodium excretion was associated with 11% higher odds of an atopic dermatitis (AD) diagnosis, 16% higher odds of having active AD, and 11% higher odds of increased severity of AD.
Those are key findings from a cross-sectional analysis of data from the United Kingdom.
“Excessive dietary sodium, common in fast food, may be associated with AD,” corresponding author Katrina Abuabara, MD, MA, MSCE, and colleagues wrote in the study, which was published online in JAMA Dermatology. They referred to recent research using sodium MRI, which showed that “the majority of the body’s exchangeable sodium is stored in the skin and that skin sodium is associated with autoimmune and chronic inflammatory conditions, including AD.” And in another study published in 2019, lesional skin sodium was 30-fold greater in patients with AD than in healthy controls.
To investigate whether there is an association between higher levels of sodium consumption and AD prevalence, activity, and severity at the population level, Dr. Abuabara, of the program for clinical research in the Department of Dermatology at the University of California, San Francisco, and coauthors drew from the UK Biobank, a population-based cohort of more than 500,000 individuals aged 37-73 years at the time of recruitment by the National Health Service. The primary exposure was 24-hour urinary sodium excretion, which was calculated by using the INTERSALT equation, a sex-specific estimation that incorporates body mass index; age; and urine concentrations of potassium, sodium, and creatinine. The primary study outcome was AD or active AD based on diagnostic and prescription codes from linked electronic medical records. The researchers used multivariable logistic regression models adjusted for age, sex, race and ethnicity, Townsend deprivation index, and education to measure the association.
Of the 215,832 Biobank participants included in the analysis, 54% were female, their mean age was 57 years, 95% were White, their mean estimated 24-hour urine sodium excretion was 3.01 g/day, and 10,839 (5%) had a diagnosis of AD. The researchers observed that on multivariable logistic regression, a 1-g increase in estimated 24-hour urine sodium excretion was associated with increased odds of AD (adjusted odds ratio [AOR], 1.11; 95% CI, 1.07-1.14), increased odds of active AD (AOR, 1.16; 95% CI, 1.05-1.28), and increased odds of increasing severity of AD (AOR, 1.11; 95% CI, 1.07-1.15).
Validating Results With US Data
To validate the findings, the researchers evaluated a cohort of 13,014 participants from the US-based National Health and Nutrition Examination Survey (NHANES), using pooled data from the 1999-2000, 2001-2002, and 2003-2004 samples. Of the 13,014 participants, 796 reported current AD, and 1493 reported AD in the past year. The mean dietary sodium intake of overall NHANES participants estimated with 24-hour dietary recall questionnaires was 3.45 g, with a mean of 3.47 g for those with current AD and a mean of 3.44 g for those without AD.
The researchers observed that a 1-g/day higher dietary sodium intake was associated with a higher risk for current AD (AOR, 1.22; 95%CI, 1.01-1.47) and a somewhat higher risk for AD in the past year (AOR, 1.14; 95% CI, 0.97-1.35).
“Future work should examine whether variation of sodium intake over time might trigger AD flares and whether it helps to explain heterogeneity in response to new immunomodulatory treatments for AD,” the authors wrote. “Reduced sodium intake was recommended as a treatment for AD more than a century ago, but there have yet to be studies examining the association of dietary sodium reduction with skin sodium concentration or AD severity,” they added. Noting that sodium reduction “has been shown to be a cost-effective intervention for hypertension and other cardiovascular disease outcomes,” they said that their data “support experimental studies of this approach in AD.”
They acknowledged certain limitations of the study, including the fact that a single spot urine sample was used in the UK Biobank cohort, “which only captures dietary intake of the last 24 hours and is not the best measure of usual or long-term intake of sodium.” They also noted that the findings may not be generalizable to other populations and that AD was based on self-report in the NHANES validation cohort.
Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the results, said the study by Dr. Abuabara and colleagues “gives us another reason to avoid salt, showing that 1 g/day of higher salt intake increases the risk of AD in an adult population and more severe AD.”
He added that, “Now, can you say that reducing salt intake will have a therapeutic effect or clinically relevant impact? No. [That is] certainly worth exploring but at a minimum, gives some more credibility to keeping it bland.”
The study was supported by a grant from the Medical Student in Aging Research Program, the National Institute on Aging, and the National Eczema Association. Dr. Abuabara reported receiving research funding for her institution from Pfizer and Cosmetique Internacional/La Roche-Posay and consulting fees from Target RWE, Sanofi, Nektar, and Amgen. No other disclosures were reported. Dr. Friedman had no relevant disclosures.
A version of this article appeared on Medscape.com.