A few newer studies on OSA and obesity--REALLY LONG

[DocWeezy]

People have very strong opinions on this matter, and I'm not trying to change anyone's mind or arrive at a definitive answer. However, newer research is making a connection between "short sleep"/OSA and metabolic syndrome. For every study posted here--it isn't many, I only searched for a couple of minutes--there are probably ten times more that only looked at it from the obesity angle, i.e., are you obese? do you have OSA? conclusion: obesity causes OSA.

Please note that I am NOT trying to say that everyone with OSA had the OSA first. I think it is pretty conclusive that obesity can cause OSA and that it does in some people; however, I also think it is erroneous for anyone to automatically conclude that obesity is the only cause of OSA. These studies also shed some light on why, when some people lose weight, their OSA does not resolve. If OSA were ONLY caused by obesity, then it should resolve upon losing weight. But as we know from many people here, OSA occurs in people of normal weight too. This review does not include any research on anatomical causes of OSA.

But now researchers are beginning to look at the effects of short sleep (whether voluntary or involuntary) and they are finding that people who are sleep deprived gain weight more easily, generally weigh more, and have more metabolic disorders. The findings are that chronic sleep deprivation plays a part in causing the weight gain and causing metabolic disorders. Most of these studies include OSA as a contributing factor to sleep deprivation; one doesn't.

This is by no means a comprehensive review, nor have I examined the articles closely to compare or critique methodology, sample size, generalizability, etc. I just want to present some recent research that contradicts the "common knowledge" that obesity causes OSA. Most earlier studies concluding that obesity causes OSA started with obesity and worked backwards to OSA; these newer studies are looking at sleep deprivation and finding the OSA/metabolic connection and that is an interesting distinction. The impacts of sleep deprivation are just now really beginning to be examined and studied, so it remains to be seen which came first---the chicken or the egg; however, the findings are interesting and consistent in that sleep deprivation impacts how a body uses insulin and how other hormones react.

These are all quotes. The articles and authors are cited.

Bonsignore, M. R., & Zito, A. (2008). Metabolic effects of the obstructive sleep apnea syndrome and cardiovascular risk. Archives of Physiology and Biochemistry, 114(4), 255-260.

p. 256:

“The effects of OSAS-associated sleep disruption are not limited to the increased risk for driving accidents, but might also involve metabolic disturbances. According to recent data, sleep loss profoundly affects metabolic pathways (Knutson et al., 2007). In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased appetite (Spiegel et al., 2004), while short sleep duration was found to be associated with altered plasma levels of leptin and ghrelin and increased BMI (Taheri et al., 2004). In young adults, a prospective study found a significant risk of obesity in subjects reporting short sleep duration (Hasler et al., 2004), leading to speculation that decreased sleeping time over the last decades in the general population may have contributed to the increasing prevalence of obesity. A modest sleep loss may also cause profound endocrinological changes, since glucose tolerance decreased after selective slow-wave sleep deprivation (Tasali et al., 2008). Finally, sleep deprivation has been found to induce a proinflammatory state, with increased release of interleukin-6 (IL-6) (Vgontzas et al., 2004; Haack et al., 2007) and production of IL-6 and tumor necrosis factor-a (TNF-a) by circulating monocytes (Irwin et al., 2006). The pro-inflammatory effects of sleep restriction may at least partly be mediated by sympathetic hyperactivity (Irwin et al., 1999; Johnson et al., 2005).
OSAS causes sleep fragmentation rather than sleep loss, making analysis of its effects more complicated compared to experimental sleep restriction (Spiegel et al., 2005). Nevertheless, OSAS-induced sleep disturbance should be considered as a potential factor negatively affecting metabolism and control of body weight.”



Alam, I., Lewis, K., Stephens, J. W., & Baxter, J. N. (2006). Obesity, metabolic syndrome and sleep apnoea: All pro-inflammatory states. Obesity Reviews, 8, 119-127.

From the abstract (p. 119):

“The contribution of OSAS to the metabolic syndrome has been under-recognized. The putative mechanisms by which OSAS causes or exacerbates these other abnormalities are discussed. We propose that activation of nuclear factor kappa B by stress hypoxia and/or by increased adipokines and free fatty acids released by excess adipose tissue is the final common inflammatory pathway linking obesity, OSAS and the metabolic syndrome both individually and, in many cases, synergistically.”

From the conclusion (p. 124):

“In recent years, there has been significant progress in the understanding of the pathophysiology of the metabolic syndrome. Recent studies have suggested a strong link between the metabolic syndrome and OSAS. The mechanism by which OSAS is associated with hypertension and contributes to IR and dyslipidaemia is not fully understood, but activation of the inflammatory cascade seems to be the common pathway for all of these disease states.




Spiegel, K., Tasali, E., Leproult, R. & Van Cauter, E. (2009). Effects of poor and short sleep on glucose metabolism and obesity risk. National Review of Endocrinology, 5, 253-261.

From the abstract:

“The importance of sleep to hormones and glucose metabolism was first documented more than four decades ago. since then, sleep curtailment has become an endemic behavior in modern society. In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has increased. OSA is very common in endocrine and metabolic disorders, but often remains undiagnosed. “

Key points (p. 254):

“Sleep loss, be it behavioral or related to sleep disorders, is an increasingly common condition in modern society.

Experimental reduction of the duration or quality of sleep has a deleterious effect on glucose metabolism.

Experimental reduction of sleep duration downregulates the satiety hormone, leptin, upregulates the appetite-stimulating hormone, ghrelin, and increases hunger and appetite

Numerous cross-sectional and prospective, epidemiologic studies have provided evidence of an association between short-duration and/or poor-quality sleep and the prevalence or incidence of diabetes mellitus or obesity

Effective treatment of obstructive sleep apnea, a sleep disorder that is highly prevalent in metabolic and endocrine disorders, has the potential to improve glucose metabolism and energy balance

Screening for habitual sleep patterns and obstructive sleep apnea might be critically important for patients with endocrine and metabolic disorders”

p. 257:

“OSA involves respiratory disturbances, hypoxic stress, poor-quality sleep (owing to sleep fragmentation and low levels of slow-wave sleep) and reduced total sleep time. The alterations in glucose regulation and/or appetite regulation observed with experimentally reduced sleep duration and quality suggest that poor-quality and short-duration sleep, in addition to hypoxia, could contribute to altered glucose homeostasis and weight gain in patients with OSA.”

p. 257

“Patients with OSA seem to be more predisposed to weight gain than control individuals with similar levels of obesity who do not have OSA. Consistent with the upregulation of ghrelin that is observed during short-duration sleep in healthy individuals, patients with OSA have high ghrelin levels, which decrease after as little as 2 days of CPAP treatment. By contrast, the decreased leptin levels that follow sleep restriction in normal individuals are not consistent with the hyperleptinemia observed in OSA. Whereas leptin levels are reduced in individuals with chronic short-duration sleep without OSA, independently of BMI and adiposity, patients with osa display higher leptin levels than BMI-matched controls.”




Patel, S. R. (2009). Reduced sleep as an obesity risk factor. Obesity Reviews, 10(2), 61-68.

p. 61:

“Besides causing fatigue and slowing neurocognitive function, recent research suggests chronic sleep restriction may also have important metabolic effects including an increased risk of obesity. Because of the rapidly growing prevalence of chronic sleep restriction, any causal association between reduced sleep and obesity would have substantial importance from a public health standpoint.”

p. 63:

“short sleep remained associated with an elevated BMI in both cohorts. After adjusting for age, race, level of education, smoking, alcohol and caffeine consumption, use of benzodiazepines and antidepressants, depression, physical activity, history of diabetes, heart disease and stroke, mean BMI was 2.5 kg m-2 greater in men and 1.8 kg m-2 greater in women sleeping less than 5 h compared with those obtaining 7–8 h of sleep. Similarly, reduced sleep was also strongly associated with obesity (Table 2). Relative to those sleeping 7–8 h, the odds of obesity associated in those sleeping less than 5 h was elevated 3.7-fold in men and 2.3-fold in women”

From the conclusion (p. 66):

“Overall, current data support an association between chronically curtailed sleep and obesity. This association is increasingly important because of the steady decline in time reserved for sleep in modern society. If the relationship is causal, treatments aimed at improving sleep may represent a novel public health approach to combating the obesity epidemic. Given the inadequacies of current treatment options for obesity prevention, further research into the role of sleep on weight homeostasis is clearly warranted.”

Interestingly, this author completely disregards OSA as a contributor to short sleep:

“At least three common causes of short sleep exist – voluntary curtailment of sleep in order to spend more time on other activities such as work, childcare or recreation despite neurocognitive effects secondary to the sleep restriction; insomnia, characterized by an inability to sleep longer despite a desire to do so; and a lack of desire to sleep longer because of subjectively feeling fully rested with less than 7–8 h of sleep.”

[avi123]

Ditto about Diabetes. You can change the word OSA with Diabetes. No wonder that more than half of Diabetics also have OSAa.