Worms Live Longer, Plague Unconfirmed · Morning Gist
Sunday, October 115 stories · 13 min
Worms Live Longer, Plague Unconfirmed
An AMPK drug passes tests in small animals, flu-shot timing for October, a Siberian lab death under scrutiny, and an aging clock built from speech.
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Compound 991, which activates the energy sensor AMPK, extended lifespan in yeast, worms and flies. In mice, it only shifted protein profiles. story 1 ↓
Get a flu shot soon if you live in the West, where cases are rising in the Pacific Northwest. Elsewhere, within weeks is fine. story 2 ↓
A worker at a Siberian plague lab died of pneumonia. Russia says no plague is confirmed, and the WHO has asked for more data. story 3 ↓
A speech-based aging clock trained on 2,928 Latin Americans tracked tau levels, brain scans and epigenetic age, making it a cheap dementia marker. story 4 ↓
Professional patient advocates help with hospital discharges and billing. The only US certification dates from 2018, and evidence they help is thin. story 5 ↓
Lawsuits say GLP-1 drugs cause blindness and pancreatitis, but there's too little adverse-event data to tell how often it happens.
1/5Fight Aging!· Reason· Oct 7
Drug that switches on energy sensor AMPK extends life in yeast, worms, flies
Researchers gave compound 991, a drug that activates the cell's energy sensor AMPK directly, to yeast, worms and flies, and it extended their lifespans. In mice it only changed protein profiles. Commentators call the gains modest.
Why it matters · AMPK is the main reason given for using metformin to slow aging, so a cleaner test of that idea helps judge whether this whole drug strategy is worth pursuing in people.
Know this first
Context from the editor, not the article · 28 sec
1 · What AMPK does
AMPK is an enzyme that senses when a cell is low on energy. It then turns on energy-saving and maintenance programmes and turns off growth. Nearly all organisms with complex cells have it, from yeast to humans.
2 · Metformin and aging
Metformin, the common diabetes drug, is widely studied as an anti-aging candidate. It activates AMPK only indirectly, by disturbing how mitochondria make energy. Its lifespan effects in animals have been inconsistent, and it acts on many other targets too.
3 · Short-lived lab species
Yeast, worms and flies are cheap and quick to test for lifespan. Metabolic tweaks extend their lives much more easily than in mammals, so a positive result there is only a first screen.
2/5STAT· Amanda Erickson· Oct 6
Flu shot timing: early in the West, within weeks elsewhere
Flu is picking up in the Pacific Northwest. Epidemiologist Michael Osterholm says people in the West should get vaccinated now and everyone else within two or three weeks. So far the season looks normal.
Why it matters · When you get a flu shot changes how protected you are at the season's peak, and this is practical advice for this month rather than hype.
Know this first
Context from the editor, not the article · 20 sec
1 · Why flu shot timing matters
A flu shot takes about two weeks to produce protective antibodies, and protection fades over the following months. US health authorities generally advise getting one in September or October, before flu usually peaks in winter.
2 · How the CDC tracks flu
The Centers for Disease Control and Prevention (CDC) publishes weekly flu activity levels by region, from 'minimal' to 'very high'. The levels come from doctor visits for flu-like illness and lab test results. Outbreaks often begin in one region before spreading.
A 28-year-old worker at a Siberian plague research institute died of unexplained pneumonia. Infectious disease physician Krutika Kuppalli argues that nothing points to a pandemic, but Russia should share its testing data.
Why it matters · It shows how to judge an early outbreak report: what is confirmed, what plague can and can't do, and which findings would actually raise the alarm.
Know this first
Context from the editor, not the article · 26 sec
1 · Pneumonic plague
Plague is caused by the bacterium Yersinia pestis. The pneumonic form infects the lungs and can spread between people through respiratory droplets. It is fatal without prompt treatment but responds to common antibiotics.
2 · Pneumonia of unknown etiology
"Etiology" means cause. The label is a standard surveillance term for lung infections whose pathogen hasn't been identified yet. It does not imply a new or exotic microbe; often the cause is never found.
3 · Soviet bioweapons legacy
The Soviet Union ran a secret biological weapons program even though it had signed the 1972 Biological Weapons Convention, which bans such weapons. The program worked with plague, anthrax and other dangerous pathogens.
4/5Fight Aging!· Reason· Oct 8
Speech recordings used to build an aging clock that tracks dementia
Researchers trained machine-learning models on voice and language features from 2,928 Latin Americans to estimate age from speech. People with dementia sounded "older" than their age, most of all those with language-dominant frontotemporal dementia.
Why it matters · A cheap, recording-based marker could widen aging and dementia research in poorer regions, though it doesn't show whether a treatment slows aging.
Know this first
Context from the editor, not the article · 25 sec
1 · What an aging clock is
A model trained on age-related data, such as DNA methylation or brain scans, to estimate a person's age. The gap between estimated and actual age is read as faster or slower biological aging.
2 · Dementia types compared
Alzheimer's disease mainly erodes memory. Frontotemporal dementia (FTD) damages the frontal and temporal lobes, changing behaviour or, in language-dominant forms, speech itself. Mild cognitive impairment is a measurable decline that falls short of dementia.
3 · Validated against other markers
p-Tau217 is a blood marker of Alzheimer's tau pathology. Epigenetic clocks such as Hannum estimate age from chemical tags on DNA. Brain clocks estimate age from MRI structure or activity.
5/5The Conversation: Health· Jennifer Schlinger, Clinical Associate Professor of Social Work, University of North Dakota· Oct 6
What professional patient advocates do, and how to find one
A social work professor explains how patient advocates help people coordinate care, sort out bills and insurance, and speak up with doctors. She also covers where to find one and what to ask. The evidence that they help is thin.
Why it matters · Hospital discharges and billing errors are where care often breaks down. Knowing that this role exists, and how far to trust claims about it, helps when a family health crisis hits.
Know this first
Context from the editor, not the article · 25 sec
1 · Why discharge is risky
When a patient moves from hospital to home or to a rehab facility, medication lists, follow-up appointments and insurance approvals all change hands at once. Mistakes and missed handoffs are common at this point.
2 · Social workers and case managers
Most US hospitals employ social workers and case managers, who plan discharges and connect patients with services. Many of them do advocacy work even if their job title doesn't say so.
3 · Informed consent
This is the principle that patients must understand the risks and options before agreeing to treatment. It became standard from the 1960s on, replacing a model in which doctors decided for patients.
A study in Aging Cell gave 1 to fission yeast, roundworms, fruit flies and mice. The drug directly switches on 2 (AMP-activated protein kinase), the cell's main energy-stress sensor. The three short-lived species lived longer. In mice, the researchers looked only at the 3, the set of proteins tissues make, and report that it shifted toward a "pro-longevity" pattern. They did not measure mouse lifespan.
Reason covered the study at the longevity site Fight Aging!, reproducing the abstract but no effect sizes. He calls the life extension modest.
Why AMPK
When a cell runs low on 4, its energy currency, AMPK detects the rise in AMP and ADP compared with ATP. It then turns on energy-producing and maintenance processes and slows growth. The enzyme looks much the same in humans, flies, worms and yeast. Several treatments that modestly slow aging in lab animals act partly through it.
The best known is 5, the diabetes drug. But metformin activates AMPK only indirectly, by disrupting energy production, and it affects many other pathways. That makes it hard to tell whether AMPK causes any benefit. Animal results for metformin have been mixed.
Why a direct activator helps
Compound 991 is a research compound, not an approved drug. It binds AMPK itself instead of starving the cell of energy. If lifespan goes up, AMPK is the likelier cause. The authors present the result as 6 that AMPK is a drug target with longevity benefits.
The caveats
Reason accepts the logic but doubts the payoff:
Even direct activation gave only a modest gain, and it came in species that respond far more readily to metabolic changes than mammals do.
The mouse data is a biomarker, not an outcome. A protein pattern that looks youthful is not longer or healthier life.
Key details are missing from the summary: the percentage gains, how they varied with dose, whether animals lacking AMPK still benefit, and any safety signals from switching AMPK on throughout the body.
His conclusion, which is his opinion: "One wouldn't expect great things to emerge from attempting this in our species."
What it means
This is clean evidence from animals without backbones that AMPK activation alone can extend life. It helps untangle the metformin story. It says nothing yet about mammalian lifespan, and nothing changes for patients.
The finding
A study published in Aging Cell tested 1 in four species. The drug activates 2 (AMP-activated protein kinase, the cell's main energy-stress sensor) by binding to it directly. Treated fission yeast (Schizosaccharomyces pombe), roundworms (Caenorhabditis elegans) and fruit flies (Drosophila melanogaster) all lived longer. Mice were treated too, but the researchers report only that their proteomic profile changed. That means the set of proteins their tissues made shifted in a way the authors call "pro-longevity". Nobody measured whether the mice lived longer.
The study was covered by Reason at the longevity site Fight Aging!. The coverage reproduces the paper's abstract but no effect sizes. How much longer each species lived, at what dose, and with how much variation is not reported here. Reason describes the effect as modest.
Why AMPK, and why go direct
AMPK sits at the centre of the cell's response to running low on fuel. When 3, the cell's energy currency, runs low, the ratio of AMP and ADP to ATP rises. AMPK detects that shift. It then turns on energy-producing and clean-up processes and slows energy-hungry ones like growth. The enzyme has three parts: an α subunit that does the work and β and γ subunits that regulate it. Full activity needs a phosphate group attached to a particular threonine on the α subunit. The enzyme looks much the same in humans, flies, worms and yeast. That similarity is the reason for testing the same drug across such distant species.
Several interventions that modestly slow aging in lab animals act partly through AMPK. They belong to a broader group of stress responses that boost cellular maintenance and repair. The best-known drug of this kind is 4. But metformin acts indirectly: it disrupts energy production, which raises the AMP/ADP-to-ATP ratio, and AMPK reacts to that. Because metformin does many other things too, a lifespan effect, or the lack of one, can't be pinned on AMPK.
The authors argue that a direct activator solves this problem. Compound 991 is a research tool compound, not an approved medicine. It binds AMPK itself instead of starving the cell of energy, so any lifespan effect is easier to put down to AMPK activation.
How to read the result
A rough analogy: metformin is like pushing a thermostat to turn on by cooling the room, while 991 is like pressing the thermostat's button. If pressing the button helps, the thermostat matters. If cooling the room helps, you can't be sure why.
By that logic, the study is what the authors call it: 5 that AMPK activation alone can extend lifespan in some organisms. Reason accepts the logic but doubts the payoff, for two reasons:
The effect is modest even in easy species. Yeast, worms and flies respond to metabolic changes much more strongly than mammals do. Many treatments that extend life in worms do little or nothing in mice.
Mammal evidence is indirect. A protein profile that looks like a long-lived one is a biomarker, not an outcome. It shows the drug changes mouse biology in a plausible direction, not that mice live longer or stay healthier.
Reason concludes that "one wouldn't expect great things" from trying this in humans. That is his judgment, though it fits the long record of metabolic interventions shrinking as they move from invertebrates to mammals.
What's missing
The excerpt leaves out several things a careful reader would want:
The percentage lifespan gain in each species, and whether it held at more than one dose.
Whether the effect disappears in animals that lack working AMPK. That is the cleanest test that 991 works through AMPK and not something else.
Which proteins changed in mice, in which tissues, and what "pro-longevity" was measured against.
Any safety signals. Turning on AMPK broadly throughout the body could have effects on the heart, muscle or metabolism, which the summary doesn't address.
Bottom line
This is early, mostly invertebrate evidence that turning AMPK on directly is enough to lengthen life in organisms where many metabolic tricks work. It removes one confounder from the metformin debate. It gives no evidence on mammalian lifespan, and the commentator who reported it doubts a large human benefit. Nothing changes for patients.
Remember
Activating AMPK directly, without metformin's side routes, was enough to lengthen life in yeast, worms and flies.
Mouse evidence is only a shift in protein profile. No mouse lifespan or healthspan was measured.
Gains in short-lived species often shrink or vanish in mammals, so expectations for humans should stay low.
Flu activity is rising in the Pacific Northwest, and some public health voices are telling people to get vaccinated now. National data from the 1 (Centers for Disease Control and Prevention) still show minimal flu in most of the country. STAT's Morning Rounds newsletter asked how to time your shot.
The timing trade-off
A flu shot takes about two weeks to produce protection, and that protection fades over the following months. If you get it too late, flu may reach you first. If you get it very early, your immunity may be weaker by the winter peak.
Michael Osterholm directs the University of Minnesota's Center for Infectious Disease Research and Policy. His advice:
In the West, or traveling there: consider getting the shot now.
Everywhere else: book one within two or three weeks. Appointments get harder to find once flu spreads.
"What I see now is a flu year starting out as a pretty normal flu year," he said. This is expert judgment based on surveillance data, not a new study, and the newsletter gives no figures on the Northwest rise.
Other items in the newsletter
2 drifted. These clip-on devices estimate blood oxygen with light. They were already known to be less accurate on darker skin. A new paper found that over five years at one hospital, they moved from overestimating oxygen to underestimating it. One author said he has "no idea" why. The finding comes from a single hospital.
Longevity clinics at nonprofit hospitals. A STAT reporter tried one. She did a treadmill test to exhaustion to measure 3 (peak oxygen use) and a smell test, because loss of smell tracks with faster aging. She also had scans and blood work. The price ranges from $5,500 to $45,000. Critics question whether tax-exempt hospitals should cater to wealthy patients and whether tests such as full-body MRIs are worth doing.
Medicare for All. A 4 poll puts US adult support at 66%, up from 53% in 2020. Six in 10 voters worry about affording care. Democrats (84%) and independents (72%) favor the policy, and 66% of Republicans oppose it.
Billing pressure. Physician Leah Pierson describes administrators asking her to record real but billable diagnoses, a practice called 5. She doesn't know how much each one adds to a patient's bill.
Nobel Prize. Optogenetics won the medicine prize. It uses a light-sensitive algae protein, 6, to switch specific brain cells on and off.
This is a STAT Morning Rounds newsletter dated October 6, 2026. It leads with a practical question for the season: when should you get a flu shot? Its answer is short. The rest of the newsletter covers several other items worth knowing about, including pulse oximeters whose readings drifted over time, the price of hospital longevity clinics, and how billing practices push up hospital charges. Most items are summaries of longer STAT stories, so the detail here is limited.
The flu shot question
Choosing when to get vaccinated is a trade-off. A flu shot takes about two weeks to produce protective antibodies, and that protection fades over the following months. If you get it too late, you may catch flu before you're protected. If you get it very early, your protection may already be fading when the season peaks in winter. US guidance usually lands on September or October for most adults. The problem is that flu is hard to predict, and outbreaks often start in one region before spreading.
STAT's Helen Branswell reports on the current situation. Flu activity is rising in the Pacific Northwest, which has prompted some calls for people to get vaccinated now. The latest national data from the 1, the Centers for Disease Control and Prevention, still show minimal activity in most of the country.
Michael Osterholm directs the University of Minnesota's Center for Infectious Disease Research and Policy, known as CIDRAP. He gives region-specific advice:
If you live in the West or plan to travel there, consider getting vaccinated now.
If you live anywhere else, book a shot within the next two or three weeks. His reason is logistical as well as medical: appointments get harder to find once flu picks up in other regions.
He sees nothing unusual so far. "What I see now is a flu year starting out as a pretty normal flu year," Osterholm said.
This is expert judgment based on surveillance data, not the result of a new study. The newsletter gives no figures for how much activity has risen in the Northwest, and it does not discuss this season's vaccine match or groups at higher risk, such as older adults.
2 drifted in both directions
Pulse oximeters are clip-on devices that estimate blood oxygen by shining light through the skin. They became common during Covid-19. Earlier research showed they are less accurate for people with darker skin, often overestimating oxygen levels, which can hide dangerously low readings. A new paper adds a separate problem. At one hospital over five years, the devices moved from overestimating blood oxygen to underestimating it. One author called the device a "black box" and said: "I have no idea why we found what we found in this paper, and why it's changing year over year." The finding comes from a single hospital, and the newsletter gives no size for the errors. It still raises the question of whether a device can be trusted as a fixed reference over time.
What hospital longevity clinics sell
STAT reporter Sarah Todd went through a longevity program at a nonprofit medical center. She ran a treadmill test to exhaustion to measure 3, the maximum rate at which her body could use oxygen. She took a scratch-and-sniff smell test, because loss of smell is associated with faster aging. She also had scans and blood draws. These programs cost $5,500 to $45,000. A Carnegie Mellon professor argued that this kind of offering makes nonprofit hospitals look like "for-profits masquerading in not-for-profit clothing." Nonprofit hospitals receive tax benefits in exchange for serving the public. Others question whether services such as full-body MRIs are scientifically sound. The newsletter doesn't say what Todd concluded.
Medicare for All polling
A 4 poll found that 66% of US adults now support Medicare for All, up from 53% in 2020. KFF is a nonpartisan health policy research group. The poll also found that 6 in 10 voters worry about affording health care, which the newsletter suggests may explain the rise. Support breaks down along party lines: 84% of Democrats and 72% of independents favor the policy, while 66% of Republicans oppose it.
How billing pressure raises costs
Physician Leah Pierson writes that after she sees a patient, hospital administrators often email her asking her to record certain additional diagnoses or complications. A more complicated patient lets the hospital bill more. The practice is called 5. The diagnoses are real ones, such as low sodium found in lab work. Pierson's concern is that doctors have no idea how much each one adds to a patient's bill. She argues the system leads hospitals to code patients as "more complicated than they truly are." The newsletter's headline for her piece blames AI tools, but the excerpt describes only the requests from administrators and doesn't explain the role of AI.
The Nobel for optogenetics
Optogenetics won the Nobel Prize in medicine. It is a technique that uses light to switch specific brain cells on or off. Karl Deisseroth shared the prize with two other scientists, whom the excerpt does not name. The method grew out of research into how a single-celled alga swims toward light. The answer was 6, a protein that makes any cell it is inserted into sensitive to light. One professor described the change it brought as going from a road atlas of the brain to "something more akin to Google Earth."
What's left open
Each item here is a pointer to a longer story. Two unknowns stand out. Will the Northwest rise turn into an early national season? And why did the hospital's oximeters drift? Neither question is answered yet.
Remember
Osterholm's advice is regional: get vaccinated now in the West and within two or three weeks elsewhere.
Pulse oximeter errors at one hospital changed direction over five years, and the authors can't explain why.
Hospital longevity programs charge $5,500 to $45,000 for tests whose value critics question.
Daria Shipilova, 28, worked at the Irkutsk Anti-Plague Research Institute of Siberia and the Far East, which studies plague, anthrax, tularemia and other dangerous pathogens. She was admitted to hospital with severe pneumonia on Sept. 29 and died about two days later. At least one hospital has reportedly been quarantined, close to 200 contacts are being monitored, and senior Russian health officials have gone to the region.
In the first column of her new STAT series, ID Consult, infectious disease physician Krutika Kuppalli argues that the case deserves scrutiny but that nothing yet supports talk of "the next Covid-19."
What is actually known
Early reports suggested 1, the lung form of plague. Russian authorities instead describe "2," meaning the cause hasn't been identified. They say tests found no pathogen linked to her work.
The World Health Organization (WHO) says Russia has reported no confirmed plague and no further infections among contacts. It has asked for more detail, including whether a second employee also has unexplained pneumonia.
A few contacts tested positive for Covid-19 or 3, a common cold virus.
Nothing reported so far suggests sustained person-to-person spread.
Why plague isn't Covid
Plague is still a possibility given where she worked. Even so, Kuppalli says it would be a very different threat from 4, the virus behind Covid-19. Plague bacteria have been studied for more than a century. Doctors can diagnose the disease, treat it with antibiotics, give preventive drugs to exposed contacts, and isolate patients. Pneumonic plague generally spreads only through close contact with someone who is actively ill. Spread from people without symptoms has never been documented. It is dangerous, but it is a known quantity.
Why transparency still matters
Kuppalli points to Sverdlovsk in 1979. Anthrax spores accidentally released from a Soviet military facility killed at least 66 people, and officials blamed contaminated meat. A 1994 study in Science traced the cases along a narrow strip downwind of the facility. She stresses there is no evidence linking today's case to weapons work. A lab exposure, an accidental release and a weapons program are separate claims, and each needs its own evidence. But that history is a reason to ask for specimens and test results, and to ask whether plague was specifically ruled out.
Her concern about the US is pointed: it is weakening the surveillance, laboratory networks and international ties that let countries check such claims for themselves.
What would change her mind
Confirmation of plague or another high-consequence pathogen, more unexplained pneumonia among contacts, evidence of spread between people, cases outside the contact network, or credible evidence of a lab exposure. None has been reported so far.
The new column is called ID Consult, and its first piece runs in STAT. In it, infectious disease physician Krutika Kuppalli, a former World Health Organization medical officer who ran an Ebola treatment unit in Sierra Leone, takes on a story that spread fast online. A young laboratory worker at a Siberian plague institute died of pneumonia, and a large quarantine followed. Kuppalli argues the case deserves attention and openness from Russia, not panic, and she sets out what we actually know.
The case
Daria Shipilova, 28, worked at the Irkutsk Anti-Plague Research Institute of Siberia and the Far East. The institute researches plague, anthrax, tularemia and other "high-consequence" pathogens, meaning those that can cause severe disease or large outbreaks. She was admitted to hospital with severe pneumonia on Sept. 29 and died about two days later.
The official response was large. At least one hospital was reportedly quarantined, close to 200 contacts are reportedly being monitored, and senior public health officials were sent to the region. A small number of tested contacts had Covid-19 or 1, a common cold virus. Neither is unusual.
Early news stories said she may have had 2. Russian authorities call it "3," a standard term meaning the cause hasn't been identified. They say testing found no pathogen associated with her work. The World Health Organization's latest assessment says Russia has reported no confirmed plague cases in Irkutsk and no further infections among contacts. The WHO has asked Russia to clarify three things: what caused her pneumonia, which pathogen prompted the public health measures, and whether a second employee also has unexplained pneumonia, as media reports suggest.
Separating signal from speculation
Kuppalli's main point is about how to read uncertain evidence. A big response, conflicting reports and little information naturally invite suspicion. But suspicion is not confirmation, and monitoring contacts doesn't mean they are infected. "Unknown etiology" does not mean a new pathogen has appeared. It means the cause hasn't been found yet, which is common with severe pneumonia.
She lists the open questions herself: the cause of death hasn't been made public, and the possible second case needs explaining. Those are reasons for continued scrutiny, not for conclusions.
If it is plague, why that still isn't Covid
Plague is caused by Yersinia pestis, a bacterium that has infected humans for thousands of years. In the pneumonic form, the infection settles in the lungs and can pass between people in respiratory droplets. Untreated, it can kill quickly. Kuppalli treats it as a live possibility given where Shipilova worked.
She argues that confirmation still wouldn't put us back in early 2020, for two reasons.
It is a known pathogen.4, the virus that causes Covid-19, was new. Nobody knew how it spread, what course the illness would take, or how to treat or prevent it. Plague has been studied for more than a century. Diagnostics exist, standard antibiotics work, and the response is well established: trace contacts, give exposed people preventive antibiotics (5), isolate patients, and apply infection control in hospitals.
It spreads differently. Spreading pneumonic plague generally takes close exposure to respiratory particles from someone who is actively sick, and transmission from people without symptoms has never been documented. Covid's ability to spread from people who felt fine is much of what made it so hard to contain. Kuppalli's illustration of the gap: with plague, finding and treating the people around a sick patient can break the chain. With an infection that spreads silently, the chain has already moved on before anyone notices. She adds that this doesn't make plague benign. The risk should be judged on what we know about this pathogen, not by analogy to the last pandemic.
Why Russia's history matters
Kuppalli doesn't dismiss the darker theories. She treats them as claims that need evidence. The Soviet Union ran a large secret biological weapons program while party to the 6, the 1972 treaty banning such weapons, and that program worked with Y. pestis.
Her main precedent is Sverdlovsk. In 1979, aerosolized spores of Bacillus anthracis, the anthrax bacterium, escaped from a military biological facility and caused an outbreak of 7 that killed at least 66 people. Soviet authorities blamed contaminated meat. Investigators later mapped the human cases and livestock deaths and found they lay along a narrow strip downwind of the facility. That pattern, published in Science in 1994, pointed clearly to an airborne release. A biological event happened, people died, the official explanation was false, and the truth took years to come out.
She is explicit that this doesn't tie the current case to weapons work, and there is no evidence that it does. A lab exposure, an accidental release and a weapons program are three separate claims, each needing its own evidence. The history justifies demanding independent verification, and she lists the questions: What specimens were collected and how were they tested? Was Y. pestis specifically ruled out? Which pathogens did Shipilova handle? Was there a lab incident or occupational exposure? Has any contact developed a similar illness? Why was the quarantine so large? And will Russia share enough with international bodies and independent experts for its conclusions to be checked?
The US angle
Kuppalli argues that the more serious worry is at home. Surveillance, in her account, is national and global security, not just case counting. It depends on laboratory networks, 8, epidemiologists, infectious disease specialists and working relationships with scientists abroad. She says the United States is weakening parts of that infrastructure, which leaves it less able to spot unusual events and more dependent on governments whose claims it may need to check independently. The column does not say which cuts she means.
What would raise concern
She names the developments that would change her view: confirmation of Y. pestis or another high-consequence pathogen, more unexplained pneumonia among contacts, evidence of spread between people, cases outside the immediate contact network, or credible evidence of a laboratory exposure. None has been reported.
This is an opinion column, and it rests on limited public information. The cause of death is unknown, the second-case report is unresolved, and Kuppalli concedes the full story may never come out. Her closing advice is to say "we don't know yet," keep asking, and not fill the gaps with fear.
Remember
"Unknown etiology" means the cause hasn't been found yet, not that a new pathogen has emerged.
Pneumonic plague is treatable with antibiotics, and spread from people without symptoms has never been documented, unlike Covid.
The 1979 Sverdlovsk anthrax cover-up is why experts want Russia's test data checked independently.
A study in Science Advances describes an 1 built from people talking. Fight Aging! writer Reason highlighted it, along with a familiar caveat about aging clocks in general.
What was built
An aging clock is a model that estimates age from biological data that change over time. Most use DNA methylation (chemical tags on DNA) or brain scans, which are costly and hard to collect at scale. This team used speech instead. The models drew on acoustic features (how the voice sounds) and linguistic features (what words and structures people use) from 2,928 people in five Latin American countries.
The sample covered healthy controls, people with mild cognitive impairment (decline short of dementia), Alzheimer's disease, and two forms of 2: one dominated by language problems and one that isn't. Supervised models learned to predict chronological age. The difference between predicted and actual age is the 3. A positive gap means the person's speech sounds older than their age.
What it found
Healthy controls had the smallest gaps. Patient groups had larger ones, ranked Alzheimer's < non-language FTD < language-dominant FTD. That ordering fits, since language-dominant FTD attacks speech directly.
Gaps tracked clinical and cognitive measures.
The summary available doesn't report effect sizes or how accurately the model predicts age.
Caveats
Every result is 7: one snapshot per person. That shows speech tracks disease status and other aging markers, but not whether it predicts future decline or responds to treatment. The authors call it a "biomarker candidate" for research, especially in underrepresented, low-resource settings.
Reason makes a broader point. Researchers have built clocks for years, yet nobody can trust that any given clock will move the right way when aging is actually treated. Only long, expensive lifespan studies can confirm that. Until that problem is solved, he argues, clocks can't do much to speed up rejuvenation research. A speech clock is cheap and easy to scale, but it faces the same gap.
A new paper in Science Advances describes an 1 built from speech recordings. Fight Aging! writer Reason covered it, and he also restated a doubt about what aging clocks can do for anti-aging research. The material available is the paper's abstract plus his commentary, so this account covers what was reported. It can't supply numbers the abstract leaves out.
The problem: clocks that are hard to scale
An aging clock is a machine-learning model trained to estimate age, or age-linked outcomes such as mortality or disease risk, from biological data. As Reason puts it, almost any complex dataset that changes with age can serve. Standard methods search for the combination of measurements that best predicts the target. The best-known clocks use DNA methylation or brain MRI. Both cost money, need equipment and trained staff, and have mostly been built on populations from wealthy countries. The authors say scalability is the main limit, and that dementia research in places like Latin America is short of cheap tools.
Speech is an appealing alternative. Recording someone talking takes a microphone and a few minutes. Voice and language also change with age and with neurodegenerative disease.
What the team did
The researchers pooled 2,928 people from five Latin American countries. Participants fell into five groups:
healthy controls;
mild cognitive impairment (MCI), a measurable decline that falls short of dementia;
Alzheimer's disease (AD);
non-language-dominant frontotemporal dementia (nldFTD), where behaviour and other functions are mainly affected;
language-dominant FTD (ldFTD), where speech and language break down first.
From each recording they extracted two kinds of features. Acoustic features describe the sound of the voice. Linguistic features describe the words and structure of what was said. The abstract doesn't list the specific features. Supervised models were trained to predict each person's chronological age. The output of interest is the 2: predicted age minus actual age. A positive SAG means the speech profile sounds older than the person is.
As an illustration (not data from the study): a 68-year-old whose speech the model reads as typical of a 75-year-old has a SAG of +7 years.
What they found
Diagnostic separation. Healthy controls had the lowest SAGs, and all patient groups had higher ones. Among the dementias the order was AD < nldFTD < ldFTD. It makes sense that language-dominant FTD scores highest, because that disease attacks the thing being measured. That also means part of the "older-sounding" signal in this group may reflect language damage more than aging in a broader sense. The abstract doesn't say where MCI falls relative to the dementias.
Clinical links. SAG was associated with clinical and cognitive measures. The specific domains aren't given in the abstract.
Molecular pathology. In Alzheimer's patients, SAG correlated with 3, a blood marker of phosphorylated tau that tracks Alzheimer's pathology. So in AD, speech that sounds older goes with more disease biology, not just older appearance.
Brain clocks. MRI-based brain-age clocks (structural, functional and combined) were associated with SAG in AD, nldFTD and ldFTD. The abstract doesn't report this link in healthy controls.
Epigenetic clocks. In healthy controls and AD, SAG correlated with three methylation-based clocks: 4 (an early clock trained on blood), Retroclock and OMICmAge. In ldFTD, only Retroclock and OMICmAge showed a link.
Social exposome. In healthy controls and AD, SAG was associated with the "5", meaning measures of a person's social and environmental exposures across life.
The abstract reports no correlation coefficients, model error, or group differences in years. Readers can't yet judge how strong any of these links are, only that they reached the authors' bar for association.
How much this shows
The authors are careful with their wording. They call SAGs "6 markers" and a "biomarker candidate". Each person was measured once. The study therefore shows that speech-derived age differs between diagnostic groups and agrees with other aging markers at one point in time. It does not show that a high SAG predicts later decline, dementia or death, or that SAG changes when health improves. That would take longitudinal follow-up.
A few other open questions follow from the design. Speech features depend on language, dialect and education. The authors describe the clock as "culturally adaptable", but a model trained on Spanish- and possibly Portuguese-speaking Latin Americans would need retraining elsewhere. Pooling patients with healthy controls may also lead the model to treat disease-related speech changes as "aging". That would explain the clean diagnostic separation but blurs what "speech age" means.
Reason's broader objection
Reason's commentary is about aging clocks in general, not this paper. He argues that after many years of clock development, the field still doesn't know how to use them to speed up therapies. The promise is a quick readout of whether a rejuvenation treatment works, without waiting years for people or animals to die. The catch is that nobody can trust a given clock to respond correctly to an intervention that actually targets aging. A treatment might shift the clock without improving health, or improve health without shifting it. Only long, expensive lifespan studies can settle that. Until it is settled, he argues, clocks add little to the pace of development.
Seen that way, the speech clock is cheaper and easier to deploy than most, and its links to tau, brain imaging and epigenetic clocks suggest it is measuring something real. But it hasn't been tested against the question Reason cares about. Its nearer-term value is probably in dementia research and screening in settings that can't afford scans or methylation assays.
Remember
Speech that sounded older tracked tau levels in Alzheimer's, plus brain-scan and epigenetic clocks in several groups.
All results are single-time-point, and the abstract gives no effect sizes, so predictive value is unproven.
Like other aging clocks, it's unknown whether it would respond correctly to a real anti-aging treatment.
Jennifer Schlinger, a social work professor at the University of North Dakota and a former 1, has written a practical guide to the role for The Conversation. A patient advocate is someone whose job is to help a patient get through the healthcare system. The piece is an explainer, not a study.
The gap advocates fill
Schlinger's example: a mother is discharged to rehab after hip replacement surgery. She doesn't know whether insurance covers the whole stay, whether she has enough pain medication, or whether her prescriptions will transfer correctly. These problems fall between the hospital, the rehab facility, the pharmacy and the insurer, and none of them necessarily owns the whole picture.
Advocates work in that gap. They:
explain medical information, such as side effects and treatment options
make sure the care team hears the patient's questions and preferences
coordinate referrals and transport between providers
before discharge, arrange support such as home-delivered meals, home healthcare and therapy
Some specialize in money. They check bills for duplicate or incorrect charges, sort out insurance coverage, appeal denied claims, and set up payment plans. Schlinger argues that even when family members are already advocating for the patient, a professional adds an outside view that isn't clouded by the emotion of the illness, plus knowledge of resources the family may not know about.
A young credential
The role started in 1966, when Ruth Ravich founded a patient representation department at Mount Sinai Hospital in New York. It grew alongside the patient rights movement and the shift to 2, the principle that patients must understand their options before agreeing to treatment.
For most of that time, anyone could call themselves an advocate. The only US certification, from the 3, dates from 2018. It requires an exam and continuing education, but it is optional. Many advocates are uncertified nurses or social workers.
The evidence is weak
The only outcome figure in the article is from a 2023 survey by the 4, a nonprofit alliance. In it, 92% of patients and providers said advocates improved care. That measures how people felt about the help, not hard outcomes such as readmissions or errors. An advocacy group ran it, and the article gives no method. Whether advocates improve measurable outcomes is still unshown.
How to find one
Ask the hospital for its social worker, 5 or staff advocate. Veterans Affairs facilities have them.
Search the Centers for Medicare and Medicaid Services website or the National Association of Healthcare Advocacy.
Expect cost to vary. The service may be free, covered by insurance, or paid out of pocket.
Before meeting one, decide your main goal, write down your questions, and bring medication lists, records and bills. Ask about their experience with cases like yours and how often you'll hear from them.
Jennifer Schlinger, a clinical associate professor of social work at the University of North Dakota, has written a practical guide to professional 1 for The Conversation. She used to work as one herself, in hospitals, home health and hospice. A patient advocate is someone whose job is to help a patient get through the healthcare system: explaining medical information, coordinating care between providers, untangling bills, and making sure the care team hears what the patient wants. The piece is an explainer, not a research report. Its one piece of outcome data is weak, as explained below.
The problem advocates address
Schlinger opens with an example. A mother is discharged to a rehabilitation center after hip replacement surgery. She has paperwork and an address, and a lot of open questions:
Will insurance cover the whole rehab stay?
Does she have enough pain medication to last until she settles in?
Will the hospital send her prescriptions over, and will they be correct?
None of these questions is medical in the narrow sense. They fall into the gaps between institutions: the hospital, the rehab facility, the pharmacy and the insurer. Each of those organizations handles its own part, and nobody necessarily owns the whole picture. That gap is what an advocate is meant to fill.
Where the role came from
Schlinger traces patient advocacy to the Civil Rights Movement's emphasis on individual rights. In 1966 Ruth Ravich founded the Department of Patient Representation at Mount Sinai Hospital in New York, which is widely considered the start of the formal role. Over the following decades, the patient rights movement made 2 the norm. Informed consent means patients must understand their options and risks before agreeing to treatment. Advocates taught patients about these rights and helped them take part in decisions that doctors had once made alone.
For most of that history, "patient advocate" was a title people gave themselves, with no standard behind it. In 2018 the 3 created a professional certification. It is the only one for this role in the US. Candidates must pass an exam covering:
medical concepts
paying for care
how the healthcare system is organized
working collaboratively with patients
They must also keep up continuing education. Certification is optional. Many people who do advocacy work are uncertified nurses or social workers, especially in rural facilities where staff cover several roles.
What advocates actually do
Schlinger groups the work into a few areas.
Explaining and representing. Advocates explain things like medication side effects and treatment options. They make sure patients' questions get answered and their concerns reach the care team. Their stated job is to keep the patient's needs, preferences, goals and values central to the care.
Coordinating care. When a patient is referred to a specialist, the advocate carries the details of the patient's condition and priorities from one provider to the next, and may arrange transport. In her own discharge-planning work, Schlinger followed a set sequence:
Learn the patient's goals.
Assess their living situation and what care they need.
Find out what worries them about the discharge plan.
Before discharge, arrange support such as home-delivered meals, home healthcare, and physical, occupational or speech therapy.
Money. Some advocates specialize in billing, coding and insurance. They can:
explain medical terms and individual charges
check bills for errors such as duplicate or incorrect charges
work out coverage and reimbursement
appeal denied claims, acting as go-between for the patient, facility and insurer
set up payment plans or find financial help
If a question is outside their expertise, they point the patient to the right person.
Working with families. Schlinger is clear that family advocacy is invaluable. She argues that a professional adds something different: an outside view that isn't clouded by the emotion of the illness, expert knowledge of the system, and awareness of resources the family may not know exist.
What the evidence shows
The only outcome figure in the article is from a 2023 survey by the 4, a nonprofit alliance. In that survey, 92% of patients and healthcare providers said working with an advocate improved patients' care. Treat this figure cautiously:
It measures perceived benefit, not outcomes such as readmissions, medication errors or money recovered on bills.
An advocacy organization ran it, so it has an interest in a positive result.
The article gives no sample size or method, and doesn't say how respondents were chosen.
The article does not show whether advocates change hard outcomes. It is plausible that they do, especially at care transitions and in disputes over bills, but this piece doesn't demonstrate it.
Finding one and what it costs
Schlinger admits it is not always easy to find an advocate. Places to start:
Ask for the hospital social worker or 5.
Ask your hospital or clinic whether it has a patient advocate on staff. Many facilities do, including Veterans Affairs.
Search the Centers for Medicare and Medicaid Services website or the National Association of Healthcare Advocacy.
Cost varies. Sometimes the healthcare organization provides the service or insurance covers it. In other cases families pay out of pocket. The article gives no price range.
An advocate employed by a hospital and an independent one you pay yourself may be in different positions when it comes to challenging that hospital. The article doesn't address this point, but it's worth weighing when you choose.
Preparing and vetting
Before a first meeting, Schlinger suggests:
Decide your main goal, such as going home, clarifying a treatment plan or understanding medication changes.
Write down your concerns and questions. The Care Partner Project publishes checklists for this.
Gather medication lists, medical records, insurance documents and bills.
To judge whether an advocate is a good fit, ask about their background and credentials, and then:
What experience do you have with cases like mine?
Can you give an example of a difficult situation you helped a family through?
How often will we be in touch?
How do you help patients raise concerns with their providers?
Remember
Advocates work in the gaps between hospital, rehab facility, pharmacy and insurer, especially at discharge and in billing disputes.
Certification has existed only since 2018 and is optional, so ask any advocate about their background.
The 92% figure comes from a satisfaction survey run by an advocacy group, not from measured outcomes.
In Alzheimer's, larger gaps went with higher 4, a blood marker of tau pathology.
Gaps were associated with MRI-based brain clocks in Alzheimer's and both FTD groups.
In healthy controls and Alzheimer's patients, gaps correlated with three epigenetic clocks: 5, Retroclock and OMICmAge. In language-dominant FTD, only two of the three showed a link.
Gaps were also associated with the "6", meaning a person's social and environmental circumstances, in healthy controls and Alzheimer's.
