Obstructive sleep apnea (OSA) is a disorder in which the upper airway obstruction is repeated during sleep. If left untreated, it causes hypoxia, daytime sleepiness, loss of concentration that can result in traffic and other accidents in the short term, and complications such as high blood pressure [1], cardiovascular disease [2], dementia [3], and depression [4] in the long run.

Obesity, age, male gender, alcohol consumption, and upper airway collapsibility are well known risk factors for OSA, and cigarette smoking has been reported to increase the risk of OSA [5]. Obesity is one of the most important risk factors for OSA, and the incidence and severity of OSA has been positively correlated with body mass index (BMI) [6]. The prevalence of OSA in obese people was shown to be twice that of normal weight people, and a 10% increase in body weight increased the apnea-hypopnea index (AHI) by 32% [7].

The most common treatment method for OSA is continuous positive airway pressure (CPAP), intraoral devices, and upper airway surgery. Among them, CPAP maintains an open airway during sleep and is known as the most effective treatment method for improving AHI and daytime sleepiness [8]. The American Academy of Sleep Medicine recommends a CPAP or oral device for the treatment of mild-to-moderate OSA patients. For patients with severe OSA, CPAP is recommended as the first-line treatment and an intraoral device is recommended as a secondary treatment method [9]. However, even among CPAP users, adherence rates during long-term follow-up were low due to inconvenience of wearing, and these low adherence rates limited the therapeutic effectiveness of CPAP [10].

Evidence suggests that weight loss or exercise may reduce the severity of OSA, and drinking and smoking have been found to be associated with an increased risk of OSA. Therefore, behavioral therapy through lifestyle modification as a means to treat OSA was investigated in this study. We will discuss lifestyle modification as a treatment method of OSA by examining the results of research on each modifiable item, including weight loss, exercise, alcohol consumption and smoking.

Many studies (Table 1) on weight-loss attempts in patients with OSA used a very low-calorie diet of only 600–800 kcal a day for the first 8 to 12 weeks, followed by diet consultation [7,11–17]. In a study of weight loss in patients with mild OSA for one year, a 10% reduction in average body weight (from 101.2 to 90.5 kg) reduced AHI by approximately 40% (from 10 to 6 events/h). Since the subjects had mild OSA patients, approximately 60% of the patients were cured with weight loss alone [15]. Despite the fact that there was no further consultation or intervention for one year thereafter, at 2-year follow-up the average BMI of patients decreased further from −3.5 kg/m² (at 1-year follow-up) to −2.5 kg/m² (at 2-year follow-up), and the average decrease of AHI was maintained at −4.0 events/h (at 1-year follow-up) and −4.6 events/h (at 2-year follow-up) [13]. In a study of weight loss during one year in moderate-to-severe OSA patients, AHI decreased by about 16.9% (from 42.5 to 32.0 events/h) with a 2.2 kg/m² reduction in BMI (from 29.8 to 27.6 kg/m²) [11]. In addition, a meta-analysis of studies examining the effects of weight loss on OSA showed that weight loss reduced the severity of OSA [18].

When the mechanism of weight loss to improve severity of OSA was examined, weight loss was found to increase the area of the upper airway by reducing velopharyngeal fat and alleviate collapsing of the upper airway by reducing mechanical burden. In addition, accumulation of abdominal visceral fat due to obesity makes ventilation difficult by increasing abdominal pressure. Weight loss can improve the severity of OSA by reducing abdominal pressure and improving thoracic exercise and ventilation. Some studies have reported that weight loss contributes to the normalization of neuromechanical control of the upper airway during sleep by reducing fat-induced inflammation-related cytokines, and resolving hormone control disorders caused by obesity [19,20].

When studies on the effects of weight-loss in patients with OSA were examined (Table 2), moderate-intensity aerobic exercise was performed 3–4 times a week for about 30 to 45 minutes for 3 months in many cases [21–25]. In a study of three-month aerobic exercise in patients with mild-to-moderate OSA, there was no reduction in body weight, but AHI decreased by about 28% (from 15.19 to 11.01 events/h) [23]. In a study of aerobic exercise for 3 months in patients with chronic heart failure, there was no weight loss but AHI decreased by 34% (from 25.2 to 16.7 events/h), and the sleep efficiency increased by 7% (from 74.4 to 79.6%) [22]. And in a study of 4-week exercise in patients with moderate-to-severe OSA and coronary artery disease, AHI decreased by 34% (from 31.1 to 20.5 events/h), overnight change in leg fluid volume decreased by 20% (from −579.0 to −465.8 mL), and overnight change in upper airway cross-sectional area increased from −0.2 cm² to +0.09 cm² [21].

Although exercise is one method of reducing body weight among life style-related treatment methods, meta-analysis of studies on the effects of aerobic exercise on OSA showed that the effects of exercise were not limited to weight loss [26,27]. In the meta-studies, there was no significant weight loss due to exercise, but AHI in patients with OSA decreased, and sleep efficiency and daytime sleepiness were improved. This means that exercise itself has a therapeutic role in OSA treatment. In dog studies, stimulation of the gastrocnemius muscle and sciatic nerve increased the activity of the genioglossus muscle [28]. In human studies, results have shown that exercise was associated with increased respiratory muscle strength [26,29]. Exercise has also been reported to reduce the fluid retention in the legs, thereby preventing rostral fluid shift to the upper body at night, where it can cause collapse of the upper airway during sleep [21,30]. The effect of exercise on OSA appears to be due to the interaction of these multiple mechanisms, rather than the effect of only one of these mechanisms.

Table 3 shows that the risk of OSA was about 1.36 to 1.56 times higher for persons who consumed alcohol than for those who did not [31–34]. In a study of 20 healthy men who consumed an excess of 1 g of alcohol per body weight, alcohol intake increased the frequency of apnea from 20 to 110 times over the entire night’s sleep, while desaturation events increased from 118 to 226 times [35]. In a study in which 0.5 g of alcohol was consumed per body weight in patients with mild-to-moderate OSA, there was no increase in the length of the apnea or aggravation of hypoxia, but the AHI increased by 37% (from 7.1 to 9.7 events/h) [36]. In a meta-analysis of studies dealing with the association between alcohol and OSA, the risk of having OSA increased by about 25% from alcohol consumption [37].

The mechanism by which alcohol induces OSA is through lowering genioglossus and hypoglossal motor nerve activities [38,39], decreased sleep arousal [35], increased nasal mucosal swelling, and increased nasal resistance [39]. In addition, alcohol is known to cause segmented sleep regardless of sleep apnea [40], and this increase in segmented sleeping by alcohol exacerbates OSA.

Some studies have reported that smoking increased the risk of OSA, but other studies have reported that smoking did not increase, or even decreased the risk (Table 4) [41–44]. However, in the Wisconsin sleep cohort study, one of the largest cohort studies of OSA in the United States, smokers were twice as likely to have OSA compared to non-smokers. The amount of smoking and the prevalence of apnea were positively correlated, and those who smoked more than 2 packs per day had a 6.7-fold risk of having mild OSA and a 40-fold risk of having moderate-to-severe OSA [44].

The mechanisms by which smoking may exacerbate OSA include changes in sleep architecture, relaxation of the upper airway muscles and decreased nerve response by nicotine, increased sleep arousal, and increased mucosal inflammation due to smoke aspiration [45]. In a study comparing the uvular mucosa of smokers and non-smokers with OSA who received uvulopalatopharyngoplasty, secretion of calcitonin gene-related peptide (inflammatory mediator) in smoker’s mucosa, lamina propria edema, and mucosal thickness were increased, and this mechanism caused smoking to narrow the area of the upper airway and exacerbate OSA [46].

Previous research has found that weight loss and exercise decreased the severity of OSA, and that alcohol and smoking increased the risk of OSA. Based on these findings, lifestyle modifications of weight loss, aerobic exercise, alcohol abstinence and smoking cessation are effective treatments for OSA (Fig. 1). However, lifestyle modification usually requires frequent individual counseling sessions to increase patient compliance, which is time consuming and costly. Despite the importance of lifestyle modification, in reality, patients with OSA are only counseled or encouraged to make lifestyle changes, and successful lifestyle modification cannot be achieved in this way.

Various research has been carried out to solve this problem, and developments in mobile technology have led to the creation of a user-oriented smartphone or wearable device app related to activity tracking [47,48]. Using these apps, each individual can easily record and confirm information about his or her dietary intake, physical activity, and sleep. Furthermore, by linking the hospital’s electronic medical record (EMR) with the smartphone app, a system is created that can summarize and present the patient’s lifestyle information, such as dietary intake, physical activity, sleep, and stress on the physician’s EMR screen [49]. That data is the life log data, which is the sum of the patient’s lifestyle information and the hospital’s clinical data, easily and conveniently constructed using the smart device and used in the medical environment.

With this system, doctors can check items such as dietary intake and physical activity during treatment through the lifestyle summary, and encourage additional lifestyle improvements based on the patient’s actual life data in the clinic. Enabling patients to schedule and coordinate activities and set diet goals for the next hospital visit can motivate the patients to evaluate his or her lifestyle data with their doctor using the hospital EMR, and is much more effective than examining it alone on their smartphone. That is, with the use of EMR-linked smartphone apps, it is now possible to boost the effectiveness of lifestyle modification [50]. In a lifestyle modification study of patients with OSA using the above system for 4 weeks, BMI was significantly lower in the experimental group that used an EMR-linked smartphone app than in the control group, and a significant improvement was shown in the lowest oxygen saturation levels and percentage of sleep time snoring at > 45 dB [50].

In the treatment of OSA, physicians are aware of the need for lifestyle modifications, but often fail to recommend them for patients using CPAP, intraoral devices, and surgery due to constraints of treatment time. Additionally, the medical staff may overlook or underestimate the effectiveness of lifestyle modification on OSA. However, considering the treatment effect that can be obtained through weight loss and exercise and the adverse effects of smoking and alcohol on OSA, lifestyle modification is the most basic and necessary treatment in the entire treatment course of OSA. As such, possible benefits of the lifestyle modification should be explained to the patients. In addition, efforts should be made to improve lifestyle using smart devices that are easily accessible to patients in real life, and the results of which can be discussed together with doctors in a treatment environment. The use of smart devices represents an improvement over the traditional method based on private counseling, which is time consuming and costly both to patients and medical staff.