As a 54-year old woman who has just had a bone density test show borderline osteoporosis, I've been doing a lot of web browsing while waiting for my followup appointment with the doc to get the official diagnosis and talk about proposed treatment plan. Among many other things that I've run across about osteoporosis, one article in particular is relevant to this thread.cre8vmynd wrote:Here are a couple studies I've found in the past regarding OSA and low t.
http://men.webmd.com/news/20110603/slee ... stosterone
http://jcem.endojournals.org/content/87/7/3394.full
Here's information regarding osteoporosis in men.
http://www.webmd.com/osteoporosis/livin ... 7/male-men
The paper is Link between obstructive sleep apnea and increased bone resorption in men and it was published in 2008 in the peer refereed journal Osteoporosis International. Bone resorption by the osteoclasts is the process by which the body takes minerals out of the bones to be used elsewhere in the body. In osteoporosis, for one reason or another, the rate of bone resorption by the osteoclasts is greater than rate of formation of new bone by the osteoblasts, and this imbalance between the rate of bone resorption and bone formation leads to the loss of bone mass over time. The paper's abstract says:
Unfortunately, the paper's copyright now belongs to Springer and requires purchasing in order to read the whole thing. The Springer link is http://www.springerlink.com/content/u67hm4j5lt576522/. However, I have also found this link to the full paper in PDF format.Abstract
The bone metabolic abnormalities in patients with obstructive sleep apnea (OSA) were examined. Severity-dependent increases in the serum/urinary levels of bone resorption markers and their attenuation following continuous positive airway pressure therapy in subjects with OSA provide the first evidence of a link between OSA and abnormal bone metabolism.
INTRODUCTION:
Hypoxia, microinflammation and oxidative stress, well-known pathophysiological features of obstructive sleep apnea (OSA), are also known to affect bone metabolism. We examined the bone metabolic abnormalities in patients with OSA and also the effects of continuous positive airway pressure (CPAP) therapy on these abnormalities.
METHODS:
A cross-sectional and prospective study was conducted in 50 consecutive male subjects visiting a sleep clinic and 15 age-matched control subjects without OSA. Plasma concentrations of IL-1beta, IL-6, TNF-alfa, 3-nitrotyrosine, osteocalcin, bone-specific alkaline phosphatase (BAP), and urinary concentrations of cross-linked C-terminal telopeptide of type I collagen (CTX) were examined before and after 3 months' CPAP in subjects with OSA.
RESULTS:
The plasma levels of the cytokines as well as the urinary CTX levels were higher in subjects with severe OSA than in those with mild OSA or control subjects. Significant decrease of the urinary excretion of CTX (before: 211+/-107 vs. after: 128+/-59 microg/mmol/creatinine; p<0.01) as well as of the plasma levels of the cytokines was observed following 3 months' CPAP.
CONCLUSIONS:
Severity-dependent increases in the serum/urinary levels of bone resorption markers and their reversal following CPAP in subjects with OSA provide the first evidence of a link between OSA and abnormal bone metabolism.
The paper makes for interesting reading.
In the Introduction section, the authors state:
In the Discussion section the authors state:Given the high prevalence of OSA and its association with multiple systemic pathological changes, it was considered likely that OSA may also have a substantial impact on other metabolic disorders. The fact that inflammatory cytokines and oxidative stress, as well as hypoxia itself are known to affect bone cell function and may be considered as risk factors for osteoporosis led us to hypothesize that OSA may also predispose oto or exacerbate osteoporosis by causing abnormalities of bone metabolism.
...
The results demonstrate that severe OSA was associated with increased bone resorption, which was reversed by CPAP therapy. To the best of our knowledge, this is the first clinical indication of the adverse effects of OSA on bone metabolism.
The authors do note limitations on the study includingThere are at least three mechanisms that may potentially mediate abnormal bone metabolism in OSA: hypoxia, increased oxidative stress and inflammation.
...
The reports that hypoxia induces osteoclast differentiation and suppresses the functions of osteoblasts are consistent with our current observation of elevation of only a bone resorption marker (urinary CTX), but not of bone formation markers (BAP and OC) in our OSA patients. These results may suggest that the abnormal bone metabolism in OSA is characterized by "an uncoupled state" between increased bone resorption and relatively suppressed bone formation.
OSA is, however, quite different from chronic hypoxia-related diseases, such as emphysema, in that the hypoxia is intermittent and that the frequent episodes of hypoxia followed by reoxygenation cause oxidative stress and inflammation, both of which have been etiologically implicated in the increased risk of cardiovascular diseases in patients with OSA. The importance of the intermittent nature of the hypoxia in OSA is probably reflected by the fact that the urinary CTX levels were weakly, but significantly, correlated with the AHI rather than the LoSO2. While elevation of the plasma levels of inflammatory cytokines is also noted in obese subjects, we were able to successfully demonstrate that the parameters of inflammation increased in our OSA patients in a severity-dependent manner in our OSA patients and that CPAP therapy attenuated these abnormalities, in the absence of any significant change of the body weight of the patients.
...
A plausible mechanism to explain the aforementioned "uncoupled state" between bone formation and bone resorption is the influence of cortisol. Elevation of the plasma level of cortisol in OSA patients and its return to normal range after CPAP therapy have been reported. Excessive cortisol levels may suppress bone formation, but not resorption. The next logical step would, therefore, be to clarify the relationship among OSA, bone metabolism and the serum levels of cortisol.
The authors conclude with:... bone mineral density was not assessed in the current study. The clinical significance of our finding of increase in the levels of bone resorption markers in OSA patients cannot be established until the bone mineral density and, ultimately, the fracture risk, is also evaluated. Thus, confirmatory evidence that OSA is indeed an independent risk factor for osteoporosis must await further clinical studies.
Because we were not able to find strong determinants of increased bone resorption in the current study, there are still other factors potentially involved in both OSA and bone metabolic abnormalities, including cortisol excess and reduced physical activity that need to be addressed. Future studies focusing on such factors may be helpful for elucidating the pathophysiological link between OSA and osteoporosis.
In conclusion, the present study was the first to demonstrate abnormalities in the markers of bone metabolism in patients with severe OSA, and reversal of these abnormalities following 3 months' CPAP therapy. Reduced inflammation and oxidative stress along with improvement in the arterial oxygen saturation associated with CPAP therapy may contribute, at least in part, to the observed beneficial effects. Larger scale clinical studies with bone mineral density and/or fracture incidence as endpoints will be needed to clarify whether or not OSA is indeed an independent risk factor for osteoporosis and whether CPAP therapy might truly have beneficial effects on the bone mass and quality and prevent fractures in subjects with OSA.
