The administration claims credit for fewer overdose deaths, children's intensive care quietly shrinks, and two aging studies look past the usual targets: splicing proteins and brain support cells.
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U.S. overdose deaths fell 27% in 2024, but researchers say the decline began before either Trump term, contradicting the administration's claim. story 1 ↓
U.S. hospitals offering any overnight pediatric care fell from 1,749 to 1,226 between 2008 and 2022. Medicaid cuts could close more. story 2 ↓
Boosting the splicing protein SRSF1 extended mouse lifespan 14% and made cells younger without erasing their identity. It's one study so far. story 3 ↓
RFK Jr. reportedly wants a ketogenic-diet researcher to run NIMH. Steven Novella says the evidence for metabolic psychiatry is still mostly preliminary. story 4 ↓
Immature brain support cells in epilepsy patients' hippocampal tissue tracked age-related reasoning decline. It's only a correlation, but it points beyond neurons. story 5 ↓
HHS will let small compounding pharmacies make six peptides the FDA hasn't approved, though the evidence behind many of them is thin.
1/5STAT· Theresa Gaffney· Oct 28
Experts dispute Trump administration's claim of credit for falling overdose deaths
The Department of Health and Human Services credited both Trump administrations for falling overdose deaths. Addiction researchers say the causes are wider: a changing drug supply, changes in how people use drugs, and harm reduction.
Why it matters · If the wrong policies get the credit, the ones that actually worked, like Medicaid-funded addiction treatment, could be cut just as the gains look secure.
Know this first
Context from the editor, not the article · 26 sec
1 · The fentanyl-era overdose crisis
U.S. overdose deaths climbed for years and hit about 110,000 a year around 2022–2023. Most of those deaths involved illicitly made fentanyl, a cheap synthetic opioid strong enough that small changes in dose can kill.
2 · What harm reduction means
Harm reduction aims to keep people who use drugs alive, without requiring them to stop first. Examples include handing out naloxone, an opioid overdose reversal drug, fentanyl test strips, and low-barrier access to buprenorphine or methadone.
3 · Medicaid and addiction treatment
Medicaid, the public insurance program for low-income Americans, is the largest payer for opioid addiction treatment in the U.S. Losing coverage often means losing access to medication.
2/5KFF Health News· Katheryn Houghton· Oct 28
US hospitals are closing intensive care units for critically ill children
Hospitals in Montana, Oregon and Missouri closed intensive care units for children this year, citing too few patients, too few specialists and low pay. The sickest children now travel farther to regional hubs.
Why it matters · Where a critically ill child can be treated is shifting quietly, one closure at a time. Nobody yet has the data to say whether longer transfers are costing children's lives.
Know this first
Context from the editor, not the article · 25 sec
1 · What a PICU is
A pediatric intensive care unit (PICU) treats critically ill children, from a few weeks old into the teens, who may need ventilators or constant monitoring. It is separate from the NICU, which cares for newborns.
2 · Why kids' care pays less
About half of US children are covered by Medicaid or the Children's Health Insurance Program (CHIP). These public programs usually pay hospitals less than private insurance, so children's units often lose money.
3 · Regionalization trade-off
Concentrating rare, complex care in a few high-volume centers can build expertise. The cost is longer transport times for patients, and less spare capacity when demand spikes.
3/5Fight Aging!· Reason· Oct 28
Boosting splicing protein SRSF1 made old cells look younger and lengthened mouse lifespan 14%
Researchers used an AI age predictor to screen genes in old human skin cells. Raising levels of SRSF1, a protein that controls RNA splicing, made the cells look younger, and it lengthened aged mice's lifespan by 14%.
Why it matters · It points to a possible route to partial cellular rejuvenation that avoids the cancer risk of Yamanaka-factor reprogramming, but so far the evidence is one mouse lifespan result.
Know this first
Context from the editor, not the article · 27 sec
1 · Yamanaka factors and reprogramming
Four genes (OCT4, SOX2, KLF4, MYC) that can turn adult cells back into stem cells. Given briefly, they reset some age-related gene activity. Given too long, cells lose their identity and can form tumors.
2 · What splicing factors do
Genes are copied into RNA, which is then cut and rejoined (spliced) before becoming protein. Splicing factors decide which pieces are kept, so a single factor can change the protein versions made from thousands of genes.
3 · Aging clocks
Statistical models trained to estimate a cell's or person's biological age from molecular data such as DNA methylation or gene expression. A lower predicted age is often used as a stand-in for rejuvenation.
4/5Science-Based Medicine· Steven Novella· Oct 28
RFK Jr. reportedly favors a ketogenic-diet researcher to lead mental health institute
Science reports that Health Secretary RFK Jr. rejected the NIH director's pick to run the National Institute of Mental Health. He favors Shebani Sethi, who studies ketogenic diets for psychiatric illness. Neurologist Steven Novella argues her field overstates thin evidence.
Why it matters · The person who runs NIMH shapes which mental-health research gets funded. Diet-based psychiatry is also reaching patients before rigorous trials have tested it.
Know this first
Context from the editor, not the article · 27 sec
1 · What NIMH does
The National Institute of Mental Health is the part of the US National Institutes of Health (NIH) that funds most federal research on mental illness. Its director sets research priorities and oversees billions in grants.
2 · Who's involved
Robert F. Kennedy Jr. is Secretary of Health and Human Services and leads the "Make America Healthy Again" (MAHA) movement, which emphasizes diet and lifestyle. Jay Bhattacharya is NIH director and reports to him.
3 · The ketogenic diet
A very low-carbohydrate, high-fat diet that pushes the body to burn fat and produce ketones. It has proven value in some childhood epilepsy. Its use for weight loss and mental illness is less established.
5/5Fight Aging!· Reason· Oct 28
In epilepsy patients, unusual immature brain support cells track age-related reasoning decline
A study of hippocampus tissue removed during epilepsy surgery found that older patients had more of an unusual type of immature support cell, and that this went along with weaker fluid intelligence, meaning reasoning ability.
Why it matters · Most drugs for cognitive decline target neurons and have done little. This study points to support cells instead, though so far it only shows a correlation, in an unusual group of patients.
Know this first
Context from the editor, not the article · 25 sec
1 · Astrocytes are not just glue
Astrocytes, also called astroglia, are star-shaped support cells in the brain. They regulate chemical messengers, blood flow and connections between neurons. Rodent studies suggest they also help control learning and memory.
2 · Living brain tissue is scarce
Most human brain tissue studied comes from autopsies, which mostly means people with advanced disease. Healthy or early-stage tissue usually comes from people having brain surgery, and those people may not represent everyone.
The 1, the federal agency that runs public health programs, has credited both Trump administrations with driving down U.S. drug overdose deaths. Its press release cited two new reports, both written by HHS's own officials and staff. Addiction experts quoted in STAT's Morning Rounds newsletter say the causes are much broader than one administration's policies.
What the numbers show
After years of steep increases that peaked during the COVID-19 pandemic, U.S. overdose deaths fell 27% in 2024. Preliminary 2025 data show another meaningful drop. The newsletter doesn't give the 2025 figure, and preliminary counts can change. Overdose deaths remain high even after the fall.
The timing problem
Epidemiologist Nabarun Dasgupta, who also advocates for 2, says the timeline undercuts the administration's claim. "The decline started years ago, with many states peaking during the COVID pandemic," he wrote. He argues the trend deserves credit from Trump's first term, the Biden administration, and Trump's second term. A policy adopted in 2025 can't explain a turn that began in 2021 or 2022.
What probably did drive it
Last week Dasgupta published a report on the likely contributors. They fall into three groups:
Changes in the drug supply, such as what is mixed into street opioids and how strong they are.
Changes in how people use drugs, not only whether they use.
Public health and harm reduction programs, which aim to keep people who use drugs alive. Examples are 3, a drug that reverses opioid overdoses, and easier access to addiction treatment.
The newsletter doesn't say how much each factor contributed. All of this evidence is observational: several things changed at once and nobody ran a controlled trial, so dividing the credit means making inferences. According to the newsletter, experts agree that one thing didn't help: closing the border.
The risk ahead
Dasgupta and others warn that 4 cuts in the 5, the 2025 budget law, could undo progress in addiction treatment. Medicaid is the public insurer for low-income Americans and a major payer for addiction medications. The law adds paperwork requirements for keeping coverage. "The paperwork burden associated with maintaining coverage is unrealistic for many in chaotic phases of drug use, namely those who need help the most," Dasgupta said. People who lose coverage can lose access to medications such as 6 and , which lower the risk of overdose death.
The 1, the federal agency that oversees public health programs, released a statement this week crediting both Trump administrations for the fall in U.S. drug overdose deaths. It cited two new reports, both written by HHS's own officials and staff. STAT's Morning Rounds newsletter reports that addiction experts see the picture as more complicated than one administration's record.
The numbers
U.S. overdose deaths rose steeply for years and spiked during the COVID-19 pandemic. In 2024 they fell 27%. Preliminary 2025 data show another meaningful decline. The newsletter doesn't give the 2025 figure, and preliminary counts often change as death investigations finish. Overdose mortality also remains high in absolute terms. A 27% drop from a record peak still leaves deaths well above where they stood before fentanyl took over the supply.
The timing argument
Nabarun Dasgupta, an epidemiologist and 2 advocate, makes the central objection: the timing doesn't fit a single-administration story. "The decline started years ago, with many states peaking during the COVID pandemic," he wrote to STAT. He argues the continued fall "deserves credit from Trump 1, Biden, and Trump 2 admins."
The reasoning is simple. If many states peaked in 2020–2022 and began declining then, policies adopted in 2025 can't explain the turn. At most they can affect whether the decline continues.
What likely drove the decline
Last week Dasgupta published a report on the likely contributing factors. The newsletter sorts them into three groups but doesn't give their relative sizes:
Changes in the drug supply. The newsletter doesn't say which changes. More broadly, researchers have pointed to shifts in what is mixed into the illicit opioid supply and how potent it is.
Behavioral changes among people who use drugs. These are changes in how people use, not only whether they use. A general example is switching from injecting to smoking, which some evidence links to lower overdose risk. The newsletter doesn't detail which changes Dasgupta's report covers.
Public health and harm reduction programs. In general these include wider 3 access, including over-the-counter sales, and easier access to addiction medicines.
One factor experts agree did not help, according to the newsletter, is closing the border. That matters because border enforcement is a central part of the administration's case on drugs.
How much weight the evidence can bear
Any attribution here is observational. No one ran a trial that assigned some states a policy and others none. Researchers have to piece together a cause from timing, differences between regions, and drug-testing data, and several things changed at once. The newsletter doesn't say what methods the two HHS reports used or how they separated their policies' effects from trends already in motion. Dasgupta's report breaks down factors that "likely" played a role, and that wording signals real uncertainty, not settled proof.
The risk ahead
Dasgupta and others warn that coming 4 cuts could undo much of the progress in addiction treatment. The cuts come from the 5, the 2025 budget and tax law. Among other changes, the law adds eligibility and paperwork requirements for some enrollees. Medicaid pays for a large share of opioid addiction treatment in the U.S.
"The paperwork burden associated with maintaining coverage is unrealistic for many in chaotic phases of drug use, namely those who need help the most," Dasgupta said. If people lose coverage, they can lose access to 6 or 7, the two main medications for opioid addiction, which lower the risk of death. That would be the mechanism for a reversal.
What's still open
The newsletter leaves the key question open: how much each factor contributed. That split decides which policies are worth protecting. It also doesn't say whether the 2025 decline is slowing, or which states, if any, are seeing deaths rise again.
Remember
Many states' overdose deaths peaked during COVID-19, before the second Trump term, which weakens any single-administration claim.
Experts say border closure didn't drive the decline. Drug supply, user behavior and harm reduction likely did.
Losing Medicaid coverage over paperwork could cut access to addiction medications and reverse the gains.
US hospitals keep closing the units that treat the sickest children. In the past year, pediatric intensive care units (1, wards for critically ill kids, separate from newborn units) closed in Montana, Oregon and Missouri. Overnight children's wings also shut in Illinois and California.
The numbers
A study led by Kenneth Michelson of Lurie Children's Hospital in Chicago counted hospitals with 2, meaning wards where children stay overnight. The number fell nearly 30% between 2008 and 2022, from 1,749 to 1,226. Three-quarters of US hospitals now have no overnight pediatric beds at all. The decline extends to routine care too: the number of hospitals that perform 3 on children fell by more than half between 2003 and 2022.
Why hospitals close them
Hospitals give several reasons:
Low volume. Few children need intensive care, and falling birth rates, vaccines and earlier treatment have reduced pediatric admissions.
Staffing. There are too few 4, who earn less than doctors who treat adults.
Money. Payers often pay less for children than for adults, and child-sized equipment adds cost.
Elizabeth Mack, a pediatric critical care doctor and spokesperson for the American Academy of Pediatrics, calls the decision for most hospitals "a spreadsheet issue."
One closure up close
Community Medical Center in Missoula, Montana, owned by for-profit Lifepoint Health, closed its PICU this month. The CEO says the unit averaged about two critically ill children a month. He expects the closure to affect about 25 patients a year. No pediatric critical care doctor has lived locally for eight years; specialists have flown in on rotation instead. Children needing a ventilator or seizure monitoring will now be stabilized and transferred. The nearest other PICU in the state is in Kalispell, about 150 miles away. The hospital keeps its newborn ICU, its general pediatric ward and its emergency care.
The worries
Raj Basu, critical care chief at Lurie, says hubs see a "creeping sense" that children arrive sicker after long transfers. He also says there isn't yet enough data to prove it. In the 2022 surge of children's illness, small emergency departments called 10 to 20 hospitals to place one child. Michelson expects that to happen again.
Mack and other researchers warn that 5 cuts will make this worse. New paperwork hurdles aimed at adults can still cost children their coverage, and fewer insured patients means less hospital revenue.
Proposed fixes include regional networks that share training and transfer protocols, federal funding for underserved areas, and higher Medicaid payment rates. None is funded yet.
Hospitals across the US are closing the units that care for the sickest children. In the past year, pediatric intensive care units (1) closed in Montana, Oregon and Missouri. These units treat critically ill patients from a few weeks old into the teens or early adulthood, separately from neonatal ICUs for newborns. Hospitals in Illinois and California also shut overnight pediatric wings. The beds are often turned into services for newborns or adults. Pediatric intensive care is becoming concentrated in large regional hubs, so critically ill children travel farther.
How large the decline is
The clearest numbers come from a study led by Kenneth Michelson, who directs emergency medicine research at the Ann and Robert H. Lurie Children's Hospital of Chicago. It counted hospitals with 2, the wards where children stay overnight. That number fell nearly 30% between 2008 and 2022, from 1,749 hospitals to 1,226. Three-quarters of US hospitals now offer no pediatric inpatient services at all.
According to Michelson, the losses spread into everyday care. The number of hospitals performing 3 on children fell by more than half between 2003 and 2022. Appendectomy is one of the most common pediatric operations, so the drop suggests routine as well as specialist care is moving to hubs.
Why hospitals are closing units
Hospitals usually point first to low volume. Few children ever need intensive care, and there are fewer young patients overall: birth rates have fallen, vaccines prevent many hospitalizations that used to be common, and doctors catch and treat illness earlier.
Staffing is the second problem. The US is short of 4, who earn less than doctors who treat adults. Money is the third. Hospitals are often paid less to treat children than adults, and they must buy separate child-sized equipment. About half of US children are covered by 5 or the related 6, public programs that generally pay less than private insurers.
Elizabeth Mack is a pediatric critical care doctor, spokesperson for the American Academy of Pediatrics and a hospital quality consultant. She calls the decision for most hospitals "a spreadsheet issue." She says the care is "very pricey" and "not sustainable," and that "there's not a great answer here."
Better medicine also makes the remaining cases harder. More children now survive complex illnesses that used to kill them. Raj Basu, critical care chief at Lurie, says that when these children do need intensive care, their conditions often require a lot of expertise. He argues that hospitals taking such cases without the right doctors or experience could put patients at risk.
A case study: Missoula
Community Medical Center in Missoula, Montana, closed its PICU this month. The article shows what that unit could do. In 2022, Darby Waldbillig's nearly 2-year-old daughter developed 7, a life-threatening infection that swells the tissue around the brain and spinal cord. Local emergency staff in Helena started antibiotics, and she was flown about 100 miles to Missoula. She spent more than a week in the PICU and survived. Her mother credits the unit's doctors.
CEO Greg Cook says the unit averaged about two children a month needing intensive care when the closure was decided. He expects it to affect about 25 patients a year. No pediatric critical care doctor has lived in Missoula since the last one retired eight years ago, so specialists have flown in on rotation. From now on, children who need a ventilator or continuous seizure monitoring will be stabilized and transferred. The next PICU in Montana is in Kalispell, about 150 miles north.
The hospital's explanations shifted. Cook said the decision was "about quality more than it is about the dollars." A spokesperson later wrote that it came down to low volume and long-standing staffing problems, not worries about current care quality. The hospital belongs to Lifepoint Health, a for-profit chain with more than $10 billion in yearly revenue. Cook said asking Lifepoint to "float the program" would not have fixed the core problem.
Portland's St. Vincent Medical Center closed its four-bed PICU last November. It belongs to the nonprofit Providence system, whose Oregon arm reported a shortfall of more than $15 million in 2024. St. Vincent also blamed low patient numbers rather than money and said the unit was often empty.
Missoula still has a lot. The hospital keeps a newborn ICU, a general pediatric ward, emergency care, surgeons, therapists and some subspecialists. Local doctors can consult remote critical care specialists. Pediatrician Lauren Wilson says she would still take her own sick child there.
What could go wrong
This is a real trade-off. Concentrating rare, complex care where staff see it often can build expertise. The costs are travel time and spare capacity. Mack's objection is blunt: families cannot be expected to cope "if the next-closest children's hospital is a flight away or an eight-hour drive." Rural areas have the biggest gaps. The cuts are happening at small nonprofits and private-equity-owned hospitals alike.
Basu says front-line doctors sense that children are "showing up a little bit sicker" because they deteriorate during transfer. He also says there isn't yet enough data to prove it. For now, harm from closures is a plausible concern, not a measured result.
Surges are the second risk. In 2022, when respiratory illness filled children's hospitals, Michelson says small emergency departments had to call 10, 15 or 20 hospitals to place one patient. He expects it to happen again.
Policy pressure
Researchers and medical groups expect Medicaid cuts to widen the gaps. The Trump administration has added administrative hurdles and narrowed who qualifies. Those changes mainly target adults, but researchers say children can lose coverage when their caregivers get caught up in paperwork. Fewer people enrolled, adults or children, means less hospital revenue.
Proposed fixes
Basu says groups such as the Society of Critical Care Medicine are exploring regional partnerships, in which specialty centers give community hospitals shared training and transfer protocols. Michelson proposes more federal funding for services in low-access areas and higher Medicaid payment rates. He argues that pediatric critical care is "more of a national necessity" than an ordinary market good.
The article leaves several questions open. It reports no outcome data comparing children treated locally with those transferred. It does not say how much regional hubs can expand. It also does not show whether any of the proposed fixes would be paid for.
Remember
Three-quarters of US hospitals now have no overnight beds for children at all.
Missoula's closed unit saw about two critically ill children a month, roughly 25 a year.
Doctors suspect longer transfers leave children sicker on arrival, but say the data don't yet show it.
Researchers at Harvard's Wyss Institute report that pushing old cells to make more 1, a protein that controls RNA splicing, made their gene activity look younger. Given to aged mice, it extended lifespan by 14%. The Fight Aging! summary describes the work, which builds on a Wyss Institute press release.
The problem being worked around
The best-known way to rejuvenate cells is partial reprogramming with 2, four genes that can turn adult cells back into stem cells. Short exposure resets some age-related changes in gene activity. Too much exposure strips cells of their identity and raises the risk of tumors. Reason, the site's author, argues that the approach is hard to turn into a therapy: different cell types in the same tissue would need different doses and timing, and that may be impossible to arrange. The researchers put it as a "fundamental tradeoff between rejuvenation and cell identity."
How they found SRSF1
The team trained a machine-learning model on 3 (the full set of genes a cell is actively using) from human skin 4, the cells that make connective tissue. The cells came from donors across a wide age range. The model accurately estimated each cell's "transcriptomic age." The team then used it as a scoring tool. They overexpressed genes from a shortlist predicted to affect aging in old fibroblast lines, and looked for genes that pushed the predicted age down.
SRSF1 scored highest. Splicing factors are attractive targets because one of them can shape how thousands of genes are expressed.
What it did
In old fibroblasts, SRSF1 reduced markers of several hallmarks of aging:
5, where damaged cells stop dividing but don't die
6, where cells struggle to keep their proteins correctly made and recycled
7, chronic low-grade inflammation
The cells kept their identity. They held their spindle shape, kept using their usual fibroblast genes, and did not switch on the stem-cell programs that Yamanaka factors trigger.
In aged mice, delivered SRSF1 ended up mostly in the liver. The researchers say it slowed the animals' rate of aging and extended lifespan by 14%.
Caveats
The summary is thin. It doesn't say how SRSF1 was delivered, how many mice were used, which sex or strain they were, or how "rate of aging" was measured. It also doesn't say whether the paper is peer-reviewed. Most of the cell evidence rests on a clock the team built themselves, and a lower clock score is not the same as better function. Because the protein built up mainly in the liver, the lifespan effect may come largely from one organ. Splicing factors are also linked to cancer in other settings, and the summary doesn't address that. Independent replication is the next thing to watch for.
A team at Harvard's Wyss Institute reports that overexpressing 1, a protein that controls how RNA is spliced, shifted old human skin cells toward a younger pattern of gene activity without turning them into something else. In aged mice it extended lifespan by 14%. The account here comes from a short Fight Aging! post by its author, Reason, which draws on a Wyss Institute press release. The article is thin on methods, so several things a reader would want to know are flagged as missing below.
The problem: rejuvenation versus identity
Partial reprogramming means briefly exposing cells to the 2, four genes (OCT4, SOX2, KLF4 and MYC) that can turn adult cells into induced pluripotent stem cells. It is the field's most-studied route to resetting age-related changes in cells. The difficulty is the dose. A little resets some of the epigenetic marks (chemical tags that govern which genes are switched on) and some of the gene-expression patterns that drift with age. Too much and cells forget what they are, dedifferentiate, and can seed tumors. The researchers call this "a fundamental tradeoff between rejuvenation and cell identity; achieving one without losing the other requires walking a fine line."
Reason argues the problem runs deeper than cancer risk. A tissue contains many cell populations, and each would probably need a different dose and timing. He calls reconciling those "somewhere between difficult and impossible" for a therapy. This has pushed researchers to look for other levers that give some rejuvenation with less risk to cell identity.
Why a splicing factor
When a gene is read, its RNA copy is cut and rejoined before it becomes a protein. Which segments are kept determines which version of the protein gets made. Splicing factors such as SRSF1 (serine/arginine-rich splicing factor 1) guide those choices. One factor can affect splicing in thousands of genes. Reason describes splicing factors as "centralized points of control over cell state," which makes them plausible single targets for broad change.
How the screen worked
The pipeline had two steps.
Build a clock. The team trained a machine-learning model on transcriptomic profiles, meaning measurements of which genes are active and how strongly. The profiles came from human skin 3, the cells that produce connective tissue, taken from donors spanning a wide age range. The model was trained across several aging-related processes, not on age alone. It then accurately predicted the "transcriptomic age" of fibroblasts from several donors.
Use the clock as a readout. The team overexpressed genes from a focused list predicted to influence aging, one candidate at a time, in old fibroblast lines. They then asked which ones lowered the predicted age.
An illustrative way to picture this, not drawn from the paper: an old cell line scores, say, 70 on the clock. Each candidate gene gets switched on harder in that line, and the line is re-scored. A gene that brings the score to 50 ranks above one that brings it to 65. The clock turns a fuzzy question ("is this cell younger?") into a number that can be ranked across many candidates. SRSF1 ranked first.
Results in cells
Old fibroblasts overexpressing SRSF1 showed fewer features of several recognized hallmarks of aging:
cellular 4, where damaged cells stop dividing but don't die and often release inflammatory signals
5, a breakdown in the normal making, folding and recycling of proteins
6, chronic low-grade inflammation that rises with age
The difference from Yamanaka factors is that the cells stayed fibroblasts. They kept their spindle shape, kept using the genes that carry out fibroblast functions, and did not activate the 7 programs (the stem-cell gene networks) that reprogramming switches on. That is the main claim: some rejuvenation without crossing the identity line.
Results in mice
When SRSF1 was delivered to aged mice, it accumulated mainly in the liver. The researchers report it slowed the animals' rate of aging and extended lifespan by 14%. They describe SRSF1 as a "geroprotective" target, meaning one that protects against aging.
What the article leaves out
Much of what would let a reader judge the mouse result is not given:
Delivery method. It isn't stated whether SRSF1 was supplied as a gene therapy, an mRNA or something else, or at what dose.
Study design. The number of mice, their sex and strain, the age at treatment, and whether 14% refers to median or maximum lifespan are not given.
Healthspan measures. "Reduced rate of aging" is not defined. It could mean clock scores, frailty indexes or physical tests.
Publication status. The journal and whether the work is peer-reviewed are not named in the summary.
Caveats worth weighing
The clock is the team's own. The cell results are judged largely by a model the researchers built. Lower transcriptomic age is a proxy, and it doesn't prove cells work better. The hallmark markers help, but the summary gives no effect sizes for them.
One organ. With SRSF1 concentrated in the liver, the lifespan gain may come mostly from liver effects, not body-wide rejuvenation. The fibroblast results may not carry over directly to the mouse result.
Cancer is not ruled out. Avoiding pluripotency removes one route to tumors. But SRSF1 has been described as a cancer-promoting gene in some human tumors in earlier research. Changing splicing across thousands of genes has many possible side effects, and the article does not address long-term safety.
Mice aren't people. A 14% lifespan extension in mice is a respectable effect for a single intervention. Many such results have not translated to humans.
Why it still matters
The approach does two things worth noting. It shows a way to screen for rejuvenation factors by scoring them against a gene-expression clock. And it adds evidence that some youthful features can be separated from loss of cell identity. Reason expects the result to encourage existing programs studying what manipulating splicing factors can achieve. Whether it holds up will depend on the full paper's methods and on other labs reproducing it.
Remember
Using a gene-expression age clock as a scoring tool let researchers rank candidate rejuvenation genes in human cells.
SRSF1 lowered markers of senescence, protein stress and inflammation while the cells kept their identity as skin fibroblasts.
The 14% mouse lifespan gain comes without published details on dosing, numbers or safety, and the protein built up mainly in the liver.
Science reports that Health and Human Services Secretary Robert F. Kennedy Jr. rejected the NIH director's choice to lead the 1 (NIMH), the main US funder of mental-health research. The NIH director, Jay Bhattacharya, had recommended neuroscientist Vikaas Sohal. Kennedy instead favors Shebani Sethi, a "metabolic psychiatrist" who, according to the report, has never held an NIH grant and was turned down by the search committee.
Yale neurologist Steven Novella, writing at Science-Based Medicine, calls this the "2" of US health agencies. Trofim Lysenko was a Soviet scientist whose politically favored pseudoscience took over Soviet biology. Novella's main subject, though, is Sethi's field.
What 3 claims
Metabolic psychiatry holds that cellular metabolism contributes to, and may even primarily cause, psychiatric illness. Its best-known treatment is the 4, a very low-carb, high-fat diet that makes the body produce ketones.
Novella describes three layers where brain function can fail:
cell biology: disease or damage in brain cells
neuronal function: neurotransmitter levels and signaling
network "wiring": how brain circuits are organized
Psychiatry mostly treats disorders as problems in the last two layers. Metabolic psychiatry moves the root cause to the first.
He agrees that exercise, nutrition, sleep and blood-pressure control matter for brain health. He calls them secondary factors: improving them can ease a disorder, but they don't cause it, so fixing them isn't a cure. His objection is to promoting them to primary causes without evidence.
The evidence
Novella describes the studies as mostly preliminary, poorly controlled and correlational. He cites a 2026 5 that pooled studies of ketogenic diets for depression and anxiety. It found "modest improvements" in depression, with inconclusive results for anxiety. The authors noted that the studies varied widely and had short follow-up, and they called for rigorous trials. His piece gives no effect sizes.
He sets this against Sethi's public claim that "we're seeing huge changes," including reversing weight gain and insulin resistance in people on antipsychotics. He argues that ketogenic diets have shown only short-term metabolic benefits.
He also recounts a case in which a psychiatrist blamed a patient's autism, mood disorder and psychosis on thyroid and vitamin problems. Blood tests showed the patient had neither. The psychiatrist's supporting studies were preclinical work or studies of severe disease.
The verdict
Novella calls Sethi's hypothesis "somewhat reasonable" but overstated. He argues she is underqualified to set research priorities for NIMH. This is an opinion piece and does not include Sethi's response.
The appointment fight
The journal Science has reported a dispute over who will lead the 1 (NIMH), the branch of the National Institutes of Health (NIH) that funds most US mental-health research. NIH Director Jay Bhattacharya recommended Vikaas Sohal, whom Steven Novella calls "a very accomplished and appropriate scientist." Health and Human Services Secretary Robert F. Kennedy Jr. reportedly rejected him. Kennedy prefers Shebani Sethi, a self-described "metabolic psychiatrist." According to the reporting, Sethi has never held an NIH grant, and the search committee rejected her.
Novella is a clinical neurologist at Yale and founder of the site Science-Based Medicine. He calls the move part of RFK Jr.'s "2" of US health agencies. The term refers to Trofim Lysenko, the Soviet agronomist whose politically favored and scientifically baseless ideas took over Soviet biology. Novella leaves the appointment details to Science. His piece is about the scientific question: what 3 claims, and why he finds it dubious.
What metabolic psychiatry claims
Metabolic psychiatry holds that metabolic health, meaning how cells produce and use energy, contributes heavily to psychiatric illness. Some proponents say it may be the primary cause, even of severe conditions. The best-known intervention is the 4, which is very low in carbohydrates and high in fat. It shifts the body toward burning fat and producing ketones.
Novella does not deny that metabolism matters for the brain. His objection is to the step from "metabolism affects brain health" to "metabolic dysfunction causes this disorder."
A three-layer model of brain disorders
Novella lays out three layers at which brain function can go wrong:
Biology. Are the brain's cells healthy, or is there pathology such as an infection? This is generally neurology's territory. Psychiatrists are expected to rule it out before calling a symptom psychiatric.
Neuronal function. The cells may be healthy but working below par. This is the "neurochemical" layer: too much or too little of a neurotransmitter, or faulty signaling.
Wiring. Even with healthy, well-functioning cells, the brain's networks can be badly organized. A circuit may be too active or too quiet, or have more complex problems of stability and self-regulation.
Mainstream psychiatry, he says, treats most diagnoses as problems in the second or third layer, or both. Metabolic psychiatry puts the root cause back in the first layer, in the cells themselves. That is why Novella calls it "a radical idea." He also says the idea is not without merit and should be researched.
Primary versus secondary factors
Novella's main distinction is between primary causes and secondary factors. Exercise, good nutrition, enough sleep, limited alcohol and blood-pressure control all support brain health, and clinicians already encourage them. They are secondary: improving them can soften a psychiatric or neurological problem, but they did not cause it, so fixing them is not a cure. Novella argues that proponents move metabolism from the secondary list to the primary one without the evidence to justify it.
He compares this to familiar errors. Acupuncture may have non-specific effects, but that does not prove meridians exist. Antidepressants raise serotonin, but that does not show low serotonin causes depression. In psychiatry he points to 5 (eye movement desensitization and reprocessing), a trauma therapy. He argues its benefit is at best non-specific, probably coming from the therapeutic relationship and the novelty of the technique, and that studies have not confirmed its proposed mechanism.
A case from practice
Novella describes helping a friend whose family member has autism, depression that is probably bipolar, and psychosis. Medication helps, but balancing benefits against side effects has been hard. A consulting psychiatrist said the symptoms came from hypothyroidism and vitamin deficiencies. Blood tests can check both easily. The patient had neither, and a later endocrinologist visit confirmed this.
The psychiatrist's working diagnosis was 6. That generally means mildly abnormal thyroid blood tests without the typical symptoms. He sent studies to support his view. Novella says they were a mix of three things:
preclinical work of doubtful relevance
studies of severe hypothyroidism, which says little about a borderline case
other material that did not show subclinical thyroid problems cause psychiatric symptoms
He calls this "extrapolating wildly" and says it typifies the field.
The evidence base
Novella describes metabolic psychiatry studies as mostly preliminary, poorly controlled, often only correlational, and not designed to establish efficacy or mechanism. As an example he cites a 2026 systematic review and 7 of ketogenic diets for anxiety and depression. A meta-analysis pools results from many studies. The review concluded:
Ketogenic diets were associated with "modest improvements in depressive symptoms." The improvements were clearer when ketosis was confirmed biochemically, which means checking that participants actually stuck to the diet.
Evidence on anxiety was "inconclusive."
The included studies varied widely, used different comparison groups, and had short follow-up.
The authors called for well-powered trials with standardized protocols and outcomes specified in advance.
Novella's piece does not give the effect sizes or the number of trials. "Modest" and "associated with" are the authors' own words.
He says such results are fine as a basis for better trials. The problem comes when people treat them as proof of efficacy and mechanism.
Sethi's claims
Novella describes Sethi's research as mostly the uncontrolled or poorly controlled ketogenic-diet work described above. He contrasts it with her public statements, such as: "We're seeing huge changes… Even if you're on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, the insulin resistance."
Antipsychotics often cause weight gain and metabolic problems, so that would be a real benefit if it held up. Novella argues the evidence for ketogenic diets shows only short-term weight and metabolic benefit, with no established long-term effect. In his reading, Sethi overstates the metabolic benefits and then extends them to mental illness on the basis of preliminary symptom data.
Judgment and open questions
Novella says Sethi is not unusual. She is pursuing "a somewhat reasonable hypothesis" while overstating it. The difference is the job. Running NIMH requires deep research experience and a critical eye for exactly these questions about causation. He argues she looks underqualified, as the search committee apparently also concluded, and that her alignment with 8 ideology is what makes her the favorite.
This is an opinion piece. It does not give Sethi's response, a full account of her publications, or Sohal's record. Whether properly controlled ketogenic-diet trials will show durable psychiatric benefit is still an open question. Novella's point is that this has not been shown yet.
Remember
A 2026 meta-analysis found only "modest" benefit for depression from ketogenic diets, from varied, short studies.
Novella argues lifestyle factors support brain health but are secondary, so fixing them is not a cure.
An NIMH director decides which psychiatric hypotheses get federal money, so the appointment affects research beyond one person.
Fluid intelligence is the ability to reason and solve new problems. It usually declines from early adulthood. Crystallized intelligence, meaning accumulated knowledge and vocabulary, tends to hold steady much longer.
Image: Fight Aging!
A new open-access paper links ageing, a decline in 1 (reasoning and solving new problems) and a type of brain cell that normally shouldn't be there. The cell is an immature form of 2, the star-shaped support cells also called astrocytes. The work comes from adults with epilepsy, and so far it shows a correlation, not a cause.
Why look at support cells
Drug development for cognitive decline has mostly targeted neurons, and the authors say those approaches have produced only modest benefits. Rodent studies show astrocytes actively regulate learning and memory, and that faulty astrocytes worsen cognition. If particular glial cells drive particular deficits in humans, treatment could target both neurons and glia.
Testing that in humans is hard because living brain tissue is rare. Autopsy tissue mostly comes from people with advanced damage.
The patient group
The team studied people with 3, the most common adult epilepsy. Its seizures start near the 4, a memory structure. When drugs fail, surgeons remove the affected hippocampal tissue. These patients get detailed cognitive tests before surgery, so researchers can compare the cells in the removed tissue with each person's measured abilities.
The team had earlier found astroglia carrying 5 (doublecortin), a protein usually seen in newborn neurons, in MTLE tissue. That suggests the cells are stuck in an immature state. These cells did not show up in control tissue from autopsies. Their numbers seemed to rise with age, but that trend wasn't shown to be significant.
What they found
The researchers first identified which mental abilities decline most with age in these patients, and fluid intelligence was one. They then found that older patients had more Dcx+ immature astroglia, and that higher counts went along with lower fluid intelligence.
The article gives no effect sizes: no patient numbers, correlation strengths or p-values. That makes the strength of the link impossible to judge.
Caveats
Correlation only. Age affects both the cell counts and the test scores. The cells could be a marker of accumulated seizure damage rather than a cause of decline. Reason, writing on the longevity blog Fight Aging!, notes the paper says little about how the cells might act.
Possibly specific to epilepsy. Healthy controls had none of these cells. People with epilepsy also show faster brain ageing. So it's unclear whether the finding applies to normal ageing, even though the authors argue it does.
Different tissue sources. Patient tissue was removed during surgery, while the controls came from autopsies.
For now this is a lead for experiments, not a treatment target.
A newly published open-access paper reports a link between ageing, worse 1 and a type of brain cell that should not be there. The cell is an immature astrocyte found in the 2 of adults with epilepsy. Reason, who writes the longevity blog Fight Aging!, flags the paper as a useful pointer. He also stresses that it says little about how the cells could cause decline.
The problem: neurons have been the main target
Drug development for cognitive decline has mostly assumed the problem lies with neurons. The authors note that therapies aimed at neurons have produced "only modest benefits." Rodent work has changed how researchers see astrocytes, or 3. These star-shaped cells, long treated as passive support for neurons, actively shape learning and memory, and when they malfunction, rodent cognition gets worse. If specific glial cells drive specific cognitive deficits in humans, treatments could combine drugs aimed at neurons with drugs aimed at glia.
Testing this in people is hard because living human brain tissue is scarce. Autopsy tissue mostly comes from people with advanced damage. Earlier stages can only be studied in people who need brain surgery anyway, and they may not be typical.
The patient group: epilepsy surgery
The researchers studied 4, the most common adult form. Seizures in MTLE start in the inner part of the temporal lobe, around the hippocampus, a structure central to memory. When drugs fail, surgeons remove the epileptic hippocampal tissue. These patients get detailed cognitive testing before surgery. That lets researchers compare cells in tissue taken from a living person with that person's measured thinking ability. The authors call this an "5 window."
There is a catch, and the authors acknowledge it. People with epilepsy show accelerated brain ageing, and cognitive decline is a known 6, meaning a condition that commonly occurs alongside epilepsy. It worsens with age. The authors argue this group can still reveal features of cognitive ageing in general. That is a claim to test, not a given.
The cell in question
The same team had previously found a pathological astroglial cell in MTLE hippocampus that carries 7, short for doublecortin. Dcx is a protein usually used to mark young, newly formed neurons. Finding it in astroglia suggests these cells are stuck in an immature state. They were undetectable in control tissue from autopsies. In that earlier work, their numbers tended to rise with age, but the trend was not shown to be significant, and no one had checked it against cognition.
What the new study did
The study had two steps:
Among the epilepsy patients, find which cognitive functions decline most strongly with age. Fluid intelligence was one.
Test whether the number of Dcx+ immature astroglia rises with age, and whether it tracks scores on those cognitive tests.
The authors report an association linking older age, lower fluid intelligence and more immature astroglia. They describe the cells as "an epilepsy-associated cellular feature corresponding to age-related cognitive decline."
What the article doesn't give
The blog post includes only the abstract and introduction. It gives no patient numbers, no correlation strengths, no p-values and no age range. It also doesn't say which tests measured fluid intelligence or whether other cognitive areas, such as memory, were linked to the cells. Without those numbers, the size of the effect can't be judged.
How much weight to put on it
It is a correlation. Age drives both the cell count and the cognitive scores. An association among the three doesn't show that the cells cause decline. They could be a marker of damage from seizures that builds up over time. They could also be a response to that damage rather than its cause. Reason notes that the mechanism is left for others to work out.
The cells may exist only in epilepsy. Healthy control tissue had no detectable Dcx+ astroglia. If so, this is not obviously a feature of normal brain ageing. Whether a related process happens in people without epilepsy is the key open question.
The comparison tissue differs. The epilepsy tissue was surgically removed from living people, while the controls came from autopsies. Differences in how tissue is collected and preserved can affect what stains positive. The article doesn't say how this was handled.
The sample is selected. Patients whose epilepsy resists drugs and who choose surgery are a narrow group.
What would move this forward
A stronger case would need several things. Experiments in animals that add or remove these cells would show whether they change cognition. Searches for similar immature astroglia in non-epileptic brains, using surgical or imaging-based methods, would test whether this is part of normal ageing. Effect sizes would show whether the link is large enough to matter. Until then, the finding is a lead. It adds to evidence that glial cells deserve attention in cognitive ageing, but it is not yet a target for treatment.
Remember
Immature astroglia carrying Dcx, a protein normally found in young neurons, appeared in epileptic hippocampus but were undetectable in autopsy controls.
No effect sizes are reported, so the strength of the link between cell counts and reasoning can't be judged.
Whether the finding applies to normal ageing, outside epilepsy, is the central untested question.
