Allergic response Conditions caused by food allergies are classified into three groups according to the mechanism of the allergic response: # IgE-mediated (classic) – the most common type, manifesting acute changes that occur shortly after eating, and may progress to anaphylaxis # Non-IgE mediated – characterized by an immune response not involving immunoglobulin E; may occur hours to days after eating, complicating diagnosis # IgE and non-IgE-mediated – a hybrid of the above two types Allergic reactions are hyperactive responses of the immune system to generally innocuous substances, such as food proteins. Why some proteins trigger allergic reactions while others do not is not entirely clear. One theory holds that proteins which resist digestion in the stomach, therefore reaching the small intestine relatively intact, are more likely to be allergenic, but studies have shown that digestion may abolish, decrease, have no effect, or even increase the allergenicity of food allergens. The heat of cooking structurally degrades protein molecules, potentially making them less allergenic. Hypersensitivities are categorized according to the parts of the immune system that are attacked and the amount of time it takes for the response to occur. The four types of hypersensitivity reaction are: type 1, immediate IgE-mediated; type 2, cytotoxic; type 3, immune complex-mediated; and type 4, delayed cell-mediated. The consequent pathophysiology of allergic responses can be divided into two time periods. The first is an acute response that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late-phase reaction" which can substantially prolong the symptoms of a response, and result in more tissue damage. In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils. Both of these are involved in the acute inflammatory response. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators called (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system while hives and eczema are localized to the skin. In addition to reacting to oral consumption, skin reactions can be triggered by contact if there are skin abrasions or cuts. Hives allergic reaction on arm After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial reaction sites. This is usually seen 2–24 hours after the original reaction. Cytokines from mast cells may also play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils. In addition to IgE-mediated responses,<unk>  can manifest as atopic dermatitis, especially in infants and young children. Some will display both, so that a child could react to an oral food challenge with allergic symptoms, followed a day or two later with a flare up of atopic dermatitis and/or gastrointestinal symptoms, including allergic eosinophilic esophagitis.<unk> nic proteins The protein parvalbumin has been identified as the major allergen causing<unk>  (but not shellfish allergy, which is caused by tropomyosin). Parvalbumin is resistant to heat and enzymatic digestion, so cooking does not diminish its allergenic potency, nor do digestive enzymes. Bony fishes manifest β-parvalbumin whereas cartilaginous fishes such as sharks and rays manifest α-parvalbumin; allergenicity to bony fishes has a low cross-reactivity to cartilaginous fishes. In addition to β-parvalbumin, fish enolase, aldolase and collagen can also trigger allergic reactions. Fish collagen is widely used in the food industry in foods such as gummy candies, jelly beans or marshmallows. It may also be marketed as a dietary supplement ingredient or as an inactive ingredient in pharmaceutical products. Standardized skin tests that incorporate parvalbumin for fish sensitivity will miss collagen allergy. People may be allergic to parvalbumin, collagen, or both. Non-allergic intolerance Histidine, the amino acid precursor to histamine Histamine, the chemical structure shown, causes a person to feel itchy during an allergic reaction Scombroid food poisoning, also referred to as scrombroid, is a reaction from consuming fish that mimics an allergic reaction. It is caused by high concentrations of histamine, synthesized by bacteria in spoiled fish. Histamine is the main natural chemical responsible for true allergic reactions, hence the confusion with<unk> . Scombroid symptoms onset is typically 10-30 minutes after consumption, and may include flushed skin, headache, itchiness, blurred vision, abdominal cramps and diarrhea. Fish commonly implicated include tuna, mackerel, sardine, anchovy, herring, bluefish, amberjack and marlin. These fish naturally have high levels of the amino acid histidine, which is converted to histamine when bacterial growth occurs during improper storage. Subsequent cooking, smoking, canning or freezing does not eliminate the histamine.
Fish allergy
Scombroid food poisoning
Poultry allergy
Shellfish allergy
Insect sting allergy
Peanut allergy
Fruit allergy
Egg allergy