The Rundown: Elon Musk’s Neuralink shared a clip of its clinical trial participants with paralysis driving a brain-computer interface-powered wheelchair — steering, reversing, and adjusting their chairs using only their thoughts.
The details:
The 1,000+ electrodes in Neuralink’s brain implant record neurons firing in the motor cortex, just as a participant thinks about moving in a particular direction. A decoding algorithm converts these brain signals into on-screen cursor movement, which appears in a custom app with a live feed of what’s ahead.As the cursor moves, custom electronics convert its position into analog signals driving the chair — up for forward, down for reverse, left/right to steer.Study participant Alex said driving became “second nature” in minutes with the BCI, and that it beats a joystick that forces his head into a hunched position.
Why it matters: Going from thought-to-cursor to actual hardware control is a step up for Neuralink, showing how its technology can help millions living with paralysis. But rivals like Synchron are chasing the same results without opening the skull, leaving open whether the richer signal from an implant is worth the operating table.
The Rundown: A rural New York school district is putting a lifelike humanoid in its high school this fall — spending nearly $58K on Sally, a silicone-skinned AI tutor that will help students with coding, robotics, and math, among other things.
The details:
Built by Realbotix, Sally stays stationary but moves its torso and makes facial expressions, guiding students through problems rather than giving answers.The school says the robot does not record audio or video, and responds only with approved knowledge — anything beyond gets an “I don’t know” response. Most of the tutoring is handled through Optio, a companion avatar that handles homework support, translations, and past sessions via student codes.The district stressed Sally won’t replace teachers, calling it an instructional tool meant to engage students and spark curiosity about emerging technologies.
Why it matters: Chatbot tutors are everywhere, but nobody has shown that giving them a body makes a difference in students’ learning experience. With Salamanca paying a hefty amount for Sally, we may soon get an early glimpse of what students actually learn (and feel) when there’s a machine nearby, trying to teach STEM concepts.
Summary: Researchers revealed that fruit flies (Drosophila melanogaster) navigate odor plumes using a sophisticated directional memory system rather than basic sensory reflexes.
Using a virtual-reality treadmill coupled with real-time neural imaging, researchers discovered that flies consistently navigate along the outer boundary of a scent plume, a strategy termed “edge tracking.” Every time a fly crosses into and out of the plume, a specialized set of neurons (FC2 neurons) within the brain’s central complex stores an angular directional memory pointing back toward the plume edge.
This internal compass allows the insect to dynamically re-orient toward the scent source even when wind conditions shift or the odor wafts away.
Key Facts
Edge Tracking Strategy: Rather than walking down the center of an odor plume or blindly heading upwind, fruit flies weave along the boundary of the scent, using the edge as a spatial guidepost.
Central Complex Neural Compass: Directional navigation is driven by FC2 neurons in the central complex, an ancient brain region responsible for spatial orientation in insects like bees and ants.
Dynamic Angular Memory: Inside an odor plume, FC2 neurons reflect the fly’s current heading. The moment the fly exits the plume, these neurons pivot to encode an angular memory pointing back to the plume boundary.
Robustness to Wind Shifts: Edge tracking allows flies to successfully reach an odor source even if the plume is angled perpendicular to the wind or rapidly shifting position.
Essential Circuitry: Silencing FC2 neurons completely abolishes the fly’s ability to turn back toward the plume after exiting, confirming that plume recovery relies on stored spatial memory rather than simple reflexes.
Source: Rockefeller University
When a fruit fly catches a whiff of a ripe peach, it quickly heads toward it. Time after time, it finds the fruit—even from many feet away and even if the scent arrives only as a few drifting, disconnected puffs.
How do they home in with such unerring accuracy? Scientists have long assumed that all insects track smells with simple reflexes, turning straight upwind when they smell something appetizing.
Fruit flies rely on FC2 neurons in the central complex to maintain an angular directional memory, enabling memory-guided edge tracking across complex, shifting odor plumes. Credit: Neuroscience News
Now, researchers in Vanessa Ruta’s lab at Rockefeller University have found that flies use a more complex navigational strategy, which relies on a sophisticated memory system.
As flies track an odor, they weave along the edge of the odor’s plume. Each time they cross into and out of the plume, they store a directional memory that points back toward the scent plume, transforming a fleeting odor encounter into a spatial memory. This stored memory is what allows them to keep navigating towards the odor source even if the plume is not aligned with the wind or wafts away.
The findings, published in Nature, show that odor tracking is not just a reflexive response but instead, flies use brain circuitry for spatial navigation to remember where a plume boundary lies and steer back to it.
“Odors are some of the richest cues animals use to navigate, but they are also some of the most difficult to navigate and to study, because they are invisible and constantly shifting,” says Ruta, head of the Laboratory of Neurophysiology and Behavior. “We wanted to understand how an animal builds a working picture of a chemical world it can’t actually see.”
Following the edge
Ruta’s team built a virtual-reality system in which a fly walks on an air-supported ball, able to turn and move forward or backward in place, like a rotating treadmill. As the fly turns, a nozzle delivering a steady air stream rotates to match, mimicking wind from a fixed direction. When the fly reaches set points on a virtual map, the researchers pipe in precise amounts of apple cider vinegar scent, allowing them to create defined odor landscapes.
“The advantage of this kind of very controlled environment is that we know exactly what the fly is smelling at every moment,” says Charles Dowell, a postdoctoral associate in the Ruta lab and an author on the study. “That is something that is very hard to pin down with real, physical plumes of odor in the natural environment.”
The team expected flies to steer upwind and track within the center of an odor plume. Instead, flies consistently tracked along just one edge of a plume, darting into the odor, quickly turning out of the plume, then walking in clean air before returning. The researchers call this pattern “edge tracking.”
To test how well this strategy worked, Ruta’s group changed the conditions that flies had to contend with—angling the plume relative to the wind or shifting the plume’s position every time a fly left it. They showed that flies could efficiently track a plume even if was perpendicular to the wind direction, underscoring edge tracking is a remarkably flexible and robust strategy.
The team also exposed flies to a recording of how a real, physical odor plume drifts and breaks apart in moving air. In the most turbulent regions of the plume, where odor encounters were too fragmented for angular memories to be reliable, flies appeared to rely on other search strategies. But closer to the odor source, where the plume became more coherent and predictable, flies transitioned to memory-guided edge tracking.
“A turbulent plume is fragmented and very complicated; flies could be facing any particular direction,” says Silas Busch, a postdoctoral fellow in the lab. “But remarkably, the flies still found their way to the region where the plume was likely to be, and tracked its edge in the same way. That was a really exciting moment for me, realizing this behavior scales across very different kinds of odor structures.”
A compass in the brain
By monitoring activity in the flies’ brain cells at the same time the insects were immersed in the virtual reality environment, the team were able to home in on the importance of the brain’s central complex—an ancient insect brain region that supports spatial navigation. They found that a set of cells called FC2 neurons that encode a fly’s navigational goals didn’t always remain fixed in one direction. While a fly was inside an odor plume, the FC2 neurons pointed in the fly’s current direction.
Once the fly left the plume, however, the cells pointed back toward its edge, suggesting that these neurons reflect the angular memory to return to the plume. Silencing FC2 neurons left flies unable to return to the scent. The results reaffirmed that the flies weren’t simply following sensory cues back to the plume, but using a form of directional memory.
“It took us a while to convince ourselves that this really relies on an angular memory,” Ruta says. Unlike a bee returning to its nest, a fly tracking a plume has no single location to aim for, since the scent itself drifts.
“The plume isn’t found in a specific location, so tracking it does not require flies to store the exact position of the plume. Instead we found they use a directional memory that allows the fly to use each odor encounter at the plume’s boundary as a chemical signpost to help them track to the source.”
The new findings reframe odor tracking as a sophisticated form of spatial memory rather than a simple reflex.The reliance on the central complex suggests that tracking a fleeting drifting plume relies on the same brain architecture that ants and bees use to find their nests. More broadly, the work highlights how flexibly the circuitry of the central complex can be used in different sensory contexts, allowing animals to use odors as dynamic spatial cues.
“When people think about fruit flies, they imagine they are simple, reflexive little creatures,” Ruta says. “But when you consider what they have to contend with in their natural environment, you find they are using strategies that are adaptive, flexible, and surprisingly sophisticated—mechanisms we might have expected only in animals with much bigger brains. The power of the fly is that we can now begin to understand how those computations are built by the brain.”
Key Questions Answered:
Q: Why was it previously assumed that insects only use reflexes to follow smells?
A: Traditional models suggested that insects use simple anemotaxis, a reflex where an animal senses a smell and automatically turns directly upwind. Because odor plumes in nature are invisible and turbulent, it was difficult to observe the precise moment-by-moment corrections insects make at the plume boundary.
Q: How do FC2 neurons act as an internal compass for the fly?
A: FC2 neurons in the brain’s central complex keep track of heading directions. While inside a scent plume, they track the fly’s real-time movement. When the fly steps out of the scent, these neurons maintain an “angular memory” vector pointing back toward where the scent was last detected, serving as a chemical signpost to steer the fly back on course.
Q: Why is “edge tracking” better than walking straight down the middle of a scent?
A: Wind constantly breaks odor plumes into disjointed puffs. By weaving along the outer edge of a plume, the fly continuously updates its spatial memory at the boundary, ensuring it can relocate the scent pathway even if the plume moves perpendicular to the wind or breaks apart.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this olfaction and memory research news
Author: Katherine Fenz Source: Rockefeller University Contact: Katherine Fenz – Rockefeller University Image: The image is credited to Neuroscience News
Original Research: Open access. “A vector-based strategy for olfactory navigation in Drosophila” by Andrew F. Siliciano, Sun Minni, Chad Morton, Charles K. Dowell, Noelle B. Eghbali, Silas E. Busch, Juliana Y. Rhee, L. F. Abbott & Vanessa Ruta. Nature DOI:10.1038/s41586-026-10827-7
Mad in Norway International Film Festival Film Review: Drunk On Too Much Life
July 10, 2026
Our Mad in America affiliate, Mad in Norway, is hosting an international film festival from September 24-26 in Lillehammer, Norway. Each week, we will feature a film. This week is Drunk On Too Much Life.
Short synopsis from the Drunk On Too Much Life webside
In a world gone crazy, a young woman discovers that her madness is a fierce and powerful gift that makes her more fully human. Drunk on Too Much Life is an intimate and powerful documentary following the filmmaker’s 21-year-old daughter’s mind-opening journey from locked-down psych wards and diagnostic labels towards expansive worlds of creativity, connection and greater meaning. On their journey, the family begins to question the widespread idea that mental illness should be understood in purely biological terms and learns the myriad ways that madness has meaning. Recovery is not a straight path to being cured but a crooked and bumpy journey and series of small awakenings.
Summary
In this documentary, we follow Corrina, a young woman from Toronto, as she navigates psychotic episodes and profound mental health challenges. Her story unfolds as a journey towards greater self-awareness and awakening, interweaving encounters with activists, conversations with family members, and archival footage from different moments in her young life. Along the way, Corrina interviews trauma expert Dr. Gabor Maté and others such as American activist Sascha DuBrul, who offer alternative, resource-oriented perspectives on unusual and extreme sensory experiences. Within the film, her path also includes multiple hospitalizations and medication treatments within the traditional biomedical system, creating a contrast between conventional psychiatry and trauma-informed, peer-based approaches to those labelled with “serious mental illness.”
Corrina’s parents, who are also the filmmakers, accompany their daughter’s journey with openness and curiosity, gradually encountering deeper spiritual and creative meanings her extreme states bring to the surface. It is Corrina’s grandmother who first offers another way of understanding what is happening to the young girl, encouraging her to give voice to her inner world through poetry and art. “You have an artistic temperament,” she tells her—words that resonate deeply with Corrina.
Tracing Corrina’s difficult passage through repeated hospitalizations, numerous medications, and her own ongoing search for meaning, Corrina finds refuge in art, poetry, music, and community. Slowly, Corrina begins to recognize herself as a deeply sensitive and creative person—someone who perceives layers of meaning and feeling that others may overlook.
What was once called illness begins to reveal itself as something more complex: a heightened sensitivity that carries vulnerability and insight, pain and possibility. Through Corrina’s personal journey, the film invites us to reconsider how our culture understands complex ‘mental illness’, and to ask whether the very qualities we often pathologize may also hold the seeds of creativity, perception, and transformation.
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This and many other films will be presented at the Mad in Norway International Film Festival in Lillehammer, Norway September 24 – 26, 2026.
Please visit Mad in Norway International Film Festival’s website at madinnorwayfilmfest.org to find out more about this film, festival programming, tickets, and other information. We hope to see you there!
And stay tuned here each week for more exciting films!
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Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
Chronic fatigue syndrome may be the result of faulty ion channels.
Karola G/Pexels/Canva
Scientists have identified a faulty cellular pathway that may help explain why people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) experience such profound exhaustion, immune dysfunction, and crashes after exertion.
Researchers at Griffith University in Australia have found that an ion channel called TRPM3 appears to malfunction in specialized “natural killer” white blood cells. The fault disrupts the movement of calcium, an important cellular messenger, into mitochondria, the tiny structures that produce energy. The finding adds weight to the idea that ME/CFS is not simply a disorder of “fatigue,” but a complex biological illness.
“First, picture that NK [natural killer] cells are a house and that TRPM3 ion channels are doorways that allow calcium to enter this house,” Professor Sonya Marshall-Gradisnik and Dr Natalie Eaton-Fitch told Refractor. “Once inside, calcium acts as a messenger essential for numerous biological processes.”
ME/CFS is a disabling multisystem illness marked by severe exhaustion, post-exertional malaise, pain, cognitive problems, dizziness, sensory sensitivity and other symptoms that can seriously limit everyday life. There is currently no cure or approved treatment.
Although ME/CFS has often been misunderstood or dismissed, research has increasingly pointed to measurable biological changes. One recurring finding is impaired natural killer cell function. These immune cells depend on carefully controlled calcium signals to do their job, including producing immune-signaling molecules called cytokines and killing infected or abnormal cells.
The new study looked at whether previously reported mitochondrial problems in ME/CFS might be downstream of earlier faults in ion-channel and calcium signaling.
The researchers focused on TRPM3, a calcium-permeable ion channel found in natural killer cells and in tissues throughout the body, including the nervous system, gastrointestinal tract, cardiovascular system and musculoskeletal system. These broad locations are important because ME/CFS symptoms are also broad, affecting multiple body systems rather than a single organ.
When TRPM3 is activated, it helps calcium enter cells and move into internal compartments such as mitochondria. In healthy cells, that calcium movement helps coordinate immune-cell activity and supports the cell’s energy demands. In the new study, the researchers used advanced live-cell imaging to watch TRPM3-dependent calcium movement in real time in natural killer cells from 10 people with ME/CFS and 10 healthy controls.
The results showed that, compared with healthy controls, ME/CFS cells had significantly reduced TRPM3-dependent calcium movement into both the cell fluid and the mitochondria. In other words, when the researchers tried to activate this ‘doorway,’ the calcium signal did not flow normally.
“This investigation by Magawa et al. demonstrates potentially impaired mitochondrial calcium influx as a result of impaired SOCE/TRPM3 ion channel activity,” said Marshall-Gradisnik and Eaton-Fitch. “This data demonstrates that impaired TRPM3 ion channel activity may result in a reduced calcium uptake by mitochondria.”
The finding is key because mitochondria do more than simply make energy. They also help buffer calcium signals and support immune-cell activation. If calcium handling is disturbed, the result may be a messy downstream chain reaction of poor signaling, impaired immune-cell function, and potentially disturbed energy production.
That “potentially” is doing a bit of heavy lifting, however. The study did not directly measure ATP, the energy-carrying molecule produced by mitochondria. The researchers say that is the next step.
“It is important to highlight that this current investigation did not determine the downstream consequences of TRPM3 activity on mitochondrial energy production by measuring ATP,” said Marshall-Gradisnik and Eaton-Fitch. “This will be undertaken in the next series of experiments.”
One of the more intriguing findings was that, after the researchers depleted and then restored calcium stores in the cells, mitochondrial calcium influx was higher in ME/CFS cells than in controls. That might sound contradictory, given that TRPM3-triggered calcium movement was reduced. The researchers say it may point to poor calcium control rather than a simple ‘too much’ or ‘too little’ problem.
“The findings suggest that the restoration of calcium resulting [sic] in an increased influx into the mitochondria in ME/CFS compared with controls,” they said. “This may be a potential compensatory mechanism whereby the mitochondria may attempt to store additional calcium reserves, acknowledging here that NK cell activity, a known calcium-dependent process, is significantly impaired in people living with ME/CFS.”
But that compensation might come at a cost. The researchers noted that increased calcium entry into mitochondria raises the risk of calcium overload, which can be toxic to cells and may impair functions such as ATP production. When TRPM3 itself was then activated, calcium entry was reduced, again pointing to an impaired signaling cascade and poor calcium balance in ME/CFS natural killer cells.
The findings are early and based on a small cohort, but they add to the growing body of work suggesting that ME/CFS may involve ion-channel dysfunction. And, clinically, the work is not yet ready to diagnose or treat patients. For a potential biomarker to move into real-world use, it would need to show reliable sensitivity and specificity across larger cohorts and across other fatigue-related conditions. Marshall-Gradisnik and Eaton-Fitch said the team is already working through that process.
“A series of criteria are required to be fulfilled prior to clinical translation,” they said. “TRPM3 ion channel activity is the only potential biomarker to be investigated at multiple levels, being genetic (DNA), protein (expression) and function.”
The therapeutic side might also be worth watching. The researchers said previous work has shown that naltrexone, a prescription medication primarily used to treat opioid overdose, can restore TRPM3 ion-channel activity in natural killer cells from people with ME/CFS, and that a clinical trial is currently underway. They are also investigating other drug targets that may directly or indirectly influence ion-channel function.
Still, the study should not be read as proof that TRPM3 dysfunction causes all mitochondrial problems in ME/CFS, or that a treatment is imminent. The more careful interpretation is that it provides another piece of a very complicated biological puzzle.
“We know from a large body of research that ME/CFS is a multidimensional physiological condition and our research adds to the growing body of international research into the pathomechanisms of ME/CFS,” Marshall-Gradisnik and Eaton-Fitch said.
The researchers said the work provides a potential mechanistic link between TRPM3 activity, poor calcium movement within cells and downstream effects such as mitochondrial dysfunction, but added that more research is needed to validate the findings and determine whether TRPM3 dysfunction directly causes poor mitochondrial activity.
For people with ME/CFS, the key message is not that a cure is around the corner. It is that researchers are continuing to identify measurable cellular abnormalities in a condition too often reduced to tiredness or psychological distress. This study points to a possible biological chain reaction: faulty calcium ‘doorways,’ poor immune-cell signaling and mitochondria that may not receive the messages they need to work properly.
There is one thing about having been a “delinquent” teen, or a “freak” as we called ourselves, in the chaos of the early 90s that really makes it seem like we were part of something special—a kind of revolution. At the very least, this time was a powerful shift in youth culture. The most amazing part of that time for me was being accompanied through my tumultuous youth by some powerful, strange, and beautiful musicians. For that I always felt very lucky. I know each era has its musical heroes, but something was really special about ’90s music, I think. And as I’ve written about before, music has been an immensely important part of my life and my healing.
The ‘90s were chock-full of brave women artists especially. But, Sinéad O’Connor, or Shuhada’ Sadaqat (the name she adopted after converting to Islam in 2018), may have been the most bold, the most unique of all the musicians of that time. She was a woman from Dublin who took on the Pope on night time television, for goodness’ sake.
When I first heard songs like Nothing Compares 2 U on the radio I was transfixed, like so many of us were, by her voice and the power of it. But when she ripped the picture of the Pope in protest of sexual abuse within the church, the rage of young girls all over the world who were experiencing patriarchal oppression was right there—right there represented on the TV. It was earth shattering as a young girl to see that kind of bravery. While my friends and I thought refusing to shave our legs and listening to Riot Grrrl bands were the best protests we could muster, she was doing something quite unimaginably, irrevocably radical.
As I entered into my young adulthood, my life quickly turned into that of a survivor of psychiatric abuse. I became an angry woman diagnosed “crazy” in my early 20s. Just like me, in the early 2000s she was diagnosed with bipolar (which she later stated was a misdiagnosis and did not identify with). I still think Sinéad is unmatched in bravery as far as public protest music and performance in our time. But not many know how she took on stigma and psychiatry, too.
When I became an activist in mental health, I encountered the video plea she released in 2017 from a hotel in New Jersey, and the thought immediately crossed my mind of how often psychiatry is used to silence a person who has strong radical views. It certainly wouldn’t be the first time that an angry woman was destroyed for her feelings, thoughts, and views through stigma, isolation, and chemical restraint. It’s really a tale as old as psychiatry itself. This quote from a review of the movie The Mad Woman’s Ball on CNN is worth including, we all know this story: “It’s a tale as old as time: A woman won’t conform to societal norms, traditional notions of femininity or what’s expected of her, and is dismissed as diseased. She’s considered hysterical. And, as such, she is locked up, burned at the stake, hidden away or placed under the supposedly steadier control of men.”
And, of course, this type of targeting is not just reserved for women. Certainly people of colour, Indigenous people, queer, and trans people all experience this.
It was when I found her video online that I started to see what had happened to this bold, immensely creative protest singer of my youth. A new light was brought to Sinéad’s life in my mind, to her music, and I had a new understanding of her suffering and mine. I felt a kinship and a solidarity with her, as many people who have struggled with isolation, suicidality, and stigma must have had.
I sometimes think about how we feel artist’s private lives are ours to judge, invade, and endlessly pontificate upon, just because they’ve offered us artwork that feels vulnerable and raw. But, I am writing this in the spirit of Sinéad’s protests of injustice.Not only did she remind me in my teens to be brave and create art that challenges the injustices of the world, she reminded me as a grown woman not to be silent about the abuses happening to people labeled mentally ill. Throughout the years, she was vocal about Israel/Palestine, abortion, sexual abuse and the church, even the corruption of the Grammys, and, in this video, she was vocal about the neglect and hardship she and so many others experience when struggling with trauma, stigma, and suicidal thoughts.
She was one of millions, she repeated in the video, one of millions.
And she was right. Just like she was right about sexual abuse in the church. She was vocal in a way I don’t know any other musicians have been about the impact of diagnosis, stigma, and psychiatry on her life, how she was dismissed and abandoned at that time by the public and her family.
This video brought me to her music again. And when she passed, I blasted her music all day. She was such a powerful creative force. In 2017, after this video came out, the media framed her emotionality as “Sinéad raises concern for her mental health.”I saw it as yet another courageous and powerful protest, a bit like ripping the Pope’s picture, but this time showing the pain and neglect that people labeled mentally ill suffer with. Many seemed to view this plea as hysterical, dramatic, something to deride or mock. But I listened carefully. It is not just a cry for help; it is a condemnation of how we treat people in mental distress.
There is probably no better tribute on the web right now to Sinéad than Amanda Palmer’s, which you can read here. And I want to add to it by remembering her experience as it is reflected in this video. That she was, in so many ways persecuted by stigma and psychiatry. “Death by a thousand paper cuts.” Palmer says. Like so many of us loud, angry women trapped in a broken system of mental health, I certainly can relate some days.
In the video, she pleads for just some compassion, and asks why we treat each other this way. She gives voice to all people labeled mentally ill who are ignored, and in her cries for justice and compassion for herself, she shows how much she felt in solidarity with others. Even crying out for a woman a few hotel rooms down who had been abandoned, too.
I listened again to the video, a day after the announcement of her death, which came shortly after her son died by suicide in 2022. It reminds me of my peers in the withdrawal community, desperately trying to get the help they need but finding so much stigma, isolation, and loneliness, not just from the medical community, but from family and friends, too.
So, in her tragic passing, I choose to honour her by raising up these words she said, by hearing and believing them. In this interview with Dr. Phil, after her raw and profoundly powerful plea to her family to take care of her after a hysterectomy which she was given no hormone replacements for, when he asked if she considered herself mentally ill.
“No,” she said confidently, “No, not unless you consider complex post-traumatic stress a mental illness.”
I often remind people of this. How the label of mental illnesses, like depression and bipolar, too, are sometimes used to mask the effects of abuse and trauma, which Sinéad had been open about having had plenty of in her life. Diagnosis like these are also so often used to dismiss someone’s feelings, as Sinéad refers to as well.
American author and queer activist Glennon Doyle raised up an important point to remember when talking about survivors of abuse and trauma, or even political targeting, who have been labeled mentally ill. She wrote on Twitter, “why is everyone saying Sinéad “battled her own demons?” she was one of very few brave enough to battle real demons: child predators, those who protected them in God’s name, homophobia, greed that kills….. she battled demons, yes- but they were us, not her.” Sinéad’s struggles were very real, and not to be dismissed by labelling her mentally ill – putting the fault in her body, her biology, instead of our society and the injustices she fought.
There are plenty of instances you can find of Sinéad referring to herself as mentally ill, but she has also said that she was misdiagnosed with bipolar in an article on the Irish Mirror. She spoke about the effects of prescription psychiatric drugs on her life, and on her hormonal health: “They are extremely debilitating drugs. Tiring to the extreme. Ironically, extremely depressing. They can cause suicidal or self-harm type thinking. They can mess up your menstrual cycle very badly and cause you to be incapacitated for a week before.”
I choose to honour her by helping others understand how common suicidal feelings are, not just in the context of trauma or drug side effects, but for everyone, especially among trauma survivors (including veterans). And to remind you how being able to talk about suicidal feelings without stigma or the threat of diagnosis, or incarceration in mental hospitals, can help people stay alive and heal. There are resources that aim to remove the stigma, like Alternatives to Suicide; you can find more information here.
I choose to remind you, too, that sometimes the best thing we can do for the people we love is to allow them to speak about their feelings without pathologising or labelling them as manifestations of illness. To honour their suffering. To listen.
Sinéad was a warrior and in many ways paid the ultimate price for her bravery. Whether it was being vilified by the public or the media for a radical protest, or by being stigmatised and dismissed as an angry woman labeled mentally ill—her songs show her brave, vulnerable openness, and her willingness to tell the truth for others. Like she says in the 2017 video, “I hope this is somehow helpful to others,” and that’s what brave artists do, they reveal inner truths, no matter how ugly, political truths, injustices, and pain we usually turn away from, and they make beautiful songs of them.
In the sprit of MIA’s Song of the Week feature, I’ve made a playlist of all the songs that I feel reveal, in her beautiful musical compositions and lyrics, the human experience of mental distress, trauma, love, loss, and healing. How art and music is a place where healing happens for all of us when warriors like her sing from the heart of it. We are blessed to have had her work, and her presence in our time.
I don’t know if there is a special place artists go to find peace when they pass away, after honouring that bargain we make to create the kind of work she did, but I do hope she is there—peaceful, with her son in that healing room.
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Just hit play below. Each song in this playlist will follow the last. The songs include: Three Babies, Drink Before the War, Thank You for Hearing Me, In This Heart, Just like U Said It Would B, The Healing Room, and Feel So Different.
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This is a repost from our affiliate site, Mad in America. The original post is avai
Illustration by Tag Hartman-Simkins / Futurism. Source: Kevin Dietsch / Getty Images; Melinda Sue Gordon / Universal Pic / Melinda Sue Gordon; Shutterstock
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Is it possible to not like a movie in a normal way? Can it simply not be “your thing” without being transposed onto some intangible, ever-raging culture war?
It certainly isn’t if you’re an anti-woke crusader like SpaceX CEO Elon Musk. Like a lot of very online right wingers who are suddenly qualified classicists, he’s very upset about the new Odyssey adaptation directed by Christopher Nolan.
Nolan, according to Musk, “desecrated Homer and groveled on his knees just to meet the woke rules required to win an Oscar.” That’s because his movie dares to do stuff like cast Black women and a trans man in prominent roles, making the director what Musk termed an “anti-White racist.” In other words, it’s supposedly not “historically accurate” — never mind the fact that the epic poem contains gods wandering the Earth and a Cyclops.
Thankfully, there’s a wonderful piece of technology called AI out there that’s perfect for realizing the juvenile aesthetic predilections of stunted creatives who want to wallow in an imagined idea of what the past was like.
“Before this year ends, Grok Imagine will make a full-length movie of The Odyssey that is historically accurate and true to the art of Homer,” Musk declared Tuesday, referring to his own AI video generator.
Musk’s post quoted, and implicitly endorsed, a three minute dialogue scene that another user generated with Grok Imagine, featuring a virtual cast that looks more Western European than Mediterranean. No comment from Musk on if this was sufficiently “historically accurate,” of course, despite previously accusing Nolan of having “total contempt for the Greek people” with his casting.
Someone should probably let Musk know that there’s already a fully AI-generated Odyssey adaptation coming out, but the creators behind that one seem to respect Nolan, so it probably won’t be anti-woke enough for his taste.
But maybe the perfect Odyssey film doesn’t have to be AI-generated, if it’s in the hands of the right director.
One Musk fanboy suggested that he should “give Mel Gibson $100 million” to create a “painstakingly historically accurate” adaptation. Musk replied, “I’m down.” (The last movie Gibson directed, “Flight Risk,” was ripped to shreds by both critics and audiences.)
Though for the past few months Musk has fought like a combatant in the Trojan War to drum up controversy over Nolan’s film, his efforts have failed spectacularly. It opened to $264 million globally and will probably make a billion dollars, if not more, by the end of its run. It’s gotten rave reviews from critics, and moviegoers seem to love it, too.
And is anyone surprised? Nolan is a beloved figure in Hollywood with legions of fans. Musk has his own army of devout followers, too, but the difference is that Musk is constantly miserable, alienating even some of his own followers with his extreme takes.
Nolan, whether you like his movies or not, is a showman that wants you to have a good time. Even Musk said Nolan was “awesome” a few years ago. Audiences will remember that they liked some of his other films and turn out for his new one. They probably won’t take notice Musk melting down about it online, even if each of his posts gets hundreds of thousands of likes on his platform he remolded to be his personal echo chamber.
I’m a tech and science correspondent for Futurism, where I’m particularly interested in astrophysics, the business and ethics of artificial intelligence and automation, and the environment.
Elon Musk: “I don’t trust OpenAI. I started that company as a non-profit open source… and it is now extremely closed source and maximizing profit… So I don’t trust Sam Altman.”
Elon Musk: “I don’t trust OpenAI. I started that company as a non-profit open source… and it is now extremely closed source and maximizing profit… So I don’t trust Sam Altman.”
Image source: Neuralink
Image source: Realbotix
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