Anxiety disorders are the most common psychiatric conditions worldwide, affecting an estimated 359 million people. Controlled breathing is widely used to ease anxious feelings, yet the precise brain pathways connecting breathing with emotion have remained unclear.
A new study in mice, published in Proceedings of the National Academy of Sciences (PNAS), describes a dedicated nose-to-brain circuit that may explain how nasal breathing can directly influence anxiety. The findings help connect ancient breathing practices with modern neuroscience.
How breathing shapes emotion
Cultures have long used breathing techniques, from pranayama in yoga to Taoist practices and meditation. Modern research increasingly supports these traditions, showing that slow, regular breathing can significantly influence emotional states and reduce anxiety symptoms.
Breathing is automatically regulated by the brainstem, but people can also consciously alter their breathing through higher brain regions. Until now, scientists have known relatively little about how either automatic or deliberate breathing patterns translate into changes within anxiety-related brain circuits.
The key role of the nose
Earlier experiments in rodents suggested that changing breathing patterns can alter emotional behavior, whether the change is voluntary or induced by manipulating brain circuits. This pointed to a nonconscious body-brain pathway that may help regulate emotion through respiration.
Intriguingly, previous work also showed that slow nasal breathing is more effective than slow mouth breathing at calming anxiety, suggesting a special role for the nose. Nasal breathing rhythms have been found to synchronize brain activity in both humans and animals.
Inside the nasal cavity, olfactory sensory neurons do more than detect odors. These cells are also sensitive to airflow, meaning that each inhalation can generate mechanical signals that travel to the olfactory bulb, a forebrain structure closely connected with emotional centers.
Mapping the nose-to-brain circuit
To investigate this mechanism, researchers used male mice and applied optogenetics to precisely control the firing of olfactory sensory neurons. They also adjusted nasal airflow through implanted cannulas, allowing them to simulate different breathing frequencies.
The team combined optogenetics, chemogenetics, electrophysiology, fiber photometry, behavioral testing and viral tracing to map the communication pathway. They found that signals begin in olfactory sensory neurons, pass to mitral cells in the olfactory bulb and then travel to long-range interneurons in the perirhinal cortex.
From the perirhinal cortex, information reaches glutamatergic neurons in the posterior basolateral amygdala, a key hub involved in processing fear and anxiety. Together, these connections form a nasal-limbic pathway that directly links inhalation with emotional regulation.
Breathing frequency and anxiety
The researchers discovered that nasal airflow regulates anxiety-like behavior in a frequency-dependent manner. When the circuit was activated at lower frequencies, mimicking slow nasal breathing, mice showed reduced anxiety-like responses during behavioral tests.
Higher-frequency stimulation, resembling rapid breathing, produced the opposite effect and increased anxiety-like behaviors. This suggests that the same pathway may either calm or intensify anxiety depending on how rapidly air moves through the nose.
When researchers chemogenetically silenced the connection between the olfactory bulb and perirhinal cortex, changes in nasal sensory frequency no longer influenced anxiety-like behavior. This indicates that the connection is essential for the emotional effects associated with nasal breathing.
Potential for noninvasive therapies
The researchers also tested a two-week program of controlled slow nasal airflow in some of the mice. The regimen restored neural activity in key parts of the circuit and reduced anxiety-like behaviors, further supporting the idea that breathing patterns can reshape emotional pathways.
The study has important limitations. It involved only male mice, relied on controlled laboratory stress models and artificial stimulation, and did not directly test humans. Translating the findings will therefore require careful clinical research and replication in other animal models.
Still, the research offers a plausible biological explanation for why slow nasal breathing appears particularly calming. The authors suggest that breathing through the nose at roughly half the normal rate could eventually be refined into a simple, noninvasive adjunct treatment for anxiety disorders.
Future studies are expected to investigate whether similar nose-to-brain circuits operate in humans, how individual differences influence responses to breathing techniques and whether targeted breathing regimens could complement psychotherapy and medication in treating anxiety.
