‘Mind over matter’ key to a healthy lifestyle?

People who want to increase their participation in regular exercise and adopt a healthier lifestyle may be best to mentally visualise it, new research by Curtin University has found.

The research, published in the leading journal Health Psychology, found that ‘mental imagery interventions’, or visualising an activity or task, may be effective in helping people change their behaviours, including moderating alcohol consumption and participating in regular physical activity.

Lead Australian author John Curtin Distinguished Professor Martin Hagger, from the School of Psychology at Curtin University, said the research aimed to explore the link between visualisation and increasing healthy behaviour.

“There are strong links between chronic illnesses like heart disease and diabetes and behaviour, and imagery-based interventions offer an inexpensive, effective way of promoting healthy behaviours such as physical activity and healthy eating,” Professor Hagger said.

“We found that people who simply visualised the steps necessary to do the healthy behaviour on a regular basis were more likely to be motivated, and actually do, the healthy behaviour.”

Mental imagery was also more effective in promoting healthy behaviours when the visualisation lasted longer, when people were reminded to do their imagery by text message, and when the person was given detailed instructions on how to conduct the imagery exercise.

Professor Hagger explained that the research could have important implications for health professionals and the broader community around the world.

“Previous studies have shown that imagery interventions have been used in various contexts including enhancing athletes’ performance, flight simulation training for aircraft pilots and for symptom relief in hospital settings. Our research shows that imagery is also effective for promoting participation in healthy behaviours,” Professor Hagger said.

“Our findings may not only be of interest to health professionals around the world, but could be of interest and potentially implemented within other industries.”

 Explore further: Research finds counting your drinks reduces alcohol consumption

More information: Dominic Conroy et al. Imagery interventions in health behavior: A meta-analysis., Health Psychology(2018). DOI: 10.1037/hea0000625

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Brain study paves way for therapy for common cause of dementia

The authors discovered more proliferating dysfunctional endothelial cells (red arrows) in diseased human brains compared to controls. Credit: R.M. Rajani et al., Science Translational Medicine (2018)

Scientists have uncovered a potential approach to treat one of the commonest causes of dementia and stroke in older people.

Studies with rats found the treatment can reverse changes in blood vessels in the brain associated with the condition, called cerebral small vessel disease.

Treatment also prevents damage to brain cells caused by these blood vessel changes, raising hope that it could offer a therapy for dementia.

Small vessel disease, or SVD, is a major cause of dementia and can also worsen the symptoms of Alzheimer’s disease. It is responsible for almost half of all dementia cases in the UK and is a major cause of stroke, accounting for around one in five cases.

Patients with SVD are diagnosed from brain scans, which detect damage to white matter—a key component of the brain’s wiring.

Until now, it was not known how changes in small blood vessels in the brain associated with SVD can cause damage to brain cells.

A team led by the University of Edinburgh found that SVD occurs when cells that line the small blood vessels in the brain become dysfunctional. This causes them to secrete a molecule into the brain.

The molecule stops production of the protective layer that surrounds brain cells—called myelin—which leads to brain damage.

Treating rats with drugs that stop blood vessel cells from becoming dysfunctional reversed the symptoms of SVD and prevented brain damage, tests found.

Researchers say that further studies will need to test whether the treatment also works when the disease is firmly established. They will also need to check if the treatment can reverse the symptoms of dementia.

Dementia is one of the biggest problems facing society, as people live longer and the population ages. Estimates indicate there are almost 47 million people living with dementia worldwide and the numbers affected are expected to double every 20 years, rising to more than 115 million by 2050.

The research, published in Science Translational Medicine, was carried out at the Medical Research Council Centre for Regenerative Medicine and the UK Dementia Research Institute at the University of Edinburgh. It was funded by the MRC, Alzheimer’s Research UK and Fondation Leducq.

Professor Anna Williams, Group Leader at the University of Edinburgh’s MRC Centre for Regenerative Medicine, said: “This important research helps us understand why small vessel disease happens, providing a direct link between small blood vessels and changes in the brain that are linked to dementia. It also shows that these changes may be reversible, which paves the way for potential treatments.”

Dr. Sara Imarisio, Head of Research at Alzheimer’s Research UK said: “Changes to the blood supply in the brain play an important role in Alzheimer’s disease as well as being a direct cause of vascular dementia. This pioneering research highlights a molecular link between changes to small blood vessels in the brain and damage to the insulating ‘white matter’ that helps nerve cells to send signals around the brain.

“The findings highlight a promising direction for research into treatments that could limit the damaging effects of blood vessel changes and help keep nerve cells functioning for longer. There are currently no drugs that slow down or stop Alzheimer’s disease and no treatments to help people living with vascular dementia. Alzheimer’s Research UK is very pleased to have helped fund this innovative research, which is only possible thanks to the work of our dedicated supporters.”

Dr. Nathan Richardson, the MRC’s Head of Molecular and Cellular Medicine, commented: “This study is a great example of how innovative discovery science into regenerative mechanisms can be applied to improve our understanding of how vascular changes contribute to dementia. This research in rats opens up new possibilities for developing therapies for cerebral small vessel disease.”

 Explore further: Vascular dementia trial of Viagra-type drug nears closing stages

More information: R.M. Rajani el al., “Reversal of endothelial dysfunction reduces white matter vulnerability in cerebral small vessel disease in rats,” Science Translational Medicine (2018). stm.sciencemag.org/lookup/doi/ … scitranslmed.aam9507

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Abivax Phase 2a HIV med data ‘mixed’

• Paris-based Abivax announced topline results from the second cohort of its Phase 2a study of ABX464 in patients with HIV, with mixed findings.
• Twelve patients were given a dose of 50 mg per day of ABX464 for three months. From the available data at 12 weeks, eight patients had completed the study.
• Four patients showed a reduction in total HIV DNA in peripheral blood CD4+ T cells, ranging from 2% to 85%, while the other four patients experienced an increase in HIV DNA, ranging from 5% to 36%.

The treatment aims to reduce the reservoirs of infected immune cells that can lay dormant in a patient’s blood, brain, gut and lymph nodes even after viral load has been reduced to undetectable levels by other regimens.

In the first cohort of the study, which included nine patients given 150 mg per day of ABX 464 for 28 days, eight patients showed a decrease in HIV DNA in peripheral blood CD4+ T cells up to 52%.

The second cohort was designed to see if a lower dose of the drug could also decrease levels — so far the results are mixed — and to see if the drug could be tolerated for a longer period of time. Abivax did not release any safety data, but said the drug was well-tolerated.

Rectal tissue biopsies were also conducted, with four patients showing a reduction in HIV DNA ranging from 16% to 71%, and four patients showing an increase in HIV DNA from 14% to 123%.

Abivax intends to present the full data at an upcoming medical meeting.

“The study results demonstrate that some HIV-infected patients receiving 50mg of ABX464 had a relevant drop in the HIV DNA reservoir. Further studies will identify the characteristics of the patients most likely to benefit from ABX464 in different dosing regimens, alone or in combination with other HIV cure strategies,” said Ian McGowan, a professor at the University of Pittsburgh School of Medicine and chair of Abivax’s Scientific Advisory Board, in a statement.

Shares of Abivax were up nearly 7% on the news in trading on the Euronext Paris stock exchange.

https://bit.ly/2KwnrkC

Unsubsidized ObamaCare enrollment dropped 20% in 2017

• The Centers for Medicare and Medicaid Services issued three new reports on the Affordable Care Act Monday, noting a 20% drop in enrollment during plan year 2017 among those not getting subsidies, and casting the data to make their case that federal and state exchanges and state individual health insurance markets are in turmoil.
• Subsidized enrollment, which makes up the vast majority of those enrolled in ACA plans, remained steady with a drop of only 3% during the same period.
• But critics noted the administration’s repeated attempts to undermine the law, including repeal of the individual mandate penalty, pullback of exchange navigators and the expansion of association health plans and short-term, limited-duration insurance, to likely result in skimpier plans and the destabilization of the ACA marketplace.

The Trump administration and Republicans in Congress have made no secret of their opposition to the ACA, attempting and failing to repeal it completely last year.

The exchanges remain stable in 2018, but more people are relying on subsidies than the prior year, according to CMS. In February 2018, approximately 10.6 million enrollees gained coverage through the exchanges, with 87% relying on advance premium tax credits, compared to 10.3 million enrolled at the same time in 2017, with 84% using tax credits.

The agency said that rising premiums have increasingly raised costs to the federal government due to the law’s subsidies.

“It is clear that many Americans are being priced out of the health insurance market, especially for employed people who earn too much to qualify for tax credits and have no access to employer-sponsored coverage,” CMS said. “This underscores the need for CMS to continue efforts to stabilize the market and provide all consumers—including those who do not qualify for large premium subsidies—with more affordable health coverage options.”

CMS Administrator Seema Verma say the new reports are evidence that the ACA is not serving the middle class and is leading to them dropping health insurance coverage.

“As the Trump Administration took office, there were warning signs that we were dealing with a crisis in the individual health insurance market and Obamacare was failing its consumers,” Verma said in a statement.

Protect Our Care, a liberal advocacy group, argued the Trump administration’s cuts to the advertising budget and navigator program amounted to sabotage of the last open enrollment.

“The Administration cut in half the number of days people could sign up for coverage; reduced the outreach budget by [90%]; and used funding to boost open enrollment to launch a propaganda campaign against the ACA. All told, these actions reduced enrollment by more than one million people,” Protect Our Care Executive Director Brad Woodhouse said in a statement.

But CMS said the actions simply shifted the burden of supporting enrollment to the private sector, noting that navigators “enrolled less than 1% of total enrollees.”

The agency also argued that its changes to the special enrollment periods improved risk pools, noting that the requirement for individuals to verify eligibility has cut the number of exceptional circumstance special enrollment periods by 56% in 2017.

https://bit.ly/2z6xasv

Empathy Matters, In Markets And In Life

Shoutout to vlogger Meir Kay, who produced an outstanding video that captures the relationship between anger and empathy.

There’s an important psychological lesson here.

Frustration is a form of anger.  It occurs when we have a goal and something prevents us from reaching that goal.  We develop an idea, place a trade based on that idea, and then a burst of volume comes into the market and moves our position against us.  Our hopes for profit are dashed with the reality of a loss.

We can voice frustration at the market or at the traders who are “obviously manipulating” the market.  We can become frustrated with ourselves and beat ourselves up over how stupid we were to place the trade.  Regardless of the object of our frustration, once we become angry, we enter fight/flight mode and stop processing the world objectively.

The good trader will catch themselves at that moment and take a step back, slow down, calm themselves, and return to their trading.

The great trader, however, will do something quite different.

Remember that markets are always speaking to us.  They tell us where participants are finding value, where participation is waxing and waning, and when participation is dominated by buyers or sellers.  The great trader is like a great listener in a conversation.  That requires empathy: the ability to not just see, but feel what other market participants are doing.

Suppose you bring up a topic in a conversation with someone you care about and they quickly change the subject and start talking about something else.  You can become frustrated, filled with a sense of injustice over being “cut off”, or you can step back and say to yourself, “That’s interesting…my friend doesn’t normally change topics like that.  This must be very important.”  That empathy makes you a better listener.  Going with the conversational flow will bring you closer to your friend.

If you have formulated a great idea for a trade and the market changes the topic on you, perhaps there is an important message there.  Doubling down on your listening skills and drawing upon your empathy opens the possibility of profiting from this new information.  It’s yet another way that developing ourselves as traders is not so different from developing ourselves as human beings.  When we replace anger with empathy, frustration with listening, we make new connections and profit from those–in markets and in life.

https://bit.ly/2tVnDQ9

Alzheimer’s may be caused by haywire immune system eating brain connections

More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons.

“It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville.

Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work.

What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity.

Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. When this system goes awry during the brain’s development, whether in the womb or later during childhood and into the teen years, it may lead to psychiatric disorders such as schizophrenia, she says.

Stevens hypothesized that the same mechanism goes awry in early Alzheimer’s disease, leading to the destruction of good synapses and ultimately to cognitive impairment. Using two Alzheimer’s mouse models—each of which produces excess amounts of the β amyloid protein, and develops memory and learning impairments as they age—she and her team found that both strains had elevated levels of C1q in brain tissue. When they used an antibody to block C1q from setting off the microglial feast, however, synapse loss did not occur, the team reports today in Science.

To Stevens, that suggests that the normal mechanism for pruning synapses during development somehow gets turned back on again in the adult brain in Alzheimer’s, with dangerous consequences. “Instead of nicely whittling away [at synapses], microglia are eating when they’re not supposed to,” she says.

The group is now tracking these mice to see whether a drug that blocks C1q slows their cognitive decline. To determine whether elevated β amyloid can cause the C1q system to go haywire, Stevens and colleagues also injected a form of the protein which is known to generate plaques into the brains of normal mice and so-called knockouts that could not produce C1q because of a genetic mutation. Although normal mice exposed to the protein lost many synapses, knockouts were largely unaffected, Stevens says. In addition, microglia only went after synapses when β amyloid was present, suggesting that the combination of protein and C1q is what destroys synapses, rather than either element alone, she says, adding that other triggers, such as inflammatory molecules called cytokines, might also set the system off.

The findings contradict earlier theories which held that increased microglia and C1q activity were merely part of an inflammatory reaction to β amyloid plaques. Instead, microglia seem to start gorging on synapses long before plaques form, Stevens says. She and several co-authors are shareholders in Annexon Biosciences, a biotechnology company that will soon start testing the safety of a human form of the antibody the team used to block C1q, known as ANX-005, in people.

Such a central role for microglia in Alzheimer’s disease is “still on the controversial side,” says Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada. One “really compelling” sign that the mechanism is important in people would be if high levels of C1q in cerebrospinal fluid early on predicted developing full-blown Alzheimer’s later in life, he says. Still, he says, “it’s difficult to argue with the strength of the study’s evidence.”

Posted in:

• Brain & Behavior
• Memory Topic

doi:10.1126/science.aaf9857

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Essilor, Delfin extend deadline for combination deal

Essilor (Euronext Paris: EI) and Luxottica (MTA: LUX), announce the extension to July 31, 2018 of the deadline of both the Combination Agreement1and Contribution Agreement2 signed between Essilor and Delfin, Luxottica’s majority shareholder.

As of today, the Chinese competition authority has not yet approved the contemplated combination between Essilor and Luxottica, such approval being a condition precedent to the closing of the combination. The parties remain confident that they will succeed in completing the antitrust processes in China and Turkey in the coming weeks.

The first General Meeting of EssilorLuxottica shareholders which was scheduled for July 25, 2018 will be reconvened by the EssilorLuxottica’s Board of Directors for a later date to be announced as soon as possible.

https://bit.ly/2u4gPik