Can Hippocrates prevent overdiagnosis?

Hippocrates' famous oath echoed around Barcelona's International Convention Centre throughout the fourth Preventing Overdiagnosis conference, held this past week. For three days, this eclectic and passionate mix of policy makers, clinicians, academics and patients discussed modern medicine's divagation from its binding principle: primum non nocere (first do no harm).

28 sept 2016--Dr. Catherine Calderwood, the Chief Medical Officer for Scotland, best encapsulated the spirit of the conference. Dr. Calderwood's keynote presentation highlighted the fundamental goal of all health care: person-centred care. Building on her Realistic Medicine report, Dr. Calderwood argued that effective, appropriate care is one that gives person preference (she prefers this term over patient preference) paramount importance. "I wanted to stand on my doorstep and talk to my neighbor," she recalls from an anecdote with a patient, "I wanted a grab rail to help me stand. I went to the doctor, I still don't have a grab rail, but I have a knee replacement and I still can't talk to my neighbor." Anecdotes such as this emphasise why we were all there: to re-focus on improving the health of people, rather than reflexively treating the conditions of patients." Clearly passionate about the health of Scottish people, Dr. Calderwood's conclusion resonated profoundly around the conference auditorium: 'Is it really part of your Hippocratic Oath to list someone for a procedure rather than talk them through why they don't need it?'
This fourth edition of the Preventing Overdiagnosis conferences felt like a landmark: 30% more abstracts were submitted than last year, and attendance was a record high. The three previous conferences focused largely on establishing whatoverdiagnosis is and its prevalence within our health care systems; cancer and incidental radiological findings dominated much of the discussion. Encouragingly, this year's meeting captured some of the successful follow up work of the previous years. Professor William (Bill) Black's insight into the influence of overdiagnosis and incidental findings on the forthcoming Fleischner Society Radiology guidelines, a USA-based organisation that produces guidance for radiologists reporting chest imaging, reflects the impact of these meetings and their surrounding research. Further, the quantification of a 'reservoir' of indolent cancer – cancer that grows, slowly and asymptomatically – via meta-analyses of autopsy studies has reinforced the hypothesis that we are finding cancer that patients will die with rather than from. We can be more assured in our belief that cancer exists on a spectrum and its natural course is not universally fatal.
New focuses at this year's conference included genetic testing, a more critical assessment of clinical practice guidelines, and strategies to reduce unnecessary care. Genetic testing has always lingered in the background of these conferences, often viewed apprehensively. Professor Chris Semsarian, a genetic cardiologist, allayed fears and offered great insight into the consideration taken when a genetic test is ordered and its results interpreted. Although genetic mutations of unknown significance (variants of unknown significance (VUS)) are still common, genetic-based care may still prove to be a solution to unnecessary care; the potential of precision medicine still beckons.
Clinical practice guidelines were also examined thoroughly. Often considered a benchmark of care quality, numerous methodological issues surrounding guidelines were raised, including panelists' conflicts of interest. The #showmorespinecampaign presented a novel and innovative approach to improve vertebral fracture guidelines. According to Teppo Järvinen and colleague's presentation, the problem is clear: '75% of osteoporosis guidelines do not take a stand on what cut-off point (criteria) should be used when diagnosing vertebral fractures', the consequences are also evident: '75% of osteoporosis treatment guidelines state that all vertebral fractures warrant osteoporosis medication'. The solutions remain difficult, but I applaud and colleagues' approach and look forward to following (and supporting) their campaign (see more here).
To truly mitigate the harm from too much medicine, effective strategies to reduce unnecessary testing and treatment must be established. Our conference hosts, Agència de Qualitat i Avaluació Sanitàries de Catalunya (AQuAS), have given these issues much thought and the sophistication of their public health campaigns within Catalonia reflect this. Their multi-level strategy to develop recommendations to improve care, based somewhat on the NICE Do Not Do guidelines, are already yielding improvements in the health of their people.
With our Hippocratic duty resonating amongst the delegates, the 2016 conference ended with a look ahead to the 2017 Preventing Overdiagnosis host, Quebec City, Canada. A year shall provide ample time for this enthused group to continue to fend off the unnecessary harms of too much medicine.

This story is republished courtesy of PLOS Blogs: blogs.plos.org.

Provided by PLOS

Multimodal everyday training and brain stimulation can help with memory problems

"By taking the correct steps, it is possible to delay or alleviate the early clinical symptoms of Alzheimer's such as forgetfulness," stresses Peter Dal-Bianco, Alzheimer's expert at MedUni Vienna's Department of Neurology, speaking on the occasion of World Alzheimer's Day on 21 September. A recent study from Finland and Sweden confirms the findings of MedUni Vienna researchers. For example, it was found that "multimodal everyday training" has a beneficial effect upon cognitive abilities such as planning and implementing projects.

27 sept 2016--In the so-called FINGER study (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability), 1,260 people aged between 60 and 77, who were already forgetful, were divided into two groups. Over a period of 24 months, one group of 631 people received regular physical exercise to fit in with their everyday lives, comprising walks with simultaneous conversation, balance and memory training on a computer, social activities, a healthy diet and monitoring of their cardiovascular status. Dal-Bianco says, "The result was a significant improvement in cognitive abilities in terms of processing speed and executive functions in the active group, as compared to the control group." The control group consisted of 629 people.
This is also corroborated by research results obtained at MedUni Vienna: "For example: inactive people have an 80 percent higher Alzheimer's risk than people who are physically active. Other factors that can accelerate the clinical onset of dementia include being overweight, diabetes mellitus, high blood pressure and smoking," says Dal-Bianco, in summary.
Currently, there are more than 30 million Alzheimer's sufferers worldwide. According to forecasts, this figure will have reached 63 million by 2030 and around 114 million by 2050. Currently 120,000 people are affected in Austria and by 2050 this is expected to be around 280,000.
Dal-Bianco: "The neurodegenerative tissue changes in the brain happen slowly and start approximately 30 years before the first clinical symptoms of dementia appear. And so, if we take the correct steps at an early stage and we also demonstrate scientifically that they work, many people would be able to delay the clinical onset of the disease so that they die from old age before they have to experience it."
The Department of Neurology at MedUni Vienna currently uses brain stimulation with ultrasound waves (currently as part of an ongoing clinical trial) – as well as drug therapy – to treat early-stage Alzheimer's. These waves are thought to supply energy to the brain tissue. This is thought to promote regeneration of structures in the nervous system: "This should improve brain performance," explains Dal-Bianco.
And another study into the early diagnosis of neurodegenerative diseases, such as Alzheimer's, is currently being conducted at MedUni Vienna, together with Gerhard Garhöfer of the Department of Clinical Pharmacology: This involves increasing the activity of the neurons in the retina of the eye by means of photo stimulation. If these neurons stop being able to transmit adequate signals for the nutrients and blood supply they require, this can be an indication of the development of Alzheimer's. The MedUni Vienna researchers hope that this study will provide another possible method for early detection of Alzheimer's.


Provided by Medical University of Vienna

Gastric reflux is common but may indicate a more serious health issue

Credit: University of Kentucky

GERD, or gastroesophageal reflux disease, is an extremely common problem seen by both primary care providers and specialists in gastroenterology. It is estimated that 10 to 20 percent of adults in the western world are suffering from this ailment at any given time.

26 sept 2016--Multiple studies have documented a direct connection between increasing body mass index and worsening symptoms of acid reflux. With the current obesity epidemic in our country, which has taken a particularly heavy toll on the population of Kentucky, GERD is sure to effect a growing number of people in our community in the near future.
Classic symptoms of GERD include a burning feeling in one's chest, the sensation of food in the back of the throat, sour/acidic taste in the mouth, cough, hoarseness or even outright regurgitation of food. These symptoms are often triggered by eating or laying down, and more particularly, poor eating habits or ingestion of foods known to trigger reflux. These easily avoidable eating habits include binge eating or ingestion of a few large meals throughout the day and eating within three hours of bedtime.
Foods which are known to be associated with reflux include citrus, tomatoes, garlic, onions, mint/peppermint, chocolate and greasy/fatty/spicy foods. Ingestion of alcohol, caffeine and smoking (even second hand) are also particularly problematic.
Many patients may self- medicate with OTC treatments such as calcium carbonate, ranitidine, omeprazole or even esomeprazole. As a general rule, it is not advisable to continue daily or long term reflux treatments without advice from a medical professional. The reasoning behind this recommendation is twofold. Persistent reflux may indicate a more serious medical issue and chronic usage of antacids can effect absorption of important vitamins and minerals in your GI tract increasing risk for problems such as osteoporosis, vitamin deficiencies and electrolyte abnormalities.
Alarm symptoms that should trigger a visit to your local health care provider include difficult or painful swallowing, vomiting, unintentional weight loss, anemia, visible bleeding or black stools. In most cases, primary care providers can adequately and effectively treat mild to moderate acid reflux without the need for referral to a specialty provider. Non-medicinal interventions such as weight loss, dietary changes and even raising the head of your bed at night can be extremely effective in preventing or minimizing recurrent episodes of reflux. Endoscopy is generally not recommended unless reflux is resistant to treatment or alarm symptoms are present.
GERD is an extremely common phenomenon that is bound to become even more prevalent with the worsening obesity epidemic in the United States. While over the counter treatments for acid reflux abound, persistent or alarm symptoms should always prompt consultation with a health care professional.
Primary care/family medicine professionals represent the front line for treatment of reflux and the gateway for referral to gastroenterology for refractory or alarm symptoms. They are also an excellent resource for behavioral/dietary management of chronic or intermittent reflux.


Provided by University of Kentucky

The diet that feeds your brain

The Mediterranean diet—rich in vegetables, fish and olive oil and featuring moderate alcohol consumption—has been shown to reduce the risk of heart disease, certain cancers and diabetes.

A study by researchers at Rush revealed that this diet is also associated with slower rates of cognitive decline in older adults. The study, which was published in the American Journal of Clinical Nutrition, looked at how well almost 4,000 older adults on the South Side of Chicago adhered to the Mediterranean diet.


23 sept 2016--The result: Those who most closely followed the diet in their eating habits showed slower rates of cognitive decline than those whose food choices were less in line with the diet.

Measuring the benefits

Every three years, study participants underwent a cognitive assessment that tested such things as memory and basic math skills. They also filled out a questionnaire on the frequency with which they ate 139 food items, such as cereal, olive oil, red meat and alcohol.
Out of a maximum score of 55, which would indicate complete adherence to the Mediterranean diet, study participants' average score was 28.
According to lead study author Christy Tangney, PhD, a faculty member in the Department of Clinical Nutrition at Rush, those with the higher scores were also the individuals whose cognitive tests showed a slower rate of decline—even when other factors that might account for the result, such as education level, were considered.
"It's always beneficial to eat healthily," says Tangney. "But we're finding more and more evidence that people who follow the Mediterranean diet have the right idea because they're actually helping to prevent some of the serious health problems that are prevalent among older adults."

A healthy approach to eating

A lot of the rules of thumb for the Mediterranean diet are true of any sensible eating plan, such as replacing whole or 2 percent milk with skim, loading up on lots of fresh fruits and vegetables, and avoiding breads, snacks and cereals made with refined white flour.
Here's a quick rundown of the diet:

• Eat seven to 10 servings a day of fresh fruits and vegetables, including legumes
• Switch to whole grain breads and cereals, and eat more whole-grain rice and pastas
• Keep almonds, cashews, pistachios and walnuts on hand for a quick snack (but because they are high in calories, limit yourself to about a handful a day and avoid candied, honey-roasted or salted nuts)
• Replace butter and margarine with healthy fats such as olive oil or canola oil
• Use herbs and spices instead of salt to flavor foods
• Limit red meat to no more than a few times a month
• Eat fish and poultry at least twice a week
• Limit higher fat dairy products, such as whole or 2 percent milk, cheese and ice cream, and switch to skim milk, fat-free yogurt and low-fat cheese
• Enjoy moderate amounts of red wine, such as a glass with lunch or dinner

The diet isn't just about what you should eat—it's also about what you shouldn't eat. As much as possible, avoid processed foods and choose foods with no trans-fats (trans-fats are responsible for increasing bad cholesterol, or LDL, and reducing good cholesterol, or HDL).


Provided by Rush University Medical Center

Dementia—catching the memory thief

Credit: CC0 Public Domain

Today (September 21) is World Alzheimer's Day, and over a hundred years since the first case of Alzheimer's disease was diagnosed. Since then we've learned a great deal about the protein 'tangles' and 'plaques' that cause the disease. How close are we to having effective treatments – and could we even prevent dementia from occurring in the first place?

21 sept 2016--You may have heard of the 'dementia tsunami'. It's heading our way. As our population ages, the number of cases of dementia is set to rocket, overwhelming our health services and placing an enormous burden on our society.
Only, it's not quite so simple. A study published last year by Professor Carol Brayne from the Cambridge Institute of Public Health suggested that better education and living standards meant people were at a lower risk of developing the disease than previously thought and so, despite our ageing population, numbers were likely to stabilise – and could even perhaps fall slightly.
Of course, even this more optimistic outlook does not hide the fact that millions of people worldwide will be diagnosed with dementia each year and millions are already living with the condition. An effective treatment for the 'memory thief' still seems like a distant prospect.
"Dementia isn't one disease: it's a constellation of changes in an individual's brain, with many underlying causes," says Brayne. "Most people, by the time they're in their eighties or nineties, have some of these changes in their brains, regardless of whether or not they ever develop dementia."
For this reason, Brayne believes we need a radical approach to tackling brain health throughout the course of our lifetime, with a greater emphasis on reduction in the risk of dementia achieved through measures in society that are related to better health in general, such as social and lifestyle changes, in addition to the focus on early therapeutic approaches to preventing or treating the disease through a pharmaceutical approach.
By far the most common and well-known form of dementia is Alzheimer's disease. Symptoms include memory problems, changes in behaviour and progressive loss of independence.
At a biological level, the disease sees a build-up of two particular types of proteins in the brain: fragments of beta-amyloid clump together in 'plaques' between nerve cells, and twisted strands of tau form 'tangles' within the nerve cells. These plaques and tangles lead to the death of nerve cells, causing the brain to shrink.
Clinical trials of Alzheimer's drugs are always going to be difficult, in part because trial participants are patients with advanced stage disease, who have already lost a significant number of nerve cells. But Professor Chris Dobson, who recently helped secure £17 million from the Higher Education Funding Council for England for a new Chemistry of Health Building, including the Centre for Misfolding Diseases, believes that most of the trials to date were destined to fail from the start because of a fundamental lack of understanding of the mechanisms that lead to Alzheimer's.
Understandably, most of the researchers tackling Alzheimer's approach the disease as a clinical – or at least a biological – problem. Dobson instead sees it as also being about chemistry and physics. He argues that the protein tangles and plaques – collectively known as aggregates – are demonstrating a physical property similar to the way in which crystals precipitate out of, say, salty water: all they need is a 'seed' to kick off the precipitation and the process runs away with itself. "In essence," he says, "biology is trying to suppress molecules behaving in a physical way." For his contributions, Dobson has been awarded the 2014 Heineken Prize for Biochemistry and Biophysics.
In 2009, Dobson, together with colleagues Professors Tuomas Knowles and Michele Vendruscolo, published a study that broke down the aggregation process into a combination of smaller steps, each of which could be tested experimentally. It became apparent to the team that drugs were failing in trials because they were targeting the wrong steps. "And this is still happening," says Vendruscolo. "Companies are still putting small molecules into clinical trials that, when we test them using our methods, we find stand no chance."
They believe there may be a role to play for 'neurostatins', which could do for Alzheimer's what statins already do to reduce cholesterol levels and prevent heart attacks and strokes. In fact, they may have already identified compounds that might fit the bill.
Professor Michel Goedert from the Medical Research Council Laboratory of Molecular Biology admits that there is a gap between our understanding of Alzheimer's and our ability to turn this into effective therapies.
"We know much about the causes of inherited forms of Alzheimer's disease, but this knowledge has so far not led to any therapies," he says. "It's clear now that abnormal protein aggregation is central to Alzheimer's disease, but we don't know the mechanisms by which this aggregation leads to neurodegeneration." Goedert himself played an instrumental part in studies that implicated the aggregation of tau protein in Alzheimer's disease and other neurodegenerative diseases, work that led to him being awarded the 2014 European Grand Prix from the Paris-based Foundation for Research on Alzheimer's Disease.
"I don't think we should talk of a cure," says Goedert. "At best, we will be able to halt the disease. Prevention will be much more important." Part of the problem, he says, lies in the fact that there is no absolute way of identifying those at risk of developing Alzheimer's disease.
The market for an Alzheimer's drug is massive, which is why pharmaceutical companies are racing to develop new drugs. Goedert doesn't believe we will ever find a single 'magic bullet', but will need to use combination therapies – in the same way that we treat other diseases, such as HIV – with each drug targeting a particular aspect of the disease.
Professor David Rubinsztein from the Cambridge Institute for Medical Research agrees with Goedert that we need to look at preventing Alzheimer's rather than just focusing on treating the disease. He, too, believes in the concept of neurostatins. "These compounds would be safe, well tolerated by most people and generally good for you; you could take them for many years before the onset of disease," he says. "Then we wouldn't need to worry about identifying people at highest risk of the disease – everyone could take them."
Rubinsztein is the academic lead for Cambridge's new Alzheimer's Research UK Drug Discovery Institute, part of a £30 million Drug Discovery Alliance that also includes the University of Oxford and University College London. This state-of-the-art institute will fast-track the development of new treatments for Alzheimer's disease and other neurodegenerative diseases. In particular, the Alliance will look at promising drug targets, assess their validity and develop small molecules that target them. These could then be taken up by pharmaceutical companies for clinical trials, removing some of the risk that results in most 'promising' drug candidates failing early on.
Rubinsztein is optimistic about our chances of fighting Alzheimer's. "If you could delay the onset of Alzheimer's, even by three to five years, that discovery would be transformative and massively reduce the number of people getting the disease," he says. "We're not asking to stop the disease, just to delay it. It's really not such a big ask."


Provided by University of Cambridge

Memory loss not enough to diagnose Alzheimer's

Diagram of the brain of a person with Alzheimer's Disease. Credit: Wikipedia/public domain.

Relying on clinical symptoms of memory loss to diagnose Alzheimer's disease may miss other forms of dementia caused by Alzheimer's that don't initially affect memory, reports a new Northwestern Medicine study.

20 sept 2016--"These individuals are often overlooked in clinical trial designs and are missing out on opportunities to participate in clinical trials to treat Alzheimer's," said first study author Emily Rogalski, associate professor at Northwestern's Cognitive Neurology and Alzheimer's Disease Center.
There is more than one kind of Alzheimer's disease. Alzheimer's can cause language problems, disrupt an individual's behavior, personality and judgment or even affect someone's concept of where objects are in space.
If it affects personality, it may cause lack of inhibition. "Someone who was very shy may go up to grocery store clerk—who is a stranger—and try to give her a hug or kiss," Rogalski said.
This all depends on what part of the brain it attacks. A definitive diagnosis can only be achieved with an autopsy. Emerging evidence suggests an amyloid PET scan, an imaging test that tracks the presence of amyloid—an abnormal protein whose accumulation in the brain is a hallmark of Alzheimer's—may be used during life to determine the likelihood of Alzheimer's disease pathology.
In the study, the authors identify the clinical features of individuals with primary progressive aphasia (PPA), a rare dementia that causes progressive declines in language abilities due to Alzheimer's disease. Early on in PPA, memory and other thinking abilities are relatively intact.
PPA can be caused either by Alzheimer's disease or another neurodegenerative disease family called frontotemporal lobar degeneration. The presence of Alzheimer's disease was assessed in this study by amyloid PET imaging or confirmed by autopsy.
The study demonstrates that knowing an individual's clinical symptoms isn't sufficient to determine whether someone has PPA due to Alzheimer's disease or another type of neurodegenerative disease. Therefore, biomarkers, such as amyloid PET imaging, are necessary to identify the neuropathological cause, the authors said.
Northwestern scientists looked at individuals in mild stages of language loss caused by Alzheimer's disease and described their brain atrophy based on MRI scans and their results on cognitive tests.
"We wanted to describe these individuals to raise awareness about the early clinical and brain features of PPA to develop metrics which would advocate for their inclusion in clinical trials targeting Alzheimer's disease," Rogalski said. "These individuals are often excluded because they don't have memory deficits, but they share the same disease [Alzheimer's] that's causing their symptoms."
The study was published online in the journal Neurology Aug. 26.

More information: Emily Rogalski et al, Aphasic variant of Alzheimer disease, Neurology (2016). DOI: 10.1212/WNL.0000000000003165


Provided by Northwestern University

Experimental zoster vaccine effective in adults aged 70+

18 sept 2016—An experimental vaccine against herpes zoster may offer lasting protection for most older adults who receive it, according to a study published in the Sept. 15 issue of the New England Journal of Medicine.

The new trial involved 13,900 adults age 70 and older. Participants were randomly assigned to receive either two doses of the herpes zoster subunit vaccine (HZ/su) containing recombinant varicella-zoster virus glycoprotein E and the AS01_B adjuvant system, or two doses of a placebo.
The researchers found that the experimental vaccine protected 89.8 percent of adults age 70 and up. During a mean follow-up of 3.7 years, only 23 vaccine recipients developed herpes zoster, compared to 223 placebo recipients. There were short-lived side effects, such as pain at the injection site, fatigue, or muscle pain; however, serious adverse events occurred with similar frequencies in the two study groups.
"In our trial, HZ/su was found to reduce the risks of herpes zoster and postherpetic neuralgia among adults 70 years of age or older," the authors write.
The study was funded by GlaxoSmithKline, the developer of HZ/su.

More information: Abstract

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Editorial

What do you know about pneumonia?

Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia.

CAUSES

17 sept 2016--Many germs can cause pneumonia. The most common are bacteria and viruses in the air you breathe. Your body usually prevents these germs from infecting your lungs. But, sometimes, these germs can overpower your immune system - even if your health is generally good.
Pneumonia is classified according to the types of germs that cause it and where you got the infection.

COMMUNITY-ACQUIRED PNEUMONIA

Community-acquired pneumonia is the most common type of pneumonia. It occurs outside of hospitals or other health care facilities. It may be caused by:
- Bacteria. The most common cause of bacterial pneumonia in the U.S. is Streptococcus pneumoniae. This type of pneumonia can occur on its own or after you've had a cold or the flu. It may affect one part (lobe) of the lung, a condition called lobar pneumonia.
- Bacteria-like organisms. Mycoplasma pneumoniae also can cause pneumonia. It typically produces milder symptoms than do other types of pneumonia. Walking pneumonia is an informal name given to this type of pneumonia, which typically isn't severe enough to require bed rest.
- Fungi. This type of pneumonia is most common in people with chronic health problems or weakened immune systems, and in people who have inhaled large doses of the organisms. The fungi that cause it can be found in soil or bird droppings, and vary depending on geographic location.
- Viruses. Some of the viruses that cause colds and the flu can cause pneumonia. Viruses are the most common cause of pneumonia in children younger than 5. Viral pneumonia is usually mild. But, in some cases, it can become serious.

TREATMENT

Treatment for pneumonia involves curing the infection and preventing complications. People who have community-acquired pneumonia usually can be treated at home with medication. Although most symptoms ease in a few days or weeks, the feeling of tiredness can persist for a month or more.
Specific treatments depend on the type and severity of your pneumonia, your age and your overall health. The options include:
- Antibiotics. These medicines are used to treat bacterial pneumonia. It may take time to identify the type of bacteria causing your pneumonia and choose the best antibiotic to treat it. If your symptoms don't improve, your doctor may recommend a different antibiotic.
- Cough medicine. This medicine may be used to calm your cough so that you can rest. Because coughing helps loosen and move fluid from your lungs, it's a good idea not to eliminate your cough completely. In addition, you should know that few studies have looked at whether over-the-counter cough medicines lessen coughing caused by pneumonia. If you want to try a cough suppressant, use the lowest dose that helps you rest.
- Fever reducers/pain relievers. You can take fever reducers/pain relievers as needed, such as aspirin, ibuprofen (Advil, Motrin IB and others) and acetaminophen (Tylenol and others).

Occupational therapy reduces hospital readmissions

An independent study published in Medical Care Research and Review found that "occupational therapy is the only spending category where additional hospital spending has a statistically significant association with lower readmission rates" for the three health conditions studied: heart failure, pneumonia, and acute myocardial infarction.

16 sept 2016--"The findings of this important study highlight just one of the many roles occupational therapy practitioners are playing in improving quality and reducing healthcare costs," said Frederick P. Somers, Chief Executive Officer of the American Occupational Therapy Association. "Occupational therapy practitioners are proving to be an essential member of any interprofessional team successfully addressing the changing demands of the health care delivery system."
Researchers Andrew Rogers (Johns Hopkins University), Ge Bai (Johns Hopkins), Robert A. Levin (University of Maryland School of Medicine), and Gerard F. Anderson (Johns Hopkins) used Medicare claims and cost data to examine the association between hospital spending for specific services and 30-day admission rates for heart failure, pneumonia, and acute myocardial infarction. They evaluated 19 distinct spending categories (including occupational therapy) in 2,791 hospitals for the heart failure analysis; 2,818 hospitals for the pneumonia analysis; and 1,595 hospitals for the acute myocardial infarction analysis.
The researchers point out that occupational therapy "focuses on a vital issue related to readmission rates—can the patient be discharged safely into her or his environment?" If not, occupational therapistsaddress issues from physical barriers to daily function to support networks. They cite six particular interventions provided by occupational therapists that could lower readmissions:

1. Provide recommendations and training for caregivers.
2. Determine whether patients can safely live independently, or require further rehabilitation or nursing care.
3. Address existing disabilities with assistive devices so patients can safely perform activities of daily living (e.g., using the bathroom, bathing, getting dressed, making a meal)
4. Perform home safety assessments before discharge to suggest modifications.
5. Assess cognition and the ability to physically manipulate things like medication containers, and provide training when necessary.
6. Work with physical therapists to increase the intensity of inpatient rehabilitation.

The researchers identify occupational therapy as "one spending category that affects both the clinical and social determinants of health" and note that "investing in occupational therapy has the potential to improve care quality without significantly increasing overall hospital spending."
The authors point out that "occupational therapy places a unique and immediate focus on patients' functional and social needs, which can be important drivers of readmission if left unaddressed."
More than 213,000 occupational therapy practitioners across the U.S. help people across the lifespan to be as independent as possible, despite illness, injury, or mental disability. Occupational therapy is the only profession that addresses the things patients want and need to do through the therapeutic use of everyday activities (occupations).

More information: A. T. Rogers et al. Higher Hospital Spending on Occupational Therapy Is Associated With Lower Readmission Rates, Medical Care Research and Review (2016). DOI: 10.1177/1077558716666981


Provided by American Occupational Therapy Association

Midlife physical activity is associated with better cognition in old age

A new study of 3050 twins finds moderately vigorous physical activity – i.e., more strenuous than walking – to be associated with better cognition in a 25-year follow-up.

15 sept 2016--A long-term follow-up study of 3050 twins from the Finnish Twin Cohort has shown that midlife, moderately vigorous physical activity is associated with better cognition at old age. The association was statistically independent of midlife hypertension, smoking, education level, sex, obesity and binge drinking. "This suggests that the beneficial influence of physical activity on the brain and cognition is not solely based on decreasing vascular risk factors", says researcher Paula Iso-Markku from the University of Helsinki.
The association was studied first in all individuals of the cohort, and then by comparing later cognition in pairs where one twin was more physically active than the other.
Increasing the volume of physical activity was not, however, associated with increased memory-protecting benefits. Instead, quite a moderate amount of physical activity was found to be sufficient for memory-protecting benefits, and only the most inactive group of twins stood out with a significantly higher risk for cognitive impairment.
"Overall, the study shows that moderately vigorous physical activity, meaning more strenuous than walking, is associated with better cognition after an average of 25 years", states Professor Urho Kujala from the University of Jyväskylä.
This finding is in accordance with earlier animal model studies, which have shown that physical activity increases the amount of growth factors in the brain and improves synaptic plasticity.
The prevalence of dementia has increased with aging populations both in Finland and globally. Although the incidence of dementia seems to have decreased in less senior generations, the total prevalence of dementia is still expected to rise. No cure for dementia exists, but during the last decade research has produced an abundance of new information on dementia prevention. The traditional vascular risk factors (elevated blood pressure, hypercholesterolemia, obesity, diabetes and lack of exercise) have also been associated with dementia risk. "However, few long-term, high-quality, follow-up studies on physical activity and cognition have been published, and it has remained unclear what type and amount of exercise is needed to safeguard cognition", Iso-Markku says.
The study, published in the Journal of Alzheimer's Disease, was conducted by scientists at the universities of Helsinki, Jyväskylä and Turku. The twins provided information on physical activity through questionnaire surveys from 1975 and 1981 (mean age in 1981: 49 years), while cognition was assessed by validated telephone interviews conducted between 1999 and 2015.

More information: Paula Iso-Markku et al. Midlife Physical Activity and Cognition Later in Life: A Prospective Twin Study, Journal of Alzheimer's Disease (2016). DOI: 10.3233/JAD-160377


Provided by University of Helsinki

Pregabalin significantly improves neuropathic pain

Pregabalin significantly improves neuropathic pain, irrespective of the time since pain onset, according to a study published online Sept. 2 in Pain Practice.

12 sept 2016--Concepción Pérez, Ph.D., from the Hospital de la Princesa in Madrid, and colleagues conducted a pooled analysis of 19 randomized placebo-controlled trials of pregabalin for peripheral neuropathic pain conditions (including diabetic peripheral neuropathy, postherpetic neuralgia, and posttraumatic/postsurgical pain). Patients were divided into five categories according to time since onset of pain. For each category, the mean change in pain score at end point was assessed versus placebo. Data were included for 5,783 patients (3,619 pregabalin-treated and 2,164 placebo-treated).
The researchers found that across pain duration categories, the mean baseline pain scores were similar. In all patients together, pregabalin significantly improved pain score at end point versus placebo (treatment difference, −0.59); similar results were seen in each pain duration category. Significantly more Patient Global Impression of Change responders were seen with pregabalin versus placebo for all patients (45 versus 30.9 percent) and for each category separately. No consistent, significant differences in treatment response were seen between the different categories of pain duration.
"Pregabalin significantly improves pain irrespective of the length of time since onset of neuropathic pain," the authors write.
Several authors disclosed financial ties to pharmaceutical companies, including Pfizer, which manufactures pregabalin and funded the study.

More information: Abstract

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Statins' benefits outweigh side-effects: science review

The heart-protecting benefits of anti-cholesterol statins far outnumber the side-effects, a scientific review said Friday blaming shoddy research for scaring people and putting lives at risk.
Much of the evidence for statins' bad rap came from trials whose very design did not allow them to draw any conclusions, said the authors of the review seeking to "help doctors, patients and the public make informed decisions."

10 sept 2016--Their own analysis, the team wrote, showed that statins prevented many more heart attacks and strokes than they caused muscle problems or diabetes.
"We've had an underestimation of the benefits and a massive overestimation of the harms," said Rory Collins of the University of Oxford's Nuffield Department of Population Health, who co-authored the review in The Lancet.
"Consequently there is a serious cost to public health from making misleading claims about high side-effect rates that inappropriately dissuade people from taking statin therapy despite the proven benefits."
Statins have been used for about 30 years to bring down "bad" LDL cholesterol, which has been linked to a risk for heart and artery disease.
It is prescribed as "secondary prevention" for people already suffering cardiovascular disease, but increasingly also as "primary prevention" for those at high risk due to high blood pressure or diabetes, for example.
As conflicting reports of statins' benefits and harms have hit the headlines in recent years, people prescribed them had stopped taking the drugs.
The new review showed that using statins to lower cholesterol would prevent "major cardiovascular events" in 1,000 out of 10,000 secondary prevention users over five years.
In people who take statins for primary prevention, 500 out of 10,000 would avoid a major event such as heart attack, stroke or coronary bypass, said the authors.

The snag

On the downside, five in 10,000 would develop myopathy—a muscle disease.
Five to ten would have a haemorrhagic stroke, which causes bleeding on the brain, and about 50-100 would develop diabetes.
However, Collins said the other type of stroke, caused by blood clots, was vastly reduce by statins—thus lowering the overall stroke risk.
The team had reviewed data from so-called randomised controlled trials, in which one group of people were given the real drug and another group a dummy "placebo" drug, without knowing who is getting what.
This is the only type of trial, the authors said, which can ascribe an effect to a drug being tested.
However, much of the evidence for statin risks came from "observational studies".
They are not designed to show a cause and effect, yet have ascribed to statins everything from memory loss, cataracts, liver disease, sleep disturbance, aggression, suicidal behaviour and erectile disfunction—none of which were borne out by randomised controlled trials, said the team.
"We hope that the impact of publishing this comprehensive scientific review will be to correct the public record about the safety and efficacy of statins," The Lancet editor Richard Horton told journalists.
A daily 40-milligram statin dose costs about £2 ($2.70, 2.6 euros) per month in Britain, where some two million people are prescribed statins for secondary prevention and four million for primary prevention.
This meant some 80,000 people in Britain alone will be spared a major cardiovascular event, said the reviewers, who received research funding from drug companies but insisted they were independent.
Other experts not involved in the study said it was a good summary of the risks and benefits.
"Statins have been unfairly demonised," Tim Chico, a cardiologist from the University of Sheffield, told the Science Media Centre.
"Statins can cause side effects, but the chance of developing these is low while the effects of suffering the heart attack that a statin might have prevented can be fatal or life-long."

More information: The Lancet, www.thelancet.com/journals/lancet/article/PIIS140-6736(16)31357-5/abstract

Canadian cardiovascular society sets new guidelines for atrial fibrillation management and treatment

A summary of the recommendations for the management of antithrombotic therapy in patients with atrial fibrillation in associationwith Non-ST-elevation acute coronary syndrome or ST-elevation myocardial infarction. ASA, acetylsalicylic acid (aspirin);CHADS2, Congestive Heart Failure, Hypertension, Age, Diabetes, Stroke/Transient Ischemic Attack; NOAC, non-vitamin K antagonist oral anticoagulant;OAC, oral anticoagulant; PCI, percutaneous coronary intervention. 

The Canadian Journal of Cardiology has just released the 2016 Focused Update to the Canadian Cardiovascular Society's (CCS) atrial fibrillation (AF) guidelines. This update provides evidence-based guidelines for Canadian practitioners and will impact how they, and the global community of cardiologists, manage and treat this serious condition.

09 sept 2016--AF is an irregular and often rapid heart rate that can increase the risk of stroke, heart failure, and other heart-related complications. It is the most common cardiac arrhythmia and the leading cause of stroke in the elderly.
"The development of guidelines has been a key activity of the CCS for over a decade," explained co-chairs Laurent Macle, MD, of the Montreal Heart Institute, Université de Montréal, Montreal, Quebec, and Atul Verma, MD, of the Southlake Regional Health Centre, Newmarket, Ontario, Canada. "Well-developed guidelines have the potential to improve the quality of cardiovascular care, lead to better patient outcomes, improve cost-effectiveness, and highlight areas for further research."
This update represents the consensus of a multidisciplinary panel of topic experts with a mandate to formulate disease-specific recommendations. The original guidelines were developed in 2010 by the Canadian Cardiovascular Society (CCS) AF Guidelines committee and are reviewed every two years. This is the third Focused Update.
This 2016 Focused Update makes important evidence-based recommendations on:

• Management of antithrombotic therapy for AF patients with various clinical presentations of coronary artery disease (CAD)
• Real-life data with non-vitamin K antagonist oral anticoagulants (NOACs)
• Use of antidotes for the reversal of NOACs
• Digoxin as a rate-control agent
• Perioperative anticoagulation management
• AF surgical therapy including the prevention and treatment of AF following cardiac surgery

An important change in this update is that for patients with AF in association with CAD who are indicated for anticoagulation therapy, a NOAC is preferred over warfarin.
For patients with AF, with an indication for primary CAD prevention or stable CAD/arterial vascular disease, the selection of antithrombotic therapy should be based on their risk of stroke.
For patients with AF and recent elective PCI, the selection of antithrombotic therapy should also be based on their risk of stroke.
For patients with AF in association with non ST-elevation acute coronary syndrome (NSTEACS) or ST-elevation myocardial infarction (STEMI), the management of antithrombotic therapy is based on the risk of stroke and whether PCI is performed.
Details of the updated recommendations are presented, along with their background and rationale. Standards, individual studies, and literature were reviewed for quality and bias. The update also includes a section on concomitant AF and coronary artery disease, which was developed in collaboration with the CCS antiplatelet (APT) guidelines committee. An updated summary of all CCS AF Guidelines recommendations, from 2010 to the present 2016 Focused Update, are provided in an Online Supplement.

More information: "2016 Focused Update of the Canadian Cardiovascular Society Guidelines for the Management of Atrial Fibrillation," by Laurent Macle, MD (Co-chair), John Cairns, MD, Kori Leblanc, PharmD, Teresa Tsang, MD, Allan Skanes, MD, Jafna L. Cox, MD, Jeff S. Healey, MD, Alan Bell, MD, Louise Pilote, MD, Jason G. Andrade, MD, L. Brent Mitchell, MD, Clare Atzema, MD, David Gladstone, MD, Mike Sharma, MD, Subodh Verma, MD, Stuart Connolly, MD, Paul Dorian, MD, Ratika Parkash, MD, Mario Talajic, MD, Stanley Nattel, MD, and Atul Verma, MD (Co-chair) for the CCS Atrial Fibrillation Guidelines Committee,

DOI: dx.doi.org/10.1016/j.cjca.2016.07.591 . Published online in advance of Volume 32/Issue 10 (October 2016) of the Canadian Journal of Cardiology.


Provided by Elsevier

Living with the risk of Alzheimer's disease

What are the expectations of persons who decide to have their risk of Alzheimer's Disease tested? What should doctors pay attention to when ascertaining individual risks? What is the benefit of risk determination for patients and their close others, while options to treat the disease remain insufficient?

08 sept 2016--According to current estimates, the number of individuals suffering from Alzheimer's Disease worldwide is 40 million – and rising. The burdens imposed on the patients, on their caregivers, and on society are considerable.
Due to recent advances in the prediction of Alzheimer's Disease, examinations for risk assessment are rapidly increasing – often by the patients' own demand. This prediction may, however, have a major psychological impact on patients and their close others, since there is no effective treatment to prevent Alzheimer's Disease.
The interdisciplinary project "Ethical and Legal Framework for Predictive Diagnosis of Alzheimer's Disease: Quality of Life of Individuals at Risk and Their Close Others (PreDADQoL)" addresses these issues and aims to close an important research gap by providing an ethical and legal framework for the predictive testing of Alzheimer's Disease. The project will be conducted under the auspices of the Center for Ethics, Rights, Economics and Social Sciences of Health (ceres) at the University of Cologne in cooperation with the Fundació ACE Barcelona, one of the largest Alzheimer's clinics in Europe.
PreDADQoL will be funded by the Federal Ministry of Education and Research for three years with an amount of 300,000 €. The coordinating supervisor is the executive director of ceres, Prof. Christiane Woopen. The research team consists of the executive director of the Institute for Medical Law of the University of Cologne, Prof. Christian Katzenmeier, the director of the Department of Psychiatry and Psychotherapy at the University Hospital Cologne, Prof. Frank Jessen, and the director of the Barcelona Alzheimer Treatment & Research Center, Mercè Boada, MD, PhD.
ceres, the Cologne Center for Ethics, Rights, Economics and Social Sciences of Health, is a cross-departmental center for interdisciplinary research, education and advanced training in the area of health. ceres also carries out advisory functions on health-related matters. The center was founded by five Faculties and the President of the University of Cologne.


Provided by University of Cologne

Post-mortem assessment guidelines for vascular cognitive impairment

New research, led by academics at the University of Bristol, has outlined the first validated set of pathological criteria for assessing the likelihood that cognitive impairment was caused by vascular disease.

07 sept 2016--The term vascular cognitive impairment (VCI) refers to a diverse group of conditions in which memory problems and other impairments of mental function result from inadequate blood flow through the brain. Vascular dementia is a severe form of VCI.
Confirmation of the clinical diagnosis of most diseases that cause dementia depends on post-mortem examination of the brain. The finding of brain tissue damaged by impaired blood supply, or of widespread hardening of the arteries in the brain suggests that the cognitive impairment was caused by vascular disease. However, these pathological abnormalities are also often found in combination with other dementing diseases such as Alzheimer's disease and, until recently, the contribution of different vascular abnormalities to cognitive impairment was difficult to quantify, as there were no validated criteria for determining this.
A large group of UK neuropathologists and other scientists, led by the University of Bristol Dementia Research Group and supported by Alzheimer's Society and Alzheimer's Research UK, has developed a set of Vascular Cognitive Impairment Neuropathology guidelines (VCING) for assessing vascular pathologies in post-mortem brain tissue. The researchers, using brains that had been donated through a scheme called Brains for Dementia Research (BDR), have identified a set of neuropathological determinants that can reproducibly be used to assign a low, intermediate or high likelihood that vascular disease contributed to cognitive impairment in an individual case.
Seth Love, Professor of Neuropathology in the University of Bristol's School of Clinical Sciences, said: "VCING represent a major advance in our ability to assess the contribution of vascular pathology to cognitive impairment and open the way to a range of studies of the determinants of VCI, including of processes that are potentially preventable or modifiable.
"More accurate determination of the contribution of cerebrovascular disease to cognitive impairment and dementia is likely to inform healthcare policy and prioritisation of resources for patients with VCI, and lead to more funding of VCI-related research. It also opens the way to a range of mechanistic studies of pathophysiological determinants of VCI, with a view to identifying processes that are potentially preventable or modifiable."
Dr Rosa Sancho, Head of Research at Alzheimer's Research UK, added: "This collaborative effort has produced a common approach for researchers working to understand the changes that take place in blood vessels that can contribute to cognitive decline. The guidelines developed through this project have the potential to help researchers and clinicians across the globe to streamline their research into dementia, taking a step forward in improving the accuracy and reliability of their work. With a growing international focus on dementia research, it's crucial that researchers are co-ordinated in their approach to studying the condition to ensure we make progress as quickly as possible for the millions affected worldwide."
It is estimated that vascular dementia accounts for around ten to 20 per cent of patients with dementia and it is the second most common cause of dementia after Alzheimer's disease.

More information: Olivia A. Skrobot et al. Vascular cognitive impairment neuropathology guidelines (VCING): the contribution of cerebrovascular pathology to cognitive impairment, Brain (2016).DOI: 10.1093/brain/aww214


Provided by University of Bristol

Italy's 100 club village reveals its secret

Scientists on Monday revealed part of the secret to why a small village in southern Italy has an unusual number of centenarians—low levels of a particular hormone that affects circulation.
Italian and US experts have spent the last six months investigating the extraordinary longevity of residents of Acciaroli, where more than one in 10—81 at the mayor's last count—of the village's population of 700 is over 100 years old.

06 sept 2016--Acciaroli is part of the Cilento coast, an area of outstanding natural beauty where the late US nutritionist Ancel Keys first established convincing evidence of the health benefits of a Mediterranean diet based on olive oil and rich in fresh fruit, vegetables and fish.
As well as reaching extremely old age, people in Acciaroli and tiny communities nearby also seem to be largely immune to dementia, heart disease and other chronic conditions associated with ageing in most of the Western world.
Researchers from Rome's Sapienza University and the San Diego School of Medicine said Monday that the explanation could lie in low levels of adrenomedullin, a hormone that acts to widen blood vessels.
Adrenomedullin is present "in a much reduced quantity in the subjects studied and seems to act as a powerful protecting factor, helping the optimal development of microcirculation", or capillary circulation, they said in a statement.
Capillary blood vessels tend to degenerate in older people, but the seniors in Cilento had capillaries of the sort found in much younger people, even those in their 20s.
The study also found "metabolites present (in the bodies of those studied) which may have a positive influence on longevity and the well-being of Cliento's centenarians", the statement said, without giving further details.
The researchers have decided to extend the study and expand their research, including by launching a fundraising campaign.
Aside from blood tests, the researchers also carried out cardiac and neurological tests, Alan S. Maisel, the San Diego cardiologist heading up the project, told AFP.
The scientists are looking into whether genetics could combine with lifestyle factors—diet and physical activity—to extend the villagers' longevity.
The Cilento locals all eat rosemary—known to improve brain function—almost every day, and also all practise some physical activity daily, such as fishing, walking or gardening, another line of enquiry for the scientists.
Before Monday's release of results, Maisel also pointed to what may be another important ingredient in the recipe for a long and happy life.
"Sexual activity among the elderly appears to be rampant," Maisel said. "Maybe living long has something to do with that, it's probably the good air and the joie de vivre."

ANTARCTIC trial antiplatelet monitoring: No benefit in elderly patients

Monitoring platelet function in order to individualize antiplatelet therapy did not improve outcomes for elderly patients after a heart attack compared to a standard, unmonitored approach, results of the ANTARCTIC trial show.

05 sept 2016--The findings, presented in a Hot Line session at ESC Congress 2016, and with simultaneous publication in the Lancet, challenge current international guidelines which recommend platelet function testing in high risk patients.
"Platelet function testing is still being used in many centres to measure the effect of antiplatelet drugs and adjust the choice of these drugs and their doses. Our study does not support this practice and these recommendations," said senior investigator Gilles Montalescot M.D, Ph.D, from Hôpital Pitié-Salpêtrière, in Paris, France.
"Although measuring the effect of antiplatelet agents makes sense in order to choose the best drugs or doses, this costly and more complex strategy does not appear to benefit patients, even when they present with extremely high risk of ischemic and bleeding events liked those enrolled in ANTARCTIC."
ANTARCTIC is the only study of platelet function testing in elderly patients at very high risk of ischemic and bleeding complications.
It enrolled 877 patients, aged 75 years or more, who presented with an acute coronary syndrome and underwent coronary stenting.
All patients were started on the antiplatelet agent prasugrel (5mg), with 442 randomised to the conventional therapy (no adjustment) and 435 to monitoring and treatment adjustment, if needed.
Patients in the monitoring arm received 14 days of the daily 5mg prasugrel dose, but then underwent a platelet function test at Day 14, followed by medication adjustment, if the test showed high or low platelet reactivity. Additional monitoring was performed at Day 28 in patients who needed treatment adjustment.
The primary end point of the trial was the composite of cardiovascular death, myocardial infarction, stroke, stent thrombosis, urgent revascularization and bleeding complication at 1-year.
This endpoint occurred at a similar rate in both arms of the study: 27.6% in the monitoring group, and 27.8% in the conventional group (hazard ratio [HR], 1.003; 95% confidence interval [CI], 0.78 to 1.29; P=0.98).
There was similarly no significant difference in rates of the main secondary end point (a composite of cardiovascular death, myocardial infarction, stent thrombosis or urgent revascularization), which occurred in 9.9% and 9.3%, respectively (HR, 1.06; 95% CI, 0.69 to 1.62; P=0.80).
"Platelet function monitoring led to a change of treatment in 44.8% of patients who were identified as being over- or under-treated, yet this strategy did not improve ischemic or safety outcomes," noted Professor Montalescot.
"ANTARCTIC confirms the ARCTIC study (NEJM 2011) in a different population with a different drug, and has addressed the potential limitations of the ARCTIC study, but finally reached the same conclusion. I expect there will be adjustments of guidelines and practice in light of this."
ANTARCTIC stands for Assessment of a Normal versus Tailored dose of prasugrel after stenting in patients Aged > 75 years to Reduce the Composite of bleeding, stent Thrombosis and Ischemic Complications.


Provided by European Society of Cardiology

Healthy ageing—longer healthspan with spermidine

Spermidine cleans the cells and could potentially prolong lifespan. Research is ongoing and some of it is presented by Professor Frank Madeo at the Healthy Ageing conference tomorrow.
Seven questions for Frank Madeo, Professor at the Institute of Molecular Biosciences at the University of Graz, and one of the speaker on the second day of the Healthy Ageing Seminar days.

What will you talk about at Healthy Ageing?

02 sept 2016--I will talk about our finding that you can, instead of fasting, have the benefits of fasting by administer the caloric restriction mimetic spermidine.

Tell us more about this?

In 2009, we discovered that spermidine induces autophagy, a cellular self cleaning process. In autophagy, damaged material that is accumulating during ageing is digested to replenish the energy need of the cell in times of starvation. Thereby also toxic junk is removed, and this explains the age-protective effect. We found that spermidine induces longevity and autophagy in different species, such as flies, worms and yeasts. It also protects against ageassociated diseases like dementia or cancer in model organisms.

That's amazing. What did your research results lead to?

Our finding has led to a "boom" in research. Many other labs are now working to defeat age-associated disease with spermidine administration. This applies to divergent fields, for instance muscle degeneration, age-induced immune dysfunction and stem cell pluripotency during aging.

Where can this take us – are we all to use spermidine in the future? And will we then live "forever"?

Who knows the future? But what is pretty clear to me is that we will not live forever, for sure. The damage that accumulates in the body is too random and too unpredictable. And in addition: Do we really want to prolong live beyond agony? Wouldn't it be better – and this is a realistic goal – to prolong healthsspan? I am quite sure that fasting regimes, or fasting mimicking diets, or fasting mimicking supplements like spermidine, may prolong healthsspan in the future. Healthy ageing is probably more dependent on lifestyle than on genes: So – it is possible that we will use these techniques to keep healthy longer.

What are the side effects?

Currently, we do not know any side effects. You can probably overdo it, like with everything. But the moderate supplementation that is used in mice by many research groups in order to defeat age-associated diseases reportedly has no side effects.

Has spermidine reached patients – is it used by humans today?

The first clinical trial, in which we administer a spermidine rich extract from wheat germs to elderly people, is currently ongoing. This is a collaboration between my lab and the Charite/Berlin. Our question is: Will age-associated decline in cognitive function be prevented by spermidine supplementation? The next clinical trial is currently being planned in Padova. They want to study if spermidine can prevent age or disease associated muscle loss.

Can I do something myself? Can I eat things that is rich in spermidine to perhaps reach some effects?

Definitely. It has been reported that consumption of spermidine rich food leads to enhancement of the polyamine – spermidine or spermine – concentration in the blood after three month. So, a change in diet towards spermidine rich food might be effective. High concentrations of spermidine are for example available in wheat germs, mushrooms, strongly fermented cheese, meat, green salad, and pears.


Provided by Chalmers University of Technology

Antipsychotic medications linked to increased risk of pneumonia in persons with Alzheimer's disease

Antipsychotic medications are associated with an increased risk of pneumonia in persons with Alzheimer's disease (AD), according to new research from the University of Eastern Finland. The risk of pneumonia was the highest at the beginning of antipsychotic treatment, remaining elevated also in long-term use. No major differences were observed between the most commonly used antipsychotics.

01 sept 2016--Pneumonia was listed as one of the leading causes of death in the FDA's 2005 warning on the use of antipsychotics for the treatment of behavioural and psychological symptoms of dementia. Since then, antipsychotics have been linked to an increased risk of pneumonia in in several studies, but studies among persons with dementia have been scarce. However, almost one third of Finns with Alzheimer's disease use antipsychotic medication.
The association between antipsychotic medication and hospitalisations or deaths due to pneumonia in 2005-2012 was investigated in the nationwide register-based cohort study MEDALZ at the University of Eastern Finland. The study included 60,584 persons with a clinically verified diagnosis of Alzheimer's disease. Persons who had used antipsychotic medication or had pneumonia within one year before the beginning of the follow- up and those who had schizophrenia and bipolar disorder were excluded from the study. The results were compared to a matched cohort of persons without Alzheimer's disease.
The age-adjusted pneumonia incidence during antipsychotic use periods was similar in the AD and non-AD cohort (9.5/100 person-years and 10.2/100 person-years, respectively) while the higher risk of pneumonia among persons with Alzheimer's disease was more evident during non-use (4.8/100 person years in those with Alzheimer's disease and 2.4/100 person-years in those without Alzheimer's disease). Thus, antipsychotic use was associated with a two-fold risk of pneumonia in persons with Alzheimer's disease and even a higher relative risk increase (3.43-fold) among those without Alzheimer's disease.
The findings indicate that antipsychotic use is linked to a higher pneumonia risk regardless of age, applied study design, treatment duration, choice of medication or comorbidities. In addition, the study only included cases of pneumonia leading to hospitalisation or death, which means that the actual risk increase may be even higher. Consequently, the risk-benefit balance should be carefully considered when antipsychotics are prescribed, and the treatment period should be as short as clinically possible.
The study also involved researchers from the University of Helsinki and Karolinska Institutet.

More information: Anna-Maija Tolppanen et al, Antipsychotic use and risk of hospitalisation or death due to pneumonia in persons with and without Alzheimer's disease, Chest (2016). DOI: 10.1016/j.chest.2016.06.004


Provided by University of Eastern Finland