Train Your Brain to Remember Anything You Learn With This Simple, 20-Minute Habit

Not too long ago, a colleague and I were lamenting the process of growing older and the inevitable increasing difficulty of remembering things we want to remember. That becomes particularly annoying when you attend a conference or a learning seminar and find yourself forgetting the entire session just days later.

But then my colleague told me about the Ebbinghaus Forgetting Curve, a 100-year-old formula developed by German psychologist Hermann Ebbinghaus, who pioneered the experimental study of memory. The psychologist’s work has resurfaced and has been making its way around college campuses as a tool to help students remember lecture material. For example, the University of Waterloo explains the curve and how to use it on the Campus Wellness website.

I teach at Indiana University and a student mentioned it to me in class as a study aid he uses. Intrigued, I tried it out too–more on that in a moment. The Forgetting Curve describes how we retain or lose information that we take in, using a one-hour lecture as the basis of the model. The curve is at its highest point (the most information retained) right after the one-hour lecture. One day after the lecture, if you’ve done nothing with the material, you’ll have lost between 50 and 80 percent of it from your memory.

By day seven, that erodes to about 10 percent retained, and by day 30, the information is virtually gone (only 2-3 percent retained). After this, without any intervention, you’ll likely need to relearn the material from scratch. Sounds about right from my experience. But here comes the amazing part–how easily you can train your brain to reverse the curve.


With just 20 minutes of work, you’ll retain almost all of what you learned.

This is possible through the practice of what’s called spaced intervals, where you revisit and reprocess the same material, but in a very specific pattern. Doing so means it takes you less and less time to retrieve the information from your long-term memory when you need it. Here’s where the 20 minutes and very specifically spaced intervals come in.

Ebbinghaus’s formula calls for you to spend 10 minutes reviewing the material within 24 hours of having received it (that will raise the curve back up to almost 100 percent retained again). Seven days later, spend five minutes to “reactivate” the same material and raise the curve up again. By day 30, your brain needs only two to four minutes to completely “reactivate” the same material, again raising the curve back up.

Thus, a total of 20 minutes invested in review at specific intervals and, voila, a month later you have fantastic retention of that interesting seminar. After that, monthly brush-ups of just a few minutes will help you keep the material fresh.


Here’s what happened when I tried it.

I put the specific formula to the test. I keynoted at a conference and was also able to take in two other one-hour keynotes at the conference. For one of the keynotes, I took no notes, and sure enough, just shy of a month later I can barely remember any of it.

For the second keynote, I took copious notes and followed the spaced interval formula. A month later, by golly, I remember virtually all of the material. And in case if you’re wondering, both talks were equally interesting to me–the difference was the reversal of Ebbinghaus’ Forgetting Curve.

So the bottom line here is if you want to remember what you learned from an interesting seminar or session, don’t take a “cram for the exam” approach when you want to use the info. That might have worked in college (although Waterloo University specifically advises against cramming, encouraging students to follow the aforementioned approach). Instead, invest the 20 minutes (in spaced-out intervals), so that a month later it’s all still there in the old noggin. Now that approach is really using your head.

Science has proven that reading can enhance your cognitive function, develop your language skills, and increase your attention span. Plus, not only does the act of reading train your brain for success, but you’ll also learn new things! The founder of Microsoft, Bill Gates, said, “Reading is still the main way that I both learn new things and test my understanding.”

By: Scott Mautz

Source: Pocket

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Critics:

Dr. John N. Morris is the director of social and health policy research at the Harvard-affiliated Institute for Aging Research. He believes there are three main guidelines you should follow when training your mind:

  1. Do Something Challenging: Whatever you do to train your brain, it should be challenging and take you beyond your comfort zone.
  2. Choose Complex Activities: Good brain training exercises should require you to practice complex thought processes, such as creative thinking and problem-solving.
  3. Practice Consistently: You know the saying: practice makes perfect! Dr. Morris says, “You can’t improve memory if you don’t work at it. The more time you devote to engaging your brain, the more it benefits.”
  4. If you’re looking for reading material, check out our guides covering 40 must-read books and the best books for entrepreneurs.
  5. Practice self-awareness. Whenever you feel low, check-in with yourself and try to identify the negative thought-loop at play. Perhaps you’re thinking something like, “who cares,” “I’ll never get this right,” “this won’t work,” or “what’s the point?” 
  6. Science has shown that mindfulness meditation helps engage new neural pathways in the brain. These pathways can improve self-observational skills and mental flexibility – two attributes that are crucial for success. What’s more, another study found that “brief, daily meditation enhances attention, memory, mood, and emotional regulation in non-experienced meditators.”
  7. Brain Age Concentration Training is a brain training and mental fitness system for the Nintendo 3DS system.
  8. Queendom has thousands of personality tests and surveys. It also has an extensive collection of “brain tools”—including logic, verbal, spatial, and math puzzles; trivia quizzes; and aptitude tests
  9. Claiming to have the world’s largest collection of brain teasers, Braingle’s free website provides more than 15,000 puzzles, games, and other brain teasers as well as an online community of enthusiasts.

 

The Cancer Custodians Hidden Truths

woman-with-headscarf-getting-chemo-treatment-article

Part of Dennis Plenker’s daily job is growing cancer. And a variety of different ones, too. Depending on the day and the project, different tumors may burgeon in the petri dishes stocked in the Cold Spring Harbor Laboratory where Plenker works as a research investigator. They might be aggressive breast cancers.

They might be glioblastomas, one of the deadliest brain tumors that rob patients of their ability to speak or read as they crowd out normal cells. Or they might be pancreatic cancers, the fast and vicious slayers that can overtake a healthy person within weeks or even days.

These tiny tumor chunks are transparent and bland—they look like little droplets of hair gel that accidentally plopped into a plastic dish and took hold. But their unassuming appearance is deceptive. If they were still in the human bodies they came from, they would be sucking up nutrients, rapidly growing and dodging the immune system defenses.

But in Plenker’s hands—or rather in the CSHL’s unique facility—these notorious killers don’t kill anyone. Instead, scientists let them grow to devise the most potent ways to kill them. These tumor chunks are called organoids. They are three-dimensional assemblages of malignant growths used to study cancer behavior and vulnerability to chemotherapy and the so-called “targeted drugs”—the next generation therapies.

Scientists used to study tumors at a single-cell level, but because tumors grow as cell clusters in the body, it proved to be inefficient. The three-dimensional structures make a difference. For example, chemo might destroy the tumor’s outer cell layer, but the inner ones can develop resistance, so where single cells may die, a 3D mass will bounce back. Organoids can provide a window into these little-known mechanisms of drug resistance.

They can reveal how normal tissues turn malignant and where the cellular machinery goes off-track to allow that to happen. As their name suggests, organoids are scientists’ windows into organs, whether healthy or stricken with disease. You need to know your enemy to beat it, Plenker says, and cancer organoids offer that opportunity.

Taken from patients currently undergoing cancer treatments, these tumor chunks will reveal their weaknesses so scientists can find the cancers’ Achilles’ heel and devise personalized treatments. “Organoids are essentially patients in a dish,” Plenker says. Only unlike real patients, the organoids can be subjected to all sorts of harsh experiments to zero in on the precise chemo cocktails that destroy them in the best possible way.

And they will likely provide a more realistic scenario than drug tests in mice or rats, as animal models aren’t perfect proxies for humans.

These notorious killers don’t kill anyone. Instead, scientists devise the most potent ways to kill them.

The way that cancer proliferates in the body is hard to reproduce in the lab. Stem-cell research made it possible. After scientists spent a decade understanding how various cells multiply and differentiate into other cell types based on molecular cues and nourishment, they were able to make cells grow and fuse into tissues.

To stick together like bricks in a nicely laid wall, cells need a biological scaffold that scientists call an extracellular matrix or ECM, which in the body is made from collagen and other materials. Today, the same collagen scaffolds can be mimicked with a gooey substance called Matrigel—and then seeded with specific cells, which take root and begin to multiply.

Some tissue types were easy to grow—Columbia University scientists grew viable bones as early as 2010.1 Others, like kidney cells, were trickier. They would grow into immature tissues incapable of performing their job of cleaning and filtering blood. It took scientists time to realize that these cells wanted more than scaffolding and food—they needed to “feel at home,” or be in their natural habitat. Kidney cells needed the feeling of liquid being washed over them, the Harvard University group found, when they first managed to grow functioning kidney tissue in 2018.2

Cancers have their own growth requirements. In the body, they manage to co-opt the organism’s resources, but keeping them happy in a dish means catering to their dietary preferences. Different cancers need different types of molecular chow—growth factors, hormones, oxygen and pH levels, and other nutrients. Pancreatic adenocarcinoma thrives in low-oxygen conditions with poor nutrients.3 Glioblastomas feed on fatty acids.4 These nutrients are delivered to organoids via a specific solution called growth medium, which the lab personnel regularly doles out into the dishes.

Plenker is charged with keeping this murderous menagerie alive and well. He is the one who designs the cancers’ dietary menu, a specific protocol for each type. And while his official title is facility manager and research investigator who works closely with David Tuveson, director of the CSHL’s Cancer Center, he is essentially a cancer custodian, a curator of a unique collection that aims to change the paradigm of cancer treatment.

Plenker’s research area is pancreatic cancer—one of the most notorious killers known. Often diagnosed late and resistant to treatment, it is essentially a death sentence—only 8 to 10 percent of patients remain alive five years after diagnosis. The chemo drugs used to treat it haven’t changed in 40 years, Plenker says. In the past decade, physicians tried combining multiple drugs together with relative success. Identifying winning combos can save lives, or at least prolong them—and that’s what the organoids will help clinicians do better.

In a groundbreaking clinical trial called PASS-01 (for Pancreatic Adenocarcinoma Signature Stratification for Treatment), Plenker’s team collaborates with other American and Canadian colleagues to identify the most effective chemo cocktails and to understand the individual patients’ tumor behaviors, which would lead to more personalized treatments.5

Scientists know the same cancer types behave differently in different patients. Typically, all malignancies have the so-called “driver mutation”— the cancer’s main trigger caused by a mutated gene. But tumors also often have “passenger mutations” that happen in nearby genes. These additional mutated genes can generate various proteins, which may interfere with treatment.

Or not. Scientists call these mutated gene combinations tumor mutational signatures, which can vary from one patient to the next. With some cancers, doctors already know what mutations signatures they may have, but with pancreatic cancer they don’t have good tale-telling signs, or biomarkers. “There aren’t many biomarkers to help clinicians decide which chemo may be better for which patient,” explains oncologist Grainne O’Kane, who treats pancreatic cancer patients at the Princess Margaret Hospital in Toronto, Canada.

That’s the reason O’Kane participates in the PASS-01 trial—it will give doctors a better view into the exact specifics of their patients’ malignancies. As they take their patients’ biopsies, they are sending little cancer snippets to the CSHL to be grown into organoids, which will be subjected to chemo cocktails of various combinations to design more personalized regiments for them.

The hospital treats all patients with the so-called standard of care chemotherapy, which is more of a one-size-fits-all approach. Some patients will respond to it but others won’t, so the goal is to define the second line of chemo defense in a more personalized fashion. “That’s where the biopsies we send to Tuveson’s lab might be useful,” O’Kane says. “They can help us find something to benefit patients after the first line of chemo stopped working.”

Organoids are patients in a dish. Unlike real patients, organoids can be subjected to experiments.

Scientists can try all kinds of combos on the tumorous organoids, which they can’t do in living people. “You can treat 100 organoids with 100 different compounds and see which one works, or which compound does a good job and which ones don’t work at all,” Plenker says. That would also allow scientists to define the precise amount of chemo, so doctors wouldn’t have to over-treat patients with harsh drugs that create sickening side effects. Ultimately, organoids should take a lot of guesswork out of the process.

With about 150 patients’ adenocarcinomas already collected, the team hopes to come up with some answers. O’Kane says her team already has three patients for which they were able to design the more personalized second line of defense chemo, based on what their organoids revealed. They haven’t yet tried it, because the trial has only started recently, but this would be the next step.

“Being able to piece all this information together in real time as patients are moving through their therapies can really improve the outcomes,” O’Kane says. And while they may not be able to save all of those who graciously donated their biopsy snippets to science, it will help build better treatments in the future. “Even if we won’t be able to help these specific patients we’re hoping to use this info in the future clinical trials,” O’Kane says.

Organoids can also help understand how cancer develops. This is particularly true for breast cancers, says Camilla dos Santos, associate professor and a member of the CSHL Cancer Center. She studies the inner life of human mammary glands, more commonly referred to as breasts, and is also part of the cancer custodian crew. The hormonal changes that women go through during pregnancy subsequently modify breast cancer risk, sometimes lowering it and sometimes increasing—a complex interplay of the body’s chemicals.

“We know that women who get pregnant for the first time before they turn 25 years old, have a 30 percent decrease in breast cancer incidents later in life,” dos Santos says. “When they turn 60 or 70, 30 percent of them will not develop cancer.” On the contrary, those who are pregnant past 38 have a 30 to 50 percent increase in developing aggressive breast cancer types. Clearly, some molecular switches are involved, but they are very hard to study within the body. That’s where organoids can provide a window into the surreptitious process.

Using breast organoids, scientists can model the complex life of mammary glands at various stages of a woman’s life. And while most women wouldn’t want their breasts poked and pierced when they are pregnant or breastfeeding, many donate their tissues after breast reduction surgery or prophylactic mastectomy due to high-risk mutations like the BRCA gene.

That’s where organoids shine because scientists can not only grow them, but also give them the pregnancy hormonal cues, which will make cells generate milk, stop lactating, or do it again—and study the complex cellular interactions that take place in real life.

There’s a lot to study. At birth, mammary glands are similar in both genders—just little patches of the mammary epithelium tissue. But when puberty hits, the female glands fill up with the so-called mammary tree—a system of ducts for future milk production, which fully “blooms” in pregnancy.

“When a woman becomes pregnant, the duct tree expands, growing two types of cells—luminal and myoepithelial ones,” explains Zuzana Koledova, assistant professor of Masaryk University in Czech Republic who also uses organoids in her work. When the baby is born, the luminal cells, which line the inside of the ducts, produce the proteins that comprise milk.

The myoepithelial cells reside outside the ducts and work as muscles that squeeze the ducts to push milk out. Dos Santos likens this pregnancy mammary gland growth to the changes of the seasons. The images of sprouting ducts look like blossoming trees in the spring while later they shrivel like plants do in the fall.

The body governs these processes via the molecular machinery of hormones, which stimulate breast cells growth during pregnancy, and later cause them to die out. The two pregnancy-related hormones, prolactin and oxytocin, are responsible for milk production. Prolactin induces the luminal cells to make milk while oxytocin makes the myoepithelial cells contract. Once the baby is weaned, the levels of these hormones drop, causing cells to shrink back to their non-pregnant state.

With organoids scientists can observe these cellular dynamics at work. Koledova’s team had watched breast organoids secrete milk based on biological cues. They even recorded movies of cells pumping tiny milk droplets in the dish they were growing in. Using tiny snippets of donated breast tissue, the team grew the organoids inside the Matrigel matrix in the growth media and then added the two pregnancy hormones into the mix, explains Jakub Sumbal, a mammary gland researcher in Koledova’s group.

As they began to secret proteins that compose milk, the organoids, which looked like little domes inside the dish, changed from translucent to opaque. “At first, you can see through them, but then as they produce these proteins, they kind of darken,” Sumbal says. “And you can see them pushing out these little droplets.”

Cancer patients would no longer have to undergo chemotherapy by trial and error.

Dos Santos’s team, who also did similar work, outlined molecular changes that follow such dish-based hormonal cues in their recent study.6 In response to hormonal messages, cells produce proteins, which they display on their surfaces, like status symbols. During pregnancy the burgeoning cells prepping for milk production display the “proteins flags” that make them look important, attracting nourishment. When it’s time to die, they commit a cellular suicide.

They signal to the bypassing macrophages—immune system cleanup crew—to devour them. “They essentially say ‘come eat me!’ to the macrophages,” dos Santos says. “Because I’m no longer needed.”

The ability to mimic these processes in a dish, allows scientists to study the molecular switches that trigger breast cancer development—or minimize it. Scientists know that cancerous cells can hide from the immune system and even co-opt it into protecting themselves. They do it by displaying their own “do not eat me” protein flags on the surface and avoid destruction.

“Sometimes cancer cells can recruit specific types of immune cells to protect them,” dos Santos says. “They can not only say ‘do not eat me,’ but say ‘come hang out with me’ to the macrophages, and the macrophages will send suppressive signals to the B-cells or T-cells, the body defenders.” It is as if the cancer requests protection—a crew of guardians around it to defend against other cells that would otherwise wipe it out.

Scientists can’t telescope into the body to peek at these interactions, but they now can watch these stealth battles unfolding in a dish. “Right now we are looking at the proteins that are secreted by the organoids—the proteins that go on the surface of the organoids’ cells and what they would communicate to the immune system,” dos Santos says.

“Even when there’s no immune system surrounding them, they would still be doing that.” There’s a way to mimic the immune system, too. Scientists can add B-cells, T-cells, macrophages, and other players into the growth medium and watch the full-blown cellular warfare in action. “That’s the next step in our research,” dos Santos says.

Understanding what hormonal fluxes trigger breast cancer, and how it recruits other cells for safekeeping, can give scientists ideas for pharmaceutical intervention. “We can find drugs that pharmacologically turn off the switches that trigger cancer or interrupt its signaling for protection,” dos Santos says. “That opens novel ways to treat people.”

Can organoid research lead to a new standard of care for cancer patients? That’s the ultimate goal, researchers say. That’s why Plenker works at keeping his collection of cancer glops alive and well and thriving—he calls it a living biobank. And he keeps a stash in the cryogenic freezer, too.

He is also developing protocols that would allow commercial companies to grow organoids the same way chemical industries make reagents or mice suppliers grow rodents for research. A benefit of organoid experiments is they don’t involve animals at all.

Hospitals may one day start growing organoids from their patients’ biopsies to design and test personalized chemo cocktails for them. Once science crosses over to that reality, the entire treatment paradigm will change. Cancer patients won’t have to undergo chemotherapy by trial and error.

Instead their cancer organoids will be subjected to this process—knocked out by a gamut of drug combinations to find the winning one to use in the actual treatment. Plenker notes that once enough data is gathered about the tumors’ mutational signatures, scientists may create a database of tumor “mugshots” matching them to the chemo cocktails that beat them best.

And then just sequencing a biopsy sample would immediately inform oncologists what drug combo the patient needs. “We may be about 10 years away from that,” Plenker says, but for now there’s a lot more research to do. And a lot more cancers to grow.

By: Lina Zeldovich

Lina Zeldovich grew up in a family of Russian scientists, listening to bedtime stories about volcanoes, black holes, and intrepid explorers. She has written for The New York Times, Scientific American, Reader’s Digest, and Audubon Magazine, among other publications, and won four awards for covering the science of poop. Her book, The Other Dark Matter: The Science and Business of Turning Waste into Wealth, will be released in October 2021 by Chicago University Press. You can find her at LinaZeldovich.com and @LinaZeldovich.

Source: The Cancer Custodians – Issue 102: Hidden Truths – Nautilus

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Critics:

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

Tobacco use is the cause of about 22% of cancer deaths. Another 10% are due to obesity, poor diet, lack of physical activity or excessive drinking of alcohol. Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants. In the developing world, 15% of cancers are due to infections such as Helicobacter pylori, hepatitis B, hepatitis C, human papillomavirus infection, Epstein–Barr virus and human immunodeficiency virus (HIV).

These factors act, at least partly, by changing the genes of a cell. Typically, many genetic changes are required before cancer develops. Approximately 5–10% of cancers are due to inherited genetic defects. Cancer can be detected by certain signs and symptoms or screening tests. It is then typically further investigated by medical imaging and confirmed by biopsy.

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment.

Further reading

How ‘Soft Fascination’ Helps Restore Your Tired Brain

Imagine shining a flashlight at a wall in a dark, empty room. If you walk toward the wall, the light will contract. The closer you get to the wall, the smaller and more concentrated the beam of light becomes. By the time the flashlight is an inch from the wall, you’ll see a tight, bright circle of light surrounded by shadow and darkness.

Your attention is a lot like the beam of that flashlight. You can focus it closely and intensely on something, or you can relax it — allowing it to grow soft and diffuse.

A lot of research — much of it recent — has examined the different types and qualities of attention and their associations with mental health and cognitive functioning. This work has revealed that certain types of attention may tire out your brain and contribute to stress, willpower failures, and other problems.

Meanwhile, activities that broaden and soften your attention may reinvigorate your brain and promote psychological and cognitive wellbeing.

Whenever you train your attention on something — an act that cognitive scientists sometimes call “directed attention” — this requires effort. More effort is needed when other things (i.e. distractions) are vying for your attention, or if the thing you’re trying to focus on is boring.

According to a 2016 review from researchers at the University of Exeter Medical School in the U.K, your ability to effortfully focus your attention is finite. Just as an overworked muscle grows weak, overworking your attention seems to wear it out. When that happens, a lot can go wrong.

For one thing, your ability to concentrate plummets. Your willpower and decision-making abilities also take a hit. According to a 2019 study in the journal Occupational Health Science, attention fatigue may also contribute to stress and burnout.

There’s even some work linking attention fatigue to attention deficit hyperactivity disorder (ADHD). “The symptoms of ADHD and ‘attention fatigue’ so closely mirror each other that the Attention Deficit Disorders Evaluation Scale has been used as a measure of attention fatigue,” wrote the authors of a 2004 study in the American Journal of Public Health.

Certain activities seem to reinvigorate the brain in ways that support directed attention and self-regulation.

Experts are still trying to figure out exactly what resource in your brain is drained by effortful directed-attention tasks. They haven’t nailed that down yet. But there’s evidence that directed attention involves frontal and parietal regions of the brain that are also involved in other “cognitive-control” processes. These are the activities that take you out of autopilot and steer you toward goal-directed thoughts and actions — the stuff that isn’t necessarily fun or engaging, but that supports your career, your relationships, and your health.

Distractions, multitasking behaviors, loud noises, bustling urban environments, poor sleep, and many other features of modern life seem to promote attention fatigue. On the other hand, certain activities seem to reinvigorate the brain in ways that support directed attention and self-regulation processes. And one of the most studied and effective of these — as you’ve probably heard — is spending time in nature.

“Getting out in nature seems to relax the brain’s frontal lobes and relieve this attention fatigue,” says Phil Stieg, MD, PhD, chairman of neurological surgery and neurosurgeon-in-chief at New York-Presbyterian/Weill Cornell Medical Center.

Exactly how nature does this is tricky. Stieg says that several overlapping mechanisms of benefit are likely at play.

But one that has garnered a lot of expert attention is termed “soft fascination.” The gist is that natural environments are just stimulating enough to gently engage the brain’s attention without unhelpfully concentrating it.

“[W]hat makes an environment restorative is the combination of attracting involuntary attention softly while at the same time limiting the need for directing attention,” wrote the authors of a 2010 study in Perspectives on Psychological Sciences. Nature, they added, seems to hit that sweet spot.

On the other hand, activities that grab and hold our attention too forcefully — books, social interactions, pretty much anything on a screen — entertaining through they may be, are unlikely to recharge our brain’s batteries. “Unlike soft fascination, hard fascination precludes thinking about anything else, thus making it less restorative,” the study authors added.

A lot of the work on soft fascination is folded into a psychological concept known as Attention Restoration Theory, or ART. While a lot of the ART research highlights time in nature as the optimal route to cognitive replenishment, it’s not the only route.

“If you’re on a cell phone for eight hours a day, your attention never gets a rest.”

Mindfulness also promotes attention restoration.

In many ways, it’s a kind of soft-fascination training. Mindfulness attempts to loosen the mind’s preoccupation with self-focused thoughts and judgments while also broadening awareness of your surroundings. This seems a lot like what spending time in nature does automatically, and there’s evidence that moving mindfulness training into natural outdoor settings may augment the practice’s benefits.

Stieg, the New York-Presbyterian/Weill Cornell neurosurgeon, recently discussed the benefits of nature on his podcast This Is Your Brain. He agrees that mindfulness may be a helpful alternative for those who don’t have access to nature (or the time to get lost in it). He also says that avoiding things that fatigue attention — loud noises, multitasking, technology — could reduce your need to escape to the outdoors.

“If you’re on a cell phone for eight hours a day, your attention never gets a rest,” he says. “I don’t think spending time in nature provides all the answers, but there’s good evidence that it support a longer, healthier, emotionally stable life.”

The bigger takeaway may be that your brain needs idle time to rest and recharge. Deprived of that time and the soft-fascination experiences that support it, your psychological and cognitive health may pay a price.

Markham Heid

By: Markham Heid

Source: How ‘Soft Fascination’ Helps Restore Your Tired Brain | by Markham Heid | Jun, 2021 | Elemental

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Hey, There’s a Second Brain In Your Gut

Scientists have known for years that there’s a “second brain” of autonomous neurons in your long, winding human digestive tract—but that’s about where their knowledge of the so-called abdominal brain ends.

Now, research published in 2020 shows that scientists have catalogued 12 different kinds of neurons in the enteric nervous system (ENS) of mice. This “fundamental knowledge” unlocks a huge number of paths to new experiments and findings.

The gut brain greatly affects on how you body works. Your digestive system has a daily job to do as part of your metabolism, but it’s also subject to fluctuations in functionality, and otherwise related to your emotions.

More: Getting the Inside Dope on Ketamine’s Mysterious Ability to Rapidly Relieve Depression

Digestive symptoms and anxiety can be comorbid, and your gut is heavily affected by stress. So scientists believe having a better understanding of what happens in your ENS could lead to better medicines and treatments for a variety of conditions, as well as improved knowledge of the connection between the ENS and central nervous system.

The research appears in Nature Neuroscience. In a related commentary, scientist Julia Ganz explains what the researchers found and why it’s so important:

“Using single-cell RNA-sequencing to profile the developing and juvenile ENS, the authors discovered a conceptually new model of neuronal diversification in the ENS and establish a new molecular taxonomy of enteric neurons based on a plethora of molecular markers.”

Neuronal diversification happens in, well, all the organisms that have neurons. Similar to stem cells, neurons develop first as more generic “blanks” and then into functional specialties. The human brain has types like sensory and motor neurons, each of which has subtypes. There are so many subtypes, in fact, that scientists aren’t sure how to even fully catalog them yet.

More: Here’s How Long Alcohol-Induced Brain Damage Persists After Drinking

Neurons of the same superficial type are different in the brain versus the brain stem—let alone in the digestive tract. So researchers had to start at the very beginning and trace how these neurons develop. They tracked RNA, which determines how DNA is expressed in the cells made by your body, to follow how neurons formed both before and after birth. Some specialties emerge in utero, and some split and form afterward.

To find this new information, the scientists developed a finer way to separate and identify cells. Ganz explains:

“Using extensive co-staining with established markers, they were able to relate the twelve neuron classes to previously discovered molecular characteristics of functional enteric neuron types, thus classifying the ENCs into excitatory and inhibitory motor neurons, interneurons, and intrinsic primary afferent neurons.”

With a sharper protocol and new information, the researchers were able to confirm and expand on the existing body of ENS neuron knowledge. And now they can work on finding out what each of the 12 ENS neuron types is responsible for, they say.

By isolating different kinds and “switching” them on or off using genetic information, scientists can try to identify what’s missing from the function of the mouse ENS. And studying these genes could lead to new treatments that use stem cells or RNA to control the expression of harmful genes.

The Mind-Gut Connection is something that people have intuitively known for a long time but science has only I would say in the last few years gotten a grasp and acceptance of this concept. It essentially means that your brain has intimate connections with the gut and another entity in our gut, the second brain, which is about 100 million nerve cells that are sandwiched in between the layers of the gut.

And they can do a lot of things on their own in terms of regulating our digestive processes. But there’s a very intimate conversation between that little brain, the second brain in the gut and our main brain. They use the same neurotransmitters. They’re connected by nerve pathways. And so we have really an integrated system from our brain to the little brain in the gut and it goes in both directions.

The little brain, or the second brain, in the gut you’re not able to see it because as I said it’s spread out through the entire length of the gut from your esophagus to the end of your large intestine, several layers of nerve cells interconnected. And what they do is even if you – and you can do this in animal experiments if you completely disconnect this little brain in the gut from your main brain this little brain can completely take care of all the digestive processes, the contractions, peristaltic reflex, regulation of blood flow in the intestine.

And it has many sensors so it knows exactly what’s going on inside the gut, what goes on in the wall of the gut, any distention, any chemicals. All of this is being picked up by these sensory nerves, fed into the interior nervous system, the second brain. And then the second brain generates these stereotypic responses. So when you vomit, when you have diarrhea, when you have normal digestion, all of this is encoded in programs in your second brain.

What the second brain can’t do it cannot generate any conscious perceptions or gut feelings. That really is the only ability that allows us to do this and perceive all the stuff that goes on inside of us is really the big brain and the specific areas and circuits within the brain that process information that comes up from the gut. Still most of that information is not really consciously perceived. So 95 percent of all this massive amount of information coming from the gut is processed, integrated with other inputs that the brain gets from the outside, from smell, visual stimuli.

And only a very small portion is then actually made conscious. So when you feel good after a meal or when you ate the wrong thing and you’re nauseated those are the few occasions where actually we realize and become aware of our gut feelings. Even though a lot of other stuff is going on in this brain-gut access all the time.

When we talk about the connection between depression and the gut there’s some very intriguing observations both clinically but also now more recently scientifically that make it highly plausible that there is an integrate connection between serotonin in the gut, serotonin in our food, depression and gut function.

By: Caroline Delbert

Caroline Delbert is a writer, book editor, researcher, and avid reader. She’s also an enthusiast of just about everything.

Source: Pocket

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Critics:

The enteric nervous system (ENS) or intrinsic nervous system is one of the main divisions of the autonomic nervous system (ANS) and consists of a mesh-like system of neurons that governs the function of the gastrointestinal tract. It is capable of acting independently of the sympathetic and parasympathetic nervous systems, although it may be influenced by them. The ENS is also called the second brain. It is derived from neural crest cells.

The enteric nervous system is capable of operating independently of the brain and spinal cord,but does rely on innervation from the autonomic nervous system via the vagus nerve and prevertebral ganglia in healthy subjects. However, studies have shown that the system is operable with a severed vagus nerve.

The neurons of the enteric nervous system control the motor functions of the system, in addition to the secretion of gastrointestinal enzymes. These neurons communicate through many neurotransmitters similar to the CNS, including acetylcholine, dopamine, and serotonin. The large presence of serotonin and dopamine in the gut are key areas of research for neurogastroenterologists.

Neurogastroenterology societies

See also

3 Simple Habits That Can Protect Your Brain From Cognitive Decline

You might think that the impact of aging on the brain is something you can’t do much about. After all, isn’t it an inevitability? To an extent, as we may not be able to rewind the clock and change our levels of higher education or intelligence (both factors that delay the onset of symptoms of aging).

But adopting specific lifestyle behaviors–whether you’re in your thirties or late forties–can have a tangible effect on how well you age. Even in your fifties and beyond, activities like learning a new language or musical instrument, taking part in aerobic exercise, and developing meaningful social relationships can do wonders for your brain. There’s no question that when we compromise on looking after ourselves, our aging minds pick up the tab.

The Aging Process and Cognitive Decline

Over time, there is a build-up of toxins such as tau proteins and beta-amyloid plaques in the brain that correlate to the aging process and associated cognitive decline. Although this is a natural part of growing older, many factors can exacerbate it. Stress, neurotoxins such as alcohol and lack of (quality and quantity) sleep can speed up the process.

Neuroplasticity–the function that allows the brain to change and develop in our lifetime–has three mechanisms: synaptic connection, myelination, and neurogenesis. The key to resilient aging is improving neurogenesis, the birth of new neurons. Neurogenesis happens far more in babies and children than adults.

A 2018 study by researchers at Columbia University shows that in adults, this type of neuroplastic activity occurs in the hippocampus, the part of the brain that lays down memories. This makes sense as we respond to and store new experiences every day, and cement them during sleep. The more we can experience new things, activities, people, places, and emotions, the more likely we are to encourage neurogenesis.

With all this in mind, we can come up with a three-point plan to encourage “resilient aging” by activating neurogenesis in the brain:

1. Get your heart rate up

Aerobic exercise such as running or brisk walking has a potentially massive impact on neurogenesis. A 2016 rat study found that endurance exercise was most effective in increasing neurogenesis. It wins out over HIIT sessions and resistance training, although doing a variety of exercise also has its benefits.

Aim to do aerobic exercise for 150 minutes per week, and choose the gym, the park, or natural landscape over busy roads to avoid compromising brain-derived neurotrophic factor production (BDNF), a growth factor that encourages neurogenesis that aerobic exercise can boost. However, exercising in polluted areas decreases production.

If exercising alone isn’t your thing, consider taking up a team sport or one with a social element like table tennis. Exposure to social interaction can also increase the neurogenesis, and in many instances, doing so lets you practice your hand-eye coordination, which research has suggested leads to structural changes in the brain that may relate to a range of cognitive benefit. This combination of coordination and socializing has been shown to increase brain thickness in the parts of the cortex related to social/emotional welfare, which is crucial as we age.

2. Change your eating patterns

Evidence shows that calorie restriction, intermittent fasting, and time-restricted eating encourage neurogenesis in humans. In rodent studies, intermittent fasting has been found to improve cognitive function and brain structure, and reduce symptoms of metabolic disorders such as diabetes.

Reducing refined sugar will help reduce oxidative damage to brain cells, too, and we know that increased oxidative damage has been linked with a higher risk of developing Alzheimer’s disease. Twenty-four hour water-only fasts have also been proven to increase longevity and encourage neurogenesis.

Try any of the following, after checking with your doctor:

  • 24-hour water-only fast once a month
  •  Reducing your calorie intake by 50%-60% on two non-consecutive days of the week for two to three months or on an ongoing basis
  • Reducing calories by 20% every day for two weeks. You can do this three to four times a year
  • Eating only between 8 a.m. to 8 p.m., or 12 p.m. to 8 p.m. as a general rule

3. Prioritize sleep

Sleep helps promote the brain’s neural “cleaning” glymphatic system, which flushes out the build-up of age-related toxins in the brain (the tau proteins and beta amyloid plaques mentioned above). When people are sleep-deprived, we see evidence of memory deficits, and if you miss a whole night of sleep, research proves that it impacts IQ. Aim for seven to nine hours, and nap if it suits you. Our need to sleep decreases as we age.

Of course, there are individual exceptions, but having consistent sleep times and making sure you’re getting sufficient quality and length of sleep supports brain resilience over time. So how do you know if you’re getting enough? If you naturally wake up at the same time on weekends that you have to during the week, you probably are.

If you need to lie-in or take long naps, you’re probably not. Try practicing mindfulness or yoga nidra before bed at night, a guided breath-based meditation that has been shown in studies to improve sleep quality. There are plenty of recordings online if you want to experience it.

Pick any of the above that work for you and build it up until it becomes a habit, then move onto the next one and so on. You might find that by the end of the year, you’ll feel even healthier, more energized, and motivated than you do now, even as you turn another year older.

By: Fast Company / Tara Swart

Dr. Tara Swart is a neuroscientist, leadership coach, author, and medical doctor. Follow her on Twitter at @TaraSwart.

Source: Open-Your-Mind-Change

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Critics:

Cognitive deficit is an inclusive term to describe any characteristic that acts as a barrier to the cognition process.

The term may describe

Mild cognitive impairment (MCI) is a neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual’s age and education but which are not significant enough to interfere with instrumental activities of daily living. MCI may occur as a transitional stage between normal aging and dementia, especially Alzheimer’s disease. It includes both memory and non-memory impairments.Mild cognitive impairment has been relisted as mild neurocognitive disorder in DSM-5, and in ICD-11.

The cause of the disorder remains unclear, as well as its prevention and treatment. MCI can present with a variety of symptoms, but is divided generally into two types.

Amnestic MCI (aMCI) is mild cognitive impairment with memory loss as the predominant symptom; aMCI is frequently seen as a prodromal stage of Alzheimer’s disease. Studies suggest that these individuals tend to progress to probable Alzheimer’s disease at a rate of approximately 10% to 15% per year.[needs update]It is possible that being diagnosed with cognitive decline may serve as an indicator of aMCI.

Nonamnestic MCI (naMCI) is mild cognitive impairment in which impairments in domains other than memory (for example, language, visuospatial, executive) are more prominent. It may be further divided as nonamnestic single- or multiple-domain MCI, and these individuals are believed to be more likely to convert to other dementias (for example, dementia with Lewy bodies).

See also

Why We Procrastinate & How To Stop It

There are days when procrastination comes for us all. You wake up, thinking about a project at work or the life admin you can no longer put off and feel a swell of dread fill your chest. You know you have to deal with it today but you start puttering around and somehow end up deep-cleaning the bin instead of replying to emails or watching sitcom bloopers rather than putting on your running shoes. The putting off of tasks is time-wasting and mindless but sometimes it feels inevitable.

The word ‘procrastination’ has deep historical roots. It derives from the Latin ‘procrastinare’ – meaning ‘to put off until tomorrow’ – but is also derived from the ancient Greek word ‘akrasia’, which means ‘acting against one’s better judgement’. The etymology says that when we procrastinate, we are well aware of what we are doing, which implies that the negative consequences of this delay rest solely on our shoulders. And yet…we do it anyway.

Why procrastination happens – and why it can feel like an inevitable part of our day – is a question that has plagued people for centuries. It’s generally assumed that this behaviour is down to a failure to self-regulate in some way: that a combination of poor time management, laziness and a lack of self-control leads us to procrastinate. In other words, it is because an individual isn’t trying hard enough. This is not just a cultural assumption but one explored by many researchers and institutions too, with studies such as this one from the University of Valencia which found that no matter how long students are given to do their work, procrastination will likely occur.

However there is a growing number of researchers countering this view. Dr Tim Pychyl is the author of popular self-help book The Procrastinator’s Digest: A Concise Guide to Solving the Procrastination Puzzle and the writer behind the Psychology Today column Don’t Delay. He believes that procrastination runs far deeper – that it is influenced by biology, our perception of time and our ability to manage our emotions.

On the biological front, procrastination comes down to ongoing tension in our brains between the limbic system and the prefrontal cortex, according to the neurosurgery department at the University of Pittsburgh Medical Center.The limbic system is a major primordial brain network and one of the oldest and most dominant parts of the brain. It supports a variety of functions, including emotions – particularly those which evolved early and play an important role in survival. This includes feelings of motivation and reward, learning, memory, the fight-or-flight response, hunger, thirst and production of hormones that help regulate the autonomic nervous system.

On the other hand, your prefrontal cortex is linked to planning complex cognitive behaviour, personality expression, decision-making and moderating social behaviour. This is where decisions, forward-planning and the rationalising of the impulsive, stimulus-based behaviour of the limbic system is centred. As the prefrontal cortex is the newer, less developed (and therefore somewhat weaker) portion of the brain, the instinctual limbic response will often win over rationalising.

This all feeds into the psychology at the heart of procrastination: what makes us feel good now (such as avoiding or delaying tasks) has a stronger hold over us than what makes us feel good in the long run. As Dr Pychyl told The New York Times: “Procrastination is an emotion regulation problem, not a time management problem.”

This is an example of ‘present bias‘, the NYT article goes on to explain: our tendency to prioritise short-term wants and needs over long-term ones, even if the short-term reward is far smaller. This feeds into a larger disconnect between the present and future self and our perception of time. We struggle to connect to our future self (aka the one who would benefit from us taking the bins out in a timely fashion) or see them as ‘us’ when the ‘us’ of today has far more immediate and pressing concerns.

At its core, procrastination is thought by Pychyl and his collaborator Dr Fuschia Sirois to be linked to an inability to regulate our emotions, which can be seen in how we prioritise short-term relief over long-term satisfaction. Putting off a task makes you feel good in the short term because it provides relief from largely negative emotions: stress, panic, disgust, anxiety, self-doubt and so on. The long-term consequences have little bearing on how good it can feel to be distracted or absorbed in something that has nothing to do with the big assignment that is making you panic. However, as all procrastinators can attest, that relief is short-lived, leading to the cycle repeating itself.

So what can you do if you’re prone to procrastination? As with anything, especially actions that regulate your emotions, you can’t just stop and expect that to work. Without learning how to regulate your emotions in other, less destructive ways, the temptation to procrastinate will once again rear its head.

Recognising that procrastination is not an act of laziness but a tool for emotional regulation can be hugely helpful, says Pychyl. It is a step towards forgiving ourselves and having self-compassion for procrastinating, both of which have been found to help procrastinators: in a 2010 study, researchers found that students who forgave themselves for procrastinating on studying for an exam were able to procrastinate less for subsequent exams. Another study, from 2012, looked at the links between procrastination, stress and self-compassion. It found that lower levels of self-compassion (aka treating ourselves with kindness and understanding when we make mistakes) may explain some of the stress that procrastinators experience. You can start to harness self-compassion by following guided meditations such as these by the founder of the Center for Mindful Self-Compassion, Dr Kristin Neff, or simply by committing to meeting challenges with kindness and understanding.

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Seeing procrastination this way can also help with the impulse towards waiting until you feel ‘ready’ to perform a certain task, as Pychyl told The Washington Post. Once we can see how our emotions have shaped how we respond to a task, it makes it easier not to let how we feel dictate whether or not we can get started. You do not need to be in the right frame of mind to start working or cleaning or studying. Instead of focusing on feelings, Pychyl recommended breaking down a task into small, component parts which can actually be accomplished. It could be as simple as writing the first sentence, dusting one surface or closing all the distracting links you have open.

Procrastination is part of life. Its impact can range from mildly irritating to life-changing but the main thing to remember is that it can’t be countered by self-flagellation. By finding ways to forgive yourself in the moment and be kind to your future self, you can slowly chip away at the habit.

By: Sadhbh O’Sullivan

Source: Why We Procrastinate & How To Stop It

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References

Scientists Find an Odd Link Between Aspirin, Air Pollution, and Male Brains

If you look at the smudged skylines of Los Angeles, California or Beijing, China, the haziness creates the illusion of cities shrouded in perpetual gray. That smog is driven by a pollutant that doesn’t just ruin the view — it worms its way into the brain, influencing the health of people exposed.

In a new study, scientists find another reason why air pollution is bad for the brain — this time zeroing in on the effect it has on men’s brain health. The study examines the negative effect of fine particulate matter, also known as PM 2.5 pollution. You might know it as black carbon or “soot.”

“Our study is the first one that demonstrates that exposure to PM2.5, even just over a few weeks, can impair cognitive performance,” lead author Xu Gao tells Inverse. Gao is an assistant professor at Peking University and a researcher affiliated with Columbia University.

What’s new — Scientists are increasingly unearthing new information about how the tainted air we breathe harms our bodies, whether it’s worsening the severity of Covid-19 or reducing men’s sperm count.

Gao and colleagues found air pollution is associated with considerable negative short-term effects on cognitive health in a sample of older white men. This finding was published Monday in the journal Nature Aging.

The study suggests PM 2.5 levels not usually considered hazardous can still cause individuals to suffer from cognitive decline due to short-term air pollution. This implies “there is no safe zone for PM 2.5,” Gao says.

Interestingly, the researchers found that men who take what’s known as non-steroidal anti-inflammatory drugs (NSAIDS) did not suffer as many harmful effects from PM 2.5 pollution. These anti-inflammatory medications include pills like aspirin.

This finding emerged although NSAIDs don’t have any known relationship to cognitive performance. The researchers suspect NSAIDs have a “modifying effect” on the inflammatory responses prompted by inhaling polluted air.

These findings are preliminary — Gao says it’s too early to endorse taking NSAIDs as a way to protect oneself from air pollution. However, he does venture to say people on these medications “may have additional benefits.”

Air pollution is associated with an ever-growing laundry list of health risks, including:

PM 2.5 pollution is especially harmful. These tiny air particles are 2.5 microns or less in size — for comparison, human hair is roughly 70 microns in diameter. This category of pollution is why you see gray horizons in cities like Los Angeles — it’s associated with smog and poor air quality. It’s arguably the greatest environmental risk factor for human mortality.

But there is some good news amidst all this doom and gloom. Some recent studies, for example, suggest exercise can offset some of the harmful effects of air pollution — even in urban areas.

Air pollution deaths have also declined by half between 1990 and 2010, correlating with improved federal regulations on air quality. But it can still do considerable short-term and long-term damage to the human mind, according to this latest Nature Aging study.

How they did it — The scientists analyzed data from 954 men in the Boston area between 1995 and 2021. The average age of a man in the study data was 69-years-old. None had chronic health conditions, but 64 percent were former smokers.

The participants were also questioned about their use of NSAIDs, including aspirin. They also took cognitive tests, including tests on their ability to remember words and repeat numbers, as well as screening exercises used to test for dementia.The researchers also analyzed this data in conjunction with information on weather patterns in the Boston area, since air pollution varies by season and is greater in the winter.

Finally, they obtained data on air pollution from a Harvard University supersite, which they used as a baseline to measure air pollution in the Greater Boston areas.

Using this information, the researchers were able to paint a picture of cognitive health that correlates with short-term air pollution and also study any potential effects of NSAIDs on cognitive performance.

Why it matters — Media and policymakers have focused, rightly so, on the number of deaths resulting from air pollution each year, which now number 200,000 annually in the U.S — and that’s just from the air that meets EPA standards.

Much less attention has been paid to air pollution’s impacts on short-term and long-term cognitive performance. The research that has been done has found air pollution can impair the cognitive performance of children, and influence cognitive decline in older adults.

Although this new study focuses on short-term effects, the researchers also conducted a sensitivity analysis to include the effects of long-term exposure to air pollution. And while preliminary, the findings don’t bode well for the human mind’s ability to withstand air pollution in the long run.

“We found that both short and long exposures were related to cognitive function,” Gao says. But the study has limitations — The study team acknowledges that their work is just a starting point. Much more research needs to be done to expand on their intriguing findings — and go beyond the scope of the study’s design.

For example, the study only focuses on older white men, “which suggests the possibility that the results might not be generalizable to other ethnic groups and/or women” the team writes. Gao would like to conduct further research involving people of different ages, races, and genders to confirm whether similar effects would occur among various demographics.

“We believe that younger people may have a better adaptive response to air pollution than the elderly. Females are also different from males with respect to health outcomes,” Gao says.

Meanwhile, scientists have long known that communities of color suffer disproportionately from air pollution. A recent Science study found Black and Hispanic individuals experience particularly high levels of PM 2.5 pollution — the subject of this study.

The researchers also analyzed this data in conjunction with information on weather patterns in the Boston area, since air pollution varies by season and is greater in the winter.

But the study has limitations — The study team acknowledges that their work is just a starting point. Much more research needs to be done to expand on their intriguing findings — and go beyond the scope of the study’s design.

What’s next — Ultimately, what’s needed is more information on both the long-term impacts of air pollution on cognitive health and the relationship between NSAIDs and air pollution. This research could be used to inform future policy, both in the U.S. and abroad.

And while Gao suggests NSAIDs could be helpful in treating the cognitive effects of air pollution, it is not a replacement for policies that reduce the actual source of pollution. Recent efforts by the Biden administration to move toward electric vehicles, as well as California’s stricter vehicle emissions standards, could help shift the tide against air pollution.

“Although our study shows that taking NSAIDs may be a solution to air pollution’s harm, [it’s] definitely not the final answer to the threats of air pollution. Changing our policies of air pollution towards a more restrictive manner is still warranted,” Gao says.

But it’s data that drives policy forward — evidence that pollution isn’t just a topic on our minds, it literally influences the brain.

By: Tara Yarlagadda

Source: Scientists find an odd link between aspirin, air pollution, and male brains

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More Contents:

Dementia and sleep deprivation linked in recent study – The Washington Post

Sleep deprivation has been linked to hypertension, obesity and diabetes and has long been suspected of having a connection to dementia. Now, a large new study has more clearly established that association by concluding that people who sleep less than six hours a night in midlife have a greater risk of developing late-onset dementia.

That doesn’t mean middle-aged short sleepers should panic, according to experts. Although the study is an important step forward, much about the connection between sleep and dementia remains unknown, they said. Still, it can’t hurt to work on your sleep habits while research continues, and you’ll find some strategies listed below.

In the study, European researchers followed nearly 8,000 people in Britain for 25 years, starting when subjects were 50. They found that those who consistently got six hours of sleep or less per night in their 50s and 60s were about 30 percent more likely to develop dementia later in life, compared to those who logged seven hours of sleep per night. That was independent of “sociodemographic, behavioural, cardiometabolic, and mental health factors,” the study authors wrote. Findings were published in the journal Nature Communications in late April.

“This is just another example of the importance of appropriate sleep for brain health,” said Michael V. Vitiello, a professor of psychiatry and behavioral sciences at the University of Washington at Seattle and member of the SleepFoundation.org medical advisory board, who wasn’t involved in the study. “It’s really important for people to be conscious of making sure that they sleep well. It’s not trivial, and it shouldn’t be the last thing you think about. It shouldn’t be the thing you sacrifice.”

Lack of sleep might increase dementia risk by impairing learning and memory development, said study author Andrew Sommerlad, an old-age psychiatrist at University College London, or it could affect the brain’s ability to clear harmful protein waste products.

Researchers have spent years trying to understand the sleep-dementia connection, a quest that becomes more urgent as the number of people with Alzheimer’s disease balloons. More than 6 million Americans are living with the disease, according to the Alzheimer’s Association, and by 2050, that number is expected to reach nearly 13 million. Yet, it’s a difficult area in which to draw conclusions.

Earlier this year, Charles Czeisler, chief of the sleep and circadian disorders division at Brigham and Women’s Hospital in Boston, co-authored a similar study that found that adults age 65 and older who got five hours or less of sleep per night had double the risk of dementia than those who clocked seven or eight hours per night. Results were published in the journal Aging.

“At this point, it’s too early to say that behavior X leads to Y,” Czeisler said. “But the association certainly reveals the importance of continuing to study the relationship.”

One of the challenges to studying the link between sleep and cognitive decline is that it’s difficult to determine what happens first: Is too little sleep a symptom of the brain changes that often begin decades before cognitive problems appear? Or does it cause those changes? So far, that’s still unclear, said Claire Sexton, director of scientific programs and outreach with the Alzheimer’s Association.

“There’s mounting evidence pointing toward the relationship between sleep and dementia,” she said. “But there are a lot of unanswered questions. There’s no one factor that would guarantee someone will develop dementia, and there’s no one factor that will guarantee someone won’t.”

Vitiello lauded the new study’s lengthy follow-up period and examination of people in their 50s (most similar research focuses on those 65 and older). But he emphasized that the findings estimate increased risk for the entire population, not for any one individual. “These are predictions,” he said. “On average, if you have this kind of disturbed sleep, your odds go up this percentage. It doesn’t mean that just because you’re a 55-year-old sleeping under six hours a night, you’re guaranteed to have an increased Alzheimer’s risk of 30 percent.”

Exactly why someone is a short sleeper — for example, if they have insomnia, hold multiple jobs that require odd hours or naturally need less sleep — likely plays a role in their unique risk, he added. The study didn’t account for those factors.

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Source: Dementia and sleep deprivation linked in recent study – The Washington Post

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More Contents:

Which fruits and vegetables don’t count toward your ‘5 a day’? New study has answers.

Morning or night? With food or without? Answers to your questions about taking supplements

What Happens To The Brain When We Experience Nostalgia

The term “nostalgia” was coined by Swiss physician Johannes Hofer derived from two Greek words, “nostos” and “algos” — meaning “suffering” and “origins”.

Nostalgia, unlike screen memory, does not relate to a specific memory, but rather to an emotional state. This idealized emotional state is framed within a past era, and the yearning for the idealized emotional state manifests as an attempt to recreate that past era by reproducing activities performed then and by using symbolic representations of the past.

Memory is really a sort of networking and synthesis and abstraction of all these experiences of our life. It’s what makes us humanly unique. It’s our autobiography. So nostalgia is a sense of being able to contact and read the book again.

According to Joseph Ledoux (an eminent neuroscientist working on emotions, fear and anxiety) nostalgia has something to do with how memory and emotions are stored in the brain.

Concept of Flashbulb memory:

But when a memory is stored at a time of emotional arousal, the imprint is more powerful, possibly due to the neurotransmitters, that the brain secretes in that moment. As per LeDoux’s conjecture, the process of forming the mental imprint of an event may be closely linked to what is known as “flashbulb memory.

In 2007, NYU psychologist Elizabeth Phelps identified the brain circuitry involved in the creation of flashbulb memories. Her team took scans of people’s brains as they recalled the events of September 11, 2001, and saw that the amygdala, the brain’s emotional center, was lit up. Her work uncovered that the closer one was to the event, the stronger the recollection and the easier it was to retrieve.

To stockpile information into our brain, we rely on a critical structure called the hippocampus. Without it, we would be blank slates with no past. This C-shaped region of the brain is highly connected to the emotional region of the brain, the amygdala.

During an experience these two structures work together and combine information from the different senses. Consequently, an experience becomes intertwined with feelings.

So when a strongly emotional event, say, like our fifth birthday party, occurs, the amygdala is helping us perceive that emotional content and our hippocampus is processing the events that occurred—the cake, the presents and all these specific details of things that compose that birthday night. We probably don’t remember much details anymore but are just nostalgic about what a terrific time we had.

Neuroimaging Studies:

fMRI studies have examined the neural substrates of listening to music that
evokes emotions such as tenderness, peacefulness and nostalgia, showing that experiencing these high valence/low arousal emotions activates various brain regions, including:

  1. Hippocampus (HPC)
  2. Parahippocampus
  3. Ventral striatum (VS)
  4. Ventromedial prefrontal cortex (VMPFC)
  5. Subgenual/rostral anterior cingulate cortex
  6. Somatosensory cortex
  7. Medial motor cortex
  8. Precuneus
  9. Medial orbitofrontal cortex

The music that many of us loved as a teenager means more to us than ever—but with each passing year, the new songs on the chartlist sound like noisy nonsense.

So, why do the songs that we heard when we were teenagers sound sweeter than anything we listen to as an adult?

This is because these songs hold disproportionate power over our emotions.

Memories are meaningless without emotion—and aside from love and drugs, nothing spurs an emotional reaction like music. Brain imaging studies show that our favorite songs stimulate the brain’s pleasure circuit (Nucleus Accumbens, Ventral Tegmental Area etc), which releases an influx of dopamine, serotonin, oxytocin, and other neurochemicals that make us feel good. The more we like a song, the more we get treated to neurochemical bliss, flooding our brains with some of the same neurotransmitters that cocaine chases after.

Olfactory Nostalgia:

The smell of chlorine wafts through the air. Suddenly, we recall childhood summers spent in a swimming pool. Or maybe it’s a whiff of apple pie, or the scent of the same perfume our mom used to wear. Our noses have a way of sniffing out nostalgia.

After a smell enters the nose, it travels through the cranial nerve through the olfactory bulb, which helps the brain process smells. The olfactory bulb is part of the limbic system, the emotional center of the brain. As a member of the limbic system, the olfactory bulb can easily access the amygdala, which plays a role in emotional memories. Olfactory bulb has a strong input into the amygdala, which process emotions. The kind of memories that it evokes are good and they are more powerful. This close relationship between the olfactory bulb and the amygdala is one of the reason odors cause a spark of nostalgia.

References:

  1. Social Cognitive and Affective Neuroscience Advance Access published June 8, 2015
  2. How the brain stores sad, glad and bittersweet recollections December 25, 2014 by Luba Ostashevsky
  3. Neuron 84, 1–10, November 19, 2014 ª2014 Elsevier Inc
  4. Smells like nostalgia: Why do scents bring back memories? by Meghan Holohan

3K viewsView 9 UpvotersRelated QuestionsMore Answers BelowWhat combination of chemicals are released in the brain when one feels nostalgic? Why do I feel nostalgic weeks before something bad happens? How exactly does the feeling of nostalgia work? How long does it take for something to trigger that specific feeling in our brain? Why do I feel nostalgic about my childhood even if I am just 14? I’m 17 yet feel nostalgia for when I was 15 and 16; is getting nostalgic this young and for such recent times normal, and what can I do about it?

Ambrose Husser, 10 years US Army. 6 years u.s. lifeguard. Amateur biologist in physicist Answered April 30, 2019 · Author has 55 answers and 7.8K answer views

We define ourselves in large part with our past experiences. So when we look at our past we look at what makes us who we are. The future often brings fourth a feeling of fear and apprehension.

You must always be careful to never dwell on the past.This will lead to depression and never fixate on the future or you will live in stress fear and apprehension.

What combination of chemicals are released in the brain when one feels nostalgic? Why do I feel nostalgic weeks before something bad happens? How exactly does the feeling of nostalgia work? How long does it take for something to trigger that specific feeling in our brain? Why do I feel nostalgic about my childhood even if I am just 14? I’m 17 yet feel nostalgia for when I was 15 and 16; is getting nostalgic this young and for such recent times normal, and what can I do about it? Why do we feel nostalgic? How can one fight nostalgia? Why do I constantly feel nostalgic? I feel like I’m wasting my life and it’s nearly over, but I’m 13. Do people like to feel nostalgic? What made you feel nostalgic recently? Why do I love the feeling of nostalgia? What do 1144 and 818 mean in a twin flame journey? What happens (scientifically) when you get heartbroken? What happens in the human brain after crying? Is it common for people to feel intense nostalgia through smell?

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Johnny Harris

What happens to the brain when it recalls good times. The first 1000 people to use the link will get a free trial of Skillshare Premium Membership: https://skl.sh/johnnyharris13 Check out Nathaniel Drew’s Video on Nostalgia: https://youtu.be/hHE1cJF3OZs I launched a Patreon. If you want to support my videos, head here: https://www.patreon.com/johnnyharris For anyone who likes smarter travel, Iz and I started a company: https://brighttrip.com/?ref=5 Subscribe to my channel: https://goo.gl/1U8Zy7 My Instagram: https://www.instagram.com/johnny.harris/ Facebook: https://www.facebook.com/JohnnyHarris Tom Fox made the music for this video: https://tfbeats.com/ I also get music from Artlist: https://bit.ly/2XfAE6C And Music Bed http://share.mscbd.fm/johnnywharris Iz’s Channel: https://www.youtube.com/iz-harris We sell our drone prints: https://backdropstock.com/collections… And we send an email once a month with a Spotify playlist. Sign up if that sounds cool: https://www.izharris.com/newsletter Gear I use: https://www.izharris.com/gear-guide Camera: https://geni.us/xK9Al Favorite Lens: https://geni.us/VrAWNG Second Favorite Lens: https://geni.us/Hcgdrb Travel Tripod: https://geni.us/Sf0bA Drone: http://geni.us/glWJhq Johnny Harris is a filmmaker and journalist. He currently is based in Washington, DC, reporting on interesting trends and stories domestically and around the globe. Johnny’s visual style blends motion graphics with cinematic videography to create content that explains complex issues in relatable ways. He holds a BA in international relations from Brigham Young University and an MA in international peace and conflict resolution from American University. Vox: https://www.vox.com/authors/johnny-ha… Spotlight: http://byupoliticalscienceblog.com/20… XYNTEO Interview: https://xynteo.com/insights/latest/po… Bonnier Talk: https://vimeo.com/232416596 Neiman Lab: https://tinyurl.com/ybjbvb7h Emmy Nomination: https://tinyurl.com/y9gjgel2 Storytelling Tips: http://chase.be/blog/5-storytelling-t… Craig Adams Podcast: https://open.spotify.com/episode/4cS0… So Money Podcast: https://tinyurl.com/ycjbl4p5

Stress Changes The Brain, And This Could Be How It Happens

The results of a new brain imaging study may have just answered a big question about how stress changes the brain. Using a combination of genetic editing and brain scanning in mice, researchers found that stress triggers a chemical cascade that radically changes how brain networks communicate, and the results could sharpen our understanding of anxiety disorders in humans.

Breaking down the research

Stress serves an important purpose in preparing us to react to danger. Anything the brain perceives as threatening triggers multiple brain networks to synchronize and communicate, all in just a fraction of a second. With systems humming, we make immediate decisions to survive the threat.

But what facilitates all of those brain networks to connect and communicate? That’s been a difficult question to answer in the human brain, because doing so would require examining brain function during the split-second window of facing a threat.

Enter our friends the mice to help solve the problem. Researchers followed a trail of previous studies and zeroed in on the neurotransmitter noradrenaline (aka norepinephrine, a chemical that floods the brain during stress) as a likely facilitator of brain-network connectivity.

The twist was that they had genetically manipulated the rodents’ brains to allow for selectively controlling when noradrenaline was released (not possible in human brains). While controlling the chemical faucet, they also scanned the mouse brains using fMRI to see what would happen.

And what happened, it turns out, was pretty amazing. The release of noradrenaline “rewired” the mouse brains, allowing different brain networks to instantly cross-communicate. But the neurotransmitter wasn’t just facilitating communication, it was restructuring neural connections beyond anyone’s expectations.

“I couldn’t believe that we were seeing such strong effects,” said the study’s first author Valerio Zerbi, a brain imaging specialist from the University of Zurich.

The researchers found the strongest rewired effects in brain areas responsible for processing sensory stimuli (auditory and visual, for example), and in the amygdala, the epicenter of the brain’s threat response system.

What does this mean for us?

It’s the part about threat response that may hold the most promise for better understanding what stress does to our brains.

Allowing for the fact that this was research in mice, the particular dynamic studied here is probably quite similar between us and our rodent counterparts. If noradrenaline rewires the human brain as it appears to rewire the brains of mice, it’s possible the long-term effects of stress are more profound than we’ve realized.

Previous research has linked the flood of noradrenaline to changes in brain connectivity, but it seems likely we’ve underestimated the effects, especially in the small but powerful part of our brain sitting at the center of anxiety disorders: the amygdala.

At a minimum, this research opens new doors for better understanding how both acute and chronic stress effects the brain, and could enlighten new ways of deconstructing anxiety conditions, now the most prevalent mental health disorders worldwide. The study was published in the journal Neuron.

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David DiSalvo is the author of the best-selling book “What Makes Your Brain Happy and Why You Should Do the Opposite”, which has been published in 15 languages, and the books “Brain Changer: How Harnessing Your Brain’s Power to Adapt Can Change Your Life” and “The Brain in Your Kitchen”. His work has appeared in Scientific American Mind, Forbes, Time, Psychology Today, The Wall Street Journal, Slate, Esquire, Mental Floss and other publications, and he’s the writer behind the widely read science and technology blogs “Neuropsyched” at Forbes and “Neuronarrative” at Psychology Today. He can be found on Twitter @neuronarrative and at his website, daviddisalvo.org. Contact him at: disalvowrites [at] gmail.com.

Source: Stress Changes The Brain, And This Could Be How It Happens