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  1. DATE: September 9, 2026 at 01:48PM
    SOURCE: SOCIALPSYCHOLOGY.ORG

    TITLE: Ozempic and Wegovy May Have an Unexpected Mental Health Benefit

    URL: socialpsychology.org/client/re

    Source: Science Daily - Top Health

    Semaglutide, the drug behind Ozempic and Wegovy, may have benefits that extend well beyond weight loss and diabetes. In a large Swedish study of nearly 15,000 people with bipolar disorder, its use was linked to a 21% lower risk of psychiatric hospitalization. Researchers think effects on inflammation and brain-related biological pathways could help stabilize mood, though other GLP-1 drugs did not show the same association.

    URL: socialpsychology.org/client/re

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #Wegovy #Semaglutide #MentalHealth #BipolarDisorder #Inflammation #MoodStability #GLP1 #PsychiatricResearch #WeightLossAndBeyond

  2. DATE: September 8, 2026 at 08:59AM
    SOURCE: SCIENCE DAILY PSYCHIATIRY FEED

    TITLE: Ozempic and Wegovy may have an unexpected mental health benefit

    URL: sciencedaily.com/releases/2026

    Semaglutide, the drug behind Ozempic and Wegovy, may have benefits that extend well beyond weight loss and diabetes. In a large Swedish study of nearly 15,000 people with bipolar disorder, its use was linked to a 21% lower risk of psychiatric hospitalization. Researchers think effects on inflammation and brain-related biological pathways could help stabilize mood, though other GLP-1 drugs did not show the same association.

    URL: sciencedaily.com/releases/2026

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #Wegovy #Semaglutide #BipolarDisorder #MentalHealthMatters #GLP1 #MoodStability #PsychiatricHealth #Inflammation #DiabetesAndWeightLoss

  3. DATE: September 8, 2026 at 08:59AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Ozempic and Wegovy may have an unexpected mental health benefit

    URL: sciencedaily.com/releases/2026

    Semaglutide, the drug behind Ozempic and Wegovy, may have benefits that extend well beyond weight loss and diabetes. In a large Swedish study of nearly 15,000 people with bipolar disorder, its use was linked to a 21% lower risk of psychiatric hospitalization. Researchers think effects on inflammation and brain-related biological pathways could help stabilize mood, though other GLP-1 drugs did not show the same association.

    URL: sciencedaily.com/releases/2026

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #Wegovy #Semaglutide #BipolarDisorder #MentalHealthBenefits #Glp1 #MoodStabilization #Inflammation #PsychiatricHospitalization #DiabetesAndWeightLoss

  4. DATE: September 5, 2026 at 06:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Over half the risk for postpartum psychosis is tied to genetics, large study finds

    URL: psypost.org/over-half-the-risk

    New research published in Molecular Psychiatry indicates that postpartum psychosis is heavily influenced by both common and rare genetic factors, with about half of the risk tied to genetics. The study also identified a specific gene involved in cholesterol production that provides evidence for shared biological pathways between postpartum psychosis, schizophrenia, and certain autoimmune conditions.

    Postpartum psychosis is a rare but severe mental health emergency that occurs in roughly 1 to 2 out of every 1,000 mothers shortly after childbirth. It involves an abrupt onset of symptoms like mania, severe depression, confusion, and psychosis, which is when a person loses touch with reality through hallucinations or delusions. The condition poses heavy risks to both the mother and the infant, often requiring immediate medical hospitalization.

    Earlier research established that this vulnerability has deep biological roots. A 2001 study showed that the tendency to experience a severe psychotic episode triggered specifically by childbirth runs strongly in families. Moving beyond familial history, a 2013 study discovered that women experiencing their first episode of postpartum psychosis show disruptions in their immune systems.

    Alongside these immune factors, metabolic changes have also been implicated, as a 2017 meta-analysis suggested that people going through their first psychotic episode tend to have altered cholesterol levels. These findings paved the way for large-scale genetic sequencing to pinpoint the exact genes and shared biological pathways involved. To build on these insights, researchers led by Seulgi Jung and study co-author Behrang Mahjani, an assistant professor at the Icahn School of Medicine at Mount Sinai who directs the Mahjani Lab, aimed to detail the specific genetic architecture of postpartum psychosis.

    “Postpartum psychosis is a severe but understudied psychiatric disorder,” Mahjani told PsyPost. “Our previous study showed that sisters of women with postpartum psychosis have a markedly elevated risk, but its heritability had not been quantified and no specific risk genes had been identified. We therefore examined the contribution of both common and rare genetic variation to the disorder.”

    The researchers first used data from Swedish national registers to estimate the overall genetic risk of the disorder. They examined health records from over 1.6 million mothers who gave birth to their first child between 1980 and 2017. Among this massive group, 2,514 mothers, or 0.15 percent, developed postpartum psychosis.

    By tracking the health records of the mothers’ sisters and cousins, the researchers estimated the heritability of postpartum psychosis to be 55 percent. This indicates that more than half of the variation in who develops the condition can be attributed to genetic factors, a rate similar to that of bipolar disorder.

    “The genetic contribution is substantial,” Mahjani explained. “Heritability in this range means that inherited variation accounts for a large share of the differences in vulnerability between individuals, comparable to what is seen for bipolar disorder and schizophrenia.”

    “This supports the view that postpartum psychosis reflects an underlying biological vulnerability rather than being simply a psychological reaction to the stress of childbirth,” he added.

    To see how much of this heritability comes from common genetic variations, the team turned to the All of Us Research Program, a large national database of genetic and health information. They focused on whole-genome sequencing data from 198 mothers of European ancestry who had experienced postpartum psychosis, comparing them to 2,013 matched controls.

    The team found that common genetic variants explained about 45.6 percent of the risk for postpartum psychosis. Because this is slightly lower than the 55 percent heritability estimated from family histories, it suggests that rarer genetic variations also play a role in the disorder.

    The researchers then looked closely at rare genetic changes, specifically focusing on protein-truncating variants. These are severe mutations that essentially break a gene, preventing it from producing a functional protein. They analyzed a larger sample of 461 cases of postpartum psychosis and 4,610 unaffected controls.

    Women with postpartum psychosis had an unusually high number of these disruptive mutations in genes that are generally highly constrained, meaning the genes do not usually tolerate mutations well without causing major biological problems. Based on these mutation patterns, the researchers estimated that there are around 81 specific genes that contribute to the risk of postpartum psychosis.

    When analyzing which individual genes were most affected, the gene HMGCR stood out strongly. This gene contains the instructions for making a key enzyme that controls how the body produces cholesterol. A second gene, DNMT1, which helps maintain how DNA is regulated and read by the body, also showed a possible, though less certain, link to the disorder.

    “The rare variants in HMGCR have large effects in the people who carry them, which is what allowed us to detect the gene despite a relatively modest sample,” Mahjani noted.

    However, he cautioned against oversimplifying this connection. “HMGCR should not be read as ‘the postpartum psychosis gene,'” he said. “It is one of the many genes contributing to risk, and like other severe psychiatric disorders the condition is highly polygenic.”

    To explore the broader impact of these genes, the researchers checked for mutations in HMGCR and DNMT1 across hundreds of thousands of individuals in two large medical biobanks. They found that rare mutations in HMGCR were also linked to conditions like vascular dementia and unspecified mental disorders, indicating the gene influences brain health outside of the postpartum period.

    Finally, the researchers compared their list of genetic risk factors for postpartum psychosis against genes known to cause other illnesses. They found that a substantial percentage of the top risk genes for bipolar disorder and schizophrenia were also linked to postpartum psychosis. Additionally, they noted a genetic overlap with autoimmune diseases like rheumatoid arthritis, myasthenia gravis, and Crohn’s disease, with HMGCR appearing as a top risk gene for both schizophrenia and rheumatoid arthritis.

    “The results were largely consistent with what genetic studies of related psychiatric disorders would predict,” Mahjani said.

    There are a few things to keep in mind regarding this study. First, definitions of postpartum psychosis can vary across different medical records. The registry data used in the study often lacked the precise end dates of episodes, which makes it harder to classify the exact duration of the illness.

    The researchers also did not separate women whose postpartum psychosis was their very first psychiatric episode from those who had a pre-existing condition, such as bipolar disorder. As a result, some of the genetic patterns they found might reflect severe mental illness in general rather than factors entirely unique to the postpartum period.

    Additionally, the genetic sequencing data relied heavily on individuals of European ancestry, meaning the results might not fully capture the genetic risk factors present in other populations. Future studies with more diverse groups will help provide a more complete picture of the condition’s genetic roots.

    “Our immediate priority is to replicate these findings in larger samples,” Mahjani said of the team’s next steps. “Beyond that, we want to understand how the genes we identified actually function in the disorder, and how genetic vulnerability interacts with the hormonal and immune changes that occur during and after pregnancy.”

    “Mainly that postpartum psychosis has been remarkably understudied relative to its severity,” he concluded. “Progress will depend on continued access to the kind of large-scale genomic resources that made this work possible, such as the All of Us Research Program, and on studies large enough to identify additional risk genes with confidence.”

    The study, “Genetic architecture of postpartum psychosis: from common to rare genetic variation,” was authored by Seulgi Jung, Madison Caballero, Adrianna Kępińska, Shelby Smout, Trine Munk-Olsen, Thalia K. Robakis, Veerle Bergink, and Behrang Mahjani.

    URL: psypost.org/over-half-the-risk

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PostpartumPsychosis #GeneticRisk #MentalHealthResearch #HMGCR #DNMT1 #CholesterolGenes #SchizophreniaOverlap #BipolarDisorder #AutoimmuneLinks #GenomicsStudy

  5. DATE: August 29, 2026 at 06:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Genetic risk for schizophrenia and bipolar disorder is linked to specific types of intelligence

    URL: psypost.org/genetic-risk-for-s

    New research suggests that the genetic links between psychiatric conditions and intelligence vary depending on the specific type of thinking skill involved. Rather than viewing intelligence as a single trait, a new genetic analysis indicates that conditions like schizophrenia and bipolar disorder share different genetic roots with problem-solving skills compared to acquired knowledge. The findings were published in Nature Communications.

    People diagnosed with certain psychiatric disorders often experience difficulties with memory, attention, and problem-solving. For instance, a 2023 review detailed how conditions like schizophrenia share overlapping genetic and environmental risk factors with cognitive challenges. Similarly, a study covered by PsyPost in 2024 found that higher general intelligence tends to be associated with fewer symptoms of attention-deficit hyperactivity disorder (ADHD) and autism, a connection partly driven by shared genetics.

    Past genetic research generally treated cognitive ability as one broad category. However, human cognition is made up of distinct skills. These include processing speed, often measured by how fast someone reacts to a prompt. Another component is fluid reasoning, which involves solving new problems and processing complex information on the spot. A third area is crystallized knowledge, representing the facts and vocabulary a person learns through culture and life experience.

    Genetic studies have historically lacked enough data to analyze these specific categories of thinking, especially crystallized knowledge. Scientists wanted to see if breaking down cognition into these specific domains might provide a more detailed picture of how mental health and intelligence are connected at a genetic level. They also wanted to account for non-cognitive skills, such as motivation and persistence, which help people succeed in educational settings.

    The research was led by Diego Londoño-Correa, a PhD and recent graduate of the Department of Psychology at The University of Texas at Austin. “There was a paradox in the behavioral and psychiatric genetics literature that I found very interesting,” he said. “People diagnosed with psychiatric disorders such as schizophrenia often show cognitive difficulties, and these negative associations are observed at both the phenotypic and genetic levels. However, genetic liability for schizophrenia and some other disorders has also been positively associated with educational attainment.”

    “In our lab, we wondered whether part of this apparent contradiction came from treating cognition as a single trait,” he explained. “We thought that part of the answer to this paradox might lie in the difference between these domains that previous studies had not accounted for.”

    The scientists analyzed genetic data from hundreds of thousands of people. Using existing genetic databases, primarily focusing on individuals of European ancestry, they gathered information on cognitive test performance and educational attainment. The total sample size for the crystallized knowledge analysis reached roughly 439,000 individuals.

    To measure specific cognitive skills, the team looked at scores from tests involving reaction time, puzzle solving, and vocabulary knowledge. “Many cognitive tests do not ‘purely’ measure a single domain such as crystallized knowledge,” Londoño-Correa explained. “For example, you still need lower-order cognitive processes such as processing speed to perform well on tests of crystallized knowledge, including vocabulary tests.”

    To address this, the researchers used a specialized statistical tool to separate the overlapping genetic influences of reaction time, fluid reasoning, and crystallized knowledge. They also isolated a non-cognitive genetic factor tied to how many years of schooling a person completed, removing any genetic effects related to actual test performance.

    The analysis identified 78 genetic regions associated with crystallized knowledge. Eight of these regions had never been linked to any cognitive trait in previous genetic research. The researchers also found that genes associated with fluid reasoning tend to be most active in the brain during early childhood development. In contrast, genes associated with crystallized knowledge show increased activity during adolescence and early adulthood, aligning with the idea that this type of knowledge builds up over time through education and experience.

    When comparing these cognitive profiles to the genetic risk for five specific psychiatric conditions, the authors found highly varied patterns. Schizophrenia and bipolar disorder showed the most similarity. The genetic risk for both conditions was associated with slower reaction times and lower fluid reasoning, but positively associated with both crystallized knowledge and non-cognitive educational skills.

    “The main takeaway is that the genetic relationship between psychiatric disorders and cognitive abilities is not uniformly positive or negative,” Londoño-Correa said. “Reducing all of cognition to a single general factor of intelligence can hide meaningful differences in how psychiatric genetic liability relates to different cognitive abilities.”

    Other conditions displayed entirely different genetic associations. The genetic risk for ADHD was associated with slightly faster reaction times, but it was also linked to lower fluid reasoning, lower crystallized knowledge, and lower non-cognitive skills. Autism spectrum disorder was positively associated only with crystallized knowledge. Alzheimer’s disease was associated only with lower fluid reasoning, matching the clinical observation that dementia often heavily impacts executive functioning and on-the-spot problem-solving.

    The researchers also compared the cognitive genetic factors to personality traits. They found that openness to experience, a trait linked to curiosity and a desire to learn, was strongly and positively associated with the genetics of crystallized knowledge.

    Londoño-Correa found this specificity particularly striking, noting that openness had a strong correlation with crystallized knowledge but much weaker associations with reaction time and fluid reasoning. “Developmental psychologists propose these genetic tendencies as ‘experience-producing drives’ so people who are more curious may seek out books, conversations, education, cultural experiences, or other cognitively rewarding environments,” he said. “Over time those experiences accumulate into crystallized knowledge, the trait that was correlated with higher risk for schizophrenia, bipolar disorder and autism.”

    These findings offer new insights, but they are subject to certain limitations. The genetic overlap between a psychiatric disorder and a cognitive trait does not mean that having a specific gene will automatically cause a mental health condition or guarantee high intelligence.

    “The most important caveat is that genetic liability is not the same thing as having a psychiatric disorder,” Londoño-Correa explained. “That is very different from saying that people diagnosed with schizophrenia have higher crystallized abilities. We are studying how genetic variation can relate to multiple traits at the same time, not describing the average characteristics of diagnosed individuals.”

    He emphasized that the study should not be interpreted as showing that clinical conditions like schizophrenia or autism improve cognition, as these disorders can have very serious cognitive and functional consequences. Furthermore, the study relied entirely on data from people of European descent to avoid statistical errors that can happen when mixing different genetic backgrounds, meaning the results might not apply to other ancestries.

    Looking ahead, the research team hopes to use these insights to explore broader evolutionary questions. “My broader interest is in understanding why genetic variation associated with psychiatric disorders persists across human evolutionary history despite the health and reproductive costs these disorders can impose, particularly for conditions that often begin relatively early in life,” Londoño-Correa said.

    He pointed to a concept known as antagonistic pleiotropy, where genetic variants that increase vulnerability to a disorder might also confer cognitive or behavioral advantages. “This study does not test natural selection directly, so we need more sophisticated analyses, for example using ancient DNA, to ask whether psychiatric-risk variants that are also associated with higher cognitive performance increased in frequency during human history,” he added.

    The study, “Crystallized and fluid cognitive abilities have different genetic associations with neuropsychiatric disorders,” was authored by Diego Londono-Correa, Javier de la Fuente, Gail Davies, Simon R. Cox, Ian J. Deary, K. Paige Harden, and Elliot M. Tucker-Drob.

    URL: psypost.org/genetic-risk-for-s

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #GeneticLinks #Schizophrenia #BipolarDisorder #CognitiveAbilities #CrystallizedKnowledge #FluidReasoning #ProcessingSpeed #NeuropsychiatricGenetics #EducationalAttainment #OpenToExperience

  6. Warum es wichtig ist, alle ernst zu nehmen:

    Eine Person in meinem Umfeld vermutete seit längerem, sie könnte ASS oder AuDHD
    ​:rosahaj_autism:​ haben. Das Umfeld nahm diese Vermutung nie ernst. Deswegen liess sie es nie abklären.

    Vor einiger Zeit vertraute sie sich mir an, weil ich selbst ADHS habe. Aus meiner Sicht zeigten sich einige passende Symptome und Verhaltensweisen, andererseits fand ich, dass irgendwie auch etwas nicht ganz passte. Aber ich bin ja keine Fachperson.

    Da die Person aber so oder so mit irgendwas zu kämpfen hatte, empfahl ich ihr, es professionell abzuklären. Ich gab ihr die Kontaktdaten meiner Psychiaterin, eine der wenigen, die neue Patientys aufnimmt und zeitnah Termine anbieten.

    Nun habe ich gestern erfahren, dass eine Diagnose gestellt wurde: bipolare affektive Störung (BAS)

    Was lernen wir daraus? Nehmt bitte alle ernst!
    🫂
    Vielleicht ist es nicht genau das, was vermutet wird. Aber wie in meiner Geschichte zeigt sich: Hilfe zu bieten ist trotzdem wertvoll, auch wenn es nicht die ursprüngliche Vermutung bestätigt
    ❤️

    #Neurodivergent #ADHS #mentalhealth #bipolardisorder #support #audhd #autismus #adhd

  7. DATE: August 21, 2026 at 04:30AM
    SOURCE: STAT NEWS MENTAL HEALTH

    TITLE: Opinion: Lil Nas X’s bipolar diagnosis and the paradox of treatment

    URL: statnews.com/2026/08/21/lil-na

    When Lil Nas X recently disclosed that he had been diagnosed with bipolar disorder, one part of his story stood out to me more than the diagnosis itself. For years, he had suspected something was wrong. Yet he resisted seeking treatment because he feared medication.

    This is a paradox that exists at the intersection of mental health, identity, and achievement. The people who are most capable of recognizing that something is wrong are often the same people most reluctant to accept help. Not because they deny their suffering, but because they have come to view suffering as an inseparable part of their success.

    Read the rest…

    URL: statnews.com/2026/08/21/lil-na

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #LilNasX #BipolarDisorder #MentalHealthAwareness #TreatmentParadox #MentalHealthInMusic #StigmaFree #TreatmentIsOk #BiPolarAwareness #ArtistsAndMentalHealth #SeekHelpEarly

  8. I’m Happy Being Bipolar

    I’m happy being bipolar

    But I am not sure others are

    I drive them crazy with my moods

    And I don’t have to try that hard

    If you get what I mean

    Everyone is zany in their own way

    All they need is a trigger

    And I am happy to be their trigger

    Life you know is more interesting

    When the world is filled

    With crazy blokes like me

    Else what is there to life

    Except boring work

    And desperate pleasure.

    #BipolarDisorder #Madness #MentalIllness #Poem #Poetry
  9. That Time I Thought All Would Be Right With The World

    It is common knowledge that I have bipolar disorder and PTSD. I write about the diagnosis a lot. I write about my history of, at times, crippling depression. I wrote ad nauseam about various traumas (though not all), mostly romantic in nature. So most people know I can get and have spent significant time depressed. And if we’ve known each other well for any length of time, you might know that the bipolar includes a sometimes difficult to control or mask variety of anger that I am ashamed […]

    carolineprice.com/2026/06/25/t

  10. The carousel, often a symbol of joy, takes on a different meaning for those who struggle with bipolar disorder. We invite you to witness the raw truth behind the smiles.

    youtube.com/shorts/01JHdCajxTU

    #MentalHealth #BiPolarDisorder #SuicideAwareness #BASICStudios

  11. Bonjour, aujourd'hui je ne serai pas présent•e sur Mastodon. Des choses que j'ai lues, adressées à ma personne ou non, m'ont soulé•e. Je souffre de problèmes de santé psychique, j'en parle souvent, alors je n'ai aucune obligation de vous répondre. Désolé•e pour celleux qui attendaient des réponses, mais aujourd'hui peut-être même demain, je me centre sur moi-même.

    Je suis actuellement en hôpital, pour un programme de 10 semaines, je sors jeudi prochain, en attendant cela me demande AUSSI du temps et de l'énergie.

    Et je dois me concentrer dessus. Ça me demande déjà assez d'énergie et de concentration.

    #TDAH #ADHD #Bipolarité #BipolarDisorder #TAG #GAD

  12. @thibaultamartin

    If I am not mistaken, I had ever read or watched somewhere that exposure to sunrise is a great method to reduce bipolar disorder symptoms.

    I remember it has something to do with circadian rhythm.

    #BipolarDisorder

  13. Selena Gomez and Benny Blanco Handle Her Mental Health Together

    Selena Gomez revealed in 2020 that she had been diagnosed with bipolar disorder. Since then, the singer and…
    #NewsBeep #News #Mentalhealth #AU #Australia #bipolar #bipolardisorder #digital_syndication #Health #MentalHealth #motherhood #SelenaGomez
    newsbeep.com/au/532046/

  14. Robert Carradine's Cause of Death: Bipolar Disorder and Suicide

    Actor Robert Carradine, known for Lizzie McGuire, died by suicide at 71 after struggling with bipolar disorder. His family confirmed the news on February 23rd.

    #RobertCarradine, #BipolarDisorder, #SuicideAwareness, #LizzieMcGuire, #MentalHealth

    newsletter.tf/robert-carradine

  15. Actor Robert Carradine, famous for his roles in Lizzie McGuire and Revenge of the Nerds, has passed away at 71. His family shared that he died by suicide after a long battle with bipolar disorder.

    #RobertCarradine, #BipolarDisorder, #SuicideAwareness, #LizzieMcGuire, #MentalHealth

    newsletter.tf/robert-carradine

  16. Completely unbeknownst to me, #RobertCarradine, whom I mentioned yesterday, took his own life a couple of weeks ago after battling #bipolardisorder for decades.

    I only knew him from #RevengeOfTheNerds, where he played alongside people like #CurtisArmstrong, but looking at some of the tribute wheels, we seemed to be a pretty awesome guy.

    Take care of yourselves, folks. #MentalHealth is serious. And in the words of Curtis Armstrong as Booger in #BetterOffDead: Suicide is never the answer, little trooper.

    deadline.com/gallery/robert-ca

  17. Hi! =) I'm an ARTIST from Calgary, Alberta who creates all Original Black and White Art - such as Face Paintings, Abstract Paintings & Poetry Paintings on Canvas as well as One-of-a-Kind Handmade Plush Art Dolls. ♡ Here's some of my Original ABSTRACT PAINTINGS on Canvas available for purchase on my Website + Art Shop at: lyndablack.ca/
    ----> All orders have FREE SHIPPING within Canada ♡

    #Art #Painting #Paintings #BlackandWhite #minimalism #Minimalist #Canvas #OriginalArt #Abstract #AbstractArt #AbstractPainting #Artist #Artists #Canada #ArtShop #ArtForSale #MastoArt #MastodonArt #Handmade #HomeDecor #Calgary #CanadianArtist #Monochrome #ModernArt #TraditionalArt #YYC #bipolar #BipolarDisorder

  18. Scientists Discover Neural Basis of Schizophrenia and Bipolar Disorder -SciTechDaily.com

    Tiny engineered brain models reveal that psychiatric disorders may arise from distinctive disruptions in neural communication rather than obvious structural damage. Credit: SciTechDaily.com

    Health

    Scientists Discover Neural Basis of Schizophrenia and Bipolar Disorder

    By Roberto Molar Candanosa, Johns Hopkins University, December 20, 2025, 8 Comments,
    5 Mins Read

    Facebook Twitter Pinterest Telegram, Share

    Using lab-grown brain tissue, researchers uncovered complex patterns of neural signaling that differ subtly between healthy brains and those linked to severe psychiatric disorders.

    For the first time, scientists have used pea-sized brain organoids grown in the laboratory to uncover how neurons may malfunction in schizophrenia and bipolar disorder. These psychiatric conditions affect millions of people around the world, yet they remain difficult to diagnose because researchers still lack a clear understanding of their underlying molecular mechanisms.

    The results could eventually help clinicians reduce diagnostic uncertainty when treating these and other mental health conditions. At present, such disorders are typically identified through clinical judgment alone, and treatment often relies on lengthy trial-and-error approaches to medication.

    A detailed account of the findings was published in the journal APL Bioengineering.

    “Schizophrenia and bipolar disorder are very hard to diagnose because no particular part of the brain goes off. No specific enzymes are going off like in Parkinson’s, another neurological disease where doctors can diagnose and treat based on dopamine levels even though it still doesn’t have a proper cure,” said Annie Kathuria, a Johns Hopkins University biomedical engineer who led the research. “Our hope is that in the future we can not only confirm a patient is schizophrenic or bipolar from brain organoids, but that we can also start testing drugs on the organoids to find out what drug concentrations might help them get to a healthy state.”

    Annie Kathuria. Credit: Will Kirk / Johns Hopkins University

    Machine learning decodes disease specific signals

    Kathuria’s team created the organoids, simplified versions of brain tissue, by reprogramming blood and skin cells from people with schizophrenia, bipolar disorder, and from healthy volunteers into stem cells capable of forming brain-like structures. They then applied machine learning tools to analyze the electrical activity of the organoids’ cells, allowing them to identify neural firing patterns associated with healthy and diseased states. In the human brain, neurons communicate through small electrical signals.

    Continue/Read Original Article Here: Scientists Discover Neural Basis of Schizophrenia and Bipolar Disorder

    Tags: Annie Kathuria, Biomedical Engineer, Bipolar Disorder, Discover, Health Research, Johns Hopkins University, Mental Health, Neural Basis, Schizophrenia, Scientists, SciTechDaily
    #AnnieKathuria #BiomedicalEngineer #BipolarDisorder #Discover #HealthResearch #JohnsHopkinsUniversity #MentalHealth #NeuralBasis #Schizophrenia #Scientists #SciTechDaily
  19. Mania Insights: AI Listens For Mood Swings In The Voices Of Those With Bipolar Disorder. “A new study from China suggests that artificial intelligence may one day help doctors spot mood swings in people with bipolar disorder just by listening to how they talk. The experimental system correctly identified manic, depressed, and stable states in Mandarin-speaking patients with around 86% […]

    https://rbfirehose.com/2025/12/09/mania-insights-ai-listens-for-mood-swings-in-the-voices-of-those-with-bipolar-disorder/

  20. CW: Hospitalization, mental health (+/-), chronic illness

    Finally coming off an ~5-day* #hypomanic stretch, which is essentially unheard of since my #MECFS worsened some years ago. One or two days is more typical.

    Guess we now know what happens when I can't take my meds for few days.

    On the upsides, I felt good for several days, even including having it probably buoy me over the post-hospital #PEM.

    There will probably be some post-mania PEM, but it's likely to be lesser.

    *I have what I call "rapid-cycling #Bipolar 1.5." It's hypomania, not full mania (Bipolar 1), but lasts longer than Bipolar 2 is "supposed to."\ It's also much more often hypomania than depression, which is good!

    #Mania #Bipolar #BipolarDisorder

  21. CW: 不专业地研究了一下双相的生物化学机制、针对各个机制现代医学层面的应对方法(GPT辅助)

    总体上来说目前的研究或许可以理解为三个方向
    (1) 遗传和环境会如何造成易感性
    (2) 发作期间大脑内生理/化学是如何失衡的
    (3) 前两者的因果关系、从易感到发病的机制(目前因果证据尚不充分,主要是相关性分析为主)
    (4)现代医学、心理学层面的应对方法

    关于研究方法,对于(1)和(2),目前大多是基于已确诊的双相患者进行病例对照式的横断面分析,通过比对基因、生活经历、神经影像、生物标志物等数据,找出一些可能的共同特征。也有部分研究采用任务态fMRI或功能连接分析来进一步细化不同状态下的大脑功能差异。而关于(3),研究相对更少,主要依赖于对高风险人群的纵向追踪(如有家族史的青少年或出现轻躁症状的个体),结合多模态数据进行建模,尝试建立从易感性到发病之间的变化路径,这个方向因果推断目前还相对弱。

    (以下内容有些是GPT生成、后续我进行了事实校验和修改,但可能还是有一些错误)

    【双相期间大脑内生理/化学是如何失衡的】

    发作期间的失衡主要集中在(1)神经递质系统的功能紊乱(2)神经营养因子水平变化(如BDNF)(3)HPA轴与应激反应异常(4)脑区功能连接失衡(前额叶-杏仁核)(5)昼夜节律的紊乱

    「神经递质系统的功能紊乱」
    * 躁期:多巴胺、谷氨酸、去甲肾上腺素等系统在部分脑区(如奖赏中枢)活性升高 → 动能强、冲动多、睡眠少
    * 抑郁期:去甲肾上腺素、血清素等调节系统功能相对减弱(可能与受体敏感性、转运机制相关)→ 情绪低落、动机缺失

    「神经营养因子BDNF变化」
    * 发作期间BDNF水平往往下降(可能是状态标志物) → 神经突触可塑性下降
    (BDNF是否是状态标志物存在争议)
    * 情绪调节系统的神经环路适应能力下降 → 更易进入极端情绪状态(具体因果机制尚不明确)

    「HPA轴与应激反应异常」
    * 慢性应激 → HPA轴过度激活 → 皮质醇节律异常
    * 长期激活可能与海马体功能下降有关 → 情绪恢复力减弱(部分研究提示结构体积变化)

    「脑区功能连接失衡」
    * 杏仁核过度活跃 + 前额叶皮层调控减弱
    * 导致情绪反应放大,自控力下降 → 冲动、攻击、反复自责等症状加剧

    「昼夜节律紊乱」
    * CLOCK、BMAL1等节律基因表达异常 → 内源性生理节律紊乱
    * 可能通过影响褪黑素/皮质醇分泌周期 → 睡眠障碍与情绪周期化(如躁/抑快速交替)

    【遗传和环境会如何造成易感性、和前者的因果关系】

    下文主要包括的部分
    (1)基因突变/表达异常如何导致BD易感性增加
    (2)早期环境可能会如何影响双相相关的大脑调节,让情绪易激惹、恢复能力下降
    (3)遗传环境共同作用于一些因素、导致双相易感性

    1. 一些基因突变或异常表达(如TLR3、LINC02449、CACNA1C、CLOCK、BDNF、ANK3基因)
    → 基因调控异常(如DNA甲基化改变)
    → 影响突触传递、神经发育与行为调节 → 情绪调节网络基础薄弱

    2. 早期环境应激(如童年创伤)可能会导致
    → HPA轴长期过度激活(皮质醇↑)
    → 神经毒性增强、神经可塑性下降,部分个体中海马体功能受损
    → 情绪易激惹 + 情绪恢复能力下降(与慢性应激适应性降低有关)

    3. 基因易感 / 环境应激可能共同影响多个系统,包括线粒体功能、神经营养、节律基因和神经递质调节机制:

    「线粒体功能变化」
    → 线粒体ATP合成效率下降(在部分双相患者中观察到)
    → 神经元能量供应不足 + 自由基累积(ROS↑)
    → 神经突触活动效率下降
    → 情绪调节能力可能受限,特别在应激情境下(机制仍在研究中)

    「神经营养因子BDNF下降」
    * 与神经元新生、突触形成减少有相关性
    * 可影响海马体 - 前额叶皮层 - 杏仁核通路的可塑性
    * 情绪调节、记忆、冲动控制可能因此受损
    (也有观点认为情绪紊乱可反过来抑制BDNF)

    「昼夜节律紊乱」
    * 节律基因表达紊乱 → 褪黑素 / 皮质醇昼夜节律异常
    * 导致睡眠剥夺 + 情绪节律失调
    * 易于发生从抑郁到躁狂的快速转换 → 快速循环或混合发作风险增加

    「神经递质调节异常」
    * 特定脑区多巴胺活性↑(躁狂) / 去甲肾上腺素活性↓(抑郁)
    * 情绪驱动系统出现波动 → 情绪极端化 + 行为不稳定
    * 部分研究指出递质失调可能受基因+应激交互影响

    「神经环路功能变化」
    * 杏仁核-前额叶皮层连接功能减弱
    * 情绪处理系统反应过强,自我控制能力下降
    * 可能表现为易怒 / 冲动 / 冲动决策 / 自杀风险增加
    (但这些功能变化也可能与早发、发作频率、神经营养下降或炎症状态本身相关)

    【调节机制以及现代医学、心理学方法的作用对象】
    1. 神经递质失衡(多巴胺↑、5-HT↓ 等)
    * 调节方式:情绪稳定剂、抗精神病药、抗抑郁药
    * 机制:调节递质释放与受体敏感性,平衡情绪驱动

    2. BDNF下降(神经营养因子减少)
    * 调节方式:锂盐、抗抑郁药、有氧运动、心理干预
    * 机制:促进突触可塑性与神经保护,提高情绪调节能力

    3. 炎症激活(如IL-6↑、TNF-α↑)
    * 调节方式:锂、ω-3脂肪酸、部分抗精神病药
    * 机制:降低神经炎症水平,减缓突触损伤

    4. 线粒体功能障碍(能量代谢↓)
    * 调节方式:锂、NAC、辅酶Q10(实验中)
    * 机制:改善神经元能量供应,降低氧化应激

    5. 昼夜节律紊乱(褪黑素/皮质醇节律异常)
    * 调节方式:锂、褪黑素补充、规律作息、光照疗法
    * 机制:重设生物钟,稳定情绪波动周期

    6. HPA轴激活(应激反应过强)
    * 调节方式:正念疗法、米氮平、情绪调节训练
    * 机制:降低皮质醇水平,增强情绪恢复能力

    7. 脑区连接异常(前额叶-杏仁核通路)
    * 调节方式:锂、CBT、经颅磁刺激(TMS)
    * 机制:增强自我控制系统对情绪中心的调节作用

    最常用的两种方法,锂被认为可以作用于除了HPA激活以外的环节,心理谈话治疗可以作用于增加神经营养因子、HPA激活和脑区链接异常。

    【参考】
    * Cai et al. (2025). Spatiotemporal dynamics in bipolar disorder. Molecular Psychiatry.
    * Yang et al. (2025). LINC02449 expression and synaptic dysfunction in BD. Nature Communications.
    * Oliveira et al. (2025). Biological rhythms disruption in latent bipolar disorder. Springer.
    * Aflouk et al. (2026). TLR3 polymorphisms and BD. Molecular Biology Reports.
    * Mezzomo et al. (2025). Metabolomics in stress-related disorders. Naunyn-Schmiedeberg’s Arch Pharmacol.
    * ENIGMA Bipolar Disorder Working Group (2025). Childhood trauma, brain morphology and BD. medRxiv.
    * Cochran et al. (2025). Modeling mood dynamics in bipolar disorder. Current Psychiatry Reports.
    * HC Kim (2025). Mitochondrial dysfunction in BD and metabolic disorders. KoreaMed.
    * Freudenberg F. (2026). Nitric oxide’s role in mood disorders. Biol Psychiatry Global Open Science.
    * Ghaemi et al. (2003). Antidepressants and rapid cycling. Am J Psychiatry.

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