What you carry at this position in your DNA and what research says about it.
Asthma Inhaler Response: 8/10 evidence, 64 publications.
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Sample genotype (not yours): G/G
Typical Asthma Inhaler Response
Standard bronchodilator treatments generally provide effective airway relaxation. Regular use of maintenance inhalers is unlikely to cause a paradoxical worsening of asthma symptoms.
What this genotype means: Standard response to common bronchodilators; Lower risk of asthma flare-ups during regular treatment.
Sample genotype (not yours): A/A
Reduced Asthma Inhaler Response and Higher Flare-Up Risk
Regular use of long-acting beta-agonist inhalers may lead to a decline in their effectiveness over time. This can paradoxically increase the risk of asthma flare-ups during daily treatment.
What this genotype means: Diminished long-term response to daily beta-agonist inhalers; Increased risk of asthma flare-ups with frequent inhaler use; Better response to beta-blocker heart medications.
Sample genotype (not yours): G/A
Slightly Reduced Asthma Inhaler Response
Standard bronchodilator treatments are generally effective, but frequent use may slightly increase the risk of reduced efficacy. Monitoring asthma control during regular inhaler use is helpful.
What this genotype means: Slightly elevated risk of declining inhaler efficacy over time; Modestly increased risk of asthma worsening with daily inhaler use.
Gene function and biological role
Gene Function: The ADRB2 gene encodes the beta-2 adrenergic receptor, a protein highly expressed in the lungs, heart, and blood vessels [1]. These receptors play a critical role in relaxing airway smooth muscle and regulating heart rate in response to adrenaline [1]. When adrenaline binds to these receptors, it triggers bronchodilation, making it easier to breathe [2]. Because of this function, beta-2 adrenergic receptors are the primary targets for common asthma rescue and maintenance inhalers [2]. Variations in this gene can alter receptor structure, affecting how they respond to both natural adrenaline and therapeutic medications [3].
Variant Impact: The rs1042713 variant represents a missense mutation in the ADRB2 gene that changes the 16th amino acid of the receptor protein from glycine to arginine [1]. This specific structural change is located in the extracellular amino-terminus of the receptor, a region that influences how the receptor is regulated and degraded [1]. The arginine-encoding A allele makes the receptor more susceptible to downregulation, meaning the receptors are cleared from the cell surface more rapidly when repeatedly stimulated [2]. Consequently, frequent exposure to beta-agonist medications can lead to a rapid loss of active receptors in carriers of this variant [2]. This molecular behavior explains why some individuals experience a declining response to their inhalers over time [4].
Key Insight: Frequent use of standard asthma rescue inhalers can paradoxically reduce their effectiveness over time in individuals carrying the A allele due to rapid receptor clearance from cell surfaces.
Location: ADRB2. Chromosome 5 · 5q32 · 148.8 Mb
Estimated prevalence by population
Global 33.3%; European 39.4%; African 25.7%; East Asian 20.8%; South Asian 30.9%; Americas 31.9%; Ashkenazi 32.5%; Finnish 30.8%; Middle Eastern 36.7%; Amish 62.9%.
Estimated GG genotype frequency.
Global 48.2%; European 46.7%; African 50.0%; East Asian 49.6%; South Asian 49.4%; Americas 49.2%; Ashkenazi 49.0%; Finnish 49.4%; Middle Eastern 47.8%; Amish 32.9%.
Estimated GA genotype frequency.
Global 18.5%; European 13.9%; African 24.4%; East Asian 29.6%; South Asian 19.7%; Americas 18.9%; Ashkenazi 18.5%; Finnish 19.8%; Middle Eastern 15.6%; Amish 4.3%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Organ Systems
Respiratory Health
Inhaler Response. Evidence: 8/10. Source: PMID 16322642. Typical Response.
Asthma Flare-Up Risk. Evidence: 8/10. Source: PMID 16772309. Typical Risk.
Pharmacogenomics
Cardiovascular Drug Response
Beta-Blocker Response. Evidence: 5/10. Source: PMID 31090079. Poorer Response.
Lifestyle, Fitness & Aging
Physical Performance & Endurance
Exercise Fat Burning. Evidence: 5/10. Source: PMID 15687340. Typical Efficiency.
Showing effects for A/A genotype
Inhaler Response. Evidence: 8/10. Source: PMID 16322642. Poorer Response.
Asthma Flare-Up Risk. Evidence: 8/10. Source: PMID 16772309. 1.7x Increased Risk.
Beta-Blocker Response. Evidence: 5/10. Source: PMID 31090079. Stronger Response.
Exercise Fat Burning. Evidence: 5/10. Source: PMID 15687340. Reduced Efficiency.
Showing effects for G/A genotype
Inhaler Response. Evidence: 8/10. Source: PMID 16322642. Slightly Reduced.
Asthma Flare-Up Risk. Evidence: 8/10. Source: PMID 16772309. 1.3x Increased Risk.
Beta-Blocker Response. Evidence: 5/10. Source: PMID 31090079. Intermediate Response.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Receptors containing glycine at position 16 maintain stable expression on the cell surface even during repeated stimulation [1]. Clinical studies show that individuals with this genotype respond well to long-acting beta-agonists like salmeterol [1]. Regular use of these medications is associated with sustained bronchodilation and a lower risk of asthma exacerbations compared to other genotypes [2]. However, some research suggests that this genotype may be associated with a higher risk of hospital visits when taking certain cardiovascular medications like beta-blockers [3]. For respiratory health, this genetic profile represents the standard, favorable response to common asthma therapies [1].
Standard response to common bronchodilators; Lower risk of asthma flare-ups during regular treatment.
Sample genotype: AA (Homozygous)
Receptors entirely composed of arginine at position 16 undergo rapid downregulation and clearance from cell membranes when repeatedly exposed to beta-agonists [1]. Clinical trials have demonstrated that regular, daily use of salmeterol or frequent albuterol can lead to a progressive loss of bronchodilator response [1]. This receptor depletion is linked to a 1.7-fold higher risk of asthma exacerbations in pediatric patients undergoing daily treatment [2]. Conversely, this genotype is associated with a more favorable response to beta-blocker medications used for heart rate control and heart failure [3]. When managing asthma, alternative or additional controller therapies, such as leukotriene modifiers, are sometimes considered [4].
Diminished long-term response to daily beta-agonist inhalers; Increased risk of asthma flare-ups with frequent inhaler use; Better response to beta-blocker heart medications.
Sample genotype: GA (Heterozygous)
Carrying one copy of the arginine variant introduces a mixture of receptor types on the cell surface, with some being more prone to downregulation [1]. Research in pediatric populations indicates a modest 1.3-fold increased risk of asthma worsening when using daily inhaled beta-agonists [2]. While rescue inhalers still provide relief, the long-term efficacy of daily controller medications may be slightly diminished [3]. This intermediate response means that while standard therapies are typically first-line, close monitoring of symptom control is beneficial [2].
Slightly elevated risk of declining inhaler efficacy over time; Modestly increased risk of asthma worsening with daily inhaler use.
Variants with shared genetic architecture
rs1800888 · ADRB2 Gene · Chr 5 · Heart and Lung Health
rs1042714 · ADRB2 Gene · Chr 5 · Cardiovascular Health
rs1042711 · ADRB2 Gene · Chr 5 · Metabolic and Airway Health
beta-Adrenergic receptor polymorphisms and response to salmeterol.
Pharmacogenetics and healthcare outcomes in patients with chronic heart failure.
Content updated August 2026.
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