all posts, eczema hacks, the eczema body, women's health

will my baby have eczema?

smiling baby lying on white mat
Photo by Victoria Borodinova on Pexels.com

A while back I wrote a post about what it’s like to have eczema and be pregnant, followed by another post after my little one was born all about living life with eczema and a baby. But today’s topic isn’t about the mom, but rather, about the baby and the baby’s risk of inheriting eczema from his/her parents.

The inspiration for this post comes from the eczema community on instagram. Many ladies have been asking about this topic, so I figured I would try to search for an answer. I apologize if it isn’t the clearest of posts. It’s a culmination of a bunch of witching hour moments over a few days, when Fiona decided that midnight, 1am, 2am, 3am, etc are equally important times to wake up each day.

Most of us know that there is a genetic component to eczema but what does that actually mean? There are a few different ideas being studied about where genes come into play with this condition that are lumped under the “outside-inside model” which look at skin barrier dysfunction (as opposed to the “inside-outside model”, which is about the gut health). Some examples of the outside-inside model, which I’ll go over individually, include:

  • FLG (a gene, that makes the protein filaggrin). I mentioned this protein in an older post, talking about how there were treatments for eczema being developed that made use of it. The gist was that a loss-of-function in the specific gene results in less filaggrin being made, and filaggrin is an essential player in keeping the skin barrier intact.
  • Tmem79/Matt (colloquially known the Matted mutant gene, so named because in mice it results in their fur having a matted look). Researchers found that mice that had this mutant MATT gene also had skin barrier issues and dermatitis issues, and that humans had a similar gene, with a common single nucleotide polymorphisms (or SNP). When there is a misstep (or a mistake) in humans’ SNP, there are significant atopic dermatitis associations.
  • Th2 (a cytokine, or a protein that impacts cell signaling). Th stands for T helper cells, and they help with host defense, but also impact inflammation. Some, like Th2 are know for being (pro)inflammatory, while Th1 is known to be anti-inflammatory. I mentioned this a little when talking about pregnancy and eczema. Research from 2015 showed there are many different Th types, that all may have their own impact on inflammation.
  • interleukin-1 (a protein from a family of inflammatory and regulatory cytokines). Many studies are still showing that breastfeeding reduces your child’s risk of eczema, because of some components (interleukin-beta specifically) in the breast milk that the child consumes. One such study went so far as to say that breastfeeding halves the risk for children between 0 and 3 years of age (and no you don’t have to breastfeed for 3 years for that to be the case!). The way interleukins work is that they are released when there is bacteria or immunological disturbances. The interleukins show up and affect cells like capillary endothelial ones, making them release chemicals and attract monocytes (large white blood cells that help kill bacteria). The problem with these is that certain types can be associated with Th2 (like IL-22 which is made by Th-22), or they can be known to be associated with inflammatory diseases like IL-17.

Then there has been a lot of research investigating if and how probiotics can help prevent eczema for babies too (even Gerber makes probiotic-included products now). In particular, Lactobacillus rhamnosus was seen to have mixed results, with some studies showing it reduced genetic susceptibility to eczema (meaning it somehow calms the baby’s risk of having eczema) for children with thirty-three eczema susceptibility SNPs. On the flip side, other studies said Lactobacillus rhamnosus had no effect on reducing the child’s risk of eczema.

To be honest, I am still a bit skeptical of the studies done that show no effect because, from what I can tell, they have the parents give the babies probiotics for say 6 months, and then continue to see if there is a benefit at some later date like 2 years of age. If a modern western diet (high carb, especially in refined sugars) can alter an adult’s gut microbiome fairly rapidly, why would the probiotics a baby takes at 6 months still be helping the gut at 2 years (the biome diversity would have changed due to diet by then, and the gut must stay healthy for it to help the skin)? Wouldn’t one expect the gut microbiome diversity to change and said “good” gut bacteria to not be able to survive the environment anymore?

So essentially I am still thinking, as the studies show no negative effects of taking probiotics, after talking with your baby’s pediatrician of course, what would be the harm in giving your baby probiotics? That and making sure to keep your baby on a diet that creates a gut environment more conducive to good bacteria flourishing.

Also note, I wasn’t able to access the whole study so I’m not sure how the probiotics were administered unfortunately. On a tangent, that’s always a frustrating point to me. I don’t think studies should cost the public to access because we should want to encourage people furthering their health in any way possible. I understand scientists need go make money too but I do wish there was another way besides charging subscriptions to databases of research. 

But I digress. So what is the takeaway for all those future mamas worrying about passing eczema on to their children? Do they have cause for concern? Perhaps. The way I see it (noting I could be interpreting this incorrectly) is for:

  • filaggrin: If the loss of function filaggrin gene is passed on, the child would probably have an increased risk.
  • Th2: the Th1/Th2 dominance seems to be more dependent on estrogen than genetics (though I could be wrong) so my guess would be that having a girl would make her more susceptible in that case (again I definitely could be wrong).
  • MATT gene: The atopic dermatitis shows up is because of that misstep (mistake) in the common SNP of the gene. As a result I think the answer is yes, it probably is a risk for one’s children, because missteps (I believe) would be passed down since they are mutations.
  • interleukins: I believe the pro-inflammatory ones that are problematic are a product more so of consistent stressors on the body (both from invaders like bacteria, and from literal stress). If the baby/child is relatively healthy and isn’t too stressed out, in tandem maybe with the mom breastfeeding her baby (so long as she is able to, aka isn’t on chemotherapy or radiation or something), then I do think the risk of eczema from this perspective, is decreased.

But the real question now is how do all these components balance out in an individual, in a baby? Does having a loss of function filaggrin gene guarantee a lifetime of eczema? Or does it just make you more susceptible but you are fine if you don’t have the MATT gene’s SNP misstep (or one of the other 33 SNPs mentioned that are related to eczema susceptibility)? It would be interesting to see a study done that investigates all these components together, so we could know which are still present when you have people with severe eczema, topical steroid withdrawal systems, etc. As for the initial question, sure, there are genetic components that you pass down to your baby, but it seems like not all the heavy hitters are genetic so your baby may still be fine.

One more thing to leave you with: the American Academy of Dermatology made a post a while back saying a few ways to reduce your baby’s chance of eczema (minus genetics naturally), which included:

  • having a dog at home before the child’s 1st birthday
  • moisturizing a newborn’s skin
  • not eliminating a bunch of things in your diet
  • eating a health diet while pregnant, and
  • breastfeeding (and having a healthy diet during it too)

All in all, know this: if you do have a baby and he/she has eczema, the research body is growing in the field and more understanding of what causes eczema are coming to light, which means better ways to treat it will follow.

REFERENCES

Bauer SM. Atopic Eczema: Genetic Associations and Potential Links to Development Exposures. International Journal of Toxicology. 2017 Mar 30: 36(3): 187-198.

Cabana MD, McKean M, Caughey AB, Fong L, Lynch S, Wong A, Leong R, Boushey HA, Hilton JF. Early Probiotic Supplementation for Eczema and Asthma Prevention: A Randomized Controlled Trial. Pediatrics. 2017 Sep; 140(3).

“Can anything prevent my child from getting eczema?” America Academy of Dermatology, https://www.aad.org/public/diseases/eczema/prevent-my-child-from-getting-eczema. Accessed 9 Jan 2019.

Hofmann A, Kiecker F, Zuberbier T. A systematic review of the role of interleukin-17 and the interleukin-20 family in inflammatory allergic skin diseases. Current Opinion in Allergy and Clinical Immunology. 2016 Oct; 16(5): 451-457.

“Interleukin 1.” R&D Systems 1999, https://www.rndsystems.com/resources/articles/interleukin-1. Accessed 18 Dec 2018.

Jepsen AA, Chawes BL, Carson CG, Schoos A-MM, Thysen AH, Waage J, Brix S, Bisgaard H. High breast milk IL-beta level is associated with reduced risk of childhood eczema. Clinical & Experimental Allergy. 2016 Jun 2; 46(10): 1344-1354.

McLean WHI. Filaggrin failure – from ichthyosis vulgaris to atopic eczema and beyond. Britist Journal of Dermatology. 2016 Sept 26; 175(52): 4-7.

Morgan AR, Han DY, Wickens K, Barthow C, Mitchell EA, Stanley TV, Dekker J, Crane J, Ferguson LR. Differential modification of genetic susceptibility to childhood eczema by two probiotics. 2014 Aug 21; 44(10): 1255-1265.

Raphael I, Nalawade S, Eagar TN, Forsthuber TG. T cell subsets and their signature cytokines in autoimmune and inflammatory diseases. Cytokine. 2015 July; 74(1): 5-17.

Saunders SP, Goh CSM, Brown SJ, Palmer CNA, Porter RM, Cole C, Campbell LE, Gierlinski M, Barton GJ, Schneider G, Balmain A, Prescott AR, Weidinger S, Baurecht H, Kabesch M, Gieger C, Lee Y, Tavendale R, Mukhopadhyay S, Turner SW, Madhok VB, Sullivan FM, Relton C, Burn J, Meggitt S, Smith CH, Allen MA, Barker JNWN, Reynolds NJ, Cordell HJ, Irvine AD, McLean WHI, Sandilands A, Fallon PG. Tmem79/Matt is the matted mouse gene and is a predisposing gene for atopic dermatitis in huma subjects. J Allergy Clin Immunol. 2013 Nov; 132 (5): 1121-1129.

all posts, treatments

my addicted (skin) life

pexels-photo-286951.jpeg

As the science of skin (dermatology) progressed, more information was understood about what this large organ is made of, how it works, and how to keep it healthy.

I won’t go into the skin anatomy today but one thing that was more or less universally accepted was: dry skin = bad skin. So in practice this meant that doctors prescribed patients to take baths and let our skin absorb lots of water and then get out, lightly pat dry, and apply the topical medication. An NEA webinar mentioned you need to get the topical medication on within 3 minutes of getting out of the water, which for a full grown adult with eczema over the entire body, proves to be a bit of a challenge.

So now let’s go more into the specifics about topical medications, let’s start with steroids. Topical steroids come in 7 classes: from Super Potent to Least Potent. A high potency topical steroid is one we’d put on our hands/feet/wrist/ankles or the areas that are more likely to have excessive thickening. A mid-strength topical steroid may be safer for the whole body but only for a 3–5 days for thin skin areas (around the eyes, mouth, genital areas). A low potency topical steroid includes the things you can get over the counter like hydrocortisone (1%).

A useful fact to keep in mind is you should know the name of the steroid you will/are using as well as the concentration (listed as a percentage). When in doubt, it doesn’t hurt to google up your specific steroid to see what strength it is if you are not sure, or ask your doctor.

Now for the more recent developments in the eczema world: the non-steroidal anti-inflammatory medications (like Protopic and Elidel). Both are types of topical calcineurin-inhibitors (TCIs), which is a big term that just means they block T cells and stop the too much cytosine (a protein that can cause redness, inflammation, and itching) from being released. TCIs are great because they help the skin without decreasing the amount of healthy cells, and without going as deeply into the skin layers (unlike topical steroids, which cause thinning of the skin if used for a long time).

Protopic is usually stronger than Elidel, but both are often seen as medications to be used after you’ve finished the course of a mid-strength topical steroid, the reason being is that the TCIs can be used for longer periods of time. They are said to be safe to use around those thin-skinned areas, but that they generally don’t work on lichenified (or thickened) skin.

An even newer development was Eucrisa. This is a non-steroidal topical ointment that works by blocking an enzyme called phosphodiesterase (which is increased in immune cells of people with eczema), which then also blocks out the production of excessive cytokines. More research is still to come, but Eucrisa seems to be another promising non-steroidal option.

Lastly, let’s talk about topical corticosteroid (TCS) withdrawal (also known as topical steroid withdrawal or TSW). The health community is still hotly torn on this issue. On the one hand, in 2015 it was stated that the TCS withdrawal is a potential adverse effect of prolonged use of topical steroids, though it was said to be a rare occurrence with not a lot of evidence backing it, and that it was probably caused by topical steroids being used incorrectly. To be honest though, it seems it would be difficult not to have misused topical steroids in the past as the research behind how much to use and how often has changed over the years.

On the other side, there are organizations like the International Topical Steroid Addiction Network (ITSAN) or individuals like Dr. Rapaport that argue that the Red Skin Syndrome (RSS) is directly because of the topical steroid use/overuse/abuse in societies.

An interesting blog post I came across talked about how much cortisol a healthy body can normally produce, and how the commonly prescribed topical corticosteroids measure up. His analysis was that the potency of prescription steroids are often so much higher than what our bodies could naturally produce, which might explain why it seems so much more common to hear about people’s skins getting addicted. He was testing out how using very low potencies and/or low doses to mirror how much cortisol our bodies could normally produce, and see if that helped him maintain his skin throughout the winter.

Also food for thought, we know that studies are incredibly expensive to fund, and so to get a lot of evidence backing up TCS withdrawal or RSS, there would need to be big companies supporting the research. However, if these studies could then have results that jeopardize major supporters (like a pharmaceutical company), it becomes less likely any such companies will want to fund said studies. I’d bet it will be a while before we get a lot of evidence around more specifics of TCS withdrawal/RSS.

 

REFERENCES

Carr WW. Topical Calcineurin Inhibitors for Atopic Dermatitis: Review and Treatment Recommendations. Pediatr Drugs. 2013 Aug;15(4):303-310.

Hajar T, Leshem YA, Hanifin JM, Nedorost ST, Lio PA, Paller AS, Block J, Simpson EL. A systematic review of topical corticosteroid withdrawal (“steroid addiction”) in patients with atopic dermatitis and other dermatoses. JAAD. 2015 Mar;72(3):543-549.e2.

Paller AS, Tom WL, Lebwohl MG, Blumenthal RL, Boguniewicz M, Call RS, Eichenfield LF, Forsha DW, Rees WC, Simpson EL, Spellman MC, Stein Gold LF, Zaenglein AL, Hughes MH, Zane LT, Hebert AA. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol. 2016 Sep;75(3):494-503.e6.

 

all posts, community, treatments

how to find dr. right (dermatology edition)

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As one of many people who sees a dermatologist for some kind of reoccurring eczema or atopic dermatitis (AD) and as someone who has cycled through the what feels like all options for treatment (often never finding that perfect product, the lifestyle management, or that patient-doctor connection), and as someone always searching to get to my dream skin, I am always hunting for ways to build a relationship with my future Dr. Right.

The most important part of having a good working relationship with your dermatologist is being able to speak your concerns. I have gotten to a point in my life where, when meeting a new dermatologist, I throw out my entire skin background in a verbal paragraph; the goal being to test the waters of this new budding relationship. Here are some examples below for personal context:

  • I have had topical steroid withdrawal (TSW) before because of my excessive use of steroidal topical ointments in my earlier years, and I am somewhat hesistant to use them now. I am also not entirely interested in oral steroids again, because of their shopping list of side effects. It is important to speak your fears of strong medications, so your derm knows what you need to discuss.
  • I have been using coconut oil on my skin and have had no problems with it except that it didn’t prevent a flare. This bit of information is shared because it’s true (and you never know when new research will come out saying that coconut oil is not as good as we thought it was… e.g. what happened with olive oil) but it also can be used to get the derm’s opinion on natural products/non-dermatologically created alternatives.
  • I have been avoiding gluten and soy (because they are common allergens and because I have other legume allergies) for a while and worry that me starting to eat them again this summer may be part of the reason for my flare. This is brought up to bridge into the field of nutrition to figure out my new derm’s opinions on diet in regards to its effect on eczema and management.
  • I know about the current new drugs on the market (Dupixent) and wonder about its effect on pre/peri/post natal women. It’s crucial to remember to bring up reproduction-related information if you are going to start a drug that hasn’t been tested on men or women for reproductive side effects, if you are interested in having children one day.
  • What is the plan for me and what will my management entail going forward? After all, I want to know she isn’t just going to prescribe me a crap ton of drugs and wish me the best with my life… continuity of care is extremely important for preventative care and management.

In the case with AD, I was hesitant about both topical and oral steroids as the major component of my management, and my derm was receptive to my initial hesitation. However, she also argued with the need for inflammation management, because in an untreated state, chronic inflammation will damage other organs and systems in time. So she walked me through the details about what she was thinking for both types of steroids- the dosages planned and how long she planned to keep me on them. If you are confused about what the drugs do or their safety, it doesn’t hurt to inquire more (for example 60mg of prednisone is on the high end of how much doctors will prescribe).

My derm told me of her roadmap for my management (an important thing you want your dermatologist to bring up!)- how long she’d want me on the oral steroids, which topical steroid was for my face versus which for the rest of my body, how we’d cycle through a 2-week steroidal/1-week non-steroidal topical cycle, and the need for more frequent bleach baths to prevent staph infections from other healthy-skinned people (because everyone carries some level of staph on their skin).

When I asked her my big question — what can I do to prevent these flares from coming back aggressively again, she also brought up diet changes, as well planning future appointments to monitor how the preventative measurements were going. All in all I left with a sense of her being committed to making sure things worked, not just prescribing me all the meds I could carry and hoping I didn’t ever need to come back.

The big takeaway from being a frequent flyer of the dermatology world is that it is okay to need to find a dermatologist who fits with you. You want someone you feel comfortable with, who you can talk to openly and feel like they both have the time to listen and are receptive to your ideas and where you are in your health literacy (i.e. do you like written or oral directions, how familiar are you with the drugs/treatments/interventions, how much you feel you understand or care to understand about the condition as a whole, how it works genetically, immunologically, neurologically, etc).

You should feel like you are leaving with enough information to get you by AND also with your questions answered, but also that you know what to expect and when to reconnect with the derm in the event that something isn’t working just right. You don’t want to feel like you’ve heard it all before, or that there is something the derm just isn’t getting about you. The relationship needs to be out on the table and the communication level high. If you have persistent remaining questions- ask them! If you are frustrated by something, voice it!

With any chronic disease, management relies on the ability to be able to communicate your feelings and symptoms, and on the ability of the provider to be able to give you the support and care contingency to make sure that you don’t falls through the cracks in the system. So when working to develop a fruitful and useful relationship with your dermatologist, don’t be afraid to be a bit selective and work through difficult questions to see if you have found your Dr. Right.

 

Here’s a photo of my own hands October 2016 (left) and March 2017 (right):

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