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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/single-gene-mutation-linked-to-increased-alcohol-tolerance-and-consumption/" 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;">Single gene mutation linked to increased alcohol tolerance and consumption</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 28th 2025, 08:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1523/JNEUROSCI.0304-25.2025" target="_blank">The Journal of Neuroscience</a></em> suggests that a specific genetic variant alters how organisms respond to alcohol. The research identifies the chrna3 gene as a primary regulator of alcohol sensitivity and indicates that defects in this gene can lead to increased tolerance.</p>
<p>Alcohol use disorders represent a significant global health burden, yet understanding the biological mechanisms behind them remains a challenge. Genetic studies in humans have frequently associated a cluster of genes known as CHRNA5-A3-B4 with nicotine and alcohol dependence. This cluster encodes subunits for nicotinic acetylcholine receptors, which are proteins involved in signaling within the nervous system. </p>
<p>While statistical associations exist, pinning down the specific contribution of the CHRNA3 gene has been difficult. Mammalian models lacking this gene typically do not survive past the neonatal stage, which prevents scientists from observing adult behaviors related to substance use. </p>
<p>The research team aimed to bypass this obstacle by using zebrafish, a model organism that shares substantial genetic similarity with humans and can survive with the mutation. They sought to determine if disabling the chrna3 gene would directly change voluntary alcohol consumption and physiological reactions to the substance.</p>
<p>To investigate this, the researchers employed CRISPR-Cas9 gene-editing technology to create a line of zebrafish with a mutation in the chrna3 gene. This mutation introduced a premature stop signal in the genetic code, resulting in a truncated and non-functional protein. </p>
<p>The team then compared the behavior of these mutant fish against wild-type fish with fully functional genes. They utilized approximately five-week-old juvenile zebrafish for the behavioral experiments. At this stage of development, the fish exhibit complex locomotor behaviors comparable to adults but allow for higher throughput testing.</p>
<p>The primary method for assessing behavior was a refined setup called the Self-Administration Zebrafish Assay. This apparatus featured a tank divided into distinct zones. A closed-loop tracking system monitored the movement of the fish. </p>
<p>When a fish entered a designated stimulus zone, the system automatically dispensed a solution containing alcohol. If the fish entered a control zone, the system dispensed water. This design allowed the animals to make active choices about their alcohol intake and regulate their exposure levels dynamically.</p>
<p>The study first established a baseline for normal behavior using wild-type fish. These animals exhibited a biphasic response to alcohol. At lower concentrations, roughly equivalent to 0.5 percent, the fish showed an initial attraction and spent more time in the alcohol-dispensing zone.</p>
<p>However, as the concentration increased or exposure time lengthened, their behavior shifted. When the effective concentration reached approximately 0.7 percent, the wild-type fish began to avoid the stimulus zone. This suggests that for typical organisms, alcohol acts as a reward at low doses but becomes aversive at higher doses.</p>
<p>The behavior of the chrna3 mutant fish presented a distinct contrast. Like the wild-type group, the mutants showed an initial attraction to the lower concentrations of alcohol. However, they did not exhibit the subsequent switch to avoidance. </p>
<p>Even as the concentration increased to levels that repelled the wild-type fish, the mutants continued to self-administer the substance. The typical aversion mechanism appeared to be blunted or absent. This resulted in the mutant fish exposing themselves to significantly higher volumes of alcohol over the course of the experiment.</p>
<p>To understand the physiological reasons for this difference, the researchers conducted a separate shoaling cohesion assay. This test measures anxiety and sedation by observing how groups of fish swim together. </p>
<p>Under normal conditions, zebrafish swim in tight groups or shoals when they feel anxious. Alcohol typically acts as an anxiolytic, which reduces anxiety and causes the shoal to loosen. At higher doses, alcohol acts as a sedative, causing the fish to swim more slowly.</p>
<p>In the wild-type groups, exposure to 0.5 percent alcohol caused the shoals to spread out, indicating reduced anxiety. Exposure to 1 percent alcohol resulted in reduced swimming speed, indicating sedation. </p>
<p>The chrna3 mutants reacted differently. They maintained tighter shoaling formations even when exposed to alcohol, suggesting they did not experience the same level of anxiety reduction. Additionally, they resisted the sedative effects of the higher dose. The mutants continued to swim actively at concentrations that significantly slowed down the wild-type fish.</p>
<p>These behavioral findings suggest that the functional chrna3 gene acts as a regulatory brake. It appears to mediate the aversive and sedative effects of alcohol that typically limit consumption. Without this genetic brake, the negative feedback loops that discourage high alcohol intake are weakened. The mutants effectively displayed a higher tolerance for the substance, requiring larger doses to elicit behavioral changes that appeared rapidly in normal fish.</p>
<p>The researchers also analyzed the gene expression profiles of adult brains to identify molecular changes. They sequenced the RNA from whole brains of both wild-type and mutant fish. The analysis revealed that the loss of chrna3 function triggered widespread compensatory changes. Approximately 1,600 genes showed significant alterations in their expression levels.</p>
<p>Among the most notable changes were alterations in genes responsible for other neurotransmitter systems. The expression of receptors for glutamate, the main excitatory neurotransmitter, and GABA, the main inhibitory neurotransmitter, was modified. </p>
<p>This indicates that the brain attempted to rebalance its signaling networks in the absence of normal cholinergic activity. Additionally, the study found downregulation of other genes in the same cluster, specifically chrna5 and chrnb4. This suggests that the function of these receptor subunits is tightly coordinated and that a defect in one can disrupt the entire system.</p>
<p>The study has certain limitations that frame the interpretation of the results. The mutation was present in all cells of the zebrafish, which prevents the researchers from pinpointing the exact brain region responsible for the behavior. </p>
<p>While the study implicates the whole brain, specific circuits likely drive the attraction and aversion responses. The researchers utilized juvenile and adult fish for different parts of the study, and while their brains are similar, developmental differences could play a role.</p>
<p>Future research aims to address these specific neural mechanisms. The team plans to investigate whether similar variants in the human CHRNA3 gene correlate with altered alcohol sensitivity in people. </p>
<p>They also intend to study the interactions between the different genes in the cluster to understand how they collectively influence addiction risk. Developing models with mutations in multiple genes will help disentangle the complex genetic architecture of substance use disorders.</p>
<p>The study, “<a href="https://doi.org/10.1523/JNEUROSCI.0304-25.2025" target="_blank">chrna3 modulates alcohol response</a>,” was authored by Joshua Raine, Caroline Kibat, Tirtha Das Banerjee, Antónia Monteiro, and Ajay S. Mathuru.</p></p>
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<td><a href="https://www.psypost.org/new-research-links-dark-triad-traits-to-the-quiet-quitting-phenomenon/" 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 research links “dark triad” traits to the quiet quitting phenomenon</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 28th 2025, 06:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.actpsy.2025.105860" target="_blank">Acta Psychologica</a></em> has found that specific personality traits may predispose senior managers to “quiet quitting.” The findings suggest that individuals with higher levels of narcissism and psychopathy are more likely to withdraw their effort at work, largely because they feel entitled to special treatment or can easily rationalize disengaging from their duties. </p>
<p>“Quiet quitting” became a popular term in recent years to describe employees who fulfill only the basic requirements of their job descriptions. While much of the public discussion has focused on external factors like poor pay or burnout, less attention has been paid to the internal personality characteristics that might drive this behavior. The authors of the new study sought to understand if the “Dark Triad” of personality traits could explain why some managers choose to psychologically detach from their work.</p>
<p>The Dark Triad consists of three distinct but related traits: narcissism, Machiavellianism, and psychopathy. Narcissism involves an inflated sense of self-importance and a need for admiration. Machiavellianism is characterized by manipulation and a focus on self-interest. Psychopathy involves a lack of empathy and a tendency toward impulsive or antisocial behavior. Previous research has linked these traits to counterproductive work behaviors, such as aggression or theft.</p>
<p>“Our study was motivated by the growing global concern surrounding quiet quitting that poses a major challenge for organizations. Not much is known about the psychological or personality-based factors that drive this behavior,” explained study author Hanfia Rahman, a senior research fellow at the Motilal Nehru National Institute of Technology Allahabad.</p>
<p>“Additionally, managers and HR leaders increasingly report difficulty identifying and addressing quiet quitting because it is subtle, hard to detect, and poorly understood. Despite this growing concern, organizations lack evidence-based guidance on which employees are most prone to quiet quitting and why.” </p>
<p>“This created a practical gap: companies had no psychological framework to anticipate or mitigate this behavior,” Rahman said. “At the same time, a theoretical gap existed because no prior research had examined whether Dark Triad personality traits predict quiet quitting. The mechanisms through which these traits influence quiet quitting was also underexplored.” </p>
<p>“Existing studies focused mainly on situational or environmental factors, overlooking personality-driven pathways. Additionally, most research came from WEIRD countries, limiting its relevance to diverse workforces. Addressing these practical and theoretical gaps, the study sought to build a clearer understanding of who is likely to quietly disengage and the psychological processes behind it, offering insights useful for managers.”</p>
<p>To test their hypotheses, the researchers recruited 402 senior-level managers from various industries in India. The sample included professionals from information technology, banking, healthcare, and manufacturing. The average age of the participants was approximately 37 years. Data collection involved a mix of face-to-face visits and online questionnaires to ensure a robust sample of high-ranking professionals.</p>
<p>Participants completed a series of standardized surveys. The Dark Triad traits were measured using a twelve-item scale that assessed tendencies toward manipulation, callousness, and attention-seeking. Psychological entitlement was measured by asking participants to rate their agreement with statements about deserving better treatment than their peers. </p>
<p>Moral disengagement was assessed through questions regarding the justification of unethical actions. Finally, the researchers measured the intention to quiet quit using a scale that evaluated enthusiasm and the willingness to go above and beyond at work.</p>
<p>The data analysis revealed that narcissism and psychopathy were significant predictors of quiet quitting intention. However, this influence was primarily indirect. Managers with high levels of narcissism or psychopathy reported much higher levels of psychological entitlement. They believed they were owed more by their organizations. When these expectations were not met, their sense of entitlement appeared to drive them toward withholding their effort.</p>
<p>Similarly, narcissism and psychopathy were strong predictors of moral disengagement. Individuals with these traits were more likely to rationalize negative behaviors. This lack of moral self-regulation allowed them to view the withdrawal of effort as acceptable or justified. The study found that this moral disengagement was a powerful precursor to the intention to quiet quit.</p>
<p>The results for Machiavellianism were distinct from the other two traits. When analyzed in isolation, Machiavellianism showed a connection to quiet quitting. However, when the researchers included all three traits in their complex statistical model, the unique influence of Machiavellianism disappeared. </p>
<p>“One result was particularly surprising,” Rahman told PsyPost. “Although Machiavellianism showed strong simple correlations with entitlement, moral disengagement, and quiet-quitting intention, these relationships were non-significant once all three Dark Triad traits were examined together in the model. This was unexpected because Machiavellianism is typically associated with manipulation and counterproductive behaviors, so we expected that it would predict quiet quitting intention.” </p>
<p>“It may be because people exhibiting Machiavellians tendencies often choose their behaviors carefully depending on what benefits them most. As quiet quitting involves withdrawing effort without gaining an advantage, it may not align with their strategic interests. Instead of disengaging quietly, Machiavellian employees may stay involved just enough to maintain influence, manage impressions, or position themselves favorably. This finding challenged the assumption that all Dark Triad traits operate similarly and highlighted the importance of examining their distinct effects.”</p>
<p>The researchers found that the combination of these personality traits and psychological mechanisms explained a substantial amount of the variance in quiet quitting intentions. The full model accounted for approximately 65 percent of the reasons why the managers in the study intended to quietly quit. This high level of predictive power indicates that personality and mindset are major factors in workplace engagement, arguably as significant as external working conditions.</p>
<p>“Quiet quitting doesn’t happen randomly: certain personality traits make employees more likely to disengage at work,” Rahman explained. “Our findings show that individuals who are more narcissistic or psychopathic tend to feel overly deserving and often justify putting in less effort, which increases their chances of quietly quitting.” </p>
<p>“The study also highlights that quiet quitting is often the result of internal psychological processes, not just workplace conditions. Feeling entitled or morally disconnected from one’s work makes it easier for someone to withdraw without guilt. The results remind us that quiet quitting is not always due to workload or culture. Sometimes, it stems from personality and how people view themselves.” </p>
<p>“For managers, this means that paying attention to personality and entitlement cues can help identify early signs of quiet quitting. For employees, it is a reminder to reflect on how personal beliefs and attitudes shape workplace behavior. Overall, the study shows that understanding ourselves, and not just our jobs, matters in how committed we feel at work.”</p>
<p>There are some limitations to this research that should be considered. The study utilized a cross-sectional design, which captures data at a single point in time. This approach prevents the researchers from proving a causal relationship. </p>
<p>It is possible that disengaging from work leads to feelings of entitlement rather than the other way around. Future research could employ longitudinal designs to track these behaviors over time to establish a clear cause-and-effect relationship.</p>
<p>The cultural context of the study is also significant. The research focused exclusively on senior managers in India. While this provides important data from a non-Western population, the results might differ in other cultural settings. </p>
<p>Cultural norms regarding hierarchy, duty, and work ethic could influence how personality traits manifest in the workplace. Future investigations should attempt to replicate these findings in different countries to see if the patterns hold true globally.</p>
<p>“A key point readers should not misunderstand is that having Dark Triad traits does not automatically mean a person will engage in quiet quitting,” Rahman noted. “Our study shows associations and psychological pathways, not inevitabilities. Personality traits increase the likelihood of psychological entitlement, moral disengagement, and quiet quitting intention, but work environments, and other factors such as leadership still play major roles.”</p>
<p>“Quiet quitting is a multifaceted behaviour, and it should not be assumed that anyone with narcissistic or psychopathic tendencies will disengage, nor that those without these traits are fully protected from doing so. The findings should be seen as identifying risk factors and not deterministic labels.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.actpsy.2025.105860" target="_blank">The dark silence: Dark triad personality traits as predictors of quiet quitting intention</a>,” was authored by Hanfia Rahman, Tripti Singh, and Mitu Mandal.</p></p>
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<td><a href="https://www.psypost.org/a-common-amino-acid-reduces-brain-plaques-in-animal-models-of-alzheimers-disease/" 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;">A common amino acid reduces brain plaques in animal models of Alzheimer’s disease</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 22:00</div>
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<p><p>A new study suggests that arginine, a common amino acid, may help reduce the brain plaques associated with Alzheimer’s disease. The researchers found that consuming this compound reduced the accumulation of toxic proteins and improved symptoms in both fruit flies and mice. These findings were published in <em><a href="https://doi.org/10.1016/j.neuint.2025.106082" target="_blank">Neurochemistry International</a></em>.</p>
<p>Alzheimer’s disease is a progressive condition characterized by the decline of memory and cognitive function. One of the primary biological markers of the illness is the buildup of amyloid beta. This protein fragment clumps together in the brain to form sticky plaques. These aggregates are thought to disrupt communication between nerve cells and trigger inflammation. Eventually, this process leads to the death of brain cells and the symptoms of dementia.</p>
<p>Medical researchers have spent decades looking for ways to stop or reverse this accumulation. Recent years have seen the approval of antibody-based therapies that target amyloid beta. </p>
<p>While these drugs represent significant progress, they come with substantial challenges. They are often expensive and require administration through intravenous lines. They also carry the risk of serious side effects, such as swelling or bleeding in the brain. There is a persistent need for treatments that are safer, more affordable, and easier to administer.</p>
<p>A team of researchers from Kindai University in Japan investigated a different approach. The group included Kanako Fujii, Toshihide Takeuchi, and Yoshitaka Nagai. They focused their attention on arginine. This is a naturally occurring amino acid that the body uses for various functions, including building proteins. </p>
<p>Arginine acts as a chemical chaperone. This means it helps other proteins fold into their correct shapes and prevents them from sticking together inappropriately. The team hypothesized that this property might stop amyloid beta from clumping into harmful plaques.</p>
<p>The investigation began with experiments in a controlled laboratory setting. The researchers mixed amyloid beta peptides with varying concentrations of arginine in test tubes. They used a special dye called Thioflavin T to measure the formation of clumps. This dye glows when it binds to amyloid fibrils. </p>
<p>The results showed that arginine prevented the protein from aggregating. The effect was stronger when higher concentrations of the amino acid were used. The scientists also used electron microscopes to look at the structures directly. They observed that the amyloid fibrils were shorter and less developed in the presence of arginine.</p>
<p>“Our study demonstrates that arginine can suppress Aβ aggregation both in vitro and in vivo,” explains Nagai. “What makes this finding exciting is that arginine is already known to be clinically safe and inexpensive, making it a highly promising candidate for repositioning as a therapeutic option for AD.”</p>
<p>Following the test tube experiments, the team tested their hypothesis on living organisms. They utilized fruit flies that had been genetically modified to produce a specific, highly toxic form of amyloid beta. This genetic variation is known as the Arctic mutation. In these flies, the toxic protein accumulates in the eyes. This causes visible tissue damage and shrinkage. The researchers fed some of these flies a diet supplemented with arginine.</p>
<p>The flies that consumed arginine showed significantly less damage to their eyes. The treatment appeared to protect the tissue from the toxicity of the amyloid protein. The researchers analyzed the tissues and found that the actual amount of accumulated protein had decreased. This suggested that the amino acid was working inside the living body just as it had in the test tube.</p>
<p>The team then moved on to a more complex animal model. They used mice that had been genetically engineered to carry human genes associated with familial Alzheimer’s disease. These mice, known as the AppNL-G-F model, are bred to develop amyloid plaques as they age. They also exhibit behavioral changes similar to the cognitive decline seen in humans. The researchers provided these mice with drinking water containing arginine.</p>
<p>The treatment began when the mice were five weeks old. The researchers monitored the animals over several months. They examined the brains of the mice at six months and nine months of age. The team found that the mice treated with arginine had significantly fewer amyloid plaques in the cortex and hippocampus. These are regions of the brain vital for memory and learning.</p>
<p>The scientists used a specialized staining technique to identify the dense cores of the plaques. This analysis confirmed that the treatment had suppressed the formation of these hardened protein deposits. The total surface area of the brain covered by plaques was reduced in the treated group. </p>
<p>The researchers also measured the levels of insoluble amyloid beta. This is the form of the protein that is hardest for the brain to clear. The treated mice had lower levels of this stubborn material compared to the untreated group.</p>
<p>Beyond looking at brain tissue, the researchers assessed the behavior of the animals. They utilized a standard assessment called the Y-maze test. This test measures a mouse’s willingness to explore new environments. It is a common way to gauge short-term memory and spatial learning in rodents. Mice with cognitive deficits tend to be less active and less likely to alternate between the different arms of the maze.</p>
<p>The untreated mice showed signs of reduced activity and exploration as they aged. In contrast, the mice that drank the arginine solution performed better. Their movement and exploration patterns were closer to those of healthy, wild-type mice. This suggested that the reduction in plaques was translating into preserved brain function.</p>
<p>The study also looked at inflammation in the brain. The accumulation of plaques typically triggers an immune response. This leads to the release of inflammatory signaling molecules called cytokines. Chronic inflammation is believed to worsen the damage caused by Alzheimer’s. </p>
<p>The researchers measured the genetic expression of several inflammatory markers. They found that the levels of these markers were lower in the mice treated with arginine. This indicated that the treatment had dampened the harmful immune response in the brain.</p>
<p>“Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation,” notes Nagai. “Given its excellent safety profile and low cost, arginine could be rapidly translated to clinical trials for Alzheimer’s and potentially other related disorders.”</p>
<p>There are important caveats to consider regarding this research. The study relied on animal models rather than human subjects. While the mouse models are sophisticated, they do not perfectly mimic the complexity of human Alzheimer’s disease. </p>
<p>For instance, the mice used in this study do not develop neurofibrillary tangles. Tangles are another major hallmark of the human disease involving a protein called tau. The mice also do not experience the extensive death of neurons that occurs in human patients.</p>
<p>The genetic mutations used in the mouse and fly models are specific to rare, familial forms of Alzheimer’s. Most human cases are sporadic and do not involve these specific mutations. It is not yet guaranteed that the treatment would work effectively for the general population. </p>
<p>Additionally, the dosage of arginine used in the experiments was quite high. It was adjusted for the metabolism of the animals. Determining the correct and safe dosage for humans would require specific clinical trials.</p>
<p>The researchers emphasize that people should not self-medicate with high doses of supplements based on these early results. The formulation used in the study was optimized for research. Commercial supplements may vary in quality and concentration. Excessive intake of any supplement can lead to imbalances in the body.</p>
<p>Future research will need to bridge the gap between these animal studies and human application. Clinical trials are necessary to verify safety and efficacy in people. Scientists will need to determine how arginine affects the progression of the disease in its later stages. </p>
<p>They will also need to see if it can help with other neurodegenerative conditions. Despite these remaining questions, the study provides a proof of concept. It suggests that supporting the body’s ability to fold proteins correctly could be a viable strategy for fighting dementia.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.neuint.2025.106082" target="_blank">Oral administration of arginine suppresses Aβ pathology in animal models of Alzheimer’s disease</a>,” was authored by Kanako Fujii, Toshihide Takeuchi, Yuzo Fujino, Noriko Tanaka, Nao Fujino, Akiko Takeda, Eiko N. Minakawa, and Yoshitaka Nagai.</p></p>
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<td><a href="https://www.psypost.org/the-booming-market-for-mushroom-edibles-has-a-hidden-and-potentially-toxic-problem/" 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;">The booming market for mushroom edibles has a hidden and potentially toxic problem</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 20:00</div>
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<p><p>Imagine you purchase a bag of gummies labeled <a href="https://www.webmd.com/vitamins-and-supplements/features/nootropics-smart-drugs-overview">nootropic</a> – a term used to describe substances that claim to enhance <a href="https://doi.org/10.3390/nu14163367">mental ability and function</a>, or “smart drugs.” However, within hours of consuming them, your heart starts racing, you’re nauseated and vomiting. Then you begin convulsing and have a seizure, resulting in a trip to the hospital.</p>
<p>You certainly did not expect to have such a severe reaction to an over-the-counter edible product, which is available online and in herbal and vape shops nationwide. What happened?</p>
<p>So-called “microdosing” of mushrooms has been on the rise over the past few years, accompanying <a href="https://theconversation.com/psilocybin-legislation-is-helping-psychedelic-drugs-make-a-comeback-a-drug-researcher-explains-the-challenges-they-face-233854">a shift in local policy</a> in some areas and <a href="https://doi.org/10.1038/s41598-022-14512-3">increasing research</a> into its potential benefits for mood and mental health. <a href="https://www.health.harvard.edu/blog/the-popularity-of-microdosing-of-psychedelics-what-does-the-science-say-202209192819">Microdosing</a> involves the ingestion of small quantities of psychoactive mushrooms, less than a regular dose and not in sufficient quantities to induce a “trip” or psychedelic experience, but to boost mood, creativity, concentration or productivity.</p>
<p>Psychedelic mushrooms are illegal at the federal level, restricted as a “Schedule 1” substance <a href="https://www.dea.gov/sites/default/files/2020-06/Psilocybin-2020.pdf">by the Food and Drug Administration</a>, though <a href="https://recovered.org/hallucinogens/psilocybin/psilocybin-legal-status">some states and local municipalities</a> have begun the process of decriminalizing the possession of these mushrooms.</p>
<p>This greater acceptance of mushrooms and psychedelics has led to a growing market for edible products containing non-hallucinogenic mushroom species that are appearing on the shelf at grocery stores, vape shops, even gas stations, with claims that these products improve mental function.</p>
<p>To meet demand, manufacturers are also turning to other types of mushrooms – including both psychoactive and non-psychedelic – some of which are potentially more toxic. But key pieces of information are often missing for consumers to make informed decisions about which products to consume.</p>
<p>I am a <a href="https://sites.psu.edu/kellogglab/">natural product scientist</a> at Pennsylvania State University, where my lab specializes in understanding the molecules found in plants, mushrooms and other natural resources and how they can benefit or harm human health. Our team actively researches these small molecules to uncover how they can address infectious and chronic diseases, but also monitors them for toxic or adverse effects on human health.</p>
<p>While nootropic products have potential to boost health, there can be little transparency surrounding many commercial mushroom products, which can have dangerous consequences.</p>
<h2>Chemistry and toxicology of psychoactive mushrooms</h2>
<p>The main psychoactive components of traditional “magic” mushrooms, found in the genus <em>Psilocybe</em>, are <a href="https://en.wikipedia.org/wiki/Psilocybin">psilocybin</a> and <a href="https://en.wikipedia.org/wiki/Psilocin">psilocin</a>. These two small molecules are alkaloids that activate receptors in the brain to trigger the main psychoactive effects of magic mushrooms.</p>
<p>Both psilocybin and psilocin have a high therapeutic index – meaning they are generally nontoxic in humans because the amount that must be ingested to be fatal or dangerous is more than 500 times the dose at which it has been <a href="https://doi.org/10.1111/j.1360-0443.2004.00744.x">shown to be therapeutically effective</a>. Therefore, psilocybin-containing mushrooms are generally considered to have a <a href="https://doi.org/10.1017/S1092852922000888">low potential for acute toxicity</a> in humans, to the point where it is believed to be nearly impossible to achieve a toxic dose from oral consumption.</p>
<h2>Demand breeds diversification in mushroom sourcing</h2>
<p>With the growth in <a href="https://www.npr.org/sections/shots-health-news/2024/06/27/nx-s1-5021788/magic-mushrooms-psilocybin-microdosing-psychedelics-trends">popularity of psychedelic mushrooms</a>, companies have been looking for ways to meet consumer demand. And in some cases, this has meant finding mushrooms that do not contain psilocybin and are therefore not restricted by the FDA. The result has been an increase in products that come without legal entanglements, which means there are products that can contain other types of mushrooms, including lions mane, chaga, reishi, maitake and a genus of mushrooms called <em>Amanita</em>, which can be hallucinogenic.</p>
<p><em>Amanita</em> mushrooms are the quintessential white-flecked, red-capped toadstools – the stereotypical image of a mushroom. These fungi contain very different compounds compared to the <em>Psilocybe</em> mushrooms, such as muscarine and ibotenic acid. These compounds function differently in the brain and, while also capable of producing psychedelic experiences, are generally considered to be more toxic.</p>
<p>Nootropic and other mushroom products are often found as edibles, including chocolates and gummies. However, there is little enforcement surrounding the ingredient labeling of such dietary supplements; products that have a proprietary blend of ingredients generally do not have to report <a href="https://ods.od.nih.gov/About/DSHEA_Wording.aspx">individual ingredients</a> to the species level. This protects trade secrets regarding unique blends of ingredients, but it can also obscure the actual composition of some edible nootropic and microdosing products. And this can have dangerous consequences.</p>
<h2>Increasing adverse effects</h2>
<p>The explosion of nootropic mushroom products has led to a wide variety of products on the market that potentially contain wildly differing levels of mushrooms, many times containing blends of multiple mushroom species. And with little reporting guidelines in effect, it can be hard to know exactly what you’re taking.</p>
<p>One <a href="http://dx.doi.org/10.15585/mmwr.mm7328a3">case study in Virginia</a> involved five people who were hospitalized after they ingested gummies from different nootropic brands that were labeled to contain muscarine, muscimol and ibotenic acid, all compounds found in <em>Amanita</em> mushrooms.</p>
<p>A follow-up analysis of locally available gummy brands that contained “mushroom nootropic” ingredients revealed the presence of psilocybin, but also caffeine, the stimulant ephedrine and mitragynin, a potential painkiller found in <a href="https://theconversation.com/nearly-2-million-americans-are-using-kratom-yearly-but-it-is-banned-in-multiple-states-a-pharmacologist-explains-the-controversy-223061">Southeast Asian plant products like kratom</a>. None of these ingredients were listed on the product label. Therefore, the cocktail of mushrooms and substances that these people were exposed to was not necessarily reflected on the label at the time of purchase.</p>
<p>The increase in use of other, potentially toxic, mushrooms in over-the-counter products has been reflected in reported poisoning cases in the United States. In 2016, out of <a href="https://doi.org/10.1080/15563650.2017.1388087">more than 6,400 mushroom-related poisoning cases</a> in the U.S., only 45 were <em>Amanita</em> mushrooms.</p>
<p>In the past few years since <a href="https://worldpopulationreview.com/state-rankings/mushroom-laws-by-state">certain states</a> began decriminalizing psilocybin, the U.S. has seen an increase in <a href="https://theconversation.com/calls-to-us-poison-centers-spiked-after-magic-mushrooms-were-decriminalized-226709">calls and reports to poison control centers</a> of people feeling nauseous and experiencing vomiting, seizures, cardiovascular symptoms and other adverse effects after ingesting edible mushroom products such as chocolates and gummies. This <a href="https://www.cdc.gov/mmwr/volumes/74/wr/mm7401a3.htm">prompted a multistate investigation</a> beginning in 2023 that uncovered over 180 cases in 34 states of people who had ingested a particular brand of mushroom-based edibles, Diamond Shruumz.</p>
<p>A <a href="https://www.fda.gov/safety/recalls-market-withdrawals-safety-alerts/prophet-premium-blends-recalls-diamond-shruumz-products-because-possible-health-risk">2024 recall</a> required that <a href="https://www.fda.gov/media/182869/download?attachment">stores remove these products</a> from their shelves. And in late 2024, the <a href="https://www.fda.gov/food/hfp-constituent-updates/fda-alerts-industry-and-consumers-about-use-amanita-muscaria-or-its-constituents-food">FDA put out a letter</a> to warn consumers and manufacturers of the dangers associated with <em>Amanita</em> mushrooms, saying they “do not meet the Generally Recognized As Safe, or GRAS, standard and that <em>Amanita</em> mushrooms are unapproved food additives.” Despite this warning, such products are still available from producers.</p>
<p>Even when a product is labeled with the relevant ingredients, mushrooms are notoriously easy to <a href="https://www.ncbi.nlm.nih.gov/books/NBK537111/">misidentify when collected</a>. Numerous mushroom species have similar shapes, colors and habits.</p>
<p>But, despite their visual similarities, these different mushrooms can have drastically different chemistry and toxicity. This even plagues foragers of culinary mushrooms, with hundreds of emergency department visits <a href="http://dx.doi.org/10.15585/mmwr.mm7010a1">due to fungal misidentification</a> every year in the U.S.</p>
<p>There is little current regulation or oversight for species identification in dietary supplements or over-the-counter mushroom edible products, leaving consumers at the mercy of producers to accurately list all raw products and ingredients on the product label.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/252866/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>
<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/the-growing-fad-of-microdosing-mushrooms-is-leading-to-an-uptick-in-poison-control-center-calls-and-emergency-room-visits-252866">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/your-brains-reaction-to-the-unknown-could-predict-how-you-vote/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Your brain’s reaction to the unknown could predict how you vote</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 18:00</div>
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<p><p>Political instability and rapid social changes often create a psychological environment where individuals crave security and predictability. A <a href="https://doi.org/10.1177/01461672251386487" target="_blank">new study</a> suggests that shifting how people perceive this sense of uncertainty can significantly influence their political behavior and social attitudes. Researchers found that when citizens view uncertainty as an opportunity rather than a threat, they exhibit greater openness to diversity and are less likely to vote for right-wing populist parties.</p>
<p>The research was conducted during the lead-up to Germany’s 2025 federal election and was led by a team from ETH Zurich in Switzerland and Goethe University Frankfurt in Germany.</p>
<p>Psychologists have recognized that the human experience of uncertainty can trigger defensive reactions. When the future feels unpredictable, individuals often seek to restore a sense of order and safety. This psychological drive frequently leads people to endorse conservative or authoritarian ideologies that promise stability.</p>
<p>These ideologies often emphasize strict social hierarchies and the preservation of the status quo. In times of crisis, the desire for predictability can make right-wing populist movements more appealing. These movements typically promote a clear distinction between an in-group and an out-group.</p>
<p>Such political groups often frame society in terms of “us versus them” to provide a sense of belonging and clarity. This dynamic tends to undermine social cohesion and can lead to hostility toward minority groups. The researchers sought to understand if there was a way to disrupt this psychological pattern.</p>
<p>The study was authored by Ruri Takizawa, Stefanie Marx-Fleck, Alina Gerlach, and Gudela Grote. They hypothesized that the link between uncertainty and exclusionary politics is not inevitable. They proposed that the problem lies not in the uncertainty itself but in how individuals interpret it.</p>
<p>The team drew upon the concept of uncertainty regulation theory. This theory suggests that people can manage the unknown in different ways. They can either close themselves off to minimize risk or open themselves up to explore new possibilities.</p>
<p>The researchers also utilized the psychological concept of mindsets. A mindset is a set of beliefs that shapes how a person processes information and views the world. The team focused on the “uncertainty-as-enabling” mindset.</p>
<p>This specific mindset characterizes uncertainty as something malleable and filled with opportunity. In contrast, an “uncertainty-as-disabling” mindset views the unknown as fixed and threatening. The researchers wanted to see if cultivating the former could promote positive intergroup relations.</p>
<p>To test this, the team designed an experiment centered around the German federal election scheduled for February 2025. This period was marked by significant political upheaval following the collapse of the country’s governing coalition. Issues regarding immigration and refugee policy were central to the national debate.</p>
<p>The study recruited a panel of seven hundred and forty-five German citizens. The participants were randomly assigned to either an intervention group or a control group. The intervention consisted of a brief online presentation designed to reshape the participants’ views on uncertainty.</p>
<p>The presentation lasted approximately seven and a half minutes. It used text, graphics, and photographs to define uncertainty as a natural part of life. The slides argued that while the unknown can be uncomfortable, it is often manageable and necessary for growth.</p>
<p>The material cited scientific findings on how uncertainty can boost creativity and memory. It also included a narrative about the late technology entrepreneur Steve Jobs. The presentation highlighted how his willingness to embrace an uncertain career path led to his success.</p>
<p>Following the presentation, participants engaged in a reflection exercise. They were asked to write a short note to a friend or family member explaining what they had learned. They also applied this new perspective to a personal situation they were currently experiencing.</p>
<p>Data collection spanned three months, from December 2024 to March 2025. The researchers measured the participants’ mindsets at multiple points after the intervention. They also assessed attitudes toward diversity and eventual voting behavior.</p>
<p>The results indicated that the brief intervention had a lasting impact. Participants who viewed the presentation reported a stronger uncertainty-as-enabling mindset compared to the control group. This shift in perspective remained stable for at least one month.</p>
<p>The researchers then examined how this mindset influenced social attitudes. They found that individuals who viewed uncertainty as an opportunity were more likely to believe in the productivity of diverse groups. These participants also reported less aversion to interacting with people from different backgrounds.</p>
<p>These diversity attitudes acted as a bridge to broader political outcomes. The study found that positive views on diversity were linked to a higher commitment to societal change. This commitment was defined as an openness to departing from the status quo.</p>
<p>Most notably, the study found a connection to voting behavior in the federal election. Participants with the enabling mindset were less likely to report voting for the Alternative for Germany (AfD). The AfD is a political party classified as right-wing populist.</p>
<p>The statistical analysis revealed a mediating effect. The intervention did not directly change voting behavior on its own. Instead, it fostered a mindset that promoted positive diversity attitudes, which then predicted a lower likelihood of supporting the populist party.</p>
<p>The researchers emphasized that this pathway held true even when accounting for the participants’ general political orientation. This suggests that the effect was not simply due to liberal participants liking the intervention more. The mindset shift appeared to operate through a specific change in how people regard social differences.</p>
<p>The authors argue that these findings highlight a potential strategy for strengthening democratic resilience. By helping citizens regulate their response to uncertainty, societies may be able to foster greater social cohesion. This approach focuses on how people process the unknown rather than directly attacking their political beliefs.</p>
<p>There are several caveats to consider regarding this research. The study relied on self-reported voting behavior, which can be subject to inaccuracies. However, the distribution of votes in the sample closely mirrored the actual election results in Germany.</p>
<p>The study was also conducted specifically within the German cultural context. Germany has been identified in previous research as a culture that tends to have high uncertainty avoidance. It is possible that the intervention might yield different results in cultures with different baseline attitudes toward ambiguity.</p>
<p>The effect sizes observed in the study were modest. While the findings were statistically significant, the intervention was a single, short exercise. The authors suggest that more intensive or repeated interventions might be necessary to achieve larger practical impacts.</p>
<p>Future research is needed to replicate these findings across different countries and political systems. The researchers also recommend investigating whether this mindset can influence attitudes toward other global challenges. Issues such as climate change or technological disruption also involve high degrees of uncertainty.</p>
<p>The study implies that the rise of right-wing populism is partly a psychological response to fear of the unknown. By reframing that fear, it may be possible to reduce the appeal of exclusionary ideologies. This offers a new perspective on how to address political polarization in unstable times.</p>
<p>The study, “<a href="https://doi.org/10.1177/01461672251386487" target="_blank">The Role of Uncertainty Mindsets in Shaping Diversity Attitudes and Their Downstream Effects on Commitment to Societal Change and Right-Wing Populist Voting</a>,” was authored by Ruri Takizawa, Stefanie Marx-Fleck, Alina Gerlach, and Gudela Grote.</p></p>
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<td><a href="https://www.psypost.org/is-sleeping-too-much-actually-bad-for-your-health/" 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;">Is sleeping too much actually bad for your health?</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 16:00</div>
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<p><p>We’re constantly being reminded by news articles and social media posts that we should be getting more sleep. You probably don’t need to hear it again – not sleeping enough is bad for your <a href="https://www.theage.com.au/lifestyle/health-and-wellness/this-kind-of-sleep-is-essential-for-a-healthy-brain-missing-out-can-be-devastating-20250514-p5lz6x.html">brain</a>, <a href="https://www.medicalnewstoday.com/articles/just-3-nights-poor-sleep-may-harm-heart-health">heart</a> and <a href="https://www.abc.net.au/news/2025-06-08/sleep-becoming-major-health-issue-in-australia/105380528">overall health</a>, not to mention your <a href="https://www.theage.com.au/lifestyle/beauty/we-all-know-the-dangers-of-poor-sleep-here-s-what-it-does-to-your-skin-20250513-p5lysy.html">skin</a> and <a href="https://www.abc.net.au/news/health/2024-09-03/not-getting-good-sleep-this-is-what-it-s-doing-to-your-body/104159716">sex drive</a>.</p>
<p>But what about sleeping “too much”? <a href="https://www.theage.com.au/lifestyle/health-and-wellness/too-little-sleep-is-bad-for-your-health-but-too-much-could-be-worse-20250620-p5m8z3.html">Recent reports</a> that sleeping more than nine hours <a href="https://www.telegraph.co.uk/news/2025/06/19/too-much-sleep-more-dangerous-not-enough/">could be worse</a> for your health than sleeping too little may have you throwing up your hands in despair.</p>
<p>It can be hard not to feel confused and worried. But how much sleep do we need? And what can sleeping a lot really tell us about our health? Let’s unpack the evidence.</p>
<h2>Sleep is essential for our health</h2>
<p>Along with nutrition and physical activity, sleep is an essential pillar of health.</p>
<p>During sleep, <a href="https://doi.org/10.1016/j.pcad.2023.02.005">physiological processes</a> occur that allow our bodies to function effectively when we are awake. These include processes involved in muscle recovery, memory consolidation and emotional regulation.</p>
<p>The <a href="https://www.sleephealthfoundation.org.au/sleep-topics/how-much-sleep-do-you-really-need">Sleep Health Foundation</a> – Australia’s leading not-for-profit organisation that provides evidence-based information on sleep health – recommends adults get seven to nine hours of sleep per night.</p>
<p>Some people are naturally <a href="https://theconversation.com/why-do-some-people-need-less-sleep-than-others-a-gene-variation-could-have-something-to-do-with-it-256342">short sleepers</a> and can function well with less than seven hours.</p>
<p>However, for most of us, sleeping less than seven hours will have <a href="https://doi.org/10.2147/NSS.S134864">negative effects</a>. These may be short term; for example, the day after a poor night’s sleep you might have less energy, worse mood, feel more stressed and find it harder to concentrate at work.</p>
<p>In the long term, not getting enough good quality sleep is a <a href="https://jcsm.aasm.org/doi/full/10.5664/jcsm.26918">major risk factor</a> for health problems. It’s linked to a higher risk of developing <a href="https://jcsm.aasm.org/doi/full/10.5664/jcsm.26918">cardiovascular disease</a> – such as heart attacks and stroke – <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2869.2011.00990.x">metabolic disorders</a>, including type 2 diabetes, poor <a href="https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(20)30136-X">mental health</a>, such as depression and anxiety, <a href="https://jcsm.aasm.org/doi/full/10.5664/jcsm.10932">cancer</a> and <a href="https://academic.oup.com/sleep/article-abstract/33/5/585/2454478">death</a>.</p>
<p>So, it’s clear that not getting enough sleep is bad for us. But what about too much sleep?</p>
<h2>Could too much sleep be bad?</h2>
<p>In a <a href="https://doi.org/10.1007/s11357-025-01592-y">recent study</a>, researchers reviewed the results of 79 other studies that followed people for at least one year and measured how sleep duration impacts the risk of poor health or dying to see if there was an overall trend.</p>
<p>They found people who slept for short durations – less than seven hours a night – had a 14% higher risk of dying in the study period, compared to those who slept between seven and eight hours. This is not surprising given the established health risks of poor sleep.</p>
<p>However, the researchers also found those who slept a lot – which they defined as more than nine hours a night – had a greater risk of dying: 34% higher than people who slept seven to eight hours.</p>
<p>This supports similar research from <a href="https://doi.org/10.1161/JAHA.118.008552">2018</a>, which combined results from 74 previous studies that followed the sleep and health of participants across time, ranging from one to 30 years. It found sleeping more than nine hours was associated with a 14% increased risk of dying in the study period.</p>
<p>Research has also shown sleeping too long (meaning more than required for your age) is linked to <a href="https://doi.org/10.2147/NSS.S163071">health problems</a> such as depression, chronic pain, weight gain and metabolic disorders.</p>
<p>This may sound alarming. But it’s crucial to remember these studies have only found a link between sleeping too long and poor health – this doesn’t mean sleeping too long is the <em>cause</em> of health problems or death.</p>
<h2>So, what’s the link?</h2>
<p>Multiple factors may influence the relationship between sleeping a lot and having poor health.</p>
<p>It’s <a href="https://pubmed.ncbi.nlm.nih.gov/18945686/">common</a> for people with chronic health problems to consistently sleep for long periods. Their bodies may need additional rest to support recovery, or they may spend more time in bed due to symptoms or medication side effects.</p>
<p>People with chronic health problems may also not be getting <a href="https://doi.org/10.1016/j.sleep.2021.10.028">high quality sleep</a>, and may stay in bed for longer to try and get some extra sleep.</p>
<p>Additionally, we know <a href="https://pubmed.ncbi.nlm.nih.gov/18945686/">risk factors</a> for poor health, such as smoking and being overweight, are also associated with poor sleep.</p>
<p>This means people may be sleeping more <em>because</em> of existing health problems or lifestyle behaviours, not that sleeping more is causing the poor health.</p>
<p>Put simply, sleeping may be a symptom of poor health, not the cause.</p>
<h2>What’s the ideal amount?</h2>
<p>The reasons some people sleep a little and others sleep a lot depend on <a href="https://www.sleephealthfoundation.org.au/sleep-topics/how-much-sleep-do-you-really-need">individual differences</a> – and we don’t yet fully understand these.</p>
<p>Our sleep needs can be related to age. <a href="https://www.sleephealthfoundation.org.au/sleep-topics/teenage-sleep">Teenagers</a> often want to sleep more and may physically need to, with sleep recommendations for teens being slightly higher than adults at eight to ten hours. Teens may also go to bed and wake up later.</p>
<p>Older adults may want to spend more time in bed. However, unless they have a sleep disorder, the amount they need to sleep <a href="https://www.sleephealthfoundation.org.au/sleep-topics/ageing-sleep">will be the same</a> as when they were younger.</p>
<p>But most adults will require seven to nine hours, so this is the healthy window to aim for.</p>
<p>It’s not just about how much sleep you get. Good quality sleep and a consistent bed time and wake time are just as important – <a href="https://www.sciencedirect.com/science/article/pii/S2352721823001663">if not more so</a> – for your overall health.</p>
<h2>The bottom line</h2>
<p>Given <a href="https://doi.org/10.1080/15402002.2021.1876693">many Australian adults</a> are not receiving the recommended amount of sleep, we should focus on how to make sure we get enough sleep, rather than worrying we are getting too much.</p>
<p>To give yourself the best chance of a <a href="https://www.sleephealthfoundation.org.au/sleep-topics/sleep-hygiene-good-sleep-habits">good night’s sleep</a>, get sunlight and stay active during the day, and try to keep a regular sleep and wake time. In the hour before bed, avoid screens, do something relaxing, and make sure your sleep space is quiet, dark, and comfortable.</p>
<p>If you notice you are regularly sleeping much longer than usual, it could be your body’s way of telling you something else is going on. If you’re struggling with sleep or are concerned, speak with your GP. You can also explore the resources on the <a href="https://www.sleephealthfoundation.org.au/">Sleep Health Foundation</a> website.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/259991/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/is-sleeping-a-lot-actually-bad-for-your-health-a-sleep-scientist-explains-259991">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/from-cold-shock-to-collapse-the-real-risks-of-the-cold-plunge-craze/" 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;">From cold shock to collapse: the real risks of the cold plunge craze</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 14:00</div>
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<p><p>Walk through any trendy suburb and you might find a new “wellness” studio offering ice baths or “<a href="https://www.sciencedirect.com/science/article/abs/pii/S1466853X08000679">contrast therapy</a>” (a sauna and ice bath combo).</p>
<p>Scroll social media, and you’re likely to come across <a href="https://www.buzzfeednews.com/article/lorencecil1/cold-plunge-pool-review">influencers preaching the cold plunge gospel</a> with cult-like zeal.</p>
<p>Ice baths have <a href="https://www.theguardian.com/society/2023/oct/01/cure-or-killer-the-rewards-and-very-real-risks-of-the-cold-water-plunge">gone mainstream</a>. Initially practised mainly among <a href="https://www.theguardian.com/environment/article/2024/jul/25/olympic-demand-for-unproven-ice-therapy-is-unsustainable-scientists-say">high-performance athletes</a>, cold water immersion is now a booming business model: sold as recovery, discipline and therapy all in one.</p>
<p>But the benefits <a href="https://theconversation.com/ice-baths-are-popular-for-exercise-recovery-and-general-wellness-but-what-does-the-science-say-250649">are questionable</a> and, importantly, ice baths can have <a href="https://bjsm.bmj.com/content/56/23/1332.abstract">health risks</a> – particularly for people who have limited experience using them.</p>
<h2>From Roman times to today</h2>
<p>Cold water immersion isn’t a new concept.</p>
<p>The “<a href="https://penelope.uchicago.edu/encyclopaedia_romana/romanurbs/baths.html">frigidarium</a>” – a room with a cold plunge pool or bath – was a feature in most Roman bathhouses.</p>
<p>For decades, athletes have used <a href="https://theconversation.com/is-a-cold-water-swim-good-for-you-or-more-likely-to-send-you-to-the-bottom-89513">cold water immersion</a>, such as swims in cold water, for recovery.</p>
<p>But in recent years, with the proliferation of <a href="https://www.news.com.au/lifestyle/health/fact-or-fad-ice-baths-are-on-the-rise-but-do-they-really-work/news-story/f9dc9afbff04f7c0ff9e597224e1ec75">commercial cold plunge centres</a>, there’s been an explosion in people using ice baths recreationally.</p>
<p>Many people are even setting up their own ice baths at home. The <a href="https://www.imarcgroup.com/cold-plunge-tub-market">global cold plunge tub market</a> was valued at close to US$338 million in 2024 and is projected to reach nearly $483 million by 2033.</p>
<p>Social media shows serene influencers meditating through the pain, claiming it boosts mental health, serotonin, testosterone, and their metabolism. But does the evidence stack up?</p>
<p>Ice baths can reduce muscle soreness after intense training, however the <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3766664/">effect is modest and short-lived</a>.</p>
<p><a href="https://onlinelibrary.wiley.com/doi/full/10.1002/lim2.53">Some research</a> shows cold water immersion can improve mood after a single exposure in young, healthy people, but <a href="https://www.sciencedirect.com/science/article/abs/pii/S0306456523002681">other research</a> doesn’t find these benefits.</p>
<p>Most claims about mental health, testosterone and weight loss aren’t backed by strong evidence. Rather, they’re anecdotal and <a href="https://theconversation.com/get-big-or-die-trying-social-media-is-driving-mens-use-of-steroids-heres-how-to-mitigate-the-risks-253110">amplified by influencers</a>.</p>
<h2>What does an ice bath involve?</h2>
<p>At commercial establishments, patrons can often use the ice baths as they please during a booked session. Ice bath temperatures often range anywhere from 3°C to 15°C. There normally isn’t actual ice in the bath, but some people add blocks of ice to their ice baths at home.</p>
<p>Businesses offering ice baths don’t always actively supervise patrons or monitor a person’s time in the ice bath. They may leave their customers to self-regulate, assuming people will know to get out of the water before they pass their body’s limits.</p>
<h2>So what are the risks?</h2>
<p>Cold water immersion <a href="https://pubmed.ncbi.nlm.nih.gov/2691172/">triggers a powerful physiological response</a>. When you hit cold water below 15°C, your <a href="https://theconversation.com/diving-into-cold-water-can-be-deadly-heres-how-to-survive-it-119341">body launches into cold shock</a>. Gasping occurs and breathing becomes rapid and uncontrollable. Heart rate spikes. Blood pressure rises.</p>
<p>Staying in the water for too long <a href="https://journals.sagepub.com/doi/full/10.1177/00258172231182601">can lead to hypothermia</a>, a condition where a person’s core body temperature drops dangerously low.</p>
<p>Shivering may <a href="https://journals.physiology.org/doi/full/10.1152/physiol.00002.2015">begin within minutes in cold water</a>. Confusion or fainting are more serious signs that hypothermia may be developing.</p>
<p>Occasionally, this “cold shock” response can lead to a heart attack <a href="https://journals.lww.com/chri/fulltext/2014/01040/stroke_after_cold_bath.16.aspx">or stroke</a> – especially if you have an undiagnosed condition affecting your heart, blood vessels or brain.</p>
<p>As far back as 1969, <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC1982576/">researchers found</a> even experienced swimmers could struggle after just a few minutes in cold water. Participants were immersed in water at 4.7°C while fully clothed and asked to swim as if trying to reach safety. Some developed serious respiratory distress and had to stop swimming within as little as 90 seconds, well before any measurable drop in core body temperature.</p>
<p>Even after you get out, your core temperature can continue to fall – a phenomenon known as <a href="https://journals.physiology.org/doi/abs/10.1152/jappl.1988.65.4.1535">afterdrop</a>. So you can encounter problems, such as collapse, even <a href="https://pubmed.ncbi.nlm.nih.gov/1815081/">after leaving the water</a>.</p>
<p>And even young, healthy people <a href="https://www.royallifesaving.com.au/about/news-and-updates/news/2024/feb/position-statement-cold-water-immersion-therapy">can be caught off guard</a>. The body isn’t designed to endure freezing water for extended periods.</p>
<p>Recently one of us (Sam Cornell) had to provide first aid at an ice bath venue in Sydney. A young man collapsed after staying in an ice bath for ten minutes. He was shivering uncontrollably and clearly suffering from cold shock.</p>
<p>Cold exposure can also cause long-term damage to nerves and blood vessels in the hands and feet, known as <a href="https://www.port.ac.uk/news-events-and-blogs/blogs/improving-health-and-wellbeing/cold-water-therapy-what-are-the-benefits-and-dangers-of-ice-baths-wild-swimming-and-freezing-showers">non-freezing cold injury</a>. This is more likely if someone spends an extended period immersed in cold water. Symptoms such as numbness, pain and sensitivity to cold can persist for years.</p>
<h2>6 tips for safer recreational ice bath use</h2>
<p>The ice bath trend is part of a broader wellness movement, promoted to young men in particular, where discomfort is repackaged as discipline. Push through <a href="https://theconversation.com/from-the-liver-king-to-ultramarathons-fitness-influencers-are-glorifying-extreme-masculinity-where-pain-is-the-point-256817">the pain</a>. Master your body. If you feel terrible, you must be doing it right.</p>
<p>But behind the hype lies a less appealing truth. Ice baths <a href="https://bjsm.bmj.com/content/56/23/1332.abstract">can be dangerous</a>.</p>
<p>We advise caution, but if you do choose to try an ice bath, treat it seriously and <a href="https://bjsm.bmj.com/content/56/23/1332.abstract">follow these tips</a> to reduce the <a href="https://www.heart.org/en/news/2022/12/09/youre-not-a-polar-bear-the-plunge-into-cold-water-comes-with-risks">risk of harm</a>.</p>
<p><strong>1. Talk to your doctor:</strong> <a href="https://www.nib.com.au/the-checkup/everyday-health/health-and-wellbeing-habits/benefits-risks-cold-water-therapy">get checked out first</a>. If you or your family have any heart, stroke or respiratory risk, skip it</p>
<p><strong>2. Know your limits:</strong> being fit doesn’t protect you <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/j.2040-4603.2016.tb00673.x">from cold shock</a></p>
<p><strong>3. Start gradually:</strong> begin with short warm to cold showers before full immersion</p>
<p><strong>4. Never go alone:</strong> always have someone with you, especially if you’re new to ice baths</p>
<p><strong>5. Keep it short and watch the temperature:</strong> limit sessions to 3–5 minutes and remember, problems can still occur after you get out</p>
<p><strong>6. Recognise the signs of danger:</strong> symptoms such as shivering, numbness and confusion can all seem like part of the experience to someone bent on pushing themselves. But these can be <a href="https://www.aafp.org/pubs/afp/issues/2004/1215/p2325.html">signs of hypothermia</a>.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/260206/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>
<p> </p>
<p>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/ice-baths-are-booming-in-popularity-but-they-come-with-health-risks-260206">original article</a>.</p></p>
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<td><a href="https://www.psypost.org/high-sugar-diets-may-mimic-alzheimers-pathology-more-closely-than-high-fat-diets/" 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;">High-sugar diets may mimic Alzheimer’s pathology more closely than high-fat diets</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 12:00</div>
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<p><p>A new study conducted on rodents suggests that while diets high in fat and diets high in sugar both lead to obesity and memory loss, they may damage the brain through different biological pathways. The researchers discovered that only chronic sugar consumption resulted in the accumulation of amyloid beta, a protein hallmark of Alzheimer’s disease, within the energy centers of brain cells. These findings were published in the journal <em><a href="https://doi.org/10.1080/1028415X.2025.2546950" target="_blank">Nutritional Neuroscience</a></em>.</p>
<p>Obesity is a growing global health concern that carries risks extending beyond cardiovascular disease and diabetes. Medical professionals recognize a strong link between metabolic disorders and the decline of cognitive functions. This connection is often characterized by a state of chronic, low-grade inflammation and oxidative stress throughout the body.</p>
<p>The brain is particularly sensitive to these metabolic disturbances. To function correctly, brain cells rely on mitochondria. These microscopic structures act as power plants within the cell to generate energy. When mitochondria malfunction, they can produce harmful byproducts known as reactive oxygen species.</p>
<p>This oxidative stress can damage neurons and has been linked to the production of amyloid beta peptide. In patients with Alzheimer’s disease, this peptide clumps together to form toxic plaques between nerve cells. It also accumulates inside the mitochondria themselves, where it disrupts energy production and triggers cell death.</p>
<p>While the association between obesity and neurodegeneration is established, the specific dietary components driving this damage remain under investigation. A research team from the Universidad Autónoma Metropolitana and the Universidad Juárez Autónoma de Tabasco in Mexico sought to clarify this relationship. They aimed to determine whether fat or sugar acts as the primary driver for these specific brain changes.</p>
<p>The researchers designed a long-term experiment using male Wistar rats. They divided the animals into three distinct groups to observe the effects of chronic consumption over a period of twelve months. The control group ate standard laboratory food and drank purified water.</p>
<p>The second group received a high-sucrose diet. These animals had access to the standard food but drank a thirty percent sucrose solution instead of water. This mimics a diet heavy in sugary beverages.</p>
<p>The third group consumed a high-fat diet. Their food was enriched with lard so that fat comprised thirty percent of their total intake. This was intended to replicate a diet rich in saturated animal fats.</p>
<p>After one year, the team assessed the animals’ physical health and cognitive abilities. They measured body weight, body fat distribution, and blood pressure. They also analyzed blood samples to check for glucose, cholesterol, and triglycerides.</p>
<p>The physical results showed that both the high-fat and high-sugar groups developed central obesity. While their total body weight was not statistically different from the control group, they carried significantly more abdominal fat. Both groups also developed high systolic blood pressure.</p>
<p>The metabolic effects differed slightly between the two experimental diets. The rats fed the high-fat diet exhibited elevated fasting glucose levels. This suggests a disruption in how their bodies managed blood sugar at rest.</p>
<p>In contrast, the rats on the high-sugar diet showed signs of insulin resistance. When given a glucose tolerance test, their bodies struggled to clear sugar from the blood efficiently over time. This group also displayed significantly higher levels of triglycerides.</p>
<p>To evaluate brain function, the researchers utilized the Morris water maze. This is a standard behavioral test where rats must swim in a pool to find a hidden platform. It assesses spatial memory and learning capabilities.</p>
<p>The cognitive results were concerning for both experimental groups. Rats fed either the high-fat or high-sugar diet took approximately twice as long to locate the safety platform compared to the control group. This indicates a significant decline in spatial memory regardless of the specific diet type.</p>
<p>Following the behavioral tests, the researchers analyzed brain tissue from the hippocampus and the cerebral cortex. These areas are critical for memory and learning and are often the first to be affected by Alzheimer’s disease. The team separated the mitochondria from the rest of the cell tissue to examine them specifically.</p>
<p>They tested for markers of oxidative stress, specifically looking for damage to lipids and proteins. Both diets caused significant damage to the mitochondrial membranes in the hippocampus. The fats and proteins within these cellular structures showed chemical signs of oxidation, similar to rusting.</p>
<p>The study then examined the activity of the electron transport chain. This is the series of protein complexes within mitochondria that actually produces energy. The activity of these complexes was altered in both diet groups, suggesting the brain cells were struggling to maintain energy levels.</p>
<p>The most distinct finding appeared when the researchers measured amyloid beta levels. They looked for this toxic peptide in both the general cell fluid and specifically inside the mitochondria. In the high-fat group, there was no significant increase in mitochondrial amyloid beta.</p>
<p>However, the high-sugar group told a different story. These animals showed a marked accumulation of amyloid beta peptide within the mitochondria of both the hippocampus and the cerebral cortex. This suggests that high sugar intake triggers a specific pathological pathway that closely resembles the molecular signature of Alzheimer’s disease.</p>
<p>This accumulation of amyloid beta is significant because the peptide is known to disrupt mitochondrial function physically. It can block the transport of essential proteins and alter the enzymes necessary for energy production. The presence of this peptide in the sugar-fed rats correlates with the unique metabolic damage observed in that group.</p>
<p>The authors suggest that while both diets lead to obesity and memory loss, the mechanisms differ. The high-fat diet appears to cause damage through general oxidative stress and inflammation. The high-sucrose diet involves these factors but also specifically promotes the buildup of neurodegenerative proteins.</p>
<p>The study indicates that fructose, a component of sucrose, may be particularly toxic to brain cells. The metabolism of fructose generates distinct byproducts that can lead to rapid cellular damage. This may explain why the amyloid accumulation was specific to the sugar-fed group.</p>
<p>There are caveats to this research that must be considered. The study was conducted on rats, and human metabolism and brain function are more complex. The results observed in animal models do not always translate directly to human clinical outcomes.</p>
<p>Additionally, the experimental diets were somewhat unbalanced regarding protein intake. The addition of lard or sugar reduced the overall percentage of protein the rats consumed. It is possible that protein deficiency contributed partially to the observed negative health effects.</p>
<p>Future research is needed to explore whether these changes are reversible. Scientists need to determine if returning to a healthy diet can clear the accumulated amyloid beta. There is also interest in whether antioxidant treatments could mitigate the mitochondrial damage caused by these diets.</p>
<p>The team also highlighted the potential role of “vitagenes,” which are genes involved in the cellular stress response. Activating these genes might offer a way to protect neurons from diet-induced damage. Understanding these pathways could lead to new preventive strategies for neurodegenerative diseases.</p>
<p>Ultimately, this research provides evidence that not all calories affect the brain in the same way. While preventing obesity is important for general health, limiting sugar intake may be specifically relevant for Alzheimer’s prevention. The data reinforces the importance of diet quality over simple calorie counting.</p>
<p>As the authors state in their conclusion: “With these findings, we show that, although excessive consumption of fat or sucrose drives to obesity, only the last could potentially bridge the gap between obesity and neurodegenerative pathogenesis, thereby highlighting the relevance of lifestyle and diet quality, bringing a way to develop preventive strategies.”</p>
<p>The study, “<a href="https://doi.org/10.1080/1028415X.2025.2546950" target="_blank">Obesity and Alzheimer´s disease: unraveling the impact of chronic consumption of high-fat or high-sucrose diets on neurodegeneration and mitochondrial dysfunction</a>,” was authored by Carlos Francisco Aguilar Gamas, Norma Edith López Diaz-guerrero, Nancy Patricia Gómez-Crisóstomo, Erick Natividad De la Cruz-Hernández, Cecilia Zazueta, Ixchel Ramírez-Camacho, Corazón de María Márquez-Álvarez, and Eduardo Martínez-Abundis.</p></p>
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<td><a href="https://www.psypost.org/repurposed-cancer-drugs-show-promise-as-combination-therapy-for-alzheimers-disease/" 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;">Repurposed cancer drugs show promise as combination therapy for Alzheimer’s disease</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 10:00</div>
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<p><p>Scientists have identified a potential new treatment strategy for Alzheimer’s disease using a combination of two existing cancer drugs. The research suggests that targeting multiple types of brain cells simultaneously offers a more effective approach than focusing on a single target. These findings were published in the journal <em><a href="https://doi.org/10.1016/j.cell.2025.06.035" target="_blank">Cell</a></em>.</p>
<p>The study was led by Yaqiao Li and Yadong Huang from Gladstone Institutes, alongside Marina Sirota from the Bakar Computational Health Sciences Institute at the University of California, San Francisco. The team initiated this research to address the high failure rate of Alzheimer’s drug development. Most current treatments focus on a single aspect of the pathology, such as amyloid plaques, or a single cell type, such as neurons.</p>
<p>However, Alzheimer’s is a complex condition that affects various biological networks. The researchers aimed to develop a strategy that acknowledges this complexity. They sought to correct the dysregulated gene expression networks across multiple cell types simultaneously. This approach relies on the idea that restoring the health of both neurons and the glial cells that support them is necessary for effective treatment.</p>
<p>“Alzheimer’s is a complex disease and currently lacks effective treatment. It affects multiple brain cell types through diverse and interconnected molecular pathways,” said study author Yaqiao Li, a postdoctoral fellow at Gladstone Institutes.</p>
<p>“Rather than focusing on a single gene or protein, our approach embraces a systems biology perspective—aiming to correct dysregulated gene expression networks across multiple cell types and restore them toward healthy-state behaviors.”</p>
<p>“Recent advances in computational power, large-scale transcriptomics, and network modeling make it possible to map these cell-type-specific regulatory programs with high resolution and design interventions that target the underlying system-level dysfunction rather than isolated components. The transformative power of combining the advancement of computational capability, real-world large clinical database, and improved animal models naturally led us to explore this topic.”</p>
<p>The researchers utilized a computational method driven by human data. They began by integrating large datasets of single-nucleus RNA sequencing from post-mortem human brains. This technology allows scientists to examine genetic activity at the level of individual cells rather than in bulk tissue.</p>
<p>This granular analysis revealed specific gene expression changes associated with Alzheimer’s across distinct cell populations. The team identified unique pathological signatures in excitatory neurons, inhibitory neurons, and glial cells like microglia and astrocytes. This step established a detailed map of the cellular dysfunction present in the disease.</p>
<p>With these disease signatures in hand, the researchers employed a computational drug repurposing pipeline. They queried a database known as the Connectivity Map, which contains information on how various drugs affect gene expression. The algorithm looked for drugs that produced gene expression patterns opposite to those seen in Alzheimer’s disease.</p>
<p>The goal was to find compounds that could essentially flip the diseased gene networks back to a healthy state. This screening process identified letrozole and irinotecan as top candidates. Letrozole is an aromatase inhibitor used to treat breast cancer, while irinotecan is a topoisomerase inhibitor used for colorectal cancer.</p>
<p>The computational prediction indicated that letrozole primarily targets defects in neurons. Conversely, irinotecan appeared to target the support networks in glial cells. The researchers hypothesized that combining these two drugs would provide a synergistic effect by addressing the disease on multiple fronts.</p>
<p>Before testing in animals, the team sought validation in real-world human data. They analyzed electronic medical records from over one million patients within the University of California health system. They looked for a correlation between the use of these specific cancer drugs and the incidence of Alzheimer’s disease.</p>
<p>The analysis compared patients who had taken letrozole or irinotecan for cancer against matched control groups who had not. The data indicated that individuals exposed to these drugs had a significantly lower risk of being diagnosed with Alzheimer’s. This real-world evidence strengthened the case for further experimental testing.</p>
<p>The researchers then proceeded to validate the combination therapy in a mouse model. They utilized mice engineered to express both amyloid beta and tau pathologies. These mice develop memory deficits and brain changes that closely mimic the human condition.</p>
<p>The mice were divided into four groups for testing. One group received a vehicle solution, two groups received either letrozole or irinotecan alone, and the final group received the combination of both. The treatment was administered over a period of three months.</p>
<p>Behavioral testing showed that the combination therapy produced the most significant benefits. Mice treated with both drugs demonstrated improved learning and memory retention in spatial navigation tasks. While single-drug treatments offered some benefit, the combination outperformed them consistently.</p>
<p>Pathological examination of the mouse brains corroborated the behavioral results. The combination treatment significantly reduced the area covered by amyloid plaques. It also lowered the levels of phosphorylated tau, a protein associated with the formation of neurofibrillary tangles.</p>
<p>The researchers also assessed the health of the neurons and glial cells. The combination therapy prevented the loss of neurons in the hippocampus, a brain region essential for memory formation. Furthermore, the treatment reduced signs of neuroinflammation driven by microglia and astrocytes.</p>
<p>To understand the molecular mechanisms, the researchers performed single-nucleus RNA sequencing on the treated mice. This analysis confirmed that the drugs worked as the computational model had predicted. The combination therapy reversed the disease-associated gene networks in a cell-type-specific manner.</p>
<p>The data provides evidence that letrozole helped correct neuronal pathways related to synaptic activity. Simultaneously, irinotecan appeared to modulate inflammatory and metabolic pathways in glial cells. This dual action likely contributes to the superior efficacy observed with the combination.</p>
<p>“We discovered that two FDA-approved cancer drugs that work together to reverse key features of Alzheimer’s disease in mouse models by targeting different brain cell types,” Li told PsyPost. “This combination therapy improved memory and reduced brain damage better than untreated or either drug alone.”</p>
<p>“The real surprise is that the top two drugs are both cancer treatment drugs. It is very exciting, with a bit of surprise, that the combination therapy with one drug targeting Alzheimer’s-related genetic changes in neurons and another targeting glia performed remarkably well in mice genetically engineered to develop aggressive Alzheimer’s-like symptoms.” </p>
<p>“It reduced brain pathology and improved memory more effectively than either drug alone or no treatment,” Li continued. “These results suggest that addressing the disease’s complexity by targeting multiple cell types and pathways simultaneously with cell-type-precision therapy may be key to unlocking a cure.”</p>
<p>Despite the promising results, the study has some limitations. The initial drug screening utilized databases based on cancer cell lines rather than brain cells. This difference means the predicted effects require extensive validation in neurological contexts.</p>
<p>Additionally, the study noted sex differences in the mouse models. Male mice showed more robust behavioral improvements compared to female mice. The researchers suggest this could be due to hormonal factors or specific characteristics of the mouse model used.</p>
<p>“Current treatment options for Alzheimer’s disease remain very limited,” Li noted. “Because these two drugs are already approved for other indications, they provide a strategic head start toward future clinical testing, and we are actively pursuing opportunities and partnerships to advance this combination therapy into clinical trials.”</p>
<p>“Looking ahead, our long-term goal is to build on this work by integrating artificial intelligence (AI) technology with large-scale molecular, clinical, and drug databases to enable a fast-track therapeutic development pipeline toward true precision medicine for Alzheimer’s—where therapies are guided not only by symptoms, but by each patient’s unique molecular and cellular signatures as well as clinical profiles.”</p>
<p>“This study exemplifies the power of interdisciplinary collaboration in biomedical research—combining large-scale drug screening and computational tools developed at UCSF with deep expertise in disease biology and experimental validation at the Gladstone Institutes,” Li added. “The seamless integration of computational and experimental biology was central to the success of this study.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.cell.2025.06.035" target="_blank">Cell-type-directed network-correcting combination therapy for Alzheimer’s disease</a>,” was authored by Yaqiao Li, Carlota Pereda Serras, Jessica Blumenfeld, Min Xie, Yanxia Hao, Elise Deng, You Young Chun, Julia Holtzman, Alice An, Seo Yeon Yoon, Xinyu Tang, Antara Rao, Sarah Woldemariam, Alice Tang, Alex Zhang, Jeffrey Simms, Iris Lo, Tomiko Oskotsky, Michael J. Keiser, Yadong Huang, and Marina Sirota.</p></p>
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<td><a href="https://www.psypost.org/playing-pickleball-at-least-three-times-a-week-linked-to-better-mental-health/" 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;">Playing pickleball at least three times a week linked to better mental health</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 27th 2025, 08:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.3389/fpsyg.2025.1676695" target="_blank">Frontiers in Psychology</a></em> provides evidence that individuals who play pickleball more frequently and for longer durations report better mental health. The findings suggest a positive “dose-response” relationship between the amount of play and wellbeing, particularly among older adults.</p>
<p>Wellbeing is a broad concept that extends beyond the simple absence of physical illness. It encompasses psychological, emotional, and social aspects of a person’s life. Public health officials increasingly view wellbeing as a primary goal of health initiatives.</p>
<p>Physical activity is widely recognized as a factor that supports wellbeing across the lifespan. However, different sports may offer varying levels of benefit depending on how often they are played. Pickleball has rapidly grown in popularity in the United States and globally.</p>
<p>This sport combines elements of tennis, badminton, and table tennis on a smaller court. The equipment includes a solid paddle and a perforated plastic ball. The game has a relatively easy learning curve and is accessible to people of various physical abilities.</p>
<p>Previous research has linked participation in organized sports to improved quality of life and reduced symptoms of depression. Some studies on tennis have hinted that playing frequency matters for mental distress levels. Yet, the specific relationship between the “dose” of pickleball and mental wellbeing remained unexplored.</p>
<p>“Pickleball has grown rapidly in popularity, yet little was known about its potential mental health benefits, especially its dose-response effect. We wanted to address this gap by examining whether playing more pickleball is associated with better mental wellbeing, and if so, how much play might be needed to see meaningful effects,” said study author Olu Owoeye, an associate professor and director of <a href="https://www.slu-tip-lab.com/" target="_blank">the Translational Injury Prevention Lab</a> at Saint Louis University.</p>
<p>Data for this research came from the Surveillance in Pickleball players to reduce INjury burden (SPIN) project. This is a larger initiative designed to understand the health impacts of the sport. The researchers distributed an online survey to active players across the United States.</p>
<p>To be eligible for the study, participants had to be residents of the U.S. and at least 18 years old. They also needed to play pickleball a minimum of once per month. Recruitment efforts utilized social media, newsletters, and flyers posted at pickleball facilities.</p>
<p>The final sample included 1,667 pickleball players. The average age of the participants was approximately 62.8 years. The ages ranged from 18 to 89 years, providing a wide view of the adult playing population.</p>
<p>Females accounted for roughly 55 percent of the respondents. The survey asked participants to report their playing habits over the past 12 months. This included how many times per week they played and how long a typical session lasted.</p>
<p>To assess mental health, the researchers employed the WHO-5 Wellbeing Index. This is a widely used questionnaire consisting of five positively worded statements. Participants rated how often they felt cheerful or in good spirits over the previous two weeks.</p>
<p>The responses were converted into a score ranging from 0 to 100. A score of 0 represents the worst possible wellbeing. A score of 100 represents the best possible wellbeing.</p>
<p>The researchers used statistical models to analyze the data. They controlled for variables such as age, sex, injury history, and participation in other sports. This allowed them to isolate the specific association between pickleball and mental health.</p>
<p>The results showed a significant association between play frequency and wellbeing. Players who engaged in the sport three or more times per week had an average wellbeing score of 77.5. Those who played two times or fewer per week had an average score of 73.5.</p>
<p>A similar pattern emerged regarding the duration of play sessions. Individuals who played for more than two hours per session had an average wellbeing score of 77.7. In contrast, those who played for two hours or less had an average score of 74.9.</p>
<p>“Engaging in more pickleball provides greater mental wellbeing, but even small doses appear to matter,” Owoeye told PsyPost. “Folks should strive to play more frequently to maximize the physical and mental wellbeing benefits of pickleball.”</p>
<p>The study also examined how personal characteristics moderated these results. Age proved to be a significant factor in the relationship between play and mental health. Older adults generally reported higher wellbeing scores than younger participants.</p>
<p>The positive link between frequent pickleball participation and wellbeing was consistent across all age groups. However, the effect appeared strongest among older adults. Specifically, the benefit peaked in the 63 to 67 age range.</p>
<p>There was a slight decline in scores for the oldest age category of players aged 78 and above. Despite this, the trend indicated that maintaining play into older age supports mental health. This aligns with theories that staying active helps mitigate age-related declines in wellbeing.</p>
<p>Injury history had a notable negative impact on the results. Players who reported sustaining an injury in the past year had substantially lower wellbeing scores. This finding held true regardless of how much they played.</p>
<p>The negative association with injury highlights the psychological toll of physical setbacks. Injuries can lead to pain and a loss of physical function. They often result in social isolation if the player can no longer participate in their community activities.</p>
<p>Sex did not appear to moderate the relationship between pickleball and wellbeing. The analysis showed no significant difference between male and female players. Both sexes experienced comparable increases in wellbeing associated with higher participation levels.</p>
<p>This suggests that the mental health benefits of the sport are equitable. It indicates that pickleball is an effective intervention for both men and women. Sex-specific modifications to programs may not be necessary to achieve these psychological gains.</p>
<p>One unexpected finding involved participation in other sports. The models showed a negative or borderline negative association between playing other sports and the wellbeing scores in this context. This requires further investigation to understand fully.</p>
<p>The authors discussed the implications of their findings for public health. The results support the idea that pickleball is a low-barrier strategy to promote mental health. Its social nature likely contributes to the observed benefits.</p>
<p>For older adults, the sport offers a way to combat loneliness and a diminished sense of purpose. The study reinforces the importance of injury prevention. Keeping players healthy allows them to sustain the participation levels that drive these mental benefits.</p>
<p>The study has several limitations that provide context for the results. The sample was skewed toward older adults, with an average age of 63. This is higher than the national average for pickleball players, which may limit how well the findings apply to younger groups.</p>
<p>The design of the study was cross-sectional. This means it captured data at a single point in time. Consequently, the researchers cannot prove that playing pickleball causes better mental health.</p>
<p>It is possible that people with higher mental wellbeing are simply more motivated to play sports. The direction of the relationship remains an open question. Additionally, the data relied on self-reports. Future research is needed to address these issues.</p>
<p>The researchers expressed an interest in conducting intervention studies. They aim to design structured pickleball programs to test these effects experimentally. </p>
<p>“We’d like to explore whether structured pickleball programs could be used as interventions for mental wellbeing,” Owoeye explained. “My team just completed a proposal for a faith-based pickleball program that will leverage the intergenerational and social connections that pickleball offers and evaluate these benefits over 12 weeks of structured pickleball exposure. We are currently looking for funding or sponsorship for this new project. Folks can support our research through our website (<a href="https://www.slu-tip-lab.com/donate" target="_blank">https://www.slu-tip-lab.com/donate</a>).”</p>
<p>The study, “<a href="https://doi.org/10.3389/fpsyg.2025.1676695" target="_blank">The more you play, the better you feel: a dose–response analysis of pickleball and mental wellbeing in U.S. adults</a>,” was authored by Oluwatoyosi B. A. Owoeye, Joseph Grese, Madeline Stenersen, Ted Yemm, Chris Sebelski, and Katie Sniffen.</p></p>
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<td><a href="https://www.psypost.org/why-you-cant-blame-your-turkeys-tryptophan-for-your-thanksgiving-food-coma/" 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;">Why you can’t blame your turkey’s tryptophan for your Thanksgiving food coma</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 26th 2025, 18:00</div>
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<p><p>Every Thanksgiving, myths of the quasi-magical powers of tryptophan rise again.</p>
<p>There’s the turkey/drowsiness myth: Eating lots of juicy turkey meat supposedly makes people feel tired because it contains an amino acid called tryptophan. This molecule travels into the brain, where it’s converted into a neurotransmitter called serotonin, which in turn is converted into a hormone called melatonin. Voila! Sleepiness.</p>
<p><a href="https://doi.org/10.1136/bmj.39420.420370.25">But science</a> and <a href="https://www.google.com/search?q=turkey+and+sleepiness">the internet</a> agree: It’s not the turkey’s tryptophan to blame for your post-feast nap. All protein sources, and even vegetables, contain some tryptophan; turkey isn’t at all special in this regard.</p>
<p>So the sleepiness myth of turkey may be fading, but other legends around tryptophan’s effects in the brain are taking hold. Some people are eyeing tryptophan supplements as an <a href="https://doi.org/10.3390/nu8010056">unconventional treatment for depression</a>. Others are curious whether <a href="https://doi.org/10.1111/j.1601-5215.2010.00508.x">eating foods that are high or low in tryptophan</a> could be useful for influencing mood. Recently, some scientists have even proposed that <a href="https://doi.org/10.1016/j.bbr.2014.07.027">gut bacteria are driving changes in emotion</a> by producing or breaking down tryptophan.</p>
<p>This tryptophan/mood connection is an area of ongoing research. And while some are captivated by tryptophan’s potential, it’s not clear whether the excitement is warranted.</p>
<h2>Looking for a tryptophan link to mood</h2>
<p>There is some scientific evidence that eating tryptophan can alter your mood.</p>
<p>For example, back in 2000, researchers found that when people ate an isolated protein that was very high in tryptophan, they <a href="https://doi.org/10.1093/ajcn/71.6.1536">felt less stress while doing math problems</a>.</p>
<p>However, placebo-controlled clinical trials haven’t, in general, shown much of a connection. A few studies have found that <a href="https://doi.org/10.1016/j.jad.2013.05.042">supplementing with pure tryptophan</a> provided little to no benefit for people with depression. Some studies have even looked at what happens when you <a href="https://doi.org/10.1038/sj.mp.4001949">remove tryptophan from people’s diets</a>, but also found little to no effect.</p>
<p>So what explains the mixed results?</p>
<h2>Serotonin itself still holds mysteries</h2>
<p>Alongside human studies, the biology of tryptophan has been well studied in rodents. Research in the early 1970s showed that taking <a href="https://doi.org/10.1126/science.178.4059.414">tryptophan supplements can boost serotonin</a>, a neurotransmitter that was historically associated with feelings of well-being and happiness.</p>
<p>Since then, scientists have learned lots of interesting facts <a href="https://www.serotoninclub.org/">about serotonin</a>. For example, there are <a href="https://doi.org/10.1523/JNEUROSCI.2830-16.2016">14 separate receptors for serotonin</a>, and they’re found all over the brain.</p>
<p>Researchers have learned how to affect this system with drugs, but not with much precision. For example, drugs like the antidepressant selective serotonin reuptake inhibitors – more widely known as SSRIs – don’t target individual receptors and they don’t restrict themselves to particular brain regions. Instead, SSRIs, the <a href="https://www.medicalnewstoday.com/kc/prozac-fluoxetine-side-effects-263773">best-known of which is Prozac</a>, bluntly boost serotonin everywhere.</p>
<p>This non-specificity is why, in my mind, it’s hard to believe that SSRIs work at all. Here’s an analogy: Say you’re Jeff Bezos and you want to increase Amazon’s revenue by speeding up your deliveries. So you decide to crank up the speed on all delivery vehicles. From now on, every truck will boost its speed by 5%. It may be a stroke of logistical genius, or it may, perhaps more likely, end up in chaos. Like ramping up serotonin all over the brain, this blunt approach might not be ideal.</p>
<p>Analogies aside, whether SSRIs affect people’s moods is an experimental question, and some research has supported the idea that these drugs work. However, especially lately, their effectiveness has <a href="https://www.newscientist.com/article/mg23931980-100-nobody-can-agree-about-antidepressants-heres-what-you-need-to-know/">come under intense scrutiny</a>. Some recent analyses cite 30 years’ worth of studies and <a href="https://doi.org/10.1186/s12888-016-1173-2">question the clinical value of SSRIs</a>, while others maintain that these drugs <a href="https://doi.org/10.1016/S0140-6736(17)32802-7">improve the symptoms of depression</a>.</p>
<p>It’s complicated, and there’s still some disagreement, but most psychiatrists agree that SSRIs are <a href="https://doi.org/10.1016/S0140-6736(17)32802-7">not effective for everyone</a>. These drugs are not psychiatric-cure-alls.</p>
<h2>More chemical fine-tuning for mood</h2>
<p>In light of all this, I’ve often found myself asking whether psychiatric researchers needed <a href="https://doi.org/10.1038/sj.mp.4001949">73 studies</a> looking at whether tryptophan depletion has an impact on mood.</p>
<p>When it comes to understanding connections between gut bacteria and the brain, or the bigger challenge of understanding and treating mental illness, should researchers really still be thinking about tryptophan?</p>
<p>It’s seems true that, similar to SSRIs, boosting tryptophan <a href="https://doi.org/10.1371/journal.pone.0035916">has a broad impact on serotonin</a>. It’s definitely possible that cranking up serotonin can influence mood, and that therefore boosting tryptophan could do the same. But it’s also possible that to manipulate something as complicated as human emotion requires a little more nuance.</p>
<p>Psychiatric research has long been moving away from the idea that <a href="https://www.ted.com/talks/david_anderson_your_brain_is_more_than_a_bag_of_chemicals?language=en">your brain is a bag of chemicals</a>; modern neuroscientists are asking for a little more specificity. From this perspective, I’m skeptical of the notion that tryptophan is the depression remedy psychiatry needs. Not only has experimental research found fairly weak results, but the theory itself isn’t very compelling.</p>
<p>Serotonin, seemingly full of psychiatric possibility, has long fascinated psychiatric researchers. But what the past half century seems to have demonstrated is that the neuroscience of human emotion is not simple. To promote lasting changes in mental health, scientists may need a little more reverence for the complex emotional beings that we all are.</p>
<p>So no, a big turkey dinner, as filled with delicious tryptophans as it might be, will likely not be the neurochemical driver for your mood on Thanksgiving.</p>
<p> </p>
<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/turning-to-turkeys-tryptophan-to-boost-mood-not-so-fast-125633">original article</a>.</em></p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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