Dementia SOS

Colorado's Dementia News and Resource Center

A new year for Dementia SOS…

You may have noticed a substantial break in the publications here at Dementia SOS this past month. The reason? In December, your author took a new position at Arapahoe Douglas Mental Health Network.

New articles will be published in the coming weeks, including a series on depression and how it may affect the progression of dementia. But we will return to the topic of antioxidants next week. Please stay tuned and thanks for your readership!

January 5, 2015 Posted by | Uncategorized | Leave a comment

The free radical theory of aging…and Alzheimer’s

The free radical theory of aging was first proposed in the 1950’s by Denham Harman, MD, PhD. Early in his career, Harman worked for Shell Oil as a research chemist and studied various free radical reactions occurring within petroleum products. He later acquired his MD at Stanford University and started to apply his research to the process of human aging.

This theory states that humans (and all organisms) age on a cellular level due to increased free radical damage over time. Free radicals are atoms that have an unpaired electron in their outer shells. They are out of balance and thus wildly seeking other electrons to bond with. In the process of mating, these particles create oxidative stress that gradually damages individual cells.

Unpaired electrons are the free radical particles that may ultimately cause us to age.

Unpaired electrons are the free radical particles that may ultimately cause us to age.

The theory first involved what are known as reactive oxygen species (ROS) – chemically reactive molecules that are a normal byproduct of the metabolism of oxygen. Cells are able to remove (scavenge) this debris normally through specific enzyme production. But when environmental circumstances become too overwhelming, ROS start to take a toll and affect the overall function of cells.

By the early 1970’s, Harman’s theory developed into the mitochondrial theory of aging. Mitochondria are small organelles that drift within cells to absorb nutrients and break them down into energy for the cells. These organelles utilize oxygen to do their work and create those ROS byproducts. A chain of events then occur where oxidative stress from the ROS damage macromolecules and basically start to compromise many different types of cells in the body.

Cardiovascular disease, diabetes, and cancer are all net effects of this oxidative stress. Cellular DNA is damaged and this starts to create abnormalities which in turn start to replicate themselves over time. This stress is also suspected of producing the pathology (plaques and tangles) of Alzheimer’s disease…

Oxygen and the Brain
Because brain tissue uses over 20% of the oxygen we consume, this area should be particularly vulnerable to oxidative stress. Chronic inflammation is another way of stating oxidative stress. The brain is exposed to inflammation across a broad spectrum of pathways, and when this inflammation escalates it can have far reaching consequences for cognitive abilities.

Oxidative stress is also suspect in the gradual disruption of the blood brain barrier (BBB). The BBB is thought of as a critical safeguard for sustaining homeostasis in brain tissue. Any evidence of BBB impairment has been associated with everything from Multiple Sclerosis, brain tumors, stroke, neuro-infections, vascular brain disease, and the neurodegenerative diseases (Alzheimer’s, Lewy Body dementia, and Fronto-Temporal dementia). Researchers are still trying to determine if oxidative stress is a precursor to this BBB deterioration, but the correlation with so many pathological disorders would be hard to dismiss.

Illustration of the endothelial cells of the blood brain barrier.  Image by Armin Kubelbeck (CC).

Illustration of the endothelial cells of the blood brain barrier. Image by Armin Kubelbeck (CC).

The BBB is primarily composed of endothelial cells. This membrane acts like a filter, allowing only specific molecules to pass in and out of the brain. It also acts as an interface between our finer (periphery) circulatory system and the central nervous system.

If the BBB is compromised, some neurotoxic substances may start to circulate into the cerebrospinal fluid. Critical nutrients may also be diminished as result of BBB impairment. And finally, the inflamed endothelial cells may generate altered protein expressions. All three of these factors are associated to Alzheimer’s disease. If oxidative stress turns out to be a trigger for a compromised blood brain barrier, prevention of inflammation becomes far more critical for cognitive health.

We’ll look at the antidote (antioxidants) next…

November 18, 2014 Posted by | Free radical theory of aging | , | Leave a comment

Aging and neurotransmitters

The speed and quality of our thoughts is dependent upon the micro-circuitry of our brain cells (neurons). The average human brain has about 86 billion neurons and they communicate directly with one another, and collectively in pathways. Sometimes we are accessing information from multiple areas of the brain to perform a given task. But let’s keep it simple…

Each brain cell has an extension called an axon. This appendage sends chemical information on to adjacent neurons that have a receptor extension called a dendrite. The spaces (or gaps) between the axons and dendrites are called synapses and chemical messengers cross these gaps with information. These messengers are called neurotransmitters.

Neurotransmitters pass between brain cells as chemical messengers.

Neurotransmitters pass between brain cells as chemical messengers.

When neurotransmitters decline
There are four NT’s in particular that affect the cognitive process as we age: Acetylcholine, Dopamine, GABA, and Serotonin. If we experience low levels for any of these neurotransmitters, we may have problems with sleeplessness, depression, anxiety, lack of motivation, memory loss, moodiness, fatigue, drug abuse, and physical ailments, such as irregular heartbeat or insulin resistance.

Acetlycholine is highly associated with memory and learning. This NT is linked with processing speed and speed of memory access. Researchers believe that Acetlycholine helps produce REM sleep and also acts as a vasodilator (relaxing blood vessels). Consequentially, low levels can affect many systems of the body: cardiovascular, urinary tract, respiratory, and gastrointestinal.

Low levels of Dopamine can often lead to lethargy and inactivity and so obesity may be a common cause (or effect) here. Dopamine is also the chief NT involved with motor function. Low levels are strongly correlated with Parkinson’s disease. But this NT is also connected with sleep disorders, addiction, memory and learning issues, and moodiness.

The full name for GABA is Gamma-aminobutyric acid. This NT controls brain rhythms and the excitability of nerve cells. When levels are low here, a person will be irritable and worry excessively. Sleep will be a problem and high levels of the damaging stress hormone coritsol will also be present.

A lack of serotonin is strongly associated with depression.  Photo by Sal Falko.

A lack of serotonin is strongly associated with depression. Photo by Sal Falko.

Finally, lack of Serotonin is highly correlated with depression. Your typical anti-depressant drug is designed to prevent the breakdown of Serotonin in the brain. So anxiety and apathy will increase when this NT is depleted and memory and learning are affected as well.

In research studies, Acetylcholine and Dopamine have clearly been shown to decrease as we age. GABA and Serotonin decrease less markedly but the loss may be exacerbated by medical conditions such as obesity, diabetes, and heart disease.

Many contributing factors
As mentioned in the previous entry, demyelinization of neurons accounts for some of the loss in neurotransmitters and death of neurons. But to make things a little more complicated, the activity of enzymes and metabolites also play a role. As enzymes increase in ratio to NT’s, they appear to wipe out NT’s or dilute their effect. Cell membranes are also compromised by the process of oxidative stress and chronic inflammation.

Because of these interacting factors (and probably many other unknown factors), much of the research on neurotransmitters cannot draw clear lines between normal aging and pathological aging due to Alzheimer’s or other types of dementia. Since oxidative stress is a major suspect, we’ll take a closer look at this process next.

October 28, 2014 Posted by | Brain Cells, Neurotransmitters, Normal Brain Aging, The Human Brain | , | Leave a comment

Brain atrophy – what is normal?

At its most basic, brain atrophy is the loss of neurons and neuronal connections. When this occurs, physical tissue shrinks up and specific areas of the brain are reduced in size and viability. The cavities of the brain [called ventricles] are also seen to enlarge over time.

Brain atrophy occurs naturally to some degree as we age. Tissue decreases in size just as muscle tissue eventually decreases in our bodies. Sarcopenia is the term for muscle loss due to aging. This loss starts to occur as early as the age of 20. By age 50, the average person can lose .4 pounds of muscle every year.

Atrophy of the brain is also thought to occur due to several neurodegenerative diseases, such as Alzheimer’s, fronto-temporal dementia, or vascular dementia. And it may be caused by traumatic brain injuries, stroke, and possibly even steroid usage, infections, or dehydration.

Model comparison of a healthy brain contrasted with the effects of Alzheimer's.

Model comparison of a healthy brain contrasted with the effects of Alzheimer’s.

Full Brain Mass
At age 25, our brains are thought to be at an optimal state. We start to lose tissue mass after this, at a fairly negligible rate until about the age of 60, when brain volume starts to drop by ½ to 1% each year. Atrophy accelerates by age 75 when the average brain volume is about 15% less compared to a 25 year old. Imagine a bike helmet with 15% less padding…

If the brain is allowed to shift inside of the skull, subtle insults to neurons may occur. Cell linings may tear or come in rough contact with other neurons. The result may be a brain herniation. This is sometimes caused by head injury, stroke, or brain tumors and the damage may be life threatening depending upon the severity of the injury. Typical signs of brain herniation include: loss of consciousness, coma, cardiac and/or respiratory arrest, headache, lethargy, one or both pupils dilated, high blood pressure, and irregular pulse or breathing.

VentriclesDiagram-wikipediaThe Cavities of the Brain
There are four interconnected cavities within the brain, known as ventricles – two lateral ventricles (one in each hemisphere of the brain), plus the third and fourth ventricle. These cavities, especially the lateral ventricles, seemingly enlarge as we age. This is thought to be occurring due to loss of neurons.

Cells die and are carried out of the brain via the ventricles. These spaces, which contain cerebrospinal fluid, then fill the void much like water seeks to fill an empty space. Some research has shown a connection between enlarged ventricles and Alzheimer’s disease. Other studies, however, indicate that loss of brain mass and enlargement of the ventricles do not necessarily correspond to cognitive decline.

The Aging of Myelin
Perhaps most significant at this point in our understanding of the aging brain, the insulation material known as Myelin has been shown to deteriorate over time. Myelin-encoated brain cells make up the “white matter” portion of our brain. This material was once thought to be just fatty insulation, but it turned out to have a much greater impact on cognition.

Myelin insulates the axons of nerve cells, helping expedite the transmission of signals.

Myelin insulates the axons of nerve cells, helping expedite the transmission of signals.

Myelin is a coating (sheath) that helps axons communicate more efficiently with dendrites. In general, white matter helps link large processing areas of our brain to communicate as a whole. Alan Peters of Boston University of Medicine describes the aging process of Myelin as follows…

There are two ways myelin is compromised: 1) dense cytoplasm builds within a myelin sheath, causing the sheath to split. 2) “balloon” formations or holes start to appear in the myelin sheaths as we age. He describes the balloon formations as a degenerative change that can also be witnessed in cases of severe diabetes. Myelin degeneration is also directly connected with Multiple Sclerosis. But some researchers estimate that as much as 50% of myelinated axons are lost in the normal aging process.

A critical byproduct of this reduced myelin content is impaired binding and signaling of neurotransmitters, the speed and quality of our thought. We’ll look at how NT’s are diminished in the aging process next.

October 14, 2014 Posted by | Brain Cells, Normal Brain Aging, The Human Brain | , | Leave a comment

Tangents on the topic of longevity

Advancing age is the number one risk factor for Alzheimer’s disease. Today, the Alzheimer’s Association estimates that 1 in 9 people over 65 have this progressive neurodegenerative disease and about 1 in 3 over 85 have AD. [That number is actually down from a 2011 annual report that concluded that 43% of those over 85 have AD]. There is also a higher incidence of AD in women than men, largely due to the fact that women tend to live longer than men.

Flashback to the early 1900’s and the average life span was 47. Higher infant mortality rates played a role in this number that is significantly lower than today (American women live an average of 81 years while men live 76 years on average). But medical advances have also made it possible for more people to live longer – treatment improvements for cardiovascular disease and the cessation of tobacco usage are two huge contributing factors here.

Longevity around the world
America actually ranks 37th in average lifespan. Japan has the highest average for a woman (87) while Iceland has the highest life expectancy for a man (81.2 years). Women in developed countries tend to live 19 years longer than those in poorer countries. Men live 16 years longer in this comparison. So ultimately, Alzheimer’s is more prevalent in developed countries where people are steadily exceeding the average age of 65.

Villagers in India have some of the lowest incidences of Alzheimer’s. Many researchers are coming to conclude that the high levels of turmeric in Indian diets may play a role there. In China, where vegetarian diets are much more common, AD was also found at a lower rate – in 2010 China had 5.7 million cases compared to 5.3 million in America (which is only one third China’s population). But the cases in China have almost doubled from just a few decades earlier…

Longevity has been increasing in China, and likewise the cases of dementia.  Photo by Miriam (CC).

Longevity has been increasing in China, and likewise the cases of dementia. Photo by Miriam (CC).

Since 1990, the average lifespan in China has increased from 70 to 76. Coincidentally, the prevalence of dementia in general there is now twice as high as reported previously by the international health community. Rapid industrialization (leading to changes in diet and lifestyle) seems to be another reason for these increasing dementia cases.

And back to Japan – here the general population consumes fish more so than meat. The incidence of dementia has been lower in comparison to Japanese-Americans (by about 4-6%). But 1 in 4 native Japanese are now over 65 and those numbers are growing. Studies have shown that Alzheimer’s has steadily been replacing vascular dementia as the critical heath issue there.

Longevity in Down Syndrome
In another unique population, people with Down Syndrome are also living longer. DS is a form of premature aging. Researchers have known for a while now that 75-100% of people with DS have the elevated pathology of Alzheimer’s disease by age 40. Early onset dementia is often observable. And yet, not all of these people go on to develop the symptoms of dementia…

People with Down Syndrome are living longer - nearly 100% exhibit the Alzheimer's  pathology by age 50.

People with Down Syndrome are living longer – nearly 100% exhibit the Alzheimer’s pathology by age 50.

Studies at the University of Wisconsin, Madison, have shown that about one third of the DS participants showed no cognitive impairment, despite having elevated levels of amyloid-beta on MRI’s and PET scans. And studies in Australia have shown that DS participants have been developing the symptoms of AD at a later age (50-60 years old), possibly due to education, early intervention, better nutrition and healthcare.

Longevity with TBI’s
Over the past few decades, significant success has been achieved in keeping people alive after traumatic brain injuries (TBI’s). While each case of TBI is unique in damage, there are some items worth noting here as well.

The symptoms of many TBI’s already overlap dementia dramatically: memory loss, impaired judgment, inappropriate behavior, attention deficits, and sometimes communication problems. Some studies have shown that moderate to severe head injuries can lead to the development of the Alzheimer’s pathology. A specific study of veterans at the University of CA, S.F. suggests that TBI’s may even be a trigger for earlier onset dementia.

The recent flurry of stories about football players and their concussions also highlight the connection between repetitive head injuries and the pathology of Alzheimer’s. These concussions are, of course, similar to dementia pugilistica, or the “punch-drunk” syndrome observed among boxers. 15-20% of all boxers are thought to develop this neurodegenerative disease.

Dementia down the road may be the price of a career in boxing.

Dementia down the road may be the price of a career in boxing.

One last tangent worth considering is that our brains are shrinking as we age. This sets the stage for increased movement of the brain inside the skull. With less protection, does this mean more vulnerability to the production of amyloid-beta protein deposits? Are these plaque build-ups a threat to the brain, or possibly the body’s best defense mechanism against subtle and sometimes not so subtle injuries to the brain? We’ll look more closely at this topic next.

September 30, 2014 Posted by | Alzheimer's Disease, Head Injury, Longevity | , , | Leave a comment

Two angles to arthritis and Alzheimer’s disease – Leukine and Etanercept

Since 2011, Dr. Huntington Potter of the CU Medical Center at Anschutz (in collaboration with the Dana Foundation) has been conducting studies on the safety and efficacy of a cancer treatment drug called Leukine, for application as an Alzheimer’s treatment. Leukine is FDA approved for bone marrow stimulation and contains a protein known as GM-CSF.

Microscopic view of microglia cells.  Photo by Grzegorz Wicher.

Microscopic view of microglia cells. Photo by Grzegorz Wicher.

The long name for this protein is Granulocyte-Macrophage Colony Stimulating Factor. GM-CSF is released naturally into the brain when a person experiences inflammation from rheumatoid arthritis. The protein stimulates production of scavenger cells (microglia) that remove beta amyloid from the brain. A connection between rheumatoid arthritis and apparent lower risk of developing Alzheimer’s is what prompted initial pilot studies.

The final collection date for this pilot phase 2 study is January of 2015, with an estimated completion date in March. This study included people ages 55-85 years old with mild to moderate Alzheimer’s, stable on all medications (including anti-dementia treatments, for at least two months), and physically able to participate in the exams.

Any clinically relevant arrhythmias, slow pulse rate (lower than 50), or active cancers would exclude candidates from the study. Other pre-existing health conditions also precluded people from the study: congestive heart disease, moderate to severe liver or lung disease, impaired kidney function, history of significant stroke or head trauma, and even sensitivity to yeast and pregnant women.

It could be a few more years before enough studies can conclude that Leukine is safe and effective at halting the progression of Alzheimer’s. Phase 3 trials may be a little ways off, but since Leukine is an existing, FDA approved drug therapy, phase 4 studies would presumably occur quickly.

Etanercept – another story…
Existing drug therapies are tempting to use for other applications not originally intended by the designers. The main advantage is that drugs are already in existence and on shelves so they save the costly development and marketing steps. “Off-label use” is the term for using a drug for a purpose not currently approved by the FDA. Enter Etanercept…

Etanercept is protein currently being manufactured by Amgen and Pfizer under the tradename Enbrel. You’ve probably seen your share of commercials for Enbrel. It comes in a powder or premixed liquid form and is FDA approved for several forms of arthritis, including rheumatoid arthritis. This molecule binds with TNF-alpha (Tumor Necrosis Factors) to neutralize these receptor cells involved with inflammation in the body and also suspected of contributing to brain cell death.

Since 2006, Edward Tobinick has been conducting case studies (not authorized by Amgen) to test the efficacy of Etanercept on Alzheimer’s, among other conditions. Etanercept comes with black-box warnings about the risk of serious infections, sepsis, and fatalities that have been reported. Many of those infections were correlated to people with immunosuppressive treatments and other underlying diseases.

Amgen has publicly distanced itself from Dr. Tobinick’s work. He has also been reprimanded by the state of California for questions on medical ethics in case studies. One big reason for the criticism has been a lack of randomized controlled trials, critical in scientific conclusions.

And so in 2011, in collaboration with the University of Southampton, England, a small randomized clinical study of 20 men and women was conducted to test Etanercept (injected in the stomach or thigh). The results were very positive, as reported by the lead, Professor Clive Holmes. The small study concluded that Alzheimer’s was not reversed but markedly prevented further progression of the disease. He is currently seeking funding for broader studies and thinks the drug could be given to dementia patients inside of five years if trials hold up.

Leukine and Etanercept are promising angles for halting the progression of Alzheimer’s: by reducing beta amyloid in the brain or reducing brain inflammation in general. But only broader studies over time will reveal the true safety and effectiveness of these two therapies.

Waiting for a cure.  (Image by Flickr user Borya)

Waiting for a cure. (Image by Flickr user Borya)

September 15, 2014 Posted by | Clinical Trials, Rheumatoid Arthritis | , , | Leave a comment

Drugs for heart rhythm problems

There are four rough classifications of antiarrhythmic drugs (as proposed by Vaughn-Williams). Some medications fall into multiple categories, while others may not be appropriate to place in any of these broad categories. While similar in many ways, each of these drugs has a different affect on the heart, whether targeting the electrical impulses or the muscles (myocardium) of the heart to restore normal rhythms.

The four classifications are:

Class I – sodium channel blockers. These drugs are also referred to as “membrane stabilizing agents.” They reduce the amount of sodium flowing into a cell to prevent that cell from activating. They in effect slow the electrical conduction rate of the heart. Class I drugs are further subdivided into moderate, weak and strong categories depending upon how they affect ventricular action potential. The most common class I drugs include: procainamide, lidocaine, and flecainide.


Class II – beta blockers. These are important drugs for preventing supraventricular tachycardia (fast heart rate in the atria, such as atrial flutter or AFib). Ultimately, they decrease electrical conduction through the AV Node.

Class III – potassium channel blockers. These drugs are used to maintain normal sinus rhythm. By reducing the flow of potassium, repolarization of cells is delayed, thus increasing action potential and refractory period durations.

Shown here, some EKG examples of re-entrant tachycardias.

Shown here, some EKG examples of re-entrant tachycardias.

The goal is to prevent re-entrant arrhythmias – arrhythmias when a tight, recurring electrical circuit develops within an area of the heart. These short circuits have a harder time existing when cellular tissue is in a refractory state. Amiodorane and sotalol are two common class III medications.

Class IV – calcium channel blockers. These drugs also decrease conduction through the AV Node, slowing atrial and ventricle contractions of the heart. But unlike beta blockers, these drugs allow the body to retain control of heart rate and contractility. Verapamil is a class IV medication.

And now Class V…
A fifth classification is also currently used to include antiarrhythmic drugs that do not fit well in the previous four categories. Some of these include: Digoxine, Adenosine, and Magnesium Sulfate. Digoxine, for instance, can slow heart rate while strengthening heart contractions.

Adenosine is also used to restore normal heart rate during an episode of supraventricular tachycardia. It has farther reaching effects though, because it plays a role in regulation of blood flow to various parts of the body in general and is an anti-inflammatory agent. Adenosine is used temporarily for ventricular heart rhythm problems.

Cautionary usage
None of these drugs are without side effects. And like any medication, dosage strength and frequency will create subtleties. Sometimes the medical condition is clearly more severe than any potential side effects, but many doctors are cautious when prescribing antiarrhythmic drugs for mild arrhythmias.

Some of these drug risks include: chance of developing an even more severe arrhythmia, trouble breathing, or severe weakness. Call 911 immediately in any of these cases. Lesser side effects, such as nausea, diarrhea, pain or weakness, may go away as you get used to taking the medication.

September 4, 2014 Posted by | Arrhythmia, Medical Conditions, Medications | , | Leave a comment

Arrhythmias and their treatments

Here are three things we know about arrhythmias:

1) If heart rate is too fast (tachycardia) this can affect the brain. Todd J Cohen, MD, author of A Patient’s Guide to Heart Rhythm Problems (A John Hopkins Press Health Book ) states: “The faster the heart rate, the greater the chance that delivery of oxygen and other nutrients to the brain and other organs will be impaired.”
2) Atrial Fibrillation (AFib) is a cyclical problem. Cohen stresses: “AFib begets AFib – the longer you are in AFib the longer you stay in AFib.”
3) Ventricular tachycardia (rapid heartbeat in the ventricles) is the most common cause of heart attacks, also known as sudden cardiac arrest.

There are several forms of arrhythmias and many interrelated causes, but the simplest way to understand this problem is by dividing them into two categories: atrial (upper heart chamber) or ventricular (lower heart chamber) arrhythmias. Then divide each of these categories into heart rate that is too slow (bradycardia) or too rapid (tachycardia).

The four chambers of the heart.  Image by Arturo J Murias (CC).

The four chambers of the heart. Image by Arturo J Murias (CC).

The symptoms of bradycardia are: dizziness, shortness of breath, depression or “feelings of impending doom,” light-headedness and passing out (syncope). Untreated high blood pressure is one of many possible causes of bradycardia. Blockages that limit blood flow are another culprit, but some medications (like beta blockers and even antiarrhythmic drugs) can lower heart rate as well. Blood thinners are often a first line of defense. Pacemakers are usually recommended when conditions are more severe.

The symptoms of tachycardia are similar to bradycardia: light-headed, dizziness, shortness of breath, and loss of consciousness. But add palpitations to that list. AFib, Atrial Flutter and atrial tachycardia are all conditions where the upper heart chambers (atria) rhythms are too fast. Antiarrhythmic drugs are sometimes prescribed for these conditions.

When tachycardia is present in the lower chambers of the heart (ventricles), conditions can become more serious. As mentioned above, ventricular tachycardia is a leading cause of sudden cardiac arrest. Surgeries such as catheter ablation may be necessary to correct your heart rate rhythm.

Shown here: a catheter ablation procedure in the atria.

Shown here: a catheter ablation procedure in the atria.

Catheter Ablation
A catheter is a medical device that is inserted into arteries or veins. For this procedure, thin wires enter the neck or groin arteries and lead to areas of the heart that need to be zapped. Electrodes on the tips of these wires emit radio waves to create heat for the ablation. They destroy any heart tissue suspected of generating tachycardia.

Catheter ablation is only recommended when a person is unresponsive to antiarrhythmic drug therapy. A person may also need to undergo a series of ablation procedures to restore normal heart rate. We’ll take a closer look at these antiarrhythmic drugs next.

August 21, 2014 Posted by | Arrhythmia, Vascular Dementia | , , | Leave a comment

The origin of arrhythmias

Arrhythmia is a term used when the heart beats irregularly. It may beat faster (known as tachycardia) or slower (bradycardia), or skip beats. Arrhythmia is not necessarily a serious condition, but certainly worth monitoring if detected.

It’s estimated that 10-15% of people 70 and older have arrhythmias. Up to 90% of people that have experienced heart attacks also had some form of heart rhythm issues. Even athletes can develop an arrhythmia – the most common known as ventricular tachycardia, whose occurrence increases with age.

Where rhythm begins
There is a cluster of cells in the upper right chamber of the heart (atria) that creates an electrical impulse for the chambers to contract. These cells are known as the sino-atrial node, or sinus node. The sinus node creates between 60-100 electrical impulses each minute in a normal heart. Does that sound familiar? It’s equivalent to your typical heart rate in beats per minute.

The electrical charge then continues from right to left atria and on to another cluster of cells called the atrioventricular node (located between the atria and ventricles). The signal splits from here to affect both the lower right and left chambers of the heart (the ventricles) via a bundle of fibers called the HIS-Purkinje system.


These electrical impulses decrease in intensity (from top to bottom of the heart) as the various chambers are set in contracting and resting motion. Atrial Fibrillation is a common source of arrhythmia, but irregularities can occur anywhere along this “wiring.” Depending upon the location, specific chambers may back up, or pool with blood.

Heart rate changes
Oxygen is a form of energy for the body. Your heart rate will naturally tend to increase when you need more energy (like during exercise or dealing with stressful situations). Your heart rate can also naturally slow down, like when you go to sleep or meditate. It’s when your rhythm is out of whack that trouble in the electrical system described above might need a review. An EKG or Electrocardiogram (ECG)is the most common way for a doctor to evaluate your heart rhythm.

You might have a heightened sense of awareness of your heartbeat, such as feeling like it is fluttering, racing, thumping. This is typically referred to as palpitations, and you will probably be more aware of them at bedtime, when you are more still and observant of your body.

Palpitations could be a symptom of arrhythmia, but they could also be caused by a number of other things:

*Stress (short or long term) – see the series on stress reduction here.
*Drugs such as caffeine, tobacco, alcohol, and other medications (like diet pills and cold or asthma medications)
*Low blood pressure
*Heart disease in other forms, such as valvular medical conditions
*Hormone changes

None of these conditions should be taken lightly and it’s possible that some of them could actually contribute to arrhythmias down the road. But you should also know that the majority of arrhythmias are considered harmless and not treated medically. We’ll discuss some of those treatments next.

August 14, 2014 Posted by | Arrhythmia, Vascular Dementia | , | Leave a comment

Atrial fibrillation and dementia

Atrial fibrillation (or AFib) is a rather common cardiovascular condition. It is estimated that one in 200 people have AFib and the numbers grow significantly (one in 20) after the age of 60. AFib can create the prime conditions for a stroke, among other health concerns.

What is AFib?
When there are inefficient or irregular contractions of the upper chambers of the heart (the atria), this area can become backed up with blood and dilate. The excess blood creates red clots that can flow into the ventricles, the aorta, and the arteries that supply blood to the brain.

The term embolized is used when a blood clot develops, breaks off from the point of origin and blocks pathways further downstream. Blood supply may be cut off entirely. But even partial blockage could cause some cognitive issues.

Congestive heart failure is also connected to AFib, In this medical condition, blood is typically pooling in the ventricles, where it may start to clot. Improper functioning of the left atria is most common in this condition, thus creating pooling issues in the left ventricle.

Valvular heart conditions can also play an interrelated role. If valves harden, blood flow can travel in the wrong direction, allowing blood to pool in the atria or the ventricles. AFib is ultimately an issue of irregular electrical impulses in the heart. It’s possible that blood backed up into the atria due to hardened valves contributes to the development of AFib (or vice versa).

Warning Signs
Fast or irregular heartbeats (arrhythmias) may be a strong indication of AFib. If these occur for minutes at a time, you should visit with your doctor immediately. It’s common to just want to ignore the symptoms. Don’t! Visit the ER immediately if you notice weakness in your left hand and leg or tingling in the whole left side of your body and/or face.

Types of AFib
There are three types of AFib: Paroxysmal, Persistent, and Chronic. Each of these has a different treatment method. Paroxysmal AFib is very sporadic and not long-lasting and usually does not call for medical treatment. Persistent AFib, however, usually means that your heart rhythm is not resuming properly and medical intervention will be necessary. Chronic AFib means the rhythms are constantly out of sync – it may not be possible to get back to normal rhythms in this condition.

Here’s a virtual guide designed by Healthline for seven effects of Atrial Fibrillation on the body.

We’ll talk more about rhythms and the heart’s natural pacemaker next…

July 31, 2014 Posted by | Uncategorized | , | Leave a comment