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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News Daily Digest (Unofficial)</span></td>
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<td><a href="https://www.psypost.org/strategic-disinvestment-from-masculinity-linked-to-poor-psychosocial-outcomes/" 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;">Strategic disinvestment from masculinity linked to poor psychosocial outcomes</a>
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<p><p>A recent study published in <a href="https://doi.org/10.1007/s11199-024-01547-1"><em>Sex Roles</em></a> reveals that “strategic masculine disinvestment,” a process where men intentionally distance themselves from traditional masculine ideals, is linked to poorer psychosocial functioning, including higher levels of distress and anger.</p>
<p>Jessica Pfaffendorf and Terrence Hill examined how changes in masculinity, including the shift away from hegemonic masculinity, marked by traits like stoicism and assertiveness, intersect with broader social changes. As structural support for traditional masculinity erodes, men are increasingly adopting alternative identity strategies.</p>
<p>The researchers analyzed data from the 2021 Crime, Health, and Politics Survey (CHAPS), which included a nationally representative sample of 803 men (ages 18-91) from the United States. To assess strategic masculine disinvestment, participants indicated whether they sometimes acted “less manly” because it helped them get ahead in the world.</p>
<p>Psychosocial functioning was evaluated through validated scales that measured variables such as mastery, anger, anxiety, depression, and nonspecific psychological distress. Mastery was assessed using items that gauged participants’ perceived sense of control over their lives, while psychological distress was measured through the K6 Psychological Distress Scale, which captures symptoms like nervousness, hopelessness, and worthlessness. Participants also provided demographic information.</p>
<p>Younger men and those with college educations were more likely to report strategic masculine disinvestment, reflecting its prevalence among demographics exposed to progressive discourses on gender and identity, particularly in educational settings. Men who reported difficulties meeting basic needs, such as paying bills or accessing healthcare, were also significantly more likely to engage in masculine disinvestment. This finding challenges prior assumptions that masculine distancing is exclusive to privileged men, demonstrating that economic precarity can play a pivotal role in shaping gendered behaviors.</p>
<p>Pfaffendorf and Hill observed consistent associations between strategic masculine disinvestment and poorer mental health. Men who engaged in disinvestment reported lower levels of mastery, feeling less control over their lives. They also experienced higher levels of anger, anxiety, and depression, along with elevated nonspecific psychological distress.</p>
<p>These findings suggest that while distancing from traditional masculinity may offer adaptive responses to changing societal norms, it also brings significant emotional and psychological challenges. The authors propose that these outcomes may stem from cognitive dissonance and identity conflicts as men navigate shifting ideals of manhood in the context of entrenched societal expectations.</p>
<p>The study’s reliance on a single-item measure for strategic masculine disinvestment may limit the reliability of findings.</p>
<p>The research, “<a href="https://doi.org/10.1007/s11199-024-01547-1">Strategic Masculine Disinvestment: Understanding Contemporary Transformations of Masculinity and Their Psychosocial Implications</a>,” was authored by Jessica Pfaffendorf and Terrence Hill.</p></p>
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<td><a href="https://www.psypost.org/scientists-reveal-the-disturbing-impact-of-wildfire-smoke-on-key-brain-cells/" 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;">Scientists reveal the disturbing impact of wildfire smoke on key brain cells</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 24th 2025, 06:00</div>
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<p><p>Wildfire smoke, long recognized as a health threat to the lungs and heart, may also pose significant risks to brain health, according to a study published in the <a href="https://www.mdpi.com/1422-0067/25/19/10288"><em>International Journal of Molecular Sciences</em></a>. The research explored how smoldering eucalyptus wood smoke extract affects human brain endothelial cells, which form the blood-brain barrier. Results showed that exposure to the smoke extract increased inflammation and reduced the levels of tight junction markers that help maintain the barrier’s integrity. These changes suggest that inhaling wildfire smoke could contribute to neuroinflammation and increase the risk of neurological disorders.</p>
<p>The study was motivated by growing evidence that wildfire smoke does more than harm respiratory and cardiovascular systems. Epidemiological research has linked wildfire exposure to cognitive deficits and a higher risk of neurodegenerative diseases like Alzheimer’s and Parkinson’s. Researchers at <a href="https://bioams.llnl.gov/">Lawrence Livermore National Laboratory</a> aimed to better understand how smoke might directly affect the brain by investigating its impact on brain endothelial cells.</p>
<p>“As we are all aware, wildfires pose significant health risks, and their frequency and intensity are increasing due to climate change,” explained postdoctoral scholar Dorothy You and senior scientist Bruce Buchholz, the corresponding authors of the study.</p>
<p>“Although many studies have examined the impact of wildfires on the lungs and heart, few have focused on potential changes in the brain resulting from wildfire smoke exposure. Some studies have suggested that wildfire smoke exposure can affect cognitive function, and we aimed to understand its potential impact on the brain at the cellular level.”</p>
<p>“Neuroinflammation is linked to the protein pathologies of neurodegenerative diseases, such as amyloid plaques and neurofibrillary tangles in Alzheimer’s disease and Lewy bodies in Parkinson’s disease,” the researchers explained. “We wanted to investigate whether exposure to wood smoke could trigger neuroinflammation. Brain endothelial cells, which line the capillaries, play a crucial role in forming the blood-brain barrier.”</p>
<p>To examine the effects of wildfire smoke, the researchers used an in vitro approach, exposing two types of human brain endothelial cells to smoldering eucalyptus wood smoke extract for 24 hours. The two cell models included primary human brain microvascular endothelial cells and an immortalized brain endothelial cell line. The smoke extract, provided by the United States Environmental Protection Agency, was prepared from eucalyptus wood burned during its smoldering phase, which produces high levels of particulate matter and toxic chemicals.</p>
<p>The study involved multiple steps to assess the cellular response. After treating the cells with varying concentrations of smoke extract, the researchers measured the production of inflammatory molecules, changes in gene expression, and markers associated with the cells’ structural integrity. They also evaluated whether the smoke extract caused cell death or oxidative stress. Advanced techniques, such as RNA sequencing, were used to identify changes in gene activity, while microscopic imaging was employed to observe structural proteins.</p>
<p>The findings revealed that the smoke extract triggered a dose-dependent increase in interleukin-8, a pro-inflammatory cytokine. Interleukin-8 plays a role in recruiting immune cells to areas of inflammation, and its elevated levels suggest that the smoke extract incites an inflammatory response in brain endothelial cells. Notably, the primary brain endothelial cells showed a stronger response compared to the immortalized cell line, indicating that the primary cells might better mimic the effects seen in living tissues.</p>
<p>“It was quite surprising to observe that two different types of brain endothelial cells responded similarly to wood smoke extracts,” You and Buchholz told PsyPost. “Although both are types of brain endothelial cells, one is an immortalized cell line intended for long-term use in the lab, whereas the other is composed of primary cells that closely mimic those found in actual tissue. Both shared very similar inflammatory pathways, suggesting that wood smoke induces a specific type of inflammation in brain endothelial cells. However, the primary cells showed a more pronounced response to the wood smoke extract.”</p>
<p>The study also uncovered that exposure to the smoke extract disrupted the expression of tight junction proteins, including ZO-1, ZO-2, and occludin, which are essential for maintaining the blood-brain barrier’s structural integrity. While changes in these proteins were more pronounced at the genetic level than at the protein level during the 24-hour exposure, this disruption could potentially make the barrier more permeable. Such permeability would allow harmful substances, including toxins and inflammatory molecules, to enter the brain more easily.</p>
<p>Additionally, the smoke extract activated specific cellular pathways related to inflammation and oxidative stress. These pathways, known as the aryl hydrocarbon receptor (AhR) pathway and the nuclear factor erythroid 2-related factor 2 (NRF2) pathway, mediate the body’s response to toxic environmental substances. Both pathways have been implicated in neuroinflammation and damage to the blood-brain barrier in prior research. The study also identified genes associated with ferroptosis, a type of cell death linked to oxidative stress and lipid damage, suggesting that smoke exposure may have broader implications for brain cell health.</p>
<p>“The main takeaway from this study is that inhaling wildfire smoke not only impacts the lungs and heart, but it can also potentially affect brain health,” the researchers said. “So, It is best to stay indoors when air quality is hazardous and wear a mask if you must go outside during poor air quality.”</p>
<p>Despite the significant findings, the study has some limitations. It focused solely on two types of brain endothelial cells and did not account for the interactions between endothelial cells and other brain cell types, such as neurons or astrocytes, which play important roles in brain health and disease. Furthermore, the study examined the effects of acute exposure to smoke extract over 24 hours.</p>
<p>“Given that many communities experiencing wildfires are exposed to wildfire smoke and poor air quality for extended periods, future studies should explore the long-term, chronic effects of repeated or prolonged exposure to wildfire smoke,” You and Buchholz said.</p>
<p>The researchers also noted that the composition of wildfire smoke varies depending on factors such as the type of biomass burned and the combustion conditions. For example, smoldering fires produce more fine particulate matter and toxic compounds than flaming fires.</p>
<p>“Smoke travels long distances and changes chemically as it ages,” the researchers noted. “The composition of smoke in exposures to firefighters is not the same as to the general population downwind.”</p>
<p>This variability underscores the importance of assessing the neurotoxicity of different types of biomass beyond smoldering eucalyptus to determine which might pose greater risks to brain health.</p>
<p>The ultimate aim of this line of research is, as the researchers put it, “to understand the impact of wildfire smoke on the brain, with a focus on identifying the potential route of entrance for wildfire smoke particles into the brain, which has been unclear to the scientific community.”</p>
<p>“Smoke consists of particles ranging from ultrafine sizes (less than 0.1 micrometers or 100 nanometers) to relatively large condensed agglomerations greater than 10 micrometers, along with thousands of chemical combustion products that tend to condense onto particles as the smoke cools,” You and Buchholz explained. “The smallest particles can be inhaled deep into the lungs and deposited there. This study examined the response of brain endothelial cells to combustion products delivered through the bloodstream. Evidence in the literature suggests that small particles can also be deposited in nasal tissues and transported to the olfactory bulb in the brain. It is likely that smoke particles and condensates can reach the brain through both routes.”</p>
<p>The study, “<a href="https://doi.org/10.3390/ijms251910288" target="_blank" rel="noopener">Eucalyptus Wood Smoke Extract Elicits a Dose-Dependent Effect in Brain Endothelial Cells</a>,” was authored by Dorothy J. You, Bria M. Gorman, Noah Goshi, Nicholas R. Hum, Aimy Sebastian, Yong Ho Kim, Heather A. Enright, and Bruce A. Buchholz.</p></p>
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<td><a href="https://www.psypost.org/men-lose-half-their-emotional-support-networks-between-30-and-90-decades-long-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;">Men lose half their emotional support networks between 30 and 90, decades-long study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 23rd 2025, 16:00</div>
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<p><p>Emotional support networks among men shrink by 50% between the ages of 30 and 90, reflecting an average decrease from two to one emotional support providers, according to research published in <a href="https://doi.org/10.1037/pag0000843"><em>Psychology & Aging</em></a>.</p>
<p>Research consistently shows that social networks tend to <a href="https://www.psypost.org/loneliness-follows-a-u-shaped-path-across-adulthood-study-finds/">shrink with age</a>. Emotional support, defined as providing comfort and understanding, is essential for well-being, particularly in older adults, where it predicts <a href="https://www.psypost.org/loneliness-linked-to-cognitive-decline-in-older-adults-study-finds/">better cognitive health</a>, emotional stability, and life expectancy. Past studies demonstrate that general social network contraction occurs globally and across genders. However, whether the decline extends to the most intimate forms of support is debated.</p>
<p>Motivated by frameworks like socioemotional selectivity theory, which proposes that older adults strategically prioritize close relationships, and theories emphasizing emotional independence with age, Kate Petrova and colleagues aimed to clarify how emotional support networks evolve and identify early predictors of their size.</p>
<p>This study utilized a unique longitudinal dataset drawn from a sample of 235 men who were originally recruited as Harvard University students between 1939 and 1942. These participants were followed for 71 years, with data collected at regular intervals to assess changes in their emotional support networks. Emotional support was defined as the number of people participants turned to for comfort and counsel during challenging times. Data collection involved seven waves of emotional support assessments conducted between 1951 and 2010.</p>
<p>Participants were asked open-ended questions about their emotional support providers, such as “Who do you turn to for emotional support?” or “With whom do you usually talk over personal problems?” The total number of support providers was calculated based on participants’ responses. However, generalized responses, such as “family” or “friends,” as well as mentions of non-human sources like pets, were excluded from formal analyses.</p>
<p>The study also examined early-life predictors of network size. Archival data from participants’ intake interviews in the late 1930s and early 1940s provided information about childhood family environments, including parental warmth and socioeconomic status (SES). Parental warmth was measured using coders’ ratings of the participants’ relationships with their mother and father, as well as the overall emotional climate of their home. Childhood SES was assessed using parental education and income levels. Life transitions, such as marriage and retirement, were also considered in the analysis, with data collected about participants’ marital and employment statuses throughout the study.</p>
<p>This comprehensive, longitudinal approach allowed the researchers to examine how emotional support networks changed over time and the factors that influenced these changes.</p>
<p>Petrova and colleagues found that emotional support networks declined significantly across the adult lifespan, with participants’ reported number of emotional support providers decreasing by approximately 50% between the ages of 30 and 90. At age 30, participants reported relying on an average of two support providers, which decreased to just one by age 90. This linear decline suggests that aging is accompanied by a reduction in the number of people individuals regularly turn to for emotional support. Interestingly, this decline was consistent across participants, indicating that the trajectory of network shrinkage was a shared experience within this cohort.</p>
<p>Results also highlighted the impact of specific life transitions on emotional support networks. Participants’ networks were smaller during periods when they were married, suggesting a consolidation of emotional reliance on their spouse. However, retirement did not appear to influence the number of emotional support providers.</p>
<p>The study also revealed that early-life experiences played a critical role in shaping network size. Participants who grew up in warmer family environments—characterized by supportive and nurturing relationships with parents—had larger emotional support networks in adulthood. In contrast, childhood SES, as measured by parental income and education, did not predict later-life network size.</p>
<p>These results emphasize the enduring influence of early family dynamics on socioemotional development, even as other life transitions occur throughout adulthood.</p>
<p>This research was limited by its all-male, predominantly White sample and its reliance on self-reported data. Additionally, the quality of emotional support and its impacts on well-being were not assessed.</p>
<p>The study, “<a href="https://doi.org/10.1037/pag0000843">Emotional support across adulthood: A 60-year study of men’s social networks</a>,” was authored by Kate Petrova, Michael D. Nevarez, Robert J. Waldinger, and Marc S. Schulz.</p></p>
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<td><a href="https://www.psypost.org/does-stress-make-people-more-susceptible-to-conspiracy-theories/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Does stress make people more susceptible to conspiracy theories?</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 23rd 2025, 14:00</div>
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<p><p>Researchers have long debated why people believe in conspiracy theories—alternative explanations for events that often challenge the mainstream narrative. These beliefs can shape public opinion on issues ranging from politics to public health, such as vaccine hesitancy and pandemic precautions. A recent study published in <em><a href="https://www.cambridge.org/core/journals/politics-and-the-life-sciences/article/effect-of-acute-stress-response-on-conspiracy-theory-beliefs/3D2B681E4E76989443B89B83ED63A153" target="_blank" rel="noopener">Politics and the Life Sciences</a></em> sought to explore whether stress—a common psychological and physiological response—could heighten an individual’s tendency to believe in conspiracy theories. The study found that while the stress procedure caused significant increases in cortisol levels (a hormone linked to stress), it did not make participants more likely to endorse conspiracy theories or interpret new information in conspiratorial terms.</p>
<p>The idea that stress might influence conspiracy thinking stems from earlier research suggesting that conspiracy beliefs often arise during crises or periods of uncertainty. Stressful situations might encourage people to search for meaning or feel a sense of control, which conspiracy theories could seem to provide. Moreover, psychological studies have linked perceived stress levels to a greater likelihood of endorsing conspiracy theories.</p>
<p>However, the exact mechanisms behind this relationship remain unclear. Could the biological effects of stress, such as the release of cortisol, play a role? The researchers behind this study aimed to address this question by isolating the physiological aspects of stress and testing their effects on conspiracy beliefs in a controlled experimental setting.</p>
<p>“Biological stress primes the body for action and can be measured physiologically, while subjective stress reflects our internal sense of unease,” said study author Vojtěch Pišl of the Department of Psychiatry at Charles University.</p>
<p>“Previous studies show that individuals who report feeling stressed are more likely to endorse conspiracy theories. This could stem from biological stress, which accelerates cognitive processing but increases the number of cognitive errors, or from social factors, where dissatisfaction with society leads people to report stress and endorse conspiracy theories as a form of protest. Our experiment aimed to confirmed the role of the biological effects. At the same time, we wanted to show that conspiracy research may benefit from physiological measurements.</p>
<p>To investigate the relationship between stress and conspiracy thinking, researchers used the Maastricht Acute Stress Test (MAST), a standardized procedure designed to induce acute stress. The study involved 143 medical students aged 20 to 25. Participants were randomly assigned to either an experimental group, which underwent the stress-inducing version of the MAST, or a control group, which experienced a non-stressful variant of the procedure.</p>
<p>The experimental stress procedure included both physical and social stressors. For example, participants submerged their hands in ice-cold water and were required to solve challenging arithmetic tasks under time pressure while receiving critical feedback. In contrast, the control group performed similar tasks but in less stressful conditions, such as using lukewarm water and receiving polite encouragement instead of criticism.</p>
<p>To measure the participants’ stress response, researchers collected salivary samples at multiple points during the study to assess cortisol levels. These samples were taken before, during, and after the MAST procedure. The participants also completed two types of surveys: one gauging their agreement with existing conspiracy theories (e.g., theories related to geopolitical events) and another measuring their likelihood of adopting conspiratorial interpretations of fictional scenarios.</p>
<p>To ensure accuracy, participants were required to follow specific guidelines before the study, such as avoiding caffeine and alcohol, refraining from smoking, and maintaining a consistent eating schedule. Additionally, the study excluded participants who did not exhibit sufficient cortisol responses to the stress procedure or whose survey responses showed inconsistencies.</p>
<p>The results confirmed that the stress procedure effectively increased cortisol levels in the experimental group, validating the biological impact of the stress induction. However, when comparing the two groups, researchers found no significant differences in their responses to either the survey of existing conspiracy theories or the fictional scenarios. In other words, the acute stress experienced by participants did not increase their likelihood of endorsing conspiracy theories or interpreting novel information in a conspiratorial way.</p>
<p>Exploratory analyses suggested that any potential effects of stress on conspiracy thinking were small or absent. The findings imply that while stress might influence cognition in other ways, it does not appear to play a significant role in shaping conspiracy beliefs—at least not in the short term or under controlled experimental conditions.</p>
<p>“Conspiracy theories might be more deeply tied to social processes and social identity than we often realize,” Pišl told PsyPost. “Moreover, many negative effects of stress could be more closely linked to our subjective interpretation of reality—such as thinking ‘everything is wrong, I feel terrible’—rather than the objective events themselves. Our experiment is just one small piece of the puzzle, but it aligns with a broader body of research showing that our perception that the world is a good place and that we are strong and resilient may be often more relevant that what is actually happening.”</p>
<p>While the study offers valuable insights, it is not without limitations. One key limitation is the sample itself. The participants were medical students—a group likely to possess higher-than-average analytical thinking skills and greater exposure to scientific reasoning. These characteristics might make them less susceptible to conspiracy thinking than the general population, potentially limiting the generalizability of the findings.</p>
<p>Additionally, the study focused on acute stress, measuring its effects within a narrow time frame (roughly 30 minutes after stress induction). Stress responses can vary over time, and it is possible that the effects on conspiracy thinking might emerge in different phases of the stress response, such as in the immediate aftermath or during prolonged stress. Future research could explore how stress affects conspiracy beliefs over longer periods or in real-world contexts.</p>
<p>“Our results were negative; we did not confirm a link between biological stress and the endorsement of conspiracy theories,” Pišl said. “However, this doesn’t imply that the link is nonexistent. Instead, it suggests that the connection is likely weaker than the link between subjectively perceived stress and conspiracy beliefs.”</p>
<p>Understanding the factors that drive conspiracy beliefs remains an important area of inquiry, especially in today’s polarized and misinformation-rich world.</p>
<p>“We plan to continue with EEG studies to explore the brain processes that may underlie the decision to endorse conspiracy theories,” Pišl said. “The study was supported by the American Association for Politics and Life Sciences, along with several Czech and European institutions. I am deeply grateful for this support, which provided not only the necessary funding but also the motivation to pursue these endeavors.”</p>
<p>The study, “<a href="https://doi.org/10.1017/pls.2024.16" target="_blank" rel="noopener">The effect of acute stress response on conspiracy theory beliefs</a>,” was authored by Vojtech Pisl, Turkay Nefes, Benjamin Simsa, Daniela Kestlerova, Pavel Kubíček, Vojtech Linka, Tatana Martynova, Rachel Sajdlova, David Sejrek, and Jan Vevera.</p></p>
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<td><a href="https://www.psypost.org/breakthrough-study-shows-how-ketamine-may-ease-dyskinesia-in-parkinsons-patients/" 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;">Breakthrough study shows how ketamine may ease dyskinesia in Parkinson’s patients</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 23rd 2025, 12:00</div>
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<p><p>A recent study published in the journal <a href="https://doi.org/10.1093/brain/awae386"><em>Brain</em></a> has revealed new insights into the neurological underpinnings of levodopa-induced dyskinesia, a common and debilitating complication of Parkinson’s disease treatment. The research explored how this condition affects the brain’s motor cortex and evaluated ketamine, an anesthetic, for its potential to alleviate symptoms.</p>
<p>By examining over 3,000 neurons in the motor cortex of rats exhibiting symptoms of dyskinesia, the study uncovered that the motor cortex becomes disconnected from movement control during dyskinesia, contrary to prior assumptions. Ketamine not only reduced dyskinesia but also partially restored the brain’s capacity to regulate movement.</p>
<p>Levodopa remains the most effective treatment for restoring motor function, but its prolonged use often leads to dyskinesia, characterized by involuntary and excessive movements. Current treatments for this condition are limited and primarily focus on symptom management rather than addressing the underlying neural mechanisms. The team sought to understand the specific changes in brain activity associated with dyskinesia and to investigate whether ketamine could offer a novel therapeutic approach.</p>
<p>“I am drawn to the question of how neurons organize and coordinate their activity with one another during learning, memory, and disease. I am also quite interested in how dopamine regulates neural activity and learning,” said study author <a href="https://psychology.arizona.edu/person/stephen-cowen">Stephen Cowen</a>, an associate professor of psychology at the University of Arizona.</p>
<p>“Consequently, I became interested in Parkinson’s disease as it is a disorder that profoundly affects both neuronal coordination and dopamine release. I became interested in ketamine the moment a student showed me their data that demonstrated the overpowering effects of low-dose ketamine on neuronal synchrony.”</p>
<p>To achieve their goals, the researchers used an established rat model of dyskinesia. They induced a Parkinsonian state in the animals by selectively damaging dopamine-producing neurons in the brain, mimicking the neurodegeneration seen in Parkinson’s disease. The rats were then treated with levodopa to provoke dyskinesia, as seen in human patients. The severity of dyskinesia was assessed using a standardized rating scale.</p>
<p>Following the induction of dyskinesia, the team recorded neural activity in the motor cortex using advanced electrode arrays capable of capturing signals from thousands of individual neurons. They specifically examined oscillatory brain activity and its relationship to movement, both before and after administering ketamine.</p>
<p>The researchers found that during dyskinesia, the motor cortex—the brain region responsible for planning and executing movement—becomes functionally disconnected from the body’s movements. This disconnection challenges the conventional belief that dyskinetic movements are directly triggered by motor cortex activity. Instead, the findings suggest that dyskinesia arises from downstream circuits in the brainstem or spinal cord, which generate pathological, involuntary movements in the absence of normal motor cortex regulation.</p>
<p>“Neurons in the motor cortex can activate or suppress movement, and it is commonly thought that unwanted movements during levodopa-induced dyskinesia result from motor cortex neurons triggering unwanted actions,” Cowen told <em>PsyPost</em>. “Contrary to this idea, results from our study, using a rat model of dyskinesia, suggest that during dyskinesia, motor cortex fails to control movement, freeing downstream motor systems to generate spontaneous abnormal involuntary movements.”</p>
<p>One of the study’s key findings was the identification of abnormal oscillatory activity in the motor cortex during levodopa-induced dyskinesia. Specifically, the researchers observed excessive neural activity in the gamma frequency range (around 80 Hz), known as finely tuned gamma oscillations.</p>
<p>These oscillations were unrelated to the animals’ physical movements, indicating a breakdown in the usual relationship between motor cortex activity and bodily actions. This abnormal activity creates a state where the motor cortex fails to control or constrain movement, potentially allowing downstream neural circuits to produce the involuntary and exaggerated movements characteristic of dyskinesia.</p>
<p>“I always assumed that the activities of motor cortex neurons would be correlated to movement in both health and disease,” Cowen said. “Observing that motor cortex was so profoundly disconnected from movement during levodopa-induced dyskinesia was a big surprise.”</p>
<p>Ketamine emerged as a promising intervention in this study. When administered to rats with dyskinesia, ketamine eliminated the pathological gamma oscillations in the motor cortex. This was accompanied by a reduction in dyskinetic movements. Additionally, ketamine partially restored the functional link between motor cortex activity and movement. While not returning entirely to normal levels, the motor cortex regained some of its ability to modulate movement-related neuronal activity. This partial restoration may be sufficient to alleviate symptoms without disrupting the therapeutic effects of levodopa on motor function.</p>
<p>Another intriguing finding was how ketamine restructured the patterns of interaction among neurons in the motor cortex. Normally, dyskinesia disrupts the network-level dynamics of the motor cortex, but ketamine induced a reorganization of these neuronal interactions. This reorganization was not uniform; rather, ketamine increased the variability in how neurons communicated, suggesting that the drug reshaped the motor cortex’s overall state. This unique neural ensemble state, induced by ketamine, may underlie its ability to reduce dyskinesia while preserving movement control.</p>
<p>“I was also surprised by how strongly ketamine altered neuron-to-neuron interactions, resulting in a novel brain state in the dyskinetic rats,” Cowen said.</p>
<p>Interestingly, the study also found that ketamine’s effects on motor cortex activity were distinct from its general impact on movement. For instance, while levodopa increased movement speed and dyskinetic behaviors, ketamine reduced dyskinesia without altering overall movement velocity. This observation indicates that ketamine’s therapeutic effects are rooted in its capacity to normalize brain activity rather than simply suppressing movement.</p>
<p>However, the study’s reliance on head-mounted inertial sensors to measure movement is a limitation. These sensors primarily captured head movements, which may not fully represent the range and complexity of dyskinetic behaviors observed in humans. “This study only looked at head movements,” Cowen noted. “It is therefore conceivable that there were other movements that were correlated with motor cortex activity that we were unable to capture.”</p>
<p>Looking forward, Cowen said he would “like to identify the specific types of neurons responsible for decoupling motor cortex from ongoing movement. I also wish to understand how low-dose ketamine disrupts interactions between neurons.”</p>
<p>The study, “<a href="https://doi.org/10.1093/brain/awae386">Decoupling of motor cortex to movement in Parkinson’s dyskinesia rescued by sub-anaesthetic ketamine</a>,” was authored by Abhilasha Vishwanath, Mitchell J. Bartlett, Torsten Falk, and Stephen L. Cowen.</p></p>
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<td><a href="https://www.psypost.org/strange-link-discovered-between-inflammation-and-orgasm-frequency/" 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;">Strange link discovered between inflammation and orgasm frequency</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 23rd 2025, 10:00</div>
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<p><p>A new study found that in individuals highly motivated to enhance connection with their partner (high approach motivation), higher levels of inflammation were associated with greater sexual satisfaction and a higher frequency of orgasms. The paper was published in <a href="https://doi.org/10.1016/j.bbi.2024.08.054"><em>Brain Behavior and Immunity</em></a>.</p>
<p>Sex is very important for most people and plays many roles in both individual lives and social relationships. People have sex to experience pleasure, reduce stress, promote relationships, create offspring, and for many other reasons. On the other hand, one’s ability to have and enjoy sex is influenced by various aspects of their physical condition, including inflammation.</p>
<p>Inflammation is the body’s natural immune response to injury, infection, or stress. It develops when the body releases immune cells and signaling molecules into the bloodstream, lymphatic system, and tissue, allowing them to travel to the site of injury or infection or create a systemic immune response. Previous studies have indicated that when under inflammation, a person often starts manifesting “sickness behavior,” characterized by social withdrawal.</p>
<p>However, more recent findings suggest that this social withdrawal might be directed only at people an individual under inflammation is not close to. It appears that heightened inflammation might increase an individual’s motivation to be with close others and affiliate with them.</p>
<p>Study author Tatum A. Jolink hypothesized that higher levels of systemic inflammation might be associated with better sexual well-being in a romantic relationship. Noting that a previous study indicated that heightened inflammation might motivate individuals to seek the company of people they love and trust, the authors hypothesized that this could extend to sexual intimacy between partners as well.</p>
<p>The study included 158 individuals between 18 and 55 years of age, 84% of whom were women. To participate, individuals were required to have been in a committed, exclusive romantic relationship for at least six months prior to the study. Participants were recruited from the community around Chapel Hill, North Carolina, United States.</p>
<p>Participants completed three lab visits, one every two weeks over the course of a month. During each visit, they provided blood samples, which the researchers used to measure C-reactive protein (CRP) levels. CRP is a protein produced by the liver in response to inflammation and is commonly used as a biomarker to assess the presence and severity of inflammatory conditions or infections in the body.</p>
<p>Additionally, participants completed a survey during each lab visit. Before coming to the lab, they also completed an online survey assessing their relational approach/avoidance motivation toward their romantic partner (how motivated they were to enhance connection with their partner versus avoid them) and their sexual satisfaction. Participants also reported how often they had sex with another person and how often they experienced orgasms in the past month.</p>
<p>The results showed that inflammation (i.e., CRP levels) was not associated with any indicator of sexual well-being (sexual satisfaction, orgasms, or frequency of sex) when all participants were considered. However, when the researchers focused on individuals with high relational approach motivation—those motivated to enhance connection with their partner—the results indicated that those with higher inflammation levels tended to report greater sexual satisfaction and more orgasms in the past month.</p>
<p>“Inflammation alone may not drive people toward – or away from – having satisfying, orgasm-filled sex. Instead, individuals highly motivated to reap the rewards of having a romantic partner may have more rewarding sexual experiences with that partner as they experience higher levels of inflammation,” the study authors concluded.</p>
<p>The study contributes to the scientific understanding of how inflammation impacts behavior. However, it should be noted that the study design does not allow causal conclusions to be drawn from the results. Additionally, all the participants were in committed romantic relationships, and the findings might differ for individuals who are single or in less satisfying relationships.</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.bbi.2024.08.054">Do inflammation and relational motivation coordinate having better sex? The interplay between C-reactive protein and relational approach motivation on sexual well-being,</a>” was authored by Tatum A. Jolink, Baldwin M. Way, Ayana Younge, and Sara B. Algoe.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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