Medically reviewed by
Dacelin St Martin, MD
Triple board-certified in Sleep Medicine,
Internal Medicine, and Pediatrics.
What is OSA? | Epidemiology | Risk Factors | Symptoms | Obesity & OSA | Diagnosis | Treatment
Overview
Obstructive sleep apnea (OSA) is a common health concern for millions of Americans. Recent studies reveal a strong link between OSA and obesity, with both acting as a cause and effect.
Obesity can contribute to the risk of OSA and exacerbate symptoms. At the same time, OSA can also lead to further weight gain and increase the risk of diseases linked to obesity.
There is a need to create awareness about how obesity and OSA are interlinked so that people can adopt healthy measures to mitigate the adverse health effects of these conditions.
Read on to know how OSA can increase your risk of obesity and vice versa.
What is OSA?
Obstructive Sleep Apnea (OSA) is a sleep disorder characterized by disturbed sleep patterns due to frequent breathing interruptions.[1]
OSA may prevent you from getting restorative sleep, increasing your risk for specific disorders. One of the most common complications of OSA is obesity.[2]
Let us have a look at how OSA affects your overall health by causing weight gain. We will also have a look at the epidemiology, risk factors, and symptoms of OSA.
Epidemiology
- OSA is more common in men above 60 years of age[3]
- Approximately 15-30% of men and 10 to 15% of North American women suffer from OSA, which is characterized by an apnea-hypopnea index of more than five events during each hour of sleep[4] [5]
Risk Factors
- Gender: OSA tends to affect men more commonly than women. The incidence of OSA rises in women after menopause[6]
- Obesity: Excessive deposition of fat around the throat and air passages can obstruct the flow of air, resulting in interrupted breathing in patients with OSA
- Genetics: The risk of OSA is higher in those having first-degree relatives diagnosed with this condition
- Larger Neck Size: A neck circumference of more than 16″ in women and 17″ in men
- Airway Obstruction due to the enlargement of the tonsils or adenoids
- Unhealthy Lifestyle Habits, such as smoking, alcohol consumption, and an unhealthy diet
Symptoms
- Frequent awakening at night with pauses in breathing
- Loud snoring
- Daytime drowsiness
- Reduced concentration or alertness during daytime
- Irritability and anger due to the lack of sleep
- Forgetfulness
- Reduced daytime productivity
- Poor academic and job performance
- Increased risk of accidents or injuries due to reduced alertness
Obesity & OSA
Excess body weight can contribute to the development of OSA by increasing the pressure on the upper airways.
The deposition of fatty tissues in the throat can cause the walls of the air passage to push inward. Due to this, the lumen of your throat, larynx, and bronchi through which the air passes while breathing becomes narrow, preventing or hindering airflow through them. These changes can significantly contribute to the development of OSA in obese patients.
Additionally, fatty deposits in the air passages may reduce the neuromuscular control in this part of your respiratory tract. These fatty deposits may also decrease lung volume making it more difficult for you to breathe.[7] [8]
These factors, when combined, can prevent you from breathing well in the lying down position, causing frequent awakening at night. The larger neck and waist circumference and skewed waist-to-hip ratio due to obesity can add to your risk of developing OSA.[9]
1) Hormonal Imbalances
Several metabolic alterations dependent on obesity are associated with OSA, including glucose intolerance and insulin resistance.
Patients with OSA are likely to have a higher risk of developing diabetes due to the imbalances in the secretion of a hormone called insulin. The reduced insulin levels can prevent the efficient metabolism of sugars in the blood, due to which the excess sugars being converted into fats, causing weight gain.
Also, disrupted sleep may worsen insulin resistance and glucose intolerance, leading carbohydrate metabolism to be hampered. This physiological response can prevent the body’s rapid utilization of calories, causing the excess energy to be converted into fats. The fat gain caused due to these metabolic changes can increase obesity and worsen your symptoms of OSA.[10]
2) Appetite and Cravings
Frequent awakening due to OSA can disrupt the production of 2 hormones that regulate hunger and cravings: leptin and ghrelin. The changes in these hormones’ levels would increase your appetite while reducing your ability to feel full after eating meals.[11] [12] As a result, these hormones can lead to you eat more, causing you to pack on the pounds.
3) Mental Stress
Lack of sleep is known to affect a person’s mental health and increase the risk of depression.
Poor emotional health might increase the secretion of a stress hormone in the brain called cortisol. This hormone, in turn, can slow down the body’s metabolic rate and reduce calorie burning. This reaction can prevent you from losing weight despite making efforts, like restricting your diet and exercising.[13]
This physiological response is how increased cortisol levels in patients with OSA can exacerbate obesity.
4) Change in Eating Habits
You can be more prone to eating junk food when you are not able to sleep well.
Reports from loved ones concerning pauses in breathing may lead to a psychological fear of sleep, disrupting sleep further. You may lay awake for long hours at night, binging on junk food just to beat boredom or to fill the late-night void.[14]
Eating junk food high in sugar and fat can create a surge in energy or cause indigestion, making relaxation difficult. These changes in the body’s functioning brought about by OSA explain how this condition can increase obesity.
How to Diagnose OSA?
OSA’s most notable symptoms include frequent awakenings at night, daytime drowsiness, and snoring; however, further physical examination and tests can help confirm a diagnosis.
During the physical check-up, the doctor will examine the mouth, back of the throat, nose for swelling, enlargement of tissues, or other abnormalities. The doctor might measure the waist and neck circumference and check blood pressure to ascertain OSA’s possible causes.
Diagnostic Tools
1. Polysomnography (sleep study at a sleep center)
2. Home sleep studies through MHSleeptesting.com
An AHI: Apnea hypopnea index of at least 5 in either polysomnography or home sleep study is required to be classified as OSA.
The Severity of Sleep Apnea Based on AHI:
1. AHI of 0-5: No Sleep Apnea
2. AHI: 5-15: Mild OSA
3. AHI: 15-30: Moderate OSA
4. AHI: >30 Severe OSA
Treatment
OSA can be managed in one of these 3 ways:
1) CPAP
Short for continuous positive airway pressure, this is considered the gold standard for all levels of severity. The CPAP machine consists of a mask that patients wear over the nose or mouth while sleeping. The machine then pumps oxygen into the airways through the mask, thus improving oxygen flow. It allows the airways to remain open while sleeping and reduces the incidences of awakening.
2) Oral Appliances
Oral Appliances or mandibular advancement devices, shaped like a mouth guard, can also be used to treat OSA. This device keeps the airways open while you are sleeping.
3) Surgery
Surgery is necessary for severe OSA cases that cannot be treated with CPAP or oral appliances, like:
- Upper pharyngeal procedures like UPP (uvulopalatopharyngoplasty), adenoidectomy, or tonsillectomy
- Nasal procedures like septoplasty, nasal valve surgery, or rhinoplasty
- Tracheostomy Maxillomandibular advancement surgery
- Lower pharyngeal procedures, like hyoid and tongue suspension, mandibular advancement, or genioglossus advancement
- Upper airway stimulation through the placement of a medical device from a company called Inspire. You simply turn on the device with the click of a button, and it helps your airways remain open, thereby preventing obstruction in the airflow.
- Upper airway stimulation through the placement of a medical device from a company called Inspire. You simply turn on the device with the click of a button, and it helps your airways remain open, thereby preventing obstruction in the airflow
Conclusion
Obesity is one of the common risk factors of OSA. If not appropriately managed, the pathophysiological and metabolic changes occurring in the body due to OSA may contribute to further weight gain.
This physiological response can create a vicious cycle with obesity causing OSA, and OSA, in turn, causing obesity. You can release yourself from this trap by talking to your doctor.
A comprehensive plan to manage both OSA and obesity is vital to avoid the health effects of these two conditions.
References:
- Arnold, J., Sunilkumar, M., Krishna, V., Yoganand, S. P., Kumar, M. S., & Shanmugapriyan, D. (2017). Obstructive Sleep Apnea. Journal of pharmacy & bioallied sciences, 9(Suppl 1), S26–S28. https://doi.org/10.4103/jpbs.JPBS_155_17
- Patil, S. P., Schneider, H., Schwartz, A. R., & Smith, P. L. (2007). Adult obstructive sleep apnea: pathophysiology and diagnosis. Chest, 132(1), 325–337. https://doi.org/10.1378/chest.07-0040
- Young, T., Palta, M., Dempsey, J., Skatrud, J., Weber, S., & Badr, S. (1993). The occurrence of sleep-disordered breathing among middle-aged adults. The New England journal of medicine, 328(17), 1230–1235. https://doi.org/10.1056/NEJM199304293281704
- Young, T., Palta, M., Dempsey, J., Peppard, P. E., Nieto, F. J., & Hla, K. M. (2009). Burden of sleep apnea: rationale, design, and major findings of the Wisconsin Sleep Cohort study. WMJ : official publication of the State Medical Society of Wisconsin, 108(5), 246–249.
- Peppard, P. E., Young, T., Barnet, J. H., Palta, M., Hagen, E. W., & Hla, K. M. (2013). Increased prevalence of sleep-disordered breathing in adults. American journal of epidemiology, 177(9), 1006–1014. https://doi.org/10.1093/aje/kws342
- Bixler, E. O., Vgontzas, A. N., Lin, H. M., Ten Have, T., Rein, J., Vela-Bueno, A., & Kales, A. (2001). Prevalence of sleep-disordered breathing in women: effects of gender. American journal of respiratory and critical care medicine, 163(3 Pt 1), 608–613. https://doi.org/10.1164/ajrccm.163.3.9911064
- Peppard, P. E., Young, T., Barnet, J. H., Palta, M., Hagen, E. W., & Hla, K. M. (2013). Increased prevalence of sleep-disordered breathing in adults. American journal of epidemiology, 177(9), 1006–1014. https://doi.org/10.1093/aje/kws342
- Young T, Skatrud J, Peppard PE. Risk Factors for Obstructive Sleep Apnea in Adults. 2004;291(16):2013–2016. doi:10.1001/jama.291.16.2013
- Peppard, P. E., Young, T., Palta, M., Dempsey, J., & Skatrud, J. (2000). Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA, 284(23), 3015–3021. https://doi.org/10.1001/jama.284.23.3015
- Romero-Corral, A., Caples, S. M., Lopez-Jimenez, F., & Somers, V. K. (2010). Interactions between obesity and obstructive sleep apnea: implications for treatment. Chest, 137(3), 711–719. https://doi.org/10.1378/chest.09-0360
- Harsch, I. A., Konturek, P. C., Koebnick, C., Kuehnlein, P. P., Fuchs, F. S., Pour Schahin, S., Wiest, G. H., Hahn, E. G., Lohmann, T., & Ficker, J. H. (2003). Leptin and ghrelin levels in patients with obstructive sleep apnoea: effect of CPAP treatment. The European respiratory journal, 22(2), 251–257. https://doi.org/10.1183/09031936.03.00010103
- Ulukavak Ciftci, T., Kokturk, O., Bukan, N., & Bilgihan, A. (2005). Leptin and ghrelin levels in patients with obstructive sleep apnea syndrome. Respiration; international review of thoracic diseases, 72(4), 395–401. https://doi.org/10.1159/000086254
- Trakada, G., Chrousos, G., Pejovic, S., & Vgontzas, A. (2007). Sleep Apnea and its association with the Stress System, Inflammation, Insulin Resistance and Visceral Obesity. Sleep medicine clinics, 2(2), 251–261. https://doi.org/10.1016/j.jsmc.2007.04.003
- Olbrich, K., Mühlhans, B., Allison, K. C., Hahn, E. G., Schahin, S. P., & de Zwaan, M. (2009). Night eating, binge eating and related features in patients with obstructive sleep apnea syndrome. European eating disorders review : the journal of the Eating Disorders Association, 17(2), 120–127. https://doi.org/10.1002/erv.908