BackgroundCompelling 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.ObjectiveWe sought to assess the association between FH of OSA and risk of obesity.MethodsThe 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).ResultsFH 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.ConclusionFamily 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 InformationResearch 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.
Background Dietary habits are critical determinants of health and especially of cardiometabolic risk status. Previous studies have examined the relationship between breakfast consumption and indices of obesity, with conflicting findings. Such discrepancy may be owed to the use of surrogate measures of adiposity such as body mass index. Furthermore, it is unknown whether frequency of breakfast consumption is associated with different patterns of regional body fat distribution. Objective In this study, we aimed at investigating the association between frequency of breakfast consumption and body fat distribution. Methods We compiled data from 184 individuals (64% males, mean age 35.8±12.6 years, ranging from 18 to 63 years old) who participated in research studies performed in the Mayo Clinic Cardiovascular/Sleep Laboratory from 2005 to 2019 and underwent whole body dual‐energy X‐ray absorptiometry (DXA) for body composition. Breakfast eating habits were assessed by questionnaire and frequency of consumption was determined as number of times per week (range 0 to 7). Responses were recoded as low frequency (0 to 2 times/week), middle frequency (3 to 4 times/week), and high frequency (5 to 7 times/week). Measures of height and weight were collected to compute body mass index (BMI, kg/m2). Total body fat percentage, fat mass, and lean mass were obtained from DXA. Regions of interest were manually adjusted with the DXA software to quantify abdominal fat and lower body fat. Abdominal fat/total body fat and lower body fat/total body fat ratios were calculated. Results Low frequency of breakfast consumption was reported by 14% of the subjects (n=26), while 18% (n=34) reported middle‐frequency of consumption. The proportion of men/women (p=0.1) and BMI values (p=0.78) were similar across breakfast eating categories. Compared to those who had breakfast with high‐frequency, those who ate it less frequently were younger (p=0.038). In age, sex, and BMI‐adjusted analysis, low‐frequency of breakfast consumption was significantly associated with greater abdominal fat mass (standardized beta=0.11, 95% CI 0.09‐ 1.29, p=0.024) and higher abdominal fat/total body fat ratio (standardized beta=0.16, 95% CI 0.003–0.024, p=0.013). Total body fat percentage (p=0.26), fat mass (p=0.26), and lean mass (p=0.22) were not associated with frequency of breakfast consumption. Similarly, no relations were seen with lower body fat (p=0.85) or lower body fat/total body fat ratio (p=0.51). Conclusion Our study showed that infrequent breakfast consumption is selectively associated with greater abdominal fat mass. As accumulation of fat in the abdominal depot is a more robust predictor of adverse outcomes than total adiposity, these findings suggest that abdominal fat may mediate the increased cardiometabolic risk previously observed in conjunction with infrequent breakfast consumption.
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