February 13, 2013
Guest post by Dr. Deborah Wardly.
Recently, my hypothesis paper on Atrial Natriuretic Peptide (ANP) was published, which discusses various actions of ANP and how they might relate to the clinical presentation of OSA and UARS. ANP is known to be elevated in OSA as a result of intrathoracic pressure changes during apneas. This has been noted to be a cause of nocturia in OSA, but there may be other previously unrecognized effects. For example, ANP is very important in lipolysis; the breakdown of fat. But in obesity, there is ANP resistance; meaning that even if there’s lots of ANP around, the body doesn’t see it, so the effect is as if the levels are low. Therefore, ANP resistance might be the key to understanding the obesity in OSA (as well as obesity in general, depending on how prevalent we believe OSA to be); there is evidence that hypoxia may lead ultimately to ANP resistance, suggesting that in OSA, it is the OSA that CAUSES the obesity, and then this becomes a vicious cycle, since we know that obesity makes OSA worse.
Other effects of ANP implicate its possible role in “adrenal fatigue”, due to the fact that ANP suppresses the hypothalamic-pituitary-adrenal axis. In the absence of hypoxia, as in UARS, this would be more prominent and ANP levels and effect should be much higher than in OSA because there would be no ANP resistance. This would also explain why those with UARS are thin, as lipolysis would be activated by the high ANP levels. A hallmark of adrenal insufficiency is orthostatic hypotension, something seen in UARS. ANP would explain the blood pressure differences seen in UARS and OSA: ANP itself lowers blood pressure, explaining lower blood pressures in UARS and then with ANP resistance in conjunction with other factors, the fact that blood pressure rises in OSA. ANP levels go up with exercise, and would explain the exercise intolerance seen in fatiguing illnesses. This theory argues that UARS underlies potentially ALL cases of adrenal fatigue, and possibly most cases of chronic fatigue syndrome. It also argues that the increase in somatic symptoms seen in UARS are mainly due to the actions of ANP.
A high level of ANP doubles the excretion rate of magnesium from the kidney, putting those with sleep disordered breathing at higher risk of magnesium deficiency. Magnesium deficiency from sleep disordered breathing may implicate its involvement in the development of obesity, insulin resistance, atherosclerosis, preeclampsia, hypertension, arrhythmia, inflammation, migraine, and asthma.
There are gender differences in ANP secretion that might explain the gender differences we see between OSA and UARS. For example, testosterone completely eliminates stretch induced release of ANP. Therefore, according to this theory, men with sleep disordered breathing and adequate testosterone levels, would have lower levels of ANP caused by their apneas, and therefore fewer somatic symptoms, compared to women.
There are also polymorphisms of ANP that would lead to much higher levels of ANP in some individuals; might these be the people we see with severe UARS?
As patients with OSA, what has been your experience? Did you have sleep problems only after you gained weight, or did your sleep problems precede your weight gain? If you are a man with UARS, do you have a low testosterone level?
March 24, 2011
There have been numerous studies that show that a major reason why people go to the bathroom to urinate frequently are doing so not because of irritable bladders or enlarged prostates, but due to an underlying sleep-breathing problem. Here’s another study that showed that about 58% of men with nocturia had obstructive sleep apnea. When treated for sleep apnea, nocturia can be significantly improved, if not completely cured in many cases. Prescription medication for this problem can’t even come close to these results.
Another recent study showed that going to the bathroom 2 or more times per night increased the mortality rate by 50% in men and 30% in women.
It’s been shown in numerous studies that the reason why you wake up is not because your bladder is too full—it’s because you’ve stopped breathing and you think your bladder is full, but it’s not. Here’s what happens: Every time you stop breathing, blood flow to the heart diminishes, but once you start breathing again, blood rushes back in your heart which dilates the heart chambers, making your heart think that you’re fluid overloaded. The heart then makes a hormone called atrial natriuretic hormone (or peptide), which makes your kidneys make more urine. At a certain point, with even a small amount of urine, you’ll feel like you have to go but only after you’ve woken up after an apnea event. Notice too, that urine volumes are typically not that large.
The thing that get me upset about all this is that despite all that we know about urinary frequency and its’ connection to obstructive sleep apnea, PCPs and urologists haven’t changed their ways at all. They continue to place patients on medications that help to relax the bladder, shrink the prostate, or even do surgery, which is like placing a band-aid. Treating with medications may help people go to the bathroom less often, but it won’t prevent cardiovascular morbidity and mortality. Treating an underlying sleep-breathing problem will not only treat nocturia effectively, it’ll also significantly lower your chances of dying.
I’m not saying that all cases of nocturia is from sleep apnea but since it’s so common, why not rule it out before looking at the more traditional options that require medications? (The same argument can be made for ADHD, depression, anxiety, heart disease, diabetes, etc.) If you have sleep apnea, treat that first, and if you still have symptoms, get checked by a urologist. What do you think about this idea?
February 7, 2009
If you’re one of the millions of men and women who have to go the the bathroom far too often, or have embarrassing leaks of urine once in a while, here’s some important information that you should know. The New York Times (Feb. 3) reported on an article from the New England Journal of Medicine which revealed that postmenopausal women with urinary incontinence issues had significant improvement after losing weight. They also benefitted in other areas such as improvements in their blood pressure, lipids, sleep and libido.
Another article in this month’s Journal SLEEP reported that OSA is associated with overactive bladder in men with or without urinary incontinence. The worse the severity of OSA, the worse the level of urinary problems. Not too surprisingly, nocturia (getting up at night to go to the bathroom frequently at night) is a known complication of obstructive sleep apnea.
Most people with these issues end up seeing a urologist initially and are placed on various medications that work to various degrees. However, a recent study suggests why you should see a sleep doctor instead—people who wake up in the middle of the night to go to the bathroom do so not because their bladders were full, but rather because they stopped breathing and then realized that they had a full bladder. OSA has also been shown to increase atrial natriuretic peptide (ANP), which is produced by the heart when it gets too much blood due to the sudden rush of blood after a lack of blood flow during an apnea episode. ANP causes you to make more urine to get rid of the excess fluid.
Something new to think about for all our senior citizens (and young adults too).