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  1. DATE: October 15, 2026 at 02:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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    TITLE: Machine learning uncovers early warning signs of depression in brain scans

    URL: psypost.org/deep-learning-mode

    A new computational model combined with brain imaging data reveals that relying too heavily on prior expectations when perceiving facial expressions can predict a person’s risk for developing depression. By analyzing how the human brain processes angry faces, researchers identified a mathematical pattern of visual distortion that appears up to four years before clinical symptoms emerge. The study was published in Science Advances.

    Major depressive disorder affects millions of people worldwide and is often difficult to treat once established. Early detection remains a high priority for public health experts, but predicting who will develop the condition relies mostly on self-reported symptoms and environmental risk factors. Identifying biological markers that indicate an individual’s vulnerability before they feel ill could improve prevention efforts.

    Mental health conditions are often characterized by altered emotional processing, such as a tendency to interpret ambiguous social cues as negative or threatening. Leading psychological theories propose that our brains construct emotional experiences by using abstract concepts stored in our memory to interpret raw sensory information, like the visual details of a face. In recent years, researchers have mapped out various brain regions associated with depression, but these descriptive patterns do not explain the exact mechanisms driving the illness.

    Han Lu and Qiang Luo, researchers at Shenzhen University and Fudan University, respectively, sought to understand how this integration of sensory input and abstract memory might go wrong in people prone to depression. They hypothesized that the visual cortex, the brain region responsible for processing sight, might act as an early bottleneck where social threat signals become distorted. To test this idea, the researchers developed a mathematical simulation to replicate how the human brain learns to recognize emotional expressions.

    The researchers first analyzed functional magnetic resonance imaging brain scans from 1,332 nineteen-year-old participants in a population-based European study known as the IMAGEN cohort. This imaging technique measures blood flow in the brain to detect areas of neural activity. The scans tracked the adolescents’ brain activity while they viewed short video clips of faces transitioning from neutral expressions to angry ones.

    Using a machine learning algorithm, the research team extracted a mathematical representation of how each participant’s visual cortex encoded the angry faces. They refer to this specific pattern of neural activity as a visual code. The team then grouped the participants based on the efficiency of these visual codes, separating them into one group with typical, highly efficient visual encoding and another with inefficient, noisy visual processing.

    Adolescents in the less efficient group reported higher levels of emotional symptoms, such as anxiety and low mood, on clinical questionnaires. This relationship indicated that a degraded visual representation of angry faces was tied to emotional distress. The researchers determined that poor visual coding in the brain was directly related to the presence of emotional symptoms.

    To understand the computational mechanism behind this degraded visual processing, the team built a deep neural network, which is an artificial intelligence model composed of interconnected algorithms modeled after the human brain. This specific model featured two distinct processing pathways. One pathway processed raw visual information from images, while the other pathway held abstract conceptual knowledge about different emotions.

    In standard human perception, the brain uses abstract knowledge to guide and speed up the processing of visual information, allowing a person to recognize a facial expression quickly. The researchers programmed their artificial network to mimic this process, allowing the conceptual pathway to regulate the visual pathway as the model learned to identify facial expressions. When the researchers compared the artificial network’s internal mathematical code to the human brain scans, they found a strong alignment.

    This similarity suggested the model successfully replicated the visual perception of angry faces. The team then conducted an experiment on the model by altering the strength of the conceptual pathway’s influence over the visual pathway. They systematically turned the regulation strength up and down to observe how the network would respond.

    When the regulation was set to an intermediate level, the model achieved optimal emotion recognition. However, when the researchers forced the model to apply excessive conceptual regulation, it began to misclassify neutral faces as angry or sad. This overreliance on abstract concepts overrode the actual visual details, producing a computational negative bias.

    The internal code of this overly regulated artificial model closely matched the inefficient, noisy brain patterns found in the adolescents with higher emotional symptoms. This suggests that overregularization, which is the act of letting preexisting beliefs overpower sensory reality, acts as a mechanism that drives negative emotional biases.

    Building on this simulation, the researchers created a computational marker that quantified each human participant’s degree of visual overregularization based on their brain scans at age nineteen. They then followed up with 725 of these participants four years later. The goal was to see if the marker could forecast the onset of mental health issues.

    Among the young adults who had no clinical symptoms at age nineteen, the mathematical marker successfully predicted which individuals would develop high levels of emotional symptoms by age twenty-three. This prediction model outperformed traditional baseline measures that rely only on demographics and basic brain activation levels. The finding suggests that the overregulation mechanism may precede the onset of emotional symptoms.

    To determine if this computational mechanism was specific to depression, the team examined genetic data from the IMAGEN participants. They checked for associations between the overregulation marker and genetic variants tied to various psychiatric conditions. The analysis showed a link between the overregulated visual marker and a specific genetic variant associated with major depressive disorder, located on a gene involved in brain development.

    The marker was also linked to the participants’ polygenic risk score for depression, which is a number that summarizes the estimated effect of many different genetic variants on a person’s risk for a disease. The visual marker did not show any links to the genetic risks for alcohol use disorder or eating disorders. This specificity supported the idea that the visual distortion mechanism is uniquely tied to depression.

    Finally, the researchers tested their marker in a separate clinical dataset of young adults to see if it persisted in established illnesses. They analyzed brain scans from 134 patients diagnosed with major depressive disorder and 62 healthy control subjects. The patients with depression exhibited higher levels of the overregulation marker compared to the healthy controls.

    The marker accurately classified whether a participant had depression or not. When applied to patients with alcohol use disorder, anorexia nervosa, and bulimia nervosa, the marker showed no group differences. The traditional brain activation measures were not statistically significant in distinguishing the depressed patients from the healthy controls.

    The study participants from both the population-based and clinical cohorts were predominantly white individuals from middle-to-high socioeconomic backgrounds. Future research will need to examine whether these specific computational patterns apply equally to populations with different ethnic, racial, and socioeconomic demographics. The differences in emotional symptoms between the high-efficiency and low-efficiency visual processing groups in the general adolescent sample were also relatively small.

    While expected in general population studies capturing subclinical distress, this small effect size means the visual clustering approach alone has limited diagnostic power for individual patients at this stage. Researchers must validate the broader clinical utility of this marker in independent patient groups. Tracking these computational markers in younger adolescents could reveal if the visual distortions appear even earlier in development.

    Tracking patients over time will also help determine if the marker can predict long-term recovery versus chronic illness. Identifying whether the visual distortion is a permanent trait or a temporary state would assist in designing targeted therapies. Interventions that aim to retrain visual processing might one day help mitigate this depression risk.

    The study, “Deep learning reveals a neurocomputational mechanism predicting depression risk in adolescents,” was authored by Han Lu, Xiaoqian Yan, Benjamin Becker, Andreas Heinz, Barbara J. Sahakian, Christelle Langley, Zhaoyu Zuo, Luolong Cao, Zuo Zhang, Lauren Robinson, Nilakshi Vaidya, Jeanne Winterer, Sinead King, Charlotte Walton, Tobias Banaschewski, Gareth J. Barker, Arun L.W. Bokde, Rüdiger Brühl, Herta Flor, Hugh Garavan, Penny Gowland, Antoine Grigis, Herve Lemaitre, Jean-Luc Martinot, Marie-Laure Paillère Martinot, Eric Artiges, Frauke Nees, Dimitri Papadopoulos Orfanos, Luise Poustka, Hedi Kebir, Ulrike Schmidt, Julia Sinclair, Michael N. Smolka, Sarah Hohmann, Nathalie Holz, Henrik Walter, Robert Whelan, Sylvane Desrivières, Gunter Schumann, Qiang Luo, STRATIFY/ESTRA Consortium, and IMAGEN Consortium.

    URL: psypost.org/deep-learning-mode

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #DepressionPrediction #Neuroimaging #MachineLearning #Brain scanBiomarkers #VisualProcessing #EmotionalBias #MentalHealthResearch #EarlyDetection #NeuralMarkers #MajorDepressiveDisorder

  2. DATE: October 9, 2026 at 02:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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    TITLE: Emotional blunting is common in depression and bipolar disorder, even after symptoms ease

    URL: psypost.org/emotional-blunting

    A study of Thai outpatients receiving treatment for depression found that more than half reported emotional blunting, a dulling of emotional responses. Rates did not differ significantly among people with major depressive disorder, persistent depressive disorder, and bipolar disorder, and emotional blunting was less common among patients whose depression was in remission, though it remained common in that group as well. The paper was published in BMC Psychiatry.

    Major depressive disorder is one of the most common mental health conditions worldwide, affecting hundreds of millions of people. Estimates suggest that its global prevalence rose by roughly 27% in 2020 alone, as the COVID-19 pandemic brought stress, isolation, and economic disruption.

    Major depression does not have a single cause but instead develops through a combination of biological, genetic, physical, behavioral, and environmental influences. Adverse childhood experiences such as abuse, neglect, bullying, and domestic violence are particularly important risk factors and are also associated with poorer treatment response and a greater chance of depression recurrence.

    One common feature of depression is emotional blunting, in which people experience reduced emotional responsiveness. The term covers experiences such as apathy, loss of motivation, anhedonia (a reduced ability to feel pleasure), emotional numbness, and diminished empathy. Emotional blunting appears to be especially common during acute episodes of depression and may persist after treatment.

    Emotional blunting is also a known side effect of some antidepressants, particularly selective serotonin reuptake inhibitors, which can leave people feeling emotionally indifferent or unable to cry. It can impair daily functioning, and in one recent study, up to 40% of patients said they had considered stopping their antidepressant because of it.

    Study author Narak Chadbunchachai and colleagues at Khon Kaen University in Thailand set out to measure how common emotional blunting is among patients whose depression was mild to moderate or in remission, and to examine its links to childhood adversity. They expected emotional blunting to be more intense among remitted patients who had experienced more adversity in childhood.

    Participants were 106 outpatients at a university hospital in Thailand who had major depressive disorder (61 of them), persistent depressive disorder (19), or bipolar I disorder (26). Persistent depressive disorder is a long-lasting form of depression in which a person has a depressed mood for most of the day, on more days than not, for at least two years, often with additional symptoms such as low energy, poor self-esteem, and hopelessness. Participants’ average age was 29 years, and 73% were women.

    To take part, patients had to have mild to moderate symptoms, could not be at risk of suicide, and had to have been on the same antidepressant treatment for at least a month. Half of the participants met the criteria for remission, meaning they had few remaining symptoms on a clinician-rated depression scale.

    Participants were first asked a single screening question from the Oxford Depression Questionnaire about whether, in the past six weeks, they had felt emotionally numbed or blunted, detached from the world around them, or as if they no longer cared about things they used to care about. They then completed the full 26-item questionnaire, which measures the intensity of emotional blunting across several dimensions, along with a questionnaire on adverse childhood experiences and two measures of depression severity.

    Based on the screening question, 56% of participants reported emotional blunting. The rate was 51% among those with major depressive disorder, 63% among those with persistent depressive disorder, and 62% among those with bipolar disorder, differences that were not statistically significant. On the full questionnaire, most participants scored in the “minimal” range, 36% scored in the “mild” range, and one person scored in the “severe” range.

    Emotional blunting was less common among participants whose depression had remitted (45%) than among those whose depression had not (66%). Across the whole sample, people with more severe depressive symptoms and more past mood episodes tended to report more intense emotional blunting, though these associations were modest. Among remitted patients, blunting was not linked to symptom severity.

    The links with childhood adversity were limited to specific parts of the questionnaire and were weak. One aspect of emotional blunting, not caring about things, tended to be stronger among participants who reported more frequent emotional or physical abuse in childhood and among those who reported less emotional support from their families. Overall emotional blunting scores were not significantly linked to any type of childhood adversity.

    Among remitted patients, the links between not caring and both emotional abuse and low emotional support held, and a second aspect, feeling emotionally detached, was associated with more frequent domestic violence in childhood. When the researchers accounted for how much participants attributed their blunting to their antidepressants, only the link between not caring and low emotional support remained statistically significant.

    “Remission was associated with a lower prevalence of EB [emotional blunting]; however, the prevalence remained high even among remitters,” the study authors concluded.

    The study contributes to the scientific knowledge about depression. However, it should be noted that the design of this study does not allow any causal inferences to be derived from the results. Additionally, the assessment of adverse childhood experiences was based on participants’ current memories of their childhood events, leaving room for recall bias to have affected the results.

    All participants were taking antidepressants, and more than 90% attributed at least some of their emotional blunting to their medication. Because the study had no comparison group of remitted patients who were not taking antidepressants, it cannot separate emotional blunting as a lingering symptom of depression from emotional blunting as a side effect of treatment.

    The paper, “Prevalence of emotional blunting and its association with childhood adverse experiences in depressive episodes,” was authored by Narak Chadbunchachai, Papan Vadhanavikkit, Sirinapa Aphisitphinyo, Pattharee Paholpak, Nawanant Piyavhatkul, Parinda Pienroj, and Pongsatorn Paholpak.

    URL: psypost.org/emotional-blunting

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #EmotionalBlunting #DepressionAwareness #BipolarDisorder #MajorDepressiveDisorder #PersistentDepressiveDisorder #AntidepressantSideEffects #MentalHealthResearch #ChildhoodAdversity #RemissionAndRecovery #BMCPsychiatry

  3. DATE: September 26, 2026 at 06:00PM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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    TITLE: Suicidal behaviors are more heritable than depression, new twin study finds

    URL: psypost.org/suicidal-behaviors

    An analysis of the Brisbane Longitudinal Twin Study data found moderate associations between genetic risk factors for suicidal thoughts and behaviors and major depressive disorder. However, environmental factors contributing to major depressive disorder were largely distinct from those contributing to suicidal thoughts and behaviors. The paper was published in Behavior Genetics.

    Suicidal thoughts and behaviors are a major public health problem. They include suicidal ideation (i.e., thinking about suicide), planning suicide, suicide attempts, and suicide deaths. Major depressive disorder is one of the strongest known risk factors for suicidal behavior, although suicide risk cannot be explained by depression alone.

    Twin and family studies indicate that suicidal thoughts and behaviors are partly heritable, suggesting that genetic differences contribute to individual vulnerability. Large genetic studies have identified many common genetic variants associated with suicide-related outcomes, but each variant contributes only a very small amount of risk. Researchers therefore increasingly use polygenic risk scores, which combine information across large numbers of genetic variants to estimate an individual’s inherited susceptibility.

    Polygenic scores for both major depression and suicidal behavior have shown modest associations with suicide-related outcomes in previous studies. The genetic overlap between suicidal behavior and psychiatric disorders suggests that some of the same biological vulnerabilities may contribute to several different forms of psychopathology. At the same time, some people who experience suicidal thoughts or engage in suicidal behavior have no clear history of psychiatric disorders, indicating that additional genetic, psychological, and environmental pathways must also be involved.

    With this in mind, study author Nathan A. Gillespie and his colleagues explored the contribution of polygenic risk scores for major depression and suicide attempt to suicidal thoughts and behaviors. They focused on three aspects of suicidal thoughts and behaviors: suicidal ideation, suicide plans, and suicide attempts. They hypothesized that polygenic risk scores for suicide attempts and major depression would explain a small amount of variation in self-reported suicidal thoughts and behaviors. These researchers also aimed to explore how much the genetic risk factors for the three aspects of suicidal thoughts and behaviors overlap.

    Study authors analyzed data from the ongoing Brisbane Longitudinal Twin Study (BLTS). While this overall study was launched in 1992 and included over 7,000 young adult twins, siblings, and parents of European ancestry, this specific analysis focused on a subset of 2,876 participants. Assessments were carried out when twins were 12, 14, 16, 21, and 25 years old.

    These analyses used data on participants’ self-reported suicidal behaviors and from a genome-wide association study (GWAS)—a study that scans the genomes of many people to find genetic variations associated with a particular disease or trait—conducted in the scope of this program. Study authors created two polygenic risk scores, one for major depression and one for suicide attempts, based on summary statistics from two large previous studies.

    The results showed that the heritability of suicidal behaviors was estimated to be between 51% and 80%. This was much higher than the estimated heritability of major depressive disorder (39% to 41%). The polygenic risk score for major depression had more consistent associations with the diagnosis of major depressive disorder, while both polygenic risk scores had modest associations with suicidal behaviors. The three types of suicidal thoughts and behaviors were strongly genetically correlated with each other, and they showed a moderate genetic correlation with major depressive disorder.

    Interestingly, non-shared environmental factors (unique individual experiences rather than shared family environments) contributing to the diagnosis of major depressive disorder were largely distinct from those influencing suicidal thoughts and behaviors.

    “This study provided compelling evidence for shared genetic architecture between DSM-IV MDD [major depressive disorder diagnosis] and STBs [suicidal thoughts and behavior]. The MD PRS [polygenic risk score for major depression] demonstrated more consistent prediction of MDD [major depressive disorder] compared to the SB PRS [polygenic risk score for suicide attempts], though both showed modest correlations with suicide outcomes,” the study authors concluded.

    The study contributes to the scientific understanding of the genetic bases of suicidal behaviors and depression. However, study authors note that they jointly analyzed data from men and women, potentially leaving some sex differences in genetic architecture unaccounted for.

    The paper, “Genetic Overlap Between DSM-IV Major Depressive Disorder and Suicidal Behaviors: Evidence from Polygenic Risk Scores in Young Adult Twins,” was authored by Nathan A. Gillespie, Mei-Hsin Su, Séverine Lannoy, Mallory Stephenson, Miguel E. Rentería, Zuriel Ceja, Ian B. Hickie, Nicholas G. Martin, and Alexis C. Edwards.

    URL: psypost.org/suicidal-behaviors

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #GeneticHeritability #SuicidalBehavior #MajorDepressiveDisorder #PolygenicRiskScores #TwinStudy #BehaviorGenetics #SuicideRisk #HeritabilityEstimates #MentalHealthResearch #DSMIVMDD

  4. DATE: September 21, 2026 at 04:53PM
    SOURCE: PSYCHIATRIC TIMES

    Direct article link at end of text block below.

    Explore evolving perspectives on the diagnosis, management and treatment considerations in major depressive disorder and bipolar I disorder. Read more: t.co/mTTIBK2U21 #Sponsored t.co/bS0wQWN2C9

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #psychotherapist #MajorDepressiveDisorder #BipolarI #MentalHealthAwareness #DepressionTreatment #BipolarDisorderCare

  5. Add-on drug lumateperone boosts sexual function in patients with depression

    Patients with major depressive disorder (MDD) and an inadequate response to standard antidepressants who received an add- on…
    #NewsBeep #News #Health #antidepressant #AU #Australia #depression #depressivedisorder #majordepressivedisorder #medicine #Placebo #psychiatry #research #SexualDysfunction #therapy
    newsbeep.com/au/893151/

  6. Depression in the US

    Depression is staggeringly common in the United States, with more than one in four adults reporting having been diagnosed with the condition in their lifetimes. In a given year, more than 8 percent of U.S. adults might report a major depressive episode. And there are more than 500,000 hospitalizations for a depressive disorder each year.

    Symptoms of depression can include sadness or low mood, feelings of worthlessness or guilt, or a loss of interest in things someone used to enjoy. But they can also involve more physical symptoms, such as slowed movements and changes in appetite or sleep, and cognitive issues, like brain fog or difficulty making decisions.

    Full article here:

    https://www.nytimes.com/2026/06/30/nyregion/depression-thomas-kean-symptoms-treatment.html?unlocked_article_code=1.uVA.jhTg.97rh3L0BgRlO&smid=url-share

    #Depression #MajorDepressiveDisorder #MentalIllness
  7. Neumora Ends Depression Drug Programme and Announces Workforce Reduction (NMRA)

    medical research red syringe NEW SIZE ©rawpixel Neumora Therapeutics (NASDAQ:NMRA) said on Monday that it will halt development…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Mentalhealth #depressiontreatment #drugcandidate #Health #majordepressivedisorder #MentalHealth #NeumoraTherapeutics
    newsbeep.com/us/706188/

  8. Depression’s “Energy Crisis”: Fatigue Starts at the Cellular Level

    Summary: Fatigue is one of the most debilitating and hardest-to-treat symptoms of major depressive disorder (MDD). New research…
    #NewsBeep #News #Mentalhealth #ATP #bioenergetics #Fatigue #Health #majordepressivedisorder #MDD #MentalHealth #Mitochondria #Neuroscience #Psychology #UK #UnitedKingdom #UniversityofQueensland
    newsbeep.com/uk/470737/

  9. DATE: August 30, 2025 at 06:00PM
    SOURCE: PSYCHIATRIC TIMES

    Direct article link at end of text block below.

    Explore MDD strategies in our Clinical Consult series. #ad For psychiatrists, NPs, and advanced practice clinicians. Watch here: t.co/G6hWN8fNK4 #PsychiatricTimes #ClinicalConsult #majordepressivedisorder t.co/jmeQ6aupsx

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #psychotherapist

  10. I ended up going down a little rabbit hole about #neurodivergence and #depression. I would consider myself #neurodivergent because my depression is lifelong and greatly impacts my daily life. I thought this article was informative as well as interesting. What do y'all think? #mentalhealth #mentalillness #mdd #majordepressivedisorder #depression #askfedi

    neurolaunch.com/is-depression-

  11. Spent time under my favorite oak tree doing, what I call, introspective work. This is the mental work of acknowledging my feelings and letting them pass. I've spent my whole life running from feelings I didn't understand, trauma I didn't know I had. It's still a hard skill to master, but I'm getting better at not running from my own feelings. I've been overwhelmed by the state of the administration in this country. The anxiety stirs up feelings from my past where I've felt the same, pressure coming in from all sides, not safe, insecurity. I finally worked on those feelings today, letting them come to the surface so I can let them leave. My work is never done. Although none of this is my fault, it is my responsibility to work through it. #majordepressivedisorder #mentalhealth #journaling #anxiety #wordvomit #thegreatoutdoors

  12. Hello friends! I think another #introduction is in order.

    I'm in my 30s and my husband and I are #childfree We live in the #roanokeva area and it's been hard making like-minded friends! I practice non-deity specific #magick and #tarot and I have an #altar that I'll frequently share. I'm a #gardener and my college degree is in #EnvironmentalStudies I'm also very open about my journey with #majordepressivedisorder , my spirituality and how I view the world. I'm an avid book #reader and I'm currently in the middle of a few books right now! I'm hoping to meet new people and maybe make some meaningful friendships ✨️😌

  13. anyone with experience with transcranial magnetic stimulation #TMS #TranscranialMagneticStimulation ?

    positive or negative results for treatment of major depressive disorder?

    or experience with #Esketamine for #depression?

    🧠 🧲 🧠 🤕 🧠 🤯 🧠 🫨 🧠 😻 🧠 🤷🏽 🧠

    #Boost #MentalHealthMetaphor #MentalHealth #Psychology #Psychiatry #Psych #MajorDepressiveDisorder #MDD #PTSD

  14. pubmed.ncbi.nlm.nih.gov/388583 Planar cell polarity proteins mediate ketamine-induced restoration of glutamatergic synapses in prefrontal cortical neurons in a mouse model for chronic stress (Freitas,et al, 2024) #ketamine #chronicstress #stress #ketaminetherapy #psychedelics #psychedelic #psychedelicresearch #research #depression #majordepressivedisorder

  15. So under normal circumstances this wud be a #Sicide night. I cannae dae that because of a promise I made, so in spite I destroyed something good that cud possibly happen tae me. I f**king hate this but it improves the odds of me being right. I donnae ken whae I am posting this, none of ye fucking ken me. I really dae hate bein meh. #MajorDepressiveDisorder #BorderlinePersonalityDisorder #SuicidalIdeations

  16. CW: Mental health issues - s*ic*de

    I am graduating. It is bittersweet. If it wasn’t for WGU, i probably wouldn’t be here today. Literally. Along with my family, my program mentor and the free counseling provided by the college saved my life.

    1 year into school my sister tried to die by overdosing on ambien, and our mom didn’t care. that drove me down into a severe mental breakdown. The guilt of not being there for her was so overwhelming, i wanted it all to end.

    My husband convinced me to use the free counseling available from school. There, i was convinced to seek professional help.

    My program mentor supported me the entire time throughout my mental health journey. Adjusting to my medication, dealing with emotions unearthed at therapy, guilt for not being able to do course work, she helped me with all of that. So i was able to finish all my coursework required to student teach. i was ready to become a math teacher.

    What we didn’t expect though was my inability to pass any of the high stakes exams required to pass for licensure.

    This lead to my first ADHD paralysis episode where my brain just disassociated when i tried to open my laptop.

    In the end i didn’t pass the tests after 6 tries. I didn’t get licensed, but my mental and physical health has been the best ever in my 40 years of life.

    #MentalHealthStory
    #WGU
    #MajorDepressiveDisorder
    #Adhd
    #LateDiagnosis
    #Disabilities

  17. Your reminder that living with #MajorDepressiveDisorder is a daily fight for survival. Even when it’s in remission. Even when you found a miraculous treatment that works for you.

    It never goes away, just recedes into the shadows because it is of the shadows. #depression #TMS

  18. last post made me want to do another #introduction.

    I am naura (she/her) 40 something wife, mom of three humans and a dog. living on stolen ohlone land.

    I joined the fedi-verse during the great red**t exodus of 2023.

    I am late diagnosed #ADHD, #TraumaSurvivor, live with #MajorDepressiveDisorder
    #AntiFascist #Leftist

    Current interests:

    #StarTrekVOY
    #WhiteoutSurvival (state 732)
    #TingusGoose
    #drawing
    #StarTrekProdigy
    #StarTrekStrangeNewWorlds
    #Cooking
    #MathEducation

    🖖🏽

  19. The end of the year is always a mentally draining part of my life.

    March is on its way. I hope to be back on more often. 🖖🏽

    #majordepressivedisorder
    #mentalhealth

  20. Just came back from a 3w social media break so i am here to introduce myself again!

    I am naura.

    40 something mom to 3 amazing #Homeschooled kids, spouse to an amazing person, #uchinanchuu, #Trekkie, #JC shipper, #MathNerd, #antifascist, #leftist, #ADHD, living with #MajorDepressiveDisorder on stolen ohlone land.

    In #ADHD fashion i have a lot of interests. My current one is #DigitalArt learning mostly manga type of drawing.

    #introduction
    #introductionV3
    #NiceToMeetYall

  21. I let my trintrellix lapse and i am once again reminded that MEDS WORK. I felt better after a few hours taking it again just like the first time i took it. It wasn’t a new me, it was like i finally could truly feel.

    I take high blood pressure meds and they work well for me too.

    They aren’t any different.

    Your mental health is just as important as your physical health.

    #MentalHealth
    #antidepressants
    #majordepressivedisorder

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