ABSTRACT
Purpose: Adolescent obesity continues to rise, with body mass index (BMI) commonly used as an adiposity surrogate. While obesity correlates with metabolic syndrome risk, individuals with the same BMI do not have equivalent health risks. In 2018, the first pediatric consensus definition for metabolically healthy obesity (MHO) was proposed. Identifying MHO patients is clinically relevant for personalizing interventions by cardiometabolic phenotype. The objective of this study was to examine baseline MHO and metabolically unhealthy obesity (MUO) prevalence and identify metabolic and anthropomorphic predictors among adolescents enrolled in weight management. Methods: This study uses baseline data from 1,316 patients ≥ 11 years of age enrolled in a weight management program for obese adolescents in Baltimore, Maryland between 2005-2018. Anthropometric measures (including body fat by bioimpedance (%fat)), vital signs, and fasting labs were performed at intake. MHO definition was: glucose <100, HDL > 40, triglycerides < 150, systolic blood pressure < 120, diastolic blood pressure < 80. MUO was defined as ≥ 1 abnormal value among MHO variables. Independent samples t-tests were used to compare mean %fat and BMI z-score of MHO and MUO groups. Bivariate logistic regression was performed to determine effects of age, sex, %fat, BMI, and BMI z-score on likelihood of MHO. Results: Mean age in the MHO group was 13.48 years (SD 1.88);mean age in the MUO group was 13.98 years (SD 2.03). 444 (33.7%) patients met criteria for MHO;872 patients had MUO. MHO teens had statistically significantly lower mean %fat (46.7% +/- 8.0% SD) vs. MUO (47.8% +/- 8.2% SD) (p = 0.034) and lower BMI z-score (2.37 +/- 0.33 SD vs 2.51 +/- 0.34 SD;p < 0.001) vs MUO. The MHO group was 66.9% female vs 54.5% females in MUO, with 38.9% lower odds of MHO for males vs. females (OR 0.611;CI 0.467 - 0.800). For every 1% increase in %fat, odds of MHO increased by 3.1%, (OR 1.031;CI 1.008 - 1.053). Each 1-year age increase led to 10.9% decrease in MHO odds (OR 0.891;CI 0.823 - 0.965). In addition, each 1 unit increase in BMI z-score was associated with a 64.5% decrease in odds of MHO (OR 0.355;CI 0.166 - 0.759). BMI change did not significantly change MHO odds. Conclusions: Among this cohort of obese adolescents enrolled in weight management, one-third had MHO. Factors associated with higher likelihood of MHO include: female sex, younger age, and lower BMI z-score. Notably, BMI was not predictive of metabolic phenotype. These findings suggest potential for risk prediction for MUO profile to tailor interventions and resources accordingly. Next, we will evaluate metabolic profiles of patients enrolled during the COVID-19 pandemic. Sources of Support: NICHD T32HD052459 (PI: Trent), The Mount Washington Foundation.
ABSTRACT
BACKGROUND: Nasal High Flow (NHF) therapy delivers flows of heated humidified gases up to 60 LPM (litres per minute) via a nasal cannula. Particles of oral/nasal fluid released by patients undergoing NHF therapy may pose a cross-infection risk, which is a potential concern for treating COVID-19 patients. METHODS: Liquid particles within the exhaled breath of healthy participants were measured with two protocols: (1) high speed camera imaging and counting exhaled particles under high magnification (6 participants) and (2) measuring the deposition of a chemical marker (riboflavin-5-monophosphate) at a distance of 100 and 500 mm on filter papers through which air was drawn (10 participants). The filter papers were assayed with HPLC. Breathing conditions tested included quiet (resting) breathing and vigorous breathing (which here means nasal snorting, voluntary coughing and voluntary sneezing). Unsupported (natural) breathing and NHF at 30 and 60 LPM were compared. RESULTS: Imaging: During quiet breathing, no particles were recorded with unsupported breathing or 30 LPM NHF (detection limit for single particles 33 µm). Particles were detected from 2 of 6 participants at 60 LPM quiet breathing at approximately 10% of the rate caused by unsupported vigorous breathing. Unsupported vigorous breathing released the greatest numbers of particles. Vigorous breathing with NHF at 60 LPM, released half the number of particles compared to vigorous breathing without NHF.Chemical marker tests: No oral/nasal fluid was detected in quiet breathing without NHF (detection limit 0.28 µL/m3). In quiet breathing with NHF at 60 LPM, small quantities were detected in 4 out of 29 quiet breathing tests, not exceeding 17 µL/m3. Vigorous breathing released 200-1000 times more fluid than the quiet breathing with NHF. The quantities detected in vigorous breathing were similar whether using NHF or not. CONCLUSION: During quiet breathing, 60 LPM NHF therapy may cause oral/nasal fluid to be released as particles, at levels of tens of µL per cubic metre of air. Vigorous breathing (snort, cough or sneeze) releases 200 to 1000 times more oral/nasal fluid than quiet breathing (p < 0.001 with both imaging and chemical marker methods). During vigorous breathing, 60 LPM NHF therapy caused no statistically significant difference in the quantity of oral/nasal fluid released compared to unsupported breathing. NHF use does not increase the risk of dispersing infectious aerosols above the risk of unsupported vigorous breathing. Standard infection prevention and control measures should apply when dealing with a patient who has an acute respiratory infection, independent of which, if any, respiratory support is being used. CLINICAL TRIAL REGISTRATION: ACTRN12614000924651.