Posts Tagged ‘mental health’


In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

They say the results advance the hope that supplementing with broccoli sprout extract, which contains high levels of the chemical sulforaphane, may someday provide a way to lower the doses of traditional antipsychotic medicines needed to manage schizophrenia symptoms, thus reducing unwanted side effects of the medicines.

“It’s possible that future studies could show sulforaphane to be a safe supplement to give people at risk of developing schizophrenia as a way to prevent, delay or blunt the onset of symptoms,” adds Akira Sawa, M.D., Ph.D., professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and director of the Johns Hopkins Schizophrenia Center.

Schizophrenia is marked by hallucinations, delusions and disordered thinking, feeling, behavior, perception and speaking. Drugs used to treat schizophrenia don’t work completely for everyone, and they can cause a variety of undesirable side effects, including metabolic problems increasing cardiovascular risk, involuntary movements, restlessness, stiffness and “the shakes.”

In a study described in the Jan. 9 edition of the journal JAMA Psychiatry, the researchers looked for differences in brain metabolism between people with schizophrenia and healthy controls. They recruited 81 people from the Johns Hopkins Schizophrenia Center within 24 months of their first psychosis episode, which can be a characteristic symptom of schizophrenia, as well as 91 healthy controls from the community. The participants were an average of 22 years old, and 58% were men.

The researchers used a powerful magnet to measure and compare five regions in the brain between the people with and without psychosis. A computer analysis of 7-Tesla magnetic resonance spectroscopy (MRS) data identified individual chemical metabolites and their quantities.

The researchers found on average 4% significantly lower levels of the brain chemical glutamate in the anterior cingulate cortex region of the brain in people with psychosis compared to healthy people.

Glutamate is known for its role in sending messages between brain cells, and has been linked to depression and schizophrenia, so these findings added to evidence that glutamate levels have a role in schizophrenia.

Additionally, the researchers found a significant reduction of 3% of the chemical glutathione in the brain’s anterior cingulate cortex and 8% in the thalamus. Glutathione is made of three smaller molecules, and one of them is glutamate.

Next, the researchers asked how glutamate might be managed in the brain and whether that management is faulty in disease. They first looked at how it’s stored. Because glutamate is a building block of glutathione, the researchers wondered if the brain might use glutathione as a way to store extra glutamate. And if so, the researchers questioned if they could use known drugs to shift this balance to either release glutamate from storage when there isn’t enough, or send it into storage if there is too much.

In another study, described in the Feb. 12 issue of the journal PNAS, the team used the drug L-Buthionine sulfoximine in rat brain cells to block an enzyme that turns glutamate into glutathione, allowing it to be used up. The researchers found that theses nerves were more excited and fired faster, which means they were sending more messages to other brain cells. The researchers say shifting the balance this way is akin to shifting the brain cells to a pattern similar to one found in the brains of people with schizophrenia. Next, the researchers wanted to see if they could do the opposite and shift the balance to get more glutamate stored in the form of glutathione. They used the chemical sulforaphane found in broccoli sprouts, which is known to turn on a gene that makes more of the enzyme that sticks glutamate with another molecule to make glutathione. When they treated rat brain cells with glutathione, it slowed the speed at which the nerve cells fired, meaning they were sending fewer messages. The researchers say this pushed the brain cells to behave less like the pattern found in brains with schizophrenia.

“We are thinking of glutathione as glutamate stored in a gas tank,” says Thomas Sedlak, M.D., Ph.D., assistant professor of psychiatry and behavioral sciences. “If you have a bigger gas tank, you have more leeway on how far you can drive, but as soon as you take the gas out of the tank it’s burned up quickly. We can think of those with schizophrenia as having a smaller gas tank.”

Because sulforaphane changed the glutamate imbalance in the rat brains and affected how messages were transmitted between the rat brain cells, the researchers wanted to test whether sulforaphane could change glutathione levels in healthy people’s brains and see if this could eventually be a strategy for people with mental disorders. For their study, published in April 2018 in Molecular Neuropsychiatry, the researchers recruited nine healthy volunteers (four women, five men) to take two capsules with 100 micromoles daily of sulforaphane in the form of broccoli sprout extract for seven days.

The volunteers reported that a few of them were gassy and some had stomach upset when eating the capsules on an empty stomach, but overall the sulforaphane was relatively well tolerated.

The researchers used MRS again to monitor three brain regions for glutathione levels in the healthy volunteers before and after taking sulforaphane. They found that after seven days, there was about a 30% increase in average glutathione levels in the subjects’ brains. For example, in the hippocampus, glutathione levels rose an average of 0.27 millimolar from a baseline of 1.1 millimolar after seven days of taking sulforaphane.

The scientists say further research is needed to learn whether sulforaphane can safely reduce symptoms of psychosis or hallucinations in people with schizophrenia. They would need to determine an optimal dose and see how long people must take it to observe an effect. The researchers caution that their studies don’t justify or demonstrate the value of using commercially available sulforaphane supplements to treat or prevent schizophrenia, and patients should consult their physicians before trying any kind of over-the-counter supplement. Versions of sulforaphane supplementsare sold in health food stores and at vitamin counters, and aren’t regulated by the U.S. Food and Drug Administration.

“For people predisposed to heart disease, we know that changes in diet and exercise can help stave off the disease, but there isn’t anything like that for severe mental disorders yet,” says Sedlak. “We are hoping that we will one day make some mental illness preventable to a certain extent.”

Sulforaphane is found in a variety of cruciferous vegetables, and was first identified as a “chemoprotective” substance decades ago by Paul Talalay and Jed Fahey at Johns Hopkins.

According to the World Health Organization, schizophrenia affects about 21 million people worldwide.

https://www.eurekalert.org/pub_releases/2019-05/jhm-bsc050619.php

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ummary: Study identifies 104 high-risk genes for schizophrenia. One gene considered high-risk is also suspected in the development of autism.

Source: Vanderbilt University

Using a unique computational framework they developed, a team of scientist cyber-sleuths in the Vanderbilt University Department of Molecular Physiology and Biophysics and the Vanderbilt Genetics Institute (VGI) has identified 104 high-risk genes for schizophrenia.

Their discovery, which was reported April 15 in the journal Nature Neuroscience, supports the view that schizophrenia is a developmental disease, one which potentially can be detected and treated even before the onset of symptoms.

“This framework opens the door for several research directions,” said the paper’s senior author, Bingshan Li, PhD, associate professor of Molecular Physiology and Biophysics and an investigator in the VGI.

One direction is to determine whether drugs already approved for other, unrelated diseases could be repurposed to improve the treatment of schizophrenia. Another is to find in which cell types in the brain these genes are active along the development trajectory.

Ultimately, Li said, “I think we’ll have a better understanding of how prenatally these genes predispose risk, and that will give us a hint of how to potentially develop intervention strategies. It’s an ambitious goal … (but) by understanding the mechanism, drug development could be more targeted.”

Schizophrenia is a chronic, severe mental disorder characterized by hallucinations and delusions, “flat” emotional expression and cognitive difficulties.

Symptoms usually start between the ages of 16 and 30. Antipsychotic medications can relieve symptoms, but there is no cure for the disease.

Genetics plays a major role. While schizophrenia occurs in 1% of the population, the risk rises sharply to 50% for a person whose identical twin has the disease.

Recent genome-wide association studies (GWAS) have identified more than 100 loci, or fixed positions on different chromosomes, associated with schizophrenia. That may not be where high-risk genes are located, however. The loci could be regulating the activity of the genes at a distance — nearby or very far away.

To solve the problem, Li, with first authors Rui Chen, PhD, research instructor in Molecular Physiology and Biophysics, and postdoctoral research fellow Quan Wang, PhD, developed a computational framework they called the “Integrative Risk Genes Selector.”

The framework pulled the top genes from previously reported loci based on their cumulative supporting evidence from multi-dimensional genomics data as well as gene networks.

Which genes have high rates of mutation? Which are expressed prenatally? These are the kinds of questions a genetic “detective” might ask to identify and narrow the list of “suspects.”

The result was a list of 104 high-risk genes, some of which encode proteins targeted in other diseases by drugs already on the market. One gene is suspected in the development of autism spectrum disorder.

Much work remains to be done. But, said Chen, “Our framework can push GWAS a step forward … to further identify genes.” It also could be employed to help track down genetic suspects in other complex diseases.

Also contributing to the study were Li’s lab members Qiang Wei, PhD, Ying Ji and Hai Yang, PhD; VGI investigators Xue Zhong, PhD, Ran Tao, PhD, James Sutcliffe, PhD, and VGI Director Nancy Cox, PhD.

Chen also credits investigators in the Vanderbilt Center for Neuroscience Drug Discovery — Colleen Niswender, PhD, Branden Stansley, PhD, and center Director P. Jeffrey Conn, PhD — for their critical input.

Funding: The study was supported by the Vanderbilt Analysis Center for the Genome Sequencing Program and National Institutes of Health grant HG009086.

https://neurosciencenews.com/high-risk-schizophrenia-genes-12021/

In a small study of patients referred to the Johns Hopkins Early Psychosis Intervention Clinic (EPIC), researchers report that about half the people referred to the clinic with a schizophrenia diagnosis did not actually have schizophrenia. People who reported hearing voices or having anxiety were the ones more likely to be misdiagnosed, according to the study published in the Journal of Psychiatric Practice.

The researchers say that therapies can vary widely for people with schizophrenia, bipolar disorder, major depression or other serious types of mental illness, and that misdiagnosis can lead to inappropriate or delayed treatment.

The findings, the researchers say, suggest that second opinions at a specialised schizophrenia clinic after initial diagnosis are wise efforts to reduce the risk of misdiagnosis, and ensure prompt and appropriate patient treatment.

“Because we’ve shined a spotlight in recent years on emerging and early signs of psychosis, diagnosis of schizophrenia is like a new fad, and it’s a problem especially for those who are not schizophrenia specialists because symptoms can be complex and misleading,” says Krista Baker, LCPC, Johns Hopkins Medicine, Baltimore, Maryland. “Diagnostic errors can be devastating for people, particularly the wrong diagnosis of a mental disorder,” she adds.

According to the National Institute of Mental Health, schizophrenia affects an estimated 0.5% of the world population, and is more common in men. It typically arises in the late adolescences, 20s and even as late as the early 30s in women. Symptoms such as disordered thinking, hallucinations, delusions, reduced emotions and unusual behaviours can be disabling, and drug treatments often create difficult side effects.

The new study was prompted in part by anecdotal evidence among healthcare providers in Baker’s specialty clinic that a fair number of people were being seen who were misdiagnosed. These patients usually had other mental illnesses, such as depression.

To see if there was rigorous evidence of such a trend, the researchers looked at patient data from 78 cases referred to EPIC for consultation between February 2011 and July 2017. Patients were an average age of 19, and about 69% were men, 74% were white, 12% African American and 14% were another ethnicity. Patients were referred to the clinic by general psychiatrists, outpatient psychiatric centres, primary care physicians, nurse practitioners, neurologists or psychologists.

Each consultation by the clinic took 3 to 4 hours, and included interviews with the patient and the family, physical exams, questionnaires, and medical and psychosocial histories.

Of the patients referred to the clinic, 54 people came with a predetermined diagnosis of a schizophrenia spectrum disorder. Of those, 26 received a confirmed diagnosis of a schizophrenia spectrum disorder following their consultation with the EPIC team, which is composed of clinicians and psychiatrists. Of the 54 cases, 51% were rediagnosed by clinic staff as having anxiety or mood disorders. Anxiety symptoms were prominent in 14 of the misdiagnosed patients.

One of the other most common symptoms that the researchers believe may have contributed to misdiagnosis of schizophrenia was hearing voices, as almost all incorrectly diagnosed patients reported auditory hallucinations.

“Hearing voices is a symptom of many different conditions, and sometimes it is just a fleeting phenomenon with little significance,” says Russell L. Margolis, MD, Johns Hopkins Schizophrenia Center, Johns Hopkins University School of Medicine, Baltimore, Maryland. “At other times when someone reports ‘hearing voices’ it may be a general statement of distress rather than the literal experience of hearing a voice. The key point is that hearing voices on its own doesn’t mean a diagnosis of schizophrenia.”

In speculating about other reasons why there might be so many misdiagnoses, the researchers say that it could be due to overly simplified application of criteria listed in the Diagnostic Statistical Manual of Mental Disorders, a standard guide to the diagnosis of psychiatric disorders.

“Electronic medical record systems, which often use pull-down diagnostic menus, increase the likelihood of this type of error,” says Dr. Margolis, who refers to the problem as “checklist psychiatry.”

“The big take-home message from our study is that careful consultative services by experts are important and likely underutilised in psychiatry,” says Dr. Margolis. “Just as a primary care clinician would refer a patient with possible cancer to an oncologist or a patient with possible heart disease to a cardiologist, it’s important for general mental health practitioners to get a second opinion from a psychiatry specialty clinic like ours for patients with confusing, complicated or severe conditions. This may minimise the possibility that a symptom will be missed or overinterpreted.”

Dr. Margolis cautioned that the study was limited to patients evaluated in 1 clinic. Nonetheless, he was encouraged by the willingness of so many patients, their families and their clinicians to ask for a second opinion from the Johns Hopkins clinic. If further study confirms their findings, it would lend support to the belief by the Johns Hopkins team that overdiagnosis may be a national problem, because they see patients from across the country who travel to Johns Hopkins for an opinion. They hope to examine the experience of other specialty consultation clinics in the future.

Reference: doi: 10.1097/PRA.0000000000000363

SOURCE: Johns Hopkins Medicine

https://dgnews.docguide.com/reported-symptoms-anxiety-hearing-voices-most-common-reasons-misdiagnosis-schizophrenia?overlay=2&nl_ref=newsletter&pk_campaign=newsletter&nl_eventid=20124


Dr. Lewis L. Judd led the National Institute of Mental Health from 1988 to 1990. (National Library of Medicine)

By Emily Langer

Lewis L. Judd, a nationally known psychiatrist who helped turn the focus of his profession from psychoanalysis to neuroscience, an approach that sought to destigmatize mental illness by treating it as cancer, heart disease or any other medical problem, died Dec. 16 in La Jolla, Calif. He was 88.

The cause was cardiac arrest, said his wife, Pat Judd.

For decades, psychiatrists were schooled in the theories of Sigmund Freud, the founder of psychoanalysis, who posited that mental disturbances could be treated through dialogue with a therapist. Practitioners sought to interpret their patients’ dreams, giving little attention to the physical functioning of the brain or the chemicals that regulate it.

Dr. Judd agreed, he once told the Associated Press, that a physician must look at patients as a “whole individual,” with all their “worries, concerns, aspirations and needs,” and not resort to simply “popping a pill in their mouth.” But he found the long-prevailing psychoanalytic approach too limiting to explain or treat afflictions such as depression, bipolar disorder, severe anxiety and schizophrenia — “these serious mental disorders that have defied our understanding for centuries,” he once told the Chicago Tribune.

Instead, he advocated a biological approach, starting at the molecular level of the brain. As director of the National Institute of Mental Health in Bethesda, Md. — a post he held from 1988 to 1990, during a hiatus from his decades-long chairmanship of the psychiatry department at the University of California at San Diego — he helped launch a federal research initiative known as the “Decade of the Brain.”

“He was obsessed with educating the public and the profession . . . that mental illnesses were biological illnesses, that schizophrenia and depression were diseases of the brain,” Alan I. Leshner, Dr. Judd’s deputy at NIMH and later chief executive of the American Association for the Advancement of Science, said in an interview. “At the time, that was a heretical thought.”

Today, the biological component of many mental illnesses is widely accepted. When Dr. Judd led NIMH, it was not; he once cited a survey in which 71 percent of respondents said mental illness was a result of personal weakness and a third attributed it to sinful behavior. Poor parenting was another common alleged culprit.

Dr. Judd argued that the biological approach to psychiatry held the promise not only of deepening understanding of the body’s most complex organ but of improving lives: If mental disorders could be shown to be a result of brain chemistry or of physical dysfunction, patients might feel less stigmatized and therefore more willing to seek treatment.

“We look at the homeless and feel that if they only got their act together, they could lift themselves up,” Dr. Judd told the Los Angeles Times in 1988, discussing the prevalence of mental illness among homeless people. “We would never believe that about someone who has cancer or some other physical disease.”

As head of NIMH, which is an arm of the National Institutes of Health and the chief federal agency for research on mental illness, Dr. Judd oversaw more than $500 million in research money. He described the Decade of the Brain — a designation conferred by Congress and President George H.W. Bush — as a “research plan designed to bring a precise and detailed understanding of all the elements of brain function within our own lifetimes.”

During his tenure at NIMH, scientists for the first time successfully grew brain tissue in a laboratory. Dr. Judd was among those scientists who touted the potential of medical imaging, such as MRIs and PET scans, to reveal the inner workings of the brain and the potential causes of diseases such as schizophrenia.

Almost 30 years after the Decade of the Brain began, much about the organ remains elusive. Leshner credited the initiative with helping bring attention to the importance of brain research as well as inspiring the Brain Initiative, a public-private research effort advanced by the Obama administration.

“The brain is really the last frontier for scientists,” Dr. Judd said.

Lewis Lund Judd was born in Los Angeles on Feb. 10, 1930. His father was an obstetrician-gynecologist, and his mother was a homemaker. Dr. Judd’s brother, Howard Judd, also became an OB/GYN and a noted researcher in women’s health at the University of California at Los Angeles.

Dr. Judd received a bachelor’s degree in psychology from the University of Utah in 1954 and a medical degree from UCLA in 1958. In the early years of his career, he served in the Air Force as a base psychiatrist.

He joined UC-San Diego in 1970 and became department chairman in 1977, helping grow his faculty into one of the most respected the country. He stepped down as chairman in 2013 and retired in 2015.

Dr. Judd’s first marriage, to Anne Nealy, ended in divorce. Survivors include his wife of 45 years, the former Patricia Hoffman, who is also a psychiatry professor at UC-San Diego, of La Jolla; three daughters from his first marriage, Allison Fee of Whidbey Island, Wash., Catherine Judd of Miami and Stephanie Judd of Chevy Chase, Md.; and four grandchildren.

Ever exploring the outer reaches of his field, Dr. Judd participated in a dialogue with the Dalai Lama in 1989 about life and the mind.

“Our model of mental health is mostly defined in terms of the absence of mental illness,” Dr. Judd told the New York Times, reflecting on the Tibetan Buddhist leader’s discussion of wisdom and compassion. “They may have more positive ones that might be worth our study.”

https://www.washingtonpost.com/local/obituaries/lewis-judd-psychiatrist-who-probed-the-science-of-the-brain-dies-at-88/2019/01/11/271e1f48-1549-11e9-b6ad-9cfd62dbb0a8_story.html?noredirect=on&utm_term=.18ed788ae8b3


Before light reaches these rods and cones in the retina, it passes through some specialized cells that send signals to brain areas that affect whether you feel happy or sad.

by Jon Hamilton

Just in time for the winter solstice, scientists may have figured out how short days can lead to dark moods.

Two recent studies suggest the culprit is a brain circuit that connects special light-sensing cells in the retina with brain areas that affect whether you are happy or sad.

When these cells detect shorter days, they appear to use this pathway to send signals to the brain that can make a person feel glum or even depressed.

“It’s very likely that things like seasonal affective disorder involve this pathway,” says Jerome Sanes, a professor of neuroscience at Brown University.

Sanes was part of a team that found evidence of the brain circuit in people. The scientists presented their research in November at the Society for Neuroscience meeting. The work hasn’t been published in a peer-reviewed journal yet, but the researchers plan to submit it.

A few weeks earlier, a different team published a study suggesting a very similar circuit in mice.

Together, the studies offer a strong argument that seasonal mood changes, which affect about 1 in 5 people, have a biological cause. The research also adds to the evidence that support light therapy as an appropriate treatment.

“Now you have a circuit that you know your eye is influencing your brain to affect mood,” says Samer Hattar, an author of the mouse study and chief of the section on light and circadian rhythms at the National Institute of Mental Health. The finding is the result of a decades-long effort to understand the elusive link between light and mood. “It is the last piece of the puzzle,” Hattar says.

The research effort began in the early 2000s, when Hattar and David Berson, a professor of neuroscience at Brown University, were studying cells in the retina.

At the time, most scientists thought that when light struck the retina, only two kinds of cells responded: rods and cones. But Hattar and Berson thought there were other light-sensitive cells that hadn’t been identified.

“People used to laugh at us if we say there are other photoreceptors distinct from rods and cones in the retina,” Hattar says.

The skeptics stopped laughing when the team discovered a third kind of photoreceptor that contained a light-sensitive substance called melanopsin not found in rods and cones. (The full name of these cells, if you’re interested, is intrinsically photosensitive retinal ganglion cells, or ipRGCs.) These receptors responded to light but weren’t part of the visual system.

Instead, their most obvious function was keeping the brain’s internal clock in sync with changes in daylight. And many scientists assumed that this circadian function also explained seasonal depression.

“People thought that the only reason you get mood problems is because your clock is misaligned,” Hattar says.

Other potential explanations included speculation that reduced sunlight was triggering depression by changing levels of serotonin, which can affect mood, or melatonin, which plays a role in sleep patterns and mood. But the evidence for either of these possibilities has been weak.

Hattar and Berson were pretty sure there was a better reason. And, after years of searching, they found one.

In September, Hattar’s team published a study about mice suggesting a direct pathway between the third kind of photoreceptor in the retina and brain areas that affect mood.

When these cells were present, an artificially shortened cycle of light and dark caused a version of depression in a mouse. But when the team removed the cells with gene-editing tools, the mouse didn’t become depressed.

Sanes knew about the research, in part because he and Berson are neuroscientists at Brown. And he was so intrigued by the discovery of the new pathway between retina and brain in mice that he decided to see whether something similar was going on in human brains.

Sanes’ team put young adults in an MRI machine and measured their brain activity as they were exposed to different levels of light. This allowed the team to identify brain areas that seemed to be receiving signals from the photoreceptors Hattar and Berson had discovered.

Two of these areas were in the front of the brain. “It’s interesting because these areas seem to be the areas that have been shown in many studies to be involved in depression and other affective disorders,” Sanes says.

The areas also appeared to be part of the same circuit found in mice.

The finding needs to be confirmed. But Hattar is pretty confident that this circuit explains the link between light exposure and mood.

So now he’s trying to answer a new question: Why would evolution produce a brain that works this way?

“You will understand why you would need light to see,” he says, “but why do you need light to make you happy?”

Hattar hopes to find out. In the meantime, he has some advice for people who are feeling low: “Try to take your lunch outside. That will help you adjust your mood.”

https://www.npr.org/sections/health-shots/2018/12/21/678342879/scientists-find-a-brain-circuit-that-could-explain-seasonal-depression

by Carly Cassella

Sticks and stones may break your bones, but name-calling could actually change the structure of your brain.

A new study has found that persistent bullying in high school is not just psychologically traumatising, it could also cause real and lasting damage to the developing brain.

The findings are drawn from a long-term study on teenage brain development and mental health, which collected brain scans and mental health questionnaires from European teenagers between the ages of 14 and 19.

Following 682 young people in England, Ireland, France and Germany, the researchers tallied 36 in total who reported experiencing chronic bullying during these years.

When the researchers compared the bullied participants to those who had experienced less intense bullying, they noticed that their brains looked different.

Across the length of the study, in certain regions, the brains of the bullied participants appeared to have actually shrunk in size.

In particular, the pattern of shrinking was observed in two parts of the brain called the putamen and the caudate, a change oddly reminiscent of adults who have experienced early life stress, such as childhood maltreatment.

Sure enough, the researchers found that they could partly explain these changes using the relationship between extreme bullying and higher levels of general anxiety at age 19. And this was true even when controlling for other types of stress and co-morbid depressive symptoms.

The connection is further supported by previous functional MRI studies that found differences in the connectivity and activation of the caudate and putamen activation in those with anxiety.

“Although not classically considered relevant to anxiety, the importance of structural changes in the putamen and caudate to the development of anxiety most likely lies in their contribution to related behaviours such as reward sensitivity, motivation, conditioning, attention, and emotional processing,” explains lead author Erin Burke Quinlan from King’s College London.

In other words, the authors think all of this shrinking could be a mark of mental illness, or at least help explain why these 19-year-olds are experiencing such unusually high anxiety.

But while numerous past studies have already linked childhood and adolescent bullying to mental illness, this is the very first study to show that unrelenting victimisation could impact a teenager’s mental health by actually reshaping their brain.

The results are cause for worry. During adolescence, a young person’s brain is absolutely exploding with growth, expanding at an incredible place.

And even though it’s normal for the brain to prune back some of this overabundance, in the brains of those who experienced chronic bullying, the whole pruning process appears to have spiralled out of control.

The teenage years are an extremely important and formative period in a person’s life, and these sorts of significant changes do not bode well. The authors suspect that as these children age, they might even begin to experience greater shrinkage in the brain.

But an even longer long-term study will need to be done if we want to verify that hunch. In the meantime, the authors are recommending that every effort be made to limit bullying before it can cause damage to a teenager’s brain and their mental health.

This study has been published in Molecular Psychiatry.

https://www.sciencealert.com/chronic-bullying-could-actually-reshape-the-brains-of-teens

by Rachel Metz

There are about 45 million people in the US alone with a mental illness, and those illnesses and their courses of treatment can vary tremendously. But there is something most of those people have in common: a smartphone.

A startup founded in Palo Alto, California, by a trio of doctors, including the former director of the US National Institute of Mental Health, is trying to prove that our obsession with the technology in our pockets can help treat some of today’s most intractable medical problems: depression, schizophrenia, bipolar disorder, post-traumatic stress disorder, and substance abuse.

Mindstrong Health is using a smartphone app to collect measures of people’s cognition and emotional health as indicated by how they use their phones. Once a patient installs Mindstrong’s app, it monitors things like the way the person types, taps, and scrolls while using other apps. This data is encrypted and analyzed remotely using machine learning, and the results are shared with the patient and the patient’s medical provider.

The seemingly mundane minutiae of how you interact with your phone offers surprisingly important clues to your mental health, according to Mindstrong’s research—revealing, for example, a relapse of depression. With details gleaned from the app, Mindstrong says, a patient’s doctor or other care manager gets an alert when something may be amiss and can then check in with the patient by sending a message through the app (patients, too, can use it to message their care provider).

For years now, countless companies have offered everything from app-based therapy to games that help with mood and anxiety to efforts to track smartphone activities or voice and speech for signs of depression. But Mindstrong is different, because it’s considering how users’ physical interactions with the phones—not what they do, but how they do it—can point to signs of mental illness. That may lead to far more accurate ways to track these problems over time. If Mindstrong’s method works, it could be the first that manages to turn the technology in your pocket into the key to helping patients with a wide range of chronic brain disorders—and may even lead to ways to diagnose them before they start.

Digital fingerprints
Before starting Mindstrong, Paul Dagum, its founder and CEO, paid for two Bay Area–based studies to figure out whether there might be a systemic measure of cognitive ability—or disability—hidden in how we use our phones. One hundred and fifty research subjects came into a clinic and underwent a standardized neurocognitive assessment that tested things like episodic memory (how you remember events) and executive function (mental skills that include the ability to control impulses, manage time, and focus on a task)—the kinds of high-order brain functions that are weakened in people with mental illnesses.

The assessment included neuropsychological tests that have been used for decades, like a so-called timed trail-­tracing test, where you have to connect scattered letters and numbers in the proper order—a way to measure how well people can shift between tasks. People who have a brain disorder that weakens their attention may have a harder time with this.

Subjects went home with an app that measured the ways they touched their phone’s display (swipes, taps, and keyboard typing), which Dagum hoped would be an unobtrusive way to log these same kinds of behavior on a smartphone. For the next year, it ran in the background, gathering data and sending it to a remote server. Then the subjects came back for another round of neurocognitive tests.

As it turns out, the behaviors the researchers measured can tell you a lot. “There were signals in there that were measuring, correlating—predicting, in fact, not just correlating with—the neurocognitive function measures that the neuropsychologist had taken,” Dagum says.

For instance, memory problems, which are common hallmarks of brain disorders, can be spotted by looking at things including how rapidly you type and what errors you make (such as how frequently you delete characters), as well as by how fast you scroll down a list of contacts. (Mindstrong can first determine your baseline by looking at how you use your handset and combining those characteristics with general measures.) Even when you’re just using the smartphone’s keyboard, Dagum says, you’re switching your attention from one task to another all the time—for example, when you’re inserting punctuation into a sentence.

He became convinced the connections presented a new way to investigate human cognition and behavior over time, in a way that simply isn’t possible with typical treatment like regularly visiting a therapist or getting a new medication, taking it for a month, and then checking back in with a doctor. Brain-disorder treatment has stalled in part because doctors simply don’t know that someone’s having trouble until it’s well advanced; Dagum believes Mindstrong can figure it out much sooner and keep an eye on it 24 hours a day.

In 2016, Dagum visited Verily, Alphabet’s life sciences company, where he pitched his work to a group including Tom Insel, a psychiatrist who had spent 13 years as director of the National Institute of Mental Health before he joined Verily in 2015.

Verily was trying to figure out how to use phones to learn about depression or other mental health conditions. But Insel says that at first, what Dagum presented—more a concept than a show of actual data—didn’t seem like a big deal. “The bells didn’t go off about what he had done,” he says.

Over several meetings, however, Insel realized that Dagum could do something he believed nobody in the field of mental health had yet been able to accomplish. He had figured out smartphone signals that correlated strongly with a person’s cognitive performance—the kind of thing usually possible only through those lengthy lab tests. What’s more, he was collecting these signals for days, weeks, and months on end, making it possible, in essence, to look at a person’s brain function continuously and objectively. “It’s like having a continuous glucose monitor in the world of diabetes,” Insel says.

Why should anyone believe that what Mindstrong is doing can actually work? Dagum says that thousands of people are using the app, and the company now has five years of clinical study data to confirm its science and technology. It is continuing to perform numerous studies, and this past March it began working with patients and doctors in clinics.

In its current form, the Mindstrong app that patients see is fairly sparse. There’s a graph that updates daily with five different signals collected from your smartphone swipes and taps. Four of these signals are measures of cognition that are tightly tied to mood disorders (such as the ability to make goal-based decisions), and the other measures emotions. There’s also an option to chat with a clinician.

For now, Insel says, the company is working mainly with seriously ill people who are at risk of relapse for problems like depression, schizophrenia, and substance abuse. “This is meant for the most severely disabled people, who are really needing some innovation,” he says. “There are people who are high utilizers of health care and they’re not getting the benefits, so we’ve got to figure out some way to get them something that works better.” Actually predicting that a patient is headed toward a downward spiral is a harder task, but Dagum believes that having more people using the app over time will help cement patterns in the data.

There are thorny issues to consider, of course. Privacy, for one: while Mindstrong says it protects users’ data, collecting such data at all could be a scary prospect for many of the people it aims to help. Companies may be interested in, say, including it as part of an employee wellness plan, but most of us wouldn’t want our employers anywhere near our mental health data, no matter how well protected it may be.

Spotting problems before they start
A study in the works at the University of Michigan is looking at whether Mindstrong may be beneficial for people who do not have a mental illness but do have a high risk for depression and suicide. Led by Srijan Sen, a professor of psychiatry and neuroscience, the study tracks the moods of first-year doctors across the country—a group that is known to experience intense stress, frequent sleep deprivation, and very high rates of depression.

Participants log their mood each day and wear a Fitbit activity tracker to log sleep, activity, and heart-rate data. About 1,500 of the 2,000 participants also let a Mindstrong keyboard app run on their smartphones to collect data about the ways they type and figure out how their cognition changes throughout the year.

Sen hypothesizes that people’s memory patterns and thinking speed change in subtle ways before they realize they’re depressed. But he says he doesn’t know how long that lag will be, or what cognitive patterns will be predictive of depression.

Insel also believes Mindstrong may lead to more precise diagnoses than today’s often broadly defined mental health disorders. Right now, for instance, two people with a diagnosis of major depressive disorder might share just one of numerous symptoms: they could both feel depressed, but one might feel like sleeping all the time, while the other is hardly sleeping at all. We don’t know how many different illnesses are in the category of depression, Insel says. But over time Mindstrong may be able to use patient data to find out. The company is exploring how learning more about these distinctions might make it possible to tailor drug prescriptions for more effective treatment.

Insel says it’s not yet known if there are specific digital markers of, say, auditory hallucinations that someone with schizophrenia might experience, and the company is still working on how to predict future problems like post-traumatic stress disorder. But he is confident that the phone will be the key to figuring it out discreetly. “We want to be able to do this in a way that just fits into somebody’s regular life,” he says.

https://www.technologyreview.com/s/612266/the-smartphone-app-that-can-tell-youre-depressed-before-you-know-it-yourself/