Mouth breathing at night is tied to snoring and sleep apnea. These repeated airway collapses trigger stress signals and intermittent drops in oxygen, which make blood pressure spike. Over time, this keeps the cardiovascular system stuck in “high alert” mode.

In Breath, James Nestor documented that when he was forced to mouth breathe at night, his blood pressure climbed dramatically, hitting hypertensive ranges. When he switched back to nasal breathing, his blood pressure fell by about 30 points overnight—a striking change for such a short timeframe (Nestor, 2020).

Clinical studies back up the link: patients with obstructive sleep apnea—a condition strongly associated with chronic mouth breathing—show higher 24-hour blood pressure compared to nasal breathers.

• Nestor, J. Breath: The New Science of a Lost Art (2020).
  
• Martínez-García et al. JAMA (2013): CPAP reduces 24-h BP in resistant hypertension (HIPARCO).
  
• Becker et al. Circulation (2003): effective CPAP lowers day & night BP by ~10 mmHg.

During sleep, opening the mouth and switching to oral breathing narrows the pharynx and increases its tendency to collapse. That raises upper‑airway resistance, promoting snoring and obstructive events that fragment sleep.

Snoring skyrockets with mouth breathing. In Breath, James Nestor showed snoring can reach 80 decibels—like a kitchen blender—when the mouth is open at night. Switching to nasal breathing dropped it to a whisper.

Clinical trials confirm: mouth breathing makes the airway more collapsible and more likely to snore. In sleeping adults, oral breathing increased upper‑airway resistance to ~12.4 vs 5.2 cmH₂O·L⁻¹·s with nasal breathing, and raised apnea–hypopnea index (AHI) from ~1.5 to 43 events/h in the same subjects.

• Nestor, J. Breath: The New Science of a Lost Art (2020).
  
• Fitzpatrick et al. Am J Respir Crit Care Med (2003): oral vs nasal breathing during sleep—oral breathing doubled resistance and raised AHI
  
• Meurice et al. Am J Respir Crit Care Med (1996): mouth opening increases upper-airway collapsibility

Saliva washes away bacteria and buffers acids. Breathing through the mouth reduces saliva, leaving teeth and gums vulnerable. Clinical studies in children and teens show mouth breathing independently raises plaque and gingivitis scores, even with good hygiene.

Late‑adolescent mouth‑breathers had a 4× higher risk of high Streptococcus mutans counts (a key cavity bacterium) over 6 months even with good hygiene.

In 201 schoolchildren (11–14 yrs), mouth breathing was independently linked with more plaque and more gingival inflammation, even after controlling for other factors.

Mummolo M. Biomed Res Int (2018): salivary markers & bacteria in mouth‑breathers.

Wagaiyu & Ashley. J Clin Periodontol (1991): mouthbreathing & gingival inflammation.

Oral-only breathing drives faster, shallower breaths. That means less efficient CO₂ exchange and wasted energy. Studies show nasal breathing slows rate, lowers ventilation relative to CO₂, and raises end-tidal CO₂—improving efficiency.

Eser et al. Front Physiol (2024): nasal breathing improved ventilatory efficiency.

Recinto et al. Sports (2017): mouth breathing drove hyperventilation but didn’t increase power.

Chronic mouth breathing shifts tongue and jaw posture, rotating the mandible downward and back. Meta-analyses show mouth-breathing kids have steeper mandibular planes, narrower airways, and more crowding.

Meta‑analysis of 10 studies: mouth‑breathing children had lower SNA/SNB angles (both jaws positioned further back), higher mandibular plane angles (SNGoGn +4.1°), and narrower airway measures (PAS −2.1 mm).

A second meta‑analysis found greater mandibular plane angles and facial height in mouth‑breathers vs nasal‑breathers—consistent with the classic “adenoid facies” pattern.

Zhao et al. BMC Oral Health (2021) meta‑analysis: craniofacial changes & airway.

Zheng et al. Exp Ther Med (2020) meta‑analysis: facial morphology differences.