Impact of Life-Threatening Childhood Food Allergies
Impact of Life-Threatening Childhood Food Allergies
Food allergy, or food hypersensitivity, can be defined as an adverse or exaggerated immunological response to food proteins resulting in a myriad of clinical symptoms (Sampson, 2004; Sicherer & Sampson, 2006). Reactions can involve the skin, gastrointestinal tract, and respiratory tract, and may be due to either an immunoglobulin E (IgE) or non-IgE mediated response (Sampson, 2004). IgE mediated responses are accountable for the allergic reactions experienced by individuals with life-threatening food allergies (Sicherer & Sampson, 2006).
Various explanations attempt to highlight the epidemiological origin of IgE and non-IgE mediated food allergies. Of the more well-known explanations, genetics has long been thought to influence sensitization and subsequent development of food allergy. Studies involving both monozygotic and dizygotic twins have provided reliable evidence to support this hypothesis (Sohi & Warner, 2008). However, the increase in prevalence of food allergies suggests that environmental factors may play a role in their development, and the hygiene hypothesis has become a new model researchers are exploring.
The hygeine hypothesis was first exposed in the late 1980s during a study on hay fever that revealed an increased number of older siblings was associated with a decreased risk of developing hay fever and eczema (Sohi & Warner, 2008). Findings from this study led scientists to believe that older siblings created an opportunity for infection to occur through unhygienic contact with younger siblings, thus creating an effective level of resistance to development of atopic disorders, such as asthma, eczema, and allergies (Sohi & Warner, 2008). Researchers have suggested that decrease in family size coupled with increased emphasis on hygienic practices in Westernized nations may explain the increasing prevalence of allergies and other atopic manifestations (Sohi & Warner, 2008).
Food allergy among children is now recognized as a worldwide issue in Westernized nations, and prevalence appears to be increasing (Nowak-Wegrzyn, 2003; Sampson, 2004; Shimamoto & Bock, 2002). In the United States alone, from 1997 to 2007, there was an 18% increase in prevalence of food allergy among children under the age of 18 years (Branum & Lukacs, 2008). More recent statistics reveal 8% of young children in the United States suffer from food allergy. Of these children, approximately 30% have multiple food allergies, and 38.7% have a history of severe food-induced reactions (Gupta et al., 2011).
Although food allergy can develop at any age, it most often appears within the first 1 to 2 years of life after the process of sensitization has occurred (Wood, 2003). Sensitization occurs in susceptible individuals during initial exposure to a food antigen. Specific IgE antibodies to that antigen form and attach to receptors on the surface of mast cells and basophils. When the food antigen is subsequently ingested, the antigen binds to the IgE antibodies and causes both mast cells and basophils to release histamine, an inflammatory mediator. Inflammatory mediators bring about the classic symptoms of swelling (especially facial), urticaria, palatal itching and tingling, throat itching and tightness, nasal pruritis and congestion, rhinorrhea, hoarseness, stridor, dry cough, dyspnea and/or wheezing, cyanosis, dizziness, hypotension, tachycardia, colicky abdominal cramps, generalized erythema, nausea, vomiting, diarrhea (often bloody), chest pain, circulatory collapse, coma, and death (Butt & Macdougall, 2008; Kagy & Blaiss, 1998; Mandell, Curtis, Gold, & Hardie, 2005; Neuget, Ghatak, & Miller, 2001; Sampson, 2004; Sicherer & Sampson, 2006; Shimamoto & Bock, 2002). Ninety percent of sensitized children react to one of eight common offenders: cow's milk, egg, wheat, soy, tree nuts, ground nut (peanut), fish, and shellfish (Anderson, 1997; Kurkowski & Boxer, 2008; O'B Hourihane, 2006; Sicherer & Sampson, 2006; Sohi & Warner, 2008). Although it is common for children to outgrow these allergies, some may endure for a lifetime (Wood, 2003).
Anaphylaxis is a serious result of an IgE mediated allergic response and can occur within minutes after ingesting a food antigen to which the child has been previously sensitized (Shimamoto & Bock, 2002). Commonly, a sensitized child need only ingest a very small amount of the food allergen to produce symptoms. Food-induced anaphylaxis (FIA) is currently the leading cause of anaphylactic reactions occurring outside of the hospital setting (Bollinger et al., 2006; Clark & Camargo, 2005; Shimamoto & Bock, 2002), and the myriad of symptoms can vary greatly in onset, presentation, and course.
Food Allergy: Overview
Food allergy, or food hypersensitivity, can be defined as an adverse or exaggerated immunological response to food proteins resulting in a myriad of clinical symptoms (Sampson, 2004; Sicherer & Sampson, 2006). Reactions can involve the skin, gastrointestinal tract, and respiratory tract, and may be due to either an immunoglobulin E (IgE) or non-IgE mediated response (Sampson, 2004). IgE mediated responses are accountable for the allergic reactions experienced by individuals with life-threatening food allergies (Sicherer & Sampson, 2006).
Various explanations attempt to highlight the epidemiological origin of IgE and non-IgE mediated food allergies. Of the more well-known explanations, genetics has long been thought to influence sensitization and subsequent development of food allergy. Studies involving both monozygotic and dizygotic twins have provided reliable evidence to support this hypothesis (Sohi & Warner, 2008). However, the increase in prevalence of food allergies suggests that environmental factors may play a role in their development, and the hygiene hypothesis has become a new model researchers are exploring.
The hygeine hypothesis was first exposed in the late 1980s during a study on hay fever that revealed an increased number of older siblings was associated with a decreased risk of developing hay fever and eczema (Sohi & Warner, 2008). Findings from this study led scientists to believe that older siblings created an opportunity for infection to occur through unhygienic contact with younger siblings, thus creating an effective level of resistance to development of atopic disorders, such as asthma, eczema, and allergies (Sohi & Warner, 2008). Researchers have suggested that decrease in family size coupled with increased emphasis on hygienic practices in Westernized nations may explain the increasing prevalence of allergies and other atopic manifestations (Sohi & Warner, 2008).
Prevalence
Food allergy among children is now recognized as a worldwide issue in Westernized nations, and prevalence appears to be increasing (Nowak-Wegrzyn, 2003; Sampson, 2004; Shimamoto & Bock, 2002). In the United States alone, from 1997 to 2007, there was an 18% increase in prevalence of food allergy among children under the age of 18 years (Branum & Lukacs, 2008). More recent statistics reveal 8% of young children in the United States suffer from food allergy. Of these children, approximately 30% have multiple food allergies, and 38.7% have a history of severe food-induced reactions (Gupta et al., 2011).
Sensitization
Although food allergy can develop at any age, it most often appears within the first 1 to 2 years of life after the process of sensitization has occurred (Wood, 2003). Sensitization occurs in susceptible individuals during initial exposure to a food antigen. Specific IgE antibodies to that antigen form and attach to receptors on the surface of mast cells and basophils. When the food antigen is subsequently ingested, the antigen binds to the IgE antibodies and causes both mast cells and basophils to release histamine, an inflammatory mediator. Inflammatory mediators bring about the classic symptoms of swelling (especially facial), urticaria, palatal itching and tingling, throat itching and tightness, nasal pruritis and congestion, rhinorrhea, hoarseness, stridor, dry cough, dyspnea and/or wheezing, cyanosis, dizziness, hypotension, tachycardia, colicky abdominal cramps, generalized erythema, nausea, vomiting, diarrhea (often bloody), chest pain, circulatory collapse, coma, and death (Butt & Macdougall, 2008; Kagy & Blaiss, 1998; Mandell, Curtis, Gold, & Hardie, 2005; Neuget, Ghatak, & Miller, 2001; Sampson, 2004; Sicherer & Sampson, 2006; Shimamoto & Bock, 2002). Ninety percent of sensitized children react to one of eight common offenders: cow's milk, egg, wheat, soy, tree nuts, ground nut (peanut), fish, and shellfish (Anderson, 1997; Kurkowski & Boxer, 2008; O'B Hourihane, 2006; Sicherer & Sampson, 2006; Sohi & Warner, 2008). Although it is common for children to outgrow these allergies, some may endure for a lifetime (Wood, 2003).
Anaphylaxis
Anaphylaxis is a serious result of an IgE mediated allergic response and can occur within minutes after ingesting a food antigen to which the child has been previously sensitized (Shimamoto & Bock, 2002). Commonly, a sensitized child need only ingest a very small amount of the food allergen to produce symptoms. Food-induced anaphylaxis (FIA) is currently the leading cause of anaphylactic reactions occurring outside of the hospital setting (Bollinger et al., 2006; Clark & Camargo, 2005; Shimamoto & Bock, 2002), and the myriad of symptoms can vary greatly in onset, presentation, and course.
