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Sleep apnea is a manifestation of obesity: Penn State Study
Sleep apnea is a manifestation of obesity: Penn State Study -- Posted by Sweet Zombie Jesus! on 06-02-05 10:14
Obstructive sleep apnea (OSA) is a prevalent disorder particularly
among middle-aged, obese men, although its existence in women as well
as in lean individuals is increasingly recognized. Despite the early
recognition of the strong association between OSA and obesity, and OSA
and cardiovascular problems, sleep apnea has been treated as a 'local
abnormality' of the respiratory track rather than as a 'systemic
illness.'
In 1997, we first reported that the pro-inflammatory cytokines
interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were
elevated in patients with disorders of excessive daytime sleepiness
(EDS) and proposed that these cytokines were mediators of daytime
sleepiness. Also, we reported a positive correlation between IL-6 or
TNFalpha plasma levels and the body-mass-index (BMI). In subsequent
studies, we showed that IL-6, TNFalpha, and insulin levels were
elevated in sleep apnea independently of obesity and that visceral fat,
was the primary parameter linked with sleep apnea.
Furthermore, our findings that women with the polycystic ovary syndrome
(PCOS) (a condition associated with hyperandrogenism and insulin
resistance) were much more likely than controls to have sleep
disordered breathing (SDB) and daytime sleepiness, suggests a
pathogenetic role of insulin resistance in OSA.
Other findings that support the view that sleep apnea and sleepiness in
obese patients may be manifestations of the Metabolic Syndrome,
include: obesity without sleep apnea is associated with daytime
sleepiness; PCOS and diabetes type 2 are independently associated with
EDS after controlling for SDB, obesity, and age; increased prevalence
of sleep apnea in post-menopausal women, with hormonal replacement
therapy associated with a significantly reduced risk for OSA; lack of
effect of continuous positive airway pressure (CPAP) in obese patients
with apnea on hypercytokinemia and insulin resistance indices; and that
the prevalence of the metabolic syndrome in the US population from the
Third National Health and Nutrition Examination Survey (1988-1994)
parallels the prevalence of symptomatic sleep apnea in general random
samples. Finally, the beneficial effect of a cytokine antagonist on EDS
in obese, male apneics and that of exercise on SDB in a general random
sample, supports the hypothesis that cytokines and insulin resistance
are mediators of EDS and sleep apnea in humans.
In conclusion, accumulating evidence provides support to our model of
the bi-directional, feed forward, pernicious association between sleep
apnea, sleepiness, inflammation, and insulin resistance, all promoting
atherosclerosis and cardiovascular disease.
Sleep Med Rev. 2005 Jun;9(3):211-24.Sleep apnea is a manifestation of
the metabolic syndrome.Vgontzas AN, Bixler EO, Chrousos GP. Department
of Psychiatry H073, Penn State College of Medicine, 500 University
Drive, Hershey, PA 17033, USA.
Re: Sleep apnea is a manifestation of obesity: Penn State Study -- Posted by Starvation on 06-02-05 15:57
Excellent post thank you.
On 2 Jun 2005 10:14:49 -0700, in alt.support.sleep-disorder "Sweet Zombie
Jesus!" wrote:
>Obstructive sleep apnea (OSA) is a prevalent disorder particularly
>among middle-aged, obese men, although its existence in women as well
>as in lean individuals is increasingly recognized. Despite the early
>recognition of the strong association between OSA and obesity, and OSA
>and cardiovascular problems, sleep apnea has been treated as a 'local
>abnormality' of the respiratory track rather than as a 'systemic
>illness.'
>
>In 1997, we first reported that the pro-inflammatory cytokines
>interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were
>elevated in patients with disorders of excessive daytime sleepiness
>(EDS) and proposed that these cytokines were mediators of daytime
>sleepiness. Also, we reported a positive correlation between IL-6 or
>TNFalpha plasma levels and the body-mass-index (BMI). In subsequent
>studies, we showed that IL-6, TNFalpha, and insulin levels were
>elevated in sleep apnea independently of obesity and that visceral fat,
>was the primary parameter linked with sleep apnea.
>
>Furthermore, our findings that women with the polycystic ovary syndrome
>(PCOS) (a condition associated with hyperandrogenism and insulin
>resistance) were much more likely than controls to have sleep
>disordered breathing (SDB) and daytime sleepiness, suggests a
>pathogenetic role of insulin resistance in OSA.
>
>Other findings that support the view that sleep apnea and sleepiness in
>obese patients may be manifestations of the Metabolic Syndrome,
>include: obesity without sleep apnea is associated with daytime
>sleepiness; PCOS and diabetes type 2 are independently associated with
>EDS after controlling for SDB, obesity, and age; increased prevalence
>of sleep apnea in post-menopausal women, with hormonal replacement
>therapy associated with a significantly reduced risk for OSA; lack of
>effect of continuous positive airway pressure (CPAP) in obese patients
>with apnea on hypercytokinemia and insulin resistance indices; and that
>the prevalence of the metabolic syndrome in the US population from the
>Third National Health and Nutrition Examination Survey (1988-1994)
>parallels the prevalence of symptomatic sleep apnea in general random
>samples. Finally, the beneficial effect of a cytokine antagonist on EDS
>in obese, male apneics and that of exercise on SDB in a general random
>sample, supports the hypothesis that cytokines and insulin resistance
>are mediators of EDS and sleep apnea in humans.
>
>In conclusion, accumulating evidence provides support to our model of
>the bi-directional, feed forward, pernicious association between sleep
>apnea, sleepiness, inflammation, and insulin resistance, all promoting
>atherosclerosis and cardiovascular disease.
>
> Sleep Med Rev. 2005 Jun;9(3):211-24.Sleep apnea is a manifestation of
>the metabolic syndrome.Vgontzas AN, Bixler EO, Chrousos GP. Department
>of Psychiatry H073, Penn State College of Medicine, 500 University
>Drive, Hershey, PA 17033, USA.
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