Case Report: Resolution of Insomnia in a 32-Year-Old Male with Generalized Anxiety Disorder Following Discontinuation of Mint-Flavored Toothpaste

Introduction

Insomnia affects up to 30% of adults in the general population and is commonly comorbid with anxiety disorders.¹ Patients with generalized anxiety disorder (GAD) frequently demonstrate heightened sensory processing and increased sympathetic activation, both of which may lower their threshold for sleep disturbances.^2,3 While psychophysiological hyperarousal is traditionally emphasized, environmental and sensory stimuli, particularly those that activate trigeminal or thermosensory pathways, are often overlooked contributors.⁴

Menthol, the active cooling compound in mint-flavored toothpaste, activates TRPM8 receptors located in oral, nasal, and central nervous system pathways.⁵ Activation of these receptors increases alertness, enhances sensory gating, and can delay sleep onset in susceptible individuals.⁶ Insomnia, possibly associated with menthol exposure, with a hypothesized contribution from TRPM8-mediated sensory activation leading to increased alertness. This case report describes an uncommon but clinically significant cause of insomnia triggered by nightly exposure to mint-flavored toothpaste, particularly in a patient with underlying anxiety.

Beyond chemical stimuli, a growing body of evidence suggests that pre-sleep sensory and environmental exposures can meaningfully influence sleep initiation and maintenance.⁷ Behavioral models of insomnia emphasize the role of conditioned arousal, in which repeated associations between wakefulness and specific environmental cues, such as light, sound, temperature, or somatosensory input, can perpetuate sleep disturbances.^8,9 Additionally, sensory stimuli that activate trigeminal or autonomic pathways may increase cortical and physiological arousal, thereby interfering with the transition to sleep.¹⁰ Emerging research also indicates that even mild sensory inputs delivered close to bedtime can alter electroencephalographic activity and delay sleep onset in susceptible individuals.¹¹ These findings support the concept that seemingly minor environmental exposures, including oral sensory stimuli, may play a contributory role in insomnia, particularly among individuals with heightened sensory sensitivity or anxiety.

Case Presentation

Patient Information: 32-year-old male

Chief Complaint: Insomnia lasting 7 months in a patient with known generalized anxiety disorder

History of Present Illness

The patient reported difficulty falling asleep (average sleep latency >1.5 hours) and frequent nighttime awakenings (2–4 episodes per night). Prior to symptom onset, the patient reported normal sleep latency (10–20 minutes) and consistent 7–8 hours of nightly sleep. Symptoms began three weeks after initiating a new mint-flavored toothpaste used exclusively at night. The patient denied new psychosocial stressors, medication changes, excessive caffeine (>150 mg/day), strenuous late-night exercise, or screen use in bed. The patient also denied regular use of other menthol-containing products, including mint-flavored mouthwash, lozenges, chewing gum, inhalants, or topical preparations, and reported no significant dietary changes involving menthol-containing foods or beverages. The patient has a 3-year history of GAD managed with escitalopram 10 mg daily, stable for over 18 months without dosage changes. No changes in medication type or dosage occurred during or after this period, and no medication-related effects on sleep were identified.

Past Medical History

● Generalized Anxiety Disorder (GAD)

● No history of sleep apnea, parasomnias, thyroid disease, or chronic pain

Social History

• Non-smoker
• No alcohol consumption
• No recreational drug use
• Regular daytime job with a stable schedule
• No recent travel or circadian disruption

Clinical Findings

• Vitals: Within normal limits
• Mental Status Exam: Mild anxiety, no depression, normal cognition
• GAD-7 score: 6 (mild anxiety)
• Insomnia Severity Index (ISI) score: 21 (moderate insomnia)
• Sleep hygiene evaluation: Adequate; no evidence of behaviors contributing to conditioned arousal
• No symptoms suggestive of obstructive sleep apnea (loud snoring, witnessed apneas, morning headaches)
• No features of restless legs syndrome
• No recent increases in caffeine, stimulant exposure, or stress

The temporal relationship strongly indicated the introduction of mint-flavored toothpaste as the precipitating factor.

Assessment and Plan

Assessment

• Insomnia, likely precipitated by menthol-induced TRPM8 activation, leading to increased alertness and sleep-onset difficulty.
• Underlying GAD may have lowered the threshold for sensory-triggered arousal, amplifying the effect.
• Other causes (eg., medication side effects, substance use, circadian disorders) were ruled out.

Plan

Advised patient to switch to a non-mint, flavor-free toothpaste (eg., baking soda or herbal base)

• Recommended continuation of current anxiety treatment.
• Suggested to implement a 2-week sleep diary to monitor progress.
• Provide education on avoiding menthol-containing evening products (mouthwash, lozenges, essential oils).
• Schedule follow-up after 2 weeks and again at 1 month.

Outcome

• Within two days of discontinuing the mint toothpaste, the patient reported:
• Reduced sleep latency from >90 minutes to ~25 minutes
• Nighttime awakenings decreased from 2–4 to 0–1 per night
• Improved perceived sleep quality and morning refreshment

This relatively short time frame of improvement should be interpreted with caution, as it may reflect an acute, stimulus-dependent effect or non-specific factors rather than a sustained therapeutic response.

At 2-week Follow-Up

• The ISI score improved from 21 to 7 (subthreshold insomnia)
• GAD-7 remained stable at 6
• No recurrence of symptoms

At 1-month Follow-Up

• Continued use of non-mint toothpaste
• Sustained remission of insomnia symptoms

Discussion

This case illustrates a probable link between nightly menthol exposure from mint-flavored toothpaste and the onset of sleep disturbance. Although menthol is widely regarded as harmless and is commonly used in oral-care products, its neurobiological effects suggest that it may influence arousal regulation in susceptible individuals.¹² The patient’s symptoms, combined with the rapid resolution of insomnia after discontinuing menthol-containing toothpaste, demonstrate a temporal relationship with reversibility but do not establish causation. Importantly, insomnia is a multifactorial condition, and a comprehensive evaluation of behavioral, psychological, and environmental factors remains essential in clinical practice. This case highlights a potentially overlooked sensory contributor while not excluding the role of other factors in the development or resolution of symptoms.

Notably, the observed short time frame of symptom improvement (within two days) may be more consistent with an acute, stimulus-dependent sensory or autonomic effect rather than a prolonged neurobiological process requiring extended washout. TRPM8 activation is known to produce immediate and reversible sensory and arousal responses, which may diminish quickly after cessation of exposure. This temporal pattern supports the possibility of a transient mechanism, although alternative explanations, including placebo or behavioral factors, should also be considered.

From a mechanistic standpoint, menthol is a well-established agonist of the TRPM8 (transient receptor potential melastatin 8) ion channel, which is responsible for cold sensation in oral, nasal, and cutaneous tissues.^13,14 Activation of TRPM8 does not merely produce a cooling feeling; it also engages sensory arousal pathways and can influence thalamocortical processing, potentially increasing cortical excitability.^15,16 However, existing evidence primarily relates to acute neurophysiological and sensory effects rather than chronic sleep disturbances. While menthol exposure has been associated with increased alertness, enhanced sensory gating, and changes in EEG activity, an electrophysiological signature associated with alertness and cognitive activation.^17–19 In addition, menthol has been reported to increase sympathetic nervous system activity.²⁰ Therefore, any proposed link between TRPM8 activation and persistent insomnia remains speculative. In this context, repeated nightly exposure to menthol may represent a potential contributing factor to sleep disruption in susceptible individuals, although this hypothesis requires further investigation.

Individuals with generalized anxiety disorder (GAD) may be especially susceptible to such effects. Patients with anxiety disorders often exhibit increased sensory hyper-responsiveness and amplified reactivity to somatosensory cues.²¹ They also demonstrate heightened baseline autonomic arousal and reduced parasympathetic tone.²² As a result, even minor sensory stimuli, such as the cooling effect of menthol before bedtime, may produce disproportionately strong arousal responses, making it more difficult to initiate or maintain sleep.¹⁹ In this case, however, the patient’s GAD-7 score remained stable over time, suggesting that anxiety severity did not change in parallel with sleep improvement. Therefore, anxiety is better interpreted as a potential predisposing factor rather than a dynamic contributor to symptom resolution. This heightened vulnerability provides a possible, rather than definitive, explanation for why the patient experienced significant sleep disruption despite a seemingly mild environmental trigger.

The clinical relevance of this case extends to everyday practice. Common nighttime exposures such as mint toothpaste, mentholated mouthwash, camphor balms, eucalyptus oil, and other TRPM8-activating substances are rarely evaluated during insomnia assessments. Yet for individuals with anxiety, heightened sensory sensitivity, or autonomic dysregulation, these exposures may meaningfully interfere with sleep quality. This case underscores the importance of obtaining a comprehensive environmental and sensory history when evaluating unexplained insomnia.

Limitations and Future Recommendations

Several limitations must be acknowledged. This is a single case report without confirmatory polysomnography, and a placebo effect cannot be completely ruled out. The rapid time course of symptom resolution may also limit interpretation, as such improvement could reflect non-specific effects rather than a direct physiological mechanism. Additionally, despite the absence of identifiable stressors or behavioral changes, unmeasured or unrecognized factors may have contributed to the improvement in sleep, and a coincidental resolution of symptoms cannot be excluded. Although the patient denied other menthol exposures, the possibility of unrecognized or intermittent sources cannot be entirely ruled out. Importantly, the improvement observed after discontinuation of menthol exposure should not be interpreted as definitive evidence of causality, as this reasoning is inherently limited in uncontrolled single-case observations. Furthermore, the lack of change in anxiety severity, as measured by the GAD-7, limits the ability to attribute the observed sleep disturbance or its resolution to fluctuations in anxiety, and alternative explanations should be considered. However, the strong temporal correlation between menthol exposure and symptom onset, combined with rapid resolution following its removal and the presence of well-supported mechanistic pathways, makes a causal relationship plausible. Further controlled studies are warranted to clarify the role of menthol and TRPM8 activation in sleep regulation, particularly among anxiety-prone populations.

This report should be interpreted within the limitations inherent to single case studies, which represent a lower level of clinical evidence and do not allow for definitive causal inference. The observed association may be influenced by unmeasured confounders or placebo effects. However, the clear temporal relationship between exposure and symptom onset, along with rapid and sustained resolution following withdrawal, provides a signal that may warrant further investigation. Rather than establishing causality, this case is intended to generate hypotheses and highlight a potentially overlooked environmental factor in insomnia, particularly among individuals with heightened sensory sensitivity. Future research could explore this hypothesis using feasible study designs, such as n-of-1 crossover trials, short-term experimental studies assessing the acute effects of menthol exposure on sleep onset and arousal, or observational studies in populations with anxiety or sensory sensitivity. Such approaches may help determine whether menthol-containing products have clinically meaningful effects on sleep in susceptible individuals.

Conclusion

In patients with anxiety-related insomnia, seemingly minor sensory exposures may have clinically significant impacts on sleep. This case describes a possible association between mint-flavored toothpaste use and insomnia, with symptom resolution following its discontinuation. While causality cannot be established from a single case, the observed temporal relationship, rapid reversibility, and biologically plausible mechanisms suggest that menthol-containing products may act as a contributing factor in susceptible individuals. Clinicians may consider including questions about oral hygiene products and other menthol-containing items when evaluating unexplained sleep disturbances, including sleep-onset insomnia, sleep-maintenance insomnia, and non-restorative sleep. Further studies are needed to investigate this potential relationship.