Introduction

If you or someone you love lives with eczema, you have probably heard the saying: “moisturize, moisturize, moisturize.” But here’s the question most people never think to ask. Why do some moisturizers work so much better than others, and why does eczema-prone skin feel so fragile in the first place?

The answer lies deep inside your skin cells, with a protein called filaggrin, one of the most important yet least talked-about players in skin health. When filaggrin does its job well, your skin stays hydrated, flexible, and resistant to irritants. When it doesn’t, often due to a genetic variation or systemic inflammation from environmental factors, the door to eczema or dermatitis for those undergoing cancer therapy swings wide open.

In this article, we’ll break down exactly what filaggrin is, what happens when it’s not working properly, and what the latest science says about repairing the damage. We’ll also cover its partner protein, corneodesmosin, (I have a hard time pronouncing it also) and explain how together they act like the bricks and mortar of your skin’s protective barrier. Along the way, we’ll use plain language and everyday analogies to make the science accessible, no dermatology degree required.

What Is Filaggrin?

The term “filaggrin” is a contraction of “filament aggregating protein.” If that sounds complicated, it is, but here’s a simple way to picture it. Imagine that your skin cells are new bricks coming off an assembly line. Filaggrin is the quality-control supervisor that shapes those bricks into the firm, flat, perfectly stacked tiles that form your skin’s outermost protective layer, the stratum corneum.

Filaggrin does this in two distinct but equally critical ways:

•       Organizing the internal skeleton of skin cells. Inside every maturing skin cell, there are long, thread-like structures called keratin filaments. Filaggrin acts like a bundle-tie, cinching these filaments together so the cell flattens out as it migrates toward the surface. This flattening creates the dense, overlapping “bricks” that form the outermost layer of skin.

•       Breaking down into natural moisturizing factor (NMF). Once those flattened cells reach the very outer layer, filaggrin is enzymatically broken down into small, water-loving molecules which include amino acids like histidine, pyrrolidone carboxylic acid (PCA), and trans-urocanic acid (UCA) which is not the same as urea. Collectively, these broken-down products are known as natural moisturizing factor (NMF), and they act like tiny sponges that hold water inside the outer skin layer and help maintain a slightly acidic pH on the skin surface.

This slightly acidic pH is more important than most people realize. It keeps the enzymes that control skin cell shedding working at the right pace and helps suppress harmful bacteria like Staphylococcus aureus, which is often found in elevated levels on eczema-prone or cancer patient skin.

So, who is most affected by filaggrin deficiency? People who carry genetic mutations in the FLG gene, i.e., the gene that encodes filaggrin, are significantly more prone to atopic eczema.

There appears to be a significant positive association between eczema and loss-of-function FLG mutations in all latitudes in the Northern hemisphere, but not in all ethnicities. The prevalence of  FLG mutations appears to be more prevalent in populations residing farther north of the Equator but is negligible in Middle Easterners and absent in most African populations (<1%). https://doi.org/10.1172/jci.insight.178258

Loss-of-function variants are found in roughly 4–15% of people with eczema of European descent, where those from Northern/Westerm Europe have a higher prevalence (~12.7% on average) compared to those from Southern/Mediterranean Europe (~4%).  However, if European patients with AD are grouped according to clinical severity, it is found that the mutations are much more common in the group with moderate or severe AD (50%) than in those with mild AD (4%-15%).

Similar mutations are found in about 4% of Asian populations but again depend on geography and health.  Among Asian patients with atopic dermatitis, the prevalence of FLG mutations is significantly higher, often cited between 15% and 27%.  Specifically, higher prevalence, with specific studies in Han Chinese and Japanese cohorts showing mutation rates in AD patients upward of 26–31% whereas southern Asians (e.g., India, Pakistan) have a much lower prevalence (<4%). 

Based on studies of admixed Latinx populations (particularly in Chile and Mexico), the prevalence of Filaggrin (FLG) loss-of-function (LoF) mutations is similar to European populations, ranging roughly between 5% and 10% in the general population, though it varies significantly by regional ancestry (European vs. Native American vs. African. https://doi.org/10.1111/ijd.15887; https://pubmed.ncbi.nlm.nih.gov/22162825/

However, research indicates that while filaggrin (FLG) mutations are common in other populations, they are rare in African populations. Instead, studies have identified that mutations in Filaggrin-2 (FLG2) gene variants——are linked to persistent atopic dermatitis in children of African ancestry, often linked to skin barrier dysfunction. https://doi.org/10.3389/falgy.2023.1203304

Carrier of this mutation are 50% more likely to have persistent eczema.  Other variants include mutations in claudin 1 (CLDN1), which encodes a structural protein in tight junctions, are related to the early onset of atopic dermatitis and a strong genetic predisposition to immune dysregulation in Th2 cytokine genes such as IL-4, IL-13, and IL-4RA.  Genetic studies suggest that the mutations present in this population contribute to more persistent and long-standing disease rather than just early-childhood transient eczema. https://pubmed.ncbi.nlm.nih.gov/34600773/

Filaggrin mutations are considered one of the single strongest known genetic risk factors for atopic eczema. They increase eczema risk by over 3-fold, frequently leading to more persistent and early-onset disease. 

Causes of Filaggrin Deficiency and Eczema

Eczema is not caused by a single factor, but rather, it’s more like a perfect storm of genetics, environment, and immune response. Filaggrin sits right at the center of that storm.  FLG mutations cause significant skin barrier defects, while Th2-driven inflammation represents the downstream immune response that drives the disease's active inflammation and itching. 

Genetics: The FLG Gene

The most well-established cause of filaggrin insufficiency is genetic. Mutations in the FLG gene reduce the amount of functional filaggrin the skin can produce. If you carry one mutated copy of the gene, your filaggrin levels may be moderately reduced. If you carry two mutated copies, the reduction is typically more severe, and so is the risk of eczema.

Think of it like a water reservoir with a crack in the wall. The smaller the crack, the slower the leak. But even a moderate leak, over time, leaves the reservoir significantly depleted.

Inflammation as a Two-Way Problem

Here’s something crucial that many people don’t know. Inflammation doesn’t just result from a weak skin barrier but also causes one. The inflammatory cytokines (chemical messengers) that flood eczematous skin can also suppress filaggrin gene expression, thereby further reducing filaggrin production even in people who started with normal (non-mutated) FLG genes. This means eczema can create a vicious cycle where inflammation reduces filaggrin, and reduced filaggrin worsens inflammation.

Environmental Triggers

Even in people with normal filaggrin genes, environmental factors can compromise the skin barrier. Common culprits include:

•       Harsh soaps and detergents that disrupt the skin’s natural pH

•       Low humidity or cold weather, which accelerates trans epidermal water loss (TEWL)

•       Frequent hand washing or prolonged water contact

•       Exposure to allergens like dust mites, pet dander, or certain foods

In people with filaggrin insufficiency, these same triggers are far more damaging because the skin barrier is already compromised, i.e., they don’t have the same protective reserve to draw from.

Symptoms and Identification

Understanding the symptoms of filaggrin-related eczema can help distinguish it from other skin conditions and point toward more targeted treatment.

Common symptoms include:

•       Persistent skin dryness and roughness, even when moisturizing regularly

•       Tightness, itching, and sensitivity, especially in cold or dry weather

•       Small cracks or fissures in the skin, particularly on the hands, fingers, and around joints

•       Redness and inflammation, often in typical locations such as the inner elbows, backs of the knees, face, and neck

•       A burning or stinging sensation experienced when water or skincare products contact the skin

How Filaggrin-Related Eczema Differs From Other Skin Conditions

Eczema is sometimes confused with psoriasis or contact dermatitis. Here are a few key distinctions:

Feature	Atopic Eczema (Filaggrin-Related)	Psoriasis / Contact Dermatitis
Onset	Usually childhood; can persist into adulthood	Psoriasis: any age; Contact Dermatitis: after specific exposure
Appearance	Dry, red, weepy, or crusted patches	Psoriasis: silvery scales; Contact Dermatitis: localized blisters or redness
Location	Inner elbows, knees, face, neck	Psoriasis: scalp, elbows, knees; Contact Dermatitis: site of contact
Itch Pattern	Intense, often worse at night	Psoriasis: milder itch; Contact Dermatitis: burning or stinging

 

Treatment Options

Treatment for eczema linked to filaggrin deficiency has evolved significantly. The best approach involves the use of multiple complimentary strategies, that address both the skin barrier and the immune response simultaneously.

Step 1: Barrier-Repair Moisturizers

The first line of defense is a well-formulated moisturizer specifically designed for atopic skin. Look for products containing:

•       Ceramides, cholesterol, and fatty acids (like linoleic acid in sunflower oil): these represent the “mortar” that fills the gaps between skin cells (bricks) to reduce water loss

•       Colloidal oatmeal or allantoin (also found in comfrey): anti-inflammatory ingredients that calm redness and irritation

•       pH-balanced formulations: a slightly acidic pH (around 4.5–5.5) supports the enzymes that control how skin cells shed while helping to suppress the growth of harmful bacteria

Step 2: Supplying NMF-like Humectants

Since filaggrin-deficient skin produces less natural moisturizing factor (NMF), a second generation of products compensates by supplying NMF-like molecules directly to the skin. These molecules include:

•       Hyaluronic acid acts as a powerful humectant, holding up to 1,000 times its weight in water

•       Glycerin acts a key humectant by drawing water into the skin, strengthening the moisture barrier, and enhancing skin softness

•       Urea, at low concentrations, is a gentle humectant that mimics part of the NMF profile, but is not the same as trans-urocanic acid (UCA) which is a NMF component

•       Pyrrolidone carboxylic acid (PCA) is another core NMF component that draws moisture into the stratum corneum

These ingredients don’t fix the underlying genetic issue, but they “fake” the outcome by keeping the outer layer hydrated even when filaggrin isn’t producing enough NMF on its own.

Step 3: L-Histidine Supplementation

L-histidine is an amino acid that serves as a direct building block for filaggrin protein. Think of L-histidine as a delivery truck stocking a depleted warehouse. If the warehouse (your skin cells) still has some capacity to produce additional filaggrin, giving it more raw material (L-histidine) allows it to make more filaggrin.

Research has explored the use of L-histidine as an oral supplement. When the skin has partially functional FLG genes, as compared to a complete loss-of-function mutation, additional L-histidine can help boost filaggrin production, which in turn increases NMF levels thereby improving moisture retention.

Step 4: Next-Generation Filaggrin-Stimulating Formulations

The most advanced barrier-repair products go beyond passive moisturizing. They combine L-histidine supplements with supportive topical ingredients specifically designed to:

•       Stimulate the skin’s own filaggrin production, not just replace its outputs

•       Support corneodesmosin production and function (the “glue proteins” discussed above) by helping outer skin cells stay firmly connected and shed at the appropriate pace

•       Create a favorable pH and lipid (oil) environment so that filaggrin-processing enzymes operate efficiently

Prescription and Medical Treatments

For moderate to severe eczema, prescription options are often necessary alongside skin barrier repair. These include:

•       Topical corticosteroids: the treatment to quickly reduce inflammation and itch during flareups; should be used for the shortest possible duration and as infrequently as possible

•       Topical calcineurin inhibitors (e.g., tacrolimus): a non-steroidal anti-inflammatory option suitable for sensitive areas like the face

•       Biologic drugs (e.g., dupilumab): target specific inflammatory pathways and have been found to be highly effective for severe atopic eczema that doesn’t respond to conventional topical treatment

You should see a dermatologist: if your eczema is unresponsive to over-the-counter treatments; if it significantly impacts your sleep or quality of life; or if you develop skin infections (a sign that your skin barrier has been severely compromised).

The Role of Corneodesmosin: The “Glue Protein”

While filaggrin gets most of the attention in eczema research, it has an equally important partner, corneodesmosin. If filaggrin shapes the bricks, corneodesmosin is the link that binds them.

Corneodesmosin is found in structures called corneodesmosomes which are tiny molecular rivets that hold adjacent skin cells together in the stratum corneum. These structures serve two opposing but coordinated functions, namely:

•       They provide cohesion and structural strength, keeping the skin barrier intact against everyday physical stress

•       They are gradually broken down by specific enzymes, allowing old skin cells to be shed in a controlled, orderly way

Think of corneodesmosin as “smart glue”. Strong enough to hold the skin barrier together but engineered to let go at exactly the right moment so old cells don’t pile up and make the skin thick and rough (like in psoriasis, a different CDSN disorder).

When it comes to eczema, corneodesmosin-related processes are frequently disrupted. When the skin’s pH rises (as it does when filaggrin is deficient), the enzymes responsible for breaking down corneodesmosomes may become overactive. This can cause the outer skin cells to shed too quickly, further weakening the barrier. Conversely, inflammation can also cause excessive corneodesmosin activity, making the skin thick and flaky.

Why This Matters: When both filaggrin and corneodesmosin are disrupted simultaneously, as they are in atopic eczema, the skin loses both its hydration (from reduced NMF) and its structural integrity (from impaired cell adhesion). The result is a skin barrier that is leaky, fragile, and easily inflamed.

Prevention Strategies

While filaggrin mutations cannot be changed, their consequences can often be minimized through consistent, science-informed skincare habits. These include:

•       Moisturize immediately after bathing. Apply moisturizer within three minutes of getting out of the shower or bath, while the skin is still slightly damp. This seals in water before it evaporates.  Depending on your origin, a moisturizer that helps stimulates filaggrin may help even more.

•       Choose fragrance-free, pH-balanced products. Fragrances are among the most common contact allergens in skincare. A pH-balanced product (pH around 4.5–5.5) supports healthy enzyme activity in the skin and discourages Staphylococcus aureus colonization.

•       Use gentle cleansers. Traditional soaps have an alkaline pH (9–10), which disrupts the skin’s natural acid mantle and accelerates corneodesmosin breakdown. pH adjusted soaps or liquid cleansers with a pH closer to skin’s natural level are far gentler.

•       Manage environmental triggers proactively. Use a humidifier in dry environments, avoid wool or synthetic fabrics directly against the skin, and wash new clothing before wearing it to remove residual irritants.  This is especially true for people of African descent where environmental factors play a key role in triggering eczema.

•       Treat skin consistently, not just during flares. The skin barrier takes time to rebuild. Barrier-repair products only work if applied regularly — waiting until a flare is already underway is far less effective than daily preventive care.  This rebuilding usually takes 2 to 6 months, depending on the severity of eczema, so patience is key.

•       Consider dietary support. Research suggests that adequate intake of essential fatty acids, vitamin D, and amino acids (including L-histidine) supports healthy skin barrier function from the inside out.

Myths and Facts About Filaggrin and Eczema

Myth: Eczema is just dry skin.

Fact: Eczema is a complex condition rooted in genetic barrier dysfunction and immune system dysregulation. Regular dry skin lacks the inflammatory component.

Myth: If your parents didn’t have eczema, you won’t get it.

Fact: Filaggrin gene mutations can appear without a strong family history of eczema, and environmental factors play a significant role even in genetically susceptible individuals.

Myth: More moisturizer means better skin barrier protection.

Fact: The formulation matters a lot more than the quantity. A well-formulated barrier-repair product with ceramides and NMF-like ingredients outperforms a generic lotion.

Myth: Topical steroids will cure eczema.

Fact: Steroids reduce inflammation during flareups, but they do not repair the underlying skin barrier defect. In fact, long-term use of topical steroids over large areas of the body will further reduce filaggrin production making future flares worse. Long-term management requires barrier focused care plus anti-inflammatory treatment.

Personal Stories

The science of filaggrin becomes most meaningful when we see how it plays out in people’s lives. The following accounts represent experiences commonly shared by individuals managing eczema with a barrier-first approach.

Mary L. – March 18, 2026

At 67 I’m still fighting chronic eczema-like skin issues. The itching was at a point of being debilitating. I have been using the eczema relief lotion, the nourishing face oil and the hydrating skin superfood for about 2 months and I am pleased to say I am having decent results. The itching is much more contained and the severely dry skin, head to foot, has been better hydrated and just so much more comfortable… even during winter. If you’ve struggled with sensitivity and product allergies like I have, you may find relief in Codex products. I certainly have.

Valentina – February 9, 2026

I received this and some other products as a gift. I was having an irritant contact dermatitis situation from my cpap mask. These products helped me with not only that but also with my little patch of eczema, and with combating the problems I experience in the winter. I put this over all my other steps under my spf, really helps protect my skin without irritation.

Tracy M. – December 2, 2025

Definitely helped: The supplement drink was good-tasting, so easy to drink. Soap smelled fine. Lotion easy to rub on. Within a couple of days, my flare up eased. It’s been unmanageable for 3 months so I was desperate to try this.Happy with the result.

Recommended Products from Codex Labs

Codex Labs Corporation is a Delaware-incorporated, science-forward skincare brand committed to developing formulations grounded in peer-reviewed research. Our eczema-focused line was specifically developed to help replenish, support and enhance the skin barrier by utilizing the biology of skin and, in particular, filaggrin and corneodesmosin science, as the technology’s primary focal point.

In addition, and what truly sets Codex Labs apart from others in the eczema space, is the inside-out approach taken to provide meaningful relief from the symptoms of eczema, i.e., dry skin, inflammation, and itch. Codex products not only tackle the issue of eczema topically (outside) but, when used in combination with our skin barrier strengthening dietary supplements (inside), provide a 360-degree treatment regimen that is sure to bring you much needed relief.

Our recommended protocol for eczema-prone, filaggrin-deficient skin addresses the barrier at multiple levels:

•       Barrier-repair lipid base — ceramide and linoleic acid (sunflower oil)-containing formulation to restore the mortar between skin cells

•       NMF-mimicking humectants — including hyaluronic acid and glycerin to compensate for reduced filaggrin breakdown products

•       L-histidine inclusion — supplying the critical building block your skin needs to produce more filaggrin where gene expression is still partially active through supplementation

•       pH-optimized formulation — maintaining a slightly acidic surface environment that supports corneodesmosin enzyme balance and suppresses bacterial colonization

Explore our full eczema collection at codexlabscorp.com. For our specific eczema product set, visit: codexlabscorp.com/collections/eczema

Frequently Asked Questions (FAQ)

Question: What is filaggrin and what does it do?

Answer: Filaggrin is a protein that helps organize the structure of skin cells and then breaks down into natural moisturizing factors (NMF) that keep the outer skin layer hydrated and slightly acidic.

Question: What is a filaggrin mutation?

Answer: A filaggrin mutation, also called an FLG loss-of-function mutation, is a genetic change that reduces how much filaggrin the skin can produce, leading to a weaker barrier and increased eczema risk.

Question: Does filaggrin deficiency cause eczema?

Answer: Filaggrin deficiency is one of the strongest genetic risk factors for atopic eczema, but eczema also involves immune dysregulation and environmental factors.

Question: How is filaggrin tested?

Answer: Filaggrin mutation status can be identified through genetic testing (e.g., a skin biopsy or blood test for FLG gene variants), though this is not yet routine in most clinical settings.

Question: Can you increase filaggrin production?

Answer: You cannot change your FLG genes, but supplying building blocks like L-histidine and using filaggrin-stimulating skincare products may support greater filaggrin output where the gene is still partially functional.

Question: What does natural moisturizing factor (NMF) do?

Answer: NMF is a mixture of small, water-binding molecules, produced when filaggrin breaks down, that keeps the outer skin layer hydrated, flexible, and slightly acidic.

Question: What is corneodesmosin?

Answer: Corneodesmosin is a protein that acts as “smart glue” between outer skin cells, keeping the barrier intact while also allowing old cells to shed at the proper rate.

Question: What ingredients help repair the skin barrier in eczema?

Answer: Key ingredients include ceramides, fatty acids, cholesterol, humectants (glycerin, hyaluronic acid, amino acids), and filaggrin-supporting amino acids like L-histidine.

 Question: Is eczema genetic?

Answer: Yes, in many cases. FLG gene mutations are a major genetic risk factor, though environment and immune factors also play important roles.

Conclusion

Filaggrin is far more than a minor footnote in dermatology. It is a cornerstone of how your skin protects you from the world. When filaggrin works well, your skin stays hydrated, flexible, and resilient. When it doesn’t, whether due to genetics, inflammation, or environmental stress, the consequences ripple outward into the chronic, relentless cycle of eczema.

The encouraging news is that understanding filaggrin gives us a roadmap for better treatment. The brick-and-mortar model of skin health, the role of natural moisturizing factor, the function of corneodesmosin as the glue holding it all together, these are no longer abstract scientific concepts. They are the rationale behind choosing the right moisturizer, using it consistently, and considering targeted ingredients like L-histidine that address the root of the problem rather than just the surface symptoms.

If you are managing eczema, you deserve more than a one-size-fits-all approach. Seek care from a dermatologist who understands the barrier model, choose products formulated with these mechanisms in mind, and know that every consistent step you take toward barrier repair is genuinely helping your skin rebuild itself.

Call to Action

At Codex Labs, our team of researchers developed an eczema-relief regimen that blew us away in terms of how well it works. The regimen involves the use of three products, namely, BIA® UNSCENTED SOAP, together with the afore-mentioned, patent-pending BIA® ECZEMA RELIEF LOTION, and ANTU® SKIN BARRIER SUPPORT SUPPLEMENT with the filaggrin-supporting amino acid L-histidine. The study’s participants used unscented soap to gently cleanse their skin, after which they topically applied the eczema relief lotion, all while taking the skin barrier support supplement. 

Codex has scientifically developed age-appropriate regimens to ensure optimized quantities of relief-generating actives are delivered. These include:

-       the BIA BABY/INFANT REGIMEN for those aged 3 – 12 months

-       the BIA TODDLER REGIMEN for those aged 1 – 3 years

-       the BIA KIDS REGIMEN for those aged 4 - 12 years

-       the BIA TEENS REGIMEN for those aged 13 - 18 years

-       the BIA ADULTS REGIMEN for those aged 18+

 These age-appropriate regimens of symptom relieving products, when used daily, yield shockingly efficacious results. How do we know? Because we have the clinical data to prove it!

Citing Sources for Medical Research

The following peer-reviewed and clinical sources support the information presented in this article:

1.     Irvine, A.D., McLean, W.H.I., & Leung, D.Y.M. (2011). Filaggrin mutations associated with skin and allergic diseases. New England Journal of Medicine, 365(14), 1315–1327. https://doi.org/10.1056/NEJMra1011040

2.     Palmer, C.N., et al. (2006). Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nature Genetics, 38(4), 441–446. https://doi.org/10.1038/ng1767

3.     Elias, P.M., & Schmuth, M. (2009). Abnormal skin barrier in the etiopathogenesis of atopic dermatitis. Current Allergy and Asthma Reports, 9(4), 265–272. https://doi.org/10.1007/s11882-009-0037-x

4.     Cork, M.J., et al. (2009). New perspectives on epidermal barrier dysfunction in atopic dermatitis: Gene–environment interactions. Journal of Allergy and Clinical Immunology, 124(3 Suppl 2), R7–15. https://doi.org/10.1016/j.jaci.2009.07.007

5.     Langan, S.M., Irvine, A.D., & Weidinger, S. (2020). Atopic dermatitis. The Lancet, 396(10247), 345–360. https://doi.org/10.1016/S0140-6736(20)31286-1

6.     Kezic, S., et al. (2012). Levels of filaggrin degradation products are influenced by both filaggrin genotype and atopic dermatitis severity. Allergy, 67(8), 1076–1084. https://doi.org/10.1111/j.1398-9995.2012.02849.x

7.     Ref: S.J. Brown, W.H.I. McLean, Eczema genetics: Current state of knowledge and future goals, J Invest Dermatol, 129 (2009), pp. 543-552