Associations Between Motor Competence, Health-Related Physical Fitness, and Mental Health Outcomes in Spanish Adolescents: The ENERGYCO Study.

Pain is a complex physiological and psychological experience arising from actual or potential tissue damage and is modulated by emotion, cognition, and memory [, ]. In recent years, various nonpharmacological approaches for pain modulation have been applied in clinical pain management, including olfactory, light, and auditory stimulation [, , , ]. Olfactory analgesia, which originates from aromatherapy, refers to the ability of odor stimuli to produce analgesic effects by modulating emotional states and the activity of the Pain Matrix of the brain [, ]. Clinical studies have shown that pleasant scents, such as lavender, vanilla, and banana, can reduce subjective pain intensity []. In particular, lavender essential oil has been widely used in clinical settings to alleviate inflammatory, cancer‐related, visceral, and neuropathic pain [, ]. Similar findings have been reported in rodents. Floral odors, such as phenylethanol and lavender essential oil, reduce nociceptive responses and suppress excessive neuronal activity in the trigeminal system []. Yang et al. [] reported that inhalation of lavender essential oil reduces hyperactivity of glutamatergic neurons in the insular cortex, thereby alleviating inflammatory pain. However, studies investigating the neural mechanisms underlying olfactory analgesia remain limited. The lateral hypothalamus (LH) functions as an integrative hub that receives inputs from feeding, emotional, and sensory systems [, ]. Increasing evidence indicates that the LH plays an important role in pain modulation []. In particular, Orexin A‐expressing neurons within the LH (LH) have been widely implicated in the regulation of nociception and are involved in several forms of nonpharmacological analgesia [, ]. Acute stress, such as restraint or forced swim stress, activates hypothalamic orexinergic neurons, which suppress nociceptive transmission through descending inhibitory pathways; accordingly, disruption of orexin signaling attenuates stress‐induced analgesia []. Similarly, electroacupuncture and voluntary exercise have been shown to reduce pain sensitivity and induce pain‐relief‐associated cue preference in mice, accompanied by activation of LH neurons. Pharmacological blockade of orexin receptors using the antagonist SB‐334867 significantly diminishes both the analgesic effect and the associated positive behavioral responses [, ]. However, whether LH neurons participate in odor‐induced analgesia remains unknown. The LH exhibits significant neural responses to odor stimuli, which is structurally supported by its extensive projection inputs from olfactory‐related brain regions []. Retrograde tracing studies using wheat germ lectin‐horseradish peroxidase (WGA‐HRP) or cholera toxin B subunit (CTB) injections into the LH revealed labeled neurons in olfactory‐related regions, including the piriform cortex (Piri), anterior olfactory nucleus (AON), olfactory tubercle (OT), and amygdala [, ]. Among these olfactory regions, the Piri serves as a major center for higher‐order olfactory processing and integration of odor information []. Recent studies by Dong et al., using anterograde viral tracing in Fos mice, further demonstrated that the LH receives projection fibers from glutamatergic neurons in the Piri []. However, some studies have suggested that olfactory information may also reach the LH through pathways independent of the Piri or OT circuits []. These discrepancies may reflect state‐ or task‐dependent recruitment of distinct olfactory pathways, as well as differences in species and experimental paradigms across studies. Despite accumulating anatomical evidence supporting olfactory‐LH connectivity, the functional relationship between the LH and the Piri has not been systematically investigated, and whether such connections contribute to odor‐induced analgesia remains largely unexplored.