Losing weight is an effective treatment for Obstructive Sleep Apnea (OSA), but why exactly this is the case has remained unclear.
Now, researchers in the Perelman School of Medicine at the University of Pennsylvania have discovered that improvements in sleep apnea symptoms appear to be linked to the reduction of fat in one unexpected body part — the tongue..
Using magnetic resonance imaging (MRI) to measure the effect of weight loss on the upper airway in obese patients, researchers found that reducing tongue fat is a primary factor in lessening the severity of OSA.
The findings were published today in the American Journal of Respiratory and Critical Care Medicine.
“Most clinicians, and even experts in the sleep apnea world, have not typically focused on fat in the tongue for treating sleep apnea,” said Richard Schwab, MD, chief of Sleep Medicine.
“Now that we know tongue fat is a risk factor and that sleep apnea improves when tongue fat is reduced, we have established a unique therapeutic target that we’ve never had before.”
Twenty-two million Americans suffer from sleep apnea, a serious health condition in which breathing repeatedly stops and starts, causing patients to wake up randomly throughout their sleep cycles.
The condition, which is usually marked by loud snoring, can increase your risk for high blood pressure and stroke.
While obesity is the primary risk factor for developing sleep apnea, there are other causes, such as having large tonsils or a recessed jaw. CPAP (continuous positive airway pressure) machines improves sleep apnea in about 75 percent of patients, studies suggest, but for the other 25 percent — those who may have trouble tolerating the machine — alternative treatment options, such as oral appliances or upper airway surgery, are more complicated.
A 2014 study led by Schwab compared obese patients with and without sleep apnea, and found that the participants with the condition had significantly larger tongues and a higher percentage of tongue fat when compared to those without sleep apnea.
The researchers next step was to determine if reducing tongue fat would improve symptoms and to further examine cause and effect.
The new study included 67 participants with mild to severe obstructive sleep apnea who were obese –those with a body mass index greater than 30.0.
Through diet or weight loss surgery, the patients lost nearly 10 percent of their body weight, on average, over six months.
Overall, the participants’ sleep apnea scores improved by 31 percent after the weight loss intervention, as measured by a sleep study.
Before and after the weight loss intervention, the study participants underwent MRI scans to both their pharynx as well as their abdomens. Then, using a statistical analysis, the research team quantified changes between overall weight loss and reductions to the volumes of the upper airway structures to determine which structures led to the improvement in sleep apnea.
The team found that a reduction in tongue fat volume was the primary link between weight loss and sleep apnea improvement.
The study also found that weight loss resulted in reduced pterygoid (a jaw muscle that controls chewing) and pharyngeal lateral wall (muscles on the sides of the airway) volumes. Both these changes also improved sleep apnea, but not to the same extent as the reduction in tongue fat.
The authors believe that tongue fat is a potential new therapeutic target for improving sleep apnea.
They suggest that future studies could be designed to explore whether certain low-fat diets are better than others in reducing tongue fat and whether cold therapies — like those used to reduce stomach fat — might be applied to reducing tongue fat.
However, Schwab notes, these types of interventions have not yet been tested.
Schwab’s team is also examining new interventions and other risk factors for sleep apnea, including whether some patients who are not obese but who have “fatty” tongues could be predisposed to sleep apnea, but are less likely to be diagnosed.
The team found that a reduction in tongue fat volume was the primary link between weight loss and sleep apnea improvement
In a recent related study, Schwab found that ethnicity may also play a role in sleep apnea severity. His research team compared the upper airway anatomy of Chinese and Icelandic patients with sleep apnea, and found that, compared to Icelandic patients of similar age, gender, and symptoms, Chinese patients had smaller airways and soft tissues, but bigger soft palate volume with more bone restrictions.
This means that Asian patients may generally be more at risk for severe sleep apnea symptoms.
The bottom line, according to Schwab, is that all patients who suffer from snoring or sleepiness should be screened for sleep apnea, whether or not they appear to fall into the typical “high-risk” obese categories.
“Primary care doctors, and perhaps even dentists, should be asking about snoring and sleepiness in all patients, even those who have a normal body mass index, as, based on our data, they may also be at risk for sleep apnea,” Schwab said.
Funding: This study was supported by grants from the National Institutes of Health. Additional Penn authors include Stephen H. Wang, Brendan T. Keenan, Andrew Wiemken, Yinyin Zang, Bethany Staley, David B. Sarwer, Drew A Torigian, Noel Williams, and Allan I. Pack.
The third edition of the International Classification of Sleep Disorders (ICSD-3) defines OSAS as a polysomnography (PSG)-determined obstructive respiratory disturbance index (RDI) ≥ 5 events/h associated with the typical symptoms of OSAS (e.g., unrefreshing sleep, daytime sleepiness, fatigue or insomnia, awakening with a gasping or choking sensation, loud snoring, or witnessed apneas), or an obstructive RDI ≥ 15 events/h (even in the absence of symptoms) .
In addition to the apneas and hypopneas that are included in the Apnea-Hypopnea Index (AHI), the RDI includes respiratory effort-related arousals (RERAs). The scoring of respiratory events is defined in the AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, Version 2.3 (AASM Scoring Manual) . However, some variability in the definition of a hypopnea event should be noted.
According to the AASM Scoring Manual recommended definition, changes in flow should be associated with a 3% oxygen desaturation or a cortical arousal, although an alternative definition that requires association with a 4% oxygen desaturation without consideration of cortical arousals is accepted.
Depending on which definition is used, the AHI may be considerably different in any given individual [5,6,7]. The discrepancy between these and other hypopnea definitions used in research studies makes the evaluation of evidence regarding the diagnosis of OSAS a complex matter.
The apnea-hypopnea index (AHI) is the average number of disordered breathing events per hour. Typically, the OSA syndrome is defined as an AHI of 5 or greater. An AHI of 5–15 is considered as mild, 15–30 is moderate and more than 30 events per hour characterizes severe sleep apnea.
The precise incidence of OSAS in adults is still unknown. It is estimated that 24 percent of men and 9 percent of women have the breathing symptoms of OSAS with or without daytime sleepiness, but about 80 percent of adults with OSAS remain undiagnosed .
On the other hand, respiratory sleep disorders (RSD) in children are characterized by a variable obstruction of the upper airway and different degrees of alteration in gas exchange during the night.
The clinical presentation goes from habitual snoring to complete obstruction of the airway [9,10]. The European Respiratory Society (ERS) taskforce for the diagnosis and management of obstructive RSD in childhood defines OSAS as “a syndrome of upper airway dysfunction during sleep, characterized by snoring and/or increased respiratory effort secondary to increased upper airway resistance and pharyngeal collapsibility” .
In childhood OSAS there is not a clear correlation between the severity of the clinical presentation and daytime symptoms, with a more nuanced range of symptoms .
Gozal et al.  proposed several criteria, classified into major and minor, for the diagnosis of OSAS in children and, above all, to assess the need for treatment. The major ones include an AHI > 2, RDI > 2, Nadir SpO2 < 90%, excessive daytime sleepiness, academic difficulties, hyperactive behavior, hypertension, enuresis, and obesity.
Among the minor ones, there are high levels of CRP, LDL, fasting insulin and low levels of HDL, recurrent middle ear otitis and adenotonsillar grade >1. The positivity of five major criteria, or three major criteria plus 3 minor criteria, indicates the need for therapeutic procedures.
According to latest guidelines, the general incidence of OSAS in the pediatric population is about 2% . Most children are around 2–8 years of age, due to the relative size of the lymphatic tissue of the upper airways . OSAS is more common in males than females. African Americans and obese children are both at increased risk for OSAS .
While many studies have addressed the etiopathogenesis of adult OSAS, many aspects of this syndrome in children remain unclear. However, there are many risk factors which can lead to a reduction or collapse of the upper airways and which may contribute to the pathogenesis of OSAS.
The diagnosis of pediatric OSAS include a detailed clinical history, focusing on physical findings, especially in the ENT district, nocturnal and diurnal symptoms and comorbidities followed by specific questionnaires administered to parents. Nocturnal oximetry and ambulatory polysomnography are mandatory. In patients with residual OSAS after surgery, DISE should be considered to detect the anatomical site of potential collapse.
To our knowledge, few papers have been published on the risk factors linked to OSAS, especially in the pediatric age [9,16]. We were able to find out 182 articles from 2012 to 2019 on Pubmed and MEDLINE using the keywords “Risk factors; Pediatric OSAS; Obesity; Adenotonsillar hypertrophy; Craniofacial abnormalities; Allergic rhinitis; Inflammation”. Only 123 articles discussed this specific topic in children.
Furthermore, it should be noted that the majority of the papers analyzed only one single risk factor and rarely multiple factors, focusing essentially on the overview of the OSAS. The very exhaustive papers published by Marcus C.L. et al.  and Li Z. et al.  are typical examples of this observation. They made a general, wonderful presentation of the pathology, but dedicated just a few paragraphs in evaluating the various risk factors.
Thus, the aim of this paper is devoted to analyzing the state of the art on this specific and its impact on diagnosis and treatment.