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Article #34

This article is not a primary research report. Rather, it is a summmary review of several different research studies, published between 1989 and 1997, in which the author participated as an investigator.Hopefully, the intrinsic interest of the topic will compensate for this variationfrom our usual recently published primary research studies. The author begins by noting the strong association of sleep apnea with disorders of metabolism or endocrine function, such as hypothyroidism. The fact that OSA appears much more common in men than women suggests several possible explanations, one of which is the different distributions of body fat in obese men and obese women. The men have more central body-fat, affecting waist and neck circumferences and depositing fat in the neck, thoracic (upper body, especially the chest), and abdominal regions. This type of obesity is associated with sleep apnea and cardiovascular illness. Hormones that affect metabolism include growth hormone, testosterone, and insulin. Growth hormone secretion is closely linked to the first slow-wave sleep period, a stage of sleep typically disrupted by OSA. In severe sleep apnea, growth hormone secretion appears to be reduced; but successful treatment with CPAP will normalize this again, concurrent with normalization of the slow-wave sleep. There is a hormone that normally stimulates growth hormone secretion, called growth hormone releasing hormone (GHRH) and this can be injected into a subject's vein to produce this effect during sleep. However, an arousal right after the injection of GHRH will interrupt the normal process of increasing Growth Hormone secretion. Thus, it is possible that fragmentation of slow-wave sleep by obstructive apneas will also interfere with the usual GH response to the subject's own GHRH. Severe OSA is associated with low testosterone levels that are also increased with CPAP. On the other hand, insulin levels are increased with OSA. This appears to be a result of both obesity and sleep apnea as independent contributing factors. The high prevalence of obesity in OSA suggests that the OSA may have a weight-promoting effect by shifting metabolism. During sleep, OSA increases energy expenditure with repetitive arousals and increased breathing effort, but during the day, sleepiness as a primary symptom of OSA may reduce physical activity--not only actual exercise, but even the kind of fidgeting and movement that goes on largely unnoticed much of the time. Finally, there has been recent research to suggest a change in the activity of serotonin neurons in untreated sleep apnea which may also contribute to weight gain.

I find this article of special value because it helps to balance the usual picture of the relationship of obesity to OSA--namely, obesity as a cause of sleep apnea.Certainly there are reasons why obesity would aggravate sleep apnea, as I'm sure it does--one obvious way being the mass of tissue pressing down on the airway.However, a person does not need to be obese to have sleep apnea, and the stereotypical picture of the "typical" sleep apneic as an obese man may contributeto failure to recognize sleep apnea when it appears, as it certainly can, in a slender young woman. Comparing subjects with different degrees of obesity (as measured by the Body Mass Index or BMI) one finds a relationship to severity of sleep apnea but not a very strong one. Within a single patient over time, weight changes may be associated with improvement or worsening of sleep apnea, and decreases or increases in necessary CPAP pressure. This was my own experience. When I was first diagnosed with OSA about six years ago, I weighed the most I ever had in my lifetime--about 220 pounds--and had given up the hobby of jogging and running road races that I had been active in several years before. I went on the Nutrisystem diet plan, resumed my jogging--to the point that I completed a couple of marathons, the first time in my life--and reduced my weight to about 175 pounds, for a net weight loss of about 45 pounds over the course of a couple years. During that time, I had some follow-up polysomnograms which led to progressive downward adjustments of my CPAP pressure. Alas, even at the point of minimum weight and maximal conditioning, I still had sleep apnea, still needed CPAP, and worst of all, still had excessive daytime sleepiness and napping. Discouraged by this limited result from a lot of effort, and deterred from keeping up my jogging regimen by a change to a much more demanding job, I regained all 45 pounds in the next couple of years. Then, in the ensuing year and a half, my weight skyrocketed to an all-time high of 286 pounds, at which point I required the highest pressure (19) I ever had. But please note that, first of all, I was not at all obese for the first 40 years of my life, including the period of time when my first symptoms of OSA emerged; and second, that I did not have a family history of obesity on either my mother's or my father's side of the family. Some points I am trying to get across with this long personal history are, that while I am now a typically obese sleep apneic, obesity did not cause my apnea in the first place (more likely it was caused by the anatomical feature of my receding chin/lower jaw). Furthermore, normalization of my weight, while it "improved" my apnea, did not come close to curing it. But I am just one individual example. I know of others with different experiences, including one woman whose OSA did clear up after a 100-pound weight loss. As a physician, I am very aware of the many dangerous health problems associated with obesity. From prior participation in a "Cardiovascular Fitness Program," as well as two years of Nutrisystem groups, I am also aware of the types of foods which are generally considered most "dangerous" and most "helpful" for obese people. I am not lacking in knowledge. But I have the same problem common to the vast majority of people with obesity, that it is enormously difficult to lose a large amount of weight and keep it off. The perspective that sees only one side of the OSA-obesity relationship, namly obesity contributing to OSA, doesn't do most people a lot of good. Rather, it serves to pin the blame for any problems on the patient. The other side of the coin, exemplified by this paper, is that OSA can cause obesity by a variety of metabolic, hormal, and symptom-related mechanisms. So, in the case of an obese sleep apneic, the poor patient told "you should lose some weight" not only faces the usual overwhelmingly difficult and usually unsuccessful task faced by most obese people, but may also be fighting multiple factors secondary to his OSA which serve to make weight loss still more difficult--with no assurance that the end result of superhuman efforts to lose weight will be relief of the OSA! Much better, I propose, to focus on successful treatment of the sleep disorders, for which we have many effective treatment approaches, and then see what happens to the weight, for which medicine still has no generally accepted, usually effective treatment to offer.

WHAT DO YOU THINK ABOUT THIS ARTICLE AND MY COMMENTS ON IT? CAN YOU RELATE IT TO ANY PERSONAL EXPERIENCES?

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