Eczema, also referred to as Atopic Dermatitis (AD), is a chronic inflammatory condition characterized by dry, intensely itchy skin. Diabetes Mellitus (DM) is a metabolic disorder defined by high blood sugar levels resulting from issues with insulin production or utilization. Although one is primarily a skin disease and the other is an endocrine condition, evidence points to a significant connection between them. This link is driven by underlying systemic processes that affect both the body’s immune system and its metabolism. Understanding how these two conditions influence one another is important for managing both skin health and overall systemic well-being.
Shared Immunological and Genetic Foundations
Both AD and diabetes share immune system dysregulation and chronic inflammation. Atopic dermatitis is largely driven by a T helper type 2 (Th2) polarization response, involving inflammatory signaling molecules like interleukin (IL)-4, IL-5, and IL-13. This Th2-driven inflammation is associated with allergic responses and compromised skin barrier function. Type 2 Diabetes (T2D) is also characterized by chronic, low-grade systemic inflammation, where elevated inflammatory factors contribute to insulin resistance. This shared inflammatory environment provides a biological bridge between the two conditions.
Genetic Overlap
Both conditions can share genetic vulnerabilities, particularly those that affect the body’s protective layers. Many individuals with AD have a variation in the gene responsible for creating filaggrin, a protein that helps maintain the skin’s outer barrier. T2D patients are also known to carry a higher incidence of filaggrin gene mutations. This suggests a shared genetic predisposition that simultaneously weakens the skin barrier and may increase susceptibility to metabolic issues.
Eczema as a Systemic Risk Factor for Diabetes
Chronic atopic dermatitis acts as a systemic disease that actively increases the risk of developing Type 2 Diabetes (T2D). The persistent inflammation releases a steady stream of inflammatory molecules into the bloodstream. These circulating cytokines, such as TNF-alpha and IL-6, interfere with the body’s ability to use insulin effectively, promoting insulin resistance throughout the tissues. This continuous low-grade systemic inflammation is a significant precursor to the onset of T2D.
Sleep Disruption
Chronic itching, a hallmark symptom of eczema, contributes to metabolic dysfunction through sleep disruption. The intense nocturnal pruritus frequently causes significant sleep disturbances, affecting many adults with AD. Poor sleep is a physiological stressor that impairs glucose metabolism and heightens insulin resistance, further accelerating the progression toward diabetes.
Corticosteroid Risk
Another risk factor comes from a common eczema treatment: corticosteroids. The long-term or widespread use of topical corticosteroids, particularly potent formulations, can lead to systemic absorption. Studies show that the cumulative dose and duration of topical corticosteroid use are associated with an increased risk of developing T2D. Clinicians must balance controlling severe skin flares against this potential iatrogenic risk to glucose regulation.
How Diabetes Affects Skin Health and Barrier Function
High blood sugar levels, or chronic hyperglycemia, have a direct effect on the skin’s structure and function, which can worsen or mimic eczema symptoms. Hyperglycemia impairs the skin’s natural barrier by altering the production and function of structural components. High glucose levels lead to the formation of Advanced Glycation End products (AGEs), which reduce the skin’s elasticity and make it more fragile.
Barrier Impairment and Dryness
The body’s attempt to excrete excess sugar pulls fluid from the cells, contributing to generalized skin dryness (xerosis), which exacerbates the dry, itchy symptoms of eczema. Hyperglycemia also disrupts the proliferation and differentiation of keratinocytes, delaying the skin’s ability to repair itself and maintain its permeability barrier. This impaired barrier function reduces the skin’s natural defense mechanisms, making it susceptible to irritants and infections.
Neuropathy and Healing
Long-term diabetes often results in damage to small blood vessels and nerves, known as diabetic neuropathy. Poor circulation and nerve damage compromise the skin’s ability to heal, turning minor scratches from eczema-related itching into slow-healing wounds prone to bacterial or fungal infections. Neuropathy can also interfere with the nerves that signal sweat production, resulting in profound dryness, especially in the extremities.
Integrated Management and Treatment Considerations
Managing both eczema and diabetes requires a coordinated, holistic approach that addresses the systemic inflammation underlying both conditions. Strict control of blood sugar levels can directly benefit skin health by reducing the detrimental effects of hyperglycemia on the skin barrier and wound healing capacity. Conversely, effective management of eczema inflammation can reduce the systemic inflammatory load, potentially improving insulin sensitivity.
Coordination between a dermatologist and an endocrinologist is paramount to avoid conflicting treatments, especially when considering corticosteroids or newer, advanced eczema therapies. For example, the use of oral Janus kinase (JAK) inhibitors for severe AD may require careful monitoring in patients with pre-existing risk factors like diabetes. Conversely, certain diabetes medications, such as SGLT2 inhibitors, have been observed to reduce the risk of developing AD. Shared lifestyle interventions, including regular physical activity and a diet focused on glucose control, are beneficial for both metabolic health and skin barrier function.