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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News</span></td>
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<td><a href="https://www.psypost.org/alcohol-shifts-the-brain-into-a-fragmented-and-local-state/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Alcohol shifts the brain into a fragmented and local state</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 1st 2026, 08:00</div>
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<p><p>A standard glass of wine or beer does more than just relax the body; it fundamentally alters the landscape of communication within the brain. New research suggests that acute alcohol consumption shifts neural activity from a flexible, globally integrated network to a more segmented, local structure. These changes in brain architecture appear to track with how intoxicated a person feels. The findings were published in the journal <em><a href="https://doi.org/10.1016/j.drugalcdep.2025.112972" target="_blank" rel="noopener">Drug and Alcohol Dependence</a></em>.</p>
<p>For decades, neuroscientists have worked to map how alcohol affects human behavior. Traditional studies often look at specific brain regions in isolation. Researchers might observe that activity in the prefrontal cortex dampens, which explains why inhibition lowers. Alternatively, they might see changes in the cerebellum, which accounts for the loss of physical coordination.</p>
<p>However, the brain does not operate as a collection of independent islands. It functions as a massive, interconnected web. Information must travel constantly between different areas to process sights, sounds, and thoughts. Understanding how alcohol impacts the traffic patterns of this web requires a different mathematical approach known as graph theory.</p>
<p>Graph theory allows scientists to treat the brain like a vast map of cities and highways. The “cities” are distinct brain regions, referred to as nodes. The “highways” are the functional connections between them, known as edges. By analyzing the flow of traffic across these highways, researchers can determine how efficiently the brain is sharing information.</p>
<p>Leah A. Biessenberger and her colleagues at the University of Minnesota and the University of Florida sought to apply this network-level analysis to social drinkers. Biessenberger, the study’s lead author, worked alongside senior author Jeff Boissoneault and a wider team. They aimed to fill a gap in the scientific literature regarding acute alcohol use.</p>
<p>While previous research has examined how chronic, heavy drinking reshapes the brain over years, less is known about the immediate network effects of a single drinking session. The researchers wanted to observe the brain in a “resting state.” This is the baseline activity that occurs when a person is awake but not performing a specific task.</p>
<p>To investigate this, the team recruited 107 healthy adults between the ages of 21 and 45. The participants were social drinkers without a history of alcohol use disorder. The study utilized a double-blind, placebo-controlled design. This method is the gold standard for removing bias from clinical experiments.</p>
<p>Each participant visited the laboratory for two separate sessions. During one visit, they consumed a beverage containing alcohol mixed with a sugar-free mixer. The dose was calculated to bring their breath alcohol concentration to 0.08 grams per deciliter, which is the legal driving limit in the United States.</p>
<p>During the other visit, they received a placebo drink. This beverage contained only the mixer but was misted with a small amount of alcohol on the surface and rim to mimic the smell and taste of a real cocktail. Neither the participants nor the research staff knew which drink was administered on a given day.</p>
<p>Approximately 30 minutes after drinking, the participants entered an MRI scanner. They were instructed to keep their eyes open and let their minds wander. The scanner recorded the blood oxygen levels in their brains, which serves as a proxy for neural activity.</p>
<p>The researchers then used computational tools to analyze the functional connectivity between 106 different brain regions. They looked for specific patterns in the data described by graph theory metrics. These metrics included “global efficiency” and “local efficiency.”</p>
<p>Global efficiency measures how easily information travels across the entire network. A network with high global efficiency has many long-distance shortcuts, allowing distant regions to communicate quickly. Local efficiency measures how well neighbors talk to neighbors. It reflects the tendency of brain regions to form tight-knit clusters that process information among themselves.</p>
<p>The analysis revealed distinct shifts in the brain’s topology following alcohol consumption. When participants drank alcohol, their brains moved toward a more “grid-like” state. The network became less random and more clustered.</p>
<p>Specifically, the study found that global efficiency decreased in several areas. This was particularly evident in the occipital lobe, the part of the brain responsible for processing vision. The reduction suggests that alcohol makes it harder for visual information to integrate with the rest of the brain’s operations.</p>
<p>Simultaneously, local efficiency increased. Regions in the frontal and temporal cortices began to communicate more intensely with their immediate neighbors. The brain appeared to fracture into smaller, self-contained communities. This structure requires less energy to maintain but hinders the rapid integration of complex information.</p>
<p>The researchers also examined a metric called “clustering coefficient.” This value reflects the likelihood that a node’s neighbors are also connected to each other. Alcohol increased the clustering coefficient across the network. This further supports the idea that the intoxicated brain relies more on local processing than global integration.</p>
<p>The team also looked at the “insula,” a region deeply involved in sensing the body’s internal state. Under the influence of alcohol, the insula showed increased connections with its local neighbors. It also displayed greater activity in communicating with the broader network compared to the placebo condition.</p>
<p>These architectural changes were not merely abstract mathematical observations. The researchers found a statistical link between the network shifts and the participants’ subjective experiences. Before the scan, participants rated how intoxicated they felt on a scale of 0 to 100.</p>
<p>The results showed that the degree of network reorganization predicted the intensity of the subjective “buzz.” Participants whose brains showed the largest drop in global efficiency and the largest rise in local clustering tended to report feeling the most intoxicated. The structural breakdown of long-range communication tracked with the feeling of impairment.</p>
<p>This correlation offers new insight into why individuals react differently to the same amount of alcohol. Even at the same blood alcohol concentration, people experience varying levels of intoxication. The study suggests that individual differences in how the brain network fragments may underlie these varying subjective responses.</p>
<p>The findings also highlighted disruptions in the visual system. The decrease in efficiency within the occipital regions was marked. This aligns with well-known effects of drunkenness, such as blurred vision or difficulty tracking moving objects. The network analysis provides a neural basis for these sensory deficits.</p>
<p>While the study offers robust evidence, the authors note certain limitations. The MRI scans did not capture the cerebellum consistently for all participants. The cerebellum is vital for balance and motor control. Because it was not included in the analysis, the picture of alcohol’s effect on the whole brain remains incomplete.</p>
<p>Additionally, the study focused on young, healthy adults. The brain changes observed here might differ in older adults or individuals with a history of substance abuse. Aging brains already show some reductions in global efficiency. Alcohol could compound these effects in older populations.</p>
<p>The researchers also point out that the participants were in a resting state. The brain rearranges its network when actively solving problems or processing emotions. Future research will need to determine if these topological shifts persist or worsen when an intoxicated person tries to perform a complex task, like driving.</p>
<p>This investigation provides a nuanced view of acute intoxication. It moves beyond the idea that alcohol simply “dampens” brain activity. Instead, it reveals that alcohol forces the brain into a segregated state. Information gets trapped in local cul-de-sacs rather than traveling the superhighways of the mind.</p>
<p>By connecting these mathematical patterns to the subjective feeling of being drunk, the study helps bridge the gap between biology and behavior. It illustrates that the sensation of intoxication is, in part, the feeling of a brain losing its global coherence.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.drugalcdep.2025.112972" target="_blank" rel="noopener">Acute alcohol intake disrupts resting state network topology in healthy social drinkers</a>,” was authored by Leah A. Biessenberger, Adriana K. Cushnie, Bethany Stennett-Blackmon, Landrew S. Sevel, Michael E. Robinson, Sara Jo Nixon, and Jeff Boissoneault.</p></p>
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<td><a href="https://www.psypost.org/social-anxiety-has-a-dark-side-that-looks-nothing-like-shyness/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Social anxiety has a “dark side” that looks nothing like shyness</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 1st 2026, 06:00</div>
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<p><p>Social anxiety is commonly associated with shyness, silence, and a tendency to withdraw from social interactions. However, new research suggests that for some adolescents, this condition manifests through aggression and impulsivity rather than avoidance. This “atypical” presentation appears linked to specific narcissistic traits. The study was published in the journal <em><a href="https://doi.org/10.1016/j.paid.2025.113581" target="_blank" rel="noopener">Personality and Individual Differences</a>.</em></p>
<p>“There is a prevailing assumption in the popular and professional literature that social anxiety is characterized solely by avoidance of tendencies and behavioral inhibition (i.e., shyness). This is likely a consequence from its formal classification of social phobia, which inadvertently shaped the way we study and understand the clinical phenomena,” explained study author <a href="https://scholar.google.ca/citations?user=EB-NaeoAAAAJ&hl=en&oi=ao" target="_blank" rel="noopener">Mollie J. Eriksson</a>, a PhD Candidate in <a href="https://www.science.mcmaster.ca/pnb/schmidt/index.html" target="_blank" rel="noopener">Louis Schmidt’s Child Emotion Lab</a> at McMaster University.</p>
<p>“Nonetheless, this prototypical inhibited presentation does not reflect the lived experience of many individuals with social anxiety symptoms (for a comprehensive review see <a href="https://doi.org/10.1177/0963721409359280" target="_blank" rel="noopener">Kashdan & McKnight</a>). And so, in the current study we aimed to examine the externalizing correlates of social anxiety that are less studied and correspondingly less understood, particularly in a population (i.e., adolescents) in which these dynamics might be especially conspicuous.”</p>
<p>The research team recruited 298 adolescents for the study. The participants ranged in age from 12 to 17 years old. The sample was nearly evenly split between boys and girls. Data was collected through a series of online self-report questionnaires.</p>
<p>Participants answered detailed questions regarding their feelings of social anxiety and their levels of narcissism. The narcissism measure distinguished between vulnerable and grandiose traits. Additional surveys assessed impulsivity and general aggression.</p>
<p>The researchers used a statistical method known as Latent Profile Analysis to group the participants. This technique identifies distinct categories of people based on patterns in their responses. “This is a very robust statistical technique because it uncovers patterns in the data that reflect individual variation in people and not simply associations between data points,” Eriksson said.</p>
<p>The analysis revealed three distinct profiles among the adolescents. The largest group comprised about 46 percent of the sample. These individuals displayed low levels of social anxiety, narcissism, and aggression. This profile appears to represent a well-adjusted or normative group with few social difficulties.</p>
<p>The second group accounted for approximately 30 percent of the participants. Adolescents in this profile reported the highest levels of social anxiety. They also scored high on vulnerable narcissism but low on grandiose narcissism and aggression. This group fits the prototypical description of social anxiety. These teens appear to manage their fear of rejection through inhibition and withdrawal.</p>
<p>The third group made up roughly 25 percent of the sample. This profile was characterized by moderate levels of social anxiety but high levels of impulsivity and aggression. Notably, these adolescents scored the highest on both vulnerable and grandiose narcissism. This combination of traits represents the “atypical” presentation of social anxiety.</p>
<p>“Social anxiety is a broad and heterogeneous mental health problem that is characterized by several features, beyond shyness,” Eriksson told PsyPost. “Recognizing its heterogeneity is the first step in identifying individuals, particularly adolescents, who may be struggling with social anxiety. By providing the tools (i.e., additional features that characterize social anxiety) we can intervene sooner, ideally before symptoms become entrenched, which will ultimately set the adolescent up for greater intra-personal and inter-personal success later in life.”</p>
<p>The researchers also found sex differences in profile membership. Boys were more likely than girls to belong to the third, aggressive profile. This suggests that boys may be more prone to expressing social fears through externalizing behaviors. This aligns with broader socialization norms where boys may be discouraged from showing vulnerability.</p>
<p>“It was exciting that these results replicated <a href="https://doi.org/10.1111/sjop.12117" target="_blank" rel="noopener">previous adult findings</a>, which really underscores the robustness of these findings,” Eriksson said. “Even though this was in line with our <em>a priori</em> hypothesis, it was also interesting that boys were more likely to be in the ‘moderate social anxiety/high externalizing profile.’ It makes me think about how sex/gender influence the expression of social anxiety.”</p>
<p>But the study, like all research, has some limitations. The data was collected at a single point in time. This prevents researchers from establishing a causal relationship between narcissism and the development of aggressive social anxiety. It is unclear if the personality traits precede the anxiety or if they develop concurrently.</p>
<p>“A common misinterpretation we would like to preempt is the assumption that these profiles represent fixed or diagnostic categories,” Eriksson explained. “Rather, they reflect patterns of co-occurring traits and symptoms within a specific developmental window. Additionally, because the data are cross-sectional, we cannot infer developmental pathways or causal mechanisms. Replication (particularly in longitudinal designs) is therefore essential for understanding how these profiles emerge and change over time.”</p>
<p>Tracking these traits from childhood into adolescence could reveal early warning signs. Identifying these patterns early could lead to more effective interventions. Standard treatments for social anxiety may not work for teens who react with aggression rather than fear.</p>
<p>“I hope to examine early childhood antecedents of atypical social anxiety symptomology both behaviorally and biologically,” Eriksson said. “This will really inform treatment and prevention efforts. I also hope to examine in more detail the novel hypothesis we articulated: social anxiety is driven by two divergent self-regulatory pathways. This hypothesis requires a longitudinal study design, which is something we plan to do in the very near future.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.paid.2025.113581" target="_blank" rel="noopener">Characterizing the dark side of social anxiety in adolescence: A replication and extension study</a>,” was authored by Mollie J. Eriksson and Louis A. Schmidt.</p></p>
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<td><a href="https://www.psypost.org/memories-of-childhood-trauma-may-shift-depending-on-current-relationships/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Memories of childhood trauma may shift depending on current relationships</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 31st 2026, 20:00</div>
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<p><p>Most people assume their memories of growing up are fixed, much like a file stored in a cabinet, but new research suggests the way we remember our childhoods might actually shift depending on how we feel about our relationships today. A study published in <em><a href="https://doi.org/10.1016/j.chiabu.2025.107873" target="_blank">Child Abuse & Neglect</a></em> reveals that young adults report fewer adverse childhood experiences during weeks when they feel more supported by their parents. This suggests that standard measures of early trauma may reflect a person’s current state of mind as much as their historical reality.</p>
<p>Adverse childhood experiences, or ACEs, refer to traumatic events such as abuse, neglect, and household dysfunction that occur before the age of 18. Medical professionals and psychologists frequently use questionnaires to tally these events because a high number of ACEs is associated with poor mental and physical health outcomes later in life. These screenings rely on the assumption that an adult’s memory of the past is stable and reliable over time.</p>
<p>However, human memory is not a static playback device. It is a reconstructive process that can be influenced by current moods, identity development, and social contexts. This is particularly true for emerging adults, who are navigating the transition from dependence on parents to establishing their own independent identities. This developmental period often requires young people to re-evaluate their family dynamics.</p>
<p>Annika Jaros, a researcher at Michigan State University, led an investigation into this phenomenon alongside co-author William Chopik. They sought to determine if fluctuations in current social relationships or stress levels corresponded with changes in how young adults remembered early adversity. They hypothesized that recollections of the past might wax and wane alongside the quality of a person’s present-day interactions.</p>
<p>The team recruited 938 emerging adults, largely undergraduate students, to complete three identical surveys. These surveys were spaced four weeks apart over a two-month period. At each interval, participants completed the Childhood Trauma Questionnaire, a standard tool used to identify histories of emotional, physical, and sexual abuse, as well as physical and emotional neglect.</p>
<p>In addition to recalling the past, participants rated the current quality of their close relationships. They reported on levels of support and strain with their parents, friends, and romantic partners. They also rated their current levels of academic stress to see if general life pressure affected their memories.</p>
<p>The researchers used statistical models to separate the data into two distinct categories of variance. They looked at differences between people, such as whether a person with a generally happy childhood reports better adult relationships. They also looked at variations within the same person over the course of the eight weeks.</p>
<p>The results showed that reports of childhood adversity were largely consistent over the two months. However, there was measurable variability in the answers provided by the same individuals from month to month. The analysis revealed that this variability was not random but tracked with changes in parental relationships.</p>
<p>When participants reported receiving higher-than-usual support from their parents, they reported fewer instances of childhood adversity. Conversely, during weeks when parental strain was higher than their personal average, recollections of emotional abuse, sexual abuse, and emotional neglect increased. This pattern suggests that a positive shift in a current relationship can soften the recollection of past transgressions.</p>
<p>The influence of friends and romantic partners was less pronounced than that of parents. While supportive friendships were generally associated with fewer reported ACEs on average, changes in friendship quality did not strongly predict fluctuations in memory from week to week. Romantic partners showed a similar pattern, where high support correlated with fewer retrospective reports of sexual abuse, but the effect was limited.</p>
<p>Academic stress also played a minor role in how participants viewed their pasts. While higher stress was linked to slight increases in reports of emotional abuse and physical neglect, the impact was small compared to the influence of family dynamics. The primary driver of change in these memories appeared to be the quality of the bond with caregivers.</p>
<p>The authors noted several limitations to the study that contextualize the results. The sample consisted primarily of university students, meaning the results may not apply to older adults or those with different socioeconomic backgrounds. The study covered only an eight-week period, leaving it unclear if these fluctuations persist or change over years.</p>
<p>There was also a pattern of attrition that affected the data. Participants with more severe histories of trauma were more likely to stop responding to the surveys over time. This may have reduced the study’s ability to capture the full range of variability in how trauma is recalled by those with the most difficult histories.</p>
<p>Despite these caveats, the findings have practical implications for therapists and researchers. A single screening for childhood adversity may capture a snapshot influenced by the patient’s current state of mind rather than a definitive history. Assessing these experiences multiple times could provide a more accurate picture of a patient’s background and current psychological state.</p>
<p>The study challenges the idea that retrospective reports are purely factual records. Instead, they appear to be dynamic interpretations that serve a function in the present. As young adults work to integrate their pasts into their life stories, their memories seem to breathe in time with their current emotional needs.</p>
<p>“People are generally consistent in how they recall their past, but the small shifts in reporting are meaningful,” said Chopik. “It doesn’t mean people are unreliable, it means that memory is doing what it does — integrating past experiences with present meaning.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.chiabu.2025.107873" target="_blank">Record of the past or reflection of the present? Fluctuations in recollections of childhood adversity and fluctuations in adult relationship circumstances</a>,” was authored by Annika Jaros and William J. Chopik.</p></p>
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<td><a href="https://www.psypost.org/aristotle-was-right-virtue-appears-to-be-vital-for-personal-happiness/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Aristotle was right: virtue appears to be vital for personal happiness</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 31st 2026, 18:00</div>
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<p><p>Virtues such as compassion, patience and self-control may be beneficial not only for others but also for oneself, according to <a href="https://doi.org/10.1111/jopy.70038">new research</a> my team and I published in the Journal of Personality in December 2025.</p>
<p>Philosophers <a href="https://plato.stanford.edu/entries/aristotle-ethics/">from Aristotle</a> <a href="https://plato.stanford.edu/entries/al-farabi/">to al-Fārābī</a>, a 10th-century scholar in what is now Iraq, have argued that virtue is vital for well-being. Yet others, such as <a href="https://plato.stanford.edu/entries/hobbes-moral/">Thomas Hobbes</a> and <a href="https://plato.stanford.edu/entries/nietzsche-moral-political/">Friedrich Nietzsche</a>, have argued the opposite: Virtue offers no benefit to oneself and is good only for others. This second theory has inspired lots of research in contemporary psychology, which often sees <a href="https://doi.org/10.1002/9780470561119.socpsy002022">morality and self-interest as fundamentally opposed</a>.</p>
<p>Many studies have found that <a href="https://doi.org/10.1177/19485506211043379">generosity is associated with happiness</a>, and that encouraging people to practice kindness <a href="https://doi.org/10.1016/j.jesp.2018.02.014">increases their well-being</a>. But other virtues seem less enjoyable.</p>
<p>For example, a compassionate person wants to alleviate suffering or misfortune, but that requires there be suffering or misfortune. Patience is possible only when something irritating or difficult is happening. And self-control involves forgoing one’s desires or persisting with something difficult.</p>
<p>Could these kinds of virtues really be good for you?</p>
<p>My colleagues and I investigated this question in two studies, using two different methods to zoom in on specific moments in people’s daily lives. Our goal was to assess the degree to which, in those moments, they were compassionate, patient and self-controlled. We also assessed their level of well-being: how pleasant or unpleasant they felt, and whether they found their activities meaningful.</p>
<p>One study, with adolescents, used the <a href="https://doi.org/10.4135/9781483381411.n173">experience sampling</a> method, in which people answer questions at random intervals throughout the day. The other, studying adults, used the <a href="https://doi.org/10.1126/science.1103572">day reconstruction</a> method, in which people answer questions about the previous day. All told, we examined 43,164 moments from 1,218 people.</p>
<p>During situations that offer opportunities to act with compassion, patience and self-control – encountering someone in need, for example, or dealing with a difficult person – people tend to experience more unpleasant feelings and less pleasant ones than in other situations. However, we found that exercising these three virtues <a href="https://doi.org/10.1111/jopy.70038">seems to help people cope</a>. People who are habitually more compassionate, patient and self-controlled tend to experience better well-being. And when people display more compassion, patience and self-control than usual, they tend to feel better than they usually do.</p>
<p>In short, our results contradicted the theory that virtue is good for others and bad for the self. They were consistent with the theory that virtue promotes well-being.</p>
<h2>Why it matters</h2>
<p>These studies tested the predictions of two venerable, highly influential theories about the relationship between morality and well-being. In doing so, they offered new insights into one of the most fundamental questions debated in philosophy, psychology and everyday life.</p>
<p>Moreover, in the scientific study of morality, lots of research has examined how people form <a href="https://doi.org/10.1146/annurev-psych-072220-104358">moral judgments</a> and how outside forces shape a person’s <a href="https://doi.org/10.1177/0146167206291006">moral behavior</a>. Yet some researchers have argued that this should be complemented by <a href="https://doi.org/10.1111/jopy.12919">research on moral traits</a> and how these are integrated into the whole person. By focusing on traits such as patience, compassion and self-control, and their roles in people’s daily lives, our studies contribute to the emerging <a href="https://doi.org/10.1177/1745691620924473">science of virtue</a>.</p>
<h2>What still isn’t known</h2>
<p>One open question for future research is whether virtues such as compassion, patience and self-control are associated with better well-being only under certain conditions. For example, perhaps things look different depending on one’s stage of life or in different parts of the world.</p>
<p>Our studies were not randomized experiments. It is possible that the associations we observed are explained by another factor – something that increases well-being while simultaneously increasing compassion, patience and self-control. Or maybe well-being affects virtue, instead of the other way around. Future research could help clarify the causal relationships.</p>
<p>One particularly interesting possibility is that there might be a “<a href="https://dictionary.cambridge.org/us/dictionary/english/virtuous-circle">virtuous cycle</a>”: Perhaps virtue tends to promote well-being – and well-being, in turn, tends to promote virtue. If so, it would be extremely valuable to learn how to help people kick-start that cycle.</p>
<p> </p>
<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/is-being-virtuous-good-for-you-or-just-people-around-you-a-study-suggests-traits-like-compassion-may-support-your-own-well-being-273641">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/adhd-diagnoses-are-significantly-elevated-among-autistic-adults-on-medicaid/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">ADHD diagnoses are significantly elevated among autistic adults on Medicaid</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 31st 2026, 16:00</div>
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<p><p>An analysis of U.S. Medicaid data found that 26.7% of autistic adults without intellectual disability had an ADHD diagnosis. This was the case for 40.2% of autistic adults with intellectual disability. The paper was published in <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2830118"><em>JAMA Network Open</em></a>.</p>
<p>Autism, or autism spectrum disorder, is a neurodevelopmental condition characterized by specificities in social communication, sensory processing, and patterns of behavior or interests. It is called a spectrum because its manifestations vary widely, from individuals who need substantial daily support to those who live independently.</p>
<p>Autism itself is not a disease and does not inherently imply poor health. However, autistic people have higher rates of certain co-occurring physical and mental health conditions compared with the general population. These commonly include anxiety, depression, ADHD, epilepsy, sleep disorders, and gastrointestinal problems.</p>
<p>Barriers to healthcare access, such as communication difficulties and lack of healthcare provider training for working with autistic individuals, can worsen overall health outcomes. Chronic stress from social exclusion, stigma, or masking autistic traits can negatively impact long-term physical and mental health. At the same time, when healthcare is accessible and appropriately adapted, autistic individuals can achieve health outcomes comparable to non-autistic peers.</p>
<p>Study author Benjamin E. Yerys and his colleagues note that attention-deficit/hyperactivity disorder (ADHD) is one of the most commonly co-occurring mental health conditions for autistic youths. At the same time, ADHD is associated with poorer health outcomes for both autistic and non-autistic children. These authors wanted to assess how often ADHD and autism occur together.</p>
<p>They analyzed Medicaid claims data from 2008 to 2019. Medicaid is a joint U.S. federal and state government health insurance program that provides free or low-cost medical coverage to people with low income, disabilities, or those meeting certain other eligibility criteria.</p>
<p>From these data, study authors constructed four groups: autistic individuals without intellectual disability, adults with intellectual disability without autism, autistic adults with intellectual disability, and (a random sample of) adult Medicaid enrollees without autism or intellectual disability. Only data of adults (i.e., 18 years of age and above) were analyzed.</p>
<p>The analysis included data belonging to a total of 3,506,661 individuals. Fifty-three percent were female, 20% were Black, 17% were Hispanic, and 60% were White.</p>
<p>The group without autism or intellectual disability had the lowest share of ADHD diagnoses at 2.7%. This percentage was 19% in the group with intellectual disabilities but without autism. In the group of autistic adults without intellectual disability, 26.7% had ADHD, and this was the case for 40.2% of autistic adults with intellectual disability.</p>
<p>Among people with an ADHD diagnosis, 36% of those without autism or intellectual disability were prescribed ADHD medication, while this was the case for 17.4% of individuals with intellectual disability (but no autism) and 26.8% of individuals who had both autism and intellectual disability. Forty-seven percent (46.7%) of participants with autism but no intellectual disability who were diagnosed with ADHD were prescribed ADHD medication.</p>
<p>“In this cohort study of Medicaid-enrolled adults, autistic adults experienced high rates of co-occurring ADHD and were more likely to receive ADHD medication prescriptions than adults in the general population. Negative health outcome rates are higher among autistic people with co-occurring ADHD, although ADHD medication prescriptions are associated with lower rates of negative health outcomes,” study authors concluded.</p>
<p>The study contributes to scientific knowledge about the co-occurrence of autism and ADHD. However, it should be noted that these data come solely from individuals enrolled in Medicaid. Results in the broader, non-Medicaid enrolled population may differ.</p>
<p>The paper, “<a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2830118">Attention-Deficit/Hyperactivity Disorder in Medicaid-Enrolled Autistic Adults,</a>” was authored by Benjamin E. Yerys, Sha Tao, Lindsay Shea, and Gregory L. Wallace.</p></p>
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<td><a href="https://www.psypost.org/long-term-antidepressant-effects-of-psilocybin-linked-to-functional-brain-changes/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Long-term antidepressant effects of psilocybin linked to functional brain changes</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 31st 2026, 14:00</div>
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<p><p>A new study suggests that the long-term antidepressant effects of psychedelics may be driven by persistent changes in how neurons fire rather than by the permanent growth of new brain cell connections. Researchers found that a single dose of psilocybin altered the electrical properties of brain cells in rats for months, even after physical changes to the neurons had disappeared. These findings were published in the journal <a href="https://doi.org/10.1038/s41386-025-02272-3" target="_blank">Neuropsychopharmacology</a>.</p>
<p>Depression is a debilitating condition that is often treated with daily medications. These standard treatments can take weeks to work and do not help every patient. Psilocybin, a compound found in certain mushrooms, has emerged as a potential alternative therapy. Clinical trials indicate that one or two doses of psilocybin can alleviate symptoms of depression for months or even years. However, scientists do not fully understand the biological mechanisms that allow a single treatment to produce such enduring results.</p>
<p>Researchers have previously focused on the concept of neuroplasticity to explain these effects. This term generally refers to the brain’s ability to reorganize itself. One specific type is structural plasticity, which involves the physical growth of new connection points between neurons, known as dendritic spines. Short-term studies conducted days or weeks after drug administration often show an increase in these spines. The question remained whether these physical structures persist long enough to account for relief lasting several months.</p>
<p>To investigate this, a team of researchers led by Hannah M. Kramer, Meghan Hibicke, and Charles D. Nichols at LSU Health Sciences Center designed an experiment using rats. They chose Wistar Kyoto rats for the study. This specific breed is often used in research because the animals naturally exhibit behaviors analogous to stress and depression in humans.</p>
<p>The investigators sought to compare the effects of psilocybin against another compound called 25CN-NBOH. Psilocybin interacts with various serotonin receptors in the brain. In contrast, 25CN-NBOH is a synthetic drug designed to target only one specific receptor known as the 5-HT2A receptor. This is the receptor believed to be primarily responsible for the psychedelic experience. By using both drugs, the team hoped to isolate the role of this specific receptor in creating long-term behavioral changes.</p>
<p>The study began with the administration of a single dose of either psilocybin, 25CN-NBOH, or a saline placebo to the male rats. The researchers then waited for a substantial period before testing the animals. They assessed the rats’ behavior at five weeks and again at twelve weeks after the injection. This timeline allowed the team to evaluate effects that persist well beyond the immediate aftermath of the drug experience.</p>
<p>The primary method for assessing behavior was the forced swim test. In this standard procedure, rats are placed in a tank of water from which they cannot escape. Researchers measure how much time the animals spend swimming versus floating motionless. In this context, high levels of immobility are interpreted as a passive coping strategy, which is considered a marker for depressive-like behavior. Antidepressant drugs typically cause rats to spend more time swimming and struggling.</p>
<p>The behavioral results indicated a lasting change. Rats treated with either psilocybin or 25CN-NBOH showed reduced immobility compared to the control group. This antidepressant-like effect was evident at the five-week mark. It remained equally strong at the twelve-week mark. The persistence of the effect suggests that the single dose induced a stable, long-term shift in behavior.</p>
<p>After the twelve-week behavioral tests, the researchers examined the brains of the animals. They focused on the medial prefrontal cortex. This brain region is involved in mood regulation and decision-making. The team utilized high-resolution microscopy to count the density of dendritic spines on the neurons. They specifically looked for the physical evidence of new connections that previous short-term studies had identified.</p>
<p>The microscopic analysis revealed that the number of dendritic spines in the treated rats was no different from that of the control group. The structural growth seen in other studies shortly after treatment appeared to be transient. The physical architecture of the neurons had returned to its baseline state after three months. The researchers also analyzed the expression of genes related to synaptic structure. They found no difference in gene activity between the groups.</p>
<p>Since structural changes could not explain the lasting behavioral shift, the team investigated functional plasticity. This refers to changes in how neurons process and transmit electrical signals. They prepared thin slices of the rats’ brain tissue. Using a technique called electrophysiology, they inserted microscopic glass pipettes into individual neurons to record their electrical activity.</p>
<p>The researchers classified the neurons into two types based on their firing patterns: adapting neurons and bursting neurons. Adapting neurons typically slow down their firing rate after an initial spike. Bursting neurons fire in rapid clusters of signals. The recordings showed that the drugs had altered the intrinsic electrical properties of these cells.</p>
<p>In the group treated with psilocybin, adapting neurons sat at a resting voltage that was closer to the threshold for firing. This state is known as depolarization. It means the cells are primed to activate more easily. The bursting neurons in psilocybin-treated rats also showed increased excitability. They required less input to trigger a signal and fired at faster rates than neurons in untreated rats.</p>
<p>The rats treated with 25CN-NBOH also exhibited functional changes, though the specific electrical alterations differed slightly from the psilocybin group. For instance, the bursting neurons in this group were not as easily triggered as those in the psilocybin group. However, the overall pattern confirmed that the drug had induced a lasting shift in neuronal function.</p>
<p>These electrophysiological findings provide a potential explanation for the behavioral results. While the physical branches of the neurons may have pruned back to normal levels, the cells “remembered” the treatment through altered electrical tuning. This functional shift allows the neural circuits to operate differently long after the drug has left the body.</p>
<p>The study implies that the 5-HT2A receptor is sufficient to trigger these long-term changes. The synthetic drug 25CN-NBOH produced lasting behavioral effects similar to psilocybin. This suggests that activating this single receptor type can initiate the cascade of events leading to persistent antidepressant-like effects.</p>
<p>There are limitations to this study that provide context for the results. The researchers used only male rats. Female rats may exhibit different biological responses to psychedelics or stress. Future research would need to include both sexes to ensure the findings are universally applicable.</p>
<p>Additionally, the forced swim test is a proxy for human depression but does not capture the full complexity of the human disorder. While it is a standard tool for screening antidepressant drugs, it measures a specific type of coping behavior. The translation of these specific neural changes to human psychology remains a subject for further investigation.</p>
<p>The researchers also noted that while spine density returned to baseline, this does not mean structural plasticity plays no role. It is possible that a rapid, temporary growth of connections acts as a trigger. This early phase might set the stage for the permanent electrical changes that follow. The exact molecular switch that locks in these functional changes remains to be identified.</p>
<p>Future studies will likely focus on the period between the initial dose and the three-month mark. Scientists need to map the transition from structural growth to functional endurance. Understanding this timeline could help optimize how these therapies are delivered.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41386-025-02272-3" target="_blank">Psychedelics produce enduring behavioral effects and functional plasticity through mechanisms independent of structural plasticity</a>,” was authored by Hannah M. Kramer, Meghan Hibicke, Jason Middleton, Alaina M. Jaster, Jesper L. Kristensen and Charles D. Nichols.</p></p>
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<td><a href="https://www.psypost.org/scientists-identify-key-brain-structure-linked-to-bipolar-pathology/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists identify key brain structure linked to bipolar pathology</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 31st 2026, 10:00</div>
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<p><p>Recent analysis of human brain tissue suggests that a small and often overlooked region deep within the brain may play a central role in bipolar disorder. Researchers found that neurons in the paraventricular thalamic nucleus are depleted and genetically altered in people with the condition. These results point toward potential new targets for diagnosis and treatment. The findings were published in the journal <em><a href="https://doi.org/10.1038/s41467-025-68094-5" target="_blank">Nature Communications</a></em>.</p>
<p>Bipolar disorder is a mental health condition characterized by extreme shifts in mood and energy levels. It affects approximately one percent of the global population and can severely disrupt daily life. While medications such as lithium and antipsychotics exist, they do not work for every patient. These drugs also frequently carry difficult side effects that cause patients to stop taking them. To develop better therapies, medical experts need a precise map of what goes wrong in the brain.</p>
<p>Past research has largely focused on the outer layer of the brain known as the cortex. This area is responsible for higher-level thinking and processing. However, brain scans using magnetic resonance imaging have hinted that deeper structures also shrink in size during the course of the illness. One such structure is the thalamus. This central hub acts as a relay station for sensory information and emotional regulation.</p>
<p>Within the thalamus lies a specific cluster of cells called the paraventricular thalamic nucleus. This area is rich in chemical messengers and has connections to parts of the brain involved in emotion. Despite these clues, the molecular details of this region remained largely unmapped in humans. A team led by Masaki Nishioka and Tadafumi Kato from Juntendo University Graduate School of Medicine in Tokyo launched an investigation to bridge this gap. They collaborated with researchers including Mie Sakashita-Kubota to analyze postmortem brain tissue.</p>
<p>The researchers aimed to determine if the genetic activity in this deep brain region differed from healthy brains. They examined brain samples from 21 individuals who had been diagnosed with bipolar disorder and 20 individuals without psychiatric conditions. They looked at two specific areas: the frontal cortex and the paraventricular thalamic nucleus. To do this, they used a technique called single-nucleus RNA sequencing.</p>
<p>This technology allows researchers to catalog the genetic instructions being used by individual cells. By analyzing thousands of nuclei, the team could identify different cell types and see which genes were active or inactive. This provided a high-resolution view of the cellular landscape. They compared the data from the thalamus against the data from the cortex to see which region was more affected.</p>
<p>The analysis revealed that the thalamus had undergone substantial changes. Specifically, the paraventricular thalamic nucleus contained far fewer excitatory neurons in the samples from people with bipolar disorder. The researchers estimated a reduction of roughly 50 percent in these cells compared to the control group. This loss was specific to the neurons that send stimulating signals to other parts of the brain.</p>
<p>In contrast, the changes observed in the frontal cortex were much more subtle. While there were some alterations in the cortical cells, they were not as extensive as those seen in the deep brain. This suggests that the thalamus might be a primary site of pathology in the disorder. The team validated these findings by staining proteins in the tissue to visually confirm the lower cell density.</p>
<p>Inside the remaining thalamic neurons, the genetic machinery was also behaving differently. The study identified a reduced activity of genes responsible for maintaining connections between neurons. These genes are essential for the flow of chemical and electrical signals. Among the affected genes were CACNA1C and SHISA9. These specific segments of DNA have been flagged in previous genetic studies as potential risk factors for the illness.</p>
<p>Another gene called KCNQ3, which helps regulate electrical channels in cells, was also less active. These channels act like gates that let electrically charged potassium or calcium atoms flow in and out of the cell. This flow is what allows a neuron to fire a signal. When the genes controlling these gates are turned down, the neuron may become unstable or fail to communicate.</p>
<p>The specific combination of affected genes suggests a vulnerability in how these cells handle calcium and electrical activity. High-frequency firing of neurons requires tight regulation of calcium levels. If the proteins that manage this process are missing, the cells might become damaged over time. This could explain why so many of these neurons were missing in the patient samples.</p>
<p>The team also looked at non-neuronal cells called microglia. These are the immune cells of the brain that help maintain healthy synapses. Synapses are the junction points where neurons pass signals to one another. The data showed that the communication between the thalamic neurons and these immune cells was disrupted.</p>
<p>A specific pattern of gene expression that usually coordinates the interaction between excitatory neurons and microglia was weaker in the bipolar disorder samples. This breakdown could contribute to the loss of synapses or the death of neurons. It represents a failure in the support system that keeps brain circuits healthy. The simultaneous decline in both neuron and microglia function suggests a coordinated failure in the region.</p>
<p>The researchers note that the paraventricular thalamic nucleus is distinct from other brain regions. It contains a high density of receptors for dopamine, a neurotransmitter involved in reward and motivation. This makes it a likely target for antipsychotic medications that act on the dopamine system. The specific genetic profile of these neurons aligns with biological processes previously linked to the disorder.</p>
<p>There are limitations to consider regarding these results. The study relied on postmortem tissue, so it represents a snapshot of the brain at the end of life. It is difficult to know for certain if the cell loss caused the disorder or if the disorder caused the cell loss. The sample size was relatively small, with only 41 donors in total.</p>
<p>Additionally, the patients had been taking various medications throughout their lives. These drugs can influence gene expression. The researchers checked for medication effects and found little overlap between drug signatures and their findings. However, they could not rule out medication influence entirely.</p>
<p>Looking ahead, the authors suggest that the paraventricular thalamic nucleus could be a target for new drugs. Therapies that aim to protect these neurons or restore their function might offer relief where current treatments fail. Advanced imaging could also focus on this region to help diagnose the condition earlier.</p>
<p>Associate Professor Nishioka emphasized the importance of looking beyond the usual suspects in brain research. “This study highlights the need to extend research to the subcortical regions of the brain, which may harbor critical yet underexplored components of BD pathophysiology,” Nishioka stated. The team hopes that integrating these molecular findings with neuroimaging will lead to better patient outcomes.</p>
<p>Professor Kato added that the findings could reshape how scientists view the origins of the illness. “We finally identified that PVT is the brain region causative for BD,” Kato said. “This discovery will lead to the paradigm shift of BD research.”</p>
<p>The study, “<a href="https://doi.org/10.1038/s41467-025-68094-5" target="_blank">Disturbances of paraventricular thalamic nucleus neurons in bipolar disorder revealed by single-nucleus analysis</a>,” was authored by Masaki Nishioka, Mie Sakashita-Kubota, Kouichirou Iijima, Yukako Hasegawa, Mizuho Ishiwata, Kaito Takase, Ryuya Ichikawa, Naguib Mechawar, Gustavo Turecki & Tadafumi Kato.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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