A food allergy is not just difficulty digesting a food but rather the immune system’s overreaction to a specific food that sparks a reaction. The actual reaction that produces symptoms involves a complex sequence of events. Although food allergies can arise at any stage in life, the vast majority have their onset in childhood, particularly in the first one to two years.

A virgin immune system has no reason to launch an all-out attack on a harmless food. It has to be properly sensitized to the food first (through an initial exposure). Sensitization is the process by which the immune system starts producing antibodies to a food that causes the immune system to overreact the next time it’s exposed to that food.

The mechanics of exactly what happens to trigger the first reaction can be somewhat complicated. In the following sections, I provide a brief overview of how sensitization leads to future reactions and how the resulting antibodies react when a problem food is reintroduced.

A food allergy is an immune system response to a food that the body mistakenly believes is harmful. Here’s a blow-by-blow description of what occurs during a typical reaction:

1. Once the immune system decides that a particular food is harmful, it creates specific IgE (Immunoglobulin E) antibodies to it. The following section introduces you to IgE.

2. The next time the individual eats that food, the immune system releases massive amounts of chemicals, including histamine, as shown in Figure below.

3. These chemicals trigger a cascade of allergic symptoms that can affect the respiratory system, gastrointestinal tract, skin, or cardiovascular system.

Although most food allergies are caused by these IgE antibodies, some do not involve IgE but rather other parts of the immune system. These are particularly common with some of the food allergies that affect the gastrointestinal tract and are referred to as non-IgE-mediated food allergies.

Your immune system produces four main classes of antibodies produced — IgG, IgA, IgM, and IgE. The first three types serve to fight infection and are critical to our health. The purpose of IgE is to fight infection, specifically parasitic infections. These IgE antibodies, however, also cause allergic reactions.

As parasitic infections have become less common in the developed world, IgE can devote more and more of its energy toward allergy. Here’s a quick overview of how IgE comes into play:

1. Once IgE is produced, it sits on the surface of the main allergy cells of the body called the mast cells and basophils.

2. The IgE that your body produces is specific for one allergen or another, and when that specific allergen reenters the body, it finds the IgE sitting on the surface of the cells.

3. Once the allergen finds the IgE, the immune system triggers the release of histamine and other chemicals that cause allergic symptoms.

The same process occurs with environmental allergens that cause hay fever and other conditions.

What causes you to develop an allergy in the first place? Is it your genetic makeup? Something in our food supply? Something you ate too much of as a kid? A great deal of research has been devoted to answering these questions, and the best answer that researchers have developed so far is that food allergies are caused by a combination of nature (your genes) and nurture (what you eat).

The best evidence available for a genetic connection comes from studies of peanut allergy in twins. The medical community knows that allergies run in families, so the genetic link is well established, but we also know that children in the same families — even twins — do not always share the same allergies.

This has led researchers to suspect that genes account only for a susceptibility to food allergies. If parents have hay fever or asthma, for example, their children are more prone to developing an allergic disease, including hay fever, asthma, eczema, or food allergy. One child may develop food allergy, another may develop hay fever, and a third may be allergy-free. Why this happens is still largely a mystery.

A genetic predisposition to a food allergy is like a genetic predisposition to bruising. Even if you bruise easily, you won’t get a bruise unless you get whacked with something. With food allergy, you’re highly unlikely to develop an allergy unless you’re predisposed to react to a particular allergen and then exposed to that allergen.

This sensitizes your immune system to the allergen, making you susceptible to future reactions. The formula that causes the onset of a food allergy is well known: Genetic Predisposition + Exposure = Sensitization. After your immune system is sensitized to a particular allergen, exposure to that allergen potentially leads to symptoms, as shown in Figure below.

The exposure piece of the equation gets pretty complicated. For those who are predisposed to developing a food allergy, the type of exposure may influence the likelihood that the exposure triggers onset, as the following general tendencies reveal:

• Repeated low-dose exposure to an allergen early in life is most likely to sensitize you to a specific allergen. In other words, you’re more likely to develop a food allergy to an allergen that repeatedly enters your system in small amounts, such as in breast feeding, trace amounts in foods, or even incidental contact.

• Large-dose exposures early in life may make you less likely to develop a food allergy. Odd, but true — increased exposure to an allergen may actually make you less sensitive to that food. Hold on. Don’t start feeing your baby peanut-based formula or advising nursing mothers to gobble up more peanuts.

At this point, doctors have no reliable way to implement this observation in a preventive treatment plan. Based on the best information currently available, the recommendation is still to avoid peanut and other common allergens early in life.

• Avoidance diets may or may not help ward off the development of a food allergy. Although my colleagues and I recommend that parents limit exposure to common food allergens early in their children’s lives, research results waffle on the conclusion.

While some studies show that avoidance diets early in life ward off the onset of food allergies, others have failed to uphold these results. We commonly see children who are born into allergic families where exposure has been virtually or completely eliminated develop the allergy.

The mother may never have eaten peanut during pregnancy or breast feeding, all peanut has been banned from the premises, and incidental contact is highly unlikely, but the child still develops a peanut allergy.

My belief is that these children are so genetically prone to developing the allergy that even inhaling a few errant molecules of peanut protein in the grocery store or shopping mall may be enough to trigger the sensitization process.