Sleep-disordered breathing and caffeine consumption: results of a community-based study.
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ABSTRACT:
SUBMITTER: Aurora RN
PROVIDER: S-EPMC3435136 | biostudies-other | 2012 Sep
REPOSITORIES: biostudies-other
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Project description:BACKGROUND AND PURPOSE:Impaired lung function is regarded as a risk factor for stroke in patients with chronic obstructive pulmonary disease. However, the association between reduced lung function and incident stroke in a community-based population with sleep-disordered breathing (SDB) remains unknown. METHODS:A prospective study was performed within the Sleep Heart Health Study cohort. Full montage home sleep testing and spirometry data on 2082 and 2072 individuals with and without SDB, respectively, were analysed. Cox proportional hazards regression models were used to estimate the association between lung function and incident stroke. RESULTS:Over 11.7 years, 183 cases of stroke were identified in participants without pre-existing cardiovascular diseases, including 71 and 112 with an apnoea-hypopnoea index <5 events/h and ?5 events/h, respectively. In the entire population, lung function was inversely associated with incident stroke [hazard ratio (HR) 0.913 (95% confidence interval 0.839-0.994) for every 10% increase in percentage of predicted forced vital capacity]. When the population was divided according to the presence/absence of SDB, the association of lung function with incident stroke became stronger in individuals with SDB [HR 0.899 (0.822-0.984) for every 10% increase in percentage of predicted forced expiratory volume in 1 s; HR 0.881 (0.787-0.987) for every 10% increase in percentage of predicted forced vital capacity] but not in individuals without SDB. CONCLUSIONS:Lung function may serve as a risk factor for incident stroke in a community-based population, especially in those with SDB. Spirometry may help improve the risk management for primary care in community-based populations.
| S-EPMC6181793 | biostudies-literature
Project description:Study objectivesSleep disordered breathing is associated with cardiovascular disease. The pathophysiologic mechanisms remain unclear, but enhanced vascular inflammation is implicated. We sought to evaluate the association of sleep disordered breathing with biomarkers of inflammation.DesignCross-sectional, observational.SettingCommunity-based.ParticipantsThere were 900 participants from the Framingham Heart Study site of the Sleep Heart Health Study (52% females, mean age 60 y, 23% ethnic minorities).InterventionsNone.MeasurementsWe assessed circulating levels of nine inflammatory biomarkers in relation to polysomnographically-derived apnea-hypopnea index and hypoxemia index (% sleep time with oxyhemoglobin saturation < 90%). Multivariable models were adjusted for demographics, smoking, cardiovascular diseases, diabetes, and other potential confounders, without and with adjustment for body mass index.ResultsWith multivariable adjustment not including body mass index, the apnea-hypopnea index was associated with C-reactive protein, inter-leukin-6, fibrinogen, intercellular adhesion molecule-1, and P-selectin levels and hypoxemia index was associated with C-reactive protein, interleukin-6, and fibrinogen levels. After adjustment for body mass index, only the association of interleukin-6 with sleep disordered breathing remained significant: the adjusted mean serum interleukin-6 level was 2.93, 3.14, 3.34, and 4.62 pg/mL, respectively, in participants with apnea-hypopnea index < 5, 5-14.9, 15-29.9, and ? 30 events/h (P = 0.01 for trend) and 2.97, 3.01, 3.35, and 4.85 pg/mL, respectively, in participants with hypoxemia index < 0.5, 0.5-4.9, 5-9.9, and ? 10% of sleep time (P = 0.02 for trend).ConclusionsIn a community-based sample, sleep disordered breathing is associated with higher levels of interleukin-6, a marker of myocardial infarction risk and mortality. Adiposity may mediate the increased levels of C-reactive protein, fibrinogen, intercellular adhesion molecule-1, and P-selectin observed in sleep disordered breathing.
| S-EPMC3622647 | biostudies-literature
Project description:RationaleSleep-disordered breathing (SDB) has been associated with total and cardiovascular mortality, but an association with cancer mortality has not been studied. Results from in vitro and animal studies suggest that intermittent hypoxia promotes cancer tumor growth.ObjectivesThe goal of the present study was to examine whether SDB is associated with cancer mortality in a community-based sample.MethodsWe used 22-year mortality follow-up data from the Wisconsin Sleep Cohort sample (n = 1,522). SDB was assessed at baseline with full polysomnography. SDB was categorized using the apnea-hypopnea index (AHI) and the hypoxemia index (percent sleep time below 90% oxyhemoglobin saturation). The hazards of cancer mortality across levels of SDB severity were compared using crude and multivariate analyses.Measurements and main resultsAdjusting for age, sex, body mass index, and smoking, SDB was associated with total and cancer mortality in a dose-response fashion. Compared with normal subjects, the adjusted relative hazards of cancer mortality were 1.1 (95% confidence interval [CI], 0.5-2.7) for mild SDB (AHI, 5-14.9), 2.0 (95% CI, 0.7-5.5) for moderate SDB (AHI, 15-29.9), and 4.8 (95% CI, 1.7-13.2) for severe SDB (AHI ≥ 30) (P-trend = 0.0052). For categories of increasing severity of the hypoxemia index, the corresponding relative hazards were 1.6 (95% CI, 0.6-4.4), 2.9 (95% CI, 0.9-9.8), and 8.6 (95% CI, 2.6-28.7).ConclusionsOur study suggests that baseline SDB is associated with increased cancer mortality in a community-based sample. Future studies that replicate our findings and look at the association between sleep apnea and survival after cancer diagnosis are needed.
| S-EPMC3406081 | biostudies-literature
Project description:RationaleWhether sleep-disordered breathing (SDB) severity and diminished lung function act synergistically to heighten the risk of adverse health outcomes remains a topic of significant debate.ObjectivesThe current study sought to determine whether the association between lower lung function and mortality would be stronger in those with increasing severity of SDB in a community-based cohort of middle-aged and older adults.MethodsFull montage home sleep testing and spirometry data were analyzed on 6,173 participants of the Sleep Heart Health Study. Proportional hazards models were used to calculate risk for all-cause mortality, with FEV1 and apnea-hypopnea index (AHI) as the primary exposure indicators along with several potential confounders.Measurements and main resultsAll-cause mortality rate was 26.9 per 1,000 person-years in those with SDB (AHI ≥5 events/h) and 18.2 per 1,000 person-years in those without (AHI <5 events/h). For every 200-ml decrease in FEV1, all-cause mortality increased by 11.0% in those without SDB (hazard ratio, 1.11; 95% confidence interval, 1.08-1.13). In contrast, for every 200-ml decrease in FEV1, all-cause mortality increased by only 6.0% in participants with SDB (hazard ratio, 1.06; 95% confidence interval, 1.04-1.09). Additionally, the incremental influence of lung function on all-cause mortality was less with increasing severity of SDB (P value for interaction between AHI and FEV1, 0.004).ConclusionsLung function was associated with risk for all-cause mortality. The incremental contribution of lung function to mortality diminishes with increasing severity of SDB.
| S-EPMC5067819 | biostudies-literature
Project description:To investigate the associations between amount of habitual alcohol consumption (HAC) and prevalence of metabolic syndrome (MetS), sleep, and sleep-disordered breathing (SDB). We enrolled 683 untreated SDB male patients (age: 54.4 ± 7.80 y, apnea-hypopnea index (AHI): 29.0 ± 21.53/h). HAC was assessed as the average number of drinks consumed per week during the past 12 months. Anthropometric and biochemical markers were used to diagnose MetS. Clinical data and MetS components were compared according to the reported amounts of HAC (no drinking, light drinking <13, heavy drinking ?13 drinks/week). As reported, 78.9% of the participants (n = 539) were regular drinkers; 33.7% (n = 230) were habitually heavy drinkers (mean: 30.7 drinks/week), and 45.2% (n = 309) were light drinkers (5.1 drinks/week). The overall prevalence of MetS was 36.9% (n = 252) and was most common in heavy drinkers (40.5%). Compared to non-drinkers and light drinkers, heavy drinkers had the greatest body mass index (BMI) and waist circumference. Central obesity, hypertension, and hyperglycemia were most prevalent in heavy drinkers. Sleep quality and severity of SDB were the worst in heavy drinkers. After adjusting for age, AHI, and BMI, heavy drinkers had a 1.71 times greater risk of MetS when compared with non-drinkers, and light and heavy drinkers had a 2.06 and 2.11 times higher risk of severe SDB than non-drinkers. HAC may increase the prevalence of MetS and deteriorate sleep in relation to amount of alcohol intake. Even light drinkers had more than twice higher risk of severe SDB than non-drinkers.
| S-EPMC4990257 | biostudies-literature
Project description:RationaleIndividuals with sleep-disordered breathing (SDB) are at increased cardiovascular risk, possibly due to SDB-related stresses contributing to atherosclerosis.ObjectivesWe postulate that pathways associated with a prothrombotic potential are up-regulated in SDB.MethodsMorning and evening plasminogen activator inhibitor-1 (PAI-1), morning fibrinogen, and morning D-dimer were measured in 537 Cleveland Family Study adults. Piecewise multivariable linear mixed models estimated relative mean change or mean change in the biomarker per 5-unit increase in apnea-hypopnea index (AHI) in two groups: AHI less than 15 and AHI greater than or equal to 15, and hypoxia defined as percentage of sleep time with Sa(O(2)) less than 90% (< 2%, ? 2%).Measurements and main resultsNonlinear associations were demonstrated: morning and evening PAI-1 increased by 12% (95% confidence interval [CI], 5-20%; P < 0.001) and 11% (95% CI, 2-20%; P = 0.01), respectively per 5-unit AHI increase until an AHI of 15, when no further increase in PAI-1 was demonstrated. The association between AHI and morning PAI-1 remained significant after adjusting for evening PAI-1 level (10%; 95% CI, 3-17%; P < 0.01). Morning fibrinogen increased on average by 8.4 mg/dl (95% CI, 3.12-13.65; P = 0.002) per five-unit AHI increase until an AHI of 15. There was no association between AHI and morning D-dimer. Hypoxia severity was not associated with thrombotic marker levels.ConclusionsPAI-1 and fibrinogen levels increase monotonically with AHI at degrees of SDB considered mildly to moderately abnormal, suggesting that even mild SDB levels may increase prothrombotic processes. There may be a plateau in this effect, occurring at levels considered to reflect only moderate SDB severity. These relationships with mild-to-moderate SDB were not observed with D-dimer.
| S-EPMC2949407 | biostudies-literature
Project description:OBJECTIVE:The objective of the Sleep Disordered Breathing substudy of the Nulliparous Pregnancy Outcomes Study Monitoring Mothers-to-be (nuMoM2b) is to determine whether sleep disordered breathing during pregnancy is a risk factor for adverse pregnancy outcomes. STUDY DESIGN:NuMoM2b is a prospective cohort study of 10,037 nulliparous women with singleton gestations that was conducted across 8 sites with a central Data Coordinating and Analysis Center. The Sleep Disordered Breathing substudy recruited 3702 women from the cohort to undergo objective, overnight in-home assessments of sleep disordered breathing. A standardized level 3 home sleep test was performed between 6(0)-15(0) weeks' gestation (visit 1) and again between 22(0)-31(0) weeks' gestation (visit 3). Scoring of tests was conducted by a central Sleep Reading Center. Participants and their health care providers were notified if test results met "urgent referral" criteria that were based on threshold levels of apnea hypopnea indices, oxygen saturation levels, or electrocardiogram abnormalities but were not notified of test results otherwise. The primary pregnancy outcomes to be analyzed in relation to maternal sleep disordered breathing are preeclampsia, gestational hypertension, gestational diabetes mellitus, fetal growth restriction, and preterm birth. RESULTS:Objective data were obtained at visit 1 on 3261 women, which was 88.1% of the studies that were attempted and at visit 3 on 2511 women, which was 87.6% of the studies that were attempted. Basic characteristics of the substudy cohort are reported in this methods article. CONCLUSION:The substudy was designed to address important questions regarding the relationship of sleep-disordered breathing on the risk of preeclampsia and other outcomes of relevance to maternal and child health.
| S-EPMC4410772 | biostudies-literature
Project description:Sleep-disordered breathing (SDB) is a common comorbidity in a number of cardiovascular diseases, and mounting clinical evidence demonstrates that it has important implications in the long-term outcomes of patients with cardiovascular disease (CVD). While recognition among clinicians of the role of SDB in CVD is increasing, it too often remains neglected in the routine care of patients with CVD, and therefore remains widely undiagnosed and untreated. In this article, we provide an overview of SDB and its relationship to CVD, with the goal of helping cardiovascular clinicians better recognize and treat this important comorbidity in their patients. We will describe the two major types of SDB and discuss the pathophysiologic, diagnostic, and therapeutic considerations of SDB in patients with CVD.
| S-EPMC4824338 | biostudies-other
Project description:Preclinical data suggest that hypoxia stimulates fibroblast growth factor 23 (FGF23) transcription and cleavage in osteocytes, resulting in elevated circulating c-terminal (cFGF23) levels but normal intact FGF23 (iFGF23) levels. We conducted a case-control study within the Hispanic Community Health Study/Study of Latinos to investigate whether sleep disordered breathing, as a model of hypoxemia, is independently associated with elevated cFGF23 levels in the general population and with elevated cFGF23 and iFGF23 levels in patients with chronic kidney disease (CKD), in whom FGF23 cleavage may be impaired. Cases (n?=?602) had severe sleep disordered breathing defined as an apnea/hypopnea index (AHI) of ?30. Controls without severe sleep disordered breathing (n?=?602) were matched for sex and CKD stage. The median AHI in the cases was 45.8 (IQR 35.5-62.5) compared to 2.6 (IQR 0.6-8.2) in the controls. Cases had higher cFGF23 levels than controls (66.2?RU/mL, IQR 52.8-98.4 vs. 61.2?RU/mL, IQR 49.5-80.1, p value <0.001). There were no differences in iFGF23 levels between cases and controls. In adjusted linear regression and multinomial regression analyses, body mass index attenuated the relationship between severe sleep disordered breathing and cFGF23 levels. No significant relationships were seen in analyses of severe sleep disordered breathing and iFGF23 levels or in analyses of iFGF23 and cFGF23 stratified by CKD status. Additional studies using other models of intermittent and chronic hypoxia are needed to confirm whether hypoxia stimulates FGF23 transcription in humans and to determine the impact on iFGF23 levels in CKD.
| S-EPMC6785996 | biostudies-literature
Project description:RationaleCross-sectional epidemiologic studies show an association between sleep-disordered breathing and hypertension, but only one cohort study has examined sleep-disordered breathing as a risk factor for incident hypertension.ObjectivesTo examine whether sleep-disordered breathing increases the risk of incident hypertension among persons 40 years of age and older.MethodsIn a prospective cohort study, we analyzed data from 2,470 participants who at baseline did not have hypertension, defined as blood pressure of at least 140/90 mm Hg or taking antihypertensive medication. The apnea-hypopnea index (AHI), the number of apneas plus hypopneas per hour of sleep, was measured by overnight in-home polysomnography. We estimated odds ratios for developing hypertension during 5 years of follow-up according to baseline AHI.Measurements and main resultsThe odds ratios for incident hypertension increased with increasing baseline AHI; however, this relationship was attenuated and not statistically significant after adjustment for baseline body-mass index. Although not statistically significant, the observed association between a baseline AHI greater than 30 and future hypertension (odds ratio, 1.51; 95% confidence interval, 0.93-2.47) does not exclude the possibility of a modest association.ConclusionsAmong middle-aged and older persons without hypertension, much of the relationship between AHI and risk of incident hypertension was accounted for by obesity. After adjustment for body mass index, the AHI was not a significant predictor of future hypertension, although a modest influence of an AHI greater than 30 on hypertension could not be excluded.
| S-EPMC2695498 | biostudies-literature