IgG food intolerance tests: do they make sense and what to do instead

The immune system produces antibodies of different classes. IgE are responsible for immediate allergic reactions: their binding to an allergen releases histamine from mast cells, which gives urticaria, swelling and sometimes anaphylaxis. IgG is a class of antibodies that appear in response to contact with almost any protein, food proteins included, and take part in normal defence and in shaping tolerance. That IgG directed against egg or milk proteins appear in the blood after eating them is an entirely physiological phenomenon.

That is why the result of an IgG panel usually has a clear logic: the highest levels concern the foods you eat most often. If you drink milk, eat eggs and bread every day, the result will show 'elevated' IgG against milk, eggs and wheat, whereas foods you never eat will be 'normal'. After a month of exclusion the elevated result often falls, which laboratories present as proof of effectiveness, although it merely reflects a change in exposure. Such a result mirrors your eating habits, not your body's reaction to a harmful ingredient.

A Polish review article from 2016 by a team from Collegium Medicum in Bydgoszcz reaches similar conclusions. The authors recall that IgG-specific reactions are a natural and normal defensive reaction of the body to food antigens, and that specific IgG antibodies to food allergens play a significant role in inducing and maintaining immunological tolerance. The statements of many scientific societies stress that specific IgG are of no significant importance in diagnosing food allergy, because their presence is associated with a normal immune response and attests to prolonged exposure to food antigens.

Fairness requires discussing the trial that supporters of the tests cite. It is one of the few randomised controlled trials that assessed an elimination diet based on an IgG result.

How should this be read? First, the trial concerned only IBS, not 'food intolerances' in general. Second, the effect was small in the analysis of all participants (10%), and larger only in people who adhered strictly to the diet, which is an analysis of lower reliability. Third, the authors themselves noted that the result needs further studies, and in the material we reviewed we did not find large trials confirming this effect. Fourth, the trial did not show that IgG are the cause of symptoms: a diet excluding several or a dozen foods can improve well-being for many other reasons, including the change in eating habits and expectations. The EAACI position was published four years after this trial and nevertheless did not consider IgG tests diagnostically useful.

The greatest risk of IgG tests lies not in the blood drawn for the test but in what follows: a long list of excluded foods. Milk, eggs, wheat, yeast and many vegetables that appear in such reports are important sources of protein, calcium, B vitamins and fibre. Their long-term exclusion from the diet can lead to deficiencies, entrench fear of eating and lower quality of life, and in real diseases (for example celiac disease) can make diagnosis harder.

The gap between the proportion of people who think they have an allergy (19%) and the proportion with convincing allergy (10.8%) shows the scale of the phenomenon: a considerable share of people avoid foods without a confirmed reason. These data concern the USA and allergy, not so-called intolerances, but the conclusion is universal: before excluding a food it is worth confirming that it is what causes the problem. IgG tests add noise here rather than information, because they generate long lists of 'suspect' foods unrelated to symptoms.

The EAACI guidelines on diagnosing IgE-mediated food allergy describe a sensible pathway: it begins with an allergy-focused history, followed by tests assessing IgE sensitisation, that is the concentration of specific IgE in serum and skin prick tests, and in selected cases the basophil activation test. The reference standard of diagnosis is the oral food challenge, performed in equivocal situations. For some foods (for example peanut and cashew) skin tests and IgE confirm the diagnosis well, for others (for example wheat and soy) their performance is poorer.

We write about specific, well-defined problems separately: lactose intolerance (lactase deficiency), fructose, histamine and celiac disease. For many of them reliable tests exist, such as breath tests or celiac-specific antibody tests, whose diagnostic value is documented. An IgG result is not a substitute for them.

Many people who switched to the diet from an IgG report sincerely say that they felt better. There is no reason to suspect them of making it up, but the fact of improvement does not mean that the specific foods named were what worked. Below we list mechanisms that can explain improvement regardless of the test result. This is general reasoning, not the result of a single study, so we treat these as probable explanations, not proven for every case.

The last mechanism is particularly important: the longer the exclusion list, the greater the chance that something that really disturbs you will be removed by accident, and the result attributed to the test. This is why well-designed studies use a sham diet (as in the cited trial in IBS), and patients' accounts based on impression alone are not proof that the test works.

If after reading the conclusions you still want to check whether some food harms you, there is a method much better than an IgG panel: controlled elimination of one or a few suspect foods followed by reintroduction. Its point is to see whether symptoms resolve after exclusion and return after the food is put back, which gives more reliable information than any blood report. If an IgE-mediated allergy is suspected, reintroduction can be dangerous and must take place under a doctor's supervision.

What we do not know: it cannot be excluded that in some people with specific diseases (such as IBS) an IgG-based elimination diet brings benefit, but the mechanism remains unexplained and the evidence is limited to a single trial from more than twenty years ago. The conclusions of this article concern commercial 'intolerance panel' tests, not IgG tests used in other justified clinical indications, for example in assessing immunity or some autoimmune diseases. We do not assess particular laboratories or products.

The need for a simple answer to the question 'what harms me' is understandable, especially when intestinal complaints or fatigue make life difficult. An IgG test promises such an answer, but has nothing to back it with. Instead of another report with a list of forbidden foods it is worth investing in diagnostics that really change management: a proper history, a diary, tests for specific diseases and a structured elimination with a controlled return.