Green prescriptions could undermine the benefits of spending time in nature
November 6, 2020
Science Daily/University of Exeter
Spending time in nature is believed to benefit people's mental health. However, new research suggests that giving people with existing mental health conditions formal 'green prescriptions', may undermine some of the benefits.
An international research team led by the University of Exeter and published in the journal Scientific Reports, investigated whether contact with nature has the potential to help people with mental health issues, such as depression and anxiety, to manage their symptoms. They found that nature is associated with a number of benefits for these individuals, but only if they chose to visit these places themselves.
The research team collected data from more than 18,000 people in 18 different countries, as part of the EU Horizons 2020 funded BlueHealth project. A key aim was to understand why people feel motivated to spend time in nature, how often they visit, and how social pressure influences their emotional experiences during visits.
The findings suggest that whilst pressure to spend time outdoors can encourage visits, it can also undermine the potential emotional and wellbeing benefits of contact with nature.
Common mental health issues are the leading cause of disability worldwide, affecting approximately 17% of the world's population each year. Although there is evidence that some people with these issues are using nature as part of their own symptom self-management, there was still much we didn't not know about how widespread this was, or whether more formal 'Green prescriptions' from medical professional to spend time in nature could aid management and potentially recovery.
The research team were surprised to find that people with depression were already visiting nature as frequently as people with no mental health issues, while people with anxiety were visiting significantly more often. On the whole, both groups also tended to feel happy and reported low anxiety during these visits.
However, the benefits of nature seem to be undermined when visits were not by choice. The more pressure people felt to visit nature by presumably well-meaning others, the less motivated people were and the more anxious they felt.
The research was led by Dr Michelle Tester-Jones, of the University of Exeter. She said: "These findings are consistent with wider research that suggests that urban natural environments provide spaces for people to relax and recover from stress. However, they also demonstrate that healthcare practitioners and loved ones should be sensitive when recommending time in nature for people who have depression and anxiety. It could be helpful to encourage them to spend more time in places that people already enjoy visiting; so they feel comfortable and can make the most of the experience."
The authors believe their paper provides evidence that careful techniques to discuss accessing nature as a means of self- or supported-management for people with mental health issues need to be integrated into these programmes if they are to offer clients the best support.
Dr Mathew White, of the University of Exeter and University of Vienna, who co-ordinated the international research team, added: "We had no idea just how much people with depression and anxiety were already using natural settings to help alleviate symptoms and manage their conditions. Our results provide even greater clarity about the value of these places to communities around the world, but also remind us that nature is no silver bullet and needs to be carefully integrated with existing treatment options."
Dr Ann Ojala, a research team member from the Natural Resources Institute Finland (Luke) said: "The results encourage further research in clinical settings. We need more information on this delicate balance between the intrinsic motivation and sometimes necessary encouragement from outside, as well as how nature visits could be integrated to mental health treatment."
Co-author Dr Greg Bratman, of the University of Washington, said: "The results highlighted the importance of taking intrinsic motivation into account when it comes to the benefits of nature visits -- and the relevance of integrating this consideration into effective green prescriptions."
Matilda van den Bosch, Assistant Professor at The University of British Columbia, said: "For green prescriptions, like with any intervention, it is important to avoid pressure to achieve compliance with the treatment. Nature cannot be forced on anyone, but must be provided at the individual's own pace and will."
https://www.sciencedaily.com/releases/2020/11/201106093024.htm
Positive outlook predicts less memory decline
Senior couple on bench (stock image). Credit: © BillionPhotos.com / stock.adobe.com
October 29, 2020
Science Daily/Association for Psychological Science
We may wish some memories could last a lifetime, but many physical and emotional factors can negatively impact our ability to retain information throughout life.
A new study published in the journal Psychological Science found that people who feel enthusiastic and cheerful -- what psychologists call "positive affect" -- are less likely to experience memory decline as they age. This result adds to a growing body of research on positive affect's role in healthy aging.
A team of researchers analyzed data from 991 middle-aged and older U.S. adults who participated in a national study conducted at three time periods: between 1995 and 1996, 2004 and 2006, and 2013 and 2014.
In each assessment, participants reported on a range of positive emotions they had experienced during the past 30 days. In the final two assessments, participants also completed tests of memory performance. These tests consisted of recalling words immediately after their presentation and again 15 minutes later.
The researchers examined the association between positive affect and memory decline, accounting for age, gender, education, depression, negative affect, and extraversion.
"Our findings showed that memory declined with age," said Claudia Haase, an associate professor at Northwestern University and senior author on the paper. "However, individuals with higher levels of positive affect had a less steep memory decline over the course of almost a decade," added Emily Hittner, a PhD graduate of Northwestern University and the paper's lead author.
Areas of future research might address the pathways that could connect positive affect and memory, such as physical health or social relationships.
https://www.sciencedaily.com/releases/2020/10/201029135501.htm
Link between sleep apnea and increased risk of dementia
November 11, 2020
Science Daily/Monash University
A new study by Monash University has found that obstructive sleep apnea (OSA) has been linked to an increased risk of dementia.
The study, published in the Journal of Alzheimer's Disease, and led by Dr Melinda Jackson from the Turner Institute for Brain and Mental Health, found that severe OSA is linked to an increase in a protein, called beta-amyloid, that builds up on the walls of the arteries in the brain and increases the risk of dementia.
The study involved 34 individuals with recently diagnosed untreated OSA and 12 individuals who were asymptomatic for sleep disorders. It explored associations between brain amyloid burden using a PET brain scan, and measures of sleep, demographics and mood.
The OSA group recorded a higher amyloid burden, poorer sleep efficiency and less time spent in stage N3 sleep (a regenerative period where your body heals and repairs itself).
OSA is a common sleep disorder, affecting about 1 billion people worldwide and is caused by the collapse of the airway during sleep, resulting in intermittent dips in oxygen levels and arousals from sleep.
"The significance of finding the association between increased brain amyloid in patients with OSA will allow for further research to explore in more detail the implications of treating OSA for reducing dementia risk," Dr Jackson said.
https://www.sciencedaily.com/releases/2020/11/201111104918.htm
Why protecting the brain against infection takes guts
November 4, 2020
Science Daily/University of Cambridge
The brain is uniquely protected against invading bacteria and viruses, but its defence mechanism has long remained a mystery. Now, a study in mice, confirmed in human samples, has shown that the brain has a surprising ally in its protection: the gut.
The brain is arguably the most important organ in the body, as it controls most other body systems and enables reasoning, intelligence, and emotion. Humans have evolved a variety of protective measures to prevent physical damage to the brain: it sits in a solid, bony case -- the skull -- and is wrapped in three layers of watertight tissue known as the meninges.
What has been less clear is how the body defends the brain from infection. Elsewhere in the body, if bacteria or viruses enter the bloodstream, our immune system kicks in, with immune cells and antibodies that target and eliminate the invader. However, the meninges form an impermeable barrier preventing these immune cells from entering the brain.
In research published today in Nature, a team led by scientists at the University of Cambridge, UK, and the National Institute of Health, USA, have found that the meninges are home to immune cells known as plasma cells, which secrete antibodies. These cells are specifically positioned next to large blood vessels running within the meninges allowing them to secrete their antibody 'guards' to defend the perimeter of the brain. When the researchers looked at the specific type of antibody produced by these cells, they got a surprise -- the antibody they observed is normally the type found in the intestine.
Plasma cells are derived from a particular type of immune cell known as a B cell. Every B cell has an antibody on its surface that is unique to that cell. If an antigen (the part of a bacterium or virus that triggers an immune response) binds to that surface antibody, the B cell becomes activated: it will divide to make new offspring that also recognise that same antigen.
During division, the B cell introduces a mutation into the antibody gene so that one amino acid is changed and its binding characteristics are slightly different. Some of these B cells will now produce antibodies that enable better binding to the pathogen -- these go on to expand and multiply; B cells whose antibodies are less good at binding die off. This helps ensure the body produces the best antibodies for targeting and destroying particular antigens.
Normally, the antibodies found in the blood are a type known as Immunoglobulin G (IgG), which are produced in the spleen and bone marrow -- these antibodies protect the inside of the body. However, the antibodies found in the meninges were Immunoglobulin A (IgA), which are usually made in the gut lining or in the lining of the nose or lungs -- these protect mucosal surfaces, the surfaces that interface with the outside environment.
The team were able to sequence the antibody genes in B cells and plasma cells in the gut and meninges and show that they were related. In other words, the cells that end up in the meninges are those that have been selectively expanded in the gut, where they have recognised particular pathogens.
"The exact way in which the brain protects itself from infection, beyond the physical barrier of the meninges, has been something of a mystery, but to find that an important line of defence starts in the gut was quite a surprise," said lead scientist Professor Menna Clatworthy from the Department of Medicine and CITIID at the University of Cambridge and the Wellcome Sanger Institute.
"But actually, it makes perfect sense: even a minor breach of the intestinal barrier will allow bugs to enter the blood stream, with devastating consequences if they're able to spread into the brain. Seeding the meninges with antibody-producing cells that are selected to recognise gut microbes ensures defence against the most likely invaders."
The team made the discovery using mice, which are commonly used to study physiology as they share many characteristics similar to those found in the human body. They showed that when the mice had no bacteria in their gut, the IgA-producing cells in the meninges were absent, showing that these cells actually originate in the intestine where they are selected to recognise gut microbes before taking up residence in the meninges. When the researchers removed the plasma cells in the meninges -- and hence no IgA was present to trap bugs -- microbes were able to spread from the bloodstream into the brain.
The team confirmed the presence of IgA cells in the human meninges by analysing samples that were removed during surgery, showing that this defence system is likely to play an important role in defending humans from infections of the central nervous system -- meningitis and encephalitis.
https://www.sciencedaily.com/releases/2020/11/201104121444.htm
Western diet impairs odor-related learning and olfactory memory in mice
November 4, 2020
Science Daily/American Chemical Society
Problems with the sense of smell appear to be an early indicator of cognitive decline in people with type 2 diabetes. However, it's unknown whether factors such as diet and obesity play a role in who develops these symptoms. Now, researchers reporting in ACS Chemical Neuroscience found that mice fed a moderate-fat, high-sugar chow (simulating a Western diet) showed a faster decline in their ability to learn and remember new odors.
Some people with type 2 diabetes (T2D) show signs of olfactory dysfunction, including problems with detecting, discriminating or recalling odors, or even a complete loss of smell. These symptoms are strongly associated with cognitive impairment, and evidence suggests they could be an early indicator of the condition in people with T2D. Obesity, which is the main risk factor for T2D, has also been associated with olfactory dysfunction, but the impact of obesity on the sense of smell specifically in these patients is unclear, as studies have produced conflicting results. Also, it's unknown whether certain nutrients in the diet, such as fat and sugar, affect the sense of smell. To find out, Grazyna Lietzau, Cesare Patrone and colleagues wanted to compare the effects of two diets on different olfactory functions in mice: a high-fat, moderate-sugar diet (HFD); and a moderate-fat, high-sugar diet (similar to a Western diet, WD). In mice, both diets cause obesity and T2D-like features.
At one, three and eight months, the team performed tests to assess different olfactory functions in the mice. By eight months, both the HFD- and WD-fed mice had impaired odor detection, odor-related learning and olfactory memory compared with the control mice. However, the WD-fed mice had a faster decline in the latter two abilities, showing olfactory dysfunction as early as 3 months after beginning the diet. These findings indicate that a high dietary sugar content, rather than hyperglycemia or weight gain, is linked with early deterioration of olfactory functions related to learning and memory, the researchers say. How sugar causes these effects, and whether they are also seen in humans, the researchers acknowledge, remains to be determined.
https://www.sciencedaily.com/releases/2020/11/201104103713.htm
New method shows great potential for the treatment of Alzheimer's disease
November 3, 2020
Science Daily/Uppsala University
In Alzheimer's disease, a protein (peptide) forms clumps in the brain and causes sufferers to lose their memory. In a recently published article, a research group at Uppsala University described a new treatment method that increases the body's own degradation of the building blocks that lead to these protein clumps.
In Alzheimer's disease, the peptide amyloid-beta begins to form clumps in the brain. This process is called aggregation and the clumps so created are called aggregates. The treatment methods for Alzheimer's disease that are currently in clinical trials are attempts to bind to these disease-causing aggregates. But they are unable to bind to the smallest aggregates, which many now believe are the most toxic to neurons.
The treatment method developed in the new Uppsala research study using mice degrades the building blocks from which these aggregates form before they have a chance to aggregate. This treatment method therefore reduces the formation of all types of aggregates.
It has long been known that the peptide somatostatin, which was used by the researchers in the Uppsala group, can activate the body's own degradation of amyloid-beta, which is the peptide that forms the aggregates. However, it has not been possible to use somatostatin as a drug in the past because it has a very short half-life in the blood of only a few minutes, and does not cross the blood-brain barrier into the brain where the aggregates are formed.
"So to be able to use somatostatin as a treatment, we fused it to a brain transport protein which allows the somatostatin to enter the brain. This has proved very effective. When we used the transport protein, we also saw that the time that the somatostatin remained in the brain increased to several days, which is fantastic," says Fadi Rofo, doctoral student at the Department of Pharmaceutical Biosciences and the study's first author.
In the study, the researchers saw the greatest effect in hippocampus, the part of the brain that forms memories and the first part to be affected by Alzheimer's disease.
"The fact that we have seen that the effect is most evident in the hippocampus in particular is very good. Our hope is that this method will be able to act in a very targeted way and have few side effects, which have been a problem in other studies," says Greta Hultqvist, assistant professor at the Department of Pharmaceutical Biosciences, who led the research study.
The study was conducted in mice, but the researchers believe that somatostatin would have the same effect in humans and that this type of treatment could be more effective than those trialled so far.
https://www.sciencedaily.com/releases/2020/11/201103104719.htm
Over 80 percent of COVID-19 patients have vitamin D deficiency
Vitamin D deficiency was more prevalent in men
October 27, 2020
Science Daily/The Endocrine Society
Over 80 percent of 200 COVID-19 patients in a hospital in Spain have vitamin D deficiency, according to a new study published in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism.
Vitamin D is a hormone the kidneys produce that controls blood calcium concentration and impacts the immune system. Vitamin D deficiency has been linked to a variety of health concerns, although research is still underway into why the hormone impacts other systems of the body. Many studies point to the beneficial effect of vitamin D on the immune system, especially regarding protection against infections.
"One approach is to identify and treat vitamin D deficiency, especially in high-risk individuals such as the elderly, patients with comorbidities, and nursing home residents, who are the main target population for the COVID-19," said study co-author José L. Hernández, Ph.D., of the University of Cantabria in Santander, Spain. "Vitamin D treatment should be recommended in COVID-19 patients with low levels of vitamin D circulating in the blood since this approach might have beneficial effects in both the musculoskeletal and the immune system."
The researchers found 80 percent of 216 COVID-19 patients at the Hospital Universitario Marqués de Valdecilla had vitamin D deficiency, and men had lower vitamin D levels than women. COVID-19 patients with lower vitamin D levels also had raised serum levels of inflammatory markers such as ferritin and D-dimer.
Other authors of the study include: Daniel Nan, José M. Olmos, Javier Crespo, and Víctor M. Martínez-Taboada of the University of Cantabria; Marta Fernandez-Ayala, Mayte García-Unzueta, Miguel A. Hernández-Hernández, Marcos López-Hoyos, Manuel Gutiérrez-Cuadra, and Juan J. Ruiz-Cubillán of the Hospital Marqués de Valdecilla-IDIVAL in Santander, Spain; Pedro Muñoz Cacho of the Servicio Cántabro de Salud in Santander, Spain;
https://www.sciencedaily.com/releases/2020/10/201027092216.htm
Study finds PTSD interacts with klotho gene, may cause premature aging in the brain
October 26, 2020
Science Daily/Boston University School of Medicine
Genetics and the environment (including psychiatric stress) may contribute to the pace of cellular aging, causing some individuals to have a biological age that exceeds their chronological age.
Researchers from the National Center for PTSD at VA Boston Healthcare System and Boston University School of Medicine (BUSM) now have found that a variant in the klotho gene, a gene previously associated with longevity, interacts with post-traumatic stress disorder (PTSD) to predict accelerated aging in brain tissue. These same researchers had previously shown this effect in living subjects when epigenetic age (biological age) was measured in blood, but this is the first time it has been studied in brain tissue.
Using data from individuals who donated their brains to the VA National PTSD Brain Bank, the researchers were able to examine how genetic variation and PTSD status interacted with each other to predict biological age and gene expression. They found that older adults with PTSD showed evidence of accelerated epigenetic aging in brain tissue if they had the "at risk" (variant) at a particular location in the klotho gene. Follow-up molecular experiments led by BUSM co-authors Cidi Chen, PhD, research associate professor and Carmela Abraham, PhD, professor of biochemistry, showed that this variant regulated the transcription of the klotho gene, suggesting functional consequences of the genetic variant.
Both PTSD and klotho impact inflammation, cardiometabolic conditions and neurodegeneration, including Alzheimer's disease. According to the researchers, better understanding how klotho and PTSD interact and the mechanisms linking both genes and traumatic stress to age-related health conditions is important for the development of novel therapeutics.
"This work allows us to better pinpoint who is at risk for accelerated cellular aging, and possibly, premature disease onset (such as neurodegeneration). This can help to identify the populations at greatest risk so that targeted treatments can be matched to the individuals who need it most. As well, the results point to potential therapeutic targets (klotho) in the development of pharmacological approaches to slow the pace of cellular aging," adds lead author Erika Wolf, PhD, clinical research psychologist for the National Center for PTSD at VA Boston Healthcare System and associate professor of psychiatry at BUSM.
https://www.sciencedaily.com/releases/2020/10/201026114208.htm
Scientists discover how a common mutation leads to 'night owl' sleep disorder
October 27, 2020
Science Daily/University of California - Santa Cruz
A new study by researchers at UC Santa Cruz shows how a genetic mutation throws off the timing of the biological clock, causing a common sleep syndrome called delayed sleep phase disorder.
People with this condition are unable to fall asleep until late at night (often after 2 a.m.) and have difficulty getting up in the morning. In 2017, scientists discovered a surprisingly common mutation that causes this sleep disorder by altering a key component of the biological clock that maintains the body's daily rhythms. The new findings, published October 26 in Proceedings of the National Academy of Sciences, reveal the molecular mechanisms involved and point the way toward potential treatments.
"This mutation has dramatic effects on people's sleep patterns, so it's exciting to identify a concrete mechanism in the biological clock that links the biochemistry of this protein to the control of human sleep behavior," said corresponding author Carrie Partch, professor of chemistry and biochemistry at UC Santa Cruz.
Daily cycles in virtually every aspect of our physiology are driven by cyclical interactions of clock proteins in our cells. Genetic variations that change the clock proteins can alter the timing of the clock and cause sleep phase disorders. A shortened clock cycle causes people to go to sleep and wake up earlier than normal (the "morning lark" effect), while a longer clock cycle makes people stay up late and sleep in (the "night owl" effect).
Most of the mutations known to alter the clock are very rare, Partch said. They are important to scientists as clues to understanding the mechanisms of the clock, but a given mutation may only affect one in a million people. The genetic variant identified in the 2017 study, however, was found in around one in 75 people of European descent.
How often this particular mutation is involved in delayed sleep phase disorder remains unclear, Partch said. Sleep behavior is complex -- people stay up late for many different reasons -- and disorders can be hard to diagnose. So the discovery of a relatively common genetic variation associated with a sleep phase disorder was a striking development.
"This genetic marker is really widespread," Partch said. "We still have a lot to understand about the role of lengthened clock timing in delayed sleep onset, but this one mutation is clearly an important cause of late night behavior in humans."
The mutation affects a protein called cryptochrome, one of four main clock proteins. Two of the clock proteins (CLOCK and BMAL1) form a complex that turns on the genes for the other two (period and cryptochrome), which then combine to repress the activity of the first pair, thus turning themselves off and starting the cycle again. This feedback loop is the central mechanism of the biological clock, driving daily fluctuations in gene activity and protein levels throughout the body.
The cryptochrome mutation causes a small segment on the "tail" of the protein to get left out, and Partch's lab found that this changes how tightly cryptochrome binds to the CLOCK:BMAL1 complex.
"The region that gets snipped out actually controls the activity of cryptochrome in a way that leads to a 24-hour clock," Partch explained. "Without it, cryptochrome binds more tightly and stretches out the length of the clock each day."
The binding of these protein complexes involves a pocket where the missing tail segment normally competes and interferes with the binding of the rest of the complex.
"How tightly the complex partners bind to this pocket determines how quickly the clock runs," Partch explained. "This tells us we should be looking for drugs that bind to that pocket and can serve the same purpose as the cryptochrome tail."
Partch's lab is currently doing just that, conducting screening assays to identify molecules that bind to the pocket in the clock's molecular complex. "We know now that we need to target that pocket to develop therapeutics that could shorten the clock for people with delayed sleep phase disorder," she said.
Partch has been studying the molecular structures and interactions of the clock proteins for years. In a study published earlier this year, her lab showed how certain mutations can shorten clock timing by affecting a molecular switch mechanism, making some people extreme morning larks.
She said the new study was inspired by the 2017 paper on the cryptochrome mutation from the lab of Nobel Laureate Michael Young at Rockefeller University. The paper had just come out when first author Gian Carlo Parico joined Partch's lab as a graduate student, and he was determined to discover the molecular mechanisms responsible for the mutation's effects.
https://www.sciencedaily.com/releases/2020/10/201027105354.htm
How exercise stalls cancer growth through the immune system
October 26, 2020
Science Daily/Karolinska Institutet
People with cancer who exercise generally have a better prognosis than inactive patients. Now, researchers at Karolinska Institutet in Sweden have found a likely explanation of why exercise helps slow down cancer growth in mice: Physical activity changes the metabolism of the immune system's cytotoxic T cells and thereby improves their ability to attack cancer cells. The study is published in the journal eLife.
"The biology behind the positive effects of exercise can provide new insights into how the body maintains health as well as help us design and improve treatments against cancer," says Randall Johnson, professor at the Department of Cell and Molecular Biology, Karolinska Institutet, and the study's corresponding author.
Prior research has shown that physical activity can prevent unhealth as well as improve the prognosis of several diseases including various forms of cancer. Exactly how exercise exerts its protective effects against cancer is, however, still unknown, especially when it comes to the biological mechanisms. One plausible explanation is that physical activity activates the immune system and thereby bolsters the body's ability to prevent and inhibit cancer growth.
In this study, researchers at Karolinska Institutet expanded on this hypothesis by examining how the immune system's cytotoxic T cells, that is white blood cells specialized in killing cancer cells, respond to exercise.
They divided mice with cancer into two groups and let one group exercise regularly in a spinning wheel while the other remained inactive. The result showed that cancer growth slowed and mortality decreased in the trained animals compared with the untrained.
Next, the researchers examined the importance of cytotoxic T cells by injecting antibodies that remove these T cells in both trained and untrained mice. The antibodies knocked out the positive effect of exercise on both cancer growth and survival, which according to the researchers demonstrates the significance of these T cells for exercise-induced suppression of cancer.
The researchers also transferred cytotoxic T cells from trained to untrained mice with tumors, which improved their prospects compared with those who got cells from untrained animals.
To examine how exercise influenced cancer growth, the researchers isolated T cells, blood and tissue samples after a training sessions and measured levels of common metabolites that are produced in muscle and excreted into plasma at high levels during exertion. Some of these metabolites, such as lactate, altered the metabolism of the T cells and increased their activity. The researchers also found that T cells isolated from an exercised animal showed an altered metabolism compared to T cells from resting animals.
In addition, the researchers examined how these metabolites change in response to exercise in humans. They took blood samples from eight healthy men after 30 minutes of intense cycling and noticed that the same training-induced metabolites were released in humans.
"Our research shows that exercise affects the production of several molecules and metabolites that activate cancer-fighting immune cells and thereby inhibit cancer growth," says Helene Rundqvist, senior researcher at the Department of Laboratory Medicine, Karolinska Institutet, and the study's first author. "We hope these results may contribute to a deeper understanding of how our lifestyle impacts our immune system and inform the development of new immunotherapies against cancer."
The researchers have received financing from the Knut and Alice Wallenberg Foundation, the Swedish Research Council, the Swedish Cancer Society, the Swedish Childhood Cancer Foundation, the Swedish Society of Medicine, Cancer Research UK and the Wellcome Trust.
https://www.sciencedaily.com/releases/2020/10/201026114229.htm
Hard physical work may significantly increase the risk of dementia
October 26, 2020
Science Daily/University of Copenhagen The Faculty of Health and Medical Sciences
Men in jobs with hard physical work have a higher risk of developing dementia compared to men doing sedentary work, new research reveals. The researchers therefore urge the health authorities to make their recommendations concerning physical activity more specific.
The muscles and joints are not the only parts of the body to be worn down by physical work. The brain and heart suffer too. A new study from the University of Copenhagen shows that people doing hard physical work have a 55-per cent higher risk of developing dementia than those doing sedentary work. The figures have been adjusted for lifestyle factors and lifetime, among other things.
The general view has been that physical activity normally reduces the risk of dementia, just as another study from the University of Copenhagen recently showed that a healthy lifestyle can reduce the risk of developing dementia conditions by half.
Here the form of physical activity is vital, though, says associate professor Kirsten Nabe-Nielsen from the Department of Public Health at the University of Copenhagen.
"Before the study we assumed that hard physical work was associated with a higher risk of dementia. It is something other studies have tried to prove, but ours is the first to connect the two things convincingly," says Kirsten Nabe-Nielsen, who has headed the study together with the National Research Centre for the Working Environment with help from Bispebjerg-Frederiksberg Hospital.
"For example, the WHO guide to preventing dementia and disease on the whole mentions physical activity as an important factor. But our study suggests that it must be a 'good' form of physical activity, which hard physical work is not. Guides from the health authorities should therefore differentiate between physical activity in your spare time and physical activity at work, as there is reason to believe that the two forms of physical activity have opposite effects," Kirsten Nabe-Nielsen says and explains that even when you take smoking, blood pressure, overweight, alcohol intake and physical activity in one's spare time into account, hard physical work is associated with an increased occurrence of dementia.
One of the study's co-authors is Professor MSO Andreas Holtermann from the National Research Centre for the Working Environment. He hopes the dementia study from the University of Copenhagen will contribute to shine a spotlight on the importance of prevention, as changes in the brain begin long before the person leaves the labour market.
"A lot of workplaces have already taken steps to improve the health of their staff. The problem is that it is the most well-educated and resourceful part of the population that uses these initiatives. Those with a shorter education often struggle with overweight, pain and poor physical fitness, even though they take more steps during the day and to a larger extent use their body as a tool. For workmen, it is not enough for example to avoid heavy lifts if they wish to remain in the profession until age 70. People with a shorter education doing manual labour also need to take preventive steps by strengthening the body's capacity via for example exercise and strength training," he says.
The study is based on data from the Copenhagen Male Study (CMS), which included 4,721 Danish men, who back in the 1970s reported data on the type of work they did on a daily basis. The study included 14 large Copenhagen-based companies, the largest being DSB, the Danish Defence, KTAS, the Postal Services and the City of Copenhagen.
Through the years, the researchers have compiled health data on these men, including data on the development of dementia conditions.
According to Kirsten Nabe-Nielsen, previous studies have suggested that hard physical work may have a negative effect on the heart blood circulation and thus also on the blood supply to the brain. This may for example lead to the development of cardiovascular diseases like high blood pressure, blood clots in the heart, heart cramps and heart failure.
The National Research Centre for the Working Environment continues to work on the results with a view to identifying healthier ways of doing hard physical work. They have therefore begun to collect data from social and healthcare assistants, child care workers and packing operatives, among others, in order to produce interventions meant to organise hard physical work in such a way that it has an 'exercise effect'.
They thus hope to see companies successfully change work procedures, ensuring for example that heavy lifts will have a positive effect rather than wear down the workers. The results will be published on an ongoing basis.
https://www.sciencedaily.com/releases/2020/10/201026114240.htm
How Does CBD Oil Make You Feel?
One of the most popular wellness ingredients today is cannabidiol (CBD). The compound is naturally found in hemp plants and is now being used for all sorts of possible therapeutic effects.
Though there is no shortage of testimonials on CBD gummies for sleep and its possible benefits, there may still be some confusion on how CBD oil makes you feel. Read more to learn about what to expect with top-shelf hemp products.
What are the Effects of CBD?
Before diving into how CBD feels, it is important to first discuss your body’s endocannabinoid system (ECS). This relatively unstudied system is made up of endocannabinoids (receptors), the cannabinoids that bind to them, and the enzymes that break them down.
THC is the cannabinoid known for producing the infamous marijuana high with its psychoactive effects. It works by activating the CB1 receptors of the ECS.
Cannabidiol, on the other hand, is non-psychoactive and has been observed to inhibit activity in these CB1 receptors and counteract THC’s effects.
Taken together, these naturally-occurring cannabinoids produce what is known as an entourage effect. This synergistic interaction is reported to produce heightened effects compared to taking just THC or CBD alone.
How CBD Feels
Ingesting hemp oil provides a more systemic effect and is the preferred method of consumers looking to benefit from its possible anti-anxiety and chronic pain-relieving effects.
Meanwhile, buying and using a CBD for pain is thought to produce more localized anti-inflammatory effects and pain relief, such as for joint pain.
Current research suggests that hemp has a very good safety profile and is well-tolerated by many people. People who have tried CBD have further compared its feeling to a runner’s high, or the natural rush of endorphins that lifts your mood.
Many consumers report feelings of relaxation and calmness after taking their cannabidiol fix. There is no standard formulation that works universally for everyone as its effects are dependent on several factors, including the type of CBD you are taking, the total cannabidiol content, and individual factors like tolerance, weight, and metabolism.
Different concentrations of hemp also influence their effects. Full-spectrum CBD is a formulation that contains up to 0.3 % THC as well as other cannabinoids like cannabinol (CBN) and cannabigerol (CBG). The level of THC in full-spectrum hemp is not enough to get you high but the presence of all-natural cannabinoids produces the desired entourage effect.
Broad-spectrum CBD produces a similar entourage effect but the formulation has the notable exclusion of THC. If you want to avoid any and all THC, then this formulation is best for you. Lastly, CBD isolates are processed to contain no other cannabinoids and terpenes but cannabidiol. This pure formulation is also popular but does not produce an entourage effect.
One formulation of hemp products that is gaining popularity contains a 1:1 CBD-to-THC ratio. Users report that this concentration is beneficial as a sleeping aid as it may produce an intoxicated feeling attributed to higher amounts of THC.
Does CBD Make You Hungry?
People curious about this cannabis substance also wonder about its other side effects like the “munchies,” a popular side effect of using marijuana. The munchies are actually effects of THC which alter the part of the brain that controls your appetite.
THC also increases levels of the ghrelin hormone, causing you to feel hungry.
As such, CBD does not cause the munchies. However, cannabidiol may relieve nausea and calm your digestive tract. By feeling less nauseated, you may end up feeling less pain overall and experience more fulfillment with your meals.
Of course, the effects of cannabidiol highly depend on how much you take. While there is a recommended CBD dosage, it’s best to consult a doctor.
Does CBD Give You Energy?
As to how CBD makes you feel, those you have tried industrial hemp oil report a mental clarity which is quite opposite from the feeling of intoxication.
According to them, cannabidiol can make you less distracted, sharpen your cognitive abilities, and make you more alert. It is this cognitive health benefit that many people desire when they take CBD.
Is CBD Oil Addictive?
It is understandable if you might think that CBD is addictive. After all, it comes from the cannabis plant. However, CBD is not addictive, and using it does not produce a “stoned” feeling that its cousin marijuana has become infamous for.
A study examined the abuse potential of CBD and it concluded that the compound does not display any signs of abuse potential.
What Happens When You Stop Using CBD Oil?
Cannabidiol may be effective in managing symptoms of anxiety but it should not replace the medications that you are already using. Frequent users of this substance who suddenly stop using it may also experience withdrawal symptoms including irritability, dizziness, nausea, and fogginess.
These statements have not been evaluated by the Food and Drug Administration. A CBD product is not intended to diagnose, treat, cure, or prevent any disease and must be taken as a supplement only.
High flavanol diet may lead to lower blood pressure
First study to use objective measure to look at 25,000 people's diet
October 21, 2020
Science Daily/University of Reading
People who consume a diet including flavanol-rich foods and drinks, including tea, apples and berries, could lead to lower blood pressure, according to the first study using objective measures of thousands of UK residents' diet.
The findings, published in Scientific Reports, studied the diet of more than 25,000 people in Norfolk, UK and compared what they ate with their blood pressure. In contrast to most other studies investigating links between nutrition and health, the researchers did not rely on study participants reporting their diet, but instead measured flavanol intake objectively using nutritional biomarkers -- indicators of dietary intake, metabolism or nutritional status that are present in our blood.
The difference in blood pressure between those with the lowest 10% of flavanol intake and those with the highest 10% of intake was between 2 and 4 mmHg. This is comparable to meaningful changes in blood pressure observed in those following a Mediterranean diet or Dietary Approaches to Stop Hypertension (DASH) diet. Notably, the effect was more pronounced in participants with hypertension.
Professor Gunter Kuhnle, a nutritionist at the University of Reading who led the study said:
"Previous studies of large populations have always relied on self-reported data to draw conclusions, but this is the first epidemiological study of this scale to objectively investigate the association between a specific bioactive compound and health. We are delighted to see that in our study, there was also a meaningful and significant association between flavanol consumption and lower blood pressure.
"What this study gives us is an objective finding about the association between flavanols -- found in tea and some fruits -- and blood pressure. This research confirms the results from previous dietary intervention studies and shows that the same results can be achieved with a habitual diet rich in flavanols. In the British diet, the main sources are tea, cocoa, apples and berries.
"The methodology of the study is of equal importance. This is one of the largest ever studies to use nutritional biomarkers to investigate bioactive compounds. Using nutritional biomarkers to estimate intake of bioactive food compounds has long been seen as the gold standard for research, as it allows intake to be measured objectively. The development, validation and application of the biomarker was only possible because of the long-term commitment of all collaborators. In contrast to self-reported dietary data, nutritional biomarkers can address the huge variability in food composition. We can therefore confidently attribute the associations we observed to flavanol intake."
An international team from the University of Reading, Cambridge University, the University of California Davis, and Mars, Incorporated studied 25,618 participants from the European Prospective Investigation into Cancer (EPIC) Norfolk study and found that the biggest difference was observed in participants with the highest blood pressure. This suggests if the general public increased its flavanol intake, there could be an overall reduction in cardiovascular disease incidence.
Hagen Schroeter, Chief Science Officer at Mars Edge, said:
"This study adds key insights to a growing body of evidence supporting the benefits of dietary flavanols in health and nutrition. But, perhaps even more exciting was the opportunity to apply objective biomarkers of flavanol intake at a large scale. This enabled the team to avoid the significant limitations that come with past approaches which rely on estimating intake based on self-reported food consumption data and the shortcomings of current food composition databases."
The study was supported with an unrestricted grant from Mars, Incorporated, and two co-authors are employees of Mars. The study worked with the EPIC Norfolk population cohort, which acknowledges funding from the Medical Research Council and Cancer Research UK.
https://www.sciencedaily.com/releases/2020/10/201021085109.htm
Scientist develops new way to test for COVID-19 antibodies
October 23, 2020
Science Daily/Seattle Children's
When Dr. Stephen Smith of Seattle Children's Research Institute came down with muscle aches, gastrointestinal distress and a sudden loss of smell in late February, he suspected he had COVID-19. The testing criteria had yet to be expanded to include individuals with Smith's symptoms and so he did what many scientists with his expertise would do: he developed a way to test himself.
The fruits of his curiosity, now published in The Journal of Infectious Diseases, offer a reliable way to quantify whether an individual has neutralizing antibodies that could prevent the novel coronavirus from infecting cells using a method that is more broadly applicable than those currently available.
"If you think you've had COVID-19 and go to the doctor, they can test your blood and tell you whether or not you have antibodies to COVID-19, but that doesn't tell you whether your antibodies are any good at functionally blocking the virus from binding to cells," Smith said. "There are tests on the market now that can tell you that, but they are expensive and take a long time to get results. We wanted to develop a way to give you additional information about your immune status without all the barriers that make it difficult to use in a community setting."
The newly developed diagnostic could have a range of potential commercial applications from broad community testing to assessing vaccine responses and screening for convalescent plasmas that have particularly high levels of neutralizing antibodies as a potential treatment.
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Cell-free test looks at protein interactions
The novel coronavirus enters cells when the viral spike protein binds to the ACE2 protein on the surface of human cells. Neutralizing antibodies that block this binding are thought to contribute to immunity to the virus in people who recover from COVID-19.
Smith applied a technique called immunoprecipitation detected by flow cytometry (IP-FCM) to study the interactions between the proteins and to look for evidence that antibodies were inhibiting the interaction and blocking the virus from binding to cells. Instead of relying on live cells and viruses like other available blood tests, IP-FCM uses recombinant -- or lab-made -- proteins and instruments commonly available in commercial serological labs.
"Other tests that provide insight into immunity work by taking antibodies from your blood and mixing them together with a virus and then exposing that mixture to live cells. Three days later they can determine immunity based on whether your blood prevented the viruses from infecting the cells or not," Smith said. "Our cell-free test can provide that same information overnight."
Collaborative science launches innovative study
Smith is among a small group of scientists in the U.S. who have pioneered IP-FCM to study the interactions between proteins. His lab in Seattle Children's Center for Integrative Brain Research uses IP-FCM to uncover new treatments for autism by studying the more than 100 genetic variations known to contribute to the condition. To apply his expertise to the current pandemic, Smith collaborated with Drs. Lisa Frenkel and Whitney Harrington from the research institute's Center for Global Infectious Global Disease Research who are following a community cohort of Seattle Children's employees who were never hospitalized and had recovered from mild to moderate COVID-19. The researchers hope by tracking their recovery and taking blood samples over time as part of the Seattle Children's Recovered SARS2 Cohort study they can shed light on the immune responses to the novel coronavirus.
Funding in part by Seattle Children's COVID-19 Research Fund helped Smith design and launch the study.
Using IP-FCM, Smith tested the blood samples from 24 cohort participants. The test showed that 92% of the participants had antibodies to the novel coronavirus at an average of a little over a month post-infection. Results were validated with 30 control samples.
"Not only did the participants have antibodies, but our test also showed that their antibodies were pretty effective at neutralizing the binding between the spike protein and the cell's receptor," he said. "It's consistent with other studies from cell-based tests showing that people who get COVID do make neutralizing antibodies."
Interestingly, when researchers looked at the test results against other data gathered from the cohort, they found that those who mounted a fever had higher levels of antibodies. The research team also plans to retest the samples to see how antibody levels change over time.
"It's going to be very important to look at people over a longer time period to track their antibody levels and whether or not they get re-infected," Smith said. "Until we do those studies, we really don't know how these clinical measures of antibody neutralization relate to susceptibility in the real world."
Identifying new drug candidates for COVID-19
In addition to exploring opportunities to commercialize the diagnostic, Smith and his team are now using the test to rapidly screen thousands of approved drugs that could potentially interfere with the binding between ACE2 and the spike protein.
Lab manager, Edward Gniffke, and Stanford University undergraduate and summer intern, Kaleb Tsegay, helped run the initial screen that could potentially identify drugs capable of preventing or treating COVID-19.
"We already have some compounds that look like they are inhibiting, which is pretty exciting," Smith said. "This first line screen will help us pinpoint the most promising agents for further tests."
https://www.sciencedaily.com/releases/2020/10/201022201404.htm
Aspirin use reduces risk of death in hospitalized COVID-19 patients
October 22, 2020
Science Daily/University of Maryland School of Medicine
Hospitalized COVID-19 patients who were taking a daily low-dose aspirin to protect against cardiovascular disease had a significantly lower risk of complications and death compared to those who were not taking aspirin, according to a new study led by researchers at the University of Maryland School of Medicine (UMSOM). Aspirin takers were less likely to be placed in the intensive care unit (ICU) or hooked up to a mechanical ventilator, and they were more likely to survive the infection compared to hospitalized patients who were not taking aspirin, The study, published today in the journal Anesthesia and Analgesia, provides "cautious optimism," the researchers say, for an inexpensive, accessible medication with a well-known safety profile that could help prevent severe complications.
"This is a critical finding that needs to be confirmed through a randomized clinical trial," said study leader Jonathan Chow, MD, Assistant Professor of Anesthesiology at UMSOM. "If our finding is confirmed, it would make aspirin the first widely available, over-the-counter medication to reduce mortality in COVID-19 patients."
To conduct the study, Dr. Chow and his colleagues culled through the medical records of 412 COVID-19 patients, age of 55 on average, who were hospitalized over the past few months due to complications of their infection. They were treated at the University of Maryland Medical Center in Baltimore and three other hospitals along the East Coast. About a quarter of the patients were taking a daily low-dose aspirin (usually 81 milligrams) before they were admitted or right after admission to manage their cardiovascular disease.
The researchers found aspirin use was associated with a 44 percent reduction in the risk of being put on a mechanical ventilator, a 43 percent decrease in the risk of ICU admission and -- most importantly -- a 47 percent decrease in the risk of dying in the hospital compared to those who were not taking aspirin. The patients in the aspirin group did not experience a significant increase in adverse events such as major bleeding while hospitalized.
The researchers controlled for several factors that may have played a role in a patient's prognosis including age, gender, body mass index, race, hypertension and diabetes. They also accounted for heart disease, kidney disease, liver disease and the use of beta blockers to control blood pressure.
COVID-19 infections increase the risk of dangerous blood clots that can form in the heart, lungs, blood vessels and other organs. Complications from blood clots can, in rare cases, cause heart attacks, strokes and multiple organ failure as well as death.
Doctors often recommend a daily low-dose aspirin for patients who have previously had a heart attack or stroke caused by a blood clot to prevent future blood clots. Daily use, however, can increase the risk of major bleeding or peptic ulcer disease.
"We believe that the blood thinning effects of aspirin provides benefits for COVID-19 patients by preventing microclot formation," said study co-author Michael A. Mazzeffi, MD, Associate Professor of Anesthesiology at UMSOM. "Patients diagnosed with COVID-19 may want to consider taking a daily aspirin as long as they check with their doctor first." Those at increased bleeding risk due to chronic kidney disease, for example, or because they regularly use certain medications, like steroids or blood thinners, may not be able to safely take aspirin, he added.
Researchers from Wake Forest School of Medicine, George Washington University School of Medicine, Northeast Georgia Health System, and Walter Reed National Military Medical Center also participated in this study.
"This study adds to the tremendous work our researchers are doing in the School of Medicine to help find new treatments against COVID-19 and save patients' lives," said E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. "While confirmatory studies are needed to prove that aspirin use leads to better outcomes in COVID-19, the evidence thus far suggests that patients may want to discuss with their doctor whether it is safe for them to take aspirin to manage potentially prevent serious complications."
https://www.sciencedaily.com/releases/2020/10/201022195637.htm
34% of older adults in the US are prescribed potentially inappropriate drugs
October 23, 2020
Science Daily/University at Buffalo
The prescription of potentially inappropriate medications to older adults is linked to increased hospitalizations, and it costs patients, on average, more than $450 per year, according to a new University at Buffalo study.
The research, which sought to determine the impact of potentially inappropriate medications on health care utilization and costs in the United States, also found that more than 34% of adults age 65 and older were prescribed these problematic drugs.
"Although efforts to de-prescribe have increased significantly over the last decade, potentially inappropriate medications continue to be prescribed at a high rate among older adults in the United States," says David Jacobs, PharmD, PhD, lead investigator and assistant professor of pharmacy practice in the UB School of Pharmacy and Pharmaceutical Sciences.
Collin Clark, PharmD, first author on the paper and clinical assistant professor in the School of Pharmacy and Pharmaceutical Sciences, adds, "The average age of the U.S. population is rising, and older adults account for a disproportionate amount of prescription medications. Harm to older adults caused by potentially inappropriate medications is a major public health challenge."
As the human body ages, the risk of experiencing harmful side effects from medications increases. Potentially inappropriate medications are drugs that should be avoided by older adults due to these risks outweighing the benefits of the medication, or when effective but lower risk alternative treatments are available.
The study, which was published in August in the Journal of the American Geriatrics Society, used the 2011-2015 Medical Expenditure Panel Survey -- conducted annually by the U.S. Public Health Service and the Centers for Disease Control and Prevention (CDC) -- to examine the prescription of 33 potentially inappropriate medications or classes of medications to adults 65 and older.
Among the potentially inappropriate medications examined were antidepressants, barbiturates, androgens, estrogens, nonsteroidal anti-inflammatory drugs, first-generation antihistamines, and antipsychotics.
Among the 218 million-plus older adults surveyed, more than 34% were prescribed at least one potentially inappropriate medication. Those patients were, on average, prescribed twice as many drugs, were nearly twice as likely to be hospitalized or visit the emergency department, and were more likely to visit a primary care physician compared to older adults who were not prescribed potentially inappropriate medication.
Patients who received these medications also spent an additional $458 on health care, including an extra $128 on prescription drugs.
"De-prescribing is currently at an early stage in the United States. Further work is needed to implement interventions that target unnecessary and inappropriate medications in older adults," says Jacobs.
https://www.sciencedaily.com/releases/2020/10/201023095850.htm
COVID-19 anxiety linked to body image issues
Study finds association between stress and anxiety, and negative body image
October 23, 2020
Science Daily/Anglia Ruskin University
A new study has found that anxiety and stress directly linked to COVID-19 could be causing a number of body image issues amongst women and men.
The research, led by Professor Viren Swami of Anglia Ruskin University (ARU) and published in the journal Personality and Individual Differences, involved 506 UK adults with an average age of 34.
Amongst women, the study found that feelings of anxiety and stress caused by COVID-19 were associated with a greater desire for thinness. It also found that anxiety was significantly associated with body dissatisfaction.
Amongst the male participants, the study found that COVID-19-related anxiety and stress was associated with greater desire for muscularity, with anxiety also associated with body fat dissatisfaction.
Negative body image is one of the main causes of eating disorders, such as anorexia and bulimia, and this new study adds to recent research indicating that fears around COVID-19, and the consequences of the restrictions introduced to help tackle it, could be contributing to a number of serious mental health issues.
Lead author Viren Swami, Professor of Social Psychology at Anglia Ruskin University (ARU), said: "In addition to the impact of the virus itself, our results suggest the pandemic could also be leading to a rise in body image issues. In some cases, these issues can have very serious repercussions, including triggering eating disorders.
"Certainly during the initial spring lockdown period, our screen time increased, meaning that we were more likely to be exposed to thin or athletic ideals through the media, while decreased physical activity may have heightened negative thoughts about weight or shape. At the same time, it is possible that the additional anxiety and stress caused by COVID-19 may have diminished the coping mechanisms we typically use to help manage negative thoughts.
"Our study also found that when stressed or anxious, our pre-occupations tend to follow gender-typical lines. During lockdown, women may have felt under greater pressure to conform to traditionally feminine roles and norms, and messaging about self-improvement may have led to women feeling dissatisfied with their bodies and having a greater desire for thinness.
"Similarly, our findings reflect the way in which stress and anxiety impact men's relationships with their bodies, particularly in terms of masculine body ideals. Given that masculinity typically emphasises the value of toughness, self-reliance, and the pursuit of status, COVID-19-related stress and anxiety may be leading men to place greater value on the importance of being muscular."
https://www.sciencedaily.com/releases/2020/10/201022201407.htm
Researchers discover neuroprotective treatment for chronic traumatic brain injury
Brief pharmacologic treatment one year after traumatic brain injury in mice reverses cognitive impairment
October 19, 2020
Science Daily/University Hospitals Cleveland Medical Center
TBI survivors are currently treated with extensive physical and cognitive rehabilitation, accompanied by medications that may mitigate symptoms yet do not halt or slow neurodegeneration. Now, researchers have found for the first time that this process can be pharmacologically reversed in an animal model of this chronic health condition, offering an important proof of principle in the field and a potential path to new therapy.
Traumatic brain injury (TBI) is a leading cause of cognitive impairment that affects millions of people worldwide. Despite growing awareness about the debilitating and lifelong progressive consequences of TBI, there are currently no treatments that slow the deteriorative process. TBI survivors are currently treated with extensive physical and cognitive rehabilitation, accompanied by medications that may mitigate symptoms yet do not halt or slow neurodegeneration.
Now, researchers have found for the first time that this process can be pharmacologically reversed in an animal model of this chronic health condition, offering an important proof of principle in the field and a potential path to new therapy. The findings from Harrington Discovery Institute at University Hospitals (UH), Case Western Reserve University (CWRU) School of Medicine, and Louis Stokes Cleveland VA Medical Center were recently published in the Proceedings of the National Academy of Sciences (PNAS) USA.
"TBI can lead to lifelong detrimental effects on multiple aspects of health," explains Andrew A. Pieper, MD, PhD, senior author on the study and Director of the Harrington Discovery Institute at UH Neurotherapeutics Center, Morley-Mather Chair in Neuropsychiatry, Professor of Psychiatry at CWRU, and Psychiatrist at the Louis Stokes Cleveland VA Medical Center Geriatrics Research Education and Clinical Center (GRECC). "Adverse long-term outcomes of TBI commonly include sensorimotor impairment, cognitive dysfunction, or emotional dysregulation, such as depression and anxiety, including worsened post-traumatic stress disorder. In addition, TBI significantly increases the risk of later developing aging-related forms of dementia, such as Alzheimer's and Parkinson's diseases."
Dr. Pieper and his team set out to test whether it was possible to reverse the lifelong chronic neurodegeneration and associated cognitive deficits after TBI, which had never been demonstrated before. They utilized a mouse model that mimicked concussive impact in middle-aged people suffering a TBI decades prior, and administered an energy-elevating neuroprotective compound, known as P7C3-A20, that they had previously shown to have therapeutic value in acute TBI. The research team waited for one year after injury and then administered the compound daily to mice for one month.
Strikingly, this brief treatment with P7C3-A20 restored normal cognitive function. They continued to observe the mice for an additional four months, during which time they did not administer any more compound. Remarkably, at the end of this period the mice still showed normal cognitive function. Thus, after just one month of treatment, cognitive function remained improved four months later.
"When we examined the brains under the microscope, we saw that chronic neurodegeneration after TBI had completely stopped in the mice that had been briefly-treated with P7C3-A20," said Edwin Vázquez-Rosa, PhD, co-first author on the study. "Then, under electron microscopy we discovered that P7C3-A20 had also facilitated repair of the endothelial cells lining the blood vessels of the brain."
"This is the first time we've seen that P7C3-A20 can protect endothelial cells at the interface of the cardiovascular system and the brain, known as the neurovascular unit (NVU)," explains Min-Kyoo Shin, PhD, co-first author on the study. Deterioration of the NVU occurs in almost all types of brain injury and disease, and is a well-known early and chronic feature of Alzheimer's disease. The team also showed that P7C3-A20 directly protects human brain microvascular endothelial cells cultured in the laboratory as well.
"Except for aging and genetics, TBI is the greatest risk factor for developing Alzheimer's disease," explains Matasha Dhar, PhD, co-first author on the study. "We speculate that preserving the blood-brain barrier at the NVU might be a way to protect TBI patients from this increased risk."
Robert A. Bonomo, MD, Associate Chief of Staff and Director of the Cleveland GRECC asserts, "These seminal findings have tremendous long-term impact on our veteran population that suffers from TBI."
There are currently no medicines available to patients that directly protect the blood brain barrier. A medicine with this property, such as one derived from the P7C3 series of compounds, would have broad applicability to numerous conditions of the brain, including TBI and Alzheimer's disease.
https://www.sciencedaily.com/releases/2020/10/201019155924.htm
Stigma impacts psychological, physical health of multiracial people
The multiracial population is one of the fastest-growing minority groups but faces stigma challenges
October 22, 2020
Science Daily/Rutgers University
Policy changes can help to fight stigmas of multiracial Americans, one of the fasting growing minority groups in the United States according to a Rutgers University-led study.
Published in the journal Policy Insights from the Behavioral and Brain Sciences, the study finds that such stigmas may be combated by legitimizing multiracial identities. Despite the increasing prominence of multiracial celebrities and leaders such as Barack Obama, Meghan Markle, and Bruno Mars, many multiracial people are physically isolated from their peers, said lead author Diana Sanchez, a Rutgers professor of psychology.
"Multiracial people encounter unique challenges because they straddle multiple racial groups," said Sanchez. "Sen. Kamala Harris is Black and South Asian, yet social media outlets vary to the extent to which they recognize her multiracial background. This lack of recognition for multiracial populations is common as is the tendency for fellow monoracial group members like South Asian or Black Americans to have trouble including a multiracial person in their group."
Multiracial people who report frequent racial identity denial also indicate more depressive symptoms, more stress, impaired motivation, and lower self-esteem -- compared with those who experience denial less frequently, according to research.
Multiracial people experience discrimination and everyday, often subtle, instances of these racist microaggressions that stem specifically from their identity -- such as being told that they cannot identify with certain racial identities or that they are not full members of their own racial communities.
The study suggests adopting policy changes that could increase population estimates that would allow for more for distribution of educational and health care resources and improve health care delivery for multiracial populations. Recommendations include:
Legitimizing multiracial identity by capitalizing the "M" in multiracial and adjusting guidelines that are set forth by, for example, the American Psychological Association and in writing style guides about race-appropriate language.
Being explicit about the consequences of listing a multiracial background on business loans and applications. There is a lack of transparency regarding how claiming a multiracial identity will affect eligibility.
Fully integrating check-all-that-apply racial measures for data collection. These have psychological benefits for multiracial people by recognizing and validating their identities.
Minority programs tailored to building community and facilitating positive racial socialization should integrate education for multiracial people by discussing how to respond to questions such as: "What are you?," "Are you sure your dad is really your dad?"
The U.S. Census 2020 marks the third assessment that allows residents to indicate belonging to more than one racial group. The 2010 U.S. Census data revealed that multiracial individuals represent one of the fastest growing minority groups in the United States, representing, at the time, roughly nine million Americans.
"Many people have argued that Harris's vice presidential nomination may be an opportunity to unite Black and South Asian communities who can jointly celebrate this candidacy, but we will first have to confront the issue that many have trouble with -- seeing multiracial people as legitimate members of their monoracial communities," said Sanchez.
https://www.sciencedaily.com/releases/2020/10/201022134725.htm
Vitamin A boosts fat burning in cold conditions
The conversion of white into brown adipose tissue is a promising target for obesity treatment
October 21, 2020
Science Daily/Medical University of Vienna
A recent study conducted by a research team led by Florian Kiefer from MedUni Vienna's Division of Endocrinology and Metabolism shows that cold ambient temperatures increase vitamin A levels in humans and mice. This helps convert "bad" white adipose tissue into "good" brown adipose tissue which stimulates fat burning and heat generation. This "fat transformation" is usually accompanied by enhanced energy consumption and is therefore considered a promising approach for the development of novel obesity therapeutics. The study has now been published in the journal Molecular Metabolism.
In humans and mammals, at least two types of fatty depots can be discerned, white and brown adipose tissue. During obesity development, excess calories are mainly stored in white fat. In contrast, brown fat burns energy and thereby generates heat. More than 90% of the body fat depots in humans are white which are typically located at the abdomen, bottom, and upper thighs. Converting white into brown fat could be a new therapeutic option to combat weight gain and obesity.
A research group led by Florian Kiefer from the Division of Endocrinology and Metabolism, Department of Medicine III at MedUni Vienna demonstrated now that moderate application of cold increases the levels of vitamin A and its blood transporter, retinol-binding protein, in humans and mice. Most of the vitamin A reserves are stored in the liver and cold exposure seems to stimulate the redistribution of vitamin A towards the adipose tissue. The cold-induced increase in vitamin A led to a conversion of white fat into brown fat ("browning"), with a higher rate of fat burning.
When Kiefer and his team blocked the vitamin A transporter "retinol-binding protein" in mice by genetic manipulation, both the cold-mediated rise in vitamin A and the "browning" of the white fat were blunted: "As a consequence, fat oxidation and heat production were perturbed so that the mice were no longer able to protect themselves against the cold," explains Kiefer. In contrast, the addition of vitamin A to human white fat cells led to the expression of brown fat cell characteristics, with increased metabolic activity and energy consumption.
"Our results show that vitamin A plays an important role in the function of adipose tissue and affects global energy metabolism. However, this is not an argument for consuming large amounts of vitamin A supplements if not prescribed, because it is critical that vitamin A is transported to the right cells at the right time," explains the MedUni Vienna researcher. "We have discovered a new mechanism by which vitamin A regulates lipid combustion and heat generation in cold conditions. This could help us to develop new therapeutic interventions that exploit this specific mechanism."
Scientists from Harvard University, Boston and Rutgers University, New Jersey were also involved in the study. The study was funded by the Austrian Science Fund (FWF), the Vienna Science and Technology Fund (WWTF) and the research fund of the Austrian Diabetes Society.
https://www.sciencedaily.com/releases/2020/10/201021112318.htm