LifeCare Chiropractic

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Alzheimer's

OTC Meds Taken by 20% of Seniors Destroying the Brain

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anti-cholinergics and dementia
Africa Studio / Dollar Photo Club

Cold medicines, anti-depressants, sleep aids, asthma/COPD drugs. You assume they’re safe because they’re readily obtained in the corner drug store or given to you by your doctor.

The list we are concerned about here are the anti-cholinergic drugs and can include some names like Amitriptyline, Dramamine, Unisom, Advil PM, Benadryl, Wellbutrin, Detrol and many cough suppressants.  The side effect may include some short-term drowsiness.  But if you just refrain from driving after taking them you’ll be just fine.

If you’re brave enough, though, you may venture to the package insert and read about all the other nasty side effects you may experience.  Things like nausea, vomiting, excessive sweating and growing an extra limb are pretty common.  But you figure there’s always times when an extra limb would be helpful, so you’re not too worried.

But what if these all-too-common seemingly-innocent drugs are actually destroying your brain?

You know that I wouldn’t be posing the question unless it had something to do with this particular study.  In it, researchers followed 3,434 older adults (average age, 73 years) who did not have dementia at the beginning of the study for an average of 7.3 years.  Shockingly, 20% of the seniors in this study were taking some form of anti-cholinergic drugs.  That’s at least 10 people in a decent sized bingo game.

Researchers compared the total cumulative dosage of the drugs and the risk of developing dementia or Alzheimers.   They broke them into four groups depending upon the total cumulative dosage.  Cumulative being the key word here.  Even at very low dosages taken over the course of 3 years put most patients into the high risk category.  Here’s the specifics:

  • There was a 19% higher risk of developing dementia or Alzheimer’s at a dosage of 91-365 (think daily use for a year).
  • The risk was 23% for dosages of 366 to 1095.
  • At cumulative dosages greater than 1095 the risk was 54% higher.

The scary thing is that the dosage were CUMULATIVE.  As in adding it all up.  Even casual use  (twice a week for a year) can put you at an increased risk.  At the high end of the dosage, 1095 cumulatively over the course of 10 years is only daily use for 3 years or 2-3 times per week for 10 years.  And many of these drugs are for chronic use, putting many users into the at-risk category.

While the focus of this article is not to go into individual uses for the anti-cholinergic drugs and how they can be better managed without destroying your brain, you at least need to understand that, if you use any of these drugs on a regular basis, you may be putting your brain at risk.  While this study was done on a senior population, you can bet that damage is still occurring in a younger brain.

And, since you’ve only got one of them to use, I personally think you should do everything possible to protect what’s inside your skull.

 

Critical Links Between Sleep Apnea, Deep Sleep and Dementia

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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 (SpO2) 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.

 

Exercise, Memory, Depression and Your Brain; Great News!

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The list of things you can do to protect your brain and improve brain function is quite long, but there is one things that is always at the top.

Exercise.

There is absolutely, positively no doubt that exercise is incredibly important for your brain.  And this is regardless of what you are worried about or what you are dealing with.  Parkinson’s, Alzheimer’s, depression, anxiety, chronic migraine headaches, seizures, multiple sclerosis…

Sadly, this tool is brought into play far too seldom.  The second you walk into your neurologist’s door, the first question he or she should be asking is how is your exercise routine going. All too frequently medications are the only item of discussion.

How exactly exercise helps the brain is yet to be figured out, but it’s likely working by several mechanisms:

  1. Improved blood flow to the brain.  More blood flow means more nutrients and healthier brain cells.
  2. Release of the hormone irisin through exercise.
  3. Muscles use glucose.  More muscle means better glycemic control and lowered risk of diabetes.  Prediabetes and diabetes destroy the brain.

And probably several more ways that I can’t think of right now.  This particular article adds to the list.  In it, researchers looked at the effect of the hormone adiponectin on the brains of mice.

Adiponectin is a hormone produced by the fat cells in the abdomen.  This hormone is essentially an anti-diabetes hormone.  As I mentioned, since diabetes is so bad for the brain, it might make sense that adiponectin would have positive effects on the cells of the brain.

But the specifics are what were so surprising:

  • Adiponectin can cross the blood–brain barrier.  Higher levels in the brain increased the number of brain cells and decreased depression-like behaviors.
  • A deficiency of adiponectin, however, cut short the beneficial effects of exercise in increasing the number of brain cells in the hippocampus (the region affected by Alzheimer’s dementia).

Because researchers were using mice, they were able to modify the hormone levels.  But, in your own brain, these same effects can be achieved through a combination of living an anti-diabetic lifestyle and exercise.

The anti-diabetic lifestyle will increase the levels of adiponectin being released by your fat cells.  The higher levels of adiponectin will give you the best possible effects of exercise on your brain.  Specifically, according the this study, the hippocampal region of your brain will benefit.  This is the region that is heavily involved with memory.

So, if you are a migraine sufferrer, it is not exercise alone that is going to protect your brain and your memory.  Exercise needs to be coupled with an anti-diabetic diet to have the full effect on protecting your brain.

Want to avoid Alzheimer’s dementia?  Same story.

Depression?  Anxiety?  Same story.

Get the point?  You cannot change or improve one aspect of your lifestyle without making changes in other areas as well.  Anything less will not give you the full benefit.

 

Pre-diabetes and the Brain—You’re Losing Brain Cells as Your Read This

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Very few patients and providers are aware of just how damaging prediabetes is. Fewer still know that it destroys the brain.

Countless times, after looking at the patient, certain lab values, patient’s history and family history it is clear that this patient is on his or her path to diabetes.  Sometimes at a slow stroll, sometimes at a full-out sprint.  When I bring this concern up to the patient the response is frequently, “Oh…my doctor checked me for diabetes and said I was ok.”  Ugh.

I equate this to the cigarette smoker stating that his or her doctor checked for lung cancer and, since nothing was found, everything is hunky-dory.  In this scenario it sounds ridiculous.

However, prediabetes is arguably more dangerous to your health than cigarette smoking.  There is not a chronic disease that is not in some way increased by prediabetes.  Some, like heart disease, neurodegenerative disorders (Alzheimer’s and Parkinson’s), stroke and many cancers are strongly linked to prediabetes, with being prediabetic almost one of the strongest risk factors.

For those of you wondering if you might just happen to be prediabetic, here’s a short list of things to look for:

  1. Abdominal obesity
  2. PCOS / menstrual problems / infertility
  3. High cholesterol (especially with low HDL, high triglycerides)
  4. Elevated liver enzymes
  5. Gout or elevated uric acid
  6. High blood pressure
  7. Anyone with heart disease or an ischemic stroke (even a TIA)
  8. Family history of diabetes, cancer, heart disease or dementia

While the list is much longer, you get the idea…

Our society has not yet adopted this level of concern with prediabetes and, as a result, few understand the level of danger that he or she is living under.  Given that over 50% of the US population can be classified as being prediabetic, this lack of fear really needs to change.

This particular article is yet another that adds to the long list of damage done to your body by being prediabetic.  In it researchers looked at 127 individuals (aged 41–86 years) and sorted out those who had high insulin resistance (most prediabetic) and those who had low a level of insulin resistance (least prediabetic).  There was a very clear association between damage to the white matter and insulin resistance.  For those neuroanatomy geeks, changes were seen in areas such as the:

  • corpus callosum, corona radiata, cerebral peduncle, posterior thalamic radiation, and right superior longitudinal fasciculus
  • white matter underlying the frontal, parietal, and temporal lobes
  • body and genu of corpus callosum
  • parts of the superior and anterior corona radiate

Basically—pretty much every area of the brain was affected by the prediabetic process.  Even more concerning was the fact that the worse the insulin resistance, the greater the white matter damage.

Brain damage from being prediabetic.  Let me repeat that in another way: Over half of the population (and there is a good chance this means YOU) is experiencing brain damage and a loss of healthy brain cells as a result of being prediabetic.

If brain cells are important to you, what changes are YOU making to be less prediabetic?

Alzheimer’s Dementia Research; We’re Throwing Money Away

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Much like the cancer scenario, it seems like dementia research is throwing money around looking for a “cure” for Alzheimer’s dementia.  I have said for years now that they ain’t going to find it.

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.  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.

The likelihood of being able to prevent Alzheimer’s dementia, on the other hand, is very strongly supported by the medical research.  While preventative measures are beyond the scope of this blog article, you can read through previous articles by clicking here.

But, much like every other chronic disease, the prevention of Alzheimer’s dementia is not sexy.  No one gets emotional over prevention.  We get emotional over miraculous cures and amazing research discoveries.  And when we get emotional, we take out our checkbooks and give money to those groups touting research for a cure.

Most of this research on a cure has focused on the abnormal proteins found in Alzheimer’s dementia victims:  amyloid plaques (AP) and neurofibrillary tangles (NFT).  While I view these two proteins as the collateral damage that occurs in the brains of Alzheimer’s dementia patients, researchers have focused on these proteins being the cause of Alzheimer’s dementia.  The thought process is that, if we can destroy these proteins, these patients will improve.  As expected, research along this pathway continues to fail.  In someone who has been given a diagnosis of Parkinson’s or Alzheimer’s dementia, the barn door was opened a long, long time ago.

This particular study is yet another reason why we need to stop spending money on a “cure.”  In this article, researchers tried to block the consequences of a molecule called AGE, or advanced glycation end-products (specifically, the drug in question was designed to block the receptor for AGE, otherwise known as RAGE).  AGEs basically come from the diabetic process.  If you’ve ever had your HbA1c checked in blood work (and you probably have) you have had one aspect of AGEs checked.

Basically, when blood sugar levels go up, they irreversibly damage proteins.  Everywhere.  This is why the diabetic process is so darn dangerous to us–every protein in your body is destroyed by the climbing blood sugar.  Kidney proteins, muscle proteins, heart proteins, brain proteins.

Because of this, the idea was that, if we could block AGEs from doing damage, we could protect the brains of those with Alzheimer’s dementia.  Here are the specifics:

  • There were 399 participants in the trial given either a high or low dose of the drug in question.
  • Halfway through the study, it was found that those on the high dose had more confusion, falls, and greater cognitive decline.
  • As a result the study was halted.  Luckily, there were no safety concerns in the low-dose group.

In summary, it was not a good idea.  Given that we know SO MUCH about how to prevent dementia, I just don’t understand why we don’t shunt more of this wasted research money into educating the general public about prevention.  Maybe it really is as simple as prevention not being “sexy.”  Maybe we should dress it up in a little black dress and heels…

 

Help for Alzheimer’s when Meds Aren’t Enough

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When symptoms progress far enough with Alzheimers dementia, there are several medications that are used. The most commonly used is Aricept, a cholinesterase inhibitor.

Acetylcholine is a neurotransmitter that our brain cells use to communicate between one another, especially those brain cells dedicated to learning and memory. Cholinesterase is the enzyme that breaks down acetylcholine. If you block the enzyme that breaks down the neurotransmitter, your brain will have more of the acetylcholine running around to make sure that a message passes from brain cell A over to brain cell B.

Namenda is another commonly used drug that blocks the action at the NMDA receptor, thereby blocking the action of the excitatory neurotransmitter glutamate. This can slow the brain activity down and keeps the brain cells from literally working themselves to death.

Beyond these medications, however, there are few options. My general answer to this concern, however, is that our understanding of what contributes to neurodegenerative disorders like Alzheimer’s dementia and Parkinson’s disease is quite detailed. While prevention is beyond the scope of this article, you can read previous articles on this topic by clicking here.

This particular article takes a fresh look at an old favorite natural compound for treatment of Alzheimer’s dementia. Ginko biloba. What is interesting here, though, is that researchers used ginko in 828 patients with mild to moderate disease who were already on cholinesterase inhibitors. This makes the results of the study that much more interesting. Here’s the details:

  • Patients were followed using the Mini Mental State Examination (MMSE), the Alzheimer’s Disease Assessment Scale-Cognitive (ADAS-Cog) subscale score, and the Activities of Daily Living (ADL) scale.
  • There was a stronger response in the MMSE score after 12-months of follow-up in those using the ginko biloba.
  • While similar improvements were also seen on the ADAS-Cog, these were not as strong.

While the improvements were not life-changing, the fact that there were definite improvements over the use of the drugs alone is a pretty important fact. The damage done to the brain cells in Alzheimer’s dementia is extensive and begins decades before symptoms are recognized. For this reason, I do not believe we will ever be able to reverse Alzheimer’s dementia—the disease is a freight train running.

However, slowing the damage down I believe is very possible. The same interventions that can help prevent Alzheimer’s dementia can also help slow down the process in the brain and hopefully increase longevity. Never a bad thing, especially when the “cost” is something as simple and safe as ginko biloba.

Protecting Your Brain from Dementia One Supplement at a Time

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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:

  1. Researchers looked at 613 patients with mild to moderate Alzheimer’s dementia who were already taking drugs for Alzheimer’s dementia (acetylcholinesterase inhibitor).
  2. 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.
  3. 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.
  4. 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

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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.