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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/does-trauma-in-childhood-influence-emotional-dynamics-in-adult-sexual-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;">Does trauma in childhood influence emotional dynamics in adult sexual relationships?</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 27th 2025, 10:30</div>
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<p><p>A study of couples in Canada found that individuals who reported greater exposure to childhood trauma tended to experience slightly fewer positive emotions and slightly more negative emotions during a sexual conflict with their partner. These individuals also tended to report slightly higher levels of attachment anxiety. The paper was published in the <a href="https://link.springer.com/article/10.1007/s10508-025-03120-7"><em>Archives of Sexual Behavior</em></a>.</p>
<p>Childhood trauma refers to serious adverse experiences during childhood that overwhelm a child’s ability to cope and can have lasting psychological effects. These may include physical, emotional, or sexual abuse; neglect; witnessing domestic violence; the loss of a parent; or chronic exposure to instability or danger.</p>
<p>Traumatic events can disrupt normal brain development and affect memory, emotion regulation, and learning. Children exposed to trauma may develop anxiety, depression, posttraumatic stress disorder, or behavioral issues. They may struggle with trust, self-esteem, and forming healthy relationships later in life. The impact of trauma often persists into adulthood, influencing physical health, mental well-being, and social functioning.</p>
<p>Study author Noémie Bigras and her colleagues set out to examine whether greater childhood trauma is associated with the duration of experienced and expressed positive and negative emotions during a sexual conflict discussion between romantic partners. They also explored whether attachment anxiety and avoidance mediate the relationship between childhood trauma and these emotional responses.</p>
<p>In this context, sexual conflict refers to an eight-minute discussion about the most important sexual problem identified by one or both partners in a couple. Attachment avoidance and anxiety are two dimensions of adult attachment. Attachment avoidance reflects discomfort with closeness, emotional distancing, and self-reliance. Attachment anxiety reflects fear of rejection, preoccupation with the relationship, and a need for reassurance and closeness.</p>
<p>Study participants were 151 couples recruited from two Canadian cities through online advertisements, posters, and word of mouth between May 2019 and January 2020. To be eligible, participants needed to be at least 18 years old, have a history of sexual activity with their partner (broadly defined), be fluent in French or English, be in a monogamous relationship, and have lived with their current partner for at least one year.</p>
<p>As part of the study, couples took part in a laboratory session that involved four discussion tasks: a five-minute warm-up discussion about everyday events; an eight-minute discussion of a previously undisclosed personal positive experience; an eight-minute discussion about their most significant sexual concern (the sexual conflict task); and a five-minute cooldown discussion about each other’s attractive qualities.</p>
<p>Participants also completed the Childhood Trauma Questionnaire (short form) and the Experiences in Close Relationships Questionnaire to assess trauma history and attachment style, respectively. After the sexual conflict discussion, they reported the emotions they experienced using the Positive and Negative Affect Schedule. In addition, the researchers assessed the duration of emotional experiences and expressions during the conflict by analyzing video footage using joystick-based continuous ratings provided by the participants and trained observers.</p>
<p>The results showed that individuals with higher levels of childhood trauma tended to report experiencing slightly fewer positive emotions and slightly more negative emotions following the sexual conflict. They were also observed and self-reported to have shorter durations of positive emotions during the interaction.</p>
<p>Greater trauma exposure was also associated with slightly higher attachment anxiety. Statistical modeling indicated that attachment anxiety helped explain (i.e., mediated) the link between childhood trauma and post-discussion emotional responses. Specifically, individuals with greater trauma histories tended to have higher attachment anxiety, which in turn was linked to more negative and fewer positive emotional experiences during the conflict.</p>
<p>“Results showed how the experience of childhood trauma both by itself and via attachment anxiety can make conflictual discussions surrounding sexuality more triggering and distressing and therefore elicit more difficult emotions to recover. As positive emotions appear to be processed differently than negative emotions, results also invite clinicians and researchers to not dwell exclusively on the manifestations of negative emotions in the aftermath of childhood trauma,” the study authors concluded.</p>
<p>The study sheds light on the links between childhood trauma and experiences in sexual conflict. However, it should be noted that the reported associations were all very weak, almost negligible. Additionally, the design of the study does not allow any causal inferences to be derived from the results.</p>
<p>The paper, “<a href="https://doi.org/10.1007/s10508-025-03120-7">Attachment Insecurity Mediates the Associations Between Childhood Trauma and Duration of Emotions During a Laboratory‑Based Sexual Confict Discussion Among Couples,</a>” was authored by Noémie Bigras, Natalie O. Rosen, Justin P. Dubé, Marie‑Ève Daspe, Myriam Bosisio, Katherine Péloquin, and Sophie Bergeron.</p></p>
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<td><a href="https://www.psypost.org/sexual-activity-before-bed-improves-objective-sleep-quality-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;">Sexual activity before bed improves objective sleep quality, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 27th 2025, 08:00</div>
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<p><p>Engaging in sexual activity—whether solo or with a partner—can lead to better sleep, according to a new pilot study published in the journal <em><a href="https://doi.org/10.1016/j.sleh.2024.11.004" target="_blank" rel="noopener">Sleep Health</a></em>. The research found that both partnered sex and solo masturbation reduced the amount of time people spent awake during the night and improved overall sleep efficiency. These effects were not reflected in subjective reports of sleep quality, but objective sleep monitoring showed consistent improvements following sexual activity compared to nights without it.</p>
<p>While many people believe that orgasm has a relaxing effect and promotes sleep, most existing evidence has relied on subjective reports. Only one study—conducted more than three decades ago—had attempted to objectively measure sleep following sexual activity, and it had significant design limitations. The present research aimed to address this gap by using a portable brain-monitoring device to measure sleep stages and sleep quality in a real-world setting.</p>
<p>“I have been investigating sleep behaviors in the adult population for several years, while this has predominantly focused on improving the sleep behaviors of elite athletes, I am always asked various questions about sleep,” said study author Michele Lastella, a senior lecturer at CQUniversity Australia.</p>
<p>“A frequent question asked ‘how come my partner falls asleep straight away after sex and I can’t’ and I thought if people are frequently asking me questions about this, then this must be indicative that there is a real lack of research evidence around it. One of the main reasons it hadn’t previously been explored in depth was related to the taboo associated with people being afraid to talk about sex. When people would ask question, a lot of the time it was associated with the males falling asleep and the women weren’t, and I thought this may be something related to the orgasm.”</p>
<p>The new study is part of a broader research effort investigating the relationship between sex and sleep. Earlier work Lastella and his colleagues <a href="https://doi.org/10.3389/fpubh.2019.00033" target="_blank" rel="noopener">surveyed 778 people and found</a> that both men and women perceived that sex with orgasm helped them fall asleep faster and sleep better. These findings prompted the current study, which provides a more detailed and objective look at how sexual activity influences sleep physiology.</p>
<p>The researchers recruited seven heterosexual couples, comprising 14 participants in total, all of whom were healthy, sexually active, and living together in South Australia. Participants were screened to ensure they had no sleep disorders, were not pregnant, and did not have children, which could affect sleep routines. All participants reported engaging in sexual activity at least twice a week. The final sample consisted of 7 males and 7 females, each around 26 years old.</p>
<p>Participants were monitored over 11 consecutive nights using a repeated-measures, crossover design. Each couple completed nights in three different conditions: no sexual activity, solo masturbation (with orgasm), and partnered sex (with orgasm). To measure sleep objectively, participants wore a wireless polysomnographic device (DREEM3 headband), which recorded brain activity, movement, and breathing during the night. Participants also completed self-report diaries each morning, detailing their sexual activity, sleep quality, mood, and readiness for the upcoming day.</p>
<p>On nights when participants engaged in sexual activity, they went to bed later than on nights with no sex. However, they also spent significantly less time awake after falling asleep and had higher sleep efficiency, meaning they spent a greater proportion of their time in bed actually sleeping. Sleep efficiency was 93.2% following solo masturbation and 93.4% after partnered sex, compared to 91.5% on nights with no sexual activity. Participants spent about 7 minutes less awake during the night following sexual activity.</p>
<p>Interestingly, the improvements in sleep were evident only in the objective data. Participants did not report significant differences in how well they thought they had slept across the three conditions.</p>
<p>“We observed that engaging in sexual activity regardless of whether it was solo masturbation or partnered sexual activity, improved objective sleep quality by reducing the amount of time spent awake throughout the night and improved overall sleep efficiency,” Lastella told PsyPost. “There were no differences in sleep duration, sleep latency and subjective sleep measures.”</p>
<p>However, they did report feeling more motivated and ready for the day following partnered sex. On average, participants rated their motivation and readiness 8–11 points higher (on a 100-point scale) after a night of partnered sex compared to nights without sex.</p>
<p>Another aspect the study examined was how sexual activity might influence the synchronization of sleep stages between partners, known as sleep stage concordance. Previous studies have shown that couples who share a bed tend to enter REM sleep at similar times, suggesting that cosleeping can influence sleep patterns. This study found that REM sleep stage concordance was significantly longer when couples slept together—regardless of whether they had engaged in sex—compared to when they slept alone. This suggests that the act of cosleeping itself may promote synchronized REM sleep, potentially due to shared environmental and physiological cues.</p>
<p>When looking at specific sleep stages, the researchers found that participants spent more time in the lightest stage of sleep (N1) on nights without sexual activity. While the difference—about 2 minutes—was statistically significant, it is unlikely to have clinical significance. Other stages of sleep, including deep sleep (N3) and REM sleep, did not show significant differences across the three conditions, although there were trends suggesting some improvements following sexual activity.</p>
<p>These findings are in line with previous research. For example, a 2023 study published in the Journal of Sleep Research used a 14-day diary method and found that partnered sex with <a href="https://www.psypost.org/partnered-sexual-activity-with-orgasm-improves-sleep-study-finds/" target="_blank" rel="noopener">orgasm was associated with shorter time to fall asleep</a> and better self-reported sleep quality. However, that study did not include objective sleep measures and found inconsistent results for solo masturbation. The current study supports the idea that orgasm, regardless of whether it occurs alone or with a partner, may have sleep-promoting effects—but these effects are more clearly captured through objective measurement.</p>
<p>The study authors suggest that hormonal changes following orgasm could explain the observed benefits to sleep. Orgasm is known to increase the release of oxytocin and prolactin while reducing cortisol levels. Oxytocin, often called the “bonding hormone,” has been linked to lower stress and better sleep, while prolactin is associated with sexual satisfaction and relaxation. These hormonal shifts may reduce arousal and promote a smoother transition into restful sleep.</p>
<p>However, the study had several limitations. The sample was small, consisting of only 14 participants, all of whom were healthy heterosexual couples. This limits the ability to generalize the findings to broader populations, such as older adults, people with sleep disorders, or those in non-heterosexual relationships. The participants also had to activate their sleep monitoring devices after sexual activity, which may have interfered with the natural transition into sleep and reduced the chance of capturing very short sleep onset latencies.</p>
<p>“One of the main challenges is setting up the device to record following sexual activity, as in an ideal real world scenario individuals would be able to simply attempt to sleep following sexual activity without having to activate/record on a device,” Lastella noted.</p>
<p>Another limitation was the potential for social desirability bias in self-reported measures. While the objective data were less susceptible to this, participants might have felt inclined to rate their sleep or sexual experiences more positively. The researchers note that future studies should aim to include a more diverse and larger sample and should explore whether sexual activity could be used as a behavioral intervention for people with poor sleep.</p>
<p>“We are actively seeking funding to support our third part of the investigation recruiting a larger sample with participants with poor sleep quality or behaviours and examine if sexual activity can help subsequent sleep behavior,” Lastella said. “This type of research is important as it provide us with a non-pharmaceutical approach toward improving not only sleep behavior but health and wellbeing as a collective. Please reach out if this research interests you, and there are funding opportunities that might support this type of research.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.sleh.2024.11.004" target="_blank" rel="noopener">Sleep on it: A pilot study exploring the impact of sexual activity on sleep outcomes in cohabiting couples</a>,” was authored by Michele Lastella, Dean J. Miller, Ashley Montero, Madeline Sprajcer, Sally A. Ferguson, Matthew Browne, and Grace E. Vincent.</p></p>
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<td><a href="https://www.psypost.org/new-research-shows-decaf-coffee-can-mimic-caffeines-effects-in-habitual-drinkers/" 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;">New research shows decaf coffee can mimic caffeine’s effects in habitual drinkers</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 27th 2025, 06:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.heliyon.2024.e41471" target="_blank" rel="noopener">Heliyon</a></em> suggests that the energizing effects of coffee might have less to do with caffeine and more to do with the ritual of drinking it. In a double-blind, placebo-controlled experiment involving habitual coffee drinkers, researchers found that ingesting decaffeinated coffee produced many of the same physiological and cognitive responses as caffeinated coffee. These findings suggest that regular coffee consumers may react to the experience of drinking coffee in ways that are independent of its caffeine content.</p>
<p>Coffee is a cornerstone of daily life for billions of people around the world. Its perceived benefits include enhanced alertness, improved focus, and a sense of readiness to take on the day. While these effects are typically attributed to caffeine, some researchers have argued that other factors—such as the smell, taste, or even the expectation of coffee—might also play a role. In particular, habitual coffee drinkers may develop conditioned responses, where the mere act of consuming coffee triggers physiological changes regardless of whether caffeine is actually present.</p>
<p>“Caffeine is something we use everyday, yet is poorly understood, and thus makes an inviting study subject. We wanted to understand what actually triggers the physical and mental effects people associate with coffee, especially in regular drinkers,” said study author Mateja Lesar, a research assistant at the <a href="https://www.fis.unm.si/?lang=en" target="_blank" rel="noopener">Faculty of Information Studies in Novo Mesto</a>.</p>
<p>“Is it the caffeine, or could it be the ritual itself? The act of drinking coffee has a clear ‘ritualistic’ dimension associated with it, but its impact is hard to separate from the impact of caffeine. To explore this, we sought to separate the effects of caffeine from the experience of drinking coffee by using decaf that looks, smells, and tastes just like regular coffee. This allowed us to investigate how much of the response is driven by expectation and habit compared to the caffeine.”</p>
<p>For their study, the researchers designed a controlled experiment focused on separating the effects of caffeine from the psychological and physiological effects of the coffee-drinking ritual. The study recruited 20 healthy university students (10 male and 10 female) who were habitual coffee drinkers, consuming one to three cups per day. All participants abstained from caffeine for at least eight hours before the experiment.</p>
<p>The participants were randomly assigned to receive either caffeinated or decaffeinated coffee. Importantly, both beverages were identical in appearance and taste, and both were made using decaffeinated coffee beans—with caffeine powder added back into the drink for the caffeine group. This approach ensured that participants in both groups believed they were drinking regular coffee. Throughout the experiment, participants underwent several assessments both before and after coffee consumption: their heart rate and blood pressure were measured, they completed a mental arithmetic test and an auditory attention task, and their brain activity was recorded using electroencephalography (EEG).</p>
<p>The researchers hypothesized that if caffeine was responsible for the alerting effects of coffee, then participants who consumed caffeinated coffee would exhibit more pronounced changes in cardiovascular and cognitive performance, as well as distinct patterns of brain activity, compared to those who received the placebo.</p>
<p>Surprisingly, the results did not fully support this expectation. Across the board, both groups showed similar physiological changes following coffee ingestion. Heart rate decreased and blood pressure increased after consuming either drink, with no significant differences between the caffeine and placebo groups.</p>
<p>“Both decaf and a high dose of caffeine produced similar cardiovascular effects,” Lesar said. “If anything, here is where we would expect a discrepancy between the two beverages, since these are harder to attribute to ritual.”</p>
<p>Cognitive performance was also largely unaffected by the presence of caffeine. In a mental arithmetic task, participants’ accuracy and number of responses did not change significantly after drinking either type of coffee. In contrast, reaction times during an auditory attention task improved slightly in both groups. However, this improvement was statistically significant only for the caffeine group. While this suggests that caffeine may enhance processing speed, the fact that the placebo group also improved—despite ingesting no caffeine—points to a possible placebo effect, fueled by the participants’ expectations.</p>
<p>The EEG data revealed more subtle distinctions. During the attention task, brain wave patterns associated with cognitive processing (specifically, the P3 component) increased in both groups after coffee consumption. However, only the caffeine group showed a statistically significant increase. Resting-state EEG data also showed a significant interaction between group and ingestion condition, with changes in alpha and beta wave activity found across several brain regions. One specific finding—the decrease in alpha power at the FC2 electrode in the caffeine group—suggests increased mental readiness, as lower alpha activity is often linked to heightened attention and reduced inhibition.</p>
<p>Taken together, these results paint a nuanced picture. While caffeine had measurable effects on brain activity and reaction time, many of the physiological and psychological responses traditionally attributed to caffeine were also present in the placebo group. This suggests that habitual coffee drinkers may be responding not just to the drug itself but also to the context and ritual of coffee consumption.</p>
<p>“Our results indicate that habitual coffee drinkers may experience conditioned responses, which are independent of the presence of caffeine,” Lesar told PsyPost. “In other words, once we are used to caffeine and expect to ingest it via a nice cup of coffee, even a cup of decaf will have (nearly) the same effect on us.”</p>
<p>The findings are consistent with a growing body of research suggesting that the experience of drinking coffee—its smell, taste, and associated expectations—can influence alertness and cognitive performance. For instance, previous studies have shown that simply smelling coffee or being told one has consumed caffeine can boost reaction times. A recent <a href="https://www.frontiersin.org/journals/behavioral-neuroscience/articles/10.3389/fnbeh.2023.1176382/full" target="_blank" rel="noopener">functional MRI study even found</a> that coffee, but not caffeine alone, activates brain regions involved in memory and goal-directed behavior.</p>
<p>Like all research, the study has limitations. The sample size was small—only 20 participants—limiting the statistical power to detect subtle effects. All participants were habitual coffee drinkers, so the results may not generalize to people who rarely consume coffee. Additionally, while decaffeinated coffee was used as a placebo, it still contains trace amounts of caffeine and other biologically active compounds, which may contribute to the observed effects.</p>
<p>Future research could build on these findings by including larger and more diverse samples, comparing habitual and non-habitual drinkers, and testing other forms of placebo. The researchers are also interested in using more advanced techniques to explore how neural responses to coffee are shaped by psychological expectations.</p>
<p>“We would like to further investigate how perceptions influence the effects of caffeine,” Lesar explained. “We suggest further research into the complex psychological and physiological effects of caffeine and coffee consumption, with a focus on habituation, placebo effects, and the impact of study design choices. Larger and more diverse samples, comparisons between habitual and non-habitual drinkers, and consideration of coffee’s other active compounds are all interesting avenues for future studies. We would also suggest analyzing the empirical data with advanced tools of data analysis, including machine learning and network analysis. In fact, we already started with the machine learning classification.</p>
<p>“Carrying out this study made us learn new things about coffee and peoples’ perception of it,” Lesar added. “We also had a chance to drink a few cups ourselves during long afternoons of EEG measurements.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.heliyon.2024.e41471" target="_blank" rel="noopener">The complexity of caffeine’s effects on regular coffee consumers</a>,” was authored by Mateja Lesar, Jakob Sajovic, Dušanka Novaković, Maša Primožič, Eva Vetrih, Martin Sajovic, Anja Žnidaršič, Peter Rogelj, Andreas Daffertshofer, Zoran Levnajić, and Gorazd Drevenšek.</p></p>
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<td><a href="https://www.psypost.org/cannabidiol-shows-promise-for-treating-alzheimers-in-mice-by-targeting-brain-hyperactivity/" 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;">Cannabidiol shows promise for treating Alzheimer’s in mice by targeting brain hyperactivity</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 26th 2025, 14:00</div>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41380-024-02789-x" target="_blank" rel="noopener">Molecular Psychiatry</a></em> provides preliminary evidence that cannabidiol, a compound derived from cannabis, may reduce cognitive decline and brain pathology in a mouse model of Alzheimer’s disease. Researchers found that chronic administration of cannabidiol improved memory performance and reduced the accumulation of amyloid-beta plaques—one of the hallmarks of Alzheimer’s. These benefits were linked to cannabidiol’s ability to regulate overactive brain cells in a key region involved in memory.</p>
<p>Cannabidiol, or CBD, is one of the main components of cannabis. Unlike tetrahydrocannabinol (THC), it does not produce a high and is generally considered safe. In recent years, researchers have been exploring its potential therapeutic effects on various neurological and psychiatric conditions, including epilepsy, anxiety, and neurodegenerative diseases such as Alzheimer’s. One area of interest is whether CBD can calm excessive brain activity, a problem observed in people and animals with Alzheimer’s disease.</p>
<p>The research team, based in China, conducted a series of experiments to test whether CBD could reduce symptoms of Alzheimer’s in genetically modified mice known as 5×FAD mice. These animals are widely used in research because they develop Alzheimer’s-like symptoms, including memory loss and the buildup of toxic amyloid-beta plaques in the brain. The researchers administered a low daily dose of CBD to these mice for just over a month and then assessed their behavior, brain activity, and the extent of brain pathology.</p>
<p>To evaluate memory function, the mice completed a series of behavioral tests. In a novel object recognition test, CBD-treated mice spent more time exploring new objects, indicating improved recognition memory. In two separate spatial memory tasks—the Morris water maze and the Barnes maze—CBD-treated mice learned the location of a hidden platform more quickly and remembered it better than untreated mice. These improvements in memory occurred without changes in general motor function or anxiety-like behavior, suggesting that CBD had specific effects on cognition.</p>
<p>Beyond behavior, the researchers looked directly at the brains of the mice. They found that CBD treatment led to a reduction in amyloid-beta plaques, particularly in the dentate gyrus, a part of the hippocampus that plays an important role in learning and memory. The reduction was most noticeable in smaller plaques, which are typically newly formed. This suggests that CBD may help slow the formation of new plaques rather than clear out existing ones. Importantly, the extent of plaque reduction in the dentate gyrus was strongly associated with the improvements in memory, highlighting the relevance of this brain region in both pathology and treatment response.</p>
<p>The study also investigated how CBD might achieve these effects at the molecular level. The researchers focused on glycine receptors, which help regulate electrical activity in the brain by dampening excessive neuronal firing. These receptors are particularly abundant in the dentate gyrus. Previous studies have shown that CBD can enhance the activity of glycine receptors by binding to a specific site on the receptor protein.</p>
<p>Using genetic techniques, the researchers disrupted glycine receptor function in some mice to test whether these receptors were necessary for CBD’s effects. In mice where glycine receptors in the dentate gyrus were either knocked down or altered to prevent CBD binding, the beneficial effects of CBD disappeared. These mice showed no improvements in memory and no reduction in amyloid-beta plaques, strongly suggesting that glycine receptors are a key mechanism behind CBD’s therapeutic action.</p>
<p>To explore how this might affect brain function, the researchers used several techniques to measure neuronal activity. In untreated Alzheimer’s model mice, neurons in the dentate gyrus were overly active, firing more rapidly than normal. Chronic CBD treatment reduced this hyperactivity, bringing the cells’ behavior closer to normal levels. This calming effect was not observed in mice with disabled glycine receptors, further reinforcing their central role.</p>
<p>The team also recorded brain activity in living mice by implanting electrodes and using calcium imaging, a technique that tracks real-time cellular activity. They found that after CBD infusion, many neurons in the dentate gyrus showed a marked drop in activity. In contrast, mice with a mutated version of the glycine receptor that could not interact with CBD showed little to no change.</p>
<p>While these findings are promising, there are several limitations to the study. First, the research was conducted in mice, not humans. Although animal models are useful for understanding disease mechanisms and testing treatments, they do not capture all aspects of human Alzheimer’s. Second, the study only used male mice, and future research will need to explore whether the same results hold true in females. Third, while the study identified glycine receptors as an important target for CBD, the compound interacts with many other receptors and systems in the brain. More work is needed to understand how these other pathways may contribute to its effects.</p>
<p>Despite these limitations, the findings add to a growing body of evidence suggesting that CBD has potential as a treatment for Alzheimer’s disease. By reducing abnormal brain activity and slowing the formation of harmful plaques, CBD may help preserve memory and cognitive function. The study also highlights the importance of glycine receptors in regulating brain activity and offers a new avenue for therapeutic intervention.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41380-024-02789-x" target="_blank" rel="noopener">Cannabidiol ameliorates cognitive decline in 5×FAD mouse model of Alzheimer’s disease through potentiating the function of extrasynaptic glycine receptors</a>,” was authored by Jin Jin, Chonglei Fu, Jing Xia, Heyi Luo, Xianglian Wang, Si Chen, Huanhuan Mao, Kai Yuan, Lin Lu, Wei Xiong, and Guichang Zou.</p></p>
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<td><a href="https://www.psypost.org/study-suggests-shared-genetic-roots-between-psychiatric-disorders-and-covid-19-risk/" 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;">Study suggests shared genetic roots between psychiatric disorders and COVID-19 risk</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 26th 2025, 12:00</div>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41380-024-02643-0" target="_blank" rel="noopener">Molecular Psychiatry</a></em> reveals that some psychiatric disorders share genetic risk factors with COVID-19 infection and severity. Using large-scale genetic data, the researchers found overlapping biological pathways—especially those related to immune system function—between disorders such as depression, attention-deficit/hyperactivity disorder, and post-traumatic stress disorder, and both COVID-19 infection and hospitalization risk. These findings suggest that the link between mental illness and vulnerability to COVID-19 may stem not only from environmental or behavioral factors, but also from shared genetic foundations.</p>
<p>The COVID-19 pandemic has had a profound impact on mental health around the world. But long before the virus disrupted daily life, researchers knew that people with psychiatric conditions tend to experience worse physical health outcomes in general. Over the course of the pandemic, several studies confirmed that individuals with pre-existing psychiatric disorders were more likely to contract the virus, experience more severe symptoms, and face higher mortality rates.</p>
<p>This raised the question: is the link between psychiatric disorders and COVID-19 outcomes solely due to environmental or lifestyle factors, such as living conditions, medications, or health behaviors—or are there shared biological underpinnings?</p>
<p>To explore this possibility, a team of researchers from institutions in Spain and Australia conducted an in-depth analysis using data from the largest available genome-wide association studies. These studies identify common genetic variants that are more frequently found in individuals with specific traits or conditions. The team focused on seven psychiatric disorders: depression, bipolar disorder, schizophrenia, attention-deficit/hyperactivity disorder, anxiety, autism spectrum disorder, and post-traumatic stress disorder. They also included a general “P-factor,” which represents a shared genetic liability across mental health conditions.</p>
<p>They compared these datasets with two COVID-19 outcomes: confirmed infection and hospitalization. Importantly, the researchers did not just look at whether the disorders and COVID-19 were linked—they tested whether there were shared genetic variants and whether those variants might play a causal role in increasing susceptibility.</p>
<p>Their analyses revealed significant genetic correlations between depression, ADHD, PTSD, and the P-factor with both COVID-19 infection and hospitalization. Anxiety also showed a positive correlation with hospitalization, but not with infection. In contrast, bipolar disorder, schizophrenia, and autism spectrum disorder did not show significant genome-wide associations with COVID-19 outcomes, though local overlaps were still detected in specific regions of the genome.</p>
<p>To understand where these overlaps occurred, the researchers divided the genome into over 1,700 independent regions and used a method called pairwise GWAS to identify which regions were shared between psychiatric disorders and COVID-19 traits. They identified several specific genomic regions that appeared to be causally shared—mostly located on chromosome 17, a region already linked to immune and neurological functions. These regions contained genes involved in immune response, stress regulation, and thyroid function.</p>
<p>One notable gene identified was <strong>THRA</strong>, which is involved in thyroid hormone signaling. It was found to be shared between depression, bipolar disorder, and COVID-19 infection. Dysfunctions in thyroid hormone receptors have been linked to mood disorders and immune deficiency, which could explain how this gene contributes to both psychiatric conditions and vulnerability to infection.</p>
<p>Another gene, <strong>CRHR1</strong>, was shared between schizophrenia, autism spectrum disorder, and COVID-19 hospitalization. CRHR1 plays a central role in the body’s stress response and also affects immune regulation. This dual role suggests that individuals with altered CRHR1 function may be more vulnerable to stress-related psychiatric disorders and at the same time experience an impaired immune response to viral infections.</p>
<p>The gene <strong>BPTF</strong>, linked to immune cell function and neurodevelopment, was shared between the general P-factor, depression, PTSD, and COVID-19 hospitalization. This convergence hints at the possibility that common disruptions in immune regulation may increase both the risk for psychiatric conditions and the likelihood of serious complications from COVID-19.</p>
<p>To go a step further, the researchers also used causal inference methods to explore whether genetic predisposition to psychiatric disorders could directly increase the risk of COVID-19 infection and hospitalization. These methods mimic randomized controlled trials by using genetic variants as natural experiments. They found evidence suggesting that depression, ADHD, and PTSD might causally increase the likelihood of COVID-19 infection. PTSD and the general P-factor also showed evidence of a causal effect on hospitalization risk. Interestingly, bipolar disorder appeared to be linked to a slightly reduced risk of hospitalization, though this finding was not consistent across all statistical tests.</p>
<p>The researchers also explored potential drug interactions with the identified genes. For example, CRHR1 interacts with medications like fluoxetine—an antidepressant that has shown anti-inflammatory effects in some studies—and corticosteroids like budesonide, which are used to treat respiratory conditions. This opens up the possibility of repurposing existing medications to improve COVID-19 outcomes among people with psychiatric conditions, especially those who may be genetically predisposed to worse illness.</p>
<p>Despite these compelling findings, the study has several limitations. All of the genetic data came from people of European ancestry, so the results may not apply to other populations. Some of the psychiatric disorders, such as anxiety and ADHD, may have lacked sufficient statistical power to detect certain effects. And while genetic methods can suggest potential causal relationships, they rely on assumptions that can be difficult to fully verify, especially when datasets share overlapping participants.</p>
<p>Sex differences were not examined due to data constraints, and other important variables like body weight or vaccination status could not be included. The study also did not examine complex interactions between genes, which may play a role in shaping both mental health and infection risk.</p>
<p>Nevertheless, this research offers a new perspective on the biological relationship between mental illness and infectious disease. Rather than viewing the increased vulnerability of people with psychiatric disorders to COVID-19 as a purely social or behavioral issue, the findings suggest that underlying genetic factors—especially those linked to immune system function—may play an important role.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41380-024-02643-0" target="_blank" rel="noopener">Genetic analyses point to alterations in immune-related pathways underpinning the association between psychiatric disorders and COVID-19</a>,” was authored by Anna Monistrol-Mula, Santiago Diaz-Torres, Mireia Felez-Nobrega, Josep Maria Haro, Sarah E. Medland, and Brittany L. Mitchell.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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