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US Law Authorizes Secretive, National ’Exercises’ Against Public Health ‘Threats’
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The ozone hole over the South Pole is now bigger than Antarctica
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The ‘melancholic joy’ of living in our brutal, beautiful world
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The tangled history of mRNA vaccines
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The Symptoms Show American Culture Is Transitioning into a Violent Oligarchy
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Facebook Has Known for Over a Year That Instagram Is Bad for Teens, Despite Claiming Otherwise
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Are we eating ourselves to extinction?
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31 Reasons Why I Won’t Take the Vaccine
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America’s Largest Windfarm: an Environmental Disaster?
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Religious exemption to vaccine mandates may be difficult to obtain, as Amish case shows
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A Letter to the Unvaccinated
Today’s Videos:
Consuming fruit and vegetables and exercising can make you happier
New research has found that fruit and vegetable consumption and exercise can increase levels of happiness
Universities of Kent and Reading (UK), September 16, 2021
New research led by the University of Kent and University of Reading has found that fruit and vegetable consumption and exercise can increase levels of happiness.
While the link between lifestyle and wellbeing has been previously documented and often used in public health campaigns to encourage healthier diets and exercise, new findings published by the Journal of Happiness Studies show that there is also a positive causation from lifestyle to life satisfaction.
This research is the first of its kind to unravel the causation of how happiness, the consumption of fruit and vegetables and exercising are related, rather than generalising a correlation. The researchers, Dr Adelina Gschwandtner (University of Kent’s School of Economics), Dr Sarah Jewell and Professor Uma Kambhampati (both from the University of Reading’s School of Economics), used an instrumental variable approach to filter out any effect from happiness to lifestyle. It showed that it is rather the consumption of fruit and vegetables and exercising that makes people happy and not the other way round.
Findings demonstrate that the ability of individuals to delay gratification and apply self-control plays a major role in influencing lifestyle decisions, which in turn has a positive impact on wellbeing. The research also shows that men appear to exercise more, and women eat more fruit and vegetables.
With it being well known that lifestyle diseases are a leading cause of ill health and mortality worldwide, and the UK having one of the highest obesity rates in Europe, these findings could have significant implications for public health policy.
Dr Gschwandtner said: ‘Behavioural nudges that help the planning self to reinforce long-term objectives are likely to be especially helpful in maintaining a healthy lifestyle. If a better lifestyle not only makes us healthier but also happier, then it is a clear win-win situation.’
Professor Kambhampati said: ‘There has been a bigger shift in recent years for healthier lifestyle choices. To establish that eating more fruit and vegetables and exercising can increase happiness as well as offer health benefits is a major development. This may also prove useful for policy campaigns around environment and sustainability.’
Greater vitamin D intake associated with increased brain cortical thickness among older individuals
Rush University (Chicago), September 10 2021.
The September 2021 issue of The Journal of Nutrition reported a study conducted by researchers at Rush University that revealed an increase in thickness of the cortex (outer layer) of the brain’s temporal lobe and regions that are vulnerable to Alzheimer’s disease among men and women with a high intake of vitamin D.
The current study included 263 cognitively unimpaired participants in the ongoing Mediterranean-DASH Intervention for Neurodegenerative Delay trial. Participants were at least 65 years of age or older. Questionnaire responses provided data concerning vitamin D intake from food and supplements.
Magnetic resonance imaging (MRI) of the brain revealed an association between total vitamin D intake and increased cortical thickness of the temporal lobe as well as in a composite measurement of areas potentially affected by Alzheimer disease. Compared to those whose vitamin D intake was among the lowest 25% of participants at less than 207 IU per day, participants whose intake was among the top 25% at 1,194 IU or more per day had an adjusted 0.038 millimeters (mm) thicker temporal lobe and a 0.043 mm increase in Alzheimer-vulnerable regions.
Among participants who reported supplementing with 800 to 1,000 IU per day vitamin D, temporal lobe measurements were an adjusted 0.039 mm thicker and Alzheimer’s regions were 0.037 mm greater in comparison with no supplementation. For participants whose supplemental vitamin D intake was 1,000 IU per day or higher, the respective increases were 0.047 mm and 0.046 mm. Vitamin D from food alone was not associated with brain cortical thickness.
“In cognitively unimpaired overweight older adults, we found an association between higher total and supplemental vitamin D intakes and greater cortical thickness in regions vulnerable to Alzheimer disease,” the authors concluded. “The results of our study should be confirmed in prospective cohort studies or clinical trials investigating the impact of vitamin D supplementation on brain outcomes.”
Body clock off-schedule? Prebiotics may help
Dietary compounds shown to protect against jet lag-type symptoms
University of Colorado, September 15, 2021
Whether it’s from jetting across time zones, pulling all-nighters at school or working the overnight shift, chronically disrupting our circadian rhythm—or internal biological clocks—can take a measurable toll on everything from sleep, mood and metabolism to risk of certain diseases, mounting research shows.
But a new University of Colorado Boulder study funded by the U.S. Navy suggests simple dietary compounds known as prebiotics, which serve as food for beneficial gut bacteria, could play an important role in helping us bounce back faster.
“This work suggests that by promoting and stabilizing the good bacteria in the gut and the metabolites they release, we may be able to make our bodies more resilient to circadian disruption,” said senior author Monika Fleshner, a professor of integrative physiology.
The animal study, published in the journal Brain, Behavior and Immunity, is the latest to suggest that prebiotics—not to be confused with probiotics found in fermented foods like yogurt and sauerkraut—can influence not only the gut, but also the brain and behavior.
Naturally abundant in many fibrous foods—including leeks, artichokes and onions—and in breast milk, these indigestible carbohydrates pass through the small intestine and linger in the gut, serving as nourishment for the trillions of bacteria residing there.
The authors’ previous studies showed that rats raised on prebiotic-infused chow slept better and were more resilient to some of the physical effects of acute stress.
For the new study, part of a multi-university project funded by the Office of Naval Research, the researchers sought to learn if prebiotics could also promote resilience to body-clock disruptions from things like jet lag, irregular work schedules or lack of natural daytime light—a reality many military personnel live with.
“They are traveling all over the world and frequently changing time zones. For submariners, who can be underwater for months, circadian disruption can be a real challenge,” said lead author Robert Thompson, a postdoctoral researcher in the Fleshner lab. “The goal of this project is to find ways to mitigate those effects.”
How a healthy gut may prevent jet lag
The researchers raised rats either on regular food or chow enriched with two prebiotics: galactooligosaccharides and polydextrose.
They then manipulated the rats’ light-dark cycle weekly for eight weeks—the equivalent of traveling to a time zone 12 hours ahead every week for two months.
Rats that ate prebiotics more quickly realigned their sleep-wake cycles and core body temperature (which can also be thrown off when internal clocks are off) and resisted the alterations in gut flora that often come with stress.
“This is one of the first studies to connect consuming prebiotics to specific bacterial changes that not only affect sleep but also the body’s response to circadian rhythm disruption,” said Thompson.
The study also takes a critical step forward in answering the question: How can simply ingesting a starch impact how we sleep and feel?
The researchers found that those on the prebiotic diet hosted an abundance of several health-promoting microbes, including Ruminiclostridium 5 (shown in other studies to reduce fragmented sleep) and Parabacteroides distasonis.
They also had a substantially different “metabolome,” the collection of metabolic byproducts churned out by bacteria in the gut.
Put simply: The animals that ingested the prebiotics hosted more good bacteria, which in turn produced metabolites that protected them from something akin to jet lag.
Are supplements worthwhile?
Clinical trials are now underway at CU Boulder to determine if prebiotics could have similar effects on humans.
The research could lead to customized prebiotic mixtures designed for individuals whose careers or lifestyles expose them to frequent circadian disruption.
In the meantime, could simply loading up on legumes and other foods naturally rich in the compounds help keep your body clock running on time? It’s not impossible but unlikely, they say—noting that the rats were fed what, in human terms, would be excessive amounts of prebiotics.
Why not just ingest the beneficial bacteria directly, via probiotic-rich foods like yogurt?
That could also help, but prebiotics may have an advantage over probiotics in that they support the friendly bacteria one already has, rather than introducing a new species that may or may not take hold.
What about prebiotic dietary supplements?
“If you are happy and healthy and in balance, you do not need to go ingest a bunch of stuff with a prebiotic in it,” said Fleshner. “But if you know you are going to come into a challenge, you could take a look at some of the prebiotics that are available. Just realize that they are not customized yet, so it might work for you but it won’t work for your neighbor.”
Magnesium status and dementia: is there a link?
Erasmus MC–University Medical Center Rotterdam, September 15, 2021
People with either low or high blood levels of magnesium may be at higher risk of developing dementia, reports a new study in Neurology.
Subjects who were in the lowest and highest quintiles of serum magnesium had a higher risk of developing dementia during the eight-year follow-up period than those in the middle three quintiles.
Among the 9,500 elderly participants in the prospective study, incidence of dementia was 30% higher in the highest and lowest blood magnesium groups, found the research team from Erasmus University, Rotterdam.
“These results need to be confirmed with additional studies, but the results are intriguing,” said first author Dr. Brenda Kieboom. “Since the current treatment and prevention options for dementia are limited, we urgently need to identify new risk factors for dementia that could potentially be adjusted. If people could reduce their risk for dementia through diet or supplements, that could be very beneficial.”
Should the study findings be confirmed, Kieboom suggested that blood tests could be used as a screening tool for people at risk of dementia.
Study details
The study measured the serum magnesium content of subjects, average age 65 who did not have dementia. Participants were followed for eight years on average. During follow-up, 823 people developed dementia, of which 662 were diagnosed with Alzheimer’s disease.
Results were adjusted for adjusted for other variables which might affect magnesium levels and dementia risk such as kidney function, alcohol intake, body mass index and smoking status.
Subjects were divided into quintiles according to their blood levels of magnesium.
The researchers proposed that the findings of increased dementia risk in the lowest and highest quintiles suggested a U-shaped risk curve.
Study limitations
As an observational study, no causality can be determined from the findings. However, the researchers acknowledged two further limitations of the study.
Firstly, magnesium levels were only measured at the start of the study and could have changed in the follow-up period. Secondly, “serum magnesium levels do not necessarily represent total body magnesium. There can still be a magnesium deficiency if serum magnesium levels are normal; therefore, misclassification could have occurred,” wrote the researchers.
Thirdly, “serum magnesium levels in our study were virtually all within the clinically defined normal range; therefore, we are unable to study the effect of hypomagnesaemia,” they added.
Previous research suggests that simple, reliable measures of magnesium status remain lacking. Serum blood levels may only be reliable in identifying severe deficiency, due to the body’s magnesium homeostasis mechanism.
The researchers also acknowledged that the ability of serum magnesium to influence neuronal levels (and thus a possible mechanism for increased dementia risk) is still the subject of debate.
Given these limitations, further work is likely to be necessary to confirm the magnesium-dementia link, using measures which reflect whole-body magnesium status (e.g. ionised magnesium).
Mayo researchers link gut microbiome to rheumatoid arthritis prognosis
Mayo Clinic, September 15, 2021
A significant indicator of whether a patient with rheumatoid arthritis will improve over the course of disease may lie in part in their gut, according to new research from Mayo Clinic’s Center for Individualized Medicine.
The study, published in Genome Medicine, found that predicting a patient’s future rheumatoid arthritis prognosis could be possible by zeroing in on the trillions of bacteria, viruses and fungi that inhabit their gastrointestinal tract, known as the gut microbiome. The findings suggest that gut microbes and a patient’s outcome of rheumatoid arthritis are connected.
“This is the first study to date that uses gut microbiome data to predict clinical improvement in rheumatoid arthritis disease activity independent of the initial measurement of their condition or prior treatment,” says Jaeyun Sung, Ph.D., a computational biologist within Mayo Clinic’s Center for Individualized Medicine and co-senior author of the study.
Rheumatoid arthritis is a chronic disorder characterized by joint inflammation and pain that can eventually lead to bone and cartilage erosion, joint deformity and loss in mobility. This complex disease affects nearly 1.3 million people in the U.S.
Zeroing in on the microbiome
For the study, the team performed a comprehensive precision genomic analysis, called “shotgun metagenomic sequencing,” on stool samples from 32 patients with rheumatoid arthritis at two separate clinical visits. The team investigated the connection between the gut microbiome and the smallest meaningful changes in clinical disease activity. The team found several traits of the gut microbiome linked to future prognosis.
“By looking at patients’ baseline gut microbiome profiles, we observed significantly different microbiome traits between patients who eventually showed improvement and those who did not,” says John M. Davis III, M.D., a clinical rheumatologist at Mayo Clinic with a specialty interest in inflammatory arthritis. Dr. Davis is co-senior author of the study.
“What was surprising is that our data suggest that depending on the eventual clinical outcome, gut microbiomes not only start at different ecological states, but also grow and develop differently,” Dr. Sung adds.
Next, by using deep-learning artificial intelligence (AI), the investigators examined if they could predict whether a patient achieves clinical improvement. Overall, the predictive performance resulted in 90% accuracy, thereby showcasing the proof of concept that the integration of gut microbiome and AI technology could theoretically be an avenue to predict disease course in rheumatoid arthritis.
Path toward treatment
“With further development, such prognostic biomarkers could identify patients who will achieve early clinical improvement with a given therapy, thereby sparing them the expense and risk of other therapies that are less likely to be effective,” Dr. Davis says. “Conversely, such tools can detect patients whose disease symptoms are less likely to improve, and perhaps allow clinicians to target and monitor them more closely. Much is left to be done, but we’re on the right path toward advancing our understanding of this disease in order to individualize medicine for patients with rheumatoid arthritis.”
Scientists have suspected for some time that the gut microbiome plays a role in rheumatoid arthritis, as well as many other inflammatory and autoimmune diseases. The enormous population of microbes help digest food, regulate the immune system and protect against pathogenic bacteria.
The researchers emphasize that every person’s microbiome is unique and consists of a complex mix of genetic, dietary and environmental influences. These differences shed light on why symptoms vary significantly among rheumatoid arthritis patients, which in turn makes it so difficult to treat and predict clinical outcome.
The study is the second recent rheumatoid arthritis investigation by Drs. Sung and Davis, highlighting the essential partnership between computational biologists and clinicians to solve complex problems in medicine. Together, they are on a path toward developing a suite of new data-driven tools to aid in early detection, diagnosis, prognosis and treatment in rheumatoid arthritis. As such, the researchers plan to explore ways to translate their findings into new biomarkers and therapies.
“Ultimately, our study reveals that modifying the gut microbiome to enhance clinical outcome may hold promise as a future treatment for rheumatoid arthritis,” Dr. Sung says. “This could revolutionize how we deliver care to our patients.”
Understanding how anxiety can drive ‘pessimistic’ decision making
Kyoto University (Japan), September 16, 2021
Is a new high-income job offer worth accepting if it means commuting an extra hour to work? People often have to make tough choices regarding whether to endure some level of discomfort to take advantage of an opportunity or otherwise walk away from the reward. In making such choices, it turns out that the brain weighs our desire to go for the reward against our desire to avoid the related hardship.
In previous research, negative mental states have been shown to upset this balance between payoff and hardship toward more ‘pessimistic’ decision making and avoidance. For example, scientists know that people experiencing anxiety have a stronger-than-normal desire to avoid negative consequences. And people with depression have a weaker desire to approach the reward in the first place. But there is still much we do not know about how the brain incorporates feelings into decision making.
Neuroscientists at Kyoto University’s Institute for Advanced Study of Human Biology (WPI-ASHBi) have connected some of the dots to reveal the brain networks that give anxiety influence over decisions. Writing in the journal Frontiers in Neuroscience, the group has published a review that synthesizes results from years of brain measurements in rats and primates and relates these findings to the human brain.
“We are facing a new epidemic of anxiety, and it is important that we understand how our anxiety influences our decision making,” says Ken-ichi Amemori, associate professor in neuroscience at Kyoto University, ASHBi. “There is a real need for a better understanding of what is happening in the brain here. It is very difficult for us to see exactly where and how anxiety manifests in humans, but studies in primate brains have pointed to neurons in the ACC [anterior cingulate cortex] as being important in these decision-making processes.”
Thinking of the brain as an onion, the ACC lies in a middle layer, wrapping around the tough ‘heart’, or corpus callosum, which joins the two hemispheres. The ACC is also well-connected with many other parts of the brain controlling higher and lower functions with a role in integrating feelings with rational thinking.
The team started by measuring brain activity in rhesus macaques while they performed a task to select or reject a reward in the form of food combined with different levels of ‘punishment’ in the form of an annoying blast of air in the face. The potential choices were visually represented on a screen, and the monkeys used a joystick to make their selection, revealing how much discomfort they were willing to consider acceptable.
When the team probed the ACC of the monkeys, they identified groups of neurons that activated or deactivated in line with the sizes of the reward or punishment on offer. The neurons associated with avoidance and pessimistic decision-making were particularly concentrated in a part of the ACC called the pregenual ACC (pACC). This region has been previously linked to major depressive disorder and generalized anxiety disorder in humans.
Microstimulation of the pACC with a low-level electrical pulse caused the monkeys to avoid the reward, simulating the effects of anxiety. Remarkably, this artificially induced pessimism could be reversed by treatment with the antianxiety drug diazepam.
With knowledge of the pACC’s involvement in anxiety-related decision-making, the team next searched for its connections to other parts of the brain. They injected viruses at the specific sites that instructed nerve cells to start making fluorescent proteins that would light up under microscope observation. The virus then spread to other connected nerve cells, revealing the pathways other areas of the brain linked to this center of ‘pessimistic’ thought.
The team found interconnections with many parts of the prefrontal cortex at the front of the human brain, which is associated with higher cogitative function and reasoning. They also noted a strong connection with labyrinth-like structures known as striosomes.
Amemori explains that “the function of the striosome structure has been something of a mystery for a long time, but our experiments point to these being an important node linking pessimistic decision-making to the brain’s reward system and dopamine regulation.”
The team noted a further connection, namely that between these striosomes and another more distant region, the caudal region of the orbitofrontal cortex (cOFC) at the front of the brain. This part is also known to be involved in cognition and decision-making.
When the team repeated their brain monitoring, microstimulation, and virus tracing studies in cOFC, they found a very similar influence on the monkey’s tendency toward pessimistic decision making. Curiously, the pACC and the cOFC also shared many of the same connections to other parts of the brain.
The team was able to generalize these findings in primates to humans by drawing comparisons with the body of knowledge in human brains studies based on magnetic resonance imaging or MRI.
Amemori says that “the many parallels in brain activation point to a common mechanism for both humans and monkeys. It’s important that we have associated striosomes and their extended network with decision making under an anxious condition, and we hope that this study will be useful toward developing brain pathway-specific treatments for neurological and psychiatric disorders in humans.”
Exercise can make cells healthier, promoting longer life, study finds
University of Virginia, September 12, 2021
Whether it’s running, walking, cycling, swimming or rowing, it’s been well-known since ancient times that doing some form of aerobic exercise is essential to good health and well-being. You can lose weight, sleep better, fight stress and high blood pressure, improve your mood, plus strengthen bones and muscles.
“Whether muscle is healthy or not really determines whether the entire body is healthy or not,” said Zhen Yan of the University of Virginia School of Medicine. “And exercise capacity, mainly determined by muscle size and function, is the best predictor of mortality in the general population.”
But why? Yan might have some answers. He and colleagues at UVA are peering inside the cell to understand, at a molecular level, why that workout – like it or not – is so vital to the body. They found that one important benefit involves the cellular power plant – the mitochondria – which creates the fuel so the body can function properly.
Exercise Stresses Mitochondria
Yan and colleagues have completed a study in mice that, for the first time, shows that just one bout of moderate-to-intense exercise acts as a “stress test” on mitochondria in muscles. They discovered that this “stress test” induced by aerobic exercise triggers a process called mitophagy, where the muscle disposes of the damaged or dysfunctional mitochondria, making the muscle healthier. Yan compares exercise-induced mitophagy to a state vehicle inspection that removes damaged cars from the streets.
“Aerobic exercise removes damaged mitochondria in skeletal muscle,” Yan said. “If you do it repeatedly, you keep removing the damaged ones. You have a better muscle with better mitochondrial quality. We clean up the clunkers, now the city, the cell, is full of healthy, functional cars.”
How Exercise Removes Mitochondria ‘Clunkers’
For this study, Yan and colleagues assessed the skeletal muscle of a mouse model where they had added a mitochondrial reporter gene called “pMitoTimer.” The mitochondria fluoresce green when they are healthy and turn red when damaged and broken down by the cell’s waste-disposal system, the lysosomes.
The mice ran on a small treadmill for 90 minutes and Yan’s team observed mitochondrial stress (signs of “state inspection”) and some mitophagy (towing of the clunkers) at six hours after exercise. Yan explained that exercise in these mice also stimulated a kinase called AMPK, which in turn switched on another kinase, Ulk1. These chemical reactions appear to be important in control of the removal of dysfunctional mitochondria.
“When its turned on, Ulk1 activates other components in the cell to execute the removal of dysfunctional mitochondria,” Yan said. “It’s analogous to a 911 call where a tow truck removes the clunkers. However, we still do not know how these activities are coordinated.”
Some Mice Didn’t Benefit From Exercise
Yan’s lab also deleted the Ulk1 gene in mouse skeletal muscle and found that, without the gene, the removal of damaged or dysfunctional mitochondria is dramatically inhibited, suggesting a new role for the Ulk1 gene in exercise and mitophagy.
“Mice that were unable to do mitophagy did not have the benefit of exercise,” explained study co-author Joshua Drake, a postdoctoral fellow in the Yan lab. “Even though, from an exercise standpoint, they still were able to run just as far as normal mice, they didn’t benefit metabolically with training.”
Drake pointed out that some people with type 2 diabetes don’t respond to exercise, which is a growing clinical problem. He hopes that continued research in the Yan lab will lead to new discoveries to help these non-responders.
The findings have been published online by the scientific journal Nature Communications.
