<p>Emerging research highlights the gut microbiome’s potential role in the development and management of atopic dermatitis (AD). While gut microbial diversity, early-life exposures, diet, and probiotics may influence disease onset and severity, individualized care and further clinical research in this area are needed to guide treatment decisions.</p>

When I talk to parents about the gut microbiome and their child’s AD, I tell them to imagine that their child’s gut is a neighborhood. In a healthy neighborhood, you have friendly neighbors and residents. Good neighbors are like good bacteria, such as Bifidobacteria and Lactobacillus. These bacteria help train the immune system and keep inflammation in check. However, in children with AD, the neighborhood has gone off the rails. The good bugs have moved out of the neighborhood, maybe because of early antibiotics, formula feeding, or cesarean delivery, and you may have troublesome new neighbors, such as Escherichia coli. It is an integrated ecosystem, and a balance helps keep the peace in the neighborhood at large.

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Probiotics, prebiotics, and synbiotics are the good neighbors you are trying to get back into the gut. So, having evaluated some of the data, I counsel every patient with AD about maintaining a healthy diet, but we do not really know everything that is going on. We know about the importance of maintaining a healthy diet and that the microbiome is integrated, but I think that the next step will be to understand not only the connections between all the microbial players but then also how they connect with the immune system. There is already a lot of thought going into this. For example, we now know that itch modulation can occur in patients with AD who have an altered gut microbiota.

We know that the gut microbiome is abnormal in patients with AD, as is, of course, the skin microbiome. There are some compelling studies suggesting that, even in infants, you can see a decreased variability in gut microbiome bacteria, and the decreased number of species correlates with the early onset of AD. However, it does not necessarily mean that we can simply replace good bacteria to fix it. It is still somewhat correlative. Nonetheless, some of the most compelling studies in terms of preventing or delaying the onset of AD are with oral probiotic supplementation.

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I think that the prevention data are strongest for L rhamnosus GG in AD. The data for this probiotic are not very compelling in terms of treating existing AD, so all we can say is that there is no doubt that something is up with the gut microbiome, and it seems possible that we can manipulate the microbiome in some way to delay or prevent eczema and, potentially, modulate it later.

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It turns out that some different strains (and mixtures of strains) may have an effect on existing disease. In particular, L salivarius is a strain with a fairly strong signal, particularly when it is mixed with other strains. I am fascinated by this but also very humbled because I think that there are a lot of interactions that we do not yet understand.

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That being said, I do recommend routine supplementation with probiotics for all of my patients with AD. I pick a product that is inexpensive, readily available, and has a mixture of strains, including L salivarius. There is probably a subgroup of patients who will respond, but I cannot select them a priori. They try it, and if they do not feel like it is helping after a few months, then they can discontinue. However, the patients who feel like it is making a difference can stay with it until we get a little further with personalized medicine to understand who is going to respond better, and to what.

It is very humbling to try to understand the relationship between the gut and skin microbiomes. There is definitely a signal there, but AD is a very complex disease, and there is not a single factor that causes it. Nonetheless, it is something that I think deserves further study, and not only in terms of the patient’s own microbiome. We are also trying to understand whether the maternal gut microbiome and alterations such as the use of antibiotics can impact a child’s risk of developing AD, since children initially acquire their microbiomes from their mothers. That is the direction we are probably going to be moving toward: to find out whether the maternal microbiome is a potential therapeutic target.

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I do not typically recommend the use of probiotics in my practice, which may reflect a bias at my clinic. I see patients who already have more severe disease; therefore, probiotics may not improve the severity of their disease much. But that does not mean that there might not be a candidate out there for whom supplements can work. We just need more data on this before we make a general recommendation.

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It is important that we educate our patients so they know that, if they try probiotics, this potentially is not going to cure their disease. So, we have to make sure that we are on the same page. We can try them for a specified period, and if they do not work, we can move on to the next thing. Could probiotics make their AD better? Maybe, and there are some data to support that. However, “don’t go it alone” would be my advice to patients. Patients appreciate a physician’s willingness to hear what they are saying. We do not want patients to feel like no one is listening to them, but we want to make sure that we get them to the point where they are feeling better.