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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/prenatal-cannabis-exposure-linked-to-blunted-brain-response-and-psychotic-like-symptoms-in-youth/" 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;">Prenatal cannabis exposure linked to blunted brain response and psychotic-like symptoms in youth</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 22nd 2025, 10:00</div>
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<p><p>An analysis of longitudinal data from the Adolescent Brain and Cognitive Development (ABCD) study has found that prenatal exposure to cannabis is associated with an increased likelihood of developing psychotic-like experiences in youth. These experiences were associated with reduced neural activation during reward anticipation in the brain’s reward-processing system, particularly in the striatum—a region involved in motivation and reward expectancy. This blunted response was more pronounced in children who had been exposed to cannabis in utero. The findings were published in <em><a href="https://doi.org/10.1016/j.biopsych.2025.05.019" target="_blank">Biological Psychiatry</a></em>.</p>
<p>Psychotic-like experiences are subclinical symptoms that resemble features of psychosis but occur in individuals who do not meet the diagnostic criteria for a psychotic disorder. Such experiences may include hearing voices, holding unusual beliefs, experiencing paranoid thoughts, or feeling detached from reality. These symptoms are relatively common during adolescence, with many young people reporting at least one such experience during this developmental period.</p>
<p>In most cases, psychotic-like experiences are temporary and do not develop into a clinical disorder. However, frequent or distressing psychotic-like experiences have been linked to increased risk for future psychiatric conditions, including schizophrenia, depression, and anxiety. Factors associated with a heightened risk for psychotic-like experiences include genetic predisposition, childhood trauma, bullying, substance use, and high levels of stress. These experiences may also reflect normative developmental processes as adolescents navigate identity formation and shifts in cognitive and emotional regulation.</p>
<p>The study, led by Carolyn M. Amir and Carrie E. Bearden, tested the hypothesis that psychotic-like experiences are associated with diminished neural activity in reward-related brain regions—specifically the striatum and the ventromedial prefrontal cortex—during anticipation of a reward. The researchers also proposed that this association would be stronger in youth who had been exposed to cannabis in utero.</p>
<p>“Our lab has been really interested in mechanisms underlying the relationship between cannabis exposure and psychosis in adolescence. Particularly concerning is the rise in cannabis use during pregnancy—and the lack of data on how this might affect brain development,” explained Bearden, a professor and director of <a href="https://capps.semel.ucla.edu" target="_blank">the Center for the Assessment and Prevention of Prodromal States (CAPPS)</a> at the University of California, Los Angeles.</p>
<p>Prenatal cannabis exposure occurs when a pregnant individual uses cannabis, allowing compounds such as tetrahydrocannabinol (THC) to cross the placenta and affect fetal development. Previous studies have linked this exposure to outcomes such as reduced birth weight, neurodevelopmental alterations, and increased risk for cognitive and behavioral difficulties in childhood.</p>
<p>The current study analyzed data from children born between 2005 and 2009 who were enrolled in the ABCD study, a large-scale longitudinal investigation of brain development and health in U.S. youth. The sample included 11,368 participants with an average age of approximately 10 years at baseline.</p>
<p>To assess psychotic-like experiences, the researchers used the Prodromal Questionnaire – Brief Child Version, a validated tool designed to measure subclinical psychosis-related symptoms in youth. Information about prenatal cannabis exposure was based on retrospective reports provided by the child’s parent or caregiver. Neural responses were assessed using task-based functional MRI while participants completed the Monetary Incentive Delay task, which measures brain activation during reward anticipation.</p>
<p>The results showed that children with prenatal cannabis exposure were more likely to report psychotic-like experiences. Across the entire sample, greater severity of psychotic-like experiences was associated with reduced activation in the striatum during reward anticipation. This effect was significantly stronger among children with prenatal cannabis exposure.</p>
<p>The researchers also tested a mediation model to examine whether blunted neural responses to reward could help explain the link between prenatal cannabis exposure and psychotic-like experiences. The findings suggest that reduced striatal activation partially mediated this relationship, indicating that altered reward processing may be one pathway through which prenatal cannabis exposure increases risk for psychotic-like experiences.</p>
<p>Additionally, the study found that psychotic-like experiences were associated with higher levels of reward motivation and impulsivity, and that these associations were more pronounced among youth with prenatal cannabis exposure. In this group, participants scored higher on measures of reward drive, reward responsiveness, and multiple dimensions of impulsivity across several assessment time points.</p>
<p>“The big finding is that youth who were exposed to cannabis before they were born were more likely to report psychotic-like experiences as teenagers,” Bearden told PsyPost. “This also appeared in how their brains responded to a reward cue — a particular part of the brain, the ventral striatum, that’s normally very reactive in response to anticipating a reward like money, was less activated in children who had been exposed to cannabis prenatally. And that brain response, in turn, was associated with more distressing psychotic-like experiences.”</p>
<p>“I was quite surprised that, when controlling for all the possible confounds we could, this association persisted. That exposure during early development would be associated with brain and behavioral differences so many years later was unexpected.”</p>
<p>The study sheds light on the links between prenatal cannabis exposure and psychological outcomes later in adolescence. However, it should be noted that the design of this study does not allow any definitive causal inferences to be derived from the results.</p>
<p>Looking forward, “we are interested in looking at the relationship of early exposure to both psychotic-like experiences over time, as well as other mental health and substance use outcomes later in life (as more timepoint data from ABCD become available),” Bearden said. “We’re also planning prospective studies with more detailed information on cannabis use—such as potency, frequency, and type of use—and how that relates to both blood biomarkers of cannabinoids as well as symptoms over time.”</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.biopsych.2025.05.019">Altered neurobehavioral reward response predicts psychotic-like experiences in youth exposed to cannabis prenatally,</a>” was authored by Carolyn M. Amir, Dara G. Ghahremani, Sarah E. Chang, Ziva D. Cooper, and Carrie E. Bearden.</p></p>
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<td><a href="https://www.psypost.org/scientist-who-linked-autism-to-chemical-and-pharmaceutical-exposures-saw-her-entire-division-shut-down-by-rfk-jr/" 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;">Scientist who linked autism to chemical and pharmaceutical exposures saw her entire division shut down by RFK Jr.</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 22nd 2025, 08:00</div>
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<p><p>A large new study published in the <em><a href="https://doi.org/10.1016/j.ijheh.2025.114613" target="_blank" rel="noopener">International Journal of Hygiene and Environmental Health</a></em> provides evidence that exposure to certain workplace chemicals among parents may influence the severity of autism spectrum disorder (ASD) symptoms and contribute to behavioral, cognitive, and adaptive challenges in their children. The findings suggest that occupational exposures—especially to plastics, ethylene oxide, phenols, and pharmaceutical agents—may have broader developmental effects beyond autism diagnosis alone.</p>
<p>Autism spectrum disorder is typically understood as a neurodevelopmental condition involving a mix of genetic and environmental factors. While previous research has associated prenatal exposure to environmental pollutants with increased autism risk, most of that work has focused on diagnosis itself, not on the range or severity of symptoms children may later experience. This study sought to expand that understanding by examining whether parental occupational exposures to potentially harmful agents before and during pregnancy are associated with the intensity of ASD symptoms and co-occurring developmental difficulties.</p>
<p>The study was conducted by former researchers from the CDC’s National Institute for Occupational Safety and Health (NIOSH), in collaboration with the University of California, Davis, as part of the <a href="https://beincharge.ucdavis.edu/" target="_blank" rel="noopener">CHARGE (Childhood Autism Risks from Genetics and Environment) study</a>. Their aim was to test whether parents’ workplace exposure to chemicals might contribute not just to ASD risk but to more severe impairments in communication, cognition, or adaptive functioning in children who are already diagnosed.</p>
<p>“My stepson was working with children with autism and we began discussing the spectrum of symptoms that children with autism experience and that little was understood about the causes of autism,” explained study author Erin C. McCanlies.</p>
<p>McCanlies had worked at NIOSH’s Health Effects Laboratory Division as a research epidemiologist, where she studied the impact of occupational exposures on health. That division was responsible for conducting research on workplace health and safety. She is now retired after <a href="https://www.propublica.org/article/rfk-jr-autism-environment-research-funding" target="_blank" rel="noopener">the division was eliminated</a> under the direction of Health and Human Services Secretary Robert F. Kennedy Jr.</p>
<p>“My job was considering how occupational exposures may result in illness or injury. This led to my thinking about the possible causes behind autism, particularly chemicals and other agents that parents might be exposed to while on the job that could potentially result in autism in their children. To better understand this potential risk I reached out to Dr. Irva Hertz-Picciotto at UC Davis, who was conducting a large study, the CHARGE study, which was designed to evaluate genetics and environmental factors that might be involved in the causes of autism.”</p>
<p>The researchers analyzed data from 532 children with confirmed ASD diagnoses and at least one parent with complete occupational history. All children were between the ages of 2 and 5 and participated in the CHARGE study, a large case-control investigation of autism and developmental delays in California. Each child’s ASD diagnosis was validated using gold-standard instruments such as the Autism Diagnostic Observation Schedule (ADOS-2) and the Autism Diagnostic Interview-Revised (ADI-R).</p>
<p>Parents completed extensive surveys about their work histories, including the types of jobs they held and any potential exposures to harmful substances during the “index period”—defined as the three months before conception through the end of pregnancy. Two industrial hygienists reviewed each job entry and assigned exposure ratings to a panel of 16 chemical categories, including disinfectants, solvents, metals, plastics, phenols, and others. These ratings were combined into a cumulative exposure score for each parent.</p>
<p>To assess ASD symptom severity, the researchers used a standardized metric called the Calibrated Severity Score (CSS), derived from ADOS-2 results. This score is intended to capture core autism features independently of age or cognitive ability.</p>
<p>In addition to the CSS, they evaluated cognitive function using the Mullen Scales of Early Learning (MSEL), adaptive functioning with the Vineland Adaptive Behavior Scales (VABS), and problem behaviors with the Aberrant Behavior Checklist (ABC). These instruments provided a broader picture of each child’s developmental profile, allowing the team to examine how parental exposures might be linked to different aspects of a child’s functioning.</p>
<p>The findings suggest that workplace exposures to several specific chemical classes were associated with worse outcomes in children with ASD. One of the strongest and most consistent patterns involved plastics and polymer chemicals. Fathers’ exposure to plastics was associated with lower scores across all cognitive and adaptive skill domains, including language, motor coordination, daily living skills, and overall functioning. When both parents were exposed, the deficits appeared to compound.</p>
<p>“I was surprised how strongly and consistently plastics and polymers stood out as being linked with multiple developmental and behavioral outcomes including irritability, hyperactivity, and daily living,” McCanlies told PsyPost.</p>
<p>Exposure to ethylene oxide—commonly used in hospital sterilization—was also linked to more severe autism symptoms, lower expressive language abilities, and poorer adaptive functioning. Similarly, parental exposure to phenol (used in construction, automotive, and some consumer products) and pharmaceuticals was associated with increased ASD severity and more pronounced behavioral challenges, especially hyperactivity and stereotyped behavior.</p>
<p>While the results do not imply that all children exposed to these chemicals will develop more severe symptoms, the patterns suggest that early life exposure to workplace toxicants may amplify certain developmental difficulties in children who already meet criteria for ASD. The study provides one of the most detailed looks to date at how parental occupation may relate not just to diagnosis, but to variation in how autism is expressed.</p>
<p>“Our findings suggest that certain parental workplace exposures may be related not just to autism, but to worse symptoms and autism behaviors,” McCanlies explained.</p>
<p>These findings are consistent with past research linking prenatal exposure to chemicals like BPA, phthalates, and metals to developmental delays, behavioral issues, and increased autism risk. The current study builds on that work by identifying specific occupational chemicals that may intensify these outcomes.</p>
<p>“These findings suggest that both men and women should follow recommended safety practices and use protective gear when working with these chemicals,” McCanlies said.</p>
<p>“This research shows that workplace safety isn’t just about protecting the worker — it’s also about protecting their future children,” added Hertz-Picciotto, a professor at the UC Davis MIND Institute. “We must consider how workplace chemicals might affect the next generation.”</p>
<p>The researchers suggest several possible biological mechanisms that could explain these associations. Many of the chemicals studied are known endocrine disruptors or immune-modulating agents, which can interfere with hormonal signaling, neural development, or inflammatory processes during pregnancy. Micro- and nano-plastics, in particular, have been shown in animal studies to cross the placenta and disrupt gene expression in the developing brain.</p>
<p>While the study offers strong statistical support for several associations, it is observational in nature and cannot prove causation. Exposure estimates were based on job descriptions rather than direct biological measurements, which may lead to some misclassification. In cases where mothers reported fathers’ job histories, the accuracy of those reports may have varied. Additionally, some chemicals had too few exposures to draw firm conclusions.</p>
<p>“More research is needed to better understand how these exposures affect brain development,” McCanlies noted. “Although we had a fairly large number of families, the number was still too small to see links with less common exposures.”</p>
<p>Nonetheless, the use of validated diagnostic tools, a large sample, expert-reviewed exposure ratings, and multiple outcome measures adds weight to the findings. The researchers note that misclassification errors in this study would most likely bias results toward the null, meaning the observed associations may underrepresent the true effects.</p>
<p>“Next steps would include longitudinal studies investigating workplace environments and specific exposures that affect both mothers and fathers that may be associated with autism and its severity,” McCanlies explained. “Research aimed at understanding the biological mechanisms underlying the link between work exposures and autism and its severity will also be important to confirm plausibility of causation and for developing effective intervention and prevention methods.”</p>
<p>“This study is unique; there are few studies that have evaluated parent work exposures and autism severity and behaviors,” McCanlies added.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.ijheh.2025.114613" target="_blank" rel="noopener">The effects of parental occupational exposures on autism spectrum disorder severity and skills in cognitive and adaptive domains in children with autism spectrum disorder</a>,” was authored by Erin C. McCanlies, Ja Kook Gu, Claudia C. Ma, Wayne T. Sanderson, Yunin J. Ludeña-Rodriguez, and Irva Hertz-Picciotto.</p></p>
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<td><a href="https://www.psypost.org/antidepressant-withdrawal-symptoms-may-be-more-common-and-more-severe-than-some-studies-suggest/" 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;">Antidepressant withdrawal symptoms may be more common and more severe than some studies suggest</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 22nd 2025, 06:00</div>
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<p><p>A newly published study in <em><a href="https://www.cambridge.org/core/journals/psychological-medicine/article/evidence-on-antidepressant-withdrawal-an-appraisal-and-reanalysis-of-a-recent-systematic-review/1E02C154EE580CA43F0EE86492B3A0E7" target="_blank" rel="noopener">Psychological Medicine</a></em> raises questions about a widely cited 2024 meta-analysis that downplayed the frequency and severity of antidepressant withdrawal symptoms. The new reanalysis suggests that when studies use systematic and appropriate methods to assess withdrawal effects, more than half of patients report experiencing symptoms—contradicting earlier claims that only about 15% are affected. The findings challenge current perceptions about the risks associated with stopping antidepressant use, particularly after short-term treatment.</p>
<p>Antidepressants are among the most commonly prescribed psychiatric medications in high-income countries, and many patients remain on them for extended periods. Yet questions remain about <a href="https://www.psypost.org/longer-antidepressant-use-linked-to-more-severe-long-lasting-withdrawal-symptoms-study-finds/">what happens when people stop taking them</a>.</p>
<p>In 2024, a large meta-analysis published in <em><a href="https://doi.org/10.1016/S2215-0366(24)00133-0" target="_blank" rel="noopener">The Lancet Psychiatry</a></em> sought to clarify just how often patients experience discontinuation symptoms after stopping antidepressants. The authors of that review, including Jonathan Henssler and colleagues based in Germany, aimed to produce what they described as a more comprehensive estimate of the incidence and severity of withdrawal effects.</p>
<p>Their study found that about 15% of people who stop taking antidepressants experience one or more withdrawal symptoms that can be directly attributed to the medication. These include issues such as dizziness, nausea, insomnia, and irritability. The researchers also reported that only about 3% of patients experienced what they considered severe symptoms—those intense enough to lead to dropout from a study or the resumption of antidepressant treatment.</p>
<p>To conduct the analysis, Henssler and colleagues systematically reviewed data from 79 studies published between 1961 and 2019, encompassing more than 21,000 participants. Their inclusion criteria were broad: the team accepted both randomized and non-randomized trials, as well as observational studies, as long as they assessed withdrawal symptoms following the discontinuation of antidepressants or placebo. They also analyzed withdrawal symptoms reported after stopping placebos in controlled trials, which they used as a baseline to subtract non-specific symptoms that might be misattributed to withdrawal.</p>
<p>Of the participants, more than 16,000 had discontinued antidepressant treatment, while nearly 4,500 had discontinued placebo. Across all groups, the researchers estimated that roughly 31% of patients experienced some form of withdrawal symptom after stopping antidepressants.</p>
<p>After accounting for the incidence of symptoms in placebo groups—estimated at about 17%—the authors concluded that roughly 15% of the symptoms could be directly tied to antidepressant withdrawal. They also identified some antidepressants, such as imipramine, paroxetine, and venlafaxine, as carrying a relatively higher risk of withdrawal symptoms.</p>
<p>The study attracted attention for its size and its conclusion that withdrawal effects, while real, were not particularly frequent or severe. But critics soon raised concerns about how the data had been collected and analyzed. In particular, several researchers questioned whether the methods used in many of the included studies were sufficient to detect withdrawal symptoms accurately.</p>
<p>That skepticism prompted the publication of a new study in <em>Psychological Medicine</em>, led by <a href="https://joannamoncrieff.com/" target="_blank" rel="noopener">Joanna Moncrieff</a> of University College London. Along with a team of researchers from Denmark, Switzerland, Austria, and the United Kingdom, Moncrieff sought to examine the data used in the original review and determine whether its conclusions were supported by more rigorous assessments.</p>
<p>“We did this research because we are concerned that some psychiatrists tend to minimize the adverse effects associated with antidepressants, particularly their dependence-inducing effects,” explained Moncrieff, a professor of critical and social psychiatry and author of <em><a href="https://amzn.to/4mV6kGZ" target="_blank" rel="noopener">Chemically Imbalanced</a></em>. “This may be because psychiatrists see the medical treatment of depression as central to the enterprise of psychiatry, and therefore feel the need to defend the reputation of antidepressants come what may.”</p>
<p>To assess the reliability of the original review, Moncrieff and her colleagues reviewed all 62 study cohorts that Henssler’s team had used to estimate the incidence of withdrawal symptoms. They examined whether those studies had used systematic and specific methods to measure symptoms, or whether they had relied on more casual observations—such as spontaneous adverse event reporting or non-specific clinician notes.</p>
<p>The researchers found that only five of the 62 studies—less than 10%—had measured withdrawal symptoms using structured questionnaires or tools specifically designed to assess the kinds of symptoms typically reported during antidepressant discontinuation. These tools, such as the Discontinuation-Emergent Signs and Symptoms (DESS) checklist, capture a range of common experiences including dizziness, emotional instability, and “brain zaps.” In contrast, most of the studies relied on vague or inconsistent methods, including open-ended questions, clinician impressions, or even retrospective chart reviews.</p>
<p>“The majority of studies were not proper studies of withdrawal but had looked at withdrawal only casually and incidentally,” Moncrieff told PsyPost. “In fact, very few of the studies had used a proper measure of withdrawal symptoms.”</p>
<p>The new team also raised concerns about other methodological features of the included studies. Many of the trials were short in duration, sometimes observing patients for only two weeks after discontinuation—a period that may not capture delayed withdrawal symptoms. The average length of antidepressant use before stopping was also less than six months in most studies, which could reduce the likelihood of detecting symptoms that become more likely with long-term use.</p>
<p>Another issue involved the way that withdrawal symptoms were sometimes misclassified as a return of the underlying mental health condition, especially in studies where symptoms of depression or anxiety were being monitored alongside withdrawal effects. This made it harder to distinguish between a relapse of the original disorder and genuine discontinuation symptoms.</p>
<p>The researchers then conducted their own meta-analysis, including only those five studies that had systematically measured withdrawal symptoms. These studies involved 601 participants, most of whom had used antidepressants for three months or less. They found that 55% of participants experienced at least one withdrawal symptom after stopping their medication. When they excluded one study in which patients did not fully stop their medication, the estimate rose to 61%. Excluding a trial of agomelatine, which is known to have lower dependence potential, pushed the estimate to 69%.</p>
<p>“We found that of the 62 studies included in the original review, only 5 used a systematic measure of antidepressant withdrawal symptoms,” Moncrieff explained. “Four of these involved people who had only used antidepressants short-term (up to 12 weeks). When we looked at the findings of these studies specifically, between 55% and 69% of participants reported experiencing withdrawal symptoms after stopping their antidepressant.”</p>
<p>“So overall, we found that the majority of evidence on antidepressant withdrawal is of poor quality and does not involve people who have taken antidepressants for long periods (those who are most at risk). The evidence that exists, however, suggests antidepressants may induce withdrawal reactions quite frequently, even after short-term use.”</p>
<p>These findings suggest that when withdrawal is measured systematically, a much larger proportion of patients report symptoms than the earlier review had indicated. The authors emphasize that their estimates do not subtract rates of withdrawal-like symptoms in placebo groups, but argue that the types and severity of symptoms reported after antidepressant discontinuation are not equivalent to those seen with placebo.</p>
<p>The new study concludes that the original 2024 review underestimates the incidence and severity of antidepressant withdrawal, in large part because of limitations in the data it relied on. These included inadequate assessment methods, short follow-up periods, and the frequent misclassification of symptoms. The researchers argue that better-designed studies are needed to understand the full scope of the problem—particularly for individuals who have used antidepressants for longer than a few months.</p>
<p>While both reviews agree that withdrawal symptoms do occur, they offer very different pictures of how often they happen and how disruptive they might be. One suggests that withdrawal is relatively rare and mild; the other indicates that it may be common, even after short-term use, and that current clinical guidelines may not reflect the full reality experienced by patients.</p>
<p>Another recent study, published in <em><a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2836262" target="_blank" rel="noopener">JAMA Psychiatry</a></em>, which involved a meta-analysis of 49 randomized clinical trials, found that people who stop taking antidepressants tend to experience only one additional discontinuation symptom, on average, compared to those who discontinue placebo or remain on the medication. The most common symptom within the first two weeks was dizziness, but the overall number and intensity of symptoms remained below the threshold typically used to define clinically significant withdrawal, and no increase in depressive symptoms was observed.</p>
<p>However, this newer study <a href="https://theconversation.com/antidepressant-withdrawal-new-review-downplays-symptoms-but-misses-the-mark-for-long-term-use-260708" target="_blank" rel="noopener">has also faced critics</a>, who argue that it downplayed the risks of antidepressant withdrawal by relying on short-term, industry-funded studies, failing to adequately account for the more severe and long-lasting symptoms experienced by long-term users and potentially repeating past mistakes that delayed recognition of the issue.</p>
<p>“Another review of antidepressant withdrawal was published recently, which also used short-term trials and poor data to come to the conclusion that antidepressant withdrawal is not a significant problem,” Moncrieff said. “However, in fact, the studies included in this latest review revealed that antidepressant withdrawal does exist, even after short-term use.”</p>
<p>“Evidence from surveys and thousands of patient reports points to the fact that antidepressant withdrawal is a significant clinical problem. Attempts to minimize it are worrying because it means that the many people who suffer from severe withdrawal reactions will not receive the understanding and support they need.”</p>
<p>As the debate continues, the need for high-quality, independent research remains urgent—particularly studies that measure withdrawal with the same level of care used to evaluate drug efficacy.</p>
<p>“There is little good quality data on antidepressant withdrawal, so it is difficult to make estimates about its frequency,” Moncrieff told PsyPost. “Also, it likely that some antidepressants have stronger dependence-inducing effects than others. Withdrawal symptoms include common symptoms such as headaches, dizziness, anxiety, and other complaints, and so far there are no studies that try to distinguish between withdrawal symptoms and ‘background’ symptoms. I hope to set up a study that can explore antidepressant withdrawal in more detail and also how to help people avoid severe withdrawal symptoms.”</p>
<p>The new study, “<a href="https://doi.org/10.1017/S0033291725100652" target="_blank">Evidence on antidepressant withdrawal: an appraisal and reanalysis of a recent systematic review</a>,” was authored by Joanna Moncrieff, Harriet Hobday, Anders Sørensen, John Read, Martin Plöderl, Michael Hengartner, Caroline Kamp, Janus Jakobsen, Sophie Juul, James Davies and Mark Horowitz.</p></p>
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<td><a href="https://www.psypost.org/birth-control-pills-reduce-the-brains-functional-individuality/" 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;">Birth control pills reduce the brain’s functional individuality</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 21st 2025, 16:00</div>
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<p><p>A new neuroimaging study suggests that oral contraceptive pills may alter how the brain is functionally organized. Researchers found that oral contraceptives reduce the individuality of brain network patterns and may influence connectivity in circuits associated with emotional regulation. The findings, published in the journal <a href="https://doi.org/10.1002/hbm.70318" target="_blank">Human Brain Mapping</a>, add to a growing body of research examining how hormonal contraceptives affect the brain.</p>
<p>Oral contraceptive pills are used by over 150 million people worldwide and represent one of the most common forms of hormonal contraception. These pills typically contain synthetic versions of the hormones estrogen and progestin, which work together to prevent pregnancy by suppressing ovulation, thickening cervical mucus, and altering the uterine lining. In doing so, they effectively interrupt the natural hormonal cycles that regulate reproductive function. </p>
<p>While they are widely regarded as safe and effective, their influence extends beyond the reproductive system. Because sex hormones also interact with brain regions involved in emotion, cognition, and reward, researchers have raised questions about whether oral contraceptives may alter brain function more broadly.</p>
<p>Some users report emotional side effects such as irritability, sadness, or mood instability, particularly during the first few months of use. In other cases, oral contraceptives are associated with mood improvements, especially for those with pre-existing hormonal mood sensitivity. Despite these individual differences, researchers still do not fully understand why some people are more vulnerable to adverse emotional effects while others are not.</p>
<p>Previous brain imaging studies have suggested that oral contraceptives may alter brain structure and connectivity, including in regions related to emotional regulation, memory, and social processing. However, these studies have often yielded conflicting results. Many relied on observational designs or small, cross-sectional samples, which limits the ability to draw conclusions about causality. </p>
<p>To address these gaps, a research team led by Gino Haase of the University of Cambridge and Nicole Petersen of UCLA conducted a randomized, double-blind, placebo-controlled crossover trial to assess whether oral contraceptive pills produce measurable changes in brain network activity and mood within individuals.</p>
<p>The researchers recruited 26 women between the ages of 20 and 33 who reported past negative mood symptoms when using hormonal contraceptives. Each participant completed two study arms: one in which they took oral contraceptive pills (30 µg ethinyl estradiol and 0.15 mg levonorgestrel) for 18–21 days, and one in which they took a matched placebo. A full menstrual cycle washout period separated the two arms. During both phases, participants underwent resting-state functional magnetic resonance imaging (fMRI) scans and provided daily self-reports of mood using the Daily Record of Severity of Problems (DRSP).</p>
<p>Blood samples confirmed that hormone levels were suppressed during the oral contraceptive phase. The researchers then analyzed brain imaging data to examine functional connectivity—patterns of synchronized activity between different brain regions over time. Unlike structural connectivity, which refers to the physical wiring of the brain through anatomical pathways, functional connectivity reflects how different regions dynamically coordinate with one another, even in the absence of an explicit task.</p>
<p>The research team first attempted to replicate specific findings from three prior studies that had identified changes in connectivity between brain regions such as the amygdala, dorsal anterior cingulate cortex, and putamen during oral contraceptive use. These regions are commonly involved in emotion regulation and reward processing.</p>
<p>The current study largely failed to replicate those findings. For instance, it did not observe a previously reported increase in connectivity between the amygdala and ventromedial prefrontal cortex. It also did not find expected changes in the dorsal anterior cingulate or parahippocampal connectivity. One partial exception was an increase in connectivity between the putamen and a region of the middle frontal gyrus, though this occurred in the opposite hemisphere compared to earlier findings.</p>
<p>The researchers suggest that methodological differences—including sample size, hormonal formulation, or analytic strategies—may account for the lack of replication. These inconsistencies led the team to explore broader, whole-brain effects of oral contraceptive use.</p>
<p>To investigate whether oral contraceptives had more diffuse effects on brain networks, the researchers applied a technique known as functional connectome fingerprinting. This method identifies patterns of connectivity that are unique to each individual and can detect changes in those patterns under different conditions.</p>
<p>The analysis revealed that oral contraceptive pills caused participants’ brain connectivity profiles to become more similar to one another, reducing between-person variability. While each participant’s brain pattern remained identifiable across conditions, the overall distinctiveness of each person’s functional connectome was lower during oral contraceptive use. This effect was strongest in networks involved in executive control, somatomotor processing, salience detection, and the default mode.</p>
<p>This convergence suggests that oral contraceptive pills may exert a normalizing or dampening effect across the brain’s functional architecture. Rather than targeting specific regions, the influence appears to be more global—altering how entire networks are configured and reducing the brain’s functional individuality.</p>
<p>In addition to these network-wide shifts, the researchers also found evidence linking brain changes to self-reported mood symptoms. Participants experienced more negative affect during the oral contraceptive phase, as measured by the DRSP. The researchers identified 13 specific connections between brain regions that significantly correlated with increases in negative mood.</p>
<p>These connections involved areas such as the frontal pole, superior frontal gyrus, posterior cingulate cortex, and precuneus—all regions known to play roles in emotional processing, self-referential thought, and regulation of internal states. The findings suggest that oral contraceptive-related changes in these circuits may underlie the mood symptoms reported by some users.</p>
<p>Rather than pointing to a single brain region responsible for these effects, the results support the idea of a distributed, hormone-sensitive network that may be involved in emotional changes during hormonal transitions—such as menstruation, postpartum periods, or contraceptive use.</p>
<p>But the study, like all research, has limitations. The sample size was relatively small (26 participants), which may limit generalizability and increase the likelihood of false positives or missed effects. Only one formulation of oral contraceptive pills was tested, so the results may not apply to other hormonal combinations. The study measured brain activity at rest, meaning it did not capture how oral contraceptives affect the brain during emotional or cognitive tasks.</p>
<p>Additionally, the intervention lasted only a few weeks. It remains unknown whether longer-term use would amplify, reduce, or change the nature of these connectivity shifts. Finally, although associations between brain connectivity and mood were observed, the study cannot establish a definitive causal pathway linking them.</p>
<p>Despite these limitations, the study suggests that oral contraceptive pills can produce measurable and widespread changes in brain connectivity. These changes are not limited to isolated regions but span across multiple major brain networks. The results also suggest that oral contraceptive pills may reduce the uniqueness of individual brain network patterns, a finding with implications for both research and clinical care.</p>
<p>The researchers propose that future studies could build on these findings by enrolling larger and more diverse samples, testing additional formulations, and using multivariate tools like connectome fingerprinting to better understand how hormonal contraceptives interact with brain function and behavior. They also suggest that the network of brain regions identified in this study could serve as a candidate for investigating mood changes across different hormone-sensitive conditions.</p>
<p>The study, “<a href="https://doi.org/10.1002/hbm.70318" target="_blank">Effects of Oral Contraceptive Pills on Brain Networks: A Conceptual Replication and Extension</a>,” was authored by Gino Haase, Jason Liu, Timothy Jordan, Andrea Rapkin, Edythe D. London, and Nicole Petersen.</p></p>
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<td><a href="https://www.psypost.org/study-uncovers-shared-and-distinct-brain-network-signatures-of-narcissistic-and-antisocial-traits/" 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 uncovers shared and distinct brain network signatures of narcissistic and antisocial traits</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 21st 2025, 14:00</div>
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<p><p>A new study provides evidence that narcissistic and antisocial personality traits are linked to both shared and distinct patterns of brain connectivity. The research, published in the journal <em><a href="https://doi.org/10.1111/psyp.70130" target="_blank">Psychophysiology</a></em>, suggests that dysfunction in three core brain networks—known as the default mode, salience, and frontoparietal networks—may play a central role in shaping these traits. These findings offer a neuroscience-based framework for understanding overlapping yet divergent features of personality pathology.</p>
<p>Narcissistic and antisocial traits often co-occur, but they manifest in different ways. Narcissism tends to involve grandiosity, a heightened focus on self-image, and a need for admiration. Antisociality, by contrast, is marked by impulsivity, rule-breaking, and disregard for the rights of others. Both types of traits can exist at subclinical levels in the general population or present more severely as part of personality disorders. Understanding their neurobiological underpinnings could help clarify how they overlap and diverge, and why they tend to cluster in certain individuals.</p>
<p>“Narcissistic and antisocial personality traits often overlap in real life and can lead to severe interpersonal and societal problems,” said study author Alessandro Grecucci, an associate professor at the University of Trento and head of <a href="http://www.alessandrogrecucci.it/clian-lab/" target="_blank">the Clinical and Affective Neuroscience Lab</a>. “While psychology has described these traits for decades, we know less about how they are represented in the brain. Recent advances in network neuroscience, and especially the study of large-scale ‘triple networks’ in the brain, offered us a unique opportunity to explore whether these traits share neural mechanisms or have distinct brain signatures.”</p>
<p>For their study, the researchers focused on three large-scale brain networks often implicated in emotional processing and self-regulation. These include the default mode network (DMN), which is active during self-referential thinking and mind-wandering; the salience network (SN), which detects emotionally relevant stimuli and helps regulate responses; and the frontoparietal network (FPN), involved in higher-order cognitive control and planning. These three systems are thought to underlie key features of personality and psychopathology.</p>
<p>The research team used graph theory and machine learning to examine how these brain networks were organized in 183 healthy adults who had completed personality assessments and resting-state functional MRI scans. Participants ranged in age from 22 to 68 and completed the Personality Styles and Disorders Inventory (PSDI), which measures dimensional traits, including narcissistic and antisocial tendencies. Importantly, these participants were not clinical patients, which allowed the researchers to explore the neural signatures of personality traits across a broad spectrum.</p>
<p>To investigate network organization, the team employed graph-theoretical metrics, which model the brain as a set of nodes and edges—akin to a social network map. These metrics allowed the researchers to quantify both local and global properties of brain function, such as how efficiently information travels between regions or how central a particular region is to the overall network.</p>
<p>The researchers built predictive models using both traditional regression and a random forest algorithm, a form of machine learning that tests how well combinations of brain metrics can predict trait scores. They focused on connections within the DMN, SN, and FPN, while also including visual and sensorimotor networks as control regions.</p>
<p>The results indicated that narcissistic and antisocial traits shared several neural features. In both cases, lower connectivity within the salience network—particularly in the anterior cingulate cortex (ACC)—was a consistent predictor. This region plays a key role in emotional awareness and integrating information about risk and reward. Reduced connectivity in this area may reflect impairments in recognizing the consequences of one’s actions or regulating emotional impulses, potentially contributing to the interpersonal difficulties seen in both traits.</p>
<p>Both traits were also associated with higher efficiency in the lateral prefrontal cortex, a hub of the frontoparietal network. This suggests increased ability to strategically plan and control behavior—potentially to achieve self-serving goals or manipulate social situations. In other words, while both traits may impair emotional regulation, they might also enhance cognitive planning when it aligns with personal motives.</p>
<p>But the patterns diverged when it came to the default mode network. For narcissistic traits, greater connectivity in the medial prefrontal cortex (MPFC)—a core DMN region—was a strong predictor. This part of the brain is associated with self-reflection, social cognition, and constructing one’s identity. The finding aligns with psychological theories suggesting that narcissism involves frequent self-focus and exaggerated fantasies of power or status.</p>
<p>In contrast, antisocial traits were linked to reduced connectivity in the DMN. This pattern may reflect lower levels of introspection or a diminished capacity to reflect on the emotional consequences of behavior. People high in antisocial traits often display impulsivity and a disregard for others, which may be rooted in diminished self-monitoring or social imagination.</p>
<p>“We expected similarities, but we were struck by how clearly the patterns diverged in the default mode network,” Grecucci told PsyPost. “This may explain why narcissistic individuals often engage in more self-reflection (even if distorted), while antisocial individuals tend to act more impulsively and with less regard for self-consequences.”</p>
<p>The study also revealed distinct features beyond the triple network. For example, antisocial traits showed stronger involvement of the visual network, which might point to heightened visual attention or sensitivity to environmental cues. This finding is tentative but aligns with other studies suggesting enhanced perceptual processing in people with high Dark Triad traits.</p>
<p>The research team confirmed their results using seed-based analyses, which track how specific brain regions communicate with others across the brain. For narcissistic traits, the medial prefrontal cortex was functionally linked to areas involved in emotion, memory, and self-related processing. For antisocial traits, the same region showed connections to sensory and occipital areas—suggesting a more externally focused processing style.</p>
<p>The anterior insula, another salience network region, was more strongly associated with narcissism than antisocial traits. This region helps integrate internal body states and emotional signals, and has been linked to experiences such as social rejection and empathy. The finding may help explain why narcissistic individuals—despite their grandiosity—often show heightened sensitivity to perceived slights or criticism.</p>
<p>Meanwhile, the right rostral prefrontal cortex, a region involved in high-level cognition and goal setting, was more strongly linked to antisocial traits. Its role may involve instrumental planning or manipulative behavior rather than reflective insight.</p>
<p>“Our study shows that narcissistic and antisocial traits are linked to changes in the same core brain networks that help us process emotions, control behavior, and think about ourselves,” Grecucci explained. “Both traits were negatively predicted by the anterior cingulate cortex of the SN, reflecting reduced danger awareness and increased risky behaviors.” </p>
<p>“Conversely, both were positively predicted by the lateral prefrontal cortex of the FPN, suggesting augmented strategic thinking to manipulate others and increased planning skills to achieve personal goals. However, they differ in the default mode network—narcissism shows more self-focused activity, antisocial traits less. This means that the same neural systems can support very different patterns of thought and behavior, depending on how they are tuned.”</p>
<p>Still, the study has limitations. The sample consisted of non-clinical participants, and results may not generalize to people with formal diagnoses like narcissistic or antisocial personality disorder. The use of resting-state MRI also means that findings reflect baseline brain activity, not responses to specific tasks. And although the researchers used advanced statistical methods, some of the findings—especially those based on uncorrected thresholds—should be interpreted with caution until replicated.</p>
<p>Future research could address these issues by including clinical populations, exploring task-based functional MRI, or distinguishing between subtypes of narcissism (such as grandiose vs. vulnerable). </p>
<p>“We aim to refine these brain-based signatures into potential biomarkers for personality pathology, and to test whether they can predict real-world behaviors or responses to interventions,” Grecucci said. “Ultimately, this could help develop neuroscience-informed strategies for prevention and treatment.”</p>
<p>The study, “<a href="https://doi.org/10.1111/psyp.70130" target="_blank">Narcissistic and Antisocial Personality Traits Are Both Encoded in the Triple Network: Connectomics Evidence</a>,” was authored by Khanitin Jornkokgoud, Richard Bakiaj, Peera Wongupparaj, Remo Job, and Alessandro Grecucci.</p></p>
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<td><a href="https://www.psypost.org/chronic-exposure-to-microplastics-impairs-blood-brain-barrier-and-damages-neurons/" 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;">Chronic exposure to microplastics impairs blood-brain barrier and damages neurons</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 21st 2025, 12:00</div>
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<p><p>A study on rats suggests that exposure to microplastics may impair the blood–brain barrier, induce oxidative stress in the brain, and damage neurons. The microplastic exposure involved oral administration of low-density polyethylene (LDPE) suspended in water for 3 and 6 weeks. The research was published in <a href="https://doi.org/10.1007/s12035-025-05157-0"><em>Molecular Neurobiology</em></a>.</p>
<p>Microplastics are tiny plastic particles, typically less than 5 millimeters in size, that originate from the breakdown of larger plastic waste or are intentionally manufactured for use in products such as cosmetics and industrial abrasives. These particles are now widespread in oceans, rivers, soil, and even the air, making them difficult to avoid.</p>
<p>Microplastics can be ingested by marine life, birds, and other animals, entering the food chain and potentially posing risks to human health. These particles are highly resistant to natural degradation, persisting in the environment for decades or even centuries. Common sources include single-use plastics, synthetic textile fibers, tire wear, and packaging materials.</p>
<p>Study author Ghasem Forutan and his colleagues note that freshwater contamination is a major route by which microplastics can enter the human body. Microplastic particles suspended in water are consumed by aquatic organisms, where they tend to accumulate. When humans eat these organisms—for example, by consuming fish—they also ingest the accumulated microplastics. However, the health effects of microplastic ingestion in humans remain poorly understood.</p>
<p>To explore these potential effects, the authors conducted a series of experiments in rats to examine whether chronic ingestion of microplastics affects brain health. They focused on neurotoxic effects, particularly the potential for microplastics to disrupt the blood–brain barrier, generate oxidative stress, and harm neurons. The blood–brain barrier is a protective layer of cells that regulates which substances can pass from the bloodstream into brain tissue.</p>
<p>In their experiments, the researchers used low-density polyethylene (LDPE), a common type of plastic. One of the key features of microplastics is their density. Plastics with higher density, such as PVC (polyvinyl chloride), tend to sink in water and may be ingested by bottom-dwelling species. In contrast, low-density plastics like LDPE float on the surface, making them more likely to be consumed by surface-feeding animals. These floating particles can also adsorb toxic pollutants from the environment, potentially serving as carriers for harmful substances into biological tissues.</p>
<p>The experiments were conducted on 80 male Wistar rats, each approximately six weeks old and weighing an average of 180 grams at the start of the study. The rats were divided into four main groups, which were further split into subgroups for specific analyses, including assessments of brain water content, blood–brain barrier permeability, biochemical markers, and histopathology.</p>
<p>Two groups were monitored for three weeks, and two for six weeks. In each pair, one group served as a control and received only double-distilled water via a gavage needle. The experimental groups received the same water, but with suspended LDPE microplastic particles smaller than 25 micrometers in diameter, at a dose of 10 mg/kg body weight per day. Gavage administration involves delivering substances directly into the stomach through a specialized needle inserted via the esophagus, ensuring consistent and controlled dosing.</p>
<p>The results indicated that the integrity of the blood–brain barrier was significantly compromised in the rats exposed to LDPE microplastics, after both 3 and 6 weeks of exposure. These rats also exhibited elevated oxidative stress, as shown by biochemical markers. In addition, levels of brain-derived neurotrophic factor (BDNF)—a protein essential for neuronal growth, function, and survival—were significantly reduced in the 6-week exposure group. Histological analyses revealed signs of neuronal damage, including cell shrinkage and necrosis, in the microplastic-exposed rats.</p>
<p>“These findings demonstrate that chronic exposure to LDPE MPs [low-density polyethylene microplastics] impairs BBB [blood-brain barrier] integrity, increases oxidative stress, and induces neuronal damage in rats. The results highlight the neurotoxic potential of MPs [microplastics] and emphasize the need for further research to address their possible health risks,” the study authors concluded.</p>
<p>The study contributes to the scientific knowledge on the health effects of low-density microplastic intake. However, it should be noted that the study was conducted on rats, not on humans. While rats and humans share many physiological similarities, they are still very different species. Results on humans might not be identical.</p>
<p>The paper “<a href="https://doi.org/10.1007/s12035-025-05157-0">Chronic Exposure to Microplastics Induces Blood–Brain Barrier Impairment, Oxidative Stress, and Neuronal Damage in Rats</a>” was authored by Ghasem Forutan, Alireza Sarkaki, Reza Dehbandi, Samireh Ghafouri, Somayeh Hajipour, and Yaghoob Farbood.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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