In a study published in Addiction Biology, researchers uncovered significant associations between use of electronic devices and signs of depression and anxiety, as well as cigarette smoking and alcohol drinking. The team also found certain genetic variants that were linked with these traits.
A review of studies on smartphone addiction found that anxiety and depression were commonly mediated mental health problems. A wide range of physical health sequelae was also associated with smartphone addiction. Furthermore, there was an association between smartphone addiction and neurological disorders.
The study included data on hundreds of thousands of individuals from the UK Biobank. Three indicators of use of electronic devices were included in the study: TV watching, computer using, and computer playing.
Their findings suggested that electronic devices use was associated with common mental traits and provided new clues for understanding genetic architecture of mental traits.
The authors wrote that the study’s findings suggest that reducing time spent using electronic devices may help reduce mental health burdens.
In a new study published in International Psychogeriatrics, researchers report that a shortened, seven-item scale can help determine a person’s level of wisdom, a potentially modifiable personality trait shown to be strongly associated with well-being.
Previously, the researchers had developed the 28-item San Diego Wisdom Scale (SD-WISE-28), which has been used in large national and international studies, biological research and clinical trials to evaluate wisdom.
But researchers found that an abbreviated seven-item version (SD-WISE-7 or Jeste-Thomas Wisdom Index), was comparable and reliable.
“Wisdom measures are increasingly being used to study factors that impact mental health and optimal aging. We wanted to test if a list of only seven items could provide valuable information to test wisdom,” said senior author Dilip V. Jeste, MD.
Past studies have shown that wisdom is comprised of seven components: self-reflection, pro-social behaviours (such as empathy, compassion and altruism), emotional regulation, acceptance of diverse perspectives, decisiveness, social advising (such as giving rational and helpful advice to others) and spirituality.
The latest study surveyed 2093 participants online, ages 20 to 82. The seven statements, selected from SD-WISE-28, relate to the seven components of wisdom and are rated on a 1 to 5 scale, from strongly disagree to strongly agree. Examples of the statements include “I remain calm under pressure” and “I avoid situations where I know my help will be needed.”
“Shorter doesn’t mean less valid,” said Dr Jeste. “We selected the right type of questions to get important information that not only contributes to the advancement of science but also supports our previous data that wisdom correlates with health and longevity.”
In addition, the SD-WISE-7 was found to strongly and positively correlate with resilience, happiness and mental well-being and strongly and negatively correlate with loneliness, depression and anxiety.
“There are evidence-based interventions to increase levels of specific components of wisdom, which would help reduce loneliness and promote overall well-being,” said Dr Jeste.
“Like the COVID vaccine protects us from the novel coronavirus, wisdom can aid in protecting us from loneliness. Thus, we can potentially help end a behavioural pandemic of loneliness, suicides and opioid abuse that has been going on for the last 20 years.”
Next steps include genetic, biological, psychosocial and cultural studies of large numbers of diverse populations to assess wisdom, as well as various factors related to mental, physical and cognitive health in people across the lifespan.
“We need wisdom for surviving and thriving in life. Now, we have a list of questions that take less than a couple of minutes to answer that can be put into clinical practice to try to help individuals,” said Dr Jeste.
The findings of a study published in Science Translational Medicine paint a new picture of how current antidepressant drugs work and suggest a new drug target in depression. As with most drugs, antidepressants were developed through trial and observation. Some 40% of patients with the disorder don’t respond adequately to the drugs, and when they do work, antidepressants take weeks to provide relief. Why this is has remained largely a mystery.
To figure out why these drugs have a delayed onset, the team examined a mouse model of chronic stress that leads to changes in behaviours controlled by the hippocampus. The hippocampus is vulnerable to stress and atrophies in people with major depression or schizophrenia. Mice exposed to chronic stress show cognitive deficits, a hallmark of impaired hippocampal function.
“Cognitive impairment is a key feature of major depressive disorder, and patients often report that difficulties at school and work are some of the most challenging parts of living with depression. Our ability to model cognitive impairment in lab mice gives us the chance to try and understand how to treat these kinds of symptoms,” said Professor Dane Chetkovich, MD, PhD, who led the study.
The study focussed on an ion transporter channel in nerve cell membranes known as the HCN channel. Previous work has shown HCN channels have a role in depression and separately to have a role in regulation of cognition. According to the authors, this was the first study to explicitly link the two observations.
Examination of postmortem hippocampal samples led the team to establish that HCN channels are more highly expressed in people with depression. HCN channel activity is modulated by a small signaling molecule called cAMP, which is increased by antidepressants. The team used protein receptor engineering to increase cAMP signaling in mice and establish in detail the effects this has on hippocampal HCN channel activity and, through that connection, on cognition.
Turning up cAMP was found to initially increase HCN channel activity, limit the intended effects of antidepressants and negatively impact cognition (as measured in standard lab tests).
However, a total reversal took place over a period of some weeks. Previous work by the researchers had established that an auxiliary subunit of the HCN channel, TRIP8b, is essential for the channel’s role in regulating animal behaviour. The new study shows that, over weeks, a sustained increase in cAMP starts to interfere with TRIP8b’s ability to bind to the HCN channel, thereby quieting the channel and restoring cognitive abilities.
“This leaves us with acute and chronic changes in cAMP, of the sort seen in antidepressant drug therapy, seen here for the first time to be regulating the HCN channel in the hippocampus in two distinct ways, with opposing effects on behaviour,” Prof Chetkovich said. “This appears to carry promising implications for new drug development, and targeting TRIP8b’s role in the hippocampus more directly could help to more quickly address cognitive deficits related to chronic stress and depression.”
To find better solutions to mental illness, a Virginia Tech researcher has found that long-banned psychedelic drugs can treat several forms of mental illness and, in mice, have achieved long-lasting results from just one dose.
Using a process his lab developed in 2015, Professor Chang Lu is helping his collaborators study the epigenomic effects of serotonergic hallucinogens, commonly known as psychedelics.
Their findings, published in Cell Reports, give insight into how psychedelic substances like psilocybin, mescaline, LSD, and similar drugs may relieve symptoms of addiction, anxiety, depression, and post-traumatic stress disorder. The drugs seem to work faster and last longer than current medications, all with fewer side effects.
Prof Lu’s genomic analysis allows researchers to use very small samples of tissue, down to hundreds to thousands of cells, and draw meaningful conclusions from them. Older processes require much larger sample sizes, so Prof Lu’s approach enables the studies using just a small quantity of material from a specific region of a mouse brain.
And looking at the effects of psychedelics on brain tissues is especially important.
While researchers can do human clinical trials with them, taking blood and urine samples and observing behaviours, Prof Lu said. “But the thing is, the behavioural data will tell you the result, but it doesn’t tell you why it works in a certain way,” he said.
But looking at molecular changes in animal models, such as the brains of mice, allows scientists to peer into what Prof Lu calls the black box of neuroscience to understand the biological processes at work. While the brains of mice are very different from human brains, Prof Lu said there are enough similarities to make valid comparisons between the two.
VCU pharmacologist Javier González-Maeso has made a career of studying psychedelics, which had previously been banned since the 1960s. Other research, primarily on psilocybin, a substance found in more than 200 species of fungi, González-Maeso said psychedelics have shown promise in alleviating major depression and anxiety disorders. “They induce profound effects in perception,” he said. “But I was interested in how these drugs actually induce behavioral effects in mice.”
To explore the genomic basis of those effects, he teamed up with Prof Lu.
In the joint study, González-Maeso’s team used 2,5-dimethoxy-4-iodoamphetamine, or DOI, a drug similar to LSD, administering it to mice that had been trained to fear certain triggers. Prof Lu’s lab then analysed brain samples. They discovered that the epigenomic variations were generally more long-lasting than the changes in gene expression, thus more likely to link with the long-term effects of a psychedelic.
After one dose of DOI, the mice that had reacted to fear triggers no longer responded to them with anxious behaviours. Their brains also showed effects, even after the substance was no longer detectable in the tissues, Prof Lu said.
As well as the science, it’s personal for him too, saying: “My older brother has had schizophrenia for the last 30 years, basically. So I’ve always been intrigued by mental health,” Lu said. “And then once I found that our approach can be applied to look at processes like that – that’s why I decided to do research in the field of brain neuroscience.”
González-Maeso said research on psychedelics is still in its early stages, and there’s much work to be done before treatments derived from them could be widely available.
Instead of being negatively impacted when looking in the mirror, it may in fact help positively alter behaviour in individuals with obesity, according to an analysis published in the Journal of Clinical Nursing.
The analysis examined the results of five studies that included 16 to 941 participants each. The results indicated that the mirror can be used to decrease anxiety and body dissatisfaction. Furthermore, investigators noted that when individuals spend a few minutes gazing at themselves in a therapeutic environment, they may attain self‐awareness that will elicit a positive change in their behaviour.
“Self-assessment and reflection are key to overall wellbeing. Our review hopes to introduce the mirror as a healthcare tool to combat obesity,” said lead author Harriet Omondi, MSN, FNP-C, of Texas Woman’s University.
New research finds no evidence that violence increases after the release of a new video game.
Violent video games like Call of Duty are often linked by the media and public to real-life violence, although there is limited evidence to support the link. Debate on the topic generally intensifies after mass public shootings, with some commentators linking these violent acts to the perpetrators’ interests in violent video games. But different factors have been pointed out as more likely explanations, such as mental health issues and/or easy access to guns.
Before governments introduce any policies restricting access to violent video games, it is important to establish whether violent video games do indeed increase players’ violence in the real world.
Taking data from the US, Dr Agne Suziedelyte at University of London, provides evidence of the effects of violent video game releases on the violent behaviour of children. Dr Suziedelyte examined the effects of violent video games on two types of violence: aggression against other people, and destruction of objects or property.
By using econometric methods which identify plausibly causal effects of violent video games on violence, rather than only associations, Dr Suziedelyte found no evidence that violence against other people increases after the release of a new violent video game. Parents reported, however, that children were more likely to destroy things after playing violent video games.
Dr Suziedelyte said: “Taken together, these results suggest that violent video games may agitate children, but this agitation does not translate into violence against other people — which is the type of violence which we care about most.
“A likely explanation for my results is that video game playing usually takes place at home, where opportunities to engage in violence are lower. This ‘incapacitation’ effect is especially important for violence-prone boys who may be especially attracted to violent video games.
“Therefore, policies that place restrictions on video game sales to minors are unlikely to reduce violence.
People who are easily distracted are more susceptible to psychological distress and mental health issues from high levels of social media use, according to a study published in the Journal of Affective Disorders. The study tracked the phone data of 69 participants ranging from 18 to 58 year-olds to see their usage of popular apps including Instagram and Reddit over a week period.
Using an eye gaze test, the researchers tracked participants’ levels of distraction and inattention. The Depression Anxiety Stress Scale, a well-known psychological scale, was used to measure and quantify measures of distress.
Lead researcher Tamsin Mahalingham, Master’s student at Curtin University, said that the results showed a strong connection with low levels of attention control and high social media use negatively impacting mental health.
“Past research has flagged concerns about the negative mental health effects from high levels of social media use, but there isn’t clear evidence about why this is, or who might be most at risk,” Miss Mahalingham said.
“Our findings suggest that if you are a very distractable person, high levels of social media use may be particularly bad for your mental health. Study results revealed that those who showed lower levels of attention control were particularly at risk of negative mental health effects of heavy social media use.”
“This inability to stay focussed may lead to exposure to more irrelevant and distracting information and potentially longer durations of social media use. On the other hand, those with higher levels of attention control may be able to more easily ignore irrelevant and potentially damaging information in news feeds such as advertising.”
Supervising researcher, Dr Patrick Clarke, said that the increased follow-on effects of greater social media use that could negatively impact emotional wellbeing.
“Social media apps are designed to draw us in and keep us engaged and the longer we spend on social media, the more we can be exposed to including negative content, or content leading to self-comparison to unattainable ideals, like those often illustrated by influencers,” Dr. Clarke said.
“More time on social media also means less time doing other, possibly more important or more productive tasks, which can also increase feelings of depression and anxiety.
“Our research helps to understand who is most at risk from the adverse mental health effects of social media use and suggests that improving attention may minimize those risks.”
New research has found that post-traumatic stress disorder symptoms in women may vary over the course of the menstrual cycle, with more symptoms during the cycle’s first few days when the hormone oestradiol is low and fewer symptoms close to ovulation, when oestradiol is high.
The results could have implications for PTSD diagnosis and treatment, said lead author Jenna Rieder, PhD, an assistant professor of psychology at Thomas Jefferson University in Philadelphia. “When in the cycle you assess women might actually affect whether they meet diagnostic criteria for PTSD, especially for people who are right on the border. And that can have real practical implications, say, for someone who is a veteran and entitled to benefits or for health insurance purposes.”
Oestradiol is a form of oestrogen that regulates the menstrual cycle. During the follicular phase, rising oestradiol levels trigger a cascade of events that result in ovulation. Studies have linked low-oestradiol portions of the cycle to greater activation in the limbic areas of the brain, which are related to emotion, and to lower activation in the prefrontal cortex when viewing emotional content. Low oestradiol has also been linked to greater stress and anxiety as well as increased fear responses.
To find out whether those links were related to traua response, researchers studied 40 women, aged 18 to 33, all of whom had experienced or witnessed a traumatic event, such as a serious injury or sexual violence. In the lab, researchers measured the participants’ level of oestradiol in their saliva, then asked them to describe the trauma that had happened to them and the PTSD symptoms they’d experienced in the past month. They found that lower oestradiol was associated with greater self-reported symptom severity in the participants.
The researchers also measured two stress biomarkers in participants’ saliva, the hormone cortisol and the enzyme salivary alpha-amylase, before and after the participants described their trauma. Salivary alpha-amylase is related to the “fight-or-flight” stress response, and cortisol is related to the body’s slower, more sustained stress response.
“In a healthy system we want a moderate, coordinated response of both of these biomarkers,” Prof Rieder said. In the women in the low-oestradiol portions of their menstrual cycles, the researchers instead found low cortisol and high salivary alpha-amylase levels resulting from recounting their trauma stories – a pattern that’s been linked in previous studies with maladaptive stress responses.
The researchers then asked the participants to answer five daily questionnaires for 10 days spanning the high- and low-oestradiol portions of their menstrual cycles. The questionnaires measured how participants were feeling at each time (from “extremely unpleasant” to “extremely pleasant” and “extremely nonstimulated or activated” to “extremely stimulated or activated”). Participants also completed a PTSD symptom checklist each evening.
Participants were found to have greater variability in their daily moods during the low-oestradiol days of their cycle and reported more severe PTSD symptoms on those days.
This could have implications for diagnosis and treatment of PTSD in women, who have long been underrepresented in PTSD research. “PTSD for a long time was mostly studied in men, in part because it was mainly studied in veterans, who were mostly men,” Prof Rieder said.
As well as its relevance to diagnosis, knowing how the menstrual cycle affects PTSD symptoms could be useful for both clinicians and patients, according to Prof Rieder. “I think this is something that clinicians would want to know, so they can impart this knowledge as part of psychoeducation,” she said. “For women who are naturally cycling, it may be useful to understand how the menstrual cycle affects their symptoms. When you can explain what’s happening biologically, it often becomes less threatening.”
A case study details three teenagers with mild or asymptomatic COVID presented with suicidal thoughts, “paranoia-like fears,” delusions and “foggy brain”, which could be explained by anti-neural antibodies – ‘turncoat’ antibodies that may attack brain tissue.
Mounting evidence points to neurological and psychiatric effects of COVID, with a UK study finding a 13% risk of a first-time diagnosis after COVID. The study, published in JAMA Neurology, is the first to look at anti-neural antibodies in paediatric patients previously infected with SARS-CoV-2.
Over five months in 2020, 18 children and teens were hospitalised with confirmed COVID at UCSF Benioff Children’s Hospital San Francisco, three of whom were the patients in the study who underwent neurological evaluations.
The researchers examined the patients’ cerebrospinal fluid (CSF) and found that two of the patients, both of whom had histories of unspecified depression and/or anxiety, had antibodies indicating that SARS-CoV-2 may have invaded the central nervous system. They also had anti-neural antibodies in their CSF, suggesting a rampant immune system accidentally targeting the brain.
The research follows a previous UCSF study that also found a high level of autoantibodies in the cerebrospinal fluid of adult patients with acute COVID, who experienced neurological symptoms, including intractable headaches, seizures and loss of smell.
“It is way too soon to know whether COVID is a common trigger for neuropsychiatric illnesses, but it does seem to be a potent trigger for the development of autoantibodies,” said co-corresponding author Samuel Pleasure, MD, PhD. “It is currently totally unknown whether patients predisposed to neuropsychiatric illnesses are more likely to develop worsened symptoms after COVID, or whether COVID infection can act as an independent trigger.”
Unlike most psychiatric presentations, the three patients in the UCSF study had symptoms with sudden onset and rapid progression, representing a marked change from their baselines, said co-first author Claire Johns, MD. “The patients had significant neuropsychiatric manifestations despite mild respiratory symptoms, suggesting potential short and long-term effects of COVID.”
After hospitalisations lasting weeks and ongoing psychiatric medications, the two UCSF patients, whose cerebrospinal fluid tested positive for SARS-CoV-2 antibodies and anti-neural antibodies, were treated with intravenous immunoglobulin, an immunomodulatory therapy that curbs inflammation in autoimmune disorders. After five days, the first patient had “more organised thoughts, decreased paranoia and improved insight.”
Autoantibodies targeting the protein TCF4 were also found, which has genetic links in some schizophrenia cases. However, “we don’t know that the antibodies are actually interfering with the protein’s function,” said co-corresponding author, Michael R. Wilson, MD, noting that the diagnosis of schizophrenia is based on a constellation of symptoms, not a biomarker. The second patient partially responded to immunotherapy with improved cognition and working memory, but continued to have “impaired mood and cognitive symptoms” six months later. The third patient, with no psychiatric history and without SARS-CoV-2 antibodies or anti-neural antibodies in their cerebrospinal fluid, recovered with psychiatric medications. Their symptoms were attributed to recreational drug use.
In another case study, a 30-year-old patient with mildly symptomatic COVID who presented at a hospital emergency department with delusions, violent outbursts, hyper-anxiety and paranoia was unresponsive to antipsychotic medication but after being diagnosed with possible “autoimmune-mediated psychosis”, responded to intravenous immunoglobulin.
Nonetheless, the researchers agree it’s unlikely that there were pre-existing autoantibodies, and they point to other disorders with psychiatric symptoms, like anti-NMDAR encephalitis syndrome, that are caused by anti-neural antibodies and respond to treatment directed at these rogue antibodies.
The researchers agree that more study is warranted, although Dr Pleasure noted that the rarity of cerebrospinal fluid samples from paediatric patients is a challenge, as they rarely have severe enough COVID to warrant a lumbar puncture.
Using mouse models, scientists have discovered a link between gut inflammation and mental comorbidities. In response to gut inflammation like that caused by inflammatory bowel disease (IBD), they observed that the vascular barrier in the brain choroid plexus closes, clamping down access to the brain. The findings were published in Science.
Though this gut-brain vascular axis deregulation is likely a protective mechanism for the brain against inflammation, the findings suggest it may also result in the various cognitive and psychiatric symptoms that are occasionally associated with IBD.
Usually associated with intestinal inflammation, IBD can also cause a wide variety of symptoms in other organs. There is a robust link between anxiety and IBD; up to 40% of patients with IBD also present with psychiatric symptoms such as anxiety or depression. While the gut-brain axis is thought to be involved in driving these symptoms, no other related mechanisms are currently known.
Using a mouse model of intestinal inflammation, Sara Carloni and colleagues identified a potential pathogenic link between IBD and its associated mental comorbidities. According to the findings, the gut vascular barrier becomes more permeable due to the inflammatory process, which allows inflammation to spread beyond the intestines.
In response to this spread, the vascular barrier in the choroid plexus of the brain shuts down, which helps to protect the brain from inflammation. However, in doing so, the process also potentially impairs communications between organs and may hinder brain function.
In a mouse model of genetically driven closure of choroid plexus endothelial cells, Carloni and colleagues observed a deficit in short-term memory and anxiety-like behaviour. Thus, the mental deficits observed alongside IBD may result from deregulation of the gut-brain vascular axis, the authors said. This finding could be used for the development of therapeutic targets in treating some behavioural disorders.
