Person:

Liu, Gang

Objectives: To estimate the prevalence of, and explore potential risk factors for, taste and smell dysfunction in the general population of the USA. Design: A cross-sectional study. Setting: A cross-sectional analysis of data collected in the National Health and Nutrition Examination Survey (NHANES 2013–2014). Participants: A total of 3519 men and women aged 40 years and older who participated in NHANES 2013–2014. Main outcome measures Using the NHANES Pocket Smell Test, smell impairment was defined as failing to correctly identify 6 or more of the 8 odours. Taste impairment was defined as failing to correctly identify quinine or sodium chloride. Results: The estimated prevalence was 13.5% for smell impairment, 17.3% for taste impairment and 2.2% for taste and smell impairment. For smell, but not taste, prevalence estimates increased with age and were higher in men and ethnic minorities. In backward stepwise logistic regression, low educational attainment, low family income and a history of asthma or cancer were independently associated with a higher prevalence of smell impairment, whereas light-to-moderate alcohol consumption (1–3 drinks/day) was associated with a lower prevalence of this condition. After multivariate adjustment, being non-Hispanic Black Americans, consuming ≥4 drinks of alcohol per day and having a history of cardiovascular disease (CVD) were independently associated with a higher prevalence of taste impairment. Conclusions: Based on a nationally representative multistage probability survey among the US population aged 40 years and older, smell and taste dysfunction affected ∼20.5 million (13.5%) and 26.3 million (17.3%) individuals, respectively. Age, gender, ethnicity, educational attainment, family income, light-to-moderate alcohol consumption and history of asthma or cancer were significant risk factors for smell dysfunction, whereas only ethnicity, heavy alcohol consumption and CVD history were associated with a higher prevalence of taste dysfunction.

Background: The potential endocrine-disrupting effects of perfluoroalkyl substances (PFASs) have been demonstrated in animal studies, but whether PFASs may interfere with body weight regulation in humans is largely unknown. This study aimed to examine the associations of PFAS exposure with changes in body weight and resting metabolic rate (RMR) in a diet-induced weight-loss setting. Methods and findings In the 2-year POUNDS Lost randomized clinical trial based in Boston, Massachusetts, and Baton Rouge, Louisiana, that examined the effects of energy-restricted diets on weight changes, baseline plasma concentrations of major PFASs were measured among 621 overweight and obese participants aged 30–70 years. Body weight was measured at baseline and 6, 12, 18, and 24 months. RMR and other metabolic parameters, including glucose, lipids, thyroid hormones, and leptin, were measured at baseline and 6 and 24 months. Participants lost an average of 6.4 kg of body weight during the first 6 months (weight-loss period) and subsequently regained an average of 2.7 kg of body weight during the period of 6–24 months (weight regain period). After multivariate adjustment, baseline PFAS concentrations were not significantly associated with concurrent body weight or weight loss during the first 6 months. In contrast, higher baseline levels of PFASs were significantly associated with a greater weight regain, primarily in women. In women, comparing the highest to the lowest tertiles of PFAS concentrations, the multivariate-adjusted mean weight regain (SE) was 4.0 (0.8) versus 2.1 (0.9) kg for perfluorooctanesulfonic acid (PFOS) (Ptrend = 0.01); 4.3 (0.9) versus 2.2 (0.8) kg for perfluorooctanoic acid (PFOA) (Ptrend = 0.007); 4.7 (0.9) versus 2.5 (0.9) kg for perfluorononanoic acid (PFNA) (Ptrend = 0.006); 4.9 (0.9) versus 2.7 (0.8) kg for perfluorohexanesulfonic acid (PFHxS) (Ptrend = 0.009); and 4.2 (0.8) versus 2.5 (0.9) kg for perfluorodecanoic acid (PFDA) (Ptrend = 0.03). When further adjusted for changes in body weight or thyroid hormones during the first 6 months, results remained similar. Moreover, higher baseline plasma PFAS concentrations, especially for PFOS and PFNA, were significantly associated with greater decline in RMR during the weight-loss period and less increase in RMR during the weight regain period in both men and women. Limitations of the study include the possibility of unmeasured or residual confounding by socioeconomic and psychosocial factors, as well as possible relapse to the usual diet prior to randomization, which could have been rich in foods contaminated by PFASs through food packaging and also dense in energy. Conclusions: In this diet-induced weight-loss trial, higher baseline plasma PFAS concentrations were associated with a greater weight regain, especially in women, possibly explained by a slower regression of RMR levels. These data illustrate a potential novel pathway through which PFASs interfere with human body weight regulation and metabolism. The possible impact of environmental chemicals on the obesity epidemic therefore deserves attention. Trial registration ClinicalTrials.gov NCT00072995