Neomi Shah

Neighborhood factors as predictors of poor sleep in the sueno ancillary study of the hispanic community health study/study of latinos

Study Objectives To evaluate whether an adverse neighborhood environment has higher prevalence of poor sleep in a US Hispanic/Latino population. Methods A cross-sectional analysis was performed in 2156 US Hispanic/Latino participants aged 18-64 years from the Sueño ancillary study of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Participants completed surveys of neighborhood environment including perceived safety, violence and noise, the Insomnia Severity Index (ISI), and 7 days of wrist actigraphy. Results In age and sex-adjusted analyses, short sleep, low sleep efficiency, and late sleep midpoint were all more prevalent among those living in an unsafe neighborhood. After adjustment for background, site, nativity, income, employment, depressive symptoms, and sleep apnea, the absolute risk of sleeping <6 hours was 7.7 (95% CI [0.9, 14.6]) percentage points greater in those living in an unsafe compared to a safe neighborhood. There were no differences in the prevalence of insomnia by level of safety or violence. Insomnia was more prevalent among those living in a noisy neighborhood. In adjusted analysis, the absolute risk of insomnia was 4.4 (95% CI [0.4, 8.4]) percentage points greater in those living in noisy compared to non-noisy neighborhoods. Conclusion Using validated measures of sleep duration and insomnia, we have demonstrated the existence of a higher prevalence of short sleep and insomnia by adverse neighborhood factors. An adverse neighborhood environment is an established risk factor for a variety of poor health outcomes. Our findings suggest negative effects on sleep may represent one pathway by which neighborhood environment influences health.

Obstructive sleep apnea and world trade center exposure

Objectives: To describe the proportion of at-risk World Trade Center (WTC)-exposed rescue/recovery workers with polysomnogram-confirmed obstructive sleep apnea (OSA) and examine the relationship between WTC exposure, physician-diagnosed gastroesophageal reflux disease (GERD), and rhinosinusitis and OSA. Methods: A total of 636 male participants completed polysomnography from September 24, 2010, to September 23, 2012. Obstructive sleep apnea was classified as mild, moderate, or severe. Associations were tested using nominal polytomous logistic regression. Results: Eighty-one percent of workers were diagnosed with OSA. Using logistic regression models, severe OSA was associated with WTC exposure on September 11, 2001 (odds ratio, 1.91; 95% confidence interval, 1.15 to 3.17), GERD (odds ratio, 2.75; 95% confidence interval, 1.33 to 5.70), and comorbid GERD/rhinosinusitis (odds ratio, 2.31; 95% confidence interval, 1.22 to 4.40). Conclusions: We found significant associations between severe OSA and WTC exposure, and with diseases prevalent in this population. Accordingly, we recommend clinical evaluation, including polysomnography, for patients with high WTC exposure, other OSA risk factors, and a physician diagnosis of GERD or comorbid GERD and rhinosinusitis.

Multiethnic meta-analysis identifies RAI1 as a possible obstructive sleep apnea-related quantitative trait locus in men

Abstract Obstructive sleep apnea (OSA) is a common heritable disorder displaying marked sexual dimorphism in disease prevalence and progression. Previous genetic association studies have identified a few genetic loci associated with OSA and related quantitative traits, but they have only focused on single ethnic groups, and a large proportion of the heritability remains unexplained. The apnea‐hypopnea index (AHI) is a commonly used quantitative measure characterizing OSA severity. Because OSA differs by sex, and the pathophysiology of obstructive events differ in rapid eye movement (REM) and non‐REM (NREM) sleep, we hypothesized that additional genetic association signals would be identified by analyzing the NREM/REM‐specific AHI and by conducting sex‐specific analyses in multiethnic samples. We performed genome‐wide association tests for up to 19,733 participants of African, Asian, European, and Hispanic/Latino American ancestry in 7 studies. We identified rs12936587 on chromosome 17 as a possible quantitative trait locus for NREM AHI in men (N = 6,737; P = 1.7 × 10‐8) but not in women (P = 0.77). The association with NREM AHI was replicated in a physiological research study (N = 67; P = 0.047). This locus overlapping the RAI1 gene and encompassing genes PEMT1, SREBF1, and RASD1 was previously reported to be associated with coronary artery disease, lipid metabolism, and implicated in Potocki‐Lupski syndrome and Smith‐Magenis syndrome, which are characterized by abnormal sleep phenotypes. We also identified gene‐by‐sex interactions in suggestive association regions, suggesting that genetic variants for AHI appear to vary by sex, consistent with the clinical observations of strong sexual dimorphism.

Sleep Apnea Is Associated with Hearing Impairment: The Hispanic Community Health Study/Study of Latinos.

STUDY OBJECTIVE Sleep apnea (SA) may promote hearing impairment (HI) through ischemia and inflammation of the cochlea. Our objective was to assess an independent association between SA and HI in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) participants. METHODS We used data from the HCHS/SOL, a multicenter population-based study of self- identifying Hispanic/Latinos 18- to 74-y-old adults from four US urban communities. We performed home SA testing and in-clinic audiometry testing in all participants. SA was defined as an apnea-hypopnea index (AHI) ≥ 15 events/h. HI was defined as a mean hearing threshold > 25 dB hearing level in either ear at the frequencies: 3,000 to 8,000 Hz for high-frequency HI (HF-HI) and 500 to 2,000 Hz for low-frequency HI (LF-HI). Combined-frequency HI (CF-HI) was defined as both conditions present, and Any-HI was considered as HI in either low or high frequencies. RESULTS Of 13,967 participants, 9.9% had SA and 32.3% had Any-HI. Adjusted for risk factors for HI, those with SA had a 30% higher odds of Any-HI (95% confidence interval [CI] = 8% to 57%), 26% higher odds of HF-HI (CI = 3% to 55%), 127% higher odds of LF-HI (CI = 21% to 326%), and 29% higher odds of CF-HI (CI = 0% to 65%). A dose-response association was observed between AHI severity and Any-HI (versus no SA, OR for AHI ≥ 15 and < 30 = 1.22, CI = 0.96 to 1.54, and OR for AHI ≥ 30 = 1.46, CI = 1.11 to 1.91, p = 0.002). CONCLUSION SA is associated with HF-HI and LF-HI, independent of snoring and other confounders. COMMENTARY A commentary on this article appears in this issue on page 641.

Sleep Apnea Is Independently Associated With Peripheral Arterial Disease in the Hispanic Community Health Study/Study of Latinos

Objective— Sleep apnea (SA) has been linked with various forms of cardiovascular disease, but little is known about its association with peripheral artery disease (PAD) measured using the ankle–brachial index. This relationship was evaluated in the Hispanic Community Health Study/Study of Latinos. Approach and Results— We studied 8367 Hispanic Community Health Study/Study of Latinos participants who were 45 to 74 years of age. Sleep symptoms were examined with the self-reported Sleep Health Questionnaire. SA was assessed using an in-home sleep study. Systolic blood pressure was measured in all extremities to compute the ankle–brachial index. PAD was defined as ankle–brachial index <0.90 in either leg. Multivariable logistic regression was used to investigate the association between moderate-to-severe SA, defined as apnea–hypopnea index ≥15, and the presence of PAD. Analyses were adjusted for covariates. The prevalence of PAD was 4.7% (n=390). The mean apnea–hypopnea index was significantly higher among adults with PAD compared with those without (11.1 versus 8.6 events/h; P=0.046). After adjusting for covariates, moderate-to-severe SA was associated with a 70% increase in the odds of PAD (odds ratio, 1.7; 95% confidence interval, 1.1–2.5; P=0.0152). This association was not modified by sex (P=0.8739). However, there was evidence that the association between moderate-to-severe SA and PAD varied by Hispanic/Latino background (P<0.01). Specifically, the odds were stronger in Mexican (adjusted odds ratio, 2.9; 95% confidence interval, 1.3–6.2) and in Puerto Rican Americans (adjusted odds ratio, 2.0; 95% confidence interval, 0.97–4.2) than in other backgrounds. Conclusions— Moderate-to-severe SA is associated with higher odds of PAD in Hispanic/Latino adults.

ATS Core Curriculum 2016: Part I. Adult Sleep Medicine

Jay S. Balachandran, Columbia St. Marys Hospital Carey C. Thomson, Mount Auburn Hospital Dezmond B. Sumter, University of Michigan Anita V. Shelgikar, University of Michigan Philippe Lachapelle, McGill University Health Centre Sushmita Pamidi, McGill University Health Centre Michael Fall, Medical University of South Carolina Chitra Lal, Medical University of South Carolina Ridhwan Y. Baba, Case Western Reserve University Neomi Shah, Icahn School of Medicine at Mount Sinai

Relationship of genetic determinants of height with cardiometabolic and pulmonary traits in the Hispanic Community Health Study/Study of Latinos

Background Associations of adult height with cardiometabolic and pulmonary traits have been studied in majority European ancestry populations using Mendelian randomization and polygenic risk score (PRS) analysis. The standard PRS approach entails creating a PRS for height using variants identified in prior genome-wide association studies (GWAS). It is unclear how well the standard PRS approach performs in non-European populations and whether height-trait associations observed in Europeans are also observed in other populations. Methods In the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), we used: (i) the standard approach to create a PRS for height (PRS1) and (ii) a novel approach to optimize the selection of variants from previously established height association loci to better explain height in HCHS/SOL (PRS2). We also estimated the extent to which PRS-trait associations were independent or mediated by the PRS effect on height. Results In 7539 women and 5245 men, PRS1 and PRS2 explained 9 and 29% of the variance in measured height, respectively. Both PRS1 and PRS2 were associated with forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1/ FVC ratio, total cholesterol and 2-hour oral glucose-tolerance test insulin levels. Additionally, PRS2 was associated with estimated glomerular filtration rate and ankle brachial index. Both PRS1 and PRS2 had pleiotropic associations with FEV1/ FVC ratio in mediation analyses. Conclusions Associations of polygenic scores of height with measures of lung function and cholesterol were consistent with those observed in prior studies of majority European ancestry populations. Mediation analysis may augment standard PRS approaches to disentangle pleiotropic and mediated effects.

Sleep Timing, Stability and Blood Pressure in the Sueño Ancillary Study of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL)

BACKGROUND: Timing and stability of the sleep‐wake cycle are potential modifiable risk factors for cardiometabolic disease. The aim of this study was to evaluate the relationship between objective measures of sleep‐wake timing and stability with cardiometabolic disease risk. METHODS: In this multicenter, cross‐sectional, population‐based study, actigraphy data were obtained from the 2,156 adults, aged 18 to 64 years, recruited from the Sueño ancillary study of the Hispanic Community Health Study/Study of Latinos (2010‐2013). These data were correlated with measures of cardiometabolic disease risk, including systolic and diastolic BPs, homeostatic assessment of insulin resistance, glycosylated hemoglobin, BMI, and hypertension and diabetes status. RESULTS: Each 10% decrease in interdaily stability was associated with a 3.0% absolute increase in the prevalence of hypertension (95% CI, 0.6‐5.3; P < .05), an increase in systolic BP by 0.78 mm Hg (95% CI, 0.12‐1.45; P < .05) and an increase in diastolic BP by 0.80 mm Hg (95% CI, 0.28‐1.32; P < .05). In addition, delaying the midpoint of sleep by 1 h was associated with an increase in systolic BP by 0.73 mm Hg (95% CI, 0.30‐1.16; P < .01) and diastolic BP by 0.53 mm Hg (95% CI, 0.17‐0.90; P < .01). These associations were not significant after adjusting for shift work status. No association was found between interdaily stability or sleep timing and diabetes, BMI, or insulin resistance. CONCLUSIONS: These results suggest that beyond sleep duration, the timing and regularity of sleep‐wake schedules are related to hypertension prevalence and BP.