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Does Having Sleep Apnea Prolong Life in the Elderly?

Here's a twist to the typical story about sleep apnea you don't see every day. A prominent sleep researcher in Israel discovered that elderly people with mild to moderate obstructive sleep apnea where less likely to die than their counterparts who didn't have sleep apnea. Their explanation is that years of hypoxia promoted increased collateral blood supply, meaning that the heart developed blood vessels that bypassed blockages. This explanation was supported by a recent German study which found similar results.

 

On first thought, it makes sense. When younger, since you don't have time to develop collateral blood vessels, you're more likely to die if you suffer a heart attack. The incidence of sleep apnea may increase as you get older, but the rate of death could go down as one gets older.

 

I wonder if chronic hypoxia in the brain causes similar protective effects. Since we know that hypoxia causes plaques that are similar to what we see in Alzheimer's, the answer is probably no. If you live long enough to beat obstructive sleep apnea, then is it more more likely you'll develop dementia?

 

What do you think about this study?

Sleep Apnea, Migraines and Multiple Sclerosis: Is There a Link?

It seems like study after study is published that links two previously unlinked conditions to one another. In this study, the presence of migraines was associated with a 47% increased risk of developing multiple sclerosis (MS) later in life. Researchers again point to a genetic wastebasket explanation, with no practical implications. In a previous post, I noted that MS was linked to heart disease. Since we know that Alzheimer's is linked to heart disease, why can't migraines be linked to heart disease or even Alzheimer's? Ultimately, if you connect all the dots of all the associations between various medical conditions, then almost every medical condition can be linked in one way or another. 

 

My sleep-breathing paradigm easily explains the link between migraines and MS via the following mechanism: Migraines are a common symptom of poor quality sleep due to an inability to breathe properly at night. By definition, all modern humans are susceptible to these events, where only the extreme end of the spectrum is called obstructive sleep apnea. If you're not able to sleep deeply, then your entire nervous system is hypersensitive, causing an over-reaction to your senses, leading to symptoms such as headaches, TMJ, sinus pain and pressure. 

 

MS is thought to be an autoimmune condition with flareups of inflammation and "plaques" in any part of the brain that are seen on MRI. Sleep apnea is known to cause not only chronic sympathetic nervous system overload, but also thickening of the blood with patients being prone to either diminished blood flow or small microscopic clots in the brain. Studies have shown that sleep apnea patients have multiple areas of decreased gray matter density in various parts of the brain. This could in theory lead to either "lesions" in the brain, neurotransmitter abnormalities, or hormonal dysfunction.

 

It makes sense that in people who have sleep-breathing problems long before they go into sleep apnea, their nervous systems are overly active (waking up too quickly), whereas sleep apnea patients' nervous systems are underactive (not waking up quickly enough). Chronic low-grade stress is also known to upregulate your immune system, leading to the classic autoimmune conditions that are often seen in people with upper airway resistance syndrome (cold hands, anxiety, fatigue, etc.). 

 

Rather then reducing human illnesses down to genetic factors or biochemical deficiencies, it makes more sense to treat the patient as a whole person. But with modern medicine, that's not allowed. Yes, there has to be progress in medical research, but as a whole, are we going in the wrong direction? I'd like to know your opinion on this issue. Please enter your opinion in the comments box below.

Sleep Apnea, Concussions and Dementia in the NFL

There's been a lot of media coverage recently about the high incidence of dementia in retired NFL pros. One report using a phone survey of retired NFL players revealed that the incidence of dementia or memory-related problems was 19 times higher than normal for men ages 30 to 49. Repeated head trauma is thought to create conditions that significantly increases the chances of developing dementia. A number of states are even enacting legislation that sets certain criteria for removing high school football players after any head injury with prompt and proper medical evaluation.

While these concerns are legitimate, I think the NFL officials are missing a very important piece of the puzzle, and that's the very high incidence of obstructive sleep apnea in current and retired pro football players. One recent Mayo Clinic study showed that 60% of all retired linemen and 46% of all other positions were found to have significant obstructive sleep apnea. Amongst active players in 2003, the overall numbers were 14% and 34% with linemen.

 

If you look at what happens to the brain with repeated episodes of hypoxia during apneas, then you'll see that the implications are profound. Untreated patients with sleep apnea are found to have multiple areas of dead or non-functioning brain tissues. Another similar study showed multiple areas of microscopic strokes, called lacunar infarcts. Chronic hypoxia in mice resulted in brain biopsy studies revealing amyloid plaques (similar to what we see with Alzheimer's disease). 

 

So with this logic, it makes sense that repeated concussions in someone with untreated obstructive sleep apnea is more likely to suffer from the cumulative effects of head trauma compared with someone without sleep apnea. As with everything else in medicine, diseases never exist alone in a vacuum. It would be interesting if they did a study looking at the incidence of obstructive sleep apnea in these ex-players with dementia. I'm willing to bet a very high percentage will have undiagnosed obstructive sleep apnea. Another, more costly and ambitious study would be to screen all current NFL players for sleep apnea and follow them for years (or decades) while undergoing proper treatment, measuring their rate of progression to developing dementia. 

 

What do you think about this issue? Should be continue treating medical conditions in isolation, or look at other co-morbid conditions that can aggravate the original diagnosis? Please enter your comments in the text area below.

Sleep Apnea, Leptin, and Alzheimer’s Disease

One of my major goals on this website is to "connect the dots" between cutting edge health research findings within the context of my sleep-breathing paradigm.

 

Here’s another not-too-surprising study about Alzheimer’s: that high levels of leptin is associated with lower rates of Alzheimer’s disease. Leptin is a hormone that’s produced by fat cells which tells your brain that your stomach is full. Over 12 years of follow-up in 785 elderly people, those with the lowest level of leptin were about 4 times more likely to develop Alzheimer’s disease than people with highest levels.

 

The study authors speculate that further research on supplementation with leptin could lead to promising new treatment options for Alzheimer’s in the future. 

 

If you step back and look at this study through the lens of my sleep-breathing paradigm, it makes perfect sense. We know that having obstructive sleep apnea makes you much more susceptible to microscopic clots and strokes in the brain, and it makes your blood thicker and more prone to stagnation and clotting. People with untreated obstructive sleep apnea are found to have multiple areas of dead or nonfunctional brain tissue. The end result is the accumulation of amyloid plaques. 

 

We also know that the physiologic effects of obstructive sleep apnea causes your leptin levels to drop (in addition to lowered levels of thyroid hormone), making you more hungry and more prone to gaining weight. Weight gain, narrows your throat even further, aggravating even more obstructions and arousals, leading to even more clots. 

 

I guarantee that you’ll continue to see many more studies associating other biochemical markers to Alzheimer’s. There are probably thousands if not millions of events that occur in the inflammatory cascade that begins with simple breathing pauses while sleeping. It’s easy to link through research any two points within this cascade, but by doing so, you’re missing the forest entirely. 

 

Can Sleeping Too Long Cause Dementia?

Alzheimer’s Risk Increased with Modest Cholesterol Elevation in Middle Age

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?

 

 

 

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.

The Value of Genetic Testing in Alzheimer’s

ABC News’ Terry Moran wrote a poignant piece on why he decided to get tested for the gene that carries markers that are linked to Alzheimer’s disease. He states that he has a strong family history of Alzheimer’s and wanted to take the test not only to know more about his future health, but also to take responsibility for his own health. He does state that this test does not definitively predict whether or not he will get Alzheimer’s. It only gives statistical information based on his innate genetic risks. It ends up that he has a 19% chance of getting Alzheimer’s. It’s about 10% greater than the average population.  

Alzheimer’s is a devastating disease, not only for the patient, but also for the immediate family members. Research so far has focused on the molecular and genetic mechanisms, with progress being made day by day. However, I can’t help but to wonder if we’re going about this the wrong way. 

 

Let me explain: We know that Alzheimer’s is linked with cardiovascular conditions such as heart disease, heart attack and stroke. Untreated obstructive sleep apnea is a major risk factor for developing heart disease and significantly increasing your risk for sudden cardiac death and stroke. Sleep apnea is something that you don’t just develop when you’re older—you’ve had some degree of it all your life. 

 

Recent sophisticated imaging studies have revealed a much higher incidence of multiple areas of brain injury or damage in people with untreated sleep apnea compared with normals. MRIs in people with sleep apnea show many more areas of "lacunar infarcts," or small areas of strokes. Rats with the Alzheimer’s gene that were subjected to chronic hypoxia were found on autopsy studies to have very similar histologic findings as in humans with Alzheimer’s. We also know that chronic hypoxia and inflammatory state that results from sleep apnea can cause microscopic areas of blood vessel clotting (rather than your more typical large vessel stroke). The authors of some of these studies were very careful in only alluding to the implications of their findings: That obstructive sleep apnea can lead to Alzhiemer’s. 

 

I’m not discrediting all the great research out there on Alzheimer’s, but at least consider the possibility that in some cases of Alzheimer’s, untreated obstructive sleep apnea can lead to Alzheimer’s, with the same clinical symptoms, biochemical and histological changes that are seen in classic Alzheimer’s patients. 

 

Mr. Moran is more likely to know about his future health if he screens himself for obstructive sleep apnea, rather than undergo genetic testing for Alzheimer’s. At least there’s something you can do about sleep apnea.

 

(See related article by guest columnist Dr. Mack Jones.)

 

 

Can A Sleep Problem Give You Alzheimer’s?

There’s been a lot of press recently about the side affects that poor sleep quality has on our cognitive functioning not to mention what it means for those who suffer from neurological problems like Alzheimers.

This month, our expert article is contributed by noted neurologist and author of Deadly Sleep, Dr. Mack Jones, who explains the reason why he thinks everyone who has Alzheimers or is at risk for this problem should get tested for a sleep breathing problem like OSA.

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 Is it possible that Obstructive Sleep Apnea (OSA) causes Alzheimer’s Disease (AD)? I believe so. As a retired clinical neurologist and former patient with Obstructive Sleep Apnea, I have a special interest in sleep disorders medicine. I am thoroughly convinced of the connection between OSA and AD and will remain so until credible studies prove otherwise. Numerous short term studies have been done on cognition (mental processes) and sleep or the lack thereof, but there are few or no long term studies to determine OSA’s relationship to Alzheimer’s Disease (AD) and/or the other dementias.

Many polysomnograms (PSGs) or in lab sleep tests have been done on patients with AD revealing an incidence of OSA of up to seventy to ninety percent.  The assumption has been that AD causes OSA, or they just happened to coincide, but I contend that OSA is the cause of AD.

There are no studies that either prove or disprove my hypothesis that long standing undiagnosed OSA is a cause of AD, but evidence is accumulating. For example, OSA is a recognized risk for Type 2 Diabetes. In the April 2008 issue of The Archives of Neurology, type 2 Diabetics had an increased risk or developing Mild Cognitive Impairment (MCI)(1) which is the earliest stage of dementia.  Fifty to sixty percent of patients with MCI progress to AD at rate of twelve percent per year.
 
Additionally, OSA is a known risk for the development of high blood pressure.  Like patients with Type 2 diabetes, those with high blood pressure were also found to have an increased risk of developing MCI.(2)  Since the majority of patients with MCI eventually progress to Alzheimer’s Disease at a rate of approximately twelve percent per year, then it’s not a stretch to conclude that OSA is a cause of Alzheimer’s Disease.
 
In 2006 a study in the Proceedings of the National Academy of Sciences showed low brain oxygen (hypoxia) raises Alzheimer’s risk in the mouse brain with a genetic susceptibility.(3) A group of mice with an Alzheimer’s gene were given a maze test in which they all performed normally. They were separated into two groups, one exposed to 16 hours of a reduced oxygen environment (hypoxia) daily for several weeks; the other group in a normal environment.

The maze test was repeated and revealed the hypoxic mice performed poorly, whereas the control groups performance remained normal as before. All the mice were sacrificed and their brains examined under the microscope. Plaques and neurofibrillary tangles typical of Alzheimer’s Disease were present in the hypoxic mouse brain specimens, whereas the controls were normal. According to investigators, the study suggests that preventing brain hypoxia (as occurs in OSA) may reduce the risk of developing Alzheimer’s Disease.
 
Reported in the June 27th issue of Neuroscience Letters, sleep apnea patients have shrunken brain structures called “mammillary bodies” involved in memory according to Rajesh Kumar, PhD and colleagues from the University of California at Los Angles (UCLA).  High resolution MRI brain scans revealed mammillary bodies to be twenty percent smaller in patients with sleep apnea than in normals.  “These findings are important because patients suffering from memory loss from other symptoms, such as alcoholism or Alzheimer’s Disease, also show shrunken mammillary bodies,” Dr. Kumar said in a press release.
 
A recent study form San Diego showed that Sleep Disordered Breathing, including OSA, is and important risk factor for cognitive impairment in older women. (4)

Neuroimaging studies have been performed on patients with OSA including CT, MRI. PET and SPECT scans, revealing a variety of defects, but none has displayed anything quiet as dramatic as in a study published in SLEEP July7, 2008, by Dr. Paul M. Macey et al. (5)  The report reveals results of a new MRI technology called DTI (Diffusion Tensor Imaging). It is an extremely sensitive method of determining damaged nerve fibers (axons). This new imaging technique reveals multiple areas of brain damage in OSA patients not known to exist until now. DTI revealed various sized color-coded yellow-orange patches of brain damage scattered throughout the brains of a group of forty-one men and women subjects with OSA. Their ages ranged from thirty-eight to fifty two years old and they had not yet been treated. The areas of nerve fiber injury were wide-spread, located in critical regions of brain including prefrontal, temporal and parietal lobes. The cerebellum and brainstem were equally involved. This is the first report of DTI imaging of a group with OSA to my knowledge. The findings have far-reaching implications.

One can anticipate finding even more areas of damage in an older population as studies are done. What problems result from each one of these areas of brain damage?  It is possible that they are responsible for difficulties with cognition, mood, behavior, memory, heart regulation, high blood pressure, breathing control, fear, anxiety and other emotional disorders including depression? Those findings are yet to be reported. Could this brain damage eventually accumulate enough to cause Alzheimer’s Disease and/or the other dementias? 

The structural changes likely represent accumulated damage over sustained periods of time.  Are they permanent or do they improve or disappear with treatment?  No one knows yet, but my guess is they may improve to some degree or even resolve with treatment, but we will have to wait and see.
 
The implications of these findings are profound. Early treatment of OSA could potentially prevent the development of Alzheimer’s Disease. Now is the time to wake up the public and our snoozing medical community and put an end to this disease.

References:

1. José A. Luchsinger, M.D. et al, Relation of Diabetes to Mild Cognitive Impairment, Arch Neurol. 2007; 64 (4):570-575.
2. Christine Reitz, M.D. PhD, et.al. Hypertension and the Risk of Mild Cognitive Impairment:, Arch Neurol. 2007; 64(12):1734-1740.
3. Xiulian Sun, et al, Hypoxia Facilitates Alzheimer’s Disease Pathogenesis By Up Regulating BACE1 Gene Expression. PNAS (Proceedings of the National Academy of
Sciences) 2006 | vol.103 | no. 49 |18727-18732
4. Adam P. Spira, et al, Disordered Breathing and Cognition in Older Women: Journal of the American Geriatrics Society. Volume 56, issue 1, January 2008, 45-50.
5. Paul M. Macey, et al, “Brain Structural Changes in Obstructive Sleep Apnea," SLEEP vol.32, Number July 7, 2008, 913-1056.

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After surviving his four year ordeal in search for a cure of his own sleep apnea, Dr. Mack Jones, a clinical neurologist, felt a need to pass on to others what he learned first-hand as a patient, so that you might avoid the pitfalls he encountered and possibly save your own life or the lives of your loved ones. Dr. Jones in his book, Deadly Sleep, expected publication date, June of 2009, discusses how this common sleep disorder is a likely cause of Alzheimer’s and possibly a host of other life threatening neurological diseases that may have been plaguing us for hundreds if not thousands of years. He can be contacted via e-mail by clicking here.
 

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