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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/how-stress-affects-us-may-depend-on-the-balance-between-testosterone-and-cortisol/" 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 stress affects us may depend on the balance between testosterone and cortisol</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 1st 2025, 10:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.psyneuen.2025.107557" target="_blank">Psychoneuroendocrinology</a></em> suggests that the way young men experience psychosocial stress may depend on the balance between two hormones: testosterone and cortisol. The researchers found that higher testosterone was linked to lower perceived stress—but only when cortisol levels were low. Conversely, high cortisol was linked to lower stress perception in those with low testosterone. These findings support the idea that it’s not just individual hormone levels that matter, but how they interact with each other.</p>
<p>Cortisol is a hormone released by the adrenal glands in response to stress. It helps the body regulate blood sugar, metabolism, and the immune response. Cortisol is often called the “stress hormone” because its levels rise when we feel threatened or under pressure. It’s also involved in how we process emotions and recover from stressful experiences.</p>
<p>Testosterone is a hormone commonly associated with male reproductive development, but it also influences behavior. Research has linked testosterone to status-seeking, competitiveness, and dominance-related behaviors. It can also affect mood and emotion regulation. While both men and women produce testosterone and cortisol, levels and their effects can differ by sex.</p>
<p>The interaction between testosterone and cortisol has been explored through the dual-hormone hypothesis, which suggests that high testosterone promotes behaviors aimed at gaining or maintaining social status—but primarily when cortisol is low. When cortisol is high, the drive for status might shift to avoiding loss or may be weakened altogether. This context-dependent version of the hypothesis suggests that cortisol shapes how testosterone affects behavior and emotional responses.</p>
<p>Given that social stress often carries a threat to status—such as being judged or evaluated—it makes sense to examine whether testosterone and cortisol interact to influence how people perceive stressful social situations. Past studies have looked at how these hormones relate to behavior and physiological stress responses, but little was known about how they affect the subjective experience of stress.</p>
<p>“It’s important to remember that dealing with psychosocial stress is often more complex than dealing with physical stress,” said study author Erik Ilkevič, a PhD candidate at Vilnius University. “Our bodies are well-equipped to handle a ‘run from the bear’ situation, but modern stressors can be more challenging and harder to understand. Since psychosocial stress is likely to increase, it’s important for people to learn how to manage it effectively, and for scientists to understand what factors affect our reactions to it.” </p>
<p>“Hormones like cortisol and testosterone, while often linked to physical reactions like stress response and reproduction, also play a significant role in our emotions and social behavior, including how we manage stress. Previous research has shown that cortisol and testosterone interactions affect certain things, but how they affect our perception of stress hadn’t been explored.”</p>
<p>For their study, the researchers recruited 40 healthy young men between the ages of 20 and 28 from Lithuania. After excluding a few participants due to preexisting health issues or sample quality concerns, the final analysis included 37 participants. All participants were screened to ensure they had no major psychological, neurological, or hormonal conditions, and none were taking steroid-based medications.</p>
<p>The participants took part in a stress-inducing experiment called the short Sing-a-Song Stress Test. In this task, they were told they would have to sing their national anthem alone, on camera, while being evaluated by expert judges. Although they were ultimately only asked to sing for three seconds, the anticipation of public singing and evaluation was designed to provoke mild psychological stress.</p>
<p>Before, during, and after the stress task, researchers measured heart rate and breathing patterns to assess physical responses. Participants also gave saliva samples to measure baseline levels of testosterone and cortisol. After the task, they rated how stressful they found the experience using a visual scale.</p>
<p>The researchers also collected information on participants’ sleep, tiredness, mood, and overall stress levels in the past month using standardized questionnaires.</p>
<p>The researchers first confirmed that the task successfully induced stress. While it didn’t significantly raise cortisol levels across the group—suggesting the stressor was relatively mild—it did cause changes in heart rate, a sign of autonomic nervous system activation.</p>
<p>The main question was whether testosterone and cortisol levels before the task could predict how stressful participants perceived the experience to be. The findings showed a clear interaction between the two hormones.</p>
<p>“We were surprised to see significant interactions between testosterone and cortisol on stress perception, even though our study had a relatively small number of participants and the stress we used was fairly mild,” Ilkevič told PsyPost. “This suggests that these hormonal interactions could be quite important, even in everyday situations.”</p>
<p>Among men with low baseline cortisol, higher testosterone was linked to lower ratings of stress. In contrast, when cortisol levels were high, testosterone had no meaningful effect on stress perception. On the other hand, among men with low testosterone, those with higher cortisol reported less stress. But when testosterone was high, cortisol no longer appeared to ease stress perception.</p>
<p>These results were consistent across both traditional statistical models and Bayesian methods, which provide a probabilistic way of interpreting data.</p>
<p>“The main takeaway is that our individual levels of cortisol and testosterone can affect how we experience stressful social situations,” Ilkevič explained. “Specifically, in men, if cortisol levels were relatively low, higher testosterone was linked to feeling less stressed, and vice versa. This suggests that it’s not just about the level of one hormone, but how they interact with each other. We think that men with higher testosterone and lower cortisol might see a stressful task as a challenge instead of a threat, which could help them feel less stressed overall.”</p>
<p>“In simple terms, how stressed you feel in a social situation might depend on the balance of cortisol and testosterone in your body.”</p>
<p>The study focused only on men, and its findings may not apply to women. The researchers chose to do this because previous work showed that testosterone and cortisol interactions are more consistently observed in men. </p>
<p>However, “it’s important to include women in this type of research because they are often underrepresented in neuroscience and health studies,” Ilkevič said. “Additionally, we only looked at testosterone. Since mood disorders are distributed unequally between men and women, and since that could be related to stress perception, future studies should include larger, more diverse groups of people (both men and women) and examine other sex hormones like estrogen and progesterone to get a more complete picture.”</p>
<p>“Our long-term goal is to better understand how stress and sex hormones interact in various social and emotional situations across both sexes. We aim to explore how these hormonal interactions are related to our emotional experiences, ability, and willingness to regulate emotions, as well as our behavior in different social settings.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.psyneuen.2025.107557" target="_blank">Testosterone and cortisol moderate perception of mild psychosocial stress in young males</a>,” was authored by Erik Ilkevič, Eglė Jašinskaitė, Rimantė Gaižauskaitė, and Ramunė Grikšienė.</p></p>
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<td><a href="https://www.psypost.org/women-who-fake-orgasm-tend-to-struggle-with-emotional-clarity-and-impulse-control-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;">Women who fake orgasm tend to struggle with emotional clarity and impulse control, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 1st 2025, 08:00</div>
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<p><p>A new study published in the <em><a href="https://doi.org/10.1080/19317611.2025.2514770" target="_blank">International Journal of Sexual Health</a></em> sheds light on the psychological reasons why women fake orgasms. The findings suggest that faking orgasm is not simply about performance, but often reflects emotional and relational dynamics. Women who struggle to manage or understand their emotions, or who engage in sex for coping reasons, are more likely to simulate sexual climax.</p>
<p>While previous studies had linked orgasm faking to social pressures or relationship concerns, little was known about how internal emotional patterns and coping motives contribute to the behavior. The researchers behind the new study sought to examine these psychological factors across two specific sexual contexts: vaginal intercourse and oral sex.</p>
<p>“We were struck by how little attention the topic of faking orgasm had received in relation to emotion regulation,” said study author <a href="https://www.meskonorbert.com/" target="_blank">Norbert Meskó</a>, a full professor at the University of Pécs. “Outside of a single doctoral dissertation, no prior studies had systematically examined this link, despite the intuitive psychological relevance.” </p>
<p>“Faking orgasm often occurs in emotionally complex relational situations, where women may struggle to express dissatisfaction, fear appearing abnormal, or wish to preserve their partner’s self-esteem. These ‘benevolent deceptions’ seemed closely tied to emotional maturity and regulation—so we set out to explore whether this everyday psychological intuition could be supported by empirical evidence.”</p>
<p>To do this, the researchers surveyed 425 Hungarian women aged 18 to 80. Participants completed a series of self-report questionnaires that assessed six types of emotional regulation difficulties and three types of sexual motivation. They also answered detailed questions about their reasons for faking orgasm in each context. The researchers used both network analysis and multiple regression models to analyze how these psychological factors were linked to the tendency to fake orgasm.</p>
<p>The results showed that emotional difficulties—especially struggling to accept emotions, problems with impulse control, and confusion about one’s feelings—were tied to faking orgasm. Women who reported these difficulties were more likely to say they had faked an orgasm, particularly during vaginal intercourse. Coping-related sexual motivation also stood out as a consistent predictor. Women who had sex to manage emotional discomfort, avoid conflict, or maintain closeness with a partner were more likely to fake climax.</p>
<p>“Our findings suggest that faking orgasm is not simply about sexual performance—it often reflects deeper emotional and relational struggles,” Meskó told PsyPost. “Women who have difficulty identifying, accepting, or managing their emotions were more likely to report faking orgasm, especially during vaginal intercourse.” </p>
<p>“For example, some women may fake orgasm because they feel anxious about disappointing their partner, guilty about not climaxing, or uncertain about how to communicate discomfort during sex. In these cases, faking orgasm may serve as a way to avoid conflict, soothe emotional tension, or protect the partner’s feelings. These findings highlight the importance of emotional awareness and honest communication in sexual relationships.”</p>
<p>The connection was stronger and more complex during vaginal intercourse than during oral sex. In the network analysis, which mapped the relationships among all variables, the psychological patterns surrounding faking orgasm during intercourse formed a denser and more interconnected structure. Key motives like partner assurance and ending the sexual encounter were linked to both emotional traits and coping goals. In contrast, the associations during oral sex were weaker and more scattered, suggesting that emotional and motivational factors may play a smaller role in that context.</p>
<p>Regression analysis confirmed these trends. During intercourse, non-acceptance of emotions and coping-related motivation were significant predictors of faking orgasm. For example, women who felt guilty or uncomfortable about not climaxing were more likely to simulate orgasm to ease tension or avoid disappointing their partner. Emotional clarity—being able to identify and understand feelings—was also linked to faking for the purpose of ending sex. In oral sex, only a few predictors emerged clearly, including non-acceptance of emotions and relationship-related sexual motives.</p>
<p>“One surprising aspect was that the psychological predictors we studied, particularly emotion regulation difficulties and coping-related sexual motives, were far more consistent and robust in the context of vaginal intercourse than in oral sex,” Meskó said. “We had expected similar patterns across both contexts, but some motives for faking orgasm during oral sex were not significantly predicted by any of the measured variables, even though the overall model was statistically significant.”</p>
<p>“This suggests that faking during oral sex may be more situational, less emotionally driven, or shaped by different social expectations. It challenged us to think more critically about how different sexual scripts and norms might influence the psychological dynamics behind this behavior. For example, a woman might fake orgasm during oral sex simply to move on from an uncomfortable moment—without it being tied to deeper emotional struggles or long-term relational concerns.”</p>
<p>The researchers note that cultural expectations likely play a role as well. In many heterosexual relationships, there is pressure on women to show sexual responsiveness or orgasm as a sign of relationship health. These scripts may contribute to a sense that faking is necessary or expected. Women may internalize the belief that their partner’s satisfaction depends on their own performance, even when that performance does not match their true experience.</p>
<p>While the study offers new insights, it is not without limitations. Because the research was based on self-report surveys, the accuracy of the data depends on participants’ willingness and ability to reflect on and describe their experiences. The design was also cross-sectional, meaning it cannot determine cause and effect. Future studies could use longitudinal or experimental designs to track how emotional states and motivations unfold in real time during sexual experiences.</p>
<p>“Our sample consisted exclusively of Hungarian women, so the findings might not fully generalize to women in other cultures or relational environments,” Meskó noted. “However, given that many psychological mechanisms are shared across societies, we believe these results can still offer valuable insight into broader patterns of female sexual behavior.”</p>
<p>Despite these caveats, the study contributes to a growing body of work emphasizing that sexual behavior is deeply intertwined with emotional life. The researchers are continuing this line of investigation. A follow-up study, currently under peer review, explores how efforts to retain a romantic partner, openness to casual sex, and satisfaction with the relationship predict faking orgasm. </p>
<p>“This new research compares different sexual contexts—vaginal intercourse versus oral sex—and shows that faking orgasm may function as a relational strategy, particularly when women are trying to preserve or strengthen their romantic bond,” Meskó explained. “Interestingly, we found that efforts to keep a partner from straying were a stronger predictor of faking orgasm than either openness to casual sex or how satisfied women felt in their relationship—especially during vaginal intercourse.”</p>
<p>“One important takeaway is that faking orgasm is not necessarily a sign of deception or manipulation—it can also reflect how a woman is trying to manage her own emotions or her partner’s feelings during sex. Some women may fake to avoid conflict, protect their partner’s self-esteem, or cope with their own discomfort, frustration, or sense of inadequacy.” </p>
<p>“Recognizing these motivations can help partners talk more openly about their sexual experiences and emotional needs,” Meskó continued. “Therapists and couples counselors might also consider exploring these patterns with clients, not to assign blame, but to build greater emotional awareness and intimacy. In this sense, understanding faking orgasm can open the door to more honest and compassionate conversations about sex.”</p>
<p>The study, “<a href="https://doi.org/10.1080/19317611.2025.2514770" target="_blank">Emotion Regulation Difficulties and Sexual Motivation Associated with Faking Orgasm among Hungarian Women</a>,” was authored by Norbert Meskó, Edit Csányi, Orsolya Inhóf, and András N. Zsidó.</p></p>
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<td><a href="https://www.psypost.org/what-we-know-about-a-person-changes-how-our-brain-processes-their-face/" 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;">What we know about a person changes how our brain processes their face</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 1st 2025, 06:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1523/JNEUROSCI.0122-25.2025" target="_blank">The Journal of Neuroscience</a></em> shows that our understanding of who someone is—beyond just what they look like—can shape how our brain processes their face. Researchers found that non-visual areas of the brain, which are typically involved in thinking about people and social knowledge, were more active and better able to distinguish face identities when participants had gained deeper knowledge about the characters during a movie.</p>
<p>The study was motivated by the question of how we come to recognize familiar people. While repeated visual exposure helps the brain build stable representations of faces, we also accumulate conceptual information—like someone’s personality or role in a story. Past research had already shown that engaging with conceptual details enhances memory for faces, but it remained unclear whether this influence affected visual processing areas or non-visual parts of the brain more involved in social understanding.</p>
<p>“Our ability to remember people we have met before is crucial for everyday social interactions,” said study author <a href="https://www-users.york.ac.uk/~ta505/" target="_blank" rel="noopener">Tim Andrews</a>, a professor at the <a href="https://www.york.ac.uk/psychology/staff/academicstaff/ta505/" target="_blank" rel="noopener">University of York</a>. “Previous research in understanding face recognition has primarily focussed on how we remember people based on what their faces look like. Visual experience clearly plays an important role in learning new faces.”</p>
<p>“However, in real life we also learn about people, not just how they look. The potential role of non-visual, conceptual information about a person has often been neglected. This conceptual information includes who a person is (semantic information), how and where we know them (episodic information) and our feelings about them (affective information). Such information could critically contribute to building a rich representation that is important for recognition.”</p>
<p>To explore this, researchers recruited 38 participants and split them into two groups. Both groups watched the same set of video clips from the British TV show Life on Mars, but with a key difference. One group watched the clips in the original order, which preserved the narrative of the episode and allowed viewers to follow the story and learn about the characters. The other group watched the same clips in a scrambled order, disrupting the storyline while keeping the visual exposure identical. This allowed researchers to isolate the effects of conceptual understanding from visual familiarity.</p>
<p>After watching the clips, participants took tests that measured how well they understood what had happened in the video. As expected, those who saw the coherent version scored much higher, confirming that they had formed a richer understanding of the characters and story.</p>
<p>About a month later, both groups returned to the lab for a brain scan using functional magnetic resonance imaging while they watched a new set of clips from the same show. These new scenes featured some of the same characters but did not form a cohesive storyline, ensuring that any differences in brain responses would reflect prior knowledge rather than differences in the new material.</p>
<p>While participants watched the new clips, researchers examined how synchronized their brain activity was using a method called inter-subject correlation. This approach measures how similar the timing of brain responses is across people watching the same video.</p>
<p>In areas of the brain associated with understanding people—like the amygdala, medial prefrontal cortex, and temporal-parietal junction—participants who had seen the original, coherent narrative showed significantly greater synchronization. This suggests that conceptual knowledge about the characters led to more consistent and robust processing of their faces in these regions.</p>
<p>In contrast, traditional face-processing areas in the visual system, such as the fusiform face area and occipital face area, showed no differences between the groups. These regions are usually responsible for analyzing the visual features of faces, and their consistent activity across both groups implies that conceptual knowledge did not affect early perceptual encoding.</p>
<p>“Our main finding was that conceptual knowledge shapes the neural representations of familiar faces in non-visual regions of the brain,” Andrews told PsyPost. “Previous theories have suggested that the ability to recognize faces is a visual process. These findings suggest that it is not just what people look like, but also what we know about them that is important for recognition.”</p>
<p>The researchers also looked at whether brain activity patterns could distinguish between specific characters. They analyzed whether the same character’s face elicited similar brain patterns across different scenes.</p>
<p>In both the visual and non-visual face-processing regions, they found stronger pattern similarity for the same character compared to different characters. But again, the enhancement was most pronounced in non-visual areas—those tied to person knowledge. These effects were more pronounced among participants who had viewed the coherent version of the video, although some patterns were present in both groups.</p>
<p>Importantly, the team ruled out the possibility that these findings were driven by low-level visual similarities between the scenes. They conducted control tests using early visual areas and brain regions not involved in face recognition, such as those that respond to places. These analyses showed that only regions specialized for face and person processing contained identity-specific patterns, and only when viewers had learned meaningful information about the characters.</p>
<p>“We had shown in a previous study (<a href="https://doi.org/10.1016/j.cortex.2024.05.016" target="_blank" rel="noopener">Noad and Andrews, 2024</a>) that associating faces with conceptual knowledge during natural viewing enhances recognition by fostering deeper processing,” Andrews said. “However, the neural level at which this occurs remains unclear. One possibility was that conceptual knowledge strengthens visual representations.”</p>
<p>“However, we found no effects in visual regions of the brain. Alternatively, conceptual knowledge may directly influence non-visual regions involved in processing semantic, episodic and affective information about the person. Consistent with this hypothesis, we found a network of non-visual regions showed significant effects of conceptual knowledge. These findings provide new insights into how real-world learning integrates perceptual and conceptual information, enriching our understanding of the neural mechanisms underlying face recognition.”</p>
<p>By using a naturalistic, narrative-rich approach, the study moved beyond previous experiments that often relied on static face images and isolated facts. This approach more closely mirrors how people encounter and learn about others in everyday life, offering new insights into the ways memory, social knowledge, and perception work together during face recognition.</p>
<p>Still, the study had some limitations. The sample size was modest, and while the trends were consistent, some group differences in identity decoding did not reach statistical significance. The use of a specific television show also limits the generalizability of the results. Future research could expand on this by using different types of narratives or testing whether the same effects occur in real-world social interactions.</p>
<p>“Most studies of face recognition have investigated the process in laboratory conditions that often lack ecological validity,” Andrews explained. “Surprisingly little is known about how we learn faces in the real world. To address this issue, we developed a naturalistic approach to understand how learning unfolds in more ecologically valid conditions and over longer time periods. Nonetheless, the time periods used in this study were shorter than those typically encountered in everyday life when we are getting to know people. Future studies should focus on studying the process over longer periods. ”</p>
<p>Despite these caveats, the findings provide evidence that understanding who someone is—beyond how they look—changes how the brain processes their face. The study suggests that memory for faces is not just stored in visual regions but is supported by a broader network of brain areas that link faces with meaning. This research helps explain why we are so good at recognizing people we know, even in changing or difficult viewing conditions: our brains don’t just see a face—they understand the person behind it.</p>
<p>“The overall aim of this research is to reveal the critical importance of conceptual knowledge in the recognition of faces,” Andrews said. “This will help develop new theoretical perspectives on how we recognize faces and to help us understand why some people have difficulty recognizing faces (see <a href="https://doi.org/10.1093/cercor/bhae285" target="_blank" rel="noopener">Noad, Watson and Andrews, 2024</a>).”</p>
<p>The study, “<a href="https://doi.org/10.1523/JNEUROSCI.0122-25.2025" target="_blank">Conceptual knowledge shapes the neural representations of learned faces in non-visual regions of the brain</a>,” was authored by Kira N. Noad, David M. Watson, and Timothy J. Andrews.</p></p>
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<td><a href="https://www.psypost.org/dementia-diagnoses-are-often-delayed-for-years-new-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Dementia diagnoses are often delayed for years, new study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 31st 2025, 19:06</div>
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<p><p>People with dementia face a long road to diagnosis, according to a comprehensive review published in the <em><a href="https://onlinelibrary.wiley.com/doi/10.1002/gps.70129" target="_blank">International Journal of Geriatric Psychiatry</a></em>. The analysis found that, on average, individuals wait 3.5 years from the time symptoms first appear until they receive a formal diagnosis. For those with early-onset dementia, the delay is even longer—averaging 4.1 years. These findings highlight ongoing gaps in timely access to care and the need for improved diagnostic strategies, particularly for younger individuals and those with less common forms of dementia.</p>
<p>Dementia is a progressive condition that affects memory, thinking, and behavior. It is not a single disease, but a group of related conditions that include Alzheimer’s disease, frontotemporal dementia, vascular dementia, and others. Symptoms usually worsen over time, eventually interfering with daily life and independence. While dementia primarily affects older adults, younger people can develop early-onset forms, often leading to misdiagnoses or delays in care.</p>
<p>A timely diagnosis is essential for planning treatment, managing symptoms, and helping families prepare for what lies ahead. It also allows individuals to access support services and medications earlier in the course of the disease. National and international health organizations have emphasized the importance of early recognition and response. Yet the actual time it takes to reach a diagnosis remains poorly understood.</p>
<p>To address this gap, a team of researchers at University College London and the University of Jaén conducted the first systematic review and meta-analysis of global evidence on time to diagnosis in dementia.</p>
<p>The researchers searched major medical databases for studies published through December 2024, identifying 13 eligible studies that together included over 30,000 people with dementia. Most of these studies recruited participants from memory clinics, hospitals, or neurology departments, and focused on individuals who had already received a formal diagnosis. The authors defined “time to diagnosis” as the interval between when symptoms first appeared—based on interviews with patients or caregivers—and the moment a diagnosis was made.</p>
<p>Using a meta-analytic approach, the team calculated that across all dementia types, the average time to diagnosis was 3.5 years. For Alzheimer’s disease specifically, the average delay was slightly longer at 3.6 years. People with frontotemporal dementia faced the longest wait, averaging 4.2 years, and those with early-onset forms of the disease had to wait even longer—around 4.1 years. In contrast, people with late-onset dementia were diagnosed more quickly, typically within 2.9 years.</p>
<p>While the overall numbers point to significant delays, the reasons behind them were complex and varied. In general, younger individuals faced longer diagnostic intervals, possibly because healthcare providers are less likely to suspect dementia in younger patients. The type of dementia also made a difference. Frontotemporal dementia, which often affects behavior and language more than memory, proved harder to identify than more typical forms like Alzheimer’s disease.</p>
<p>Some studies suggested that people with lower cognitive test scores or who had difficulty with daily activities were diagnosed more quickly, possibly because their symptoms were more severe or obvious. Other factors that appeared to delay diagnosis included having multiple consultations with different providers, receiving an initial diagnosis of mild cognitive impairment, or undergoing more complex diagnostic procedures like brain scans.</p>
<p>Socioeconomic and racial disparities also played a role. In one U.S.-based study, Black participants and those with less education waited longer to receive a diagnosis, suggesting barriers related to access, healthcare literacy, or provider bias.</p>
<p>The review also found that access to specialist services could make a difference. In Australia, people with early-onset dementia who were seen at a dedicated diagnostic clinic received their diagnosis faster than those who were not. This points to the potential benefits of specialized centers that focus on diagnosing and managing dementia in younger adults.</p>
<p>Despite these insights, the researchers noted that data on the causes of delayed diagnosis were limited and often inconsistent across studies. Many of the factors associated with longer or shorter diagnostic intervals were identified in only a single study, making it hard to draw firm conclusions. The studies also used different methods to define and measure the time to diagnosis, which could have affected the results.</p>
<p>The authors emphasized the need for more research to understand how diagnostic delays affect patients and families, and what can be done to improve the process. They called for the development of standard definitions and criteria for measuring time to diagnosis, as well as better tracking of the steps patients go through from first symptoms to final diagnosis.</p>
<p>While delays in dementia diagnosis are partly due to the gradual onset and vague nature of early symptoms, the findings suggest that the healthcare system itself plays a major role. Long referral pathways, limited access to specialists, and inadequate training for general practitioners may all contribute to the problem.</p>
<p>The authors concluded that improving the timeliness of dementia diagnosis should be a public health priority. This is particularly true for younger patients and those with frontotemporal dementia, who currently face the longest delays. Establishing specialist diagnostic centers, standardizing care pathways, and training healthcare professionals to recognize the wide range of dementia symptoms could help close the gap.</p>
<p>The study, “<a href="https://doi.org/10.1002/gps.70129" target="_blank">Time to Diagnosis in Dementia: A Systematic Review With Meta-Analysis</a>,” was published July 27, 2025 and authored by Olubunmi Kusoro, Moïse Roche, Rafael Del-Pino-Casado, Phuong Leung, and Vasiliki Orgeta.</p></p>
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<td><a href="https://www.psypost.org/are-zombie-cells-in-your-blood-vessels-driving-long-covid-and-chronic-fatigue/" 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;">Are “zombie cells” in your blood vessels driving long-COVID and chronic fatigue?</a>
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<p><p>Millions of people who recover from infections like COVID-19, influenza and glandular fever are affected by long-lasting symptoms. These include chronic fatigue, brain fog, exercise intolerance, dizziness, muscle or joint pain and gut problems. And many of these symptoms worsen after exercise, a phenomenon known as post-exertional malaise.</p>
<p>Medically the symptoms are known as myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS). The World Health Organization classifies this as a post viral fatigue syndrome, and it is <a href="https://www.cdc.gov/me-cfs/about/index.html">recognised</a> by both the WHO and the United States Centers for Disease Control and Prevention as a brain disorder.</p>
<p>Experiencing illness long after contracting an infection is not new, as patients have reported these symptoms for decades. But COVID-19 has amplified the problem worldwide. Nearly half of people with ongoing post-COVID symptoms – a condition known as long-COVID – now meet the criteria for ME/CFS. Since the start of the pandemic in 2020, it is estimated that more than 400 million people have developed <a href="https://www.context.news/socioeconomic-inclusion/long-covid-costs-countries-billions-of-dollars">long-COVID</a>.</p>
<p>To date, no widely accepted and testable mechanism has fully explained the biological processes underlying long-COVID and ME/CFS. Our work offers a new perspective that may help close this gap.</p>
<p>Our research group studies blood and the cardiovascular system in inflammatory diseases, as well as post-viral conditions. We focus on coagulation, inflammation and endothelial cells. Endothelial cells make up the inner layer of blood vessels and serve many important functions, like regulating blood clotting, blood vessel dilation and constriction, and inflammation.</p>
<p>Our latest <a href="https://www.preprints.org/manuscript/202505.1875/v1">review</a> aims to explain how ME/CFS and long-COVID start and progress, and how symptoms show up in the body and its systems. By pinpointing and explaining the underlying disease mechanisms, we can pave the way for better clinical tools to diagnose and treat people living with ME/CFS and long-COVID.</p>
<h2>What is endothelial senescence?</h2>
<p>In our review, our international team proposes that certain viruses drive endothelial cells into a half-alive, “zombie-like” state called cellular senescence. Senescent endothelial cells stop dividing, but continue to release molecules that awaken and confuse the immune system. This prompts the blood to form clots and, at the same time, prevent clot breakdown, which could lead to the constriction of blood vessels and limited blood flow.</p>
<p>By placing “zombie” blood-vessel cells at the centre of these post-viral diseases, our hypothesis weaves together microclots, oxygen debt (the extra oxygen your body needs after strenuous exercise to restore balance), brain-fog, dizziness, gut leakiness (a digestive condition where the intestinal lining allows toxins into the bloodstream) and immune dysfunction into a single, testable narrative.</p>
<h2>From acute viral infection to ‘zombie’ vessels</h2>
<p>Viruses like SARS-CoV-2, Epstein–Barr virus, HHV-6, influenza A, and enteroviruses (a group of viruses that cause a number of infectious illnesses which are usually mild) can all infect endothelial cells. They enable a direct attack on the cells that line the inside of blood vessels. Some of these viruses have been shown to trigger endothelial senescence.</p>
<p>Multiple <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC9533263/">studies</a> show that SARS-CoV-2 (the virus which causes COVID-19 disease) has the ability to induce senescence in a variety of cell types, including endothelial cells. Viral proteins from SARS-CoV-2, for example, sabotage DNA-repair pathways and push the host cell towards a senescent state, while senescent cells in turn become even more susceptible to <a href="https://www.nature.com/articles/s41556-023-01097-w">viral entry</a>. This reciprocity helps explain why different pathogens can result in the same chronic illness. Influenza A, too, has shown the ability to drive endothelial cells into a senescent, <a href="https://pubmed.ncbi.nlm.nih.gov/39841412/">zombie-like state</a>.</p>
<h2>What we think is happening</h2>
<p>We propose that when blood-vessel cells turn into “zombies”, they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained.</p>
<p>During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness.</p>
<p>In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these “zombie” cells found in the blood vessels can create the mix of symptoms seen in long-COVID and ME/CFS.</p>
<h2>Immune exhaustion locks in the damage</h2>
<p>Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-COVID and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction.</p>
<p>Senescent endothelial cells may also send out a chemical signal to repel <a href="https://biologyinsights.com/hla-e-its-role-in-immunity-pregnancy-and-cancer/">immune attack</a>. So the “zombie cells” actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist.</p>
<p>In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-COVID, and this may enable the “zombie cells” to survive and the disease to progress.</p>
<h2>Where the research goes next</h2>
<p>There is a registered clinical trial in the US that is investigating senescence in <a href="https://clinicaltrials.gov/study/NCT04903132?tab=history&a=4">long-COVID</a>. Our consortium is testing new ways to spot signs of ageing in the cells that line our blood vessels. First, we expose healthy endothelial cells in the lab to blood from patients to see whether it pushes the cells into a senescent, or “zombie,” state.</p>
<p>At the same time, we are trialling non‑invasive imaging and fluorescent probes that could one day reveal these ageing cells inside the body. In selected cases, tissue biopsies may later confirm what the scans show. Together, these approaches aim to pinpoint how substances circulating in the blood drive cellular ageing and how that, in turn, fuels disease.</p>
<p>Our aim is simple: find these ageing endothelial cells in real patients. Pinpointing them will inform the next round of clinical trials and open the door to therapies that target senescent cells directly, offering a route to healthier blood vessels and, ultimately, lighter disease loads.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/261108/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/long-covid-viruses-and-zombie-cells-new-research-looks-for-links-to-chronic-fatigue-and-brain-fog-261108">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/prenatal-bpa-exposure-linked-to-schizophrenia-like-brain-changes/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Prenatal BPA exposure linked to schizophrenia-like brain changes</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 31st 2025, 14:00</div>
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<p><p>A new animal study has found that prenatal exposure to bisphenol A — a chemical commonly found in plastics — can lead to lasting brain changes and behavior associated with schizophrenia. The research, published in <em><a href="https://doi.org/10.1016/j.physbeh.2025.114933" target="_blank" rel="noopener">Physiology & Behavior</a></em>, revealed that female rats exposed to BPA in the womb showed impaired sensorimotor function and a reduction in key brain cells linked to psychiatric illness. Surprisingly, however, male rats were unaffected.</p>
<p>Bisphenol A, or BPA, is a synthetic compound widely used in manufacturing polycarbonate plastics and epoxy resins. These materials appear in everyday items such as food containers, water bottles, the lining of metal cans, and thermal paper receipts. BPA can leach from products and enter the human body through ingestion, skin contact, or inhalation. Studies have detected BPA in the blood, urine, and tissue of more than 90 percent of people tested, including pregnant women. BPA also crosses the placenta and blood-brain barrier, meaning it can reach the developing brain during pregnancy.</p>
<p>BPA is known to interfere with hormone systems and is considered an endocrine-disrupting chemical. Because of its widespread presence and links to health concerns, BPA has become the focus of major scientific and regulatory efforts. The U.S. National Toxicology Program, along with the Food and Drug Administration and the National Institute of Environmental Health Sciences, established the CLARITY-BPA project to better understand its biological effects.</p>
<p>The developing brain is particularly sensitive to environmental toxins, and prenatal exposure to endocrine disruptors like BPA may permanently alter brain structure and function. Previous studies have linked early BPA exposure to problems with learning, memory, mood, and social behavior in animals, and to neurodevelopmental disorders such as anxiety, depression, and autism in humans.</p>
<p>Some research has also raised concerns about a possible link between BPA and schizophrenia, a severe mental disorder involving hallucinations, delusions, and disrupted thinking. One theory of schizophrenia points to dysfunction in a specific set of brain cells that use the chemical messenger GABA. These cells include parvalbumin-positive interneurons in the prefrontal cortex — a brain region central to planning, decision-making, and social behavior.</p>
<p>Given this background, the researchers set out to test whether prenatal BPA exposure could affect markers of schizophrenia in rats, including behavior linked to psychosis and changes in GABA-related brain genes and cells.</p>
<p>Scientists at the Iran University of Medical Sciences used pregnant Sprague-Dawley rats and assigned them to one of four groups. From the first day of pregnancy until delivery, each group received a daily oral dose of either low-dose BPA (0.25 mg/kg), high-dose BPA (2.5 mg/kg), a reference estrogen (ethinyl estradiol), or a control solution.</p>
<p>After birth, the pups were raised by their mothers and weaned at three weeks old. They were housed until early adulthood. On days 62 and 63 after birth, both male and female offspring were tested for behavioral changes. Researchers examined two main outcomes: locomotor activity and a test called prepulse inhibition (PPI), which measures how well the brain filters sensory information. Deficits in PPI are commonly seen in schizophrenia.</p>
<p>On day 64, the researchers collected brain tissue from a subset of the animals. They used immunohistochemistry to examine the density of parvalbumin-positive neurons in the prefrontal cortex. They also used a genetic technique to measure levels of three genes associated with schizophrenia: GAD67, NRG1, and ERbB4.</p>
<p>Female rats exposed to either dose of BPA in the womb showed a significant drop in PPI, indicating impaired sensorimotor gating. This deficit was not seen in male rats or in those exposed to the reference estrogen. PPI is often used in animal models to assess psychotic-like behavior, and reductions in this measure have been linked to schizophrenia-like brain dysfunction.</p>
<p>The researchers also found a sharp reduction in the number of parvalbumin-positive neurons in the prefrontal cortex of female rats exposed to BPA. These neurons play a key role in controlling brain rhythms and maintaining the balance between excitatory and inhibitory signals. Loss or dysfunction of these cells has been consistently reported in the brains of people with schizophrenia.</p>
<p>Interestingly, BPA exposure did not significantly change the expression of GAD67, NRG1, or ERbB4 — genes involved in GABA signaling and neural development — in either male or female rats. Nor did it affect general locomotor activity in either sex.</p>
<p>These results suggest that BPA may disrupt the development or survival of specific neuron types in a sex-dependent way, without altering all aspects of GABAergic gene expression.</p>
<p>Although this study did not find changes in the three measured genes, other research has shown that BPA can interfere with multiple brain development pathways. BPA has been found to affect neural stem cells, reduce cell proliferation and differentiation, and disturb important growth signals such as the Wnt/β-catenin and BDNF pathways. These disruptions may impair neurogenesis and synaptic development during key stages of brain formation.</p>
<p>The current study adds to this body of work by linking prenatal BPA exposure to long-lasting structural and functional changes in a brain region implicated in schizophrenia. The authors suggest that BPA’s hormone-like activity may interfere with estrogen receptor signaling, which plays a role in brain development and is different between males and females.</p>
<p>The researchers acknowledged several limitations. First, they focused only on the prenatal period, although postnatal exposure could also influence brain outcomes. Second, they examined the rats in early adulthood but did not assess whether the effects emerged earlier or evolved over time. Third, only two BPA doses were tested. Other effects might be found with lower or higher exposures. Finally, the analysis of brain tissue was limited to a small number of thin sections, which may not reflect the full extent of changes in the prefrontal cortex.</p>
<p>Even so, the findings point to a potential mechanism by which prenatal BPA exposure could increase the risk of schizophrenia-related features, at least in females. Future research should explore how BPA influences other brain regions and behavioral systems, and whether similar effects occur in other species, including humans.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.physbeh.2025.114933" target="_blank" rel="noopener">Prenatal exposure to Bisphenol A sex-specifically disrupts prepulse inhibition and decreases parvalbumin-positive neurons in the prefrontal cortex of adult rats</a>,” was authored by Abdolhakim Ghanbarzehi, Soraya Mehrabi Abbas Piryaei, Fereshteh Azedi, Ali Mohammadi, and Ali Shahbazi.</p></p>
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<td><a href="https://www.psypost.org/new-study-links-low-self-efficacy-to-bedtime-procrastination/" 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 links low self-efficacy to bedtime procrastination</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 31st 2025, 12:00</div>
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<p><p>A study of college students in China found that those with lower self-efficacy are more prone to bedtime procrastination—that is, putting off going to bed. This relationship was partially explained by fear of missing out and increased social media use. The findings were published in <a href="https://doi.org/10.1177/00332941251329864"><em>Psychological Reports</em></a>.</p>
<p>Many people struggle with poor sleep quality. Some studies estimate that one in three individuals believes they need better or more sleep, indicating widespread sleep problems. These issues include difficulties falling asleep, staying asleep, or achieving restful, restorative sleep. Common sleep disorders include insomnia, sleep apnea, and restless legs syndrome, all of which can lead to fatigue, irritability, poor concentration, and diminished physical and mental health.</p>
<p>One behavior that contributes to sleep problems is bedtime procrastination. This occurs when a person delays going to bed without any external reason, often despite feeling tired. It is commonly linked to poor self-control, digital distractions, or a desire to reclaim personal time at night—a phenomenon known as “revenge bedtime procrastination.”</p>
<p>People who procrastinate at bedtime often spend late-night hours scrolling through social media, watching videos, or engaging in other non-essential activities. This behavior can lead to chronic sleep deprivation and create a self-reinforcing cycle of exhaustion and disrupted sleep habits. Stress, anxiety, and irregular daily routines can exacerbate these problems.</p>
<p>Researchers Han Bao and Shichuan Li set out to clarify the relationship between self-efficacy and bedtime procrastination in a sample of Chinese university students. They also examined whether fear of missing out and social media use might mediate that relationship. They hypothesized that students with lower self-efficacy would be more likely to use social media excessively and experience fear of missing out. In turn, these factors might increase bedtime procrastination, partially explaining why it is associated with low self-efficacy. Fear of missing out refers to the anxiety that others are having rewarding experiences without the person experiencing the fear. It is often triggered by viewing social media posts or updates.</p>
<p>The researchers conducted an online survey with 468 university students from the Chinese provinces of Jilin, Liaoning, and Shandong. Participants received the equivalent of approximately one U.S. dollar as compensation. Among them, 253 were male.</p>
<p>The survey included several standardized psychological assessments: the 10-item General Self-Efficacy Scale, the 10-item Fear of Missing Out Scale, the Facebook Intensity Scale (to assess social media use), and the Bedtime Procrastination Scale.</p>
<p>The results showed that students with lower self-efficacy were more likely to procrastinate at bedtime, used social media more frequently, and reported higher levels of fear of missing out. The researchers tested a statistical model proposing that low self-efficacy leads to greater social media use and heightened fear of missing out, which in turn contribute to increased bedtime procrastination. The results supported this model, but also indicated that fear of missing out and social media use only partially explain the connection between self-efficacy and bedtime procrastination.</p>
<p>“Our results indicate that FoMO [fear of missing out] and social media use act as indirect influencing factors, impacting the relationship between self-efficacy and bedtime procrastination. This finding helps to better understand the complex relationship between emotional and behavioral regulation,” the study authors concluded.</p>
<p>The study sheds light on the factors associated with bedtime procrastination. However, it should be noted that the design of this study does not allow any causal inferences to be derived from the results. Causal relationships tested in the statistical models created by study authors remain only a possibility for now.</p>
<p>The paper, “<a href="https://doi.org/10.1177/00332941251329864">Self-Efficacy, Fear of Missing out, Social Media Use, and Bedtime Procrastination in Chinese College Students,</a>” was authored by Han Bao and Shichuan Li.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
<p><strong>This information is taken from free public RSS feeds published by each organization for the purpose of public distribution. Readers are linked back to the article content on each organization's website. This email is an unaffiliated unofficial redistribution of this freely provided content from the publishers. </strong></p>
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