Regarding hypertension and antihypertensives, a physician plays a role in diagnosing patients and guiding them so that they could control their hypertension by taking antihypertensives after excluding some curable causes for elevated blood pressure such as weight gain, salty food, stress, and smoking [3]. Physicians will guide patients to take antihypertensives when high blood pressure still persists after correcting reversible causes. Sleep physicians should correct reversible causes for insomnia such as daily life activities, sleep-wake patterns, and other sleep disorders before prescribing sleeping pills [4]. And, physicians should guide patients to control their sleep problems with a certain tool when insomnia still remains after correcting reversible causes. From this point of view, we need to ask ourselves whether insomnia is a transient symptom or functional impairment. If we consider insomnia as a transient symptom, it is reasonable to instruct patients to take their sleeping pills transiently and guide them to quit sleeping pills as early as possible. On the other hand, if insomnia is a long-lasting functional impairment of the brain and if patients cannot sleep by themselves without certain materials (pills, vegetables, or herbal remedies), we can guide patients to control their sleep disturbance by taking sleeping pills.

Insomnia can occur temporarily when an individual suffers from severe stress or has a psychiatric or medical disease [5,6]. Vice versa, if precipitating factors in 3P model [5] can be elucidated, insomnia can resolve easily. However, if the precipitating factor cannot be easily elucidated, insomnia can last for a long time (chronic insomnia). If a woman suffers sleep disturbance while living with a husband who is stressful to her, insomnia may last unless she gets away from her husband.

On the other hand, we can find some evidence suggestive of more organic impairment and requirement of a longer time for recovery rather than a transient symptom. First, the proportion of N3 stage decreases with age [7]. It has been reported that delta activity (slow-wave sleep) decreases with aging. Aging is associated with a gradual loss of neurons such as the prefrontal cortex and the thalamus known to play key roles in generating and regulating delta waves [8]. Neurotransmitters such as gamma-aminobutyric acid (GABA) known to promote slow-wave sleep or serotonin and acetylcholine known to influence sleep architecture can be altered. Furthermore, cortical thickening in the region involved in sleep regulation can result in less pronounced delta wave activity. It means that the chance of sleeplessness is higher with increasing age.

Second, the peak level of melatonin can be decreased. It has been well reported that melatonin peak level can be decreased with aging. It is a basic reason for developing prolonged-release melatonin (PRM) as a sleeping pill [9]. However, paradoxically, PRM itself can be a evidence showing that insomnia can be a functional impairment, since patients cannot sleep well without the help of PRM, which can replenish the age-related decreased melatonin. Furthermore, among children with autism spectrum disorder or brain development disorder, nocturnal melatonin level is reduced. Such reduction is one of the causes for sleep disturbance in children [10]. It is related to pineal gland hypofunction, which can impair its ability to produce melatonin. Neurodevelopmental disorders are often associated with imbalances in neurotransmitters and neurochemicals, which can affect the function of the pineal gland and melatonin production. Certain genetic mutations associated with neurodevelopmental disorders may directly or indirectly affect melatonin synthesis.

From this point of view, some of insomnia patients suffer from lifelong insomnia and may require sleep aids for long-term, and that these patients should not be given the same one unified rule—quit sleep aids as early as possible. We should not tell patients to stop or quit their sleeping pills without considering characteristics of insomnia itself. Rather, clinicians should classify patients into “patients who can sleep without medication” and “patients who cannot sleep without medication.” Without this classification, our guidance to reduce or quit the sleeping pills can be a sword to some patients who cannot sleep without medication due to functional impairment of brain. Sleep physicians should guide “patients who can sleep without medications” to get the help. Non-pharmacological treatments, such as cognitive-behavioral therapy for insomnia (CBT-I), are effective for many “patients who can sleep without medication.” However, for “those who cannot sleep without medication,” we need to develop optimal strategies for the safe and effective use of sleeping pills. Understanding the characteristics of insomnia can help in creating these strategies, guiding patients on the scientific use of sleeping pills, including when to take them and how to discontinue their use appropriately.