Reducing the risk of sudden unexpected infant death: the caffeine hypothesis

Thomas Hegyi; Barbara M. Ostfeld

doi:10.1038/s41372-025-02333-x

Reducing the risk of sudden unexpected infant death: the caffeine hypothesis

Thomas Hegyi, Barbara M. Ostfeld

Robert Wood Johnson Medical School (RWJMS), Pediatrics, Division of Neonatology

Rutgers, The State University

Research output: Contribution to journal › Review article › peer-review

Abstract

This review proposes that intermittent hypoxia is the primary pathogenic mechanism driving Sudden Infant Death Syndrome (SIDS). Intermittent hypoxia is a powerful source of molecular and cellular injury and is frequently experienced by infants, especially under conditions associated with known SIDS risk factors such as prone sleeping, respiratory infections, and prenatal nicotine exposure. These factors often trigger hypoxic episodes that may impair autonomic regulation, hinder arousal from sleep, and damage critical neural circuits. By integrating current data, this review highlights the central role of intermittent hypoxia in SIDS pathophysiology. Additionally, it evaluates the potential of caffeine, a respiratory stimulant and adenosine receptor antagonist, as a protective intervention to reduce SIDS risk by enhancing respiratory stability and arousal capacity.

Original language	American English
Journal	Journal of Perinatology
DOIs	https://doi.org/10.1038/s41372-025-02333-x
State	Accepted/In press - 2025

ASJC Scopus subject areas

Pediatrics, Perinatology, and Child Health
Obstetrics and Gynecology

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10.1038/s41372-025-02333-x

Cite this

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title = "Reducing the risk of sudden unexpected infant death: the caffeine hypothesis",

abstract = "This review proposes that intermittent hypoxia is the primary pathogenic mechanism driving Sudden Infant Death Syndrome (SIDS). Intermittent hypoxia is a powerful source of molecular and cellular injury and is frequently experienced by infants, especially under conditions associated with known SIDS risk factors such as prone sleeping, respiratory infections, and prenatal nicotine exposure. These factors often trigger hypoxic episodes that may impair autonomic regulation, hinder arousal from sleep, and damage critical neural circuits. By integrating current data, this review highlights the central role of intermittent hypoxia in SIDS pathophysiology. Additionally, it evaluates the potential of caffeine, a respiratory stimulant and adenosine receptor antagonist, as a protective intervention to reduce SIDS risk by enhancing respiratory stability and arousal capacity.",

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AB - This review proposes that intermittent hypoxia is the primary pathogenic mechanism driving Sudden Infant Death Syndrome (SIDS). Intermittent hypoxia is a powerful source of molecular and cellular injury and is frequently experienced by infants, especially under conditions associated with known SIDS risk factors such as prone sleeping, respiratory infections, and prenatal nicotine exposure. These factors often trigger hypoxic episodes that may impair autonomic regulation, hinder arousal from sleep, and damage critical neural circuits. By integrating current data, this review highlights the central role of intermittent hypoxia in SIDS pathophysiology. Additionally, it evaluates the potential of caffeine, a respiratory stimulant and adenosine receptor antagonist, as a protective intervention to reduce SIDS risk by enhancing respiratory stability and arousal capacity.

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Reducing the risk of sudden unexpected infant death: the caffeine hypothesis

Abstract

ASJC Scopus subject areas

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