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  • Waseda Researchers Apply Attachment Theory to Human-AI Bonds: What EHARS Reveals About Anxiety and Avoidance

    As AI chatbots and digital assistants become part of daily life, researchers are looking beyond trust and usefulness to understand the emotional side of human-AI interaction. A team at Waseda University argues that attachment theory, long used to explain human bonds, can also help explain why some people turn to AI for comfort and guidance.

    The researchers developed a new self-report measure called the Experiences in Human-AI Relationships Scale, or EHARS, to capture how users relate to AI in ways that resemble attachment patterns. The work, based on two pilot studies and a formal study, was published in Current Psychology in May 2025.

    Measuring attachment anxiety and avoidance

    EHARS focuses on two dimensions: attachment anxiety and attachment avoidance toward AI systems. Higher anxiety is linked to seeking reassurance and worrying that an AI will respond inadequately, while higher avoidance reflects discomfort with emotional closeness and a preference for distance.

    In the study, nearly 75% of participants reported turning to AI for advice, suggesting that many people already treat AI as a source of guidance. About 39% described AI as a constant, dependable presence, a finding the authors say is relevant to how emotional security can be sought through technology.

    What the findings do and do not mean

    The authors emphasize that the results do not prove people are forming genuine human-like attachments to AI. Instead, the study indicates that established psychological frameworks may help describe patterns in human-AI relationships as these tools become more conversational and socially responsive.

    That distinction matters because AI systems can simulate empathy without experiencing it, potentially shaping user expectations and dependency. Researchers and ethicists have increasingly warned that emotionally persuasive interfaces can heighten risks for vulnerable users, particularly in loneliness and mental health contexts.

    Implications for ethical AI design

    The team suggests EHARS could help designers and researchers evaluate how different users emotionally engage with AI, informing safer interaction patterns. In practice, that could mean more transparent disclosures, careful use of relational language, and guardrails to reduce overreliance where attachment anxiety appears high.

    As AI companions, coaching bots, and therapy-adjacent apps expand, measuring emotional dynamics may become as important as testing accuracy and security. The Waseda study positions attachment-informed evaluation as one tool for aligning AI behavior with user well-being and responsible product design.

  • New Swedish study flags delayed paternal depression surge around baby’s first year

    New Swedish study flags delayed paternal depression surge around baby’s first year

    Fathers in Sweden are less likely to receive a psychiatric diagnosis during their partner’s pregnancy and in the months right after their child is born. But this pattern reverses over time. A new study published in JAMA Network Open reports that diagnoses of depression and stress-related conditions rise about a year after childbirth. The research was led by scientists at Karolinska Institutet in Sweden and Sichuan University in China.

    “The transition to fatherhood often involves both positive experiences and a range of new stresses,” says Jing Zhou, PhD student at the Institute of Environmental Medicine, Karolinska Institutet, and co-first author of the paper. “Many cherish the intimate moments with their child, whilst at the same time the relationship with their partner may be affected and sleep quality may deteriorate, which can contribute to an increased risk of mental ill-health.”

    Study Tracks Over 1 Million Fathers Across Sweden

    The researchers analyzed data from more than one million fathers whose children were born in Sweden between 2003 and 2021. Using linked national registers, they followed when men received new psychiatric diagnoses, beginning one year before pregnancy and continuing until the child reached one year of age.

    Depression and Stress Diagnoses Increase After One Year

    The findings show that psychiatric diagnoses became less common during pregnancy and in the early months after birth compared with the year before pregnancy. By one year after birth, diagnoses related to anxiety and substance use had returned to levels seen before pregnancy. In contrast, depression and stress-related disorders showed a clear increase. These diagnoses rose by more than 30 percent compared with rates before pregnancy.

    “The delayed increase in depression was unexpected and underscores the need to pay attention to warning signs of mental ill-health in fathers long after the birth of their child,” says Donghao Lu, senior lecturer and associate professor at the Institute of Environmental Medicine, Karolinska Institutet, and the paper’s corresponding author.

    Timing Support for Fathers’ Mental Health

    The researchers note that their results are based on clinical diagnoses, meaning men who did not seek care may not be included. Even so, the study highlights when fathers may be most vulnerable during early parenthood.

    “By identifying periods of increased vulnerability, healthcare providers and other stakeholders can more easily offer support,” says Jing Zhou. “Postnatal depression is often discussed for new mothers, but fathers’ well-being is also important, both for themselves and for the whole family.”

    The study was conducted in collaboration with Sichuan University in China and Uppsala University in Sweden. It was funded by Karolinska Institutet’s strategic research area in epidemiology and biostatistics, the Swedish Research Council and the European Research Council. The researchers report no conflicts of interest.

  • Scientists pinpoint metformin’s brain pathway, offering new clues for targeted type 2 diabetes treatment

    Scientists pinpoint metformin’s brain pathway, offering new clues for targeted type 2 diabetes treatment

    After more than 60 years as a first-line drug for type 2 diabetes, metformin is yielding a clearer explanation for how it lowers blood sugar. Researchers report that part of its glucose-lowering effect depends on a specific brain circuit, not only the liver or the gut.

    The study, led by Baylor College of Medicine and international collaborators, was published in Science Advances. It focuses on the ventromedial hypothalamus, a brain region known to help regulate whole-body metabolism.

    A protein switch in the hypothalamus

    The team centered on Rap1, a small signaling protein active in the ventromedial hypothalamus. They found that clinically relevant metformin dosing relied on suppressing Rap1 activity in this brain area to reduce blood glucose.

    To test the mechanism, the researchers used mice engineered to lack Rap1 in the ventromedial hypothalamus and then fed them a high-fat diet to model diabetes. In those mice, low-dose metformin did not improve blood sugar, while insulin and GLP-1–based drugs still worked.

    Why tiny brain doses mattered

    In another experiment, researchers delivered extremely small amounts of metformin directly into the brains of diabetic mice. Even at doses thousands of times lower than typical oral exposure, blood glucose fell markedly, supporting a central nervous system effect.

    The study also identified SF1 neurons in the ventromedial hypothalamus as key responders, becoming activated when metformin reached the brain. Electrophysiology data suggested metformin increased activity in most of these neurons, but only when Rap1 signaling was intact.

    What it could mean next

    The findings add to a growing view that metformin’s benefits may come from multiple organs working together, with the brain reacting at comparatively low drug levels. The authors argue that mapping this pathway could help guide future diabetes therapies that more precisely target glucose control.

    The researchers also pointed to broader interest in metformin’s neurological effects, including ongoing questions about brain aging. They plan to examine whether the same Rap1-linked signaling helps explain other observed effects of the drug beyond diabetes.

  • New research shows when eye contact matters most, and why robots can read it too

    New research shows when eye contact matters most, and why robots can read it too

    For the first time, a new study has revealed how and when we make eye contact — not just the act itself — plays a crucial role in how we understand and respond to others, including robots.

    Led by cognitive neuroscientist Dr Nathan Caruana, researchers from the HAVIC Lab at Flinders University asked 137 participants to complete a block-building task with a virtual partner.

    They discovered that the most effective way to signal a request was through a specific gaze sequence: looking at an object, making eye contact, then looking back at the same object. This timing made people most likely to interpret the gaze as a call for help.

    Dr Caruana says that identifying these key patterns in eye contact offers new insights into how we process social cues in face-to-face interactions, paving the way for smarter, more human-centered technology.

    “We found that it’s not just how often someone looks at you, or if they look at you last in a sequence of eye movements but the context of their eye movements that makes that behavior appear communicative and relevant,” says Dr Caruana, from the College of Education, Psychology and Social Work.

    “And what’s fascinating is that people responded the same way whether the gaze behavior is observed from a human or a robot.

    “Our findings have helped to decode one of our most instinctive behaviors and how it can be used to build better connections whether you’re talking to a teammate, a robot, or someone who communicates differently.

    “It aligns with our earlier work showing that the human brain is broadly tuned to see and respond to social information and that humans are primed to effectively communicate and understand robots and virtual agents if they display the non-verbal gestures we are used to navigating in our everyday interactions with other people.”

    The authors say the research can directly inform how we build social robots and virtual assistants that are becoming ever more ubiquitous in our schools, workplaces and homes, while also having broader implications beyond tech.

    “Understanding how eye contact works could improve non-verbal communication training in high-pressure settings like sports, defense, and noisy workplaces,” says Dr Caruana.

    “It could also support people who rely heavily on visual cues, such as those who are hearing-impaired or autistic.”

    The team is now expanding the research to explore other factors that shape how we interpret gaze, such as the duration of eye contact, repeated looks, and our beliefs about who or what we are interacting with (human, AI, or computer-controlled).

    The HAVIC Lab is currently conducting several applied studies exploring how humans perceive and interact with social robots in various settings, including education and manufacturing.

    “These subtle signals are the building blocks of social connection,” says Dr Caruana.

    “By understanding them better, we can create technologies and training that help people connect more clearly and confidently.”

    The HAVIC Lab is affiliated with the Flinders Institute for Mental Health and Wellbeing and a founding partner of the Flinders Autism Research Initiative.

    Acknowledgements: Authors were supported by an Experimental Psychology Society small grant.

  • Evolutionary anthropologists warn modern life is outpacing human biology, fueling chronic stress and fertility declines

    Evolutionary anthropologists warn modern life is outpacing human biology, fueling chronic stress and fertility declines

    Evolutionary anthropologists Colin Shaw of the University of Zurich and Daniel Longman of Loughborough University argue that human biology is struggling to keep up with the speed of industrial and urban change. In a recent analysis, they describe a growing mismatch between the bodies shaped by evolution and the environments many people now inhabit.

    For most of human history, daily life involved frequent movement, natural light cycles and intermittent threats that triggered short, intense stress responses. The researchers say modern living has shifted those conditions within just a few centuries, adding prolonged sedentary time and near-constant stimulation.

    Why stress no longer turns off

    Shaw and Longman point to the stress response as a key example of this mismatch. They argue that the same biological systems once used to survive predators now activate in response to traffic, workplace pressure, social media and persistent urban noise.

    Unlike an acute threat that ends quickly, many modern stressors linger or recur throughout the day. Longman suggests that repeated activation without adequate recovery can keep the nervous system on high alert, which may contribute to long-term wear on multiple body systems.

    Health and fertility trends under scrutiny

    The analysis links the modern environment to concerns such as rising inflammatory and autoimmune conditions, alongside global fertility declines. The authors frame these patterns as potential signs that industrial exposures and lifestyles can undermine both wellbeing and reproduction.

    They also highlight research documenting declines in sperm count and sperm motility since the mid-20th century. Shaw notes that scientists have investigated potential connections with chemical exposures, including pesticides and herbicides, as well as emerging concerns about microplastics.

    What solutions could look like

    Because genetic adaptation typically unfolds over many generations, the researchers argue the mismatch is unlikely to resolve through evolution on any near-term timeline. Instead, they suggest the focus should be on redesigning environments to better fit human physiology.

    That could include treating access to nature as a public health priority and adjusting city design to reduce harmful exposures such as noise, air pollution and disruptive light at night. The authors say evidence on which stimuli most affect blood pressure, heart rate and immune function could help guide policy and planning.

  • Study suggests a part of the human auditory cortex is uniquely tuned to chimpanzee calls

    Study suggests a part of the human auditory cortex is uniquely tuned to chimpanzee calls

    The human brain is not limited to recognizing our own voices. Research from the University of Geneva (UNIGE) has revealed that specific parts of the auditory cortex react strongly to chimpanzee vocalizations. Chimpanzees are our closest relatives both genetically and in the types of sounds they produce. The study, which appears in the journal eLife, indicates that certain subregions of the brain may be especially tuned to the calls of particular primate species. This insight offers a new way to explore how voice recognition emerged and how it may relate to the development of language.

    Human voices play a central role in social communication, and a significant portion of the auditory cortex is devoted to interpreting them. Researchers wanted to know whether these abilities have deeper evolutionary origins. To investigate this question, scientists from UNIGE’s Faculty of Psychology and Educational Sciences used a comparative approach grounded in species evolution. By examining how the human brain processes the vocalizations of closely related species, such as chimpanzees, bonobos and macaques, they aimed to identify traits shared with other primates. This approach helps shed light on how the neural foundations of vocal communication began to emerge long before language existed.

    Studying How the Brain Responds to Primate Calls

    In the experiment, 23 human volunteers listened to vocal sounds from four species. Human voices served as the control group. Chimpanzee calls were included because these primates are closely related to us both genetically and acoustically. Bonobo vocalizations were also tested, even though they often sound more like birdsong. Macaque calls were added because these primates are more distantly related to humans both evolutionarily and acoustically. Researchers used functional magnetic resonance imaging (fMRI) to examine activity across the auditory cortex. “Our intention was to verify whether a subregion sensitive specifically to primate vocalizations existed,” explains Leonardo Ceravolo, research associate at UNIGE’s Faculty of Psychology and Educational Sciences and first author of the study.

    A Distinct Neural Response to Chimpanzee Vocalizations

    The results confirmed their expectations. A part of the auditory cortex known as the superior temporal gyrus, which plays a key role in processing sounds related to language, music and emotional cues, showed increased activation when participants heard certain primate calls. “When participants heard chimpanzee vocalizations, this response was clearly distinct from that triggered by bonobos or macaques.”

    This pattern is particularly striking because bonobos are just as genetically close to humans as chimpanzees, yet their vocalizations differ greatly in acoustic structure. The findings suggest that both evolutionary closeness and similarity in sound features influence how the human brain reacts.

    What the Findings Suggest About Language Evolution

    This discovery offers new directions for understanding how the neural basis of communication evolved. It indicates that some parts of the human brain may have preserved a sensitivity to the calls of our closest primate relatives. “We already knew that certain areas of the animal brain reacted specifically to the voices of their fellow creatures. But here, we show that a region of the adult human brain, the anterior superior temporal gyrus, is also sensitive to non-human vocalizations,” notes Leonardo Ceravolo.

    These results support the idea that humans and great apes share vocal processing abilities that existed before spoken language emerged. They may also help explain how voice recognition develops in early life. For instance, this line of research could clarify how babies begin recognizing familiar voices while still in utero.

  • MIT study links GRIN2A mutation to slower reality updating in schizophrenia, pointing to a treatable brain circuit

    MIT study links GRIN2A mutation to slower reality updating in schizophrenia, pointing to a treatable brain circuit

    Researchers at MIT report that a mutation in the gene GRIN2A may interfere with how the brain updates beliefs when new information arrives, a cognitive difficulty often seen in schizophrenia. In mouse experiments, the change was tied to slower, less adaptive decision-making in a shifting environment.

    Schizophrenia affects about 1% of people and has a strong genetic component, though the biology connecting risk genes to symptoms has been hard to pin down. Large genomic studies have identified many associated variants, but many sit in non-coding DNA, making their functional impact difficult to interpret.

    From genetic signal to mechanism

    To narrow in on mutations that directly alter proteins, the team drew on large-scale exome sequencing that compares protein-coding regions across people with schizophrenia and unaffected controls. That work has helped highlight a smaller set of genes where rare disruptive mutations can substantially increase risk.

    GRIN2A stands out because it encodes a subunit of the NMDA receptor, a key component of glutamatergic signaling involved in learning, plasticity and cognitive control. NMDA receptor dysfunction has long been considered relevant to schizophrenia, but linking specific mutations to circuit-level effects has remained challenging.

    Decision task reveals slower adaptation

    In the study’s behavioral task, mice chose between two levers with different reward sizes and different effort costs that changed over time. Typical mice shifted to the more efficient option once the higher-reward choice became too costly, reflecting flexible updating as conditions evolved.

    Mice carrying the GRIN2A-related mutation took longer to commit, continuing to alternate between choices after the balance of effort and reward had effectively changed. The researchers interpret the pattern as reduced ability to incorporate new evidence quickly, leaving prior expectations to dominate behavior for longer.

    A circuit that can be nudged

    Brain measurements pointed to altered activity in the mediodorsal thalamus and its connections with the prefrontal cortex, a pathway central to executive function and decision-making. The team reports that this thalamocortical circuit appeared to represent changing option values differently in the mutated mice.

    Using optogenetics to activate neurons in the mediodorsal thalamus, the researchers were able to push behavior toward the more adaptive pattern seen in control animals. While only a subset of patients would be expected to carry GRIN2A mutations, the results suggest the same circuit could contribute to cognitive symptoms across broader groups.

    The authors frame the work as a step toward treatments that target cognition, an area where many patients continue to experience impairment even when hallucinations or delusions are reduced. Next efforts focus on identifying druggable nodes in the thalamus–prefrontal pathway that might restore more flexible updating without invasive methods.

  • UC Berkeley study points to oxytocin as the fast track to friendship, and why some bonds take longer to form

    UC Berkeley study points to oxytocin as the fast track to friendship, and why some bonds take longer to form

    New research from the University of California, Berkeley suggests the hormone oxytocin helps speed up the early stages of friendship formation, sharpening the sense of preferring a familiar peer over a stranger. The work, published in Current Biology, adds nuance to oxytocin’s popular image by focusing on how quickly and selectively social bonds take shape.

    Oxytocin is released during a range of social and bodily experiences, including touch, sex, childbirth and breastfeeding, and it acts in the brain as a neuromodulator. While it is often linked with closeness and trust, scientists have also associated oxytocin signaling with social defensiveness, including stronger in-group and out-group behavior.

    The team studied prairie voles, a species widely used to examine social bonding because individuals form stable, selective relationships. Instead of focusing only on mating pairs, the researchers emphasized peer bonds that resemble human friendships, such as choosing to huddle and groom with one familiar partner rather than spending time with strangers.

    What changed without oxytocin receptors

    Using prairie voles engineered to lack oxytocin receptors, the researchers found the animals were slower to form a peer preference. In tests where typical voles show a strong preference after about 24 hours, the receptor-deficient animals often needed up to a week to reliably choose a familiar partner.

    The difference was not simply that the animals became less social overall. The findings point to reduced selectivity, meaning the altered animals were less consistent about who they sought out and were quicker to lose track of established partners when placed into new group settings.

    Friendship selectivity, not just sociability

    In a mixed-group, multi-room setup designed to mimic a party-like environment, typical voles spent early time near known companions before gradually mingling. Voles without oxytocin receptors mixed more freely from the start, behaving as if prior peer connections carried less weight.

    In another test measuring social motivation, female voles usually worked harder to access a familiar peer than a stranger. The receptor-deficient animals still showed motivation for a mate, but not for a friend, indicating that oxytocin signaling may matter more for the reward value of peer bonds than for mating bonds.

    A new look with oxytocin nanosensors

    To examine whether the brain compensated for missing receptors by releasing more oxytocin, researchers used an oxytocin nanosensor that fluoresces when it detects the molecule. Measurements indicated no excess oxytocin release and, instead, lower release from fewer sites in the nucleus accumbens, a region central to social reward.

    The results help explain why friendships formed more slowly and were less stable in challenging social conditions. Researchers say the work could inform future studies of psychiatric conditions where social bonding is disrupted, while underscoring that oxytocin’s role is complex and context-dependent.

    The study also fits into a growing body of vole research suggesting oxytocin is not strictly required for bonds to exist, but can strongly affect how efficiently they form. By separating friendship-like bonds from mating behavior, the authors argue that the biology of peer relationships deserves attention in its own right.

  • Gut microbiome study points to inflammatory sugars as a potential trigger for ALS and frontotemporal dementia

    Gut microbiome study points to inflammatory sugars as a potential trigger for ALS and frontotemporal dementia

    Researchers at Case Western Reserve University say they have identified a gut-driven immune mechanism that may help explain why brain damage progresses in amyotrophic lateral sclerosis and frontotemporal dementia. The work focuses on specific sugars produced by certain gut bacteria and how they may spark harmful inflammation.

    The study, published in Cell Reports, links bacterial glycogen molecules to immune activation that can injure neurons in models of ALS and FTD. The authors suggest the pathway could become both a diagnostic clue and a target for treatments aimed at the gut rather than the brain alone.

    How the proposed gut pathway works

    According to the researchers, some gut microbes can generate an inflammatory form of glycogen, a complex sugar, that appears to provoke immune responses tied to neurodegeneration. In the study’s patient samples, 70% of 23 people with ALS or FTD showed elevated levels of the implicated bacterial glycogen, compared with about one-third of people without the conditions.

    Aaron Burberry, an assistant professor at Case Western Reserve School of Medicine, said the team found that these microbial sugars can trigger immune reactions that ultimately damage brain cells. The results point to a potential way to interrupt the process by reducing or degrading the inflammatory glycogen.

    Why genes may not be the whole story

    The findings could be especially relevant for carriers of the C9orf72 mutation, the most common known genetic cause of ALS and FTD. Many carriers never develop disease, and the study adds evidence that environmental factors such as the gut microbiome may influence whether symptoms emerge.

    The researchers propose that certain bacterial communities may act as a switch that worsens inflammation in genetically susceptible people. That idea aligns with a growing body of research connecting immune activity, the microbiome, and neurodegenerative disease risk.

    What comes next for treatment research

    In experiments described by the team, lowering levels of the harmful glycogen improved brain health measures and extended lifespan in model systems. Alex Rodriguez-Palacios, also at Case Western, said reducing these sugars was associated with better outcomes, supporting efforts to design therapies that target the compounds in the gut.

    The group plans larger studies to track microbiome changes in ALS and FTD patients, including before and after disease onset where possible. Burberry said the results support clinical trials testing whether glycogen-degrading approaches could slow progression, though timelines and trial designs will depend on additional validation.

  • Study suggests strong social ties may slow biological aging, with epigenetic clocks offering new clues

    Study suggests strong social ties may slow biological aging, with epigenetic clocks offering new clues

    Building strong relationships throughout life — from loving parents in childhood to close friends, active communities, and faith involvement in adulthood — may actually slow how the body ages. Researchers suggest that these “social advantages” can influence biological aging markers known as epigenetic clocks, which track changes in DNA methylation. People who enjoy more supportive and connected lives often appear biologically younger than their chronological age.

    Long-Term Study Links Social Advantage to Youthful Biology

    The findings were published in the October issue of Brain, Behavior and Immunity — Health and draw on data from over 2,100 adults who participated in the long-running Midlife in the United States (MIDUS) study.

    Anthony Ong, a psychology professor at Cornell University, and his colleagues discovered that people with greater “cumulative social advantage” — a measure of lifelong social and emotional support — tended to show slower biological aging and reduced chronic inflammation.

    Measuring the Pace of Aging

    The study examined two leading measures of biological age, called GrimAge and DunedinPACE. Both are epigenetic clocks that scientists use to predict health risks and life expectancy. Participants with richer and more consistent social relationships displayed younger biological profiles on both measures.

    “Cumulative social advantage is really about the depth and breadth of your social connections over a lifetime,” Ong said. “We looked at four key areas: the warmth and support you received from your parents growing up, how connected you feel to your community and neighborhood, your involvement in religious or faith-based communities, and the ongoing emotional support from friends and family.”

    The Biology of Connection

    The researchers hypothesized that sustained social advantage becomes reflected in core regulatory systems linked to aging, including epigenetic, inflammatory and neuroendocrine pathways. Remarkably, they found that higher social advantage was linked to lower levels of interleukin-6, a pro-inflammatory molecule implicated in heart disease, diabetes and neurodegeneration. Interestingly, however, there were no significant associations with short-term stress markers like cortisol or catecholamines.

    Why Lifelong Relationships Matter

    Unlike many earlier studies that looked at social factors in isolation — whether a person is married, for example, or how many friends they have — this work conceptualized “cumulative social advantage” as a multidimensional construct. And by combining both early and later-life relational resources, the measure reflects the ways advantage clusters and compounds.

    “What’s striking is the cumulative effect — these social resources build on each other over time,” Ong said. “It’s not just about having friends today; it’s about how your social connections have grown and deepened throughout your life. That accumulation shapes your health trajectory in measurable ways.”

    Connection as a Form of Investment

    This doesn’t mean a single friendship or volunteer stint can turn back the biological clock. The authors suggest that the depth and consistency of social connection, built across decades and different spheres of life, matters profoundly. The study adds weight to the growing view that social life is not just a matter of happiness or stress relief but a core determinant of physiological health.

    “Think of social connections like a retirement account,” Ong said. “The earlier you start investing and the more consistently you contribute, the greater your returns. Our study shows those returns aren’t just emotional; they’re biological. People with richer, more sustained social connections literally age more slowly at the cellular level. Aging well means both staying healthy and staying connected — they’re inseparable.”