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More Connections Between Alzheimer’s and Sleep Apnea

This is a study that Dr. Mack Jones mentioned during my interview with him a few months ago about a mice developing Alzheimer’s-like brain findings after chronic oxygen deprivation. 

 

Amyloid plaques and neurofibrillary tangles are the two hallmark findings on autopsy studies in patients with Alzheimer’s. Accumulation of amyloid-β protein is the major component of plaques, which is derived from a breakdown of β-amyloid precursor protein (APP) by an enzyme called β-site APP cleavage enzyme (BACE1). It turns out that hypoxia (lowered levels of oxygen) stimulates BACE1 activity, which cleaves APP, leading to more accumulation of β-amyloid protein. This was reported in The Proceedings of the National Academy of Sciences journal in 2006. The study authors placed mice in hypoxic environments (16 hrs/dy for one month) and looked at their brains after being sacrificed. They found significantly increased numbers of amyloid plaques compared with control mice. These plaques were also histologically very similar to what humans have with Alzheimer’s.

 

My question to you is: What common medical condition that I mention all the time causes hypoxia for 8 hours every night for years or decades?

 

 

 

Chicken or the Egg? Diabetes or Obstructive Sleep Apnea

Here’s another study that strengthens the connections between the dots in my sleep-breathing paradigm. About 87% of obese type II diabetics were found to have undiagnosed obstructive sleep apnea. Most diabetes studies give the impression that having diabetes can lead to obstructive sleep apnea due to gradual weight gain, but what I propose is that having even very mild sleep-breathing problems can predispose to elevated glucose levels, insulin resistance, and weight gain. I talk about the specific mechanism  in my book, Sleep, Interrupted. What I want to emphasize is the fact that an underlying sleep-breathing condition is what can predispose you to obesity AND diabetes, not the other way around.

Ulcerative Colitis, Chron’s, and Sleep Deprivation

Here’s more evidence that sleep deprivation can exacerbate inflammatory bowel disease, which includes ulcerative colitis and Chron’s disease. A study was published in Sleep Medicine where rats who were given a substance to induce colitis (DSS, dextran sodium sulfate). Control rats that were deprived of acute sleep deprivation or chronic sleep deprivation had no signs of colitis. Rats on DSS developed colitis, but acute sleep deprivation showed histologic signs of additional inflammation on histology, but showed no clinical symptoms such as weight loss. However, rats subjected to chronic sleep deprivation showed increased histologic inflammation, as well as clinical symptoms. This study is a follow-up to a previous study that showed that patients with inflammatory bowel disease had significantly more sleep disturbances.

Disappointing Results for Valerian as a Sleep Aid

In this month’s issue of Sleep Medicine, researchers reported that valerian, a popular herbal remedy that’s promoted as a sleep aid, was found no better than a placebo. Sixteen older women with insomnia were randomized and given either 300 mg of concentrated valerian extract or placebo before bedtime. Sleep quality was assessed at baseline and after the treatment phase by using a questionnaire, sleep study, daily sleep logs and actigraphy (nighttime movement analysis). After 2 weeks of treatment, no difference was found in all these assessments between valerian and placebo. 

Interestingly, people taking valerian had significantly more nighttime awakenings seen on sleep studies. This may be explained by the fact that valerian may have stimulant, rather than sedative properties. Herbalists have noted this apparent paradoxical effect of valerian. There have been many conflicting studies on using valerian as a sleep aid, and this study only adds more fuel to the fire. 

My take on this? If valerian works for you, keep using it. Even if its’ beneficial effect is a placebo response, it may be worth using. If not, try something else.

Can Taking Sleeping Pills Increase Your Chance of Dying?

A landmark study from Sweden revealed that taking sleeping pills long term is associated with a significantly increased chance of dying. In men, it was 4.5x higher overall and in women it was 2x. They followed about 3500 men and women for 20 years, and found that 379 men and 278 women died during this period. Breaking down cause-specific reasons for dying, regular sleeping pill use in men was a risk factor for cardiac death, cancer death, suicide death, and death from "all remaining causes." In women it was a risk factor only for suicide. Notably, using sleeping pills in men was a better predictor of dying from cancer than from smoking.

 This study support previous studies that found that short or long sleep duration is associated with increased mortality. It’s important to note that this study doesn’t prove that taking sleeping pills per sé increased your chances of dying. It’s more likely that people with illnesses such as cancer or depression are more likely to use sleeping pills. However, what if it can be shown that poor quality or quantity of sleep can cause depression, heart disease or even cancer? Come to think of it, I think there are already many studies that suggest show these results. 

Sudden Infant Death Syndrome & Obstructive Sleep Apnea

I recently stumbled upon a handful of studies about sudden infant death syndrome (SIDS) in a book on sleep apnea by Dr. Allan Pack. SIDS is a tragic condition where an infant dies suddenly in the first year of life or no apparent reason. Apparent life threatening events (ALTEs, or near-miss SIDS) are episodes then a child stops breathing, but comes back to life. Not too surprisingly, Dr. Christian Guilleminault (who published the original paper on upper airway resistance syndrome, and the link between sleep apnea and cluster headaches and sleep walking) and colleagues reported that in 3/5 families of children with SIDS or near-miss SIDS, parents and grandparents had elevated AHIs and excessive sleepiness. All seven children in this study with near-miss SIDS were found to have obstructive sleep apnea at 12 months. 

In a follow-up study, Guilleminault followed 25 children with near-miss SIDS (by 4.5 months) in a group of 700 that required sleep studies for over one year. All 25 were found to have obstructive sleep apnea by age 5. Deray, et al found that loud snoring frequency in fathers of SIDS or near-miss SIDS children was over 2 times that of control. It was stated clearly that this is a subgroup of all children with SIDS, but my gut feeling is that it’s much bigger than they think it is.

I alluded to another study in a past post where breast-feeding was found to lower SIDS rates. I’ve presented evidence that bottle-feeding may increase the chances of developing obstructive sleep apnea. It’s interesting to note that the peak incidence of SIDS occurs around 4-6 months. This is also the time that the infant’s voice box descends and separates away from the soft palate. This transitional period can be a dangerous time for infants, as they go from obligate nasal breathers (when they can suckle and breathe in parallel) to nasal and mouth breathers. 

Should All Older People Be On High Blood Pressure Pills?

A recent article published in the British Medical Journal concluded that all older people should be placed routinely on blood pressure lowering pills, regardless of whether or not they have high blood pressure. You can read a summary here.

It’s one thing to conclude that lowering blood pressure even incrementally has potential health benefits, but to say that all older people should be placed routinely on a cocktail of high blood pressure medications is going too far. Also, the fact that the authors have financial interest in what they’re recommending does not support their stance.

What they should be asking is what’s actually causing hypertension. One major cause that’s been proven but virtually ignored by the medical community is the presence of obstructive sleep apnea. It’s safe to say that most seniors will have some degree of obstructed breathing. Despite all that we know about the cause and effect relationship between hypertension and sleep apnea, 90% of people who have it are not diagnosed. Instead, they get treated for their hypertension, diabetes, depression, anxiety, weight gain, heart disease, heart attack and stroke.

 

Read the summary article and let me know your thoughts on this. Has research, in the name of science, gone too far?

 

 

 

Sleep Apnea, Hearing Loss, and Thick Blood

I came across this interesting article in Sleep Medicine, where they showed that in patients with obstructive sleep apnea, a significant number were hemodynamically hyperviscosity positive (282/610 patients). Hyperviscous means that blood is thicker and more prone to clog arteries. Of these 282 patients, 239 had brainstem AEP abnormalities. AEPs are tests for ear neurologic reflexes where clicks are given in one ear and brain waves are measured in response. It tests for inner ear and brainstem function.

Ones that didn’t have hyperviscosity all had normal AEPs. Of these 239 patients, 57 had bilateral sensorineural hearing changes (no waves at all), and 182 patients had significant bilateral signal changes. After 6 months of CPAP, hyperviscosity was normalized in 159 patients. In 112 of these 159 patients a repeat AEP became normal. Of the 80 patients on CPAP that did not normalize, hemodilution therapy resulted in normalization in 61 patients. Hemodilution is when blood is made thinner by removing some blood and adding some saline.

This paper talks about bilateral conditions but also brings up the possibility of unilateral sudden sensorineural hearing loss being explained by this mechanism. It’s in line with my personal observation that every patient that I see with sudden sensorineural hearing loss has a history and exam consistent with an underlying sleep-breathing disorder. The handful that agreed to undergo sleep studies showed significant obstructive sleep apnea in all cases. I think the implications of this paper are enormous.

Sleep Doctors vs. Patients: CPAP Data Monitoring

It’s common knowledge that one important way of increasing effectiveness of CPAP therapy is to constantly monitor the data that the machine records, which includes time used, lead rates, effective AHI, and other variables. Traditionally, this data is somehow taken to or transmitted to the patient’s sleep medicine doctor who analyzes the data to monitor compliance and effectiveness, in light of how the patient is doing. 

 

There’s been a growing movement amongst CPAP users to analyze their own data, and some people are even changing their own pressure settings. What I’ve noticed is that these are the most committed users, willing to do anything to get a better night’s sleep. In many cases these people know more about their xPAP machines than the DME vendors (durable medical equipment) or even their sleep doctors. Patients will know all about the latest xPAP models and try new mask models, in many cases paying extra beyond what insurance pays for.

 

There are many vocal arguments for and against this type of self-monitoring, but the issue I want to bring up is a sense that not all, but many sleep doctors are reluctant to have the patient take an active part in monitoring their own therapy. They’re not being told to go elsewhere, but the essential message that patients seem to hear is, "if you do this, you’re on your own." DME vendors are also caught in the middle.

 

Sleep doctors argue that self monitoring is good, but changing pressures should always be done after consulting the treating physician, since improper pressure can lead to problems such as ineffectiveness or even central sleep apnea. Patients argue that they should be able to manage their own condition for the most part, like what a diabetic does. 

 

There’s no black or white issue here—there are some patients that are fully capable and responsible enough to do this on their own, and others that are not. An ideal situation is to have a system in place where patients that want to take more responsibility can do so without feeling like they’re being frowned upon. This takes extra effort on the part of the sleep doctor and a trusting relationship with good communication. 

 

If you’re a CPAP user, where do you lie along this continuum? How much extra effort do you take to maximize your results?

 

Sleep Apnea Can Cause Brain Damage

A recent review of the literature in the Journal of the American Dental Association concluded that episodes of hypoxia (low oxygen levels) due to sleep-breathing problems can lead to permanent brain damage, and can even occur in early childhood. These findings are not too surprising, with a number of studies in recent years that support this finding. What’s troubling, however, is that no one is making the possible connection between brain injury due to sleep apnea and other well known neurologic conditions such as ADHD and Alzheimer’s.

Numerous studies have shown that sleep apnea patients have more areas of injured or dead brain tissue than patients without sleep apnea. This can occur in the gray and white matter (which serve memory and cognition), and even in the lower areas that control breathing, sensation and movement. One sleep researcher at a meeting that I went to many years ago stated that in young children who undergo tonsillectomies for obstructive sleep apnea, they catch up pretty dramatically in terms of cognition, memory, reaction times and intelligence scores. But they never catch up fully with age matched control children that don’t have obstructive sleep apnea. What this implies is that there may be a slight, but permanent brain injury.

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