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.

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