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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/childhood-curiosity-might-be-somewhat-protective-against-depression-in-adulthood-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Childhood curiosity might be somewhat protective against depression in adulthood, study finds</a>
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<p><p>An analysis of data from the 2020 China Family Panel Study found that childhood curiosity was associated with adult depression, with individuals who recalled being curious as children tending to report slightly fewer depressive symptoms on average. The study also found that this relationship might be explained in part by future confidence, a component of optimism. The paper was published in the <a href="https://www.sciencedirect.com/science/article/abs/pii/S0022395625000718"><em>Journal of Psychiatric Research</em></a>.</p>
<p>Depression is a common mental health disorder characterized by persistent feelings of sadness, hopelessness, and a loss of interest or pleasure in daily activities. It can also involve physical symptoms such as fatigue, changes in sleep or appetite, and difficulty concentrating.</p>
<p>Although the causes of depression are not fully understood, research has identified many contributing factors, including both genetic and environmental influences. In particular, some psychological characteristics appear to offer protection against depression and anxiety. One such trait is curiosity, which plays a key role in knowledge acquisition, skill development, and social relationships. Studies suggest that curiosity in childhood fosters psychological and cognitive flexibility, qualities that may help individuals maintain positive thinking when facing complex or stressful situations in adulthood.</p>
<p>Study author Chengbin Zheng and his colleagues sought to explore the relationship between childhood curiosity and depression in adulthood. They analyzed data from the 2020 wave of the China Family Panel Study.</p>
<p>The China Family Panel Study is a nationally representative, longitudinal survey designed to capture changes in Chinese society, including shifts in health, education, population, and economic conditions. It is one of the largest and most comprehensive social panel studies in China. The project began in 2010 and has conducted five biannual follow-up surveys. The data used in this study came from the fifth wave, completed in 2020, and included responses from 17,162 participants with valid data.</p>
<p>The researchers assessed participants’ self-reported childhood curiosity using the item: “At 14 years old, I was curious and exploratory and enjoyed new experiences.” They also measured future confidence by asking, “How would you rate your confidence in the future?” Subjective social status was assessed with the question, “How would you rate your social status in your local area?” Depression symptoms were measured using the 8-item version of the Center for Epidemiologic Studies Depression Scale (CES-D-8), a widely used screening tool.</p>
<p>Results indicated that participants who recalled higher levels of curiosity at age 14 tended to report slightly lower levels of depressive symptoms in adulthood. In addition, individuals who expressed higher confidence about the future — defined as the belief that the future will bring positive outcomes — reported fewer symptoms of depression.</p>
<p>The researchers tested a statistical model suggesting that childhood curiosity leads to greater future confidence, which in turn lowers depression risk. Their analysis supported this model, particularly for women.</p>
<p>“Childhood curiosity was negatively associated with depression in adulthood. For men, future confidence partially mediated the relationship between childhood curiosity and depression in adulthood; while for women, future confidence had a full mediation effect on the relationship between childhood curiosity and depression in adulthood,” the study authors concluded.</p>
<p>The study sheds light on the links between childhood curiosity and depression. However, it should be noted that the association between childhood curiosity and depression reported in the study is very weak, almost negligible in strength and only detectable because the number of study participants was very large. Additionally, childhood curiosity assessment was based on adults recalling their curiosity level when they were children. This leaves room for recall bias to have affected the results.</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.jpsychires.2025.02.003">Does childhood curiosity influence depression in adulthood?</a>”, was authored by Chengbin Zheng, Leilei Liang, Tongshuang Yuan, Junsong Fei, Xixi Zhao, Huimin Wang, Jiaying Gao, Xiaoying Liu, and Songli Mei.</p></p>
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<td><a href="https://www.psypost.org/authoritarian-beliefs-predict-whether-voters-see-trump-or-clinton-as-psychopathic/" 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;">Authoritarian beliefs predict whether voters see Trump or Clinton as psychopathic</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jun 4th 2025, 08:00</div>
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<p><p>New research published in <a href="https://ejop.psychopen.eu/index.php/ejop/article/view/14475/14475.html" target="_blank" rel="noopener">Europe’s Journal of Psychology</a> reveals that voters’ beliefs about authority and social hierarchy can shape how they perceive psychopathic traits in political candidates. The study, which focused on the 2016 United States presidential election, found that people tend to see more psychopathy in the opposing candidate and less in the one they support—particularly if they hold authoritarian views. These perceptions were strongly linked to vote choice, and the pattern held even three years later, suggesting a durable influence of psychological beliefs on political judgments.</p>
<p>Psychopathy is a personality construct characterized by traits such as callousness, manipulation, lack of remorse, and impulsivity. While the term often evokes images of criminal behavior, psychologists view psychopathy as a spectrum. In politics, some traits associated with psychopathy—such as fearlessness and social boldness—can be seen as assets, while others—like deceitfulness or a lack of empathy—can be viewed as disqualifying. Yet research shows that the average person struggles to recognize psychopathy and other personality disorders, often relying on vague impressions rather than accurate psychiatric knowledge.</p>
<p>Against this backdrop, the researchers set out to investigate whether voters’ own personality-related beliefs—particularly their level of authoritarianism—might influence how they judge psychopathic tendencies in political candidates. Authoritarianism is a long-studied belief system marked by a preference for order, obedience to authority, and social conformity.</p>
<p>People who score high in authoritarianism or related constructs such as social dominance orientation are often drawn to strong, hierarchical leadership styles. The researchers hypothesized that authoritarian voters would be less likely to see psychopathy in a dominant candidate like Donald Trump and more likely to see it in a candidate like Hillary Clinton, who campaigned on more moderate and inclusive themes.</p>
<p>“I began the study shortly after the election in 2016 because I realized that the election of Donald Trump would be consequential in many ways. I have followed his career from the time he was merely a real estate developer from Queens because he evidenced from early on a keen, almost obsessive, interest in being in the public eye,” explained study author Paul E. Jose, a professor of psychology at Victoria University of Wellington.</p>
<p>“When he entered politics and eventually became a presidential candidate, I did not take him seriously because he evidenced many dark and politically questionable traits, which I thought would be perceived as disqualifying for office. I, along with a lot of other observers, were surprised that he was elected President in 2016, and since I follow politics through the lens of psychological theory and research, I wanted to understand this phenomenon better.”</p>
<p>The study involved two large samples of voters who reported having voted for either Trump or Clinton in the 2016 election. In the first study, conducted shortly after Trump’s inauguration, 313 participants (159 Trump voters and 154 Clinton voters) completed surveys measuring their authoritarian beliefs and their perceptions of psychopathic traits in each candidate. The psychopathy ratings were based on a modified version of the Psychopathy Checklist–Revised, a widely used clinical tool. Participants also completed the Right-Wing Authoritarianism Scale and the Social Dominance Orientation scale to assess their ideological beliefs.</p>
<p>A second study, conducted three years later shortly after Trump’s acquittal in his first impeachment trial, used the same design with a different sample of 297 voters. This allowed the researchers to test whether perceptions and their links to vote choice remained consistent over time.</p>
<p>The findings showed that perceptions of psychopathy were highly polarized and depended strongly on political alignment. In both studies, Clinton voters tended to rate Trump as highly psychopathic and Clinton as low on psychopathy. Trump voters, by contrast, rated Clinton as higher in psychopathy and Trump as lower. This “mirror image” pattern was remarkably strong: voters consistently attributed psychopathy to the candidate they did not support while seeing little or none of it in their preferred candidate. The effect was especially pronounced among Clinton voters, who rated Trump’s psychopathic tendencies higher than Trump voters rated Clinton’s.</p>
<p>“The most powerful finding of the study was that attributions of psychopathology were hugely influenced by political choice,” Jose told PsyPost. “Clinton voters attributed far more psychopathic traits to Trump than their own candidate, and Trump voters attributed much more psychopathic traits to Clinton than their own candidate. The aphorism ‘beauty is in the eye of the beholder’ applies here in that voters tend to minimize flaws in their own candidate and maximize flaws in their disfavored candidate.”</p>
<p>Interestingly, when responses were averaged across political groups, there was only a small difference between the candidates in perceived psychopathy, and this emerged only in the second study. On the whole, voters were not uniformly more likely to see psychopathy in Trump than in Clinton or vice versa. Instead, perceptions were shaped by partisanship and, more specifically, by underlying authoritarian beliefs.</p>
<p>“We found that voters, as a large and heterogeneous group, did not attribute psychopathic traits and behaviors to Trump more than to Hillary Clinton at the time of his inauguration,” Jose explained. “Three years later at the time of his first impeachment, however, a slight increase in attributed psychopathology to Trump was found, indicating that the American public was increasingly noticing his unsavory traits.”</p>
<p>To explore how authoritarian beliefs shaped these patterns, the researchers constructed a path model that examined how scores on the Right-Wing Authoritarianism and Social Dominance Orientation scales predicted perceptions of psychopathy in the candidates and how those perceptions influenced vote choice. Individuals who scored high on authoritarianism tended to see Clinton as more psychopathic and Trump as less so. These perceptions, in turn, predicted their vote for Trump. Conversely, people with lower authoritarian scores tended to see Trump as more psychopathic and Clinton as less, and were more likely to vote for Clinton.</p>
<p>The analysis also showed that the link between authoritarian beliefs and vote choice was partly mediated by these perceptions of psychopathy. In other words, authoritarian voters didn’t just vote for Trump because of shared ideology—they also saw him as psychologically healthier than Clinton, while Clinton voters with low authoritarian beliefs saw Trump as psychologically more dangerous.</p>
<p>“Voters who held authoritarian views (i.e., we should follow tradition and aggressively suppress non-conforming people) strongly supported Trump’s candidacy,” Jose told PsyPost. “He evidenced some authoritarian tendencies in his first term, but his second term is marked by a dramatic increase in authoritarian policies, actions, and stances.”</p>
<p>The second study confirmed and extended these findings. Even three years after the election, the same patterns held. Participants continued to show a strong tendency to perceive the opposing candidate as highly psychopathic. Moreover, perceptions of Trump’s psychopathy had increased slightly overall by 2020, even among his own voters. This may reflect how his behavior during his presidency, including actions related to immigration, race, and executive power, affected people’s judgments.</p>
<p>Despite the passage of time and political events such as impeachment, the core relationships between authoritarianism, psychopathy perception, and vote choice remained stable. This suggests that these are not fleeting political impressions but deeply rooted psychological dynamics that shape how people interpret the actions and personalities of political figures.</p>
<p>The study also connects with a broader literature on mental health literacy—people’s ability to accurately recognize signs of psychological disorders. Prior research has shown that while many laypeople can identify common conditions like depression, few can accurately recognize personality disorders such as psychopathy. In one study, only about 39 percent of respondents correctly identified a description of psychopathy.</p>
<p>This lack of knowledge likely contributes to the strong role that ideological filters play in shaping perceptions. People tend to interpret candidates’ actions in ways that confirm their preexisting beliefs, rather than making judgments based on accurate diagnostic understanding.</p>
<p>“I thought that we would find at least a small difference in overall attributed psychopathy at the outset of the study,” Jose said. “However, the patterns in the data that we obtained suggest that my experiences with psychological theory and research in combination with a long, rich, and varied media exposure (from Fox to MSNBC) provided an unusual lived experience in comparison to that of average American voters.</p>
<p>“As a psychologist, I noticed certain behaviors as possibly diagnostically salient, whereas the average person is not trained to notice these characteristics. The ability to discern mental disorders in everyday life is termed ‘mental health literacy,'” and discussion of its relevance to voters perceiving mental health characteristics in public persons features strongly in the final version of the paper.”</p>
<p>As with all research, there are limitations. The cross-sectional nature of the data means that the direction of influence between beliefs, perceptions, and vote choice cannot be definitively established. And although the samples were large and demographically diverse, they were drawn from an online platform and may not fully represent the general population of voters.</p>
<p>“From samples of about 300 voters at each time point, we made claims about how millions of U.S. voters felt and thought about the two presidential candidates at those two times,” Jose noted. “It is important to realize that our statistical findings are probabilistic, i.e., we believe with a reasonably high level of confidence that our conclusions fairly accurately reflect the views of voters at those time-points. To support this claim, it is relevant that we replicated the findings from our first time-point with findings from a second time-point obtained three years later. Still, larger-scale studies of voters followed over time are needed to verify the key findings of this work.”</p>
<p>Future research could also examine whether the same patterns hold for other political figures, including those outside the United States or on different points of the political spectrum. It may also be helpful to investigate how media framing, exposure to expert commentary, and education in mental health affect voters’ ability to recognize or misrecognize traits like psychopathy in political leaders.</p>
<p>“I would like to encourage American voters and institutions to devote more time and effort to obtaining and disseminating critical information about candidates’ views, policies, and behavioral tendencies,” Jose said. “It is perhaps naive to expect that voters as a block will become familiar with behavioral indices of psychiatric disorders, but I would like voters as a block, media as an industry, and American institutions at large to rely more upon the expertise and knowledge base of our psychological and psychiatric communities of clinicians and academic researchers.”</p>
<p>“The U.S. government is a representative democracy, and, in order for it to function well, the citizenry needs to be well educated, informed about the critical issues of the day, and knowledgeable about where candidates stand on these issues. I would add that voters need to possess a the ability to identify disqualifying personal traits of candidates so that good choices are made for the good of the country. We are presently in a real world test of whether American voters possess this important skill. As I noted at the outset of my comments, the outcome is and will be consequential.”</p>
<p>The study, “<a href="https://ejop.psychopen.eu/index.php/ejop/article/view/14475/14475.html" target="_blank" rel="noopener">Voters’ Attributions of Psychopathic Traits to Donald Trump and Hillary Clinton After the 2016 U.S. Presidential Election and the 2020 Trump Impeachment Trial</a>,” was authored by Paul E. Jose, Ira J. Roseman, Anna Geiserman, Taylor Winter, and Boris Bizumic.</p></p>
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<td><a href="https://www.psypost.org/antidepressant-use-in-pregnancy-not-linked-to-child-mental-health-problems-after-accounting-for-maternal-depression/" 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 use in pregnancy not linked to child mental health problems after accounting for maternal depression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jun 4th 2025, 06:00</div>
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<p><p>Children born to mothers who used antidepressants during pregnancy do not appear to face higher risks of developing depression or anxiety by adolescence, according to a large study published in the Journal of the <em><a href="https://doi.org/10.1016/j.jaac.2025.03.026" target="_blank">American Academy of Child & Adolescent Psychiatry</a></em>. After accounting for maternal mental health and other relevant factors, researchers found no significant difference in psychiatric outcomes between children exposed to selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors during pregnancy and those who were not.</p>
<p>Antidepressants known as selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors are commonly prescribed to treat depression and anxiety. These medications work by increasing levels of neurotransmitters, such as serotonin and norepinephrine, which play a role in mood regulation. They are widely used, especially among women of childbearing age. In the United States, up to 15% of reproductive-aged women and 6% to 8% of pregnant women are prescribed one of these medications.</p>
<p>The question of whether antidepressants taken during pregnancy might affect a child’s long-term mental health has been a topic of ongoing concern. Some earlier studies suggested that children exposed to these medications before birth may be at higher risk for conditions like depression or anxiety. However, distinguishing the effects of the medication from the effects of maternal depression itself has proven challenging. Depression during pregnancy is a known risk factor for a wide range of child developmental issues, so it has remained unclear whether observed risks were due to the medications or to the illness being treated.</p>
<p>“My training is in both epidemiology and neuroscience so I have been interested in studying long-term development from a brain and behavioral perspective,” said study author Ardesheer Talati, a professor of clinical neurobiology and co-director of the Columbia Psychiatry Grand Rounds at Columbia University and the New York State Psychiatric Institute. “I am also interested in translational research. Preclinical studies had suggested some risks associated with antidepressant exposure in mice, but it is critical to test whether such findings also apply to human populations, where depression does not occur randomly or in a vacuum.”</p>
<p>The researchers conducted a retrospective cohort study using health records from the Rochester Epidemiology Project, a population-based data resource in Olmsted County, Minnesota. They followed a group of children born between 1997 and 2010 and tracked their psychiatric diagnoses through 2021. The study included 837 children whose mothers used either selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors during pregnancy, along with comparison groups of 863 children whose mothers did not use antidepressants during pregnancy and 399 whose mothers had discontinued use before becoming pregnant.</p>
<p>The research team extracted data from the mothers’ and children’s medical records, including information about medication use, psychiatric diagnoses, delivery outcomes, and demographic characteristics. Two board-certified psychiatrists independently verified whether mothers had taken the medications during pregnancy and adjudicated whether children had been diagnosed with depression or anxiety. Children were followed from birth until either a mental health diagnosis was made or the study period ended.</p>
<p>Initial analyses showed that children exposed to antidepressants during pregnancy had higher rates of depression or anxiety diagnoses compared to children of nonusers. But once the researchers adjusted for whether the mother had experienced depression during pregnancy, the association disappeared. The adjusted hazard ratio for developing depression or anxiety was 1.00, meaning there was no increased risk. Children whose mothers had used antidepressants before but not during pregnancy showed a similar pattern. These results suggest that the increased rates of psychiatric diagnoses in exposed children may be explained by maternal depression itself rather than by any direct effect of the medications.</p>
<p>The researchers also looked at exposure to selective serotonin reuptake inhibitors specifically and found the same result: no increased risk after adjusting for maternal mental health. Additional analyses showed that these findings held true when limiting follow-up to the first 15 years of life, excluding early childhood diagnoses, or excluding mothers who experienced depression in the decade after childbirth.</p>
<p>Importantly, the researchers found no differences in psychiatric outcomes between children whose mothers used antidepressants during pregnancy and those whose mothers had only used them beforehand. This further supports the idea that maternal illness—not in utero medication exposure—is likely the driving factor behind the association between maternal antidepressant use and child mental health. Sensitivity analyses that examined differences by the child’s sex, timing of antidepressant exposure during pregnancy, and other factors yielded similar results.</p>
<p>“We show the complexity that studies testing the long-term effects of prenatal exposures such as depression have,” Talati told PsyPost. “Indeed if we just look overall, the children exposed to antidepressant medications in pregnancy do have higher rates of psychopathology themselves (so you would be tempted to say, antidepressants cause risk in the kids).” </p>
<p>“However, once you adjust for potential confounding factors, these findings whittle away. Moreover, the children of the women who used antidepressant medications <em>before</em>, but not during pregnancy had comparable rates, suggesting that it is either maternal depression or some underlying vulnerability that is driving the increased psychopathology (called “confounding by indication”), rather than the medication <em>per se</em>.”</p>
<p>These findings align <a href="https://doi.org/10.1186/s13034-023-00624-9" target="_blank">with an earlier study published in 2023</a> that used data from over 1 million births in Denmark. That study also found a modest association between prenatal antidepressant exposure and emotional disorders in children, including depression and anxiety. However, it similarly showed that the association was greatly reduced or disappeared after adjusting for maternal mental health and other confounding factors. In fact, the Danish study found that maternal antidepressant use after pregnancy and paternal use during the mother’s pregnancy were also associated with increased child risk—further pointing to shared familial or genetic influences rather than a causal effect of medication use during pregnancy.</p>
<p>Both studies relied on large, population-based cohorts and advanced statistical techniques to minimize bias. The Minnesota study, in particular, included rigorous manual review and psychiatrist adjudication of medical records, which helped ensure that both medication exposure and psychiatric diagnoses were accurately captured. But the authors acknowledge some limitations. The study relied on prescription records rather than pharmacy fill data, so it’s possible that some mothers prescribed antidepressants did not take them. </p>
<p>Because the research is observational, it cannot definitively prove that antidepressants during pregnancy have no effect. “We cannot really randomize pregnant women to medications or not, so must rely on ‘real world’ use and data,” Talati noted. “While we do our best to account for all the confounders, there are always going to be differences that you cannot see or measure.”</p>
<p>Looking ahead, the researchers plan to continue exploring how antidepressant exposure during pregnancy might affect child development beyond emotional disorders, including gut health and disorders involving brain-gut interactions. </p>
<p>“We have been following in different cohorts using different approaches; moreover, because these antidepressant medications work by altering serotonin levels, and the vast majority of the serotonin resides in the gut, we also have an arm of the study showing the effects of prenatal SSRI use on offspring gut development and disorders of brain-gut interaction,” Talati said. “Finally, we want to get a better handle on timing of mechanisms—> e.g., are there particular periods in pregnancy that confer the greatest risk.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.jaac.2025.03.026" target="_blank">Prenatal Antidepressant Exposure and Risk of Depression and Anxiety Disorders: An Electronic Health Records–Based Cohort Study</a>,” was authored by Ardesheer Talati, Jennifer L. Vande Voort, Launia J. White, David Hodge, Cynthia J. Stoppel, Myrna M. Weissman, Jay A. Gingrich, and William V. Bobo.</p></p>
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<td><a href="https://www.psypost.org/neuroscientists-discover-brain-rhythms-slow-down-during-sleep-in-two-distinct-ways/" 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;">Neuroscientists discover brain rhythms slow down during sleep in two distinct ways</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jun 3rd 2025, 16:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1523/JNEUROSCI.1845-24.2025" target="_blank" rel="noopener">The Journal of Neuroscience</a></em> has uncovered how the human brain’s internal timing mechanisms shift during sleep. Researchers analyzed electrical recordings from 106 patients and found that two different kinds of brain timescales—based on broad and gamma-frequency brain signals—both became longer during sleep. However, these timescales followed opposite organizational patterns across the cortex. While broadband timescales increased along a known sensory-to-association hierarchy, gamma timescales decreased. The study suggests that the brain’s natural rhythms slow during sleep, but in distinct ways depending on the type of signal and brain region.</p>
<p>The researchers were interested in a fundamental question: how does the timing of brain activity—its so-called “timescales”—change during sleep? In neuroscience, timescales refer to how long neural signals remain autocorrelated, or how long a signal “remembers” its past. These timescales vary across the brain and are thought to be linked to how information is processed and integrated.</p>
<p>Sensory areas, for example, usually show shorter timescales, suitable for quickly responding to external input, while association areas, involved in more complex processing, typically display longer ones. Previous studies had shown that timescales lengthen during sleep, but the nature of these changes and how they are organized across the brain remained unclear.</p>
<p>To investigate this, the research team analyzed intracranial electroencephalography (iEEG) recordings from 106 individuals with epilepsy, who had electrodes implanted for clinical purposes. The data came from a publicly available database and included brain activity recorded during wakefulness, deep non-REM sleep (also called NREM3), and REM sleep. The participants ranged in age from 13 to 62 years, with 48 women in the sample. Researchers focused on 1-minute recordings during each state and examined activity from over 1,000 electrode sites distributed across the cortex.</p>
<p>The team extracted two distinct kinds of timescales from the data. One came from the broadband iEEG signal, which captures a wide range of brain activity from slow to fast frequencies (0.5–80 Hz). The other was derived from gamma-band power (40–80 Hz), a faster rhythm associated with sensory processing and cognitive functions. They measured the timescales using the autocorrelation function, which shows how long a signal is similar to itself over time, and fitted these with an exponential decay model. They also assessed spatial correlations between brain regions by calculating how synchronized signals were across different electrode pairs.</p>
<p>The researchers found that both broadband and gamma timescales became longer during sleep compared to wakefulness. In deep non-REM sleep, broadband timescales increased on average by about 105 milliseconds across brain areas, while gamma timescales increased by around 31 milliseconds. During REM sleep, both also showed slight increases, but the effects were much smaller. Importantly, these changes followed different patterns depending on the signal type.</p>
<p>Broadband timescales followed a known hierarchy in the brain. In both wakefulness and deep sleep, they increased from sensory areas like the visual cortex to higher-order regions such as the medial temporal lobe and orbitofrontal cortex. This pattern matched previous findings and supports the idea that association areas naturally operate on slower timescales, integrating information over longer periods.</p>
<p>Gamma timescales, however, followed the opposite trend. During sleep, they became longer in sensory regions like the visual and auditory cortices, and shorter in associative areas. This reversal of the typical hierarchy suggests that gamma-based timescales may serve different functions during sleep, possibly related to the reprocessing of sensory input or memory consolidation.</p>
<p>To understand what might be causing the increase in timescales during sleep, the researchers focused on slow waves—large, slow oscillations that are a hallmark of deep sleep. Using a separate 10-minute recording of NREM3 sleep, they identified over 85,000 individual slow wave events. They found that both types of timescales increased during these events, especially broadband ones.</p>
<p>Broadband timescales rose by 171% around the trough of slow waves, while gamma timescales increased by only 51%. Moreover, brain regions with higher overall densities of slow waves showed longer broadband timescales, suggesting a direct link between slow-wave activity and temporal dynamics.</p>
<p>The study also looked at how brain regions interact across space during different states. By measuring spatial correlations—how much two brain regions fluctuate together—they found that long-range synchronization was strongest during deep sleep, particularly for broadband signals. Interestingly, while broadband spatial correlations were highest over long distances during wakefulness, gamma spatial correlations peaked during NREM sleep but only at short distances. These findings indicate that the brain’s ability to integrate information across space and time varies depending on the sleep state and type of neural activity.</p>
<p>One of the key takeaways from this work is that the brain’s intrinsic timing mechanisms are more complex than previously thought. Rather than a single timescale that lengthens during sleep, the study reveals the presence of multiple timescales that vary by frequency range and cortical location. This layered organization suggests that different rhythms may serve distinct functions, even within the same brain region.</p>
<p>The researchers also highlight that while sleep is often thought of as a disconnected state, their findings complicate this view. Deep sleep showed increased spatial correlations and longer timescales in several areas, indicating enhanced local coordination rather than global shutdown. However, REM sleep showed reduced spatial correlations, possibly reflecting a more fragmented or internally focused mode of activity.</p>
<p>Like all research, this study has limitations. The sample consisted of individuals with epilepsy, which may affect brain dynamics, though the researchers used resting-state recordings outside of seizure activity. In addition, while intracranial recordings offer high spatial and temporal precision, electrode placement is limited by clinical needs, meaning some brain areas are underrepresented. Future studies could explore how timescales change over longer periods or during specific cognitive tasks, as well as whether similar patterns are seen in non-clinical populations.</p>
<p>The study, “<a href="https://doi.org/10.1523/JNEUROSCI.1845-24.2025" target="_blank" rel="noopener">Sleep Modulates Neural Timescales and Spatiotemporal Integration in the Human Cortex</a>,” was authored by Riccardo Cusinato, Andrea Seiler, Kaspar Schindler, and Athina Tzovara.</p></p>
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<td><a href="https://www.psypost.org/dna-methylation-may-explain-how-childhood-adversity-shapes-depression-risk/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">DNA methylation may explain how childhood adversity shapes depression risk</a>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s44220-024-00345-8" target="_blank">Nature Mental Health</a></em> provides evidence that early-life adversity can leave lasting biological imprints that help explain why some children develop depression later in life, while others seem to be more resilient. By examining changes in DNA methylation—a chemical process that influences how genes are expressed—the researchers identified specific biological pathways that mediate the link between early hardship and later mental health outcomes.</p>
<p>The study shows that DNA methylation patterns can either increase or reduce the impact of adversity on depressive symptoms during adolescence. These findings suggest that epigenetic changes not only mark biological vulnerability but may also serve as indicators of psychological resilience. Some of these changes may even offer future avenues for intervention or prediction of mental health outcomes.</p>
<p>Depression is one of the most common mental health conditions worldwide, affecting more than 260 million people. Exposure to adversity in childhood—such as abuse, neglect, poverty, or family instability—is one of the most powerful known risk factors for developing depression later in life. However, the biological mechanisms that explain this connection are not fully understood.</p>
<p>One promising explanation lies in epigenetics, a field that studies how environmental influences can change gene activity without altering the underlying genetic code. DNA methylation is a key epigenetic process that acts like a dimmer switch, turning gene expression up or down in response to experience. </p>
<p>Prior studies have shown that stressful or traumatic experiences in early life can alter DNA methylation levels, and some research has also linked these changes to mental health conditions. But until now, few studies have used large, long-term datasets to directly test whether DNA methylation serves as a bridge between childhood adversity and later depression.</p>
<p>The researchers used data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a long-term project tracking the health and development of families in the United Kingdom. They focused on a subset of 627 to 675 children who had complete data on adversity exposure, DNA methylation levels, depressive symptoms, and relevant demographic factors.</p>
<p>The children were assessed for seven different types of adversity between birth and age seven. These included caregiver abuse, exposure to violence or sexual abuse, maternal mental illness, living in a single-adult household, family instability, financial hardship, and neighborhood disadvantage. To understand when adversity might matter most, the researchers tested five different models based on the timing and accumulation of these experiences.</p>
<p>Blood samples collected when the children were seven years old were used to assess DNA methylation across over 278,000 sites in the genome. Depressive symptoms were then measured at age 10.6 using a widely used self-report questionnaire.</p>
<p>To analyze the data, the team applied advanced statistical techniques to identify which DNA methylation sites served as mediators—meaning they helped explain the link between adversity and later depressive symptoms. They also replicated their findings in two additional studies: the Future of Families and Child Wellbeing Study in the United States and the Generation R Study in the Netherlands.</p>
<p>The team identified 70 specific DNA methylation sites that helped explain between 10% and 73% of the connection between early adversity and depressive symptoms. These sites showed two distinct patterns. About 44% appeared to increase risk—meaning that adversity led to DNA methylation changes that were associated with higher depression scores. The remaining 56% had protective effects, where DNA methylation changes seemed to reduce the negative impact of adversity.</p>
<p>Interestingly, some types of adversity were more strongly linked to protective DNA changes. For example, all six methylation sites related to physical or sexual abuse had protective effects. Similarly, most of the sites associated with maternal mental illness appeared to buffer against depression. In contrast, adversity related to financial hardship or family instability was more likely to be linked with risk-increasing methylation patterns.</p>
<p>The researchers also found that the timing of adversity mattered. Sensitive periods during early childhood—particularly between birth and age five—were especially important in shaping DNA methylation patterns that later influenced mental health.</p>
<p>These findings were partially replicated in the two independent studies, which included samples from more diverse backgrounds and used different tissues for DNA methylation assessment. While the exact methylation sites did not always match across datasets, the overall patterns of risk and protection were consistent. Notably, protective effects were more reliably replicated than risk-increasing ones.</p>
<p>Biological analyses showed that many of the DNA methylation sites identified in this study are located near genes involved in brain development, immune function, and stress responses. Some had been previously linked to other early-life conditions, such as preterm birth or maternal depression. Although none overlapped with genes identified in genetic studies of depression, the researchers suggest that DNA methylation may offer a different, environmentally responsive layer of biological insight.</p>
<p>The study offers new insights into how early-life experiences become biologically embedded, but there are limitations. First, the primary dataset (ALSPAC) included mostly white participants from the United Kingdom, which limits how well the findings generalize to other racial and ethnic groups. More diverse samples are needed to confirm these results across populations.</p>
<p>Second, DNA methylation was measured in blood or saliva, not brain tissue. Although some methylation patterns in the blood may reflect those in the brain, they are not perfect proxies. Future studies using postmortem tissue or experimental models could help clarify whether these changes directly influence brain function.</p>
<p>Third, the study’s statistical models cannot prove causation. Even though the design was longitudinal, other unmeasured factors could still influence both adversity and later depression. Additionally, the biological role of specific methylation sites remains unclear, and more work is needed to understand how they interact with other genetic and environmental influences.</p>
<p>Despite these limitations, the study represents an important step forward in understanding how childhood adversity influences mental health at the molecular level. It introduces the idea that DNA methylation may not just mark vulnerability but also play a role in resilience.</p>
<p>Lead author Alexandre Lussier emphasized this point: “If confirmed, these epigenetic markers could serve as biomarkers of risk and resilience for mental illness throughout the lifespan. From a broader perspective, this work could lay the foundation for new strategies and tools to predict and prevent depression and other mental and physical disorders that can arise from exposures to childhood adversity.”</p>
<p>“Over the next five years, we plan to extend our research work to larger and more diverse datasets, since most of this work was completed in European-based populations, which limits its generalizability and interpretability.”</p>
<p>The study, “<a href="https://doi.org/10.1038/s44220-024-00345-8" target="_blank">DNA methylation mediates the link between adversity and depressive symptoms</a>,” was authored by Alexandre A. Lussier, Brooke J. Smith, Jonah Fisher, Mannan Luo, Janine Cerutti, Lisa Schneper, Trey Smith, Charlotte A. M. Cecil, Janine F. Felix, Colter Mitchell, Daniel A. Notterman, Kerry J. Ressler, Daniel J. Schaid, Andrew J. Simpkin, Matthew J. Suderman, Esther Walton, Andrew D. A. C. Smith, and Erin C. Dunn.</p></p>
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<td><a href="https://www.psypost.org/how-are-dark-triad-traits-associated-with-emotional-functioning/" 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;">How are dark triad traits associated with emotional functioning?</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jun 3rd 2025, 12:00</div>
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<p><p>A study of ethnic Hungarians living in Serbia suggests that psychopathy and narcissism are the key traits connecting the Dark Triad with aspects of emotional functioning. Individuals high in psychopathy tended to be less emotionally reactive and showed deficits in both trait-based and ability-based emotional functioning. Those high in narcissism, on the other hand, were more likely to report using emotions to facilitate performance, but showed reduced ability to recognize negative emotional states in others. The study was published in the <a href="https://doi.org/10.1002/ijop.70011"><em>International Journal of Psychology</em></a>.</p>
<p>The Dark Triad refers to a cluster of three socially aversive personality traits: narcissism, Machiavellianism, and psychopathy. Narcissism is marked by grandiosity, entitlement, and a need for admiration. Machiavellianism is defined by manipulation, cynicism, and strategic self-interest. Psychopathy includes traits such as impulsivity, emotional detachment, and a lack of empathy.</p>
<p>Although these traits are distinct, they overlap in their propensity for interpersonal exploitation. High levels of Dark Triad traits have been linked to aggression, unethical behavior, and relationship difficulties. Some studies suggest that these traits also involve the manipulation of others’ emotions, indicating possible links between dark traits and emotional processing skills.</p>
<p>Study author Beata Grabovac and her colleagues sought to examine how the Dark Triad traits relate to specific domains of emotional functioning. They hypothesized that individuals high in psychopathy and Machiavellianism would exhibit lower emotional intelligence and reduced ability-based cognitive empathy, and that all three traits would be associated with lower affective empathy.</p>
<p>Emotional intelligence refers to the ability to perceive, understand, regulate, and use emotions effectively. Cognitive empathy involves understanding another person’s mental and emotional perspective, while affective empathy is the capacity to emotionally resonate with others’ feelings.</p>
<p>The sample included 359 ethnic Hungarians living in Serbia, with an average age of 25 years. About 46% were women, and approximately 40% were university students, while 52% had a high school education or lower. All participants completed assessments in Hungarian.</p>
<p>Participants completed several measures: the Short Dark Triad (to assess narcissism, Machiavellianism, and psychopathy), the Reading the Mind in the Eyes Test (to measure ability-based cognitive empathy), the Wong and Law Emotional Intelligence Scale, and the Empathy Quotient, which includes trait-based subscales of empathy and social skills.</p>
<p>The results showed that psychopathy was associated with reduced emotional reactivity and impaired recognition of others’ emotions, especially positive emotions. These findings point to both self-reported and performance-based emotional deficits.</p>
<p>Narcissism was linked to a greater tendency to use emotions to facilitate goal-directed behavior. Narcissistic individuals also reported better social skills and cognitive empathy. However, they were less able to recognize negative emotional states in others and tended to be slightly less emotionally reactive, suggesting a disconnect between their self-perception and actual emotional abilities.</p>
<p>Machiavellianism was weakly related to emotional functioning overall but showed small positive associations with cognitive empathy and the use of emotions to enhance performance. However, individuals high in Machiavellianism did not perform better on tasks that required accurately identifying emotional states, suggesting a possible gap between perceived and actual emotional skill.</p>
<p>“This study offers an important insight into the affective world of dark individuals and gives parallel information about how individuals see themselves and how they actually perform in the context of emotional functioning. It also gives a more detailed picture about the unique affective style of the specific dark traits and about the variability in their success in emotion recognition using a task that is more difficult than just reading emotions from whole faces, because of fewer visual cues (e.g., only the eye regions are presented without the mouth). Our results have shown that there are pervasive difficulties for the Dark Triad across various emotion categories, and that they manifest diverse and specific patterns in impaired emotional functioning,” study authors concluded.</p>
<p>The results shed light on the links between the Dark Triad traits and the way individuals process and use emotions. However, it should be noted that all data were based on self-reports, leaving room for reporting bias to have affected the results. Additionally, all study participants were Hungarians. Results on other ethnic and cultural groups might differ.</p>
<p>The paper, “<a href="https://doi.org/10.1002/ijop.70011">A Network Analysis of the Associations Between the Dark Triad Traits and Domains of Emotional Functioning,</a>” was authored by Beata Grabovac, Bojana M. Dinić, Aleksandar Tomašević, Grace Carroll, and Tom Burke.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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