Results from an Australian study linking peanut allergies to a skin genetic defect were released this week. A group of scientist from the Dundee University found that the gene, filaggrin, found in human skin can triple the risk of a child developing a peanut allergy. According to the study, "a fifth of all peanut allergy sufferers have a filaggrin defect. Those with the defect can be three times more likely to suffer peanut allergy than people with normal filaggrin." Here's the link to the article so that you can read the details.
I did a little more research on filaggrin because I'd never heard of it. In an article on the New York Times website, I found that "filaggrin is a skin protein that serves as a natural moisturizer. Without it, the usually impervious barrier formed by the skin is compromised by cracking." This article, dated back in 2006, reports how a group of scientist from the Dundee University (the same research team from the first article I linked) found the defective gene for filaggrin while researching the cause of chronic eczema. Evidently, having shown that filaggrin was a significant factor in causing eczema and asthma, the scientist next decided to investigate whether the gene might also be a cause of peanut allergy.
Here's a couple of interesting sections from the 2006 article stating that eczema might not be a side-effect from allergies, but that allergies might be a side-effect from a skin defect:
For decades, allergists embraced the idea that eczema arose from an immune overreaction inside the body, leading to inflammation and cracked, itchy skin. Skin cracking, in turn, let in more allergens, irritants and microbes that further fueled the cycle. The theory was supported by the observation that eczema sufferers show high blood levels of an immune defense protein called IgE and often develop immune-related ailments like asthma, food allergies and hay fever.
Many dermatologists, on the other hand, have argued that allergies do not cause chronic eczema. Over the last decade, some proposed that an intrinsic defect of the skin occurs first and then causes immunological weirdnesses. In other words, trouble develops from the outside in.
I've have never heard the theory that skin can be defective (with a dry, filaggrin-deficient barrier) and let in environmental pollutants, food proteins, bacteria, dust mites, etc., and that those "foreign intrusions might activate immune cells to respond and crank out IgE, causing the inflamed skin lesions. That process may also prime the immune system to overreact to specific allergens, leading eventually to asthma, hay fever and food allergies."
If you're dealing with children that have eczema, it might be worthwhile to read these articles. It's always interesting to hear different theories even if it does often confuse an already confusing issue. This article goes on to quote a dermatologist not related to the study. Here's an excerpt: "the genetic studies magnify the need to protect the dry, damaged skin barrier and keep out irritants and allergens by hydrating it and keeping it intact. That means that along with using anti-inflammatory medications, it is crucial for eczema patients to follow the basic advice on moisturizing to prevent flare-ups. For infants, the research even raises the possibility of prevention and points out that maybe we can reduce the impact of asthma and allergic rhinitis by treating the skin in kids with eczema early by moisturizing right from day one.”
I find it an interesting coincidence that Abigail had eczema, but her younger brother did not. I should mention too that both her dad and I have also had minor boughts of eczema in the past, and that I suffer from really dry skin. Too bad that filaggrin screening tests are a ways away.
