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Atopic dermatitis (AD), a common chronic itchy inflammation of the upper skin, is typically caused by genetic defects in the skin barrier, making the skin more prone to inflammation. Individuals with AD often have family members who suffer from asthma or hay fever. Currently, it is widely believed that AD is a genetic disorder. Affecting up to 20% of children and 4-5% of adults globally, this widespread condition has garnered significant attention from researchers.

A recent article published in the Journal of the American Medical Association - Dermatology, titled "Sodium Intake and Atopic Dermatitis," has revealed that the occurrence of AD might be related to the amount of sodium intake.

Although salt is an essential seasoning in human diet, excessive intake has been linked to elevated blood pressure, leading to cardiovascular diseases. This has been widely acknowledged, and thus, clinicians often advise patients to reduce their salt consumption. Previous studies have indicated a correlation between fast food consumption and an increased risk of AD, with sodium being a primary component of fast food, possibly serving as a significant dietary trigger for AD. Sodium magnetic resonance imaging studies have shown that exchangeable sodium is primarily stored in the skin, further suggesting a link between sodium and AD.

To investigate the relationship between sodium and AD, Katrina Abuabara and her colleagues from the University of California, San Francisco, analyzed the 24-hour urinary sodium excretion of 215,832 adult participants aged 37-72 from the UK Biobank. Using the International Study of Salt, Other Factors, and Blood Pressure equation, they considered factors such as body mass index, age, urinary potassium, sodium, and creatinine concentrations.

The median 24-hour urinary sodium excretion among these participants was 3.6 g/day. The researchers found that for every additional gram of sodium excreted over 24 hours, the likelihood of being clinically diagnosed with eczema increased by 11%, and the risk of developing eczema rose by 16%.

The exact mechanism by which high sodium intake might increase the risk of AD remains unclear. Researchers hypothesize that it may involve sodium's effects on skin barrier function, immune response, and microbiome. Abuabara, a member of the research team, noted that previous studies have shown that sodium can activate cells in the immune system, triggering inflammatory pathways. AD patients often have an overactive immune response to allergens or irritants, leading to skin inflammation and subsequent symptoms. Another team member, Brenda Chiang, mentioned that while the study demonstrates a link between high urinary sodium levels and eczema, further research is needed to determine whether high sodium intake causes AD. Carsten Flohr from King's College London also cautioned that it is too early to conclude that reducing dietary sodium levels could lower the severity or risk of AD.

Addressing these concerns, the research team plans to further explore the relationship and evaluate the impact of sodium intake restriction as an intervention for AD.

Reference:

Chiang BM, Ye M, Chattopadhyay A, Halezeroglu Y, Van Blarigan EL, Abuabara K. Sodium Intake and Atopic Dermatitis. JAMA Dermatol. 2024 Jun 5:e241544. doi: 10.1001/jamadermatol.2024.1544. Epub ahead of print. PMID: 38837130; PMCID: PMC11154362.