How Anemia Can Be Caused By Upper Airway Resistance Syndrome

I just saw Kim (name changed for privacy), who is a 24 year old graduate student for her recurrent sinus infections. She tried multiple antibiotics which helped only temporarily. She also mentioned that she was chronically tired, which she blamed on her anemia. As I see in many women (and men) with upper airway resistance syndrome, she also had frequent headaches, cold hands and feet, low blood pressure, and cannot sleep on her back.
 
One of the most common explanations by doctors for fatigue in younger women is said to be from anemia. It’s thought that losing regular amounts of blood during the normal menstrual cycle can lower blood count levels. There are a number of other explanations for anemia, including Vitamin B12 and folate deficiency.
 
One of my guest bloggers, Dr. Deborah Wardly, recently published a review article a few years back on the effects of atrial natriuretic peptide (ANP) on various aspects of your body. ANP is created in your heart muscles every time it’s subjected to obstructed breathing. The heart thinks that the body has too much fluid, and creates ANP which goes to the kidneys to create more urine, lowering blood volume. She also points out that ANP has been shown to lower your blood pressure, keep you thin, make your nervous system more excitable, make you chronically tired, and makes you pee more than usual. In particular, ANP is also known to lower the angiotensin-aldosterone pathway in the kidneys.
 
So how does lowering angiotensin-aldosterone cause anemia? A quick review of the renin-angiotensin-aldosterone system (RAAS) is in order. I know it sounds a bit complicated, but take a look at the referenced figures, and you’ll see how everything in the body is so well interconnected.
 
The RAAS is a hormone system that regulates blood pressure and fluid balance. If the kidneys sense that you’re dehydrated (lower blood flow through the kidneys), the cells in your kidneys convert an already circulating protein (prorenin) into renin, which converts angiotensinogen (made by the liver) into angiotensin I. Angiotensin I is then converted into angiotensin II by angiotensin converting enzyme (ACE) in the lungs. Angiotensin II constricts your blood vessels, raising your blood pressure. It also stimulates the hormone aldosterone, which is made in the adrenal cortex (which also makes epinephrine). Aldosterone causes the kidneys to reabsorb sodium and water, causing you to hold onto sodium, raising your blood pressure. 
 
As you can see in this diagram, there are a number of steps that can be blocked by certain prescription medications.
 
ANP has the opposite effect of angiotensin II, lowering renin and aldosterone in the kidneys. One review article states that angiotensin II acts to stimulate erythropoietin, which is made in the kidneys to stimulate red blood cell production in your bone marrow. So by lowering the salt and fluid conserving properties of angiotensin II, you can in theory lower erythropoietin levels. This supports the observation that you can have mild anemia if you’re taking ACE inhibitors for high blood pressure or in certain people with chronic kidney disease. Now you can add upper airway resistance syndrome to the list (via ANP production).
 
If you have been diagnosed with anemia, do you also have cold hands, low blood pressure, headaches or chronic fatigue? Do you also prefer to sleep on your side or stomach? Please tell us your story in the box below.

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2 thoughts on “How Anemia Can Be Caused By Upper Airway Resistance Syndrome

  1. that’s interesting. so this stimulus would have to be unopposed by the hypoxia stimulus to increase EPO. this would be seen only in those who really don’t drop their oxygen levels. I have some anecdotes that relate to this. I have noticed all my life that I tend to have a higher iron level and a borderline high hematocrit for a woman. after jaw surgery, my baseline hematocrit is a few points lower than it used to be. my sleep studies never showed me dropping below 90%, but I think that this is an artificial cutoff that may not be as benign as we think. I have a friend who has always had an unexplained reticulocytosis. she has SDB by history but won’t get a study. I know others with unexplained borderline polycythemia, with untreated SDB by history. so I think that “mild” SDB may be responsible for elevated counts with desats that we would otherwise blow off. do you see this?

    on the other side, I have a friend who has horrible excessive daytime sleepiness to the point she falls asleep in the middle of writing me emails (and then sends them), but after two sleep studies the docs just call it benign snoring. (and will not treat her even though she can hardly get to the appointments with them without falling asleep while driving.) so she is obviously not desaturating “significantly”. she cannot sleep for more than a few hours at a time, and this is not benign. she has a lot of other problems and ended up getting a transfusion accidentally because of a lab error. she was obviously upset but I said: I’m willing to bet you are sleeping better, due to increased oxygen carrying capacity. and I was right; she can now sleep for 6 hours straight. part of my ability to predict this was her sudden ability to get through an email to me without falling asleep: her EDS is better. so this argues that desats that we think are within normal, are not at all, and that they are waking people up and causing pathology, outside of simply the sensation of airway collapse being the trigger to microarousal.

    so, the people you have seen with UARS and anemia, what do they desaturate to? do they have milder desats than others with UARS and no anemia? the other side of it is that maybe their UARS is only symptomatic because of their anemia from another cause. if you correct the anemia, do the UARS symptoms improve?

    anemia is known to be associated with developmental problems in children, and worse outcome in autism. I have to wonder if this is solely related to poorer oxygen carrying capacity combined with SDB, which of course goes undetected. such that the hypoxic insult is causative for the brain dysfunction. and guess what? the autism gets better if you supplement iron to correct the anemia…..

  2. I fit the UARS pattern pretty closely and have macrocytic anemia that no experts have been able to figure out (looks like pernicious but doesn’t respond to B12 shots or folate etc). What kind of anemia would your theory predict? Thank-you!