A baby’s skin may hold clues about future food allergies before any symptoms appear.

In a study of infants in Australia, researchers found that some babies who later developed both eczema and food allergies had different mixes of microbes living on their skin at just 2 to 3 months old. At that point, none had been diagnosed with eczema or had a history of itchy skin. The findings suggest skin microbes could someday help doctors spot children who may be at higher risk earlier, but the research is still a long way from becoming a screening test.

“We actually saw skin microbiome changes in infants who hadn't even been diagnosed with these diseases yet,” said Zeyang Shen, an assistant professor at Washington State University and one of the study’s lead authors. “That was one of the most exciting findings because those changes could potentially be used as biomarkers to help clinicians diagnose disease earlier.”

The study, published in Allergy, included 429 infants. Researchers analyzed more than 1,000 skin samples collected from babies’ cheeks and the creases of their elbows. Samples were taken when some of the babies were 2 to 3 months old and again around age 1.

By age 1, 95 infants had been diagnosed with at least one food allergy, and most of those children also had eczema. Another group had food sensitization, meaning allergy tests showed an immune response to a food even though the child could still eat that food without an allergic reaction. That distinction is important because food sensitization is not the same as food allergy.

The researchers were especially interested in whether differences in the skin microbiome appeared before eczema or food allergy had been diagnosed.

Among babies who later developed eczema alone, they did not find an early microbial pattern that clearly set them apart from healthy infants. But babies who later developed both eczema and food allergy had higher levels of several types of bacteria on their skin at 2 to 3 months. One of them was Staphylococcus aureus, a common bacterium that has previously been linked to eczema and allergic disease.

That may help researchers understand why some babies with eczema also develop food allergies while others do not.

The differences became more noticeable by about age 1. Babies with eczema alone had a different mix of skin microbes from babies who had both eczema and food allergy, suggesting those conditions may not follow exactly the same biological path.

But the study cannot tell us whether those microbes actually contribute to eczema or food allergies. It is also possible that very early changes related to allergic disease were already affecting the skin before parents or doctors noticed symptoms.

The researchers also looked at genetics. They focused on variations in a gene called FLG, which helps the skin maintain its protective barrier and is strongly linked to eczema risk. Among babies with eczema, those genetic differences were tied to additional changes in the skin microbiome by age 1. However, those differences were not seen in the earlier samples taken at 2 to 3 months.

Another finding involved mothers and babies sharing microbes. Researchers found that some of the same bacterial strains were present on both, which is not surprising given how much close contact parents and infants have.

“The microbial strains are very much shared between infants and their mothers,” Shen said. “That gives us another layer to this story, suggesting that the people we live around and continuously exchange microbes with could also be contributing to our skin microbiome.”

That does not mean mothers are passing along bacteria that cause food allergies. Microbial sharing was found regardless of whether the infant developed eczema or food allergy, and the study was not designed to determine whether those shared microbes affect disease risk.

There are other reasons to interpret the results cautiously. All of the infants were born in Australia, and most cases of eczema were mild. Researchers did not have information about antibiotic exposure, which could affect skin microbes. The early samples also came from a much smaller group than the samples collected around age 1.

The infants were also part of an ongoing clinical trial studying vitamin D supplementation. Because researchers still did not know which children had received vitamin D and which had received a placebo when this analysis was done, they could not rule out the possibility that supplementation affected the skin microbiome.

For parents, the study does not suggest changing a baby’s skin care routine, using probiotics or trying to alter the skin microbiome. None of those approaches were tested.

Instead, the findings offer scientists another clue about how eczema and food allergies may begin. If future studies find the same patterns in other children, a simple skin sample might one day help identify babies who need closer monitoring before symptoms develop.

“Today, these diseases are diagnosed after symptoms appear,” Shen said. “If we can validate these microbial signals in other groups of children, they could potentially serve as early biomarkers that help identify disease risk much earlier.”

The research received support from the National Institutes of Health, Washington State University, Australia’s National Health and Medical Research Council, the Victorian government and several charitable and philanthropic organizations. One author reported research grants and consulting relationships involving several pharmaceutical and biotechnology companies outside this study and serves as a nonexecutive director of OmnisOva.