Parkinson's drug may help treat cancer: Study

29 September 2017 

WASHINGTON: A drug used to treat Parkinson's disease has significant anticancer effects in human cells and could pave the way for novel treatments against the deadly disease, scientists have found.

The findings may also explain the low incidence of many cancers in patients with Parkinson's disease.

"Carbidopa is a FDA-approved drug for treating Parkinson's disease. Hence, clinical trials can be conducted right away to evaluate its efficacy in humans as an anticancer drug," said Yangzom Bhutia from Texas Tech University in the US.

Parkinson's disease is a degenerative neurological disorder that mostly influences a person's movement and motor skills, with symptoms including shaking, rigidity and difficulty in walking.

These effects are a result of lower than normal production of dopamine, a chemical that sends behavioural signals from the brain to the body.

While there is currently no cure for the condition, there are a number of treatments that act to reduce the severity of the symptoms of Parkinson's disease. Dopamine itself cannot be used as a drug, as it will not cross the blood-brain barrier.

However, one of the chemicals that forms dopamine levodopa or L-DOPA - can cross into the brain and is converted into dopamine once there.

L-DOPA has been used to treat Parkinson's disease symptoms for many years, but when used alone can result in side effects such as nausea.

This is because only 5-10 per cent of levodopa taken as a drug crosses the blood-brain barrier, with the rest being converted into dopamine elsewhere in the body.

The drug carbidopa does not cross into the brain, but when taken with L-DOPA prevents its conversion into dopamine outside the brain and reduces side effects for patients.

Many studies show that patients with Parkinson's disease have a lower rate of most cancers compared with the general population.

As most patients in these studies were treated with a combination of L-DOPA and carbidopa, it is possible that one or both of these drugs could exhibit anti-cancer properties and contribute to the lower incidence of cancer observed in these patients.

Earlier studies showed that L-DOPA does not have anticancer properties, but until now the potential anticancer properties of carbidopa have not been investigated.

"Carbidopa is never used by itself as a drug for any disease. But our data show that carbidopa by itself possesses the anticancer effect," said Bhutia, lead author of the study published in the Biochemical Journal.

"We believe that the reduced incidence of most cancers in Parkinson's disease patients is due to carbidopa," she said.

"We also postulate that the increased incidence of melanoma in Parkinson's disease patients is most likely due to L-DOPA, and not due to carbidopa, because L-DOPA is the precursor for melanin synthesis, a metabolic pathway that occurs exclusively in melanocytes," she added.

http://www.newindianexpress.com/lifestyle/health/2017/sep/29/parkinsons-drug-may-help-treat-cancer-study-1664546.html

Walk to Stamp Out Parkinson's 2017

JOIN US ON SATURDAY, OCTOBER 14, 2017, AS WE WALK TO STAMP OUT PARKINSON'S AT THE PHILADELPHIA ZOO!  

We are SO proud that the Walk to Stamp Out Parkinson’s remains one of the biggest grassroots community fundraising events to support people with Parkinson’s and their families in the Delaware Valley. And, we are proud to host our 2017 Walk to Stamp Out Parkinson's at the Philadelphia Zoo, America's First Zoo. 

In 2016, over 2,000 walkers, donors, friends, colleagues, healthcare professional came together for the Walk to Stamp Out Parkinson's in support of families impacted by the disease. 

As a fundraising event, Stamp Out Parkinson’s has raised over $2.4 million dollars over the last 15 years that are reinvested back into our region for research and quality of life programs and services.

What’s New This Year? It’s all about IMPACT!

When you join us for our Walk to Stamp Out Parkinson’s, you make an impact in the lives of families living with Parkinson’s disease through your fundraising efforts.

That’s why we are asking all participants to make a financial commitment to attend the Walk on Saturday, October 14th. And, if you can’t be with us in person, you can still make an impact gift as a donor and virtual walker.  

When you join us at the zoo, you and your team will have access to the zoo for the entire day and you can explore at your own pace. A schedule of events:

7:45 AM - 8:30 AM REGISTRATION 

• Visit 98.1 WOGL and our partners!

7:45 AM – 9:30 AM SPONSOR FAIR AND TEAM PHOTOS

8:00 AM - 9:00 AM PHILLY PHANATIC

8:30 AM – 9:15 AM A WALK TO STAMP OUT PARKINSON'S 

8:45 AM – 9:30 AM MOVEMENT CENTRAL! TENTATIVE SCHEDULE:

• 8:45 – 9:00 am:  Dance for PD with Keila Cordova
• 9:00 – 9:15 am:   Rock Steady Boxing with Heather Cianci
• 9:15 – 9:30 am:   Rhythm of Life Percussion Experience with Jim Mobile

9:15 AM 2017 WALK CONCLUDES

HANG OUT AT THE PHILADELPHIA ZOO FOR POST-WALK FUN ACTIVITIES!

How to Participate

There are several ways to support the walk – as an individual, as a family, as a team captain, or as a virtual walker.  And, you can always donate! 

Click here for steps to register as a returning team and as a participant by going to:

https://www.dropbox.com/s/l900hfs5qua13rw/2017%20Team%20Captain%20Guide%20FINAL%20PDF%20VERSION.pdf?dl=0 

 As an Individual

• Register as an a participant (Participants 18 years of age and over).Your registration fee gives you day-long access to the zoo (in and out privileges), an official walk T-shirt, snacks, entertainment AND supports one individual to attend 5 Dance for PD classes. On October 14th, the fee to attend is $50 per person.  Children under 10 years of age are free.

As a Team Captain

• If you register as the Team Captain, ask your family, friends or colleagues to join your team. Teams that raise $1500 or more will be added to the Champions Circle with the team name included on the official walk T-shirt. Raise $2500 or more and you and your team will be invited to a special "post-event party" hosted by our Presenting Sponsor, AbbVie, featuring food, fun and games. 

As a Family

• The Family 4-Pack for $100 allows a family of 4 (children 10 to 17 years of age) day-long access to the zoo, four official walk T-shirts, snacks and entertainment. 

As a Virtual Walker

• If you can’t be at the walk but would still want to fundraise for the event, sign up as a virtual walker. You can share your fundraising efforts with friends and family so that they can support your efforts! If you raise $50 or more, you will receive an official walk T-shirt!

Make an Impact Gift

• Find a level of support, identify a team or walker (if you prefer) and give to make an impact. Your donation is 100% tax-deductible and will go towards programs that keep people with Parkinson’s active and engaged.

Get Inspired! Create, join, donate or support a team!

https://youtu.be/Sog30hCgbac

http://events.theparkinsoncouncil.org/site/TR/Events/General?fr_id=1090&pg=entry

New Orleans Ballet Association: Parkinson's dance class

September 29, 2017

NEW ORLEANS (AP) — The New Orleans Ballet Association has begun free dance classes for people with Parkinson's disease and their families, caregivers and friends.

The chronic neurological disorder causes tremors and movement difficulties.

Organizers say Dance for Parkinson's instructors will deal with symptom-specific concerns related to balance, cognition, motor skills, depression and physical confidence, but the classes are designed as an enjoyable aesthetic experience rather than as therapy.

A spokeswoman says 80 people registered for Wednesday's kickoff. There's no limit on the number who can sign up. Classes begin Oct. 4, and will be Wednesdays at 11 a.m. at the Jewish Community Center.

The Oscar J. Tolmas Charitable Trust is presenting the program modeled after the Mark Morris Dance Group's Dance for PD program, which is based in New York with affiliates worldwide.

http://www.beaumontenterprise.com/news/article/New-Orleans-Ballet-Association-Parkinson-s-dance-12239946.php

Cognitive Dysfunction Linked to Increased Parkinson's Risk

Deborah Brauser

September 29, 2017

Dr Sirwin K.L. Darweesh

Early cognitive dysfunction may be a significant risk factor for future risk for parkinsonian disorders, including Parkinson's disease (PD), new research suggests.

Among more than 7300 study participants, those with low overall cognitive scores at baseline were at significantly greater risk for incident parkinsonism and for probable PD 8 years later than those with higher baseline scores.

Risk for parkinsonism was also increased for those with poor scores on a range of different types of tests, including letter-digit substitution and verbal fluency.

"The findings suggest that cognitive dysfunction can be considered a sign of prodromal PD," the investigators, led by Sirwin K.L. Darweesh, MD, Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, the Netherlands, write.

Dr Darweesh told Medscape Medical News that although the investigators were not surprised to see the association between poor cognitive function and "short-term risk" of parkinsonism, it was interesting to see that the risk went beyond an 8-year interval.

"Furthermore, our observation that diverse domains of cognition, including executive, attention, cognitive speed, and memory, are already implicated in prodromal parkinsonism patients extends prior observations" in those with clinical parkinsonism, he said.

The findings were published online September 25 in JAMA Neurology.  

"Growing Urgency"        

Although previous research has shown that patients with PD often have cognitive dysfunction, "there is a scarcity of data on cognitive functioning before parkinsonism diagnosis," the authors write.

"In clinical parkinsonism patients, most notably those with Parkinson's disease, damage to the brain is already quite advanced at the time of diagnosis, rendering them less susceptible to putative disease-modifying interventions," added Dr Darweesh.

"As a consequence, there is a growing sense of urgency to unravel the prodromal phase of common parkinsonism diseases."

For the current analysis, the investigators assessed 7386 participants in the prospective, population-based Rotterdam Study (57.4% women; mean age, 65.3 years). Baseline cognition was assessed between January 2002 and December 2008 by using a battery of tests.

In the study cohort, 1.1% developed incident parkinsonism during a mean follow-up of 8.3 years. Of these participants, 72.2% were diagnosed with probable PD, and 30.4% had comorbid dementia.

In the 24 patients who had comorbid dementia, 10 developed it before onset of parkinsonism, while the others developed it afterwards.

Results showed that the participants who had low global cognition scores at baseline were more likely to have incident probable PD than those with higher scores at baseline (adjusted hazard ratio [HR], 1.52; 95% confidence interval [CI], 1.11 - 2.08). Changes in semantic fluency were also associated with probable PD (HR, 1.35).

The following table shows that low scores on several cognitive tests were significantly associated with increased risk for parkinsonism.

Table. Risk Factors for Incident Parkinsonism

Low Baseline Scores for:	HR (95% CI)
Global cognition	1.79 (1.37 - 2.33)
Letter-digit substitution	1.59 (1.22 - 2.04)
Verbal fluency	1.61 (1.23 - 2.08)
Inverted interference task on Stroop color word test	1.56 (1.25 - 1.96)

The association between poor baseline global cognition scores and incident parkinsonism remained significant past 8 years (HR, 1.59; 95% CI, 1.01 - 2.59). Even after exclusion of the participants who developed dementia, the HR was still a significant 1.72.

he likelihood ratio for parkinsonism development was 2.66 for those who had both cognitive impairment and "subtle motor signs" at baseline (95% CI, 1.64 - 4.32).

"Our data provide important insight" into the link between cognitive dysfunction and risk of parkinsonism within the general population, "especially given the fact that, to our knowledge, only 2 community-based studies have previously published data on this topic," write the investigators.

Changing the Disease Course

In an accompanying editorial, Ethan G. Brown, MD, and Caroline M. Tanner, MD, PhD, both from the Movement Disorders and Neuromodulation Center at the University of California, San Francisco, write that the Rotterdam Study "provides an excellent setting" for looking into these issues.

"Because this is a large, community-wide cohort with low attrition, the results are broadly applicable," the editorialists write.

However, noted limitations include the following: "the neuropsychological assessment was not as thorough as currently recommended" for assessing cognition in PD; the primary outcome was development of parkinsonism, including vascular and medication-induced versions, instead of development of PD; and "the study design precluded specialist adjudication of all PD diagnoses."

Still, "these findings have numerous implications," Dr Brown and Dr Tanner write.

They note that the association between changes in semantic fluency and probable PD echoes previous results and underlines the importance of giving this type of test early on. Another key finding was that patients with mild cognitive impairment, especially those with subtle motor signs, may have prodomal PD.

"This recognition can allow physicians to screen for falls or other nonmotor aspects of PD in these cases and provide early treatment for these symptoms," they write.

"Intervening at the earliest stage of PD may provide the best chance for slowing disease progression and maintaining function. Clarification of the early course of PD with studies such as this may allow identification in time to change the course of disease."

The analysis was supported by Stichting ParkinsonFonds. The Rotterdam Study is supported by the Erasmus MC University Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Ministry of Education, Culture and Science; the Ministry of Health, Welfare and Sports; the European Commission; the Netherlands Genomics Initiative; and the Municipality of Rotterdam. The study authors have disclosed no relevant financial relationships. Dr Brown receives compensation for serving on the Fellowship Advisory Board for AbbVie Inc. Dr Tanner reports receiving grants from the Michael J Fox Foundation, the Parkinson's Disease Foundation, the Department of Defense, Sage Bionetworks, and the National Institutes of Health; compensation for serving on Data Monitoring Committees for Biotie Therapeutics, Voyager Therapeutics; and Intec Pharma; and consulting fees from Neurocrine Biosciences, Adamas Therapeutics, and PhotoPharmics.

http://www.medscape.com/viewarticle/886336#vp_2

The food ingredient hordenine in beer activates the reward centre in the brain

September 29, 2017

FAU-based researcher Thomas Sommer preparing a sample of beer. After processing, the level of hordenine in the sample is determined using high-performance liquid chromatography and mass spectrometry. Credit: FAU/Katharina Götz

Visitors to the Oktoberfest have always known it and now it has been scientifically proven – beer can lift your spirits. Scientists at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) examined 13,000 food components to find out whether they stimulate the reward centre in the brain and make people feel good. Hordenine which is found in malted barley and beer seems to do the job quite well.

Some foods make us happy. Well, maybe not happy but they make us feel good. That is why we cannot stop eating when we have had enough. Scientists call this hedonic hunger – the drive to eat for pleasure rather than to satisfy an actual biological need. This feel-good effect is caused by the neurotransmitter dopamine – tempting foods stimulate the reward centre in the brain where the dopamine D2 receptor is located. Researchers of the Chair of Food Chemistry at FAU investigated whether there are special substances in foods that activate the dopamine D2 receptor in the same way as dopamine.

The team worked with FAU's Computer Chemistry Centre using a virtual screening approach which is often used in pharmaceutical research. This process analyses food components in a computer simulation rather than in the laboratory. Using computer simulations means that all types of known substance can be investigated. In the laboratory, it is only feasible to test a small selection of foodstuff extracts using standard screening techniques. 

13,000 molecules, 17 hits

Initially, the scientists set up a database of 13,000 molecules which are present in foodstuffs. Using this database, the objective was to find those molecules that fit the dopamine D2 receptor – rather like finding the right key for a lock. The system was then used to identify which molecules could interact with the dopamine D2 receptor; these might be present in synthetic substances already known to interact with the receptor, such as medicines for treating Parkinson's and schizophrenia, or which might be candidates for interaction due to the three-dimensional structure of the receptor. In the end, 17 of the original 13,000 options were selected and these were analysed in the laboratory in cooperation with the Division of Medicinal Chemistry at FAU.

Beer – a surprise finding

The most promising results were obtained for hordenine, a substance present in malted barley and beer. 'It came as a bit of surprise that a substance in beer activates the dopamine D2 receptor, especially as we were not specifically looking at stimulant foodstuffs,' explains Prof. Dr. Monika Pischetsrieder.

Just like dopamine, hordenine stimulates the dopamine D2 receptor, however it uses a different signalling pathway. In contrast with dopamine, hordenine activates the receptor solely through G proteins, potentially leading to a more prolonged effect on the reward centre of the brain. The team is now investigating whether hordenine levels in beer are sufficient to have a significant effect on the reward centre. All things considered, the results indicate that hordenine may well contribute to the mood-boosting effect of beer.

The researchers have published their findings in an article in Scientific Reports.

More information: Thomas Sommer et al. Identification of the Beer Component Hordenine as Food-Derived Dopamine D2 Receptor Agonist by Virtual Screening a 3D Compound Database, Scientific Reports (2017). DOI: 10.1038/srep44201 

Journal reference: Scientific Reports 

Provided by: Friedrich-Alexander University

https://medicalxpress.com/news/2017-09-food-ingredient-hordenine-beer-reward.html

Researchers get a lead on how to detect degenerative neurological diseases sooner

September 29, 2017

TSRI postdoctoral researcher Joseph D. Schonhoft and graduate student Cecilia Monteiro. Credit: TSRI

Researchers at The Scripps Research Institute (TSRI) may have found a way to help doctors diagnose diseases like Alzheimer's and Parkinson's earlier in their progression. A special peptide probe being developed in Jeffery Kelly's lab at TSRI is showing promise as a tool for detecting the early signs of transthyretin (TTR) polyneuropathy, a progressive neurological disease. This probe could enable doctors to implement interventions before degeneration becomes too severe, allowing treatments to be more effective. This probe may also increase our understanding regarding which aggregate structure(s) disrupts the normal functions of neurons.

Misfolded proteins misassemble into amyloid in a defined insoluble 3D structure. Since amyloid deposits are a common feature of most neurodegenerative diseases, this structure is considered responsible for a variety of amyloid diseases, from cardiomyopathies to neurodegenerative diseases including Alzheimer's, without much direct evidence. Recent evidence suggests that soluble oligomeric aggregates rather than amyloid may, in fact, be the culprit.

This TSRI study, focused on making peptide probes for aggregates other than amyloid fibrils, was conducted by postdoctoral researcher Joseph D. Schonhoft and graduate student Cecilia Monteiro. Prior to joining the Kelly Lab as a graduate student, Monteiro was a practicing neurologist in Portugal, where she treated neurodegenerative disease patients, including TTR amyloid polyneuropathy patients. The TTR amyloidoses are amyloid diseases where misfolded TTR assemblies cause neurodegeneration or cardiomyopathy, depending on the sequence of TTR that aggregates.

"Cecilia is a physician scientist and came to TSRI with a clinical background, and I am a biophysicist and biochemist. Together we formed a unique interdisciplinary team for this research," said Schonhoft.

Some diagnostic strategies detect insoluble amyloids using antibodies designed to bind to them and make them visible to scientists. But before amyloid develops, the body may produce soluble misfolded oligomeric aggregates in a non-amyloid conformation. The TSRI team developed a peptide-based probe that can detect non-native TTR oligomers earlier in the disease progression, before amyloid is easily detected (the probe does not recognize amyloid).

The researchers used their peptide probe to detect non-native TTR oligomers in the plasma of a group of patients diagnosed with TTR amyloid polyneuropathy, alongside samples from a healthy control group and asymptomatic carriers of the mutation that causes the majority of TTR polyneuropathy cases. The study revealed that patients with the disease had higher levels of non-native TTR oligomers than either of the two control groups. In addition, a subset of patients who had been treated for the disease with the drug tafamidis (discovered by the Kelly Lab and sold by Pfizer), as well as liver transplant-mediated gene therapy showed lower levels of non-native TTR oligomers. These results demonstrate proof of concept for using the peptide probe for early diagnosis and as a response to therapy biomarker.

The researchers are now scrutinizing the utility of their peptide probe in larger numbers of patients in order to correlate the levels of the non-native TTR oligomers with disease initiation and progression. Little is known about which aggregate structure causes these degenerative diseases.

"One of the biggest questions in the field is whether the soluble oligomers are a driver of disease. Our approach may be able to answer that question," said Monteiro.

Provided by: The Scripps Research Institute 

https://medicalxpress.com/news/2017-09-degenerative-neurological-diseases-sooner.html

Elderly who have trouble identifying odors face risk of dementia

September 29, 2017

For both studies, the researchers used a well-validated tool, known as 'Sniffin'Sticks.' Credit: Rob Kozloff, for the University of Chicago Medicine

A long-term study of nearly 3,000 adults, aged 57 to 85, found that those who could not identify at least four out of five common odors were more than twice as likely as those with a normal sense of smell to develop dementia within five years.

Although 78 percent of those tested were normal - correctly identifying at least four out of five scents - about 14 percent could name just three out of five, five percent could identify only two scents, two percent could name just one, and one percent of the study subjects were not able to identify a single smell.

Five years after the initial test, almost all of the study subjects who were unable to name a single scent had been diagnosed with dementia. Nearly 80 percent of those who provided only one or two correct answers also had dementia, with a dose-dependent relationship between degree of smell loss and incidence of dementia.

"These results show that the sense of smell is closely connected with brain function and health," said the study's lead author, Jayant M. Pinto, MD, a professor of surgery at the University of Chicago and ENT specialist who studies the genetics and treatment of olfactory and sinus disease. "We think smell ability specifically, but also sensory function more broadly, may be an important early sign, marking people at greater risk for dementia."

"We need to understand the underlying mechanisms," Pinto added, "so we can understand neurodegenerative disease and hopefully develop new treatments and preventative interventions."

"Loss of the sense of smell is a strong signal that something has gone wrong and significant damage has been done," Pinto said. "This simple smell test could provide a quick and inexpensive way to identify those who are already at high risk."

The study, "Olfactory Dysfunction Predicts Subsequent Dementia in Older US Adults," published September 2?, 2017, in the Journal of the American Geriatrics Society, follows a related 2014 paper, in which olfactory dysfunction was associated with increased risk of death within five years. In that study, loss of the sense of smell was a better predictor of death than a diagnosis of heart failure, cancer or lung disease.

For both studies, the researchers used a well-validated tool, known as "Sniffin'Sticks." These look like a felt-tip pen, but instead of ink, they are infused with distinct scents. Study subjects smell each item and are asked to identify that odor, one at a time, from a set of four choices. The five odors, in order of increasing difficulty, were peppermint, fish, orange, rose and leather.

Losing the ability to smell can have a substantial impact on lifestyle and wellbeing. Credit: Wikimedia Commons

Test results showed that:

• 78.1 percent of those examined had a normal sense of smell; 48.7 percent correctly identified five out of five odors and 29.4 percent identified four out of five. 
• 18.7 percent, considered "hyposmic," got two or three out of five correct. 
• The remaining 3.2 percent, labelled "anosmic," could identify just one of the five scents (2.2%), or none (1%).

The olfactory nerve is the only cranial nerve directly exposed to the environment. The cells that detect smells connect directly with the olfactory bulb at the base of the brain, potentially exposing the central nervous system to environmental hazards such as pollution or pathogens. Olfactory deficits are often an early sign of Parkinson's or Alzheimer's disease. They get worse with disease progression.

Losing the ability to smell can have a substantial impact on lifestyle and wellbeing, said Pinto, a specialist in sinus and nasal diseases and a member of the Section of Otolaryngology-Head and Neck Surgery at UChicago Medicine. "Smells influence nutrition and mental health," Pinto said. People who can't smell face everyday problems such as knowing whether food is spoiled, detecting smoke during a fire, or assessing the need a shower after a workout. Being unable to smell is closely associated with depression as people don't get as much pleasure in life."

"This evolutionarily ancient special sense may signal a key mechanism that also underlies human cognition," noted study co-author Martha K. McClintock, PhD, the David Lee Shillinglaw Distinguished Service Professor of Psychology at the University of Chicago, who has studied olfactory and pheromonal communication throughout her career.

McClintock noted that the olfactory system also has stem cells which self-regenerate, so "a decrease in the ability to smell may signal a decrease in the brain's ability to rebuild key components that are declining with age, leading to the pathological changes of many different dementias."

In an accompanying editorial, Stephen Thielke, MD, a member of the Geriatric Research, Education and Clinical Center at Puget Sound Veterans Affairs Medical Center and the psychiatry and behavioral sciences faculty at the University of Washington, wrote: "Olfactory dysfunction may be easier to quantify across time than global cognition, which could allow for more-systematic or earlier assessment of neurodegenerative changes, but none of this supports that smell testing would be a useful tool for predicting the onset of dementia."

"Our test simply marks someone for closer attention," Pinto explained. "Much more work would need to be done to make it a clinical test. But it could help find people who are at risk. Then we could enroll them in early-stage prevention trials."

"Of all human senses," Pinto added, "smell is the most undervalued and underappreciated - until it's gone."

More information: Dara R. Adams et al, Olfactory Dysfunction Predicts Subsequent Dementia in Older U.S. Adults, Journal of the American Geriatrics Society (2017).  DOI: 10.1111/jgs.15048 

Journal reference: Journal of the American Geriatrics Society

Provided by: University of Chicago Medical Center

https://medicalxpress.com/news/2017-09-elderly-odors-dementia.html

Will binge-watching TV increase your risk for Alzheimer's disease and diabetes?

September 28, 2017 by Josephine Chau And Melody Ding, The Conversation

This study didn’t actually measure sitting and its relationship to inflammation - which causes disease. Credit: D.Reichardt/Flickr, CC BY

A recent study published in the journal Medicine and Science in Sports and Exercise was reported in many media outlets as a bringer of "bad news" to television watchers, with the Herald Sun noting:

Every hour you spend sitting watching TV makes you more likely to die from inflammation-related diseases, Melbourne researchers have found."

The Melbourne research made it all the way to the US. A Philadelphia-based publication ran the headline: 

"This new study will convince you to stop binge-watching TV after work"

And a site for fans of the show Game of Thrones appropriated the study, claiming watching the show itself could increase risk of early death from inflammatory-related conditions. The Daily Mail took it further saying "binge-watching Game of Thrones could kill."

Of course the study, conducted by researchers from the Baker Heart and Diabetes Institute, did not have anything to do with Game of Thrones, and fans can rest assured watching the show will not kill them. Rather, the study showed an association between increased hours of television viewing and higher risk of certain inflammatory diseases.

Inflammation is a response our immune system launches to fight infection. But when this inflammation becomes chronic, it can be complicit in conditions like heart disease and depression. 

The inflammatory-related conditions most relevant to the recent study include respiratory diseases, influenza and pneumonia, Alzheimer's disease, Parkinson's disease, motor neuron disease, diabetes and kidney disease. While cardiovascular disease (such as heart disease and stroke) and cancer are also associated with inflammation, they were not included in this study.

Despite the headlines, including the Institute's own press release about the dangers of "sitting down to binge watch" TV, this study did not actually measure sitting down during TV-viewing. This means the findings should not be interpreted as indicating that TV-viewing is harmful to health due to sitting involved.

And most of the media reports failed to mention that the association between television viewing and increased risk of disease was reversed for those who were active. So, how should we interpret the study?

How was the study conducted?

This study analyses data from the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) first collected in 1999-2000 from 11,247 participants (the baseline study). The study aimed to provide national data on the number of people with diabetes, obesity, high blood pressure and kidney disease in Australia. A proportion of these participants filled out a follow-up questionnaire in 2004-2005 and a third survey was conducted in 2011-2012.

The recent paper used data from 8,933 baseline participants who had responded to a questionnaire delivered by a trained interviewer. They were asked how much time they spent watching TV or videos in the last seven days, and about their social and economic characteristics (such as age, gender, education and household income), medical history (such as type 2 diabetes and heart disease), and health-related behaviours (such as smoking, physical activity and diet).

The study followed participants to November 30, 2013. For those who had died, the research team obtained information from the Australian National Death Index about their cause of death, which was coded based on a standard called the International Classification of Diseases (version 10).

Out of 896 deaths, 130 were attributable to inflammatory-related causes that were not cancer or cardiovascular diseases over a median follow-up period of 13.6 years.

Cardiovascular disease and cancer were excluded in this study as associations between these conditions and TV-viewing had already been explored in AusDiab and other cohorts. 

Researchers then specifically calculated the association between TV-viewing and other diseases for which inflammation is an accompanying characteristic.

What were the results?

When not taking physical activity (of moderate to vigorous intensity) into account, the authors found for every extra hour of TV watched per day, there was a 12% increased risk of inflammatory-related death in the overall sample. This was after adjusting for the role of age, sex, education, household income, alcohol intake, energy intake, diet, and markers for heart and metabolic health risk (including waist circumference, blood pressure, smoking status, fast blood sugar and cholesterol). 

Interestingly, the increased risks observed were eliminated when physical activity was taken into account. 

In analyses with the overall sample, adults who watched TV for four or more hours per day had a 74% higher risk of dying from an inflammatory-related disease compared to those watching less than two hours per day. This result was found after taking into account a range of factors including age, sex, education, household income, smoking status (ex or current), alcohol intake, energy intake, diet, heart and metabolic health risks, and physical activity.

What does it mean?

This study didn't actually measure sitting and its relationship to inflammation. As acknowledged by the authors, TV-viewing is a commonly used but problematic proxy for sedentary (sitting) behaviour. Researchers do not know if the health risks linked with TV-viewing are due to sitting and watching TV itself or other factors. Nor do they know the fundamental differences between those who binge watch TV and those who do not. 

For example, TV-viewing is associated with consumption of unhealthy foods and drinks, and people who watch TV for long hours are more likely to be of lower socioeconomic backgrounds, be unemployed, have poor mental health, and possibly suffer from underlying chronic diseases. In other words, despite a possible association between high amounts of TV-viewing and inflammatory-related death, we do not know if one actually causes the other.

Second, excluding cancer and cardiovascular diseases in the definition of inflammatory disease-related can confuse the actual risk percentages for some participants, due to an issue known as "competing risks". These exist when a person is at risk of dying from several causes, but they can only die from one cause. For instance, bowel and liver cancer are associated with inflammatory conditions. Similarly, inflammatory-related diseases such as type 2 diabetes are associated with higher risk for cardiovascular diseases.

A strength of this study is that the analyses adjusted for a wide range of social and economic, health and behavioural factors. The authors also excluded people who died in the first two years after the survey, in case they had unknown or undiagnosed illnesses.

What else should we take into account?

A growing body of evidence suggests too much sitting, especially prolonged periods of unbroken sitting, is linked with poorer heart health and higher risk of developing chronic diseases, dying prematurely, and being hospitalised. Some studies suggest the associations of prolonged sitting with negative health outcomes are independent of physical activity, but others show physical activity may eliminate the harmfulness of sitting.

A key finding that received little attention in the reporting was the role of physical activity which, when taken into account, eliminated the link between TV-viewing and higher risk of inflammatory-related death. This suggests activities like brisk walking, jogging, football, or dancing on most days of the week, will keep risk of inflammatory-related diseases associated with TV-viewing at bay.

So, our take home message is if you are going to watch TV (while sitting down or otherwise), make sure you fit in an exercise session to counteract the possible harms to your health. —Josephine Chau, Melody Ding

Peer review

TV viewing time is related to nearly half a dozen influences that could explain its damaging associations with early death and many other health outcomes. So, I agree the study tells us hardly anything about sitting.

But inflammatory-related death is also a nonspecific mishmash of causes. Searching the International Classification of Diseases for the term "inflammatory" returns over 185 hits. Such conditions range from infectious diseases to respiratory, nervous system, digestive, endocrine, musculoskeletal, genital and urinary, and metabolic disorders. Each condition has completely different causation, pathology, and symptoms. 

Does this make them a distinct class of disorders one can reasonably expect to be affected by a behaviour like TV-watching and the sitting it involves? Unlikely.

It's hard to tell if interventions to reduce TV time would be a good investment. The recreational screen media landscape has changed dramatically in the last few years and TV is now one of the many screen options people have during leisure time, so we could end up replacing one screen with another. Perhaps it is a safer investment to motivate people to be physically active daily and enable them to do so by making the environment friendlier to physical activity. —Emmanuel Stamatakis

Response from study author

The study's lead author Megan Grace, Research Fellow at the Baker Heart and Diabetes Institute, said researchers exploring links between sedentary behaviour and health were building a "convincing argument that sitting is bad for health and that simple, practical, short periods of activity throughout the day may help to reduce the long-term risk of disease."

She said this study needed to be considered in context with others in the area. Read Megan Grace's full response to media coverage of their study here. —Megan Grace

Provided by: The Conversation

https://medicalxpress.com/news/2017-09-binge-watching-tv-alzheimer-disease-diabetes.html