Family History of Obstructive Sleep Apnea and Risk of Obesity
Authors: Rajendran Aiswarya , Danyluk Alexandria B , Smith Kevin L. , Boeve Angelica R. , Bukartyk Jan , Singh Prachi R. , Somers Virend K. , Covassin Naima K 
Published: June 2021

Background

Compelling evidence links obstructive sleep apnea (OSA), a prevalent sleep disorder, to heightened morbidity and mortality. Individuals with family history (FH) of OSA exhibit increased risk of developing this sleep disorder, suggesting that genetics, in addition to demographic and lifestyle factors, are likely implicated in the pathogenesis of OSA. However, it is unclear whether a positive FH of OSA predisposes to other unfavorable health outcomes. In this regard, data on its impact on vulnerability to obesity, both a precursor and a consequence of OSA, are lacking.

Objective

We sought to assess the association between FH of OSA and risk of obesity.

Methods

The study population consisted of 612 individuals (66% male, age 48.1±17.3 years) who took part in research studies performed in the Cardiovascular/Sleep Laboratory at Mayo Clinic and had complete family history data. FH of OSA and obesity were determined from questionnaires. Demographics and medical comorbidities including OSA diagnosis were obtained from self‐reports. Body mass index (BMI, kg/m2) was calculated from height and weight measures and used to determine obesity status as follows: normal weight (BMI <25 kg/m2), overweight (BMI 25–29.9 kg/m2), and obese (BMI ≥30 kg/m2). Measurements of waist circumference were obtained to determine central obesity (defined as waist circumference ≥88 cm in women and ≥102 cm in men).

Results

FH of OSA was reported by twelve percent of the sample (n=72). Individuals with FH of OSA were younger and more likely to be female than those without (age: 40.8±12.6 years vs 49.1±17.6 years, P<0.0001; sex: 48.6% vs 32.2%, P=0.008). Those with positive FH had higher BMI (31.5±6.8 kg/m2 vs 29.2±7 kg/m2, P=0.009), were more frequently obese (59.7% vs 39.8%, P=0.007), and had higher prevalence of central obesity (67.7% vs 53.8%, P=0.036). Multivariable regression models showed the FH of OSA was associated with 3.2‐times greater risk of obesity (95% CI 1.7–5.9, P=0.0002) and with 2.3‐times greater risk of central obesity (95% CI 1.2–4.5, P=0.011) after correcting for age, sex, OSA diagnosis, and FH of obesity.

Conclusion

Family history of OSA is accompanied by an increased likelihood of obesity, especially central obesity, even if subjects with FH of OSA are much younger. This relationship is independent of conventional risk factors, including OSA diagnosis, suggesting that comorbid OSA in the offspring is unlikely to be implicated. Research addressing the potential pathophysiological mechanisms underlying our findings is warranted.

Support or Funding Information

Research support: VKS and PS are supported by NIH HL65176. NC is supported by American Heart Association grant 16SDG27250156, and Mayo Clinic CCaTS grant Marie Ingalls Cardiovascular Research Career Development Fund.

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.