For a long time, allergies such as eczema, hay fever and asthma have been known to occur due to a combination of genetic and environmental factors. However, wellness experts have been unclear about which genes are responsible – until now. According to a new study, published in Nature Genetics, there are ten genetic variants that increase your risk of developing allergies, and the more variants you have, the more likely it is that these health concerns will affect your wellbeing.
You develop allergies because your immune system incorrectly believes a harmless substance called an allergen – which includes dust or pollen – is a threat. A particular type of cell from your immune system, B lymphocyte, then produces antibodies against an allergen. This process, known as sensitisation, often happens when you’re very young and from then on, every time you are exposed to that allergen the antibodies produced by the B cells will bind to the allergen. This is what triggers the inflammation on your skin (eczema), nose (hay fever) or lungs (asthma), and causes symptoms such as itching, sneezes and wheezes.
According to study leader Manuel Ferreira, Queensland Institute of Medical Research, ‘We believe there are many genes that determine who becomes sensitised to an allergen and who doesn’t. If you inherit from your parents enough “faulty versions” of these genes, then not only are you more likely to become sensitised to an allergen as a child, but you will also be at an increased risk of developing eczema, hay fever or asthma later in life. Our study – the largest of its kind – compared the DNA of 12,000 people with allergies and 20,000 people without allergies. We found 10 regions of the DNA that were different between people with and without allergies.’
However, Ferreira explained that this research has only just begun. ‘In this study we have only identified ten regions of the DNA that increase the risk of having allergies, but there are hundreds more yet to be identified,’ he said. ‘We will conduct larger, similar studies to identify the remaining regions. For most of these ten regions, we still don’t quite understand how or why the faulty versions of the genes increase the risk of allergies. How do these genes work? Are there specific environmental factors, such as smoking or diet, that turn on the faulty gene? We will be conducting new studies to answer these questions.’
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