Can dementia drugs cause fainting?

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Cholinesterase inhibitors and hospitalization for bradycardia: a population-based study.
PLoS Med. 2009 Sep;6(9):e1000157. PubMed. SOURCE:

Memory drugs for Alzheimer's cause slower heart rates and even fainting. The magnitude of these risks are not always made clear to patients. Learn about side-effects, avoiding a pacemaker and injuries from falls.

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Side effects associated with several commonly-prescribed dementia drugs may be putting elderly Canadians at risk, says Queen's University Geriatrics professor Sudeep Gill.

Cholinesterase inhibitors are often prescribed for people with Alzheimer's disease and related dementias because they increase the level of a chemical in the brain that seems to help memory. These include Aricept^®, Exelon^® and Reminyl, known generically as donepezil, rivastigmine and galantamine.

Drugs for Early to Midstage

Brand Name	Generic Name
Aricept®	donepezil
Exelon®	rivastigmine
Remynil or Razadyne®	galantamine

Although such drugs are known to provoke slower heart rates and fainting episodes, the magnitude of these risks are not always made clear to patients.

"This is very troubling, because the drugs are marketed as helping to preserve memory and improve function," says Dr. Gill, who is an Ontario Ministry of Health and Long-term Care Career Scientist, working at Providence Care's St. Mary's of the Lake Hospital in Kingston. "But for a subset of people, the effect appears to be the exact opposite."

In a large study using province-wide data, Dr. Gill and his colleagues discovered that people who used cholinesterase inhibitors were hospitalized for fainting almost twice as often as people with dementia who did not receive these drugs. Experiencing a slowed heart-rate was 69 per cent more common amongst cholinesterase inhibitor users. In addition, people taking the dementia drugs had a 49 per cent increased chance of having permanent pacemakers implanted and an 18 per cent increased risk of hip fractures.

Unfortunately, Dr. Gill continues, this class of drugs is one of the few effective dementia treatments available today. Acknowledging that these drugs do have an important role in the management of dementia, he suggests that people who are already at a higher risk (for example, those who have had previous episodes of fainting or slowed heart rate) may want to ask their doctors to reassess the value of taking the drugs.

Slowing of the heart rate from cholinesterase inhibitors, if significant, may cause a person to faint and suffer fall-related injuries such as a broken hip - often debilitating and sometimes fatal for seniors. ( See the related article: 14 Ways to Prevent Falling at Home ) However, many physicians aren't aware of the connection between these problems and the dementia drugs, Dr. Gill notes.

If the association with dementia drugs is not identified, people who faint may be prescribed a permanent pacemaker: an invasive procedure that can involve serious complications for seniors. Both the injuries incurred from falling and the risks from pacemaker implants are "downstream consequences" of not recognizing this drug-induced phenomenon. 

REFERENCE: Park-Wyllie LY, Mamdani MM, Li P, Gill SS, Laupacis A, Juurlink DN.
Cholinesterase inhibitors and hospitalization for bradycardia: a population-based study.

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Use DICE method for dementia

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SOURCE:
University of Michigan
An innovative technique called "DICE" empowers caregivers, patients & professionals to work together and reduce dementia's behavioral problems. Learn how it can help cut antipsychotic drugs and make life easier for everyone. 

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ANN ARBOR, Mich. — A novel approach to handling agitation, aggression and other unwanted behaviors by people with dementia may help reduce the use of antipsychotics and other psychiatric drugs in this population, and make life easier for them and their caregivers, a team of experts says.

The new DICE model - for Describe, Investigate, Evaluate, and Create - seeks to reduce psychotropic medication use in dementia patients.

Publishing their recommendations under the easy-to-remember acronym of “DICE”, the panel of specialists in senior mental health hope to spark better teamwork among those who care for dementia patients at home, in residential facilities and in hospitals and clinics.

In fact, the federal agency that runs Medicare and funds much dementia-related care has made the DICE approach an official part of its toolkit for reducing the use of antipsychotic drugs and other mental health medications in people with dementia.

D: Describe - Asking the caregiver, and the patient if possible, to describe theThough these drugs may still help some patients, the important paper in the Journal of the American Geriatrics Society says, many non-medication approaches could also help reduced unwanted behaviors, also known as neuropsychiatric symptoms of dementia. But it will take teamwork and communication to do it.

Most people with Alzheimer’s disease and other memory-affecting conditions also get aggressive, agitated, depressed, anxious, or delusional from time to time, says senior author Helen C. Kales, M.D., head of the U-M Program for Positive Aging and Geriatric Psychiatry at the University of Michigan Health System and investigator at the VA Center for Clinical Management Research . Or, they might have delusions, hallucinations, or lose inhibitions.

“Often more than memory loss, behavioral symptoms of dementia are among the most difficult aspects of caring for people with dementia. These symptoms are experienced almost universally, across dementia stages and causes,” she says. “Sadly, these symptoms are often associated with poor outcomes including early nursing home placement, hospital stays, caregiver stress and depression, and reduced caregiver employment.”

Doctors often prescribe these patients medications often used in patients with mental health disorders, despite little hard evidence that they work well and despite the risks they can pose -- including hastening death. Meanwhile, studies have shown promise from non-medication approaches to changing dementia patients’ behavior and reducing triggers for behavioral symptoms in their environment and daily life. But too few health teams are trained in their use.

Kales and her colleagues Laura N. Gitlin, Ph.D. and Constantine G. Lyketsos, M.D. from Johns Hopkins University authored the new paper on behalf of a group of experts, called the Detroit Expert Panel on the Assessment and Management of the Neuropsychiatric Symptoms of Dementia, who developed the DICE approach.

Sponsored by Kales’ program, the national multidisciplinary panel of experts met in Michigan to create a comprehensive approach to behavioral management.

Dubbed “DICE” for Describe, Investigate, Evaluate, and Create, it details key patient, caregiver and environmental considerations with each step of the approach and describes the “go-to” behavioral and environmental interventions that should be considered.

Briefly described, the components are: 

• 1. Who
  2. What
  3. When
  4. Where
  of situations where problem behaviors occur and the physical and social context for them. Caregivers could take notes about the situations that led to behavior issues, to share with health professionals during visits.

• I: Investigate – Having the health provider look into all the aspects of the patient’s
  1. health
  2. Dementia symptoms
  3. Current medications
  4. Sleep habits
  that might be combining with physical, social and caregiver-related factors to produce the behavior.

• C: Create – Working together, the patient’s caregiver and health providers develop a plan to prevent and respond to behavioral issues in the patient, including everything from
  1. Changing the patient’s activities
  2. Adjusting the environment
  3. Care education
  4. Support for the caregiver.

• E: Evaluate – Giving the provider responsibility for assessing
  1. How well the plan is being followed
  2. how it’s working
  3. What might need to be changed.

The authors say that doctors should prescribe psychotropic drugs only after they and the patient and caregiver have made significant efforts to change dementia patients’ behavior through environmental modifications and other interventions, with three exceptions related to severe depression, psychosis or aggression that present risk to the patient or others. 

Now, the authors say, health providers of all kinds who care for dementia patients should familiarize themselves with the DICE approach – as should the spouses, adult children and others who care for dementia patients at home.

“Innovative approaches are needed to support and train the front-line providers for the burgeoning older population with behavioral symptoms of dementia,” says Kales, a professor in the U-M Medical School’s Department of Psychiatry and member of the U-M Institute for Healthcare Policy & Innovation . “We believe that the DICE approach offers clinicians an evidence-informed structured clinical reasoning process that can be integrated into diverse practice settings.” 

Gitlin, who directs the Center for Innovative Care in Aging at the Johns Hopkins School of Nursing, adds, “The DICE approach is inherently patient- and caregiver-centered because the concerns of individuals with dementia and their caregivers are integral to each step of the process. DICE also enables clinicians to consider the roles of nonpharmacologic, medical and pharmacologic treatments concurrently.”

Lyketsos, chair of the Department of Psychiatry at Johns Hopkins Bayview, stresses that the approach “has tremendous utility in clinical trials of treatments for behavioral symptoms, particularly in testing new medications. DICE can be used to better subtype behaviors, or focus on particular behaviors at randomization coupled with systematic treatment approaches”.

MORE INFORMATION:

Reference: Journal of the American Geriatrics Society, Volume 62, Issue 4, pp 762–769, April 2014

Learn more about the U-M Program for Positive Aging , including its resources for health care providers to assist with management of behavioral aspects of dementia

Where Alzheimer's Begins

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Columbia University Medical Center.

ROOTS OF ALZHEIMER'S: 

Columbia University researchers have pinpointed 3 discoveries about Alzheimer's:

• Where it starts
• Why it starts there
• How it spreads.

Learn why this can help researchers treat Alzheimer's sooner and better. 

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Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer's disease and in mouse models of the disease, Columbia University Medical Center (CUMC) researchers have clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads. In addition to advancing understanding of Alzheimer's, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journalNature Neuroscience.

Alzheimer's disease starts in the entorhinal cortex (yellow). Using fMRI in mouse (left) and human (right) brains, the researchers provide evidence that the disease spreads from the entohrinal cortex (yellow) to other cortical regions (red) -- the perirhinal cortex and posterior parietal cortex. (Credit: Usman Khan/lab of Scott A. Small, MD, Columbia University Medical Center.)

"It has been known for years that Alzheimer's starts in a brain region known as the entorhinal cortex," said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer's Disease Research Center. "But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected."

The study also shows that, over time, Alzheimer's spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer's spreads "functionally," that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.

A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. "The LEC is especially vulnerable to Alzheimer's because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer's," said co-senior author Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.

In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP). All of the adults were free of dementia at the time of enrollment.

"Dr. Richard Mayeux's WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer's disease," said Dr. Small. "This study has given us a unique opportunity to image and characterize patients with Alzheimer's in its earliest, preclinical stage."

The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer's disease. An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) -- a measure of metabolic activity -- in the LEC compared with that of the 84 adults who were free of dementia.

A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer's.

To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small's lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.

The study has implications for both research and treatment. "Now that we've pinpointed where Alzheimer's starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer's at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions," said Dr. Small. In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer's drugs during the disease's early stages.

Why More Skinny People Have Alzheimer's

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

REFERENCE:

• “Body Mass Index and Risk of Alzheimer Disease: a Mendelian Randomization Study of 399,536 Individuals,” https://academic.oup.com/jcem/article-

Studies have found an association between Alzheimer’s and the low BMI of thin people. New findings suggest this is not a causal relationship. Find out more. 

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Washington, DC - A new large-scale genetic study found that low body mass index (BMI) is likely not a causal risk factor for Alzheimer’s disease, as earlier research had suggested, according to a study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism. 

”Although prior studies found an association between Alzheimer’s disease and low BMI, the new findings suggest this is not a causal relationship,” said the study’s senior author, Ruth Frikke-Schmidt, M.D., D.M.Sc., Ph.D., Chief Physician at Rigshospitalet in Copenhagen, Denmark, and Associate Research Professor at the University of Copenhagen. “The association can likely be explained by the fact that individuals with Alzheimer’s disease are more likely to have low BMIs due to loss of appetite and weight loss in the early stages of the disease.” 

To examine the association between Alzheimer’s disease and low BMI, the researchers analyzed blood and DNA samples from 95,578 participants in the Copenhagen General Population Study (CGPS). Of the participants, 645 individuals developed Alzheimer’s disease. 

The researchers analyzed the study participants’ DNA for the presence of five genetic variants that have strong associations with BMI. Based on how many variants were found, participants were divided into four groups to reflect the likelihood of low BMI. The researchers also analyzed data from up to 249,796 individuals participating in the Genetic Investigation of ANthropometric Traits (GIANT) consortium for the genetic variants closely linked to low BMI. 

The analysis found the presence of the genetic variants tied to low BMI was not associated with increased risk of Alzheimer’s disease. For comparison, the researchers examined if individuals with genetic variants connected to high BMI were more likely to have type 2 diabetes and did find the expected causal relationship. 

“We found individuals with lifelong low BMI due to genetic variation were not at increased risk of Alzheimer’s disease,” Frikke-Schmidt said. “Since genetic variants are not affected by other risk factors or diseases, this is a clean measure that can help to determine causality. The findings highlight that testing causality of a risk factor is pivotal before considering changing public health recommendations based on observational data alone.” 

THE STUDY:

• Other authors of the study include: Liv Tybjærg Nordestgaard and Anne Tybjærg-Hansen, of Rigshospitalet; and Børge G. Nordestgaard, of Herlev and Gentofte Hospital. All three also are affiliated with the University of Copenhagen.

SUPPORT:

• The research was supported by the Danish Medical Research Council, the Lundbeck Foundation, the Alzheimer Research Foundation, and the Research Fund at the Capital Region of Denmark.

SOURCE:

• The Endocrine Society
  Endocrinologists are at the core of solving the most pressing health problems of our time, from diabetes and obesity to infertility, bone health, and hormone-related cancers. The Society has more than 18,000 members, including scientists, physicians, educators, nurses and students in 122 countries. To learn more about the Society and the field of endocrinology, visit our site at www.endocrine.org

Alzheimer's & Incontinence

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Alzheimers&Demantia Weekly

SOURCE:
The Alzheimer's Disease Education and Referral (ADEAR) Center 

Here are some good ways you can deal with incontinence in dementia care. 

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A person with Alzheimer’s disease may have other medical problems over time. These problems can cause more confusion and behavior changes. The person may not be able to tell you what is wrong.

One problem, incontinence, means a person can’t control his or her bladder and/or bowels. This may happen at any stage of Alzheimer’s disease, but it is more often a problem in the later stages. Signs of this problem are leaking urine, problems emptying the bladder, and soiled underwear and bed sheets. Let the doctor know if you see any of these signs. He or she may be able to treat the cause of the problem.

Causes of Incontinence

1. Incontinence has several possible causes. Some can be treated:
2. Urinary tract infection
3. Enlarged prostate gland
4. Too little fluid in the body (dehydration)
5. Diabetes that isn’t being treated
6. Taking too many water pills
7. Drinking too much caffeine
8. Taking medicines that make it hard to hold urine

When you talk to the doctor, be ready to answer the following questions:

• What medicines is the person with Alzheimer’s taking?
• Does the person leak urine when he or she laughs, coughs, or lifts something?
• Does the person urinate often?
• Can the person get to the bathroom in time?
• Is the person urinating in places other than the bathroom?
• Is the person soiling his or her clothes or bed sheets each night?
• Do these problems happen each day or once in a while?

What To Do About Incontinence

Here are some ways you can deal with incontinence:

1. Remind the person to go to the bathroom every 2 to 3 hours. Don’t wait for him or her to ask.
2. Show the person the way to the bathroom, or take him or her.
3. Watch for signs that the person may have to go to the bathroom, such as restlessness or pulling at clothes. Respond quickly.
4. Make sure that the person wears loose, comfortable clothing that is easy to remove.
5. Limit fluids after 6 p.m. if problems happen at night. Do not give the person fluids with caffeine, such as coffee or tea.
6. Give the person fresh fruit before bedtime instead of fluids if he or she is thirsty.

Here are some other tips:

• Mark the bathroom door with a big sign that reads “Toilet” or “Bathroom.”
• Use a stable toilet seat that is at a good height. Using a colorful toilet seat may help the person identify the toilet. You can buy raised toilet seats at medical supply stores.
• Plan ahead if you are going out with the person. Know where restrooms are located. Take an extra set of clothing in case of an accident.
• Help the person when he or she needs to use a public bathroom. This may mean going into the stall with the person or using a family or private bathroom.

Accidents Happen

Be understanding when bathroom accidents occur. Stay calm and reassure the person if he or she is upset. 

Incontinence supplies, such as adult disposable briefs or underwear, bed protectors, and waterproof mattress covers, may be helpful. You can buy these items at drugstores and medical supply stores. A drainable pouch may be useful for the person who can’t control his or her bowel movements. Talk to a nurse about how to use this product. 

Some people find it helpful to keep a record of how much food and fluid the person with Alzheimer’s takes in and how often he or she goes to the bathroom. You can use this information to make a schedule for going to the bathroom. 

Aluminum linked directly to early onset of Alzheimer’s disease

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Natural News

Aluminum is everywhere: it contaminates vaccines, it’s in a variety of medications, baby products, cosmetics, and it’s even in the food you eat. And like several other metals, it isn’t really all that great for the human brain (or the rest of the body).

Even the CDC’s Agency for Toxic Substances and Disease Registry (ATSDR) notes that aluminum can elicit negative effects in the musculoskeletal, neurological, and respiratory systems. This is especially worrisome because some research indicates that aluminum is capable of building up in bodily tissues, which would greatly increase its potential to cause harm. [RELATED: Keep up with the latest CDC headlines at CDC.news]

Research has suggested that there may be a link between aluminum exposure and Alzheimer’s disease for several years. That link, however, has always been somewhat murky. The evidence to support their claims has often been lacking. Recently, however, scientists have found a direct link between the metal and the onset of the neurological disorder.

Connecting the dots: aluminum and Alzheimer’s

According to scientists from Keele University, located in Staffordshire, aluminum actually plays a role in most — if not all– cases of Alzheimer’s. Professor Exley, a scientist from the university, has been studying this connection at length. In a recent article for The Hippocratic Post, Exley explained, “We already know that the aluminium content of brain tissue in late-onset or sporadic Alzheimer’s disease is significantly higher than is found in age-matched controls. So, individuals who develop Alzheimer’s disease in their late sixties and older also accumulate more aluminium in their brain tissue than individuals of the same age without the disease.”

Exley went on to say that even higher levels of aluminum have been found in individuals with certain forms of Alzheimer’s disease and notes that these high amounts of exposure are often attributed to the environment these people live in, or their workplace. “This means that Alzheimer’s disease has a much earlier age of onset, for example, fifties or early sixties, in individuals who have been exposed to unusually high levels of aluminium in their everyday lives,” contends Exley.

High aluminum content in Alzheimer’s patients

In 2016, Exley published his most revealing study yet in the Journal of Trace Elements in Medicine and Biology. This study is believed to be of exceptional value because it is the first to measure aluminum content in the brain tissue of individuals that have been diagnosed with familial Alzheimer’s disease.

Alzheimer’s is considered to be “familial” when two or more people in the same family are stricken by the condition.

Exley and his team found that people who had passed away with diagnosed familial Alzheimer’s disease had the highest concentrations of aluminum in their brain tissue that had ever been recorded.

“We now show that some of the highest levels of aluminium ever measured in human brain tissue are found in individuals who have died with a diagnosis of familial Alzheimer’s disease,” Exley wrote. He went on to note that the amount of aluminum found in the brain tissue of the individuals with familial Alzheimer’s disease were almost identical to those seen in individuals who died of aluminum-induced encephalopathy while undergoing renal dialysis. [RELATED: Learn more about toxic metals and other damaging compounds at Toxins.news]

Exley and his team concluded that their research indicates that the genetic predisposition for Alzheimer’s disease is likely tied to the accumulation of aluminum in brain tissue. The researchers note that aging is a risk factor for Alzheimer’s and that the human brain tends to accumulate more aluminum as we get older. Because of aluminum’s neurotoxic effects, its accumulation in brain is going to exacerbate or contribute to any ongoing disease or toxicity.

Sources:

GreenMedInfo.com

ATSDR.CDC.gov

Self reported cognitive decline as an early warning sign of cognitive impairment or even Alzheimer'

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Barbara (Bobbi) Kolonay RN BSN MS CCM HNB-BC

Expert in Holistic Aging & Care Management, Speaker, Author, Consultant, Entrepreneur, "Assuring Dignified Aging"

Dementia Weekly

Recent data from several research groups have provided evidence that self-experienced decline in cognitive performance in elderly people, even those with normal performance on cognitive tests, is a risk factor for future dementia and Alzheimer's disease, and may indicate an increased likelihood for the presence of preclinical Alzheimer's.

However, research on SCD is limited by lack of a common research framework, which prevents comparability across studies and hinders deeper research into the topic. 

In response, Frank Jessen, Ph.D., of the University of Bonn, Germany, led an international group of Alzheimer's researchers to form the Subjective Cognitive Decline Initiative (SCD-I). The working group includes the primary authors of the recently presented diagnostic criteria as well the lead investigators of prominent biomarker initiatives (ADNI, AIBL, DESCRIPA, Dementia Competence Network) and large population-based cohort studies. The group concluded that, "The currently available data is too limited and too heterogeneous to define SCD… as a clear-cut entity and highlights the need for intensified research on this topic." 

The initial goal of the SCD-I then became to develop and disseminate a research framework for SCD, with a focus on SCD during the preclinical stage of Alzheimer's. 

"This framework provides guidelines on terminology and assessment of SCD in various research settings," said Jessen. "It also describes key features that increase the likelihood that SCD in an individual is related to preclinical Alzheimer's." 

Jessen says the new research framework "will greatly support research on the earliest stage of Alzheimer's."