Eczema, food allergies, and summer travel

Midsummer it's hard to find time to post. We're taking two weeklong family vacations not so far apart and with planning and packing and then getting swamped with work when you get back there's not much time to write.

Two aspects of traveling are relevant to this blog: how to take your eczema pharmacy along with you, and how to handle your kid's food allergies.

Last Saturday we got back from a trip to a family camp in the Sierra Nevada. It was awesome. I didn't think about work for a whole week and was so stress-free that I could jump in the pool whenever I felt like it and strut around in just my bathing suit. You've got to enjoy these times when you have them.

We ate in the camp mess hall. The staff were great about telling us what the ingredients were in all the food. Often they could give us a special dish without nuts or dairy, which are the two things my daughter's allergic to. But of course, she's a picky eater, and you can never tell what she's going to go for.

When we got back, I read about a tragic incident at a summer camp near Sacramento where a 13-year-old girl died after one bite of a Rice Krispies square containing peanuts. My daughter doesn't have an anaphylactic reaction to anything--not yet--but this was a sober reminder of how deadly nut allergies can be.

Our next trip starts on Wednesday when we fly to Nova Scotia for my parents' 50th wedding anniversary. We often go to NS in August and last year, coming back, we spent an extra day in Newark airport thanks to United Airlines, which we are NEVER FLYING AGAIN. I had run out of any moisturizer or steroid, which was my fault--but try finding fragrance-free moisturizer in the airport shops. Not going to happen. By the time we got home, my eczema was out of control and took several days to cool down to a point where I could appear in public.

Also, being out of food and having a kid with allergies in an airport was a different kind of nightmare. You can't find an ingredient list anywhere and everything seems to have nuts or dairy or whatever. My daughter was essentially reduced to eating potato chips for the better part of 24 hours, but we did gamble on getting her noodles from a random Asian restaurant. Just glad, now that I know she's allergic to sesame, that Asian restaurants in airports are far from authentic.

So this year? I'm going to bring too much moisturizer. And we're going to pack a day's worth of safe food for my daughter.

Hopefully we won't need it--we're flying Air Canada.

New NEA blog post on allergy tests for eczema

I just wrote a new post on the NEA blog, about food allergy tests for eczema. I interviewed Jon Hanifin, a professor at Oregon Health Sciences University and one of the giants in the field of eczema research and practice. (Eczema is commonly diagnosed using the "Hanifin and Rajka" criteria.) Read the post if you are wondering how useful allergy tests are for food triggers of eczema.

The last few weeks my family has been under a lot of stress because my five-year-old son just started kindergarten. He has been unhappy about moving to a new school--where he's in a class of 28 (his preschool had 14 kids) and about 500 students attend total. He cries when we drop him off, when we mention school, and at night when he protests that he doesn't want to go. Plus there's homework--four pages a day, for a kindergartner! and Dad's Club and PTA. So you can understand why my posts have been a bit sparse. The pace will pick up again, I'm sure.

Wheat opens up a whole new universe of food

For the first year of my daughter Voov's life, her face and hands were a red mess of eczema. Blood laced her stool. The combination of symptoms led us and her doctor to think that some allergen was to blame. Skin prick tests registered positive for almost everything--which wasn't much help! Voov was breastfed, so my wife began to cut out foods in her own diet for two weeks at a time to see if anything changed. Removing dairy improved things; so that was it for cow-based milk and ice cream for my wife for a long time.

Then we started Voov on solid foods. At first she had only 12 options, several of which she refused outright. And so most of the atoms now composing her body lived previous lives as chicken, tofu, rice, apple, peas, and banana.

After three years, we redid the skin prick test, and while the technician made a hash of reading the results, we took the apparent improvement as a license to start trying a host of new things. We began with high-value, low-risk items like carrots, potato, chard, and quinoa. It was marvelous: Voov had no reaction to any of them. Eggs, even.

The problem was that she didn't like to eat any of them. She was set in her ways. It seems that three years is precisely the wrong age to start introducing a kid to new foods. However, there was one notable exception: ketchup. We ran trials of tomato and onion, and then Heinz--and bingo, we'd found something she liked and didn't react to.

I immediately realized that I could cover any food in ketchup and there'd be a good chance she'd eat it.

This past week, though, has seen a revolution.

Still standing as major potential villains were the big four: fish, dairy, nuts, and wheat. My wife is a fish-phobe so it's not worth worrying about fish because I can never cook it for the family. We know Voov is allergic to milk, because she threw up shortly after she drank some by accident (her skin test showed major allergy to milk and beef). And we're leaving nuts as something to try in the doctor's office when we have an epi-pen handy. That left one thing to try: wheat.

One week ago, we began giving Voov slices of wheat bread (after carefully checking the ingredient list; it's amazing how many breads contain milk products). She loves it, and she loves wheat noodles, and so far she hasn't had the slightest apparent reaction. Awesome! It has opened up a whole new universe of food.

In the space of a few weeks, we've completely inverted our food restrictions. Instead of Voov only being able to eat a few things, she's suddenly able to eat all BUT a few things. We'll be reading ingredient labels for years to come, but our lives have gotten much simpler and easier.

Coincidentally, Selena over at Amazing & Atopic started her daughter on wheat this week. Things didn't go so well for her, unfortunately.

The three-year allergy test: a comedy of error and opinion

It’s a schizophrenic experience to write a blog covering research on a medical condition while at the same time being a patient and a parent of a child with that disease. Some days I’m writing about what’s possible at the cutting edge. Other days I’m dealing with the imperfections of medicine when it’s applied by real people.

Yesterday it was the latter. My daughter Voov had her 3-year allergy checkup at Kaiser Permanente. First time around, we saw an allergist who barely spoke English. She administered a skin prick test that showed Voov reacting to virtually every food allergen. She advised us to feed her nothing but three things (rice, broccoli, and bananas) for two years.

Can you believe that? Where did this allergist learn about nutrition? Fortunately we, as Voov’s parents, had heard of fat and protein and the idea of a balanced diet. We negotiated a list of ten or so items—including meat—and the possibility of trying a few others.

Voov eats boring food, but she doesn’t care. Her absolute favorite is potato chips. She can go through a party bowl of chips like a school of piranhas through a pig.

Two years later, Voov has her second allergy test—again, a battery of skin-prick tests—with a different allergist, because we weren’t going to put up with the first one again. Voov squirms as the pricks are made and writhes as the itch sets in. She appears to register positive only to dairy. Hooray!

But wait. After consultation it appears that Voov is not allergic to dust mites, which virtually every eczema patient reacts to. Is she really not allergic to dust mites? Let’s look at her back again. Oops—there’s a big red wheal about where the dust mite allergen was applied. Or is it?

It turns out that the tech who read the results didn’t do so in a rigorous manner. She just noted the few spots that showed positive reactions, rather than going through every spot to verify the negative locations. And immediately after reading in this shortcut fashion, she erased all the pen markings on Voov’s back with alcohol.

The allergist is left advising us that Voov is probably allergic to dust mites and dairy. But, she adds, the results of skin prick tests don’t bear much relation to what foods people really react to. Just feed the kid stuff and see if she reacts, the allergist says—and no need to wait the usual two weeks; three days is enough.

I like this idea—let’s just get on with trying foods and seeing if there’s a problem. But it’s unnerving to run into medical professionals who have different opinions—not to mention the odd opinion that is clearly wrong. I’d like to think there was something close to truth out there regarding food allergies and eczema. Unfortunately, while scientists can agree that barrier problems with eczema somehow predispose kids to develop food triggers, the best practice in the clinic seems to be to leave it up to the parents to figure out what’s causing the problem.

Jon Hanifin: Barrier defects come first in eczema; allergies follow

Atopic dermatitis is a disease that arises primarily because of a breakdown in the barrier properties of the skin, and allergic reactions typical of AD are a consequence of this breakdown, Jon Hanifin told an audience last week at the annual meeting of the American Academy of Dermatology, held in San Diego.

Hanifin is one of the US's leading dermatologists, and practices at Oregon Health and Science University in Portland. He was kind enough to send me the Powerpoint of his talk, which I wanted to read because I figured from its title ("AD Pathogenesis: What's New") that it would give me a good picture of the field.

His talk was encyclopedic and technical and I'm not going to attempt to cover the whole thing. But it did make clear to me that the standard model for how eczema arises and develops is in a state of flux.

For a long time, it was thought that allergy was the dominant factor in eczema. But a key paper in 2006 linked higher risk of developing eczema and asthma to mutations in the gene coding for the protein filaggrin. Filaggrin is a long protein, consisting of a string of subunits, that has an important structural role in skin cells, especially in the uppermost layer (the stratum corneum), and also gets broken down at the surface into something called "natural moisturizing factor." From that first paper came a flood of research into filaggrin, which has helped paint a fuller picture.

One thing that jumped out at me from Hanifin's talk was that the relationship between filaggrin mutation and eczema is not simple. The severity of eczema depends on where mutations are within the protein; it's possible to have more than one mutation, which greatly increases the likelihood that you'll get eczema.

Hanifin cautions that filaggrin is not the only genetic culprit in the origins of eczema. Mutations in certain other proteins can compromise the skin barrier.

If filaggrin is messed up, your skin barrier will be too--it'll be leaky--and this means that your body gets exposed early on to a wide variety of antigens that it otherwise wouldn't be. Recently I wrote about the "hygiene hypothesis," which posits that it's good for kids to get exposed to germs because that helps prevent allergies later on, but it seems that it's not good to get exposed to too many germs, because that leads to allergies later on. There's a Goldilocks-just-right amount of germs that your immune system needs to encounter to develop properly. Hanifin laid out the current thinking, which goes as follows:

• Defects in skin cell proteins let in irritants, microbes, allergens
• This causes skin cells to release a signaling molecule called "TSLP"
• TSLP stimulates white blood cells to develop an immune system dominated by type 2 helper T cells (which act via antibodies and inflammation, rather than by macrophages that eat pathogens)
• Th2 cells induce production of IgE antibodies, and then you have classic allergies linked to eczema.

It's just a logical progression. Allergy caused by skin defects seems generally to make more sense to clinicians and researchers these days than skin defects caused by allergy.

Now, is it possible to have atopic dermatitis without abnormal IgE/Th2? Hanifin replied by email:

Yes, roughly 20% of AD patients have typical eczema without any Th2/IgE abnormalities or asthma, etc. ( I call that "pure AD" but allergists tend to call it "intrinsic.") It's been known for years and is the reason we've always doubted that allergy was causative for the skin disease--IgE is clearly involved with hay fever, food allergy and some cases of asthma that usually accompany AD.

Hanifin lays a lot of stress on the precise definition of food allergy, which is specifically defined as an adverse health effect, rather than an adverse immune response. (He refers you, and me, to the NIAID Food Allergy Guidelines.) A positive IgE test for a food doesn't necessarily mean you're allergic. You have to get ill after eating something to be truly allergic to it. Hanifin clarifies:

Not necessarily ill, but usually rapid onset of hives, maybe nausea, cough--sometimes anaphylaxis...The tests are often imprecise and not everyone with high specific IgE levels reacts to that food. Whether they have become tolerant or never were allergic can only be speculated.

My guess is that Hanifin and other dermatologists are increasingly under siege from overinformed patients such as myself who have garnered information from the internet and are now demanding that their doctors conduct allergy tests to nail down the one or two things they're convinced must be causing their eczema. In his email, he comments that there are currently "enormous financial incentives associated with the belief of allergy causation of AD." Patients, and the insurance system, are paying a lot of money for test results that aren't useful.

What I'd like to see an explanation of is why most children grow out of eczema. What is it that's happening to their skin barrier and immune systems as they mature over the ages of 3-8 or so that is freeing them from the disease? Maybe, if we knew, we could capture and intensify that process and apply it to at-risk children and adults who have remained affected.

"Me no like carrots"/Protein fragment could be target for treatment of eczema itch

Saturday--double swimming lessons again. We're getting dried off afterward, me and the two kids, and in the men's changing room they're getting some lessons in anatomy as a number of hirsute and moderately obese men shower. One of them lathers himself head to toe with soap. I kid you not, I have never seen someone so completely covered with suds, as if he'd been dipped like a sheep. What must it be like to be able to use soap like that without consequences? For me and Voov soap is something to be used sparingly if at all.

Voov, as you may know, has been on a restricted diet. For about a year or so she has eaten about eight things (others are allowed but not always available as organic produce--e.g. asparagus). So three weeks ago we were given the green light to start trying a small roster of new foods. The first candidate was carrots, which we chose for their nutritional punch. We were excited as we placed the first plate of chopped, boiled carrots in front of Voov. She picked up a piece and stuck it in her mouth.

"Me no like them. Me not eat them," she said.

And so it proved, after we offered them every day for two weeks: she doesn't like carrots. Fortunately she liked the next two items, apple and pork; we are on week two of pork and next week on to something else.

Hidden B went away last week to a veterinary conference and chose the opportunity to wean Voov off breastfeeding. That's two and a quarter years Voov has been breastfed (Hidden B is ecstatic to be able to eat dairy again) and I hope that her eczema and potential asthma are less severe because of it. I myself was fed on formula pretty much from birth. My mother says that that was what mothers were told to do in those days. I suspect but cannot prove that my food-related eczema has been nastier because of the formula--Hidden B tells me the opinion of doctors at her vet practice (now there's authority for you) is that it's better for kids to be exposed to tiny amounts of allergens through their mothers' milk, rather than be completely deprived of exposure and then hit all at once when they eat real food.

* * * 

I thought I would write a bit about a recent paper in the Journal of Neuroscience. Scientists at Yale and Johns Hopkins have found, in experiments with human volunteers, that BAM8-22, a common protein fragment found in the body can produce itch by a neural pathway independent of histamine.

Histamine is a small molecule that some foods (pickles, aged cheese, red wine) contain a lot of; it is also stored in white blood cells called mast cells that release it in response to food allergies. There are neurons with receptors for histamine, and these neurons send itch impulses to the central nervous system. This is why I scratch like a demented monkey after I eat Parmigiano-Reggiano.

But it is also known that there are other neural pathways for itch; researchers don't know many details yet. For this new paper, the scientists showed that when they poked volunteers' forearms with little plant spines coated with BAM8-22, the forearms got itchy, even if they had been rubbed with antihistamine cream beforehand.

The plant spines are called "cowhage spicules." Cowhage is famous for making people itchy, and it has tiny spines covered with an enzyme that triggers itch. A group of scientists has decided that cowhage spicules are the perfect instruments for applying chemicals that induce itch. Is that weird or what? Apparently if you autoclave (treat at high temperature & pressure) the spicules for an hour, the original enzyme is destroyed and the spicules don't make you itchy.

So the upshot of this new research is that BAM8-22 and the receptor it interacts with (its identity is known too) could be a major pathway by which chronic itch signals, like those that operate in eczema, are sent to the central nervous system. It's possible that pharmacologists may now search for drugs that inactivate the BAM8-22 receptor, and conduct clinical trials to find out whether the drugs relieve chronic itch. My guess is that such drugs could emerge in a decade or so, if a pharma company--or startup--decides that the pathway could be profitable.

An immune link between the gut and the skin in eczema

New research led by Raif Geha at Children's Hospital Boston has revealed how the immune system connects the gut to the skin, and thus how food allergies may affect the skin.

The connection is made by helper T cells. Geha and his team were investigating, in mice, how it is that an allergic reaction that the body has to a food--and we all know that the usual way that food enters the body is when we eat it--can manifest as an eczema-type reaction when the food is rubbed on the skin. Not eaten; rubbed on the skin.

The authors of the paper claim that this is a common occurrence but I beg to differ. I've never heard of it. But they put a lot of work (and taxpayers' money) into their experiments, and their results are intriguing.

Helper T cells are white blood cells whose job it is to detect foreign material in the body, and when it's detected, to stimulate B cells to produce antibodies. What I didn't know was that there are distinct populations of T cells, determined by molecules embedded in their outer membranes, which home in on different regions of the body. Some go to the gut; some to the skin; presumably, some to the lungs, etc. What happens is that the molecules in their membranes will bind specifically to "adhesion molecules" that are found in these different regions. A T cell that homes to the gut will stick to the adhesion molecules in the gut but not the skin.

And Geha and colleagues find that T cells that originally home to the gut can be reprogrammed to head to the skin instead. They immunized mice with the egg protein ovalbumin, and then later observed what happened when ovalbumin was applied to the skin of the mice. Normal mice developed eczema-like inflammation at that spot. Mice that had been genetically engineered with T cells that did not have the skin-homing surface molecule CCR4 did not show signs of eczema. In a truly gruelling series of experiments carried out late at night by grad student slaves, the authors showed that the initial immunization generated a bunch of gut T cells specifically programmed to hunt down ovalbumin; the body then modified these T cells to head to the skin. The reprogramming takes place in the lymph nodes.

I find this fascinating; I didn't know there was such a pathway. It could be that (in the way distant future) someone will develop a way to treat eczema patients with well-defined food allergies, and in these patients prevent the food-antigen-specific T cells from homing to the skin.

The research raises one huge question for me, though. Most eczema related to food allergy does not occur because we rub food on our skin. (At least, I know that I'm allergic to parmesan, but I sure as hell don't go rubbing it on the backs of my knees.) So what is going on to connect the gut to the skin and cause inflammation in the majority of eczema patients?

In which the author does something dumb

I heard recently from a reader, Jon, who related how his wife was able to clear up her hand eczema by quitting dairy and eggs. Jon sent me a photo of her palm. To anyone with normal skin, it would have appeared inflamed, but to me or anyone else living with eczema, it was obvious that her hand was in recovery. Yikes--I've never had it on my palms before, and hope I never do. I'm sure we all wish Jon's wife the best in controlling her hand eczema. It's a bummer to have to give up dairy and eggs, especially with Christmas looming, but a remission from itch is a fine present to get in exchange.

Even though I often write about eczema and food reactions, I'm not immune to doing dumb things myself. Here's one. I was barely able to type out that last post of mine (on Friday) because I was scratching the hell out of my arms. Recently, I've been missing real Parmesan cheese. Since I discovered that Parmesan gives me a terrible reaction, I've been making do with the Kraft version, which any Italian would consider an abomination. But it had been three years since I'd last had Parmigiano-Reggiano, and you know how food reactions can be maddeningly inconsistent. I thought I would try it again. I bought a hefty chunk at the cheese shop a couple weeks ago and started grating it onto pasta dishes. For a while, my body let me get away with it. But last Friday, BAM! after I'd eaten some, an otherworldly itch revved up in my forearms that scratching just made worse. (But try not scratching.) It was pretty funny, typing my eczema blog and stopping every few minutes to claw away like a demented monkey.

But somehow, I felt in control, knowing exactly what was causing the itch--the histamines in the aged Parmesan--and that it would ebb away to nothing overnight, as it did.

Won't do that again in a hurry.

* * *

Some relevant news out of the University of California, San Francisco last week, for anyone interested in that story about how children are less likely to develop eczema if their mothers, while pregnant with them, worked on a farm or lived with cats. UCSF researchers have found that the fetus has an immune system of its own independent of its mother's; and that the fetal immune system develops a tolerance to most foreign antigens to which it is exposed. (This prevents a reaction to the mother's cells.) Once the baby is born, its immune system switches over to fighting foreign antigens.

Maybe if you expose the fetus to cat dander while it's still in the mother's body, it develops a tolerance for it that persists after the child is born. I know that cat and dog dander are pervasive in our environment, so much so that virtually everyone is constantly exposed to them. Could cat dander by itself be responsible for a significant fraction of eczema?

* * *

This week, I'm proud to observe that End Eczema has passed 1,000 pageviews. Any blog of real standing gets several thousand pageviews per post, so I've got a long way to go!

Also, at least a few people are finding this blog on Google, which is good to know. For a while, it was completely invisible.

If you're wondering who your fellow readers are, here's the breakdown by pageviews:

United States    792
Canada        49
United Kingdom    40
Germany        34
Australia        31
Denmark        18
Malaysia        18
Singapore        10
Netherlands        8
South Africa        5

Thank you all for reading.  It's an hono(u)r to write for you.

Allergies: Better to eat foods than to waste away

So I read through the new NIAID guidelines for doctors on how to diagnose and handle food allergies.

It's complicated. There are so many kinds of allergies.

But, in short: many parents are needlessly restricting their kids' diets because of the fear of allergies, or the fear that the kids will develop allergies. As a result, I infer, some kids are growing up with unbalanced diets that can have knock-on effects on development.

The authors of the guidelines say that blood IgE tests for specific allergens are not, by themselves, enough to identify an allergy; nor are skin prick tests. Instead--as most of us already knew--the only true test is to eat the stuff and see if anything happens. And it's best if you eat the stuff in a double-blind trial in which neither the doctor nor the patient know, at the time, whether the patient is eating the candidate food or a placebo.

Alternatively, especially for non-IgE food allergies, you can drop a suspect food from your diet for a while and see if there are any changes. The authors recommend only dropping one or two foods at a time.

The authors make a number of intriguing points.

• Food allergies and eczema are highly associated; but you can develop tolerance to a food and it won't cause problems thereafter.
• Conversely, it's possible to become desensitized to a food if you eat a lot of it, but this desensitization can wear off. The authors only briefly touch on this point and don't list a reference.
• You can have a lot of IgE that binds a food, but not have an allergy. This is why blood IgE isn't so useful, and implies that there are other factors downstream of IgE that are altered in eczema patients: possibly a mast cell imbalance.
• You can have a non-immune reaction to food that can affect your quality of life. (E.g. lactose intolerance. I myself have reactions to aged cheese and pickles and concentrated tomato paste, which contain a lot of histamine; I have reactions to hot peppers and alcohol, which dilate blood vessels in my skin and somehow cause irritation.)
• Most kids will eventually tolerate all foods but tree nuts and peanuts.
• The authors do NOT recommend using allergen-specific immunotherapy to treat food allergies arising from IgE. I'm guessing this is because of the risk of anaphylactic shock. However, a large meta-study just found that sublingual immunotherapy was effective and virtually risk-free for treatment of hay fever. It must be that the allergens from pet dander, pollen, and dust mites are somehow less dangerous.

Where is the science going on this? At the moment, antihistamines are considered the way to manage non-lethal food allergies. (Epinephrine for anaphylaxis.) The authors say

Drugs that alter the immune response to the allergen are commonly considered the most likely candidates for such therapy in the future, but these treatments are not currently recommended.

I wonder whether there are any drug candidates in the pipeline.

NIAID lays down the law for food allergies

Voov's got this red inflammation on her face, around her mouth. Suddenly broke out today. It looks like she's having a reaction to something, maybe food, except that she's been eating the same stuff she has been eating for many months. Zucchini, broccoli, sweet potato, corn, tofu, rice, chicken, turkey, pear, banana-- and that's it. She doesn't avoid certain foods, she excludes everything but.

It just occurred to me that maybe she ate something off the floor. Shmoop, at 3.75 years, doesn't have a spotless record in conveying food from plate to mouth. Maybe he dropped a noodle or piece of omelet or something that Voov hoovered up when we weren't watching.

Anyway, although her skin was good for a long while, it's flaring up just in time for her dermatology appointment on Thursday. That's the way it should be. Much better than right afterward.

You've probably seen this all over the news: a panel of experts vetted by the National Institute of Allergy and Infectious Diseases (NIAID) has just released guidelines for clinical diagnosis and treatment of food allergies. There's what appears to be a decent writeup in the Wall Street Journal health section (I saw several other instances, but this was the best).

1. The original paper is--guess where--in the Journal of Allergy and Clinical Immunology, my favorite eczema mag. The paper is a doorstopper. (At 14 pages, it appears to be a shortened version of the real guidelines!) I'm only a little way into it, but I do mean to go through it and find what parts of it are specifically applicable to eczema. I want to comment on a couple things that jumped out at me though. they're defining a food allergy as "an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food"-- that is, at first glance, they're not considering the magnitude of the reaction
2. they're distinguishing between a patient just having IgE antibodies to food allergens and having an actual allergic reaction. Having antibodies is called "sensitization" and doesn't necessarily imply an allergy.
3. this from the WSJ piece: "It's especially hard to pinpoint a true food allergy in young children with eczema, since they make IgE antibodies to many foods. 'If you did 100 food tests, all 100 would be positive. That's what we see from patients coming in from around the country,' says David Fleischer" of National Jewish Health in Denver.

That's in line with what I heard when I requested a RAST test for allergies about 5 years ago. My allergist told me that people like me, with eczema, just overwhelmed the assay because we had so much IgE floating around.

I'll be interested to see if there's anything new in these guidelines that can help me and my daughter. It's hard to imagine, because I'm a trained scientist, but after 40 years of living in this body I am still not sure exactly what it's allergic to.