Scientists Defend Findings Linking Childhood Snoring to Microbiome Imbalance

A quiet but consequential scientific exchange is unfolding in the pages of the Journal of Clinical Sleep Medicine, and it touches one of the most intriguing questions in pediatric sleep research: whether children who snore, or who struggle with obstructive sleep apnea, carry a distinctly altered community of microbes in their throats and guts. The latest installment is an author reply from a team of Australian researchers led by Jennifer Hudson and Chee Y. Ooi of the University of New South Wales and Sydney Children’s Hospital, responding to a formal correspondence from Dr. Hyun Jin Min that raised pointed methodological questions about their original study. The exchange matters because the original work reported that children with obstructive sleep apnea and even simple primary snoring show oropharyngeal dysbiosis, a disruption of the microbial communities lining the upper airway, alongside a mild compositional imbalance in the gastrointestinal tract.

The original study, published in the same journal, set out to answer a question that has been building in the literature for years: are the microbiome alterations previously reported in children with obstructive sleep apnea confined to the severe end of the sleep-disordered breathing spectrum, or do they extend to children who merely snore without measurable drops in oxygen? The researchers found that the airway microbiomes of children with obstructive sleep apnea and those with primary snoring were broadly similar to each other and distinct from healthy controls. That similarity is the conceptual heart of the work, because it suggests that whatever is reshaping the microbial landscape is not simply the severity of the apnea itself, nor the hypoxic burden of repeated nighttime oxygen desaturation, but something shared across the whole spectrum of sleep-disordered breathing.

Dr. Min’s correspondence, published as a formal comment on the paper, highlighted several considerations that anyone who works with sequencing-based microbiome data will recognize immediately. Oropharyngeal microbial communities are notoriously sensitive to their immediate surroundings. Recent food intake can seed the mouth with transient organisms. Oral hygiene practices, from toothbrushing to mouthwash use, can shift the balance of species detectable on a swab. Even the time of day at which a sample is collected matters, as high-frequency saliva sampling studies have demonstrated clear diurnal and eating-associated microbial patterns. Any one of these factors, if it differs systematically between patient groups and controls, could masquerade as a disease-associated dysbiosis when it is really just a difference in when the children last brushed their teeth.

In their reply, the authors addressed this concern with unusual transparency about their sampling protocol. All oropharyngeal swabs in the study were collected during daytime clinic hours, at approximately four in the afternoon, and always before the children began their overnight sleep study. That standardization of timing removes one source of variability. But the team acknowledged a more difficult limitation: information about recent dietary intake and oral hygiene practices was not collected at all, owing to the practical challenges of enforcing strict oral protocols in a young pediatric cohort. The authors conceded that some of the taxa identified in the oropharyngeal microbiome may therefore reflect transient environmental exposures rather than stable colonization, and they called for longitudinal sampling studies to properly characterize the stable microbial community in children with sleep-disordered breathing.

The second major issue raised in the correspondence concerns allergies and upper airway inflammation, and here the confounding problem is arguably even more serious. Allergic rhinitis is extraordinarily common in children, and it is also plausibly linked to both snoring and to measurable changes in the nasal and oral microbiome. Systematic reviews of the nasal mucosal microbiome in children and adolescents with allergic rhinitis have documented distinct microbial signatures, and separate work on the adenotonsillar microbiome of snoring children has shown correlations between microbial composition and clinical characteristics. If allergic children are overrepresented in the sleep-disordered breathing group, an apparent association between snoring and dysbiosis could in fact be an association between allergy and dysbiosis, with sleep merely along for the ride.

The authors agreed that allergic and upper airway inflammatory conditions may influence oral microbial communities, but they were candid that such information was not systematically collected prospectively in their cohort and therefore could not be evaluated in the analysis. This is a genuine gap, and the team did not attempt to paper over it. Instead, they framed the original study’s ambition more narrowly: the goal was to determine whether previously reported microbiome alterations in children with obstructive sleep apnea occurred across the full spectrum of sleep-disordered breathing, including primary snorers, and whether those alterations tracked with objective measures of disease severity such as the obstructive apnea/hypopnea index or the oxygen saturation nadir during sleep. Disentangling the relative contributions of sleep-disordered breathing and upper airway inflammation, they wrote, and identifying the underlying mechanisms of oropharyngeal dysbiosis, will require further investigation.

The third thread of the exchange concerns anatomy, and in particular adenotonsillar hypertrophy, the enlargement of the tonsils and adenoids that is the single most common cause of obstructive sleep apnea in children. Dr. Min argued that adenotonsillar size is a relevant factor in shaping the airway microbiome, and the authors agreed, adding other anatomical variables to the list: tongue position and craniofacial differences between individuals, both of which have been linked to oral microbiome changes in prior studies of craniofacial conditions. The logic is straightforward. The physical architecture of the upper airway determines airflow patterns, tissue surfaces, secretions, and local oxygen tension, all of which are ecological variables for the bacteria that live there. A child with massively enlarged tonsils presents a fundamentally different habitat to microbes than a child with a wide, unobstructed airway.

Yet the authors explained why they could not stratify their participants by adenotonsillar size, and their reasoning exposes a stubborn problem in pediatric sleep research. Reliable and objective assessments of adenotonsillar size were not routinely available for the cohort. Visual grading of tonsillar size using standard grading scales remains observer-dependent, with documented variation across raters, a limitation that has been quantified in studies of clinical tonsil grading reliability. Otolaryngology review and radiological studies were not undertaken in all children in the study, particularly those classified as primary snorers, who in routine clinical practice often do not undergo such examinations. The result is a study that can compare microbiomes across diagnostic groups but cannot yet pinpoint which anatomical features within those groups are doing the microbial heavy lifting.

What emerges from the reply is a careful, measured defense that doubles as a research roadmap. The similarity of microbial profiles between children with obstructive sleep apnea and primary snorers, the authors argue, points toward factors common to both conditions as the important determinants of airway microbial composition. Their candidate list includes altered breathing patterns, upper airway anatomy including adenotonsillar hypertrophy, and local inflammatory processes. Identifying which of these shared features drives the dysbiosis, they write, represents the important next step in determining the mechanisms underpinning airway dysbiosis in children with sleep-disordered breathing. The sequencing data from the original publication have been deposited in the NCBI Sequence Read Archive under BioProject PRJNA1312271, allowing other teams to interrogate the findings independently, and the correspondence itself generated no new data.

For the broader field, the exchange is a textbook illustration of how microbiome science matures. The era of simply cataloging which microbes are present in a disease state is giving way to a harder and more valuable enterprise: ruling out confounders, standardizing collection protocols, accounting for anatomy and inflammation, and distinguishing transient passengers from stable residents. The Australian team’s willingness to enumerate the limitations of their own cohort, from unrecorded toothbrushing habits to ungraded tonsils, is precisely the kind of candor that allows follow-up studies to be designed well. Children who snore are often dismissed as harmless noise in the family bedroom, but if even primary snoring is accompanied by a measurable shift in the microbial ecology of the airway and gut, the humble snore may prove to be a window into a systemic biological process, one that researchers are only now learning to read.

Subject of Research: Microbiome alterations in children with obstructive sleep apnea and primary snoring

Article Title: Reply to “Correspondence regarding ‘Obstructive sleep apnea and primary snoring in children are associated with oropharyngeal dysbiosis and a mild compositional imbalance in the gastrointestinal tract’”

Article References: Hudson, J., Akhand, A., Nwe, M. T., Coffey, M. J., van Dorst, J., Chuang, S., & Ooi, C. Y. (2026). Reply to “Correspondence regarding ‘Obstructive sleep apnea and primary snoring in children are associated with oropharyngeal dysbiosis and a mild compositional imbalance in the gastrointestinal tract’”. Journal of Clinical Sleep Medicine, 22(1), Article 120. https://doi.org/10.1007/s44470-026-00141-4

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00141-4

Keywords: obstructive sleep apnea, primary snoring, children, microbiome, oropharyngeal dysbiosis, gut microbiota, adenotonsillar hypertrophy, sleep-disordered breathing, allergic rhinitis, sequencing, pediatric sleep disorders, author reply