What Happens To Our Brains When We Get Depressed

In the ’90s, when he was a doctoral student at the University of Lausanne, in Switzerland, neuroscientist Sean Hill spent five years studying how cat brains respond to noise. At the time, researchers knew that two regions—the cerebral cortex, which is the outer layer of the brain, and the thalamus, a nut-like structure near the centre—did most of the work. But, when an auditory signal entered the brain through the ear, what happened, specifically?

Which parts of the cortex and thalamus did the signal travel to? And in what order? The answers to such questions could help doctors treat hearing loss in humans. So, to learn more, Hill, along with his supervisor and a group of lab techs, anaesthetized cats and inserted electrodes into their brains to monitor what happened when the animals were exposed to sounds, which were piped into their ears via miniature headphones. Hill’s probe then captured the brain signals the noises generated.

The last step was to euthanize the cats and dissect their brains, which was the only way for Hill to verify where he’d put his probes. It was not a part of the study he enjoyed. He’d grown up on a family farm in Maine and had developed a reverence for all sentient life. As an undergraduate student in New Hampshire, he’d experimented on pond snails, but only after ensuring that each was properly anaesthetized. “I particularly loved cats,” he says, “but I also deeply believed in the need for animal data.” (For obvious reasons, neuroscientists cannot euthanize and dissect human subjects.)

Over time, Hill came to wonder if his data was being put to the best possible use. In his cat experiments, he generated reels of magnetic tape—printouts that resembled player piano scrolls. Once he had finished analyzing the tapes, he would pack them up and store them in a basement. “It was just so tangible,” he says. “You’d see all these data coming from the animals, but then what would happen with it? There were boxes and boxes that, in all likelihood, would never be looked at again.” Most researchers wouldn’t even know where to find them.

Hill was coming up against two interrelated problems in neuroscience: data scarcity and data wastage. Over the past five decades, brain research has advanced rapidly—we’ve developed treatments for Parkinson’s and epilepsy and have figured out, if only in the roughest terms, which parts of the brain produce arousal, anger, sadness, and pain—but we’re still at the beginning of the journey.

Scientists are still some way, for instance, from knowing the size and shape of each type of neuron (i.e., brain cell), the RNA sequences that govern their behavior, or the strength and frequency of the electrical signals that pass between them. The human brain has 86 billion neurons. That’s a lot of data to collect and record.

But, while brain data is a precious resource, scientists tend to lock it away, like secretive art collectors. Labs the world over are conducting brain experiments using increasingly sophisticated technology, from hulking magnetic-imaging devices to microscopic probes. These experiments generate results, which then get published in journals. Once each new data set has served this limited purpose, it goes . . . somewhere, typically onto a secure hard drive only a few people can access.

Hill’s graduate work in Lausanne was at times demoralizing. He reasoned that, for his research to be worth the costs to both the lab that conducted it and the cats who were its subjects, the resulting data—perhaps even all brain data—should live in the public domain. But scientists generally prefer not to share. Data, after all, is a kind of currency: it helps generate findings, which lead to jobs, money, and professional recognition. Researchers are loath to simply give away a commodity they worked hard to acquire. “There’s an old joke,” says Hill, “that neuroscientists would rather share toothbrushes than data.”

He believes that, if they don’t get over this aversion—and if they continue to stash data in basements and on encrypted hard drives—many profound questions about the brain will remain unanswered. This is not just a matter of academic curiosity: if we improve our understanding of the brain, we could develop treatments that have long eluded us for major mental illnesses.

In 2019, Hill became director of Toronto’s Krembil Centre for Neuroinformatics (KCNI), an organization working at the intersection of neuroscience, information management, brain modelling, and psychiatry. The basic premise of neuroinformatics is this: the brain is big, and if humans are going to have a shot at understanding it, brain science must become big too. The KCNI’s goal is to aggregate brain data and use it to build computerized models that, over time, become ever more complex—all to aid them in understanding the intricacy of a real brain.

There are about thirty labs worldwide explicitly dedicated to such work, and they’re governed by a central regulatory body, the International Neuroinformatics Coordinating Facility, in Sweden. But the KCNI stands out because it’s embedded in a medical institution: the Centre for Addiction and Mental Health (CAMH), Canada’s largest psychiatric hospital. While many other neuroinformatics labs study genetics or cognitive processing, the KCNI seeks to demystify conditions like schizophrenia, anxiety, and dementia. Its first area of focus is depression.

Fundamentally, we don’t have a biological understanding of depression.

The disease affects more than 260 million people around the world, but we barely understand it. We know that the balance between the prefrontal cortex (at the front of the brain) and the anterior cingulate cortex (tucked just behind it) plays some role in regulating mood, as does the chemical serotonin. But what actually causes depression? Is there a tiny but important area of the brain that researchers should focus on?

And does there even exist a singular disorder called depression, or is the label a catch-all denoting a bunch of distinct disorders with similar symptoms but different brain mechanisms? “Fundamentally,” says Hill, “we don’t have a biological understanding of depression or any other mental illness.”

The problem, for Hill, requires an ambitious, participatory approach. If neuroscientists are to someday understand the biological mechanisms behind mental illness—that is, if they are to figure out what literally happens in the brain when a person is depressed, manic, or delusional—they will need to pool their resources. “There’s not going to be a single person who figures it all out,” he says. “There’s never going to be an Einstein who solves a set of equations and shouts, ‘I’ve got it!’ The brain is not that kind of beast.”

The KCNI lab has the feeling of a tech firm. It’s an open-concept space with temporary workstations in lieu of offices, and its glassed-in meeting rooms have inspirational names, like “Tranquility” and “Perception.” The KCNI is a “dry centre”: it works with information and software rather than with biological tissue.

To obtain data, researchers forge relationships with other scientists and try to convince them to share what they’ve got. The interior design choices are a tactical part of this effort. “The space has to look nice,” says Dan Felsky, a researcher at the centre. “Colleagues from elsewhere must want to come in and collaborate with us.”

Yet it’s hard to forget about the larger surroundings. During one interview in the “Clarity” room, Hill and I heard a code-blue alarm, broadcast across CAMH, to indicate a medical emergency elsewhere in the hospital. Hill’s job doesn’t involve front line care, so he doesn’t personally work with patients, but these disruptions reinforce his sense of urgency. “I come from a discipline where scientists focus on theoretical subjects,” he says. “It’s important to be reminded that people are suffering and we have a responsibility to help them.”

Today, the science of mental illness is based primarily on the study of symptoms. Patients receive a diagnosis when they report or exhibit maladaptive behaviours—despair, anxiety, disordered thinking—associated with a given condition. If a significant number of patients respond positively to a treatment, that treatment is deemed effective. But such data reveals nothing about what physically goes on within the brain.

“When it comes to the various diseases of the brain,” says Helena Ledmyr, co-director of the International Neuroinformatics Coordinating Facility, “we know astonishingly little.” Shreejoy Tripathy, a KCNI researcher, gives modern civilization a bit more credit: “The ancient Egyptians would remove the brain when embalming people because they thought it was useless. In theory, we’ve learned a few things since then. In relation to how much we have left to learn, though, we’re not that much further along.”

Joe Herbert, a Cambridge University neuroscientist, offers a revealing comparison between the way mental versus physical maladies are diagnosed. If, in the nineteenth century, you walked into a doctor’s office complaining of shortness of breath, the doctor would likely diagnose you with dyspnea, a word that basically means . . . shortness of breath.

Today, of course, the doctor wouldn’t stop there: they would take a blood sample to see if you were anemic, do an X-ray to search for a collapsed lung, or subject you to an echocardiogram to spot signs of heart disease. Instead of applying a Greek label to your symptoms, they’d run tests to figure out what was causing them.

Herbert argues that the way we currently diagnose depression is similar to how we once diagnosed shortness of breath. The term depression is likely as useful now as dyspnea was 150 years ago: it probably denotes a range of wildly different maladies that just happen to have similar effects. “Psychiatrists recognize two types of depression—or three, if you count bipolar—but that’s simply on the basis of symptoms,” says Herbert. “Our history of medicine tells us that defining a disease by its symptoms is highly simplistic and inaccurate.”

The advantage of working with models, as the KCNI researchers do, is that scientists can experiment in ways not possible with human subjects. They can shut off parts of the model brain or alter the electrical circuitry. The disadvantage is that models are not brains. A model is, ultimately, a kind of hypothesis—an illustration, analogy, or computer simulation that attempts to explain or replicate how a certain brain process works.

Over the centuries, researchers have created brain models based on pianos, telephones, and computers. Each has some validity—the brain has multiple components working in concert, like the keys of a piano; it has different nodes that communicate with one another, like a telephone network; and it encodes and stores information, like a computer—but none perfectly describes how a real brain works. Models may be useful abstractions, but they are abstractions nevertheless.

Yet, because the brain is vast and mysterious and hidden beneath the skull, we have no choice but to model it if we are to study it. Debates over how best to model it, and whether such modelling should be done at the micro or macro scale, are hotly contested in neuroscience. But Hill has spent most of his life preparing to answer these questions.

Hill grew up in the ’70s and ’80s, in an environment entirely unlike the one in which he works. His parents were adherents of the back-to-the-land movement, and his father was an occasional artisanal toymaker. On their farm, near the coast of Maine, the family grew vegetables and raised livestock using techniques not too different from those of nineteenth-century homesteaders. They pulled their plough with oxen and, to fuel their wood-burning stove, felled trees with a manual saw.

When Hill and his older brother found out that the local public school had acquired a TRS-80, an early desktop computer, they became obsessed. The math teacher, sensing their passion, decided to loan the machine to the family for Christmas. Over the holidays, the boys became amateur programmers. Their favourite application was Dancing Demon, in which a devilish figure taps its feet to an old swing tune. Pretty soon, the boys had hacked the program and turned the demon into a monster resembling Boris Karloff in Frankenstein. “In the dark winter of Maine,” says Hill, “what else were we going to do?”

The experiments spurred conversation among the brothers, much of it the fevered speculation of young people who’ve read too much science fiction. They fantasized about the spaceships they would someday design. They also discussed the possibility of building a computerized brain. “I was probably ten or eleven years old,” Hill recalls, “saying to my brother, ‘Will we be able to simulate a neuron? Maybe that’s what we need to get artificial intelligence.’”

Roughly a decade later, as an undergraduate at the quirky liberal arts university Hampshire College, Hill was drawn to computational neuroscience, a field whose practitioners were doing what he and his brother had talked about: building mathematical, and sometimes even computerized, brain models.

In 2006, after completing his PhD, along with postgraduate studies in San Diego and Wisconsin, Hill returned to Lausanne to co-direct the Blue Brain Project, a radical brain-modelling lab in the Swiss Alps. The initiative had been founded a year earlier by Henry Markram, a South African Israeli neuroscientist whose outsize ambitions had made him a revered and controversial figure.

In neuroscience today, there are robust debates as to how complex a brain model should be. Some researchers seek to design clean, elegant models. That’s a fitting description of the Nobel Prize–winning work of Alan Hodgkin and Andrew Huxley, who, in 1952, drew handwritten equations and rudimentary illustrations—with lines, symbols, and arrows—describing how electrical signals exit a neuron and travel along a branch-like cable called an axon.

Other practitioners seek to make computer-generated maps that incorporate hundreds of neurons and tens of thousands of connections, image fields so complicated that Michelangelo’s Sistine Chapel ceiling looks minimalist by comparison. The clean, simple models demystify brain processes, making them understandable to humans. The complex models are impossible to comprehend: they offer too much information to take in, attempting to approximate the complexity of an actual brain.

Markram’s inclinations are maximalist. In a 2009 TED Talk, he said that he aimed to build a computer model so comprehensive and biologically accurate that it would account for the location and activity of every human neuron. He likened this endeavour to mapping out a rainforest tree by tree. Skeptics wondered whether such a project was feasible. The problem isn’t merely that there are numerous trees in a rainforest: it’s also that each tree has its own configuration of boughs and limbs. The same is true of neurons.

Each is a microscopic, blob-like structure with dense networks of protruding branches called axons and dendrites. Neurons use these branches to communicate. Electrical signals run along the axons of one neuron and then jump, over a space called a synapse, to the dendrites of another. The 86 billion neurons in the human brain each have an average of 10,000 synaptic connections. Surely, skeptics argued, it was impossible, using available technology, to make a realistic model from such a complicated, dynamic system.

In 2006, Markram and Hill got to work. The initial goal was to build a hyper-detailed, biologically faithful model of a “microcircuit” (i.e., a cluster of 31,000 neurons) found within the brain of a rat. With a glass probe called a patch clamp, technicians at the lab penetrated a slice of rat brain, connected to each individual neuron, and recorded the electrical signals it sent out.

By injecting dye into the neurons, the team could visualize their shape and structure. Step by step, neuron by neuron, they mapped out the entire communication network. They then fed the data into a model so complex that it required Blue Gene, the IBM supercomputer, to run.

In 2015, they completed their rat microcircuit. If they gave their computerized model certain inputs (say, a virtual spark in one part of the circuit), it would predict an output (for instance, an electrical spark elsewhere) that corresponded to biological reality. The model wasn’t doing any actual cognitive processing: it wasn’t a virtual brain, and it certainly wasn’t thinking.

But, the researchers argued, it was predicting how electrical signals would move through a real circuit inside a real rat brain. “The digital brain tissue naturally behaves like the real brain tissue,” reads a statement on the Blue Brain Project’s website. “This means one can now study this digital tissue almost like one would study real brain tissue.”

The breakthrough, however, drew fresh criticisms. Some neuroscientists questioned the expense of the undertaking. The team had built a multimillion-dollar computer program to simulate an already existing biological phenomenon, but so what? “The question of ‘What are you trying to explain?’ hadn’t been answered,” says Grace Lindsay, a computational neuroscientist and author of the book Models of the Mind. “A lot of money went into the Blue Brain Project, but without some guiding goal, the whole thing seemed too open ended to be worth the resources.”

Others argued that the experiment was not just profligate but needlessly convoluted. “There are ways to reduce a big system down to a smaller system,” says Adrienne Fairhall, a computational neuroscientist at the University of Washington. “When Boeing was designing airplanes, they didn’t build an entire plane just to figure out how air flows around the wings. They scaled things down because they understood that a small simulation could tell them what they needed to know.” Why seek complexity, she argues, at the expense of clarity and elegance?

The harshest critics questioned whether the model even did what it was supposed to do. When building it, the team had used detailed information about the shape and electrical signals of each neuron. But, when designing the synaptic connections—that is, the specific locations where the branches communicate with one another—they didn’t exactly mimic biological reality, since the technology for such detailed brain mapping didn’t yet exist. (It does now, but it’s a very recent development.)

Instead, the team built an algorithm to predict, based on the structure of the neurons and the configuration of the branches, where the synaptic connections were likely to be. If you know the location and shape of the trees, they reasoned, you don’t need to perfectly replicate how the branches intersect.

But Moritz Helmstaedter—a director at the Max Planck Institute for Brain Research, in Frankfurt, Germany, and an outspoken critic of the project—questions whether this supposition is true. “The Blue Brain model includes all kinds of assumptions about synaptic connectivity, but what if those assumptions are wrong?” he asks. The problem, for Helmstaedter, isn’t just that the model could be inaccurate: it’s that there’s no way to fully assess its accuracy given how little we know about brain biology.

If a living rat encounters a cat, its brain will generate a flight signal. But, if you present a virtual input representing a cat’s fur to the Blue Brain model, will the model generate a virtual flight signal too? We can’t tell, Helmstaedter argues, in part because we don’t know, in sufficient detail, what a flight signal looks like inside a real rat brain.

Hill takes these comments in stride. To criticisms that the project was too open-ended, he responds that the goal wasn’t to demystify a specific brain process but to develop a new kind of brain modelling based in granular biological detail.

The objective, in other words, was to demonstrate—to the world and to funders—that such an undertaking was possible. To criticisms that the model may not work, Hill contends that it has successfully reproduced thousands of experiments on actual rats. Those experiments hardly prove that the simulation is 100 percent accurate—no brain model is—but surely they give it credibility.

And, to criticisms that the model is needlessly complicated, he counters that the brain is complicated too. “We’d been hearing for decades that the brain is too complex to be modelled comprehensively,” says Hill. “Markram put a flag in the ground and said, ‘This is achievable in a finite amount of time.

The specific length of time is a matter of some speculation. In his TED Talk, Markram implied that he might build a detailed human brain model by 2019, and he began raising money toward a new initiative, the Human Brain Project, meant to realize this goal. But funding dried up, and Markram’s predictions came nowhere close to
panning out.

The Blue Brain Project, however, remains ongoing. (The focus, now, is on modelling a full mouse brain.) For Hill, it offers proof of concept for the broader mission of neuroinformatics. It has demonstrated, he argues, that when you systemize huge amounts of data, you can build platforms that generate reliable insights about the brain. “We showed that you can do incredibly complex data integration,” says Hill, “and the model will give rise to biologically realistic responses.”

When Hill was approached by recruiters on behalf of CAMH to ask if he might consider leaving the Blue Brain Project to start a neuroinformatics lab in Toronto, he demurred. “I’d just become a Swiss citizen,” he says, “and I didn’t want to go.” But the hospital gave him a rare opportunity: to practice cutting-edge neuroscience in a clinical setting. CAMH was formed, in 1998, through a merger of four health care and research institutions.

It treats over 34,000 psychiatric patients each year and employs more than 140 scientists, many of whom study the brain. Its mission, therefore, is both psychiatric and neuroscientific—a combination that appealed to Hill. “I’ve spoken to psychiatrists who’ve told me, ‘Neuroscience doesn’t matter,’” he says. “In their work, they don’t think about brain biology. They think about treating the patient in front of them.” Such biases, he argues, reveal a profound gap between brain research and the illnesses that clinicians see daily. At the KCNI, he’d have a chance to bridge that gap.

The business of data-gathering and brain-modelling may seem dauntingly abstract, but the goal, ultimately, is to figure out what makes us human. The brain, after all, is the place where our emotional, sensory, and imaginative selves reside. To better understand how the modelling process works, I decided to shadow a researcher and trace an individual data point from its origins in a brain to its incorporation in a KCNI model.

Last February, I met Homeira Moradi, a neuroscientist at Toronto Western Hospital’s Krembil Research Institute who shares data with the KCNI. Because of where she works, she has access to the rarest and most valuable resource in her field: human brain tissue. I joined her at 9 a.m., in her lab on the seventh floor. Below us, on the ground level, Taufik Valiante, a neurosurgeon, was operating on an epileptic patient. To treat epilepsy and brain cancer, surgeons sometimes cut out small portions of the brain. But, to access the damaged regions, they must also remove healthy tissue in the neocortex, the high-functioning outer layer of the brain.

Moradi gets her tissue samples from Valiante’s operating room, and when I met her, she was hard at work weighing and mixing chemicals. The solution in which her tissue would sit would have to mimic, as closely as possible, the temperature and composition of an actual brain. “We have to trick the neurons into thinking they’re still at home,” she said.

She moved at the frenetic pace of a line cook during a dinner rush. At some point that morning, Valiante’s assistant would text her from the OR to indicate that the tissue was about to be extracted. When the message came through, she had to be ready. Once the brain sample had been removed from the patient’s head, the neurons within it would begin to die. At best, Moradi would have twelve hours to study the sample before it expired.

The text arrived at noon, by which point we’d been sitting idly for an hour. Suddenly, we sprang into action. To comply with hospital policy, which forbids Moradi from using public hallways where a visitor may spot her carrying a beaker of brains, we approached the OR indirectly, via a warren of underground tunnels.

The passages were lined with gurneys and illuminated, like catacombs in an Edgar Allan Poe story, by dim, inconsistent lighting. I hadn’t received permission to witness the operation, so I waited for Moradi outside the OR and was able to see our chunk of brain only once we’d returned to the lab. It didn’t look like much—a marble-size blob, gelatinous and slightly bloody, like gristle on a steak.

Under a microscope, though, the tissue was like nothing I’d ever seen. Moradi chopped the sample into thin pieces, like almond slices, which went into a small chemical bath called a recording chamber. She then brought the chamber into another room, where she kept her “rig”: an infrared microscope attached to a manual arm.

She put the bath beneath the lens and used the controls on either side of the rig to operate the arm, which held her patch clamp—a glass pipette with a microscopic tip. On a TV monitor above us, we watched the pipette as it moved through layers of brain tissue resembling an ancient root system—tangled, fibrous, and impossibly dense.

Moradi needed to bring the clamp right up against the wall of a cell. The glass had to fuse with the neuron without puncturing the membrane. Positioning the clamp was maddeningly difficult, like threading the world’s smallest needle. It took her the better part of an hour to connect to a pyramidal neuron, one of the largest and most common cell types in our brain sample.

Once we’d made the connection, a filament inside the probe transmitted the electrical signals the neuron sent out. They went first into an amplifier and then into a software application that graphed the currents—strong pulses with intermittent weaker spikes between them—on an adjacent computer screen. “Is that coming from the neuron?” I asked, staring at the screen. “Yes,” Moradi replied. “It’s talking to us.”

A depressive brain is a noisy one. What if scientists could locate the neurons causing the problem?

It had taken us most of the day, but we’d successfully produced a tiny data set—information that may be relevant to the study of mental illness. When neurons receive electrical signals, they often amplify or dampen them before passing them along to adjacent neurons. This function, called gating, enables the brain to select which stimuli to pay attention to. If successive neurons dampen a signal, the signal fades away.

If they amplify it, the brain attends more closely. A popular theory of depression holds that the illness has something to do with gating. In depressive patients, neurons may be failing to dampen specific signals, thereby inducing the brain to ruminate unnecessarily on negative thoughts. A depressive brain, according to this theory, is a noisy one. It is failing to properly distinguish between salient and irrelevant stimuli. But what if scientists could locate and analyze a specific cluster of neurons (i.e., a circuit) that was causing the problem?

Etay Hay, an Israeli neuroscientist and one of Hill’s early hires at the KCNI, is attempting to do just that. Using Moradi’s data, he’s building a model of a “canonical” circuit—that is, a circuit that appears thousands of times, with some variations, in the outer layer of the brain. He believes a malfunction in this circuit may underlie some types of treatment-resistant depression.

The circuit contains pyramidal neurons, like the one Moradi recorded from, that communicate with smaller cells, called interneurons. The interneurons dampen the signals the pyramidal neurons send them. It’s as if the interneurons are turning down the volume on unwanted thoughts. In a depressive brain, however, the interneurons may be failing to properly reduce the signals, causing the patient to get stuck in negative-thought loops.

Etienne Sibille, another CAMH neuroscientist, has designed a drug that increases communication between the interneurons and the pyramidal neurons in Hay’s circuit. In theory, this drug should enable the interneurons to better do their job, tamp down on negative thoughts, and improve cognitive function.

This direct intervention, which occurs at the cellular level, could be more effective than the current class of antidepressants, called SSRIs, which are much cruder. “They take a shotgun approach to depression,” says Sibille, “by flooding the entire brain with serotonin.” (That chemical, for reasons we don’t fully understand, can reduce depressive symptoms, albeit only in some people.)

Sibille’s drug, however, is more targeted. When he gives it to mice who seem listless or fearful, they perk up considerably. Before testing it on humans, Sibille hopes to further verify its efficacy. That’s where Hay comes in. He has finished his virtual circuit and is now preparing to simulate Sibille’s treatment. If the simulation reduces the overall amount of noise in the circuit, the drug can likely proceed to human trials, a potentially game-changing breakthrough.

Hill’s other hires at the KCNI have different specialties from Hay’s but similar goals. Shreejoy Tripathy is building computer models to predict how genes affect the shape and behaviour of neurons. Andreea Diaconescu is using video games to collect data that will allow her to better model early stage psychosis.

This can be used to predict symptom severity and provide more effective treatment plans. Joanna Yu is building the BrainHealth Databank, a digital repository for anonymized data—on symptoms, metabolism, medications, and side effects—from over 1,000 CAMH patients with depression. Yu’s team will employ AI to analyze the information and predict which treatment may offer the best outcome for each individual.

Similarly, Dan Felsky is helping to run a five-year study on over 300 youth patients at CAMH, incorporating data from brain scans, cognitive tests, and doctors’ assessments. “The purpose,” he says, “is to identify signs that a young person may go on to develop early adult psychosis, one of the most severe manifestations of mental illness.”

All of these researchers are trained scientists, but their work can feel more like engineering: they’re each helping to build the digital infrastructure necessary to interpret the data they bring in.

Sibille’s work, for instance, wouldn’t have been possible without Hay’s computer model, which in turn depends on Moradi’s brain-tissue lab, in Toronto, and on data from hundreds of neuron recordings conducted in Seattle and Amsterdam. This collaborative approach, which is based in data-sharing agreements and trust-based relationships, is incredibly efficient. With a team of three trainees, Hay built his model in a mere twelve months. “If just one lab was generating my data,” he says, “I’d have kept it busy for twenty years.” Read more……

Simon Lewsen, a Toronto-based writer, contributes to Azure, Precedent, enRoute, the Globe and Mail, and The Atlantic. In 2020, he won a National Magazine Award.

Source: What Happens to Our Brains When We Get Depressed? | The Walrus

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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

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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Beauty Is In The Brain: AI Reads Brain Data, Generates Personally Attractive Images

Researchers have succeeded in making an AI understand our subjective notions of what makes faces attractive. The device demonstrated this knowledge by its ability to create new portraits on its own that were tailored to be found personally attractive to individuals. The results can be utilised, for example, in modelling preferences and decision-making as well as potentially identifying unconscious attitudes.

Researchers at the University of Helsinki and University of Copenhagen investigated whether a computer would be able to identify the facial features we consider attractive and, based on this, create new images matching our criteria. The researchers used artificial intelligence to interpret brain signals and combined the resulting brain-computer interface with a generative model of artificial faces. This enabled the computer to create facial images that appealed to individual preferences.

“In our previous studies, we designed models that could identify and control simple portrait features, such as hair color and emotion. However, people largely agree on who is blond and who smiles. Attractiveness is a more challenging subject of study, as it is associated with cultural and psychological factors that likely play unconscious roles in our individual preferences. Indeed, we often find it very hard to explain what it is exactly that makes something, or someone, beautiful: Beauty is in the eye of the beholder,” says Senior Researcher and Docent Michiel Spapé from the Department of Psychology and Logopedics, University of Helsinki.

The study, which combines computer science and psychology, was published in February in the IEEE Transactions in Affective Computing journal.

Preferences exposed by the brain

Initially, the researchers gave a generative adversarial neural network (GAN) the task of creating hundreds of artificial portraits. The images were shown, one at a time, to 30 volunteers who were asked to pay attention to faces they found attractive while their brain responses were recorded via electroencephalography (EEG).

“It worked a bit like the dating app Tinder: the participants ‘swiped right’ when coming across an attractive face. Here, however, they did not have to do anything but look at the images. We measured their immediate brain response to the images,” Spapé explains.

The researchers analysed the EEG data with machine learning techniques, connecting individual EEG data through a brain-computer interface to a generative neural network.

“A brain-computer interface such as this is able to interpret users’ opinions on the attractiveness of a range of images. By interpreting their views, the AI model interpreting brain responses and the generative neural network modelling the face images can together produce an entirely new face image by combining what a particular person finds attractive,” says Academy Research Fellow and Associate Professor Tuukka Ruotsalo, who heads the project.

To test the validity of their modelling, the researchers generated new portraits for each participant, predicting they would find them personally attractive. Testing them in a double-blind procedure against matched controls, they found that the new images matched the preferences of the subjects with an accuracy of over 80%.

“The study demonstrates that we are capable of generating images that match personal preference by connecting an artificial neural network to brain responses. Succeeding in assessing attractiveness is especially significant, as this is such a poignant, psychological property of the stimuli.

Computer vision has thus far been very successful at categorising images based on objective patterns. By bringing in brain responses to the mix, we show it is possible to detect and generate images based on psychological properties, like personal taste,” Spapé explains.

Potential for exposing unconscious attitudes

Ultimately, the study may benefit society by advancing the capacity for computers to learn and increasingly understand subjective preferences, through interaction between AI solutions and brain-computer interfaces.

“If this is possible in something that is as personal and subjective as attractiveness, we may also be able to look into other cognitive functions such as perception and decision-making. Potentially, we might gear the device towards identifying stereotypes or implicit bias and better understand individual differences,” says Spapé.

By: University of Helsinki

Source: Beauty is in the brain: AI reads brain data, generates personally attractive images — ScienceDaily

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Anjan Chatterjee uses tools from evolutionary psychology and cognitive neuroscience to study one of nature’s most captivating concepts: beauty. Learn more about the science behind why certain configurations of line, color and form excite us in this fascinating, deep look inside your brain. Check out more TED talks: http://www.ted.com The TED Talks channel features the best talks and performances from the TED Conference, where the world’s leading thinkers and doers give the talk of their lives in 18 minutes (or less). Look for talks on Technology, Entertainment and Design — plus science, business, global issues, the arts and more. Follow TED on Twitter: http://www.twitter.com/TEDTalks Like TED on Facebook: https://www.facebook.com/TED Subscribe to our channel: https://www.youtube.com/TED
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Journal Reference:

  1. Michiel Spape, Keith Davis, Lauri Kangassalo, Niklas Ravaja, Zania Sovijarvi-Spape, Tuukka Ruotsalo. Brain-computer interface for generating personally attractive images. IEEE Transactions on Affective Computing, 2021; 1 DOI: 10.1109/TAFFC.2021.3059043
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Starting Your Day on the Internet Is Damaging Your Brain

I’ve said before the first 3 hours of your day can dictate how your life turns out. And this often begins with the very first thing that you decide to put in your brain. You can either start you day with junk food for the brain (the internet, distracting apps, etc) or you can start the day with healthy food for the brain (reading, meditation, journaling, exercising, etc). When you start the day with junk food for the brain, you put yourself at a self imposed handicap that inhibits your ability to get into flow and prevents you from doing deep work. When you start the day with health food for your brain, the exact opposite happens.

Anytime I start my day with junk food for the brain, the quality of the day goes down. I’m less happy, focused, and productive. I spend a ton of time on the internet and don’t get any real work done. But if I start my day with health food for the brain, I find that my mood is better, I’m happier, more focused and productive.

Why Junk Food for the Brain is Toxic

If you woke up in the morning, smoked a cigarette, ate 2 donuts, and washed it down with 2 cups of coffee, it wouldn’t be surprising that your physical performance is subpar. You’re probably not going to go out and run 2 miles or win a prize fight after that kind of breakfast.

But when it comes to our brain, we’re not nearly as mindful about the idea that we should treat the information we consume like the food we eat.

“When you wake up you’re in this theta alpha state and you’re highly suggestible. Every like, comment, share, you get this dopamine fix and it’s literally rewiring your brain. What you’re smart device is doing especially if that’s the first thing you grab when you wake up and you’re in this alpha theta state, is rewiring your brain to be distracted.” — @Jim Kwik

If we start our days by checking email, instagram, or the internet, we keep reinforcing the behavior of distraction until it becomes our new habit. Some of the smartest behavioral scientist and designers in the world have worked really hard to make sure that their products are addictive, habit forming, and only provide you with a temporary sense of fulfillment so the you are always jonesing for your next fix. As Mark Manson so brilliantly said, cell phones are the new cigarettes, And a significant amount of what’s on the internet is nothing more than junk food for the brain.

Why Healthy Food for the Brain is So Powerful

If you woke up in the morning and had a really healthy breakfast, that revitalized and energized you, you’d likely hit the gym or a morning run expecting to be at your peak. The same goes for our brains.

When we start the day with health food for the brain, instead of a self imposed handicap, we give ourselves a massive competitive advantage. On the days when I religiously follow through on the 8-step daily routine that allowed me to write multiple books and 100’s of articles, my productivity goes through the roof, flow happens effortlessly, and I end up doing a lot of deep work. The idea for this article was actually the result of giving my brain some health food to start the day.

  • I did 20 minutes of meditation
  • I did almost an hour of reading
  • I wrote in my journal for 30 minutes
  • When I turned on my computer, I blocked distractions and started writing.

When you start the day with health food for your brain, you don’t end up depleting your willpower, and as a result you get more done in far less time.

So how exactly do you start the day with health food for your brain? To wean ourselves off of junk food for the brain, we have to actually replace it with something else.

Don’t use your devices in the morning

Smartphones distract us whether they are on, off, in our pockets, or on a table, and they command our attention even when they are not our own. The best solution for preventing smartphone distraction is to remove it from the picture altogether — Steve Magness

If your refrigerator or pantry is filled with junk food, you’re going to be much more likely to eat it. Same goes for your devices. If you turn them on first thing in the morning, you’re going to be much more likely to give into the sources of distraction that they make accessible. The only thing that I use my phone for in the morning is a 20 minute meditation with the Calm app. After that, I take it out of the room I’m working in.

Set aside 20 minutes to meditate

Reality as we know it occurs in the space between stimulus and response. An event happens and we make it mean something. But this happens so fast that we don’t question the validity of the meaning we’ve assigned to an event, situation or circumstance. The way to take control of the meaning is to slow that process down, and the way to slow that process down is with meditation.

I have a natural tendency to overreact or make situations more stressful than they really are. But as my meditation practice has deepened, I’ve noticed a profound energetic shift. Many of the things that would have previously rattled me don’t. On the mornings that I follow through with my 20 minutes of meditation, I’m able to focus more easily, and I don’t crave sources of distraction nearly as much

The most successful people I’ve interviewed on Unmistakable Creative, all of the peak performance books I’ve read, spiritual teachings, and many billionaires all reference the role that a daily meditation habit is played in their life. That was convincing enough evidence for me to make it a daily habit.

Read books, not the internet

When we read on the internet, we tend to scan more than we read. How often do you sit around at a dinner party discussing the amazing article you read on the internet? Almost all of my ideas for what I want to write about have come from books. Almost none of them have come from reading articles on the internet. I’ve even found in my cases that when I read a physical book that I previously read on Kindle, I tend to get far more value out of it.

Years ago when I interviewed Julien Smith, he said “I don’t read blogs. I read books.” And he had one of the most popular blogs on the internet. I stopped reading blogs, started reading books, and as a result became a more prolific writer. After watching the prolific career that Ryan Holiday has built, and observing his reading habits, I decided to follow his lead. Believe me the irony that you’re reading this on the internet is not lost on me.

Do 1 hour of Deep Work

One hour of deep work is a form of self care. It’s incredibly fulfilling. It’s an affirmation to yourself and to the universe that you value yourself and your time. You can accomplish extraordinary things in just one focused hour a day of uninterrupted creation time. With deep work, you get disproportionate results from your efforts. It’s the 80–20 rule at work. 80% of your output will come from 20 percent of your effort.

Just some food for thought. When I started writing this article I set my distraction blocker for 45 minutes. As I wrote this sentence I decided to do a check on my word count and realized I’d written over 1200 words in about 35 minutes. That’s what happens when you combine flow and deep work together

One last thing to consider. What are you really getting out of checking Facebook, instagram, or anything on your phone when you wake up in the morning? Is it making you happier or more successful in any way at all? If you added up all the time you possibly waste over the course of a year on this behavior, it’s likely you could write a book, build a business, or learn an instrument, all of which are going to do far more for the quality of your life than the temporary dopamine fix your phone provides.

Source: Starting Your Day on the Internet Is Damaging Your Brain

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Slowly Losing Your Mind in Lockdown? 5 Apps to Boost Your Mental Health

It should come as no surprise to learn being stuck inside for months on end with minimal human contact is not good for your well-being. As the COVID-19 pandemic continues to disrupt any semblance of normalcy throughout the U.S. and elsewhere, many people are feeling the effects of reduced employment and other disruptions of daily life—compounded by more visible instances of targeted police brutality and racial discrimination.

If you’re stressed out, exhausted by the stream of bad news, or just fell off whatever good habits you had in 2019, here’s how you can use your mobile device to get back on track. With apps that make chores fun, simple meditation tools, or services to address your mental health issues, you can, maybe, better prepare yourself for whatever else this year has in store.

Get your sleep schedule back on track with Pzizz

There’s a good chance you’ve got a lot on your mind right now—which means counting sheep might not cut it when it comes to getting to sleep, and staring at your phone while doomscrolling is almost certainly even worse. And while there are a handful of apps designed to track your sleep, getting one meant to help you get to bed is just as important.

Pzizz is a sleep app that uses audio cues based on sleep research to help you fall asleep. It uses a mixture of speech, music, and audio to get you relaxed and prime your body for some down time, be it for a few minutes or a whole night. You can adjust the mix as well, leaning toward a more talkative or musical sleep aid for the allotted time period. Subscribing to the premium version of the app nets you access to a wider variety of sounds and guided sleep experiences.

Gamify your routines with Habitica

If you need a little motivation to get done what you need to get done on a daily basis, and don’t mind adding a little fantastical vibe to the mix, try out Habitica, a task management and to-do list service that gamifies the work you accomplish. You create an RPG-esque character, which “defeats enemies” and levels up whenever you confirm that you’ve accomplished on of your IRL tasks—whether those are daily activities, errands to run, or habits to build. You can play by yourself or team up with friends for a more social element (and to add accountability to the mix); in either case, you can obtain prizes and gear for your fictional avatar by checking off boxes on your to-do list.

Reflect for a moment with Enso

If you’re like me, and just want to practice sitting for a few minutes with no distractions, you should try out Enso. It’s a minimal but elegant iOS meditation app perfect for both beginning students or experienced practitioners. There are no voices to distract you, and no music to focus on or tolerate. Just set a timer, hit start, and wait until it runs out.

You can customize your session with multiple bells to signify prep time, sitting time, and intervals for those engaging in a more advanced meditation practice. Buying Enso’s $2.99 pro version will net you some much-needed features, like Apple Health integration, an in-app audio player for custom meditation tunes, and extra alert tones you can pick to ease yourself in and out of your sitting practice.

For some good bedtime white noise, use Dark Noise

Trying to read a book or focus on some work while the outside world honks, shouts, and distracts is no fun. That’s why white noise is so useful, drowning out other sounds with a more predictable, familiar tone. That’s what Dark Noise is for.

The app features a wide array of sounds, from white, brown, pink, and grey noises, to heavy rains and waterfalls, crickets, wind chimes, and coffee shops. With such a selection, you’re sure to find a noise to keep you distracted, focused, or drowsy—whatever you need. And there’s a timer, so you can have the app shut down on its own after you finish work (or fall asleep).

Talk to someone with BetterHelp

Everyone needs someone to talk to—especially now. With in-person therapy currently out of reach for many thanks to the coronavirus, those seeking mental-health treatment might want to consider BetterHelp. Using the app, you can speak to a licensed psychologist or counselor via text, phone, or video. With no insurance necessary, pricing ranges from $40 to $70 per month, and there are over 10,000 therapists and counselors—all with over three years of therapy experience—to choose from (you’ll take a quiz to see which one is the best fit for you).

By Patrick Lucas Austin

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Multiple Sclerosis Risk 29% Higher for People Living in Urban Areas, New Research Reveals

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Air pollution could be a risk factor for the development of multiple sclerosis (MS), a new study conducted in Italy has found.The research, presented today at the European Academy of Neurology (EAN) Virtual Congress, detected a for MS in individuals residing in that have lower levels of air pollutants known as particulate matter (PM).

It showed that the MS risk, adjusted for urbanization and deprivation, was 29% higher among those residing in more urbanized areas.The study sample included over 900 MS patients within the region, and MS rates were found to have risen 10-fold in the past 50 years, from 16 cases per 100,000 inhabitants in 1974 to almost 170 cases per 100,000 people today.

Whilst the huge increase can partly be explained by increased survival for MS patients, this sharp increase could also be explained by greater exposure to .The analysis was conducted in the winter, given that this is the season with the highest pollutant concentrations, in the north-western Italian region of Lombardy, home to over 547,000 people.

Commenting on the findings at the EAN Virtual Congress, lead researcher Professor Roberto Bergamaschi explained, “It is well recognized that immune diseases such as MS are associated with multiple factors, both genetic and environmental. Some environmental factors, such as vitamin D levels and smoking habits, have been extensively studied, yet few studies have focused on air pollutants. We believe that air pollution interacts through several mechanisms in the development of MS and the results of this study strengthen that hypothesis.”

Particulate matter (PM) is used to describe a mixture of solid particles and droplets in the air and is divided into two categories. PM10 includes particles with a diameter of 10 micrometers of smaller and PM2.5 which have a diameter of 2.5 micrometers or smaller.Both PM10 and PM2.5 are major pollutants and are known to be linked to various health conditions, including heart and lung disease, cancer and respiratory issues.

According to the World Health Organization, 4.2 million deaths occur every year because of exposure to ambient (outdoor) air pollution.Three different areas were compared within the study region based on their levels of urbanization, of which two areas were found to be above the European Commission threshold of . “In the higher risk areas, we are now carrying out specific analytical studies to examine multiple possibly related to the heterogeneous distribution of MS risk”, added Professor Bergamaschi.

The number of people living with MS around the world is growing, with more than 700,000 sufferers across Europe. The vast majority (85%) of patients present with relapsing remitting MS, characterized by unpredictable, self-limited episodes of the central nervous system. Whilst MS can be diagnosed at any age, it frequently occurs between the ages of 20-40 and is more frequent in women. Symptoms can change in severity daily and include fatigue, walking difficulty, numbness, pain and muscle spasms.

By European Academy of Neurology

Source: https://medicalxpress.com

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Am I Having an RMS Relapse Again? See Some Common Signs

You’re doing everything right—you visit your healthcare provider regularly, you take your relapsing MS medication exactly as it is prescribed—so why does it feel like that’s still not enough? It could be that you’re continuing to experience frequent relapses—a sign that your treatment may not be working well enough.

Knowing when it’s a relapse

Relapses, also known as flare-ups, are when new or existing symptoms appear or worsen, lasting for at least 24 hours and sometimes for as long as several weeks or months. While MS affects everyone differently, there are some common symptoms that people may experience during a relapse. Perhaps you’ve experienced one or more of the following symptoms.

Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.

LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.

Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.

LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.

Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.

LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.

Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.

LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.

Accepting frequent relapses as “just part of living with relapsing MS” is not a good plan. If you’re on a treatment but still feel like you’re experiencing too many relapses, it could be time for you to learn about LEMTRADA.

LEMTRADA is not approved to treat individual symptoms of a relapse. Click below to read about the LEMTRADA study and plan to have a discussion with your healthcare provider about your relapsing MS and treatment goals.

IMPORTANT SAFETY INFORMATION

LEMTRADA can cause serious side effects including:

Serious autoimmune problems: Some people receiving LEMTRADA develop a condition where the immune cells in your body attack other cells or organs in the body (autoimmunity), which can be serious and may cause death. Serious autoimmune problems may include:

  • Immune thrombocytopenic purpura (ITP), a condition of reduced platelet counts in your blood that can cause severe bleeding that may cause life‑threatening problems. Call your healthcare provider right away if you have any of the following symptoms: easy bruising; bleeding from a cut that is hard to stop; coughing up blood; heavier menstrual periods than normal; bleeding from your gums or nose that is new or takes longer than usual to stop; small, scattered spots on your skin that are red, pink, or purple
  • Kidney problems called anti‑glomerular basement membrane disease, which, if not treated, can lead to severe kidney damage, kidney failure that needs dialysis, a kidney transplant, or death. Call your healthcare provider right away if you have any of the following symptoms: swelling of your legs or feet; blood in the urine (red or tea‑colored urine); decrease in urine; fatigue; coughing up blood

It is important for you to have blood and urine tests before you receive, while you are receiving and every month for 4 years or longer, after you receive your last LEMTRADA infusion.

Serious infusion reactions: LEMTRADA can cause serious infusion reactions that may cause death. Serious infusion reactions may happen while you receive, or up to 24 hours or longer after you receive LEMTRADA.

  • You will receive your infusion at a healthcare facility with equipment and staff trained to manage infusion reactions, including serious allergic reactions, and urgent heart or breathing problems. You will be watched while you receive, and for 2 hours or longer after you receive, LEMTRADA. If a serious infusion reaction happens while you are receiving LEMTRADA, your infusion may be stopped.

Tell your healthcare provider right away if you have any of the following symptoms of a serious infusion reaction during the infusion, and after you have left the healthcare facility:

  • swelling in your mouth or throat
  • trouble breathing
  • weakness
  • fast, slow, or irregular heartbeat
  • chest pain
  • rash

To lower your chances of getting a serious infusion reaction, your healthcare provider will give you a medicine called corticosteroids before your first 3 infusions of a treatment course. You may also be given other medicines before or after the infusion to try to reduce your chances of having these reactions or to treat them if they happen.

Stroke and tears in your arteries that supply blood to your brain (carotid and vertebral arteries): Some people have had serious and sometimes deadly strokes and tears in their carotid or vertebral arteries within 3 days of receiving LEMTRADA. Get help right away if you have any of the following symptoms that may be signs of a stroke or tears in your carotid or vertebral arteries:

  • drooping of parts of your face
  • weakness on one side
  • sudden severe headache
  • difficulty with speech
  • neck pain

Certain cancers: Receiving LEMTRADA may increase your chance of getting some kinds of cancers, including thyroid cancer, skin cancer (melanoma), and blood cancers called lymphoproliferative disorders and lymphoma. Call your healthcare provider if you have the following symptoms that may be a sign of thyroid cancer:

  • new lump
  • swelling in your neck
  • pain in front of neck
  • hoarseness or other voice changes that do not go away
  • trouble swallowing or breathing
  • cough that is not caused by a cold

Have your skin checked before you start receiving LEMTRADA and each year while you are receiving treatment to monitor for symptoms of skin cancer.

Because of risks of autoimmunity, infusion reactions, and some kinds of cancers, LEMTRADA is only available through a restricted program called the LEMTRADA Risk Evaluation and Mitigation Strategy (REMS) Program.

Do not receive LEMTRADA if you are infected with human immunodeficiency virus (HIV).

Thyroid problems: Some patients taking LEMTRADA may get an overactive thyroid (hyperthyroidism) or an underactive thyroid (hypothyroidism). Call your healthcare provider if you have any of these symptoms:

  • excessive sweating
  • unexplained weight loss
  • fast heartbeat
  • eye swelling
  • nervousness
  • unexplained weight gain
  • feeling cold
  • worsening tiredness
  • constipation

Low blood counts (cytopenias): LEMTRADA may cause a decrease in some types of blood cells. Some people with these low blood counts have increased infections. Call your doctor right away if you have symptoms of cytopenias such as:

  • weakness
  • chest pain
  • yellowing of the skin or whites of the eyes (jaundice)
  • dark urine
  • fast heartbeat

Inflammation of the liver: Call your healthcare provider right away if you have symptoms such as unexplained nausea, stomach pain, tiredness, loss of appetite, yellowing of skin or whites of eyes, or bleeding or bruising more easily than normal.

Serious infections: LEMTRADA may cause you to have a serious infection while you receive and after receiving a course of treatment. Serious infections may include:

  • listeria. People who receive LEMTRADA have an increased chance of getting a bacterial infection called listeria, which can lead to significant complications or death. Avoid foods that may be a source of listeria or make sure foods are heated well.
  • herpes viral infections. Some people taking LEMTRADA have an increased chance of getting herpes viral infections. Take medicines as prescribed by your healthcare provider to reduce your chances of getting these infections.
  • tuberculosis. Your healthcare provider should check you for tuberculosis before you receive LEMTRADA.
  • hepatitis. People who are at high risk of, or are carriers of, hepatitis B (HBV) or hepatitis C (HCV) may be at risk of irreversible liver damage.

These are not all the possible infections that could happen while on LEMTRADA. Call your healthcare provider right away if you have symptoms of a serious infection such as fever or swollen glands. Talk to your healthcare provider before you get vaccinations after receiving LEMTRADA. Certain vaccinations may increase your chances of getting infections.

Progressive multifocal leukoencephalopathy (PML): A rare brain infection that usually leads to death or severe disability has been reported with LEMTRADA. Symptoms of PML get worse over days to weeks. It is important that you call your doctor right away if you have any new or worsening medical problems that have lasted several days, including problems with:

  • thinking
  • eyesight
  • strength
  • balance
  • weakness on 1 side of your body
  • using your arms or legs

Inflammation of the gallbladder without gallstones (acalculous cholecystitis): LEMTRADA may increase your chance of getting inflammation of the gallbladder without gallstones, a serious medical condition that can be life-threatening. Call your healthcare provider right away if you have any of the following symptoms:

  • stomach pain or discomfort
  • fever
  • nausea or vomiting

Swelling of lung tissue (pneumonitis): Some people have had swelling of the lung tissue while receiving LEMTRADA. Call your healthcare provider right away if you have the following symptoms:

  • shortness of breath
  • cough
  • wheezing
  • chest pain or tightness
  • coughing up blood

Before receiving LEMTRADA, tell your healthcare provider if you:

  • have bleeding, thyroid, or kidney problems
  • have a recent history of infection
  • are taking a medicine called Campath® (alemtuzumab)
  • have received a live vaccine in the past 6 weeks before receiving LEMTRADA or plan to receive any live vaccines. Ask your healthcare provider if you are not sure if your vaccine is a live vaccine
  • are pregnant or plan to become pregnant. LEMTRADA may harm your unborn baby. You should use birth control while receiving LEMTRADA and for 4 months after your course of treatment
  • are breastfeeding or plan to breastfeed. You and your healthcare provider should decide if you should receive LEMTRADA or breastfeed.

Tell your healthcare provider about all the medicines you take, including prescription and over‑the‑counter medicines, vitamins, and herbal supplements. LEMTRADA and other medicines may affect each other, causing side effects. Especially tell your healthcare provider if you take medicines that increase your chance of getting infections, including medicines used to treat cancer or to control your immune system.

The most common side effects of LEMTRADA include:

  • rash
  • headache
  • thyroid problems
  • fever
  • swelling of your nose and throat
  • nausea
  • urinary tract infection
  • feeling tired
  • trouble sleeping
  • upper respiratory infection
  • herpes viral infection
  • hives
  • itching
  • fungal infection
  • joint pain
  • pain in your arms or legs
  • back pain
  • diarrhea
  • sinus infection
  • mouth pain or sore throat
  • tingling sensation
  • dizziness
  • stomach pain
  • sudden redness in face, neck, or chest
  • vomiting

Tell your healthcare provider if you have any side effect that bothers you or that does not go away. These are not all the possible side effects of LEMTRADA.

You may report side effects to the FDA at 1-800-FDA-1088.

Please see full Prescribing Information/Medication Guide, including serious side effects, for additional Important Safety Information.

©2019 Genzyme Corporation. All rights reserved.

Source: Am I having an RMS relapse again? See some common signs.

Listen as Dr. Daniel Ontaneda, Cleveland Clinic Mellen Center for Multiple Sclerosis Treatment and Research, reviews relapses in the MS disease course, what a relapse is, and why it is important to better understand them with one of his patients. For more information about MS relapse or other related MS questions, visit http://my.clevelandclinic.org/service….

“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says

Lea Grinberg, a neuropathologist and associate professor at the UCSF Memory and Aging Center in San Francisco’s Mission Bay, holds slides of brain tissue used for research on August 15, 2019. (Lindsey Moore/KQED)

People who donate their bodies to science might never have dreamed what information lies deep within their brains.

Even when that information has to do with sleep.

Scientists used to believe that people who napped a lot were at risk for developing Alzheimer’s disease. But Lea Grinberg with the UCSF Memory and Aging Center started to wonder if “risk” was too light a term — what if, instead, napping indicated an early stage of Alzheimer’s?

About a decade ago, Grinberg — a neuropathologist and associate professor — was working with her team to map a protein called tau in donated brains. Some of their data, published last week, revealed drastic differences between healthy brains and those from Alzheimer’s patients in the parts of the brain responsible for wakefulness.

Lea Grinberg uses a program that takes a microscope’s magnification of brain tissue on a slide and projects it on a computer screen on August 15, 2019. The different colors represent different biological features in the brain tissue sample, including neurons and tau protein. (Lindsey Moore/KQED)

Wakefulness centers in the brain showed the buildup of tau — a protein that clogs neurons, Grinberg says, and lets debris accumulate. Gradually, these clogged neurons die. Some areas of the diseased brains had lost as much as 75% of their neurons. That may have led to the excessive napping scientists had observed before. Although the team only studied brains from 13 Alzheimer’s patients and 7 healthy individuals, Grinberg says that the degeneration caused by Alzheimer’s was so profound they were sure of its significance.

“We are kind of changing our understanding of what Alzheimer’s disease is,” she says. “It’s not only a memory problem, but it’s a problem in the brain that causes many other symptoms.”

Although these symptoms aren’t as severe as complete loss of memory or motor functions, Grinberg says they can still hold real consequences for a person’s quality of life. “Because if you don’t sleep well every day and if you… are not in the mood to do things like you were before, it’s very disappointing, right? My grandparents were like this.”

Grinberg says it’s important to know whether napping could be an early sign of Alzheimer’s, for treating symptoms and developing drugs that could slow the progression of the disease. Although there are no prescription drugs available to treat tau buildup, she says, a few are in clinical trials.

Lea Grinberg holds boxes filled with samples of brain tissue for study on August 15, 2019. (Lindsey Moore/KQED)

A public health professor and neuroscientist at UC Berkeley says the new information offers hope to researchers. William Jagust, who has studied Alzheimer’s for over 30 years, says the results could help select patients for clinical trials of new drugs that require early treatment. “It’s also just very important for understanding the evolution of Alzheimer’s disease with the hope that we eventually will have a drug,” he adds.

It’ll be awhile before doctors can diagnose anyone with Alzheimer’s based on how often they doze off. “There’s no practical application of this to clinical medicine as of today,” Jagust says, “but I think it’s on the cutting edge of the very, very important questions.”

By:

Source: “Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says

What is Alzheimer’s disease? Alzeimer’s (Alzheimer) disease is a neurodegenerative disease that leads to symptoms of dementia. Progression of Alzheimer’s disease is thought to involve an accumulation of beta-amyloid plaque and neurofibrillary tangles in the brain. Find more videos at http://osms.it/more. Study better with Osmosis Prime. Retain more of what you’re learning, gain a deeper understanding of key concepts, and feel more prepared for your courses and exams. Sign up for a free trial at http://osms.it/more. Subscribe to our Youtube channel at http://osms.it/subscribe. Get early access to our upcoming video releases, practice questions, giveaways and more when you follow us on social: Facebook: http://osms.it/facebook Twitter: http://osms.it/twitter Instagram: http://osms.it/instagram Osmosis’s Vision: Empowering the world’s caregivers with the best learning experience possible.
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