Are food allergies becoming more common?
This is one of the biggest questions in allergy medicine.
There is substantial evidence that food allergy has become an increasingly important health problem, particularly over recent decades, but establishing the precise size and causes of any increase is surprisingly difficult.
The updated European systematic review found increases in several measures compared with earlier estimates, including self-reported food allergy and sensitisation.
But the researchers themselves highlighted several possible explanations.
There may be a real increase.
Awareness may have increased.
Researchers may now investigate more foods.
More studies may come from countries that were previously underrepresented.
Diagnostic practice has changed.
The population being studied has changed.
All of those things can move the number.
This is another situation where science is much more interesting than a headline saying:
"Food allergies have risen by X%."
The headline may be directionally correct.
Understanding what produced the number is harder.
Why would allergy increase at all?
If food allergy genuinely has increased over only a few generations, human genetics cannot be the whole explanation.
Our gene pool simply does not transform that quickly.
Something about the environment interacting with genetic susceptibility must matter.
Researchers have investigated numerous possibilities.
Changes in microbial exposure.
The gut microbiome.
Vitamin D.
Pollution.
Dietary patterns.
Skin-barrier dysfunction.
Infant feeding.
Timing and route of allergen exposure.
Antibiotic use.
Reduced exposure to certain infections.
Modern indoor lifestyles.
None provides a single universal explanation.
Some have much stronger evidence behind them than others.
And different mechanisms may interact.
The old popular idea that allergy exists simply because modern life is "too clean" is an enormous oversimplification of a much richer field of research.
One discovery in particular has transformed thinking about food-allergy prevention.
For years, parents were often encouraged to delay giving allergenic foods to babies.
Then a landmark clinical trial involving peanut asked whether doing almost the opposite might protect high-risk children.
The result changed international guidance.
That isn't specifically a mustard story.
But it is such an important development in our understanding of how food allergy begins that it belongs in a definitive guide to allergy.
The skin may be teaching the immune system before the stomach gets a chance
One of the most intriguing modern ideas concerns how the immune system first encounters food proteins.
Food is supposed to enter through the mouth and digestive system.
But tiny amounts of food protein exist in the environment.
They can get onto hands.
Onto surfaces.
Into household dust.
Onto damaged skin.
Babies with eczema can have an impaired skin barrier — rather like a brick wall whose mortar has developed gaps.
That may allow environmental allergens to interact with the immune system through inflamed skin.
Meanwhile, eating a food through the gut during an appropriate developmental window may help teach the immune system that the food belongs in the category:
harmless — tolerate this.
This concept is sometimes called the dual-allergen exposure hypothesis.
In greatly simplified terms:
Exposure through damaged skin may encourage sensitisation, while appropriate early oral exposure can encourage tolerance.
The biology is considerably more complicated than that sentence, and the evidence is much stronger for some foods than for others.
Nobody should therefore take peanut research and invent their own mustard-feeding programme for a baby.
But the underlying idea represents a profound change in how scientists think about food allergy.
We used to concentrate overwhelmingly on what happened after somebody became allergic.
Increasingly, researchers are asking:
Can we stop the allergy developing in the first place?
Mustard remains something of an epidemiological mystery
And here we arrive back where we started.
For Britain today, we cannot responsibly give a neat figure such as:
"One person in every 2,743 has mustard allergy."
The evidence does not justify that precision.
Current UK guidance describes mustard allergy as thought to be rare and acknowledges that we do not know how many people are affected.
European clinical research tells us mustard can be an important allergen in particular populations.
Challenge studies tell us that sensitisation alone can substantially overestimate true clinical mustard allergy.
Molecular research tells us mustard participates in complicated patterns of cross-reactivity.
And epidemiology tells us geography, diet and environment matter.
Sometimes the most knowledgeable answer is not the most precise-looking one.
For EatSafe UK, that should be a rule:
If science doesn't know the number, we don't invent one to make the article look authoritative.
The question behind the question
Knowing how many people have mustard allergy is useful for public health.
For the individual who actually has it, however, another question may matter more:
Will I always have it?
Children famously outgrow some food allergies.
Cow's-milk and egg allergy often behave differently over time from peanut and tree-nut allergy.
So where does mustard fit?
Can mustard allergy disappear?
Does the age at which it begins matter?
Should somebody ever be retested?
And could future treatments make avoiding mustard for life unnecessary?
Those questions take us from epidemiology into the natural history and rapidly changing world of food-allergy treatment.