Asthma is a chronic inflammatory disease that affects the airways, causing them to narrow, swell, and produce extra mucus, which leads to difficulty breathing, wheezing, and coughing. The condition is influenced by a combination of inherited genetic susceptibility and external environmental factors. While the answer to whether asthma is hereditary is yes, it is not caused by inheriting a single gene.
Quantifying the Genetic Risk
The likelihood of developing asthma increases significantly with a family history of the condition. For an individual with no family history, the baseline risk of developing asthma is approximately 5%.
The risk profile shifts based on the closeness of the affected relative. If one parent has asthma, the child’s risk rises substantially to about 25%. This risk doubles to roughly 50% if both parents have been diagnosed with asthma. Having a full sibling with the condition also results in a risk of roughly 25%.
The Polygenic Nature of Asthma
Asthma is classified as a polygenic disorder, meaning it is caused by the cumulative effect of variations across multiple genes, not a single defective gene. These gene variants, or single nucleotide polymorphisms, each contribute a small amount to the overall risk. This complex genetic architecture explains why the condition does not follow the clear-cut inheritance patterns seen in single-gene disorders.
Scientists have identified numerous genetic regions associated with asthma susceptibility that influence different biological processes. Some gene variants affect the immune system’s regulation, predisposing the body to allergic responses and inflammation. Other variants influence the structure and function of the airways, making them more prone to hyperresponsiveness and muscle constriction.
The cumulative effect of these risk variants is often quantified using a polygenic risk score, which predicts susceptibility based on the total genetic load. A highly studied region is the 17q21 locus, which contains the ORMDL3 and GSDMB genes, strongly linked to childhood-onset asthma. Other genes, such as IL33 and IL1RL1, are involved in the signaling pathways of inflammatory proteins that drive the allergic response in the lungs.
How Environment Interacts with Genes
Genetic susceptibility alone is rarely enough to cause asthma, which is why the condition is considered a gene-environment interaction disorder. The inherited genetic factors create the biological predisposition, but external environmental exposures often serve as the “trigger” for the disease to manifest. This interaction is a central concept in understanding the development of the condition.
Specific gene variants can make an individual uniquely sensitive to common environmental irritants. For instance, some genes involved in detoxification, like the Glutathione-S-transferase (GSTM1) family, interact with air pollutants. Individuals with certain variants in these genes may have a reduced ability to neutralize the effects of traffic-related air pollution or nitrogen dioxide from indoor sources like gas stoves.
Early-life exposure to environmental tobacco smoke (ETS), also known as secondhand smoke, is another powerful example of this interaction. Studies show that genes located on chromosome 5q, which are linked to immune and inflammatory responses, increase asthma risk only when an infant is exposed to ETS. Exposure to high levels of common allergens or viral respiratory infections in early childhood can similarly interact with inherited immune-regulating genes.
Inherited Risk Versus Certainty
A family history of asthma establishes a higher baseline risk, but it does not predetermine a diagnosis. Identical twins, who share 100% of their DNA, have a concordance rate of only about 70-75% for asthma. This confirms that genetics are powerful but not the sole determinant, as the remaining difference is attributable to the unique environmental exposures and life experiences of each twin.
Individuals with a high genetic predisposition can mitigate their risk by actively controlling their environment. Reducing exposure to known environmental triggers, such as avoiding smoking during pregnancy and minimizing a child’s exposure to indoor air pollutants, can modify how the inherited genes are expressed. This focused management provides a practical avenue for risk reduction, even when a genetic susceptibility exists.