Alzheimers dementia

Critical Links Between Sleep Apnea, Deep Sleep and Dementia

February 7, 2015 by James Bogash

sleep apnea and dementia — karuka/Dollar Photo Club

Hundreds of millions of dollars are spent on dementia research annually. While many may not like my opinion, I think we’re throwing this money away.

To date, we have had very little in the way of a “cure.” The research dollars continue to hit dead ends.

Here’s the problem. By the time that someone is diagnosed with a neurodegenerative disorder, it is likely that he or she has already lost a large chunk of the dopaminergic cells of the substantia nigra (Parkinson’s) or the cells of the hippocampal region and the neocortex (Alzheimer’s dementia). In these patients, the loss of brain cells has been going on for decades. DECADES.

The process is a freight train going.

I do not think we will ever be able to stop this freight train. Slow it down maybe: studies on coenzyme Q10, magnesium, exercise and ginko biloba have demonstrated the ability to slow the progression of neurodegenerative disorders.

One thing, however, is very, very clear.

Prevention is possible. We now have very clear cut risk factors for Alzheimer’s dementia. And the vast majority of them are modifyable. Very modifyable. Smoker? Quit. Don’t exercise? Start. On your way to diabetes? Change your diet and exercise. Too much brainless TV? Shut it off and challenge your mind.

This particular study adds yet another preventable risk factor to the list.

Sleep. And lack of it.

And not just the take-a-pill-so-you-can-sleep sleep, but good quality, slow-wave sleep (SWS, non-REM stage N3). Ironically, some drugs that you may take to help you sleep are actually interfering with your ability to hit the SWS stage of sleep. Drugs like fluoxetine (Prosac) and paroxetine (Paxil) have been shown to interfere with SWS sleep.

Researchers looked at a group of 167 Japanese American men in Honolulu, HI who were followed until their death and had their brains examined at autopsy. Specifically, researchers were looking for signs of brain damage associated with cognitive loss and Alzheimer’s (Braak stage, neurofibrillary tangle and neuritic plaque counts, microinfarcts, generalized brain atrophy, lacunar infarcts, Lewy bodies, neuronal loss and gliosis in the locus ceruleus).

This brain damage was then compared to the results of a sleep study (polysomnography) done at the beginning of the study. Here’s what they found: and died through 2010 (mean 6.4 years to death). Polysomnography measures included the apnea-hypopnea index, duration of apnea or hypopnea, duration of hypoxemia, minimum oxygen saturation (SpO₂), duration of slow-wave sleep (SWS, non-REM stage N3), and arousals.

Sleep duration with oxygen saturation levels (SpO_{2) less than}95% was associated with a whopping 388% higher levels of microinfarcts (small strokes).
Greater SWS duration (in other words, better deep sleep) was associated with less 68% less atrophy in the brain.
Lewy bodies were 83% less common in those who had more sleep at 95% oxygen saturation or more.
Higher minimum oxygen saturation during REM sleep was associated with less gliosis and neuronal loss in the locus ceruleus (in English–less inflammatory cells and less dead brain cells were found in the region of the brain stem that deals with stress and our ability to respond to stress).
Cognitive scores declined less among men with greater SWS duration.

These are some pretty serious associations. And it all fits into the picture of what we already know. Prediabetes and diabetes are very closely associated with cognitive loss, dementia and Alzheimer’s. Prediabetes and diabetes are also closely associated with sleep apnea. So it just makes sense that sleep apnea and poor quality sleep would be linked to brain damage.

Brain damage.

That sounds serious. AND, it sounds like it’s finally time to go get that sleep study done and find out if you need to be using a CPAP or BiPAP machine. Your brain will thank you.

Brain Damage in Epilepsy—Can it be Avoided?

January 16, 2015 by James Bogash

brain damage in seizures — abhijith3747/Dollar Photo Club

I don’t need to go into how epilepsy is a condition not limited to the brain, because I have covered this many times in the past.

This is also just one of the areas where migraines and seizures have similarities—migraines are also a brain condition that is not limited to the brain. Both are an indication that something is very, very wrong.

All of the evidence points to an underlying problem with the way the brain cells are able to produce and use energy. This problem is referred to as mitochondrial dysfunction (which just so happens to be one of my favorite phrases and, coincidentally, the root of all that is evil in chronic disease…).

In seizures, this problem generating energy leads to the brain cells firing before they are supposed to fire, resulting in a domino effect on other brain cells, producing the uncontrolled brain firing of a seizure.

In migraines, it is unclear whether the mitochondrial dysfunction creates the headaches by affecting the way blood vessels react in the brain, or whether a problem with the way blood vessels react (called flow mediated dilation) starves the brain for the nutrients it needs to generate energy. Luckily, the lifestyle changes for both conditions are the same.

Regardless, researchers seem to agree that there is a serious problem with the blood vessels in both migraines and seizures. Ultimately, blood vessel problems play a role in dementia and Alzheimer’s disease as well.

To clarify what I mean by “blood vessel problems,” you need to understand that your blood vessels are very dynamic. They expand and contract as needed based on signals they get from the cells they feed to provide nutrients. As an example, if you took a racquetball and started squeezing it repeatedly, the muscles cells in your hand and wrist will quickly need more nutrients to continue. As a result a signal is sent to the blood vessels of the arms, causing them to dilate (open) and increase blood flow into the forearm and hand.

Picture this same action in the brain. When the brain cells in an area need more oxygen, glucose or micronutrients, blood flow to this area of the brain increases. No imagine if the blood vessels were no longer as responsive. You end up with starving brain cells. Not a good scenario.

With this as background, I’d like to throw this particular article into the mix. In it, researchers reviewed the dangerous relationship between blood vessel function and damage and cognitive decline. They open with identifying findings that are common between chronic epilepsy, Alzheimer’s dementia and age-related cognitive decline. These include:

Increased plaquing in the carotid arteries (CA–IMT)
Elevated homocysteinemia levels
Lipid abnormalities (cholesterol, triglycerides, VLDL, low HDL, etc…)
Weight gain and obesity
Insulin resistance / prediabetes
High levels of inflammation
High levels of oxidative stress

All of these factors wreak havoc on blood vessel health. Poor vessel health not only damages the brain cells that it feeds, but the long-term dysfunction in the blood vessels ultimately damages the blood vessels themselves, leading to hardening of the arteries, making the starvation of the brain cells permanent.

All of this damage to the blood vessels lead to brain damage. The authors note a few of the well-accepted brain changes as a result of this damage. These include:

Decreased volume of the hippocampus (an area also shrunk by chronic stress and one of the areas that are damaged in Alzheimer’s dementia)
Increased cortical thinning of the frontal lobe (the area of the brain that deals with personality).
Ventricular expansion and increased white matter ischemic disease (a sign of brain cells dying)
Total brain atrophy (basically a shrinking brain)
β-amyloid protein in the brain (one of the principle proteins found in the brains of Alzheimer’s dementia patients)

If you’re still reading this far, then you now understand just how critically important it is to go beyond seizure control to making whatever lifestyle changes you need to make. A true anti-seizure treatment protocol needs to include a lifestyle that is anti-diabetic and anti-heart disease. Luckily, these lifestyles are pretty much the same.

And you may find that, once you have adopted a healthier lifestyle, your seizures will also improve. You’ve got nothing to lose.

Except your brain cells.

Protecting Your Brain from Dementia One Supplement at a Time

January 13, 2014 by James Bogash

While teasing one another that we’ve lost our mind may be funny, the literal experience of losing your mind to dementia is not likely as entertaining.

However, the rates continue to increase at a startling rate and no hope is in sight for a cure. Some pharmaceutical companies have even given up the fight to find a cure because the failures have been too expensive.

The ability to prevent dementia with lifestyle, however, is very solidly proven in the medical research. This may include higher education (or, in lieu of a degree, continual challenging your brain by reading this blog several times through on a daily basis), exercise, a plant based diet and maintaining an anti-diabetic lifestyle.

Personally, I do not feel that we will ever find a cure for Alzheimer’s dementia or Parkinson’s disease (the other neurodegenerative disorder that shares many of the same underlying damage to the brain). By the time a diagnosis is made, the brain has lost a very large chuck (upwards of 70%) of the cells in the affected region. In other words, it’s a freight train moving at a high rate of speed.

I do, however, believe that we can slow the freight train down, even if it’s just a little bit. Antioxidants like CoQ10, magnesium threonate and n-acetyl cysteine (NAC) may play a role here. Another very powerful antioxidant for the brain is vitamin E.

I have an entire eBook dedicated to vitamin E (that can be found by clicking here) and the benefits it has been shown to have on the heart and brain. This particular study supports vitamin E’s ability to protect the brain yet again and compares it to the effects of memantine (aka Namenda—one of the newest classes of drugs used to treat Alzheimer’s dementia). Here are the details:

Researchers looked at 613 patients with mild to moderate Alzheimer’s dementia who were already taking drugs for Alzheimer’s dementia (acetylcholinesterase inhibitor).
Participants took either 2000 IU/day of alpha tocopherol, 20 mg/d of memantine, both of these or a placebo for an average of 2.27 years.
ADCS-ADL (Alzheimer’s Disease Cooperative Study/Activities of Daily Living) scores declined by 3.15 units less in the alpha tocopherol group compared with the placebo group, who showed greater declines in the scores over the time of the study). This corresponded to 19% slower decline, or about 6.2 months delay in cognitive decline.
Caregiver time increased the least in the alpha tocopherol group (about 2 hours less).

While these changes aren’t life altering, this is still a very powerful advantage from something as simple, safe and inexpensive as vitamin E. I must, however, interject that the form used here, alpha-tocopherol, is definitely not the most potent of the vitamin E family to be using to protect your brain. This honor goes to gamma-tocopherol, the form of vitamin E found more often in nature (such as in nuts and seeds).

It makes me wonder just how much stronger the results of the study would have been had the researchers used a mixed tocopherol product high in gamma tocopherol…

Alzheimer’s Dementia: Forget a Cure and Move on Prevention

December 12, 2013 by James Bogash

The loss of the mind when the body is still intact is a difficult thing. Fear of dementia is universal.

Much like every other chronic disease we know of, countless dollars are poured from the private sector, the government and the drug companies to find that miraculous cure. For a time, the spotlight was on therapies to use the immune system to destroy the amyloid plaques that accumulate in the brains of those with dementia, but this pathway has borne no fruit. As a result of this failed endeavor, many of the drug companies trying to find a cure based on the amyloid protein have halted funding in this direction.

Meanwhile, for over a decade there has been strong evidence about lifestyle habits that can protect your brain from Alzheimer’s dementia. Over a decade of blocking the information on how incredibly protective lifestyle can be for Alzheimer’s dementia. Even the Alzheimer’s Association website has nothing on the homepage about prevention. You would think that there is no way to prevent Alzheimer’s disease.

This couldn’t be further from the truth. The list of protective factors is quite long and beyond the scope of this post, but you can begin to read some of these by clicking here (hint: exercise alone has been shown to lower risk some 90%).

All of this leads to this particular article. In it, Dr. Gandy basically reviews the current evidence on Alzheimer’s, both in the realm of treatment and prevention. He notes that the FDA is now leaning towards therapies that will lower the risk in those known to be at high genetic risk. The hints of an answer from clinical trials will begin to be seen as early as 2018.

2018?? Some 20+ years after the research began to emerge on how to prevent Alzheimer’s dementia we’ll begin to admit that we can prevent it? There are times that I’m sure the medical research I review and comment on is available to me and me alone and no other researcher or clinician has access to it. How else could we remain so incredibly disconnected?

Either way, don’t wait another 20 or more years. We already know that damage to the brains of the children of Alzheimer’s patients begin to show up decades earlier than anyone thought. If you have a close family member that has been diagnosed with Alzheimer’s, the 20+ year lag is going to be too late for you. You need to start now.

Worried About Alzheimer’s Dementia or Parkinsons? You NEED to Add This

May 24, 2013 by James Bogash

With any chronic condition such as Alzheimer’s dementia, whether talking about prevention or treatment, I never advocate a one disease: one cure model. The natural approach necessitates a complete lifestyle change. This is where the power of lifestyle comes in–the benefits of hundreds of positive choices adding together to produce a massive improvement.

I have certainly addressed the mitochondrial dysfunction model of neurodegenerative disorders in previous blog posts and will not go into this model in detail here (although previous blog posts on the topic can be read by clicking here). However, it can be summarized by saying that anything that helps with the way your brain cells make energy is good while anything that harms the way your brain cells make energy is bad. Too much of a loss in the ability of your brain to make energy and you start to lose brain cells. While we can all tolerate the loss of a few here and there, too many brain cells lost can lead to the diagnosis of Alzheimer’s dementia or Parkinson’s disease.

Antioxidants clearly benefit our brain and protect the mitochondria within your brain cells, and thus, in general, will lower your risk of developing neurodegenerative disorders. Antioxidants can come internally, such as cellular made coenzyme Q10 (CoQ10) or the enzymes superoxide dismutase or glutathione peroxidase, or they can come from the foods you eat or what you drink. Examples can include:

Vitamin E (ONLY as mixed tocopherols)
Coenzyme Q10 supplements
Coffee or tea
Other phytonutrients (the thousands of compounds that make up the colors, scents, smells and tastes of the plant world)

Some phytonutrients are more potent than others, which brings us to this particular study.

Researchers looked at a mouse model of Alzheimer’s disease to see how well an extract from pomegranates could halt or slow the progression of the disease. The results were pretty good in the group of mice prone to the formation of amyloid plaques (like those seen in Alzheimer’s dementia) given the pomegranate extract compared to the same type of mice not give the extract:

The pomegranate feeding shortened the distance it took for the mice to get out of a maze.
The extract group had less inflammation in the brain (based on TNF-alpha and NFAT levels).
The pomegranate fed group had less “turning on” of the immune system in the brain (termed microgliosis).
The pomegranate group had less amyloid plaque formation.
2 polyphenol components of pomegranate extract, punicalagin and ellagic acid, seemed to do the bulk of the work.

Overall, while this was a mouse study, the results were pretty strong in suggesting that the mere addition of a pomegranate extract was able to protect the brain in multiple ways from the Alzheimer’s progression.

As always, you should never follow a one-cause, one-cure model, but a sip or two of pomegranate juice may not be a bad idea. Better yet, as the summer rolls around I’ll be able to pick my own pomegranates from my backyard trees and eat the seeds directly.

I’m sure my brain will thank me.

Powerhouse Vitamin Plays Role in Alzheimer’s Dementia Diagnosis

March 7, 2013 by James Bogash

As far as I’m concerned, the medical dementia research strongly points to an oxidative stress/mitochondrial dysfunction model of neurodegenerative disorders like Alzheimer’s dementia and Parkinson’s disease. The idea that we really don’t have any idea what causes it is just not true.

The likely reason why mainstream medicine hasn’t accepted this model is because it puts much of the responsibility smack dab in the middle of the patient’s lap. Genetics play a role, but it’s likely a small one. Lifestyle is key to both preventing and causing Alzheimer’s dementia.

Pivotal in prevention is protecting my favorite organelle, the mitochondria. This little factory within each of our cells generate energy in the form of ATP. (Are we dredging up bad memories from high school biology yet?) Since brain cells require extremely high amounts of energy, the mitochondria are critical for your brain cells to function correctly. Not enough energy in the brain cells and they begin to break down and, when things get bad enough, your brain cells commit suicide (a process called apoptosis).

Too many suicidal cells in the neocortex or hippocampal regions of your brain and you begin to develop what we call Alzheimer’s dementia. Unfortunately, by the time symptoms are noticed, the condition has been progressing for decades and a very large chunk of the brain cells in this region are already dead.

So how can we protect our brain from this suicidal pathway?

In two ways.

The first is to stop abusing the mitochondria in our brain cells. The list of items that damage our brain is quite long, but should not drop any jaws. Here are a few of the more dangerous risks:

After you’ve cleaned up the mess, the next thing to focus on is aspects of lifestyle that are well know to protect the brain. The general recommendations that I promote for all chronic diseases remains the same and can be found by clicking here. Besides lifestyle, there are numerous supplements that have some pretty good support for protecting the brain. These include:

However, there is another strong player. Vitamin E.

And not your normal, run of the mill, cheap vitamin E supplement. Vitamin E is actually a combination of 8 different forms–4 tocopherols and 4 tocotrienols. Nature provides us with these multiple forms of tocopherols and tocotrienols. Any good supplemental form of vitamin E is going to have a this mix of all 8 forms. Giving high levels of just one form of vitamin E can actually drive down levels of other forms of vitamin E in the bloodstream.

Vitamin E, as a blend of all 8 forms, is very protective to our body, especially the heart and blood vessels. And if you protect your blood vessels, you’re protecting your brain.

But just how protective is it??

You might want to sit down for this one, or if you’re driving, pull over (actually…you shouldn’t really be driving trying to read this anyway..).

Diagnosing Alzheimer’s using a MRI alone is not without its problems and faults. Currently, it is not used as a sole measure to make the diagnosis. In this particular study, researchers looked at what happened when they added blood levels of these 8 vitamin E forms to an MRI for differentiating Alzheimer’s dementia from cognitive impairment from normal brains. Here’s what they found:

MRI and plasma vitamin E measures increased accuracy to 98.2% for differentiating Alzheimer’s dementia from normal brains.
For telling mild cognitive impairment from normal brains, the accuracy was 90.7%.
In addition, also identified 85% of individuals with cognitive loss who converted to Alzheimer’s dementia at 1 year follow-up (Tweet this).

Basically, the serum levels of the vitamin E family made the MRI diagnosis far more powerful, especially when it came to predicting who was going to progress to full blown Alzheimer’s dementia. Isn’t your brain worth a little vitamin E? Plan on spending $15-20 / month. Do NOT buy the cheap forms with only alpha tocopherol–it may make things worse.

Parents With Dementia? This May Be Happening in Your Brain

June 29, 2012 by James Bogash

It may be generations before rising rates of Alzheimer’s dementia and Parkinson’s rates will stop increasing. One of my pet peeves in the average medical practice today is that we continue to remain decades behind research. It is this delay that will keep the next generation from avoiding Alzheimers dementia.

Why is this? Because it is very clear that the damage to the brain that occurs in Alzheimer’s and Parkinson’s begin decades before symptoms appear. For Parkinson’s, we know that, by the time symptoms are present, 70% of the brain cells in a specific region of the brain have died. 70%.

That means that, in anyone who has had a family history of these neurodegenerative conditions, there is a high likelihood that damage has already begun.

So, while patients I have come across who have this family history and are concerned about also developing the disease, none understand that the process has already begun.

Hopefully, this particular article will make this a little more clear. Basically, researchers looked at the hippocampal region of the brain (the area principally affected in Alzheimer’s) and found that this region had begun to atrophy (shrink).

Even more to the point, the brain had begun to shrink WITHOUT any cognitive loss. Clearly, the damage was already occurring, but it would yet be years before symptoms are evident.

If you have a family history of Alzheimer’s, or if you do not want to be the one to start the family history in your family tree, changes need to start now. These changes have been addressed in prior posts and can be viewed here.

In the meantime, if you have a family history of Alzheimer’s, have you been told that your brain may already been at risk?

Drug to Lower Cholesterol Drug Can Destroy Your Brain

June 27, 2012 by James Bogash

I’ll admit it. I’m no fan of drugs to lower cholesterol. 30+ blog posts on the topic should convict me. But linking statins to dementia is new news even to me.

To understand this association, there are two things you need to understand.

First, statins like Lipitor, Crestor and Zocor block an enzyme called HMG-CoA reductase. This is the enzyme that produces cholesterol in our bodies. However, this enzyme also produces a tiny little compound called Coenzyme Q10.

You may have heard of CoQ10 before because it is absolutely essential to make energy in every one of our cells. CoQ10 has been shown to play a role in various chronic diseases and conditions. They may include:

The other factor to understand for this post is that Alzheimer’s disease is associated with the presence of two abnormal proteins in the brain, called neurofibullary tangles (NFT) and amyloid plaques (AP) made up of tau proteins. It is pretty clear that these proteins are the result of damage to the brain, rather than creating the disease.

So, we can understand that anything that increases the production of tao protein is probably not a good thing.

By now, you can probably guess what prescription medication was shown to increase the production of tao protein in this particular study.

Yep.

The statin class of drugs was shown to increase the presence of tao protein. If you combine this fact with the well accepted fact that statins reduce blood levels of CoQ10 and CoQ10 plays a distinct role in Alzheimer’s disease progression, you can see a serious problem here.

The bottom line? Lowering your cholesterol with statins may make your cholesterol levels look better, but the list of problems this class of drugs contributes to get longer all the time. This leaves lifestyles changes as the only viable option.

If you are taking statins to lower your cholesterol, tell me some concerns you may have over the long term damage that may be occurring…