Egg Allergy
Introduction
Section titled “Introduction”Egg allergy is one of the most common food allergies, particularly prevalent in infancy, and represents a significant global public health concern.[1] Its prevalence has shown a consistent increase over the past two decades in many regions, including Europe and Australia.[1]This condition involves an adverse immune response to proteins found in hen’s eggs. It is a complex disease influenced by both genetic predispositions and environmental factors.[1]Twin studies have estimated the heritability of food allergy, including egg allergy, to be substantial, around 80%.[1]
Biological Basis
Section titled “Biological Basis”The biological basis of egg allergy involves intricate genetic mechanisms. Genome-wide association studies (GWAS) have begun to unravel the genetic architecture underlying this condition. For instance, suggestive maternal genetic effects on egg allergy have been observed, with specific single nucleotide polymorphisms (SNPs) likers4572450 and rs1343795 on chromosome 17 showing associations.[2] These SNPs are located in the ZNF652gene, which has previously been linked to atopic dermatitis.[2] It is hypothesized that maternal genetic variations in the ZNF652gene might be associated with maternal eczema during pregnancy, subsequently influencing the development of egg allergy in the offspring.[2]While some studies did not find genome-wide significant associations specifically for egg allergy alone, broader food allergy GWAS have identified susceptibility loci, such as theSERPINBgene cluster, which are relevant given that hen’s egg allergy is a specific type of food allergy.[1]
Clinical Relevance
Section titled “Clinical Relevance”Clinically, egg allergy can manifest with a range of symptoms, from mild reactions to severe, life-threatening anaphylaxis.[1] Accurate diagnosis is crucial and typically relies on a convincing history of clinical allergic reaction upon ingesting eggs, coupled with evidence of sensitization. This evidence can include a detectable level of food-specific IgE (≥ 0.10 kU L−1) and/or a positive skin prick test (with a mean weal diameter ≥ 3 mm) to the specified food.[3]Given its potential for severe reactions, understanding and managing egg allergy is paramount for affected individuals and their families.
Social Importance
Section titled “Social Importance”The rising prevalence of egg allergy worldwide underscores its social importance. It impacts the daily lives of affected children and their families, necessitating careful dietary management and emergency preparedness. Research into the genetic underpinnings of egg allergy aims to provide a deeper understanding of its etiology, potentially leading to improved diagnostic tools, targeted prevention strategies, and more effective treatments.
Sample Size and Statistical Power
Section titled “Sample Size and Statistical Power”Genetic studies of complex traits like egg allergy are often constrained by sample size, which significantly impacts the ability to detect subtle genetic effects. Despite some studies representing the largest genome-wide association studies (GWAS) on food allergy to date, the number of individuals, particularly for specific subtypes such as egg allergy, remains relatively small Within this cluster, thers1243064 variant, an intergenic polymorphism near SERPINB7 and SERPINB2, has shown a strong association with hen’s egg allergy, reaching genome-wide significance in meta-analyses.[1] SERPINB7 (serpin peptidase inhibitor, clade B, member 7) is highly expressed in the upper layers of the epidermis, and its proper function is vital for maintaining skin barrier integrity; loss-of-function mutations can lead to skin barrier deficiencies, suggesting its role in preventing allergen entry.[1] The risk allele for rs1243064 is identified as a tissue-specific expression quantitative trait locus (eQTL), meaning it can influence the expression levels of genes like SERPINB10 in whole blood, thereby potentially modulating immune responses relevant to the development of allergic conditions.[1]Further genetic insights into egg allergy involve variants in genes such asZNF652 and GRIN2B. The rs1343795 variant, an intronic SNP within the ZNF652gene, has been suggestively associated with egg allergy.[2] ZNF652encodes a zinc finger protein, which functions as a transcription factor regulating gene expression, and variations in this gene may influence maternal eczema during pregnancy, potentially impacting offspring’s risk of egg allergy.[2] Separately, the rs12227569 variant is linked to the GRIN2Bgene, which codes for a subunit of the N-methyl-D-aspartate (NMDA) receptor, a crucial component in neurotransmission.[2] While GRIN2Bis primarily recognized for its role in brain function, alterations in NMDA receptor signaling could indirectly affect the complex interplay between the nervous and immune systems, including interactions along the gut-brain axis, which are relevant to the development and manifestation of allergic diseases.[2]Other variants under investigation for their potential roles in egg allergy and related traits includers17023017 in BMPR1B, rs7717393 in SGCD, rs5961136 in ITIH6, rs16823014 in ABCB11, rs250585 in COG7, rs6498482 associated with TMF1P1 and ERCC4, and rs2303921 linked to TAF1B. The BMPR1Bgene encodes a receptor involved in bone and cartilage development and cell differentiation, processes that can intersect with immune system regulation.[1] SGCDis important for muscle membrane integrity, and its broader cellular functions might influence inflammatory pathways relevant to allergic responses.[2] ITIH6 contributes to extracellular matrix organization and inflammation, which could impact tissue remodeling during allergic reactions.[1] ABCB11is crucial for bile acid transport and liver function, potentially influencing the gut microbiome and immune tolerance, whileCOG7 plays a role in glycosylation and protein trafficking, critical for cell surface receptor function and immune cell signaling.[2] Lastly, TMF1P1, ERCC4, and TAF1B are involved in diverse cellular processes, including transcriptional regulation and DNA repair, which can indirectly affect immune cell development and responses, thereby modulating an individual’s susceptibility to allergies.[1]
Defining Egg Allergy and its Phenotypic Spectrum
Section titled “Defining Egg Allergy and its Phenotypic Spectrum”Egg allergy is precisely defined as a specific type of food allergy (FA) characterized by an adverse immunological reaction to proteins found in hen’s egg. This condition is distinguished from other adverse food reactions by the involvement of the immune system, often mediated by immunoglobulin E (IgE) antibodies.[3]The conceptual framework for diagnosing egg allergy typically involves a two-pronged approach: a convincing history of a clinical allergic reaction upon ingestion of egg, coupled with objective evidence of sensitization to egg components.[3] This rigorous definition is crucial, as studies indicate a significant discrepancy between self-reported food allergies and those confirmed by objective diagnostic methods, with self-reported prevalence often being substantially higher than challenge-proven prevalence.[1]The classification of egg allergy places it as one of the most common and distinct phenotypes within the broader category of “any FA,” alongside peanut and cow’s milk allergies.[3]Individuals are categorized as having egg allergy if they meet the established diagnostic criteria for this specific food. Conversely, normal controls are defined by the absence of both clinical allergic reactions and evidence of sensitization to any of the common food allergens, including egg.[3] The term “uncertain FA phenotypes” is used when a definitive history of clinical allergic reaction following specific food ingestion is unavailable, highlighting the importance of comprehensive clinical data for precise classification.[3]
Diagnostic Criteria and Approaches
Section titled “Diagnostic Criteria and Approaches”The diagnosis of egg allergy relies on a combination of clinical criteria and specific approaches to confirm both a reaction history and immunological sensitization. Key diagnostic criteria include a convincing history of an allergic reaction after egg ingestion and evidence of sensitization, typically measured by detectable food-specific IgE (sIgE) levels and/or a positive skin prick test (SPT).[3] Operational definitions for sensitization often specify thresholds; for instance, a detectable sIgE is commonly defined as ≥ 0.10 kU L−1, while a positive SPT to egg is defined by a mean wheal diameter (MWD) of ≥ 3 mm.[3] For SPT, additional criteria ensure reliability, such as a negative control MWD < 3 mm, a positive control MWD ≥ 3 mm, and a difference between positive and negative controls ≥ 3 mm.[3]The gold standard for diagnosing food allergy, including egg allergy, is the Oral Food Challenge (OFC), with double-blind placebo-controlled OFCs (DBPCFC) being the most definitive approach.[1]A positive OFC is scored based on objective cutaneous, gastrointestinal, respiratory, or cardiovascular reactions attributable to the allergen, distinct from any placebo effect.[1] In cases where OFC is contraindicated due to the risk of severe allergic reactions, a diagnosis can be made based on a convincing history of an immediate, severe allergic reaction combined with specific sensitization, such as an IgE level > 0.35 kU l−1.[1] Research studies often explore the robustness of these definitions by performing sensitivity tests using alternative cut-off values for sIgE (e.g., ≥ 0.35 kU L−1) and SPT (e.g., MWD ≥ 5 mm or 95% positive predictive value) to assess the impact of different thresholds on diagnostic outcomes.[3]
Genetic and Environmental Factors in Egg Allergy Phenotypes
Section titled “Genetic and Environmental Factors in Egg Allergy Phenotypes”While the core definition of egg allergy is based on clinical and immunological responses, research acknowledges the influence of genetic and environmental factors in shaping its phenotype. Genetic studies, such as genome-wide association studies (GWAS), investigate potential susceptibility loci associated with egg allergy. Although specific genome-wide significant or suggestive single nucleotide polymorphisms (SNPs) for egg allergy were not consistently identified in some studies, suggestive maternal genetic effects have been observed.[3] For instance, SNPs like rs4572450 and rs16948048 in or near the ZNF652gene have shown marginal maternal genetic effects on egg allergy, potentially linking maternal eczema during pregnancy to offspring egg allergy risk.[2]These findings suggest that the manifestation and severity of egg allergy may involve complex interactions between a child’s genotype, maternal genetic contributions, and environmental exposures. The term “phenotype definition” in this context encompasses not only the presence or absence of the allergy but also potential underlying genetic predispositions that could inform future classifications or subtyping of egg allergy. Understanding these related concepts and their nomenclature is essential for advancing research into the etiology and prevention of food allergies.
Clinical Evaluation and Oral Food Challenges
Section titled “Clinical Evaluation and Oral Food Challenges”The diagnosis of hen’s egg allergy typically commences with a comprehensive clinical evaluation, emphasizing a convincing history of an allergic reaction immediately following the ingestion of egg-containing foods. This detailed history is paramount for pinpointing potential allergens and understanding the presentation of the allergic response . This complex condition involves an interplay of genetic predispositions, specific immunological pathways, and environmental factors that disrupt normal immune tolerance and lead to hypersensitivity. The heritability of food allergy, including egg allergy, is estimated to be approximately 80%, indicating a strong genetic component.[1]Understanding the underlying biological mechanisms is crucial for better diagnosis, management, and potential prevention strategies for egg allergy.
Immunological Basis of Egg Allergy
Section titled “Immunological Basis of Egg Allergy”Egg allergy manifests through a dysregulated immune response where the body mistakenly identifies egg proteins as harmful, leading to allergic reactions that can range from mild to life-threatening anaphylaxis.[1]A key biomolecule in this process is food-specific Immunoglobulin E (IgE), an antibody that plays a central role in sensitizing immune cells. Upon initial exposure to egg allergens, antigen-presenting cells process the proteins and present them to T helper cells, which then promote B cell differentiation into plasma cells that produce allergen-specific IgE. This IgE then binds to high-affinity receptors on mast cells and basophils, priming them for a rapid response upon subsequent allergen exposure.[3]Upon re-exposure, egg allergens cross-link the IgE antibodies on the surface of these primed cells, triggering their degranulation and the release of pre-formed mediators such as histamine, as well as newly synthesized mediators like leukotrienes and prostaglandins. This cascade of molecular and cellular events leads to the characteristic symptoms of an allergic reaction, affecting various tissues and organs including the skin, gastrointestinal tract, respiratory system, and cardiovascular system, potentially leading to systemic consequences like anaphylaxis.[1] Furthermore, Innate Lymphoid Cells Type 2 (ILC2s) have been implicated in promoting food allergy by blocking the generation of mucosal allergen-specific regulatory T cells, which are crucial for maintaining immune tolerance and suppressing allergic responses.[1]
Genetic Contributions to Allergic Predisposition
Section titled “Genetic Contributions to Allergic Predisposition”Genetic mechanisms play a substantial role in an individual’s susceptibility to egg allergy, with several gene loci identified as contributing factors. TheSERPINBgene cluster, located on chromosome 18q21.3, has been identified as a significant susceptibility locus for food allergy, and specific variants within this cluster, such asrs12964116 and rs1243064 , have shown associations with hen’s egg allergy.[1]Serine protease inhibitors (SERPINs) are a superfamily of proteins that regulate proteolytic cascades involved in inflammation, immunity, and tissue remodeling, suggesting that genetic variations in these genes can disrupt immune homeostasis and contribute to the allergic phenotype. Additionally, while primarily associated with peanut allergy, theHLA-DQB1 locus, a component of the Major Histocompatibility Complex (MHC) on chromosome 6, is critical for presenting antigens to T cells and is broadly involved in immune recognition, suggesting its general relevance in the genetic architecture of food allergies.[1] Other genetic regions, such as those on chromosome 1q21.3 (rs12123821 ) and 5q31.1 (rs11949166 ), have also shown genome-wide significant associations with general food allergy and some evidence of association with hen’s egg allergy.[1] These loci likely contain genes or regulatory elements that influence various molecular and cellular pathways involved in immune cell development, function, and the regulation of inflammatory responses. Genetic variations in these regions can alter gene expression patterns or protein functions, thereby modulating an individual’s propensity to develop an allergic reaction to egg proteins.
Barrier Function and Environmental Modulators
Section titled “Barrier Function and Environmental Modulators”The integrity of biological barriers, particularly the skin, plays a critical role in preventing allergen sensitization and is influenced by specific genetic mechanisms. Loss-of-function mutations in the epidermal barrier gene FLG (filaggrin) have been shown to increase the risk for allergen sensitization, including peanut, by compromising the skin barrier.[1]A defective skin barrier allows allergens to penetrate more easily, initiating an immune response through the skin rather than the gut, which can skew the immune system towards an allergic phenotype. This pathophysiological process underscores the interconnectedness of different organ systems in allergy development.
Environmental factors, often interacting with genetic predispositions, further modulate the risk of egg allergy. For instance, theC11orf30/LRRC32 region, which contains the rs2212434 SNP, is a known risk locus for eczema, asthma, and other inflammatory diseases, and has also been replicated for food allergy.[1] Eczema, characterized by skin barrier dysfunction, can serve as a gateway for allergen exposure, contributing to sensitization. This highlights how systemic conditions and tissue interactions, such as those between the skin and the immune system, can significantly influence the development and severity of food allergies.
Maternal Genetic Effects and Offspring Risk
Section titled “Maternal Genetic Effects and Offspring Risk”Maternal genetic factors have been observed to exert suggestive influences on the risk of egg allergy in offspring. Specifically, maternal genetic effects, such as those associated withrs4572450 and rs1343795 on chromosome 17, located within the ZNF652gene, have been linked to egg allergy.[2] The ZNF652 gene encodes a zinc finger protein, which typically functions as a transcription factor, suggesting its involvement in regulating gene expression patterns that could influence immune development or inflammatory processes. Genetic variations in ZNF652may alter its regulatory networks, thereby affecting cellular functions relevant to allergy.
Research indicates that maternal eczema during pregnancy is associated with an increased risk of offspring egg allergy.[2] This observation supports the hypothesis that maternal genetic variations in genes like ZNF652could be linked to maternal eczema, which in turn contributes to the development of egg allergy in the child. These findings highlight the complex interplay of maternal genetics, maternal health conditions, and the subsequent impact on developmental processes and homeostatic disruptions in the offspring’s immune system, influencing their susceptibility to specific food allergies like egg allergy.[2]
Genetic Modulators of Epithelial Barrier Integrity
Section titled “Genetic Modulators of Epithelial Barrier Integrity”Genetic variations play a crucial role in predisposing individuals to egg allergy by influencing key biological pathways, particularly those governing epithelial barrier function. TheSERPINBgene cluster, identified as a susceptibility locus for food allergy, includes genes likeSERPINB7, which is highly expressed in the upper layers of the epidermis and other stratified epithelia.[1] Loss-of-function mutations in SERPINB7 are linked to conditions characterized by skin barrier deficiency, suggesting that variations in this gene cluster can compromise the integrity of epithelial barriers in the skin and potentially the digestive tract.[1]This compromised barrier function may facilitate increased allergen penetration, serving as an initial step in sensitizing the immune system to egg proteins and contributing to the development of egg allergy.[1]Specific single nucleotide polymorphisms (SNPs) within this cluster, such asrs12964116 and rs1243064 , are implicated in this process.[1] rs1243064 acts as a tissue-specific expression quantitative trait locus (eQTL), where the risk allele is negatively correlated with gene expression, potentially altering the levels of proteins critical for epithelial maintenance.[1]Such genetic predispositions directly impact the physical barrier, which is a primary defense against allergens, and illustrate how gene regulation can influence disease susceptibility at a fundamental level.
Immune Cell Activation and Cytokine Dysregulation
Section titled “Immune Cell Activation and Cytokine Dysregulation”The development of egg allergy involves complex immune signaling pathways, particularly the regulation of T helper type 2 (Th2) cell responses. The genetic variant rs12964116 , located within the SERPINB gene cluster, alters binding sites for critical transcription factors, including CEBPB and STAT3.[1] CEBPB is known to regulate the expression of Th2 effector cytokines such as interleukin-13 (IL-13), interleukin-4 (IL-4), and interleukin-5 (IL-5), which are central to allergic inflammation, and also plays a role in promoting mucosal immunity.[1] Concurrently, STAT3 binding at this locus is essential for Th2 cell development in allergic inflammation models, indicating that altered binding due to rs12964116 can lead to dysregulated Th2 responses.[1]This intricate interplay between genetic variations, transcription factor activity, and cytokine production highlights a core mechanism through which immune cells become aberrantly activated, driving the allergic reaction to egg proteins.
Maternal and Epigenetic Contributions to Allergy Risk
Section titled “Maternal and Epigenetic Contributions to Allergy Risk”Maternal genetic factors and the intrauterine environment represent significant pathways influencing offspring susceptibility to egg allergy. Suggestive maternal genetic effects on egg allergy have been observed, with SNPs likers4572450 and nearby variants located in the ZNF652 gene.[2] It is hypothesized that maternal genetic variations in ZNF652may be associated with maternal eczema during pregnancy, which in turn increases the risk for the development of egg allergy in the offspring.[2] This suggests a pathway where maternal health conditions, potentially genetically mediated, can directly influence the child’s allergic predisposition. Furthermore, maternal metabolic alterations or environmental triggers experienced during pregnancy, such as stress or weight gain, may interact with maternal genetic variants to influence the intrauterine environment or induce infant epigenetic variations from the prenatal period onwards.[2]These epigenetic modifications could alter gene expression patterns in the developing fetus, establishing a heightened susceptibility to food allergies like egg allergy.
Integrated Network Dysregulation in Allergic Disease
Section titled “Integrated Network Dysregulation in Allergic Disease”The pathogenesis of egg allergy represents a systems-level integration of genetic, environmental, and immunological pathways, where dysregulation at multiple points contributes to the emergent allergic phenotype. The genetic susceptibility loci, such as theSERPINB gene cluster and the C11orf30/LRRC32region, which is also associated with inflammatory diseases like eczema and asthma, illustrate pathway crosstalk and shared genetic underpinnings across allergic conditions.[1] Disruptions in epithelial barrier function, as mediated by SERPINB7, create an entry point for allergens, which then interact with a genetically predisposed immune system.[1] The altered regulation of transcription factors like CEBPB and STAT3 further propagates this dysregulation by skewing the immune response towards an allergic Th2profile, characterized by excessive cytokine production.[1]This hierarchical regulation, from genetic variants influencing barrier integrity to altered immune signaling and the impact of maternal factors, collectively forms a complex network where pathway dysregulation leads to the characteristic symptoms of egg allergy.
Genetic Predisposition and Risk Stratification
Section titled “Genetic Predisposition and Risk Stratification”Research into the genetic factors influencing egg allergy aims to uncover specific genetic variants that contribute to an individual’s susceptibility. While genome-wide association studies (GWAS) have identified significant genetic loci for other food allergies, large-scale analyses have yet to find genome-wide significant or highly suggestive single nucleotide polymorphisms (SNPs) directly associated with egg allergy in populations of European ancestry.[3]This suggests that the genetic architecture for egg allergy may involve numerous variants with smaller individual effects, necessitating even larger study cohorts for their robust identification, as current study power may be insufficient to detect variants with moderate effect sizes.[1] The eventual identification of such genetic markers could pave the way for more personalized medicine approaches, enabling early risk stratification and potentially guiding targeted preventive strategies for high-risk individuals.
Diagnostic Considerations and Phenotype Characterization
Section titled “Diagnostic Considerations and Phenotype Characterization”The accurate diagnosis of egg allergy is fundamental for effective clinical management, relying on established criteria that encompass a convincing history of a clinical allergic reaction upon egg ingestion, alongside objective evidence of sensitization. This evidence typically includes a detectable food-specific IgE level (≥ 0.10 kU/L) and/or a positive skin prick test (SPT) with a mean wheal diameter of 3 mm or greater.[3] In situations where oral food challenges (OFCs) are contraindicated due to the risk of severe reactions, a strong history combined with a specific IgE level greater than 0.35 kU/L may be sufficient for diagnosis.[1] Thus, while genetic insights continue to evolve, current clinical practice remains centered on established immunological and historical diagnostic methods.
Maternal Factors and Associated Conditions
Section titled “Maternal Factors and Associated Conditions”Emerging research indicates a role for maternal genetic influences in the development of egg allergy in offspring. Studies have observed suggestive maternal genetic effects, with specific SNPs such asrs4572450 and rs1343795 located within the ZNF652gene demonstrating associations with egg allergy.[2] Notably, genetic variants in ZNF652have also been associated with atopic dermatitis, a frequently co-occurring condition in individuals with allergies, and maternal eczema during pregnancy has been linked to an elevated risk of offspring egg allergy.[2]These findings suggest that maternal genetic variations, possibly by influencing maternal atopic conditions, could serve as an important prognostic indicator for offspring egg allergy risk, offering potential avenues for early life interventions or enhanced monitoring strategies based on maternal health and family history.[2] Further investigation is essential to fully elucidate these complex maternal-fetal genetic interactions and their comprehensive clinical implications.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs1243064 | SERPINB7 - SERPINB2 | egg allergy |
| rs17023017 | BMPR1B | egg allergy |
| rs7717393 | SGCD | egg allergy |
| rs5961136 | ITIH6 | egg allergy |
| rs16823014 | ABCB11 | egg allergy |
| rs250585 | COG7 | egg allergy |
| rs6498482 | TMF1P1 - ERCC4 | egg allergy heart rate |
| rs1343795 | ZNF652 | cancer egg allergy |
| rs12227569 | GRIN2B | egg allergy |
| rs2303921 | TAF1B | egg allergy |
Frequently Asked Questions About Egg Allergy
Section titled “Frequently Asked Questions About Egg Allergy”These questions address the most important and specific aspects of egg allergy based on current genetic research.
1. If I have egg allergy, will my children get it too?
Section titled “1. If I have egg allergy, will my children get it too?”Yes, there’s a strong genetic link. Twin studies show that egg allergy heritability is substantial, around 80%. This means your children have a higher chance of developing it if you have it, though it’s not a guarantee as environmental factors also play a role.
2. Why did my sibling get egg allergy, but I didn’t?
Section titled “2. Why did my sibling get egg allergy, but I didn’t?”Egg allergy is complex. Even with a strong genetic component, specific gene variations, like those in theSERPINB cluster or other yet-to-be-identified genes, can differ between siblings. Also, environmental factors interact with your genes, leading to different outcomes even within the same family.
3. Could my health during pregnancy affect my baby’s egg allergy risk?
Section titled “3. Could my health during pregnancy affect my baby’s egg allergy risk?”Yes, your health during pregnancy might play a role. Research suggests maternal genetic variations, particularly in the ZNF652gene, could be linked to maternal eczema during pregnancy. This, in turn, is hypothesized to influence the development of egg allergy in your offspring.
4. Is a blood test enough to know if I’m allergic to eggs?
Section titled “4. Is a blood test enough to know if I’m allergic to eggs?”It depends, but usually, a blood test for food-specific IgE levels (detectable at ≥ 0.10 kU L−1) is part of it. However, a definitive diagnosis also requires a convincing history of a clinical allergic reaction after eating eggs, often coupled with a positive skin prick test (weal diameter ≥ 3 mm).
5. Why is it hard for doctors to definitively diagnose egg allergy?
Section titled “5. Why is it hard for doctors to definitively diagnose egg allergy?”Diagnosing egg allergy precisely is challenging because it requires strict criteria, often including oral food challenges, which are hard to do widely. Also, different doctors might use slightly varied cutoffs for IgE levels or skin prick test results, which can lead to some inconsistency or misclassification if your full clinical history isn’t available.
6. Does my family’s ethnic background affect my egg allergy risk?
Section titled “6. Does my family’s ethnic background affect my egg allergy risk?”Yes, your ethnic background can matter. Many genetic studies on egg allergy have primarily focused on people of European ancestry. While findings from these groups are important, their relevance and specific genetic risk factors for other ancestral populations are often still being investigated and may differ.
7. Can I prevent my child’s egg allergy even if it runs in our family?
Section titled “7. Can I prevent my child’s egg allergy even if it runs in our family?”While genetics play a significant role with about 80% heritability, environmental factors are also crucial. Current research aims to understand these gene-environment interactions better. This understanding could eventually lead to targeted prevention strategies, but more research is needed to provide specific actionable advice.
8. Why do some people have really severe egg allergy reactions?
Section titled “8. Why do some people have really severe egg allergy reactions?”Egg allergy can manifest very differently, from mild reactions to severe, life-threatening anaphylaxis. This wide range of symptoms is part of the complex biological basis of the condition, influenced by the interplay of various genetic predispositions and environmental factors.
9. Can a DNA test tell me if my baby will have egg allergy?
Section titled “9. Can a DNA test tell me if my baby will have egg allergy?”A DNA test can identify some genetic susceptibility loci, like those in the SERPINB gene cluster or maternal ZNF652variations. However, current genetic variants only explain a modest fraction of the total heritability, meaning a DNA test cannot fully predict if your baby will develop an egg allergy, as much of the genetic picture is still unknown.
10. Is my own eczema linked to my child’s egg allergy?
Section titled “10. Is my own eczema linked to my child’s egg allergy?”Yes, there’s a hypothesized link. Specific maternal genetic variations in the ZNF652gene, which has been linked to atopic dermatitis (eczema), are thought to be associated with maternal eczema during pregnancy. This, in turn, is proposed to influence the development of egg allergy in your child.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Marenholz I et al. “Genome-wide association study identifies the SERPINB gene cluster as a susceptibility locus for food allergy.”Nat Commun, vol. 8, no. 1, 2017, p. 1056.
[2] Liu X et al. “Genome-wide association study of maternal genetic effects and parent-of-origin effects on food allergy.” Medicine (Baltimore). 2018 Feb;97(7):e9655. PMID: 29489655.
[3] Hong X et al. “Genome-wide association study identifies peanut allergy-specific loci and evidence of epigenetic mediation in US children.”Nat Commun, vol. 6, 2015, p. 6304.