From the Allergic Living Archives. First published in the magazine in 2008.
If you have a child with peanut allergies, other parents will say to you: “Nobody was allergic to peanut butter when I was a kid.” If a cat swishing through a room starts you wheezing, you’ll get asked: “How come so many people have asthma?” Both are reasonable questions, variants on the broader million-dollar one: “Why do so many people have allergies today?”
If you want an easy answer, allergy experts will simply say they don’t know. But what they mean is – they don’t know entirely. The fact is that scientists understand a lot more about allergic disease than they did a decade ago. There are still gaping holes in their knowledge, but as they continue to fill in the pieces to the puzzle, what they are finding is fascinating and often surprising. In the following investigation, Allergic Living examines what science knows so far about why allergies occur.
In the Beginning
When a baby is born, its immune system is a work in progress. “You’re born with a naïve, allergic-skewed immune system,” explains Dr. Michael Cyr, an allergist and immunologist at McMaster University in Hamilton, Ontario. This is what scientists call the Th2 mode.
During the first days, weeks and months of life, as the baby comes into contact with various germs, bacteria, viruses and infection, the system is supposed to start learning to distinguish between what is harmful and what is benign.
Some allergists liken the emerging immune system to a toggle switch or a reset button: we’re all born in that Th2 mode and then that first bout of sniffles at eight weeks or the ear infection at four months begins to “switch” the immune system over from Th2 to Th1 mode or fighting bacterial infection mode.
But in the person with a genetic inclination to allergy, something misfires and the switchover doesn’t happen properly. Cyr, who’s a researcher with AllerGen (the Allergy, Genes and Environment Network), says that why this process happens easily for some people but not for others remains unclear, and may depend on a confluence of factors.
The young child who doesn’t get switched over is now atopic – predisposed to developing an allergic response to a trigger such as cat dander or ragweed pollen or peanuts. After breathing in or consuming one of those, the child’s immune system creates allergy antibodies – specifically Immunoglobulin E or IgE antibodies – to guard against the offending trigger. The next time the immune system encounters it, the IgE will go on the defensive, setting off a cascade of allergic symptoms.
Though genetics are a large contributing factor to whether a person becomes allergic, scientists haven’t found one specific allergy gene. “It’s becoming clear that it’s not a gene, it’s a whole series of genes,” says Cyr. Something has changed to increase the number of us who are developing allergies, says Dr. Dennis Ownby, a professor of pediatrics and the head of allergy and immunology at the Medical College of Georgia in Augusta.
“What seems to have happened over the last three decades, at least in developed countries, is that genetic ability [to be allergic] has become more prominent,” he says.
Just how much have allergies and asthma grown? Figures from the World Allergy Organization reveal the global prevalence of asthma has increased by an astounding 50 per cent every decade for the past 40 years. In North America today, leading allergy organizations estimate that about 24 million Americans and three million Canadians have asthma.
In the past decade alone, the prevalence of food allergy, once an uncommon condition, has skyrocketed. The Food Allergy & Anaphylaxis Network*, the U.S. education group, estimates that about 12 million Americans – 4 per cent of the population – now contend with the disease. The Canadian rate of food allergy is estimated to be comparable. Peanut allergy alone has doubled in young American kids.
In our modern world, allergy has spread like wildfire. Scientists are certain that genes alone can’t be the whole reason why. “The genetic pool does not dramatically change over decades,” notes Cyr. “So it’s obvious there’s something else going on.” And that something appears to be our environment.
Getting to the Dirt
While references to asthma date back to ancient Chinese medical texts, the real story of our modern understanding of allergy begins in earnest in 1989. It was a heady year, with the fall of Berlin Wall and the beginning of the opening up of the former East bloc. A team of German scientists decided this presented a great opportunity to compare the prevalence of asthma in Leipzig (former East Germany) and Munich (former West Germany).
Here were two highly similar gene pools of people who had been living in very different societies and conditions. “At that stage, everyone, including us, believed that air pollution was causing asthma and allergies,” says Dr. Erika von Mutius, who was then a young pediatrician and team leader, and who today is a professor and head of the asthma and allergy department of Munich University’s Children’s Hospital.
When the findings began coming back showing that there was considerably more asthma in modern, Western, hygienic Munich than among the study group living in Leipzig with its billowing factory smokestacks, the researchers were incredulous.
“It was so opposite what we’d anticipated,” recalls von Mutius on the phone from Munich. “We didn’t believe it, so we thought it was a mistake in data entry and re-entered all the data.” But the data were right, and the results were published in 1992.
*Update: The organization FAAN has been renamed FARE.