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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/your-social-status-has-a-surprising-influence-on-your-biological-stress-responses/" 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;">Your social status has a surprising influence on your biological stress responses</a>
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<p><p>A new comprehensive analysis of experimental research suggests that feeling lower in social rank due to socioeconomic factors like income or education can heighten the body’s cardiovascular stress responses. While temporarily feeling low-status based on task performance did not consistently produce this effect, the findings point to a potential biological pathway connecting social inequality to heart health. The research was published in the journal <em><a href="https://doi.org/10.1037/hea0001493" target="_blank" rel="noopener">Health Psychology</a></em>.</p>
<p>The study was motivated by a long-observed and persistent pattern in public health: people with lower socioeconomic position experience higher rates of chronic disease and tend to live shorter lives. These health disparities are widespread and appear to involve more than just differences in access to medical care or material resources. Researchers have hypothesized that the psychological experience of being lower on the social ladder might itself be a form of chronic stress that can damage the body over time.</p>
<p>Adrian C. Williams and his colleagues at the University of Alabama sought to test a specific part of this hypothesis by looking for a direct, causal link between the feeling of low social rank and physiological changes relevant to cardiovascular disease.</p>
<p>To address this question, the researchers conducted a meta-analysis. Rather than running new experiments with participants, this approach systematically collects and statistically integrates findings from previously published studies on a given topic. The team searched scientific databases for laboratory experiments that had been published up to September 2023.</p>
<p>They included studies that experimentally manipulated a participant’s sense of social rank, making them feel either higher or lower than someone else, and then measured their physiological responses. These responses included changes in heart rate, blood pressure, and the stress hormone cortisol, all of which are linked to cardiovascular health when repeatedly activated. The final analysis included 25 separate studies, representing a total of 2,005 participants.</p>
<p>When the researchers pooled the data from all 25 studies, they did not find a consistent, overall effect. On average, being randomly assigned to feel lower in social rank did not reliably cause a greater physiological stress reaction compared to being assigned to feel higher in rank. The average effect size was near zero and not statistically significant. This initial result suggests that simply making someone feel temporarily subordinate in a lab setting is not, by itself, a reliable way to trigger a measurable stress response in the body.</p>
<p>However, the team suspected that the way social rank was manipulated in the experiments might be an important factor. To explore this, they conducted a moderator analysis, which involves splitting the studies into categories to see if the results differ between them. They identified two main types of manipulations used by researchers.</p>
<p>One category involved performance-based tasks, where participants were made to feel superior or inferior based on their performance on a cognitive test, a game, or a puzzle. The other category involved manipulations based on socioeconomic factors, where participants were given information suggesting they were of lower or higher standing based on indicators like family income, parental education, or even how they were dressed.</p>
<p>This analysis revealed a clear and significant pattern. In the group of studies that used performance-based manipulations, there was no consistent link between assigned rank and physiological reactivity. But in the seven studies that used socioeconomic-based manipulations, the results were different.</p>
<p>Participants who were made to feel that they had a lower socioeconomic position showed heightened cardiovascular reactivity. This means their bodies, specifically their heart and blood vessels, had a stronger response when they were subsequently exposed to a stressful task. This finding provides experimental evidence for the idea that the psychological awareness of one’s socioeconomic standing can directly influence biological processes tied to disease risk.</p>
<p>Another pattern emerged when the researchers examined the sex of the participants. In the small number of studies that included only female participants, there was a significant association where lower manipulated status led to higher physiological reactivity. In contrast, the studies that included only male participants did not show this effect. This suggests that men and women might respond differently to manipulations of social rank, although the small number of studies in each category means this finding should be interpreted with caution.</p>
<p>The researchers offer an explanation for why socioeconomic-based manipulations had a stronger effect than performance-based ones. They propose that socioeconomic status is a more stable, socially meaningful, and persistent indicator of a person’s position in the social hierarchy. Information about one’s income or educational background may tap into deeply internalized feelings about social value, opportunity, and security.</p>
<p>In contrast, performing poorly on a single, artificial lab task is a fleeting event that may not carry the same psychological weight or be seen as a genuine threat to one’s overall social standing. The biological systems that monitor social threats might be more sensitive to cues related to enduring social structures like socioeconomic position.</p>
<p>The authors identified several limitations in the available research. The total number of studies was relatively small, particularly the number using socioeconomic manipulations. The participants in these studies were predominantly white college students from North America, which limits how broadly the findings can be applied to other age groups, cultures, and racial or ethnic backgrounds.</p>
<p>The experimental designs also varied, with many studies including additional manipulations beyond social rank, which could add complexity to the results. Another key limitation is that these lab studies capture only a brief, acute reaction. They cannot fully represent the chronic and cumulative nature of stress that individuals with lower socioeconomic status may experience throughout their lives from factors like financial strain, discrimination, and environmental hardships.</p>
<p>Future research could build on these findings by conducting more experiments that specifically manipulate social rank using socioeconomic cues. Using larger and more diverse samples will be important for understanding how these effects might differ across various populations. Researchers could also design studies to examine the cognitive and emotional processes, such as rumination or vigilance, that might occur after a person experiences a threat to their social standing. Such work could help clarify the psychological mechanisms that connect the perception of social rank to physiological outcomes.</p>
<p>The study concludes that while not all temporary experiences of low status trigger a physical response, the feeling of having a lower socioeconomic position appears to be a plausible contributor to the biological wear and tear that can lead to disparities in cardiovascular health.</p>
<p>The study, “<a href="https://doi.org/10.1037/hea0001493" target="_blank" rel="noopener">Perceived Social Rank and Physiology: A Meta-Analysis of Experimental Manipulations</a>,” was authored by Adrian C. Williams, Jenny M. Cundiff, Riley M. O’Neill, Katie E. Garrison, and Jennifer Morozink Boylan.</p></p>
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<td><a href="https://www.psypost.org/slow-processing-speed-linked-to-school-difficulties-even-in-bright-children/" 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;">Slow processing speed linked to school difficulties even in bright children</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 2nd 2025, 08:00</div>
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<p><p>A new study suggests that some children who are highly verbal and intellectually advanced may still face notable challenges in school if they process information more slowly than expected. Despite their cognitive strengths, these children were more likely to be seen by teachers and parents as disorganized, less responsible, and struggling with study-related tasks. The findings come from a research team based at Massachusetts General Hospital and Harvard Medical School and were published in the journal <em><a href="https://doi.org/10.1080/09297049.2025.2539695" target="_blank" rel="noopener">Child Neuropsychology</a></em>.</p>
<p>Processing speed refers to how quickly and accurately a person can take in information, make sense of it, and respond. It affects how efficiently someone can complete tasks that involve thinking, attention, and coordination.</p>
<p>While slower processing speed is a known difficulty for many children with neurodevelopmental or psychiatric conditions, less is known about how this issue affects children who appear cognitively gifted in some areas. Processing speed refers to how quickly someone can perceive information, make sense of it, and respond.</p>
<p>Earlier studies have linked slower processing to academic struggles, social communication problems, and even job performance in adulthood. But in children who are otherwise cognitively strong—especially in verbal skills—researchers have been curious to learn whether a lag in processing speed might still carry risks.</p>
<p>A 2022 study by the same lead author, <a href="https://www.drginaforchelli.com/" target="_blank" rel="noopener">Gina Forchelli</a>, pointed toward this possibility. That earlier work showed that children with high verbal intelligence but slower processing had worse outcomes in reading and math than their peers with faster processing. This raised new questions: Even if a child has strong verbal skills, could slower processing hinder how they function day-to-day in school or with peers? And are teachers or parents more likely to notice these struggles?</p>
<p>The current study was designed to explore those questions. The researchers hoped to better understand the “real world” impact of this uneven cognitive profile—strong verbal comprehension paired with slower processing.</p>
<p>“Processing speed difficulties in children has been a growing area of interest in the field and a strong interest of one of my mentors, Dr. Ellen Braaten,” explained Forchelli, a pediatric neuropsychologist and the co-director of postdoctoral training at the Learning and Emotional Assessment Program (LEAP) at Massachusetts General Brigham Hospital.</p>
<p>“Through my clinical training and work as a neuropsychologist, I have found processing weaknesses in the children and adolescents have been a marker for difficulty in the ‘real world.’ Sometimes children with processing speed difficulties have a clinical diagnosis and sometimes they do not, but the majority of them are struggling in some functional capacity. I sought out to explore how processing speed difficulties present across the cognitive spectrum.”</p>
<p>For their study, the researchers analyzed data from 679 children and adolescents between the ages of 6 and 17, all referred to a child psychiatry clinic for evaluation. Each had a verbal comprehension score above 110, placing them in the high-average to superior range for verbal reasoning. The researchers then divided the children into two groups: those with relatively slower processing speed (a 15-point or greater gap between verbal and processing scores) and those without such a gap.</p>
<p>To explore real-world impacts, the researchers looked at parent and teacher responses to questions about academic performance, adaptive behavior, social interactions, and risky behaviors such as substance use. These responses came from standardized behavioral questionnaires and from open-ended clinical history forms.</p>
<p>The findings suggest that slower processing speed, even in otherwise bright children, tends to influence how they manage school tasks. According to parent reports, children with slower processing were more likely to repeat a grade. They were also seen as less organized and less responsible with their schoolwork.</p>
<p>Teachers were even more likely than parents to notice differences. On standardized rating scales, teachers reported that children with slower processing had more problems with leadership, study skills, and functional communication. These children also showed more attention and learning problems, as rated by teachers. Notably, these teacher ratings showed meaningful differences even though most children in the study were not considered clinically impaired overall.</p>
<p>“This study suggests that a relatively lower performance on a measure of processing speed compared to verbal ability is a legitimate concern, even for children with higher cognitive abilities when processing speed falls within the average range for their age,” Forchelli told PsyPost. “In these cases, individuals with higher cognitive ability and relatively lower processing speed were found to be more vulnerable to struggles in their school performance, particularly in approach to academic work, and may be a marker for underperformance compared to peers without processing speed weaknesses in clinically-referred populations (see Forchelli et al., 2022). Results also suggest the need to collaborate and communicate with schools effectively, as teachers reported most concern in our study and may be the first to notice problems in this population.”</p>
<p>The researchers did not find significant differences between the two groups when it came to making friends, social behavior, or risky activities such as substance use or trouble with the law. Even among adolescents, slower processing did not appear linked to higher rates of substance use or legal concerns.</p>
<p>This was somewhat unexpected, given earlier studies that have connected slower processing to weaker social communication and emotional regulation, especially in youth with autism or attention problems. The authors note that their sample was younger on average, and social challenges related to processing speed may emerge more strongly in later adolescence or in broader community samples.</p>
<p>While the findings provide new insight into a subgroup of bright children who may still face challenges, the authors caution that the study has limitations. Most notably, it relies on observations reported by parents and teachers, rather than direct reports from the children themselves. Children and teens may not always share their struggles openly with adults, especially when it comes to internal experiences or risky behavior.</p>
<p>Another limitation is the nature of the sample. All participants were referred to a child psychiatry clinic, so they may already represent a group with more complex or concerning behaviors. It remains unclear whether the same patterns would hold in children who are not receiving clinical evaluations.</p>
<p>“We would benefit from more information from children themselves to possibly learn additional things (e.g. whether processing speed relates to risky behaviors),” Forchelli said. “Our sample was also taken from a clinically-referred population, which makes us also want to understand whether results generalize to children who haven’t been referred for evaluations.”</p>
<p>“Ultimately, my hope is to better understand how to best support success in these individuals. The current literature also has great variability in how processing speed difficulties are operationalized and measured. I am working on another paper currently that hopes to illuminate more recent trends in the literature and the implications for what directions we can take in the field.”</p>
<p>The study, “<a href="https://doi.org/10.1080/09297049.2025.2539695" target="_blank" rel="noopener">Influence of slower processing speed (PS) in children with high cognitive ability on parent- and teacher-reported psychosocial outcomes</a>,” was authored by Gina A. Forchelli, Pieter J. Vuijk, Mary K. Colvin, Lauren E. Wolfe, Maya R. Koven, Emily N. Tetreau, Alysa E. Doyle, and Ellen B. Braaten.</p></p>
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<td><a href="https://www.psypost.org/new-psychology-research-suggests-voters-respond-more-to-feelings-than-facts/" 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 psychology research suggests voters respond more to feelings than facts</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 2nd 2025, 06:00</div>
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<p><p>A recent study published in <em><a href="https://doi.org/10.3389/fpos.2025.1640408" target="_blank" rel="noopener">Frontiers in Political Science</a></em> provides evidence that emotions influence voting decisions more strongly than policy preferences. By analyzing data from five United States presidential elections between 2000 and 2016, the researchers found that voters are not only swayed by how closely a candidate’s views align with their own, but also by how the candidate makes them feel. Emotional reactions—especially positive feelings toward one candidate over another—tend to have a larger effect on vote choice than rational evaluations based on ideology.</p>
<p>Voting is often thought of as a rational act, one in which citizens weigh the pros and cons of candidates based on issues, policies, and competence. This perspective is shaped by long-standing theories such as rational choice theory, which suggest voters make calculated decisions to maximize their self-interest. In this view, individuals compare party platforms to their own policy preferences and vote for the option that promises the greatest benefit.</p>
<p>However, emotions have long been part of the political experience. Campaigns use music, imagery, slogans, and personal stories to connect with voters emotionally. Political scientists have increasingly recognized that affect (feelings like hope, pride, anger, or fear) plays a role in shaping political behavior. While emotions have been shown to mobilize voters and strengthen partisan identity, fewer studies have directly compared their influence with that of rational thinking in determining how people vote.</p>
<p>The new study set out to do just that. The researchers aimed to assess the extent to which emotional reactions and rational evaluations independently and jointly predict vote choice. More importantly, they wanted to understand whether emotional factors have a stronger effect than rational ones.</p>
<p>“I published a paper entitled ‘<a href="https://doi.org/10.1177/0192512113490365" target="_blank" rel="noopener">Why Do People Vote? Rationality or Emotion</a>‘ in the <em>International Political Science Review</em>, where I examined how rationality and emotion shape voter turnout. Building on this work, Professor Costas Panagopoulos and I extended the analysis to explore how these two factors influence individuals’ vote choices. Because little scholarly attention has been devoted to examining the effects of rationality and emotion on vote choice simultaneously, our study seeks to address this gap in the literature,” explained study author Ching-Hsing Wang, an associate professor at National Cheng Kung University.</p>
<p>For their study, Panagopoulos and Wang analyzed voter data from the American National Election Studies, which collects information from nationally representative surveys conducted around each presidential election. They focused on the five elections from 2000 to 2016, encompassing contests won by George W. Bush, Barack Obama, and Donald Trump.</p>
<p>The researchers built a statistical model that included two main components. The first was a “party differential,” a measure of how ideologically close a voter felt to each major political party. This represented the rational side of vote choice. The second was the “emotion differential,” which reflected how positively or negatively a voter felt about the two major party candidates. This served as the emotional side of the equation.</p>
<p>By using a method called binary probit regression, the authors estimated how much each factor contributed to a voter’s decision to choose one candidate over another. They also included other variables, such as presidential approval, views on the economy, party identification, education, income, age, race, and gender, to account for other known influences on voting.</p>
<p>The findings suggest that both rational evaluations and emotional responses independently affect how people vote. In every election examined, voters who felt ideologically closer to a candidate’s party were more likely to vote for that candidate. At the same time, those who felt more positive emotions toward a candidate—such as hope, pride, or affection—were also more likely to vote for them.</p>
<p>However, the researchers found that emotional reactions were typically more powerful predictors than rational assessments. In the combined analysis across all five elections, a one standard deviation increase in emotional preference led to a 9.2% increase in the likelihood of voting for a candidate. In contrast, a similar increase in policy agreement led to only a 3.1% increase. The emotional effect was nearly three times larger.</p>
<p>“Our study shows that emotions carry sufficient weight to influence voting behavior across the electorate, implying that campaigns that build emotional connections may be more persuasive than those relying solely on policy arguments,” Wang told PsyPost. “At the same time, because emotions are such powerful drivers, voters should make a conscious effort to reflect on their own reactions. By recognizing when their emotions are triggered and then assessing whether those feelings are supported by a candidate’s record or policy positions, voters can better balance emotional influence with rational judgment.”</p>
<p>This pattern held in every election year studied. For example, in the 2016 contest between Donald Trump and Hillary Clinton, the emotional differential had the largest influence of all. The study found that those who felt more positive emotions toward Trump were significantly more likely to vote for him, regardless of whether they aligned with his policy positions.</p>
<p>The data also suggest that emotions matter more in elections without an incumbent. In open-seat contests—when no sitting president is running—voters appeared even more emotionally driven. Emotional preferences had a stronger impact in 2000, 2008, and 2016 than in 2004 and 2012, when incumbents George W. Bush and Barack Obama sought reelection.</p>
<p>Another way the researchers evaluated the importance of emotions was by comparing how well different models fit the data. They found that models including both rational and emotional factors fit the data best. Models that excluded emotional considerations performed more poorly. This suggests that ignoring emotions in studies of voter behavior leaves out an essential part of the picture.</p>
<p>Finally, the researchers tested whether rationality and emotion interact—whether emotional responses shape the way people interpret policy positions, or vice versa. With one exception in the 2016 election, the data showed little support for this idea. Instead, emotion and rationality appeared to influence vote choice separately.</p>
<p>“Although both rational thinking and emotions shape how people decide their vote, emotions tend to carry greater weight than rational considerations,” Wang said. “Our findings suggest that voters should be mindful of whether a candidate is appealing more to their feelings than to their judgment and recognize how these emotions affect their choices.”</p>
<p>“When experiencing an emotional reaction, it is advisable to review the candidate’s track record, policies, or debate performance to see whether the feelings are grounded in substance. Voters should also remain cautious of emotional appeals, as campaigns often use music, imagery, and storytelling to influence public sentiment, and being aware of these tactics can lead to more balanced decision-making.”</p>
<p>The study provides robust evidence across multiple elections, but the authors acknowledge there are still some limitations. For instance, their analysis focused on direct effects and did not explore the many ways emotions might also influence vote choice indirectly. For example, emotions can shape how people seek out information, interpret news, or process campaign messages. These subtler dynamics were beyond the scope of the current study.</p>
<p>In addition, the measures used for rationality and emotion relied on self-reported survey responses, which may not capture all dimensions of how people form political judgments. Future research could explore alternative ways of measuring both cognitive and emotional inputs, including how they change over time or respond to specific campaign tactics.</p>
<p>“Our next steps are to explore whether rationality and emotion play significant roles in shaping individuals’ political behaviors, such as participation in protests, and to examine their effects in contexts beyond the United States,” Wang said.</p>
<p>The study, “<a href="https://www.frontiersin.org/journals/political-science/articles/10.3389/fpos.2025.1640408/full" target="_blank" rel="noopener">Rationality, affect, and vote choice</a>,” was published August 18, 2025.</p></p>
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<td><a href="https://www.psypost.org/women-with-adhd-are-three-times-more-likely-to-experience-a-severe-premenstrual-disorder/" 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;">Women with ADHD are three times more likely to experience a severe premenstrual disorder</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 1st 2025, 18:00</div>
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<p><p>Attention-deficit hyperactivity disorder (ADHD) has historically been <a href="https://acamh.onlinelibrary.wiley.com/doi/10.1111/jcpp.13480">under-studied in women</a>. This means we still have a limited understanding of how the condition may uniquely affect women – and what effect monthly hormonal changes may have on women with ADHD.</p>
<p>But a recent study conducted by me and my colleagues has shown that women with ADHD are at <a href="https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/increased-risk-of-provisional-premenstrual-dysphoric-disorder-pmdd-among-females-with-attentiondeficit-hyperactivity-disorder-adhd-crosssectional-survey-study/CD1DC6B31D4B009AB04F580C1189BC86">higher risk for mental health struggles</a> associated with the menstrual cycle. We found that having ADHD makes women around three times more likely to experience premenstrual dysphoric disorder.</p>
<p>Premenstrual dysphoric disorder (PMDD), is a serious condition that affects about <a href="https://www.sciencedirect.com/science/article/pii/S0165032724000764?via%3Dihub">3% of women worldwide</a>. The condition can seriously interfere with a person’s everyday life, causing symptoms such as mood swings, irritability, depressed mood and anxiety.</p>
<p>These symptoms occur in the days before menstruation, and resolve after the period starts. For some, PMDD may lead to severe outcomes, such as being at an <a href="https://www.liebertpub.com/doi/10.1089/jwh.2021.0185">increased risk of attempting suicide</a>.</p>
<p>We conducted an online survey of 715 women aged 18 to 34 in the UK. We asked them whether they experienced different symptoms of ADHD or PMDD, whether they’d received an ADHD diagnosis from a doctor and how symptoms interfered with their lives.</p>
<p>We found that about 31% of women with a clinical ADHD diagnosis also had PMDD, as did around 41% of women who scored high for ADHD symptoms (whether they had been formally diagnosed with ADHD or not). In comparison, only about 9% of women without ADHD met the criteria for PMDD. We also found that women who had ADHD and a clinical diagnosis of depression or anxiety had an even greater risk of PMDD.</p>
<p>The research showed that the most common PMDD symptoms women experienced were irritability, feeling overwhelmed and depression. But women with ADHD may also be more likely to experience insomnia when they have PMDD.</p>
<h2>The PMDD and ADHD link</h2>
<p>Our study <a href="https://www.sciencedirect.com/science/article/abs/pii/S0022395620311134?via%3Dihub">isn’t the first</a> to show a link between the two conditions, but it is the first to identify a similar PMDD risk among women with ADHD symptoms, not just among those who were in treatment. We’re also the first to show that people who have ADHD plus depression or anxiety are at an even greater risk of PMDD.</p>
<p>Other research suggests that women with ADHD may also be at higher risk for mental health problems during other times of hormonal change. For instance, one study found women with ADHD experienced higher rates of depression and anxiety after starting <a href="https://www.jaacap.org/article/S0890-8567(22)01894-9/fulltext">combined oral hormonal contraceptives</a>. Another study found that women with ADHD were more likely to experience depression <a href="https://www.sciencedirect.com/science/article/pii/S016503272300085X?via%3Dihub">after giving birth</a> than those without the condition.</p>
<p>More research is now needed to understand why women with ADHD appear to be more vulnerable to PMDD, and whether this affects what treatments work best.</p>
<p>It should be noted that our study assesses “provisional PMDD diagnosis”. An official diagnosis requires two months of symptom tracking across the menstrual cycle. But we asked women to remember how they felt across their menstrual cycle rather than tracking how they feel in real-time.</p>
<p>This means we could be over- or under-estimating PMDD prevalence as we’re relying on participants to recall their symptoms.</p>
<p>Future research should assess PMDD symptoms among women in real-time as they experience their menstrual cycles to more accurately assess symptoms without having to rely on people’s memory. Additionally, it may be difficult to distinguish PMDD from other disorders that may worsen during the premenstrual period, <a href="https://link.springer.com/article/10.1007/s11920-021-01286-0">such as depression or anxiety</a>. Tracking symptoms across the menstrual cycle in real-time would help to disentangle this.</p>
<p>PMDD can have profoundly negative effects on women’s lives. Some women even report it can make them feel <a href="https://www.tandfonline.com/doi/full/10.1080/23293691.2024.2436925">“physically unable to see the joy in things”</a>. Although symptoms can be managed with prescription treatments, this can only happen if the condition is diagnosed by a doctor.</p>
<p>Our new research shows us that women with ADHD are an at-risk group for PMDD, especially if they also have depression or anxiety. This suggests doctors should consider screening for PMDD among women with ADHD to reduce distress and adverse outcomes associated with the condition.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/260222/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/women-with-adhd-three-times-more-likely-to-experience-premenstrual-dysphoric-disorder-new-research-260222">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/standardized-cannabis-extract-safely-relieves-chronic-back-pain/" 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;">Standardized cannabis extract safely relieves chronic back pain</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 1st 2025, 16:00</div>
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<p><p>A new large-scale clinical trial has found that a standardized, full-spectrum cannabis extract can effectively and safely reduce chronic low back pain. The study, published in <em><a href="https://doi.org/10.1038/s41591-025-03977-0" target="_blank">Nature Medicine</a></em>, showed that the treatment, known as VER-01, provided meaningful pain relief and improved physical function and sleep quality without signs of causing dependence or withdrawal.</p>
<p>Chronic low back pain is a leading cause of disability worldwide, affecting over half a billion people and diminishing their quality of life. Current drug treatments offer limited help and come with significant risks. Nonsteroidal anti-inflammatory drugs are not suited for long-term use because of potential gastrointestinal and cardiovascular side effects. Opioids are frequently prescribed but carry a high risk of abuse, dependence, and overdose, which has fueled a global health crisis. </p>
<p>Researchers led by Matthias Karst of Hannover Medical School in Germany recognized an urgent need for new, non-addictive pain relievers. They focused on cannabis-based medicines, which have generated public interest but often lack high-quality scientific evidence. To address this gap, the team designed a rigorous, large-scale trial to test a chemically well-defined and consistent cannabis extract.</p>
<p>The research was a complex, multi-phase trial conducted at 66 sites in Germany and Austria. In the first phase, 820 adults with chronic low back pain were randomly assigned to receive either the oral cannabis extract VER-01 or a placebo for 12 weeks. This phase was double-blind, meaning neither the participants nor the investigators knew who was receiving the active treatment. The primary goal was to measure the change in average pain intensity, which participants rated on a 0-to-10 scale. For a subgroup of participants whose pain had a nerve-related component, the researchers also assessed changes in neuropathic pain symptoms using a specific questionnaire.</p>
<p>After the initial 12 weeks, the study found that VER-01 was significantly more effective than the placebo at reducing pain. The group receiving the cannabis extract reported an average pain reduction of 1.9 points on the 10-point scale, compared to a 1.4-point reduction in the placebo group. The difference between the two groups was statistically significant. The treatment was especially effective for participants who started with severe pain and for those who had nerve-related pain. The study also met its secondary goal, showing a significant decrease in neuropathic pain symptoms for those taking VER-01 compared to placebo.</p>
<p>The benefits extended beyond simple pain reduction. Participants taking the active treatment reported significant improvements in their sleep quality and physical function. A higher percentage of people in the VER-01 group achieved at least a 30% reduction in their pain, a level considered clinically meaningful. They also used about half as much rescue medication, like ibuprofen, as the participants in the placebo group. Overall, these improvements translated into a better quality of life and a more positive global impression of their condition.</p>
<p>Following the 12-week controlled phase, the trial entered a long-term open-label extension, where participants could continue taking VER-01 for an additional six to twelve months. During this period, the pain relief was not only sustained but continued to improve. Participants did not show signs of needing higher doses over time to achieve the same effect, suggesting a lack of tolerance development.</p>
<p>A final phase of the study involved a randomized withdrawal. Some participants who had benefited from the treatment were unknowingly switched from VER-01 to a placebo to see if their pain would return. The primary measurement for this phase, which was the time it took for the treatment to be considered a failure, did not show a statistically significant difference between the groups. The study authors suggest this may be due to the limited number of participants in this part of the trial. A secondary analysis did show, however, that participants who were switched to the placebo experienced a significant increase in their pain compared to those who continued taking VER-01.</p>
<p>Regarding safety, adverse events were more common in the VER-01 group than in the placebo group. The most frequent side effects were dizziness, headache, fatigue, nausea, and dry mouth. Most of these events were mild to moderate in intensity and tended to occur during the first few weeks of treatment before subsiding. While more participants on VER-01 discontinued the study due to side effects, the rate of serious adverse events was similar between the two groups. A central finding of the safety analysis was the complete absence of signs related to drug abuse, dependence, or withdrawal symptoms, even after treatment was stopped abruptly.</p>
<p>Jan Vollert, a lecturer in neuroscience at the University of Exeter, told <a href="https://www.sciencemediacentre.org/expert-reaction-to-phase-3-trial-of-cannabis-extract-ver-01-for-chronic-low-back-pain/" target="_blank">the Science Media Centre</a>: “This is an excellent study. We have long argued that studies on cannabis or cannabis-based substances need to provide high level of evidence: this is it. It is only one trial, and we will need further studies to confirm the findings, but this is a good signal that the compound could help patients.”</p>
<p>Vollert also emphasized the importance of using a specific, controlled product. “This is in no way comparable to smoking cannabis…this study does not make a case for smoking cannabis, as smoking cannabis and taking VER-01 are probably as similar as eating hazelnuts and eating Nutella: they might share a similar basis, but they just are not comparable.”</p>
<p>David Nutt, the head of the Centre for Neuropsychopharmacology at Imperial College London, also weighed in. “This is an elegant study using a placebo design with later cross over from placebo to active that confirms what we at DrugScience and other have been saying for some time based on our T21 initiative and Multi-Criteria Decision Analysis – that whole plant extract cannabis-based products have a role in chronic pain treatment.”</p>
<p>The researchers acknowledge some limitations of their work. The study did not directly compare VER-01 to other pain medications like opioids, though a follow-up study on that topic is planned. Cognitive function was not formally assessed, which could be included in future investigations of cannabinoid treatments. The lack of a statistically significant result in the withdrawal phase suggests that future studies of this kind may require a larger sample size to confirm the maintenance of effect. The findings position VER-01 as a promising therapeutic option that could play an important part in the future of pain management.</p>
<p>The study, “<a href="https://www.nature.com/articles/s41591-025-03977-0" target="_blank">Full-spectrum extract from Cannabis sativa DKJ127 for chronic low back pain: a phase 3 randomized placebo-controlled trial</a>,” was authored by Matthias Karst, Winfried Meissner, Sabine Sator, Jens Keßler, Volker Schoder, and Winfried Häuser.</p></p>
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<td><a href="https://www.psypost.org/new-study-identifies-gut-bacteria-product-that-can-trigger-parkinsons-like-brain-damage/" 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 study identifies gut bacteria product that can trigger Parkinson’s-like brain damage</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 1st 2025, 14:00</div>
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<p><p>A new study has identified a specific substance produced by a common gut bacterium that can travel to the brain and cause the loss of dopamine-producing neurons, a hallmark of Parkinson’s disease. The research, published in the journal <em><a href="https://www.nature.com/articles/s41467-025-63473-4" target="_blank">Nature Communications</a></em>, establishes a direct chemical link from a gut microbe to neurodegeneration, suggesting a new avenue for understanding and potentially treating the condition.</p>
<p>The investigation was led by a collaborative team of scientists, with joint supervision by Yunjong Lee from Sungkyunkwan University School of Medicine and Ara Koh from Pohang University of Science and Technology in the Republic of Korea. They were joined by researchers from institutions in China and Sweden. The team’s work was motivated by a growing body of evidence connecting the gut microbiome, the vast community of microorganisms living in our digestive tracts, to Parkinson’s disease. </p>
<p>While previous studies have shown that the gut bacteria composition is different in individuals with Parkinson’s disease, the specific microbes and the mechanisms by which they might influence the brain have remained largely unknown. The researchers aimed to identify a particular bacterial product, known as a metabolite, that could cross from the gut into the brain and directly contribute to the disease’s pathology.</p>
<p>To begin their investigation, the researchers re-analyzed genetic data from a large group of 491 individuals with Parkinson’s disease and 234 healthy controls. This analysis confirmed that people with Parkinson’s disease had higher levels of a bacterium called <em>Streptococcus mutans</em> in their gut. They also found that the gene for an enzyme called urocanate reductase was more abundant in the gut microbiomes of the patient group. </p>
<p>This enzyme is responsible for producing a metabolite called imidazole propionate. Consistent with these genetic findings, when the team measured imidazole propionate levels in blood plasma from a separate cohort of 65 patients and 65 healthy controls, they found significantly higher concentrations in the individuals with Parkinson’s disease.</p>
<p>Having established a correlation in humans, the researchers turned to animal models to determine if this link was causal. They introduced <em>Streptococcus mutans</em> into the guts of germ-free mice, which are raised in a sterile environment and have no native gut bacteria. Another group of mice received heat-killed, or pasteurized, <em>Streptococcus mutans</em> to test if the bacterium’s metabolic activity was necessary for any effects. </p>
<p>Mice colonized with live <em>Streptococcus mutans</em> showed a significant loss of dopamine-producing neurons in a specific area of the midbrain. They also developed signs of brain inflammation, including the activation of brain support cells called astrocytes and microglia. These brain changes were accompanied by motor impairments, as measured by a pole-climbing test. In contrast, mice given the inactive, pasteurized bacteria showed no such symptoms.</p>
<p>The scientists then measured metabolite levels in the mice. They found that animals colonized with live <em>Streptococcus mutans</em> had elevated levels of imidazole propionate in both their blood and their brain tissue, confirming that the substance produced in the gut could cross the blood-brain barrier and enter the central nervous system. This finding suggested that imidazole propionate itself could be the agent driving the brain damage. </p>
<p>To isolate its effect, the team engineered a harmless strain of <em>Escherichia coli</em>, which does not naturally produce imidazole propionate, to carry the gene for urocanate reductase from <em>Streptococcus mutans</em>. When these engineered bacteria were introduced into germ-free mice, the animals began to produce imidazole propionate and subsequently developed the same Parkinson’s-like symptoms: loss of dopamine neurons, brain inflammation, and motor deficits. This experiment demonstrated that the enzyme and its chemical product were sufficient to induce the pathology.</p>
<p>The research team also explored the molecular mechanism inside brain cells. They discovered that imidazole propionate activates a key cellular signaling pathway known as mTORC1, which is involved in cell growth, aging, and neurodegeneration. In the brains of mice colonized with <em>Streptococcus mutans</em>, the mTORC1 pathway was specifically activated in dopamine-producing neurons. </p>
<p>To confirm that this pathway was responsible for the damage, the researchers treated mice with a drug called rapamycin, which inhibits mTORC1. When mice were given both <em>Streptococcus mutans</em> and rapamycin, they were protected from the loss of dopamine neurons and motor problems, even though imidazole propionate levels in their brains remained high. This showed that imidazole propionate causes its toxic effects by acting through the mTORC1 pathway.</p>
<p>Parkinson’s disease is also characterized by the clumping of a protein called alpha-synuclein in the brain. The scientists investigated whether imidazole propionate could affect this process. They used a mouse model where small “seeds” of alpha-synuclein are injected into the brain to start the clumping process. When these mice were also colonized with <em>Streptococcus mutans</em>, the formation of alpha-synuclein clumps was significantly accelerated, the loss of dopamine neurons was more severe, and their motor problems worsened. This suggests that the bacterial metabolite can exacerbate the core protein-related pathology of the disease. </p>
<p>Finally, to prove that imidazole propionate alone was the culprit, the researchers administered the purified chemical directly to mice, either through injections into the bloodstream or directly into the brain. In both cases, the administration of imidazole propionate by itself was enough to cause the selective loss of dopamine neurons and motor deficits, and this damage was prevented by the mTORC1 inhibitor rapamycin.</p>
<p>While these findings provide a compelling link, the study has some limitations. The experiments were conducted in mice, and the mechanisms may not be identical in humans. Future research is needed to understand why dopamine-producing neurons appear to be particularly vulnerable to imidazole propionate. The researchers also note that long-term studies in human populations are necessary to determine if elevated levels of imidazole propionate are a risk factor that predicts the future development of Parkinson’s disease or simply a consequence of it. </p>
<p>These results open the door to new therapeutic strategies. For instance, developing a drug that could inhibit the urocanate reductase enzyme in the gut might lower the production of imidazole propionate and offer a way to slow or prevent the progression of the disease.</p>
<p>“Our study provides a mechanistic understanding of how oral microbes in the gut can influence the brain and contribute to the development of Parkinson’s disease,” said Professor Ara Koh. “It highlights the potential of targeting the gut microbiota as a therapeutic strategy, offering a new direction for Parkinson’s treatment.”</p>
<p>The study, “<a href="https://www.nature.com/articles/s41467-025-63473-4" target="_blank">Gut microbial production of imidazole propionate drives Parkinson’s pathologies</a>,” was authored by Hyunji Park, Jiwon Cheon, Hyojung Kim, Jihye kim, Jihyun Kim, Jeong-Yong Shin, Hyojin Kim, Gaeun Ryu, In Young Chung, Ji Hun Kim, Doeun Kim, Zhidong Zhang, Hao Wu, Katharina R. Beck, Fredrik Bäckhed, Han-Joon Kim, Yunjong Lee, and Ara Koh.</p></p>
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<td><a href="https://www.psypost.org/semaglutide-shows-potential-to-curb-cocaine-addiction-behaviors/" 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;">Semaglutide shows potential to curb cocaine addiction behaviors</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 1st 2025, 12:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.euroneuro.2025.07.001" target="_blank">European Neuropsychopharmacology</a></em> suggests that semaglutide, a drug already used to treat type 2 diabetes and obesity, may also help reduce cocaine use, drug-seeking behavior, and relapse in preclinical models. The research found that semaglutide lowered both the motivation to consume cocaine and the amount taken by rats, while also dampening the brain’s response to cocaine. These findings indicate that semaglutide may be a potential candidate for future clinical trials targeting cocaine use disorder, a condition for which no approved medication currently exists.</p>
<p>Cocaine use disorder is a chronic condition marked by strong cravings, loss of control over drug use, and a tendency to relapse after periods of abstinence. Despite its severe public health impact, there are no approved medications specifically designed to treat it. Psychosocial therapies often yield limited success, which has led scientists to explore pharmaceutical alternatives.</p>
<p>One area of interest involves a class of drugs known as glucagon-like peptide-1 receptor agonists. These compounds were originally developed to regulate blood sugar levels in people with type 2 diabetes. More recently, research has shown that they may also influence the brain’s reward systems, which are heavily involved in addiction. One such compound, exendin-4, has been shown to reduce drug-seeking behavior in rodents. However, it has not demonstrated effectiveness in humans, possibly due to its short duration of action and relatively weak binding to its target receptors.</p>
<p>Semaglutide, sold under brand names such as Ozempic, is a longer-acting and more potent version of these drugs. It has become widely known for its use in treating type 2 diabetes and for promoting weight loss. Importantly, earlier studies found that semaglutide reduces alcohol consumption in both animals and people diagnosed with alcohol use disorder. These findings raised the possibility that semaglutide might also reduce other forms of addictive behavior. The present study aimed to investigate whether that potential extends to cocaine use.</p>
<p>“There are currently no treatments for cocaine use disorder, raising the need for new treatments,” said study author Elisabet Jerlhag, a professor of pharmacology at the University of Gothenburg. “Previous studies have shown that GLP-1 receptor agonists like exenatide reduce cocaine responses in animals, but to a low extent. We recently showed that semaglutide, a GLP-1 receptor agonist with higher potency, reduces alcohol-related responses with a high magnitude, and these data were verified in a human clinical trial where semaglutide reduced alcohol drinking in humans with alcohol use disorder. We therefore wanted to investigate if semaglutide reduces cocaine responses with a higher magnitude.”</p>
<p>The researchers conducted a series of experiments in male rats and mice to examine how semaglutide affects cocaine-related behaviors. First, they used a self-administration model in rats, where the animals were trained to press a lever to receive doses of cocaine. After the behavior was well established, rats were given different doses of semaglutide to see whether it would reduce cocaine intake.</p>
<p>Two of the three doses tested (0.026 and 0.039 milligrams per kilogram) significantly lowered the number of lever presses for cocaine. The lowest dose (0.013 milligrams per kilogram) did not have a noticeable effect. The reduction in cocaine-taking was not due to sedation or reduced movement, as overall activity levels remained stable in most cases. Food and water intake did decrease with semaglutide, but these changes were expected and did not indicate nausea, based on a specific test involving kaolin consumption.</p>
<p>The researchers also examined how semaglutide influenced motivation to consume cocaine by using a progressive-ratio schedule, which gradually increases the number of lever presses required to receive each cocaine dose. Both effective doses of semaglutide reduced the animals’ willingness to work for the drug, suggesting a drop in motivation.</p>
<p>Next, the team tested semaglutide’s effect on relapse-like behavior. In this part of the study, rats first learned to self-administer cocaine, then underwent extinction training where cocaine was no longer available. Later, after a single dose of cocaine was given to trigger a craving, the rats were tested to see if they would resume lever pressing. Semaglutide significantly reduced this reinstatement of drug-seeking behavior at the higher doses. Again, the lowest dose had no measurable effect.</p>
<p>In a separate line of experiments, the researchers looked at how semaglutide affected dopamine signaling in the brain. Dopamine is a key neurotransmitter involved in the brain’s reward system and is strongly activated by cocaine use. In both mice and rats, semaglutide reduced the spike in dopamine typically seen after cocaine administration. These reductions were observed using techniques that measure chemical levels in real time within the nucleus accumbens, a region linked to drug reward and reinforcement.</p>
<p>Additional tests in mice showed that semaglutide also blunted the increase in locomotor activity caused by cocaine, a behavior often used as a proxy for the drug’s stimulant effects. Notably, semaglutide by itself did not change baseline dopamine levels or locomotor activity, suggesting that it specifically interferes with the effects of cocaine rather than broadly dulling brain activity or causing fatigue.</p>
<p>To rule out the possibility that semaglutide was simply making the animals feel sick or disoriented, the researchers measured intake of kaolin clay, a behavior in rodents that reflects nausea. Across all experiments, semaglutide did not increase kaolin intake, suggesting that the behavioral changes observed were not caused by malaise.</p>
<p>“We found that semaglutide reduces cocaine intake, motivation to consume cocaine, relapse to cocaine taking behaviors possibly by blocking the cocaine induced reward,” Jerlhag told PsyPost. In particular, there was a “26% reduction in cocaine intake, 52% reduction in motivation to consume cocaine, and 62% reduction in relapse to cocaine taking behaviors.”</p>
<p>While these findings are promising, the researchers emphasize that the study has limitations. Most notably, the behavioral experiments were conducted only in male rats. Although semaglutide has been shown to reduce alcohol and food intake in both male and female rodents, further work is needed to confirm whether the same effects apply to females in the context of cocaine use.</p>
<p>Another limitation is that the exact mechanisms behind semaglutide’s effects on cocaine behavior are not fully understood. Although the reduction in dopamine response provides one clue, the brain’s reward and motivation systems are complex and involve multiple interacting circuits. Future research may explore how semaglutide interacts with these systems, particularly the gut-brain axis, where it is believed to have multiple signaling roles.</p>
<p>There is also a need to determine whether these results translate to humans. Prior studies with similar drugs have shown mixed outcomes in clinical settings, likely due to differences in potency, treatment schedules, and individual variation in patients. Given semaglutide’s longer duration of action and stronger receptor affinity, it may overcome some of the limitations observed with earlier compounds.</p>
<p>Finally, the authors point out that while semaglutide caused some reductions in food and water intake, these effects did not seem to produce significant discomfort in the animals. Even so, understanding how the drug affects patients who are already underweight or have other health complications will be important for evaluating its clinical potential.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.euroneuro.2025.07.001" target="_blank">Semaglutide suppresses cocaine taking, seeking, and cocaine-evoked dopamine levels in the nucleus accumbens</a>,” was authored by Cajsa Aranäs, Antonia Caffrey, Christian E. Edvardsson, Heath D. Schmidt, and Elisabet Jerlhag.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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