Snoring and sleeping apnea are reportedly associated with morbidity. We used home monitoring (MESAM IV) to measure snoring and sleep apnea in 294 men aged 40 to 65 yr from the volunteer register of the Busselton (Australia) Health Survey. In this group, 81% snored for more than 10% of the night and 22% for more than half the night; 26% had a respiratory disturbance index (RDI) > or = 5, and 10% had an RDI > or = 10. There was a relatively low correlation between percentage of night spent snoring and RDI (rho = 0.47, p < 0.005). Subjective daytime sleepiness plus RDI > or = 5 occurred in a minimum of 3%. Obesity was related to snoring, RDI, and minimum SaO2 (all p < 0.0001). There was no relationship between age and either RDI or snoring, but increased age was related to minimum SaO2 < 85% (p < 0.05). Alcohol consumption was not related to sleep-disordered breathing. Smokers snored for a greater percentage of the night than nonsmokers (41 versus 31%, p = 0.01). We conclude that, in middle-aged men, both snoring and sleep apnea are extremely common, and in this age range both are associated with obesity but not with age. However, a high percentage of snoring is not essential for the occurrence of sleep apnea, nor does it necessarily indicate that apnea is present.

Objective: To ascertain whether objectively measured obstructive sleep apnea (OSA) independently increases the risk of all cause death, cardiovascular disease (CVD), coronary heart disease (CHD), stroke or cancer Design: Community-based cohort Setting and Participants: 400 residents of the Western Australian town of Busselton Measures: OSA severity was quantifi ed via the respiratory disturbance index (RDI) as measured by a single night recording in November-December 1990 using the MESAM IV device, along with a range of other risk factors. Follow-up for deaths and hospitalizations was ascertained via record linkage to the end of 2010. Results: We had follow-up data in 397 people and then removed those with a previous stroke (n = 4) from the mortality/ CVD/CHD/stroke analyses and those with cancer history from the cancer analyses (n = 7). There were 77 deaths, 103 cardiovascular events (31 strokes, 59 CHD) and 125 incident cases of cancer (39 cancer fatalities) during 20 years follow-up. In fully adjusted models, moderate-severe OSA was signifi cantly associated with all-cause mortality (HR = 4.2; 95% CI 1.9, 9.2), cancer mortality (3.4; 1.1, 10.2), incident cancer (2.5; 1.2, 5.0), and stroke (3.7; 1.2, 11.8), but not signifi cantly with CVD (1.9; 0.75, 4.6) or CHD incidence (1.1; 0.24, 4.6). Mild sleep apnea was associated with a halving in mortality (0.5; 0.27, 0.99), but no other outcome, after control for leading risk factors. Conclusions: Moderate-to-severe sleep apnea is independently associated with a large increased risk of all-cause mortality, incident stroke, and cancer incidence and mortality in this community-based sample.

Undiagnosed OSA is highly prevalent in the Western Australian general population. While the complete BQ is a sub-optimal screening instrument for the general population, snoring frequency or hypertension can be used to screen out moderate-severe OSA from general population samples with limited reduction in sample size. As there are few general population samples available for epidemiological or genetic studies of OSA and its associated phenotypes, these results may usefully inform future case-control studies.

No measure of snoring was associated with all-cause mortality, or incident cardiovascular disease or stroke over 17 yr in this community-based sample.

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We are in broad agreement with Drs. Kezirian and Chang's letter 1 regarding our publication describing no statistically discernible increase in the risk for death, incident cardiovascular disease, or stroke that can be linked to snoring over 17 years observation in the Busselton Sleep Cohort. 2 They have quite rightly highlighted the fact that as a small cohort study, we were unable to rule out the possibility that snoring has subtle effects on cardiovascular health because our confidence intervals were quite wide. But as our editorialist noted, 3 there do not appear to be any other community-based cohort studies with sufficient follow-up that might provide additional high-quality data. So even with all of the problems highlighted by us 2 and by the letter, 1 our study seems to be the only one of its type. The study by Rich and colleagues did report a subtle association between a measured snoring index and all-cause mortality, but only in a subset of patients (n = 5,955) without sleep apnea and with a BMI < 30 (OR = 1.16; 95% CI, 1.01-1.32) when the background mortality rate in the whole cohort was 2.1% in n = 77,260 patients. 4 But that study was not a community-based cohort, and the authors regretted being unable to control for basic risk factors such as cholesterol and smoking. And so we must be left wondering whether those explain the risk in that subgroup analysis.Because of the relatively small size of our study we chose to provide the power we had to detect quite large increases in the relative risk (i.e., 3 times the risk). Whilst some cardiovascular risk factors have a relatively small relative increase in risk, they tend to have important increases in absolute risk for bad outcomes if the risk factor and the outcome are common-but the stroke outcome in our study was quite rare. We still agree with Kezirian and Chang that the Busselton cohort shows that there probably is not a strong association, but there may be a weak association (i.e., an odds ratio of 1.2-1.5 between the lowest and highest quartile of snoring). As we stated in the paper, 2 we were severely underpowered to detect subtle associations, particularly with a rare occurrence such as the biologically plausible stroke association.To borrow their legal metaphor: in both law and medicine the burden of proof is on the accuser. So far there is still very little reliable evidence from studies of the right scientific design that snoring is a killer. The fatal snoring hypothesis seems unlikely to us given the difficulty in showing that mild sleep apnea deleterious consequences. [5][6][7][8] In addition, the influential Spanish

Background: Urinary incontinence has been experienced as a problem since 1500 BC. In the twentieth century it is still a major problem that remains a source of distress for many sufferers. A lack of literature regarding the prevalence  of stress urinary incontinence (SUI) amongst chronic obstructive pulmonary disease (COPD) patients lead to this studyObjective: To determine the prevalence of stress urinary incontinence in female COPD patients between the ages of 30 and 70 years.Methods: This cross-sectional study included 67 female COPD patients (aged 30-70 years) who were interviewed during a three month period. A structured COPD / incontinence questionnaire was used to obtain data. Statistical analysis of results included Fisher’s exact test and two-tailed t-tests. A p-value of < 0,05 was considered to be statistical significant.Results: The prevalence of SUI in female COPD patients was estimated as 82,1%. Smoking history was the only variable with a significant positive correlation regarding the patients presenting with SUI (p < 0,05). The proportion of smokers in the subjects presenting with SUI (SUI group - 29/55) is significantly higher than the subjects with no symptoms of SUI (normal group - 2/12).Discussion and Conclusion: The outcome of this study revealed a high prevalence of SUI in female COPD patients. Cigarette smoking, as the major contributing factor, revealed a strong statistical correlation between COPD and SUI.

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