Eczema is caused by a combination of genetic predisposition, immune system dysfunction, and environmental triggers that together compromise the skin’s protective barrier. There isn’t a single cause. Instead, multiple factors interact: your genes determine how well your skin can hold moisture and block irritants, your immune system overreacts to substances that wouldn’t bother most people, and external conditions like cold weather or air pollution can tip the balance toward a flare. Understanding these layers helps explain why eczema runs in families, why it often appears alongside allergies and asthma, and why it behaves so differently from person to person.
A Faulty Skin Barrier Starts the Problem
Healthy skin works like a brick wall. Skin cells are the bricks, and a mortar of fats (called lipids) seals the gaps between them. In eczema, both the bricks and the mortar are defective.
The most important genetic factor identified so far involves a gene called FLG, which provides instructions for making a protein called filaggrin. Filaggrin does two critical jobs: it bundles structural proteins together to create flat, tightly packed skin cells that form a strong outer barrier, and as it breaks down, it produces molecules that act as the skin’s natural moisturizing system. These breakdown products also maintain the skin’s slightly acidic pH, which helps fight off bacteria. About 40 mutations in the FLG gene have been identified in people with eczema. These mutations produce a shortened, nonfunctional version of the protein, leaving the skin unable to hold water properly or keep irritants out.
The fat composition of eczematous skin is also measurably different. Total levels of ceramides, the most important fats in that “mortar” layer, are significantly reduced compared to healthy skin. The ratio of ceramides to cholesterol drops, and the specific types of ceramides shift: longer-chain varieties that provide the strongest waterproofing decrease, while shorter-chain versions that correlate with increased water loss increase. The structural consequence is that the organized, dense fat layers found in healthy skin become disordered and porous in eczema. Very long-chain fatty acids (24 carbons or more) also decline, replaced by shorter fatty acids that don’t seal the barrier as effectively. The result is skin that loses water too quickly, dries out, cracks, and lets allergens and bacteria slip through.
The Immune System Overreacts
A leaky skin barrier alone doesn’t fully explain eczema. The immune system plays an equally central role, and in eczema it’s skewed toward a particular type of inflammatory response.
In healthy immune function, different branches of the immune system balance each other. In eczema, immune cells called Th2 cells dominate, producing signaling molecules that drive allergic-type inflammation. These signals recruit eosinophils, mast cells, and basophils into the skin, all of which release compounds that cause itching, redness, and swelling. They also push other immune cells called B cells to produce large amounts of IgE, the antibody most associated with allergic reactions. This creates a self-reinforcing cycle: Th2 cells produce signals that encourage even more immune cells to become Th2 cells, amplifying the inflammatory response with each round.
These same inflammatory signals actively damage the skin barrier further. They suppress the production of filaggrin and ceramides, meaning the immune response itself makes the barrier worse, which lets more irritants in, which triggers more immune activity. This vicious cycle is why eczema tends to flare and persist rather than resolve on its own.
Bacteria on the Skin Play a Bigger Role Than Expected
Everyone’s skin is home to a diverse community of bacteria, but in eczema that diversity collapses. During flares, one species dominates: Staphylococcus aureus. Colonization by S. aureus is nearly universal in people with active eczema, and the timing is telling. Microbiome studies show that the bacterial takeover precedes and accompanies flares, then diversity rebounds during remission.
Research in mice with a disrupted skin barrier (lacking filaggrin, just like many eczema patients) shows that S. aureus applied to the skin triggers a strong inflammatory response that wouldn’t occur in animals with an intact barrier. Specialized immune cells in the outer skin layer called Langerhans cells detect the bacteria and set off the immune cascade. Without these sentinel cells, the inflammatory response doesn’t happen, confirming they’re essential to how the skin reacts to bacterial overgrowth. The practical takeaway is that a damaged barrier allows bacteria to trigger inflammation that a healthy barrier would prevent entirely.
Childhood Environment Shapes the Risk
Eczema affects an estimated 84 million children worldwide, and prevalence has been rising, particularly in low-income regions and Sub-Saharan Africa, while holding steady or declining in parts of Europe. This pattern points to environmental and lifestyle factors beyond genetics.
The hygiene hypothesis, first proposed in 1989, offers one explanation. The observation was straightforward: children with older siblings got hay fever and eczema less often. The reasoning is that early exposure to a wide range of microbes trains the immune system toward tolerance rather than overreaction. Without that microbial education, the immune system tilts toward the Th2-dominated, allergy-prone state that drives eczema. Modern extensions of this idea focus specifically on the gut microbiome. Factors like antibiotic use in early life, cesarean birth, and a low-fiber diet can disrupt the bacterial communities in a child’s intestines. These gut bacteria normally help calibrate the immune system, and when they’re thrown off balance, the risk of allergic conditions, including eczema, increases.
This doesn’t mean dirt prevents eczema or that hygiene is bad. It means the developing immune system benefits from diverse microbial exposure, the kind that comes naturally from living with siblings, pets, or in rural environments, and that disrupting the body’s microbial communities during critical windows in infancy can have lasting immunological consequences.
Environmental Triggers That Cause Flares
Once someone has eczema-prone skin, a range of external conditions can provoke or worsen flares. Cold, dry weather is one of the most consistent triggers. Data from Northern Europe shows that colder temperatures, lower humidity, and stronger winds all correlate with increased eczema-related healthcare visits. Each 10% drop in humidity is associated with a 10% increase in flare risk. The International Eczema Council identifies cold, dry weather as a key environmental trigger, with children disproportionately affected.
Air pollution is another significant factor. A large U.S. study found that exposure to fine particulate matter (PM2.5) more than doubled the odds of having eczema. These tiny particles are small enough to penetrate the skin, where they generate oxidative stress, impair the barrier, increase water loss, and trigger inflammatory signaling. A meta-analysis spanning 42 studies across 14 countries confirmed that elevated levels of particulate matter, nitrogen dioxide, and sulfur dioxide are all linked to more eczema-related emergency and outpatient visits. For sulfur dioxide specifically, each 10 microgram-per-cubic-meter increase corresponded to a 6% rise in eczema visits.
Indoor environments matter too. Visible mold in the home increases the risk of eczema by about 35%, with stronger effects from prolonged exposure. Dust mites and their waste products are another common indoor trigger, particularly in humid climates where they thrive. Heat and sweating can also provoke flares, meaning eczema sufferers often struggle at both temperature extremes.
Eczema Often Leads to Other Allergic Conditions
Eczema isn’t just a skin problem. It’s frequently the first step in a progression called the atopic march, where eczema in infancy leads to food allergies, then asthma and hay fever in later childhood. About one in three children with eczema goes on to develop asthma. Among children with severe eczema, that number jumps to roughly 70%, compared to about 8% of the general population.
The timing and severity of eczema matter. Children who develop eczema before age two, particularly those who also show IgE antibodies to common environmental allergens by ages two to four, are at the highest risk of progressing through the atopic march. The mechanism appears to work through the skin itself: a dysfunctional barrier allows allergens to penetrate and sensitize the immune system. That sensitization then becomes systemic, priming the airways to overreact to the same types of allergens. In this way, early eczema essentially trains the immune system to be allergic, with consequences that extend well beyond the skin.
Why It Runs in Families
Eczema has a strong hereditary component, but it doesn’t follow a simple pattern. Having one parent with eczema, asthma, or hay fever increases a child’s risk substantially. Having two affected parents raises it further. The filaggrin gene mutations are the best-studied genetic factor, but they only account for a portion of cases. Many people with eczema have no identifiable filaggrin mutation, and some people who carry the mutation never develop the condition.
What’s inherited isn’t eczema itself so much as a collection of vulnerabilities: a tendency toward a thinner lipid barrier, an immune system that leans toward Th2 responses, lower baseline production of ceramides, and skin that’s more permeable to irritants. Whether these vulnerabilities translate into actual disease depends on the environmental exposures, microbial encounters, and triggers a person faces throughout life. This is why identical twins don’t always share the condition, and why eczema prevalence varies so dramatically between countries with similar genetic backgrounds but different lifestyles and climates.