If you have eczema or a child with eczema, you may wonder if the condition is hereditary, or passed along by genes in your family. Researchers are still uncertain about exactly what causes eczema. The condition is likely caused by a combination of genetic and environmental factors that lead the skin to become more sensitive.
Chronic eczema, also called atopic dermatitis, is associated with certain genes. However, having these genes does not necessarily mean you will develop eczema. Twin studies, for instance, which examine people who have the same genes, show that the rate of eczema between twins is not 100 percent. While genetics make up a significant portion of susceptibility to eczema, this finding suggests that environmental factors are also key in the condition’s development.
Atopic dermatitis tends to run in families with a history of the condition. In fact, childhood eczema is two to three times higher in children whose mother or father has a history of eczema.
Eczema also tends to occur in families with a history of other atopic (allergy-related) conditions, such as asthma, hay fever, and food or environmental allergies (such as to pollen and pet hair). Approximately 70 percent of people living with atopic dermatitis have a family history of atopic conditions. About 30 percent of people diagnosed with atopic dermatitis also have food allergies. The risk of developing atopic dermatitis increases if both parents have atopic conditions. Because asthma, atopic dermatitis, and seasonal allergies often occur together, they are known as the atopic triad.
According to The Journal of Pediatrics, studies have found that certain inheritable genetic mutations may play a role in the development of eczema. These genes control the immune system as well as proteins that help keep the skin barrier healthy and functioning properly.
Currently, two theories explain how the genes FLG and CARD1 may lead to eczema. Other genes may also be involved. Much more research is needed to clarify the role of these genes and other gene mutations on the development of atopic dermatitis. Atopic dermatitis likely involves multiple genes, with environmental factors affecting the severity of a person’s condition.
The outside-inside theory supports the idea that the skin barrier has a mutation in the filaggrin gene (FLG) associated with contact dermatitis and atopic dermatitis. FLG is a gene that codes for the profilaggrin protein, which makes up the epidermal layer of the skin. The epidermal layer protects the body from environmental toxins and infections. Researchers estimate that 50 percent of eczema cases can be explained by an FLG gene mutation. This mutation is also the strongest genetic risk factor for the development of early-onset atopic dermatitis.
The inside-outside theory supports the idea that the immune system has an imbalance of T cells, which are immune cells that make up the dermis layer of the skin. T cells play an important role in the skin’s allergic responses. A gene called CARD11 helps T cells and other cells in the skin identify foreign substances and defend the body against infections. Genetic studies have found several mutations in the CARD11 gene of T cells associated with atopic dermatitis. Poor skin barrier function due to this mutation may allow for allergens and microbes to enter the skin and create an inflammatory or allergic reaction.
Another gene, KIF3A, has been found to decrease moisture in the skin barrier and lead to atopic dermatitis. Gene mutations allowing for more moisture to be lost from the skin to the atmosphere are associated with atopic dermatitis.
One study in The Journal of Allergy and Clinical Immunology found that the MTHFR gene, which codes for an enzyme that helps the body process the vitamin folate, may be associated with the development of asthma. The role of MTHFR mutations on the development of eczema is less clear, however. Another study cited in the International Journal of Epidemiology found that people with MTHFR mutations were more likely to have allergic conditions like eczema. On the other hand, a study in the journal Clinical and Experimental Allergy found no connection between MTHFR mutations and allergic conditions. More research is needed to understand the role MTHFR mutations can play in the development of conditions like eczema.
There is currently no cure for eczema, but there are ways you can prevent flare-ups and treat symptoms. In infants, it is important to treat eczema as early as possible. Applying topical moisturizers routinely and avoiding irritants such as harsh soaps and detergents, dyes and fragrances, itchy fabrics, dust, pollen, and extreme hot or cold temperatures are effective ways to prevent eczema flares.
Avoiding or removing known inflammatory foods from your diet may also help prevent eczema symptoms. These foods may include eggs, dairy, wheat, corn, and soy. It is important to talk with your doctor about identifying food allergies. While many people with atopic dermatitis have food allergies, the role of food in exacerbating the skin condition remains unclear.
Genetic tests and screening may be an option for people with a family history of eczema or atopic diseases. Blood and saliva tests can help identify mutations in the CARD11, FLG, or MTHFR genes. Talk with your doctor about genetic testing options.
Your dermatologist may also prescribe a steroid cream or other topical treatments to help control itching and repair the skin barrier. Antibiotic creams can help to fight bacterial infections from open sores or cracks. It is best to avoid scratching or rubbing the affected area of skin to help prevent infections or worsening of eczema symptoms. A newer medicine called dupilumab (sold as Dupixent) can help control more severe forms of the disease.
Read more about treatments for eczema here.
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