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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/psychedelic-retreats-show-promise-in-easing-depression-ptsd-and-reintegration-struggles-among-veterans/" 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;">Psychedelic retreats show promise in easing depression, PTSD, and reintegration struggles among veterans</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 16th 2025, 10:00</div>
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<p><p>A new study has found that military veterans who attended retreats involving psychedelic substances like psilocybin or ayahuasca experienced substantial short-term improvements in mental health, including symptoms of depression and post-traumatic stress disorder. The study, published in <em><a href="https://doi.org/10.1002/brb3.70660" target="_blank">Brain and Behavior</a></em>, also found that these retreats helped veterans with the often difficult transition back into civilian life.</p>
<p>The researchers set out to explore whether combining psychedelic therapy with communal retreat programs could offer an effective alternative for veterans facing mental health challenges. Veterans returning from combat deployments are at heightened risk for conditions like post-traumatic stress disorder and depression, and many report feelings of isolation and difficulty reintegrating into civilian society. </p>
<p>The study was conducted by researchers in collaboration with Heroic Hearts Project, a nonprofit that connects veterans with psychedelic retreat programs. </p>
<p>“At Heroic Hearts Project, in collaboration with researchers at Imperial College London, we set out to evaluate the impact of psychedelic-assisted retreats as a more accessible and scalable approach to supporting military veterans. Through observational research, we aimed to assess the real-world effectiveness of these naturalistic settings in addressing treatment-resistant PTSD and broader mental health challenges,” said study author Grace Blest‑Hopley, a research associate at King’s College London, chief scientific officer at NWPharma Tech, research director at the <a href="https://heroicheartsproject.org/" target="_blank">Heroic Hearts Project</a>, and founder of <a href="https://hystelica.com/" target="_blank">Hystelica</a>.</p>
<p>“Importantly, we used validated clinical measures commonly applied in veteran populations—allowing us to compare outcomes against standard benchmarks. We also focused on post-deployment reintegration and the transition from military to civilian life, recognizing this as a critical and often overlooked aspect of veterans’ long-term recovery.”</p>
<p>The research team recruited 58 military veterans who had signed up for either a psilocybin retreat in Jamaica or an ayahuasca retreat in Peru. Participants completed a range of mental health questionnaires before the retreat and again four weeks after returning home. These assessments measured symptoms of PTSD, depression, anxiety, sleep disturbance, post-concussion issues, quality of life, overall well-being, and success in reintegration after military service.</p>
<p>Before being accepted to participate in the retreat programs, all individuals underwent medical and psychological screening to ensure they were physically and mentally stable and not taking medications that might interact negatively with psychedelic substances. They also had to be free from a history of psychotic disorders. Most of the participants were male, in their 40s, and over 80% had a prior PTSD diagnosis. Many had additional diagnoses, including depression, anxiety, and chronic pain. Nearly one-third had never used a psychedelic substance before.</p>
<p>Retreats typically lasted five to seven days. In the psilocybin group, participants drank tea brewed from psychedelic mushrooms in two separate sessions, spaced 48 hours apart. Ayahuasca participants took part in three ceremonies led by indigenous facilitators. Before and after the retreat, participants engaged in group and individual coaching sessions designed to help them prepare for and integrate their experiences. These sessions were a core part of the healing process, encouraging reflection, emotional processing, and connection with fellow veterans.</p>
<p>After four weeks, the researchers found consistent and statistically significant improvements across all eight measured outcomes. The most pronounced effects were seen in depression and PTSD symptoms. On average, depression scores dropped by 29%, while PTSD scores declined by 26%. Participants also showed major gains in anxiety, sleep quality, post-concussion symptoms, and overall mental well-being. Improvements in civilian reintegration were also noted, with an 18% reduction in self-reported difficulties transitioning to post-military life.</p>
<p>“Our study found that psychedelic-assisted retreats can lead to significant early improvements in veterans’ mental health—particularly in depression and PTSD—as well as sleep, anxiety, and overall well-being,” Blest‑Hopley told PsyPost. “Veterans with more severe symptoms often saw the greatest benefit. These results suggest that psychedelic retreats could offer a holistic and scalable approach to supporting veterans, addressing both psychological healing and reintegration into civilian life.”</p>
<p>The researchers also examined how different psychedelic substances and participant characteristics influenced outcomes. Participants who attended psilocybin retreats generally showed greater overall improvement, particularly in measures like depression, anxiety, and post-concussion symptoms. However, veterans who attended ayahuasca retreats saw slightly greater reductions in PTSD symptoms.</p>
<p>Veterans who entered the program with high levels of depression or PTSD experienced the largest drops in their scores four weeks later. This suggests that the retreats may be especially helpful for veterans whose symptoms have not responded well to traditional treatments.</p>
<p>“Veterans with the most severe symptoms showed some of the largest gains,” Blest‑Hopley said. “It underscores the transformative potential of these interventions for those who’ve not responded well to conventional care.”</p>
<p>When the results were broken down by gender, male participants experienced greater improvements across most outcomes—including depression, anxiety, and reintegration—but female participants showed larger reductions in PTSD symptoms. But the researchers noted that the number of women in the study was small, which limits the ability to draw strong conclusions about gender differences.</p>
<p>Despite these encouraging results, the study had several limitations. It was observational in nature and lacked a placebo or control group, which makes it difficult to determine how much of the improvement was due to the psychedelic substances versus other factors, such as the group support or the retreat environment itself. Participants also volunteered for the study and many held positive beliefs about psychedelic therapy beforehand, which may have influenced their responses. In addition, the outcomes were measured only four weeks after the retreat, leaving open the question of whether the benefits would persist over time.</p>
<p>“We can’t disentangle the active psychedelic effect from the therapeutic retreat environment,” Blest‑Hopley noted. “Future randomized studies or control group comparisons are essential.”</p>
<p>The study also did not include data on the specific psychedelic doses administered, nor did it systematically track adverse effects. While the researchers noted that psychedelics are generally considered non-addictive and well-tolerated in clinical settings, the lack of detailed safety data limits the ability to fully assess the risks.</p>
<p>“Our long-term vision is to expand access to psychedelic-assisted retreats for more veterans, grow the healing community, and learn from our collective experiences to inform best practices,” Blest‑Hopley explained. “We aim to conduct meaningful research that helps us understand the real-world impact of these retreats and use that evidence to support advocacy—accelerating access for deserving groups like veterans and their families. Ultimately, we hope this work contributes to a framework for how psychedelic healing can be safely and effectively implemented across the wider population.”</p>
<p>“It’s incredibly encouraging to see such positive outcomes supporting the widespread impact of Heroic Hearts’ work. We remain deeply committed to responsibly expanding access to psychedelics for military veterans—bridging their immediate need for real-world healing with rigorous psychedelic science.”</p>
<p>The study, “<a href="https://doi.org/10.1002/brb3.70660" target="_blank">Exploring the Therapeutic Effects of Psychedelics Administered to Military Veterans in Naturalistic Retreat Settings</a>,” was authored by Megan Calnan, Grace Blest-Hopley, Chris Busch, Milly Adams, Simon G. D. Ruffell, Theodore Piper, Leor Roseman, Hannes Kettner, and Robin Carhart-Harris.</p></p>
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<td><a href="https://www.psypost.org/neurons-in-an-autism-model-fail-to-distinguish-social-from-non-social-touch/" 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;">Neurons in an autism model fail to distinguish social from non-social touch</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 16th 2025, 08:00</div>
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<p><p>New research provides a potential brain-based explanation for social touch aversion in some forms of autism. A study published in <a href="https://www.nature.com/articles/s41467-025-59852-6"><em>Nature Communications</em></a> finds that in a mouse model of Fragile X syndrome, a leading genetic cause of autism, neurons in key sensory and emotional brain regions fail to differentiate between being touched by another mouse and being touched by a plastic object. This apparent neural confusion is mirrored in the animals’ behavior, as they treat both social and non-social interactions as equally unpleasant, especially when the contact is unsolicited.</p>
<p>For most social animals, including humans, touch is a fundamental channel of communication and bonding. From a comforting hug to a friendly pat on the back, physical contact can convey emotion, build relationships, and offer solace. Brain circuits have evolved to recognize the unique significance of social touch, often prioritizing it over contact with inanimate things. However, for some individuals with neurodevelopmental conditions like autism spectrum disorder, social touch can be perceived not as pleasant, but as overwhelming or aversive.</p>
<p>This difference in sensory experience is a major focus for scientists seeking to understand the neural basis of autism. A team of UCLA researchers, led by Trishala Chari and <a href="https://porteralab.dgsom.ucla.edu/" target="_blank" rel="noopener">Carlos Portera-Cailliau</a>, set out to investigate the neural underpinnings of social touch aversion. They started with a specific question: Could it be that for individuals who find social touch unpleasant, their brains are not processing the unique “social value” of that touch? Perhaps, at a neural level, the brain fails to distinguish between a social interaction and a non-social one, leading to a negative or avoidant response to both.</p>
<p>“My lab is interested in understanding what is different at the circuit level in neurodevelopmental conditions. Fragile X syndrome is the most common inherited cause of intellectual disability and the leading single‑gene contributor to autism, and there is a very good mouse model for it (because it reproduces many of the same symptoms of the human disease), so we have focused on it,” explained Portera-Cailliau, a professor of neurology and neurobiology at the David Geffen School of Medicine at UCLA.</p>
<p>“I like to say we follow a symptom-to-circuit approach, meaning that we start with a specific symptom of autism, like sensory hypersensitivity and then record from neurons in circuits that would be responsible for that symptom. For example, in the past we discovered that aversion to repetitive whisker stimulation in Fragile X mice is associated with reduced habituation of neurons in the somatosensory cortex that process those whisker stimuli, whereas in control healthy mice (wild-type mice) the same neurons reduce their firing gradually because the whisker stimulation is not bothersome to them – it is non-threatening and non-salient – so they ignore it.”</p>
<p>“In this study, we wanted to investigate the circuit basis of another related symptom in Fragile X syndrome, aversion to social touch (hugging, kissing, tickling),” Portera-Cailliau said. “The ultimate goal of our symptom-to-circuit approach to neurodevelopmental conditions is to eventually identify an intervention at the neuronal level that might restore circuit function to wild type control levels, as a therapy for that symptom.”</p>
<p>To explore this, the researchers used a special strain of mice, known as Fmr1 knockout mice, which exhibit behaviors that are similar to Fragile X symptoms in humans, including sensory hypersensitivity and social avoidance. The scientists aimed to connect a specific behavior—aversion to social touch—directly to the activity of neurons in the brain circuits responsible for processing it.</p>
<p>The research was conducted in two main phases. First, the researchers needed to identify which brain regions were most active during social touch. To do this, they used a sophisticated genetic tool in a group of wild-type mice. This technique permanently marks any neurons that become highly active during a specific time window.</p>
<p>The researchers placed these mice in an apparatus where they were held comfortably in place but could run on a ball. A motorized platform then repeatedly presented them with either another mouse for a social interaction or a plastic tube for a non-social one.</p>
<p>By analyzing the brains of these mice afterward, the scientists could create a map of the brain regions that became active in response to these different types of touch. This mapping confirmed the involvement of the somatosensory cortex, a region that processes touch from the whiskers, and also highlighted two other key areas: the basolateral amygdala, known for its role in processing emotions like fear and pleasure, and the tail of the striatum, which is involved in making decisions based on sensory information.</p>
<p>In the second, and primary, phase of the study, the scientists conducted a more complex experiment with both wild-type mice and the Fmr1 knockout mice, the model for Fragile X syndrome. They surgically implanted state-of-the-art Neuropixels probes into the brains of these mice. These incredibly fine probes contain hundreds of electrodes, allowing the researchers to simultaneously record the individual electrical signals, or “spikes,” from hundreds of neurons across all three target brain regions: the somatosensory cortex, the tail of the striatum, and the basolateral amygdala.</p>
<p>With these probes in place, the mice were again placed in the behavioral apparatus. This time, the experiment was designed to test two different factors. The first was the context of the touch: social (another mouse) versus non-social (a plastic object). The second was the element of choice. In “voluntary” interactions, the platform would bring the other mouse or object close enough for the test mouse to reach out and explore it with its whiskers. In “forced” interactions, the platform moved closer, bringing the other mouse or object into direct contact with the test mouse’s snout, invading its personal space.</p>
<p>Throughout these trials, high-resolution cameras recorded the mice’s faces and bodies. The researchers used specialized software to analyze these videos for signs of aversion, such as running to avoid the interaction, squinting the eyes (orbital tightening), or moving the whiskers in a specific way.</p>
<p>“Our novel assay also allowed us to compare situations in which the interactions were voluntary (meaning the test mouse could choose to interact by whisking to palpate the other mouse or object) and situations where the test animal was forced to interact because the other mouse or object was brought into direct contact with its snout (basically being brought into its ‘personal space’ which we imagined would be more aversive than voluntary interactions),” Portera-Cailliau explained.</p>
<p>“This assay is pretty sophisticated: it involves a motor that moves the platform where the visitor mouse or object is placed, several high resolution cameras that focus on the mouse’s head, pupil, body, a bunch of electronics to keep track of when things happen, and custom code written in MATLAB and Python to run it all smoothly. Trishala built it all from scratch.”</p>
<p>The findings revealed a stark contrast between the two groups of mice, both in their behavior and their underlying brain activity. The wild-type mice behaved as expected for a social animal. They showed clear signs of aversion to the inanimate object, especially when it was forced upon them. They would run to avoid it and display negative facial expressions. When presented with another mouse, however, they were much more tolerant and did not show these same aversive behaviors. Their actions indicated that they could distinguish between a meaningless object and a meaningful social partner.</p>
<p>The Fmr1 knockout mice behaved very differently. They failed to make this distinction. They showed just as much aversion to the social touch of another mouse as they did to the non-social touch of the plastic object. Their behavior suggested that both experiences were equally unpleasant to them. This was particularly evident during forced interactions. When social touch was forcefully imposed onto them within their personal space, the Fmr1 knockout mice showed more aversive facial expressions than the wild-type mice, indicating that unsolicited social contact was especially bothersome for them.</p>
<p>“Wild-type mice clearly differentiated between social and non-social stimuli because they showed aversion to being brought in contact with an object, but not a mouse,” Portera-Cailliau told PsyPost. “We know this because we video-recorded their faces and used machine-vision approaches to analyze their facial expressions. Control mice showed squinting of their eyes and unusual posturing of their whiskers (whisker protraction) only when presented with an object, but they tolerated social interactions very well. We interpret this to mean that control mice seem to enjoy social interactions, but don’t like repeated interactions with a plastic object or a furry toy mouse, particularly when we forced it onto their personal space.”</p>
<p>“In contrast, Fmr1 knockout mice showed similar degrees of aversion to both object and social touch (even voluntary touch), as if they couldn’t tell them apart or felt that social touch was just as unpleasant as non-social touch. In other words, we could reproduce what is seen in the clinic with human Fragile X syndrome patients in the mouse model.”</p>
<p>The recordings from the Neuropixels probes provided a direct window into the brain activity driving these behaviors. In the wild-type mice, the neurons clearly reflected the animals’ behavioral preferences. Neurons in the somatosensory cortex showed different patterns of activity for social versus object touch, with a general preference for social stimuli. This suggests the sensory cortex does not just register the physical sensation of touch, but also its context.</p>
<p>In the tail of the striatum and basolateral amygdala, activity seemed less about the identity of the stimulus and more about the choice; neurons in these regions fired most intensely during the most aversive condition for the wild-type mice: forced object touch. This suggests these areas are involved in processing unwanted or unpleasant interactions.</p>
<p>In the brains of the Fmr1 knockout mice, this organized and discriminating neural response was largely absent. Neurons in their somatosensory cortex and tail of the striatum were much less able to tell the difference between social and object touch, especially during voluntary interactions. The distinct neural signature that signified “social” in the wild-type mice was blunted or missing.</p>
<p>Using computational models, the researchers confirmed that they could accurately predict whether a wild-type mouse was experiencing social or object touch just by looking at its neural activity. For the Fmr1 knockout mice, this prediction was far less accurate, because the neural signals for the two conditions were so similar. This suggests that the behavioral inability to distinguish social value stems from an inability of the underlying brain circuits to represent that value.</p>
<p>Finally, the researchers used a linear encoding model, a computational method to determine how strongly the activity of a neuron is related to different behaviors. In wild-type mice, the activity of neurons in the somatosensory cortex was strongly linked not only to the type of touch but also to the aversive facial expressions the mice made. In the Fmr1 knockout mice, this relationship between neural activity and aversive behavior was weaker and altered. This finding reinforces the idea that in this model of autism, the entire chain of processing, from representing a social stimulus to generating a behavioral response, is different.</p>
<p>“We found that neurons in the somatosensory cortex of control mice fired differently to social touch compared to object touch,” Portera-Cailliau said. “Most neurons showed greater modulation of their activity with social touch than with object touch, meaning they fired more to social interactions.”</p>
<p>“In contrast, neurons from Fmr1 knockout mice fired more similarly to both presentations, implying that at the network level the brain could not discriminate between social and non-social stimuli. This was further confirmed with a linear encoding model that determined how well each behavior variable (eye squinting, whisker protraction, pupil size, etc.) was encoded by the activity of a particular neuron.”</p>
<p>“The take home message is that neurons in mice with Fragile X symptoms seem less able to differentiate between social and non-social interactions, which could explain why at the behavior level they find both similarly annoying/aversive. Therefore, social avoidance in Fragile X syndrome/autism could relate to differences in the activity of neurons. By tweaking that activity it may be possible to restore a preference of certain neurons for social touch, which could help individuals better tolerate social interactions they find uncomfortable.”</p>
<p>The study does have some limitations. While behaviors like facial squinting and avoidance are strong indicators of a negative experience, it is impossible to know for certain what a mouse is subjectively feeling. The results will also need to be reproduced in other laboratories and with other animal models of autism to understand how broadly they apply.</p>
<p>“One worry is that we sometimes fall into the habit of anthropomorphizing too much what we see in mouse behavior. We are interpreting the facial expressions of certain Fmr1 knockout mice to social touch as reflecting aversion, unpleasantness, discomfort, but we can’t tell for sure what they experience,” Portera-Cailliau noted.</p>
<p>“There is also a lot of variability between individual mice, with some showing a lot of aversion and others less, and there was no universal way by which mice showed aversion: some mice that showed a lot of squinting to social interactions showed little whisker protraction or running avoidance, and vice versa. This may not be surprising. Humans don’t always respond the same way to certain irritating stimuli (like nails on a chalkboard).”</p>
<p>“It will also be important for other labs to reproduce similar results, not just in Fmr1 knockout mice, but in other models of autism spectrum disorder,” Portera-Cailliau added.</p>
<p>Despite these caveats, the research provides a powerful insight into the brain mechanisms of social touch processing. The team’s next steps include recording from other brain regions that may be involved and testing whether existing drugs could restore a more typical pattern of neural activity. They also plan to enhance the experiment by giving mice more control, for instance by letting them press a lever to bring a social partner closer or keep them away. This could help explore more nuanced aspects of social preference.</p>
<p>The study, “<a href="https://www.nature.com/articles/s41467-025-59852-6">A reduced ability to discriminate social from non-social touch at the circuit level may underlie social avoidance in autism</a>,” was authored by Trishala Chari, Ariana Hernandez, João Couto, and Carlos Portera-Cailliau.</p></p>
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<td><a href="https://www.psypost.org/medicinal-cannabis-may-actually-worsen-sleep-a-new-study-finds/" 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;">Medicinal cannabis may actually worsen sleep, a new study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 16th 2025, 06:00</div>
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<p><p>You might have heard cannabis and <a href="https://www.psypost.org/new-study-provides-first-objective-evidence-of-cannabinols-potential-to-improve-sleep/">cannabinoid</a> products can help people sleep. <a href="https://www.tga.gov.au/products/unapproved-therapeutic-goods/medicinal-cannabis-hub/medicinal-cannabis-access-pathways-and-usage-data">Data</a> shows one of the <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC9127064/">top reasons</a> people use cannabis is to help them sleep.</p>
<p>But there’s a dearth of high-quality research on how medicinal cannabis products actually affect sleep.</p>
<p>To find out more, our research team conducted a small pilot study involving 20 people. We wanted to compare how they slept after using a medicinal cannabis product, compared to a placebo.</p>
<p>The results of the <a href="https://onlinelibrary.wiley.com/doi/10.1111/jsr.70124">study</a>, published in the <em><a href="https://onlinelibrary.wiley.com/doi/10.1111/jsr.70124">Journal of Sleep Research</a></em>, surprised us.</p>
<p>We found a single oral dose of a cannabinoid product decreased total sleep time and the time spent in REM sleep (rapid eye movement, which is when we tend to dream). We didn’t observe any change in objective alertness the day after the treatment.</p>
<p>Our study is small and only measured the effect of a single dose, so more research is clearly needed.</p>
<p>But overall, our findings suggest cannabinoids may acutely influence sleep, primarily by suppressing REM sleep, without noticeable next-day impairment.</p>
<h2>What we did</h2>
<p>All 20 people (16 of whom were female) involved in our study had a clinical diagnosis of insomnia disorder.</p>
<p>This means they reported having challenges falling asleep and/or maintaining sleep and that these disturbances impact day-to-day functioning socially, at work, or in other important areas of life.</p>
<p>The average age of our study participants was about 46 years.</p>
<p>At our lab, the study participants were interviewed by a doctor and had their medical history taken. All participants also underwent an overnight diagnostic sleep study. This was done to confirm their sleeplessness was truly insomnia and not other conditions such as sleep apnoea.</p>
<p>Once the participant was able to start the study, they were asked to sleep for two nights at our lab, with at least one week between those two visits.</p>
<p>On one of their visits, they were given a placebo.</p>
<p>On the other, they were given a single oral dose of a medical-grade cannabis oil containing 10 mg THC (tetrahydrocannabinol, the compound responsible for the psychoactive effects of cannabis) and 200 mg CBD (cannabidiol, which does not produce a “high”).</p>
<p>Using a product with a precise, known dose ensures the results are relevant to what doctors in Australia are already prescribing.</p>
<p>The order in which participants received either the treatment or the placebo was randomised, so they didn’t know which one they were taking.</p>
<p>After taking either the treatment or the placebo, they slept at our lab while wearing a special cap with 256 monitors on it. This high-density electroencephalogram or EEG allowed us to record the electrical activity of the brain while the person slept.</p>
<p>The next morning, after they either woke or were woken, they performed a driving simulation test around the time of their normal morning commute.</p>
<p>They also underwent a test that assessed their ability to stay awake in a quiet, dimly lit environment. To track their alertness throughout the day, they repeated this test four times while wearing the high-density EEG cap. This was so we could test their alertness the day after either the treatment or the placebo.</p>
<h2>What we found</h2>
<p>Our results were not what we expected.</p>
<p>We found the THC/CBD treatment decreased total sleep time by an average of 24.5 minutes. This was largely driven by a significant impact on REM sleep (the phase associated with dreaming), which not only decreased by an average of 33.9 minutes but also took significantly longer for participants to enter. The treatment also offered no benefit in helping participants stay asleep throughout the night.</p>
<p>Perhaps most intriguingly, this objective worsening of sleep wasn’t reflected in the participants’ own perceptions; they reported no change in their subjective sleep quality. This disconnect continued into the next day.</p>
<p>While participants noted feeling slightly more sleepy after the treatment, their objective alertness – measured by their ability to stay awake in a quiet, dimly lit room – was reassuringly unchanged, as was their cognitive and simulated driving performance.</p>
<p>This leads to a crucial question: if a single dose produces these changes, what are the cumulative effects on a person’s sleep after weeks, months, or years of nightly use?</p>
<p>We simply don’t have the answers yet, especially with a medical-grade cannabis product.</p>
<h2>A growing body of research</h2>
<p>Our findings underscore a significant gap between the widespread public perception of cannabis for sleep and the complex scientific reality. As highlighted by a <a href="https://pubmed.ncbi.nlm.nih.gov/39612156/">review</a> we published in the journal <a href="https://pubmed.ncbi.nlm.nih.gov/39612156/">Current Psychiatry Reports</a>, the evidence base remains thin.</p>
<p>We reviewed 21 recent studies (published between 2021 and 2024) of cannabinoids being used for insomnia, subjective sleep impairment, obstructive sleep apnoea, rapid eye movement sleep behaviour disorder, and restless legs syndrome.</p>
<p>We found that, despite its widespread use, there’s not enough research yet to support the use of medical cannabis to treat sleep disorders.</p>
<p>This is why this kind of research is so vital. It provides the first pieces of a much larger puzzle.</p>
<p>To give doctors and patients the clear guidance they need, there is an urgent need for adequately funded, well-designed clinical trials with larger sample sizes and longer treatment durations to truly understand the long-term impacts of medicinal cannabis on sleep and daytime functioning.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/256467/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<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/cannabinoid-products-may-reduce-total-sleep-time-in-adults-with-insomnia-new-study-256467">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/scientists-identify-the-brains-built-in-brake-for-binge-drinking/" 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 the brain’s built-in brake for binge drinking</a>
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<p><p>Despite the profound human, social and economic costs of alcohol abuse, existing treatments have failed to provide meaningful relief. Excessive alcohol consumption remains a leading cause of <a href="https://www.who.int/publications/i/item/9789240096745">death and disability worldwide</a>. In the U.S. alone, <a href="https://www.samhsa.gov/data/data-we-collect/nsduh-national-survey-drug-use-and-health/national-releases/2023">16.4 million people</a> age 12 and older reported binge drinking on five or more days in the past month.</p>
<p>Although there are several drugs available to those seeking to stop or lower their alcohol consumption, their <a href="https://doi.org/10.1080/08897077.2015.1133472">effectiveness is limited</a>, and they often have significant side effects. Over the past three decades, efforts to treat excessive drinking have focused primarily on developing drugs that target proteins that can control how neurons respond to stimuli. Because these proteins are present in almost every neuron throughout the brain, the drugs also affect neurons that aren’t directly responsible for regulating alcohol’s effects. This often leads to unwanted side effects like headache, fatigue, drowsiness or insomnia.</p>
<p>In my work <a href="https://www.researchgate.net/profile/Gilles-Martin-3">as a neurobiologist</a>, I study the idea that pinpointing the specific brain circuits that play a role in suppressing alcohol consumption is critical to developing targeted treatments with limited side effects. In my newly published research, my team and I identified a small cluster of <a href="https://www.nature.com/articles/s41593-025-01970-x">neurons responsible for suppressing binge drinking</a>.</p>
<h2>A map of binge drinking neurons</h2>
<p>Researchers have <a href="https://doi.org/10.1038/sj.mp.4000206">identified several brain regions</a> that play a key role in alcohol abuse. But there has been strong evidence that only a very small number of neurons within these regions underpinned the effects of the drug on brain function.</p>
<p>Small populations of neurons, called <a href="https://theconversation.com/memories-of-the-good-parts-of-using-drugs-can-keep-people-hooked-altering-the-neurons-that-store-them-could-help-treat-addiction-245529">neuronal ensembles</a>, have been shown to play a <a href="https://doi.org/10.1016/j.conb.2015.07.009">key role</a> in <a href="https://doi.org/10.1038/nature11028">memory formation</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/35379803">experiencing fear</a>. However, researchers haven’t known whether the neuronal ensembles activated during binge drinking also influence binge drinking behavior.</p>
<p>Considering the <a href="https://doi.org/10.1159/000437413">billions of neurons</a> contained in the brain, the task of identifying these neurons is akin to finding a needle in a haystack. To solve this challenge, my colleagues and I used a genetically modified mouse model that, upon exposure to alcohol, activates a gene coding for a red fluorescent protein that is selectively expressed in alcohol-sensitive neurons. By tracing these fluorescent neurons, we were able to make a <a href="https://www.nature.com/articles/s41593-025-01970-x">map of the precise locations of affected neurons</a>.</p>
<p>We identified a discrete number of neurons that respond to binge drinking in a brain region called the <a href="https://doi.org/10.1016/j.pnpbp.2018.01.010">medial orbitofrontal cortex</a>. This area is known for its key role in controlling decision-making and adapting behavior to a changing environment.</p>
<p>We also found that turning this neuronal ensemble off resulted in a <a href="https://www.nature.com/articles/s41593-025-01970-x">sharp increase of alcohol consumption</a> in mice. This means that the brain has, in essence, a built-in regulation system that is activated during alcohol drinking to act as a brake on its consumption. Should these neurons misfire, the regulatory system would fail, possibly leading to uncontrolled drinking.</p>
<h2>Future treatments</h2>
<p>Although this study advances our understanding of how and where binge drinking modulates brain function in mice, it remains unclear whether human brains are also equipped with the same neuronal ensemble. If they are, stimulating these neurons may provide a path toward helping people who experience difficulty controlling their alcohol intake.</p>
<p>Although selective control of neuronal activity is a formidable challenge, <a href="https://www.umassmed.edu/news/news-archives/2016/04/newsweek-umass-medical-school-develops-gene-therapy-for-rare-neurodegenerative-disease/">progress in gene therapy</a> for patients with cancer and other rare diseases offers hope for more effective alcohol use disorder treatments with fewer side effects.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/257217/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<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/binge-drinking-brake-found-in-mouse-brains-offering-future-path-to-treating-alcohol-abuse-new-research-257217">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/trumps-speeches-stump-ai-study-reveals-chatgpts-struggle-with-metaphors/" 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;">Trump’s speeches stump AI: Study reveals ChatGPT’s struggle with metaphors</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 15th 2025, 12:00</div>
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<p><p>President Donald Trump’s political speeches recently served as a testing ground for the capabilities and limitations of large language models. By analyzing the metaphors embedded in four major speeches, researchers not only gained insight into Trump’s rhetorical strategies but also exposed key weaknesses in artificial intelligence systems like ChatGPT when it comes to understanding figurative language in political contexts. Their findings are published in <em>Frontiers in Psychology</em>.</p>
<p>Large language models, or LLMs, are computer programs trained to understand and generate human language. They work by analyzing vast amounts of text—such as books, websites, and conversations—and learning statistical patterns in how words and sentences are used. LLMs like ChatGPT can write essays, summarize documents, answer questions, and even hold conversations that feel natural.</p>
<p>However, they do not truly understand language the way humans do. Instead, they rely on pattern recognition to predict what words are likely to come next in a sentence. This can lead to convincing results in many situations, but it also means the models can misinterpret meaning, especially when language is abstract or emotionally charged.</p>
<p>To test how well a large language model can detect metaphors in political speech, the researchers selected four of Donald Trump’s speeches from mid-2024 to early 2025. These included his Republican nomination acceptance speech after surviving an assassination attempt, his post-election victory remarks, his inaugural address, and his speech to Congress. These texts, totaling over 28,000 words, were chosen because they are filled with emotionally charged and ideologically driven language, often using metaphor to frame political issues in ways that resonate with supporters.</p>
<p>The researchers used a method called critical metaphor analysis to examine the text. This method focuses on how metaphors influence political thinking and shape public attitudes. They then adapted this method for use with ChatGPT-4, prompting the model to go through a step-by-step process: understand the context of the speech, identify potential metaphors, categorize them by theme, and explain their likely emotional or ideological impact.</p>
<p>The large language model was able to detect metaphors with moderate success. Out of 138 sampled sentences, it correctly identified 119 metaphorical expressions, giving it an accuracy rate of around 86 percent. But a closer look revealed several recurring problems in the model’s reasoning. These issues provide insight into the limitations of artificial intelligence when it tries to interpret complex human communication.</p>
<p>One of the most common mistakes was confusing metaphors with other forms of expression, such as similes. For example, the model misinterpreted the phrase “Washington D.C., which is a horrible killing field” as metaphorical when it is more accurately described as a literal, emotionally charged comparison. The model also tended to overanalyze simple expressions.</p>
<p>In one case, it flagged the phrase “a series of bold promises” as metaphorical, interpreting it as a spatial metaphor when no such figurative meaning was intended. The model also struggled to correctly classify names and technical terms. For instance, it treated “Iron Dome,” the name of Israel’s missile defense system, as a metaphor instead of a proper noun.</p>
<p>These missteps show that while LLMs can detect surface-level patterns, they often lack the ability to understand meaning in context. Unlike humans, they do not draw on lived experience, cultural knowledge, or emotional nuance to make sense of language. This becomes especially apparent when analyzing political rhetoric, where metaphor is often used to tap into shared feelings, histories, and identities.</p>
<p>The study also tested the model’s ability to categorize metaphors based on shared themes or “source domains.” These categories include concepts like Force, Movement and Direction, Health and Illness, and the Human Body. For example, Trump frequently used phrases like “We rise together,” “Unlock America’s glorious destiny,” and “Bring law and order back,” which were successfully classified as Movement or Force metaphors. These metaphors help convey ideas of progress, strength, and control—key themes in campaign messaging.</p>
<p>However, the model performed poorly in less common or more abstract categories, such as Cooking and Food or Plants. In the Plants category, it failed to detect any relevant metaphors at all. In Cooking and Food, it produced several false positives, identifying metaphors that human reviewers judged to be literal. These results suggest that LLMs are more reliable when working with familiar, frequently used metaphor types and less reliable in areas that require nuanced understanding or cultural context.</p>
<p>To verify their findings, the researchers compared the AI-generated results with those produced by traditional metaphor analysis tools, such as Wmatrix and MIPVU. The results were strongly correlated overall, but some differences stood out. ChatGPT was faster and easier to use, but its accuracy varied widely across metaphor categories. In contrast, the traditional methods were slower but more consistent in identifying metaphors across all categories.</p>
<p>Another issue the study uncovered is that LLM performance depends heavily on how prompts are written. Even small changes in how a question is asked can affect what the model produces. This lack of stability makes it harder to reproduce results and undermines confidence in the model’s reliability when dealing with sensitive material like political speech.</p>
<p>The researchers also noted broader structural problems in how LLMs are trained. These models rely on enormous datasets scraped from the internet, much of which is uncurated and not annotated for meaning. As a result, LLMs may lack exposure to metaphorical language in specific cultural, historical, or political contexts. They may also pick up and reproduce existing biases related to gender, race, or ideology—especially when processing emotionally or politically loaded texts.</p>
<p>The researchers conclude that while large language models show promise in analyzing metaphor, they are far from replacing human expertise. Their tendency to misinterpret, overreach, or miss subtleties makes them best suited for assisting researchers rather than conducting fully automated analysis. In particular, political metaphors—which often rely on shared cultural symbols, deep emotional resonance, and implicit ideological framing—remain difficult for these systems to understand.</p>
<p>The study, “<a href="https://doi.org/10.3389/fpsyg.2025.1591408" target="_blank" rel="noopener">Large language models prompt engineering as a method for embodied cognitive linguistic representation: a case study of political metaphors in Trump’s discourse</a>,” was authored by Haohan Meng, Xiaoyu Li, and Jinhua Sun.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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