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The authors point out that apneic and hypopneic episodes during sleep are known to cause brief rises of blood pressure. Moreover, 50-90% of patients with sleep-disordered breathing have hypertension, suggesting a strong association of the two disorders. It is quite plausible, from a physiological basis, that sleep-disordered breathing could cause sustained hypertension. Adverse physiological effects of sleep apnea include low blood oxygen, high carbon dioxide, frequent arousals from sleep, and high negative pressures within the chest. There is also evidence for increased sympathetic nerve activity (the "fight or flight" response of the body), decreased sensitivity of body receptors monitoringblood pressure, increased response of blood vessel musculature, and abnormal salt and water metabolism. Several hormones, such as insulin and growth hormone, are also disturbed in sleep apnea.Furthermore, blood pressure decreases after treatment of sleep apnea with CPAP or tracheostomy.
All this would seem to weigh heavily in favor of sleep disordered breathing causing hypertension, but the case for this remains inconclusive because of "potential confounding factors" like obesity and age. This study undertook to use a general population sample of 1069 middle-aged men and women, enrolled in a longitudinal study of the natural history of sleep-disordered breathing, the Wisconsin Sleep Cohort Study, which is unique in having a large population-based sample subjected to in-laboratory assesment of sleep-disordered breathing with polysomnography.
The sample was obtained as follows: all employees aged 30 to 60 of five state agencies in south-central Wisconsin received sleep questionnaires, and 79% completed them. About half accepted an overnight sleep study. The final study sample resembled the nonparticipants except for: having more education; a higher Body Mass Index (BMI, a measure of obesity); more frequent reports of snoring; and less frequent reports of hypertension. Statistical techniques were used to determine that these sampling biases did not significantly affect the results. Of the total of 1069 subjects, 833 (78%) had Apnea/Hypopnea Indices (AHI) less than 5, indicating an absence of sleep apnea; 141 (13%) had AHIs between 5 and 15, suggesting mild sleep apnea; 58 (5%) had AHIs between 15 and 30, consistent with moderate sleep apnea, and 37 (3%) had AHIs over 30, consistent with severe sleep apnea.
Blood pressures increased with severity of sleep-disordered breathing, as did diagnosed hypertension and use of antihypertensive medications. Also increasing with greater severity of sleep-disordered breathing were: obesity, age, and proportion of males, so these factors had to be taken into account. Statistical analyses which accomplished this continued to show a relationship between high blood pressure and severity of sleep-disordered breathing. There was a tendency for this relationship to be a bit stronger in less obese individuals. Each additional one-point increase in the Apnea/Hypopnea Index (indicating one additional apnea or hypopnea per hour of sleep) increased the risk of hypertension by about 4%. Males represented 57% of the total sample but 81% and 86% of the moderate and severe sleep apneics, respectively. Smokers comprised only 14% of the sample and did not appear overrepresented among the moderate-severe sleep apneics. Body Mass Index increased steadily from the group with no sleep apnea through the group with severe sleep apnea, from an average BMI of 28 in the first group to 38 in the last group.
The authors described theirs as the "largest community sample that has been studied with in-laboratory polysomnography." Their findings showed that undiagnosed and untreated sleep apnea was associated with elevated blood pressure and hypertension, independently of age, sex, and obesity. There was a consistent dose-response relationship between blood pressure and severity of sleep apnea, but even mild sleep-disordered breathing (AHI 5-15) carried an increased risk of elevated blood pressure.
They considered their study's major limitation to be the cross-sectional nature of the data: that is, they studied their subjects at a single point in time, preventing exmination of the relationship in time between the development of sleep-disordered breathing and that of high blood pressure. It is therefore possible--though it seems less likely--that high blood pressure may be causing sleep apnea, rather than the reverse. In fact, some antihypertensive drugs such as beta-blockers reduce apneas and hypopneas and hypertension increases the sensitivity of bodily receptors to levels of oxygen and carbon dioxide. In fact, the causal relationship may proceed in both directions at once.
The independent association of sleep-disordered breathing with high blood pressure, while consistent and statistically significant, is not large in magnitude, so that it does require a large sample such as this to detect, especially when confounding factors must be taken into account. This problem may underly the negative results derived from some clinic-based studies when they adjusted data for age and obesity. Also, some clinic-based studies have used symptomatic patients without clear-cut sleep apnea as controls, whereas these may represent the mild sleep apneics who were in this study found to have an increased risk of high blood pressure, making differentiation from the sample of severer sleep apneics more difficult in those other studies.
The authors made a special point about their finding of a stronger relationship of sleep-disordered breathing with high blood pressure in non-obese individuals. So powerful is the stereotype of the obese sleep apneic that a non-obese patient may never even get questioned about symptoms related to sleep-disordered breathing, whereas these may be the most important group for intervention, with the most beneficial effect of apnea treatment on blood pressure.
To give an idea of the public health significance of their findings, the authors calculated from their data that, among middle-aged adults, sleep-disordered breathing contributes to hypertension in about 400,000 women and 2 million men!
Hopefully, the concluding sentence of the Summary above startled some readers.We should all know by now that sleep apnea is much more common than was thought a couple of decades ago, before the advent of effective treatments made the disorder more popular to diagnose. However, we may have yet to appreciate the full range of catastrophic health problems that stem from this common disorder. Each such problem--heart attacks, strokes, chronic obstructive pulmonary disease, auto accidents, cognitive impairment, mood disturbances--needs study in the exhaustive way that these authors have done with high blood pressure. When good data on all these complicationsis in, we may have to add sleep disordered breathing as a new item on our list of "most important public health problems"--along with alcohol and drug abuse, depression, suicide, cancer, Alzheimer's Disease, AIDS, etc. Even those of us who "carry the banner" of raising sleep apnea awareness may still be far from comprehending the full extent of the problem.
I really have no major issues to take with this study, except that I wish, as the authors do, for more longitudinal data, which one hopes might eventually be forthcoming from a sample such as this involved in a longitudinal study already. It seems a bit regrettable to have cut off the youngest and oldest age groups from inclusion. Otherwise, I found their results convincing, even though a bit unexpected.
I was particularly receptive to their advice to not restrict routine questioning about sleep disordered breathing to the stereotypical obese patient. The patient with sleep apnea who doesn't fit the stereotype is at special risk for going unrecognized and untreated. Moreover, the stereotype perpetuates the "blaming the victim" psychology of finding a causal factor in an illness which can be seen as a "lifestyle" variable under the supposed voluntary control of the patient. Then the doctor may feel justified in limit his treatment to advising the patient to correct the "bad habit"--when the fact is that obesity is one of the least treatment-responsive conditions known to medicine, and it would be a rare doctor willing to take on the patient's obesity as his responsibility to treat and cure! It is not enough to tell the obese patient to "just say no to food" or, paraphrased in a more politic way, "eat a nutritious and healthy diet." It is patently absurd to think that such doctorly advice constitutes effective treatment for obesity, and most likely it serves to wash the "cause" of the medical problem from the doctor's hands. It is well to inform the doctor that many factors unrelated to overeating or underexercising, but amenable to medical treatment like sleep apnea, may be as much the cause of obesity and hypertension as obesity is a cause of the other conditions. (As a recently transformed "fatty" I have become quite militant about fat people's rights not to be blamed for everything that goes wrong with them, including their obesity!)
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