Thank you AI or SI: Traumatic Brain Injury (TBI) amnesia deeply damages a person’s ability to trust what others say because it destroys the internal benchmarks used to verify reality. When a brain injury compromises memory, individuals are left without a reliable personal record to compare against external information.

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Traumatic Brain Injury (TBI) amnesia deeply damages a person’s ability to trust what others say because it destroys the internal benchmarks used to verify reality. When a brain injury compromises memory, individuals are left without a reliable personal record to compare against external information.

This breakdown in belief and the resulting pervasive doubt happen through several primary neurological and cognitive mechanisms:

1. The Erasure of Personal Reality (Anterograde Amnesia)

When a person experiences anterograde amnesia from a TBI, their brain loses the ability to form or store new memories. [1]

  • The Mechanism: If someone tells a TBI survivor, “We already talked about this an hour ago,” or “You promised you would handle that bill today,” the survivor’s internal timeline contains absolutely zero record of that event.
  • The Core Doubt: Because the conversation is entirely absent from their mind, being told it occurred feels like a distortion of reality. It creates a harrowing choice for the survivor: believe that their own mind is profoundly failing them, or suspect that the other person is mistaken, misremembering, or actively lying.

2. Confabulation (“Honest Lying”)

TBI frequently causes damage to the frontal lobes, leading to confabulation—the brain’s unintentional creation of false memories to fill in blank spaces. [1, 2]

  • The Mechanism: Confabulation is not intentional deception; the brain genuinely believes these fabricated memories are true.
  • The Core Doubt: When a family member or caregiver corrects a confabulated memory with the actual facts, the TBI survivor experiences a sharp psychological conflict. Because their false memory feels 100% vivid and real, external corrections feel like gaslighting. The survivor stands firm in their “memory,” viewing the other person’s version of events with heavy skepticism. [1]

3. Poor Source Monitoring

Source monitoring is the cognitive ability to remember how or where you learned a piece of information. TBI impairs this function. [1]

  • The Mechanism: A survivor might dream something, imagine a scenario, or see a fleeting thought, and their brain later catalogs it as a factual, real-world event.
  • The Core Doubt: When others try to tell them that the event never happened (e.g., “You didn’t actually go to the store yesterday, you were in bed”), the survivor cannot discern why their brain holds that image unless it actually happened. They naturally doubt the validator rather than their own vivid internal experience.

4. Overload and Information Processing Delays

A brain recovering from a TBI processes information at a much slower speed. [1, 2]

  • The Mechanism: When people speak quickly or deliver complex details, the survivor’s brain experiences cognitive overload. They miss pieces of the conversation or fail to synthesize the meaning in real time. [1, 2]
  • The Core Doubt: This gap in comprehension creates immediate insecurity. When they cannot fully grasp or track what is being told to them, their natural defense mechanism is to withdraw into doubt or rejection of the information to protect themselves from confusion.

5. Neurogenic Paranoia and Lack of Insight (Anosognosia)

Structural damage to specific brain systems can alter emotional regulation and self-awareness. [1, 2]

  • Anosognosia: Some TBI survivors suffer from a clinical lack of insight, meaning they are neurologically incapable of recognizing their own cognitive deficits. If they do not believe their memory is damaged, they will naturally conclude that everyone else is lying to them. [1, 2]
  • Paranoia: TBI can cause a dysregulation of neurotransmitters (like dopamine) or damage the frontal and temporal lobes, occasionally triggering organic paranoia or persecutory delusions. This creates a baseline psychological state of suspicion where the survivor feels that others are manipulating them or taking advantage of their confusion. [1]

The Emotional Impact: Living with TBI amnesia means navigating a world where your own mind feels like an unfaithful narrator, but everyone else’s version of reality feels completely foreign. This exhausting dynamic naturally breeds protective skepticism and profound isolation.

Are you exploring this to help support a loved one who is recovering from a TBI, or are you managing these memory symptoms yourself? Knowing the context can help me provide tailored communication strategies or coping mechanisms.

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Psychiatric Times: Schizophrenia and Dissecting Algorithms of the Mind

News|Articles|September 28, 2026

Dissecting Algorithms of the Mind: Toward Precision Psychiatry in Schizophrenia

Author(s)Jessica Walters

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Key Takeaways

  • Computational phenotyping reframes schizophrenia as separable algorithmic failures, using structured tasks to extract latent variables mapping onto frontal-cortical and striatal targets and yielding clinically meaningful subtypes.
  • Xanomeline-trospium pairs central muscarinic agonism with peripheral antagonism, preserving M1/M4 efficacy while mitigating cholinergic adverse events and avoiding weight gain, sedation, and extrapyramidal symptoms typical of D2 blockade.

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Experts highlight biomarker-driven schizophrenia care—computational subtypes, muscarinic drugs, sharper negative-symptom scoring, and KCC2 targets—reducing trial-and-error prescribing.

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How can clinicians move schizophrenia treatment from trial and error toward a principled, mechanism-based match between patient and medication? At the inaugural Precision Therapeutics in Schizophrenia symposium, Michael Halassa, MD; Steve Brannan, MD; Srihari Gopal, MD, MHS; and Zhong Zhong, PhD; sought to answer this question. Halassa opened, framing the problem frankly: an estimated 30% of patients with schizophrenia do not have medications that adequately address their symptoms.1

Halassa argued that psychiatry lacks the objective biomarkers available in fields like cardiology, forcing clinicians to combine noisy clinical measurements into idiosyncratic treatment decisions. He reframed precision psychiatry as an engineering problem: reducing a high-dimensional feature space into a smaller set of latent variables that map onto specific treatment targets. Those latents, he said, should cluster around 3 disease-generative processes relevant to psychotic disorders—model building, model revision, and credit assignment—which correspond loosely to frontal-cortical and striatal circuits. “If you take seriously the idea that the brain runs algorithms just like machines do, then you have the opportunity to put people in structured tasks and environments to expose that algorithm,” Halassa said.¹ Using a cue-switching task administered to patients with schizophrenia and healthy controls, his lab identified 2 patient subtypes based on how sensory uncertainty was incorporated into decision-making; the subtypes did not differ in positive symptom burden but did differ in negative symptoms.

Brannan then detailed the development of xanomeline-trospium (Cobenfy), approved for schizophrenia in 2024 as the first new antipsychotic mechanism in roughly 70 years. Xanomeline, derived from arecoline found in betel nuts, produced dose-dependent psychosis remission in a 1990s Alzheimer disease trial but was shelved due to cholinergic adverse events. Pairing xanomeline, which crosses into the brain, with trospium, which does not, cut adverse events roughly in half while preserving central efficacy at the M1 and M4 muscarinic receptors—M4 enriched in the striatum, and M1 in the frontal cortex, the seat of executive function. Unlike haloperidol or clozapine, which act on dopamine D2 receptors, xanomeline-trospium avoided weight gain, sedation, and extrapyramidal symptoms, Brannan emphasized. Phase 1 dosing settled on 20 mg and 40 mg of xanomeline, and phase 2 and 3 trials enrolled patients with schizophrenia in inpatient settings to ensure medication adherence. In the phase 3 EMERGENT trials, xanomeline-trospium produced statistically significant reductions in PANSS total score versus placebo, with effect sizes of 0.6 or greater.2 Post hoc analysis also showed a numerically larger placebo-controlled response among patients with prominent negative symptoms at baseline, and cognitive improvement was concentrated in the subgroup with baseline impairment.

Gopal continued with clinical insights since approval: “We would hear these reports of people who were awakening, who were brightening up, who were opening up that they hadn’t been before,” he said, describing patients who had been treatment-resistant for decades.2 Because the 30-item PANSS was developed in the 1980s and may not fully capture this phenomenon, a colleague, Ken Kramer, constructed a 6-item PANSS Clarity Composite combining anhedonia, social interaction, and motivation items. Across the pooled EMERGENT dataset, the composite showed a numerically larger treatment effect than PANSS total score or established factor scores such as the Marder negative factor, though Gopal cautioned the analysis was exploratory and unpublished. He noted the composite’s basis was clinical intuition rather than formal factor analysis, and that confirmatory work remains needed to determine whether it captures a construct distinct from existing negative-symptom measures.

For You

References

1. Halassa M, Brannan S, Gopal S, et al. Theme I: Innovative Pharmacology and Next Generation Therapeutics. Presented at: Precision Therapeutics in Schizophrenia Symposium; September 23-24, 2026; Roanoke, VA.

2. Kaul I, Sawchak S, Walling DP, et al. Efficacy and safety of xanomeline-trospium chloride in schizophrenia: a randomized clinical trial. JAMA Psychiatry. 2024;81(8):749-756.

3. Arion D, Lewis DA. Altered expression of regulators of the cortical chloride transporters NKCC1 and KCC2 in schizophrenia. Arch Gen Psychiatry. 2011;68(1):21-31.

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Trinity College Dublin: Your voice may reveal how fast and how well you’re aging. Comment: Post TBI I had aphasia, then brocas, tone change in speech. This finding for me makes a lot of common sense. I will look forward to its progress

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Your voice may reveal how fast and how well you’re aging

Posted on: 30 September 2026

A new study shows that machine-learning clocks based on speech can estimate chronological age and may also offer a window into brain aging, biological aging, cognitive health, cumulative burden, and dementia.

The study, just published in leading international journal Science Advances, outlines that researchers have developed a “speech clock” that can estimate a person’s chronological age from hundreds of acoustic and linguistic characteristics of their speech.

The difference between a person’s actual age and their speech-predicted age (called the speech age gap) was also associated with multiple independent markers of biological aging, brain health, cognition, social adversity, and dementia.

The study analysed 2,928 Spanish-speaking participants from Argentina, Chile, Colombia, Mexico, and Peru, including healthy adults and people with mild cognitive impairment, Alzheimer’s disease, and different forms of frontotemporal dementia.

Rather than looking at a single property of the voice, the researchers used machine learning to analyse hundreds of features capturing how people speak and what they say: incorporating speech rate and pauses, pitch, emotional content, vocabulary, semantic precision, and the amount and organisation of verbal output. Machine-learning models combined these features to estimate chronological age and generate an individual speech age gap.

People whose speech appears older than expected for their chronological age also showed signs of accelerated aging across several biological and clinical systems. The speech age gap was associated with brain age measured using structural and functional neuroimaging. It was also related to epigenetic aging, measured through three independent DNA-methylation clocks, that estimate how biologically “old” the body appears based on age-related chemical changes in DNA. 

Additionally, greater speech-age acceleration was associated with poorer global cognition, executive function, functional abilities, and several forms of memory. Importantly, these relationships were not restricted to language tests: speech age was also related to performance on non-linguistic cognitive measures.

The speech clock also differentiated healthy individuals from people with dementia. Healthy participants showed the lowest speech age gaps, while progressively larger gaps were observed across Alzheimer’s disease and forms of frontotemporal dementia.

The complete speech-age measure discriminated clinical groups better than individual acoustic or linguistic features considered separately. In Alzheimer’s disease, it was associated with higher levels of plasma p-tau217, one of the most important blood biomarkers of Alzheimer’s pathology. The same speech-derived measure also tracked cognitive and clinical functioning.

Speech also carried a social signal. Among healthy individuals and people with Alzheimer’s disease and other dementia, accelerated speech aging was associated with a more adverse social exposome: a combination of lifelong factors such as education, financial conditions, food insecurity, healthcare access, and early-life experiences.

“Our voice appears to contain much more information about aging than we previously recognised,” said Agustin Ibanez, Professor in Brain Health at the Global Brain Health Institute and School of Medicine, Trinity, and senior author of the study. 

“It captures both the passage of chronological time and signals coming from cognition, the brain, systemic biology, and even our accumulated social environment. This raises the possibility that something as simple and accessible as speech clocks, maybe combined with biomarkers, could eventually complement much more expensive measures of aging.”

What is the potential impact of this research?

The potential implications are substantial. Many current measures of biological aging require MRI scanners, blood samples, molecular assays, or specialised clinical assessments. Speech, in contrast, can be recorded remotely, repeatedly, non-invasively, and at very low cost. This could be particularly important in countries and communities where advanced diagnostic technologies are difficult to access. 

Because the study was conducted across five Latin American countries (a region historically underrepresented in dementia research) it also provides evidence that sophisticated biomarkers of aging do not necessarily need to depend exclusively on expensive technologies developed in high-resource settings.

The researchers emphasise, however, that the speech clock is not yet a diagnostic test for dementia. The study was primarily cross-sectional, meaning that it cannot establish whether an older-appearing speech profile predicts who will subsequently develop cognitive decline or dementia. Longitudinal studies, validation in additional languages and cultures, and testing in more naturalistic speech settings will be required before clinical implementation.

“The broader finding is nevertheless striking in that a person’s voice may provide a remarkably compact readout of multiple dimensions of aging,” added Prof. Ibanez. 

“From chronological age to brain aging, epigenetic aging, cognition, Alzheimer’s-related pathology, social exposures, and dementia phenotypes, information traditionally obtained through very different and often expensive measurements appears to converge, at least partly, in the way we speak. 

“If confirmed longitudinally and across populations, speech could ultimately become one of the most scalable tools for monitoring healthy and accelerated aging—potentially transforming an everyday human behaviour into a window onto the biology of aging.”

The journal article can be read on the Science Advances website (DOI: https://doi.org/10.1126/sciadv.aef.9864)

Media Contact:

Thomas Deane | Media Relations | deaneth@tcd.ie | +353 1 896 4685

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Nature: AI ‘speech clock’ assesses how fast you’re ageing from your voice. Comment: As a person who sustained TBI aphasia, broca’s – this is part of an explanation for people who sustain TBI or strokes

AI ‘speech clock’ assesses how fast you’re ageing from your voice

The pitch and emotional content of your speech are important predictors of accelerated ageing, researchers find.

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Older adult speaking into a handheld microphone with a bright background.
A new ‘speech clock’ analyses characteristics of a person’s voice, including pitch, to assess how quickly they are ageing.Credit: Cheschhh/Getty

A ‘speech clock’ developed by scientists can predict how well a person is ageing based on characteristics of their voice and how they talk. The clock draws on hundreds of vocal features, including pitch and talking speed, to estimate a person’s age.

‘Inflammation clock’ can reveal body’s biological age

Using the clock, the scientists calculated a ‘speech age gap’ for individuals: the difference between a person’s age as predicted by the speech clock and their chronological age. Large speech age gaps were strongly associated with cognitive issues in people, such as those that arise in dementia, suggesting that the new clock could be a useful tool for determining whether a person is growing older faster than expected.

The findings were published today in the journal Science Advances1.

“We can see a huge predictive value, just with a very simple four minutes of speech recordings,” says neuroscientist Agustín Ibáñez at Adolfo Ibáñez University in Santiago, who is a co-author of the study.

The speech clock could be a boon for tracking the ageing of people in low-resource regions, because it doesn’t rely on expensive or invasive technologies, such as brain scans and blood tests, says Jed Meltzer, a cognitive neuroscientist who specializes in language at the University of Toronto in Canada and was not involved in the study. “It is a very impressive piece of work.”

Predicting age with speech

Ageing clocks often use biological markers to assess how rapidly a person’s body is declining. For instance, ‘brain clocks’ use signatures from neuroimaging to determine whether an individual’s brain is ageing faster than their chronological age suggests. And ‘epigenetic clocks’ look at the patterns of methyl tags on a person’s DNA to estimate their biological age. But so far, researchers hadn’t developed a clock based on speech. Such a tool could offer a useful window into the ageing process because speaking involves a “huge amount of brain work”, Ibáñez says.

How quickly are you ageing? What molecular ‘clocks’ can tell you about your health

To create their clock, Ibáñez and his colleagues recorded 2,928 Spanish speakers from Argentina, Chile, Colombia, Mexico and Peru while they completed various speech tasks. The group was a mixture of healthy individuals and people with mild cognitive impairment, Alzheimer’s disease or other forms of dementia. The researchers used machine-learning algorithms to extract more than 700 speech characteristics that can change with ageing and dementia, such as pitch and vocabulary range, from the audio recordings. They then used these data to train their speech-clock model to predict each study participant’s age.

Overall, the speech clock could distinguish between healthy individuals and those with some form of cognitive impairment. The clock, for instance, categorized the speech of people with cognitive issues as being older than would be expected for their chronological age. Healthy people were generally assessed as having speech that matched their chronological age.

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New Atlas: Drug 10 times stronger than fentanyl claiming lives in the US

Society & Community

Drug 10 times stronger than fentanyl claiming lives in the US

By Mike McRae

September 29, 2026

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Opioid epidemic has a new threat.

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A synthetic opioid up to 10 times stronger than fentanyl is attracting attention as an emerging global threat, having been officially tied to more than 40 fatal overdoses over the past two years in the US alone.

That figure is likely to be far greater, with authorities and researchers finding themselves in the dark on just how widespread the use of the compound cychlorphine may already be.

Like morphine and fentanyl, cychlorphine locks onto the brain’s mu-opioid receptors, reducing pain and increasing euphoria. Its structure puts it into a completely separate class of synthetic opioid agonists, though, one that preclinical studies suggest may affect breathing and blood flow at far lower doses than even fentanyl.

If you’ve never heard of the drug, you’re far from alone. First identified just two years ago by the US Center for Forensic Science Research and Education, cychlorphine still lacks a standardized test that can quickly detect its presence in clinical samples.

Nonetheless, global surveillance programs suggest the market for the novel synthetic opioid (NSO) is increasing, especially in North America, with cychlorphine since detected in close to 200 drug seizures across 10 countries, and considered to be responsible for at least 78 deaths.

In April this year, the White House Office of National Drug Control Policy issued a drug threat notice on the drug, emphasising its proliferation through regions in the South, Midwest, and Northeast.

And an editorial published in the Journal of Pain Research makes it clear just how serious the threat could be.

“The lethality and speed of cychlorphine’s emergence make it an urgent NSO threat currently facing clinicians, first responders, and public health practitioners,” writes a team of authors led by Temple University pharmacologist Robert B Raffa.

While the drug’s appearance is new, the pattern of its emergence is anything but.

For decades, the illicit distribution and use of opioids has become an increasing public health problem. Fuelled in part by the overprescription of painkillers like OxyContin in the 1990s, the market for unregulated substitutes exploded into what became regarded as an epidemic by the turn of the millennium.

Efforts to curb the distribution and use of opioids have since resulted in an arms race between drug manufacturers and surveillance programs.

Fentanyl – a pharmaceutical developed in the 1960s as a safer alternative to morphine – proliferated as a cheaper, more convenient additive. Its potency made it easier to transport in smaller quantities, leading to a surge in its distribution in the 2010s.

Since the international control of a class of synthetic opioids called brorphines in 2022, and China’s blanket ban on another class known as nitazenes in 2025, a window of opportunity has opened for new opioid agonists – one quickly filled by cychlorphine.

While authorities bring themselves up to speed on the extent of the problem in the community, medical specialists are still determining the most effective method for treating overdoses.

First responders typically treat opioid overdoses with a drug called naloxone, which temporarily blocks the mu-opioid receptors.

“We do know it’s more powerful than fentanyl and that naloxone, or Narcan, does not completely block the effects of the drug and multiple doses may be needed to prevent an overdose,” chief medical examiner at Knox County Regional Forensic Center Darinka Mileusnic-Polchan said in February.

Raffa and his colleagues argue that the reasoning behind the advice isn’t based on solid evidence. What’s more, cychlorphine’s tendency to be detected in association with other drugs that interfere with naloxone suggests it may not be the synthetic opioid that’s the problem.

There’s no doubt we’ll be hearing more about this novel opioid and the dangers it poses to the wider community.

The editorial was published in the Journal of Pain Research.

Source: MedicalXpress

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Mike McRae

Mike McRae

Mike is a highly respected science journalist, having written and edited news on innovation, discovery, and technology for more than 20 years. He is also a published author with the University of Queensland Press (Tribal Science: Brains, Beliefs, and Bad Ideas and Unwell: What Makes a Disease a Disease?), and has worked extensively teaching science and producing educational resources.

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Nature: How to spend $25 billion on science: OpenAI’s staggeringly rich research charity gets under way

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  • 30 September 2026

How to spend $25 billion on science: OpenAI’s staggeringly rich research charity gets under way

Jacob Trefethen, who leads life sciences at the OpenAI Foundation, speaks to Nature about the organization’s ambitions to cure disease.

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OpenAI launched a non-profit foundation that it says is one of best resourced philanthropic organizations ever.Credit: doomu/Shutterstock

The OpenAI Foundation — the charity arm of the artificial-intelligence behemoth — is on track to become one of the wealthiest non-profit organizations on the planet. And, with a 26% stake in OpenAI, which is seeking a valuation of around US$1.4 trillion, it could even become the richest. The foundation was created in October 2025, after a tumultuous shake-up of OpenAI’s governance and structure. It has so far committed to giving away at least $25 billion.

This month, the foundation cut a round of cheques as part of a $125-million commitment to fund the creation of freely available data for health and life-sciences research. The grants included $40 million for a project at the University of North Carolina at Chapel Hill to develop cancer vaccines; $500,000 for a pilot project to repurpose data from bankrupt biotechnology companies; and $15 million to an effort to better predict how drugs cross the blood–brain barrier and other membranes. Those awards follow a tranche of $100 million for Alzheimer’s disease research.

Jacob Trefethen, who previously worked at Coefficient Giving, a billionaire-funded foundation, is now head of life sciences at the OpenAI Foundation in San Francisco, California. He tells Nature that this is only the start, and the foundation plans to move fast.

A headshot of Jacob Trefethen smiling.
Jacob Trefethen leads life sciences at the OpenAI Foundation.Credit: Jacob Trefethen

Why is the OpenAI Foundation funding health and life sciences?

Our mission is to ensure AI benefits all of humanity. Part of the reason that we’re starting in the life sciences and health is that we think that’s one of the areas where AI can have the most benefit.

The non-profit Chan Zuckerberg Initiative announced in 2016 that its aim was to cure all disease by the end of the century. Does the OpenAI Foundation have a similar goal?

We intend to be ambitious. We have started with three areas in the life sciences to focus: AI for Alzheimer’s; public data for health; and high-burden diseases — which for us means any disease that leads to over half a million deaths around the world each year or similarly massive ill health.

We’re going to try and ask the question, what’s newly possible, for example, in tuberculosis — the largest infectious killer — that may help people who don’t currently have good-enough options. We have a kind of unifying philosophy and a hope to move quickly.

How do biological data fit in?

We think that the combination of intelligence and more observations of the world is what will deliver breakthroughs for people against disease. And those observations mean scientific data.

We think a lot of these problems that we’re working on, like Alzheimer’s, we collectively don’t know enough to deliver treatments that are excellent for patients. And so that requires more data of various forms to get there, probably. We want to support that underlying scientific infrastructure so that all researchers can build on it and all patients can benefit.

Is it a bit self-serving for the OpenAI Foundation to support projects that will generate data that could make OpenAI’s model more capable?

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Axios: Scoop: Rubio kicked out Iranian delegation

 🥾 Scoop: Rubio kicked out Iranian delegation
 
Secretary of State Marco Rubio speaks during a UN Security Council meeting in New York last week. Photo: Charly Triballeau/AFP via Getty Images

Secretary of State Marco Rubio demanded on Monday that the Iranian delegation to the UN General Assembly immediately leave the country after negotiations stalled, a U.S. official and a second source with knowledge of the matter told Axios’ Barak Ravid.

Why it matters: Though the Iranians were likely to depart soon anyway, Rubio’s move was a highly unusual diplomatic rebuke and laid bare the deep distrust between the two countries amid fruitless efforts to broker an end to the war.

Qatari mediators tried to secure a diplomatic breakthrough between the U.S. and Iran but made little progress, with neither side willing to budge.

Among those ordered to leave New York was Rubio’s Iranian counterpart, Foreign Minister Abbas Araghchi.

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Fortune: Gen Z … Skilled trades can pay 32% more

Carhartt CEO warns schools are steering Gen Z students away from a lucrative career path: Skilled trades can pay 32% more

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Carhartt’s CEO Linda Hubbard believes students need more guidance on skilled trades as employers face a widening shortage of electricians, plumbers, and other workers. Jeff Kowalsky/Bloomberg via Getty Images

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Corporate America is slowly waking up to a crisis facing America’s blue-collar workforce: There aren’t enough skilled workers to fill the jobs already available—and the gap is expected to widen.

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About 1.7 million skilled-trades job openings are projected each year through 2035 as employers contend with both new demand, including the rapid build-out of data center infrastructure, and an aging workforce. But current training pipelines are producing just 55% of the skilled workers needed to fill those jobs.

That’s according to a new report from the Alliance for America’s Skilled Trades, a coalition formed earlier this summer by Ford, Carhartt, BlackRock and Google—and has since expanded to 14 other corporations, including Meta, Microsoft, and The Hershey Company.

But perhaps more troubling, according to Linda Hubbard, CEO of the 137-year-old workwear brand Carhartt, is what happens before workers ever enter the trades full-time: Too many students aren’t being given a clear path toward success. Fewer than half of people who start a trades apprenticeship finish it, while just 29% of starters are working in a trade within five years of leaving their apprenticeship.

“I can’t imagine how frustrating that would be to someone who really had all this enthusiasm to learn, goes into a program, and it’s just really not delivering what it needs to get them to success,” Hubbard told Fortune.

The skilled-trades pipeline starts long before the job site

Hubbard, who came from a blue-collar family, pointed to practical barriers, including a lack of reliable transportation and childcare, that can cause workers to drop out of training programs. But she also pointed to another problem that starts much earlier: the guidance students receive in school.

“We’ve been investing in high school training programs, but maybe we don’t have guidance counselors that are necessarily encouraging people to connect and explore a career in the skilled trades,” Hubbard said. 

While 95% of counselors agree trade school is valuable and a credible post-high school option, just 54% say they often recommend vocational or trade school and only 28% often recommend an apprenticeship, according to the report.

“I would encourage just counselors to think about it more broadly: ‘What are the skills you need to develop and how those can be fulfilling in developing a lifelong career?’” Hubbard said.

For students, the appeal of the career can be both practical and financial. Many vocational programs provide on-the-job training, allowing workers to earn money while they learn to become an electrician, plumber, or HVAC technician. Skilled trades careers pay 32% more than other jobs that don’t require a college degree and offer a later path to entrepreneurship. 

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But the work comes with trade-offs, too: Beyond the long-standing stigma that skilled trades are less respected than white-collar careers, some jobs can be physically demanding and require significant travel as projects start and finish.

Hubbard hopes the new data and workforce alliance can be a first step toward improving the programs that prepare workers for the trades—and making sure more of them actually lead to successful careers.

The attention on skilled trades is something Mike Rowe has sought for decades

While the skilled trades are now catching the attention of many C-suite executives, it’s an issue Mike Rowe has been focused on for decades. Known for his TV show Dirty Jobs, Rowe has long argued that America has overlooked a huge class of essential jobs that don’t require a four-year degree.

“The basic argument was you got a couple million good jobs that don’t require a four-year degree that employers are struggling to fill,” Rowe told Fortune Daily. “The jobs are essential, but for whatever reason, they’re not lauded. They’re not celebrated, and most of them are out of sight and out of mind.”

Now, he said the stigma around the trades is colliding with surging demand for workers—from the construction of data centers to the expansion of the defense industrial base.

“There is a massive—it’s a knife fight in a phone booth—to get the talent that you need right now on a construction site,” he told Fortune’s Ellie Austin.

And those jobs can come with six-figure paychecks. Rowe recently spoke with three electricians working at a data center in Plano, Texas, he said, all under 30 and all earning more than $200,000 a year.

His advice to young people considering their career options was simple: “Pick the tires on everything,” Rowe said. “Look at all of it. Try not to get pulled into the inertia and the suppositions and the pre-existing ideas that a lot of well-intended people in your life might have.”

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Preston Fore

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