Paper: Clarke L, McQueen J, Samild A, Swain A. The dietary management of food allergy and food intolerance in children and adults. Australian Journal of Nutrition and Dietetics. 1996;53(3):89–98.
Available from: https://www.sswahs.nsw.gov.au/rpa/allergy/research/daareview.pdf
Overview of paper: This review paper, written for dietitians, covers the definition, symptoms, and diagnosis of food allergies and (pharmacological) food intolerance. The only way to diagnose food intolerance is through an elimination diet and subsequent food challenges, and “all patients with suspected food intolerance need to be assessed by a physician to exclude any other disorder” before starting down this path.
The quote:
In most patients [on an elimination diet], clinical improvement occurs gradually over a two- to four-week period. If there is no change in symptoms after four weeks of strict adherence to the elimination diet, then food intolerance is unlikely to be the main factor in causing the patient’s symptoms. A normal diet should then be resumed by reintroducing one suspect food or chemical group at a time (e.g. milk, wheat, salicylate, amines, preservatives and colours) in gradually increasing amounts, up to high doses for three to seven days to determine if symptoms are exacerbated.
Significance of quote: Even though pharmacological food intolerance reactions are often delayed, elimination diets only need to last for four weeks to rule out food intolerance.
Let’s talk some more about whether it’s a good idea to try an elimination diet on your own to check for sensitivities to milk, eggs, fish, crustacean shellfish, tree nuts, peanuts, wheat and soybean. As I explained in an earlier post, these foods are known as the Big 8 food allergens in the US, and anyone who suspects that they have ever had an allergic reaction to one of these foods should talk with their doctor. As we saw, food allergies often diminish over time, but they will never cross over into a food sensitivity or intolerance.
With that established, we can move on to another issue: Can the Big 8 allergenic foods also cause intolerances? Well, it is true that wheat, milk, soy, and eggs can trigger flare-ups in people with irritable bowel syndrome (IBS), but to date, no one has established that this is related to allergy or to pharmacological food intolerance. We also know that lactose intolerance is real, and egg whites, soy sauce, and spoiling fish have the potential to cause adverse reactions by way of biogenic amines (including histamine). But, for the most part, the answer to my question is “No.”
This is not to say that people cannot have other problems with these foods. In fact, outside food allergies and the limited examples of food intolerance I just mentioned, doctors have identified several disorders in adults where the immune system unnecessarily reacts to certain food proteins – these are listed in the table below under ‘Other immune system reactions.’ These problems can be quite serious, so they are not something you should try to diagnose on your own.
Table 1. Possible reactions to the Big 8 food allergens in adults. When dealing with these foods, there are a lot of reasons to see a doctor and not many reasons to do an elimination diet on your own.
Foods
Allergic reactions
Other immune system reactions
Food intolerances
Milk
Cow’s milk protein allergy
Cow’s milk protein intolerance (unknown mechanism)
Soy protein intolerance (only in children) Possible aggravation in celiac disease (?)
Possible amine intolerance to soy sauce (?)
Eggs
Egg allergy (to whites, yolk, or both)
–
Egg white intolerance (histamine)
Crustacean shellfish
Shellfish allergy
Food protein induced entercolitis syndrome – FPIES (rare but serious)
–
Fish
Fish allergy
–
Scombroid poisoning (histamine)
Peanuts
Peanut allergy
–
–
Tree nuts
Tree nut allergy
–
–
Any food protein (varies by person)
–
Eosinophilic esophagitis (usually males)
–
One more thing: In the table above, I have classified reactions to the Big 8 foods as food allergy, food intolerance, and other immune system reactions; however, you might also run into the term ‘food sensitivity’ on the Internet. It’s important to be clear about what this phrase implies. In many contexts, ‘food sensitivity’ can be used as a generic term to describe any type of adverse reaction to food. I’m often guilty of using it this way. However, when someone recommends that you try an elimination diet or take a blood test to see whether you have ‘food sensitivities’ to the Big 8 foods, they are probably referring to something very specific – and very incorrect – namely, the idea that you may have some kind of chronic, low-level allergic reaction to food that is undermining your health. These IgG-based ‘food sensitivities’ don’t actually exist and so are not listed in my table of possible reactions.
To summarize, most reactions to the Big 8 foods are serious problems that require proper medical care; light-weight allergic ‘food sensitivities’ do not exist, so there is no need to test for them on your own. Even in the case of gluten sensitivity, you need to be checked for possible celiac disease before you go gluten free. And you certainly shouldn’t try to test yourself for egg white or fish/histamine intolerance without having properly ruled out allergies to eggs or fish. If you do feel that you are experiencing symptoms related to food, the best thing to do (after seeing your doctor) is talk to a registered dietitian about other foods that can cause food intolerance.
I have mixed emotions whenever I see an article on the Internet that instructs people on using an elimination diet to discover their food sensitivities. Of course, it’s not the idea of an elimination diet that bothers me – I have said many times that a properly done elimination diet and food challenges are the only way to diagnose food intolerance. These articles worry me when they suggest testing for sensitivities to foods that are on the list of Big 8 allergens. Simply put, don’t mess with these foods without consulting your doctor.
The Big 8 foods account for 90% of the food allergies in the US. (Interestingly, the most common food allergens vary by country.) The Big 8 foods are milk, eggs, fish, crustacean shellfish, tree nuts, peanuts, wheat and soybean. Other notable allergens include buckwheat, sesame, celery, mustard, and even corn. Fruits can also cause allergic reactions, and, quite frankly, it is possible to be allergic to any food, even if it isn’t commonly thought of as an allergen. Deadly anaphylactic reactions in adults are most often caused by peanuts, but any allergen can lead to a life-threatening reaction, even when your previous reactions were mild.
Adult-onset allergies
Did you know that it is possible for adults to develop food allergies after a lifetime of being able to eat anything? Allergies can start at any age, and adult-onset food allergies come with an increased risk for severe reactions.
Recently, doctors from Northwestern University [1] wanted to learn more about adult-onset food allergies, so they looked at the medical records of 1,111 patients from their allergy clinics. Fifteen percent of these patients were newly diagnosed as adults. In this group, the average age of onset was 31 years old, and 64% of patients were women. Shellfish and fish were the most common allergens, but all of the major allergens were represented.
If you think that you may have experienced an allergic reaction to a food in the past – even something as small as tingling in the mouth or a delayed reaction – ask your doctor for help in ruling out food allergies. For each person, the minimum amount of allergen required to produce a reaction is different. While the minimum amount for some foods is generally small (think peanuts), others often require larger amounts. When you ‘challenge’ yourself with a food to see whether you have a reaction, you don’t want to get into trouble by eating a large amount of something you wouldn’t normally eat. Even if your doctor allows you to do the food challenges on your own, it’s better to have asked than to be sorry later.
You might wonder why certain Internet MDs and nutritionists are giving out bad advice on testing for sensitivities to these allergenic foods. Unfortunately, they are basing their advice on misinformation from the alternative medicine community. Alternative medicine will have you believe that there is a lower grade of allergic reaction – originally referred to as food intolerance but now most often called a ‘sensitivity’ – that occurs when your IgG antibodies try to protect you from harmful foods. (A different antibody, IgE, is responsible for true allergic reactions.) As the story goes, IgG-based symptoms are delayed but never deadly. The truth is, these reactions don’t exist, and IgG antibodies are present in all of us as a sign that we can tolerate the foods that we commonly eat, like wheat, milk, eggs, soy, etc. Don’t mistake your mild but true allergic reactions for one of these ‘sensitivities.’ Even though food allergies often diminish over time, they will never cross over into a food sensitivity.
For more information on the common foods that produce allergic reactions (and for some interesting reading, too), check out these websites:
Stay tuned for a second article on this topic, where I will discuss the other conditions associated with these food allergens that you should talk to your doctor about.
1. Kamdar TA, Peterson S, Lau CH, Saltoun CA, Gupta RS, Bryce PJ. Prevalence and characteristics of adult-onset food allergy. The Journal of Allergy and Clinical Immunology: In Practice. 2015 Jan;3(1):114–115.e1.
No blood test can detect food intolerance, not even the IgG/IgG4 ELISA tests that check for ‘hidden food intolerances’ to over a hundred common foods.
How do I get help, then?
Depending on where you live, it may be difficult to find a doctor or registered dietitian who has experience diagnosing food intolerance. Provided that your doctor has already ruled out other health problems, you can always contact the professional dietitics association in your country or visit their website. These associations maintain lists of dietitians by location and specialty. Depending on your medical history, some dietitians may be willing to consult with you from a distance.
Remember, the only way to diagnose food intolerance is through an elimination diet and food challenges. Even if you are concerned about a dairy or gluten sensitivity, IgG blood tests are of no value. (1-3)
In fact, allergy and immunology associations around the world have issued position statements warning against IgG blood tests, which they see as leading to potentially dangerous dietary restrictions, overlooked conditions (including true allergies), and unnecessary costs. Immunologists have found no evidence that IgG antibodies cause delayed food allergies or intolerances. As we’ll see later, it also turns out that the main demonstration of ‘successful’ IgG-based exclusion diets was not really so successful.
Still, you’re probably here because you have heard (from testing companies or the alternative medicine community, no doubt) that science supports not only the assumption behind IgG blood tests – that IgG antibodies are linked to delayed food sensitivities and chronic symptoms – but also the reported ability of IgG-based exclusion diets to relieve chronic illness. You may have also seen these tests in pharmacies or in the offices of doctors who practice functional or integrative medicine. You may be wondering, “Why are these tests being sold if they don’t work?”
“Why” involves motivation, so I’d rather focus on “how.” In the case of IgG blood tests, “how they can be sold” is an unfortunate melding of a few facts taken out of context plus some flawed research, with a few misrepresentations about how the immune system works thrown in. I must be clear, though – the problem isn’t one with consensus in the medical community. As I said, immunologists have not found any evidence of IgG-based food sensitivities, and it’s not as if they wouldn’t have noticed – for sure, IgG antibodies come up in research on immunotherapy, and this is a hot topic these days.
The alleged medical credibility of IgG blood tests is really coming from researchers in other specialties who hear about these tests and decide to give them a try for whatever condition they study (migraines, IBS, ADHD, etc.). This doesn’t seem particularly wise, but under the tenets of evidence-based medicine, a high-quality study should weed out bad ideas. However, in debunking the myths used to support food intolerance blood tests, we’ll see that not all studies are high quality.
Antibodies and allergies
Before we dive into the myths, let’s start with some background on antibodies and allergies. Antibodies, also known as immunoglobulins (Ig), are proteins produced by the immune system that help protect our bodies from foreign materials. There are several different classes of antibodies. For example, IgE antibodies bind to allergens (proteins from plants, animals, and fungi that should otherwise be of no threat to the body) and trigger histamine release from mast cells in what we think of as classical allergies (like to pollen or peanuts). Specialists refer to classical allergies as IgE-mediated reactions.
Allergy, intolerance, or sensitivity?
You may see different terms used to describe IgG blood tests – some say they detect food intolerance, others say delayed allergies, and others say food sensitivities. Since IgG antibodies are not involved in any adverse reactions to food, it doesn’t matter which label you choose – they’re all incorrect. Historically, though, these tests were advertised as detecting food intolerance, but the recent trend is to use the term food sensitivity. By medical convention, however, if IgG-based reactions were real, they would actually be a type of allergy. I prefer to speak of them as IgG-mediated reactions, but I do vary it a bit depending on the context.
The symptoms of IgE-mediated allergy come on rather abruptly after eating an offending food, often within 30 minutes to an hour. Other types of reactions – like cow’s milk protein intolerance – involve different aspects of the immune system and take longer to develop. Supporters of food intolerance blood tests believe that IgG antibodies cause yet another delayed type of allergic reaction, one which the medical community has failed to notice. Often this reaction is incorrectly labeled as food intolerance.
The IgG antibody class has several specialties, one of which is protective immunity. Protective immunity refers to our immune system’s ability to recognize and remove invaders like bacteria or viruses. This is also what keeps us from getting chicken pox twice. Blood is routinely screened for IgG antibodies to check for prior infections or vaccinations, but this is not the kind of blood test we’re talking about here.
IgG antibodies also support tolerance. Tolerance occurs when the immune system remembers to suppress its reaction to a foreign substance or to the body itself – in other words, tolerance is why the majority of us can eat whatever we want without fear of an allergic reaction. There are different mechanisms behind tolerance, but in many cases we have regulatory T cells to thank. Regulatory T cells invoke several helpers to suppress the immune response, and these include IgG antibodies. (4) IgG blocks IgE antibodies from combining with allergens and producing an allergic reaction, although the precise mechanics are under debate.
Even with this brief introduction, we can start to see that IgG antibodies are unlikely to be behind adverse reactions to food. The most advanced scientific knowledge points to the conclusion that food-specific IgG antibodies in our blood indicate exposure and tolerance, not in-tolerance, to those foods. (5) In other words, IgG antibodies are just a normal part of life. Unfortunately, commercial laboratories and alternative medicine still perpetuate the notion of IgG-mediated food reactions.
Taking on the myths behind IgG blood tests
We’ll debunk six myths that are used to support food intolerance blood tests:
Myths 1 and 2 cover the (lack of a) relationship between food-specific IgG antibodies and symptoms. Myths 3 through 5 get technical as they explore the mechanisms by which IgG antibodies (supposedly) cause illness. Myth 6 is the big one – it covers the claim that exclusion diets based on an individual’s food-specific IgG levels can successfully treat chronic symptoms. We’ll become amateur scientists to deal with this myth, and, in the process, we’ll see that sometimes it only takes a basic understanding of the scientific method and a little logic to evaluate medical studies.
Myth 1: High levels of IgG antibodies mean that you have a hidden or delayed reaction to food
Everyone produces IgG antibodies to food. Even though food intolerance blood tests rank your IgG antibody concentrations for various foods as low, medium, and high, there is actually no such thing as a ‘correct’ level. IgG concentrations vary from person to person and depend on diet – perhaps even on how one was fed as an infant (4) – so even healthy people will have high IgG levels for some foods. This means that a healthy person could get the same diet recommendations from an IgG blood test as a person with symptoms.
The same thing happens in classic food allergies, where there is no question that IgE antibodies are responsible. Some allergy-free people have elevated IgE levels, so doctors will not diagnose someone as having a classic (IgE-mediated) allergy without some sort of secondary evidence. This evidence could include a personal history, a physical exam, a skin-prick test, or an elimination diet and food challenge; of these, the strongest evidence is the elimination diet and food challenge.
Some supporters of IgG blood tests do acknowledge this situation indirectly by saying that the tests should only be used to “guide” a standard elimination diet and food challenge. So, then, how well do these tests perform as guides? Promotional materials almost always include testimonials by people who believe that an IgG blood test helped them find the foods behind their symptoms, and this is not surprising. As Brostoff and Gamlin (6) point out, alternative therapies could not make viable businesses if there were no successes. But these authors go on to explain that success stories are far from evidence that a test is worth your money:
“Given that the most common sources of food intolerance are wheat and milk, such therapists can achieve a reasonable success rate by diagnosing sensitivity to these two foods in all their patients. If eggs, oranges, chocolate, tea, and coffee are added to the list, they may well achieve success with 50 percent or more, and some patients will benefit from the placebo effect alone.” (p. 141)
So it seems that common sense would have about a 50% chance of finding at least some of the relevant foods for people who, we assume, actually have a food sensitivity. That’s the same odds as flipping a coin – any blood test would certainly need to do better than that. But in a 2001 survey of UK residents who had taken the YorkTest IgG blood test, only about 50% saw significant improvement in symptoms after eliminating their reported foods. (7) [The survey was repeated in 2007 (8), but its write-up contains a hole: it does not give us enough information to calculate an analogous success rate to compare with the first survey (9).] All in all, it looks like IgG blood tests, common sense, and luck offer about the same amount of help for guiding an elimination diet.
Myth 2: Food-specific IgG antibody levels correlate with chronic symptoms
You may be surprised to learn that no one has shown that food-specific IgG levels correlate with symptoms. The few studies that looked for a relationship gave mixed results – for example, testing of over 5,000 people with self-reported food reactions (10) found positive correlations for antibodies to certain foods and negative correlations for others. A negative correlation means that high antibody levels are associated with health, which certainly goes against pro-IgG claims. Most importantly, only one of these studies ensured that the participants actually had food sensitivities in the first place, and this small study found no relationship between IgG levels and, in their case, irritable bowel syndrome. (11)
Confirming up-front that participants have food sensitivities (and to which foods) is a fundamental requirement of any study on food allergy or intolerance – without it, all conclusions are meaningless. Moreover, the verification of food sensitivities must be done in some way that is independent of what is being researched. After all, you can’t diagnose someone as having food sensitivity using the IgG blood test when it is the blood test itself that you are investigating. And you can’t just ask someone if they experience adverse reactions to food, because more people think that they have a food sensitivity (up to 10 times more) than actually do. Food sensitivities can only be verified through careful elimination diets and food challenges.
In scientific terms, the strictest elimination diet/food challenge protocol is called the double blind placebo controlled food challenge (DBPCFC), because there is an additional requirement that both participants and researchers be ‘blind’ to whether a person is given a placebo or a real food challenge. The DBPCFC is the gold standard of food allergy and food intolerance diagnosis, which means that it is the standard to which the validity of any new test, like a blood test, must be compared. All good research on food sensitivities requires the DBPCFC, but most studies that look for IgG-mediated reactions fail to use it. This will come into play again when we consider Myth 6.
Myth 3: IgG antibodies degranulate basophils
Basophils and mast cells are closely-related immune cells that lie at the heart of allergic reactions. These cells are first ‘sensitized’ when IgE antibodies attach to their surface; later, when multiple IgE antibodies link up with an allergen, the cells ‘degranulate’ to release histamine and other chemicals that are responsible for allergy symptoms. Over 30 years ago, researchers entertained the possibility that IgG antibodies could also operate in this manner, but this was based on an observation that has since been discounted (12). That’s the short answer — IgG antibodies do not degranulate basophils. The long answer is more complex.
In 1982, Fagan et al. (13) observed that a subclass of IgG antibody (IgG4) degranulated basophils in vitro – this is why some food intolerance tests look at IgG4 levels specifically. After Fagan’s observation, IgG antibodies became a hot research topic. As the 1990s rolled around, immunologists had accepted that IgG was not a direct cause of allergic reactions, and IgG4 in particular was cleared of its alleged involvement; still, though, the initial observation needed to be explained. (14-16) In 1992, Lichtenstein et al. (17) revisited Fagan’s work and uncovered the reason why IgG had appeared to be a reagin.
Author’s note
I included this myth for people who want to pull out the old research and claim that IgG antibodies degranulate basophils. However, you shouldn’t read too much into this explanation of anti-IgE antibodies: there is nothing here to imply that IgG is a sign of classical (IgE-mediated) allergies.
It turned out that IgG did not degranulate the basophils directly. Using the blood of allergic donors, Lichtenstein showed that IgE antibodies were really responsible, as one would expect. However, the IgE antibodies had IgG antibodies attached to them, and this IgG had hidden the IgE in earlier experiments. It may sound strange, but it is possible to have antibodies against antibodies, and that is what these IgG antibodies were – anti-IgE antibodies. Hidden IgE antibodies are not uncommon: in certain tests, the presence of IgG anti-IgE antibodies can give the appearance of increased IgG levels and decreased IgE levels for the same allergen. (18)
Myth 4: IgG antibodies cause inflammation
To say that IgG antibodies cause inflammation is like trying to name a tune from just one note. There are four subclasses of IgG (IgG1 through IgG4), each with different roles. From the study of protective immunity, we know that some IgG antibodies have pro-inflammatory effects while others are anti-inflammatory. (19) However, the protective immune response involves a finely choreographed balance between these players, along with many other antibodies and cells. IgG4 antibodies help to wrap things up at the end of the immune response and have an anti-inflammatory effect. (19) Overall, IgG antibodies are necessary to keep our immune system in check, and singling out one type of IgG to conclude that IgG antibodies cause inflammation is a gross oversimplification – and just plain wrong.
Myth 5: IgG blood tests detect Type III hypersensitivities
Promotional materials from some laboratories will try to convince you of IgG’s role in food sensitivities by bringing up an unrelated point – that IgG antibodies are involved in Type III hypersensitivities. That is true, but it has nothing to do with what we are talking about here.
Type III hypersensitivities occur when immune complexes, made from IgG antibodies bound to other proteins, deposit in tissues like the kidneys, the joints, or blood vessel walls. This activates the immune system and leads to tissue damage. Type III hypersensitivities are caused by chronic infections, by inhaling dusts from hay or mold, or by your own body in autoimmune disorders, but not by foods. If you have a chronic Type III hypersensitivity reaction, you’re sick, you know it, and your doctor knows it – you might have a type of arthritis, breathing problems, or lupus.
Myth 6: Diets based on IgG levels have been shown to successfully treat symptoms
In debunking Myths 1 through 5, we have seen that there is no evidence to support the existence of IgG-mediated food reactions. In spite of this, a handful of clinical studies have attempted to determine whether diets based on IgG levels can reduce symptoms by looking at two specific groups of people – patients with migraine or patients with irritable bowel syndrome (IBS). Some studies found no benefit (see reference 20, for example), while others saw mild effectiveness (see reference 21).
These diet studies compare the effectiveness of test diets – ones that exclude the foods for which an individual has high IgG levels – against “sham” diets that serve as placebo controls. The best known of these studies, and the one regarded by alternative medicine as the pivotal study for legitimizing IgG blood tests, is a randomized controlled trial conducted by Atkinson et al. in 2004 (21). In order to blind participants to the nature of their diet, both diets in the Atkinson study excluded the same number of foods, but the control diets excluded foods for which a person did not have high IgG levels. Here, the group of IBS sufferers that received the test diet saw a 26% improvement in symptoms over the group that received the control diet.
The Atkinson study may look promising, but we’ll see that it suffers from inherent design flaws that essentially nullify its results. Before we get into this, though, we need to discuss how the scientific method is supposed to be applied to clinical studies. The scientific method is a procedure used to ensure that we make valid conclusions about the world around us. Observations are used to formulate a hypothesis about the way things work, and the hypothesis leads to predictions of cause and effect. This is where we hit the first problem with the Atkinson study – no one has observed that food-specific IgG antibodies are related to symptoms, so there should really be no hypothesis to proceed with.
When there is a reasonable hypothesis, it can be validated by testing its predictions in an experiment. Experiments are controlled situations where one and only one factor is varied and the outcome is recorded – if two or more factors are varied at one time, you would not know which is responsible for the outcome. If the outcome is the same as the prediction, and if the same result is obtained when other researchers repeat the experiment, then the hypothesis is true for that situation. In our case, if the Atkinson study really did have a valid hypothesis, it would only be true for IBS sufferers.
The scientific method is harder to apply in medicine than in branches of science like chemistry or physics where experimental conditions can be completely controlled. Some medical experiments that might seem ideal in terms of controlled conditions are unethical to perform on humans because the procedures might do harm. Moreover, people are people – participants in clinical studies have different histories, different environments, and different genes, and they don’t always follow directions. They are also susceptible to the placebo effect, where their own expectations of success or failure influence the outcome of a medical intervention.
To deal with human variability and unpredictability, medical science has developed its own arsenal of experimental techniques, the most notable of which is the use of a control group to serve as a reference for interpreting results. People in the control group might not have the illness in question or might not be subjected to the factor being studied. The selection of the control group can make or break an investigation, so care must be taken to match the characteristics of the people in the control group to those in the test group. When people are randomly assigned to each group, which is the ideal situation, the experiment is called a randomized controlled trial.
Getting back to the Atkinson study, we can see that it was not a well-designed experiment because multiple foods were excluded from the test diet or included in the control diet – in other words, more that one factor was varied at a time. Some might counter that this was necessary in order to see the full effects of the diets, and maybe that’s true, but the proper procedure would have been to conduct a DBPCFC on multiple and individual foods. While the test and control diets were both problematic, the most significant problem came from the control diet, as three independent researchers pointed out in letters to the journal that published the Atkinson results (22). One commenter noted, “regardless of IgG antibody status, the dietary restrictions in one group are not controlled for by the other group, and hence the conclusion may not be valid.” (23) Ironically, the control group added more uncertainty to the experiment than it took away.
Here is an example of this uncertainty. Most participants had high IgG levels for wheat and milk, so the test diets ended up being wheat-free and milk-free while the control diets generally contained these foods. This difference between the diets is significant because wheat and milk are known to aggravate IBS. Was the control group accidentally sabotaged by being given unfriendly foods? We just don’t know. It might be tempting to wonder whether IgG antibodies are the reason why wheat and milk aggravate IBS symptoms, but remember, there is no proof that IgG levels are related to any adverse effects. Moreover, Hunter (11) pointed out that significantly more participants in the Atkinson study had high IgG levels for milk than had been previously observed, so IgG levels are most likely not a factor in IBS.
The main lesson here is that experiments like the Atkinson study are too fraught with uncertainty for us to draw any conclusions from their results. One of the study’s investigators countered criticism of the control diets by arguing that the control diets did successfully compensate for the placebo effect because the test group improved on their diet to a statistically greater extent than the control group. (24) Statistical results are only as good as the experiment, though. The improvement of the control group may not have all been due to the placebo effect – their diet may have inadvertently removed some REAL food intolerance triggers, although we will never know because no one bothered to check the participants for food sensitivities using a DBPCFC.
Experimental flaws aside, it is also worthwhile to get a sense of just what a “26% improvement in symptoms” means for an IBS study. In a different measure of success, called the number needed to treat (NNT), the test diets in the Atkinson study performed much worse than other dietary interventions used in IBS. (11) The NNT is the number of people that need to be treated in order to find one who benefits from the treatment, calculated with respect to the control group. The NNT for this study was 9, while for most IBS diet studies, the NNT is around 2. Again, as we saw in Myth 1, diets based on IgG blood tests just don’t measure up.
Conclusions
In order to prove that food-specific IgG antibodies cause delayed reactions and chronic symptoms, one fundamental question would need to be answered: “do high levels of IgG against a food predict an adverse reaction to that food” (11). In debunking the myths used to justify food intolerance blood tests, we have seen that no research has provided a positive answer to that question. The evidence actually points to there being no association between IgG antibodies and adverse reactions, making IgG blood tests useless.
Some might personalize the argument against IgG-mediated food sensitivities and see it as dismissing their symptoms or delayed reactions in general. This is not true. The issue here is whether IgG blood tests are worth 500 to 1000 USD and the inconvenience, risk, and expense of modifying one’s diet – all possibly for nothing or for less improvement than could have been gained using a proper elimination diet and food challenges.
Remember that elimination diets and food challenges are already reliable means of diagnosing food sensitivities, even though spending a month or so tracking and testing your diet may not seem as attractive as a single blood test. Fortunately, the diet investigation process is not a shot in the dark – an experienced doctor or dietitian can use your personal history and your own suspicions to guide you through the process. Even though testing companies use rhetoric about ‘hidden food intolerances,’ there is usually nothing ‘hidden’ about food sensitivities at all.
1. Hochwallner H, Schulmeister U, Swoboda I, Twaroch TE, Vogelsang H, Kazemi-Shirazi L, et al. Patients suffering from non-IgE-mediated cow’s milk protein intolerance cannot be diagnosed based on IgG subclass or IgA responses to milk allergens. Allergy. 2011 Sep;66(9):1201–7. PubMed
2. Philpott H, Nandurkar S, Lubel J, Gibson PR. Alternative investigations for irritable bowel syndrome. J Gastroenterol Hepatol. 2013 Jan;28(1):73–7. PubMed
3. Carroccio A, Mansueto P, D’Alcamo A, Iacono G. Non-Celiac Wheat Sensitivity as an Allergic Condition: Personal Experience and Narrative Review. The American journal of gastroenterology. 2013;108(12):1845–52. PubMed
4. Akdis CA, Akdis M. Mechanisms of allergen-specific immunotherapy. Journal of Allergy and Clinical Immunology. 2011 Jan;127(1):18–27. PubMed
6. Brostoff J, Gamlin L. Food Allergies and Food Intolerance: The Complete Guide to Their Identification and Treatment. Inner Traditions/Bear; 2000. 486 p.
7. Sheldon TA. Audit of the York Nutritional Laboratory Survey. Townsend Letter for Doctors and Patients [Internet]. [cited 2014 Mar 4];2002(August/September). Available from: http://webcache.googleusercontent.com/search?q=cache:QMG_H0UxZqIJ:www.drbralyallergyrelief.com/baf-report.doc
8. Hardman G, Hart G. Dietary advice based on food-specific IgG results. Nutrition & Food Science. 2007;37(1):16–23.
9. Are we missing something? 5,286 people responded to the 2007 survey of YorkTest users. Of these respondents, 75.8% indicated that they had experienced a ‘noticeable improvement’ in their condition after excluding foods from their diet. This may be true, but there are two things that are misleading about this figure. First, the definition of ‘noticeable improvement’ was expanded in the 2007 analysis to include people with only moderate improvement – this was not the case in the 2001 survey, so the 2007 results look better. More importantly, the 2007 survey does not tell us the total number of people who originally received the survey; in other words, we know how many people responded, but we don’t know how many people didn’t. When survey results are analyzed, it is important to have some idea of how non-respondents would have answered, because these people are more likely to have a negative attitude about the survey topic. As in the 2001 survey, the 2007 survey did include phone follow-ups with a sample of non-respondents, and, as expected, these people were less successful than the respondents with their diets after the YorkTest. In 2001, the inclusion of non-respondents in the analysis gave an overall success rate that was lower than the rate for respondents alone. The same would be true for the 2007 survey, but since the report did not tell us how many people failed to respond, we have no way of calculating the overall success rate. In other words, the 75.8% figure does not mean what we are led to think it means, and the true percentage would be lower.
10. Zeng Q, Dong S-Y, Wu L-X, Li H, Sun Z-J, Li J-B, et al. Variable Food-Specific IgG Antibody Levels in Healthy and Symptomatic Chinese Adults. PLoS One [Internet]. 2013 Jan 3 [cited 2014 Feb 16];8(1). Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536737/
11. Hunter JO. Food elimination in IBS: the case for IgG testing remains doubtful. Gut. 2005 Aug;54(8):1203. PubMed
12. Hamilton RG. Relevance of (IgG anti-IgE)-IgE complexes, IgG subclass and modern IgG antibody autoanalyzers in the dying IgG reagin story. Allergy. 2009 Feb;64(2):317–8. PubMed
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How common is pharmacological food intolerance? Several million people are currently suffering from this problem in the West, and more – perhaps 5-10% – will have experienced it in their lifetime. You might see figures out there, however, that vary widely, from less than a percent to 20% and upwards, but this isn’t so surprising considering that it has also been difficult to get good prevalence estimates for food allergies (1,2). In this article we will sort through the available data and see why 5-10% is a fair estimate for the lifetime prevalence of food intolerance.
What is prevalence?
Prevalence tells us how many people are suffering from a disorder at a single point in time, given as a percentage of the total population. Since it is impossible to ask every person whether they have a certain condition, researchers work instead with a sample of people who will represent the entire population. The size of this sample will dictate the reliability of the results. The best studies also verify a person’s response by having them go through a medical examination or some other diagnostic procedure.
What data is out there on food intolerance?
For conditions like food intolerance, where the prevalence is expected to be only a few percent (or less than a percent), the most reliable data will come from studies where the sample size is in the hundreds (or thousands). From among these studies, we only want to consider the ones that use a double blind placebo-controlled food challenge (DBPCFC) to check whether a person really suffers from food intolerance. It turns out that just a handful of investigations meet our requirements (see Table 1), and four out of five of these focus only on the effects of food additives like artificial colors and sodium benzoate.
Table 1. Large-scale prevalence studies for food intolerance
Country
Study type
Population
Prevalence
Denmark (4) N = 4274
Additives DBPCFC
All children
1-2%
Denmark (5) N = 379
Additives OC, DBPCFC
Atopic children
2-7%
Denmark (6) N = 1094
Additives DBPCFC
22 year olds
0.5%
UK (7) N = 18,582
Additives DBPCFC
Adults
0.01%-0.23%
Germany (8) N = 4093
Foods, additives & salicylate DBPCFC
Adults
0.78-1.1%
N is the sample size
DBPCFC is double-blind placebo-controlled food challenge, an elimination diet and food challenge where the researchers and participants are unaware of who is receiving a real food challenge or a placebo
OC is open challenge, where the challenge food is known to all involved
Overall, it appears that food additive intolerance occurs in a few percent of children and a fraction of a percent of adults; when more foods are included, as in the German study, the prevalence increases to about one percent. The studies given in Table 1 also verify what has been observed elsewhere, namely that:
Food intolerance is more common in women than in men.
Children are more likely to suffer from food additive intolerance than adults.
Atopic individuals (people with allergies and often asthma) are more likely to see adverse reactions to food, which often exacerbate flare-ups of their existing conditions.
Unfortunately, the data that we have falls short in several ways, most notably in scope. As mentioned, the studies in Table 1 focused on food additives, not naturally-occurring trigger chemicals in food. Even in terms of additives, each study differed in the number and amounts of additives that were tested, and common preservatives, such as sulphites, were absent in many cases. Madsen (3) pointed out that these studies also differed in their inclusion criteria, that is, the symptoms that people could have and still participate in a study. Furthermore, many symptoms, including migraine, gastrointestinal symptoms, and hyperactivity in children, were not considered. Thus, the reported prevalence rates are slightly lower than what should be expected for pharmacological food intolerance when it is more completely defined.
Towards a more inclusive prevalence rate
Is there any other data that we can use to improve our estimate? Numerous smaller studies have been done on food intolerance in specific groups – like sufferers of chronic skin reactions, respiratory symptoms, and gastrointestinal problems – and it is tempting to extend the numbers found there to the rest of the population. Unfortunately, we cannot rely on studies that were not originally designed to establish prevalence rates because the results may be biased. For example, specialized clinics are likely to have reputations that attract specific types of patients, and these may or may not be representative of all patients with those conditions. This is called spectrum bias, a well-known cause of variation in clinical studies.
Alternatively, we could look at prevalence estimates for sensitivities to individual food chemicals, or at the co-occurrence of food intolerance and certain illnesses, and add it all up. For example, histamine intolerance, defined as two or more non-allergic symptoms that improve through antihistamine use and a low histamine diet, is thought to have a prevalence rate of at least 1% and perhaps higher (9). In the US alone, about 12% of the population suffers from migraines, and food triggers are involved in about half the cases (10). Indirect evidence (11) suggests that irritable bowel syndrome is aggravated by foods that contain or cause the release of histamine in the body – this could affect as much as 5-10% of the population, but this has not been clinically verified. The picture is even less clear for other food triggers and conditions, and we are missing information on sensitivities to naturally-derived salicylate and benzoate, other biogenic amines, etc.
Looking at the numbers that we do have, it seems reasonable, if not conservative, that the overall prevalence of food intolerance would be at least several percent. This consistent with the lifetime prevalence estimate of 5-10% from Loblay and Swain of the RPAH Allergy Clinic in Australia (12); they based this estimate on their experience with thousands of patients, although experience does not carry the same scientific weight as epidemiological studies. Still, we can double check if these numbers make sense by considering lifetime prevalence and self-reported prevalence rates.
Lifetime prevalence
When scientists give prevalence rates, they are actually talking about point prevalence, which is how I defined prevalence at the beginning of this article: the fraction of people suffering from a disorder at a single point in time. Lifetime prevalence is the fraction of people who will suffer from a disorder at some point in their lifetime. For life-long illnesses, the point prevalence and the lifetime prevalence will be equal; for disorders that last for relatively brief periods, the lifetime prevalence can be several or even many tens of times higher than the point prevalence, depending on exactly what it is that predisposes a person to developing a disorder. We can expect that the lifetime prevalence of food intolerance will be higher than the point prevalence values we have been discussing, but we don’t know by how much.
If we have some idea of how long food intolerance lasts, we can put some limits on how many times higher lifetime prevalence could be. Food intolerance is thought of as a transient and individualized problem (13, 14). Different people will experience food intolerance for different lengths of time, and, after undergoing a period of avoiding their personal triggers, will have varying success in reintroducing these food chemicals to their diet. There are limited follow-up reports on individuals who have undergone food intolerance testing. Swain (15) found that 81% of respondents to a follow-up questionnaire still experienced a recurrence of symptoms as much as five years after having identified their trigger chemicals. We can make some assumptions and use a probability calculation to estimate that for this group, food intolerance lasts for 14 years – this means that the lifetime prevalence for adults would be about three times higher than the point prevalence. (16) This keeps us in line with our lifetime prevalence estimate of 5-10%.
Self-reported rates
Doctors and researchers often note that people perceive more adverse reactions to foods than can be verified through double-blind placebo-controlled food challenges. Self-reported prevalence rates from surveys of the general population are as much as 10 times higher than the rates determined through controlled testing – this goes for all types of food reactions, even allergies. For example, in the German study included in Table 1, which also looked at food allergy, the self-reported lifetime prevalence for all food hypersensitivities was 34.9%, while the point prevalence was found to be 3.6% based on food challenges. (8) Surveys conducted in different countries give different self-reported rates (17), which can be explained by different diets, different genetic make-ups, and cultural differences.
The discrepancy between clinical and self-reported rates causes some medical professionals to be suspicious about the existence of food intolerance. But does this discrepancy really mean that food intolerance is, for the most part, ‘all in the mind?’ Let’s consider some possible reasons for the higher self-reported rates:
Depending on the survey questions, the self-reported rates could be representing the lifetime prevalence instead of the point prevalence – we need to be careful not to compare apples and oranges.
The respondents could simply be wrong about what caused their symptoms. Most of the self-reported rates were recorded before the current media focus on food allergies and food intolerance, but, today, heightened awareness is increasing the perception that food is the source of symptoms that are otherwise unexplained.
Food aversion is a real phenomenon – you begin to associate a food with an illness and then any exposure to that food makes you feel ill – and this could be mistaken for food intolerance.
Some people may experience a food sensitivity reaction once or twice in their lives, never to be repeated. Large-scale diagnostic studies like the ones listed in Table 1 do have procedures for screening out such events (for example, see reference 7) and only inviting individuals who have a history of reproducible food-related symptoms to participate in the food challenge phase. Studies that present only self-reported rates may or may not use such procedures, so we need to look carefully at each figure to see exactly what it includes.
Another possibility is that there is something about how food intolerance is verified in clinical studies that leads to an underestimation of the true prevalence. Next we will look at the difficulties involved in diagnosing food intolerance to see if this has any effect on point prevalence.
Diagnostic challenges
While it is possible to diagnose food intolerance by elimination diets alone and by open food challenges, only the double-blind placebo-controlled food challenge (DBPCFC) is viewed by researchers as providing a definitive result. This makes it the ‘gold standard’ among test procedures, but, unlike many other gold standard tests, the accuracy of the DBPCFC is not known. (18) In other words, since the process has not been standardized, the accuracy will vary from study to study depending on how the test was conducted.
The DBPCFC was developed with food allergies in mind, where a single food is expected to produce a fairly rapid reaction. These reactions are often easy to see – an asthmatic patient experiences a decrease in breathing ability or a patient develops hives. However, even with food allergies, the results are not always clear cut. (19-21) Take chronic eczema that has not cleared before the test – how much of a change in skin irritation is needed for a positive result? How long should you wait for a response? How do you grade subjective symptoms like headache? How many times should you repeat the test if the patient responds to the placebo? Should you stop medications during the test? Etc.
The diagnosis of food intolerance shares these uncertainties and more, and it can be difficult to reproduce positive food challenge results even in people with good evidence of food intolerance. (7) Several things come into play here:
It is not uncommon for someone to need to be exposed to a combination of food chemicals before they see symptoms. For example, Di Lorenzo et al. (22) found that few patients with chronic urticaria (hives) reacted to challenges with a single food additive but that many reacted to mixtures. Something like this could result from a true sensitivity to each of the triggers (12, 15) (even ones that are not chemically related) or from the unique effects that mixtures have on the processes that rid the body of foreign chemical substances.
Food intolerance reactions are dose-dependent, so a person will only see symptoms if the accumulated amount of food chemical in their body exceeds their threshold dose. Each person has a different threshold dose and this threshold can change over time. Researchers have trouble addressing these issues in food intolerance studies. For example, high challenge doses do not necessarily guarantee more positive reactions and, in any case, might not be representative of normal consumption. Incremental challenges might seem to mimic real life, but they could also lead a person to become more tolerant of a food chemical.
Similarly, some sufferers will be more sensitive to food triggers when they are also under stress, suffering from an illness, or exposed to certain chemicals (cleaning chemicals, fragrances, etc.) in their environment. (23) These additional factors may not be present at the time of the food challenge. Hormonal changes can also play a role in food sensitivity, but I have yet to see a study account for menstrual cycle, even though more women suffer from food intolerance than men.
Patients with chronic or allergic conditions need to be experiencing symptoms at the time of the food challenge in order for any worsening effect to be observed.
Researchers could simply be testing for sensitivity to the wrong chemicals. While salicylate or histamine intolerance is most often associated with fruit, German researchers reported that patients who failed to react to those substances still reacted to tomato extract, pointing to other unknown trigger chemicals. (24, 25). In another example, Lessof (26) pointed out years ago that a reaction to pesticide residue on unwashed fruit can also mimic food intolerance.
Trying to prove an association between food intolerance and a specific condition is like a shot in the dark if the condition that you are looking at is not uniform. As an example, consider the association between attention deficit hyperactivity disorder (ADHD) in children and food additives. For decades, scientists and the public have gone back and forth over whether behavior in these children is influenced by food chemicals. In 2010, one group of researchers found that food additives affected ADHD-like symptoms in children who possessed a gene that decreased their ability to break down histamine. (27) This result has yet to be replicated, but, if verified, it would go a long way to explaining why different studies had been finding different results – only a subgroup of children with ADHD (those with a certain gene) are sensitive to food chemicals. If a study did not happen to include any of these children, then it would have found no connection between behavior and food.
Right now we do not know the extent to which these diagnostic challenges might impact clinically-determined prevalence rates for food intolerance, but we can say that there is more uncertainty in these rates than is currently understood. From the examples that I have given, you might conclude that point prevalences could only go up if researchers addressed these issues; however, it all depends on how you define food intolerance and its impact on health. Increasing the specificity of the DBPCFC would certainly benefit individuals with hard-to-diagnose food sensitivities; at the same time, large-scale prevalence studies might also find more people who experience occasional reactions that do not lead to significant impairment. In the latter case, better diagnostics would not give us any more useful information on food intolerance as a public health problem.
Since self-reported prevalence rates vary more between countries than clinically-verified rates do (see ref 16 for examples), the inflation seen in self-reported rates is probably related more to cultural effects than to limitations of the DBPCFC. Based on self-reported rates, the real lifetime prevalence of food intolerance should never be more than 20-30%, which still supports our estimate of 5-10%. If we knew more about the mechanisms behind food intolerance, we could set upper limits on the prevalence rates for sensitivities to individual trigger chemicals; however, this will not necessarily be an easy task, because for each chemical sensitivity, there are still likely to be different mechanisms at work in different people.
Conclusions
A lifetime prevalence estimate of 5-10%, as given by Loblay and Swain, is probably a good, and perhaps conservative, estimate of the true prevalence of food intolerance. Better prevalence rates will not be available until researchers standardize the double blind placebo-controlled food challenge, define food intolerance consistently in terms of trigger chemicals and recognized symptoms, and make progress uncovering the mechanisms behind food intolerance.
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16. Assumptions: The disappearance of symptoms follows a fixed probability and can be modelled by an exponential distribution; 81% still experience symptoms after 3 years. The rate of decline would be 0.07 events/year, which would lead to an expectation of 1/0.07 ≈ 14 years/event. For adults, assume a lifetime period of 40 years: 40/14 ≈ 3.
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Non-celiac gluten sensitivity is not the same as food intolerance: gluten sensitivity may turn out to be a type of immune system reaction, while food intolerance is a non-allergic sensitivity to food chemicals. They do share one thing, though: the only proper way to diagnose them is through an elimination diet and food challenges.
Elimination diets and food challenges are not rocket science, but they do need to be done right. Here, I’d like to give you an example of how to do them WRONG. This comes from an episode of The Dr. Oz Show, in a segment titled “The New Warning Signs for Gluten Sensitivity.” Let’s look at why Dr. Oz’s advice is not a good way to go about investigating your diet.
“The New Warning Signs for Gluten Sensitivity”
In this episode, Dr. Oz warns that anyone who experiences migraine, brain fog, depression, joint pain, arthritis, or skin rashes could actually be suffering from gluten sensitivity (1). His guest, Dr. Amy Myers, agrees.
Dr. Myers is introduced as a specialist in functional medicine, which means that she is a licensed MD who practices alternative medicine. This is far from the first time that “America’s doctor” has promoted alternative medicine on his show; there are many good articles out there on his mixture of scientific and non-scientific beliefs – search on his name at Science-Based Medicine for more than a few – so I’m not going to get into that here. But I will say that much of what is said on his show should be taken with a grain of salt, including Dr. Myers’ thoughts on the prevalence of gluten sensitivity.
Dr. Myers first states that gluten sensitivity affects 18 million people in the US. She doesn’t explain this, but this figure corresponds to 6% of the US population, which is what some quote as the maximum possible prevalence for non-celiac gluten sensitivity (2). She then states that her personal suspicion is that 1 out of 2 people have gluten sensitivity, but this goes directly against what the researchers who originated the disorder think. She and Dr. Oz then tell us that people who suspect gluten sensitivity can do a gluten-free trial at home.
What’s wrong here?
The first problem with Dr. Oz’s advice is a matter of motivation. How likely is it that someone has gluten sensitivity? If the prevalence is 6%, then gluten sensitivity is a problem of similar size to food intolerance, but it’s not that likely for people who suffer from migraine, brain fog, depression, joint pain, or rashes – which are fairly common problems – to have gluten sensitivity. If the prevalence is 50%, as is presented on the show, then it’s quite a different story – you’d be crazy not to go gluten-free, right? And you might think, “Well, it’s only a two week diet. It won’t hurt and it might help.” But it could hurt, and it’s important to get it right.
Even for people who do have a deep suspicion that their symptoms are related to food, it is hard to know exactly which food or foods are causing the problem because we don’t eat single ingredients all day long. This leads me to the second problem with Dr. Oz’s advice – he doesn’t explain that an elimination diet and food challenges must be done in a systematic way.
Theoretically, you could just remove one food from your diet and keep the rest of your diet entirely the same. But this is difficult, if not impossible, to do in reality, especially with a foundation food like wheat. For example, if you stop eating pasta, you will probably also stop eating tomato sauce, and if you stop eating bread, you might also stop eating jam. You might still eat tomatoes and you might eat fruit, but tomato sauce and jam are concentrated versions of these foods and more likely to cause food intolerance. (3) Or you might inadvertently cut down on sugar and carbs or dairy or some other common trigger. (In fact, there is an idea floating around that high-sugar diets can lead to the same health effects as described by Dr. Oz.) So, if you started a two week gluten-free diet and felt better, could you really blame gluten for your symptoms? No.
All you can conclude from a poorly-done elimination diet is that your symptoms might be caused by something in your usual diet. Food challenges are the necessary second step to determine whether a specific food is causing your symptoms. After your symptoms subside, you must try eating that food again (the ‘challenge’) – if your symptoms return, then you can blame that food. But the food challenge is not as simple as it sounds, and you should be working with a doctor or dietitian on this. First, you should challenge with every food or trigger chemical that you excluded during the elimination diet phase – which, as I said, will probably include more substances than just gluten. Second, you should not only test yourself with the foods in question but also with a placebo. In an informal setting, a placebo could be any meal for which you do not know the ingredients (of course, you need to be working with someone else to pull this off). As you can see, coming up with the right foods or meals to challenge with does take some research and planning.
The placebo test is important to make sure that you find the truth and not just what you expect to find. In some cases, a doctor or dietitian might omit this step, especially in open challenges where it is obvious which food is being tested; however, the placebo effect could be significant for someone who goes into the process believing that they have a 50/50 chance of being sensitive to gluten. On top of this, specialists think that for patients with subjective symptoms (symptoms that can’t be measured by a third-party, like headache, brain fog, etc.), the food challenge and placebo tests should be repeated three times each, with a sufficient ‘wash out’ or break period in between, in order to get the best results.
So far I have been talking about avoiding results that are false positives – that is, thinking that you have gluten sensitivity when you don’t. It is also conceivable that you could get a false negative result, where you really are sensitive to gluten but your symptoms didn’t go away during the elimination diet. One way this could happen is if you also have a food intolerance – either you kept eating other foods that contributed to your symptoms or you added more of them to your diet through gluten substitutes. For example, sweet potato flour, sesame seeds, coconut flour, fava bean flour (and ‘garfava flour’), and almond flour are reported to be high in salicylate and/or amines. Most other grains and substitutes are not. Something similar could happen if you also suffer from a food allergy that you don’t know about (many gluten sensitive people also report food allergies). In order to avoid false negatives, the elimination diet should remove as many possible allergens or trigger chemicals as possible.
The price for getting it wrong
Those who suffer from celiac disease must to be extremely careful to avoid even trace amounts of gluten or else risk serious complications. This is a hard life to lead, to say the least, and not something to get into unnecessarily just because we are in the middle of a gluten-free fad. People on gluten-free diets also have problems meeting certain nutritional requirements, such as for folate and fiber. Doctors do not yet know whether gluten-sensitive people would need to follow the same level of adherence to a gluten-free diet as celiac suffers do.
Health problems should be approached more carefully than a 10 minute TV segment can convey. Doctors diagnose people with gluten sensitivity by ruling out all other causes and by looking at several different gastrointestinal test results that are easiest to interpret before you go gluten free. Self-diagnosis is dangerous because you can miss a serious medical problem; you also do yourself a disservice if you do have gluten sensitivity, because a doctor could provide you with ongoing advice as new risk factors, diagnostics, and treatments are discovered in this active area of research. You’ve waited long enough to sort out your symptoms – find a medical professional to help you get it right the first time.
1. The New Warning Signs for Gluten Sensitivity [Internet]. The Dr. Oz Show. 2013 [cited 2013 Dec 27]. Available from: http://www.doctoroz.com/episode/gluten-warning-signs-next-epidemic (Archived by WebCite® at http://www.webcitation.org/6OjaH1MXG).
2. Catassi C, Bai J, Bonaz B, Bouma G, Calabrò A, Carroccio A, et al. Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders. Nutrients. 2013 Sep 26;5(10):3839–53.
3. Swain A. The role of natural salicylates in food intolerance [PhD Dissertation]. University of Sydney; 1988. Available from: http://www.sswahs.nsw.gov.au/rpa/allergy/research/students/1988/AnneSwainPhDThesis.pdf
In this day and age, it’s hard to imagine medical tests that don’t draw blood or that don’t involve expensive, room-filling equipment; however, for food intolerance and some immune-mediated reactions, the tried and true diagnostic requires only a pencil, paper, and food. Doctors, dietitians, and medical researchers rely on elimination diets and food challenges to identify food sensitivities, which can be used regardless of the underlying mechanism – this is important because right now we have only rough ideas of how these some of these reactions might work.
Diet investigations are deceptively simple – start from scratch and add only one potential trigger at a time until the culprit is found – but they also require a detailed knowledge of food chemicals. For this and for safety reasons – after all, you need to rule out if you actually have an allergy or another condition – you should always undergo a diet investigation with the help of a doctor or a registered dietitian. To help you prepare, let’s look at the three phases of the process: the elimination diet, the food challenges, and the modified diet. Before you start, your dietitian may also ask you to briefly keep a food and symptom journal to provide a baseline on the severity and frequency of your symptoms.
The information here is provided to give you an idea of the diet investigation process; it is not a set of instructions to carry out the procedure yourself. Always check with a doctor or a registered dietitian before modifying your diet. The elimination diet/food challenge process is not appropriate for pregnant women. People with asthma or laryngeal edema (swelling in the throat/upper airways) should only undergo food challenges in a clinic where resuscitation facilities are available. People with Crohn’s disease should not try an elimination diet without medical supervision.
Phase 1: Elimination diet
The elimination diet consists of only a few foods that are unlikely to cause symptoms in most people; depending on your history, it might be less restrictive. You must adhere to the diet even if you think that you know which food chemical makes you ill because you might be sensitive to more than one chemical. In most people, symptoms improve after two to four weeks on the elimination diet. You may experience a withdrawal reaction (a flare-up of symptoms) after the first or second week.
The elimination diet is necessary for several reasons. First, it indicates whether you are on the right track: if there is no change in symptoms after four weeks of strict adherence to the diet, then food intolerance is unlikely. Second, it removes the variability (the ‘noise’) in your symptoms so that changes can be detected during the food challenge phase. Finally, it lowers the amount of trigger chemical that you need to eat in order to see symptoms.
The food challenges determine which food chemicals are triggering symptoms. After at least two weeks on the elimination diet, specific foods are reintroduced into your diet one at a time – these are the ‘challenges.’ If a reaction occurs after a challenge, then you must wait until the symptoms subside, plus a few days, before moving on to the next food. Such challenges are referred to as ‘open’ challenges because you are aware of what you are eating. In research studies, participants are given food chemicals in capsules so they do not know which chemical is being tested or whether they are getting a placebo – these ‘blind’ challenges provide the most reliable diagnosis.
Wheat and milk are often tested first because reactions to these foods are just as common as pharmacological food intolerance reactions; then salicylate, benzoate, amines, MSG, artificial colors, etc. are tested on the advice of your dietitian. Ideally, challenge foods would only contain one trigger chemical, but this is not always possible. When challenge foods contain more than one trigger, the ordering of the challenges is important to systematically rule out all possibilities.
Your dietitian will design a modified diet for you based on your challenge results. You will be reevaluated in 1 or 2 months to see how well the restricted diet is working and to decide whether it is safe to liberalize what you eat. In this part of the process, you will be checking to see whether you have a high or low dose threshold for symptoms; you may also be able to gradually increase the amount of triggers that you eat, but, for your safety, you should always work on this with a dietitian or doctor. Since threshold doses can decrease after avoiding a food chemical, sensitive people could experience dangerous reactions when reintroducing foods to their diet, even in amounts that previously did not cause symptoms.
More information
Consult these books if you are interested in learning more about diet investigations:
Brostoff J, Gamlin L. Food Allergies and Food Intolerance: The Complete Guide to Their Identification and Treatment. Inner Traditions/Bear; 2000. 486 p.
Clarke L, McQueen J, Samild A, Swain A. The dietary management of food allergy and food intolerance in children and adults. Australian Journal of Nutrition and Dietetics. 1996;53(3):89–98.
